Fig. 6.

Proposed pathomechanisms triggered by noise, PM or combined exposure. While PM confers most of its detrimental effects via damage of the lung (inflammation and oxidative stress), noise initiates systemic adverse health effects primarily by causing neuronal activation, cerebral oxidative stress and stress hormone release. The primary target organ damage by PM and noise converges at the cardiovascular level showing additive exacerbation of some functional (endothelial dysfunction) and biochemical markers (oxidative stress by 3-NT, SODs, HO-1). The source of reactive oxygen species (ROS) in the vasculature was not yet entirely identified but may be a mixture of different NADPH oxidase enzymes and mitochondrial ROS sources. The elevated ACE-2 expression in the lungs of PM and noise co-exposed mice may not only increase the risk and severity of COVID-19 infections but also have general effects on cardiovascular health. Scheme was created using Biorender program.