Low doses of environmental chemicals can make animals gain weight. Whether they do the same to humans is a thorny issue.

In 2005, Mike Skinner’s group at Washington State University published a disturbing observation: pregnant rats exposed to high levels of a commonly used fungicide had sons with low sperm counts as adults. When the males did succeed in impregnating a female, they bore sons who also had fewer sperm, and the gametes were less viable. The problem perpetuated through multiple generations, as Skinner’s lab observed the rats over several years.¹

“We sat on [the results] for four years because it was a major observation, so we wanted to get as much on the mechanism as possible,” Skinner says. He and his colleagues found that altered DNA methylation patterns in the germ line were to blame.

To see if other environmental chemicals could have the same effect, they screened a host of potentially toxic chemicals: jet fuel, plastics ingredients, and more pesticides. Again, exposed animals had offspring with reproductive problems, which were passed down for generations. The researchers also saw another phenotype pop up again and again: obesity. Skinner first saw fat rats in his experiments after he’d injected females with a mixture of bisphenol A (BPA) and phthalates, substances used to make plastic products and, like the fungicide the researchers originally tested, known to be endocrine disruptors. The rats’ pups and their pups’ pups—animals that had direct exposure to the chemicals—showed other abnormalities, but were of normal weight. However, roughly 10 percent of third-generation (F3) rats descended from exposed females became obese.²

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