David H. Groth

Carcinogenic effects of antimony trioxide and antimony ore concentrate in rats

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.

Carcinogenicity of beryllium: Review of the literature☆

The carcinogenicity of beryllium (Be) is reviewed. At least 17 different senior authors have published 27 different scientific articles which demonstrate the carcinogenicity of 13 different beryllium compounds. Osteogenic sarcomas can be induced in rabbits by the intravenous injection or by the inhalation of Be compounds. Lung cancer can be induced in rats and monkeys by intratracheal injections and inhalation exposures. The first published report on the carcinogenicity of Be was in 1946.

Identification of stainless steel welding fume particulates in human lung and environmental samples using electron probe miciroanalysis

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.

Carcinogenicity of beryllium hydroxide and alloys

Animal experiments are presented which show that Be metal, BeAl alloy, passivated Be metal, and beryllium hydroxide are pulmonary carcinogens in rats. These findings are supported by successful transplantation experiments. In addition, other alloys of Be, VBe12, TiBe12, TaBe12, NbBe12, Be2B, and Be4B were found to produce pulmonary metaplasia, frequently a preneoplastic lesion in rats. Old rats are shown to be more susceptible to the induction of pulmonary metaplasia than young adult rats. These results indicate that a lower dose of Be would be required to produce cancer in old animals compared to young adult animals. A discussion on the lung cancer incidence in beryllium production workers is presented.

Vinyl Chloride Propellant in Hair Spray and Angiosarcoma of the Liver among Hairdressers and Barbers : Case Reports

Abstract Two cases of angiosarcoma of the liver (ASL) are, to the best of our knowledge, the first literature reports of such cases identified among hairdressers and barbers who used hair sprays containing vinyl chloride (VC) as a propellant. The cases were exposed to VC aerosols between 1966 and 1973, for 4–5 year periods. Modeling indicates estimated peak levels of VC exposure ranging from 129 ppm to 1234 ppm, and average exposure ranging from 70 ppm to 1037 ppm, based upon assumptions of use and number of air exchanges per hour. As ASL is a sentinel cancer for exposure to VC, identification of these cases raises concern about the contribution of VC to hepatocellular carcinoma (HCC), a much more common type of liver cancer, as well as other VC-related cancers among hairdressers and barbers. Had manufacturers acted in a responsible manner, VC never would have been introduced as a propellant into consumer products such as hair sprays, pesticides, and paints.

Chronic Effects of Inhaled Amorphous Silicas in Animals

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/m 3 concentrations of three types of synthetic amorphous silicas: fume, gel, and precipitated. Autopsieson 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.

Comparative Changes in Serum Enzyme Levels in Beryllium- or Carbon Tetrachloride-Induced Liver Necrosis

Summary Four serum enzymes (ICD, GOT, GPT, LDH) and one liver enzyme (acid phosphatase) were used to evaluate the difference in the rat response to Be-induced midzonal liver necrosis and CCl4induced centrolobular necrosis. Be produced a maximum elevation of liver free acid phosphatase 8 hr after injection, but the elevation of the serum enzymes ICD, GOT, or GPT were not observed until 48 hr after Be injection. LDH was not elevated at any time period. At equivalent doses in the CCl4-injected animals, serum ICD, GOT, and GPT were all elevated by 48 hr, but no elevation of liver acid phosphatase was observed at any time period. These differences in response indicate a biochemical as well as an anatomical difference between these two types of chemically induced liver necrosis. The authors thank Mr. Lee Bland and Carl Hopper for technical assistance in this study.

An evaluation of the inhalation toxicity of one commercial proteolytic enzyme preparation.

The inhalation toxicity of a commercial proteolytic enzyme preparation containing 12% subtilisin Carlsberg was studied in experimental animals. Guinea pigs that had been pretreated by a series of intradermal injections of the enzyme preparation in saline solution died as a result of a single 6-hour exposure to the enzyme preparation at an air concentraion of 41.2 mg/m-3, while normal guinea pigs and pretreated guinea pigs that were dosed with an antihistamine immediately prior to exposure survived. The 6-hour LC50 for pretreated guinea pigs was determined as 24.7 mg/m-3. Normal rats, normal rabbits, and pretreated rabbits survived exposures to the enzyme preparation at concentrations as high as 36.8 mg/m-3. Pathologic examinations revealed changes only in the lungs of the exposed animals. These pulmonary alterations appear to be reversible. A histamine release is suggested as the primary effect of a secondary exposure to this proteolytic enzyme preparation.