Serum cotinine as a marker of environmental tobacco smoke exposure in epidemiological studies: the experience of the MATISS project

To describe serum cotinine levels in a rural Italian population and to examine its usefulness as an epidemiologic biomarker of nicotine exposure, cross-sectional data collected in 1993 for the MATISS Project (2098 men and 1352 women, aged 20–79 years) were used. The study population consisted of 977 current smokers, 882 nonsmokers reporting exposure to environmental tobacco smoke (ETS) and 1520 nonsmokers reporting no ETS exposure. Mean values of serum cotinine measured by radioimmunoassay for never smokers, ex-smokers and current smokers (including four categories of cigarette consumption), and for categories of ETS exposure in all nonsmokers were calculated. In univariate analysis, there was a positive association between self-reported nicotine exposure and serum cotinine levels in all groups. Using self-reported status as truth, sensitivity and specificity for various cotinine cutoff points were estimated to distinguish nonsmokers from smokers. The value of 15 ng/mL represented the best combined levels of sensitivity (95%) and specificity (96%). Using this cutoff point, the overall misclassification rate for self-reported nonsmokers was 2.1% and about two times greater for the more vs. the less educated. In multivariate analysis, reported ETS exposure among nonsmokers was significantly associated with serum cotinine even after adjusting for age, socio-demographic and behavioural factors, though the strength of the association was not strong. In conclusion, serum cotinine represents a reliable epidemiological marker of nicotine intake and may be helpful when studying ETS exposure. Improved information collection is needed to reduce misclassification among nonsmokers and enhance our understanding of the relationship between ETS and cotinine measures.     

Measuring exposure to environmental tobacco smoke (ETS): a developing country's perspective

AIMS: To assess exposure to ETS among nonsmokers in the community and examine the relation between various subjective and objective measures of exposure to ETS in a developing country's setting. METHODS: An interviewer-administered population-based survey of adults 18-65 years residing in Aleppo, Syria. From a total number of 2038 participants, a sub-sample of 419 nonsmokers (27.2% men, 72.8% women, mean age 34 years) underwent subjective and objective assessment of exposure to ETS (saliva cotinine, breath CO, self-reported measures of exposure combined into ETS exposure scale). RESULTS: Overall, 97.6% of adults nonsmokers assessed in this study, 72.9% of whom were women, have detectable saliva cotinine levels (mean +/- SD 1.7 +/- 1.5 ng/ml). Correlation between self-reported exposure measures and saliva cotinine was moderate with the strongest observed for number of cigarette smokers in the house, average number of cigarettes smoked daily in the house, house policy regarding smoking, and total ETS score (r 0.3-0.4). These same variables were among the best predictors of saliva cotinine according to stepwise linear regression analysis, but their individual relevance differed between men and women reflecting underlying differences in gender-based behavior-mobility patterns. Generally, subjective measures could explain 22% of the variability in cotinine levels in men and 19% in women. CONCLUSIONS: Exposure to ETS is universal among adult nonsmokers in Syria. Saliva cotinine correlated moderately with self-reported measures, whereby selected subjective measures can be as informative as composite scores incorporating multiple measures. Even in this environment of omnipresence of smoking, household restrictions seem to offer protection against ETS exposure.     

Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma

The impact of environmental tobacco smoke (ETS) exposure on adult pulmonary function has not been clearly determined. Because adults with asthma have chronic airway inflammation, they may be a particularly susceptible group. Using data from the Third National Health and Nutrition Examination Survey (NHANES III), I examined the cross-sectional relationship between serum cotinine, a biomarker of ETS exposure, and pulmonary function among 10,581 adult nonsmokers and 440 nonsmoking adults with asthma whose cotinine and spirometry data were available. I generated residuals, which are observed minus predicted values (based on Crapo equations), for forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio to adjust for age, sex, and height. In addition, I used multivariate linear regression to control for sociodemographic characteristics and previous smoking history. Most adults with and without asthma had detectable serum cotinine levels, indicating recent ETS exposure (85.7% and 83.4%, respectively). Among nonsmoking male participants, I found no evidence that ETS exposure was related to decreased pulmonary function. In the nonsmoking female stratum, the highest cotinine tertile was associated with a lower FEV1 [-100 mL; 95% confidence interval (CI), -143 to -56 mL], FVC (-119 mL; 95% CI, -168 to -69 mL), and FEV1/FVC ratio (-1.77%; 95% CI, -2.18% to -1.36%). Among women with asthma, the highest cotinine tertile was also associated with decreased FEV1 (-261 mL; 95% CI, -492 to -30 mL), FVC (-291 mL; 95% CI, -601 to 20 mL), and FEV1/FVC ratio (-1.6%; 95% CI, -3.3% to 0.19%). In conclusion, ETS exposure is associated with decreased pulmonary function in adult females, especially those with asthma. This analysis should provide further impetus for public policies that promote smoke-free environments.     

