Chloropicrin - Extension Toxicology Network
TRADE OR OTHER NAMES
Some trade names for products containing chloropicrin include "Chlor-O- Pic," "Metapicrin" "Timberfume" and "Tri-Clor." A partial list of trade names for chloropicrin mixtures with methyl bromide includes "Tri-Con," "Terr- O-Gas," "Preplant Soil Fumigant" and "Pic-Brom." Chloropicrin mixtures with 1,3-Dichloropropene include "Telone C-17," "Tri-Form" and "Pic-Clor."
REGULATORY STATUS
Chloropicrin is currently undergoing USEPA FIFRA reregistration. It is a Class I toxicity, Restricted Use Pesticide (RUP), labeled with the signal word "Danger" (1). The U.S. Department of Transportation (DOT) proper shipping name is "Chloropicrin, 6.1, UN 1580, PGI, Poison Inhalation Hazard, Hazard Zone B." The Emergency Response Guide (ERG) number is 56. NFPA designations are 4- Health, 0-Fire, 3-Reactivity. Chloropicrin is not listed under the EPA Clean Air Act, EPA Clean Water Act or the EPA Marine Pollutant List (2). A tolerance is not required for preplant soil fumigation uses of chloropicrin.
INTRODUCTION
Chloropicrin is a clear, colorless, oily liquid with a strong, sharp, highly irritating odor. It is a strong lachrymator (1). Chloropicrin has been used as an insecticide since 1917 and as a soil fumigant since 1920 (3). The primary use today is for preplant soil fumigation to control soil borne fungi, diseases and nematodes (1). It also is used to treat wood poles and timbers for internal decay by fungi and insects; as a warning/clearing agent for sulfuryl fluoride (structural fumigant) and methyl bromide (soil and structural fumigant); and is also used in organic synthesis.
For soil fumigation and wood treatment, chloropicrin is packaged in DOT 4BW240 steel cylinders and bulk tanks which may be pressurized. When used as a warning agent for methyl bromide, chloropicrin is packaged along with the methyl bromide in steel cylinders. When used as a structural fumigation warning agent for sulfuryl fluoride, chloropicrin is packaged in small plastic bottles in DOT approved overpacks.
Chloropicrin has a moderate vapor pressure (18.3 mmHg at 20 degrees C) and exists as a liquid at room temperature. Chloropicrin/methyl bromide mixtures will volatilize readily upon opening of the cylinder valve. Materials incompatible with chloropicrin are PVC, fiberglass, aluminum and magnesium and their alloys (1, 4).
TOXICOLOGICAL EFFECTS
Acute Toxicity
Undiluted chloropicrin is highly toxic by ingestion or direct contact with the skin or eyes. According to the American Conference of Governmental Industrial Hygienists (5), 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) (5). Inhalation exposure to 4 ppm (26 mg/meters cubed) for a few seconds may cause some degree of incapacitation (5) and an exposure of a few seconds to 15 ppm (100 mg/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 (5). The American Industrial Hygiene Association Emergency Response Planning Guideline for one hour exposure to chloropicrin is 3 ppm (20 mg/meters cubed)(6).
Animal studies established that the 4-hour inhalation LC50 for chloropicrin vapor in rats is 11.9 ppm (79.7 mg/meters cubed)(37) and the respiratory irritation potential threshold (RD50) in mice is 7.98 ppm (53.5 mg/meters cubed)(37). 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 (7) and male Fisher 344 rats exposed to chloropicrin (8) 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 (9). 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 (10). 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 (11). 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 (12, 15). 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 (16, 20). 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 (Log10 Kow) is 2.50 at 25 degrees C indicating that chloropicrin would not be expected to bioaccumulate in mammalian cells (21).
ECOLOGICAL EFFECTS
Effects on Birds
Little information is available about the effects of chloropicrin on bird life. A feeding study in chickens (22) 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 (22).
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 (23) and 4.5 days (24) with carbon dioxide being the terminal breakdown product (24). Chloropicrin moves rapidly in soils within twelve inches of injection but may diffuse to a maximum depth of four feet in sandy soil (25). 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 (26). In the absence of sunlight or microorganisms, chloropicrin does not undergo hydrolysis (27, 28). The calculated Henry's Law Constant is 2.51 x 10 to the minus 3 atm meters cubed mole-1 (29). The Koc for silt loam and agricultural sand soils was 5.29 and 93.59 respectively (33).
