Dataset Information

The behavioral ecology of secondhand smoke exposure: A pathway to complete tobacco control.

ABSTRACT:

Introduction

This article outlines a theoretical framework for research concerning secondhand smoke exposure (SHSe) prevention as a means to curtail the tobacco industry.

Methods

The Behavioral Ecological Model (BEM) assumes interlocking social contingencies of reinforcement (i.e., rewards or punishments) from the highest level of society (e.g., taxing cigarette sales) to physiological reactions to nicotine that influence smoking and SHSe. We review selected research concerning both policy and clinical efforts to restrict smoking and/or SHSe.

Results

Research to date has focused on smoking cessation with modest to weak effects. The BEM and empirical evidence suggest that cultural contingencies of reinforcement should be emphasized to protect people from SHSe, especially vulnerable children, pregnant women, the ill, the elderly, and low-income adults who have not "elected" to smoke. Doing so will protect vulnerable populations from industry-produced SHSe and may yield more and longer-lasting cessation.

Conclusions

Interventions that reduce SHSe may serve as a Trojan horse to counter the tobacco industry. Future studies should: (a) guide policies to restrict SHSe; (b) develop powerful community and clinical interventions to reduce SHSe; (c) test the degree to which policies and other contexts enhance the effects of clinical interventions (e.g., media programs disclosing the disingenuous marketing by the industry); and (d) investigate the effects of all health care providers' ability to reduce SHSe and generate an antitobacco culture, by advising all clients to avoid starting to smoke, to protect their children from SHSe, and to quit smoking.

SUBMITTER: Hovell MF

PROVIDER: S-EPMC2782259 | biostudies-literature | 2009 Nov

REPOSITORIES: biostudies-literature

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Publications

The behavioral ecology of secondhand smoke exposure: A pathway to complete tobacco control.

Hovell Melbourne F MF Hughes Suzanne C SC

Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco 20090923 11

<h4>Introduction</h4>This article outlines a theoretical framework for research concerning secondhand smoke exposure (SHSe) prevention as a means to curtail the tobacco industry.<h4>Methods</h4>The Behavioral Ecological Model (BEM) assumes interlocking social contingencies of reinforcement (i.e., rewards or punishments) from the highest level of society (e.g., taxing cigarette sales) to physiological reactions to nicotine that influence smoking and SHSe. We review selected research concerning bo ...[more]

PMID: 19776346

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Project description:BackgroundAirports may represent significant sources of secondhand smoke (SHS) exposure for both travelers and employees. While previously common smoking rooms have largely disappeared from US airports, smoking continues to occur outdoors at terminal entrances. SHS may be especially high at arrival areas, since they oftentimes are partially enclosed by overhead departures, creating stagnant microenvironments. This study assessed particulate matter <2.5 microns in diameter (PM2.5), a common surrogate for SHS, at airport terminal locations to evaluate both outdoor exposure risk and possible indoor drift of SHS from outdoor sources.MethodsA convenience sample of nine airport terminal arrival areas in the US state of Florida was surveyed between February and July 2018. PM2.5 levels were assessed outdoors and indoors at terminal entrances and at control areas far into terminal interiors. We also examined the impact of smoking location on SHS exposure by correlating cigarette and passing vehicle counts with PM2.5 levels at terminals with contrasting proximity of designated smoking locations to terminal entrances.ResultsAlthough outdoor PM2.5 levels (mean 17.9, SD 6.1 µg/m3) were significantly higher than indoors (p < 0.001), there was no difference between indoor areas directly inside terminal entrances and areas much further interior (mean 8.8, SD 2.6 vs mean 8.5, SD 3.0 µg/m3, p=0.49). However, when smoking areas were in close proximity to terminal entrances, the number of lit cigarettes and vehicular traffic per minute predicted 70% of the variance of PM2.5 levels (p < 0.001), which was attributable mostly to the cigarette number (β = 0.83; 95% CI (0.55 to 1.11); p < 0.001). This effect was not observed at smoking areas further away.ConclusionPM2.5 data did not suggest indoor drift from outside smoking. Nevertheless, absolute exposure outdoors was high and correlated with the location of designated smoking areas. Further studies are needed to examine the effect of microclimate formation on exposure risk.

