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DECALIN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Decalin is a dicyclic paraffin.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C10-H18

Available Forms Sources

    A) FORMS
    1) While Decalin can occur as the cis- or trans- isomer, commercial preparations are generally either essentially pure trans- or a mixture of up to 60% cis- (Budavari, 1989).
    B) SOURCES
    1) Decalin is a component of crude oil (Clayton & Clayton, 1994). It also occurs in urban air, estuarine sediments, industial waste water, sewage sludge, wood stove emissions, motor vehicle exhaust, and leaches into drinking water from asphalt-lined pipes (HSDB , 1996).
    C) USES
    1) Decalin is used as a solvent, turpentine substitute, as an ingredient in fuels and lubricants, and as a fuel for stoves (Clayton & Clayton, 1994; Budavari, 1989).
    2) In pharmacological and toxicological research, decalin has been used as a vehicle for chronic skin painting studies in animals and in short-term genetic assays (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) Decalin is a skin, eye, and mucous membrane irritant. Systemic poisoning has not been reported in humans. Inhalation may cause CNS depression. Prolonged or repeated skin exposure may produce defatting dermatitis and eczema. Aspiration of the liquid into the lungs may cause potentially fatal chemical pneumonitis and noncardiogenic pulmonary edema. The urine may be blue or greenish-brown.
    B) Liver and kidney damage have been seen in experimental animals, but there is no evidence for these effects in humans. Decalin has caused kidney and endocrine tumors in experimental animals.
    0.2.4) HEENT
    A) Cataracts have been produced in experimental animals.
    B) Eye, nose, and throat irritation may be seen.
    0.2.6) RESPIRATORY
    A) Aspiration of the liquid into the lungs may present a risk for potentially fatal chemical pneumonitis or noncardiogenic pulmonary edema.
    0.2.7) NEUROLOGIC
    A) Numbness and headache can occur.
    0.2.8) GASTROINTESTINAL
    A) Vomiting can occur following ingestion.
    0.2.9) HEPATIC
    A) Liver pathology was seen in experimental animals.
    0.2.10) GENITOURINARY
    A) Blue and brownish-green urine have been reported in exposed humans.
    B) Kidney damage was induced in male rats.
    0.2.14) DERMATOLOGIC
    A) Defatting dermatitis with a subsequent increased risk for skin infections can occur.
    B) Eczema has been reported from prolonged skin contact.
    0.2.19) IMMUNOLOGIC
    A) Eczema has occurred with occupational exposure.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Laboratory Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) In general, gastric emptying is NOT INDICATED. Do NOT induce emesis.
    B) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    C) Activated charcoal adsorbs kerosene, turpentine, and benzene in vitro and in animal models. Activated charcoal may cause vomiting, which may increase the risk of aspiration. Activated charcoal may be indicated in patients who have coingested an adsorbable toxic substance.
    1) 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.
    D) IN SYMPTOMATIC PATIENTS - (coughing, choking, tachypnea, etc) monitor blood gases to assure adequate ventilation. Admit the patient for observation.
    1) Observe all patients for 6 hours. If vital signs become abnormal or symptoms develop admit patient to the hospital and obtain a chest x-ray. Patients who remain asymptomatic for 6 hours can usually be discharged.
    E) 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.
    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.
    B) Respiratory tract irritation, if severe, can progress to pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    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.
    E) CATECHOLAMINES -
    1) Inhalation of some volatile hydrocarbons has been associated in experimental animals with a lowering of the arrhythmogenic threshold for injected catecholamines, especially epinephrine.
    2) If a patient poisoned with this agent should require administration of catecholamines, EKG monitoring should be done and the drug initially administered at the lower recommended doses, with titration to the desired effect.
    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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    3) 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.

Range Of Toxicity

    A) The lowest effective dose for producing irritation in humans is 100 ppm. The maximum tolerated dose in humans is not known.

Clinical Effects

Summary Of Exposure

    A) Decalin is a skin, eye, and mucous membrane irritant. Systemic poisoning has not been reported in humans. Inhalation may cause CNS depression. Prolonged or repeated skin exposure may produce defatting dermatitis and eczema. Aspiration of the liquid into the lungs may cause potentially fatal chemical pneumonitis and noncardiogenic pulmonary edema. The urine may be blue or greenish-brown.
    B) Liver and kidney damage have been seen in experimental animals, but there is no evidence for these effects in humans. Decalin has caused kidney and endocrine tumors in experimental animals.

