Aerosol Science and Technology 32:93- 105 (2000) © 2000 American Association for Aerosol Research Published by Taylor and Francis
0278-6826 /00 /$12.00 +.00
a
Incidence and Apparent Health Significance of Brief Airborne Particle Excursions
Robert A. Michaels and Michael T. Kleinman RAM TRAC CORPORATION, 3100 ROSENDALE ROAD, SCHENECTADY, NY 12309-1510 AND DEPARTMENT OF COMMUNITY AND ENVIRONMENTAL MEDICINE, UNIVERSITY OF CALIFORNIA COLLEGE OF MEDICINE, IRVINE, CA 92717-1825
ABSTRACT. The U.S. EPA has tightened control of fine particles primarily by limiting maximum 24 h average airborne concentrations. The present investigation used real-time monitoring to record short-term PM excursions and literature evaluation to determine whether PM levels reached in excursions might be health significant. Data recorded in Birmingham, AL, Penticton, British Columbia, and Zeebrugge, Belgium revealed numerous excursions, one reaching 2,000 Ug /M?. Toxicology and clinical studies involving brief exposures to particle levels in the range of observed excursions elicited adverse effects in both animals and humans. The area of lung surface developing lesions was elevated in rats breathing the same 4h dose of aerosols when the 4 h average rate of aerosol delivery included a short-term (= 5 min) burst (= 50%) above the average dose rate. Elevations were observed with each of two aerosols tested. The magnitude of the effect was higher with one of the two aerosols, whose dose rate included four excursions rather than just one excursion. Symptom severity in asthmatics was associated with PM elevations, but the strength of the association depended upon the PM averaging time: the strength of the PM association with symptom severity increased as the PM averaging time varied from 24 h to 8 h to 1 h. Three hundred people were overcome after wind lofted particles into the air during a 4 day outdoor music festival in Queen Creek, AZ in April 1997. More research is necessary, but evidence presented here suggests that greater risk reduction might be achievable via controlling 1 h and 24 h PM averages than via tightening control of 24 h averages without controlling the 1 h average.
INTRODUCTION
This paper reports information presented at the 17th Annual Meeting of the American Association for Aerosol Research (AAAR 798) and updates information presented earlier at the 14th Annual Meeting (AAAR 795). At Court direction, the U.S.
EPA has reviewed the National Ambient Air Quality Standard (NAAQS) for airborne particles (American Lung Association 1993, 1994; U.S. District Court 1994; U.S. EPA 1987, 1995a, b). The old and new NAAQS limits PM with diameter <10 microns (PM,,) to a time-weighted average mass
94 RA. Michaels and M. T. Kleinman
limit of 150 ug /M® of air over 24 h, but the new NAAQS also controls 24 h PM, ; to 65 ug /M°, which is generally lower than the PM, fraction of PM,, at 150 wg /M®?. Increased stringency was primarily based upon epidemiological associations of particle elevations during air pollution episodes with elevated mortality and morbidity in communities (for example, see Dockery and Pope 1994; Pope et al. 1992; Pope and Dockery 1992). 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; PM,, < 1,200 ug /M?). Recent studies associate significant elevations of morbidity and mortality with particle levels well within PM,)=150 pg/M? (reviewed by U.S. EPA 1995b) and below levels which have been explainable by known toxicological mechanisms. The present study inquires whether 24 h average particle levels educed via the U.S. EPA reference gravimetric monitoring method might encompass undetected, health significant, shorter-term excursions sufficient to explain the observed adverse effects (Michaels 1996, 1997, 1998; Michaels and Kleinman 1997a, 1997b).
METHODS
The method of investigation consisted of evaluating available analytical data and literature and recent experiments. First, the study quantified short-term excursions of particle mass contributing to 24 h averages well within the NAAQS. Second, it assessed the toxicological and epidemiological literature to evaluate the possibility that such excursions, notwithstanding their relatively brief persistence, might cause mortality and /or morbidity. Third, it examined data from experiments conducted by Kleinman et al. involving rats inhaling equal timeweighted average aerosol concentrations,
Aerosol Science and Technology 32:2 February 2000
with or without excursions, to determine whether the severity of adverse effects elicited by constant aerosol delivery might be augmented by excursions. Two aerosols were investigated in this manner. The methods used in these studies are described in detail in Kleinman et al. (1989).
