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INTRODUCTION: INHALATION EXPOSURE AND SYSTEMIC IMMUNOTOXICITY: MECHANISMS LINKING THE LUNG AND IMMUNE SYSTEM
Citation:
Selgrade, MJK. INTRODUCTION: INHALATION EXPOSURE AND SYSTEMIC IMMUNOTOXICITY: MECHANISMS LINKING THE LUNG AND IMMUNE SYSTEM. Presented at Society of Toxicology Annual Meeting, New Orleans, LA, March 06 - 10, 2005.
Description:
Concerns regarding inhaled compounds, immune suppression and increased risk of disease have focused primarily on suppression of local immune responses in the lung and susceptibility to respiratory infections. However, a number of studies have shown that both gaseous (O3, NO2) and particulate (diesel, Cd-coated fly ash, cigarette smoke) air pollutants, as well as soluble metals (NiCl2 and CdCl2) and a pesticide (carbaryl) administered by inhalation suppress systemic immune responses. Studies have most often assessed the antibody response to sheep red blood cells, lymphoproliferative responses to non-specific mitogens, and/or peripheral blood lymphocyte phenotypes. Although limited data is available, enhanced susceptibility to systemic infections has also been observed. Systemic immune suppression following inhalation exposure has been reported in both rodent and human studies. Results often varied depending on the exposure protocol. Because results via other routes of exposure were not always positive, mechanisms linking the lung and systemic immune system have been proposed. Inflammatory responses are thought to be involved. Potential mechanisms include production of long-lived free radicals, production of immunosuppressive mediators such as prostaglandin E2 and interleukin-10, and a shift in the balance of T helper (Th)1 and Th2 lymphocytes in favor of Th2 responses. This latter possibility is attractive, because many of these same agents have adjuvant effects on the induction of allergic sensitization or are themselves allergenic. Also, as described in later talks, mechanisms have been suggested that involve effects on the nervous and/or endocrine system. Systemic immune suppression following inhalation exposure has been reported in studies dating back 30 years. However, until recently the mechanisms responsible for these effects have been largely speculative. The papers presented at this symposium represent some of the first studies to systematically assess the mechanisms (immunologic and metabolic) underlying these effects. (This abstract does not reflect EPA policy).