RESUMO
The global issue of ozone pollution is becoming increasingly prominent. Previous epidemiological studies suggested that ozone might cause respiratory system damage and increase the risk of mortality from all causes, as well as respiratory diseases such as chronic obstructive pulmonary disease and pneumonia. It results in severe illness and economic burden. Ozone can also lead to lung inflammation, asthma, and chronic obstructive pulmonary disease, increasing susceptibility to pathogen infections and affecting lung development. Some studies have observed upregulated of serum amyloid-like protein A and neutrophil chemotactic keratinocyte chemoattractant in mice exposed to ozone, along with increased percentage of polymorphonuclear leukocytes, total protein, oxidative proteins, lactate, and phospholipids in bronchoalveolar lavage fluid. Ozone exposure could cause enlarged alveolar spaces, granulocyte infiltration, type 2 inflammation, mucus obstruction, and metaplasia of mucus cells in the lungs of mice. When mass concentration of ozone was 1.962 mg/m3, rats showed necrosis and detachment of bronchial ciliated cells, swelling of type 1 alveolar epithelial cells, disruption of endothelium in capillaries, and increased emptying of type 2 alveolar epithelial cells. At a mass concentration of 5.886 mg/m3, monkeys showed degeneration or complete loss of the inner layers of alveolar epithelium, partial pulmonary interstitial edema, and thickening of the blood-air barrier. Ozone could induce oxidative stress, leading to increased oxidative stress response in cells. Particular attention should be paid to personal protection for workers exposed to ozone, researches on the mechanisms related to ozone, as well as the development of corresponding treatments, preventive drugs, and medical devices.