Factors Associated with Second-Hand Smoke Exposure in Young Inner-City Children with Asthma
Arlene ButzJill S. HaltermanMelissa H. BellinMona TsouklerisMichele DonithanJoan KubRichard E. ThompsonCassia LandJennifer WalkerMary E. Bollinger
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Abstract:
Objectives. To examine the association of social and environmental factors with levels of second-hand smoke (SHS) exposure, as measured by salivary cotinine, in young inner-city children with asthma. Methods. We used data drawn from a home-based behavioral intervention for young high-risk children with persistent asthma post-emergency department (ED) treatment (N = 198). SHS exposure was measured by salivary cotinine and caregiver reports. Caregiver demographic and psychological functioning, household smoking behavior, and asthma morbidity were compared with child cotinine concentrations. Chi-square and ANOVA tests and multivariate regression models were used to determine the association of cotinine concentrations with household smoking behavior and asthma morbidity. Results. Over half (53%) of the children had cotinine levels compatible with SHS exposure and mean cotinine concentrations were high at 2.42 ng/ml (SD 3.2). The caregiver was the predominant smoker in the home (57%) and 63% reported a total home smoking ban. Preschool aged children and those with caregivers reporting depressive symptoms and high stress had higher cotinine concentrations than their counterparts. Among children living in a home with a total home smoking ban, younger children had significantly higher mean cotinine concentrations than older children (cotinine: 3–5 year olds, 2.24 ng/ml (SD 3.5); 6–10 year olds, 0.63 ng/ml (SD 1.0); p < .05). In multivariate models, the factors most strongly associated with high child cotinine concentrations were increased number of household smokers (β = 0.24) and younger child age (3–5 years) (β = 0.23; p < .001, R2 = 0.35). Conclusion. Over half of the young inner-city children with asthma were exposed to SHS, and caregivers are the predominant household smokers. Younger children and children with depressed and stressed caregivers are at significant risk of smoke exposures, even when a household smoking ban is reported. Further advocacy for these high-risk children is needed to help caregivers quit and to mitigate smoke exposure.Keywords:
Cotinine
Tobacco smoke
Secondhand Smoke
Objectives: Occupational health studies often rely on self-reported secondhand smoke (SHS) exposure. This study examines the accuracy of self-reported tobacco use and SHS exposure. Methods: Data on serum cotinine, self-reported tobacco use, and SHS exposure for US workers were extracted from three National Health and Nutrition Examination Surveys (n = 17,011). Serum cotinine levels were used to classify workers into SHS exposure categories. The percent agreement between self-reported tobacco use and SHS exposure with the cotinine categories was calculated. Results: Workers reporting tobacco use were 88% accurate whereas workers reporting work, home, or home+work exposures were 87% to 92% accurate. Workers reporting no SHS exposure were only 28% accurate. Conclusions: Workers accurately reported their smoking status and workplace-home SHS exposures, but substantial numbers reporting "no exposures" had detectable levels of cotinine in their blood, indicating exposure to SHS.
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Background This study examined whether thirdhand smoke (THS) persists in smokers' homes after they move out and non-smokers move in, and whether new non-smoking residents are exposed to THS in these homes. Methods The homes of 100 smokers and 50 non-smokers were visited before the residents moved out. Dust, surfaces, air and participants' fingers were measured for nicotine and children's urine samples were analysed for cotinine. The new residents who moved into these homes were recruited if they were non-smokers. Dust, surfaces, air and new residents' fingers were examined for nicotine in 25 former smoker and 16 former non-smoker homes. A urine sample was collected from the youngest resident. Results Smoker homes' dust, surface and air nicotine levels decreased after the change of occupancy (p<0.001); however dust and surfaces showed higher contamination levels in former smoker homes than former non-smoker homes (p<0.05). Non-smoking participants' finger nicotine was higher in former smoker homes compared to former non-smoker homes (p<0.05). Finger nicotine levels among non-smokers living in former smoker homes were significantly correlated with dust and surface nicotine and urine cotinine. Conclusions These findings indicate that THS accumulates in smokers' homes and persists when smokers move out even after homes remain vacant for 2 months and are cleaned and prepared for new residents. When non-smokers move into homes formerly occupied by smokers, they encounter indoor environments with THS polluted surfaces and dust. Results suggest that non-smokers living in former smoker homes are exposed to THS in dust and on surfaces.
