To investigate whether the exposure to fine particulate matter (PM2.5) in a rat model can impair erectile function and the possible mechanism. Sprague-Dawley rats were distributed into 4 groups (n = 9 each): 1 control group and 3 groups exposed to different levels of PM2.5. Rats were exposed to PM2.5 (0.0 [saline control], 0.8, 1.6, and 3.2 mg/rat). After exposure period, the ratio of maximum intracavernosal pressure to mean arterial pressure, molecular-biological indicators in corpus cavernosum tissue and plasma, and the pathologic changes of the lung tissue and penile tissue were detected and compared between the control group and the 3 exposure groups. The ratio of maximum intracavernosal pressure to mean arterial pressure in 2 groups exposed to PM2.5 was significantly lower than that of the control group only (P <.05). Exposure to PM2.5 could trigger the significant increase of plasma malondialdehyde, vascular endothelial growth factor, C-reactive protein, and tumor necrosis factor-α in experimental groups than that of the control group (P <.05). Expression of endothelial nitric oxide synthase (NOS), neuronal NOS, cyclic guanosine monophosphate, NOS activity, and content of reactive oxygen species in penile tissue were higher than that of the control group in a dose-response way (P <.05). The function of penile erection is impaired by exposure to PM2.5. The decrease in the expression of endothelial NOS and NOS activity in penile cavernous tissue caused by systemic inflammatory and oxidative stress status induced by exposure to PM2.5 may be one of the important risk factors of erectile dysfunction. Copyright © 2016 Elsevier Inc. All rights reserved.