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A single exposure to photochemical smog causes airway irritation and cardiac dysrhythmia in mice
Citation:
Hazari, M., R. Chesnutt, K. Stratford, N. Coates, Todd Krantz, C. King, A. Farraj, AND Ian Gilmour. A single exposure to photochemical smog causes airway irritation and cardiac dysrhythmia in mice. Society of Toxicology, San Diego, CA, March 22 - 26, 2015.
Impact/Purpose:
The data presented here shows that a single exposure to photochemical smog causes adverse cardiac and ventilatory effects. This work addresses Agency needs with respect to determining the health effects of air pollution and contributing to the risk assessment process.
Description:
The data presented here shows that a single exposure to photochemical smog causes airway irritation and cardiac dysrhythmia in mice. Smog, which is a complex mixture of particulate matter and gaseous irritants (ozone, sulfur dioxide, reactive aldehydes), as well as components which react with sunlight to form secondary pollutants, has recently been linked to increased risk of adverse cardiopulmonary responses. We hypothesized that a single exposure to photochemical smog would cause cardiac electrical and ventilatory changes in mice. Female C57BL/6 mice were surgically implanted with radiotelemeters for the measurement of heart rate (HR), electrocardiogram (ECG) and heart rate variability (HRV). Following recovery mice were exposed whole-body to either smog or filtered air (FA) for 4hrs. A photochemical reaction chamber was used to generate smog from a precursor mixture of hydrocarbons and nitric oxides which achieved concentrations of 337 µg/m3 secondary organic aerosol, 0.072 ppm O3, and 0.131 ppm NO2. Ventilatory function was assessed before, and one and 24hrs after exposure in a plethysmograph while HR and ECG were measured continuously. Mice exposed to smog experienced a significant increase in HR during exposure when compared to FA; however, there were no differences or changes in ECG or HRV. Exposure to smog caused significant increase in breathing frequency and decreased in inspiratory time (i.e. rapid shallow breathing) and a significant decrease in HR 1hr post-exposure; these effects were gone 24hrs later. Mice exposed to smog also had cardiac dysrhythmia as well as non-conducted p-waves, which were not present in the FA group. The results of this study show that a single exposure to smog causes acute cardiac and ventilatory effects which reverse over time. Although these responses likely do not represent serious or permanent underlying deficits, they clearly indicate the potential toxicity of complex multipollutant mixtures, particularly for those with cardiopulmonary disease. (This abstract does not reflect USEPA policy)