Figure 4.

Mechanisms Underlying PM-Induced Cardiovascular Disease

Inhaled PM localizes within pulmonary tissues, eliciting oxidative stress and systemic inflammation. This in turn triggers secondary effector pathways including the activation of the HPA axis, platelet activation, autonomic dysfunction, and the generation of biological intermediates such as modified phospholipids. These pathways result in endothelial and vascular injury, atherothrombosis, inflammation, epigenomic changes, and ultimately lead to the development of cardiovascular disease. HPA = hypothalamic-pituitary-adrenal.