Background: Effects of air pollution on pulmonary toxicity have been reported. The objective of this study was to investigate the regulation of angiotensin system caused by particulate matter (PM) in lungs. We examined the effects of traffic‐related particulate matter with an aerodynamic diameter of <1 μm (PM1), high‐efficiency particulate air (HEPA)‐filtered air, and clean air on the underlying pathways of angiotensin system in lungs after 3 and 6 months of whole‐body exposure in 6‐month‐old Sprague Dawley rats.Results: The rats were exposed to 16.3 ± 8.2 (4.7~68.8) μg/m3 of PM1 during the study period. We observed that angiotensin‐converting enzyme (ACE) was significantly decreased with 6 months of PM1 exposure. Angiotensin II (AngII) was significantly increased after 3‐months exposure of PM1. Angiotensin type 1 (AT1) receptor was significantly decreased with 6 months of PM1 exposure; however, we did not observed significant change in angiotensin type 2 (AT2) receptor or AT1/AT2 ratio in lung tissue after exposure. RAS was activated by 3‐months exposure of PM1 in lung. Conclusions: Our results suggest the pathways related to angiotensin system may be
