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Morphology of neoplastic lesions induced by 1,3-butadiene in B6C3F1 mice.

1,3-Butadiene (CAS No. 106-99-0) was studied for potential carcinogenicity and chronic toxicity by inhalation in B6C3F1 mice. Groups of 50 mice of each sex were exposed to 0, 625, or 1250 ppm 1,3-butadiene for 6 hr/day, 5 days/week for 60 weeks (male) or 61 weeks (female). The study was scheduled for 104 weeks of exposure but was terminated early because of reduced survival related to induction of a variety of tumors in 1,3-butadiene-exposed mice. A second chronic inhalation study was conducted in which male and female mice were exposed to 0, 6.25, 20, 62.5, 200, or 625 ppm for up to 2 years. Additional groups of 50 male mice were exposed to 625 ppm for 13 or 26 weeks, 312 ppm for 52 weeks, or 200 ppm for 40 weeks, then held without exposure until scheduled sacrifice 104 weeks after initial exposure. 1,3-Butadiene-exposed mice from both studies had increased incidences of malignant lymphomas that were observed as early as week 20 in the first study and week 23 in the second study. The lymphomas were primarily lymphocytic and originated in the thymus, although generalized lymphoma was often present. Exposed mice in both studies developed cardiac hemangiosarcomas that were observed as early as week 32 in the first study and week 41 in the second study. Also present were foci of endothelial hyperplasia in the myocardium that were regarded as early evidence of developing hemangiosarcoma. Alveolar epithelial hyperplasia, alveolar/bronchiolar adenomas and alveolar/bronchiolar carcinomas represented the spectrum of proliferative lung lesions induced by exposure to 1,3-butadiene in both studies. Exposure-related proliferative forestomach lesions observed in both studies included epithelial hyperplasia, squamous cell papillomas, and squamous cell carcinomas. 1,3-Butadiene-exposed female mice in both studies developed mammary gland neoplasms at increased incidences. Most of the mammary tumors were pleomorphic adenocarcinomas, but several adenoacanthomas were also seen. Granulosa cell tumors of the ovary were exposure-related neoplasms in both studies. Occasionally the granulosa cell tumors were malignant as evidenced by vascular invasion or pulmonary metastasis. Although there was an increased incidence of hepatocellular neoplasms in exposed females in the first study, by week 65 of the second study there was not evidence of a clear response of liver neoplasms. The preliminary results of the second study indicate there was induction of tumors similar to those seen in the first study but occurring in response to lower concentrations of 1,3-butadiene.

Animals↗

Carcinogenicity and chronic toxicity of para-chloronitrobenzene in rats and mice by two-year feeding.

Carcinogenicity and chronic toxicity of para-chloronitrobenzene (p-CNB) were examined by feeding diets containing p-CNB to rats and mice of both sexes for two years. The dietary concentration of p-CNB was 0 (control), 40, 200, or 1000 ppm (w/w) for rats and 0, 125, 500, or 2000 ppm for mice. Survival rates of the high-dosed male rats and male mice were significantly decreased compared with those of the respective controls, and this was attributed to the increased number of cancer deaths. Therefore, the high-dose levels were considered not to exceed the maximum tolerated dose. Significant decreases in red blood cell counts and hematocrit value and an increase in mean corpuscular volume were noted in the p-CNB-fed rats and mice. Nonneoplastic splenic lesions were characterized by capsule hyperplasia, fibrosis, fatty metamorphosis, and increased extramedullary hematopoiesis in rats, and congestion, increased extramedullary hematopoiesis, hemosiderin deposition, and ossification in mice. Incidences of fibromas, fibrosarcomas, osteosarcomas, sarcomas (NOS), and hemangiosarcomas in males and fibrosarcomas in females were significantly increased in the spleen of high-dosed rats. The most frequently observed splenic tumor was fibrosarcomas, followed by fibromas. The tumor incidences were increased in a dose-related manner and were more prevalent in males than in females. The malignant tumors metastasized mainly to the liver, peritoneum, and pancreas. Adrena/medullary hyperplasia and pheochromocytomas were significantly increased in the p-CNB-fed females. No tumor was induced in any of the p-CNB-fed mice of either sex except hepatic hemangiosarcomas in the 2000 ppm-fed females. Causative factors of p-CNB-induced carcinogenicity and chronic toxicity are discussed in light of the subchronic and chronic hematotoxicity reported in our present and previous studies and in the literature.

Administration, Oral↗

Evaluation of ifosfamide for treatment of various canine neoplasms.

lfosfamide (3-[2-chloroethyl]-2[(2 chloroethyl)amino]tetrahydro-2H-1,3,2-oxazaphosphorine 2-oxide) is an alkylating agent with a broad spectrum of antitumor activity. The efficacy and toxicity of ifosfamide were evaluated in 72 dogs with spontaneously occurring tumors. Forty dogs (56%) had lymphoma, 31 (43%) had sarcomas, and 1 had a metastatic carcinoma. Five dogs received ifosfamide at dosages <350 mg/m2 IV. Neither toxicity nor response were observed, and the remaining dogs received ifosfamide at 350 mg/m2 (n = 18) and 375 mg/m2 body surface area IV (n = 49). Saline diuresis and the thiol compound mesna were used to prevent urothelial toxicity. Fifty-two dogs had measurable tumors and could be evaluated for response. Complete responses were seen in 1 dog with metastatic leiomyosarcoma of the urinary bladder and in 1 dog with metastatic cutaneous hemangiosarcoma. One dog with lymphoma had a partial response for 112 days. Six dogs with splenic hemangiosarcoma received ifosfamide postsplenectomy and their median survival time was 147 days. The acute dose limiting toxicity was neutropenia 7 days after administration of ifosfamide. The median and mean neutrophil counts 7 days after ifosfamide at 350 mg/m2 were 2,035 cells/microL and 4,773 cells/microL, respectively (n = 12). The median and mean neutrophil counts 7 days after ifosfamide at 375 mg/m2 were 2,500 cells/microL and 3,594 cells/microL, respectively (n = 37). No dog developed clinical or microscopic evidence of hemorrhagic cystitis. Ifosfamide appears safe to use in tumor-bearing dogs, and the evaluation of combination chemotherapy protocols that include ifosfamide should be considered.

Animals↗

Acute hemoperitoneum in horses: a review of 19 cases (1992-2003).

The medical records of 19 horses with acute hemoperitoneum were reviewed. The causes for the hemoperitoneum were idiopathic (8 horses), splenic hematoma with capsular tear (7), bleeding from the reproductive tract (3), multicentric hemangiosarcoma (1), and systemic amyloidosis (1). The affected horses were between 4 and 32 years of age (median 11.5 years). The most consistent findings on initial examination were depression, tachycardia, tachypnea, pale mucous membranes, prolonged capillary refill time, colic, and abdominal discomfort. Less common clinical signs included abdominal distention, profuse sweating, ataxia, and broad ligament mass palpated on rectal examination. Clinicopathologic abnormalities commonly detected were anemia, neutrophilia, lymphopenia, thrombocytopenia, hypoproteinemia, hypocalcemia, azotemia, increased creatinine kinase, and sorbitol dehydrogenase activity. Hemoperitoneum was diagnosed on the basis of abdominocentesis, transabdominal ultrasonography, and postmortem examination. Sixteen horses were treated, and 3 horses were euthanized at owners' request because of severe clinical signs. The treatment consisted of the administration of intravenous fluids, plasma or blood transfusion, nonsteroidal drugs, antimicrobial drugs, and antifibrinolytic and procoagulant agents. Rapid clinical deterioration was observed in 2 horses, necessitating euthanasia. The remaining 14 horses survived the abdominal bleeding (survival rate 74%) and were discharged 3-15 days (median 7.0 days) after presentation. Postmortem examination of the 6 nonsurvivors showed massive abdominal hemorrhage from splenic hematoma with capsular tear (2 horses), multicentric hemangiosarcoma with liver rupture (1), systemic amyloidosis with splenic hematoma and capsular tear (1), and bilateral ruptured ovarian hematomas (1). In one horse, no origin of the bleeding could be determined during postmortem examination.

Animals↗

Frequency of and risk factors associated with lingual lesions in dogs: 1,196 cases (1995-2004).

