Passive Tobacco Smoke Exposure Research Articles

Atopic dermatitis and tobacco smoke exposure during childhood and adolescence

Tobacco smoke may affect atopic dermatitis (AD) because of its known effects on humoral and cellular immunity, but prior studies lack data on disease severity and biomarkers over time. We investigated the association between passive and active tobacco smoke exposure (TSE) during childhood and adolescence and the activity and severity of AD. A birth cohort of 10,521 individuals was followed through adolescence as part of the Avon Longitudinal Study of Parents and Children. We used mixed-effect models to determine the risk of AD (based on repeated assessments) with passive smoke exposure during childhood, active TSE during adolescence, and using a serum biomarker of tobacco exposure (cotinine) at 3 time points. After adjusting for confounding factors, there was no evidence of a relationship between passive TSE and concurrent AD activity in childhood (adjusted odds ratio, 0.95; 95% confidence interval, 0.83, 1.07) or of an increased risk between active smoking and AD activity in adolescence (adjusted odds ratio, 0.57; 95% confidence interval, 0.44, 0.75). Secondary analyses demonstrated no dose-response relationship and no increased severity of AD with passive or active TSE. Furthermore, we found no increased risk of AD with a cumulative measure of passive TSE across childhood (adjusted relative risk ratio, 0.98; 95% confidence interval, 0.96, 1.00). Neither active nor passive TSE was associated with AD during childhood and adolescence.

Associations of active and passive tobacco exposure with elevated blood pressure in Korean adolescents.

To test the hypothesis that tobacco exposure is associated with elevated blood pressure (EBP) in Korean adolescents, and that the association is dose dependent. This cross-sectional study used data from the 2011-2020 Korea National Health and Nutrition Survey (KNHANES). Subjects were eligible if they were 13-18 years at the time of participation in KNHANES. Tobacco exposure was defined by urine cotinine level. The main outcomes were EBP and hypertension. Statistical analyses were conducted using SAS version 9.4 with appropriate sampling weights to account for the complex survey design, stratification, and cluster variable. A total of 2,518 adolescents was included in the analysis, representing 2.5 million Korean adolescents. The mean± standard deviation participant age was 15.3±1.7 years, and 55.3% were male. The number of participants with active tobacco smoke exposure was 283 (11.2%), passive tobacco smoke exposure was 145 (5.8%), and no smoke exposure was 2,090 (83.0%). Analysis of the 2,518 urine-cotinine-verified participants showed that tobacco smoke exposure had a significant effect on EBP: with an odds of elevated blood pressure of 3.00 (95% confidence interval [CI], 1.14 to 7.89). The odds of hypertension were 3.61 (95% CI, 1.13 to 11.49) in the active smoking group compared with the no tobacco exposure group after adjustment for potential confounders. It is necessary to present a range of public health plans to reduce tobacco exposure that affects adolescents' blood pressure, and further research with a larger number of participants using urine cotinine as a biomarker is needed.

Effect of prenatal passive tobacco smoke exposure on full-term birth weight of born neonates:SR

Abstract Prenatal smoking increases the risks of pre-term birth, stillbirth, neonatal death, and perinatal death as well as neurodevelopmental disorders in children. However, there is a lack of consistency in research published about association/impacts of passive smoking and low birth weight (LBW). Hence, we carried out this systematic review to determine whether or not there is a relation between prenatal tobacco smoke exposure and full-term LBW infants. Following PRISMA guidelines, we carried out systematic searches with PubMed, CINAHL, PsycInfo, and Embase for cohort case-control studies the 31-year period from 1991 - 2022. Of the 2,877 articles identified, 835 duplicates were removed. Title screening was done for 2,126 articles. 25 articles met the inclusion criteria that were Peer reviewed full-text articles in the English language and related to LBW due to passive smoking only. We found 20/25 articles showed a significant relationship with an OR ranging between 2.14 and 54.9 respectively between exposure to environmental tobacco smoke (ETS) and LBW infants at term and 5 articles showed no association with an OR ranging between 0.48 and 1.51. A significant difference found between the sample size among the studies included influencing the outcome of the study (ranging from smallest (n = 208) and largest (n = 17412). Mean age of mother was 29.6±3.8 and mean birth weight was 3,212±467.1. Nicotine level > 4.1 ng/mL or duration of exposure 24.4 hours/week gives strong evidence of prevalence of LBW among SHS exposed mothers. Compiled evidence suggests that, there is a significant association between prenatal passive smoke exposure and neonatal birth-weight at full term. There is a need for health researchers and public health experts to design and implement targeted programmes to reduce LBW due to passive smoke in our societies. Key messages • Exposure to ETS from domestic sources has a substantial influence on birth weight. • Combining educational programmes and legislative interventions is required to eliminate infants’ contact with tobacco smoke in utero and throughout childhood.

