Dianna J Magliano1, Fanny Rancière2, Rémy Slama3, Ronan Roussel4, Hannu Kiviranta5, Xavier Coumoul6, Beverley Balkau7, Jérémie Botton8. 1. Baker Heart and Diabetes Institute, Diabetes and Population Health, Melbourne, Australia; Monash University, Department of Epidemiology and Preventive Medicine, Melbourne, Australia. Electronic address: dianna.magliano@baker.edu.au. 2. Université de Paris, Centre of Research in Epidemiology and Statistics (CRESS), Inserm, F-75004 Paris, France; Université de Paris, Faculté de Pharmacie de Paris, Paris, France. 3. Inserm-Centre National de la Recherche Scientifique (CNRS) and Université Grenoble-Alpes Joint Research Center, Institute for Advanced Biosciences (IAB), U1209, Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Grenoble, France; Université Grenoble-Alpes, IAB, Grenoble, France. 4. Inserm, UMRS 1138, Centre de Recherche des Cordeliers, Paris, France; Assistance Publique-Hôpitaux de Paris, Bichat Hospital, DHU FIRE, Diabetology, Endocrinology and Nutrition, Paris, France; Université de Paris, UFR de Médecine, Paris, France. 5. National Institute of Health and Welfare, Kuopio, Finland. 6. Université de Paris, T3S, Inserm UMR S-1124, F-75006 Paris, France. 7. Université Paris-Saclay, UVSQ, Univ. Paris-Sud, Inserm, Clinical Epidemiology, CESP, Villejuif, France. 8. EPI-PHARE Scientific Interest Group in Epidemiology of Health Products, French National Agency for the Safety of Medicines and Health Products and the French National Health Insurance, Saint-Denis, Ile-de-France, France; IRSA, La Riche, France.
Abstract
AIMS: To explore exposure to 22 persistent organic pollutants (POPs) and incident type 2 diabetes in a population-based, prospective cohort. METHODS: This case-cohort study on 753 participants without type 2 diabetes at baseline, was followed-up over nine years, as part of the French D.E.S.I.R. cohort. We measured 22 POPs in fasting serum at baseline. The associations between baseline POP concentrations, pre-adjusted for lipids, BMI, age and sex, with incident type 2 diabetes, were assessed using Prentice-weighted Cox regression models (time scale: age), adjusted for traditional confounding factors. POPs were also modelled summed in functional groups: polychlorinated biphenyls (∑PCB) and organochlorines (∑OC) and also individually, after log-transformation, in adjusted Cox models. RESULTS: There were 200 incident diabetes cases over nine years. Pre-adjusted POP concentrations were not related to diabetes risk for any of the 22 POPs examined. The fully-adjusted hazard ratios (HRs) per interquartile range of the pre-adjusted POPs, ranged from 0.87 (95% CI: 0.64,1.19) to 1.22 (0.93,1.59,). For dichlorodiphenyldichloroethylene (p, p'-DDE) and dichlorodiphenyltrichloroethane (p, p'-DDT), the HRs were 1.09 (0.83,1.43) and 0.89 (0.70,1.13), respectively. The HRs for PeCB, HCB, β-HCH, γ-HCH, oxychlordane, trans-nonachlor were 0.98 (0.85,1.13), 1.06 (0.84,1.33), 1.22 (0.93,1.59), 1.13 (0.89,1.42), 1.00 (0.76,1.31), 0.86 (0.66,1.13), respectively. HRs for ∑PCB, ∑OC and for individual log-transformed POPs did not differ significantly from one. CONCLUSION: We did not observe any relations between exposure to POPs and diabetes in this population-based cohort. These results do not support causal inferences reported in previous studies linking serum POP concentrations and diabetes risk.
AIMS: To explore exposure to 22 persistent organic pollutants (POPs) and incident type 2 diabetes in a population-based, prospective cohort. METHODS: This case-cohort study on 753 participants without type 2 diabetes at baseline, was followed-up over nine years, as part of the French D.E.S.I.R. cohort. We measured 22 POPs in fasting serum at baseline. The associations between baseline POP concentrations, pre-adjusted for lipids, BMI, age and sex, with incident type 2 diabetes, were assessed using Prentice-weighted Cox regression models (time scale: age), adjusted for traditional confounding factors. POPs were also modelled summed in functional groups: polychlorinated biphenyls (∑PCB) and organochlorines (∑OC) and also individually, after log-transformation, in adjusted Cox models. RESULTS: There were 200 incident diabetes cases over nine years. Pre-adjusted POP concentrations were not related to diabetes risk for any of the 22 POPs examined. The fully-adjusted hazard ratios (HRs) per interquartile range of the pre-adjusted POPs, ranged from 0.87 (95% CI: 0.64,1.19) to 1.22 (0.93,1.59,). For dichlorodiphenyldichloroethylene (p, p'-DDE) and dichlorodiphenyltrichloroethane (p, p'-DDT), the HRs were 1.09 (0.83,1.43) and 0.89 (0.70,1.13), respectively. The HRs for PeCB, HCB, β-HCH, γ-HCH, oxychlordane, trans-nonachlor were 0.98 (0.85,1.13), 1.06 (0.84,1.33), 1.22 (0.93,1.59), 1.13 (0.89,1.42), 1.00 (0.76,1.31), 0.86 (0.66,1.13), respectively. HRs for ∑PCB, ∑OC and for individual log-transformed POPs did not differ significantly from one. CONCLUSION: We did not observe any relations between exposure to POPs and diabetes in this population-based cohort. These results do not support causal inferences reported in previous studies linking serum POP concentrations and diabetes risk.