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Sources and Biomarkers of Secondhand Tobacco Smoke Exposure in Urban Adolescents
Abstract
Objective:
In an urban adolescent population, we evaluated sources of exposure to secondhand tobacco smoke (SHS), examined differences in exposure by race/ethnicity, age and sex, and determined the relationship between exposure source(s) and the biomarkers cotinine and NNAL.
Methods:
Participants were recruited from a public hospital-based outpatient clinic in San Francisco, CA, USA.
Results:
Of a sample of N=298 adolescents screened, 235 were biologically confirmed to be exposed to tobacco smoke. Of those, N=16 were active smokers and N=219 were exposed to SHS; 91(39%) were heavily SHS exposed (median cotinine=0.76 ng/mL) and 128 (54%) had light SHS exposure (median cotinine=0.11ng/mL). Within those SHS exposed, the most common source of exposure was in a public area. No significant racial/ethnic differences were found, although African American adolescents were more likely to live in a home that allowed smoking. Older adolescents were more likely to be exposed across several difference sources, and females more likely to be exposed in a car and in public areas. Past 7-day exposure in the home, in a car, and current blunt use were significantly related to biomarkers of exposure.
Conclusions:
Urban adolescents are exposed to SHS across a variety of sources. Although exposure in a public area is most common, exposure in the home and in cars significantly influences tobacco biomarker levels. Interventions to reduce exposure would have the greatest impact in this population if they focused on reducing exposure in the home and in cars. History of blunt use is a strong determinant of tobacco exposure.
... In a study of adolescents of low socioeconomic status (SES) in San Francisco, California, 76% were found to have recent light or heavy SHS exposure based on biochemical screening of the major nicotine metabolite, cotinine, with ranges of 0.05-30 ng/mL [5]. In a follow-up study, these adolescents reported common exposure to SHS in public areas; however, reported SHS in homes and cars significantly predicted biochemical exposure [6]. Interventions targeted at reducing SHS may improve adolescent health. ...
... Participants of the ages of 12-21 years were recruited from July 2017 to May 2018. Recruitment occurred through (1) invitation from prior research studies [5,6], if the individual's cotinine level was within the heavy SHS range (urinary cotinine 0.25-30 ng/mL) during their prior study involvement; (2) social media ads on Facebook and Instagram; and (3) flyers posted in the Children's Health Center (CHC) at the Zuckerberg San Francisco General Hospital. We included participants over the age of 18 years, as the CHC services adolescent patients up to the age of 21 years. ...
... We included participants over the age of 18 years, as the CHC services adolescent patients up to the age of 21 years. A screening measure assessed tobacco use and SHS exposure [6]. Self-reported active use of cigarettes, electronic cigarettes, or other tobacco products was an exclusion. ...
Background
Secondhand smoke (SHS) exposure in children and adolescents has adverse health effects. For adolescents of lower socioeconomic status (SES), exposure is widespread, evidenced in the measurement of urinary cotinine, a major metabolite of nicotine. Direct intervention with exposed children has been proposed as a novel method, yet there is minimal evidence of its efficacy. Combining this approach with a mobile health (mHealth) intervention may be more time and cost-effective and feasible for adolescent populations.
Objective
In this pilot study, we assessed the feasibility and preliminary evidence of efficacy of a 30-day text message–based mHealth intervention targeted at reducing SHS exposure in adolescent populations of low SES.
Methods
For the study, 14 nonsmoking and nonvaping participants between the ages of 12-21 years exposed to SHS were enrolled. The intervention consisted of a daily text message sent to the participants over the course of a month. Text message types included facts and information about SHS, behavioral methods for SHS avoidance, or true-or-false questions. Participants were asked to respond to each message within 24 hours as confirmation of receipt. Feasibility outcomes included completion of the 30-day intervention, receiving and responding to text messages, and feedback on the messages. Efficacy outcomes included a reduction in urinary cotinine, accuracy of true-or-false responses, and participants’ perceptions of effectiveness.
Results
Of the 14 participants that were enrolled, 13 completed the intervention. Though not required, all participants had their own cell phones with unlimited text messaging plans. Of the total number of text messages sent to the 13 completers, 91% (372/407) of them received on-time responses. Participant feedback was generally positive, with most requesting more informational and true-or-false questions. In terms of efficacy, 54% (6/11) of participants reduced their cotinine levels (however, change for the group overall was not statistically significant (P=.33) and 45% (5/11) of participants increased their cotinine levels. Of the total number of true-or-false questions sent across all completers, 77% (56/73) were answered correctly. Participants’ ratings of message effectiveness averaged 85 on a scale of 100.
Conclusions
In this pilot study, the intervention was feasible as the majority of participants had access to a cell phone, completed the study, and engaged by responding to the messages. The efficacy of the study requires further replication, as only half of the participants reduced their cotinine levels. However, participants answered the majority of true-or-false questions accurately and reported that the messages were helpful.