Association of tobacco smoke exposure with metabolic profile from childhood to early adulthood: the Special Turku Coronary Risk Factor Intervention Project.

To investigate the associations between passive tobacco smoke exposure and daily smoking with a comprehensive metabolic profile, measured repeatedly from childhood to adulthood. Study cohort was derived from the Special Turku Coronary Risk Factor Intervention Project (STRIP). Smoking status was obtained by questionnaire, while serum cotinine concentrations were measured using gas chromatography. Metabolic measures were quantified by nuclear magnetic resonance metabolomics at 9 (n = 539), 11 (n = 536), 13 (n = 525), 15 (n = 488), 17 (n = 455), and 19 (n = 409) years. Association of passive tobacco smoke exposure with metabolic profile compared participants who reported less-than-weekly smoking and had serum cotinine concentration <1 ng/mL (no exposure) with those whose cotinine concentration was ≥10 ng/mL (passive tobacco smoke exposure). Associations of daily smoking with metabolic profile in adolescence were analysed by comparing participants reporting daily smoking with those reporting no tobacco use and having serum cotinine concentrations <1 ng/mL. Passive tobacco smoke exposure was directly associated with the serum ratio of monounsaturated fatty acids to total fatty acids [β = 0.34 standard deviation (SD), (0.17-0.51), P < 0.0001] and inversely associated with the serum ratios of polyunsaturated fatty acids. Exposure to passive tobacco smoke was directly associated with very-low-density lipoprotein particle size [β = 0.28 SD, (0.12-0.45), P = 0.001] and inversely associated with HDL particle size {β = -0.21 SD, [-0.34 to -0.07], P = 0.003}. Daily smokers exhibited a similar metabolic profile to those exposed to passive tobacco smoke. These results persisted after adjusting for body mass index, STRIP study group allocation, dietary target score, pubertal status, and parental socio-economic status. Both passive and active tobacco smoke exposures during childhood and adolescence are detrimentally associated with circulating metabolic measures indicative of increased cardio-metabolic risk.

Covariation between serum cotinine and blood lead levels among US pediatric populations: Trends from 1999 to 2018

BackgroundTobacco smoke, including both active and passive smoke, can be an important source of lead exposure. However, the relationship between passive tobacco smoke exposure (PTSE) and blood lead levels (BLL), especially in vulnerable populations, needs to be further explored. The present study was to assess the covariation between serum cotinine, a measure of PTSE, and BLL in a pediatric population during 1999–2018. MethodsData on 21,817 children, aged 3–19 years, was extracted from the biennial nationally representative surveys. The trends of the prevalence of lead exposure (BLL ≥ 3.5 µg/dL) and PTSE (cotinine ≥ 1 ng/mL but < 10 ng/mL) were determined, and the covariation between BLL and cotinine was assessed. The population attributable fraction (PAF) of PTSE to the BLL was proxied using the partial R2 of the hierarchical linear regression. The association between PTSE and lead exposure was estimated using multivariate logistic regression. ResultsA parallel decreasing trend in the prevalence of lead exposure and PTSE was observed. Similarly, the means of both BLL and cotinine declined simultaneously. Overall, the PAF from PTSE towards blood lead was 7 %, doubling the PAF from race/ethnicity and family income combined. Stratified by race/ethnicity, PAF from PTSE was 8 % in Blacks and Whites and 4 % for Hispanics. The odds ratio of PTSE with lead exposure was 2.45 (95 % CI, 1.75, 3.44), 2.00 (1.21, 3.33), and 1.16 (0.64, 2.13) for Black, White, and Hispanic children, respectively. Cotinine mean remained two times higher in Blacks than non-Black children at the end of the study period. ConclusionSerum cotinine and BLL may have a significant association in children that persists even as both have been steadily declining in recent years. The contribution from PTSE to blood lead variations could be greater than that from socioeconomic factors. Further reducing lead exposure might be achieved by eliminating PTSE, particularly for the Black pediatric population.