FINDINGS
Airborne Particle Excursions
Data sets were screened to identify those which 1. exhibited short-time resolution, 2. encompassed at least one 24 h period, and 3. revealed 24 h airborne particle levels within the current NAAQS. Screening identified 3 locations, and 10 days, during which 24 h average PM, < 150 mg /M’. At all 3 locations, and in 6 of the 10 identified cases meeting the screening criteria, excursions exceeding 150 ug/M? were noted (Michaels 1996).
In Birmingham, AL on 16 April 1990, 24 h average PM,) was 70 wg /M®, but 2 1 h average excursions exceeding 200 wg /M? were recorded. In Penticton, British Columbia on approximately 8 days between 30 July and 7 August 1994, 24 h average PM, varied from close to 0 to close to 150 ug/M?, but excursions exceeding 150 ug/M? were recorded on 4 of the 8 days. These included 3 1 h average excursions to 300 ug/M? and 2 excursions to approximately 500 wg /M?. In Zeebrugge, Belgium on 15 March 1993, 24 h average PM, was 101 ug /M?, but several 15 min average excursions exceeding 200 ug/M? were recorded. In one excursion, the 15 min average reached 2,000 ug/M®, significantly exceeding the estimated magnitude, though not the persistence, of the 1952 London fog (< 1,200 wg /M?; Schwartz 1993).
Michaels (1996) summarizes the observed excursions and quantifies their mag-
Aerosol Science and Technology 32:2 February 2000
nitude relative to the London fog and 24 h averages. Excursions attained levels 0.1 to 1.6 times the London fog. Four of 27 excursions (15%) 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.
Toxicological Significance
Numerous studies of short-term effects exerted by PM during controlled acute human exposures were identified (Anderson et al. 1992; Aris et al. 1991a,b; Avol et al. 1988a,b, 1990; Balmes et al. 1988; Culp et al. 1995; Fine et al. 1987a,b; Frampton et al. 1992, 1995; Green et al. 1989; Hanley et al. 1992; Koenig et al. 1989, 1992, 1993, 1994; Kulle et al. 1986; Laube et al. 1993; Linn et al. 1989; Morrow et al. 1994; Utell et al. 1982, 1989; Yang and Yang 1994). Many of these (16/25) reported positive results (Avol et al. 1988a,b; Balmes et al. 1988; Fine et al. 1987a,b; Frampton et al. 1992; Green et al. 1989; Hanley et al. 1992; Koenig et al. 1989, 1992, 1994; Linn et al. 1989; Morrow et al. 1994; Utell et al. 1982, 1989; Yang and Yang 1994). Table 1 includes the positive and negative studies. It ranks the tabulated studies, along with findings of epidemiology studies of daily mortality (for example, see Dockery and Pope 1994). Ranking is in increasing order of the product of concentration (c) times exposure duration (1) (Haber’s rule states that cx t=constant; Ten Berge’s adjustment states that c” x t=constant, but the value of n is substance specific and species specific, and undefined for generic PM). Table 1 indicates that adverse particleassociated health effects have been demonstrated beginning at levels as low as 202
Brief Airborne Particle Excursions 95
ug /M (Yang and Yang 1994) and at exposure durations as short as 30 min (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). Asthmatics have been found to be among the populations most sensitive to PM based upon observations of pulmonary function changes occurring during controlled PM exposures of short duration. Most studies of this kind involving nonasthmatics have revealed no significant effects.
Participant ages in the clinical 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 (Balmes et al. 1988; Frampton 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 | and 3 min (FEV,, FEV;), forced vital capacity (FVO), and peak flow; as well as such symptoms as throat irritation and coughing (see references cited in Table 1).
