News Release

UC studies links between air pollution and childhood anxiety

Researchers at UC and Cincinnati Children's investigate traffic-related air pollution and symptoms of childhood anxiety, through neuroimaging

Peer-Reviewed Publication

University of Cincinnati

Exposure to air pollution is a well-established global health problem associated with complications for people with asthma and respiratory disease, as well as heart conditions and an increased risk of stroke, and according to the World Health Organization, is responsible for millions of deaths annually. Emerging evidence now suggests that air pollution may also impact the metabolic and neurological development of children.

A new study from researchers at the University of Cincinnati and Cincinnati Children's Hospital Medical Center looks at the correlation between exposure to traffic-related air pollution (TRAP) and childhood anxiety, by looking at the altered neurochemistry in pre-adolescents.

"Recent evidence suggests the central nervous system is particularly vulnerable to air pollution, suggesting a role in the etiology of mental disorders, like anxiety or depression," says Kelly Brunst, PhD, assistant professor in the Department of Environmental Health at the College of Medicine, and lead author on the study.

"This is the first study to use neuroimaging to evaluate TRAP exposure, metabolite dysregulation in the brain and generalized anxiety symptoms among otherwise healthy children," says Brunst.

The study was published by the journal Environmental Research and is available online.

The researchers evaluated imaging of 145 children at an average age of 12 years, looking specifically at the levels of myo-inositol found in the brain through a specialized MRI technique, magnetic resonance spectroscopy. Myo-inositol is a naturally-occurring metabolite mainly found in specialized brain cells known as glial cells, that assists with maintaining cell volume and fluid balance in the brain, and serves as a regulator for hormones and insulin in the body. Increases in myo-inositol levels correlate with an increased population of glial cells, which often occurs in states of inflammation.

They found that, among those exposed to higher levels of recent TRAP, there were significant increases of myo-inositol in the brain, compared to those with lower TRAP exposure. They also observed increases in myo-inositol to be associated with more generalized anxiety symptoms. "These findings suggest that the neurotoxic effect of high TRAP exposure on generalized anxiety is partially (12%) due to increases in myo-inositol," says Brunst.

Brunst noted however, that the observed increase in reported generalized anxiety symptoms in this cohort of typically developing children was relatively small and are not likely to result in a clinical diagnosis of an anxiety disorder. "However, I think it can speak to a bigger impact on population health ... that increased exposure to air pollution can trigger the brain's inflammatory response, as evident by the increases we saw in myo-inositol," says Brunst. "This may indicate that certain populations are at an increased risk for poorer anxiety outcomes."

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Co-authors on the study include Patrick Ryan, PhD, associate professor; and Mekibib Altaye, PhD, research professor, both with dual appointments in the departments of pediatrics and environmental health at the College of Medicine, and with Cincinnati Children's; Grace LeMasters, PhD, emeritus professor, Department of Environmental Health, UC College of Medicine; Kimberly Yolton, PhD, director of Research Section, General and Community Pediatrics at Cincinnati Children's, and a professor of pediatrics in the College of Medicine; Kim Cecil, PhD, research professor of radiology, pediatrics and environmental health with UC and Cincinnati Children's; and Thomas Maloney and Travis Beckwith, PhD, with the Department of Radiology at Cincinnati Children's.

Funding for this project was provided by the National Institutes of Environmental Health Sciences (P30 ES006096, R00 ES024116, R01 ES019890, R01 ES11170, and R01 ES027224) and the National Center for Advancing Translational Sciences (NCATS, UL1 TR001425).

The authors cite no conflicts of interest.


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