Breastfeeding and infant acute otitis media: A comprehensive analytical study

Significance of the study acute otitis media (AOM) is an infection of the middle ear usually caused by a complication of viral infection in the upper respiratory tract 1. The interaction of virus and bacteria plays an important role in the development of AOM and in the latter case can be treated with antibiotics . Due to limited space in the middle ear and relatively poor drainage through the Eustachian tube, especially in young children, AOM is often accompanied by significant pain and other characteristics including fever, acute loss of hearing and general lethargy. The factors currently identified as associated with a reduced risk of AOM include breastfeeding, avoidance of in utero and childhood passive tobacco smoke exposure, and avoidance of indoor air pollution. Evidence from the literature supports a reduction in AOM risk from breastfeeding. However, there has been no recent comprehensive analytical review, particularly addressing issues related to the effect of duration and exclusivity of breastfeeding on the risk of AOM. Therefore, we aimed to study the relation between Breastfeeding and acute otitis media.

Effects of life-stage and passive tobacco smoke exposure on pulmonary innate immunity and influenza infection in mice

ABSTRACT Limited data are available on the effects of perinatal environmental tobacco smoke (ETS) exposure for early childhood influenza infection. The aim of the present study was to examine whether perinatal versus adult ETS exposure might provoke more severe systemic and pulmonary innate immune responses in mice inoculated with influenza A/Puerto Rico/8/34 virus (IAV) compared to phosphate-buffered saline (PBS). BALB/c mice were exposed to filtered air (FA) or ETS for 6 weeks during the perinatal or adult period of life. Immediately following the final exposure, mice were intranasally inoculated with IAV or PBS. Significant inflammatory effects were observed in bronchoalveolar lavage fluid of neonates inoculated with IAV (FA+IAV or ETS+IAV) compared to PBS (ETS+PBS or FA+PBS), and in the lung parenchyma of neonates administered ETS+IAV versus FA+IAV. Type I and III interferons were also elevated in the spleens of neonates, but not adults with ETS+IAV versus FA+IAV exposure. Both IAV-inoculated neonate groups exhibited significantly more CD4 T cells and increasing numbers of CD8 and CD25 T cells in lungs relative to their adult counterparts. Taken together, these results suggest perinatal ETS exposure induces an exaggerated innate immune response, which may overwhelm protective anti-inflammatory defenses against IAV, and enhances severity of infection at early life stages (e.g., in infants and young children).

Gender differences in the associations between tobacco smoke exposure and depressive symptoms among U.S. adults: NHANES 2007–2018

BackgroundFindings concerning gender differences in the associations between tobacco smoke exposure (TSE) and depression are inconsistent. This study aimed to investigate the gender-specific associations between active and passive TSE with depressive symptoms in a large, nationally representative sample of U.S. adults. MethodsData were from 27,175 adults aged ≥20 years in the 2007–2018 National Health and Nutrition Examination Survey (NHANES). Depressive symptoms were assessed using the Patient Health Questionnaire-9 (PHQ-9). Multivariable logistic regression was used to adjust for possible confounders. Whether the TSE-depression relationships may differ by age, race/ethnicity, socioeconomic status, body mass index (BMI), and self-reported health status was examined. ResultsAfter adjustment for lifestyle- and health-related variables, no significant associations between active (OR, 1.16 [95% CI, 0.87–1.55]) and passive TSE (OR, 0.84 [95% CI, 0.59–1.19]) and depressive symptoms were found among men. Among women, active TSE was associated with depressive symptoms (OR, 1.90 [95% CI, 1.51–2.39]), while the association for passive TSE was nonsignificant (OR, 1.11 [95% CI, 0.91–1.34]) after adjusting for lifestyle- and health-related variables. Interaction and subgroup analyses showed that self-reported health status could modify the relationship between passive TSE and depressive symptoms among women. Furthermore, a dose-response relationship between serum cotinine and depressive symptoms was found in women, but not in men. ConclusionsThis study suggests a stronger TSE-depression association in women than in men. Understanding these gender-specific patterns and identifying the potential moderators of such relationships will enable better targeting of public health interventions.