... Recent papers by Li and Hecht [2] and Nardone et al. [18] provide a valuable characterization of toxic substances in cigarette smoke. All components of tobacco smoke undergo subsequent changes during smoking, e.g., by oxidation, reduction, pyrolysis, or hydrolysis. ...
... Each of these substances often has a complex biological effect that harms smokers. In addition to nicotine, the primary alkaloid responsible for tobacco's effects and addictive properties, a wide range of carcinogens and mutagens have been detected in cigarette smoke, including carbon monoxide, hydrogen cyanide, sulfur oxide, ammonia, formaldehyde, acrolein, benzene, vinyl chloride, heavy metals such as lead, nickel, toluidine, arsenic, naphthylamine, dimethyl nitrosamine, dibenzo acridine, polycyclic aromatic hydrocarbons (PAHs) [2,18]. ...
Acrolein, a highly reactive unsaturated aldehyde, is a ubiquitous environmental pollutant that seriously threatens human health and life. Due to its high reactivity, cytotoxicity and genotoxicity, acrolein is involved in the development of several diseases, including multiple sclerosis, neurodegenerative diseases such as Alzheimer’s disease, cardiovascular and respiratory diseases, diabetes mellitus and even the development of cancer. Traditional tobacco smokers and e-cigarette users are particularly exposed to the harmful effects of acrolein. High concentrations of acrolein have been found in both mainstream and side-stream tobacco smoke. Acrolein is considered one of cigarette smoke’s most toxic and harmful components. Chronic exposure to acrolein through cigarette smoke has been linked to the development of asthma, acute lung injury, chronic obstructive pulmonary disease (COPD) and even respiratory cancers. This review addresses the current state of knowledge on the pathological molecular mechanisms of acrolein in the induction, course and development of lung diseases and cancers in smokers.
... Specifically, hand nicotine levels at T2 were almost five times higher than that of adult nonsmokers who lived with smokers (121.8 ng/wipe in enrolled children vs. 25.6 ng/wipe in adult nonsmokers) (Matt et al., 2016). Median levels of urinary cotinine and NNAL were also much higher in enrolled children compared to adolescents who were nonsmokers or light smokers in studies by others Benowitz et al., 2018;Nardone et al., 2020). Over a six-week period, hand nicotine and the four urinary TSE markers showed similar correlations between T1 and T2. ...
... Firstly, tobacco use is of interest to male reproductive researchers as it contains over 7000 compounds, of which approximately 70 have been identified as carcinogenic (Hecht 2003;IARC 2012). Different toxicants present in tobacco smoke is reviewed in detail by Shihadeh et al. (Shihadeh et al. 2015;Nardone et al. 2019). Combustible tobacco products cause the emission, and hence exposure to gases, vaporized liquids, and particles through the processes of hydrogenation, pyrolysis, oxidation, decarboxylation, and dehydration ). ...
Despite the association between tobacco use and the harmful effects on general health as well as male fertility parameters, smoking remains globally prevalent. The main content of tobacco smoke is nicotine and its metabolite cotinine. These compounds can pass the blood-testis barrier, which subsequently causes harm of diverse degree to the germ cells. Although controversial, smoking has been shown to cause not only a decrease in sperm motility, sperm concentration, and an increase in abnormal sperm morphology, but also genetic and epigenetic aberrations in spermatozoa. Both animal and human studies have highlighted the occurrence of sperm DNA-strand breaks (fragmentation), genome instability, genetic mutations, and the presence of aneuploids in the germline of animals and men exposed to tobacco smoke. The question to be asked at this point is, if smoking has the potential to cause all these genetic aberrations, what is the extent of damage? Hence, this review aimed to provide evidence that smoking has a mutagenic effect on sperm and how this subsequently affects male fertility. Additionally, the role of tobacco smoke as an aneugen will be explored. We furthermore aim to incorporate the epidemiological aspects of the aforementioned and provide a holistic approach to the topic.
The aim of this research was to investigate the therapeutic effects of Kencur (Kaempferia galanga L.) extract on kidney histopathological damage in male mice exposed to cigarette smoke. Twenty 8-week-old male mice were randomly divided into five treatment groups (n=5). The negative control group (C-) consisted of mice not given kencur extract or exposed to cigarette smoke, while the positive control group (C+) comprised mice exposed to cigarette smoke without kencur extract. Treatment groups included Treatment 1 (T1) administered 150 mg/kg BW of kencur extract, Treatment 2 (T2) administered 300 mg/kg BW, and Treatment 3 (T3) administered 600 mg/kg BW. Mice were exposed to cigarette smoke for 14 days. The data were analyzed using the Kruskal-Wallis test to evaluate overall differences among the treatment groups. Where significant differences were found (p<0.05), further pairwise comparisons were conducted using the Mann-Whitney test, confirming statistically significant differences between specific treatment groups. Treatment 3 (T3) was found to be the most effective in reducing histopathological damage in the kidneys of male mice. This study demonstrates that kencur extract effectively reduces histopathological damage in the kidneys of mice exposed to cigarette smoke, highlighting its potential as a protective agent against smoke-induced tissue injury.
