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1.  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.
PMCID: PMC3113654  PMID: 20401688
Asthma; Children; Cotinine; Particulate matter; Air Nicotine
2.  Screening for Environmental Tobacco Smoke Exposure among Inner City Children with Asthma 
Pediatrics  2008;122(6):1277-1283.
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.
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.
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.
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).
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.
PMCID: PMC2597221  PMID: 19047246
Environmental tobacco smoke; asthma; children; primary care; screening
3.  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
4.  Does passive smoking increase the frequency of health service contacts in children with asthma? 
Thorax  2001;56(1):9-12.
BACKGROUND—Passive smoking is a major cause of respiratory morbidity in children. However, few studies give accurate estimates of the health effects of passive smoking in children with asthma using an objective measure of exposure. The effects of passive smoking using salivary cotinine levels to measure exposure were investigated.
METHODS—A sample of 438 children aged 2-12 years with asthma who had a parent who smoked were recruited in Tayside and Fife, Scotland. Health service contacts for asthma, assessed from GP case records, were used as a proxy for morbidity.
RESULTS—A weak U-shaped relationship was found between the salivary cotinine level and health service contacts for asthma: compared with low cotinine levels those with moderate cotinine levels had a reduced contact rate (relative rate (RR) = 0.91, 95% confidence interval (CI) 0.80 to 1.05), whereas high cotinine levels were associated with an increased rate of contact (RR = 1.19, 95% CI 1.05 to 1.37). In contrast, a strong association was seen with the amount the parent reported smoking in front of the child: the higher the level the fewer visits were made for asthma (RR for everyday exposure = 0.66, 95% CI 0.56 to 0.77). This effect was not seen for non-respiratory visits. Demographic factors, age of child, and number of children in the family all had a powerful effect on the number of visits for asthma. The parents' perception of asthma severity was associated with visit frequency independent of actual severity (derived from drug treatment).
CONCLUSION—High levels of parental smoking in the home are associated with a reduction in health care contacts for asthma. This could be due to a lack of awareness of asthma symptoms among heavy smokers or a reluctance to visit the GP. Children with asthma who have parents who smoke heavily may not be receiving adequate management.

PMCID: PMC1745908  PMID: 11120897
5.  Environmental Tobacco Smoke and Behaviors of Inner-City Children With Asthma 
To explore the relationship between environmental tobacco smoke (ETS) exposure and behavior among inner-city children with significant asthma.
We analyzed baseline data for 200 children 4 to 10 years old who were enrolled in an asthma program. Environmental tobacco smoke exposure was measured by the child’s salivary cotinine level. Caregivers completed the 28-item Behavior Problem Index (BPI). Positive responses were summed for a total BPI score, and children with scores >14 were considered to have significant behavior problems. We conducted Student t tests and multivariate regression analyses to determine the association of children’s cotinine levels with BPI scores.
Overall, 56% of children were male, 65% were black, and 72% had Medicaid. Mean cotinine level was 1.47 ng/mL. Overall, 30% of children had total BPI scores >14. Children with cotinine values >1.47 ng/mL had significantly higher scores compared with children with lower cotinine values on total BPI (12.5 vs 10.2), as well as externalizing (9.0 vs 7.2), antisocial (2.3 vs 1.7), and immature (2.1 vs 1.6) subscales. In a multivariate model, log cotinine remained independently associated with externalizing (P = .04), headstrong (P = .04), and antisocial behavior (P = .04).
Cotinine levels are independently associated with problem behaviors among this sample of urban children with asthma.
PMCID: PMC2597107  PMID: 18922501
behavior; childhood asthma; environmental smoke exposure; inner-city
6.  Advising parents of asthmatic children on passive smoking: randomised controlled trial 
BMJ : British Medical Journal  1999;318(7196):1456-1459.
To investigate whether parents of asthmatic children would stop smoking or alter their smoking habits to protect their children from environmental tobacco smoke.
Randomised controlled trial.
Tayside and Fife, Scotland.
501 families with an asthmatic child aged 2-12 years living with a parent who smoked.
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.
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.
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
7.  A survey of schoolchildren's exposure to secondhand smoke in Malaysia 
BMC Public Health  2011;11:634.
