年度环境细颗粒物质量及其成分与线粒体 DNA 丰度的相关性研究。
Associations of Annual Ambient Fine Particulate Matter Mass and Components with Mitochondrial DNA Abundance.
机构信息
From the aChanning Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; bVocational Health College, Canakkale Onsekiz Mart University, Çanakkale, Turkey; cDepartment of Developmental Neurobiology, National Institute of Perinatology, Mexico City, Mexico; dDepartment of Environmental Health, Harvard T. H. Chan School of Public Health, Boston, MA; eDepartment of Statistics, Colorado State University, Fort Collins, CO; fDepartment of Environmental Health Sciences, Columbia Mailman School of Public Health, New York, NY; gDepartment of Biostatistics, Harvard School of Public Health, Boston, MA; and hNormative Aging Study, Veterans Affairs Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, Boston, MA.
出版信息
Epidemiology. 2017 Nov;28(6):763-770. doi: 10.1097/EDE.0000000000000717.
BACKGROUND
Fine particulate matter (PM2.5) represents a mixture of components with potentially different toxicities. However, little is known about the relative effects of PM2.5 mass and PM2.5 components on mitochondrial DNA (mtDNA) abundance, which may lie on the pathway of PM2.5-associated disease.
METHODS
We studied 646 elderly male participants in the Normative Aging Study from Greater Boston to investigate associations of long-term exposure to PM2.5 mass and PM2.5 components with mtDNA abundance. We estimated concentrations of pollutants for the 365-day preceding examination at each participant's address using spatial- and temporal-resolved chemical transport models. We measured blood mtDNA abundance using RT-PCR. We applied a shrinkage and selection method (adaptive LASSO) to identify components most predictive of mtDNA abundance, and fit multipollutant linear mixed-effects models with subject-specific intercept to estimate the relative effects of individual PM component.
RESULTS
MtDNA abundance was negatively associated with PM2.5 mass in the previous year and-after adjusting for PM2.5 mass-several PM2.5 components, including organic carbon, sulfate (marginally), and nitrate. In multipollutant models including as independent variables PM2.5 mass and PM2.5 components selected by LASSO, nitrate was associated with mtDNA abundance. An SD increase in annual PM2.5-associated nitrate was associated with a 0.12 SD (95% confidence intervals [CI] = -0.18, -0.07) decrease in mtDNA abundance. Analyses restricted to PM2.5 annual concentration below the current 1-year U.S. Environmental Protection Agency standard produced similar results.
CONCLUSIONS
Long-term exposures to PM2.5-associated nitrate were related to decreased mtDNA abundance independent of PM2.5 mass. Mass alone may not fully capture the potential of PM2.5 to oxidize the mitochondrial genome.See video abstract at, http://links.lww.com/EDE/B274.
背景
细颗粒物（PM2.5）代表了具有潜在不同毒性的成分混合物。然而，对于 PM2.5 质量和 PM2.5 成分对线粒体 DNA（mtDNA）丰度的相对影响知之甚少，而 mtDNA 丰度可能处于与 PM2.5 相关疾病的发生途径上。
方法
我们研究了来自大波士顿地区的规范老化研究中的 646 名老年男性参与者，以调查 PM2.5 质量和 PM2.5 成分的长期暴露与 mtDNA 丰度的关联。我们使用时空分辨的化学输送模型，在每个参与者的地址处估计前 365 天污染物的浓度。我们使用 RT-PCR 测量血液 mtDNA 丰度。我们应用收缩和选择方法（自适应 LASSO）来识别最能预测 mtDNA 丰度的成分，并拟合多污染物线性混合效应模型，以估计每个 PM 成分的相对影响。
结果
mtDNA 丰度与前一年的 PM2.5 质量呈负相关，并且在调整 PM2.5 质量后，与几种 PM2.5 成分呈负相关，包括有机碳、硫酸盐（略有）和硝酸盐。在包含 LASSO 选择的独立变量 PM2.5 质量和 PM2.5 成分的多污染物模型中，硝酸盐与 mtDNA 丰度相关。每年 PM2.5 相关的硝酸盐增加 1 个标准差与 mtDNA 丰度降低 0.12 个标准差（95%置信区间 [CI]：-0.18，-0.07）相关。将分析限制在当前美国环境保护署 1 年标准以下的 PM2.5 年浓度时，得到了类似的结果。
结论
与 PM2.5 相关的硝酸盐的长期暴露与 mtDNA 丰度降低独立相关，而 PM2.5 质量可能无法完全捕捉 PM2.5 氧化线粒体基因组的潜力。
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