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1.贵州医科大学公共卫生与健康学院,环境污染与疾病监控教育部重点实验室,贵州贵阳
2.陆军军医大学(第三军医大学)军事预防医学系毒理学教研室,重庆
3.重庆医科大学附属妇女儿童医院(重庆市妇幼保健院)妇女保健科,重庆
王童,E-mail: wangtong@tmmu.edu.cn
曹佳,E-mail: caojia@tmmu.edu.cn
收稿:2025-12-13,
修回:2026-03-21,
录用:2026-03-29,
纸质出版:2026-05-30
移动端阅览
吴冬艳,张海燕,银晨然,等.PM2.5暴露导致精子总数与浓度下降:基于队列研究与TRAEC策略系统评估的双重证据[J].陆军军医大学学报,2026,48(10):1433-1443.DOI:10.16016/j.2097-0927.202512067.
WU D Y,ZHANG H Y,YIN C R,et al.PM2.5 exposure causes decreases in total sperm count and concentration: dual evidence from a cohort study and systematic evaluation with TRAEC strategy[J].J Army Med Univ,2026,48(10):1433-1443.DOI:10.16016/j.2097-0927.202512067.
吴冬艳,张海燕,银晨然,等.PM2.5暴露导致精子总数与浓度下降:基于队列研究与TRAEC策略系统评估的双重证据[J].陆军军医大学学报,2026,48(10):1433-1443.DOI:10.16016/j.2097-0927.202512067. DOI:
WU D Y,ZHANG H Y,YIN C R,et al.PM2.5 exposure causes decreases in total sperm count and concentration: dual evidence from a cohort study and systematic evaluation with TRAEC strategy[J].J Army Med Univ,2026,48(10):1433-1443.DOI:10.16016/j.2097-0927.202512067. DOI:
目的
2
当前关于细颗粒物(fine particulate matter, PM
2.5
)暴露是否影响男性精液质量的研究存在较大的异质性,且缺乏对PM
2.5
精液毒性的系统评估。本研究基于代表性育龄人群为生精周期PM
2.5
暴露与精液参数的关联提供新的证据,并在此基础上对现有的人群、动物和细胞实验研究证据开展系统评估。
方法
2
基于重庆市孕前生殖健康与出生结局队列,对重庆市妇幼保健院2018年11月到2023年9月招募的有备孕计划的男性志愿者进行问卷调查,同时采集1次精液样本,并按照标准化流程完成精液参数分析,包括精液量、精子总数、精子浓度、精子前向运动、精子总运动和精子正常形态。通过中国大气成分近实时追踪数据集获取PM
2.5
暴露数据,根据问卷地址信息匹配生精周期不同阶段的个体暴露,采用多重线性回归评估PM
2.5
暴露与精液参数的剂量-反应关系。采用环境化学物目标风险评估(Targeted Risk Assessment of Environmental Chemicals, TRAEC)策略进行系统评估,通过Pubmed、Web of Science和ScienceDirect 3个数据库检索符合标准的研究论文,同时纳入前述队列分析结果,共同评估PM
2.5
暴露的生殖毒性,得出综合定量得分,并按照标准判定风险等级。
结果
2
队列研究结果显示,纳入2018年1月至2023年9月期间入组男性志愿者5 735名,平均年龄为(31.42±4.58)岁,生精周期PM
2.5
暴露每升高四分位间距浓度,精子总数和精子浓度分别下降12.30% (95%
CI
:-16.21~-8.22,
P
<
0.000 1)和10.25% (95%
CI
:-13.64~-6.72,
P
<
0.000 1)。基于TRAEC策略共纳入41项研究证据,结果显示,生精周期PM
2.5
暴露对精子总数和精子总运动的影响风险处于中等风险水平,精子浓度、精子前向运动、精液量和精子正常形态处于低等风险水平。
结论
2
队列研究和TRAEC评估结果一致显示,PM
2.5
暴露主要引起精子总数与精子浓度下降,提示PM
2.5
具有潜在生精毒性。对策 建议卫生行政部门依托现有妇幼保健网络和孕前检查体系,在空气质量预警期间同步发布生殖健康防护提示,对备孕男性开展针对性的健康宣教和风险告知。
Objective
2
Current evidence on whether exposure to fine particulate matter (PM
2.5
) affects male semen quality exhibits considerable heterogeneity
and a systematic evaluation of PM
2.5
spermatotoxicity is lacking. This study aims to provide new evidence on the association between PM
2.5
exposure during the spermatogenic cycle and semen parameters in a representative population of reproductive age men
and to conduct a systematic evaluation integrating existing evidence from population
animal
and cellular studies.
Methods
2
Based on the Chongqing Preconception Reproductive Health and Birth Outcome Cohort
a questionnaire survey was conducted on male volunteers with pregnancy plans recruited in Chongqing Maternal and Child Health Hospital from November 2018 to September 2023. Their semen samples were collected and analyzed following st
andardized procedures
including semen volume
total sperm count
sperm concentration
progressive motility
total motility
and normal sperm morphology. PM
2.5
exposure data were obtained from the Tracking Air Pollution in China (TAP) dataset. Individual-level exposure during different stages of the spermatogenic cycle was estimated based on the residential addresses from the recovered questionnaires. Multiple linear regression analysis was employed to estimate the dose-response relationships between PM
2.5
exposure and semen parameters. Targeted Risk Assessment of Environmental Chemicals (TRAEC) strategy was adopted for systematic evaluation. Eligible studies were retrieved from PubMed
Web of Science
and ScienceDirect databases. The findings from the cohort analysis were also incorporated to jointly assess the reproductive toxicity of PM
2.5
exposure
yielding a comprehensive quantitative score
and determine the risk level according to predefined criteria.
Results
2
The cohort study enrolled 5 735 male volunteers subjected from January 2018 to September 2023
with a mean age of 31.42±4.58 years. Each interquartile range increase in PM
2.5
exposure during the spermatogenic cycle was associated with a 12.30% (95%
CI
: -16.21 to -8.22
P
<
0.000 1) decrease in total sperm count and a 10.25% (95%
CI
: -13.64 to -6.72
P
<
0.000 1) decrease in sperm concentration. The TRAEC-based evaluation incorporated 41 studies
revealing that PM
2.5
exposure during the spermatogenic cycle posed a moderate risk for total sperm count and total motility
and a low risk for sperm concentration
progressive motility
semen volume
and normal sperm morphology.
Conclusion
2
Both the cohort study and the TRAEC-based systematic evaluation consistently demonstrate that PM
2.5
exposure primarily causes decreases in total sperm count and sperm concentration
suggesting potential spermatogenic toxicity of PM
2.5
exposure. Countermeasures It is recommended that health authorities should leverage the existing maternal and child healthcare networks and preconception screening systems to simultaneously issue reproductive health protection alerts during air pollution episodes
and to provide targeted health education and risk communication for men planning pregnancy.
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