Chronic Exposure to PM2.5 Nitrate, Sulfate, and Ammonium Causes Respiratory System Impairments in Mice
Chronic Exposure to PM2.5 Nitrate, Sulfate, and Ammonium Causes Respiratory System Impairments in Mice
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长期暴露于 PM2.5 硝酸盐、硫酸盐和铵会导致小鼠呼吸系统受损
DOI：
10.1021/acs.est.0c05814
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发表时间：
2021
影响因子：
11.4
通讯作者：
Hao Ke
中科院分区：
文献类型：
--
作者：
Zhang Jushan;Cheng Haoxiang;Wang Dongbin;Zhu Yujie;Yang Chun;Shen Yuan;Yu Jing;Li Yuanyuan;Xu Shunqing;Zhang Shumin;Song Xiaolian;Zhou Yang;Chen Jia;Jiang Jingkun;Fan Lihong;Wang Changhui;Hao Ke
水溶性无机离子（WSI）是环境空气PM2.5（直径≤2.5 μm的颗粒物）的主要组成部分，但其潜在的健康效应尚未得到充分研究。在C57 BL/6小鼠上，我们量化了三种主要的PM2.5WSIs（NO3-、SO 42-和NH 4+）对呼吸系统的影响。暴露情景包括不同的WSI类型、浓度、动物发育阶段（幼年与成年）和性别。全面评估暴露效应，特别关注呼吸功能和组织/细胞水平的变化。慢性PM2.5NO3暴露导致呼吸功能明显下降，主要表现为气流阻塞。年轻小鼠的下降比成年小鼠更严重。在幼龄小鼠中，暴露于22 μg/m3PM2.5NO3-使FEV0.05（0.05 s用力呼气量）降低11.3%（p= 9.6 × 10-3），并使肺中性粒细胞浸润增加7.9%（p= 7.1 × 10-3）。因果关系检验表明，中性粒细胞浸润参与了PM2.5NO3毒性的生物学机制。相比之下，PM2.5SO42-的影响比NO3-弱得多。PM2.5NO3-暴露导致呼气峰流速降低的作用是PM2.5SO42-暴露的3.4倍。PM2.5NH4+暴露对呼吸功能无显著影响。总之，这项研究提供了强有力的证据，对PM2.5WSIs的不利影响，其中的影响是最深刻的年轻小鼠暴露于PM2.5NO3-。如果在人体中得到证实，PM2.5WSI的毒性将在环境健康和政策制定方面产生广泛的影响。
Water-soluble inorganic (WSI) ions are major components of ambient air PM2.5(particulate matter of diameter ≤2.5 μm); however, their potential health effects are understudied. On C57BL/6 mice, we quantified the effect of three major PM2.5WSIs (NO3–, SO42–, and NH4+) on respiratory systems. Exposure scenarios include different WSI types, concentrations, animal development stages (young vs adult), and sex. The exposure effects were comprehensively assessed, with special focus on the respiratory function and tissue/cell level changes. Chronic PM2.5NO3–exposure produced significant respiratory function decline, mainly presented as airflow obstruction. The decline was more profound in young mice than in adult mice. In young mice, exposure to 22 μg/m3PM2.5NO3–reduced FEV0.05(forced expiratory volume in 0.05 s) by 11.3% (p= 9.6 × 10–3) and increased pulmonary neutrophil infiltration by 7.9% (p= 7.1 × 10–3). Causality tests identified that neutrophil infiltration was involved in the biological mechanism underlying PM2.5NO3–toxicity. In contrast, the effects of PM2.5SO42–were considerably weaker than NO3–. PM2.5NO3–exposure was 3.4 times more potent than PM2.5SO42–in causing reduction of the peak expiratory flow. PM2.5NH4+exposure had no statistically significant effects on the respiratory function. In summary, this study provided strong evidence on the adverse impacts of PM2.5WSIs, where the impacts were most profound in young mice exposed to PM2.5NO3–. If confirmed in humans, toxicity of PM2.5WSI will have broad implications in environment health and policy making.