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News article30 November 2022Directorate-General for Environment

Exposure to chemicals from plastic and other sources: a possible causal factor in obesity?

Issue 590: Do chemicals, including environmental contaminants, contribute to obesity? A review looks at the evidence with implications for policy and research

Exposure to chemicals from plastic and other sources: a possible causal factor in obesity?
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Although genetic susceptibility and stress are believed to contribute to obesity1, the prevailing view is that it is chiefly caused by an imbalance between energy intake and expenditure, or more simply – overeating and lack of exercise. Addressing the problem – now a worldwide pandemic – focuses on individual action or medical intervention to counter these factors. However, this approach has not even slowed the rise of obesity. A growing number of studies indicate that certain endocrine-disrupting chemicals may be important causative factors – primarily when exposure occurs during early development.

The obesogen hypothesis holds that these chemicals can increase susceptibility to obesity by influencing human health through eating behaviour, fat storage, gut microbiota and other aspects of metabolism. For example, experimental work shows that certain chemicals can increase white adipose tissue mass (white fat) in animals. A recent review of the literature by 43 researchers with expertise in obesogens2 examined which chemicals are implicated, looking at more than 700 relevant publications.

They found some 50 chemicals and classes of chemicals that can be classified as obesogens, based on animal, in vitro and epidemiological studies. These include:

  • phthalates (found in PVC);
  • bisphenols (including A, F and S: industrial chemicals used to make certain plastics and resins since the 1950s);
  • fine particulate matter (air pollutant particles) ;
  • perfluoroalkyl and polyfluoroalkyl substances (PFAS – used in food packaging and cookware);
  • flame retardants (PBDEs and OPFRs – found in furniture and consumer electricals);
  • dichlorodiphenyltrichloroethane (DDT) and other pesticides, some food additives and emulsifiers;
  • di- and tributyltin (DBT and TBT – most uses of these chemicals are now restricted) – found in PVC and often used in antifouling paints);
  • polychlorinated biphenyls (PCBs – used in past industrial processes); and
  • parabens (used as preservatives in pharmaceuticals, cosmetics and the food industry).

The list is of concern for human and ecosystem health. For example, traffic-related air pollution has been positively associated with increased body mass index in children. Bisphenol A (BPA) is among the highest production-volume chemicals detected in ecosystems. The European Food Safety Authority (EFSA) previously set a tolerable daily intake for BPA at four micrograms (µg) per kilogram (kg) bodyweight. However, the EFSA has proposed to lower this by 100 000-fold based on a revised risk assessment, and its use has been restricted. Furthermore, the many bisphenol chemicals similar to BPA are likely to have similar health impacts and require equal attention.

Tributyltin (TBT) was the first chemical designated an obesogen based on findings in mice exposed to it. TBT, once widely used in industry, is a known seafood contaminant due to its use in shipping and is present in PVC plastic and dibutyltin. While there are strong in vivo findings of the effects of TBT, few studies have detected TBT in human blood. However, recent research has shown that this may be because TBT binds strongly to the plastic specimen containers used in such studies.

Some obesogens, such as BPA, phthalates and TBT, can cause obesity over three or more generations in animal models, say the researchers. This transgenerational inheritance is of even more profound concern because the affected individuals were never exposed to the chemicals. Thus the inheritance is epigenetic (arising from non-genetic influences on gene expression) and likely to be permanent. This highlights the need for caution, say the researchers, because most chemicals have not been tested for their ability to cause adverse health effects across multiple generations.

Several studies featured in the review showed that the early stages of human development are a vulnerable window for exposure. Effects may not become apparent until later in life, yet they can be inherited by offspring and are not reversible with current technologies. Compounding the health hazard, obesity is a risk factor for diseases including cancer, diabetes and cardiovascular diseases.

The researchers make some policy recommendations, firstly that obesogens should be classified separately from endocrine disruptors as a substance of great concern. As with carcinogens, they propose two categories: obesogens and potential obesogens. They propose that Class 1 obesogens – those evidenced as harmful through data from in vitro, animal models and human studies – should be banned, or exposure significantly reduced. The researchers also suggest that people should be better informed about the sources and risks of obesogenic chemicals, for example, through product labelling.

In terms of future research, the study suggests that more work is needed on what levels can be considered safe for environmental exposure to obesogens, and that data from biomonitoring would enhance understanding of human exposure. The researchers also note there has been little research on the benefits of reducing children’s exposure to obesogenic pesticides.

Footnotes:

  1. Obesity is commonly defined as a BMI above 30 kg/m2 in western countries.
  2. This project received funding from the European Union’s Horizon 2020 research and innovation programme.

Source:

Heindel, J.J., Howard, S., Agay-Shay, K., Arrebola, J.P., Audouze, K., Babin, P.J., Barouki, R., Bansal, A., Blanc, E., Cave, M.C., Chatterjee, S. et al. (2022) Obesity II: Establishing causal links between chemical exposures and obesity. Biochemical Pharmacology, 199: 115015.

To cite this article/service:

Science for Environment Policy”: European Commission DG Environment News Alert Service, edited by the Science Communication Unit, The University of the West of England, Bristol.

Notes on content:

The contents and views included in Science for Environment Policy are based on independent, peer reviewed research and do not necessarily reflect the position of the European Commission. Please note that this article is a summary of only one study. Other studies may come to other conclusions

Details

Publication date
30 November 2022
Author
Directorate-General for Environment

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