Volume 2 Issue 4
July-September 1997
AIRBORNE PARTICULATE MATTER

INTRODUCTION

Airborne particles have long been known to be a health hazard, ever since major cities became filled with soot in the early days of the industrial revolution. Historical pollution episodes like those in London in 1952 and Donora, Pennsylvania in 1948 raised awareness of the potential health threat of pollution. Approximately 4000 people died during the two-week London episode, and the deaths have been attributed to a combination of particles, SO2 and acid aerosols. More recently, scientists have turned their attention to smaller particles as a potential health threat, including "fine" and "ultrafine" particles (PM2.5 and PM0.1, respectively). One concern with particle sizes is the ability of the particles to enter the respiratory tract and penetrate deeply into the lungs. Larger particles are more likely to be trapped in the nasal passages or the trachea, but smaller particles can be carried into the lung and enter the alveoli, or air exchange sacs.

On July 18, 1997, the U.S. Environmental Protection Agency established new air quality standards for particulate matter, adding new standards for PM2.5 while retaining PM10 standards. Environment Canada is also considering revisions to the air quality guidelines for particulate matter, and it is expected that proposed guidelines for PM10 and PM2.5 will be published in Fall 1997.



PARTICULATE MATTER TERMS

There are a number of terms for particulate matter that are all based on the sampling method used. An historical PM measure that is still in use is Total Suspended Particles (TSP), in which airborne particles are captured on a filter and weighed; particles ranging in size from 0 to about 40 microns are included.

In the U.S. and Canada, PM standards or guidelines are now based on PM10 or PM2.5, where the "cut-off" diameter of the captured particles is 10 or 2.5 microns, respectively. Coarse Particles (CP or PM10-2.5) is determined by subtracting the fine particle concentration from PM10. The particles are still collected on a filter and weighed, but the collection devices first exclude particles of larger sizes. TSP, PM10 and PM2.5 are all measured as mass per volume of air, usually ug/m3.

Two historical PM measures that are still commonly used are Coefficient of Haze (COH) and Black Smoke or British Smoke (BS). Both are measured by collecting particles on a filter or tape, and determining the quantity of particles by reflectiveness or opacity; BS is a measure of the "blackness" of the particle stain on the filter paper. These more indirect measures can be converted to ug/m3 if the monitors can be calibrated to another nearby collection device that measures PM by mass (such as PM10).

Note: All particle sizes are described in terms of "aero-dynamic diameter" or the functional diameter equivalent to that of a spherical particle which settles at the same rate as the particles considered.

COMMUNITY HEALTH STUDIES

The results of numerous epidemiological studies indicate that an increase in PM concentration is associated with increased mortality, increased hospitalization for respiratory or cardiovascular diseases, increases in respiratory symptoms and decreased lung function.1 In one review article, a 10 ug/m3 increase in PM10 concentration was found to be associated with a 1% increase in daily mortality, and a 3% increase in asthma attacks, bronchodilator use and lower respiratory symptoms.2

Mortality: There are numerous studies that link exposure to PM with increased mortality. Two recent publications from the U.S. show associations with both long-term and short-term exposures. Pope et al.,3 using data from surveys of American Cancer Society volunteers from 151 U.S. metropolitan areas, found a relative risk ratio of 1.17 (1.09 to 1.26) for mortality from all causes with long-term exposure to PM2.5. The availability of questionnaire data allowed the authors to adjust for factors such as cigarette smoking and occupational exposures. In the short-term study, Schwartz et al.4 found that a 10 ug/m3 increase in PM2.5 (from two days previously) was associated with a 1.5% (1.1% to 1.9%) increase in total mortality in six U.S. cities. For both studies, higher risk levels were found when considering mortality from cardiopulmonary diseases.

