The effects of low-level environmental tobacco smoke exposure on pulmonary function tests in preschool children with asthma

Objectives: Though parents of children with asthma smoke, they often avoid smoking in their homes or near their children, thus limiting exposure. It is not known if such low-level environmental tobacco smoke (ETS) results in measurable exposure or affects lung function. The objectives of this study were to measure urinary cotinine in preschool children with asthma, and to examine the relationship between low-level ETS exposure and pulmonary function tests (PFTs). Methods: Preschool children with asthma were enrolled. Parents completed questionnaires on ETS exposure and asthma control, urinary cotinine concentrations were measured and PFTs were compared between subjects with and without recent ETS exposure. Results: Forty one subjects were enrolled. All parents denied smoking in their home within the last 2 weeks, but 14 (34%) parents admitted to smoking outside their homes or away from their children. Fifteen (37%; 95%CI: 23–53) of the children had urinary cotinine levels ≥1?ng/ml, of which seven (17%; 95%CI: 8–32) had levels ≥5?ng/ml. FEV₁ and FEV_0.5 were lower in subjects with a urinary cotinine level ≥5?ng/ml as compared to those with levels <1?ng/ml or between 1 and 5?ng/ml; both at baseline and after inhalation of albuterol. Five of seven subjects with urinary cotinine levels ≥5?ng/ml had FEV_0.5 less than 65% of predicted values. There were no significant differences in IOS measures. Conclusions: Despite parental denial of smoking near their children, preschool children may be exposed to ETS. Such low-level ETS exposure may affect lung function, possibly in a dose-dependent manner.     

Salivary cotinine levels in children presenting with wheezing to an emergency department

We set out to evaluate salivary cotinine concentrations to judge tobacco smoke exposure among infants and children, and to examine the results in relation to age and wheezing. This was a case-control study of wheezing children (n = 165) and children without respiratory tract symptoms (n = 106) who were enrolled in the Pediatric Emergency Department at the University of Virginia. The age range of both wheezing and control patients was 2 months to 16 years. Questionnaires were combined with cotinine assays in saliva to evaluate exposure to environmental tobacco smoke (ETS) for each child. The prevalence of exposure to one or more smokers at home was high (68%); and 43% of the children enrolled were exposed to ETS from their mothers. According to the questionnaires, and after adjusting for age and race, a wheezing child in this study was more likely than a control to be exposed to at least one smoker at home (odds ratio = 1.9; 95% CI = 1.1-3.4). However, the odds of exposure to ETS from smoking mothers did not differ significantly between wheezing and control patients, and no significant association was found between the presence of wheezing and salivary cotinine levels. Among children exposed to ETS at home, cotinine levels were significantly higher in saliva from those under the age of two years, and from toddlers aged 2 and 3 years, compared to values from children over age 4 years. Moreover, the number of smokers in the home strongly influenced cotinine levels from children under age 4 years. In addition, higher cotinine levels were observed in saliva from children under age 2 years who were exposed to ETS from their mothers. Cotinine levels were similar and significantly correlated in paired samples of saliva and serum from children under 4 years of age (n = 54), (r = 0.92, P < 0.001). Based on information gathered from questionnaires, the results indicate that wheezing children were more likely than controls to be exposed to ETS at home. However, significant differences in ETS exposure between wheezing and control groups with respect to maternal smoke exposure or comparisons of salivary cotinine levels were not apparent. It was clear that determinations of salivary cotinine for monitoring the prevalence and intensity of household smoke exposure in this study were most valuable during the first 4 years of life.     

Passive smoking in asthmatic children: effect of a "smoke-free house" measured by urinary cotinine levels.

