Final Report of the Human Health Work Group of the New York State Department of Environmental Conservation Comparative Risk Project

Final Report

of the

Human Health Work Group of the

New York State Department of Environmental Conservation Comparative Risk Project

May 2001

Table of Contents

Lists of Appendices and Tables ...............00.. 000000 c cece eects Page iii Members of the Human Health Work Group ..............-.-.-.0000000000 222s ees Page v Acknowledgments ........... 00... eee eee eee cece ee ee Page vi Abbreviations .... 2.2... 202 eee eee eee eee ee Page vii Executive Summary) ..... 2.62222 Page ix I. Charge to the Human Health Work Group ............2.-.-.5-00000000 00 ee eee eeee Page | IL Introduction ...........0. 00.0000 cece eens Page | Ill. Methods ............0 00.00 Page 2 A. Selection of stressor groups ......... 2... Page 2 B. Selection of individual stressors within stressor groups ..............---- Page 3 C. Toxicity assessment ..........0..00 000002 e cee Page 5 D. Exposure assessment ............000 0000000 e cece eee eee Page 10 E. Risk characterization .............0000 000000 c cece es Page 13 F. Comparative ranking of stressor groups ..........-.-----00000000000-5 Page 14 IV. Attributes, Uncertainties, and Limitations ..................0..0.000-00005- Page 17 A. Inclusion of all known chemicals within a stressor group ................ Page 17 B. Incomplete toxicological profiles for stressor chemicals ................. Page 17 C. Information on environmental presence and concentration ............... Page 18 D. Human exposure ...............0. 000000 c cece cet Page 18 E. Animal vs. human data ........02000000 00000002 cece Page 18 F. Uncertainty factors ............ 00000000 cece Page 19 G. Additivity, antagonism, and synergism ................-.------------ Page 19 H. Conclusions ..............0 000000 c cece eee Page 19 V. Risk Characterization for Stressors .........05.0000 000000 c cece eee eee eee Page 21 A. Acidic and alkaline substances ............0000.0 000002 e eee eee eee Page 21 B. Atmospheric gases ..............0 000000 c eee t eee Page 29 C. Halogens/Disinfectant Residuals/Byproducts ...............---------- Page 37 D. Metals and cyanide ................. 000002 c cece Page 45 E. Non-volatile halogenated organic compounds (NVHOCs) ............--- Page 63 F. Non-volatile and semi-volatile organic compounds ...................-- Page 82 G. Nutrients 2.0.2.2 2222s Page 82 H. Particulates .......00 0022s Page 87 I. Pesticides ....... 00202 Page 101

J. Petroleum products ............. 0.00002 Page 124

K. Polynuclear aromatic hydrocarbons (PAHs) ..............----------- Page 132

L. Ionizing Radiation ................. 000002 c eee Page 138 M. Suspended and settleable solids ................000000000000000055 Page 148 N. Volatile (VOCs) & semi-volatile (SVOCs) organic compounds ......... Page 151 VI. Conclusions and Recommendations ...............-.-.000000000 eee eee eee Page 161 A. Conclusions ......... 0... eee ee eee eee Page 161 B. Recommendations .................0 000000 c cece eee eee Page 162

Lists of Appendices and Tables

Appendices

Appendix A . . Data Tables

Appendix B . NVHOCs Risk Calculations Appendix C Pesticides Risk Calculations Appendix D Summary of Data Sources Appendix E... 2.2... 02. Evaluation of Phthalate Esters Tables

Table III-1: Number of substances evaluated by the HHWG compared to number of

substances released to the environment or in commercial production Table III-2: Toxicity data parameters ............2.00000 0000002 e cece Table III-3: Non-cancer effects .... 2.2. .... 0.0.0 c eee eee eee eee Table Ill-4: Cancer effects .......... 2.0.0.0. Table III-5: Exposure data parameters ............02000000 000000 e cere eee eee Table III-6: Exposure ranking ................0 00000000 c eee eee Table III-7: Risk characterization matrix ...........00..000 0000000 c cece Table V-A.1: Risk characterization matrix for acidic and alkaline substances Table V-A.2: Individual stressor ranks for acidic and alkaline substances . Table V-B.1: Criteria for ranking atmospheric gases ................. Table V-B.2: Atmospheric gases and relevant toxicity/exposure information Table V-B.3: Individual stressor ranks for atmospheric gases ..................--- Table V-C.1: Halogens/drinking water disinfectant residuals/byproducts ............ Table V-C.2: Risk matrix for halogens, disinfectant residuals and disinfectant

byproducts... 2... eee eee eee eee eee Page 42 Table V-D.1: Mean daily dietary intake of selected metals ....................... Page 46 Table V-D.2: Detection of metals in drinking water samples from NYSDOH,

January 1980-January 1994.22.00 2 2222s Page 47

Table V-D.3a: 1994 Air sampling results (ug/m’) for metals at New York locations ... Page 48

Table V-D.3b: 1994 Air sampling results for metals at New York locations converted to mg/kg/d... 2.2.2.2 2 cee Page 48

Page iii

Table V-D.4: Concentrations of metallic elements in clean, undisturbed soil samples,

Eastern United States .........20..0.0020.02020.0200000020200202020200202020202020200200-- Page 49 Table V-D.5: Concentrations of selected metals in four home garden fertilizers

compared to concentrations in clean soil ................-0-0-000000000000-5 Page 50 Table V-D.6: Concentrations of selected metals in two agricultural fertilizers

compared to concentrations in clean soil ................-0-0-000000000000-5 Page 50 Table V-D.7: Concentrations of selected metals in municipal sewage sludge ......... Page 51

Table V-D.8: Concentrations of selected metals in surface soil from major agricultural production areas of the US (Holmgren et al., 1993) and typical

agricultural soil in New York (Harrison et al., 1997) ...................--. Page 51 Table V-D.9: Ranking of metals by exposure and toxicity ......................-. Page 58 Table V-D.10: Metals ranked for toxicity but not for exposure ...................- Page 58 Table V-D.11: Metals with neither exposure nor toxicity rankings ................. Page 58 Table V-D.12: Ranking of metals by category ................-5.00000000002+--5 Page 59 Table V-E.1: Risk characterization matrix for cancer and non-cancer effects caused

by non-volatile halogenated organic compounds ......................2-- Page 69 Table V-G.1: New York drinking water data from January 1980 to January 1994 ..... Page 83 Table V-G.2: Ingestion health guidelines for nutrients ....................------ Page 84 Table V-G.3: Reference doses for nutrients from IRIS .................--.-.-.------ Page 85 Table V-H.1: Levels of PM, ;, PM,) and TSP measured in NY in 1997 ............. Page 91 Table V-H.2: Asbestos concentrations in air .............-0.000000 00002 e ee eee ee Page 92 Table V-H.3: Ranking matrix for asbestos ............0..00000 000000 e cece eeee Page 97

Table V-I.1: Summary of estimated pesticide use (in thousands of pounds) in New York where use is greater than 100,000 pounds of active ingredient per year .. Page 104 Table V-I.2: Risk characterization matrix for cancer and non-cancer effects of

pesticides... eee eee eee eee Page 106 Table V-I.3: Cancer classifications of pesticides used extensively in New York ...... Page 117 Table V-J.1: Risk characterization matrix for petroleum products ................ Page 128 Table V-J.2: Individual stressor ranks for petroleum products ................---- Page 129 Table V-K.1: Risk characterization matrix for PAHs ....................--+---- Page 135 Table V-K.2: Individual stressor ranks for PAHs ...............-------2-+--+---5 Page 136 Table V-L.1: Breakdown of average radiation exposure to U.S. population ......... Page 140 Table V-N.1: Relative risk for VOCs based on toxicity and potential inhalation

EXPOSUTE . 2... Page 154 Table V-N.2: Relative risk for VOCs based on toxicity and potential ingestion

EXPOSUTE . 2... Page 155 Table V-N.3: Relative risk for Semi-VOCs based on toxicity and potential

inhalation exposure ..............0 000002 c cece ee Page 155 Table V-N.4: Relative risk for Semi-VOCs based on toxicity and potential

ingestion exposure .............00 00000 e cece Page 156 Table VI-1: Results of stressor group ranking for human health risk ............... Page 161

Page iv

Members of the Human Health Work Group

Dr. John Conway State University of New York at Albany, School of Public Health

Ms. Diana Hinchcliff New York State Chemical Alliance

Dr. Nancy Kim, Chair New York State Department of Health

Mr. Robert Majewski New York State Department of Environmental Conservation

Dr. Robert Michaels RAM TRAC Corporation, Schenectady, NY

Mr. Carlos Montes New York State Department of Environmental Conservation

Dr. Samuel Morris Brookhaven National Laboratory

Mr. Kenneth Pokalsky The Business Council of New York State

Mr. Lawrence Skinner New York State Department of Environmental Conservation

Mr. Gregory Smead New York State Department of Health

Ms. Patricia Whitman New York State Governor’s Office of Regulatory Reform

Mr. John Zeh New York State Department of Environmental Conservation

Page v

Acknowledgments:

The Human Health Work Group would like to acknowledge the contributions of the following people who assisted the work group in this project.

Mr. Kernan Davis New York State Department of Environmental Conservation

Ms. Marilyn DuBois New York State Legislative Commission on Toxic Substances and Hazardous Wastes

Dr. Daland Juberg International Center for Toxicology and Medicine

Ms. Tonya Lowery St. John New York State Department of Health

Ms. Elizabeth Meer New York State Legislative Commission on Toxic Substances and Hazardous Wastes

Dr. Mary Jo Miller Exxon Biomedical Services

Mr. John Stouffer Sierra Club

Page vi

Abbreviations

ACGIH AGC ATSDR CDC DBP DECSIS EU FUSRAP HHWG HI

HSDB HSEES IARC IPM

IRIS

LD5 LLRW LOEL mCi MCL mg/l mg/kg/day mg/m mrem/yr NAAQS NCI NESHAPS ng/g ng/m* NIOSH NOEL NVHOCs NYSDEC NYSDOH OSHA PAHs pCi/L PEL

PM

ppb

ppm PTDI

American Conference of Governmental Industrial Hygienists Annual Guideline Concentration

Agency for Toxic Substances and Disease Registry

Centers for Disease Control

Disinfection Byproduct

NYS Department of Environmental Conservation Spill Information System

European Union

Formerly Utilized Remediation Program

Human Health Work Group

Hazard Index

Hazardous Substances Data Base

Hazardous Substance Emergency Events Surveillance International Agency for Research on Cancer Integrated Pest Management

Integrated Risk Information System

Lethal Dose (50%)

Low Level Radioactive Waste

Lowest Observed Effect Level

Millicuries

Maximum Contaminant Level

milligrams per liter

milligrams per kilogram per day

milligrams per cubic meter

millirems per year

National Ambient Air Quality Standard

National Cancer Institute

National Emissions Standards for Hazardous Air Pollutants nanograms per gram

nanograms per cubic meter

National Institutes of Occupational Safety and Health No Observed Effect Level

Non Volatile Halogenated Organic Hydrocarbons New York State Department of Environmental Conservation New York State Department of Health

Occupational Health and Safety Administration Polynuclear Aromatic Hydrocarbons

picocuries per liter

Permissible Exposure Limit

Particulate Matter

parts per billion

parts per million

Provisional Tolerable Daily Intake

Page vii

RfC RfD SVOCs THM TLV TRI TSCA CUS TSP

UF

ug/g ug/l ug/m* USDA USDOE USEPA USFDA USGS USNRC VOCs WHO

Reference Concentration

Reference Dose

Semi Volatile Organic Compounds

Trihalomethane

Threshold Limit Value

Toxics Release Inventory

Toxic Substances Control Act Chemical Update System Total Suspended Particulates

Uncertainty Factor

micrograms per gram

micrograms per liter

micrograms per cubic meter

United States Department of Agriculture

United States Department of Energy

United States Department of Environmental Protection United States Food and Drug Administration

United States Geological Survey

United States Nuclear Regulatory Commission Volatile Organic Compounds

World Health Organization

Page viii

Executive Summary

The Human Health Work Group (HHWG) was asked by the Steering Committee to evaluate all known health risks, including both cancer and non-cancer effects, for each group of stressors. Health risk is the probability that human health effects may occur. The determination of whether or not a substance poses a health risk to humans is based on the potency (or strength) of a substance and the type and amount of exposure to that substance.

The final composition of the HHWG included members of state agencies, academic institutions and industry. The original composition of the work group also included members from environmental groups, federal and local government agencies and the state legislature.

The work group organized its analysis into six steps. At each step of the analysis, the work group tried to reach consensus on major decisions. Many decisions, including the final rankings, were the result of a process of debate in which opinions sometimes differed. The six steps were:

1. Selection of stressor groups. The steering committee defined fourteen stressor groups to be evaluated. The groups were defined based on chemical and physical properties.

2. Selection of individual substances within stressor groups. Many stressor groups contain a large number of substances. Not all of the substances within a stressor group could be analyzed due to time and resource limitations, so the work group selected a subset of the substances in each stressor group for analysis. The HHWG selected substances that would be of particular concern to human health, rather than attempt to represent the entire range of stressors within a group. For each stressor group, the HHWG identified a long list of potential stressors, developed criteria for choosing a smaller final list of stressors, and then used those criteria to select the stressors that would be evaluated in detail for each stressor group. Most stressor groups included criteria on toxicity, environmental concentrations, release or production. The HHWG used a variety of types of data to decrease the possibility of overlooking documented exposures associated with individual stressors.

3. Toxicity assessment. The toxicity of a substance is characterized by the health effects it can cause and its relative potency (strength). The dose of a chemical is the amount of chemical per body weight to which one is exposed. The potency of a substance is determined by how the degree of health effects changes with increasing dose. Stressor rankings for non-carcinogens were based on potency; rankings for carcinogens were based on potency and weight-of-evidence classifications. Weight-of-evidence classifications are based on the certainty of the evidence showing that the substance is a human carcinogen. The work group did not assign or adjust rankings based on the type of health effect; the work group’s intent was to treat all types of health effects (acute, chronic, non-cancer and cancer) equally.

4. Exposure assessment. Exposure to environmental pollutants can occur by eating food or

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soil, drinking water, breathing air or dust, and direct contact with skin. Exposure to higher levels of a substance or for a longer time can result in a higher risk of health effects. The actual dose to which a person is exposed from environmental pollutants is rarely known. However, pollutant levels in various environmental media (such as air, water, food and soil) can be measured and then human exposure can be estimated based on assumptions about how much air, water, food or soil a person might take in.

The HHWG ranked substances from “1” (highest) to “4” (lowest) using a hierarchy of data categories to assess exposure. Stressors were first ranked based on environmental levels of substances reported in state and federal monitoring studies. When environmental monitoring data were not available, the HHWG assessed data on release of these substances into the environment, primarily from industrial sources or accidental releases such as spills. These data are a surrogate for possible exposure; they do not provide direct evidence of exposure resulting from these releases. When environmental monitoring and release data were not available, commercial production data were used to compare possible human exposures. However, because of the limitations in data availability and the difficulty of translating commercial production into environmental exposure, there was a great deal of uncertainty regarding the usefulness of these data as a surrogate for human exposure.

J. Risk characterization. The HHWG combined data from its toxicity and exposure assessments to assess the health risks associated with current exposures. A matrix was used to show the toxicity rank and the exposure rank (on a scale of 1 to 4) assigned to each stressor. In addition, the matrix combined these two ranks into an overall health risk rank. For example, those stressors ranked highest in toxicity and exposure received the highest health risk rank (A), and those ranked lowest in toxicity and exposure received the lowest health risk rank (C).

6. Comparative ranking of stressor groups. The final step in the HHWG’s comparative risk process was to compare the health risks posed by one stressor group to the health risks posed by other stressor groups. The steering committee asked the HHWG to rank stressor groups into three risk categories; A, B and C. The work group agreed it was not possible to define absolute, quantitative measures of risk for groups of stressors. Each work group member who was assigned a stressor group first proposed a recommendation of A (highest), B or C (lowest) rank for the entire stressor group based on the risk characterizations for the individual stressors. Then the recommendation was reviewed by the work group. The work group then sought to reach consensus on an A, B or C rank for each stressor group, judging the relative risk associated with the stressor group compared to other stressor groups. Final ranks were debated and opinions sometimes differed, usually because of the variability of health risks for individual stressors within the same stressor group. These differences were resolved when the work group agreed that three stressor groups should be ranked as A/B (lower than A but higher than B) and one stressor group as B/C (lower than B but higher than C). Consensus was reached on the ranking for each stressor group.

There are several assumptions and limitations in the process of comparative risk

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assessment. There are many substances in commercial use that do not have adequate data for toxicity and exposure. There are also so many substances in use that we could not possibly evaluate all known substances in detail. Because of these and other limitations, one should not view the results of this process as statements of absolute certainty. On the other hand, these limitations did not prevent us from using technically sound methods and data sources to achieve a reasonable assessment of relative risk.

The work group ranked stressor groups based on the risk of health effects relative to other stressor groups. The ranking was not a quantitative measure of human health risk. For most stressor groups, the ranks for individual stressors varied within the group, regardless of the rank for the entire group. Therefore, it is important to review the report for each stressor group to see where individual stressors may have been ranked differently than the rest of the stressor group. The work group ranked the stressor groups as A, B or C, with A the highest human health risk and C the lowest. Because of the variability of individual stressor ranks within a group, some groups were judged to be A/B (lower than A, but higher than B) or B/C (lower than B but higher than C).

Stressor groups ranked as A: non-volatile halogenated compounds

Stressor groups ranked as A/B: metals

particulates

petroleum products

Stressor groups ranked as B: acidic & alkaline substances atmospheric gases

halogens

pesticides

volatile organic compounds semi-volatile organic compounds

Stressor groups ranked as B/C: polynuclear aromatic hydrocarbons

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Stressor groups ranked as C: nutrients

ionizing radiation

suspended & settleable solids

It is important to note that these rankings were determined from exposure data which are influenced by the current federal, state and local regulations in place. If this ranking were used to relax regulation or other efforts to control exposure to a stressor group that was ranked low, then the health risks associated with that stressor group may be much higher than estimated in this project. For example, ionizing radiation is ranked low because there is very little exposure to this stressor. The lack of exposure is due to stringent regulations. Relaxation of regulations to control ionizing radiation would not be justified because of its low ranking in this project.

Each stressor group report includes recommendations that are specific to that stressor group. The following recommendations are included in this section because they were either applicable to more than one stressor group or to emphasize their importance. More specific recommendations for each stressor group can be found in the individual stressor group reports.

1. General recommendations

° Efforts should be made to encourage and use pollution prevention techniques, especially to reduce hazards posed by those substances the HHWG identified as having the greatest health risks.

° Where data indicate that continued or additional controls on certain substances are

needed to protect human health (for example, if cancer or non-cancer risks associated with a given exposure are unacceptably high), the state should make efforts to control sources and reduce potential exposure.

° This assessment should be re-evaluated periodically to determine whether new exposure data or health effects data are available.

° Because of the numerous substances which exist in commerce today, only a subset could be evaluated through this comparative risk process. If there are particular compounds of interest to New York regulators and health officials that were not included in this project, these compounds should be evaluated. For example, comments received during the public comment period suggested an evaluation of polybrominated diphenyl ethers (PBDEs) and phthalates. The supporting documentation submitted justifies recommending that PBDEs be evaluated. Based on the uses, potential for exposure and possible health effects, phthalates should also be evaluated.

° Monitoring of contaminants in drinking water should continue and necessary actions be

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taken so that drinking water of acceptable quality is available to residents.

Recent data from USEPA and NYSDEC indicate that mobile non-point sources of PM, VOCs and metals are important contributors to air pollution. The Risk Reduction Strategies Work Group should consider this data in developing their recommendations.

2. Recommendations on specific stressor groups

Because of the very large radiation doses that may result from indoor radon, both USEPA and NYSDOH encourage New York residents to measure radon in their homes and to reduce the radon levels if they exceed 4 pCi/L.

The potential for exposure to some atmospheric gases (ozone, nitrogen oxides, carbon monoxide) is high in urban areas. Pollution prevention would help to reduce the potential exposure to some of these gases.

The exposure to disinfectant byproducts should be re-evaluated once data is available from New York drinking water utilities pursuant to the USEPA’s “information collection tule.” This rule became effective in early 1997, and requires the generation of 18 months

of monitoring data.

Although there exist extensive programs for blood-lead surveillance, reducing lead levels in older homes, and public information, it is recommended that additional effort be made to reduce lead exposure via pollution prevention. The reasons for this are that (1) the effects of lead are irreversible; (2) young children are at the highest risk; (3) currently, much of the current effort identifies children at risk only after their blood lead levels are above the recommended value; and (4) there is no certainty that the currently recommended values are sufficiently low.

Additional effort to reduce exposure to mercury is also recommended. There appears to be an excessive number of emergency events associated with mercury (63 in the period 1992-96). A greater effort to reduce these events seems warranted. Also, mercury is found in high concentrations in fish and shell fish in New York waters. Cadmium, and in some cases, other metals are also found in high concentrations. NYSDOH issues fish advisories based on NYSDEC’s extensive monitoring and NYSDEC is working on approaches to eliminate sources. This is a long-term problem that requires continuing effort. Greater efforts are needed to identify and aid populations that subsist almost entirely on fish.

The major problem with nutrients in water and human health seems to be primarily with private wells. It is not likely that the New York State Department of Health or county health departments will start monitoring private wells. Since the human health problem is primarily with infants, a method for notifying families with newborn infants should be developed. If their primary source of potable water is a private well, it should be tested

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for nitrate-nitrogen levels. If the MCL is exceeded, an alternative source of water should be found or adequate treatment should be utilized to reduce the nitrate-nitrogen level.

° The state should review its methods for developing health advisories for recreationallycaught fish. ° Efforts should continue to reduce the possibility of human exposure to NVHOCs in the

state. Appropriate measures should be taken to reduce contaminant levels in fish to below those which would require restrictive advisories.

° The relationship between one-hour average levels of PM in New York and human morbidity and mortality should be studied and pollution prevention should be used to control short-term excursions of PM.

° The continued use of Integrated Pest Management should be supported.

° A program to educate residential pesticide users in proper application and safe handling of pesticides should be developed.

° Air monitoring data at gas stations indicate that people who refuel their vehicles can be exposed to high levels of petroleum products. Measures to control such exposures may be addressed by pollution prevention.

3. Research needs

° Subpopulations with the potential for higher exposure to certain substances (in particular, NVHOCs, metals, pesticides, VOCs and SVOCs) should be identified and assessed for health risks.

. More and better environmental monitoring data, specific to New York, are needed to

properly characterize human exposure to most stressors. In some cases, data on urban environments are available, but not for rural areas. Studies on indoor air in homes, schools and non-industrial workplaces are needed to evaluate potential exposure to stressors such as pesticides and NVHOCs. Drinking water, surface water and groundwater monitoring for pesticides should continue. Also, studies of multi-pathway exposures for some substances would be useful. Better personal monitoring (measurement of contaminants by a monitor attached to a person) for human exposure to some stressors (PM, VOCs/SVOCs) would be useful.

° More and better health effects data associated with both acute- and chronic-duration exposure to many substances are needed.

° Reference concentrations, reference doses and cancer potency factors need to be developed for many stressors.

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° Additional and more complete body burden information on some substances would be useful to assist in benchmarking body burdens against other indices (e.g., biomarkers of effect and exposure, blood levels considered to be safe or adverse) which may assist in evaluating potential impacts to human health.

4. Data use/availability

° TRI data show that some stressors are released into the air in significant quantities by certain facilities, often in or near urban areas. TRI data should be used to focus pollution prevention techniques to reduce these releases.

° New York spill data should be evaluated to better determine how and where spills of toxic substances occur (in particular, petroleum products, acidic and alkaline substances and mercury) so that action may be taken to reduce the number of spills and related injuries.

° New York should make existing environmental monitoring and biomonitoring data more accessible and easier to use.

° For many chemicals, there are enough data to make a reasonable evaluation of health tisk. However, there are chemicals for which we have very limited or no information. It is recommended that a review of chemicals that are produced or used in high volumes in New York be made to identify any chemicals that need further study to determine their toxicological properties and their potential for exposure to humans. With USEPA guidance, the chemical industry has begun a screening program of high production chemicals to identify those that need further study.

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I. Charge to the Human Health Work Group

The Steering Committee charged the Human Health Work Group (HHWG) with the following task: “The Human Health Work Group will evaluate for each problem area all known health risks, including both cancer and non-cancer effects. The socio-economic and hardship impacts of health effects will be evaluated by the Quality of Life Work Group.”

II. Introduction

The determination of whether or not a substance poses a health risk to humans is based on clinical, epidemiological, and/or animal studies that demonstrate exposure to a substance is associated with health effects. In the context of human health, “risk” is the probability that health effects may occur. Health effects range in type and severity from lethal effects to subtle non-adverse biochemical effects. To evaluate the risk of health effects, the HHWG used the results of standard risk assessment methods, but differed slightly in its approach compared to other comparative risk projects.

Most regulatory agencies use the following steps in the risk assessment process:

Hazard identification. Determine what substances are involved, what types of health effects these substances may cause, and what exposure pathways are relevant (how are people exposed to a substance from a given source).

Dose-response assessment. Characterize the relationship between the different doses of a toxic substance and the degree of health effect associated with those doses. Generally, as the dose of a substance increases, the health effect becomes more probable or severe in nature.

Exposure assessment. Characterize the magnitude, duration and frequency of human exposure to a substance for an individual and/or a population. Characterize the various pathways of exposure and the number of people exposed.

Risk characterization. Combine the information obtained from hazard identification, doseresponse assessment, and exposure assessment to estimate the health risks associated with current exposures and describe the confidence in this assessment.

The HHWG used a risk assessment process similar to the standard process described above, with some modifications. The work group organized its analysis into six steps.

Selection of stressor groups. To coordinate how each work group in the project would look at problem areas, the steering committee decided to define problem areas as stressor groups. Stressor groups were defined by the steering committee as groups of substances with similar chemical and physical properties.

Selection of individual substances within stressor groups. The work group selected a subset of

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the substances in each stressor group for analysis. This was necessary because not all of the substances within a stressor group could be analyzed due to time and resource limitations.

Toxicity assessment. This step combined both dose-response assessment and some elements of hazard identification. The HHWG characterized substances based on the types of health effects for each individual substance as well as dose-response data.

Exposure assessment. The work group combined elements of standard exposure assessment and hazard identification. The HHWG characterized potential human exposure based on environmental concentrations, release to the environment, or production/use data. The primary route(s) of exposure were identified.

Risk characterization. A standard risk assessment calculates a quantitative estimate of risk based on the information from hazard identification, dose-response assessment, and exposure assessment. The HHWG combined data from its toxicity and exposure assessments in a semi-

quantitative approach to characterize the health risks associated with current exposures.

Comparative ranking of stressor groups. The work group examined the results for all substances within a stressor group, and used its best judgment to rank the health significance of each problem area relative to other problem areas.

Many comparative risk assessment projects have attempted to use the best available scientific data and standard risk assessment methods to assess and rank risks to human health posed by environmental stressors. However, ranking results are not determined by quantitative analyses alone. Selecting the problem areas and the data used, adopting risk assessment methods, and evaluating the risks of an entire problem area all involve some degree of judgment. This project reflects the best judgment of the members of the HHWG, all of whom brought their own areas of experience and expertise to the project.

III. Methods

This section describes the methods that the HHWG used to rank most of the stressors and stressor groups. However, the type of data available for some stressor groups did not allow the use of these methods. For these stressor groups, a different ranking method was used and the method was explained in the individual section on that stressor group.

A. Selection of stressor groups

The Steering Committee, with input from the HHWG and the other work groups, determined how the project would characterize the environmental problem areas to be evaluated by the working groups. Problem areas can be characterized in a variety of different ways: for example, by sources of pollution, by environmental stressors, by impact on environmental media, or by some combination of the above. Each way of characterizing environmental problem areas could produce different results when the final ranking of problem areas is

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completed. For example, if problem areas were characterized by sources of pollution, the substances from a source would be grouped, rather than grouping substances by chemical and physical properties, or some other method. Or, if a single substance, such as lead, was identified as one problem area while other chemicals (like other metals) were grouped together, the risks posed by lead would be more readily apparent than risks from other individual substances.

The Steering Committee decided to characterize problem areas by grouping substances into stressor groups based, in most cases, on physical and chemical properties of the substances. The HHWG then reviewed these groupings and suggested modifications to the Steering Committee.

B. Selection of individual stressors within stressor groups

Many stressor groups contain a large number of substances. Because the HHWG had finite human and financial resources and a limited amount of time, not all substances within a stressor group could be evaluated. Even if more time or resources were available, there are little or no published data concerning the health effects and environmental exposures for many substances. Table III-1 shows a large number of substances in commercial production for which we did not have toxicological or exposure information. However, we were able to find useful data for many of the chemicals that we selected for evaluation.

Table III-1: Number of substances evaluated by the HHWG compared to number of substances released to the environment or in commercial production

approximate # of chemicals With Chemical Abstract Numbers 17,878,000 In Registry of Toxic Effects of Chemical Substances _| 112,900 In commercial production 70,000 In NYSDEC List of Hazardous Substances 1360 In USEPA Toxics Release Inventory 650 In USEPA Integrated Risk Information System 530 In NYS Hazardous Substances Emergency Events 500 Surveillance Evaluated by the work group 315

The HHWG decided to select a subset of substances to evaluate for each stressor group. Several considerations went into choosing the method of selecting individual substances, or stressors. If the subsets chosen were large, the HHWG would not be able to evaluate the stressors in detail due to resource limitations. If the subsets were small, the work group may have missed stressors that were important to evaluate. The HHWG decided to select substances that are of particular concern to human health, rather than attempt to represent the entire range of stressors within a group. The work group recognized the importance of evaluating stressors known to be potentially hazardous as well as of identifying stressors which are produced or used

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in large quantities but have limited hazard data. These stressors of unknown hazard could then be recommended for further study.

Individual stressors were selected in a two step process. First, the HHWG attempted to identify the stressors in a stressor group by reviewing as many different types of data sources as possible. Data sources on toxicity, human exposure, environmental monitoring, environmental release, emergency events, production and use, and regulatory and analytical lists were all reviewed to identify a large subset for each stressor group. Second, the large subset was culled to a smaller list of stressors that would be evaluated in more detail. In this step, work group members attempted to include not only substances known to be highly toxic or with high environmental levels, but also those with high production volumes or involved in high numbers of emergency events (such as spills).

The HHWG assigned the evaluation of each stressor group to an individual work group member. Some work group members evaluated more than one stressor group. Because the available data for each stressor group varied, a universal set of criteria to select individual stressors within stressor groups was not identified. Instead, the work group adopted the following set of principles to guide each HHWG member in selecting the final list of stressors to evaluate in their respective stressor group.

° Establish and use criteria to develop an initial stressor list from data sources.

° Establish and use criteria to select a final stressor list from the initial list.

° Explain and justify the criteria used for selecting stressors for each stressor group.

° Use data sources that are relevant to the stressor group.

° Use both hazard and exposure data for each stressor group.

° Use as broad a range of hazard and exposure data as relevant and appropriate for each specific stressor group.

° Use production or release data.

° Use data sources that provide good quality data.

° Use special knowledge of individual stressors, when appropriate.

° Consider background environmental levels, when appropriate.

° Review and reach consensus for the stressor selection for each stressor group.

Each work group member used the above guidelines to identify a potential list of stressors, develop criteria for selecting a final list of stressors, and to select the stressors that would be evaluated in detail for their stressor group. For each stressor group, the criteria used by the HHWG are described in the results section for that stressor group. Most stressor groups included criteria on toxicity, environmental concentrations, release or production to identify the substances of greatest potential exposure and health concern. Because there were gaps in the existing data, the HHWG used a variety of data sources and data types to decrease the potential for overlooking documented exposures associated with individual stressors.

Once each work group member selected the criteria and individual stressors for a stressor group, the results were presented to the HHWG, comments were addressed, and consensus was

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reached to accept the selection criteria and results.

C. Toxicity assessment

Identification of the human health hazards posed by different toxic substances is a complex process involving evaluations of both human and animal data. While the strongest evidence of potential hazard is derived from well-conducted clinical or epidemiological studies that link specific chemical exposures to adverse impacts in human populations, this type of information is not available for many substances of concern. In the absence of human data, one must rely on toxicological data from animal experiments. The necessity of extrapolating from animals to humans introduces some uncertainty into the process of human health risk assessment. Also, toxicological profiles for many substances are incomplete, meaning that all potential health endpoints have not been evaluated. However, this does not preclude the development of a toxicological profile for a substance of concern. Information about human variability in susceptibility to toxic substances is often times unavailable, although uncertainty factors (which are included in the establishment of guidelines or standards for exposure) account for this variability.

The HHWG generally used readily available data from government and international health and environmental organizations (New York State Department of Health, New York State Department of Environmental Conservation, US Environmental Protection Agency, US Agency for Toxic Substances and Disease Registry, International Agency on Research for Cancer, World Health Organization, European Union). Most of these data are internally peer-reviewed.

HHWG members were not expected to review original research; however, some HHWG members did so when they had the resources and desire. Appendix D presents a description of the data sources that were often used. Relying on these data sources, the HHWG attempted to find and report information for the categories in Table III-2. The results of the data collection for each stressor are presented in Appendix A. For many of the individual stressors chosen, there were adequate data to allow a reasonable prediction of their toxicity to humans. For other stressors, there were data gaps that made the toxicity assessment more uncertain.

The toxicity of a substance is often characterized by the health effects it can cause and its relative potency. Toxic substances can have different human health effects, and the effects vary in severity and organ system affected. The HHWG attempted to identify the health effects of greatest concern, as well as the health effect that was associated with the RfD, RFC, LOEL or NOEL.

After readily available data on individual stressors were collected, the HHWG attempted to assign stressor rankings for non-carcinogens based on an assessment of dose-response and, for carcinogens, weight-of-evidence classifications and cancer potency. The work group did not assign or adjust ranking based on the type of health effect, whether it be cancer, effects on the respiratory system or some other effect.

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Table III-2: Toxicity data parameters

Parameter

Description

Reference dose (RfD or RfC)

An estimate (with uncertainty spanning perhaps an order of magnitude) of a daily exposure to humans (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime.

Cancer potency factor (CPF)

An estimated factor derived from animal data used to calculate increased human cancer risk associated with a given exposure.

Weight-of-evidence determination

The extent to which the available biomedical data support the hypothesis that a substance causes a particular health effect in humans.

No observed effect level (NOEL)

Lowest observed effect level (LOEL)

The level of a chemical which, when given to test animals, produced no observed health effect (NOEL) or the lowest level that produced an observed health effect (LOEL).

Health endpoint of greatest concern

Considered to be the most significant human health effect.

Health endpoint associated

The particular health effect from which the RfD, RFC, LOEL

with RfD/RfC/LOEL/NOEL | or NOEL were derived.

LD,, The dose in food or water at which half of the test animals exposed to a substance died.

LCs The concentration in air at which half of the test animals

exposed to a substance died.

Understanding what dose (amount of chemical per body weight) of a toxic substance will cause different health effects is critical to the determination of health risk. Dose-response relationships assist in defining the potency (or strength) of toxic substances, indicating how the degree of health effects changes with increasing dose. Risk assessments can produce different results depending on the choice of models and assumptions that characterize the dose-response relationship. Some scientists disagree as to whether standard risk assessments underestimate or overestimate risk. There is also disagreement on whether there is or is not a threshold for carcinogenic effects. The HHWG decided that consistent use of standard risk assessment methods would provide the best comparison between stressor groups and generally adopted the risk assessment approach of state and federal regulatory agencies. The HHWG used reference doses, NOELs, LOELs and cancer potency factors from the US Environmental Protection Agency’s Integrated Risk Information System (IRIS), when available, for evaluating potency.

The HHWG ranked substances from “1” (highest) to “4” (lowest) based on cancer and non-cancer effects. Table III-3 shows the criteria that were used to rank non-cancer effects. The

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criteria were a modification of the European Union (EU) classification system as described in the European Inventory of Existing Commercial Chemical Substances (EINECS). The three types of criteria were:

° Acute toxicity: oral LD<), dermal LD,, and inhalation LC, data were compared to the dose-response criteria in Table III-3.

° Subchronic and chronic effects toxicity: LOELs (or NOELS if LOELs were not available) were compared to the dose-response criteria in Table III-3.

° Corrosive and irritant effects: ranked based on the type of effect, with corrosive

substances (those that can burn skin) ranked “2” and irritants (to eyes, skin, respiratory system) ranked “3”.

For each substance, the highest rank resulting from any of the three categories (acute, chronic or corrosive/irritant) determined the final non-cancer rank.

The HHWG judged the cutoff points used in Table III-3 to be reasonable, but other cutoffs could also have been reasonably chosen and the results would have been different. The EU system was chosen as a model because it used data generated by standard risk assessment methods, it had classifications available for many stressors, its criteria were available (so the HHWG could rank stressors not already classified by the EU) and its assignment of stressors to classifications were peer-reviewed. Three modifications were made to the EU system:

1. The classification names from the EU were changed to the numbers | through 4.

2. The EU system did not classify any substances as category “1” based on the subchronic/chronic effects. Criteria were added by the HHWG to allow ranking a substance category “1” based on the subchronic/chronic effects.

3. The EU system was modified to classify “irritant” substances as category “3” and “corrosive” substances as category “2”. However, for each substance, the HHWG reviewed acute, subchronic and chronic toxicity data to determine if a higher ranking was justified.

The workgroup decided not to rank non-cancer effects by severity of effect. A substance may produce a severe effect (death) at one level of exposure and a mild effect (irritation) at a lower level. With the EU system, the rank was typically determined by a LOEL, which is often associated with a less severe effect. The work group decided that attempting to rank the severity of the effects associated with the LOEL was too subjective. Both the effects associated with the LOEL and the health effects of greatest concern were documented in the appendices.

Table III-3: Non-cancer effects

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Rank | Acute effects Subchronic/Chronic effects | Corrosive Irritant 1 oral LDsy < 25 mg/kg Danger of cumulative dermal LD, < 50 mg/kg effects or serious damage inhalation LCs, (4 hr) after repeated or prolonged -aerosol/particulate < 250mg/m? exposure at the following -gas/vapor < 500 mg/m? dose levels: strong evidence of irreversible oral < 0.5 mg/kg/day damage after single exposure dermal < 1 mg/kg/day at above dose ranges inhalation < 2.5 mg/m*/day 2 oral LDsy 25 - 200 mg/kg Danger of cumulative corrosive dermal LD.) 50 - 400 mg/kg effects or serious damage (causes inhalation LCs, (4 hr) after repeated or prolonged | burns to -aerosol/particulate 250 - 1,000 mg/m? | exposure at the following the skin) -gas/vapor 500 - 2,000 mg/m? dose levels: strong evidence of irreversible oral < 5 mg/kg/day damage after single exposure dermal < 10 mg/kg/day at above dose ranges inhalation < 25 mg/m’*/day 3 oral LD, 200 - 2,000 mg/kg Danger of cumulative irritating dermal LD.) 400 - 2,000 mg/kg effects or serious damage to eyes, inhalation LCs, (4 hr) after repeated or prolonged | skin, -aerosol/particulate 1,000-5,000 mg/m? | exposure at the following respiratory -gas/vapor 2,000 - 20,000 mg/m? dose levels: tract: strong evidence of irreversible oral < 50 mg/kg/day may damage after single exposure dermal < 100 mg/kg/day sensitize at above dose ranges inhalation < 250 mg/m*/day 4 oral LD, > 2,000 mg/kg No effects not dermal LD., > 2,000 mg/kg after repeated or prolonged | irritating inhalation LCs, (4 hr) exposure at the following to skin, -aerosol/particulate > 5,000 mg/m? dose levels: eyes, or -gas/vapor > 20,000 mg/m? oral < 50 mg/kg/day respiratory strong evidence of irreversible dermal < 100 mg/kg/day tract: damage after single exposure inhalation < 250 mg/m*/day | nota at above dose ranges sensitizer

to evaluate these effects:

Carcinogens were ranked using the criteria in Table III-4. Two types of data were used

Carcinogens were ranked based on weight-of-evidence (for example, known carcinogens ranked higher than probable or possible carcinogens). These weight-of-evidence data

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were gathered from the EU, the US Environmental Protection Agency (USEPA) and the International Agency for Research on Cancer (IARC). These classifications are based on the evidence indicating that the substance is a human carcinogen.

sufficient human evidence: category 1 sufficient animal evidence: category 2

some, but insufficient animal evidence: category 3

no evidence or not classifiable: category 4

e Carcinogens were also ranked by potency using oral slope factors or inhalation unit risks reported by the USEPA’s Integrated Risk Information System (IRIS), when available. These are cancer potency factors based on modeled dose-response relationships assuming lifetime exposure.

Table III-4: Cancer effects

Rank EU USEPA IARC Oral slope | Inhalation factor unit risk (evidence) (mg/kg/ per ug/m? dayy' 1 1. Human A. Human 1. Human >10 >1x 10° sufficient human 2 2. Suspected | Bl and B2. 2A and 2B. 1 to 10 1x 10% to sufficient human Probable human | Probable and 1x 10° animal Possible human 3 3. Possible C. Possible 0.1 to 1.0 | 1x 10° to some human human 1x 10" animal 4 D. Not 3. Not <0.1 <1x 10° not classi- classifiable classifiable fiable or E. Evidence of | 4. Probably none non-carcinogen | nota carcinogen

The highest rank resulting from either weight-of-evidence data or potency was used to determine the final cancer rank. However, some judgement was used if a chemical ranked high in potency, but low by weight-of-evidence. In such cases, if the HHWG member could reasonably use the lower weight-of-evidence ranking, the cancer rank could be lowered with proper justification.

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The highest rank resulting from either the non-cancer or cancer criteria was used to determine the final overall toxicity rank.

The HHWG did not consider the additive, antagonistic or synergistic effects that might occur in humans potentially exposed to multiple substances. Further discussion of these effects can be found in section IV.

D. Exposure assessment

Exposure to environmental pollutants can occur via ingestion, inhalation or dermal contact. The HHWG typically considered exposures from ingestion of contaminated food or drinking water, from inhalation of contaminated air or from ingestion of contaminated soil. For most of the stressor groups there was incomplete information on the presence of individual stressors in some types of environmental media. The HHWG attempted to identify the most important route contributing to human exposure for each individual stressor and to obtain environmental concentration or presence data for these media. However, these data were unavailable in many cases, clearly indicating that better monitoring data are needed. The work group did not evaluate exposure data for occupational exposures and exposures that result from lifestyle choices (such as smoking, method of home heating, and cooking methods).

Many of the available data sets used by the HHWG to assess exposure had inherent limitations because of the type of data or the way data were collected or reported. For example, some data sets were limited to a selected list of chemicals that is required by a particular regulation, or they may not include data that are considered confidential business information. Most data sets used by the HHWG are described in Appendix D.

One source of information concerning exposure is human monitoring data. These data describe the chemical body burden of humans and are collected through national surveys and targeted state programs, such as the NYSDOH blood lead sampling program. These data document actual body burden, but such data are few and generally limited to persistent chemicals. Therefore, the work group attempted to assess human exposure with environmental monitoring levels.

The work group’s exposure assessments made use of state and federal monitoring programs that describe pollutant levels in various environmental media (such as air, water, food and soil). Many substances may be present in more than one environmental media. However, in the final analysis, one exposure route often dominates the total exposure. Where possible, the HHWG focused on the exposure route that would pose the dominant risk. If two routes made significant contributions to human exposure, the HHWG attempted to assess both. In some cases, data were not available to assess exposure routes that may be important. Often, environmental monitoring data are limited to a relatively small number of substances that are routinely analyzed. The HHWG also tried to identify average levels to which the general population is exposed, as well as a reasonable “worst case” concentration to which a subpopulation may be exposed. For example, the indoor and outdoor air levels of

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perchloroethylene are generally low, but the indoor air levels in apartments above dry cleaners are often quite high and are likely to pose a significantly greater risk to human health. When evaluating environmental concentrations, the HHWG found it difficult to determine whether they resulted from past or present releases. For example, banned substances such as PCBs are still released into the environment from transformer leaks, fires and landfills. Therefore, we did not consider when the stressor was released or the source of the stressor. The HHWG decided to rank exposure based on current environmental concentrations and let the Risk Reduction Strategies Work Group analyze what problems could be addressed by pollution prevention. Of the four types of media considered (air, water, food and soil), soil was the medium least used for ranking because of either lack of data or it was judged not to be a major route of exposure.

When environmental monitoring data were not available, the HHWG assessed data on release of these substances into the environment, primarily using the Toxics Release Inventory (TRI). Although these data are a poor surrogate for actual human exposure, they provide evidence of potential exposure in New York. Relying on release data to compare potential human exposures increases the uncertainty associated with characterizing risk. For some stressor groups, there are more data on release than there are on environmental monitoring. However, TRI data are limited to certain types of facilities releasing more than specified amounts of certain substances (see Appendix D). After the rankings had been completed, data on release became available from the National-scale Air Toxics Assessment (USEPA, 2000) (NATA). NATA is a compilation of national air toxic emissions from 1996 sources and estimated concentrations across the United States. NATA includes more types of emission sources than TRI, such as major stationary sources (factories, municipal incinerators) and other sources (cars, trucks, small businesses, fires). This is a new database and USEPA is still making corrections to it. Although the HHWG did not use NATA to rank stressors, the data would be useful for the Risk Reduction Strategies Work Group to consider after the information is checked for accuracy.

When release data were not available, production data (primarily from the Toxic Substances Control Act (TSCA) Chemical Update System (CUS)) were used to compare potential human exposures. However, only non-confidential business information was available. Also, data were not found on how much of what is manufactured is used in-state, how much is exported or how much is imported. Many compounds that are made are immediately used for another process, thereby limiting the number of people exposed to a potential hazard. Therefore, there was a great deal of uncertainty regarding the usefulness of these data as a surrogate for human exposure.

The HHWG collected available data for each of the parameters in Table III-5. The results of the data collection for each stressor are presented in Appendix A.

The size of the exposed population was not used by the workgroup to rank stressors. Most monitoring studies were applicable to the general population of New York, but some studies identified subpopulations with the potential for greater exposure, such as residents near dry cleaners or people who regularly eat freshwater fish that they catch. The work group

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identified these subpopulations, but did not try to quantify the actual number of persons potentially exposed. The HHWG decided not to rank the size of the population exposed for several reasons. First, the estimates of exposed population sizes were quite subjective. Second, population data were available for some stressors, but not others. Third, the workgroup judged that the level of exposure was a more important factor than the size of the population.

Table III-5: Exposure data parameters

Parameter Description

Typical exposure Average levels of the chemical in air, water, soil or food to which people are generally exposed

‘Reasonable’ worst case Maximum levels of the chemical in air, water, soil or food to

exposure which the general population is exposed or levels associated

with a highly exposed sub-population.

Size of exposed populations | A qualitative description of the exposed population.

Route of exposure How people are exposed to a chemical (inhalation, ingestion, skin contact). Release Amount of the substance released by facilities to the

environment (reported in pounds per year to a specific media, such as air).

Production/use Amount of a substance produced or used by facilities (reported in pounds per year). Emergency events Number of times per year a substance was reported to be

involved in emergency events such as spills or evacuations.

Substances were assigned an exposure rank using the criteria shown in Table III-6. As explained above, the HHWG used a hierarchy of data categories to assess exposure. If environmental concentrations of substances in air, water, soil or food were available, they were used to rank exposure. In Table III-6, the cutoff points for dividing substances into the four exposure categories (“1” is the highest and “4” is the lowest) for environmental media were chosen so that doses would be equal across environmental media for a particular category (for example, the dose for category “1” for air would be the same as the dose for category “1” for food).

If available, environmental concentration data are presented for both average levels to which the general population is exposed and a reasonable “worst case” or maximum concentration to which a subpopulation is exposed. However, environmental data were not available for many substances. In these cases, release data from the Toxics Release Inventory were used to rank the potential exposure. For other substances, data on spills or other emergency events involving the release of substances into the environment were used as a surrogate for exposure. When no other exposure surrogates were available, production/use data from the

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Toxic Substances Control Act Chemical Update System were used. For some stressor groups, all types of exposure surrogate data were used to rank stressors, resulting in several rankings for each stressor. This allowed comparison of the rankings using different exposure data types.

As with the cutoffs for the toxicity assessment, one could reasonably choose other cutoffs that would result in a different ranking. The cutoffs appeared reasonable to the work group, but it was difficult to equate the cutoffs for one category (release, for example) with the cutoffs from another category (such as production). When different exposure surrogates are used to rank different stressors, comparisons between these stressor rankings is more uncertain.

Table III-6: Exposure ranking

Number of Emissions | Production Environmental Concentrations E umber 0 (TRI media TSCA Exposure ‘Fuente specific to CUS Catego: 4: athwa Ibs/1994 gory Drinking (NYS fos 199) ( ) Air Water Soil Food HSEES, (ug/m*)! (ppb) (ppm)’_|_(ppb)_|_ 1992-1996) 1 >10 >100 >1400 | >1000 > 1000 >1,000,000 >108 (highest) 2 1 to 10 10 to 140 to | 100to | 50to 1000 | 100,000 to 10’ to 108 100 1400 1000 1,000,000 0.1 to 1 1 to 10 14 to 10 to 5 to 50 10,000 to 10° to 107 140 100 100,000 <0.1 <l <14 <10 <5 <10,000 <10° (lowest)

' micrograms per cubic meter of air ? parts per billion > parts per million

E. Risk characterization

Risk characterization involves combining the information from the toxicity and exposure assessments and presenting this information on each substance in a way so that one can evaluate the relative risks posed by various stressors.

In a standard risk assessment, the potency (as indicated by a reference dose or cancer potency factor) is compared to the estimated exposure or dose (determined from concentrations in the media to which the population may be exposed) to produce a quantitative estimate of risk. In this evaluation, the work group, based on the criteria described for toxicity and exposure assessments, assigned a rank of “1” (highest) to “4” (lowest) for toxicity and another rank of 1 to 4 for exposure for each stressor. The matrix shown in Table III-7 was then used to combine

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these toxicity and exposure ranks into an overall evaluation. Those stressors ranked near the top left corner would receive an A rank (highest), those across a diagonal from the lower left to the upper right would receive a B rank, and those near the lower right corner would receive a C rank (lowest). This method allowed the work group to use data on environmental levels when available, and to use alternate indicators for exposure (release or production) when environmental concentrations were not available.

Table III-7: Risk characterization matrix

toxicity 1 (highest) | 2 3 4 (lowest) exposure 1 (highest) | A A A B 2 A A B C 3 A B B C 4 (lowest) B C C Cc

If one were to calculate the quantitative risk associated with each stressor (where data were available), one would find that there is some overlap in the risk estimate between adjacent boxes in Table III-7. This is because each box represents a product of a range of toxicity values multiplied by a range of exposure values. However, the degree of uncertainty associated with the toxicity and exposure data in this assessment may be a more important factor to consider than the mathematical overlap between boxes in Table III-7.

F. Comparative ranking of stressor groups

The final step in the HHWG’s comparative risk process was to compare the health risks posed by one stressor group to the health risks posed by other stressor groups. The Steering Committee asked the HHWG to rank stressor groups into three risk categories (A, B and C). The HHWG agreed it was not possible to define absolute, quantitative measures of health risk for an entire group. Not all of the potential health impacts of a stressor group could be determined given the data and resource constraints. To provide a final evaluation of the human health risks posed by stressor groups, the HHWG examined its results on a limited number of individual stressors and used its best judgment to reach a final ranking.

Comparative rankings were based on the results of the risk characterizations produced by the HHWG which combined both toxicity and exposure assessments. Each work group member who was assigned a stressor group first proposed a recommendation of A, B or C rank for the entire stressor group based on the risk characterizations for the individual stressors. For example, if most of the stressors in a group were ranked B, then the recommendation would be to rank the group B. The recommendation was then reviewed by the work group. The HHWG then sought to reach consensus on an A, B or C rank for each stressor group, judging the relative risk

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associated with the stressor group compared to other stressor groups. Final ranks were debated and opinions sometimes differed, usually because of the variability of health risks for individual stressors within the same stressor group. These differences were resolved when the work group agreed that three stressor groups should be ranked as A/B (lower than A but higher than B) and one stressor group as B/C (lower than B but higher than C). Consensus was reached on the ranking for each stressor group.

The HHWG also decided to point out any individual stressor that was ranked A even though its stressor group was ranked B or C. Other individual stressors could be identified to illustrate where further data is needed to adequately evaluate their potential health risks.

A draft report was prepared and distributed for public review and comment. Comments from 14 reviewers were received and all were carefully considered. Several changes to the report were made based on the comments submitted. None of the final stressor group ranks were changed as a result of the comments.

References

Agency for Toxic Substances and Disease Registry. Various dates. Toxicological Profiles for selected substances. US Public Health Service. Atlanta, GA.

California Comparative Risk Project. 1994. Toward the 21st Century; Planning for the Protection of California’s Environment. California Public Health Foundation, Berkeley, CA.

EINECS Plus CD. 1996. European inventory of existing commercial chemical substances and European list of notified chemical substances. Silver Platter Information, Ltd. London, UK.

National Institute for Occupational Safety and Health. 1987. Registry of Toxic Effects of

Chemical Substances. 1985-86 edition. US Government Printing Office. Washington, DC.

New York State Department of Environmental Conservation. 1996a. SARA Title III, Section 313, 1994 TRI Data as of 11/18/96. Chemical list by total amount. NYSDEC. Albany, NY.

New York State Department of Environmental Conservation. 1998. 6 NYCRR, Chapter V, Part 597, List of hazardous substances. www.dec.state.ny.us

New York State Department of Health. 1997. Hazardous Substances Emergency Events Surveillance (HSEES). 1992-1996. Bureau of Toxic Substance Assessment. Albany, NY.

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RTK Network, 1997. TSCA Chemical Update System (CUS). www.rtk.net (or telnet to ttk.net). The Right to Know Network. Washington, DC.

US Environmental Protection Agency. 1997. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, OH.

World Health Organization. Various dates. IARC Monographs on the evaluation of carcinogenic risks to humans. Selected substances. International Agency for Research on Cancer. Lyon, France.

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IV. Attributes, Uncertainties, and Limitations Associated with a Comparative Risk Project

Comparative risk is a relative term and in the context of the Human Health Work Group effort, the intent was to identify, evaluate, and prioritize those environmental chemicals or elements of greatest potential concern and to provide the public with a general sense of those chemical stressors that may present a risk given sufficient exposure. However, because of the vast number of inadequately tested chemicals, chemical mixtures, and products in commercial use today, there are numerous assumptions and limitations that must be described so that results of a comparative risk effort are not construed to represent statements of absolute certainty.

Risk assessment (and comparative risk) can serve as a qualitative and/or quantitative tool for decision making, yet is a method of analysis that uses numerous assumptions in the absence of available and substantiated toxicological and exposure information. In risk assessment, default assumptions are initially used in the absence of otherwise available information. Common to the majority of stressor groups within the Human Health section are the following areas of uncertainty and limitations with regard to how broadly the results and conclusions of this risk project can be extrapolated to all people in New York.

A. Inclusion of all known chemicals within a stressor group

The HHWG determined that it would be unrealistic for each stressor group to include and evaluate all known chemicals within that group given time, monetary, and information-related constraints. The HHWG decided to identify those chemicals of greatest potential exposure and subsequent health concern based on production, emission, environmental concentration, and human exposure data. While this process does not preclude the omission of a toxic or hazardous material or exposure of concern, using a variety of different databases (hazard, emission, environmental concentration) helps to minimize those omissions.

B. Incomplete toxicological profiles for stressor chemicals

The toxicological profiles for many industrial or commercial chemicals in existence today are often incomplete. For some chemicals, there are little or no toxicological data. However, we do have adequate toxicological information for many highly hazardous chemicals and can reasonably predict their toxicity to humans. While not having complete information for all acute and chronic endpoints associated with a chemical is limiting, it does not prevent our ability to get some perspective on the relative risks chemicals pose to humans and should not be sufficient reason to undermine the utility or results of the present effort.

A related concern within the HHWG was how to assess and characterize the risk associated with chemicals for which there is an absence of toxicological data. The HHWG recognized this as a general concern across stressor groups. When the HHWG identified chemicals with little toxicological data but a high potential for human exposure, these chemicals

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were recommended for further study.

C. Information on environmental presence and concentration

For most of the stressor groups, there was incomplete information on the environmental presence of stressors, particularly across environmental media (i.e., air, water, soil, sediments). An attempt was made to ascertain environmental concentration or presence data for the medium/media most relevant for each respective stressor group. However, this task revealed that environmental data are often unavailable and it is recommended that additional effort and resources be dedicated to providing better monitoring data in the future. For purposes of this effort, in cases where environmental data were not available, the HHWG used emission or production data (if available) as a surrogate for environmental monitoring data. Although these types of data are not direct measures of human exposure, they may provide some indirect indication of the potential for human exposure. Similar to information on environmental concentrations of contaminants in various environmental media, HHWG members attempted to collect data on various routes of human exposure (inhalation, ingestion of contaminated drinking water, intake from residual contaminants on food), although in the final analysis and evaluation of potential risk, rankings were based on the single highest potential exposure route. For many stressor groups, the HHWG did not evaluate potential exposure from soil or sediment. Efforts should be made to obtain accurate measurement of those contaminants with significant hazard potential to provide some indication of environmental concentration.

D. Human exposure

An uncertainty for most stressor groups is the degree or amount of actual human exposure (and, in toxicological terms, the bioavailable dose to the target tissue or organ) from identified stressors. This represents an area where future biomonitoring or exposure data would be beneficial. Even if data are available for contaminant concentrations in air, water, or soil, information on the extent of actual human exposure is often unavailable and thus human exposure must be estimated based on assumptions regarding human behavior. Market basket surveys are often helpful in identifying concentrations of residual contaminants such as pesticides and trace metals in food products. This information may be useful in estimating human exposure and intake through food consumption.

E. Animal vs. human data

Another common area of uncertainty is related to the toxicity potential of stressor chemicals on human health. Testing of humans is not conducted for moral and ethical reasons. It is only through occupational surveys, epidemiological data, and/or case reports that toxic effects in humans are ascertained. Animal toxicity data are often used as a surrogate for the estimation of human health effects. The USEPA states: “The inference that humans and animals (mammals) are similar, on average, in intrinsic susceptibility to toxic chemicals and that data from animals can in many cases be used as a surrogate for data from humans is the basic premise of modern toxicology” (USEPA, 1989).

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F. Uncertainty factors

The HHWG used available toxicological data (RfDs, NOELs, LOELs) to assess human health risk to stressors. It is important to understand that RfDs are calculated from NOELs or LOELs and incorporate a judgement of uncertainty and that NOELs and LOELs do not. When deriving an estimate such as an RfD from a NOEL or a LOEL from an animal study, uncertainty factors are used to address the uncertainty associated with various limitations of the study. An uncertainty factor (UF) of 10 is used to reduce the RfD when it is based on studies using prolonged exposure to average healthy humans to account for the variability in human populations. An additional UF of 10 is used when RfDs are based on studies using long-term exposure to animals to account for the uncertainty of using animal data as a surrogate for human data. Another UF of 10 is used when RfDs are based on a LOEL instead of a NOEL. An additional UF of 10 is used when RfDs are based on short-term animal studies to account for the uncertainty of using short-term data to assess health risks from long-term exposure. A modifying factor (from 1 to 10) is also used to reduce the R£D to reflect the professional judgement of the completeness of the database and the number of species tested (ATSDR, 1992). Understanding the assumptions and data used in a risk assessment allows one to identify the limitations when extrapolating the hazard or risk potential from animal data to humans.

G. Additivity, antagonism, and synergism

The HHWG did not consider the principles of additivity, antagonism, or synergism of effect for chemicals to which humans may be exposed. Additivity is the combined effect of two or more chemicals equal to the sum of their individual effects. Antagonism is the combined action of two or more substances to produce an effect less than the sum of their individual effects. Synergism is the combined action of two or more substances to produce an effect greater than the sum of their individual effects. This is a very difficult task and an aspect of risk assessment that remains largely undeveloped. There is knowledge on the interactions of some chemical mixtures, but even a crude analysis is complex. Humans are exposed not only to trace levels of environmental contaminants in foods, water and air, but also to pharmaceutical drugs and other chemicals as a result of lifestyle (alcohol and tobacco smoke). While potential interactions of these chemicals are possible, one must also take into account the human body’s natural processes, which include metabolism, detoxification and DNA repair. Ultimately, the assessment of exposure to mixtures and the potential effects resulting from such exposures was beyond the capabilities of this work group.

H. Conclusions

Despite the various sources of uncertainty and recognized limitations that accompany efforts related to evaluation of human health risk from environmental contaminants, the HHWG has identified those individual stressors and stressor groups that appear to constitute the greatest potential risk to humans under certain exposure conditions. While additional sources of information and increased data availability will aid future comparative risk efforts of this type, the HHWG used technically sound methods and data sources to make a reasonable assessment of

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relative risk and has identified:

1. contaminants of concern based on hazard and/or exposure potential;

2. scenarios that deserve additional attention (e.g., indoor settings for humans with appreciable inhalation exposure to a volatile organic compound); and

3. data voids (e.g., exposure or monitoring data for a given contaminant) that will benefit

from increased attention in the future. References

Agency for Toxic Substances and Disease Registry (ATSDR). 1992. Public Health Assessment Guidance Manual. Lewis Publishers. Chelsea, MI.

USS. Environmental Protection Agency (USEPA). 1989. Risk Assessment Guidance for Superfund; Volume I; Human Health Evaluation Manual (Part A); Interim Final. Office of Emergency and Remedial Response. Washington, DC. EPA/540/1-89/002.

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V. Risk Characterization for Stressors

This section describes the process and the results of characterizing the human health risk associated with each individual stressor within a stressor group.

A. Acidic and alkaline substances 1. Steering Committee definition

“This category includes substances that have a pH less than 2 or greater than 12.5. It does not include substances that react once in the environment to form acids or bases, or to cause acid rain.” The HHWG decided to include some weaker acids and bases as well, because they are produced, used or released in New York in significant quantities.

2. What are acidic and alkaline substances?

Acids are substances that, when dissolved in water, release hydrogen ions (H*). The greater the hydrogen ion concentration, the lower the pH. Bases, when dissolved in water, release hydroxyl ions (OH). The greater the hydroxyl concentration, the greater the pH. A neutral solution (neither acid nor base) has a pH of 7 and has an equal number of hydrogen ions and hydroxy] ions (an example is pure water). Acids and bases can neutralize one another. If the number of hydrogen ions from a strong acid equals the number of hydroxyl ions from a strong base, then the mixture of the two will form water and a salt and the mixture will have a pH of 7. Concentrated acids and bases can be corrosive. Acids and bases can be solid, liquid or gas, depending on the substance. Some can also be small liquid droplets attached to particles in the air. Commonly used acids are hydrochloric acid, sulfuric acid, nitric acid and hydrofluoric acid. Commonly used bases include ammonia, sodium hydroxide and potassium hydroxide.

3. Sources of acids and bases

Acids and bases are some of the most widely produced substances and are used ina variety of industries. Acids and bases are used in manufacturing other chemicals. Acids are also used for pickling steel, making fertilizer, dyes, and pigments, refining fats and oils, electroplating, leather tanning and adjusting pH in swimming pools and drinking water. Bases are used in pulp and paper mills, textile, detergent and soap manufacturing, etching, electroplating and agriculture. Acids may be released into the environment from chemical manufacturing, combustion of fuels and solid waste incineration. Bases may be released from paper industries, brewing industries, and chemical and soap manufacturing. Acids are also released from natural sources like volcanoes. One might be exposed to acids or bases in jobs where these chemicals are used or when using household products such as oven cleaners and drain cleaners. One may also be exposed to low levels of some acids in outdoor air in heavily polluted areas. Exposure to higher levels of acids or bases could occur from accidental spills.

4. Environmental fate

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Acids and bases will react quickly with other substances in the air, water or soil to form salts. They do not persist a long time in the environment. Some acids, such as sulfuric acid, may be transported in the air as liquid droplets attached to particles. They are removed from the air when it rains, resulting in acid rain.

5. Health effects

Exposure to acids and bases can occur through breathing, swallowing or skin contact. Health effects from exposure to acids and bases vary depending on the concentration of the substance and the length of time one is exposed to the substance. Concentrated acids and bases are corrosive to the surface that they contact. Direct contact with high concentrations can burn the eyes, skin and throat. Inhaling high concentrations of acids or bases can damage the respiratory system and swallowing them can damage the digestive system. Direct contact with low concentrations can cause mild irritation, but long term inhalation of low levels of some acids and bases in the air can cause tooth erosion and aggravate pre-existing respiratory diseases. Hydrogen fluoride poses a different health concern than other acids and bases. It has the same corrosive properties as other strong acids, but it can also can penetrate the skin to cause systemic effects such as decalcification of bones. Exposure to hydrofluoric acid can result in immediate health effects or effects may be delayed for several hours after exposure.

6. Selecting stressors a. Identification of substances

There are too many acids and bases to evaluate all of them in this project, so a method of selecting compounds that would be of particular concern for human health was devised. Several sources of information were used to identify possible stressors that could be included in this group. All acids and bases that appeared in the data sources listed below were screened for inclusion in this group. These compounds are listed in Appendix A, Table A.1 along with any available values from those sources.

° US Environmental Protection Agency (EPA) Integrated Risk Information System (IRIS): values listed are reference doses (RfD) or reference concentrations (RfC).

° American Conference of Governmental Industrial Hygienists (ACGIH): values listed are threshold limit values (TLV).

. New York State Department of Environmental Conservation (NYSDEC) Air Guide 1: values listed are air guideline concentrations (AGC).

e Toxic Substances Control Act (TSCA) Chemical Update System (CUS): values listed are non-confidential volumes reported for chemicals that are manufactured, distributed, processed, used or disposed in New York. (The 100 substances with the highest volumes were screened.)

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e New York State Department of Environmental Conservation (NYSDEC) Toxics Release Inventory (TRI): values are total releases (air, water, land).

° New York State Department of Health (NYSDOH) Hazardous Substances Emergency Events Surveillance (HSEES): values listed are number of emergency events in New York involving these substances from 1992 to 1996.

b. Criteria for selecting stressors

The following criteria were used to select substances from the data sources listed above for further evaluation.

° Any substance with a reported TRI release for New York.

° Any substance with more than 3 reported HSEES events in the past five years.

. Any substance with a TLV less than 5 mg/m’.

. Any substance with a TSCA CUS volume more than 1,000,000 pounds/year for New York.

All selected stressors are identified in Table V-A.1 as well as in Appendix A, Table A.1. The goal was to select those compounds which present a greater risk of exposure to the public and those compounds with higher toxicity. There were little data on environmental monitoring for acids and bases. Release data (TRI ), spill data (HSEES) and production data (TSCA CUS) were used as surrogates for exposure when screening and selecting stressors. The ACGIH TLV was used as a data source for toxicity screening because it evaluated the most acids and bases.

7. Ranking the selected stressors

The selected stressors were ranked by toxicity and exposure using the approach described in the methods section. Data used to rank each substance are shown in Appendix A, Table A.2. In Table V-A.1, each stressor is ranked based on toxicity data and either environmental data, release data (TRI), production/use data (TSCA) or emergency events (HSEES), whenever these data were available. There was no single measure of environmental exposure which had data available for all substances. Some stressors are shown more than once in Table V-A.1 because more than one type of exposure-related data was available.

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Table V-A.1: Risk characterization matrix for acidic and alkaline substances

toxicity rank

1 (highest) 2 3 4 (lowest) exposure | | ammonia (TRI) rank hydrochloric acid (TRI) lis _ _ , highest, 2 | hydrofluoric acid (TRI) acetic acid (average air) sulfuric acid ammonia (HSEES, average air) 4is (TRI, HSEES, average air) | sodium hydroxide (HSEES) lowest hydrochloric acid (HSEES, average air) 3 | hydrofluoric acid nitric acid (HSEES, TRI) m-toluic acid (TSCA) sorbic acid (TSCA) (HSEES, average air) acetic acid (HSEES) oxalic acid (TSCA) 2-amino-|-naphthalene formic acid (TRI) p-toluenesulfonic acid -sulfonic acid potassium hydroxide (HSEES) (TSCA) (TSCA) phosphoric acid (HSEES, TRI) 4 | acrylic acid formic acid (HSEES) calcium oxide (HSEES) (HSEES, TRI, TSCA) sodium hydroxide (TSCA) oxalic acid (HSEES) hydrochloric acid (TSCA) peracetic acid (HSEES, TRI)

8. Discussion

* data source used for final ranking (see text) Could not rank due to lack of exposure data:

cesium hydroxide picric acid

Table V-A.1 displays the matrix that combines the toxicity and exposure rankings. Not only does it show that this process can

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produce different results when more than one measure of exposure is used, but some routes of exposure (for example, direct contact through spills or inhalation of average concentrations) may be of more concern than other pathways for some stressors. Because there are sparse toxicological or exposure-related data for many substances, a lower rank should not mean that a substance should be ignored. However, there are enough data to make a reasonable comparison within this group to point out where pollution prevention could be useful.

