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Stachybotrys chartarum: current knowledge of its role in disease.

Stachybotrys chartarum is one of several species of filamentous fungi capable of producing mycotoxins under certain environmental conditions. In some observational studies, the growth of this toxigenic mold in the indoor environment has been implicated as a cause of building-related illness. Following reports of a cluster of cases of pulmonary hemosiderosis and hemorrhage associated with exposure to Stachybotrys, public health measures have been recommended which have far-reaching implications. Although the hazards associated with exposure to some mycotoxins have been well studied, the health risks from environmental exposure to Stachybotrys remain poorly defined. The purpose of this review is to critically evaluate the current body of epidemiologic knowledge regarding Stachybotrys and to increase physician awareness regarding this emerging environmental health issue.

Animals↗

Intravenous ascorbic acid in hemodialysis patients with functional iron deficiency: a clinical trial.

BACKGROUND: Hemodialysis (HD) patients with functional iron deficiency (FID) often develop resistance to recombinant human erythropoietin (rHuEpo). In these patients, iron therapy may be a hazard, leading to iron overload and consequently to hemosiderosis. Recent studies suggest that intravenous ascorbic acid (IVAA) may circumvent rHuEpo resistance. The aim of our study was to show the effects of IVAA on FID and whether this results in a better correction of anemia in HD patients with stable hemoglobin (Hb) concentration and FID. METHODS: Twenty-seven HD patients with serum ferritin >300 microg/l, transferrin saturation (TS) <20% and hemoglobin (Hb) <10 g/dL were selected andrandomly divided into two groups to enter a cross-over trial with IVAA. In group I IV vitamin C 500 mg was administered three times a week for three months and discontinued in the next three months of the study. Vitamin C was not given the first three months in group II (control group, first three months of the study), who then received 500 mg IV three times a week for the next three months. RESULTS: Hb and TS% significantly increased (baselines vs 3 months, Hb 9.2 +/- 0.2 vs 10.0 +/- 0.3 g/dL, TS% 17.5 +/- 0.6 vs 25.7 +/- 1.7, respectively p < 0.01 and p <0.001) in group I after three months; ferritin fell significantly from 572 +/- 40 to 398 +/- 55 microg/L (p<0.004). Ten patients completed the study: mean Hb and TS% fell significantly (3 months vs final, Hb 9.9 +/- 0.3 vs 8.9 +/- 0.2 g/dL, TS% 25.1 +/- 1.2 vs 19.1 +/- 1.1, respectively p < 0.01 and p <0.001), while mean ferritin did not change. Mean Hb, ferritin and TS% remained unchanged in group II after three months. Hb and TS% mean values rose significantly (3 months vs final, Hb 9.0 +/- 0.2 vs 9.9 +/- 0.2 g/dl, TS% 18.4 +/- 1.0 vs 27.0 +/- 1.0, respectively p < 0.005 and p <0.001), and ferritin markedly decreased from 450 +/- 50 to 206 +/- 24 microg/L (p < 0.001) at the end of the study. The rHuEpo dose was kept unchanged throughout the study. Differences were analyzed after three months. Mean Hb rose (0.8 +/- 0.2 g/dL) in group I but dropped (-0.1 +/- 0.1 g/dL) (p< 0.009) in group II. Ferritin dropped in both groups (group I vs group II, -173 + /-48 vs - 33 +/- 21 microg/L) (p < 0.01) while TS% increased (group I vs group II, 8.2 +/- 1.5 vs 0.4 +/- 0.7) (p < 0.001). CONCLUSION: IVAA may partially correct FID and consequently help rHuEpo hyporesponsive anemia.

Adult↗

Iron metabolism, sickle cell disease, and response to cyanate.

In an attempt to understand the variability of the hematologic response to oral sodium cyanate, iron metabolism was studied in a group of 39 patients with sickel cell disease. Eleven of the 39 patients were found to have no stainable iron in the marrow despite the fact that patients with sickle cell disease are generally considered to have hemosiderosis. The mean per cent saturation and total iron-binding capacity were in the low-normal range in sickle cell patients whether or not stainable iron was present in the bone marrow aspirate. Serum ferritin concentrations, on the other hand, were found to be high in both groups (greater than 500 mu g/liter) when compared to controls (60 mu g/liter). The high serum ferritin levels denoted significant total-body iron deposition which may be unavailable for normal metabolic processes. One patient with no stainable iron in the bone marrow aspirate did respond to iron therapy alone with an increase in hemoglobin concentration. Serum ceruloplasmin levels were also found to be high in sickle cell disease patients. The ability to respond to oral cyanate therapy was correlated with the amount of stainable iron in the bone marrow aspirate. These studies emphasize the necessity of a reevaluation of iron metabolism in the pathophysiology and treatment of sickle cell disease.

Administration, Oral↗

[Liver biopsy: the mandatory test in liver diagnosis in adults].

The aim of the study was clinical and morphological analysis patients with liver biopsy. In this work technique of percutaneous liver biopsy, indications, contraindications and complications were presented. Among 547 liver biopsy 56% patients was HCV infected and a 14% patient was HBV infected. Microscopic examination was performed the similar percentage the stage of inflammation and fibrosis. Among patients without viral infection (HBV and HCV) the most finding was steatosis and liver cirrhosis. Agreement of clinical diagnosis with results of microscopic investigations with reference to of inflammable changes carried out 90%, the less agreement with steatosis, cholestasis and hemosiderosis. In 30% patients after biopsy were pains in place executed of intervention and right arm for 6 hours. 0.5% of patients was sub capsular bleeding after intervention. We no observed dangerous complications after liver percutaneous biopsy. Liver biopsy is very important investigation in liver diagnosis, comparatively safety if contraindications are complains.

Adolescent↗

Neonatal (perinatal) hemochromatosis.

Autopsy findings are described of six cases (from four families) of neonatal hemochromatosis, a defect featured by severe prenatal iron storage in the liver and in a number of visceral organs similarly as in the hereditary adult-type hemochromatosis. Genetically, the two disorders are different, however. All the cases showed a characteristic liver damage with heavy iron deposits in the liver cells, lobular disarray and intralobular fibrosis, tendency towards multinuclear hepatocyte formation, ultimately resulting in pigmented cirrhosis and liver failure. In five instances the cirrhosis present was atrophic, in one case it was hepatomegalic. Death occurred prenatally in one case (31st week), perinatally in three, and two cases died as young infants. The mechanism of the liver disorder, mainly that of iron accumulation, has remained unresolved. Extrahepatally, hemosiderosis affected various epithelia (in particular, thyreocytes, renal distal tubular epithelia and those of pancreatic acini) and myocardial cells which, however, did not show any damage. In two instances the placenta was conspicuously hyperplastic, in one case it showed prominent hydropic transformation of its villi. In one case there was simultaneous cytomegaly. Entities which must be considered in the differential diagnosis of neonatal hemochromatosis because of considerable hepatic and extrahepatic iron accumulation have been discussed.

