Source of Biomass Cooking Fuel Determines Pulmonary Response to Household Air Pollution
Source of Biomass Cooking Fuel Determines Pulmonary Response to Household Air Pollution
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DOI：
10.1165/rcmb.2013-0201oc
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发表时间：
2014-03-01
影响因子：
6.4
通讯作者：
Biswal, Shyam
中科院分区：
文献类型：
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作者：
Sussan, Thomas E.;Ingole, Vijendra;Biswal, Shyam
约有30亿人-占世界人口的一半-由于在低效率的炉灶上燃烧生物质燃料而暴露在极高浓度的家庭空气污染中，全球每年有400万人死亡。然而，我们对家庭空气污染暴露的肺反应以及潜在的分子和细胞事件的理解是有限的。印度最普遍的两种生物质燃料是木材和牛粪，使用这些燃料的家庭中典型的24小时平均颗粒物（PM）浓度为300至5，000 mg/m3。我们解剖了小鼠急性或亚慢性暴露于从印度农村家庭收集的木材或牛粪PM生物质烹饪过程中肺反应的机制。急性暴露导致强烈的促炎细胞因子产生、嗜酸性炎症、气道阻力和高反应性，所有这些在暴露于来自牛粪的PM的小鼠中显著更高。相反，亚慢性暴露诱导嗜酸性粒细胞炎症，PM特异性抗体反应，肺泡破坏是最高的木材PM暴露小鼠。为了理解触发生物质PM诱导的炎症的分子途径，我们将Toll样受体（TLR）2-、TLR 3-、TLR 4-、TLR 5-和IL-1 R缺陷小鼠暴露于PM，并发现IL-1 R、TLR 4和TLR 2是暴露于木材或牛粪PM的小鼠中通过MyD 88引起炎症反应的主要受体。总之，这项研究表明，亚慢性暴露于从燃烧生物质燃料的家庭收集的PM，主要通过激活TLR和IL-1 R途径，这可能会增加慢性呼吸道疾病的风险，从而导致持续性肺部炎症。
Approximately 3 billion people-half the worldwide populationare exposed to extremely high concentrations of household air pollution due to the burning of biomass fuels on inefficient cookstoves, accounting for 4 million annual deaths globally. Yet, our understanding of the pulmonary responses to household air pollution exposure and the underlying molecular and cellular events is limited. The two most prevalent biomass fuels in India are wood and cow dung, and typical 24-hour mean particulate matter (PM) concentrations in homes that use these fuels are 300 to 5,000 mg/ m(3). We dissected the mechanisms of pulmonary responses in mice after acute or subchronic exposure to wood or cow dung PM collected from rural Indian homes during biomass cooking. Acute exposures resulted in robust proinflammatory cytokine production, neutrophilic inflammation, airway resistance, and hyperresponsiveness, all of which were significantly higher in mice exposed to PM from cow dung. On the contrary, subchronic exposures induced eosinophilic inflammation, PM-specific antibody responses, and alveolar destruction that was highest in wood PM-exposed mice. To understand the molecular pathways that trigger biomass PM-induced inflammation, we exposed Toll-like receptor (TLR)2-, TLR3-, TLR4-, TLR5-, and IL-1R-deficient mice to PM and found that IL-1R, TLR4, and TLR2 are the predominant receptors that elicit inflammatory responses via MyD88 in mice exposed to wood or cow dung PM. In conclusion, this study demonstrates that subchronic exposure to PM collected from households burning biomass fuel elicits a persistent pulmonary inflammation largely through activation of TLR and IL-1R pathways, which could increase the risk for chronic respiratory diseases.