Lee Alison, Kinney Patrick, Chillrud Steve, Jack Darby
Division of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY.
Mailman School of Public Health, Department of Environmental Health Sciences, Columbia University, New York, NY.
Ann Glob Health. 2015 May-Jun;81(3):368-74. doi: 10.1016/j.aogh.2015.08.006.
Household air pollution (HAP)-associated acute lower respiratory infections cause 455,000 deaths and a loss of 39.1 million disability-adjusted life years annually. The immunomodulatory mechanisms of HAP are poorly understood.
The aim of this study was to conduct a systematic review of all studies examining the mechanisms underlying the relationship between HAP secondary to solid fuel exposure and acute lower respiratory tract infection to evaluate current available evidence, identify gaps in knowledge, and propose future research priorities.
We conducted and report on studies in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. In all, 133 articles were fully reviewed and main characteristics were detailed, namely study design and outcome, including in vivo versus in vitro and pollutants analyzed. Thirty-six studies were included in a nonexhaustive review of the innate immune system effects of ambient air pollution, traffic-related air pollution, or wood smoke exposure of developed country origin. Seventeen studies investigated the effects of HAP-associated solid fuel (biomass or coal smoke) exposure on airway inflammation and innate immune system function.
Particulate matter may modulate the innate immune system and increase susceptibility to infection through a) alveolar macrophage-driven inflammation, recruitment of neutrophils, and disruption of barrier defenses; b) alterations in alveolar macrophage phagocytosis and intracellular killing; and c) increased susceptibility to infection via upregulation of receptors involved in pathogen invasion.
HAP secondary to the burning of biomass fuels alters innate immunity, predisposing children to acute lower respiratory tract infections. Data from biomass exposure in developing countries are scarce. Further study is needed to define the inflammatory response, alterations in phagocytic function, and upregulation of receptors important in bacterial and viral binding. These studies have important public health implications and may lead to the design of interventions to improve the health of billions of people daily.
家庭空气污染(HAP)相关的急性下呼吸道感染每年导致45.5万人死亡,损失3910万个伤残调整生命年。人们对HAP的免疫调节机制了解甚少。
本研究旨在对所有研究进行系统综述,这些研究探讨了固体燃料暴露所致HAP与急性下呼吸道感染之间关系的潜在机制,以评估现有证据,找出知识空白,并提出未来研究重点。
我们按照PRISMA(系统评价和Meta分析的首选报告项目)指南开展并报告研究。共对133篇文章进行了全面评审,并详细阐述了主要特征,即研究设计和结果,包括体内研究与体外研究以及所分析的污染物。对36项研究进行了非详尽综述,这些研究涉及环境空气污染、交通相关空气污染或来自发达国家的木烟暴露对先天免疫系统的影响。17项研究调查了HAP相关固体燃料(生物质或煤烟)暴露对气道炎症和先天免疫系统功能的影响。
颗粒物可能通过以下方式调节先天免疫系统并增加感染易感性:a)肺泡巨噬细胞驱动的炎症、中性粒细胞募集以及屏障防御破坏;b)肺泡巨噬细胞吞噬作用和细胞内杀伤的改变;c)通过上调参与病原体入侵的受体增加感染易感性。
生物质燃料燃烧所致的HAP改变先天免疫,使儿童易患急性下呼吸道感染。来自发展中国家生物质暴露的数据稀缺。需要进一步研究来确定炎症反应、吞噬功能改变以及在细菌和病毒结合中起重要作用的受体上调情况。这些研究具有重要的公共卫生意义,可能会促成旨在改善数十亿人日常健康状况的干预措施设计。