Exposure to environmental tobacco smoke in pregnant women: the association between self-report and serum cotinine

The risk of delivering a low-birth-weight infant as the result of exposing a nonsmoking pregnant woman to environmental tobacco smoke (ETS) is not well defined. The method of ascertaining ETS exposure during pregnancy may explain the lack of consistent study findings. In a large sample of pregnant women, we compared distributions between two methods of ETS exposure: self-report and cotinine, a nicotine metabolite, from serum. At livery, subjects were asked about duration and location of exposure to ETS during their second trimester. A single cotinine measurement was assayed from serum collected at 15-19 weeks gestation (limit of detection=0.05 ng/mL). Self-reported (hours per day) ETS exposure was correlated (r=0.38) with cotinine concentration. Regression analysis revealed that while self-reported ETS was significantly associated with (log) cotinine, it did not explain a large amount of total variation. While 72% of subjects reported no exposure to ETS, almost all had measurable levels of cotinine. Studies of pregnant women based upon an hours per day ETS question have likely misclassified a sizable portion of ETS-exposed women as "unexposed." Since there is recent evidence that low levels of ETS exposure result in unfavorable pregnancy outcomes, these studies have underestimated the effect of ETS.     

Tobacco smoke exposure and serum cotinine in a random sample of adults living in Verona,Italy

In this study, the authors attempted to validate answers to smoking-habit questions contained in the European Community Respiratory Health Survey questionnaire. The respondents were invited to visit the chest clinic at Verona, Italy, and their serum cotinine levels were measured. The authors invited each of 504 subjects to complete a respiratory interview and to give a blood sample for a radioimmunoassay serum cotinine measurement. A total of 375 subjects responded, of whom 129 were smokers (34.4%), 79 were exsmokers (21.1%), and 167 (44.5%) had never smoked. Exposure to environmental tobacco smoke was reported by 216 subjects (57.6% [mean exposure = 3.8 hr/day (+/- 3.4 hr/day standard deviation)]). In smokers, serum cotinine levels were directly related to the number of cigarettes smoked/day. The authors excluded from analysis nonsmokers who had serum cotinine levels that were > or = 14 ng/ml, and the resulting mean values were 1.7 ng/ml (+/- 2.1 ng/ml standard deviation) in nonsmokers unexposed to environmental tobacco smoke and 2.6 ng/ml (+/- 2.6 ng/ml standard deviation) (p < .002) in nonsmokers exposed to environmental tobacco smoke. There was a relationship between serum cotinine levels and hours of exposure to environmental tobacco smoke (R2 = .136, p < .05). Serum cotinine, which is an objective and accepted measure of tobacco exposure, confirmed the validity of the European Community Respiratory Health Survey questionnaire with respect to smoking habits and environmental tobacco smoke exposure.     

Exposure to secondhand smoke outside of a bar and a restaurant and tobacco exposure biomarkers in nonsmokers