The association of active and passive tobacco smoke exposure with chronic rhinosinusitis symptom severity: A cross-sectional study.

Chronic rhinosinusitis (CRS) causes a great deal of morbidity. There are a multitude of causal factors, though their precise contribution to symptom severity has yet to be defined.We hypothesized that exposure to both primary and secondhand tobacco smoke would correlate with more severe symptoms of CRS. This is a prospective cross-sectional study performed at an academic tertiary care medical center from 2010 to 2013. A total of 85 consecutive patients with chronic sinusitis were screened;70 withmedically refractory CRS requiring functional Endoscopic sinus surgery (FESS) were enrolled. Recent tobacco exposure was assessed using serum cotinine levels. Sinonasal mucosa was biopsied to assess ciliary architecture. Demographics, medical history, tobacco and environmental exposures, and computed tomography (CT) imaging were also collected. Two quality of life (QOL) surveys were administered: one disease specific, Sinonasal Outcomes Test-20 (SNOT-20), and one general, Short Form-12 (SF-12). Results were correlated with the aforementioned exposures. The 70 patients had an average age of 46 years, and 42% were male.Variables that correlated with worse SNOT-20 scores included serum cotinine (r=0.43, p=0.002), number of cigarettes smoked daily (r=0.27, p=0.03), and number of secondhand cigarettes exposed to per day (r=0.29, p=0.04). There were no significant correlations between SNOT-20 scores and Lund-MacKay or axonemal ultrastructural abnormalities (AUA)-ciliary scores. The two five-variable models best predicted disease-specific QOL. Increased amounts of serum cotinine and primary and secondhand smoke exposure were associated with worse sinonasal QOL. This study establishes an objective relationshipbetween smoke exposure and patient-perceived severity of CRS, emphasizing the importance of tobacco cessation counseling as part of management.

Passive smoking and knowledge of its health hazards in the Kingdom of Saudi Arabia

Abstract Introduction Exposure to secondhand smoke is a major public health issue that requires assessing its magnitude. This study assesses the current status of passive smoking and its determinates in the Kingdom of Saudi Arabia. Methods This national study conducted in the 13 regions of Saudi Arabia through web-based-computer assisted telephone interviews. The two main measurements were passive smoking among nonsmokers and smoking behaviors in microenvironments among smokers. Data on socio-economic and demographical data, smoking status, attitude, and knowledge on passive smoking impacts were also collected. Data was weighted by age, gender, and region to account for the different probabilities of selection. Results Exposure to secondhand smoke among non-smokers was 44%. Smoking at home with the presence of children in the same room was prevalent (25% cigarettes smokers, 30% waterpipe smokers). About 18% of smokers smoke inside their cars while children on-board. Only 34.4% of smokers perceived, “to a very large extent”, the harms of their smoking might be doing to others. As the knowledge on secondhand smoking exposure health risks increases the smokers were less likely to smoke in microenvironment (R= -0.16, p value&amp;lt; 0.01). Almost half of the population (49.1wt.%) were “extremely concerned” about the effect of passive smoking on their health in the future. Conclusions Passive smoking is prevalent in the Saudi population and a proportion of smokers smokes in microenvironments with the presence of children. Further preventive and promotion strategies are needed to protect the public from the hazards of passive smoking with special attention to vulnerable populations. Key messages Identify the association between knowledge of the associated health risks with exposure to passive smoking and smoker behaviors that expose nonsmokers to tobacco smoke in private micro-environments. Assess the impact of individual knowledge of passive smoking associated health risks and vulnerability to passive tobacco smoke exposure.

