Acrylonitrile exposure incurs lung function decline: Insights from lifestyle intervention and mechanistic pathway in
Shuhui Wan1, Jiahao Song1, Yongfang Zhang1
1Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China; Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China.
Background:
Acrylonitrile (AN), a prevalent Urban Air Toxic Pollutant, has drawn growing worldwide attention due to its alarming health threat. Evidence regarding the respiratory effect of AN exposure and its interaction with lifestyle in the general population remains limited, and the underlying mechanisms are largely unexplored.
Methods:
In this urban population-based prospective cohort study (baseline: 2011-2012; two follow-ups: 2014-2015 and 2017-2018), urinary AN metabolite N-Acetyl-S-(2-cyanoethyl)-L-cysteine (CYMA) and lung function were repeatedly measured for 6236 observations of 3515 participants. We utilized linear mixed models to evaluate the cross-sectional and longitudinal relationships between CYMA and lung function. Interaction plots were depicted to estimate the interaction of CYMA with healthy lifestyle score (HLS). Biomarkers of inflammation (plasma transforming growth factor-β [TGF-β], C-reactive protein, and club cell secretory protein) and oxidative damage to DNA (urinary 8-hydroxy-deoxyguanosine [8-OHdG]), lipid (urinary 8-iso-prostaglandin-F2α [8-iso-PGF2α]), and protein (plasma protein carbonyl) were conducted to investigate their mediation mechanistic roles.
Results:
Cross-sectionally, each one-unit increase in log10-transformed CYMA was associated with a -30.66 mL (95 % CI: 57.99, -3.34), -32.11 mL (-53.20, -11.02), and -173.04 mL/s (-279.99, -66.09) alterations in FVC, FEV1, and PEF, respectively. Longitudinally, each one-unit increase in log10-transformed CYMA was associated with a -10.18 mL/year (-17.98, -2.38), -6.37 mL/year (-11.96, -0.78), and -33.68 mL/(s·year) (-62.63, -4.73) alterations in FVC, FEV1, and PEF, respectively. Increased HLS interactively attenuated the effect of CYMA on FEV1. Furthermore, TGF-β, 8-OHdG, and 8-iso-PGF2α mediated 5.78 %-36.17 % of the CYMA-associated lung function reduction.
Conclusion:
Daily life exposure to AN was associated with lung function decline. Mitigating AN pollution, promoting healthy lifestyles, and targeting fibro-inflammation, oxidative DNA damage, and lipid peroxidation pathways could be effective strategies to safeguard the public respiratory health.
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