Yinan Zheng1, Marco Sanchez-Guerra2, Zhou Zhang3, Brian T Joyce4, Jia Zhong5, Jacob K Kresovich4, Lei Liu6, Wei Zhang6, Tao Gao7, Dou Chang8, Citlalli Osorio-Yanez9, Juan Jose Carmona5, Sheng Wang10, John P McCracken5, Xiao Zhang11, Yana Chervona12, Anaite Díaz13, Pier A Bertazzi14, Petros Koutrakis5, Choong-Min Kang5, Joel Schwartz5, Andrea A Baccarelli15, Lifang Hou16. 1. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA; Health Sciences Integrated PhD Program, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. 2. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Department of Developmental Neurobiology, National Institute of Perinatology, Mexico City, Mexico. 3. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA; Driskill Graduate Program in Life Sciences, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. 4. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA; Division of Epidemiology/Biostatistics, School of Public Health, University of Illinois-Chicago, Chicago, IL, USA. 5. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 6. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA; Robert H. Lurie Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. 7. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. 8. Department of Safety Engineering, China Institute of Industrial Relations, Beijing, China. 9. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 10. Department of Occupational and Environmental Health, Peking University Health Science Center, Beijing, China. 11. Clinical Research Unit, Khoo Teck Puat Hospital, Singapore. 12. Department of Environmental Medicine, New York University Langone Medical Center, Tuxedo, NY, USA. 13. Center for Health Studies, Universidad del Valle de Guatemala, Guatemala City, Guatemala. 14. Department of Clinical Sciences and Community Medicine, University of Milan and IRCCS Fondazione Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy. 15. Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY, USA. Electronic address: ab4303@cumc.columbia.edu. 16. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA; Robert H. Lurie Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. Electronic address: l-hou@northwestern.edu.
Abstract
BACKGROUND: Airborne particulate matter (PM) may induce epigenetic changes that potentially lead to chronic diseases. Histone modifications regulate gene expression by influencing chromatin structure that can change gene expression status. We evaluated whether traffic-derived PM exposure is associated with four types of environmentally inducible global histone H3 modifications. METHODS: The Beijing Truck Driver Air Pollution Study included 60 truck drivers and 60 office workers examined twice, 1-2 weeks apart, for ambient PM10 (both day-of and 14-day average exposures), personal PM2.5, black carbon (BC), and elemental components (potassium, sulfur, iron, silicon, aluminum, zinc, calcium, and titanium). For both PM10 measures, we obtained hourly ambient PM10 data for the study period from the Beijing Municipal Environmental Bureau's 27 representatively distributed monitoring stations. We then calculated a 24h average for each examination day and a moving average of ambient PM10 measured in the 14 days prior to each examination. Examinations 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 collected after work. We used adjusted linear mixed-effect models to examine percent changes in histone modifications per each μg/m3 increase in PM exposure. RESULTS: In all participants each μg/m3 increase in 14-day average ambient PM10 exposure was associated with lower H3K27me3 (β=-1.1%, 95% CI: -1.6, -0.6) and H3K36me3 levels (β=-0.8%, 95% CI: -1.4, -0.1). Occupation-stratified analyses showed associations between BC and both H3K9ac and H3K36me3 that were stronger in office workers (β=4.6%, 95% CI: 0.9, 8.4; and β=4.1%, 95% CI: 1.3; 7.0 respectively) than in truck drivers (β=0.1%, 95% CI: -1.3, 1.5; and β=0.9%, 95% CI: -0.9, 2.7, respectively; both pinteraction <0.05). Sex-stratified analyses showed associations between examination-day PM10 and H3K9ac, and between BC and H3K9me3, were stronger in women (β=10.7%, 95% CI: 5.4, 16.2; and β=7.5%, 95% CI: 1.2, 14.2, respectively) than in men (β=1.4%, 95% CI: -0.9, 3.7; and β=0.9%, 95% CI: -0.9, 2.7, respectively; both pinteraction <0.05). We observed no associations between personal PM2.5 or elemental components and histone modifications. CONCLUSIONS: Our results suggest a possible role of global histone H3 modifications in effects of traffic-derived PM exposures, particularly BC exposure. Future studies should assess the roles of these modifications in human diseases and as potential mediators of air pollution-induced disease, in particular BC exposure.
BACKGROUND: Airborne particulate matter (PM) may induce epigenetic changes that potentially lead to chronic diseases. Histone modifications regulate gene expression by influencing chromatin structure that can change gene expression status. We evaluated whether traffic-derived PM exposure is associated with four types of environmentally inducible global histone H3 modifications. METHODS: The Beijing Truck Driver Air Pollution Study included 60 truck drivers and 60 office workers examined twice, 1-2 weeks apart, for ambient PM10 (both day-of and 14-day average exposures), personal PM2.5, black carbon (BC), and elemental components (potassium, sulfur, iron, silicon, aluminum, zinc, calcium, and titanium). For both PM10 measures, we obtained hourly ambient PM10 data for the study period from the Beijing Municipal Environmental Bureau's 27 representatively distributed monitoring stations. We then calculated a 24h average for each examination day and a moving average of ambient PM10 measured in the 14 days prior to each examination. Examinations 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 collected after work. We used adjusted linear mixed-effect models to examine percent changes in histone modifications per each μg/m3 increase in PM exposure. RESULTS: In all participants each μg/m3 increase in 14-day average ambient PM10 exposure was associated with lower H3K27me3 (β=-1.1%, 95% CI: -1.6, -0.6) and H3K36me3 levels (β=-0.8%, 95% CI: -1.4, -0.1). Occupation-stratified analyses showed associations between BC and both H3K9ac and H3K36me3 that were stronger in office workers (β=4.6%, 95% CI: 0.9, 8.4; and β=4.1%, 95% CI: 1.3; 7.0 respectively) than in truck drivers (β=0.1%, 95% CI: -1.3, 1.5; and β=0.9%, 95% CI: -0.9, 2.7, respectively; both pinteraction <0.05). Sex-stratified analyses showed associations between examination-day PM10 and H3K9ac, and between BC and H3K9me3, were stronger in women (β=10.7%, 95% CI: 5.4, 16.2; and β=7.5%, 95% CI: 1.2, 14.2, respectively) than in men (β=1.4%, 95% CI: -0.9, 3.7; and β=0.9%, 95% CI: -0.9, 2.7, respectively; both pinteraction <0.05). We observed no associations between personal PM2.5 or elemental components and histone modifications. CONCLUSIONS: Our results suggest a possible role of global histone H3 modifications in effects of traffic-derived PM exposures, particularly BC exposure. Future studies should assess the roles of these modifications in human diseases and as potential mediators of air pollution-induced disease, in particular BC exposure.
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