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1.  What determines levels of passive smoking in children with asthma? 
Thorax  1997;52(9):766-769.
BACKGROUND: Children with parents who smoke are often exposed to high levels of environmental tobacco smoke, and children with asthma are particularly susceptible to the detrimental effects of passive smoking. Data were collected from parents who smoke and from their asthmatic children. The families are currently taking part in a randomised controlled trial to test an intervention designed to reduce passive smoking in children with asthma. This paper reports on the baseline data. Questionnaire data and cotinine levels were compared in an attempt to assess exposure and to identify factors which influence exposure of the children. The aim of the study was to identify the scope for a reduction in passive smoking by these children. METHODS: A sample of 501 families with an asthmatic child aged 2-12 years was obtained. Factors influencing passive smoking were assessed by interviewing parents. Cotinine levels were measured from saliva samples using gas liquid chromatography with nitrogen phosphorous detection. RESULTS: Cotinine levels in children were strongly associated with the age of the child, the number of parents who smoked, contact with other smokers, the frequency of smoking in the same room as the child, and crowding within the home. Parental cotinine levels, the amount smoked in the home, and whether the home had a garden also exerted an independent effect on cotinine levels in the children. CONCLUSIONS: Many children are exposed to high levels of environmental tobacco smoke and their cotinine levels are heavily dependent upon proximity to the parent who smokes. Parents who smoke have a unique opportunity to benefit their child's health by modifying their smoking habits within the home. 



PMCID: PMC1758643  PMID: 9371205
2.  Association of Maternal Smoking With Child Cotinine Levels 
Nicotine & Tobacco Research  2013;15(12):2029-2036.
Introduction:
Our aim was to understand the strength of association between parental smoking and child environmental tobacco smoke (ETS) exposure in order to inform the development of future tobacco control policies. ETS was measured using child cotinine levels below the active smoking threshold.
Methods:
Participants were drawn from the Avon Longitudinal Study of Parents and Children and included 3,128 participants at age 7 years and 1,868 participants at age 15 years. The primary outcome was cotinine levels of nonsmoking children, to investigate the relationship between maternal smoking and child cotinine levels. The secondary outcome was cotinine levels of all individuals to investigate the relationship between child smoking and child cotinine levels. Maternal and child smoking behavior was assessed by self-report questionnaire. We adjusted for several sociodemographic variables.
Results:
We found an association between maternal smoking and child cotinine at age 7 years (mean cotinine = 1.16ng/ml serum, ratio of geometric means = 3.94, 95% CI = 2.86–5.42) and at age 15 years (mean cotinine = 0.94ng/ml serum, ratio of geometric means = 5.26, 95% CI = 3.06–9.03), after adjustment for potential confounders.
Conclusions:
The magnitude of this association for children whose mothers were heavy smokers was comparable with the quantity of half the levels of cotinine observed among children who were irregular (i.e., nonweekly) active smokers, and it was greater than five times higher than that seen in nonsmoking children whose mothers didn’t smoke. This provides further evidence for the importance of public health interventions to reduce smoking exposure in the home.
doi:10.1093/ntr/ntt094
PMCID: PMC3819976  PMID: 23880896
3.  Comparison of parental reports of smoking and residential air nicotine concentrations in children 
Background
Using questionnaires to assess children's residential exposure to environmental tobacco smoke (ETS) may result in misclassification from recall and response bias. Questionnaire data have frequently been validated against urinary cotinine measurements, but rarely against actual measurements of residential air nicotine.
Objective
To compare questionnaire reported smoking with air nicotine concentrations in a large population of children and with urinary cotinine levels in a subpopulation; and to assess the potential impact of the symptom status of the children on the agreement between different measures of exposure.
Methods
The authors assessed residential exposure to ETS in 347 German, 335 Dutch, and 354 Swedish preschool and schoolchildren by questionnaire and air nicotine measurements, and in a subset of 307 German children by urinary cotinine measurements. They then compared the different measures of ETS exposure.
Results
In all countries, air nicotine concentrations increased with increasing questionnaire reported smoking in a dose‐response fashion. Specificity and negative predictive values of questionnaire reports for nicotine concentrations were excellent. Sensitivity and positive predictive values were moderate to good. Excluding occasional smokers, the overall percentage of homes misclassified was 6.9%, 6.7%, and 5.1% in Germany, the Netherlands, and Sweden, respectively. Similar results were found for the agreement of urinary cotinine concentrations with questionnaire reports and air nicotine levels. There was no indication of underreporting by parents of symptomatic children.
Conclusion
Despite some misclassification, questionnaire reports are an inexpensive and valid estimate of residential ETS exposure among preschool and school children.
doi:10.1136/oem.2006.027151
PMCID: PMC2077986  PMID: 16912089
environmental tobacco smoke; questionnaire; air nicotine; urinary cotinine
4.  Screening for Environmental Tobacco Smoke Exposure among Inner City Children with Asthma 
Pediatrics  2008;122(6):1277-1283.
Background
Environmental tobacco smoke (ETS) causes increased morbidity among children with asthma, however pediatricians do not consistently screen and counsel families of asthmatic children regarding ETS. An index score based on parent report of exposure could help providers efficiently screen for ETS.
Objective
1) To develop an index measure of ETS based on parent self-report of smoking behaviors; 2) To determine whether the index score is associated with children’s present and future cotinine levels.
Methods
Data were drawn from a community intervention for inner-city children with persistent asthma (n=226, response rate 72%). Measures of child salivary cotinine and parent self-reported ETS-related behaviors were obtained at baseline and 7–9 months later. To develop the index score, we used a 15-fold cross-validation method on 70% of our data that considered combinations of smoke exposure variables, controlling for demographics. We chose the most parsimonious model that minimized the mean square predictive error. The resulting index score included primary caregiver smoking and home smoking ban status. We validated our model on the remaining 30% of data. ANOVA and multivariate analyses were used to determine the association of the index score with children’s cotinine levels.
Results
54% of asthmatic children lived with ≥1 smoker and 51% of caregivers reported a complete home smoking ban. The children’s mean baseline cotinine was 1.55ng/ml (range 0.0–21.3). Children’s baseline and follow-up cotinine levels increased as scores on the index measure increased. In a linear regression, the index score was significantly and positively associated with children’s cotinine measurements at baseline (p<.001, model R2=.37) and 7–9 months later (p<.001, R2=.38).
