Biomarkers of Secondhand Smoke Exposure in Waterpipe Tobacco Venue Employees in Istanbul, Moscow, and Cairo.

Background: Most smoke-free legislation to reduce secondhand smoke (SHS) exposure exempts waterpipe (hookah) smoking venues. Few studies have examined SHS exposure in waterpipe venues and their employees. Methods: We surveyed 276 employees of 46 waterpipe tobacco venues in Istanbul, Moscow, and Cairo. We interviewed venue managers and employees and collected biological samples from employees to measure exhaled carbon monoxide (CO), hair nicotine, saliva cotinine, urine cotinine, urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and urine 1-hydroxypyrene glucuronide (1-OHPG). We estimated adjusted geometric mean ratios (GMR) of each SHS biomarker by employee characteristics and indoor air SHS measures. Results: There were 73 nonsmoking employees and 203 current smokers of cigarettes or waterpipe. In nonsmokers, the median (interquartile) range concentrations of SHS biomarkers were 1.1 (0.2, 40.9) µg/g creatinine urine cotinine, 5.5 (2, 15) ng/mL saliva cotinine, 0.95 (0.36, 5.02) ng/mg hair nicotine, 1.48 (0.98, 3.97) pg/mg creatinine urine NNAL, 0.54 (0.25, 0.97) pmol/mg creatinine urine 1-OHPG, and 1.67 (1.33, 2.33) ppm exhaled CO. An 8-hour increase in work hours was associated with higher urine cotinine (GMR: 1.68, 95% CI: 1.20, 2.37) and hair nicotine (GMR: 1.22, 95% CI: 1.05, 1.43). Lighting waterpipes was associated with higher saliva cotinine (GMR: 2.83, 95% CI: 1.05, 7.62). Conclusions: Nonsmoking employees of waterpipe tobacco venues were exposed to high levels of SHS, including measurable levels of carcinogenic biomarkers (tobacco-specific nitrosamines and PAHs). Implications: Smoke-free regulation should be extended to waterpipe venues to protect nonsmoking employees and patrons from the adverse health effects of SHS.

Foucault, surveillance, and carbon monoxide testing within stop-smoking services.

Health professionals have adopted proactive testing for early evidence of disease. Researchers have identified that this leads to enumerated understandings and shapes behavior in productive ways. Smoking-cessation advisors regularly test clients for carbon monoxide (CO), but client views of this had not previously been explored. We interviewed 23 clients of a United Kingdom-based stop-smoking service regarding their experiences of CO testing. The majority of participants were successful quitters. We used ATLAS.ti 7 as a data-management tool during structured qualitative analysis. Our findings reveal that clients believed the results of their CO tests. Many became enumerated in their understanding, and thus placed themselves in a hierarchy with other members of their group. Almost all clients found that knowing their CO test score was motivating. We conclude that additional research is needed to understand the experiences of CO testing among clients who do not quit.

Factors associated with smoking abstinence among smokers and recent-quitters with lung and head and neck cancer.

