Health Effects of Airborne Particulate Matter: Role of Short-Term
Exposures In Producing Chronic Effects
ROBERT A. MICHAELS, Ph.D., C.E.B
RAM TRAC Corporation Schenectady, New York, U.S.A.
Synopsis BIOGRAPHY ACKNOWLEDGMENT EDITORS’ COMMENTARY SUMMARY INTRODUCTION METHODS FINDINGS 1. Identification of Monitoring Technologies 2. Airborne Particle Excursions 8. Toxicological Significance 4. Regulatory Significance E. CONCLUSIONS REFERENCES
DOwP
118 Sourcebook on Asbestos Diseases
BIOGRAPHY
Robert A. Michaels, Ph.D., C.E.R is a Board Certified Environmental Assessor and Chair, Academy of Board Certified Environmental Professionals, Elected Life Member, New York Academy of Sciences; Admitted Member, American College of Toxicology, and Admitted Member, Society of Toxicology. Dr. Michaels is President of the Schenectady, NY-based RAM TRAC Corporation. His clients have included the U. S. Congress and California Governor, and he is past Chair of the State of Maine Scientific Advisory Panel. Dr. Michaels now chairs the Academy of Board Certified Environmental Professionals, and serves on two National Fire Protection Association (NFPA) committees revising industrial emergency response guidelines. He received his doctorate from the State University of New York at Stony Brook in 1979, was admitted as a Member of the American College of Toxicology and of the Society of Toxicology, and in 1986 was elected Life Member of the New York Academy of Sciences. He may be contacted at the RAM TRAC Corp., 3100 Rosendale Road, Schenectady, New York 12309, U.S.A. Telephone: 518-785-0976.
Health Effects of Airborne Particulate Matter 119
ACKNOWLEDGMENT
This research was supported in part by Rupprecht & Patashnick, Inc., Albany, NY.
120 Sourcebook on Asbestos Diseases
EDITORS’ COMMENTARY
The level of asbestos exposure is rarely stable. In the real world, the direction, velocity, and aerodynamics of windblown asbestos may cause extreme variations even in a short time period. Those who sample airborne asbestos fibers know about “upwind sampling” and very “aggressive sampling” (as possible extremes in terms of results). In asbestos mines and fabricating facilities, a worker may pass through “clean” areas and “dirty” areas. In other words, the typical exposures are not predictably chronic, but are acute or episodic in character. In the following chapter, the focus on “repetitive acute exposures” may help to explain some of the adverse health effects and mechanisms of disease pathogenesis that are presently confounding or confusing both clinical and field studies.
Supplemental information, in this book series, may be found in: Asbestos Monitoring for Airborne Fibers: Preabatement Through Final Clearance (Chapter 11 in Volume 5); Analysis of Airborne Asbestos (Chapter 10 in Volume 5); Measurement of Airborne Asbestos Fibers (Chapter 2 in Volume 9); Effectiveness of Respirators (Chapter 4 in Volume 10); and Pathogenic Mechanisms in Pulmonary Fibrosis (Chapter 1 in Volume 6).
A. SUMMARY
Asbestos-related disease increasingly is being viewed within the broader context of health effects exerted by airborne particulate matter (PM). Likewise, health effects exerted by chronic exposure to PM are increasingly being viewed as the products of repetitive acute exposures, possibly including toxicologically significant individual exposure episodes. To help elucidate the place of respiratory disease caused by asbestos within the context of related effects caused by acute and chronic exposure to PM gener-
Health Effects of Airborne Particulate Matter 121
ally, this paper addresses the potential health significance of repetitive acute exposures to PM.
