Road Repairs: Does Exposure to Traffic Affect Mechanisms of Vascular Injury and Repair?

stimates of the health effects of air pollution are alarming , with up to 7 million attributable deaths worldwide each year. Although the pulmonary effects of air pollution are widely recognized, it is only in the last few decades that the adverse cardiovascular effects of air pollution have become apparent. Exposures to diesel exhaust, a prominent source of urban air pollution and a pollutant rich in combustion-derived nanoparticles, has multiple detrimental actions on the cardiovas-cular system. Brief exposure to diesel exhaust at concentrations encountered at the roadside of heavily polluted cities promotes vasoconstriction, 4 causes impaired relaxation of blood vessels, 5 increases arterial stiffening, 6 promotes blood clotting, 7 inhibits the release of fibrinolytic factors, 5 and promotes myocar-dial ischemia. 8 Parallel animal studies have shown that diesel exhaust particles also generate free radicals, 9,10 increase blood pressure, 11 promote atherosclerosis, 12,13 induce arrhythmia, 14 and increase the susceptibility of the heart to injury 15 (Figure). In this edition of the journal, DeJarnett et al 16 elaborate on another potentially important mechanism through which traffic-derived air pollution could promote cardiovascular disease. The authors studied 316 individuals with cardiovascular risk factors and examined whether angiogenic cells in blood are related to the proximity of their residence to major roadways. The investigators demonstrate that volunteers living within 300 m of a major road have higher numbers of circulating cells with characteristics of early stem cells and vascular endothelial cells. The association was not linked to evidence of a systemic inflammatory response. The thoroughness of the study design is commendable: using a large sample group for the degree of cell profiling (15 different cell populations), detailed evaluation of roadside proximity and traffic density, and accounting for multiple potential confounding variables, including cigarette smoking and socioeconomic factors. The present study expands on their earlier findings, 17 whereby exposure to fine particulate matter (PM 2.5) during a high air pollution episode was associated with a decrease in circulating progenitor cells. The current findings seem to contradict these earlier observations. The authors suggest that the seemingly opposing effects of roadside proximity, and therefore exposure to traffic-derived air pollutants, with those of ambient PM exposure is resolved by noting that roadside proximity was associated with an increase in distinct CD133 + and CD31 + cell populations, but not those specific populations that were decreased by PM 2.5 exposure in their earlier study. It is perhaps premature though …