On the pulmonary tumorigenicity of arsenic trisulfide and calcium arsenate in hamsters.

The pulmonary tumorigenicity of arsenic trisulfide and calcium arsenate was explored following 15 intratracheal instillations in male Syrian golden hamsters at weekly doses of about 3 mg/kg body weight (as arsenic). One lung adenoma appeared in 28 animals examined in the arsenic trisulfide group and 4 adenomas in 35 animals surviving the treatment with calcium arsenate. No adenomas were seen in 26 animals instilled with the vehicle (0.9% saline solution). The results show that calcium arsenate is tumorigenic (P less than 0.05), while the evidence is inconclusive for arsenic trisulfide.

Carcinomas of the respiratory tract in hamsters given arsenic trioxide and/or benzo[a]pyrene by the pulmonary route.

The pulmonary carcinogenicity of arsenic trioxide (As) alone and in combination with benzo[a]pyrene (BP) was studied in male Syrian golden hamsters given 15 weekly intratracheal instillations. The animals were divided into four groups: As, BP, As + BP, and controls. At each instillation about 3 mg/kg body wt as arsenic and/or 6 mg/kg body wt of BP was administered. All groups received a carrier dust (charcoal carbon), which increased the lung retention of arsenic, as well as sulfuric acid. Carcinomas of the larynx, trachea, bronchi, or lungs were found in 3, 17, and 25 of 47, 40, and 54 animals examined in the As, BP, and As + BP groups. No respiratory tract carcinomas were found in 53 control animals. The incidence of pulmonary adenomas, papillomas, and adenomatoid lesions was markedly higher in the As group than in the control group (P less than 0.01). Taken together the data provide strong evidence that arsenic trioxide can induce lung carcinomas. Furthermore, there was some evidence of a positive interaction between arsenic and BP in relation to adenomatous lung tumors, which could be of importance for the synergism between arsenic and smoking observed in smelter workers.

Ochratoxin A as the cause of spontaneous nephropathy in fattening pigs.

At a number of slaughters nephropathy and high ochratoxin A contents in kidneys have been observed in fattening pigs from two Swedish farms. In one herd the source of contamination was barley grown on the home farm and stored under such conditions that the growth of fungal species (Penicillium verrucosum var. verrucosum) producing ochratoxin A occurred, with the subsequent formation of the toxin. In this case high ochratoxin A levels in fattening pigs were found during a period of about 18 months. In the second herd, where compounded feed was used, it was impossible to locate the source of contamination. It was presumed that a consignment of feed was damaged by rain during storage at the farm. Ochratoxin A was found in fattening pigs from this herd for a period of about 2 months. Ochratoxin A appeared in the kidneys of all investigated pigs. In some animals the livers, whole blood, and plasma were analyzed, too. The livers contained somewhat lower amounts of ochratoxin A than the kidneys, whereas the content in whole blood and plasma, respectively, was 5 and 13 times greater. Kidneys spontaneously contaminated with ochratoxin A, when stored for 10 months at -70 degrees C, showed no systematic decrease in toxin content.