INTRODUCTION: Smoking cessation among cancer patients is critical for improving outcomes. Understanding factors associated with smoking abstinence after the diagnosis of cancer can provide direction to develop and test interventions to enhance cessation rates. The purpose of this study was to identify determinants of smoking outcomes among cancer patients. METHODS: Standardized questionnaires were used to collect data from 163 smokers or recent-quitters (quit≤6 months) at study entry of which 132 and 121 had data collected at 3 and 6 months. Biochemical verification was conducted with urinary cotinine and carbon monoxide. Descriptive statistics, Cronbach alpha coefficients, Pearson correlations, Fisher's exact test, and multivariable logistic regression were used for analyses. RESULTS: Seven-day-point-prevalence-abstinence (PPA) rates were 90/132 (68%) at 3 months; 46/71 (65%) among lung and 44/61 (72%) among head and neck cancer patients, whereas 7-day-PPA rates were 74/121 (61%) at 6 months; 31/58 (53%) among lung and 43/63 (68%) among head and neck cancer patients. Continuous abstinence rates were 63/89 (71%) at 3 months; 32/45 (71%) among lung and 31/44 (70%) among head and neck cancer patients, whereas continuous abstinence rates were 46/89 (52%) at 6 months; 18/45 (40%) among lung and 28/44 (64%) among head and neck cancer patients. Lower cancer-related, psychological and nicotine withdrawal symptoms were associated with increased 7-D-PPA abstinence rates at 3 and 6 months in univariate models. In multivariable models, however, decreased craving was significantly related with 7-day-PPA at 3 months and decreased craving and increased self-efficacy were associated with 7-D-PPA at 6 months. Decreased craving was the only factor associated with continuous abstinence at 6 months. CONCLUSIONS: Smoking outcomes among lung and head and neck cancer patients appear to have remained the same over the last two decades despite the availability of an increased number of pharmacotherapy options to treat tobacco dependence. Decreased craving and increased self-efficacy were the most consistent factors associated with improved smoking outcomes but symptom control may also play a role in optimal management. Use of combined, and/or higher doses of pharmacotherapy along with behavioral interventions that increase self-efficacy and manage symptoms may promote enhanced cessation rates.

Factors affecting exposure to nicotine and carbon monoxide in adult cigarette smokers.

Exposure to cigarette smoke among smokers is highly variable. This variability has been attributed to differences in smoking behavior as measured by smoking topography, as well as other behavioral and subjective aspects of smoking. The objective of this study was to determine the factors affecting smoke exposure as estimated by biomarkers of exposure to nicotine and carbon monoxide (CO). In a multi-center cross-sectional study of 3585 adult smokers and 1077 adult nonsmokers, exposure to nicotine and CO was estimated by 24h urinary excretion of nicotine and five of its metabolites and by blood carboxyhemoglobin, respectively. Number of cigarettes smoked per day (CPD) was determined from cigarette butts returned. Puffing parameters were determined through a CreSS® micro device and a 182-item adult smoker questionnaire (ASQ) was administered. The relationship between exposure and demographic factors, smoking machine measured tar yield and CPD was examined in a statistical model (Model A). Topography parameters were added to this model (Model B) which was further expanded (Model C) by adding selected questions from the ASQ identified by a data reduction process. In all the models, CPD was the most important and highest ranking factor determining daily exposure. Other statistically significant factors were number of years smoked, questions related to morning smoking, topography and tar yield categories. In conclusion, the models investigated in this analysis, explain about 30-40% of variability in exposure to nicotine and CO.

Evaluation of exposure reduction to indoor air pollution in stove intervention projects in Peru by urinary biomonitoring of polycyclic aromatic hydrocarbon metabolites.

Burning biomass fuels such as wood on indoor open-pit stoves is common in developing regions. In such settings, exposure to harmful combustion products such as fine particulate matter (PM(2.5)), carbon monoxide (CO) and polycyclic aromatic hydrocarbons (PAHs) is of concern. We aimed to investigate if the replacement of open pit stoves by improved stoves equipped with a chimney would significantly reduce exposure to PAHs, PM(2.5) and CO. Two stove projects were evaluated in Peru. Program A was part of the Juntos National Program in which households built their own stoves using materials provided. In Program B, Barrick Gold Corporation hired a company to produce and install the stoves locally. A total of 30 and 27 homes participated in Program A and B, respectively. We collected personal and kitchen air samples, as well as morning urine samples from women tasked with cooking in the households before and after the installation of the improved stoves. Median levels of PM(2.5) and CO were significantly reduced in kitchen and personal air samples by 47-74% after the installation of the new stoves, while the median reduction of 10 urinary hydroxylate PAH metabolites (OH-PAHs) was 19%-52%. The observed OH-PAH concentration in this study was comparable or higher than the 95th percentile of the general U.S. population, even after the stove intervention, indicating a high overall exposure in this population.

