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Photochemical Reaction Altered Cardiac Toxicity of Diesel Exhaust Inhalation
Citation:
Tong, H., R. McIntosh-Kastrinsky, K. Sexton, AND D. Diaz-Sanchez. Photochemical Reaction Altered Cardiac Toxicity of Diesel Exhaust Inhalation. American Thoracic Society (ATS) Meeting, Denver, CO, May 15 - 20, 2015.
Impact/Purpose:
This study demonstrated the cardiac toxicity of diesel exhaust and photochemical reaction processes might alter the toxicity.
Description:
Rationale: Epidemiological studies have indicated an association between urban air pollution exposure and cardiovascular morbidity and mortality. The present study was designed to evaluate the cardiac effects of inhaled diesel exhaust and compared with photochemically altered diesel exhaust in a murine model.Methods: Four-month old mice were exposed to freshly emitted diesel exhaust (DE), photochemically aged DE in an outdoor irradiation chamber, or filtered air (FA) for 4 hours. DE was generated from 1980 Mercedes-Benz engine. Aged DE was generated by photochemical reaction of DE with Urban Mixture in a photochemical reaction chamber. The Urban Mixture composition (50+ hydrocarbons) is based on EPA analyses of 40+ cities and was used to create two test mixtures of different concentrations but of the same composition of the primary organics. Eight hours after exposure cardiac effects were assessed by Langendorff-method of cardiac perfusion. Isolated mouse hearts were perfused for 25 min prior to 20 min of global ischemia followed by 2 hours of reperfusion. Left ventricular developed pressure (LVDP), heart rate, and cardiac contractility were measured at baseline and 60 min after reperfusion.Results: Hearts from the DE-exposed groups had significantly lower baseline LVDP (79.7±10.7 cmH2O) compared to FA-group (157.7±21.3 cmH2O; p<0.01). Baseline left ventricular contractility was also significantly depressed by the DE inhalation. The maximum +dP/dt was significantly lower in the DE groups (3127±561 cmH2O/s vs. 5421±868 cmH2O/s in the FA group; p<0.05) and the minimum –dP/dt was also decreased by the DE inhalation (-2300±353 cmH2O/s vs. -4023±588 cmH2O/s for FA; p<0.05). Aged DE inhalation also resulted in significant reduction of baseline LVDP (102.5±11.2 cmH2O; p<0.05) but without effects on the cardiac contractility. There was no statistically significant difference of heart rate, coronary artery flow rate, and recovery of cardiac function after ischemia/reperfusion in the exposed groups compared to FA control. Conclusions: This study demonstrated that inhalation of freshly emitted DE significantly decreased baseline LVDP and cardiac contractility in mice, and aged DE inhalation had less reduction of LVDP. This study suggests that the cardiac toxicity of DE may be influenced by the photochemical reaction processes. This abstract does not necessarily reflect US EPA policy.