There were outdoor air concentration data for five stressors (hydrogen fluoride, sulfuric acid, acetic acid, ammonia and hydrochloric acid). These data were either from the U.S. or from other states; none were specific to New York. Also, many of the air data were reported as not detected. Table V-A.1 shows that the ranks that resulted from outdoor air data are the same as ranks based on TRI data (which are specific to New York). TRI data were used to determine the final rank of most stressors. Some compounds were ranked A and may have high concentrations in air near facilities that emit them. Populations near these facilities have potential exposure via inhalation.

For stressors where no TRI data were available, HSEES or TSCA data were used to rank stressors. The data source used for the final ranking for each stressor is marked with an asterix in Table V-A.1. Two substances (cesium hydroxide and picric acid) could not be ranked due to the lack of exposure-related data.

Emergency event data from HSEES indicate that several substances present possible exposures to populations near accidental releases, such as spills. Direct contact or inhalation of high concentrations are possible exposure routes for nearby populations. Sulfuric acid, ammonia, hydrochloric acid and sodium hydroxide were ranked A by this measure. According to HSEES data from 1992 to 1995, six (ammonia, hydrochloric acid, phosphoric acid, sodium hydroxide and sulfuric acid) out of the ten compounds associated with the most injuries resulting from spills in New York were acids or bases. A study done by the New York State Department of Health HSEES group on ammonia-related emergency events found that over half of ammonia spills involved piping, as opposed to other places within facilities (transport, storage, process vessels).

Since much of the exposure ranking for acids and bases is based on release, emergency event, or production data, there is a significant amount of uncertainty as to actual exposure for the general population. However, outdoor air data from other states support the ranks based on TRI data from New York. Because acids and bases are not very persistent in the environment, populations near releases or spills are more likely to be exposed.

There were very little toxicological or exposure data for some substances with high production volumes (2-amino-1-naphthalene sulfonic acid, p-toluene sulfonic acid, m-toluic acid). Although the limited data indicate these substances may not be extremely toxic, the uncertainty associated with ranking these substances is high. The final ranking for the twenty substances included in this stressor group are shown in Table V-A.2.

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Table V-A.2: Individual stressor ranks for acidic and alkaline substances

Rank Stressor A sulfuric acid, hydrofluoric acid, hydrochloric acid, ammonia, sodium hydroxide B acrylic acid, nitric acid, potassium hydroxide, phosphoric acid, acetic acid,

formic acid, m-toluic acid, p-toluene sulfonic acid

Cc calcium oxide, oxalic acid, peracetic acid, sorbic acid, 2-amino-1-naphthalene sulfonic acid

Not ranked | cesium hydroxide, picric acid

9. Recommendations

° HSEES data indicate that acids and bases are among the substances with the highest number of accidental releases (spills) and injuries resulting from these spills. Studies should be done to investigate how and why these spills occur and measures be taken to reduce the number of spills and injuries.

. TRI data show that some acids and bases (ammonia, hydrochloric acid, hydrofluoric acid and sulfuric acid) are released into the air in significant quantities by certain facilities, often in or near urban areas. These substances have been found in outdoor air in other states. Reduction of these releases may be a worthwhile goal for pollution prevention.

. Of the 20 acids and bases evaluated, three with high production volumes had little toxicological data (2-amino-1-naphthalene sulfonic acid, p-toluene sulfonic acid, mtoluic acid). Further research should be done to investigate toxicological properties of these compounds.

° More and better environmental monitoring data are needed to properly characterize possible human exposure to these substances.

10. Ranking acidic and alkaline substances as a group

It is recommended that this stressor group be ranked B. Acids and bases are corrosive substances and short-term, high level exposures can cause significant injury. These types of exposures have occurred during accidental spills and acids and bases are some of the most commonly spilled substances in New York. Long-term, low level exposures to acids and bases released into the air can aggravate existing respiratory disease, but acids and bases are not persistent in the environment. Because there are documented injuries to the public resulting from exposure to these substances, a rank of at least B is necessary.

11. References

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Agency for Toxic Substances and Disease Registry. 1997. Toxicological Profile for sulfur trioxide and sulfuric acid. US Public Health Service. Atlanta, GA.

Agency for Toxic Substances and Disease Registry. 1993. Toxicological Profile for Fluorides, Hydrogen fluoride and Fluorine. US Public Health Service. Atlanta, GA.

Agency for Toxic Substances and Disease Registry. 1990. Toxicological Profile for Ammonia. US Public Health Service. Atlanta, GA.

American Conference of Governmental Industrial Hygienists, Inc. 1991. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. ACGIH. Cincinnati, OH.

EINECS Plus CD. 1996. European inventory of existing commercial chemical substances and European list of notified chemical substances. Silver Platter Information, Ltd. London, UK.

Howard, P.H., ed. 1990. Handbook of Environmental Fate and Exposure Data for Organic Chemicals. Vol II. Lewis Publishers. Chelsea, MI.

National Institute for Occupational Safety and Health. 1987. Registry of Toxic Effects of

Chemical Substances. 1985-86 edition. US Government Printing Office. Washington, DC.

National Toxicology Program. 1992. NTP Technical report on toxicity studies of formic acid. National Institutes of Health. NIH pub # 92-3342. Research Triangle Park, NC.

New York State Department of Environmental Conservation. 1996a. SARA Title III, Section 313, 1994 TRI Data as of 11/18/96. Chemical list by total amount. NYSDEC. Albany, NY.

New York State Department of Environmental Conservation. 1996b. 1995 Annual New York State Air Quality Report. Ambient Air Monitoring System. Executive Summary. Division of Air Resources. Albany, NY.

New York State Department of Environmental Conservation. 1991. Draft New York State Air Guide-1; Guidelines for the Control of Toxic Ambient Air Contaminants. Division of Air Resources. Albany, NY.

New York State Department of Health. 1997. Hazardous Substances Emergency Events Surveillance (HSEES). 1992-1996. Bureau of Toxic Substance Assessment. Albany, NY.

Occupational Safety and Health Administration. 1978a. Occupational Health Guideline for

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Acetic Acid. US Department of Labor. Washington, DC.

Occupational Safety and Health Administration. 1978b. Occupational Health Guideline for Calcium Oxide. US Department of Labor. Washington, DC.

Occupational Safety and Health Administration. 1978c. Occupational Health Guideline for Nitric Acid. US Department of Labor. Washington, DC.

Occupational Safety and Health Administration. 1978d. Occupational Health Guideline for Oxalic acid. US Department of Labor. Washington, DC.

Occupational Safety and Health Administration. 1978e. Occupational Health Guideline for Phosphoric acid. US Department of Labor. Washington, DC.

Occupational Safety and Health Administration. 1978f. Occupational Health Guideline for Sodium hydroxide. US Department of Labor. Washington, DC.

RTK Network, 1997. TSCA Chemical Update System (CUS). www.rtk.net (or telnet to ttk.net). The Right to Know Network. Washington, DC.

Sax, N.I. and R.J. Lewis, ed. 1989. Dangerous Properties of Industrial Materials. Van Nostrand Reinhold. New York, NY.

US Environmental Protection Agency. 1997. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, OH.

US Environmental Protection Agency. 1994. OPPT Chemical Factsheet. Chemicals in the

Environment: Acrylic acid. Office of Pollution Prevention and Toxics. EPA 749-F-94006. Washington, DC.

US Food and Drug Administration. 1980. Sodium hydroxide and potassium hydroxide; proposed affirmation of GRAS status as direct human food ingredients. Federal Register: 45(37): 11842 - 11846.

World Health Organization. 1992. IARC Monographs on the evaluation of carcinogenic risks to humans. Occupational exposures to mists and vapours from strong inorganic acids and other industrial chemicals. Vol 54. International Agency for Research on Cancer. Lyon, France.

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B. Atmospheric gases

The individual stressors in this group do not share a common structure or properties that make them a distinct group (e.g., volatile organic compounds). Their grouping is based solely on their shared location in the atmosphere. It is not practical to discuss them as a group so they will be dealt with individually as they interact in an urban setting. The selection of the following chemicals was based on their ubiquitous presence in the environment.

1. Steering Committee definition

“This category includes nitrogen oxides and sulfur dioxide, which are common byproducts of combustion and which contribute to acid rain. They are also precursors to ambient ozone, which is considered in this category. Greenhouse gases, except for chlorofluorocarbons (CFCs), are also included in this category. Carbon monoxide and carbon dioxide are combustion by-products and methane is emitted from various sources, including landfills.”

2. Carbon monoxide

Carbon monoxide (CO) is a colorless, odorless gas which, if inhaled in sufficient concentration, may cause serious health effects. As the most prevalent among all air pollutants normally found in urban atmospheres, carbon monoxide is produced primarily by the incomplete combustion of fuels and other organic materials. Although mobile sources (motor vehicles) constitute by far the largest single anthropogenic source of CO, space heating, refuse and agricultural burning, and industrial processes also contribute to carbon monoxide emissions (ACGIH, 1991; HSDB, 1998).

Carbon monoxide concentrations in urban areas are usually highest during the morning and evening rush hours when the volume of slow moving or idling motor vehicles is the greatest. This problem worsens when it occurs in street canyons where atmospheric dispersion is poor and pollutants become trapped near the ground level. Cold weather starts and poor engine performance, together with an increase in space heating and nocturnal inversions, tend to make the CO problem more prevalent during the winter months.

The most serious health effect of carbon monoxide is its ability to enter the blood stream by displacing the oxygen that is carried to the cells. Carbon monoxide has an affinity for hemoglobin that is 200 times that of oxygen, which normally combines with hemoglobin. This CO/hemoglobin combination, known as carboxyhemoglobin impedes the proper distribution of oxygen to all parts of the body. CO laden blood can weaken heart contractions thereby decreasing the volume of blood being pumped and can significantly reduce an otherwise healthy person’s ability to perform tasks such as walking (USEPA, 1991).

Especially susceptible to carbon monoxide are individuals who suffer from angina, lung disease, anemia, or cerebral-vascular problems. The human fetus can also be adversely affected

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by carbon monoxide as can cigarette smokers and those exposed to long-term CO concentrations such as daily commuters sitting in idling cars.

2. Carbon dioxide

Carbon dioxide is a colorless gas with a faintly pungent odor. It is shipped as a liquefied compressed gas and in solid form is utilized as dry ice. Naturally occurring carbon dioxide is found in solution in spring water which is sometimes so charged with gas under pressure that it is effervescent. It is evolved in large quantities from vents and fissures in the earth’s volcanic regions. For industrial use, carbon dioxide is recovered from synthesis gas in ammonia production, from substitute natural gas production, from cracking of hydrocarbons, and from natural springs or wells. For laboratory purposes it is obtained by the action of an acid ona carbonate. It is also a by-product of the fermentation of carbohydrates and an end product of combustion and respiration (HSDB, 1998).

As with carbon monoxide, carbon dioxide levels increase in heavily populated areas from mid-morning to mid-afternoon from sources such as motor vehicles, and residential heating, ventilating, and air conditioning systems.

When inhaled in elevated concentrations, carbon dioxide may act to produce narcotic effects at 30,000 ppm, stimulation of the respiratory center at 50,000 ppm, and asphyxiation depending on the concentration and duration of exposure (ACGIH, 1991).

3. Sulfur dioxide

Like carbon monoxide, sulfur dioxide (SO,) is also a colorless gas, but unlike CO, it has a clearly detectable pungent odor and taste. It is highly soluble in water, forming sulfurous acid. The major sources of SO, emissions are fossil fuel (coal, oil) fired power plants and boilers, ore smelters, and oil refineries. Smaller stationary combustion sources such as space heating also contribute to the problem, especially in urban areas during the winter (HSDB, 1998; USEPA 1994).

Human exposure to sulfur dioxide can result in irritation of the respiratory system which can cause both temporary and permanent damage. The degree of harm would probably be higher in the presence of airborne particulates. Particulates tend to catalyze the atmospheric conversion of SO, to sulfur trioxide (SO,) which combines with water vapor to form sulfuric acid mist.

4, Nitrogen dioxide

Nitrogen dioxide (NO,), a reddish brown gas with a highly detectable pungent odor, is highly corrosive and a strong oxidizing agent. It is produced from the reaction of atmospheric nitrogen and oxygen during high temperature combustion processes such as the burning of fuel (coal, oil, gas) and internal combustion (motor vehicles). Nitric oxide (NO), a colorless, odorless gas, is also a product of combustion and the combination of NO and NO, is commonly

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referred to as NO, (HSDB, 1998; Fed Reg, 1995).

While NO by itself is not usually considered a health hazard, NO, can cause inflammation of the lungs and bronchial tubes at high concentrations and less severe respiratory problems at lower concentrations.

5. Sulfates and nitrates

Sulfates and nitrates are secondary pollutants formed in the atmosphere primarily by the reaction between sulfur or nitrogen dioxide (primary pollutants) with other airborne substances and, to a lesser extent, can be traced to natural sources. Sulfates and nitrates are essentially fine particulate compounds often transported in the air over long distances and are capable of deep penetration into the human respiratory tract.

Both sulfates and nitrates contribute to the acid deposition problem via their atmospheric conversion into acids that are deposited as rain or snow on ground receptors that may be miles downwind of the original source (NYSDEC, 1996).

6. Ozone

In its pure state, ozone is a naturally occurring form of oxygen normally found in high concentrations at very high altitudes as a blue, unstable gas with a characteristically pungent odor. It can also be readily detected at ground level near arcing electrical motors and during lightning storms. Ozone at high altitudes or in the stratosphere serves as a shield against harmful, cancer-causing ultra-violet light. At the ground-level, ozone is colorless and odorless and is the major constituent of photochemical smog (HSDB, 1998).

Ground-level ozone is considered a secondary pollutant, formed in the atmosphere by the photochemical reaction of nitrogen oxides and reactive hydrocarbons (volatile organic compounds) in the presence of high temperatures and ultraviolet light. These primary pollutants (precursors) are emitted from motor vehicle exhaust, gasoline and oil storage/transfer and operations involving solvents, degreasing agents, and cleaning fluids.(USEPA, 1992)

Ozone concentrations at ground level are usually higher during hot summer afternoons when the photochemical activity is most pronounced. Ambient ozone concentrations are a product of local precursors and long-range transport of ozone and its precursors from upwind sources.

With regard to chronic health effects, toxicological data indicate that ozone-induced lung injury is roughly similar across species (including monkeys, rats, and mice) with responses that are concentration dependent. The currently available scientific information provides at least a biologically plausible basis for considering the possibility that repeated inflammation associated with exposure to O; over a lifetime may result in reduced lung function by making the lung tissue less elastic. (Fed Reg, 1997)

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7. Methane

The major sources of methane are biological in origin. Methane is a highly volatile constituent of crude oil and natural gas. It is released to the environment via the manufacture, use, and disposal of many products associated with the petroleum and gasoline industries. Methane may be released to the environment as emissions from coal outgassing, combustion and liquefaction. Two other important sources include the rumen of domestic animals, especially of cattle, and the emission of methane during the growing of rice. Data document the release of methane into the environment from hazardous waste disposal sites, landfills and waste incinerators; and the combustion of gasoline and diesel fueled engines.

Methane is neither irritating to the skin, eyes, nose, throat, or lungs nor it is considered poisonous. The major hazards associated with methane handling, transport, and control are due to its explosiveness and flammability (ACGIH, 1991).

8. Ranking individual stressors

The chemicals in this group cannot be ranked using the matrix developed by the HHWG. Neither reference doses nor cancer potency factors have been derived for these chemicals. Instead these stressors were ranked using a hazard index where peak air concentrations from monitoring stations in New York were averaged and then divided by the concentration that was determined to be a NOEL or LOEL (see Table V-B.2). The resulting ratio was compared to the criteria in Table V-B.1 to assign a rank for each stressor.

Table V-B.1: Criteria for ranking atmospheric gases

Hazard Index Rank >1 A (highest) 0.1>x<1 B <0.1 C (lowest)

Peak values reported in the NYS Air Quality Report Ambient Air Monitoring System, Annual 1996 (NYSDEC, 1996) were used to obtain air concentration for sulfur dioxide, nitrogen dioxide, ozone, and carbon monoxide. The air concentrations for carbon dioxide were reported from analyses of air in temperate zones as reported in the Merck Index.

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Table V-B.2: Atmospheric gases and relevant toxicity/exposure information

potency/toxicity

exposure

Hazard index

Chemical Name EU NOEL LOEL ACGIH NYSDEC Air Concentration NYS air conc (max) (CAS number) class “? TLV Ambient Air (1996) HEES® | +NOEL/LOEL mg/m? Standards # spills 1997” 1992-96 Sulfur Dioxide Toxic, 0.2 ppm/S5m 0.5 ppm/S5m 5.2, A4 lyr 0.03 ppm | 0.009 ppm annual avg. | 19 0.009=0.2=0.045 7446-09-5 irritant exercising exercising asthmatics 24hr 0.14 ppm | 0.06 ppm 24hr high {ancual average) asthmatics 0.75ppm 3hr 0.50 ppm 0.146 ppm 3hr high (24hr high) 0.6 ppm/15m exercising healthy adults 0.146+0.2=0.73 healthy adults increase airway resistance (3hr high) Nitrogen Dioxide | Very toxic, 0.2 - 0.3 ppm/3hr 5.6, A4 lyr 0.05 ppm | 0.029 ppm annual avg. | 3 0.029+0.2=0.145 10102-44-0 irritant airway responsiveness 0.133 Lhr high (annual average) in asthmatics” P0067 (Jhr high) Ozone none 0.12 ppm/1hr exposure - Heavy work | 1 hr 0.12 ppm | 0.026 ppm annual avg. | none 0.026+0.12=0.217 10028-15-6 decrease in lung function® | 0.1 0.134 ppm Ihr high (annual average) 0.134=0.12=1.08 Mod. work (Ihr high) 0.16 Light work 0.2 Carbon Monoxide } Toxic, 9 ppm 8hr exposure 29 8 hr 9 ppm 0.9 ppm annual avg. 1 0.9+9=0.1 630-08-0 extremely 35 ppm Ihr exposure” 1 hr 35 ppm 6.5 ppm 8hr high {ama verse) flammable carboxyhemoglobin levels 11.7 ppm Ihr high (Shr high) at 5% or less 11.7235=0.3 (Jhr high) Carbon Dioxide none 5000 ppm provided 9000 270-360 ppm” 1 360=5000=0.07 124-38-9 normal amounts of O, inhaled air” Methane extremely Simple none reported none NA 74-82-8 flammable asphyxiant see footnotes next page NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page 33

Footnotes for Table V-B.2:

1 Office for Official Publications of the European Community. European Listing of Notified Chemical Substances. 2 1997 American Conference of Governmental and Industrial Hygienists TLVs and BEIs Booklet. (A4-Not

Classifiable as a Human Carcinogen: There are inadequate data on which to classify the agent in terms of its carcinogenicity in humans and/or animals.

3 NYSDEC Draft New York State Air Guide-1. Guidelines for the Control of Toxic Ambient Air Contaminants 1991. Table I Summary of Federal and State Ambient Air Standards

4 NYSDEC New York State Air Quality Report Ambient Air Monitoring System. 1996 Annual DAR 97-1. July 1997.

5 NYS Hazardous Substances Emergency Events Surveillance. NYSDOH, 1997.

6 U.S. EPA, 1994. Supplement to the Second Addendum (1986) to Air Quality Criteria for Particulate Matter and Sulfur Oxides (1982). EPA/600/FP-93/002.

7 Federal Register: October 11, 1995 (Volume 60, Number 196) National Ambient Air Quality Standards for Nitrogen Dioxide: Proposed Decision [Page 52874-52889]

8 U.S. EPA, 1992. Summary of Selected New Information on Effects of Ozone on Vegetation: Supplement to 1986 Air Quality Criteria for Ozone and Other Photochemical Oxidants. EPA/600/8-88/105F

9 U.S. EPA, 1991. Air Quality Criteria for Carbon Monoxide. Office of Research and Development.

Research Triangle Park, NC. EPA600/8-90/045F. As cited in “Testimony of Wanda Lizak Wells, Ph.D., Research Scientist. Bureau of Toxic Substance Assessment NYSDOH on Carbon Monoxide to the Health Committee of the Albany Common Council.”

10 Analyses of air in the temperate zones of the earth show 0.027-0.036% (v/v) of CO2. MERCK INDEX. 10TH ED 1983, p. 251

The no observable effect level (NOEL) or lowest observable effect level (LOEL) are values reported for sulfur dioxide, nitrogen dioxide, carbon monoxide and ozone and used by the US Environmental Protection Agency to develop air quality standards for these chemicals. The American Conference of Governmental and Industrial Hygienists (ACGIH, 1991) has recommended a threshold limit value-time weighted average (TLV-TWA) of 5000 ppm for carbon dioxide that will provide a good margin of safety from asphyxiation, provided normal amounts of oxygen are present in the inhaled air. A NOEL/LOEL could not be determined for methane. The major hazards associated with methane are due to its explosiveness and flammability. Neither the Occupational Safety and Health Administration (OSHA) nor the National Institute for Occupational Health and Safety (NIOSH) have established a permissible exposure level (PEL) or recommended exposure limit (REL) for methane.

The individual stressors and their ranks are shown in Table V-B.3.

Table V-B.3: Individual stressor ranks for atmospheric gases

Category | Stressor

A ozone (hr high)

B SO2 (24hr & 3hr high), CO (8hr & lhr high), NO2 (annual average & lhr high), ozone (annual average), carbon monoxide (annual average)

Cc SO2 (annual average), carbon dioxide, methane

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9. Recommendations

Data for these gases for the exception of carbon dioxide and methane were obtained from monitoring stations in urban areas along the New York State Thruway corridor and New York City and Long Island metro areas. The available information indicates that the potential for exposure to these gases is high in these urban areas. It is not certain if the populations in rural areas are exposed to these gases at above background levels. Better environmental monitoring data, especially in rural areas, are needed to properly characterize possible human exposure to these substances.

10. Ranking atmospheric gases as a group

It is recommended that this stressor group be ranked B. These atmospheric gases are naturally occurring. However, concentration of these gases increases above background levels in urban areas where machinery such as automobiles, boilers, air conditioning, etc. are used in relation to population density. Short-term and long-term exposure can aggravate existing respiratory disease. Because the populations exposed to high concentrations of these gases are primarily in large urban areas, a rank of B is considered appropriate.

11. References

ACGIH, 1991. Documentation of the Threshold Limit Values and Biological Exposure Indices. Sixth Edition 1991. American Conference of Governmental and Industrial Hygienists. (ACGIH)

Federal Register: October 11, 1995. (Volume 60, Number 196) National Ambient Air Quality Standards for Nitrogen Dioxide: Proposed Decision [Page 52874 - 52889].

Federal Register: July 18, 1997. (Volume 62, Number 138)] 40 CFR Part 50 National Ambient Air Quality Standards for Ozone; Final Rule [Page 38855-38896].

Hazardous Substances Data Bank (HSDB), 1998. National Library of Medicine on-line. Bethesda MD.

Merck, 1983. Merck Index, 10th edition, p. 251. M. Windholz, ed. Merck & Co. Rahway, NJ.

New York State Department of Environmental Conservation, (NYSDEC), 1996. New York State Air Quality Report Ambient Air Monitoring System. 1995 Annual DAR 96-1. November 1996.

USS. Environmental Protection Agency (USEPA), 1991. Air Quality Criteria for Carbon Monoxide. Office of Research and Development. Research Triangle Park, NC. EPA600/8-90/045F. As cited in “Testimony of Wanda Lizak Wells, Ph.D., Research Scientist. Bureau of Toxic Substance Assessment NYSDOH on Carbon Monoxide to the Health Committee of the Albany Common Council.”

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USS. Environmental Protection Agency (USEPA), 1992. Summary of Selected New Information on Effects of Ozone on Vegetation: Supplement to 1986 Air Quality Criteria for Ozone and Other Photochemical Oxidants. EPA/600/8-88/105F.

U.S. Environmental Protection Agency (USEPA), 1994. Supplement to the Second Addendum (1986) to Air Quality Criteria for Particulate Matter and Sulfur Oxides (1982). EPA/600/FP-93/002.

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C. Halogens/Disinfectant Residuals/Byproducts 1. Steering Committee definition

This stressor category was defined by the steering committee as: “Elemental halogens, such as chlorine and bromine; drinking water chlorination byproducts and wastewater disinfection byproducts, such as trihalomethanes.”

2. What are “elemental halogens,” and “disinfection byproducts”

“Elemental halogens” are group VIIB on the periodic table, and includes fluorine (F;), chlorine (Cl,), bromine (Br,) and iodine (I,). The term “chlorination byproducts” and the more general term of “disinfection byproducts” or DBPs, refer to chemicals that are produced when disinfectants that are added to public water supplies react with other substances, such as organic carbons and bromide, in the source water. This is a large group of substances; for example, a 1989 study of 10 public water supply utilities identified nearly 200 compounds attributed to the chlorination of public drinking water. It also refers to chemicals that are produced when disinfectants are used in municipal waste water treatment plants for the treatment of sanitary wastewater.

3. Selection of individual stressors

The selection of disinfectant/residuals was based on the use of drinking water disinfectants in New York. These include chlorine, chloromines and chlorine dioxide. According to data provided by the New York State Department of Health, chlorine is the drinking water disinfectant used by virtually all public water utilities serving more than 10,000 persons. In addition to New York City’s system, which serves about 7.3 million persons, all other large systems in the state (serving an additional 6.5 million persons) use chlorine, with the exception of one system (120,000 persons) using chloromine and one system (22,000 persons) using chlorine dioxide. The NYSDOH data indicated no public water utility is employing ozone as a disinfectant.

Several information sources were used to establish a list of disinfection byproducts for this report. The principal source of information used was the preamble to the U.S. Environmental Protection Agency’s 1994 proposed national drinking water standards for disinfectants and disinfection byproducts. This rule, which focuses on public drinking water supplies, established maximum concentration limits and maximum concentration goals for 14 disinfectant residuals and disinfectant byproducts that were determined to be of the most significant public health concern by the USEPA, and that were determined to have adequate health and exposure data on which to base standards.

In addition, experts at the New York State Department of Environmental Conservation and New York State Department of Health, within the wastewater management industry, and within the disinfection product manufacturing industry were interviewed for additional information on stressors of concern, particularly regarding DBPs related to wastewater

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treatment. The New York State Department of Environmental Conservation’s Division of Water was contacted for information about sanitary wastewater disinfectant residuals of significant human health concerns. The response was that the Division of Water did not focus on any wastewater DBPs in their wastewater permitting program.

Various other reports (e.g., the International Joint Commission annual report) and other literature sources were also reviewed, but they did not provide information on specific stressors in this category.

As the result of this process, the list of DBPs adopted for this report consists of those DBPs for which a standard or guidance value has been established by the USEPA in its disinfectant/disinfectant byproducts rule. The disinfectant residuals, DBPs and the four elemental halogens are identified in Table V-C.1.

4. Halogens, Disinfection Residuals, Disinfection Byproducts

The following provides a brief description of possible human health effects, exposure routes and sources of halogens, water disinfection residuals and disinfection byproducts from drinking water and waste water treatment.

a. Elemental Halogens

. Chlorine — Major uses include manufacturing of pharmaceuticals, plastics, pesticides, solvents and refrigerants, paper manufacturing, and in drinking water treatment and wastewater treatment. It is also used in the manufacture of flame-retardant compounds and lithium and zinc batteries; and is also used in the processing of meat, fish, vegetables and fruit.

Human health risks primarily reflect the risk of direct exposure, and include occupational exposure risks as well as off-site risks due to accidental releases. Elemental chlorine poses acute human health risks through inhalation or exposure to skin or eyes due to its highly corrosive nature. It can cause chemical pneumonia, or even death in high concentrations, and can cause severe irritation to skin, eyes and the respiratory tract. Liquid chlorine can burn eyes and skin. Chlorine is not known to pose carcinogenic or reproductive risks, nor to cause effects from chronic exposure. With regard to other potential risks to humans, chlorine is nonflammable, but can react explosively with certain chemicals. Chlorine is not a persistent, bioaccumulative substance and once released to the environment it tends to form salts like sodium chloride.

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Table V-C.1: Halogens/drinking water disinfectant residuals/byproducts

(trichloroacetaldeyhde)*

Group Chemical/Compound CAS # halogens fluorine 7782-41-4 bromine 7726-95-6 chlorine! 7782-50-5 iodine 7553-56-2 disinfection chloromines (monochloramine)* 10599-90-3 residuals chlorine dioxide 10049-04-4 disinfection trihalomethanes total trihalomethanes (TTHM) na byproducts , chloroform (trichloromethane) 67-66-3 bromodichloromethane 75-27-4 dibromochloromethane 124-48-1 bromoform (tribromomethane)* 75-25-2 haloacetic acids monochloroacetic acid 79-11-8 (five) (HAAS) ° — dichloroacetic acid ? 79-43-6 trichloroacetic acid “ 76-03-9 monobromoacetic acid 79-08-3 dibromoacetic acid 631-64-1 bromate (BrO,) 4 potassium bromate 7758-01-2 sodium bromate 7789-38-0 chlorite * 7758-19-2 chloral hydrate 302-17-0

1. chlorine is also regulated as a disinfectant residual

2. chloromines are also a chlorine DBP

3. chlorine disinfection byproduct 4. ozone disinfection byproduct/ICR 5. chlorine dioxide disinfection byproduct/ICR

The most likely source of human exposure to elemental chlorine is acute exposure through accidental releases, which pose a health concern due to chlorine’s highly

corrosive nature. Ingestion of chlorinated drinking water has been associated with an increased risk of bladder and colon cancer in humans, and research is being conducted to

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assess the carcinogenic effects of chlorination byproducts in drinking water. Therefore, drinking water chlorination is an important concern because of the high degree of human exposure. However, it is important to note that the risk of health effects from chlorine disinfection byproducts must be judged against the risks posed by drinking water that has not been disinfected. Wastewater disinfection byproducts are of minor concern from a human health perspective because of the limited potential for exposure.

. Fluorine — Fluorine is used in the production of metallic and other fluorides, in the production of fluorocarbons, and are an active constituent of fluoridating compounds used in drinking water and toothpastes. It is a powerful oxidizing agent, and reacts vigorously with most oxidizable substances at room temperature, frequently with ignition.

. Iodine — Iodine is used in the manufacture of dyes, alkylation and condensation catalysts, antiseptics and germicides, x-ray contrast media, food and feed additives, pharmaceuticals and other products. It is toxic by ingestion and inhalation, and a strong irritant to eyes and skin.

. Bromine — Bromine is used in the manufacture of “anti-knock” gasoline (ethylene dibromide), fire-retardants for plastics, dyes, pharmaceuticals, and other products, and used as a bleaching agent, intermediate for fumigants, and as a solvent. It is toxic by ingestion and inhalation, and a severe skin irritant. It is a strong oxidizing agent that may ignite combustible materials on contact.

b. Disinfectant residuals

Common chlorine-based disinfectants include chlorine, chloromines and chlorine dioxide. These are commonly used in water treatment to kill bacteria and other disease-causing microorganisms. They are also added to water supplies to provide continuous disinfection throughout the water distribution system.

The USEPA has found that chorine and chlorine dioxide, at high doses over extended periods, have been shown to damage blood in lab animals; chloramines have been shown to damage blood and the liver in lab animals. Chlorine dioxide, when given to pregnant lab animals in drinking water, has been shown to cause delays in development of the nervous system of their offspring.

c. Drinking water chlorination byproducts

Drinking water disinfectants combined with organic and inorganic matter present in water can form a wide range of chemicals referred to generally as disinfection byproducts. The USEPA has determined that a number of DBPs are a human health concern at certain levels of exposure. For example, several DBPs resulting from chlorination have been classified by the USEPA as possible human carcinogens. Further, some trihalomethanes and haloacetic acids have been shown to cause cancer in rats. Other DBPs have been shown to damage the liver and

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nervous system, and cause reproductive or developmental effects, in lab animals. 5. Ranking the selected stressors

Toxicity and exposure data were collected on the individual stressors in accordance with general guidelines developed by the HHWG. The toxicity research was based on five principal data sources:

. the USEPA’s “National primary drinking water regulations: Disinfectants and disinfectant byproducts proposed rule, FR July 29, 1994"

. the USEPA’s “Integrated Risk Information System,” or IRIS,

. the “Registry of Toxic Effects of Chemical Substances”

. the “Chemical Hazard Response Information System” and

. the World Health Organization’s “Guidelines for Drinking Water Quality.”

The exposure data were derived from:

. New York State Department of Environmental Conservation’s 1996 summary report on “toxic release inventory” data,

. Water supply monitoring data provided by the New York State Department of Health.

. US. Environmental Protection Agency TSCA production database, and

. the USEPA’s “National primary drinking water regulations: Disinfectants and disinfectant byproducts proposed rule, FR July 29, 1994"

The detailed toxicity and exposure data are presented in Appendix A, Tables C.1 and C.2, respectively. Table V-C.2 presents a summary of the toxicity and exposure ranks for seventeen individual stressors in this stressor group; iodine and fluorine are not included due to a lack of exposure data.

6. Ranking the stressor group

The HHWG agreed that combined hazard rankings would be assigned based on a stressor’s location on the toxicity/exposure matrix shown in Table V-C.2. The six squares in the upper left portion of the matrix were assigned a combined ranking of A (highest level of hazard based on risk and exposure), the six squares in the lower right portion of the matrix were assigned a combined ranking of C (lowest level of hazard based on risk and exposure), and all other squares in the matrix were assigned a combined ranking of B.

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Table V-C.2: Risk matrix for halogens, disinfectant residuals and disinfectant byproducts

toxicity rank

1 (highest) 2 3 4 (lowest) exposure 1 chlorite chlorine rank li 2 chloroform monochloromine dibromoacetic highest monochloroacetic acid | trichloroacetic acid | acid monobromoacetic acid | bromate Ais dichloroacetic acid lowest bromodichloromethane | chlorine dioxide bromoform dibromochloro3 methane chloral hydrate bromine

Not Ranked = fluorine, iodine

Based on this approach, the individual stressors received combined rankings as follows:

. five of the individual stressors received a combined rank of A . six of the individual stressors received a combined rank of B . five of the individual stressors received a combined rank of C

If these alpha rankings were assigned numeric values of A=1, B=2 and C=3, then the mathematical mean of these scores is 2.0 (equivalent to a B). For this reason, it is recommended that this stressor group receive a combined hazard ranking of B. However, HHWG members raised issues as to the appropriateness of assigning a single hazard ranking to this contamination class. Issues were raised as to whether this approach sufficiently reflects the body of epidemiological studies regarding the relationship between the human cancers and the ingestion of disinfection products and/or byproducts. Specifically, it was recommended that this hazard ranking be modified to reflect epidemiological studies of the relationship between chlorinated drinking water and cancers in humans.

A report on cancer risks to humans, published by the World Health Organization’s (WHO) International Agency for Research on Cancer (1991), provides a discussion of major studies. The WHO’s final evaluation states that “there is inadequate evidence for the carcinogenicity of chlorinated drinking water in humans” or “in experiment animals,” and that “chlorinated drinking water is not classifiable as to its carcinogenicity to humans.” On the one

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hand, the WHO cites studies that found significant increase in risks for colon cancer, rectal cancer and urinary bladder cancer, as well as moderate increases in risk of lung and stomach cancer, in populations with long-term exposure to disinfected drinking water. On the other hand, the WHO found that these studies generally did not document exposure, and did not adequately address possible confounding variables such as population migrations, the constituents of local water supplies, and characteristics of the local population. Based on this further consideration, the work group retained the overall hazard ranking of B for this stressor group.

7. Discussion

The following additional information relates to the risk/exposure assessment data discussed above.

. As has been the case for most of the stressor group assessment efforts, the limited amount of health effects data limited the number of individual stressors included in this analysis, and in some cases has limited the thoroughness of this assessment.

. The USEPA determined that drinking water is the predominant source of human exposure to chlorine. In doing its drinking water standard assessment, the USEPA assigned a relative source contribution value of 80% to drinking water (the USEPA’s then-current exposure assessment policy ceiling).

. The USEPA reported that the level of total organic carbon (TOC) in source water is a good indication of the likely production of total trihalomethanes and other DBPs from the disinfection of drinking water. TOC in surface waters within USEPA Region 2 are near the national average (comparing 25th, 50th and 75th percentiles of samples taken from source waters within USEPA Region 2.)

The following issues are presented for consideration by the Risk Reduction Strategies Work Group.

. According to the U.S. Environmental Protection Agency, risk reduction strategies related to DBPs include: use of alternative disinfectant products/processes; removal of DBP precursors from source water; treatment/removal of DBPs post-disinfection.

. A large number of DBPs related to chlorination have been identified, along with a lesser number of DBPs related to alternative disinfectants. Generally speaking, more health data is available for significant chlorination DBPs than for DBPs related to alternative disinfectants. For example, the USEPA determined that there was insufficient health data to include aldehydes, a principal DBP of ozonation, in its residual/byproducts rule.

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. In its 1994 rulemaking preamble, the USEPA expressed concern about promoting a largescale shifting away from chlorine to alternative disinfectants due to uncertainties about the efficacy of other disinfectants (a possible increase in microbial exposure or exposure to pathogenic organisms could increase, rather than decrease public health risk) and the occurrence and health effects of DBPs related to alternative disinfectants.

8. Recommendations The following recommendations apply to this assessment process:

. The exposure numbers for disinfectant residuals and disinfectant byproducts should be revisited once data is available from New York drinking water utilities pursuant to the USEPA’s “information collection rule.” This rule became effective in early 1997, and requires the generation of 18 months of monitoring data.

. This assessment should be reassessed periodically to determine whether sufficient health data has been developed to reflect new health effects data.

9. References

National Institute for Occupational Safety and Health. 1987. Registry of Toxic Effects of

Chemical Substances. 1985-86 edition. US Government Printing Office. Washington, DC.

National Research Council. 1987. Drinking Water and Health: Disinfectants and Disinfectant Byproducts, Volume 7. Subcommittee on Disinfectants and Disinfectant Byproducts; Safe Drinking Water Committee; Board on Environmental Studies and Toxicology; Commission on Life Sciences. National Academy Press. Washington D.C.

US Environmental Protection Agency. 1994. National Primary Drinking Water Regulations. 40 CER Part 141.

USS. Environmental Protection Agency. 1998. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, OH.

World Health Organization, International Agency for Research on Cancer. 1990. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Chlorinated Drinkingwater, Chlorination Byproducts; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds. Volume 52. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, Lyons, France.

World Health Organization. 1996. Guidelines for drinking-water quality, Second edition. Volume 2. Health criteria and other supporting information. World Health Organization. Geneva.

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D. Metals and cyanide 1. Steering Committee definition

“This category includes both elemental and organic forms of metals. Lead, mercury, and cadmium are the three that are most often cited as posing environmental risk. Other metals, such as silver, nickel, chromium, and manganese, have sometimes been implicated as causing harm and may be considered as well. In addition, cyanide will be considered here because of its similar properties. These substances enter the environment through a wide variety of sources, including combustion, wastewater discharges and manufacturing facilities.”

2. What are metals?

About three-fourths of all elements are metals. An understanding of metals and how to use them was crucial to the development of civilization. Today, millions of tons of metals are produced and used every year. Clearly, there are great differences among metals, but as a group they are identified by characteristics that they share to some degree. The most common characteristics of metals are that they are good conductors of electricity and heat and that they can be worked. That is, they can be hammered into shapes or drawn into wire. The degree to which any given metal carries these characteristics varies. There are great differences among metals. Mercury, for example, is a liquid at room temperature.

Metal atoms in general have a lower ionization potential than other elements. That is, the electrons of a metal atom are held more weakly and have a greater range of motion. Metals can conduct electricity, which is simply a flow of electrons, because of the mobility of electrons. Most metals can oxidize easily. Moreover, one metal ion can be substituted for another without changing the overall bonding in a major way, so that metals can form an incredible variety of compounds.

Different metals can be fused together to form alloys, such as brass (copper and zinc), bronze (copper and tin) and stainless steel (iron, chromium, nickel and carbon). Metals also combine with non-metals forming many different compounds. For example, the metallic element sodium combines with chlorine to form common table salt.

3. Sources of Metals

Metal ores are resources found in the earth's crust. Ores are mined, smelted, and refined. The metals are then forged, cast or drawn into useful forms and made into products. Metals are also combined into a wide variety of compounds and mixtures. As natural parts of soil and water, metals are incorporated into plant and animal life.

4. Environmental Fate and Human Exposure

Metals oxidize readily and combine with other substances. The metals themselves do not degrade, but may be transported by wind or water. Some metals are bio-accumulated in plants

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and animals. People are exposed to metals in the environment through air, water, soil and food. Metals released to the air will eventually deposit in soil. Metals in soil can seep into groundwater, can be carried overland into surface water, can be re-entrained into the air to be inhaled, can be ingested by children, and can be taken up into plants.

a. Diet

The U.S. Food and Drug Administration's Total Diet Study (1986-1991) estimated mean daily dietary intake of selected metals in terms and compared them to "Provisional Tolerable Daily Intake (PTDI) established by the United Nations Food and Agriculture Organization and the World Health Organization (Gunderson, 1995). These are summarized in Table V-D.1. Arsenic and mercury are derived primarily from seafood, cadmium from grain, potatoes and lettuce, and lead from dispersed sources.

Table V-D.1: Mean daily dietary intake of selected metals, mg/kg/day (Gunderson, 1995).

Metal PTDI Range of intake Arsenic 0.0021 0.00036 - 0.00081 Cadmium 0.001 0.00016 - 0.00046 Lead 0.0036 0.0001 - 0.00037 Mercury 0.0071 0.00003 - 0.00007

Excessive exposures through diet may result from ingestion of fish from contaminated waters. Contamination in commercially sold fish is regulated, but consumption of fish taken by sport fishers is not. The New York State Department of Health (NYSDOH) publishes health advisories for waters where sport fish have contaminant levels greater than federal standards. These advisories provide an indication of the extent of contamination in New York waters and fish. There are currently 79 New York waters with advisories. Of these, 15 are associated with mercury and two with cadmium (New York State Department of Health, 1998a).

b. Drinking Water

Since metals are naturally found in the earth, they are also a natural component of our drinking water. In some cases, the natural level of a metal in water may be hazardous, requiring that the water be treated or not used for drinking. In other cases, water may be contaminated through spills or from waste sites. An indication of the extent of contaminated water can be found in a database of private and public well water samples analyzed by the New York State Department of Health from January 1980 to January 1994. Since many of these wells were sampled because of suspected contamination, they probably represent an overestimate of the extent of well-water contamination in the state. The data are summarized in Table V-D.2. Unfortunately, the database provided only fraction of samples above the detection limit and the maximum value found. For metals with a health-based standard and a maximum value given, eight out of 10 exceeded the standard. These included all the metals with over 50% detects. On the other hand, there is no way to determine from these data what percentage of the detects were above the standard. Except for barium, copper, manganese, and zinc, only a small fraction of tested wells were above the level of detection.

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Table V-D.2: Detection of metals in drinking water samples from NYSDOH, January 1980-

January 1994.

Metal | Number of | Number of | Fraction Detection Maximum |MCL (ug/L) samples Detects detects limits (ug/L) | result (ug/L)

Al 2311 120 0.05 0.5 to 100 7,850 200* As 3072 105 0.03 10 170 50 Sb 2312 6 0.00 1 to 80 50 Ba 3295 1951 0.59 0.5 to 5 8,050 2,000 Cd 3322 23 0.01 2 to5 ll 5 Co 2238 14 0.01 0.1 to 5 171 100 Cu 2808 1785 0.64 5 5,450 1,300 Cr 3355 92 0.03 5 to 10 870 100 Pb 3685 345 0.09 5 to 10 7,000 15 Mn 3233 1919 0.59 0.02 18,000 50* Hg 3333 35 0.01 0.2 to 0.4 5.7 2 Ni 2308 148 0.06 0.5 to 5 316 Se 3042 26 0.01 5 30 50 Ag 3111 39 0.01 0.02 34 100* Vv 2235 25 0.01 1to5 221 Zn 2740 1780 0.65 0.05 to 10 8.350 5,000*

MCLs are national primary and secondary drinking water standards except for tin,

which is a New York MCL. MCLs with an "*" indicate standard is not health

related but addresses cosmetic or aesthetic effects, e.g., taste or tooth discoloration.

c. Air

The New York State Department of Environmental Conservation's ambient air monitoring system monitors for a limited number of metals in the air. Values are reported in

microgram per cubic meter of air. Data are shown in Table V-D.3a.

Using comparative risk values in Smith (1996), the air concentration data in Table VD.3a were expressed in terms of milligram metal per kilogram body weight per day for comparison with exposures from other sources. These are provided in Table V-D.3b.

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Table V-D.3a: 1994 Air sampling results (ug/m*) for metals at New York locations (NYSDEC, 1995).

Station Arsenic Cadmium Mercury Nickel Vanadium Albany 0.0017 0.0049 0.0001 0.0153 0.0019 St. Regis, 0.0017 0.0041 0.0001 0.0065 0.0061 Franklin County

Niagara Falls 0.0021 0.0033 0.0008 0.0087 0.0065. Midtown 0.0018 0.0035 0.0002 0.0571 0.0178 Manhattan

Greenpoint, 0.0019 0.0047 0.0002 0.0392 0.0133 Brooklyn

Susan Wagner, | 0.0017 0.0034 0.0001 0.0205 0.0119 Staten Island

PS 26, Staten 0.0020 0.0039 0.0001 0.0247 0.0137 Island

Table V-D.3b: 1994 Air sampling results for metals at New York locations converted to

mg/kg/day. Station Arsenic Cadmium __| Mercury Nickel Vanadium Albany 0.0000005 0.0002 0.0000002 | 0.000004 _| 0.0000005 St. Regis, 0.0000005 0.0002 0.0000002 | 0.000002 | 0.000002

Franklin Co. Niagara Falls _| 0.0000006 0.0002 0.000001 0.000002 0.000002

Midtown 0.0000005 0.0002 0.0000003 | 0.00002 0.000005 Manhattan

Greenpoint, 0.0000006 0.0002 0.0000003 =| 0.00001 0.000003 Brooklyn

Susan Wagner | 0.0000005 0.0002 0.0000002 | 0.000006 =| 0.000003 Staten Island PS 26, Staten | 0.0000006 0.0002 0.0000002 | 0.000007 | 0.000004 Island

The National-scale Air Toxics Assessment (USEPA, 2000) (NATA) is a compilation of national air toxic emissions from 1996 sources and estimated concentrations across the United States. This report became available after the ranking was completed, but illustrates an important point. NATA includes more types of emission sources than TRI, such as major stationary sources (factories, municipal incinerators) and other non-point sources (cars, trucks, small businesses, fires). The percentage of New York statewide emissions of metals from nonpoint sources ranged from 47% for chromium compounds to 94% for manganese compounds. More than half of the emissions for lead, mercury and cadmium were from non-point sources. These data may be useful to the Risk Reduction Strategies Work Group when they conduct their analysis.

d. Soil

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Metals and metal compounds are a natural part of soil. Metals in airborne particles deposit in soil. Clean background levels in soil are given in Table V-D.4. People can be exposed to metals in soil by direct consumption of soil. Children, especially, ingest dirt and dust, but adults also ingest some dirt.

Plants take up metals from soil and airborne deposition of metals contaminate plant surfaces. Home grown vegetables are a possible route of exposure to metals in soil. Fertilizers can add additional metals to soils. Table V-D.5 provides concentrations of various metals in home garden fertilizers while Table V-D.6 provides concentrations in agricultural fertilizers. Clean soil concentrations from Table V-D.4 are included in Tables V-D.5 and V-D.6 as a comparison. Depending on the character of the soil, rainfall, plant uptake rates and the specific metal, continual application of fertilizers can lead to accumulation of the metal in the soil.

Table V-D.4: Concentrations of metallic elements in clean, undisturbed soil samples, Eastern United States. Concentrations in j1g/g dry weight of soil unless indicated as percent (%) (Shacklette and Boerngen, 1984)

Metal Geometric mean_} Standard deviation Observed range Aluminum (%) 3.3 2.87 0.7 - >10 Arsenic 4.8 2.56 <0.1 - 73 Barium 290 2.35 10 - 1,500 Beryllium 0.55 2.53 <1-7 Chromium 33 2.6 1 - 1,000 Cobalt 5.9 2.57 <0.3 - 70 Copper 13 2.80 <1 - 700 Tron (%) 1.4 2.87 0.01 ->10 Lead 14 1.95 <10 - 300 Magnesium (%)__| 0.21 3.55 0.005 - 5 Manganese 260 3.82 <2 - 7,000 Mercury 0.081 2.52 0.01 - 3.4 Molybdenum 0.32 3.95 <3 - 15 Nickel 11 2.64 <5 - 700 Selenium 0.30 2.44 <0.1 -3.9 Sodium (%) 0.25 4.55 <0.05 - 5 Strontium 53 3.61 <5 - 700 Thallium 717 1.58 2.2 - 23 Tin 0.86 2.81 <0.1- 10 Titanium (%) 0.28 2.00 0.007 - 1.5 Vanadium 43 2.51 <7 - 300 Zinc 40 2.11 <5 - 2,900

In some cases, natural concentrations of a metal in soil may be above levels thought to produce health effects. More generally, however, toxic levels of metals in soil result from spills, disposal of wastes, or deposition from nearby industries or heavily trafficked roads. Hazardous waste sites frequently have toxic levels of arsenic, cadmium, mercury, and other metals in soil. Sometimes municipal sewage sludge is disposed by spreading on land. Table V-D.7 provides

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concentrations of metals in sewage sludge. As with fertilizers, continual applications over time can lead to accumulation of metals in the soil. Orchards and some agricultural lands may have excessive concentrations of metals. Table V-D.8 provides concentrations of metal in soil from major agricultural production areas of the US. Localized sites where hazardous materials have been disposed or materials containing metals were used are the principal locations of high metal

concentrations in soil.

Table V-D.5: Concentrations of selected metals in four home garden fertilizers compared to dry weight (S. Rowland, NYSDEC)

concentrations in clean soil from Table V-D.4, yg/:

Metal Product 1 Product 2 Product 3 Product 4 Clean Soil Arsenic 2.1 2.1 <0.8 13.8 48 Cadmium <0.5 2.6 0.7 0.7 - Chromium 11.9 24.6 41 22.3 33 Copper 1,000 19.6 1,360 52 13 Lead 28.6 6.3 0.8 103 14 Mercury <0.1 <0.1 <0.5 <0.09 0.08 Molybdenum <2 <2.1 10.1 <4.3 0.32 Nickel 46 <4.2 5.6 15.1 11 Selenium <0.5 <0.5 20.2 <0.5 0.30 Zinc 1,210 373 8,580 208 40

concentrations in clean

Table V-D.6: Concentrations of selected metals in two agricultural fertilizers compared to soil from Table V-D.4, ug/;

dry weight (S. Rowland, NYSDEC)

Metal Product 1 Product 2 Clean Soil Arsenic 8.0 5.3 48 Cadmium 1.0 3.1 - Chromium 23 55 33 Copper 64 <1.2 13. Lead 227 74 14 Mercury 0.41 <0.12 0.08 Molybdenum <4.2 5.3 0.32 Nickel 25.7 19 11 Selenium <0.5 <2.3 0.30 Zinc 285 28.4 40

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Table V-D.7: Concentrations of selected metals in municipal sewage sludge (Rowland, NYSDEC and Harrison et al., 1987) compared to concentrations in clean soil from Table V-D.4,

ug/g dry weight Metal Sewage Typical sludge | Recommended | Clean Soil sludge concentration Soil Maximum (Harrison et al.) | Concentration (Rowland) (Harrison et al.) Arsenic 3.4 3-10 1-10 48 Cadmium 1.1 2-15 2 - Chromium 17.2 50 - 500 52 33 Copper 51 300 - 1500 20 13 Lead 105 100 - 300 15 14 Mercury 0.34 1-10 0.1 0.08 Molybdenum <4 5 - 50 1 0.32 Nickel 25.7 10 - 150 16 11 Selenium <4 2-6 0.4 0.30 Zinc 715 500 - 2500 60 40

Table V-D.8: Concentrations of selected metals in surface soil from major agricultural production areas of the US (Holmgren et al., 1993) and typical agricultural soil in New York (Harrison et al., 1997), compared to concentrations in clean soil from Table V-D.4 and recommended maximum concentrations from Harrison et al., ug/g dry weight

Metal Holmgren et al. data Cornell data | Table V-D.4 | Cornell comparison recommended Geometric Geometric | Typical NY | Geometric Recommend mean -USA_ | standard Agricultural | mean - clean | Maximum deviation - | Soil soil (Table Concentration USA (Cornell) V-D.4) Arsenic : : <9 4.8 1-10 Cadmium 0.175 2.70 0.2 : 2 Chromium : : 52 33 See note Copper 18 2.65 20 13. 40 - 100 Lead 10.6 1.74 15 14 300 Mercury : : 0.1 0.68 1 Nickel 16.5 2.31 16 ll 25-50 Selenium : : 0.4 0.3 5 Thallium : - 0.2 7.7 1 Zinc 42.9 2.35 60 40 75-200

Note: The chemical form of chromium is critical. Cr-III is of little concern while Cr-VI is

highly toxic.

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5. Health Effects of Metals

Many metals are essential for life in trace amounts because they are used in essential biochemical reactions. These include iron, manganese, chromium, zinc, copper, cobalt, molybdenum, selenium and vanadium. Some of these same metals can be toxic if absorbed in excessive amounts. If exposures are too high, metals can cause a variety of different diseases. The specific disease and the level of toxicity varies greatly among different metals and among different compounds of the same metal. Metals with higher rankings are discussed in more detail below.

a. Arsenic

Arsenic is a naturally occurring element in the earth's crust. It is usually found combined with oxygen, chlorine, or sulfur. Arsenic combined with these elements is called inorganic arsenic, whereas arsenic combined with carbon and hydrogen is referred to as organic arsenic. The organic forms are usually less toxic than the inorganic. In some places natural deposits of arsenic result in toxic concentrations of arsenic in drinking water. This has been observed in Taiwan, India, and Pakistan with disastrous results. Smelting of copper and other metals often releases inorganic arsenic into the air. Low levels of arsenic also are produced by burning fossil fuel, wood, and cigarettes. In New York, an important source of arsenic in soil has been pesticides used in agriculture, especially in orchards and potato farms. In the past, inorganic arsenic was contained in many household products such as paints, dyes and rat poisons, but these products are no longer in general use.

Inorganic arsenic has been recognized as a poison since ancient times. Large doses can produce death. The most characteristic systemic effect of oral exposure is the appearance of dark and light spots on the skin and small "corns" on the palms, soles, and trunk. Low concentrations taken by mouth may cause irritation of the digestive tract, pain, nausea, vomiting and diarrhea. Higher concentrations or longer exposure can cause liver and kidney damage and impaired nerve function.

Total arsenic concentrations in the New York Harbor in winter flounder, bivalves and crustaceans are commonly greater then 1,000 nanograms per gram (ng/g). The greatest values are in American lobster with average values in muscle of 5,697 ng/g. These concentrations are characteristic of contaminated areas. Based on current understanding of arsenic chemistry in marine organisms, however, arsenic in edible marine fish, bivalves and crustaceans are unlikely to be a significant human health concern since it is present primarily as nontoxic organoarsenicals (NYSDEC, 1997).

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b. Cadmium

Cadmium is a naturally occurring element in the earth's crust. It is most often combined with oxygen, chlorine or sulfur. Cadmium is used mostly in metal plating, pigments, batteries and plastics. It is obtained as a by-product of smelting other metals. Small quantities occur naturally in air, water, soil and food. The largest source of cadmium released to the environment is the burning of fossil fuels or incineration of municipal waste. Food is the primary source of human exposure to cadmium. Phosphate fertilizers can add cadmium to soil and the cadmium is then taken up by crops. This route applies also to tobacco, where the cadmium is then inhaled. A single cigarette may contain 1-2 ug of cadmium.

Cadmium is not often found in water at levels of concern, although it can leach into water from pipes and solder. Water may also be contaminated from hazardous waste sites. Unlike arsenic or mercury, cadmium does not undergo methylation or form volatile compounds in the aquatic environment.

Cadmium bioaccumulates in humans, especially in the kidney and liver. Chronic oral or inhalation has been associated with renal dysfunction, bone damage, hypertension anemia, endocrine alternations and immuno-suppression. Animal experiments and epidemiological studies have demonstrated that cadmium is a probable human carcinogen when inhaled. Although no beneficial health effects of cadmium are known, typical exposures through food, water, and air (i.e., 0.0004 milligrams per kilogram body weight per day) is believed to pose little risk. The World Health Organization has set a tolerable daily intake of 0.001 milligrams per kilogram per day (mg/kg/day) and recommends a drinking water guideline of 0.005 milligrams per liter (mg/l). USEPA has established an interim maximum contaminant level in drinking water of 0.01 mg/l, with a goal of 0.005 mg/l.

c. Chromium

Chromium is found in three primary states: chromium(0), chromium(III) and chromium(VI). Chromium(0) is the pure metal, which is used in making steel and other alloys. Chromium compounds, mostly in chromium(III) and chromium(VI) forms, are used for chrome plating, pigments, leather tanning, wood treatment and water treatment. Chromium(III) is an essential element for life. Chromium in food is mostly chromium(III), which is generally not harmful, although very large doses may be harmful. Chromium(VI), however, can cause kidney and liver damage and has been designated as a known human carcinogen when inhaled (ATSDR, 1989; USEPA, 1998).

Chromium contamination has been found in about one-third of the hazardous waste sites on the USEPA Superfund National Priorities List. It is found in agricultural soils, presumably from use of fertilizers rich in chromium. It is emitted to air by a number of industrial processes and by the combustion of fossil fuels.

d. Mercury

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Mercury can combine with other elements to form compounds that are organic or inorganic. Air naturally contains about 2.4 parts per trillion (ppt) of mercury, but near mercury refineries or mines can be nearly 1,800 ppt. Mercury in air is usually inorganic. Mercury levels in water are usually less than 25 ppt. Water found at Superfund sites average 200 ppt and levels greater than 500 ppt have been found in groundwater. Some people, dentists for example, may be exposed to mercury vapor occupationally. Spills of mercury can also lead to exposure to the vapor. Mercury ranks eighth in New York on the number of emergency events (such as spills). There were 63 emergency events involving mercury from 1992 through 1996. Mercury can also enter the body through the skin. People who eat large amounts of tuna or swordfish may be exposed to high levels of mercury. In New York, mercury was present at concentrations of less than 250 ng/g in most aquatic species. Two exceptions were tautog and striped bass, with average concentrations of 267 and up to 517 ng/g respectively. Mercury concentrations in striped bass appeared to be size or age dependent. Fish from the East River and the Arthur Kill - Kill Van Kull - Newark Bay complex most frequently contained the greatest concentrations of mercury (NYSDEC, 1996).

Long-term exposure to mercury can damage the brain, kidneys and affect the development of fetuses. Breathing inorganic mercury vapor causes greater harm to the brain. Inorganic mercury salts eaten in contaminated food or drunk in water will have more of an effect on the kidneys. Organic mercury affects the brain and developing fetuses. In fact, the developing fetus appears to be the most sensitive target for organic mercury. Mercury concentrations in hair are often used to assess the level of mercury in the body. ATSDR categorized 5.9 ppm in hair as the "no adverse effects level," equivalent to 0.024 mg/l in blood (ATSDR, 1990a; ITER, 1998).

e. Lead

Lead and its compounds can be found in air, water, dust, soil, plants and animals. It is emitted from active volcanoes. Exhausts from motor vehicles using leaded gasoline was the largest source of environmental lead from the 1920s until banned by USEPA. The most common source for lead exposure for children is lead-based paint in older homes that has deteriorated into paint chips and dust. Over 80% of homes built before 1978 have lead-based paint in them. Homes built before 1950 are more likely to have lead-based paint and pose the greatest hazard to children. In addition, children may be exposed directly to soil contaminated from vehicle exhaust and weathered paint from buildings or soil may be tracked or blown into the home adding to household dust. Lead clings to fingers, toys and other objects that children normally put into their mouths. While natural levels of lead in soil are usually below 50 parts per million (ppm), soils adjacent to houses with exterior lead-based paints may have levels of over 10,000 ppm. Young children may also chew on exposed lead paint on surfaces in homes such as windowsills. Another source of lead in the home is when lead-based paint is disturbed during remodeling. The principal source of exposure of lead to adults is occupational, although adults may also be exposed in some hobbies, in lead contained in some "folk" medicines and cosmetics, and from lead in plumbing.

Lead from soil can wash into surface water during heavy rainstorms. Downward

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leaching to groundwater, however, is very slow under most conditions. The major source of lead in drinking water is not from the outdoor environment, but is lead solder in plumbing and lead in plumbing fixtures. The standard for lead in tap water is 15 parts per billion (ppb). A 1997 New York City survey of "worst case" homes found 10% of the homes had over 24 ppb. Plants can take up lead from soil in waste sites or areas with heavy automobile traffic.

Lead provides no known biological benefit to humans. It can produce adverse effects on virtually every system in the body. Pregnant women exposed to lead have a greater risk of premature birth, a low birth weight infant or abortion. Young children exposed to lead have a greater risk of impaired mental and physical development. These effects persist even after blood lead levels are reduced. Exposure to high levels of lead can damage the brain and kidneys. The New York City Health Department recommends all children from 6 months to 6 years be given blood tests for lead. The Centers for Disease Control recommend that a child's lead level should be below 10 micrograms/deciliter (tg/dl) and that children with blood lead levels over 20 g/dl need a physician's care. Typical blood lead levels in children age 1 - 5 years range from 2.5 to 3.0 g/dl. Very high blood lead levels (70 g/dl or higher), such as when a child repeatedly eats lead paint (pica) can lead to seizures, coma and death. Among children born in 1997 in New York, about 68% were tested by age two. Of these children, 4.1% had blood lead levels greater than or equal to 10 ug/dL (NYSDOH, 2000). Nationwide samples reported by the US Centers for Disease Control in the Third National Health and Nutrition Examination Survey 1991-94 found an average of 4.4% of children aged 1-5 had blood lead levels over 10 g/dL. The percentage varied by race, income, urban status, and age of housing (CDC, 1997b).

There have been great strides in reducing exposure to lead. Due to mandated and voluntary bans on the use of lead in gasoline, paint, food containers and plumbing systems and on state and local surveillance systems, there has been a dramatic decline in blood lead levels in the United States. Despite this, the risk of lead exposure remains high in children who are poor, living in older housing and/or in large metropolitan areas. In the period 1991-1994, nearly one million children age 1-5 years had elevated blood lead levels (CDC, 1997a; CDC, 1997b; ATSDR, 1990b; Xintaras, 1992; NYC, undated; NYC, 1998).

f. Silver

USEPA assigns a "no adverse effects level" of 0.014 mg/kg/day to silver. The "effect" upon which this is based is argyria, a cosmetic pigmentation of the skin, mucous membranes, and eyes. Silver has not been associated with any adverse health effects or chronic toxicity in humans and there is no evidence for carcinogenicity, neurotoxicity or reproductive or developmental toxicity resulting from exposure to silver. Because of this, the maximum contaminant level goal (MCL) for silver in drinking water was deleted in 1991. Moreover, argyria has not been reported for, and is not expected to occur as a result of, environmental exposures. Based on these data, silver poses little environmental hazard to human health.

g. Copper

Copper naturally occurs in rock, soil, water, sediment, air, plants and animals. Its

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average concentration in the earth's crust is about 50 ppm. Copper is an essential element for all known living organisms. The concentration of copper in air ranges from a few nanograms per cubic meter (ng/m*) to 200 ng/m’, although near smelters air concentrations may reach 5,000 ng/m’. Average concentration of copper in tap water ranges from 20 to 75 ppb. Many homes have copper concentrations in tap water of more than 1,000 ppb (1 ppm), picked up while sitting in copper pipes. These high concentrations decrease after the water is allow to run awhile. The average concentration of copper in surface and groundwater is 4 ppb, although some groundwater contains high levels of copper. Drinking water with 30 ppm can cause vomiting, diarrhea, or stomach cramps. Drinking water with 3 ppm over a year can cause liver damage in infants (ATSDR, 1990c).

h. Manganese

Manganese is an essential element for all living organisms. Disease states may be associated with both deficiencies and excesses of manganese. The National Research Council Estimated Safe and Adequate Daily Dietary Intake is 2 to 5 mg/day. Average dietary intakes of manganese in the U.S. are 2.3 - 8.8 mg/day, although 10 mg/day may be normal for a vegetarian diet. While the actual intakes in the vegetarian diet are higher, the availability of manganese is lower. There is some evidence that combinations of diet and drinking water intake totaling in the teens of mg/kg/day may cause neurological effects. There is some concern (although no evidence) that powdered baby formula containing manganese may pose a risk to neonates when mixed with tap water that has elevated manganese levels. This concern is based on limited evidence that neonates absorb more manganese through the gastrointestinal tract and are less able to excrete absorbed manganese (USEPA, 1997). Inhalation exposure to manganese can cause impairment of neurobehavioral function (USEPA, 1997).

i. Zinc

Zinc is an essential element, required in small doses. Insufficient zinc results in poor health and lowered immune response. Most zinc intake is through the diet. Dietary zinc intake in the US averages 7 - 16 mg/day. Potatoes contain 6 ppm zinc while fish, meat and poultry may contain 24 ppm zinc. Increased intake of zinc may result from water stored in galvanized metal containers, flowing through galvanized pipes, or contaminated by waste zinc. Excessive exposure may also occur by taking too many zinc dietary supplements. Zinc concentrations in air are generally less than 1 ug/m’, but range from 0.1 to 1.7 ug/m* near cities. Levels of zinc that are detrimental to health are well above recommended daily allowances of 15 mg/day for men and 12 mg/day for women. Doses 10 to 15 times higher than this cause digestive problems. Greater amounts of zinc may lead to interference with the immune system and the ability to take in other essential minerals. Inhalation of zinc fumes or dust from smelting or welding can produce metal fume fever. The USEPA oral RfD for zinc is 0.3 mg/kg/day, which does not meet the US Recommended Daily Allowance (RDA) for infants, preadolescent children and lactating women. Therefore, it is necessary to consider the potential health effects of deficiency as well as excess of zinc intake.

6. Identification of substances

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There are too many metallic compounds to evaluate them all in the scope of this project.

Since chemists generally can identify the elemental metal easier then metal compounds, concentrations and effects are often reported in terms of the pure metal. Metals were included in the screening if:

listed in the European Union database,

an RfD or RfC was assigned by USEPA in the Integrated Risk Information System (IRIS),

there was an OSHA or NIOSH recommended level,

there was a reported release to air, water or land in the Toxics Release Inventory (TRI) for New York.

7. Selection of stressors

The following criteria were used to select stressors for further evaluation.

Any substance with a reported TRI release

Any substance with more than 3 reported spills on the NYS HSEES in the past 5 years Any substance with an OSHA Recommended Exposure Limit (REL) less than 5 mg/m* Any substance with a Toxic Substances Control Act Chemical Update System (TSCA CUS) production for New York more than 1,000,000 pounds/year.

Any substance with EU rank greater than "harmful"

Any substance with an oral cancer slope > 0.1 per mg/kg/day

Any substance with an RfD <0.1

. Ranking the selected stressors

The data on which rankings were based are given in Appendix A, Table D.1. Metals

were ranked by chronic effects or by probability of carcinogenic effects. Concentrations in edible portions of fish above 1 ppm increased the exposure factor by one unit. Because so many metals fell into the highest toxicity ranking category, it was divided into two parts, (1a) and (1b). The division line was an oral effect at 0.1 mg/kg/day. Results are provided in Tables V-D.9 through V-D.11.

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Table V-D.9: Ranking of metals by exposure and toxicity

Toxicity Rank la 1b 2 3 4 (highest) (lowest) Exposure | 1 Lead Rank (highest) 2 Mercury Manganese Zinc (air) 3 Arsenic Barium Aluminum | Manganese | Silver Chromium (VI) Copper (water) Cadmium Iron 4 Cobalt Antimony Vanadium (lowest) Molybdenum | Nickel

Table V-D.10: Metals ranked for toxicity but not for exposure Toxicity rank

1 (highest) 2 3 4 (Lowest)

Beryllium | Chromium (III) Cyanide

Selenium | Tin

Thallium Uranium (soluble salts)

Table V-D.11: Metals with neither exposure nor toxicity rankings Magnesium | Titanium

Platinum Tungsten

Sodium Uranium (insoluble)

9. Conclusions

Among the metals with both exposure and toxicity information (Table V-D.9), there were seven metals in the "A" category: arsenic, barium, cadmium, chromium(VI), lead, manganese (in air), and mercury. Of these, only lead fell into the highest exposure category, due to exposure to children. All fell into the highest toxicity category. Aluminum, copper, iron, manganese (in water), and zinc fell into the "B" category. Nickel, silver, and vanadium were in the "C" category. Chromium, manganese, and zinc are essential elements for which too little intake can be as harmful as too much. The toxicity rank for zinc was lowered one category because the Rf£D for zinc does not provide the RDA for children and lactating women.

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Table V-D.12: Ranking of metals by category Rank | Metal

A Arsenic, Barium. Cadmium, Chromium VI, Lead, Manganese (in air), Mercury

B Aluminum, Antimony, Cobalt, Copper, Iron, Molybdenum, Manganese (in water), Zinc

Cc Nickel, Silver, Vanadium

There were no metals with information only on exposure. Of the metals with information only on toxicity (Table V-D.10), three were in the highest toxicity category, beryllium, selenium and thallium. Beryllium is highly toxic, but significant exposure is limited to beryllium workers and their associates. Selenium, on the other hand, while toxic in excessive amounts, is an essential element. Selenium deficiency results in serious disease. There were three metals in the second toxic category, chromium IIL, tin, and uranium. Chromium is relatively common in the earth's crust and is an essential element for health. Uranium is also commonly found in the earth's crust and in people, although it is not thought to be an essential element for life.

