Personal exposure to fine particulate matter and blood pressure: A role of angiotensin converting enzyme and its DNA methylation

The underlying intermediate mechanisms about the association between fine particulate matter (PM2.5) air pollution and blood pressure (BP) were unclear. Few epidemiological studies have explored the potential mediation effects of angiotensin-converting enzyme (ACE) and its DNA methylation. We design...

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Bibliographic Details
Published in:Environment international 2016-09, Vol.94, p.661-666
Main Authors: Wang, Cuicui, Chen, Renjie, Cai, Jing, Shi, Jingjin, Yang, Changyuan, Tse, Lap Ah, Li, Huichu, Lin, Zhijing, Meng, Xia, Liu, Cong, Niu, Yue, Xia, Yongjie, Zhao, Zhuohui, Kan, Haidong
Format: Article
Language:English
Subjects:
Air Pollutants - analysis
Angiotensin-converting enzyme
Biomarkers - analysis
Blood pressure
Blood Pressure - drug effects
Blood Pressure - genetics
China
DNA methylation
DNA Methylation - drug effects
Fine particulate matter
Humans
Hypertension - chemically induced
Hypertension - enzymology
Hypertension - genetics
Inhalation Exposure - adverse effects
Inhalation Exposure - analysis
Linear Models
Longitudinal Studies
Male
Panel study
Particle Size
Particulate Matter - analysis
Particulate Matter - toxicity
Peptidyl-Dipeptidase A - blood
Peptidyl-Dipeptidase A - genetics
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Summary:The underlying intermediate mechanisms about the association between fine particulate matter (PM2.5) air pollution and blood pressure (BP) were unclear. Few epidemiological studies have explored the potential mediation effects of angiotensin-converting enzyme (ACE) and its DNA methylation. We designed a longitudinal panel study with 4 follow-ups among 36 healthy college students in Shanghai, China from December 17, 2014 to July 11, 2015. We measured personal real-time exposure to PM2.5, serum ACE level, and blood methylation of ACE gene and the repetitive elements. We applied linear mixed-effects models to examine the effects of PM2.5 on ACE protein, DNA methylation and BP markers. Furthermore, we conducted mediation analyses to evaluate the potential pathways. An interquartile range increase (26.78μg/m3) in 24-h average exposure to PM2.5 was significantly associated with 1.12 decreases in ACE average methylation (%5mC), 13.27% increase in ACE protein, and increments of 1.13mmHg in systolic BP, 0.66mmHg in diastolic BP and 0.82mmHg in mean arterial pressure. ACE hypomethylation mediated 11.78% (P=0.03) of the elevated ACE protein by PM2.5. Increased ACE protein accounted for 3.90~13.44% (P=0.35~0.68) of the elevated BP by PM2.5. Repetitive-element methylation was also decreased but did not significantly mediate the association between PM2.5 and BP. This investigation provided strong evidence that short-term exposure to PM2.5 was significantly associated with BP, ACE protein and ACE methylation. Our findings highlighted a possible involvement of ACE and ACE methylation in the effects of PM2.5 on elevating BP. •Personal exposure to PM2.5 was significantly associated with elevated BP.•The first study examining the mediation of ACE protein in the effects of PM2.5 on BP.•The first study examining the effects of PM2.5 on ACE methylation.•ACE and ACE methylation may mediate the effects of PM2.5 on BP.
ISSN:0160-4120
1873-6750
DOI:10.1016/j.envint.2016.07.001