Polyaromatic hydrocarbons in pollution: a heart-breaking matter.

Area of Science:

• Environmental Health
• Cardiovascular Toxicology
• Ecotoxicology

Background:

• Air pollution poses significant risks to human cardiovascular function.
• The precise mechanisms driving pollution-induced cardiotoxicity remain incompletely understood.
• Particulate matter (PM) and polycyclic aromatic hydrocarbons (PAHs) are implicated as key mediators.

Purpose of the Study:

• To review epidemiological, clinical, and experimental evidence linking air pollution to cardiovascular dysfunction.
• To elucidate the conserved mechanisms of cardiotoxicity across vertebrate species.
• To establish a framework for understanding the global impact of cardiotoxic pollution.

Main Methods:

• Review of epidemiological studies on air pollution and cardiovascular disease.
• Analysis of experimental evidence from fish exposed to PAHs (e.g., Deepwater Horizon spill).
• Examination of mechanistic knowledge on PM and PAH exposure in mammalian cardiovascular pathologies.

Main Results:

• Growing epidemiological data link air pollution exposure to cardiovascular dysfunction in humans.
• PAHs from oil spills demonstrate cardiotoxic effects in fish, indicating conserved pathways.
• PM and PAH exposure are associated with mammalian atherosclerosis, cardiac hypertrophy, arrhythmias, and contractile dysfunction.

Conclusions:

• Mechanisms of air pollution-induced cardiotoxicity are conserved across vertebrate hearts.
• Understanding these conserved pathways is crucial for addressing the global burden of cardiovascular disease linked to pollution.
• The aryl hydrocarbon receptor (AhR) is a key target in pollution-mediated cardiotoxicity.