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PROPYLENE DICHLORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Propylene dichloride is a volatile solvent and has been used as a chemical intermediate, fumigant and gasoline scavenging agent. Its use as a solvent is significantly limited due to its flammability.

Specific Substances

    1) 1,2-dichloropropane
    2) Bichlorure de Propylene (French)
    3) DCP
    4) alpha, beta-Dichloropropane
    5) Dwuchloropropan (Polish)
    6) ENT 15,406
    7) NCI-c 55141
    8) Propylene Chloride
    9) Propylene Dichloride
    10) alpha, beta-Propylene Dichloride
    11) RCRA WASTE NUMBER: U083
    12) Molecular Formula: C3-H6-Cl2
    13) NIOSH/RTECS TX 9625000
    14) CAS 78-87-5
    15) DICHLOROPROPANE (CAS 78-87-5)
    1.2.1) MOLECULAR FORMULA
    1) C3-H6-Cl2

Available Forms Sources

    A) FORMS
    1) Propylene dichloride has been mixed with 1,3 dichloropropene to create DD, a fumigant mixture that is an intense eye, skin, and pulmonary irritant (Finkel, 1983).
    2) Industrial Grade: 99% to 99.5% (IARC , 1986)
    B) SOURCES
    1) It is derived from the "action of chlorine on propylene" (Lewis, 1997).
    2) The substance is a propylene oxide byproduct and can be produced through hypochlorination/dehydrochlorination by mixing propylene, chlorine, and calcium hydroxide (Ashford, 1994).
    3) It is manufactured from antimony pentachloride and propyl chloride (HSDB , 2001).
    C) USES
    1) Propylene dichloride is used as a perchloroethylene and carbon tetrachloride intermediate; as an intermediate in rubber processing; as a gasoline scavenging agent; as a fat, oil, resin, gum, wax, plastic, and metal solvent; as a cellulose esters and ethers solvent; and in scouring compounds and metal degreasing and spotting agents (ACGIH, 1991; HSDB , 2001; Lewis, 1997). It also is used in furniture finish, in solutions for dry cleaning, and in insecticidal fumigant mixtures, specifically as a fungicide, nematocide, herbicide, insecticide, and soil fumigant (Budavari, 2000; IPCS, 1993; Zenz, 1994).
    2) Because it is a good and relatively cheap solvent, propylene dichloride has been used in the past with high frequency and in high concentrations as a stain remover. This has led to sniffing of this chlorinated hydrocarbon for abuse purposes (Pozzi et al, 1985).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Most exposures are via inhalation, although ingestions have occurred. Both chronic and acute exposures may cause liver and kidney damage.
    B) Ingestion can cause nausea, vomiting, diarrhea, abdominal pain, disseminated intravascular coagulation, hemolytic anemia, hepatic injury, renal failure, headache, and CNS depression.
    C) Effects from inhalation may include respiratory tract irritation, anorexia, abdominal pain, vomiting, ecchymoses, and hematuria. In severe cases hepatic injury, renal failure, hemolysis, and coagulopathy may develop.
    D) Repeated or prolonged skin contact with propylene dichloride may result in skin irritation due to defatting.
    E) The liquid is moderately irritating to the eye but does not cause serious or permanent injury.
    0.2.4) HEENT
    A) CONJUNCTIVITIS - This chemical is moderately irritating to the eyes but is not expected to cause serious or permanent injury.
    0.2.6) RESPIRATORY
    A) At high concentrations the vapors are irritating to the respiratory tract.
    0.2.7) NEUROLOGIC
    A) Very high concentrations are depressant in animals.
    0.2.9) HEPATIC
    A) Hepatotoxicity has been seen in humans both after ingestion and inhalation.
    0.2.10) GENITOURINARY
    A) Acute renal failure was seen in humans after both ingestion and inhalation. Renal biopsy in one case showed acute renal necrosis.
    0.2.13) HEMATOLOGIC
    A) Disseminated intravascular coagulation and hemolytic anemia have been reported in human cases.
    0.2.20) REPRODUCTIVE
    A) Although this agent has shown some teratogenicity in microbial studies, its effect among mammalian systems is still yet to be determined.
    B) Testicular degeneration, reduction in sperm, and/or increased number of degenerate spermatogonia in the epididymis were noted in rats gavaged with 1,2-dichloropropane.