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.
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.
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).
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.
PMCID: PMC3162528  PMID: 21824403
Secondhand smoke; salivary cotinine; schoolchildren; self-reported smoke exposure; smoke-free legislation; enzyme-immunoassay method
8.  Residential smoking restrictions are not associated with reduced child SHS exposure in a baseline sample of low-income, urban African Americans 
Health  2010;2(11):1264-1271.
Second hand smoke exposure (SHSe) relates to many chronic and acute illnesses. Low income African American (AA) maternal smokers and their children have disproportionately higher tobacco-use and child SHSe-related morbidity and mortality than other populations. While public health officials promote residential smoking restrictions to reduce SHSe and promote smoking cessation, little is known about the impact of restrictions in changing smoking behavior and SHSe in this population. Thus, the purpose of this study was to examine associations between residential smoking restrictions, maternal smoking, and young children’s SHSe in the context of other factors known to influence low income AA mothers’ smoking behavior. For this study, we used cross-sectional, baseline data from 307 AA maternal smokers’ pre-treatment interviews completed as part of a subsequent behavioral counseling trial to reduce their young (< 4 years old) children’s SHSe. Residential smoking restriction was dichotomized as 0 = no restrictions and 1 = some restrictions. Child urine cotinine provided a biomarker of SHSe. Mothers reported cigarettes/day smoked, cigarettes/day exposed to child, and intention to quit. Multivariate regressions modeled effects of restriction as the primary predictor of smoking and exposure outcomes. Maternal smoking patterns such as cigarettes per day (β = 0.52, p < 0.001) and years smoked (β = −0.11; p = 0.03) along with presence of additional smokers in the home (β = 0.10; p = 0.04), but not residential restriction (β = −0.09, p = 0.10), predicted reported SHSe. Restriction did not relate to baby cotinine or maternal intention to quit. Thus, residential smoking restrictions may contribute to efforts to reduce children’s SHSe and promote maternal smoking change; but alone, may not constitute a sufficient intervention to protect children. Multi-level intervention approaches that include SHSe-reduction residential smoking policies plus support and cessation assistance for smokers may be a necessary approach to smoke-free home adoption and adherence.
PMCID: PMC3715960  PMID: 23875066
Home Smoking Policy; Second Hand Smoke; Underserved Populations
9.  Racial Differences in Exposure to Environmental Tobacco Smoke among Children 
Environmental Health Perspectives  2004;113(3):362-367.
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 (β = 0.34, p = 0.03) than in white children (β = 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.
PMCID: PMC1253766  PMID: 15743729
African American; asthma; cotinine; ETS; housing
10.  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
11.  Salivary cotinine concentration versus self-reported cigarette smoking: Three patterns of inconsistency in adolescence 
The present study examined the extent and sources of discrepancies between self-reported cigarette smoking and salivary cotinine concentration among adolescents. The data are from household interviews with a cohort of 1,024 adolescents from an urban school system. Histories of tobacco use in the last 7 days and saliva samples were obtained. Logistic regressions identified correlates of three inconsistent patterns: (a) Pattern 1—self-reported nonsmoking among adolescents with cotinine concentration above the 11.4 ng/mg cutpoint (n=176), (b) Pattern 2—low cotinine concentration (below cutpoint) among adolescents reporting having smoked within the last 3 days (n=155), and (c) Pattern 3—high cotinine concentration (above cutpoint) among adolescents reporting not having smoked within the last 3 days (n=869). Rates of inconsistency were high among smokers defined by cotinine levels or self-reports (Pattern 1=49.1%; Pattern 2=42.0%). Controlling for other covariates, we found that reports of nonsmoking among those with high cotinine (Pattern 1) were associated with younger age, having few friends smoking, little recent exposure to smokers, and being interviewed by the same interviewer as the parent and on the same day. Low cotinine concentration among self-reported smokers (Pattern 2) was negatively associated with older age, being African American, number of cigarettes smoked, depth of inhalation, and exposure to passive smoke but positively associated with less recent smoking and depressive symptoms. High cotinine concentrations among self-reported nonsmokers was positively associated with exposure to passive smoke (Pattern 3). The data are consonant with laboratory findings regarding ethnic differences in nicotine metabolism rate. The inverse relationship of cotinine concentration with depressive symptoms has not previously been reported. Depressed adolescent smokers may take in smaller doses of nicotine than nondepressed smokers; alternatively, depressed adolescents may metabolize nicotine more rapidly.
