Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction.

Area of Science:

• Environmental Health
• Cardiovascular Toxicology
• Toxicology

Background:

• Benzene is a common environmental pollutant and known carcinogen.
• Cardiovascular toxicity of benzene is not well understood.
• Population studies link benzene exposure to increased heart failure risk.

Purpose of the Study:

• To investigate the effects of benzene exposure on heart failure.
• To determine if benzene exacerbates pressure overload-induced heart failure in mice.

Main Methods:

• Male C57BL/6J mice underwent transverse aortic constriction (TAC) or sham surgery.
• Mice were exposed to benzene (50 ppm) or filtered air for 6 weeks.
• Cardiac function, gene expression (RNA-seq), and neutrophil infiltration were analyzed.
• In vitro studies used benzene metabolites (hydroquinone, catechol) on endothelial cells.

Main Results:

• Benzene exposure significantly worsened cardiac function (reduced fractional shortening and ejection fraction) in TAC mice.
• RNA-seq revealed increased genes related to adhesion, inflammation, and stress response in TAC/benzene hearts.
• Neutrophil infiltration (CD11b+/S100A8+/MPO+) in the heart increased 3-fold with TAC/benzene exposure.
• Benzene metabolites increased P-selectin expression and neutrophil adhesion to endothelial cells in vitro.

Conclusions:

• Benzene exacerbates heart failure in a mouse model of pressure overload.
• Benzene promotes endothelial activation and neutrophil recruitment to the heart.
• This mechanism contributes to benzene-induced cardiovascular toxicity.