Objective
A systematic review was conducted to evaluate the use patterns, health perceptions, and cardiopulmonary health effects of cigars.
Data sources
PubMed and Google Scholar were searched for peer-reviewed articles published between June 2014 and February 2021. Search keywords included cigars, cigarillos, little cigars, and cardiopulmonary health outcomes.
Study selection
Of 782 papers identified, we excluded non-English articles, review articles, commentaries, and those without empirical data on cigars. Three coders independently reviewed all articles and compared codes to resolve discrepancies. 93 articles met the inclusion criteria and were included.
Data synthesis
Cigars have evolved from premium cigars to encompass little cigars and cigarillos (LCCs). LCCs are available in an array of flavors and at a price advantage, and as a result, are used by different groups compared to premium cigars. LCCs are more frequently used by youth, young adults, and those who identify as Black/African American. LCCs are often used in combination with other tobacco products, alcohol, and cannabis. Despite limited regulation, cigars generate smoke of a similar composition as cigarettes. Among the studies identified, evidence suggests that cigar use is associated with cardiovascular and pulmonary toxicity. Higher all-cause and cancer-related mortalities are associated with cigar use, particularly with more frequent and deeper inhalation, compared to non-tobacco users.
Conclusions
LCCs are used more frequently by at-risk groups compared to premium cigars. Recent studies evaluating cigar cardiopulmonary health effects are limited but suggest cigars have similar health risks as conferred by cigarette smoking. With the use of LCCs and targeted marketing on the rise among high-risk groups, there is a critical need for continued research in this area.
Objective:
Environmental tobacco smoke exposure (ETSE) was race/ethnicity-specific, but how the race/ethnicity-specific ETSE has changed over time, diverging or converging, remains unclear. We examined ETSE trends by race/ethnicity in US children aged 3-11 years.
Methods:
We analyzed the data of 9678 children who participated in the biennial National Health and Nutrition Examination Surveys, 1999-2018. ETSE was defined as serum cotinine ≥ 0.05 ng/ml, with ≥ 1 ng/ml as heavy exposure. For trend description, adjusted biennial prevalence ratios (abiPR: the ratio associated with a 2-year increase in time) were estimated by race/ethnicity. The prevalence ratios between races/ethnicities were used to quantify ethnoracial differences in different survey periods. Analyses were performed in 2021.
Results:
The overall ETSE prevalence was cut by almost half, from 61.59% (95% confidence interval = 56.55%, 66.62%) in the 1999-2004 survey to 37.61% (33.90%, 41.31%) in 2013-2018, exceeding the national 2020 health target (47.0%). However, the decrease occurred unequally between races/ethnicities. Heavy ETSE declined significantly in white [abiPR = 0.80 (0.74, 0.86)] and Hispanic children [0.83 (0.74, 0.93)], but insignificantly in black children [0.97 (0.92, 1.03)]. Consequently, the adjusted prevalence ratio between black children and white children increased from 0.82 (0.47, 1.44) in 1999-2004 to 2.73 (1.51, 4.92) in 2013-2018 for heavy ETSE. Hispanic children remained at the lowest risk throughout the study period.
Conclusion:
Overall ETSE prevalence was cut by half between 1999 and 2018. However, due to uneven declines, the gaps between black children and others have expanded in heavy ETSE. Special vigilance is needed in preventive medicine practice with black children.
Purpose of the Review
To summarize the findings of published works supported by the Human Health Exposure Analysis Resource (HHEAR) program and provide recommendations to advance the field of environmental epidemiology.Recent FindingsWe identified 41 papers that have used HHEAR-generated laboratory results. Metals, phthalates, and phenol biomarkers were the most common biomarkers measured.SummaryThis review highlights numerous associations found between environmental exposures and a range of human health outcomes building on existing studies using HHEAR resources. The HHEAR repository has helped participating investigators expand the breadth of their research and bridge gaps in the existing literature. In the future, combining and harmonizing data in the repository will broaden the scope of the research published and improve sample size and power in these projects.
High levels of NNAL, the tobacco smoke exposure (TSE) biomarker of the carcinogen 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), indicate future cancer risk. A prior study of smokers’ children revealed NNAL levels as high as active smokers. Therefore, we conducted a case series to examine the sociodemographics, TSE and clinical patterns, and other TSE biomarker levels in 9 children with extreme NNAL levels of >200 pg/ml to generate hypotheses and explore potential causes and implications. We identified 0 to 4-year-olds who presented to an emergency setting and lived with ⩾1 smoker who were part of a parental tobacco cessation trial (n = 461). Of these children, 52 had urinary NNAL, cotinine, and N-oxides results (n = 52). Nine children (17.3%) had NNAL levels >200 pg/ml, ranging from 206.4 to 1399.0 pg/ml (Median (Mdn) = 489.2 pg/ml; Interquartile Range (IQR) = 222.7-1289.3 pg/ml). The cotinine Mdn (IQR) was 38.5 (10.3-102.2) ng/ml and the N-oxides Mdn (IQR) = 93.8 (24.7-109.6) pg/ml. While all biomarker levels were alarmingly high, these young children would not have been flagged for very high cancer risk based on urinary cotinine levels alone. This underscores the critical role of comprehensive TSE biomarker measurement in capturing different TSE exposure patterns and assessing children’s future risk for cancer and other TSE-related morbidities.