Adult↗

[Antibodies against human recombinant erythropoietin: an unusual cause of erythropoietin resistance].

In a 70 year old man with primary glomerulonephritis, severe anemia occurred after 4 years on hemodialysis and rHu-EPO. The usual mechanisms of EPO-resistance were excluded. A bone marrow sample showed red all aplasia. No circulating EPO could be detected; the serum inhibited the growth of erythroid precursors in bone marrow cultures. Immunoprecipitation identified an IgG anti-EPO, still active against deglycosylated EPO, i.e. directed against the peptidic matrix. Its high neutralising capacity and the absence of any immune abnormality rule out an auto-antibody. Anti-rHu EPO immunisation is a very rare occurrence, made severe by transfusion-dependence and the risk of hemosiderosis. An immuno-modulating treatment can therefore be justified.

Aged↗

NTP technical report on the toxicity studies of Acetone in F344/N Rats and B6C3F1 Mice (Drinking Water Studies) (CAS No. 67-64-1).

Toxicity studies were conducted by administering acetone (greater than 99%percnt; pure) in drinking water to groups of F344/N rats and B6C3F1 mice of each sex for 14 days or 13 weeks. Fourteen-Day Studies: All rats and mice receiving concentrations as high as 100,000 ppm acetone in drinking water lived to the end of the 14-day studies. The mean body weights of male rats receiving 50,000 or 100,000 ppm and female rats given 100,000 ppm were lower than those of controls. Body weights of all groups of mice were similar. Kidney and liver weight to body weight ratios for exposed rats and mice were greater than those for controls. Histopathologic changes were not seen in these organs in rats or in the kidney in mice. Centrilobular hepatocellular hypertrophy was noted in male and female mice receiving 20,000 and 50,000 ppm acetone, respectively. Thirteen-Week Studies: All rats lived to the end of the 13-week studies (drinking water concentrations as high as 50,000 ppm). The final mean body weights of rats receiving 50,000 ppm were 19%percnt; lower than that of controls for males and 7%percnt; lower for females. Water consumption by all rats that received 50,000 ppm acetone and females that received 20,000 ppm or more was notably lower than that by controls. Liver and kidney weight to body weight ratios were increased for male and female rats receiving 20,000 ppm or greater. Caudal and right epididymal weights and sperm motility were decreased for male rats given 50,000 ppm, and the percentage of abnormal sperm was increased. Leukocytosis and thrombocytopenia were observed at 20,000 ppm and above (males and females), and reticulocytopenia and erythrocytopenia were seen at 5,000 ppm and above (males). These changes, in addition to increase in erythrocyte size (MCV), are consistent with macrocytic anemia. Splenic pigmentation (hemosiderosis) noted in dosed male rats was apparently related to these changes. The increased incidence and severity of nephropathy observed in dosed male rats were considered the most prominent chemically related findings in this study. All mice lived to the end of the 13-week studies (drinking water concentrations up to 20,000 ppm for males and up to 50,000 ppm for females). The final mean body weights of dosed and control mice were similar. Water consumption by female mice that received 50,000 ppm acetone was notably lower than that by controls. The absolute liver weight and the liver weight to body weight ratio were significantly increased for females receiving 50,000 ppm, and the absolute spleen weight and the spleen weight to body weight ratio were significantly decreased. Results from the hematologic analyses did not show any biologically significant effects. Centrilobular hepatocellular hypertrophy of minimal severity was seen in 2110 female mice receiving 50,000 ppm. No compound-related lesions were found in male mice. In summary, the results from these studies show that acetone is mildly toxic to rats and mice when administered in drinking water for 13 weeks. Minimal toxic doses were estimated to be 20,000 ppm acetone for male rats and male mice and 50,000 ppm acetone for female mice. No toxic effects were identified for female rats. The testis, kidney, and hematopoietic system were identified as target organs in male rats, and the liver was the target organ for male and female mice. Synonyms: 2-propanone; dimethyl ketone; pyroacetic acid. (NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.)

Journal Article↗

[The significance of immunologic phenomenons in pulmonary diseases of children (author's transl)].

Under special conditions the lung develops reactions of hypersensitivity, e.g. by the contact with antigens consisting of foreign proteins, organic dusts or different pathogen organisms. It must be distinguished between uncomplicated allergic and autoimmune diseases. The exact separation is difficult, because transitions from one state to the other are possible. The autoimmunisation is a very complicated phenomenon, where endogensou cells are effective as auto-antigens and induce the development of auto-antibodies. From the pathological-anatomical point of view thate are no typical structural changes in the lung, which define a disease as a special autoimmune disease. But the prevalence of round cells in inflamed tissue, the appearance of granuloma with epithelial cells point to immunological phenomenons. Examples for allergic diseases are: "Asthma bronchiale, pigeon-breeder disease, mite-allergy, farmer's lung, drug-induced allergy", and for autoimmune diseases: "Lupus erythematosus, rheumatoid arthritis, polyarteritis nodosa, idiopathic pulmonary hemosiderosis, idiopathic pulmonary fibrosis." The drug-therapy consists of corticoids and immune-suppressive drugs.

Adolescent↗

Intestinal mucosal changes in thalassaemia major.

Ten infants and children suffering from Thalassaemia major, proven by clinical, hematological and biochemical criteria, were subjected to intestinal biopsy. Specimens were studied for histological and histochemical patterns. The histological picture showed shortening and fusion of villi with cellular infiltration. Reduced mucopolysaccharides and relatively normal alkaline phosphatase activity were demonstrated. The degree of histological and histochemical changes correlates with the degree of anemia. The effects of these changes on the iron absorption and the tissue hemosiderosis are aroused. The possibility of these changes, being non-specific and secondary to anemia and tissue hypoxia is also postulated.

Child↗

[The prevention programs for beta thalassemia in the Jezreel and Eiron valleys: results of fifteen years experience].

