Health Risks Support A One-Hour Airborne Particle Standard with Data Acquisition Via Rapid Automated Monitoring Instrumentation’ -
Robert A. Michaels RAM TRAC Corporation 3100 Rosendale Road Schenectady, NY 12309
ABSTRACT
Recently evinced associations of mortality and morbidity in communities with currently permissible particle mass levels have motivated reconsideration of EPA’s particle standard. EPA must decide whether to regulate lower levels, challenging toxicological plausibility. This study inquires whether 24-hour average particle levels might encompass undetected, toxicologically significant excursions.
‘Two monitoring technologies--inertial and beta attenuation--were found for measuring particle excursions. Data revealed numerous excursions, one reaching 2,000 g/M3, twice that of the 1952 London fog. Toxicology literature confirmed the harmfulness of brief exposure to particles in the range of observed excursions. However, EPA has focused upon protracted rather than short-term toxicological causes. This study suggests that short-term mechanisms may cause the unexplained effects. Particle excursions are followed by prolonged internal exposure of lungs which cannot efficiently clear fine particles. Prolonged internal exposure may correlate with prolonged, potentially lethal, cardiopulmonary stress, especially for the frail elderly and infirm.
This study supports the recommendation that EPA further consider a one-hour particle standard, despite Agency uncertainty that “the majority of effects” observed after daily exposure would occur after
briefer exposures. A one-hour mass limit of 300 pg might enhance protection against acknowledged short-term effects, avoiding a burdensome change in the 150 ug 24-hour mass limit.
INTRODUCTION
At Court direction, the U. S. Environmental Protection Agency (EPA) is reviewing the National Ambient Air Quality Standard (NAAQS) for airborne particles (1, 2, 54, 55). The present NAAQS limits particulate matter within a diameter of 10 microns (PM ) to a time-weighted average mass limit of 150
pg of air over 24 hours (and 50 pg annually). It is based primarily upon epidemiological associations of particle elevations during air pollution episodes with elevated mortality and morbidity in communities (for example, see 18, 44, 45). Particle levels during the 1952 London fog have been
estimated at 1,200 pg (53; PMyg $1,200 gM). Recent studies associate significant elevations of
morbidity and mortality with particle levels well within the NAAQS (reviewed most recently by EPA, 1995; 60), and below levels which can be explained by known toxicological mechanisms. The EPA must soon decide whether to control airbome particles to levels below those of demonstrated toxicological significance, and risk further legal challenge.
EPA’s Clean Air Science Advisory Committee (CASAC) advised the EPA to explain the basis for averaging times specified in the airborne particle standard (14):
“A number of the Panel members noted the absence of a sixth link, namely, the rationale for using a 24-hour averaging time for the NAAQS... The justification for using any specific averaging time, including a 24-hour averaging time, is not established” (source document, page 3).
———————— . This research was supporied by Ruprecht & Patashnick, Inc.; Albany, New York.
In response, the Agency considered applying a longer averaging time of up to several days and a shorter averaging time, such as one hour (57-60). The present study inquires whether 24-hour average particle levels educed via the U. S. EPA reference gravimetric monitoring method might encompass undetected shorter-term excursions sufficient to explain the observed adverse effects.
METHODS
The method of investigation consisted of evaluation of available analytical data and literature to resolve three technical issues. First, the study determined whether instrumentation is available to reliably and economically measure particle levels over short intervals. Second, it quantified short-term excursions of particle mass contributing to 24-hour averages well within the NAAQS. Third, it assessed the likely toxicological adequacy of such excursions, considering their relatively brief persistence, to cause mortality and/or morbidity.
The findings regarding the three issues elucidated above were evaluated relative to EPA policies and procedures for air pollutant standard setting under the Clean Air Act (3, 56) based upon the weight of evidence for the existence, nature, and magnitude of public health risks. Ultimately, the findings were evaluated relative to a major regulatory issue facing state health departments and the U. S. EPA. That issue is, in view of currently available data and instrumentation technologies, whether public health protection can be assured via the current airborne particle risk management approach, which limits particle excursions only to the degree that they produce exceedances of 24-hour and annual mass limits.
FINDINGS
Identification of Monitoring Technologies
Tworelatively new particle monitoring technologies were found to be capable of reliably measuring airborne particle levels in real time or over short intervals (15, 16, 35-38, 43, 46-51, 58). Inertial monitors can measure particles virtually continuously, whereas beta attenuation monitors can do so over intervals of an hour or less under realistic conditions. Both technologies represent alternatives to the reference gravimetric method for monitoring airborne particles. The technologies reflect evolution of the older technologies most notably in three directions: 1. toward greater sensitivity associated with utilizing non-gravimetric physical principles for measurement; 2. toward continuous monitoring and reduced sampling time; and 3. toward greater automation and reduced expense of operation. Indeed, inertial instruments are deployed in the U. K. Automatic Urban Network (AUN), gathering particle data with a 15-minute time resolution (50). Using this short time resolution, AUN posts on the Internet one-houraverage values, updated hourly, at monitors in 18 cities (http:/ /www.aeat.co.uk/products/centres/netcen/ airqual/bulletins/pm10.html), adding power to ongoing U. K. studies of particle health effects.
