We aimed to assess the influence of long-term exposure to POPs on the risk of metabolic syndrome, combining a cross-sectional with a 10-year longitudinal follow-up design. Residues of eight POPs were quantified in adipose tissue samples from 387 participants recruited between 2003 and 2004 in Granada province (Spain). The outcome (“metabolically compromised”) was defined as having ≥1 diagnosis of type 2 diabetes, hypertension, hypertriglyceridemia, and/or low HDL cholesterol. The cross-sectional analysis was conducted in the initial cohort, while the 10-year longitudinal analysis was conducted in those 154 participants free of any of the somentioned metabolic diseases and classified as “metabolically healthy” at recruitment. Statistical analyses were performed using single and multi-pollutant approaches through logistic and Cox regression analyses with elastic
net penalty. After adjusting for confounders, β-hexachlorocyclohexane (β-HCH) and hexachlorobenzene (HCB) were independently associated with an increased risk of being metabolically compromised (unpenalized ORs = 1.17, 95% CI = 1.01–1.36 and 1.17, 95% CI = 0.99–1.38, respectively). Very similar results were found in the 10-year longitudinal analysis [HRs = 1.28, 95% CI = 1.01–1.61 (β-HCH); 1.26, 95% CI = 1.00–1.59 (HCB)] and were in line with those obtained using elastic net regression. Finally, when the arithmetic sum of both compounds was used as independent variable, risk estimates increased to OR = 1.25, 95% CI = 1.03–1.52
and HR = 1.32, 95% CI = 1.02–1.70. Our results suggest that historical exposure to HCB and β-HCH is consistently associated with the risk of metabolic disorders, and that these POPs might be partly responsible for the morbidity risk traditionally attributed to age and obesity.