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XTONNI:T PIP - CI ILl)ROPICRIN http://ace.orst.eduicgi-bin/ints/0I /pipsichloropt. hun or eyes. According to the American Conference of Governmental Industrial Hygienists (261), airborne exposure to 0.3-0.37 ppm (2-2.5 mg/meters cubed) for 3-30 seconds results in eye irritation. This response is reported to be highly variable among individuals and tearing (lachrymation) may occur at airborne exposures of 0.15-0.3 ppm (1-2 mg/meters cubed) (261). Inhalation exposure to 4 ppm (26 mg/meters cubed) for a few seconds may cause some degree of incapacitation (261) and an exposure of a few seconds to 15 ppm (100 rn /meters cubed) can cause injury to the respiratory track. Exposure to concentrations above 15 ppm can result in lacrimation, vomiting, and if allowed to continue for a minute or longer, can cause pulmonary edema and possibly death (261). The American Industrial Hygiene Association Emergency Response Planning Guideline for one hour exposure to chloropicrin is 3 ppm (20 mg/meters cubed)(262). Animal studies established that the 4 -hour inhalation LC50 for chloropicrin vapor in rats is 11.9 ppm (79.7 mg/meters cubed)(293) and the respiratory irritation potential threshold (RD50) in mice is 7.98 ppm (53.5 mg/meters cubed)(293). The FIFRA Toxicity Classification for chloropicrin acute effects is Category I and the signal word for that classification is "Danger." Signs and Symptoms of Poisoning: Undiluted chloropicrin is severely and immediately irritating to the 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 1 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 ppm 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 ot' ;:I' nig 1 114 I'�i