UMLS:C0596263 - FACTA Search

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Query: UMLS:C0596263 (carcinogenesis)
64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

(-)Epigallocatechin-3-gallate (EGCG), the major polyphenolic component of green tea, inhibits experimental chemical and physical carcinogenesis, yet little toxicological data has been reported. Therefore, we performed studies on the dermal toxicity of EGCG applied in an ointment formulation in mice. Female BALB/c mice were dehaired with a topical depilatory and administered 75 microl EGCG in hydrophilic Ointment U.S.P. at three concentrations (10, 3, and 1%, all w/w) daily for 30 days. At the 10% concentration, gross toxicity was manifested by the formation of erythema and papular lesions by day 5. A 7% reduction in weight was observed by day 15. No toxicity was observed at the two lower concentrations or in the vehicle control group. Also, no toxicity was observed when mice were dehaired by shaving. This study was repeated in female SKH1 mice, an outbred hairless strain that does not require depilation. No toxicity was observed in the SKH1 mice, indicating that daily topical EGCG appears non-toxic in normal skin. However, use of topical depilatories may potentiate dermal toxicity of EGCG.
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PMID:Dermal toxicity of topical (-)epigallocatechin-3-gallate in BALB/c and SKH1 mice. 1094 May 8

Chromosomal defects are frequently present in malignant and premalignant skin disorders; however, it is not known whether ultraviolet radiation from sunlight plays a role in their induction. To obtain information on the ability of ultraviolet A and ultraviolet B to induce chromosomal aberrations, cultured melanocytes and fibroblasts were exposed to physiologic doses of ultraviolet A or ultraviolet B and, for comparison, to gamma rays. As a measure of chromosomal aberrations, the formation of micronuclei was determined. To obtain sufficient statistical data on induced micronuclei and cell kinetics, a flow cytometry method has been modified and applied. The flow cytometry method analysis is based on staining the DNA with ethidium bromide and the cell membranes with 1,6-diphenyl-1,3,5,-hexatriene. We observed dose-dependent micronuclei formation after gamma or ultraviolet B irradiation in both cell types and also for ultraviolet A in fibroblasts. The yield of micronuclei induced in fibroblasts by ultraviolet A was only a factor 15 smaller than that induced by ultraviolet B (313 nm). The results indicate that 10 kJ per m2 (equivalent to 1 minimal erythema dose) of ultraviolet B and 150 kJ per m2 of ultraviolet A (0.2 minimal erythema dose) can induce 1% of micronuclei in fibroblasts, equivalent to the induction due to 0.6 Gy of gamma radiation. In conclusion, physiologic doses of sunlight can induce chromosomal aberrations at a level comparable with that observed after exposure to approximately 1 Gy of ionizing radiation. Therefore, sunlight can be considered a potential inducer of chromosomal aberrations in skin cells, which may contribute to skin carcinogenesis.
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PMID:Low doses of UVB or UVA induce chromosomal aberrations in cultured human skin cells. 1095 Dec 80

Protection against sun-induced damage leading to photocarcinogenesis in skin is a highly desirable goal. Among various strategies, chemopreventive approaches utilizing non-toxic agents to prevent the occurrence of precancerous lesions or their surrogate markers are potentially attractive. Epidemiological and experimental studies provide evidence that some naturally occurring chemical agents in the human diet can diminish cancer risk. Aside from water, tea is the most common beverage consumed worldwide. Black tea accounts for nearly 80% of total tea production. Black tea and green tea are derived from the same plant, Camelia sinensis. Green tea contains monomeric polyphenols known as flavanols and black tea contains dimeric flavanols and polymeric polyphenols known as theaflavins (TFs) and thearubigins (TRs). Over the past fifteen years our laboratory has been exploring the feasibility of using tea and its constitutents as an approach to skin cancer prevention. We demonstrated that green tea, black tea and constituent polyphenols protect against chemical- and ultraviolet B (UVB)-induced carcinogenesis and reduce the growth of established tumors in skin. We have also shown the efficacy of green and black tea extracts against UVB and psoralen + ultraviolet A (PUVA)-induced early damage in skin. Although PUVA is highly effective in treating certain skin diseases, careful follow-up studies of cohorts of patients have shown that similar to UVB, PUVA treatment increases the risk for cutaneous squamous cell carcinoma and melanoma. We have found that oral administration of a standardized green tea extract (SGTE) prior to and during treatment of SKH-1 mice diminished PUVA-induced skin hyperplasia and hyperkeratosis. SGTE-treatment also inhibited PUVA-induced accumulation of c-fos and p53 proteins and epithelial hyperproliferation. Both topical application and oral administration of SGTE after PUVA-treatment reduced skin inflammation and cell hyperproliferation. Topical application of SGTE to human skin prior to PUVA-treatment inhibited the delayed skin inflammatory response. Similarly, oral and topical administration of standardized black tea extract (SBTE) and its two major polyphenolic sub-fractions protect against UVB-induced erythema in SKH-1 mice. Furthermore, topical application of tea extracts to human volunteers protects against UVB-induced erythema. In summary, these studies indicate that tea extracts are effective in reducing UVB- and PUVA-mediated DNA damage, expression of early response genes and early inflammatory changes in skin. These studies verify a conceptual rationale for employing naturally occurring dietary constitutents as an approach to cancer chemoprevention.
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PMID:Novel approaches to chemoprevention of skin cancer. 1113 32

