This study was initiated because of a suspected increase in incidence of lung cancer in antimony smelter workers in England. Three groups of 8-mo-old Wistar-derived rats (90 males and 90 females per group) were exposed by inhalation to either Sb2O3 [time-weighted average (TWA) 45 mg/m3], Sb ore concentrate (TWA 36 + 40 mg/m3), or filtered air (controls) for 7 h/d, 5 d/wk, for up to 52 wk and sacrificed 20 wk after terminating exposures. Serial sacrifices (5 rats/sex/group) were performed at 6, 9, and 12 mo. Autopsies and histopathological examinations were performed on all animals. The dusts and animal tissues were analyzed for Sb, arsenic, and other inorganic elements by atomic absorption and proton-induced X-ray emission methods. The most significant findings were the presence of lung neoplasms in 27% of females exposed to Sb2O3 and 25% of females exposed to Sb ore concentrate (p less than 0.01). None of the male rats in any group or the female controls developed lung neoplasms. There were no significant differences in incidences of cancer of other organs between exposed and control rats. These results were compared with other published results, including an animal inhalation study with Sb2O3 in which lung tumors were also induced. Higher concentrations of arsenic were found in tissues from female rats than from male rats. For example, arsenic levels in blood of control males, control females, Sb2O3 males, Sb2O3 females, Sb ore males, and Sb ore females were 60, 123, 115, 230, 71, and 165 micrograms arsenic/g dry blood, respectively, 9 mo after initiating exposures.

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Warts remain one of the most common reasons for dermatology and primary care visits, yet no definitive therapy is available. Treatment of pediatric patients adds additional challenges, as the adept provider must effectively manage parents' expectations and patients' fears. This article provides an update on research in the field of viral cutaneous wart therapies with a focus on pediatric patients. Safety issues and potential complications of therapy are also addressed.

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Fisher F344 rats and B6C3F1 mice were exposed to concentrations of 0, 150, 300, 600 and 1200 ppm of dimethylformamide (DMF) for 6 hours a day, 5 days a week for 12 weeks. Detailed clinical observations were obtained weekly and body weights biweekly on all animals. Clinical chemistry and hematology evaluations were made on all rats and approximately half the mice at terminal sacrifice. Gross necropsy examinations were made on all animals. Histopathologic evaluations were conducted on selected tissues of animals of both species at all dose levels. Few overt signs of toxicity were seen in either rats or mice. There was a dose related depression in body weight gain in rats that was significant at the 1200 ppm level from the second week of study onwards. A total of 11 mice died or were sacrificed moribund during the study, 8 from the high dose and 2 from the 600 ppm dose level. Both clinical chemistry (in rats only) and gross necropsy observations, and histopathology of tissues indicate the possibility that liver may be the target in specific organ toxicity. The no-effect DMF dose was below the 150 ppm level for both rats and mice and the maximum tolerated dose was below the 600 ppm level.

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Open lung biopsy specimens from two welders and air samples from their workplace environments were examined with the electron probe microanalyzer. X-ray analysis showed that the majority of particles found in the lung tissue from both workers and in the air samples to be composed of varying amounts of iron, chromium, manganese and nickel, the major components of some types of stainless steel. Based upon these analyses, it was concluded that the majority of the particles in both biopsy specimens were a result of the workplace environment.

Rats, guinea pigs, and monkeys were exposed by inhalation (5.5 to 6 h/day, 5 days/week) for up to 18 months at 15 mg/m3 concentrations of three types of synthetic amorphous silicas: fume, gel, and precipitated. Autopsies on rats were performed after 3, 6, and 12 months of exposure, and on guinea pigs and monkeys after 10 to 18 months of exposure. The most significant finding was the deposition of large quantities of amorphous silica in macrophages in the lungs and tracheal lymph nodes of exposed monkeys. Relatively few or no macrophages containing particles of amorphous silica were found in the lungs and lymph nodes of the guinea pigs and rats. It is also significant that fume silica induced early nodular fibrosis in the lungs of the monkeys. Correlating these histological findings, lung-function studies indicated statistically significant differences in lung volume and ventilatory mechanics measurements between those monkeys exposed to fume silica and the control group. In addition, monkeys exposed to precipitated silica demonstrated significantly lower lung volumes compared with controls, while monkeys exposed to silica gel had significant changes in ventilatory performance and mechanical properties.