ASPHYXIANTS, SIMPLE

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Classification | Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

Specific Substances

1) Acetylen (synonym)
2) Ethine (synonym)
3) Ethyne (synonym)
4) Narcylen (synonym)
5) CAS 74-86-2 (synonym)

1) Argon-40 (synonym)
2) CAS 7440-37-1 (synonym)

1) n-Butane (synonym)
2) Diethyl (synonym)
3) Methylethylmethane (synonym)
4) CAS 106-97-8 (synonym)

1) Carbonic Acid Gas (synonym)
2) Carbonic Anhydride (synonym)
3) Dry Ice (synonym)
4) CAS 124-38-9 (synonym)

1) Bimethyl (synonym)
2) Dimethyl (synonym)
3) Ethyl Hydride (synonym)
4) Methylmethane (synonym)
5) CAS 74-84-0 (synonym)

1) Acetene (synonym)
2) Bicarburretted Hydrogen (synonym)
3) Elayl (synonym)
4) Ethene (synonym)
5) Liquid Ethyene (synonym)
6) Olefiant Gas (synonym)
7) CAS 74-85-1 (synonym)

1) CAS 7440-59-7 (synonym)

1) CAS 1333-74-0 (synonym)

1) LPG (synonym)
2) L.P.G. (synonym)
3) LP Gas (synonym)
4) Bottle Gas

1) Fire Damp (synonym)
2) Marsh Gas (synonym)
3) Methyl Hydride (synonym)
4) CAS 74-82-8 (synonym)

1) CAS 7440-01-9 (synonym)

1) CAS 7727-37-9 (synonym)

1) Dimethylmethane (synonym)
2) Propyl Hydride (synonym)
3) CAS 74-98-6 (synonym)

1) Methylethene (synonym)
2) Methylethylene (synonym)
3) Propene (synonym)
4) 1-Propene (synonym)
5) CAS 115-07-1 (synonym)

1) NITROGEN OXIDE (CAS 10102-44-0) (synonym)
2) NOX (synonym)
3) NITROGEN PEROXIDE, LIQUID (CAS 10102-44-0) (synonym)
4) NITROGEN TETROXIDE (CAS 10102-44-0) (synonym)
5) PETROLEUM GAS, LIQUID (synonym)
6) PROPANE MIXTURES
7) SIMPLE ASPHYXIANTS
8) TRIMETHYLMETHANE (synonym)
9) NATURAL GAS, COMPRESSED (WITH HIGH
10) -----METHANE CONTENT)
11) ETHYLENE, REFRIGERATED LIQUID (CRYOGENIC
12) ----- LIQUID)
13) CARBON DIOXIDE, COMPRESSED
14) METHANE GAS (synonym)
15) ARGON, COMPRESSED
16) ANHYDRIDE CARBONIQUE
17) CARBON DIOXIDE (LIQUIFIED)
18) CARBON DIOXIDE, REFRIGERATED LIQUID
19) -----(CRYOGENIC LIQUID)
20) COMPRESSED PETROLEUM GAS
21) DINITROGEN TETROXIDE (CAS 10102-44-0) (synonym)
22) ETHANE, REFRIGERATED LIQUID (CRYOGENIC
23) ----- LIQUID)
24) HELIUM, CRYOGENIC LIQUID
25) HELIUM GAS (synonym)
26) HELIUM, LIQUID
27) HYDROGEN, COMPRESSED
28) HYDROGEN GAS (synonym)
29) HYDROGEN, REFRIGERATED LIQUID
30) ------(CRYOGENIC LIQUID)
31) LIQUIFIED NATURAL GAS (synonym)
32) LIQUIFIED HYDROCARBON GAS
33) LIQUEFIED GAS, FLAMMABLE, N.O.S. (synonym)

Available Forms Sources

1) All the agents included are colorless gases (Student, 1981). Argon, carbon dioxide, ethane, helium, hydrogen, methane, neon, and nitrogen are odorless (Student, 1981). Acetylene has a faint garlic odor (Student, 1981). Ethylene has a sweet odor and taste (Student, 1981). Butane, liquefied petroleum gas, propane, and propylene have a faint petroleum-like odor and may be stenched with mercaptans for transport and storage (Student, 1981).

1) Some volatile solvents currently being abused via inhalation route include glues, cleaning substances, nail polish remover, hair sprays, fire extinguishing agents, typewriter correction fluid, butane lighter fluid, deodorant propellants, and other aerosol contents (McBride & Busuttil, 1990).
2) Carbon dioxide may accumulate deep in a lake that lies in a volcanic crater. Release of carbon dioxide from rising colder, deep water can produce a deadly cloud of gas that has been postulated to explain the deaths associated with the Lake Nyos disaster of August 21, 1986 (Baxter et al, 1989; Freeth, 1992), Lake Monoun disaster of August 1984 (Sigurdsson et al, 1987), and Dieng Plateau, Indonesia disaster of February 20, 1979 (LeGuern et al, 1982).

a) Volcanic gases may contain water vapor, carbon dioxide, sulfur dioxide, hydrogen sulfide, hydrogen chloride, hydrogen fluoride, and carbon monoxide (Thorarinsson, 1979).
b) Lack of lung and skin findings ruled out involvement of acidic volcanic gases. Plants and animals in the area did not suggest exposure to acidic volcanic gases.

3) Elevated carbon dioxide levels were reported in a home that had been built on a reclaimed surface coal mine with an abandoned deep coal mine beneath the property. Carbon dioxide levels in the home ranged from 1% on the upper floors to 12% in a basement floor drain (normal air is 0.035% CO2). Oxygen levels in the basement crawlspace were 14% (CDC, 2004).
4) HELIUM - is readily available from party and welding suppliers. It has been used in conjunction with a tight fitting homemade mask as a suicide agent (Gallagher et al, 2003).
5) CARBON DIOXIDE - Carbon-dioxide asphyxiation following the evaporation of special-effect dry ice has been reported (Hsieh et al, 2005).

1) ACETYLENE is used in welding, metal cutting, and as a raw material for carbon black and vinyl compounds such as vinyl chloride, vinylidene chloride, neoprene, acrylonitrile, acrylic acid, perchlene, trichlene, and tetrahydrofuran (ITI, 1985).
2) ARGON is an inert, colorless gas used in neon signs (Sax, 1984). Argon lasers are an alternative light source that can be used for photopolymerization of resin-based dental materials and for teeth bleaching (Cassoni & Rodrigues, 2007), and argon plasma coagulation (APC) therapy may be used for treatment of certain tumors (Ogata et al, 2007).
3) BUTANE is used as a raw material for automobile fuels, in organic synthesis, and as a solvent, refrigerant, and aerosol (ITI, 1985).
4) CARBON DIOXIDE is used in the synthesis of urea, for dry ice, and in soft drinks, fire extinguishers, and organic synthesis (ITI, 1985).
5) ETHANE is used in organic synthesis, and as a fuel and a freezing agent (ITI, 1985).
6) ETHYLENE is used in the manufacture of polyethylene, acetaldehyde, ethyl chloride (which is further processed into anesthetics, cooling mediums, solvents, and tetraethyl lead), ethylenechlorohydrin, and ethylene oxide, and is used to mature fruits (ITI, 1985).
7) HELIUM is used as an inactive gaseous atmosphere in soldering, in gelmanium and silicon crystal growth operations, as a filler for balloons, as a heating medium, for gas leakage checking operations, and in neon signs (ITI, 1985).

a) Right-to-die groups have proposed suicide by asphyxiation using helium pumped into a plastic bag placed over the head as a means of hastening death. Seven cases have been reported using this method (Gilson et al, 2003).

8) HYDROGEN is used in oil hardening, metallurgy, plumbing materials, vacuum tubes, electric bulbs, glass fusion, atmospheric phenomena observation, oxygen-hydrogen welding procedures, platinum and quartz machining, as a cooling or reducing agent, and in the synthesis of ammonia, methanol, and hydrochloric acid (ITI, 1985).
9) LIQUIFIED PETROLEUM GAS is used as a domestic, industrial, and automotive fuel (ITI, 1985).
10) METHANE is used as a fuel and as a raw material for hydrogen, hydrogen cyanide, ammonia, acetylene, and formaldehyde production (ITI, 1985).
11) NEON is an inert, colorless gas used in neon signs (Sax, 1984).
12) NITROGEN is a colorless, odorless gas, sometimes combined with oxides of nitrogen which may appear brownish and produce respiratory irritation. It is used in the manufacture of ammonia, to provide a non-oxidizing atmosphere to some manufacturing processes and is found as "black damp", a nitrogen-dioxide mixture in some coal mines.
13) PROPANE is used as a raw material in organic synthesis, as a component of industrial and domestic fuels, as an extractant, a solvent, a refrigerant, and in the manufacture of ethylene (ITI, 1985).
14) PROPYLENE is a raw material in polypropylene, isopropyl alcohol, isopropylbenzene, acetone, and propylene oxide manufacturing (ITI, 1985).

