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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.