The use of naturally occurring botanicals with substantial antioxidant activity to afford protection to human skin against UV damage is receiving increasing attention. The green tea constituent (-)-epigallocatechin-3-gallate (EGCG) is a potent antioxidant and has shown remarkable preventive effects against photocarcinogenesis and phototoxicity in mouse models. In this study we have investigated the effects of topical application of EGCG, the major polyphenol present in green tea, to human skin before UV irradiation on UV-induced markers of oxidative stress and antioxidant enzymes. Using immunohistochemistry and analytical enzyme assays, we found that application of EGCG (mg/cm(2) skin) before a single UV exposure of 4x minimal erythema dose (MED) markedly decreases UV-induced production of hydrogen peroxide (68-90%, P < 0.025-0.005) and nitric oxide (30-100%, P < 0.025-0.005) in both epidermis and dermis in a time-dependent manner. EGCG pretreatment also inhibits UV-induced infiltration of inflammatory leukocytes, particularly CD11b(+) cells (a surface marker of monocytes/macrophages and neutrophils), into the skin, which are considered to be the major producers of reactive oxygen species. EGCG treatment was also found to inhibit UV-induced epidermal lipid peroxidation at each time point studied (41-84%, P < 0.05). A single UV exposure of 4x MED to human skin was found to increase catalase activity (109-145%) and decrease glutathione peroxidase (GPx) activity (36-54%) and total glutathione (GSH) level (13-36%) at different time points studied. Pretreatment with EGCG was found to restore the UV-induced decrease in GSH level and afforded protection to the antioxidant enzyme GPx. Further studies are warranted to study the preventive effects of EGCG against multiple exposures to UV light of human skin.
Carcinogenesis 2001 Feb
PMID:Green tea polyphenol (-)-epigallocatechin-3-gallate treatment of human skin inhibits ultraviolet radiation-induced oxidative stress. 1118 50

It is not very clear why oral submucous fibrosis (OSF) is prone to develop squamous cell carcinoma (SCC). Experimental studies on hamster have shown that wounding of oral mucosa promotes induction of epithelial dysplasia (ED) initiated with carcinogens. Hence, a study was undertaken to find the effect of intraoral traumatic factors (ITF) in OSF. Randomly selected 110 OSF patients were divided into 2 groups: Traumatic group (TG), having tooth/malposed impacted third molar/appliance/calculus; and Non-traumatic group (NTG). Clinico-pathological features of traumatic mucosa of TG were compared with non-traumatized mucosa of NTG. It was found that amongst 60 TG cases there were 8 cases of SCC, 4 cases of leukoplakia and 1 case of lichenoid dysplasia and erythema, erosion and ulcer were mostly observed with sharp tooth (28) cases and malposed impacted tooth (19) cases. Further, various degrees of ED were seen in more cases of TG (23%) than in NTG (8%). This study concludes that traumatised mucosa in OSF due to various ITF may concentrate the carcinogens which by penetrating cause carcinogenesis of susceptible cells.
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PMID:Malignant potential of oral submucous fibrosis due to intraoral trauma. 1121 27