Overview

Life Support

Clinical Effects

0.2.1)

A) USES: There is no medical use. Simple asphyxiants include, among many others, carbon dioxide (CO2), helium (He), and gaseous hydrocarbons (ie, methane (CH4), ethane (C2H6), propane (C3H8), and butane (C4H10)).
B) TOXICOLOGY: In contrast to cellular asphyxiants (ie, cyanide (CN) or carbon monoxide (CO)), simple asphyxiants act mainly by displacing oxygen from the atmosphere, leading to decreased alveolar partial oxygen pressure and, consequently, hypoxemia. CNS dysfunction and anaerobic metabolism are the hallmark of serious toxicity. Symptoms and signs of toxicity depend on duration of asphyxiant concentration in the ambient air, exposure duration, respiratory effort, and individual vulnerability (eg, older age, cardiovascular disease). Initial euphoria due to hypoxemia may impair the patient's ability to escape from the toxic environment.
C) EPIDEMIOLOGY: Exposure to asphyxiants mainly occurs in industrial settings, occasionally in outbreaks from a natural or industrial disaster. Gaseous hydrocarbons are occasionally abused for euphoric effects.
D) WITH POISONING/EXPOSURE

1) MILD TO MODERATE POISONING: Decreased night vision, headache, nausea, compensatory increase of respiration and pulse. Oxygen saturation may be below 90%, even in asymptomatic or mildly symptomatic patients.
2) SEVERE POISONING: Decreased alertness, somnolence, dizziness, fatigue, euphoria, memory loss, decreased visual acuity, cyanosis, loss of consciousness, dysrhythmias, myocardial ischemia, pulmonary edema, seizures, and death. Oxygen saturation may be 80% or lower.

0.2.3)

A) WITH POISONING/EXPOSURE

1) Hyperventilation and tachycardia may be noted following exposure to simple asphyxiants.

0.2.20)

A) Sequelae of oxygen deprivation in the unborn are controversial. Cerebral palsy, previously thought to be due to acute hypoxia during labor and/or childbirth, remains poorly understood.

0.2.21)

A) Although the numbers are too small to draw definite conclusions, an excess of deaths from cancer was noted at an acetylene production plant. Lung, stomach, and pancreatic cancer were the most common.
B) It has been postulated that ethene exposures, especially in urban areas, may be expected to lead to a lifetime cancer risk in humans. It was estimated that approximately 70 cancer deaths per 100,000 may occur.

Laboratory Monitoring

Treatment Overview

0.4.3)

A) MANAGEMENT OF MILD TO MODERATE TOXICITY

1) Primarily supportive care. Supplemental oxygen is the mainstay of treatment, and most patients recover rapidly once exposure ceases and oxygen is administered.

B) MANAGEMENT OF SEVERE TOXICITY

1) Supportive treatment. Administer supplemental oxygen. In cases of severe CNS depression, consider orotracheal intubation. Anxiety and euphoria are signs of hypoxemia. Avoid benzodiazepines or other respiratory depressant agents. Patients who do not recover rapidly have likely sustained hypoxic end organ damage, which may be irreversible. Cerebral edema with increased intracranial pressure (ICP) may be managed by ventilation and the administration of mannitol; persistent elevation of ICP may require mechanical decompression (eg, decompressive craniectomy).

C) DECONTAMINATION

1) PREHOSPITAL: Remove the patient from the hypoxic environment as quickly as possible and administer supplemental oxygen.

D) AIRWAY MANAGEMENT

1) Early orotracheal intubation in patients with signs of severe poisoning (ie, severe CNS depression, insufficient respiratory effort, seizures).

E) ANTIDOTE

1) Oxygen is the antidote for asphyxiant poisoning. Administer high flow oxygen to all symptomatic patients.

F) PATIENT DISPOSITION

1) HOME CRITERIA: Patients with minimal symptoms after inadvertent exposure can be managed at home with termination of exposure.
2) OBSERVATION CRITERIA: Symptomatic patients and those with deliberate exposures should be referred to a healthcare facility.
3) ADMISSION CRITERIA: Patients with CNS depression, seizures, or other signs of severe hypoxemia should be admitted to the hospital.
4) CONSULT CRITERIA: Consult a poison control center or a medical toxicologist for assistance in managing patients with severe toxicity (ie, CNS depression, seizures) or in whom the diagnosis is not clear.

G) PITFALLS

1) Failure to recognize concurrent toxicity (ie, carbon monoxide or pulmonary irritants), resulting in morbidity from untreated poisoning. Frostbite may occur due to rapid evaporation of some of these agents.

H) DIFFERENTIAL DIAGNOSIS

1) Differential diagnosis is wide given the non-specific symptoms and signs in asphyxiant exposure. The hallmark of severe asphyxiant poisoning is CNS dysfunction in conjunction with hypoxemia and low oxygen saturation. History of exposure is the key to diagnosis.
2) Consider carbon monoxide poisoning, methemoglobinemia, poisoning with other CNS depressants, drugs associated with seizures or other CNS affections. Consider cellular asphyxiants (oxygen saturation will be high in patients with cyanide poisoning).

0.4.4)

A) Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes.

0.4.5)

A) OVERVIEW

1) Rewarming and a variety of topical treatments are indicated for frostbite injury. SEE MAIN SECTION FOR MORE INFORMATION.

Range Of Toxicity

Clinical Effects

Summary Of Exposure

Vital Signs

3.3.1)

A) WITH POISONING/EXPOSURE

1) Hyperventilation and tachycardia may be noted following exposure to simple asphyxiants.

3.3.2)

A) WITH POISONING/EXPOSURE

1) HYPERVENTILATION: Air hunger and hyperventilation may be noted, especially in the later stages of hypoxia (Langford, 2005; Kizer, 1984; AFP 161-18, 1968).

3.3.5)

A) WITH POISONING/EXPOSURE

1) TACHYCARDIA: An increased pulse rate may be seen (Wong et al, 2012; Leikin et al, 2009; Langford, 2005; AMPC, 1984).

Heent

3.4.3)

A) WITH POISONING/EXPOSURE

1) DECREASED VISION

a) Decreases in night vision, visual acuity, and visual fields (tunnel vision) may occur (AMPC, 1984). These effects can be factors in impaired ability to escape from the toxic environment.
b) Transient blurring of vision has been noted with direct spraying of butane on the eye (Grant, 1986).
c) Serious adverse ocular effects were not noted in one reported case of dry ice (carbon dioxide) direct eye contact (Grant, 1986).
d) Mydriasis, proptosis, yellow vision, transient blindness, and CNS and retinal cell damage have occurred from hypoxia following severe or prolonged asphyxia (Grant, 1986).

2) INCREASED INTRAOCULAR PRESSURE: Slight and brief elevations of intraocular pressure may be seen in human eyes with inhalation of 10% carbon dioxide (Grant, 1986).

3.4.6)

A) WITH POISONING/EXPOSURE

1) Frothy mucous may be seen in the throat or upper airways of persons inhaling various volatile solvents (McBride & Busuttil, 1990).

Cardiovascular

3.5.2)

A) TACHYARRHYTHMIA

1) WITH POISONING/EXPOSURE

a) An increased pulse rate may develop (Wong et al, 2012; Leikin et al, 2009; CDC, 2004; AMPC, 1984).

B) CONDUCTION DISORDER OF THE HEART

1) WITH POISONING/EXPOSURE

a) In cases of severe or prolonged hypoxia, cardiac manifestations can include atrial and ventricular dysrhythmias, hypotension, myocardial ischemia, and eventual asystole (El-Menyar et al, 2005; Safar & Caroline, 1978).
b) Repeated ventricular tachycardia and seizures were reported following accidental inhalation of an aerosol deodorant propellant containing isobutane, n-butane, and propane (Wason et al, 1986).
c) CASE REPORT: A 14-year-old boy who habitually inhaled butane, developed severe chest pain and collapsed 15 minutes after sniffing 7 canisters of butane. He was pulseless and apneic with ventricular fibrillation. Following resuscitation, marked anterolateral ST elevation was observed, along with sinus tachycardia. Despite aggressive care, the patient died 4 days later following multiple organ failure and the development of asystole (El-Menyar et al, 2005).
d) CASE REPORT: A 15-year-old boy who inhaled butane once a week experienced severe chest pain and collapsed after one episode. He was found pulseless and apneic, with ventricular fibrillation. After resuscitation, an EKG showed sinus tachycardia with left-bundle-branch block. Signs of myocardial ischemia (high serial enzymes, ST segment elevation) were present and he had evidence of cerebral edema (Gunn et al, 1989).
e) CASE REPORT: A 25-year-old woman developed cardiac arrest after unintentionally spraying air freshener into her nostrils while at a supermarket. Her husband began to immediately perform cardiopulmonary resuscitation and she was brought to an emergency department. An initial ECG showed ventricular fibrillation which was successfully electrically cardioverted. Four hours following resuscitation, cardiac monitoring indicated frequent ventricular ectopy, which was treated with an esmolol infusion. With continued supportive care, the patient recovered and was discharged on hospital day 5 without sequelae. Toxicological analysis of the air freshener revealed that it contained isobutane (Senthilkumaran et al, 2012).
f) Bradycardia progressing to asystole may occur in the absence of signs of cyanosis following inhalation exposure to 99.97% carbon dioxide. The authors suggest hypercapnia and acidosis may contribute to the cause of cardiac arrest (Jawan & Lee, 1990).
g) CARBON DIOXIDE: In an industrial incident, a container of liquid carbon dioxide was unintentionally opened in an enclosed working environment. Symptoms included chest pain, dyspnea, cough, and dizziness. ECGs in 15 patients revealed atrial fibrillation in 2 patients, ST-segment changes in 2 patients, and non-Q wave myocardial infarction in 1 patient (Halpern et al, 2004).