Greater sensitivity of non-gravimetric instrumentation. Technologies for measuring particles have traditionally involved collection on a filter and measurement of the difference in filter weight before and after a known volume of air has been drawn through it. This traditional technology relies upon gravity to cause particles to affect a balance in proportion to their mass. The technology requires a relatively long period of time for sampling, depending upon the ambient particle level, to assure collection of particle mass sufficient to register accurately using an instrument of specified sensitivity known as a mass balance (or microbalance, for small samples).
One relatively new technology utilizes an inertial system of mass measurement (35, 36-38, 43, 46, 47, 50, 51). Inertial mass measurement relies upon the naturally constant frequency of an oscillator, like a tuning fork, of fixed length and mass (43). A filter of known area is placed at the free end of a hollow tapered glass tube which is mechanically oscillated in a clamped-free mode. A detector quantifies redaction in the frequency of the oscillator, which occurs in proportion to the particle mass captured on the filter.
Another relatively new technology utilizes the phenomenon of beta radiation attenuation to measure particle mass. Beta attenuation utilizes a source which emits beta particles, which are either electrons (in practice) or positrons (in principle). A detector is placed at some distance from the source, and the source is measured while a strip filter is interceded to collect particles. As particles accumulate, they absorb beta emissions, attenuating the signal detected in proportion to the particle mass.
Increased automation. Both the inertial and beta decay detectors described above are relatively more automated than gravimetric detectors. The trend toward increased automation of monitoring _ equipment applies more broadly than to mass measurement alone. Indeed, reduced manual labor in particle sampling and analysis might enable routine monitoring of (non-speciated) particle-borne volatile and semivolatile organics along with mass measurements at a cost comparable to that of labor-intensive sampling now prevalent for use in particle measurement. According to the U. S. EPA (58):
“The initial cost of an automated sampler is typically 2-3 times that of a manual, single channel PM jg sampler, but can be offset by the savings in operator labor costs” (source document, page 4-30).
Continuous monitoring and reduced sampling time. The inertial and beta attenuation detectors selected for description above are both essentially continuous particle mass monitors. The inertial instrument appears to be more sensitive than the beta attenuation instrument because the amount of particle mass accumulation needed by the latter to accurately measure beta attenuation is greater than that required by the former to detect oscillation frequency reduction. Relative to the beta detector, therefore, the inertial instrument represents a more perfect continuous monitor, inasmuch as it requires less sampling time to elapse before a significant mass response will be recorded. Nonetheless, both detector types respond in minutes compared with the gravimetric hi-vol detector, which may require hours to collect a reliably measurable sample under ordinary ambient conditions. The trend toward reduced sampling time and continuous monitoring facilitates routine and economical short-term airborne particle mass monitoring with respect to selected particle size windows in the respirable range.
Airborne Particle Excursions
Data sets were screened to identify those which 1. were obtained using one or both of the identified technologies, 2. exhibited short time resolution, 3. encompassed at least one 24-hour period, and 4. revealed 24-hour airborne particle levels well within the current NAAQS. Screening identified
three locations, and 10 days, during which 24-hour average PMjq < 150 mg/M3, At all three locations,
and in six of the 10 identified cases meeting the screening criteria, excursions exceeding 150 pgs were noted (Table 1; Figs. 1-3).
In Birmingham, Alabama on 16 April 1990 24-hour average PMj9 was 70 pe/M3, but two one-
hour-average excursions exceeding 200 pgyM3 were recorded (Table 1; Fig. 1). In Penticton, British Columbia on approximately eight days between 30 July and 7 August 1994 24-hour average PMjq varied from close to zero to close to 150 ne/M3, but excursions exceeding 150 pg were recorded on four of the eight days (Table 1; Fig. 2). These included three one-hour-average excursions to 300 pg3 and two excursions to approximately 500 pe/M3. In Zeebrugge, Belgium on 15 March 1993 24-hour average PM4q was 101 pg/M3, but several 15-minute-average excursions exceeding 200 pg/M3 were recorded
(Table 1; Fig. 3). In one excursion, the 15-minute average reached 2,000 gM, significantly exceeding the estimated magnitude, though not the persistence, of the 1952 London fog (S1,200-ug/M3; 53).
Toxicological Significance
Toxicology literature was evaluated, confirming that high particle levels in the observed range of measured fine particle excursions can cause adverse respiratory effects. Numerous studies of short-term effects exerted by airbome particles during controlled acute human exposures were identified. Many of these reported positive results (4, 7-12, 17, 19-22, 25-32, 34, 40, 61, 62, 64). Table 2 exemplifies the positive studies, ranking the tabulated examples, along with findings of daily mortality studies (for example, see 18) and the current PM 1 standard (55), in order of increasing dose times exposure duration.
Table 2 indicates that adverse particle-associated health effects have been demonstrated beginning at levels as low as 202 pg (64) and at exposure durations as short as 30 minutes (62, 64). These effects
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Fig. 1. Hourly PM16 April 1990 with a 2
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Data provided by Rupprecht & measurements. Conf. on The Role of Meteorology in Managing the Environment of the 90s. Scottsdale, Arizona; 26-28 January 1993.