Laboratory Monitoring

    A) If there is a known exposure, monitor liver, kidney, and hematologic functions.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    B) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
    C) Do not give oils by mouth. They may increase absorption.
    D) Do not administer adrenergic amines or atropine.
    E) Support respiration, observe for CNS depression and pulmonary irritation.
    F) Monitor liver and kidney function after an exposure.
    G) HEMODIALYSIS - May be effective supportive care in renal and hepatic failure.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) No toxic blood or serum concentration has yet been established.
    B) The TLV is 75 ppm, and the STEL is 110 ppm.
    C) Short-term exposures to 400 to 500 ppm were tolerated by workmen without adverse effects.

Clinical Effects

Summary Of Exposure

    A) Most exposures are via inhalation, although ingestions have occurred. Both chronic and acute exposures may cause liver and kidney damage.
    B) Ingestion can cause nausea, vomiting, diarrhea, abdominal pain, disseminated intravascular coagulation, hemolytic anemia, hepatic injury, renal failure, headache, and CNS depression.
    C) Effects from inhalation may include respiratory tract irritation, anorexia, abdominal pain, vomiting, ecchymoses, and hematuria. In severe cases hepatic injury, renal failure, hemolysis, and coagulopathy may develop.
    D) Repeated or prolonged skin contact with propylene dichloride may result in skin irritation due to defatting.
    E) The liquid is moderately irritating to the eye but does not cause serious or permanent injury.

Heent

    3.4.1) SUMMARY
    A) CONJUNCTIVITIS - This chemical is moderately irritating to the eyes but is not expected to cause serious or permanent injury.
    3.4.3) EYES
    A) Propylene dichloride is moderately irritating and causes some pain when splashed into eyes. However, it is not expected to result in serious or permanent injury (Clayton & Clayton, 1994).
    1) CASE REPORT - CONJUNCTIVITIS persisted for several hours following an ocular exposure in a workman, resulting from a ruptured pipeline. Corneal epithelium was damaged, which resolved spontaneously with no special treatment (Grant & Schuman, 1993).
    2) ANIMAL - Propylene dichloride is moderately irritating to eyes, but is not expected to cause serious or permanent injury (ACGIH, 1986). Guinea pigs repeatedly exposed to 2200 ppm for 7 hours developed serious conjunctival swelling (Proctor et al, 1988).

Respiratory

    3.6.1) SUMMARY
    A) At high concentrations the vapors are irritating to the respiratory tract.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) CASE SERIES - Six men developed severe respiratory complications following a tank car explosion. The tank car contained 4 parts o-dichlorobenzene, 2 parts propylene dichloride, and 1 part ethylene dichloride. Coughing and choking occurred initially, followed by 4 to 6 hours of quiescence. Over 2 to 3 days pulmonary edema, atelectasis, emphysema, and bronchopneumonia developed secondary to destruction of much of the lining of the respiratory tract. Three patients subsequently died and one of the remaining 3 survivors showed residual impairment of respiratory tract function (Gosselin et al, 1984; HSDB , 2000).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Respiratory irritation was seen in guinea pigs exposed to 2200 ppm for several 7 hour exposures. Repeated exposures to 1000 ppm produced respiratory irritation in rats and mice (Proctor et al, 1988). One animal study with mice determined that respiratory injury rather than hepatic injury was the primary cause of acute death (Clayton & Clayton, 1994).

Neurologic

    3.7.1) SUMMARY
    A) Very high concentrations are depressant in animals.
    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) CASE REPORT - Coma with CNS preservation of reaction to noxious stimuli has occurred after intentional oral ingestion in one patient (Thorel et al, 1986).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) In very high concentrations this agent was found to be a depressant in animals (Proctor et al, 1988).
    2) COORDINATION ABNORMAL
    a) Incoordination was seen in guinea pigs exposed to 2200 ppm for several 7 hour exposures. Rats given several exposures to 1000 ppm developed weakness and general debility which led to death (Proctor et al, 1988).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) CASE SERIES - Abdominal pain, anorexia, and vomiting have been reported following inhalation and ingestion exposures in 3 human cases (HSDB , 2000).

Hepatic

    3.9.1) SUMMARY
    A) Hepatotoxicity has been seen in humans both after ingestion and inhalation.
    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) Hepatotoxicity has been seen in humans, both after ingestion and inhalation. Damage may manifest itself several days after an ingestion (Pozzi et al, 1985).
    B) PORTAL HYPERTENSION
    1) CASE REPORT - One case of severe, early hepatocellular necrosis with late appearance of portal hypertension and fibrosis following an intentional suicidal oral ingestion has been reported (Thorel et al, 1986).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) Hepatic damage has been seen in fatally poisoned animals (Proctor et al, 1988; Clayton & Clayton, 1994). Dogs and guinea pigs who inhaled 1000 ppm for 22 to 24 exposures developed severe liver damage and died. This experiment ranked propylene dichloride hepatotoxicity to be somewhat more acute than carbon tetrachloride, but less than ethylene dichloride.
    2) LACK OF EFFECT
    a) Another study where animals inhaled 400 ppm for 128 to 140 daily 7-hour exposures, showed no histologic changes (Proctor et al, 1988).

