Retrospective assessment of radon progeny and pollution effects in COPD

氡（Rn）是一种放射性气体，其衰变成能够诱导细胞凋亡的放射性子代。 吸入后的伤害。住宅暴露于Rn是常见的;然而，目前的健康问题， 法规仅基于其作为肺癌致癌物的影响。目前尚不清楚暴露在Rn衰变中是否 产品导致其他非癌症的不良健康影响，如我们在慢性阻塞性肺疾病中提出的 慢性阻塞性肺病（COPD）患者。在这个探索性和发展性的应用中，我们将评估暴露是否 Rn衰变产物，如使用铅-210（210 Pb）评估的，具有最长半衰期的后代，增强了 空气污染颗粒物的毒性（和健康影响）。 在170名东马萨诸塞州COPD患者中，我们先前评估了室内家庭暴露于PM2.5 和黑碳，在一年的时间里季节性地收集多达四个7天的样本。由于210 Pb是 在与存档的PM2.5过滤器样品上的α（α）发射子体平衡时， 从它们发出的辐射将允许反算住宅210 Pb水平（作为替代措施， Rn子代）在取样时存在。因此，我们将研究暴露于Rn子代是否 （as 210 Pb）改变（增加）PM2.5和炭黑对以下方面的影响：1）全身性疾病的血浆生物标志物 炎症（C-反应蛋白和白细胞介素-6）; 2）脂质氧化损伤的尿生物标志物 （丙二醛）和DNA（8-羟基-2 '-脱氧鸟苷）;和3）肺功能（FEV 1、FVC和 FEV 1/FVC）。这项研究设计包括一个强有力的和新颖的暴露组成部分， 相关和机械的结果。这些与COPD患者的健康有关，这是一种常见的 这种疾病影响了大约11%的55岁以上的美国人口。

Radon (Rn) is a radioactive gas that decays into radiation-emitting progenies capable of inducing cellular damage once inhaled. Residential exposure to Rn is common; however, current health concerns and regulations are based only on its effects as a lung carcinogen. It is not known whether exposure to Rn decay products results in other, non-cancer, adverse health effects, as we propose in chronic obstructive pulmonary disease (COPD) patients. In this exploratory and developmental application, we will assess whether exposure to Rn decay products, as assessed using lead-210 (210Pb), the progeny with the longest half-life, enhances the toxicity (and health effects) of air pollution particles. In 170 Eastern Massachusetts COPD patients, we have previously assessed indoor-home exposures to PM2.5 and black carbon by collecting up to four 7-day samples seasonally over the period of one year. Since 210Pb is in equilibrium with alpha (α)-emitting progeny on archived PM2.5 filter samples, the measurement of total α- radiation emitted from them will permit back-calculation of residential 210Pb levels (as a surrogate measure of Rn progeny) present at the time of sampling. Therefore, we will investigate whether exposure to Rn progeny (as210Pb) modifies (increases) the effect of PM2.5 and black carbon on: 1) plasma biomarkers of systemic inflammation (C-reactive protein and interleukin-6); 2) urinary biomarkers of oxidative damage to lipids (malondialdehyde) and DNA (8-hydroxy-2'-deoxyguanosine); and 3) pulmonary function (FEV1, FVC, and FEV1/FVC). This research design encompasses a strong and novel exposure component linked to clinically relevant and mechanistic outcomes. These are relevant to the health of COPD patients, which is a common disease affecting approximately 11% of the US population older than age 55 years.