Environmental tobacco smoke (ETS) decreases pulmonary function and increases both airway reactivity and frequency of child asthma exacerbations. True exposure is related not only to parents smoking and to the number of cigarettes that they smoke, but also to involuntary smoking in public places. The aim of this study was to evaluate, by measuring urinary cotinine levels, the exposure to ETS in asthmatic children and the contribution of unapparent smoke exposure. Twenty asthmatic children (aged 7-12 years) were evaluated on the 1st day (TO) and after a week (T1) in a "smoke-free house." The mean level of urinary cotinine in children was 15.8 +/- 2.7 ng/mg of creatinine at TO and 4.2 +/- 0.6 ng/mg of creatinine at T1 (p < 0.0001). The urinary cotinine concentrations were higher in children living with smoking parents (21.8 +/- 3.4 ng/mg creatinine) compared with children not exposed to parental smoke (6.8 +/- 3.0 ng/mg creatinine; p = 0.017). The number of cigarettes smoked by parents correlates with the urinary cotinine levels (p = 0.005; r = 0.64). Urinary cotinine levels significantly decreased after the avoidance of ETS in children exposed to parental smoke (21.8 +/- 3.4 ng/mg at TO; 5.0 +/- 0.8 ng/mg at T1; p < 0.001) and also in children whose parents declared to be nonsmokers (6.8 +/- 1.2 ng/mg at TO; 3.0 +/- 0.8 ng/mg at T1; p = 0.006). Our data confirm the widespread indirect and undetected tobacco smoke exposure in children with chronic asthma and the relevance of an evaluation with an objective method of the exposure to second-hand smoke.     

Predictors of cotinine levels in US children: data from the Third National Health and Nutrition Examination Survey

STUDY OBJECTIVE: To determine what factors predict cotinine levels in US children. DESIGN: Cross-sectional study. SUBJECTS: Nationally representative sample of 5,653 US children, both with and without reported tobacco smoke exposure in their homes. METHODS: We stratified the children into those with reported passive smoke exposure at home and those without this exposure. We used regression models to predict the log of the cotinine level of the participants with the following independent covariates: age; race/ethnicity; number of rooms in the home; sex; parental education; family poverty index; family size; region; and, among children with reported passive smoke exposure, the number of cigarettes smoked in the home. RESULTS: Children exposed to passive smoke had a mean cotinine level of 1.66 ng/mL, and children not exposed to passive smoke had a mean level of 0.31 ng/mL. Among children with reported smoke exposure, non-Mexican-American race/ethnicity, young age, low number of rooms in the home, low parental education, and an increasing number of cigarettes smoked in the home were predictors of increased serum cotinine levels. Among children with no reported smoke exposure, significant predictors of increased cotinine levels included black race, young age, Midwest region of the United States, low number of rooms in the home, low parental education, large family size, and low family poverty index. CONCLUSION: While the reported number of cigarettes smoked in the home is the most important predictor of cotinine levels in children exposed to smoke and may provide an opportunity for clinical intervention, other demographic factors are important among children both with and without reported smoke exposure.     

Assessing smoking status in children, adolescents and adults: cotinine cut-points revisited

AIMS: To reassess saliva cotinine cut-points to discriminate smoking status. Cotinine cut-points that are in use were derived from relatively small samples of smokers and non-smokers 20 or more years ago. It is possible that optimal cut-points may have changed as prevalence and exposure to passive smoking have declined. DESIGN: Cross-sectional survey of the general population, with assessment of self-reported smoking and saliva cotinine. PARTICIPANTS: A total of 58 791 respondents aged 4 years and older in the Health Survey for England for the years 1996-2004 who provided valid saliva cotinine specimens. MEASURES: Saliva cotinine concentrations, demographic variables, self-reported smoking, presence or absence of smoking in the home, a composite index of social disadvantage derived from occupation, housing tenure and access to a car. FINDINGS: A cut-point of 12 ng/ml performed best overall, with specificity of 96.9% and sensitivity of 96.7% in discriminating confirmed cigarette smokers from never regular smokers. This cut-point also identified correctly 95.8% of children aged 8-15 years smoking six or more cigarettes a week. There was evidence of substantial misreport in claimed ex-smokers, especially adolescents (specificity 72.3%) and young adults aged 16-24 years (77.5%). Optimal cut-points varied by presence (18 ng/ml) or absence (5 ng/ml) of smoking in the home, and there was a gradient from 8 ng/ml to 18 ng/ml with increasing social disadvantage. CONCLUSIONS: The extent of non-smokers' exposure to other people's tobacco smoke is the principal factor driving optimal cotinine cut-points. A cut-point of 12 ng/ml can be recommended for general use across the whole age range, although different cut-points may be appropriate for population subgroups and in societies with differing levels of exposure to secondhand smoke.     