OBJECTIVE: To categorize histologic lesions affecting the tongue, determine the frequency with which they develop, and identify risk factors associated with their development in dogs. DESIGN: Retrospective case series. ANIMALS: 1,196 dogs. PROCEDURES: Diagnostic reports of lingual biopsy specimens from dogs evaluated from January 1995 to October 2004 were reviewed. RESULTS: Neoplasia comprised 54% of lingual lesions. Malignant tumors accounted for 64% of lingual neoplasms and included melanoma, squamous cell carcinoma, hemangiosarcoma, and fibrosarcoma. Large-breed dogs, especially Chow Chows and Chinese Shar-Peis, were at increased risk for melanoma. Females of all breeds and Poodles, Labrador Retrievers, and Samoyeds were more likely to have squamous cell carcinomas. Hemangiosarcomas and fibrosarcomas were commonly diagnosed in Border Collies and Golden Retrievers, respectively. Benign neoplasms included squamous papilloma, plasma cell tumor, and granular cell tumor. Small-breed dogs, especially Cocker Spaniels, were at increased risk for plasma cell tumors. Glossitis accounted for 33% of diagnoses; in most cases, the inciting cause was not apparent. Whereas large-breed dogs were more likely to have lingual neoplasia, small-breed dogs were more likely to have glossitis. Calcinosis circumscripta accounted for 4% of lingual lesions and predominately affected young large-breed dogs. The remaining submissions consisted mostly of various degenerative or wound-associated lesions. CONCLUSIONS AND CLINICAL RELEVANCE: The frequency of lingual lesions was not evenly distributed across breeds, sexes, or size classes of dogs. Veterinarians should be aware of the commonly reported lingual lesions in dogs so that prompt diagnosis and appropriate management can be initiated.

Age Factors↗

Indications and Role of Liver Transplantation for Malignant Tumors.

PURPOSE: The indication for liver transplantation in malignant liver tumors has been controversial due to disappointing results and shortage of donor organs. The authors evaluated the experience and results of a single center in order to define present indications and selection criteria in hepatobiliary malignancy. PATIENTS AND METHODS: Retrospective analysis of 212 patients who underwent liver transplantation for malignant tumors between 1972 and 1995: Primary hepatobiliary tumors: hepatocellular carcinoma, n = 124 (with underlying cirrhosis, n = 86; fibrolamellar subtype, n = 8); intrahepatic bile duct (cholangiocellular) carcinoma, n = 24; proximal bile duct carcinoma, n = 29; other uncommon entities (n = 15); secondary liver tumors: neuroendocrine, n = 11, and nonendocrine, n = 9. RESULTS: Survival rates in primary liver cancer were correlated to International Union Against Cancer (UICC) tumor stage. For hepatocellular and proximal bile duct carcinoma significantly better outcome was found in UICC-tumor stage I and II versus III and IV. No long-term survival was found after transplantation for intrahepatic bile duct carcinoma, hemangiosarcoma and nonendocrine liver metastases. Comparison of transplant and resected patients with hepatocellular carcinoma stage I and II with underlying cirrhosis showed better survival after transplantation: 1-, 3-, 5-year survival rate of 83.3% versus 76.9%, 75.8% versus 44.0%, 60.6% versus 44.0%, and median survival 96.5 versus 23.2 months. Although this difference was not significant, no patient died from tumor recurrence in the transplant group versus three in the resection group. DISCUSSION AND CONCLUSIONS: Patients with malignant tumors can be selected for transplantation with predictable likelihood for long-term survival. According to the present data, liver transplantation can be considered in unresectable UICC-stage II hepatocellular and proximal bile duct carcinoma, the uncommon entities fibrolamellar carcinoma, epitheliod hemangioendothelioma and hepatoblastoma as well as liver metastases from neuroendocrine tumors. UICC-stage II and IV hepatocellular carcinoma as well as intrahepatic bile duct carcinoma, hemangiosarcoma and metastases from nonendocrine tumors should be excluded from transplantation alone. For hepatocellular carcinoma, multimodality treatment protocols have had a proven impact on the prevention of early recurrence and prolongation of survival. There is evidence that liver transplantation in still resectable hepatocellular carcinoma with underlying cirrhosis might be more appropriate in order to cure the cancer-bearing disease.

Journal Article↗

Comparative stochastic effects of inhaled alpha- and beta-particle-emitting radionuclides in beagle dogs.

The stochastic effects of inhaled, insoluble particles of alpha- or beta-particle-emitting radionuclides were compared in dogs. Male and female beagle dogs were exposed briefly by nasal inhalation to relatively insoluble aerosols of (239)PuO(2) or (144)Ce in fused aluminosilicate particles (FAP) and observed for cancer for their lifetimes. The initial lung burden and retention of each radionuclide was determined by whole-body counting of the emissions from (144)Ce-(144)Pr- or (169)Yb-labeled (239)PuO(2). Lung doses were calculated for each dog from these data. The lung doses ranged from 0.21 to 1200 Gy for (144)Ce FAP and 1.6 to 58 Gy for (239)PuO(2). Dogs with doses to the lung of about 60 Gy or greater from (144)Ce or about 2 Gy or greater from (239)PuO(2) had an increased incidence of lung carcinomas. In dogs exposed to (144)Ce FAP, three organs were targets for neoplasia: lung, tracheobronchial lymph nodes, and heart. The insoluble FAP carried to the lymph nodes draining the lung delivered high radiation doses to the nodes and adjacent heart, resulting in hemangiosarcomas of these organs. In the lung, high radiation doses induced hemangiosarcomas and carcinosarcomas. At lower doses, carcinomas of various histological patterns were induced in the lung. In dogs exposed to (239)PuO(2), the lung was the sole target organ for neoplasia. Nearly all of these neoplasms were carcinomas of various histological patterns. These results indicated that relatively low doses of alpha-particle radiation can induce pulmonary cancers, but relatively large doses of beta-particle radiation are required. In addition, inhaled beta-particle emitters can also induce cancers in lung-associated lymph nodes and heart at these larger absorbed radiation doses.

Administration, Inhalation↗

1998 results of the first series of follow-up studies on Japanese thorotrast patients and their relationships to an autopsy series.

The 1998 survey of the first series of epidemiological studies of Japanese Thorotrast patients revealed that 18 (6.9%) were alive and 244 (93.1%) had died among 262 war-wounded veterans to whom Thorotrast had been administered intravascularly. Of 1,630 age- and sex-matched controls, 525 (32.2%) were alive and 1,105 (67.8%) had died. These results indicated a shortening of the life span in patients who had received Thorotrast compared to their controls. Of the patients in the Thorotrast group, the main causes of death were liver malignancies (79, 30.2%), liver cirrhosis (20, 7.6%), blood diseases (9, 3.4%), and cancers of the extrahepatic bile duct (5, 1.9%). Statistical analyses by the chi(2) test and estimation of the relative risk (risk ratio) showed that the incidences of these disorders were significantly higher in the Thorotrast group than in the controls. In the 54-year period from 1945 to 1998, our autopsy series was enlarged to include 398 individuals: 386 injected with Thorotrast intravascularly and 12 injected by other routes. Results of analyses of the 386 autopsy cases given Thorotrast intravascularly were as follows: 263 cases (68.1%) of liver malignancies, 28 cases (7.3%) of liver cirrhosis, 29 cases (7.5%) of blood diseases, 16 cases (4.1%) of lung cancer, 4 cases (1.0%) of malignant peritoneal tumors, 2 cases (0.5%) of bone sarcomas, and 1 case (0.3%) of hemangiosarcoma of the spleen. The relative risks of liver malignancies, blood diseases, bone sarcomas, malignant peritoneal tumors, and hemangiosarcoma of the spleen manifested significantly higher ratios in the Thorotrast autopsy cases (ratio of proportion) than in the autopsy control cases. Histological studies of these autopsied cases revealed that Thorotrast-induced liver malignancies showed remarkable differences in the proportions of histological types of tumors from those of non-Thorotrast liver malignancies since 1975. However, in this survey, we noted a remarkable increase in the incidence of liver malignancy of multiple histological types compared to that in histological controls. Based on the results of our 1998 survey, we estimated attributable risks of Thorotrast-inducedliver malignancies and blood diseases in the life span. Results showed 523 liver malignancies per 10(4) person Gy and 150 blood diseases per 10(4) person Gy for Japanese male Thorotrast carriers (wasted dose 10 years).

Adolescent↗

Toxicology and carcinogenesis studies of o-nitrotoluene sulfone (CAS no. 88-72-2) in F344/N rats and B6C3F(1) mice (feed studies).