C) DEAD - SUDDEN DEATH

1) WITH POISONING/EXPOSURE

a) "Sudden sniffing death", or cardiac arrest, has been reported following the intentional inhalation of hydrocarbons and is associated with high mortality and morbidity (LoVecchio, 1998).
b) CASE REPORTS: Two cases of sudden death associated with inhalation of butane and propane by previously healthy 11-year-old and 15-year-old boys have been described. Postmortem examination found no evidence of anatomical cause or organic disease. Butane in the 11-year-old and propane in the 15-year-old were confirmed by toxicologic analysis (Siegel & Wason, 1990).
c) CASE REPORT: A 15-year-old boy was found unresponsive after inhalation of antiperspirant deodorant containing n-butane. He was pronounced dead 75 minutes later. Autopsy findings included cerebral edema, pulmonary edema, and congestion of the organs. The cause of death was presumed to be n-butane-induced fatal cardiac arrhythmia (Ago et al, 2002).
d) CASE REPORT: A 17-year-old boy lost consciousness and suffered a cardiac arrest after repeatedly inhaling gaseous spray from a lighter refill can containing butane. Defibrillation attempts were unsuccessful and he was pronounced dead after 60 minutes. Autopsy findings included tiny hemorrhagic ruptures of the myocardial fibers (Hirt et al, 2004).
e) CASE REPORT: A 16-year-old boy suffered cardiac arrest ("sudden sniffing death") following the intentional inhalation of Glade(R) aerosolized air freshener (butane, isobutane). Thirteen minutes after cardioversion, lidocaine, and epinephrine treatment, a return to sinus rhythm occurred. Anteroseptal myocardial infarction complicated his hospital course. The patient was discharged 16 days after admission (LoVecchio, 1998).

D) MYOCARDIAL INFARCTION

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 14-year-old boy who habitually inhaled butane, developed severe chest pain and collapsed 15 minutes after sniffing 7 canisters of butane. He was pulseless and apneic with ventricular fibrillation. Following resuscitation, marked anterolateral ST elevation and sinus tachycardia were observed. Evidence of an extensive anterior myocardial infarction was noted by an abnormal echocardiogram (LV ejection fraction of 25%; decreased LV contractility) and cardiac catheterization (dyskinetic apex, akinetic anterior and lateral walls, normal coronary arteries), along with elevated cardiac enzymes. Despite aggressive care, the patient died 4 days later following multiple organ failure and the development of asystole (El-Menyar et al, 2005).
b) CASE REPORT: A 15-year-old sustained an anterolateral myocardial infarction secondary to deliberate inhalational abuse of butane. His cardiac status improved during his hospitalization, but he remains with obvious decorticate posturing, cognitive memory personality problems, and derangement of central thermal regulating mechanism (Bauman et al, 1991).

E) SHOCK

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Coma, shock, rhabdomyolysis, metabolic acidosis, hyperkalemia, and suspected pneumonitis were reported in a 21-year-old woman following exposure to liquefied petroleum gas (Sampson et al, 2015).

3.5.3)

A) ANIMAL STUDIES

1) DYSRHYTHMIA

a) Epinephrine-induced cardiac dysrhythmias have been intensified by propane in dog and mice studies, but not in monkeys (Wheeler et al, 1992).

2) ECG ABNORMAL

a) ECG complexes, observed in a canine model of carbon dioxide poisoning, resembled severe hypokalemia. Specifically, inverted T wave, depressed ST segment, and the prominent U wave were noted (Ikeda et al, 1989). The ST segment and T wave changes are not uncommon in the presence of acidosis.

Respiratory

3.6.2)

A) HYPERVENTILATION

1) WITH POISONING/EXPOSURE

a) A feeling of breathlessness, and rapid respirations may develop (Wong et al, 2012; CDC, 2004; AMPC, 1984).

1) Serum pH falls as carbon dioxide is dissolved in plasma stimulating chemoreceptors in the brain and carotid bodies to increase alveolar ventilation. Hyperventilation increases with exposure to increasing concentrations of carbon dioxide and may lead to dyspnea (Langford, 2005).

b) CASE REPORT: A 70-year-old man with a history of obstructive sleep apnea was found unresponsive, but regained consciousness following administration of 100% oxygen. Prior to losing consciousness, the patient reported experiencing light-headedness, a bitemporal throbbing headache, and hyperventilation. On presentation to the emergency department, the patient was drowsy, and hypotensive (93/55 mmHg). With supportive care, he recovered and was discharged 2 days later. Questioning of the patient revealed that he had been traveling in his vehicle with the windows rolled up while transporting 500 pounds of odorless dry ice. It is suspected that the patient's history of obstructive sleep apnea contributed to the development of carbon dioxide-induced asphyxia (Leikin et al, 2009).

B) CYANOSIS

1) WITH POISONING/EXPOSURE

a) Cyanosis may be noted (AMPC, 1984).

C) APNEA

1) WITH POISONING/EXPOSURE

a) Apnea may result if the exposure is not terminated (Proctor & Hughes, 1978).

D) ACUTE LUNG INJURY

1) WITH POISONING/EXPOSURE

a) Pulmonary edema was reported in a case of asphyxia caused by dry ice (Takaoka et al, 1988). Deodorant sprays, butane inhalation, and inhalation of other propellants has resulted in pulmonary edema and lung congestion (McBride & Busuttil, 1990; Ago et al, 2002; Hirt et al, 2004; Ago et al, 2002).
b) In an industrial incident, a container of liquid carbon dioxide was unintentionally opened in an enclosed working environment. Symptoms included chest pain, dyspnea, cough, and dizziness. Chest x-rays in 2 of 22 patients revealed pulmonary edema (Halpern et al, 2004).
c) CASE REPORT: A 35-year-old man was found dead with a hose in his mouth, sealed with packing tape, and connected to a gas wall outlet. An autopsy, performed 48 hours later, revealed pulmonary edema and congestion, as well as cerebral edema, and pleural and epicardial petechiae. Toxicologic analysis of his tissues indicated the presence of methane (eg, brain 14 mcL/g, heart 17 mcL/g, lung 56 mcgL/g), suggesting a cause of death of asphyxia due to oxygen displacement secondary to methane gas inhalation (Rossi et al, 2013).

E) PNEUMONITIS

1) WITH POISONING/EXPOSURE

a) Two cases have been reported where butane-isobutane lighter fluid has been sprayed into the mouth, then ignited when exhaled (Cartwright et al, 1983; Marsh, 1984).

1) Progressive bilateral pulmonary infiltrates developed and resolved in 4 to 5 days after treatment with oxygen and antibiotics.

b) In an industrial incident, a container of liquid carbon dioxide was unintentionally opened in an enclosed working environment. Symptoms included chest pain, dyspnea, cough, and dizziness. Chest x-rays in 6 of 22 patients revealed diffuse or patchy alveolar patterns consistent with pneumonitis (Halpern et al, 2004).
c) CASE REPORT: A 44-year-old welder became dizzy and weak with progressive dyspnea after exposure to acetylene during aluminum welding. Twenty-two hours post-exposure, he presented to the emergency department with severe dyspnea. Physical examination revealed shallow breathing with inspiratory bilateral basal crackles on auscultation. Arterial blood gas analysis indicated respiratory insufficiency (pH 7.4, pCO2 4.8 kPa, pO2 6.7 kPa, HCO3 21.8 mmol/L), a chest x-ray demonstrated interstitial infiltration and pulmonary function and gas diffusion tests revealed impaired diffusion capacity and severe restriction (FVC 2.75 [57% predicted capacity], FEV 2.04 [54% predicted volume], CO2 diffusing capacity 4.7 [47% predicted capacity]), indicative of interstitial pneumonitis. With supportive treatment, including corticosteroids, beta-agonists, and oxygen therapy, the patient gradually recovered and was discharged 9 days post-exposure (Brvar, 2014).
d) CASE REPORT: Coma, shock, rhabdomyolysis, metabolic acidosis, hyperkalemia, and suspected pneumonitis were reported in a 21-year-old woman following exposure to liquefied petroleum gas (Sampson et al, 2015).