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Fig. 2. Hourly and Daily PM,9 Concentration In Penticton, British Columbia, 30 July to 7 August 1994*
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Rupprecht, E., M. B. Meyer, and H. Patashnick. Performance characteristics of a near realtime particulate mass monitor. Presentation at Conference on Particulate Matter: Health and Regulatory Issues. Pittsburgh, Pennsylvania 4-6 April 1995.
ig. 3. Time Variation of 15-Minute Average PM-10; Zeebrugge,
um; 15 March 1993 (24-Hour Averag 01 j1g/cu Meter)*
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1 time of day (24-hour clock) Pic 7s
With permission from the source: Institute of Hygiene & Epidemics, Belgium yy
Table 1. Short-Term Particle Excursions Without Exceedance of the 24-Hour PM-10 Standard -
24-hour airborne excursion excursion- ‘excursionaverage particle averaging to-24-hour——to-1952 particle mass time ‘mass London-Fog mass excursion ratio ratios
agicoM) GgfeuM) (minutes)
1gge, Belgium 1 3/53 101 1,898 15 18.8 16 Penticton, British Columbia 3 Tp1pA 50 500 60 100 04 gge, Belgium 1 31Sp3 101 780 15 1 07
ge, Belgium 1 3nsp3 101 os 15 64 0s
sege, Belgium 1 3nss3 101 353 15 5S os Penticton, British Columbia 3 ans 100 460 60 46 4 gge, Belgium 1 3583 101 425 15 42 04 ebrugge, Belgium 1 3/593 101 355 15 35 03 Penticton, British Columbia 3 sips 100 320 60 32 03 Birmingham, Alabama 2 46/90 70 m2 60 32 02 Birmingham, Alabama 2 4/1690 0 208 60 30 02 Penticton, British Columbia 3 8np4 120 350 60 29 03 enticton, British Columbia 3 84 100 280 60 28 02 -brugge, Belgium 1 3593 101 283 15 28 02 Birmingham, Alabama 2 4/1690 70 116 60 25 01 Penticton, British Columbia 3 814 120 290 60 24 02 e, Belgium 1 3/1593 101 28 15 24 02
-brugge, Belgium 1 3593 101 230 15 23 02 brugge, Belgium 1 3/1593 101 20 15 22 02 -brugge, Belgium i 3593 101 20 15 22 02 Penticton, British Columbia 3 82/94 120 250 60 24 02 Penticton, British Columbia 3 8894 120 240 60 20 02 brugge, Belgium 1 3/1593 101 195 15 19 02 sage, Belgium 1 3593 101 193 15 19 02 brugge, Belgium 1 3s93 101 185 15 18 02 nticton, British Columbia 3 80194 120 210 60 18 02 3c, Belgium 1 3SB3 101 153 15 15 on
Birmingham, 3/1 day; Penticton, 9/9 day 15/1 day
ean excursion (ig/cu M) 99 373 03 standard deviation (jug/cu M) 7 342 03 ficient of variation z 7 1 2
fraction exhibiting excursions 1.00 days examined 10 fraction exkibiting excursions
1. Institute of Hygiene and Epidemics, Belgium;
lo. Meyer, M. B. Applications of continuous PM-10 measurements. Conference on the Role of Meteorology In Managing the Environment of the 90s. Scottsdale, Arizona; 26-28 January 1993;
1s. Rupprecht, E.; M. B. Meyer, and H. Patashnick. Performance charactetistcs of a near real-time particulate mass moniter. Conference on Particulate Matter: Health and Regulatory Issues; Pittsburgh, Pennsylvania; 4-6 April 1995.
I++ Conservatively assumes London fog = 1,200 pg/cu M, but this estimate is probably total particulates rather than only PM-10.
‘The deaths of approximately 4,000 people over 10 days in 1952 have been attributed to the London fog (see text for source).
Table 2. Particle Effects Revealed In Controlled Acute Human Exposures
[citation] healthy ] asthmatic | activity | subject [particle MMAD dose] duration dosex Jeffect(s) tol subjects | subjects | level_| age span |type(s) i) duration = Y_f- (eM) | ug/euM) | Grind [ug min/ca MO) 4 F healthy: no effects aa ona] 25 atrest | 23-48 |TSP 202 30 6,060 asthmatic: reduced lung ang, function (FEV1)_ peste G 15 exercise 19-50 |Nacl, H2S04,NH3 | 0.80 700 30 21,000 reduced lung function (FEV1) pore ar) 7 exercise | 20-57 |NaCl, H2S04 190 120 22,800 —_|reduced lung function (FEV1)] Green, _et| . factivated carbon + cough, reduced hung fanction| 2 24 0 exercise 18-35 formaldehyde 14 1,020 120 122,400 (FVC, FEV3, peak flow) 72,000 -|daily mortali id i i [om fom | wm tow yo | 50-100| 1,440 |, 7 y mo an 144,000 ‘morbidity begin ove a ase ae wee oy 10 150 1,440 216,000 |NAAQS for PM-10 ee we 0 exercise} 20-39 |Nacl+ H2s04 09 2,000 120 et =o en ane et al, 1992 lung function Balmes, et] 641 (9,900,000 to} = increased specific airway al. 1988 0 12 at rest 25-41 |NaCl,30mOsm 53-61 187,100,000 25,900,000 aletancs ‘citations:
1. Balmes, J. R., et al. Acidity potentiates bronchoconstriction induced by hypoosmolar aerosols. American Reviews of Respiratory Disease, 138:35-9, 1988; 2. Framptom, M. W., etal. Sulfuric acid aerosol exposure in humans assessed by bronchoalveolar lavage. American Reviews of Respiratory Disease, 146:626-32, 1992; 3. 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; 4. 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; 5. 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;
6. Yang, SC, and S-P. Yang. Respiratory function changes from inhalation of polluted air. Archives of Environmental Health, 49:182-7, 1994,
[=MMAD: mass median aerodynamic diameter
were documented in asthmatics at rest (64) or engaged in exercise (62). Participant ages in these studies varied from 19 to 50 (62) and 23 to 48 (64). Thus, no frail elderly, elderly, or infirm subjects were included in the studies. Other positive studies likewise involved asthmatic subjects exercising or at Test, of ages up to 57 years (12, 21, 25, 40). For obvious 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 (FEV, 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, one epidemiological study will be cited, constituting evidence favoring short-term toxicological mechanisms for inducing morbidity and mortality which may persist for days after an air pollution episode. Specifically, Lawther, et al. (1970; 33) used a diary method in which bronchitis patients recorded daily changes in the severity of their symptoms telative 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” (source document, page 538), which may be several times the 24-hour average (63) which served merely as a surrogate parameter for such excursions.