UNLABELLED: [structure: see text] o-Nitrotoluene is used to synthesize agricultural and rubber chemicals, azo and sulfur dyes, and dyes for cotton, wool, silk, leather, and paper. o-Nitrotoluene was nominated for study by NIOSH and the NTP based on its considerable human exposure as well as the absence of long-term studies of carcinogenicity in rodents. Male and female F344/N rats and B6C3F1 mice were exposed to o-nitrotoluene (greater than 99% pure) in feed for 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, rat and mouse bone marrow cells, and mouse peripheral blood erythrocytes. 2-YEAR STUDY IN RATS: In the core study, groups of 60 male and 60 female rats were fed diets containing 625, 1,250, or 2,000 ppm o-nitrotoluene (equivalent to average daily doses of approximately 25, 50, or 90 mg o-nitrotoluene/kg body weight to males and 30, 60, or 100 mg/kg to females) for 105 weeks. In a 3-month stop-exposure study, groups of 70 male rats were fed diets containing 2,000 or 5,000 ppm o-nitrotoluene (equivalent to average daily doses of approximately 125 or 315 mg/kg) for 13 weeks followed by undosed feed for the remainder of the study. A group of 70 male rats receiving undosed feed served as a control group for both male rat studies; 60 female rats receiving undosed feed were the control group for the female core study. Ten control males and 10 males from each stop-exposure group were sacrificed at 3 months. Survival, Body Weights, and Feed Consumption: All 2,000 ppm core study, all 5,000 ppm stop-exposure, and all but three core study 1,250 ppm male rats died before the end of the studies. Survival of 625 ppm core study and 2,000 ppm stop-exposure males and of 2,000 ppm females was significantly less than that of the controls. Mean body weights of all exposed groups of males except the 625 ppm group were generally less than those of the controls throughout the study. Mean body weights of 2,000 ppm females were less than those of the controls during year 2 of the study. Feed consumption by exposed groups of rats was similar to that by the controls. Biomarkers of Exposure: Three urinary metabolites were followed during the study as biomarkers of exposure. The ratios of o-nitrobenzoic acid to creatinine and of o-nitrobenzylmercapturic acid to creatinine determined at 2 weeks and at 3, 12, and 18 months were linearly related to exposure concentration in males and females. The ratio of o-aminobenzoic acid to creatinine was not related to exposure concentration. Pathology Findings: The incidences of malignant mesothelioma in male rats occurred with positive trends in both the core and stop-exposure studies and were significantly greater in exposed groups than in the controls. Incidences of subcutaneous skin neoplasms (fibroma, fibrosarcoma, and lipoma) were increased in exposed groups of males, while the incidences of fibroma or fibrosarcoma (combined) were increased in exposed females. In all exposed groups of males and females except 2,000 ppm core study males, the incidences of mammary gland fibroadenoma were significantly increased. The incidences of mammary gland hyperplasia were significantly increased in 625 and 1,250 ppm females. Increased incidences of mesothelioma, skin neoplasms, and mammary gland fibroadenoma in the stop-exposure males indicated that 3 months of dosing were sufficient to produce a carcinogenic effect. Liver weights of 5,000 ppm stop-exposure males were significantly greater than those of the controls at 3 months. The incidences of hepatocellular adenoma in 2,000 ppm core study males and females and of hepatocellular adenoma or carcinoma (combined) in 2,000 ppm core study and 5,000 ppm stop-exposure males were significantly increased. Cholangiocarcinoma occurred in three 5,000 ppm stop-exposure males, and a single hepatocholangiocarcinoma occurred in a 625 ppm male and in a 2,000 ppm core study male. Nonneoplastic lesions of the liver included eosinophilic, mixed cell, and clear cell foci in exposed groups of males and females and mixed cell infiltrate in exposed males and basophilic focus in exposed females. The incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) were significantly increased in 5,000 ppm stop-exposure males, as were alveolar/bronchiolar hyperplasia in most exposed groups of males and females. The incidences of hematopoietic cell proliferation of the spleen and of hyperplasia of the mandibular lymph node (females) and bone marrow were increased in exposed groups of males at 3 months and/or 2 years and in exposed groups of females at 2 years. The incidences of mononuclear cell leukemia were significantly decreased in all groups of males exposed to 1,250 ppm or greater and in all exposed groups of females; the incidence of testicular interstitial cell adenoma was significantly decreased in 5,000 ppm stop-exposure males. 2-YEAR STUDY IN MICE: Groups of 60 male and 60 female mice were fed diets containing 0, 1,250, 2,500, or 5,000 ppm o-nitrotoluene (equivalent to average daily doses of approximately 165, 360, or 700 mg/kg to males and 150, 320, or 710 mg/kg to females) for 105 weeks. Survival, Body Weights, and Feed Consumption: All 2,500 and 5,000 ppm males died before the end of the study. Survival of 1,250 ppm males and 5,000 ppm females was significantly less than that of the controls. Mean body weights of exposed males and 5,000 ppm females were generally less than those of the controls throughout the study, and those of 2,500 ppm females were less during the second year of the study. Feed consumption by 5,000 ppm males was less than that by the controls. Biomarkers of Exposure: Three urinary metabolites were followed during the study as biomarkers of exposure. The ratios of o-nitrobenzoic acid to creatinine determined at 2 weeks and at 3, 12, and 18 months were linearly related to exposure concentration in males and females. The concentrations of o-nitrobenzylmercapturic acid and o-aminobenzoic acid were below the limit of quantitation at most time points. Pathology Findings: The incidences of hemangiosarcoma in all exposed groups of males and in 5,000 ppm females were significantly greater than those in the controls. Large intestine (cecum) carcinomas were observed in all exposed groups except 5,000 ppm males. The incidences of hepatocellular neoplasms were significantly increased in 2,500 and 5,000 ppm females. Nonneoplastic liver lesions including eosinophilic and basophilic foci and minimal to mild necrosis were enhanced in exposed males and females. Also present were focal hepatocyte syncytial alteration in exposed males and hepatocyte necrosis and focal hepatocyte cytoplasmic vacuolization in 5,000 ppm females. Renal tubule pigmentation occurred more frequently in exposed groups of males and in 5,000 ppm females than in the controls. Olfactory epithelial degeneration occurred in every male and female mouse exposed to 2,500 or 5,000 ppm, and the severity of this lesion increased with increasing exposure concentration. GENETIC TOXICOLOGY: o-Nitrotoluene was not mutagenic in any of several strains of S. typhimurium, with or without metabolic activation enzymes (S9). Sister chromatid exchanges were significantly increased in cultured Chinese hamster ovary cells following exposure to o-nitrotoluene in the presence of S9; an equivocal response was seen without S9. o-Nitrotoluene did not induce chromosomal aberrations in cultured Chinese hamster ovary cells, with or without S9. o-Nitrotoluene did not induce a significant increase in the frequency of micronuclei in bone marrow polychromatic erythrocytes of male rats or male mice when administered by intraperitoneal injection. Results of a peripheral blood micronucleus test were equivocal for male mice and negative for female mice administered o-nitrotoluene in feed for 13 weeks. CONCLUSIONS: Under the conditions of these studies, there was clear evidence of carcinogenic activity* of o-nitrotoluene in male rats based on increased incidences of malignant mesothelioma, subcutaneous skin neoplasms, mammary gland fibroadenoma, and liver neoplasms. The increased incidences of lung neoplasms in male rats were also considered to be exposure related. There was clear evidence of carcinogenic activity of o-nitrotoluene in female rats based on increased incidences of subcutaneous skin neoplasms and mammary gland fibroadenoma. The increased incidence of hepatocellular adenoma in female rats was also considered to be exposure related. There was clear evidence of carcinogenic activity of -o-nitrotoluene in male and female mice based on increased incidences of hemangiosarcoma, carcinoma of the large intestine (cecum), and hepatocellular neoplasms (females only). Exposure to o--nitrotoluene caused increased incidences of nonneoplastic lesions of the mammary gland (females only), liver, bone marrow, spleen, lung, and mandibular lymph node (females only) in male and female rats and of the liver, kidney, and nose in male and female mice. Decreased incidences of mononuclear cell leukemia occurred in exposed groups of rats; the incidence of testicular interstitial cell adenoma was decreased in exposed male rats. [tables: see text]

Administration, Oral↗

NTP Toxicology and Carcinogenesis Studies 2-Butoxyethanol (CAS NO. 111-76-2) in F344/N Rats and B6C3F1 Mice (Inhalation Studies).

