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The Reproductive Toxicity of Microplastics: From Environmental Contamination to Organ Distribution and Reproductive Hazards.

Environmental toxicology 2026
Shubhradeep Chakraborty, Abhratanu Ganguly, Satadal Adhikary, Suchandra Bhattacharya, Prem Rajak

Summary

This review pulls together existing research showing that tiny plastic particles from our environment—found in water, food, and air—are turning up in reproductive organs like ovaries, testicles, and semen. Scientists believe these particles may disrupt hormone signaling, trigger inflammation, and even damage reproductive cells, potentially affecting fertility in both men and women. While the science is still developing and more long-term studies are needed, this is an early warning sign that everyday plastic exposure could have hidden costs for reproductive health.

Models
Study Type Environmental

Microplastics (MPs) are ubiquitous in nature, contaminating various environmental media such as soil, air, and water. Moreover, they can be found in drinking water and foods, increasing the risks of human exposure. Studies have reported that MPs can be detected in various human organs, including the reproductive ones. Ovarian follicular fluids and uterine tube tissue have been documented to contain up to 7181 particles/mL and 1.40 particles/g, respectively. Similarly, samples associated with the male reproductive system are also reported with MPs. Specifically, semen and testicular tissue samples contain up to 17 and 11.60 particles/g of MPs, respectively. Growing evidence suggests that MPs can potentially harm the reproductive system by adversely affecting the development and maturation of gametes. They can modulate the cAMP/PKA/StAR pathway to affect FSH and LH. MP-induced ROS production alters the Akt/ESR1/NRF pathway to upregulate IL-1β, IL-6, and TNF-α proinflammatory cytokines. MP-mediated NLRP-3 activation promotes pyroptosis of gonadal germ cells. Therefore, in this comprehensive literature review, the latest data on the environmental distribution of MPs, their entry into the human body, and their accumulation in reproductive tissues are critically examined. The roles of oxidative stress, endocrine disruption, inflammation, and cellular apoptosis in MP-induced reproductive toxicity are also discussed. This review emphasizes the need for further toxicological evaluations and long-term epidemiological studies to fully understand the range of associated risks and highlights knowledge gaps regarding the mechanistic pathways by which MPs trigger reproductive toxicity.

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