Influence of persistent organic pollutants on the complement system in a population-based human sample

• TEQ value is positively associated with levels of C3a and C3a/C3 ratio.
• Association between TEQ and C3a/C3 ratio indicates rising C3a production from C3.
• The associations observed point toward activation of innate immune system.

BackgroundPersistent organic pollutants (POPs) are toxic compounds generated through various industrial activities and have adverse effects on human health. Studies performed in cell cultures and animals have revealed that POPs can alter immune-system functioning. The complement system is part of innate immune system that helps to clear pathogens from the body. We performed a large-scale population-based study to find out associations between summary measures of different POPs and different complement system markers.MethodsIn this cross-sectional study, 16 polychlorinated biphenyls (PCBs), 3 organochlorine (OC) pesticides, octachloro-p-dibenzodioxin, and 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) were analyzed for their association with levels of protein complement 3 (C3), 3a (C3a), 4 (C4) and C3a/C3 ratio. A total of 992 individuals (all aged 70 years, 50% females) were recruited from the Prospective Investigation of the Vasculature in Uppsala Seniors cohort. Regression analysis adjusting for a variety of confounders was performed to study the associations of different POP exposures (total toxic equivalency value or TEQ and sum of 16 PCBs) with protein complements.ResultsThe TEQ values were found to be positively associated with C3a (β = 0.07, 95% CI = 0.017–0.131, p = 0.01) and C3a/C3 ratio (β = 0.07, 95% CI = 0.015–0.126, p = 0.01) taking possible confounders into account. The association observed was mainly driven by PCB-126.ConclusionIn this study involving 992 elderly individuals from the general population, we showed that POPs, mainly PCB-126, were associated with levels of complement system markers indicating that the association of these toxic compounds with downstream disease could be mediated by activation of immune system.