The studies described above demonstrate adverse health effects induced by short-term exposure to particles. However, the evaluation of the toxicological significance of responses which were precluded from progressing to clinical significance will also benefit from an inquiry into the possible mechanism(s) of toxicological action producing the demonstrated effects. Elucidation of plausible mechanisms might enable prediction of the clinical significance of similar exposures, or of exposures which are not terminated in a timely manner (as part of an experimental protocol), to more susceptible individuals.
Only a single toxicological principle need be invoked to demonstrate that brief airborne exposures may be more toxicologically, and more clinically, significant for some individuals. Briefly intense airborne exposures may deposit an overwhelming number of particles per alveolar macrophage cell, inhibit particle clearance, and result in protracted intemal pulmonary exposures. The duration of such exposures will be inversely proportional to the fine particle clearance rate. Individuals whose lung function is compromised may clear fine particles less efficiently and less rapidly than normal individuals under identical exposure conditions, increasing their effective exposure to fine particles, as indicated by Miller, et al. (1995; 39). They reported differentials favoring higher exposure of individuals having compromised respiratory systems, including approximately three-fold increases in the number of 1-11 particles deposited per unit of respiratory surface area, per ventilatory unit, per alveolus, and per alveolar macrophage cell. They also reported similar findings with respect to 0.1-11 particles.
Prolonged internal exposure to fine particles may correlate with irritation and prolonged, potentially lethal, reductions in the alveolar surface area available for gas exchange, and therefore in the efficiency and rate of gas exchange. These challenges may result in cardiopulmonary stress, possibly provoking episodes of apnea and cardiac arrhythmias, especially for the frail elderly, the infirm, and generally for individuals suffering from preexisting respiratory disease (especially if severe). These factors, and possibly increased susceptibility to airborne pathogens (52), suggest the likelihood that short-term adverse effects observed at subclinical intensities in young asthmatics whose cardiopulmonary health is otherwise robust may be exacerbated in older individuals suffering from preexisting health deficits.
Elucidation of toxicological mechanisms by which fine particles induce adverse health effects observed clinically has been incomplete because of a dearth of animal models (53). However, investigations into airborne particle-induced effects on rats and dogs are reported under way at Harvard University’s School of Public Health, and are closing this data gap. The ongoing research has been published in abstract form (24, 41, 42), and more completely in oral and written reports by John Godleski to CASAC (23). The findings implicate short-term, possibly electrophysiological mechanisms of fineparticle-induced cardiopulmonary malfunctioning, shown via electrocardiograms (EKGs).
Nearing, et al. (42) induced ST segment elevation and periods of apnea in dogs inhaling fly ash at 1,000 pe/M3 for 3d, 4 h/d. Nearing, et al. (41) also demonstrated increased T-wave alternans amplitude,
indexing vulnerability to ventricular fibrillation, in dogs inhaling fly ash at 3,000 pe/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.
Godleski, et al. (23, 24) used rats exhibiting either monocrotyline-induced pulmonary inflammation or SO-induced chronic bronchitis. Rats with respiratory pathology then inhaled particles
concentrated from Boston air at 228 to 288 pgm for 3 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 (23) 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.
CONCLUSION AND DISCUSSION
The findings of this study form the basis for drawing one principal conclusion about the airborne particle issue, Specifically, this study suggests that known toxicological mechanisms may explain observed associations of airborne particles with mortality and morbidity if exposure is scrutinized over an appropriately short time frame. Several implications arise from this conclusion.
The U. S. EPA’s current NAAQS requires averaging PM mass over 24 hours and one year,
precluding both detection and control of shorter-term exposures, which appear to be toxicologically significant. However, the Agency has not proposed to incorporate an airborne particle mass limit averaged over a shorter time than 24 hours (57). Indeed, the Agency’s response to CASAC’s advice to justify its averaging times suggests confusion between the averaging time appropriate for health effect causation (and prevention) vs. health effect detection:
“The current 24-hour averaging time is consistent with the majority of the results from community epidemiological studies, which have reported associations of 24-hour concentrations of PM 19, fine particles, and TSP {total suspended
particulates] with an array of health effects. Nevertheless, because some such studies have found g stronger association with a multiple day average... the Staff considered whether a multiple day averaging time would be more appropriate... The 24-hour averaging time effectively protects against episodes lasting for several days while also protecting sensitive individuals who may experience effects after a single day of exposure. Thus, the staff concludes that a longer averaging time, such as 3 to 5 days, would not provide more effective protection than a 24-hour average” (source document, page VI-2; emphasis added).