Metals combine with other elements to form thousands of compounds of alloys and compounds. Many of these are commonly found in homes, while others provide little or no exposure to the public.

10. Ranking the Stressor Group

Ranking metals against the other stressor groups is a subjective decision. Most groups are, like the metals group, broad and include highly toxic substances and much less toxic substances as well as substances to which many people are exposed and substances to which only a few people are exposed. Moreover, the kinds of effects differ substantially, from death or fatal diseases such as cancer to much less severe effects. Specific subjective judgements in ranking metals among stressor groups include (1) the relative importance of exposure vs. toxicity; (2) the relative seriousness one attributes to different diseases; (3) the relative weight one put on who is affected, e.g., children or adults; and (4) on a judgement of the relative weighting of the different substances within the range of substances in each stressor group.

Thirty-nine percent of the metals for which toxicity and exposure information were available fell into the "A" category. Among children born in 1997 in New York, about 68% were tested by age two. Of these children, 4.1% had blood lead levels indicating that they are at risk to the harmful effects of the highest ranked metal, lead. In the judgment of the author, there are only three stressor groups that might equal the risk posed by metals to the public in New York. The metal stressor group should certainly be in the "A" category.

11. Recommendations

There are six metals in the "A" category. Of these, the ones with the highest ranking are

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lead and mercury.

° Although there exist extensive programs for blood lead surveillance, reducing lead levels in older homes, and public information, it is recommended that additional effort be made to reduce lead exposure. The reasons for this are that (1) the effects of lead are irreversible; (2) young children are at the highest risk; (3) currently, much of the current effort identifies children at risk only after their blood lead levels are above the recommended value; and (4) there is no certainty that the currently recommended values are sufficiently low.

° Additional effort to reduce exposure to mercury is also recommended. There appears to be an excessive number of emergency events associated with mercury (63 in the period 1992-96). A greater effort to reduce these events seems warranted. Also, mercury (and to a lesser extent, cadmium) is found in high concentrations in fish and shell fish in New York waters. NYSDOH issues fish advisories based on NYSDEC’s extensive monitoring, and NYSDEC is working on approaches to eliminate sources. This is a longterm problem that requires continuing effort. Greater efforts are needed to identify and aid populations that subsist almost entirely on fish.

12. References

ATSDR. 1989. Chromium Public Health Statement, Agency for Toxic Substances and Disease Registry, Atlanta, GA.

ATSDR. 1990a. Mercury Public Health Statement. Agency for Toxic Substances and Disease Registry, Atlanta, GA.

ATSDR. 1990b. Lead Public Health Statement. Agency for Toxic Substances and Disease Registry, Atlanta, GA.

ATSDR. 1990c. Copper Public Health Statement. Agency for Toxic Substances and Disease Registry, Atlanta, GA.

CDC. 1997a. Facts on ... Lead. Centers for Disease Control and Prevention, National Center for Environmental Health, Atlanta, GA.

CDC. 1997b. Update: blood lead levels -- United States, 1991-1994. Morbidity and Mortality Weekly Report 46(07) 141-146, Centers for Disease Control and Prevention, National Center for Environmental Health, Atlanta, GA.

Gunderson, E.L. 1995. FDA Total Diet Study, July 1986- - April 1991, dietary intakes of

pesticides, selected elements, and other chemicals. Journal of OAC International 78: 1353-1363.

Harrison, E.Z., M.B. McBride, D.R. Bouldin. 1997. The case for caution, recommendations for land application of sewage sludges and an appraisal of the US EPA's Part 503 Sludge

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Rules, Cornell Waste Management Institute, Cornell University, Ithaca, NY.

Holmgren, G.G.S., M.W. Meyer, R.L. Chaney, R.B. Daniels. 1993. Cadmium, lead, zinc, copper and nickel in agricultural soils of the United States of America, J. Environ. Qual. 22: 335-348.

ITER. 1998. International Toxicity Estimates for Risk Database file on Methylmercury. www.tera.org.

New York State Department of Environmental Conservation. 1995. New York State Air Quality Report, Ambient Air Monitoring System. Albany, NY.

New York State Department of Health. November 1996. Chemicals in fish, shellfish and crustaceans from the New York - New Jersey Harbor Estuary, PCB, organochlorine pesticides and mercury. Albany, NY.

New York State Department of Health. November 1997. Chemicals residues in fish, bivalves and crustaceans from the New York - New Jersey Harbor Estuary, arsenic, cadmium and lead. Albany, NY.

New York State Department of Health. 1998a. Chemicals in sport fish and game. Albany, NY.

New York State Department of Health. 2000. Personal communication from Thomas Talbot, Bureau of Environmental and Occupational Epidemiology. Albany, NY.

NYC. 1998. Press Release: City making progress against lead in drinking water. New York City Department of Environmental Protection, NY.

NYC. Undated. A guide to lead poisoning. New York City Department of Health, NY.

Shacklette, H.T. and J.G. Boerngen. 1984. Element concentrations in soils and other surficial material of the conterminous United States, U.S. Geological Survey Professional Paper 1270, U.S. Government Printing Office, Washington, D.C.

Smith, R.L. 1996. Risk-based concentrations: prioritizing environmental problems using limited data, Toxicology 106: 243-266.

USEPA. 1998. Integrated Risk Information System, Chromium(VI), US Environmental Protection Agency.

USEPA. 1997. Manganese. Integrated Risk Information system. US Environmental Protection Agency.

Xintaras, C. 1992. Analysis paper: impact of lead-contaminated soil on public health. Agency for Toxic Substances and Disease Registry, Atlanta, GA.

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E. Non-volatile halogenated organic compounds (NVHOCs) 1. Steering Committee definition:

“This category includes dioxin, certain pesticides, PCBs, and a variety of other compounds that are generally of high molecular weight and contain at least one halogen atom. These compounds are likely to be both highly bioaccumulative and toxic.”

2. What are they?

Non-volatile halogenated organic compounds are a class of chemical compounds having varying degrees of halogenation; the halogen in most NVHOCs in the environment is chlorine. They are insoluble, or of extremely low solubility, in water but are readily soluble in octanol or lipids. Generally, NVHOCs are persistent in the environment and readily accumulate in biological tissues.

Examples of NVHOCs include the banned pesticides (i.e., DDT, aldrin, dieldrin, chlordane, endrin, heptachlor, mirex and toxaphene), several pesticides currently used (i.e., dicofol, endosulfan, methoxychlor, pentachloronitrobenzene), combustion byproducts or byproducts of chemical production (i.e., chlorinated dioxins, furans and quaterphenyls), insulating products (i.e., PCBs), fire retardants (i.e., mirex, PBBs), and pesticide precursors (i.e., chlorophenols, hexachlorobutadiene, hexachorocyclopentadiene), among others.

3. Sources of NVHOCs

One class of NVHOCs, the chlorinated cyclodiene pesticide group of compounds (including DDT, dieldrin, aldrin, endrin, chlordane, etc.) were produced for application as insecticides from the mid-1940's through the mid-1970's. Most uses of these substances have been banned in the United States and/or New York. However, some of these materials continue to be used in other countries and may enter the United States on foods or other products, or via global air transport. Due to their persistence and accumulative ability, residues remaining from past usage continue to accumulate in biota, in some cases to levels which exceed criteria for protection of human consumers for edible species.

Chlorinated dioxins and dibenzofurans originate as contaminants during the production of certain chemicals (such as chlorinated phenols and polychlorinated biphenyls (PCBs)), or products made from chlorinated phenols, e.g., the pesticides silvex and 2,4,5-T. Current technology has dramatically reduced or eliminated dioxin concentrations during production processes, and silvex and 2,4,5-T production and use have been banned. A current major source of dioxins and furans is the incomplete combustion of wastes (e.g., burn barrels), PCBs, chlorophenols, and certain other compounds where chlorine is present. Well-operated incinerators release little dioxin or furans. Lemieux (1997) showed that burning | to 5 days worth of a household’s waste (5 to 40 pounds) in a burn barrel could produce as much dioxins and furans as a 200 ton (400,000 pound) per day incinerator; similar findings were made for a number of other chemicals. Further, chlorinated dioxins may be present in waste oils from diesel

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engines if fuel or oil additives containing chlorine are present. Wildfires have also been documented as producing low concentrations of dioxins.

Historically, PCBs were used in a wide array of applications, including as an insulator in capacitors and transformers, in carbonless carbon paper, printing inks, immersion oils, sealants, hydraulic fluids, and fluorescent light ballasts. Production of PCBs in the United States has been discontinued and most uses have been phased out. However, PCB residuals exist in many areas of the environment in soil, sediment and water. PCBs have been disposed in many landfills, and are in over 30 permitted discharges, following activated carbon treatment, to New York waters. These contaminated areas continue to affect some biota residing in those environments and taint species used for human consumption. In addition, aerial transport of PCBs around the globe has been well documented and persists due to continued use in other countries. However, aerial sources are rarely the primary source of PCBs in New York waters, therefore, biota are seldom adversely affected by aerial sources of PCB.

4. Environmental fate

Most of these compounds are persistent in the environment, and frequently have degradation half-lives greater than one year. These compounds are fat soluble thus they readily accumulate in biological tissues, in some cases to concentrations which exceed criteria for the protection of human consumers of edible biota. In some areas of the state, NVHOC residues continue to produce mortality of birds and other organisms in the wild (Ward Stone, Wildlife Pathologist, NYSDEC, numerous memoranda). A large volume of scientific literature delves into the impacts of NVHOCs on fish, wildlife and other biota (reviews by Eisler, 1985a, 1985b, 1986a, 1986b, 1990; Eisler and Belisle, 1996; Fitchko, 1986; Gilbertson, 1988; Nessel and Gallo, 1992; Cook et al., 1993; Blus, 1996; Peakall, 1996; Niimi, 1996; Kamrin and Ringer, 1996; Hoffman et al., 1996; Sijm and Opperhuizen, 1996, and others including US Environmental Protection Agency water quality standards documents). Many of these compounds (e.g., DDT, PCB, dioxins, dieldrin, dicofol) are well known for their ability to disrupt reproduction of birds, mink, fish or other wildlife, and cause production of teratogenic responses in some organisms. Further, some compounds have been documented as causing reductions in growth, behavioral changes (including Secord and McCarty, 1997), impairment of liver or kidney functions, egg shell thinning, and changes in susceptibility to disease.

5. Health effects

Exposure to NVHOCs can occur through breathing, eating, drinking or skin contact. Health effects from exposure to these chemicals vary depending on the concentration of the substance and the length of time one is exposed to the substance. For this summary of health effects associated with NVHOCs, the stressor group has been divided into three groups: chlorinated pesticides, PCBs and dioxins and furans. Not all of the substances in this section have been associated with all of the health effects discussed here, nor are all of the health effects for each chemical discussed.

a. Chlorinated pesticides (chlordane, aldrin, dieldrin, DDT, DDD, DDE, mirex, and others)

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Swallowing large amounts of some of these pesticides have caused serious nervous system effects as well as kidney and liver damage in humans. Long-term feeding of these pesticides to animals caused liver, nervous system, kidney and reproductive system effects. All of these pesticides can cause cancer in laboratory animals; most of them cause liver cancer. None are known to cause cancer in humans (ATSDR, 1993, 1994a, 1994b and 1995a). Most of these pesticides are classified by IARC and the USEPA to be probable or possible human carcinogens.

b. PCBs

Animals fed PCBs over several weeks or months had many serious health effects, including liver, stomach, and thyroid gland damage, anemia, acne, and impaired reproduction. Some PCBs also can alter the endocrine system of animals and suppress thyroid levels, lactation and testosterone levels. Breathing very high levels of some PCBs over several months caused liver effects in animals.

Skin conditions, such as acne and rashes, can occur in people exposed to PCBs. These effects may be due to PCDD/F contaminants in the PCB mixtures. Some studies in the workplace raise concerns that exposure to PCBs may cause respiratory irritation, digestive system discomfort, changes in the blood and liver, and depression and fatigue. Human studies often have shortcomings which make it difficult to establish a clear association between PCB exposure levels and health effects (ATSDR, 1997 and 1998a).

There is sufficient evidence to conclude that PCBs cause cancer in animals. Rats fed PCBs throughout their lives developed liver cancer. Some epidemiological studies of workers raise concerns about cancer in humans but the results are not sufficient to determine if PCBs cause cancer in humans. Both IARC and the USEPA have classified PCBs as probable human carcinogens.

PCBs can cross the placenta and enter the fetus from the exposed mother. PCBs can concentrate in breast milk, so infants can be exposed to higher levels of PCBs than adults. There is sufficient evidence to conclude that PCBs impair reproduction and development in animals. Animal studies have shown harmful effects on infant behavior, increased prenatal death, and changes in infants’ thyroid and reproductive organs when mothers were exposed to PCBs. Because the nervous system, thyroid, and reproductive organs are still developing in the fetus and infant, the effect of PCBs on these systems may be greater when exposed before and shortly after birth. Some studies of human infants have associated possible exposure to PCBs with changes in birth weight or behavior; these effects are consistent with effects seen in animals exposed to PCBs (ATSDR, 1997 and 1998a).

c. Dioxins and furans (PCDD/Fs) The health effects of 2,3,7,8-TCDD and some other PCDD/Fs have been extensively

studied in animals. Some of the PCDD/Fs (such as 2,3,7,8-TCDD) are much more potent than others, and can cause health effects at much lower doses. Also, some kinds of animals are much

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more sensitive to PCDD/Fs than others. In a sensitive species, 2,3,7,8-TCDD can cause death after a single exposure to small amounts. PCDD/Fs are found as mixtures in the environment, and 2,3,7,8-TCDD is rarely the main PCDD/F found. Exposure to 2,3,7,8-TCDD can cause death, chloracne, birth defects (and other effects on the fetus) and damage to the liver, immune system and reproductive system in animals. Other PCDD/Fs are less studied; those with chlorine at the 2,3,7 and 8 positions have similar effects to 2,3,7,8-TCDD but the effects occur at higher doses.

There have been many studies of humans exposed to PCDD/Fs from accidents, workplace manufacture of pesticides, and Agent Orange spraying in Vietnam. Many of the human studies have shortcomings which make it difficult to establish an association between PCDDFF levels and health effects. People exposed to large amounts of PCDD/Fs can have chloracne, a skin disease. Changes in liver function in people exposed to PCDD/Fs have been

reported (ATSDR, 1998b). These effects are consistent with effects seen in animals exposed to PCDD/Fs.

There is sufficient evidence to conclude that 2,3,7,8-TCDD causes cancer in animals. Rats and mice fed small amounts of 2,3,7,8-TCDD for a long time developed liver and thyroid cancers. Several studies of workers exposed to high levels suggest that PCDD/F exposure may increase the risk of cancer in humans. IARC has determined that 2,3,7,8-TCDD can cause cancer in humans, but it is not possible to classify other PCDD/Fs (McGregor, et al., 1998). The USEPA has classified 2,3,7,8-TCDD and other PCDD/Fs mixtures as probable human carcinogens.

PCDD/Fs can cross the placenta from the mother to the fetus. PCDD/Fs are also found in human milk, cows milk and infant formulas. It is not known if PCDD/Fs can cause birth defects in human infants, but birth defects have been associated with exposure to PCDD/Fs in animal studies (ATSDR, 1998b).

6. Exposure

The primary sources of human exposure (80 to 90 percent) for several of these compounds are through ingestion of food (Birmingham et al., 1989; Newhook, 1988) with fish consumption being a principal food pathway for some of these compounds (Schwartz et al., 1983; Fitzgerald et al., 1996). The fish containing greatest concentrations of NVHOCs come from fresh and estuarine waters; fish from marine waters seldom have elevated NVHOC levels. PCBs are the dominant contributor to non-cancer health risks from Great Lakes fish consumption (Dourson and Clark, 1990), although certain organochlorine pesticides, dioxins and furans could contribute to the overall risk. Statewide, PCBs are the most frequent cause for health advisories to restrict consumption of freshwater sport fish (New York State Department of Health, 1998). ATSDR and USEPA (1996) consider consumption of fish containing PCBs to be a national problem with significant health consequences. In human adipose tissue, “background” PCB concentrations of 0.5 to 10 parts per million were recorded in the 1970's (Wasserman et al., 1979), but concentrations in the 1990's are expected to be lower due to reductions in PCB concentrations in food by more than an order of magnitude (Gunderson, 1988, 1995).

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PCBs in indoor air may deserve further attention since average concentrations ranging from about 90 ng/m’ to over 400 ng/m’ have been reported in buildings where PCB use has been confirmed (e.g., from fluorescent light ballasts, PCB containing sealants, natural gas use) (NYSDOH, 1982; MacLeod, 1981; Oatman and Roy, 1986; Balfanz et al., 1993; Wallace et al., 1996). The most recent data for New York are from 1982, but there are studies of PCBs in indoor air in New York underway. PCB concentrations in rural outdoor air are typically less than | ng/m* (ATSDR, 1995) while urban outdoor air averages are | to 10 ng/m*? PCB (ATSDR, 1997).

Human exposure to dioxins and furans is broader than for other NVHOCs. Nessel and Gallo (1992) indicate consumption of fish, dairy products, and meats are the primary sources of exposure to the general population while exposures to dioxins and furans in soil, air and water are much smaller or negligible sources. Occupational exposures or accidental releases represent the remaining significant potential for human exposures. The human population in North America has 6 to 7 parts per trillion of TCDD in adipose tissue (Jensen, 1987 and 1989).

7. Identification of substances

The substances for initial evaluation include: 1) all organochlorine pesticide compounds for which a U. S. Food and Drug Administration tolerance, or U. S. Environmental Protection Agency action limit has been established; 2) halogenated biphenyls and related substances; and 3) other halogenated compounds with a potential for accumulation in tissues which have been noted in scientific literature (e.g., Kuehl, 1981; Endicott and Cook, 1994; Wiemeyer, 1996). These substances, and some of their important characteristics, are included in Appendix A, Table El.

8. Selection of stressors

The stressors selected for hazard evaluation or evaluation of potential carcinogenic risk include those compounds documented to be present in New York fish, the US food supply, or in air.

9. Discussion

The concentrations of some NVHOCs, principally PCB and chlordane, in some recreationally caught fish (freshwater sport fish) exceed criteria for the protection of human consumers of fish. NVHOCs, along with mercury, are the principal cause of health advice to limit consumption of fish taken from New York waters (New York State Department of Health, 1998). As a consequence of NVHOC presence in freshwater sport fish, approximately 74.5 percent (based on surface water acreage) of the fresh waters of the state, including Lakes Ontario, Erie and Champlain, are considered use impaired. Further, about 550 miles of rivers and streams (excluding tributaries) in New York and nearly 30 percent the state’s marine district are use impaired by NVHOCs.

One dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin, is the most toxic man-made chemical

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compound known. The dose lethal to 50 percent of exposed sensitive laboratory animals (LD.)) is in the range of 1 to 50 g/kg (Hutzinger et al., 1985). Other than for several related dioxins and furans, these LD.) values are at least three orders of magnitude more toxic than values for other NVHOCs and pesticides (Tucker and Crabtree, 1970; Cook et al., 1993; Meister Publishing Company, 1997).

10. Areas not evaluated

° Soil and sediment exposures were not evaluated except as they may affect fish that are consumed. Therefore, dermal exposures were not evaluated, but they are believed to be minor compared to recreationally caught fish.

° The lack of European Union or U. S. Environmental Protection Agency classifications of several chemicals prevented human health characterization. The compounds included chloroanilines, methoxychlor, tetrachlorobenzenes, and trichlorobenzenes. All have been detected in the U. S. food supply.

° Dicofol and toxaphene have been detected in the U. S. food supply; however, no Rf{D was available for hazard characterization.

° Concentrations of many compounds in water were either not measured or not detected. Where measured, analytical techniques used were frequently inadequate for determination of these chemical residues in water at the low concentrations that are meaningful for human health evaluation. Therefore, these exposures, if any, were not evaluated.

11. Stressor ranking

Where data or information are available, each stressor has been classified or ranked by two methods. The first method employs the methodology used for all other stressors included within this Human Health Work Group report as provided in the Methods sections of this report. The findings of these assessments are provided in Table V-E1.

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Table V-E.1: Risk characterization matrix for cancer and non-cancer effects caused by non-

volatile halogenated organic compounds based on the federal limits for fish, and via consumption of food or New York fish, or inhalation of indoor air.

Toxicity Exposure 1 (highest) 2 4 (lowest) NYS fish DDT & metabolites 1 (some waters) (highest) PCBs Federal limit for fish* DDT & metabolites PCBs Toxaphene 2 Federal limit for fish NYS fish Dieldrin Chlordane (some waters) Endrin DDT & metabolites (most waters) Mirex (Lake Ontario) Federal limit for fish Aldrin Chlordane Chlordecone Heptachlor Heptachlor epoxide 3 NYSDOH limit NYS fish TCDD (as TEQs)** Chlordane (most waters) NYS fish Federal limit for fish Dieldrin (some waters) Mirex TCDD (as TEQs) (New York Harbor and Indoor air Lake Ontario fish)** Chlordane Heptachlor PCBs

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Exposure

Toxicity

1 (highest)

(lowest)

NYS fish Dieldrin (most waters) Endrin

TCDD (as TEQs) (most waters)**

Indoor air Dieldrin

NYS fish Aldrin Chlordecone Heptachlor Heptachlor epoxide HCCHs Mirex (waters other than Lake Ontario)

4 (lowest)

Indoor air Methoxychlor

Toxaphene

Indoor air Aldrin DDT & metabolites Dicofol Heptachlor epoxide HCB HCCHs

Ambient air PCBs

Federal limits for fish are the US Food and Drug Administration tolerance for PCBs and the US Environmental Protection Agency action limits for pesticides. * The scale for exposure assessment of food was reduced by three orders of magnitude for TCDD, i.e., the units

became ppt (parts per trillion).

The second method employs calculation of: a) the Hazard Index for non-carcinogenic effects, and b) the cancer risk for carcinogenic effects of each stressor for which data are available. The calculations were conducted using federal or state limits which define fish acceptable for commercial sale and serve as the basis for state health advice on consumption of fish, representative chemical residue concentrations in New York fish, chemical residues concentrations reported in the U. S. food supply, and chemical residues concentrations detected in air. The calculated hazard indices or cancer risks were then characterized in a manner similar to that provided in the standard procedures noted in the methods section of this report. The details of the assumptions and methods used for the calculation of hazard indices and cancer risks, and the findings that are derived, are provided in Appendix B.

The calculated risks for both cancer and non-cancer human health effects from consumption of the NVHOCs reported in the U. S. food supply are provided in Appendix B, Section 1. The classification of NVHOCs based on hazard indices (Appendix B, Tables B1 and B2) indicates most compounds represent a low level of risk. Moderate dietary non-cancer risks were found for adult exposure to dioxins and furans and for children’s exposure to dieldrin.

Based on the calculations in Appendix B, Tables B1 and B2, the cancer risks to adults of reproductive age are moderate to low. In general, children are exposed to greater doses of

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chemicals than adults because their intake per unit of body weight is greater than that of adults. If children had the same sensitivity to these chemicals as adults, it could be assumed that the cancer risks for children would be higher than for adults. However, calculating cancer risks for children is very uncertain because cancer potency factors that have been developed for adults have limited applicability to children. The animal studies from which cancer potency factors are derived test only adult animals; young animals and children may have different sensitivities than adults. Therefore, children’s sensitivity to carcinogens is too uncertain and the cancer risks for children were not calculated.

The consumption of fish, particularly freshwater sport fish, is a primary route of exposure for several NVHOCs. Appendix B, Sections 2 and 3 present estimates of cancer and non-cancer risks, respectively, to three populations (the general population, avid anglers and subsistence anglers) via consumption of NVHOCs in freshwater sport fish.

A description of the various populations of fish consumers used in this evaluation is necessary to lend perspective to the risk or hazard indices. In national surveys of food or fish consumption, the average adult consumes about one-quarter pound of fish per week, of which two-thirds is less contaminated marine fish. However, 75% of the general population was reported to eat no freshwater fish. Therefore the risks in Appendix B, Sections 2 and 3 are calculated separately for the 25% of the population that eats freshwater sport fish. The risks for the rest of the population are also presented and are lower. For the general population, NVHOC concentrations in freshwater sport fish were estimated by choosing the typical upper bound concentrations of these compounds in fish taken from freshwaters in New York without restrictive health advisories (New York State Department of Environmental Conservation files).

There are about 1.2 million freshwater anglers (based on license sales) and 2 million marine anglers in New York (based on national angler surveys); a small portion of anglers fish both areas. In many cases, the fish these anglers catch are consumed by their families, and, in some cases, sold to local people or markets. The avid angler is assumed to consume one-half pound of fish per week, based on national surveys, with fish consumption primarily from freshwaters having fish with NVHOC levels at federal limits for specific compounds. The characterization is the likely worst case scenario for most anglers, or their families. Regular consumption of fish having chemical concentrations at or above the federal limits is of low likelihood. Angler surveys indicate approximately 80% percent of freshwater anglers follow Department of Health’s advice regarding fish consumption (Connelly et al., 1992). Many anglers modify their fish consumption to incorporate trimming techniques which reduce chemical exposure, choose alternate species of fish containing lower concentrations of chemical residues, or use other methods to reduce chemical exposures. The remaining anglers (20 percent) choose to ignore the health advice, or are unaware of the health advice. Statewide, 85% to 90% of licensed anglers are aware of health advisories (Connelly et al., 1992). In waters not requiring a fishing license (i.e., marine waters and the tidal portion of the Hudson River), angler awareness of the health advisories is poor. Only 48% of the anglers fishing the Hudson River and 22% of anglers fishing Jamaica Bay were aware of the health advisories (Barclay, 1993).

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It is likely that there is a limited population, such as Native Americans, that because of their culture or perhaps economic status, are likely to consume a larger quantity of freshwater sport fish per week than the avid angler. The term “subsistence anglers” has been used to describe such populations. Barclay (1993) states that 10% of the surveyed population on the Hudson River indicated fishing for food was a primary reason for fishing the Hudson and these people tended to be in the lowest income categories. NYSDOH (2000) cites similar data. Connelly et al. (1992) indicated that people consuming larger quantities of fish tended to consume primarily those species with lower concentrations of chemical contaminants (e.g. panfish). To estimate risks for subsistence anglers, the typical upper bound NVHOC concentrations in fish from freshwaters without health advisories (used for the general population) were used. The USFDA estimated that the average subsistence angler consumes slightly more than 1 pound of freshwater fish per week (Bolger et al., 1990). Because the definition of a subsistence angler is still being developed, and their fish consumption patterns and possible exposure to contaminants from fish is not well known, these calculations should be updated when more data become available.

Based on Tables B-3 and B-4, cancer risk for the general population exposed to NVHOCs in fish is within acceptable ranges of risk for all organochlorine pesticides, and at the upper bound of acceptability for PCBs. However, for avid anglers, the cancer risk is greater than the acceptable range for PCBs and several organochlorine pesticides if the recreationally caught fish eaten contained these chemicals at the federal limits. The hazard indices for noncarcinogenic effects of these compounds (Tables B-5, B-6 and B-7) provides a similar relationship. Almost uniformly, the hazard index for PCB is at least an order of magnitude greater than for the several organochlorine pesticides. For avid anglers and subsistence anglers, the uncertainty factors built into the reference dose for PCBs are largely eliminated.

Cancer risk from inhalation of indoor air is estimated in Appendix B, section 4. Based on studies of indoor air in homes in Massachusetts by Zimmerman and Schaum (1990), exposure to chlordane, dieldrin, heptachlor and the lindane group of compounds may represent a moderate cancer risk in homes. However, the data must be used with caution, since the studies were conducted in the 1980s at locations outside New York. They may not represent current New York conditions where use of all these compounds have been banned. Chlordane, and dieldrin to a lesser extent, was commonly used for termite and ant control around buildings in areas with sandy soils (e.g., Long Island). Improper use of chlordane and dieldrin is known to have been made in homes (based on unpublished 1983 NYSDEC studies of over 1000 homes). Therefore, the continued presence of chlordane and dieldrin in some New York homes is expected.

PCB in air was further examined using data reported in the “Exposure” section (also see Appendix B, section 4). PCBs in outdoor air are believed to represent a low cancer risk whereas PCBs in the indoor air of homes and other buildings with significant PCB sources (such as burned-out fluorescent light ballasts) may represent a moderate cancer risk. As new New York data become available, these risks will be evaluated further.

The consolidated ranking based on cancer risks and hazard indices is presented as Appendix B, section 5. Note that the classifications derived by computation of cancer risk and

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hazard indices (Appendix B, section 5) when compared to the standard method of the HHWG (Table V-E1) are comparable in that exposure to NVHOCs via freshwater sport fish poses the greatest risk of health effects.

12. Conclusions

In developing conclusions relating to cancer risk, it is assumed that cancer risk levels in the range of 10“ to 10° may be within an acceptable range for humans although this range of cancer risk is classified as a moderate cancer risk. The following findings were developed by this assessment.

a. In general, concentrations of non-volatile halogenated organic compounds in the U. S. food supply present moderate or low levels of cancer risk to consumers. For non-cancer effects, NVHOCs in the U. S. food supply generally provide a low level of risk. Dioxins and furans in foods present a moderate risk.

b. Despite all uses being banned in New York and/or nationally, PCBs and some organochlorine pesticides continue to be present in recreationally caught fish at concentrations which exceed federal limits for fish in commercial markets. These limits are also the values used as the basis for development of health advice for consumers of freshwater sport fish.

c. The fish having elevated concentrations of NVHOCs are found primarily in fresh and estuarine waters of the state.

d. Chemical concentrations in freshwater sport fish provide the primary route of NVHOC exposure to humans. Exceptions occur for dioxins and furans where meat and dairy products also contribute to human exposures.

e. For the general population, concentrations of organochlorine pesticides found in freshwater sport fish in New York have, at most, a moderate cancer risk.

f. Typical concentrations of PCBs and dieldrin in freshwater sport fish statewide provide an elevated cancer risk to human consumers of those fish.

g. Limits for organochlorine pesticides in fish established by the U. S. Environmental Protection Agency, or the tolerance for PCBs established by the U. S. Food and Drug Administration, are uniformly too high to provide adequate protection of children and adults that consume fish. Avid anglers, subsistence anglers, and their families who frequently consume fish with elevated concentrations of PCB and/or certain organochlorine pesticides have very high risks of health effects.

h. Concentrations of some organochlorine pesticides in indoor air in homes in Massachusetts (in 1986-88) posed a moderate cancer risk (10 to 10°). Since the information is at least 10 years old and no studies are known to have been conducted in

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homes (or workplaces) within New York, there is a need to conduct studies of current exposures to people in homes and workplaces within New York.

1. There are no current data on indoor air levels of PCB in New York. Older data (over 10 years old) mostly from other states suggest that PCB in indoor air of homes, schools, and workplaces with significant sources of PCB may pose a moderate level of cancer risk.

j. Production of dioxins and furans, and other chemicals, from well-operated incinerators is far less than that from burning similar quantities of wastes in backyard burn barrels. Efficient incinerator operations are an effective means of reducing exposures to NVHOCs, particularly dioxins and furans.

13. Recommendations

Based on the findings above, several recommendations for improved management of NVHOCs include:

a. The state and federal governments should continue to review the latest toxicological and epidemiological data for NVHOCs and re-evaluate regulatory limits for NVHOCs as appropriate.

b. The state should review its methods for developing health advisories for recreationally caught fish.

c. Efforts should continue to reduce the possibility of human exposure to NVHOCs in the

state. Appropriate measures should be taken to reduce contaminant levels in fish to below those which would require restrictive advisories.

d. Studies of indoor air in homes, schools and non-industrial workplaces in New York should be done to evaluate human exposures to NVHOCs. If significant exposures are found, efforts should be considered to reduce those exposures.

14. Stressor group categorization

It is recommended that this stressor group be ranked category A for the following reasons:

a. For some stressors in the NVHOC group, particularly PCBs, the data suggest the possibility of elevated levels of cancer and non-cancer risk to avid and subsistence anglers and of health effects in newborns and children born from mothers that consumed fish containing elevated residue levels;

b. The ubiquity, persistence, and accumulation in tissues (or soils and sediments) of many NVHOCs provides a repository for continuing human exposures, even when all usage is precluded;

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c. The ability of these chemicals to be passed by the mother to the fetus via cord blood, or to the newborn via maternal milk, and the risk of adverse effects are a special concern for future generations of people; and

d. The abundance of sources of these compounds may provide some of the greatest opportunities and rewards for control efforts. However, these opportunities may also represent some of the most difficult to manage and effectively implement.

15. References

ACGIH Worldwide. 1996. 1996 TLVs and BEIs. Threshold limit values for chemical substances and physical agents, biological exposure indices. American Conference of Governmental Industrial Hygienists. 39 p.

Agricultural Profile Project Team. 1996. An agricultural profile of the Great Lakes basin: Characteristics and trends in production, land-use and environmental impacts. Great Lakes Commission, Ann Arbor, MI. 184 p. + appendices.

Aspelin, A. L. 1997. Pesticide industry sales and usage: 1994 and 1995 market estimates. 733R-97-002. Office of Pesticide Programs, U. S. Environmental Protection Agency, Washington, DC. 35 p.

ATSDR. 1993. Toxicological Profile for Aldrin/Dieldrin. Agency for Toxic Substances and Disease Registry. US Department of Health and Human Services. Atlanta, GA.

ATSDR. 1994a. Toxicological Profile for Chlordane. Agency for Toxic Substances and Disease Registry. US Department of Health and Human Services. Atlanta, GA.

ATSDR. 1994b. Draft Toxicological Profile for 4,4'-DDT, 4,4'-DDE, 4,4'-DDD. Agency for Toxic Substances and Disease Registry. Atlanta, GA.

ATSDR. 1995a. Draft Toxicological Profile for Mirex and Chlordecone. Agency for Toxic Substances and Disease Registry. Atlanta, GA.

ATSDR. 1995b. Toxicological Profile for Polychlorinated Biphenyls. Agency for Toxic Substances and Disease Registry. Atlanta, GA.

ATSDR. 1997. Toxicological Profile for Polychlorinated Biphenyls, Update. Agency for Toxic Substances and Disease Registry. Atlanta, GA.

ATSDR. 1998a. Draft Toxicological Profile for Polychlorinated Biphenyls (PCBs). Agency for Toxic Substances and Disease Registry. Atlanta, GA.

ATSDR. 1998b. Toxicological Profile for Chlorinated dibenzo-p-dioxins. Agency for Toxic

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Substances and Disease Registry. US Department of Health and Human Services. Atlanta, GA.

ATSDR and USEPA. 1996. Public Health Implications of PCBs Exposures. Agency for Toxic Substances and Disease Registry, Atlanta, GA, and U. S. Environmental Protection Agency, Washington, DC. 21 p.

Balfanz, C., J. Fuchs, and H. Kieper. 1993. Sampling and analysis of polychlorinated biphenyls (PCB) in indoor air due to permanently elastic sealants. Chemosphere 26:871-880.

Barclay, B. 1993. Hudson River Angler Survey. Hudson River Sloop Clearwater. Poughkeepsie, NY. 56 p.

Birmingham, B., A. Gilman, D. Grant, J. Salminen, M. Boddington, B. Thorpe, I. Wile, P. Tofe, and V. Armstrong. 1989. PCDD/PCDF multimedia exposure analysis for the Canadian population: detailed exposure estimation. Chemosphere 19(1-6):637-642.

Blus, L. J. 1996. DDT, DDD, and DDE in birds. Pages 49 - 71, In: Beyer, W. N., G. H. Heinz, and A. W. Redmon-Norwood (Eds.), Environmental Contaminants in Wildlife: Interpreting Tissue Concentrations, Lewis Publishers, Boca Raton, FL.

Bolger, M. M. Adams, L. Sawyer, J. Burke, C. Coker, and R. Scheuplein. 1990. Risk assessment methodology for environmental contaminants in fish and shellfish. Center for Food Safety and Applied Nutrition, U.S. Food and Drug Administration, Washington, D.C.

Cook, P. M., R. J. Erickson, R. L. Spehar, S. P. Bradbury, and G. T. Ankley. 1993. Interim report on data and methods for assessment of 2,3,7,8-tetrachlorodibenzo-p-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055, Office of Research and Development, U. S. Environmental Protection Agency, Washington, DC.

Connelly, N.A., B.A. Knuth and C.A. Bisogni. 1992. Effects of the health advisory and advisory changes on fishing habits and fish consumption in New York sport fisheries. HRDU Series No. 92-9, Human Dimensions Research Unit, NYS College of Agriculture and Life Sciences, Cornell University, Ithaca, NY. 120 p.

Dourson, M., and M. Clark. 1990. Fish Consumption Advisories: Toward a Unified Scientifically Credible Approach. Reg. Toxicol. Pharm. 12:161-178.

Endicott, D. D., and P. M. Cook. 1994. Modeling the partitioning and bioaccumulation of TCDD and other hydrophobic organic chemicals in Lake Ontario. Chemosphere 28(1):75-87.

Eisler, R. 1985a. Mirex hazards to fish, wildlife, and invertebrates: A synoptic review. Biol. Rep. 85(1.1), U. S. Fish and Wildlife Service, Laurel, MD. 42 p.

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Eisler, R. 1985b. Toxaphene hazards to fish, wildlife, and invertebrates: A synoptic review. Biol. Rep. 85(1.4), U.S. Fish and Wildlife Service, Laurel, MD. 26 p.

Eisler, R. 1986a. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic review. Biol. Rep. 85(1.7), U. S. Fish and Wildlife Service, Laurel, MD. 72 p.

Eisler, R. 1986b. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. Biol. Rep. 85(1.8), U. S. Fish and Wildlife Service, Laurel, MD. 37 p.

Eisler, R. 1990. Chlordane hazards for fish, wildlife, and invertebrates: A synoptic review. Biol. Rep. 85(1.21), U. S. Fish and Wildlife Service, Laurel, MD. 49 p.

Eisler, R., and A. A. Belisle. 1996. Planar PCB hazards to fish, wildlife, and invertebrates: A synoptic review. Biol. Rep. 31, U.S. Fish and Wildlife Service, Washington, DC. 75 p.

Fitchko, J. 1986. Literature review of the effects of persistent toxic substances on Great Lakes biota. Report of the Health of Aquatic Communities Task Force. International Joint Commission, Windsor, Ontario. 256 p.

Fitzgerald, E. F., K. A. Brix, D. A. Deres, S. A. Hwang, B. Bush, G. L. Lambert, and A. Tarbell. 1996. Polychlorinated biphenyl (PCBs) and dichlorodipheny! dichloroethylene (DDE) exposures among Native American men from contaminated Great Lakes fish and wildlife. Toxicol. Ind. Health 12:361-368.

Gartrell, M. J., J. C. Craun, D. S. Podrebarac, and E. L. Gunderson. 1986. Pesticides, selected elements, and other chemicals in infant and toddler total diet samples, October 1980March 1982. J. Assoc. Off. Anal. Chem. 69(1):123-145.

Gianessi, L. P., and J. E. Anderson. 1995. Pesticide use in New York crop production. National Center for Food and Agriculture Policy, Washington, DC. 64 p.

Gilbertson, M. 1988. Epidemics in birds and mammals caused by chemicals in the Great Lakes. Pages 133 - 152, Jn: Evans, M. S. (Ed.), Toxic Contaminants and Ecosystem Health: A Great Lakes Focus, John Wiley & Sons, New York.

Gunderson, E. L. 1988. FDA Total Diet Study, April 1982-April 1984, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc. Off. Anal. Chem. 71(6):1200-1209.

Gunderson, E. L. 1995. FDA Total Diet Study, July 1986-April 1991, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc Off. Analyt. Chem. Intl. 78(6):1353-1363.

Hoffman, D. J., C. P. Rice, and T. J. Kubiak. 1996. PCBs and dioxins in birds. Pages 165-207, In: Beyer, W. N., G. H. Heinz, and A. W. Redmon-Norwood (Eds.), Environmental

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Contaminants in Wildlife: Interpreting Tissue Concentrations, Lewis Publishers, Boca Raton, FL.

Hutzinger, O., M. V. D. Berg, K. Olie, A. Opperhuizen, and S. Safe. 1985. Dioxins and furans in the environment: Evaluating toxicological risk from different sources by multi-criteria analysis. Pages 9 to 32, Jn: Kamrin, M. A., and P. W. Rodgers (Eds.), Dioxins in the Environment, Hemisphere Publishing Corporation, Washington, DC.

Jacobs, H. L., H. D. Kahn, K. A. Stralka, and D. B. Phan. 1998. Estimates of per capita fish consumption in the U. S. Based on the continuing survey of food intake by individuals (CSFII). Risk Anal. 18:283-291.

Jensen, A. A. 1987. Polychlorobiphenyls (PCBs), polychlorodiobenzo-p-dioxins (PCDDs) and polychlorodibenzofurans (PCDFs) in human milk, blood and adipose tissue. Sci. Total Environ. 64:259-293.

Jensen, A. A. 1989. Background levels in humans. Pages 345-380, Jn: Kimbrough, R. D., and A. A. Jensen (Eds.), Halogenated Biphenyls, Terphenyls, Naphthalenes, Dibenzodioxins and Related Compounds, Elsevier, Amsterdam.

Kamrin, M. A., and R. K. Ringer. 1996. Toxicological implications of PCB residues im mammals. Pages 153-163, In: Beyer, W. N., G. H. Heinz, and A. W. Redmon-Norwood (Eds.), Environmental Contaminants in Wildlife: Interpreting Tissue Concentrations, Lewis Publishers, Boca Raton, FL.

Kuehl, D. W. 1981. Unusual polyhalogenated chemical residues identified in fish tissue from the environment. Chemosphere 10(3):231-242.

Lemieux, P.M. 1997. Evaluation of emissions from the open burning of household waste in barrels. Volume | - Technical Report. EPA-600/R-97-134a. Control Technology Center, U. S. Environmental Protection Agency, Research Triangle Park, NC. 69 p.

MacLeod, K. 1979. Sources of emissions of polychlorinated biphenyls into the ambient atmosphere and indoor air. EPA-600/4-78-022. Office of Research and Development, U. S. Environmental Protection Agency, Research Triangle Park, NC.

MacLeod, K. 1981. Polychlorinated biphenyls in air. Environ. Sci. Technol. 15:926-928.

McGregor, D. B., C. Partensky, J. Willbourn, and J. M. Rice. 1998. An IARC evaluation of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans as risk factors in human carcinogensis. Environ. Health Perspec. 106(Suppl. 2):755-760.

Meister Publishing Company. 1994. Farm Chemicals Handbook ‘94. Meister Publishing Company, Willoughby, OH.

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Meister Publishing Company. 1997. Farm Chemicals Handbook ‘97. Meister Publishing Company, Willoughby, OH.

Nessel, C. S., and M. A. Gallo. 1992. Dioxins and related compounds. Pages 163-183, Jn: Lippman, N. (Ed.), Environmental Toxicants: Human Exposures and Their Health Effects, Van Nostrand Reinhold, New York.

Newhook, R. C. 1988. Polybrominated biphenyls: multimedia exposure analysis. Contract report to the Department of National Health and Welfare, Ottawa, Canada.

Niimi, A. J. 1996. PCBs in aquatic organisms. Pages 117-152, Jn: Beyer, W. N., G. H. Heinz, and A. W. Redmon-Norwood (Eds.), Environmental Contaminants in Wildlife: Interpreting Tissue Concentrations, Lewis Publishers, Boca Raton, FL.

NYSDEC. 1991. Draft New York State Air Guide - 1: Guidelines for the control of toxic ambient air contaminants. Division of Air Resources, New York State Department of Environmental Conservation, Albany, NY.

NYSDEC. 1991. Water quality standards and guidance values. Division of Water, New York State Department of Environmental Conservation, Albany, NY. 59 p.

NYSDOH. 2000. Health Consultation: 1996 Survey of Hudson River Anglers, Hudson Falls to Tappan Zee Bridge at Tarrytown, New York. CERCLIS No. NYD980763841, New York State Department of Health, Troy, NY. 61 p.

NYSDOH. 1998. Health advisories: Chemicals in Sportfish and Game; 1998-1999. New York State Department of Health, Albany, NY. 18 p.

NYSDOH. 1997. Compilation of octanol-water partition coefficients (Draft). Bureau of Toxic Substance Assessment, New York State Department of Health, Albany, NY. 11 p.

NYSDOH, 1982. An Assessment of the Possible Impact of Natural Gas Use on PCB Levels in Indoor Air: A Study Conducted by the New York State Natural Gas Utilities. Bureau of Toxic Substance Assessment, New York State Department of Health. Albany, NY. 48 p.

Oatman, L., and R. Roy. 1986. Surface and indoor air levels of polychlorinated biphenyls in public buildings. Bull. Environ. Contam. Toxicol. 37:461-466.

Pao, E. K. Fleming, P. Guenther, and S. Mickle. 1982. Foods Commonly Eaten by Individuals: Amount Per Day and Per Eating Occasion. Consumer Nutrition Center, U.S. Department of Agriculture. Hyattsville, MD.

Peakall, D. B. 1996. Dieldrin and other cyclodiene pesticides in wildlife. Pages 73-97, In: Beyer, W. N., G. H. Heinz, and A. W. Redmon-Norwood (Eds.), Environmental Contaminants in Wildlife: Interpreting Tissue Concentrations, Lewis Publishers, Boca

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Raton, FL.

Schwartz, P. M., S. W. Jacobson, G. Fein, J. L. Jacobson, and H. A. Price. 1983. Lake Michigan fish consumption as a source of polychlorinated biphenyls in human cord serum, maternal serum, and milk. Am. J. Public Health 73:293-296.

Secord, A. L., and J. P. McCarty. 1997. Polychlorinated biphenyl contamination of tree swallows in the upper Hudson River valley, New York. Effects on breeding biology and implications for other bird species. U.S. Fish and Wildlife Service, Cortland, NY. 50 p. + tables, figures and appendix.

Seyler, L. A., J. W. Allan, D. A Rutz, and M. A. Kamrin. 1994. EXTOXNET Pesticide Information Notebook. Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and the University of California at Davis.

Sijm, D. T. H. M., and A. Opperhuizen. Dioxins: an environmental risk for fish? Pages 209228, In: Beyer, W. N., G. H. Heinz, and A. W. Redmon-Norwood (Eds.), Environmental Contaminants in Wildlife: Interpreting Tissue Concentrations, Lewis Publishers, Boca Raton, FL.

Tucker, R. K., and D. G. Crabtree. 1970. Handbook of toxicity of pesticides to wildlife. U.S. Fish and Wildlife Service, Denver, CO.

USEPA. 1996. PCBs: Cancer dose-response assessment and application to environmental mixtures. EPA/600/P-96/001F. National Center for Environmental Assessment, U. S. Environmental Protection Agency, Washington, DC. 74 p.

USEPA. 1997. Exposure Factors Handbook. Volume II. National Center for Environmental Assessment, U.S. Environmental Protection Agency, Washington, DC.

Vorhees, D. J., A. C. Cullen, and L. M. Altshul. 1997. Exposure to polychlorinated biphenyls in residential indoor air and outdoor air near a Superfund site. Environ. Sci. Technol. 31:3612-3618

Wallace, J. C., I. Basu, and R. A. Hites. 1996. Sampling and analysis artifacts caused by elevated indoor air polychlorinated biphenyl concentrations. Environ. Sci. Technol. 30:2730-2734.

Wasserman, M., D. Wasserman, S. Cucos, and H. J. Miller. 1979. World PCBs map: Storage and effects in man and his biologic environment in the 1970s. Ann. N. Y. Acad. Sci. 320:69-124.

Wiemeyer, S. N. 1996. Other organochlorine pesticides in birds. Pages 99-115, Jn: Beyer, W. N., G. H. Heinz, and A. W. Redmon-Norwood (Eds.), Environmental Contaminants in Wildlife: Interpreting Tissue Concentrations, Lewis Publishers, Boca Raton, FL.

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Zimmerman, F. W., and J. L. Schaum. 1990. Final report of the nonoccupational pesticide exposure study (NOPES). EPA/600/3-90/003. Exposure Assessment Research Division, U. S. Environmental Protection Agency, Research Triangle Park, NC.

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F. Non-volatile and semi-volatile organic compounds

The evaluation of non-volatile and semi-volatile organic compounds can be found in section N, with the volatile organic compounds.

G. Nutrients 1. Steering Committee definition:

“This category includes substances containing various elements, such as phosphorous, potassium, and nitrogen, that act to promote growth of certain unwanted aquatic species, often to the detriment of other beneficial species. These primarily reach the environment through nonpoint sources, including agricultural activities.”

2. What are nutrients?

Nutrients are included in the substances that are essential to the existence of living organisms. Many of the nutrients are fairly abundant and are needed in relatively large quantities by plants and animals. Such substances are termed macronutrients and include nitrogen, phosphorus, and potassium. An overabundance of these nutrients in an aquatic environment can promote unwanted growth of algae and other aquatic plants.

3. Sources of nutrients:

Nitrates, nitrites and phosphates are naturally occurring substances that are often found in groundwater, especially in rural areas. Nutrients are also added to the environment as a result of human activities. Major sources of nutrients are fertilizer, septic systems and manure storage and spreading. Fertilizers are also a source of trace metals and perchlorate. Other sources of nutrients include domestic waste, industrial waste, nonagricultural rural runoff, urban runoff and rainfall.

Several studies in New York State have clearly documented nitrate-nitrogen levels in drinking water. A study conducted in 1995-96 in upstate New York by Gelberg et al. included testing 419 wells supplying drinking water to farms. Overall, nitrates were detected in 95 percent of the wells tested (concentration levels greater than 0.05 mg/l) and 15.7 percent had levels which exceeded the maximum contaminant level (MCL) of 10 mg/l. Fifteen percent of the wells tested from farms where infants resided were also elevated. Wells that were shallow, dug, springs, or were located on large farms were more likely to have elevated concentrations of nitrates.

Groundwater quality monitoring was carried out in 10 wells in Suffolk County from 1975 to 1996. There were 330 analyses over the 22-year period; the average nitrate concentration for all 10 wells was 11.3 mg/l. There were periods lasting several years that had different trends in

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nitrate concentrations. The monitoring data for the period 1979 to 1984 indicate that the combined 10-well average nitrate concentration was generally decreasing to levels below the MCL, with the exception of 1981, which averaged 9.8 mg/l for this period. Conversely, from 1986 to 1991 the combined average nitrate concentration in the wells was 12.9 mg/l, or 31% greater than the 1979 to 1984 average. A specific reason for this variation was not determined.

The New York State Sanitary Code requires that a groundwater source be placed on quarterly monitoring if the nitrate level is above 50% of the MCL. When a source appears to exceed the MCL, it is taken off line and either remedial action is taken or a new source is developed. A public water system is not allowed to supply water that exceeds the MCL. Water quality is routinely monitored at the point of entry to the distribution system.

The following drinking water data were generated from a database of private and public well water samples in New York analyzed by the New York State Health Department from January 1980 to January 1994. The reasons for the sampling varied; many were sampled because of suspected contamination. Nitrites were not detected in most samples, so the median value for nitrite is somewhere below the detection limits. Wells in which nitrate in the water exceeded the MCL were predominately from private wells.

Table V-G.1: New York drinking water data from January 1980 to January 1994.

nitrites (as nitrogen) nitrates (as nitrogen) total number of samples 96 1654 number of detects 17 1061 range of detection limits (g/l) <5 <20 to <400 median result (ug/l) <5 320 maximum result (g/l) 369 58,000

There is considerable disagreement and controversy about the principal source of phosphate found in water ecosystems. Today phosphate fertilizers are thought to be the major contributors to the levels of phosphate found in water; in the past phosphate detergents were a major contributor. Phosphate detergents have been banned in New York since the 1970's.

Nitrites and nitrates are intentionally added to food, eg. to preserve bacon, ham, hot dogs, pastrami, smoked fish and cured poultry. Nitrite curing is more rapid than nitrate curing and therefore, is used more often. Nitrites are effective microbial inhibitors.

4. Environmental fate:

Most nutrients end up in water, i.e., rivers, streams, and lakes. The nitrate form of nitrogen is of concern because of the high water solubility of this ion and consequent leaching,

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diffusion, and environmental mobility in soil and water. Nitrate can contaminate groundwater to unacceptable levels. Nitrite is formed from nitrate or ammonium ions by certain microorganisms in soil, water, sewage, and the alimentary tract. Thus, the concern in the environment relates to its conversion by biologic systems to nitrite.

Phosphotus applied to the soil as fertilizer moves primarily by erosion because phosphate strongly adsorbs (sticks) on soil particles. However, some soluble phosphorus compounds do move in runoff water. Phosphate is a major contributor to eutrophication (an increase in nutrients in lakes or streams which leads to increased algal or bacterial growth).

5. Health effects:

Two health hazards associated with consumption of water containing large concentrations of nitrate or nitrite are methemoglobinemia and the potential formation of carcinogenic nitrosamines. Nitrate-nitrogen (NO,-N) is a frequently found contaminant in groundwater. The major reason for concern is the possibility of methemoglobinemia, a disease which can lead to impairment of oxygen transport in the blood. The problem is most acute in infants less than three months of age.

Epidemiological correlations have been shown to exist for an increase in the incidence of gastric cancer and the concentration of nitrate in drinking water. This evidence comes from work in Worksop, England and the mountainous areas of Columbia. This work is only suggestive and additional research is needed.

Table V-G.2: Ingestion health guidelines for nutrients

Chemical | Drinking Water MCL SDWA Reference Carcinogen Health Advisories (ug/L) Minimum — | Dose Class Longer-term and (mg/kg/day)

10 day (ug/L) Guideline Nitrate 10,000 10,000 10,000 1.0E+00 D PMCLG chronic Nitrite 1,000 1,000 1.0E-01 D subchronic 1.0E-01 chronic

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Table V-G.3: Reference doses for nutrients from IRIS

Nitrite CAS 14797-65-0 Crit dose 1 mg/kg-day

UF 1 MF 10 RfD 1.0E-01 Confid High Nitrate CAS 14797-55-8 Crit dose 1.6 mg/kg-day

UF 1 MF 1 RfD 1.6E+00 Confid High

6. Conclusions:

For the most part nutrients would appear to be more of a problem from an environmental standpoint than from a human health perspective. Increased nutrients in surface waters have been associated with an increased rate of eutrophication and algal blooms. Overproduction and ultimate decay of algae causes oxygen depletion in the deep and shallow water near the shore of lakes. This rapid growth of algae gives rise to a number of undesirable effects on treatment of the water for consumption, on fisheries, and on the use of lakes for recreational purposes.

Blue-green algae, the Cyanophyta, are known to produce exotoxins (toxic chemicals released outside the cell). When waterblooms of the Cyanophyta are present in a reservoir, lake, pond or slough, the cells and toxins can become concentrated enough to cause illness or death in almost any mammal, bird or fish that ingests enough of the toxic cells or extracellular toxin. Acute oral toxicity to humans has not been documented but there is increasing evidence that the toxins cause gastroenteritis and contact irritations in users of certain recreational and municipal water supplies.

Although the use of nitrites in food as a preservative is tangential to discussion of nutrients, the reaction of nitrite with secondary amines to form nitrosamines is worthy of mention. Nitrites are not in themselves carcinogenic but rather are precursors. Nitrosamines have produced liver damage, hemorrhagic lung lesions, and convulsions in rats.

7. Ranking the stressor group

Based on available information, this stressor group (nutrients) should be ranked in the lowest category (C). The major potential human effect of drinking water high in nitrate-nitrogen is methemoglobinemia and this occurs only in infants. Recent monitoring of water in New York has documented wells that exceed the 10 mg/l MCL of nitrate-nitrogen but a review of current literature has not documented any cases of methemoglobinemia. It is important to point out that private wells are not routinely monitored and are the major source of water containing nitratenitrogen. Caveat emptor or “let the buyer beware” applies to the consumer using a private well as a source of potable water.

8. Recommendation The major problem with nutrients in water and human health seems to be primarily with

private wells. It is not likely that the New York State Department of Health or county health departments will start monitoring private wells. Since the human health problem is primarily

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with infants, a recommendation is:

° A system for notifying individuals who expect to start a family or have infants less than three months of age should be developed. If their primary source of potable water is a private well, it should be tested for nitrate-nitrogen levels. If the MCL is exceeded, an alternative source of water should be found or adequate treatment should be utilized to reduce the nitrate-nitrogen level.

9. References

ATSDR. 1991. Nitrate/Nitrite Toxicity. Case studies in Environmental Medicine. Agency for Toxic Substances and Disease Registry, Public Health Service, U. S. Department of health and Human Services, Atlanta, Georgia. 23 pp

Amdur, M. O., Doull, J., and Klaassen, C. D. 1993. Casarett and Doull’s Toxicology. The Basic Science of Poisons. Fourth Edition. McGraw-Hill, Inc., New York. 1033 pp.

Baier, J. H., Hibbard, M. E., and Trent, M. 1996. Nitrate and Pesticide Impacts of Agriculture on Groundwater Quality, Suffolk County, New York. Suffolk County Department of Health Services, New York. 19pp.

New York State Department of Health.. 1998. Table of private and public well water samples in New York analyzed by the New York Department of Health from January 1980 to January 1994. Provided by Greg Smead.

Gelberg, K. H., Church, L., Casey, G., London, M., Roerig, D. S., Boyd, J. and Hill M. (1998?) Nitrate levels in Drinking water in rural New York State. New York State Department of Health, Bureau of Occupational Health, Two University Place, Albany, New York. 21

Pp.

Heath, D. F. and McGee, P. N. 1962. Toxic properties of dialkylnitrosamines and some related compounds. Br. J. Ind. Med., 19:276-82.

Koren, H. 1991. Handbook of Environmental health and Safety. Principles and Practices. Volume I. Second Edition. Lewis Publishers, Chelsea, Michigan. 604 pp.

Nadakavukaren, A. 1995. Our Global Environment. A Health prospective. Fourth Edition. Waveland Press, Inc., Prospect Heights, Illinois. 711 pp.

Straub, C. P. 1989. Practical Handbook of Environmental Control. CRC Press, Inc., Boca Raton, Florida. 537 pp.

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H. Particulates 1. Steering Committee definition

“This category includes dust, soot, and other small particles (PM,,) that become suspended in the air. Asbestos will be considered as well. Combustion is the primary source of particulates. Toxic substances that are associated with particulates, such as benzo(a)pyrene, are not included here.”

2. What are particulates?

Particulate matter (PM) is a complex mixture of particles of varying size, shape and chemical composition, that come from various sources. PM consists of a mineral core and, often, adsorbed substances. PM may include solid particles as well as droplets, together termed “aerosols”. Often, particles are classified by their size. Total Suspended Particulate (TSP) includes a broad range of particle sizes including up to diameters of 40 microns or greater. Particles with a diameter of 10 microns or less are called PM,, and consist of a “fine” fraction (particles with an diameter of 2.5 microns or less) and a “coarse” fraction (particles with diameters between 2.5 and 10 microns). The particles with a diameter less than 2.5 microns are called PM, ; and are able to penetrate into the respiratory tract more deeply than coarse particles. About one percent of PM,, is respirable (can penetrate to areas of the lung where gas exchange occurs) while about 80% of PM, , is respirable.

PM can also be classified by composition, physical state, or source. Dusts are solid particles arising from grinding, milling, or blasting. Fumes arise from combustion, sublimation (change from solid directly to gas), or vapor condensation. Smoke arises from combustion of organic matter. Mists and fogs are liquid droplets arising from condensation of liquid on airborne particles. Smog is the complex mixture of particles and gases arising from solar irradiation of automotive exhausts.

3. Sources of particulates

In general, particles are generated through natural processes and as byproducts of industrial practices. Fine particles are primarily generated by volatilization and condensation of combustion products. They can also be formed from coagulation or condensation of atmospheric gases. Sulfate, strong acid, ammonium, nitrate, organic compounds, trace elements, elemental carbon, and water constitute the bulk of the fine particles. Sulfur dioxide, nitrogen oxides and organic compounds can react with ozone or other chemicals in the air to form acids, ammonium sulfates and nitrates. Because many of these reactions occur more rapidly with sunlight and heat, higher concentrations of PM are common during the summer.

Coarse particles are primarily generated from mechanical processes such as crushing, grinding, blasting and scraping of surfaces. Mining and agricultural practices are sources of coarse particles. The natural components of coarse PM are wind blown dust and sea salt. The coarse particle fraction contains components from minerals in the earth’s crust, dust from human

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activities, fly ash from combustion of fossil fuels and particles of biological origin, such as pollen, fungal spores and plant and insect parts. A recent study of particulate emissions in midtown Manhattan found that diesel exhaust was the major source of PM,). Personal exposure to particles occurs both indoors and outdoors. A portion of the particles found indoors originate from outdoor sources. Examples of indoor sources of particles are cooking, smoking, vacuuming, sweeping and dusting.

4. Environmental fate

Particles are removed from the atmosphere by precipitation and gravitational settling. PM may react chemically with volatile components of the atmosphere. PM may also interact with water, causing particles to swell. Swelling can alter PM size and density, changing the dynamics of deposition. Once deposited, PM may be resuspended. However, the size distribution of PM which is resuspended is likely to differ from that of PM which precipitates, because the larger particles are more difficult to resuspend.

Fine particles are transported longer distances and have a longer residence time in air compared to coarse particles. This results in the more uniform distribution of fine particles across large geographical areas and contributes to the problem of regional haze. The regional transportation of fine particles makes controlling air levels difficult to address on a purely local basis. Coarse particles, although not entirely attributable to local sources, are more amenable to local control.

5. Health effects

Exposure to particles can occur through breathing, swallowing, and skin contact. The exposure route of greatest concern is inhalation. Factors that may contribute to health effects are the amount, shape, surface area and size of the particle. Current research indicates that health effects may arise from exposure to particles and/or chemicals adsorbed to their exterior surfaces. Large particles are deposited in the mouth, larynx and nose. Smaller particles are able to travel further and may deposit in the tracheal and bronchial regions and still smaller particles can reach the bronchioles and alveoli of the lungs. An individual’s age, gender, ventilation rate and expiratory force are personal factors that affect the deposition pattern of particles. Particle retention in the respiratory tract can vary depending on the deposition rate and the body’s efficiency of clearing particles from the system.

Currently, the biological mechanisms by which particles produce health effects are only partly understood, but epidemiological studies have associated PM with numerous public health impacts. These have included increases in mortality, elevated hospital emergency room visits, elevated hospital admissions; increased severity of respiratory symptoms and incidence of respiratory diseases, such as asthma, reduced lung function, lung tissue alterations, reduced respiratory tract particle clearance efficiency and reduced resistance to respiratory pathogens. Sensitive subpopulations have been recognized, including individuals with pre-existing respiratory and/or cardiovascular disease. The association between higher ambient particulate levels and adverse health effects has been reported following both short and long term

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exposures.

PM is complex and variable, making it difficult to determine the biological mechanism(s) and specific etiological agents underlying the associations found in the epidemiological studies. Many factors, such as the size and the chemical composition of the PM, the presence and role of other air contaminants, the relationship between outdoor and indoor air concentrations of PM, and the age and existing health status of those effected, must be considered. Currently there are many studies, such as the Health Effects Institute Particles Program (sponsored by the USEPA and the motor vehicle industry), underway to investigate these factors.

6. Asbestos

Asbestos is the name of a group of six different minerals (amosite, chrysotile, tremolite, actinolite, anthophyllite, and crocidolite) that occur naturally in the soil and rocks in some areas. These minerals are made of fibers that are tasteless and odorless. Asbestos fibers are resistant to heat and most chemicals and have been used in a wide range of man-made products such as building materials (shingles, ceiling and floor tiles, insulation, cement), brake and clutch linings and heat-resistant fabrics. Asbestos fibers may be suspended in the air from natural weathering and the break down of man-made asbestos products. Fibers may be carried long distances before settling. Asbestos does not move through soil and does not break down into other chemicals in the environment.

One is most likely to be exposed to asbestos by breathing fibers in the air. Indoor air in buildings with crumbling asbestos materials can have high levels. Fibers that are inhaled can deposit in air passages and in the lungs. Asbestos workers exposed to high levels of asbestos in the air may develop a scarring of the lungs called asbestosis. This lung disease leads to difficulty breathing and possible heart disease. Asbestos workers were also found to have two types of cancer; lung cancer and mesothelioma, a cancer of the lining that surrounds the lung and other organs. The risk of cancer increases with the level of asbestos fibers in the air, the length of time exposed, and cigarette smoking. Mesotheliomas have also been diagnosed in family members of asbestos workers. Asbestos is classified as a known human carcinogen by the USEPA (1998) and IARC (1998). There is a scientific debate about the potency of different fiber types and sizes. There are some studies which suggest that tremolite, amosite and crocidolite may be more potent than chrysotile. Most studies show that long fibers are more likely to cause cancer than short fibers.

There are both federal and New York regulations to minimize exposure to asbestos. New uses of asbestos are banned, and there are regulations on the release of asbestos from factories or during building demolition or renovation. The disposal of asbestos is regulated. Schools are required to inspect for and remediate asbestos materials. There are regulations to protect workers who work with asbestos-containing materials. There are also regulations to limit asbestos in drugs, food packaging and drinking water.

7. Selection of Stressors

Particulate matter can be categorized into various fractions based on particle density

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(size) or chemical composition (sulfate, strong acid, ammonium, nitrate, organic compounds, trace elements). The steering committee definition specifically excluded consideration of chemical composition from this stressor group. Most epidemiological studies have characterized the size of the PM studied. Therefore, stressors were selected based on particle size: TSP, PM,, and PM, ;. Asbestos was considered as a separate stressor.

8. Ranking the selected stressors

Background levels (from biological and geological sources) of PM are estimated to be above the highest category in the HHWG’s exposure classification scheme. For this reason, the ranking scheme described in the methods section was not used. PM was ranked by comparison of monitored levels in New York to levels associated with health effects in epidemiological studies and to USEPA standards. Asbestos was ranked using the standard classification scheme.

9. National Ambient Air Quality Standard for particulate matter

New York is subject to federal regulations of PM. The National Ambient Air Quality Standard (NAAQS) for particulate matter was 150 ug/m? for the PM,, 24-hour average and 50 ug/m? for the PM,, annual average. The new NAAQS, which went into effect in September of 1997, retains the annual average and 24-hour average standards for PM,, and establishes a new 15 ug/m* PM, ; annual average and 65 ug/m? PM, , 24-hour average (USEPA, 1997, 40 CFR Part 50).

10. PM concentrations in air a. Annual and 24 hour averages

PM levels have been measured by various agencies at a number of rural, suburban and urban sites across the US. The USEPA has collected and reported summaries of these data. Annual average non-urban levels of PM,, in the northeastern US have ranged from 12 to 25 ug/m*. The annual average PM,, concentration in urban areas in the northeastern US in 1994 was 23 ug/m*. In 1986, annual average levels of PM, ; in the northeastern US have ranged from 9 to 16 ug/m? in non-urban areas and 20 to 28 ug/m? in urban areas. On an annual average basis, the ratio of PM, ; to PM), is often near 0.6, but these values are highly variable and can be higher or lower on individual days or in specific locales (USEPA, 1996).

The NYSDEC measures levels of TSP at 27 sites and PM,, at 50 sites in various areas around the state. Most of the sites are located in urban areas; a few are located in rural or remote areas. The composite annual average of PM,, for all sites in New York has decreased steadily from 32 ug/m* in 1986 to 20 ug/m? in 1997. Annual average levels in 1997 were below the state and federal standard of 50 ug/m’ at all but one site (51 ug/m? at a Manhattan site). Annual averages ranged from 11 ug/m? at Whiteface mountain to 51 ug/m* on Broadway in Manhattan. The highest 24-hour average PM,, level was 105 ug/m? measured on Madison Ave. in Manhattan (the state and federal standard is 150 ug/m*) (NYSDEC, 1998).

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Composite annual average TSP levels for all sites in New York were generally between 40 and 50 ug/m’ during the 1980s and between 30 and 40 ug/m’ in the 1990s. The composite annual average for 1997 for all sites was 35 ug/m*. The annual averages for individual sites ranged from 23 ug/m? in Hudson to 117 ug/m? on Madison Ave. in Manhattan (the only site that exceeded the state standard). The Madison Ave. monitor is a special purpose monitor located at the curb rather than at roof level like most other monitors. Levels at curbside do not measure the same exposure as those at roof level. The highest 24-hour average TSP level was 185 ug/m’ also measured on Madison Ave. in Manhattan; the state standard is 250 ug/m? (NYSDEC, 1998).

The NYSDEC began monitoring for PM, ; at four sites in New York City in 1997 and is in the process of implementing more monitoring sites across the state. The measurements made in 1997 did not use the USEPA method that is required for comparison to the new standard. In addition, three of the four sites were at ground level and more likely to be impacted by vehicle emissions. For these reasons, it may not be valid to compare these data to the new standard. However, a comparison does provide a preliminary indication of whether the new standard will be met in 1999. The annual averages for PM, ; in 1997 for the four sites in New York City ranged from 21 to 37 ug/m’ with a composite average for all 4 sites of 29 ug/m’. These averages exceeded the NAAQS of 15 ug/m’. The maximum 24-hour average was 91 ug/m’. Three out of four sites had at least one 24-hour average above the NAAQS of 65 ug/m’.

