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Diss Factsheets

Toxicological information

Direct observations: clinical cases, poisoning incidents and other

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Administrative data

Endpoint:
direct observations: clinical cases, poisoning incidents and other
Type of information:
other: Review report clinical cases
Adequacy of study:
supporting study
Reliability:
4 (not assignable)
Rationale for reliability incl. deficiencies:
other: Data cited by the Netherlands Health Council. Reliability of each reference not known but the overview is a reliable source and data cited contribute to weight of evidence assessment.

Data source

Reference
Reference Type:
publication
Title:
Unnamed
Year:
2004
Report date:
2004

Materials and methods

Study type:
other: poisoning incidents and studies with volunteers
Endpoint addressed:
acute toxicity: inhalation
Principles of method if other than guideline:
This document is an overview .
GLP compliance:
not specified

Test material

Constituent 1
Chemical structure
Reference substance name:
Butane
EC Number:
203-448-7
EC Name:
Butane
Cas Number:
106-97-8
Molecular formula:
C4H10
IUPAC Name:
butane
Constituent 2
Reference substance name:
n-butane, methylethylmethane, butyl hydride
IUPAC Name:
n-butane, methylethylmethane, butyl hydride
Details on test material:
- Name of test material (as cited in study report): butane
- Physical state: colourless and flammable gas with a gasoline-like odour

Method

Type of population:
other: general and occupational
Subjects:
see below
Ethical approval:
not applicable
Route of exposure:
inhalation
Reason of exposure:
intentional
Exposure assessment:
not specified
Details on exposure:
No details
Examinations:
Mostly found dead.
Medical treatment:
None. One case involved involving cardiopulmonary resuscitation, 6-day catecholamine treatment, and 11-day mechanic ventilation.

Results and discussion

Clinical signs:
Ranged from found dead to severe acute neurological (seizure, somnolence, coma) or cardiovascular (ventricular fibrillation, asystole, collapse) complications and minor symptoms such as nausea, dizziness, vomiting, headache and sore throat
Results of examinations:
At very high concentrations, butane can cause asphyxiation and CNS depression. Numerous cases of fatal inhalation of butane have been reported; a direct consequence of inhalant abuse.   Butane is reported to induce severe acute neurological (seizure, somnolence, coma) or cardiovascular (ventricular fibrillation, asystole, collapse) complications and minor symptoms such as nausea, dizziness, vomiting, headache and sore throat.
Effectivity of medical treatment:
Limited
Outcome of incidence:
High acute exposure through misuse can result in death.

Any other information on results incl. tables

The Netherlands Health Council summarise several individual cases or retrospective studies in which butane was identified as the toxic agent have been reported. They mostly concern its abuse as an inhalant, from lighters or hair/deodorant sprays, by teenagers and adolescents. Butane abuse is often fatal due to heart failure (arrhythmias, ventricular fibrillation, asystole) (Bland et al 1998,Bowen et al 1999, Chaudrey et al 2002, Döring et al 2002, Field-Smith et al 2003, Graefe et al 1999, Roberts 1990, Rohrig et al 1997, Wehner et al 2002). In one reported case, death was due to multiple organ failure involving the central nervous system, cardiovascular and pulmonary systems, and the liver (Rieder-Scharinger et al 2000).

Of 39 cases where death was considered to be a direct consequence of inhalant abuse, 13 were associated with butane (Bowen et al 1999). Butane is reported to induce severe acute neurological signs such as seizure, somnolence, coma or cardiovascular complications e.g. ventricular fibrillation or asystole. Minor symptoms include nausea, dizziness, vomiting, headache and sore throat (Döring et al 2002, Edwards et al 2000, O’Neill 99).

Döring et al. 2002 described a case of severe encephalopathy of a 15-year-old girl, having inhaled butane repeatedly for 4 weeks when an acute abuse incident occurred. Treatment involved cardiopulmonary resuscitation, 6-day catecholamine treatment, and 11-day mechanic ventilation; however the girl was left with severe brain damage with vigil coma and spastic quadriplegia. Repetitive MRI-imaging revealed disintegration of grey matter, increasing cerebral atrophy, and destruction of basal ganglia while EEG revealed diminished basal activity with flat amplitude.

Gray and Lazarus, 1993 report a case of a right-sided hemiparesis in the right arm and leg, flaccid tone, and absent reflexes with an extensor plantar reflex.

Frangides et al. 2003, reported a rare case of non-fatal acute massive rhabdomyolysis in a 27-year-old man following accidental inhalation of liquid gas fumes leaking from a tank which contained a mixture of butane (80%), propane (20%), ethanethiol, and olefines.

Two cases are reported of butane exposure in pregnant women, one accidentally exposed in pregnancy week 27, the other intentionally as a suicide attempt in week 30 (Fernàndez et al 1986). The first woman gave birth to a child with hydranencephaly, while the second woman gave birth to a child that died after 11 hours with severe encephalomalacia and hypoplastic kidneys (Gosseye et al 1982). In both cases, the brain effects were not considered to be caused by butane but by intrauterine anoxia. In neither of these cases were estimations of the concentrations inhaled made, also, as the history prior to the exposures is unknown, the relationship of the developmental outcomes to butane exposure this study is highly uncertain.

