Background: Mechanisms of cardiovascular injuries from exposure to gas and particulate air pollutants are unknown.
Objective: We sought to determine whether episodic exposure of rats to ozone or diesel exhaust particles (DEP) causes differential cardiovascular impairments that are exacerbated by ozone plus DEP.
Methods And Results: Male Wistar Kyoto rats (10-12 weeks of age) were exposed to air, ozone (0.
Aging adults are a growing segment of the U.S. population and are likely to exhibit increased susceptibility to many environmental toxicants.
View Article and Find Full Text PDFBackground: Exposure to diesel exhaust (DE) is linked to vasoconstriction, endothelial dysfunction, and myocardial ischemia in compromised individuals.
Objective: We hypothesized that DE inhalation would cause greater inflammation, hematologic alterations, and cardiac molecular impairment in spontaneously hypertensive (SH) rats than in healthy Wistar Kyoto (WKY) rats.
Methods And Results: Male rats (12-14 weeks of age) were exposed to air or DE from a 30-kW Deutz engine at 500 or 2,000 microg/m3, 4 hr/day, 5 days/week for 4 weeks.
Zinc is a common metal in most ambient particulate matter (PM), and has been proposed to be a causative component in PM-induced adverse cardiovascular health effects. Zinc is also an essential metal and has the potential to induce many physiological and nonphysiological changes. Most toxicological studies employ high levels of zinc.
View Article and Find Full Text PDFTire and brake wear particles contain transition metals, and contribute to near-road PM. We hypothesized that acute cardiopulmonary injury from respirable tire particles (TP) will depend on the amount of soluble metals. Respirable fractions of two types of TP (TP1 and TP2) were analyzed for water and acid-leachable metals using ICP-AES.
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