Mehrdad Arjomandi, MD

My primary research interest is studying the physiologic and inflammatory mechanisms of airway remodeling in various exposure-response models such as ozone-induced oxidative injury, allergic airway inflammation, and wood or tobacco smoke-induced airway injury.   Dr. Arjomandi is Assistant Professor of Medicine In-residence in the Division of Pulmonary and Critical Care at UCSF with a joint appointment at San Francisco Veterans Affairs Medical Center. He is the Associate Director of the Human Exposure Laboratory at the UCSF Lung Biology Center, and an investigator at the UCSF Center for Tobacco Control Research and Education. Dr. Arjomandi received his bachelor degree in molecular biology from University of California San Diego in 1991, and his MD degree from Stanford University School of Medicine in 1996. He completed his residency in Internal Medicine at UCLA Medical Center (1999) and his fellowship in Pulmonary and Critical Care Medicine at UCSF (2003). Dr. Arjomandi is currently funded through a NIH/NHLBI Mentored Patient-oriented Career Development Award (K23), and the UCSF Flight Attendants Medical Research Institute (FAMRI) Center of Excellence Research Award.

Dr. Arjomandi is also the Co-Principal Investigator on two state grants through the California Air Resources Board. The lung is constantly exposed to various environmental pollutants, allergens, and toxins, which interact with airways and alveoli and result in inflammation, injury, and disease. Exposure-related pulmonary diseases are increasingly recognized as a growing global problem; however, our understanding of their clinical spectrum and underlying pathophysiology has remained limited. Although exposures to various environmental agents cause a range of airway and lung diseases, evidence exists to suggest that many of these agents share common pathways of inflammation and injury. For example, long-term exposure to tobacco smoke, wood smoke, ozone, or allergen, alone or in combination, can cause chronic obstruction and remodeling of airways. The nature and extent of these pathologic processes may be dependent on the type and amount of exposure, and on individual factors such as genetics, age, co-morbid conditions, and diet.