Chloropicrin can be produced during chlorination of drinking water if nitrated organic contaminants are present (30, 31). In a sampling of 1,386 wells in California between 1984 and 1989, no chloropicrin was detected (32). In a sampling of 15,175 wells in Florida, chloropicrin was found in three wells at 0.035-0.068 Hg/L (32).
Breakdown of Chemical in Surface Water
Since chloropicrin has a higher density than water (1.65 g/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 (28).
Breakdown of Chemical in Plants
No chloropicrin or nitromethane was detected in crops grown in soil treated with radiolabelled chloropicrin (34). Carbon dioxide, as the terminal breakdown product, was metabolized by plants and incorporated into natural plant biochemical compounds via the single carbon pool (35).
Breakdown of Chemical in Air
Chloropicrin is efficiently photolyzed in the atmosphere. The half-life of chloropicrin in air exposed to simulated sunlight was 20 days (36). The photoproducts were phosgene (which will hydrolyze to carbon dioxide and hydrogen chloride), nitric oxide, chlorine, nitrogen dioxide and dinitrogen tetroxide.
Analytical Methods
The concentration of chloropicrin in air may be measured using Kitagawa direct reading gas detector tube#l72 (Matheson-Kitagawa, East Rutherford, NJ). Gas chromatography methods are available to measure chloropicrin in air (27) and may utilize XAD-4 solid sorbent tubes (SKC Inc., Eighty Four, PA).
PHYSICAL PROPERTIES AND GUIDELINES
Exposure Guidelines:
ACGIH TLV: 0.1 ppm TWA
OSHA PEL: 0.1 ppm
Physical Properties:
Appearance: Heavy, colorless, liquid with a sharp odor
Chemical names: Trichloronitromethane; Methane,trichloronitro; Nitrotrichloro-methane, Nitrochloroform
CAS # 76-06-2
Molecular Formula: CC13NO2
Molecular Weight: 164.38
Melting Point: -64 degrees C
Boiling Point: 112 degrees C
Vapor Pressure: 18.3 mmHg @ 20 degrees C, 24 mmHg @ 25 degrees C
Solubility in water: 1.6 g/L @ 25 degrees C
Solubility in other solvents: Miscible in most organic solvents.
BASIC MANUFACTURERS
Niklor Chemical Corp.
2060 E. 220th Street
Long Beach, CA 90810
Review by Basic Manufacturer:
Comments solicited: May and October, 1995
Comments received: not received
REFERENCES
Some trade names for products containing chloropicrin include "Chlor-O- Pic," "Metapicrin" "Timberfume" and "Tri-Clor." A partial list of trade names for chloropicrin mixtures with methyl bromide includes "Tri-Con," "Terr- O-Gas," "Preplant Soil Fumigant" and "Pic-Brom." Chloropicrin mixtures with 1,3-Dichloropropene include "Telone C-17," "Tri-Form" and "Pic-Clor."
REGULATORY STATUS
Chloropicrin is currently undergoing USEPA FIFRA reregistration. It is a Class I toxicity, Restricted Use Pesticide (RUP), labeled with the signal word "Danger" (1). The U.S. Department of Transportation (DOT) proper shipping name is "Chloropicrin, 6.1, UN 1580, PGI, Poison Inhalation Hazard, Hazard Zone B." The Emergency Response Guide (ERG) number is 56. NFPA designations are 4- Health, 0-Fire, 3-Reactivity. Chloropicrin is not listed under the EPA Clean Air Act, EPA Clean Water Act or the EPA Marine Pollutant List (2). A tolerance is not required for preplant soil fumigation uses of chloropicrin.
INTRODUCTION
Chloropicrin is a clear, colorless, oily liquid with a strong, sharp, highly irritating odor. It is a strong lachrymator (1). Chloropicrin has been used as an insecticide since 1917 and as a soil fumigant since 1920 (3). The primary use today is for preplant soil fumigation to control soil borne fungi, diseases and nematodes (1). It also is used to treat wood poles and timbers for internal decay by fungi and insects; as a warning/clearing agent for sulfuryl fluoride (structural fumigant) and methyl bromide (soil and structural fumigant); and is also used in organic synthesis.
