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Here goes another one - PCP: WT <<<<<< Attached TEXT file named "Commercial Products" follows >>>>>> Commercial Products PCP, Penta, Penchlorol, Santophen, Chlorophen, Pentacon, Penwar, Sinituho. The sodium salt is sodium pentachlorophenate. In various products, pentachlorophenol has been used as an herbicide, algacide, defoliant, wood preservative, germicide, fungicide, and molluscicide. As a wood preservative, it is commonly applied as a 0.1% solution in mineral spirits, No. 2 fuel oil, or kerosene. It is used in pressure treatment of lumber at 5% concentration. Weed killers contain higher concentrations. PCP is no longer available for over-the-counter sale in the United States. Pentachlorophenol volatilizes from treated wood and fabric. It is virtually odorless. Excessively treated interior surfaces may be a source of exposure sufficient to cause irritation to eyes, nose, and throat. Technical PCP contains lower chlorinated phenols (4-12%) plus traces of chlorobenzodioxins, chloro-benzofurans, and chlorobenzenes. <<<<<< Attached TEXT file named "Symptoms and Signs of Poisoning" follows >>>>>> Symptoms and Signs of Poisoning IRRITATION of the nose, throat, and eyes is the most common symptom of airborne PCP, causing stuffy nose, scratchy throat, and tearing. Dermal exposure may lead to contact dermatitis, or more rarely, diffuse urticaria or chloracne. Commonly reported symptoms of systemic poisoning by PCP are profuse SWEATING, weakness, dizziness, anorexia, nausea and - in workers exposed over long periods - weight loss. Indications of severe acute poisoning are HYPERTHERMIA, muscle spasms, tremor, labored breathing, a sense of constriction in the chest, abdominal pain and vomiting, restlessness, excitement, and mental confusion. Tachycardia and increased respiratory rate are usually apparent. Intense THIRST is characteristic. <<<<<< Attached TEXT file named "Toxicology" follows >>>>>> Toxicology PCP is efficiently absorbed across the skin, the lung, and the gastro-intestinal lining. It is rapidly excreted, mainly in the urine as unchanged PCP and as PCP glucuronide. In the blood, a large fraction of absorbed PCP is protein-bound. The residence half-life of PCP in humans is about 27-36 hours. Because minute amounts of PCP are consistently detectable in the blood and urine of the general population, a continuing low-level intake (micrograms per day) of PCP by virtually everyone is implied. In adequate concentration, PCP is irritating to mucous membranes and skin. Contact dermatitis occurs commonly in workers having contact with PCP. Internally, large doses are toxic to the liver, kidneys, and nervous system. An important mechanism of toxic action is increased cellular oxidative metabolism resulting from the uncoupling of oxidative phosphorylation. This leads to increased heat production (hyperthermia). Severe poisoning and death have occurred as a result of intensive PCP exposure. Dermal absorption has been the basis of virtually all occupational poisonings. Most adult fatalities have occurred in persons working in hot environments where hyperthermia is poorly tolerated. Several infant deaths have occurred in a nursery where a PCP-containing diaper rinse had been used. Chloracne has occurred in production workers, possibly due to chlorodioxin contaminants. Individual cases of exfoliative dermatitis of the hands and diffuse urticaria and angioedema of the hands have been reported in intensively exposed workers. Cases of aplastic anemia, peripheral neuropathy, and leukemia have been reported which were associated temporally with PCP exposure. Causal relationships in these cases were not established. Albuminuria, glycosuria, and aminoaciduria, and elevated BUN reflect renal injury. Liver enlargement, anemia and leukopenia have been reported in some intensively exposed workers. Elevated serum alkaline phosphatase, GOT, and LDH enzymes indicate significant insult to the liver, including both cellular damage and some degree of biliary obstruction.