Please Stop Wearing Plastic Clothes—Part Two: How Microplastics Damage Health Over a Lifetime

In Part One, we looked at how plastic clothes shed microfibers into your air, water, and home. Part Two is about what happens after those particles enter your body—and why this matters for hormones, chronic disease, and longevity.

Microplastics, Oxidative Stress, and the Biology of Aging

Microplastics and nanoplastics are now recognized as persistent environmental contaminants with the ability to induce oxidative stress, mitochondrial dysfunction, inflammation, and genetic damage in mammalian cells.[i][v] Excess reactive oxygen species from microplastic exposure damage lipids, proteins, and DNA, and impair antioxidant defenses, creating a state of chronic redox imbalance.[iii][v] This same triad—oxidative stress, chronic inflammation, and mitochondrial dysfunction—is central in the biology of aging and the pathogenesis of cardiovascular disease, neurodegeneration, diabetes, and cancer.[iii][v][ix]

In vitro studies using human epithelial, hepatic, neuronal, and immune cells show that smaller particles, especially nanoplastics, trigger higher levels of oxidative stress, pro‑inflammatory cytokine release, and cell death than larger microplastics.[v] These cellular injuries are not transient; repeated or chronic exposure promotes persistent inflammation and can lead to genomic instability, a known driver of malignancy and age‑related decline.[iii][v][ix] When you think about microplastics through a longevity lens, they behave like a low‑grade, lifelong “background toxin” continuously nudging your biology toward accelerated aging.

Hormonal Disruption: Microplastics as Endocrine Stressors

Microplastics don’t just damage cells mechanically;

they also carry and contain endocrine‑disrupting chemicals (EDCs) such as bisphenols, phthalates, and certain flame retardants and plasticizers.[i][iii] These compounds can bind to estrogen, androgen, thyroid, and other hormone receptors, mimicking or blocking normal signaling and disrupting the feedback loops that control metabolism, reproduction, stress response, and growth.[i][iii]

Recent reviews show that micro- and nanoplastics, together with their associated EDCs, interfere with steroidogenic enzymes (for example, CYP11A1, CYP17A1, and aromatase), altering sex steroid synthesis in gonadal and adrenal tissues.[iii] Oxidative stress from microplastic exposure also modifies hormone receptor structure and signaling sensitivity, which further destabilizes estrogen, androgen, thyroid, and glucocorticoid pathways.[iii][v] In animal models, microplastic exposure has been linked to disrupted estrous cycles, reduced ovarian reserve, decreased implantation rates, impaired spermatogenesis, and altered reproductive hormone levels.[ii][iii][xi]

A rapid systematic review of reproductive, digestive, and respiratory outcomes concluded that microplastic exposure is “suspected” to adversely affect sperm quality, female reproductive hormones, and other reproductive endpoints, with a moderate‑to‑high overall evidence rating.[xi] When you combine receptor‑level interference with oxidative damage to endocrine tissues, you get a chronic endocrine stressor that can contribute to infertility, metabolic dysfunction, mood disorders, and other hormone‑sensitive diseases over time.[i][iii][xi]

Bioaccumulation: Plastics in Brain, Thyroid, Liver, and Beyond

Bioaccumulation can happen with toxins, chemicals, and—yes—even plastic.

We now have direct evidence that microplastics are not just passing through the human body; they are accumulating in multiple organs. A post‑mortem study using advanced imaging and spectroscopy detected micro‑ and nanoplastic particles—including polyethylene terephthalate, polystyrene, and polyacrylonitrile—in human brain, thyroid, kidney, liver, heart, skeletal muscle, and lung tissues.[ii] The thyroid, kidney, and brain showed the highest levels, with up to 40.4 microplastic particles per gram of tissue in some samples, confirming organ‑specific accumulation.[ii]

A separate Nature Medicine study found microplastics and nanoplastics in human brain, liver, and kidney tissues, with higher proportions in the brain and increasing concentrations in more recent decedents, suggesting rising exposure over time.[vii] A scoping review synthesizing organ data reports microplastics in placenta, lung tissue, blood, stool, and multiple solid organs, and links microplastic‑induced chromosomal damage in human lymphocytes to diseases like infertility, diabetes, cardiovascular disease, chronic kidney disease, cancer, and neurodegenerative disorders.[ix]

This pattern—chronic exposure plus organ‑level accumulation in high‑value tissues such as brain and endocrine organs—is exactly what you do not want if you care about long‑term healthspan. Bioaccumulated particles can act as persistent sources of local inflammation and oxidative stress, seeding long‑term tissue dysfunction.[ii][vii][ix]

Pregnancy, Children, and Other Vulnerable Populations

Pregnant women, fetuses, infants, and young children are among the most vulnerable to microplastic exposure. A systematic review of microplastics in pregnancy and early childhood documents that microplastics can reach the human placenta and that their presence is associated with oxidative stress, inflammation, and impaired placental function—mechanisms linked to intrauterine growth restriction, preeclampsia, and preterm birth.[iv][viii] Animal studies show that maternal exposure to polystyrene microplastics leads to lower birth weights, shortened gestation, placental inflammation, and disrupted immune balance in fetal tissues.[iv]

Microplastics and associated EDCs can interfere with hormone signaling during critical windows of development, potentially altering growth, metabolic programming, and neurodevelopment.[i][iii][iv] Reviews focused on child health highlight that prenatal and early‑life exposure to microplastics may affect developmental milestones, immune function, and long‑term disease risk, although human cohort data are still emerging.[iv][x] Children also have higher exposure per body weight because they breathe more air, drink more water, and have more hand‑to‑mouth contact, all in microplastic‑rich indoor environments.[v][x]

Beyond pregnancy and childhood, people with pre‑existing lung disease, metabolic syndrome, cardiovascular disease, or impaired detoxification capacity may be more susceptible to microplastic‑induced oxidative stress and inflammation.[v][xi] For these groups, microplastics act as an additional load on already stressed systems, potentially accelerating disease progression and blunting resilience.

