Monday, February 21, 2005

(Don't) Be Still My Heart

BrooklynDodger believes that community studies of the last decade showing increased mortality and illness from cardiovascular causes with increases in particulate exposure present the biggest opportunity in occupational and environmental health.

At the outset, there was limited or no experimental toxicology to support the observation that particles could cause cardiovascular effects. This presented laboratory scientists with a problem equivalent to proving that tobacco smoke could cause cancer. Gradually the problem of replicating health effects in free living humans in the laboratory is being solved.

Key is the recognition that an 0.3 micron particle can penetrate from the lungs into the systemic circulation. Once scientists know it's there, they can devise many studies to measure effects which can't be directly observed in people.

In this study, diesel particulate matter intilled into the lungs affected blood clotting, a key change related to heart disease.

Toxicol Lett. 2004 Apr 1;149(1-3):243-53.

Possible mechanisms of the cardiovascular effects of inhaled particles: systemic translocation and prothrombotic effects.

Nemmar A, Hoylaerts MF, Hoet PH, Nemery B.Laboratory of Pneumology, Unit of Lung Toxicology, K.U. Leuven, Herestraat, 49, Leuven 3000, Belgium.

Particulate air pollution is associated with cardiovascular morbidity and mortality. Fine particles with a diameter <2.5>Recently, we have demonstrated that ultrafine particles are able to translocate from the lung into the systemic circulation in hamsters and humans. In urban areas, diesel engines are considered to be the major source of PM2.5. We therefore evaluated the acute effect (1 h) of diesel exhaust particles (DEP) in a hamster model of peripheral vascular thrombosis induced by free-radical mediated endothelial injury, using intravenous Rose Bengal and local illumination. Intratracheal doses of 5-500 microg of DEP per animal induced inflammation with elevation of neutrophils, total proteins and histamine in bronchoalveolar lavage. DEP enhanced experimental arterial and venous platelet rich-thrombus formation in vivo. Blood samples taken from hamsters 30 and 60 min after instillation of DEP caused platelet activation, when analyzed in the Platelet Function Analyser (PFA-100). The direct addition of DEP to untreated hamster blood also caused platelet aggregation. These effects persisted up to 24 h after instillation. Our results provide plausible mechanistic explanations for the epidemiologically established link between air pollution and acute cardiovascular effects.

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