Concept: Passive smoking
Exposure to secondhand smoke from burning tobacco products causes premature death and disease, including coronary heart disease, stroke, and lung cancer among nonsmoking adults and sudden infant death syndrome, acute respiratory infections, middle ear disease, exacerbated asthma, respiratory symptoms, and decreased lung function in children (1,2). The U.S. Surgeon General has concluded that there is no risk-free level of exposure to secondhand smoke (1). Previous CDC reports on airport smoke-free policies found that most large-hub airports in the United States prohibit smoking (3); however, the extent of smoke-free policies at airports globally has not been assessed. CDC assessed smoke-free policies at the world’s 50 busiest airports (airports with the highest number of passengers traveling through an airport in a year) as of August 2017; approximately 2.7 billion travelers pass through these 50 airports each year (4). Among these airports, 23 (46%) completely prohibit smoking indoors, including five of the 10 busiest airports. The remaining 27 airports continue to allow smoking in designated smoking areas. Designated or ventilated smoking areas can cause involuntary secondhand smoke exposure among nonsmoking travelers and airport employees. Smoke-free policies at the national, city, or airport authority levels can protect employees and travelers from secondhand smoke inside airports.
BACKGROUND: Successful cancer prevention policies and programming for youth must be based on a solid understanding of youth’s conceptualization of cancer and cancer prevention. Accordingly, a qualitative study examining youth’s perspectives of cancer and its prevention was undertaken. Not surprisingly, smoking (i.e., tobacco cigarette smoking) was one of the dominant lines of discourse in the youth’s narratives. This paper reports findings of how youth conceptualize smoking with attention to their perspectives on parental and family-related smoking issues and experiences. METHODS: Seventy-five Canadian youth ranging in age from 11–19 years participated in the study. Six of the 75 youth had a history of smoking and 29 had parents with a history of smoking. Youth were involved in traditional ethnographic methods of interviewing and photovoice. Data analysis involved multiple levels of analysis congruent with ethnography. RESULTS: Youth’s perspectives of parents and other family members' cigarette smoking around them was salient as represented by the theme: It’s not fair. Youth struggled to make sense of why parents would smoke around their children and perceived their smoking as an unjust act. The theme was supported by four subthemes: 1) parenting the parent about the dangers of smoking; 2) the good/bad parent; 3) distancing family relationships; and 4) the prisoner. Instead of being talked to about smoking it was more common for youth to share stories of talking to their parents about the dangers of smoking. Parents who did not smoke were seen by youth as the good parent, as opposed to the bad parent who smoked. Smoking was an agent that altered relationships with parents and other family members. Youth who lived in homes where they were exposed to cigarette smoke felt like a trapped prisoner. CONCLUSIONS: Further research is needed to investigate youth’s perceptions about parental cigarette smoking as well as possible linkages between youth exposed to second hand smoke in their home environment and emotional and lifestyle-related health difficulties. Results emphasize the relational impact of smoking when developing anti-tobacco and cancer prevention campaigns. Recognizing the potential toll that second-hand smoke can have on youth’s emotional well-being, health care professionals are encouraged to give youth positive messages in coping with their parents' smoking behaviour.
BACKGROUND: Despite efforts to reduce exposure to secondhand smoke (SHS), only 5% of the world’s population enjoy smoke-free restaurants and bars. METHODS: Lifetime excess risk (LER) of cancer death, ischaemic heart disease (IHD) death and asthma initiation among non-smoking restaurant and bar servers and patrons in Minnesota and the US were estimated using weighted field measurements of SHS constituents in Minnesota, existing data on tobacco use and multiple dose-response models. RESULTS: A continuous approach estimated a LER of lung cancer death (LCD) of 18×10(-6)(95% CI 13 to 23×10(-6)) for patrons visiting only designated non-smoking sections, 80×10(-6)(95% CI 66 to 95×10(-6)) for patrons visiting only smoking venues/sections and 802×10(-6)(95% CI 658 to 936×10(-6)) for servers in smoking-permitted venues. An attributable-risk (exposed/non-exposed) approach estimated a similar LER of LCD, a LER of IHD death about 10(-2) for non-smokers with average SHS exposure from all sources and a LER of asthma initiation about 5% for servers with SHS exposure at work only. These risks correspond to 214 LCDs and 3001 IHD deaths among the general non-smoking population and 1420 new asthma cases among non-smoking servers in the US each year due to SHS exposure in restaurants and bars alone. CONCLUSIONS: Health risks for patrons and servers from SHS exposure in restaurants and bars alone are well above the acceptable level. Restaurants and bars should be a priority for governments' effort to create smoke-free environments and should not be exempt from smoking bans.
Smoking cessation was examined among a subset of current smokers who were high-risk participants in the UK Lung Cancer Screening (UKLS) pilot trial of low-dose CT screening.
