Hydrocarbons

152 Hydrocarbons






Pathophysiology


A hydrocarbon is an organic compound composed mainly of carbon and hydrogen atoms. In modern society, these compounds are virtually everywhere. Hydrocarbons are so common in our society that exposures—even illnesses related to exposures—are not usually documented. Hydrocarbons derive most commonly from distillation and processing of petroleum, but many derive from plants (pine oil, essential oils), animal fats, and natural gas. An example is gasoline, which is a mixture of alkanes, alkenes, naphthenes, and aromatic hydrocarbons. Commercial gasoline contains hundreds—up to 1500—individual chemical species.


The term solvent is often used to refer to an organic solvent—typically a hydrocarbon mixture—that is used to dissolve other substances. Occupational literature often uses the terms solvent and hydrocarbon interchangeably. Organic solvents are common in industry, and workers may suffer dermal or inhalational exposures. Children may suffer unintentional hydrocarbon exposures, often ingestions, with a risk of pulmonary hydrocarbon aspiration. More concerning is a trend toward greater intentional abuse of volatile hydrocarbon inhalants by adolescents and young adults. This form of substance abuse, often termed volatile substance abuse (VSA), is a growing problem worldwide.


One can predict many of the physical properties of hydrocarbons by knowing the molecular shape and size (number of carbon atoms in the molecule’s chain). The nonpolar, covalent bonds between carbon-carbon and carbon-hydrogen atoms produce dispersion forces, which result in the attraction between hydrocarbon molecules. These same forces repel polar molecules (e.g., water) and make hydrocarbons generally hydrophobic. Once dissolved in aqueous solution, nonpolar hydrocarbons can transit rapidly through lipid membranes, including cell membranes and the blood-brain barrier. Small, light, aliphatic hydrocarbons with up to 4 carbons are gases at room temperature; those with 5 to 19 carbon molecules are liquids; and longer molecules form solids or paraffins. Branching in the molecule destabilizes intermolecular forces, so less energy is required to separate molecules. This makes it easier for a molecule to leave the liquid phase and enter the vapor phase (to volatilize). Therefore, for a given molecular size, more branching means a lower boiling point, and the compound is typically more volatile. Gaseous or volatilized hydrocarbons are likely to cause toxicity by inhalation.


Lipid-soluble solvents (aromatic, aliphatic, or halogenated hydrocarbons) are more likely than water-soluble hydrocarbons (alcohols, ketones, or esters) to cause acute central nervous system (CNS) effects. Clinicians are familiar with these effects from experience with inhaled anesthetic agents, which cause CNS sedation similar to that resulting from other hydrocarbons. The Meyer-Overton hypothesis suggests that inhaled anesthetics dissolve into some critical lipid compartment of the CNS and cause generalized inhibition of neuronal transmission. This mechanism is probably oversimplified, but it helps to explain partly the nonspecific inhibition of neuronal transmission that hydrocarbons produce in the CNS. Specific membrane interactions may also contribute to this process,1 and several receptor-mediated interactions are known to occur.


Specific physical properties of ingested hydrocarbons help to predict the risk of pulmonary aspiration (Table 152.1). In particular, viscosity, surface tension, and volatility determine aspiration potential and the contribution to pulmonary toxicity.2 Viscosity is a measure of a fluid’s resistance to flow, commonly described in units of Saybolt universal seconds (SUS). This property is not the same as the fluid’s density; in fact, these two properties correlate poorly.



Low-viscosity substances (less than 60 SUS), such as turpentine, gasoline, or naphtha, have higher tendency for aspiration in animal models. A lower viscosity value predicts a higher risk. The U.S. Consumer Products Safety Commission now requires child-resistant packaging for products that contain 10% or more hydrocarbons and have a measured viscosity less than 100 SUS.


