Assessment of prenatal tobacco smoke exposure by determining nicotine and its metabolites in meconium

Meconium samples collected from 115 neonates were analysed for nicotine, cotinine and trans -3-hydroxycotinine (OH-cotinine) by means of high-performance liquid chromatography (HPLC) to identify prenatal smoke exposure. The self-reported maternal smoking status during pregnancy was determined by means of a questionnaire and verified by measurements in urine prior to childbirth. The total sum of nicotine and its metabolites (Sum(tot)) of the first passed meconium samples was 1560 +/- 1024 pmol/g in newborns of smoking mothers. Smoking of less than five cigarettes was clearly detected. Sum(tot) remained constant in all meconium samples passed by a neonate in succession. However, the proportion of nicotine decreased with the time of passage after birth and the OH-cotinine proportion increased, whereas cotinine hardly changed. Nicotine or its metabolites were not detectable in meconium (detection limit < 20 pmol/g), when the mothers were only exposed to environmental tobacco smoke (ETS) using the HPLC method. The hypothesis that the content of nicotine metabolites in meconium reflects long-term smoke exposure could not be confirmed in newborns whose mothers had quit smoking during the latter half of pregnancy. Determining Sum(tot) enables the intensity of continuous smoking during pregnancy to be estimated in all meconium samples passed by a newborn.     

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.     

Urinary hydroxyproline excretion in smokers, non-smokers and passive smokers

The hydroxyproline/creatinine ratio in urine was investigated in 200 cigarette smokers, 199 pipe and/or cigar smokers and 24 non-smokers. For cigarette smokers a statistically significant positive correlation is found between this ratio and daily cigarette consumption, COHb, serum cotinine and nicotine excretion in urine. This smoking-related increase in the hydroxyproline/creatinine ratio is, for the most part or completely, due to the fact that creatinine urine concentrations inversely correlate with the smoke uptake variables. Neither pipe and/or cigar smoking nor passive smoke exposure of non-smokers seem to affect the hydroxyproline/creatinine ratio. A seasonal influence is found in these studies as well as in two experiments with limited numbers of subjects: the hydroxyproline/creatinine ratio is higher in winter than in summer for both smokers and non-smokers. Our data do not favour the idea that measuring hydroxyproline/creatinine ratios in urine is an accurate method of investigating early effects of smoking, passive smoking and air pollution in man.     

Estimation of smoke dosage and mortality of non-smokers from environmental tobacco smoke

This paper shows how biochemical markers can be used to estimate smoke intake from passive smoking to complement epidemiological studies on the health risks and mortality to non-smokers. Using data from slow nicotine infusions given over 1 h, we estimated that the nicotine intake from passive smoking averages about 0.014 mg/h among urban non-smokers leading their usual daily lives. This compares with 0.23 mg/h in a smoke-filled public house, 0.36 mg/h during maximum exposure in an unventilated room, and 1.0 to 1.4 mg nicotine per cigarette taken in by active smokers. Data from several studies on urinary nicotine concentrations and those of cotinine in blood, urine and saliva were collated. The results show that the concentrations in non-smokers averaged about 0.7% (for nicotine) and 0.6% (for cotinine) of the levels found in smokers. From this we estimate that the mortality from passive smoking is about 1000 non-smokers per year in Britain and about 4000 per year in the United States, assuming that the relation of dose to risk is linear.     

Determination of nicotine and cotinine in human serum and urine: an interlaboratory study

An interlaboratory study aimed at determining nicotine and cotinine in human serum and urine was carried out. 11 laboratories from 6 countries, all experienced in performing nicotine and cotinine determinations in biological fluids by radioimmunoassay (RIA) and/or gas chromatography (GC) were involved. Each of them received 18 serum and 18 urine samples. The specimens were obtained from 8 smokers and 10 non-smokers; 2 samples from non-smokers were spiked with defined amounts of nicotine and cotinine. All the laboratories distinguished perfectly between the smokers and the non-smokers and according to cotinine levels in serum the laboratories ranked the samples with good agreement. There were systematic differences in the absolute values between the laboratories. The ratios of urinary cotinine concentrations between active and passive smokers differed widely from laboratory to laboratory. The reasons for this are not yet known and necessitate further investigation.     

