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1,6-HEXAMETHYLENEDIAMINE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) 1,6 Hexamethylenediamine is solid (anhydrous) at 15 degrees C and 1 atm and has rhombic bipyrimidal plates.

Specific Substances

    1) 1,6-Diamino-N-hexane
    2) 1,6-Diaminohexane
    3) 1,6-Hexanediamine
    4) 1,6-Hexylenediamine
    5) Hexamethylenediamine
    6) Hexane-1,6-diamine
    7) Hexane-1,6-diamino-
    8) HMD(A)
    1.2.1) MOLECULAR FORMULA
    1) C6-H16-N2
    2) NH2(CH2)6NH2
    3) H2N(CH2)6NH2

Available Forms Sources

    A) FORMS
    1) HMDA is solid (anhydrous) at 15 degrees C and 1 atm. It has a weak, fishy odor similar to piperdine and exists as colorless leaflets or platelets and as long needles from sublimation. It has also been described as a white crystalline solid with an ammonia-type odor. Closer examination of the solid indicates rhombic bipyrimidal plates. Anhydrous HMDA is 99.8% pure, while HMDA in solution is 70% pure. HMDA solution is a clear, colorless liquid (AAR, 2000; ACGIH, 1996; CHRIS, 2002; HSDB , 2002; Lewis, 2000).
    B) SOURCES
    1) Methods of Manufacturing/Derivation:
    a) Reduction of adiponitrile with sodium and alcohol (Budavari, 2000).
    b) HMDA may be formed by reacting catalytic vapor-phase ammonia with adipic acid to yield adiponitrile. This step is then followed by liquid-phase catalytic hydrogenation (Lewis, 2001a).
    c) HMDA may also be formed by chlorinating butadiene, followed by a reaction with sodium cyanide (cuprous chloride catalyst) to produce 1,4-dicyanobutylene, and hydrogenation (Lewis, 2001a).
    C) USES
    1) 1,6-Hexamethylenediamine (HMDA) is used as a chemical intermediate in the manufacture of resins, such as nylon-type polyamide and nylon. The polyamides formed from HMDA are used in printing inks, dimer acids, paints, and textiles. HMDA is used in the manufacture of oil-modified and moisture-area types of urethane coatings. It is also used to prepare hexamethylene diisocyanate. The diamines, including HMDA, are industrially used as corrosion inhibitors through their application as an additive in oils and lubricants and as curing agents for epoxide resins and plastic articles (ACGIH, 1996; Budavari, 2000; HSDB , 2002; Sittig, 1991a).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) 1,6-hexamethylenediamine (HMDA) is corrosive to the eyes, skin, and respiratory tract. Inhalation may cause coughing, labored breathing, and shortness of breath. Contact with liquid HMDA may be caustic to the skin and eyes causing redness and pain. First-degree burns may result from short-term exposure to the skin, and prolonged exposure may cause secondary burns. Symptoms of HMDA ingestion may include abdominal cramps and pain.
    B) Chronic or repeated exposure can cause anemia, kidney or liver damage. Other signs and symptoms of prolonged contact may include skin damage, allergic rhinitis, bronchial asthma, impairment of bronchial permeability, toxicoallergic hepatitis, gastritis, colitis, hypergammaglobulinemia, increased transaminase activity, and eosinophilia.
    C) Inhalation may be fatal as a result of spasm, inflammation and edema of the larynx and bronchi, chemical pneumonitis, and acute lung injury.
    0.2.4) HEENT
    A) Eye, nasal and throat irritation may occur following exposure to HMDA vapors.
    0.2.6) RESPIRATORY
    A) Respiratory signs and symptoms following exposure to HMDA may include: shortness of breath, cough, wheezing, bronchial and tracheal irritation, and laryngitis. Inhalation of the vapors may progress to serious lung injury as a result of laryngospasm, bronchospasm, chemical pneumonitis and pulmonary edema.
    0.2.8) GASTROINTESTINAL
    A) Hexamethylenediamine may cause abdominal cramping and pain if ingested.
    0.2.9) HEPATIC
    A) Although information is limited, there have been reports of acute hepatitis following occupational exposure to HMDA. Variables, such as airborne concentration and exposure to other chemicals at the occupational site are unknown.
    0.2.10) GENITOURINARY
    A) Although information is limited, there have been reports of decreased kidney function following occupational exposure to HMDA. Variables, such as airborne concentration and exposure to other chemicals at the occupational site are unknown.
    0.2.13) HEMATOLOGIC
    A) Anemia, hypergammaglobulinemia, eosinophilia and increased transaminase activity have been reported, although information is limited.
    0.2.14) DERMATOLOGIC
    A) Skin irritation, including first and second-degree burns have been seen with acute exposure.
    0.2.20) REPRODUCTIVE
    A) Although human studies of teratogenicity and reproductive effects were not found, several animal studies have shown minimal reproductive effects. Mortality has been seen, but only at maternally toxic doses. Slight skeletal development retardation and slightly decreased litter size have been seen in rats and mice.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic effects of HMDA in humans.

