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Effects of Photochemically-Aged Atmospheres on Allergic Responses in Mice
Citation:
McGee, M., E. Boykin, Todd Krantz, C. King, J. Krug, N. Modak, C. Wood, Ian Gilmour, AND S. Gavett. Effects of Photochemically-Aged Atmospheres on Allergic Responses in Mice. Society of Toxicology, San Diego, CA, March 22 - 26, 2015.
Impact/Purpose:
The health effects of diverse air pollutants which contribute to the EPA air pollution alert system (code orange,red, purple) may be achieved by any one pollutant (ozone, PM, volatile organic compounds,etc.) reaching the designated action level, and it is not known whether the effects of combined pollutants reaching each of these levels will have a more detrimental effect than the effects of the individual air pollutants. This research begins to ascertain the effects of combined or single pollutants in a new experimental chamber which can mimic realistic pollutant scenarios mimicing smog. The benefits of understanding realistic combinations of airborne pollutants on respiratory health in animal models are substantial in providing insight into potential human health effects.
Description:
Although air pollution is a complex mixture consisting of multiple gaseous and particulate components, current regulations and research approaches often focus on single pollutants. To better assess the impact of air pollution mixtures on respiratory health, we investigated the effects of a smog mixture on allergic airway disease in mice. A photochemical reaction chamber was used to generate smog from a precursor mixture of hydrocarbons and NO which achieved concentrations of 337 µg/m3 secondary organic aerosol, 0.072 ppm O3, and 0.131 ppm NO2. Healthy and house dust mite (HDM)-sensitized (allergic) BALB/cJ mice were exposed 4 hr/day for 1 or 5 days to smog or clean air. Two days after HDM challenge, airway mechanics were tested in anesthetized ventilated mice. Airway resistance following methacholine aerosol challenge was significantly increased in HDM-allergic mice, but smog exposure did not further enhance the response. Bronchoalveolar lavage (BAL) macrophages, eosinophils, and cytokines (IL-4 and IL-5) were also significantly increased in HDM-allergic mice compared to non-allergic mice. Five days of smog exposure induced an increase in macrophages and eosinophils, and 1 day smog exposure induced an increase in BAL lactate dehydrogenase in the HDM-allergic mice, but these differences were not significant. Lung histopathology showed that 5 day smog exposure increased the incidence of intracytoplasmic particulate matter within alveolar macrophages, but did not alter allergic-induced inflammatory changes. No significant effects of allergic challenge or smog treatment were observed on nasal histopathology. Future studies will examine alternative mixtures of smog at different air quality levels to further explore which realistic atmospheres affect the severity of allergic lung disease. (This abstract does not represent U.S. EPA policy.)