Microplastics and Fertility: What the Research Says in 2026

Concerns about microplastics and reproductive health have grown sharply in recent years, driven by a series of widely covered studies and increased public awareness through documentary coverage. The question many people are now asking — particularly those trying to conceive or planning a family — is straightforward: can the plastic particles found throughout the human body actually affect fertility?

The evidence is still developing, but what has been published in peer-reviewed journals is worth understanding carefully. This article summarises the current state of research on microplastics and reproductive health, covers both male and female fertility, explains the mechanisms through which harm may occur, and provides practical steps for reducing exposure.

The Study That Made Headlines: Microplastics in Human Testes

In 2024, a study led by researchers at the University of New Mexico, published in Toxicological Sciences, reported finding microplastics in every human testicular tissue sample tested. The study examined 23 human testes and 47 dog testes, finding microplastics in all of them.

Key findings from the study:

• The average concentration of microplastics in human testicular tissue was approximately 330 micrograms per gram of tissue — nearly three times the concentration found in dog testes
• Polyethylene (PE) was the most prevalent polymer type detected, followed by PVC and other common plastics
• The study found a statistically significant negative association between certain types of microplastic contamination and sperm count in dogs, though the human sample size was too small to draw definitive conclusions about human fertility impacts
• All human samples came from men aged 16 and over at autopsy, indicating that microplastic accumulation in reproductive tissue is widespread

This study received extensive media coverage and was a catalyst for broader public concern. A subsequent commentary in Current Urology called the findings “a call to action for urological research,” noting that microplastics crossing the blood-testis barrier raises significant questions about long-term reproductive consequences.

Male Fertility: What the Research Shows

The Yan et al. study was not the first to connect microplastics with male reproductive concerns. A broader body of research has been building over several years.

Sperm Count and Quality

A 2021 review published in the International Journal of Environmental Research and Public Health by D’Angelo and Meccariello examined the evidence linking microplastics to male fertility impairment. The review found that:

• Animal studies consistently showed that microplastic exposure reduced sperm count, motility (movement), and morphology (shape)
• The effects were dose-dependent — higher microplastic exposure correlated with more pronounced impacts on sperm parameters
• Microplastics appeared to cause oxidative stress in testicular tissue, damaging sperm DNA and reducing the viability of sperm cells

Microplastics in Semen

A 2025 clinical study published in International Urology and Nephrology found significantly higher microplastic concentrations in the semen of men with varicocele (a condition associated with reduced fertility) compared to fertile controls. This was among the first studies to directly measure microplastics in human semen and correlate concentrations with a clinical fertility condition.

Declining Sperm Counts

It is worth noting the broader context: global sperm counts have been declining for decades. A large meta-analysis by Levine et al. (2017, updated 2022), published in Human Reproduction Update, found that average sperm counts among Western men declined by approximately 50% between 1973 and 2018. The causes of this decline are likely multifactorial, and microplastic exposure is one of several environmental factors under investigation alongside pesticides, air pollution, and lifestyle changes.

Female Fertility: What the Research Shows

Research on microplastics and female fertility is at an earlier stage than for male fertility, but emerging findings are concerning.

Ovarian Function

Animal studies have shown that microplastic exposure can impair ovarian function. Research in mouse models has demonstrated that ingested microplastics can reach ovarian tissue and cause inflammation, reduce the number of viable follicles (the structures that release eggs), and disrupt normal ovarian hormone production.

IVF and Assisted Reproduction

While no large-scale human clinical studies have yet conclusively linked microplastic exposure to IVF outcomes, the biological plausibility is established. The chemicals carried by microplastics — particularly BPA and phthalates — have been independently shown to affect oocyte (egg) quality and embryo development. Several IVF clinics have begun advising patients to reduce plastic exposure as part of preconception care, reflecting a precautionary stance ahead of definitive clinical evidence.

Endocrine Disruption in Women

The endocrine-disrupting potential of plastic chemicals is particularly relevant for female fertility. Oestrogen signalling is central to ovulation, implantation, and early pregnancy. BPA, which is structurally similar to oestradiol (the primary female sex hormone), can bind to oestrogen receptors and interfere with normal hormonal regulation. Phthalates have been associated with disrupted menstrual cycles and reduced anti-Mullerian hormone (AMH) levels — a marker of ovarian reserve.

The Mechanism: How Plastic Chemicals Affect Reproduction

Microplastics themselves are concerning, but much of the reproductive harm may come from the chemical additives that microplastics carry. Understanding this distinction is important.

Endocrine Disruptors

Many plastic additives are classified as endocrine-disrupting chemicals (EDCs). The Endocrine Society has identified plastic-associated chemicals as a significant category of EDCs, capable of interfering with hormones at very low concentrations.

The key chemicals of concern for fertility include:

• Bisphenol A (BPA): Used in polycarbonate plastics and can linings. Mimics oestrogen and has been shown to affect both male and female reproductive function in animal studies. Although BPA has been restricted in baby bottles in the UK since 2011, it remains present in many other food-contact materials.

• Phthalates (DEHP, DBP, BBP): Used as plasticisers to make PVC and other plastics flexible. Found in food packaging, personal care products, and household items. Phthalates have been linked to reduced testosterone, lower sperm quality, and disrupted ovarian function.

• PFAS (per- and polyfluoroalkyl substances): Used in non-stick coatings and food packaging. Some PFAS compounds have been associated with reduced fertility and longer time-to-pregnancy in epidemiological studies.

The “Trojan Horse” Effect

Microplastics can act as carriers for environmental pollutants — absorbing persistent organic pollutants, heavy metals, and other contaminants from the environment and concentrating them on their surface. When ingested, these contaminated microplastic particles can release their chemical payload in the body, delivering concentrated doses of harmful substances directly to tissues including reproductive organs.