2-Butoxyethanol is a member of a family of ethylene glycol monoalkyl ethers. It is used extensively as a solvent in surface coatings such as lacquers, enamels, varnishes, and latex paint; in paint thinners, paint stripping formulations, and inks; and in degreasers and industrial and household cleaners. 2-Butoxyethanol was nominated for study because of its widespread use in industrial and consumer applications, the potential for exposure to workers and the general population, and the absence of chronic toxicity data. Male and female F344/N rats and B6C3F1 mice were exposed to 2-butoxyethanol (greater than 99% pure) by inhalation (primary route of human exposure) for 14 weeks or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, and the bone marrow of male F344/N rats and B6C3F1 mice. 14-WEEK STUDY IN RATS: Groups of 10 male and 10 female rats were exposed to 2-butoxyethanol by inhalation at concentrations of 0, 31, 62.5, 125, 250, or 500 ppm, 6 hours per day, 5 days per week for 14 weeks. One female rat in the 250 ppm group was killed moribund during week 8; four females in the 500 ppm group were killed moribund during week 1 and one during week 5. Final mean body weights of females exposed to 500 ppm were significantly less than those of the chamber controls. Clinical findings included abnormal breathing, pallor, red urine stains, nasal and eye discharge, lethargy, and increased salivation and/or lacrimation. Due to vascular thrombosis and infarction in the tail vertebrae of 500 ppm female rats, the tails became necrotic and either sloughed off or were chewed off. The primary effect on the hematopoietic system was an anemia characterized as macrocytic, normochromic, and regenerative in males exposed to 125 ppm or greater and, to a greater extent, in all exposed groups of females. Compared to the chamber controls, kidney weights of males exposed to 500 ppm and females exposed to 125 ppm or greater and liver weights of males exposed to 250 or 500 ppm and females exposed to 125 ppm or greater were significantly increased, and thymus weights of females exposed to 500 ppm were significantly less. In female rats killed moribund, there was considerable histologic evidence of thrombosis in tissues and organs including the nasal cavity, incisors, liver, lung, and heart. In addition to thrombosis, infarction occurred in the vertebrae of the tail resulting in necrosis and loss of the distal portion of the tail. There were also inflammation, necrosis, and ulceration of the forestomach; necrosis and centrilobular degeneration of the liver; renal tubule degeneration; and atrophy of the spleen and thymus. Exposure-related increases in the incidences of Kupffer cell pigmentation, forestomach inflammation and epithelial hyperplasia, bone marrow hyperplasia, splenic hematopoietic cell proliferation, and renal tubule pigmentation were observed in male and/or female rats surviving to the end of the study. 14-WEEK STUDY IN MICE: Groups of 10 male and 10 female mice were exposed to 2-butoxyethanol by inhalation at concentrations of 0, 31, 62.5, 125, 250, or 500 ppm, 6 hours per day, 5 days per week for 14 weeks. Two male and two female mice exposed to 500 ppm died and two males and two females were killed moribund during the first 2 weeks of the study. Final mean body weights of 125, 250, and 500 ppm male mice were significantly less than those of the chamber controls. Clinical findings were observed only in 500 ppm males and females that died or were killed moribund and included abnormal breathing, red urine stains, and lethargy. Hematologic evaluation indicated an anemia that was characterized as normocytic, normochromic, and regenerative in mice exposed to 62.5 ppm or greater; the anemia was more pronounced in females. Liver weights of males exposed to 500 ppm were significantly greater than the chamber controls. In mice either dying early or killed moribund, there were inflammation, necrosis, and ulceration of the forestomach; mediastinal pleura and peritoneal inflammationmmation associated with the forestomach lesions; liver necrosis; renal tubule degeneration; atrophy of the spleen, thymus, and mandibular and mesenteric lymph nodes; and degeneration of the testis. Exposure-related increases in the incidences of hematopoietic cell proliferation and hemosiderin pigmentation of the spleen, Kupffer cell hemosiderin pigmentation of the liver, inflammation and epithelial hyperplasia of the forestomach, and renal tubule hemosiderin pigmentation occurred in male and/or female mice surviving to the end of the study. 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were exposed to 2-butoxyethanol by inhalation at concentrations of 0, 31.2, 62.5, or 125 ppm, 6 hours per day, 5 days per week for 104 weeks. For hematology and bone marrow analyses, additional groups of 27 male and 27 female rats were exposed to 0, 62.5, or 125 ppm for evaluation at 3, 6, and 12 months and nine male and nine female rats were exposed to 31.2 ppm for evaluation at 3 (hematology only) and 6 months. Survival and Body Weights: Survival of exposed male and female rats was similar to the chamber control groups. The mean body weights of females exposed to 125 ppm were generally less than the chamber control group. Hematology and Bone Marrow Cellularity: The most consistent exposure-related effect on the hematopoietic system was an exposure concentration-related mild macrocytic, normochromic, regenerative anemia present at 3, 6, and 12 months, with females more affected than males. Significant increases in bone marrow cellularity and decreases in the myeloid/erythroid ratio relative to the chamber controls were observed at all time points in females exposed to 125 ppm, and a decrease in the myeloid/erythroid ratio was observed in males exposed to 125 ppm at 12 months. Pathology Findings: The incidence of benign or malignant pheochromocytoma (combined) of the adrenal medulla in females exposed to 125 ppm was not significantly increased compared to the chamber controls but exceeded the historical control range. Exposure-related increases in the incidences of hyaline degeneration of the olfactory epithelium and Kupffer cell pigmentation of the liver were observed in male and female rats. 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female mice were exposed to 2-butoxyethanol by inhalation at concentrations of 0, 62.5, 125, or 250 ppm, 6 hours per day, 5 days per week for 104 weeks. For hematology and bone marrow analyses, additional groups of 30 male and 30 female mice were exposed to 0, 62.5, 125, or 250 ppm for evaluation at 3, 6, and 12 months. Survival and Body Weights: Survival of male mice exposed to 125 or 250 ppm was significantly less than that of the chamber control group. The mean body weights of exposed males were generally less than those of the chamber control group during the last 6 months of the study. The mean body weights of exposed female mice were less than those of the chamber control group; the reductions were greater and occurred earlier than those observed in males. Hematology: The most consistent exposure-related effect on the hematopoietic system was an exposure concentration-related minimal normocytic, normochromic, regenerative anemia present at 3, 6, and 12 months, with females affected slightly more than males. Pathology Findings: In females exposed to 250 ppm, incidences of forestomach squamous cell papilloma and squamous cell papilloma or carcinoma (combined) were significantly increased relative to the chamber controls, and these incidences exceeded the ranges in historical chamber controls. In 2-butoxyethanol exposed males, there were possible exposure-related increases in the incidences of squamous cell papilloma of the forestomach, although the increases were not significant and the incidences were within the historical control range for chamber controls. Accompanying these neoplasms in females and, to a lesser extent, in males were exposure-related increases in the incidences of ulcer and epithelial hyperplasia of the forestomach. In male mice exposed to 250 ppm, the incidence of hemangiosarcoma of the liver was significantly increased relative to chamber controls and exceeded the range in historical controls; in addition, there were possible exposure-related increases in the incidence of hepatocellular carcinoma. Incidences of hemosiderin pigmentation in the Kupffer cells were significantly increased in 125 and 250 ppm males and all exposed groups of females. The incidences of splenic hematopoietic cell proliferation and hemosiderin pigmentation were generally increased in males and females, and the incidences of bone marrow hyperplasia were increased in males. The incidences of hyaline degeneration of the olfactory and respiratory epithelia of the nose were increased in female mice. GENETIC TOXICOLOGY: 2-Butoxyethanol did not induce mutations in any of the S. typhimurium strains tested, with or without induced hamster or rat liver S9. 2-Butoxyethanol induced cycle delay but did not induce either sister chromatid exchanges or chromosomal aberrations in cultured Chinese hamster ovary cells with or without S9. 2-Butoxyethanol did not induce micronuclei in bone marrow cells of male rats or mice administered the chemical by intraperitoneal injection three times at 24-hour intervals. CONCLUSIONS: Under the conditions of these 2-year inhalation studies, there was no evidence of carcinogenic activity of 2-butoxyethanol in male F344/N rats exposed to 31.2, 62.5, or 125 ppm. There was equivocal evidence of carcinogenic activity of 2-butoxyethanol in female F344/N rats based on the increased combined incidences of benign or malignant pheochromocytoma (mainly benign) of the adrenal medulla. There was some evidence of carcinogenic activity of 2-butoxyethanol in male B6C3F1 mice based on increased incidences of hemangiosarcoma of the liver. A marginal increase in the incidences of forestomach squamous cell papilloma and an increase in the incidences of hepatocellular carcinoma may have been exposure related. There was some evidence of carcinogenic activity of 2-butoxyethanol in female B6C3F1 mice based on increased incidences of fore stomach squamous cell papilloma or carcinoma (mainly papilloma). Increased incidences of forestomach neoplasms in male and female mice occurred in groups in which ulceration and hyperplasia were also present. Exposure to 2-butoxyethanol caused a mild regenerative anemia and effects secondary to the anemia. Synonyms: 2-Butoxy-1-ethanol; m-butyl ether; butyl glycol; ethylene glycol monobutyl ether Trade name: Butyl Cellosolve

Journal Article↗

NTP Toxicology and Carcinogenesis Studies of Pentachloroanisole (CAS No. 1825-21-4) in F344 Rats and B6C3F1 Mice (Feed Studies).

