Impact of declining exposure to secondhand tobacco smoke in public places to decreasing smoking-related cancer mortality in the US population.
ABSTRACT: BACKGROUND:The major decrease in exposure to secondhand smoke (SHS) in public places in recent decades could have contributed to the decline in smoking-related cancer mortality observed in the US population. METHODS:Prospective study among 11,856 non-smoking adults aged ?40?years who participated in NHANES 1988-1994 or 1999-2004 and were followed for mortality through 2006. We estimated the amount of change in cancer mortality over time attributed to the intermediate pathway of changes in SHS exposure in public places, after adjustment for risk factors and SHS exposure at home. RESULTS:The adjusted smoking-related cancer mortality rate ratios (95% CI) for a two-fold increase in serum cotinine and a 1-hour increase in occupational SHS exposure time were 1.10 (1.03, 1.17) and 1.14 (1.06, 1.24) for all-cancer, and 1.13 (1.03, 1.24) and 1.14 (1.02, 1.26) for smoking-related cancer, respectively. The absolute reduction in mortality comparing 1999-2004 to 1988-1994 was 75.8 (-25.5, 177.0) and 77.0 (2.6, 151.4) deaths/100,000 person-years, for all-cancer and smoking-related cancer, respectively. Among these avoided all-cancer deaths, 45.8 (2.8, 89.5) and 18.1 (-1.2, 39.6)/100,000 person-year were attributable to changes in serum cotinine concentrations and occupational SHS exposure time, respectively. The corresponding numbers of smoking-related cancer avoided deaths were 36.4 (0.7, 72.8) and 9.9 (-3.8, 24.9)/100,000?person-year. CONCLUSIONS:Declines in SHS exposure were associated with reductions in all-cancer and smoking-related cancer mortality, supporting that smoking bans in public places may have reduced cancer mortality among non-smoking adults.
Project description:INTRODUCTION:We report on second-hand smoke (SHS) exposure based on saliva cotinine levels among children in Bangladesh-a country with laws against smoking in public places. METHODS:A survey of primary school children from two areas of the Dhaka district was conducted in 2015. Participants completed a questionnaire and provided saliva samples for cotinine measurement to assess SHS exposure with a cut-off range of ?0.1ng/mL. RESULTS:Four hundred and eighty-one children studying in year-5 were recruited from 12 primary schools. Of these, 479 saliva samples were found sufficient for cotinine testing, of which 95% (453/479) were positive for recent SHS exposure. Geometric mean cotinine was 0.36 (95% CI = 0.32 to 0.40); 43% (208/479) of children lived with at least one smoker in the household. Only 21% (100/479) reported complete smoking restrictions for residents and visitors; 87% (419/479) also reported being recently exposed to SHS in public spaces. Living with a smoker and number of tobacco selling shops in the neighborhood had positive associations with recent SHS exposure. CONCLUSIONS:Despite having a ban on smoking in public places, recent SHS exposure among children in Bangladesh remains very high. There is an urgent need to reduce exposure to SHS in Bangladeshi children. IMPLICATIONS:Children bear the biggest burden of disease due to SHS exposure than any other age group. However, children living in many high-income countries have had a sharp decline in their exposure to SHS in recent years. What remains unknown is if children living in low-income countries are still exposed to SHS. Our study suggests that despite having a ban on smoking in public places, most primary school children in Dhaka, Bangladesh are still likely to be exposed to SHS.
Project description:<h4>Background</h4>The association between smoking and suicide is still controversial, particular for early life cigarette smoking exposure. Few studies have investigated this association in adolescents using population-based cohorts, and the relationship with second hand smoking (SHS) exposure has not been addressed.<h4>Methods and findings</h4>In this study, we followed a large population-based sample of younger people to investigate the association between smoking, SHS exposure and suicide mortality. Between October 1995 and June 1996, 162,682 junior high school students ages 11 to 16 years old living in a geographic catchment area in Taiwan were enrolled and then followed till December 2007 (1,948,432 person-years) through linkage to the National Death Certification System. Participants who were currently smoking at baseline had a greater than six-fold higher suicide mortality than those who did not smoke (29.5 vs. 4.8 per 100,000 person-years, p<0.001) as well as higher natural mortality (33.7 vs. 10.3 per 100,000 person-years, p<0.001). After controlling for gender, age, parental education, asthma, allergic rhinitis, and alcohol consumption, the adjusted hazard ratios for suicide were 3.69 (95% CI 1.85-7.39) in current smokers, and 1.47 (95% CI 0.94-2.30) and 2.83 (95% CI 1.54-5.20) respectively in adolescents exposed to SHS of 1-20 cigarettes and >20 cigarettes/per day. The estimated depression-adjusted odds ratio did not change substantially. The population attributable fractions for suicide associated with smoking and heavy SHS exposure (>20 cigarettes/per day) were 9.6% and 10.6%, respectively.<h4>Conclusions</h4>This study showed evidence of excess suicide mortality among young adults exposed to active or passive early life cigarette smoking.