The role of air nicotine in explaining racial differences in cotinine among tobacco-exposed children

OBJECTIVE: African-American children have higher rates of tobacco-associated morbidity. Few studies have objectively measured racial differences in the exposure of children to tobacco smoke. The objective of this study was to test whether African-American children have higher levels of cotinine compared to white children while accounting for ambient measures of tobacco smoke. SETTING: Community-based sample of asthmatic children (n = 220) enrolled in an environmental tobacco smoke (ETS) reduction trial. PARTICIPANTS: A biracial sample (55% African American) of children with asthma aged 5 to 12 years who were routinely exposed to ETS. MEASUREMENTS: We measured cotinine levels in serum and hair samples at baseline, 6 months, and 12 months. We measured the level of ETS exposure over a 6-month period by placing air nicotine dosimeters in the homes of the children at baseline and at 6-month study visits. RESULTS: African-American children had significantly higher levels of cotinine at all time points in the study. At the 12-month visit, African-American children had higher levels of serum cotinine (1.39 mug/dL vs 0.80 mug/dL, p = 0.001) and hair cotinine (0.28 ng/mg vs 0.08 ng/mg, p < 0.0001) when compared with white children. In a repeated-measures analysis, African-American children had significantly higher levels of serum cotinine (beta = 0.28, p = 0.04) and hair cotinine (beta = 1.40, p < 0.0001) compared with white children. Air nicotine levels and housing volume were independently associated with higher levels of cotinine. CONCLUSIONS: Among children with asthma, African-American children have higher levels of serum and hair cotinine compared with white children.     

The relationship of salivary cotinine to respiratory symptoms, spirometry, and exercise-induced bronchospasm in seven-year-old children

The effects of passive tobacco smoke exposure upon respiratory symptoms and lung function were assessed in a cross-sectional survey of 770 children 7 yr of age, using cotinine as a quantitative biochemical marker of exposure. Salivary cotinine levels were strongly related to the number of smokers in the home, but three-quarters of children from nonsmoking households had detectable salivary cotinine, and 10% of this group were in the upper two-fifths of the distribution of measured tobacco smoke exposure. Smoking by persons other than members of the household may deserve greater attention in future studies of young children. After adjustment for housing tenure, most respiratory symptoms were unrelated to salivary cotinine, but a "tendency for colds to go to the chest" was twice as prevalent in the upper two-fifths as in the lower two-fifths of the cotinine distribution. No association was found between salivary cotinine and reports of wheeze or measured reduction in FEV1 after 6 min of free running. After adjustment for sex, height, test conditions, and housing tenure, all baseline spirometric indices except FVC were inversely associated with salivary cotinine. Only FEF75-85 and FEF75 were significantly reduced, the difference for each index between the top and bottom quintiles of the cotinine distribution being about 7%, equivalent to a reduction of 1.1% (95% CL, 0.1 to 2.1%) per doubling of cotinine concentration. These changes may be evidence of small airways damage, which could later progress to more severe respiratory impairment.     

Tobacco smoke exposure in children and adolescents with diabetes mellitus.

AIMS: To examine active and passive tobacco smoke exposure in children and adolescents attending a diabetic clinic. METHODS: Salivary cotinine concentrations were measured by gas chromatography and questionnaire data on the smoking habits of patients, families and friends were analysed as well as recording of glycosylated haemoglobin (HbA1c), body mass index (BMI) and social deprivation score. RESULTS: Salivary cotinine concentrations identified 7% of the patients as active smokers and 72% as passive smokers. The mean cotinine concentration in those with no identifiable source of exposure was 0.10 (95% confidence interval 0.05-0.14) ng/ml, 2.81 (2.24-3.38) ng/ml in the passive smoking group and 1003.69 (55.96-151.41) ng/ml in the active smokers. Cotinine concentrations in passive smokers increased with the number of sources of exposure. The mean cotinine concentration was also higher when the mother was the sole source compared to other sources. There was no statistically significant correlation to smoking exposure and HbA1c BMI and deprivation scores. CONCLUSION: Tobacco smoke exposure may pose serious health risks to children and adolescents with diabetes and additional public health measures are required to reduce overall exposure.     