Pentachloroanisole is a chlorinated aromatic compound which is widely distributed at low levels in the environment and in food products. Formation of pentachloroanisole in the environment may result from the degradation of structurally related, commercially important, ubiquitous chlorinated aromatic compounds such as pentachlorophenol and pentachloronitrobenzene which are known rodent toxins or carcinogens. Toxicology and carcinogenesis studies were conducted by administering pentachloroanisole (>99% pure) in corn oil by gavage to groups of male and female F344/N rats and B6C3F1 mice for 16 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium strains, mouse lymphoma cells, and Chinese hamster ovary cells. 16-DAY STUDIES IN RATS: Groups of five male and five female F344/N rats were administered pentachloroanisole in corn oil by gavage once per day, 5 days per week, for 16 days at doses of 0, 100, 125, 150, 175, or 200 mg/kg body weight. Deaths occurred during days 2 and 3 in rats receiving doses of 125 mg/kg or greater; these deaths were considered directly related to pentachloroanisole administration. No biologically significant changes in mean body weight gains or final body weights were noted in the 100 mg/kg groups of rats. Because of the high early mortality rate, valid comparisons of body weight differences in other dose groups could not be made. Inactivity was noted in all dose groups. Rats administered doses of 125 mg/kg or greater also exhibited dyspnea. 16-DAY STUDIES IN MICE: Groups of five male and five female B6C3F1 mice were administered pentachloroanisole in corn oil by gavage once per day, 5 days per week, for 16 days at doses of 0, 100, 175, 250, 325, or 400 mg/kg. Deaths occurred during days 2 and 3 in mice receiving doses of 175 mg/kg or greater; these deaths were considered directly related to chemical administration. No biologically significant changes in mean body weight gains or final body weights were noted in 100 mg/kg males or 100 or 175 mg/kg females. Because of the high early mortality rate, valid comparisons of body weight differences in other dose groups could not be made. Inactivity was noted in dosed mice. 13-WEEK STUDIES IN RATS: Groups of 10 male and 10 female rats were administered pentachloroanisole in corn oil by gavage once per day, 5 days per week, for 13 weeks at doses of 0, 40, 80, 120, 140, or 180 mg/kg body weight. Most rats receiving doses of 120 mg/kg or greater died during the first week of the study as a direct result of pentachloroanisole administration. Mean body weight gains of males administered 40 or 80 mg/kg and of females administered 40, 80, or 120 mg/kg pentachloroanisole were significantly lower than those of the controls. Most dosed rats exhibited temporary inactivity for several hours after dosing. Relative liver and kidney weights of males administered 40 or 80 mg/kg and absolute and/or relative liver and kidney weights of females administered 40 to 120 mg/kg were significantly greater than those of the controls. Lesions observed in males administered 80 mg/kg or more and in females administered 120 mg/kg or more included pulmonary congestion, hemorrhage, and/or edema, meningeal congestion, and hepatocellular necrosis, glycogen depletion, and degeneration of biliary epithelium in the liver. 13-WEEK STUDIES IN MICE: Groups of 10 male and 10 female mice were administered pentachloroanisole in corn oil by gavage once per day, 5 days per week, for 13 weeks at doses of 0, 40, 80, 120, 140, or 180 mg/kg body weight. Most mice administered doses of 120 mg/kg or higher died during the first week of the study as a direct result of pentachloroanisole administration. Mean body weight gains of females administered 40 to 140 mg/kg were significantly greater than that of the controls, but those of dosed males were similar to that of the controls. Most dosed mice exhibited temporary inactivity for several hours after dosing. Absolute and relative liver weights of males administered 80 mg/kg, absolute and relative liver weights of femats of females administered 40 to 180 mg/kg, and absolute and relative kidney weights of females administered 80 to 180 mg/kg pentachloroanisole were also significantly greater than those of the controls. Lesions observed in males administered 40 mg/kg or more and in females administered 80 mg/kg or more included pulmonary congestion and/or edema, adrenal congestion, lymphoid depletion of lymph nodes and thymus, hepatocellular cytomegaly and karyomegaly, and pigment accumulation in hepatocytes and Kupffer cells. 2-YEAR STUDIES IN RATS: Based on the chemical-related mortality and liver lesions seen in the 16-day and 13-week studies, doses selected for the 2-year studies were 0, 10, 20, and 40 mg/kg for males and 0, 20, and 40 mg/kg for females. Groups of 70 male and 70 female rats were administered pentachloroanisole in corn oil by gavage 5 days per week for up to 2 years. At 9 and 15 months, up to 10 animals per group were selected for interim evaluations. Survival, Body Weights, and Clinical Findings: The survival of high-dose males was significantly decreased (vehicle control, 24/50; low-dose, 20/50; mid-dose, 24/50; high-dose, 14/50); most deaths in the high-dose group occurred at or before week 16. The majority of deaths in the mid- and high-dose groups may have been due to pentachloroanisole-related hyperthermia. The survival of dosed females was greater than that of the controls (29/50, 35/50, 44/50). Final mean body weights of mid- and high-dose males were 7&percnt; and 10&percnt; lower than that of the controls; final mean body weight of high-dose females was 11&percnt; lower than that of the controls. Final mean body weights of other dose groups were similar to those of the vehicle controls. At the 9-month interim evaluation, mean rectal temperature of males administered 40 mg/kg was significantly greater than that of the controls. Relative liver and kidney weights of males and females administered 20 or 40 mg/kg were significantly greater than those of controls. At the 15-month interim evaluation, relative liver weights of dosed females and absolute liver weights of 40 mg/kg females were significantly greater than those of the controls, as were relative liver and kidney weights of 40 mg/kg males. Pathology Findings: In the 2-year studies, administration of pentachloroanisole to males was associated with significant increases in the incidences of benign adrenal medulla pheochromocytomas. The incidence of benign adrenal medulla pheochromocytomas was marginally increased in high-dose females and slightly exceeded the range of the historical controls. Incidences of adrenal medulla hyperplasia were increased in dosed female rats, but not in dosed males. The incidences of pancreatic adenomas and focal hyperplasia were decreased in dosed males. The incidences of mammary gland fibroadenomas and uterine stromal polyps and sarcomas (combined) were decreased in high-dose females. Treatment-related increased incidences of intracytoplasmic pigmentation occurred in renal tubule epithelium, olfactory epithelium, and hepatocytes of males and females. Congestion and hemorrhage of the lungs, lymph nodes, thymus, adrenal cortex, and meninges, as well as hepatocellular centrilobular necrosis occurred almost exclusively in mid- and high-dose males that died or were killed moribund before the end of the studies. 2-YEAR STUDIES IN MICE: Based on the chemical-related mortality and liver lesions seen in the 16-day and 13-week studies, doses selected for the 2-year studies were 0, 20, and 40 mg/kg. Groups of 70 male and 70 female mice were administered pentachloroanisole in corn oil by gavage 5 days per week for up to 2 years. At 9 and 15 months, up to 10 animals per group were selected for interim evaluations. Survival, Body Weights, and Clinical Findings: The survival of dosed males was similar to that of the controls; survival of high-dose females was lower than that of the controls (24/50, 25/50, 16/50). The decreased survival of the high-dose females was attributed primarily to ovarian abscesses which were observed after moribund sacrifice. At the 9-month interim evaluation, the mean body weight of males administered 40 mg/kg was significantly lower than that of the vehicle controls. Absolute and relative liver weights of females and the relative liver weight of males administered 40 mg/kg were significantly greater than those of the controls. Final mean body weights of low- and high-dose males were 11&percnt; and 17&percnt; lower than that of the controls. Final mean body weights of dosed females were similar to that of the controls. There were no clinical findings attributed to pentachloroanisole administration. Pathology Findings: Centrilobular hepatocyte cytomegaly and pigment accumulation in hepatocytes and Kupffer cells were seen in dosed mice, but not in controls at the 9- and 15-month interim evaluations. In the 2-year studies, the incidence of benign pheochromocytomas was significantly increased in high-dose males. Dosed males also exhibited increased incidences of adrenal medulla hyperplasia and hypertrophy. The incidences of hemangiosarcomas of the liver were significantly increased in dosed males. Increased incidences of hepatocellular cytologic alteration, biliary tract hyperplasia, and Kupffer cell pigmentation occurred in dosed males and females; the incidences of mixed cell foci were also increased in dosed males. Cytologic alteration encompassed hepatocellular cytomegaly, karyomegaly, hepatocyte degeneration and necrosis, and multinucleated giant cell formation, and was considered an advanced stage of the pathologic process observed at 13 weeks. GENETIC TOXICOLOGY: Pentachloroanisole was mutagenic in Salmonella typhimurium strains TA98 and TA1537 in the absence but not in the presence of exogenous metabolic activation (S9). No clear mutagenic activity was observed in TA100 with hamster S9, without S9, or in TA1535 with or without S9. An equivocal response was observed in TA100 with rat S9. Pentachloroanisole was positive for induction of trifluorothymidine resistance in mouse lymphoma L5178Y cells with S9; the response observed without S9 was weak and inconsistent. In cytogenetic tests with Chinese hamster ovary cells, pentachloroanisole induced sister chromatid exchanges, but not chromosomal aberrations, with and without S9. TOXICOKINETICS: Male and female F344/N rats and B6C3F1 mice were administered 10, 20, or 40 mg/kg pentachloroanisole by gavage or 10 mg/kg pentachloroanisole intravenously (Appendix H). A rapid elimination of pentachloroanisole and a rapid formation of its main metabolite, pentachlorophenol, were seen in both species after an intravenous or an oral dose of pentachloroanisole. The area under the concentration-versus-time curve of pentachloroanisole increased with dosage in each species but the dose proportionality was lost above 20 mg/kg. No sex-related differences were found in the rate of absorption of pentachloroanisole from the GI tract, in the area under the concentration-versus-time curve, or in the overall rate elimination of pentachloroanisole. However, in female rats the area under the concentration-versus-time curve of pentachlorophenol was significantly larger than in male rats. No such difference was observed in mice. CONCLUSIONS: Under the conditions of these 2-year gavage studies, there was some evidence of carcinogenic activity of pentachloroanisole in male F344/N rats based on increased incidences of benign pheochromocytomas of the adrenal medulla. There was equivocal evidence of carcinogenic activity of pentachloroanisole in female F344/N rats based on marginally increased incidences of benign pheochromocytomas of the adrenal medulla. There was some evidence of carcinogenic activity of pentachloroanisole in male B6C3F1 mice based on increased incidences of benign pheochromocytomas of the adrenal medulla and hemangiosarcomas of the liver. There was no evidence of carcinogenic activity of pentachloroanisole in female B6C3F1 mice given doses of 20 or 40 mg/kg. Pentachloroanisole administration was associated with increased incidences of adrenal medulla hyperplasia in female rats and increased incidences of pigmentation in the renal tubule epithelium, olfactory epithelium, and hepatocytes of male and female rats. In addition, decreased incidences of pancreatic adenomas and focal hyperplasia in male rats and decreased incidences of mammary gland fibroadenomas and uterine stromal polyps and sarcomas (combined) in female rats were observed. Hyperthermia-related lesions in male rats receiving 20 or 40 mg/kg were considered indirectly related to pentachloroanisole administration. Pentachloroanisole administration was associated with increased incidences of adrenal medulla hyperplasia and hypertrophy and hepatocellular mixed cell foci in male mice. In male and female mice, nonneoplastic liver lesions associated with pentachloroanisole administration included hepatocellular cytologic alteration, Kupffer cell pigmentation, biliary tract hyperplasia, and subacute inflammation. Synonyms: 2,3,4,5,6-pentachloroanisole; methyl pentachlorophenate; methyl pentachlorophenyl ether; o-methylpentachlorophenol; pentachloromethoxybenzene; pentachlorophenyl methyl ether

