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首页> 外文会议>Annual conference of the International Society of Exposure Science >Environmental Exposures to PM and Resultant Metabolomic Perturbations in Humans
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Environmental Exposures to PM and Resultant Metabolomic Perturbations in Humans

机译：环境暴露于人类的PM和导致的代谢组学扰动

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Studies have shown the adverse pulmonary and cardiovascular Impacts of human exposures to airborne particulate matter (PM2.5). Epidemiological studies, primarily the cardiovascular studies, drive much of the risk assessment for ambient PM standards. Although PM concentration is the most common metric of exposure and risk, this measure fails to define the chemical variations that underlie potential differences in toxicity. Chemical species in PM, measured by EC/OC, ions, elements, and extractable organics, clearly demonstrate source-dependent variability in the chemical composition of PM. Such chemical variability would be expected to result in different biochemical perturbations in those people exposed, as assessed through a broad-spectrum metabolomics analysis. This study draws on PM filters and associated biological samples (urine, plasma, exhaled breath condensate or EBC) archived from two earlier PM exposure studies. One study collected samples (EBC, urine) in both Butte, MT, and Fairbanks, AK. The fractional contribution from wood smoke is higher in MT and the contribution from fuel oil is higher in AK. The second study utilized chamber-based exposures of people to PM and PM + NO2, or not, with the collection of blood plasma after exposure. PM filters from both studies were solvent-extracted and the extracts were analyzed by 2-D GC/TOF-MS.The SVOC profiles were subjected to multivariate analysis and visualization using SIMCA 13.0 (Umetrics, Umea, Sweden) which revealed several SVOCs that differentiated MT-based from the AK-based samples. Analysis of data derived from the EPA filter analysis is in process. Differences in exposure, such as high/low PM mass in a given location, relative concentrations of discriminators, and location, will be used to establish groups for planned metabolomics investigations. This work was sponsored by RTI, NIEHS (5R01ES016336), NIH Common fund (11010737) and the US EPA. This abstract does not necessarily reflect EPA policy.
机译：研究表明，人体暴露于空气中的颗粒物（PM2.5）对肺和心血管有不利影响。流行病学研究（主要是心血管研究）推动了环境PM标准的大部分风险评估。尽管PM浓度是最常见的暴露和风险指标，但该措施无法定义潜在的毒性差异所基于的化学变化。通过EC / OC，离子，元素和可萃取的有机物测量的PM中的化学物质清楚地证明了PM的化学成分具有源依赖性。如通过广谱代谢组学分析所评估的，这种化学变异性将导致所接触人群的不同生物化学扰动。这项研究利用了从两项较早的PM暴露研究中存档的PM过滤器和相关的生物样品（尿液，血浆，呼出气冷凝物或EBC）。一项研究在MT的Butte和AK的Fairbanks收集了样本（EBC，尿液）。 MT中来自木烟的分数贡献较高，而AK中来自燃料油的贡献较高。第二项研究利用人们基于室的暴露于PM和PM + NO2（或不暴露），并在暴露后收集血浆。两项研究的PM过滤器均经过溶剂萃取，提取物通过2-D GC / TOF-MS分析.SVOC谱图使用SIMCA 13.0（Umetrics，Umea，Sweden）进行了多变量分析和可视化，揭示了几种可以区分的SVOC来自基于AK的样本的基于MT的样本。正在进行从EPA过滤器分析得出的数据分析。暴露的差异（例如给定位置的高/低PM质量，鉴别剂的相对浓度和位置）将用于建立计划的代谢组学研究的组。这项工作是由RTI，NIEHS（5R01ES016336），NIH共同基金（11010737）和美国EPA赞助的。此摘要不一定反映EPA政策。

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