Table V-H.1: Levels of PM, ;, PM,, and TSP measured in NY in 1997 (ug/m’) PM,y TSP PM, ;*

measured | federal | measured state measured | federal levels standard levels standard levels* standard

composite annual

average (all NY 20 50 35 75 29* 15 sites)

annual average 23 to

(range for individual | 11 to 51 50 117** 75 21 to 37* 15 sites)

24-hour average (maximum for an 105 150 185 250 91* 65 individual site)

* PM, ; levels were measured only at 4 sites in New York City. Three of the four sites were at ground level. These levels were not measured using the USEPA method.

**Madison Ave. in Manhattan (annual average TSP of 117 ug/m’) was the only site above the standard, this monitor was located at the curb instead of roof level.

b. Short-term excursions

The scientific literature was reviewed to identify data sets where 24-hour average PM.) levels were within the current NAAQS, but which exhibited shorter term PM levels exceeding

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150 ug/m*. Screening identified three locations, and 10 days, which met these criteria (Michaels, 1996; Michaels, 1998; Michaels and Kleinman, 1997; Michaels and Kleinman, 2000).

In Birmingham, Alabama on April 16, 1990, 24-hour average PM,, was 70 ug/m’, but two one-hour average excursions exceeding 200 ug/m’ were recorded (Meyer, 1993). In Penticton, British Columbia on approximately eight days between 30 July and 7 August 1994 24-hour average PM,, varied from close to zero to close to 150 ug/m’, but excursions exceeding 150 ug/m? were recorded on four of the eight days. These included three one-hour average excursions to 300 ug/m’ and two excursions to approximately 500 ug/m* (Rupprecht, et al., 1995). In Zeebrugge, Belgium on 15 March 1993 24-hour average PM, was 101 ug/m’, but several 15-minute average excursions exceeding 200 ug/m’ were recorded (IHE Belgium, 1993). In one excursion, the 15-minute average reached 2,000 ug/m’, significantly exceeding the estimated magnitude, though not the persistence, of the 1952 London fog. Particle levels during the 1952 London fog, during which some 4,000 people died over a period of 10 days, have been estimated at 1,200 ug/m? (Schwartz, 1993).

Excursions attained levels from 0.1 to 1.6 times the London fog benchmark. Four of 27 excursions (15 percent) reached at least 0.5 of the London fog level. These estimates are based upon the conservative assumption that the average London fog particle mass estimate consisted of only PM,,, whereas PM,, may have represented only a fraction of this estimate. These data indicate that short-term excursions above the 150 ug/m’ level can occur even when the 24-hour average PM,, level is below the federal standard.

c. Asbestos

Many measurements of asbestos fibers in air have been made. The following table shows typical ranges of concentrations in certain types of locations.

Table V-H.2: Asbestos concentrations in air

location asbestos concentration* (ug/m*)

Outdoor air, remote from any asbestos sources 10° to 10*

Outdoor air, urban areas 10* to 107

Outdoor air, industrial asbestos operations 5x 10° to5

Indoor air, variety of locations 10° to 2 x 10"

Indoor air, buildings with asbestos containing materials | 2 x 10° to9 x 10°

* Data from ATSDR, 1993

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11. Toxicity a. Epidemiological studies of PM

Several epidemiological studies conducted within the last decade show increases in daily mortality are associated with increased 24-hour concentrations of particulate matter. The studies were conducted at multiple locations in the United States and abroad and evaluated monitored levels of ambient particles using various measures of particulate concentrations. Statistically significant increases in the risk for mortality are associated with increases in PM,, of 50 ug/m* above baseline in air over a 24-hour period. The average levels of PM, in these studies were often below the 150 ug/m’ federal standard for a 24-hour period. Several studies found similar results for TSP. Relatively little information on mortality associated with PM, ; levels is available; one recent study in six US cities suggests increased risk of mortality associated with an increase of 25 ug/m? above baseline over a 24-hour period (USEPA, 1996).

Morbidity effects have been studied to examine their relationship with PM exposure. Several studies have found that increases in hospitalization due to chronic obstructive pulmonary disease (COPD) and pneumonia are associated with increases of 50 ug/m’ in PM,, above background. Also, some studies indicate possible associations between increased PM exposure and increases in respiratory symptoms and lung function (assessed by measuring airflow while subjects exhale). Sensitive populations such as the elderly and those with pre-existing respiratory diseases may be at higher risk than the general population (USEPA, 1996).

b. Studies assessing short-term exposure to PM

Some studies of health effects associated with short-term exposure to PM report the following:

e Asthmatics in clinical studies with controlled exposures to short-term (30 minutes) concentrations of PM (202 ug/m*) exhibited measurable respiratory effects.

. In studies of asthmatics and PM concentrations in ambient air, asthmatics reported more severe respiratory symptoms associated with uncontrolled daily, 8-hour and 1-hour exposures to elevated PM levels.

° Dogs exposed to high levels (1,000 to 3,000 ug/m*) of PM for 3 to 4 hours/day exhibited abnormal electrocardiograms (EKGs) and temporary absence of breathing (apnea). Rats with pre-existing respiratory pathology exposed to lower levels (228 to 288 ug/m*) of PM for 3 hours/day exhibited apnea, broncho constriction, decreased breathing rates and increased mortality.

° Rats exposed to 5-minute excursions above a steady-state concentration of PM exhibited an increased area of lesions in the lung compared to rats exposed to a steady-state concentration with no excursions. Rats exposed to four excursions exhibited increased areas of lesions compared to rats exposed to one excursion.

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These studies are summarized below. Further details on these studies are available in Appendix A, Table H.1.

Two studies have reported respiratory effects in asthmatics at rest (Yang and Yang, 1994) or engaged in exercise (Utell, et al, 1989) beginning at levels as low as 202 ug/m’ and at exposure durations as short as 30 minutes. Health effects included increased airway resistance, reduced lung function and symptoms such as throat irritation and coughing. Other positive studies likewise involved asthmatic subjects exercising or at rest, of ages up to 57 years (Balmes, et al, 1988; Framptom, et al, 1992; Green, et al, 1989; Morrow, et al, 1994).

In addition to the clinical studies described above, in which exposure of asthmatics to PM was controlled, are two studies in which exposure to PM was uncontrolled. Lawther, et al. (1970) reported a clear association of symptom severity with daily concentrations of smoke or sulfuric acid in London. They concluded, however, that this association could not be attributed to the measured 24-hour average concentrations, but more likely to "the effects of brief exposures to the maximum concentrations occurring during the day", which may be several times the 24-hour average (Waller and Commins, 1966). A second clinical study in which exposure of asthmatics to PM was uncontrolled was conducted by Delfino, et al. (1997). Asthma symptom severity was found to be associated with PM levels. Significantly, the strength of the association increased as PM averaging time decreased from 24 hours to eight hours to one hour.

The studies described above demonstrate adverse health effects in humans induced by short-term exposure to particles. Investigations into airborne particle-induced effects on rats and dogs implicate short-term, possibly electrophysiological mechanisms of fine-particle-induced cardiopulmonary malfunctioning, shown via electrocardiograms (EKGs). Nearing, et al. (1996b) induced abnormal EKGs and periods of apnea (temporary absence of breathing) in dogs inhaling fly ash at 1,000 ug/m? for 3 days, 4 hours/day. Nearing, et al. (1996a) also demonstrated apnea and abnormal EKGs, indicating vulnerability to heart attacks, in dogs inhaling fly ash at 3,000 ug/m* for 3 days, 3 hours/day.

PM lethality has been demonstrated empirically in animal models. Godleski, et al. (1995, 1996) used rats with respiratory pathology previously produced in the laboratory. These rats then inhaled particles concentrated from Boston air at 228 to 288 ug/m’ for 3 hours/day. Apnea, broncho constriction and a decrease in breathing rate occurred in exposed rats compared to controls. Deaths occurred on all exposure days, possibly as a result of heart or respiratory malfunction.

Two bioassays were conducted in which aerosols were delivered either constantly at the average concentration, or included excursions. The bioassays represent results obtained in an investigation by Kleinman, et al. (1989), but excluded from that report because it did not address the issue of excursions. In both bioassays, rats were exposed for four hours to either of two aerosols using the published methods. However, in the unpublished bioassays, the rates at which the aerosols were delivered included either one or four excursions, defined as elevations of at least 50 percent above an otherwise steady state concentration, lasting for at least five minutes.

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Except for the excursions, treated and control rats experienced identical exposures. Greater lesion area in the lung was found in rats exposed to aerosol excursions. In the bioassay with four excursions, the increased lesion area in exposed rats over control rats was greater than in the bioassay with only one excursion.

12. Discussion

Numerous epidemiological studies indicate that exposure to TSP, PM,, or PM, ; is associated with increases in human morbidity and mortality. However, conclusions drawn from epidemiological studies can be limited by numerous factors, including potential confounders, applicability and quality of the environmental monitoring data, and assessment of health endpoints. Further study may answer some the following questions:

° What are the toxicological effects of PM in relation to size and chemical composition?

° How applicable are ambient air data from a single monitor to personal exposures (which do not occur at the monitoring site)?

° What is the role of indoor air vs. outdoor air exposures and what fraction of indoor PM is from outdoor sources?

° To what degree are health effects correlated with chronic exposures and/or short-term excursions that are above the average daily concentrations?

° What is the effect of other variables (such as levels of other air contaminants, subjects’

health status and age, lifestyle choices such as exposure to tobacco smoke) on mortality and morbidity measures?

Short-term PM,, levels can exceed 24-hour average levels by an order of magnitude even though the 24-hour average is below the 150 ug/m* NAAQS (Michaels, 1996; Michaels, 1998; Michaels and Kleinman, 1997; Michaels and Kleinman, 2000). PM levels of 202 ug/m* over thirty minutes have exerted toxicological effects upon asthmatics. These levels are comparable to short-term levels of PM measured in ambient air. Such excursions might constitute a previously unrecognized cause of mortality and morbidity revealed by epidemiology studies based upon 24-hour average PM levels. USEPA's decision to change the PM standard may be justified by residual health risks associated with the old standard. However, the time required for PM to cause adverse effects may be briefer than the time interval over which the effects commonly have been observed (Michaels, 1997). Effects exerted by PM may be caused by exposure to brief PM excursions which may be obscured by dilution within 24-hour PM averages routinely reported.

Greater reduction of residual risks posed by PM within the old NAAQS may be achievable via control of one-hour PM averages than by control of 24-hour averages. Recommending that further study is desirable should not imply that controlling one-hour average PM should be delayed until further information is available. Pollution prevention strategies could be useful in controlling short-term excursions of PM. Companies should be encouraged to explore ways of complying with a one-hour PM limit, and compare estimated compliance costs of a one-hour vs. 24-hour limit. In many, if not most, industries controlling PM excursions to a one-hour mass limit of, say, 300 ug/m’ can be achieved more economically than controlling

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24-hour averages, because industrial processes often include brief periods of reduced PM control, when excursions occur.

Although NYSDEC monitoring data did not indicate what the major sources of PM are, high PM concentrations from curbside locations in New York indicate that vehicle emissions can be a significant source of PM. This is another area where pollution prevention should be considered.

13. Ranking the stressors a. PM

Epidemiological and clinical studies have reported associations between exposure to PM and human health effects. Air monitoring in New York indicates that the levels of PM,, and TSP are declining and are generally below the federal standard. However, monitoring for PM,; was recently implemented at a limited number of New York City sites. These data were not collected using the USEPA method and therefore are not directly comparable to the new NAAQS. However, these data give a preliminary indication that PM, ; levels may exceed the new federal standard in coming years. Therefore, PM,, and TSP are ranked B, and PM, is ranked A in light of the recent monitoring data.

b. Asbestos

Asbestos was ranked in the following matrix using the standard method developed by the HHWG. Typical exposures in indoor or outdoor air are ranked B. Asbestos is a known human carcinogen but it is typically found at very low levels in air, even in buildings with asbestoscontaining materials. However, occupational exposures to asbestos are higher and would justify an A rank.

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Table V-H.3: Ranking matrix for asbestos.

toxicity rank

1 (highest) 2 3 4 (lowest)

exposure rank 1

1 is highest, 2 | outdoor air

4 is lowest near industrial asbestos

operations

4 | typical indoor and outdoor air

14. Recommendations

More research is needed on both exposure to PM and the toxicity of PM. Data are needed to assess:

° Relationship between ambient air levels of PM and personal exposures,

° Exposures to the PM components and characteristics that are most associated with health effects,

° Relationship between PM, other air pollutants and human health effects,

e Those features of PM (size, composition) that are most related to health effects,

° The biological mechanism(s) by which PM may cause health effects.

Of particular importance is the question of exposure to short-term high levels of PM that are masked by the reporting of 24-hour averages. The relationship between one-hour average levels of PM in New York and human morbidity and mortality should be studied and pollution prevention should be used to control short-term excursions of PM.

Pollution prevention should also consider the feasibility of further control of PM from mobile sources. This stressor group should be reassessed as more information becomes available.

15. Ranking the stressors as a group

It is recommended that particulate matter be assigned a rank of A/B. Evidence indicates that certain human populations exposed to PM at levels above a threshold dose over a particular time period have a higher risk of experiencing adverse health effects. An A rank is difficult to justify given that much research still is needed to determine what types of PM, what levels and what exposure periods are most associated with potential effects. A lower ranking is

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inappropriate because increases in human mortality have been associated with increased exposure to PM and one of the sensitive subpopulations (the elderly) is a large part of the population.

16. References:

ACGIH. 1996. Threshold Limit Values for Chemical Substances and Physical Agents, Biological Exposure Indices. American Conference of Governmental Industrial Hygienists. Technical Affairs Office. Cincinnati, OH.

ATSDR. 1993. Toxicological Profile for Asbestos. Update. Draft for Public Comment. Agency for Toxic Substances and Disease Registry. US Department of Health and Human Services. Atlanta , GA.

Balmes, J. R., et al. 1988. Acidity potentiates broncho constriction induced by hypo- osmolar aerosols. American Reviews of Respiratory Disease, 138:35-9.

Delfino, R. J.; et al. 1997. Effects of PM-10 and ozone on symptoms and peak expiratory flow in asthmatics living at the inversion base. Abstract. Proceedings of the American Lung Association and American Thoracic Society International Conference; San Francisco, California; 17-21 May 1997.

Framptom, M. W., et al. 1992. Sulfuric acid aerosol exposure in humans assessed by bronchoalveolar lavage. American Reviews of Respiratory Disease, 146:626-32.

Godleski, J. J. 1995. Oral and written report to the PM10 Review Panel, USEPA Clean Air Science Advisory Committee (CASAC). Research Triangle Park, North Carolina; 14 December 1995;

Godleski, J. J., et al. 1996. Death from inhalation of concentrated ambient air particles in animal models of pulmonary disease. ; American Thoracic Society 1996 International Conference, New Orleans, Louisiana, 11-15 May, Am. J. Respir. Crit. Care Med. 153:A543..

Green, D. J., et al. 1989. Acute pulmonary response in healthy, non-smoking adults to inhalation of formaldehyde and carbon. Journal of Toxicology and Environmental Health, 28:261-75.

Health Effects Institute Particles Program. 1999. HEI Program Summary: Research on the effects of particulate air pollution on mortality and morbidity. www.healtheffects.org/particle

IARC. 1998. International Agency for Research on Cancer. Lists of IARC evaluations. www.iarc.fr World Health Organization. Lyon, France.

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Institute of Hygiene and Epidemics (IHE) Belgium. 1993. Unpublished data.

Kleinman, M. T., et al. 1989. Health effects of acid aerosols formed by atmospheric mixtures. Environmental Health Perspectives, 79:137-45.

Lawther, P. J., R. E. Waller, and M. Henderson. 1970. Air pollution and exacerbations of bronchitis. Thorax, 25:525-539.

Meyer, M. B. 1993. Applications of continuous PM,) measurements. Paper presented at the Conference on the Role of Meteorology in Managing the Environment, Scottsdale, AZ. 26-28 January 1993. Air and Waste Management Association 45(5):320-382.

Michaels, R. A. 1998. Permissible daily airborne particle mass levels encompass brief excursions to the 'London fog' range which may contribute to daily mortality and morbidity in communities. Applied Occupational and Environmental Hygiene, 13(6):385-394.

Michaels, R.A. 1997. Particulate matter policy. Science. 278:1696. (Letter)

Michaels, R.A. 1996. Airborne particle excursions contributing to daily average particle levels may be managed via a |-hr standard, with possible public health benefits. Aerosol Science and Technology. 25:437-444.

Michaels, R.A. and M.T. Kleinman. 1997. Health risks support a one-hour airborne particle standard with data acquisition via rapid automated monitoring instrumentation. Proceedings of the 90th Annual Meeting and Exhibition of the Air& Waste Management Association, June 8-13, 1997. Toronto, Ontario, Canada. 21 pp.

Michaels, R.A. and M.T. Kleinman. 2000. Incidence and apparent health-significance of brief airborne particle excursions. Aerosol Science and Technology. 32:93-105.

Morrow, P. E., et al. 1994. Effects of near ambient levels of sulphuric acid aerosol on lung function in exercising subjects with asthma and chronic obstructive pulmonary disease. Annals of Occupational Hygiene, 38(Supplement 1):933-938.

Nearing, B. D., et al. 1996a. Inhaled fly ash results in alteration in cardiac electrophysiologic function. New Orleans, Louisiana; American Thoracic Society 1996 International Conference, 11-15 May, abstract in press, 1996.

Nearing, B. D., et al. 1996b. Exposure to inhaled environmental air particles results in significant ST-segment elevation in dogs with normal coronary arteries. American College of Cardiology 45th Annual Scientific Session, Abstract No. 075548, abstract in press, 1996.

NYSDEC, 1996. New York State Air Quality Report Ambient Air Monitoring System, 1995

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Annual DAR 96-1. New York State Department of Environmental Conservation, Division of Air Resources. Albany, NY.

NYSDEC, 1998. Aerometric Information Retrieval System for NYS, 1997. Provided by Robert Majewski, New York State Department of Environmental Conservation, Division of Air Resources. Albany, NY.

Rupprecht, E., Meyer, M.B., Patashnick, H. 1995. Performance characteristics of a near realtime ambient particulate mass monitor. Paper presented at the USEPA and Air & Waste Management Assoc. Conference on Particulate Matter: Health and Regulatory Issues, Pittsburgh, PA, 1-6 April 1995.

Schwartz, J. 1993. Environmental pollution and human health: an epidemiology perspective. Chapter 11 in: C. R. Cothern and N. P. Ross (editors), Environmental Statistics, Assessment, and Forecasting; Boca Raton, Florida; Lewis, pp. 209-222.

US Environmental Protection Agency. 1996. Air Quality Criteria Document. Air Quality Criteria for Particulate Matter. Volume I of III. Office of Research and Development. EPA 600/P-95/001aF. Washington, DC.

US Environmental Protection Agency. 1997. 40 CFR Part 50, National Ambient Air Quality Standards for Particulate Matter; Final Rule. Federal Register. Vol 62 (138): 38652.

US Environmental Protection Agency. 1998. Integrated Risk Information System. Asbestos. www.epa.gov.

Utell, M. J., et al. 1989. Effect of inhaled acid aerosols on respiratory function: the role of endogenous ammonia. Journal of Aerosol Medicine, 2:141-147.

Waller, R. E., and B. T. Commins. 1966. Episodes of high pollution in London, 1952-1966. In: National Society for Clean Air, London, Proceedings of the International Clean Air Congress, London, 1966, Part I, p. 228.

Yang, S.C., and S.P. Yang. 1994. Respiratory function changes from inhalation of polluted air. Archives of Environmental Health, 49:182-7.

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I. Pesticides 1. Steering Committee definition:

“This category includes all pesticides, herbicides, fungicides, and others, that are not included in other categories ... Certain pesticides are found in the non-volatile halogenated organic compounds and heavy metals categories. This category includes carbamates and organophosphates.”

2. What are pesticides?

Pesticides are agents, most often chemical compounds, which are used to kill or control pests. Pests most often targeted include insects, unwanted plants, fungi, mites, rodents and bacteria. Pesticides encompass several thousand chemical compounds having a wide array of structures. These structural groups include amides, carbamates, dithiocarbamates, organophosphates, synthetic pyrethroids, triazines, inorganics, organometallics, chlorophenoxy acids, aldehydes, chlorophenolics, substituted ureas, pyrazoles and uracils.

Several pesticide groups have not been included in this chapter. Unless used for crop purposes, those pesticide products excluded are bactericides and medicines used for animal and human health maintenance, slime control agents for cooling water and water treatment systems, disinfection products for water and wastewater treatment facilities (included in the “Halogens/Disinfection Residuals/Byproducts” section) and food preservatives. Chlorinated cyclodiene pesticides (e.g., DDT, aldrin, dieldrin, chlordane and endrin) and chlorinated camphenes (1.e., toxaphene) are included in the “Non-volatile halogenated organic compounds” (NVHOCs) section. This section does not include inert ingredients unless those chemicals are also used as active ingredients or synergists (chemicals that increase the effect of the active ingredient).

3. Sources of pesticides

Pesticides are manufactured products, primarily chemical compounds, which are purposely applied for specific uses in agriculture, homes, gardens, lawn and tree care, right-ofway maintenance for utilities and roads, nuisance control, and health maintenance. In New York, approximately 12,500 pesticide products are registered for sale and use (New York State Department of Environmental Conservation, Bureau of Pesticide Management, personal communication). The most commonly used pesticide products are herbicides (46%), insecticides (11%), fungicides (6%), fumigants and nematocides (14%), conventional pesticides (e.g., sulfur, petroleum products) (13%), and all other pesticides (10%). Approximately 1.24 billion pounds of these pesticides were used in the United States annually in 1994 and 1995 (Aspelin, 1997). In New York during 1995, an estimated 10.5 million pounds of agricultural pesticides were applied to crops (Gianessi and Anderson, 1995); it is estimated that a substantial additional quantity is applied for other uses (e.g., turf, indoor pest control, right-of-way, home and garden, disinfection and health maintenance). Table V-I.1 provides estimates for some pesticide uses where the amount used exceeds 100,000 pounds active ingredient.

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4. Environmental fate

The environmental fate of pesticides is variable. Some pesticides do not degrade readily. Some, particularly organochlorine pesticides such as DDT, chlordane and endrin, were banned 10 to 20 years ago because they persist in the environment, bioaccumulate and cause adverse ecological or human health effects (see “Non-volatile halogenated organic compounds (NVHOCs)” section). Recently, chemical manufacturers have focused on developing pesticides that degrade more readily, sometimes within several days, in the environment and do not accumulate in organisms or soils. However, since they do not bind as much to soils and biota, they may be more mobile in soils and transfer to water more readily. Some pesticides are highly mobile in soil and have been shown to leach to groundwater. Some pesticides (e.g., atrazine, organophosphates), although they may be short-lived, degrade to products of similar toxicity.

5. Health effects

Pesticides are used in agriculture, homes, gardens, lawn and tree care, right-of-way maintenance for utilities and roads, nuisance control, and health maintenance. Exposure may occur through any of these uses. There are many different classes of chemical compounds that are used as pesticides. Many of these chemicals can affect the nervous system. Potential health effects depend on the amount of exposure. Low exposure may have no or minimal short term effects, but high exposures can cause many effects, including weakness, dizziness, headache, nausea, vomiting, respiratory and nervous system failure and death. High exposures to some pesticides may also affect other organs such as the kidney and liver.

Some pesticides have been identified as probable or possible human carcinogens. In the Great Lakes basin, an estimated 33 million pounds of these pesticides were used in agriculture in 1995. Alachlor (a probable human carcinogen) and metolachlor, atrazine and cyanazine (possible human carcinogens) comprise two-thirds of that amount (Agricultural Profile Project Team, Great Lakes Commission, 1996). In New York, probable or possible carcinogens represent approximately 43 percent of the total quantity of agricultural pesticides used (calculated from Appendix A, Table I.1). Most (86%) of this 43% are alachlor, atrazine, metolachlor, cyanazine and mancozeb (a possible human carcinogen). The European Union classifies atrazine as a mutagen (the only such classification for the 109 pesticides examined by the HHWG).

6. Identification of pesticides

The pesticides selected for initial evaluation included all the chemical compounds listed in the following publications as used or potentially used in New York, or found in food or water that may be consumed by people in New York. The list is not exhaustive since it excludes bactericides and other pesticide chemicals that may be registered for use in New York but for which a citation was not found. A limited number of additional substances were added based on the knowledge of members of the HHWG. The 358 chemicals initially selected are found in Appendix A, Table I.1 along with available data from these sources.

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Aspelin, A. L. (1997); provides pesticide sales and usage values for 1994 and 1995.

Gartrell, M. J., J.C. Craun, D. S. Podrebarac, and E. L. Gunderson (1986); provides pesticide residue data for foods in a total diet study as sampled from 1980 to 1982.

Gianessi, L. P., and J. E. Anderson (1995); provides pesticide use data for crops in New York state.

Gunderson, E. L. (1988); provides pesticide residue intake estimates for the total diet as sampled from 1982 to 1984.

Gunderson, E. L. (1995); provides pesticide residue intake estimates for the total diet as sampled from 1986 to 1991.

Zimmerman, F. W., and J. L. Schaum (1990); provides indoor air pesticide exposure data for homes in Massachusetts and Florida during Spring 1986 thru Winter 1988.

New York State Department of Health, Bureau of Toxic Substances Assessment (1997, draft); provides a compilation of octanol-water partition coefficients for pesticides and other chemicals.

Seyler, L. A., J. W. Allan, D. A. Rutz, and M. A. Kamrin (1994); provides summaries of information for agricultural pesticides frequently used in New York, Michigan, Oregon and California.

Suffolk County Department of Health Services (1999); provides a report on pesticide residues found in groundwater of Long Island from October 1997 through March 1998.

U. S. Environmental Protection Agency Integrated Risk Information System (IRIS); provides reference doses and reference concentrations for pesticides and other chemicals.

7. Selection of pesticides

Criteria for selecting pesticides for further evaluation are listed in Appendix A, Table I.2. Pesticides selected were those reported in New York drinking, surface or groundwaters, pesticides in nationwide food basket surveys, and pesticides present in an indoor air study from Massachusetts and Florida. The 109 pesticides selected for further evaluation are listed in Appendix A, Table I.2 along with their toxicity and cancer classification by the European Union, the U. S. Environmental Protection Agency, or in cases where the cancer classification is more stringent, the International Agency for Research on Cancer (IARC).

8. Data for ranking the selected pesticides Ranking matrices were developed by two methods: by the “standard” method provided in

the Methods section of this report, and by calculating cancer risks and hazard indices based on pesticide residues reported in food, water or indoor air.

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A variety of data were used to classify pesticides by the “standard” method. Data on pesticide residues in indoor air and crop use of pesticides are provided in Appendix A, Table I.1. Pesticide residues detected in surface waters or groundwaters of limited areas of New York are provided in Appendix A, Table 1.3. Table V-I.1 summarizes estimates of crop use, home and garden use, and industrial, commercial and government use of pesticides in New York where known total annual use estimates are 100,000 pounds or more. It should be noted that Table VI.1 provides only information on the top 10 pesticides used in homes and gardens, or in industrial, commercial and government applications.

Table V-I.1: Summary of estimated pesticide use (in thousands of pounds) in New York where use is greater than 100,000 pounds of active ingredient per year.

Pesticide Agriculture Home & Garden Ind./Comm./Govt. Total p-Dichlorobenzene 2 2,450 - 2,450 Glyphosate 591 490 770 1,851 2,4-D 142 630 910 1,682 Atrazine 1,426 - - 1,426 Chlorpyrifos 219 280 910 1,409 Petroleum 1,304 - R-NG 1,304 oil/distillates Metolachlor 1,199 - - 1,199 1,4-Dithiane 724 - - 724 Methyl bromide 112 - 560 672 Cyanazine 648 - - 648 Alachlor 610 - - 610 Diazinon 16 280 280 576 Copper sulfate 66 - 490 556 Sulfur 501 - R-NG 501 DEET - 490 - 490 Dicamba 135 350 - 485 MCPP 2 350 - 352 Captan 328 - - 328 Diuron 34 - 280 314 Carbaryl 93 210 - 303 MSMA - - 280 280 Naphthalene - 280 - 280 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page 103

Pesticide Agriculture Home & Garden Ind./Comm./Govt. Total DCPA (Dacthal) 39 210 - 249 EPTC 252 - - 252 Malathion 18 - 210 228 Benefin - 210 - 210 Carbofuran 158 - - 158 Cryolite 146 - - 146 Chlorothalonil 130 - - 130 Maneb 125 - - 125

' Estimates for average agriculture usage are from Gianessi and Anderson (1995) for the years 1990-1993. For home and garden usage plus industrial/commercial/government usage the estimates are based on 1994-1995 market estimates published by USEPA (1997). In the latter document, estimates are on a national scale. The estimates for New York were derived based on population and assuming a states’ population would use the pesticides proportionate to the national population. It was estimated that New York has seven percent of the US population and all national estimates were prorated by that percentage. The maximum national use estimates were used.

? A dash (-) indicates amounts were not estimated. Usage is known to occur for some pesticides indicated by a dash. > R-NG = Reported but amounts were not given.

The Methods section of this report classifies chemicals by volume produced or volume released to the environment as a surrogate for human exposure. The Methods section has no criteria for classifying pesticides based on the amounts used in New York. Although the amount of pesticides used is not directly correlated with exposure, particularly in agricultural settings, “amount used” is a surrogate for potential exposure similar to classifying chemicals based on production or release. The following criteria were used to classify pesticides based on amount used.

Rank Estimated pounds of pesticide active ingredient used annually in New York 1 (highest) > 1,000,000

2 100,000 to 1,000,000

3 10,000 to 100,000

4 (lowest) <10,000 9. Ranking results using “standard” method

The ranking from using the “standard” method as described in the Methods section is shown in Table V-I.2. This provides a classification based on both cancer and non-cancer endpoints. The toxicity or potency classification of most pesticides in Table V-I.2 was determined by toxic non-carcinogenic effects; in only four instances (atrazine, Captan, propargite and pronamide) were toxicity or potency classifications increased due to carcinogenic potential.

Commercial applicators in New York began reporting pesticide use to NYSDEC in 1997, as required by a new law. The information required includes the USEPA registration number of

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the product, registered product name, and quantity used. In 1997, over 2600 pesticide products

were reported used (NYSDEC, 1998). The registered product name does not include the

chemical names of the active ingredients. The product quantity reported is the amount of the

pesticide product in gallons or pounds, not the amount of active ingredient used. For this

chapter, the amount and kind of active ingredient in each pesticide product applied would be important classification variables, but as this information was not included in the NYSDEC report, it was not used.

Table V-I.2: Risk characterization matrix for cancer and non-cancer effects of pesticides.

Toxicity or Potency

Exposure 1 (highest) 2 3 1 NYS groundwater | Crop Use DCPA (Dacthal) Metolachlor (highest) or TCPA Petroleum (Long distillates Island maximum) Homeowner use Crop Use pAtrazine Dichlorobenzene

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Toxicity or Potency

Exposure 1 (highest) 2 3 2 NYS groundwater | NYS groundwater | NYS surface Aldicarb DCPA (Dacthal) water (Long Island) or TCPA (Long Metolachlor Island average) Crop Use Ethylene NYS groundwater Carbofuran dibromide 1,2Chlorpyrifos (Long Island) Dichloropropane Simazine (Long Island) Homeowner use (Long Island) Metolachlor Chlorpyrifos (Long Island) Crop Use Ind./Comm/ Alachlor Crop Use Govt. use Captan Cyanazine Chlorpyrifos Chlorothalonil Glyphosate Malathion 2,4-D Dicamba Homeowner use EPTC Benefin Maneb Carbaryl Methyl bromide DEET Glyphosate Homeowner use 2,4-D Ind./Comm./ DCPA (Dacthal) Govt. use Diazinon Copper sulfate Dicamba Glyphosate Ind./Comm./ Govt. use 2, 4-D Diazinon Diuron Methyl bromide

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Toxicity or Potency

Exposure 1 (highest) 2 3 3 Crop Use NYS surface NYS surface Azinphos-methyl | water water Dimethoate Atrazine Carbaryl Ethoprop Cyanazine Fonofos NYS groundwater | Metolachlor Malathion Alachlor Methomyl (Long Island) NYS groundwater Phorate Atrazine (upstate) | Cyanazine Terbufos 2,4-D (upstate) Dinoseb Metolachlor NYS groundwater | (Long Island) (upstate) Carbofuran Endosulfan Metalaxyl Methomyl (Long Island) (Long Island) (Long Island) Prometon Oxamyl! Crop Use (Long Island) (Long Island) DCPA (Dacthal) Diazinon Crop Use Diuron Carbaryl Endosulfan Chloramben Iprodione Copper sulfate Linuron Pendimethalin Methyl bromide Permethrin Methyl parathion Metribuzin Oxamyl Phosmet Propargite Simazine Vinclozolin

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Toxicity or Potency Exposure 1 (highest) 2 3 4 4 NYS surface NYS surface NYS surface Crop use (lowest) | water water water DCNA Carbofuran Alachlor Pendimethalin (Dichloran) Chlorpyrifos DCPA (Dacthal) Prometon Malathion Diazinon Pronamide Molinate EPTC Tebuthiuron Metribuzin Crop use Simazine Crop use Acephate Terbacil Dicofol Disulfoton Fenvalerate Mevinphos NYS groundwater | Methoxychlor Atrazine Indoor air (Long Island) Indoor air Chlorpyrifos Metribuzin Carbaryl Dichlorvos (Long Island) Permethrin Malathion Resmethrin Crop use Ronnel PCNB Pronamide Terbacil Indoor air Atrazine Bendiocarb Captan Chlorothalonil 2, 4-D Diazinon DCPA (Dacthal) Folpet o-Phenylphenol Propoxur

10. Ranking based on cancer risk and hazard index calculations

Since people can be exposed to pesticides by inhalation or ingestion, concentrations of pesticide residues in food and water or in indoor air were used to estimate exposure. Dermal exposure can also occur but data for evaluating that route of exposure were not readily available. Hazard indices for non-carcinogenic effects were calculated for food and indoor air and cancer risk estimates were calculated for food and water. For some pesticides in some media, lack of reference doses, cancer potency factors or environmental concentrations prevented calculation of

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hazard indices or cancer risks. The basis and results of calculations of cancer risk and hazard indices are provided in Appendix C and the rankings are summarized in Appendix C, Table C.3. Ten of 17 pesticides detected in indoor air are classified as possible carcinogens by USEPA, IARC or the EU, but cancer potency factors were not available for these ten pesticides. A reference dose was available for dichlorvos only.

11. Areas not evaluated This evaluation has not examined all human exposure pathways or exposed populations. Exposure from the following pathways or to the following populations could exceed that to the

general population as assessed by consumption of food and water and inhalation of indoor air:

° dermal exposure through contact with pesticides or inert ingredients applied to turf and soil, or found in sediment;

° pesticide applicator exposure, especially of farmers, nursery workers, migrant laborers, and turf applicators;

° families of pesticide applicators and residents living close to lands on which pesticides have been applied;

° residents in buildings constructed in areas where persistent pesticides have been applied,

particularly orchards or vineyards;

° personnel involved in pesticide manufacturing, formulation, transport and sales; ° reported instances of pesticide poisoning; ° sensitive populations such as children, the sick and elderly, and the facilities where these

people spend a considerable portion of their lives (e.g., schools, hospitals, nursing facilities); and

° individuals exposed to more than one pesticide at the same time, or to pesticides with similar effects through multiple routes.

There is information in the scientific literature that could be used to evaluate the exposures and populations listed above. However, this effort was beyond the resources of the HHWG.

Calculations of cancer risk or hazard indices for many pesticides cannot be made because information on cancer potency, reference doses and reference concentrations are not available. For many pesticides, there is not enough information to evaluate whether they may cause cancer in humans. The ongoing reevaluation of pesticides by the U. S. Environmental Protection Agency, particularly for those pesticides registered prior to the 1988 amendments of the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), should improve the database for many

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pesticides. These data may result in changes of registered uses of these pesticides. Because new information on the effects of pesticides will become available, it will be necessary to update the ranking of individual pesticides in this comparative risk approach.

12. Discussion Many people are very interested in pesticides because of several factors:

° The intended use of pesticides is to kill or control certain target organisms; however, nontarget organisms (including people) may be adversely affected also. The potential impacts on people are estimated, with uncertainty, based on animal experiments, and the limited epidemiological studies of human populations.

° Pesticides may produce, depending on the amount of exposure, a number of health impacts including, among others, reproductive impairment, neurological disorders, liver or kidney damage, and cancer.

° Since there are about 12,500 pesticide products registered in New York, there is a potential for simultaneous exposure to multiple pesticides. The probability of simultaneous exposures depends on many factors, including diet, pesticide use in and outside the home and occupation. Simultaneous exposure may enhance, alter or reduce effects attributed to individual pesticides. These interactions can complicate investigations of health effects.

° Compared to many other groups of compounds, there is a relative abundance of published information on the effects of pesticides. Despite the availability of these data, there may be a lack of understanding of the relative risks of pesticide use and exposure by the general public.

° There are a limited number of reports that suggest an increased incidence of some adverse human health effects associated with exposure to pesticides (Zahm and Ward, 1998).

The following discussion provides additional data and further rationale for the conclusions and recommendations.

a. Pesticides in groundwater and surface water

The contamination of groundwater in Long Island by agricultural pesticides has been a health concern, particularly in Suffolk County, where residents rely on groundwater as the sole source for drinking water. Past pesticide use has impacted the groundwater quality in agricultural areas of Suffolk County, prompting the ban of pesticides such as aldicarb, carbofuran, oxamyl, ethylene dibromide and dacthal from the county. However, residues from these pesticides and others are still found in groundwater in agricultural areas of the county. In addition, several of the pesticides detected in groundwater were formerly predicted to degrade,

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volatilize or adhere to soil, making it unlikely they would migrate to water. When untreated groundwater samples from public water supply wells were found to exceed state or federal maximum contaminant levels for public drinking water supplies (MCL), the wells were taken out of service or treated to prevent the contaminants from reaching consumers. For private wells that are impacted, water is usually treated with filters or in some cases, public water systems have been extended. Groundwater contamination remains in these areas, and continued monitoring is necessary.

In the Water Quality Monitoring for Pesticides Program, the Suffolk County Department of Health Services (SCDHS), the US Geological Survey (USGS) and the NYSDEC have monitored waters throughout the state for a wide variety of pesticide residues, concentrating on areas of known contamination or high pesticide use, public water supplies, and on the Long Island sole source aquifer (NYSDEC, 1998). Groundwater monitoring for pesticides on Long Island has focused on areas of concentrated pesticide use such as agricultural areas. Some findings of groundwater monitoring on Long Island:

° Pesticides and their metabolites were found in untreated water from both public and private wells in Nassau and Suffolk counties in 1998 (Appendix A, Table I.4). The sampling locations were not random, but were in areas of high pesticide use. They are not representative of all conditions on Long Island.

° Of the nearly 900 wells sampled by the SCDHS (Appendix A, Table 1.4), 26 percent had detectable levels of pesticide(s) and 10% had a level of a pesticide which, if the raw water was used for drinking, would exceed drinking water standards.

° Fifteen different pesticides were found in Nassau County and 30 different pesticides were found in Suffolk County. Some pesticides levels in untreated water exceeded MCLs. Six of the 10 pesticides exceeding MCLs on Long Island were removed from the market between 10 and 20 years ago, indicating the persistence of these chemicals in groundwater.

° Private wells in the eastern end of Suffolk County, where there is the most agriculture, had the highest percentage of wells containing pesticides. The vast majority of the pesticide impacted wells were shallow.

In upstate monitoring, many commonly used pesticides have been detected in the surface waters of New York (Appendix A, Table I.3). However, concentrations are generally well below all applicable health standards. Short-lived peaks above these levels occur in certain rivers and streams during high spring flows, typically in areas where pesticides have recently been applied. No surface water intakes used for public water supply were found to exceed MCLs. Some findings:

° In upstate New York in 1997, the USGS sampled surface water at six sites 8 to 20 times per year and 64 sites once in the spring. Generally, low concentrations of 34 pesticides or breakdown products were found. Some of the pesticides detected do not have surface

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water quality standards.

° The detection of pesticides in surface water was clearly related to pesticide use in the watershed. The highest concentrations of simazine were in rivers and streams that drain orchards and vineyards. The highest concentrations of corn herbicides (atrazine and metolachlor) were in waters draining areas with high corn production. Insecticides were more commonly found in waters draining urban areas and orchards and vineyards.

° Some pesticides were found frequently in surface water samples (atrazine (97%), metolachlor (80%), simazine (72%), alachlor (50%) and cyanazine (41%)).

b. Pesticides in indoor air

Pesticide concentrations in indoor air were measured from 1986 through 1988 in Massachusetts and Florida during three seasons (Zimmerman and Schaum, 1990; also known as the NOPES study). Indoor air samples were collected from 173 homes in Florida and from 86 homes in Massachusetts. Minimum and maximum average concentrations of 32 pesticides or pesticide degradation products were reported. Pesticide levels in New York would probably be more similar to levels in Massachusetts than in Florida. Therefore, the maximum average concentrations of pesticides found in Massachusetts homes were compared to the ranking guidelines in the “standard” method. All the pesticides (excluding NVHOCs) reported were classified in the lowest exposure category. The NOPES data were collected over ten years ago in a relatively small study in other states. The study focused on general seasonal concentrations, rather than potentially higher concentrations shortly after pesticide applications. A study of short-term (directly after pesticide applications) and long-term pesticide concentrations in indoor air in New York residences and other buildings would be more useful to characterize possible exposures, including simultaneous exposures to multiple pesticides.

Cancer potency factors and reference concentrations are lacking for 16 of the 17 pesticides measured in indoor air of homes. Therefore, health risks could not be evaluated for these pesticides, except for dichlorvos, which had a low Hazard Index (from 0.01 to 0.02 for the range of average indoor air concentrations in Massachusetts homes). There are indoor air standards for some pesticides in industrial settings, but they do not apply to residences, where exposures may occur for longer periods and where there are more sensitive populations (elderly, ill, children).

c. Pesticides in food

The U. S. Food and Drug Administration conducts chemical analyses on food samples representative, both in kind and proportion, of those purchased by consumers, called “market baskets” (Gartrell et al. 1986; Gunderson, 1988 and 1995). The market baskets are purchased several times each year in selected major metropolitan areas of the United States, including four market baskets in New York. Their findings are periodically reported, usually about once every five years, since trends in food ingestion and chemical levels change slowly. In the most recent reported survey (Gunderson, 1995), nearly 300 pesticides, pesticide-related and industrial

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chemical residues were measured in 4,914 individual food samples; the data reported included all 113 compounds found and was reported as the calculated total daily exposure concentrations (based on body weight) for different age groups of people. Except for NVHOCs, the pesticides detected in five percent or more of the samples were malathion, diazinon, chlorpyrifos, chlorpyrifos-methyl, endosulfan, methamidophos, and DCNA (dichloran). The daily exposure concentrations of these seven pesticides were generally very low.

The data for all pesticides detected in food were used to calculate hazard indices or cancer risks for an adult 25 to 30 years old. This age category typically contains the greatest pesticide consumption for adult age groups reported and represents the period in life with greatest reproductive potential. Based on the calculations, on a market basket basis, human exposure to individual pesticides in food seldom represents a significant hazard or cancer risk (Appendix C, Table C.1). However, Gunderson (1995) acknowledged that occasionally individual foods may contain pesticide residues which exceed regulatory guidelines. When this occurs, the food product may be subject to regulatory or enforcement actions to prevent its presence in U.S. markets, or to reduce pesticide residues through changes in pesticide use or harvest restrictions.

d. Pesticide use

Quantitative estimates of the major (greater than 100,000 pounds) pesticide active ingredients used annually in New York are presented in Table V-I.1 (based on Gianessi and Anderson, 1995, and Aspelin, 1997). Estimates for all crop uses of pesticides in New York are included in Appendix A, Table I.1. Commercial pesticide applicators, importers and manufacturers are now required to report to the NYSDEC annually on the application or sale of pesticides in New York. These data should be used in any future evaluations of pesticide use in New York.

Pesticides are used widely in urban, rural and forested areas of New York. In New York, agricultural pesticide use is dominated by pesticides used on corn and, to a lesser extent, on fruits, vegetables, soybeans and potatoes. Atrazine, metolachlor, cyanazine and alachlor are primarily used on corn, with more than one million pounds of each of the first two compounds used. The use of herbicides in agriculture far exceeds that of insecticides and fungicides. Long term efforts to develop crop plants resistant to disease have resulted in large reductions in the need for fungicides. The fungicide 1,4-dithiane (Mancozeb) is used on fruit crops, and dormant sprays containing petroleum distillates are used on fruit trees and vines. Alachlor and metolachlor are used on soybeans, and metolachlor on potatoes. Many pesticide products use petroleum distillates as carriers or as the active ingredient and are applied to a wide array of crops.

In home and garden use (Table V-I.1), the dominant pesticide used is p-dichlorobenzene which is an insect repellant (home use as moth balls or flakes), or a fumigant of clothes and leather. Glyphosate and 2,4-D are used for weed control in lawns and gardens, diazinon for insect control in lawns and gardens, and DEET as an insect repellant applied to human skin. On a unit area basis, pesticide use in homes and gardens is frequently reported to be in greater

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concentrations than agricultural uses of the same materials.

Major industrial, commercial and government uses of pesticides (Table V-I.1) include glyphosate and 2,4-D for weed control, chlorpyrifos and methyl bromide for insect control in buildings, including food and grain storage areas, methyl bromide for rodent control in granaries, and copper sulfate for algae control in water supplies.

The Agricultural Profile Project Team 1996 draft report of the Great Lakes Commission classified pesticide use rates in five levels for counties within the Great Lakes basin. Wayne County, New York had the greatest rate of pesticide application in the entire Great Lakes basin. Of the 28 counties in New York partly or entirely within the basin, Wayne and Orleans counties had the greatest use of pesticides classified as probable or potential carcinogens and of pesticides with potential for reproductive or endocrine system disruption. Crops in Wayne County receiving the greatest pesticide applications were corn, apples, peaches, pears and potatoes. To better understand pesticide use in New York, the New York State Department of Environmental Conservation is collecting data on pesticide applications from across the state as part of the Pesticide Reporting Law. These data may be used to provide direction for further study of potential for human exposure.

It is likely that not enough attention has been paid to residential pesticide use by homeowners. Many residential pesticide users may not follow use directions, may not wear protective clothing, may not take necessary safety precautions, may use more than the recommended dose, and may improperly store pesticides. In such cases, there may be increased contact with pesticides during application and pesticide residuals may be more readily available in the home, on lawns and in gardens. There is an opportunity to educate residents about the proper use of pesticides and the potential health impacts of exposure.

Past pesticide use continues to present potential exposure to humans since many of the pesticides used persist for many years. Many compounds were NVHOCs, which are addressed elsewhere. Others (e.g., mercurial compounds and lead arsenate) were applied to orchards, vineyards and other locations for insect, fungus and scab control. As orchards and vineyards have gone out of production, especially in areas of urban/suburban growth such as the lower Hudson River valley, residential development creates new human exposures. For example, dermal contact with contaminated soil may be increased. Little information is available on these potential exposures but they are worthy of investigation. Local government agencies (e.g., county health departments, town zoning boards, etc.) have regulatory jurisdiction over various aspects of residential subdivision development. Some county health departments require an evaluation of the need for a soils management plan on former agricultural properties proposed for residential development. This may include surface soil sampling for pesticide residues and a management plan to address areas of elevated contamination. This practice should be encouraged.

e. Inert ingredients

Most pesticide products contain inert ingredients. In many cases the inert ingredients are

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recognized as having no toxicity or other deleterious effects to humans or the environment in the amounts present. However, some inert ingredients are of toxicological concern and may pose an increased and potentially unacceptable risk to humans and the environment. These chemicals, in combination with the pesticide’s active ingredients, should be considered together for evaluation of potential human impacts. Current USEPA policy will result in the phase-out of inert ingredients with toxicological significance.

f. Children and pesticides

The National Research Council (1993) examined pesticides in the diets of infants and children. They concluded that because children and infants are not the same as adults, the assessment of impacts on children should not be treated in the same way as for adults. Children have immature organ systems, differing body composition, differing dietary (including water) intakes, and differing exposures to chemicals. There are specific periods during child development when chemical exposures may permanently alter organ system functions.

Acute toxicity and chronic effects studies of pesticides are predominantly conducted on adult animals; few studies compare the toxicity with immature individuals of a test species. The NRC recommended further research on the effects of pesticides in infants and children, including:

° assessment of pesticide impacts on sensitive organ systems in young test organisms,

° metabolism of pesticides in young test animals,

° exposure during early developmental stages (after the second trimester) through adolescence and their sequelae in later life,

° development of validated animal models for assessing risks to infants and children,

° an improved assessment of the diets of infants and children and of chemical concentrations in foods consumed by infants and children,

° assessment of concurrent exposures to pesticides with similar modes of action.

The causes of childhood cancers are largely unknown. Recent reviews on potential associations between pesticide use and the incidence of childhood cancer have noted that frequent occupational exposure to pesticides (farm exposure), or home use of pesticides may be associated with leukemia and brain cancer (Daniels et al., 1997; Zahm and Ward, 1998). Leukemia and brain cancer comprise approximately 75% of childhood cancers (Grufferman, 1998). Parental occupational exposure to pesticides was also associated with Wilms’ tumor, Ewing’s sarcoma, and germ cell tumors. However, environmental causes of childhood cancer have been difficult to pin down, partly because childhood cancer is rare and partly because it is difficult to estimate past exposures after children develop cancer.

g. Potential carcinogenic pesticides used in New York

Table V-I.3 presents a tally of the pesticides used extensively in New York (Table V-L.1 was used as the basis) that were classified by their potential to cause cancer.

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Table V-I.3: Cancer classifications of pesticides used extensively in New York

c ; Agriculture Home & Industrial/Commercial ancer Classification Garden /Government Number examined 25 12 11

Probable human carcinogen 6 0 1

Possible human carcinogen 5 3 0

Not assessed 6 4 4

Not classifiable 6 3 4

Evidence for non- 2 2 2 carcinogenicity

This information suggests the need to understand exposure to carcinogenic pesticides used extensively in New York. Other pesticides used in New York may require a similar assessment.

h. Regulation of potentially carcinogenic pesticides in food

The Delaney Clause of the Food, Drug and Cosmetic Act, adopted in 1958, was a zero risk policy that prohibited any food additive if it caused cancer in humans or animals. Food additives were defined by the Act as substances which may by their intended uses become components of food. Pesticides in or on raw agricultural products were excluded from this definition (USFDA, 1984). In 1992, a federal judge, in settlement of a case brought by the Natural Resources Defense Council and the state of California, ordered the USEPA to enforce the Delaney Clause by 1997. More than 80 pesticides would be affected by the decision. By passage of the Food Quality Protection Act of 1996, Congress and the President eliminated the Delaney Clause of the Food, Drug and Cosmetic Act in favor of standards based on acceptable tisk developed from scientific evidence. New standards for these pesticides are to be developed.

A reevaluation of all existing tolerances for pesticides is to be conducted within 10 years of enactment of the Food Quality Protection Act of 1996. All existing and new tolerances must be “safe” which is defined as “reasonable certainty that no harm will result from aggregate exposure” to the pesticide, including exposures through diet, drinking water, nondietary and nonoccupational exposures (e.g., indoor air, dermal) where those exposures can be reasonably and reliably determined. Additional testing is mandated, e.g., endocrine system disruption. The Food Quality Protection Act of 1996 explicitly requires the USEPA to address risks to infants and children, while placing less emphasis on benefits of pesticides used to maintain the food

supply.

i. Integrated Pest Management (IPM)

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Integrated Pest Management is a sustainable approach to managing pests by combining biological, cultural, physical and chemical tools in a way that minimizes economic, health and environmental risks. The desired results from IPM are reduced pesticide use, expense and impacts, and crops and livestock of equal or better quantity and quality to that achieved through pesticide use alone. IPM has been extensively promoted by Cornell University’s College of Agriculture and Life Sciences and state, regional and county cooperative extension services. The agriculture community has been an effective supporter and user of IPM practices for many years. The use of IPM in agriculture has been an important factor in reducing use of pesticides in this sector.

IPM is a process which includes several components. First, the grower must understand how the crop grows, how different pest populations develop, what control options are available, and the relative benefits and costs of control actions. Crops are carefully monitored to determine the potential impact of pest populations. The farmer can then determine how serious a problem is and what options are available before taking action. This contrasts with routine preventative chemical treatments or chemical treatments in response to any pest presence regardless of how small the infestation (Northeast Integrated Pest Management, 2000).

IPM uses a combination of controls to reduce the impact of pests, such as:

° biological control - using beneficial organisms (predators, parasites, diseases) to suppress pests,

. cultural control - using rotations, cultivation, and sanitation to reduce pests,

° physical control - using barriers, traps, trap crops and adjusting planting location or timing to evade pests,

° genetic control - choosing disease resistant plants,

° chemical control - using conventional pesticides, biopesticides, pheromones and other

chemicals to suppress pests. An attempt should be made to choose chemical controls that are specific to the pest species (as nearly as possible), short-lived in the environment, least toxic to humans and beneficial species, used at the lowest effective rate, and alternated with other chemicals to help prevent resistance.

13. Conclusions

The following conclusions are based on the “standard” method of risk characterization (Table V-I.2).

a. Large amounts of some pesticides are used in New York. For several pesticides, the use is more than one million pounds of active ingredients annually. Studies have shown pesticides present in drinking water, food and indoor air. Residues are found in turf and soils after application. Some of these pesticides have been classified by USEPA as probable or possible human carcinogens. There has been limited scientific investigation of potential adverse health impacts caused by simultaneous exposure to pesticides by more than one route or to those pesticides having similar modes of action.

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b. Concentrations of pesticides in surface waters are generally well below water quality criteria. Pesticides applied in agriculture and in some urban areas can migrate to surface water; herbicides applied to corn and row crops (atrazine, metolachlor, cyanazine) are the most frequently found.

c. Concentrations of some pesticides in untreated water from a few public drinking water wells on Long Island have exceeded drinking water MCLs. All of these wells were removed from service or were treated to reduce concentrations below the MCL. These pesticides were primarily older pesticides that have been banned for use on Long Island for as much as 20 years. These pesticides have also been found in shallow private water wells in areas of Long Island with a past history of application. Private wells found to be contaminated are most often treated with filters to remove pesticides. Groundwater monitoring in Long Island is continuing.

d. Pesticides commonly used in or around residences (e.g., p-dichlorobenzene, DEET, diazinon, glyphosate, chlorpyrifos, and 2,4-D) may present a potential for increased human exposure. Little evaluation has been done of pesticide use in home and work environments in New York.

The following conclusions are based on estimates of cancer risk and hazard indices (Appendix C, Table C.3).

e. Based on USDA market basket studies, adult consumers of food have a low risk of cancer from pesticide residues. There is no method available to calculate cancer risk to children from exposure to pesticides in food. There is a moderate risk for non-cancer health effects from exposure to diazinon (for children) and methamidophos (for children and adults) in the market basket foods. Consumption of all other pesticide residues in food for which calculations could be made presented a low risk of non-cancer effects.

f. Concentrations of some pesticides in groundwater (ethylene dibromide and dacthal in Long Island) would present moderate to very high cancer risks if these groundwaters were used for drinking without treatment. All public water supply wells with such concentrations are removed from service or are treated to reduce concentrations. Concentrations of some pesticides in some surface waters (atrazine, cyanazine and simazine) would present moderate cancer risks if the waters were used for drinking water without treatment.

g. Several possible exposure scenarios were not evaluated due to lack of data or resources. These include exposure through home, lawn and garden use of pesticides; occupational exposures to farmers, pesticide applicators and manufacturers; exposure to pesticides in indoor air and soil; and sensitive subpopulations.

h. There is a lack of information about health risks from multiple exposures, i.e., exposures to the same pesticides repeatedly, to several pesticides simultaneously and to pesticides by multiple routes of exposure.

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i. Reference doses or concentrations, and cancer potency factors are lacking for many pesticides.

j. There is a general lack of monitoring data for many pesticides in most media. 14. Recommendations

a. Continue to monitor pesticides in drinking water and take actions as necessary so that drinking water of acceptable quality can be available to residents.

b. Continue to monitor pesticides in groundwater and surface water in the NYSDEC Water Quality Monitoring for Pesticides Program. Continue to assess pesticide use in areas with sensitive aquifers.

c. Examine the scientific literature, including that developed under the FQPA and the NYSDEC pesticide registry, to refine risk characterizations and evaluate the potential exposures in the “Areas not evaluated” section.

d. Identify monitoring programs and studies to better define human pesticide exposures and health impacts, especially for children, farmers and pesticide applicators. Where significant exposures are identified, implement appropriate action to reduce or eliminate the exposure.

e. Evaluate pesticide contamination of indoor air in residences and other buildings. f. Develop a program to educate residential users of pesticides in proper application and

safe handling of pesticides. Encourage the use of non-toxic alternatives where possible and practical.

g. Support the continued use of Integrated Pest Management in agriculture and livestock management. h. Develop water quality standards, cancer potency factors, and reference doses or

concentrations for pesticides. Characterize the risks associated with exposure to pesticides via indoor air.

i. If cancer or non-cancer risks associated with exposures to a given pesticide are unacceptably high, the state should take action (eg., regulatory, legislative) to control sources and reduce potential exposure.

15. Stressor categorization

Pesticides are used to eliminate or control insects, rodents, other pests, unwanted vegetation and diseases in the environment, in homes and workplaces, in food, in water supplies,

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and in medicine. In some cases, these activities may have adverse impacts on non-target organisms, including people. This stressor group should be ranked group B. Based on the environmental or use data available to the HHWG, several pesticides could be ranked as group A. However, a larger number of pesticides are ranked as B or C. The large number of chemicals used as pesticides, the known and likely exposures to pesticides, and the possibility of interactions of pesticides causing potentially adverse human health effects which are not understood supports the proposed stressor group categorization.

16. References

ACGIH Worldwide. 1996. 1996 TLVs and BEIs. Threshold limit values for chemical substances and physical agents, biological exposure indices. American Conference of Governmental Industrial Hygienists. 39 p.

Agricultural Profile Project Team. 1996. An agricultural profile of the Great Lakes basin: Characteristics and trends in production, land-use and environmental impacts. Great Lakes Commission, Ann Arbor, MI. 184 p. + appendices.

Aspelin, A. L. 1997. Pesticide industry sales and usage: 1994 and 1995 market estimates. 733R-97-002. Office of Pesticide Programs, U. S. Environmental Protection Agency, Washington, DC. 35 p.

Daniels, J. L., A. F. Olshan, and D. A. Savitz. 1997. Pesticides and childhood cancers. Environ. Health Perspec. 105(10):1068-1077.

Entringer, R. A. 1997. Memoranda to District Staff, Field Coordinators dated September 3, 1997 and October 22, 1997.

Gartrell, M. J., J. C. Craun, D. S. Podrebarac, and E. L. Gunderson. 1986. Pesticides, selected elements, and other chemicals in infant and toddler total diet samples, October 1980March 1982. J. Assoc. Off. Anal. Chem. 69(1):123-145.

Gianessi, L. P., and J. E. Anderson. 1995. Pesticide use in New York crop production. National Center for Food and Agriculture Policy, Washington, DC. 64 p.

Grufferman, S. 1998. Methodologic approaches to studying environmental factors in childhood cancer. Environ. Health Perspec. 106 (Suppl. 3):881-886.

Gunderson, E. L. 1988. FDA Total Diet Study, April 1982-April 1984, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc. Off. Anal. Chem. 71(6):1200-1209.

Gunderson, E. L. 1995. FDA Total Diet Study, Jule 1986-April 1991, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc. Off. Analyt. Chem. Intl.

78(6):1353-1363.

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Meister Publishing Company. 1994. Farm Chemicals Handbook ‘94. Meister Publishing Company, Willoughby, OH.

Meister Publishing Company. 1997. Farm Chemicals Handbook ‘97. Meister Publishing Company, Willoughby, OH.

National Research Council. 1993. Pesticides in the Diets of Infants and Children. Committee on Pesticides in the Diets of Infants and Children, Board on Agriculture, and Board on Environmental Studies and Toxicology, National Research Council. National Academy Press, Washington, DC. 386 p.

Northeast Integrated Pest Management. 2000. The Integrated Pest Management Approach. http://www.nysaes.cornell.edu/ipmnet/ipm.prim.psu2.html.

Nosenchuck, N. H. 1997. Memorandum to Acting Commissioner John P. Cahill dated April 18, 1997.

NYSDEC. 1991. Draft New York State Air Guide - 1: Guidelines for the control of toxic ambient air contaminants. Division of Air Resources, New York State Department of Environmental Conservation, Albany, NY.

NYSDEC. 1998. Ambient water quality standards and guidance values. TOGS 1.1.1. Division of Water, New York State Department of Environmental Conservation, Albany, NY. 59p.

NYSDEC. 1997. Combined Regulatory Impact and Draft Environmental Impact Statement Title 6, Chapter X, Parts 700-706, Volume 1 of 3. New York State Department of Environmental Conservation, Albany, NY.

NYSDEC. 1998. Annual Report: New York State 1997 Pesticide Sales and Applications. Pesticides Management Program. New York State Department of Environmental Conservation, Albany, NY.

NYSDEC. 1999. Annual Report: New York State 1998 Pesticide Sales and Applications. Pesticides Management Program. New York State Department of Environmental Conservation, Albany, NY.

NYSDOH. 1997. Compilation of octanol-water partition coefficients (Draft). Bureau of Toxic Substance Assessment, New York State Department of Health, Albany, NY. 11 p.

Seyler, L. A., J. W. Allan, D. A Rutz, and M. A. Kamrin. 1994. EXTOXNET Pesticide Information Notebook. Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and the University of California at Davis.

Suffolk County Department of Health Services. 1999. Water Quality Monitoring Program to Detect Pesticide Contamination in Groundwaters of Nassau and Suffolk Counties, NY.

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Final Report for the NYSDEC Water Quality Program. Hauppage, NY.

Trent, M., and S. F. Robbins. 1996. Nitrate and pesticide impacts of agriculture on groundwater quality of Suffolk County, NY. Bureau of Groundwater Resources, Suffolk County Department of Health Services, Hauppage, NY. 19 p.

USEPA. 1996. Office of Pesticide Programs List of Chemicals Evaluated for Carcinogenic Potential (dated July 15, 1996). U. S. Environmental Protection Agency, Washington, DC. 31 p.

USEPA. 1997. Pesticides Industry Sales and Usage, 1994 and 1995 Market Estimates. Office of Prevention, Pesticides and Toxic Substances. U. S. Environmental Protection Agency, Washington, DC.

USEPA. 1998. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, U. S. Environmental Protection Agency. Cincinnati, OH.

USFDA. 1984. Requirements of Laws and Regulations Enforced by the U.S. Food and Drug Administration. Food and Drug Administration, U.S. Department of Health and Human Services. Rockville, MD. HHS Publication No. (FDA)85-1115.

USGS. 1997a. Pesticides in surface waters of the Hudson River basin, New York and adjacent states. Fact Sheet FS 238-96. U.S. Geological Survey, Troy, NY. 4p.

USGS. 1997b. Pesticides in surface waters of the Hudson River basin - Mohawk River subbasin. Fact Sheet FS 237-96. U.S. Geological Survey, Troy, NY. 4 p.

Zahm, S. H., and M. A. Ward. 1998. Pesticides and childhood cancer. Environ. Health Perspec. 106 (Suppl. 3):893-908.

Zimmerman, F. W., and J. L. Schaum. 1990. Final report of the nonoccupational pesticide exposure study (NOPES). EPA/600/3-90/003. Exposure Assessment Research Division, U. S. Environmental Protection Agency, Research Triangle Park, NC.

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J. Petroleum products 1. Steering Committee definition:

“This category includes petroleum product mixtures such as oil, gasoline and diesel fuel. It does not include the substances that are released when these products are burned or the individual components such as benzene, toluene and xylene, which are considered in the VOC category.”

2. What are petroleum products?

Petroleum products are derived from the distillation of crude oil. Examples are gasoline, fuel oil, diesel fuel, kerosene and motor oil. These products are mixtures of many different hydrocarbon compounds refined from crude petroleum. Many of these products also contain additives such as octane enhancers, antioxidants, icing inhibitors, detergents and corrosion inhibitors. Some of these products are liquid at room temperature and evaporate into the air easily. Many of these products are flammable. “Waste oil” in this document refers to used motor oil, which may contain substances (such as metals) not present in the original product.

3. Sources of petroleum products:

Petroleum products are among the most widely produced substances. Out of the 40 substances reported to have the highest non-confidential production volumes in 1994 in New York by the Toxic Substances Control Act (TSCA) chemical update system, 19 were petroleum products. Petroleum products are used as fuels (gasoline, diesel fuel, kerosene, heating oil), solvents (stoddard solvent, ligroine) and lubricants (motor oil). Exposure to these products occurs from breathing vapors (such as when filling a gas tank or using an oil-based paint or spraying a pesticide), through skin contact (using products such as paint thinner) or from drinking contaminated water. A spill of a petroleum product can contaminate indoor air, a drinking water well or the soil.

4. Environmental fate:

Some components of petroleum products can evaporate into the air, where they may be broken down by exposure to sunlight and other chemicals in the air. When spilled on soil, some components may leach into the groundwater. Some components are not soluble in water and may sit just above the water table in the soil. Petroleum compounds may be broken down by living organisms in soil or water. However, this may take years to occur. Some components can attach to the soil and remain in the environment for many years.

5. Health effects: Exposure to petroleum products can occur through breathing, swallowing or skin contact.

Health effects from exposure to petroleum products vary depending on the concentration of the substance and the length of time that one is exposed to the substance. Breathing petroleum

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vapors can cause nervous system effects (such as headache, nausea, and dizziness) and respiratory irritation. Very high exposures can cause coma and death. Liquid petroleum products which come into contact with the skin can cause irritation and some can be absorbed through the skin. Chronic exposure to petroleum products may affect the nervous system, blood and kidneys. Animals exposed to high levels of some petroleum products have developed liver and kidney tumors. Whether specific petroleum products can cause cancer in humans is not known; however, there is evidence that occupationally exposed humans in the petroleum refining industry have an increased risk of skin cancer and leukemia.

6. Selection of stressors a. Identification of substances:

There are too many petroleum products to evaluate all of them in this project, so a method of selecting compounds that would be of particular concern for human health was devised. Several sources of information were used to identify possible stressors that could be included in this group. All petroleum products that appeared in the data sources listed below were screened for inclusion in this group. These compounds are listed in Appendix A, Table J.1 along with any available values from those sources.

° American Conference of Governmental Industrial Hygienists (ACGIH): values listed are threshold limit values (TLV).

. New York State Department of Environmental Conservation (NYSDEC) Air Guide 1: values listed are air guideline concentrations (AGC).

e Toxic Substances Control Act (TSCA) Chemical Update System (CUS): values listed are non-confidential volumes reported for chemicals that are manufactured, distributed, processed, used or disposed in New York State. (The 5 substances with the highest volumes were used.)

° New York State Department of Environmental Conservation Spill Information System (DECSIS): values listed are number of spills and number of gallons spilled in New York State in the 1995-1996 fiscal year.

° Farm Chemicals Handbook, 1997: Meister Publishing Company: an ‘X’ denotes the product was listed as a pesticide component (active ingredient or inert) in this publication.

b. Criteria for selection of stressors

The following criteria were used to select stressors to be ranked from the substances identified in the data sources listed above.

° Any substance reported by the NYSDEC Oil spill information system.

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° Any substance with a NYSDEC Air Guide 1 guidance value. ° Any substance reported in the Farm Chemicals Handbook. ° The 5 substances with the highest TSCA CUS production for New York in 1994.

All selected stressors are identified in Table V-J.1 and in Appendix A, Table J.1. The goal was to select those compounds which present a greater potential for human exposure. There were few data on environmental monitoring or release for petroleum products, so spill data (DECSIS), production data (TSCA CUS) and use data (Farm Chemicals Handbook, Air Guide 1) were used as surrogates for exposure data when screening and selecting stressors.

7. Grouping stressors

Petroleum products are mixtures of many different hydrocarbon compounds. Many products have a significant overlap in composition with each other. For this reason, the American Petroleum Institute (API) was consulted to determine if any of the selected products were similar enough in composition to justify considering them as a group rather than as individual stressors. Based on the judgement of the API, several petroleum products were grouped together to be considered as a single category, as shown in Appendix A, Table J.1. For example, diesel fuel and fuel oil #2 were ranked together as “#2 fuel oils” because their components and properties are quite similar.

8. Ranking the stressors

The stressors were ranked by toxicity and exposure using the approach described in the methods section. Some products were grouped into categories based on their similar compositions, and each category was considered to be a single stressor. Data used to rank each substance are shown in Appendix A, Table J.2. First, data were sought for each product, regardless of whether it was grouped into a larger category. Second, each product was ranked based on these data. Third, the rank for a category of products was determined by selecting the highest ranking from the individual products within that category.

