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.
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.
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.
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.
Despite some misclassification, questionnaire reports are an inexpensive and valid estimate of residential ETS exposure among preschool and school children.
environmental tobacco smoke; questionnaire; air nicotine; urinary cotinine
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.
Secondhand smoke is a major cause of morbidity and mortality. It has been associated with serious health problems in both children and adults. Efforts to reduce exposure to secondhand smoke in Nebraska have included programs to prevent tobacco use among young people and campaigns for smoke-free workplaces and homes. Despite these interventions, young people continue to be exposed to secondhand smoke at an unacceptably high rate. The objective of this study was to examine the extent to which Nebraska public middle and high school students were exposed to secondhand smoke in 2002 and 2006, to evaluate factors associated with this exposure, and to propose interventions.
The Nebraska Youth Tobacco Survey was administered in 2002 and 2006 to a representative sample of students from public middle and high schools. All students who chose to participate completed an anonymous, self-administered survey that included questions on demographics, tobacco use, tobacco-related knowledge and attitudes, and exposure to secondhand smoke. Data were weighted to account for nonresponses at both student and school levels and to ensure generalizability of the estimates for public school students in Nebraska according to their grade, sex, and race/ethnicity. This study analyzed a subset of responses on secondhand smoke exposure, which was defined as being in a room or vehicle during the previous 7 days with someone who was smoking cigarettes.
Secondhand smoke exposure in a room, a vehicle, or both declined significantly among all students from 2002 (69.0%) to 2006 (61.3%). In both 2002 and 2006, students were significantly more likely to be exposed to secondhand smoke in a room than in a vehicle (64.4% vs 48.2% in 2002 and 56.9% vs 40.2% in 2006). Among racial and ethnic groups, only white students experienced a significant decline in exposure from 2002 (70.0%) to 2006 (61.4%). Girls were significantly more likely to be exposed to secondhand smoke in 2006 than were boys, and only boys experienced a significant overall decline in exposure from 2002 (69.3%) to 2006 (57.7%). Smoking behaviors and attitudes continued to influence secondhand smoke exposure from 2002 to 2006, although students experienced significant declines whether they were smokers or nonsmokers, and whether they lived with a smoker or not. Those with close friends who smoked and those who did not perceive secondhand smoke as harmful, however, did not benefit.
These data indicate reductions in exposure to secondhand smoke among Nebraska's middle and high school students, but exposure remains a problem, particularly in rooms. Adoption of a comprehensive statewide smoke-free policy will contribute to significantly reduced exposure to secondhand smoke among young people in public places, but other measures to address exposure in the home and private vehicles are needed or should be strengthened. These include physician counseling based on behavioral change theory to encourage cessation and home-based no-smoking rules, in addition to interventions that target minorities, who are disproportionately affected by secondhand smoke exposure. Evaluation of existing measures, such as programs to prevent tobacco use among young people and campaigns to collect pledges for smoke-free homes, will be required to determine their effectiveness in reducing exposure to secondhand smoke among youth in Nebraska.
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.
behavior; childhood asthma; environmental smoke exposure; inner-city
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
Purpose. Adult active smoking is a risk factor for dry eye. We hypothesize that passive smoking in children can also produce the same effects. Methods. We included 112 school children presenting with eye discomfort. Assessment of eye dryness and its severity levels depending on symptoms of dry eye, visual symptoms, tear breakup time (TBUT), Schirmer-1 test, and corneal fluorescein staining were done for all of them. Exposure to cigarette smoking was assessed by history-taking and urinary cotinine levels. Results. Dry eye was found in 80/112 children. Passive smoking was documented in 76/112 children. Number of cigarettes to which the child was exposed per day and the duration of exposure to passive smoking were significantly higher in children with dry eye compared to those without. Urinary cotinine, and cotinine/creatinine ratio (CCR) was significantly higher in children with dry eye compared to those without dry eye. Multiregression analysis showed that the most important determinants of dry eye were CCR and number of cigarettes/day. Conclusion. Passive smoking represents a significant risk factor of dry eye in children comparable to that shown with active adult smoking. Male children are more prone to this effect.
