Concentrations of the Carcinogen 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone in Sidestream Cigarette Smoke Increase after Release into Indoor Air: Results from Unpublished Tobacco Industry Research

@article{Schick2007ConcentrationsOT,
  title={Concentrations of the Carcinogen 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone in Sidestream Cigarette Smoke Increase after Release into Indoor Air: Results from Unpublished Tobacco Industry Research},
  author={Suzaynn F. Schick and Stanton A. Glantz},
  journal={Cancer Epidemiology Biomarkers \& Prevention},
  year={2007},
  volume={16},
  pages={1547 - 1553}
}
  • S. SchickS. Glantz
  • Published 1 August 2007
  • Medicine
  • Cancer Epidemiology Biomarkers & Prevention
Research has shown that the toxicity of sidestream cigarette smoke, the primary constituent of secondhand smoke, increases over time. To find potential mechanisms that would explain the increase in sidestream smoke toxicity over time, we analyzed unpublished research reports from Philip Morris Co. using the internal tobacco industry documents now available at the University of California San Francisco Legacy Tobacco Documents Library and other Web sites. Unpublished research from Philip Morris… 
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Evaluation of tobacco specific nitrosamines exposure by quantification of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in human hair of non-smokers

For the first time, NNK is present in hair samples from non-smokers in concentrations much higher than any other tobacco specific nitrosamine, and may provide a good estimation of cancer risk associated with exposure to secondhand smoke.

Urine Cotinine Underestimates Exposure to the Tobacco-Derived Lung Carcinogen 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone in Passive Compared with Active Smokers

Cotinine measurement leads to an underestimation of exposure to the carcinogen NNK from secondhand smoke when compared with active smoking, suggesting a nonlinear tobacco smoke dose-response and/or that cotinine is not providing an accurate measure to the toxic constituents of secondhand tobacco smoke.

Thirdhand smoke causes DNA damage in human cells.

It is demonstrated for the first time that exposure to THS is genotoxic in human cell lines, suggesting that THS exposure is related to increased oxidative stress and could be an important contributing factor in THS-mediated toxicity.

Cotinine Underestimates Exposure to the Tobacco-ived Lung Carcinogen 4-( Methylnitrosamino )-1-( 3-Pyridyl )-B & P utanone in Passive Compared with Active Smokers

The discrepancy between cotinine levels in relation to disease risk comparing versus passive smoking suggests a nonlinear tobacco smoke dose-response and/or that c nicotine is oviding an accurate measure of exposure to the toxic constituents of secondhand tobacco smoke.

Extensive Metabolic Activation of the Tobacco-Specific Carcinogen 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone in Smokers

The results of this study show for the first time that NNK metabolic activation is a quantitatively significant pathway in smokers, accounting for ∼86% of total urinary excretion of NNK metabolites.

Comparison of urine cotinine and the tobacco-specific nitrosamine metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and their ratio to discriminate active from passive smoking.

Both urine cotinine and NNAL are sensitive and specific biomarkers for discriminating the source of tobacco smoke exposure when biomarkers are measured while a person has ongoing exposure to tobacco smoke.

Toxicity of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in early development: A wide-scope metabolomics assay in zebrafish embryos.

Toxicity of 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NKK) in early development: a wide-scope metabolomics assay in zebrafish embryos

The results confirm NNK as a harmful embryonic agent and demonstrate zebrafish embryos to be a suitable early development model to monitor NNK toxicity.

Exposure to nitrosamines in thirdhand tobacco smoke increases cancer risk in non-smokers.

...

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