Conclusion
An index measure with combined information regarding primary caregiver smoking and household smoking restrictions helps to identify asthmatic children with the greatest exposure to ETS, and can predict children who will have elevated cotinine levels 7–9 months later.
doi:10.1542/peds.2008-0104
PMCID: PMC2597221  PMID: 19047246
Environmental tobacco smoke; asthma; children; primary care; screening
5.  Advising parents of asthmatic children on passive smoking: randomised controlled trial 
BMJ : British Medical Journal  1999;318(7196):1456-1459.
Objective
To investigate whether parents of asthmatic children would stop smoking or alter their smoking habits to protect their children from environmental tobacco smoke.
Design
Randomised controlled trial.
Setting
Tayside and Fife, Scotland.
Participants
501 families with an asthmatic child aged 2-12 years living with a parent who smoked.
Intervention
Parents were told about the impact of passive smoking on asthma and were advised to stop smoking or change their smoking habits to protect their child’s health.
Main outcome measures
Salivary cotinine concentrations in children, and changes in reported smoking habits of the parents 1 year after the intervention.
Results
At the second visit, about 1 year after the baseline visit, a small decrease in salivary cotinine concentrations was found in both groups of children: the mean decrease in the intervention group (0.70 ng/ml) was slightly smaller than that of the control group (0.88 ng/ml), but the net difference of 0.19 ng/ml had a wide 95% confidence interval (−0.86 to 0.48). Overall, 98% of parents in both groups still smoked at follow up. However, there was a non-significant tendency for parents in the intervention group to report smoking more at follow up and to having a reduced desire to stop smoking.
Conclusions
A brief intervention to advise parents of asthmatic children about the risks from passive smoking was ineffective in reducing their children’s exposure to environmental tobacco smoke. The intervention may have made some parents less inclined to stop smoking. If a clinician believes that a child’s health is being affected by parental smoking, the parent’s smoking needs to be addressed as a separate issue from the child’s health.
Key messagesMany asthmatic children are exposed to high levels of environmental tobacco smokeA brief intervention informing parents of asthmatic children on the harmful effects of passive smoking did not lead to a reduction in exposure of their children to tobacco smokeLow rates of smoking cessation were found in both the intervention group and the control groupSome parents may have been less inclined to stop smoking after the interventionBrief interventions requesting smokers to stop for another person’s health seem ineffective
PMCID: PMC27890  PMID: 10346773
6.  A survey of schoolchildren's exposure to secondhand smoke in Malaysia 
BMC Public Health  2011;11:634.
Background
There is a lack of data describing the exposure of Malaysian schoolchildren to Secondhand Smoke (SHS). The aim of this study is to identify factors influencing schoolchildren's exposures to SHS in Malaysia.
Method
This cross-sectional study was carried out to measure salivary cotinine concentrations among 1064 schoolchildren (10-11 years) attending 24 schools in Malaysia following recent partial smoke-free restrictions. Parents completed questionnaires and schoolchildren provided saliva samples for cotinine assay.
Results
The geometric mean (GM) salivary cotinine concentrations for 947 non-smoking schoolchildren stratified by household residents' smoking behaviour were: for children living with non-smoking parents 0.32 ng/ml (95% CI 0.28-0.37) (n = 446); for children living with a smoker father 0.65 ng/ml (95% CI 0.57-0.72) (n = 432); for children living with two smoking parents 1.12 ng/ml (95% CI 0.29-4.40) (n = 3); for children who live with an extended family member who smokes 0.62 ng/ml (95% CI 0.42-0.89) (n = 33) and for children living with two smokers (father and extended family member) 0.71 ng/ml (95% CI 0.40-0.97) (n = 44). Parental-reported SHS exposures showed poor agreement with children's self-reported SHS exposures. Multiple linear regression demonstrated that cotinine levels were positively associated with living with one or more smokers, urban residence, occupation of father (Armed forces), parental-reported exposure to SHS and education of the father (Diploma/Technical certificate).
Conclusions
This is the first study to characterise exposures to SHS using salivary cotinine concentrations among schoolchildren in Malaysia and also the first study documenting SHS exposure using salivary cotinine as a biomarker in a South-East Asian population of schoolchildren. Compared to other populations of similarly aged schoolchildren, Malaysian children have higher salivary cotinine concentrations. The partial nature of smoke-free restrictions in Malaysia is likely to contribute to these findings. Enforcement of existing legislation to reduce exposure in public place settings and interventions to reduce exposure at home, especially to implement effective home smoking restriction practices are required.
doi:10.1186/1471-2458-11-634
PMCID: PMC3162528  PMID: 21824403
Secondhand smoke; salivary cotinine; schoolchildren; self-reported smoke exposure; smoke-free legislation; enzyme-immunoassay method
7.  Changes in child exposure to secondhand smoke after implementation of smoke-free legislation in Wales: a repeated cross-sectional study 
BMC Public Health  2009;9:430.
Background
Smoke-free legislation was introduced in Wales in April 2007. In response to concerns regarding potential displacement of smoking into the home following legislation, this study assessed changes in secondhand smoke (SHS) exposure amongst non-smoking children.
Methods
Approximately 1,750 year 6 (aged 10-11) children from 75 Welsh primary schools were included in cross-sectional surveys immediately pre-legislation and one year later. Participants completed self-report questionnaires and provided saliva samples for cotinine assay. Regression analyses assessed the impact of legislation on children's SHS exposure at the population level, and amongst subgroups defined by parental figures who smoke within the home.
Results
Geometric mean salivary cotinine concentrations were 0.17 ng/ml (95% CI 0.15,0.20) pre-legislation and 0.15 ng/ml (95% CI 0.13,0.17), post-legislation, although this change was not statistically significant. Significant movement was however observed from the middle (0.10-0.50 ng/ml) to lower tertile, though not from the higher end (>0.51 ng/ml) to the middle.
Reported exposure to SHS was greatest within the home. Home-based exposure did not change significantly post-legislation. Reported exposure in cafés or restaurants, buses and trains, and indoor leisure facilities fell significantly.
The proportion of children reporting that parent figures smoked in the home declined (P = 0.03), with children with no parent figures who smoke in the home significantly more likely to provide saliva with cotinine concentrations of <0.10 ng/ml post-legislation.
