Nina Iszatt1, Hein Stigum1, Eva Govarts2, Lubica Palkovicova Murinova3, Greet Schoeters4, Tomas Trnovec3, Juliette Legler5, Cathrine Thomsen6, Gudrun Koppen2, Merete Eggesbø7. 1. Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway. 2. VITO, Unit of Environmental Risk and Health, Mol, Belgium. 3. Slovak Medical University, Faculty of Public Health, Department of Environmental Medicine, Bratislava, Slovakia. 4. VITO, Unit of Environmental Risk and Health, Mol, Belgium; University of Southern Denmark, Department of Environmental Medicine, Odense, Denmark; University of Antwerp, Department of Biomedical Sciences, Antwerp, Belgium. 5. VU University Amsterdam, Institute for Environmental Studies, Amsterdam, The Netherlands. 6. Division of Environmental Medicine, Norwegian Institute of Public Health, Oslo, Norway. 7. Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway. Electronic address: merete.eggesbo@fhi.no.
Abstract
BACKGROUND: Dioxins and dioxin-like compounds are endocrine disrupting chemicals (EDCs). Experimental studies suggest perinatal exposure to EDCs results in later obesity. However, the few epidemiological investigations on dioxins are inconclusive. We investigated perinatal exposure to dioxins and dioxin-like compounds, infant growth and body mass index (BMI) in childhood. METHODS: We pooled data from 3 European birth cohorts (Belgian, Norwegian, Slovak) with exposure assessment in cord blood or breast milk. Two cohorts had dioxin-like toxicity assessed using dioxin-responsive chemical-activated luciferase expression (DR-CALUX) bioassay and one cohort had measured concentrations of dioxins, furans and dioxin-like polychlorinated biphenols with CALUX relative potency values applied. Growth was cohort- and sex-specific change in weight-for-age z-score between birth and 24months (N=367). BMI was calculated at around 7years (median 7.17, interquartile range [IQR] 7.00-7.37years, N=251), and overweight defined according to international standards for children equivalent to adult BMI >25kg/m(2) (Cole and Lobstein, 2012). We fitted multivariate models using generalized estimating equations, and tested effect modification by sex, breastfeeding and cohort. Results per 10pgCALUXTEQ/g lipid increase in exposure. RESULTS: Dioxin exposure was highest in the Belgian and lowest in the Norwegian cohort; median (IQR) of the pooled sample 13 (12.0) pgCALUXTEQ/g lipid. Perinatal exposure to dioxins and dioxin-like compounds appeared associated with increased growth between 0 and 24months (adjusted estimate for change in z-score: β=0.07, 95% CI: -0.01, 0.14). At 7years, dioxins exposure was associated with a statistically significant increase in BMI in girls (adjusted estimate for BMI units β=0.49, 95% CI: 0.07, 0.91) but not in boys (β=-0.03, 95% CI: -0.55, 0.49) (p-interaction=0.044). Furthermore, girls had a 54% (-6%, 151%) increased risk of overweight at 7years (p-interaction=0.023). CONCLUSION: Perinatal exposure to dioxin and dioxin-like compounds was associated with increased early infant growth, and increased BMI in school age girls. Studies in larger sample sizes are required to confirm these sex-specific effects.
BACKGROUND:Dioxins and dioxin-like compounds are endocrine disrupting chemicals (EDCs). Experimental studies suggest perinatal exposure to EDCs results in later obesity. However, the few epidemiological investigations on dioxins are inconclusive. We investigated perinatal exposure to dioxins and dioxin-like compounds, infant growth and body mass index (BMI) in childhood. METHODS: We pooled data from 3 European birth cohorts (Belgian, Norwegian, Slovak) with exposure assessment in cord blood or breast milk. Two cohorts had dioxin-like toxicity assessed using dioxin-responsive chemical-activated luciferase expression (DR-CALUX) bioassay and one cohort had measured concentrations of dioxins, furans and dioxin-like polychlorinated biphenols with CALUX relative potency values applied. Growth was cohort- and sex-specific change in weight-for-age z-score between birth and 24months (N=367). BMI was calculated at around 7years (median 7.17, interquartile range [IQR] 7.00-7.37years, N=251), and overweight defined according to international standards for children equivalent to adult BMI >25kg/m(2) (Cole and Lobstein, 2012). We fitted multivariate models using generalized estimating equations, and tested effect modification by sex, breastfeeding and cohort. Results per 10pgCALUXTEQ/g lipid increase in exposure. RESULTS:Dioxin exposure was highest in the Belgian and lowest in the Norwegian cohort; median (IQR) of the pooled sample 13 (12.0) pgCALUXTEQ/g lipid. Perinatal exposure to dioxins and dioxin-like compounds appeared associated with increased growth between 0 and 24months (adjusted estimate for change in z-score: β=0.07, 95% CI: -0.01, 0.14). At 7years, dioxins exposure was associated with a statistically significant increase in BMI in girls (adjusted estimate for BMI units β=0.49, 95% CI: 0.07, 0.91) but not in boys (β=-0.03, 95% CI: -0.55, 0.49) (p-interaction=0.044). Furthermore, girls had a 54% (-6%, 151%) increased risk of overweight at 7years (p-interaction=0.023). CONCLUSION: Perinatal exposure to dioxin and dioxin-like compounds was associated with increased early infant growth, and increased BMI in school age girls. Studies in larger sample sizes are required to confirm these sex-specific effects.
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