Project description:Importance:The World Health Organization estimates that the 1 billion individuals who smoke worldwide contribute to the 880 000 secondhand smoke (SHS)-related deaths among individuals who do not smoke each year. A better understanding of the scale of harm of SHS to those who do not smoke could increase awareness of the consequences of smoking and help to design measures to protect individuals who do not smoke, especially children. Objective:To calculate the number of individuals who smoke associated with the death of 1 individual who died of SHS exposure both on a global scale and in various World Bank regions. Design, Setting, and Participants:In this cross-sectional epidemiologic assessment, data from Our World in Data were used to tabulate the number of individuals who smoke in each country and number of premature deaths related to SHS in that country from 1990 to 2016. The mean number of cigarettes consumed in all countries was also included in analyses. Data were collected for the following World Bank regions: North America, Latin America and the Caribbean, Europe and Central Asia, the Middle East and North Africa, sub-Saharan Africa, South Asia, and East Asia and the Pacific from 1990 and 2016. Statistical analysis was conducted in July 2019. Exposure:Secondhand smoke. Main Outcomes and Measures:The pack-year index, calculated as the number of pack-years associated with the death of 1 individual who does not smoke but was exposed to SHS, and the SHS index, calculated as the number of individuals who smoked for 24 years (ie, the mean duration of smoking) associated with the death of 1 individual who does not smoke. Results:Globally, the SHS index changed favorably, from 31.3 (95% CI, 30.6-32.0) individuals who smoked associated with the death of 1 individual who did not smoke in 1990 to 52.3 (95% CI, 51.2-53.5) individuals who smoked in 2016. There was a wide regional variation in the 2016 secondhand smoke index, from 42.6 (95% CI, 41.6-43.5) individuals who smoked in the Middle East and North Africa to 85.7 (95% CI, 83.8-87.7) individuals who smoked in North America. Worldwide, the pack-year index also changed favorably from 751.9 (95% CI, 736.3-770.7) pack-years associated with 1 death in 1990 to 1255.9 (95% CI, 1227.2-1284.4) pack-years in 2016. Conclusions and Relevance:In this study, the substantial disparity among regions in both the SHS index and pack-year index reflected large differences in the scale of the harm of SHS on those who do not smoke. This information may help local policy makers implement measures to better protect those who do not smoke and increase public engagement. Although the number of pack-years and the number of individuals who smoke associated with the death of 1 individual who did not smoke favorably changed over the study period, as of 2016, 52.3 individuals who smoked were associated with the death of 1 individual who did not smoke.

Project description:Introduction:Cigarette smoking is inversely associated with DNA methylation of the aryl hydrocarbon receptor repressor (AHRR; cg05575921). However, the association between secondhand tobacco smoke (SHS) exposure and AHRR methylation is unknown. Methods:DNA methylation of AHRR cg05575921 in CD14+ monocyte samples, from 495 never-smokers and 411 former smokers (having quit smoking ?15 years) from the Multi-Ethnic Study of Atherosclerosis (MESA), was cross-sectionally compared with concomitantly ascertained self-reported SHS exposure, urine cotinine concentrations, and estimates of air pollutants at participants' homes. Linear regression was used to test for associations, and covariates included age, sex, race, education, study site, and previous smoking exposure (smoking status, time since quitting, and pack-years). Results:Recent indoor SHS exposure (hours per week) was inversely associated with cg05575921 methylation (? ± SE = -0.009 ± 0.003, p = .007). The inverse effect direction was consistent (but did not reach significance) in the majority of stratified analyses (by smoking status, sex, and race). Categorical analysis revealed high levels of recent SHS exposure (?10 hours per week) inversely associated with cg05575921 methylation (? ± SE = -0.28 ± 0.09, p = .003), which remained significant (p < .05) in the majority of stratified analyses. cg05575921 methylation did not significantly (p < .05) associate with low to moderate levels of recent SHS exposure (1-9 hours per week), urine cotinine concentrations, years spent living with people smoking, years spent indoors (not at home) with people smoking, or estimated levels of air pollutants. Conclusions:High levels of recent indoor SHS exposure may be inversely associated with DNA methylation of AHRR in human monocytes. Implications:DNA methylation is a biochemical alteration that can occur in response to cigarette smoking; however, little is known about the effect of SHS on human DNA methylation. In the present study, we evaluated the association between SHS exposure and DNA methylation in human monocytes, at a site (AHRR cg05575921) known to have methylation inversely associated with current and former cigarette smoking compared to never smoking. Results from this study suggest high levels of recent SHS exposure inversely associate with DNA methylation of AHRR cg05575921 in monocytes from nonsmokers, albeit with weaker effects than active cigarette smoking.

Dataset Information

The behavioral ecology of secondhand smoke exposure: A pathway to complete tobacco control.

Introduction

Methods

Results

Conclusions

Publications

The behavioral ecology of secondhand smoke exposure: A pathway to complete tobacco control.

Similar Datasets

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