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Hydrocarbon Toxicity

  • Author: Michael D Levine, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Apr 21, 2015
 

Background

Hydrocarbons are a heterogenous group of organic substances that are primarily composed of carbon and hydrogen molecules. They are quite abundant in modern society. Some of the most commonly ingested hydrocarbons include gasoline, lubricating oil, motor oil, mineral spirits, lighter fluid/naphtha, lamp oil, and kerosene.[1] Other common sources of hydrocarbons include dry cleaning solutions, paint, spot remover, rubber cement, and solvents. In addition, many volatile substances that contain hydrocarbons (eg, glue, propellants) are commonly abused for their euphoric effects.

Hydrocarbons can be classified as being aliphatic, in which the carbon moieties are arranged in a linear or branched chain, or aromatic, in which the carbon moieties are arranged in a ring. Halogenated hydrocarbons are a subgroup of aromatic hydrocarbons, in which one of the hydrogen molecules is substituted by a halogen group. The most important halogenated hydrocarbons include carbon tetrachloride, trichloroethylene, tetrachloroethylene, trichloroethane, chloroform, and methylene chloride.

The hydrocarbons can be derived from either petroleum or wood. Petroleum distillates include kerosene, gasoline, and naphtha, whereas wood-derived hydrocarbons include turpentine and pine oil. The length of the chains as well as the degree of branching determine the phase of the hydrocarbon at room temperature; most are liquid, but some short-chain hydrocarbons (eg, butane) are gas at room temperature, whereas other long-chain hydrocarbons (eg, waxes) are solid at room temperature.

Toxicity from hydrocarbon ingestion can affect many different organs, but the lungs are the most commonly affected organ. The chemical properties of the individual hydrocarbon determine the specific toxicity, while the dose and route of ingestion affect which organs are exposed to the toxicity. Unlike the aromatic or aliphatic hydrocarbons, the halogenated hydrocarbons tend to cause a wider range of toxicity.

The recreational use of inhaling hydrocarbons and other volatile solvents for the purposes of creating a euphoric state is becoming increasingly common. Several methods are used for this abuse, including "sniffing" (directly inhaling vapors), "huffing" (placing a hydrocarbon-saturated rag over the mouth and nose and then inhaling), or "bagging" (inhaling via a plastic bag filled with hydrocarbon vapors).

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Pathophysiology

The toxicity of hydrocarbons is directly related to their physical properties, specifically the viscosity, volatility, surface tension, and chemical activity of the side chains. The viscosity is a measure of resistance to flow and is measured in Saybolt Seconds Universal (SSU). Substances with a lower viscosity (SSU < 60, eg, turpentine, gasoline, naphtha) are associated with a higher chance of aspiration. The surface tension is a cohesive force created by van der Waals forces between molecules and is a measure of a liquid's ability to "creep." Like the viscosity, the surface tension is also inversely related to aspiration risk; the lower the viscosity, the higher the risk of aspiration. The viscosity is the single most important chemical property associated with the aspiration risk.[2]

Volatility is the tendency for a liquid to change phases and become a gas. Hydrocarbons with a high volatility can vaporize and displace oxygen, which can lead to a transient state of hypoxia. Not surprisingly, the degree of volatility is directly related with the risk of aspiration. The amount of hydrocarbon ingested has not consistently been linked to the degree of aspiration and hence pulmonary toxicity.

Toxicity from hydrocarbon exposure can be thought of as different syndromes, depending on which organ system is predominately involved. Organ systems that can be affected by hydrocarbons include the pulmonary, neurologic, cardiac, gastrointestinal, hepatic, renal, dermatologic, and hematologic systems. The pulmonary system is the most commonly involved system.[3]

Pulmonary

Pulmonary complications, especially aspiration, are the most frequently reported adverse effect of hydrocarbon exposure. While most aliphatic hydrocarbons have little GI absorption, aspiration frequently occurs, either initially or in a semidelayed fashion as the patient coughs or vomits, thereby resulting in pulmonary effects. Once aspirated, the hydrocarbons can create a severe pneumonitis.