Laboratory Monitoring

    A) Monitor CBC, urinalysis, and liver and kidney function tests in patients with significant exposure.
    1) Toxic serum or blood levels for HMDA have not been established.
    B) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Because of the possibility of gastrointestinal tract irritation, do NOT induce emesis.
    B) Effects of exposure (inhalation, ingestion, or skin contact) may be delayed.
    C) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    1) 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).
    a) 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.
    b) 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).
    D) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    E) 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.
    F) ENDOSCOPY: Early endoscopy allows patients without gastrointestinal injury to be medically cleared, and provides important prognostic information in patients who do have varying degrees of gastrointestinal burns. In addition, it facilitates the safe placement of enteral feeding tubes thereby shortening the period of time that patients with burns are without enteral nutritional support. Endoscopy should be performed within the first 24 hours post-ingestion, and should be avoided from 2 days to 2 weeks post-ingestion since wound tensile strength is lowest and the risk of perforation highest during this time. Endoscopy is indicated for all adults with deliberate ingestion or any signs or symptoms attributable to ingestion, and for children with stridor, vomiting, or drooling. Consider endoscopy in children with dysphagia, refusal to swallow, significant oral burns, or abdominal pain. If second or third degree burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    0.4.3) INHALATION EXPOSURE
    A) ACUTE LUNG INJURY
    1) Effects of exposure (inhalation, ingestion, or skin contact) may be delayed.
    B) 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.
    C) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    D) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    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) Effects of exposure (inhalation, ingestion, or skin contact) may be delayed.
    2) 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).
    3) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) Upper respiratory tract and eye irritation have been noted at concentrations greater than 100 mg/m(3). The minimum lethal human dose to this agent has not been delineated.

Clinical Effects

Summary Of Exposure

    A) 1,6-hexamethylenediamine (HMDA) is corrosive to the eyes, skin, and respiratory tract. Inhalation may cause coughing, labored breathing, and shortness of breath. Contact with liquid HMDA may be caustic to the skin and eyes causing redness and pain. First-degree burns may result from short-term exposure to the skin, and prolonged exposure may cause secondary burns. Symptoms of HMDA ingestion may include abdominal cramps and pain.
    B) Chronic or repeated exposure can cause anemia, kidney or liver damage. Other signs and symptoms of prolonged contact may include skin damage, allergic rhinitis, bronchial asthma, impairment of bronchial permeability, toxicoallergic hepatitis, gastritis, colitis, hypergammaglobulinemia, increased transaminase activity, and eosinophilia.
    C) Inhalation may be fatal as a result of spasm, inflammation and edema of the larynx and bronchi, chemical pneumonitis, and acute lung injury.

Heent

    3.4.1) SUMMARY
    A) Eye, nasal and throat irritation may occur following exposure to HMDA vapors.
    3.4.3) EYES
    A) CONJUNCTIVITIS
    1) Irritation of the eyes and upper respiratory tract have been found in workers exposed to HMDA vapors at concentrations greater than 100mg/m(3) (Grant & Schuman, 1993).
    2) Eye exposure to the solid form of HMDA is alkalotic and may be caustic and strongly irritating to the eyes (NIOSH ICSC, 1998; Grant & Schuman, 1993).
    3.4.5) NOSE
    A) Rats and mice exposed to HMDA by inhalation at varying concentrations 6 hours per day, 5 days a week for 90 days, showed signs of epithelial atrophy of the nose, degeneration of the olfactory nerves and ulcerations of the nasal mucosa at the higher concentrations (ACGIH, 2001).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory signs and symptoms following exposure to HMDA may include: shortness of breath, cough, wheezing, bronchial and tracheal irritation, and laryngitis. Inhalation of the vapors may progress to serious lung injury as a result of laryngospasm, bronchospasm, chemical pneumonitis and pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) TOXIC EFFECT OF GAS, FUMES AND/OR VAPORS
    1) Respiratory signs and symptoms following exposure to HMDA may include: shortness of breath, cough, wheezing, bronchial and tracheal irritation, and laryngitis. Inhalation of the vapors may progress to serious lung injury as a result of laryngospasm, bronchospasm, chemical pneumonitis and pulmonary edema (NTP , 2002).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) In a rat inhalation study where Sprague-Dawley rats were exposed to aerosol solutions of aqueous HMDA in concentrations of 0, 12.8, 51 or 215 mg/m(3)for six hours a day, five days a week for 13 weeks, results varied depending on the concentration of the dose (Johannsen et al, 1987).
    1) At the highest dose of 215 mg/m(3), 13 of 15 male and 10 of 15 female rats died. The rats showed signs of respiratory distress, debilitation, eye irritation and weight loss before death, although the cause of death was not determined. Rats in this group also showed increased red blood cell counts, hematocrits, hemoglobin, blood urea nitrogen concentrations and serum-glutamic-pyruvic-transaminase (SGPT) activity. On autopsy these rats showed tracheal and nasal passage inflammation, collapsed alveoli, interstitial fibrosis and squamous metaplasia (Johannsen et al, 1987).
    2) The rats exposed to 51 mg/m(3) concentration showed signs of respiratory irritation, decreased body weight and eye irritation, but no hematologic signs or histological changes (Johannsen et al, 1987).
    b) In another rat inhalation study, heated HMDA vapors at a concentration of 2100 ppm for two 6-hour exposures caused respiratory irritation, lethargic behavior, lung congestion and death in 2 of 8 rats. A lesser concentration of 210 ppm over fifteen 6-hour exposures showed no adverse effects (ACGIH, 2001).

