Hydrocarbon Inhalation Injury

Updated: Mar 29, 2017
  • Author: Rakesh Vadde, MBBS; Chief Editor: Denise Serebrisky, MD  more...
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Inhalation injury due to hydrocarbons can occur as a result of either accidental or intentional exposure. Inhalant abuse, the deliberate inhalation of hydrocarbons as a form of recreational drug use, has become a significant health issue affecting children. Epidemiologic data state that, among adolescents, inhalants are the second most widely used class of illicit drugs; more than 2 million children aged 12-17 years report using inhalants at least once in their lifetime. Death from intentional inhalation of hydrocarbon fumes is not uncommon and is usually due to sudden cardiac events or CNS depression. The recognition and treatment of inhalant abuse remain challenges for pediatricians and emergency physicians.

Deliberate inhalation of volatile hydrocarbons for their mood-altering effects is popular among adolescents. Their low cost, ready availability, and ease of use contribute to this problem. Volatile hydrocarbons are contained in glues, solvents, lighter fluid, gasoline, and paints. Most inhalants are composed of several compounds, and almost all pressurized aerosol products can be abused because the propellants are volatile hydrocarbons. Inhalation is most commonly achieved by sniffing, huffing, or bagging. [1, 2]

In young children, ingestion typically occurs as an exploratory behavior. The hydrocarbon is frequently unsecured or improperly stored in a drinking container. Since 2001, The US Consumer Product Safety Commission has required child-resistant packing of products that have low viscosity and contain greater than 10% hydrocarbon by weight. [3]

The majority of intoxication reports of hydrocarbons are due to inhalation or ingestion, but a few case reports have described intravenous ingestion of gasoline for suicide. [4]



The exact mechanism of action for the volatile substances on the whole is unknown. Two theories have been postulated for the mechanism of action of inhalants. One hypothesis is that the volatile solvents produce a generalized slowing of axonal ion-channel transport by altering the membranes, similar to anesthetic gasses. [5] The second theory suggests that potentiation of the GABA receptors occurs; a cross-tolerance between 1,1,1-trichloroethane, toluene, ethanol, barbiturates, and benzodiazepines is noted. [6]

Recreational abuse of hydrocarbons by inhalation is accomplished in 3 ways: sniffing, huffing, and bagging. Sniffing, the least potent delivery method, is the inhalation of the volatile substance through the nostrils (ie, sniffing glue). Huffing is the placing of a rag soaked with an inhalant such as gasoline or lighter fluid over the nose and mouth. Bagging involves repeated deep inhalations from a plastic or paper bag filled with a particular hydrocarbon such as spray paint or another propellant.

Chronic abusers generally inhale 3-4 times daily for 10-15 minutes each time, although prolonged sessions of inhaling 6-7 hours a day as a group activity have been described. Tolerance and physical dependence can occur, although withdrawal symptoms are only infrequently reported.

Two primary organ systems are affected by inhalation hydrocarbon toxicity: the CNS and the cardiopulmonary system. Volatile hydrocarbons are highly lipid soluble and readily cross the blood-brain barrier. Rapid absorption occurs across the large surface area of the pulmonary vascular bed, and peak blood levels are noted approximately 15-30 minutes after inhalation. Confusion, disorientation, disinhibition, and euphoria are exhibited early. Speech becomes slurred, and motor function becomes impaired, with gait becoming staggered. Hallucinations are frequently described, followed by CNS depression, drowsiness, and sleep. Coma can occur with prolonged or repeated exposures; however, this is unusual because the intentional exposure ceases as the user becomes drowsy.

Sudden sniffing death syndrome was first described by Bass in 1970. [7] Death occurs after the user is startled during or soon after inhalation. Hydrocarbons can sensitize the myocardium to endogenous and exogenous catecholamines, which can precipitate ventricular dysrhythmias and sudden death. [8, 9] In addition, some limited data have shown toxic effects of hydrocarbons directly on the myocardium, and excess catecholamine concentrations may cause an increase in oxygen demand, coronary artery spasm, platelet aggregation, and thrombus formation. [10] Numerous case reports also detail acute myocardial infarction as a complication following hydrocarbon inhalation. [11, 12, 13]

With acute intoxication, deaths due to asphyxiation from a plastic bag over the head or from aspiration of stomach contents are not unusual. Also, trauma-related injury and motor vehicle accidents have been reported, resulting from disinhibition and disorientation following inhalation.

Other reported complications include renal tubular acidosis with subsequent hypokalemia and hyperchloremia; frostbite with facial injury and burns to the trachea, mainstem bronchi, esophagus, and oral cavity due to intentional inhalation of fluorinated hydrocarbon; bone marrow damage, aplastic anemia, and leukemia due to benzene exposure; and toxic hepatitis due to toluene exposure. [14, 15, 13, 16, 17] In contrast to pulmonary injury from aspiration of liquid hydrocarbons, direct pulmonary injury from acute inhalation exposure has not been described.

