Genotoxicity biomarkers associated with exposure to traffic and near-road atmospheres: a review

Diesel and gasoline emissions, which are the primary components of traffic exhaust, are known or possible human carcinogens, respectively, and working or living near high-traffic roads is associated with various health effects, including cancer. To help understand the mechanistic basis for this observation, the present article reviews 63 studies on genotoxicity biomarkers in traffic-exposed subjects, with office workers being the typical control subjects. The six primary biomarkers used in these studies were the traditional cytogenetic end points, chromosome aberrations (CAs), micronucleus (MN) and sister chromatid exchange, and the standard molecular end points for DNA damage, P-32-postlabeling, the comet assay and urinary 8-hydroxydeoxyguanosine. These six assays accounted for 74 of the 87 biomarker assessments reported in the studies; all six effectively distinguished traffic-exposed from control populations, giving an average 89% positive results among exposed versus control subjects. In addition, three genomic biomarkers effectively distinguished between the exposed and control populations; these assays measured changes in gene expression, leukocyte telomere length and DNA methylation. Nearly half of all of the studies included exposure assessments involving blood (primarily protein adducts), urine (primarily 1-hydroxypyrene) or air (primarily polycyclic aromatic hydrocarbons); these assays distinguished the exposed from the control subjects for the vast majority of the studies. All but three of the 63 reports were environmental studies that investigated 18 general exposure categories, such as traffic police and automobile/bus mechanics. The studies were performed in 20 countries; however, nearly all of the environmental studies were performed in Europe and Asia, with only one each from Africa, North America and South America. Given that several of the biomarkers are associated with increased cancer risk, including CAs, MNs and altered telomere length, the data reviewed here provide strong mechanistic support for the ability of chronic exposure to traffic exhaust to increase cancer risk.