PMCID: PMC2538943  PMID: 16920650
12.  A Second Reporter Matters 
Home and car smoking bans implemented by caregivers are important approaches to reducing children’s secondhand smoke (SHS) exposure and attendant health risks. Such private smoking bans are usually informal and are subject to individuals’ interpretation, observation, and recall. Relying on a single reporter may lead to misclassification of bans in families.
To determine (1) proportion of families with discordant reports of bans; (2) association between parent–child report agreement and SHS exposure; and (3) whether including a second reporter of bans improves prediction of child SHS exposure.
In each of 386 participating families a preteen and a parent reported separately on their home and car smoking bans, and agreement was determined. ANOVA, chi-square, and multiple regression were used to determine relationships between SHS exposure (measured by urine cotinine and reported exposure) and home/car smoking bans reported by preteens and parents.
In 19% of families, reports disagreed for home smoking bans; 30% for car smoking bans. Families who agreed on the presence of a ban had the lowest exposure, families who agreed on the absence of a ban had the highest exposure, and intermediate exposure for those who disagreed. Parent and child reports of bans each explained significant, unique variance in child SHS exposure.
Due to relatively high prevalence of discordant reporting, a more accurate classification of home/car bans may result from including multiple reporters.
PMCID: PMC3107008  PMID: 21496758
13.  Self-Reported Exposure to Second-Hand Smoke and Positive Urinary Cotinine in Pregnant Nonsmokers 
Yonsei Medical Journal  2009;50(3):345-351.
This cross-sectional study aimed to examine the association between self-reported exposure status to second-hand smoke and urinary cotinine level in pregnant nonsmokers.
Materials and Methods
We recruited pregnant nonsmokers from the prenatal care clinics of a university hospital and two community health centers, and their urinary cotinine concentrations were measured.
Among a total of 412 pregnant nonsmokers, the proportions of self-reported exposure to second-hand smoke and positive urinary cotinine level were 60.4% and 3.4%, respectively. Among those, 4.8% of the participants who reported exposure to second-hand smoke had cotinine levels of 40 ng/mL (the kappa value = 0.029, p = 0.049). Among those who reported living with smokers (n = 170), "smoking currently permitted in the whole house" (vs. not permitted at home) was associated with positive urinary cotinine in the univariable analysis. Furthermore, this variable showed a significant association with positive urinary cotinine in the stepwise multiple logistic regression analysis [Odds ratio (OR), 15.6; 95% Confidence interval (CI) = 2.1-115.4].
In the current study, the association between self-reported exposure status to second-hand smoke and positive urinary cotinine in pregnant nonsmokers was poor. "Smoking currently permitted in the whole house" was a significant factor of positive urinary cotinine in pregnant nonsmokers. Furthermore, we suggest that a complete smoking ban at home should be considered to avoid potential adverse effects on pregnancy outcomes due to second-hand smoke.
PMCID: PMC2703756  PMID: 19568595
Passive smoking; pregnant women; cotinine
14.  Changes in exposure of adult non-smokers to secondhand smoke after implementation of smoke-free legislation in Scotland: national cross sectional survey 
BMJ : British Medical Journal  2007;335(7619):549.
Objective To measure change in adult non-smokers' exposure to secondhand smoke in public and private places after smoke-free legislation was implemented in Scotland.
Design Repeat cross sectional survey.
Setting Scotland.
Participants Scottish adults, aged 18 to 74 years, recruited and interviewed in their homes.
Intervention Comprehensive smoke-free legislation that prohibits smoking in virtually all enclosed public places and workplaces, including bars, restaurants, and cafes.
Outcome measures Salivary cotinine, self reported exposure to smoke in public and private places, and self reported smoking restriction in homes and in cars.