UNLABELLED: beta thalassemia is an hereditary disease caused by mutations in the beta globin gene. The clinical course is characterized by chronic hemolytic anemia that required regular blood transfusions. Secondary to the blood transfusions, patients developed severe hemosiderosis that can cause death in the early twenties unless appropriate iron chelator therapy is given. Due to the severity of the disease and the expensive treatment, a prevention program should be instituted. We report our experience in a prevention program among pregnant women in the Jezreel and Eiron Valleys during a period of fifteen years. RESULTS: A total of women were screened for beta thalassemia. Within this group, 928 were found to be carriers and 180 couples were found to be at risk to deliver an affected baby. Two hundred and fifty nine prenatal diagnoses were performed and in 45 cases the parents decided to abort the affected child. In ten cases the parents choose to deliver an affected baby. Fifteen different beta globin mutations were detected in the area covered by the program. CONCLUSIONS: A prevention program among pregnant women is feasible and prevents most of the new cases of hemoglobinopathies in the covered area. RECOMMENDATIONS: Based on our experience, and the relative low cost of this program, we recommend instituting a national prevention program for beta thalassemia throughout the country.

Abortion, Induced↗

Rituximab for refractory childhood autoimmune hemolytic anemia.

BACKGROUND: Chronic childhood autoimmune hemolytic anemia is an uncommon disorder that is associated with significant morbidity. Treatment with high dose steroids, splenectomy and frequent blood transfusions results in a myriad of complications including growth failure, bone demineralization, Cushing's syndrome, immunosuppression, and transfusional hemosiderosis. OBJECTIVES: To investigate the efficacy of the monoclonal anti-CD20 antibody, rituximab, in treating children with AIHA. METHODS: Four children with chronic AIHA, including two with prior splenectomy, who were dependent on high dose steroids and refractory to other immunosuppressive regimens were treated with four to six weekly doses of rituximab at a dose of 375 mg/m2. RESULTS: All four patients became transfusion-independent and were taken off prednisone completely. Adverse effects included infusion-related reactions that were mild, and infectious complications of Pneumocystis carinii pneumonia and varicella pneumonia. CONCLUSIONS: Treatment with rituximab appears promising for refractory AIHA; if may obviate the need for prednisone and may result in sustained disease remissions in some patients.

Adolescent↗

NTP Toxicology and Carcinogenesis Studies of Isobutyl Nitrite (CAS No. 542-56-3) in F344 Rats and B6C3F1 Mice (Inhalation Studies).