Evaluation of biomarkers of exposure in adult cigarette smokers using Marlboro snus.

INTRODUCTION: It has been reported that adult smokers (AS) may be considering smokeless tobacco products as an alternative to smoking. The objective of this study was to evaluate the change in exposure in AS using Marlboro snus (MSNUS) (a tobacco pouch product in test market in June 2007). METHODS: AS were randomized into the following groups--CS: subjects (n = 30) continue smoking their own brand; DU: subjects (n = 60) reduced their daily cigarette consumption by >or=50% and were allowed to use MSNUS; SN: subjects (n = 15) stopped smoking their cigarettes but were allowed to use MSNUS; NT: subjects (n = 15) were not allowed to use any tobacco products for the entire duration of the 8-day study. Biomarkers of smoke exposure (BOE) measured at baseline and postbaseline were 24-hr urinary excretion of metabolites of N-nitrosamines, nicotine (urine and plasma), aromatic amines, benzene, and polycyclic aromatic hydrocarbon; urine mutagenicity; and carboxyhemoglobin at various timepoints. RESULTS: Statistically significant (p < .05) reductions in all the urinary BOE were observed in the DU group compared with the CS group. After correcting for the residual effect, a proportionate reduction (approximately 50%) in most of the biomarkers was observed. Even larger reductions, similar to the NT group, were observed in the SN group. DISCUSSION: The proportionate reduction in exposure when reducing the number of cigarettes by 50% and using MSNUS, under the consumption patterns observed, suggest that the AS did not appear to alter their smoking behavior. The added exposure from MSNUS usage in this group was minimal. The AS sustained substantial reductions in exposure when using MSNUS exclusively.

A cross-sectional investigation of biomarkers of risk after a decade of smoking.

Two groups of 20 healthy volunteers with cigarettes of different tar yield were compared with a group of 20 never smokers over 24 h for several biomarkers. All groups were of similar mean ages and the smokers had smoked for a homogeneous period of approximately 10 yr. The groups were assessed using routine medical parameters as well as biomarkers of recent smoke exposure and other biomarkers that were under evaluation as possible markers of risk for smoking-associated diseases. All biomarkers of exposure-carbon monoxide, nicotine plus its five major metabolites, and 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanol (NNAL)-were significantly elevated in smokers. For biomarkers of potential risk evaluated in the blood, white cells and immunoglobulin (Ig) G showed a decrease related to smoking status (p < .01). Interleukin 6 levels were higher in smoker groups compared to never smokers, with a significant increasing trend across the groups (p < .05). Among the urinary biomarkers studied, 11-deydro-thromboxane B2, 2,3-dinor-thromboxane B2, and thymidine glycol showed significant increasing trends across the groups (p < .01). The results suggest that after the first decade or less of smoking, changes in inflammatory, immunological, and cardiovascular function can be observed. However, further studies on larger groups will be required to better understand the kinetics of these subtle effects observed early in smokers and their relationship with the potential risk of subsequent smoking-associated disease.

Exhaled carbon monoxide screening for environmental tobacco smoke exposure in preanesthetic children.

OBJECTIVE: Exposure to environmental tobacco smoke (ETS) is associated with an increased risk of perioperative adverse events in children. The purpose of this study was to evaluate exhaled carbon monoxide (CO) as a preoperative ETS screening tool in children. METHODS: Five hundred and one children aged 6-15 years were enrolled. The child's guardian completed a questionnaire that surveyed environmental exposures to CO and ETS. A preoperative urine sample was obtained from children who assented and were able to void, and urine cotinine values were measured. Exhaled CO was measured using the EC50-Micro Smokerlyzer (Bedfont Scientific Ltd, UK). RESULTS: Four hundred and fifty-one subjects completed the study, and urine samples were obtained from 83. 25% of subjects were classified as exposed to ETS based on questionnaire results. Exhaled CO values did not correlate with either the qualitative (questionnaire) or quantitative (urine cotinine) measurements of ETS exposure. Exhaled CO predicted a urine cotinine/creatinine ratio >10 with a sensitivity of 10% and a specificity of 85%. CONCLUSION: Exhaled CO measured by this device is not a useful preoperative screening tool for ETS exposure in children. Because exhaled CO has been used successfully to monitor ETS exposure in adolescents, we believe that its failure in our population is as a result of the limited ability of small children to perform vital capacity maneuvers in order to provide an adequate endtidal sample.

