CUMULATIVE PM2.5 EXPOSURE AND TELOMERE LENGTH IN WORKERSEXPOSED TO WELDING FUMES

摘要

Telomeres are genomic structures that reflect both mitotic history and biochemical trauma to the genome. Metals inherent in fine particulate matter (PM2.5) were shown to be genotoxic via oxidative damage. However, few studies investigated the induction time of cumulative PM2.5 exposure on telomere length in a longitudinal setting. Therefore, the purpose of this study was to assess the association between occupational PM2.5 exposure in various time windows and telomere length. The study population consisted of 48 boilermakers and the follow-up period was 8 yr. The main exposures were cumulative occupational PM2.5 in the month, year, and career prior to each blood draw, assessed via work history questionnaires and area air measures. Repeated telomere length measurements from leukocytes were assessed via real-time quantitative polymerase chain reaction (qPCR). Analysis was performed using linear mixed models controlling for confounders and white blood cell differentials. Cumulative PM2.5 exposure was treated continuously and categorized into quartiles, in separate analyses. At any follow-up time, for each milligram per cubic meter per hour increase in cumulative PM2.5 exposure in the prior month, there was astatistically significant decrease in relative telomere length of −0.04units. When categorizing the exposure into quartiles, there was a significantnegative association between telomere length and highest quartile of cumulativePM2.5 exposure in the prior month (−0.16). These findingssuggest that genomic trauma to leukocyte telomeres was more consistent withrecent occupational PM2.5 exposure, as opposed to cumulative exposureextending into the distant past.