The time frames over which adverse health effects are caused vs. manifested commonly bear little if any relation to one another. For example, a bullet wound may represent a nearly instantaneous cause of death. Alternatively, death may occur days after the instantaneous causal event. Likewise, diseases may result from instantaneous exposures to pathogens, but pathology typically develops after a significantly longer incubation period, and death (if it occurs) may occur over still longer time frames bearing no relation to the duration of the exposure event.
In the case of airborne particle associated health effects, exposure occurs at some background intensity over long periods, and episodically at sometimes lower and sometimes higher intensities. To
illustrate, Figure 4 depicts exposure to a 24-hour average PM of 100 ug with a brief (15-minute) excursion to 1,000 ng, approximately equivalent to that attained during the 1952 London fog (53), and approximately half that actually observed in the present study (Fig. 3). Figure 4 also illustrates the
ensuing process of particle accumulation in the lungs, and the slower rate of particle clearance. Finally, alternative time courses for the manifestation of adverse health effects are shown.
Three similar peaks represent possible one-day, two-day, or three-day delays in postexposure mortality, similar to delays reported in some epidemiological studies. Inasmuch as no prior knowledge
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may be assumed of the occurrence or length of any delay, a shallower curve is also depicted showing the statistical effect of averaging (‘curve smoothing’) over a three-day period. The curve illustrates that the longer-term averaging strategy offers a higher probability of encompassing a delayed mortality peak, if it occurs, whether it occurs after one, two, or three days postexposure. However, this benefit is offset by the reduced height of the curve, showing that each 24-hour mortality peak will be diluted over a 72-hour period. This will reduce the probability of statistically identifying a 24-hour peak due to its dilution with (ideally) a 48-hour period of background mortality incidence.
The purpose of the airborne particle standard, as suggested by Figure 4 and the above analysis of multiple-day averaging, is not to assist epidemiologists to detect health effects, but to prevent health effects from occurring. This should reduce attention to curve smoothing and the time frame for health effect detection, focusing it instead upon shorter time frames for health effect causation and prevention. EPA’s Criteria Document addresses the time frame issue for health effect causation (58). However, short-term health effects are excluded from consideration. Indeed, the document prefers the hypothesis of long-term
causation:
“One of the best indications that there is a longer-term effect of PM is that the relative risks estimated in the long-term mortality studies are considerably larger than those in the acute mortality studies... This suggests that the long-term studies include the excess deaths inferred in acute studies, and also include some of the excess deaths attributable to air pollution that may occur during low-pollution baseline periods, and would not be inferred by the acute mortality studies” (source document, page 1-36),
Clearly, particle-induced health effects must be cumulative, so that exposures of longer duration will be associated with greater risks. This is widely accepted to be the case, for example, with respect to cigarette smoking. However, the issue of whether long-term or short-term risks are greater is irrelevant. The relevant issues are 1. whether excursion-associated relative risks correlate with sufficiently high absolute risks to public health to merit management via the NAAQS (already decided), and 2. whether observed mortality and morbidity can be plausibly explained without invoking short-term mechanisms of causation.
One implication of the present investigation is that the Agency should further consider the shortterm causation scenario in the context of standard setting, and indeed it does in the Staff Paper (57), as follows:
“The staff has also considered the evidence regarding effects nae with PM exposures of durations less than 24 hours. Some investigators ta the 1987 review Lawnher. tal. 1970) speculated ta the observed heath effects might be largely due to short-term peaks on the order of an hour. Controlled human and animal exposures to specific components of fine Particles, such as acid aerosols, also suggest that some effects, such as bronchoconstriction, can occur after exposures of minutes to hours. Some epidemiological studies of exposures to acid aerosols have also found changes in respiratory symptoms in children using averaging times less than a 24-hour period (e.g., 12 hours). However, it is not clear whether the majority of effects that have been associated with daily exposure to PM, including mortality and various measures of morbidity, would occur after only short duration exposures. Moreover, q 24-hour average can be expected to provide
significant protection from potential effects associated with short-duration beaks in most urban atmospheres.” (pp. VI-2 to VI-3, emphasis added).
Thus, EPA rejects short-term causation and, concomitantly, a one-hour mass limit, based upon three incorrect premises: 1. that Lawther, et al. (33) merely “speculated” that peak exposure rather than 24-hour exposure exacerbated bronchitis among the subjects of their investigation, 2. that standards for air pollutants must be based upon a “majority” of observed effects rather than just the one effect occurring at the lowest exposure level, and 3. that a 24-hour averaging time will protect against excursions, which is refuted by the present investigation. The Lawther, et al. study is further evaluated below.
