Hydrocarbons Toxicity 

Updated: Dec 17, 2019
Author: Mityanand Ramnarine, MD, FACEP; Chief Editor: Stephen L Thornton, MD 


Practice Essentials

Exposure to hydrocarbons is common in modern society. Hydrocarbons are easily accessible in products such as gasoline, turpentine, furniture polish, household cleansers, propellants, kerosene, and other fuels. Although hydrocarbons include all compounds composed predominantly of carbon and hydrogen, the compounds of interest are derived from petroleum and wood. Most of the dangerous hydrocarbons are derived from petroleum distillates and include aliphatic (straight-chain) hydrocarbons and aromatic (benzene-containing) hydrocarbons. Other hydrocarbons such as pine oil and turpentine are derived from wood.

Types of exposure include unintentional ingestion, intentional recreational abuse, unintentional inhalation, and dermal exposure or oral ingestion in a suicide attempt. The highest rates of morbidity and mortality result from accidental ingestion by children younger than 5 years. Aspiration pneumonitis is the most common complication of hydrocarbon ingestion, followed by central nervous system (CNS) and cardiovascular complications.


Halogenated hydrocarbons, like carbon tetrachloride, and trichloroethylene, are more likely than others to be absorbed systemically, leading to varied effects depending on their toxic potential.The toxic potential of hydrocarbons is directly related to both the dose and the compound’s physical properties: volatility, solubility, viscosity, and surface tension.

Viscosity refers to the compound’s resistance to flow (eg, gasoline and mineral oil have low viscosity). As the viscosity increases, the aspiration potential decreases.

Volatility refers to the compound’s ability to vaporize. The higher the volatility, the easier the compound is to inhale. Thus, highly volatile compounds with low viscosity are more likely to be inhaled or aspirated. Simple petroleum distillates such as kerosene, mineral oil, gasoline, and furniture polish are examples of such substances that are easily aspirated.

Compounds that are lipophilic are able to cross the blood-brain barrier, leading to CNS effects.  Halogenated hydrocarbons (eg, methylene chloride, chloroform, carbon tetrachloride) and aromatic hydrocarbons (eg, benzene, toluene, xylene) are easily absorbed through respiratory and gastrointestinal mucosa, often leading to CNS toxicity.

Pulmonary effects

Pulmonary toxicity is the result of hydrocarbon aspiration causing direct effects on lung parenchyma. Low-viscosity, highly volatile hydrocarbons, such as kerosene and mineral oils, are easiest to aspirate. The hydrophobic nature of hydrocarbons allows them to penetrate deep into the tracheobronchial tree, producing inflammation and bronchospasm. These volatile chemicals can displace alveolar oxygen, leading to hypoxia.

Direct contact with alveolar membranes can lead to hemorrhage, hyperemia, edema, surfactant inactivation, leukocyte infiltration, and vascular thrombosis, resulting in poor oxygen exchange, atelectasis, and pneumonitis. Hypoxia ensues secondary to ventilation/perfusion mismatch, shunt formation, and bronchospasm. Respiratory symptoms generally begin in the first few hours after exposure and usually resolve in 2–8 days.

Complications include hypoxia, barotrauma due to mechanical ventilation, and acute respiratory distress syndrome (ARDS). Prolonged hypoxia may result in encephalopathy, seizures, and death.

Gastrointestinal effects

Local irritation is the usual GI manifestation of hydrocarbon ingestion. Abdominal pain and nausea are common complaints. Vomiting increases the likelihood of pulmonary aspiration. Hepatotoxicity occurs more frequently with occupational exposure and is less likely to result from inhalant use.

CNS effects

Hydrocarbon toxicity produces various CNS effects. After inhalation, hydrocarbons are absorbed through the lungs into the bloodstream. Most of these chemicals are CNS depressants, with Initial effects similar to the disinhibition observed in patients with alcohol intoxication. Effects occur in a dose-dependent manner. Narcotic-like depression may also be observed. Euphoria may develop, as in alcohol or narcotic toxicity. Eventually, lethargy, headache, obtundation, and coma may follow. Seizures are uncommon and are believed to be due to hypoxia.