435 The association between tobacco smoke exposure during childhood and adolescence and atopic dermatitis activity and severity

Atopic dermatitis (AD) is the most common chronic inflammatory skin disease worldwide, yet the triggers of disease activity and persistence are still not completely understood. Tobacco smoke exposure (TSE) is an environmental factor that deserves particular attention because of its known effects on humoral and cellular immunity. The objective of our study was to investigate the extent to which TSE during childhood and adolescence is associated with AD activity and severity. Data were obtained from the Avon Longitudinal Study of Parents and Children, a longitudinal population-based cohort from the UK with 10,518 individuals followed from birth through adolescence. AD was based on a validated measure of maternal-reported flexural dermatitis activity at 10 time points and severity at 9 time points between the ages of 2.5 and 18 years. TSE was measured using a standardized maternal-reported measure at 8 time points between the ages of 6 months and 9 years. Child serum cotinine levels (a nicotine metabolite and validated TSE biomarker) were available at 7, 15.5, and 17 years of age. After adjusting for demographic and socioeconomic confounding, there was no significant association between TSE level and the risk of ever having AD using cross-sectional multinomial regression models (RRR: 0.80-1.19; p>0.05 at all time points) and no significant association between TSE and AD severity (RRR: 0.69-1.52; p>0.05 at all time points). At 7 years old, there was no significant association between child serum cotinine level and AD severity. In contrast, at 15.5 years, a 1 ng/mL increase in serum cotinine showed a small but statistically significant association with severe AD compared to no AD (RRR: 1.007; 95% CI: 1.000, 1.013), suggesting that active rather than passive TSE may be most relevant to disease activity and severity.

Prenatal tobacco exposure and ADHD symptoms at pre-school age: the Hokkaido Study on Environment and Children\u2019s Health

BackgroundThere have been inconsistent findings reported on maternal passive smoking during pregnancy and child risk of ADHD. In this study, ADHD symptoms at pre-school age children in association with prenatal passive and active tobacco smoke exposure determined by maternal plasma cotinine levels in the third trimester were investigated.MethodsThis was a follow-up study of the birth cohort: the Hokkaido Study on Environment and Children’s Health. Children whose parents answered Strengths and Difficulties Questionnaire (SDQ) to identify child ADHD symptoms (hyperactivity/inattention and conduct problems) and total difficulties at age 5 years with available maternal plasma cotinine level at the third trimester were included (n = 3216). Cotinine levels were categorized into 4 groups; ≦ 0.21 ng/ml (non-smoker), 0.22–0.51 ng/ml (low-passive smoker), 0.52–11.48 ng/ml (high-passive smoker), and ≧ 11.49 ng/ml (active smoker).ResultsMaternal cotinine levels of active smokers were significantly associated with an increased risk of total difficulties (OR = 1.67) and maternal low- and high-passive smoking also increased the risk (OR = 1.11, 1.25, respectively) without statistical significance. Similarly, maternal cotinine levels of active smokers were associated with an increased risk of hyperactivity/inattention (OR = 1.49). Maternal low- and high-passive smoking and active smoking increased the risk of hyperactivity/inattention (OR = 1.45, 1.43, and OR = 1.59, respectively) only in boys.ConclusionOur findings suggested that maternal active smoking during pregnancy may contribute to the increased risk of child total difficulties and hyperactivity/inattention at pre-school age. Pregnant women should be encouraged to quit smoking and avoid exposure to tobacco smoke.

Environmental risk factors for cleft lip and palate in low-resource settings: a case-control study

Abstract Background Cleft lip with or without palate is the most common birth defect with a global prevalence of 1 in 700 births. Although there is a clear algorithm of care in developed countries, the lack of access to surgery in low-income and middle-income countries (LMICs) means that millions of people live with this easily treated condition. Although smoke exposure from unsafe cooking practices no longer occurs in the developed world and is not routinely studied, exposure to smoke from cooking remains an important challenge to health in LMICs. We aimed to understand whether exposure to cooking smoke is associated with cleft lip and palate in these low-resource settings. Methods We conducted a case–control study of mothers of a child with cleft lip with or without palate (cases) and population-matched mothers of children who do not have the condition (controls) in partnership with Operation Smile. Participants were from Vietnam, the Philippines, Honduras, Nicaragua, Morocco, Democratic Republic of the Congo, and Madagascar. Participants provided written consent and the University of Southern California gave ethical approval for the study. The primary exposure of interest was smoke inhalation in the form of smoking before or during pregnancy, paternal (ie, the father of the child) smoking, living with any smoker, or cooking indoors over a fire. We used logistic regression with multiple adjustment models to assess these smoke exposures as possible risk factors for cleft lip and palate. Findings We included data from 2168 cases and 2080 controls, recruited between 2011 and 2017. We found that Interpretation Exposure to smoke while cooking is a well-established health risk in LMICs for a wide variety of diseases, but has never been studied with respect to cleft lip and palate. We have shown that it may play a role in the risk of cleft lip and palate, and that it may be a larger risk factor than active or passive tobacco smoke exposure. Exposures specific to low-resource settings must be taken into account when we study preventable risk factors in order to develop strategies that will address the populations at the highest risk of having to live with this condition. Funding None.