Objectives: Cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and N-oxides are biomarkers of tobacco smoke exposure (TSE) used to assess short- and longer-term TSE. The objective of this study was to assess the associations between these TSE biomarkers, sociodemographics, parental smoking, and child TSE patterns among 0–17-year-olds. Methods: A convenience sample of 179 pediatric patients (mean (SD) age = 7.9 (4.3) years) who lived with ≥1 smoker and who had parental assessments completed and urine samples analyzed for the three TSE biomarkers of interest were included. Biomarker levels were log-transformed, univariate regression models were built and Pearson correlations were assessed. Results: In total, 100% of children had detectable levels of cotinine and >96% had detectable NNAL and N-oxide levels. The geometric means of cotinine, NNAL, and N-oxide levels were 10.1 ng/mL, 25.3 pg/mL, and 22.9 pg/mL, respectively. The mean (SD) number of daily cigarettes smoked by parents was 10.6 (6.0) cigarettes. Child age negatively correlated with urinary cotinine (r = −0.202, p = 0.007) and log NNAL levels (r = −0.275, p < 0.001). The highest log-cotinine levels were in children who were younger, of African American race, and whose parents had a lower education, an annual income ≤USD15,000, and no smoking bans. The highest log-NNAL and N-oxide levels were in children whose parents had a lower education, had no smoking bans, and were around higher numbers of cigarettes. Conclusion: Children of smokers who were younger, African American, and had no smoking bans had the highest TSE biomarker levels. Targeted interventions are needed to reduce TSE levels among high-risk children.
Introduction:
Tobacco use is the leading cause of preventable disease and death in the United States; nearly all tobacco product use begins during youth and young adulthood.
Methods:
CDC, the Food and Drug Administration, and the National Cancer Institute analyzed data from the 2011-2018 National Youth Tobacco Surveys to estimate tobacco product use among U.S. middle and high school students. Prevalence estimates of current (past 30-day) use of seven tobacco products were assessed; differences over time were analyzed using multivariable regression (2011-2018) or t-test (2017-2018).
Results:
In 2018, current use of any tobacco product was reported by 27.1% of high school students (4.04 million) and 7.2% of middle school students (840,000); electronic cigarettes (e-cigarettes) were the most commonly used product among high school (20.8%; 3.05 million) and middle school (4.9%; 570,000) students. Use of any tobacco product overall did not change significantly during 2011-2018 among either school level. During 2017-2018, current use of any tobacco product increased 38.3% (from 19.6% to 27.1%) among high school students and 28.6% (from 5.6% to 7.2%) among middle school students; e-cigarette use increased 77.8% (from 11.7% to 20.8%) among high school students and 48.5% (from 3.3% to 4.9%) among middle school students.
Conclusions and implications for public health practice:
A considerable increase in e-cigarette use among U.S. youths, coupled with no change in use of other tobacco products during 2017-2018, has erased recent progress in reducing overall tobacco product use among youths. The sustained implementation of comprehensive tobacco control strategies, in coordination with Food and Drug Administration regulation of tobacco products, can prevent and reduce the use of all forms of tobacco products among U.S. youths.
Background:
Many adolescents are exposed to tobacco smoke, from either active smoking (CS) or secondhand smoke (SHS) exposure. Tobacco-specific biomarkers of exposure include cotinine (detects use in past 2-4 days) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL; detects use for a month or longer). NNAL is expected to detect more intermittent tobacco exposure. We compared NNAL and cotinine as biomarkers of exposure to tobacco in urban adolescents and determined the optimal NNAL cutoff point to distinguish CS from SHS exposure.Methods:Surplus urine samples, collected from 466 adolescents attending pediatric well or urgent care visits at Zuckerberg San Francisco General Hospital in 2013 to 2014, were assayed for cotinine and NNAL.Results:Ninety-four percent of adolescents had measurable levels of NNAL compared with 87% for cotinine. The optimal NNAL cutoff point to distinguish CS from SHS was 9.6 pg/mL by latent class or 14.4 pg/mL by receiver-operating characteristic analysis. Cotinine and NNAL were strongly correlated, but the correlation slopes differed for active versus SHS-exposed adolescents. Among nonsmokers, NNAL levels were significantly higher in African American (median, 3.3 pg/mL) compared with other groups (0.9-1.9 pg/mL), suggesting greater exposure to SHS.Conclusions:Urine NNAL screening finds a large majority (94%) of urban adolescents are exposed to tobacco. African Americans are exposed to higher levels of SHS than other ethnic/racial groups.Impact:SHS is associated with significant medical morbidity in adolescents. Routine biochemical screening with NNAL or cotinine detects high prevalence of SHS exposure and should be considered as a tool to reduce SHS exposure in high-risk populations.Cancer Epidemiol Biomarkers Prev; 27(3); 1-8. ©2018 AACR.