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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. Key words: Tobacco smoke pollution, Nicotine, Cotinine, Child, Hair
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In Reply.—
Concerning the comments of Mr Jones, the intention of the study was not to demonstrate the hazardous nature of passive smoke exposure, which has been amply documented elsewhere.1,2Our study demonstrated exposure during the flight to cigarette smoke, which was absorbed and later excreted in the form of cotinine, a metabolite of nicotine. Furthermore, both the degree of exposure to nicotine and the levels of cotinine subsequently excreted were correlated with symptoms of physical irritation as well as annoyance. Second, the purpose of measuring nicotine in the air was because it is a marker of exposure to cigarette smoke. It was not to imply that particular levels of nicotine per se are deleterious. Environmental tobacco smoke contains several thousand chemicals, of which at least 40 are demonstrated carcinogens. These carcinogens are the species of interest for risk-assessment studies. Third, although health information on environmental tobacco smoke isCotinine
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Background and Aims: In the absence of comprehensive smoking bans in public places, bars and nightclubs have the highest concentrations of secondhand tobacco smoke, posing a serious health risk for workers in these venues. The objective of this study was to assess exposures of bar and nightclub employees to secondhand smoke, including non-smoking and smoking employees. Methods: Between 2007 and 2009, we recruited around 10 venues per city and up to 5 employees per venue in 24 cities in the Americas, Eastern Europe, Asia and Africa. Air nicotine concentrations were measured for 7 days in 238 venues. To evaluate personal exposure to secondhand smoke, hair nicotine concentrations were measured for 625 non-smoking and 311 smoking employees. The relationship between hair nicotine and air nicotine concentrations was estimated using mixed-effect models with country specific intercepts. Results: Median (interquartile range) air nicotine concentrations were 3.5 (1.5, 8.5) μg/m3 and 0.2 (0.1, 0.7) μg/m3 in smoking and smoke-free venues, respectively. Median (interquartile range) hair nicotine concentrations were 1.7 (0.5, 5.5) ng/mg and 6.0 (1.6, 16.0) ng/mg in non-smoking and smoking employees, respectively. After adjustment for age, sex, education, living with a smoker, hair treatment and region, a 2-fold increase in air nicotine concentrations was associated with a 29% (95% confidence interval 22%, 37%) increase in hair nicotine concentrations in non-smoking employees and with a 10% (2%, 19%) increase in smoking employees. Conclusions: Exposure to secondhand smoke in the workplace, assessed by air nicotine, resulted in elevated concentrations of hair nicotine among both smoking and non-smoking bar and nightclub employees. Legislation measures that ensure complete protection from secondhand smoke exposure in indoor public places are urgently needed.
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Environmental tobacco smoke (ETS), also referred to as secondhand smoke (SHS), is a major threat to public health and is increasingly recognized as an occupational hazard to workers in the hospitality industry. Therefore, several countries have implemented smoke-free regulations at hospitality industry sites. In Portugal, since 2008, legislation partially banned smoking in restaurants and bars but until now no data have been made available on levels of indoor ETS pollution/exposure at these locations. The aim of this study was to examine the occupational exposure to ETS/SHS in several restaurants in Lisbon, measured by indoor fine particles (PM(2.5)) and urinary cotinine concentration in workers, after the partial smoking ban in Portugal. Results showed that the PM(2.5) median level in smoking designated areas was 253 μg/m³, eightfold higher than levels recorded in canteens or outdoor. The nonsmoking rooms of mixed restaurants exhibited PM(2.5) median level of 88 μg/m³, which is higher than all smoke-free locations studied, approximately threefold greater than those found in canteens. Importantly, urinary cotinine concentrations were significantly higher in nonsmoker employees working in those smoking designated areas, confirming exposure to ETS. The proportion of smokers in those rooms was found to be significantly positively correlated with nonsmoker urinary cotinine and indoor PM(2.5) levels, establishing that both markers were occupational-ETS derived. The use of reinforced ventilation systems seemed not to be sufficient to decrease the observed ETS pollution/exposure in those smoking locations. Taken together, these findings demonstrate that the partial restrictions on smoking in Portuguese venues failed to provide adequate protection to their employees, irrespective of protective measures used. Therefore, a smoke-free legislation protecting individuals from exposure to ETS/SHS in all public places and workplaces is urgently needed in Portugal.
