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Quantitative and objective measurement of exposure to cigarette smoke by assays of chemical markers is desirable, especially in preventive medicine, since the negative health effects of tobacco smoke are well documented. Chemical markers include nicotine and cotinine in plasma, urine, and saliva; carbon monoxide in exhaled air; carboxyhemoglobin in blood and thiocyanate in biological fluids. Ease of use, cost, specificity, and sensitivity vary across markers. Determination of the thiocyanate/creatinine ratio in urine is a reliable, noninvasive, and inexpensive test for evaluating exposure to cigarette smoke. No marker for cumulative exposure to cigarette smoke is available to date. The plasma level of fluorescent lipoperoxides may provide an estimation of the in vivo toxicity of exposure to cigarette smoke.

After a brief review of the concepts of free radical and enzymatic lipid peroxidation, spontaneous peroxidation (initiation, propagation, termination, end-products) is described in detail on the basis of the latest published studies shedding new light on the role of this process in a wide variety of disease states. Toxic effects of lipid peroxidation and physiologic protective mechanisms are described. Currently available routine methods for evaluating lipid peroxidation, particularly in plasma, although imperfect, are nevertheless valuable in clinical practice in view of the many human disease states involving lipid peroxidation.

A simple, inexpensive spectrofluorometric ultramicroassay for determining the plasma lipid peroxidation index is described. Plasma is incubated for 60 minutes at 95 degrees C in a thiobarbituric acetate buffer medium (pH 3,5) with butylhydroxytoluene and Fe . The chromogen is then extracted in butanol 1-pyridine and quantified by spectrofluorometry (exc.: 532 nm; em: 553 nm). The mean value of the plasma thiobarbituric lipid peroxidation index determined by this method in 101 healthy non-smokers (age 39.1 +/- 8.7 years) was found to be 1.61 +/- 0.72.

Transferrin structure, metabolism and physiological functions (iron transport, activation of cellular growth, bacteriostatic effect) are described with reference to the last informations available from the literature. This analysis results in a better understanding of the mechanisms involved in its physiopathological variations. Decreased serum transferrin levels are the result of a reduction of the biosynthesis (hepatic deficiencies, malnutrition), or an increase of catabolism (acute, chronic and malignant infections), or an increase of intestinal or renal losses, or very infrequently genetic disorders. Increased serum transferrin levels are the result of either hyposiderosis or an oestrogenic impregnation. Alcoholism and diabetes are responsible of qualitative modifications of this protein.

A simple accurate and very reproducible procedure for measuring serum iron concentration without precipitating serum proteins is described. In the same time, iron is released from serum transferrin, reduced and determined at 535 mn by incubation in a water bath at 55 degrees for five minutes within a formate buffered system (pH 2,6; i = 0,05) including bathophenanthroline sulfonate. This method yields values very similar to those obtained by that of the International Committee for Standardization in Hematology (ICSH).

Ghosts are adsorbed on extemporaneously formed tricalcium phosphate precipitate in lytic medium. They are free of hemoglobin and chemical characteristics are in good agreement with those obtained by Dodge (3) and Hanahan (5).