Long-term psoralen plus ultraviolet A radiation (PUVA) therapy is associated with an increased risk of squamous cell carcinoma and malignant melanoma. Genistein (4',5,7-trihydroxyisoflavone), a major isoflavone in soybeans and a specific inhibitor of protein tyrosine kinase, has been shown to inhibit UVB induced skin carcinogenesis in hairless mice. For this study we examined the protective effects of topical genistein on PUVA-induced photodamage. In two separate experiments, genistein in a dimethyl sulfoxide/acetone (1:9) solution was applied to SKH-1 female mice 1 h post 8-methoxy-psoralen dosing and 1 h prior to UVA irradiation. Application of genistein significantly decreased PUVA-induced skin thickening, and greatly diminished cutaneous erythema and ulceration in a dose-dependent manner. Histological examination showed that PUVA treatment of mouse skin induced dramatic inflammatory changes throughout the epidermis; topical genistein prevented these changes without noticeable adverse effects. Cells containing cleaved poly(ADP-ribose) polymerase (PARP) and active caspase-3 were significantly increased in PUVA-treated skin (P < 0.05 and P < 0.0001, respectively) as compared with unexposed control skin. Topical genistein completely inhibited cleavage of PARP and caspase-3. Proliferating cell nuclear antigen (PCNA) positive cells were observed in suprabasal areas of the epidermis and were significantly decreased in PUVA-treated skin compared with both control samples and samples treated with PUVA plus topical genistein (P < 0.005). These results indicate that genistein protects the skin from PUVA-induced photodamage.
Carcinogenesis 2002 Feb
PMID:Effects of the isoflavone 4',5,7-trihydroxyisoflavone (genistein) on psoralen plus ultraviolet A radiation (PUVA)-induced photodamage. 1187 39

Inflammatory stimuli result in the production of cutaneous eicosanoids, which are known to contribute to the process of tumor promotion. Cyclooxygenase (COX), the rate-limiting enzyme for the production of prostaglandins (PG) from arachidonic acid, exists in at least two isoforms, COX-1 and COX-2. COX-1 is constitutively expressed in most tissues and plays various physiological roles, whereas increased COX-2 expression is known to occur in several types of epithelial neoplasms. Enhanced PG synthesis is a potential contributing factor in UVB-induced nonmelanoma skin cancers (NMSC). Increased COX-2 staining occurs in murine skin neoplasms after chronic exposure to carcinogenic doses of UVB. In this study, immunohistochemical and Western blot analyses were employed to assess longitudinally COX-2 expression in a standard mouse UVB complete carcinogenesis protocol and in human basal cell carcinomas (BCC) and squamous cell carcinomas (SCC). During UVB irradiation of mice, COX-2 expression consistently increased in the hyperplastic skin, the benign papillomas and the SCC. COX-2 expression was also increased in human actinic keratoses, SCC and BCC as well as in murine SCC and BCC. The pattern of COX-2 expression was quite variable, occurring in a patchy distribution in some lesions with staining confined mainly to suprabasal cell layers. In general, COX-2 expression progressively became more extensive in benign papillomas and well-differentiated murine SCC. The staining was predominantly cytoplasmic and perinuclear in some focal areas in tissue stroma around both murine and human tumors. Western blot analysis confirmed negative COX-2 expression in normal skin, whereas acute UVB exposure resulted in increased enzyme expression, which continued to increase in developing papillomas and SCC. Because of the evidence indicating a pathogenic role for eicosanoids in murine and human skin neoplasms, we performed studies to assess the anti-inflammatory and anticarcinogenic effects of green tea extracts, which are potent antioxidants. Acute exposure of the human skin to UVB (minimum erythema dose x 4) caused a transient enhancement of the COX-2 expression, which reverted to baseline within hours; however, in murine skin the expression persisted for several days. Pretreatment with the topically applied green tea extract (1 mg/cm2) largely abrogated the acute COX-2 response to UVB in mice or humans. In summary, enhanced COX-2 expression serves as a marker of epidermal UVB exposure for murine and human NMSC. These results suggest that COX-2 inhibitors could have potent anticarcinogenic effects in UVB-induced skin cancer.
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PMID:Cyclooxygenase-2 expression in murine and human nonmelanoma skin cancers: implications for therapeutic approaches. 1212 10