F) SUDDEN INFANT DEATH SYNDROME

1) WITH POISONING/EXPOSURE

a) Excess levels of carbon dioxide, ammonia, and other asphyxiant gases have been theorized to accumulate at the face of a sleeping infant. If the infant is unable to change its position or breathing pattern, SIDS may result from asphyxiation (Corbyn, 1993; Malcolm et al, 1994). Asphyxia may be due to an excess of carbon dioxide and abnormal reflex actions connected with breathing and swallowing.

3.6.3)

A) ANIMAL STUDIES

1) BRONCHOSPASM

a) Bronchoconstriction and respiratory depression have been reported in animal studies with propane (Wheeler et al, 1992).

Neurologic

3.7.2)

A) CENTRAL NERVOUS SYSTEM FINDING

1) WITH POISONING/EXPOSURE

a) Various disturbances of normal neurologic functioning including dizziness, headache, blurry vision, belligerence, euphoria, numbness and tingling of the extremities, sleepiness, mental confusion, memory loss, speech impairment, and decreased coordination, concentration, and judgement may occur (Langford, 2005; Harris & Mirza, 2005; CDC, 2004; AMPC, 1984; AFP 161-18, 1968).

B) ANOXIC ENCEPHALOPATHY

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 13-year-old, markedly obese adolescent with habitual butane use was found unconscious and developed agitation and confusion after reportedly inhaling 2 cans of a propellant deodorant that contained butane and hydrofluorocarbon 152A. The patient became alert with episodes of drowsiness 24 hours after exposure. Over the next 3 days, periods of disorientation, along with ataxia and slurred speech occurred. On day 4, EEG showed abnormal delta and theta waveforms consistent with drug-induced encephalopathy; MRI was normal. Despite prolonged symptoms, the patient recovered without sequelae (Harris & Mirza, 2005).
b) Twenty-four hours after asphyxiant-induced cardiac arrest with cardioversion recovery, an EEG revealed organic or metabolic encephalopathy (diffuse slow delta activity). At a 6-month follow-up, the patient had returned to his baseline mental capacity (LoVecchio, 1998).
c) CASE REPORT: A 16-year-old boy developed confusion, lethargy, and visual hallucinations approximately 1 day after inhaling a 300-mL can of butane lighter fluid. On examination, he exhibited akinetic mutism with abulia. He also appeared to have mild ataxia in his upper extremities bilaterally. An EEG performed 2 days after admission showed diffuse background slowing with intermittent bilateral frontal delta waves and an abnormal arousal response pattern. An MRI revealed abnormal hyperintensity in both thalami, as well as in the right cerebellum and the subinsular tissues, all of which are indicative of an encephalopathy due to toxic or metabolic causes. Three months after admission, the patient continued to exhibit severe mutism and apathy (Kile et al, 2006).

C) COMA

1) WITH POISONING/EXPOSURE

a) Prolonged hypoxemia may result in loss of consciousness (Kizer, 1984; Weiss & Lakshminarayan, 1994). Incapacitation with loss of ability for self-rescue may occur before complete unconsciousness (AFP 161-18, 1968).
b) CASE REPORT: A 70-year-old man with a history of obstructive sleep apnea was found unresponsive, but regained consciousness following administration of 100% oxygen. Prior to losing consciousness, the patient reported experiencing light-headedness, a bitemporal throbbing headache, and hyperventilation. On presentation to the emergency department, the patient was drowsy and hypotensive (93/55 mmHg). With supportive care, he recovered and was discharged 2 days later. Questioning of the patient revealed that he had been traveling in his vehicle with the windows rolled up while transporting 500 pounds of odorless, dry ice. It is suspected that the patient's history of obstructive sleep apnea contributed to the development of carbon dioxide-induced asphyxia (Leikin et al, 2009).
c) CASE REPORT: Coma, shock, rhabdomyolysis, metabolic acidosis, hyperkalemia, and suspected pneumonitis were reported in a 21-year-old woman following exposure to liquefied petroleum gas (Sampson et al, 2015).

D) NEUROPATHY

1) WITH POISONING/EXPOSURE

a) Prolonged asphyxia may result in CNS injury (Proctor & Hughes, 1978).
b) Neurological deficit may occur following rupture of an intraaortic balloon catheter secondary to arterial gas (helium) embolization (Frederiksen et al, 1988).

E) SEIZURE

1) WITH POISONING/EXPOSURE

a) Seizures may be seen during serious cases of asphyxia (Takaoka et al, 1988).
b) Seizures and rhabdomyolysis (CPK greater than 18,000 International Units/L) following intentional inhalation of butane and isobutane have been reported (LoVecchio, 1998).

F) HEMIPLEGIA

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Hemiparesis has been reported following acute volatile substance abuse in a 15-year-old adolescent who inhaled butane gas and a 12-year-old boy who inhaled glue (Gray & Lazarus, 1993).

G) CEREBRAL EDEMA

1) WITH POISONING/EXPOSURE

a) Acute cerebral edema with brainstem herniation has been found on autopsy in several cases involving inhalation of deodorant spray and butane (McBride & Busuttil, 1990).
b) CASE REPORT: An 18-year-old man became comatose and developed cardiac arrest, that was successfully resuscitated, after inhaling butane from an aerosol container for cigarette lighter fluid. At hospital admission, the patient's intracranial pressure (ICP) was measured as 14 mmHg. An MRI showed high signal changes symmetrically in both putamen with less predominant changes in the occipital and frontal lobes. Two days later, a repeat ICP measurement indicated that his ICP increased to greater than 20 mmHg, and was refractory to mannitol treatment, necessitating bilateral decompressive craniectomy. A post-operative CT revealed bilateral decompression, and repeat ICP monitoring demonstrated values that were consistently below 20 mmHg. However, the patient's hemodynamic status deteriorated and he died approximately 5 days post-admission due to multi-organ failure and cardiogenic shock (Peyravi et al, 2012).
c) CASE REPORT: A 35-year-old man was found dead with a hose in his mouth, sealed with packing tape, and connected to a gas wall outlet. An autopsy, performed 48 hours later, revealed pulmonary edema and congestion, as well as cerebral edema, and pleural and epicardial petechiae. Toxicologic analysis of his tissues indicated the presence of methane (eg, brain 14 mcL/g, heart 17 mcL/g, lung 56 mcgL/g), suggesting a cause of death of asphyxia due to oxygen displacement secondary to methane gas inhalation (Rossi et al, 2013).

Gastrointestinal

3.8.2)

A) NAUSEA AND VOMITING

1) WITH POISONING/EXPOSURE

a) Nausea, vomiting, and prostration may occur, but usually resolve within 24 to 48 hours following termination of exposure (AFP 161-18, 1968).
b) Two cases have been reported where butane-isobutane lighter fluid has been sprayed into the mouth, then ignited when exhaled (Cartwright et al, 1983; Marsh, 1984).

1) Coffee grounds emesis, abdominal pain, gastritis, and hemorrhagic esophagitis were present.
2) Gastrointestinal symptoms resolved spontaneously within 10 days after treatment with antacids.

Acid-Base

3.11.2)

A) ACIDOSIS

1) WITH POISONING/EXPOSURE

a) An elevated pCO2 may develop from carbon dioxide retention (Saltzman, 1986; Clayton & Clayton, 1982).
b) A combined respiratory and metabolic acidosis was seen in a serious exposure to dry ice (Takaoka et al, 1988).
c) Commercial acetylene may be in solution with acetone. The amount of acetone released increases as acetylene decreases in the tanks. Therefore, inhaled industrial acetylene may mimic ketoacidosis (acidosis, hyperglycemia, and ketonuria) (Foley, 1985).
d) CASE REPORT: Coma, shock, rhabdomyolysis, metabolic acidosis, hyperkalemia, and suspected pneumonitis were reported in a 21-year-old woman following exposure to liquefied petroleum gas (Sampson et al, 2015).

