Air pollution exposure and histone 3 methylation and acetylation in highly exposed individuals in Beijing, China: A repeated-measures study

Background: Particulate matter (PM) induces epigenetic changes including histone modifications which influence chromatin structure and gene expression. We evaluated whether ambient PM exposure is associated with modifications of histone 3 (H3) in individuals exposed to high levels of air pollution in Beijing, China. Methods: The Beijing Truck Driver Air Pollution Study included 60 truck drivers and 60 office workers examined 1-2 weeks apart in 2008. Our study examined three measures of PM exposure: personal PM exposure, including PM2.5 and black carbon (BC), measured during eight work hours using portable monitors; acute ambient PM10 exposures using examination-day data averaged from 27 monitoring stations; and recent (14-day moving average) ambient PM10 exposure, also based on the monitoring station data. For histone modifications we measured global levels of H3 lysine 9 acetylation (H3K9ac), H3 lysine 9 tri-methylation (H3K9me3), H3 lysine 27 tri-methylation (H3K27me3), and H3 lysine 36 tri-methylation (H3K36me3) in blood leukocytes. Results: In all participants combined, one unit increase in recent PM10 exposure was inversely associated with H3K27me3 (β = -1.1%; 95% CI: -1.6, -0.6) and H3K36me3 (β = -0.8%; 95% CI, -1.4; -0.1). In office workers only, one unit increase in personal BC exposure was positively associated with H3K9ac (β = 4.6%; 95% CI: 0.9, 8.4), H3K9me3 (β = 5.8%; 95% CI: 0.6, 11.4), and H3K27me3 (β = 4.1%; 95% CI, 1.3; 7.0). In women, ten unit increase in acute PM10 exposure was associated with H3K9ac (β = 10.7%; 95% CI: 5.4, 16.2) whereas in men the effect was smaller and insignificant. Conclusions: Exposure to fine PM and traffic-related pollutants is associated with H3 modifications. H3 modification levels among less-exposed participants and women are more responsive to PM fluctuations. Future studies should assess the role of H3 modification in human diseases and as a potential mediator of air pollution-induced disease.