Background: With an increase in indoor smoking bans, many smokers smoke outside establishments and near their entrances, which has become a public health concern.Objectives: We characterized the exposure of nonsmokers to secondhand smoke (SHS) outside a restaurant and bar in Athens, Georgia, where indoor smoking is banned, using salivary cotinine and urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL).Methods: In a crossover study, we assigned 28 participants to outdoor patios of a restaurant and a bar and an open-air site with no smokers on three weekend days; participants visited each site once and stayed for 3 hr. We collected saliva and urine samples immediately before and after the visits (postexposure) and on the following morning and analyzed samples for cotinine and total NNAL, respectively. Regression models were fitted and changes in biomarkers were contrasted between locations.Results: Postexposure and preexposure geometric mean salivary cotinine concentrations differed by 0.115 ng/mL [95% confidence interval (CI): 0.105, 0.126)] and by 0.030 ng/mL (95% CI: 0.028, 0.031) for bar and restaurant visits, respectively. There were no significant post- and preexposure differences in cotinine levels after control site visits, and changes after bar and restaurant site visits were significantly different from changes after control site visits (p < 0.001). Results comparing next-day and preexposure salivary cotinine levels were similar. Next-day creatinine-corrected urinary NNAL concentrations also were higher than preexposure levels following bar and restaurant visits [1.858 pg/mg creatinine higher (95% CI: 0.897, 3.758) and 0.615 pg/mg creatinine higher (95% CI: 0.210, 1.761), respectively], and were significantly different from changes after the control visits (p = 0.005).Conclusion: Salivary cotinine and urinary NNAL increased significantly in nonsmokers after outdoor SHS exposure. Our findings indicate that such exposures may increase risks of health effects associated with tobacco carcinogens.     

Personal exposure to environmental tobacco smoke: salivary cotinine, airborne nicotine, and nonsmoker misclassification.

A large study was conducted to assess exposure to environmental tobacco smoke (ETS) in a geographically dispersed study population using personal breathing zone air sampling and salivary cotinine levels. Approximately 100 self-reported nonsmoking subjects in each of 16 metropolitan areas were recruited for this investigation. Cumulative distributions of salivary cotinine levels for subjects in smoking and nonsmoking homes and workplaces exhibited a general trend of decreasing salivary cotinine levels with decreasing time spent in smoking environments. Median salivary cotinine levels for the four experimental cells in the study (product of smoking and nonsmoking home and workplaces) were comparable to those reported for a large national study of serum levels of cotinine (Third National Health and Nutrition Examination Survey, NHANES III), when the latter was corrected for expected differences between serum and saliva concentrations. However, the most highly exposed group in this study had a median salivary cotinine concentration approximately a factor of 2 greater than that of the comparable group in the NHANES III study. Misclassification rates, both simple (for self-reported nonsmokers) and complex (self-reported lifetime never smokers), were near the median of those reported for other studies. Estimated misclassification rates for self-reported lifetime never-smoking females are sufficiently high (2.95% using a discrimination level of 106 ng/ml) that, if used in the Environmental Protection Agency (EPA) risk assessment related to ETS and lung cancer, would place the lower 90% confidence interval (CI) for relative risk at nearly 1.00, i.e., no statistically significant increased risk. For the 263 most highly exposed subjects in the study whose self-reported nonsmoking status was accurate, the correlation between airborne exposure to nicotine and average salivary cotinine is so small, on an individual basis, that it makes the relationship useless for estimating exposure on a quantitative basis. When subjects are grouped according to likely categories of nicotine exposure, correlation between group median airborne nicotine exposure and salivary cotinine level increases dramatically. The comparison improves for the most highly exposed subjects, suggesting that such quantitative comparisons are useful for only those subjects who are exposed to the higher levels of ETS. However, airborne nicotine exposure for most of the subjects does not account for estimated systemic levels of nicotine, based on salivary cotinine levels.     

Factors associated with discrepancies between self-reports on cigarette smoking and measured serum cotinine levels among persons aged 17 years or older: Third National Health and Nutrition Examination Survey, 1988-1994

The discrepancy between cigarette smoking status reported during an interview and measured level of serum cotinine, a nicotine biomarker, was investigated in a representative sample of the US population aged >/=17 years (N = 15,357). Data were collected from participants in the Third National Health and Nutrition Examination Survey (1988-1994). Among self-reported smokers, 7.5% (95% confidence interval: 6.3, 8.7) had a serum cotinine level less than or equal to 15.0 ng/ml, the selected cutoff point for identifying nonsmokers. Age (p < 0.01), race/ethnicity (p < 0.01), and average number of cigarettes smoked per day (p < 0.01) were associated with these discrepant findings. Among self-reported nonsmokers, 1.4% (95% confidence interval: 1.1, 1.7) had a serum cotinine level greater than 15.0 ng/ml, the selected cutoff point for identifying smokers. Race/ethnicity (p < 0.01), education (p < 0.01), number of household members who smoked in the home (p = 0.03), and self-reported smoking status from an earlier home interview (p < 0.01) were associated with these discrepant findings. Differences in smoking patterns, including the extent of nicotine dosing, may explain most of the discrepancy observed among self-reported smokers, whereas deception regarding smoking status may explain most of the discrepancy among self-reported nonsmokers. This study provides evidence that self-reported smoking status among adult respondents to a population-based survey conducted in a private medical setting is accurate.     

