Identifying and quantifying secondhand smoke in source and receptor rooms: logistic regression and chemical mass balance approaches.

Identifying and quantifying secondhand tobacco smoke (SHS) that drifts between multiunit homes is critical to assessing exposure. Twenty-three different gaseous and particulate measurements were taken during controlled emissions from smoked cigarettes and six other common indoor source types in 60 single-room and 13 two-room experiments. We used measurements from the 60 single-room experiments for (i) the fitting of logistic regression models to predict the likelihood of SHS and (ii) the creation of source profiles for chemical mass balance (CMB) analysis to estimate source apportionment. We then applied these regression models and source profiles to the independent data set of 13 two-room experiments. Several logistic regression models correctly predicted the presence of cigarette smoke more than 80% of the time in both source and receptor rooms, with one model correct in 100% of applicable cases. CMB analysis of the source room provided significant PM2.5 concentration estimates of all true sources in 9 of 13 experiments and was half-correct (i.e., included an erroneous source or missed a true source) in the remaining four. In the receptor room, CMB provided significant estimates of all true sources in 9 of 13 experiments and was half-correct in another two.

Secondhand smoke exposure and risk following the Irish smoking ban: an assessment of salivary cotinine concentrations in hotel workers and air nicotine levels in bars.

OBJECTIVE: To investigate whether the Irish smoking ban has had an impact on secondhand smoke (SHS) exposures for hospitality workers. DESIGN, SETTING, AND PARTICIPANTS: Before and after the smoking ban a cohort of workers (n = 35) from a sample of city hotels (n = 15) were tested for saliva cotinine concentrations and completed questionnaires. Additionally, a random sample (n = 20) of city centre bars stratified by size (range 400-5000 square feet), were tested for air nicotine concentrations using passive samplers before and after the ban. MAIN OUTCOME MEASURES: Salivary cotinine concentrations (ng/ml), duration of self reported exposures to secondhand smoke, air nicotine (microg/cubic metre). RESULTS: Cotinine concentrations reduced by 69%, from 1.6 ng/ml to 0.5 ng/ml median (SD 1.29; p < 0.005). Overall 74% of subjects experienced decreases (range 16-99%), with 60% showing a halving of exposure levels at follow up. Self reported exposure to SHS at work showed a significant reduction from a median 30 hours a week to zero (p < 0.001). There was an 83% reduction in air nicotine concentrations from median 35.5 microg/m3 to 5.95 microg/m3 (p < 0.001). At baseline, three bars (16%) were below the 6.8 microg/m3 air nicotine significant risk level for lung cancer alone; at follow up this increased to 10 (53%). CONCLUSIONS: Passive smoking and associated risks were significantly reduced but not totally eliminated. Exposure to SHS is still possible for those working where smoking is still allowed and those working where smoke may migrate from outdoor areas. Further research is required to assess the true extent and magnitude of these exposures.

The smoke you don't see: uncovering tobacco industry scientific strategies aimed against environmental tobacco smoke policies.

OBJECTIVES: This review details the tobacco industry's scientific campaign aimed against policies addressing environmental tobacco smoke (ETS) and efforts to undermine US regulatory agencies from approximately 1988 to 1993. METHODS: The public availability of more than 40 million internal, once-secret tobacco company documents allowed an unedited and historical look at tobacco industry strategies. RESULTS: The analysis showed that the tobacco industry went to great lengths to battle the ETS issue worldwide by camouflaging its involvement and creating an impression of legitimate, unbiased scientific research. CONCLUSIONS: There is a need for further international monitoring of industry-produced science and for significant improvements in tobacco document accessibility.

Health risks associated with cigar smoking.

This article summarizes principal findings from a conference convened by the American Cancer Society in June 1998 to examine the health risks of cigar smoking. State-of-the-science reports were presented and 120 attendees (representing government and private agencies, academia, health educators, and tobacco control experts) participated in panels and summary development discussions. The following conclusions were reached by consensus: (1) rates of cigar smoking are rising among both adults and adolescents; (2) smoking cigars instead of cigarettes does not reduce the risk of nicotine addiction; (3) as the number of cigars smoked and the amount of smoke inhaled increases, the risk of death related to cigar smoking approaches that of cigarette smoking; (4) cigar smoke contains higher concentrations of toxic and carcinogenic compounds than cigarettes and is a major source of fine-particle and carbon monoxide indoor air pollution; and (5) cigar smoking is known to cause cancers of the lung and upper aerodigestive tract. JAMA. 2000;284:735-740

The effect of cigar smoking on indoor levels of carbon monoxide and particles.

To provide new information on environmental tobacco smoke (ETS) levels from cigars, we conducted three types of experiments: (1) Measurements of carbon monoxide (CO) during 15 controlled experiments in an office where several cigar brands were machine-smoked; (2) Measurements of CO or respirable suspended particles (RSP) and particle-bound polycyclic aromatic hydrocarbons (PAH) in a residence where two cigars were smoked by a person; and (3) Measurements of CO during two studies at cigar social events (where there were up to 18 cigars being smoked at a time) in which an investigator wore a concealed personal exposure monitor. Average concentrations of CO at the cigar social events were comparable to, or larger than, those observed on a freeway during rush hour traffic. A mass balance model that has been used successfully to predict ETS from cigarettes is used in this paper to obtain CO, RSP, and PAH emission factors (emission rate [mg/min], total mass emitted [mg], and emissions per mass smoked [mg/g]). The calculated emission factors show that the cigar can be a stronger source of CO than the cigarette. In contrast, the cigar may have fewer emissions of RSP and PAH per gram of consumed tobacco than the cigarette, but its size and longer smoking time results in greater total RSP and PAH emissions than for a single cigarette.