Quantitation of urinary cotinine, a major metabolite of nicotine, by an enzyme-linked immunosorbent assay (ELISA), was performed in parallel with questionnaires containing items on smoking status, such as active and/or passive smokers, the number of cigarettes smoked, and the presence or absence of active smokers in the surroundings in a department store (517 employees). The cotinine values corrected by creatinine (cotinine-creatinine ratios, CCRs) approximately conformed to the extent of self-recognition of their exposure status to tobacco-smoke, and were low in the order of active smokers, passive smokers and non-smokers who felt they were not exposed to tobacco-smoke. Occupational differences of the CCRs were not found in the employees.
In the active smokers, the CCRs were increasing according to the number of cigarettes per day they smoked, and the values were nearly proportional to nicotine contents of cigarette in the moderate smokers who smoked 11-20 cigarettes per day. The CCRs of males were higher than those of females in the active smokers, which also agreed well with the numbers of cigarettes they smoked per day. In the passive smokers, the CCRs were remarkably and significantly higher in subjects who felt they were exposed to tobacco-smoke both in their workplaces and homes.
Urinary CCRs measured by ELISA are thus found to be a reliable and excellent objective indicator of both active and passive exposure-status to tobacco-smoke.
Urinary cotinine; Exposure status to tobacco-smoke; Relationship between subjective recognition and cotinine values; ELISA; Department store employees
This article reviews data from experimental and epidemiologic studies on passive smoking and makes 12 recommendations for further study. The physicochemical nature of passive smoke, the smoke inhaled by nonsmokers, differs significantly from the mainstream smoke inhaled by the active smoker. At present, measurement of urinary cotinine appears to be the best method of assessing exposures to passive smoking. Data indicate that the greater number of lung cancers in nonsmoking women is probably related to environmental tobacco smoke. Exposures in utero and very early in life to passive smoking may be important in relationship to the subsequent development of cancer and need further consideration. The short-term effects of environmental tobacco smoke on the cardiovascular system, especially among high-risk individuals, may be of greater concern than that of cancer and requires further study. Further study of increased risks of lung cancers in relation to environmental tobacco smoke exposure requires larger collaborative studies to identify lung cancer cases among nonsmokers, better delineation of pathology, and more careful selection of controls. In addition, studies of epithelial cells or specific cytology should be undertaken to determine evidence of cellular changes in relation to environmental tobacco smoke exposure. Animal inhalation studies with passive smoke should be initiated with respect to transplacental carcinogenesis, the relationship of sidestream smoke exposure with lung cancer, the induction of tumors in the respiratory tract and other organs, and the differences in the physicochemical natures of sidestream and mainstream smoke.
Passive exposure to tobacco smoke significantly contributes to morbidity and mortality in children. Children, in particular, seem to be the most susceptible population to the harmful effects of environmental tobacco smoke (ETS). Paternal smoking inside the home leads to significant maternal and fetal exposure to ETS and may subsequently affect fetal health. ETS has been associated with adverse effects on pediatric health, including preterm birth, intrauterine growth retardation, perinatal mortality, respiratory illness, neurobehavioral problems, and decreased performance in school. A valid estimation of the risks associated with tobacco exposure depends on accurate measurement. Nicotine and its major metabolite, cotinine, are commonly used as smoking biomarkers, and their levels can be determined in various biological specimens such as blood, saliva, and urine. Recently, hair analysis was found to be a convenient, noninvasive technique for detecting the presence of nicotine exposure. Because nicotine/cotinine accumulates in hair during hair growth, it is a unique measure of long-term, cumulative exposure to tobacco smoke. Although smoking ban policies result in considerable reductions in ETS exposure, children are still exposed significantly to tobacco smoke not only in their homes but also in schools, restaurants, child-care settings, cars, buses, and other public places. Therefore, more effective strategies and public policies to protect preschool children from ETS should be consolidated.
Tobacco smoke pollution; Nicotine; Cotinine; Child; Hair
Four metrics were used to assess exposure to environmental tobacco smoke (ETS) for a probability sample (n = 152) of elementary school-age children in two economically disadvantaged neighborhoods: a) caregiver responses to a baseline questionnaire (BQ) about smoking status and behavior; b) 48-hr time-activity (T-A) data on location and time spent by children in the presence of tobacco smoke; c) total urinary cotinine as a marker for nicotine uptake; and d) urinary NNAL [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol] + NNAL-Gluc [4-(methylnitrosamino)-1- (3-pyridyl)-1-(O-beta-D-glucopyranuronosyl)butane] as a marker for uptake of the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Consistent differences in ETS exposure by ethnicity and race were observed. Although data were insufficient to determine differences for NNAL + NNAL-Gluc, BQ responses, T-A data, and cotinine levels all indicated that average ETS exposure was highest for African-American children, moderately high for those designated "other" (white, Southeast Asian, Native American), moderately low for Hispanic children, and lowest for Somali immigrant children. For example, in February 2000, mean cotinine levels were 14.1 ng/mL for African Americans, 12.2 ng/mL for other, 4.8 ng/mL for Hispanics, and 4.4 ng/mL for Somalis. The BQ and T-A data together were reasonably good predictors of total cotinine levels (adjusted r2 = 0.69), and based on limited data, measured total cotinine values were a relatively good predictor of NNAL + NNAL-Gluc (adjusted r2 = 0.73). The results suggest that when children are exposed to ETS primarily in their homes, questionnaires and T-A logs might be effective screening tools for identifying those likely to experience higher uptake of nicotine.
