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Respiratory Exposure to Thirdhand Cigarette Smoke Increases Concentrations of Urinary Metabolites of Nicotine
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Abstract
Introduction
The aims of this study were to characterize particle size in a thirdhand smoke (THS) aerosol and measure the effects of controlled inhalational exposure to THS on biomarkers of tobacco smoke exposure, inflammation, and oxidative stress in human subjects. Secondhand cigarette smoke changes physically and chemically after release into the environment. Some of the resulting chemicals persist indoors as thirdhand cigarette smoke. THS that is sorbed to surfaces can emit particles back into the air.
Aims and Methods
Smoke particle size was measured with a scanning mobility particle sizer and condensation particle counter. Using a crossover study design, 18 healthy nonsmokers received a 3-hour inhalational exposure to THS and to filtered, conditioned air. THS was generated with a smoking machine and aged overnight in a chamber. The chamber was flushed with clean air to create the THS aerosol. The tobacco smoke metabolites cotinine, 3-hydroxycotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) were measured in urine. Vascular endothelial growth factor and interleukin-6 in plasma, and 8-isoprostane in urine, were measured using enzyme-linked immunosorbent assay kits.
Results
Mean smoke particle size increased with aging (171 to 265 nm). We found significant increases in urinary cotinine and 3-hydroxycotinine after 3 hours of exposure to THS and no significant increases in NNAL, interleukin-6, vascular endothelial growth factor or 8-isoprostane.
Conclusions
Acute inhalational exposure to 22-hour old tobacco smoke aerosol caused increases in the metabolites of nicotine but not the metabolites of the tobacco-specific nitrosamine NNK (4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone). This corroborates the utility of cotinine and NNAL for secondhand and THS exposure screening.
Implications
This study shows that a 3-hour inhalational exposure to the tobacco smoke aerosol that forms in a room that has been smoked in and left unventilated overnight causes increases in urinary metabolites of nicotine, but not of the tobacco-specific nitrosamine NNK. This suggests that cleaning personnel and others who live and work in rooms polluted with aged or thirdhand cigarette smoke regularly may have inhalational exposures and potential health effects related to their exposure to nicotine and other smoke toxicants.
Oxford University Press (OUP)
Title: Respiratory Exposure to Thirdhand Cigarette Smoke Increases Concentrations of Urinary Metabolites of Nicotine
Description:
Abstract
Introduction
The aims of this study were to characterize particle size in a thirdhand smoke (THS) aerosol and measure the effects of controlled inhalational exposure to THS on biomarkers of tobacco smoke exposure, inflammation, and oxidative stress in human subjects.
Secondhand cigarette smoke changes physically and chemically after release into the environment.
Some of the resulting chemicals persist indoors as thirdhand cigarette smoke.
THS that is sorbed to surfaces can emit particles back into the air.
Aims and Methods
Smoke particle size was measured with a scanning mobility particle sizer and condensation particle counter.
Using a crossover study design, 18 healthy nonsmokers received a 3-hour inhalational exposure to THS and to filtered, conditioned air.
THS was generated with a smoking machine and aged overnight in a chamber.
The chamber was flushed with clean air to create the THS aerosol.
The tobacco smoke metabolites cotinine, 3-hydroxycotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) were measured in urine.
Vascular endothelial growth factor and interleukin-6 in plasma, and 8-isoprostane in urine, were measured using enzyme-linked immunosorbent assay kits.
Results
Mean smoke particle size increased with aging (171 to 265 nm).
We found significant increases in urinary cotinine and 3-hydroxycotinine after 3 hours of exposure to THS and no significant increases in NNAL, interleukin-6, vascular endothelial growth factor or 8-isoprostane.
Conclusions
Acute inhalational exposure to 22-hour old tobacco smoke aerosol caused increases in the metabolites of nicotine but not the metabolites of the tobacco-specific nitrosamine NNK (4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone).
This corroborates the utility of cotinine and NNAL for secondhand and THS exposure screening.
Implications
This study shows that a 3-hour inhalational exposure to the tobacco smoke aerosol that forms in a room that has been smoked in and left unventilated overnight causes increases in urinary metabolites of nicotine, but not of the tobacco-specific nitrosamine NNK.
This suggests that cleaning personnel and others who live and work in rooms polluted with aged or thirdhand cigarette smoke regularly may have inhalational exposures and potential health effects related to their exposure to nicotine and other smoke toxicants.
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