Assessment of the exposure of children to environmental tobacco smoke (ETS) by different methods.

1. In order to elucidate the role of exposure to environmental tobacco smoke (ETS) in various acute and chronic illnesses in children, it is important to assess the degree of exposure by suitable methods. For this purpose, we determined the exposure to ETS in 39 children (4-15 years) and 43 adults (16+ years) by questionnaires, personal diffusion samplers for nicotine, and cotinine measurements in saliva and urine. In addition, the influence of the smoking status and the location of the home (urban or suburban) on the benzene exposure of the children was investigated. 2. On average, the 24 children living in homes with at least one smoker were exposed to ETS for 3.1 h/d. This is significantly longer (P<0.001) than the daily exposure time of the 15 children from nonsmoking homes (0.3 h/d). The nicotine concentrations on the personal samplers worn over 7 days were 0.615 and 0.046 microg/m3 for children from smoking and nonsmoking homes, respectively (P<0.001). Average salivary cotinine levels were 1.95 ng/ml in children from smoking homes and 0.11 ng/ml in children from nonsmoking homes (P< 0.01). The corresponding urinary cotinine levels were 29.4 and 4.5 ng/mg creatinine (P< 0.001). There was no difference in the extent of ETS exposure between children and adults from smoking households. Adults from nonsmoking homes tended to have higher ETS exposure than children from nonsmoking homes. 3. Exposure to benzene, which was determined by means of personal samplers, measurements of benzene in exhaled air and of the urinary benzene metabolite trans, trans-muconic acid, was not significantly related to the smoking status of the home but primarily dependent on the location of the home.     

Quantitation of cotinine in nonsmoker saliva using chip-based nanoelectrospray tandem mass spectrometry

A new analytical procedure was developed for the quantitation of nonsmoker salivary cotinine. Small volumes of saliva were diluted with water, fortified with cotinine-d3 (internal standard), then passed through small extraction columns. The analyte and internal standard were eluted with 0.1% (v/v) acetic acid/acetonitrile. Aliquots of each extract were analyzed directly, without chromatographic separation, using chip-based (NanoMate) nanospray tandem mass spectrometry. The calculated detection limit was 0.49 ng cotinine/mL saliva. This method was used to quantify salivary cotinine collected from nonsmoking human subjects living in one of three environmental tobacco smoke (ETS) exposure categories or "cells": 1. smoking home/smoking workplace; 2. smoking home/nonsmoking workplace; and 3. nonsmoking home/smoking workplace. Samples were collected during five sequential days, including Saturday, as part of a larger study to evaluate potential variability in exposure to ETS. Salivary cotinine measurements were made for the purpose of excluding misclassified smokers and for comparison with known levels of exposure to airborne nicotine in each exposure category. The concentrations observed were consistent with those reported from other large studies reported elsewhere. A non-parametric statistical test was applied to the data within each cell. No statistically significant differences were found between the mean cotinine concentrations collected on a weekday as compared to those collected on a weekend day. When the non-parametric test was applied to the three cells, a statistically significant difference was observed between cell 1 compared to cells 2 and 3. The salivary cotinine concentrations were thus statistically invariant over a five-day exposure period, and they were greatest under the conditions of smoking home and smoking workplace.     

Environmental tobacco smoke at home and in public places prior to smoking ban enforcement: Assessment by hair analysis in a population of young adult students