Hydrocarbon pneumonitis results from a direct toxic affect by the hydrocarbon on the lung parenchyma. The type II pneumocytes are most affected, resulting in decreased surfactant production. This decrease in surfactant, results in alveolar collapse, ventilation-perfusion mismatch, and hypoxemia. Hemorrhagic alveolitis can subsequently occur, which peaks 3 days after ingestion.[4] The end result of hydrocarbon aspiration is interstitial inflammation, intra-alveolar hemorrhage and edema, hyperemia, bronchial necrosis, and vascular necrosis. Rare pulmonary complications include the development a pneumothorax, pneumatocele, or bronchopleural fistula.[5]

Nervous system

CNS toxicity can result from several mechanisms, including direct injury to the brain or indirectly as a result of severe hypoxia or simple asphyxiation.

Many of the hydrocarbons that affect the CNS directly can make their way across the blood-brain barrier because certain hydrocarbons are highly lipophilic. In addition, for individuals who are huffing or bagging, the act of rebreathing can result in hypercarbia, which can contribute to decreased level of arousal.

Prolonged abuse of hydrocarbons can result in white matter degeneration (leukoencephalopathy) and atrophy.[6, 7] In addition, prolonged exposure to certain hydrocarbons (eg, n -hexane or methyl-n -butyl ketone [MnBK]) can result in peripheral neuropathy, blurred vision, sensory impairment, muscle atrophy, and parkinsonism.[8]

Cardiovascular

Exposure to hydrocarbons can result in cardiotoxicity.[9]

Most importantly, the myocardium becomes sensitized to the effects of catecholamines, which can predispose the patient to tachydysrhythmias, which can result in syncope or sudden death.

Gastrointestinal

Many of the hydrocarbons create a burning sensation because they are irritating to the GI mucosa. Vomiting has been reported in up to one third of all hydrocarbon exposures.

Hepatic [10]

The chlorinated hydrocarbons, in particular carbon tetrachloride, are hepatotoxic. Usually, the hepatotoxicity results after the hydrocarbon undergoes phase I metabolism, thereby inducing free radical formation. These free radicals subsequently bond with hepatic macromolecules and ultimately cause lipid peroxidation. This metabolite creates a covalent bond with the hepatic macromolecules, thereby initiating lipid peroxidation.

The common histopathologic pattern is centrilobular (zone III) necrosis.

Liver function test results can be abnormal within 24 hours after ingestion, and clinically apparent jaundice can occur within 48-96 hours.

Methylene chloride, a hydrocarbon commonly found in paint remover, is metabolized via the P450 mixed function oxidase system in the liver to carbon monoxide (CO). Unlike other cases of CO exposure, with methylene chloride, CO formation can continue for a prolonged period of time.

Renal

Chronic exposure to toluene, an aromatic hydrocarbon, can result in a distal renal tubular acidosis and present with an anion gap acidosis (see the Anion Gap calculator). A patient may have chronic exposure either via an occupational environment or by repeated recreational inhalation.

Hematologic

Prolonged exposure to certain aromatic hydrocarbons (especially benzene) can lead to an increased risk of aplastic anemia, multiple myeloma, and acute myelogenous leukemia. In addition, hemolysis has been reported following the acute ingestion of various types of hydrocarbons.[11]

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Epidemiology

Frequency

United States

In 2012, 31,031 cases of hydrocarbon poisoning were reported to US poison control centers. Of those, 13,422 were in patients aged 19 years or younger.[1]

International

In developing nations, kerosene is implicated in approximately one third of pediatric poisonings.

Mortality/Morbidity

In 2012, 18 deaths due to hydrocarbons were reported to US poison control centers.[1] However, several other deaths are classified as being due to "chemicals, cleaning substances, fumes/gases/vaporizers," and "pesticides." Thus, the true number is probably slightly higher. In addition, the poison control data are widely known to be an underestimate of the true incidence because of underreporting.