Heent

    3.4.1) SUMMARY
    A) Cataracts have been produced in experimental animals.
    B) Eye, nose, and throat irritation may be seen.
    3.4.3) EYES
    A) IRRITATION - Decalin is an eye irritant (Clayton & Clayton, 1994).
    B) CATARACTS - Decalin in unspecified amounts produced cataracts in guinea pigs when applied to the eye for 30 minutes per day for approximately 6 days. Cataracts did not occur in weanling rats given 2% decalin in the diet (Snyder, 1987).
    3.4.5) NOSE
    A) IRRITATION - Decalin is irritating to the mucous membranes (Clayton & Clayton, 1994).
    3.4.6) THROAT
    A) IRRITATION - Decalin is irritating to the mucous membranes (Clayton & Clayton, 1994).

Respiratory

    3.6.1) SUMMARY
    A) Aspiration of the liquid into the lungs may present a risk for potentially fatal chemical pneumonitis or noncardiogenic pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) Aspiration of the liquid into the lungs can cause pulmonary edema, pneumonitis, and hemorrhage (HSDB , 1996).

Neurologic

    3.7.1) SUMMARY
    A) Numbness and headache can occur.
    3.7.2) CLINICAL EFFECTS
    A) PARESTHESIA
    1) Decalin can cause numbness (CHRIS , 1996).
    B) HEADACHE
    1) Headache has been reported from exposure to decalin (CHRIS , 1996).

Gastrointestinal

    3.8.1) SUMMARY
    A) Vomiting can occur following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Gastrointestinal upsets can occur following ingestion (CHRIS , 1996).

Hepatic

    3.9.1) SUMMARY
    A) Liver pathology was seen in experimental animals.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Pathological changes including fatty hepatocellular cytoplasmic vacuolization were seen in the livers of mice exposed to 5 and 50 ppm by inhalation for 90 days (Snyder, 1987). Atrophy of the liver was seen in guinea pigs exposed by the oral, inhalation and cutaneous routes (HSDB , 1996). These effects have not been reported in exposed humans.

Genitourinary

    3.10.1) SUMMARY
    A) Blue and brownish-green urine have been reported in exposed humans.
    B) Kidney damage was induced in male rats.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL COLOR
    1) Exposure to decalin can turn the urine blue (CHRIS , 1996).
    2) Workers exposed to a mixture of decalin and tetralin reported brownish-green urine (HSDB , 1996).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Focal necrosis of tubular epithelial cells at the corticomedullary junction was seen in the kidneys of male rats exposed to 5 or 50 ppm for 90 days, at doses as low as 25 ppm for 35 days; hyaline droplet formation in the proximal tubular epithelial cells was usually present. Females did not show these effects (Snyder, 1987; Stone et al, 1987a).
    b) Hyaline droplets consisting of alpha-2u-globulin were also formed after only 2 days of oral dosing at 10 to 100 mg/kg per day; kidney effects were reversible within 1 week after cessation of treatment (Alden et al, 1984).
    c) Formation of hyaline droplets reached a maximum within 5 days after initiation of inhalation exposure at 125 ppm (Kanerva et al, 1987a).
    d) Higher doses caused tubular cellular necrosis and chronic glomerulonephrosis after 12 to 19 days of dosing (Alden et al, 1984).
    e) Decalin was slightly more potent than d-limonene in inducing kidney abnormalities in rats by the oral route (Kanerva et al, 1987).
    f) Four specific decalin-induced proteins were seen in the cortexes of male rats; they were not present in immature males or treated females (Kanerva et al, 1987b).
    g) Formation of hyaline droplets from exposure to decalin is similar to effects seen in male rats exposed to branched-chain linear paraffins (Phillips & Cockrell, 1984; Gaworski et al, 1985).
    h) Of rats, dogs, mice, and guinea pigs, only male rats developed hyaline droplets after exposure to decalin (Alden et al, 1984; Bruner, 1984; Gaworski et al, 1985).
    i) Because of the peculiarities of the kidney system in the male rat, these findings may have little or no relevance to humans (Stone et al, 1987).
    j) These effects have not been reported in exposed humans.

