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Background information


Volatile substances are chemical compounds that give off fumes at room temperature [1][2][3]. They are also called ‘inhalants’ in recognition of their route of administration. Volatile substance use (VSU) is the ‘practice of deliberately inhaling (“sniffing”, “huffing”, “bagging” or “chroming”) substances that are vaporous at ambient temperatures for the purpose of becoming intoxicated’ ([4], p.23).

Volatile substances are central nervous system depressants which produce an immediate and intense intoxication for users. The onset of effect occurs rapidly because the extensive capillary surface of the lungs readily absorbs the vapour, causing blood levels to peak within minutes of use [5].

There are approximately 250 household, medical and industrial products that contain potentially intoxicating volatile substances [1]. Many of these are readily available and inexpensive.

Types of volatile substances

Volatile substances are usually classified into four groups [6]:

Methods of use

While the chemicals used in VSU are diverse, as is the broad range of effects, the main characteristic linking all of these substances is that they are almost exclusively inhaled [6]. Inhaling methods include:

Demographic information about volatile substance use

VSU is most commonly used by young people in ‘socioeconomically deprived and marginalised groups’ ([4], p.24). The four demographic groups most commonly identified are [1][4]:

Reasons why people use volatile substances

Volatile substances are used by people for a variety of reasons, including [7][8][9]:

Physical effects of volatile substance use

The psychoactive effects of inhaling volatile substances occur rapidly but only last for a short time (5 to 45 minutes after ceasing use) [3]. However, the fat soluble nature of volatile substances means that they can be stored in neurological tissues and have a prolonged effect on the level of consciousness for a much longer time period.

Many of the harmful physical effects from VSU are reversible, especially for infrequent users [3][4]. The damage caused by VSU is cumulative; chronic VSU is associated with an increased likelihood of permanent brain injury [1], although the extent of VSU-caused brain injury is debated in the literature [1][3].

There are short-term and long-term physical effects of VSU [1][3][6]:

Short-term physical effectsLong-term physical effects
  • a feeling of wellbeing
  • fatigue
  • headache
  • blurred vision
  • slurred speech
  • nausea and vomiting
  • increased risk-taking and loss of inhibition
  • agitation and aggression
  • confusion
  • hallucinations
  • loss of coordination
  • abdominal pain
  • heart palpitations
  • loss of consciousness
  • death
  • red, watery eyes
  • nosebleeds
  • lack of energy
  • indigestion
  • dizziness
  • frequent cough
  • shortness of breath
  • tinnitus (ringing in the ears)
  • angina (temporary chest pain)
  • stomach ulcers
  • chronic headache
  • sinusitis (inflammation of the area around the nose)
  • attention, memory and problem solving issues
  • depression
  • loss of hearing and sight
  • ataxia (lack of coordination of muscle movements)
  • seizures and epilepsy
  • reduced bone density
  • damage to the heart, lungs, liver and kidneys

Sudden sniffing death

Some inhalants can indirectly cause sudden death by cardiac arrest in a syndrome known as ‘sudden sniffing death’ [1][10]. The hydrocarbon gases present in the inhalants appear to sensitise the myocardium to adrenaline. In this state, a sudden surge of adrenaline (for example, from a frightening hallucination or intense physical activity) can cause a fatal cardiac arrhythmia. Sudden sniffing death can occur after a single use and is associated with the inhalation of butane, propane, and the chemicals found in aerosols [6].


Individuals who inhale petrol can die as a result of asphyxiation. The oxygen in the lungs is displaced by the inhaled petrol vapour which may stop the user from breathing [1][11]. Inhaling petrol from a bag or in a confined space (such as under a blanket) increases the risk of death from asphyxiation. The risk of death from asphyxiation also applies to Opal fuel [12]. Spraying volatile substances directly into the mouth is thought to cause asphyxiation since the cooling agents in the aerosol propellant freeze the larynx [13].

Cognitive and neurological impairments

Cognitive impairments

Cognitive impairments from VSU include a reduced attention span, short-term memory deficits, problem solving difficulties, and impairments to visual-spatial skills. The severity can range from mild impairment to severe dementia [14]. Cognitive impairments associated with VSU appear to be cumulative, but one study found that when controlling for socioeconomic disadvantage the differences in cognitive skills among people reporting VSU were not statistically significant [15].

Neurological impairments

Forms of neurological disorders, including Parkinson’s disease, appear to be linked to VSU [16][17][18]. The neurological damage caused by VSU is considered to be cumulative; chronic, long-term VSU is more likely to cause permanent brain injury or death than is infrequent VSU. Early studies suggested that brain injury associated with VSU was permanent [19][20], but recent evidence suggests that significant recovery from the effects of VSU is possible where abstinence occurs prior to the development of cerebellar atrophy [21][22][23][24].