Pilot study on lower nitrosamine smokeless tobacco products compared with medicinal nicotine.

Smokeless tobacco (ST) products have the potential to be used as a harm reduction method for cigarette smokers. These products can deliver significantly less toxicants than cigarettes, although they are not toxicant free nor harmless. It is important to examine potential health risks and benefits of these products. These two small pilot studies examined the effects of two different ST products (Exalt and Ariva) compared with medicinal nicotine, another potential harm reduction product. Dependent, healthy adult cigarette smokers, who were motivated to quit smoking, underwent 1 week of baseline smoking measurement. They were then asked to quit smoking and were randomly assigned to use either an ST product or a medicinal nicotine lozenge (MNL, Commit) for 2 weeks, then crossed over to use the other product for 2 weeks. In the last week, following the sampling phase, subjects could choose the product they wished to use. Assessments were made repeatedly during baseline cigarette use and throughout the 5 weeks of treatment. Outcome measures included biomarkers for tobacco exposure and subjective, physiological, and behavioral responses. Tobacco-specific carcinogen uptake was greater from Exalt than from the MNL, and was comparable between the MNL and Ariva. Physiological effects and subjective effects on withdrawal and craving were comparable among Exalt, Ariva, and the MNL. Ariva was preferred over the MNL, which was preferred over Exalt. With the exception of medicinal nicotine products, low-nitrosamine ST products have the greatest potential to result in reduced toxicant exposure compared with other combustible reduced exposure products and have promise for reducing individual risk for disease. However, the population effect of marketing of such products as reduced exposure/reduced risk is unknown. The need for further research in this area and regulation of tobacco products is evident.

Clinical laboratory evaluation of potential reduced exposure products for smokers.

Smoking-related cancer and other disease account for more than 400,000 U.S. deaths annually. Smoking cessation reduces smoking-related disease rates, but relapse rates are high. Thus, interest in reducing the harm of continued smoking is growing. Potential reduced exposure products (PREPs) are marketed to reduce smokers' exposure to smoke toxicants such as carbon monoxide (CO) and carcinogens and may be harm reduction tools. New PREPs are proliferating, but past experience with "low-yield" cigarettes that failed to reduce smokers' toxicant exposure suggests that comprehensive evaluation is necessary to predict if these new products are likely to alter the harm caused by smoking. The purpose of the study was to develop clinical laboratory methods for PREP evaluation. Smokers (N = 35) completed four, 5-day conditions that differed by product used: Advance, Eclipse, own brand cigarettes, or no cigarettes. Carcinogen (as assessed by one nitrosamine and one polycyclic aromatic hydrocarbon biomarker) and nicotine exposure were assessed via thrice-weekly urine sampling. Withdrawal symptoms were measured daily, and smoking behavior was assessed on the first and last day of each condition. Relative to own brand, Advance reduced exposure to the nitrosamine NNK and CO, and Eclipse reduced exposure to nicotine and the nitrosamine NNK, increased exposure to CO, and resulted in larger, longer, and more frequent puffs. No smoking reduced exposure to the nitrosamine NNK, CO, and nicotine, whereas withdrawal was elevated (all p values <.05). Clinical laboratory evaluation of PREPs for smokers is valuable for measuring users' smoke toxicant exposure, withdrawal, and smoking behavior and should be incorporated into a comprehensive PREP evaluation strategy.