Gastrointestinal

    3.8.1) SUMMARY
    A) Hexamethylenediamine may cause abdominal cramping and pain if ingested.
    3.8.2) CLINICAL EFFECTS
    A) ABDOMINAL PAIN
    1) Hexamethylenediamine may cause abdominal cramping and pain if ingested (ILO , 1998).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Rats and mice given HMDA in their drinking water for 14 days showed no toxic effects, other than the mice showing a slight decrease in body weight at the higher concentrations. This was attributed to the unpleasant taste of the HMDA in water and not to toxicity (ACGIH, 2001).
    b) A group of rats given dietary HMDA in varying doses resulted in a minimal retardation of weight gain at the higher doses. Necropsy and microscopic evaluation of 30 different tissues and organs revealed no other treatment related changes (Johannsen & Levinskas, 1987).

Hepatic

    3.9.1) SUMMARY
    A) Although information is limited, there have been reports of acute hepatitis following occupational exposure to HMDA. Variables, such as airborne concentration and exposure to other chemicals at the occupational site are unknown.
    3.9.2) CLINICAL EFFECTS
    A) TOXIC HEPATITIS
    1) Although information is limited, there have been reports of acute hepatitis following occupational exposure to HMDA. Variables, such as airborne concentration and exposure to other chemicals at the occupational site are unknown (Bingham et al, 2001).

Genitourinary

    3.10.1) SUMMARY
    A) Although information is limited, there have been reports of decreased kidney function following occupational exposure to HMDA. Variables, such as airborne concentration and exposure to other chemicals at the occupational site are unknown.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) Although information is limited, decreased kidney function has been reported following occupational exposure to HMDA. Variables, such as airborne concentration and exposure to other chemicals at the occupational site are unknown (ACGIH, 2001).

Hematologic

    3.13.1) SUMMARY
    A) Anemia, hypergammaglobulinemia, eosinophilia and increased transaminase activity have been reported, although information is limited.
    3.13.2) CLINICAL EFFECTS
    A) DISORDER OF HEMATOPOIETIC STRUCTURE
    1) Anemia, hypergammaglobulinemia, eosinophilia and increased transaminase activity have been reported, although information is limited (NTP , 2002).

Dermatologic

    3.14.1) SUMMARY
    A) Skin irritation, including first and second-degree burns have been seen with acute exposure.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Contact with HMDA liquid or solid is corrosive to the skin. Short term exposure may cause first-degree burns. Longer exposure may cause second-degree burns (CHRIS , 2002; NIOSH ICSC, 1998).
    B) ECZEMA
    1) CASE HISTORY - Four male workers at a nylon manufacturing plant developed an eczema-like dermatitis after exposure to hexamethylenediamine. They were employed at the plant from 2 to 27 months. The workers were treated and returned to their jobs, only to have the eczema reappear. Complete recovery did not occur until the workers were transferred to other jobs (Duverneuil & Buisson, 1952).

Reproductive

    3.20.1) SUMMARY
    A) Although human studies of teratogenicity and reproductive effects were not found, several animal studies have shown minimal reproductive effects. Mortality has been seen, but only at maternally toxic doses. Slight skeletal development retardation and slightly decreased litter size have been seen in rats and mice.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential teratogenic effects of exposure to HMDA in humans.
    B) ANIMAL STUDIES
    1) In a study of pregnant rats given dietary HMDA at doses of 112, 184, and 300 mg HMDA/kg body weight, minimal developmental effects were seen only at maternally toxic doses. One mortality was noted in a rat given the 300 mg dose. No maternal effects were seen at the 112 and 184 mg doses. No teratogenic effects were seen, but pups that received the 184 and 300 mg/kg doses showed slight skeletal development retardation (ACGIH, 2001).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to HMDA in human pregnancy or lactation.
    B) ANIMAL STUDIES
    1) ANIMAL STUDIES
    a) Pregnant female rats that received HMDA 200 mg/kg/day by gavage during the first 2 weeks of gestation were not found to have any fetal effects or changes in litter size (David & Heck, 1983) ACGIH, 2001).
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) Reproduction and fertility were not affected over two generations of rats that received dietary administration of HMDA in doses up to 150 mg/kg/day. Litter size was slightly decreased in a group that received 500 mg/kg/day, but there were no adverse effects on survival during lactation in this group or in any of the lower dose groups (Short et al, 1991).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS124-09-4 (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) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic effects of HMDA in humans.