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NTP Toxicology and Carcinogenesis Studies of 1,3-Butadiene (CAS No. 106-99-0) in B6C3F1 Mice (Inhalation Studies).

1,3-Butadiene is produced in large volumes for use in the manufacture of synthetic rubber and of thermoplastic resins. In previous inhalation studies conducted by the NTP (NTP, 1984) there was clear evidence of multiple organ carcinogenicity in male and female mice exposed to 625 or 1,250 ppm 1,3-butadiene for 60 or 61 weeks. To better characterize exposure-response relationships for neoplasms and nonneoplastic lesions, toxicology and carcinogenesis studies were conducted by exposing groups of male and female B6C3F1 mice to air containing 1,3-butadiene (greater than 99% pure) for up to 2 years. An additional study in male B6C3F1 mice, in which exposure to 1,3-butadiene was stopped after limited exposure periods (13, 26, 40, or 52 weeks), was performed to assess the effects of varying concentration and duration of exposure on the incidences of 1,3-butadiene-induced neoplasms. In vitro genetic toxicology studies were conducted in Salmonella typhimurium and mouse lymphoma cells. In vivo genetic effects were assayed in germ cells of male Drosophila melanogaster and in bone marrow and peripheral blood cells of B6C3F1 mice. 2-Year Studies: Groups of 70 male and 70 female mice were exposed to air containing 0, 6.25, 20, 62.5, or 200 ppm 1,3-butadiene for 6 hours per day, 5 days per week for up to 2 years; groups of 90 male and 90 female mice were exposed to 625 ppm 1,3-butadiene on the same schedule. Up to 10 animals from each group were examined after 9 and 15 months of exposure. Survival and Body Weight in the 2-Year Studies: Two-year survival was decreased for males and females exposed to concentrations of 20 ppm or above, primarily due to the development of chemical-related malignant neoplasms. No female mice exposed to 200 or 625 ppm or males exposed to 625 ppm survived to the end of the studies (males: 35/50, 39/50, 24/50, 22/50, 4/50, 0/70; females: 37/50, 33/50, 24/50, 11/50, 0/50, 0/70). Mean body weights of exposed male and female mice were similar to those of the controls. Hematologic Effects in the 2-Year Studies: Hematologic parameters were evaluated after 9 and 15 months of exposure. At 9 months, decreases in erythrocyte counts, hemoglobin concentration, and packed red cell volume were observed in male mice exposed to 62.5 ppm or above and in female mice exposed to 200 or 625 ppm. Mean erythrocyte volume was increased in male mice exposed to 625 ppm and in females exposed to 200 or 625 ppm. At 15 months, decreases in erythrocyte counts, hemoglobin concentration, and packed red cell volume and increases in mean erythrocyte volume were observed in male and female mice exposed to 625 ppm. Neoplasms and Nonneoplastic Lesions in the 2-Year Studies: Exposure of mice to 1,3-butadiene induced benign and malignant neoplasms at multiple sites. Statistically significant increases in the incidences of neoplasms at one or more sites were seen at concentrations of 20 ppm and higher in males and 6.25 ppm and higher in females. There was no exposure level in this study at which a significant carcinogenic response was not observed. Statistically significant increases occurred in the incidences of malignant lymphoma; histiocytic sarcoma; cardiac hemangiosarcoma; harderian gland adenoma; hepatocellular adenoma and carcinoma; alveolar/bronchiolar adenoma and carcinoma; mammary gland carcinoma, adenoacanthoma, and malignant mixed tumor (females only); benign and malignant ovarian granulosa cell tumor; and forestomach squamous cell papilloma and carcinoma. Low incidences of uncommon neoplasms also occurred in exposed male and female mice, including intestinal carcinomas in males, renal tubule adenomas in males and females, skin sarcomas (all types combined) in females, and Zymbal's gland adenomas and carcinomas in females. Lymphocytic lymphomas appeared as early as week 23 and were the principal cause of death of male and female mice exposed to 625 ppm 1,3-butadiene. The early and extensive development of lethal lymphocytic lymphomas in mice exposed to 625 ppm resulted in a reduced number of mice at risk for neoplasms developing laterg later at other sites. Exposure-response relationships for 1,3-butadiene-induced neoplasms were more clearly characterized at concentrations below 625 ppm and after adjustment for intercurrent mortality. Increased incidences of nonneoplastic lesions in exposed mice included bone marrow atrophy; testicular atrophy; ovarian atrophy, angiectasis, germinal epithelial hyperplasia, and granulosa cell hyperplasia; uterine atrophy; cardiac endothelial hyperplasia and mineralization; alveolar epithelial hyperplasia; forestomach epithelial hyperplasia; and harderian gland hyperplasia. Stop-Exposure Study: The stop-exposure study consisted of groups of 50 male mice exposed to 1,3-butadiene at concentrations of 200 ppm for 40 weeks, 625 ppm for 13 weeks, 312 ppm for 52 weeks, or 625 ppm for 26 weeks. After the exposures were completed, these groups were placed in control chambers for the remainder of the 2-year study. The total exposure of 1,3-butadiene (concentration times duration of exposure) of the 13- and 40-week stop-exposure groups was approximately 8,000 ppm-weeks, while that of the 26- and 52-week stop-exposure groups was approximately 16,000 ppm-weeks. The survival of all stop-exposure groups was markedly lower than that of the controls. The incidences of lymphocytic lymphoma, histiocytic sarcoma, cardiac hemangiosarcoma, alveolar/bronchiolar adenoma and carcinoma, forestomach squamous cell papilloma and carcinoma, hepatocellular adenoma, harderian gland adenoma and adenocarcinoma, and preputial gland carcinoma were significantly increased. Neoplasms were induced at most of these sites after only 13 weeks of exposure to 1,3-butadiene. Additionally, low numbers of malignant gliomas and neuroblastomas of the brain and Zymbal's gland carcinomas occurred in one or more stop-exposure groups. At similar total exposures, the incidence of lymphocytic lymphoma was greater with exposure to a higher concentration of 1,3-butadiene for a short time compared with exposure to a lower concentration for an extended period (34&percnt; at 625 ppm for 13 weeks versus 12&percnt; at 200 ppm for 40 weeks; 60&percnt; at 625 ppm for 26 weeks versus 8&percnt; at 312 ppm for 52 weeks). Genetic Toxicology: 1,3-Butadiene has been tested both in vitro and in vivo for mutagenic activity. In vitro, positive results were obtained in the Salmonella typhimurium gene mutation assay with strain TA1535; mutagenic activity was not observed in other S. typhimurium strains (TA100, TA97, and TA98). 1,3-Butadiene was negative in the mouse lymphoma assay for induction of trifluorothymidine resistance in L5178Y cells with and without S9. In vivo, 1,3-butadiene did not induce sex-linked recessive lethal mutations in germ cells of male Drosophila melanogaster; however, it did induce significant increases in chromosomal aberrations and sister chromatid exchanges in bone marrow cells of mice exposed for 2 weeks by inhalation. In addition, significant increases in micronucleated erythrocytes were observed in peripheral blood samples obtained from male and female mice exposed to 1,3-butadiene for 2 or 13 weeks or 15 months by inhalation. Conclusions: The previous inhalation studies of 1,3-butadiene (TR-288) in male and female B6C3F1 mice provided clear evidence of carcinogenicity at exposure concentrations of 625 or 1,250 ppm. The present inhalation studies - 2-year exposures of 6.25, 20, 62.5, 200, or 625 ppm or shorter duration exposures of 200, 312, or 625 ppm - provide a better characterization of the concentration-dependent responses for 1,3-butadiene-induced neoplasms and nonneoplastic lesions. The present studies confirmed the clear evidence of carcinogenicity of 1,3-butadiene in male B6C3F1 mice based on increased incidences of neoplasms in the hematopoietic system, heart, lung, forestomach, liver, harderian gland, preputial gland, brain, and kidney. There was clear evidence of carcinogenicity of 1,3-butadiene in female B6C3F1 mice based on increased incidences of neoplasms in the hematopoietic system, heart, lung, forestomach, liver, harderian gland, ovary, and mammary gland. Low incidences of intestinal carcinomas in male mice, Zymbal's gland carcinomas in male and female mice, and renal tubule adenomas and skin sarcomas in female mice may also have been related to administration of 1,3-butadiene. Synonyms: alpha,gamma-Butadiene; bivinyl; divinyl; erythrene; vinylethylene; biethylene; pyrrolylene