There has been an increased trend among school children to start smoking early. Majority of the smokers began smoking before 18 years of old. School programmes design to prevent tobacco use becomes one of the most effective strategies available to reduce smoking. Before initiating this school programme, a pilot study is needed to know the KAP towards smoking among school children in this community.
A school based study was conducted in a rural area involving 2 clusters samples involving 8 years old and 13 years old children representing samples of lower and secondary school student. The school children were asked to complete a self-administrated questionnaire that includes question concerning KAP about tobacco smoking. A total score for the questionnaire primary and the secondary school is rated separately for knowledge (0–14), (22–47) attitude (0–5), (18–84) practice (0–8), (8–22) respectively.
A total of 187 primary school student and 174 secondary school student participated in the study. They are mainly Malay students (95%) and only 30% of the fathers are working in government sector. The score of primary school student on knowledge (Mean 11.0, SD 1.8), attitude (Mean 3.7, SD 4.0) and practice (Mean 6.7, SD 8.0). The score of secondary school student on knowledge (Mean 41.5, SD 4.7), attitude (Mean 63.8, SD 8.0) and practice (Mean 18.5, SD 2.1).
Finding suggests that there are still a proportion of children who have poor knowledge, attitudes and bad practices of smoking. This demonstrates that school based preventive education is still needed to increase the awareness and also prevention of smoking among schoolchildren.
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.
environmental tobacco smoke (ETS) during childhood and in utero
exposure to maternal smoking are associated with adverse effects on
lung growth and development.
METHODS—A study was
undertaken of the associations between maternal smoking during
pregnancy, exposure to ETS, and pulmonary function in 3357 school
children residing in 12 Southern California communities. Current and
past exposure to household ETS and exposure to maternal smoking in
utero were assessed by a self-administered questionnaire completed by
parents of 4th, 7th, and 10th grade students in 1993.Standard linear
regression techniques were used to estimate the effects of in utero and
ETS exposure on lung function, adjusting for age, sex, race, Hispanic
ethnicity, height, weight, asthma, personal smoking, and selected
exposure to maternal smoking was associated with reduced peak
expiratory flow rate (PEFR) (-3.0%, 95% CI -4.4 to -1.4), mean mid
expiratory flow (MMEF) (-4.6%, 95% CI -7.0 to -2.3), and forced
expiratory flow (FEF75) (-6.2%, 95% CI -9.1 to -3.1),
but not forced expiratory volume in one second (FEV1). Adjusting for household ETS exposure did not substantially change these
estimates. The reductions in flows associated with in utero exposure
did not significantly vary with sex, race, grade, income, parental
education, or personal smoking. Exposure to two or more current
household smokers was associated with reduced MMEF (-4.1%, 95% CI
-7.6 to -0.4) and FEF75 (-4.4%, 95% CI -9.0 to 0.4).
Current or past maternal smoking was associated with reductions in PEFR and MMEF; however, after adjustment for in utero exposure, deficits in
MMEF and FEF75 associated with all measurements of ETS were substantially reduced and were not statistically significant.
exposure to maternal smoking is independently associated with decreased
lung function in children of school age, especially for small airway flows.
In Western countries, active maternal smoking during pregnancy is recognized as the most important preventable risk factor for adverse birth outcomes. However, the effect of passive maternal smoking is less clear and has not been extensively studied. In Japan, there has been only one epidemiological study which examined the effects of active smoking during early pregnancy on birth outcomes although the effects of passive smoking were not assessed.