Oral contraceptives (OCs) can affect the skin through their hormonal effects or through iatrogenic effects associated with their toxicity in certain individuals. They may also be beneficial in certain androgen-dependent dermatoses. Toxic effects of OCs are rare but potentially serious; they should be diagnosed early and require permanent termination of OC use. The clinical manifestations are variable and not specific to the medication. The most frequently reported manifestations are allergic vascularities which may lead to serious renal complications, fixed pigmented erythema, urticaria, which may have other etiologic factors, and lichenoid eruptions. Combined OCs, because of their estrogen content, may cause sensitivity to light in susceptible women. Other dermatoses can be initiated or aggravated by OCs without direct relation to their hormonal effects. OCs are therefore contraindicated if there is a personal or family history of porphyries or a personal history of systemic lupus erythematosus, erythema nouex, herpes gestationis, or malignant melanoma. Hormonal-related dermatological effects caused by either progestins or estrogens have become less frequent as dose levels have declined. Chloasma, either melasma or a poorly defined spotty pigmentation, accounts for 2/3 of cases of OC-related dermatoses. It is more common in women of Mediterranean background. 80% of affected OC users have a history of "mask of pregnancy", but the condition is also found in nulliparas. Exposure to sunlight is a factor. Women with a history of chloasma of pregnancy and dark coloring should not use OCs. Seborrhea is directly related to the androgen effect of OCs and is less likely to occur with 17 OH progesterone derivatives than with 19 norsteroid derivatives. The role of androgens in acne is well known, but 2 other factors are necessary: an anomaly in keratinization and proliferation of corynebacterium acnes, a saprophyte of the follicles. OCs do not necessarily need to be suspended during well-conducted acne treatment. Alopecia is rare but difficult to diagnose because of its psychological aspects. Androgenic alopecia is aggravated by progestins derived from 19 norsteroids. True hirsutism caused by an androgen-producing ovarian pathology is not related to OC use. Estrogens are incriminated in the etiology of telangiectasies, permanent dilatations of the arterioles. Once developed the condition does not regress and requires treatment with sclerosing agents, electrocoagulation, or laser. The various dermatological risk factors should be ruled out before prescription of an OC. Classic contraceptive pills are not commonly used in treatment of common acne because the strongly estrogenic climate required for therapeutic utility carries the risk of hypertriglyceridemia, thrombophlebitis, and possibly carcinogenesis. The recent development of pills containing the antiandrogen cyproterone acetate instead of a progestin in combination with ethinyl estradiol reduces androgenic effects in women. This pill may be useful in cases of severe acne, severe seborrhea, androgenic alopecia, or excessive facial hair.
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PMID:[Cutaneous effects in hormonal contraception]. 1228 Dec 76