In Table V-J.1, each stressor is ranked based on toxicity data and either environmental data (air, water or soil concentrations), production/use data (TSCA) or spill data (DECSIS), whenever these data were available. There was no single measure of environmental exposure which had data available for all substances. Some stressors are shown more than once in Table V-J.1 because more than one type of exposure related data was available. There were air, soil or water data for four stressors ( gasoline range, #2 fuel oils, kerosene range and waste oils). Some of these data were from New York; some were from other states. These environmental data were used to determine the final stressor rank. For stressors without environmental data, spill data or production/use data were used to determine the final rank. The data source used for the final rank is marked with an asterisk in Table V-J.1. Three substances (fuel oil #4, crude oil and ligroine) could not be ranked due to the lack of toxicity data or exposure-related data.

9. Discussion

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Table V-J.1 displays the matrix that combines the toxicity and exposure rankings. Not only does it show that this process can produce different results when more than one measure of exposure is used, but some pathways of exposure (for example, direct contact through spills or inhalation of air concentrations) may be of more concern than other pathways for some stressors.

Because there are sparse toxicological or exposure-related data for many petroleum products, a lower rank should not mean that a substance should be ignored. However, there are enough data to make a reasonable comparison within this group to point out where pollution prevention might begin.

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Table V-J.1: Risk characterization matrix for petroleum products

toxicity rank

1 (highest)

4 (lowest)

*petroleum residues, light vacuum

(TSCA) 2 fuel oil #6 (DECSIS) gasoline range (DECSIS) 3 4 stoddard solvent (TSCA)

indoor air after spill) *kerosene range (TSCA,

air during aircraft fueling) *lubricating base stock (TSCA)

*waste oil (roadside soil)

1 (highest) | 2 3 4 (lowest) exposure 1 gasoline range #2 fuel oils (DECSIS, *asphalt rank (gas station air, TSCA) ground water spill, (TSCA)

kerosene range (DECSIS) waste oil (DECSIS)

* data source used in final ranking (see text) Could not rank due to lack of data:

fuel oil #4 - no toxicity data petroleum (crude oil) - no exposure data ligroine - no exposure data

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The Toxics Release Inventory (TRI) does not require the reporting of petroleum products, so it is difficult to compare the release of these products against other substances. However, 19 of the 40 substances reported to have the highest non-confidential production volumes in 1994 in New York by the Toxic Substances Control Act Chemical Update System were petroleum products. Clearly, petroleum products are among the most widely produced and used substances in New York. Considering the widespread use of these products as automotive fuels, home heating fuels, solvents in paints, pesticides, other household products, and as lubricating oils, combined with the ability of many of their components to evaporate into the air, the potential for exposure to the general population is very high. However, there is more uncertainty related to actual human exposure when stressors are ranked based on production data as opposed to environmental monitoring data.

There is only limited information on the concentration of petroleum products in the air, water and soil. This is partly because investigators usually test for the individual components of these products rather than attempting to quantify the total product. However, the available data indicate that petroleum products can be found in high concentrations in air at gasoline stations, in soil along roads and in groundwater and indoor air following spills. The NYSDEC Spill Information System (DECSIS) data indicate that about five million gallons of petroleum products were spilled in fiscal year 1995-96 in New York. There were over 5000 spills of #2 fuel oil during that period. Populations potentially exposed to petroleum products would be those near spills and those refueling automobiles. Although no data were available, there are potential exposures to petroleum products in the use of some household products and to waste oil for those people who change engine oil.

The final ranking for the nine stressors in this group are shown in Table V-J.2.

Table V-J.2: Individual stressor ranks for petroleum products

Rank Stressor

A (highest) | gasoline range, petroleum residues (light vacuum), #6 fuel oil, #2 fuel oils, kerosene range, lubricating base stock

B waste oil, asphalt

C (lowest) | stoddard solvent

Not ranked | #4 fuel oil, crude oil, ligroine

10. Recommendations

° DECSIS data indicate that there were five million gallons of petroleum products spilled in fiscal year 1995-96 in New York. Many of these spills can impact groundwater or indoor air. Studies should be done to investigate how and why these spills occur and measures should be taken to reduce the number of spills.

° Air monitoring data at gas stations indicate that people who refuel their vehicles can be exposed to high levels of petroleum products. Measures to control such exposures may

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be addressed by pollution prevention. ° More and better environmental monitoring data are needed to properly characterize possible human exposure to these substances.

11. Ranking petroleum products as a stressor group

The volume of petroleum products used and spilled in New York is very large compared to other stressor groups. The few monitoring data available indicate that when these products are used (such as at gasoline stations) or when spills occur, human exposure to petroleum products can increase. Some components of petroleum products can remain in the environment for many years after a spill. Petroleum products can cause central nervous system and respiratory effects. Some have been classified as possible human carcinogens (based on animal data and occupational exposures). Because of their widespread use, the frequency and volume of spills, and the potential for health effects, this stressor group should be ranked A/B.

12. References

Agency for Toxic Substances and Disease Registry. 1997. Toxicological Profile for Mineralbased Crankcase Oil. US Public Health Service. Atlanta, GA.

Agency for Toxic Substances and Disease Registry. 1996. Toxicological Profile for JP-5 and JP-8. US Public Health Service. Atlanta, GA.

Agency for Toxic Substances and Disease Registry. 1995a. Toxicological Profile for Fuel Oils. US Public Health Service. Atlanta, GA.

Agency for Toxic Substances and Disease Registry. 1995b. Toxicological Profile for Gasoline. US Public Health Service. Atlanta, GA.

Agency for Toxic Substances and Disease Registry. 1995c. Toxicological Profile for Stoddard Solvent. US Public Health Service. Atlanta, GA.

EINECS Plus CD. 1996. European inventory of existing commercial chemical substances and European list of notified chemical substances. Silver Platter Information, Ltd. London, UK.

International Agency for Research on Cancer. 1989. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Occupational Exposures in Petroleum Refining; Crude Oil and Major Petroleum Fuels. Volume 45. World Health Organization. Lyon, France.

National Institute for Occupational Safety and Health. 1987. Registry of Toxic Effects of Chemical Substances. 1985-86 edition. US Government Printing Office. Washington, DC.

New York State Department of Environmental Conservation. 1996. Spill Information System

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Annual Report, April 1995 - March 1996. Bureau of Spill Prevention and Response. Albany, NY.

New York State Department of Health. 1998. Personal Communication. Bureau of Toxic Substance Assessment, Special Investigations Section. Albany, NY.

RTK Network, 1997. TSCA Chemical Update System (CUS). www.rtk.net. The Right to Know Network. Washington, DC.

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K. Polynuclear aromatic hydrocarbons (PAHs) 1. Steering Committee definition:

“This category includes aromatic compounds that contain three or more closed rings. A typical example is benzo(a)pyrene, which is a potent carcinogen. The primary source of these compounds in the environment is combustion. Styrene, a PAH, and alkylphenol, a substituted non-halogenated aromatic, are also included in this category.”

2. What are PAHs?

PAHs are a class of chemicals consisting of three or more fused rings. They comprise a large number (several hundred) of substances, many of which have been minimally characterized. PAHs generally occur as complex mixtures, not as single compounds.

3. Sources of PAHs:

PAHs are released to the environment primarily through incomplete combustion, both natural (wildfires) and man-induced (residential coal burning, residential fireplaces, incineration, power generation and tobacco smoking). More than 90% of environmental releases were due to combustion with the remainder due to other sources such as production of coal tar, asphalt and creosote. Also, more than 90% of the PAHs released is to the air.

4. Environmental fate:

Because of their low water solubility and high affinity for organic materials, PAHs released to the atmosphere are expected to bind to airborne particles such as soot.

Due to their very low vapor pressure and low water solubility, PAHs deposited on land will remain bound to soil materials. Since minimal desorption of PAH into water would be expected, erosion and surficial runoff are the most likely processes for movement of PAH from land to water where they would most likely remain on, or become bound to, sediments.

PAHs can chemically decompose to longer lasting products by reacting with sunlight and other chemicals in the air, generally over a period of days to weeks. Breakdown in soil and water generally takes weeks to months and is caused primarily by the actions of microorganisms.

5. Health effects:

There are limited chronic toxicological data for most PAHs. Most information comes from studies of experimental animals and must be extrapolated to humans. However, this information is too limited to draw specific conclusions about noncarcinogenic endpoints on humans. Reliable health-based information exists only on a few of the PAHs and the potential health effects of the other less well-studied PAHs must be inferred from this information.

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There is limited evidence in humans and sufficient evidence from bioassays and shortterm tests that certain PAHs are carcinogenic. Human studies show that some individuals exposed through inhalation or from skin contact for long periods to mixtures that contain PAHs and other compounds have developed cancer.

6. Selection of individual stressors a. Identification of substances

There are several hundred PAHs. The selection of specific PAHs was based on the extensive evaluation previously conducted on this stressor group by the New York State Department of Health and the U.S. Department of Health and Human Services. All PAHs

appearing in the documents listed below were screened for inclusion in this evaluation:

. Ambient Air Criteria Document, Polynuclear Aromatic Hydrocarbons, New York State Department of Health, November, 1989

° Toxicological Profile for Polycyclic Aromatic Hydrocarbons, U.S. Department of Health and Human Services, August, 1995

b. Criteria for selection of stressors

The following criteria were used to select the stressors from the substances identified in the two documents:

° Toxicity of the substance ° Potential for human exposure ° Extent of information available to evaluate substance

Based on these criteria 17 substances were selected for evaluation. Although the Steering Committee’s definition of PAHs included both styrene and alkylphenol (cresol), these substances are being addressed by the Human Health Work Group as a volatile organic compound (VOC) and semi-volatile compound (SVOC) respectively.

7. Ranking the selected stressors

The selected stressors were ranked by toxicity and exposure using the approach described in the methods section. Data used to rank each substance are shown in the attached table. The toxicity ranking assigned to a substance represents the highest rank assigned to the substance in any of the health effects. The selected stressors were evaluated for carcinogenic potential based on the classification of the European Union, the International Agency for Research on Cancer (IARC) and the U.S. Environmental Protection Agency (USEPA). Six of the selected stressors were identified as Category 2 carcinogens (suspected human carcinogen) by the European Union. The IARC classified two of the selected stressors as Group 2A (probable human carcinogen), four as Group 2B (possible human carcinogens) and seven as Group 3 (not

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classifiable). The USEPA classified seven of the selected stressors as Group B2 (probable human carcinogen) and seven as Group D (not classifiable).

A quantitative cancer risk estimate has only been developed for benzo[a]pyrene. USEPA and others have developed a relative potency estimate (toxicity equivalence factor) for PAHs based on their relative potency to benzo[a]pyrene. By using these toxicity equivalence factors, the cancer potency factor for the other carcinogenic PAHs was estimated.

Data on noncancer health effects have been derived from animal studies for acenaphthene, anthracene, fluoranthene, fluorene, and pyrene. The animal studies were for oral exposure of an intermediate duration. There are no adequate dose-response data that identify threshold levels for noncancer health effects in humans or animals for any other substance or duration of exposure.

There is a relatively large body of data characterizing PAH levels in the environment; however, most of the data were derived from studies outside New York. Caution must be used in interpreting and comparing results of different studies due to the use of different sampling times, periods and methods. Rather than trying to reconcile the differences, the data were evaluated and compared with the threshold values established for the exposure ranking for the various environmental concentrations. A specific value was used only when the data clearly showed that it exceeded the respective threshold value for that particular environmental medium. Otherwise, the threshold value was used to represent the respective environmental concentration.

The toxicity and exposure rankings were combined in Table V-K.1 to indicate the individual stressors overall ranking. In general, none of the PAHs were in the upper left corner of the table which represents an A rank. The confidence for the rankings were low for all the substances, except for acenaphthene, because they do not have a LOEL (lowest observed effect level). Acenaphthene is given a moderate confidence ranking since it has a LOAEL derived from a mouse oral subchronic study.

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Table V-K.1: Risk characterization matrix for PAHs

Toxicity Rank 1 (highest) 2 3 4 (lowest) 1 Benzo[a]pyrene L 2 Fluoranthene L E “posure Pyrene L Benzo[a]anthracene L Chrysene L_ | Benzo[e]pyrene L Benzo[b]fluoranthene L Benzo[g,h,i]perylene L 3 Benzo[k]fluoranthene L Ideno[1,2,3-c,d]pyrene L Dibenz[a,hJanthracene L_ | Benzo[j]fluoranthene L Acenapthene L Acenaphthylene M 4 Anthracene L Fluorene L Phenanthrene L Confidence M = moderate L=low

8. Discussion

There are limited environmental exposure data for PAHs in New York. The 1996 Toxic Release Inventory data show air releases of 9400 pounds for phenanthrene and 580 pounds for anthracene. There were no reported spills or emergency releases of PAHs in New York. The New York State Department of Health conducted a surface soil sampling study in the SenecaBabcock neighborhood in Buffalo. Results of this study indicated a minimal increase in health risk from soil ingestion attributed to the concentrations of benzo(a)pyrene. The New York State Department of Health has taken subsequent subsurface soil samples to assess the additional health risk from eating vegetables grown in this soil. Results of the potential risk from eating homegrown vegetables has not been completed. The New York State Department of Health also participated in a recently completed study of emissions from the open burning of household waste in barrels. The study found that the mass emitted per mass of waste burned to be substantial for many compounds including PAHs. The exposure to humans from these emissions has not been determined. Additional exposure data used in this evaluation for PAHs were derived from various studies throughout the United States. As noted earlier, caution must be used in interpreting and comparing results of different studies due to the use of different sampling times, periods and methods.

In selecting exposure concentration data, the highest reported value in the references was used only if it exceeded the respective threshold value for that particular medium. This highest value was used regardless when it was collected. This approach in all likelihood would lead to a

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more conservative ranking for a particular PAH.

The greatest sources of exposure to PAHs for most of the US population are active or passive inhalation of the compounds in tobacco smoke, wood smoke, and contaminated air, and ingestion of these compounds in foodstuffs. Ingestion of foodstuff and tobacco smoke can be more significant pathways of exposure to PAHs than contaminated air depending on personal habits and preferences. Primarily due to emissions from tobacco smoke, unvented space heaters, and food preparation, indoor air can be an important source of human exposures to PAHs.

The final ranking for the 17 stressors in this group are shown in Table V-K.2.

Table V-K.2: Individual stressor ranks for PAHs

Rank Stressor A Benzo[a]pyrene B Dibenz[a,h]anthracene, Benzo[a]anthracene, Benzo[b]fluoranthene, Benzo[k]fluoranthene, Ideno[1,2,3-c,d]pyrene, Chrysene, Fluoranthene, Pyrene Cc Benzo[j]fluoranthene, Benzo[e]pyrene, Benzo[g,h,i]perylene, Acenapthene, Acenaphtylene, Anthracene, Fluorene, Phenanthrene

9. Recommendations

. More and better environmental monitoring data, specific to New York, are needed to properly characterize human exposure to PAHs.

° More and better health effects data associated with acute-duration and chronic-duration exposure to PAHs are needed.

10. Ranking PAHs as a stressor group

It is recommended that this stressor group be ranked C but the individual stressor, benzo(a)pyrene, be ranked as B due to higher than average soil concentrations in New York. The recommendation is based on the conservative approach used in the evaluation of this stressor group and the opportunity for pollution prevention to reduce health risks. The exposure values used in this evaluation represented maximum values reported in the references. In all likelihood, exposure to concentrations of PAHs in New York would be much lower except for soil concentrations. Since personal habits (tobacco smoker, whether windows were kept open, how frequently doors were opened, and home improvements) and individual preferences (method of home heating, cooking methods, diet, etc.) are significant factors in determining the level of exposure to PAHs, pollution prevention would offer limited opportunity to reduce known health effects from PAHs.

11. References

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American Conference of Governmental Industrial Hygienists, Inc. 1997. 1997 Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. ACGIH. Cincinnati, OH.

EINECS Plus CD. 1996. European inventory of existing commercial chemical substances and European list of notified chemical substances. Silver Platter Information Ltd. London, UK.

New York State Department of Environmental Conservation. 1986. New York State Toxics Air Monitoring Report 1982-1984. Division of Air Resources. Albany, NY.

New York State Department of Environmental Conservation. 1991. Draft New York State Air Guide-1; Guidelines for the Control of Toxic Ambient Air Contaminants. Division of Air Resources. Albany, NY.

New York State Department of Environmental Conservation. 1996. SARA Title III, Section 313, 1996 TRI Data as of 1/98. Chemical list by total amount. NYSDEC. Albany, NY.

New York State Department of Health. 1989. Ambient Air Criteria Document, Polynuclear Aromatic Hydrocarbons. Bureau of Toxic Substance Assessment. Albany, NY.

New York State Department of Health. 1996. Revised Draft- Technical Report; Seneca-Babcock Neighborhood Soil Sampling Program, Results of December 1994 Sampling. Bureau of Environmental Exposure Investigation. Albany, NY.

U.S. Department of Health & Human Services. 1995. Toxicological Profile for Polycyclic Aromatic Hydrocarbons. Agency for Toxic Substances and Disease Registry. Atlanta, GA.

US Environmental Protection Agency. 1997. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, OH.

United States Environmental Protection Agency. 1997. Evaluation of Emissions From the Open Burning of Household Waste in Barrels. Washington, DC.

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L. Ionizing Radiation 1. Steering Committee definition

“This category includes radiation released by human activities, but not radon or other naturally-occurring radiation.” The Human Health Work Group included a discussion of radon in this section for informational purposes even though it is not officially a part of this stressor group .

2. What is Ionizing Radiation?

Ionizing radiation is any radiation capable of displacing electrons from atoms or molecules, thereby producing ions. Examples of ionizing radiation are alpha, beta, gamma, X-rays, neutrons and ultraviolet light. High doses of ionizing radiation may produce severe skin or tissue damage (USNRC, 1981).

There are five types of ionizing radiation associated with radioactive materials which can affect humans. These types are alpha, beta, gamma , X-rays and neutron radiation. Alpha particles are composed of two neutrons and two protons. Beta particles are high-speed electrons. Gamma radiation, like medical X-rays, is composed of photons. However, gamma radiation is emitted from the nucleus of atoms whereas X-rays are of lower energy and are either emitted by electrons orbiting the nucleus or emitted by X-ray generating machines.

Radioactive materials are used in certain manufacturing and industrial processes such as measuring the thickness of products, elimination of static electricity, and increasing the shelf life of food products. Radioactive materials are also used in oil drilling, geologic exploration, weld examinations, laboratory non-destructive testing, and jet engine inspections. Radioactive materials can be found in consumer products such as smoke detectors, luminous dial watches and exit signs. Radioactive materials are employed in medical diagnosis and treatment, medical and scientific research, and in the production of electricity at nuclear power plants.

3. Definition of terms used

Maximally Exposed Individual. A hypothetical person who remains in an uncontrolled area who would, when all potential routes of exposure from a facility’s operation are considered, receive the greatest possible dose equivalent.

Millicurie (mCi). A millicurie is one-thousandth of a curie (3.7 x 10’ transformations per second).

Millirem (mrem). A unit of radiation dose equivalent that is equal to one one-thousandth of a rem. Rem. The acronym for roentgen equivalent man. The special unit of any of the quantities expressed as dose equivalent. The dose equivalent in rem is equal to the absorbed dose in rad multiplied by the quality factor.

4. Environmental fate

Regulated Discharges

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Most radioactive materials are not discharged to the environment. However, certain regulated amounts of radioactive material are allowed to be discharged to the air and water environment by governmental agencies such as the United States Department of Energy (DOE), the Nuclear Regulatory Commission (NRC), the United States Environmental Protection Agency (USEPA) and the New York State Department of Environmental Conservation (NYSDEC). Regulated discharges and potential doses to the maximally exposed member of the public which might result from those discharges are shown in Appendix A, Table L.1.

Accidental Releases in Transport

Radioactive materials are rarely spilled (released) during the normal course of transportation. There is however, the potential to release radioactive materials to the environment in transportation accidents involving the transport of low-level radioactive waste (LLRW) or radioactive isotopes used for medical, research or industrial purposes. In New York, the safety record for LLRW transport has been very good. Only six transportation accidents involving LLRW occurred in New York during the period 1971 to 1997 and none of these involved any release of radioactive material. There were eleven incidents of minor radioactive contamination of LLRW transport casks which exceeded federal standards during this period (Sandia, 1997).

Some transportation incidents have involved the transport of radioactive pharmaceuticals or sealed radioactive sources en route to the products users. There have been ten incidents involving these types of radioactive materials during the period 1971 to 1997 in New York. Only one of these incidents resulted in an environmental release (Sandia, 1997). This release occurred in July 1992 when a Trans World Airline aircraft aborted takeoff at Kennedy Airport and caught fire. The plane was carrying 3 molybdenum / Technetium generators designated for medical use which were

damaged by the fire. All three generators sustained some release of radioactive materials (Sandia, 1997).

FUSRAP Sites/Facilities

There are 46 formerly utilized remedial action program (FUSRAP) sites nationwide, of which 24 have been remediated. There are at least seven sites located in New York that require remediation (Pena, 1997). These sites are owned by the federal government, private industry, or individuals and most were used by the Manhattan Engineering District and the Atomic Energy Commission for research development, production of uranium and thorium feed materials or storage of radioactive ores and residues and became contaminated as a result of these activities (DOE, 1992). The seven major FUSRAP sites in New York are, with one exception, secured/restricted sites located adjacent to uncontrolled public areas. The radioactive contamination at these sites is being remediated with federal funding. There are presently no discharges to the off-site environment that result in any measurable dose to the public. One goal of the FUSRAP program is to effectively cleanup any residual radioactive contamination to allow for future use of the sites.

Brookhaven National Labs (BNL)

In 1997, the Agency for Toxic Substances and Disease Registry (ATSDR) of the U.S. Department of Health & Human Services performed a health consultation of the groundwater contamination at BNL (ATSDR, 1997b). The report states, "the radionuclides strontium-90 and

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tritium have appeared above drinking water standards in on-site monitoring wells. Strontium-90 and tritium have not been detected off site at levels above drinking water standards." In the conclusions of the consultation, conclusion number five states, "the levels of strontium-90 and tritium detected in residential wells are below their respective drinking water standards and are not expected to cause adverse health effects." Other than airborne radionuclide releases, which are detailed in another section of this report, the only other pathway for public exposure is discharges from the sewage treatment plant (STP) to the Peconic River. A recent discharge from the STP, from July 25 to July 28, 1997, discharged approximately 300 mCi of tritium into the on-site portion of the Peconic River at a maximum concentration of 65,000 picocuries per liter (pCi/l). However, the portion of the Peconic River on-site which receives the STP effluent is entirely lost to the groundwater system before it reaches the eastern BNL site boundary (Geraghty & Miller, 1996). Thus the STP effluent drains from the stream channel and recharges the underlying water table, becoming part of the groundwater system. Therefore this discharge is not expected to lead to public exposure due to dilution and decay in the groundwater system, and since the homes whose wells are most likely to be impacted by this release have been connected to the public water supply system.

5. Natural background radiation

The world is continually exposed to low levels of ionizing radiation and this exposure is called background radiation. The average annual radiation exposure to the United States population from background and other sources is 360 millirem (mrem). This average radiation exposure is tabulated in Table V-L.1.

Most of this exposure is from radon (55%) which is found in all air, but at higher levels in indoor environments. People are exposed to radiation from cosmic sources (8%), terrestrial sources (8%) and natural internal sources (11%). Humans may also be exposed to ionizing radiation from x-ray and nuclear medicine tests and from radiation therapy (15%). Less than 0.1% of the public’s exposure is from the regulated discharge of radioactive material to the environment (NCRP, 1987).

Table V-L.1: Breakdown of average radiation exposure to U.S. population

Source Dose % of mrem/yr Total

Cosmic - Radiation entering the earth’s atmosphere from sources in outer 26 8 space. Main radionuclides produced include C-14, H-3 and Na-22 which are isotopes of major elements in the body. Essentially constant, although does vary with altitude.

Terrestrial - Radiation from radionuclides naturally present in the earth’s 28 8 soil, rocks, etc. Radionuclides include U-238, U-235 and Th-232. Essentially constant.

Internal - Mainly consists of C-14, K-40, Pb-210/Po-210, U, Th, and Ra 39 11 which are maintained within the body at a constant level.

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Inhaled (Radon) - Largest natural radiation source and most variable. 200 55 Due to natural radon and its short lived decay products.

Medical - Includes diagnostic tests (e.g. x-rays) and nuclear medicine 53 15 therapy (e.g. cancer treatment).

Consumer Products - Various radionuclides included in and radiation 10 3 from domestic water supplies, building materials, combustible fuels (coal, natural gas) highway construction materials and television receivers.

Occupational - Various jobs routinely use or produce radioactive 1 0.3 sources/materials such as medical, mining, well logging etc.

Fallout - Includes radioactive fallout from the past atmospheric nuclear <l <0.3 weapons tests. Most of current exposure is from C-14, with smaller amounts from external sources and internal Sr-90 sources. This value will continue to decrease.

Nuclear Fuel Cycle - Includes the exposure to radiation from mining, <0.5 0.1 fuel processing, power production, waste management and disposal.

Totals - The total average annual effective dose equivalent exposure to a 360 100 member of the U.S. population.

Source: NCRP Report No. 93 and NCRP Report No. 94

6. Radon

Radon is a naturally occurring radioactive gas that results from the radioactive decay of radium which occurs in varying concentrations in all types of soil. Radon atoms that reach the ground surface disperse readily into the atmosphere and produce an ambient concentration of about 0.2 - 0.5 picocuries per liter (pCi/L) of air. Radon is carried into buildings with soil gas entering the building through openings and cracks in the basement walls and floors and can accumulate to high concentrations indoors. The average radon concentration in New York single family homes has been measured at 1.1 pCi/L in the first floor and 2.7 pCi/L in the basement. Radon concentrations in homes depend on the surficial soil characteristics (radium concentration and soil permeability), the house construction (degree of communication between indoor air and surrounding soil gas) and house ventilation characteristics (ventilation rate, sources of indoor pressure reduction). Indoor concentration varies considerably from one home to another and from area to area in the state. Radon is also dissolved in groundwater and can be carried into homes with well water. Some of the radon in water escapes into the house atmosphere when water is aerated as in the showers and washing machines, thus, contributing to the indoor air concentration.

Radon decays into a series of short lived radioactive isotopes of polonium, lead and bismuth. As one breathes, these decay products which are suspended in the air, deposit on the inner surface of the lungs leading to radiation exposure to the lung tissue. Exposure to indoor radon has been estimated by a National Research Council committee to result in 15,400 or 21,800 lung cancer deaths per year in the US, depending on which model is used.

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7. Health effects of ionizing radiation

Radiation exposure can result from radiation sources which emit penetrating radiation, such as x-ray machines and gamma emitting radioactive sources. It also can result from the intake through ingestion, inhalation or absorption through the skin, of radioactive materials, which are deposited in the body. As these materials decay, the emitted radiation delivers a dose to the tissue. The radiation dose received depends on the type of radiation emitted, the type and amount of the radioactive material deposited, its distribution within different organs and tissues, and how rapidly it decays and is eliminated from the body. The nature of the health effects that can result from radiation depends upon a number of factors which include the radiation dose received, the period over which the dose is received, and the part of the body receiving the dose. At high doses, radiation can cause a variety of injuries whose severity increases with the absorbed dose. At very high doses, radiation results in killing a sufficient number of cells to cause death or to impair the function of the exposed organ within a short time after exposure. At low radiation doses, similar to those likely to result from environmental exposure, these acute effects do not occur, but the radiation dose increases the probability of cancer induction in the exposed individual. Radiation has been found to increase cancer risk in most body tissues. The added probability of cancer mortality from radiation exposure increases with dose, and is estimated to be about 5 x 10“ per rem. Different tissues have differing sensitivities for radiation induced cancer. Bone marrow (leukemia), thyroid, female breast and lungs are among the most sensitive organs. On the other hand, there is little, or no evidence that radiation causes prostate or cervical cancer.

8. Regulatory standards

State and federal agencies have established strict regulatory standards that limit the radiation doses received by humans. These health-based standards have been established to limit the risk associated with exposure to radiation. The possession and use of radiation sources and radioactive materials are regulated in New York by the New York State Departments of Health and Labor and by the New York City Department of Health. The NYSDEC regulates the discharge of radioactive material to the environment from State-regulated facilities under its 6 NYCRR Part 380 regulations, "Prevention and Control of Environmental Pollution by Radioactive Materials" (NYSDEC, 1994). Part 380 limits potential public doses that may result from these discharges to 100 millirem per year (mrem/yr), which is approximately 28% of an individual’s background exposure.

When the NYSDEC revised 6 NYCRR Part 380, in 1994, a new section was added requiring Part 380 permittees to develop discharge minimization programs. Subpart 380-7 requires all permittees to develop, document, and implement a discharge minimization program for maintaining discharges of licensed material to the environment as low as reasonably achievable (ALARA). ALARA is a basic principle of radiation safety and means making every reasonable effort to maintain exposures to radiation as far below the regulatory dose limits as is practical consistent with the purpose for which the radioactive material is used. The concept of ALARA includes evaluating the application of pollution prevention techniques . Most facilities holding Part 380 permits in New York now have discharge minimization programs, and by March of 1999, all Part 380 permittees will have them.

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Within three years, the Part 380 regulations will be revised to include a 10 mrem dose constraint for radioactive emissions to the air, to be compatible with federal regulations (10 CFR 20). Currently, there are 33 Part 380 permits authorizing the discharge of radioactive material to the environment (via air, water, and incineration). The dose to the public that could result from these permitted discharges would be less than 10 mrem/yr if permittees discharged the maximum quantities allowed under their permits. Most permittees did not discharge their maximum permit limits and the potential dose to the public that could have resulted from the 1996 discharges is less than 1 mrem/yr.

The current federal and state regulations limit radiation workers’ doses to 5.0 rem/yr (5,000 mrem/year). The limit to the public is 100 mrem/yr. The USEPA National Emissions Standards for Hazardous Air Pollutants (NESHAPS) contain requirements that limit the dose from radionuclides discharged to the air to 10.0 mrem/yr. Based on the Safe Drinking Water Act, the USEPA has issued drinking water standards in 40 CFR that limit the dose from radionuclides to 4.0 mrem/year for man made sources of beta and photon emitters. The USEPA has adopted a cleanup standard of 15 mrem/year dose to the public for radioactively contaminated sites. The NRC’s criterion for unrestricted use of facilities and sites following decommissioning is 25 mrem/yr. New York state agencies will adopt a comparable requirement. Finally, for nuclear power plants, the NRC has sets ALARA goals in Appendix I to 10 CFR Part 50 to limit air discharges so that the maximum dose does not exceed 5.0 mrem/yr to individuals in unrestricted areas (USNRC, 1997).

9. Identification of radionuclides

Appendix A, Table L.1 lists 64 radionuclides (sources of ionizing radiation) which were permitted to be discharged (1996 data) by either state or federal regulatory agencies. The total discharge in millicuries (mCi) for each radionuclide can be found at the bottom of the spread sheet in the row entitled “total activity”. The numeric threshold for entry on the spread sheet was an annual discharge of 10“ mCi (0.1 microcurie) or greater. Therefore, some extremely small annual discharges are not listed. The predicted annual dose to maximally exposed members of the public (off-site) for all 36 facilities is listed in the column “Dose mrem/yr”. Specific doses for certain facilities were developed through computer modeling. Where available, the dose from air and water pathways are given separately.

10. Selection of stressors

Since all the radionuclides listed in Appendix A, Table L.1 are sources of ionizing radiation and since biological effects of ionizing radiation are primarily dependent on dose, pathway and duration of exposure, it is difficult to select one radionuclide over another in any kind of specific ranking. The best method of evaluating ionizing radiation as a stressor is to look at the overall dose given to members of the public by radioactive materials discharged to the environment as compared to natural sources of ionizing radiation. These doses, resulting from regulated facility discharges, can be found in the “Dose mrem/yr” column in Appendix A, Table L.1.

11. Ranking man-made discharges of ionizing radiation as a stressor

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Radioactive materials discharged to the environment, either through regulated discharges or through accidental releases, qualify as environmental stressors. All but one of the largest regulated discharges to the environment are noble gases which are not incorporated into the body and are readily dispersed in the atmosphere (Ar-41, Kr-85, Kr-85m, Kr-87,

Kr-88, Xe-133, and Xe-135). The only other radionuclide that was discharged in any significant amount was tritium (H-3). The doses to the maximally exposed individual from these discharges however, were very small. The doses from regulated facility discharges are minimal when compared to the internal dose for the average American due to C-14, K-40, Pb-210, Po-210, U, Th, and Ra (39 mrem/yr). The radionuclides that contribute to this internal dose are normally found in the body. When facility discharge doses are compared to the overall dose the average person receives a year from background and other sources (360 mrem/yr, see Table V-L.1), they are very small.

Since the doses from these discharges are extremely small and the overall potential for exposure is low, the ranking of man-made discharges of ionizing radiation as a stressor is therefore Cc.

12. Natural sources of ionizing radiation as an area of concern

Natural sources of radiation can be grouped into four main groups: cosmic, terrestrial, internal and radon. Combined, these sources contribute about 82% of the total annual radiation dose to the average US resident.

Cosmic radiation, which originates outside the earth is attenuated by the atmosphere before reaching the earth’s surface. Thus, its contribution to dose increases with elevation, due to the reduced thickness of the protective atmospheric layer. At sea level, it results in an annual dose of about 26 mrem. The dose doubles at an elevation of about 1,500 meters (about 5,000 feet).

Terrestrial radiation arises from radionuclides with very long half-life, referred to as primordial radionuclides, which existed in the earth’s crust since its formation. These include potassium-40 (“K) and different uranium (U) and thorium (Th) isotopes. The U and Th isotopes form decay chains of shorter lived decay products which include radium and radon. Exposure to gamma radiation emitted by these radionuclides results in an average dose to the US resident of 28 millirem per year. The terrestrial dose varies from one area to another depending upon the concentration of the different radionuclides in the soil and the surficial rock formations. For example, the terrestrial radiation dose in parts of Bear Mountain park in New York is more than 100 mrem/yr for a person continuously present at that location.

Internal radiation dose results from the incorporation of primordial and cosmogonic radionuclides and their decay products into body tissues following their intake, primarily with food or water. The average annual dose from internal sources is about 39 mrem. The largest contribution to internal dose comes from “°K and Polonium-210 (*'°Po). “°K contributes about 19 mrem/yr and !°Po, which occurs in the decay chain of Uranium-238 (* U), contributes about 16 mrem/yr. Cosmic radiation also produces radioactive materials in the atmosphere including Tritium CH), Beryllium-7 (’ Be), Carbon-14 ('*C), and Sodium-22 (??Na). The intake of ’Be and '*C

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contribute about 1.2 mrem/yr each to an individual’s dose. Contributions from H and Na are much smaller.

Assuming an indoor air radon concentration of 1.1 pCi/L, the National Council on Radiation Protection and Measurements (NCRP) estimated the inhalation of radon decay products to result in an average radiation dose of 2400 mrem7/yr to the bronchial epithelium of the lungs and an effective dose equivalent of 200 mrem/yr. Thus, exposure to indoor radon contributes about two thirds of the average total radiation dose from natural sources. Indoor radon concentrations show large variability. The concentrations measured by NYSDOH in indoor air in New York range from about 0.5 to 520 pCi/L. Concentrations over 2000 pCi/L have been reported in homes in Pennsylvania and in New Jersey.

The National Research Council committee used two different models to estimate that 15,400 or 21,800 of the lung cancer deaths that occurred in 1995 in the US can be attributed to exposure to indoor radon. The US population was 270 million in 1995 , so the risk of death from exposure to radon is 5.7 x 10° or 8.1 x 10° per year. Assuming a 72 year lifespan, the risk of death is approximately 4.1 x 10° or 5.8 x 10° for a lifetime. Since exposure to existing levels of indoor radon are estimated to result in these levels of risk, exposure to radon in indoor air should be considered an area of concern.

13. Recommendations

Because of the very large radiation doses that may result from indoor radon, both USEPA and NYSDOH encourage New York residents to measure radon in their homes and to reduce the radon levels if they exceed 4 pCi/L.

14. References

Agency for Toxic Substances and Disease Registry (ATSDR). 1997a. Draft Toxicological Profile For Ionizing Radiation. U.S. Department of Health and Human Services. Atlanta, GA.

Agency for Toxic Substances and disease Registry (ATSDR). 1997b. Health Consultation Addendum, CERCLIS No. NY7890008975. U.S. Department of Health and Human Services. Atlanta, GA

Geraghty & Miller, Inc. 1996. Regional Groundwater Model Brookhaven National Laboratory.

Mettler, Jr., Fred A.,MD, and Upton, Arthur C., MD, Medical Effects of Ionizing Radiation, Second Edition, W.B.Saunders Company, Philadelphia, PA. 1995.

National Council on Radiation Protection and Measurements (NCRP). 1987. Ionizing Radiation Exposure of the Population of the United States. No. 93. NCRP, Bethesda, MD.

National Council on Radiation Protection and Measurements (NCRP). 1987. Exposure of the Population in the United States and Canada from Natural Background Radiation. No. 94.

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NCRP, Bethesda, MD.

National Research Council. 1998. Committee on Health Risks of Exposure to Radon (BEIR VD), Health Effects of Exposure to Radon; Washington DC. National Academy Press.

Niagara Mohawk Power Corporation (NMPC). 1997. January-June 1996 Semi-Annual Effluent Release Report Nine Mile Point Unit 1. NMPC, Lycoming, NY.

Niagara Mohawk Power Corporation. (NMPC) 1997. July-December 1996 Semi-Annual Effluent Release Report Nine Mile Point Unit 1. NMPC, Lycoming, NY.

Niagara Mohawk Power Corporation (NMPC) 1997. January-June 1996 Semi-Annual Effluent Release Report Nine Mile Point Unit 2. NMPC, Lycoming, NY.

Niagara Mohawk Power Corporation (NMPC) 1997. July-December 1996 Semi-Annual Effluent Release Report Nine Mile Point Unit 2. NMPC, Lycoming, NY.

New York Power Authority (NYPA). 1997. James A. Fitzpatrick Nuclear Power Plant SemiAnnual Radioactive Effluent Release Report January-June 1996. NYPA, Lycoming, NY.

New York Power Authority (NYPA). 1997. James A. Fitzpatrick Nuclear Power Plant SemiAnnual Radioactive Effluent Release Report July-December 1996. NYPA, Lycoming, NY.

New York Power Authority (NYPA). 1997. Indian Point Nuclear Power Plant Semi-Annual Effluent Release Report January-June 1996. Lycoming, NY.

New York Power Authority (NYPA). 1997. Indian Point Nuclear Power Plant Semi-Annual Effluent Release Report July-December 1996. Lycoming, NY.

New York State Department of Environmental Conservation (NYSDEC). 1994. 6 NYCRR Part 380 rules and Regulations for Prevention and Control of Environmental Pollution by Radioactive Materials.

Pena, Federico, Secretary of Energy, 1997. Correspondence sent to Honorable William S. Cohen, Secretary of Defense. Washington, DC.

Rochester Gas and Electric Corporation (RG & E). 1996. R.E. Ginna Nuclear Power Plant SemiAnnual Effluent Release Report January-June 1995. Rochester, NY.

Rochester Gas and Electric Corporation (RG & E). 1996. R.E. Ginna Nuclear Power Plant SemiAnnual Effluent Release Report July-December 1995. Rochester, NY.

Sandia National Laboratories (Sandia) 1997. Radioactive Materials Incident Report Database 1971-1997. Sandia National Laboratories, Albuquerque, NM .

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U.S. Department of Energy (USDOE). 1992. Environmental Restoration and Waste Management Site-Specific Plan for DOE Oak Ridge Field Office Formerly Utilized Sites Remedial Action Program. USDOE, Oak Ridge, TN. U.S.

United States Department of Energy (USDOE). 1994. Niagara Falls Storage Site Environmental Surveillance Report for Calendar Year 1993. Lewiston, NY

U.S. Department of Energy (USDOE). 1996. Brookhaven National Laboratory (BNL) Site Environmental Report for Calendar Year 1995. U.S. DOE, Upton, NY.

Department of Energy (USDOE). 1997. U.S. Department of Energy Air Emissions Annual Report Calendar Year 1996 Colonie Interim Storage Site (CISS), U.S. DOE, Colonie, NY.

U.S. Department of Energy (USDOE). 1997. U.S. Department of Energy Report of Radionuclide Emissions for Calendar Year 1996 for the Knolls and Kesselring Sites of the Knolls Atomic Power Laboratory. Schenectady, NY.

United States Nuclear Regulatory Commission (USNRC). 1997. 10 CFR Part 50 Domestic Licensing of Production and Utilization Facilities, Appendix I to Part 50

United States Nuclear Regulatory Commission (USNRC). 1981. Glossary of Terms. NUREG0770. Washington, D.C.

West Valley Nuclear Services Company, Inc./ Dames & Moore. 1997. West Valley Demonstration Project Site Environmental Report 1996. WVNS, West Valley, NY.

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M. Suspended and settleable solids 1. Steering Committee definition

“This category includes nontoxic solid particles, such as silt, that have the ability to cause physical or mechanical damage to surface waters.”

2. What are they?

Settleable solids are defined as solids in water that may, in quiescent waters, settle within a given period of time, usually one hour. Suspended solids are fine grained solids in water that remain suspended in the water for periods greater than one hour. These solids may include soil particles and biological particles such as algae, but not include pathogens. With additional more prolonged periods of quiescence, a portion of these solids may also settle. The most evident characteristic of water with elevated levels of solids is the lack of water clarity and having turbid brown or gray appearance, unless biological materials predominate giving the water another color

(e.g., green). 3. Sources of solids

The greatest amount of solids (more than 90%) originate from erosion of soils, particularly during rainfall and high water events. Additional quantities of suspended and settleable solids derive from natural biological materials (e.g., algae) and wastewater control facilities. The concentration of suspended or settleable solids in water is dependent on several factors including water velocity, the amounts of rainfall or snow melt, temperature, the relative ability of soil to be eroded, and soil cover. The level of solids of biological origin is also affected by nutrient concentrations, the amount of sunlight, and the concentrations of herbivores or planktivores within the water.

4. Environmental fate

Settleable solids are readily deposited at any location with quiet or relatively quiet waters, e.g., flood plains, wetlands, pools, lakes, reservoirs, and other impoundments. These solids may not be resuspended except during major flow events. These solids are most responsible for filling of impoundments thereby reducing their water holding capacity.

A portion of suspended solids may settle if prolonged quiescence is encountered. These solids are most readily resuspended during storm or other high flow events. The organic portion of suspended solids are normally a part of natural biological cycles. Those solids that do not settle may eventually be transported downstream to the ocean.

5. Health effects

The quantification of health effects does not follow methods for evaluation of chemical compounds, yet the presence of suspended or settleable solids in water may have dramatic effects

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on the use of water by humans. For example, solids may impart a disagreeable taste and color to water necessitating solids removal, at substantial expense for construction and operation of treatment facilities, to make water acceptable for drinking. During swimming season, excessive suspended solids may preclude use of water by bathers. Settleable solids may have a long term impact on reservoir or water supply capacity. While immediate threats to water supply capacity are seldom experienced in New York, water supplies of several small communities must be regularly maintained to assure appropriate capacity.

A substantial concern in some waters is the ability of harmful chemicals (e.g., polychlorinated biphenyls, heavy metals) to adhere to fine particles (suspended solids) which then act as a concentrating mechanism for chemical residues and as a transport mechanism for contaminants within a waterway. The adherence of chemicals to suspended solids creates opportunities for enhanced human exposure to these chemicals through several mechanisms:

a) drinking water exposure,

b) direct skin contact with sediments,

c) inhalation of chemicals desorbed from sediments, and

d) ingestion of edible biota (e.g., fish, shellfish and crustaceans) that have acquired their

contaminants via direct or indirect exposure to chemicals on suspended or settled solids.

Adhered chemicals would have to be removed from public drinking water supplies via filtration and/or coagulation of solids. The dermal and inhalation exposure pathways are minor exposure routes in most cases. Only in the case of consumption of aquatic organisms can potentially harmful concentrations of chemical residues derived from suspended or settled solids represent a human health concern. In the known instances where this may occur (e.g., polychlorinated biphenyls, DDT, dioxins), institutional controls on the consumption of fish or other aquatic organisms would reduce the human health risks.

6. Ranking the stressor group

It is recommended that the stressor group be classified as C. Several factors were considered as follows:

a) Where suspended or settleable solids may be a factor for drinking water, filtration and/or treatment with alum is conducted to remove the solids prior to distribution of the water to the public.

b) For public bathing areas, regulations controlling the level of acceptable turbidity, one measure of suspended solids levels, are enforced to provide for improved public safety. Swimming at sites that are unregulated may pose some additional risk when water clarity is reduced.

c) Chemical residues adhered to suspended or settleable solids are largely removed by solids removal in water supply systems. For waters not in water supply systems, dermal contact with, inhalation of, or incidental ingestion of, chemical residues adhered to suspended solids normally represent a minuscule health risk. Institutional controls of chemical residues in foods would reduce the risk posed by chemicals which are transferred from suspended solids to edible biota.

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N. Volatile (VOCs) & semi-volatile (SVOCs) organic compounds

1. Steering Committee definitions

(VOCs): This category includes many low molecular weight solvents used in a variety of commercial processes, such as dry cleaning, degreasing, manufacturing, painting and printing. Common solvents include perchloroethylene, TCE, and benzene.

(SVOCs): This category includes phthalates, alkylphenols, and glycol ethers, among other compounds, that may produce harmful effects such as endocrine disruption.

2. Human Health Work Group definition

VOCs and SVOCs are man-made compounds with the common characteristic that they contain carbon as a fundamental part of their structure. VOCs and SVOCs are distinguished analytically from each other principally on the basis of their volatility and relative boiling points with VOCs possessing boiling points below 100°C and SVOCs boiling in excess of 100°C. VOCs also typically have higher vapor pressures than SVOCs. There are hundreds of both VOCs and SVOCs that are presently used in commercial and industrial applications.

3. Sources

Transient VOC and SVOC presence in the environment results both from human activities (e.g., trace concentrations of benzene from gasoline) and from direct or fugitive release from industrial processes (e.g., cleaning solvents from dry cleaners). Of the total material derived from human activities that is emitted to the atmosphere on an annual basis, VOCs as a class have been estimated to contribute approximately 15%. SVOCs, as compared to VOCs, do not have as significant an atmospheric presence due to physical/chemical properties which limit their use in industrial applications.

4. Environmental fate

The primary environmental medium (e.g., air, water, soil) in which many VOCs are initially found is the atmosphere as a result of their relatively high vapor pressures. Atmospheric half-life of VOCs, however, is short as a result of transformation and reaction with hydroxyl radicals in air and degradation precipitated by sunlight and other atmospheric processes. If contained in surface waters, VOCs will rapidly volatilize, while their relative presence in soil, sediment, and water bodies is limited. SVOCs, with lower vapor pressures, will distribute more readily to soil, surfaceand groundwater, and to a lesser extent, air, although SVOCs in air tend to be rapidly removed by photochemical reactions. In surface water and soil, non-chlorinated VOCs and SVOCs are generally rapidly removed as a result of biodegradation by microorganisms, although rate of degradation is dependent on environmental temperature, microbial acclimation, and mixing conditions (in water). As a class, both VOCs and SVOCs will not persist in the environment for long periods of time as do some other more persistent chemicals (e.g., metals, polychlorinated aromatics such as dioxin).

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5. Health effects

There are acute and chronic toxicity data for some VOCs and SVOCs, particularly those with known carcinogenic properties (e.g., benzene, vinyl chloride, formaldehyde). The sentinel health effect of many VOCs is Central Nervous System (CNS) depression and sensory irritation following overexposure, typically in occupational settings. Other toxicities (kidney, liver damage) are associated with VOCs and SVOCs, although these effects have either been evaluated through animal laboratory studies or reported in occupational settings and human case reports. There are limited data suggestive of chronic adverse effects resulting from environmental exposures to VOCs or SVOCs, most likely a result of the limited duration and concentration of exposure potential to humans. Ingestion and dermal contact (the other potential pathways of exposure) of most VOCs and SVOCs is negligible from environmental media and these routes of exposure are not anticipated to contribute to adverse health effects.

6. Initial screening of VOCs and SVOCs

VOCs and SVOCs were distinguished from each other based on the standard USEPA analytical methodologies (8240A for VOCs and 8270A for SVOCs) that are used to detect these respective classes of compounds in numerous media types. It was important to consider as much relevant information as possible for purposes of identifying initial lists from which individual stressors could be selected. Therefore, three different data sets involving environmental emissions, two data sets involving environmental exposures (one set for SVOCs), and production data were used. In addition, biological sampling data were used for SVOCs. Emphasis was placed on those compounds with the largest emissions, highest environmental concentrations, or greatest production volume (See Appendix A, Tables N.1 and N.2).

7. Selection of stressor VOCs and SVOCs

Given the robust parameters (production, emissions, exposure) initially used to derive the beginning lists, priority was placed on those compounds that (1) were common to numerous lists, (2) possess known toxicity potential given sufficient exposure (e.g., benzene and leukemia), (3) have substantial exposure potential in the ambient environment, and (4) are generally wellrecognized chemicals with respect to human and ecosystem health risk. This is a step that involved some subjectivity and professional judgment, although the hallmarks of risk (i.e., exposure combined with toxicity) were prominently considered when developing the final list of VOC and SVOC stressors. Based upon frequency of presence on various lists, coupled with toxicity characteristics and potential exposure, the following compounds were selected for further evaluation as stressor chemicals:

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Volatile Organic Compounds:

Benzene Carbon Tetrachloride Chloroform Formaldehyde

Methanol Methylene Chloride Perchloroethylene Toluene

1,1,1 Trichloroethane Trichloroethylene

Vinyl! Chloride Xylenes (mixed isomers)

Semi-Volatile Organic Compounds:

1,4-Dichlorobenzene p-Dioxane 2-Ethoxyethanol Ethylene Glycol 2-Methoxyethanol Phenol

1,2,4-Trimethylbenzene

It is important to note that VOCs and SVOCs as classes contain hundreds of compounds and for the scope of this project, it would have been time- and resource-intensive to evaluate each and every one. Therefore, professional judgment and criteria (toxicity potential, exposure potential, presence in New York commerce and presence in the environment) were used to identify those compounds for further evaluation and ranking. Certainly, other VOCs and SVOCs could be evaluated for risk ranking purposes should that be the desire of NYSDEC and NYSDOH management and staff.

8. Development of exposure and toxicity profiles for selected stressors

All available and pertinent information for each stressor was included in developing exposure and toxicity profiles. Much of the data and information was obtained from USEPA or New York state agency databases. The thought process was to include all pertinent information so that transparency in the risk ranking step was evident (see Appendix A, Tables N.3 and N.4).

The National-scale Air Toxics Assessment (USEPA, 2000) (NATA) is a compilation of national air toxic emissions from 1996 sources and estimated concentrations across the United States. This report became available after the ranking was completed, but illustrates an important point. NATA includes more types of emission sources than TRI, such as major stationary sources (factories, municipal incinerators) and other non-point sources (cars, trucks, small businesses, fires). The percentage of New York statewide emissions of VOCs in this report from non-point sources ranged from 24% for vinyl chloride to 99% for benzene. More than half of the emissions for benzene, formaldehyde, perchlorethylene, chloroform, carbon tetrachloride, and methylene chloride were from non-point sources. These data may be useful to the Risk Reduction Strategies Work Group when they conduct their analysis.

9. Ranking the stressors with relative risk tables

Four-year ambient (outdoors) air averages were used for the VOC stressors and a value of

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50 ppb taken from NYSDOH data was used for those VOCs that have been detected at this concentration in well samples near hazardous waste sites. For SVOCs, ambient air or water concentrations were not available and thus, exposure was based on 1995 New York Total TRI Emissions. It should be noted that these data are not as preferable as actual environmental media data and are potentially less representative and relevant to human exposure.

To simulate a worst-case exposure scenario, particularly in the absence of robust environmental concentration data for all stressors, a conservative approach was taken which included the decision to use a maximum exposure data point for each stressor, if it existed. By doing this, evaluation of cancer and noncancer risks would identify any potential health risks. It should be noted and encouraged that where risks are identified, further refinements in the exposure area (i.e., seeking additional data or using average concentrations) should be considered (see Tables V-N.1 to V-N.4).

Table V-N.1: Relative risk for VOCs based on toxicity and potential inhalation exposure

Toxicity 1 (highest) 2 3 4 (lowest) Exposure! Methanol* 1 Perchloroethylene (highest) (residential near dry cleaners) 2 Benzene Formaldehyde* Toluene Methylene Chloride Xylene Perchlorgethylene 1,1,1-TCA 3 Vinyl Chloride* Carbon Tetrachloride Chloroform Trichloroethylene 4 (lowest)

' Exposure Criteria, based on ambient air concentrations, are as follows for VOCs:

Ambient Air Concentration > 10 ug/m* = 1

Ambient Air Concentration 1-10 ug/m’ = 2

Ambient Air Concentration 0.1 - < 1 ug/m’ = 3

Ambient Air Concentration < 0.1 ug/m’ = 4

* Exposure Potential based on TRI emissions; no ambient measurements available

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Table V-N.2: Relative risk for VOCs based on toxicity and potential ingestion exposure Toxicity 1 2 3 4 (highest) (lowest) Exposure!* 1 (highest) 2 3 Carbon Tetrachloride | Xylene Benzene Chloroform Trichloroethylene Perchloroethylene 1,1,1-TCA 4 (lowest) Vinyl Chloride Methylene Chloride Toluene

' Exposure Criteria, based on NYSDOH public/private well data, are as follows for VOCs:

Drinking water

> 100 ppb = 1

Drinking water > 10 to 100 ppb = 2

Drinking water Drinking water

1-10 ppb =3 <1 ppb =4

?Note: All stressors could be placed in higher exposure categories if maximum well concentrations were used. However, median levels were either much lower than maximum levels or non-detectable.

Table V-N.3: Relative risk for Semi-VOCs based on toxicity and potential inhalation exposure

Toxicity 1 (highest) 2 3 4 (lowest) Exposure! 1 (highest) 2 Phenol 3 2-Ethoxyethanol Ethylene Glycol

4 (lowest)

2-Methoxyethanol

1,2,4Trimethylbenzene p-Dioxane

1,4-Dichlorobenzene*

I Exposure Criteria, based on 1995 NYS TRI Total Emissions, are as follows for Semi-Volatiles

Total TRI Emissions > 1,000,000 Ibs = 1 Total TRI Emissions > 100,000 - 1,000,000 Ibs = 2

Total TRI Emissions > 10,000 - 100,000 Ibs = 3

Total TRI Emissions < 10,000 lbs = 4

* Exposure based on actual ambient air concentrations

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Page 154

Table V-N.4: Relative risk for Semi-VOCs based on toxicity and potential ingestion exposure

Toxicity 1 (highest) 2 3

4 (lowest)

Exposure!” 1 (highest)

Ethylene Glycol

1,4Dichlorobenzene 1,2,4- (lowest) Trimethylbenzene

' Exposure Criteria, based on NYSDOH public/private well data, are as follows for Semi-VOCs:

Drinking water > 100 ppb = 1 Drinking water > 10 to 100 ppb = 2 Drinking water 1-10 ppb = 3 Drinking water < 1 ppb =4

?Note: All identified stressors could be placed in higher exposure categories if maximum well concentrations were used. However, median levels were either much lower than maximum levels or non-detectable.

10. Conclusions

A review of the comparative risk results, which includes the relative risk tables for VOC and SVOC stressors, reveals the following:

a. Relative risk for VOC stressors resulting from potential inhalation exposure shows that benzene, methanol, formaldehyde, and vinyl chloride appear to stand out as stressors that may be deserving of further evaluation for relative health risk potential. It should be noted that exposure potential for all of these compounds (except benzene) was based on TRI emissions and as such, no ambient data were utilized in estimating relative risk. Of these four compounds, formaldehyde is perhaps best known as a ubiquitous air contaminant, particularly indoors, while methanol is not typically associated with substantial inhalation exposures. Benzene and vinyl chloride represent the most toxic of the VOC stressors which drives their inclusion in the higher-risk compounds. It is noteworthy that the NYSDOH has collected monitoring data on specific indoor air contaminants in several occupational settings (e.g., shoe repair, furniture stripping, autobody repair) which show that indoor air concentrations can be significantly higher than the outdoor ambient concentrations used here within. Additionally, perchloroethylene air concentrations in some residential homes near dry cleaners may be significant and this represents an area where pollution prevention or exposure control measures should be considered.

b. Concerning relative risk for VOC stressors resulting from potential ingestion exposure, benzene, vinyl chloride, and carbon tetrachloride predominate as the ones of highest

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concern. These are reasonable compounds on which to focus given sufficient exposure, as the toxicity and health concerns with these compounds is well-established.

c. With regard to SVOCs, only phenol stands out as a higher risk compound, which may not be surprising given the relatively lower vapor pressure (and therefore ambient air concentration) associated with SVOCs.

d. In assessing the noncancer risk from inhalation exposure using USEPA RfCs or RfDs (if Rf£C not available) benchmarked against maximum exposure data, carbon tetrachloride and perchloroethylene represent the compounds of greatest potential concern given the ranking system (A-C) employed in this comparative risk project. For carbon tetrachloride, however, its inclusion as a higher potential risk is driven by its rather low RfD (RfC not available), the lowest by several orders of magnitude of those compounds evaluated. Moreover, carbon tetrachloride is not typically associated with those ambient air contaminants that are often associated with human health concerns. Assessment of noncancer risk from ingestion exposure reveals that carbon tetrachloride represents a compound posing higher potential risk and thus potable or drinking water sources containing substantial concentrations of this compound represent a focal point for continued investigation.

e. Evaluation of cancer risk from both inhalation and ingestion exposure reveals that benzene and chloroform (inhalation exposure) and benzene, carbon tetrachloride, and vinyl chloride (ingestion exposure) represent the stressors of greatest potential concern. Of these, only chloroform stands out as perhaps not deserving of the higher risk ranking as it is not typically associated with significant health risk from inhalation exposures. Conversely, the compounds identified as potential carcinogenic risks from ingestion exposure are appropriately identified as contaminants of concern.

11. Ranking of VOCs as a stressor group

A weight-of-evidence assessment of VOCs as a group indicates that they should be placed in the B, or middle category in terms of overall risk to human health. Human exposure is primarily by inhalation and occupational settings generally represent higher exposure scenarios than ambient environmental exposures.

12. Ranking of SVOCs as a stressor group

A weight-of-evidence assessment of SVOCs as a group indicates that they should be placed in the B, or middle category in terms of overall risk to human health. In general, there is very limited exposure to the general population from this class of compounds, which may be largely a result of the low vapor pressure and physical state which preclude significant airborne concentrations.

13. Recommendations One of the more critical aspects involved in assessing human health risk from environmental contaminants is that of accurately determining or predicting exposure to a

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substance(s). For many VOCs and SVOCs there are limited data around actual human exposure, both from occupational and ambient scenarios. This comparative risk effort has identified a need for additional, accurate human exposure monitoring data for VOCs and SVOCs, particularly for the inhalation route of exposure.

Additionally, while human exposure to SVOCs is considered to be less than to VOCs due to the differences in physical/chemical properties, it would be helpful to have additional and more complete body burden information on SVOCs. These types of data would assist in benchmarking body burdens against other indices (e.g., biomarkers of effect and exposure, blood levels considered to be safe or adverse) which may assist in evaluating potential impacts to human health.

A theme that emanated throughout this project and one that is relevant to VOC and SVOC stressors is that of subpopulations of higher risk. For example, occupational workers in the drycleaning industry or residents in mixed-zone areas (i.e., dwellings above or proximal to drycleaners) may be at higher risk of exposure to perchloroethylene and thus this particular group of individuals should be further assessed for potential health impact. There may be a need for assessment of this type for multiple VOCs and SVOCs and for multiple occupational settings (dry cleaners, shoe repair, textile screen painting, furniture stripping, etc.), an effort which hopefully will reveal those at highest potential risk of exposure.

Finally, because of the numerous VOCs and SVOCs which exist in commercial application today, only a subset could be evaluated through this comparative risk process. It is recommended that if there are particular compounds of interest to New York regulators and health officials, that these compounds be evaluated in a manner consistent with the VOCs and SVOCs ranked in the present chapter.

14. References

Alliance of Chemical Industries of New York State, Inc. 1996. Report on Chemical Emissions of the Members of the Alliance of Chemical Industries of New York State, Inc.

American Conference of Governmental Industrial Hygienists (ACGIH). 1997. 1997 Threshold Limit Values for Chemical Substances and Physical Agents: Biological Exposure Indices. Cincinnati, OH.

California OEHHA. 1997. Technical Support Document for the Determination of Noncancer Chronic Reference Exposure Levels.

EINECS Plus CD. 1996. European inventory of existing commercial chemical substances and European list of notified chemical substances. Silver Platter Information, Ltd. London, UK.

Method 8240A (Volatile Organics by GC/MS) and Method 8270A (Semivolatile Organic Compounds by GC/MS).

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New York State Department of Environmental Conservation. 1986. New York State Toxics Air Monitoring Report, 1982-84. Bureau of Air Quality Surveillance. Albany, NY.

New York State Department of Environmental conservation. 1995. Draft NYS Air Guide-1. Guidelines for the Control of Toxic Ambient Air Contaminants. Division of Air Resources, Albany, NY.

New York State Department of Environmental Conservation. 1995. New York State Ambient Toxic Air Monitoring Network, 1992/93 Data Addendum for Volatile Organic Compounds. Division of Air Resources. Albany, NY.

New York State Department of Environmental Conservation. 1996. 1995 Annual New York State Air Quality Report, Ambient Air Monitoring System. Division of Air Resources, Albany, NY.

New York State Department of Environmental Conservation. 1997. NYS Toxic Release Inventory (TRI) Review, 1995. Albany, NY.

New York State Department of Health. 1997. Background Indoor/Outdoor Air Levels of Volatile Organic Compounds in Homes Sampled by the New York State Department of Health, 1989-1996. Bureau of Toxic Substance Assessment, Albany, NY.

New York State Department of Health. 1997. Cumulative Report, 1992-1995. Hazardous Substances Emergency Events Surveillance (HSEES). Bureau of Toxic Substance Assessment, Albany, NY.

New York State Department of Health. 1999. Residential Exposure to Volatile Organic Compounds from Nearby Commercial Facilities: Draft Report. Bureau of Toxic Substance Assessment, Albany, NY.

Schreiber, J.S. et al. 1993. An investigation of indoor air contamination in residences above dry cleaners. Risk Analysis. 13:335-344.

Smead, G. Personal Communication. Discussions on volatile organic chemical concentrations in indoor air.

US Environmental Protection Agency. 1988. USEPA National Ambient Volatile Organic Compounds Database Update. Research Triangle Park, NC. EPA/600/3-88/101a.

US Environmental Protection Agency. 1995. Health Effects Assessment Summary Tables. FY 1995 Annual.

US Environmental Protection Agency. 1997. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, OH. (www.epa.gov/iris)

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VI. Conclusions and Recommendations

A. Conclusions

The workgroup ranked stressor groups based on the risk of health effects relative to other stressor groups. The ranking was not a quantitative measure of human health risk. For most stressor groups, the ranks for individual stressors varied within the group, regardless of the rank for the entire group. Therefore, it is important to review the report for each stressor group to see where individual stressors may have been ranked differently than the rest of the stressor group. The work group ranked the stressor groups as A, B or C, with A the highest human health risk and C the lowest. Because of the variability of individual stressor ranks within a group, some groups were judged to be A/B (lower than A, but higher than B) or B/C (lower than B but higher than C).

Table VI-1: Results of stressor group ranking for human health risk

Risk of Human Health Effects Stressor Groups A (highest) non-volatile halogenated compounds A/B metals

particulates

petroleum products

B acidic and alkaline substances atmospheric gases

halogens

pesticides

volatile organic compounds semi-volatile organic compounds

B/C polynuclear aromatic hydrocarbons

C (lowest) nutrients ionizing radiation suspended and settleable solids

It is important to note that these rankings were determined from exposure data which are influenced by the current federal, state and local regulations in place. If this ranking were used to relax regulation or other efforts to control exposure to a stressor group that was ranked low, then the health risks associated with that stressor group may be much higher than estimated in this project. For example, ionizing radiation is ranked low because there is very little exposure to this stressor. The lack of exposure is due to stringent regulations. Relaxation of regulations to control ionizing radiation would not be justified because of its low ranking in this project.

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B. Recommendations

Each stressor group report includes recommendations that are specific to that stressor group. The following recommendations are included in this section because they were either applicable to more than one stressor group or to emphasize their importance. More specific recommendations for each stressor group can be found in the individual stressor group reports.

1. General recommendations

° Efforts should be made to encourage and use pollution prevention techniques, especially to reduce hazards posed by those substances the HHWG identified as having the greatest health risks.

° Where data indicate that continued or additional controls on certain substances are needed

to protect human health (for example, if cancer or non-cancer risks associated with a given exposure are unacceptably high), the state should make efforts to control sources and reduce potential exposure.

° This assessment should be re-evaluated periodically to determine whether new exposure data or health effects data are available.

° Because of the numerous substances which exist in commercial application today, only a subset could be evaluated through this comparative risk process. If there are particular compounds of interest to New York regulators and health officials that were not included in this project, these compounds should be evaluated. For example, a comment received during the public comment period suggested an evaluation of polybrominated diphenyl ethers (PBDEs). The supporting documentation submitted justifies recommending these compounds be evaluated.

° Monitoring of contaminants in drinking water should continue and necessary actions be taken so that drinking water of acceptable quality is available to residents.

° Recent data from USEPA’s NATA and NYSDEC curbside PM monitoring indicate that mobile non-point sources of PM, VOCs and metals are important contributors to air pollution. The Risk Reduction Strategies Work Group should consider this data in developing their recommendations.

2. Recommendations on specific stressor groups ° Because of the very large radiation doses that may result from indoor radon, both USEPA and NYSDOH encourage New York residents to measure radon in their homes and to

reduce the radon levels if they exceed 4pCi/L.

° The potential for exposure to some atmospheric gases (ozone, nitrogen oxides, carbon monoxide) is high in urban areas. Pollution prevention would help to reduce the potential

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exposure to some of these gases.

The exposure to disinfectant byproducts should be re-evaluated once data is available from New York drinking water utilities pursuant to the USEPA’s “information collection rule.” This rule became effective in early 1997, and requires the generation of 18 months of

monitoring data.

Although there exist extensive programs for blood-lead surveillance, reducing lead levels in older homes, and public information, it is recommended that additional effort be made to reduce lead exposure via pollution prevention. The reasons for this are that (1) the effects of lead are irreversible; (2) young children are at the highest risk; (3) currently, much of the current effort identifies children at risk only after their blood lead levels are above the recommended value; and (4) there is no certainty that the currently recommended values are sufficiently low.

Additional effort to reduce exposure to mercury is also recommended. There appears to be an excessive number of emergency events associated with mercury (63 in the period 199296). A greater effort to reduce these events seems warranted. Also, mercury is found in high concentrations in fish and shell fish in New York waters. Cadmium, and in some cases, other metals are also found in high concentrations. NYSDEC does extensive monitoring and issues fish advisories and is working on approaches to eliminate sources. This is a long-term problem that requires continuing effort. Greater efforts are needed to identify and aid populations that subsist almost entirely on fish.

The major problem with nutrients in water and human health seems to be primarily with private wells. It is not likely that the New York State Department of Health or county health departments will start monitoring private wells. Since the human health problem is primarily with infants, a method for notifying families with newborn infants should be developed. If their primary source of potable water is a private well, it should be tested for nitrate-nitrogen levels. If the MCL is exceeded, an alternative source of water should be found or adequate treatment should be utilized to reduce the nitrate-nitrogen level.

The state should review its methods for developing health advisories for recreationally caught fish.

Efforts should continue to reduce the possibility of human exposure to NVHOCs in the state. Appropriate measures should be taken to reduce contaminant levels in fish to below those which would require restrictive advisories.

The relationship between one-hour average levels of particulate matter in New York and human morbidity and mortality should be studied and pollution prevention should be used to control short-term excursions of particulate matter.

The continued use of Integrated Pest Management should be supported.

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A program to educate residential pesticide users in proper application and safe handling of pesticides should be developed.

Air monitoring data at gas stations indicate that people who refuel their vehicles can be exposed to high levels of petroleum products. Measures to control such exposures may be addressed by pollution prevention.

. Research needs

Subpopulations with the potential for higher exposure to certain substances (in particular, NVHOCs, metals, pesticides, VOCs and SVOCs) should be identified and assessed for health risks.

More and better environmental monitoring data, specific to New York, are needed to properly characterize human exposure to most stressors. In some cases, data on urban environments are available, but not for rural areas. Studies on indoor air in homes, schools and non-industrial workplaces are needed to evaluate potential exposure to stressors such as pesticides and NVHOCs. Drinking water, surface water and groundwater monitoring for pesticides should continue. Also, studies of multi-pathway exposures for some substances would be useful. Better personal monitoring (measurement of contaminants by a monitor attached to a person) for human exposure to some stressors (PM, VOCs/SVOCs) would be useful.

More and better health effects data associated with both acute- and chronic-duration exposure to many substances are needed.