Journal Article↗

NTP Toxicology and Carcinogenesis Studies of Commercial Grade 2,4 (80%)- and 2,6 (20%)- Toluene Diisocyanate (CAS No. 26471-62-5) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

Toluene diisocyanate (TDI) is commercially produced as an approximate 80:20 mixture of the 2,4- and 2,6-isomers. In 1980, 580,000 pounds of this chemical were produced in the United States, primarily for use in the manufacture of flexible polyurethane foams. These foam elastomers are found in furniture and automobile cushions, carpet underlays, pillow filling, mattresses, insulation, shoes, purses, and toys. TDI is also used to produce polyurethane coatings for lacquers and wood finishes. Groups of 50 female F344/N rats and 50 B6C3F1 mice were administered commercial grade toluene diisocyanate (80% 2,4- and 20% 2,6-) in corn oil by gavage at doses of 60 or 120 mg/kg body weight, 5 days per week for 105 or 106 weeks. Groups of 50 male F344/N rats received 30 or 60 mg/kg and groups of 50 male B6C3F1 mice received 120 or 240 mg/kg on the same schedule. Dosage analyses of toluene diisocyanate indicated that the chemical had reacted in the corn oil vehicle, resulting in actual gavage concentrations 77% to 90% of theoretical values. Groups of 50 rats and 50 mice of each sex received corn oil only and served as vehicle controls. Survival in all groups of dosed rats in the 2-year studies were shorter (P</=0.005) than that of the controls; depressions of the mean body weight gain relative to controls were greater than 10% in all dosed rat groups throughout most of the study. A dose-dependent pattern of cumulative toxicity began at 70 weeks and culminated in excessive mortality, indicating the estimated tolerated dose had been exceeded for rats. Acute bronchopneumonia occurred at increased incidences in groups of dosed male and female rats (males: control, 2/50; low dose, 6/50; high dose, 14/50; females: 1/50, 10/50, 25/49). Subcutaneous tissue fibromas or fibrosarcomas (combined) in male rats occurred with a positive trend (P<0.01; 3/50, 6/50, 12/50). The incidence in the high dose group was higher than that in the controls (P</=0.01). The same tumor comparisons were significant (P<0.001) in female rats by the life table analysis. Mammary gland fibroadenomas in female rats occurred with a positive trend (P<0.001), and the incidences in low and high dose groups were significantly higher than that in controls (P</=0.01). Pancreatic acinar cell adenomas in male rats occurred with a positive trend (P<0.05; 1/47, 3/47, 7/49). The incidence in the high dose group was higher than that in the controls (P<0.05). The incidences of pancreatic islet cell adenomas in female rats were higher by the incidental tumor test (P</=0.01) in low dose (6/49) and high dose (2/47) groups than in controls (0/50). An islet cell carcinoma was also observed in a low dose female rat. The incidences of female rats with neoplastic nodules in the liver occurred with a positive trend (P<0.05; 3/50, 8/50, 8/48), and the incidence in the high dose group was higher (P<0.05) than that in the controls. Survival of high dose male mice in the 2-year study was significantly shorter than that of the controls (P<0.001). During the second year of the study, mean body weight gains of high dose male mice were less than those of the controls. Cytomegaly of kidney tubular epithelium was found in 45/48 (94%) low dose male mice and 41/50 (82%) high dose male mice but not in any of the controls. Hemangiomas or hemangiosarcomas (combined) of the circulatory system in female mice occurred with a positive trend (P</=0.01; control, 0/50; low dose, 1/50; high dose, 5/50). The incidence in the high dose group was significantly higher than that in the controls (P<0.05). Hepatocellular adenomas in female mice occurred with a positive trend (P</=0.001; 2/50, 3/50, 12/50), and the incidence in the high dose group was higher than that in the controls (P<0.01). Toluene diisocyanate was mutagenic in Salmonella typhimurium strains TA98 and TA100 in the presence (but not the absence) of Aroclor 1254-induced male Sprague-Dawley rat or male Syrian hamster liver S9; it was not mutagenic in strains TA 1535 or 1537. An audit of the experimental data for these 2-year toxicological and carcinogenicity An audit of the experimental data for these 2-year toxicological and carcinogenicity studies on commercial grade 2,4- and 2,6-toluene diisocyanate was conducted. There were no data discrepancies that influenced the final interpretations. Under the conditions of these gavage studies, commercial grade toluene diisocyanate in corn oil was carcinogenic for F344/N rats, causing subcutaneous fibromas and fibrosarcomas (combined) in males and females, pancreatic acinar cell adenomas in males, and pancreatic islet cell adenomas, neoplastic nodules of the liver, and mammary gland fibroadenomas in females. Toluene diisocyanate was not carcinogenic for male B6C3F1 mice. TDI was carcinogenic for female B6C3F1 mice, causing hemangiomas or hemangiosarcomas (combined), as well as hepatocellular adenomas. Levels of Evidence of Carcinogenicity: Male Rats: Positive Female Rats: Positive Male Mice: Negative Female Mice: Positive Synonym: TDI

Journal Article↗

Bioassay of 5-Chloro-o-toluidine for Possible Carcinogenicity (CAS No. 95-79-4).

5-Chloro-o-toluidine, an aromatic amine and dye intermediate, was selected for bioassay by the National Cancer Institute because of the high incidence of bladder cancer observed among dye manufacturing industry workers. A bioassay for the possible carcinogenicity of 5-chloro-o-toluidine was conducted using Fisher 344 rats and B6C3F1 mice. 5-Chloro-o-toluidine was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. Twenty animals of each sex and species were placed on test as controls. The high and low dietary concentrations of 5-chloro-o-toluidine were 5,000 and 2,500 ppm for rats and 4,000 and 2,000 ppm for mice. The compound was administered in the diet for 78 weeks, followed by an observation period of 26 weeks for rats and 13 weeks for mice. There were significant positive associations between the concentrations of 5-chloro-o-toluidine administered and mortality among male and female mice, but not among rats of either sex. Adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. Distinct mean body weight depression was apparent when dosed female rats and dosed mice of both sexes were compared to their controls, indicating that the concentrations administered to these animals in this bioassay may have approximated the maximum tolerated concentrations. Since no mean body weight depression, relative to controls, no significantly accelerated mortality, and no signs of toxicity other than fatty metamorphosis of the liver were associated with administration of 5-chloro-o-toluidine to male rats, it is possible that these animals may have been able to tolerate a higher dietary concentration of the compound. There was a significant positive association between the concentration of 5-chloro-o-toluidine administered to male rats and the incidence of adrenal pheochromocytomas in these animals; however, neither of the Fisher comparisons was significant. None of the other statistical tests fortumors at any site in male and female rats indicated a significant positive association between dosage and incidence. In mice of both sexes there were significant positive associations between concentration administered and the incidence of hemangiosarcomas. In addition, the high dose to control Fisher exact comparisons for both sexes were significant. The Cochran-Armitage tests were also significant and positive for the incidences of hepatocellular carcinomas in both sexes of mice. For males and females the high dose to control Fisher exact comparisons were significant, and for females the low dose to control comparison was also significant. Under the conditions of this bioassay, 5-chloro-o-toluidine was carcinogenic to B6C3F1 mice, inducing hemangiosarcomas and hepatocellular carcinomas in both males and females. There was no conclusive evidence of the carcinogenicity of the compound in Fisher 344 rats. Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats: Negative Male Mice: Positive Female Mice: Positive Synonyms: 5-chloro-2-methylbenzeneamine; p-chloro-o-aminotoluene; 4-chloro-2-aminotoluene; 2-amino-4-chlorotoluene; o-amino-p-chlorotoluene; 5-chloro-2-methylaniline; 2-methyl-5-chloroaniline; 1-amino-2-methyl-5-chlorobenzene; 1-amino-3-chloro-6-methylbenzene; Fast Red KB Base; Azogene Fast Red KB; Brentamine Fast Red KB Base; Naphthosol Fast Red Base; Naphthanil Red KB Base

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Bioassay of Michler's Ketone for Possible Carcinogenicity (CAS No. 90-94-8).