Acute exposure leads to an increase in gamma-aminobutyric acid (GABA) and glycine function. With more chronic exposure, these effects become blunted as tolerance develops. Activation of the mesolimbic dopaminergic system is also thought to be responsible for the addictive properties of these agents.

Hydrocarbon inhalation induces oxygen radicals that persist for up to 24 hours, exerting the greatest effect on the hippocampus. The most pronounced effects are seen in the developing brain; this would account for the learning and memory deficits experienced by adolescents who abuse hydrocarbons.

Cardiac effects

 Dysrhythmias are a major concern, especially in adolescents. It is thought that exposure sensitizes the myocardium to endogenous catecholamines, leading to ventricular arrhythmias with virtually no warning. By inhibiting calcium influx and sodium potassium channels, they facilitate after-depolarization, leading to enhanced automaticity. Halogenated hydrocarbons are thought to put patients at greater risk for such arrythmias.

Hypoxia and direct myocardial damage from inhalation may also put patients at risk. Prolonged use may lead to structural damage, including edema, intramyocardial hemorrhages, contraction band necrosis, rupturing of myofibrils, interstitial fibrosis, and myocarditis, which may impede normal cardiac function. Some hydrocarbons may also act as negative inotropes via direct effects on conduction through the atrioventricular node and chronotropic effects. Sudden death has been reported as a result of coronary vasospasm following inhalation

Renal effects

Hydrocarbon toxicity can lead to metabolic acidosis, hyperchloremia, and hypokalemia resulting from distal renal tubular acidosis. Anion gap acidosis occurs as the compounds are metabolized, and sodium and potassium are lost via renal excretion along with these metabolites.

Dermal effects

Skin exposure can result in mild inflammation or chemical burns. The ability of a particular hydrocarbon to permeate the skin depends on the agent’s size, lipophilicity, and structure. Repeated exposure to an agent can also cause sensitization resulting in allergic dermatitis. Injection may cause skin necrosis, thrombophlebitis, abscess formation, necrotizing fasciitis, and compartment syndrome. Mucous membrane exposure may result in irritation or chemical burns

Other effects

Up to 60% of patients exposed to hydrocarbons will present with fever, which typically resolves within 48 hours. Hydrocarbons are reported to cause bone marrow toxicity and hemolysis. Leukocytosis may occur early on in the clinical course, with or without pneumonitis, with resolution typically within 1 week. Chlorinated hydrocarbon toxicity may cause hepatic and renal failure, and toluene toxicity may lead to renal tubular acidosis. Direct contact with the skin and mucous membranes may cause effects ranging from local irritation to extensive chemical burns.

Frequent users are more likely to experience depressed mood. Recreational or occupational exposure can lead to memory loss, attention deficits, and learning and judgment deficits.


Aliphatic hydrocarbons include the following:

  • Fuels [1, 2]
  • Solvents
  • Furniture polish and paints

Aromatic hydrocarbons include the following[3, 4, 5, 6] :

  • Plastics
  • Solvents
  • Glues

Halogenated hydrocarbons include the following:

  • Refrigerants
  • Propellants
  • Cleaning products
  • Paint strippers
  • Solvents

Wood distillates include the following:

  • Turpentine
  • Pine oil


In 2017, 27,613 single exposures to hydrocarbon poisoning were reported to US poison control centers. Of those, 9001 were in children younger than 6 years of age, and another 3289 were in older children and teenagers. Moderate outcomes were reported in 1628 cases overall, major outcomes in 123, and death in 16 cases. Hydrocarbons account for 5% of all single-substance fatalities in children yournger than 6 years and is the second most common cause of nonpharmaceutical exposure fatality in adolescents ages 13 to 19 years of age.[7]

Unintentional ingestion usually occurs in children younger than 5 years.[8] Improper storage and mislabeled containers of hydrocarbons are common contributing factors. Abuse by inhalation is most common in adolescents and young adults.


