|IDENTIFICATION AND USE: 2,4,6-Trichlorophenol (2,4,6 -TCP) is a colorless needle or yellow solid that has a strong phenolic odor. This germicidal agent was used as a fungicide, bactericide, wood preservative, biocide, and intermediate in production of higher chlorinated phenols. It is not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses. HUMAN EXPOSURE AND TOXICITY: Trichlorophenols produce redness and edema on skin contact and on prolonged exposure mild to moderate chemical burns of skin of man. In eye they induce conjunctival irritation and sometimes corneal injury and iritis. Dusts are irritating to nose and pharynx and systemic effects presumably resemble phenol. Trichlorophenols can have an irritating effect on the lung, and it cannot be excluded that long-term exposure may produce pulmonary fibrosis. Children with low levels (<3.58 ug/g) and high levels (=3.58 ug/g) of urinary 2,4,6-TCP had a higher risk of parent-reported ADHD compared to children with levels below the limit of detection after adjusting for covariates. It was concluded that exposure to TCP may increase the risk of behavioral impairment in children. The potential neurotoxicity of these chemicals should be considered in public health efforts to reduce environmental exposures/contamination, especially in countries where organochlorine pesticides are still commonly used. 2,4,6-Trichlorophenol is reasonably anticipated to be a human carcinogen according to NTP. ANIMAL STUDIES: In rats lethal doses of chlorophenols produce restlessness, increased rate of respiration, rapidly developing motor weakness, tremors, clonic convulsions, dyspnea, and coma. 2,4,6-TCP produces these signs but decreased activity and motor weakness do not appear quite so promptly. 2,4,6-TCP was not hepatotoxic in rats as assessed by measurement of hepatic glucose-6-phosphatase and serum sorbitol dehydrogenase. Carcinogenesis bioassays were conducted by giving 2,4,6-TCP in feed to groups of male and female rats and male mice for two years. Adverse effects at two years were leukocytosis and monocytosis of peripheral blood and hyperplasia of bone marrow in both sexes of rats. In mice, liver toxicity, including individual liver cell abnormalities, focal areas of cellular alteration, and focal and nodular areas of hyperplasia were commonly present. TCP caused leukemias/lymphomas in male rats, and possibly in female rats and female mice as well, and induced liver tumors in male and female mice. 2,4,6-TCP, a non-mutagen to Salmonella, was negative in tests for chromosome breakage in vitro, but did produce numerical chromosome changes and micronuclei in V79 cells. 2,4,6-TCP induces structural chromosome aberrations in CHO cells and in V79 cells using a 3-hr treatment and 20-hr sampling time (17-hr recovery). Positive results were obtained when a recovery time of 4-12 hr was allowed after the 24-hr treatment with 2,4,6-TCP, and when 2,4,6-TCP was tested with S9. ECOTOXICITY STUDIES: 2,4,6-TCP was applied at single doses of into compartments of a natural experimental pond to study the effect on biota. Changes seen included a rapid decline of daphnia concentration to zero after phytoplankton, a continuous increase of contamination indicators like flagellates and microorganisms, and a significant decrease in O2 concentration as a secondary effect of the changed balance between autotrophic and heterotrophic populations.