Age

Proportionately, more fatalities are associated with children younger than 5 years who often accidentally ingest hydrocarbons, and among adolescents, who are more likely to abuse volatile hydrocarbons.

Inhalant abuse is becoming increasingly common among adolescents. It is estimated that approximately 20% of students in middle school and high school have abused volatile substances.[12]

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Contributor Information and Disclosures
Author

Michael D Levine, MD Assistant Professor, Department of Emergency Medicine, Section of Medical Toxicology, Keck School of Medicine of the University of Southern California

Michael D Levine, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Phi Beta Kappa, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Coauthor(s)

Chip Gresham, MD, FACEM Emergency Medicine Physician and Medical Toxicologist, Department of Emergency Medicine, Clinical Director of Medication Safety, Middlemore Hospital; Senior Lecturer, Auckland University Medical School, New Zealand

Chip Gresham, MD, FACEM is a member of the following medical societies: American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

David A Peak, MD Associate Residency Director of Harvard Affiliated Emergency Medicine Residency; Attending Physician, Massachusetts General Hospital; Assistant Professor, Harvard Medical School

David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, American Medical Association

Disclosure: Partner received salary from Pfizer for employment.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Timothy P Barron, DO, and Jeremiah J Johnson, MD, to the development and writing of this article.

References
  1. Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 31st Annual Report. Clin Toxicol (Phila). 2014 Dec. 52(10):1032-283. [Medline]. [Full Text].

  2. Seymour FK, Henry JA. Assessment and management of acute poisoning by petroleum products. Hum Exp Toxicol. 2001 Nov. 20(11):551-62. [Medline].

  3. Lifshitz M, Sofer S, Gorodischer R. Hydrocarbon poisoning in children: a 5-year retrospective study. Wilderness Environ Med. 2003. 14(2):78-82. [Medline].

  4. Gross P, McNerney JM, Babyak MA. Kerosene pneumonitis: an experimental study with small doses. Am Rev Respir Dis. 1963 Nov. 88:656-63. [Medline].

  5. Rodricks A, Satyanarayana M, D'Souza GA, Ramachandran P. Turpentine-induced chemical pneumonitis with broncho-pleural fistula. J Assoc Physicians India. 2003 Jul. 51:729-30. [Medline].

  6. Borne J, Riascos R, Cuellar H, Vargas D, Rojas R. Neuroimaging in drug and substance abuse part II: opioids and solvents. Top Magn Reson Imaging. 2005 Jun. 16(3):239-45. [Medline].

  7. Filley CM, Halliday W, Kleinschmidt-DeMasters BK. The effects of toluene on the central nervous system. J Neuropathol Exp Neurol. 2004 Jan. 63(1):1-12. [Medline].

  8. Garrettson LK. n-Hexane and 2-Hexanone. Sullivan JB, Krieger GR, eds. Clinical Environmental Health and Toxic Exposure. 2nd ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 2001. 1211-14; chap110.

  9. Klein BL, Simon JE. Hydrocarbon poisonings. Pediatr Clin North Am. 1986 Apr. 33(2):411-9. [Medline].

  10. Palmer RB, Phillips SD. Chlorinated hydrocarbons. Shannon MW, Borron SW, Burns MJ, eds. Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose. 4th ed. Philadelphia, Pa: Saunders; 2007. 1347-61.

  11. Algren JT, Rodgers GC Jr. Intravascular hemolysis associated with hydrocarbon poisoning. Pediatr Emerg Care. 1992 Feb. 8(1):34-5. [Medline].

  12. Anderson CE, Loomis GA. Recognition and prevention of inhalant abuse. Am Fam Physician. 2003 Sep 1. 68(5):869-74. [Medline].

  13. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). 2008 Dec. 46(10):927-1057. [Medline]. [Full Text].

 
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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.
 
 
 
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