Isobutyl nitrite is used to a limited extent as an intermediate in the syntheses of aliphatic nitrites. It is also an ingredient of various incenses or room odorizers and is used as a euphoric. The chemical has also been used as a jet propellant and in the preparation of fuels. Isobutyl nitrite was nominated by the Consumer Product Safety Commission to the NTP for toxicology and carcinogenicity studies because of its possible contribution to the high incidence of Kaposi's sarcoma among male homosexual acquired immune deficiency syndrome patients and because of the lack of available data on the potential carcinogenicity of isobutyl nitrite. Male and female F344/N rats and B6C3F1 mice were exposed to isobutyl nitrite (purity of 93% or greater) by inhalation for 16 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, Drosophila melanogaster, and mouse peripheral blood. 16-DAY STUDY IN RATS: Groups of five male and five female F344/N rats were exposed to 0, 100, 200, 400, 600, or 800 ppm (approximately 420, 840, 1,700, 2,500, or 3,300 mg/m(3)) isobutyl nitrite by inhalation for 6 hours per day, 5 days per week for a total of 12 exposures during a 16-day period. All males and females exposed to 600 or 800 ppm and one 400 ppm female died on the first day of the study. Final mean body weights and mean body weight gains of 400 ppm males and females were significantly lower than those of the controls. Clinical findings observed in 400 ppm males and females included ocular discharge, lethargy, hunched posture, and rough coats. Absolute and relative lung weights of all exposed groups of males and of 200 and 400 ppm females were less than those of the controls. Chemical-related hyperplasia of the bronchial epithelium was observed in 200 and 400 ppm males and females and hyperplasia of the nasal turbinate epithelium was observed in rats exposed to 400 ppm or less. Hemosiderin pigmentation was observed in the spleen of 200 and 400 ppm males and females and bone marrow hematopoietic hyperplasia was observed in rats exposed to 400 ppm or less. 16-DAY STUDY IN MICE: Groups of five male and five female B6C3F1 mice were exposed to 0, 100, 200, 400, 600, or 800 ppm (approximately 420, 840, 1,700, 2,500, or 3,300 mg/m(3)) isobutyl nitrite by inhalation for 6 hours per day, 5 days per week for a total of 12 exposures during a 16-day period. Three males and four females exposed to 800 ppm died before the end of the study. Final mean body weights and mean body weight gains of 600 and 800 ppm males and females were significantly lower than those of the controls. Mice exposed to 400 ppm or greater were lethargic and exhibited hunched posture and rough coats. Absolute and relative lung weights of 600 and 800 ppm males and the relative lung weight of 600 ppm females were significantly greater than those of the controls. Chemical-related hyperplasia of the bronchiolar epithelium was observed in all exposed groups of males and females. Lymphocytic atrophy of the spleen and thymus was observed in males and females exposed to 400 ppm or greater. 13-WEEK STUDY IN RATS: Groups of 10 male and 10 female F344/N rats were exposed to 0, 10, 25, 75, 150, or 300 ppm (approximately 42, 105, 315, 630, or 1,260 mg/m(3)) isobutyl nitrite by inhalation for 6 hours per day, 5 days per week for 13 weeks. All rats survived to the end of the study. Final mean body weights and mean body weight gains of 300 ppm males and females were significantly lower than those of the controls, as was the mean body weight gain of 150 ppm females. Clinical findings observed during the study included ruffled fur in 300 ppm males and females, hypoactivity in 300 ppm males, and hyperactivity in 150 and 300 ppm females. A very mild chemical-related methemoglobinemia and anemia occurred in male and female rats in the 75, 150, and 300 ppm groups. Hematopoietic hyperplasia occurred in the bone marrow of all exposed groups of males and females and was considered to be a secondary response to the anemia and methed methemoglobinemia. There was minimal hemosiderin pigment accumulation in the spleens of males and females exposed to 75 ppm or greater, mild to moderate epithelial cell hyperplasia of the nasal mucosa was observed in 300 ppm males and females, and minimal hyperplasia occurred in 150 ppm males and females. Hyperplasia of the bronchial epithelium was observed in 300 ppm males and females. 13-WEEK STUDY IN MICE: Groups of 10 male and 10 female B6C3F1 mice were exposed to 0, 10, 25, 75, 150, or 300 ppm (approximately 42, 105, 315, 630, or 1,260 mg/m(3)) isobutyl nitrite by inhalation for 6 hours per day, 5 days per week for 13 weeks. There were no chemical-related deaths. Final mean body weights and mean body weight gains of 150 and 300 ppm females were significantly less than those of the controls. Final mean body weights and mean body weight gains of exposed groups of males were similar to those of the controls. There were no chemical-related clinical findings. A very mild chemical-related methemoglobinemia occurred in male and female mice in the 150 and 300 ppm groups. A very mild anemia occurred in the 300 ppm groups. In the lung, increased incidences of mild to moderate hyperplasia of the bronchiolar epithelium occurred in males and females exposed to 300 ppm. Minimal hyperplasia occurred in males exposed to 75 ppm or greater and in females exposed to 150 ppm. Minimal epithelial cell hyperplasia of the nasal mucosa was observed in 300 ppm males. Increased hematopoiesis of the spleen, secondary to the hematotoxicity, occurred in males exposed to 75 ppm or greater and in females exposed to 150 or 300 ppm. Increased hemosiderosis of the spleen occurred in males exposed to 300 ppm and in females exposed to 75 ppm or greater. 2-YEAR STUDY IN RATS: Based on the low final mean body weights, anemia, and the mild to moderate nasal mucosal lesions and the hyperplastic bronchial lesions observed in 300 ppm males and females, isobutyl nitrite exposure concentrations selected for the 2-year inhalation study in rats were 37.5, 75, and 150 ppm. Groups of 56 male and 56 female rats were exposed to 0, 37.5, 75, or 150 ppm (equivalent to 0, 158, 315, or 630 mg/m(3)) isobutyl nitrite by inhalation for 6 hours per day, 5 days per week, for 103 weeks. Ten male and 10 female rats from each group were evaluated at 15 months for clinical pathology and histopathology. Survival, Body Weights, Clinical Findings, Hematology, and Clinical Chemistry: Survival rates of exposed groups of rats were greater than those of the controls, and the survival rates of 75 and 150 ppm males were significantly greater than that of the control. Mean body weights of 150 ppm males and females were 3&percnt; to 11&percnt; lower than those of the controls throughout the course of the study. There were no clinical findings considered to be related to isobutyl nitrite exposure. A very mild methemoglobinemia and anemia occurred in male and female rats exposed to 75 or 150 ppm. Pathology Findings: Incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) occurred with significant positive trends in exposed males and females, and the incidences of these neoplasms in 75 ppm males and in 150 ppm males and females were significantly greater than those in the controls. The incidence of alveolar/bronchiolar carcinoma was significantly greater in 150 ppm male rats than that in the controls. The incidences of alveolar epithelial hyperplasia were also increased in 75 and 150 ppm males and in all exposed groups of females. The incidences of mononuclear cell leukemia in exposed groups of males and females were significantly less than those in the controls. 2-YEAR STUDY IN MICE: Based on the low final mean body weight of 300 ppm females and the mild to moderate bronchiolar hyperplasia observed in 300 ppm males and females, isobutyl nitrite exposure concentrations selected for the 2-year inhalation study in mice were 37.5, 75, and 150 ppm. Groups of 60 male and 60 female mice were exposed to 0, 37.5, 75, or 150 ppm (equivalent to 0, 158, 315, or 630 mg/m(3)) isobutyl nitrite by inhalation for 6 hours per day, 5 days per week, for 103 weeks. As many as 10 male and 10 female mice from each group were evaluated at 15 months for clinical pathology and histopathology. Survival, Body Weights, Clinical Findings, and Hematology and Clinical Chemistry: Survival rates of exposed groups of males were similar to those of the controls. Survival rates of exposed groups of females were greater than those of the controls, and the survival rate in 37.5 ppm females was significantly greater than that of the controls. Mean body weights of exposed groups of males and of 37.5 and 75 ppm females were similar to those of the controls throughout the study. Mean body weights of 150 ppm females were lower than those of the controls from week 20 until the end of the study. There were no biologically significant clinical findings noted in the 2-year study in mice. A very mild methemoglobinemia and anemia occurred in male and female mice exposed to 75 or 150 ppm. Pathology Findings: Incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) occurred with significant positive trends in exposed males and females, and the incidences of these neoplasms were significantly greater than those in the controls in 75 ppm males and in 150 ppm males and females. Incidences of alveolar epithelial hyperplasia were significantly increased in 75 and 150 ppm male and female mice. Thyroid gland follicular cell adenoma occurred with a significant positive trend in male mice; the incidences of thyroid gland follicular cell hyperplasia were increased in all exposed groups of males, and the incidences in males exposed to 37.5 or 150 ppm were significantly greater than those in the controls. Incidences of serous exudate and olfactory epithelium atrophy in the nose of 150 ppm females were significantly greater than those in the controls. Incidences of minimal to mild hemosiderin pigment in the spleen of 75 and 150 ppm male mice were significantly greater than those in the controls. GENETIC TOXICOLOGY: Isobutyl nitrite was found to be mutagenic in vitro and in vivo. It induced base-pair substitution mutations in Salmonella typhimurim strains TA100 and TA1535 and sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells. Positive responses in the S. typhimurium tests required S9 activation, but isobutyl nitrite induced chromosomal effects in cultured Chinese hamster ovary cells with and without S9. In vivo, no induction of sex-linked recessive lethal mutations was noted in the germ cells of male Drosophila melanogaster exposed to isobutyl nitrite via feeding or injection. However, significant increases in micronucleated normochromatic erythrocytes were observed in the peripheral blood of male and female mice treated with isobutyl nitrite for 90 days by inhalation. CONCLUSIONS: Under the conditions of these 2-year inhalation studies, there was clear evidence of carcinogenic activity of isobutyl nitrite in male and female F344/N rats based on the increased incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined). There was some evidence of carcinogenic activity of isobutyl nitrite in male and female B6C3F1 mice based on the increased incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) in males and females. The increased incidence of thyroid gland follicular cell adenoma in male mice may have been related to isobutyl nitrite exposure. Exposure of rats and mice to isobutyl nitrite by inhalation for 2 years resulted in increased incidences of alveolar epithelial hyperplasia (male and female rats and mice), thyroid gland follicular cell hyperplasia and splenic hemosiderin pigmentation (male mice), and serous exudate and atrophy of the olfactory epithelium of the nose (female mice). Exposure of rats to isobutyl nitrite by inhalation for 2 years resulted in decreased incidences of mononuclear cell leukemia in males and females.

Journal Article↗

[Several clinic-morphologic aspects and problems concerning the pathogenesis of the Marchiafava-Miche li syndrome (paroxysmal nocturnal hemoglobinuria].