Viau et al. 1987 reported no clinically significant effects on biochemical and immunological markers of kidney (function) in 53 male refinery workers occupationally exposed for an average of 11 years to a number of hydrocarbons, including butane (concentration ranged from 0.4 to 17.8mg/m3).

Assuming a correlation between the anaesthetic potency of a gas and its air/olive oil partition coefficient, Drummond expected that a concentration of butane of 17,000 ppm (40,290 mg/m3) would induce narcosis in man (Drummond 1993).

Bland JM, Taylor J. Deaths from accidental drug poisoning in teenagers. Deaths due to volatile substance misuse are greatly underestimated. BMJ 1998; 316: 146

Bowen SE, Daniel J, Balster RL. Deaths associated with inhalant abuse in Virginia from 1987 to1996. Drug Alcohol Depend 1999; 53: 239-45.Chaudhry S. Deaths from volatile substance misuse fall. BMJ 2002; 325: 122.134-18 Health-based Reassessment of Administrative Occupational Exposure Limits

Döring G, Baumeister FAM, Peters J, et al. Butane abuse associated encephalopathy. Klin Pädiatr 2002; 214: 295-8.

Drummond I. Light hydrocarbon gases: a narcotic, asphyxiant, or flammable hazard? Appl Occup Environ Hyg 1993; 8: 120-5.

Edwards KE, Wenstone R. Successful resuscitation from recurrent ventricular fibrillation secondary to butane inhalation. Br J Anaesth 2000; 84: 803-5.

Fernàndez F, Pèrez-Higueras A, Hernàndez R, et al. Hydranencephaly after maternal butane-gas intoxication during pregnancy. Dev Med Child Neurol 1986: 28: 361-3.

Field-Smith ME, Butland BK, Ramsey JD, et al. Trends in death associated with abuse of volatile substances. London, UK: St George’s Hospital Medical School, Department of Community Health Sciences, 2003;http://www.vsareport.org.

Frangides CY, Tzortzatos GV, Koulouras V, et al. Acute massive rhabdomyolysis due to prolonged inhalation of liquid gas. Eur J Emerg Med 2003; 10: 44-6.

Gosseye S, Golaire MC, Larroche JC. Cerebral, renal and splenic lesions due to fetal anoxia and their relationships to malformations. Dev Med Child Neurol 1982; 24: 510-8.

Graefe A, Müller RK, Vock R, et al. Tödliche Intoxikationen durch Propan-Butan. Arch Kriminol 1999; 203: 27-31

Gray MY, Lazarus JH. Butane inhalation and hemiparesis. Clin Toxicol 1993; 31: 483-5.

O'Neill J, McCarthy C. Myocardial infarction in a 14-year old boy after butane inhalation (letter). Ir Med J 1999; 92: 344.

Rieder-Scharinger J, Peer R, Rabl W, et al. Multiorganversagen nach Butangasinhalation: Ein Fallbericht. Wien Klin Wochenschr 2000; 112: 1049-52.

Roberts MJD, McIvor RA, Adgey AAJ. Asystole following butane gas inhalation. Br J Hosp Med 1990; 44: 294.

Rohrig TP. Sudden death due to butane inhalation. Am J Forensic Med Pathol 1997; 18: 299-302.134-20 Health-based Reassessment of Administrative Occupational Exposure Limits

Viau C, Bernard A, Lauwerys R, et al. A cross-sectional survey of kidney functioning in refinery employees. Am J Ind Med 1987; 11: 177-87.

Wehner F, Benz D, Wehner HD. Tödliche Inhalation von Butan-Propan-Gas. Arch Kriminol 2002; 205: 164-8.  

 

Applicant's summary and conclusion

Conclusions:
At very high concentrations, butane can cause asphyxiation and CNS depression. Several cases of fatal inhalation of butane have been reported, a direct consequence of inhalant abuse.

Executive summary:

At very high concentrations, butane can cause asphyxiation and CNS depression. Numerous cases of fatal inhalation of butane have been reported; a direct consequence of inhalant abuse.   Butane is reported to induce severe acute neurological (seizure, somnolence, coma) or cardiovascular (ventricular fibrillation, asystole, collapse) complications and minor symptoms such as nausea, dizziness, vomiting, headache and sore throat.

Two cases are reported of butane exposure in pregnant women, one accidentally exposed in pregnancy week 27, the other intentionally as a suicide attempt in week 30. The first woman gave birth to a child with hydranencephaly, while the second woman gave birth to a child that died after 11 hours with severe encephalomalacia and hypoplastic kidneys. In both cases, the brain effects were not considered to be caused by butane but by intrauterine anoxia. In neither of these cases were estimations of the concentrations inhaled made, also, as the history prior to the exposures is unknown, the relationship of the developmental outcomes to butane exposure this study is highly uncertain.

Assuming a correlation between the anaesthetic potency of a gas and its air/olive oil partition coefficient, it is reported that a concentration of butane of 17,000 ppm (40,290 mg/m3) would induce narcosis in man.