Amongst children with no parent figures who smoke in the home, the likelihood of 'not knowing' or 'never' being in a place where people were smoking increased post-legislation.
Conclusion
Smoke-free legislation in Wales did not increase SHS exposure in homes of children aged 10-11. Reported SHS exposure in public places fell significantly. The home remained the main source of children's SHS exposure. The legislation was associated with an unexpected reduction in cotinine levels among children with lower SHS exposure pre-legislation. The findings indicate positive rather than harmful effects of legislation on children's SHS exposure, but highlight the need for further action to protect those children most exposed to SHS.
doi:10.1186/1471-2458-9-430
PMCID: PMC2789068  PMID: 19930678
8.  How to minimize children’s environmental tobacco smoke exposure: an intervention in a clinical setting in high risk areas 
BMC Pediatrics  2013;13:76.
Background
Despite the low prevalence of daily smokers in Sweden, children are still being exposed to environmental tobacco smoke (ETS), primarily by their smoking parents. A prospective intervention study using methods from Quality Improvement was performed in Child Health Care (CHC). The aim was to provide nurses with new methods for motivating and supporting parents in their efforts to protect children from ETS exposure.
Method
Collaborative learning was used to implement and test an intervention bundle. Twenty-two CHC nurses recruited 86 families with small children which had at least one smoking parent. Using a bundle of interventions, nurses met and had dialogues with the parents over a one-year period. A detailed questionnaire on cigarette consumption and smoking policies in the home was answered by the parents at the beginning and at the end of the intervention, when children also took urine tests to determine cotinine levels.
Results
Seventy-two families completed the study. Ten parents (11%) quit smoking. Thirty-two families (44%) decreased their cigarette consumption. Forty-five families (63%) were outdoor smokers at follow up. The proportion of children with urinary cotinine values of >6 ng/ml had decreased.
Conclusion
The intensified tobacco prevention in CHC improved smoking parents’ ability to protect their children from ETS exposure.
doi:10.1186/1471-2431-13-76
PMCID: PMC3660282  PMID: 23672646
Children; Child Health Care; Tobacco smoke prevention; Passive smoking
9.  Relation of passive smoking as assessed by salivary cotinine concentration and questionnaire to spirometric indices in children. 
Thorax  1993;48(1):14-20.
BACKGROUND: Previous studies of the effects of passive exposure to smoke on spirometric indices in children have largely relied on questionnaire measures of exposure. This may have resulted in underestimation of the true effect of passive smoking. Biochemical measures offer the opportunity to estimate recent exposure directly. METHODS: The relation between spirometric indices and passive exposure to tobacco smoke was examined in a large population sample of 5-7 year old children from 10 towns in England and Wales. The effects of passive exposure to smoke on lung function were assessed by means of both salivary cotinine concentration and questionnaire measurements of exposure. Analyses of the relation between spirometric values and cotinine concentrations were based on 2511 children and of the relation between spirometric values and questionnaire measures on 2000 children. RESULTS: Cotinine concentration was negatively associated with all spirometric indices after adjustment for confounding variables, which included age, sex, body size, and social class. The strongest association was with mid expiratory flow rate (FEF50), the fall between the bottom and top fifths of the cotinine distribution being 6%, equivalent to a reduction of 14.3 (95% confidence limits (CL) 8.6, 20.0) ml/s per ng/ml cotinine. Salivary cotinine concentrations were strongly related to exposure to cigarette smoke at home but 88% of children who were from non-smoking households and not looked after by a smoker had detectable cotinine concentrations, 5% being in the top two fifths of the cotinine distribution. A composite questionnaire score based on the number of regular sources of exposure was as strongly related to mid and end expiratory flow rates as the single cotinine measure. The fall in FEF50 per smoker to whom the child was exposed was 51.0 (26.5, 75.5) ml/s. The relationships between the questionnaire score and forced vital capacity (FVC) or forced expiratory volume in one second (FEV1) were not statistically significant. CONCLUSIONS: These effects of passive smoking on respiratory function are consistent with the results of previous studies and, although small in absolute magnitude, may be important if the effects of exposure are cumulative. In children aged 5-7 years the use of a single salivary cotinine concentration as a marker of passive exposure to smoke resulted in clear relationships between exposure and FVC and FEV1, whereas the associations were much weaker and not significant when based on the questionnaire score. The associations between exposure and mid or end expiratory flow rates were of similar magnitude for cotinine concentration and the questionnaire score. The use of salivary cotinine concentration in longitudinal studies may help to determine the extent to which these effects are cumulative or reversible.
PMCID: PMC464228  PMID: 8434347
10.  Passive exposure to tobacco smoke in children aged 5-7 years: individual, family, and community factors. 
BMJ : British Medical Journal  1994;308(6925):384-389.
OBJECTIVE--To examine the importance of parental smoking on passive exposure to tobacco smoke in children and the social and geographical patterns of exposure. DESIGN--Cross sectional study. SETTING--Schools in 10 towns in England and Wales; five towns with high adult cardiovascular mortality and five with low rates. SUBJECTS--4043 children aged 5-7 years of European origin. MAIN OUTCOME MEASURES--Salivary cotinine concentration and parents self reported smoking habits. RESULTS--1061 (53.0%) children were exposed to cigarette smoke at home or by an outside carer. Geometric mean cotinine rose from 0.29 (95% confidence interval 0.28 to 0.31) ng/ml in children with no identified exposure to 4.05 (3.71 to 4.42) ng/ml in households where both parents smoked and 9.03 (6.73 to 12.10) ng/ml if both parents smoked more than 20 cigarettes a day. The effect of mothers' smoking was greater than that of fathers', especially at high levels of consumption. After adjustment for known exposures geometric mean cotinine concentrations rose from 0.52 ng/ml in social class I to 1.36 ng/ml in social class V (P < 0.0001); and were doubled in high mortality towns compared with the low mortality towns (P = 0.002). In children with no identified exposure similar trends by social class and town were observed and the cotinine concentrations correlated with the prevalence of parental smoking, both between towns (r = 0.69, P = 0.02) and between schools within towns (r = 0.50, P < 0.001). CONCLUSIONS--Mothers' smoking is more important that fathers' despite the lower levels of smoking by mothers. Children not exposed at home had low cotinine concentration, the level depending on the prevalence of smoking in the community.