Genitourinary

    3.10.1) SUMMARY
    A) Acute renal failure was seen in humans after both ingestion and inhalation. Renal biopsy in one case showed acute renal necrosis.
    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) Acute renal failure was seen in humans after both ingestion and inhalation. Renal biopsy in one case showed acute renal necrosis. This symptom may not manifest itself for several days after an exposure (Pozzi et al, 1985).

Hematologic

    3.13.1) SUMMARY
    A) Disseminated intravascular coagulation and hemolytic anemia have been reported in human cases.
    3.13.2) CLINICAL EFFECTS
    A) DISSEMINATED INTRAVASCULAR COAGULATION
    1) Disseminated intravascular coagulation was reported by Pozzi et al (1985) in three patients, but in only one was it clinically significant. This was a case of chronic inhalation-abuse. This effect has not previously been reported in either human or animal studies.
    B) HEMOLYTIC ANEMIA
    1) Hemolytic anemia had not been previously reported, but was seen in the patients of Pozzi et al (1985).
    C) BLOOD COAGULATION PATHWAY FINDING
    1) CASE REPORT - Coagulopathy with prolonged prothrombin time, decreased Factor V levels and platelet count, and elevated levels of fibrin split products was reported in a case of severe hepatocellular necrosis following suicidal oral ingestion (Thorel et al, 1986).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) This agent is mildly irritating to the skin but does not cause serious or permanent injury (ACGIH, 1980; (Lewis, 1996; Clayton & Clayton, 1994). Repeated or continued contact with skin may produce defatting and subsequent irritation (Proctor et al, 1988; Hathaway et al, 1991).
    2) Delayed allergic contact dermatitis resulting from exposure to 1,2-dichloropropane, with positive patch test has been reported (Baruffini et al, 1989). Repeated occupational contact with the solvent and preexisting skin lesions may have predisposed these workers to dermatitis.
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PERCUTANEOUS ABSORPTION
    a) RABBITS - Percutaneous absorption has been observed in rabbits (Pozzi et al, 1985).

Endocrine

    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ADRENAL INSUFFICIENCY
    a) Animal experiments indicate a potential for adrenal injury at high oral doses (Clayton & Clayton, 1994).

Reproductive

    3.20.1) SUMMARY
    A) Although this agent has shown some teratogenicity in microbial studies, its effect among mammalian systems is still yet to be determined.
    B) Testicular degeneration, reduction in sperm, and/or increased number of degenerate spermatogonia in the epididymis were noted in rats gavaged with 1,2-dichloropropane.
    3.20.2) TERATOGENICITY
    A) CONGENITAL ANOMALY
    1) Although this agent has shown some teratogenicity in microbial studies, its effect among mammalian systems is still yet to be determined (Clayton & Clayton, 1994).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS78-87-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: 1,2-Dichloropropane
    b) Carcinogen Rating: 1
    1) The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
    3.21.4) ANIMAL STUDIES
    A) HEPATOMA
    1) MICE - Hepatomas were seen in mice given 128 to 140 exposures to 400 ppm (ACGIH, 1986; Clayton & Clayton, 1994).
    B) CARCINOMA
    1) RATS - There was equivocal evidence of mammary gland carcinogenicity in female rats given 250 mg/kg/day by gavage (NTP, 1986).
    C) NEOPLASM HEPATIC
    1) MICE - There was some evidence of carcinogenicity in male and female mice for hepatocellular neoplasms, primarily adenomas (NTP, 1986).
    D) LACK OF EFFECT
    1) RATS - There was no evidence of carcinogenicity in rats given 62 or 125 mg/kg/day by gavage (NTP, 1986).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) If there is a known exposure, monitor liver, kidney, and hematologic functions.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No specific lab work (CBC, electrolytes) is needed unless otherwise clinically indicated.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) If there is a known exposure, monitor liver, kidney, and hemotologic functions. With chronic low-dose exposures in industry, an annual evaluation of liver and kidney functions is recommended (Pozzi et al, 1985; Plunkett, 1976).

