Fouks Yuval, Vaughan Denis A, Bortoletto Pietro, Chang Jeffrey Che-Wei, Lantsberg Daniel, Datta Vivekananda X, McSweeney Brian, Schwartz Joel David, Sakkas Denny
Boston IVF-IVIRMA Global Research Alliance, Waltham, MA, USA.
Reproductive Services Unit, The Royal Women's Hospital, Parkville, VIC, Australia.
Hum Reprod. 2025 Sep 2. doi: 10.1093/humrep/deaf173.
Does exposure to fine particulate matter (PM2.5) impact sperm DNA fragmentation?
Higher PM2.5 exposure was associated with increased sperm DNA fragmentation, with greater effects observed in men of lower socioeconomic status (SES).
Environmental air pollutants such as PM2.5 have been linked to adverse reproductive and perinatal outcomes. However, their impact on sperm chromatin integrity remains underexplored, particularly in the context of geographic and sociodemographic modifiers.
STUDY DESIGN, SIZE, DURATION: This was a cross-sectional study including 21 851 semen samples collected between 2005 and 2022 from men undergoing fertility evaluation across multiple US regions.
PARTICIPANTS/MATERIALS, SETTING, METHODS: Semen samples were obtained from men older than 18 years, with testing performed in a single reference laboratory. Exposure to PM2.5 was estimated using validated satellite-derived models and aligned with the 70-80 day spermatogenic window prior to sample collection. Spatial linear mixed-effects models incorporating natural splines and geographic correlation structures were used to assess nonlinear associations between PM2.5 and sperm DNA fragmentation index (DFI), while adjusting for age, SES, population density, and racial composition. Interaction terms were used to evaluate effect modification.
Higher PM2.5 exposure was associated with increased DFI (estimate = 0.45; P = 0.0025), with a clear nonlinear dose-response pattern peaking at ∼11 µg/m³. A significant interaction was observed between PM2.5 and SES (estimate = 0.45; P = 0.0148), indicating that men from lower SES areas experienced stronger pollution-related DNA damage. Age remained a strong independent predictor: men ≥50 years showed markedly elevated DFI (estimate = 14.36; P < 0.0001).
LIMITATIONS, REASONS FOR CAUTION: The sample was derived from men seeking fertility evaluation and may not represent the general population. ZIP-code level SES and exposure proxies may not reflect to the full extent an individual-level exposures, and residual confounding is possible.
These results underscore the reproductive health consequences of environmental air pollution and its intersection with social inequality. PM2.5 exposure may disproportionately affect sperm chromatin quality in disadvantaged populations; this finding supports targeted environmental and reproductive health interventions. Sperm DNA fragmentation may serve as a biomarker of environmental and social stress.
STUDY FUNDING/COMPETING INTEREST(S): This study was internally funded. V.X.D. and B.M. are employees of ReproSource, which provided laboratory testing, and Quest Diagnostics. No other conflicts of interest were reported.
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暴露于细颗粒物（PM2.5）是否会影响精子DNA碎片化？
更高的PM2.5暴露与精子DNA碎片化增加有关，在社会经济地位较低（SES）的男性中观察到的影响更大。
环境空气污染物如PM2.5已与不良生殖和围产期结局相关联。然而，它们对精子染色质完整性的影响仍未得到充分研究，特别是在地理和社会人口统计学修饰因素的背景下。
研究设计、规模、持续时间：这是一项横断面研究，包括2005年至2022年间从美国多个地区接受生育评估的男性中收集的21851份精液样本。
参与者/材料、环境、方法：精液样本取自18岁以上男性，在单一参考实验室进行检测。使用经过验证的卫星衍生模型估算PM2.5暴露，并与样本采集前70 - 80天的生精窗口对齐。采用纳入自然样条和地理相关结构的空间线性混合效应模型来评估PM2.5与精子DNA碎片化指数（DFI）之间的非线性关联，同时调整年龄、SES、人口密度和种族构成。交互项用于评估效应修饰。
更高的PM2.5暴露与DFI增加相关（估计值 = 0.45；P = 0.0025），呈现出明显的非线性剂量反应模式，在约11µg/m³时达到峰值。在PM2.5与SES之间观察到显著的交互作用（估计值 = 0.45；P = 0.0148），表明来自SES较低地区的男性经历了更强的污染相关DNA损伤。年龄仍然是一个强有力的独立预测因素：50岁及以上的男性DFI明显升高（估计值 = 14.36；P < 0.0001）。
局限性、谨慎的原因：样本来自寻求生育评估的男性，可能不代表一般人群。邮政编码层面的SES和暴露代理可能无法充分反映个体层面的暴露情况，可能存在残余混杂因素。
这些结果强调了环境空气污染及其与社会不平等的交叉对生殖健康的影响。PM2.5暴露可能对弱势群体的精子染色质质量产生不成比例的影响；这一发现支持有针对性的环境和生殖健康干预措施。精子DNA碎片化可能作为环境和社会压力的生物标志物。
研究资金/利益冲突：本研究由内部资助。V.X.D.和B.M.是ReproSource的员工，该公司提供实验室检测，以及Quest Diagnostics。未报告其他利益冲突。
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