Abstract

Background: Persistent organochlorine pollutants (POPs) include several groups of synthetic compounds with high lipophilic and bioaccumulative potential that accumulate in the food chain. Despite their long-term ban, they are still of concern and the general population is constantly exposed to these pollutants at low doses through diet. POPs are proposed to be involved in the atherosclerotic process and to cause endothelial cell dysfunction. We assess longitudinally whether plasma concentrations of different POPs were associated with blood pressure (BP) and risk of hypertension in middle-aged women and men. Methods: Study subjects were 850 participants in the Västerbotten Intervention Programme with two blood samples and BP measurements, 10 years apart, during 1990 to 2003 (baseline) and during 2001 to 2013 (follow-up). The POP measured were the fungicide hexachlorobenzene (HCB), the insecticide dichlorodiphenyl-trichloroethane (DDT) –and its persistent metabolite p,p′-dichlorodiphenyl-dichloroethylene (DDE)– and the dioxin-like and non-dioxin-like polychlorinated biphenyls (DL-PCBs, NDL-PCBs). We used generalized estimated equations to assess the associations. Results: At both sampling occasions, about 50% had hypertension. DL-PCBs and DDE, but not NDL-PCBs or HCB, were associated with hypertension, while only the association for DL-PCB remained statistically significant after lipid-standardization and adjustment for BMI and total plasma lipids. The multivariable-adjusted OR of hypertension based on repeated measurements were 1.50 (95% CI: 1.07-2.11) for DL-PCBs (3 rd vs. 1 st tertile of lipid-standardized POPs). In stratified adjusted analyses, ORs for those born after 1950 increased : 3.99 (95% CI: 2.15-7.43), while no association was observed among those born earlier. For DEE, when non-adjustment for BMI, the OR of hypertension were 1.43 (95% CI: 1.04, 1.97). Conclusions: Based on repeated measurements, the accumulated exposure to the pollutants DL-PCBs and DDE, although less clear for the latter, may disrupt the normal BP levels. Individuals born after 1950 –when early-life exposure to these substances became common– may be pre-disposed for these effects.

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