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Genotoxicity Biomarkers Associated with Exposure to Traffic And Near-Road Atmospheres: A Review
Citation:
DeMarini, D. Genotoxicity Biomarkers Associated with Exposure to Traffic And Near-Road Atmospheres: A Review. MUTAGENESIS. Oxford University Press, Cary, NC, 28(5):485-505, (2013).
Impact/Purpose:
Genotoxicity Biomarkers Associated with Exposure to Traffic And Near-Road Atmospheres: A Review This review highlights two important observations. One is that >80% of the genotoxicity biomarker studies found genotoxic effects in populations exposed to traffic compared with control populations (typically office workers). All 6 of the primary, established biomarkers that were used predominantly in these studies were effective and sensitive, as were 3 genomic biomarkers that were used in just a few recent studies. Thus, there is compelling data that chronic, daily exposure to traffic exhaust is genotoxic and a risk factor for cancer. This is because studies have shown that having elevated frequencies of 3 of the biomarkers (chromosomal aberrations, micronuclei, and shortening oftelomers) is a risk factor for cancer Such data also provide mechanistic support for emerging epidemiology indicating that traffic exposure is a cancer risk. Second, this review highlights the fact that only 1 out of the 60 studies involved traffic exposure in the U.S.; all ofthe rest of these environmental studies were performed in Europe and Asia, with one each from South American and Africa. Thus, this review also identifies an important gap in our understanding of the ge:notoxicity of traffic exhaust and near-road exposures in the U.S. This is important given the known differences in traffic fleet (e.g., proportion of gasoline versus diesel) in the U.S. compared with Europe or Asia. This review will provide guidance regarding future research directions of the field and the Agency with regard to traffic and near-road studies.
Description:
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 paper reviews the 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 endpoints, chromosome aberrations (CAs), micronuclei (MN), and sister chromatid exchange (SCEs); and the standard molecular endpoints for DNA damage, 32P-postlabeling, the comet assay, and urinary 8-hydroxydeoxyguanosine. These six assays accounted for 72 of the 84 biomarker assessments reported in the studies; all six effectively distinguished traffic-exposed from control populations, giving an average 84% 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 19 countries; however, nearly all of the environmental studies were performed in Europe and Asia, with only 1 each from Africa, North America, and South America. Given that several of the biomarkers are associated with increased cancer risk, including CAs, MNs, and shortened telomere length, the data reviewed here provide strong mechanistic support for the ability of chronic exposure to traffic exhaust to increase cancer risk.