Source-to-receptor pathways of anthropogenic PM2.5 in Detroit, Michigan: Comparison of two inhalation exposure studies

Masako Morishita, Gerald J. Keeler, Jacob D. McDonald, James G. Wagner, Li Hao Young, Satoshi Utsunomiya, Rodney C. Ewing, Jack R. Harkema

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Recent studies have attributed toxic effects of ambient fine particulate matter (aerodynamic diameter ≤ 2.5 μm; PM2.5) to physical and/or chemical properties rather than total mass. However, identifying specific components or sources of a complex mixture of ambient PM2.5 that are responsible for adverse health effects is still challenging. In order to improve our understanding of source-to-receptor pathways for ambient PM2.5 (links between sources of ambient PM2.5 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 PM2.5 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 PM2.5 and CAPs, identification of major emission sources of PM2.5, 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 PM2.5, 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 PM2.5-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 PM2.5 emitted from refineries and incinerators and biologically relevant dose, which in turn may be associated with observed health effects.

Original languageEnglish
Pages (from-to)1805-1813
Number of pages9
JournalAtmospheric Environment
Volume43
Issue number10
DOIs
Publication statusPublished - Mar 1 2009
Externally publishedYes

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air
meteorology
trace metal
chemical property
animal
asthma
metal
toxicology
aerodynamics
point source
particulate matter
combustion
comparison
particle
exposure
trace element
modeling
effect
health
dose

All Science Journal Classification (ASJC) codes

  • Environmental Science(all)
  • Atmospheric Science

Cite this

Source-to-receptor pathways of anthropogenic PM2.5 in Detroit, Michigan : Comparison of two inhalation exposure studies. / Morishita, Masako; Keeler, Gerald J.; McDonald, Jacob D.; Wagner, James G.; Young, Li Hao; Utsunomiya, Satoshi; Ewing, Rodney C.; Harkema, Jack R.

In: Atmospheric Environment, Vol. 43, No. 10, 01.03.2009, p. 1805-1813.

Research output: Contribution to journalArticle

Morishita, Masako ; Keeler, Gerald J. ; McDonald, Jacob D. ; Wagner, James G. ; Young, Li Hao ; Utsunomiya, Satoshi ; Ewing, Rodney C. ; Harkema, Jack R. / Source-to-receptor pathways of anthropogenic PM2.5 in Detroit, Michigan : Comparison of two inhalation exposure studies. In: Atmospheric Environment. 2009 ; Vol. 43, No. 10. pp. 1805-1813.
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