Garcia Erika, Stratakis Nikos, Valvi Damaskini, Maitre Léa, Varo Nerea, Aasvang Gunn Marit, Andrusaityte Sandra, Basagana Xavier, Casas Maribel, de Castro Montserrat, Fossati Serena, Grazuleviciene Regina, Heude Barbara, Hoek Gerard, Krog Norun Hjertager, McEachan Rosemary, Nieuwenhuijsen Mark, Roumeliotaki Theano, Slama Rémy, Urquiza Jose, Vafeiadi Marina, Vos Miriam B, Wright John, Conti David V, Berhane Kiros, Vrijheid Martine, McConnell Rob, Chatzi Lida
Department of Preventive Medicine, University of Southern California, Los Angeles, CA.
Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY.
Environ Epidemiol. 2021 May 11;5(3):e153. doi: 10.1097/EE9.0000000000000153. eCollection 2021 Jun.
Nonalcoholic fatty liver disease is the most prevalent pediatric chronic liver disease. Experimental studies suggest effects of air pollution and traffic exposure on liver injury. We present the first large-scale human study to evaluate associations of prenatal and childhood air pollution and traffic exposure with liver injury.
Study population included 1,102 children from the Human Early Life Exposome project. Established liver injury biomarkers, including alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, and cytokeratin-18, were measured in serum between ages 6-10 years. Air pollutant exposures included nitrogen dioxide, particulate matter <10 μm (PM), and <2.5 μm. Traffic measures included traffic density on nearest road, traffic load in 100-m buffer, and inverse distance to nearest road. Exposure assignments were made to residential address during pregnancy (prenatal) and residential and school addresses in year preceding follow-up (childhood). Childhood indoor air pollutant exposures were also examined. Generalized additive models were fitted adjusting for confounders. Interactions by sex and overweight/obese status were examined.
Prenatal and childhood exposures to air pollution and traffic were not associated with child liver injury biomarkers. There was a significant interaction between prenatal ambient PM and overweight/obese status for alanine aminotransferase, with stronger associations among children who were overweight/obese. There was no evidence of interaction with sex.
This study found no evidence for associations between prenatal or childhood air pollution or traffic exposure with liver injury biomarkers in children. Findings suggest PM associations maybe higher in children who are overweight/obese, consistent with the multiple-hits hypothesis for nonalcoholic fatty liver disease pathogenesis.
非酒精性脂肪性肝病是最常见的儿童慢性肝病。实验研究表明空气污染和交通暴露对肝脏损伤有影响。我们开展了第一项大规模人体研究,以评估产前和儿童期空气污染及交通暴露与肝脏损伤之间的关联。
研究人群包括来自人类早期生活暴露组项目的1102名儿童。在6至10岁时测量血清中已确立的肝脏损伤生物标志物,包括丙氨酸转氨酶、天冬氨酸转氨酶、γ-谷氨酰转移酶和细胞角蛋白-18。空气污染物暴露包括二氧化氮、粒径小于10微米(PM10)和小于2.5微米的颗粒物。交通指标包括最近道路的交通密度、100米缓冲区内的交通负荷以及到最近道路的反比距离。暴露赋值基于孕期的居住地址(产前)以及随访前一年的居住和学校地址(儿童期)。还对儿童期室内空气污染物暴露进行了检查。采用广义相加模型并对混杂因素进行校正。研究了性别和超重/肥胖状态的交互作用。
产前和儿童期的空气污染及交通暴露与儿童肝脏损伤生物标志物无关。产前环境PM与超重/肥胖状态之间对于丙氨酸转氨酶存在显著交互作用,在超重/肥胖儿童中关联更强。没有证据表明与性别存在交互作用。
本研究未发现产前或儿童期空气污染或交通暴露与儿童肝脏损伤生物标志物之间存在关联的证据。研究结果表明,超重/肥胖儿童中PM的关联可能更高,这与非酒精性脂肪性肝病发病机制的多重打击假说一致。