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美国成年人环境多环芳烃暴露及促炎活性对2型糖尿病的影响

Effects of Environmental Polycyclic Aromatic Hydrocarbons Exposure and Pro-Inflammatory Activity on Type 2 Diabetes Mellitus in US Adults.

作者信息

Srivastava Shweta

机构信息

Christina Lee Brown Envirome Institute, University of Louisville, Louisville, United States of America.

出版信息

Open J Air Pollut. 2022 Jun;11(2):29-46. doi: 10.4236/ojap.2022.112003. Epub 2022 Jun 24.

Abstract

Polycyclic aromatic hydrocarbons (PAHs) are formed due to natural and anthropogenic activities and known for their potential impact and persistence in the environment. PAHs exposure has been linked to cause adverse health effect including lung cancer, heart conditions and genetic mutations. The understanding of metabolic effects of PAHs exposure is less clear especially in the presence of pro-inflammatory stress like alcoholism or diabetes. The aim of this article is to understand the metabolic effects of PAHs exposure on Type 2 Diabetes Mellitus (T2DM) by analyzing the clinical biomarkers data retrieved from the National Health and Nutrition Examination Survey, Center for Disease Control (CDC NHANES) (2015-16). This study has also accessed the interactive impact of PAHs and other proinflammatory factors, like alcohol intake on the metabolic syndrome on T2DM. We investigated urinary levels of hydroxylated PAHs metabolites (OH-PAHs) along with demographic, clinical and laboratory data. Generalize linear model Univariate factorial ANOVA was used to evaluate the group differences in the demographics, PAH exposure, drinking patterns, clinical data, and biomarker levels. Linear regression model was used to analyze the association of biomarkers, PAH exposure and drinking data. Multivariable regression model was used for multi-independent model to assess comorbidity association and their effect sizes on the clinical outcomes. The results indicated that BMI (p = 0.002), and age (≤0.001) are independent demographic risk factors for T2DM in high PAHs exposure. Acute proinflammatory activity characterized by CRP, is augmented by elevated monocyte levels (p ≤ 0.001) and stepwise addition of 1-Hydroxynapthelene (p = 0.005), and 2-Hydroxynapthelene (p = 0.001) independently. Prevalence of highest average drinks over time is observed in the high PAHs exposure; with males drinking almost twice compared to females in highly exposed population. Pathway response of T2DM shows sexual dimorphism; with males showing association with triglycerides (p ≤ 0.001), and females with CRP (p = 0.015) independently with HbA1C. The arrangement of CRP, absolute monocyte levels, serum triglycerides and average drinks over time predict the HbA1C levels (adjusted R = 0.226, p ≤ 0.001) in individuals with high PAHs exposure. Findings from this investigation support the pathological role of high exposure of PAHs in the exacerbation of metabolic disorder syndrome involving T2DM. Sexual dimorphism is reflected in alcohol drinking, with males drinking more in the high PAHs exposure group. Alcohol drinking as an independent factor was associated with the T2DM indicator, HbA1C in individuals with high PAHs exposure.

摘要

多环芳烃(PAHs)是由自然活动和人为活动形成的,因其在环境中的潜在影响和持久性而闻名。接触PAHs与包括肺癌、心脏疾病和基因突变在内的不良健康影响有关。对PAHs接触的代谢影响的了解尚不清楚,尤其是在存在酗酒或糖尿病等促炎应激的情况下。本文的目的是通过分析从疾病控制中心国家健康与营养检查调查(CDC NHANES)(2015 - 16年)中检索到的临床生物标志物数据,来了解PAHs接触对2型糖尿病(T2DM)的代谢影响。本研究还探讨了PAHs与其他促炎因素(如酒精摄入)对T2DM代谢综合征的交互影响。我们调查了羟基化PAHs代谢物(OH - PAHs)的尿液水平以及人口统计学、临床和实验室数据。使用广义线性模型单因素方差分析来评估人口统计学、PAHs接触、饮酒模式、临床数据和生物标志物水平的组间差异。使用线性回归模型分析生物标志物、PAHs接触和饮酒数据之间的关联。多变量回归模型用于多独立模型,以评估共病关联及其对临床结局的效应大小。结果表明,在高PAHs接触人群中,体重指数(BMI)(p = 0.002)和年龄(≤0.001)是T2DM的独立人口统计学风险因素。以C反应蛋白(CRP)为特征的急性促炎活性,通过单核细胞水平升高(p ≤ 0.001)以及1 - 羟基萘(p = 0.005)和2 - 羟基萘(p = 0.001)的逐步添加而增强。随着时间推移,在高PAHs接触人群中观察到最高平均饮酒量的患病率;在高暴露人群中,男性饮酒量几乎是女性的两倍。T2DM的通路反应表现出性别差异;男性与甘油三酯(p ≤ 0.001)相关,女性与CRP(p = 0.015)独立相关且与糖化血红蛋白(HbA1C)有关。CRP、绝对单核细胞水平、血清甘油三酯和随着时间推移的平均饮酒量的排列可预测高PAHs接触个体的HbA1C水平(调整后R = 0.226,p ≤ 0.001)。本调查结果支持高暴露PAHs在涉及T2DM的代谢紊乱综合征加重中的病理作用。性别差异体现在饮酒方面,在高PAHs接触组中男性饮酒更多。饮酒作为一个独立因素与高PAHs接触个体的T2DM指标HbA1C相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2923/9283753/1d7ffd81b247/nihms-1821051-f0001.jpg

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