Obesogens in action

Exposure to obesogens at any age can lead to obesity, but foetuses and young children have been found to be the most vulnerable. The chemicals enter the developing foetus through the mother’s blood and cause modifications in the expression of genes. These are called epigenetic changes and lead to “foetal programming”. For example, under the influence of the toxins the stem cells may be programmed to make fat cells instead of bone cells, predisposing the unborn child to be plump. A study published in the May issue of PNAS found that epigenetic changes caused by a fungicide, vinclozolin, can be passed on to as many as three generations.

In children and adults, however, the obesogenic effect of chemicals manifests as changes in metabolism through regulation of hormones. For instance, the chemicals affect the functioning of the thyroid gland, which controls metabolism. This lowers the metabolic rate and the body burns fewer calories. Other hormones affected by obesogens are leptin that regulates the feeling of satiety and resistin that reduces insulin sensitivity and leads to type 2 diabetes. These hormones are produced by the adipose tissue which till recently was believed to be just a storage space for fat. Studies have found that this tissue too has become a target of obesogens such as the fungicide, tolylfluanid. It increases the formation of fat cells and reduces leptin secretion and results in higher food intake. Another chemical, tributyltin chloride affects production of fat cells by controlling a receptor protein on the nucleus of the stem cells called peroxisome proliferator-activated receptor gamma (PPARγ). It stimulates the receptor and predisposes stem cells to become fat cells.

The WHO’s health statistics reveal that women are more likely to be obese than men. This was established by a study published in the May issue of Environmental Health Perspectives where the researchers studied 665 Danish women who reported pregnancy in the late 1980s. The levels of perfluorooctanoate (PFOA)—a chemical used to make non-stick cookware—were measured in their blood. The researchers analysed Body Mass Index (BMI), an indicator of body fat, of their offspring 20 years later in 2009. They found daughters of women, who had about 6 nanogram/millilitre (ng/ml) of PFOA in their serum, had on average 1.6 kg/m2 higher BMI compared to daughters of women who had about 2 ng/ml of the chemical in their blood. They did not find the BMI difference in male offspring.

Researchers say the reason behind women being more susceptible could be that they have more fat deposits in the body. This makes them more vulnerable to the fat-soluble environmental toxins. Women have 25-31 per cent body fat, while men have 18-25 per cent, according to American Council on Exercise.

What is more worrisome is the fact that the obesogenic effect of the chemicals is evident even at very low doses. The same chemical at high doses becomes toxic and leads to weight loss. The obesogens do not follow the long held principle of toxicology which suggests that chemicals follow a linear curve—the larger the amount of the chemical, the more the effect on people. In case of obesogens lower doses can have more effect. This means regulators are unlikely to set appropriate safe limits for chemicals since they test them taking into consideration their linear pathway.

Frederick S vom Saal, professor at the University of Missouri in the US, who has done pioneering work on BPA, including analysing its association with obesity, says that most of the studies show that the human body carries between 0.5 and 4 ng/ml (parts per billion) of BPA in the serum. This range can be harmful, he says. The chemical can mimic estradiol and cause breast cancer even at amounts below one part per trillion, 1,000 times lower than found in the human body, he explains.