Urinary cotinine levels of electronic cigarette (e-cigarette) users

The popularity of electronic cigarettes (e-cigarettes) is rapidly increasing in many countries. These devices are designed to imitate regular cigarettes, delivering nicotine via inhalation without combusting tobacco but currently, there is a lack of scientific evidence on the presence or absence of nicotine exposure. Such research relies on evidence from e-cigarette users urine samples. In this study, we aimed to determine the levels and compare the amount of nicotine to which e-cigarette users, cigarette smokers and passive smokers are exposed. Therefore, urine samples were collected from e-cigarette users, cigarette smokers, passive smokers, and healthy nonsmokers. The urinary cotinine levels of the subjects were determined using gas chromatography–mass spectrometry. The mean (±SD) urinary cotinine levels were determined as 1755?±?1848?ng/g creatinine for 32 e-cigarette users, 1720?±?1335?ng/g creatinine for 33 cigarette smokers and 81.42?±?97.90?ng/g creatinine for 33 passive smokers. A significant difference has been found between cotinine levels of e-cigarette users and passive smokers (p?<?0.05). There were no statistically significant differences between e-cigarette users and cigarette smokers (p?>?0.05). This is a seminal study to demonstrate the e-cigarette users are exposed to nicotine as much as cigarette smokers.     

Passive smoke exposure in infants and children with respiratory tract diseases.

1. The adverse effect of passive smoke exposure on the respiratory tract, particularly in infants and children, is not an issue of dispute. It was the objective of this study to analyse the extent and the intensity of passive smoke exposure in infants and children with respiratory tract diseases, and compare the information obtained with parents' subjective assessment. At the time of admission to the hospital, the parents of 295 infants and children (aged 1 month to 11 years) were questioned by the physician as to the smoking habits in the families' homes. An HPLC method was employed to determine simultaneously nicotine, cotinine and trans-3'-hydroxycotinine in the children's urine. 2. The sum of the nicotine metabolites turned out to be a sensitive marker in determining passive smoke exposure. Measurements revealed passive smoke exposure in 66% of the children, the frequency in younger children being significantly (P < 0.001) higher than in children over 5 years (84% vs 52%). The average concentration of nicotine metabolites in younger passive smokers was significantly (P < 0.001) higher when compared to the older ones (193 nmol/l vs 86 nmol/l). Forty-nine per cent of the parents assessed that their children had experienced passive smoke exposure, and another 10% emphasised that they only smoked in the absence of their child. In children with cystic fibrosis and bronchial asthma, the number of passive smokers as assessed by their parents were lower by 65% and 29% respectively when compared to the findings obtained from measurements. In children without respiratory diseases, the difference was as little as 18%. 3. Parents when questioned in conjunction with an illness of their children, tended to understate, or even withhold the truth about, passive smoke exposure. Therefore, reliable information on passive smoke exposure of patients can only be obtained through objective measurements.     

Exposure and kinetics of polycyclic aromatic hydrocarbons (PAHs) in cigarette smokers

