Health effects of outdoor air pollution. Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society.
Particles, SOx, and acid aerosols are a complex group of distinct pollutants that have common sources and usually covary in concentration. During the past two decades, the chemical characteristics and the geographic distribution of sulfur oxide and particulate pollution have been altered by control strategies, specifically taller stacks for power plants, put in place in response to air pollution regulations adopted in the early 1970s. While the increasing stack heights have lowered local ambient levels, the residence time of SOx and particles in the air have been increased, thereby promoting transformation to various particulate sulfate compounds, including acidic sulfates. These sulfate particles constitute a large fraction of the total mass of smaller particles (< 3 microns in aerodynamic diameter). Epidemiologic studies have consistently provided evidence of adverse health effects of these air pollutants. Particulate and SO2 pollution were strongly implicated in the acute morbidity and mortality associated with the severe pollution episodes in Donora (Pennsylvania), London, and New York in the 1940s, 1950s, and 1960s. There is new evidence that even current ambient levels of PM10 (30 to 150 micrograms/m3) are associated with increases in daily cardiorespiratory mortality and in total mortality, excluding accidental and suicide deaths. These associations have been shown in many different communities, as widely different in particle composition and climate as Philadelphia, St. Louis, Utah Valley, and Santa Clara County, California. It has recently been shown in a long-term prospective study of adults in the United States that chronic levels of higher PM10 pollution are associated with increased mortality after adjusting for several individual risk factors. Daily fluctuations in PM10 levels have also been shown to be related to acute respiratory hospital admissions in children, to school and kindergarten absences, to decrements in peak flow rates in normal children, and to increased medication use in children and adults with asthma. Although some epidemiologic studies suggest that acid aerosols are an important toxic component of PM10, other studies do not support this hypothesis. Dockery and Pope (408) recently reviewed the epidemiologic literature for adverse effects, assuming that reported associations can be attributed to acute particle mass exposures. Combined effects were estimated as percent increase in comparable measures of mortality and morbidity, associated with each 10 micrograms/m3 increase in daily mean PM10 exposure (Table 7). While total mortality increased by 1% for each 10 micrograms/m3 increase in PM10, respiratory mortality increased by 3.4% and cardiovascular mortality increased by 1.4%. Hospital admissions and emergency department visits increased approximately 1% for all respiratory complaints, and 2% to 3% for asthma. Exacerbation of asthma increased by about 3%, as did lower respiratory symptoms. Small decreases in lung function, approximately 0.1%, have also been observed. This review suggests that the epidemiologic studies of adverse morbidity measures are coherent with the mortality studies showing quantitatively similar adverse effects of acute exposures to particulate pollution. Despite these epidemiologic findings for acute and chronic adverse health effects from air pollution associated with relatively low levels of inhalable particles, there are no complementary data from toxicologic studies or from acute human exposures to similar levels of respirable particles. Thus, controlled human exposures to various particles, including H2SO4, at relevant levels (< 150 micrograms/m3) have not identified significant alterations in respiratory function in healthy individuals.(ABSTRACT TRUNCATED)
D000328:Adult; D000336:Aerosols / Q000633:toxicity; D000393:Air Pollutants / Q000633:toxicity; D000397:Air Pollution / Q000009:adverse effects* / Q000517:prevention & control; D000818:Animals; D001249:Asthma / Q000150:complications; D015415:Biomarkers; D016535:Bronchial Hyperreactivity; D002248:Carbon Monoxide / Q000633:toxicity; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000401:mortality; D002417:Cattle; D002478:Cells, Cultured; D002648:Child; D004630:Emergencies; D004782:Environmental Health / Q000331:legislation & jurisprudence; D005260:Female; D006760:Hospitalization; D006801:Humans; D007854:Lead / Q000633:toxicity; D008173:Lung Diseases, Obstructive / Q000150:complications; D008297:Male; D008954:Models, Biological; D009585:Nitrogen Dioxide / Q000633:toxicity; D016272:Occupational Health / Q000331:legislation & jurisprudence; D010126:Ozone / Q000633:toxicity; D011247:Pregnancy; D011817:Rabbits; D051381:Rats; D012129:Respiratory Function Tests; D012140:Respiratory Tract Diseases / Q000453:epidemiology* / Q000401:mortality; D013458:Sulfur Dioxide / Q000633:toxicity; D014481:United States
D000336:Aerosols; D000393:Air Pollutants; D015415:Biomarkers; D013458:Sulfur Dioxide; D007854:Lead; D010126:Ozone; D002248:Carbon Monoxide; D009585:Nitrogen Dioxide