PMCID: PMC2539482  PMID: 8124146
11.  A longitudinal study of environmental tobacco smoke exposure in children: Parental self reports versus age dependent biomarkers 
BMC Public Health  2008;8:47.
Background
Awareness of the negative effects of smoking on children's health prompted a decrease in the self-reporting of parental tobacco use in periodic surveys from most industrialized countries. Our aim is to assess changes between ETS exposure at the end of pregnancy and at 4 years of age determined by the parents' self-report and measurement of cotinine in age related biological matrices.
Methods
The prospective birth cohort included 487 infants from Barcelona city (Spain). Mothers were asked about maternal and household smoking habit. Cord serum and children's urinary cotinine were analyzed in duplicate using a double antibody radioimmunoassay.
Results
At 4 years of age, the median urinary cotinine level in children increased 1.4 or 3.5 times when father or mother smoked, respectively. Cotinine levels in children's urine statistically differentiated children from smoking mothers (Geometric Mean (GM) 19.7 ng/ml; 95% CI 16.83–23.01) and exposed homes (GM 7.1 ng/ml; 95% CI 5.61–8.99) compared with non-exposed homes (GM 4.5 ng/ml; 95% CI 3.71–5.48). Maternal self-reported ETS exposure in homes declined in the four year span between the two time periods from 42.2% to 31.0% (p < 0.01). Nevertheless, most of the children considered non-exposed by their mothers had detectable levels of cotinine above 1 ng/mL in their urine.
Conclusion
We concluded that cotinine levels determined in cord blood and urine, respectively, were useful for categorizing the children exposed to smoking and showed that a certain increase in ETS exposure during the 4-year follow-up period occurred.
doi:10.1186/1471-2458-8-47
PMCID: PMC2276212  PMID: 18254964
12.  Factors Associated with Second Hand Smoke Exposure In Young Inner City Children with Asthma 
Objectives
To examine the association of social and environmental factors with levels of second hand smoke (SHS) exposure, as measured by salivary cotinine, in young inner city children with asthma.
Methods
We used data drawn from a home-based behavioral intervention for young high risk children with persistent asthma post emergency department (ED) treatment (N=198). SHS exposure was measured by salivary cotinine and caregiver report. Caregiver demographic and psychological functioning, household smoking behavior and asthma morbidity were compared with child cotinine concentrations. Chi-square and ANOVA tests and multivariate regression models were used to determine the association between cotinine concentrations with household smoking behavior and asthma morbidity.
Results
Over half (53%) of the children had cotinine levels compatible with SHS exposure and mean cotinine concentrations were high at 2.42 ng/ml (SD 3.2). The caregiver was the predominant smoker in the home (57%) and (63%) reported a total home smoking ban. Preschool age children, and those with caregivers reporting depressive symptoms and high stress had higher cotinine concentrations than their counterparts. Among children living in a home with a total home smoking ban, younger children had significantly higher mean cotinine concentration than older children (Cotinine: 3–5 year olds, 2.24 ng/ml (SD 3.5); 6–10 year olds, 0.63 ng/ml (SD 1.0); p <0.05). In multivariate models, the factors most strongly associated with high child cotinine concentrations were increased number of household smokers (β = 0.24) and younger child age (3–5 years) (β = 0.23; P <0.001, R2 = 0.35).
Conclusion
Over half of young inner-city children with asthma were exposed to second hand smoke and caregivers are the predominant household smoker. Younger children and children with depressed and stressed caregivers are at significant risk of smoke exposures, even when a household smoking ban is reported. Further advocacy for these high-risk children is needed to help caregivers quit and to mitigate smoke exposure.
doi:10.3109/02770903.2011.576742
PMCID: PMC3113681  PMID: 21545248
asthma; children; cotinine; second hand smoke
13.  Household Smoking Behavior: Effects on Indoor Air Quality and Health of Urban Children with Asthma 
Maternal and child health journal  2011;15(4):460-468.
The goal of the study was to examine the association between biomarkers and environmental measures of second hand smoke (SHS) with caregiver, i.e. parent or legal guardian, report of household smoking behavior and morbidity measures among children with asthma. Baseline data were drawn from a longitudinal intervention for 126 inner city children with asthma, residing with a smoker. Most children met criteria for moderate to severe persistent asthma (63%) versus mild intermittent (20%) or mild persistent (17%). Household smoking behavior and asthma morbidity were compared with child urine cotinine and indoor measures of air quality including fine particulate matter (PM2.5) and air nicotine (AN). Kruskal–Wallis, Wilcoxon rank-sum and Spearman rho correlation tests were used to determine the level of association between biomarkers of SHS exposure and household smoking behavior and asthma morbidity. Most children had uncontrolled asthma (62%). The primary household smoker was the child's caregiver (86/126, 68%) of which 66 (77%) were the child's mother. Significantly higher mean PM2.5, AN and cotinine concentrations were detected in households where the caregiver was the smoker (caregiver smoker: PM2.5 μg/m3: 44.16, AN: 1.79 μg/m3, cotinine: 27.39 ng/ml; caregiver non-smoker: PM2.5: 28.88 μg/m3, AN: 0.71 μg/m3, cotinine:10.78 ng/ml, all P ≤ 0.01). Urine cotinine concentrations trended higher in children who reported 5 or more symptom days within the past 2 weeks (>5 days/past 2 weeks, cotinine: 28.1 ng/ml vs. <5 days/past 2 weeks, cotinine: 16.2 ng/ml; P = 0.08). However, environmental measures of SHS exposures were not associated with asthma symptoms. Urban children with persistent asthma, residing with a smoker are exposed to high levels of SHS predominantly from their primary caregiver. Because cotinine was more strongly associated with asthma symptoms than environmental measures of SHS exposure and is independent of the site of exposure, it remains the gold standard for SHS exposure assessment in children with asthma.
doi:10.1007/s10995-010-0606-7
PMCID: PMC3113654  PMID: 20401688
Asthma; Children; Cotinine; Particulate matter; Air Nicotine
14.  Validity of self reports in a cohort of Swedish adolescent smokers and smokeless tobacco (snus) users 
Tobacco Control  2005;14(2):114-117.
Objective: To validate self reports of cigarette and smokeless tobacco (snus) use in a prospective cohort of adolescents.
Design: A cross sectional analysis of a cohort sub-sample.
