Assessment of environmental tobacco smoke exposure in children with asthmatic symptoms by questionnaire and cotinine concentrations in plasma, saliva, and urine

doi:10.1016/S0895-4356(99)00212-7

Journal of Clinical Epidemiology

Volume 53, Issue 7, July 2000, Pages 715-721

https://doi.org/10.1016/S0895-4356(99)00212-7 Get rights and content

Abstract

To validate a detailed questionnaire for assessment of environmental tobacco smoke (ETS) exposure by the biomarker cotinine in various media, a population-based study in the urban area of Malmö, Sweden was performed in children aged 8–13 years with and without asthmatic symptoms. There were strong correlations between urinary and saliva cotinine concentrations and also, though to a lesser extent, between these media and plasma. Even a detailed questionnaire gave only a rough picture of the ETS exposure, as indicated by the biomarkers. In a multivariate model, the most significant questionnaire-derived predictor of the cotinine levels was the maternal smoking habits; other questionnaire variables gave only a minimal explained variance. Children with a history of asthmatic symptoms had statistically significantly lower median cotinine levels in urine and saliva compared to referent children, most likely because of the antismoking information to their parents. This should be considered in epidemiological studies of ETS risks.

Introduction

Increased prevalence of maternal smoking as well as levels of the nicotine metabolite cotinine in urine was found in consecutive new cases of severe childhood asthma, compared to referent children, indicating that ETS exposure is a risk factor [1]. However, the relationship between ETS exposure and asthma in different studies has not been consistent [2]. This could be due to different study designs. For example, we know little about the smoking behavior of parents of children with asthma after the onset of symptoms.

Further, the exposure assessment in most investigations are based on self-reports [3]; hence, they could be biased [4]. For example, there is a possibility of deceptive underreporting of exposure in children by smoking parents. Further, several factors are of importance for the exposure, such as the amount of tobacco smoked, room size, ventilation, and proximity to smokers. Also, exposure may occur outside the home, for example, in cars [5]. It may be difficult to estimate these factors in a questionnaire. Biomarkers of ETS exposure may be used for validation of ETS questionnaire.

We found that cotinine, determined in saliva [6] and in urine [7], were useful as biomarkers of ETS exposure. Plasma levels have also been used [8]. However, the relationship between concentrations of cotinine in plasma, saliva, and urine and ETS exposure has not been investigated.

Therefore, in the present study, the relationships between information on ETS exposure in a detailed ETS questionnaire, on the one hand, and cotinine concentrations in plasma, saliva, and urine on the other were investigated in children who suffered asthma and in referents.

Section snippets

Subjects

Out of a population sample of urban children (N = 2684) living in southern part of Sweden [9], who had answered a questionnaire on airways symptoms and exposures, all 137 children with asthmatic symptoms living in Malmö, Sweden were, during the winter (November–January), invited to a medical examination, including sampling of plasma, saliva, and urine. However, 52 children [mean age: 10.3 (8–13) years, 31 (60%) were boys] did not participate for different reasons, including acute illness. There

Cotinine and questionnaire data on ETS exposure

The median levels of cotinine in children were low (plasma 0.60 μg/l; saliva 0.30 μg/l; urine 0.53 μg/g crea) in homes who reported no indoor smoking, and increased considerably with smoking in the home by parents or others (Table 1). If both parents (with or without other smokers) reported that they were currently smoking in their home, the median cotinine concentrations in children were about 3, 9, and 17 times higher for plasma, saliva, and urine, respectively, compared to homes with no

Discussion

The most interesting findings of the present study were: a detailed questionnaire on ETS exposure only explained a limited fraction of the variance in the biomarkers of ETS exposure; maternal smoking was most important; plasma, saliva, and urinary cotinine concentrations in children were closely associated, but with a variation; and children with a history of asthmatic symptoms had lower current ETS exposure than referent children, in spite of the fact that the latter were few.

Selection biases

Acknowledgements

This study has been supported by grants from the Swedish Association against Asthma and Allergy, the National Swedish Environment Protection Agency, the Swedish Work Environment Fund, the Medical Faculty at Lund University and the European Commission (Biomed 1). Thanks to Ms. Inger Bensryd, RN, Anita Nilsson, RN, Ms. Kerstin Diab, RN, and Ms. Pia Aprea.