Children's exposure to secondhand smoke (SHS) has been causally linked to a number of childhood morbidities and mortalities. Over 50% of UK children whose parents are smokers are regularly exposed to SHS at home. No previous review has identified the factors associated with children's SHS exposure in the home.
AIM: To identify by systematic review, the factors which are associated with children's SHS exposure in the home, determined by parent or child reports and/or biochemically validated measures including cotinine, carbon monoxide or home air particulate matter.
METHODS: Electronic searches of MEDLINE, EMBASE, PsychINFO, CINAHL and Web of Knowledge to July 2014, and hand searches of reference lists from publications included in the review were conducted.
FINDINGS: Forty one studies were included in the review. Parental smoking, low socioeconomic status and being less educated were all frequently and consistently found to be independently associated with children's SHS exposure in the home. Children whose parents held more negative attitudes towards SHS were less likely to be exposed. Associations were strongest for parental cigarette smoking status; compared to children of non-smokers, those whose mothers or both parents smoked were between two and 13 times more likely to be exposed to SHS.
CONCLUSION: Multiple factors are associated with child SHS exposure in the home; the best way to reduce child SHS exposure in the home is for smoking parents to quit. If parents are unable or unwilling to stop smoking, they should instigate smoke-free homes. Interventions targeted towards the socially disadvantaged parents aiming to change attitudes to smoking in the presence of children and providing practical support to help parents smoke outside the home may be beneficial.
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.
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.
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, R(2) = 0.35).
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.
Cotinine is the most widely used biomarker to distinguish active versus passive smoking. However, there is an overlap in cotinine levels when comparing light or occasional smokers versus heavily exposed passive smokers. 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) is a tobacco-specific nitrosamine measurable in urine with a much longer half-life than cotinine. The aim of the study was to determine optimal cutoff points to discriminate active versus passive smokers and to compare sensitivity and specificity for the use of cotinine, NNAL, and the ratio of the NNAL/cotinine in urine.
Cotinine and NNAL were measured in urine of 373 active smokers and 228 passive smokers.
Geometric mean cotinine levels were 2.03 ng/ml (interquartile interval: 0.43-8.60) and 1,043 ng/ml (658-2,251) and NNAL levels were 5.80 pg/ml (2.28-15.4) and 165 pg/ml (90.8-360) pg/ml in passive and active smokers, respectively. NNAL/cotinine ratio in urine was significantly higher for passive smokers when compared with active smokers (2.85 vs. 0.16, p < .01). The receiver operating characteristics analysis determined optimal cutoff points to discriminate passive versus active smokers: 31.5 ng/ml for cotinine (sensitivity: 97.1% and specificity: 93.9%), 47.3 pg/ml for NNAL (87.4% and 96.5%), and 0.74 x 10⁻³ for NNAL/cotinine ratio (97.3% and 87.3%).
Both urine cotinine and NNAL are sensitive and specific biomarkers for discriminating the source of tobacco smoke exposure. Cotinine is the best overall discriminator when biomarkers are measured while a person has ongoing exposure to tobacco smoke. NNAL because of its long half-life would be particularly useful when there is a delay between exposure and biomarker measurement. The NNAL/cotinine ratio provides similar sensitivity but poorer specificity at discriminating passive versus active smokers when compared with NNAL alone.
There is no safe level of secondhand tobacco-smoke exposure, and no previous studies have explored multiunit housing as a potential contributor to secondhand tobacco-smoke exposure in children. We hypothesized that children who live in apartments have higher cotinine levels than those who live in detached homes, when controlling for demographics.
We analyzed data from the 2001-2006 National Health and Nutrition Examination Survey. The housing types we included in our study were detached houses (including mobile homes), attached houses, and apartments. Our study subjects were children between the ages of 6 and 18 years. Cotinine levels were used to assess secondhand tobacco-smoke exposure, and those living with someone who smoked inside the home were excluded. χ(2) tests, t tests, and Tobit regression models were used in Stata. Sample weights accounted for the complex survey design.
Of 5002 children in our study, 73% were exposed to secondhand tobacco smoke. Children living in apartments had an increase in cotinine of 45% over those living in detached houses. This increase was 212% (P < .01) for white residents and 46% (P < .03) for black residents, but there was no significant increase for those of other races/ethnicities. At every cutoff level of cotinine, children in apartments had higher rates of exposure. The exposure effect of housing type was most pronounced at lower levels of cotinine.
Most children without known secondhand tobacco-smoke exposure inside the home still showed evidence of tobacco-smoke exposure. Children in apartments had higher mean cotinine levels than children in detached houses. Potential causes for this result could be seepage through walls or shared ventilation systems. Smoking bans in multiunit housing may reduce children's exposure to tobacco smoke.
