The rate of obesity in very young children — even infants — continues to climb. Evidence is building that obesity-promoting chemicals called obesogens are contributing to this alarming trend.
Some of these obesogens are pesticides that — as the ongoing study of endocrine disruption clarifies — can act at very low doses to interfere with all kinds of physiological processes. This includes, it turns out, triggering increased fat cell production.
With children affected so early in life, it's become increasingly clear that genetic and behavioral factors alone cannot explain the rising rates of obesity. Scientists are now examining the contribution of environmental factors, researching whether chemical exposures may be promoting obesity, and if so, how.
A recent study of triflumizole (TFZ) suggests that this fungicide is a likely obesogen. In 2010, over 40,000 pounds of TFZ's active ingredient was used in over 6,000 agricultural applications in the state of California alone. Widely used on food and ornamental crops, TFZ is not particularly toxic nor carcinogenic — but it does promote fat cells.
Researchers found that TFZ treatment of human stem cell cultures activated the pathway leading to fat cell production. Stem cells have the potential to become different kinds of cells (i.e., a stem cell can become a bone cell or fat cell).
The study also examined pre-birth exposure to TFZ in the drinking water of female mice. The lowest dose produced a significant increase in stored fat, while higher doses had no effect. This type of dose response — when different levels of exposure lead to different effects — is showing up in more and more studies, leading EPA to rethink how it evaluates pesticide risk.
In addition, stem cells prepared from the fat of female mice exposed to TFZ had significant genetic changes. Expression of a genetic marker that inhibits fat cell production was reduced, while genes known to promote fat cell production had increased expression.
Findings from this study suggest that exposure to a widely used fungicide may promote the rate of fat cell production from stem cells, and that female offspring exposed to TFZ in utero may have genetic changes that lead to increased fat cell production.
And the TFZ paper is just one of many recent studies on pesticides and obesogens. While this is a fairly new field of study, evidence is accumulating that chemicals are likely contributors to the obesity epidemic.
In our recent report, A Generation in Jeopardy, we discussed recent epidemiological studies focusing on children's health and putative obesogens. At this point, most of the studies focus on adult and teenage obesity.
The widespread public health consequences of the obesity epidemic suggest that we should pay very close attention to this rapidly emerging science.