Variability of measures of exposure to environmental tobacco smoke in the home

We assessed the variability of four markers of environmental tobacco smoke exposure in 10 homes with 20 nonsmoking and 11 smoking household members. We obtained exposure questionnaires, saliva and urine for cotinine, and air particle samples for respirable particles and nicotine on 10 sampling days: every other day over 10 days, and then 1 day every other week over 10 wk. The mean concentrations of respirable particles in the 10 homes ranged from 32.4 to 76.9 micrograms/m3, and concentrations of nicotine ranged from 0.6 to 6.9 micrograms/m3. Linear regression models that included indicator variables for self-reported exposure explained 9 and 6% of the variability of the respirable particle and the nicotine concentrations, respectively. The individual mean urinary cotinine levels standardized to creatinine concentration ranged from 3.9 to 55.8 ng/mg Cr, and for salivary cotinine the mean levels ranged from 0.9 to 4.3 ng/ml. Indicator variables for self-reported exposure explained 8 and 23% of the variability of the urinary and salivary cotinine levels, respectively. We conclude that because of the marked variability of these measures, multiple measurements are needed to establish a stable profile of exposure to environmental tobacco smoke in the home.     

Low-level environmental tobacco smoke exposure and inflammatory biomarkers in children with asthma

Objective: The effects of low-level environmental tobacco smoke (ETS) exposure, on asthma control, lung function and inflammatory biomarkers in children with asthma have not been well studied. The objective of the study was to assess ETS exposure in school-age children with asthma whose parents either deny smoking or only smoke outside the home, and to assess the impact of low-level ETS exposure on asthma control, spirometry and inflammatory biomarkers. Methods: Forty patients age 8–18 years with well-controlled, mild-to-moderate persistent asthma treated with either inhaled corticosteroids (ICS) or montelukast were enrolled. Subjects completed an age-appropriate Asthma Control Test and a smoke exposure questionnaire, and exhaled nitric oxide (FeNO), spirometry, urinary cotinine and leukotriene E₄ (LTE₄) were measured. ETS-exposed and unexposed groups were compared. Results: Only one parent reported smoking in the home, yet 28 (70%) subjects had urinary cotinine levels ≥1?ng/ml, suggesting ETS exposure. Seven subjects (18%) had FeNO levels >25parts per billion, six of whom were in the ETS-exposed group. In the ICS-treated subjects, but not in the montelukast-treated subjects, ETS exposure was associated with higher urinary LTE₄, p?=?0.04, but had no effect on asthma control, forced expiratory volume in 1?s or FeNO. Conclusions: A majority of school-age children with persistent asthma may be exposed to ETS, as measured by urinary cotinine, even if their parents insist they don’t smoke in the home. Urinary LTE₄ was higher in the ETS-exposed children treated with ICS, but not in children treated with montelukast.     

Pharmacokinetic Predisposition to Nicotine from Environmental Tobacco Smoke: A Risk Factor for Pediatric Asthma

