THE POTENTIAL OF THE HYDROCARBON BREATH TEST AS A MEASURE OF LIPID-PEROXIDATION

The straight chain aliphatic hydrocarbons ethane and pentane have been advocated as noninvasive markers of free-radical induced lipid peroxi dation in humans. In in vitro studies, the evolution of ethane and pen tane as end products of n-3 and n-6 polyunsaturated fatty acids, respe ctively, correlates very well with other markers of lipid peroxidation and even seems to be the most sensitive test available. In laboratory animals the use of both hydrocarbons as in vivo markers of lipid pero xidation has been validated extensively. Although there are other poss ible sources of hydrocarbons in the body, such as protein oxidation an d colonic bacterial metabolism, these apparently are of limited import ance and do not interfere with the interpretation of the hydrocarbon b reath test. The production of hydrocarbons relative to that of other e nd products of lipid peroxidation depends on variables that are diffic ult to control, such as the local availability of iron(II)) ions and d ioxygen. In addition, hydrocarbons are metabolized in the body, which especially influences the excretion of pentane. Because of the extreme ly low concentrations of ethane and pentane in human breath, which oft en are not significantly higher than those in ambient air, the hydroca rbon breath test requires a flawless technique regarding such factors as: (1) the preparation of the subject with hydrocarbon-free air to wa sh out ambient air hydrocarbons from the lungs, (2) the avoidance of a mbient air contamination of the breath sample by using appropriate mat erials for sampling and storing, and (3) the procedures used to concen trate and filter the samples prior to gas chromatographic determinatio n. For the gas chromatographic separation of hydrocarbons, open tubula r capillary columns are preferred because of their high resolution cap acity. Only in those settings where expired hydrocarbon levels are sub stantially higher than ambient air levels might washout prove to be un necessary, at least in adults. Although many investigators have concen trated on one marker, it seems preferable to measure both ethane and p entane concurrently. The results of the hydrocarbon breath test are no t influenced by prior food consumption, but both vitamin E and beta-ca rotene supplementation decrease hydrocarbon excretion. Nevertheless, t he long-term use of a diet high in polyunsaturated fatty acids, such a s in parenteral nutrition regimens, may result in increased hydrocarbo n exhalation. Hydrocarbon excretion slightly increases with increasing age. Short-term increases follow physical and intellectual stress and exposure to hyperbaric dioxygen. Several other factors require furthe r evaluation, including normal ranges in infants and children and the effects on the test of altered diffusion and local lipid peroxidation as a consequence of lung disease. The test seems to be unreliable in s mokers, because smoking cigarettes results in impressive increases in ethane and pentane exhalation. Hydrocarbon excretion is increased in a great variety of conditions in which lipid peroxidation was thought t o be involved, which confirms both the reliability and the nonspecific nature of the test. Abnormal excretion has been documented in alcohol ic and choletatic liver disease, vitamin E deficiency, pulmonary disea se, autoimmune disease, inflammatory bowel disease, ischemia-reperfusi on injury, and neurologic disease. In many, if not most, conditions, i ncreased lipid peroxidation is an epiphenomenon instead of playing a p athogenetic role. Therefore, the results of the hydrocarbon breath tes t should not be regarded in isolation but in the light of clinical and laboratory parameters, including other markers of lipid peroxidation.