Association of benzene exposure and atrial fibrillation in a national cohort: The modifying effect of genetic susceptibility

Background: Exposure to benzene poses significant health risks, with cardiovascular toxicity emerging as a primary adverse effect. However, the exact influence of benzene on the development of atrial fibrillation (AF) remains unclear. The occurrence of AF is influenced by environmental factors and genetic factors that should not be overlooked. Previous studies have found an association between accelerated biological aging and benzene and AF. This study explored the effects of benzene exposure on the risk of incident AF later in life, examining the interaction with genetic susceptibility and the mediating role of accelerated biological aging. Methods: From 2006 to 2010, 432,522 participants in the UK Biobank who were free of cardiovascular disease at baseline were included. The annual average benzene concentrations during the follow-up period were assessed using air dispersion models. AF patients were identified using the International Classification of Diseases 10th Revision (ICD-10) code. Cox proportional hazard models were employed to explore the association between benzene exposure and incident AF. Restricted cubic spline models were utilized to estimate the exposureresponse relationships. The polygenic risk score (PRS) for AF was used to examine the gene–environment interactions related to AF risk. Results: Exposure to benzene significantly increased the risk of AF, with the hazard ratio (95 % confidence interval) for a standard deviation increase in benzene concentration reaching 1.02 (1.00, 1.04). Participants with high benzene exposure and high genetic risk had a greater risk of AF than those with low benzene exposure and low genetic risk (HR, 3.12; 95 % CI, 2.82, 3.46). Accelerated biological aging significantly mediated the association between benzene exposure and AF. Conclusions: Exposure to benzene is associated with an increased risk of AF, particularly in populations at high genetic risk. Accelerated biological aging partially mediated these associations.

Abstract licence: CC BY-NC

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