Exposure to environmental tobacco smoke and cognitive abilities among U.S. children and adolescents

We used the Third National Health and Nutrition Examination Survey (NHANES III), conducted from 1988 to 1994, to investigate the relationship between environmental tobacco smoke (ETS) exposure and cognitive abilities among U.S. children and adolescents 6-16 years of age. Serum cotinine was used as a biomarker of ETS exposure. Children were included in the sample if their serum cotinine levels were less than or equal to 15 ng/mL, a level consistent with ETS exposure, and if they denied using any tobacco products in the previous 5 days. Cognitive and academic abilities were assessed using the reading and math subtests of the Wide Range Achievement Test-Revised and the block design and digit span subtests of the Wechsler Intelligence Scale for Children-III. Analyses were conducted using SUDAAN software. Of the 5,365 6- to 16-year-olds included in NHANES III, 4,399 (82%) were included in this analysis. The geometric mean serum cotinine level was 0.23 ng/mL (range, 0.035-15 ng/mL); 80% of subjects had levels < 1 ng/mL. After adjustment for sex, race, region, poverty, parent education and marital status, ferritin, and blood lead concentration, there was a significant inverse relationship between serum cotinine and scores on reading (beta = -2.69, p = 0.001), math (beta = -1.93, p = 0.01), and block design (beta = -0.55, p < 0.001) but not digit span (beta = -0.08, p = 0.52). The estimated ETS-associated decrement in cognitive test scores was greater at lower cotinine levels. A log-linear analysis was selected as the best fit to characterize the increased slope in cognitive deficits at lower levels of exposure. These data, which indicate an inverse association between ETS exposure and cognitive deficits among children even at extremely low levels of exposure, support policy to further restrict children's exposure.     

Tobacco Smoke Exposure and Serum Cotinine in a Random Sample of Adults Living in Verona,Italy

In this study, the authors attempted to validate answers to smoking-habit questions contained in the European Community Respiratory Health Survey questionnaire. The respondents were invited to visit the chest clinic at Verona, Italy, and their serum cotinine levels were measured. The authors invited each of 504 subjects to complete a respiratory interview and to give a blood sample for a radioimmunoassay serum cotinine measurement. A total of 375 subjects responded, of whom 129 were smokers (34.4%), 79 were exsmokers (21.1%), and 167 (44.5%) had never smoked. Exposure to environmental tobacco smoke was reported by 216 subjects (57.6% [mean exposure = 3.8 hr/day {± 3.4 hr/day standard deviation}]). In smokers, serum cotinine levels were directly related to the number of cigarettes smoked/day. The authors excluded from analysis nonsmokers who had serum cotinine levels that were ≥ 14 ng/ml, and the resulting mean values were 1.7 ng/ml (± 2.1 ng/ml standard deviation) in nonsmokers unexposed to environmental tobacco smoke and 2.6 ng/ml (± 2.6 ng/ml standard deviation) (p < .002) in nonsmokers exposed to environmental tobacco smoke. There was a relationship between serum cotinine levels and hours of exposure to environmental tobacco smoke (R ² = .136, p < .05). Serum cotinine, which is an objective and accepted measure of tobacco exposure, confirmed the validity of the European Community Respiratory Health Survey questionnaire with respect to smoking habits and environmental tobacco smoke exposure.     

