Dr. Arjomandi is Assistant Professor of Medicine in the Division of Lung Biology Center with dual appointments in the Divisions of Pulmonary and Critical Care and Occupational and Environmental Medicine. He is the Associate Director of the Human Exposure Laboratory at the UCSF Lung Biology Center. 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 at UCSF (2003). Dr. Arjomandi has been a recipient of the American Lung Association and the Chest Foundation research fellowships in the past. He is currently funded through an NIH/NHLBI Mentored Patient-oriented Career Development Award (K23). He is also the co-Principal Investigator on two state grants through the California Air Resources Board.
Dr. Arjomandi’s general research interests include the respiratory health effects of various environmental air pollutants and oxidant gases (e.g., ozone, O3, and environmental tobacco smoke) and various occupational exposures (e.g., beryllium). He is currently studying the effects of O3-induced oxidative injury and secondhand tobacco smoke (SHS) including the following specific topics:
1) The immunologic mechanisms of oxidative injury in airways through studying the patterns of gene expression in an O3-induced oxidative injury model in parallel human and mouse experiments. Recent data from Human Exposure Laboratory suggest that OPN and alveolar macrophages may play a role in airway remodeling caused by O3-induced oxidative injury. OPN is a cytokine involved in tissue repair and remodeling which has chemotactic properties as well as pro-fibrotic activities. In a pilot study of four human subjects, we found that the expression of OPN in BAL cells and the recruitment of alveolar macrophages into airways increase by several folds in an O3-induced oxidative injury model in asthmatic subjects (Arjomandi et al. 2005). Furthermore, epidemiologic studies involving our research team and others have shown that long-term exposure to O3 is associated with chronic air flow obstruction and decreased lung function, i.e., airway remodeling (Galizia et al. 1999; Tager et al. 2005), a finding that has been confirmed in animal O3 exposure studies (Schelegle et al. 2003). Together, these studies suggest a possible role for OPN and alveolar macrophages in airway remodeling due to oxidative injury.
2) The impact of antioxidant enzyme genetic polymorphisms on the susceptibility to oxidative injury through studying the role of antioxidant enzyme genotypes in O3-induced airway responses. Considerable inter-subject variability is observed in respiratory responses to O3-induced oxidative injury, potentially due to differential antioxidant and xenobiotic metabolizing enzyme function and innate immune responses. Understanding genetic and host determinants of the responses to O3 will be important to reducing the burden of diseases characterized by oxidative stress such as asthma or COPD. Recently, our research group has found that certain antioxidant enzyme genotypes have sex specific effects on chronic effects of O3-induced oxidative injury. Specifically, the GSTP1 Val105 variant allele was found to be protective against the chronic airflow obstruction that is associated with lifetime exposure to ambient O3 in females. Currently, we are studying the effects of other antioxidant enzyme genotypes as well as the effects of race/ethnicity on the respiratory effects of O3-induced oxidative injury.
3) The acute airway physiologic and immunologic responses to secondhand tobacco smoke (SHS) in controlled and parallel human and mouse models of SHS exposure. Exposure to SHS causes diverse adverse health effects in nonsmokers such as sinusitis and other upper airway problems, asthma flares, COPD, heart disease, and lung cancer. With heavier SHS exposure, there appear to be more adverse health outcomes in adults, suggesting a dose-dependent response to SHS exposure. In a collaborative study with Dr. Kent Pinkerton in UC Davis, we are attempting to characterize the lung responses to SHS exposure. In addition, similar to the O3 exposure study above, we are studying the underlying mechanisms of these respiratory effects by studying the gene expression of airway cells in parallel human and mouse studies.
4) The effect of chronic SHS exposure on lung function in human. When flight attendants who worked on commercial aircraft before the ban on cigarette smoking were monitored, SHS concentrations on these aircraft resulted in easily measured levels of urinary cotinine (a major metabolite of nicotine) indicating they had been exposed to significant levels of tobacco smoke (Samet et al. 1987). Therefore, it is very likely that flight attendants exposed to SHS have suffered from SHS-related long-term damage to their lungs. In collaboration with Dr. Warren Gold at UCSF, we have performed lung function and cardiopulmonary exercise testing on a small cohort of pre-smoking ban flight attendants. Our preliminary findings show that about 40% of these flight attendants have abnormal resting diffusion capacity and curvilinear flow-volume loops suggestive of mild COPD.