Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Hospital Los Angeles, Los Angeles, CA, USA.
Department of Pediatrics, The Saban Research Institute, Children's Hospital Los Angeles, Los Angeles, CA, USA; Department of Psychology, University of Oregon, Eugene, OR, USA.
Ecotoxicol Environ Saf. 2024 Nov 1;286:117234. doi: 10.1016/j.ecoenv.2024.117234. Epub 2024 Oct 24.
Exposure to ambient air pollutants has emerged as a risk for metabolic-dysfunction associated steatotic liver disease (MASLD).
We sought to examine associations between short-term (prior month) and long-term (prior year) ambient air pollution exposure with hepatic fat fraction (HFF) and liver stiffness in Latino youth with obesity. A secondary aim was to investigate effect modification by patatin-like phospholipase domain-containing protein 3 (PNPLA3) genotype and liver disease severity.
Data was analyzed from 113 Latino youth (age 11-19) with obesity in Southern California. Individual exposure to particulate matter with aerodynamic diameter ≤ 2.5μm (PM), ≤ 10μm (PM), nitrogen dioxide (NO), 8-hour maximum ozone (8hrMax-O), 24-hr O, and redox-weighted oxidative capacity (O) were estimated using residential address histories and United States Environmental Protection Agency air quality observations. HFF and liver stiffness were measured using magnetic resonance imaging. Linear models were used to determine associations between short-term and long-term exposure to air pollutants with HFF and liver stiffness. Modification by PNPLA3 and liver disease severity was then examined.
Short-term exposure to 8hrMax-O was positively associated with HFF. Relationships between air pollution exposure and HFF were not impacted by PNPLA3 genotype or liver disease severity. Long-term exposure to 8hrMax-O and O were positively associated with liver stiffness. Associations between air pollution exposure and liver stiffness depended on PNPLA3 genotype, such that individuals with GG genotypes exhibited stronger, more positive relationships between short-term exposure to PM, 8hrMax-O, 24-hr O and O and liver stiffness than individuals with CC/CG genotypes. In addition, relationships between short-term exposure to NO and liver stiffness were stronger in those with severe liver disease.
Air pollution exposure may be a risk factor for liver disease among Latino youth with obesity, particularly in those with other preexisting risks for liver damage.
环境空气污染物暴露已成为代谢功能障碍相关脂肪性肝病（MASLD）的一个风险因素。
我们旨在研究短期（前一个月）和长期（前一年）环境空气污染暴露与拉丁裔肥胖青少年肝脂肪分数（HFF）和肝硬度之间的关系。次要目的是研究 patatin-like phospholipase domain-containing protein 3（PNPLA3）基因型和肝病严重程度的作用修饰。
分析了来自南加州 113 名拉丁裔肥胖青少年（年龄 11-19 岁）的数据。使用居住地址历史记录和美国环境保护署空气质量观测值，估算个体对空气动力学直径≤2.5μm（PM）、≤10μm（PM）、二氧化氮（NO）、8 小时最大臭氧（8hrMax-O）、24 小时 O 和氧化还原加权氧化能力（O）的暴露。使用磁共振成像测量 HFF 和肝硬度。线性模型用于确定短期和长期暴露于空气污染物与 HFF 和肝硬度之间的关系。然后检查 PNPLA3 和肝病严重程度的修饰作用。
8hrMax-O 的短期暴露与 HFF 呈正相关。空气污染暴露与 HFF 之间的关系不受 PNPLA3 基因型或肝病严重程度的影响。8hrMax-O 和 O 的长期暴露与肝硬度呈正相关。空气污染暴露与肝硬度之间的关系取决于 PNPLA3 基因型，即 GG 基因型个体的短期暴露于 PM、8hrMax-O、24 小时 O 和 O 与肝硬度之间的关系比 CC/CG 基因型个体更强、更积极。此外，NO 短期暴露与肝硬度之间的关系在严重肝病患者中更强。
空气污染暴露可能是拉丁裔肥胖青少年肝病的一个危险因素，特别是在那些有其他潜在肝脏损伤风险的患者中。