Pulmonary toxicity is the major cause of morbidity and mortality. Approximately 20 deaths per year result from hydrocarbon poisoning; most of these deaths occur in children younger than 5 years. Long-term exposure may result in significant morbidity. Cardiomyopathy, cerebellar atrophy, dementia, cognitive deficits, and peripheral neuropathy have all been reported with long-term hydrocarbon inhalant abuse. Sudden death has been reported as a result of coronary vasospasm due to hydrocarbon inhalation.

Aspiration pneumonitis is the most common complication of hydrocarbon ingestion, followed by CNS and cardiovascular complications. The major respiratory complications are aspiration and lung injury secondary to pneumonitis.[9] Pneumothoraces and barotrauma are potential complications of mechanical ventilation. Most patients improve after 24 hours, and symptoms resolve within 1 week.

CNS complications include seizures, encephalopathy, and memory loss. These sequelae are usually believed to be secondary to a hypoxic insult. Myocarditis and cardiomyopathy are reported cardiovascular complications of hydrocarbon toxicity.

Patient Education

Patient education is crucial in the prevention of unnecessary or accidental exposure. Most exposures in young children are accidental and can be prevented. Teaching points include the following:

  • Parents should teach young children about the dangers of poisons, beginning at an early age

  • Advise the parents about the proper storage and labeling of harmful chemicals

  • Inform parents about common household products that may be dangerous, and recommend steps that they can take to minimize the possibility of an accidental exposure

  • Educate parents that they need to supervise their children when they are in high-risk areas (eg, kitchen, garage, laundry room) where toxic substances may be present.

  • Provide the parents with the telephone number of their local poison control center

For patient education information, see Poisoning Treatment and Childproof Your Home.




Typical features of unintentional hydrocarbon ingestion include the following:

  • The most common scenario involves a young child whose ingestion is often not witnessed; the parent may smell the chemical on the child's skin, clothing, or breath, or they may report that their child is coughing, choking, cyanotic, or vomiting

  • If the ingestion is unwitnessed, the amount ingested is usually impossible to quantify

  • Sources of ingested hydrocarbons range from cleaning products in the kitchen to solvents in the garage; often, these chemicals are not properly labeled, or they are inadvertently stored in a beverage container

  • A history of coughing, choking, vomiting, or cyanosis is highly correlated with the likelihood of pulmonary aspiration

Intentional inhalation of volatile hydrocarbons uses the following techniques:

  • Sniffing involves inhaling the fumes of a liquid from an open container

  • Huffing involves applying the chemical to a cloth or rag and then inhaling the hydrocarbon by covering the nose and mouth with the cloth or rag

  • Bagging involves placing the hydrocarbon in a bag and then placing the bag over the face to inhale the fumes

Physical Examination

In cases of hydrocarbon aspiration, the patient's temperature may be elevated due to the body's reaction to the foreign substance. Respiratory, central nervous system (CNS), and gastrointestinal (GI) findings may be present, as well as cardiac arrhythmias, mucosal irritation, and chemical burns of the skin.

Respiratory findings may include the following:

  • Coughing
  • Choking
  • Tachypnea
  • Grunting
  • Cyanosis
  • Rales
  • Wheezing

CNS findings may include the following:

  • Dizziness
  • Lethargy
  • Ataxia
  • Seizures
  • Coma

GI findings may include the following:

  • Nausea
  • Vomiting
  • Abdominal pain

Acute Inhalation

CNS intoxication occurs in three stages.[10]  Stage 1 includes mild effects that users may find enjoyable, and thus lead to chronic abuse.These effects include euphoria, excitability, disinhibition, and impulsive behavior. However, stage 1 also commonly features headache, dizziness, and nausea, followed by dysesthesia of tongue, numbness of legs, muscular weakness, tinnitus, blurry vision/diplopia, tremors, and ataxia. Some users may also exhibit aggressive behavior, irritability, amnesia, and slurred speech.

Stage 2 involves CNS depression. Slurred speech, confusion, and hallucination are the most common findings in this stage. In stage 3, the CNS depression seen in stage 2 further progresses to obtundation, coma, seizures, and possibly death.