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In this study, the author examined (a) levels of airborne pollutants from environmental tobacco smoke in 8 restaurants, and (b) changes in urinary cotinine and nicotine levels among 97 nonsmoking subjects (i.e., 40 restaurant employees, 37 patrons, and 20 referents). Airborne pollutant levels were significantly lower in the control environments than in the nonsmoking dining rooms in which smoking was not permitted, and the levels were significantly lower in the dining rooms in which smoking was not permitted than in the dining rooms in which smoking was permitted. Levels of urinary cotinine and nicotine increased among subjects in the dining rooms in which smoking was permitted, and the increase was significantly greater in employees than patrons. There was a significant positive correlation between levels of urinary nicotine increase and the levels of airborne nicotine and solanesol. The results of this study support the restriction of smoking to designated areas that have separate ventilation systems, or the prohibition of smoking in restaurants.
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Introduction
This study examined tobacco smoke pollution (also known as thirdhand smoke, THS) in hotels with and without complete smoking bans and investigated whether non-smoking guests staying overnight in these hotels were exposed to tobacco smoke pollutants.Methods
A stratified random sample of hotels with (n=10) and without (n=30) complete smoking bans was examined. Surfaces and air were analysed for tobacco smoke pollutants (ie, nicotine and 3-ethynylpyridine, 3EP). Non-smoking confederates who stayed overnight in guestrooms provided urine and finger wipe samples to determine exposure to nicotine and the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone as measured by their metabolites cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), respectively.Findings
Compared with hotels with complete smoking bans, surface nicotine and air 3EP were elevated in non-smoking and smoking rooms of hotels that allowed smoking. Air nicotine levels in smoking rooms were significantly higher than those in non-smoking rooms of hotels with and without complete smoking bans. Hallway surfaces outside of smoking rooms also showed higher levels of nicotine than those outside of non-smoking rooms. Non-smoking confederates staying in hotels without complete smoking bans showed higher levels of finger nicotine and urine cotinine than those staying in hotels with complete smoking bans. Confederates showed significant elevations in urinary NNAL after staying in the 10 most polluted rooms.Conclusions
Partial smoking bans in hotels do not protect non-smoking guests from exposure to tobacco smoke and tobacco-specific carcinogens. Non-smokers are advised to stay in hotels with complete smoking bans. Existing policies exempting hotels from complete smoking bans are ineffective.Cotinine
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In this pilot study, we examined the validity and usefulness of hair nicotine–cotinine evaluation as a biomarker of monitoring exposure to tobacco. Head hair samples were collected from 22 infants (<2 years of age) and 44 adults with different exposures to tobacco (through either active or passive smoking) and analyzed by liquid chromatography–mass spectrometry (LC-MS) for nicotine and cotinine. Hair samples were divided into three groups, infants, passive smoker adults and active smoker adults, and into eight subgroups according to the degree of exposure. The limit of quantification (LOQ) was 0.1 ng/mg for nicotine and 0.05 ng/mg for cotinine. Mean recovery was 69.15% for nicotine and 72.08% for cotinine. The within- and between-day precision for cotinine and nicotine was calculated at different concentrations. Moreover, hair nicotine and cotinine concentrations were highly correlated among adult active smokers ( R 2 = 0.710, p < 0.001), among adult nonsmokers exposed to secondhand smoke (SHS; R 2 = 0.729, p < 0.001) and among infants ( R 2 = 0.538, p = 0.01). Among the infants exposed to SHS from both parents the noted correlations were even stronger ( R 2 = 0.835, p = 0.02). The above results identify the use of hair samples as an effective method for assessing exposure to tobacco, with a high association between nicotine and cotinine especially among infants heavily exposed to SHS.
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A commercially available enzyme-linked immunosorbent assay was used to quantitate cotinine, a nicotine metabolite, in the plasma of caged birds exposed to environmental tobacco smoke. Birds in smoking households were found to have significantly higher plasma cotinine levels (4.3–37.8 ng/ml) than control birds from nonsmoking households (0–3.6 ng/ml) (P < .001). These high levels of cotinine are similar to those reported in humans with clear evidence of clinical alteration and resultant disease from environmental tobacco smoke.
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