During the last decade several studies have shown that children whose parents smoke have higher rates of asthma. Recently, hair concentrations of cotinine have been shown to reflect systemic exposure to this constituent of smoke in both children and adults. At the present time it is not known, however, why some children exposed to passive smoking have asthma while others, similarly exposed, do not. The present study aimed at verifying whether asthmatic children are different from nonasthmatic children exposed to similar degrees of passive smoking in the way their bodies handle nicotine, a constituent of cigarette smoke. Seventy-eight asthmatic children were compared to 86 control children, all attending a consulting pediatric clinic in Toronto. A questionnaire completed by the parents and children detailed the daily number of cigarettes the child was exposed to and the identity of the smokers. Clinical data were extracted from the patients' charts. Urinary (corrected for creatinine) and hair concentrations of cotinine were measured by radioimmunoassays. The asthmatic and control children were of similar age, gender, and ethnic distribution, parental education, and socioeconomic status. Parents of asthmatic children tended to report a lower daily number of cigarettes (7.4 ± 1.3/day vs. 11.2 ± 2.3/day, p = 0.14), and this report agreed with the trend of urinary cotinine (47.1 ± 9.1 ng/mg vs. 62.6 ±11.5 ng/mg, respectively). Conversely, children with asthma had on average twofold higher concentrations of cotinine in their hair (0.696 ± 0.742 ng/mg) than control children (0.386 ± 0.383) (p = 0.0001). In a similar manner, the hair.urine concentration ratio was significantly higher in children with asthma (0.028 ± 0.002) than in their controls (0.18 ± 0.003) (p = 0.0001). These results suggest that under exposure to similar amounts of nicotine, children with asthma have on average twofold higher systemic exposure to this constituent of cigarette smoke. These data suggest that out of all children passively exposed to environmental tobacco smoke, those who exhibit asthma have a higher systemic exposure to nicotine, possibly due to lower clearance rate. This is the first evidence of pharmacokinetic predisposition to environmental tobacco smoke as an etiological factor in pediatric asthma.     

Relationship between Exhaled Nitric Oxide and Exposure to Low-Level Environmental Tobacco Smoke in Children with Asthma on Inhaled Corticosteroids

Objectives. The relationship between exhaled nitric oxide (FeNO) and asthma severity or control is inconsistent. Active smoking lowers FeNO, but the relationship between passive smoking and FeNO is less clear. Children may be exposed to low-level environmental tobacco smoke (ETS) or thirdhand smoke, even if parents avoid smoking in the presence of their children. Our hypothesis was that FeNO is lower in children with asthma exposed to low-level ETS when compared with those who are not exposed. Methods. Children with stable asthma, 8-18 years of age, on low- or medium-dose inhaled corticosteroids (ICS) were enrolled. Spirometry, Asthma Control Questionnaire (ACQ), FeNO, exhaled breath condensate pH (EBC pH), and EBC ammonia were compared between children with and without ETS exposure as determined by urinary cotinine. Results. Thirty-three subjects were enrolled, of which 10 (30%) had urinary cotinine levels ≥1 ng/ml. There were no significant differences between the two groups in age, sex, BMI percentile, atopy status, FEV(1), EBC pH, or EBC ammonia. Median ACQ was 0.29 (IQR: 0.22-0.57) for those with cotinine levels <1 ng/ml and 0.64 (IQR: 0.57-1.1) for those with cotinine levels of ≥1 ng/ml, p = .02. Median FeNO (ppb) was 23.9 (IQR: 15.2-34.5) for unexposed subjects and 9.6 (IQR: 5.1-15.8) for exposed subjects, p = .008. Conclusions: Children with asthma on low to medium doses of ICS and recent low-level ETS exposure have lower FeNO levels when compared with non-ETS-exposed subjects. Exposure to low-level ETS or thirdhand smoke may be an important variable to consider when interpreting FeNO as a biomarker for airway inflammation.     

Changes in environmental tobacco smoke (ETS) exposure over a 20-year period: cross-sectional and longitudinal analyses

