OBJECTIVES: To determine the effects of aging on the toxicity of sidestream tobacco smoke, the complex chemical mixture that enters the air from the lit end of burning cigarettes and constitutes the vast bulk of secondhand smoke. DESIGN: Statistical analysis of data from controlled experimental exposures of Sprague Dawley rats to fresh and aged (for more than 30 minutes) sidestream smoke for up to 90 days followed by histological sectioning of the respiratory epithelium. The data were obtained from a series of experiments conducted at Philip Morris' formerly secret INBIFO (Institut für Biologische Forschung) laboratory in Germany. RESULTS: Using total particulate material as the measure of smoke exposure, aging sidestream cigarette smoke for at least 30 minutes increases its toxicity fourfold for 21 day exposures and doubles the toxicity for 90 day exposures, relative to fresh sidestream smoke. CONCLUSIONS: These results help explain the relatively large biological effects of secondhand smoke compared to equivalent mass doses of mainstream smoke.

Thirdhand cigarette smoke is the fraction of cigarette smoke that remains in the environment long after a cigarette is extinguished.

The Truth Tobacco Industry Documents collection at the University of California San Francisco was searched for information on thirdhand smoke.

In 1991, scientists at Philip Morris Inc conducted some of the first studies on thirdhand cigarette smoke. For 110 days, 8 hours a day, they ran sidestream cigarette smoke through a 30 m3 room that contained carpet, curtain, and textured wallpaper. The room was ventilated with clean air every night. By comparing the chemicals in the air during the 8-hour smoking period and during the clean air ventilation period, they showed that some smoke chemicals persist in the air 12 hours after smoking. By extracting the nicotine and nitrosamines from samples of the carpet, curtain, and wallpaper, they found that high concentrations of nicotine and the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) persisted in the room for more than 50 days; that surface chemistry affected nitrosamine concentrations; and that the concentration of NNK in the room, 110 days after the last cigarette was extinguished, could exceed the mass of NNK that entered the room as smoke.

These data, from a controlled environment where the total number of cigarettes smoked is known, provide further evidence that cigarette smoke chemicals remain in the environment for months after smoking, that they reemit back into the air, and that they react to form new toxins and carcinogens. Smoke-free policies are the best method to reduce exposure to thirdhand smoke.

This unpublished, original research from Philip Morris Inc demonstrates that majority of the nicotine and tobacco-specific nitrosamines in the secondhand smoke from each cigarette smoked indoors remains on indoor surfaces for months after the cigarette is extinguished. It also demonstrates that elevated concentrations of nicotine, ammonia, formaldehyde, and the gas-phase nitrosamine, N-nitrosopyrrolidine, can be found in the air for more than 12 hours after smoking; that surface chemistry affects nitrosamine formation and persistence; and that the amount of the carcinogenic nitrosamine NNK that persists months after smoking ends can exceed the amount that actually came out of the cigarettes.

When, as a condition of the Master Settlement Agreement (MSA) in 1998, US tobacco companies disbanded the Council for Tobacco Research and the Center for Indoor Air Research, they lost a vital connection to scientists in academia and the private sector. The aim of this paper was to investigate two new research projects funded by US tobacco companies by analysis of internal tobacco industry documents now available at the University of California San Francisco (San Francisco, California, USA) Legacy tobacco documents library, other websites and the open scientific literature. Since the MSA, individual US tobacco companies have replaced their industry-wide collaborative granting organisations with new, individual research programmes. Philip Morris has funded a directed research project through the non-profit Life Sciences Research Office, and British American Tobacco and its US subsidiary Brown and Williamson have funded the non-profit Institute for Science and Health. Both of these organisations have downplayed or concealed their true level of involvement with the tobacco industry. Both organisations have key members with significant and long-standing financial relationships with the tobacco industry. Regulatory officials and policy makers need to be aware that the studies these groups publish may not be as independent as they seem.

Introduction

Methods

Results

Conclusions

Implications

Introduction.  The aims of this study were to characterize particle size in a thirdhand smoke aerosol and measure the effects of controlled inhalational exposure to thirdhand smoke 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.  Thirdhand smoke that is sorbed to surfaces can emit particles back into the air.

Methods.  Smoke particle size was measured with a scanning mobility particle sizer/condensation particle counter. Using a crossover study design, 18 healthy nonsmokers received a three-hour inhalational exposure to thirdhand smoke and to filtered, conditioned air.  Thirdhand smoke 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 nm to 265 nm). We found significant increases in urinary cotinine and 3-hydroxycotinine after three hours of exposure to thirdhand smoke 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 thirdhand smoke exposure screening.

Introduction: Cannabis regulation and use are undergoing dramatic changes. New cannabis products and new ways of using are emerging.  These changes have the potential to affect exposure to cannabis smoke and other emissions from cannabis use.  Cannabis smoke is known to contain fine, respirable particles (PM_2.5) and other toxicants and carcinogens. 

Objectives: To assess the potential for exposure to PM2.5 from novel cannabis aerosols, we measured PM_2.5 concentrations in a cannabis retail outlet (a dispensary) that permits on-site consumption of cannabis via non-combustion methods including vaporization and dabbing.

Methods: PM2.5 concentrations in the dispensary were measured around the clock for five weeks using 2 laser photometer instruments (429,604 data points collected over 38.69 days).  The instruments were calibrated gravimetrically using a controlled cigarette generation system at regular intervals during the experiment. Outdoor PM_2.5 concentrations were taken from a nearby EPA monitoring station.

Results: The average PM_2.5 concentration in the dispensary retail space, during business hours, was 84 ± 124 µg/m³, with a median of 47 µg/m³.  The average PM_2.5 concentration when the business was closed was 3 ± 7 µg/m³ with a median of 2 µg/m³.   The highest daily concentrations correlated with the hours with the most customers.

Conclusion: Our results suggest that the use of cannabis products indoors, even by non-combustion methods, increases the concentration of PM_2.5. These findings are of concern to the public health because the business studied was in compliance with local laws and because PM_2.5 exposure is a known cause of cardiopulmonary and metabolic disease.