Methods

    A) CHROMATOGRAPHY
    1) Gas chromatography may be used to analyze propylene dichloride. The usefulness of doing this is questionable, since 80 to 90% of this compound is excreted in expired air, urine, or feces within 24 hours and symptoms may not manifest until after this period of time.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) If there is a known exposure, monitor liver, kidney, and hematologic functions.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) Propylene chloride was adsorbed on granular activated charcoal when evaluated as an effective technique for removing this compound from drinking water (HSDB , 2000).
    2) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) DIETARY FINDING
    1) Do not give oils by mouth. They tend to increase intestinal absorption of these lipophilic toxicants.
    B) CONTRAINDICATED TREATMENT
    1) Do not administer adrenergic amines or atropine, which may further increase mild cardioirritability.
    C) SUPPORT
    1) Support respiration, observe for CNS depression and pulmonary irritation. Pulmonary edema has not been reported. Observe for possible aspiration.
    2) No specific treatment or antidote exists. Provide symptomatic and supportive care.
    D) MONITORING OF PATIENT
    1) Studies of liver and kidney function should be done if there is chronic low-dose exposure, abuse, or if a significant acute exposure has occurred.
    2) HEMODIALYSIS - May be effective supportive care in renal and hepatic failure.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) HEMODIALYSIS
    1) Dialysis or any other methods of extracorporeal elimination have not proved useful in hastening the elimination of this chemical.

Abstracts

Case Reports

    A) ADULT
    1) A 49-year-old patient reported by Thorel et al (1986) ingested an unknown amount of pure propylene dichloride in a suicide attempt. Coma with preservation of reaction to noxious stimuli and respiratory depression requiring mechanical ventilation were seen on admission. Initial liver function tests were normal. Three days after ingestion, icterus, elevated aminotransferase levels, and prolonged prothrombin time were noted. There was no prior history of alcoholism or chronic hepatic diseases. Viral serologies were negative. A coagulopathy developed requiring heparin infusion and platelet and fresh frozen plasma infusions.
    2) An erosive esophagitis was seen on gastroscopy. Hepatocellular necrosis was found on liver biopsy. The patient improved, but at follow up one month later had developed hepatomegaly, splenomegaly, and ascites. Seven months after ingestion, hepatomegaly and splenomegaly persisted. A repeat gastroscopy showed esophageal varices. Measurement of intrahepatic pressures showed a pressure gradient consistent with portal hypertension. A repeat liver biopsy showed portal fibrosis without hepatocellular necrosis.

Range Of Toxicity

Summary

    A) No toxic blood or serum concentration has yet been established.
    B) The TLV is 75 ppm, and the STEL is 110 ppm.
    C) Short-term exposures to 400 to 500 ppm were tolerated by workmen without adverse effects.

Minimum Lethal Exposure

    A) ACUTE LETHAL STUDIES
    1) An adult male died following consumption of 50 mL of propylene dichloride (ACGIH, 1991).
    2) One reported death followed ingestion of DCP in a human, but the ingested amount could not be verified (Pozzi et al, 1985).
    3) Six men were hospitalized and seven men died within 24 hours after a spill of 3000 gallons of DOW 421, a mixture containing 2 parts propylene dichloride, 4 parts o-dichlorobenzene, and 1 part ethylene dichloride in a rail way tank car accident. Three of the six hospitalized men also died (ACGIH, 1991).
    4) Death resulted following a man's ingestion of 50 mL of a cleaning solution containing propylene dichloride. Other substances in the solution were not known (IPCS, 1993).
    B) CHRONIC EXPOSURE STUDIES
    1) "1,2-Dichloropropane is not classifiable as to its carcinogenicity to humans (Group 3)" (IARC, 1999).
    C) ANIMAL DATA
    1) INHALATION - A four-hour exposure to 2000 ppm was fatal to rats. 22-24 exposures to 1000 ppm caused death in some animals (Heppel et al, 1946).
    2) GAVAGE - Over 50 percent of the male rats gavaged with 750 mg/kg of 1,2-dichloropropane five times weekly, died within 10 days (Bruckner et al, 1989).
    3) "There is limited evidence in experimental animals for the carcinogenicity of 1,2-dichloropropane" (IARC, 1999).
    4) NTP CARCINOGENESIS STUDIES NTP, 1991
    a) "(Gavage); No Evidence: Male Rat"
    b) "(Gavage); Equivocal Evidence: Female Rat"
    c) "(Gavage); Some Evidence: Male and Female Mouse"

