杨硕1, 李黄佳琪1, 刘卉萌2a, 冯蓉3, 徐红梅2b, 杜伟1, 孙健2b, 吴少伟2a
1. 昆明理工大学 环境科学与工程学院, 云南 昆明 650500; 2.西安交通大学 a.公共卫生学院, 陕西 西安 710061, b.能源与动力工程学院, 陕西 西安 710049; 3.山西大学 环境与资源学院, 山西 太原 030031
引用格式:
杨硕, 李黄佳琪, 刘卉萌, 等. 细颗粒物健康效应研究进展[J]. 中国粉体技术, 2027, 33(2): 1-14.
Yang Shuo, Li Huangjiaqi, Liu Huimeng, et al. Research progress on health effects of fine particulate matter[J]. China Powder Science and Technology, 2027, 33(2): 1-14.
DOI:10.13732/j.issn.1008-5548.2027.02.005
收稿日期: 2026-07-28, 修回日期: 2026-08-22, 上线日期: 2026-09-27。
基金项目: 国家自然科学基金项目,编号:82273587、42277422。
第一作者: 杨硕(1994—),男,特聘副教授,博士,硕士生导师,研究方向为环境毒理学与健康。E-mail:Alonzoy@foxmail.com。
通信作者: 孙健(1989—),男,副教授,博士,硕士生导师,研究方向为大气污染与人体健康。E-mail:sunjian0306@mail.xjtu.edu.cn。
通信作者:吴少伟(1983—),男,教授,博士,研究方向为环境因素对人群健康的影响。E-mail:shaowei_wu@xjtu.edu.cn。
摘要: 【目的】 系统梳理我国细颗粒物健康效应研究在暴露评估、人群流行病学、早期亚临床损伤及细胞与动物毒理机制方面的进展,明确各类证据的衔接关系,为健康导向的大气污染防控提供依据。 【研究现状】 综述固定站点、高分辨率模型、时间-活动模式和个体暴露监测等暴露评估方法,概括队列、时间序列、病例交叉及定组研究(panel study)证据,总结气溶胶及其组分与心血管、呼吸、代谢、神经、肾脏和生殖等多系统健康结局的关联,以及氧化应激、炎症反应、内皮损伤和代谢紊乱等机制。 【结论与展望】 提出协同应用高时空分辨率个体暴露监测、多组分检测、多组学和人工智能分析;认为未来应加强组分毒性异质性的人群验证,探索基于氧化潜势和毒性权重的健康风险评价与差异化控制。
关键词: 细颗粒物; 健康效应; 个体暴露评估; 人群流行病学; 早期亚临床损伤; 细胞与动物毒理学; 健康风险防控
Abstract
Significance Exposure to fine particulate matter (PM2.5) remains an important environmental health concern in China despite sustained improvements in ambient air quality. Research has progressed beyond estimating disease burdens under severe haze conditions to assessing risks at lower pollution levels, characterizing component-specific toxicity, identifying early biological responses, and evaluating health benefits from exposure reduction. This review summarizes progress in China across four interconnected fields: exposure assessment, large-scale epidemiology, early subclinical injury, and cellular and animal toxicology. It clarifies how evidence from environmental concentrations, personal exposure, biological responses, population health outcomes, and mechanistic experiments can support health-oriented strategies for air pollution prevention and control.
Progress For exposure assessment, fixed-site monitoring and outdoor concentrations at residential locations remain important for describing regional pollution backgrounds and long-term trends. High-resolution spatiotemporal models, time-activity information, microenvironmental measurements, portable sensors, positioning data, and inhaled-dose estimation enable more detailed characterization of individual exposure. However, uncertainties remain because of challenges related to sensor calibration, humidity interference, compliance with device-wearing protocols, limitations of indoor positioning, and limited comparability between modeled and measured exposure estimates. Evidence from household solid-fuel use, cooking emissions, and air quality improvement scenarios shows that indoor sources and activity patterns can influence exposure levels and health benefits. Large-scale epidemiological evidence has been generated from nationwide time-series analyses, case-crossover studies, and major prospective cohorts. Long-term exposure to PM2.5 and its components has been associated with cardiovascular, respiratory, renal, metabolic, neurological, and reproductive outcomes, as well as mortality, among both general and susceptible populations. Associations vary among black carbon, nitrate, sulfate, ammonium, organic matter, chloride, soil particles, sea salt, metals, and polycyclic aromatic hydrocarbons, indicating that health effects cannot be fully represented by particle mass concentration alone. A study covering 292 Chinese cities and nearly 49 million hospital admissions reported that black carbon was consistently associated with higher risks of hospital admission across multiple organ systems, with associations generally stronger than those observed for PM2.5 mass concentration. Healthy lifestyles and physical activity may modify selected pollution-related risks, although these effects vary depending on exposure window and population. Small-scale longitudinal and panel studies provide temporally resolved evidence of biological changes preceding clinical disease. Repeated personal exposure measurements have been combined with measurements of blood, urine, saliva, exhaled breath condensate, lung function testing, and multi-omics analyses. Reported early responses include oxidative DNA damage, lipid peroxidation, systemic and airway inflammation, coagulation changes, endothelial dysfunction, altered sphingolipid metabolism, and impaired lung function. Intervention studies suggest that long-term indoor air purification may lower diastolic blood pressure in older adults, while fish oil supplementation may attenuate PM2.5-related inflammatory responses. Studies conducted in rural areas of the Fenwei Plain have linked solid-fuel-related PM2.5 and organic components to changes in biomarkers and pulmonary function. Toxicological evidence is increasingly generated using exposure systems that more closely approximate inhalation under real-world conditions. Earlier approaches based on particle extraction, submerged-cell exposure, and intratracheal instillation are complemented by inhalation exposure to concentrated ambient particles and air-liquid interface exposure systems. These systems better preserve particle size, chemical composition, deposition characteristics, and biologically active constituents. Major pathways include oxidative stress, mitochondrial dysfunction, inflammatory signaling, epithelial and endothelial injury, vascular smooth muscle cell phenotypic switching, impaired air-blood barrier function, neuroinflammation, and interorgan crosstalk. Component-specific toxicity has been demonstrated for transition metals, black carbon, polycyclic aromatic hydrocarbons, mixed metal components, and environmentally persistent free radicals. Reactive oxygen species generation, p38 mitogen-activated protein kinase signaling, Toll-like receptor 4-nuclear factor kappa B activation, barrier injury, and neurodegenerative changes contribute to these effects. Oxidative potential is emerging as an integrative indicator linking aerosol composition with biological activity, although broader validation in human populations remains necessary.
Conclusions and Prospects Evidence generated in China increasingly connects regional pollution, personal exposure, early biological responses, clinical outcomes, and toxicological mechanisms. However, limitations remain in personal exposure assessment, the comparability of component-specific exposure estimates, the evaluation of multipollutant mixtures, and the translation of toxicological findings into air quality management. Future research should integrate wearable multipollutant monitoring, high-resolution exposure modeling, cohort resources, exposomics, multi-omics, and artificial intelligence. Greater attention should be given to susceptible populations, low-level exposure, indoor-outdoor source interactions, and population-based validation of component-specific toxicity. Health risk assessment and air quality management should incorporate source-specific effects, oxidative potential, and toxicity weighting to support differentiated emission control and maximize population health benefits.
Keywords: fine particulate matter; health effect; personal exposure assessment; population epidemiology; early subclinical injury; cellular and animal toxicology; health risk prevention and control
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