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Division of Pulmonary, Allergy and Critical Care Medicine

SarcoidosisTeamRanu Surolia, Ph.D.

Ranu Surolia, Ph.D., assistant professor in the UAB Division of Pulmonary, Allergy, and Critical Care Medicine, has received an R01 grant  for the project, “Environmental cadmium, persistent inflammation, and airways disease.” Surolia’s grant builds on her past work as part of the National Institute of Environmental Health Sciences P42 Superfund Award project, “Impact of Airborne Heavy Metals on Lung Disease and the Environment.” This project will investigate how cadmium toxicity is responsible for persistent inflammation and airway remodeling.

Cadmium is a heavy metal pollutant that has no biological function in the human body.  Cadmium is emitted from sources like smelters, coal-fired plants, coke factories, and forest fires. Environmental cadmium is associated with a higher risk of development of small airway diseases like COPD and Asthma, however, the mechanism by which this happens remains unclear.

Surolia’s laboratory research has found that biological samples from UAB Superfund Site residents have high levels of cadmium in their lung tissue, along with twice the incidence of chronic airway diseases than the general population. Environmental exposure to cadmium can induce dysregulated resolution pathways related to persistent inflammation, which may be a reason for the increased incidences of airway diseases.

Surolia observed that the Cadmium exposed alveolar macrophages demonstrated decreased efferocytosis ability, the presence of increased protein arginine deiminase 4 (PAD4), and citrullinated calcium-calmodulin-dependent protein kinase II (CaMKII). Her research team will investigate cadmium toxicity-mediated effects of PAD4-related downstream pathways for impaired efferocytosis for the persistent inflammation and airway remodeling. Surolia's research team hopes to determine if cadmium-exposure-mediated dysfunctional efferocytosis is associated with airway disease in vivo animal models and ex-vivo organoid models. She will expand the outcomes of these mechanistic studies to corelate with dysfunction of efferocytosis in the biological samples from patients with COPD and North Birmingham residents at the Superfund Site.

For full details on this project, please visit the NIH RePorter.