Exposure to hexachlorobenzene during pregnancy increases the risk of overweight in children aged 6 years.
Smink, A, N Ribas-Fito, M Torrent, MA Mendez, JO Grimalt and J Sunyer. 2008.
Acta Pediactrica, in press.
Synopsis by Dr. Pete Myers
In the first prospective study exploring how fetal exposures may affect the risk of childhood obesity, scientists from Spain report that children born to mothers with higher levels of the pesticide hexachlorobenzene (HCB) in cord blood were significantly more likely to be overweight and obese by the age of six. These results add to growing evidence that fetal exposure to contaminants can interfere with hormonal mechanisms that control weight later in life, thereby contributing to the world-wide epidemic of metabolic disorder.
What did they do? Smink et al. measured HCB and other persistent organic pollutants in cord blood from 405 infants at birth from a cohort study in Menorca, Spain. At the age of 6.5 years, they measured the children's weight and height. They classified children as overweight if they were at the 85th percentile or higher of the US National Center for Health Statistics/WHO reference BMI index (body mass index; kg/height).
In addition to HCB, they measured total PCBs, p,p'-DDE and p,p'-DDT.
At the time mothers were recruited into the study, prior to the child's birth, interviewers obtained information about the mother, including age, education, socio-economic status, how many children they had had, smoking, alcohol use, weight, height and diet. After birth they gather data on the infant's height and weight as well as infant-feeding practices. Smink et al. then used a series of multivariate statistical analyses to explore the relationship between HCB exposure and the likelihood of overweight in children.
What did they find? All of the 405 children had organchlorine contaminants in their cord blood. Of the organochlorine contaminants measured, p,p'-DDE had the highest median level (1.03 ng/mL) while p,p'-DDT (0.08 ng/mL) had the lowest. Total PCBs were 0.70 ng/mL. The median for HCB was 0.68 ng/mL (0.46-1.02 interquartile range).
After dividing the children into 4 groups based on HCB levels, they found that children in the highest HCB exposure group had higher average values for the other organochlorines. Also, their mothers were older and had higher BMI. These children were also heavier with a higher BMI. Overweight and obesity were higher in the children with higher HCB exposure.
The multivariate statistical analyses then allowed them to sort out how different factors like mother's weight during pregnancy interacted with HCB levels. After controlling for these variables, the association between HCB levels and overweight/obesity remained statistically significant. Children in the higher exposure group had a risk of being overweight of 1.7 compared to the low exposure group, and of 2 for obesity. These results are independent of socio-economic status, maternal education, number of prior births, maternal obesity and birth weight. The result was stronger for children whose mothers had smoked during pregnancy.
What does it mean? These data come from the first prospective epidemiological study to explore links between fetal exposures to contaminants the risk of childhood obesity. The study establishes the first link for exposure HCB during pregnancy and childhood overweight and obesity.
The mechanism(s) of action by which HCB might cause this effect is not known. No animal studies have been published on HCB's potential role as an obesogen (see discussion to left). Smink et al. speculate that one pathway may involve HCB increasing the risk of Type 2 diabetes during pregnancy, and that this medical condition then increases the odds for childhood obesity.
Whatever the mechanism, this prospective study adds significantly to the weight of evidence implicating fetal exposures in the causation of childhood obesity. Smink et al. go so far as to conclude:
"The prevalence of obesity has increased at an alarming level of at least 300 million people worldwide. Additionally, other diseases like diabetes will increase in prevalence as well. Protection for this possible diabetes epidemic is needed. The risk on increased BMI at young age, caused by prenatal exposure to OCs like HCB, has to be minimized. Therefore, it is important that pregnant women are informed about the possible effects on prenatal exposure to HCB on the BMI of the child later in life."
CDC 2000. CDC Growth Charts, United States. National Center for Health Statistics.
Colborn, T, D Dumanoski and JP Myers. 1996. Our Stolen Future. Dutton.
Grün F and B Blumberg. 2006. Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling. Endocrinology 147 (6 Suppl): S50-5.
Grün F and B Blumberg. 2007. Perturbed nuclear receptor signaling by environmental obesogens as emerging factors in the obesity crisis. Reviews in Endocrine and Metabolic Disorders 8:161-171.
Hatch, EE, JW Nelson, MM Qureshi, J Weinberg, LL Moore, M Singer and TF Webster. 2008. Association of urinary phthalate metabolite concentrations with body mass index and waist circumference: a cross-sectional study of NHANES data, 1999-2002. Environmental Health doi: 10.1186/1476-069X-7-27.
Heindel JJ. 2003. Endocrine disruptors and the obesity epidemic. Toxicolological Sciences 76:247-249.
Keith, SW, DT Redden, PT Katzmarzyk, MM Boggiano, EC Hanlon, RM Benca, D Ruden, A Pietrobelli, JL Barger, KR Fontaine, C Wang, LJ Aronne, SM Wright, M Baskin, NV Dhurandhar, MC Lijoi, CM Grilo, M DeLuca, AO Westfall and DB Allison. 2006. Putative contributors to the secular increase in obesity: exploring the roads less traveled. International Journal of Obesity 30:1585-1594.
Newbold RR, E Padilla-Banks, RJ Snyder and WN Jefferson. 2007. Perinatal exposure to environmental estrogens and the development of obesity. Molecular Nutrition & Food Research 51:912-917.
Stahlhut, RW, E van Wijngaarden, TD Dye, S Cook and SH Swan. 2007. Concentrations of Urinary Phthalate Metabolites Are Associated with Increased Waist Circumference and Insulin Resistance in Adult U.S. Males. Environmental Health Perspectives 115:876-882.
© Environmental Health Sciences. Articles may be used for educational and other not-for-profit purposes with credit to Environmental Health Sciences.