Our study objectives were (1) to investigate the selectivity of polycyclic aromatic hydrocarbon (PAH) metabolites for tobacco smoke exposure and (2) to determine half-lives of PAH metabolites in smokers. There were 622 participants from the United States (US) and Poland, and of these, 70% were smokers. All subjects provided spot urine samples, and 125 smokers provided blood samples. Urinary PAH metabolite half-lives were determined in 8 smokers. In controlled hospital studies of 18 smokers, the associations between various measures of nicotine intake and urinary excretion of PAH metabolites were investigated. Plasma nicotine was measured by GC. LC-MS/MS was used to measure the plasma levels of cotinine and trans-3'-hydroxycotinine, and urine levels of nicotine and its metabolites, total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and PAH metabolites (2-naphthol, 1-, 2-, and 3-hydroxyfluorenes, 1-, 2-, 3-, and 4-hydroxyphenanthrenes, and 1-hydroxypyrene). Regardless of smoking status, PAH metabolite excretion was higher in Polish subjects than in US subjects (p-values <0.001). 1-Hydroxyfluorene exhibited the greatest difference between smokers and nonsmokers, with a 5-fold difference in Polish subjects and a 25-fold difference in US subjects, followed by 3- and 2-hydroxyfluorenes, 2-naphthol, and 1-hydroxypyrene. The differences for hydroxyphenanthrenes were small or nonsignificant. 1-Hydroxyfluorene had the highest correlation with urine nicotine equivalents (r = 0.77) and urine NNAL (r = 0.64). While the half-lives of PAH metabolites were <10 h in smokers, 1-hydroxyfluorene had the largest ratio of initial to terminal urine concentration (58.4 ± 38.6, mean ± SD) after smoking. Receiver Operating Characteristic (ROC) analysis of PAHs among Polish and US subjects further showed that hydroxyfluorenes are most highly discriminative of smokers from nonsmokers followed by 2-naphthol and 1-hydroxypyrene. In conclusion, hydroxyfluorenes, particularly 1-hydroxyfluorene, and 2-naphthol are more selective of tobacco smoke than 1-hydroxypyrene and hydroxyphenanthrenes. Characterization of hydroxyfluorene and 2-naphthol metabolites in urine may improve the characterization of PAHs from tobacco smoke and related disease risks among smokers and nonsmokers.     

Total cotinine in plasma: a stable biomarker for exposure to tobacco smoke

Determination of plasma cotinine concentration is the predominant assay employed to quantify smoking and exposure to environmental tobacco smoke in epidemiological studies. However, cotinine is biotransformed into secondary metabolites. This pilot study determined plasma concentrations of cotinine, cotinine glucuronide, 3-hydroxycotinine, and 3-hydroxycotinine glucuronide. Total cotinine concentration was determined by summation of all four metabolites. The goals of this study were (1) to explore the stability and validity of total cotinine concentration as a measure of tobacco smoking and as a measure of exposure to environmental tobacco smoke in nonsmokers, (2) to explore the stability of plasma concentrations of each of the four nicotine metabolites in smokers by performing a.m. and p.m. measures, and (3) to explore the stability of indices of glucuronidation as measures of possible markers for enzymatic activity. The subject sample included 76 white volunteers (32% smokers and 68% nonsmokers). Plasma total cotinine concentration appeared to be very stable, suggesting that total cotinine concentration may be a good measure for epidemiological studies employing a single plasma sample. Moreover, plasma total cotinine concentration also reflected exposure to environmental tobacco smoke more accurately than did plasma cotinine concentration, which would have not identified 27% of passive smokers. 3-Hydroxycotinine glucuronide and 3-hydroxycotinine plasma concentrations were almost as stable as cotinine concentrations. However, cotinine glucuronide and its indices of glucuronidation were unstable, suggesting that cotinine glucuronide undergoes deconjugation. New studies of total cotinine in plasma using more than two blood collections during the day are needed to definitively establish that it is a stable biomarker for epidemiological studies.     

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.     

Passive and active exposure to cigarette smoke in a smoking experiment

Six volunteer female habitual smokers were exposed during a 2-wk experimental period to cigarette smoke, both actively and passively, in an exposure chamber (volume 10 m3, average air exchange rate 6.8 times/h), where the ambient carbon monoxide, particle, and aldehyde concentrations were monitored. Three of the six subjects were smoking at the time, 2 cigarettes (filtered, self-burning low tar brand) per person per hour, 30 cigarettes altogether during each of the 5-h experimental days in the chamber. Samples of blood and urine were taken from each subject after 3 nonsmoking days and after each day of active or passive smoking. Among the parameters tested, blood carboxyhemoglobin, plasma cotinine, and urinary mutagenicity were higher in samples taken after active smoking than after nonsmoking periods. Although the exposure conditions were similar for all subjects, the parameters measured showed quite high interindividual variation. Thioethers and thiocyanates were not significantly elevated in the active smoking samples; neither were there any differences during this short experimental period in the sister chromatid exchange frequencies. The only parameters showing an increasing trend after passive exposure, as compared with nonsmoking samples, were urinary mutagenicity and plasma cotinine, the main metabolite of nicotine.     

