# Angiotensin-Converting Enzyme (ACE) Inhibitors and Statins Mitigate Negative Cardiovascular and Pulmonary Effects of Particulate Matter in a Mouse Exposure Model

## TL;DR

This study shows that ACE inhibitors and statins can reduce the harmful effects of air pollution on the heart and lungs in mice.

## Contribution

The study demonstrates that common cardiovascular drugs can mitigate PM2.5-induced damage in a mouse model.

## Key findings

- Atorvastatin and captopril reduced PM2.5-induced systolic blood pressure increases and endothelial dysfunction.
- Both drugs decreased ROS and NOX-2 expression in the vasculature of PM2.5-exposed mice.
- Only captopril showed anti-inflammatory effects in the heart and lung, but neither reduced systemic inflammation.

## Abstract

Particulate matter (PM) is a significant contributor to air pollution-associated negative health effects, and cardiovascular disease patients are more susceptible to air pollution-mediated damage of the heart and vessels. The present study investigated the protective effects against PM-induced cardiovascular damage by classic cardiovascular drugs, as used for the standard therapy of cardiovascular disease patients. Male C57BL/6J mice were exposed to ambient PM2.5 (<2.5 µm) for 3 days with or without treatment with the cholesterol-lowering drug atorvastatin (20 mg/kg/d) or the angiotensin-converting enzyme (ACE) inhibitor captopril (50 mg/kg/d). Both drugs mitigated PM2.5-induced systolic blood pressure increases and partially prevented endothelial dysfunction, as reflected by a mixed effect on endothelial nitric oxide synthase phosphorylation. Both drugs ameliorated reactive oxygen species (ROS) formation and phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX-2) expression in the vasculature of PM2.5-exposed mice. Pulmonary ROS levels showed a minor improvement by the treatments, whereas Nox2 mRNA expression was not diminished. Only captopril showed some anti-inflammatory effects in the heart and lung of PM2.5-exposed mice, whereas both drugs failed to reduce systemic inflammation measured in plasma. These findings offer new insights into potential mitigation strategies for PM2.5-induced cardiovascular complications, particularly for patients at higher cardiovascular risk, like those with coronary artery or ischemic heart disease or hypertension.