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Epidemiological studies have shown that air pollution increases cardiovascular morbidity and mortality. Objective markers of cardiovascular risk have also been associated with increases in ambient pollution. This study was designed to assess whether prolonged exposure to ambient levels of air pollution may induce structural alterations of pulmonary and cardiac vessels. Mice were chronically exposed to ambient levels of air pollution in downtown São Paulo, Brazil. The animals were maintained in exposure chambers, 24 h/day, 7 days/wk, during 4 mo. One group was exposed to ambient air, and the control group was exposed to filtered air. Morphometric measurements of the ratio between the lumen and wall (L/W) areas were performed on transverse sections of renal, pulmonary, and coronary arteries. As expected, lumen/wall ratios increased with arterial caliber (p.001). A significant decrease of L/W with exposure to air pollution was detected in pulmonary (p = .03) and coronary (p = .021) arteries, whereas no effects of air pollution were observed in renal vessels. Our results indicate that animals chronically exposed to ambient air pollution develop a significant thickening of the arterial wall in the coronary and pulmonary circulation.

Exposure to air pollution can elicit cardiovascular health effects. Children and unborn fetuses appear to be particularly vulnerable. However, the mechanisms involved in cardiovascular damage are poorly understood. It has been suggested that the oxidative stress generated by air pollution exposure triggers tissue injury. To investigate whether prenatal exposure can enhance oxidative stress in myocardium of adult animals, mice were placed in a clean chamber (CC, filtered urban air) and in a polluted chamber (PC, São Paulo city) during the gestational period and/or for 3 mo after birth, according to 4 protocols: control group-prenatal and postnatal life in CC; prenatal group-prenatal in PC and postnatal life in CC; postnatal group-prenatal in CC and postnatal life in PC; and pre-post group-prenatal and postnatal life in PC. As an indicator of oxidative stress, levels of lipid peroxidation in hearts were measured by malondialdehyde (MDA) quantification and by quantification of the myocardial immunoreactivity for 15-F2t-isoprostane. Ultrastructural studies were performed to detect cellular alterations related to oxidative stress. Concentration of MDA was significantly increased in postnatal (2.45 +/- 0.84 nmol/mg) and pre-post groups (3.84 +/- 1.39 nmol/mg) compared to the control group (0.31 +/- 0.10 nmol/mg) (p.01). MDA values in the pre-post group were significantly increased compared to the prenatal group (0.71 +/- 0.15 nmol/mg) (p = .017). Myocardial isoprostane area fraction in the pre-post group was increased compared to other groups (por = .01). Results show that ambient levels of air pollution elicit cardiac oxidative stress in adult mice, and that gestational exposure may enhance this effect.