Genetic Predisposition May Boost Link Between Air Pollution and Obesity, Study Says

Genetic Predisposition May Boost Link Between Air Pollution and Obesity, Study Says
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Air pollution may be associated with obesity and body fat percentage, according to a comprehensive new study from the United Kingdom.

The link between certain air pollutants and obesity may be stronger among individuals who are genetically predisposed to have a higher body mass index (BMI), the findings suggested.

The study, “Associations of air pollution with obesity and body fat percentage, and modification by polygenic risk score for BMI in the UK Biobank,” was published in the journal Environmental Research.

The prevalence of obesity has tripled in the U.S. for the past 40 years. Although much emphasis has been placed on personal behaviors and genetic factors that increase a person’s susceptibility to develop obesity, its rapid rise also most likely results from environmental factors.

In particular, air pollution may affect metabolism, adipose (fat) deposition, food craving and/or satiety (feeling full), as well as inflammation and oxidative stress — the damage to cells caused by toxic free radicals. All of those conditions are closely related to obesity.

Studies investigating the possible relationship between air pollution and obesity mostly have used BMI as a proxy for body fat percentage, even though BMI itself is unable to distinguish between lean and fat body mass. No study of this possible association has used body fat percentage, even though it is an excellent predictor of subsequent health outcomes, the scientists stated in their study.

In addition, it is still unclear if one’s genetic predisposition for obesity also may contribute to greater effects of air pollutants on body fat.

To tackle these issues and explore the relationship between air pollution and body fat, investigators at the University of Arizona used longitudinal data from 473,026 individuals, age 40–69 (mean age 56), part of the UK Biobank. Enrollment in the Biobank took place from 2006 to 2010, and follow-up from 2012 to 2013.

Investigators used classical measures of obesity, such as BMI and waist-hip ratio (WHR), along with body fat percentage. They also assessed the potential affect of genetic background on the relationship between air pollutants and obesity.

The team used annual estimates of average air pollution gathered in 2010 that included exposure to gaseous — nitrogen dioxide (NO2) and nitrogen oxides (NOx) — and particle matter pollutants of various sizes, along with indirect measures of pollution, such as traffic intensity (vehicles per day) and distance to road. Statistical analyses were used to evaluate possible associations between the different parameters. (Notably, particulate matter pollutants refer to mixtures of solid particles and liquid droplets found in the air.)

Nearly all enrolled individuals (95%) were white, 54% were women, and approximately a third (32%) had at least a college degree. Follow-up data were available only from 19,518 individuals.

With the exception of IDTR, all measures of air pollution were directly associated with at least one measure of body fat at enrollment. However, both exposure to NO2 and greater IDTR correlated with lower BMI at enrollment.

At follow-up, statistical analyses revealed that higher levels of air pollution were associated with greater BMI and body fat percentage.

Among the study’s limitations were the fact that annual estimates of air pollution preceded follow-up data collection, and that analyses of genetic predisposition to obesity were based mostly on information from Caucasians in the U.K., and as such may not be applicable to other populations.

Joana holds a BSc in Biology and a MSc in Evolutionary and Developmental Biology from Universidade de Lisboa. She is currently finishing her PhD in Biomedicine and Clinical Research at Universidade de Lisboa. Her work has been focused on the impact of non-canonical Wnt signaling in the collective behavior of endothelial cells — cells that made up the lining of blood vessels — found in the umbilical cord of newborns.
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José holds a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.

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Joana holds a BSc in Biology and a MSc in Evolutionary and Developmental Biology from Universidade de Lisboa. She is currently finishing her PhD in Biomedicine and Clinical Research at Universidade de Lisboa. Her work has been focused on the impact of non-canonical Wnt signaling in the collective behavior of endothelial cells — cells that made up the lining of blood vessels — found in the umbilical cord of newborns.
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