Setting: County of Stockholm, Sweden.
Subjects: 520 adolescents in the final grade of junior high school (mean age 15.0 years).
Main outcome measure: Concordance between self reported tobacco use and saliva cotinine concentration.
Results: Using a cut point of 5 ng/ml saliva cotinine to discriminate active tobacco use, there was a 98% concordance between self reported non-use in the past month and cotinine concentration. The sensitivity of the questionnaire compared to the saliva cotinine test, used as the gold standard, was 90% and the specificity 93%. One hundred and fifteen out of 520 subjects (22%) reported monthly tobacco use. Among these, 67% (46/69) of the exclusive cigarette smokers, 82% (23/28) of exclusive snus users, and 94% (15/16) of mixed users (cigarettes + snus) had cotinine concentrations above 5 ng/ml. Among subjects reporting daily use 96% (64/67) had saliva cotinine concentrations above the cut point. Exclusive current cigarette users were more likely to be classified discordantly by questionnaire and cotinine test compared to snus users (odds ratio 3.2, 95% confidence interval 1.2 to 8.6).
Conclusion: This study confirms the reliability of adolescents' self reported tobacco use. In a context of low exposure to environmental tobacco smoke a cut off for saliva cotinine of 5 ng/ml reliably discriminated tobacco users from non-users. Irregular use of tobacco in this age group probably explains the discrepancy between self reported use and cotinine concentrations.
doi:10.1136/tc.2004.008789
PMCID: PMC1747998  PMID: 15791021
15.  Cord serum cotinine as a biomarker of fetal exposure to cigarette smoke at the end of pregnancy. 
Environmental Health Perspectives  2000;108(11):1079-1083.
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.
PMCID: PMC1240166  PMID: 11102300
16.  A motivational interviewing intervention to PREvent PAssive Smoke Exposure (PREPASE) in children with a high risk of asthma: design of a randomised controlled trial 
BMC Public Health  2013;13:177.
Background
Especially children at risk for asthma are sensitive to the detrimental health effects of passive smoke (PS) exposure, like respiratory complaints and allergic sensitisation. Therefore, effective prevention of PS exposure in this group of vulnerable children is important. Based on previous studies, we hypothesized that an effective intervention program to prevent PS exposure in children is possible by means of a motivational interviewing tailored program with repeated contacts focussing on awareness, knowledge, beliefs (pros/cons), perceived barriers and needs of parents, in combination with feedback about urine cotinine levels of the children. The aim of the PREPASE study is to test the effectiveness of such an intervention program towards eliminating or reducing of PS exposure in children at risk for asthma. This article describes the protocol of the PREPASE study.
Methods
The study is a one-year follow-up randomized controlled trial. Families with children (0–13 years of age) having an asthma predisposition who experience PS exposure at home are randomized into an intervention group receiving an intervention or a control group receiving care as usual. The intervention is given by trained research assistants. The intervention starts one month after a baseline measurement and takes place once per month for an hour during six home based counselling sessions. The primary outcome measure is the percentage of families curtailing PS exposure in children (parental report verified with the urine cotinine concentrations of the children) after 6 months. The secondary outcome measures include: household nicotine level, the child’s lung function, airway inflammation and oxidative stress, presence of wheezing and questionnaires on respiratory symptoms, and quality of life. A process evaluation is included. Most of the measurements take place every 3 months (baseline and after 3, 6, 9 and 12 months of study).
Conclusion
The PREPASE study incorporates successful elements of previous interventions and may therefore be very promising. If proven effective, the intervention will benefit the health of children at risk for asthma and may also create opportunity to be tested in other population.
Trial registration number
NTR2632
doi:10.1186/1471-2458-13-177
PMCID: PMC3599824  PMID: 23442389
Children; Asthma; Passive smoke exposure; Motivational interviewing; Intervention
17.  Association of Secondhand Smoke Exposure with Pediatric Invasive Bacterial Disease and Bacterial Carriage: A Systematic Review and Meta-analysis 
PLoS Medicine  2010;7(12):e1000374.
Majid Ezzati and colleagues report the findings of a systematic review and meta-analysis that probes the association between environmental exposure to secondhand smoke and the epidemiology of pediatric invasive bacterial disease.
Background
A number of epidemiologic studies have observed an association between secondhand smoke (SHS) exposure and pediatric invasive bacterial disease (IBD) but the evidence has not been systematically reviewed. We carried out a systematic review and meta-analysis of SHS exposure and two outcomes, IBD and pharyngeal carriage of bacteria, for Neisseria meningitidis (N. meningitidis), Haemophilus influenzae type B (Hib), and Streptococcus pneumoniae (S. pneumoniae).
Methods and Findings
Two independent reviewers searched Medline, EMBASE, and selected other databases, and screened articles for inclusion and exclusion criteria. We identified 30 case-control studies on SHS and IBD, and 12 cross-sectional studies on SHS and bacterial carriage. Weighted summary odd ratios (ORs) were calculated for each outcome and for studies with specific design and quality characteristics. Tests for heterogeneity and publication bias were performed. Compared with those unexposed to SHS, summary OR for SHS exposure was 2.02 (95% confidence interval [CI] 1.52–2.69) for invasive meningococcal disease, 1.21 (95% CI 0.69–2.14) for invasive pneumococcal disease, and 1.22 (95% CI 0.93–1.62) for invasive Hib disease. For pharyngeal carriage, summary OR was 1.68 (95% CI, 1.19–2.36) for N. meningitidis, 1.66 (95% CI 1.33–2.07) for S. pneumoniae, and 0.96 (95% CI 0.48–1.95) for Hib. The association between SHS exposure and invasive meningococcal and Hib diseases was consistent regardless of outcome definitions, age groups, study designs, and publication year. The effect estimates were larger in studies among children younger than 6 years of age for all three IBDs, and in studies with the more rigorous laboratory-confirmed diagnosis for invasive meningococcal disease (summary OR 3.24; 95% CI 1.72–6.13).