Air nicotine and saliva cotinine as indicators of workplace passive smoking exposure and risk.

We model nicotine from environmental tobacco smoke (ETS) in office air and salivary cotinine in nonsmoking U.S. workers. We estimate that: an average salivary cotinine level of 0.4 ng/ml corresponds to an increased lifetime mortality risk of 1/1000 for lung cancer, and 1/100 for heart disease; > 95% of ETS-exposed office workers exceed OSHA's significant risk level for heart disease mortality, and 60% exceed significant risk for lung cancer mortality; 4000 heart disease deaths and 400 lung cancer deaths occur annually among office workers from passive smoking in the workplace, at the current 28% prevalence of unrestricted smoking in the office workplace.

Smoking behavior, workplace policies, and public opinion regarding smoking restrictions in Maryland.

The Maryland Occupational Safety and Health (MOSH) advisory board recently proposed a smoking ban in most Maryland workplaces, including bars and restaurants, unless smoking is restricted to a separately ventilated area where nonsmoking workers cannot be required to enter. Results from the 1992-1993 Current Population Survey strongly suggest that there is broad support among Maryland residents for such restrictions and that the MOSH rules would merely extend an already widespread practice in the state. Efforts by the tobacco industry to gain an injunction against the proposed MOSH regulations would not appear to be supported by a clear majority of Maryland residents.

An enforceable indoor air quality standard for environmental tobacco smoke in the workplace.

Environmental tobacco smoke (ETS) has recently been determined by U.S. environmental and occupational health authorities to be a human carcinogen. We develop a model which permits using atmospheric nicotine measurements to estimate nonsmokers' ETS lung cancer risks in individual workplaces for the first time. We estimate that during the 1980s, the U.S. nonsmoking adult population's median nicotine lung exposure (homes and workplaces combined) was 143 micrograms (micrograms) of nicotine daily, and that most-exposed adult nonsmokers inhaled 1430 micrograms/day. These exposure estimates are validated by pharmacokinetic modeling which yields the corresponding steady-state dose of the nicotine metabolite, cotinine. For U.S. adult nonsmokers of working age, we estimate median cotinine values of about 1.0 nanogram per milliliter (ng/ml) in plasma, and 6.2 ng/ml in urine; for most-exposed nonsmokers, we estimate cotinine concentrations of about 10 ng/ml in plasma and 62 ng/ml in urine. These values are consistent to within 15% of the cotinine values observed in contemporaneous clinical epidemiological studies. Corresponding median risk from ETS exposure in U.S. nonsmokers during the 1980s is estimated at about two lung cancer deaths (LCDs) per 1000 at risk, and for most-exposed nonsmokers, about two LCDs per 100. Risks abroad appear similar. Modeling of the lung cancer mortality risk from passive smoking suggests that de minimis [i.e., "acceptable" (10(-6))], risk occurs at an 8-hr time-weighted-average exposure concentration of 7.5 nanograms of ETS nicotine per cubic meter of workplace air for a working lifetime of 40 years. This model is based upon a linear exposure-response relationship validated by physical, clinical, and epidemiological data. From available data, it appears that workplaces without effective smoking policies considerably exceed this de minimis risk standard. For a substantial fraction of the 59 million nonsmoking workers in the U.S., current workplace exposure to ETS also appears to pose risks exceeding the de manifestis risk level above which carcinogens are strictly regulated by the federal government.

Risk assessment methodologies for passive smoking-induced lung cancer.

Risk assessment methodologies have been successfully applied to control societal risk from outdoor air pollutants. They are now being applied to indoor air pollutants such as environmental tobacco smoke (ETS) and radon. Nonsmokers' exposures to ETS have been assessed based on dosimetry of nicotine, its metabolite, continine, and on exposure to the particulate phase of ETS. Lung cancer responses have been based on both the epidemiology of active and of passive smoking. Nine risk assessments of nonsmokers' lung cancer risk from exposure to ETS have been performed. Some have estimated risks for lifelong nonsmokers only; others have included ex-smokers; still others have estimated total deaths from all causes. To facilitate interstudy comparison, in some cases lung cancers had to be interpolated from a total, or the authors' original estimate had to be adjusted to include ex-smokers. Further, all estimates were adjusted to 1988. Excluding one study whose estimate differs from the mean of the others by two orders of magnitude, the remaining risk assessments are in remarkable agreement. The mean estimate is approximately 5000 +/- 2400 nonsmokers' lung cancer deaths (LCDSs) per year. This is a 25% greater risk to nonsmokers than is indoor radon, and is about 57 times greater than the combined estimated cancer risk from all the hazardous outdoor air pollutants currently regulated by the Environmental Protection Agency: airborne radionuclides, asbestos, arsenic, benzene, coke oven emissions, and vinyl chloride.