Reference concentrations, reference doses and cancer potency factors need to be developed for many stressors.

Additional and more complete body burden information on some substances would be useful to assist in benchmarking body burdens against other indices (e.g., biomarkers of effect and exposure, blood levels considered to be safe or adverse) which may assist in evaluating potential impacts to human health.

4. Data use/availability

TRI data show that some stressors are released into the air in significant quantities by certain facilities, often in or near urban areas. TRI data should be used to focus pollution prevention techniques to reduce these releases.

New York spill data should be evaluated to better determine how and where spills of toxic substances occur (in particular, petroleum products, acidic and alkaline substances and mercury) so that action may be taken to reduce the number of spills and related injuries.

New York should make existing environmental monitoring and biomonitoring data more

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accessible and easier to use.

° For many chemicals, there are enough data to make a reasonable evaluation of health risk. However, there are chemicals for which we have very limited or no information. It is recommended that a review of chemicals that are produced or used in high volumes in New York be made to identify any chemicals that need further study to determine their toxicological properties and their potential for exposure to humans. With USEPA guidance, the chemical industry has begun a screening program of high production chemicals to identify those that need further study.

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Appendix A Data Tables Final Report of the Human Health Work Group

New York State Department of Environmental Conservation

Comparative Risk Project

May 2001

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-1

Appendix A, Table A.1: Acidic and alkaline substances: Stressor selection

potency/toxicity exposure stressor

Chemical CAS NYSDEC selected name number EPA EPA | ACGIH Air TSCA |TRI NYS

IRIS IRIS TLV | Guide 1 CUS Total HSEES

RfD RfC mg/m3 | AGC production |releases | # spills

mg/kg-d | mg/cu.m ug/m3. Ibs/1994 __|Ibs/yr 1992-96

acetic acid 64-19-7 25 7 yes acrylic acid 79-10-7 0.5 1.00E-03 5.9 14 141,019 510 2 yes 2-amino-1-naphthalene 81-16-3 1,880,501 0 yes sulfonic acid adipic acid 124-04-9 5 0 no ammonia 7664-41-7 1.00E-01 17 360 1,226,80 74 yes calcium hydroxide 1305-62-0 5 2 no calcium oxide (lime) 1305-78-8 2 1 yes cesium hydroxide 21351-79-1 2 0 yes formic acid 64-18-6 94 22 14,336 1 yes fumaric acid 110-17-8 299,829 0 no hydrobromic acid 10035-10-6 9.9 s 240 0 no hydrochloric acid 7647-01-0 2.00E-02 | 7.5 s 7 33,100 3,859,70 B yes hydrofluoric acid 7664-39-3 2.3 s 2.85 276,734 11 yes metanilic acid 121-47-1 289,184 0 no nitric acid 7697-37-2 5.2 0.12 98,124 17 yes oleic acid 112-80-1 3500 1 no oxalic acid 144-62-7 1 24 4,942,692 1 yes palmitic acid 57-10-3 44,080 0 no peracetic acid 79-21-0 2,100 2 yes phosphoric acid 7664-38-2 1.00E-02 1 11,711 13 yes phosphorous acid 10294-56-1 121,898 0 no NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-2

potency/toxicity exposure stressor Chemical CAS NYSDEC selected name number EPA EPA | ACGIH Air TSCA {TRI NYS IRIS IRIS TLV | Guide 1 CUS Total HSEES RfD RfC mg/m3 | AGC production |releases | # spills mg/kg-d | mg/cu.m ug/m3. Ibs/1994 __|Ibs/yr 1992-96 picric acid 88-89-1 0.1 0.24 0 yes potassium hydroxide 1310-58-3 2s 12 yes sodium carbonate 497-19-8 50 3 no sodium hydroxide 1310-73-2 2s 310,848 61 yes sorbic acid 110-44-1 2,370,000 0 yes stearic acid 57-11-4 811,072 0 no sulfuric acid 7446-09-5 1 24 197,917 113 [yes toluenesulfonic (p-)acid 104-15-4 1,840,245 0 yes toluic (m-) acid 99-04-7 1,944,484 0 yes s= stel Selection criteria: Any chemical reported as a TRI release Any chemical with more than 3 spills reported by HSEES Any chemical with a TLV less than 5 mg/m3 Any chemical with production greater than 1 million pounds reported by TSCA NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-3

Appendix A, Table A.2: Acidic and alkaline substances: Data for ranking stressors

potency/toxicity exposure EPA health health Average | Maximum | NYS TRI TSCA Chemical CAS EU IRIS LOEL LDS50 effects effects annual outdoor | HSEES | Total air CUS name number class RfD or | inhale mg/kg of assoc. outdoor | airconc. | #spills | releases | production (1) RfC mg/m? LC50 greatest with airconc. | ug/m* | 1992-96 | Ibs/yr | Ibs/1994 (2) mg/m concern LOEL ug/m? (3) (4) (5) acetic acid | 64-19-7 | corrosive | none 25 oral rat | corrosive | eye irrit 1 to 10 80 7 (toxic)* LOEL 3,530 |to skin, eye} human urban auto human (7) resp (6) California} exhaust (6) (8) (9) (9) acrylic acid | 79-10-7 | corrosive | 0.5 0.33 corrosive |damageto| none none 2 510 141,019 (very | mg/kg- | LOEL to skin, eye} nasal found found toxic)* | 1.00E- | mouse resp mouse mg/m3 (2) (10) (2) 2-amino-1- | 81-16-3 none none oral rat | eye irritant none none 0 1,880,501 naphthalene (none 19,400 (11) found found sulfonic acid required)* (7) ammonia | 7664-41- toxic 1.00E- 1.9 corrosive |pneumoni | 0.1 to 3.8 90 74 1,056,40 mg/m3 | LOEL rat to skin, eye} respirator | urban & dairy (2) resp lesions | rural US feedlot (12) rat (2) (12) (12) NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-4

potency/toxicity exposure EPA health health Average |Maximum} NYS TRI TSCA Chemical CAS EU IRIS LOEL LDS50 effects effects annual outdoor | HSEES | Total air CUS name number class RfD or | inhale mg/kg of assoc. outdoor | airconc. | #spills | releases | production (1) RfC mg/m LC50 greatest with airconc. | ug/m*> | 1992-96 | Ibs/yr | Ibs/1994 (2) mg/m concern LOEL ug/m? (3) (4) (5) calcium 1305-78- none none 25 corrosive nasal none none 1 (lime) (harmful) LOEL to skin, eye | irritation found found human resp human (6) (13) (6) cesium 21351- none none oral rat | corrosive none none 0 hydroxide (harmful) 570 to skin, eye found found (7) resp (6) formic acid | 64-18-6 | corrosive | none 38 LCS50 corrosive liver, none none 1 14,336

(toxic)* LOEL rat] mouse |to skin, eye] enzyme found found (14) 6200 resp rat ) (14) (14)

hydrochloric | 7647-01- | corrosive | 2.00E- 6.1 corrosive |hyperplasi} 0.1 to 2 none 73 3,854,70} 33,100 acid (toxic)* | mg/m3 |LOEL rat to skin, eye }upper resp} rural & found (2) resp system | Michigan (6) (2) (15) NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-5

potency/toxicity exposure EPA health health Average |Maximum} NYS TRI TSCA Chemical CAS EU IRIS LOEL LDS50 effects effects annual outdoor | HSEES | Total air CUS name number class RfD or | inhale mg/kg of assoc. outdoor | airconc. | #spills | releases | production (1) RfC mg/m LC50 greatest with airconc. | ug/m*> | 1992-96 | Ibs/yr | Ibs/1994 (2) mg/m concern LOEL ug/m? (3) (4) (5) hydrofluoric | 7664-39- | very toxic] none 0.1 corrosive | nerve cell <1.0 none 11 276,734 acid LOEL rat to skin, eye} effects | urban US found (16) resp rats 1.1 can affect nasal <0.05 LOEL lung, heart | irritation | rural US human bones (16) | human (16) nitric acid | 7697-37- | corrosive | none 63 LCS0 rat | corrosive not none none 17 98,100 (toxic)* NOEL rat 600 to skin, eye| reported found found © @) resp em) oxalic acid | 144-62-7 | harmful | none oral rat | corrosive none none 1 4,942,692 375 to skin, eye found found (7) resp can affect kidney (18) peracetic 79-21-0 | harmful | none rat LC50 | corrosive none none 2 2,100 acid corrosive 450 to skin, eye found found (7) resp a) NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-6

potency/toxicity exposure EPA health health Average |Maximum} NYS TRI TSCA Chemical CAS EU IRIS LOEL LD50 effects effects annual outdoor | HSEES | Total air CUS name number class RfD or | inhale mg/kg of assoc. outdoor | airconc. | #spills | releases | production (1) RfC mg/m LC50 greatest with airconc. | ug/m*> | 1992-96 | Ibs/yr | Ibs/1994 (2) mg/m concern LOEL ug/m? (3) (4) (5) phosphoric | 7664-38- | corrosive | 1.00E- 180 corrosive | bronchiol none none 13 11,194 acid (toxic)* | mg/m3 | LOEL rat to skin, eye} fibrosis found found o) resp @ (19) picric acid | 88-89-1 toxic none | 0.009 to sensitizatio | sensitiz. none none 0 (very 0.19 dermatitis | dermatitis | found found toxic)* LOEL eye irrit human human kidney (6) (6) effects (6) potassium | 1310-58- | corrosive | none oral rat} corrosive none none 12 hydroxide (toxic)* 365 to skin, eye found found (7) resp (6) sodium 1310-73- | corrosive | none oral corrosive none none 61 310,848 hydroxide (toxic)* rabbit |to skin, eye found found 147 (20) | mucous mem. (21) sorbic acid | 110-44-1 none none oral rat |skin irritant none none 0 2,370,000 (none 7360 (11) found found required)* (7) NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-7

potency/toxicity exposure EPA health health Average | Maximum | NYS TRI TSCA Chemical CAS EU IRIS LOEL LDS50 effects effects annual outdoor | HSEES | Total air CUS name number class RfD or | inhale mg/kg of assoc. outdoor | airconc. | #spills | releases | production qd) RfC mg/m LC50 greatest with air conc. ug/m> =| 1992-96 | Ibs/yr | Ibs/1994 (2) mg/m concern LOEL ug/m? (3) (4) (5) sulfuric acid | 7664-93- | corrosive | none 0.21 corrosive |decreased | US <5 50 113 195,611 (very LOEL to skin, eye| forced (22) Ontario toxic)* human resp capacity | sulfates, (22) (22) (22) human | 4.1 (24) p- toluene | 104-15-4 | irritant none oral skin, eye, none none 0 1,840,245 sulfonic acid (harmful) 400 mucous found found (7) irritant (11) m-toluic acid | 99-04-7 none none oral irritant none none 0 1,944,484 (harmful) 1630 (7) (11) found found * EU rank assigned or modified based on displayed data references (see main body of report for full citations) 1 EINECS, 1996 7 NIOSH, 1987 13 OSHA, 1978b 19 OSHA, 1978e 2 USEPA, 1997 8 OSHA, 1978a 14 NTP, 1992 20 USFDA, 1980 3 NYSDOH, 1997 |9 Howard, 1990 15 WHO, 1992 21 OSHA, 1978f 4 NYSDEC, 1996a_ {10 USEPA, 1994 16 ATSDR, 1993 22 ATSDR, 1997 5 RTK Network, 11 Sax, 1989 17 OSHA, 1978c 23 NYSDEC, 1991 6 AGGIH, 1991 12 ATSDR, 1990 18 OSHA, 1978d 24 NYSDEC, 1996b

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-8

Appendix A, Table C.1: Health effects data for halogens

Halogens

Fluorine CAS# 7782-41-4

Oral NOEL .06 mg/kg/d (dental fluorosis)*

R£D 6E-2

(Note: IRIS database stated that .12 mg/kg/d is considered “a safe exposure level” for crippling skeletal fluorosis.)

Source: IRIS

Toxicity Ranking 1 (basis: Oral NOEL)

Bromine CAS# 7726-95-6

Oral LD, 14 mg/kg (human)

Oral LD, 440 mg/kg (“unspecified species”)

Oral LD, 2600 mg/kg (rat)

Source: Registry of Toxic Effects of Chemical Substances

Toxicity Ranking 3 (basis: oral NOEL/unspecified species)

Chlorine CAS# 7782-50-5

Oral NOEL 14.4 mg/kg/d (no observed effects) RfD 1E-1 mg/kg/d

EPA Cancer Classification - D

Source: IRIS

Toxicity ranking 3 (basis: oral NOEL)

Iodine CAS# 7553-56-2

Oral LD,, 28 mg/kg (human)!

Oral TD,, 26 mg/kg/1Y (intermittent) (evidence of thyroid hyperfunction)!

Oral LD,, 14 gm/kg (rat)!

Acute Oral LD,, 4340 mg/kg (rat)?

Sources: 1. Registry of Toxic Effects of Chemical Substances; 2. World Health Organization “Guidelines for Drinking Water Quality,” Second Edition, 1996 (WHO)) Toxicity ranking 4 (basis: Acute oral LD.)

Disinfection Residuals

Monochloromine (Chloromines) CAS# 10599-90-3

Oral NOEL 9.5 mg/kg/d (rat/no observed effects)

RfD 1E-1 mg/kg/d

EPA Cancer classification - D

Source: IRIS

Note that EPA’s maximum residual disinfection level also includes trichloramine, CAS # 10025-85-1)

Toxicity ranking 3 (basis: oral NOEL)

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-9

. Chlorine dioxide CAS# 1004-90-4 Oral LOEL 10 mg/kg/d (rat) Oral NOEL 3 mg/kg/d (rat) RfD 1E-2 mg/kg/d EPA cancer classification - D Source: EPA “National Primary Drinking Water Regulations: Disinfectants and Disinfectant Byproducts Proposed Rule, FR July 29, 1994 Toxicity ranking 3 (basis: Oral NOEL/rat)

Disinfection Byproducts

. Chloroform (trichloromethane) CAS# 67-66-3 Oral LOEL 12.9 mg/kg/d (dog, chronic oral bioassay)! RfD 1E-2 mg/kg/d EPA cancer classification - B2 Oral slope factor 6.1E-3 Drinking water unit risk factor 1.7E-07

Source: IRIS

(Note 1. “Converted from 15 mg/kg/d, conversion factors: 15 mg/kg/day x 6 days/7 days = 12.9 mg/kg/d)

Toxicity ranking 2 (basis: EPA cancer classification)

. Bromodichloromethane CAS# 75-27-4 Oral LOEL 17.9 mg/kg/d (chronic mouse gavage bioassay) R£D .02 mg/kg/d (critical effect: renal cytomegaly) EPA cancer classification - B2 Oral slope factor 6.2E-3 Drinking water unit risk 1.8E-06 Source: IRIS Toxicity ranking 2 (basis: EPA cancer classification)

. Dibromochloromethane CAS# 124-48-1 Oral LOEL 42.9 mg/kg/d (rat) (subchronic gavage bioassay)! Oral NOEL 21.4 mg/kg/d (hepatic lesions) RfD 2E-2 mg/kg/d EPA cancer classification - C Oral slope factor 8.4E-2 Drinking water unit risk 2.4E-06 Source: IRIS (Note 1. “Converted from 60 mg/kg/d” Note 2. “Converted from 30 mg/kg/d”) Conversion factors: dose adjusted for gavage schedule 5\day/week) Toxicity ranking 3 (basis: Oral NOEL/hepatic lesions)

. Bromoform CAS# 75-25-2

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-10

Oral LOEL 35.7 mg/kg/d (rat)!

Oral NOEL 17.9 mg/kg/d (rat) (hypatic lesions)”

RfD 2E-2 mg/kg/d

EPA cancer classification - B2

Oral slope factor 7.9 E-3

Drinking water unit risk 2.3E-07

Source: IRIS

(Note 1. “Converted from 50 mg/kg/d” Note 2. “Converted from 25 mg/kg/d”) Conversion factors: dose have been adjusted for treatment schedule (5 days/week) Toxicity ranking 2 (basis: EPA cancer classification)

. Monochloroacetic acid CAS# 79-11-8 Oral LD.) 55 mg/kg (mouse)! Oral LD.y 76.2 (rat)? Sources: 1.Registry of Toxic Effects of Chemical Substances, 2. Chemical Hazard Response Information System Toxicity ranking 2 (basis: oral LD,)/mouse)

. Monobromoacetic acid CAS# 79-08-3 Oral LD, 50mg/kg (rat) Oral LD,, 100 mg/kg (mouse) Source: Registry of Toxic Effects of Chemical Substances Toxicity ranking 2 (basis: oral LD;)/rat)

. Dichloroacetic acid CAS# 79-43-6 Oral LOEL 12.5 mg/kg/d (dog)! R{D 4E-3 mg/kg/d ' EPA cancer classification - B2? Sources: 1. EPA “National Primary Drinking Water Regulations: Disinfectants and Disinfectant Byproducts Proposed Rule, FR July 29, 1994, 2. IRIS Toxicity ranking 2 (basis: EPA cancer classification)

. Trichloroacetic acid CAS# 76-03-9 Oral LOEL 330 mg/kg/d (rat)' R{fD 1E-2 mg/kg/d ' EPA cancer classification - C? Sources: 1. EPA “National Primary Drinking Water Regulations: Disinfectants and Disinfectant Byproducts Proposed Rule, FR July 29, 1994, 2. IRIS Toxicity ranking 3 (basis: EPA cancer classification)

. Dibromoacetic acid CAS# 631-64-1 Note: Reproductive effects in rats at oral dose of 3500 mg/kg Source: Registry of Toxic Effectsof Chemical Substances Toxicity ranking 4 (basis: reproductive effects data)

. Bromate

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-11

Potassium bromate CAS# 7758-01-2

Acute oral LD,, 223 mg/kg (mouse)

“Estimated” LD,, 200 mg/kg

Source: “Guidelines for Drinking Water Quality,” Second edition, World Health Organization

Sodium bromate CAS# 7789-38-0

Oral LD, 280 mg/kg (rat)

Source: “Guidelines for Drinking Water Quality,” Second edition, World Health Organization

Toxicity ranking 3 (basis: acute oral LD,9/mouse)

. Chlorite CAS# 7758-19-2

Oral LOEL 3 mg/kg/d (rat) (depressed exploratory behavior)

EPA cancer classification - D

Source: EPA “National Primary Drinking Water Regulations: Disinfectants and Disinfectant Byproducts Proposed Rule, FR July 29, 1994

Toxicity ranking 2. (basis: oral LOEL)

. Chloral hydrate CAS# 302-17-0 Oral LOEL 16 mg/kg/d (mouse) Source: EPA “National Primary Drinking Water Regulations: Disinfectants and Disinfectant Byproducts Proposed Rule, FR July 29, 1994 Toxicity ranking 3 (basis: oral LOEL)

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-12

Appendix A, Table C.2: Exposure data/rankings for halogens

Halogens

DOH)

Fluorine CAS# 7782-41-4 No data Exposure Ranking NA

Bromine CAS# 7726-95-6 96 NYS TRI = 1592 lbs. total releases Exposure Ranking 4

Chlorine CAS# 7782-50-5 96 NYS TRI = 100,288 Ibs. to air Typical range/residual chlorine in drinking water = .2 to 1.0 ppm (source: NYS

US production (TSCA) = 1.07 x 10° Ibs lower bounds, 1.49 x 10° Ibs upper bounds Population served/chlorinated water systems 3.6 million + NYC (source: NYS DOH, Bureau of Public Water Supply Protection)

Exposure Ranking 1 Iodine CAS# 7553-56-2

No data

Exposure ranking NA

Disinfection Residuals

Monochloromine (Chloromines) CAS# 10599-90-3

Mean concentrations = 1.1 to 1.8 ppm (source: EPA “DBP rule”)

Population served/chloromine-treated water systems = 120,000 (source: NYS DOH, Bureau of Public Water Supply Protection)

Exposure ranking 1

Chlorine dioxide CAS# 1004-90-4

Population served/chloride dioxide treated water systems = 21,700 (source: NYS DOH, Bureau of Public Water Supply Protection) Exposure ranking 3

Disinfection Byproducts

Chloroform (trichloromethane) CAS# 67-66-3 NYS DOH average detect = 43.5 ppb

NYS DOH maximum detect = 7,205 ppb

96 NYS TRI = 7 lbs total releases

Exposure ranking 2 (basis: average detect)

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-13

. Bromodichloromethane CAS# 75-27-4 NYS DOH average detect = 5.3 ppb NYS DOH maximum detect = 44.5 ppb Exposure ranking 3 (basis: average detect)

. Dibromochloromethane CAS# 124-48-1 NYS DOH average detect = 2.6 ppb NYS DOH maximum detect = 24 ppb Exposure ranking 3 (basis: average detect)

. Bromoform CAS# 75-25-2 NYS DOH average detect = 3.3 ppb NYS DOH maximum detect = 34 ppb Exposure ranking 3 (basis: average detect)

. HAAS Monochloroacetic acid CAS# 79-11-8 Monobromoacetic acid CAS# 79-08-3

Dichloroacetic acid CAS# 79-43-6 Trichloroacetic acid CAS# 76-03-9 Dibromoacetic acid CAS# 631-64-1 Mean concentrations range from 4 ppb to 97 ppb (source EPA) Exposure Ranking 2 . Bromate

Potassium bromate CAS# 7758-01-2

Sodium bromate CAS# 7789-38-0 Maximum concentration reported = 60 ppb (source EPA) Exposure Ranking 2

. Chlorite CAS# 7758-19-2 Mean concentrations range from .4 to 1.2 ppm (source EPA) Exposure Ranking 1

. Chloral hydrate CAS# 302-17-0 Mean concentrations range from 5.0 to 7.8 ppb (source EPA) Exposure Ranking 3

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-14

Appendix A, Table D.1: Stressor data for metals

Chemical EU] NOAEL, | NOAEL Health] Health [EPA Cancer [NIOSH [Children | NYS | NYS | NYS | NYS [Emergency | Fish] Concen- | Stressor | Tox- | Exponame Class } LOAEL | (mg/kg/d) | LOAEL | effect | effect [Cancer |mutagen, OSHA [(%with | Avg | Max | TRI | TRI [Events Advisory | tration | selected | icity | sure CAS base on (mg/kg/d) | assoc | greatest | slope reproduc- |TLV __| blood outdoor | outdoor | Air | water |(HSEES 1998” | in fish or class number Oral, concer | factor tive. (mg/m3) | lead air cone. | air cone. | release | release |1992-96) shellfish dermal, (mg/kg/d) |teratogen over 10 | (ug/m3) | (ug/m3) | (Ibs/y) | (Ibs/y) (ng/g) inhalation evidence ug/dL) ‘Aluminum oral T 3 33600 0 yes z 3 (Al) Regional superfund from Smith ‘Antimony oral O35 | aaa, 3587 | 481 yes T 7 (Sb) blood ‘Arsenic toxic | oral 0.0008 Karatosis F30E-03 | sufficient 0.002 31 2 285 to [yes T 3 (As) human 16,000 7440-38-2 Barium oral 02 Tnereased T9497 | 8925 T yes T 3 (Ba) blood pressure Berylium oral 0:46 [0.01-0.1 intestine a 3 yes T (Be) ugim3 kidney. (sulfate) (Soluble (inhale) _ | liver, salts) spleen 7440-41-7, Cadmium oral 0.005 provem- [Kidney [0.16 probable 7.00310 1125 w z TT yes T 3 (Cd) uria (1.8E-3. human 0.005 4,800 ug/m3) | (inhale) (inhale) Cobalt Tahalation [0.03 0.05 730 Eo) yes T 4 (Co) (ATSDR | mg/m3 dust 7440484 MHR) fume 0.1 carbonyl Copper oral, 04 01 30308] 15795 yes Z 3 (Cu) regional (fume) superfund 10 from (mist) Smith Chromium oral 25 0.012 20083 3 yes T 3 (VD (Cr) ug/m3 (inhalation only) Chromium oral 1468 Suspected z (itt) human insoluble salts Cyanide oral 108 Wis, yes 3 (free) thyroid, 57-12-5 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-15

Chemical NOAEL Health [EPA Cancer NIOSH Children] NYS] NYS | NYS | NYS Jbmergency | ish] Concen- | Stressor | Tos name (mg/kg/d) | LOAEL effect |Cancer mutagen, OSHA |(%with | Avg Max | TRI | TRI [Events Advisory | tration | selected CAS (mg/kg/d) greatest | slope reproduc- |TLV __| blood outdoor | outdoor | Air | water |(HSEES 1998 | in fish or number concer | factor tive. (mg/m3) | lead air cone. | air cone. | release | release |1992-96) (mg/kg/d) |teratogen over 10 | (ugim3) | (ug/m3) | (Ibs/y) | (Ibs/y)

inhalation evidence ug/dL) Tron oral, 03 T 7 (femic yes 2 3 (salts) regional chloride)

Smith Lead oral from | 0.0036 Sufficient )0.1=0.02 TUT O15 | 35708 7 Tato yes T T (Pb) Gunderso human | mg/kg/d o. 8,780

n+note Manganese inhalation (0.05 | neuroTogicar T 221862 | 375 T 2 (Mn) mg/m3 7439-96-5 Magnesium oral 0.005 chronic T (Mg) idegestion Mercury Tahalation 0.009____[ tremor, 0.05 TE=ti6 261 6 oe 75 7 z (Hg) (Vapor) mg/m3 memory vapor SE4 Molybdenum Oral 0.14 [increased 3 239 0 yes 7 7 (Mo) uric acid 7439-98-7 Nickel carcin | Oral 3 Possible T O02 12062 yes 2 q (Ni) 3 human 0.06 (soluble salts) Platinum T (Pt) Selenium Oral T0Is clinical 02 yes T (Se) Jeno: 7782-49-2 Silver Oral 0.014 fargyra__| none O01 TI291 | 5978 7 yes q 3 (Ag) (PEL) Sodium Thallium oral, IRIS 024 yes T (Th) w Tin oral 06 z z (Sn) HEAST,

from

Smith Titanium 10 nO (Ti) dioxide Tungsten 3 yes (Ww) insoluble

1 soluble Uranium Oral, 28 yes z (U) based on (soluble hexasalts hydrate uranium 02 (insoluble) NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-16

Chemical EU] NOAEL, | NOAEL Health] Health [EPA Cancer [NIOSH [Children | NYS] NYS] NYS] NYS [Emergency | Fish] Concen- | Stressor | Tox- ] Exponame Class | LOAEL | (mg/kg/d) | LOAEL | effect | effect [Cancer |mutagen, OSHA [(%with | Avg | Max | TRI | TRI [Events Advisory | tration | selected | icity } sure cAS base on (mg/kg/d) | assoc | greatest | slope reproduc- |TLV __| blood outdoor | outdoor | Air | water |(HSEES 1998” | in fish or class | class number Oral, concer | factor tive, (mg/m3) | lead air cone. | air cone. | release | release |1992-96) shellfish dermal, (mg/kg/d) |teratogen over 10 | (ugim3) | (ug/m3) | (Ibs/y) | (Ibs/y) (ng/g) inhalation evidence ug/dL) Vanadium oral 0.89 deorease in 0.01 to yes z 4 (v) hair cystine 002 pentoxide 1314-62-1 Zine Tight | oral T [inereasetm [interferes T T34542] 43305 yes 3 Z (Zn) y : rthreyte wih we (fume) 7440-66-6 | flam dismutase | minerals 5-10 mable (oxide) (dust) > NOAEL and LOAEL values from EPAMIRIS unless otherwise stated > Smith, RL. 1996. Risk-based concentrations. prioritizing environmental problems using limited data, Toxicology 106, 243-266 Gunderson, EL. 1995. FDA total diet study, July 1986-Apnil 1991, dietary intakes of pesticides, selected elements and other chemicals, J_ of AOAC Intl 18, 1353-1363 Sw = withdrawn fom IRIS NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-17

Appendix A, Table E.1

Characteristics of potency or toxicity, environmental standards or criteria, potential or actual human exposure, and European

Union classifications of toxic or bioaccumulative chemicals as they apply to selected semi-

olatile halogenated organic

chemicals. Chari European Union or Potency - Toxicity! Standards or Criteria Exposure USEPA Chemical classifications"” (Synonyms) CAS Number RIS et EPA ecto NYS USEPA. USFDA NOAEL/ EPA drinking ACGIH USFDA EGS market NYS NYSDOH 0 -, LOAEL IRIS R{D (me/ke/d)"s water TLV? limit NOPES basket® DOH # fish health NHATS Toxicity Carcinoinhalation 2 > f (ng/m’) s (ng/g fat) genicity (mg/kg- (mg/kg/d) standard? (mg/m’) in fish (ng/kg- advisories’ day) cancer potency (ug/l) (ug/g) bw/day) factor (unit risk ° eee per ug/m’) Aldrin’ 0.025 L 3.00E-05 17 ND G' 0.25 03 ND-39 <0.1/<0.1* 1.99E+05 <10 T B2 309-00-2 4.9E-03 0.001 (sum with dieldrin) Chlordane’ 0.055 N 6.00E-05 13 0.05 Gws; 0S 1.20E+00 03 36-253 1.6/0.8 1.69E+03 13 <10 Xn B2 57-74-9 3.7E-04 2x10 Sws Chlordecone 2.40E-03 04 1,00E+02 T 3 (Kepone) 143-50-0 Chloroalkylsilanes - Chloroanilines 12.5L 4.00E-03 5.0GWS 6.00E+00 6.0/5.1* 2- 95-51-2 (4) (each) (4) (tetra + 3- 108-42-9 penta) 4 106-47-8 Chlorofluorotoluenes Chloronaphthalenes 10 SWS, 4.80E-01 - 2- 91-58-7 (2-) (hexa) 2.40E-01 (octa) Chlorophenols (mono) 5.0N 5.00E-03 1.0 GWS + Xn - 2- 95. 8 (2-) (2-) Sws 3- (total) 4 Chlorophenyl phenyl ether Chlorophthalates NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-18

Characteristic European Union or Potency - Toxicity! Standards or Criteria Exposure USEPA Chemical fications (Synonyms) CAS Number EPA IRIS oral slope He EPA f NYS ¢ ~ factor “4 NYSDEC 7 re NOAEL/ EPA kg/d drinking ACGIH ‘s NYSDOH NHATS' c: LOAEL IRIS RfD (mee water DOH # fish health (nels fat) Toxicity senicity (mgkg- (mg/kg/d) standard? (mg/m’) kK,” advisories* e/g genicity cancer potency day)’ . (ugh) factor (unit risk per ug/m') DDD’ 0.24 0.3 GWS; ND 0.7/0.3 1.05E+06 <10 - B2 (TDE) 8x 10° 72-54-8 sws DDE 0.34 0.2 GWSs; 5.0 (sum 0.5-5 42.0/11.9 3.24E+06 <9-6800 - B2 72-55-9 7x 10° with Sws DDT) DDT 0.05 N 0.34 0.2 GWS; 1 5.0 1.1/0.5 5.7SE+0S 3 <9-540 T B2 50-29-3 9.TE-0S 1x 10° (total DDT) Sws Dichlorobenzidine 0.45 5.0GWS 3.16E+03, T B2 91-94-1 Dicofol ND-7 35.5/8.3 2.83E+04 Xn, Xi - 115-32-2 Dieldrin 0.005 N 5.00E-05 16 0.004 0.25 03 7.228 1.45E+03 <44-4100 T B2 60-57-1 4.6E-03 6x 10 sw Endosulfan 0.6N 6.00E-03 01 46.0/17.7 1 T, Xi - hiodan) 115-29-7 Endrin 0.025 N 1 03 <0.1/<0.1 1.45E+05 <50 T+ - 72-20-8 0.002 SWS. Heptachlor’ O.1SN 45 0.04 Gws; 0.05 03 5-134 <0.1/<0.1 2.50E+04 <10 T B2 76-44-8 13E-03 2x 10% Sws Heptachlor epoxide 0.0125 L 1.30E-05 91 0.03 GWs; 0.05 03 ND-0.6 2.5/0.9 5.00E+02 <10-310 T B2 1024-57-3 2.6E-03 3x 10* Sws Hexachlorobenzene 0.08 N 16 0.04 Gws; 0.025* 2.20E-03 ND-0.9 2.1/0.8 1.70E+05 <12-1300 T B2 (HCB; No Bunt) 4.6E-04 3x10 118-74-1 Sws Hexachlorobutadiene 0.5 GWS; 0.21 5.00E-02 6.03E+04 - 3 91001-50-2 0.01 SWS Hexachlorocyclopen-tadiene 7.0N 7.00E-03 0.078 5.0GWS O11 7.00E-02 1.10E+05, - - T1-41-4 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-19

Characteristic

Potency - Toxicity!

Standards or Criteria

Exposure

European Union or USEPA

Chemical classifications"® (Synonyms) CAS Number IRIS oral slope EPA ctor NYS USEPA USFDA NOAEL EPA drinking | ACGIH USFDA . market NYSDOH . : LOAEL IRIS RD omy water TLV? limit NOPES basket® DOH # fish health wae Toxicity Caring” (mg/kg- (mg/kg/d) standard? (mg/m’) in fish (ng/kg- Ky advisories* ee & day) cancer potency (ug!) (ug/g) bw/day) y factor (unit risk 2 we y per ug/m') Hexachloroethane LON 1.00E-03, 0.014 97 3.98E+04 - 67-721 4.0E-06 a-HCCH 63 0.01 Gws 6.00E-04 ND-09 2.7108 7.94E+03 - B2 (-HCH; a-BHC) 1.8E-03 4x10" 319-84-6 sws b-HCCH 18 0.04 GW 2.00E-03, <0.1/0.1 7.94E+03 <19-570 - B2; (B-HCH; b-BHO) 53E-04 0.001 SWS 3-IARC 319-850.04 GWs: B2 0.001 SW Lindane 033 3.00E-04 - 0.05 GW 0s 6.00E-04 07. 3.2/1.0 4.57403 1, Xi B2 (g-HCCH; -HCH; fe 0.001 SWS BHC) 58-89-9 Methoxychlor 5.01N 5.00E-03 10 ND-06 0.903 2.00E+04 - D 243-5 Mirex 0.07N 2.00E-04 0.03 Gws; 0.1 (sum 7.76E+06 3 Xn B2; (Dechlorane) 1x 10° with (includes 3 (IARC) 2385-85-5 sws photo- photomirex) mirex) Octachlorostyrene 02GWs; 6x 10° sws Pentachlorobenzene 83N 8.00E-04 0.12 5.0GWS 1.55E+05 <10 Xn - 608-93-5 Pentachloronitro-benzene 0.75N 3.00E-03, ND GWS 0s 25108 LSIE+O4 Xi c (PCNB; Quintozene) 82-68-8 Photomirex 0.1 (sum with mirex) Polybrominated biphenyls 5.0GWS (PBBs)

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-20

Chemical

(Synonyms) CAS Number

Characteristic

Potency - Toxicity!

Standards or Criteria

Exposure

European Union or USEPA

classifications"®

EPA NOAEL LOAEL (mg/kgday)

EPA IRIS oral slope factor EPA IRIS RID (mg/kg/d)"; (me/ke/d) inhalation

cancer potency factor (unit risk per ug/m’)

NYS. drinking water standard® (ugil)

ACGIH TLV (mg/m’)

USEPA USEDA NOPES*

int (ag/m’) in fish e (ugig)

USFDA market basket* (ng/kgbw/day)

DOH

NYSDOH # fish health advisories*

NHATS' (ng/g fat)

Carcino-

Toxicity genicity

Polychlorinated biphenyls 2.00E-05 2 0.09 (sum) 0S 4.S0E-04 2.0 (sum) ND-7' 1.9/0.9 6.20E+07 37 <15-1700 Xn B2 (PCBs) 1.0E-4 Gws; 1336-36-3 1x 10° (sum) SWS: ~Aroclor 1016/1242 0.007 N 7.00E-05 10 3.80E+05 53469-21-9 Aroclor 1248 12672-29-6 2.02E+06 0.005 L. 2.00E-05 0S 6.20E+07 Aroclor 1260 11096-82-5 1.29E+06 Polychlorinated dioxins 6200 7x 107 3.00E-08 0.00001 1 41E+06 6 0.047 1 for (PCDDs) as TCDD HxCDD GWS and 6 (as 2,3,7,813 x10" SW 2,3,7,8- TCDD HxCDD expressed as TCDD 3 for all 2,3,7,8- toxic others. TCDD toxic equival- (IARC)? equivalents ents) Polychlorinated dibenzofurans 3 for all (PCDFs) ‘compounds (IARC)? Polychlorinated diphenyl ethers (PCDEs) Polychlorinated naphthalenes Polychlorinated quaterphenyls Polychlorinated terphenyls (PCTs) -Aroclor 5442 12642-23-8 -Aroclor 5460 11126-42-4 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-21

Tetrachlorobenzenes 0.34N 3.00E-04 5.0 (each) <0.1/<0.1* 4.70E+04 -

Characteristic

European Union or

Potency - Toxicity! Standards or Criteria Exposure USEPA Chemical classifications" (Synonyms) CAS Number 1Ris onl slope EPA ~ factor P NYS: USFDA NOAEL/ EPA 1 drinking ACGIH EGS market NYS: NYSDOH 09 ~. LOAEL IRIS R‘D (me/ke/dys water TLV wid NOPES basket* DOH # fish health | NHATS Toxicity | Carcinoinhalation ° 5 AGC (ng/m’) 0 : (ng/g fat) genicity (mg/kg- (mg/kg/d) uncer polency standard’ (mg/m’*) (ug/m) (ng/kg- Koy advisories" day)’ tk (ugh) “e bw/day)

factor (unit risk per ug/m’)

Gws; 10 SWS (sum)

Toxaphene’ MW 0.06 Gws; 05 1.20E+00 50 2.4/6.7 1.90E+03 T.Xi B2 8001-35-2 3.2E-4 6x 10°

SWS Trichlorobenzenes 148N 1.00E-02 5.0 (each) 9.00E+00 0.2/<0.1* 1.50E+04 - D 12,4 120-82-1 Gws

50F

' Source: U. S. Environmental Protection Agency IRIS database. NOAEL/LOAEL = No observed adverse effect level/Lowest observed adverse effect level; Rf£D = Reference Dose; cpf = Cancer potency factor. ? Source: NYSDEC (1997) Combined Regulatory Impact and Draft Environmental Impact Statement Title 6, Chapter X, Parts 700-706, Volume | of 3. ND = None detected by sensitive analytical techniques;

GWS = Groundwater standard; SWS = Surface water standard; F = To prevent flavor impairment in edible fish tissues. > Source: American Conference of Governmental Industrial Hygienists (ACGIH) (1996). 1996 TLVs and BEIs. Threshold limit values for chemical substances and physical agents; Biological Exposure Indices. A revised ACGIH TLV value for hexachlorobenzene of 0.002 mg/m’ is proposed. Source: NYSDEC (1991) Draft New York State Air Guide - 1; Guidelines for the control of toxic ambient air contaminants. Division of Air Resources, New York State Department of Environmental Conservation, Albany, NY. 20 p. + appendices. > Source: Immerman, F. W., and J. L. Schaum. (1990) Final report of the nonoccupational pesticide exposure study (NOPES). EPA/600/3-90/003. U. S. Environmental Protection Agency, Research Triangle Park, NC. The values provided are the minimum average and maximum average concentrations in indoor air. ° Sources: Gunderson, E. L. (1995) FDA Total Diet Study, July 1986-April 1991, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc. Off. Analyt. Chem. Intl. 78(6):1353-1363. If the entry is followed by an asterisk (*), then the source is either: Gartrell et a/. (1986) Pesticides, selected elements, and other chemicals in infant and toddler diet samples, October 1980-March 1982. J. Assoc. Off. Anal. Chem. 69(1):123-145; or, Gunderson, E. L. (1988) FDA Total Diet Study, April 1982-April 1984, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc. Off. Anal. Chem. 71(6):1200-1209. The values given are the total dietary intake for 2-year old children/25 to 30 year old adults (greatest value; sex ignored). None of the chemicals exceeded the FAO/WHO ADI’s then in effect. 7 Source: New York State Department of Health, Bureau of Toxic Substance Assessment (1997) Compilation of octanol-water partition coefficients (draft). 11

P.

Source: New York State Department of Health (1998) Health advisories: Chemicals in sportfish and game, 1998-1999. 18 p. ° Sources: For all compounds except dioxins and furans: Stanley, J. S. (1986) Broad scan analysis of the FY82 National Human Adipose Tissue Survey

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-22

specimens; Volume I - Executive Summary. Final Report for | EPA Prime Contract No. 68-02-4252, Office of Toxic Substances, U. S. Environmental Protection Agency, Washington, DC. For dioxins and furans: Stanley, J. S., and J. Orban. (Undated) Chlorinated dioxins and furans in the general U. S. population: NHATS FY87 results. Final report for EPA Contract No. 68-DO-0137, Office of Toxic Substances, U. S. Environmental Protection Agency, Washington, DC.

'° Classifications are: T+ = Very toxic; T = Toxic; Xn = Harmful; Xi = Irritant; - = No classification assigned; blank cell = not determined (in most instances this is a group of chemical compounds with varying toxicity and undetermined carcinogenicity). Cancer classifications are: 1 or A= Known human

carcinogen; B2 or 2A (IARC) = Probable Human carcinogen; C or 2B = Possible human carcinogen; D or 3 = Not classifiable; E = Evidence of noncarcinogenicity for humans.

" Source: New York State Department of Environmental Conservation 1982-1984 air monitoring.

® Source: McGregor, D. B., C. Partensky, J. Wilbourn, and J. M. Rice. 1998. An IARC evaluation of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans as risk factors in human carcinogenesis. Environ. Health. Perspect. 106(Suppl. 2):755-760.

+ Production, formulation, sale and use is prohibited in New York State, or the United States.

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Appendix A, Table H.1 Review of recent studies on toxicity of PM from short-term exposures

Adverse particle-associated health effects have been demonstrated beginning at levels as low as 202 g/M3 (Yang and Yang, 1994) and at exposure durations as short as 30 minutes (Utell, et al. 1989; Yang and Yang, 1994). These effects were documented in asthmatics at rest (Yang and Yang, 1994) or engaged in exercise (Utell, et al. 1989). Participant ages in these studies varied from 19 to 50 (Utell, et al. 1989) and 23 to 48 (Yang and Yang, 1994). Thus, no frail elderly, elderly, or infirm subjects were included in the studies. Other positive studies likewise involved asthmatic subjects exercising or at rest, of ages up to 57 years (Ruprrecht, et al. 1995; Framptom, et al. 1992; Green, et al. 1989; Morrow, et al. 1994). For ethical reasons, adverse effects, when observed, could not be allowed to progress to clinical significance. However, reported effects included increased airway resistance; reduced values of lung function parameters such as forced expiratory volume at one and three minutes (FEV1, FEV3), forced vital capacity (FVC), and peak flow; as well as such symptoms as throat irritation and coughing.

In addition to the clinical studies described above, in which exposure of asthmatics to PM was controlled, are two studies in which exposure to PM was uncontrolled. A study conducted by Lawther, et al. (1970) employed a diary method, in which bronchitis patients recorded daily changes in the severity of their symptoms relative to their recollection of previous-day symptom severity. The diary method required participants to make an entry pertaining to a full day of symptom experience. Lawther, et al. reported a clear association of symptom severity with daily concentrations of smoke or sulfuric acid in London. They concluded, however, that this association could not be attributed to the measured 24-hour average concentrations, but more likely to "the effects of brief exposures to the maximum concentrations occurring during the day" (page 538), which may be several times the 24-hour average (Waller and Commins, 1966) which served merely as a surrogate parameter for such excursions. The basis for the Lawther, et al. conclusion included their (uncited) experimental work on normal subjects:

"... the measurements quoted in the present paper relate only to 24-hour average concentrations of sulphur dioxide and other pollutants. The evidence that we have from experimental work on normal subjects suggests that the effects of inhaling prepared mixtures of pollutants are of rapid onset, and peak concentrations encountered during the day may therefore be more relevant than 24-hour averages. The effects that we have reported cannot be considered as the result of 24-hour exposures to at least 500 g/M3 of sulphur dioxide together with 250 g/M3 of smoke: they are more likely to reflect the effects of brief exposures to the maximum concentrations occurring during the day, and these may be several times the 24-hour averages" (page 538).

A second clinical study in which exposure of asthmatics to PM was uncontrolled was conducted by Delfino, et al. (1997). Asthma symptom severity was found to be associated with PM levels. Significantly, the strength of the association increased as PM averaging time decreased from 24 hours to eight hours to one hour. The strength of the association actually increased with increasing exposure duration, as would be expected. However, as also shown, this trend was reversed unambiguously when equivalent exposure metrics were used, specifically, inhaler use per unit of exposure time (per hour) rather than per total exposure time.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-24

A short time frame for human response to PM also was evident when 300 people were overcome shortly after wind lofted fine particles into the air during four-day outdoor music festival attended by an estimated 40,000 people in Queen Creek, Arizona in April 1997. Arizona has a high concentration of residents with respiratory conditions. Examination of data reported by emergency medical personnel operating a treatment station at the concert revealed the approximate time course of visitations to the station. A significant elevation, indeed a peak, in the rate of visitation for emergency medical treatment, and a similar increase in the rate at which individuals seeking medical attention were transported to area hospitals. In fact, the rate increased so sharply that ambulances quickly saturated the local hospital, necessitating airlifting of patients to more distant health care facilities.

The studies described above demonstrate adverse health effects induced by short-term exposure to particles. However, exposure was routinely terminated to preclude symptoms from progressing to clinical significance. This ethical constraint has been overcome, however, in investigations using animal models. Investigations into airborne particle-induced effects on rats and dogs, under way at Harvard University's School of Public Health, have been published in abstract form (Godleski, et al. 1996; Nearing, et al. 1996a; Nearing, et al. 1996b), and more completely in oral and written reports by John Godleski to CASAC (Godleski, 1995). The findings implicate short-term, possibly electrophysiological mechanisms of fine-particle-induced cardiopulmonary malfunctioning, shown via electrocardiograms (EKGs).

Nearing, et al. (1996b) induced ST segment elevation and periods of apnea in dogs inhaling fly ash at 1,000 g/M3 for 3 d, 4 h/d. Nearing, et al. (1996a) also demonstrated increased T-wave alternans amplitude, indexing vulnerability to ventricular fibrillation, in dogs inhaling fly ash at 3,000 g/M3 for 3 d, 3 h/d. ST segment elevation and T-wave alternans effects began soon after exposure and became most prominent by day three. Apnea for 20 to 30 seconds occurred during hour four on day 3. As a frequent precursor to heart attacks, T-wave alternans represents a clinically serious cardiological event suggestive of PM lethality.

PM lethality also has been demonstrated empirically in animal models. Godleski (1995) and Godleski, et al. (1996) used rats exhibiting either monocrotyline-induced pulmonary inflammation or SO2-induced chronic bronchitis. Rats with respiratory pathology then inhaled particles concentrated from Boston air at 228 to 288 g/M3 for 3 h/d, 6 h/d. Breathing rates declined from 17.1/min. in controls to 9/min. in exposed rats. Apnea for up to 22 seconds occurred. Bronchoconstriction occurred in 80 percent of rats exhibiting respiratory disease, compared with 25 percent of controls. Rats exhibited no signs of distress, but deaths occurred on all exposure days, possibly as a result of particle-induced arrhythmias or other EKG-related cardiopulmonary malfunction. Godleski (1995) indicated that mortality might also be consistent with systemic effects following particle induction of proinflammatory mediators, such as the cytokines interleukin-1 and tumor necrosis factor-alpha (TNFa).

Two bioassays were conducted in which aerosols were delivered either constantly at the average concentration, or included excursions. The bioassays, though unpublished, represent results obtained in an investigation by Kleinman, et al. (1989) which was published, but excluded from that report, which did not address the issue of excursions. In both bioassays, rats

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-25

were exposed for four hours to either of two aerosols using the published methods (Kleinman et al., 1989). However, in the unpublished bioassays, the rates at which the aerosols were delivered included either one or four excursions. Excursions were defined as elevations of at least 50 percent above an otherwise constant steady state aerosol concentration, lasting for at least five minutes. Unpublished Kleinman, et al. bioassays involved microscopic examination of rat lungs 48 hours after four-hour controlled exposures of groups of six rats to either of two sulfate aerosols, designated AMS and SAM.

The fraction of microscopically examined rat lung area exhibiting aerosol-induced lesions was evaluated in groups of rats exposed to excursions vs. no-excursion controls exposed to the same aerosol. Thus, except for the excursions, treated and control rats experienced identical exposures. Greater lesion area was found in rats exposed to aerosol excursions. However, in the case of AMS, the increment over control rats was greater, reflecting the occurrence of four excursions, compared with only one excursion in the case of rats exposed to the SAM aerosol.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-26

Appendix A, Table H.2. Particle Effects Revealed In Controlled Acute Human Exposures

citation | healthy | asthmatic | activity} age other particle dose |duration] dose x effect(s) subjects| subjects | level factor(s) type(s) duration years mg/m min. mg min/m? studies emphasizing inert mineral particles Yang and 30 25 atrest | 23 - 48 we ITSP 202 30 6,060 healthy: no effects; asthmatic: Yang, 1994 reduced lung function (FEV1) Anderson, 15 15 exercise | 18 - 45 carbon black 200 60 12,000 Jno effects etal. 1992 Framptom, 30 30 exercise | 20 - 42 we NaCl or H2SO4, 100 180 18,000 Jno particle effects (ozone effect et al., 1995 then ozone noted Utell, et al., 0 15 exercise | 19 - 50 NaCl, H2S04, 700 30 21,000 — |reduced lung function (FEV1) 1989 INH3 Anderson, 0 15 exercise | 18 - 45 carbon black + 358 60 21,480 |no effects etal. 1992 H2S04 aerosol Morrow, et 0 17 exercise | 20 - 57 NaCl, H2SO4 190 120 22,800 |reduced lung function (FEV1) al., 1994 Morrow, et 0 0 exercise | 52 - 70 |17 subjects |NaCl, H2SO4 190 120 22,800 |no effects al., 1994 with COPD Anderson, 15 0 exercise | 18 - 45 carbon black + 505 60 30,300 |no effects fetal 1992} 2S O4 aerosol ft Aris, et al. 0 18 exercise | 23 - 37 NaCl 3,000 16 48,000 |no effects 1991b Laube, et 7 0 exercise | 20 - 31 NaCl, H2SO4 1,000 60 60,000 no effects al., 1993

Green, et 24 0 exercise | 18 - 35 we activated carbon 1,020 120 122,400 Jcough, reduced lung function al. 1989 + formaldehyde FVC, FEV3, peak flow Kulle, et al., 20 0 exercise | 20 - 35 activated carbon, 517 240 124,080 Jno effects 1986 SO2 100 1,440 | 144,000 |daily mortality and morbidity observed 150 1,440 | 216,000 INAAQS for PM-10

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

acids and/or othe

1 toxicologically active moieties

studies emphasizing £ ly

lemonade

citation | healthy | asthmatic | activity} age other particle dose |duration] dose x effect(s) subjects| subjects | level factor(s) type(s) duration wee we we years . mg/m min. mg min/m? Culp, et al., 16 0 exercise | 20 - 39 NaCl + H2S04 2,000 120 240,000 |no effects on lung function 1995 Framptom, 12 0 exercise | 20 - 39 NaCl + H2S04 2,000 120 240,000 throat irritation; no effect on lung et al., 1992 function Balmes, et 0 12 atrest | 25-41 NaCl, 30 mOsm_ | 5,900,000 5,900,000 |increased specific airway al. 1988 to resistance 87,100,000

Koenig, et 0 14 exercise | 13 - 18 IH2S04 35 45 1,575 |reduced lung function (FEV1) al., 1992 Koenig, et 0 9 exercise | 12 - 18 H2S04, SO2, 68 40 2,720 Ino clinical symptoms; reduced al., 1989 H2S04 + SO2, lung function (FEV1)

IHNO3 Avol, et al. 0 32 exercise | 8-16 we H2SO04 134 40 5,360 Ino effect (one subject: increased 1990 specific airway resistance) Koenig, et 8 9 exercise | 60 - 76 (NH4)2S04; 152 40 6,080 Ino effects (airway resistance noted al., 1993 H2S04 +/- to be correlated with oral

7,200

9,000

12,240

Utell, et al., we we we we we H2S04 450 16

1982 y Hanley, et 0 22 exercise | 12 - 19 oe H2S04 +/- 200 45

al., 1992 lemonade ) Koenig, et 0 28 exercise | 12 - 19 lozone, NO2, 68 180

al., 1994 H2S04, HNO3

Utell, et al., H2S04 1,000 16

16,000

Aris, et al. 0 18 exercise | 23 - 37 H2SO04 3,000 16 48,000 |no effects 1991b Aris, et al. 10 0 exercise | 20 - 40 ozone HNO3 fog 500 120 60,000 —_|no effects 199la sensitive,

Inon-smoker

ammonia in asthmatics

reduced lung function (specific airway conductance) in asthmatics

reduced lung function (FEV1, FVC2, FVC3

Ino effect (6 asthmatics did not complete protocol

reduced lung function (specific airway conductance) in asthmatics

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

citation | healthy | asthmatic | activity} age other particle dose |duration] dose x effect(s) subjects| subjects | level factor(s) type(s) duration _ a years oe mg/m min. | mg min/m*

Linn, et al., 15 30 exercise | 18 - 50 H2S04, ozone 100 780 78,000 — jincremental, marginal acid-

1989 induced lung function decrease (FEV 1) and airway responsiveness increase

Aris, et al. 0 18 exercise | 23 - 37 H2SO04 1,400 60 84,000 _|no effects

1991b

Avol, et al. 21 21 exercise | 18 - 45 H2SO04 1,460 60 87,600 |dose-related lower respiratory

1988a symptoms in asthmatics; reduced lung function (FEV1)

Aris, et al. 10 0 exercise | 20-40 Jozone HNO3 fog 500 180 90,000 Ino effects

199la sensitive,

Inon-smoker Linn, et al., 22 19 exercise | 18 - 48 H2SO04 2,000 60 120,000 _Jincreased symptoms with larger 1989 acid particles (4 asthmatics unable

to complete protocol due to symptoms

Avol, et al. 22 22 exercise | 18 - 45 H2SO04 2,193 60 131,580 |dose-related lower respiratory 1988b symptoms in asthmatics; reduced lung function (peak flow 100 1,440 | 144,000 |daily mortality and morbidity observed 150 1,440 | 216,000 INAAQS for PM-10 Balmes, et 0 12 atrest | 25-41 H2S04, 30 5,900,000 5,900,000 |increased specific airway al. 1988 mOsm to resistance fo 87100, 000 ff Balmes, et 0 12 atrest | 25-41 HNO3, 30 mOsm | 5,900,000 5,900,000 |increased specific airway al. 1988 to resistance 87,100,000 Balmes, et 0 12 atrest | 25-41 H2SO04 + HNO3, | 5,900,000 5,900,000 |increased specific airway al. 1988 30 mOsm to resistance 87,100,000

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

citation | healthy | asthmatic | activity} age other particle dose |duration| dose x effect(s) subjects| subjects }| level factor(s) type(s) duration wes wes wes wes years _ _ mg/m? min. | mg min/m* ve Balmes, et 0 12 atrest | 25-41 we H2S04 300 5,900,000 a 5,900,000 |increased specific airway al. 1988 mOsm to resistance 87,100,000 Fine, et al., 0 10 atrest | 22-34 we INa2SO3 + acetic | 0.25 to 8 a ? bronchoconstriction 1987a acid + SO2 ppm Fine, et al., 0 8 atrest | 22-29 we HCl + H2S04 we a ? cough, increased airway resistance 1987b

1. Anderson, K. R., et al. Controlled exposures of volunteers to respirable carbon and sulfuric acid aerosols. Journal of the Air & Waste Management Association, 42:770-6, 1992;

2. Aris, R., et al. The effects of sequential exposure to acid fog and ozone on pulmonary function in exercising subjects. American Reviews of Respiratory Disease, 143:85-91, 1991a;

3. Aris, R., et al. Lack of bronchoconstrictor response to sulfuric acid aerosols and fogs. American Reviews of Respiratory Disease, 143:744-50, 1991b;

4. Avol, E. L., et al. Respiratory dose-response study of normal and asthmatic volunteers exposed to sulfuric acid aerosol in the sub-micrometer size range. Toxicology and Industrial Health, 4:173-84, 1988a;

5. Avol, E. L., et al. Short-term respiratory effects of sulfuric acid in fog: a laboratory study of healthy and asthmatic volunteers. Journal of the Air Pollution Control Association, 38:258-63, 1988b;

6. Avol, E. L., et al. Respiratory responses of young asthmatic volunteers in controlled exposures to sulfuric acid aerosol. American Reviews of Respiratory Disease, 142:343-8, 1990;

7. Balmes, J. R., et al. Acidity potentiates bronchoconstriction induced by hypoosmolar aerosols. American Reviews of Respiratory Disease, 138:35-9, 1988;

8. Culp, D. L., et al. Composition of human airway mucins and effects after inhalation of acid aerosols. American Journal of Physiology, 269(3, Part 1):L358-70, September 1995;

9. Fine, J. M., et al. The roles of pH and ionic species in sulfur dioxide- and sulfite-induced bronchoconstriction. American Reviews of Respiratory Disease, 136:1,122-6, 1987b;

10. Fine, J. M., et al. The role of titratable acidity in acid aerosol-induced bronchoconstriction. American Reviews of Respiratory Disease, 135:826-30, 1987a;

11. Framptom, M. W., et al. Sulfuric acid aerosol exposure in humans assessed by bronchoalveolar lavage. American Reviews of Respiratory Disease, 146:626-32, 1992;

12. Framptom, M. W., et al. Sulfuric acid aerosol followed by ozone exposure in healthy and asthmatic subjects. Environmental Research, 69:1-14, 1995;

13. Green, D. J., et al. Acute pulmonary response in healthy, non-smoking adults to inhalation of formaldehyde and carbon. Journal of Toxicology and Environmental Health, 28:261-75, 1989;

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-30

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

Hanley, Q. S., et al. Response of young asthmatic patients to inhaled sulfuric acid. American Reviews of Respiratory Disease, 145:326-31, 1992;

Koenig, J. Q., et al. Effects of inhalation of acidic compounds on pulmonary function in allergic adolescent subjects. In: Symposium on Health Effects of Acid Aerosols. Research Triangle Park, NC, October 1987. Environmental Health Perspectives, 79:173-8, 1989;

Koenig, J. Q., et al. The effect of duration of exposure on sulfuric acid-induced pulmonary function changes in asthmatic adolescent subjects a dose-response study. Toxicology and Industrial Health, 8:285-96, 1992;

Koenig, J. Q., et al. Respiratory effects of inhaled sulfuric acid on senior asthmatics and nonasthmatics. Archives of Environmental Health, 48:171-5, 1993;

Koenig, J. Q., et al. Oxidant and acid aerosol exposure in healthy subjects and subjects with asthma. Part 1: effects of oxidants, combined with sulfuric or nitric acid, on the pulmonary function of adolescents with asthma. Cambridge, MA; Health Effects Institute, Research Report No. 70, 36 pp., 1994;

Kulle, T. J., et al. Pulmonary effects of sulfur dioxide and respirable carbon aerosol. Environmental Research, 41:239-50, 1986;

Laube, B. L., et al. Acute exposure to acid fog: effects on mucociliary clearance. American Reviews of Respiratory Disease, 147:1,105-11, 1993;

Linn, W. S., et al. Effect of droplet size on respiratory responses to inhaled sulfuric acid in normal and asthmatic volunteers. American Reviews of Respiratory Disease, 140:161-6, 1989;

Morrow, P. E., et al. Effects of near ambient levels of sulphuric acid aerosol on lung function in exercising subjects with asthma and chronic obstructive pulmonary disease. Annals of Occupational Hygiene, 38(Supplement 1):933-8, 1994;

Utell, M. J., et al. Comparison of normal and asthmatic subjects' responses to sulphate pollutant aerosols. In: W.H. Walton, Editor. Inhaled Particles. V. Proceedings of an International Symposium organized by the British Occupational Hygiene Society, Cardiff, Wales; September 1980. Annals of Occupational Hygiene, 26:691-7, 1982;

Utell, M. J., et al. Effect of inhaled acid aerosols on respiratory function: the role of endogenous ammonia. Journal of Aerosol Medicine, 2:141-7, 1989;

Yang, S.-C., and S.-P. Yang. Respiratory function changes from inhalation of polluted air. Archives of Environmental Health, 49:182-7, 1994.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-31

Appendix A: Table I.1: Characteristics of potency or toxicity, regulatory values, and human or environmental exposure for pesticides.

Characteristic

Potency - Toxicity! Regulatory Values Exposure Chemicals jonyms) EPA NYS CAS Number; EPA EPA IRIS Cancer NYS DEC USFDA Solubility NYS. Cancer NOAEV | RED (oral) | Potency Drinking ‘Air’ | Nopess | ™atket NYS in waters Koct Type 1990- NYS classification’ LOAEL | (mg/kg/d); Oral water Gaidet | (ngim | basket” DOW’ (neil @ (eml) of | 1993 Avg. | SW/GW (mg/kg- | RC (air) | (mg/kg/dy' | standard? AGC! 8 (ng/kg- Kow 30), 8 Use? use!” Survey" day) (mg/m*) Inhale (ug/l) vale? bw/day) S°C) (lb/yr) (ug/my! g/m name/CAS/eancer drinking | 1 C | nopes usfda Kow water Koe type mean water solubility use use survey Abameetin . 0.0004E; 0.0078 I 20 71751-41-2 - Acephate 0.004; 9.9/8.2 0E+00 I 4,235 30560-19-1; C - Acetochlor 0.02E; H “ 34256-82-1; B2 - Aciflourfen 0.013E; 0E+00 >250 H 150 aa (Blazer; Tackle) - 62476-59-9; B2 Acrolein = 0E+00 HR (Magnicide H) 0.00002E 107-02-8: C Alachlor r 0.01E; 0.5 SW-S 8.30E+02 240 H 610,485 ++ (Lasso) +GW-S; 15972-60-8; B2 2.0 MCL Aldicarb 7.0 SW-S: 0.1/0.1 1.4E+01 6000 N ay, (Temik) 0.35 GW116-06-3; D $ (sum with methomyl: 3.0 MCL Allethrin insol I (Pynamin) 584-79-2

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-32

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Ametryn 8.6N 0.009E; 50 SW- 0E+00 185 H 834-12-8 - GV+ 20°C GW-S 4-aminopyridine 3N 0.0002E; 1.0 SW- 2E+00 80000 - BR (Avitrol) - GV 500000 504-24-5; D (HCI salt) Amitraz 0.25 N 0.0025E; 4.97E-2; 3.45E+04 I 2,557 33089-61-1; C - - Amitrole 0.0005 1.13E-0; 0.2 280 100 H 61-82-5; B2 WHO; - Ammonium sulfamate 2143N 0.2E; 10 240 648000 H (Ammate) - 7773-06-2 Anilazine 0.0004 F 1,071 (Dyrene) OPP; 101-05-3 - ANTU 03 R(*) 86-88-41 Apollo 1.25N 0.013E; 3.45E+04 A (Clofentezine) - 74115-24-5; C Aramite 2.5E-2; A(*) 140-57-8; B2 7.1E-6 Asulam SOL 0.05E; 0E+00 H 3337-71-1;C - Atrazine 3.5N 0.035E; 3.0 SW- 5 nd-0.3 2.14E+02 33 100 H 1,426,474 +/+ (Aatrex) - - GV; 7.5 1912-24-9; C/2B- GW-S; 3.0 IARC MCL Azinphos methyl 0.0015 0.07 SW- 0.2 31.1/6.1 8.96E+02 30 1000 I 78,007 +0/- (Guthion) OPP; GV; 4.4 (skin) 86-50-0; E = GW-S NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-33

name/CAS/cancer

NOAEL, LOAEL

R{D, REC

cancer potency

drinking water

TLV

AGC

nopes

usfda

Kow

water solubility

Koc

type use

mean use

water survey

Azobenzene 103-33-3; B2

5.0 SWGV+ GW-S

6.61E+03

Azocyclotin (Peropal; Tricyclotin) 41083-11-8

0.001 WHO;

3.45E+04

Azoxystrobin (Abound; Heritage) 131860-33-8

Baythroid (Cyfluthrin) 68359-37-5

2.5N

0.025E;

1.63E+04

Benalaxyl (Galben) 71626-11-4

3.45E+04

Bendiocarb 22781-23-3

6.32E+02

Benefin (Benfluralin) 1861-40-1

35 GW-S

4.20E+05

Benomyl (Benlate) 17804-35-2: C(q)

SN

1.29E+03

11,295

Bensulide (Betasan) 741-58-2

12.5

0.0066 OPP;

25 @ 20°C

14,080

Bentazon (Basagran) 25057-89-0; E

2.5N

0.0025E;

2.20E+02

3.4

6,629

Bidrin

(Dicrotophos) 141-66-2

0.1N

0.0001E;

0.25 (skin)

Biphenthrin (Bifenthrin; Talstar) 82657-04-3; C

15N

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-34

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey phthalate +GMES ingre H+8+-482 & Brodifacoum R 56073-10-0 Bromacil >250 0.1 44 GW-S 10 2.8E+01 815 109 H -/+ 314-40-9; C <1250 OPP; Bromadiolone R 28772-56-7 Bromophos 0.04 <0.1 2.91E+05 40 I 2104-96-3 WHO; <0.1 Bromoxynil SN 0.02E; 1.03E-1 5.35E+05 130 H 66,271 “| 1689-84-5: C(q) - 4.1E-1 Butachlor 0.037 3.5 GW-S 1.150E+03 H + 23184-66-9 OPP: Butylate SN 0.05E; 50 SW- 5.70E+02 44 @ 20°C 540 H 41,018 -l- (Sutan) - GV+ 2008-41-5; E GW-S Cacodylic acid 0.01E; 6.23E-2 0.2 1E+00 667000 H 75-60-5; B2 - - Captafol 2L 0.002E: 5.1E-2; 0.1 2.40E+04 F [- (Difolatan) - - (skin) 2425-06-1; B2/2AIARC Captan 12.5N 0.13E; 2.4E-3; 18 GW-S 5 nd-0.1 47.0/13. 2.24E+02 5.1 F 327,640 133-06-2; B2 - - 9 Carbaryl 9.6N 0.1E; 2.27E-2; 29 GW-S 5 nd-28 127.3/33 1E+00 50 205-457 I 92,945 +/- (Sevin) - - 8 63-25-2: C(q) Carbendazim 0.01 3.63E+03 10,000 F 10605-21-7 WHO; NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-35

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Carbofuran 0.5N 0.005E; 15 SW-S + 0.1 0.24 0.1/0.1 4.0E+01 25700 I 157,906 +h (Furadan) - GW-GV; 1563-66-2 40 MCL Carbon disulfide 0.1E; 6E+00 FM 75-15-0 0.7E Carbon tetrachloride 0.0007E; 1.3E-1; 0.4 SW- 4.37E+02 F [- 56-23-5; B2 - 1SE-5 GV; 5.0 GW-S; 5.0

MCL Carbophenthion 0.00013 0.1/0.1* 1.11E+05 LA (Trithion) OPP; 786-19-6 - Carbosulfan 1.0N 0.01E; 1.27E+05 LN, (Marshal) - M 55285-14-8 Carboxin 10N 0.1E; 50 SW- 1.13E+02 195 F 5234-68-4 - GV+

GW-S Chloral 15.7L 0.002E; ? 75-81-6 - Chloramben. ISL 0.015E; 50 SW- 799 13 H 15,098 -/- (Amiben; Vegiben) - GV+ 133-90-4 GW-S Chloranil 5.0 GW-S 1.55E+05 F 118-75-2 Chlordimeform 0.001 9.4E-1; 0E+00 LA 6164-98-3; B2 OPP; - Chlorfenvinphos 0.002 1.56E+02 Miscible LA 470-90-6 WHO; Chlorimuron-ethyl 6.25N 0.02E; 1.6E+01 H 210 (Classic) - 90982-32-4

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-36

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Chlorobenzilate SN 0.02E; 4.4/0.8 3.24E+03 ~ insol. 1065 A -/+ 510-15-6; 3-IARC - Chloroform 0.01E; 6.1E-3; 7.0 SW-S 9.3E+01 FM 67-66-3; B2 - 2.3E-5 +GW-S Chloropicrin 0.67 SF 49,335 76-06-2 Chlorothalonil 1.5N 0.015E: 7.7E-3; 5.0 GW-S <0.1-3 <0.1 7.62E+02 0.6 F 130,838 +/- (Bravo) - - <0.1 1897-45-6; B2 Chlorpropham SON 0.2E; 597) 2.66E+02 89 1150 H -/+4 101-21-3; E - 188.6 Chlorpyrifos 0.03 N 0.003E: 0.2 6-280 13.8/3.8 9.33E+04 2.0 6070 I 218,597 (Dursban, Lorsban) - (skin) 2921-88-2; E Chlorpyrifos-methyl 0.01 323 1.50E+04 I 5598-13-0 OPP; 11.6 Chlorsulfuron. 5.0N 0.05E; 6E+00 300-2800 H 64902-72-3 - Clomazone 43 0.043 1100 274 H 748 (Command; OPP; Dimethazone) - 81777-89-1 Clopyralid 05 2 - (Lontrel) OPP; 1702-17-6 - Copper hydroxide F (Champ; Champion) 20427-59-2; D Copper sulfate 1.0 143,000 F 66,257 7758-99-8; D Coumaphos 0.00025 1.35E+04 R 56-72-4; E OPP; NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-37

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Crufomate 0.1 5.0 ? (Ruelene) WHO; 299-86-5 - Cryolite I 146,054 - (Kryocide) 15096-52-3; D Cyanazine 1.25 0.002E; 1.0E-0; 1.50E+02 171 190 H 647,756 +/+ (Bladex) - - 21752-46-2: C(q) Cycloate 0.005 H 12,985 (Ro-Neet) OPP; 1134-23-2 - Cyclohexanone 462 N 5.0E; PC 108-94-1 - Cyhalothrin 0.5N 0.005E; 0.24 LA (Karate, lambda- - Cyhalothrin) 91465-08-6; D Cyhexatin 0.00075 2.46E+05 A 13121-70-5 OPP; Cypermethrin 1.0N 0.01E; 2.95E+04 0.009 160,000 I 46 (Ammo) - 52315-07-8; C Cyromazine 0.75 N 0.0075E; 1E+00 IGR (Larvadex) - 66215-27-8; E Cytokinins PGR 47 2,4-D 1.0N 0.01E; 50 SW-S+ 10 nd-3 <0.1 3.7E+01 890 H 141,665 -/+ 94-75-7; D - GW-S; 50 <0.1 MCL 2,4-DB 8N 0.008E; 5.43E+02 46 H 32,000 -l- (2,4-D is a metabolite) - 94-28-6 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-38

name/CAS/cancer NOAEL RED, cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey

Dalapon 8.45N 0.03E; 50 SW- 5.8 6E+00 502,000 1.0 H, -

75-99-0 - GV+ PGR GW-S

Daminozide 15N 0.15E; 8.7E-3; 0E+00 100,000 PGR (Alar) - - 1596-84-5; B2

Danitol 2.5N 0.025E; Al (Fenpropathrin) - 39515-41-8; E

DCNA 0.025 258.6) F 1,478 (Botran; Dichloran) OPP; 7713 99-30-9 -

DCPA IN O.O1E; 1.49E-3; nd-3 1.8/1.0 6.80E+03 0.5 H 38,861 ++ (Dacthal) ~ ~ 1861-32-1; C(q)

DEET 0.9E; IR + (N, N-Diethyl-meta- - toluamide)

134-62-3; D

Deltamethrin 0.01 2.92E+07 ~ insol. I 52918-63-5 OPP;

Demeton 0.04L | 0.00004E; 0.11 4.07E+02 LA (Systox) - (skin) 8065-48-3

Demeton-s-methyl 05 5E+00 LA (Metasystox) (skin) 919-86-8

Desmedipham 0.04 H 13684-56-5; E OPP;

Dialifor 4.90E+04 LA (Torak) 10311-84-9

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-39

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Diallate 0.005 SE+00 H (Avadex) OPP; 2303-16-4 - Diazinon 0.01 0.00009 0.7 GW-S 0.1 1-322 10.6/3.7 2.04E+04 60 I 16,241 +/+; (Spectracide) OPP: (skin) found in 333-41-5 - L. Erie & Ontario Dibromochloro — 1.4E-0; 0.04 SW-S 1.95E+02 SF [- propane (DBCP) 0.0002E 8.3E-0 +GW-S; 96-12-8; B2 0.2 MCL Dicamba 3.0N 0.03E; 0.44 GW- 1.02E+03 500,000 2.0 H 134,531 -/+ (Banvel) - Ss 1918-00-9; D Dicapthon I - 2463-84-5 Dichlobenil 0.013 1.26E+03 H + 1194-65-6; C OPP; 1,2-Dichlorobenzene 0.09E; 3.0 SW-S 3.98E+03 HL 95-50-1; D - + GW-S; SF, 5.0 MCL solvent 1,4-Dichlorobenzene — 3.0 SW-S 2.45E+03 F (Paracide) 0.8E + GW-S; 106-46-7; C 5.0 MCL 1,2-Dichloroethane 9.1E-2; 0.6 SW-S FM, HK (Ethylene dichloride) 2.6E-5 +GW-S; Inert 107-06-2; B2 5.0 MCL ingred solvent 1,2-Dichloropropane ~~ 1.0 SW-S SF,N 44 (DD; Propylene 0.004E +GW-S; dichloride) 5.0 MCL 78-87-5 1,3-Dichloropropene 0.0003E; 5.33E-2 0.4 SW-S SF,N (- (Telone) 0.02E - +GW-S; 542-75-6; B2 5.0 MCL NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-40

name/CAS/cancer NOAEL, LOAEL

R{D, REC

cancer potency

drinking water

TLV

AGC

nopes

usfda

Kow

water solubility

Koc

type use

mean use

water survey

Dichlorprop (2,4-DP) 120-36-5

0.005 OPP;

-/+

Dichlorvos 0.05 N (DDVP)

62-73-7; C(q)/2BIARC/B2-CRAVE

0.0005E;

0.0005E

0.9 (skin)

2-148

<0.1 <0.1

2.5E+01

10,000

LF

Diclofop methyl (Hoelon) 51338-27-3; C(q)

1.05E+04

Dicofol (Kelthane) 115-32-2; C

0.0012 OPP;

2.83E+04

7,597

Dienochlor 6.25 (Pentac) 2227-17-0

1411-2011

Diethatyl-ethyl (Antor) 58727-55-8

4,097

Difenzoquat 25N (Avenge) 43222-48-6; E

Diflubenzuron 2.0N (Dimilin) 35367-38-5; E

6.61E+03

0.08

Dimethipin 2.0N (Harvade) 55290-64-7; C

6E+00

Dimethoate 0.05 N

(Cygon) 60-51-5;C

6.9/7.2

1E+00

46,450

Dimethylformamide 68-12-2

50 SWGV+ GW-GV

0E+00

Solvent for pesticides

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-41

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey

Dinitrocresol 5.00E+02 LF, : (DNOC) H,D 534-52-1 Dinocap 0.5 0.004 4 630 F 861 (Karathane) OPP; 39300-45-3; E - Dinoseb IL 0.001E; 7.0 MCL 4.90E+03 52 H,D -/+4 (Dinitro) - (*) 88-85-7; C Dioxathion 0.0015 0.2 LA 78-34-2 WHO; (skin) Diphacinone 03 R 82-66-6 Diphenamid 3.0m N 0.03E; 50 SW- 8.3E+01 H 957-51-7 - GV+

GW-S Diphenylamine 0.025E; 41.0/7.4 3.98E+03 Treat 122-39-4 - apple

pear scald

Diquat dibromide 0.22 N 0.0022E; 20 SW-S+ | 0.1,0.5 0E+00 700,000 @ 100,000 H 3,831 [- 2764-72-9; E - GW-S; 20 (skin) 20°C

MCL Disulfiram 2.0 ? 97-17-8 Disulfoton 0.04 L 0.00004E; ND GW-S 0.1 0.3/0.4 1.05E+03 25 @ 23°C I 3,438 -l- (Di-Syston) - (skin) 298-04-4; E 1,4-Dithiane 105 L 0.01E; 6.0E-2; 1.8 GW-S 5 ~ insol F 724,111 (- (Mancozeb; Manzate) - - (ETU is metab.) 8018-01-7; B2 Diuron 0.625 N 0.002E; 10 9.4E+01 H 34,332 + 330-54-1; B2 -

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-42

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey

Dodine 1.25N 0.004: 3.62E+03 100,000 F 14,120

2439-10-3 -

Endosulfan 0.6N 0.006E: 0.1 46.0, 1E+00 I 48,463 +

(Thiodan) - (skin) 17.7 (degrad.

