Environmental Tobacco Smoke Measuring Exposures and Assessing Health Effects (1986) / Chapter Skim
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8 Assessing Exposures to Environmental Tobacco Smoke Using Biological Markers
8 Assessing Exposures to Environmental Tobacco Smoke Using Biological Markers
Pages 133-160
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From page 133... ...
The development of new biochemical methods enables us to obtain measurements of exposure to ETS by determining the uptake of specific agents in body fluids and calculating the risk relative to that of the exposure of active smokers. The uptake of individual agents from ETS can be determined by biochemical measures that have been developed for assessment of active smoking behavior, as long as these measures are sensitive and specific enough for quantitating exposure to such agents by nonsmokers.
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From page 134... ...
explain why some investigators were unable to distinguish between nonsmokers exposed to ETS and those without any exposure to tobacco smoke (Hoffmann et al., 1984; Jarvis, 1985~. Similarly, the mean serum level of SCN- in healthy pregnant women at term who were exposed to ETS (35.9 mom/ was not distinctly different from that in those without ETS exposure (32.3 gwol/~)
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From page 135... ...
The authors of the latter stiffly also reported a weak correlation between thiocyanate concentration and number of cigarettes smoked per family (Poulton et al., 1984~. This study was criticized because some of the determined thiocyanate levels were within the range reported for heavy cigarette smokers.
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From page 136... ...
In the case of cigarette smokers who have inhaled puffs of smoke containing 20,000-50,000 ppm of CO, the correlation between exhaled CO and COHb is also in good agreement (r = 0.97; Heinemann et al., 1984~. The COHb levels are of value for comparing degrees of smoke inhalation.
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From page 137... ...
Nicotine and Cotinine Disregarding nicotine-containing chewing gum and nicotine aerosol rods as aids for smoking cessation, the presence of nicotine and that of its major metabolite, cotinine, in biological fluids is entirely due to the exposure to tobacco, tobacco smoke, or environmental tobacco smoke. The determination of nicotine and cotinine in saliva, blood, or urine of active and passive smokers is done primarily by gas chromatography (GC)
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From page 138... ...
Table S-3 compares nicotine and cotinine levels as determined in one laboratory in plasma, saliva, and urine of nonsmokers with and without ETS exposure and of active smokers. This comparison shows that, generally, concentrations of nicotine and cotinine in plasma, saliva, and urine of nonsmokers exposed to ETS amount
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From page 139... ...
~ 4 ~ ~ ~ ~V ~ ~ r, '= - ~ =._ ~ ~ ~ ~ =._ 3 _ ._ C~ ._ ._ ._ ._ ._ O o oo ~ oo oo ~ ~ ~ 0 ~ £ I I I 1 7 1 1 1 1 x e~ r~ c-~ ~ ~> ~ ~ ~ · s ~x x ~ ;^ ;- ~ ~ ~ ^~ a~ 0 0 c Ct Ct ~ Ct ~ Ct Ct Ct Ct C~ G)
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From page 141... ...
In the case of cigarette smokers, they found conning levels of 8.57 ~ 0.39 ~g/mg of creatinine in urine. This study has been questioned because its findings of cotinine in urine of both active and passive smokers indicate levels substantially higher than those reported in other studies (AdIkofer et al., 1985; Pittenger, 1985)
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From page 142... ...
o U, o o Z Z LU U' o ~xO & ~ ~ C,~ o ~ o ~ ~; ~7 ~s ~ ~o ~ ~ _ _ ~_ _ o o _ ~ · & , o .= Co, ~, , ~ : e ~ ' ~ E ~ e E 7 ~ 2 ~ I ~ ' ~ '~' ~ ~ ~9 i ' ~ ' ~ ct D ~ ~ ~D ~ ~ ~ U)
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From page 143... ...
o ed ct ct c:S 5- s ._ U
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From page 144... ...
Cotinine elimination in the plasma of nonsmokers exposed to ETS was reported to be slower than Cotinine elimination in the plasma of active smokers. Cotinine elimination from urine was also significantly slower.
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From page 145... ...
Urinalysis for cotinine is the preferred method for assessment of long-term ETS exposure, because the sampling is noninvasive, the excretion rate of cotinine is only slightly dependent on the pH of urine, ant] assessment of the average daily exposure on the basis of cotinine levels is independent of the restrictions posed by variations of the hal£life of nicotine in smokers and nonsmokers (Beckett et al., 1971; Klein and Gorrod, 1978~.
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From page 146... ...
At present, the question of quantitative aspects of urinary hydroxyproline excretion in nonsmokers exposed to ETS is not settled. It will require additional studies before this compound and its ratio to creatinine can be used as indicators for the degree of ETS exposure.
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From page 147... ...
It has been shown that endogenous formation of NPRO is significantly increased in cigarette smokers (Hoffmann and Brunnemann, 1983; Ladd et al., 1984; Scherer and AdIkofer, in press)
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From page 148... ...
Since 1975, the most widely used assay for genotoxicity of human urine is the determination of mutagenicity in bacterialtested strains with and without activation by enzyme-induced liver homogenate. In 1977, Yamasaki and Ames reported the presence of mutagens in the urine of cigarette smokers, thus suggesting a correlation between mutagens in smokers' urine and increased risk for bladder cancer.
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From page 149... ...
and tested for mutagenicity with tested strain TB98 using rat liver homogenate for metabolic activation (Sorsa et al., 1985~. As is evident from the data in Table B-4, COHb values for nonsmokers and passive smokers were indistinguishable, while there wan a trend for higher plasma cotinine values in the passive smokers.
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From page 151... ...
AdOucts Formed In Passive Smokers upon Exposure to ETS Since about 1975, highly sensitive methods have been developed for the determination of protein- or DNA-adJucts of environmental carcinogens and toxic agents in circulating blood. Methods probing these reactions for the toxic agents known to occur in tobacco smoke and ETS include determination of hemoglobin abducts of nitrosodimethylamine, methyl chloride, viny} chIoricle, and benzene (National Institute of Environmental Health Sciences, 1984)
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From page 152... ...
This fact underlines the urgent need for the development of highly sensitive dosimetric methods for ETS-specific carcinogens that can be applied In field studies. SUMMARY AND RECOMMENDATIONS Passive smokers are exposed to trace amounts of toxic agents including tumor initiators, tumor promoters, carcinogens, and organ-specific carcinogens when inhaling ETS.
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From page 153... ...
During the last decade, immunoassays and postiabell~g methods have been developed for tracing toxic and carcinogenic agents in circulating blood. These methodologies should be used for the development of dosimetry studies in nonsmokers exposed to ETS.
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From page 154... ...
2. A study on the urinary excretion of aromatic amines in nonsmokers exposed to ETS is needed in order to correlate the total amounts of individual armies and their metabolites in the urine of nonsmokers exposed to ETS.
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From page 155... ...
Salivary cotinine levels and passive tobacco smoke exposure in the home.
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From page 156... ...
Die analytische und diagnostische Validitat der Bestimmung Ron Carboxyhamoglobin im Blut und Kohlenmonoxid in der Atemlult Iron Rauchern und Nichtrauchern.
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From page 157... ...
Thiocyanat im Serum ails Indikator fur die SchadstoRbelastung durch Tabakrauch. Arbeitsmed.
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From page 158... ...
Detection of benzo~a~pyrene: DNA adducts in human white blood cells. Cancer Res.
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From page 159... ...
Billings. Smoking cessation program: Baseline carbon monoxide and serum thiocyanate levels as predictors of outcome.
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