Genotoxicity

    A) At the time of this review, no data are available to assess the mutagenic potential of this agent in humans. No mutagenic effects have been found in studies of salmonella typhimurium, mice or hamsters.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor CBC, urinalysis, and liver and kidney function tests in patients with significant exposure.
    1) Toxic serum or blood levels for HMDA have not been established.
    B) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    4.1.2) SERUM/BLOOD
    A) Monitor CBC, urinalysis, and liver and kidney function tests in patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) Workers who are occupationally exposed to HMDA should have an annual physical examination, including liver enzyme and hepatic function testing. Workers who have allergies and liver diseases should be excluded from handling HMDA (ITI, 1995).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor CBC, urinalysis, and liver and kidney function tests in patients with significant exposure.
    1) Toxic serum or blood levels for HMDA have not been established.
    B) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    1) 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).
    a) 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.
    b) 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).
    6.5.2) PREVENTION OF ABSORPTION
    A) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    B) 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.
    6.5.3) TREATMENT
    A) ENDOSCOPY OF STOMACH
    1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    2) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
    3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992; Nuutinen et al, 1994)
    4) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    5) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.

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.
    6.7.2) TREATMENT
    A) 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).
    B) BRONCHOSPASM
    1) BRONCHOSPASM SUMMARY
    a) Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.
    2) ALBUTEROL/ADULT DOSE
    a) 2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    3) ALBUTEROL/PEDIATRIC DOSE
    a) 0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    4) ALBUTEROL/CAUTIONS
    a) The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.
    5) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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) 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).
    B) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    6.9.2) TREATMENT
    A) SUPPORT
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) BURN OF SKIN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) Upper respiratory tract and eye irritation have been noted at concentrations greater than 100 mg/m(3). The minimum lethal human dose to this agent has not been delineated.

Minimum Lethal Exposure

    A) ADULT
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) ADULT
    1) Upper respiratory tract and eye irritation have been noted at concentrations greater than 100 mg/m(3) (Grant & Schuman, 1993).
    2) Workers handling HMDA in an atmosphere containing 2 to 5.5 mg/m(3) under normal operations and 131.5 mg/m(3) during autoclave operations developed conjunctival and upper respiratory tract irritation. One worker out of 20 studied developed acute hepatitis followed by dermatitis, and the effects were attributed to HMDA. No anemia was observed (Bingham et al, 2001).

Workplace Standards

    A) ACGIH TLV Values for CAS124-09-4 (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) 1,6-Hexanediamine
    a) TLV:
    1) TLV-TWA: 0.5 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): URT and skin irr
    d) Molecular Weight: 116.21
    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 CAS124-09-4 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS124-09-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: 1,6-Hexanediamine
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS124-09-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ACGIH, 1996a OHM/TADS, 2002 RTECS, 2002)
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 320 mg/kg
    2) LD50- (SUBCUTANEOUS)MOUSE:
    a) 1300 mg/kg
    3) LD50- (ORAL)RAT:
    a) 750 mg/kg
    b) 980 mg/kg (ACGIH, 1996a)
    4) TCLo- (INHALATION)RAT:
    a) 5 g/m(3) for 6H/2W- intermittant -- changes to lung, thorax, or respiration; hemorrhage; death
    b) 215 mg/m(3) for 6H/13W- intermittant -- structural/functional change in trachea or bronchi; weight loss/decreased weight gain, death
    c) 360 mcg/m(3) for 17W- intermittant -- cardiac and vascular changes

Physicochemical

Physical Characteristics

    A) HMDA is solid (anhydrous) at 15 degrees C and 1 atm. It will absorb water and carbon dioxide from air and is soluble in water, alcohol, benzene, and ether. It has a weak, fishy odor similar to piperdine and exists as colorless leaflets or platelets and as long needles from sublimation. It has also been described as a white crystalline solid with an ammonia-type odor. Closer examination of the solid indicates rhombic bipyrimidal plates. HMDA solution is a clear, colorless liquid (AAR, 2000; (ACGIH, 1996a; CHRIS , 2002; HSDB , 2002; Lewis, 2000).

Molecular Weight

    A) 116.21

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