Exposure to secondhand tobacco smoke (SHS) has been linked to increased risk for a number of diseases, including lung cancer. The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is of particular interest due to its potency and its specificity in producing lung tumors in animals. The NNK metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in urine is frequently used as a biomarker for exposure. Due to its long half-life (40-45 days), NNAL may provide a long-term, time-averaged measure of exposure. We developed a highly sensitive liquid chromatography-tandem mass spectrometry method for determination of NNAL in human urine. The method involves liquid-liquid extraction followed by conversion to the hexanoate ester derivative. This derivative facilitates separation from interfering urinary constituents by extraction and chromatography and enhances detection with electrospray ionization mass spectrometry. The lower limit of quantitation is 0.25 pg/mL for 5-mL urine specimens. Applications to studies of people with a range of different SHS exposure levels is described.
Nicotine is of importance as the addictive chemical in tobacco, pharmacotherapy for smoking cessation, a potential medication for several diseases, and a useful probe drug for phenotyping cytochrome P450 2A6 (CYP2A6). We review current knowledge about the metabolism and disposition kinetics of nicotine, some other naturally occurring tobacco alkaloids, and nicotine analogs that are under development as potential therapeutic agents. The focus is on studies in humans, but animal data are mentioned when relevant to the interpretation of human data. The pathways of nicotine metabolism are described in detail. Absorption, distribution, metabolism, and excretion of nicotine and related compounds are reviewed. Enzymes involved in nicotine metabolism including cytochrome P450 enzymes, aldehyde oxidase, flavin-containing monooxygenase 3, amine N-methyltransferase, and UDP-glucuronosyltransferases are represented, as well as factors affecting metabolism, such as genetic variations in metabolic enzymes, effects of diet, age, gender, pregnancy, liver and kidney diseases, and racial and ethnic differences. Also effects of smoking and various inhibitors and inducers, including oral contraceptives, on nicotine metabolism are discussed. Due to the significance of the CYP2A6 enzyme in nicotine clearance, special emphasis is given to the effects and population distributions of CYP2A6 alleles and the regulation of CYP2A6 enzyme.
An important part of blunt (marijuana in a cigar shell) smoking is the ritual of the preparation process and the selection of tobacco product for the blunt. This article explores reasons for selection from the different tobacco products available in the legal commercial market. Based upon three years of ethnographic research with 92 focal subjects, the analysis focuses upon the practical, subcultural, and symbolic reasons that blunt smokers give for choosing tobacco products (cigars for blunts-CFBs) employed in the blunt preparation process. The blunt ritual also functions within the marijuana subculture to differentiate blunt smokers from joints/pipes smokers. This analysis explores the reasons users give for selecting among the most popular inexpensive cigar brands (Dutch Masters, Phillies Blunts, and Backwoods) all owned and marketed by a single cigar conglomerate. Blunt chasing--the smoking of a cigarillo or cigar following a blunt--is an emergent phenomenon that further expands the market for tobacco products among blunt smokers. Recently, many different flavors have been added to these tobacco products in order to attract young and minority blunt consumers.
Objectives:
Our objective was to examine the relationship between distinct tobacco smoke exposure (TSE) measures and TSE-related symptoms and emergency department (ED) and/or urgent care (UC) use among nonsmoking adolescents without asthma diagnoses.
Methods:
We performed a secondary analysis of 7389 adolescents who completed the Population Assessment of Tobacco and Health Study wave 2. Logistic regression and Poisson regression models were built.
Results:
Adolescents with TSE were at increased risk of reporting: shortness of breath, finding it hard to exercise, wheezing during or after exercise, and dry cough at night. Adolescents who lived with a smoker and had home TSE were at increased odds of reporting wheezing or whistling in the chest, and only adolescents with home TSE were at increased risk of reporting wheezing that disturbed sleep. Adolescents with TSE were less likely to report very good or excellent overall health and physical health but were more likely to report they sometimes, often, or very often missed school because of illness. Participants who lived with a smoker and had TSE ≥1 hour were more likely to have had an ED and/or UC visit. Participants with any TSE were at increased risk of having a higher number of ED and/or UC visits.
Conclusions:
Different TSE measures uniquely increased the risk of TSE-related symptoms, but any TSE increased the risk of having a higher number of ED and/or UC visits. The providers at these high-volume settings should offer interventions to adolescents who are exposed to tobacco smoke and their families to decrease these symptoms and related morbidity.
Introduction:
Routine biochemical assessment of tobacco smoke exposure could lead to more effective interventions to reduce or prevent secondhand smoke (SHS)-related disease in adolescents. Our aim was to determine using urine cotinine (major nicotine metabolite) measurement the prevalence of tobacco smoke exposure among adolescents receiving outpatient care at an urban public hospital.
Methods:
Surplus urine was collected in 466 adolescents attending pediatric or urgent care clinics at San Francisco General Hospital, serving families with lower levels of income and education, in 2013-14. The majority were Hispanic or African American. Urine cotinine cut points of 0.05 to 0.25 ng/ml, 0.25 to 30 ng/ml and 30 ng/ml were used to classify subjects as light SHS or thirdhand smoke exposed, SHS or light/intermittent active users, and active tobacco users, respectively.