For soil fumigation and wood treatment, chloropicrin is packaged in DOT 4BW240 steel cylinders and bulk tanks which may be pressurized. When used as a warning agent for methyl bromide, chloropicrin is packaged along with the methyl bromide in steel cylinders. When used as a structural fumigation warning agent for sulfuryl fluoride, chloropicrin is packaged in small plastic bottles in DOT approved overpacks.
Chloropicrin has a moderate vapor pressure (18.3 mmHg at 20 degrees C) and exists as a liquid at room temperature. Chloropicrin/methyl bromide mixtures will volatilize readily upon opening of the cylinder valve. Materials incompatible with chloropicrin are PVC, fiberglass, aluminum and magnesium and their alloys (1, 4).
TOXICOLOGICAL EFFECTS
Acute Toxicity
Undiluted chloropicrin is highly toxic by ingestion or direct contact with the skin or eyes. According to the American Conference of Governmental Industrial Hygienists (5), 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) (5). Inhalation exposure to 4 ppm (26 mg/meters cubed) for a few seconds may cause some degree of incapacitation (5) and an exposure of a few seconds to 15 ppm (100 mg/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 (5). The American Industrial Hygiene Association Emergency Response Planning Guideline for one hour exposure to chloropicrin is 3 ppm (20 mg/meters cubed)(6).
Animal studies established that the 4-hour inhalation LC50 for chloropicrin vapor in rats is 11.9 ppm (79.7 mg/meters cubed)(37) and the respiratory irritation potential threshold (RD50) in mice is 7.98 ppm (53.5 mg/meters cubed)(37). 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 (7) and male Fisher 344 rats exposed to chloropicrin (8) 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 (9). 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 (10). 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 (11). 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 (12, 15). 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 (16, 20). 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 (Log10 Kow) is 2.50 at 25 degrees C indicating that chloropicrin would not be expected to bioaccumulate in mammalian cells (21).
ECOLOGICAL EFFECTS
Effects on Birds
Little information is available about the effects of chloropicrin on bird life. A feeding study in chickens (22) 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 (22).
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 (23) and 4.5 days (24) with carbon dioxide being the terminal breakdown product (24). Chloropicrin moves rapidly in soils within twelve inches of injection but may diffuse to a maximum depth of four feet in sandy soil (25). 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 (26). In the absence of sunlight or microorganisms, chloropicrin does not undergo hydrolysis (27, 28). The calculated Henry's Law Constant is 2.51 x 10 to the minus 3 atm meters cubed mole-1 (29). The Koc for silt loam and agricultural sand soils was 5.29 and 93.59 respectively (33).
Chloropicrin can be produced during chlorination of drinking water if nitrated organic contaminants are present (30, 31). In a sampling of 1,386 wells in California between 1984 and 1989, no chloropicrin was detected (32). In a sampling of 15,175 wells in Florida, chloropicrin was found in three wells at 0.035-0.068 Hg/L (32).
Breakdown of Chemical in Surface Water
Since chloropicrin has a higher density than water (1.65 g/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 (28).
Breakdown of Chemical in Plants
No chloropicrin or nitromethane was detected in crops grown in soil treated with radiolabelled chloropicrin (34). Carbon dioxide, as the terminal breakdown product, was metabolized by plants and incorporated into natural plant biochemical compounds via the single carbon pool (35).
Breakdown of Chemical in Air
Chloropicrin is efficiently photolyzed in the atmosphere. The half-life of chloropicrin in air exposed to simulated sunlight was 20 days (36). The photoproducts were phosgene (which will hydrolyze to carbon dioxide and hydrogen chloride), nitric oxide, chlorine, nitrogen dioxide and dinitrogen tetroxide.
Analytical Methods
The concentration of chloropicrin in air may be measured using Kitagawa direct reading gas detector tube#l72 (Matheson-Kitagawa, East Rutherford, NJ). Gas chromatography methods are available to measure chloropicrin in air (27) and may utilize XAD-4 solid sorbent tubes (SKC Inc., Eighty Four, PA).