Surface tension indirectly measures dispersion forces between molecules in a fluid, but it also characterizes the interaction with the surface that the fluid contacts. This property can be quantified on a modified Wilhelmy balance, which measures adherence of the fluid along a surface (“the inability to creep”). In theory, the lower the surface tension is, the higher is the aspiration risk.2 A lower surface tension value predicts a higher risk.


Volatility is the tendency for a liquid to enter the gas phase. Hydrocarbons that are highly volatile have a high vapor pressure and so tend to vaporize, enter the lungs, displace oxygen, and cause hypoxia. A higher volatility value predicts a higher risk.



Mechanisms of Toxicity


Although organ-specific pathophysiology is often unique to individual agents, much of the toxicity of hydrocarbons results from their ability to dissolve fats or, similarly, to diffuse across hydrophobic barriers intended to protect anatomic structures (e.g., lipid bilayers, myelin). Hydrocarbon solvents cause irritation of skin and mucous membranes. Recurrent or prolonged contact results in “defatting” of skin, dissolving lipid components, and disrupting the normal architecture of the stratum corneum.3


Most hydrocarbons are flammable or combustible. Under appropriate conditions, most hydrocarbons can explode. The widespread availability of hydrocarbons and their use as organic solvents account for the frequent finding of stored quantities of these solvents in clandestine illicit drug laboratories and other places. Storage and use of these flammable agents appreciably contribute to the health hazards of these facilities.






Cardiac Effects


Many hydrocarbons are acutely cardiotoxic. Especially important is their propensity to induce tachyarrhythmias. The mechanism by which hydrocarbons cause malignant rhythms is poorly characterized, but some of these agents can precipitate ventricular tachycardia or fibrillation and can cause sudden death.


Endogenous or exogenous catecholamines (e.g., epinephrine) are proarrhythmic. Hydrocarbons enhance this potential and are said to sensitize the myocardium to the arrhythmogenic effects of catecholamines. Essentially every class of hydrocarbon compounds, including general anesthetic agents, can sensitize the heart. Some classes carry a high risk, however, and others sensitize the myocardium modestly, if at all. The ability of these substances to sensitize the heart constitutes an accepted system for grading halocarbon (e.g., Freon) toxicity. Unsaturated, aliphatic hydrocarbons (e.g., ethylene) and aliphatic ethers have been studied but do not appear to be sensitizers. Other unsaturated compounds (e.g., acetylene), are weak sensitizers. Aromatic hydrocarbons and, especially, halogenated hydrocarbons are often potent sensitizers.6


Sensitization appears to be mediated by slowed conduction velocity, possibly by chemical and functional changes in the membrane transport proteins at gap junctions. The major ventricular gap junction protein is composed of connexin 43. This protein is regulated by phosphorylation, such that the dephosphorylated state of the hexamers in the channel is associated with greater gap junction resistance. In the presence of epinephrine, halocarbons increase gap junction resistance in myocardial tissue and slow conduction velocity.7



Nervous System Effects


The mechanism by which hydrocarbons depress consciousness is unknown. Diffusion across the blood-brain barrier with neuronal membrane stabilization provides the foundation of the Meyer-Overton hypothesis. To date, no specific receptor wholly explains this generalized effect. In cases of pulmonary toxicity, hypoxemia may contribute to depressed consciousness.8


Chronic solvent abuse leads to irreversible CNS toxicity, best described in the setting of toluene abuse. Volitional abusers demonstrate loss of cerebral white matter, with a characteristic syndrome of cognitive and motor deficits. Autopsied brains of long-term toluene abusers show profound atrophy and mottling of the white matter, as though the lipid-based myelin had been dissolved away. Microscopic examination shows a consistent pattern of demyelination, with relative preservation of axons. These pathologic features correlate with the clinical syndrome of subcortical dementia.9 Mild cognitive deficits show improvement after 6 months of abstinence. In patients with advanced disease, regardless of the exposure history, full recovery is unlikely.10

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Jun 14, 2016 | Posted by in EMERGENCY MEDICINE | Comments Off on Hydrocarbons

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