Mitchell D. Cohen, PhD

Inhaled polluted air may account for a large number of respiratory diseases; with each breath, local lung cell populations are directly exposed to the various metals present. Individual metals can then, in turn, trigger a wide variety of biological effects that may be involved in the diseases’ pathogeneses. Among these is an impaired pulmonary immunocompetence evolving from modified structural, functional, or biochemical properties of local immune cells, i.e., alveolar macrophages (AM). Our studies have clearly shown that, (A) apart from dose (i.e., amount of metal delivered to lung), the potential for a metal (at fixed dose) to be a pulmonary immunotoxicant depends on select physicochemical properties and that (B) valency and redox behavior are key factors governing if a metal affects AM function and determinative in the magnitude of effect(s) imparted on overall pulmonary immune responses. Our findings also revealed that select metals caused shifts in lung iron (Fe) homeostasis that appeared to correspond with changes in host ability to resist/clear an infection.

Most recently, Dr. Cohen initiated studies to investigate the toxicities of World Trade Center (WTC) dusts and how select properties of the dusts (such as particle diameter, alkalinity, etc.) were likely to have been key factors underlying the increased incidence of airway hyper-responsiveness, as well as sarcoid-like granulomatous pulmonary disease (SLGPD) development, documented in exposed first responders. Collaborative studies with investigators in the department, NYU Grossman School of Medicine, and outside universities are being designed to take advantage of various tissue/biologic samples to be generated in the dust-exposed model systems utilized.