Trends in passive smoking in cystic fibrosis, 1993-1998

We set out to study trends in exposure to passive smoking in children with cystic fibrosis over a 5-year period. We also evaluated the effects of this exposure on lung function. Cross-sectional data were collected on 52 children in 1998 and compared with similar data collected on 56 children in 1993. Within these two groups, there were 34 children who were studied on both occasions. Data collected included: questionnaire information about family smoking habits; forced expiratory volume in 1 sec (FEV1); forced vital capacity (FVC); and measurements of urinary and salivary cotinine levels. Salivary cotinine was more closely related to family smoking behavior than urinary cotinine concentrations (r for salivary cotinine = 0.54, P < 0.001; r for urinary cotinine = 0.37, P = 0.008). In 1993, 26/56 (46%) households contained at least one smoker (smoking households) compared with 23/52 (44%) in 1998. In 1993, a median of 15 cigarettes was smoked/day in smoking households compared to 20 cigarettes/day in 1998. In the longitudinal group, there was a small, nonsignificant reduction in mean urinary cotinine levels (geometric mean, 1993 = 5.03 ng/mL; 1998 = 4.76 ng/mL; P = 0.4). There was no significant difference between the smoking and nonsmoking households in change in lung function over 5 years (fall in FEV1 in smoking households, 10.3% vs. 11.2% in nonsmoking households; P = 0.87). We conclude that in a group of children with cystic fibrosis followed over 5 years, there was little reduction in passive smoking exposure. We did not show a relationship between such exposure and decline in lung function. A larger study will be necessary to determine whether such an effect is present. .     

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.     

Parental smoking behavior and the urinary cotinine levels of asthmatic children.

To determine whether parental reports of smoking habits and modifications in smoking behavior are associated with urinary cotinine levels (UCLs), UCLs were measured in 77 asthmatic children. Parental reports and UCLs agreed for 58 of the 77 children (75%). Although UCLs of children whose parents smoked indoors and outdoors were significantly higher than UCLs of children whose parents did not smoke (p<0.0001, p<0.002, respectively), there was no statistically significant difference between the UCLs of children whose parents smoked indoors and outdoors (p = 0.286). We concluded that encouraging smoking parents of asthmatic children to smoke outdoors may not be an effective way to lessen exposure.     

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.     

Evaluation of hair cotinine and toxic metal levels in children who were exposed to tobacco smoke

Tobacco or tobacco products (TTP) are harmful because they contain nicotine and some heavy metals. In this study, it was aimed to evaluate whether the responses of parents to questionnaires were compatible with the hair cotinine levels of their children, and to investigate whether exposure to environmental tobacco smoke (ETS) and living conditions increased the levels of cotinine, lead (Pb), arsenic (As), and cadmium (Cd) in the hair samples of the children. Questionnaires were administered to the parents questioning household consumption of TTP and living conditions. Children were grouped as “exposed to ETS” (E‐ETS) and “not exposed to ETS” (NE‐ETS). This grouping was performed through a questionnaire‐based evaluation, and a hair cotinine cut‐off value‐based evaluation. According to the questionnaire‐based evaluation, there were no significant differences in hair Pb, As, and Cd levels between the groups (P‐values: .337, .994, and .825, respectively). The hair cotinine of the E‐ETS group was higher (0.24 ± 0.21 vs 0.22 ± 0.15 ng/mg), but the difference was not statistically significant (P = .317). According to the cotinine evaluation, cotinine, Pb, and As levels were statistically higher in the E‐ETS group (P < .001, <.001, and .036, respectively), but there was no statistical difference between the groups in terms of Cd levels (P = .238). Our results showed that exposure to ETS increased the levels of cotinine, Pb, and As in the hair samples of children, and the questionnaire responses of the parents about their smoking habits might not be compatible with the hair cotinine levels of the children.     

Increased severity of respiratory syncytial virus airway infection due to passive smoke exposure

Objective

Aim of this study was to analyze whether children with objectively measured second‐hand cigarette smoke (SHS) exposure suffer from a more severe course of disease when hospitalized with lower respiratory tract infection (LRTI) due to respiratory syncytial virus (RSV).

Methods

This prospective study was conducted at the Department of Pediatrics, Wilhelminen‐Hospital, Vienna, Austria in children aged below 1 year without a history of preceding lung disease and with acute symptoms of LRTI and a positive nasopharyngeal swab for RSV. On admission, urinary cotinine was measured as a marker of recent SHS and clinical severity of LRTI was assessed by oxygen saturation SpO₂ and the “admission clinical severity score” (CSSA). Parents/caregivers were asked to complete a customized questionnaire assessing risks for SHS and demographic characteristics.