2-Chloroacetophenone is a potent lacrimator that has been used as a riot control agent and in tear gas formulations for personal protection devices. NTP Toxicology and Carcinogenesis studies were conducted by exposing groups of F344/N rats and B6C3F1 mice of each sex to air containing 2-chloroacetophenone vapor for 14 days, 13 weeks, 15 months, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium and Chinese hamster ovary (CHO) cells. Fourteen-Day Studies: In 14-day studies, exposure concentrations of 2-chloroacetophenone ranged from 4.8 to 64 mg/m3. All rats exposed to 19, 43, or 64 mg/m3 died during the first week of the studies and 1/5 male rats exposed to 10 mg/m3 died during the second week of the study. Rats exposed to 10 mg/m3 lost weight; the final mean body weights of male or female rats exposed to 4.8 mg/m3, the lowest concentration used, were 23% or 15% lower than that of controls. During the exposure, rats showed partial closure of the eyelids, excessive lacrimation (dacryorrhea), dyspnea, and erythema. All mice exposed to 10 mg/m3 or higher concentrations of 2-chloroacetophenone died during the first week of the studies. The final mean body weights of mice exposed to 4.8 mg/m3 were similar to those of controls. Dacryorrhea was observed in exposed mice. Thirteen-Week Studies: The exposure concentrations of 2-chloroacetophenone ranged from 0.25 to 4 mg/m3 for rats and mice. All rats lived to the end of the studies. The final mean body weights of rats exposed to 4 mg/m3 were 9% lower than those of controls. Eye irritation during exposure was evident in rats exposed to 0.5 mg/m3 or higher concentrations of 2-chloroacetophenone. One of 10 female mice exposed to 4 mg/m3 and 1/10 female mice exposed to 0.5 mg/m3 died before the end of the study. The final mean body weights of exposed mice were 7%-12% lower than that of controls for males and 12%-15% lower for females. No chemical-related gross or microscopic lesions were observed in rats or mice. In the 2-year studies, groups of 60 rats of each sex were exposed to a vapor of 0 (chamber control), 1, or 2 mg/m3 (0, 0.15, or 0.3 ppm) 2-chloroacetophenone, 6 hours per day, 5 days per week. Groups of 60 mice of each sex were exposed to 0 (chamber control), 2, or 4 mg/m3 (0, 0.3, or 0.6 ppm) on the same schedule. Ten animals from each group were killed and examined at 15 months; the remaining animals continued on study for 2 years. Fifteen-Month Studies: In the 15-month studies, minimal-to-mild focal squamous metaplasia and hyperplasia of the respiratory epithelium were seen at increased incidences in rats exposed to 2 mg/m3. No exposure-related lesions were observed in mice of either sex. Body Weight and Survival in the Two-Year Studies: Mean body weights and survival of exposed and chamber control rats were similar throughout most of the studies (survival-male: control, 14/50; 1 mg/m3, 22/50; 2 mg/m3, 17/50; female: 23/50; 20/50; 24/50). Mean body weights of male mice exposed to 4 mg/m3 were about 5%-12% lower than those of controls after week 30; small differences between mean body weights of exposed and control female mice were not clearly exposure related. The survival of female mice exposed to 2 mg/m3 was significantly lower than that of chamber controls after week 98. No other differences in survival were observed between any groups of mice (male: control, 34/50; 2 mg/m3, 36/50; 4 mg/m3, 33/50; female: 40/50; 28/50; 32/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Fibroadenomas of the mammary gland occurred in female rats with positive trends, and the incidence in the 2 mg/m3 group was greater than that in chamber controls (control, 12/50; 1 mg/m3, 19/50; 2 mg/m3, 23/50). The incidences of adenomas or adenocarcinomas of the mammary gland were not increased in the exposed groups. Minimal-to-mild suppurative inflammation of the nasal mucosa was observed at increased incidences in exposed male rats. Hyperplasia and squamous metaplasia of the nasal respiratory epithelium were observed at increased incidences in exposed ry epithelium were observed at increased incidences in exposed male and female rats. In mice, squamous metaplasia of the respiratory epithelium of the nasal passage was seen in four females and two males exposed to 4 mg/m3 2-chloroacetophenone. Inflammation, ulcers, and squamous hyperplasia of the forestomach were observed at increased incidences in exposed female rats. Genetic Toxicology: 2-Chloroacetophenone was not mutagenic in S. typhimurium strains TA98, TA100, TA1535, or TA1537 with or without exogenous metabolic activation. In cytogenetic tests with CHO cells, 2-chloroacetophenone did not induce sister chromatid exchanges with or without activation, but a weak positive increase in chromosomal aberrations was observed in the absence of metabolic activation. Conclusions: Under the conditions of these 2-year inhalation studies, there was no evidence of carcinogenic activity of 2-chloroacetophenone for male rats exposed to 1 or 2 mg/m3. There was equivocal evidence of carcinogenic activity for female F344/N rats, based on a marginal increase in fibroadenomas of the mammary gland. There was no evidence of carcinogenic activity for male or female B6C3F1 mice exposed to 2 or 4 mg/m3 2-chloroacetophenone. Synonyms: a-chloroacetophenone; 2-chloro-1-phenylethanone; CN; phenacyl chloride; phenylchloromethylketone Trade Names: Mace®.; Chemical Mace®.
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PMID:NTP Toxicology and Carcinogenesis Studies of 2-Chloroacetophenone (CAS No. 532-27-4) in F344/N Rats and B6C3F1 Mice (Inhalation Studies). 1269 42