Despite inititatives to reduce tobacco consumption, smoking remains a primary cause of death for both smokers and nonsmokers exposed to environmental tobacco smoke (ETS). The characteristics of some specific groups can make them more exposed to ETS or limit the benefit of prevention measures. This study investigated determinants of ETS in a population of young adult students, considered at higher risk of exposure due to their specific lifestyle. This cross-sectional study involved 90 students aged 20 ± 1.7 years, from the University of Luxembourg, prior to the smoking ban enforcement in public places in the country. Participants reported their tobacco consumption and exposure to ETS at home and/or in public places, and provided a hair sample analyzed for nicotine and cotinine. Nicotine and cotinine were significantly higher in smokers than in nonsmokers' hair in general (median: 2.6 vs. 0.9 ng/mg and 87.1 vs. 22.5 pg/mg respectively). However, nonsmokers exposed to ETS at home and in public places had comparable concentrations to smokers (nic = 2.2 ng/mg; cot = 56.2 pg/mg), whereas unexposed nonsmokers presented significantly lower values (nic = 0.4 ng/mg, cot = 8.5 pg/mg). Nonsmokers exposed to ETS only at home presented higher values than nonsmokers only exposed in public places (nic: 1.3 vs. 0.8 ng/mg, cot: 70.4 vs. 15.0 pg/mg). The study shows the widespread exposure to ETS in this population, the importance of exposure assessment, and the relevance of hair analysis for this purpose. Results suggest that ETS can lead to equivalent exposure to active smoking and that exposure at home can highly contribute to ETS, which is not solved by smoking ban in public places.     

Reference values for hair cotinine as a biomarker of active and passive smoking in women of reproductive age, pregnant women, children, and neonates: systematic review and meta-analysis

Exposure to environmental tobacco smoke (ETS) is most often estimated using questionnaires, but they are unreliable. Biomarkers can provide valid information on ETS exposure, the preferred biomarker being cotinine. However, no reference range of hair cotinine exists to distinguish among active, passive, and unexposed nonsmokers. This study identifies cutoffs to validate cotinine as a marker for exposure to ETS. Data were obtained from six databases (four US, one Canada, one France). Active smoking and exposure to ETS were measured in the hair of women of reproductive age, pregnant women, their children, and neonates. Subjects were classified into active smokers, passively exposed to ETS, and unexposed nonsmokers. A total of 1746 cases were available for analysis. For active smokers, mean hair cotinine concentrations (95% confidence interval) were 2.3 to 3.1 ng/mg for nonpregnant women and 1.5 to 1.9 ng/mg for pregnant women. In the group of passive smokers, mean hair cotinine concentrations were 0.5 to 0.7 ng/mg for nonpregnant women, 0.04 to 0.09 ng/mg for pregnant women, 0.9 to 1.1 for children, and 1.2 to 1.7 for neonates. Among unexposed nonsmokers, mean hair cotinine was 0.2 to 0.4 ng/mg in nonpregnant women, 0.06 to 0.09 ng/mg in pregnant women, and 0.3 to 0.4 ng/mg in children. Cutoff values for hair cotinine were established to distinguish active smokers from passive or unexposed (0.8 ng/mg for nonpregnant women and 0.2 ng/mg for pregnant women). A cutoff value of 0.2 ng/mg was accurate in discriminating between exposed children and unexposed. These new values should facilitate clinical diagnosis of active and passive exposure to tobacco smoke. Such diagnosis is critical in pregnancy and in a large number of tobacco-induced medical conditions.     

Saliva cotinine and exhaled carbon monoxide levels in natural environment waterpipe smokers

The purpose of this study is to evaluate the variations in exhaled CO and saliva cotinine in natural environment waterpipe smokers and compare them with cigarette smokers and absolute nonsmokers. Three groups were included in the study: nonsmokers (n = 20), waterpipe smokers (n = 15), and cigarette smokers (n = 20). A questionnaire was completed for each participant, exhaled CO was measured before and after waterpipe or cigarette smoking, and saliva cotinine was measured immediately after. We excluded from our study mixed smokers of both waterpipe and cigarettes. Mean values of saliva cotinine in waterpipe and cigarette smokers were very close: 77.8 ng/ml (SD = 110.4) and 87.1 (SD = 82.7) respectively. The weight and height of the persons as well as the size of the waterpipe bottle affected saliva cotinine. However, in waterpipe smokers, CO increased by 300% after 1 h of smoking, while in cigarette smokers, it only increased by 60%. In nonsmokers, exhaled CO was similar to environmental CO (10.2 ppm). The results of our study confirm that waterpipe device water does not filter nicotine and that the smoker him- or herself, by the frequency and the depth of inhalation, controls smoke inhalation. Like cigarette smokers, waterpipe smokers are exposed to harmful substances, such as CO, which was found to be quite high. The levels of expired CO and salivary cotinine could be good tools to detect exposure to waterpipe smoking.     