Conclusions
When considered together with evidence from direct smoking and biological mechanisms, our systematic review and meta-analysis indicates that SHS exposure may be associated with invasive meningococcal disease. The epidemiologic evidence is currently insufficient to show an association between SHS and invasive Hib disease or pneumococcal disease. Because the burden of IBD is highest in developing countries where SHS is increasing, there is a need for high-quality studies to confirm these results, and for interventions to reduce exposure of children to SHS.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
The deleterious health effects of smoking on smokers are well established, but smoking also seriously damages the health of nonsmokers. Secondhand smoke (SHS), which is released by burning cigarettes and exhaled by smokers, contains hundreds of toxic chemicals that increase the risk of adults developing lung cancer and heart disease. Children, however, are particularly vulnerable to the effects of SHS exposure (also known as passive smoking) because they are still developing physically. In addition, children have little control over their indoor environment and thus can be heavily exposed to SHS. Exposure to SHS increases the risk of ear infections, asthma, respiratory symptoms (coughing, sneezing, and breathlessness), and lung infections such as pneumonia and bronchitis in young children and the risk of sudden infant death syndrome during the first year of life.
Why Was This Study Done?
Several studies have also shown an association between SHS exposure (which damages the lining of the mouth, throat, and lungs and decreases immune defenses) and potentially fatal invasive bacterial disease (IBD) in children. In IBD, bacteria invade the body and grow in normally sterile sites such as the blood (bacteremia) and the covering of the brain (meningitis). Three organisms are mainly responsible for IBD in children—Streptococcus pneumoniae, Haemophilus influenzae type B (Hib), and Neisseria meningitidis. In 2000, S. pneumonia (pneumococcal disease) alone killed nearly one million children. Here, the researchers undertake a systematic review and meta-analysis of the association between SHS exposure in children and two outcomes—IBD and the presence of IBD-causing organisms in the nose and throat (bacterial carriage). A systematic review uses predefined criteria to identify all the research on a given topic; meta-analysis is a statistical method that combines the results of several studies. By combining data, it is possible to get a clearer view of the causes of a disease than is possible from individual studies.
What Did the Researchers Do and Find?
The researchers identified 30 case-control studies that compared the occurrence of IBD over time in children exposed to SHS with its occurrence in children not exposed to SHS. They also identified 12 cross-sectional studies that measured bacterial carriage at a single time point in children exposed and not exposed to SHS. The researchers used the data from these studies to calculate a “summary odds ratio” (OR) for each outcome—a measure of how SHS exposure affected the likelihood of each outcome. Compared with children unexposed to SHS, exposure to SHS doubled the likelihood of invasive meningococcal disease (a summary OR for SHS exposure of 2.02). Summary ORs for invasive pneumococcal disease and Hib diseases were 1.21 and 1.22, respectively. However, these small increases in the risk of developing these IBDs were not statistically significant unlike the increase in the risk of developing meningococcal disease. That is, they might have occurred by chance. For bacterial carriage, summary ORs for SHS exposure were 1.68 for N. meningitidis, 1.66 for S. pneumonia (both these ORs were statistically significant), and 0.96 for Hib (a nonsignificant decrease in risk).
What Do These Findings Mean?
These findings indicate that SHS exposure is significantly associated with invasive meningococcal disease among children. However, the evidence that SHS exposure is associated with invasive pneumococcal and Hib disease is only suggestive. These findings also indicate that exposure to SHS is associated with an increased carriage of N. meningitidis and S. pneumoniae. The accuracy and generalizability of these findings is limited by the small number of studies identified, by the lack of studies from developing countries where SHS exposure is increasing and the burden of IBD is high, and by large variations between the studies in how SHS exposure was measured and IBD diagnosed. Nevertheless, they suggest that, by reducing children's exposure to SHS (by, for example, persuading parents not to smoke at home), the illness and death caused by IBDs among children could be greatly reduced. Such a reduction would be particularly welcome in developing countries where vaccination against IBDs is low.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1000374.
The US Centers for Disease Control and Prevention provides information on secondhand smoke, on children and secondhand smoke exposure, on meningitis, and on Hib infection
The US Environmental Protection Agency also provides information on the health effects of exposure to secondhand smoke (in English and Spanish) and a leaflet (also in English and Spanish) entitled Secondhand Tobacco Smoke and the Health of Your Family
The US Office of the Surgeon General provides information on the health consequences of involuntary exposure to tobacco smoke
The World Health Organization provides a range of information on the global tobacco epidemic
The World Health Organization has information on meningococcal disease (in English only) and on Hib (in several languages)
The US National Foundation for Infectious Diseases provides a fact sheet on pneumococcal disease
doi:10.1371/journal.pmed.1000374
PMCID: PMC2998445  PMID: 21151890
18.  Passive smoking and lung function in α1-antitrypsin heterozygote schoolchildren 
Thorax  2003;58(3):237-241.
Methods: The effect of passive smoking on lung function was investigated in a cross sectional study of 997 primary and secondary schoolchildren aged 11–13 years categorised by Pi phenotype as either PiM homozygotes or Pi heterozygotes. Data on respiratory health and risk factors were collected by questionnaire, lung function was measured by spirometric tests, bronchial hyperresponsiveness was evaluated by methacholine test, atopic status was evaluated by skin prick testing, and a blood sample was collected to determine Pi phenotype. Urinary cotinine and creatinine concentrations were determined and assessment of exposure was made from questionnaire data and urinary cotinine concentrations. The results were analysed by multiple regression analysis.
Results: Sixty one subjects (6.1%) were found to be Pi heterozygotes. Lung function did not differ between homozygotes and heterozygotes. There was a reduction in lung function in subjects exposed to parental smoking in the overall sample: FEV1/FVC ratio (-0.78%), FEF25-75 (-0.11 litres), and FEF75 (-0.13 litres). Interaction terms between parental smoking and Pi status were significant with regard to FEV1/FVC ratio (p=0.035) and FEF50 (p=0.023). In subjects exposed to parental smoking the decrement in lung function in Pi heterozygotes tended to be greater (FEV1/FVC ratio = -2.57, FEF25–75 = -0.30, FEF50 = -0.43, and FEF75 = -0.29) than in PiM homozygotes. These results did not change significantly when the urinary cotinine concentration was used as an exposure variable.
Conclusions: The detrimental effect of environmental tobacco smoke on lung function in schoolchildren is confirmed. This harmful effect is greater in Pi heterozygotes than in PiM homozygotes.
doi:10.1136/thorax.58.3.237
PMCID: PMC1746588  PMID: 12612303
19.  Passive smoking by self report and serum cotinine and the prevalence of respiratory and coronary heart disease in the Scottish heart health study. 