Effect of indoor air quality on the natural history of asthma in an urban population in Poland.

Background: Indoor air pollution may have an impact on asthma. Objective: To evaluate the influence of indoor air pollution on the natural history of asthma. Methods: Data collection by using the European Community Respiratory Health Survey and International Study of Asthma and Allergies in Childhood standardized questionnaire (N = 18,617) and medical examinations (N = 4783) in selected Polish regions was used. Statistical analysis was performed by using the χ² test. A value of p < 0.05 was considered statistically significant. Results: Questionnaire results demonstrated that people who used the central heating system were less likely to declare the occurrence of asthma (odds ratio [OR] 0.84) and were corroborated with clinical findings of moderate asthma (OR 0.35). Symptomatic asthma occurred more frequently in people who used a solid-fuel heating device (OR 1.36) and electric heaters (OR 1.54). The use of cooking appliances with municipal natural gas (OR 1.77) and gas storage tanks (OR 2.03) was correlated with more frequent declarations of asthma. Symptomatic asthma was more common among people who smoked for at least 1 year (OR 2.26) and those who smoked over the course of the preceding month (OR 1.60). Passive exposure to tobacco smoke provided for a 1.5-fold increase in the incidence of symptomatic asthma (OR 1.53), regardless of the time of exposure. Conclusion: Both active and passive tobacco smoke exposure as well as the use of certain types of heating and cooking appliances have a significant impact on the incidence of asthma and the intensification of its symptoms in rooms with limited air exchange. Highlights of the study included the following: (1) central heating had an amelioratory effect on asthma, (2) heating technologies used at home had a significant impact on the incidence of asthma, and (3) devices used for cooking (municipal and cylinder gas stoves) played an important role in the intensification of asthma symptoms.

Pregnancy-Associated Plasma Protein A (PAPP-A) Concentration in Population of Healthy Young People: Interactions with Tobacco Smoke and Anti-oxidative Status

Pregnancy-associated plasma protein A (PAPP-A) is a high-molecular zinc-binding metalloproteinase that was first detected in the serum of pregnant women. It can also be detected in men and non-pregnant women. Recently, a growing interest in determining the concentration of PAPP-A as a marker of oxidative stress and atherosclerotic processes has been observed. Among the factors that could potentially influence the PAPP-A formation is the exposure to tobacco smoke. Some components of tobacco smoke have an immediate effect on the body and also direct influence on the cardiovascular system. The aim of this study was to evaluate the relation between PAPP-A concentration and either passive or active exposure to tobacco smoke in the population of medicine students (n = 152). The relation between PAPP-A concentration and chosen markers of inflammatory response and anti-oxidative processes was analyzed. The samples of serum, urine, and saliva were collected and main nicotine metabolites in urine samples were determined using ELISA technique. Comparison of the PAPP-A concentrations in the study group revealed that in the group of active smokers, the concentration of the protein was significantly higher than in the group of passive smokers (p = .04) and the group of not-exposed students (p = .006). PAPP-A concentration showed significant positive correlation with the values of FRAP and main nicotine metabolites. The evident influence of both active and passive tobacco smoke exposure on PAPP-A levels in the studied population of young people who in general are not included in the group of high-risk cardiovascular incidents, shows how important early prevention of anti-health behaviors is.