Results Overall, geometric mean cotinine concentrations in adult non-smokers fell by 39% (95% confidence interval 29% to 47%), from 0.43 ng/ml at baseline to 0.26 ng/ml after legislation (P<0.001). In non-smokers from non-smoking households, geometric mean cotinine concentrations fell by 49% (40% to 56%), from 0.35 ng/ml to 0.18 ng/ml (P<0.001). The 16% fall in cotinine concentrations in non-smokers from smoking households was not statistically significant. Reduction in exposure to secondhand smoke was associated with a reduction after legislation in reported exposure to secondhand smoke in public places (pubs, other workplaces, and public transport) but not in homes and cars. We found no evidence of displacement of smoking from public places into the home.
Conclusions Implementation of Scotland's smoke-free legislation has been accompanied within one year by a large reduction in exposure to secondhand smoke, which has been greatest in non-smokers living in non-smoking households. Non-smokers living in smoking households continue to have high levels of exposure to secondhand smoke.
PMCID: PMC1976488  PMID: 17827485
15.  Association of Maternal Smoking With Child Cotinine Levels 
Nicotine & Tobacco Research  2013;15(12):2029-2036.
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.
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.
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.
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.
PMCID: PMC3819976  PMID: 23880896
16.  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
17.  Changes in child exposure to environmental tobacco smoke (CHETS) study after implementation of smoke-free legislation in Scotland: national cross sectional survey  
BMJ : British Medical Journal  2007;335(7619):545.
Objective To detect any change in exposure to secondhand smoke among primary schoolchildren after implementation of smoke-free legislation in Scotland in March 2006.
Design Comparison of nationally representative, cross sectional, class based surveys carried out in the same schools before and after legislation.
Setting Scotland.
Participants 2559 primary schoolchildren (primary 7; mean age 11.4 years) surveyed in January 2006 (before smoke-free legislation) and 2424 in January 2007 (after legislation).
Outcome measures Salivary cotinine concentrations, reports of parental smoking, and exposure to tobacco smoke in public and private places before and after legislation.
Results The geometric mean salivary cotinine concentration in non-smoking children fell from 0.36 (95% confidence interval 0.32 to 0.40) ng/ml to 0.22 (0.19 to 0.25) ng/ml after the introduction of smoke-free legislation in Scotland—a 39% reduction. The extent of the fall in cotinine concentration varied according to the number of parent figures in the home who smoked but was statistically significant only among pupils living in households in which neither parent figure smoked (51% fall, from 0.14 (0.13 to 0.16) ng/ml to 0.07 (0.06 to 0.08) ng/ml) and among pupils living in households in which only the father figure smoked (44% fall, from 0.57 (0.47 to 0.70) ng/ml to 0.32 (0.25 to 0.42) ng/ml). Little change occurred in reported exposure to secondhand smoke in pupils' own homes or in cars, but a small decrease in exposure in other people's homes was reported. Pupils reported lower exposure in cafes and restaurants and in public transport after legislation.
Conclusions The Scottish smoke-free legislation has reduced exposure to secondhand smoke among young people in Scotland, particularly among groups with lower exposure in the home. We found no evidence of increased secondhand smoke exposure in young people associated with displacement of parental smoking into the home. The Scottish smoke-free legislation has thus had a positive short term impact on young people's health, but further efforts are needed to promote both smoke-free homes and smoking cessation.
PMCID: PMC1976539  PMID: 17827487
18.  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.
PMCID: PMC4276627  PMID: 25469922
smoking; caregiver; environmental tobacco smoke (ETS); children; gas chromatography-triple quadrupole mass spectrometry (GC-MS/MS); cotinine
19.  Is the hair nicotine level a more accurate biomarker of environmental tobacco smoke exposure than urine cotinine? 
Study objective: The aim of this study was to compare the two biomarkers of exposure to environmental tobacco smoke (ETS); urine cotinine and hair nicotine, using questionnaires as the standard.
Design: A cross sectional study of children consecutively admitted to hospital for lower respiratory illnesses during the period of the study.
Settings: Three regional hospitals in the larger Wellington area, New Zealand.
Participants: Children aged 3–27 months and admitted to the above hospitals during August 1997 to October 1998. A total of 322 children provided 297 hair samples and 158 urine samples.