PMyp levels within EPA’s 24-hour, 150-ug/M® standard have been associated with mortality and morbidity, which remain causally unexplained. EPA’s standard, refocused on PMgs, has been downwardly adjusted, assuming that effects observed daily are caused by daily exposures. Real-time PM monitoring was used to inquire whether 24-hour-average PM levels might encompass brief, health-significant excursions. Data from Birmingham, Alabama, Penticton, British Columbia, and Zeebrugge, Belgium revealed many excursions; one reaching 2,000 ug/M’, twice the level in the lethal 1952 London fog. Harm from brief exposure to PM in the range of observed excursions was demonstrated experimentally in people, dogs, and rats. In rats, the area of lung surface developing lesions was elevated when the four-hour average aerosol dose rate included a short-term burst. Elevations were observed with each of two aerosols, and were more pronounced with four excursions than with one excursion. In another study, short-term PM exposure killed rats. In dogs, short-term PM exposure caused serious electrocardiogram changes. In humans, asthma symptoms were associated with PM levels, but the strength of the association increased as PM averaging time decreased from 24 hours to eight hours to one hour. Short-term human response to PM also was evident when 300 people were overcome after wind lofted particles into the air during a four-day outdoor music festival in Queen Creek, Arizona in April 1997. These findings support four conclusions: (1) EPA’s decision to change the PM standard may be justified by residual health risks associated with the old standard; (2) the time required for PM to cause adverse effects may be briefer than the time interval over which the effects are observed; (3) greater risk reduction would appear to be achievable via control of one-hour PM averages than 24-hour averages; and (4) additional study of PM excursions is needed.
B. INTRODUCTION
Asbestos-related disease increasingly is being viewed within the broader context of health effects exerted by airborne PM. Likewise, health effects exerted by chronic exposure to PM are increasingly being viewed as the products of repetitive acute exposures, possibly including toxicologically significant individual exposure episodes. To help elucidate the place of respiratory disease caused by asbestos within the context of related effects caused
122 Sourcebook on Asbestos Diseases
by acute and chronic exposure to PM generally, this paper addresses the potential health significance of repetitive acute exposures to PM.
This paper reports and updates information presented at the Second Colloquium on Particulate Air Pollution & Human Health, held in Park City, Utah in May 1996. At Court direction, the U.S. Environmental Protection Agency (EPA) has reviewed the National Ambient Air Quality Standard (NAAQS) for airborne particles (1,2,49,50). The old and new NAAQS limit particulate matter within a diameter of 10 microns (PMj)) to a time-weighted average mass limit of 150 yg/ME of air over 24 hours, but the new NAAQS also controls one-hour PM,,5 to 65 wg/M®, which is generally lower than the PM,; fraction of PMyy at 150 pg/M?.
The increase in stringency primarily was based upon epidemiological associations of particle elevations during air pollution episodes with elevated mortality and morbidity in communities (for example, see 14,43,44). 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® (48; PMy) < 1,200 pe/M®). Recent studies associate significant elevations of morbidity and mortality with particle levels well within PMi = 150 wg/MP (reviewed by EPA, 1995; 53), and below levels which have been explainable by known toxicological mechanisms. 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.
Cc. METHODS
The method of investigation consisted of evaluating 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 possible 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 (3,51) based upon the weight of evidence for the existence, nature, and magnitude of public health risks. Ultimately, the findings were evaluated rela-
Health Effects of Airborne Particulate Matter 123
tive to a major regulatory issue facing state health departments and the U.S. EPA. That issue is whether adequate public health protection can be secured via the 24-hour NAAQS, which limits particle excursions only to the insignificant degree to which they produce exceedances of 24-hour PM limits.
D. FINDINGS
1. Identification of Monitoring Technologies
Two PM monitoring technologies were found to be capable of reliably measuring PM mass levels in real time or over short intervals (11,32-35,42,45-47,53). 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.
2. 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 within the current NAAQS. Screening identified three locations, and 10 days, during which 24-hour average PMj) < 150 mg/M®. At all three locations, and in six of the 10 identified cases meeting the screening criteria, excursions exceeding 150 wg/M* were noted (36; Fig. 5-1, Table 5-1).
In Birmingham, Alabama on 16 April 1990 24-hour average PM,y was 70 wg/M°, but two one-hour-average excursions exceeding 200 ug/M® were recorded. In Penticton, British Columbia on approximately eight days between 30 July and 7 August 1994 24hour average PM) varied from close to zero to close to 150 wg/M’, but excursions exceeding 150 ug/M’ were recorded on four of the eight days (Fig. 5-1). These included three one-hour-average excursions to 300 wg/M® and two excursions to approximately 500 wg/M®. In Zeebrugge, Belgium on 15 March 1993 24-hour average PM,) was 101 ywg/M’, but several 15-minute-average excursions exceeding 200 g/M’ were recorded. In one excursion, the 15-minute average reached 2,000 yg/M®, significantly exceeding the estimated magnitude, though not the persistence, of the 1952 London fog (< 1,200-ug/M*; 48).
