Determination of cyanide and thiocyanate in humans
1992 (English)Doctoral thesis, comprehensive summary (Other academic)
Cyanide exposure from several sources may cause chronic diseases or acute lethal intoxication in humans. Accurate and specific methods for determination of cyanide and its metabolite thiocyanate are therefore needed for clinical and epidemiological purposes. An improved method for determination of thiocyanate in serum and urine was developed by adsorption of thiocyanate on a weakly basic anion-exchange resin by a chaotropic effect, followed by colorimetrical determination by a modified Konig reaction. Dietary intake of cyanide and sulfur was estimated by determination of urinary thiocyanate and inorganic sulfate in a Mozambican population affected by the paralytic disease konzo. Konzo was found to be associated with a high cyanide and low sulfur intake from a diet dominated by cassava roots that were consumed without removal of the naturally occurring cyanogen compounds. A low intake of sulfur containing proteins was supposed to enhance toxic effects of cyanide by reducing cyanide to thiocyanate conversion.
For determination of blood cyanide in field studies an analytical method that enabled transport of samples was developed. Cyanide was stabilized in blood by adding silver ions and after distillation determined by the Konig reaction. A 30-fold increase in sensitivity was obtained by fluorometric determination of the Konig chromogen, which enabled determination of physiological blood cyanide levels 0.117 ± 0.038 J..Ullol/L (mean± SD), and blood cyanide after smoking a cigarette 0.424 ± 0.173 f.tmol/L. A rapid method for determination of toxic blood cyanide levels could be developed by separating the cyanide containing erythrocytes from thiocyanate containing plasma by washing with saline and thereafter protein precipitation followed by direct spectrophotometric determination of the König chromogen.
Measurement of hydrogen cyanide in breath showed no correlation with blood levels of cyanide. Experiments revealed that most of the hydrogen cyanide found in breath from normal human beings originates from oxidation of thiocyanate by salivary peroxidase in the oropharynx.
In a study of fire casualties 9 out of 18 victims had toxic blood cyanide levels (> 40 J..Ullol/L) and one had a blood cyanide level of 101 J..UllOI/L but a nontoxic blood carboxyhemoglobin, which suggests a lethal effect of cyanide exposure. Blood cyanide levels in two suicidal intoxications were found to be 105 and 139 J..UllOl/L. A lethal outcome in one of the cases that received insufficient antidotal treatment indicates that immediate laboratory verification of cyanide intoxication may be life-saving.
Place, publisher, year, edition, pages
Linköping: Linköpings universitet , 1992. , 92 p.
Linköping University Medical Dissertations, ISSN 0345-0082 ; 355
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-25684Local ID: 10060ISBN: 91-7870-647-5OAI: oai:DiVA.org:liu-25684DiVA: diva2:246232
1992-05-07, Aulan, Administrationsbyggnaden, Universitetssjukhuset, Linköping, 09:00 (Swedish)
Papers, included in the Ph.D. thesis, are not registered and included in the posts from 1999 and backwards.2009-10-082009-10-082012-07-19Bibliographically approved