In addition to the clinical studies described above, in which exposure of asthmatics to PM was controlled, are 4 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. (1970) reported a clear association of symptom severity with daily concentrations of smoke
TABLE 1. Particle effects revealed in controlled acute human exposures
Citation Healthy Asthmatic Activity Other Particle Dose x
Citation no. Subjects Subjects Level Age Factor(s) Type(s) Dose Duration Duration Effect(s)
wee wee wee wee wee (y) wee wee (ug/cuM) (min) (gmin /cu M) wee
Koenig et al. 29 0 14 exercise 13-18 H,SO, 3545 1,575 reduced lung function (FEV 1) 1992
Koenig et al. 28 0 9 exercise 12-18 H,SO,,S0O,, 68 40 2,720 no clinical symptoms; reduced 1989 H,SO, +SO,, lung function (FEV 1)
HNO,
Avolet al. 9 0 32 exercise 8-16 H,SO, 134 40 5,360 no effect (one subject: increased 1990 specific airway resistance) Yang and 60 30 25 atrest 23-48 TSP 202 30 6,060 healthy: no effects; asthmatic:
Yang 1994 reduced lung function (FEV 1) Koenig et al. 30 8 9 exercise 60-76 (NH,).SO4; 152. 40 6,080 no effects (airway resistance 1993 H,SO, noted to be correlated with + /—lemonade oral ammonia in asthmatics) Utell et al. 57 H,SO, 450 16 7,200 reduced lung function (specific 1982 airway conductance) in asthmatics Hanley et al. 25 0 22 exercise 12-19 H, SO, +/- 200 45 9,000 reduced Jung function (FEV 1, 1992 lemonade FVC2, FVC3) Anderson 4 15 15 exercise 18-45 carbon black 200 60 12,000 no effects et al. 1992 Koenig et al. 31 0 28 exercise 12-19 ozone, NO, 68 180 12,240 no effect (6 asthmatics did not 1994 H,SO,, HNO; complete protocol) Utell et al. 57 H,SO, 1,000 16 16,000 reduced lung function (specific 1982 airway conductance) in asthmatics Frampton 19 30 30 exercise 20-42 NaCl or H,SO,, 100 180 18,000 no PM effects (ozone effect et al. 1995 then ozone noted) Utell et al. 58 0 15 exercise 19-50 NaCl, NH;, 700 ~=—30 21,000 reduced lung function (FEV 1) 1989 H,SO, Anderson 4 0 15 exercise 18-45 carbon black + 358 60 21,480 no effects et al. 1992 H,SO, aerosol Morrow et al. 44 0 17 exercise 20-57 NaCl, H,SO, 190 120 22,800 reduced lung function (FEV 1)
L6
Morrow etal. 1994 Anderson etal. 1992 Aris et al. 1991b Aris et al. 1991b Aris et al. 199la
Laube et al.
1993 Linn et al. 1989
Aris et al. 1991b Avolet al. 1988a
Aris et al. 1991a
Linn et al. 1989
Green et al.
1989 Kulle et al. 1986
exercise
exercise
exercise
exercise
exercise
exercise
exercise
exercise
exercise
exercise
exercise
exercise
exercise
52-70
18-45
23-37
23-37
20-40
20-31
18-50
23-37
18-45
20-40
18-48
18-35
20-35
17 subjects with COPD
ozone sensitive, nonsmoker
ozone sensitive, nonsmoker
NaCl, H,SO,
carbon black + H,SO, aerosol
NaCl
H, SO,
HNO; fog
NaCl, H,SO,
H,SO,, ozone
H,SO,
H,SO,
HNO, fog
H,S0,
activated carbon +
formaldehyde
activated carbon, so,
3,000 3,000
1,000
1,400
1,460
2,000
1,020
22,800
30,300
48,000 48,000
60,000
60,000
78,000
84,000
87,600
90,000
120,000
122,400
124,080
no effects
no effects
no effects no effects
no effects
no effects
incremental, marginal acidinduced lung function decrease (FEV, ) and airway responsiveness increase
no effects
dose-related lower respiratory symptoms in asthmatics; reduced lung function (FEV 1)
no effects
increased symptoms with larger acid particles (4 asthmatics unable to complete protocol due to symptoms)
cough, reduced lung function (FVC, FEV3, peak flow)
no effects
TABLE 1. Particle effects revealed in controlled acute human exposures (continued).