The authors present a broad pathoanatomic picture and concise clinical-laboratory characteristics of Marchiafava-Micheli's disease on the basis of their studies of case record date of 31 patients, data of 13 autopsies and findings of 27 treanobiopsies. Changes in the organs observed in Marchiafava-Micheli's disease were first of all morphological manifestations of massive intravascular hemolysis and associated with latter complications The most characteristic pathoanatomic feature was changes in the bone marrow which manifested themselves in hyperplasis of nuclear forms of the red series and in drastically pronounced disorders of the microcirculation. Necrobiotic changes in the kidney accompanied by massive hemosiderosis, dystrophic changes in the liver with the development of cirrhosis, inhibition of lymphopoiesiis in the spleen and lymph nodes were detected most often...

Biopsy↗

Toxicology and Carcinogenesis Studies of Bromoethane (Ethyl Bromide) (CAS No. 74-96-4) in F344/N Rats and B6C3F1 Mice (Inhalation Studies).

Bromoethane is an alkylating agent used primarily as a chemical intermediate in various organic syntheses. In toxicology and carcinogenesis studies, groups of F344/N rats and B6C3F1 mice of each sex received whole-body exposure to bromoethane (greater than 98% pure) once for 4 hours or for 6 hours per day, 5 days per week, for 14 days, 14 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium and Chinese hamster ovary (CHO) cells. Single-Exposure, Fourteen-Day, and Fourteen-Week Studies: Single-exposure inhalation studies were conducted in rats and mice at target concentrations of 625, 1,250, 2,500, 5,000, or 10,000 ppm bromoethane. All rats exposed to 10,000 ppm bromoethane and 3/5 female rats exposed to 5,000 ppm died before the end of the single-exposure studies. All mice exposed to 5,000 or 10,000 ppm bromoethane and 2/5 female mice exposed to 1,250 ppm died before the end of the studies. Fourteen-day inhalation studies were conducted in rats and mice at target concentrations of 0, 250, 500, 1,000, 2,000, or 4,000 ppm bromoethane. All rats and mice exposed to 2,000 or 4,000 ppm died before the end of the 14-day studies. Final mean body weights of exposed and control rats were similar. Fourteen-week inhalation studies were conducted in rats and mice at target concentrations of 0, 100, 200, 400, 800, or 1,600 ppm bromoethane. Four of 10 male and 2/10 female rats exposed to 1,600 ppm died before the end of the 14-week studies. The final mean body weights of rats exposed to 1,600 ppm were lower than the initial mean body weights. Compound-related lesions observed in rats at 1,600 ppm, but not at lower concentrations, included minimal atrophy of the thigh muscle, minimal-to-moderate multifocal mineralization in the cerebellum of the brain, minimal-to-severe hemosiderosis of the spleen, marked atrophy of the testis, and minimal-to- mild atrophy of the uterus. The effects in the testis and uterus are probably due to chemical-related loss in body weight during the studies. In mice, compound-related deaths included 3/10 male and 1/10 female mice exposed to 1,600 ppm, 1/9 males exposed to 800 ppm, and 1/10 males exposed to 400 ppm. The final mean body weights of male and female mice exposed to 1,600 ppm were about 15% lower than those of controls. Compound-related effects included atrophy of the uterus and involution of the ovary in females exposed to 1,600 ppm bromoethane. Based on these results, 2-year studies were conducted by exposing groups of 49 or 50 rats or mice of each sex to bromoethane at 0, 100, 200, or 400 ppm, 6 hours per day, 5 days per week. Body Weight and Survival in the Two-Year Studies: Mean body weights of exposed and control rats were generally similar throughout the studies. No significant differences in survival were observed between any groups of male rats (control, 17/49; 100 ppm, 26/50; 200 ppm, 27/50; 400 ppm, 21/50); survival of the 100-ppm group of female rats was greater than that of controls (19/50; 29/50; 24/49; 23/50), and the number of control and 400-ppm male rats and control female rats surviving to the end of the studies was low. Mean body weights of the 400-ppm group of male mice were up to 9% lower than those of controls throughout the study. Mean body weights of the 400-ppm group of female mice were generally 6%-16% lower than those of controls after week 29. No differences in survival were observed between any group of male mice (35/50; 37/50; 30/50; 34/50). The survival of the 400-ppm group of female mice was lower than that of controls at the end of the study (36/50; 37/50; 37/49; 23/49). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: The incidences of pheochromocytomas or malignant pheochromocytomas (combined) of the adrenal medulla were increased in exposed male rats (control, 8/40; 100 ppm, 23/45; 200 ppm, 18/46; 400 ppm, 21/46). Granular cell neoplasms of the brain were seen in exposed male rats but not in controls (0/49; 3/50; 1/50; 1/50). A glioma, an astrocytoma, or an oligodendroglioma was seen in 3/50 male rats exposed to 100 p in 3/50 male rats exposed to 100 ppm. Gliomas were not observed in control female rats, but they occurred in exposed female rats with a significant positive trend (0/50; 1/50; 1/48; 3/50). The historical incidence of granular cell tumors in male F344/N rat chamber controls at the study laboratory is 0/297. The incidences of gliomas in the exposed female groups were not significantly greater than that in the controls and were within the historical incidence range for glial cell neoplasms for untreated controls in NTP studies (mean: 23/1,969, 1&percnt;; range: 0/50-3/50), but they exceeded the historical incidence range for chamber controls at the study laboratory (mean: 1/297, 0.3&percnt;; range: 0/50-1/50). Alveolar epithelial hyperplasia was increased in rats exposed to 400 ppm bromoethane (male: 3/48; 7/49; 7/48; 18/48; female: 5/50; 4/48; 5/47; 10/49). Alveolar/bronchiolar adenomas or carcinomas (combined) were seen in four male rats exposed to 200 ppm and in one exposed to 400 ppm. Alveolar/bronchiolar adenomas were observed in 3/49 female rats at 400 ppm but not at lower concentrations or in controls. The incidences in exposed male and female rats were not significantly greater than those in controls; however, the historical incidence in rat chamber controls for alveolar/bronchiolar adenomas or carcinomas (combined) at the study laboratory is 6/299 (2&percnt;) for males and 4/297 (1.3&percnt;) for females. The incidences of epithelial hyperplasia and squamous metaplasia of the nasal cavity were increased in rats exposed to 400 ppm. The incidence of suppurative inflammation of the nasal cavity was increased in exposed male rats, and the incidences of suppurative inflammation of the larynx and metaplasia of the olfactory sensory epithelium were increased in exposed male and female rats. An adenoma of the nose was seen in one 400-ppm male rat and in one 400-ppm female mouse. Suppurative inflammation and dilatation of the salivary gland ducts were observed at increased incidences in the 200- and 400-ppm groups of female rats. Animals were found to be positive for rat coronavirus/sialodacryoadenitis virus antibodies. The incidence of mammary gland neoplasms was significantly lower in female rats at 400 ppm than in controls (18/50; 15/50; 10/48; 7/50). Adenomas (0/50; 1/50; 1/47; 6/48), adenocarcinomas (0/50; 2/50; 3/47; 19/48), and squamous cell carcinomas (0/50; 1/50; 1/47; 3/48) of the uterus occurred in exposed female mice and not in control mice. The incidence of alveolar/bronchiolar neoplasms was greater in male mice at 400 ppm than in controls (adenomas or carcinomas, combined: 7/50; 6/50; 12/50; 15/50). Acute/chronic inflammation of the lung was observed at increased incidences in female mice at 200 and 400 ppm. Genetic Toxicology: Bromoethane, tested in a closed environment of a desiccator, was mutagenic in S. typhimurium strain TA100 with and without exogenous metabolic activation; it was not mutagenic in strain TA98. In cultured CHO cells, bromoethane induced sister chromatid exchanges (SCEs) but not chromosomal aberrations in both the presence and absence of exogenous metabolic activation. Conclusions: Under the conditions of these 2-year inhalation studies, there was some evidence of carcinogenic activity of bromoethane for male F344/N rats, as indicated by increased incidences of pheochromocytomas of the adrenal gland; neoplasms of the brain and lung may also have been related to exposure to bromoethane. For female F344/N rats, there was equivocal evidence of carcinogenic activity, as indicated by marginally increased incidences of neoplasms of the brain and lung. For male B6C3F1 mice, there was equivocal evidence of carcinogenic activity, based on marginally increased incidences of neoplasms of the lung. There was clear evidence of carcinogenic activity for female B6C3F1 mice, as indicated by neoplasms of the uterus. Synonyms: monobromoethane; bromic ether; hydrobromic ether

