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Hydrocarbons Toxicity

  • Author: Mityanand Ramnarine, MD, FACEP; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Aug 17, 2015
 

Background

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.

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Pathophysiology

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.

GI 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.

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Epidemiology

Frequency

United States

In 2013, 31,031 cases of hydrocarbon poisoning were reported to US poison control centers. Of those,  9622 were in children younger than 6 years of age, and another 3800 were in older children and teenagers. Moderate outcomes were reported in 1700 cases overall, major outcomes in 122, and death in 18 cases.[1] Hydrocarbons account for 1-2% of nonpharmacologic exposures in children under 6 years of age and 10% of all single-substance fatalities in children.

Mortality/Morbidity

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.

Age

Unintentional ingestion usually occurs in children younger than 5 years.[2] Improper storage and mislabeled containers of hydrocarbons are common contributing factors. Abuse by inhalation is most common in adolescents and young adults.

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Contributor Information and Disclosures
Author

Mityanand Ramnarine, MD, FACEP Assistant Professor of Emergency Medicine, Program Director, Emergency/Internal Medicine/Critical Care, Hofstra Northwell School of Medicine at Hofstra University; Attending Physician, Department of Emergency Medicine, Long Island Jewish Medical Center

Mityanand Ramnarine, MD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Physicians, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Lisa M Santoriello, MD Resident Physician, Departments of Emergency Medicine and Internal Medicine, Long Island Jewish Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Received salary from Merck for employment.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

William T Zempsky, MD Associate Director, Assistant Professor, Department of Pediatrics, Division of Pediatric Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center

William T Zempsky, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Acknowledgements

Randy J Goldstein, MD  Medical Director of Emergency Department, Las Palmas Medical Center

Randy J Goldstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.  

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