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Smog exposure and host resistance to respiratory pathogens
Citation:
Luebke, R., C. Copeland, L. Copeland, W. Williams, C. Wood, D. Morgan, S. McCullough, J. Krug, S. Gavett, K. Gowdy, AND Ian Gilmour. Smog exposure and host resistance to respiratory pathogens. Society of Toxicology Amnnual Meeting, Baltimore, MD, March 12 - 16, 2017.
Impact/Purpose:
The US EPA is evaluating the health effects of photochemical smog on respiratory, cardiovascular and metabolic health (https://www.epa.gov/air-research/secondary-organic-aerosol-soas-research). Smog exposure has been associated with an increased risk of allergy and decreased resistance to respiratory infections; we therefore investigated the effects of smog on the host response to respiratory pathogens.
Description:
The US EPA is evaluating the health effects of photochemical smog on respiratory, cardiovascular and metabolic health (https://www.epa.gov/air-research/secondary-organic-aerosol-soas-research). Smog exposure has been associated with an increased risk of allergy and decreased resistance to respiratory infections; we therefore investigated the effects of smog on the host response to respiratory pathogens. Atmospheres were generated in a chamber fed with selected hydrocarbons (gasoline + -pinene-“smog A” or gasoline +isoprene-“smog B”), and subjected to ultraviolet light. Final chamber concentrations were 252 ppb NO2, 104 ppb O3, and 1070 ug/m3 secondary organic aerosol, SOA) (Smog A) or 617 ppb NO2, 376 ppb O3, and 53 ug/m3 SOA (Smog B). Balb/C female mice were exposed to filtered air or smog for 4 h/d X 5 d; subgroups of control and exposed mice were either immunized with heat-killed Streptococcus pneumoniae (HKSP; smog A) or infected with mouse-adapted influenza A/Puerto Rico/8/34 (H1N1) on the first or last day of exposure. Mice were necropsied 7 d after immunization or infection and markers of lung damage and resistance to infection were assessed. Exposure to smog A did not alter the concentration of antibody to HKSP in the serum or concentrations of protein, lactate dehydrogenase or leukocyte concentrations in the bronchoalveolar lavage fluid (BALF),although the % neutrophils was greater in the post-exposure air group. Virus burdens were similar in air- and smog B-exposed mice, as were BALF constituents. Body weight loss and lung lobe weights were significantly greater in both air and smog B mice infected at the end of exposure, as were lung lobe weights and % macrophage while neutrophils were decreased. Expression of inflammatory cytokine genes in these groups of mice tended to be significantly lower, particularly in mice exposed to smog. Although apical measures of host immunocompetence (antibody to HKSP, virus burdens) were not compromised at the whole animal level, exposure to smog containing a high concentration of O3 following infection did reduce expression of key cytokine genes in the lung. O3 can reduce the severity of influenza infection, independent of virus titers, suggesting that the O3 component of smog may have had the greatest impact in these studies when present for multiple days prior to infection.