Journal Article↗

Epidermoid cancers that masquerade as venous ulcer disease.

Many lesions originally diagnosed as venous ulcers exhibit characteristics that are strikingly similar to skin cancers and might represent sites of primary carcinomas. To ascertain the frequency of malignancy in patients previously diagnosed with venous ulcer disease, a retrospective cohort review of patients evaluated at a Wound Healing Center in Florida was conducted. Charts of all patients with IDC-9 codes for varicose veins with stasis ulcer, varicose veins with ulcer and inflammation, and venous peripheral insufficiency were reviewed. Only charts of patients with one of these diagnoses and documented clinical varicosities, hemosiderosis, brawny edema, and lesions located at the medial or lateral lower leg were included. Sixty (60) patients were identified. Of these, 20 had lesions that were clinically suspicious for epidermoid skin cancers (ie, showing raised borders and chronic scaling). Biopsies confirmed malignancy in 15 of the 60 ulcers (25%). Of these, eight were squamous cell cancers. Given the high rate of malignancies in this cohort of patients, it is postulated that primary epidermoid cancers may mimic venous ulcers in appearance, location, and symptoms; that Marjolin's ulcers are rare despite their propensity to develop in many different types of wounds; and that patients with a history of venous ulcers and prolonged exposure to ultraviolet rays may benefit from lesion biopsies to test for epidermoid cancers.

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NTP Toxicology and Carcinogenesis Studies of n-Butyl Chloride (CAS No. 109-69-3) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

Toxicology and carcinogenesis studies of n-butyl chloride (greater than 99.5% pure), a solvent as well as an alkylating agent, were conducted by exposing groups of F344/N rats and B6C3F1 mice to n-butyl chloride in corn oil by gavage for 14 days, 13 weeks, and 2 years. In the 14-day studies, no compound-related gross pathologic effects were observed in groups of five male or female rats or mice administered doses of up to 3,000 mg/kg body weight. However, deaths occurred in the groups administered 750, 1,500, or 3,000 mg/kg. Tremors and convulsions following gavage administration were observed. In the 13-week studies, groups of 10 male and 10 female rats were administered up to 500 mg/kg n-butyl chloride, and similar groups of mice received up to 1,000 mg/kg, Three of 10 male rats in the 500 mg/kg dose group and one female mouse in the 120 mg/kg dose group died before the end of the studies. Mild to moderate extramedullary hematopoiesis was observed in 3/10 male rats receiving 500 mg/kg. Mean body weights of male and female rats receiving 250 or 500 mg/kg were lower than those of the vehicle controls. Convulsions were observed in male and female rats receiving 250 mg/kg or higher and in 2/10 female mice receiving 1,000 mg/kg. Based on these results, 2-year toxicology and carcinogenesis studies of n-butyl chloride were conducted by administering doses of 0, 60, or 120 mg/kg in corn oil by gavage to groups of 50 male and 50 female rats and doses of 0, 500, or 1,000 mg/kg to groups of 50 male and 50 female mice. In the 2-year studies, survival relative to that of vehicle controls was significantly lower in high dose male rats (40/50 vs 17/50) and high dose female rats (35/50 vs 11/50) and in male mice receiving 1,000 mg/kg (33/50 vs 10/50). Due to excessive mortality in the 1,000 mg/kg female mice, the group was terminated in the 45th week and a second series of 2-year studies in mice of each sex was started at concentrations of 0 and 250 mg/kg. Male mice in the 1,000 mg/kg group had 10% lower mean body weights than the vehicle control group. No adverse effects on survival or body weights in other dosed groups of rats and mice were observed. Convulsions were observed before or after gavage administration on several occasions during the rat studies. These observations were noted primarily in the high dose groups (male: vehicle control, 1/50; low dose, 3/50; high dose, 27/50; female: vehicle control, 0/50; low dose, 7/50; high dose, 45/50). Hemorrhage of the brain and alveoli were observed primarily in high dose male and female rats dying from convulsions. Lymphoid depletion of the spleen and splenic hemosiderosis were also observed inthese animals. In mice, convulsions were observed only in the first studies (in the high dose female mice that were terminated early and in 6/50 high dose male mice). Pheochromocytomas of the adrenal gland occurred at marginally increased incidence in low dose female rats (1/50; 6/50; 1/49). Hyperplasia was observed in 3/50 vehicle controls, 7/50 low dose females, and 4/49 high dose females. The incidence of pheochromocytomas was low, not dose related, and not seen in males, and thus it was not considered to be compound related. Cytoplasmic vacuolization of the adrenal cortex occurred at increased incidences in males (5/50; 10/50; 20/50) but not in female rats. Nephropathy of the kidney occurred at increased incidences in female rats (13/50; 25/50; 20/50) but not in male rats. Additional nonneoplastic lesions such as congestion, inflammation, or nephrosis were not present to any degree in either vehicle control or dosed female rats. An increased incidence of alveolar/bronchiolar adenomas or carcinomas (combined) was observed in the 500 mg/kg group of female mice (3/50 vs 9/50), but little effect was seen in the 250 mg/kg group (6/50 vs 8/50). The incidences of adenomas or carcinomas (combined) in dosed female mice were not significantly different from that in the pooled vehicle control group from the first and second studies (pooled controls, 9/100; 250 mg/kg, 8/50; 500 mg/kg, 9/50). The lack o0). The lack of hyperplasia in female mice and the negative trend in male mice suggest that these marginal effects were probably not related to the administration of n-butyl chloride. An increased incidence of hepatocellular adenomas or carcinomas (combined) was observed in the 500 mg/kg dose group of female mice (3/50 vs 8/50) but not in the 250 mg/kg dose group (9/50 vs 7/50). An increased incidence of hemangiosarcomas was observed in male mice in the first study (1/50; 3/50; 4/50) but not in the second study (4/50 vs 2/50). Neither of these marginal effects was regarded as compound related. n-Butyl chloride was not mutagenic in Salmonella typhimurium strains TA98, TA1535, or TA1537 in the presence or absence of Aroclor 1254-induced male Sprague-Dawley rat liver S9 or in the presence of male Syrian hamster liver S9. n-Butyl chloride was mutagenic in the mouse lymphoma L5178Y/TK&plusmn; assay in the absence of Aroclor-induced male rat liver S9 and was not tested in the presence of S9. n-Butyl chloride did not induce sister-chromatid exchanges or chromosomal aberrations in Chinesehamster ovary cells in the presence or absence of Aroclor-induced male rat liver S9. An audit of the experimental data was conducted for the 2-year studies of n-butyl chloride. No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenicity of n-butyl chloride for male and female F344/N rats at daily doses of 60 or 120mg/kg, for male B6C3F1 mice at doses of 250, 500, or 1,000 mg/kg, or for female B6C3F1 mice at doses of 250 or 500 mg/kg. Chemical-induced toxicity in high dose rats (primarily females) reduced the sensitivity of the study for determining carcinogenicity. Synonyms: 1-chlorobutane; butyl chloride; n-propylcarbinyl chloride

