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EXTOXNET PIP - CHLOROPICRIN Page 2 of 4 upper respiratory tract, eyes and skin upon direct contact. Exposure to airborne concentrations of chloropicrin exceeding 0.15 ppm (1 mg/meters cubed) can cause tearing and eye irritation which is reversible upon termination of exposure. Prolonged inhalation exposures at airborne concentrations above I ppm may cause symptoms of respiratory system damage including irritation of the airways, shortness of breath and/or tightness in chest and difficulty in breathing. Inhalation exposure to very high levels, even if brief, can lead to pulmonary edema, unconsciousness and even death. . Chronic Toxicity/Subchronic Effects: Studies with male and female CD rats and CD-1 mice exposed to chloropicrin vapor in whole body inhalation chambers at concentrations of 0.3, 1.0, or 3.0 ppm for six hours per day, five days per week for thirteen weeks (263) and male Fisher 344 rats exposed to chloropicrin (264) indicated that respiratory tissue is the target for chloropicrin inhalation toxicity. Portal-of-entry effects occurred in the upper respiratory tissue of animals inhaling chloropicrin vapor for 90 days at concentrations at or above 0.1 ppm (0.67 mg/meters cubed). . Reproductive Effects: A study utilizing chloropicrin vapor administered by whole body inhalation for six hours per day, seven days per week to male and female CD rats at concentrations of 0.5, 1.0, or 1.5 ppm through two generations of animals indicated that reproduction fitness is not adversely affected by chloropicrin inhalation even at systemically toxic levels (265). The No Observable Adverse Effect Level (NOAEL) was 1.0 ppm for systemic toxicity and greater than 1.5 ppm for developmental toxicity and reproductive parameters. Teratogenic Effects: In a study with sexually mature virgin female Sprague-Dawley rats exposed by whole body inhalation to chloropicrin vapor for six hours per day for days 6-15 of gestation, there were no treatment- related fetal malformations (266). The incidence of developmental variations in the mid- and high-dose groups increased over the control group and was statistically significant in the high-dose group. The NOAEL for maternal toxicity was 0.4 pprn and the NOAEL for fetal toxicity was 1.2 ppm indicating that the developing fetus is not a target tissue for chloropicrin.The developmental toxicity of chloro-picrin in sexually mature virgin female New Zealand White SPF rabbits was evaluated by whole body exposure/inhalation to chloropicrin vapor for six hours per day for days 7-20 of gestation (267). There were no treatment related fetal malformations reported, the incidence of developmental variations in the mid- and high-dose groups was increased over the control group and was considered to be treatment related but was not dose related nor was it statistically significant. The NOAEL for maternal toxicity was 0.4 ppm and the NOAEL for fetal toxicity was 1.2 ppm indicating that the developing fetus is not a target tissue. . Mutagenic Effects: Chloropicrin has been evaluated in several in vitro genetic toxicity test systems (268, 271). Bacterial cell testing for gene mutation produced some evidence of genetic toxicity in 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. ENVIRONMENTAII FATE