TY - JOUR
T1 - Exposure to air pollution is associated with an increased risk of metabolic dysfunction-associated fatty liver disease
AU - Guo, Bing
AU - Guo, Yuming
AU - Nima, Qucuo
AU - Feng, Yuemei
AU - Wang, Ziyun
AU - Lu, Rong
AU - Baimayangji, null
AU - Ma, Yue
AU - Zhou, Junmin
AU - Xu, Huan
AU - Chen, Lin
AU - Chen, Gongbo
AU - Li, Shanshan
AU - Tong, Huan
AU - Ding, Xianbin
AU - Zhao, Xing
AU - on behalf of the China Multi-Ethnic Cohort (CMEC) collaborative group
N1 - Funding Information:
This work was supported by the National Key Research and Development Program of China (Grant No. 2017YFC0907305 ). This work was also supported by the National Natural Science Foundation of China (Grant No. 81973151 , 81773548 ) and China Postdoctoral Science Foundation (Grant No. 2020M683335 ). YG was supported by a Career Development Fellowship of the Australian National Health and Medical Research Council ( APP1163693). SL was supported by an Early Career Fellowship of the Australian National Health and Medical Research Council ( APP1109193). The funders had no role in the study design, data collection, data analysis and interpretation, writing of the report or decision to submit the article for publication.
Publisher Copyright:
© 2021 The Author(s)
PY - 2022/3
Y1 - 2022/3
N2 - Background & Aims: Accumulating animal studies have demonstrated the harmful contribution of ambient air pollution (AP) to metabolic dysfunction-associated fatty liver disease (MAFLD), but corresponding epidemiological evidence is limited. We examined the associations between long-term AP exposure and MAFLD prevalence in a Chinese population. Methods: We conducted a cross-sectional study of 90,086 participants recruited in China from 2018 to 2019. MAFLD was assessed based on radiologically diagnosed hepatic steatosis and the presence of overweight/obese status, diabetes mellitus, or metabolic dysregulation. Residence-specific levels of air pollutants, including particulate matter with aerodynamic diameters of ≤1 μm (PM1), ≤2.5 μm (PM2.5), and ≤10 μm (PM10), and nitrogen dioxide (NO2), were estimated by validated spatiotemporal models. We used logistic regression models to examine the AP–MAFLD associations and further evaluated potential effect modifications by demographics, lifestyle, central obesity, and diabetes status. Results: Increased exposure levels to all 4 air pollutants were significantly associated with increased odds of MAFLD, with odds ratios (ORs) of 1.13 (95% CI 1.10–1.17), 1.29 (1.25–1.34), 1.11 (1.09–1.14), and 1.15 (1.12–1.17) for each 10 μg/m3 increase in PM1, PM2.5, PM10, and NO2, respectively. Further stratified analyses revealed that individuals who are male, alcohol drinkers, and current and previous smokers, those who consume a high-fat diet, and those with central obesity experience more significant adverse effects from AP exposure than other individuals. Conclusions: This study provides evidence that long-term exposure to ambient PM1, PM2.5, PM10, and NO2 may increase the odds of MAFLD in the real world. These effects may be exacerbated by unhealthy lifestyle habits and central obesity. Lay summary: We conducted an epidemiological study on the potential effect of ambient air pollution on the risk of metabolic dysfunction-associated fatty liver disease (MAFLD) in approximately 90 thousand adults in China. We found that long-term exposure to ambient air pollution may increase the odds of MAFLD, especially in individuals who are male, smokers, and alcohol drinkers, those who consume a high-fat diet, and those with central obesity.
AB - Background & Aims: Accumulating animal studies have demonstrated the harmful contribution of ambient air pollution (AP) to metabolic dysfunction-associated fatty liver disease (MAFLD), but corresponding epidemiological evidence is limited. We examined the associations between long-term AP exposure and MAFLD prevalence in a Chinese population. Methods: We conducted a cross-sectional study of 90,086 participants recruited in China from 2018 to 2019. MAFLD was assessed based on radiologically diagnosed hepatic steatosis and the presence of overweight/obese status, diabetes mellitus, or metabolic dysregulation. Residence-specific levels of air pollutants, including particulate matter with aerodynamic diameters of ≤1 μm (PM1), ≤2.5 μm (PM2.5), and ≤10 μm (PM10), and nitrogen dioxide (NO2), were estimated by validated spatiotemporal models. We used logistic regression models to examine the AP–MAFLD associations and further evaluated potential effect modifications by demographics, lifestyle, central obesity, and diabetes status. Results: Increased exposure levels to all 4 air pollutants were significantly associated with increased odds of MAFLD, with odds ratios (ORs) of 1.13 (95% CI 1.10–1.17), 1.29 (1.25–1.34), 1.11 (1.09–1.14), and 1.15 (1.12–1.17) for each 10 μg/m3 increase in PM1, PM2.5, PM10, and NO2, respectively. Further stratified analyses revealed that individuals who are male, alcohol drinkers, and current and previous smokers, those who consume a high-fat diet, and those with central obesity experience more significant adverse effects from AP exposure than other individuals. Conclusions: This study provides evidence that long-term exposure to ambient PM1, PM2.5, PM10, and NO2 may increase the odds of MAFLD in the real world. These effects may be exacerbated by unhealthy lifestyle habits and central obesity. Lay summary: We conducted an epidemiological study on the potential effect of ambient air pollution on the risk of metabolic dysfunction-associated fatty liver disease (MAFLD) in approximately 90 thousand adults in China. We found that long-term exposure to ambient air pollution may increase the odds of MAFLD, especially in individuals who are male, smokers, and alcohol drinkers, those who consume a high-fat diet, and those with central obesity.
KW - air pollution
KW - epidemiologic study
KW - MAFLD
KW - Metabolic-associated fatty liver disease
UR - http://www.scopus.com/inward/record.url?scp=85122966403&partnerID=8YFLogxK
U2 - 10.1016/j.jhep.2021.10.016
DO - 10.1016/j.jhep.2021.10.016
M3 - Article
C2 - 34883157
AN - SCOPUS:85122966403
SN - 0168-8278
VL - 76
SP - 518
EP - 525
JO - Journal of Hepatology
JF - Journal of Hepatology
IS - 3
ER -