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This review introduces a potential unifying concept involving the risk of chronic diseases in which early-life exposure to endocrine-disrupting chemicals (EDCs) can program host responses for misregulated inflammation. Inflammation is a part of host defense against pathogenic challenges and one of the processes necessary for normal tissue homeoregulation and for reproduction (e.g., implantation, labor). Deviations from tightly regulated inflammation present a significant health risk because unresolved inflammation can compromise tissue function and increase the risk for later-life cancer in the affected target tissue. The critical windows of innate immune vulnerability during prenatal and neonatal maturation are when developmental programming and the trajectory for childhood and adult inflammatory responses are largely established. Misregulated inflammation is a common thread that links most significant chronic diseases and conditions across all physiologic systems as well as the associated comorbid conditions. As a result, chronic diseases exist both as a myriad of conditions and as an integrated, dysfunctionally connected unit. Because the hormone microenvironment exerts a significant effect on resident innate immune cell function, endocrine disruption is likely to produce misregulated inflammation in tissues. Among the factors determining specific health risks and disease outcomes across a lifetime are the age of exposure, sex, genetic background, and transgenerational epigenetic experiences. Additional research into early-life EDC exposure and misregulation of inflammation appears to be a useful avenue for reducing environmental health risks.

Misregulated inflammation as an outcome of early-life exposure to endocrine-disrupting chemicals