Dermatologic

    3.14.1) SUMMARY
    A) Defatting dermatitis with a subsequent increased risk for skin infections can occur.
    B) Eczema has been reported from prolonged skin contact.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Decalin is a skin irritant (Clayton & Clayton, 1994).
    B) DERMATITIS
    1) Decalin can cause a defatting dermatitis with cracking and subsequent increased risk for secondary infection (CHRIS , 1996).
    2) Painters exposed to decalin experienced dermatitis in the absence of systemic effects (Clayton & Clayton, 1994).
    C) ECZEMA
    1) A vesicular eczema accompanied by intensive pruritus occurred on areas of the skin in closest contact with exposure to decalin (Snyder, 1987).

Immunologic

    3.19.1) SUMMARY
    A) Eczema has occurred with occupational exposure.
    3.19.2) CLINICAL EFFECTS
    A) ECZEMA
    1) A vesicular eczema accompanied by intensive pruritus occurred on areas of the skin in closest contact with exposure to decalin (Snyder, 1987). It is not clear whether this eczema was due to immunological or purely defatting mechanisms.

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    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 this agent during pregnancy or lactation.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS91-17-8 (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
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Decalin was carcinogenic by RTECS criteria via the inhalation route in mice; 50 ppm given continuously for 90 days was associated with endocrine tumors (RTECS , 1996).
    2) Decalin was neoplastic by RTECS criteria via the inhalation route in rats; 5 ppm given continuously for 90 days was associated with endocrine tumors (RTECS , 1996).
    3) Decalin was not carcinogenic or a promoter in skin painting studies in mice (Horton et al, 1957; Bingham & Falk, 1969; Horton & Christian, 1974).
    a) It has been used as a "neutral" vehicle for other compounds in chronic skin painting studies (Horton et al, 1976).
    4) Male rats exposed to decalin by inhalation for 1 year developed renal cell tumors, while female rats and mice of both sexes did not (Bruner, 1984).
    5) Pituitary tumors were seen in mice and rats exposed to decalin for 90 days by inhalation; however, these were not dose-related (Gaworski et al, 1985).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) Urinalysis and kidney function tests are suggested in cases of significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Chest x-ray may be indicated if there is evidence of aspiration or pulmonary irritation.

Methods

    A) CHROMATOGRAPHY
    1) Decalin can be monitored in the air by trapping on glass fiber filters and polyurethane foam, followed by elution and quantitation by high-resolution gas or liquid chromatography (HSDB , 1996).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    6.3.5) DISPOSITION/DERMAL EXPOSURE
    6.3.5.5) OBSERVATION CRITERIA/DERMAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Gastric decontamination is NOT indicated in the majority of ingestions, since systemic toxicity is unlikely from ingestion of a pure hydrocarbon. Do NOT induce emesis in most cases. Ipecac-induced emesis is preferable to gastric lavage in an alert patient who requires gastric emptying. Lavage should be reserved for a patient who is lethargic or obtunded.
    B) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    C) ACTIVATED CHARCOAL/CATHARTIC
    1) Activated charcoal adsorbs kerosene, turpentine, and benzene in vitro and in animal models (Chin et al, 1969; Laass, 1974; Laass, 1980) Raush, 1935; (Decker et al, 1981). Its efficacy for other hydrocarbons is not documented. Activated charcoal may cause vomiting, which may be hazardous to patients who have ingested hydrocarbons.
    a) Activated charcoal may be indicated in patients who have coingested adsorbable toxic substances. Do not give cathartics if the patient already has diarrhea or increased bowel sounds.
    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) MONITORING OF PATIENT
    1) If the patient is symptomatic upon arrival at the medical facility, pulmonary aspiration has probably already occurred. Monitor arterial blood gases in cases of aspiration pneumonitis to ensure adequate ventilation.
    2) CHEST X-RAY - Admit and obtain chest x-ray in all symptomatic patients.
    a) Observe patients for 6 hours. If vital signs become abnormal or symptoms develop admit patient to the hospital and obtain a repeat chest x-ray. Patients who remain asymptomatic for 6 hours can usually be discharged.
    B) 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).
    C) CORTICOSTEROID
    1) Have not been shown to be of benefit in treating hydrocarbon pneumonitis.
    D) INJECTION
    1) PARENTERAL INJECTION - Close medical follow-up for potential pneumonitis or local reaction is imperative. Aggressive management of local abscess with incision, drainage and appropriate antibiotic usage is indicated.
    E) EXTRACORPOREAL MEMBRANE OXYGENATION
    1) Extracorporeal membrane oxygenation (ECMO) has been reported to be successful therapy in two cases of pediatric hydrocarbon aspiration involving mineral oil and mineral seal oil. These two children received standard therapy for hydrocarbon aspiration without success prior to the institution of extracorporeal membrane oxygenation (Jaeger et al, 1987).

