Studies link pervasive 'obesogens' to weight gain in frogs, mice
For the most part, the blame for the obesity epidemic has fallen on diet and exercise, with particular emphasis on familiar evils such as the proliferation of junk food, the advent of the remote control, trans fat, ever-longer commutes and even the disappearance of physical education in schools.
But now some researchers have identified a new suspect: pollution.
Attributing obesity to diet and exercise is "practically scientific dogma at this point," says Bruce Blumberg, associate professor of developmental and cell biology at UC Irvine. But, he continues, "diet and exercise are simply not adequate to explain the explosion of obesity in Western countries."
Instead, Blumberg believes the obesity epidemic actually is due, in part, to industrial pollution — specifically to low levels of toxic compounds he calls "obesogens."
Just as exposure to carcinogens can trigger cancer, Blumberg and other researchers say exposure to obesogens can trigger a dramatic increase in the amount of fat produced in a person's body, leading to excess weight and obesity.
Blumberg and his co-workers exposed female frogs to extremely low levels of TBT; as expected, TBT did indeed cause sexual mutation among frogs. But what was really striking, he says, was that the hapless amphibians got fat — really fat. "To be honest, I will have to say we stumbled on this," he says.
Tiny doses had a big effect - Although most of the research on endocrine disrupters has focused on their potential effects on sexual development, fat production also is regulated by the hormone system and is, theoretically at least, just as susceptible to disruption.
Blumberg injected mice with TBT and observed similar results: fat rodents. Even more significant, the compound triggered obesity in ridiculously min-uscule quantities. In fact, Blumberg and his colleagues demonstrated effects from TBT at 27 parts per billion — the rough equivalent of 4 tablespoons in an Olympic-sized swimming pool.
Toxicology experts concur that some compounds are so potent that they can indeed trigger changes at minute concentrations, at least in the test tube.
"It sounds absurd, but it's not inconsistent with what we see in the lab," says Fred Berman, director of the Toxicology Information Center at the Center for Research on Occupational and Environmental Toxicology at Oregon Health & Science University.
Organotins are everywhere
The disruptive effects of organotins stem from their propensity to stimulate a particular hormone receptor that plays a key role in maintaining the body's metabolism, in effect telling the body which kind of cells are in short supply and need to be grown.
Organotins somehow encourage that receptor to manufacture fat cells — which in turn promotes that ominous abdominal bulge feared by statisticians and movie stars alike.
Organotins first came into widespread use in the 1960s in the shipbuilding industry, where they were mixed with paint to deter barnacles and mollusks from accumulating on the hulls of ships.
They also have been used as soil fungicides for crops such as nuts, potatoes, rice and celery; as "slimicide" to clean up the goop that accumulates in underground water wells; and in the manufacture of polyvinyl chloride, or PVC, a hard plastic found in drainpipes, vinyl flooring, window frames and hundreds of other places.
These widespread uses suggest several possible routes of human exposure, Blumberg says. Organotins may contaminate crops, seep into wells or leach into drinking water from PVC pipes.