Implications of nicotine detected in autopsy cases of newborn babies and infants from the perspective of social medicine

Smoking by pregnant and parturient women is generally suspected to increase nicotine levels in fetal and infant blood. Supportive data of nicotine levels in infants is, however, inadequate. We investigated blood and muscle nicotine and cotinine levels in 14 autopsy cases of newborn babies and infants using gas chromatography. Among the 14 cases investigated, nicotine or cotinine was detected in six cases (42.9%). In each of these six cases, the mother was a smoker. Route of exposure to nicotine originating from smoking was transplacental in three cases, via breast milk in one case and secondhand smoke in two cases. Nicotine and cotinine levels in blood from the two cases with placental exposure were 10.6-84.4 ng/ml and 20.3-183 ng/ml, and levels in muscle from one case were 43.9 ng/g and 308 ng/g, respectively. Nicotine and cotinine levels in blood from exposure via breast milk were 19.1 ng/ml and 87.1 ng/ml, and from secondhand smoke were 0 ng/ml and 14.6-20.1 ng/ml. Mean concentrations of blood nicotine and cotinine in 68 autopsy cases of adult habitual smokers were 30.0 ng/ml and 247 ng/ml. Our data for nicotine and cotinine levels in infant blood seem to indicate that some infants who are born and develop under exposure to smoking by family members, particularly the mother, may show high nicotine levels in blood and experience possible health risks.     

Hubble-bubble (water pipe) smoking: levels of nicotine and cotinine in plasma,saliva and urine

OBJECTIVES: The purpose of the present study was to assess the levels of nicotine and cotinine in biological fluids (plasma, saliva, and urine) following hubble-bubble (HB) smoking. METHODS: Fourteen healthy male volunteers, aged 28 +/- 8 years, body weight of 82.7 +/- 13.53 kg, participated in the study. All volunteers were habitual HB smokers for 3.29 +/- 1.90 years who smoked at least 3 runs per week with an average of 20 g Mua'sel per run. Volunteers were requested to avoid smoking, at least 84 hours prior to the time of the study. After baseline samples were taken, volunteers started smoking 20 g of Mua'sel for a period of 45 minutes. Heparinized blood samples (5 or 10 ml each) were drawn for nicotine and cotinine analysis before, during and after the smoking period. Saliva samples were collected just before smoking (time 0) and at the end of smoking (45 min). Urine also was collected at time 0 and 24-hour urine collection was also taken to measure nicotine and cotinine excretion. Nicotine and cotinine were extracted from samples and assayed by gas chromatography. All data are presented as mean +/- SEM throughout the text, Tables and Figures unless indicated otherwise. RESULTS: Plasma nicotine levels rose from 1.11 +/- 0.62 ng/ml at baseline to a maximum of 60.31 +/- 7.58 ng/ml (p < 0.001) at the end of smoking (45 min). Plasma cotinine levels increased from 0.79 +/- 0.79 ng/ml at baseline to its highest concentration of 51.95 +/- 13.58 ng/ml (p < 0.001) 3 hours following the end of smoking. Saliva nicotine levels significantly rose from 1.05 +/- 0.72 to 624.74 +/- 149.3 ng/ml and also saliva cotinine levels significantly increased from 0.79 +/- 0.79 ng/ml to 283.49 +/- 75.04 ng/ml. Mean amounts of nicotine and cotinine excreted in urine during the 24-hour urine collection following smoking were equal to 73.59 +/- 18.28 and 249 +/- 54.78 microg, respectively. CONCLUSION: Following a single run of HB smoking, plasma, saliva and urinary nicotine and cotinine concentration increased to high values. This observation suggests that HB may not be an innocent habit, as people believe.     

