| Abstract [eng] |
Aim: To critically evaluate and systematically synthesise the available research evidence on the effects of microplastics on male reproductive health. Objectives: To characterise microplastic exposure routes and toxicokinetics; to describe their detection in the male reproductive system; to elucidate the dominant molecular toxicity mechanisms; to evaluate effects on semen parameters including sperm deoxyribonucleic acid integrity; and to critically assess the quality of human evidence while identifying existing knowledge gaps. Methods: A literature search was conducted across four electronic databases — PubMed/MEDLINE, Web of Science, Scopus and ScienceDirect — covering January 2018 to March 2025. The following search string was applied: ("microplastic*" OR "nanoplastic*") AND ("male fertility" OR "sperm" OR "spermatogenesis" OR "testis" OR "testosterone" OR "semen quality"). Only full-text articles written in English were eligible for inclusion. The final synthesis drew on more than 57 peer-reviewed publications, spanning systematic reviews, meta-analyses, in vivo animal studies and human observational studies. Results: The literature makes one thing fairly clear: microplastics are now essentially everywhere: in the environment and, increasingly, in the human body. Most relevant here is that since 2023, six independent research groups have confirmed microplastic presence in testicular tissue and semen, in some cases across every sample tested. Their effects on semen quality appear to be statistically significant and multidirectional: sperm concentration, motility and viability all tend to decline, while the rate of morphological abnormalities rises. The dominant toxicity mechanism seems to be reactive oxygen species generation as the molecular initiating event, triggering a downstream cascade of oxidative stress, inflammation, blood-testis barrier disruption and impaired steroidogenesis. Polymer type also appears to matter: Polytetrafluoroethylene and polyethylene show the strongest associations with semen quality impairment in human studies, though precisely why different polymers behave differently remains incompletely understood. One of the more striking recent findings is that sperm deoxyribonucleic acid fragmentation indices can increase up to fivefold in animal models following microplastic exposure, with six distinct molecular pathways identified at the cellular level linking oxidative stress to deoxyribonucleic acid damage. There is also some evidence that these changes are at least partially reversible after exposure ends but morphological defects do not appear to fully normalise. In short, microplastics seem to act on the male reproductive system through a reasonably well-characterised biological cascade, yet direct epidemiological evidence linking the human microplastic body burden to clinically confirmed infertility is still lacking. Conclusions: Microplastics accumulate in the male reproductive system and likely impair spermatogenesis through an oxidative stress cascade, this is currently the most biologically plausible hypothesis. Direct causality in humans remains unestablished, as all existing human studies are cross-sectional and methodologically limited. Sperm deoxyribonucleic acid fragmentation testing should be considered as an additional clinical biomarker in men from high-pollution environments, and future research needs to integrate simultaneous measurement of microplastic burden and DNA fragmentation indices within the same samples that gap is arguably the most important one the field currently faces. |
