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

摘要

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.rnThis 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.