The effects of tobacco smoke on plasma alpha- and gamma-tocopherol levels in passive and active cigarette smokers

Tobacco smoke is one of the causes of oxidative stress that is leading to attenuation of the antioxidative body protective barrier by means of decreasing the levels of intra- and extracellular antioxidants. The effect of tobacco smoke on plasma levels of two main forms of Vitamin E, alpha- and gamma-tocopherol, in passive smokers (urinary cotinine concentration 50-500 microg/L) and active smokers (urinary cotinine concentration >500 microg/L) were studied. Slight, but statistically significant decreases in plasma alpha-tocopherol level in passive and active smokers in comparison with non-smokers (by 5.7% and 9.2%, respectively) were found. The plasma gamma-tocopherol levels remained unchanged. The Pearson's correlation coefficient for the plasma alpha-tocopherol level and the urinary cotinine concentration in passive and active smokers was -0.431, P = 0.004 and -0.534, P < 0.001, respectively, and for gamma-tocopherol in similar conditions -0.190, P = 0.217 and 0.346, P = 0.027, respectively. The obtained results indicate the secondary role that alpha- and gamma-tocopherol play in the process of tobacco smoke free radical scavenge, or they may also reflect the body increased anti-oxidative mobilization in response to oxidative stress evoked by tobacco smoke.     

Urinary cotinine levels of smokeless tobacco (Maraş powder) users

Smokeless tobacco is used in various forms in some countries of the world. "Mara? otu" is a kind of smokeless tobacco usage in the Southeastern region of Turkey. The use of smokeless tobacco causes nicotine addiction and dependence. Moreover this type of smokeless tobacco usage is one of the risk factors for oral cancers and genotoxic damages for users. Cotinine is widely used as a biomarker of tobacco consumption and intake of nicotine. Therefore, urine samples were collected from people who are using Mara? powder and smoking cigarettes, and passive smokers, and the levels of cotinine investigated. The purpose of this study is to determine the cotinine levels of Mara? powder users and to compare the results with cigarette smokers and passive smokers. Urinary cotinine levels of subjects were determined by using capillary gas chromatography with FID detection. The mean (+/- SD) urinary cotinines have been determined as 6467.35+/-3198 microg/g creatinine for 26 Mara? powder users, 1943.92+/-1443 microg/g creatinine for 26 cigarette smokers and 198.62+/-420.82 microg/g creatinine for 26 passive smokers. A significant difference has been found between cotinine levels of Mara? powder users and cigarette smokers, which is three times higher in Mara? powder users (p<0.001). The present study suggests that smokeless tobacco poses a threat to public health and it should not be viewed as a safe alternative to cigarettes.     

Direct analysis of tobacco-specific nitrosamine NNK and its metabolite NNAL in human urine by LC–MS/MS: evidence of linkage to methylated DNA lesions

4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and its urinary metabolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), are the most investigated carcinogenic biomarkers of tobacco-specific nitrosamines. Here, we report the development of a sensitive and selective assay based on liquid chromatography–tandem mass spectrometry (LC–MS/MS) to simultaneously measure urinary NNK and NNAL. With the use of isotope internal standards and online solid-phase extraction, urine samples were directly analyzed without prior sample purification. The detection limits of this method were 0.13 and 0.19 pg on column for NNK and NNAL, respectively. Inter- and intra-day imprecision was <10 %. Mean recovery of NNK and NNAL in urine was 99–100 %. This method was applied to measure urinary NNK and NNAL in 101 smokers and 40 nonsmokers to assess tobacco exposure. Urinary nicotine, cotinine, N3-methyladenine (N3-MeA), and N7-methylguanine (N7-MeG) were also measured by isotope-dilution LC–MS/MS methods. The results showed that urinary NNK was not observed in all smokers. Urinary free NNAL (0.10 ± 0.09 ng/mg creatinine) and total NNAL (0.17 ± 0.14 ng/mg creatinine) were detected in all smokers. Urinary concentrations of NNAL were significantly correlated with nicotine, cotinine, N3-MeA, and N7-MeG in smokers (P < 0.001). This method enables the direct and simultaneous measurement of NNK and NNAL in urine using only 50 μL of urine. This study first demonstrated in human that urinary tobacco-specific nitrosamines metabolite (NNAL) are highly correlated with their resulting methylated DNA lesions in urine, which may help to substantiate an increased cancer risk associated with tobacco smoke exposure.     

