Hydrocarbon toxicity: A review

Context: Clinical effects of hydrocarbon exposure have been reported since 1897. These substances are ubiquitous, and their exposures are common. The specific hydrocarbon and route of exposure will determine the clinical effect, and an understanding of this is helpful in the care of the hydrocarbon-exposed patient.

Objective: To complete a comprehensive review of the literature on hydrocarbon toxicity and summarize the findings.

Methods: Relevant literature was identified through searches of Medline (PubMed/OVID) and Cochrane Library databases (inclusive of years 1975-2013), as well as from multiple toxicology textbooks. Bibliographies of the identified articles were also reviewed. Search terms included combinations of the following: hydrocarbons, inhalants, encephalopathy, coma, cognitive deficits, inhalant abuse, huffing, sudden sniffing death, toluene, renal tubular acidosis, metabolic acidosis, arrhythmia, dermatitis, and aspiration pneumonitis. All pertinent clinical trials, observational studies, and case reports relevant to hydrocarbon exposure and published in English were reviewed. Chronic, occupational hydrocarbon toxicity was not included.

Results: Exposure to hydrocarbons occurs through one of the following routes: inhalation, ingestion with or without aspiration, or dermal exposure. Inhalational abuse is associated with central nervous system depression, metabolic acidosis, and arrhythmia. The exact mechanism of the CNS depression is unknown, but experimental evidence suggests effects on NMDA, dopamine, and GABA receptors. Chronic toluene inhalation causes a non-anion gap metabolic acidosis associated with hypokalemia. Halogenated hydrocarbon abuse can cause a fatal malignant arrhythmia, termed "sudden sniffing death". Individuals who regularly abuse hydrocarbons are more likely to be polysubstance users, exhibit criminal or violent behavior, and develop memory and other cognitive deficits. Heavy, long-term use results in cerebellar dysfunction, encephalopathy, weakness, and dementia. Neuroimaging may demonstrate leukoencephalopathy in these cases. Acute exposures improve with cessation of exposure. Electrolyte and fluid replacement will improve metabolic acidosis. Arrhythmias are precipitated via catecholamine surge, and beta blockers are presumed protective. Aspiration of hydrocarbons causes a potentially fatal pneumonitis. Symptoms may include cough, wheezing respiratory distress, and hypoxia. Bilateral interstitial infiltrates may be delayed for several hours after the development of pneumonitis. Treatment consists of supportive care, supplemental oxygen, and may require intubation and admission to an intensive care unit in severe cases. Unfortunately, aspiration pneumonitis remains a leading cause of poisoning mortality in children. Dermal exposure can cause dermatitis, chemical burns, and defatting injury. Oral exposure can cause local irritation as well as vomiting, diarrhea, and abdominal pain.

Conclusion: Acute hydrocarbon exposure can result in a wide array of pathology, such as encephalopathy, pneumonitis, arrhythmia, acidosis, and dermatitis. Intentional inhalational and accidental ingestion exposures with aspiration lead to the greatest morbidity and mortality.