Decreasing trend in passive tobacco smoke exposure and association with asthma in U.S. children

In this study, we assessed trends of serum cotinine levels over time among US children ages 3–11 years and compared the risk of asthma in groups exposed to passive tobacco smoke. We utilized National Health and Nutrition Examination Survey (NHANES) data collected from 2003 to 2014 (n = 8064). Serum cotinine level, household smoker status, asthma status, and sociodemographic information were extracted for multiple regression analyses. The adjusted biannual change in log (cotinine) in comparison to earlier NHANES survey cycles was − 0.196 (p < 0.001) overall, − 0.055 (p = 0.089) among children with household smoker(s), and − 0.129 (p < 0.001) among children without. The proportion of children living with household smokers decreased from 24.9% in the 2003–2004 cycle to 11.4% in the 2013–2014 cycle. The adjusted odds ratios (ORs) for asthma were 1.34 (95% confidence interval (CI): 1.00–1.80; 2nd tertile vs 1st tertile) and 1.69 (95%CI: 1.25–2.29; 3rd tertile vs1st tertile), respectively. Highly exposed asthmatic children, in the 3rd cotinine tertile (>0.13 ng/mL), were primarily Non-Hispanic Black (61.0%) and whose family incomes were below poverty guidelines. Overall results reveal passive smoke exposure level among children ages 3–11 in the US decreased over the study period. Nevertheless, higher exposure to passive smoke is still associated with higher odds of childhood asthma. Targeted smoking cessation interventions in clinical practices are needed to reduce tobacco smoke exposure and related asthma risk in children, particularly in low-income and minority groups.

Smoke-induced neuromuscular junction degeneration precedes the fibre type shift and atrophy in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is largely caused by smoking, and patient limb muscle exhibits a fast fibre shift and atrophy. We show that this fast fibre shift is associated with type grouping, suggesting recurring cycles of denervation-reinnervation underlie the type shift. Compared to patients with normal fat-free mass index (FFMI), patients with low FFMI exhibited an exacerbated fibre type shift, marked accumulation of very small persistently denervated muscle fibres, and a blunted denervation-responsive transcript profile, suggesting failed denervation precipitates muscle atrophy in patients with low FFMI. Sixteen weeks of passive tobacco smoke exposure in mice caused neuromuscular junction degeneration, consistent with a key role for smoke exposure in initiating denervation in COPD. A neurological basis for the fast fibre shift and atrophy seen in limb muscle of patients with chronic obstructive pulmonary disease (COPD) has not been considered previously. The objective of our study was: (1) to determine if denervation contributes to fast fibre shift and muscle atrophy in COPD; and (2) to assess using a preclinical smoking mouse model whether chronic tobacco smoke (TS) exposure could initiate denervation by causing neuromuscular junction (NMJ) degeneration. Vastus lateralis muscle biopsies were obtained from severe COPD patients [n=10 with low fat-free mass index (FFMI), 65years; n=15 normal FFMI, 65years) and healthy age- and activity-matched non-smoker control subjects (CON; n=11, 67years), to evaluate morphological and transcriptional markers of denervation. To evaluate the potential for chronic TS exposure to initiate these changes, we examined NMJ morphology in male adult mice following 16weeks of passive TS exposure. We observed a high proportion of grouped fast fibres and a denervation transcript profile in COPD patients, suggesting that motor unit remodelling drives the fast fibre type shift in COPD patient limb muscle. A further exacerbation of fast fibre grouping in patients with low FFMI, coupled with blunted reinnervation signals, accumulation of very small non-specific esterase hyperactive fibres and neural cell adhesion molecule-positive type I and type II fibres, suggests denervation-induced exhaustion of reinnervation contributes to muscle atrophy in COPD. Evidence from a smoking mouse model showed significant NMJ degeneration, suggesting that recurring denervation in COPD is probably caused by decades of chronic TS exposure.

The 500-year Cultural & Economic Trajectory of Tobacco: A Circle Complete.