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Third, caregiver report of childhood TSE varies across provider types (i.e. nurses, residents and ED providers) when compared to biomarkers of TSE (Kruse and Rigotti, 2014). Although some studies have confirmed TSE self-report with biochemical validation of TSE using cotinine (Irvine et al., 1997; Willers et al., 2000), widespread use of biochemical validation in the PED is impractical. Thus, changing assessment procedures, such as using structured caregiver interviews which are sensitive for assessing TSE during pediatric visits (Kruse and Rigotti, 2014), may offer improved findings in the PED.
Tobacco smoke exposure causes significant childhood morbidity and is associated with a multitude of conditions. National organizations recommend tobacco smoke exposure screening at all pediatric clinical encounters. Data regarding tobacco smoke exposure screening in the pediatric emergency department is sparse, although children with tobacco smoke exposure-associated conditions commonly present to this setting. We aimed to determine the frequency and outcome of tobacco smoke exposure screening in the pediatric emergency department, and assess associated sociodemographic/clinical characteristics.
This retrospective review included pediatric patients presenting to a large pediatric emergency department in Cincinnati, Ohio between 2012 and 2013. Variables extracted included: age, sex, race/ethnicity, insurance, child's tobacco smoke exposure status, triage acuity, diagnosis, and disposition. Regression analyses examined predictors of tobacco smoke exposure screening and tobacco smoke exposure status.
A total of 116,084 children were included in the analysis. Mean child age was 6.20 years (SD ± 5.6); 52% were male. Nearly half of the children in the study did not undergo tobacco smoke screening; only 60% of children with tobacco smoke exposure-related illnesses were screened. Predictors of tobacco smoke exposure screening were: younger age, male, African American, non-commercial insurance, high acuity, tobacco smoke exposure-related diagnoses and non-intensive care admission. Of children screened for tobacco smoke exposure, 28% were positive. Children more likely to screen positive were non-Hispanic, had non-commercial insurance, and had tobacco smoke exposure-related diagnoses. NonAfrican American children triaged as low acuity were more likely to have tobacco smoke exposure, yet were less likely to be screened.
Despite national recommendations, current tobacco smoke exposure screening rates are low and fail to identify at-risk children. Pediatric emergency department visits for tobacco smoke exposure-associated conditions are common, thus further research is needed to develop and assess standardized tobacco smoke exposure screening tools/interventions in this setting.
Effects of cigarette smoking and nicotine metabolite ratio on leukocyte telomere length.
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Several approaches have been employed to study the effect of tobacco smoke in LTL (Li et al., 2011; Morla et al., 2006; Savale et al., 2009). Studies have estimated exposure with the reported number of CPD (Kannel, 1981), which has accuracy limitations (Oddoze et al., 1999; Willers et al., 2000). Although asking the number of CPD is actually regarded as the standard measure of exposure, may not be a good indicator.
Studies of the effects of smoking on leukocyte telomere length (LTL) using cigarettes smoked per day or pack years smoked (PYS) present limitations. Reported high levels of smoking may not increase toxin exposure levels proportionally. Nicotine metabolism ratio (NMR) predicts total cigarette puff volume and overall exposure based on total N-nitrosamines, is highly reproducible and independent of time since the last cigarette. We hypothesized that smokers with higher NMRs will exhibit increased total puff volume, reflecting efforts to extract more nicotine from their cigarettes and increasing toxin exposure. In addition, higher levels of smoking could cause a gross damage in LTL. The urinary cotinine, 3-OH cotinine and nicotine levels of 147 smokers were analyzed using a LC/MS system Triple-Q6410. LTL and CYP2A6 genotype was determined by PCR in blood samples. We found a significant association between NMR and CYP2A6 genotype. Reduction in LTL was seen in relation to accumulated tobacco consumption and years smoking when we adjusted for age and gender. However, there were no significant differences between NMR values and LTL. In our study the higher exposure was associated with lower number of PYS. Smokers with reduced cigarette consumption may exhibit compensatory smoking behavior that results in no reduced tobacco toxin exposure. Our results suggest that lifetime accumulated smoking exposure could cause a gross damage in LTL rather than NMR or PYS. Nevertheless, a combination of smoking topography (NMR) and consumption (PYS) measures may provide useful information about smoking effects on health outcomes.
Association of time-location patterns with urinary cotinine among asthmatic children under household environmental tobacco smoke exposure
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Environmental tobacco smoke (ETS) is a hazardous component of indoor air, and may increase the risk of respiratory diseases, atherosclerosis and otitis media in children. In this study, we explored the relationship between time inside the house, ETS exposure and urinary cotinine level, and also determined the association of time inside the house on asthma phenotypes when children exposed to ETS.