Figure 5-1 Hourly and daily PMyo concentration in Penticton, British Columbia, 30 July to 7 August 1994.*
1-Hour Average PM-10
100 24-Hout Average PM-10
4-Hour and 24-Hour PM-10 Cone [yg/m"] 8 8 I —>
eee)
100 i ae S0-JULGS 31-Jul-94 1-Aug-94 2-Aug-94 — S-Aug-94 4-Aug-94 S-Aug,94 6-Aug-94 77-Aug-98
*source: Rupprecht, E., M. B. Meyer, and H. Patashnick. Performance characteristics of a near-real-time particulate mass
monitor. Conference on Particulate Matter: Health and Regulatory Issues. Pittsburgh, Pennsylvania 4-6 April 1995.
vor
HOMMORTCT FOJHOGHY UO ooqodanog
3/15/93 7TBUA 3/15/93 3/15/93 3/15/93 8/1/94 3/15/93 3/15/93 8/1/94 4/16/90 4/16/90 8/2/94 8/1/94 3/15/93 4/16/90 8/3/94 3/15/93 3/15/93 3/15/93 3/15/93 8/2/94 8/3/94 3/18/93 3/15/93 3/15/93 8/3/94 3/15/93
BLESSRRSPRERSBSSENSARSBESE BSBGESSUGTTSSASSSSSRGSAUASS
SSRSSRRSRERKE
27 Birmingham, 3/1 day; Penticton, 9/9 days; Zeebrugge, 15/1 day os 9 373 3 39 7 “ 36
‘Conference on Particulate Matter: ‘Health and Regulatory Issues; Pittsburgh, Pennsylvania; 4-6, 0 M, but this estimate is probably total \ttributed
Table 5-1 Short-term particle excursions without exceedance of the 24-hour PM-10 standard.
Table 5-1 summarizes the observed excursions and quantifies their magnitude relative to 24-hour average and London fog particle mass benchmarks. 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,o, whereas PM,o may have represented only a fraction of this estimate.
Table 5-2 Particle effects revealed in controlled acute human exposures.
dosex —_|effect(s) duration (ug min/cu M))... healthy: no effects; 202 6,060 asthmatic: reduced lu function (FEV1)
NaCl, H2SO4, NH3 0.80 700 reduced lung function (FEV1)
NaCl, H2S04 = 190 22,800
activated carbon +} formaldehyde bn bees 122400 _|eVC, FEV3, peak flow) : 72,000 -|daily morbidity and
144,000 __|mortality begin 10 150 216,000 |NAAQS for PM-10
10 50-100
=
throat irritation; no effect on| 240,000) lung function
q 641 [9900,000. to] increased specific airway atrest | 25-41 |NaCl,30 mOsm 53-61 ro to0,000 = 25,900,000 increased!
exercise | 20-39 |NaCl+H2SO4 09 2,000
tations: . Balmes, J. R., etal. Acidity potentiates bronchoconstriction induced by hypoosmolar aerosols. American Reviews of Respiratory Disease, 138:35-9, 1988; Framptom, M. W, et al. Sulfuric acid aerosol exposure in humans assessed by bronchoalveolar lavage. American Reviews of Respiratory Disease, 146:626-32, 1992; 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; 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,, etal. 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 SP. Yang. Respiratory function changes from inhalation of polluted air. Archives of Environmental Health, 49:182-7, 1994. mass median aerodynamic diameter
96T
sesBasiq] SOSegsy UO Yooqeo1no0g
Health Effects of Airborne Particulate Matter 127
3. Toxicological Significance
Numerous studies of short-term effects exerted by PM during controlled acute human exposures were identified (23,35,38,58, 59). Many reported positive results (4,5-10,12,15-18,21,22,24-29, 31,39,54,55,57). Table 5-2 exemplifies the positive studies, ranking the tabulated examples, along with findings of daily mortality studies (for example, see 14) and the current PM,, standard (50), in increasing order of concentration (c) times exposure duration. (t) product (Haber’s rule states that c x t = constant; Ten Berge’s adjustment states that c® x t = constant, but the value of n is species specific, and unknown for PM).