Study subjects were 1565 mothers with singleton pregnancies and the babies born from these pregnancies. Data on active maternal smoking status in the first, second, and third trimesters and maternal environmental tobacco smoke (ETS) exposure at home and work were collected with self-administered questionnaires.
Compared with children born to mothers who had never smoked during pregnancy, children born to mothers who had smoked throughout their pregnancy had a significantly increased risk of small-for-gestational-age (SGA) (adjusted odd ratio [OR] = 2.87; 95% confidence interval: 1.11 − 6.56). However, active maternal smoking only in the first trimester and active maternal smoking in the second and/or third trimesters but not throughout pregnancy were not significantly associated with SGA. With regard to the risk of preterm birth, the adjusted ORs for the above-mentioned three categories were not significant; however, the positive linear trend was significant (P for trend = 0.048). No significant association was found between active maternal smoking during pregnancy and the risk of low birth weight. There was a significant inverse relationship between active maternal smoking during pregnancy and birth weight; newborns of mothers who had smoked throughout pregnancy had an adjusted mean birth weight reduction of 169.6 g. When classifying babies by gender, a significant positive association between active maternal smoking throughout pregnancy and the risk of SGA was found only in male newborns, however, the interaction was not significant. Maternal ETS exposure at home or work was not significantly associated with any birth outcomes.
This is the first study in Japan to show that active maternal smoking throughout pregnancy, but not during the first trimester, is significantly associated with an increased risk of SGA and a decrease in birth weight. Thus, women who smoke should quit smoking as soon as possible after conception.
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.
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.
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.
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.
Exposure to environmental tobacco smoke (ETS) is one of the major factors of predisposing children to develop several hazardous health problems. We decided to investigate the association between nicotinine, one of the nicotine metabolites and esophagitis in children with gastroesophageal reflux disease (GERD).
In a case control study 46 children suffering from esophagitis referred to endoscopy ward were recruited. The control group consisted of 45 healthy children. Urine samples were collected and urinary cotinine level (UCL) measured.
The mean age of esophagitis and control groups were 5.11±2.93 and 6.72±2.8 respectively. Sixty children were passive smokers; 31 of them had non-smoker parents. In control group, 32 (71.1%) children and in esophagitis group 29 (63%) children had non-smoker parents. The mean value of UCL in patients suffering from esophagitis was significantly higher than those in normal group (P=0.04, 24.98±6.4 ng/ml vs. 15.16 ± 3.9 ng/ml). Considering 50ng/ml as a cutoff point for UCL, it was significantly higher in passive smoker group than in non smoker group (P=0.02). The mean cotinine level differed significantly in esophagitis and control group.
Our results indicate the increased risk of developing esophagitis in children with ETS exposure.
Cotinine; Children; Esophagitis; Passive Smoking
Exposure to household Secondhand Smoke (SHS) poses a major health threat to children after an indoor smoking ban was imposed in Taiwan. This study aimed to assess the household SHS exposure in elementary school children in southern Taiwan and the factors associated with their avoidance of SHS exposure before and after the implementation of Taiwan's new Tobacco Hazards Prevention Act in 2009.
In this cross-sectional school-based study, data on household SHS exposure, avoidance of SHS and related variables was obtained from the 2008 and 2009 Control of School-aged Children Smoking Study Survey. A random sample of 52 elementary schools was included. A total of 4450 3-6 graders (aged 8-13) completed the questionnaire. Regression models analyzed factors of children's self-confidence to avoid household SHS exposure.
Over 50% of children were found to have lived with a family member who smoked in front of them after the new law enacted, and 35% of them were exposed to household SHS more than 4 days a week. Having a positive attitude toward smoking (β = -0.05 to -0.06) and high household SHS exposure (β = -0.34 to -0.47) were significantly associated with a lower avoidance of SHS exposure. Comparing to girls, boys had lower scores in their knowledge of tobacco hazards; and this factor was significantly related to their SHS avoidance (β = 0.13-0.14).
The intervention program should enhance school children do actively avoid exposure to SHS in home settings, and more importantly, provide tobacco hazard knowledge to male students to avoid exposure to household SHS for themselves. The results also provide further evidence that Tobacco Hazards Prevention Act should perhaps be extended to the family environment in order to protect children from the hazards of household SHS exposure.
Children; Secondhand smoke
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.
To test the efficacy of behavioural counselling for smoking mothers in reducing young children's exposure to environmental tobacco smoke.
Randomised double blind controlled trial.
Low income homes in San Diego county, California.