A total of 222 asthmatic children and 205 non-asthmatic controls were recruited in the Genetic and Biomarker study for Childhood Asthma (GBCA). Structured questionnaires and time–location pattern questionnaires were administered by face-to-face interview. Urinary cotinine was measured by liquid chromatography tandem mass spectrometry (LC/MS/MS). The level of household ETS exposure was assessed using the cotinine/creatinine ratio (CCR).
In general, urinary cotinine and CCR were higher in subjects exposed to household ETS than those who never had ETS at home. A significant positive relationship was found between average time inside the house and urinary CCR in asthmatic children with current ETS at home (β=0.278, p=0.02). After adjustment for age and gender, average time inside the house was positively related to severe wheeze in asthmatic children with household ETS within 1 month (OR: 1.26, 95%: 1.02–1.64).
Our study suggests that the major source of ETS exposure for children is due to longer period of exposures among children living with adult smokers at home. Home-smoking restrictions that effectively prevent children from being exposed to ETS would be worthwhile.
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To investigate parental smoking patterns and their association with wheezing in children.
We performed a case-control study that included 105 children between 6 and 23 months of age who were divided into two groups: cases (children with 3 previous episodes of wheezing) and controls (healthy children without wheezing). The children's exposure to cigarette smoking was estimated using a questionnaire completed by the mothers and by the children's urinary cotinine levels.
Based on both the questionnaire results and cotinine levels, exposure to cigarette smoking was higher in the households of cases in which the incidence of maternal smoking was significantly higher than that of paternal smoking. Children in this group were more affected by maternal smoking and by the total number of cigarettes smoked inside the house. Additionally, the questionnaire results indicated that the risk of wheezing was dose dependent. The presence of allergic components, such as atopic dermatitis and siblings with allergic rhinitis and asthma, greatly increased the odds ratio when wheezing was associated with cotinine levels.
Children exposed to tobacco smoke have an increased risk of developing wheezing syndrome. This risk increases in association with the number of cigarettes smoked inside the house and the presence of other allergic components in the family.
The school-based preventive asthma care trial: Results of a pilot study
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In addition, we measured standard variables known to influence asthma outcomes, including demographic variables (race, sex, ethnicity, insurance, caregiver's age and education level), medical variables (allergy), and caregiver depression using the Kessler Psychological Distress scale.14 We also measured smoke exposure by caregiver interview15 and obtained salivary cotinine levels (at baseline and the final assessment) using a standardized technique.16,17 At the end of the school year, we administered a structured survey with Likert-scale questions to assess feasibility and acceptability of this program from caregivers, school nurses, and providers.
To test the feasibility and preliminary effectiveness of the School-Based Preventive Asthma Care Technology (SB-PACT) program, which includes directly observed therapy of preventive asthma medications in school facilitated by Web-based technology for systematic symptom screening, electronic report generation, and medication authorization from providers.
We conducted a pilot randomized trial of SB-PACT versus usual care with 100 children (aged 3-10 years) from 19 inner-city schools in Rochester, New York. Outcomes were assessed longitudinally by blinded interviewers. Analyses included bivariate statistics and linear regression models, adjusting for baseline symptoms.
There were data for 99 subjects for analysis. We screened all children using the Web-based system, and 44 of 49 treatment group children received directly observed therapy as authorized by their providers. Treatment group children received preventive medications 98% of the time they were in school. Over the school year, children in the treatment group experienced nearly 1 additional symptom-free day over 2 weeks versus the usual care group (11.33 vs 10.40, P = .13). Treatment children also experienced fewer nights with symptoms (1.68 vs 2.20, P = .02), days requiring rescue medications (1.66 vs 2.44, P = .01), and days absent from school due to asthma (0.37 vs 0.85, P = .03) compared with usual care. Further, treatment children had a greater decrease in exhaled nitric oxide (−9.62 vs −0.39, P = .03), suggesting reduction in airway inflammation.
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Original articlesAssessment of environmental tobacco smoke exposure in children with asthmatic symptoms by questionnaire and cotinine concentrations in plasma, saliva, and urine

Abstract

Introduction

Section snippets

Subjects

Cotinine and questionnaire data on ETS exposure

Discussion

Acknowledgements

J Chromatogr

Mutat Res

Environ Res

Addict Behav

Environ Res

Toxicol Lett

Lancet

Passive smoking and childhood asthma—urinary cotinine levels in children with asthma and referents

Allergy

Passive smoking as a risk factor for development of obstructive respiratory disease and allergic sensitization