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Microplastics and the Immune System - A Hidden Driver of Modern Disease
Summary
This preprint hypothesises that accumulation of microplastics in tissues acts as a chronic activator of innate immunity via sustained IL-1β, IL-6, and TNF-α signalling, and proposes that this mechanism may contribute to fibromyalgia, infertility, and dementia. The hypothesis identifies APOE ε4 status as a potential risk modifier and calls for polymer-specific tissue load studies.
Microplastics are now documented in human blood, placenta, testes, and brain. Their persistence, surface chemistry, and ability to cross biological barriers make them plausible chronic activators of innate immunity. This preprint hypothesizes that tissue microplastic burden contributes to fibromyalgia, infertility, and dementia via sustained IL-1, IL-6, and TNF-α signalling, with risk modified by APOE ε4 status. The hypothesis is falsifiable through polymer-specific load quantification, cytokine profiling, and prospective clinical cohorts. A pilot trial framework using curcumin and omega-3 supplementation is outlined to reduce inflammatory tone and test for clinical benefit. The paper calls for coordinated, large-scale studies integrating exposure measurement (ng/mL serum), genetics, and longitudinal outcomes. Whether results are positive or null, they carry immediate implications for clinical practice and environmental policy. Microplastic exposure is presented as a candidate driver of modern inflammatory disease and a potential extinction-scale risk if unaddressed.