title: National Particle Component Toxicity (NPACT) Initiative: integrated epidemiologic and toxicologic studies of the health effects of particulate matter components.
abstract: Particulate matter (PM*), an ambient air criteria pollutant, is a complex mixture of chemical components; particle sizes range from nanometer-sized molecular clusters to dust particles that are too large to be aspirated into the lungs. Although particle composition is believed to affect health risks from PM exposure, our current health-based air quality standards for PM are limited to (1) the mass concentrations of PM2.5 (particles 2.5 microm or smaller in aerodynamic diameter), which are largely attributable to combustion products; and (2) PM10 (10 microm or smaller), which includes larger-sized mechanically generated dusts. Both of these particle size fractions are regulated under the National Ambient Air Quality Standards (NAAQS) and both have been associated with excess mortality and morbidity. We conducted four studies as part of HEI's integrated National Particle Component Toxicity (NPACT) Initiative research program. Since 1999, the Chemical Speciation Network (CSN), managed by the U.S. Environmental Protection Agency (U.S; EPA), has routinely gathered air monitoring data every third or sixth day for the concentrations of numerous components of PM2.5. Data from the CSN enabled us to conduct a limited time-series epidemiologic study of short-term morbidity and mortality (Ito study); and a study of the associations between long-term average pollutant concentrations and annual mortality (Thurston study). Both have illuminated the roles of PM2.5 chemical components and source-related mixtures as potentially causal agents. We also conducted a series of 6-month subchronic inhalation exposure studies (6 hours/day, 5 days/week) of PM2.5 concentrated (nominally) 10 x from ambient air (CAPs) with apolipoprotein E-deficient (ApoE(-/-)) mice (a mouse model of atherosclerosis) (Chen study). The CAPs studies were conducted in five different U.S. airsheds; we measured the daily mass concentrations of PM2.5, black carbon (BC), and 16 elemental components in order to identify their sources and their roles in eliciting both short- and long-term health-related responses. In addition, from the same five air-sheds we collected samples of coarse (PM10-2.5), fine (PM2.5-0.2), and ultrafine (PM0.2) particles. Aliquots of these samples were administered to cells in vitro and to mouse lungs in vivo (by aspiration) in order to determine their comparative acute effects (Gordon Study). The results of these four complementary studies, and the overall integrative analyses, provide a basis for guiding future research and for helping to determine more targeted emission controls for the PM components most hazardous to acute and chronic health. Application of the knowledge gained in this work may therefore contribute to an optimization of the public health benefits of future PM emission controls. The design of each NPACT study conducted at NYU was guided by our scientific hypotheses, which were based on our reviews of the background literature and our experience in conducting studies of associations between ambient PM and health-related responses. These hypotheses guided the development and conduct of the four studies. Hypothesis 1. Coarse, fine, and ultrafine PM are each capable of producing acute health effects of public health concern, but the effects may differ according to particle size and composition. (Applies to all studies.) Hypothesis 2. Long-term PM2.5 exposures are closely associated with chronic health effects. (Applies to studies 1 and 4.) Hypothesis 3. The source-apportionment techniques that we have developed and refined in recent years provide a useful basis for identifying major categories of sources of PM in ambient air and specific chemical components that have the greatest impacts on a variety of acute and chronic health effects. (Applies to all studies.) Hypothesis 4. The health effects due to ambient PM exposures can best be seen in sensitive subgroups within overall human populations and in animal models of such populations. (Applies to studies 1, 3, and 4.) Overall, the studies have demonstrated that the toxicity of PM is driven by a complex interaction of particle size range, geographic location, source category, and season. These findings suggest that the components of PM--associated with certain categories of sources--are responsible for the observed adverse health effects. Most importantly, the responsible components and source categories vary with the health-related endpoints being assessed. Across all studies, fossil-fuel combustion source categories were most consistently associated with both short- and long-term adverse effects of PM2.5 exposure. The components that originate from the Residual Oil Combustion and Traffic source categories were most closely associated with short-term effects; and components from the Coal Combustion category were more closely associated with long-term effects.
authors.affiliation: Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY 10987, USA. morton.lippmann@nyumc.org
authors.forename: Morton
authors.initials: M
authors.lastname: Lippmann
authors.affiliation: Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY 10987, USA.
authors.forename: Lung-Chi
authors.initials: LC
authors.lastname: Chen
authors.affiliation: Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY 10987, USA.
authors.forename: Terry
authors.initials: T
authors.lastname: Gordon
authors.affiliation: Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY 10987, USA.
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Ito
authors.affiliation: Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY 10987, USA.
authors.forename: George D
authors.initials: GD
authors.lastname: Thurston
mesh_terms: D000393:Air Pollutants / Q000032:analysis* / Q000633:toxicity*; D000397:Air Pollution / Q000009:adverse effects*; D000818:Animals; D015984:Causality; D002648:Child; D004781:Environmental Exposure / Q000706:statistics & numerical data*; D006801:Humans; D051379:Mice; D052638:Particulate Matter / Q000633:toxicity*; D011634:Public Health / Q000592:standards*; D012140:Respiratory Tract Diseases / Q000453:epidemiology* / Q000209:etiology; D015996:Survival Rate; D013997:Time Factors; D014481:United States / Q000453:epidemiology
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter