Host: The Japanese Society of Toxicology
Ozone generators have been exponentially installed in medical institutions for viral inactivation of COVID-19. However, an acceptable concentration of ozone (0.1 ppm) is regulated based on the effects on the healthy people, and toxic effects in the patient with serious respiratory dysfunction is still uncertain. Therefore, the aim of this study is to compare the toxic effects of ozone exposure between a normal mouse and a mouse model of acute respiratory distress syndrome (ARDS). Ozone (0.1 ~ 0.3 ppm) exposure was performed 6 hours/day for 5 consecutive days in BALB/c mouse. ARDS was induced by intranasal administration of lipopolysaccharide 72 hours before data sampling. Percutaneous oxygen saturation (SpO2) was measured by pulse oximeter. Lung tissue, bronchoalveolar lavage fluid (BALF) and hilar lymph nodes (LN) were collected for pathological and immunological evaluations. SpO2 was significantly reduced by ozone exposure in ARDS groups, while there was no influence in normal groups. Ozone exposure also exacerbated the histological evaluation including neutrophil infiltration and epithelial cell necrosis in ARDS groups, while no significant changes were observed in normal groups. In BALF, ozone exposure significantly enhanced cytokine (IL-1β and RANTES) levels in ARDS groups, however, no change was observed in normal groups. Cytokine (IL-5 and IL-17) production in LN was also significantly upregulated by ozone exposure in ARDS groups. Our findings indicate that current acceptable concentration of ozone has a possible adverse effect in the patient with ARDS.