How is antimony dust deposition caused? Briefly described as follows:
1. Etiology
Antimony pneumoconiosis is a lung disease caused by long-term inhalation of metallic antimony and antimony trioxide fumes during the production process. In industry, antimony is mainly used to make alloys, and its oxides can be made into pigments for use in enamel, ceramics, paints, and rubber industries. The mining of antimony ore, especially during the smelting, refining, and alloy production processes, can produce a large amount of antimony fumes.
2. Pathogenesis
There are different opinions on the role of antimony in causing pneumoconiosis. Karajovic (1957) first reported that among workers exposed to antimony trioxide dust in a smelter in Yugoslavia, 31 cases of antimony pneumoconiosis were found. Subsequently, many scholars reported nearly a hundred cases of antimony pneumoconiosis. Bouffont (1987) reported two cases of lung biopsy specimens from patients diagnosed with antimony dust deposition, where fibrosis was found around the dust lesions. China has abundant antimony reserves, and in the 1960s and 1970s, Guangxi, Guizhou, and Hunan reported more than 300 cases of antimony pneumoconiosis in succession, and conducted in-depth research on the biological effects of antimony. In 1983, Chinese scholars believed that antimony dust has a more serious impact on the lungs than tin dust, and can cause acute or chronic interstitial pneumonia.
There is little pathological data on antimony pneumoconiosis. In 1967, Mecallum reported on a case of a smelter worker who died of lung cancer, where the pathological examination found a large amount of antimony dust deposition around alveolar spaces, alveolar septa, and small blood vessels, as well as a reaction of dust-laden macrophages, without fibrosis. China has reported four cases of pathological changes in smelter workers who were not diagnosed with antimony pneumoconiosis before death, including chronic bronchitis, bullous emphysema, fibrosis around small bronchi and alveolar septa, and dust deposition in hilar lymph nodes. In 1984, several Chinese scholars repeatedly injected antimony dust into rats through the trachea, 50mg per rat each time. Three months after the second dust exposure, nodules in the lungs appeared with reticular fibers but no collagen fibers; after the fourth dust exposure six months later, nodules appeared with collagen fibers; but by nine months, the dust lesions decreased, showing regression or disappearance of lesions, with most of the dust in the lungs being cleared.