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in Sidestream Cigarette Smoke Increase after Release into Indoor Air: Results from Unpublished Tobacco Industry Research

Schick, Suzaynn F.; Glantz, Stanton A.

doi:10.1158/1055-9965.epi-07-0210

Cited by 60 publications

(52 citation statements)

References 33 publications

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“…In addition, NNK levels increase as SHS ages, presumably related to the reaction of tobacco-specific alkaloid nicotine with nitric oxide in SHS (Schick & Glantz, 2007;Sleiman et al, 2010). Consistent with these changes in the composition of SHS over time, we recently reported that cotinine measurement leads to an underestimation of exposure to NNK from SHS compared with active smoking (N. Benowitz et al, 2010).…”

mentioning

confidence: 60%

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

Goniewicz

Eisner

Lazcano‐Ponce

et al. 2011

Nicotine &Amp; Tobacco Research

137

126

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Conclusions:Both urine cotinine and NNAL are sensitive and specific biomarkers for discriminating the source of tobacco smoke exposure. Cotinine is the best overall discriminator when biomarkers are measured while a person has ongoing exposure to tobacco smoke. NNAL because of its long half-life would be particularly useful when there is a delay between exposure and biomarker measurement. The NNAL/cotinine ratio provides similar sensitivity but poorer specificity at discriminating passive versus active smokers when compared with NNAL alone. IntroductionBiomarkers are useful in assessing both active and passive smokers' exposure to tobacco smoke. Self-reported exposure such as cigarettes smoked per day by active smokers and hours per day exposed to secondhand smoke (SHS) in passive smokers is imprecise. Exposure patterns differ significantly from person to person due to differences in how cigarettes are smoked, differences in tobacco products, room ventilation, proximity of smokers to nonsmokers, and many other environmental factors (N. L. Benowitz, 1996).Biomarkers are used to discriminate active from passive smokers in epidemiological studies, population surveillance of tobacco use, and research on the health risks of active and passive smoking. Determination of optimal biomarker cutoff Abstract Objectives: Cotinine is the most widely used biomarker to distinguish active versus passive smoking. However, there is an overlap in cotinine levels when comparing light or occasional smokers versus heavily exposed passive smokers. 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) is a tobacco-specific nitrosamine measurable in urine with a much longer half-life than cotinine. The aim of the study was to determine optimal cutoff points to discriminate active versus passive smokers and to compare sensitivity and specificity for the use of cotinine, NNAL, and the ratio of the NNAL/cotinine in urine.Methods: Cotinine and NNAL were measured in urine of 373 active smokers and 228 passive smokers.Results: Geometric mean cotinine levels were 2.03 ng/ml (interquartile interval: 0.43-8.60) and 1,043 ng/ml (658-2,251) and NNAL levels were 5.80 pg/ml (2.28-15.4) and 165 pg/ml (90.8-360) pg/ml in passive and active smokers, respectively. NNAL/cotinine ratio in urine was significantly higher for passive smokers when compared with active smokers (2.85 vs. 0.16, p < .01). The receiver operating characteristics analysis determined optimal cutoff points to discriminate passive versus active smokers: 31.5 ng/ml for cotinine (sensitivity: 97.1% and specificity: 93.9%), 47.3 pg/ml for NNAL (87.4% and 96.5%), and 0.74 × 10 −3 for NNAL/cotinine ratio (97.3% and 87.3%).

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confidence: 60%

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

Goniewicz

Eisner

Lazcano‐Ponce

et al. 2011

Nicotine &Amp; Tobacco Research

137

126

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“…Given the low volatility of TSNAs and the high levels of nicotine typically found in environments contaminated with tobacco smoke, these carcinogens can persist indoors (42) and on the human envelope. Because of their frequent contact with surfaces and dust, infants and children are particularly at risk.…”

Section: Resultsmentioning

confidence: 99%

Formation of carcinogens indoors by surface-mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards

Sleiman

Gundel

Pankow

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

372

365

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This study shows that residual nicotine from tobacco smoke sorbed to indoor surfaces reacts with ambient nitrous acid (HONO) to form carcinogenic tobacco-specific nitrosamines (TSNAs). Substantial levels of TSNAs were measured on surfaces inside a smoker's vehicle. Laboratory experiments using cellulose as a model indoor material yielded a >10-fold increase of surface-bound TSNAs when sorbed secondhand smoke was exposed to 60 ppbv HONO for 3 hours. In both cases we identified 1-(N-methyl-N-nitrosamino)-1-(3-pyridinyl)-4-butanal, a TSNA absent in freshly emitted tobacco smoke, as the major product. The potent carcinogens 4-(methylnitrosamino)-1-(3-pyridinyl)-1-butanone and N-nitroso nornicotine were also detected. Time-course measurements revealed fast TSNA formation, with up to 0.4% conversion of nicotine. Given the rapid sorption and persistence of high levels of nicotine on indoor surfaces-including clothing and human skin-this recently identified process represents an unappreciated health hazard through dermal exposure, dust inhalation, and ingestion. These findings raise concerns about exposures to the tobacco smoke residue that has been recently dubbed "thirdhand smoke." Our work highlights the importance of reactions at indoor interfaces, particularly those involving amines and NO x /HONO cycling, with potential health impacts.exposure | indoor environment | nitrosamine | nitrogen oxides | heterogeneous chemistry

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“…Recent evidence, from our laboratory and others, has shown that SHS undergoes numerous chemical and physical changes after it is released into the air. Nicotine and other semivolatile organic compounds in smoke adsorb to surfaces where they can react with oxidant gases present in SHS and ambient air to form new chemical compounds (Singer et al 2002(Singer et al , 2003Destaillats et al 2006;Schick and Glantz 2007;Petrick et al 2011). …”

mentioning

confidence: 99%

An Apparatus for Generating Aged Cigarette Smoke for Controlled Human Exposure Studies

Schick

Farraro

Fang

et al. 2012

Aerosol Science and Technology

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Research has shown that cigarette smoke changes chemically and physically after it is released into indoor air, that these changes can increase secondhand smoke (SHS) toxicity, and that acute exposures to even low levels of SHS increase the risk of cardiopulmonary disease. We designed a system to reproduce realistic SHS exposures in the laboratory for use in controlled human exposure studies. We generated cigarette smoke with a smoking machine, diluted it and conducted it through a 6 m 3 stainless steel flow reactor at rates equivalent to the upper ranges of normal residential air exchange rates, to create aged cigarette smoke as a model for secondhand cigarette smoke. We observed that approximately 50% of the particle mass deposited within the system and that particle deposition percentage was higher when absorbent materials were placed within the system. The particle size ranges and deposition percentages, coefficients and velocities observed for this smoke aerosol are in good agreement with published values for SHS observed in residences and vehicles. This apparatus also permits the study of the physical and chemical interactions between SHS and indoor surfaces. The apparatus delivers stable aerosol concentra- Health and Human Services 2006). However, the mechanisms by which SHS exposure causes diseases other than cancer are still unclear. SHS is a complex and dynamic mixture made up of particles and gases that includes smoke from the burning end of the cigarette (sidestream smoke) and exhaled mainstream smoke (U.S. Department of Health and Human Services 1986). Recent evidence, from our laboratory and others, has shown that SHS undergoes numerous chemical and physical changes after it is released into the air. Nicotine and other semivolatile organic compounds in smoke adsorb to surfaces where they can react with oxidant gases present in SHS and ambient air to form new chemical compounds (Singer et al. 2002(Singer et al. , 2003Destaillats et al. 2006;Schick and Glantz 2007;Petrick et al. 2011).Subchronic and chronic exposure studies using laboratory animals have demonstrated that, when quantified on the basis of 1246 AGED CIGARETTE SMOKE FOR HUMAN EXPOSURE STUDIES 1247 particulate material mass, aged cigarette smoke is more toxic to the respiratory epithelium than fresh smoke (Schick and Glantz 2006). Thus, studies that use freshly generated cigarette smoke may not capture the health effects caused by SHS in the real world. We created an aged-cigarette-smoke generation system to reproduce human exposures to secondhand cigarette smoke in the real world as accurately as possible in the laboratory. Controlled exposure studies are an important tool for assessing the acute health effects of exposure to pollutant exposures in humans and the biological mechanisms underlying these health effects. By using human subjects, it is possible to eliminate the doubt and dispute involved when animal exposure data are used to set exposure limits for humans. Previous human exposure studies have used two essential methods to ge...

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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

Abstract: 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,

Cited by 60 publications

References 33 publications

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

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

Formation of carcinogens indoors by surface-mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards

An Apparatus for Generating Aged Cigarette Smoke for Controlled Human Exposure Studies

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