Relationships between cigarette consumption and biomarkers of tobacco toxin exposure.

Epidemiologic studies show a dose-response relationship between cigarettes per day and health outcomes such as heart and lung disease, and health outcomes are related to some biomarkers of tobacco exposure. The objective of this study was to examine the relationships between cigarettes per day and levels of selected biomarkers of tobacco toxin exposure: carbon monoxide (CO), metabolites of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and polycyclic aromatic hydrocarbons [total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and 1-hydroxypyrene (1-HOP), respectively], and total cotinine (cotinine plus cotinine-N-glucuronide). We did a cross-sectional analysis of merged data from (a) two clinical trials and (b) two cohorts of light smokers (total n = 400). The mean age of participants was 50.4 years and the range of cigarette consumption was 1 to 100/d; however, few subjects smoked >45 cigarettes/d (n = 12). Results show that levels of the biomarkers CO, total NNAL, and total cotinine increase with an increase in the number of cigarettes smoked per day, but not in a linear fashion. 1-HOP is a less discriminating biomarker as levels are relatively stable regardless of the number of cigarettes smoked per day. There is considerable variability in toxin measurement, especially at high levels of smoking. There was a significant correlation between cigarettes per day and total NNAL, 1-HOP, total cotinine, and CO. Total NNAL was highly significantly correlated with total cotinine and CO and also significantly correlated with 1-HOP. These findings suggest that the number of cigarettes smoked per day is not necessarily a reliable measure of toxin exposure and may underestimate tobacco toxin exposure at low levels of smoking or overestimate exposure at high levels of smoking.

Nitric oxide synthesis inhibition promotes renal production of carbon monoxide.

We tested the hypothesis that the status of NO synthesis influences the renal heme-heme oxygenase system. Studies were conducted in untreated rats and rats treated with the NO synthesis inhibitor N(G)-nitro-L-arginine methyl ester for 2 days. Treated and untreated rats were contrasted in terms of renal expression of heme oxygenase-1 and -2, renal carbon monoxide (CO)-generating activity, and urinary CO concentration and excretion rate. Heme oxygenase-1 and -2 proteins were similarly expressed in the kidneys of untreated and treated rats. In contrast, the NADPH-dependent component of the CO-generating activity of renal homogenates incubated with heme (a measure of heme oxygenase activity) was higher (P<0.05) in kidneys from rats treated with the NO synthesis inhibitor relative to corresponding data in untreated rats (1015+/-95 versus 379+/-111 pmol CO/mg per hour). Similarly, relative to corresponding data in untreated rats, rats treated with the NO synthesis inhibitor displayed increased (P<0.05) urinary CO concentration (920+/-174 versus 2286+/-472 pmol/mL) and urinary CO excretion (4.7+/-0.4 versus 14.3+/-2.7 pmol/min). This study demonstrates that NO synthesis inhibition upregulates the urinary concentration and excretion rate of CO, and the HO-dependent generation of CO by renal homogenates, without affecting the expression of renal heme oxygenase isoforms. Our findings imply that endogenous NO is an inhibitory regulator of renal CO generation by HO.

Effects of exogenous heme on renal function: role of heme oxygenase and cyclooxygenase.

We examined the effects of heme administration (15 mg/kg IV) on indexes of renal carbon monoxide production and contrasted the renal functional response to heme in anesthetized rats pretreated and not pretreated with stannous mesoporphyrin (40 micromol/kg IV) to inhibit heme oxygenase or sodium meclofenamate (5 mg/kg IV plus infusion at 10 microg/kg per minute) to inhibit cyclooxygenase. In rats without drug pretreatment, heme administration decreased renal vascular resistance and increased renal blood flow, urine volume, and sodium excretion associated with augmented urinary excretion of 6-keto-PGF1alpha and enhanced concentration of carbon monoxide in the renal cortical microdialysate. Pretreatment with stannous mesoporphyrin did not prevent heme from producing renal vasodilation and increasing renal blood flow but abolished the diuretic and natriuretic responses. Conversely, pretreatment with sodium meclofenamate blunted the renal vasodilatory effect of heme but affected neither the diuretic nor the natriuretic effect. We conclude that heme-induced renal vasodilation is a cyclooxygenase-dependent response involving increased synthesis of PGI2, whereas heme-induced diuresis and natriuresis are heme oxygenase-dependent responses involving inhibition of tubular reabsorption of sodium and water through undefined mechanisms.