Michler's ketone, a dye intermediate and derivative of dimethylaniline, was selected for bioassay by the National Cancer Institute because of the elevated incidence of bladder cancer noted among dye manufacturing industry workers. A bioassay for the possible carcinogenicity of technical-grade Michler's ketone was conducted using Fischer 344 rats and B6C3F1 mice. Michler's ketone was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. Twenty animals of each sex and species were placed on test as controls. The high and low dietary concentrations of Michler's ketone were respectively, 500 and 250 ppm for male rats, 1,000 and 500 ppm for female rats, and 2,500 and 1,250 ppm for mice of both sexes. The compound was administered to rats and mice for 78 weeks. The period of compound administration was followed by an observation period of 28 weeks for male and high dose female rats, 29 weeks for low dose female rats and 13 weeks for mice. There were significant positive associations between the concentrations of Michler's ketone administered and mortality in rats and mice of both sexes. Adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. There was distinct dose-related mean body weight depression in female rats and in mice of both sexes, and the mean body weight among dosed male rats was slightly lower than that in controls, indicating that the concentrations of Michler's ketone administered tothese animals in this bioassay may have approximated the maximum tolerated concentrations. There were significant positive associations between the concentrations of Michler's ketone administered and the incidences of hepatocellular carcinomas in both sexes of rats and in female mice and hemangiosarcomas in male mice. In all of these cases the high dose to control Fisher exact comparison was also significant. Under the conditions of this bioassay, dietary administration of Michler's ketone was carcinogenic to male and female Fischer 344 rats and female B6C3F1 mice, causing hepatocellular carcinomas, and to male B6C3F1 mice, causing hemangiosarcomas. Levels of Evidence of Carcinogenicity: Male Rats: Positive Female Rats: Positive Male Mice: Positive Female Mice: Positive Synonyms: bis[4-(dimethylamino)phenyl]methanone; 4,4'-bis(dimethylamino)benzophenone; p,p'-bis(dimethylamino)benzophenone; bis[p-(N,N'-dimethylamino)phenyl]ketone; tetramethyldiaminobenzophenone

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Bioassay of aniline hydrochloride for possible carcinogenicity.

A bioassay of aniline hydrochloride for possible carcinogenicity was conducted using Fischer 344 rats and B6C3F1 mice. Aniline hydrochloride was administered in the feed, at either of two concentrations, to groups of 50 male and female animals of each species, with the exception of 49 female mice in the high dose group. The high and low dietary concentrations of aniline hydrochloride were, respectively, 0.6 and 0.3 percent for rats and 1.2 and 0.6 percent for mice. After a 103-week period of compound administration, observation of the rats and mice continued for up to an additional 5 weeks. For rats and mice, respectively, 25 and 50 animals of each sex were placed on test as controls and fed only the basal diet. In male rats there were several types of mesenchymal tumors, primarily of the spleen, associated with administration of the compound. Hemangiosarcomas of the spleen and the combined incidence of fibrosarcomas and sarcomas NOS of the spleen were each statistically significant in male rats. The combined incidence of fibrosarcomas and sarcomas NOS of multiple body organs was also significant in male rats. The number of female rats having fibrosarcomas or sarcomas NOS of either the spleen alone or multiple organs of the body cavity was significantly associated with increased dietary concentration of aniline hydrochloride. This result was not supported by the Fischer exact tests, but because of the rarity of these tumors, the observed incidences (0/24 in the control group, 1/50 [2 percent] in the low dose group, 7/50 [14 percent] in the high dose group) were considered indicative of a compound-related carcinogenic effect. In mice of both sexes no tumors occurred in statistically significant increased incidences among dosed groups when compared to controls. Under the conditions of this bioassay, dietary administration of aniline hydrochloride was carcinogenic to male and female Fischer 344 rats, inducing hemangiosarcomas and a combination of fibrosarcomas and sarcomas NOS of the spleen and a combination of fibrosarcomas and sarcomas NOS of multiple body organs. There was no evidence of compound-induced carcinogenicity in B6C3F1 mice of either sex.

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Bioassay of 2,7-dichlorodibenzo-p-dioxin (DCDD) for possible carcinogenicity.

A bioassay of 2,7-dichlorodibenzo-p-dioxin (DCDD) for possible carcinogenicity was conducted by administering the test chemical in feed to Osborne-Mendel rats and B6C3F1 mice. Groups of 35 rats of each sex were administered DCDD at one of two doses, either 5,000 or 10,000 ppm, for 110 weeks. Groups of 50 mice of each sex were administered these same doses for 90 weeks. Controls consisted of 35 untreated rats of each sex and 50 untreated mice of each sex. All surviving male rats were killed at 110 to 112 weeks, all surviving female rats at 110 to 117 weeks, all surviving male mice at 92 to 101 weeks, and all surviving female mice at 91 to 98 weeks. Mean body weights of most of the dosed groups of rats and mice were lower than those of corresponding controls both when placed on study and for much of the study period; however, survival of any group was not significantly affected by administration of the test chemical. Sufficient numbers of dosed and control rats and mice of each sex were at risk for the development of late-appearing tumors. No tumors were induced in male or female rats or female mice at incidences that were significantly higher in the dosed groups than in the corresponding control groups. Both low-and high-dose rats had toxic hepatic lesions characterized by centrilobular fatty metamorphosis and/or necrosis. In the male mice, hepatocellular adenomas or carcinomas occurred at incidences that were dose related (P=0.008), and, in direct comparisons, were higher in the low-dose group (P=0.008) and the high-dose group (P=0.010) than in the control group (controls 8/49, low-dose 20/50, high-dose 17/42). However, the historical incidence of this lesion in control male B6C3F1 mice at this laboratory does not permit a clear association of the lesion with the administration of the test compound. There were also significant increases in the incidence of combinations of leukemias and lymphomas and of hemangiosarcomas and hemangiomas in the low-dose male mice, but these findings were not supported by the high-dose animals. It is concluded that under the conditions of this bioassay, DCDD was not carcinogenic for Osborne-Mendel rats of either sex or for female B6C3F1 mice. The marginal increased incidences of combinations of leukemias and lymphomas, of hemangiosarcomas and hemangiomas, and of hepatocellular carcinomas and adenomas in male B6C3F1 mice are, however, considered as suggestive of a carcinogenic effect of 2,7-dichlorodibenzo-p-dioxin in these animals.

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Bioassay of calcium cyanamide for possible carcinogenicity.

A bioassay of formulated calcium cyanamide for possible carcinogenicity was conducted by administering the test chemical in feed to F344 rats and B6C3F1 mice. Groups of 50 rats of each sex were administered a commercial formulation containing 63% calcium cyanamide in the diet at one of two doses, either 100 or 200 ppm for the males and either 100 or 400 ppm for the females, for 107 weeks. Groups of 50 mice of each sex were administered the test chemical at one of two doses, either 500 or 2,000 ppm, for 100 weeks. Matched controls consisted of 20 untreated rats and 20 untreated mice of each sex. All surviving animals were killed at the end of administration of the test chemical. Mean body weights of the dosed rats and mice were only slightly lower than those of corresponding controls, except for the low-dose female mice, whose mean body weights were unaffected by the test chemical. Mortality was dose related only in male mice. Survival was 70% or greater in all dosed and control groups of each species and sex at the end of the bioassay, and sufficient numbers of animals were at risk in all groups for the development of late-appearing tumors. Both rats and mice may have been able to tolerate higher doses. No tumors occurred in the dosed rats of either sex at incidences that could clearly be related to administration of the calcium cyanamide. However, in the subchronic studies performed with the rats, calcium cyanamide was found to cause diffuse follicular hyperplasia of the thyroid, with periglandular fibrosis and prominent periglandular vascularity. In male mice, hemangiosarcomas were dose related in the males (P=0.006); however, in direct comparisons, incidences in the individual dosed groups were not significantly higher than those in the control group (controls 1/20 (5%); low-dose 2/50 (4%); high-dose 10/50 (20%)). The incidence of these tumors in historical-control male B6C3F1 mice was (13/323 (4%)), and the highest incidence observed was 2/19 (10%). In female mice, lymphomas or leukemias were dose related (P=0.009), and in a direct comparison the incidence of these tumors in the high-dose group was significantly higher (P=0.006) than that in the control group (controls 1/20 (5%); low-dose 11/46 (24%); high-dose 18/50 (36%)); however, the incidence of the lymphomas or leukemias in historical-control female B6C3F1 mice was 67/324 (21%), suggesting that the incidence of these tumors in the matched-control group of the present bioassay may have been abnormally low. Thus, neither the incidences of hemangiosarcomas of the circulatory system in male mice nor of lymphomas or leukemias in the female mice can clearly be related to administration of the test chemical. It is concluded that under the conditions of this bioassay, the test formulation of calcium cyanamide was not carcinogenic for F344 rats or B6C3F1 mice of either sex.

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