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 ≤ 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 (PM_2.5) concentration was determined gravimetrically; hearts were analyzed by morphometry. There was a reduction of the PM_2.5 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.