Journal Article↗

NTP Toxicology and Carcinogenesis Studies of Dichloromethane (Methylene Chloride) (CAS No. 75-09-2) in F344/N Rats and B6C3F1 Mice (Inhalation Studies).

Dichloromethane is widely used in industrial processes, food preparation, and agriculture. In industry, dichloromethane is used as a solvent in paint removers, degreasing agents, aerosol propellants, and triacetate solutions; as a blowing agent in flexible urethane foams; and as a process solvent in the manufacture of steroids, antibiotics, vitamins, and tablet coatings. The use of dichloromethane as an extraction solvent for spice oleoresins, hops, and caffeine from coffee has been approved by the U.S. Food and Drug Administration. Dichloromethane has been used as an inhalation anesthetic and as a fumigant for grain and strawberries. Toxicology and carcinogenesis studies of dichloromethane (99% pure) were conducted by inhalation exposure of groups of 50 male and 50 female F344/N rats and B6C3F1 mice 6 hours per day, 5 days per week, for 102 weeks. The exposure concentrations used (0, 1,000, 2,000, or 4,000 ppm for rats and 0, 2,000, or 4,000 ppm for mice) were selected on the basis of results from 13-week inhalation studies in which groups of 10 rats and 10 mice of each sex were exposed to dichloromethane at concentrations of 525-8,400 ppm 6 hours per day, 5 days per week. During the 2-year studies in rats, body weight gains for exposed males and females were comparable to those of the chamber controls. The survival of exposed male rats was comparable to that of the chamber controls; however, the survival of all groups of males at the termination of the study was low (control, 16/50; low dose, 16/50; mid dose, 17/50; high dose, 9/50). Most of the early deaths among male rats occurred during the final weeks of the study; the survival of male rats through week 86 of the study was 36/50, 39/50, 37/50, and 33/50. This decreased survival is believed to be related to the high incidence of leukemia (34/50; 26/50; 32/50; 35/50). Survival of female rats exposed at 4,000 ppm was reduced relative to that of the chamber controls (30/50; 22/50; 22/50; 15/50); leukemia occurred frequently in all female rat groups. Final mean body weights of high dose male mice and low and high dose female mice were 10%-17% lower than those of the chamber controls; these reductions occurred during the last 16 weeks of the study. The survival of dosed male mice and high dose female mice was reduced relative to that of the chamber controls (male: control, 39/50; low dose, 24/50; high dose, 11/50; female: 25/50; 25/50; 8/50). This reduced survival may have been due to the chemically induced development of liver and lung neoplasia in male and female mice. Increased incidences of benign mammary gland lesions (adenomas and fibroadenomas) occurred in male and female rats exposed to dichloromethane (male: 0/50; 0/50; 2/50; 5/50; female: 5/50; 11/50; 13/50; 23/50). The incidence of malignant mammary gland neoplasms was not increased in female rats (2/50; 2/50; 2/50; 0/50); none was observed in male rats. In addition, integumentary system tumors in the area of the mammary chain occurred with a positive trend in male rats (subcutaneous tissue fibroma or sarcoma: 1/50; 1/50; 2/50; 5/50); the combined incidence of all tumors in the mammary area in male rats was 1/50, 1/50, 4/50, and 9/50. Exposure to dichloromethane was associated with increased incidences of hepatic hemosiderosis, cytomegaly, cytoplasmic vacuolization, necrosis, granulomatous inflammation, and bile duct fibrosis in both male and female rats. There was a positive but marginal trend in the incidence of hepatocellular neoplastic nodules or hepatocellular carcinomas (combined) in female rats (2/50; 1/50; 4/50; 5/50). The incidence of squamous metaplasia of the nasal cavity was increased in female rats exposed at 4,000 ppm (1/50; 2/50; 3/50; 9/50) but not in males (4/50; 5/50; 3/50; 3/50). No nasal cavity tumors were observed in rats. The increased incidences of mononuclear cell leukemia in mid dose and high dose female rats (17/50; 17/50; 23/50; 23/50) were statistically significant by age-adjusted analyses. In male rats, mesotheliomas (arising primarily from the tunica vaginalis) occurred at increas) occurred at increased incidences (0/50; 2/50; 5/50; 4/50). Lung tumors occurred at increased incidences in male and female mice exposed to dichloromethane (alveolar/bronchiolar adenomas: male - 3/50; 19/50; 24/50; female - 2/50; 23/48; 28/48; alveolar/bronchiolar carcinomas: male - 2/50; 10/50; 28/50; female - 1/50; 13/48; 29/48). Cytologic degeneration of the liver was observed at increased incidences in high dose male and dosed female mice (male: 0/50; 0/49; 22/49; female: 0/50; 23/48; 21/48). Incidences of hepatocellular adenomas or hepatocellular carcinomas (combined) were increased in high dose male and dosed female mice (male: 22/50; 24/49; 33/49; female: 3/50; 16/48; 40/48). There were also dose-related increases in the numbers of mice bearing multiple lung or liver neoplasms. Dose-related increases were observed in the incidences of testicular atrophy in male mice and uterine and ovarian atrophy in female mice; these effects are considered to be secondary responses to neoplasia. An audit of the experimental data was conducted for the 2-year studies of dichloromethane. No data discrepancies were found that influenced the final interpretations. Under the conditions of these inhalation studies, there was some evidence of carcinogenicity of dichloromethane for male F344/N rats as shown by an increased incidence of benign neoplasms of the mammary gland. There was clear evidence of carcinogenicity of dichloromethane for female F344/N rats as shown by increased incidences of benign neoplasms of the mammary gland. There was clear evidence of carcinogenicity of dichloromethane for male and female B6C3F1 mice, as shown by increased incidences of alveolar/bronchiolar neoplasms and of hepatocellular neoplasms. Synonyms: DCM; methylene chloride

