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Environmental pollutants as emerging risk factors in osteoarthritis: Mechanistic and epidemiological evidence
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This review synthesized mechanistic and epidemiological evidence linking environmental pollutants — including microplastics — to osteoarthritis pathogenesis. The authors found accumulating in vitro, animal, and human data suggesting that chemical exposures accelerate cartilage degradation and joint inflammation through multiple pathways.
Osteoarthritis (OA) is a multifactorial degenerative joint disease with increasing evidence implicating environmental pollutants as underrecognized contributors to its pathogenesis. This review EditedbyDr.CaterinaFaggiostematically synthesizes in vitro, animal, computational, and human epidemiological studies to elucidate the mechanistic and population-level effects of chemical exposures on OA. Airborne pollutants, including PM2.5, PM10, NO2, O3, and trihalomethanes, are associated with increased OA incidence, promoting cartilage degradation through oxidative stress, inflammatory cytokine overproduction, and epigenetic or developmental programming. Heavy metals such as cadmium, lead, arsenic, mercury, and copper induce reactive oxygen species (ROS), chondrocyte apoptosis, extracellular matrix (ECM) breakdown, and systemic inflammation, with both experimental and epidemiological studies demonstrating dose-dependent relationships. Persistent organic pollutants, including polychlorinated biphenyls (PCBs) and per-/polyfluoroalkyl substances (PFAS), disrupt autophagy, endocrine signaling, and cartilage homeostasis, with evidence of bioaccumulation in synovial fluid and modulation of gene expression relevant to bone-cartilage metabolism. Endocrine-disrupting chemicals, including phthalates, brominated flame retardants, and acetyl tributyl citrate, further exacerbate OA susceptibility via MAPK and NF-κB pathway activation, ROS generation, and ECM dysregulation. Epidemiological data consistently demonstrate associations between these exposures and OA prevalence, incidence, and symptom severity, often showing additive or synergistic effects for multiple pollutants. Despite these advances, research is limited by cross-sectional designs, high-dose experimental models, incomplete assessment of pollutant mixtures, and geographic and joint-specific biases. Future studies should prioritize longitudinal cohort designs, repeated biomonitoring, mechanistic exploration of mixture effects, and inclusion of emerging pollutants such as microplastics. Integrating environmental exposure assessment with advanced imaging, omics technologies, and computational modeling will enhance understanding of pollutant-induced OA mechanisms. Collectively, this evidence underscores the need for environmental interventions, public health strategies, and preventive approaches aimed at mitigating pollutant-driven joint degeneration, highlighting environmental exposures as a critical, yet modifiable, determinant of OA risk.
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A translational synthesis of clinical and experimental data examined the role of microplastic exposure in osteoarthritis (OA) development, finding evidence that MPs bioaccumulate in joint tissues and may promote inflammation and oxidative damage that disrupts cartilage homeostasis. The review identified MP exposure as a plausible but underexplored contributor to OA progression.
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