Abstract
As an important risk factor of respiratory disorders, traffic-related air pollution (TRAP) has caused extensive concerns. Epigenetic change has been considered a link between TRAP and respiratory diseases. However, the exact effects of TRAP on epigenetic changes are still unclear. Here we investigated the dose- and time- effect responses of TRAP on DNA methylations and H3K9 acetylation (H3K9ac) in both blood and lung tissues of rats. The findings showed that every 1 μg/m3 increase of TRAP components were associated with changes in %5 mC (95% CI) in LINE-1, iNOS, p16CDKN2A, and APC ranging from −0.088% (−0.150, −0.026) to 0.102 (0.049, 0.154), as well as 0.276 (0.053, 0.498) to 0.475 (0.103, 0.848) ng/mg increase of H3K9ac. In addition, every 1 more day exposure at high level of TRAP (in tunnel) also significantly changed the levels of DNA methylation (ranging from −0.842% to 0.248%) and H3K9ac (16.033 and 15.718 ng/mg pro in PBMC and lung tissue, respectively) changes. Season and/or sex could interact with air pollutants in affecting DNA methylation and H3K9ac. The findings showed that TRAP exposure is dose- and time- dependently associated with the changes of DNA methylation and H3K9ac.
Highlights
Air pollution is an important risk factor of respiratory disorders[1]
Those studies mainly investigated the effects of single air pollutant, while the effects of traffic-related air pollution (TRAP) as a mixture were not investigated[5,34,35,36,40]; in addition, most studies investigated epigenetic effects in different white blood cells[5,30,31,32,33,34,37,38,40,41,42], which represent the overall results from all the organs of the whole body, while the effects in the target organ, namely lung, were not been well studied; ambient air monitoring data were from central air monitoring stations adopted in most studies to estimate the air pollution level[30,32,33,36,39,41,42], which may not loyally represent the TRAP level
Season, SO2 level, temperature, and age were adjusted, the results showed that every 1 μg/m3 increase of PM2.5 resulted in 0.04% increase of p16CDKN2A promoter methylation in blood DNA, 0.02% and 0.06% decrease of long interspersed nucleotide elements-1 (LINE-1) and inducible nitric oxide synthase gene (iNOS) methylation in lung tissue DNA, 0.01% and 0.01% increase of APC and p16CDKN2A promoter methylation in lung tissue DNA, and 0.64 and 0.66 ng/mg protein increase of H3K9 acetylation (H3K9ac) from peripheral blood mononuclear cells (PBMCs) and lung tissue histone, respectively
Summary
Air pollution is an important risk factor of respiratory disorders[1]. With the accelerated urbanization and rapid economic development in China, air pollution level increased rapidly in the past several decades[2]. In addition to global hypomethylation, studies have shown that air pollutant exposure could induce abnormal methylation of the promoters of specific genes including inducible nitric oxide synthase gene (iNOS)[25,26]. Studies have demonstrated that PM exposure could induce the changes of histone acetylation; for instance, NO2 and PM could affect the DNA methylation and histone acetylation[27,28,29] All these findings suggest from both disease and air pollution aspects that epigenetic changes may be an important link between air pollution and respiratory diseases. Global DNA methylation, methylation of 3 gene-specific genes, and acetylation of histone H3K9 were measured in both blood and lung tissues to investigate the epigenetic effects of TRAP exposure
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