Results:
Among subjects 87% were exposed, including 12% active smoking, 46% SHS and 30% lightly exposed. The SHS exposed group adjusted geometric mean cotinine values were significantly higher in African Americans (1.48 ng/mL) compared to other groups (0.56 - 1.13 ng/ml).
Conclusions:
In a city with a low smoking prevalence (12%), a large majority (87%) of adolescents seen in a public hospital clinic are exposed to tobacco. This is much higher than reported in national epidemiological studies of adolescents, which used a plasma biomarker. Since SHS is associated with significant respiratory diseases and parents and adolescents underreport exposure to SHS, routine biochemical screening should be considered as a tool to reduce SHS exposure. The clinical significance of light exposure needs to be investigated.
Implications:
Urine biomarker screening found that a large majority (87%) of adolescents treated in an urban public hospital are exposed to tobacco. Since secondhand smoke (SHS) is associated with significant respiratory diseases and parents and adolescents underreport exposure to SHS, routine biochemical screening should be considered as a tool to reduce SHS exposure.
Introduction:
An increasingly popular method of consuming marijuana is through the smoking of "blunts," cigar products in which some or all of the tobacco filler is removed and repacked with marijuana. Even if all tobacco filler is removed from the cigar product in the process of making blunts, nicotine may be present in the wrapper of the cigar product. This preliminary analysis quantified the nicotine content in wrappers of cigar products commonly used for blunt smoking.
Methods:
Five cigar products (3 large cigars, 2 cigarillos) were tested, yielding physical characteristics of cigar length, diameter, weight, and wrapper weight. Nicotine concentration in the wrapper of each cigar product was analyzed via gas chromatography/mass spectrometry. Total nicotine content in the wrapper of each cigar product was computed as the product of cigar wrapper weight and nicotine concentration in wrapper.
Results:
Depending on the product, the cigar wrapper contributed between 8 and 18% of the weight of the entire cigar article. Total nicotine content in the cigar wrapper ranged from 1.2 to 6.0mg per cigar.
Discussion:
All 5 tested cigar products had wrappers that contain quantifiable levels of nicotine, indicating that users of blunts may expose themselves to some degree of nicotine, the addictive component of tobacco. Future experimental studies that examine the efficiency of nicotine delivery from typical blunt smoking, as well as surveillance studies that quantify the number of blunts smoked by an individual per day, are needed to evaluate the contribution of blunt smoking to nicotine dependence.
Breathing secondhand smoke (SHS) causes heart disease and lung cancer in adults and increased risks for sudden infant death syndrome, acute respiratory infections, middle-ear disease, worsened asthma, respiratory symptoms, and slowed lung growth in children. No risk-free level of exposure to SHS exists. The Global Youth Tobacco Survey (GYTS), initiated in 1999 by the World Health Organization (WHO), the Canadian Public Health Association, and CDC includes questions related to tobacco use, including exposure to SHS. This report examines data collected from 137 jurisdictions (i.e., countries and territories) during 2000-2007, presents estimates of exposure to SHS at home and in places other than the home among students aged 13-15 years who had never smoked, and examines the association between exposure to SHS and susceptibility to initiating smoking. GYTS data indicated that nearly half of never smokers were exposed to SHS at home (46.8%), and a similar percentage were exposed in places other than the home (47.8%). Never smokers exposed to SHS at home were 1.4-2.1 times more likely to be susceptible to initiating smoking than those not exposed. Students exposed to SHS in places other than the home were 1.3-1.8 times more likely to be susceptible to initiating smoking than those not exposed. As part of their comprehensive tobacco-control programs, countries should take measures to create smoke-free environments in all indoor public places and workplaces.
Background
Environmental tobacco smoke (ETS) negatively affects children with asthma. The prevalence of ETS exposure among children with poor asthma control may be changing. Importantly, the mechanisms by which ETS worsens asthma control are poorly understood.
Objective
We describe how ETS affects gastroesophageal reflux (GER), respiratory infections, and leukotriene production among children with poor asthma control.
Methods
We analyzed data from 306 children between 6 and 17 years of age with poorly controlled asthma enrolled in a 6-month clinical trial. We evaluated prevalence and determinants of ETS exposure by interview, questionnaire, and urinary cotinine and the association of ETS exposure on leukotriene production, respiratory infections, GER, lung function, and asthma control. We used multivariable linear, logistic, and Poisson regressions to assess outcomes.
Results
ETS prevalence estimates ranged from 6% to 30%. Children with domestic indoor exposure had worse asthma control (c-Asthma Control Test, 17.8 vs 21.5; P = .04), worse FEV1 % predicted (84.1 vs 90.7; P = .02), and a trend for increased mean urinary leukotriene E4. ETS from any setting was associated with increased symptomatic respiratory infections (adjusted incidence rate ratio: 1.30; P = .02). However, children exposed to ETS did not have symptoms or pH probe results, suggestive of heightened GER.
Conclusions
Domestic smoking exposure was associated with both higher rates of symptomatic respiratory infection and poorer asthma control despite generally intensive controller therapy. ETS exposure is common among asthmatic children with poor control and may worsen asthma control by promoting respiratory infections. Further investigation is required to elucidate ETS mechanisms in poor asthma control.