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) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
    a) However, based on anecdotal experience, some clinicians do recommend early administration of corticosteroids (such as methylprednisolone 1 gram intravenously as a single dose) in an attempt to prevent the later development of pulmonary edema.
    1) Anecdotal experience with dimethyl sulfate inhalation showed possible benefit of methylprednisolone in the TREATMENT of noncardiogenic pulmonary edema (Ip et al, 1989).
    3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
    4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.
    B) 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).
    C) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    D) MONITORING OF PATIENT
    1) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    E) CONDUCTION DISORDER OF THE HEART
    1) CATECHOLAMINES - Inhalation of some volatile hydrocarbons has been associated in experimental animals with a lowering of the arrhythmogenic threshold for injected catecholamines, especially epinephrine.
    2) If a patient poisoned with this agent should require administration of catecholamines, ECG monitoring should be done and the drug initially administered at the lower recommended doses, with titration to the desired effect.
    F) 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) 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).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    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) SKIN ABSORPTION
    1) 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.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EFFICACY
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) DERMAL: A man who used decalin mixed with detergents to clean paving stones developed vesicular eczema in skin areas closest to contact with the cleaners. Small amounts of albumin and urobilin were seen in the urine, suggesting possible kidney involvement (Snyder, 1987).

Range Of Toxicity

Summary

    A) The lowest effective dose for producing irritation in humans is 100 ppm. The maximum tolerated dose in humans is not known.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) Rats inhaling saturated vapor died within 2 hours (Clayton & Clayton, 1994).
    2) Four of six rats died when exposed to 500 ppm for 4 hours (Clayton & Clayton, 1994; RTECS , 1996).
    a) Tremors and convulsions occurred prior to death; lung congestion was seen at postmortem examination (Snyder, 1987).
    3) When three guinea pigs were exposed to 319 ppm for 8 hours per day, one died on the first day, another on day 21, and the third on day 23 (Clayton & Clayton, 1994).
    a) Liver and kidney injury and lung congestion were noted in the guinea pigs at postmortem examination (Clayton & Clayton, 1994; RTECS , 1996).
    4) When applied to a 6 cm(2) area of skin of guinea pigs on two successive days, decalin caused deaths 10 days after exposure with a similar pattern of tissue injury as that seen with inhalation (Clayton & Clayton, 1994).
    5) The lowest published lethal concentration by inhalation in mice was 993 ppm for 4 hours (RTECS , 1996).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) No serious industrial poisonings from decalin have been documented (Snyder, 1987).
    2) The maximum tolerated human exposure to this agent has not been delineated.
    B) ANIMAL DATA
    1) No apparent toxicity was seen in rats exposed to 200 ppm for 6 hours each for 20 exposures (Snyder, 1987).
    2) No apparent effects on the liver, kidney, brain, spleen, or blood forming organs were seen in beagle dogs exposed to 5 or 50 ppm for 90 days (Gaworski & Leahy, 1979).

Workplace Standards

    A) ACGIH TLV Values for CAS91-17-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS91-17-8 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS91-17-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    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 CAS91-17-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Clayton & Clayton, 1994 RTECS, 1996 Snyder, 1987
    1) LD50- (ORAL)RAT:
    a) 4.17 grams/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Acute toxicity from decalin appears to follow a typical pattern seen with low-viscosity hydrocarbons. In general, its toxic effects are related to its lipophilic properties.
    B) Formation of hyaline droplets in the kidneys from decalin exposure is similar to effects seen in male rats exposed to branched-chain linear paraffins (Phillips & Cockrell, 1984; Gaworski et al, 1985; Stone et al, 1987a; Read et al, 1988).
    C) Formation of hyaline droplets depends on alpha sub(2u)-globulin: strains of rats which are genetically deficient in this protein do not respond to decalin, and female rats make hyaline droplets in response to decalin when injected with the globulin protein (Ridder et al, 1990).

Physicochemical

Physical Characteristics

    A) Decalin is a colorless liquid with a mild, aromatic odor similar to that of menthol or turpentine (Lewis, 1993; Budavari, 1989; CHRIS , 1996).
    B) Decalin occurs as cis- and trans-isomers (Lewis, 1993; Budavari, 1989).

Molecular Weight

    A) 138.24

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