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The pulmonary health effects of diesel exhaust and diesel exhaust particles: Evidence from cellular in vitro and human exposure studies.

机译：柴油机废气和柴油机废气颗粒对肺部健康的影响：来自细胞体外和人体暴露研究的证据。

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The adverse health effects resulting from ambient air pollution exposure is an increasing concern worldwide. Globally, over two-hundred epidemiologic studies report that human exposure to ambient particulate matter (PM) has a deleterious effect on cardiopulmonary mortality and morbidity, including the exacerbation of pre-existing lung disease and the development of new respiratory infections. The contribution of diesel exhaust exposure to the observed health effects is a particular concern because diesel exhaust particles (DEP) are a significant portion of fine ambient PM in many US and international cities. Previous research demonstrates that DEP exposure may enhance pulmonary vulnerability to infection by suppressing innate lung responses and enhancing allergic inflammation, but the cellular pathways involved in these processes remain unclear. The goal of the research described herein was two-fold: (1) to investigate the effects of particulate matter (PM) and diesel exhaust particle (DEP) exposure on human pulmonary inflammation; and (2) evaluate the general pathways that may be involved in DEP-induced effects. To this end, we conducted a series of in vitro experiments on human alveolar macrophages (AM) as well as a human controlled DE exposure study in order to evaluate oxidative, inflammatory mediator, and phospholipid endpoints that may be involved in DEPinduced effects. We found that DEP and ambient PM may enhance human vulnerability to lung infection by modulating alveolar macrophage (AM) oxidative and inflammatory cytokine responses to bacterial exposure. Our in vivo results demonstrated that DE exposure down-regulates TH1 cytokine concentration and stimulates TH2 cytokine concentrations in the bronchial fluid of exposed human volunteers, indicating that DE shifts pulmonary defense toward allergic-type mechanisms. DE exposure also decreased calcium concentration, a metal important to many immune mechanistic pathways, measured in human exhaled breath condensate. Finally, we demonstrate that in vivo DE exposure and DEP exposure in vitro alters AM phospholipid concentrations, thus potentially generating unique "fingerprints" of exposure. The results of our studies will contribute significantly to other toxicological, controlled exposure, and epidemiological studies, providing a strong data pool from which to determine the national standards that best protect public health and welfare.
机译：暴露于环境空气污染中对健康造成的不利影响在世界范围内日益引起关注。在全球范围内，超过两百项流行病学研究报告表明，人体暴露于环境颗粒物（PM）对心肺疾病的死亡率和发病率具有有害影响，包括加剧先前存在的肺部疾病和发展新的呼吸道感染。柴油机废气暴露对观察到的健康影响的贡献特别令人担忧，因为在许多美国和国际城市中，柴油机废气颗粒（DEP）是环境PM的重要组成部分。先前的研究表明，DEP暴露可能会通过抑制先天性肺反应和增强变态反应性炎症而增强肺部对感染的脆弱性，但涉及这些过程的细胞途径尚不清楚。本文所述研究的目的有两个方面：（1）研究颗粒物（PM）和柴油机排气颗粒（DEP）暴露对人肺部炎症的影响； （2）评估可能与DEP诱导的效应有关的一般途径。为此，我们对人肺泡巨噬细胞（AM）进行了一系列体外实验以及一项人为控制的DE暴露研究，以评估可能与DEP诱导的作用有关的氧化，炎症介质和磷脂终点。我们发现，DEP和环境PM可能通过调节肺泡巨噬细胞（AM）对细菌暴露的氧化性和炎症性细胞因子反应而增强人类对肺部感染的脆弱性。我们的体内结果表明，DE暴露可下调人类志愿者支气管液中TH1细胞因子的浓度，并刺激TH2细胞因子的浓度，这表明DE可使肺部防御转向过敏型机制。在人体呼出的呼吸道凝结物中测得的DE暴露也降低了钙浓度，钙浓度是许多免疫机制中重要的金属。最后，我们证明体内DE暴露和DEP体外暴露会改变AM磷脂浓度，从而潜在地产生独特的暴露“指纹”。我们的研究结果将对其他毒理学，控制暴露和流行病学研究做出重大贡献，为确定最能保护公众健康和福利的国家标准提供强大的数据库。

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