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DICHLOROPROPENE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Dichloropropene is a halogenated hydrocarbon, and is primarily a soil fumigant used as a nematocide, but small amounts are also used as a chemical intermediate.

Specific Substances

    1) Alpha, gamma dichloropropylene
    2) 1,3-dichloropropene
    3) 1,3-dichloropropylene
    4) Alpha-chloroallyl chloride
    5) Gamma-chloroallyl chloride
    6) CAS 542-75-6
    7) Molecular Formula: C3-H4-Cl2
    8) DICHLOROPROPENE (TRANS-)
    1.2.1) MOLECULAR FORMULA
    1) C3-H4-Cl2

Available Forms Sources

    A) FORMS
    1) Some brand names of this agent include Telone(R), Verlex(R) and D-D(R). D-D(R) is a mixture of this agent and propylene dichloride, a fumigant mixture that is an intense eye, skin, and pulmonary irritant. The mixture has a yellow color and a pungent garlic-like odor (Finkel, 1983).
    B) USES
    1) Dichloropropene is primarily a soil fumigant used as a nematocide, but small amounts are also used as a chemical intermediate (Clayton & Clayton, 1994).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Exposures occur primarily during production of this agent and in its bulk handling. The fumigant is usually injected 15 to 30 cm into the soil so concentrations are low at the surface and exposure risks are minimal. Early data gathered on the initial commercial product indicated significant hepatotoxicity, but more recent data on the current commercial product would indicate less hepatotoxicity.
    B) Ingestion has resulted in tachycardia, ARDS, acute renal failure, hepatorenal syndrome, severe coagulopathies, gastrointestinal hemorrhage, pancreatitis, and multiorgan system failure.
    0.2.4) HEENT
    A) This chemical is irritating to the eyes of test animals. Severe to moderate injury occurred to the eyes of rabbits after splash contact. Prompt washing decreased the degree of irritation. Vapors are irritating to the eyes of animals tested. Nasal irritation also occurred at concentrations greater than 1000 ppm.
    0.2.6) RESPIRATORY
    A) ARDS has been reported after ingestion. Animals exposed to 2700 ppm developed severe lung injury.
    0.2.9) HEPATIC
    A) Hepatorenal syndrome has been reported after acute oral exposure.
    B) Rats given 400 to 700 mg/kg developed hepatotoxicity. Older literature based on an earlier commercial product suggests more hepatic damage than tests on the newer preparations.
    0.2.10) GENITOURINARY
    A) Acute renal failure has been reported after ingestion. Rats given 400 to 700 mg/kg developed kidney abnormalities on gross pathological examination. The newer preparations may be less nephrotoxic.
    0.2.14) DERMATOLOGIC
    A) Necrosis and edema were present when the agent was confined to rabbit skin, but were much reduced when the product was allowed to evaporate.
    0.2.20) REPRODUCTIVE
    A) Based on animal data, this agent does not appear to be a mammalian teratogen at doses that would not also cause severe toxicity.

Laboratory Monitoring

    A) Toxic serum levels have yet been established.
    B) Monitor renal and liver function tests, serum electrolytes, glucose, amylase or lipase, INR or PT/PTT and platelet count after significant exposure.
    C) Monitor arterial blood gases and/or pulse oximetry and chest radiograph in patients with respiratory distress.

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) Monitor liver and kidney function. Elevations may not be seen for several days.
    C) Respiratory support may be indicated in significant exposures. Monitor for pulmonary edema.
    D) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    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) 2700 ppm is said to be extremely irritating to the lungs and caused renal and hepatic damage to animals. Human data is not available. The TLV is 1 ppm.

Clinical Effects

Summary Of Exposure

    A) Exposures occur primarily during production of this agent and in its bulk handling. The fumigant is usually injected 15 to 30 cm into the soil so concentrations are low at the surface and exposure risks are minimal. Early data gathered on the initial commercial product indicated significant hepatotoxicity, but more recent data on the current commercial product would indicate less hepatotoxicity.
    B) Ingestion has resulted in tachycardia, ARDS, acute renal failure, hepatorenal syndrome, severe coagulopathies, gastrointestinal hemorrhage, pancreatitis, and multiorgan system failure.