Main results: Hair nicotine levels were better able to discriminate the groups of children according to their household's smoking habits at home (no smokers, smoke only outside the home, smoke inside the house) than urine cotinine (Kruskall-Wallis; χ2=142.14, and χ2=49.5, respectively (p<0.0001)). Furthermore, hair nicotine levels were more strongly correlated with number of smokers in the house, and the number of cigarettes smoked by parents and other members of the child's households. Hair nicotine was better related to the questionnaire variables of smoking in a multivariate regression model (r2=0.55) than urine cotinine (r2=0.31).
Conclusions: In this group of young children, hair nicotine was a more precise biomarker of exposure to ETS than urine cotinine levels, using questionnaire reports as the reference. Both biomarkers indicate that smoking outside the house limits ETS exposure of children but does not eliminate it.
PMCID: PMC1732006  PMID: 11801622
20.  Prevalence and predictors of home and automobile smoking bans and child environmental tobacco smoke exposure: a cross-sectional study of U.S.- and Mexico-born Hispanic women with young children 
BMC Public Health  2006;6:265.
Detrimental effects of environmental tobacco smoke (ETS) exposure on child health are well documented. Because young children's primary exposure to ETS occurs in homes and automobiles, voluntary smoking restrictions can substantially reduce exposure. We assessed the prevalence of home and automobile smoking bans among U.S.- and Mexico-born Hispanics in the southwestern United States, and examined the influence of mother's country of birth and smoking practices on voluntary smoking bans and on child ETS exposure.
U.S.- and Mexico-born Hispanic mothers of children aged 2 through 12 years were systematically sampled from health clinics in Albuquerque, New Mexico. In-person interviews were conducted with 269 mothers (75.4% response rate) to obtain information on main study outcomes (complete versus no/partial home and automobile smoking bans; child room and automobile ETS exposure) and risk factors (mother's country of birth, maternal and household smoking behaviors). Data were analyzed with chi square tests and logistic regression models.
Three-fourths (74–77%) of U.S.-born and 90–95% of Mexico-born mothers reported complete automobile and home smoking bans. In multivariate analyses, mother's U.S nativity, mother's current smoking, and presence of other adult smokers in the home were associated with significantly increased odds of not having a complete home or automobile smoking ban. Mother's smoking was associated with child ETS exposure both indoors (odds ratio [OR] = 3.31) and in automobiles (OR = 2.97). Children of U.S.-born mothers had increased odds of exposure to ETS indoors (OR = 3.24; 95% confidence interval [CI]: 1.37–7.69), but not in automobiles. Having complete smoking bans was associated with substantially reduced odds of child ETS exposure both indoors (OR = 0.10; 95% CI: 0.04–0.27) and in automobiles (OR = 0.14; 95% CI: 0.05–0.36).
This study of Hispanic mothers in the southwestern U.S. indicates that there are substantial differences between U.S.- and Mexico-born mothers in the prevalence of home and automobile smoking bans, and resulting child ETS exposure. Tobacco interventions to increase smoke-free environments for U.S. Hispanic children should focus on both home and automobile smoking practices, especially among U.S.-born mothers, and utilize strategies that impact smoking practices of all household members.
PMCID: PMC1636637  PMID: 17069652
21.  Passive smoking, salivary cotinine concentrations, and middle ear effusion in 7 year old children. 
BMJ : British Medical Journal  1989;298(6687):1549-1552.
