Student Research: Mark Sullivan
Lung diseases as a whole are the third leading cause of mortality in the US, with an estimated 16 million Americans living with chronic lung disease such as asthma and chronic obstructive pulmonary disease. The etiologies of chronic lung disease are wide-ranging from occupational, environmental and modifiable exposures such as smoking. While some risk factors for development and progression of chronic lung disease are well known, the role of chronic low-level exposure to air pollution association in lung disease remains uncertain. Transition metals (TM) represent a small portion of elemental species found within Fine Particulate Matter (PM2.5), but are important as they have high potential for chemical reactivity in vivo. TM have been shown to react with cellular components leading to creation of reactive oxygen species (ROS) such as superoxide anion, hydrogen peroxide, and hydroxyl radical or contribute to depletion of glutathione and protein-bound sulfhydryls, all of which may increase potential for end organ tissue damage. Because of their ubiquitous distribution in PM2.5 and potential for metal-induced ROS formation, TM exposures are of increasing interest for their potential role in the development of lung disease. For this study we chose four transition metal elements for their known association with lung disease; Chromium, Cobalt, Cadmium and Nickel. Obstructive lung disease etiology is a growing concern due to increasing incidence and prevalence in never smokers. The reactive nature of transition metals, and their presence in PM2.5 may point to an association with prevalence of obstructive lung disease. In this cross sectional study using the MESA Air population based cohort, we demonstrate that exposure to ambient air pollution levels of 4 specific transition metals (Ni, Cr, Cd, Co) is associated with decreased lung density by CT scan and decreased lung function by spirometry.