Development and Characterization of an Elisa for Cotinine in Biological Fluids

Abstract

Cotinine is a major metabolite of nicotine and serves as an important biomarker of tobacco smoke exposure. To monitor exposure to tobacco smoke or nicotine, a sensitive enzyme-linked immunosorbent assay (ELISA) for cotinine was developed. The test had an 1–50 of between 0.5 and 1.0 ng/ml for cotinine and about 500-fold less affinity for nicotine. Few matrix effects were not detectable in human saliva, although relatively small matrix effects (1–50 for cotinine, 2.8 ng/ml) were observed in human serum and urine. The test accurately measured the levels of cotinine in NI5T standards in freeze-dried human urine derivative material (r = .9999) indicating its reliability for measurement of cotinine. The test readily detected low levels (5–500 nglml) of cotinine in human saliva and serum samples. Also, the levels of cotinine in plasma and urine samples from smoke-exposed mice and rats could be rapidly analyzed for cotinine. This ELISA is therefore a sensitive and accurate test for the determination of cotinine in plasma, serum, saliva, and urine samples from humans and animals, and can be successfully used for monitoring and quantifying exposure to tobacco smoke or nicotine.     

Hair analysis--a biological marker for passive smoking in pregnancy and childhood.

Passive smoking has been shown to adversely affect the health of infants and children. We used hair analysis for nicotine and its metabolite cotinine as a biological marker for exposure to smoking in these two groups. Using radioimmunoassay we measured maternal and fetal hair concentrations of nicotine and cotinine in the mother-infant pairs belonging to three different groups based on the mother's smoking habits. The three groups were: active smokers, passive smokers and nonsmokers. There was a significant correlation between maternal and neonatal hair concentration for both, nicotine and cotinine. Mothers and infants in the smoking groups, both active and passive, had significantly higher hair concentrations of both, nicotine and cotinine than in the control, nonsmoking group. In an older cohort, we compared two groups: 78 asthmatic children were compared to 86 healthy children exposed to similar degrees of passive smoking. By using objective, biological markers, our study aimed at verifying whether asthmatic children are different from nonasthmatic children in the way their bodies handle nicotine. Our results show, that, despite the fact that parents of asthmatic children tend to smoke a lower number of cigarettes per day, their children had an average twofold higher concentrations of cotinine in their hair then the control, nonasthmatic children. These studies document the importance of hair analysis as a tool for measuring exposure to cigarette smoke.     

Saliva Cotinine and Exhaled Carbon Monoxide Levels in Natural Environment Waterpipe Smokers

The purpose of this study is to evaluate the variations in exhaled CO and saliva cotinine in natural environment waterpipe smokers and compare them with cigarette smokers and absolute nonsmokers. Three groups were included in the study: nonsmokers (n = 20), waterpipe smokers (n = 15), and cigarette smokers (n = 20). A questionnaire was completed for each participant, exhaled CO was measured before and after waterpipe or cigarette smoking, and saliva cotinine was measured immediately after. We excluded from our study mixed smokers of both waterpipe and cigarettes. Mean values of saliva cotinine in waterpipe and cigarette smokers were very close: 77.8 ng/ml (SD = 110.4) and 87.1 (SD = 82.7) respectively. The weight and height of the persons as well as the size of the waterpipe bottle affected saliva cotinine. However, in waterpipe smokers, CO increased by 300% after 1 h of smoking, while in cigarette smokers, it only increased by 60%. In nonsmokers, exhaled CO was similar to environmental CO (10.2 ppm). The results of our study confirm that waterpipe device water does not filter nicotine and that the smoker him- or herself, by the frequency and the depth of inhalation, controls smoke inhalation. Like cigarette smokers, waterpipe smokers are exposed to harmful substances, such as CO, which was found to be quite high. The levels of expired CO and salivary cotinine could be good tools to detect exposure to waterpipe smoking.     