Lawther, et al. (1970)
Lawther, et al. (1970; 33) did not merely “speculate” that exacerbation of bronchitis symptoms among their patients was caused by peak rather than 24-hour exposure. Rather, consistent with (later) EPA airbome pollutant standard setting under the Clean Air Act (see below), they drew the conclusion based upon clinical data on normal subjects. The relevant portion of the Lawther, et al. report follows:
“One further reservation is that 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 gia of sulphur dioxide
together with 250 pgiM3 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” (source document, page 538; emphasis added).
Finally, the EPA Criteria Document (60) accepts as valid the Lawther, et al. findings:
“The analysis of the Lawther et al. (1970) study was made prior to the availability of current statistical methods such as Poisson regression using generalized estimating equations. The large differences seen by Lawther et al, (1970) at high levels would undoubtedly remain significant regardless of the analysis technique” (subject document, pp. 12-109 to 12-110).
EPA Airborne Pollutant Standard Setting
The findings reported in epidemiological and controlled human exposure studies must be evaluated relative to EPA policies and procedures for air pollutant standard setting (3, 56) based upon the weight of evidence for the existence, nature, and magnitude of public health risks. The Agency requested the American Thoracic Society to define toxicological effects, and degrees of effect, which might qualify as forming the basis for limiting air pollutants, and both the American Thoracic Society (1985; 3) and the U. S. EPA (1989; 56) have published these guidelines. Their implementation leaves much to the discretion of the implementer, but the guidelines are prescriptive and valuable nonetheless.
According to U. S. EPA policy (56), air pollution limits must be set based upon a clinically significant adverse effect, not any effect, as defined by American Thoracic Society (3):
"We define ‘adverse respiratory health effects’ as medically significant physiologic or pathologic changes..." (source document, page 666).
Many of the controlled human exposure studies focus upon asthmatics during exercise and at rest. These studies, described earlier in Table 2 and associated text, reveal symptoms of asthma exacerbation such as bronchoconstriction, increased airway resistance, reduced FEV and FEV3, reduced FVC, and
reduced peak flow. The issue of whether these effects can form the basis for air pollutant standard setting under EPA’s Clean Air Act implementation policies and procedures is resolved by the American Thoracic
Society:
"[I]t is important to consider differences between statistical significance and medical or biological significance... Not all [statistically significant] changes (e. g., physiologic) are necessarily adverse... [For example, according to the US EPA] the eye, nose, and throat irritation associated with ... urban ‘smog’ or photochemical oxidant air pollution is not medically important and is, therefore, not considered an ‘adverse health effect’ in relation to the Clean Air Act. This irritation certainly is annoying or bothersome, which puts it in the category of an effect on human welfare. However, irritation that triggers an asthmatic attack is an
adverse health effect. The EPA has portrayed this pollution burden (figure 1) by indicating the proportion of the population that might be affected... [and] anarea of responses that might be considered adverse” (American Thoracic Society 1985, page 666; 3; emphasis added).
Clearly, the symptoms evoked by controlled clinical exposures as described and tabulated (Table 2) above do not include triggering an asthmatic attack. However, according to EPA and American Thoracic Society guidelines, this clinical endpoint need not be experimentally induced to be used in standard setting. Rather, the guidelines justify inferring greater severity of response with greater exposure. The American Thoracic Society, quoted above, continues as follows:
This spectrum of biologic responses would be evoked more strongly as the concentrations of pollutants are increased" (American Thoracic Society 1985, page 666; 3; emphasis added).
The U. S. EPA has proposed to regulate PM) 5 rather than PMy (57). This proposal is irrelevant
to the present findings made or conclusions drawn. Effects exerted by particles are widely acknowledged to result predominantly from the most respirable (fine) fraction. PM 49 excursions undoubtedly
encompass excursions of PM 5. Thus, the 24-hour PMj9 standard of 150 pe can be expressed as
an equivalent one-hour standard of about 300 pg/M3, which may be in turn formulated as a one-hour PM2_5 mass equivalent if the NAAQS focus changes.
The present investigation has revealed that 1. significant airborne particle excursions occur over brief intervals of duration 15 minutes to one hour, 2. such excursions are potentially significant toxicologically, and 3. the effects caused by short-term exposure to particles constitute appropriate clinical bases for standard setting under the Clean Air Act. These findings add to the risk management options available to the EPA. The EPA must soon decide whether to risk further legal challenge by managing airbome particles to levels below those of demonstrated toxicological significance. The present investigation enables the Agency to reject standard setting in the absence of demonstrated statistical and clinical significance of the health risks being managed. Alternatively, the Agency can manage airbome particle risks based upon statistically and clinically significant public health endpoints, avoidance of which i consistent with EPA policies and procedures for airborne pollutant standard setting under the Clean Air
Ct.
The cost of NAAQS compliance is large, and will increase if the 24-hour airborne particle mass limit is revised downward. The cost to the Agency will be large if the proposed standard is legally challenged, and larger if it does not prevail. Compliance with a one-hour mass limit would be less burdensome because it would primarily affect equipment start-up and shutdown rather than constant facility operation. The present study suggests that a one-hour limit may eliminate the need to strengthen longer-term limits while being: 1. more effective at protecting health, 2. justified by available data, and 3. economically feasible.
LITERATURE CITED .
1.
10.
ll.
12.
14,
15.
16.
is 18. 19. 20. 21. 22; 23.
24,
25.
