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Nonalcoholic Fatty Liver Disease (MAFLD) and Long-Term Ambient Air Pollution Exposure: The Multi-Ethnic Study of Atherosclerosis (MESA)

机译:非酒精性脂肪性肝病(MAFLD)和长期环境空气污染暴露:动脉粥样硬化(MESA)的多民族研究

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Background: Animal studies have suggested that air pollution may cause metabolic changes including hepatic fat accumulation characteristic of insulin resistance in Type Ⅱ diabetes. This outcome has not previously been assessed in relation to air pollution. Aims: We performed a cross-sectional analysis to estimate the association between long-term ambient NOx and PM2.5 and fatty liver, as measured via computed tomography (CT). Methods: The Multi-Ethnic Study of Atherosclerosis (MESA) is a population based cohort from 6 sites (n=6814). Participant exposures were annual average ambient PM2.5 and NOx concentrations estimated at year 2000 participant addresses using a likelihood-based land-use regression spatiotemporal model. The outcome was CT assessed liver density in Hounsfield units (HU), where liver attenuation less than 42 HU was considered to be non-alcoholic fatty liver disease (NAFLD). Logistic regression was used to assess the relationship between participant exposure and NAFLD. Individuals with excess alcohol consumption were excluded (men >14 drinks/wk and women >7 drinks/wk; remaining=6469). Primary models were adjusted for age at baseline, recruitment site, gender, race/ethnicity, educational attainment, BMI, waist circumference, smoking status, diabetes, HOMA-IR, HDL, and triglycerides. Results: Participants missing covariate values were excluded, resulting in a final sample size of 5558 for PM2.5 and 5484 for NOx. The adjusted OR of NAFLD for PM2.5 was 0.92 (95% CI: -0.84,1.00) for a 1 μg/m3 difference in PM2.5 (p=.O52). The adjusted OR for NOx was 0.99 (95% CI: 0.98,1.00) HU for a 1 ppm difference in NOx (p=.24). Site-adjusted models with fewer covariates were non-significant. Liver attenuation was also evaluated as a linear outcome and the results were similarly non-significant. In contrast, the adjusted OR of NAFLD for untreated diabetes was 2.28 (95% CI: 1.35, 3.85) compared to non-diabetics (p < .01). Conclusions: Estimated air pollution exposure was not associated with fatty liver in this cross-sectional analysis.
机译:背景:动物研究表明,空气污染可能会导致代谢变化,包括Ⅱ型糖尿病患者胰岛素抵抗的肝脂肪蓄积特征。以前尚未对与空气污染有关的结果进行评估。目的:我们进行了一项横截面分析,以评估长期环境NOx和PM2.5与脂肪肝之间的联系,这是通过计算机断层扫描(CT)测量的。方法:多族裔动脉粥样硬化研究(MESA)是一个基于人群的队列研究,来自6个地点(n = 6814)。参与者的暴露量是使用基于可能性的土地利用回归时空模型在2000年参与者地址处估算的年平均环境PM2.5和NOx浓度。结果是CT评估的Hounsfield单位(HU)的肝脏密度,其中肝衰减小于42 HU被认为是非酒精性脂肪性肝病(NAFLD)。使用逻辑回归分析评估参与者暴露与NAFLD之间的关系。排除过量饮酒的人(男性> 14杯/周,女性> 7杯/周;剩余= 6469)。调整了主要模型的基线年龄,征募地点,性别,种族/民族,教育程度,BMI,腰围,吸烟状况,糖尿病,HOMA-IR,HDL和甘油三酸酯。结果:排除了缺少协变量值的参与者,导致PM2.5的最终样本量为5558,NOx的最终样本量为5484。对于PM2.5而言​​,NAFLD的调整后OR值为0.92(95%CI:-0.84,1.00),其中PM2.5差异为1μg/ m3(p = .O52)。对于NOx的1 ppm差异,调整后的NOx OR为0.99(95%CI:0.98,1.00)HU(p = 0.24)。协变量较少的现场调整模型不显着。肝衰减也被评估为线性结果,结果相似地无统计学意义。相比之下,未经治疗的糖尿病患者的NAFLD调整后OR为2.28(95%CI:1.35,3.85),而非糖尿病患者则为(p <.01)。结论:在该横断面分析中,估计的空气污染暴露与脂肪肝无关。

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