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Effects of Isoprene- and Toluene-Generated Smog on Allergic Inflammation in Mice
Citation:
Gavett, S., M. McGee, A. Ledbetter, J. Dye, Todd Krantz, C. King, Ian Gilmour, AND J. Krug. Effects of Isoprene- and Toluene-Generated Smog on Allergic Inflammation in Mice. Society of Toxicology, Baltimore, MD, March 12 - 16, 2017.
Impact/Purpose:
The effects of complex regional multipollutant mixtures on the expression of disease in susceptible populations are dependent on multiple exposure and susceptibility factors. This study examines the characteristics of complex mixtures that lead to development and exacerbation of acute and chronic disease endpoints in a mouse model of allergic asthma.
Description:
Reactions of organic compounds with nitric oxide (NO) and sunlight produce complex mixtures of pollutants including secondary organic aerosol (SOA), ozone (O3), nitrogen dioxide (NO2), and reactive aldehydes. The health effects of these photochemical smog mixtures in susceptible populations including asthmatics are unclear. We assessed effects of smog generated from mixtures of NO with isoprene (IS) or toluene (TL) on allergic inflammatory responses in Balb/cJ mice. House dust mite (HDM)-sensitized or control mice were all challenged with HDM intranasally 1 d prior to whole-body inhalation exposure to IS (chamber average 509 ppb NO2, 246 ppb O3, and 160 g/m3 SOA), TL (217 ppb NO2, 129 ppb O3, and 376 g/m3 SOA), or HEPA-filtered air (4 h/d for 2 days). Mice were necropsied within 3 h after the second exposure (2 d post-HDM challenge). Assessment of breathing parameters during exposure with double-chamber plethysmography showed a trend for increased specific airway resistance and decreased minute volume during the second day of TL exposure in both non-allergic and HDM-allergic mice. HDM-allergic air-exposed mice had significant increases in numbers of bronchoalveolar lavage (BAL) alveolar macrophages (AM) and eosinophils (EO), and trends for increases in BAL indices of lung injury in comparison with non-allergic air-exposed mice. Exposure to either IS or TL attenuated the increases in AM, EO, and lung injury markers in HDM-allergic mice. The results of this study suggest that photochemically-derived smog from IS or TL precursors may inhibit markers of allergic inflammation, but worsen some indices of pulmonary function. These findings are consistent with those reported with mixtures of O3 and the cyclic terpene limonene which inhibited allergic lung inflammation in mice (Hansen, J Immunotoxicol 2016), suggesting that complex interactions of pollutants present in smog may provide both detrimental and protective effects on pulmonary responses. (This abstract does not reflect USEPA policy)