Journal Article↗

Carcinogenesis Bioassay of 2-Biphenylamine Hydrochloride (CAS No. 2185-92-4) in F344/N Rats and B6C3F1 Mice (Feed Study).

2-Biphenylamine (2-aminobiphenyl) is a chemical intermediate used in the manufacture of C.I. Acid Red 15. It is present as a contaminant in 4-biphenylamine (a rubber antioxidant) and in diphenylamine (a dye intermediate, stabilizer for nitrocellulose explosives, and a topical agent for prevention of screwworm infestation in animals). Single-dose, 14-day, and 13-week studies were conducted using technical-grade 2-biphenylamine (2-aminobiphenyl) containing up to 2.5% of the carcinogenic contaminant, 4-biphenylamine. When the contamination was recognized, analytical development was begun to purify the material. The salt, 2-biphenylamine hydrochloride, was prepared to obtain a more pure test product, which contained 0.006%-0.049% 4-biphenylamine. The prechronic tests were completed by the time purification was accomplished, so data from a second 14-day study with 2-biphenylamine hydrochloride were used to help set dose levels for the chronic study. The results of the comparative 14-day studies showed that technical-grade 2-biphenylamine was more toxic to mice than rats than 2-biphenylamine hydrochloride as evidenced by greater incidence of splenomegaly and greater weight gain depression. The technical-grade 2-biphenylamine caused a dose-related decrease in hemoglobin concentration and a dose-related increase in leukocyte count in male and female mice in the 13-week study. Hemosiderosis, congestion, and extramedullary hematopoiesis were present in the spleens of nearly all rats receiving 3,000 ppm or more of the chemical, and in nearly all mice with 1,000 ppm or more 2-biphenylamine in their diets. The chronic study was conducted with the purified 2-biphenylamine hydrochloride by feeding diets containing 1,000 or 3,000 ppm 2-biphenylamine hydrochloride to groups of 49 or 50 F344/N rats and 50 B6C3F1 mice of each sex for 103 weeks. Groups of 50 rats and 50 mice of each sex served as controls. Survival of dosed male and female rats and dosed female mice was comparable with that of the corresponding controls. Survival of high-dose male mice was significantly (P<0.010) less than that of low-dose and control male mice. There were little or no differences in body weight changes for rats or mice between dosed and control groups, although there was a slight decrease in body weight gain at the end of the study for high-dose male (-11%) and female (-8%) rats. Inflammatory cells and interstitial fibrosis were found in increased incidence in the kidneys of dosed male rats as compared with controls and were considered to be compound related. In addition to the increase in renal inflammation and fibrosis, dosed male rats had more focal cellular changes of the liver than did the controls. There were no increased or decreased incidences of tumors in rats that could be associated with chemical administration. Myelomonocytic leukemia in male rats (control, 14/50; low-dose, 1/50; high-dose, 4/50) and fibroadenomas of the mammary gland in female rats (22/50, 10/49, 9/50) occurred with significantly (P<0.03) decreasing trends and the incidences in the dosed groups were significantly (P<0.02) lower than that in the controls. There were no increased or decreased incidences of tumors in rats that could be associated with chemical administration. Hemangiosarcomas from all sites occurred in female mice with a statistically significant (P</=0.002) positive trend. The observed incidence of hemangiosarcomas was 0/49, 1/50, and 7/50 in the control, low-dose, and high-dose groups, respectively. The incidence in the high-dose group was significantly (P<0.01) higher than that in controls. The conclusion that this was due to 2-biphenylamine rather than the contaminant, 4-biphenylamine, is supported by the absence of urinary bladder tumors, which are common to 4-biphenylamine. Hemangiosarcomas also occurred in male mice with a statistically significant positive trend (P=0.040 by a life table test), with incidences of 0/50, 2/50, and 3/50. None of the pairwise comparisons were statistically different. The development of hemangiosarcomas may have been curtailedment of hemangiosarcomas may have been curtailed in the high-dose group of male mice, since only 21/50 survived until the termination of the study. The hemangiosarcomas found in female mice are uncommon with only 6/816 (0.7&percnt;) previously seen in controls at the same laboratory. The rate for control male mice is equally low: 7/803 (0.9&percnt;). Alveolar/bronchiolar adenomas of the lung occurred at a significantly (P<0.01) decreased rate in male mice with an incidence in dose groups lower (P<0.05) than that in controls. Under the conditions of the bioassay, 2-biphenylamine hydrochloride was not carcinogenic for F344/N rats of either sex. 2-Biphenylamine hydrochloride was carcinogenic for B6C3F1 female mice, inducing hemangiosarcomas at various sites. The evidence for an association between the administration of 2-biphenylamine hydrochloride and the increased incidence of hemangiosarcomas in male mice was equivocal. Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats: Negative Male Mice: Equivocal Female Mice: Positive

Journal Article↗