Environmental tobacco smoke and pregnancy outcome

BACKGROUND: Recent reviews conclude that environmental tobacco smoke (ETS) leads to diminished birth weight. However, the threshold and magnitude of that effect is uncertain. We aimed to determine the magnitude and shape of the relations between ETS and various adverse pregnancy outcomes using a highly sensitive biochemical assay. METHODS: Maternal serum specimens were collected from more than 3000 women enrolled in California's prenatal screening program in 1992 and analyzed for cotinine. Information on pregnancy outcomes was obtained from live birth/fetal death records and hospital questionnaires. We conducted analyses on 2777 woman-live birth pairs and 19 woman-fetal death pairs in which the mother was presumed to be a nonsmoker (midtrimester cotinine levels < or =10 ng/mL). RESULTS: In multiple logistic regression analyses, the odds ratios of fetal death, preterm delivery, and term-low birth weight were 3.4, 1.8, and 1.8, respectively, in the highest cotinine quintile (0.236-10 ng/mL), compared with the lowest quintile (<0.026 ng/mL). In adjusted linear models, there was a linear dose-dependent effect of log cotinine on mean birth weight (-109 g) and mean infant length (-0.84 cm) over the range of cotinine values. Linear relations were not found with respect to infant head circumference or the ratio of brain weight to body weight. Infant's body mass index declined with exposures above approximately 0.5 ng/mL cotinine. We estimated that ETS levels at or above 0.05 ng/mL (experienced by 62% of the study population) accounted for 12% of all adverse outcomes. CONCLUSIONS: ETS exposure in pregnant women adversely affects pregnancy by increasing fetal mortality and preterm delivery at higher exposure levels and slowing fetal growth across all levels of ETS exposure.     

Environmental tobacco smoke and risk of spontaneous abortion

BACKGROUND: Studies of exposure to environmental tobacco smoke (ETS) and risk of spontaneous abortion are limited to a few studies of self-reported exposure, and the results have been inconsistent. The aim of this study was to investigate risk of early spontaneous abortion related to ETS and active smoking as defined by plasma cotinine levels. METHODS: We conducted a population-based case-control study in Uppsala County, Sweden, between January 1996 and December 1998. Cases were 463 women with spontaneous abortion at 6 to 12 completed weeks of gestation, and controls were 864 pregnant women matched to cases according to the week of gestation. Exposure status was defined by plasma cotinine concentrations: nonexposed, <0.1 ng/mL; ETS-exposed, 0.1-15 ng/mL; and exposed to active smoking, >15 ng/mL. Multivariable analysis was used to estimate the relative risk of spontaneous abortion associated with exposure to ETS and active smoking. RESULTS: Nineteen percent of controls and 24% of cases were classified as having been exposed to ETS. Compared with nonexposed women, risk of spontaneous abortion was increased among both ETS-exposed women (adjusted odds ratio = 1.67; 95% confidence interval = 1.17-2.38) and active smokers (2.11; 1.36-3.27). We could not show a differential effect of exposure to ETS or active smoking between normal and abnormal fetal karyotype abortions. CONCLUSIONS: Nonsmoking pregnant women exposed to ETS may be at increased risk of spontaneous abortion. Given the high prevalence of ETS exposure, the public health consequences of passive smoking regarding early fetal loss may be substantial.     

Relative sensitivity and specificity of salivary and serum cotinine in identifying tobacco-smoking status of self-reported nonsmokers and smokers of tobacco and/or marijuana

Serum and salivary cotinine levels were measured in 327 smoking and nonsmoking participants in a study of the health effects of marijuana with and without tobacco. These individuals had no reason to misrepresent their current tobacco-smoking status. The sensitivity, specificity, and predictive values positive and negative of the cotinine levels in distinguishing self-reported current tobacco smokers from nonsmokers was high (88-100%) and essentially the same for both fluids. Agreement between self-report and cotinine levels was not influenced by the presence or absence of marijuana smoking. A good correlation was found between serum and salivary cotinine levels in self-reported tobacco smokers (r = 0.84, p less than 0.001). Mean average levels were 279 +/- 144 ( +/- standard deviation) ng/ml for serum and 360 +/- 195 ng/ml for saliva. In a separate group of seven tobacco smokers, cotinine levels in saliva were found to be essentially independent of salivary flow rate. An analogous relationship has been observed by others for various compounds that are filtered to saliva from the blood. This may explain the close relationship observed between serum and salivary cotinine levels, and the observation made by others that the half-life of salivary cotinine is similar to that of serum cotinine.     