Many solvents, particularly toluene, are lipophilic and readily cross the placenta, resulting in characteristic fetal anomalies that include microcephaly, narrow bifrontal diameter, short palpebral fissures, hypoplastic mid face, wide nasal bridge, abnormal palmar creases, and blunt fingertips. The syndrome of toluene embryopathy closely resembles the phenotypic features found in fetal alcohol syndrome. [18, 19]

With long-term hydrocarbon inhalation, CNS damage occurs, including loss of cognitive functions, gait disturbances, and loss of coordination. Radiographic tests have demonstrated loss of brain mass and white-matter degeneration. Additionally, certain chemicals have been shown to have associations with specific CNS injuries, including peripheral neuropathy, deafness, and optic neuropathy. Other, less common complications of long-term hydrocarbon inhalation include restrictive pulmonary disease, pulmonary hypertension, and reduced diffusion capacity. [20, 21, 22]

Pulmonary toxicity can occur as a result of hydrocarbon aspiration. This injury differs from hydrocarbon inhalation injury. The most common clinical scenario of hydrocarbon aspiration is a young child unintentionally ingesting a hydrocarbon-containing compound such as lamp oil or a cleaning solvent (see the image below). [23]

Anteroposterior view of the chest of 14-month-old Anteroposterior view of the chest of 14-month-old boy 30 hours after ingesting lamp oil. Note the central right lower lobe infiltrate obscuring the right heart border.

Hydrocarbons cause direct injury to the respiratory epithelium, producing inflammation and bronchospasm. Direct contact with alveolar membranes can lead to hemorrhage, hyperemia, edema, surfactant inactivation, leukocyte infiltration, and vascular thrombosis. The result is poor oxygen exchange, atelectasis, and pneumonitis. [24] For more information, see Toxicity, Hydrocarbons.




United States

National surveys of adolescents in the United States have revealed that, after marijuana, inhalants are the most commonly used class of illicit drugs for 8th and 10th graders; inhalants are the third most widely used illicit drugs for 12th graders. [25] The low cost, ease of use, and ready availability of organic solvents perpetuate their abuse. Epidemiologic data suggest a decrease in the prevalence of inhalant abuse, but overall abuse rates remain high.

Inhalant abuse by adolescents in the United States is common. In 2000, more than 2 million adolescents aged 12-17 years reported using inhalants at least once in their lifetime. [26] Since 1975, the National Institute on Drug Abuse annual survey of high-school seniors has documented a lifetime incidence of inhalant abuse of 15-20%, with the highest prevalence of use being in 8th graders. [27, 28]

Although the trend of lifetime use decreases between the 8th and 12th grades, these data may underestimate the true lifetime use of older adolescents because many students have dropped out of school by the 12th grade and, thus, are no longer included in the survey.

The typical person who abuses inhalants is a young male of lower socioeconomic class. Overall, males are twice as likely to abuse inhalants as females; however, between the 8th and 12th grades, the difference is less pronounced. Immigrants from Latin America and American Indians have a higher prevalence of use, and blacks have a low prevalence of inhalant abuse. Although inhalant abuse is typically thought of as being most common among adolescents, abuse among adults is also well described, and abuse in children as young as age 4-6 years has been reported. [29, 30, 27]

A study reported that inhalant use prevalence rates generally declined from 1991 to 2011, however, the proportion of females and Hispanics among lifetime users increased. [31]

According to the National Institute on Drug Abuse, research shows that inhalant users initiate use of cigarettes, alcohol, and almost all other drugs at younger ages than those who did not use inhalants. In addition, early inhalant users are more likely to develop substance abuse disorders, including abuse of prescription drugs, compared with other substance abusers with no history of inhalants use. [32]


The United Kingdom is the only major country in the Western world that tracks inhalant abuse fatalities; an incidence of 2 deaths per week has been documented. In Canada, the patterns of inhalant use are similar to those associated with other illicit substances for experimenters, intermittent users, and long-term abusers. Long-term use tends to be endemic in both the inner-city areas and remote communities, and data show an association between chronic use, lower socioeconomic class, and family dysfunction.


Although hydrocarbon inhalation was previously thought to be a benign fad, permanent and significant pulmonary and neurologic sequelae clearly may persist even after abuse has discontinued. Recreational solvent inhalation may account for as much as 2% of all deaths among adolescent males. In the United Kingdom, 15% of deaths caused by inhalants occur as a result of suffocation, 15% are a result of accidental trauma, and 15% are a result of aspiration, whereas the remaining 55% are a result of sudden sniffing death syndrome. [33, 34] The fact that 22% of victims of sudden sniffing death syndrome had no history of inhalant abuse is of significant concern, demonstrating that death can result from any episode of inhalant abuse.

In the United States, inhalant abuse was responsible for 12.2% of the deaths reported to poison control centers in the group aged 13-19 years. Given that many inhalant-related deaths are never reported to poison control centers, this statistic grossly underestimates the true mortality due to inhalant abuse. [27]

Ongoing inhalant use has been associated with significant psychosocial pathology, including failure in school and delinquency; a high correlation between poor academic performance and inhalant abuse is noted. In patients with neurologic symptoms who abused toluene as an inhalant, nearly one third showed deficits in orientation, attention, learning, arithmetic calculation, abstraction, construction, and recall. [35, 29]

As solvent abuse becomes chronic, damage to the CNS becomes irreversible, with changes occurring in the cerebellar and cerebral white matter, including demyelination and gliosis. [36] Psychiatric disorders, spasticity, cognitive changes, and secondary Parkinson disease have been reported. Attention deficit and decreased memory retrieval may also occur. [37]


Previous data suggested the highest inhalant abuse to be among Latin American immigrants. In adolescents aged 12-17 years, inhalant users were more likely to be American Indian or Alaskan Native (13.2%), followed by multiracial (11.2%) and white (9.5%). [38, 27] Lowest reported rates were among blacks (5.3%) and Asians (6.5%).


According to data from Wu et al in 2004, the lifetime prevalence rates of inhalant abuse were not significantly different for males and females aged 12-17 years. [27]


Peak age of inhalant abuse is 14-15 years, with onset of abuse occurring from ages 6-8 years. Use typically declines by the late teenage years; however, some users continue to abuse inhalants into adulthood.