The health effects of ambient fine
particulate matter (PM(2.5)) and its potential impact on vascular
endothelial function have not been thoroughly investigated. As
endothelial dysfunction plays an important role in the
pathogenesis of
atherosclerosis and its complications, we examined the effects of concentrated fine ambient particles (CAPs) on the plasma level of
asymmetric dimethylarginine (
ADMA) in a pilot study.
ADMA is a circulating endogenous inhibitor of
nitric oxide synthase (NOS) that is associated with
impaired vascular function and increased risk for
cardiovascular events. A mobile air research laboratory (AirCARE 1) was used to provide "real-world" CAPs exposures for this study conducted in Detroit, MI. Fourteen Brown
Norway rats were exposed to
filtered air (FA) (n = 7) or CAPs (0.1-2.5 microm) (n = 7) for 3 consecutive days (8 h/day) in July 2002. Rats were exposed during these periods to
average particle mass concentrations of 354 microg/m(3). Rat plasma samples were collected 24 h postexposure. Plasma concentrations of
ADMA were significantly elevated in rats exposed to CAPs versus those exposed to FA (
mean +/-
standard deviation = 1.49 +/- 0.18 vs. 1.29 +/- 0.26 microM, p =.05 by
one-tailed t-test). Analyses of meteorological data and CAPs trace element composition suggest that local particle emission sources contributed largely to overall mass of CAPs. Results of this pilot study suggest that exposure to PM(2.5) at high concentrations may trigger an acute increase in circulating
ADMA level. This finding has implications for the regulation of vasomotor tone by
particulate pollutants and the
propensity for adverse
cardiovascular events.