Heent

    3.4.1) SUMMARY
    A) This chemical is irritating to the eyes of test animals. Severe to moderate injury occurred to the eyes of rabbits after splash contact. Prompt washing decreased the degree of irritation. Vapors are irritating to the eyes of animals tested. Nasal irritation also occurred at concentrations greater than 1000 ppm.
    3.4.2) HEAD
    A) IRRITATION of the mucous membranes may be noted (IARC, 1986).
    3.4.3) EYES
    A) Highly irritating to eyes and mucous membranes (Grant & Schuman, 1993).
    B) SPLASH CONTACT is irritating to the eyes of test rabbits (ACGIH, 1991). Severe to moderate injury occurred to eyes of rabbits after splash contact. Prompt washing decreased the degree of irritation (Clayton & Clayton, 1994).
    C) Vapors at 2700 ppm are irritating to the eyes in animals tested. Concentrations of 1000 ppm cause lacrimation (ACGIH, 1991).
    D) CONJUNCTIVITIS is a common finding (IARC, 1986).
    3.4.5) NOSE
    A) Vapors at 2700 ppm were irritating to the nose and caused severe nasal injury to rats. Even concentrations of 1000 ppm were irritating to exposed animals (ACGIH, 1991).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) CASE REPORT - Tachycardia (130 beats/min) developed 2 hours after exposure in a 27-year-old man with a fatal dichloropropene ingestion (Hernandez et al, 1994).
    B) HYPOTENSIVE EPISODE
    1) CASE REPORT - Severe hypotension secondary to hypovolemia was reported in a 27-year-old man who developed multiorgan system failure and died after ingesting dichloropropene (Hernandez et al, 1994).

Respiratory

    3.6.1) SUMMARY
    A) ARDS has been reported after ingestion. Animals exposed to 2700 ppm developed severe lung injury.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Dyspnea may be reported after inhalation exposure (IARC, 1986).
    2) In a group of 80 people exposed to dichloropropene because of a truck spill, 4 complained of chest discomfort (Hathaway et al, 1996). Five of 28 patients interviewed 12 weeks after exposure complained of chest discomfort, one of whom was diagnosed with pneumonia.
    B) ACUTE LUNG INJURY
    1) CASE REPORT - Adult respiratory distress syndrome was reported in a 27-year-old man with a fatal dichloropropene ingestion (Hernandez et al, 1994).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) RATS exposed to 2700 ppm developed severe lung injury (ACGIH, 1991). Pulmonary edema was not mentioned.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) FATIGUE
    1) Weakness has been reported after exposure (IARC, 1986).
    B) HEADACHE
    1) Headache and dizziness are commonly reported symptoms (IARC, 1986).
    2) In a group of 80 people exposed to dichloropropene because of a truck spill, 6 complained of headache (Hathaway et al, 1996). Twelve of 28 patients interviewed 12 weeks after exposure complained of headache.
    C) DIZZINESS
    1) In a group of 80 people exposed to dichloropropene because of a truck spill, 5 complained of dizziness (Hathaway et al, 1996).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea and vomiting may occur (IARC, 1986).
    B) HEMORRHAGIC DIARRHEA
    1) CASE REPORT - Bloody diarrhea developed in a 27-year-old may after ingesting dichloropropene (Hernandez et al, 1994). The patient also developed thrombocytopenia and a severe coagulopathy.
    C) PANCREATITIS
    1) Pancreatitis has been reported in one fatal case (Hernandez et al, 1994).
    D) ABDOMINAL PAIN
    1) Six of 28 patients interviewed 12 weeks after exposure to dichloropropene because of a truck spill complained of abdominal discomfort (Hathaway et al, 1996).

Hepatic

    3.9.1) SUMMARY
    A) Hepatorenal syndrome has been reported after acute oral exposure.
    B) Rats given 400 to 700 mg/kg developed hepatotoxicity. Older literature based on an earlier commercial product suggests more hepatic damage than tests on the newer preparations.
    3.9.2) CLINICAL EFFECTS
    A) HEPATORENAL SYNDROME
    1) CASE REPORT - Hepatorenal syndrome developed in a 27-year-old male following ingestion of dichloropropene. He developed multiorgan system failure and died. Necropsy results showed liver congestion and a yellowish soft hepatic parenchyma (Hernandez et al, 1994).
    B) ABNORMAL LIVER FUNCTION
    1) In a prospective study in the Dutch flower bulb industry, workers who applied dichloropropene had lower levels of total bilirubin at the end of the four month season than they did at the beginning (7.0 vs 9.5 micromol/liter) (Brouwer et al, 1991). Other liver function tests (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, g-glutamyltranspeptidase) did not change significantly. The authors speculated that this resulted from induction of hepatic enzymes.
    2) In a group of 41 people who had liver enzymes levels assayed after being exposed to dichloropropene because of a truck spill, 11 had slightly elevated SGOT and/or SGPT levels (Hathaway et al, 1996).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) RATS - Minimal human or animal data are available, but rats given 400 to 700 mg/kg developed hepatotoxicity demonstrated by gross pathological examination (ACGIH, 1991). The older literature, based on an earlier commercial product, suggests more hepatic damage than tests on the newer preparations (Clayton & Clayton, 1994).