PHYSICAL PROPERTIES AND GUIDELINES
Exposure Guidelines:
ACGIH TLV: 0.1 ppm TWA
OSHA PEL: 0.1 ppm
Physical Properties:
Appearance: Heavy, colorless, liquid with a sharp odor
Chemical names: Trichloronitromethane; Methane,trichloronitro; Nitrotrichloro-methane, Nitrochloroform
CAS # 76-06-2
Molecular Formula: CC13NO2
Molecular Weight: 164.38
Melting Point: -64 degrees C
Boiling Point: 112 degrees C
Vapor Pressure: 18.3 mmHg @ 20 degrees C, 24 mmHg @ 25 degrees C
Solubility in water: 1.6 g/L @ 25 degrees C
Solubility in other solvents: Miscible in most organic solvents.
BASIC MANUFACTURERS
Niklor Chemical Corp.
2060 E. 220th Street
Long Beach, CA 90810
Review by Basic Manufacturer:
Comments solicited: May and October, 1995
Comments received: not received
REFERENCES
- Meister, R.T. 1995. Farm Chemicals Handbook '95. Meister Publishing Company. Willoughby, OH.
- Chemtox Online. 1995. Resource Consultants, Inc. Brentwood, TN.
- Roark, R.C. 1934. USDA Miscellaneous Publication No. 176. A Bibliography of Chloropicrin 1848- 1932. United States Department of Agriculture. Washington, DC.
- Thomson, W.T. 1991-2. Agricultural Chemicals Book III. Miscellaneous Agricultural Chemicals. Thomson Publications Fresno, CA.
- American Conference of Governmental Industrial Hygienists. 1992. Documentation of Threshold Limit Values and Biological Exposure Indices, Sixth Ed. Cincinnati, pp. 299-300.
- American Industrial Hygiene Association. 1987. Emergency Response Planning Guidelines: Chloropicrin. AIHA, Washington, DC.
- Chun, J.S. and W.J. Kintigh. 1993. Chloropicrin: Ninety-Day Inhalation Toxicology Study in Rats and Mice. Bushy Run Research Center. Export, PA. (Unpublished study submitted to USEPA).
- Yoshida, M. et. al. 1987. Subchronic Inhalation Toxicity of Chloropicrin Vapor in Rats. J. Pesticide Sci., 12:673-681.
- Schardein, J.L. 1994. Two Generation Inhalation Reproduction/ Fertility Study in Rats. International Research and Development Corp. Mattawan, MI. (Unpublished study submitted to USEPA)
- Schardein, J.L. 1993. Inhalation Developmental Toxicity Study in Rats. International Research and Development Corp. Mattawan, MI. (Unpublished study submitted to USEPA)
- Schardein, J.L. 1993. Inhalation Developmental Toxicity Study in New Zealand White Rabbits. International Research and Development Corp. Mattawan, MI. (Unpublished study submitted to USEPA)
- San, R.H. and Valentine Wagner III. 1990. Salmonella/Mammalian- Microsome Plate Incorporation Mutagenicity Assay (Ames Test) with a Confirmatory Assay. Microbiological Associates, Inc. Rockville MD. (Unpublished study submitted to USEPA)
- Putman, D.L. and Marcia Morris. 1990. Chromosome Aberrations in Chinese Hamster Ovary (CHO) Cells With Confirmatory Assay. Microbiological Associates, Inc. Rockville, MD. (Unpublished study submitted to USEPA)
- San, R.H. and Cynthia Sigler. 1990. L5178Y TK+/- Mouse Lymphoma Mutagenesis Assay With Confirmation. Microbiological Associates, Inc. Rockville, MD. (Unpublished study submitted to USEPA)
- Curren, R.D. 1990. Unscheduled DNA Synthesis in Rat Primary Hepatocytes With a Confirmatory Assay. Microbiological Associates, Inc. Rockville, MD. (Unpublished study submitted to USEPA)
- Ulrich, C.E. 1995. Two Year Oral (Gavage) Chronic Toxicity Study of Chloropicrin in Rats. International Research and Development Corp. Mattawan, MI. (Unpublished study submitted to USEPA)
- Wisler, J.A. 1994. Evaluation of Chloropicrin in a One Year Oral (Capsule) Toxicity Study in Dogs. International Research and Development Corp. Mattawan, MI. (Unpublished study submitted to USEPA)
- Burleigh-Flayer, H.D., W.J. Kintigh and C.L. Benson. 1995. Chloropicrin: Vapor Inhalation Oncogenicity Study in CD-1 Mice. Bushy Run Research Center. Export, PA. (Unpublished study submitted to USEPA)
- Burleigh-Flayer, H.D., W.J. Kintigh and C.L. Benson. 1995. Chloropicrin: Vapor Inhalation Oncogenicity Study in CD-1 Rats. Bushy Run Research Center. Export, PA. (Unpublished study submitted to USEPA)
- National Institutes of Health. 1978. Bioassay of Chloropicrin for Possible Carcinogenicity. NCI Technical Report No. 65, DHEW Publication No. (NIH) 78-1315.