Recently-published studies from other countries support these findings. Researchers in England4 found that a 10 ug/m3 increase in PM10 was associated with a 1.1% increase in mortality for all causes (p=0.03), as well as with a 5% increase in death due to chronic obstructive pulmonary disease and a 1.7% increase in deaths from circulatory diseases. In Mexico City, an increase in total mortality was associated with a 100 ug/m3 increase in TSP (rate ratio 1.058, 95% CI 1.033-1.083).5

While many previous studies have found associations between PM exposure and mortality in adults, a recent report suggests that increased mortality among infants is associated with increased exposure to PM.6 Woodruff et al. obtained data on almost 4 million infants from 86 U.S. metropolitan areas, and the infants' PM10 exposures during the first two months of life were classified as high, low or medium using ambient monitoring data (PM10 range 11.9-68.8 ug/m3). In normal birth weight infants, high PM10 exposure was associated with death from respiratory causes (OR 1.40, 95% CI 1.05, 1.85) and sudden infant death syndrome (OR 1.26, 95% CI 1.14, 1.39). An increased in death from respiratory causes was also found in low birth weight infants, though not statistically significant.

Hospital Admissions: Many, but not all, studies have found associations between PM exposure and hospitalization. In England,5 a 10 ug/m3 increase in PM10 was associated with 2 to 6% increases in hospital admissions for asthma, bronchitis, pneumonia, all respiratory causes and cerebrovascular diseases. A recent study in Tucson, Arizona8 found an increase in admissions for cardiovascular disease (2.75%, 95% CI 0.52-5.04) for a change from 28 to 51 ug/m3 PM10. A similar association was found with CO concentration, and the PM10 and CO effects were found to be independent and additive. In the winter months in Santa Clara County, California,9 where wood stoves are commonly used as a heat source, significant increases in emergency room visits for asthma were found with a 60 ug/m3 increase in PM10 when temperatures were below, but not when above, 41 degrees. Relative risks in different temperature categories ranged from 1.11 (95% CI 1.03-1.19) to 1.43 (95% CI 1.18-1.69).

However, in a reanalysis of data from an earlier study, Moolgavkar and colleagues10 found no associations between admissions for respiratory disease with pollutants in Birmingham, Alabama, and, in Minneapolis-St. Paul, only a small increase in admissions (3.4% increase) with PM10 was found and that association was not statistically significant when other pollutants were considered. Mixed findings have also been reported in Canadian studies, though it should be noted that both used only data from the summer months, while PM levels can be higher in the winter. In Montreal,11 ozone was found to be the strongest predictor of emergency room visits for respiratory illness but positive associations were also found with particles, with significant increases of 16%, 12% and 6% predicted for mean increases in PM10, PM2.5 and sulfate concentration, respectively. The authors conclude that relative mass

COMMUNITY HEALTH STUDIES (continued)

effects are PM2.5 > PM10 >> sulfates. In contrast, Burnett et al.12 found associations with admissions for respiratory or cardiac causes and numerous PM measures (PM10, PM2.5, COH, CP, sulfates and acid aerosols), but statistical significance was generally lost when additional pollutants (especially ozone and nitrogen dioxide) were considered in the models.

Respiratory Symptoms or Pulmonary Function Changes: Researchers in California13 found a significant increase in inhaler use with a 10 ug/m3 increase in PM10 (p<0.02) in a panel of asthmatic subjects (9 to 46 years of age); no significant effect on peak flow rate was found with PM exposure. Lower respiratory illness in children was found to increase with both a 20 ug/m3 increase in PM10 (1.08, 95% CI 1.04-1.15) and a 10 ug/m3 increase in PM2.5 (1.21, 95% CI 1.08-1.35) in Mexico City.14 In Amsterdam, decreases in morning and evening peak flow rate (4% and 3%, respectively) and significant increases in 3 of 4 symptom categories were found over the range of 4 to 40 ug/m3 BS; smaller effects were seen for ozone and PM10.15 A recent report from the large Swiss study (nearly 10,000 adult subjects) indicates that a 3.4% decrease in FVC (a lung function measure) is associated with a 10 ug/m3 increase in PM10.16 In contrast, Thurston17 found ozone to be more strongly associated with pulmonary function changes than measures of acid aerosols and sulfates in a Connecticut asthma summer camp.