Cord serum cotinine as a biomarker of fetal exposure to cigarette smoke at the end of pregnancy

This study investigated the association between biomarkers of fetal exposure to cigarette smoke at the end of pregnancy, cotinine in cord serum and in maternal and newborn urine samples, and quantitative measurement of smoking intake and exposure evaluated by maternal self-reported questionnaire. Study subjects were 429 mothers and their newborns from a hospital in Barcelona, Spain. A questionnaire including smoking habits was completed in the third trimester of pregnancy and on the day of delivery. Cotinine concentration in cord serum was associated with daily exposure to nicotine in nonsmokers and with daily nicotine intake in smokers. The geometric mean of cotinine concentration in cord serum statistically discriminated between newborns from nonexposed and exposed nonsmoking mothers, and between these two classes and smokers, and furthermore was able to differentiate levels of exposure to tobacco smoke and levels of intake stratified in tertiles. Urinary cotinine levels in newborns from nonsmoking mothers exposed to more than 4 mg nicotine daily were statistically different from levels in two other categories of exposure. Cotinine concentration in urine from newborns and from mothers did not differentiate between exposure and nonexposure to environmental tobacco smoke (ETS) in nonsmoking mothers. Cord serum cotinine appeared to be the most adequate biomarker of fetal exposure to smoking at the end of pregnancy, distinguishing not only active smoking from passive smoking, but also exposure to ETS from nonexposure.     

Racial differences in exposure to environmental tobacco smoke among children

Exposure to environmental tobacco smoke (ETS) is a major cause of morbidity and mortality among U.S. children. Despite African-American children's having a lower reported exposure to tobacco compared to whites, they suffer disproportionately from tobacco-related illnesses and have higher levels of serum cotinine than white children. The goal of this study was to test whether African-American children have higher levels of serum and hair cotinine, after accounting for ETS exposure and various housing characteristics. We investigated the level of cotinine in both hair and serum in a sample of 222 children with asthma. Using a previously validated survey for adult smokers, we assessed each child's exposure to ETS. We collected detailed information on the primary residence, including home volume, ventilation, and overall home configuration. Despite a lower reported ETS exposure, African-American children had higher mean levels of serum cotinine (1.41 ng/mL vs. 0.97 ng/mL; p = 0.03) and hair cotinine (0.25 ng/mg vs. 0.07 ng/mg; p < 0.001) compared with white children. After adjusting for ETS exposure, housing size, and other demographic characteristics, serum and hair cotinine levels remained significantly higher in African-American children (ss = 0.34, p = 0.03) than in white children (ss = 1.06, p < 0.001). Housing volume was significantly associated with both serum and hair cotinine but did not fully explain the race difference. Our results demonstrate that, despite a lower reported exposure to ETS, African-American children with asthma had significantly higher levels of both serum and hair cotinine than did white children. Identifying causes and consequences of increased cotinine may help explain the striking differences in tobacco-related illnesses.     

Biochemical validation of self-reported exposure to environmental tobacco smoke

Biochemical validation of reported exposure to environmental tobacco smoke (ETS) lends credibility to epidemiological studies investigating the association of passive inhalation of smoke to respiratory disease or lung cancer. In the current study, a series of questions regarding ETS exposure was self-administered to nonsmokers and self-reported intensity of exposure was compared with cotinine levels in urine samples obtained on site. The target population of this study was a group of municipal workers who reported exposure in a domestic setting and/or in the workplace. When asked if they were exposed to ETS on social occasions, both males and females who responded positively had higher urinary cotinine levels (P less than 0.02) than those who gave a negative response. Mean urinary cotinine concentrations were found to be elevated in both men and women who reported that they lived with a smoker. Cotinine levels in the urine of those reporting exposure were over twice as high as those in the urine of respondents who denied having been exposed. ETS exposure in the home was the greatest contributor to increased urinary cotinine levels in both men and women. Among individuals who were exposed at work only, the reported degree of exposure agreed well with the mean urinary cotinine values. Those findings emphasize that the validation of exposure status with a biomarker is an essential prerequisite for epidemiological studies investigating passive smoking.     