Genitourinary

    3.10.1) SUMMARY
    A) Acute renal failure has been reported after ingestion. Rats given 400 to 700 mg/kg developed kidney abnormalities on gross pathological examination. The newer preparations may be less nephrotoxic.
    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) CASE REPORT - Acute renal failure was reported in a 27-year-old man who developed hypotension, multiorgan system failure and died after ingesting dichloropropene (Hernandez et al, 1994).
    B) ABNORMAL RENAL FUNCTION
    1) In a prospective study in the Dutch flower bulb industry, workers who applied dichloropropene had higher urinary concentrations of albumin at the end of the four month season than they did at the beginning (5.2 vs 7.6 milligrams/liter) (Brouwer et al, 1991). In the same workers the concentration of retinol binding protein in urine was higher at the end of the season (20 vs 26.9 micrograms/liter) while serum creatinine was lower (93 vs 87.5 micromol/liter).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEPHROPATHY TOXIC
    a) RATS - Minimal animal and human data are available, but rats given 400 to 700 mg/kg developed kidney abnormalities on gross pathological examination (ACGIH, 1991). Older literature based on an earlier commercial product suggested more renal damage than tests on the newer preparation (Clayton & Clayton, 1994).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) BLOOD COAGULATION PATHWAY FINDING
    1) CASE REPORT - Severe coagulopathy with incoaguable blood and a platelet count of 55,000 was reported in a 27-year-old man who developed multiorgan system failure and died after ingesting dichloropropene (Hernandez et al, 1994).

Dermatologic

    3.14.1) SUMMARY
    A) Necrosis and edema were present when the agent was confined to rabbit skin, but were much reduced when the product was allowed to evaporate.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) Smarting of the skin and first-degree burns may occur with short-term exposure; second-degree burns may be seen after prolonged contact (CHRIS , 1999).
    B) SKIN IRRITATION
    1) Irritation of the mucous membranes may be noted (IARC, 1986; Grant & Schuman, 1993).
    C) ERUPTION
    1) CASE REPORT - Sensitization occurred in a 20-year-old man. Erythematous, pruritic papular lesions developed on the hands and feet. The lesions disappeared after topical corticosteroid therapy. Patch testing was positive (van Joost & de Jong, 1988).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) RABBITS - This liquid is irritating to the skin of rabbits (ACGIH, 1991). Necrosis and edema were present when the agent was confined to rabbit skin, but were much reduced as the product was allowed to evaporate (Clayton & Clayton, 1994).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) Hyperglycemia associated with pancreatitis and insulin resistance, has been reported after ingestion in one fatal case (Hernandez et al, 1994).

