Using an e-cigarette in indoor environments may involuntarily expose nonusers to nicotine but not to toxic tobacco-specific combustion products. More research is needed to evaluate health consequences of secondhand exposure to nicotine, especially among vulnerable populations, including children, pregnant women, and people with cardiovascular conditions.

4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) is tobacco specific and has a longer half-life than other tobacco biomarkers studied thus far. An accurate measurement of the NNAL half-life is important for optimal use to assess exposure to tobacco smoke. We determined the half-life of NNAL in urine in eight daily smokers on a clinical research ward and in five occasional smokers in a real-life environment. Total NNAL in urine was monitored for 14 days in daily smokers after stopping smoking and for up to 60 days in occasional smokers. The average half-life for the terminal phase in the daily smoker group using a two-compartmental body model was 10.3 days (beta phase), and using a noncompartmental model, it was 9.1 days. In the occasional group, these values were 17.6 and 16.0 days, respectively. The alpha-phase half-lives were 14.3 and 27.8 hours for the two groups, respectively. The inter-subject coefficient of variation of the NNAL terminal half-life ranged from 14% to 30%, and the intra-subject coefficient of variation ranged from 3% to 18%. There was very good agreement between the plasma and urinary halflives in two subjects with plasma analyses: 7.4 versus 7.9 days and 9.2 versus 10.7 days. Mean renal clearance of NNAL was 13 ± 2.3 mL/min. The terminal half-life of NNAL of 10 to 18 days indicates that this biomarker can be used to detect tobacco smoke exposure for 6 to 12 weeks after cessation of exposure and requires a similar time to assess the steady levels of NNAL after switching from one tobacco product to another. (Cancer Epidemiol Biomarkers Prev 2009;18(12):3421-5)

SUMMARY Carbon monoxide (CO) is one of the more toxic agents present in the gas phase of second-hand tobacco smoke. There is sufficient evidence suggesting that passive smokers are involuntarily poisoned by low CO concentrations. At lower doses, CO affects the central nervous system leading to deterioration in visual perception, manual dexterity, learning, driving performance, and attention level. The effects of chronic inhalation of CO at doses corresponding to tobacco smoking on the cardiovascular system are not well investigated but might involve myocardial hypertrophy and arrhythmias. In people with pre-existing disease, CO pollution alone may result in increased morbidity and mortality. In the study CO levels were monitored in 22 Polish pubs. The temporary CO concentration varied in examined pubs varied from 0 to 33.11 ppm. The average 8-hours CO concentration varied from 0.21 to 10.20 ppm. Nine percent of pubs exceeded the WHO or EU limit value at some point during the monitoring process. The average weekly CO concentration in all examined microenvironments varied from 0 to 4.80 ppm. The most important factor influencing CO concentration was air-exchange through open doors and windows. In pubs where doors and windows were closed, the following statistical important factors influencing CO concentration were found: 1) the number of smokers present in the pub, 2) the pub’s capaciousness, and 3) and the pub’s location. The results of the study show that second-hand tobacco smoke is a significant source of CO in Polish pubs. Passive smokers in Polish pubs might be exposed to very high CO concentration exceeding UE reference value.

Carbon monoxide (CO) is one of the toxic constituents in tobacco smoke. The aim of the study was to evaluate a complex analytical method that allows quantification of the exposure of passive smokers to CO. The exposed volunteers were placed in the model room where portions of cigarettes (5, 10, or 15 cigarettes every 30 or 60 min over 4 h) were smoked using a homemade smoking machine. The concentrations of CO and of the ventilation marker (methane) were monitored for the duration of each experiment. CO and methane were analyzed on-line using GC-FID with methanization. Carboxyhemoglobin (COHb) was analyzed twice: just before and after the experiment. After hemolysis of a 100-microL blood sample, CO was quantitatively released by adding 10% K3[Fe(CN)6] inside a small reactor and under stable pressure transported through a microtube with an absorbing agent on a chromatography loop. The proposed analytical method allows us to quantify exposure of passive smokers by measuring the dose-effect correlation. We observed that increasing COHb levels were directly correlated with the CO concentration in the air, but were also intermediately correlated with the frequency and number of smoked cigarettes and with the ventilation coefficient.

In Poland, 38.0% of men and 25.6% of women smoke daily. One method for expanding access to smoking cessation services is through community-based pharmacists. Surveys were administered in [2007][2008] to (a) current smokers, (b) members of a pharmacy association, and (c) pharmacy students in their final year of training. Pharmacists were the highest ranked health professionals to whom Polish smokers reported they would turn for information about pharmacological support for smoking cessation. Most pharmacists (79%) reported their knowledge allowed them to provide basic smoking cessation information to their patients. Pharmacy students reported being more able to provide information about the health consequences of tobacco smoking than to help patients quit smoking (85% vs. 61%). In Poland, community-based pharmacists are positioned to provide smoking cessation interventions to all segments of the population. To extend and promote smoking cessation efforts, comprehensive tobacco cessation training should be a required component of the pharmacy school curriculum.