Is DDT a time-bomb behind the obesity epidemic? | Grist

ddt_adMichael Skinner didn’t start the experiment with the hypothesis that he’d find a connection between the insecticide DDT and obesity.

“We didn’t expect to find that,” he said. “In fact, the frequency of obesity really came as a surprise.”

Skinner, a scientist at Washington State University, wanted to take a close look at the way DDT affected inheritance. So his team injected DDT into pregnant rats and watched first their children, and then their grandchildren (or is it grandrats?). It was only in the third generation, the great-grand-rat, that they saw it: Fully half of these rats were obese. The implication is that the same thing could be happening with humans.

Michael Skinner
Michael Skinner.

“Is there a correlation between the fact that we were all exposed to DDT in the 1950s for 10 years, and the fact that we are now seeing high levels of obesity?” Skinner asked. His work suggests that there could be.

Of course, the more immediate cause of obesity is too many calories. But there may be more going on here than too much food. Humans are getting fat, so are our pets, so are wild animals. There’s a trend toward obesity in nearly every species scientists have studied.

Of course it’s too early to lay the blame on DDT. This study simply raised the possibility. But the findings are plausible.

“I do believe that the observed obesity is real,” emailed Andrea Gore, a professor of pharmacology and toxicology at the University of Texas Austin. Other experiments have already shown that endocrine-disrupting chemicals can cause obesity generations after exposure, Gore said.

Skinner had already seen that he could trigger the inheritance of disease with various chemicals. There’s a narrow window during the gestation, where an exposure to lots of things can cause heritable epigenetic changes.

“The majority of things we’ve tested came up positive,” he said.

So the obvious question: Is this a problem specific to DDT, or would we have seen similar results if Skinner’s team had decided to inject the rats with vitamin C? In other words, is this about the chemical, or just the timing of the exposure?

If the DDT had caused kidney disease, Skinner said, he would have been reassured. A lot of things seem to have epigenetic effects that lead to kidney disease. But obesity is unusual — that suggests a problem with DDT itself, Skinner said.

Skinner started this experiment after the World Health Organization lifted the ban on DDT to help fight malaria. That was a good decision based on the available information, Skinner said, but no one had looked to see if DDT had an effect on subsequent generations. “On the one hand, there are 2 million deaths per year in Africa from malaria. On the other hand, we’re looking at the possibility of metabolic disease in every generation to come,” Skinner said.

The word “possibility” there is key. This wasn’t a risk assessment study, and we don’t know if we’d see something similar in humans from environmental exposure to DDT, as opposed to direct injection. But this study should give pause to the people arguing to reintroduce DDT to places even without a malaria problem, Skinner said. It’s now being used in France, among other places. And once you spray DDT, it’s out there for a long time.

“If you go to any river in the U.S., and push your finger down into the mud one or two inches, the primary contaminant you will find there is DDT,” Skinner said. The stuff just takes a really long time to break down, and Skinner’s research suggests that its effects could last much longer.


Study finds no link between kids' obesity and DDT, PCBs …

July 4, 2013

U.S. children who were exposed in the womb to high levels of DDT, PCBs and other chlorinated chemicals in the 1960s were not more likely to be obese, according to new research.

One substance, dieldrin, was linked to higher odds of obesity in children but the number of children studied was small.

Fhardseen/flickr Multiple causes of childhood obesity may include prenatal exposure to chemicals.

It is the largest study examining the link between organochlorine chemicals and childhood obesity, and the first to associate obesity with prenatal exposure to the pesticide dieldrin. Previous studies have reached conflicting conclusions.

Organochlorines were widely used as pesticides and industrial compounds in the 1940s through 1970s. Most uses have been banned for decades. However, traces of these chemicals are still found in most people’s bodies today because they persist in the environment and accumulate in fatty tissues.

Childhood obesity is an increasing problem worldwide. In the United States, 4 percent of children aged 6 to 11 were obese in the early 1970s compared with 20 percent in 2008. Researchers have been examining the role that prenatal exposure to potentially hormone-altering chemicals – such as organochlorines – may play.

The epidemiologists used data from the U.S. Collaborative Perinatal Project, which enrolled pregnant women from 1959-1965. The women’s blood was measured in their third trimester for DDT, polychlorinated biphenyls (PCBs) and other chlorinated chemicals. Then the researchers checked records for 1,915 of the women’s children to determine how many were obese at the age of 7.

Prenatal exposure to all but one of the chemicals was not associated with obese or overweight children. However, for dieldrin, children in the two groups of highest exposure were 3.6 and 2.3 times more likely to be obese than those in the lowest exposure group.

Only 89 children were in the two highest exposure groups. “The suggestive association between dieldrin and childhood obesity was perhaps a chance finding given the number of analyses we performed,” the authors wrote in the paper published in Environmental Health Perspectives.

Dieldrin was widely used as a pesticide from about 1950 to 1974 but was banned from almost all uses in the United States in 1985, according to the U.S. Environmental Protection Agency.

The pregnant women in this study had much higher levels of all the chemicals tested (hexachlorocyclohexane, DDE, DDT, dieldrin, heptachlor epoxide, hexachlorobenzene, trans-nonachlor, oxychlordane and PCBs) than people do today.

The researchers controlled for mothers’ race, education, pre-pregnancy weight, smoking status and the child’s birth order.

Previous research linking the chemicals to children’s body weight has been inconsistent. DDE exposure was linked to a higher body mass index for children, according to a 2011 study, but the link was dependent upon maternal smoking. HCB exposure was linked to obesity and higher body mass index for children in a 2008 study. The children were exposed to higher levels than in the current study.

On the contrary, PCBs were linked to decreased weight among exposed children in studies in 2002 and 2006. This association was not found in the present study.

It is unclear how organochlorine chemicals might affect a child’s body weight. But previous research has suggested that they could alter the hormones that regulate growth or alter the functioning of the central nervous system.

Most studies have focused on high levels of exposure. In light of this, the authors of the current study said they could not rule out the possibility that prenatal exposure to low levels of organochlorines could spur obesity. Some research has shown that small doses of hormone-like substances can have effects that large doses do not.

The study was a collaboration of scientists from Mexico’s National Institute of Public Health, the U.S. Centers for Disease Control and Prevention, the National Institute of Environmental Health Sciences and Ohio State University.