Estimating Cotinine Associations and a Saliva Cotinine Level to Identify Active Cigarette Smoking in Alaska Native Pregnant Women

Studies indicate nicotine metabolism varies by race and can change during pregnancy. Given high rates of tobacco use and limited studies among Alaska Native (AN) women, we estimated associations of saliva cotinine levels with cigarette use and second-hand smoke (SHS) exposure and estimated a saliva cotinine cutoff to distinguish smoking from non-smoking pregnant AN women. Using questionnaire data and saliva cotinine, we utilized multi-variable linear regression (n = 370) to estimate cotinine associations with tobacco use, SHS exposure, demographic, and pregnancy-related factors. Additionally, we estimated an optimal saliva cotinine cutoff for indication of active cigarette use in AN pregnant women using receiver operating characteristic (ROC) curve analysis (n = 377). Saliva cotinine significantly decreased with maternal age and significantly increased with cigarettes smoked per day, SHS exposure, and number of previous full term pregnancies. Using self-reported cigarette use in the past 7 days as indication of active smoking, the area under the ROC curve was 0.975 (95 % CI: 0.960–0.990). The point closest to 100 % specificity and sensitivity occurred with a cotinine concentration of 1.07 ng/mL, which corresponded to sensitivity of 94 % and specificity of 94 %. We recommend using a saliva cotinine cutoff of 1 ng/mL to distinguish active smoking in pregnant AN women. This cutoff is lower than used in other studies with pregnant women, most likely due to high prevalence of light or intermittent smoking in the AN population. Continued study of cotinine levels in diverse populations is needed.     

Accuracy of self-reported smoking status among participants in a chemoprevention trial

BACKGROUND: Exposure to tobacco products is readily assessed through self- or interview-administered questionnaires. Degree of misreporting among participants in chemoprevention trials is unknown. We assessed the level of discrepancy between self-reported smoking exposure and plasma cotinine among participants in a chemoprevention trial. METHODS: Analyses were conducted among 824 men and women who participated in a dietary trial of adenoma recurrence. Smoking exposure was ascertained through self-administered questionnaires at three time-points. Plasma cotinine was measured by gas chromatography among 283 never, 446 former and 95 current self-reported smokers. Sensitivity and specificity were assessed using various plasma cotinine cut-points. RESULTS: Degree of misclassification for self-reported current smokers was minor (0-3%), regardless of cotinine cut-point used. Using a cut-point of 20 ng/ml, which takes into account exposure to environmental tobacco smoke among nonsmokers, sensitivity and specificity were 98.9% and 80.2%, respectively. CONCLUSIONS: These data indicate that degree of misreport for current smokers is extremely low; however, approximately 20% of self-reported never smokers misreport their exposure, suggesting that validation of self-report is needed for these individuals.     

Exposure to environmental tobacco smoke in the nonsmoking population of Cambodia

OBJECTIVE: To estimate the extent of environmental tobacco smoke (ETS) exposure among nonsmokers in the adult population of Cambodia. METHODS: A cross-sectional survey was conducted on a nationally representative sample of 13,988 Cambodian adults in 2005. Information on smoking and exposure to ETS was obtained by trained interviewers using a standard questionnaire. RESULTS: Overall, 37.4% of the 10,263 nonsmoking responders, or an estimated 1,629,700 nonsmoking Cambodians, were exposed to ETS. One third of pregnant women (31.4%) were exposed to ETS at home. In both unadjusted and adjusted models, men were less likely to be exposed to ETS at home (OR=0.34; 95% CI=0.29-0.41) and more likely to be exposed to ETS at work and in public places (OR=3.08; 95% CI=2.14-4.43 and OR=2.17; 95% CI=1.82-2.59, respectively). Education was inversely related to ETS exposure at home (OR=0.51; 95% CI=0.27-0.96 for 10 years of education vs 5 years or less). Legislators, senior officials, and managers were less likely to be exposed to ETS at home than professionals (OR=0.13; 95% CI=0.04-0.46), but more likely to be exposed at work or in public places. Rural residence was associated with higher ETS exposure in the home (OR=2.52; 95% CI=1.71-3.71) and lower ETS exposure at work (OR=0.42; 95% CI=0.24-0.76) compared to urban residence. CONCLUSIONS: The high prevalence of ETS exposure among adult Cambodians indicates an urgent need for specific measures such as public awareness campaigns, policies, and regulations to protect nonsmokers in Cambodia.