Relative contributions of PM2.5 chemical constituents to acute arterial vasoconstriction in humans.

Inhal Toxicol

Gage Occupational and Environmental Health Unit, St. Michael's Hospital, and Public Health Sciences, University of Toronto, Toronto, Ontario, Canada.

Published: June 2004

Studies have shown associations between acute ambient particulate matter (PM) levels and increases in morbidity and mortality from cardiovascular diseases. We have previously reported in 24 healthy adults that exposure to concentrated ambient particles plus ozone (CAP + O(3)) caused a mean decrease of 0.09 mm in brachial artery diameter (BAD), which was significantly larger than a mean increase of 0.01 mm among the same individuals exposed to filtered air (FA). Our current objective is to examine the relationship between total and constituent PM(2.5) mass concentrations and the acute vascular response. We have analyzed both ambient and exposure filters from the brachial artery study for major chemical constituents, allowing us to compare the strength of the associations between each constituent and an individual's arterial response. We determined gravimetric PM(2.5) mass concentration and inorganic ion content from exposure filters. Twenty-three-hour ambient PM(2.5) filters collected from the same site and on the same day were used to estimate exposure concentrations of trace elements and organic and elemental carbon. We performed linear regression analyses on the levels of measured or estimated PM constituents using each subject's FA exposure as a control. We found, from our regression analyses, a significant negative association between both the organic and elemental carbon concentrations and the difference in the postexposure change in the BAD (Delta BAD) between and CAP + O(3) and FA exposure days. An understanding of the PM constituents most responsible for adverse health outcomes is critical for efforts to develop pollution abatement strategies that maximize benefits to public health.

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http://dx.doi.org/10.1080/08958370490439489DOI Listing

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