The reliability of Thiocyanate measurement of smoking exposure

Prue, Donald M.; Martin, John E.; Hume, Arthur S.; Davis, Norman S.

doi:10.1016/0306-4603(81)90002-2

Cited by 18 publications

(9 citation statements)

References 11 publications

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“…The measurement of the gases ingested during smoking not only provides information on the absorption of harm fur gases to the blood stream but, by extrapolation, may also provide information on nicotine absorption. These gas measures include expired carbon monoxide (CO; Jaffe et al,1978;Prue, Krapfl, & Martin, 1981) measured with a mechanical device such as an Ecolyzer (Energetics Science, Inc., Elmsford, NY), carboxyhemoglobin (COHb) measured in blood samples (Hill & Marquardt, 1980;Russell, Wilson, Patel, Cole, & Feyerabend, 1973), and thiocyanate (SCN), a metabolite of hydrogen cyanide gas, measured in blood, urine, or saliva (Frederiksen, Martin, & Webster, 1979;Prue, Martin, & Hume, 1980;Prue, Martin, Hume, & Davis, 1981). We consider these measures to be indirect, since nicotine exposure can only be inferred from them.…”

Section: Dependent Measuresmentioning

confidence: 99%

“…Fourth, the results may have been influenced by the bodily fluid assessed for nicotine content (i.e., plasma, urine, or saliva) as well as the type of chemical analysis used (i.e., gas chromatography or spectrophotometrics). The measurement of nicotine and other constituents of tobacco smoke in biological fluids is a relatively new and highly sophisticated endeavor involving potential confounding during collection, storage, and analysis (Prue, Martin, Hume, & Davis, 1981), and as yet no standard form of biochemical measurement has been established. With respect to this issue, Ashton et al (1979) used several measures including urinary and plasma nicotine, urinary cotinine, and mouth-level exposure, and the measure in Russell et al (1975) was plasma nicotine.…”

Section: Brand Switchingmentioning

confidence: 99%

See 1 more Smart Citation

Nicotine's role in smoking: An analysis of nicotine regulation.

McMorrow

Foxx²

1983

Psychological Bulletin

111

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Nicotine regulation refers to a smoker's maintenance of a characteristic level of nicotine in the body. It implies that changes in smoking behavior (i.e., compensation) will accompany either increases or decreases in nicotine availability. Research on regulation has been inconclusive because of (a) a failure to distinguish between regulation and compensation, (b) the use of indirect rather than direct measures of nicotine exposure, and (c) a number of methodological problems. This review addresses these issues by (a) clarifying definitional ambiguities, (b) presenting a classification strategy that differentiates the indirect and direct evidence for regulation, (c) quantifying the direct evidence, (d) discussing measurement and methodological problems, and (e) suggesting future research.

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Section: Dependent Measuresmentioning

confidence: 99%

Section: Brand Switchingmentioning

confidence: 99%

Nicotine's role in smoking: An analysis of nicotine regulation.

McMorrow

Foxx²

1983

Psychological Bulletin

111

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“…Others have examined this phenomenon and have reported no significant effect following a twofold increase in chloride excretion rate (Schulz et al, 1979). The conditions under which both blood (Ballantyne, 1977) and saliva (Prue et al, 1981) are stored have been shown to significantly alter SCN concentrations in these samples. Similar effects may be present for serum samples as well.…”

Section: Discussionmentioning

confidence: 95%

Relationship of serum thiocyanate concentrations to smoking characteristics

1984

Journal of Toxicology and Environmental Health

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Thiocyanate (SCN) concentrations were determined in serum samples from 130 young healthy persons (60 smokers) and related to their smoking and physiologic characteristics. Serum thiocyanate correlated strongly and approximately equally with the number of cigarettes/d X kg of ideal body weight (IBW) (r = 0.748), total nicotine intake in mg/d X kg IBW (r = 0.735), and total tar intake in mg/d X kg IBW (r = 0.731). Multiple linear regression analysis that included these factors as well as sex, marijuana use, menthol, and degree of inhalation only increased the multiple r to 0.803. A more sensitive statistical method (NYBAID) was also used to determine the most significant influences of these variables on serum SCN. The association with depth of inhalation (i.e., smoking versus nonsmoking) was dominant among the relationships considered. The highest SCN levels were exhibited in heavy nicotine users (8.58 +/- 3.00 mg/l), while average users had slightly lower concentrations (6.49 +/- 2.37 mg/l) (p less than 0.03). In nontobacco smokers, those who smoked marijuana several times weekly had higher SCN levels (4.66 +/- 2.16 mg/l) than noncannabis users (2.38 +/- 1.38 mg/l) (p less than 0.03). These studies confirm the utility of serum SCN as an index of smoking rate and demonstrate the role of secondary variables in accounting for the chemical in serum.

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“…First, consumption of leafy vegetables produces substantial increases in saliva thiocyanate leading to false positives (Pechacek et al 1984b). Thiocyanate samples have been found to deteriorate if they are not stored in airtight containers (Prue et al 1981). Expired air CO has been found to have a half-life as short as 4 hours (Benowitz 1982), making it difficult to use in studies with large samples.…”

Section: Physiological Measuresmentioning

confidence: 99%