The associations between endocrine disrupting chemicals and markers of inflammation and immune responses: A systematic review and meta-analysis.

Exposure to endocrine disrupting chemicals (EDCs) may lead to dysregulated inflammatory responses, however, the detailed relationship between different EDCs and inflammation remains unclear. A systematic review and meta-analysis was conducted to evaluate the associations between four types of EDCs (bisphenol A (BPA), phthalates (PAEs), organochlorine pesticides (OCPs), and polychlorinated biphenyls (PCBs)) and markers of inflammation and immune responses in humans. Three databases were searched, and 36 studies with a total of 22055 participants were included. The associations between EDCs and 26 inflammation-related acute phase proteins and cytokines were analyzed. The results demonstrated that exposure to BPA was positively associated with circulating levels of C-reactive protein (CRP) and interleukin (IL)-6. Exposure to PAEs was associated with elevated levels of CRP, IL-6 and IL-10. Subgroup analysis found that three PAE metabolites mono-benzyl phthalate (MBzP), mono-isobutyl phthalate (MiBP), and mono-n-butyl phthalate (MnBP) were directly associated with a higher level of CRP, and two other PAE metabolites mono-carboxyisononyl phthalate (MCNP) and mono-3-carboxypropyl phthalate (MCPP) were positively associated with IL-6. The positive associations between PAEs and CRP, IL-6 and IL-10 were significant in the high-molecular-weight phthalate (HMWP) exposure group, not the low-molecular-weight phthalate (LMWP) exposure group. Exposure to OCPs was positively associated with CRP, IL-1β, IL-2, and IL-10. No significant association was found between PCBs and inflammatory markers. These findings demonstrate that exposure to EDCs is closely linked to dysregulated inflammatory responses. More studies should be conducted in the future to get a comprehensive view of the associations between different EDCs and inflammation, and investigations on the underlying mechanisms are needed.