Dermatologic

3.14.2)

A) FROSTBITE

1) WITH POISONING/EXPOSURE

a) Several of the agents included are gases stored in compressed or liquid forms (ITI, 1985; Sax, 1984). Dermal exposure to these agents can cause frostbite injury (Corn et al, 1991; James & Moss, 1989; Elliott, 1991; ITI, 1985).
b) Gangrene due to cold injury may be a complication following exposure to these agents (Leu & Clodius, 1989).
c) CASE REPORT: A 44-year-old oil refinery worker received second-degree frostbite injury after being sprayed with liquid propylene through his insulated work-suit. Physical examination revealed discoloration with blistering on both thighs medially. The patient also developed shortness of breath, tachycardia, hypertension, and tachypnea. With supportive care, the patient's vital signs normalized and, after further observation and evaluation at a burn center, the patient was discharged (Wong et al, 2012).
d) CASE REPORT: A 50-year-old man developed superficial frostbite of his right hand following exposure to carbon dioxide leaking from a damaged fire extinguisher. Initially, the patient's fingers were pale, cold, and numb; however, the pain became throbbing, with significant erythema and edema of his second, third, and fourth fingers, and subsequent development of clear superficial blisters. With supportive therapy, the patient recovered without sequelae (Arbab & Mirfazaelian, 2014).

B) CHEMICAL BURN

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 13-year-old girl acutely exposed to propane gas became unconscious with gas continuing to spray on her left shoulder for several minutes. Upon initial examination, the wound appeared superficial, but cellulitis developed and her clinical condition worsened. The wound was explored and liquefied, purulent, subcutaneous fat, necrotic muscle tissue, and a mixed second- and third-degree burn were found. The patient recovered completely after further debridement and grafting (VanGelder & Sheridan, 1999).
b) Superficial flash burns have been reported secondary to sniffing butane from a cigarette lighter refill aerosol can. Butane fumes accumulated in the enclosed space (automobile) and were ignited when one of the occupants attempted to light a cigarette. All burns healed spontaneously. There were no respiratory problems, behavioral changes, confusion, or hallucinations noted on examination at admission (Scerri et al, 1992).

Musculoskeletal

3.15.2)

A) RHABDOMYOLYSIS

1) WITH POISONING/EXPOSURE

a) Rhabdomyolysis (CPK greater than 18,000 International Units/L) and seizures have been reported following intentional inhalation of hydrocarbons (LoVecchio, 1998).
b) CASE REPORT: Coma, shock, rhabdomyolysis, metabolic acidosis, hyperkalemia, and suspected pneumonitis were reported in a 21-year-old woman following exposure to liquefied petroleum gas (Sampson et al, 2015).

Endocrine

3.16.2)

A) HYPERGLYCEMIA

1) WITH POISONING/EXPOSURE

a) Commercial acetylene may be in solution with acetone. The amount of acetone released increases as acetylene decreases in the tanks. Therefore, inhaled industrial acetylene may mimic ketoacidosis (acidosis, hyperglycemia, and ketonuria) (Foley, 1985).

Reproductive

3.20.1)

A) Sequelae of oxygen deprivation in the unborn are controversial. Cerebral palsy, previously thought to be due to acute hypoxia during labor and/or childbirth, remains poorly understood.

3.20.3)

A) HYPOXIA

1) The agents included are biologically inert gases. A potential could exist for fetal hypoxia during maternal hypoxemia from exposure.

B) HYDROCEPHALUS

1) The birth of an infant with hydranencephaly at 39 weeks was associated with the accidental maternal intoxication from butane gas at week 27 of gestation. The authors state that it is highly probable that the fetus was hypoxic during the period of maternal hypoxemia and this resulted in massive brain tissue necrosis. The severe radiological abnormalities were the result of subsequent cavitation and resorption of the necrotized tissue (Fernandez et al, 1986).

Carcinogenicity

3.21.1)

A) IARC Carcinogenicity Ratings for CAS74-86-2 (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

B) IARC Carcinogenicity Ratings for CAS7440-37-1 (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

C) IARC Carcinogenicity Ratings for CAS106-97-8 (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

D) IARC Carcinogenicity Ratings for CAS124-38-9 (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

E) IARC Carcinogenicity Ratings for CAS74-84-0 (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

F) IARC Carcinogenicity Ratings for CAS74-85-1 (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: Ethylene
b) Carcinogen Rating: 3

1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.

G) IARC Carcinogenicity Ratings for CAS7440-59-7 (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

H) IARC Carcinogenicity Ratings for CAS1333-74-0 (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

I) IARC Carcinogenicity Ratings for CAS74-82-8 (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

J) IARC Carcinogenicity Ratings for CAS7440-01-9 (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

K) IARC Carcinogenicity Ratings for CAS7727-37-9 (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

L) IARC Carcinogenicity Ratings for CAS74-98-6 (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) Not Listed

M) IARC Carcinogenicity Ratings for CAS115-07-1 (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: Propylene
b) Carcinogen Rating: 3

3.21.2)

3.21.3)

A) CARCINOMA

1) An excess of deaths from cancer was noted at an acetylene production plant. Lung, stomach, and pancreatic cancer were the most common. Risk appeared to be concentrated to one of 15 plants studied in England (Newhouse et al, 1988). The numbers are too small to draw definite conclusions.
2) It has been postulated that ethene exposures, especially in urban areas, at a concentration of 1 part per billion, may be expected to lead to a lifetime cancer risk in humans. In a risk assessment model, it was estimated that approximately 70 cancer deaths per 100,000 may occur (Tornqvist, 1994). This information is speculative.

Genotoxicity

Laboratory Monitoring

Monitoring Parameters Levels

4.1.1)

A) Monitor vital signs and mental status.
B) Obtain initial serum lactate and arterial blood gases as needed to diagnose and monitor respiratory and metabolic acidosis.
C) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity.
D) MRI or CT of the brain are indicated if there are signs or symptoms of cerebral edema or coma or if there is a persistent abnormal neurologic exam.

4.1.2)

A) ACID/BASE

1) Obtain initial serum lactate and arterial blood gases as needed to diagnose and monitor respiratory and metabolic acidosis.

4.1.4)

A) OTHER

1) Monitor vital signs and mental status.
2) MAGNETIC RESONANCE IMAGING

a) Magnetic resonance imaging may be useful when there is a suspicion of encephalopathy secondary to inhalant abuse.

1) CASE REPORT: A 16-year-old boy developed confusion, lethargy, and visual hallucinations approximately 1 day after inhaling a 300-mL can of butane lighter fluid which was 2 days prior to his admission. Family members were not immediately aware of the exposure. Signs and symptoms included akinetic mutism with abulia. An EEG performed 2 days after admission, showed diffuse background slowing with intermittent bilateral frontal delta waves, and an abnormal arousal response pattern. An MRI revealed abnormal hyperintensity in both thalami, as well as in the right cerebellum and the subinsular tissues, all of which are indicative of an encephalopathy due to toxic or metabolic causes (Kile et al, 2006).

3) AMBIENT LEVELS

a) Atmospheric oxygen concentration monitoring may be advisable when entry into enclosed spaces that may contain asphyxiant gases is considered (Clayton & Clayton, 1982).

4) ECG

a) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity.

5) CT SCAN

a) Obtain a CT scan of the brain if there are signs or symptoms of cerebral edema or coma or if there is a persistent abnormal neurologic exam.

Methods

1) A method of providing evidence for lethal solvent abuse is to sample head space above lung tissue and perform cryogenically focused gas-liquid chromatography, as the pleural cavity acts as an efficient trap for aspirated substances (Kirkbride & Manock, 1992).

1) Collection and storage of tissues and body fluids for toxicologic analysis require special techniques to prevent the loss of these highly volatile substances (Imami & Kemal, 1986).

Treatment

Life Support

Patient Disposition

6.3.3)

6.3.3.1) ADMISSION CRITERIA/INHALATION

A) Patients with CNS depression, seizures, or other signs of severe hypoxemia should be admitted to the hospital.

6.3.3.2) HOME CRITERIA/INHALATION

A) Patients with minimal symptoms after inadvertent exposure can be managed at home with termination of exposure.

6.3.3.3) CONSULT CRITERIA/INHALATION

A) Consult a poison control center or a medical toxicologist for assistance in managing patients with severe toxicity (ie, CNS depression, seizures) or in whom the diagnosis is not clear.

6.3.3.5) OBSERVATION CRITERIA/INHALATION

A) Symptomatic patients and those with deliberate exposures should be referred to a healthcare facility.

Monitoring

Oral Exposure

6.5.1)

A) SUMMARY

1) Remove the patient from the hypoxic environment as quickly as possible and administer supplemental oxygen.

Inhalation Exposure

6.7.2)

A) OXYGEN

1) Administer 100% humidified supplemental oxygen with assisted ventilation, as required.

B) SUPPORT

1) If hypoxia has been severe or prolonged, carefully evaluate for neurologic sequelae and provide supportive treatment as indicated.

C) MONITORING OF PATIENT

1) Monitor vital signs and mental status.
2) Obtain initial serum lactate and arterial blood gases as needed to diagnose and monitor respiratory and metabolic acidosis.
3) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity.
4) MRI or CT of the brain are indicated if there are signs or symptoms of cerebral edema or coma or if there is a persistent abnormal neurologic exam.