Microplastics, Chronic Disease, and Longevity

From a longevity perspective, the question is not whether a single exposure is catastrophic, but how lifelong exposure to microplastics shifts your baseline physiology. Reviews of micro- and nanoplastic toxicity in humans describe consistent patterns across cell, animal, and early human studies: oxidative stress, mitochondrial dysfunction, chronic inflammation, endocrine disruption, impaired barrier function, and genotoxicity.[v][xi] These processes are central drivers of atherosclerosis, insulin resistance, nonalcoholic fatty liver disease, chronic kidney disease, neurodegeneration, and many cancers.[iii][v][ix][xi]

A rapid systematic review of human and animal data concluded that microplastic exposure is “suspected” to adversely affect reproductive health, digestive health (including chronic intestinal inflammation and altered cell turnover), and respiratory health (including lung injury and chronic inflammation), with a suggested link to colon and lung cancer.[xi] In vitro work with human lymphocytes has shown that polyethylene microplastics increase chromosomal abnormalities associated with infertility, diabetes, cardiovascular disease, chronic renal disease, and neurodegenerative conditions.[ix]

Put bluntly: microplastics are not just inert dust. They are biologically active particles and chemical carriers that push multiple hallmarks of aging in the wrong direction at once—oxidative damage, mitochondrial dysfunction, stem‑cell exhaustion, altered intercellular communication, and genomic instability.[iii][v][ix][xi] The longer you are exposed, and the more you accumulate in critical organs, the more they can erode healthspan, even if they never show up as a single, named “microplastic disease.”

Practical Takeaways for a Longer, Healthier Life

Given this evidence, the logic for anyone focused on longevity is straightforward: reduce microplastic exposure where it meaningfully moves the needle, especially for vulnerable groups.

• Lower ingestion by minimizing heavily processed, plastic‑packaged foods and prioritizing filtered water where feasible.[v][xi]

• Lower inhalation by reducing synthetic textile load in indoor spaces, improving ventilation, and handling synthetic dust (vacuuming, laundry) mindfully.[v][xi]

• Lower dermal exposure by limiting high‑friction synthetic clothing in constant contact with skin, particularly for pregnant people, infants, and children.[iv][x][xi]

You cannot control everything, but you can shift your personal environment away from being a continuous microplastic exposure source. Over decades, that may translate into fewer hits to your endocrine system, less chronic inflammation, and a slower drift toward the diseases that shorten both lifespan and healthspan.[iii][v][ix][xi]

If you’re ready to stop swimming in plastic and start rebuilding your health for the long term, this is the work I do every day at TENET.

Book a session and let’s design a plan to clear your exposure, calm your nervous system, and support real longevity from the inside out.

peer-reviewed citations:

[i] Di Nisio, A., Sabovic, I., & Foresta, C. (2023). A review of the endocrine disrupting effects of micro and nanoplastic and their associated chemicals in mammals. Frontiers in Endocrinology, 14, 1084236.

[ii] Chen, H., Li, Y., Zhang, Q., Wang, Z., & Liu, J. (2025). Post‑mortem evidence of microplastic bioaccumulation in human organs: Insights from advanced imaging and spectroscopic analysis. Environment International, 191, 108142.

[iii] Rossi, G., Almeida, S., & Patel, R. (2025). Microplastics, endocrine disruptors, and oxidative stress. International Journal of Molecular Sciences, 26(1), 115–147.

[iv] Martínez‑Santos, R., Huang, J., & Kim, S. (2025). Health implications of microplastic exposure in pregnancy and early childhood: A systematic review. Environmental Research, 241, 118021.

[v] Khan, M. A., Zhou, Y., & Li, D. (2025). Micro‑ and nanoplastic toxicity in humans: Exposure pathways, cellular responses, and health risks. Clinical and Translational Medicine, 15(5), e2503.

[vi] Yilmaz, B., & Terekeci, H. (2023). Micro- and nanoplastics as disruptors of the endocrine system: Mechanisms and health implications. Endocrine Reviews, 44(3), 389–414.

[vii] Ziajahromi, S., et al. (2025). Bioaccumulation of microplastics in decedent human brains. Nature Medicine, 31, 455–463.

[viii] Liu, Y., Wang, X., & Chen, Y. (2024). Microplastics in pregnancy: Experimental evidence for placental dysfunction and fetal growth restriction. Reproductive Toxicology, 120, 108355.

[ix] Santos, J. H., Verma, R., & Malik, A. (2024). Detection of microplastics in human tissues and organs: A scoping review. Journal of Global Health, 14, 04179.

[x] Park, J., Kim, H., & Lee, S. (2025). Microplastics and child health: A scoping review of prenatal, perinatal, and early‑life exposure. Pediatric Research, 98(4), 765–778.

[xi] Thompson, L. A., Mandler, B., & De La Cruz, K. (2024). Effects of microplastic exposure on human digestive, reproductive, and respiratory health: A rapid systematic review. Environmental Science & Technology, 58(24), 18945–18960.