Inhalant Abuse

Intentional misuse of volatile substances (or inhalants) is a significant risk for morbidity and mortality in youth worldwide. According to the findings of the 2008 National Survey on Drug Use and Health, 729,000 persons aged 12 or older used inhalants for the first time within the past 12 months; 70.4 percent were under age 18 when they first used. Annual estimates of first-time users have decreased since 2003, although the average age at first use among recent initiates has decreased from 17.1 years in 2007 to 15.9 years in 2008. [Office: 2009] While national survey data suggest the use is equal in males and females, more males were involved in cases reported to poison control suggesting that boys engage in riskier behaviors. Propellants, gasoline, and paint are the products most commonly reported to poison control centers; butane, propane, and air fresheners have the highest fatality rates.[Marsolek: 2010]

Volatile substances are attractive to youth because they are inexpensive, legal, and often readily available in the household or local stores. The “high” achieved occurs and resolves relatively quickly in comparison with other drugs of abuse, allowing the user to sniff after school and still return home sober.[Kurtzman: 2001] As inhalants are readily available in household products or purchased easily, they are often the first drug of abuse tried.[Young: 1999] Inhalant abuse has been shown to be a predictor of abuse of other substances, intravenous drugs in particular.[Dinwiddie: 1991] Adolescents who have abused inhalants are also at risk for depression and suicidality.[Sakai: 2004] Individuals with inhalant use disorders are more likely to exhibit interpersonal violence with physical cruelty to other people and animals as well as use of dangerous weapons.[Howard: 2010]

Individuals inhale substances such as glue, paints, correction fluid, butane, and gasoline to induce a “high” or state of euphoria. Volatile inhalation results in rapid delivery of the lipophilic inhalant to the central nervous system. Methods of inhalation include “sniffing,” in which the inhalant is directly sniffed, “bagging,” in which the substance is inhaled from a paper or plastic bag, and “huffing,” in which the substance is inhaled orally from a cloth saturated with the inhalant held close to the nose and mouth. Habitual users typically begin “sniffing” and progress to “huffing” to induce a more rapid and prolonged euphoria.[Kurtzman: 2001]

Toxic effects of inhalant abuse have been identified in multiple organ systems:
  • Neurologic. All inhalants have the potential for CNS toxicity, and toluene (found in glues and solvents) is particularly damaging. Prolonged use of toluene may result in encephalopathy, cognitive dysfunction, dementia; cortical atrophy and cerebellar changes may be seen upon neuroimaging.[Malm: 1980] [Fornazzari: 1990] In some cases, CNS impairment is permanent. Peripheral neuropathy has been reported as a consequence of habitual inhalant abuse.
  • Cardiovascular. Hypotension and tachycardia occur at low doses; bradycardia seen at higher doses.[Zee-Cheng: 1985] Lethal arrhythmia (sudden sniffing death syndrome (SSDS)) has been reported.[Bass: 1970]
  • Renal. Renal tubular acidosis (RTA), urinary calculi, and glomerulonephritis have been associated with inhalant use, particularly toluene.[Batlle: 1988]
  • Pulmonary. Volatiles displace oxygen in the alveoli causing hypoxia. Inhaled solvents can cause a chemical pneumonitis, exacerbating hypoxia. Asphyxia may occur during “bagging.”
  • Hepatic. Toxin-mediated hepatitis progressing to liver failure has been reported.[Kaplan: 1979]
  • Hematologic. Bone marrow suppression and leukemia have been associated with chronic occupational solvent inhalation.[Vigliani: 1976]
  • Intrauterine exposure. Inhaled solvents readily cross the placenta and are known teratogens. Prenatal toluene exposure, in particular, is associated with oral clefts, micrognathia, microcephaly, growth deficiency, and developmental delay.[Pearson: 1994] Features may be similar to those associated with fetal alcohol exposure. Neonatal renal tubular acidosis has also been reported with prenatal toluene exposure.

Clinical presentations are classified in four stages ranging from immediate euphoric effects through severe CNS depression:[Kurtzman: 2001]
  • Immediate effects include excitation, eurphoria, and disinhibition; respiratory (cough, wheeze, sneezing) and gastrointestinal (salivation, abdominal pain, nausea, vomiting, diarrhea) symptoms may be present.These effects generally resolve within 2 hours.
  • Second stage: progressive CNS depression with slurred speech, delusions, disorientation, tremor, visual changes, weakness, headache, and visual hallucinations
  • Third stage: severe CNS depression is present with ataxia, obtundation, hyporeflexia, nystagmus
  • Fourth stage: stupor, seizures, coma, arrhythmia, and death (many individuals who die from SSDS have no previous known history of inhalant abuse) may occur.

Management of acute intoxication with inhaled solvents is supportive with attention to respiratory status and oxygenation, providing support for airway, breathing, and circulation as appropriate.[Kurtzman: 2001] Close attention must be paid to vital signs as well as neurologic status. Cardiopulmonary monitoring is recommended due to the risk of arrhythmia and respiratory depression. Oxygen should be administered as needed along with intravenous hydration and decontamination of skin and clothes.

Authors & Reviewers

Initial publication: June 2010; last update/revision: June 2010
Current Authors and Reviewers:
Author: Catherine Jolma, MD

Page Bibliography

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