© 2006 American Thoracic Society doi: 10.1164/rccm.2601003
Small Particles with Big EffectsNew York University School of Medicine, New York, New York
Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland The Clean Air Act directs the Environmental Protection Agency (EPA) to promulgate National Ambient Air Quality Standards (NAAQS) for particulate matter (PM) that are evidence-based and that protect the public health with "an adequate margin of safety," regardless of cost. The PM NAAQS, last revised in 1997, has recently been reviewed in a multi-year process, and initial recommendations for the next NAAQS were just made by the EPA. The latest proposal includes a slight tightening of the existing fine particle standard (for PM2.5, i.e., particles < 2.5 µm in aerodynamic diameter) and the addition of a standard for coarse PM in urban areas in the size range PM10–2.5. The new recommendations, however, are not as stringent as recommended by the Agency staff and the Clean Air Scientific Advisory Committee (CASAC), which provides peer review and guidance on the NAAQS. We call for, as has the American Thoracic Society, a more stringent NAAQS than Administrator Johnson's proposal. The PM NAAQS has a central role in the management of air quality in the United States. Particles have multiple sources, both natural and related to human activities, and the consequences of a new NAAQS are potentially sweeping. Consequently, the PM NAAQS is of great interest to stakeholders that include affected industries, municipalities, environmental groups, and nongovernmental organizations, particularly the American Lung Association, and the public generally. Over the six-year process leading to the most recent proposal for revision of the NAAQS, there has again been substantial discussion and controversy concerning the new scientific evidence since the prior NAAQS and the extent to which key uncertainties have been addressed. The new evidence is substantial, in part because Congress called for a national research agenda on PM that was to be developed by the EPA with guidance from a committee of the National Research Council (1). PM has now been linked to a broad range of adverse health effects, both respiratory and cardiovascular, in epidemiologic and toxicologic research. The diversity of effects may reflect the complexity of airborne PM, which is made up of a rich mixture of primary and secondary particles. Combustion sources—vehicles, power generation, and industry—are major contributors to urban PM. Monitoring data show that PM2.5 differs in concentration and characteristics across regions of the country, within urban areas and by season. The U.S. median annual average PM2.5 concentration is 13 µg/m3 (range, 4–28 µg/m3), with higher levels in urban areas and in the eastern United States and California. Physical and chemical properties of PM have been postulated to be determinants of toxicity: for example, metal content, oxidative potential, or being in the ultrafine size mode (< 0.10 µm). Consequently, management of sources of more toxic particles may be critical to public health and effects of PM on health may vary across the country. The primary impetus for the 1997 PM NAAQS and the current proposed revision has been epidemiologic evidence that associates PM with increased risk for mortality (2). Time-series studies reported in the early 1990s showed that day-to-day variation in PM concentration was associated with mortality counts (3). These studies in selected cities have now been followed by national-level time-series analyses in the United States and Europe that pool data from broad regions to produce national estimates of the effect of PM on daily mortality. For example, in 90 U.S. cities, the National Morbidity and Mortality Air Pollution Study (NMMAPS) estimated a 0.2% increase of all-cause mortality per 10 µg/m3 increase in PM10 (4). Risk was highest in the northeast and for cardiovascular and respiratory causes of death. Findings of follow-up studies, including most notably the Harvard Six Cities Study (5) and the American Cancer Society's Cancer Prevention (CPS) II Study (6), show that the resulting loss of life may be substantial. The World Health Organization estimated that inhalation of PM in ambient air causes 500,000 premature deaths per year. The time-series studies show a linear relationship between PM concentration and risk at concentrations measured routinely in many U.S. cities (7). There is a now a substantial, parallel literature on PM and morbidity. Studies have addressed PM and risk for hospitalization and other clinical outcomes and preclinical biomarkers (8). Since the 1997 PM NAAQS, there has been an explosion of research on cardiovascular consequences of exposure to PM (9) indicating short-term and long-term effects of PM on cardiovascular health.
Expanding toxicologic research indicates multiple mechanisms by which PM might cause disease. The evidence on PM2.5 and cardiovascular health effects is illustrative of the complexity of underlying pathogenetic mechanisms (9): cardiovascular effects of PM exposure may result from systemic inflammation, autonomic effects, or accelerated atherosclerosis. Particles mobilize monocytes, band cells, and neutrophils from the bone marrow, elevate serum 1L-1
Numerous studies have shown that PM exposure activates inflammatory pathways in the respiratory system. For example, in vitro exposure of normal human bronchial epithelial (NHBE) cells stimulates release of oxidants, hemeoxygenase, cytokines, and upregulation of NF- In the face of the extensive evidence on PM and health and the strong mandate of the Clean Air Act for public health protection, the PM NAAQS proposed by Administrator Johnson appear lax. Based on the same evidence, the American Thoracic Society and other health organizations have recommended 12 and 25 µg/m3 for the average annual and 24-h PM2.5 standards, respectively. The proposed, less stringent standard does not protect the nation's health, as required by the Clean Air Act. FOOTNOTES Conflict of Interest Statement: Neither author has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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