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Inflammatory and oxidative stress responses of healthy adults to changes in personal air pollutant exposure.
Environmental Pollution ( IF 7.6 ) Pub Date : 2020-04-03 , DOI: 10.1016/j.envpol.2020.114503 Xinyan Hu 1 , Linchen He 2 , Junfeng Zhang 3 , Xinghua Qiu 1 , Yinping Zhang 4 , Jinhan Mo 4 , Drew B Day 5 , Jianbang Xiang 6 , Jicheng Gong 1
Environmental Pollution ( IF 7.6 ) Pub Date : 2020-04-03 , DOI: 10.1016/j.envpol.2020.114503 Xinyan Hu 1 , Linchen He 2 , Junfeng Zhang 3 , Xinghua Qiu 1 , Yinping Zhang 4 , Jinhan Mo 4 , Drew B Day 5 , Jianbang Xiang 6 , Jicheng Gong 1
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Exposure to air pollutants has been associated with respiratory and cardiovascular mortality, but the underlying molecular mechanisms remain inadequately understood. We aimed to examine molecular-level inflammatory and oxidative stress responses to personal air pollutant exposure. Fifty-three healthy adults aged 22-52 were measured three times for their blood inflammatory cytokines and urinary malondialdehyde (MDA, an oxidative stress biomarker) within 2 consecutive months. Pollutant concentrations monitored indoors and outdoors were combined with the time-activity data to calculate personal O3, PM2.5, NO2, and SO2 exposures averaged over 12 h, 24 h, 1 week, and 2 weeks, respectively, prior to biospecimen collection. Inflammatory cytokines and MDA were associated with pollutant exposures using linear mixed-effects models controlling for various covariates. After adjusting for a co-pollutant, we found that concentrations of proinflammatory cytokines were significantly and negatively associated with 12-h O3 exposures and significantly but positively associated with 2-week O3 exposures. We also found significant and positive associations of proinflammatory cytokines with 12-h and 24-h NO2 exposures, respectively. However, we did not find clear associations of PM2.5 and SO2 exposure with proinflammatory cytokines and with MDA. The removal of an O3-generating electrostatic precipitator in the mechanical ventilation systems of the offices and residences of the subjects was associated with significant decreases in IL-1β, IL-2, IL-6, IL-8, IL-17A, and TNF-α. These findings suggest that exposure to O3 for different time durations may affect systemic inflammatory responses in different ways.
中文翻译：
健康成年人对个人空气污染物暴露变化的炎性和氧化应激反应。
暴露于空气污染物与呼吸道疾病和心血管疾病的死亡率有关，但对潜在的分子机制仍知之甚少。我们旨在研究分子水平的炎症和氧化应激反应对个人空气污染物的暴露。在连续2个月内，对53名22-52岁的健康成年人进行了3次血液炎症细胞因子和尿液丙二醛（MDA，一种氧化应激生物标记物）的测量。在收集生物样本之前，将室内和室外监测的污染物浓度与时间活动数据相结合，以分别计算平均12小时，24小时，1周和2周的个人O3，PM2.5，NO2和SO2暴露量。使用控制各种协变量的线性混合效应模型，炎症细胞因子和MDA与污染物暴露相关。在调整了共污染物后，我们发现促炎细胞因子的浓度与12小时O3暴露显着负相关，与2周O3暴露显着正相关。我们还发现促炎细胞因子分别与12小时和24小时NO2暴露有显着正相关。但是，我们没有发现PM2.5和SO2暴露与促炎细胞因子和MDA有明确的关联。受试者办公室和住所的机械通风系统中产生O3的静电除尘器的移除与IL-1β，IL-2，IL-6，IL-8，IL-17A和TNF的显着降低有关-α。
更新日期：2020-04-03
中文翻译：
健康成年人对个人空气污染物暴露变化的炎性和氧化应激反应。
暴露于空气污染物与呼吸道疾病和心血管疾病的死亡率有关，但对潜在的分子机制仍知之甚少。我们旨在研究分子水平的炎症和氧化应激反应对个人空气污染物的暴露。在连续2个月内，对53名22-52岁的健康成年人进行了3次血液炎症细胞因子和尿液丙二醛（MDA，一种氧化应激生物标记物）的测量。在收集生物样本之前，将室内和室外监测的污染物浓度与时间活动数据相结合，以分别计算平均12小时，24小时，1周和2周的个人O3，PM2.5，NO2和SO2暴露量。使用控制各种协变量的线性混合效应模型，炎症细胞因子和MDA与污染物暴露相关。在调整了共污染物后，我们发现促炎细胞因子的浓度与12小时O3暴露显着负相关，与2周O3暴露显着正相关。我们还发现促炎细胞因子分别与12小时和24小时NO2暴露有显着正相关。但是，我们没有发现PM2.5和SO2暴露与促炎细胞因子和MDA有明确的关联。受试者办公室和住所的机械通风系统中产生O3的静电除尘器的移除与IL-1β，IL-2，IL-6，IL-8，IL-17A和TNF的显着降低有关-α。
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