This carrier effect means that the reproductive risk from microplastics may be greater than the plastic particles alone would suggest. The combination of the physical presence of microplastics in tissue and the chemical burden they carry creates what some researchers describe as a “double hit” to reproductive health.

What the Research Does NOT Yet Prove

Honest assessment of the evidence requires acknowledging what remains unknown. This matters both for public understanding and for the credibility of the claims being made (a principle known as E-E-A-T in search quality guidelines — but more importantly, a matter of scientific integrity).

No proven direct causation in humans

While the Yan et al. study found microplastics in human testes, and the varicocele study found higher concentrations in subfertile men, these are correlational findings. They show that microplastics are present in reproductive tissue and that their concentration may be associated with reduced fertility markers — but they do not prove that microplastics directly caused the fertility impairment. Other confounding factors (diet, lifestyle, environmental exposures) could contribute.

Animal studies may not translate directly

Much of the strongest evidence comes from animal studies using controlled exposure levels. The doses used in laboratory studies sometimes exceed typical human exposure, meaning the observed effects may not occur at the concentrations humans actually experience.

No established safe threshold

We do not yet know what level of microplastic exposure is “safe” for reproductive health — or whether such a threshold exists. This makes it difficult to quantify individual risk.

Long-term human data is lacking

The field of microplastic health research is less than a decade old. Long-term epidemiological studies — the kind that would definitively answer whether microplastic exposure impairs human fertility at population level — have not yet been completed.

Documentary and media coverage

The surge in public interest around microplastics and fertility has been partly driven by documentary coverage. While this has been valuable for raising awareness, media coverage can sometimes compress nuance. The research is genuinely concerning, but “microplastics found in testicles” (a factual statement) is importantly different from “microplastics are causing an infertility crisis” (an unsupported conclusion at this stage).

For a broader view of microplastics and health beyond reproductive effects, see our article on what the science says about microplastics and human health.

Practical Steps to Reduce Reproductive Exposure

While the research matures, the precautionary principle suggests reducing unnecessary microplastic exposure — particularly for those planning a family. The good news is that the most impactful changes map directly to the exposure pathways identified in the research.

Reduce Ingestion (Food and Drink)

Food contact is a primary exposure route, and the chemicals of greatest concern for fertility (BPA, phthalates) are concentrated in food packaging and containers.

• Switch to glass food storage: Replace plastic food containers with glass alternatives. Pyrex Round Storage Set containers are made from borosilicate glass — chemically inert with zero microplastic or chemical migration risk.
• Never heat food in plastic: Microwaving or heating food in plastic containers dramatically increases microplastic and chemical release. Transfer to glass or ceramic before reheating.
• Use a stainless steel or glass water bottle: Klean Kanteen Classic 800ml eliminates the ongoing microplastic contribution from single-use plastic bottles.
• Choose plastic-free tea: If you drink multiple cups daily, switching to loose leaf tea or brands with certified plastic-free bags removes a significant exposure source.

Reduce Dermal Absorption (Personal Care)

Personal care products are applied directly to skin, and many contain synthetic polymers and EDCs including phthalates (often listed as “fragrance” on ingredient labels).

• Choose natural-ingredient products: Weleda Skin Food uses plant-based ingredients with no synthetic polymers. Faith in Nature Shampoo is free from phthalates and synthetic fragrances.
• Check ingredient lists: Look for and avoid polyethylene, polypropylene, nylon, and ingredients listed as PEG compounds. Products listing “parfum” or “fragrance” without further specification may contain phthalates.
• Be especially cautious with products used on intimate areas where absorption rates are higher and proximity to reproductive organs is greatest.

Reduce Inhalation

Airborne microplastic fibres — primarily from synthetic textiles and household dust — are another exposure route.

• Ventilate your home regularly to reduce indoor microplastic fibre concentrations
• Choose natural-fibre clothing and bedding where practical (cotton, linen, wool)
• Vacuum regularly with a HEPA filter to remove settled microplastic-containing dust

For Those Actively Trying to Conceive

If you are currently trying to conceive or about to start IVF treatment, the precautionary case for reducing microplastic exposure is at its strongest. The changes listed above are most impactful in the 3-6 months before conception, as this is the period during which sperm develop (spermatogenesis takes approximately 74 days) and egg maturation occurs.

Some fertility clinics now include plastic exposure reduction as part of their preconception lifestyle advice, alongside more established recommendations around diet, alcohol, and folic acid supplementation.

For parents already concerned about children’s exposure, our guide on microplastics and children covers age-specific risks and practical steps for families.

Sources

1. Microplastic presence in dog and human testis and its potential association with sperm count and weights of testis and epididymis — Toxicological Sciences, 2024
2. Microplastics crossing the blood-testis barrier: A call to action for urological research — Current Urology, 2025
3. Microplastics: A Threat for Male Fertility — International Journal of Environmental Research and Public Health, 2021
4. Increased seminal microplastic burden in men with varicocele — International Urology and Nephrology, 2025
5. Temporal trends in sperm count: a systematic review and meta-regression analysis of samples collected globally in the 20th and 21st centuries — Human Reproduction Update, 2022
6. Plasticenta: First evidence of microplastics in human placenta — Environment International, 2021
7. Endocrine-Disrupting Chemicals — The Endocrine Society

Information in this article is based on published peer-reviewed research and does not constitute medical advice. If you have concerns about fertility, consult a healthcare professional. Research in this field is progressing rapidly — findings described here reflect the state of evidence as of early 2026.