STUDY OBJECTIVE--To explore the relationship between self reported environmental tobacco smoke exposure (or passive smoking), the serum cotinine concentration, and evidence of respiratory or coronary disease in men and women who have never smoked. DESIGN--Cross sectional random population survey identifying disease markers and relating them to measures of passive smoking. Disease markers were previous medical diagnoses, response to standard symptom questionnaires, and electrocardiographic signs. SETTING--Samples of men and women aged 40-59 years drawn from general practitioner lists in 22 local government districts of Scotland, between 1984 and 1986. PARTICIPANTS--A total of 786 men and 1492 women who reported never having smoked tobacco, and who had serum cotinine concentrations below 17.5 ng/ml, the cut off point for smoking "deceivers", took part. RESULTS--Fewer than one third of never smokers reported no recent exposure to environmental tobacco smoke and the same proportion had no detectable cotinine. Women had lower cotinine values than men but reported more exposure to smoke. The correlation between the measures of exposure was poor. Self-reported exposure showed strong, statistically significant, dose response relationships with respiratory symptoms and with the coronary disease markers. These relationships were weak or absent for serum cotinine, except for diagnosed coronary heart disease. Here the dose response gradient was as strong as that for self report, with an odds ratio of 2.7 (95% CI 1.3, 5.6) for the highest v the lowest exposure group, adjusted for age, housing tenure, total cholesterol, and blood pressure, and not explained by fibrinogen. CONCLUSIONS--The validity of different measures of tobacco smoke exposure needs further investigation. The gradient of diagnosed coronary heart disease with both self reported exposure and serum cotinine was, however, surprisingly strong, statistically significant, and unexplained by other factors. These findings reinforce current policies to limit passive tobacco smoke exposure.
PMCID: PMC1060097  PMID: 7798040
20.  Effect of counselling mothers on their children's exposure to environmental tobacco smoke: randomised controlled trial 
BMJ : British Medical Journal  2000;321(7257):337-342.
Objective
To test the efficacy of behavioural counselling for smoking mothers in reducing young children's exposure to environmental tobacco smoke.
Design
Randomised double blind controlled trial.
Setting
Low income homes in San Diego county, California.
Participants
108 ethnically diverse mothers who exposed their children (aged <4 years) to tobacco smoke in the home.
Intervention
Mothers were given seven counselling sessions over three months.
Main outcome measures
Children's reported exposure to environmental tobacco smoke from mothers in the home and from all sources; children's cotinine concentrations in urine.
Results
Mothers' reports of children's exposure to their smoke in the home declined in the counselled group from 27.30 cigarettes/week at baseline, to 4.47 at three months, to 3.66 at 12 months and in the controls from 24.56, to 12.08, to 8.38. The differences between the groups by time were significant (P=0.002). Reported exposure to smoke from all sources showed similar declines, with significant differences between groups by time (P=0.008). At 12 months, the reported exposure in the counselled group was 41.2% that of controls for mothers' smoke (95% confidence interval 34.2% to 48.3%) and was 45.7% (38.4% to 53.0%) that of controls for all sources of smoke. Children's mean urine cotinine concentrations decreased slightly in the counselled group from 10.93 ng/ml at baseline to 10.47 ng/ml at 12 months but increased in the controls from 9.43 ng/ml to 17.47 ng/ml (differences between groups by time P=0.008). At 12 months the cotinine concentration in the counselled group was 55.6% (48.2% to 63.0%) that of controls.
Conclusions
Counselling was effective in reducing children's exposure to environmental tobacco smoke. Similar counselling in medical and social services might protect millions of children from environmental tobacco smoke in their homes.
PMCID: PMC27449  PMID: 10926589
21.  Measuring environmental tobacco smoke exposure in infants and young children through urine cotinine and memory-based parental reports: empirical findings and discussion 
Tobacco Control  1999;8(3):282-289.
OBJECTIVE—This study examined the reliability and potential biases of two urine collection methods from which cotinine measures were obtained and the validity of memory-based parental reports of their children's exposure to environmental tobacco smoke (ETS).
DESIGN—Structured interviews were conducted with mothers of infants and young children to obtain memory-based estimates of recent ETS exposure. Urine samples were collected through standard and cotton roll collection methods for cotinine analysis.
SETTING—All interviews took place at an off-campus research facility. Urine samples were collected at the study office or the subjects' homes.
PARTICIPANTS—Mothers were recruited from San Diego county sites of the Women, Infants, and Children (WIC) Supplemental Food and Nutrition Program. Sample 1 (infants) consisted of eight boys and eight girls aged 1-44 months (mean = 12.6 months). Sample 2 (children) included 10 boys and 10 girls aged 3-8 years (mean = 61.2 months).
MAIN OUTCOME MEASURES—Urine cotinine and memory-based parent reports of ETS exposure from structured interviews.
RESULTS—There was overall high reliability for urine cotinine measures and no effect of collection method on urine cotinine levels. Memory-based reports obtained from smoking mothers showed moderately strong and consistent linear relationships with urine cotinine measures of their infants and children (r = 0.50 to r = 0.63), but not for reports obtained from non-smoking mothers.
CONCLUSIONS—Memory-based parental reports of short-term ETS exposure can play an important role in quantifying ETS exposure in infants and children.


Keywords: environmental tobacco smoke; parental smoking; passive smoking
PMCID: PMC1763950  PMID: 10599573
22.  Relationship between Caregivers’ Smoking at Home and Urinary Levels of Cotinine in Children 
Objective: To assess the impact of different smoking behaviors of caregivers on environmental tobacco smoke (ETS) exposure in children aged 5–6 years in Changsha, China. Methods: We conducted a cross-sectional, random digit-dial telephone survey of caregivers (n = 543) between August and October 2013. Caregivers’ smoking behaviors were collected by a questionnaire. Exposure assessment was based upon determination of urinary cotinine levels in children employing gas chromatography–triple quadrupole mass spectrometry (GC-MS/MS). Results: In children not living with a smoker, children living with one smoker, and children living with more than one smoker at home, median urinary cotinine concentrations (ng/mL) were 0.72, 2.97, and 4.46, respectively. For children living with one smoker, median urinary cotinine levels of children exposed to ETS were associated with caregiver smoking behaviors, i.e., if a caregiver consumed more cigarettes (>20 compared with ≤10; 7.73 versus 2.29 ng/mL, respectively). Conclusions: The magnitude of ETS exposure in children is correlated with the smoking behaviors of the caregiver. Counseling for smoking cessation and educational interventions are needed urgently for smoking caregivers to increase their awareness about ETS exposure and to encourage smoking cessation at home or to take precautions to protect children’s health.
doi:10.3390/ijerph111212499
PMCID: PMC4276627  PMID: 25469922
smoking; caregiver; environmental tobacco smoke (ETS); children; gas chromatography-triple quadrupole mass spectrometry (GC-MS/MS); cotinine
23.  The influence of parental smoking and family type on saliva cotinine in UK ethnic minority children: a cross sectional study 
BMC Public Health  2010;10:262.