Citation Healthy Asthmatic Activity Other Particle Dose x Citation no. Subjects Subjects Level Age Factor(s) Type(s) Dose Duration Duration Effect(s) see see see see see (y) see eee (ug/cuM) (min) (ug min /cu M) eee Avolet al. 8 22 22 exercise 18-45 H,SO, 2,193 60 131,580 dose-related lower 1988b respiratory symptoms in asthmatics; reduced lung function (peak flow) Culp et al. 12 16 0 exercise 20-39 NaCl +H,SO, 2,000 120 240,000 no effects on lung 1995 function Frampton 18 12 0 exercise 20-39 NaCl +H,SO, 2,000 120 240,000 throat irritation; no effect etal. on lung function 1992 Balmes et al. 10 0 12 atrest 25-41 30 milliOsmolar 5,900,000 to = 5,900,000 increased specific airway 1988 (mOsm) NaCl 87,100,000 resistance Balmes et al. 10 0 12 atrest 25-41 H,SO,, 5,900,000 to = 5,900,000 increased specific airway 1988 30 mOsm 87,100,000 resistance Balmes et al. 10 0 12 atrest 25-41 HNO,, 5,900,000 to = 5,900,000 increased specific airway 1988 30 mOsm 87,100,000 resistance Balmes et al. 10 0 12 atrest 25-41 H,SO, +HNO,, 5,900,000 to = 5,900,000 increased specific airway 1988 30 mOsm 87,100,000 resistance Balmes et al. 10 0 12 atrest 25-41 H,SO, 5,900,000 to = 5,900,000 increased specific airway 1988 300 mOsm 87,100,000 resistance Fine et al. 16 0 10 atrest 22-34 Na,SO, +acetic 0.25 to 2 bronchoconstriction 1987a acid +0, 8 ppm Fine et al. 17 0 8 atrest 22-29 HCl +H,SO, ? cough, increased airway
1987b
Aerosol Science and Technology 32:2 February 2000
or sulfuric acid in London. They concluded, however, that this association might not be attributed to the measured 24 h average concentrations, but more likely to “the effects of brief exposures to the maximum concentrations occurring during the day” (Lawther et al. 1970, p. 538), which may be several times the 24 h 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.
A second clinical study in which exposure of asthmatics to PM was uncontrolled was conducted by Delfino et al. (1997, 1998). Asthma symptom severity was found to be associated with PM levels. The strength of the association actually increased with increasing exposure duration, as would be expected. However, correcting for inhaler use per unit of exposure time (per hour) rather than per total exposure time (which had varied between 1 and 24 hours) revealed increased strength of the association with PM concentration as PM averaging time decreased from 24 h to 8h to lh (Michaels 1998).
In two clinical studies conducted in Australia, exposure to PM also was uncontrolled. Simpson et al. (1997) reported that daily mortality in Brisbane was associated with daily maximum 1 h, but not 24 h, average PM concentrations. PM was associated with mortality from cardiovascular but not respiratory conditions. In Sydney, Morgan et al. (1998) reported that admissions of people over age 65 into hospitals for treatment of chronic obstructive pulmonary disease (COPD) was associated more strongly with daily maximum 1 h PM concentrations (3.01% increase) than with 24h concentrations (2.41% increase). The rate at which people over age 65 were admitted to hospitals for treatment of heart conditions was associated with both maximum
Brief Airborne Particle Excursions 99
1 h and 24 h average PM concentrations. This latter association was reported to be of similar magnitude (2.7-2.8% increase in admissions), notwithstanding the averaging time difference.