Maximum Tolerated Exposure

    A) Workmen tolerated short-term exposures to 400 to 500 ppm workmen without adverse effects (Hathaway et al, 1996).
    B) IARC Carcinogenicity Classification: Group 3, not classifiable as to its carcinogenicit to humans
    C) ANIMAL DATA
    1) INHALATION - Some animals survived over 100, 7 hour exposures to 1000 ppm while repeated exposure was fatal to others (ACGIH, 1991). 400 ppm given for 140 daily, 7 hour exposures produced no negative effects in rats, dogs, or guinea pigs(Hathaway et al, 1996).
    2) GAVAGE - Morphological changes in liver centrilobular cells were noted in rats gavaged with 500 or 1000 mg/kg of 1,2-dichloropropane in corn oil once daily for 10 days (Bruckner et al, 1989).
    3) Guinea pigs survived 200 mg/kg, but liver injury did result (Bingham et al, 2001a).
    4) Areas of focal necrosis were observed to be isolated and decrease with duration of treatment following both oral and parenteral administration of DCP in short- and long-term studies in rats (Bruckner et al, 1989; Trevisan et al, 1989).
    D) OTHER
    1) Lewis (2000) suggests the following relation between chlorinated hydrocarbons and the toxicity they produce, beginning with the most toxic.
    1) Dichloroethane
    2) Dichloropropane
    3) Carbon tetrachloride
    4) Trichloroethylene
    5) Dichloromethane

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) No toxic blood or serum concentration has yet been established.

Workplace Standards

    A) ACGIH TLV Values for CAS78-87-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Propylene dichloride
    a) TLV:
    1) TLV-TWA: 10 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: SEN
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT irr; body weight eff
    d) Molecular Weight: 112.99
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS78-87-5 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Propylene dichloride
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix A
    3) IDLH:
    a) IDLH: 400 ppm
    b) Note(s): Ca
    1) Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

    C) Carcinogenicity Ratings for CAS78-87-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Propylene dichloride
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: 1,2-Dichloropropane
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 1 ; Listed as: 1,2-Dichloropropane
    a) 1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Propylene dichloride
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    5) MAK (DFG, 2002): Category 3B ; Listed as: 1,2-Dichloropropane
    a) Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS78-87-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Propylene dichloride
    2) Table Z-1 for Propylene dichloride:
    a) 8-hour TWA:
    1) ppm: 75
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 350
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ACGIH, 1991 Bingham et al 2001 Budavari, 2000 CHRIS, 2001 Hathaway et al, 1996 HSDB, 2001 IPCS, 1993 Lewis, 2000 NTP, 1991 OHM/TADS, 2001 RTECS, 2001
    1) LD50- (SKIN)HUMAN:
    a) 8.15 g/kg (Bingham et al, 2001)
    2) LD50- (ORAL)MOUSE:
    a) 860 mg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 1100 mg/kg
    4) LD50- (ORAL)RAT:
    a) 2196 mg/kg (Lewis, 2000)
    b) 1.7-2.1 g/kg (Bingham et al, 2001)
    c) 1947 mg/kg
    d) 1.19 mL/kg (Budavari, 2000; HSDB, 2001)
    e) 1.9 g/kg (IPCS, 1993)
    f) 1947 mg/kg (NTP, 1991)
    g) 1900 mg/kg (OHM/TADS, 2001)
    5) LD50- (SKIN)RAT:
    a) 9 mL/kg (HSDB, 2001)
    6) TCLo- (INHALATION)MOUSE:
    a) 400 ppm for 7H/7W- intermittent -- degeneration of fatty liver; death
    7) TCLo- (INHALATION)RAT:
    a) 9 mg/m(3) for 24H/94D-continuous -- specific arc-as recordings of CNS; respiration, lung, or thorax changes; true cholinesterase
    b) 10 mg/m(3) for 24H/60D- intermittent -- liver changes; phosphatases; dehydrogenases
    c) 1000 ppm for 7H/20W-intermittent -- spleen changes; fatty liver degeneration; death

Pharmacology Toxicology

Toxicologic Mechanism

    A) Propylene dichloride appears to have a direct toxic effect on renal tubular cells. It is also thought that this agent creates centrilobular hepatic necrosis (Pozzi et al, 1985) that may progress to fibrosis and the development of portal hypertension (Thorel et al, 1986).

Physicochemical

Physical Characteristics

    A) Propylene dichloride is a colorless, stable, mobile liquid with a sweet, chloroform-like odor. The substance sinks in water (Bingham et al, 2001; Budavari, 2000; CHRIS , 2001; Lewis, 1997; NIOSH , 2001).
    B) "Human subjects described the odor as 'strong' at 130 to 190 ppm and 'not noticeable' at 15 to 23 ppm" (HSDB , 2001).

Molecular Weight

    A) 112.99

Other

    A) ODOR THRESHOLD
    1) 0.25 ppm (ACGIH, 1991)
    2) 50 ppm (NTP , 1991)
    3) 420 mg/(m3) (Sittig, 1991)

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