Results

After inclusion of 217 patients, data of 185 patients with a mean (SD) age of 106 days (80) were analyzed. Twenty‐five patients (13.5%) were “cotinine‐positive” (COT+) defined as a urinary cotinine level of ≥7 μg/L. SpO₂ on admission was significantly lower in children recently exposed to SHS defined objectively by COT+ (94.8% ±2.0) in urine on admission compared to children not recently exposed (COT−) (96.8% ±3.0; P < 0.01). Disease severity, assessed via mean clinical severity score on admission (CSSA) for COT+ and COT− was 2.56 and 1.71, respectively (P = 0.03).

Conclusions

Recent exposure to SHS was associated with lower O₂ saturation and higher clinical severity score, measured by urine cotinine levels in children hospitalized for RSV infection under 1 year of age.

     

Tobacco smoke exposure, wheeze, and atopy

We investigated the effect of in utero and postnatal environmental tobacco smoke (ETS) exposure on respiratory symptoms and atopy in the first 3 years of life in children at high risk of allergic disease (both parents atopic). Three hundred and sixty-nine children were followed from birth and reviewed at ages 1 and 3 years (respiratory questionnaire, skin testing). Parental smoking questionnaires were administered, and plasma cotinine in cord and peripheral blood (at age 1 year) was measured (capillary column gas-liquid chromatography). Wheezing starting in the first year of life was significantly more common in children of smoking mothers (54.2% vs. 39.5%, P = 0.017), but not wheezing starting after age 1 year (10.8% vs. 10.9%, smoking and nonsmoking mothers, P = 0.99). Detectable cord cotinine was not associated with wheeze. More frequent wheeze in infancy was significantly more common in those with detectable 1-year cotinine (e.g., wheeze without colds, 17.8% vs. 5.6%, P = 0.02; wheeze most days, 6.5% vs. 0%, P = 0.04). ETS exposure was not associated with atopy. In the multivariate regression analysis, maternal smoking during pregnancy and/or in the first year of life remained associated with wheeze in the first year of life (odds ratio, 1.88; 95% confidence interval, 1.14-3.12; P = 0.01). ETS exposure in "high-risk" infants increases the risk of wheezing starting in the first year of life, but not after age 1 year. However, ETS exposure has little or no effect on the development of atopy. Measurement of plasma cotinine was no more useful than tobacco exposure assessment by questionnaire in our cohort.     

Promoting smoke-free environments in Latin America: a comparison of methods to assess secondhand smoke exposure

Secondhand smoke (SHS) contains toxicants and carcinogens that are known to cause premature death and disease. Objectively measuring SHS exposure can support and evaluate smoke-free legislation. In Latin America, the most commonly used methods to measure SHS exposure are airborne nicotine and respirable suspended particles (PM?.?). Here we present results from studies conducted in public places and homes across Latin American countries. Airborne nicotine was detected in most locations between 2002-2006, before the implementation of 100% smoke-free legislation in Uruguay, Panama, Guatemala and other large cities within Latin America. Between 2006 and 2008, PM?.? levels were found to be five times higher in places where smoking was present at the time of sampling compared to those without smoking. Measuring SHS exposure across Latin America has increased our understanding of the magnitude of exposure in this region and results have been used to effectively promote smoke-free legislation.     

Association between second hand smoke (SHS) exposure and caregiver stress in children with poorly controlled asthma

Objective: Urban children with asthma experience high rates of second hand smoke (SHS) exposure. The objective was to examine whether SHS exposure is associated with symptom frequency in children with poorly controlled asthma. Methods: Children were enrolled in a RCT to test the efficacy of an environmental control behavioral intervention versus an attention control group and followed over 12 months. SHS exposure assessed using salivary cotinine measurement. Frequency of child asthma symptoms, healthcare utilization, household smoking and caregiver daily life stress were obtained via caregiver report. Time of enrollment was recorded to assess seasonal factors. Symptom days and nights were the primary outcomes. Multivariable models and odds ratios examined factors that best predicted increased frequency of daytime/nighttime symptoms. Results: Children (n?=?222) with a mean age of 6.3 (SD 2.7) years, were primarily male (65%), African American (94%), Medicaid insured (94%), and had poorly controlled asthma (54%). The final multivariable model indicated symptoms in the fall (OR 2.78; 95% CI 1.16, 6.52) and increased caregiver daily life stress (OR 1.13, 95% CI 1.02, 1.25) were significantly associated with increased symptom days when controlling for cotinine level, intervention status, child age and home and car smoking restrictions. Conclusions: There was no impact of SHS exposure on increased symptom frequency. High caregiver daily life stress and symptoms in fall season may place children with asthma at risk for increased day/nighttime symptoms. Close monitoring of symptoms and medication use during the fall season and intervening on caregiver life stress may decrease asthma morbidity in children with poorly controlled asthma.     