American Lung Association. Complaint ina civil case: American Lung Association Vs. Carol Browner, U. S. EPA; U. S. District Court, District of Arizona, Case No. CIV-93643-TUC-ACM, 11 pp., 12 October 1993;
american Lung Association. The Perils of Particulates. New York City, 24 pp., March 1994;
American Thoracic Society. Guidelines as to what constitutes an adverse respiratory health effect, with specific reference to epidemiologic studies of air pollution. American Reviews of Respiratory Disease, 131:666-8, 1985;
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;
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;
Aris, R., et al. Lack of bronchoconstrictor response to sulfuric acid aerosols and fogs. American Reviews of Respiratory Disease, 143:744-50, 1991b;
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, 1988;
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;
Avol, E. L., ef al. Respiratory responses of young asthmatic volunteers in controlled pate to sulfuric acid aerosol. American Reviews of Respiratory Disease, 142:343-8, 1990;
Balmes, J. R., et al. Acidity potentiates bronchoconstriction induced by hypoosmolar aerosols. American Reviews of Respiratory Disease, 138:35-9, 1988;
CASAC. Letter from George T. Wolff, CASAC Chairperson, to EPA Administrator Carol M. Browner transmitting CASAC comments on the April 1995 draft Air Quality Criteria for Particulate Master. Washington, DC; Clean Air Science Advisory Committee (CASAC), EPA-SAB-CASAC-LTR-95-005, 4 pp., 31 August 1995;
Chow, J. C. Measurement methods to determine compliance with ambient air quality standards ‘for suspended particles--summary of critical review. Environmental Manager, 1:12-5, May 1995;
Chow, J. C. Measurement methods to determine compliance with ambient air quality standards ‘for suspended particles--critical review. Journal of the Air & Waste Management ‘Association, 45(5):320-82, May 1995
Culp, D. L., et al. Composition of human airway mucins and effects after inhalation of acid aerosols. American Journal of Physiology, in press, 1995;
Dockery, D. W., and C. A. Pope III. Acute respiratory effects of particulate air pollution. Annual Reviews of Public Health, 15:107-32, 1994;
Fine, J. M., et al. The role of titratable acidity in acid aerosol-induced bronchoconstriction. American Reviews of Respiratory Disease, 135:826-30, 1987a;
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;
Framptom, M. W., et al. Sulfuric acid aerosol exposure in humans assessed by bronchoalveolar lavage. American Reviews of Respiratory Disease, 146:626-32, 1992;
Framptom, M. W., et al. Sulfuric acid aerosol followed by ozone exposure in healthy and asthmatic subjects. Environmental Research, in press, 1995;
Godleski, J. J. Oral and written report to the PMjq Review Panel, U. S. EPA Clean Air
Science Advisory Committee (CASAC). Research Triangle Park, North Carolina; 14 December 1995;
Godleski, J. J., et al. Death from inhalation of concentrated ambient air particles in animal models of pulmonary disease. New Orleans, Louisiana; American Thoracic Society 1996 International Conference, 11-15 May, abstract in press, 1996;
Green, D. J., et al. Acute pulmonary response in healthy, non-smoking adults to inhalation
215)
26. 27.
28.
29. 30.
31. 32. 33; 34.
35.
36.
37.
38.
39).
41.
42.
43.
44,
45.
of} Jormaldeloiie and carbon. Journal of Toxicology and Environmental Health, 28:26175, 1989;
Hanley, Q. S., et al. Response of young asthmatic patients to inhaled sulfuric acid. Américan 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 the Health Effects of Acid Aerosols. Rescue Triangle Park, NC, October 1987. Environmental Health Perspectives, 79:173-
1989;
Koenig, J. Q., et al. The effect of duration of exposure on sulfuric acid-induced pulmonary Sunction 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;
Lawther, P. J., R. E. Waller, and M. Henderson. Air pollution and exacerbations of bronchitis. Thorax, 25:525-39, 1970;
Linn, W. S., et al. Effect of droplet size on respiratory responses to inhaled sulfuric acid in nol and asthmatic volunteers. American Reviews of Respiratory Disease, 140:161-6,
Meyer, M. B. Applications of continuous PM 1g measurements. Paper presented at the
Conference on the Role of Meteorology in Managing the Environment. Scottsdale, Arizona; 12 pp., 26-28 January 1993;
Meyer, M. B., E. Rupprecht, and H. Patashnick. Considerations for the sampling and measurement of ambient particle mass. Paper presented at the U. S. EPA and Air & Waste Management Association Conference on Particulate Matter: Health and Regulatory Issues. Pittsburgh, Pennsylvania; 8 pp., 4-6 April 1995;
Michaels, R. A. Response to Chow (see citations 15, 16; above). In: J. G. Watson. Measurement methods to determine compliance with ambient air quality standards for suspended particles. Journal of the Air & Waste Management Association, 45:666-84, September 1995;
Michaels, R. A. Health risks and particle monitoring: new technologies to meet emerging data needs. AAAR ‘95. Pittsburgh, Pennsylvania; 14th Annual Meeting of the American Association for Aerosol Research, 9 - 13 October, 1995; Abstract, page 338, 1995;
Miller, F. J., et al. Dosimetric issues relating to particulate toxicity. In: R. F. Phalen and D. V. Bates (editors), Proceedings of the Colloquium on Particulate Air Pollution and Human Mortality and Morbidity, Part I, Irvine, California; Inhalation Toxicology, 7:615-32, 1995;
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;
Nearing, B. D., et al. Inhaled fly ash results in alteration in cardiac electrophysiologic Junction. New Orleans, Louisiana; American Thoracic Society 1996 International Conference, 11-15 May, abstract in press, 1996;
Nearing, B. D., et al. 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;
Patashnick, H., and E. G, Rupprecht. Continuous PM-10 measurements using the tapered element oscillating microbalance. Journal of the Air & Waste Management Association, 41(8):1,079-83, August 1991;
Pope, C. Arden, J. Schwartz, and M. R. Ransom. Daily mortality and PM 19 pollution
in Utah Valley. Archives of Environmental Health, 47(3):211-7, May/June 1992; Pope C. Arden, and D. W. Dockery.. Acute health effects of PM 19 pollution on
symptomatic and asymptomatic children. American Reviews of Respiratory Disease,
46.
