Diesel exhaust, which is emitted from on- and off-road sources, is a complex mixture of toxic gaseous and particulate components that results in triggered adverse cardiovascular effects like arrhythmias. We hypothesized that increased risk of triggered arrhythmias one day after diesel exhaust exposure is mediated by airway sensory nerves bearing transient receptor potential (TRP) channels (e.g., TRPA1) that, when activated by noxious chemicals, can cause a centrally-mediated autonomic imbalance and heightened risk of arrhythmia.