Table 5-2 indicates that adverse particle-associated health effects have been demonstrated beginning at levels as low as 202 yg/Me (57) and at exposure durations as short as 30 minutes (55,57). These effects were documented in asthmatics at rest (57) or engaged in exercise (55). Participant ages in these studies varied from 19 to 50 (55) and 23 to 48 (57). Thus, no frail 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 (10,17,21,39). 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 (FEV,, FEVs), 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; 30) 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 24hour average (56) 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:
128 Sourcebook on Asbestos Diseases
“.. . 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 yg/M? of sulphur dioxide together with 250 g/M° 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; 13). They used frequency of medicinal inhaler use by asthmatic subjects as a surrogate indicator of symptom severity. 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. Figure 5-2 shows that 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.
Ashort time frame for human response to PM was also 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 (Fig. 5-3). Figure 5-3 illustrates 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. Indeed, 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 (Fig.
5-2 Dependence of PM,,/asthma-symptom association upon PM» averaging time.*
Delfino, R.J.,etal. Effects of PMy and ozone on symptoms and peak
03. g 3 “_ eS BY 024 ee go 2g 33 SE a Ey e asthma symptom increase per 50 pg/cu M 3 00. asthma symptom increase per 50 yg /cu M.h 1h max PM-10 &hmax average PM-10 2th average PM-10 average “Adapted from:
‘expiratory flow in asthmatics living at the inversion base, Abstract.
American Lung Association/ American Thoracic Association International Conference, San Francisco, 17-21 May, 1997.
Assumption: Haber's rule applies: concentration x time = constant, C*t = constant, where n=
sOHeY eyeTNoIeg susoqary Jo sey yITeSH
&R
a
number of individuals per hour 3
a
—— patients ———hospitalizations
&
SSERS9 988825
$8 oO
elapsed time (minutes)
Assumes reporting period beginning 12 noon Thursday 24 April and ending 8:00 p.m. Sunday 27 April 1997. D)
Figure 5-3 Approximate emergency visit and hospitalization rates, Country Thunder Concert; Queen Creek, Ari-
zona; 24-27 April 1997.*
O8T
HONVORTC] HOJFOGHY UO Yooqooanog
Health Hffects of Airborne Particulate Matter 181
6-4) and dogs (Fig. 5-5), under way at Harvard University’s School of Public Health, have been published in abstract form (20,40,41), and more completely in oral and written reports by John Godleski to CASAC (19). The findings implicate short-term, possibly electrophysiological mechanisms of fine-particle-induced cardiopulmonary malfunctioning, shown via electrocardiograms (EKGs; Fig. 5-5).
Nearing, et al. (41) induced ST segment elevation and periods of apnea in dogs inhaling fly ash at 1,000 ug/M? for 3 d, 4 h/d (Fig. 5-5). Nearing, et al. (40) also demonstrated increased T-wave alternans amplitude, indexing vulnerability to ventricular fibrillation, in dogs inhaling fly ash at 3,000 wg/M? 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 (Fig. 5-5). Asa 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, et al. (19,20) 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 ug/M? 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 (19) indicated that mortality also might be consistent with systemic effects following particle induction of proinflammatory mediators, such as the cytokines interleukin-1 and tumor necrosis factor-alpha.
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. which was published (1989; 23), but excluded from that report, which 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 (23). However, in the unpublished bioassays, the rates at which the aerosols were delivered included either one or four excursions (Fig. 5-6). 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
132 Sourcebook on Asbestos Diseases
2 E io) § 228 to 288 g/cuM. airborne particle rmal 7 monocrotal- regimen disease bronchitis model "Adapted from:
Godleski, J.J. Death from inhalation of concentrated ambient air particles in animal models of pulmonary disease. Abstract No, 615051. American Thoracic Society International Conference; New Orleans, Louisiana; 11-15 May 1996.
Figure 5-4 Mortality induced by six-hour exposures of rats to airborne particles on three consecutive days.*
lungs 48 hours after four-hour controlled exposures of groups of
six rats to either of two sulfate aerosols, designated AMS and SAM, with the compositions as set forth in Table 5-3.