Clinical correlation between the consumption of nicotine and cotinine concentrations in urine and serum by competitive enzyme-linked immunosorbent assay

Different negative effects of smoking are known (e.g. postoperative complications), which lead, especially in plastic surgery, to unsatisfactory results. The aim of this study was to examine the appropriateness of a cotinine enzyme-linked immunosorbent assay (ELISA) for routine usage in operative disciplines. By correlation of smoking habits and concentration of cotinine in serum and urine, we tried to ascertain reference values for smokers, passive smokers and non-smokers. The reliability and sensitivity of the cotinine ELISA concerning nicotine exposure need to be proven. 165 (108 men, 57 women) test persons were examined by detecting cotinine in serum and urine by ELISA. The study shows a very good sensitivity, precision and reproducibility of the cotinine ELISA according to the laboratory criteria. The test shows significance of a good differentiation between smokers, passive smokers and non-smokers in urine. In serum, cotinines are excellent to differentiate between smokers and non-smokers/passive smokers. Urine and serum tests demonstrate valid and comparable results.     

Evidence for urinary excretion of glucuronide conjugates of nicotine, cotinine, and trans-3'-hydroxycotinine in smokers.

Urinary nicotine metabolic output was profiled for 11 smokers who smoked their regular cigarette brands ad libitum. Thermospray liquid chromatography/mass spectrometry was used to monitor nicotine and eight metabolites, including glucuronide conjugates of nicotine, cotinine, and trans-3'-hydroxycotinine that were determined indirectly using enzyme hydrolysis. These results were used to estimate an average, steady-state concentration in a 24-hr urine sample during ad libitum smoking and to assess interindividual variability in the excretion of these metabolites. The variability in absolute amount among the nine analytes ranged from 35 to 70% for these smokers. The glucuronide conjugates constituted an average of 29% of all urinary metabolites monitored in this study. trans-3'-Hydroxycotinine in the free form constitutes the largest single metabolite in smokers' urine, with an average of 35% of the total. The sums of nicotine metabolites determined here are very close to the Federal Trade Commission yields of nicotine for the total number of cigarettes smoked by these subjects during the urine collection interval. These results indicate that a large proportion of the nicotine absorbed while smoking can be accounted for as urinary metabolites of nicotine, including glucuronide conjugates of nicotine, cotinine, and trans-3'-hydroxycotinine.     

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.     

Smoking and passive smoking during pregnancy and early infancy: effects on birth weight, lactation period, and cotinine concentrations in mother's milk and infant's urine

The extent of smoke exposure via mother's milk and passive smoking was investigated in a prospective, longitudinal matched-pair study by comparison between children, whose mothers smoked substantially throughout pregnancy and nursing period and children whose mothers did not smoke. Our preliminary results show that not only infants of smoking mothers but also those of smoking fathers show reduction of birth weight. Smoking mothers weaned their babies earlier than non-smokers. Cotinine concentrations in breast milk depended on the number of cigarettes smoked. The highest urinary excretion of cotinine (as expressed by ng cotinine/mg creatinine ratios) were observed in infants fully breast-fed by smoking mothers. After weaning the values were in the same range as those of formula-fed infants of smoking mothers (exposed to passive smoking only). In the group of non-smokers only small or undetectable amounts of cotinine were found. Thus it is demonstrated that both nursing and--to a lower degree--passive smoking contribute to the exposure of infants to nicotine and its metabolite cotinine.     

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.     

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.