Other health effects: In a comprehensive research project currently underway in the Teplice region of the Czech Republic,18 the effects of air pollution on numerous health endpoints is being studied. Preliminary findings indicate that recent exposures to both SO2 and TSP are associated with decreases in sperm viability, though not total sperm count. In Beijing,19 a study of approximately 75,000 births (mother's first child) indicates an association between low birth weight and both SO2 and TSP exposure during the third trimester; the authors report that the proportion of low birth weight attributable to air pollution is 13%. The increased Odds Ratios for low birth weight (<2500 g) for a 100 ug/m3 change in pollutant were 1.11 (95% CI 1.06-1.16) for SO2 and 1.10 (95% CI 1.05-1.14) for TSP.

AIRBORNE PARTICLES IN THE U.S. AND CANADA

The PM standards recently established by the U.S. EPA are 15 ug/m3 for the annual mean and 65 ug/m3 for a daily mean concentration of PM2.5. For PM10, the levels of 50 ug/m3 (annual mean) and 150 ug/m3 (24-hour) remain in place. (For each standard there are different averaging times or other parameters used in determining compliance.)

Scientists from Environment Canada and Health Canada20 recently published a report on PM measurements from 19 Canadian locations. For 14 urban areas, the average TSP level was 55.2 ug/m3, with a maximal concentration of 572 ug/m3. Average daily concentrations of PM10 and PM2.5 were 27.6 ug/m3 (maximum 175 ug/m3) and 13.9 ug/m3 (maximum 89 ug/m3), respectively. Approximately 44% of TSP was found to be PM10, and PM2.5 comprises about 49% of PM10. Levels of PM2.5 increased from summer to winter, presumably due to increases from combustion sources in the heating season. PM10 was slightly increased during the winter months; CP levels decreased somewhat in winter.

Using monitoring data from 42 non-urban sites in he U.S.,21 PM2.5 concentrations were found to increase from west to east, with annual mean concentrations of 4 and 12 ug/m3, respectively, while PM10 annual mean concentrations ranged from 18 ug/m3 in southeastern states to 8 ug/m3 in central western states. The ratio of PM2.5 to PM10 ranged from 45% in the western states to 65% in eastern U.S. states.

BIOLOGICAL MECHANISMS FOR PM EFFECTS

Numerous toxicological studies and several clinical studies have been published recently that offer insight into the biological means by which PM exposure would result in adverse respiratory or cardiovascular effects.

Increased inflammatory response with PM exposure is indicated in several recent studies. U.S. EPA researchers22 have found evidence for effects mediated by the transition metal (iron, nickel, vanadium, etc.) content of particles. Effects seen included recruitment of immune cells (neutrophils, eosinophils, monocytes) and inflammation of the lung tissue. German researchers23 have found both the water-soluble (i.e. metals) and solvent-soluble (i.e. polynuclear aromatic hydrocarbons) components of particles can exacerbate inflammatory reactions, though the effects were somewhat different. The aqueous component of particles was associated with increased immune chemical levels (PGE2 and IL-8), while increased production of reactive oxygen species was found with the organic PM component. Studies have also suggested that PM exposures may exacerbate allergic responses, and a recent study reports that grass pollen allergen binds to diesel exhaust particles, which could allow allergens to become concentrated in polluted air and thus trigger attacks of allergic asthma.24

It was hypothesized that inflammatory reactions may result in changes in blood chemistry that result in the cardiac effects found in epidemiological studies of PM exposure. Recently, German researchers25 reported significant increases in plasma viscosity in men during an air pollution episode during Winter 1984-5. Increases were found to be associated with three measured pollutants, TSP, SO2 and CO, but the associations were only statistically significant for SO2 and CO among women.