Nicotine exposure can be detected in cerebrospinal fluid of active and passive smokers

A simple, rapid and sensitive liquid chromatography/mass spectrometry (LC/MS) method has been utilized for the quantitative determination of nicotine and its major metabolite cotinine (COT) in human cerebrospinal fluid (CSF) of active and passive smokers. CSF samples from 18 smokers, 15 non-smokers, 15 children, 15 infants, and 9 neonatal were analyzed for nicotine (NIC) and cotinine content. Cotinine levels in the CSF of smokers ranged from 27.3 to 457.1 ng/ml, whereas nicotine levels were considerably lower (6.0–215.1 ng/ml). Cotinine could be detected in 4 of the 15 CSF samples from non-smokers (3.5–30.4 ng/ml), and a few other passive smokers, including neonates from smoking mothers (15.6–81.1 ng/ml). The concentrations of cotinine in CSF samples suggests that nicotine easily passes into the CSF, which makes it an excellent CSF marker for tobacco-smoke exposure.     

Household smoking behavior and ETS exposure among children with asthma in low-income,minority households

Environmental tobacco smoke (ETS) exposure was measured among 242 children with asthma who live in homes where at least one person smokes. Subjects were identified through clinics, schools, community agencies, and hospitals serving low-income, medically underserved communities in Los Angeles. Parents were surveyed about smoking behaviors in the household, children's ETS exposure, and attitudes towards smoking and smoking behavior change. Validation measures included urine cotinine for the child with asthma and passive air nicotine monitors placed in the subjects' homes. Overall reported levels of household smoking and ETS exposure were low, with a significant amount of household smoking taking place outside rather than inside the home. Over 47% of the respondents reported absolute restrictions against smoking in the home, and these restrictions were associated with lower reported levels of smoking, ETS exposure, and air nicotine and urine cotinine concentrations.     

High performance liquid chromatographic determination of nicotine and cotinine in plasma and nicotine and cotinine, simultaneously, in urine

Three analytical procedures were developed to determine nicotine in plasma, cotinine in plasma and, simultaneously, nicotine and cotinine in urine. After liquid or solid-phase extraction, the purified aqueous phase is injected into a high performance liquid chromatograph equipped with an ultra-violet detector using a CN Spheri-5 micron cartridge-column with an inner diameter of 4.6 mm and a length of 10 or 22 cm. The limit of quantitation for nicotine in plasma was around 8 to 15 ng/ml, that of cotinine in plasma around 50 ng/ml and that of nicotine and cotinine in urine around 170 ng/ml and 70 ng/ml, respectively. The limit of detection of nicotine in plasma was around 1 ng/ml and that of nicotine and cotinine in urine around 20 ng/ml and 10 ng/ml, respectively. The passive exposure to cigarette smoke by non-smokers and the "resting levels" of nicotine in plasma and urine of smokers were studied. The analytical methods were set up to study the pharmacokinetics and bioavailability of nicotine in healthy volunteers following single and repeated administrations of different doses of transdermal nicotine systems.     

Occupational exposure to environmental tobacco smoke: a study in Lisbon restaurants

Environmental tobacco smoke (ETS), also referred to as secondhand smoke (SHS), is a major threat to public health and is increasingly recognized as an occupational hazard to workers in the hospitality industry. Therefore, several countries have implemented smoke-free regulations at hospitality industry sites. In Portugal, since 2008, legislation partially banned smoking in restaurants and bars but until now no data have been made available on levels of indoor ETS pollution/exposure at these locations. The aim of this study was to examine the occupational exposure to ETS/SHS in several restaurants in Lisbon, measured by indoor fine particles (PM(2.5)) and urinary cotinine concentration in workers, after the partial smoking ban in Portugal. Results showed that the PM(2.5) median level in smoking designated areas was 253 μg/m3, eightfold higher than levels recorded in canteens or outdoor. The nonsmoking rooms of mixed restaurants exhibited PM(2.5) median level of 88 μg/m3, which is higher than all smoke-free locations studied, approximately threefold greater than those found in canteens. Importantly, urinary cotinine concentrations were significantly higher in nonsmoker employees working in those smoking designated areas, confirming exposure to ETS. The proportion of smokers in those rooms was found to be significantly positively correlated with nonsmoker urinary cotinine and indoor PM(2.5) levels, establishing that both markers were occupational-ETS derived. The use of reinforced ventilation systems seemed not to be sufficient to decrease the observed ETS pollution/exposure in those smoking locations. Taken together, these findings demonstrate that the partial restrictions on smoking in Portuguese venues failed to provide adequate protection to their employees, irrespective of protective measures used. Therefore, a smoke-free legislation protecting individuals from exposure to ETS/SHS in all public places and workplaces is urgently needed in Portugal.     

