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Effects of Chronic Exposure to Air Pollution from Sao Paulo City on Coronary of Swiss Mice, from Birth to Adulthood
1 Experimental Air Pollution Laboratory, School of Medicine, University of São Paulo, Brazil Correspondence: Maria Lúcia Bueno Garcia, PhD, MD, School of Medicine, University of São Paulo, Av. Dr. Arnaldo 455, Sao Paulo, Brazil, CEP: 1246-903; e-mail:gajugu{at}terra.com.br.
To explore the hypothesis that air pollution promotes cardiovascular changes, Swiss mice were continuously exposed, since birth, in two open-top chambers (filtered and nonfiltered for airborne particles
Key Words: vascular remodeling • air pollution • particulate matter • collagen • elastic fiber • coronary arteries Abbreviations: ABNT, Associação Brasileira de Normas Técnicas • CETESB, State of Sao Paulo Sanitation Agency • ECM, extracellular matrix • HEPA, High Efficiency Particulate Air • LV, left ventricle • PM, particulate matter • RV, right ventricle • SHR, spontaneous hypertensive rats • VEGF, vascular endothelial growing factor
This version was published on April
1, 2009 Toxicologic Pathology, Vol. 37, No. 3,
306-314 (2009) |
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0.3 µm) placed 20 m from a street with heavy traffic in downtown Sao Paulo, twenty-four hours per day for four months. Fine particle (PM2.5) concentration was determined gravimetrically; hearts were analyzed by morphometry. There was a reduction of the PM2.5 inside the filtered chamber (filtered = 8.61±0.79 µg/m3, nonfiltered = 18.05±1.25 µg/m3, p < .001). Coronary arteries showed no evidence of luminal narrowing in the exposed group but presented higher collagen content in the adventitia of LV large-sized and RV midsized vessels (p = .001) and elastic fibers in both tunicae adventitia and intima-media of almost all sized arterioles from both ventricles (p = .03 and p = .001, respectively). We concluded that chronic exposure to urban air since birth induces mild but significant vascular structural alterations in normal individuals, presented as coronary arteriolar fibrosis and elastosis. These results might contribute to altered vascular response and ischemic events in the adulthood.