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Purpose <p>Fine particulate matter (PM<sub>2.5</sub>) negatively impacts the reproductive system. Yet, the impact of water-insoluble PM<sub>2.5</sub> (WI-PM<sub>2.5</sub>) particles and water-soluble PM<sub>2.5</sub> (WS-PM<sub>2.5</sub>) extracts on male fertility is not fully elucidated. The current research is aimed to identify and analyze individual toxic effect patterns of WI-PM<sub>2.5</sub> and WS-PM<sub>2.5</sub> exposures.</p> Methods <p>This investigation involved the intratracheal instillation of both low (20&#xa0;μg) and high (200&#xa0;μg) doses of WS-PM<sub>2.5</sub> and WI-PM<sub>2.5</sub> in male C57BL/6 mice (n = 6 in each group). PM<sub>2.5</sub> samples were collected adjacent to polluted industrial complex in southern Taiwan in 2020–21. To elucidate the influence of PM<sub>2.5</sub> composition on reproductive toxicity, a comprehensive range of health measures was analyzed (body and gonadal organ weights, sperm count, motility, morphology, mitochondrial membrane potential [MMP], reactive oxygen species generation, sperm chromatin DNA fragmentation index [DFI], testicular DNA content during spermatogenesis, and testicular histopathology).</p> Results <p>Exposure to WS-PM<sub>2.5</sub> and WI-PM<sub>2.5</sub> reduced rates of normal sperm morphology, with each also presenting unique toxic effects. WI-PM<sub>2.5</sub> exposure can cause reduction in the cauda epididymis weight, while raising the percentage of abnormal sperm heads, MMP, and DFI in both low- and high-dose groups. Also, it increased the rate of tetraploid cells in the low-dose group. Conversely, exposure to WS-PM<sub>2.5</sub> resulted in a decline in the weight of the cauda epididymis, coupled with elevated levels of elongating spermatids, round spermatids, and diploid cells at both doses. The testicular histopathological alterations were observed in both dose groups.</p> Conclusions <p>Our study unequivocally demonstrated that being exposed to PM<sub>2.5</sub>, even at modest levels of air contaminants, can negatively impact the male reproductive system through causing biological impairments and cellular dysfunctions, including disturbances in sperm MMP, among other testicular effects. With separate hazard profiles associated with WI-PM<sub>2.5</sub> and WP-PM<sub>2.5</sub> exposures, it is imperative to consider the distinct features of PM<sub>2.5</sub> when examining its toxic hazards.</p> Graphical Abstract <p></p>

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Impact of PM2.5 Exposure on Reproductive Health and Sperm Functions in Mice from a High-Pollution Industrial Environment

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月19日

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  • Fu-Jen Cheng,
  • Chung-Shin Yuan,
  • Xin Chen,
  • Yu-Sheng Lin,
  • Ping-Hsun Wu,
  • Ping-Chi Hsu

摘要

Purpose

Fine particulate matter (PM2.5) negatively impacts the reproductive system. Yet, the impact of water-insoluble PM2.5 (WI-PM2.5) particles and water-soluble PM2.5 (WS-PM2.5) extracts on male fertility is not fully elucidated. The current research is aimed to identify and analyze individual toxic effect patterns of WI-PM2.5 and WS-PM2.5 exposures.

Methods

This investigation involved the intratracheal instillation of both low (20 μg) and high (200 μg) doses of WS-PM2.5 and WI-PM2.5 in male C57BL/6 mice (n = 6 in each group). PM2.5 samples were collected adjacent to polluted industrial complex in southern Taiwan in 2020–21. To elucidate the influence of PM2.5 composition on reproductive toxicity, a comprehensive range of health measures was analyzed (body and gonadal organ weights, sperm count, motility, morphology, mitochondrial membrane potential [MMP], reactive oxygen species generation, sperm chromatin DNA fragmentation index [DFI], testicular DNA content during spermatogenesis, and testicular histopathology).

Results

Exposure to WS-PM2.5 and WI-PM2.5 reduced rates of normal sperm morphology, with each also presenting unique toxic effects. WI-PM2.5 exposure can cause reduction in the cauda epididymis weight, while raising the percentage of abnormal sperm heads, MMP, and DFI in both low- and high-dose groups. Also, it increased the rate of tetraploid cells in the low-dose group. Conversely, exposure to WS-PM2.5 resulted in a decline in the weight of the cauda epididymis, coupled with elevated levels of elongating spermatids, round spermatids, and diploid cells at both doses. The testicular histopathological alterations were observed in both dose groups.

Conclusions

Our study unequivocally demonstrated that being exposed to PM2.5, even at modest levels of air contaminants, can negatively impact the male reproductive system through causing biological impairments and cellular dysfunctions, including disturbances in sperm MMP, among other testicular effects. With separate hazard profiles associated with WI-PM2.5 and WP-PM2.5 exposures, it is imperative to consider the distinct features of PM2.5 when examining its toxic hazards.

Graphical Abstract