Sudden cardiac death may occur after an acute heavy exposure to high concentrations of hydrocarbons, followed by physical exertion or extreme excitation due to the myocardial sensitization to the surge in epinephrine circulating during such instances. Coronary vasospasm may also occur, leading to acute myocardial infarction.

Chronic Inhalation

The most common sequelae of long-term use include muscle weakness, tremor, and peripheral neuropathy. No definite timeframe of use has been determined for onset of signs of chronic inhalation, with no clear cumulative dose-response relationship. However, most of the signs do not develop until the persons has been inhaling hydrocarbons two to three times weekly for about 6 months.[10]

Chronic use leads to memory impairment and may place users at higher risk of psychiatric disorders. In one study of adult inhalant users, the prevalence of such disorders was as follows[10] :

  • Mood disorders – 48%
  • Anxiety disorders – 36%
  • Personality disorders – 45%

Disorders that result from long-term hydrocarbon inhalation may be reversible with discontinuation of use. Resolution of the disorder may be incomplete, however.





Laboratory Studies

After acute inhalation, hydrocarbons are not typically detected on routine drug screens, though specific inhalants can be detected on gas chromatography performed within 10 hours of exposure. With methylene chloride exposure (eg, occupational exposure from paint stripping), carboxyhemoglobin concentrations will be elevated. If the history suggests halogenated hydrocarbon exposure, liver function tests should be perofrmed to evaluate for signs of hepatic injury.

Arterial blood gas analysis is useful in documenting hypoxemia in severely affected patients. Hypercarbia may be observed in patients with respiratory depression and decreased gas exchange.

In the acute phase, serum chemistry results are expected to be within the normal ranges. An increased anion gap (see the Anion Gap calculator) may indicate co-ingestion of another toxin.

In chronic inhalant abuse, elevated creatine phosphokinase (CPK) concentrations with rhabdomyolysis can occasionally be seen. Laboratory studies generally reveal low bicarbonate and low potassium levels, with no anion gap. Hematuria and pyuria have also been reported.

Imaging Studies

In cases of acute exposure, no definite radiographic changes will be seen on chest x-ray, head computed tomography (CT), or brain magnetic resonance imaging (MRI). With aspiration, however, hydrocarbon pneumonitis may ensue, with chest x-ray findings developing over the course of hours (see the image below). Such findings may include bilateral interstitial infiltrates, usually in the middle and lower lobes, air bronchograms, pneumatocele, atelectasis, and pleural effusions. These abnormalities can persist for months.

Hydrocarbon pneumonitis. Hydrocarbon pneumonitis.

Nonfatal cases of pneumonitis typically resolve within 1 week. However, cases resulting from mineral or lamp oil ingestion may require 5-6 weeks for resolution. Repeat chest films should be obtained if any acute change in a patient’s respiratory status occurs, because a pneumothorax and pneumomediastinum may develop. If discharge is being considered for an asymptomatic patient, a chest radiograph should be obtained 6 hours after the ingestion to document the negative findings.

On brain MRI, abnormalities suggested to be related to cumulative inhalant exposure most commonly include white matter changes and subcortical abnormalities in the thalamus, basal ganglia, pons, and cerebellum. These abnormalities are possibly the result of axonal damage and gliosis, although the mechanism is not clearly defined. These findings tend to start in the periventricular region, then extend into the subcortical white matter.

Other findings on brain scans in chronic inhalant abusers include the following[10] :

  • Cerebral and cerebellar atrophy
  • Atrophic dilatation of the ventricles
  • Widening of the cerebral/cerebellar sulci
  • Hypointensity of the thalami
  • Hypointensity of the red nuclei and substantia nigra
  • Hyperintensity of the dentate


Other Tests

Bedside pulse oximetry is useful in the emergency department because hypoxia is a direct result of hydrocarbon aspiration.