Hair nicotine/cotinine concentrations as a method of monitoring exposure to tobacco smoke among infants and adults

In this pilot study, we examined the validity and usefulness of hair nicotine-cotinine evaluation as a biomarker of monitoring exposure to tobacco. Head hair samples were collected from 22 infants (<2 years of age) and 44 adults with different exposures to tobacco (through either active or passive smoking) and analyzed by liquid chromatography-mass spectrometry (LC-MS) for nicotine and cotinine. Hair samples were divided into three groups, infants, passive smoker adults and active smoker adults, and into eight subgroups according to the degree of exposure. The limit of quantification (LOQ) was 0.1 ng/mg for nicotine and 0.05 ng/mg for cotinine. Mean recovery was 69.15% for nicotine and 72.08% for cotinine. The within- and between-day precision for cotinine and nicotine was calculated at different concentrations. Moreover, hair nicotine and cotinine concentrations were highly correlated among adult active smokers (R (2) = 0.710, p < 0.001), among adult nonsmokers exposed to secondhand smoke (SHS; R (2) = 0.729, p < 0.001) and among infants (R (2) = 0.538, p = 0.01). Among the infants exposed to SHS from both parents the noted correlations were even stronger (R (2) = 0.835, p = 0.02). The above results identify the use of hair samples as an effective method for assessing exposure to tobacco, with a high association between nicotine and cotinine especially among infants heavily exposed to SHS.     

Correlation between urinary nicotine, cotinine and self-reported smoking status among educated young adults

The objective of this study was to correlate, differentiate and validate the self-reported smoking status of educated young adults with urinary biomarkers (i.e. nicotine and cotinine). Freshmen students were recruited on voluntary basis. They filled-up self-administered questionnaire and their urine samples were collected for analysis. The urinary nicotine (UN) and cotinine (UC) were measured by gas chromatograph-mass spectrometry. Smokers, non-smokers and ex-smokers were found to be both significantly correlated and different in their UN and UC levels. UC level of 25ng/ml was the optimal cut-off to differentiate smokers from non-smokers. Using this cut-off value, the prevalence of smoking among the students was found to be higher (15.4%) than the self-reported data (14.3%). UC is useful in validating individual recent smoking history and the cut-off could serve as a marker for assessing the clinical impact of smoking and environmental tobacco smoke (ETS) exposure on human health.     

Comparison of serum and salivary cotinine measurements by a sensitive high-performance liquid chromatography-tandem mass spectrometry method as an indicator of exposure to tobacco smoke among smokers and nonsmokers

Exposure to tobacco smoke, both from active smoking and from passive exposure to environmental tobacco smoke, can be monitored by measuring cotinine, a metabolite of nicotine, in a variety of biological sources including blood, urine, and saliva. Previously, a sensitive atmospheric-pressure ionization, tandem mass spectrometric (LC-API-MS-MS) method for cotinine measurements in serum was developed in support of a large, recurrent national epidemiologic investigation. The current study examined the application of this LC-API-MS-MS method to both serum and saliva cotinine measurements in a group of 200 healthy adults, including both smokers and nonsmokers. The primary objective of this study was to evaluate the relationship between serum and saliva cotinine concentrations to facilitate the linking of results from epidemiologic studies using salivary cotinine measurements to existing national data based on serum cotinine analyses. The results indicate that a simple, linear relationship can be developed to describe serum and saliva cotinine concentrations in an individual, and the expression describing this relationship can be used to estimate with reasonable accuracy (approximately +/- 10%) the serum cotinine concentration in an individual given his or her salivary cotinine result. It was further confirmed that saliva cotinine samples are generally quite stable during storage after collection, even at ambient temperatures, and this sample matrix appears to be well-suited to the requirements of many epidemiologic investigations.     