Scottish smoke‐free legislation and trends in smoking cessation

Aim To investigate trends in smoking cessation before and after the introduction of Scottish smoke‐free legislation and to assess the perceived influence of the legislation on giving up smoking and perceptions of the legislation in smokers. Design, setting and participants Longitudinal data on smoking cessation were obtained from 1998 to 2007 on a cohort of 3350 Scottish adults aged between 50 and 75 years at baseline. All members of the cohort were participating in a clinical trial of aspirin in people at moderately increased risk of cardiovascular events. A subgroup of 474 participants who had smoked in the year prior to the introduction of legislation in March 2006 also completed a questionnaire on the influence and perceptions of the smoke‐free legislation following its introduction. Measurements Smoking status was recorded yearly, including dates of quitting and restarting. Participants who gave up smoking for at least 3 months were recorded as having quit smoking. The questionnaire included scales on whether the smoke‐free legislation had helped/influenced cessation, made the individual think about/prompt them to quit and perceptions of the legislation. Findings The odds of smokers quitting annually increased throughout the 7‐year period prior to introduction of the smoke‐free legislation to 2 years afterwards (odds ratio 1.09, 95% confidence interval 1.05–1.12, P < 0.001). During 2006, the pattern of quarterly quitting rates changed, with an increase in quit rates (to 5.1%) in the 3‐month period prior to introduction of the legislation (January–March 2006). Socio‐economic status was not related to smoking cessation. In the subgroup completing the questionnaire (n = 474), 57 quit smoking between June 2005 and May 2007 and 43.9% of these said that the smoke‐free legislation had helped them to quit. Most (>70%) smokers were positive about the legislation, especially those from more affluent compared with more deprived communities (P = 0.01). Conclusions The Scottish smoke‐free legislation was associated with an increase in the rate of smoking cessation in the 3‐month period immediately prior to its introduction. Overall quit rates in the year the legislation was introduced and the subsequent year were consistent with a gradual increase in quit rates prior to introduction of the legislation. Socio‐economic status was not related to smoking cessation, but individuals from more affluent communities were more positive about the legislation.     

Changes in smoking prevalence in 16–17‐year‐old versus older adults following a rise in legal age of sale: findings from an English population study

Aim To assess smoking prevalence before and after the rise in legal age of sale of cigarettes in England and Wales from age 16 to age 18 in October 2007. Design A series of monthly cross‐sectional household surveys: the ‘Smoking Toolkit Study’. Setting England. Participants A total of 53 322 adults aged 16 and over interviewed between October 2006 and May 2009, 1136 of whom were aged 16 or 17 years. Measurements Change in smoking prevalence from pre‐ to post‐legislation, assessed by self‐reported smoking status, among the 16–17‐year‐old group and older adults. Findings The prevalence change following the legislation among those aged 16 and 17 was 7.1 percentage points (denominator = 1136) compared with 2.4 percentage points (denominator = 52 186) for older adults (odds ratio 1.36, P = 0.024, 95% confidence interval = 1.04–1.77 for the interaction). There was no difference within older age categories. Conclusions There was a greater fall in prevalence in 16–17‐year‐olds following an increase in age of sale than in older age groups. This provides some support to the view that raising the age of sale can, at least in some circumstances, reduce smoking prevalence in younger age groups.     

Does passive smoke exposure trigger acute asthma attack in children?