Aims   To examine long-term changes in environmental tobacco smoke (ETS) exposure in British men between 1978 and 2000, using serum cotinine.
Design   Prospective cohort: British Regional Heart Study.
Setting   General practices in 24 towns in England, Wales and Scotland.
Participants   Non-smoking men: 2125 studied at baseline [questionnaire (Q1): 1978–80, aged 40–59 years], 3046 studied 20 years later (Q20: 1998–2000, aged 60–79 years) and 1208 studied at both times. Non-smokers were men reporting no current smoking with cotinine < 15 ng/ml at Q1 and/or Q20.
Measurements   Serum cotinine to assess ETS exposure.
Findings   In cross-sectional analysis, geometric mean cotinine level declined from 1.36 ng/ml [95% confidence interval (CI): 1.31, 1.42] at Q1 to 0.19 ng/ml (95% CI: 0.18, 0.19) at Q20. The prevalence of cotinine levels ≤ 0.7 ng/ml [associated with low coronary heart disease (CHD) risk] rose from 27.1% at Q1 to 83.3% at Q20. Manual social class and northern region of residence were associated with higher mean cotinine levels both at Q1 and Q20; older age was associated with lower cotinine level at Q20 only. Among 1208 persistent non-smokers, cotinine fell by 1.47 ng/ml (95% CI: 1.37, 1.57), 86% decline. Absolute falls in cotinine were greater in manual occupational groups, in the Midlands and Scotland compared to southern England, although percentage decline was very similar across groups.
Conclusions   A marked decline in ETS exposure occurred in Britain between 1978 and 2000, which is likely to have reduced ETS-related disease risks appreciably before the introduction of legislation banning smoking in public places.     

Pharmacokinetic Predisposition to Nicotine from Environmental Tobacco Smoke: A Risk Factor for Pediatric Asthma

During the last decade several studies have shown that children whose parents smoke have higher rates of asthma. Recently, hair concentrations of cotinine have been shown to reflect systemic exposure to this constituent of smoke in both children and adults. At the present time it is not known, however, why some children exposed to passive smoking have asthma while others, similarly exposed, do not. The present study aimed at verifying whether asthmatic children are different from nonasthmatic children exposed to similar degrees of passive smoking in the way their bodies handle nicotine, a constituent of cigarette smoke. Seventy-eight asthmatic children were compared to 86 control children, all attending a consulting pediatric clinic in Toronto. A questionnaire completed by the parents and children detailed the daily number of cigarettes the child was exposed to and the identity of the smokers. Clinical data were extracted from the patients' charts. Urinary (corrected for creatinine) and hair concentrations of cotinine were measured by radioimmunoassays. The asthmatic and control children were of similar age, gender, and ethnic distribution, parental education, and socioeconomic status. Parents of asthmatic children tended to report a lower daily number of cigarettes (7.4 ± 1.3/day vs. 11.2 ± 2.3/day, p = 0.14), and this report agreed with the trend of urinary cotinine (47.1 ± 9.1 ng/mg vs. 62.6 ±11.5 ng/mg, respectively). Conversely, children with asthma had on average twofold higher concentrations of cotinine in their hair (0.696 ± 0.742 ng/mg) than control children (0.386 ± 0.383) (p = 0.0001). In a similar manner, the hair.urine concentration ratio was significantly higher in children with asthma (0.028 ± 0.002) than in their controls (0.18 ± 0.003) (p = 0.0001). These results suggest that under exposure to similar amounts of nicotine, children with asthma have on average twofold higher systemic exposure to this constituent of cigarette smoke. These data suggest that out of all children passively exposed to environmental tobacco smoke, those who exhibit asthma have a higher systemic exposure to nicotine, possibly due to lower clearance rate. This is the first evidence of pharmacokinetic predisposition to environmental tobacco smoke as an etiological factor in pediatric asthma.     

Secondhand tobacco smoke and severity in wheezing children: Nasal oxidant stress and inflammation

Objectives: Prenatal and postnatal smoke exposures are associated with many lung diseases in children due to impaired lung function, increased inflammation, and oxidative stress. We aimed to determine the influence of secondhand tobacco smoke exposure on the levels of nasal glutathione, IL-8, IL-17, MMP-9, and TIMP-1, as well as serum surfactant protein-D (SP-D) in wheezy children. Methods: We enrolled 150 children with recurrent wheezing and recorded wheezing characteristics at enrollment. We measured the levels of serum cotinine, SP-D, nasal glutathione, IL-8, IL-17, MMP-9, and TIMP-1. Serum cotinine levels between 3 and 12 ng/mL, and above 12 ng/mL were defined as lower and higher level secondhand tobacco smoke exposure, respectively. The ANOVA test, Pearson's correlation analysis and multivariate analysis with a linear regression test were used for the statistical analysis. Results: Ninety-one children had been exposed to lower level secondhand tobacco smoke, while 24 children were exposed to higher level secondhand tobacco smoke. Thirty-five children were not exposed to cigarette smoke. Wheezing symptom scores were higher in exposed children (p = 0.03). Levels of other biomarkers showed no significant difference. Conclusions: Secondhand tobacco smoke exposure is associated with more severe respiratory symptoms in wheezing children. However, levels of nasal or serum inflammatory markers fail to explain this association, either because of different mechanical factors in the process or due to low levels of the biomarkers especially in nasal secretions.     