D) 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).

E) SEIZURE

1) SUMMARY

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

2) DIAZEPAM

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

3) NO INTRAVENOUS ACCESS

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

4) LORAZEPAM

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).

5) PHENOBARBITAL

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

6) OTHER AGENTS

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).

F) RHABDOMYOLYSIS

1) SUMMARY: Early aggressive fluid replacement is the mainstay of therapy and may help prevent renal insufficiency. Diuretics such as mannitol or furosemide may be added if necessary to maintain urine output but only after volume status has been restored as hypovolemia will increase renal tubular damage. Urinary alkalinization is NOT routinely recommended.
2) Initial treatment should be directed towards controlling acute metabolic disturbances such as hyperkalemia, hyperthermia, and hypovolemia. Control seizures, agitation, and muscle contractions (Erdman & Dart, 2004).
3) FLUID REPLACEMENT: Early and aggressive fluid replacement is the mainstay of therapy to prevent renal failure. Vigorous fluid replacement with 0.9% saline (10 to 15 mL/kg/hour) is necessary even if there is no evidence of dehydration. Several liters of fluid may be needed within the first 24 hours (Walter & Catenacci, 2008; Camp, 2009; Huerta-Alardin et al, 2005; Criddle, 2003; Polderman, 2004). Hypovolemia, increased insensible losses, and third spacing of fluid commonly increase fluid requirements. Strive to maintain a urine output of at least 1 to 2 mL/kg/hour (or greater than 150 to 300 mL/hour) (Walter & Catenacci, 2008; Camp, 2009; Erdman & Dart, 2004; Criddle, 2003). To maintain a urine output this high, 500 to 1000 mL of fluid per hour may be required (Criddle, 2003). Monitor fluid input and urine output, plus insensible losses. Monitor for evidence of fluid overload and compartment syndrome; monitor serum electrolytes, CK, and renal function tests.
4) DIURETICS: Diuretics (eg, mannitol or furosemide) may be needed to ensure adequate urine output and to prevent acute renal failure when used in combination with aggressive fluid therapy. Loop diuretics increase tubular flow and decrease deposition of myoglobin. These agents should be used only after volume status has been restored, as hypovolemia will increase renal tubular damage. If the patient is maintaining adequate urine output, loop diuretics are not necessary (Vanholder et al, 2000).
5) URINARY ALKALINIZATION: Alkalinization of the urine is not routinely recommended, as it has never been documented to reduce nephrotoxicity, and may cause complications such as hypocalcemia and hypokalemia (Walter & Catenacci, 2008; Huerta-Alardin et al, 2005; Brown et al, 2004; Polderman, 2004). Retrospective studies have failed to demonstrate any clinical benefit from the use of urinary alkalinization (Brown et al, 2004; Polderman, 2004; Homsi et al, 1997).

G) CEREBRAL EDEMA

1) CLINICAL IMPLICATIONS

a) Cerebral edema and elevated intracranial pressure (ICP) may occur. Emergent management includes head elevation and administration of mannitol; hyperventilation should be performed if there is evidence of impending herniation.

2) MONITORING

a) Patients will usually require endotracheal intubation and mechanical ventilation. Monitor intracranial pressure, cerebral perfusion pressure and cerebral blood flow.

3) TREATMENT

a) Most information on the treatment of cerebral edema is derived from studies of traumatic brain injury.

4) MANNITOL

a) ADULT/PEDIATRIC DOSE: 0.25 to 1 gram/kilogram intravenously over 10 to 15 minutes (None Listed, 2000).
b) AVAILABLE FORMS: Mannitol injection (5%, 10%, 15%, 20%, 25%).
c) MAJOR ADVERSE REACTIONS: Congestive heart failure, hypernatremia, hyponatremia, hyperkalemia, renal failure, pulmonary edema, and allergic reactions.
d) PRECAUTIONS: Contraindicated in well-established anuria or impaired renal function not responding to a test dose, pulmonary edema, CHF, severe dehydration; caution in progressive oliguria and azotemia. Do not add to whole blood for transfusions; enhanced neuromuscular blockade has occurred with tubocurarine. Keep serum osmolarity below 320 mOsm.
e) MONITORING PARAMETERS: Renal function, urine output, fluid balance, serum potassium levels, serum osmolarity, and CVP.

5) HYPERTONIC SALINE

a) Preliminary studies suggest that hypertonic saline (7.5% saline/6% dextran) 100 ml reduced ICP more effectively than 200 mL of 20% mannitol in adults with elevated ICP after traumatic brain injury(Battison et al, 2005).

6) ELEVATION

a) Elevation of the head of the bed to approximately 30 degrees decreases ICP and improves cerebral perfusion pressure (Meixensberger et al, 1997; Schneider et al, 1993; Feldman et al, 1992).

7) MECHANICAL DECOMPRESSION

a) Early surgical decompression, ventriculostomy with CSF drainage, or craniectomy may be useful in patients with persistent elevation of ICP (Sahuquillo & Arikan, 2006; Sakai et al, 1998; Polin et al, 1997; Taylor et al, 2001). Most experience with these modalities has been in patients with traumatic brain injury.

8) HYPERVENTILATION

a) SUMMARY: Hyperventilation has been associated with adverse outcomes and should not be performed routinely (Muizelaar et al, 1991). It is indicated in patients who have clinical evidence of herniation or if there is intracranial hypertension refractory to sedation, paralysis, CSF drainage and osmotic diuretics (None Listed, 2000a).
b) RECOMMENDATION:

1) The PCO2 must be controlled in the range of 25 torr; further lowering of PCO2 may create undesirable effects secondary to local tissue hypoxia.
2) End-tidal CO2 tension, correlated with an initial ABG measurement, provides a noninvasive means of monitoring PCO2 (Mackersie & Karagianes, 1990).
3) Most authorities advise that hyperventilation should be considered a temporizing measure only; SUSTAINED hyperventilation should be avoided (Am Acad Neurol, 1997; Bullock et al, 1996; Kirkpatrick, 1997).

9) CASE REPORT: An 18-year-old man became comatose and developed cardiac arrest, that was successfully resuscitated, after inhaling butane from an aerosol container for cigarette lighter fluid. At hospital admission, the patient's intracranial pressure (ICP was measured as 14 mmHg. An MRI showed high signal changes symmetrically in both putamen with less predominant changes in the occipital and frontal lobes. Two days later, a repeat ICP measurement indicated that his ICP increased to greater than 20 mmHg, and was refractory to mannitol treatment, necessitating bilateral decompressive craniectomy. A post-operative CT revealed bilateral decompression, and repeat ICP monitoring demonstrated values that were consistently below 20 mmHg. However, the patient's hemodynamic status deteriorated and he died approximately 5 days post-admission due to multi-organ failure and cardiogenic shock (Peyravi et al, 2012).

Eye Exposure

6.8.1)

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

6.9.2)

A) FROSTBITE

1) Freeze injury associated with dermal exposure to compressed or liquid forms (ie, propane) is unlike frostbite in that the damage occurs within seconds and rewarming is not beneficial (US Department of Labor, 1988).

a) It is suggested that freeze injuries of this nature be managed much like a thermal burn (Corn et al, 1991).
b) Burn surgeons should be consulted in the more severe cases (Corn et al, 1991).

2) PREHOSPITAL

a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).

3) REWARMING

a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).

4) WOUND CARE

a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
c) The injured extremities should be elevated and should not be allowed to bear weight.
d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).

Abstracts

Case Reports

1) CARBON DIOXIDE: A 37-year-old man was found unconscious in a car fully loaded with 40 kg of dry ice. He developed seizures and pulmonary edema. Blood gases showed serious hypoxia with combined respiratory and metabolic acidosis. He was ventilated mechanically for 12 hours, improved rapidly, and fully recovered in two weeks (Takaoka et al, 1988).
2) CARBON DIOXIDE: Survivors of the Lake Nyos disaster in August of 1986 were noted to have superficial blisters which healed rapidly. Characteristics of the blisters suggested that they were the result of depriving the skin of oxygen. Hospitalized and outpatient survivors had symptoms compatible with exposure to a suffocating gas (Freeth, 1992). Many survivors had lost consciousness for hours (6 to 36 hours) after the incident (Wagner et al, 1988). Cough, headache, fever, weakness or malaise, and limb swelling were frequently noted (10% or more incidence) among the victims (Baxter et al, 1989).

a) Autopsies were not performed at the time of the disaster or soon after and linguistic and cultural barriers prevented any detailed retrospective study. Evidence after the incident suggested a slow buildup of carbon dioxide deep in the lake, followed by its release as a cold, suffocating aerosol.
b) Dogs, cats, cattle, goats, chickens, snakes, and frogs were also found dead in their tracks. Insect life was noted to be absent for approximately 24 hours following the incident (Wagner et al, 1988).