CS2 (94% o-chlorobenzalmalononitrile [CS]; 5% Cab-O-Sil(R). colloidal silica; 1% hexamethyldisilizane), an eye and respiratory irritant, is used as an aerosol to control riots. NTP Toxicology and Carcinogenesis studies were conducted by exposing groups of F344/N rats and B6C3F1 mice of each sex for 6 hours per day, 5 days per week for 2 weeks, 13 weeks, or 2 years, to a CS2 aerosol. Genetic toxicology studies with CS2 were conducted in Salmonella typhimurium, mouse lymphoma cells, and Chinese hamster ovary (CHO) cells. Fourteen-Day Studies: At exposure concentrations of 0, 1, 3, 10, 30, or 100 mg/m3 CS2, all rats exposed to 30 or 100 mg/m3 and all mice exposed to 10, 30, or 100 mg/m3 died before the end of the studies. Compound-related clinical signs observed included erythema, blepharospasm, listlessness, nasal discharge, and mouse breathing. Thirteen-Week Studies: At exposure concentrations of 0, 0.4, 0.75, 1.5, 3, or 6 mg/m3, 1/10 male rats exposed to 6 mg/m3 died before the end of the studies. Final mean body weights of rats exposed to 1.5 mg/m3 or more were 17%-44% lower than that of controls for males and 10%-24% lower for females. The absolute and relative thymus weights were reduced for exposed male and female rats, particularly at 6 mg/m3. Compound-related lesions of the nasal passage in rats included focal erosion with regenerative hyperplasia and squamous metaplasia of the respiratory epithelium and suppurative inflammation. Acute inflammation and hyperplasia of the respiratory epithelium were seen in the larynx and trachea of some exposed rats. All mice exposed to 6 mg/m3 and 1/10 males and 1/10 females exposed to 3 mg/m3 died before the end of the studies. Final mean body weights of mice exposed to 3 mg/m3 were 13% lower than that of controls for males and 9% lower for females. Compound-related lesions of the nasal passage in mice included squamous metaplasia of the nasal respiratory epithelium and inflammation. Based on these results, CS2 exposure concentrations for the 2-year studies were 0, 0.075, 0.25, or 0.75 mg/m3 for 6 hours per day, 5 days per week for 105 weeks for groups of 50 rats of each sex. Groups of 50 mice of each sex were exposed to 0, 0.75, or 1.5 mg/m3 on the same schedule. Body Weights and Survival in the Two-Year Studies: Final mean body weights of rats exposed to 0.75 mg/m3 were 7%-11% lower than those of controls. Final mean body weights of mice exposed to CS2 were lower than those of controls (male: 5% and 9%; female: 10% and 17%). No compound-related clinical signs were observed. No significant differences in survival were seen for any group of rats or mice of either sex. Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Compound-related nonneoplastic lesions occurred in the nasal passage of exposed rats and mice. In exposed rats, hyperplasia and squamous metaplasia of the respiratory epithelium and degeneration of the olfactory epithelium with ciliated columnar and/or squamous metaplasia were observed. Focal chronic inflammation and proliferation of the periosteum of the turbinate bones were increased slightly in rats at the top exposure concentration. Suppurative inflammation with hyperplasia and squamous metaplasia of the respiratory epithelium occurred in exposed mice. There were no compound-related increased incidences of neoplasms in rats or mice exposed to CS2. In exposed female mice, there were pronounced decreases in the incidences of adenomas of the pituitary pars distalis (control, 13/47; 0.75 mg/m3, 5/46; 1.5 mg/m3, 1/46) and decreased incidences of malignant lymphomas (21/50; 12/50; 8/50). Genetic Toxicology: The responses in Salmonella gene mutation tests with CS2 were equivocal in one laboratory for strain TA100 in the absence of exogenous metabolic activation (S9) and equivocal in another laboratory for TA97 with S9; in all other strains tested, CS2 was clearly negative with or without S9. CS2 induced trifluorothymidine resistance in mouse L5178Y/TK lymphoma cells in the absence of S9; it was not tested with S9. CS2 induced both sister chromatid exchangeslymphoma cells in the absence of S9; it was not tested with S9. CS2 induced both sister chromatid exchanges and chromosomal aberrations in CHO cells with and without S9. Conclusions: Under the conditions of these inhalation studies, there was no evidence of carcinogenic activity of CS2 for male or female F344/N rats exposed to 0.075, 0.25, or 0.75 mg/m3 in air for up to 2 years. There was no evidence of carcinogenic activity for male or female B6C3F1 mice exposed to 0.75 or 1.5 mg/m3 in air for up to 2 years. Concentration-related decreases in the incidences of pituitary gland adenomas and lymphomas were observed in female mice. Exposure to CS2 caused degeneration and squamous metaplasia of the olfactory epithelium, hyperplasia and metaplasia of the respiratory epithelium, and proliferation of the periosteum of the nasal passage of rats. In mice, exposure to this compound caused suppurative inflammation and hyperplasia and squamous metaplasia of the respiratory epithelium of the nasal passage.
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PMID:NTP Toxicology and Carcinogenesis Studies of CS2 (94% o-Chlorobenzalmalononitrile, CAS No. 2698-41-1) in F344/N Rats and B6C3F1 Mice (Inhalation Studies). 1269 44

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