Exposure to volatile substances during pregnancy

Volatile substances can cross the placental barrier, and prenatal exposure is associated with: spontaneous abortion; low birthweight; prematurity; developmental delays; neurobehavioral problems; physical malformations; and behavioural issues later in life [25].

Social effects of volatile substance use

VSU is associated with a variety of social harms that involve the individuals who use volatile substances, their families, their communities, and wider society [1]. While it is not possible to draw a causal relationship between VSU and the social effects, VSU is associated with social issues, including [1][4]:


  1. d'Abbs P, Maclean S (2008) Volatile substance misuse: a review of interventions. Barton, ACT: Australian Government Department of Health and Ageing
  2. MacLean S, D'abbs PH (2006) Will modifying inhalants reduce volatile substance misuse? A review. Drugs: Education, Prevention, and Policy; 13(5): 423-439
  3. Parliament of Victoria Drugs and Crime Prevention Committee (2002) Inquiry into the inhalation of volatile substances: final report. Melbourne: Parliament of Victoria
  4. Consensus-based clinical practice guideline for the management of volatile substance use in Australia (2011) National Health and Medical Research Council
  5. Wille SMR, Lambert WEE (2004) Volatile substance abuse—post-mortem diagnosis. Forensic Science International; 142(2-3): 135-156
  6. National Institute on Drug Abuse (2005) Research report series – inhalant abuse. Maryland: National Institute on Drug Abuse
  7. Carroll A, Houghton S, Odgers P (1998) Volatile solvent use among Western Australian adolescents. Adolescence; 33(132): 877–889
  8. Cheverton J, Schrader T, Scrogings Z (2003) Sniffing around the valley: chroming in Brisbane's inner-city. Brisbane: Brisbane Youth Service
  9. Brady M (1992) Heavy metal: the social meaning of petrol sniffing in Australia. Canberra: Aboriginal Studies Press
  10. Bass M (1970) Sudden sniffing death. Journal of the American Medical Association; 212(12): 2075-2079
  11. National Institute on Drug Abuse (2012) NIDA InfoFacts: inhalants. Retrieved 2010 from
  12. Cavanagh G (2008) Inquest into the death of Kenny Malthouse. Hermannsburg, NT: Coroner's Court, Northern Territory
  13. Chalmers E (1991) Volatile substance abuse. Medical Journal of Australia; 154(Feb 18): 269-274
  14. National Inhalant Abuse Taskforce (2005) National Directions on Inhalant Abuse: consultation paper. Melbourne: National Inhalant Abuse Taskforce
  15. Chadwick O, Yule W, Anderson R (1990) The examination attainments of secondary school pupils who abuse solvents. British Journal of Educational Psychology; 60(part 2): 180-191
  16. Hageman G, van der Hoek J, van Hout M, van der Laan G, Steur EJ, de Bruin W, Herholz K (1999) Parkinsonism, pyramidal signs, polyneuropathy, and cognitive decline after long-term occupational solvent exposure. Journal of Neurology, Neurosurgery and Psychiatry; 246(3): 198-206
  17. Pezzoli G, Canesi M, Antonini A, Righini A, Perbellini L, Barichella M, Mariani CB, Tenconi F, Tesei S, Zecchinelli A, Leenders KL (2000) Hydrocarbon exposure and Parkinson's disease. Neurology; 55(5): 667-673
  18. Ramón MF, Ballesteros S, Martinez‐Arrieta R, Jorrecilla JM, Cabrera J (2003) Volatile substance and other drug abuse inhalation in Spain. Clinical Toxicology; 41(7): 931–936
  19. Maruff P, Burns CB, Tuyler P, Currie BJ, Currie J (1998) Neurological and cognitive abnormalities associated with chronic petrol sniffing. Brain; 121(10): 1903-1917
  20. White RF, Proctor SP (1997) Solvents and neurotoxicity. The Lancet; 349(9060 (April 26)): 1239–1243
  21. Cairney S, Maruff P, Burns CB, Currie J, Currie B (2004) Neurological and cognitive impairment associated with leaded gasoline encephalopathy. Drug and Alcohol Dependence; 73(2): 183-188
  22. Cairney S, Maruff P, Burns CB, Currie J, Currie BJ (2004) Saccade dysfunction associated with chronic petrol sniffing and lead encephalopathy. Journal of Neurology, Neurosurgery and Psychiatry; 75(3): 472-476
  23. Cairney S, Maruff P, Burns CB, Currie J, Currie BJ (2005) Neurological and cognitive recovery following abstinence from petrol sniffing. Neuropsychopharmacology; 30(5): 1019-1027
  24. Rosenberg NL, Sharp CW (1997) Solvent toxicity: a neurological focus. Substance Use & Misuse; 32(12-13): 1859-1864
  25. Jones H, BalsterR (1998) Inhalant abuse in pregnancy. Obstetrics & Gynecology Clinics of North America; 25(1): 153-167

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Last updated: 2 April 2014
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