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Fig. 1 | Environmental Health

Fig. 1

From: Potential role of polycyclic aromatic hydrocarbons as mediators of cardiovascular effects from combustion particles

Fig. 1

Possible mechanisms linking PM2.5/ DEP/ OC/ PAH with CVD. Three general lines of causality are suggested: i) Distortion of autonomic nerve endings in the lungs causing loss of vascular control reflexes via the autonomic nervous system (ANS; red), ii) Pulmonary inflammation and “systemic spill over” (green) and iii) direct effects of organic chemicals (OC) and polycyclic aromatic hydrocarbons (PAHs), affecting blood/vascular system directly (blue). Possible links include: oxidative stress, inflammation, vasoconstriction, endothelial dysfunction, coagulation, thrombosis, heart rate, heart rate variability (HRV), redox imbalance, impaired high density lipoproteins (HDL)-function as well as effects during embryonic development - via reactive metabolites, reactive oxygen species (ROS), aryl hydrocarbon receptor (AhR)-genomic and/or non-genomic pathways including [Ca2+]I and G protein-coupled receptors (GPCRs). Partly modified from [3]

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