Project description:To investigate the link between smoking exposure, telomere length and mortality, with emphasis on second-hand smoke (SHS) exposure and the duration of smoking cessation.A total of 1,018 participants died during follow-up (mean: 10.3 years). A 50 base-pair decrease in LTL was shown among cotinine-confirmed current versus never smokers. The 90th quantile of LTL decreased with increasing cotinine among never smokers, indicating a role of SHS. Longer telomeres with smoking cessation were indicated but limited to a 3-16 year period of abstaining smoking. When assessing mortality, we observed a lower risk of all-cause death for the second quintile compared to the first among never smokers (HR: 0.67, 95% CI: 0.52-0.87), and a higher risk was found among current smokers (HR: 1.89, 1.19-2.92).We studied 6,456 nationally representative U.S. respondents with mortality follow-up through to 31 December 2011. Smoking status was assessed by interviews and cotinine levels. Relative leukocyte telomere length (LTL) was quantified by polymerase chain reaction (PCR). Multivariable linear regression was performed to examine LTL by smoking exposure, adjusted for age, sex, race/ethnicity, socioeconomic status, education, body mass index, alcohol consumption, and physical activity. We further estimated the association of LTL with cotinine levels using quantile regression, and with smoking cessation dynamics. Cox regression was used to estimate mortality by smoking status and LTL.Our findings indicated a complex association between smoking, telomere length, and mortality. LTL alterations with SHS and smoking cessation warrant further investigation for translation to public health measures.
Project description:Secondhand smoke (SHS) exposure is associated with elevated CHD risks. Yet the pathways through which this may operate have not been investigated in epidemiologic studies with objective SHS exposure measures and a wide range of CHD risk factors associated with active smoking. Therefore we investigate associations between SHS exposure and CHD risk factors, to clarify how SHS exposure may raise risk of CHD.Cross-sectional population-based study of 5029 men and women aged 59-80 years from primary care practices in Great Britain. Smoking, behavioural and demographic information was reported in questionnaires; nurses made physical measurements and took blood samples for analysis of serum cotinine and markers of inflammation, hemostasis and endothelial dysfunction.Active cigarette smokers had lower albumin and higher triglycerides, CRP, IL-6, white cell count, fibrinogen, blood viscosity, factor VIII, VWF and t-PA than non-smokers. Among non-smokers, serum cotinine levels were independently positively associated with CRP, fibrinogen, factor VIII, VWF and t-PA and inversely associated with albumin, after adjustment for age, gender, social and behavioural factors. The differences in CRP, fibrinogen and albumin between cotinine < or =0.05 and >0.7 ng/ml were one-third to one half the size of differences between cotinine < or =0.05 ng/ml and current smokers, but were of similar magnitude for VWF and t-PA.Endothelial, inflammatory and haemostatic markers related to CHD risk showed independent associations with SHS exposure in the same direction as those for active smoking. Results aid understanding of the associations between SHS exposure and elevated CHD risks.
Project description:Pregnant women often underreport their smoking status and extent of secondhand smoke (SHS) exposure. Biomarker confirmation is the recommended method to assess smoking behaviors and SHS exposure in both mothers and infants.The primary aims are to (a) examine the relationship between smoking behaviors and SHS exposure in mother-baby couplets using maternal and infant hair nicotine and maternal urine cotinine analyses and (b) determine whether there is an association between maternal and infant hair nicotine samples obtained shortly after birth.A cross-sectional study with a multiethnic sample of 210 mother-baby couplets assessing SHS exposure.The level of maternal hair nicotine (MHN) was significantly different among three groups: nonsmoking, nonsmoking/passive exposed, and smoking (p < .0001), with nonsmoking and nonexposed women having the lowest level. Urine cotinine was strongly associated with self-reported smoking status (rho = .88; p < .0001). Maternal and infant hair nicotine were correlated, although MHN correlated more strongly with smoking status (rho = .46, p < .0001) than infant hair nicotine (rho = .39, p < .0001).MHN was a more precise biomarker of prenatal SHS exposure than infant hair nicotine; mothers' urine cotinine was strongly correlated with self-reported smoking status.