Table 5-3 Composition of Aerosols Used In Study Demonstrating Exeursion Effect on Rat Lungs*
component AMS SAM
varied components
ammonium 0.5 mg/M8 0.0 mg/Me sulfuric acid 0.0 mg/M3 0.5 mg/M8 invariant components
iron sulfate 1.0 mg/M? 1.0 mg/M® manganese sulfate 0.2 mg/MS 0.2 mg/M? nitrogen dioxide 2.6 ppm 2.6 ppm ozone 0.6 ppm 0.6 ppm sulfur dioxide 5.0 ppm 5.0 ppm
“See Kleinman, M. T., et al. Health effects of acid aerosols formed
atmospheric mixtures, Environmental Health Perspectives, 79:187+ 6, 1989,
Health Effects of Airborne Particulate Matter 133
o7. 06: Hie tS 24 01 7 control 1,680 pg/cu M 3,040 ug/cu M airborne particle regimen
\
g s & 2. 18: t: 05. q control 1,680 ug/cu M 3,040 pg/cu M airbome particle regimen
Apnea In Dogs Induced By Four-Hour Exposures To Airborne Particles on Three Consecutive Days
33 af 4 i ai control 1,680 pg/euM — 3,040ug/cuM airborne particle regimen
Adapted from: Nearing, B.D, et al, Inhaled ly ash results in alteration in cardiac electrophysiologic function. Abstract ‘New Orleans, Loulalana; International Conference of the American Thoracic Society, 11-15 May 1996; Nearing, B.D, et al. Exposure to inhaled environmental air particles results in significant ST-segment elevations in dogs with normal coronary arterles, Abstract No, 075548, American College of Cardiology, 45th Anewal Scientific Sesaion, 1996,
Figure 5-6 EKG changes in dogs induced by three-hour exposures to airborne particles on three consecutive days,"
134 Sourcebook on Asbestos Diseases
The fraction of microscopically examined rat lung area exhibiting aerosol-induced lesions was evaluated in groups of rats exposed to excursions versus no-excursion controls exposed to the same aerosol. Thus, except for the excursions, treated and control rats experienced identical exposures. Results are presented in Fig. 5-6, which consists of two sets of paired columns. In both sets, the column to the right indicates greater lesion area 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.
4, Regulatory Significance
The findings reported in bioassays, controlled human exposure studies, and epidemiology studies in which PM exposure is uncontrolled must be evaluated relative to EPA policies and procedures for air pollutant standard setting (3,51) based upon the weight of evidence for the existence, nature, and magnitude of public health risks. The Agency requested the American Thoracic Society (AT'S) to define toxicological effects, and degrees of effect, which might qualify as forming the basis for limiting air pollutants, and both ATS (1985; 3) and the U. S. EPA (1994; 51) have published these guidelines.
According to U. S. EPA policy (51), air pollution limits must be
set based upon a clinically significant adverse effect, not any effect, as defined by ATS (8):
“We define ‘adverse respiratory health effects’ as medically significant physiologic or pathologic changes . . .” (page 666).
Many of the controlled human exposure studies focus upon asthmatics during exercise and at rest. These studies, described earlier in Table 5-2 and associated text, reveal symptoms of asthma exacerbation such as bronchoconstriction, increased airway resistance, reduced FEV, and FEVs;, reduced FVC, and reduced peak flow (for example, see Fig. 5-7). 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 ATS (3):
“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
lesion area at 48 hours| (percent of area examined) | |
[rat lung
n=6rats SAM, one excursion, n=6rats
"dala source: Michael "AMS: ammonium, Fe +M GAM: sulfuric acid, Fe+Mn sulfates) (ALL: ozone, NO2, $02 (0, 2.6, { Kleinman, UC/Irvine, ) (_ sulfates (05,10, 02'mg/eu ty ) (05, 1.0, 02 mg/cuM) $0 ppm) |
Figure 5-6 Pulmonary effect of five-to 10-min. sulfate aerosol excursions during four-hour controlled exposures of rats.*
se oyeMNoAVg ouIOgaTY Jo spay yIeeH
GéT
136 Sourcebook on Asbestos Diseases
on human welfare. However, irritation that triggers an asthmatic attack is an adverse health effect” (page 666; emphasis added).
Clearly, the symptoms evoked by controlled clinical exposures as described and tabulated (Table 5-2) above do not include trig-
gering an asthmatic attack. However, according to EPA and ATS guidelines, this clinical endpoint need not be (and for ethical reasons, cannot be) experimentally induced to be used in standard setting. Rather, the guidelines justify inferring greater severity of response with greater exposure. AT'S continues:
This spectrum of biologic responses would be evoked more strongly as the concentrations of pollutants are increased” (page 666; emphasis added).
