Unmasking the hazy link between wildfire particulate air pollution and cardiopulmonary health.
Unmasking the hazy link between wildfire particulate air pollution and cardiopulmonary health.
复制标题
揭示野火颗粒空气污染与心肺健康之间的模糊联系。
DOI：
10.1016/j.explore.2023.06.012
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发表时间：
2023
期刊：
影响因子：
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通讯作者：
Zelikoff,JudithT
中科院分区：
文献类型：
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作者：
Saporito,AntonioF;Zelikoff,JudithT
Wildfires and their effects are an unfamiliar sight to most East Coast individuals, unless they have been employed as a firefighter, were a West Coast transplant, or present for the eerie, orange haze that asphyxiated much of the Northeastern Seaboard on June 7th, 2023. The emigration of Nova Scotian wildfire smoke to the US resulted in peak fine-size particulate matter (PM2. 5) concentration of 460 μg/m3 (micrograms per cubic meter) in New York City (1), with similar concentrations in other East Coast locations, such as Newark, Philadelphia, and Washington DC In comparison, the US Environmental Protection Agency (EPA) sets a daily limit of PM2. 5 exposure at 35 μg/m3 which is considered a safe level for most populations (2). Health experts, therefore, echoed the advice to avoid exposure and isolate from the hazard, and in lieu of this recommendation, to use personal protective equipment (PPE), such as N95 masks. However, exposure may have been unavoidable, and this event raises the question of the possible adverse health effects, both acute and chronic, associated with exposure to particulate-laden wildfire smoke.PM2. 5 denotes fine particulate matter with a maximum aerodynamic diameter of 2.5 micrometers, a size at least 20 times smaller than the width of a human hair. The minute size of PM2. 5 confers numerous advantages to this particle in being able to penetrate deep into the respiratory system. Once inspired, PM2. 5 can avoid impacting on the numerous turns and bifurcations of the bronchus, where it would be swept up and disposed of through coughing by the mucociliary elevator (3). Thus, its small size and mass enable the particle to coast along respired air directly to the air-exchanging alveolar sacs in the deep lung, where it deposits on the surface of alveolar cells. PM2. 5 that are not consumed by residing alveolar macrophages—and subsequently disposed of—can exert their toxicity by promoting inflammatory environments and ultimate damage to the alveolar space (3). Moreover, such tiny particles can diffuse through the alveolar walls and become absorbed
