DDT breakdown product appears to be an ‘obesogen,’ but only in youngsters of normal-weight moms
One-quarter of babies born to women who had relatively high concentrations of a DDT-breakdown product in their blood grew unusually fast for at least the first year of life, a study finds. Not only is this prevalence of accelerated growth unusually high, but it’s also a worrisome trend since such rapid growth during early infancy has — in other studies — put children on track to become obese.
Affected babies in the new study weighed no more than normal at birth, so growth in the womb was unaffected. Their moms were also normal weight — which is significant because babies born to overweight and obese women sometimes undergo rapid growth.
Carried out in Spain, the new — and still ongoing — study recruited more than 500 women to take part, beginning in the first trimester of their pregnancies. Blood collected upon entry was assayed for the presence of several common persistant chlorinated pollutants: DDT, its breakdown product DDE, hexachlorobenzene (a now-banned fungicide that still occurs inadvertently as a byproduct during the manufacturing of other chlorinated compounds), beta-hexachlorohexane (a contaminant of the insecticide lindane), and any of several dioxinlike polychlorinated biphenyls (fluids used as electrical insulators). Researchers continue to follow the babies born into the study (most of whom are now around 4 years old).
The study probed for correlations between pollutants in the moms’ blood and growth differences among their children. Only DDE exhibited such an association.
Babies born to normal-weight moms who had exhibited elevated blood-DDE levels (in the upper 25 percent of all participants) were twice as likely to grow rapidly during their first 6 months than were infants born to the least-exposed women (with DDE concentrations in the lowest 25 percent). By 14 months old, children whose exposures to DDE in the womb had been in the top 50 percent were four times as likely to be overweight — as indicated by a high body-mass-index, or BMI, score — when compared to children with lower exposures.
Although the heavier children were not obese, they will be followed to see if they become so, notes Michelle Mendez of the Center for Research in Environmental Epidemiology, in Barcelona, who led the new analyses.
Her team’s findings appeared online October 5, ahead of print, in Environmental Health Perspectives.
Finding no DDE link to growth among children of overweight and obese women was a surprise, Mendez says. “We didn’t actually expect this interaction between maternal weight and DDE’s impacts,” she explains, but the study’s analyses point to less than a 5 percent chance that such a finding was due to chance.
If the association is confirmed in followup studies, she says, “there is still this big mystery: why some infants would start to grow more rapidly than others immediately after birth. Are they eating more? Are they less active? We just don’t know.” Presumably, she says, some type of fetal reprogramming — maybe to neural wiring, maybe in switches affecting the activity of particular genes — has altered the way these children metabolize their food.
In fact, a growing body of data has been indicating that some pollutants — known colloquially as obesogens — can trigger the body to put on the pounds. In animals, these pollutants will sometimes lead a mouse to become rotund despite eating no more and exercising no less than its lean cousins.
Many obesogens — including DDE — have a hormonal alter ego. In the body, DDE can either turn on or block the activity of natural estrogens, female sex hormones. This pollutant also can block the activity of male sex hormones. Such properties lead scientists to describe this pesticide derivative as an endocrine disrupter.
This new paper “is very interesting because the authors have linked the extensive literature on rapid early infancy weight gain [and] later increased BMI with endocrine disrupter exposure in a population of significant size,” says
Bruce Blumberg of the University of California, Irvine. Although there have been few studies investigating endocrine disrupters of any type with weight-regulation issues in children, he notes that “DDE levels are consistently associated with increased BMI in adults. Therefore, the current study provides another link between DDE and the risk of obesity.”
Data on chemicals showing obesogenic activity in animals “are already very strong and we should be concerned,” maintains Ana Soto of the Tufts University School of Medicine in Boston. But this endocrinologist acknowledges that plenty of people remain skeptical of animal data. And for them, she says, the new study’s findings from children make a good case that endocrine disrupters can be human obesogens.
As to where people might encounter DDE: Its parent, DDT, is still used for malaria control in some parts of the world. As persistent organic pollutants, DDT and DDE can leapfrog around the world for years after the insecticide was first released (Science News, March 16, 1996, p. 174). Some researchers have found DDE tainting plush toys (Science News, Dec. 10, 2005, p. 381). Root vegetables, such as carrots, may pick up DDE from soil even years after DDT was last used, and residues of the pesticide have been found tainting produce and meat from countries where DDT’s use remains legal.
M.A. Mendez, et al. Prenatal organochlorine compound exposure, rapid weight gain and overweight in infancy. Environmental Health Perspectives, in press, 2010. doi:10.1289/ehp.1002169
J. Raloff. Organic doesn't mean free of pesticides. Science News Online, May 21, 2005. [Go to]
J. Raloff. The Case for DDT: What do you do when a dreaded environmental pollutant saves lives? Science News, Vol.158, July 1, 2000, p. 12.
J. Raloff. The Pesticide Shuffle, Science News, Vol. 149, March 16, 1996, p. 174.
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