Introduction:
Secondhand smoke (SHS) exposure is associated with numerous adverse health effects, including cancer, cardiovascular disease, asthma, respiratory infections, and decreased pulmonary function. This study provides population estimates of SHS exposure among the Canadian nonsmoking population based on self-report and urinary cotinine concentrations.
Methods:
The 2007-2009 Canadian Health Measures Survey, a nationally representative cross-sectional survey, collected data from Canadians aged 6-79 years, and it includes self-report and urinary cotinine measures of tobacco smoke exposure (n = 4,455).
Results:
An estimated 22% of nonsmokers reported being exposed to SHS every day or almost every day. Of those, 70% of children (6-11 years) and 48% of adolescents (12-19 years) had detectable cotinine levels compared with 23% of adults (20-79 years). An estimated 77% of nonsmokers exposed to SHS only in the home had detectable cotinine levels compared with 11% of nonsmokers exposed to SHS only outside the home. Of those exposed to SHS only in the home, a higher percentage of children (5.1%) had detectable cotinine levels compared with adults (3.1%).
Conclusions:
Despite well-known health risks associated with exposure to tobacco smoke, a substantial proportion of the Canadian population continues to be exposed to SHS. Higher percentages of certain subpopulations had detectable cotinine concentrations, including children, adolescents, and those exposed to SHS in the home.
The nicotine metabolite cotinine is widely used to assess the extent of tobacco use in smokers, and secondhand smoke exposure in non-smokers. The ratio of another nicotine metabolite, trans-3'-hydroxycotinine, to cotinine in biofluids is highly correlated with the rate of nicotine metabolism, which is catalyzed mainly by cytochrome P450 2A6 (CYP2A6). Consequently, this nicotine metabolite ratio is being used to phenotype individuals for CYP2A6 activity and to individualize pharmacotherapies for tobacco addiction. In this paper we describe a highly sensitive liquid chromatography-tandem mass spectrometry method for determination of the nicotine metabolites cotinine and trans-3'-hydroxycotinine in human plasma, urine, and saliva. Lower limits of quantitation range from 0.02 to 0.1ng/mL. The extraction procedure is straightforward and suitable for large-scale studies. The method has been applied to several thousand biofluid samples for pharmacogenetic studies and for studies of exposure to low levels of secondhand smoke. Concentrations of both metabolites in urine of non-smokers with different levels of secondhand smoke exposure are presented.
To estimate the prevalence of self-reported exposure to secondhand smoke (SHS) in different settings and to describe salivary cotinine concentration and its determinants among non-smokers.
Cross-sectional study of a representative sample (N=775) of adult non-smokers in Barcelona, Spain (years 2004-2005). We assessed exposure to SHS using a questionnaire and measurement of salivary cotinine concentration. We calculated prevalence rates of self-reported exposure and medians and geometric means of salivary cotinine concentration. We adjusted for potential confounding factors with multinomial logistic regression models.
The prevalence rate of self-reported exposure to SHS among non-smokers in any setting was 75.7% (95% CI: 72.7%-78.8%). The prevalence of exposure to SHS tended to decrease with age. The geometric mean of cotinine concentrations among non-smokers was 1.49 ng/ml (95% CI: 1.39-1.60 ng/ml) among all subjects, and 1.80 ng/ml (95% CI: 1.37-2.35 ng/ml) in subjects who reported exposure to SHS in all settings. In bivariate and multivariate analyses, the cotinine concentration increased with the number of smokers and the number of cigarettes smoked per day in the presence of non-smokers in the household.
In this population, self-reported exposure to SHS is very high. Salivary cotinine concentrations in non-smokers are associated with exposure at home.
The complexity of tobacco smoke leads to some confusion about the mechanisms by which it causes lung cancer. Among the multiple components of tobacco smoke, 20 carcinogens convincingly cause lung tumors in laboratory animals or humans and are, therefore, likely to be involved in lung cancer induction. Of these, polycyclic aromatic hydrocarbons and the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone are likely to play major roles. This review focuses on carcinogens in tobacco smoke as a means of simplifying and clarifying the relevant information that provides a mechanistic framework linking nicotine addiction with lung cancer through exposure to such compounds. Included is a discussion of the mechanisms by which tobacco smoke carcinogens interact with DNA and cause genetic changes--mechanisms that are reasonably well understood--and the less well defined relationship between exposure to specific tobacco smoke carcinogens and mutations in oncogenes and tumor suppressor genes. Molecular epidemiologic studies of gene-carcinogen interactions and lung cancer--an approach that has not yet reached its full potential--are also discussed, as are inhalation studies of tobacco smoke in laboratory animals and the potential role of free radicals and oxidative damage in tobacco-associated carcinogenesis. By focusing in this review on several important carcinogens in tobacco smoke, the complexities in understanding tobacco-induced cancer can be reduced, and new approaches for lung cancer prevention can be envisioned.
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