Reproductive

    3.20.1) SUMMARY
    A) Based on animal data, this agent does not appear to be a mammalian teratogen at doses that would not also cause severe toxicity.
    3.20.2) TERATOGENICITY
    A) LACK OF EFFECT
    1) Based on animal data, this agent does not appear to be a mammalian teratogen at doses that would not also cause severe toxicity (Clayton & Clayton, 1994; Hanley et al, 1987).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS542-75-6 (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: 1,3-Dichloropropene (technical-grade)
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.3) HUMAN STUDIES
    A) IARC CATEGORY
    1) 1,3-dichloropropene IARC group 2B; Human: inadequate evidence; Animal: sufficient evidence (Lewis, 1996).
    B) CARCINOMA
    1) Two cases of non-Hodgkins lymphoma and one of acute myelomonocytic leukemia have been associated with exposure to 1,3-dichloropropene. The relationship has not yet been proven (Markovitz & Crosby, 1984).
    3.21.4) ANIMAL STUDIES
    A) BENIGN TUMOR
    1) LUNG TUMORS - An increased incidence of benign bronchioalveolar lung tumors was seen in RATS exposed to 60 ppm chronically (Lomax et al, 1989).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Toxic serum levels have yet been established.
    B) Monitor renal and liver function tests, serum electrolytes, glucose, amylase or lipase, INR or PT/PTT and platelet count after significant exposure.
    C) Monitor arterial blood gases and/or pulse oximetry and chest radiograph in patients with respiratory distress.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No toxic blood or serum levels have yet been established.
    2) Monitor renal and liver function tests in substantial exposures.
    3) Monitor serum electrolytes, glucose and amylase or lipase in substantial exposures.
    B) HEMATOLOGY
    1) Monitor CBC, platelets, INR or PT/PTT after substantial exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) Complete urinalysis is advisable following significant exposures.
    B) OTHER
    1) In exposed humans, mercapturic acid adducts are found in the urine (IARC, 1986) Van Welie et al, 1989).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor pulmonary function studies and arterial blood gases in all symptomatic exposures.
    b) ECG should be monitored in all symptomatic exposures.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Toxic serum levels have yet been established.
    B) Monitor renal and liver function tests, serum electrolytes, glucose, amylase or lipase, INR or PT/PTT and platelet count after significant exposure.
    C) Monitor arterial blood gases and/or pulse oximetry and chest radiograph in patients with respiratory distress.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) 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) 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.
    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).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor liver and kidney function after an exposure. Elevations may not be seen for several days.
    B) IRRITATION SYMPTOM
    1) In significant exposures, pulmonary irritation may be severe. This is based on animal studies and not human data.
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).

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).

Range Of Toxicity

Summary

    A) 2700 ppm is said to be extremely irritating to the lungs and caused renal and hepatic damage to animals. Human data is not available. The TLV is 1 ppm.

Maximum Tolerated Exposure

    A) ANIMAL DATA
    1) 2700 parts per million is said to be extremely irritating to the lungs and caused renal and hepatic damage in rats. A one hour exposure to 1000 parts per million was survived by rats, but a two hour exposure killed these animals.
    2) Guinea pigs died after a single exposure of 400 parts per million. Lung injury in surviving animals lasted up to eight days. Rats given up to 30 milligrams/kilogram orally developed no significant symptoms (Clayton & Clayton, 1994).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) A blood 1,3-dichloropropene level was 1.13 micromol/L 2 hours after ingestion in a 27-year-old man who ultimately died of multiorgansystem failure (Hernandez et al, 1994). The blood level obtained at autopsy was 0.33 micromol/L.

Workplace Standards

    A) ACGIH TLV Values for CAS542-75-6 (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) 1,3-Dichloropropene
    a) TLV:
    1) TLV-TWA: 1 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: Skin
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    b) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): Kidney dam
    d) Molecular Weight: 110.98
    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 CAS542-75-6 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: 1,3-Dichloropropene
    2) REL:
    a) TWA: 1 ppm (5 mg/m(3))
    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: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s): See Appendix A
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS542-75-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: 1,3-Dichloropropene
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: 1,3-Dichloropropene
    a) B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.
    3) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: 1,3-Dichloropropene
    a) B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.
    4) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: 1,3-Dichloropropene
    a) B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.
    5) 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): 2B ; Listed as: 1,3-Dichloropropene (technical-grade)
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    6) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: 1,3-Dichloropropene
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    7) MAK (DFG, 2002): Category 2 ; Listed as: 1,3-Dichloropropene (cis- and trans-)
    a) Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.
    8) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): R ; Listed as: 1,3-Dichloropropene (Technical Grade)
    a) R : RAHC = Reasonably anticipated to be a human carcinogen

    D) OSHA PEL Values for CAS542-75-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1999
    1) LD50- (ORAL)MOUSE:
    a) 640 mg/kg
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 175 mg/kg
    3) LD50- (ORAL)RAT:
    a) 470 mg/kg

Physicochemical

Physical Characteristics

    A) cis-trans, mixture: A light-straw colored liquid with a sharp, sweet penetrating and irritating odor.

Molecular Weight

    A) 111 (Budavari, 1996)

Other

    A) ODOR THRESHOLD
    1) At 1-3 ppm the odor was faint and fatigued rapidly. It apparently reacts with rubber, leather and fur to produce a strong smell. The odor has been described as skunk or garlic-like (ACGIH, 1991; Clayton & Clayton, 1994).

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