3) CARBON DIOXIDE: Bradycardia progressing to asystole was the presenting arrhythmia in a 21-month-old child who received 99.97% carbon dioxide during anesthesia . Cyanosis was not noted at any time. No neurological sequelae occurred secondary to the incident suggesting that hypercapnia and acidosis must have been at least contributory and hypoxemia was not the most likely cause of the cardiac arrest (Jawan & Lee, 1990).
4) ISOBUTANE, BUTANE, and PROPANE: A 2-year-old child was presented to the emergency room with hypotension, pale skin, cyanosis, pulse rate of 120, and a generalized tonoclonic seizure (that subsided after a dose of diazepam) after inhaling the propellant of an aerosolized deodorant . ECG showed a wide QRS-complex tachycardia which probably represented ventricular tachycardia. She was cardioverted a total of 10 times. Her blood pressure dropped, she developed apnea and central cyanosis and was administered cardiopulmonary resuscitation and endotracheal intubation. Blood gas values revealed a pH of 7.37, pCO2 of 33 mmHg, and PO2 greater than 400 mmHg on 5 L/min of oxygen. Cardiac rhythm was ventricular tachycardia at a rate of 225. The patient was put on a lidocaine drip which produced sinus rhythm. She was also started on prophylactic phenobarbital after experiencing another tonoclonic seizure. The patient was discharged after 7 days at which time her cardiac rhythm and clinical status was normal. One month later on examination, all findings were normal (Wason et al, 1986).
5) BUTANE GAS: A 15-year-old adolescent who inhaled approximately half the contents (amount unknown) of butane gas from a cigarette lighter fuel canister was admitted to the hospital 10 hours post-inhalation. On admission, he was alert and oriented but found to have a right-sided hemiparesis with greatly reduced power in both right arm and leg, flaccid tone, and absent reflexes with an extensor planter reflex on the right side. Otherwise, his physical examination was normal. CT head scan on day 2 of hospital admission was normal as was a drug screen for alcohol, full blood count, urea, electrolytes, and glucose. At discharge on day 5, hemiparesis had improved, but he still had upper limb proximal muscle weakness and a hemiplegic gait (Gray & Lazarus, 1993).

Range Of Toxicity

Summary

Minimum Lethal Exposure

1) Unconsciousness leading to death will occur when the atmospheric oxygen concentration is reduced to 6% to 8% or less (Kizer, 1984).

Maximum Tolerated Exposure

1) INHALATION: Signs of asphyxia will be noted when atmospheric oxygen is displaced such that the oxygen concentration is 15 to 16% or less (Sax, 1984; Kizer, 1984).
2) INHALATION: A previously healthy 16-year-old boy suffered a cardiac arrest, which reversed to sinus rhythm after more than 6 cardioversions. He admitted to inhaling Glade(R) air freshener and using a plastic bag over his face. The patient admitted to previous use of "huffing" air freshener. The contents of the air freshener included butane and isobutane (LoVecchio, 1998).
3) DERMAL: Epidermal necrosis was noted from spraying propane for 12 seconds duration to the skin of animals. Dermal necrosis was noted at 24 hours and damage to the superficial muscle was noted at five days following application of sprayed propane to the skin of animals for 30 seconds duration (Hicks et al, 1979).

Serum Plasma Blood Concentrations

7.5.2)

A) TOXIC CONCENTRATION LEVELS

1) CONCENTRATION LEVEL

a) Hypoxemia is defined as a pO2 less than 75 mmHg (Safar & Caroline, 1978), although at higher altitudes, physiologic compensation needs to be taken into account.
b) The DISTURBANCE STAGE of hypoxia where significant symptomatology may be seen that can impair the ability for self-rescue occurs when the arterial oxygen saturation is 64% to 82% (AMPC, 1984).
c) The CRITICAL STAGE of hypoxia where total incapacitation and unconsciousness may occur within 3 to 5 minutes is seen with arterial oxygen saturations of 60% to 70% or less (AMPC, 1984).
d) CARBON DIOXIDE: Concentrations up to 35% carbon dioxide have an exciting effect upon both circulation and respiration (Hill & Flack, 1908). Concentrations above 35% carbon dioxide have a depressing effect upon both circulation and respiration (Hill & Flack, 1908).

2) CASE REPORT: A 35-year-old man was found dead with a hose in his mouth, sealed with packing tape, and connected to a gas wall outlet. An autopsy, performed 48 hours later, revealed pulmonary edema and congestion, as well as cerebral edema, and pleural and epicardial petechiae. Toxicologic analysis of his tissues and fluids indicated the presence of methane at the following concentrations: peripheral blood 16 mcL/g, brain 14 mcL/g, heart 17 mcL/g, kidneys 19 mcL/g, liver 14 mcL/g, and lungs 56 mcL/g. The cause of death was attributed to asphyxia due to oxygen displacement secondary to methane gas inhalation (Rossi et al, 2013).

Workplace Standards

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) Acetylene

a) TLV:

1) TLV-TWA:
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: D
3) Definitions:

a) D: Simple asphyxiant; see discussion covering Minimal Oxygen Content found in the "Definitions and Notations" section following the NIC tables (in TLV booklet).

c) TLV Basis - Critical Effect(s): Asphyxia
d) Molecular Weight: 26.02

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) ACGIH TLV Values for CAS7440-37-1 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Argon

a) TLV:

1) TLV-TWA:
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: D
3) Definitions:

a) D: Simple asphyxiant; see discussion covering Minimal Oxygen Content found in the "Definitions and Notations" section following the NIC tables (in TLV booklet).

c) TLV Basis - Critical Effect(s): Asphyxia
d) Molecular Weight: 39.95

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:

C) ACGIH TLV Values for CAS106-97-8 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Aliphatic hydrocarbon gases, Alkanes (C1-C4)

a) TLV:

1) TLV-TWA: 1000 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): Card sens; CNS impair
d) Molecular Weight: Varies

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) Under Study

1) Aliphatic hydrocarbon gases

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

c) Under Study

1) Butane

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

D) ACGIH TLV Values for CAS124-38-9 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Carbon dioxide

a) TLV:

1) TLV-TWA: 5000 ppm
2) TLV-STEL: 30,000 ppm
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): Asphyxia
d) Molecular Weight: 44.01

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:

E) ACGIH TLV Values for CAS74-84-0 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Ethane

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

1) See Aliphatic Hydrocarbon Gases: Alkane [C1-C4]

b) Under Study

1) Ethane

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

F) ACGIH TLV Values for CAS74-85-1 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Aliphatic hydrocarbon gases, Alkanes (C1-C4)

a) TLV:

1) TLV-TWA: 1000 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): Card sens; CNS impair
d) Molecular Weight: Varies

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) Under Study

1) Aliphatic hydrocarbon gases

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

c) Adopted Value

1) Ethylene

a) TLV:

1) TLV-TWA: 200 ppm
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: A4
2) Codes: Not Listed
3) Definitions:

a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

c) TLV Basis - Critical Effect(s): Asphyxia
d) Molecular Weight: 28.05

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:

G) ACGIH TLV Values for CAS7440-59-7 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Helium

a) TLV:

1) TLV-TWA:
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: D
3) Definitions:

a) D: Simple asphyxiant; see discussion covering Minimal Oxygen Content found in the "Definitions and Notations" section following the NIC tables (in TLV booklet).

c) TLV Basis - Critical Effect(s): Asphyxia
d) Molecular Weight: 4.0

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:

H) ACGIH TLV Values for CAS1333-74-0 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Hydrogen

a) TLV:

1) TLV-TWA:
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: D
3) Definitions:

a) D: Simple asphyxiant; see discussion covering Minimal Oxygen Content found in the "Definitions and Notations" section following the NIC tables (in TLV booklet).

c) TLV Basis - Critical Effect(s): Asphyxia
d) Molecular Weight: 1.01

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:

I) ACGIH TLV Values for CAS74-82-8 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Aliphatic hydrocarbon gases, Alkanes (C1-C4)

a) TLV:

1) TLV-TWA: 1000 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): Card sens; CNS impair
d) Molecular Weight: Varies

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) Under Study

1) Aliphatic hydrocarbon gases

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

c) Adopted Value

1) Methane

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

1) See Aliphatic Hydrocarbon Gases: Alkanes [C1-C4]

d) Under Study

1) Methane

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

J) ACGIH TLV Values for CAS7440-01-9 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Neon

a) TLV:

1) TLV-TWA:
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: D
3) Definitions:

a) D: Simple asphyxiant; see discussion covering Minimal Oxygen Content found in the "Definitions and Notations" section following the NIC tables (in TLV booklet).

c) TLV Basis - Critical Effect(s): Asphyxia
d) Molecular Weight: 20.18

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:

K) ACGIH TLV Values for CAS7727-37-9 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Nitrogen

a) TLV:

1) TLV-TWA:
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: D
3) Definitions:

a) D: Simple asphyxiant; see discussion covering Minimal Oxygen Content found in the "Definitions and Notations" section following the NIC tables (in TLV booklet).

c) TLV Basis - Critical Effect(s): Asphyxia
d) Molecular Weight: 14.01

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:

L) ACGIH TLV Values for CAS74-98-6 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Propane

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

1) See Aliphatic Hydrocarbon Gases: Alkanes [C1-C4]

b) Under Study

1) Propane

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

c) Adopted Value

1) Aliphatic hydrocarbon gases, Alkanes (C1-C4)

a) TLV:

1) TLV-TWA: 1000 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): Card sens; CNS impair
d) Molecular Weight: Varies

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:

d) Under Study

1) Aliphatic hydrocarbon gases

a) TLV:

1) TLV-TWA:
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):
d) Molecular Weight:

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:

M) ACGIH TLV Values for CAS115-07-1 (American Conference of Governmental Industrial Hygienists, 2010):

a) Adopted Value

1) Propylene

a) TLV:

1) TLV-TWA: 500 ppm
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: A4
2) Codes: Not Listed
3) Definitions:

c) TLV Basis - Critical Effect(s): Asphyxia; URT irr
d) Molecular Weight: 42.08

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:

N) NIOSH REL and IDLH Values for CAS74-86-2 (National Institute for Occupational Safety and Health, 2007):

1) Listed as: Acetylene
2) REL:

a) TWA:
b) STEL:
c) Ceiling: 2500 ppm (2662 mg/m(3))
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

3) IDLH: Not Listed

O) NIOSH REL and IDLH Values for CAS7440-37-1 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

P) NIOSH REL and IDLH Values for CAS106-97-8 (National Institute for Occupational Safety and Health, 2007):

1) Listed as: n-Butane
2) REL:

a) TWA: 800 ppm (1900 mg/m(3))
b) STEL:
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

3) IDLH: Not Listed

Q) NIOSH REL and IDLH Values for CAS124-38-9 (National Institute for Occupational Safety and Health, 2007):

1) Listed as: Carbon dioxide
2) REL:

a) TWA: 5000 ppm (9000 mg/m(3))
b) STEL: 30,000 ppm (54,000 mg/m(3))
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

3) IDLH:

a) IDLH: 40,000 ppm
b) Note(s): Not Listed

R) NIOSH REL and IDLH Values for CAS74-84-0 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

S) NIOSH REL and IDLH Values for CAS74-85-1 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

T) NIOSH REL and IDLH Values for CAS7440-59-7 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

U) NIOSH REL and IDLH Values for CAS1333-74-0 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

V) NIOSH REL and IDLH Values for CAS74-82-8 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

W) NIOSH REL and IDLH Values for CAS7440-01-9 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

X) NIOSH REL and IDLH Values for CAS7727-37-9 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

Y) NIOSH REL and IDLH Values for CAS74-98-6 (National Institute for Occupational Safety and Health, 2007):

1) Listed as: Propane
2) REL:

a) TWA: 1000 ppm (1800 mg/m(3))
b) STEL:
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

3) IDLH:

a) IDLH: 2100 ppm
b) Note(s): [10%LEL]

1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

Z) NIOSH REL and IDLH Values for CAS115-07-1 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

AA) Carcinogenicity Ratings for CAS74-86-2 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Acetylene
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 ; Listed as: Acetylene
5) MAK (DFG, 2002): Not Listed
6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

AB) Carcinogenicity Ratings for CAS7440-37-1 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Argon
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

AC) Carcinogenicity Ratings for CAS106-97-8 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Aliphatic hydrocarbon gases, Alkanes (C1-C4)
2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Aliphatic hydrocarbon gases
3) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Butane
4) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
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): Not Listed
6) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: n-Butane
7) MAK (DFG, 2002): Not Listed
8) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

AD) Carcinogenicity Ratings for CAS124-38-9 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Carbon dioxide
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 ; Listed as: Carbon dioxide
5) MAK (DFG, 2002): Not Listed
6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

AE) Carcinogenicity Ratings for CAS74-84-0 :

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

AF) Carcinogenicity Ratings for CAS74-85-1 :

a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

4) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
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): 3 ; Listed as: Ethylene

a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.

6) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
7) MAK (DFG, 2002): Category 3B ; Listed as: Ethylene

a) Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)

8) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

AG) Carcinogenicity Ratings for CAS7440-59-7 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Helium
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

AH) Carcinogenicity Ratings for CAS1333-74-0 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Hydrogen
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

AI) Carcinogenicity Ratings for CAS74-82-8 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Aliphatic hydrocarbon gases, Alkanes (C1-C4)
2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Aliphatic hydrocarbon gases
3) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methane
4) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methane
5) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
6) 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
7) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
8) MAK (DFG, 2002): Not Listed
9) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

AJ) Carcinogenicity Ratings for CAS7440-01-9 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Neon
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

AK) Carcinogenicity Ratings for CAS7727-37-9 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Nitrogen
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

AL) Carcinogenicity Ratings for CAS74-98-6 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Propane
2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Propane
3) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Aliphatic hydrocarbon gases, Alkanes (C1-C4)
4) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Aliphatic hydrocarbon gases
5) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
6) 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
7) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Propane
8) MAK (DFG, 2002): Not Listed
9) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

AM) Carcinogenicity Ratings for CAS115-07-1 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Propylene

a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

2) EPA (U.S. Environmental Protection Agency, 2011): Not 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): 3 ; Listed as: Propylene

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

AN) OSHA PEL Values for CAS74-86-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AO) OSHA PEL Values for CAS7440-37-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AP) OSHA PEL Values for CAS106-97-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AQ) OSHA PEL Values for CAS124-38-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Listed as: Carbon dioxide
2) Table Z-1 for Carbon dioxide:

a) 8-hour TWA:

1) ppm: 5000

a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

2) mg/m3: 9000

a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

3) Ceiling Value:
4) Skin Designation: No
5) Notation(s): Not Listed

AR) OSHA PEL Values for CAS74-84-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AS) OSHA PEL Values for CAS74-85-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AT) OSHA PEL Values for CAS7440-59-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AU) OSHA PEL Values for CAS1333-74-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AV) OSHA PEL Values for CAS74-82-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AW) OSHA PEL Values for CAS7440-01-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AX) OSHA PEL Values for CAS7727-37-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

AY) OSHA PEL Values for CAS74-98-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Listed as: Propane
2) Table Z-1 for Propane:

a) 8-hour TWA:

1) ppm: 1000

a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

2) mg/m3: 1800

a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

3) Ceiling Value:
4) Skin Designation: No
5) Notation(s): Not Listed

AZ) OSHA PEL Values for CAS115-07-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

Toxicity Information

7.7.1)

A) ACETYLENE
B) BUTANE
C) CARBON DIOXIDE
D) ETHANE

1) LD50- (INHALATION)HUMAN:

a) 1000 parts per million (ITI, 1985a)

E) ETHYLENE
F) LIQUEFIED PETROLEUM GAS

1) LD50- (ORAL)RAT:

a) 850 mg/kg (Sax, 1984)

G) METHANE

Pharmacology Toxicology

Toxicologic Mechanism

Physicochemical

Physical Characteristics

Molecular Weight

Animal Toxicology

Range Of Toxicity

11.3.2)

A) SWINE

1) The recommended maximal concentration of carbon dioxide in environmental air as contaminant is 1,540 ppm according to a cross-sectional epidemiologic study associating air quality with disease and productivity in swine in southern Sweden (Donham, 1991).

References

General Bibliography

10)

11)

12)

13)

14)

15)

16)

17)

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19)

20)

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22)

23)

24)

25)

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ASPHYXIANTS, SIMPLE

Classification | Detailed evidence-based information

Therapeutic Toxic Class

Specific Substances

Available Forms Sources

Life Support

Clinical Effects

Laboratory Monitoring

Treatment Overview

Range Of Toxicity

Summary Of Exposure

Vital Signs

Heent

Cardiovascular

Respiratory

Neurologic

Gastrointestinal

Acid-Base

Dermatologic

Musculoskeletal

Endocrine

Reproductive

Carcinogenicity

Genotoxicity

Monitoring Parameters Levels

Methods

Life Support

Patient Disposition

Monitoring

Oral Exposure

Inhalation Exposure

Eye Exposure

Dermal Exposure

Case Reports

Summary

Minimum Lethal Exposure

Maximum Tolerated Exposure

Serum Plasma Blood Concentrations

Workplace Standards

Toxicity Information

Toxicologic Mechanism

Physical Characteristics

Molecular Weight

Range Of Toxicity

General Bibliography