Project description:: No study has reported the relationship between secondhand smoke (SHS) exposure and hypertension in self-reported never-smokers verified by nicotine metabolite. The aim of this study is to determine the relationship between SHS exposure and hypertension in self-reported and cotinine-verified never-smokers. A total of 106,268 self-reported never-smokers, verified as nonsmokers by urinary cotinine, who participated in Kangbuk Samsung Cohort study (KSCS) between 2012 and 2016 were included. Cotinine-verified nonsmokers were defined as individuals having urinary cotinine <50 ng/mL. SHS exposure was defined as current exposure to passive smoke indoors at home or the workplace. The multivariate regression model revealed that SHS exposure was associated with hypertension (odds ratio (OR) (95% confidence interval (CI)), 1.16 (1.08, 1.24)). Current SHS exposure that has been exposed to home SHS (1.22 (1.11, 1.33)) as well as current SHS exposure only at the workplace (1.15 (1.02, 1.29)) significantly increased the ORs for hypertension compared to no SHS exposure. There was no significant gender interaction for the relationships between SHS exposure and hypertension. This study showed that SHS exposure was significantly associated with hypertension in self-reported never-smokers verified as nonsmokers by urinary cotinine, suggesting necessity of health program and stricter smoking regulation to reduce the risk of hypertension.
Project description: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 (? = 0.24) and younger child age (3-5 years) (? = 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.
Project description:Smoking is the leading preventable disease worldwide and passive smoking is estimated to be the cause of about 1.0% of worldwide mortality. The determination of tobacco smoke biomarkers in human biological matrices is key to assess the health effects related to the exposure to environmental tobacco smoke. The biomonitoring of cotinine, the main nicotine metabolite, in human biofluids-including urine, serum or saliva-has been extensively used to assess this exposure. However, the simultaneous determination of cotinine together with other tobacco biomarkers and the selection of alternative biological matrices, such as hair, skin or exhaled breath, would enable a better characterization of the kind and extent of tobacco exposure. This review aims to perform a critical analysis of the up-to-date literature focused on the simultaneous determination of multiple tobacco smoke biomarkers studied in different biological matrices, due to the exposure to secondhand smoke (SHS) and thirdhand smoke (THS). Target biomarkers included both tobacco-specific biomarkers-nicotine and tobacco specific nitrosamine biomarkers-and tobacco-related biomarkers, such as those from polycyclic aromatic hydrocarbons, volatile organic compounds, metals and carbon monoxide. To conclude, we discuss the suitability of determining multiple biomarkers through several relevant examples of SHS and THS exposure.
Project description:<h4>INTRODUCTION</h4> Adolescents are at increased risk of secondhand smoke exposure (SHS) due to the limited control that they have over social and physical environments. Yet, knowledge regarding determinants of SHS among non-smoking adolescents is limited. This study identifies social and environmental factors associated with SHS among non-smoking adolescents. <h4>METHODS</h4> To be included, parents and adolescents (aged 11–17 years) of the Adolescents, Place, and Behavior Study had to have completed surveys between March 2019 and May 2020. Adolescents had to have not reported smoking within the past 30 days and provided a saliva sample assayed for cotinine (?3 ng/mL). A series of stepwise linear regression models were fit to the data to identify social and environmental determinants of SHS, using log-transformed salivary cotinine. <h4>RESULTS</h4> Of the 105 adolescent and parent dyads included, 90.3% were African American, 26.9% of parents reported smoking, 33.3% resided in multi-unit housing, and 67.7% lived in homes where smoking was not permitted. Significant associations were found between parent tobacco use (?=2.56, SE=0.98, p=0.0082) and residing in multi-unit housing (?=1.72, SE=0.86, p=0.0460) with increased log-transformed cotinine levels among non-smoking adolescents. Adolescent age, gender, and race/ ethnicity, parental education, peer tobacco use, the number of adults and children in the home, average number of days of self-reported SHS within public spaces outside of the home, and home smoking policies were not significantly associated with cotinine. <h4>CONCLUSIONS</h4> Results emphasize the importance of reducing secondhand smoke exposure by reducing parental smoking and altering exposures within social and home environments. Parental tobacco use and residential setting should be considered when developing interventions to reduce secondhand smoke exposure among non-smoking adolescents.