Carbon monoxide regulates blood pressure cooperatively with nitric oxide in hypertensive rats.

Both carbon monoxide (CO), the product of heme oxygenase (HO), and nitric oxide (NO) elevate cyclic guanosine monophosphate levels in smooth muscle cells, leading to relaxation of the vessels. We examined the hypothesis that the effect of CO in regulating blood pressure could be augmented in hypertension where the function and/or production of NO is impaired. We used two hypertensive models, a spontaneously hypertensive rat (SHR), and a Wistar Kyoto rat (WKY) which was given the NO synthase (NOS) inhibitor N(omega)-nitro- L-arginine (L-NNA). In these hypertensive rats, we examined HO gene expression with Northern blot analysis, guanosine 3',5'-monophosphate (cGMP) levels with enzyme-linked immunosorbent assay of each organ, and the response of blood pressure to treatment with an HO substrate (hemin, 23 micromol/kg body weight, i.p.) or HO inhibitor (zinc or tin protoporphyrin-IX; ZnPP or SnPP, 50 micromol/kg body weight i.p. or s.c.), for 4 or 8 consecutive days with plethysmography. Northern blot analysis showed that HO-1 and -2 mRNA levels in the left ventricle, aorta, kidney, and soleus muscle in the hypertensive rats were 2-5 times higher than those in control normotensive WKYrats. In contrast, both HO mRNA levels in the gastrocnemius muscle in the hypertensive rats were similar to those in control WKYrats. As to whether the HO/CO system contributes to the regulation of blood pressure, ZnPP or SnPP increased and hemin decreased systolic blood pressure (SBP), respectively, in the hypertensive rats (P < 0.01), but not in WKYrats, accompanied with changes in cGMP in each organ of the hypertensive rats. The effect of CO in the regulation of blood pressure is augmented, resulting in increased expression of HO gene when the function and/or production of NO is impaired.

Smoking during pregnancy and intention to quit: a profile of methadone-maintained women.

The present study characterized cigarette smoking patterns (self-report, carbon monoxide, and cotinine), health-risk perceptions, attitudes, and quitting intentions among pregnant methadone-maintained women (n = 50) enrolled in comprehensive perinatal drug treatment. At baseline, women expressed only moderate motivation and self-efficacy for smoking cessation, and 60% were in the precontemplation stage of change for quitting. Follow-up assessment during pregnancy (n = 40) showed no change in self-reported cigarettes per day or cotinine values. Despite recognition of the personal and fetal health risks of smoking and high social support for quitting, none of the women stopped smoking and few demonstrated reduction. Compared to other pregnant smokers, this sample is characterized by many of the factors associated with difficulty in quitting. Innovative harm-reduction strategies and nicotine replacement medications deserve scientific attention in this high-risk group of tenacious smokers.

Smoking behaviour and compensation: a review of the literature.