OBJECTIVE--To assess the contribution of passive exposure to tobacco smoke to the development of middle ear underpressure and effusion. DESIGN--Cross sectional observational study. SETTING--One third of the primary schools in Edinburgh. SUBJECTS--892 Children aged 6 1/2 to 7 1/2 were examined, and satisfactory tympanograms were obtained in 872. Results of assay of salivary cotinine concentrations were available for 770 children, and satisfactory tympanograms were available for 736 of these. END POINT--Correlation of the prevalence of middle ear underpressure and effusion with concentrations of the marker of nicotine, cotinine, in the saliva of the children. MEASUREMENTS AND MAIN RESULTS--Middle ear pressure and compliance were measured in both ears by impedance tympanometry. Salivary cotinine concentrations were assayed by gas-liquid chromatography. Cotinine concentrations increased with the number of smokers in the household. Girls had higher concentrations than boys, and children living in rented housing had higher concentrations than those living in housing owned by their parents. There was a trend towards more abnormal tympanometric findings with increasing cotinine concentration, the odds ratio for a doubling of the cotinine concentration being 1.14 (95% confidence interval 1.03 to 1.27). After adjustment for the sex of the child and housing tenure the odds ratio for a doubling of the cotinine concentration was 1.13 (1.00 to 1.28). CONCLUSIONS--The results of this study are consistent with those of case-control studies of children attending for an operation to relieve middle ear effusion. They indicate that the disease should be added to the list of recognised hazards associated with passive smoking. About one third of the cases of middle ear effusion in this study were statistically attributable to exposure to tobacco smoke.
PMCID: PMC1836817  PMID: 2503113
22.  Impact of the Spanish Smoking Law on Exposure to Second-Hand Smoke and Respiratory Health in Hospitality Workers: A Cohort Study 
PLoS ONE  2009;4(1):e4244.
A smoke-free law came into effect in Spain on 1st January 2006, affecting all enclosed workplaces except hospitality venues, whose proprietors can choose among totally a smoke-free policy, a partial restriction with designated smoking areas, or no restriction on smoking on the premises. We aimed to evaluate the impact of the law among hospitality workers by assessing second-hand smoke (SHS) exposure and the frequency of respiratory symptoms before and one year after the ban.
Methods and Finding
We formed a baseline cohort of 431 hospitality workers in Spain and 45 workers in Portugal and Andorra. Of them, 318 (66.8%) were successfully followed up 12 months after the ban, and 137 nonsmokers were included in this analysis. We obtained self-reported exposure to SHS and the presence of respiratory symptoms, and collected saliva samples for cotinine measurement. Salivary cotinine decreased by 55.6% after the ban among nonsmoker workers in venues where smoking was totally prohibited (from median of 1.6 ng/ml before to 0.5 ng/ml, p<0.01). Cotinine concentration decreased by 27.6% (p = 0.068) among workers in venues with designated smoking areas, and by 10.7% (p = 0.475) among workers in venues where smoking was allowed. In Portugal and Andorra, no differences between cotinine concentration were found before (1.2 ng/ml) and after the ban (1.2 ng/ml). In Spain, reported respiratory symptom declined significantly (by 71.9%; p<0.05) among workers in venues that became smoke-free. After adjustment for potential confounders, salivary cotinine and respiratory symptoms decreased significantly among workers in Spanish hospitality venues where smoking was totally banned.
Among nonsmoker hospitality workers in bars and restaurants where smoking was allowed, exposure to SHS after the ban remained similar to pre-law levels. The partial restrictions on smoking in Spanish hospitality venues do not sufficiently protect hospitality workers against SHS or its consequences for respiratory health.
PMCID: PMC2621339  PMID: 19165321
23.  Can parents of children with cancer accurately report their child's passive smoking exposure? 
Nicotine & Tobacco Research  2009;11(11):1289-1295.
This study examined whether children with cancer are exposed to measurable levels of passive smoke as assessed by parent report and laboratory measures of urine cotinine, an established biomarker of passive smoke exposure (PSE). It also determined whether parents/caretakers of young cancer patients can provide valid reports of their child's PSE during the child's treatment, by examining their association with urine cotinine measures.
Participants included 124 parents of a child with cancer who lived with at least one adult smoker in the home and was exposed to tobacco smoke in the home and/or car. Eligible patients were younger than 18 years of age, were receiving active treatment for cancer at a large pediatric oncology institution, were at least 30 days postdiagnosis, and did not smoke. Parents provided information about smoking and their child's PSE by responding to a series of questionnaires. Patients provided urine samples for cotinine analyses.
Findings showed that parents provided valid short-term accounts of their child's PSE in the context of their child's cancer treatment. Parent reports of PSE showed moderately strong positive relationships with urine cotinine levels which were stronger for reports provided by parents who smoked compared with nonsmoking parents.