The relationship between asthma and passive smoking has been well established. However, it is still not clear whether an acute asthma attack can be induced by acute smoke exposure. The specific aims of this study were: 1- To assess the degree of smoke exposure through urinary cotinine levels in asthmatic children during and 4 weeks after asthma attacks and, 2- To evaluate the reliability of parental questionnaires in asthmatic children by comparing the data obtained from cotinine measurements and parental reports. Thirty-two consecutive asthmatic children who were admitted to the emergency clinic were included in the study. Parents were asked to complete a questionnaire about their smoking habits and housing conditions. Urinary cotinine and creatinine levels were measured in children during and 4 weeks after the acute asthma attack. The mean age of the patients was 5.7 +/- 3.2 years. The mean attack rate was 3.5 +/- 3.8 per year. Thirty-eight percent of the patients were taking no preventive treatment. In 80 % of patients, urinary cotinine and creatinine ratios (CCR) were significantly above the non-exposed, non-smoker levels. However, CCR levels during acute asthma attacks were not higher than those measured 4 weeks after the acute attack (314.6 +/- 299.1 vs. 203.8 +/- 165.2 ng/mg respectively, p > 0.05). Although parental reports of passive smoke exposure was 71 %, CCR levels revealed that 81 % and 97 % of children were exposed to passive smoke during acute attacks and asymptomatic periods, respectively. In conclusion, although the proportion of children with acute asthma attacks who were exposed to passive smoking was high, the degree of passive smoke exposure was not higher during acute attacks. Parental questionnaires were found to be unreliable in reporting passive smoke exposure in asthmatic children during acute attacks.     

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.     

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.     

Determination of environmental tobacco smoke in primary school children with urine cotinine measurements

Environmental tobacco smoke (ETS) has been regarded as one of the most important public health issues. It has been estimated that approximately 75% of Turkish children are exposed to ETS. In this study the parental smoking habits were determined. Then, the relationship between parent-reported estimates of children's exposure to ETS in the home and children's urinary cotinine levels was examined. According to the reports of parents, 57.8% of the fathers and 23.3% of the mothers were current smokers, 69.8% of the children came from homes with smokers, and 53.4% had daily exposure to ETS. Urinary cotinine levels were significantly higher in the exposed group than the nonexposed group. This data showed that ETS exposure was prevalent and a combination of a parent-report and a biological measures is suggested as the most informative estimate of ETS exposure in children.     

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.     

Household Smoking and Bronchial Hyperresponsiveness in Children with Asthma

This study investigated whether household environmental tobacco smoke (ETS) exposure is associated with increased bronchial hyperresponsiveness (BHR) in children with asthma. Two hundred forty-nine children, ages 7–11 years, sampled from a larger group with reported asthma or multiple asthma symptoms identified in a community survey in Cape Town, underwent histamine challenge testing and had urinary cotinine measured. Parents were interviewed for information on smoking habits and a variety of covariates. Children with asthma whose mothers smoked had a lower frequency of BHR than asthmatic children of nonsmoking mothers, particularly if the mother smoked ≥15 cigarettes daily. BHR was also less common among children sharing a house with four or more smokers vs. fewer or none. BHR was unrelated to paternal smoking. In contrast, FEV₁ was lower among children whose mothers currently smoked. The findings do not support a mechanism whereby ETS exposure aggravates existing childhood asthma by increasing BHR. This association may be masked, however, by the degree to which mothers of asthmatic children adjust their smoking. The results are consistent with an adverse effect of maternal smoking on lung function in asthmatic children.     

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.     

Secondhand smoke (SHS) exposure is associated with circulating markers of inflammation and endothelial function in adult men and women

AimsSecondhand smoke (SHS) exposure is associated with elevated CHD risks. Yet the pathways through which this may operate have not been investigated in epidemiologic studies with objective SHS exposure measures and a wide range of CHD risk factors associated with active smoking. Therefore we investigate associations between SHS exposure and CHD risk factors, to clarify how SHS exposure may raise risk of CHD.MethodsCross-sectional population-based study of 5029 men and women aged 59–80 years from primary care practices in Great Britain. Smoking, behavioural and demographic information was reported in questionnaires; nurses made physical measurements and took blood samples for analysis of serum cotinine and markers of inflammation, hemostasis and endothelial dysfunction.ResultsActive cigarette smokers had lower albumin and higher triglycerides, CRP, IL-6, white cell count, fibrinogen, blood viscosity, factor VIII, VWF and t-PA than non-smokers. Among non-smokers, serum cotinine levels were independently positively associated with CRP, fibrinogen, factor VIII, VWF and t-PA and inversely associated with albumin, after adjustment for age, gender, social and behavioural factors. The differences in CRP, fibrinogen and albumin between cotinine ≤0.05 and >0.7 ng/ml were one-third to one half the size of differences between cotinine ≤0.05 ng/ml and current smokers, but were of similar magnitude for VWF and t-PA.ConclusionsEndothelial, inflammatory and haemostatic markers related to CHD risk showed independent associations with SHS exposure in the same direction as those for active smoking. Results aid understanding of the associations between SHS exposure and elevated CHD risks.