- Secara, S.R. 1990. Chloropicrin - Octanol/Water Partition Coefficient. Bolsa Research Associates Inc. Hollister, CA. (Unpublished study submitted to USEPA)
- United States Department of Agriculture Forest Service. 1986. Pesticide Background Statements. Volume II. Fungicides and Fumigants. Agriculture Handbook Number 661.
- U.S. Environmental Protection Agency. 1992. Pesticide Environmental Fate One Line Summary: Chloropicrin. USEPA Environmental Fate and Effects Division. Washington, DC.
- Shepler, K., C. Hatton and L. Ruzo. 1995. Aerobic Soil Metabolism of [14C]Chloropicrin. PTRL West Inc. Richmond, CA. (Unpublished study submitted to USEPA)
- Ivancovich, A. 1987. Chloropicrin - Field Dissipation Study. Bolsa Research Associates. Hollister, CA. (Unpub-lished study submitted to USEPA)
- Shepler, K., C. Hatton and L. Ruzo. 1995. Anaerobic Aquatic Metabolism of [14C]Chloropicrin. PTRL West Inc. Richmond, CA. (Unpublished study submitted to USEPA)
- Hazardous Substances Data Bank (HSDB). Accession Number 977. National Library of Medicine, Bethesda, MD. 1993 CD ROM version: Micromedix Inc., Denver CO.
- Lee, H. and T. Moreno. 1993. Photohydrolysis of Chloropicrin. Bolsa Research Associates. Hollister, CA. (Unpublished study submitted to USEPA)
- Evaluation Summary, Ground Water Protection Data, Record No. 63408. 1989. California Department of Food and Agriculture Pesticide Registration Branch.
- Duguet, J.P., Y. Tsutsumi and A. Bruchet. 1988. Chloropicrin in Potable Water: Conditions of Formation and Production During Treatment Processes. Environ. Technol. Lett. 9(4) 299-310.
- Fair, P. S., R.C. Barth and J. Flesch. 1988. Measurement of Disinfection By-Products in Chlorinated Drinking Water. Proc.- Water Qual. Technol. Conf:, 15:339-53. Office of Drinking Water, USEPA Cincinnati, OH.
- U.S. Environmental Protection Agency. 1992. Pesticides in Groundwater Database, A Compilation of Monitoring Studies: 1971-1991, National Summary. EPA 734-12-92-0001.
- Craine, E.M. 1985. An Adsorption Study With Soil and Chloropicrin. Wil Research Laboratories, Inc. Ashland, OH. (Unpublished study submitted to USEPA)
- Lawrence, L.J. 1990. Quantitative Characterization of [14C]Residues Present in Soil, Strawberries, Green Beans and Red Beets Grown Under Actual Field Conditions Following Treatment of Soil with [14C]Chloropicrin. PTRL East Inc., Richmond, KY. (Unpublished study submitted to USEPA)
- Wilhelm, S. et. al. 1995. Environmental Fate of Chloropicrin. American Chemical Society Division of Agrochemicals Picogram and Abstracts Vol 49.
- Moilanen, K.W., D.G. Crosby and J. Humphrey. 1978. Vapor-Phase Photodecomposition of Chloropicrin. Tetrahedron, 34, pp. 3345-3349.
- Handbook of Environmental Data on Organic Chemicals. 1983. Verschueren Publishing Co. p. 384