Background
In the United Kingdom, there has been an increase in cigarette smoking in ethnic minority adults since the 1970s; in some groups levels are now similar to that of White British people. We aimed to examine the determinants of exposure to secondhand smoke in ethnic minority children. We hypothesised that exposure to secondhand smoke in children will vary across ethnic groups, but that the correlates of exposure would be similar to that of Whites.
Methods
The Determinants of Adolescent Social well-being and Health sample comprises 3468 White United Kingdom and ethnic minority (Black Caribbean, Black African, Indian, Pakistani, Bangladeshi) pupils aged 11-13 yrs. Outcome was saliva cotinine concentration. Explanatory variables collected by self-complete questionnaire included ethnicity, child reported household smoking and socio-economic circumstances. Data were analysed using linear regression models with a random intercept function.
Results
Ethnic minority children had lower saliva cotinine than Whites, partly explained by less smoking among parents. White and Black Caribbean children had higher cotinine levels if they lived in a household with a maternal smoker only, than with a paternal smoker only. Living in a lone compared to a dual parent household was associated with increased cotinine concentration of 45% (95%CI 5, 99%) in Whites, 27% (95%CI 5,53%) in Black Caribbeans and 21% (95%CI 1, 45%) in Black Africans after adjusting for household smoking status. Material disadvantage was a significant correlate only for White children (40% (95%CI 1, 94%) increase in cotinine in least compared to most advantaged group).
Conclusions
Ethnic minority children were less exposed to secondhand smoke than Whites, but the variations within groups were similarly patterned. These findings suggest that it is important not to be complacent about low smoking prevalence in some minority groups.
doi:10.1186/1471-2458-10-262
PMCID: PMC2885335  PMID: 20482885
24.  Smoking prevention and cessation programme in Cystic Fibrosis: integrating an environmental health approach 
Journal of Cystic Fibrosis  2011;11(1):34-39.
Background
There have been several studies assessing the epidemiology and effects of tobacco smoke in the cystic fibrosis (CF) population, but few address the efforts of smoking cessation interventions. Our objective is to present one tobacco prevention and cessation programme targeting patients with CF in the Mediterranean region of Murcia (Spain).
Methods
All registered patients in the Regional CF unit (n=105) in 2008 were included in a cross-sectional and prospective uncontrolled study of tobacco use and exposure in CF patients using a baseline and one-year follow-up. Target population includes both patients and other family members living at home. The study included an initial telephone questionnaire, measurement of lung function, urinary cotinine levels, and several telephone counselling calls and/or personalized smoking cessation services.
Results
Of the 97 contacted patients, 59.8% (n=58) were exposed to environmental tobacco smoke (ETS), 12.4% (n=12) had smoked at one time, and 14.3% (n=8) of patients over the age of 15 actively smoked. The mean age was 31.13 (range: 19-45). Of the non-smokers (n=89), 56.2% reported ETS and 26.9% live with at least one smoker at home. 49.2% had urinary cotinine levels >10 ng/ml. The correlation found between patients’ cotinine levels and their reported tobacco exposure was (0.77, p<0.0001). Active smoking by mothers during pregnancy was associated with significantly lower lung function in young CF patients (-0,385, p= 0.04). At the one-year follow-up, 13 individuals made attempts to stop smoking, 6 of which are now ex-smokers (12.5% of all smokers).
Conclusions
Smoking during pregnancy adversely affects lung function in individuals with CF. Tobacco he targeted tobacco prevention and cessation programmes are an effective and vital component for CF disease management. The trained professionals in prevention and smoking cessation services could provide patients with adequate follow-up, integrating an environmental health approach into CF patients’ healthcare
doi:10.1016/j.jcf.2011.09.005
PMCID: PMC3260390  PMID: 22000068
Environmental tobacco smoke; cystic fibrosis; smoking prevention
25.  Counseling to reduce children's secondhand smoke exposure and help parents quit smoking: A controlled trial 
Nicotine & Tobacco Research  2009;11(12):1383-1394.
Introduction:
We tested a combined intervention to reduce children's secondhand smoke exposure (SHSe) and help parents quit smoking.
Methods:
After baseline, mothers who exposed their children younger than 4 years to 10 or more cigarettes/week were randomized to the intervention (n = 76) or usual care control condition (n = 74). Outcomes were assessed at 3, 6, 12, and 18 months. Intervention families were offered 10 in-person at home and 4 telephone counseling sessions over 6 months, and additional pre- and postquit telephone sessions. Counseling procedures included behavioral contracting, self-monitoring, and problem solving.
Results:
Parents’ reports of their smoking and children's exposure showed moderate and significant correlations with children's urine cotinine levels and home air nicotine (r = .40–.78). Thirteen (17.1%) intervention group mothers and 4 (5.4%) controls reported that they quit smoking for 7 days prior to 1 or more study measurements, without biochemical contradiction (p = .024). Results of generalized estimating equations showed significantly greater decrease in reported SHSe and mothers’ smoking in the counseled group compared with controls. Reported indoor smoking and children's urine cotinine decreased, yet group differences for changes were not significant.
Discussion:
Nicotine contamination of the home and resulting thirdhand exposure may have contributed to the failure to obtain a differential decrease in cotinine concentration. Partial exposure to counseling due to dropouts and lack of full participation from all family members and measurement reactivity in both conditions may have constrained intervention effects. Secondhand smoke exposure counseling may have been less powerful when combined with smoking cessation.
doi:10.1093/ntr/ntp148
PMCID: PMC2784487  PMID: 19875762

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