Simultaneous determination of mecamylamine, nicotine, and cotinine in plasma by gas chromatography-mass spectrometry

The nicotine receptor antagonist mecamylamine has been shown to increase the efficacy of transdermal nicotine as a pharmacotherapy for tobacco addiction. A product for simultaneous transdermal administration of nicotine and mecamylamine is undergoing clinical trials. In order to carry out pharmacokinetic studies, quantitation of low nanogram per milliliter levels of mecamylamine and nicotine was required. This paper describes a method for simultaneous determination of mecamylamine, nicotine, and the nicotine metabolite, cotinine, in human plasma using gas chromatography-mass spectrometry (GC-MS). Limits of quantitation for mecamylamine, nicotine and cotinine are 2, 1 and 2 ng/ml, respectively.     

Risks for heart disease and lung cancer from passive smoking by workers in the catering industry.

Workers in the catering industry are at greater risk of exposure to secondhand smoke (SHS) when smoke-free workplace policies are not in force. We determined the exposure of catering workers to SHS in Hong Kong and their risk of death from heart disease and lung cancer. Nonsmoking catering workers were provided with screening at their workplaces and at a central clinic. Participants reported workplace, home, and leisure time exposure to SHS. Urinary cotinine was estimated by enzyme immunoassay. Catering facilities were classified into three types: nonsmoking, partially restricted smoking (with nonsmoking areas), and unrestricted smoking. Mean urinary cotinine levels ranged from 3.3 ng/ml in a control group of 16 university staff through 6.4 ng/ml (nonsmoking), 6.1 ng/ml (partially restricted), and 15.9 ng/ml (unrestricted smoking) in 104 workers who had no exposures outside of work. Workers in nonsmoking facilities had exposures to other smoking staff. We modeled workers' mortality risks using average cotinine levels, estimates of workplace respirable particulates, risk data for cancer and heart disease from cohort studies, and national (US) and regional (Hong Kong) mortality for heart disease and lung cancer. We estimated that deaths in the Hong Kong catering workforce of 200,000 occur at the rate of 150 per year for a 40-year working-lifetime exposure to SHS. When compared with the current outdoor air quality standards for particulates in Hong Kong, 30% of workers exceeded the 24-h and 98% exceeded the annual air quality objectives due to workplace SHS exposures.     

Good relationship between saliva cotinine kinetics and plasma cotinine kinetics after smoking one cigarette

This study investigated the relationship between plasma and saliva cotinine kinetics after smoking one cigarette and the relationship between cotinine kinetics and estimated nicotine intake, which was calculated as mouth level exposure (MLE) of nicotine, from smoking two test cigarettes with different nicotine yields. This study was conducted in 16 healthy adult Japanese smokers, who did not have null nor reduced-activity alleles of CYP2A6, with a quasi-randomized crossover design of smoking a low-tar cigarette or a high-tar cigarette. Saliva cotinine showed similar concentration profiles to plasma cotinine, and all of the calculated pharmacokinetic parameters of cotinine showed the same values in plasma and saliva. The C_max and AUC of cotinine showed almost the same dose-responsiveness to the estimated MLE of nicotine between plasma and saliva, but the t_max and t_1/2 of cotinine were not affected by the estimated MLE of nicotine in either plasma or saliva. The results show that saliva cotinine kinetics reflects plasma cotinine kinetics, and measurement of saliva cotinine concentration gives the same information as plasma cotinine on the nicotine intake. Thus, saliva cotinine would be a good and less-invasive exposure marker of cigarette smoke, reflecting the plasma cotinine concentration and kinetics.