Pollutants, including Organophosphorus and Organochloride Pesticides, May Increase the Risk of Cardiac Remodeling and Atrial Fibrillation: A Narrative Review

Abstract

Highlights: What are the main findings? Abnormally increased concentrations of ingested or inhaled pollutants can lead to cardiac oxidative stress and inflammation. Untreated cardiac inflammation promotes myocardial fibrosis and cardiac arrhythmias. What is the implication of the main findings? Patients hospitalized for acute pesticide poisoning often suffer from episodes of atrial or ventricular fibrillation. Management of pollutant poisoning associated with AF includes detoxification (i.e., gastric lavage) and prompt rhythm control. Atrial fibrillation (AF) is the most common type of cardiac rhythm disorder. Recent clinical and experimental studies reveal that environmental pollutants, including organophosphorus–organochloride pesticides and air pollution, may contribute to the development of cardiac arrhythmias including AF. Here, we discussed the unifying cascade of events that may explain the role of pollutant exposure in the development of AF. Following ingestion and inhalation of pollution-promoting toxic compounds, damage-associated molecular pattern (DAMP) stimuli activate the inflammatory response and oxidative stress that may negatively affect the respiratory, cognitive, digestive, and cardiac systems. Although the detailed mechanisms underlying the association between pollutant exposure and the incidence of AF are not completely elucidated, some clinical reports and fundamental research data support the idea that pollutant poisoning can provoke perturbed ion channel function, myocardial electrical abnormalities, decreased action potential duration, slowed conduction, contractile dysfunction, cardiac fibrosis, and arrhythmias including AF.