Source-to-receptor pathways of anthropogenic PM 2.5 in Detroit, Michigan: Comparison of two inhalation exposure studies

Abstract

Recent studies have attributed toxic effects of ambient fine particulate matter (aerodynamic diameter ≤ 2.5 μm; PM 2.5) to physical and/or chemical properties rather than total mass. However, identifying specific components or sources of a complex mixture of ambient PM 2.5 that are responsible for adverse health effects is still challenging. In order to improve our understanding of source-to-receptor pathways for ambient PM 2.5 (links between sources of ambient PM 2.5 and measures of biologically relevant dose), integrated inhalation toxicology studies using animal models and concentrated air particles (CAPs) were completed in southwest Detroit, a community where the pediatric asthma rate is more than twice the national average. Ambient PM 2.5 was concentrated with a Harvard fine particle concentrator housed in AirCARE1, a mobile air research laboratory which facilitates inhalation exposure studies in real-world settings. Detailed characterizations of ambient PM 2.5 and CAPs, identification of major emission sources of PM 2.5, and quantification of trace elements in the lung tissues of laboratory rats that were exposed to CAPs for two distinct 3-day exposure periods were completed. This paper describes the physical/chemical properties and sources of PM 2.5, pulmonary metal concentrations and meteorology from two different 3-day exposure periods—both conducted at the southwest Detroit location in July 2003—which resulted in disparate biological effects. More specifically, during one of the exposure periods, ambient PM 2.5-derived trace metals were recovered from lung tissues of CAPs-exposed animals, and these metals were linked to local combustion point sources in southwest Detroit via receptor modeling and meteorology; whereas in the other exposure period, no such trace metals were observed. By comparing these two disparate results, this investigation was able to define possible links between PM 2.5 emitted from refineries and incinerators and biologically relevant dose, which in turn may be associated with observed health effects.