115-29-7; E prod.)

Endothall 2.0N 0.02E; 8.1E+01 H [-

129-67-9 -

Epichlorohydrin ~~ 9.9E-3; 0E+00 LF

106-89-8; B2 0.001E 1.2E-6

EPN 0.1 0.3/ ne* LA

2104-64-5

EPTC 2.5N 0.025E: 5.8E+01 280 H 252,056 +/-

(Eptam) ~

759-94-4

Esfenvalerate 2.5N 0.02 I 3,045 _

(Asana XL; Pydrin) OPP;

66230-04-4; E -

Ethalfluralin 0.04 8.9E-2; H _

(Sonalan) OPP; -

55283-68-6; C(q) -

Ethephon 0.5L 0.005E: PGR 238

16672-87-0; D -

Ethiofencarb 2.2E+01 I

(Croneton)

29973-13-5

Ethion 0.05 N 0.000SE; 04 22.2/4.5 3.12E+04 ~ insol. 8890 LA [-

563-12-2; E - (skin)

Ethofumesate 04 H

26225-79-6; D OPP;

Ethoprop 0.0001 2.81E-2; 2.6E+01 I 20,555 -/+

(Mocap; Ethoprophos) OPP; -

13194-48-4 -

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-43

name/CAS/cancer

NOAEL, LOAEL

R{D, REC

cancer potency

drinking water

TLV

AGC

nopes

usfda

Kow

water solubility

Koc

type use

mean use

water survey

Ethyl dibromide

0.008 (child)

0.045

53.7 - 61.7

4040 @ 20°C

14-160

Ethylene 74-85-1; 3-IARC

PGR

Ethylene chlorobromide 107-04-0

SF

Ethylene dibromide (EDB; 1,2dibromoethane) 106-93-4; B2/2AIARC

1.0 WHO;

8.SE+1; 2.2E-4

0.0006

SW-S +

GW-S; 0.05 MCL

5.8E+01

FM

Ethylene oxide 75-21-8; 1-IARC

0.05 SWGV+ GW-GV

1E+00

FM

ETU (Ethylene thiourea) 96-45-7; B2

0.25 L

0.00008E;

ND - GWSs

0E+00

Etradiazole 2593-15-9

4.96E+02

SF

Etrimfos (Ekamet) 38260-54-7

6.32E+02

Express (Tribenuron-methyl) 101200-48-0

0.79 N

Fenamiphos (Nemacur) 22224-92-6; E

0.025 N

0.00025E;

0.1 (skin)

5.2E+01

700 @ 20°C

Fenarimol (Rubigan) 60168-88-9; E

0.065 OPP;

1.97E+03

3,861

Fenbutatin oxide (Vendex) 13356-08-6; E

0.05 OPP;

4,109

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-44

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Fenitrothion 0.0013 1.4/0.8 2.40E+03 LA (Sumithion) OPP; 122-14-5; E - Fenoxaprop-ethyl 0.0025 4.40E+04 H (Depon; Excel; OPP; Furore) - 6644 1-23-4 Fenoxycarb 0.08 6 IGR 79127-80-3; B2 OPP; Fensulfothion 0.00025 0.1 9E+00 (*) 115-90-2 OPP; Fenthion 0.0007 0.2 1.45E+03 55 I (Baytex) OPP; (skin) 55-38-9; E - Fenuron 1.4/0.2 H _ 101-42-8 Fenvalerate 0.025E; 44/19 2.63E+04 I 6 (Pydrin) - 51630-58-1; E Ferbam 0.02 4.2 GW-S 10 1.92E+02 F 34,588 14484-64-1 WHO; Flucythrinate 1.58E+06 I 70124-77-5 Fluazifop-p-butyl 0.01E: 0.48 100,000 H 1,507 (Fusilade) - 79241-46-6 Fluchloralin 6.17E+04 H (Basalin) 33245-39-5 Fluometuron 12.5N 0.013E; 50 SW- 2.2E+01 90 175 H “| 2164-17-2; C - GV+ GW-S NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-45

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Fluridone 8.0N 0.08E; H (Sonar) - 59756-60-4; E Flurprimidol 18N 0.02E; 1.62E+02 PGR (Cutless) - 56425-91-3 Flusilazole 0.2N 0.0007E: 5.56E+02 F (NuStar) - 85509-19-9 Flutolanil 63.7L 0.06E; F (Moncut) - 66332-96-5; E Fluvalinate, tau IN 0.01E; 0.1 mg/; 1.08E+07 ~ insol. I 102851-06-9 - 100 ug/ (skin) Folpet 10N 0.10 E; 3.5E-3; 50 GW-S nd-0.8 3.1/1.0 3.45E+04 F 133-07-3; B2 - - Fomesafen 0.0025 1.9E-1; 4.96E+02 H (Flex) OPP; - 72178-02-0; C(q) - Fonofos 0.2N 0.002E: 0.1 0.2/<0.1 2.14E+03 I 89,225 “| (Dyfonate) - (skin) 944-22-9: E Formaldehyde 0.02E; — F 50-00-0; B1 - 1.3E-5 Formetanate 0.002 0E+00 I 8,362 hydrochloride OPP; (Carzol) - 23422-53-9; E Fosetyl-al 250N 3.0E; 0E+00 ?- (Aliette) - Not 39148-24-8; C mark eted in US Furfural 79L 0.003E: 79 0E+00 ? 98-01-1 - NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-46

name/CAS/cancer

NOAEL, LOAEL

R{D, REC

cancer potency

drinking water

TLV

AGC

nopes

usfda

Kow

water solubility

Koc

type use

mean use

water survey

Furmecyclox (Epic 500; Xyligen B) 60568-05-0; B2

3.0E-2;

F(*)

Gibberellic acid 71-06-5

PGR

Glufinosinateammonium

77182-82-2

04N

0.0004E;

0E+00

Glyphosate (Roundup) 1071-83-6; E

10N

1E+00

900,000

591,372

Haloxyfop-methyl (Verdict) 69806-40-2; B2

0.005 N

Hexachlorophene 70-30-4

5.0 GW-S

8.51E+03

Hexazinone 51235-04-2; D

10N

50 SWGV+ GW-S

0E+00

21,600

Hydramethylnon (Amdro) 67485-29-4; C

7.51E+06

Imazalil 35554-44-0; C(q)

1.25N

73E+01

Imazapyr (Arsenal) 81334-34-1; E

Imazaquin (Scepter) 81335-37-7

2.62E+02

Imazethapyr (Pursuit) 81334-34-1

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-47

name/CAS/cancer

NOAEL, LOAEL

cancer potency

drinking water

TLV

AGC

nopes

usfda

Kow

water solubility

Koc

type use

mean use

water survey

Iprodione (Glycophene) (Vinclozolin is metab.) 36734-19-7; B2

42N

4.39E-2;

5.18

1.99E+03

13 @20°C

18,100

Isodrin (isomer of aldrin) 465-73-6

5.0 GW-S

1)

Isofenphos (Oftanol, Amaze) 25311-71-1

1.10E+03

Isopropalin (Paarlan) 33820-53-0

5.0 GW-S

4.20E+05

H(*)

Isoxaben (Gallery; Snapshot) 82558-50-7; C

1.63E+04

Lactofen (Cobra) 77501-63-4; B2

1.5L

4.39E+05

Linuron (Lorox) 330-55-2; C

0.625 L

2.4/0.8

1.54E+02

17,003

Londax (Bensulfuron-methyl) 83055-99-6

19.9N

1.6E+01

Malathion 121-75-5; D

7.0 GW-S

nd-17

218.4) 70.4

7.76E+02

+/+

Maleic hydrazide 123-33-1; E

0E+00

PGR

Maneb (Bravo) (ETU is metab.) 12427-38-2; B2

1.8 GW-S

0.5

MCPA (Weedone) 94-74-6

0.15N

0.0005E;

1.18E+02

866,000 for salt; 5 for ester

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-48

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey MCPB 12N 0.01E; H 2,944 _ 94-81-5 - MCPP 0.001E: 3.2E+01 H 1,980 -/+ (Mecoprop) - 1929-86-8 Mepiquat chloride 25N 0.03 E; PGR 24307-26-4; E - Mecarbam 0.002 1.9E+01 ? 2595-54-2 WHO; Merphos 0.1N 0.00003E; 0.1/<0.1 0.0023 @ D (DEF; Folex; - 20°C Tribufos) 78-48-8; C Metalaxyl 6.25N 0.06E; 2E+00 8400 F 8,932 -/+ 5$7837-19-1; E - Metaldehyde 23 240 MO 108-62-3 Metam-sodium 1.98E-1; SF, (- 137-42-8; B2 - F,I, N,H Methamidophos 0.05 L 0.00005E; 19.9, 0E+00 I 16,336 (- (Monitor) - 16.7 10265-92-6; E Methidathion 0.1N 0.001E; - 0.8/0.2 1.00E+02 240 LA 950-37-8; C - Methiocarb 0.005 <0.1/1.4 2.84E+03 LA, -l- (Mesurol) OPP; M, 2032-65-7; D - BR Methomyl 2.5N 0.025E; 0.35 25 12.3/3.7 2E+00 5800 or 160 I 54,911 SK (Lamate) - GW-S 58000 16752-77-5 (sum with aldicarb) NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-49

name/CAS/cancer

NOAEL, LOAEL

cancer potency

drinking water

TLV

AGC

nopes

usfda

Kow

water solubility

Koc

type use

mean use

water survey

Methoprene (Altosid) 40596-69-8

2.42E+04

1.39

IGR

Methoxychlor 72-43-5; D

5.01N

35 SW-S + GW-S; 40 MCL

0.9/0.3

2.00E+04

0.1

1,140

Methyl bromide 74-83-9; D

5 (skin)

1E+00

SF, FM

112,047

Methyl isothiocyanate (MITC; Trapex; Vorlex)

556-61-6

(*)

Methyl parathion (Penn-Cap M) 298-00-0

0.025 N

0.00025E;

1.5 GW-S (sum with parathion)

0.2 (skin)

0.1/<0.1

8.1E+01

28,018

Methylene bromide (Dibromomethane) 74-95-3

5.0 MCL

2.40E+03

Metiram (ETU is metab.) 9006-42-2

0.0003 OPP;

~ insol.

we o te ay &

Metobromuron 3060-89-7

<0.1 <0.1

Metolachlor (Dual; Pennant) 51218-45-2; C

3.8E+01

1,199,364

+/+

Metribuzin (Sencor) 21087-64-9; D

25N

50 SWGV+ GW-S

1.6E+01

1200 @ 20°C

+/+

Metsulfuron-methyl (Ally) 74223-64-6

8.0E+01

Mevinphos (Phosdrin) 7786-34-7

0.00025 OPP;

0.092 (skin)

7.8/3.0

Miscible

1.0

1,194

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-50

name/CAS/cancer NOAEL RED, cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey

Molinate 02N 0.002E; LIE-1; 2.2E+01 800 at 50 H + (Ordram) - - 21°C 2212-67-1; C(q)

Monocrotophos 0.00005 0.25 <0.1/0.1 LA (Azodrin) OPP; (skin) 6923-22-4 -

MSMA 0.01 H (Monosodium OPP;

methanearsonate) - 2163-80-6

Myclobutanil 2.49 N 0.025 1.60E+02 F 12,444 (Systhane; Rally) opp; 88671-89-0; E -

NAA 0.05 PGR 679 (1-Naphthaleneacetic opp; acid; alpha- - naphthylacetic acid) 86-87-3

Nabam 1.8 GW-S F 142-59-6

NAD PGR 416 (Naphthaleneacetamide) 86-86-2

Naled 0.2N 0.002E; 3 (skin) 2.4E+01 ~ insol. 180 I 436 - (Dibrom) - 300-76-5; E

Naphthalene 10 SW-S + 2.46E+03 F - 91-20-3 GW-GV

Napropramide 30N 0.1E; 3.24E+02 73 @20°C H 14,906 - 15299-99-7 -

Naptalam 0.053 H 4,656 (Alanap-1) OPP; 132-66-1; D -

Neburon <0.1/<0. H - 555-37-3 1

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-51

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Nitralin 0.03E; 35 GW-S 6.01E+04 H(*) (Planavin) - 4726-14-1 Nitrapyrin 10 2.59E+03 NI 1929-82-4; D Nitrofen 3.45E+04 H 1836-75-5; 2B-IARC 4-Nitrophenol 1.0 (sum Inert “i 100-02-7 phenols) ingred SW-S + GW-S Norflurazon 3.75N 0.04E; 9.31E+02 H 6,715 “| 27314-13-2; C - Oils I 1,304,034 Omethoate 0.0003 4.8/5.3 miscible LA (Folimat) WHO; 1113-02-6 - Oryzalin SN 0.05E; 1.3E-1; 1.28E+04 2.5 600 H 266 + (Surflan) - - 19044-88-3: C(q) Oxadiazon 0.5N 0.005E: 1.4E-1; 1.23E+04 H 19666-30-9; C(q) - - Oxamyl 2.5N 0.025E: 50 GW-S 0.1/0.2 0E+00 280,000 44 I 13,738 HK (Vydate) - 23135-22-0 Oxydemeton-methy! 0.0005 I 327 - (Metasystox R) OPP; 301-12-2 - Oxyfluorfen 0.3N 0.003E: 1.28E-1; 4.20E+05 0.1 100,000 H 1,004 (Goal) - - 42874-03-3: C(q) Oxytetracyeline 0.005 F 530 (Terramycin) OPP; 79-57-2: D - NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-52

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Oxythioquinox 0.006 3.42E-2 I 4,195 (Morestan) OPP; 2439-01-2; B2 - Paclobutrazol 12.5N 0.013E; 7.31E+02 PGR 76738-62-0; D - Paraquat 0.45N 0.0045E; 3.0 GW-S 0.5 0.24 0E+00 very 15,473 to H 29,413 (- (Cyclone; Gramoxone) -- (dust), soluble 51,856 4685-14-7; E 0.1 respirable fraction Parathion 0.00033 1.5 GW-S 0.1 0.12 3.7/1.1 6.46E+03 12.4 I -l- (Ethyl parathion) OPP: (sum with | (skin) 56-38-2: C - methyl parathion) PCNB 0.75 N 0.003E: ND GW-S 0.5 2.5/0.8 1.51E+04 0.44 F 1,036 (Pentachloronitro- - benzene; Quintozene) 82-68-8; C Pebulate 0.007 4.07E+02 H + (Tillam) OPP; 1114-71-2 - Pendimethalin 12.5N 0.04E; 5.0 GW-S 1.27E+05 0.275 24,300 H 61,818 + (Prowl: Squadron) - 40487-42-1; C Pentachlorophenol 3.0N 0.03E; 1.29E-1; 1.0 SW-S 0.5 1.4/0.8 1.32E+05 20 @ 30°C 3 to 4000 I, WP -/+ (PCP; Penta) - - +GW-S (skin) 608-93-5; B2 (sum of phenols); 1.0 MCL Permethrin SN OSE; 1.84E-2; 12 nd-1.5 34.8) 3.02E+03 02@ 86,000 I -l- (Pounce; Ambush; - - 28.3 20°C Torpedo; Outflank) 52645-53-1; C(q) Perthane 0.7/0.4 I (Ethylan) 72-56-0 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-53

name/CAS/cancer NOAEL RED, cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Phenmedipham 25N 0.25E; 1.6E+01 H 637 (Betanal) - 13684-63-4; D d-Phenothrin 0.071 1.63E+04 Miscible I (Sumithrin) OPP: 26046-85-5 - Phenthoate 0.003 2.56E+03 LA 2597-03-7 OPP; Phenylmercuric 4E+00 H,F, acetate (PMA) I 62-38-4 (bann edin NYS) o-Phenylphenol 0.02 27-80 2.29E+03 F(*) (2-biphenylol; 2- WHO; hydroxybiphenyl; - Dowicide 1) 90-43-7; B2/2B-IARC Phorate 0.66 0.0005 ND GW-S 0.05 0.1/0.1 5.01E+04 50 I 29,879 “| (Thimet) OPP: (skin) 298-02-2; E - Phosalone 0.0025 4.2/0.7 2.01E+04 AI l- (Zolone) OPP: 2310-17-0 - Phosmet 2N 0.02E; 8.1/2.0 6.76E+02 20 I 37,168 (Imidan) - 732-11-6; C Phosphamidon 0.0002 3.9/0.7 2.2E+01 I 13171-21-6; C OPP; Phosphine 0.026 N 0.0004E; 0.42 I, FM (Aluminum 0.0003E. phosphide) 20859-73-8; D

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-54

name/CAS/cancer

NOAEL,

cancer drinking potency water

TLV

Kow

water solubility

mean use

Phoxim (Baythion; Volaton) 14816-18-3

4.19E+03

Picloram (Tordon) 1918-02-1; E

50 SWGV+ GW-S

2E+00

430 (salt 200,000)

Pindone (Pivalyn) 83-26-1

0.1

Pinnacle (Harmony; Thifensulfuronmethyl) 79277-27-3

0.013E;

Piperazine dihydrochloride 142-64-3

Piperonyl butoxide 51-03-6;C

Pirimicarb (Rapid) 23103-98-2

7E+00

Pirimiphos-methyl 29232-93-7

2.53E+02

Primisulfuron-methyl (Beacon) 86209-51-0; D

70 @ 20°C

Prochloraz (Prelude; Omega; Mirage) 67747-09-5; C(q)

0.009E;

5.44E+03

Profenofos

(Curacron) 41198-08-7; E

0.00005 OPP;

9.31E+02

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-55

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Profluralin 4.20E+05 H (Tolban) 26399-36-0 Prometon 15N 0.015E; 50 SW- 2.8E+01 H +/+ (Pramitol) - GV+ 1610-18-0; D GW-S Prometryn 3.75N 0.004E; 7.T9E+02 48 @ 20°C 500 H 454 7287-19-6; E - Pronamide 7.5N 0.075E; 1.54E-2; 1.83E+03 15 218 H 2,326 + (Kerb; Propyzamide) - - 23950-58-5; B2 Propachlor 13.3N 0.013E; 35 GW-S 5.60E+02 H 5,715 -l- (Ramrod) - 1918-16-7 Propamocarb 0.1 0E+00 F hydrochloride OPP: (Banol; Prevex) - 25606-41-1; D Propanil SN 0.005E; 7.0 GW-S 9.7E+01 225 188 H + (Stampede) - 709-98-8 Propargite 22.5N 0.02E; 1.71E-2; 221.1 7.33E+04 I 70,829 + (Omite) - - 8. 2312-35-8; B2 Propazine SN 0.02E; 4 45E-2 16 GW-S 7.85E+02 8.6@ H 139-40-2: C(q) -- 20°C Propetamphos 0.005 110 I 31218-83-4 OPP; Propham SON 0.02E; 50 SW- 8.7E+01 H, + 122-42-9 - GV+ PGR GW-S Propiconazole 1.25N 0.013E; F 3,348 (Tilt; Orbit; Alamo; - Banner) 60207-90-1; C NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-56

name/CAS/cancer

NOAEL, LOAEL

cancer potency

drinking water

TLV

AGC nopes

usfda

Kow

water solubility

Koc

type use

mean use

water survey

Propoxur (Baygon) 114-26-1; B2

0.36 L

3.69E-3;

0.5

11-316

1E+00

-/+

Pyrazon (Chloridazon, Pyramin) 1698-60-8

2,719

Pyrethrins (Pyrethrum) 8003-34-7

0.064 OPP;

insol

Quinalphos 13593-03-8

0.05 N

0.0005E;

1.21E+03

LA

Quinoline (Oxyquinoline citrate)

1.1E+01

Pr

Quizalofop-p-ethyl (Assure) 100646-51-3; D

0.9N

1.27E+05

04@ 20°C

Resmethrin 10453-86-8

nd-0.4

<1@ 20°C

Ronnel (Fenchlorphos) 299-84-3

nd-0.1

<0.1 <0.1*

3.45E+04

Rotenone (Noxfish; Pro-noxfish) 83-79-4; E

0.38N

1.83E+03

0.02 @ 20°C

Ryania 15662-33-6

Savey (Hexythiazox) 78587-05-0

2.5N

0.025E;

4.96E+02

Sesone 136-78-7

0E+00

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-57

name/CAS/cancer NOAEL RED, cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey

Sethoxydim 8.86N 0.09E; 6.45E+03 4700 50 H 291 74051-80-2 -

Siduron H 475 1982-49-6

Silvex 0.75 N 0.008E; 10 MCL 9.1E+01 H(*) -l- (2,4,5-TP) - 93-72-1; D

Simazine 0.52N 0.005E; 1.2E-1; 0.5 SW-S 1.66E+02 | 5@22°C 138 H 88,913 40/4 (Princap; Princep; - - + GW-S; Caliber 90; Aquazine) 4.0 MCL 122-34-9; C(q)

Sodium chlorate H,D 77175-09-9

Sodium fluoracetate 0.05 N 0.00002E; 0.05 PC

(Compound 1080) - (*) 62-74-8

Streptomycin 0.05 F 1,879 57-92-1 opp;

Strychnine 25L 0.0003E; 0.15 8.5E+01 R 57-24-9 -

Sulfallate 2.34E+02 H (Vegedex) 95-06-7; 2B-IARC

Sulfometuron-methyl 5 0.84 244 H (Oust) 74222-97-2

Sulfotepp 0.000SE; 02 117 Al (TEDP; Bladafum; - (skin) 41* Thiotepp) 3689-24-5

Sulfur 36.8/5.3 F 501,071 7704-34-9

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-58

name/CAS/cancer

NOAEL, LOAEL

cancer potency

drinking water

TLV

AGC

nopes

usfda

Kow

water solubility

Koc

type use

mean use

water survey

Sulfuryl fluoride (Vikane) 2699-79-8

100,000 @ 9°C

Sulprofos (Bolstar; Merafos) 35400-43-2; E

1.08E+05

2,4,5-T 93-76-5

3.0N

35 GW-S

0.3/0.2

4E+00

H(*)

TCPA (tetrachloro terephthalic acid) (metab. of DCPA)

50 GW-S

Metab of DCPA

Tebuthiuron (Spike) 34104-18-1; D

7N

0.07E;

50 SWGV+ GW-S

6.2E+01

Tecnazene (Fusarex; TCNB) 117-18-0

0.01 WHO;

0.2/0.1

PGR

Temephos 3383-96-8

0.3

0.0005 OPP;

0.03

TEPP. 107-49-3

0.047

Terbacil 5902-51-2; E

1.25N

0.013E;

50 GW-S

2.8E+01

6,987

Terbufos

(Counter) 13071-79-9; E

0.00005 OPP;

0.09 SWGV+ GW-GV

<0.1 0.1*

6.03E+03

IN

86,400

Terbutryn 886-50-0; C

0.1N

0.001E;

1.21E+03

Tetrachloroethylene 127-18-4

0.7 SWGV; 5.0 GW-S

FM )

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-59

name/CAS/cancer NOAEL RED, cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey

Tetrachlorvinphos 3.13N 0.03E; 1.83E-3; 0.1/<0.1 2.56E+03 I

(Gardona) - -

22248-79-9: C(q)

Tetradifon 0.1/<0.1 0.08 A

(Tedion)

116-29-0

Tetramethrin I

7696-12-0; C

Thallium sulfate 0.25 N 0.00008E; R

7446-18-6; D -

Thiabendazole 0.1 668.5, 4.96E+02 50

148-79-8 OPP; 151

Thiobencarb 1.0N 0.01E; 8.64E+02 H +

(Saturn; Bolero) -

28249-77-6; D

Thiodicarb 0.03 7.31E+02 I 32,587

(Larvin) OPP:

59669-26-0; B2 -

Thiofanox 0.0003 3E+00 I

(Decamox) OPP: (soil)

39196-18-4 -

Thiophanate-methyl 8N 0.08E; F 20,096

23564-05-8 -

Thiram SN 0.005E; 1.8 GW-S 1.0 24 8.64E+02 30 383 F 3,685

(ETU is metab.) -

137-26-8

Tralomethrin 0.75 N 0.0075E; 3.44E+02 I

66841-25-6 -

Triadimefon 2.5N 0.03 E; 5.89E+02 F 4,786

(Bayleton) -

43121-43-3; C

Triallate 1.275N 0.013E; 8.32E-2; <0.1 7.68E+03 4 2220 H +

(Far-Go) - - <0.1

2303-17-5; C

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-60

name/CAS/cancer NOAEL RD cancer drinking TLV AGC nopes usfda Kow water Koc type mean water

LOAEL RFC potency water solubility use use survey Triasulfuron 12N 0.01E; H (Amber; Logran) - 82097-50-5; E Triazophos 0.001 6.50E+02 IM, [- (Hostathion) WHO; N 24017-47-8 -- Tributyltin oxide 0.025 N 0.00003E; 50 SW- 10 5500 1 1000 to MO +in (TBTO) - GV+ 8000 Great 56-35-9 GW-GV Lakes Trichlorfon 0.002 3E+00 120,000 2 I (Dipterex; Dylox; OPP; Pronto) - (DDVP is metab.) 52-68-6; E 1,2,3- 5.0 GW-S; 0.2/<0.1 Trichlorobenzene 5.0 MCL 1,2,4- 14.8N 0.01E; 5.0 GW-S; 1.50E+04 H Trichlorobenzene - 5.0 MCL 120-82-1; D 1,1,2-Trichloroethane 3.9N 0.004E; 5.7E-2; 1.0 SW-S 2.95E+02 FM 79-00-5; C - 1.6E-5 + GW-S; (*)

5.0 MCL Trichlorophenol 1.1E-2; 1.0 SW-S 5.25E+03 F,B (Dowicide) 3.1E-6 +GW-S (2,4,5-); (*) 25167-82-2; B2 (sum of 4.90E+03 phenols) (2,4,6-) Triclopyr 25 0.05 23 (ester); H - 55335-06-3; D OPP; 2,100,000 - (salt) Tridiphane 0.33 N 0.003E; H (Tandem) - 58138-08-2; C Trifluralin 0.75 N 0.075E; 7.TE-3: 35 GW-S 0.1 2.14E+05 24 @27°C 7000 H 41,246 -l- (Treflan) - - 1582-09-8: C(q) NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-61

name/CAS/cancer NOAEL RED, cancer drinking TLV AGC nopes usfda Kow water Koc type mean water LOAEL RFC potency water solubility use use survey Triforine 0.025 8.64E+02 F 698 (Funginox) OPP: 26644-46-2 - Triphenyl phosphate 50 SW- 34.8 115-86-6 GV+ 18.4 GW-GV Triphenyltin hydroxide 0.0003 2.8E-0; 3.62E+03 F (Fentin hydroxide) OPP: - 76-87-9; B2 - Vamidothion 0.008 4E+00 A,M (Kilval) WHO; 2275-23-2 - Vernolate 1.0N 0.001E; 2.15E+02 H (Vernam; Surpass) - 1929-77-7 Vinclozolin 2.5N 0.025E; 11.0/3.5 1.9E+01 34 F 10,655 (Ronilan) - 50471-44-8; C Warfarin 0.029 L 0.0003E; 0.1 1.60E+03 R 81-81-2 - Zinc phosphide 3.48L 0.0003E; 0.3 0.95 ~ insol. R 1314-84-7; D - Zineb (Cumene) 25L 0.05E; 1.8 GW-S 246 2.84E+03 10 F [- (ETU is metab.) - (skin) 12122-67-7; 3-IARC Ziram 0.02 4.2 GW-S 3.73E+02 65 F 43,414 137-30-4 WHO;

° Cancer classifications are: 1= Carcinogenic to humans; B1, B2 or 2A = Probable human carcinogen; 2B, C or C(q) = Possible human carcinogen; D or 3 = Not classifiable; E = Evidence of noncarcinogenicity for humans.

' Source: U. S. Environmental Protection Agency IRIS database, the USEPA Office of Pesticide Programs List of Chemicals Evaluated for Carcinogenic Potential dated June 10, 1998, the Office of Pesticides Programs Reference Dose Tracking Report dated February 19, 1997. NOAEL/LOAEL = No observed adverse effect level/Lowest observed adverse effect level; RfD = Reference dose, E = from IRIS data for RfD values, OPP = Office of Pesticides Programs proposed RfD, WHO = World Health Organization RfD cited in the Reference Dose Tracking Report.

* Sources: Water quality standards are from Title 6 of the New York Codes, Rules and Regulations (Environmental Conservation Law), Chapter X, Parts 700-

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-62

706; water quality guidance values are from NYSDEC (1998) Division of Water Technical and Operational Guidance Series (1.1.1) Ambient Water Quality Standards and Guidance Values and Groundwater Effluent Limitations; maximum concentration limits (MCL) in potable water are from Part 5, Subpart 5-1 of Public Health Law. SW = surface water standard; GW = groundwater; S = standard; GV = guidance value. For each compound without an assigned MCL, the MCL of 50 ug/l is assigned by Part 5 to unspecified organic compounds (UOCs), and the total concentration of all unspecified organic contaminants plus several principal organic contaminants shall not exceed 100 g/l.

* Source: American Conference of Governmental Industrial Hygienists (ACGIH) (1996). 1996 TLVs and BEIs. Threshold limit values for chemical substances and physical agents; Biological exposure indices.

* NYSDEC (1991) Draft New York State Air Guide - 1, Guidelines for the control of toxic ambient air contaminants. Division of Air Resources, New York State Department of Environmental Conservation, Albany, NY. 20 p. + appendices.

> Source: Immerman, F. W., and J. L. Schaum (1990) Final report of the nonoccupational pesticide exposure study (NOPES). EPA/600/3-90/003. U. S. Environmental Protection Agency, Research Triangle Park, NC.

° Sources: Gunderson, E. L. (1995) FDA Total Diet Study, July 1986-April 1991, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc. Off. Analyt. Chem. Intl. 78(6):1353-1363. Where values are followed by an asterisk (*), the data sources are: Gartrell et al. (1986) Pesticides, selected elements, and other chemicals in infant and toddler total diet samples, October 1980-March 1982. J. Assoc. Off. Anal. Chem. 69(1):123-145; or, Gunderson, E. L. (1988) FDA Total Diet Study, April 1982-April 1984, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc. Off. Anal. Chem. 71(6):1200-1209. Dietary intakes are for 2-year old children/25 - 30 year old adults; for adults, the greastest value (which in most cases was for women) was used.

7 New York State Department of Health, Bureau of Toxic Substances Assessment (1997) Compilation of octanol-water partition coefficients (draft). 11 p.

* Source: Meister Publishing Company, Inc. (1994) Farm Chemicals Handbook ‘94. Meister Publishing Company, Inc., Willoughby, OH.; Seyler, L. A., J. W. Allan, D. A. Rutz, and M. A. Kamrin. 1994. EXTOXNET Pesticide Information Notebook. Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and the University of California at Davis.

° Chemical used as: A = Acaracide;

B = Bactericide; BR = Bird repellant;

D = Defoliant; F = Fungicide;

FM = Fumigant; H = Herbicide;

I= Insecticide; IGR = Insect growth regulator; IR = Insect repellant; M = Miticide;

Mo = Molluscicide N= Nematocide;

NI = Nitrification inhibitor; P = Piscicide;

PC = Predator control; PGR = Plant growth regulator; Pr = Preservative; PS = Pesticide solvent;

SF = Soil fumigant; T = Termiticide;

R = Rodenticide; WP = Wood preservative; and

(*) = discontinued pesticide. ' Source: Gianessi, L. P., and J. E. Anderson (1995) Pesticide use in New York crop production. National Center for Food and Agricultural Policy, Washington, DC. Reported as pounds active ingredient per year. " Sources: See table titled “Concentrations of pesticides detected in surface water or groundwater of New York State” for data sources. In addition, Seyler eg al. (1994), as provided in footnote 8, was the source for diazinon and tributlytin oxide information in the Great Lakes. - = Measured but not detected; + = Detected; © = Maximum concentration is greater than the New York State surface water or groundwater standards or guidance values, as appropriate, or greater than the federal Safe Drinking Water Act MCL.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-63

Appendix A, Table I.2: Selection of pesticides of concern in New York State Criteria:

1. Chemical has been reported as present in surface water or groundwater of New York State during 1994 to 1997 (USGS NAWQA survey of the Hudson River drainage basin; Suffolk County groundwater assessment; NYSDOH municipal drinking water assessments); or

Chemical has been reported as present in air of homes during 1985 to 1988 (NOPES study); or

Chemical has been reported as present in human food (USFDA market basket survey for 1982 to 1984); and

2. Chemical was reported as being used in New York State since 1990 (National Center for Food and Agriculture Policy; The Chemical Specialties Manufacturers Association).

The pesticides selected for further evaluation and their classification by the European Union, the U. S. Environmental Protection Agency, or other agencies, are noted below.

European Union classifications USEPA Classification

Pesticide Toxicity! Carcinogenicity” Potency? Carcinogenicity” Acephate Xn - Vh Cc Alachlor Xn, R40,R43. 3 H B2* Aldicarb T+ - Vh D* Atrazine Xn, Xi, R40, 3, Mu H C(q)*;

R43 2B, IARC Azinphos-methyl T+ - E* Bendiocarb T - Benefin - - M Bromophos Xn - Captan Xn, Xi, R40, 3 M B2*

R43 Carbaryl Xn - M C(q)* Carbofuran T+ - H Carbophenthion T, R24 - Chloramben - - M Chlorobenzilate Xn - M 3, IARC Chlorothalonil Xn, R40 3 H B2*

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-64

Chlorpropham -

Chlorpyrifos T Chlorpyrifos-methyl - Copper sulfate Xn, Xi Cupric hydroxide - Cyanazine Xn 2, 4-D Xn, Xi DCNA (Dichloran) - DCPA (Dacthal) - DDVP (Dichlorvos) T, R24 Diazinon Xn Dicamba - p-Dichlorobenzene Xn, Xi 1,2-Dichloropropane Xn Dicofol Xn, Xi, R43 Dimethoate Xn Dinoseb T, Xi, R2, R3, R24 Diphenylamine T, R33 Disulfoton T+, R27 Diuron Xn Endosulfan T, Xi, R24 EPN T+, R27 EPTC Xn Ethion T Ethoprop T+, R27 Ethylene dibromide T, Xi, R23, R24 Fenitrothion Xn Fenuron Xi Fenvalerate - Folpet Xn, Xi, R40, R43 Fonofos T+, R27 Glyphosate - Iprodione - Linuron Xn, R40 Malathion Xn

Vh

Vh

came?

Vh

mre <

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

E* E*

D* D*

C(q)* D*

C(q)* B2

D* c* c*

c* c*

E*

E*

E*

2B, IARC E*

E* B2

E* E* B2* Cc D*

Page A-65

MCPP - -

Merphos (Tribufos) - - Vh

Methamidophos T+, Xi, R24 - Vh

Methidathion T+ - Vh

Methiocarb T -

Methomyl T+ - H

Methoxychlor - - M

Methyl bromide T, Xi -

Methyl! parathion T+, R24 - Vh

Metobromuron - -

Metolachlor - - M

Metribuzin Xn - H

Mevinphos T+, R27 -

Molinate Xn - Vh

Monocrotophos T+ -

MSMA - -

Naphthalene - -

Neburon - -

N,N-diethyl-meta-toluamide = Xn, Xi -

Omethoate T -

Oxamyl T+, R26 - H

Parathion T+, R27 -

PCNB Xi, R26 - H

Pendimethalin Xn - M

Pentachlorophenol T+, Xi, R24, 3 H R26, R40

Permethrin Xn, R27 - M

Perthane - -

Petroleum distillates/oils

o-Phenylphenol Xi -

Phorate T+ -

Phosalone T -

Phosmet Xn -

Phosphamidon T+, R24,R40 = -, Mu

Picloram - - M

Pirimiphos-methyl Xn - Vh

Profenofos Xn -

Prometon - - M

Pronamide - - M

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

C(q)* E*

D*

c* D*

c(q)*

D*

ce ce B2

c(q)*

E*

c* c* E*

E* D* B2*

Page A-66

Propargite Xn, Xi - M B2*

Propoxur T - B2* Resmethrin Xn - M

Ronnel Xn -

Simazine Xn, R40 3 H C(q)* Sodium chlorate Xn -

Sulfotep T+, R27 -

Sulfur - -

2,4,5-T Xn, Xi - H

Tebuthiuron Xn - M D* Tecnazene Xi, R43 -

Terbacil - - H E* Terbufos T+, R27 - E* Tetrachlorvinphos - - H C(q)* Tetradifon - -

Thiabendazole - -

Triallate Xn - H ct Tributyltin oxide - - Vh 1,2,3-Trichlorobenzene - -

Triphenyl phosphate - -

Vinclozolin - - H E*

' Toxicity codes are: T+ = Highly toxic; T = Toxic; Xn = Harmful; Xi = Irritant; R2 = May cause damage to unborn child; R3 = May impair fertility; R23 = Toxic by inhalation; R24 = Toxic in contact with skin; R26 = Very toxic by inhalation; R27 = Very toxic in contact with skin; R40 = Possible risk of irreversible effects; R43 = May cause sensitization by skin contact; - = Not reported or determined by the European Union.

? Carcinogenicity codes are: 2 or B2 or 2B = Probable human carcinogen; 3 or C or C(q) = Possible human carcinogen; D = Not classifiable as to human carcinogenicity; E = Evidence of noncarcinogenicity for humans; Mu = Mutagenic; - = Not reported or determined by the European Union; * = Proposed classification which lacks full agency concurrence.

> Based on USEPA oral NOAEL (preferred) or LOAEL values applied to potency categories as follows: Vh = very high potency (<0.5 mg/kg/d); H = high potency (<5.0 mg/kg/d); M = moderate potency (<50 mg/kg/d); L = low potency (>50 mg/kg/d).

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-67

Appendix A, Table I.3: Pesticide residues in surface and ground waters of New York State.

Concentration in water (ug/l)

Hud Ri basi Mohawk Af Son Ver 19949! River basin Suffolk Upstate LILCO Pesticide surface water ( ) surface County - New York . homeowner water 10 Wells wells well (1997); Median of (1994- (1996)°; (1997)*; Maximum ’ Maximum 1995)’; Maximum | Maximum detects . Maximum Alachlor* 0.013 0.022 0.021 Aldicarb 8.9 (1.0 average) Atrazine* 0.015 0.38 43 11 Carbaryl 0.044 1.6 0.86 Carbofuran 0.021 0.021 nd 1.6 Chlorpyrifos 0.01 0.01 Cyanazine 0.030 0.2 21 >3.0 2,4-D 1.25 DCPA (Dacthal) 0.01 0.011 499 (62 average)" Diazinon 0.008 0.056 0.55 EPTC 0.004 Malathion 0.1 0.1 Metolachlor 0.012 0.16 1.3 2.0 Metribuzin 0.033 Molinate 0.016 Pendimethalin 0.035 Prometon 0.023 0.024 0.071 Pronamide 0.052 0.052 Simazine 0.013 0.55 0.018 34 Tebuthiuron 0.01 Terbacil 0.023

* Excludes metabolite concentration. + Initially incorrectly identified. Reported here as originally reported by authors. Later correctly identified as the DCPA metabolite tetrachloroterephthalic acid (TCPA).

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Page A-68

' USGS. 1997a. Pesticides in surface waters of the Hudson River basin, New York and adjacent states. Fact Sheet FS 238-96. U.S. Geological Survey, Troy, NY. 4p.

? USGS. 1997b. Pesticides in surface waters of the Hudson River basin - Mohawk River Subbasin. Fact Sheet FS 237-96. U.S. Geological Survey, Troy, NY. 4 p.

> Trent, M., and S. F. Robbins. 1996. Nitrate and pesticide impacts of agriculture on groundwater quality Suffolk County, NY. Bureau of Groundwater Resources, Suffolk County Department of Health Services, Hauppage, NY. 19 p.

* Entringer, R. A. 1997. Memoranda to District Staff, Field Coordinators dated September 3, 1997 and October 22, 1997.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-69

Appendix A, Table I-4: Pesticide residues in groundwater of Long Island, New York.!

Pesticides and Maximum Concentrations Detected Nassau County Suffolk County NYS Result Max. ground MCL Max. Pesticide Cone. Pesticide water ans Cone. (ugil) standara | “8/) (ugil) (ug!) Greater than TCPA (1) 89.0 alachlor (2)? 0.5 2.0 6.66 MCL* aldicarb sulfoxide & sulfone (47) 0.35 7.0 41.0 bis(2-ethylhexyl) phthalate (2) 5.0 6.0 14.0 1,2-dichloropropane (4) 1.0 5.0 11.0 EDB (20) 6E-4 0.05 778 simazine (3) 0.5 40 12.3 TCPA (29) 50 50.0 766.0 1,2,3-trichloropropane (1) 0.04 5.0 6.0 Greater than arsenic (6) 30.9 alachlor (2) 0.5 2.0 0.28 MDL but less atrazine (3) 0.2 aldicarb sulfoxide & sulfone (74) 0.35 7.0 6.9 than MCL* cadmium (9) 11.2 arsenic (10) 25.0 50.0 11.0 2,4-D (1) 0.97 | atrazine (5) 15 3.0 0.77 dieldrin (1) 0.78 | bis(2-ethylhexyl) phthalate (5) 5.0 6.0 3.9 dinoseb (1) 0.59 | carbofuran (3) 15.0 40.0 47 prometon (1) 0.2 2,4-D (6) 50.0 50.0 1.08 simazine (1) 0.4 1,2-dichloroethane (4) 0.6 5.0 1.0 TCPA (2) 33.0 1,2-dichloropropane (31) 1.0 5.0 40 1,3-dichloropropane (1) 5.0 5.0 1.0 dinoseb (5) - 7.0 2.61 EDB (1) 6E-4 0.05 0.03 endosulfan sulfate (1) - 50.0 1.99 MCPP (1) - 50.0 1.8 metalaxyl (7) - 50.0 1.2 methomyl (1) 0.35 50.0 1.7 metolachlor (19) - 50.0 11.4 metribuzin (2) 50.0 50.0 0.21 4-nitrophenol (4) 1.0 50.0 241 oxamyl (8) 50.0 50.0 11.0 prometon (2) 50.0 50.0 3.8 simazine (7) 0.5 40 3.0 TCPA (18) 50 50.0 33.0 1,2,3-trichloropropane (10) 0.04 5.0 40 Unquantified DEET (1) bromacil (1) positives dicamba (1) butachlor (1) dichloroprop (1) chlorobenzilate (1) oxamyl (1) diazinon (1) pentachlorophenol (1) dichloroprop (2) propoxur (1) pentachlorophenol (5) propoxur (2)

' Adapted from: Suffolk County Department of Health Services (1998)

? Parenthetic values are number of wells containing the indicated pesticide in the sampling period from October 1997 through March 1998. A total of 898 wells were sampled.

> MCL = Maximum Contaminant Level established by the Safe Drinking Water Act.

* All pesticides with residue concentrations in excess of the MCL also exceed NYS groundwater standards; indeed, the groundwater standards are more stringent than the MCL in each case. In addition, the maximum concentrations of 1,2dichloroethane and methomyl exceed NYS groundwater standards.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-70

Appendix A, Table J.1: Stressor selection, petroleum products

potency/toxicity exposure ACGIH | Air Guide 1 TSCA NYSDEC | NYSDEC Farm TLV AGC CUS Oil Oil Chemicals mg/m3 ug/m3 production spills spills Handbook Ibs/1990 gal 95-96 # 95-96 1997 asphalt (petroleum) 8052-42-4 5 4.95E+08 #2 fuel oils diesel fuel 68334-30-5 1.20E+05 1205 X (present) #2 fuel oils fuel oil #2 68476-30-2 2.23E+08 | 4.20E+06 5369 Xx fuel oil #4 68476-31-3 1.30E+04 239 fuel oil #6 68553-00-4 2.50E+05 369 X | gasoline range gasoline 8006-61-9 890 1.00E+05 1751 gasoline range naphtha (benzin) 8030-30-6 1590 4.38E+07 xX | gasoline range naphtha (heavy aromatic) 64742-94-5 0.1 | gasoline range naphtha (light) 64742-95-4 0.1 | gasoline range petroleum naphtha (heavy catalytic cracked) 64741-54-4 3.60E+08 | gasoline range petroleum naphtha (full-range reformed) 68919-37-9 5.50E+08 gasoline range petroleum naphtha (light catalytic cracked) 64741-55-5 3.60E+08 Ligroine (VM&P naphtha) 8032-32-4 1370 33000 kerosene range jet fuel (JP-5) kerosene is major constituent 8008-20-6 1.20E+04 118 kerosene range kerosene 8008-20-6 2400 1.59E+08 _| 1.40E+04 265 stoddard solvent (mineral spirits) 8052-41-3 525 1.69E+05 X petroleum (crude oil) 8002-05-9 0.1* lubricating base stocks | petroleum distillates (hydrotreated light) 64742-47-8 9.70E+08 lubricating base stocks | petroleum distillates (solvent refined light 64741-89-5 Xx paraffinic) lubricating base stocks | petroleum distillates (solvent refined heavy 64741-88-4 Xx paraffinic) petroleum residues (light vacuum) 68512-62-9 4.90E+08 waste oil (used mineral-based crankcase oil) 1.00E+04 942 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-71

Appendix A, Table J.2: Stressor data for petroleum products

potency/toxicity exposure Chemical CAS name number NYS NYSDEC | NYSDEC EU IARC LOEL LDS50 health health | TSCA CUS Oil Oil average maximum class class or effect effect production spills spills environ. environ. (2) (1) LC50 assoc greatest Ibs/1990 | gal 95-96 | #95-96 | concent concent. LOEL concern @Q) (4) (4) asphalt (petroleum) 8052-42-4 none skin skin cancer 4.95E+08 (none mouse. tumors (1) Teq.)** 905,000 (1) mg/kg/d (1) diesel fuel 68334-30-5 harmful 3 inhal rat oral rat decreased cancer 1.20E+05 1205 carc-3 250 mg/m3 9,000 body (2, 6) (6) mg/kg (1) _| weight (6) fuel oil #2 68476-30-2 harmful 3 inhal mice ataxia cancer 2.23E+08 | 4.20E+06 5369 1232 ug/L carc-3 65 mg/m3 (6) (2) groundwater (6) near spill (6) >10 ug/m3 indoor air near spill (10) fuel oil #4 1.30E+04 239 fuel oil #6 68553-00-4 toxic 2B 2.50E+05 369 care-2 | gasoline 8006-61-9 toxic 2B inhal rat inhal rat kidne cancer 1.00E+05 1751 3 to 25 mg/m3 carc-2 44 mg/m3 300,000 effects (7) gas stations oral rat mg/m3 (1) (7) (7) 30 mg/kg/d 7) | jet fuel (JP-5) 8008-20-6 harmful 3 1.20E+04 118 kerosene 8008-20-6 harmful inhal mice guinea liver cancer 1.59E+08 | 1.40E+04 265 12 mg/m3 150 mg/m3 pig CNS (8) aircraft fueling | oral rat 20,000. kidne (8) 9600 mg/kg/d mg/kg effects (8) skin mice (1) 21 mg/kg (8) NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-72

potency/toxicity exposure Chemical CAS name number NYS NYSDEC | NYSDEC EU IARC LOEL LDS50 health health | TSCA CUS Oil Oil average maximum class class or effect effect production spills spills environ. environ. (2) (1) LC50 assoc greatest Ibs/1990 | gal 95-96 | #95-96 | concent concent. LOEL concern @Q) (4) (4)

naphtha (benzin) 8030-30-6 toxic inhal rat 2 cancer 4.38E+07

care-2 1600 ppm (1) (2) naphtha (heavy aromatic) [64742-94-5 harmful naphtha (light) 64742-95-4 none | petroleum (crude oil) 8002-05-9 toxic skin mice skin cancer

carc-2 210 mg/kg tumors (2)

Q) Q) | petroleum distillates 64742-47-8 harmful 9.70E+08 (hydrotreated light) petroleum distillates 64741-89-5 toxic cancer (2) (solvent refined light care-2 | paraffinic) | petroleum distillates 64741-88-4 toxic cancer (2) (solvent refined heavy care-2 paraffinic) | petroleum naphtha 64741-54-4 toxic cancer (2) | 3.60E+08 (heavy catalytic cracked) care-2 petroleum naphtha 68919-37-9 toxic cancer (2) |_5.50E+08 (full-range reformed) care-2 | petroleum naphtha 64741-55-5 toxic cancer (2) | 3.60E+08 | (light catalytic cracked) carc-2 | petroleum residues 68512-62-9 toxic cancer (2) | 4.90E+08 | (light vacuum) care-2 stoddard solvent 8052-41-3 toxic inhal rat metaplasia | cancer (2) |_1.69E+05 (mineral spirits) care-2, 214 mg/m3 trachea NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-73

potency/toxicity exposure Chemical CAS name number NYS NYSDEC | NYSDEC EU IARC LOEL LDS50 health health | TSCA CUS Oil Oil average maximum class class or effect effect production spills spills environ. environ. (2) (1) LC50 assoc greatest Ibs/1990 | gal 95-96 | #95-96 | concent concent. LOEL concern @Q) (4) (4) (9) () VM&P naphtha 8032-32-4 toxic eye human inhal rat eye cancer (2) | (ligroine) care-2 880 ppm 3400 ppm | irritation Q) Q) Q) waste oil (used none skin mice skin cancer 1.00E+04 942 39 to 860 mineral-based crankcase (harmful)** 60 mg/kg tumors (5) meg/g oil) (5) (5) roadside soil (5) references _|(full references available in main report) 1 NIOSH, 1987. ATSDR, 1997 9 ATSDR, 1995c EINECS, 1996 ATSDR, 1995a. 10 NYSDOH, 1998.

RTK Network, 1997

5 6 7 8

ATSDR, 1995b.

TARC, 1989.

2 3 4

NYSDEC, 1996

ATSDR, 1996.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-74

Appendix A, Table K.1: Polycyclic Aromatic Hydrocarbons: Data for ranking stressors

Compound EU EPA End RfD NOAEL Cancer Ambient | Drinking Soil Food

CAS Number Class or point | (mg/kg/d) | (mg/kg/day) Potency Air Water Conc. | Conc. IARC Factor Conc. Conc. (ppm) | (ppb) Class (mg/ke/dy" | (ue/m') | (pb)

Acenapthene Liver 6E-2 175 .0073 <0.1 <1 <l

83-32-9

Acenaphthylene D .0073 42 <1 <l

208-96-8

Anthracene /3 Liver 3E-1 1000 .073 <0.1 <1 <l

120-12-7 (NOEL)

Benz[a]Janthracene 2 B2/2B .73 <0.1 <l 59 50

56-55-3

Benzo[a]pyrene 2 B2/2B 7.3 <0.1 <1 7 1600

50-32-8

Benzo[e]pyrene /3 <0.1 <1 14 20

192-97-2

Benzo[b]fluoranthene 2 B2/2B .73 <0.1 <l 62 30

205-99-2

Benzo[j|fluoranthene 2 /2B <0.1 <l

205-82-3

Benzo[g,h,i]perylene D/3 .073 <0.1 <1 47 <5

191-24-2

Benzo[k]fluoranthene 2 B2/2B .73 <0.1 <l 26 <l

207-08-9

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-75

Compound EU EPA End RfD NOAEL Cancer Ambient | Drinking Soil Food

CAS Number Class or point | (mg/kg/d) | (mg/kg/day) Potency Air Water Conc. | Conc. IARC Factor Conc. Conc. (ppm) | (ppb) Class (mg/ke/dy" | (ue/m') | (pb)

Chrysene B2/3 .073 <0.1 <1 <l 28

218-01-9

Dibenz[a,h]anthracene 2 B2 36.5 <0.1 <1 <3

53-70-3

Fluoranthene D/3 Liver 4E-2 3000 .0073 <0.1 <l 166 14

206-44-0

Fluorene D/3 Blood 4E-2 125 .0073 <0.1 <l

86-73-7

Ideno[1,2,3-c,d]pyrene B2/2B 73 <0.1 <1 61 10

193-39-5

Phenanthrene D/3 .0073 <0.1 <1

85-01-8

Pyrene /3 Kidney 3E-2 75 <0.1 <1 147 11

129-00-0

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-76

Appendix A, Table L.1: Activity of nuclides in mCi discharged to NYS environment Dose in mrem /year to maximally exposed person off-site (1996)

FACILITY Dose mrem/yr | Am-241 | Am-243 Aral Ba-128] Ba-l33] Be-7 | Bre? | Br77 ene Ce-T4T KAPL-Kno 0.0014 KAPL - Kess 0.0300 TS20,0000 TOOT.0000 BNL-Air 0.0600 TS0000.0000 | 0.007 T2000 | 21300 | 0.4263 BNL -H20, 0.1200 03200 0.1100 0.0420 V.00TU V.000T 0.0087 00002 [0.0670 0.0125 04590 <10 T1080 0-Incin- U of R =10 33140 0-Incin - Trud =10* 0-Incin - Brist =10* 34200 0-120 - Proct =10* 310.0000 0-20 - Koda =10 0.1700 0-Air - Alban =10 0-Arr- Bris =10* 0.0006 0- Air- Come =10* 0-Air - Columb =10* ZO2F 0000 0-Air - ICN =10 0-Aur- Malin =10 0-Aur- MPT =10* 0-Air- NRD =10* T.000T 0-Air- Progen =10* -Air- SPL =10 0-Aur- Bult =10 TS.1000 0-Air - Sync =10* 0-Air - Sync =10* 0-Air- Sync =10* 0-Air - Sync =10 0-Air- Sync =10 0-Air - Sync =10* 0-Air - Sync =10* 0-Air- Wyet =10* 0.1300 0.0153 T588.1000 0.0126 30 T350.7000 5.0 TAFizpat_Ar 02400 ZEIZ0-0000 TAFitzpat_H20 0.0001 bares 0.0722 3097-7000 NMP Teo EF SSA TO UU0UUTT FFF TOTAL ACTIVITY TUS TS95276.5000 | 0.0098 | V.000T | 05200 | 21300 | 0.4203 | 26421000 | 1322T0TS [IN MILLICURIES NOTE: ¥ All Part 380 permittees are significantly below 10 mrem/year in their dose to the pul

ble - <5.0 represents standards in Appendix | of 10 CFR Part 50

Air Dose above’

e note: 25 of the 33 Part 380 permittees are shown here. The rem microcurie threshold established for this spreadsheet.

ng 8 permittees either had no discharges or the levels were below the 0.1

¥¥** Specific radionuclide release data is not available

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-77

FACILITY

CI-36

Co-S7

Co-58

Co-60

Cr-51

Cs-134

Cs-137

Eu-154

F-18

Fe-55

Fr-223

H-3

1-125

KAPL-Knolls site

0.0020

KAPL - Kesselring

0.0006

273.0000

BNL-Air

0.0274

0.0300,

0.0080

5.6757

104819.0000

0.0400

BNL -H20

0.0600

0.0300

0.0300

0.8600

CISS

EML

0.0021

0.0015

0.0002

West Valley - Air

0.0915

0.0001

West Valley -H20

0.1770

6.3800,

752.0000

380-Incin - Wad

6.6160

0.0003

380-Incin - U of R

0.0640

128.7360

0.0140

380-Incin - Trud

16.0120

380-Incin - Brist

380-H20 - Proct

86.9600

380-H20 - Koda

1.6300

380-Air - Alban

0.0750

380-Air - Brist

380- Air - Corne

118.4000

380-Air - Columb

826.0000

5.7500

380-Air - ICN

6.3400

380-Air - Malin

380-Air - MPI

380-Air - NRD

4390.0000

380-Air - Progen

0.0018

380-Air - SPL

502320.0000

380-Air - Buff

79.3000

380-Air - Syne

380-Air - Syne

380-Air - Sync 380-Air C

380-Air

380-Air - Syne

380-Air - Sync

380-Air - Wyet

0.1800

Ginna - Air

0.0037

Ginna - H20

1.0000.

0.4000

0.0313

1.7000.

3.9000

3.4000

Indian Pt 2/3 Air

2303.0000

Indian Pt 2/3 H20

12.1000

6.5000

8.7000

8.0000,

3.3000

J.A-Fitzpat_ Air

0.0420

0.0021

0.0288

18894.0000

J.A.Fitzpat _H20

0.1720

2.3500

1.0200

0.0945

NMP | & 2 Air

0.5000

0.3006

0.0299

0.6043

109774.0000

NMP 1 & 2 H20

26.31

5.64

0.36

5476.00

NESS - Air/H20

TOTAL ACTIVITY

0.0640

0.0874

13.3320

36.3197

6.9919

10.4000

25.0409

0.0001

905.3000

7.6911

130.6211

IN MILLICURIES

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-78

FACILITY

1-126

1-129

I-13]

1-133

1-135

K-40

Kr-83m

Kr-85

Kr-85m

Kr-87

Kr-88

Mn--34

KAPL-Knolls site

362.0000

KAPL - Kesselring

3.0400,

0.0369

14.0000

8.8400

20.0400

BNL-Air

1.5600

0.0014

4.9250

BNL -H20

0.1400

CISS

EML

West Valley - Air

1.2928

West Valley -H20

0.1250

1.3800

380-Incin - Wad

380-Incin - U of R

380-Incin - Trud

380-Incin - Brist

380-H20 - Proct

380-H20 - Koda

380-Air - Alban

0.0950

380-Air - Brist

380- Air - Corne

380-Air - Columb

380-Air - ICN

380-Air - Malin

0.0080

380-Air - MPI

380-Air - NRD

380-Air - Progen

0.0373

380-Air - SPL

380-Air - Buff

0.1500

380-Air - Sync 380-Air C

0.3200

380-Air

0.0400

0.0800

380-Air - Syne 380-Air C

0.3400

380-Air

0.0020

380-Air - Sync

0.1300

380-Air - Wyet

Ginna - Air

0.1000

172.3000

235.5000

356.5000

453.8000

Ginna - H20

8.5000,

4.8000

35.9000

0.0459

Indian Pt 2/3 Air

0.2000

3533.8000

22.4000

3.3000

Indian Pt 2/3 H20

0.2000

0.1000,

J.A.Fitzpat Air

1.9000.

10.4000

7.9000

18480.0000

65690.0000

44184.0000

0.0435

J.A-Fitzpat_ _H20

3.1400

NMP | & 2 Air

1.0000.

6.8000

0.1000

25.5000

483.0000

6150.0000

0.1000

NMP 1 & 2 H20

16.20

NESS - Air/H20

TOTAL ACTIVITY

1.5600.

1.4178

13.2437

22.0000

13.8000

6.3050,

3.0400,

4068.2369

18777.4000

66538.3400

19.6294

IN MILLICURIES

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-79

FACILITY

Mn-56

Na-22

N-13

Ni-63

O-15

P-32

Pa-231

Pa-234

Pb-210

Po-209

Po-210

Pu-236

Pu-238

Pu-239

KAPL-Knolls site

0.0001

0.0002

KAPL - Kesselring

BNL-Air

0.0057

0.0005

BNL -H20

0.1100

CISS

0.0069

EML

0.0004

West Valley - Air

West Valley -H20

0.0371

0.0103

380-Incin - Wad

380-Incin - U of R

0.0310,

380-Incin - Trud

380-Incin - Brist

380-H20 - Proct

380-H20 - Koda

380-Air - Alban

380-Air - Brist

380- Air - Corne

380-Air - Columb

50.0000

768.0000

380-Air - ICN

380-Air - Malin

380-Air - MPI

380-Air - NRD

0.0003

380-Air - Progen

380-Air - SPL

380-Air - Buff

54.9000

265.3000

380-Air - Sync

380-Air - Sync

380-Air - Sync

380-Air - Syne

380-Air - Syne

380-Air - Sync

380-Air - Sync

380-Air - Wyet

Ginna - Air

Ginna - H20

Indian Pt 2/3 Air

Indian Pt 2/3 H20

8.8000

J.A.Fitzpat Air

J.A.Fitzpat _H20

NMP 1 & 2 Air

NMP 1 & 2 H20

NFSS - Air/H20

TOTAL ACTIVITY

0.0057,

0.1105

104.9000

8.8310,

1033.3000

0.0069

0.0004

0.0003

0.0372

0.0105

IN MILLICURIES

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-80

FACILITY

Pu-242

Ra-223

Ra-226

Rb-83

Rb-84

Rb-86

8-35

Sb-124

Sb-125

Sr-90

Te-99

Th-227

Th-230

KAPL-Knolls site

0.0115

0.0020

KAPL - Kesselring

BNL-Air

0.0053

0.0078

6.5700

0.0589

BNL -H20

0.1300

CISS

0.0020

EML

0.0020

West Valley - Air

0.0034

West Valley -H20

5.4400

38.5000

380-Incin - Wad

380-Incin - U of R

0.0090

380-Incin - Trud

380-Incin - Brist

380-H20 - Proct

380-H20 - Koda

380-Air - Alban

380-Air - Brist

380- Air - Corne

380-Air - Columb

380-Air - ICN

380-Air - Malin

380-Air - MPI

380-Air - NRD

380-Air - Progen

380-Air - SPL

380-Air - Buff

380-Air - Sync

380-Air - Sync

380-Air - Sync

380-Air - Syne

380-Air - Sync

380-Air - Sync

380-Air - Sync

380-Air - Wyet

Ginna - Air

Ginna - H20

0.9000

5.0000,

0.1000

Indian Pt 2/3 Air

Indian Pt 2/3 H20

4.3000

6.9000,

J.A.Fitzpat Air

J.A.Fitzpat H20

0.1020

NMP | & 2 Air

0.2023

NMP 1 & 2 H20

0.01

NFSS - Air/H20

TOTAL ACTIVITY

0.0053

0.0078

6.5700

0.0090

5.3609

11.9115

5.8851

38.5000

0.0020

IN MILLICURIES

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-81

FACILITY

Th-231

Th-234

U-232

U-234

U-235

U-236

U-238

Xe-127

Xe-131m

Xe-133

Xe-133m

Xe-135

Y-90

KAPL-Knolls site

0.0015

0.0001

0.0000

0.0000

0.0021

KAPL - Kesselring

1.9800.

365.0000

12.8000

240.0000

BNL-Air

0.0056

0.0083

0.0006

0.0051

BNL -H20

CISS

0.0069

0.0020

0.0069

EML

West Valley - Air

West Valley -H20

0.6630

0.3130

0.0117

0.1780

380-Incin - Wad

380-Incin - U of R

380-Incin - Trud

380-Incin - Brist

380-H20 - Proct

380-H20 - Koda

380-Air - Alban

380-Air - Brist

380- Air - Corne

380-Air - Columb

380-Air - ICN

380-Air - Malin

288.9100

380-Air - MPI

341.0000

380-Air - NRD

380-Air - Progen

380-Air - SPL

380-Air - Buff

380-Air - Sync

306.4800

380-Air - Sync

184.2600

380-Air - Sync

380-Air - Syne

274.3000

380-Air - Sync

88.2900

380-Air - Sync

5.7840

380-Air - Sync

19.1300

380-Air - Wyet

Ginna - Air

105.8000

26985.0000

66.9000

9643.9000

Ginna - H20

1.8000

1.4000

Indian Pt 2/3 Air

678.1000

Indian Pt 2/3 H20

J.A.Fitzpat Air

5557.0000

57661.0000

J.A.Fitzpat H20

NMP | & 2 Air

0.0044

1224.0000

NMP 1 & 2 H20

NFSS - Air/H20

TOTAL ACTIVITY

0.0069

0.6630

0.3165

0.0118

0.0000

0.1849

0.0056

107.7800

34416.9667

79.7006

69448 4051

0.0021

IN MILLICURIES

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-82

Appendix A, Table N.1: Initial Screening of Candidate Volatile Organic Compounds

Emission Data

Emission Data

Emission Data

Exposure Data

Exposure Data

Production Data

1995 NYS TRI

NYS Chemical

OAQPS Priority

NYS Indoor Air

NYS Ambient

1995 NYS TSCA

(> 50,000 Ibs/yr)* | Alliance Member Hazardous Air Contaminant Monitoring 1993 Production Data (emissions > Pollutant (present > 10% of (detected at > (for chemicals 50,000 Ibs/yr)* (> 5000 Ibs/yr NYS samples) 1/100th of AGC) with > 4,000,000 emissions)* Ibs annual production) Toluene Methylene Chloride }| Acetaldehyde Benzene Methylene Chloride Benzene 130,000,000 Methanol Methanol Benzene Carbon Chloroform Methanol Tetrachloride 108,000,000 Methylene Chloride | Toluene Formaldehyde Chloroform 1,2-Dichloroethane Toluene 51,000,000 Xylene Xylene Methylene Chloride Chloromethane Carbon Tetrachloride 2-Butanone 25,000,000 n-Butyl Alcohol 1,2- Xylene Hexane Trichloroethylene Perchloroethylene Dichloropropane 8,000,000 MEK Cyclohexane Vinyl Chloride Ethylbenzene 1,1,2-Trichloroethane Formaldehyde 6,000,000 Trichloroethylene tert-Butyl Alcohol Toluene Methylene Chloride | Tetrachloroethylene Xylene 6,000,000. Carbon Disulfide n-Butyl Alcohol Trichloroethylene Tetrachloroethylene Benzene Trichloroethylene 4,000,000 Carbonyl Sulfide Formaldehyde Tetrachloroethylene Toluene Xylenes (m,p) MIBK Methyl Styrene 1,1,1Methacrylate Trichloroethane 1,1,1- MEK Xylene Trichloroethane Acetaldehyde Vinyl! Chloride Trichlorofluoromethane Formaldehyde MIBK Chlorodifluoromethane Methyl methacrylate Tetrachloroethylene Cyclohexane 1,1-dichloro-1fluoroethane Styrene Hexane Ethylbenzene Vinyl Chloride Benzene 1,2-Dichloropropane Chloromethane sec-Butyl Alcohol * Chemicals are listed in decreasing order relative to total environmental release Note: Biological sampling data (human) not available for VOCs NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-83

Appendix A, Table N.2: Initial Screening of Candidate Semi-Volatile Organic Compounds

Emission Data

Emission Data

Emission Data

Exposure Data

Production Data

Biological Data

1995 NYS TRI NYS Chemical OAQPS NYS Indoor Air 1995 NYS Frequency of (> 5000 Ibs/yr)* Alliance Member Priority Contaminant Production Data (for Detection of (emissions > 5000 | Hazardous Air (present > 10% of chemicals with > Semi-VOCs Ibs/yr)* Pollutant samples) 2,000,000 Ibs annual NHATS FY82 (> 5000 Ibs/yr production NYS emissions)* Glycol Ethers p-Dioxane Glycol Ethers 1,4-Dichlorobenzene Ethylene Glycol Dichlorobenzene 128,000,000 9% Phenol Phenol 4-Isopropyltoluene Alkyl Benzene Trichlorobenzene Derivatives 4% 14,000,000 Ethylene Glycol 2-Methoxyethanol 1,2,4-Trimethylbenzene | 0-Cresol Napthalane 10,000,000 40% 1,2,4- 1,3,5-Trimethylbenzene } Benzoyl Chloride Diethyl Phthalate Trimethylbenzene 9,000,000 42% N,N- p-Cresol Hexachlorobenzene Dimethylformamide 3,000,000 76% N-Methyl-2- 2,3,6-Trimethyl Phenol | B-BHC pyrolidinone 2,000,000 87% Aniline Phenanthrene 13%

2-Ethoxyethanol

Dibuty! Phthalate 44%

Acetophenone Butylbenzyl Phthalate 69%

Pyridine Dioctyl Phthalate

2-Methoxyethanol

31%

Napthalene

p-Dioxane

Di-n-Butyl Phthalate

Isopropylbenzene

Cresol

o-Toluidine

Benzoyl Chloride

* Chemicals are listed in decreasing order relative to total environmental release

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001

Page A-84

Appendix A, Table N.3: Selected VOC Stressors and Relevant Toxicity/Exposure Information

EU Hazard RfD RfC Effect (in Oral Inhalation Sentinel NOAEL TLV- NYS Measured NYS NYSDOH Chemical Classification/ | (mg/kg/ | (mg/m3) animals) Slope Unit Risk Health (mg/kg/ TWA Ambient NYS Ave/Max | [water] at IARC* day) Associated Factor | per ug/m3 Effect day) unless | (ppm) | Exposure Ambient Indoor private Cancer with per specified (4-yr. ave Maximum Air or public Classification RfD/RFC mg/kg/ in ppb) (ppb) Levels wells day (ppb) (ppb) Methylene Harmful/2B 0.06 3 Hepatocell. | 0.0075 | 4.7 E-7 Narcosis; | 5.85 (2-yr., 50 0.33 18 <2 Chloride Carcinoma CNS d.w., rat) 0.5-1.0 effects 695 mg/m3 14.1 (inhal.) Benzene Toxic/1 Leukemia 0.029 8.6 E-6 Narcosis; 10 0.95 1.67 0.9 1.0-10 (human) leukemia 5.6 Carbon Toxic/2B 0.0007 Hepatocell. 1.3E-1 | 15E-5 CNS, 5 0.12 0.31 <0.5 Tetrachloride Carcinoma; systemic 10= 0.5-5.0 kidney effects STEL <15 effects Xylenes Harmful 2 CNS effects CNS 100 1.01 2.19 1.2 (mixed) effects; 1 sens irrit. 5.1 Perchloro- Harmful/2B 0.01 Hepato- sensory, 14 (6-wk., 25 0.34 3.22 <i ethylene toxicity anesth. oral, mouse) | 100 = 0.5 - 2.0 effects STEL 3.2 Formalde- Toxic/2A 0.2 Squamous 1.3 E-5 severe 15 (2-yr., 0.3C | 245749 Ib 0.36 hyde cell carc.; sens. d.w., rat) TRI g.i. lesions wrt. irrit. emissions 5.5 Methanol Toxic 0.5 Altered visual 500 (90 200 4149567 enzymes effects, days, 250= | Ib- TRI resp. gavage, rat; | STEL | emissions acidosis NOEL) Chloroform Harmful/2B 0.01 Liver, 0.006 2.3 E-5S clinical 12.9(7.5 yr, | 10 0.07 0.12 <1 kidney anesth. dog) 0.5 - 5.0 tumors LOAEL 2.1 Trichloro- Harmful/Not CNS, 50 0.06 0.11 <1 ethylene classifiable sensory 100 = 0.5 - 5.0 effects STEL <19 1,1,1-Tri- Harmful/Not CNS, 350 0.47 0.94 0.9 chloroethane | Classifiable sensory 450= 0.5 - 5.0 effects STEL 6.4 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-85

EU Hazard RfD RfC Effect (in Oral Inhalation Sentinel NOAEL TLV- NYS Measured NYS NYSDOH Chemical Classification/ | (mg/kg/ | (mg/m3) animals) Slope Unit Risk Health (mg/kg/ TWA Ambient NYS Ave/Max | [water] at IARC* day) Associated Factor | per ug/m3 Effect day) unless | (ppm) | Exposure Ambient Indoor private Cancer with per specified (4-yr. ave Maximum Air or public Classification RfD/RFC mg/kg/ in ppb) (ppb) Levels wells day (ppb) (ppb) Toluene Harmful 0.2 0.4 liver/kidney CNS 223 (13 wk., | 50 2.76 3.7 4 wt. changes; depress. gavage, rat) 0.5- 1.0 neurotox. 13 Vinyl Toxic/1 1.9 8.4 E-5 CNS 5 66607 Ib Chloride depress., TRI 0.5-1.0 death emissions * | = known human carc.; 2A = probably carcinogenic to humans; 2B = possibly carcinogenic to humans NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-86

Appendix A, Table N.4 Selected Semi-Volatile Stressors and Relevant Toxicity/Exposure Information

EU Hazard RfD RfC Effect (in Oral Sentinel NOAEL TLV- NYS 1995 NYS NYSDOH Chemical Classification | (mg/kg | (mg/m3) animals) Slope Health (mg/kg/day) | TWA | Ambient | Total TRI | Ave/Max | [water] at & IARC /day) Associated | Factor Effect unless (ppm) | Exposure | Emissions Indoor private or Cancer with (mg/kg specified (4-yr ave. (Ib) Air public Classification RfD/RFC /day) in ppb) Levels wells (ppb) (ppb)

Harmful CNS 25 71172 <13 1,2,4-Trimethyl depress., 0.5-1.0 benzene sens. irrit <2

Toxic; 0.6 decr. fetal syst. tox., 60 (rat, 5 154740 Phenol Corrosive body wt. sens. gavage) 10 irrit. Toxic; 0.4 0.2 repro./dev. CNS 380 mg/m3 5 18306 2-Ethoxyethanol Repro. Cat. 2 toxicity effects; (rabbit, repro. inhal., 13 tox. wk) Toxic; 0.02 repro./dev. CNS 93 mg/m3 5 21506 2- Repro. Cat. 2 toxicity effects; (rabbit, Methoxyethanol repro. inhal., 13 tox. wk)

Harmful 0.8 incr. liver | 0.024 | neurotox. | 75 mg/m3 10 0.01 <0.3 1,4- wt. irritation (rat, inhal., 0.5-5.0 Dichlorobenzene multi-gen) 0.8

Harmful 2.0 kidney- wrt. irrit. | 200 (NOEL, | 39-C 93563 Ethylene Glycol and feto- renal tox. rat, diet, 50

toxicity dev. study) Harmful/2B nasal sq. 0.011 sens. 25 78733 p-Dioxane cell care. irrit. NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page A-87

Appendix B NVHOCs Risk Calculations Final Report of the Human Health Work Group New York State Department of Environmental Conservation Comparative Risk Project

May 2001

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page B-1

APPENDIX B Section 1

Cancer risk and hazard indices for consumption of food from U. S. markets.

Data sources:

Gunderson, E. L. 1995. FDA Total Diet Study, July 1986-April 1991, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc Off. Analyt. Chem. Intl. 78(6):13531363.

Gunderson, E. L. 1988. FDA Total Diet Study, April 1982-April 1984, dietary intakes of pesticides, selected elements, and other chemicals. J. Assoc. Off. Analyt. Chem. 71(6):1200-1209.

Gartrell, M. J., J. C. Craun, D. S. Podrebarac, and E. L. Gunderson. 1986. Pesticides, selected elements, and other chemicals in infant and toddler total diet samples, October 1980-March 1982. J. Assoc. Off. Analyt. Chem. 69(1):123-145.

US Environmental Protection Agency. 2000. Draft Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Related Compounds. Part III. National Center for Environmental Assessment. Washington, DC. EPA/600/P-00/001Bg.

Brief study description:

The U. S. Food and Drug Administration determined chemical residue concentrations in foods representing typical market baskets in cities throughout the United States, including four cities in New York state. The resulting data were converted to average daily intakes for the specific chemical compounds examined for selected age groups of people. In the most recent study, concentrations of nearly 300 compounds or elements were determined in each food product. Only non-volatile halogenated organic compounds (NVHOCs) are examined here. Data for dioxins and furans are from USEPA (2000).

Assumptions:

The risk of adverse health impacts caused the NVHOCs is greatest with exposure to the fetus and young children but declines as the individual becomes an adult. To approximate the potential range of cancer risk or non-cancer hazard, computations are made for two-year old children and adults of reproductive age (25 to 30 year old adults, sex ignored). Other assumptions are:

1. Calculations are based on computed average daily intake of specific chemicals in a representative composite of food taken from U. S. markets nationwide. Of the values reported, the most current values are used for computations.

2. Cancer potency quotients and reference doses published by the U. S. Environmental

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page B-2

Protection Agency are used in cancer risk or hazard index calculations, respectively. Calculations:

Cancer risk = USFDA market basket chemical intake rate (ng/kg/d) X 10°mg/ng X Oral cancer potency quotient (mg/kg/d)!

Hazard index = USFDA market basket chemical intake rate (ng/kg/d) X 10% mg/ng R£D (mg/kg/d)

The results of the computations are presented in Table B-1.

Classification of NVHOCs: See Table B-2.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page B-3

Table B-1: Cancer risks and hazard indices for human consumption of food from the U. S. market (based on values reported by Gunderson, 1995, Gunderson, 1988, Gartrell et al., 1986 or USEPA, 2000).

Two-year old child (10 kg)

Adult (25 to 30 year old; 70 kg)

Chemical(s) Market basket Hazard Market basket Cancer Hazard value Index value Risk Index (ng/kg/d) (ng/kg/d)

Aldrin <0.1 <5.88E-3 <0.1 <1.70E-6 <5.88E-3 Chlordane 1.6 2.66E-2 0.8 1.04E-6 1.33E-2 Chloroanilines 6.0 1.50E-3 5.1 - 1.27E-3 DDD 0.7 1.40E-3° 0.3 4.08E-8 6.00E-4° DDE 42.0 8.40E-2° 11.9 4.04E-6 2.38E-2° DDT 11 2.20E-3 0.5 1.70E-7 1.00E-3 Dieldrin 7.2 1.44E-1 2.8 4. 48E-5 5.60E-2 Dioxins and furans - - 0.00059 9.2E-5 5.9E-1 (TEQ) Endosulfan 46.0 7.66E-3 17.7 - 2.95E-3 Endrin <0.1 <3.33E-4 <0.1 - <3.33E-4 Heptachlor <0.1 <2.00E-4 <0.1 <4.5E-7 <2.00E-4 Heptachlor epoxide 2.5 1.92E-1 0.9 4.05E-6 6.92E-2 HCB 2.1 4.20E-3 0.8 7.28E-6 1.00E-3 a-HCCH 2.7 9.00E-3° 0.8 1.28E-6 2.66E-3° B-HCCH <0.1 <3.33E-4° <0.1 <1.80E-7 <3.33E-4°

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Two-year old child (10 kg) Adult (25 to 30 year old; 70 kg) Chemical(s) Market basket Hazard Market basket Cancer Hazard value Index value Risk Index

(ng/kg/d) (ng/kg/d) y-HCCH 3.2 1.06E-2 1.0 - 3.33E-3 Methoxychlor 0.9 1.80E-4 0.3 - 6.00E-5 PCB 1.9 9.50E-2 0.9 9.00E-7 4.50E-2 PCNB 2.5 8.33E-4 0.8 - 2.66E-4 Tetrachlorobenzenes <0.1 <3.33E-4 <0.1 - <3.33E-4 Toxaphene 22.4 - 6.7 7.37E-6 - Trichlorobenzenes 0.2 2.00E-5 <0.1 : <1.00E-5

“ A hyphen (-) indicates either a cancer potency value or an RfD value were lacking. ° The calculated hazard index used the RfD value for DDT.

* The calculated hazard index used the RfD value for y-HCCH.

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Table B-2: Classification of cancer risk and hazard indices for chemical residues in food taken from U. S. markets

Cancer Risk Hazard Index Classification adult 2-yr old child adult Very high CR>107, or HI>10 High 10?>CR>10%, or 102HI>1 Moderate Aldrin* Dieldrin Dioxins and furans 107>CR>10°, or Chlordane Heptachlor epoxide 1>HP>0.1 DDE Dieldrin Dioxins and furans HCB Heptachlor epoxide a-HCCH Toxaphene Low DDD Aldrin Aldrin CR<10°, or DDT Chlordane Chlordane HI<0.1 Heptachlor Chloroanilines Chloroanilines B-HCCH DDD DDD PCB DDE DDE DDT DDT Endosulfan Dieldrin Endrin Endosulfan Heptachlor Endrin HCB Heptachlor HCCHs Heptachlor epoxide Methoxychlor HCB PCB HCCHs PCNB Methoxychlor Tetrachlorobenzenes PCB Trichlorobenzenes PCNB Tetrachlorobenzenes

Trichlorobenzenes

* May be classified as “Low” since the market basket value was <0.1 ng/kg/day.

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APPENDIX B SECTION 2

Cancer risk to adults from consumption of fish containing residues of certain non-volatile halogenated organic compounds.

Background:

Cancer risk from exposure to NVHOCs through the consumption of fish was calculated for three populations: the general population, avid anglers, and subsistence anglers.

General Assumptions:

A two-year old child weighs 13 kg, and an adult weighs 70 kg For the general population:

a. Adult consumption rate of freshwater fish is 6 g/day (USEPA, 1997; Jacobs, et al., 1998). b. Adult consumption rate of marine fish is 12.5 g/day (USEPA, 1997; Jacobs, et al., 1998). c. Concentrations are mean levels found in marine fish and upper bound levels in freshwater fish from NY waters without health advisories (NYSDEC files). 1. For avid anglers: a. Adult consumption rate of freshwater fish is 32.4 g/day (USEPA, 1997; Jacobs, et al., 1998). b. Concentrations are regulatory limits or guidelines 1. For subsistence anglers: a. Adult consumption rate of freshwater fish is 71 g/day (Bolger, et al., 1990). b. Concentrations are mean levels found in marine fish and upper bound levels in freshwater fish from NY waters without health advisories (NYSDEC files). 1. Use oral potency quotient values published in IRIS, or by the US Environmental Protection

Agency’s Office of Pesticide Programs, whichever is more recent. Calculation: cancer risk =

Consumption rate (kg/d) X_ residue concentration (mg/kg) X Oral potency quotient (mg/kg/d)" body weight (kg)

The results of the calculations are presented in Table B-3 and B-4.

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Table B-3: Cancer risk for three populations consuming fish with NVHOC residues.

concentrations (mg/kg) oral potency cancer risk Compound i factor i . i regulatory fresh marine (mg/kg/dayy" avid subsistence general population limit water angler angler eat freshwater fish | no freshwater fish Aldrin 0.3 <0.005 <0.005 17.0 2.3E-3 <8.6E-5 <2.2E-5 <1.5E-5 Chlordane 0.3 0.015 <0.01 0.35 4.8E-5 5.3E-6 1.0E-6 <6.2E-7 DDT & 5.0 0.2 0.03 0.34 7.8E-4 6.9E-5 7.6E-6 1.8E-6 metabolites Dieldrin 0.3 0.007 <0.005 16.0 2.2E-3 1.1E-4 2.3E-5 <1.4E-5 Heptachlor 0.3 <0.005 <0.005 4.5 6.2E-4 <2.2E-5 <5.9E-6 <4.0E-6 Heptachlor 0.3 <0.005 <0.005 9.1 1.2E-3 <4.6E-5 <1.2E-5 <8.1E-6 epoxide HCB* 0.05 0.005 <0.002 1.6 3.7E-5 8.1E-6 1.2E-6 <5.7E-7 a-HCCH <0.005 <0.005 6.3 <3.2E-5 <8.3E-6 <5.6E-6 B-HCCH <0.005 <0.005 1.8 <9.1E-6 <2.3E-6 <1.6E-6 Mirex 0.1 0.03 <0.002 PCB 2.0 0.2 <0.05 2.0 1.8E-3 4.0E-4 5.2E-5 <1.7E-5 Toxaphene 5.0 <0.05 <0.05 1.1 2.5E-3 <5.5E-5 <1.4E-5 <9.8E-6 TCDD (TEQ) 1E-5 4E-6 <2E-6 1.56E5** 7.2E-4 6.3E-4 1.0E-4 <5.5E-5

There is no regulatory limit for HCB; concentrations in NY waters are usually below 0.05 mg/kg. * The cancer potency factor for TCDD is being re-evaluated; the previous factor (from 1985) is reported here.

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Table B-4: Classification of cancer risk for adults from consumption of fish containing NVHOCs.

Risk Avid angler Subsistence angler General population Classification eat freshwater fish eat no freshwater fish Very high CR>10? High Aldrin* Dieldrin 10°>CR>104 DDT & metab. PCB Dieldrin TCDD Heptachlor* Heptachlor epoxide* PCB TCDD Toxaphene* Moderate Chlordane Aldrin* Aldrin* Aldrin* 10“>CR>10° HCB Chlordane DDT & metab DDT & metab. DDT & metab. Dieldrin Dieldrin* HCB Heptachlor* Heptachlor* Heptachlor* Heptachlor epoxide* | Heptachlor epoxide* Heptachlor epoxide* | HCB a-HCCH* a-HCCH* a-HCCH* B-HCCH* B-HCCH* B-HCCH* PCB* Toxaphene* PCB TCDD* Toxaphene* Toxaphene* TCDD Low Chlordane Chlordane* CR< 10° HCB*

* For this chemical, detection limits are rarely exceeded. The appropriate classification may be one class lower.

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APPENDIX B SECTION 3 Non-cancer risk to adults and children from consumption of fish containing residues of certain non-volatile halogenated organic compounds.

Background:

Non-cancer risk from exposure to NVHOCs through the consumption of fish was calculated using hazard indices for three populations: the general population, avid anglers, and subsistence anglers.

General Assumptions:

1. A two-year old child weighs 13 kg, and an adult weighs 70 kg 1. The fish consumption rate for a 2 year old child is 42% of the adult rate, based on USDA food consumption survey (Pao, 1982). 1. For the general population: a. Adult consumption rate of freshwater fish is 6 g/day (USEPA, 1997; Jacobs, et al., 1998). b. Adult consumption rate of marine fish is 12.5 g/day (USEPA, 1997; Jacobs, et al., 1998). c. Concentrations are mean levels found in marine fish and upper bound levels in freshwater fish from NY waters without health advisories (NYSDEC files). 1. For avid anglers: a. Adult consumption rate of freshwater fish is 32.4 g/day (USEPA, 1997; Jacobs, et al., 1998). b. Concentrations are regulatory limits or guidelines 1. For subsistence anglers: a. Adult consumption rate of freshwater fish is 71 g/day (Bolger, et al., 1990). b. Concentrations are mean levels found in marine fish and upper bound levels in freshwater fish from NY waters without health advisories (NYSDEC files). 1. Use Reference Doses (RfD) published in IRIS by the US Environmental Protection Agency. Calculation: hazard index = consumption rate (kg/d) X residue concentration (mg/kg)

body weight (kg) X RfD (mg/kg/day)

The results of the calculations are presented in Tables B-5 and B-6.

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Table B-5: Hazard Indices for adults and 2-year old children in two populations consuming fish with NVHOC residues.

concentrations (mg/kg) RfD hazard index Compound i (mg/kg/day) i i regulatory fresh marine avid angler subsistence angler limit water

adult child adult child Aldrin 0.3 <0.005 <0.005 3E-5 46 10. <0.17 <0.38 Chlordane 0.3 0.015 <0.01 6E-5 2.3 5.2 0.25 0.57 DDT & 5.0 0.2 0.03 SE-4 46 10. 0.41 0.92 metabolites Dieldrin 0.3 0.007 <0.005 SE-5 2.8 6.3 0.14 0.32 Heptachlor 0.3 <0.005 <0.005 5E-4 0.28 0.63 <0.01 <0.02 Heptachlor 0.3 <0.005 <0.005 1.3E-5 11. 24. <0.39 <0.88 epoxide HCB* 0.05 0.005 <0.002 8E-4 0.03 0.07 0.01 0.01 a-HCCH <0.005 <0.005 B-HCCH <0.005 <0.005 Mirex 0.1 0.03 <0.002 2E-4 0.23 0.52 0.15 0.34 PCB 2.0 0.2 <0.05 2E-5 46. 104. 10. 23. Toxaphene 5.0 <0.05 <0.05 TCDD (TEQ) 1E-5 4E-6 <2E-6 1E-9 46 10. 41 9.2

* There is no regulatory limit for HCB; concentrations in NY waters are usually below 0.05 mg/kg.

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Table B-6: Hazard Indices for adults and 2-year old children in the general population consuming fish with NVHOC residues.

concentrations (mg/kg) RfD hazard index for general population

Compound (mg/kg/day)

regulatory fresh marine eat freshwater fish eat no freshwater fish

limit water adult child adult child

Aldrin 0.3 <0.005 <0.005 3E-5 <0.04 <0.1 <0.03 <0.07 Chlordane 0.3 0.015 <0.01 6E-5 0.05 0.1 <0.03 <0.07 DDT & 5.0 0.2 0.03 5E-4 0.04 0.1 0.01 0.02 metabolites Dieldrin 0.3 0.007 <0.005 5E-5 0.03 0.07 <0.02 <0.04 Heptachlor 0.3 <0.005 <0.005 5E-4 <0.003 <0.006 <0.002 <0.004 Heptachlor 0.3 <0.005 <0.005 1.3E-5 <0.1 0.2 <0.07 <0.2 epoxide HCB* 0.05 0.005 <0.002 8E-4 0.001 0.002 <0.0004 <0.001 a-HCCH <0.005 <0.005 B-HCCH <0.005 <0.005 Mirex 0.1 0.03 <0.002 2E-4 0.01 0.03 <0.002 <0.004 PCB 2.0 0.2 <0.05 2E-5 1.3 2.9 <0.4 <1. Toxaphene 5.0 <0.05 <0.05 TCDD (TEQ) 1 E-5 4E-6 <2E-6 1E-9 0.7 1.6 <0.4 <0.8

* There is no regulatory limit for HCB; concentrations in NY waters are usually below 0.05 mg/kg.

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Table B-7: Classification of non-cancer risk for adults and children from consumption of fish containing NVHOCs.

General population Hazard Avid angler Subsistence angler Class eat freshwater fish eat no freshwater fish adult child adult child adult child adult child Very High Heptachlor Heptachlor PCB HI>10 epoxide* epoxide* PCB PCB High Aldrin* Aldrin* PCB TCDD PCB PCB 10>HI>1 Chlordane Chlordane TCDD TCDD ~ DDT & DDT & metab. metab. Dieldrin Dieldrin TCDD TCDD Moderate Heptachlor* | Heptachlor* | Aldrin* Aldrin* TCDD Heptachlor PCB* Heptachlor 1>HE-0.1 Mirex Mirex Chlordane Chlordane epoxide* TCDD* epoxide* ~ DDT& metab DDT& metab PCB* Dieldrin Dieldrin TCDD* Heptachlor Heptachlor epoxide* Mirex | epoxide* Mirex Low HCB HCB HCB HCB Aldrin* Aldrin* Aldrin* Aldrin* 0.1>HI Heptachlor* Heptachlor* Chlordane Chlordane Chlordane* Chlordane* ~ DDT & metab. DDT & DDT & metab. DDT & Dieldrin metab. Dieldrin* metab. Heptachlor* Dieldrin Heptachlor* Dieldrin* Heptachlor Heptachlor* | HCB* Heptachlor* epoxide* HCB Heptachlor HCB* HCB Mirex epoxide* Mirex* Mirex Mirex* * For this chemical, detection limits are rarely exceeded. The appropriate classification may be one class lower. NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page B-13

APPENDIX B Section 4 Cancer risk for indoor air exposures to non-volatile halogenated organic compounds’.

Data sources: See Tables B-8 and B-9.

Brief description of study:

The study measured pesticide concentrations in indoor air from 1986 through 1988 in homes in Florida, a relatively high pesticide use area, and Massachusetts, a relatively low to moderate pesticide use area. Indoor air samples were collected from 173 homes in Florida and from 86 homes in Massachusetts. Minimum and maximum average concentrations of 32 pesticides or pesticide degradation products were reported. Pesticide levels in New York would most likely be more similar to levels in Massachusetts than in Florida. Therefore the Massachusetts data were used for this analysis.

Assumptions: 1. Respiratory characteristics of children and adults are approximately the same or proportionate

2. Maximum average and minimum average chemical residue concentrations are used 3. Use inhalation cancer potency quotients published by the US Environmental Protection Agency for calculation of cancer risk.

Calculation: The results of the computations are presented inTables D-1 and D-2.

Cancer risk = Residue concentration (ng/m*) X 10° g/ng X Inhalation potency quotient (ug/m*)y'

Classification of cancer risk: See Table B-10.

' Reference concentrations were not available for computation of hazard indices.

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Table B-8: Cancer risk for inhalation of chemical residues in residential indoor air.

Concentration’ and cancer risk Chemicals) | Sverage vwernge | concentration Cancer risk concentration Cancer risk (ng/m°) (ng/m*)

Aldrin ND? - 0.2 9.8E-7 Chlordane 36 1.3E-5 253 9.4E-5 DDD ND - ND - DDE 0.5 4.9E-8° 5 4.9E-7> DDT 0.7 6.8E-8 0.9 8.7E-8 Dicofol ND - 7 NC* Dieldrin 0.7 3.2E-6 0.8 3.7E-6 Heptachlor 5 6.5E-6 35 4.6E-5 Heptachlor epoxide ND - ND - Hexachlorobenzene ND - ND - a-HCCH ND ND

3.6E-7° 2.7E-6 > y-HCCH 0.7 5 Methoxychlor ND - ND -

' Data source: Immerman, F. W., and J. L. Schaum. 1990. Final report of the nonoccupational pesticide exposure study (NOPES). EPA/600/3-90/003. Exposure Assessment Research

Division, U. S. Environmantal Protection Agency, Research Triangle Park, NC.

> ND = Not detected; detection limits were not specified in the materials available. Therefore, cancer risk was not calculated.

> The cancer potency quotient for DDT was used for DDE cancer risk calculation.

+ NC = Not calculated due to lack of a cancer potency quotient. > The cancer potency quotient is for total HCCHs. The calculated cancer risk is for total HCCHs.

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Table B-9: Cancer risk for polychlorinated biphenyl (PCB) concentrations in ambient air and indoor air from non-New York settings.

Environmental Setting

Average concentration range (ng/m’)

Cancer Risk

References

non-residential

Ambient air, rural 0.3 - 1.9 3.0E-08 to 1.9E-07 | ATSDR, 1995b Buckley, 1983 Urban air 1-10 1.0E-07 to 1.0E-06 | ATSDR, 1997 Macleod, 1979, 1981 Vorhees et al., 1997 Indoor air, residential | 10 - 275 1.0E-06 to 2.8E-05 | Macleod, 1979, 1981 Indoor air, 90 - 457 9.0E-06 to 4.6E-05 | Balfanz, 1993

Macleod, 1979, 1981

Oatman & Roy, 1986 Wallace et al., 1996

Data sources: ATSDR. 1995b. Toxicological profiles on polychlorinated biphenyls. Agency for Toxic Substances and Disease Registry, Atlanta, GA.

ATSDR. 1997. Toxicological profiles on polychlorinated biphenyls: Update. Agency for Toxic Substances and Disease Registry, Atlanta, GA.

Balfanz, E., J. Fuchs, and H. Kieper. 1993. Sampling and analysis of polychlorinated biphenyls (PCB) in indoor air due to permanently elastic sealants. Chemosphere 26:87 1-880.

Buckley, E. H., and T. J. Tofflemire. 1983. Uptake of airborne PCBs by terrestrial plants near the tailwater ofadam. 1983 National Conference on Environmental Engineering, Proceedings of the ASCE Specialty Conference, Hilton Harvest House, Boulder, CO.

Macleod, K. 1979. Sources of emissions of polychlorinated biphenyls into the ambient atmosphere and indoor air. EPA-600/4-78-022. Office of Research and Development, U. S. Environmental Protection Agency, Research Triangle Park, NC.

Macleod, K. 1981. Polychlorinated biphenyls in air. Environ. Sci. Technol. 15:926-928.

Oatman, L., and R. Roy. 1986. Surface and indoor air levels of polychlorinated biphenyls in public buildings. Bull. Environ. Contam. Toxicol. 37:461-466

Vorhees, D. J., A. C. Cullen, and L. M. Altshul. 1997. Exposure to polychlorinated biphenyls in residential air and outdoor air near a Superfund site. Environ. Sci. Technol. 31:3612-3618.

Wallace, J. C., 1. Basu, and R. A. Hites. 1996. Sampling and analysis artifacts caused by elevated indoor air polychlorinated biphenyl concentrations. Environ. Sci. Technol. 30:2730-2734.

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Table B-10: Classification of cancer risk due to inhalation of indoor air.

Indoor air concentration

Risk Classification we . Minimum average Maximum average Very High CR>10? High 10?>CR>107 Moderate Chlordane Chlordane 10*>CR>10° Dieldrin Dieldrin Heptachlor Heptachlor HCCHs PCB Low DDT & metabolites Aldrin CR< 10° HCCHs DDT & metabolites PCB

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APPENDIX B Section 5

Summary of cancer risk and hazard indices for non-volatile halogenated organic compounds

Exposure route

Cancer Risk (CR) US Food Fish Indoor air Hazard Index (HI) avid angler subsistence general (eat no angler freshwater fish) Very high Heptachlor epoxide PCB CR>10”, or PCB HI>10 High Aldrin Dieldrin 10°>CR=210*, or Chlordane TCDD 10>HI>1 DDT & metabolites Dieldrin Heptachlor TCDD Toxaphene Moderate Aldrin HCB Aldrin Aldrin Chlordane 10*>CR210°, or Chlordane Mirex Chlordane DDT & metabolites | Dieldrin 12HI20.1 DDE DDT & metabolites Dieldrin Heptachlor Dieldrin Heptachlor Heptachlor HCCHs HCB Heptachlor epoxide Heptachlor epoxide | PCB Heptachlor epoxide HCB PCB a-HCCH a-HCCH TCDD Toxaphene B-HCCH Toxaphene Mirex Toxaphene

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Cancer Risk (CR) or Hazard Index (HI)

Low CR<10°, or HI<0.1

Exposure route

US Food

Cloranilines

DDD

DDT

Endosulfan Endrin

Heptachlor HCCHs Methoxychlor PCB

PCNB Tetrachlorobenzenes Trichlorobenzenes

avid angler

Fish

subsistence angler

general (eat no freshwater fish)

Chlordane HCB Mirex

Indoor air

Aldrin DDT & metabolites

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Appendix C

Pesticides Risk Calculations

Final Report of the Human Health Work Group New York State Department of Environmental Conservation

Comparative Risk Project

May 2001

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APPENDIX C Pesticide risk calculations

Section 1

Calculation of the cancer risk and hazard indices for pesticides in food from U. S. markets

Assumptions:

1. Calculations are based on computed average daily intake of specific chemicals in a representative composite of food taken from U. S. markets nationwide. These values are

reported in Gunderson (1995), Gunderson (1988), or Gartrell et a/. (1986). Of the reported values, the most current values are used.

2. The representative food intakes are those for two-year old children and the greatest

values reported for 25 to 30 year old adults (sex ignored). For cancer risk calculations, the 25 to 30 year old adult intake rate is assumed for lifetime exposure.

3. Cancer potency quotients and reference doses published by the U. S. Environmental Protection Agency are used in cancer risk or hazard index calculations, respectively.

Computations: Cancer risk = USFDA market basket chemical intake rate (ng/kg/d) X 10° mg/ng X Oral cancer potency quotient (mg/kg/day)"

Hazard index = USFDA market basket chemical intake rate (ng/kg/d) X_ 10° mg/ng R£D (mg/kg/d)

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Table C-1: Calculated cancer risk and hazard indices for pesticides detected in U. S. food.

Daily Amount Hazard Index Pesticide Child/Adult Cancer Risk Child (ng/ke/d)" (2-year old) Adult Acephate 9.9/8.2 7.13E-8 2.47E-3 2.05E-3 Aldicarb <0.1/<0.1 - <1.00E-4 <1.00E-4 Azinphos-methyl 31.1/6.1 - 2.07E-2 4.07E-3 Bromophos <0.1/<0.1 - <2.50E-6 <2.50E-6 Captan 47.0/13.9 3.34E-8 3.61E-4 1.07E-4 Carbaryl 127.3/33.8 7.67E-7 1.27E-3 3.38E-4 Carbofuran 0.1/0.1 - 2.00E-5 2.00E-5 Carbophenthion 0.1/0.1 - 7.69E-4 7.69E-4 Chlorobenzilate 4.4/0.8 - 2.20E-4 4.00E-5 Chlorothalonil <0.1/<0.1 <7.70E-10 <6.66E-6 <6.66E-6 Chlorpropham 597.0/188.6 - 2.98E-3 9.43E-4 Chlorpyrifos 13.8/3.8 - 4.60E-3 1.27E-3 Chlorpyrifos-methy] 32.2/11.6 - 3.22E-3 1.16E-3 2,4-D <0.1/<0.1 - <1.00E-5 <1.00E-5 DCNA (Dichloran) 258.6/77.3 - 1.03E-2 3.09E-3 DCPA (Dacthal) 1.8/1.0 1.49E-9 1.80E-4 1.00E-4 Diazinon 10.6/3.7 - 1.18E-1 4.11E-2 Dichlorvos <0.1/<0.1 <2.90E-8 <2.00E-4 <2.00E-4 Dicofol 35.5/8.3 - 2.96E-2 6.92E-3 Dimethoate 6.9/7.2 - 3.45E-2 3.60E-2 Diphenylamine 41.0/7.4 - 1.64E-3 2.96E-4 Disulfoton 0.3/0.4 - 7.50E-3 1.00E-2 Endosulfan 46.0/17.7 - 7.67E-3 2.95E-3 EPN 0.3/nc? - - - Ethion 22.2/4.5 - 4.44E-2 9.00E-3 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page C-3

Daily Amount Hazard Index Pesticide Child/Adult Cancer Risk Child (ng/kg/d)* (2-year old) Adult Fenitrothion 1.4/0.8 - 1.08E-3 6.15E-4 Fenuron 1.4/0.2 - - - Fenvalerate 44/1.9 - 1.76E-4 8.00E-6 Folpet 3.1/1.0 3.50E-9 3.10E-5 1.00E-5 Fonofos 0.2/<0.1 - 1.00E-4 <5.00E-5 Iprodione 5.1/1.8 7.90E-8 1.27E-4 4.50E-5 Linuron 2.4/0.8 - 1.20E-3 4.00E-4 Malathion 218.4/70.4 - 1.09E-2 3.52E-3 Merphos 0.1/<0.1 - 3.33E-3 <3.33E-3 Methamidophos 19.9/16.7 - 3.98E-1 3.34E-1 Methidathion 0.8/0.2 - 8.00E-4 2.00E-4 Methiocarb <0.1/1.4 - <2.00E-5 2.80E-4 Methomyl 12.3/3.7 - 4.92E-4 1.48E-4 Methoxychlor 0.9/0.3 - 1.80E-4 6.00E-5 Methyl! parathion 0.1/<0.1 - 4.00E-4 <4.00E-4 Metobromuron <0.1/<0.1 - - - Mevinphos 7.8/3.0 - 3.12E-2 1.20E-2 Monocrotophos <0.1/0.1 - <2.00E-3 2.00E-3 Neburon <0.1/<0.1 - - - Omethoate 4.8/5.3 - 1.60E-2 1.77E-2 Oxamyl 0.1/0.2 - 4.00E-6 8.00E-6 Parathion 3.7/1.1 - 1.12E-2 3.33E-3 PCNB 2.5/0.8 - 8.33E-4 2.67E-4 Pentachlorophenol 1.4/0.8 1.03E-7 4.67E-5 2.67E-5 Permethrin 34.8/28.3 5.21E-7 6.96E-4 5.66E-4 NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page C-4

Daily Amount Hazard Index Pesticide Child/Adult Cancer Risk Child (ng/kg/d)* (2-year old) Adult

Perthane 0.7/0.4 - - -

Phorate 0.1/0.1 - 2.00E-4 2.00E-4 Phosalone 4.2/0.7 - 1.68E-3 2.80E-4 Phosmet 8.1/2.0 - 4.05E-4 1.00E-4 Phosphamidon 3.9/0.7 - 1.95E-2 3.50E-3 Pirimiphos-methyl 4.1/1.6 - 4.10E-4 1.60E-4 Profenofos 0.1/<0.1 - 2.00E-3 <2.00E-3 Propargite 221.1/38.5 6.58E-7 1.11E-2 1.93E-3 Ronnel <0.1/<0.1 - <6.67E-6 <6.67E-6 Sulfotepp 11.7/4.1 - 2.34E-2 8.20E-3 Sulfur 36.8/5.3 - - -

2, 4, 5-T 0.3/0.2 - 3.00E-5 2.00E-5 Tecnazene 0.2/0.1 - 2.00E-5 1.00E-5 Terbufos <0.1/0.1 - <2.00E-3 <2.00E-3 Tetrachlorvinphos 0.1/<0.1 <1.83E-10 3.33E-6 <3.33E-6 Tetradifon 0.1/<0.1 - - -

Thiabendazole 668.5/151.0 - 6.69E-3 1.51E-3 Triallate <0.1/<0.1 <8.32E-9 <7.69E-6 <7.69E-6 1,2,3-Trichlorobenzene 0.2/<0.1 - - -

Triphenyl phosphate 34.8/18.4 - - -

Vinclozolin 11.0/3.5 - 4.40E-4 1.40E-4

“Sources: The most recent data published by Gunderson (1995), Gunderson (1988), or Gartrell et

al. (1986).

nc = Not calculated by Gunderson (1995).

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APPENDIX C

Section 2

Calculation of the cancer risk for pesticides in water from New York State sources.

Assumptions:

1. The calculations are based on concentrations of specific pesticides detected in New York State surface waters or groundwaters from 1994 through March 1998 (see Appendix A, Tables I.3 and I.4). Maximum concentrations are used for computations except for DCPA (Dacthal) in groundwaters where the average concentrations were used.

2. Computations were made for an adult with an average lifetime body weight of 70 kg and

ingestion of two liters of water per day over a 70 year lifetime.

3. Cancer potency quotients published by the US Environmental Protection Agency are used

in computations.

Note:

Hazard indices could not be calculated due to the lack of reference concentrations for all the

pesticides detected in water.

Computations:

Calculated cancer risk =

Water consumed (I/d) X Pesticide concentration (ug/l) X 10° mg/wg X Oral cancer potency factor (mg/kg/dy"

Body weight (kg)

Table C-2: Calculated cancer risk to an adult from the consumption of pesticides detected in

New York State surface water or groundwater.

Pesticide Surface water Groundwater Alachlor -* - Aldicarb and metabolites nd° - Atrazine 2.7E-5 7.0E-6 Carbaryl 1.0E-6 nd Carbofuran - - Chlorpyrifos - nd Cyanazine 6.0E-5 8.6E-5 2,4-D nd - DCPA (Dacthal) 4.7E-10 2.6E-6 °

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Diazinon

1,2-Dichloropropane nd - Dinoseb nd - EPTC - nd Ethylene dibromide nd 1.9E-1 Malathion - nd MCPP nd - Metalaxyl nd - Methomyl nd - Metolachlor - - Metribuzin - - Molinate 5.0E-8 nd 4-Nitrophenol nd - Oxamyl] nd - Pendimethalin - nd Prometon - - Pronamide 2.2E-8 nd Simazine 1.9E-6 1.2E-4 (4.2E-5)4 TCPA nd 3.3E-5 © Tebuthiuron - nd Terbacil - nd

* A dash (-) indicates the absence of a cancer potency factor with which to calculate a cancer risk. In most instances, the pesticide has inadequate information from which to determine its carcinogenicity. In a few instances, there is evidence a pesticide is non-

carcinogenic.

° nd indicates the chemical was not detected

© Initial reports of DCPA (Dacthal) were erroneous. TCPA, a metabolite of DCPA (Dacthal), was the actual compound detected.

The cancer potency factor for DCPA (Dacthal) was used for computations in both cases.

¢ The parenthetic value reflects the more recent and extensive data represented in Appendix A, Table I-4, and is used as the basis

for categorization in Appendix C, Table C-3

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Appendix C Table C-3: Cancer risk (CR) and hazard indices (HI) for pesticides in US food, New York surface waters or groundwaters, and indoor air of Massachusetts homes.

Risk Classification

Adult Cancer Risk

Hazard Index

2-year old child

adult

Very high NYS groundwater CR>107 Ethylene dibromide HI>10 High 10°>CR>107 102HIz1 Moderate NYS surface water US food US food 107>CR>10° Atrazine Diazinon Methamidophos 12HI20.1 Cyanazine Methamidophos Simazine NYS groundwater Atrazine Cyanazine DCPA (Dacthal) and TCPA Simazine Low US food US food US food CR<10° All pesticides (13) for | All other pesticides All other pesticides HI<0.1 which calculations (60) for which (61) for which were possible calculations were calculations were possible possible NYS surface water Carbaryl Indoor air Indoor air DCPA (Dacthal) Dichlorvos Dichlorvos Molinate Pronamide Indoor air Dichlorvos

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Appendix D

Summary of Data Sources

Final Report of the Human Health Work Group New York State Department of Environmental Conservation

Comparative Risk Project

May 2001

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page D-1

Summary of Data Sources Used

This summary provides a brief description of the data sources that were commonly used for many of the stressor groups. This list does not include every data source used for each stressor.

1. American Conference of Governmental Industrial Hygienists . 1996. 1996 TLVs and BEIs: Threshold Limit Values for Chemical Substances and Physical Agents: Biological Exposure Indices. Cincinnati, OH.

Guidelines for about 1,000 substances in workplace air to assist in control of health hazards.

2. Chemical Exchange Directory, SA. 1996. EINECS Plus CD. European Inventory of Existing Chemical Substances and European List of Notified Chemical Substances. Silver Platter Information, Ltd. London, UK.

Provides toxicological classifications for about 100,000 substances evaluated by the European Union. These classifications are based on acute and chronic effects as well as carcinogenic properties.

3. Gartrell, MJ, JC Craun, DS Podrebarac and EL Gunderson. 1986. Pesticides, selected elements and other chemicals in adult total diet samples, October 1980 - March 1982. J Assoc Off Anal Chem. 69(1): 146-161.

The US Food and Drug Administration’s total adult diet studies estimate the dietary intake of selected pesticides, chemicals and elements by retail purchase and analysis of foods representative of adult diets. The results are reported by food groups. Average concentrations and maximum concentrations are reported.

4. National Institutes for Occupational Safety and Health. 1987. Registry of Toxic Effects of Chemical Substances. 1985-1986 edition. US Government Printing Office, Washington, DC.

Reports limited toxicological data (primarily acute exposure data such as LDS0s) and cites sources of toxicological data for about 88,000 substances.

5. New York State Department of Environmental Conservation. 1986. New York State Toxics Air Monitoring Report, 1982-1984. Bureau of Air Quality Surveillance. Albany, NY.

Reports maximum air concentrations of total PCBs, lindane and benzo(a)pyrene for 11 monitoring

sites across New York state.

6. New York State Department of Environmental Conservation. 1991. Draft New York

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State Air Guide - 1: Guidelines for the Control of Toxic Ambient Air Contaminants. Division of Air Resources. Albany, NY.

Provides guidance on concentrations in ambient air for about 470 chemicals. Both short-term and annual average concentrations are provided.

7. New York State Department of Environmental Conservation. 1995. New York State Ambient Toxic Air Monitoring Network 1992/1993 Data Addendum for Volatile Organic Compounds. Division of Air Resources, Albany, NY.

Outdoor air data for seventeen volatile organic compounds measured by the New York State Department of Environmental Conservation in 1992 and 1993. Samples were collected from ten air monitoring stations in rural, suburban, urban and industrial areas in New York State. Monthly, quarterly and annual averages are reported.

8. New York State Department of Environ Aldrin Chlordane

DDT & metabolites mental Conservation. 1996. 1994 Toxic Release Inventory (TRI) Data. (www.dec.state.ny.us/website/ppu/p2tri)

The TRI is a publicly available database that contains toxic chemical release and transfer data from manufacturing facilities in the U.S. Each year, certain facilities in New York State must report estimated releases and transfers of listed toxic chemicals to the US Environmental Protection Agency and to New York State. The TRI list includes 643 chemicals. Manufacturing facilities that meet the following criteria must report releases and transfers of listed chemicals.

. 10 or more full-time employees

. manufacturing or processing of 25,000 pounds of a listed chemical

° other use of 10,000 pounds of a listed chemical

. facilities in the Standard Industrial Classification (SIC) primary codes 20-39

The TRI provides data on releases to air, water and soil from these facilities for the listed chemicals. However, facilities who do not meet the above criteria do not have to report any releases and chemicals that are not on the TRI list do not have to be reported. There may also be problems with the accuracy of self-reported data.

9. New York State Department of Environmental Conservation. 1996. 1995 Annual New York State Air Quality Report, Ambient Air Monitoring System. Division of Air Resources. Albany, NY

Reports annual average outdoor air data for carbon monoxide, ozone, particulates, sulfur dioxide, nitrogen oxides, lead, arsenic, cadmium, mercury, nickel and vanadium. Air samples were collected at both continuous and manual (every sixth day) air monitoring stations throughout New York State in 1995 as well as, for some analytes, historical data from 1964 through the present.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page D-3

10. | New York State Department of Environmental Conservation. 1996. Spill Information System Annual Report, April 1995 - March 1996. Bureau of Spill Prevention and Response. Albany, NY.

Reports the number of spills and number of gallons spilled for 12 classes of petroleum products in New York state reported to the NYS DEC in fiscal year 1995-1996.

11. New York State Department of Health. 1997. Background Indoor/Outdoor Air Levels of Volatile Organic Compounds in Homes Sampled by the New York State Department of Health, 1989-1996. Bureau of Toxic Substance Assessment, Albany, NY.

Indoor and outdoor air levels for 57 VOCs are reported for 53 residences considered to have background levels of VOCs in air. Residences were selected as control homes after surveys to determine there were no unusual sources of VOCs in the home. Median, Sth percentile and 95th percentile values are reported.

12. New York State Department of Health. 1997. Cumulative Report, 1992 - 1995. Hazardous Substances Emergency Events Surveillance (HSEES). Bureau of Toxic Substance Assessment, Albany, NY.

A summary of the investigations of about 7,800 emergency events involving non-petroleum compounds resulting in spill data on 1,462 releases. Reports the number of spills, the amount spilled and the number of people injured for selected substances. Selected fields from the entire database (not published) were made available to the workgroup.

13. New York State Department of Health. 1998. Environmental Laboratory Data and Reporting System (ELDARS). Maintained by the Wadsworth Center for Laboratories and Research, Albany, NY.

Searches were made of the ELDARS database for results of drinking well water analyses for VOCs, metals, disinfection by-products and nutrients for the years 1980 to 1994. These well water samples were analyzed by the NYS Department of Health usually because of suspected contamination for some, but not all substances analyzed. Results are limited to those substances that are routinely analyzed. These data are not published.

14. New York State Department of Health. 1998. Health Advisories: Chemicals in Sportfish and Game, 1998-1999. Bureau of Toxic Substance Assessment, Albany, NY.

Advisories on consuming sportfish and game due to levels of chemicals that may be harmful to health. Reports specific water bodies in New York with advisories and the chemical(s) of concern for these water bodies.

15. Right-To-Know Network. 1994. TSCA Chemical Update System, 1990 (updated

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1994). (www.rtk.net)

Contains production levels of chemicals listed by the Toxics Substances Control Act. Data was collected from producers in 1990 and updated in 1994. Data on production volumes, chemical names, or company name and site can be claimed by the submitter as confidential business information (CBI or “trade secret”). CBI information is not available through this database. There are 25,000 records in the database and 16,500 do not report the production volume because it is CBI.

16. Shacklette, HT and JG Boerngen. 1984. Element Concentrations in Soils and Other Surficial Materials of the Conterminous United States. US Geological Survey Professional Paper 1270. US Government Printing Office. Washington, DC.

Reports the number of samples, averages and ranges of elements in the surface soils in the eastern US. Sampling sites were selected about 50 miles apart and with surface materials that were very little altered from their natural condition.

17. Suffolk County Department of Health. 1989. Status: Pesticide Sampling Programs 1980-1988. Bureau of Drinking Water.

Results of analyses of drinking water from wells in Suffolk County for 75 pesticides from 1980 to 1988. The number of samples analyzed are reported and the range and averages for detected pesticides are reported.

18. United States Agency for Toxic Substances and Disease Registry. (Various dates.) ATSDR Toxicological Profiles (for selected chemicals). (www.atsdr.cdc.gov/toxpro2)

These peer-reviewed documents are produced by the ATSDR to provide reviews on toxic chemicals. They provide summaries of data from the scientific literature on the toxicity, health effects, production, release, environmental levels and body burden for selected chemicals.

19. United States Environmental Protection Agency, 1988. National Ambient Volatile Organic Compounds (VOCs) Database Update. Research Triangle Park, NC. EPA/600/3-88/010a.

Data on 320 volatile organic compounds were compiled, critically evaluated and presented. Outdoor and indoor data are reported primarily form 1970 to 1987 from locations throughout the U.S. Averages, medians and quartile ranges are provided. The outdoor sites include remote, rural, suburban, urban and source-dominated. The indoor sites include residential, non-industrial workplace, and personal monitors. Differences in the studies (study design, laboratory procedures and equipment, sampling procedures) can affect the results.

20. United States Environmental Protection Agency. 1990. Final report of the nonoccupational pesticide study (NOPES) . Office of Health and Environmental

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Assessment. Research Triangle Park, NC.

Provides ranges of mean concentrations of 32 pesticides in indoor air in homes in Jacksonville, FL and Springfield/Chicopee, MA. Homes with high, medium and low pesticide use were sampled

21. United States Environmental Protection Agency. 1992. Pesticides in Ground Water Database: A Compilation of Monitoring Studies: 1971-1991, Region 2. Office of Pesticide Programs.

Groundwater monitoring data on pesticides from a collection of studies conducted by federal, state and local governments, the pesticide industry and private institutions. Samples were usually taken at the well, not at a consumer’s drinking water tap. Differences in the studies (study design, laboratory procedures and equipment, sampling procedures and well use) can affect the results. This is not a complete data set of all wells or studies.

22. US Environmental Protection Agency. 1998. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, OH. (www.epa.gov/iris)

Toxicological information on 536 chemicals maintained by the USEPA. Includes reference doses or concentrations, cancer potency factors, and supporting data and rationale used to develop these values.

23. World Health Organization. (Various dates). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans (various topics). International Agency for Research on Cancer. Lyon, France. (Database available at www.iarc.fr)

Provides classifications of carcinogenic properties of chemical substances that have been evaluated by IARC.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page D-6

Appendix E

Evaluation of Phthalate Esters by the New York State Department of Health

Final Report of the Human Health Work Group New York State Department of Environmental Conservation

Comparative Risk Project

May 2001

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Phthalate esters

As a result of public comment on the draft report of the HHWG, the steering committee requested the New York State Department of Health (NYSDOH) to evaluate phthalate esters. These compounds fall into the Semi-Volatile Organic Compounds stressor group, but the HHWG did not select any phthalate esters for evaluation. The NYSDOH evaluated phthalate esters using the same procedure as for other stressors. This evaluation was not reviewed or approved by the HHWG.

1. Steering Committee definition None 2. What are phthalate esters?

Phthalate esters are manufactured chemicals used to make plastics more flexible. They are oily liquids that evaporate slowly. Examples of phthalate esters include butyl benzyl phthalate (BBP), di-(2-ethylhexyl) phthalate (DEHP), diethyl phthalate (DEP), dimethyl phthalate (DMP), di-n-butyl phthalate(DNBP), and di-n-octyl phthalate (DNOP).

3. Sources of phthalate esters

Phthalate esters are found in plastic products such as table cloths, shower curtains, rainwear, shoes, baby pants, dolls, toys, food packaging, tools, garden hoses, pipes, wallpaper, floor tiles, furniture, carpet backing, automobile upholstery, paints, insecticides, cosmetics, hair spray, fingernail polish, toothbrushes, medical tubing and blood storage bags. Phthalate esters can be released very slowly from products, but environmental levels (air, water) are low. Exposure could come from children chewing on plastic toys and from food. Dialysis patients or people who need many blood transfusions have the highest exposures.

4. Environmental fate

Phthalate esters can evaporate very slowly from products and can be transported in air by sticking to dust particles. In the environment, phthalate esters can be released slowly from plastic products into the soil. They attach to soil and do not move far away from where they were released. They are oily liquids that dissolve very slowly into water or groundwater. In the presence of oxygen, bacteria in the soil and water can break down some phthalate esters into simpler chemicals. Some phthalate esters have been found to build up in animals that live in the water (algae, molluscs, crustaceans, insects and fish). However, organisms higher in the food chain more readily break down these compounds, reducing the accumulation of phthalate esters in the food chain.

The U.S. Centers for Disease Control (CDC) recently released monitoring data on seven phthalate metabolites in urine from a sample of the U.S. population. Levels of metabolites of

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page E-2

diethyl phthalate and di-n-butyl phthalate were higher than metabolites of other phthalates that are produced in greater quantities. These data have prompted CDC to focus research on the exposure to and health effects associated with these two phthalate esters. Phthalate metabolites were also found in higher concentrations than metals and organophosphate pesticide metabolites.

5. Health effects

Exposure to phthalate esters can occur through breathing, eating food, drinking water, receiving blood transfusions and chewing on plastic toys. The skin can absorb only a small amount of phthalate esters. Health effects from exposure to phthalate esters vary depending on the concentration of the substance and the length of time one is exposed to the substance. Phthalate esters are broken down by the body and most of the phthalate ester and the breakdown products leave the body. This process is not well understood for some phthalate esters. A small amount of the phthalate ester will remain in the body.

There are very few studies on human exposure to phthalate esters. Most data on health effects comes from studies of rats and mice. One concern about exposure to phthalate esters is cancer. The USEPA has classified di-(2-ethylhexyl) phthalate (DEHP) as a probable human carcinogen and butyl benzyl phthalate as a possible human carcinogen. Eating high doses of DEHP has caused liver cancer in rats and mice; however, studies show that the human liver reacts in a different way to DEHP than rodent livers. IARC has recently downgraded its classification of DEHP from a possible human carcinogen to “not classifiable” based on these studies. Some phthalate esters have not been thoroughly studied with respect to cancer.

Exposure to large amounts of phthalate esters have caused non-cancer effects in rodents. Large amounts of DNBP applied repeatedly to the skin may cause irritation. Exposure to large amounts of some phthalate esters (DEHP, DNBP, DEP ) in food has caused effects on reproduction and development (decreased sperm formation, delayed sexual maturity, decreased fertility, birth defects) and effects on the liver and kidney in rodents. The mechanism of toxicity on reproduction and development is not understood. There is some evidence that DEHP and, to a lesser extent, DNBP can effect the endocrine system. It is not clear if the reproductive and developmental effects seen after exposure to DEHP are caused by endocrine disruption.

6. Selecting stressors a. Identification of substances Several sources of information were used to identify possible stressors that could be

included in this group. All phthalate esters that appeared in the data sources listed below were screened for inclusion in this group.

. US Environmental Protection Agency (EPA) Integrated Risk Information System (IRIS): values listed are reference doses (RfD). . Toxic Substances Control Act (TSCA) Chemical Update System (CUS): values listed are

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page E-3

non-confidential volumes reported for chemicals that are manufactured, distributed, processed, used or disposed in New York. (The 100 substances with the highest volumes were screened.)

. New York State Department of Environmental Conservation (NYSDEC) Toxics Release Inventory (TRI): values are total releases (air, water, land). . New York State Department of Health (NYSDOH) Hazardous Substances Emergency

Events Surveillance (HSEES): values listed are number of emergency events in New York involving these substances from 1992 to 1996.

. International Agency for Research on Cancer, Monographs on the evaluation of carcinogenic risks to humans. 2001. . Agency for Toxic Substances and Disease Registry. Toxicological Profiles.

b. Criteria for selecting stressors

The following criteria were used to select substances from the data sources listed above for further evaluation.

. Any substance with a reported TRI release for New York.

. Any substance with a reported HSEES event in the past five years.

. Any substance with a TSCA CUS volume of any amount for New York

. Any substance with an IARC, EU, or EPA carcinogen rank above “not classifiable”. . Any substance with an ATSDR toxicological profile.

All selected stressors are identified in Table E.1 The goal was to select those compounds which present a greater risk of exposure to the public and those compounds with higher toxicity. There were little data on environmental monitoring for many phthalate esters. Release data (TRI), spill data (HSEES) and production data (TSCA CUS) were used as surrogates for exposure when screening and selecting stressors.

7. Ranking the selected stressors

The selected stressors were ranked by toxicity and exposure using the approach described in the methods section of the HHWG report. Data used to rank each substance are shown in Table E.1. In Table E.2, each stressor is ranked based on toxicity data and either environmental data (food), release data (TRI), production/use data (TSCA) or emergency events (HSEES), whenever these data were available. There was no single measure of environmental exposure which had data available for all substances. DEHP is shown more than once in Table E.2 to show the difference in rank based on the USEPA carcinogen classification versus the LOEL.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page E-4

Table E.1 Phthalate ester data table

Chemical EU | EPA |LOAEL | Health | Health EPA Cancer Air concen- Food Water NYS NYS | NYS |Emerg. | Tox- | Exponame Class | IRIS oral effect | effect | Cancer | weight of tration concen- | concen- | TSCA | TRI TRI |Events | icity | sure CAS (1) RfD | mg/kg/d | assoc | greatest | slope evidence ug/m3 tration tration CUS air water |HSEES | class | class number mg/kg/d | (2) with |concern | factor (EPA, ppb ug/L | production | release | release | 1992-96 (2) LOAEL (mg/kg/d) | IARC) Ibs/1994 J (Ibs/y) | (Ibs/y) |(5) (2) (2) (2,10) (3) (4) | 4 butyl none | 2E-1 470 | increase |cancer,} none |C possible 0 3 4 benzyl m Iver liver human, EPA | tri phthalate weight C not care 85-68-7 classifiable di-(2-ethyl | none | 2E-2 19 | increase | repro- | 1.4E-2 B2 2E-3 most 10 2238 1 0 3 2 hexyl) m Iver ductive, probable Outdoor | samples US loel | food phthalate weight’ I kidney, human, | Great Lakes | less than | surface 2 117-81-7 cancer onsite (6) 1000 water EPA ; (6) (6) care di-n-buty! none | 1E-1 | 600 [increased] repro- | none D not 3E-3 to — 140 to 570 ] 0.1 to 0.5 6520 | 2000 0 4 2 phthalate mortality | ductive classifiable 6E-3 fish and | US loel | food 84-74-2 (rats) Outdoor NY | seafood | drinking 40 (7) water (7) Indoor (7) diethyl none | 8E-1 | 3160 [decrease | develop-| none D not |4E-1 toS5E-1| 400to | 0.01 to 526 0 0 4 1 phthalate growth, ment classifiable | outdoor NJ | 1700 1.0 loel | food 84-66-2 in orean 1.6 to 2 fish MI US weights indoor NJ >1000 |drinking (8) foods in water plastic (8) (8) dimethyl none | none a repro- | none D not 3610 | 3 0 4 4 phthalate 6800 ductive classifiable LDSO| tri 131-11-3 mg/kg (1) diallyl none ora wat none none 403067 0 3 4 phthalate 770 mg/kg LDS50] tsca 131-17-9 a) tri di-n-octyl none | none | 2078 liver liver none none |6E-5 to 9E-4 <0.5 4 4 phthalate necrosis | reprod. Oregon EPA est loel | air, 117-84-0 (9) (9) water

Table E-2: Risk characterization matrix for phthalate esters

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toxicity rank

1 (highest) 2 3 4 (lowest)

exposure | | diethyl phthalate rank (food) lis highest 2 di-(2-ethylhexyl) phthalate di-(2-ethylhexyl) phthalate | *di-n-butylphthalate

> (food, USEPA carcinogen rank) | (food, LOEL) (food) 4is lowest 3

4 butyl benzyl phthalate di-n-octyl phthalate

(TRI) *diallyl phthalate (TRI, TSCA)

(water, air) *dimethy! phthalate (TRI)

* data source used for final ranking (see text)

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Page E-6

8. Discussion

Table E-2 displays the matrix that combines the toxicity and exposure rankings. Because there are sparse toxicological or exposure-related data for many substances, a lower rank should not mean that a substance should be ignored.

The USEPA and IARC classify di-(2-ethylhexyl) phthalate (DEHP) differently with respect to carcinogenicity (see the discussion in section 5). Because the IARC classification is based on more recent data, the NYSDOH used the IARC classification. However, the LOEL gave a higher rank for DEHP than did the IARC cancer classification, so the LOEL was used for the final ranking. The most common health effects of concern are on reproduction (affecting both males and females), the kidney, and the liver.

In general, the data indicate that the two highest routes of human exposure to phthalate esters are from blood transfusions (or dialysis) and from food (in fish, other seafood or from food in plastic packaging). When environmental data were available for a stressor, the exposure ranking was high, primarily due to levels in food. When environmental levels were not available, the exposure ranking was low, because release and use data were not high or they were unavailable. The rankings for the seven substances included in this group are shown in Table E-3.

Table E-3: Individual stressor ranks for phthalate esters

Rank Stressor

A

B di-(2-ethylhexyl) phthalate, diethyl phthalate

Cc butyl benzyl phthalate, diallyl phthalate, di-n-butyl phthalate, dimethyl phthalate, di-n-octyl phthalate

The CDC recently reported that phthalate metabolites were also found in higher concentrations in human urine than metals and organophosphate pesticide metabolites. Although the HHWG did not have criteria for ranking exposure based on human biomonitoring, these data indicate that human exposure to phthalates is higher than exposure to many metals and pesticides, and also higher than the exposure rank suggested by the limited environmental and other surrogate exposure data cited above. If the exposure ranking for each phthalate ester was increased by one increment based on the human monitoring data, the ranking would appear as in Table E-4.

NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page E-7

Table E-4: Individual stressor ranks for phthalate esters, increased due to human monitoring data

Rank Stressor

A di-(2-ethylhexyl) phthalate

B diethyl phthalate, butyl benzyl phthalate, diallyl phthalate, di-n-butyl phthalate Cc dimethyl phthalate, di-n-octyl phthalate

9. Recommendations

. More toxicological data would be useful to better evaluate the potential effects of these substances, particularly on human reproduction.

. More and better environmental monitoring data (including levels in food and in stored blood for transfusions) are needed to properly characterize possible human exposure to these substances.

. Three phthalates (di-(2-ethylhexyl) phthalate, di-n-butyl phthalate, and diethyl phthalate) should be given special attention because of their potential for exposure or potential to cause health effects.

10. Ranking phthalate esters as a group

Given the limited exposure information on phthalate esters, human monitoring data should be taken into account and the ranking should be as shown in Table E-4. The data indicate that although there may be a considerable amount of exposure to phthalate esters, the toxicity of these compounds has not been shown to be as high as some other stressor groups. Therefore, a group rank of “B” is justified. However, some individual phthalates (di-(2-ethylhexyl) phthalate, di-nbutyl phthalate, and diethyl phthalate) are of greater concern than the group as a whole.

11. References 1. EINECS Plus CD. 1996. European inventory of existing commercial chemical substances and European list of notified chemical substances. Silver Platter Information, Ltd. London,

UK.

2. US Environmental Protection Agency. 1997. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, OH. (www.epa.gov/iris)

3. RTK Network, 1997. TSCA Chemical Update System (CUS). The Right to Know Network. Washington, DC. (www.rtk.net)

4. New York State Department of Environmental Conservation. 1996a. SARA Title III, Section 313, 1994 TRI Data as of 11/18/96. Chemical list by total amount. NYSDEC. Albany,

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NY. (www.dec.state.ny.us/website/ppu/p2tri)

5. New York State Department of Health. 1997. Hazardous Substances Emergency Events Surveillance (HSEES). 1992-1996. Bureau of Toxic Substance Assessment. Albany, NY.

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NYSDEC Comparative Risk Project - Human Health Work Group Final Report May 2001 Page E-9

Publication citation

Human Health Work Group, including RA Michaels. Final Report of the Human Health Work Group of the New York State Department of Environmental Conservation Comparative Risk Project. Albany, New York; NYS DEC, 308 pages, May 2001;

Robert A. Michaels on ResearchGate