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`X 0XNI.T 1'll' - C111,01M'ICRIN http://ace.orst.cdu/cgi-bin/mts/01 /pipsichloropt.lit m one of five tester strains in the presence of an exogenous metabolic activation system but testing in higher order cells (mammalian cells) did not confirm the potential for chloropicrin to produce gene mutation. Chloropicrin did not cause damage to mammalian cell DNA. In vitro testing of mammalian cell chromosomes for damage (breaks, exchange figures, fragments, etc.) produced evidence suggestive of a clastogenic effect but the data were equivocal. • Carcinogenic Effects: Six long-term bioassays have been performed to evaluate the potential of chloropicrin to cause chronic and/or carcinogenic effects by inhalation, oral, and gavage dosing (272, 276). Chronic toxicity was limited to inflammatory and other degenerative changes associated with chronic wound healing at the portal -of -entry and at associated tissues (i.e. rodent forestomach following life-long oral dosing). No neoplastic or tumorigenic response was produced by chloropicrin in any species tested by the three routes of exposure. • Organ Toxicity: Target organs for chloropicrin toxicity include eyes, skin, respiratory tract and tissue associated with portal -of -entry into the body. • Fate in Mammals: The octanol/water partition coefficient (Log 10 Kow) is 2.50 at 25 degrees C indicating that chloropicrin would not be expected to bioaccumulate in mammalian cells (277). ECOLOGICAL EFFECTS Effects on Birds: Little information is available about the effects of chloropicrin on bird life. A feeding study in chickens (278) demonstrated no adverse effects at doses as high as 100 ppm for 120 days. This was the highest dose tested. Effects on Aquatic Organisms: Chloropicrin is toxic to fish. For trout and bluegill the 96 -hour LC50 was 0.0165 mg/L and 0.105 mg/L respectively (278). Effects on Other Animals (Nontarget species): When used according to label, exposure to nontarget species is unlikely. However, because of its toxicity to mammals and invertebrates, it can be assumed that chloropicrin may be harmful to many nontarget organisms. ENVIRONMENTAL FATE Breakdown of Chemical in Soil and Groundwater: The half-life of chloropicrin in sandy loam soil was 8-24 hours (279) and 4.5 days (280) with carbon dioxide being the terminal breakdown product (280). Chloropicrin moves rapidly in soils within twelve inches of injection but may diffuse to a maximum depth of four feet in sandy soil (281). Since it is only slightly soluble in water, it will not move rapidly in aquatic environments. In an anaerobic aquatic/soil system, chloropicrin was converted to nitromethane with a half-life of 1.3 hours (282). In the absence of sunlight or microorganisms, chloropicrin does not undergo hydrolysis (283, 284). The calculated Henry's Law Constant is 2.51 x 10 to the minus 3 atm meters cubed mole -1 (285). The Koc for silt loam and agricultural sand soils was 5.29 and 93.59 respectively (289). Chloropicrin can be produced during chlorination of drinking water if nitrated organic contaminants are present (286, 287). In a sampling of 1,386 wells in California between 1984 and 1989, no chloropicrin was detected (288). In a sampling of 15,175 wells in Florida, chloropicrin was found in three wells at 0.035-0.068 Hg/L (288). Breakdown of Chemical in Surface Water: Since chloropicrin has a higher density than water (1.65 9/ml) and is only slightly soluble, it will sink to the bottom of surface water. The half-life of chloropicrin in water exposed to light was 31.1 hours with carbon dioxide, bicarbonate, chloride, nitrate and nitrite being the breakdown products (284). Breakdown of Chemical in Plants: No chloropicrin or nitromethane was detected in crops grown in soil treated with radiolabelled chloropicrin (290). Carbon dioxide, as the terminal breakdown product, was metabolized by plants and incorporated into natural plant biochemical compounds via the single carbon pool (291). ol'-1 5/1'_ 00 104 1) NI