108 ethnically diverse mothers who exposed their children (aged <4 years) to tobacco smoke in the home.
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.
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.
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.
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.
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.
Environmental tobacco smoke; asthma; children; primary care; screening
The National Social Life, Health, and Aging Project (NSHAP) assessed smoking behaviors and alcohol use as factors directly related to physical health, well-being, and social relationships. We describe self-report measures of tobacco and alcohol use, as well as an established biological marker of tobacco exposure, cotinine, collected in Wave 1 of NSHAP.
We compare smoking behaviors and alcohol use by gender and age group. We report on derived measures of alcohol consumption and tobacco exposure widely used in medical and substance use literature, compare current and past users, and describe associations between self-reported smoking status and cotinine.
Men are more likely than women to report alcohol use, potential problem drinking, and ever smoking. Alcohol use and smoking are lower among older age groups. Although current smoking is less prevalent than in the general U.S. adult population, 50% of current and 29% of past smokers have lifetime exposure of 40 pack-years or more. Cotinine is directly related to number of cigarettes per day but with considerable unexplained variation. Cotinine levels contradict self-report in fewer than 4% of nonsmokers.
NSHAP provides data useful for investigation of smoking and alcohol use and their association with health and social factors.
Smoking behavior; Tobacco; Alcoholuse; Cotinine; Older adult
Cigarette tobacco smoke is a potent environmental contaminant known to adversely affect health including fertility and pregnancy.
To examine the associations between second-hand cigarette tobacco-smoke exposure, or active smoking and serum concentrations of steroid hormones using tandem mass spectrometry.
Healthy women (18–45 y) from the general community in the Metropolitan Washington, DC were recruited at the follicular stage of their menstrual cycle. Participants were assigned to one of three study groups: active smokers (N= 107), passive smokers (N= 86), or non-smokers (N= 100). Classifications were based on a combination of self-reporting and serum cotinine concentrations.
Serum androgens, estrogens, progestins, androstenedione, aldosterone, cortisol, corticosterone, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), 11-deoxycortisol and 25-hydroxy-vitamin D3 (25-OHVitD3) and cotinine were measured by isotope dilution tandem mass spectrometry (LC/MS/MS) (API-5000). Kruskal–Wallis tests were used to assess median differences among the three groups, with Dunn’s multiple comparison test for post hoc analysis.
Serum estrone, estradiol, and estriol concentrations were lower in active and passive smokers than in non-smokers. The three study groups differed significantly in serum concentrations of 16-OHE1, aldosterone and 25-OHVitD3, as well as in the ratios of many of the steroids. Pair-wise comparison of the groups demonstrated significant differences in hormone concentrations between (i) smokers and nonsmokers for aldosterone: (ii) passive smokers and non-smokers for aldosterone, progesterone and estriol. Moreover, for smokers and passive smokers, there were no significant differences in these hormone concentrations.
Smoke exposure was associated with lower than normal median steroid hormone concentrations. These processes may be instrumental in explaining some adverse effects of tobacco smoke on female health and fertility.
Environmental toxicants; Cigarette tobacco smoke exposure; Mineralocorticoids; Sex hormones; Stress hormones; Tandem mass spectrometry
Despite knowledge of the adverse health effects of passive smoking, children are still being exposed. Children's nurses play an important role in tobacco preventive work through dialogue with parents aimed at identifying how children can be protected from environmental tobacco smoke (ETS) exposure. The study describes the experiences of Child Health Care (CHC) nurses when using the validated instrument SiCET (Smoking in Children's Environment Test) in dialogue with parents.
In an intervention in CHC centres in south-eastern Sweden nurses were invited to use the SiCET. Eighteen nurses participated in focus group interviews. Transcripts were reviewed and their contents were coded into categories by three investigators using the method described for focus groups interviews.
The SiCET was used in dialogue with parents in tobacco preventive work and resulted in focused discussions on smoking and support for behavioural changes among parents. The instrument had both strengths and limitations. The nurses experienced that the SiCET facilitated dialogue with parents and gave a comprehensive view of the child's ETS exposure. This gave nurses the possibility of taking on a supportive role by offering parents long-term help in protecting their child from ETS exposure and in considering smoking cessation.
Our findings indicate that the SiCET supports nurses in their dialogue with parents on children's ETS exposure at CHC. There is a need for more clinical use and evaluation of the SiCET to determine its usefulness in clinical practice under varying circumstances.
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.
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.
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.
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.