Relationship between Exhaled Nitric Oxide and Exposure to Low-Level Environmental Tobacco Smoke in Children with Asthma on Inhaled Corticosteroids

Objectives. The relationship between exhaled nitric oxide (FeNO) and asthma severity or control is inconsistent. Active smoking lowers FeNO, but the relationship between passive smoking and FeNO is less clear. Children may be exposed to low-level environmental tobacco smoke (ETS) or thirdhand smoke, even if parents avoid smoking in the presence of their children. Our hypothesis was that FeNO is lower in children with asthma exposed to low-level ETS when compared with those who are not exposed. Methods. Children with stable asthma, 8–18 years of age, on low- or medium-dose inhaled corticosteroids (ICS) were enrolled. Spirometry, Asthma Control Questionnaire (ACQ), FeNO, exhaled breath condensate pH (EBC pH), and EBC ammonia were compared between children with and without ETS exposure as determined by urinary cotinine. Results. Thirty-three subjects were enrolled, of which 10 (30%) had urinary cotinine levels ≥1 ng/ml. There were no significant differences between the two groups in age, sex, BMI percentile, atopy status, FEV₁, EBC pH, or EBC ammonia. Median ACQ was 0.29 (IQR: 0.22–0.57) for those with cotinine levels <1 ng/ml and 0.64 (IQR: 0.57–1.1) for those with cotinine levels of ≥1 ng/ml, p = .02. Median FeNO (ppb) was 23.9 (IQR: 15.2–34.5) for unexposed subjects and 9.6 (IQR: 5.1–15.8) for exposed subjects, p = .008. Conclusions: Children with asthma on low to medium doses of ICS and recent low-level ETS exposure have lower FeNO levels when compared with non-ETS-exposed subjects. Exposure to low-level ETS or thirdhand smoke may be an important variable to consider when interpreting FeNO as a biomarker for airway inflammation.     

Relationship of endotoxin and tobacco smoke exposure to wheeze and diurnal peak expiratory flow variability in children and adolescents

Background and objective: The relationship between endotoxin exposure and asthma severity (wheeze and airways obstruction) is not well described. The effects of endotoxin and tobacco smoke exposure on self‐reported wheeze and diurnal PEF variability (DV‐PEF) were examined in children aged 6–18 years with asthma or wheeze. Methods: A cross‐sectional study was performed in a rural area. From this study, children who reported wheeze in the previous 12 months or a physician diagnosis of asthma (n = 98) were selected for a case–control study. These subjects, who were the basis for the present analysis, completed: (i) a home environmental assessment, including dust collection to measure endotoxin levels: (ii) a clinic visit, including saliva collection to measure cotinine levels; and (iii) 2 week monitoring of twice daily symptom records, including wheeze, and PEF to calculate DV‐PEF. Results: Among these children, 22.4% reported wheeze during the monitoring period. Greater DV‐PEF was associated with higher endotoxin loads in play areas (P < 0.05). The association between salivary cotinine levels and high DV‐PEF was modified by gender. In females, higher cotinine levels were associated with an increased risk of high DV‐PEF compared with lower cotinine levels (P < 0.05), but this was not observed among males. Conclusions: Higher endotoxin exposure was associated with greater DV‐PEF among children with asthma or wheeze. While previous studies have suggested that endotoxin exposure protects against the development of asthma, individuals with the disease should avoid high exposure levels to limit exacerbations. The effect of tobacco smoke exposure on lung health may differ between male and female children.     

