The influence of passive smoking on the cardiovascular system.

Cardiovascular effects of tobacco smoke have been studied in passive smokers far less extensively than in active smokers. Under real-life conditions, passive smokers inhale approximately 0.02 to 0.01 of the amount of particulate matter taken up by active smokers. Their nicotine concentration in serum is within a range that is barely distinguishable from the background level. The increase in carboxyhemoglobin rarely exceeds 1%. In healthy subjects heavily exposed to tobacco smoke, no or only slightly acute effects on the cardiovascular system are found. Whether or not passive smoking is likely to aggravate symptoms in patients with advanced coronary heart disease has not yet been unequivocally established and requires further investigation. From a few studies on occupational groups exposed to carbon monoxide (CO) and from experiments with animals chronically treated with CO or nicotine, the conclusion can be drawn that neither CO nor nicotine is likely to play a role in the development and progression of coronary heart disease in those concentrations normally found in passive smokers.

[Analytic and diagnostic validity of the determination of carboxyhemoglobin in blood and carbon monoxide in the breath of smokers and non-smokers]. / Die analytische und diagnostische Validität der Bestimmung von Carboxyhämoglobin im Blut und Kohlenmonoxid in der Atemluft von Rauchern und Nichtrauchern.

The analytic and diagnostic validity of the determination of carboxyhaemoglobin and carbon monoxide in smokers and non-smokers was investigated. Both methods are of high analytic and diagnostic validity. Precision and accuracy fullfil the essential requirements. Comparison of the methods shows good correlation (= 0.97) and linear regression (y = 51.5 X 10(-3)x + 6.26 X 10(-6] within the investigated range. Values for the conditional probabilities of sensitivity, specificity, predictive values, and efficiency are higher 0.80. Taking into account the standardized sample collection for the CO determination, the two methods are of comparable validity when used in clinical and epidemiological investigations on smokers and non-smokers.

Effect of cigarette smoking on white blood cells and erythrocyte enzymes.

Healthy volunteers smoked 21 to 26 cigarettes containing different amounts of condensate (tar) and nicotine for 16 wk. Enzymes and metabolites of erythrocyte metabolism were not influenced, with the exception of a slight inhibition of delta-aminolevulinic acid dehydratase. Hematological parameters were normal except the white blood count, which was elevated in smokers but remained within the normal range.

[The influence of different diets and smoking on the clinical chemical diagnosis of pheochromocytoma, neuroblastoma, and carcinoid syndrome (author's transl)]. / Der Einfluss von Nahrungsmitteln und Rauchen auf die klinisch-chemische Diagnostik von Phäochromozytom, Neuroblastom und Karzinoid-Syndrom.

The interference of various foodstuffs on methods to determine epinephrine (E), norepinephrine (NE), vanillylmandelic acid (VMA), metanephrines (MN), homovanillic acid (HVA), and 6-hydroxyindole acetic acid (5-HIA) in the 24 h urine for diagnosis of pheochromocytoma and carcinoid syndrome, respectively, was investigated. The foodstuffs included were: tea, coffee, almonds, pineapples, cheese, walnuts, vanilla pudding, bananas, tomatoes, and chocolate. Further, the interference of cigarette smoking on the determination of E, NE, VMA, and MN was also investigated. Walnuts caused a rather high elevation of 5-HIA in the urine. After eating bananas elevated excretion of E, NE, VMA, MN, and 5-HIA was observed. Small increases of the MN values were noticed after coffee and pineapples. Smoking of 20-30 cigarettes/day had no influence on the variables measured. If the methods described are used, thus, only bananas and walnuts have to be restricted some days before and during urine sampling, but not coffee and pineapples if consumed in the usual small quantities. There is no reason to insist on diet restriction except for bananas and walnuts.

Comparative evaluation of different spectrophometric methods for the determination of small amounts of carboxyhaemoglobin.

Four spectrophotometric methods measuring HbCO were investigated in comparison with an analyzer (CO-Oximeter) in order to find a method determining HbCO fractions) below 0.10 with sufficient reliability. The CO-Oximeter was chosen as "reference" method because results of other authors with this instrument yielded good agreement with other methods, e.g. IR-spectrometry, GLC, van Slyke. Only the five wavelength method of Commins & Lawther (1965) Brit. J. Industr. Med. 22, 139--143) can be recommended, for it yielded CV's and sensitivities comparable to the CO-Oximeter. The within-run precision had CVs of 2.3% to 4.7%, the sensitivity was 0.0021 to 0.0028. The method is suited even for HbCO measurements of shorter series.

Hereditary deficiency of triosephosphate isomerase in four unrelated families.

Triosephosphate isomerase deficiencies in erythrocytes and leucocytes were discovered in three unrelated families by a heterozygote screening of 3000 blood samples. In addition, a family found by Schroter et al. [not published] was studied. In these four families, only heterozygote carriers were found. In the family described by Freycon et al. with hetero- and homozygote carriers of triosephosphate isomerase deficiency, the heterozygotes were reinvestigated. There was 51% of normal enzyme activity in three of the families. In the other two families the enzyme activity was 64% and 71% of normal. Two of the eleven heterozygotes, both children, were diseased, but it seems unlikely that the disorders resulted from the deficiencies. The activities of thirteen enzymes, the Km of triosephosphate isomerase for glyceraldehyde phosphate and the concentrations of metabolites were normal. Antibody titration showed normal specific activities in four families and 50% of normal in one family. No electrophoretic variant was detected. From the proved heredity, a heterozygous frequency of at least 1/1000 is indicated. A maximal frequency of 5/1000 is estimated by using further instances of triosephosphate isomerase deficiency where heredity has not yet been investigated. An explanation for the small number of known cases is that this enzyme is not routinely assayed.

Toxicological and clinical aspects of cyanide metabolism.

This contribution deals with the occurrence of cyanide and its biological pathways in the body. Especially possibilities of detoxification are pointed out. Intoxications are caused by acute and chronical cyanide uptake. Tobacco amblyopia, retrobulbar neuritis in pernicious anaemia, Leber's optic atrophy, Nigerian nutritional neuropathy, and sterility in female heavy smokers are attributed to cyanide intoxication. Various methods for treating acute and chronic cyanide intoxication are discussed.