Who smokes, and why do they do it? What factors discourage and otherwise reward or incentivize smoking? Tobacco use has been accompanied by controversy from the moment of its entry into European culture, and conflicting opinions regarding its potentially adverse influence on health have coexisted for hundreds of years. Its use in all forms represents the world’s single greatest cause of preventable disease and death. Tobacco was introduced to Europe by Christopher Columbus, who in October 1492 discovered the crop in Cuba. While the next four centuries would see tobacco as the most highly traded economic commodity, by 1900, the now familiar cigarette remained obscure and accounted for only 2% of total tobacco sales. Global tobacco consumption rose sharply after 1914 and became especially prevalent following World War II, particularly among men. Indeed, overall tobacco sales increased by more than 60% by the mid-20th century, and cigarettes were a critical driver of this growth. Cigarettes dominated the tobacco market by 1950, by then accounting for more than 80% of all tobacco purchases. In the absence of clinical and scientific evidence against tobacco, moral and religious arguments dominated opposition voices against tobacco consumption in the 1800s. However, by the mid-20th century, advancements in medical research supported enhanced government and voluntary actions against tobacco advertising and also raised awareness of the dangers associated with passive tobacco smoke exposure. Solid epidemiological work connecting tobacco use with “the shortening of life span” began to appear in the medical literature in the 1950s, linking smoking with lung cancer and related conditions. In subsequent years, these developments led to significant curtailment of tobacco use. This monograph explores aspects of the intersection of tobacco with themes of behavioral incentives, religion, culture, literature, economics, and government over the past five centuries.

Tobacco Smoke Exposure Association With Lipid Profiles and Adiposity Among U.S. Adolescents

PurposeWe investigated the association between tobacco smoke exposure (TSE) as measured by serum cotinine and lipoprotein cholesterols and adiposity in adolescents. MethodsWe performed a secondary analysis of 1999–2012 National Health and Nutrition Examination Survey data including participants 12–19 years old. We examined TSE: unexposed (<.05 ng/mL), passively exposed (.05–2.99 ng/mL), and actively exposed (≥3 ng/mL); lipid profiles: total cholesterol, high-density lipoprotein cholesterol (HDL-C), non-HDL-C, low-density lipoprotein cholesterol (LDL-C), and triglycerides; and adiposity: body mass index z-score (BMIZ), waist circumference (WC), and waist-to-height ratio (WHtR). Covariates were age, sex, race/ethnicity, income, diet, and physical activity. Multiple regression models were used to assess the association between TSE and lipid profile variables separately, and then TSE and adiposity measures separately, adjusting for covariates. We performed logistic regression to examine the association of TSE with body mass index and WHtR classifications. ResultsOf the 11,550 participants, 41.7% were unexposed to tobacco smoke, 40.5% were passively exposed, and 17.8% were actively exposed. Compared with unexposed, participants with active TSE had lower total cholesterol, lower HDL-C, and higher triglycerides; higher BMIZ, higher WC, and higher WHtR; participants with passive TSE had lower HDL-C, higher total cholesterol, and higher LDL-C; higher BMIZ, higher WC, and higher WHtR. Participants actively exposed were at increased odds of being obese or WHtR ≥.65, and those passively exposed were at increased odds of being overweight, obese, or WHtR ≥.65. ConclusionsActive TSE and passive TSE are differentially associated with factors within the lipid profile and adiposity, independent of covariates. TSE prevention efforts should start as early as childhood and continue throughout adolescence and adulthood.

The effect of passive exposure to tobacco smoke on perioperative respiratory complications and the duration of recovery

The incidence of perioperative respiratory complications and postoperative care unit recovery time investigated in patients with passive tobacco smoke exposure according to the degree of exposure. Total 270 patients ranging in age from 18 to 60 years with the ASA physical status I or II exposed and not exposed to passive tobacco smoke received general anesthesia for various elective surgical operations evaluated for the study. Patients divided into two groups as exposed and non-exposed to passive tobacco smoke, those exposed to passive smoke are also divided into two groups according to the degree of exposure. Patients taken to the postoperative care unit (PACU) at the end of the operation and monitorized until Modified Aldrete's Scores became 9 and more. Respiratory complications evaluated and recorded in intraoperative and postoperative period. A total of 251 patients were enrolled; 63 (25.1%) patients had airway complications, 11 (4.4%) had complications intraoperatively and 52 (20.7%) patients had complications postoperatively. There has been found significant relation with passive tobacco smoke exposure and high incidences of perioperative and postoperative respiratory complications. The risk of cough, desaturation and hypersecretion complications were found to be increased depending on the degree of exposure. There was significant relation between the degree of passive smoke exposure and the duration of PACU stay. Passive tobacco smoke exposed general anesthesia receiving patients also regarding to the degree of exposure having high rates of perioperative respiratory complications and prolongation of PACU stays when compared with unexposed patients.