Trends in and predictors of second‐hand smoke exposure indexed by cotinine in children in England from 1996 to 2006

Aims To explore trends in and predictors of second‐hand smoke (SHS) exposure in children. To identify whether inequalities in SHS exposure are changing over time. Design Repeated cross‐sectional study with data from eight annual surveys conducted over an 11‐year period from 1996 to 2006. Setting England. Participants Nationally representative samples of children aged 4–15 years living in private households. Measurements Saliva cotinine (4–15‐year‐olds), current smoking status (8–15‐year‐olds), smoking status of parents and carers, smoking in the home, socio‐demographic variables. Findings The most important predictors of SHS exposure were modifiable factors—whether people smoke in the house on most days, whether the parents smoke and whether the children are looked after by carers who smoke. Children from more deprived households were more exposed and this remained the case even after parental smoking status has been controlled for. Exposure over time has fallen markedly among children (59% decline over 11 years in geometric mean cotinine), with the most marked decline observed in the period immediately preceding smoke‐free legislation. Declines in exposure have generally been greater in children most exposed at the outset. For example, in children whose parents both smoke, median cotinine declined annually by 0.115 ng/ml compared with 0.019 ng/ml where neither parent smokes (P < 0.05). Conclusions In the 11 years leading up to smoke‐free legislation in England, the overall level of SHS exposure in children as well as absolute inequalities in exposure have been declining. Further efforts to encourage parents and carers to quit and to avoid smoking in the home would benefit child health.     

The elimination half-life of urinary cotinine in children of tobacco-smoking mothers

Exposure to environmental tobacco smoke (ETS) is strongly associated with childhood morbidity. Cotinine, the major metabolite of nicotine, is a useful marker of tobacco smoke exposure. Cotinine levels in infants are higher than in older children or adults exposed to the same reported quantity of ETS. One hypothesis to explain this difference is that the urinary elimination half-life of cotinine is different between infants and older children. Urine was collected at admission, 12, 24 and 48 h, cotinine levels were subsequently measured and then standardized by correcting for creatinine excretion. Urinary elimination half-life of cotinine was calculated in 31 infants and 23 older children. The median half-life was 28.3 h (range 6.3-258.5 h) in infants, and 27.14 h (range 9.7-99.42 h) in older children. A Mann-Whitney U test showed no significant difference in the median half-life of cotinine between the two age groups (P = 0.18). Multivariate linear regression analysis demonstrated no significant relationship between half-life of cotinine and corrected cotinine level (P = 0.24). Our results support the hypothesis that higher cotinine levels in infants is due to greater exposure, rather than slower metabolism of cotinine.     

Real-life environmental tobacco exposure does not affect exhaled nitric oxide levels in asthmatic children.

Serial measurement of exhaled nitric oxide (eNO) has been shown to be a good noninvasive marker of asthma control. Active smoking decreases eNO levels. The effect of real-life environmental exposure to tobacco smoke (ETS) on eNO levels is not known. Our objective was to study the impact of environmental tobacco exposure on eNO levels in asthmatic and non-asthmatic children. Single breath off-line collection of eNO was performed in asthmatic and non-asthmatic children with and without ETS. Urine was collected for cotinine/nicotine analysis. Fifty-seven children were enrolled, of which 25 were asthmatic and 32 had smoke exposure. One active smoker was excluded from the data analysis. The mean eNO was 11.1 ppb (n = 31; SD = 18.5) in those passively exposed vs. 11.1 ppb (n = 25; SD = 19.9) among the unexposed (not statistically significant). The mean eNO was 6.1 (n = 32; SD = 4.4) among the non-asthmatics and 17.8 (n = 24; SD = 27.4) among the asthmatics (p = 0.02; CI: 1.9-21.6). Real-life environmental tobacco exposure does not appear to decrease eNO levels in asthmatic children. Off-line collection of exhaled nitric oxide with a Mylar collection device helps differentiate asthmatics from non-asthmatics.