Research examines how linoleic acid intake changes lung inflammation following ozone exposure in susceptible populations

Author: Kelli Trinoskey

A glowing representation of human lungs in light blue against a black background, showcasing intricate bronchial structures.

Featured expert

  • Kymberly Gowdy, MS, PhD, associate professor of Internal Medicine in the Division of Pulmonary, Critical Care and Sleep Medicine at The Ohio State University College of Medicine.

Globally, air pollution is responsible for premature deaths and economic loss. Kymberly Gowdy, MS, PhD, associate professor of Internal Medicine in the Division of Pulmonary, Critical Care and Sleep Medicine at The Ohio State University College of Medicine, just received an R21 grant from the National Institute of Environmental Health Sciences to expand research on the health effects of ozone, a criteria air pollutant, on lung injury and infection in people with obesity.

Forty-two percent of people in the United States have a body mass index that is considered obese, leading to them exhibit enhanced sensitivity to air pollution, including ozone. People with obesity also have an increase of n-6 polyunsaturated fatty acids (PUFAs) circulating in their bodies. One PUFA abundant in the western diet is linoleic acid (LA), which is a fatty acid only taken in through diet.

LA in the diet has been associated with both beneficial and detrimental health effects, but its influence on lung inflammation is currently understudied. Dr. Gowdy and her team will examine if a high intake of LA increases distinct oxidized linoleic acid metabolites (OXLAMs) that drive inflammation, with the aim to develop ways to mitigate obesity-exacerbated lung inflammation and injury following ozone exposure.

In this study, they will rely on mouse models and human bronchoalveolar lavage and plasma samples from individuals with a differential of body mass indexes to show:

  • How dietary LA intake in obesity leads to the generation of distinct pulmonary oxidized linoleic acid metabolites (OXLAMs) and drives inflammation following ozone exposure.
  • That decreasing consumption of LA will reduce lung LA accumulation and production of OXLAMs, metabolites which are further metabolized by enzymes including soluble epoxide hydrolase (sEH), driving inflammation.
  • The contribution of individual OXLAMs on ozone-induced pulmonary inflammation.
  • If specific dietary interventions could mitigate obesity-exacerbated lung inflammation and injury.

This research and any of its resulting findings have the potential to pave the way for innovative, precision nutrition approaches and the ability to combat the adverse health effects of air pollution, and more broadly to impact other types of lung inflammation or injury.