E. CONCLUSIONS
Excursions of airborne particle mass may elevate PM, by an order of magnitude relative to 24-hour average levels within the 150-yg/M*® NAAQS (36). PM levels comparable to those reached during documented excursions can exert toxicological effects upon humans and animals, including mortality in animals (38,58). Such excursions might constitute a previously unrecognized cause of mortality and morbidity revealed by epidemiology studies based upon 24-hour average PM levels. Toxicological effects reported in association with PM in the range of observed excursions are of types determined to be appropriate for air pollutant standard setting under the Clean Air Act, according to U. S. EPA criteria. Thus, EPA’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. A corollary is that threshold effects exerted by PM may be caused by brief exposure to PM excursions exceeding effect thresholds.
Non-cancer effects typically exhibit thresholds when caused by agents other than PM. Failure of PM epidemiology studies to discern such thresholds need not suggest their absence, if the effects are caused by brief exposure to high PM concentrations. PM data averaged over 24 hours may have supported NAAQS revision, but relevant averaging time(s) still must be selected based upon exposure durations eliciting observed effects. Constraining the NAAQS to control 24-hour average PM is illogical when observed effects seem equally consistent with causation by briefer excursions to high PM concentrations (59),
Health Effects of Airborne Particulate Matter 137
Thus, EPA’s preference for managing 24-hour average PM concentrations, reflecting availability of 24-hour average PM data, is technically unjustified. Additional study of the epidemiology of PM excursions is needed. However, data already available and presented herein suggest that 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.
In many if not most industries, controlling PM excursions to a one-hour mass limit of, say, 300 wg/M* can be achieved more economically than controlling 24-hour averages, because industrial processes often include brief periods of reduced PM control, when excursions occur. For example, plastics factories may produce several types of plastics using the same (extrusion) equipment operated with resins at different temperatures. Shifting to a new plastic type requires purging the previous resin, changing the temperature, and running the equipment with the new resin. PM emissions during these transitional phases of operation can be controlled more economically because they require improvements to only a small part of overall operations. For example, plastics factories can run resins requiring higher temperatures after first running lower-temperature resins, or they can assure adequate extruder temperature reduction prior to introducing lowertemperature resins.
Figure 5-7 Effects of breathing polluted Taipei Tunnel air upon asthmatics
at rest.*
respiratory conductivity, FEV,,/FVC, FEVis provacative cum. dose, men women men women men women men ‘women. —f10/(emH,O/L9)) a) ‘Giters) (methacholine units) [clean alr control ia 12 08S O797 301 250 55 47 [Taipei tunnel air”* 07 0s 0773 0761 278 269 36 33 fististica significance | <n001 <0.001 <0.05 <005 <0.05 <0.05 <0.001 <0.001 fe) —L 6050- E | Provacative cum, dose, women (methacholine units) 404 Bee Provacative cum. dose, men (methacholine units) eo FEVI.O, women (liters) = 30. FEVLO, men (liters) > FEVLO/EVG, women (..) 20. FEVLO/EVG, men(.) 10. respiratory conductivity, women {10/(emH20/L3)] op. respiratory conductivity, men {10/(anEZO/Ls)1 dean Talpel alr emit “met Adapted from: Yang, S-C.,and SP. Yang. Respiratory function changes from inhalation of polluted air. Archives of Environmental Health, 49(3):182-7, May /June 1994. treatments: ‘Suspended particulates (ug/cu M)|__CO (ppm) SO; (ppb) NO, (ppb)
Clear-air ComtrOl | emrenenmnne H+/9 164/07 84/3 464/15 Taiped tunnel air | wmmovommm 202 +/-33 343/48 1124/19 488-4 /-24
‘iin
Poanoae@rrr GO1WHanEe TH WAAnNAA MAR
Health Effects of Airborne Particulate Matter 139
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Publication citation
Michaels, RA. Health effects of airborne particulate matter: role of short-term exposures in producing chronic effects. In: Current Asbestos Issues, Sourcebook on Asbestos Diseases; George A. Peters and Barbara J. Peters, Editors. Charlottesville, Virginia; Reed Elsevier, Inc.; Lexis Law Publishing Division; Volume 18, pp. 117-43, 1998;