47. 48. 49.
50.
51.
52.
53.
54.
55. 56.
57.
58.
59.
60.
61.
62. 63.
145:1,123-8, 1992;
RAM TRAC. Health Risks and Particle Monitoring: New Technologies To Meet Emergin,
Data Needs, Including A One-Hour Upper Mass Limit In the Next National Ambient Air Quality Standard. Robert A. Michaels, PhD, CEP; Project Director. Schenectady, New York; RAM TRAC Corporation, 169 pp., 17 July 1995;
R&P. TEOM® Series 1400A ambient particulate monitor. Albany, New York; Rupprecht and Patashnick Company, product technical literature 4 pp. plus attachments, undated;
R&P. Partisol Model 2000 air sampler. Albany, New York; Rupprecht and Patashnick Company, product technical literature 4 pp. plus attachments, undated;
R&P. Summary: Series 5400 ambient carbon particulate monitor. Albany, New York, Rupprecht and Patashnick Company, product technical literature 11 pp. plus attachments, September 1994;
Rupprecht, E., M. B. Meyer, and H. Patashnick. Performance characteristics of a near real-time ambient particulate mass monitor. Paper presented at the U. S. EPA and Air & Waste Management Association Conference on Particulate Matter: Health and Regulatory Issues. Pittsburgh, Pennsylvania; 11 pp., 4-6 April 1995;
Rupprecht, G., et al. A new automated monitor for the measurement of particulate carbon in the atmosphere. Paper presented at the U. S. EPA and Air & Waste Management Association Conference on Particulate Matter: Health and Regulatory Issues. Pittsburgh, Pennsylvania; 11 pp., 4-6 April 1995;
Rylander, R. Alterations of lung defense mechanisms against airborne bacteria. Archives of Environmental Health, 18:551-5, April 1969;
Schwartz, J. Environmental pollution and human health: an epidemiology perspective. Chapter 11 in: C. R. Cothem and N. P. Ross (editors), Environmental Statistics, Assessment, and Forecasting; Boca Raton, Florida; Lewis, pp. 209-22, 1993;
U. S. District Court. Judgment ina civil case: American Lung Association Vs. Carol Browner, U. S. EPA; U. S. District Court, District of Arizona, Case No. CIV-93-643TUC-ACM, 11 pp., 6 October 1994;
U. S. EPA. Ambient Air Quality Standards for Particulate Matter; Final Rules. Federal Register, 52(126):24,633-68, 1 July 1987;
U. S. EPA. Interim Methods for Development of Inhalation Reference Doses. Washington, DC; Office of Health and Environmental Assessment, EPA/600/8-88/066F, PB90-145 723, i. p., August 1989;
U. S. EPA. Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment of Scientific and Technical Information: OAQPS Staff Paper. Research ‘Triangle Park, North Carolina; Office of Air Quality Planning and Standards (OAQPS), External Review Draft, i.p., November 1995;
U. S. EPA. Air Quality Criteria for Particulate Mater, Review Draft. Washington, DC; Office of Research and Development, EPA/600/AP-95/001a, Vol. 1 of 3 volumes, i. p., 5 December 1995,
U. S. EPA. Air Quality Criteria for Particulate Matter, Review Draft. Washington, DC; Office of Research and Development, EPA/600/AP-95/001b, Vol. 2 of 3 volumes, i. p., 5 December 1995;
U. S. EPA. Air Quality Criteria for Particulate Matter, Review Draft. Washington, DC; Office of Research and Development, EPA/600/AP-95/001c, Vol. 3 of 3 volumes, i. p., 5 December 1995;
Utell, M. J., et al. Comparison of normal and asthmatic subjects’ responses to sulphate pollutant aerosols. \n: 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., ef al. Effect of inhaled acid aerosols on respiratory function: the role of endogenous ammonia. Journal of Aerosol Medicine, 2:141-7, 1989;
Waller, R. E., and B. T. Commins. 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, 1966;
Yang, SC, and S.-P. Yang. Respiratory function changes from inhalation of polluted air. Archives of Environmental Health, 49:182-7, 1994.
Publication citation
Michaels, RA. Health risks support a one-hour airborne particle standard with data acquisition via rapid automated monitoring instrumentation. In: Measurement of Toxic and Related Air Pollutants, U. S. EPA and Air and Waste Management Association; Research Triangle Park, North Carolina; 7-9 May 1996; pp. 201-7, 1996;