The systematic review examined peer-reviewed research published in English through December 2025. Its search covered PubMed, the Web of Science Core Collection and Scopus, with two reviewers independently screening titles and abstracts. Eligible work addressed environmental exposure, human biomonitoring, mammalian toxicopathology, cellular and molecular mechanisms, intergenerational effects, and possible preventive or therapeutic strategies. Preprints, conference abstracts, editorials, case reports, non-English publications, duplicate datasets and studies without essential particle characterization were excluded.

Human exposure occurs mainly through gastrointestinal ingestion, respiratory inhalation and dermal contact. The review reports that adults may ingest an estimated 0.1–5 g of microplastics per week, although laboratory exposure doses and particle characteristics do not necessarily correspond to real-world exposure. Bottled water has contained an average of 325 particles per liter in the cited research, with a maximum of 10,000 particles per liter, while up to 94% of commercial salt products contained detectable microplastics. Dermal exposure occurs through products such as cosmetics and textiles, but the review notes a lack of direct evidence that dermal exposure causes human tissue damage.

Human monitoring has detected micro- and nanoplastics in blood, semen, testicular tissue, penile tissue and other sites. One study cited by the review reported a mean testicular concentration of 329.44 μg/g, with polyethylene the most prevalent polymer. A canine-and-human study found higher testicular concentrations than measurements from organs such as the liver and lungs under its tested conditions, suggesting possible tissue-specific accumulation rather than proving a reproductive effect. In human semen, reported concentrations reached 15.34 μg/mL, and particles have included fibers, fragments and films.

The strongest mechanistic evidence comes from animal and cell experiments. In mice and rats, exposure to polystyrene micro- or nanoplastics produced testicular histological changes, seminiferous-tubule damage, apoptosis, reduced sperm counts and motility, increased sperm abnormalities and lower testosterone. Co-exposure with cadmium, sodium fluoride or microcystin-LR produced more severe reproductive injury in the reported models than microplastic exposure alone. These findings demonstrate toxicity under the specified laboratory conditions; they do not establish equivalent effects from typical human exposure.

Oxidative stress occupies the center of the proposed mechanism. Exposure can increase reactive oxygen species and lipid peroxidation while reducing antioxidant enzymes and glutathione. Reactive oxygen species activate MAPK and NF-κB signaling, damage mitochondria, impair energy production and contribute to inflammation, ferroptosis and apoptosis. Experimental studies also associate microplastic exposure with disruption of the blood-testis barrier, impaired hypothalamic-pituitary-testicular signaling, disturbed steroidogenesis, altered glucose and lipid metabolism, and changes in intestinal microbial communities that can intensify inflammatory pathways.

Animal findings extend beyond the testes. In a mouse experiment, daily oral administration of 200 nm polystyrene nanoplastics at 2 mg/L for 35 days was followed by lower body weight, testicular weight and body length in first-generation offspring, as well as testicular histological damage and reduced sperm count and motility. The experiment did not establish that heritable sperm DNA damage or a particular epigenetic process caused those outcomes. Human placental microplastics and altered embryonic-cell metabolism have also been reported, but these observations do not by themselves demonstrate developmental harm in exposed pregnancies.

Human findings remain mainly observational and correlational. A meta-analysis summarized in the review reported that micro- or nanoplastic exposure was associated with a 5.99 million/mL reduction in sperm concentration, a 10.65% increase in sperm abnormality rate and a 14.62% decrease in motility, although the supplied review does not identify the included populations clearly enough to label it exclusively as a human analysis. Polytetrafluoroethylene detection in semen has also been associated with lower total sperm count, concentration and progressive motility. Small samples, limited population coverage, crude exposure assessment and unresolved confounding prevent causal conclusions.

The review identifies no clinically validated treatment for micro- or nanoplastic-induced male infertility. Environmental measures, reduced use of plastic packaging and utensils, boiled or filtered water, natural-fiber products, cleaning, occupational protection, chitosan, antioxidants and anti-inflammatory agents have been investigated at environmental, behavioral or preclinical levels, with no established human reproductive benefit. It calls for standardized dose and particle-characterization methods, experiments using environmentally relevant mixtures, and prospective cohorts with robust exposure assessment before the animal and human evidence can be used to estimate reproductive risk or guide clinical prevention.

Subject of Research: Experimental and human evidence on micro- and nanoplastic exposure and male reproductive toxicity

Article Title: Micro- and nanoplastic exposure: male reproductive toxicity, underlying mechanisms, and research prospects

Article References: Wang, M., Zheng, J., Shen, C., Liu, C., Ma, S., Wang, Y., Fan, M., & Sheng, M. (2026). Micro- and nanoplastic exposure: male reproductive toxicity, underlying mechanisms, and research prospects. Frontiers in Endocrinology, 17, Article 1940055. https://doi.org/10.3389/fendo.2026.1940055

Image Credits: AI Generated

DOI: 10.3389/fendo.2026.1940055

Keywords: microplastics, nanoplastics, male infertility, reproductive toxicity, sperm quality, testicular damage, oxidative stress, endocrine disruption, human biomonitoring, systematic review, Micro-, nanoplastic