Exposure to hexachlorobenzene during pregnancy increases the risk of overweight in children aged 6 years

Center for Research in Environmental Epidemiology, Institut Municipal Investigació Mèdica, Barcelona, Spain.
Acta Paediatrica (Impact Factor: 1.67). 11/2008; 97(10):1465-9. DOI: 10.1111/j.1651-2227.2008.00937.x
Source: PubMed


To determine whether prenatal exposure to hexachlorobenzene (HCB) has potential adverse effects on child's weight and body mass index (BMI) in a general population with no local pollution sources.
Starting from mid 1997, all mothers presenting for antenatal exposure in Menorca were recruited. Subsequently, 482 children were enrolled. HCB was measured in cord blood. Weight and height were measured at birth and at age 6.5 years.
Children with HCB levels higher than 1.03 ng/mL in cord blood were 1.14 kg (0.38) heavier and had a higher BMI (beta= 0.80 (0.34)) than children with HCB levels lower than 0.46 ng/mL. No statistically significant associations were found in height. Children in the higher exposure group of HCB had an increased risk of 2.5 and 3.0 of being overweight and obese. Children from normal weight mothers also presented an increased risk of having higher BMI with increasing concentrations of HCB in cord serum.
Prenatal exposure to HCB is associated with an increase in BMI and weight at age 6.5 years. Further studies with larger samples and longer follow-up are needed to confirm these results.

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Available from: Agnes J Smink
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    • "HCB has previously been associated with restricted fetal growth such as low birth weight, low birth length and lower head circumference (Eggesbo et al., 2009) (Brucker-Davis et al., 2010; Ribas-Fito et al., 2002; Schade and Heinzow, 1998). The reported associations between prenatal HCB exposure and postnatal child growth are conflicting: one study found increased risk of overweight at six years (Smink et al., 2008), however, no associations were found between prenatal exposure to HCB and child growth up to six months (Mendez et al., 2011) or body mass index (BMI) at 3 years (Verhulst et al., 2009). One problem in the studies of prenatal exposure is how to appropriately account for the postnatal exposure, since if HCB is exerting any effect also postnatally this will affect the estimated prenatal effect. "
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    ABSTRACT: Background: Infants are exposed to persistent environmental contaminants through breast milk, yet studies assessing the health effects of postnatal exposure are lacking. Existing postnatal exposure assessment is either too simple (lactation exposure model, LEM) or requires complex physiologically-based pharmacokinetic (PBPK) models. Objectives: We present equations for postnatal exposure calculations. We applied these equations to study the effect of hexachlorobenzene (HCB) on infant growth in the two first years of life. Methods: HCB was measured in breast milk samples in 449 mother-child pairs participating in the Norwegian birth cohort study HUMIS. We used these concentrations, mother's weight, height and age, together with child's weight at 8 age points, and proportion of milk consumed each month, to calculate HCB concentrations in the infant over age. We then estimated the association between HCB and infant growth using a linear mixed model. Results: Children exposed to HCB via mother's milk reached concentrations 1-5 times higher than the mother. HCB was associated with lower weight gain in the first 2years (-33g per unit HCB and month, 95% CI: -38, -27 at 6months). Associations were stronger during the first 3months (-57g per unit HCB and month, 95% CI: -67, -49 at 1month), indicating a critical window of effect. Our equations gave more precise estimates than the LEM. Conclusion: Our equations for postnatal exposure of lipophilic environmental toxicants give better results than the LEM and are easier to implement than the complex PBPK models. HCB exposure, especially during the first three months of life, has a negative effect on infant growth up to 2years.
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    • "We found that higher prenatal HCB and DDE concentrations were significantly associated with increased BMI z-scores and adiposity at 4 years of age. Our findings for HCB are consistent with previous studies that reported positive associations with offspring obesity at 14 months (Valvi et al. 2014) and 6 years (Smink et al. 2008). On the contrary,Delvaux et al. (2014)reported no significant association of HCB measured in cord blood and markers of abdominal obesity at 7–9 years. "
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    ABSTRACT: Prenatal exposure to endocrine disrupting chemicals such as persistent organic pollutants (POPs) may increase risk of obesity later in life. We examined the relation of in utero POPs exposure to offspring obesity and cardiometabolic risk factors at 4 years in the Rhea mother-child cohort in Crete, Greece (n=689). We determined concentrations of polychlorinated biphenyls (PCBs), dichlorodiphenyldichloroethene (DDE), and hexachlorobenzene (HCB) in first trimester maternal serum. We measured child weight, height, waist circumference, skinfold thicknesses, blood pressure (BP), blood levels of lipids, C-reactive protein, and adipokines at 4 years of age. Childhood obesity was defined using age- and sex-specific cut points for BMI as recommended by the International Obesity Task Force. On multivariable regression analyses, a 10-fold increase in HCB was associated with a higher BMI z score (adj. β=0.49; 95% CI: 0.12, 0.86), obesity (RR=8.14; 95% CI: 1.85, 35.81), abdominal obesity (RR=3.49; 95% CI: 1.08, 11.28), greater sum of skinfold thickness (β=7.71 mm; 95% CI: 2.04, 13.39) and higher systolic BP (β=4.34 mmHg; 95% CI: 0.63, 8.05) at 4 years of age. Prenatal DDE exposure was associated with higher BMI z score (β=0.27; 95% CI: 0.04, 0.5), abdominal obesity (RR=3.76; 95% CI: 1.70, 8.30) and higher diastolic BP (β=1.79 mmHg; 95% CI: 0.13, 3.46). PCBs were not significantly associated with offspring obesity or cardiometabolic risk factors. Prenatal exposure to DDE and HCB was associated with excess adiposity and higher blood pressure levels in early childhood.
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    • "It has been suggested that EDCs can affect adipocyte differentiation and weight homeostasis (Baillie-Hamilton, 2002; Grun and Blumberg, 2007; Heindel, 2003), possibly through activation of nuclear receptors such as the PPARs (Grun and Blumberg, 2007), and various chemicals have been linked to obesity and metabolic disorders including tributyltin (TBT), polychlorinated biphenyls (PCBs), bisphenol A (BPA) (Langer et al., 2007; Miyawaki et al., 2007; Smink et al., 2008; Vasiliu et al., 2006; vom Saal et al., 2012). Especially exposure of the fetus to EDCs is considered to increase the risk of obesity in adult life as developmental programming of metabolic set points may be disturbed (Frontera et al., 2008; Levin, 2006; vom Saal et al., 2012). "

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