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| Toxicity Summary |
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| Link to the Distributed Structure-Searchable Toxicity (DSSTox) Database |
| IDENTIFICATION AND USE: Catechol is a tablet or colorless crystal, prism or aqueous solution, which discolors to brown on exposure to air and light. It has a faint characteristic odor. It is used as antioxidant in the rubber, chemical, photographic, dye, fat, and oil industries. It was formerly used as an antiseptic. Catechol was found unsafe for use in cosmetics. HUMAN EXPOSURE AND TOXICITY: Catechol contact with the skin has been known to cause an eczematous dermatitis. It is highly irritating upon direct contact; severe eye and deep skin burns result. Well absorbed by skin. Systemic toxicity similar to that of phenol however, catechol may be more likely to cause convulsions and hypertension. At high doses, renal and liver injury may occur. Absorption through the skin, in a few instances, has resulted in symptoms of illness resembling closely those induced by phenol, except for certain central effects (convulsions) that were more marked. Death apparently is initiated by respiratory failure. Catechol was found to be a more harmful toxin than phenol in human blood cells in vitro, since it provokes statistically significant changes in the function of erythrocytes even at low doses. Both compounds induced methemoglobin formation, glutathione depletion and conversion of oxyhemoglobin to methemoglobin, which is associated with superoxide anion production and lead to formation of ferryl hemoglobin, hydrogen peroxide or hydroxyl radicals. It is known that oxidation of catechol leads to formation of semiquinone radicals. Catechol induced DNA damage in human peripheral blood lymphocytes, and in proliferating human T-lymphocytes. Catechol is confirmed animal carcinogen with unknown relevance to humans. ANIMAL STUDIES: Instillation of 100 mg of catechol into the eyes of rabbits caused a moderate conjunctivitis with exudate and corneal opacity that progressed to a severe conjunctivitis, iritis, and widely diffuse corneal opacity at 72 hours. Fourteen days after instillation, the corneas were vascularized, had infiltration of granulation tissue, and were protruding (keratoconus). Hyperemia of the stomach and intestines was reported after lethal oral doses in rats. Repeated absorption of sublethal doses by animals has induced methemoglobinemia, leucopenia and anemia. Death is apparently initiated by respiratory failure. Catechol clearly induced increases in DNA synthesis in rat forestomach epithelium independent of sex. In the glandular stomach, catechol treatment for 4 weeks increased crypt height due to elevation of DNA synthesis and caused submucosal growth of pyloric mucosal cells. Administration of catechol (1.5% in the diet) for 20 weeks induced mild to moderate hyperplasia in the forestomach. Rats fed catechol in the diet at concentrations of 0 or 1.5% for four weeks followed by 0.8% for 47 weeks either with no other exposure or one week after exposure to N-methyl- N"-nitro-N-nitrosoguanidine increased the incidence of forestomach papillomas, glandular stomach adenocarcinomas, squamous-cell carcinomas of the forestomach, and adenocarcinomas in the pyloric region of the glandular stomach in rats. Regenerative cell proliferation due to toxicity plays an important role in catechol-induced glandular stomach carcinogenesis. Catechol also exhibited developmental toxicity in rats. Litter size and weights were reduced at the maternally toxic doses. Malformations involving limbs, tail and urogenital systems were reported at all doses. Catechol was negative in the Ames assay, but induced sister chromatid exchanges in Chinese hamster ovary V79 cells. In in vivo mouse micronucleus assays, in which the conjugation enzymes responsible for detoxication were present, both positive and negative results were reported. ECOTOXICITY STUDIES: Catechol-treated sea bass showed disorders in the metabolic toxicity indicators such as hypoglycemia, low blood urea nitrogen level and decrease of alkaline phosphatase activity. |
| Source: DrugBank or Hazardous Substances Data Bank (HSDB) |