REFERENCES:

1) Vedal S. 1997. J Air Waste Manage Assoc 47:551-581

2) Dockery DW, Pope CA III. 1994. Annu Rev Public Health 15:107-132

3) Pope CA III, Thun MJ, Namboori MM et al. 1995. Am J Respir Crit Care Med 151:669-674

4) Schwartz J, Dockery DW, Neas LM. 1996. J Air Waste Manage Assoc 46:927-939

5) Wordley J, Walters S, Ayres JG. 1997. Occup Environ Med 54:108-116

6) Borja-Aburto VH, Loomis DP, Bangdiwala SI, Shy CM, Rascon-Pacheco RA. 1997. Am J Epidemiol 145:258-268

7) Woodruff TJ, Grillo J, Schoendorf KC. 1997. Environ Health Perspect 105:608-612.

8) Schwartz J. 1997. Epidemiol 8:371-377

9) Lipsett M, Hurley S, Ostro B. 1997. Environ Health Perspect 105:216-222

10) Moolgavkar SH, Luebeck EG, Anderson EL. 1997. Epidemiol 8:364-370

11) Delfino RJ, Murphy-Moulton AM, Burnett RT, Brook JR, Becklake MR. 1997. Am J Respir Crit Care Med 155:568-576

12) Burnett RT, Cakmak S, Brook JR, Krewski D. 1997. Environ Health Perspect 105:614-620

13) Delfino RJ, Zeiger RS, Seltzer JM, et al. 1997. Environ Health Perspect 105:622-635

14) Romieu I, Meneses F, Ruiz S, et al. 1996. Am J Respir Crit Care Med 154:300-307

15) Gielen MH, van der Zee SC, Wijnen JH, van Steen CJ, Brunekreef B. 1997. Am J Respir Crit Care Med 155:2105-2108

16) Ackermann-Liebrich U, Leuenberger P, Schwartz J, et al. 1997. Am J Respir Crit Care Med 155:122-129

17) Thurston GD, Lippmann M, Scott MB, Fine JM. 1997. Am J Respir Crit Care Med 155:654-660

18) Wang X, Ding H, Ryan L, Xu X. 1997. Environ Health Perspect 105:514-520

19) Sram RJ, Benes I, Binkova B, et al. 1996. Teplice program - the impact of air pollution on human health. Environ Health Perspect 104:699-714

20) Brook JR, Dann TF, Burnett RT. 1997. J Air Waste Manage Assoc 47:2-19

21) Eldred RA, Cahill TA, Flocchini RG. 1997. J Air Waste Manage Assoc 47:194-203

23) Dreher KL, Jaskot RH, Lehmann JR et al. 1997. J Toxicol Environ Health 50:285-305

24) Hitsfeld B, Friedrichs KH, Ring J, Behrendt H. 1997. Toxicol 120:185-95

25) Peters A, Doring A, Wichmann H-E, Koenig W. 1997. Lancet 349:1582-1587

26) Knox RB, Suphioglu C, Taylor P, et al. 1997. Clin Exp Allergy 27:246-251

PREPARED BY:

Great Lakes Center for Occupational and Environmental Safety and Health
School of Public Health
University of Illinois at Chicago
2121 West Taylor Street
Chicago, Illinois 60612-7260
(312) 996-7887
email: mross1@uic.edu

 

Project Coordinator:
Mary A. Ross, PhD
Senior Science Advisor:
Daniel O. Hryhorczuk, MD, MPH

 

A quarterly summary of recent findings in the scientific literature on human health effects and environmental pollutants, with an emphasis on pollutants of the Great Lakes ecosystem. Prepared under the direction of the Health Professionals Task Force of the International Joint Commission. This does not represent the official position of the International Joint Commission.

 

Health Professionals Task Force Secretary: Jim Houston
International Joint Commission
Canada Section
100 Metcalfe Street
Ottawa, Ontario K1P 5M1
phone (613) 995-0230
fax (613) 993-5583
email houstonj@ijc.achilles.net


Revised October 6, 1997

Maintained by Kevin Stone, kstone@magi.com