A short time frame for human response to PM also was evident when 300 people required emergency medical attention on 24 April 1997, shortly after wind lofted fine particles into the air during a 4 day outdoor music festival attended by an estimated 40,000 people in Queen Creek, AZ (Michaels 1998). Arizona has a high concentration of residents with respiratory conditions. The incident primarily involved local bioaerosols including dried alfalfa fragments and the dominant pollen, which was probably mesquite during the incident although oak pollen might have been present as well even though it had peaked the week before the incident, according to University of Arizona faculty member Mary Kay O’Rourk (telephone communication 2 May 1997). Concentrations of competing PM,, originating from urban (predominantly combustion) sources were low, as reported by a letter dated 22 May 1997 from Bryan J. Sundblom of the Pinal County Air Quality Control District, which presumably also maintains these records for public scrutiny. Monitors were operating at 2 contiguous sites: Apache Junction North and Apache Junction South. Twenty-four hour average PM, concentrations were 28.88 and 31.01 yg /M°, respectively, on 22 April 1997; and 24.87 and 25.83 ug /M)?, respectively, on 28 April.
The studies described above demonstrate adverse health effects induced by shortterm exposure to particles. However, controlled exposures were 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
100 R.A. Michaels and M. T. Kleinman
rats and dogs, at Harvard University’s School of Public Health, have been published in abstract form (Godleski et al. 1996; Nearing et al. 1996a,b) and more completely in oral and written reports (Godleski 1995, 1996, 1999, 2000; Killingsworth et al. 1997). The findings implicate short-term, possibly electrophysiological mechanisms of fine-particle-induced cardiopulmonary malfunctioning, shown via electrocardiograms (EKGs).
Godleski et al. (2000) and Nearing et al. (1996b) induced ST segment elevation and periods of apnea in dogs inhaling fly ash at 1,000 wg/M?* for 3 days, 4 h per day. Nearing et al. (1996a) also demonstrated increased amplitude of T-wave alternans, an electrophysiological indicator of vulnerability to ventricular fibrillation, in dogs inhaling fly ash at 3,000 wg /M? for 3 days, 3 h per day. ST segment elevation and T-wave alternans effects began soon after exposure and became most prominent by day 3. Apnea for 20 to 30 s occurred during hour 4 on day 3. As a frequent precursor to potentially fatal heart attacks, T-wave alternans represents a clinically serious cardiological predictor of PM lethality.
PM lethality also has been demonstrated in animal models. Godleski (1995), Godleski et al. (1996, 2000), and Killingsworth et al. (1997) used rats exhibiting either monocrotaline-induced pulmonary inflammation or SO,-induced chronic bronchitis. Rats with such respiratory pathology then inhaled particles concentrated from Boston air at 228 to 288 wg /M? for 3 days, 6 h per day. Six h average PM concentration for the control group was 245+ /—70; for the monocrotaline-treated group, 228 + /— 89; and for the chronic bronchitis group, 288 + /—64 pg/M?. Although daily observations lasted 3 days, effects were observed beginning on day 1. Effects included increased bronchoconstriction, apnea, and mortality in treated groups compared with
Aerosol Science and Technology 32:2 February 2000
controls. The question of whether or not these short-term effects associated with PM exposure would have been mitigated if the same concentration-time product were attained over a 24 h period was not addressed.
At AAAR ’98, Godleski reported on a collection of PM transported to a concentrator from different compass directions (Godleski et al. 1999). Directions of PM origin were determined by wind direction. Electrophysiological parameters in dogs varied in real time with variation in the source direction of PM delivered to the test animals, augmenting evidence for shortterm physiological response to PM exposure.