Parent reports of PSE were validated by positive and significant associations with urine cotinine. Reports provided in the context of possible verification by biomarker assays can provide sufficiently accurate estimates of PSE to serve as outcome measures for clinical research and clinical care in a pediatric cancer setting.
PMCID: PMC2762928  PMID: 19696308
24.  Simultaneous measurement of urinary total nicotine and cotinine as biomarkers of active and passive smoking among Japanese individuals 
Measuring urinary cotinine is a popular and established method of biologically monitoring exposure to tobacco smoke. However, the lower detection limit of cotinine often impedes the evaluation of passive (second-hand) smoking and this, together with unconverted nicotine, does not reflect actual levels of exposure. Furthermore, a portion of the Japanese population might have decreased ability to metabolize nicotine. The present study was therefore carried out to validate the simultaneous analysis of total concentrations of free nicotine and cotinine and their glucuronides to determine actual levels of voluntary and involuntary exposure to cigarette smoke.
Urine samples from 118 Japanese smokers and 117 non-smokers were analyzed using gas chromatography–mass spectrometry. Voluntary and involuntary smoking status was self-reported and workplace smoking restrictions were objectively evaluated.
The integrated sum of all concentrations showed 2.2- and 2.4-fold higher total levels (free and glucuronide) of nicotine and cotinine relative to the free levels. Median (quartiles) of total nicotine and cotinine were 1635 (2222) and 3948 (3512) ng/mL in smokers, and 3.5 (5.3) and 2.8 (4.2) ng/mL in non-smokers. Concentrations of urinary nicotine were higher than those of cotinine in 21 % of smokers and in 54 % of non-smokers. Nicotine and cotinine levels were significantly associated with a smoking habit, as well as being significantly associated with the workplace and home environments of non-smokers.
The present method can monitor voluntary and involuntary exposure to tobacco smoke. Measuring total urinary nicotine levels might be useful for analyzing exposure to cigarette smoke among non-smokers.
PMCID: PMC3650179  PMID: 23011941
Tobacco smoke; Nicotine; Cotinine; GC–MS; Japanese
25.  Second Hand Smoke is Associated with Sensorineural Hearing Loss in Adolescents 
Second hand smoke (SHS) exposure, either in utero or during childhood, has been linked to low birth weight, sudden infant death syndrome, upper and lower respiratory infections, increased asthma severity, dental caries, behavioral problems, ADHD, emotional problems, and otitis media (OM).To our knowledge, no previous study has examined the possible association between SHS and sensorineural hearing loss (SNHL) in adolescent.
The study objectives were to (1) exam risk factors for sensorial hearing loss in different age, gender, race, and income/poverty groups among adolescents (age 12 to 19) in the U.S. using data from most recent waves of NHANES (2005–2006); and, (2) evaluate the independent association between SHS and sensorial hearing loss among adolescents.
Cross-sectional analysis of nationally representative data.
National Health and Nutrition Examination Survey 2005–2006.
1533 non-institutionalized adolescents age 12–19 who underwent audiometric testing, had serum cotinine levels available, and were not actively smoking.
The serum cotinine levels, presence of household smokers, and self-report of smoking were used to determine SHS exposure and active smoking. Low frequency hearing loss was defined as the average pure tone level greater than 15 dB for 500, 1000, and 2000 Hz; high frequency hearing loss was defined as the average pure tone level greater than 15 dB for 3, 4, 6, and 8 kHz.
SHS exposure was associated with elevated pure tone hearing levels at 2, 3 and 4 kHz. and 1.8 fold increased risk of unilateral low frequency SNHL in multivariate analyses (95% C.I.: 1.08-3.46). The incidence of SNHL was directly related to level of SHS exposure as reflected in serum cotinine levels. In addition, nearly 82% of adolescents with low frequency SNHL did not report hearing difficulty.
SHS is associated with increased incidence of LFSNHL that is directly related to level of exposure. The affected individuals are unaware of the hearing loss. Therefore, early identification and prevention of hearing loss related to SHS may produce significant public health benefits.
PMCID: PMC4117391  PMID: 21768409
Second hand smoke (SHS); low frequency sensorineural hearing loss; high frequency sensorineural hearing loss; serum cotinine levels

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