An electrocardiogram (ECG) should be obtained in all patients thought to have exposure to hydrocarbons. ECG changes may include the following:

  • Atrioventricular (AV) blockade
  • Atrial fibrillation
  • Premature ventricular contractions
  • Supraventricular tachycardia
  • QT interval prolongation
  • ST segment elevation
  • Sinus bradycardia
  • Ventricular fibrillation


Medical Care

Stabilization of the airway is always the first priority of treatment in patients with hydrocarbon poisoning. Give supplemental oxygen to all patients, and perform bedside pulse oximetry. Early intubation, mechanical ventilation, and use of positive end-expiratory pressure may be warranted in a patient with inadequate oxygenation, severe respiratory distress, or a decreased level of consciousness. Take all precautions to minimize the patient's risk of vomiting and further aspiration. A trial of bronchodilators may prove useful in patients with suspected bronchospasm.

Routine use of steroids or antibiotics is not generally advocated, however, some studies have demonstrated beneficial effects of prophylactic use of steroids and antibiotics to prevent chemical pneumonitis.[9]

Cutaneous decontamination is indicated in cases of cutaneous exposure: Decontaminate the skin as soon as possible by removing the involved clothing and thoroughly washing the skin with soap and water. Vapor inhalation and cutaneous absorption may occur long after the exposure. Health care providers must take precautionary action to minimize their own exposure to the toxic substance.

Gastric decontamination in cases of oral ingestion is controversial. Ipecac-induced emesis is contraindicated in patients who have ingested a low-viscosity hydrocarbon (eg, gasoline, kerosene, furniture polish, mineral spirits) because the aspiration risk is high.[11]

Before gastric decontamination is performed, the airway must be stabilized to minimize the risk of aspiration if the patient vomits. Because aspiration is a major complication of hydrocarbon ingestion, reserve gastric decontamination for patients with large intentional ingestions or those at increased risk of systemic toxicity.

Regarding gastric lavage, the risk and complications of aspiration generally outweigh the benefits. Lavage is useful in cases in which the hydrocarbon has an inherent systemic toxicity or contains additives with known toxicity. A useful mnemonic for remembering such hydrocarbons is CHAMP, which stands for camphor, halogenated hydrocarbons, aromatic hydrocarbons, (heavy) metal-containing hydrocarbons, and pesticide-containing hydrocarbons. If lavage is attempted, nasogastric lavage is advised because the ingested substance is a liquid, and the use of a large-caliber orogastric tube greatly increases the risk of vomiting and aspiration.

Activated charcoal has a limited role in the management of hydrocarbon ingestion. Charcoal poorly adsorbs most hydrocarbons. Furthermore, charcoal tends to distend the stomach and cause vomiting, increasing the aspiration potential. The use of activated charcoal is indicated in cases of a suicide attempt or in cases in which another adsorbable toxic substance have been co-ingested.

Patients who have respiratory symptoms consistent with hydrocarbon aspiration should be observed or admitted to the hospital for at least 12 hours.

Patients whose respiratory symptoms improve during this time may be safely discharged home. Patients who have respiratory distress and require mechanical ventilation should be admitted to an intensive care unit.

Patients with hydrocarbon poisoning may be safely discharged home if all of the following conditions are met:

  • They have been observed in the emergency department for at least 6 hours
  • They are asymptomatic
  • Their chest radiography findings are normal
  • They are instructed to return if respiratory symptoms develop


Contact the local poison control center in all hydrocarbon ingestions. Consult a psychiatrist, psychologist, or other mental health professional if the exposure was a result of a suicide attempt. A substance abuse professional may provide assistance in cases of recreational or long-term hydrocarbon abuse.


For primary prevention, see Patient Education.

Inhalant abuse occurs in adolescents and adults and should be deterred. Hydrocarbons may be inhaled for recreation, similar to drugs and alcohol. Hydrocarbons might also be inhaled as part of suicidal gestures and attempts. Considerations include the following:

  • Treatment of the underlying causes of these behaviors might help in preventing hydrocarbon use.
  • Maintain a high index of suspicion with any adolescent who has signs of alcohol intoxication or recreational drug use.
  • Immediately address any suspicions of inhalation abuse with the patient's parent or regular physician.


Medication Summary

No specific antidotes are available for hydrocarbon poisoning. Treatment with prophylactic antibiotics is not beneficial.[12] Corticosteroid therapy is also not beneficial, and may be harmful in some cases.