Two bioassays were conducted in which aerosols were delivered either constantly at the average concentration or with excursions. The bioassays were conducted as part of a larger investigation by Kleinman et al. (1989). Although the report excludes from its scope the bioassays involving aerosol excursions, it includes the bioassay methods. In both bioassays, rats were exposed for 4 h to either of 2 aerosols, designated AMS and SAM. However, the rates at which the aerosols were delivered included no excursions, 1 excursion, or 4 excursions (Figure 1). An excursion was defined as an elevation of at least 50% above an otherwise constant steady state aerosol concentration, lasting for at least 5 min. The Kleinman et al. bioassays involved microscopic examination of rat lungs 48 h after 4h controlled exposures of groups of 6 rats to AMS or SAM, which are sulfate aerosols with the compositions listed in Table 2.
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.
rat lung lesion area at 48 hours (percent of area examined) —
excursions,
n=6rats AMS, four excursions, n= 6rats n=6rats SAM, one excursion, n=6rats “data source: Michael AMS: ammonium, Fe + Mn SAM: sulfuric acid, Fe + Mn sulfates ALL: ozone, NO2, SO2 (0.6, 2.6, Kleinman, UC/Irvine sulfates (0.5, 1.0, 0.2 mg/cu M) eC (0.5, 1.0, 0.2 mg/cu M) 5.0 ppm)
FIGURE 1. Pulmonary effect of 5- to 10-min sulfate aerosol excursions during 4-hour controlled exposures of rats.*
102 R.A. Michaels and M. T. Kleinman
TABLE 2. Composition of aerosols delivered to rats with or without excursions.*
AMS SAM Component Aerosol Aerosol Varied Components Ammonium 0.5mg/M? 0.0 mg /M? Sulfuric Acid 0.0 mg/M? 0.5 mg/M> Invariant Components Iron Sulfate 1.0 mg/M? 1.0 mg/M? Manganese 0.2mg/M? 0.2 mg /M? Sulfate Nitrogen 2.6 ppm 2.6 ppm Dioxide Ozone 0.6 ppm 0.6 ppm Sulfur 5.0 ppm 5.0 ppm Dioxide
*Source: Kleinman et al. (1989).
Results are presented in Figure 1, which consists of 2 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, both absolutely and proportionately, reflecting the effect of 4 excursions, compared with only 1 excursion in the case of rats exposed to the SAM aerosol.
CONCLUSIONS
Excursions of airborne particle mass may elevate PM, by an order of magnitude relative to 24 h average levels within the 150 ug /M? NAAQS. PM levels comparable to those reached during documented excursions can exert toxicological effects upon humans and animals, including mortality in animals. Such excursions might constitute a previously unrecognized cause of mortality and morbidity revealed by epidemiology studies based upon 24 h average PM levels. Toxicological effects reported in association with PM in the range of concentrations and durations of observed excursions are of types determined to be ap-
Aerosol Science and Technology 32:2 February 2000
propriate for air pollutant standard setting under the Clean Air Act, according to applicable criteria (American Thoracic Society 1985) adopted by the U.S. EPA (1994). Thus, the 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 (Michaels 1997).
To reduce residual risks posed by PM within the old NAAQS, the EPA has tightened control of fine particles, primarily by limiting maximum 24 h average airborne PM concentrations. A potentially complementary approach to further reduce risks is to maintain 24 h PM limits, while also controlling excursions, for example, by limiting 1 h average PM concentrations. A 1 h PM,, value in the range of 300 wg /M® has been suggested (Michaels 1996, 1998). Technical justification for the EPA’s preference for managing 24 h average PM, but not 1 h average PM concentrations (reflecting availability of 24 h average PM data), has also been questioned (Michaels 1997). Although additional study of the epidemiology of PM excursions is needed, the
complementary approach of limiting both 24 h and 1 h PM should be considered.
This research was supported by Rupprecht & Patashnick, Inc. (Albany, New York).
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104 R.A. Michaels and M. T. Kleinman
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Received November 4, 1998; accepted August 27, 1999.
Publication citation
Michaels, RA; and Michael T. Kleinman. Incidence and apparent health-significance of brief airborne particle excursions. Aerosol Science & Technology, 32:93-105, Feb. 2000;