RATIONALE: Compensation or compensatory smoking, accurately defined, deals with the question of whether switching to cigarette brands with different smoke yields is associated with a change in smoke uptake proportional to the change in machine-derived yields. The issue of compensation is important because it bears on whether switching to "lighter" brands means lower overall smoke intake or not. OBJECTIVES: The present review investigated whether and to what extend low yield cigarettes are smoked more intensively. In addition, published data on whether nicotine, "tar", or any other smoke constituent or property influence compensational smoking are summarized. METHODS: The studies on compensation were classified as follows: (1) studies on smoking behaviour in relation to cigarette yields (with and without brand switching); (2) studies on compensation for nicotine (switching between cigarettes which differ "only" in their nicotine yield, nicotine supplementation, manipulation of renal nicotine excretion, administration of nicotine agonists or antagonists); (3) studies on compensation for other factors (influence of tar, taste, irritation, draw resistance). In order to quantify the degree of compensation, an index is defined and applied to selected brand switching studies. This compensation index determines, in relative units, the degree to which a smoker responds to a change in smoke yields with a change in smoke uptake measured by suitable biomarkers. The role of vent blocking is also briefly discussed. RESULTS: Most of the studies which compare the smoking behaviour when smoking cigarettes with different smoke yields supply evidence for "partial" compensation, suggesting that cigarettes with lower yields are smoked more intensively than those with higher yields. These studies also show that a change in the daily number of cigarettes is not a common mechanism of compensation. Effective vent blocking during smoking is a rare event and can therefore also be regarded as an uncommon mechanism of compensation. Evaluation of a suitable subset of brand-switching studies revealed an average compensation of 50-60% of the nicotine yield. Compensation tended to be more complete when changing to cigarettes with higher yields than when changing to cigarettes with lower yields. In general, brand-switching studies do not supply information on the underlying causal factors responsible for compensatory smoking. Results of the nicotine supplementation studies are not conclusive: some report evidence of nicotine titration, others do not. A general problem with this type of investigation is that continuous nicotine application does not mimic the spike-wise application with cigarette smoking, and may lead to nicotine tolerance. There is limited evidence that cigarettes were smoked more intensively when the urinary clearance of nicotine was increased. A small number of studies provide some evidence that smoking intensity increased after smokers were administered a nicotine antagonist. Several reports indicate that tar, taste and sensory properties of the smoke as well as the draw resistance of the cigarette may play a role in compensatory smoking. Low-yield cigarettes usually have reduced pressure drops which smoke researchers have suggested leads to increased puff volume. This effect seems to be independent of the smoke yield of the cigarette. There is also some evidence that some smokers maintain a consistent pattern of smoking which works independent of any changes in nicotine or tar yields, taste or design features of the cigarette ("functional autonomy"). CONCLUSIONS: The available data suggest that smokers partially compensate for a different smoke yield. While the factors and their interaction responsible for compensational smoking are not fully understood, there are data suggesting that a subgroup of smokers may partially compensate for nicotine. Even in this subgroup of smokers, however, the relative importance of the pharmacological versus

A burning issue. The Japanese "fire basin".

This article presents two deaths due to acute carbon monoxide poisoning that occurred when charcoal-burning hibachis were used as heating sources in enclosed camping facilities. In both deaths, the levels of blood carbon monoxide saturation were at or slightly below the expected lethal level. Coronary arteriosclerosis may have contributed to one death, while oxygen depletion may have been a contributing factor in the other. These cases illustrate the danger of using such heating sources in enclosed spaces, due to their carbon monoxide-generating capability. We suggest that suitable warnings be placed on the hibachis themselves.

[Gas chromatographic determination of formic acid in urine as carbon monoxide (author's transl)]. / Gaschromatographische Bestimmung von Ameisensäure im Harn in Form von Kohlenmonoxid

A gas chromatographic method for determining formic acid in human urine is described. The analytical reliability of this method fullfills the criteria of statistical quality control. The rate of recovery is 101.2 to 105.7% the variability coefficients lie between 2.9 and 7.2%. The selectivity of this method is demonstrated by analysing a group of components normally occuring in urine which did not interfere with the determination of formic acid. The detection limit of about 4.3 mumol/1 formic acid in urine permits the determination of the concentration of formic acid in the urine of normal persons. The concentrations of formic acid in the urine of a group of normal persons lies between 0 and 2.79 mmol/1. The average concentration was 0.39 +/- 0.60 mmol/1.