This study was performed to quantify the association between mortality and known and unknown second hand smoke (SHS) exposure as measured by cotinine levels in non-smokers.Data collected from 1999 to 2010 in the National Health and Nutrition Examination Survey (NHANES) were linked to the National Death Index. Self-reported non-smokers aged ≥ 20 years (N=20,175) were studied. Serum cotinine was measured at recruitment; non-smokers were those with cotinine below the reported race-specific cut-off points (5.92 ng/mL, 4.85 ng/mL, and 0.84 ng/mL for non-Hispanic blacks, non-Hispanic whites, and Mexican Americans, and 3.08 ng/mL for all other groups).Serum cotinine levels were significantly associated with overall survival (HRadj 1.17, 95% CI: 1.13-1.22 per natural-log unit change in cotinine), death for all medical causes, lung cancer, all cancers, and heart diseases, after adjustment for gender, race/ethnicity, body mass index (BMI), smoking history, and education. Similar results were observed when non-smokers reporting no SHS exposure at home or work were analyzed. There was a statistically significant trend in years of life lost, adjusted for confounders, across cotinine categories both in non-smokers (YLLadj: 5.8, 6.4, 6.9, 7.4; p for trend <0.0001) and non-smokers reporting no SHS exposure (YLL adj: 5.7, 6.2, 6.4, and 6.6; p for trend =0.03).Serum cotinine levels identify SHS-attributable mortality in subjects who would have otherwise been overlooked by questionnaire data, providing further evidence that the economic toll of SHS may be substantially higher than what was reported based on questionnaires.
Parental smoking is known to worsen asthma symptoms in children and make them refractory to asthma treatment, but the molecular mechanism is unclear. Recently, oxidative stress from tobacco smoke has been reported to impair histone deacetylase-2 (HDAC2) via phosphoinositide-3-kinase (PI3K)/Akt activation and thus to reduce corticosteroid sensitivity. The aim of this study is to investigate passive smoking dependent molecular abnormalities in alveolar macrophages by comparing passive smoke exposed children and non-passive smoke exposed children with uncontrolled severe asthma.
The present exploratory study examined the role of acculturation in the perception of the risks of smoking following a smoking cessation induction intervention among Latino caregivers of children with asthma. The sample consisted of 131 Latino smokers (72.9 % female; 18.3 % born in the U.S.) who were caregivers of a child with asthma. Caregivers were randomized to one of two smoking cessation interventions that were part of a home-based asthma program. Self-report measures of risk-perception were assessed at baseline, end of treatment (2 months after baseline), and 2- and 3-months post-treatment. At baseline, caregivers, regardless of level of acculturation, reported moderate to high levels of concern about the effects of secondhand smoke on their child’s health as well as perceived risk regarding the effect of smoking on their own health. However, caregivers who were low in acculturation had a greater increase in concern about the effects of smoking on their child from pre-to post treatment compared to those who were high in acculturation (p = .001). Lastly, level of acculturation moderated the association between caregivers' concern about smoking on their child’s health and their motivation to quit smoking (p < .05), but not cessation rates or reduced secondhand smoke exposure (p > .05). Specifically, motivation to quit at 3 months was greater for those with low acculturation. Though exploratory, these findings suggest that risk perception may be more easily influenced in low versus high acculturated populations and this should be considered in the design of clinical interventions and potentially mass media campaigns seeking to influence risk of caregiver behavior on child health with ethnic and racial minorities.
Secondhand smoke (SHS) in US casinos is common, but little is known about the residue of tobacco smoke pollutants left behind in dust and on surfaces, commonly referred to as thirdhand smoke (THS). We examined SHS and THS pollution and exposure before and during a casino smoking ban and after smoking resumed.
Objective To understand whether the impact of smoking on chronic rhinosinusitis (CRS) is reversible after smoking cessation. Study Design Cross-sectional study. Setting Academic tertiary care rhinology clinic. Subjects and Methods A total of 103 former-smoker CRS patients and 103 nonsmoker CRS patients were prospectively recruited. The primary outcome measure was sinonasal symptom severity measured with the 22-item Sinonasal Outcomes Test (SNOT-22), and secondary outcome measures were general health-related quality of life (QOL) measured with the 5-dimensional EuroQol visual analog scale (EQ-5D VAS) and patient-reported CRS-related antibiotic and oral corticosteroid usage in the past year. Outcome measures were compared between cohorts and checked for association with time since cessation of smoking for former smokers. Results Compared with nonsmokers, former smokers had worse SNOT-22 score ( P = .019) and EQ-5D VAS score ( P = .001) and reported using more CRS-related antibiotics ( P = .003) and oral corticosteroids in the past year ( P = .013). In former smokers, every year was associated with a statistically significant improvement in SNOT-22 score (β = -0.48; 95% CI, -0.91 to -0.05; P = .032), EQ-5D VAS score (β = 0.46; 95% CI, 0.02-0.91; P = .046), and CRS-related oral corticosteroid use (relative risk = 0.95; 95% CI, 0.91-0.98; P = .001). Given the differences in our study outcome measures between former smokers and nonsmokers, we estimate that the reversible impacts of smoking on CRS may resolve after 10 to 20 years. Conclusions CRS patients who are former smokers have worse sinonasal symptomatology, QOL, and CRS-related medication usage than nonsmokers. Every year since cessation of smoking is associated improvements in sinonasal symptomatology, QOL, and CRS-related oral corticosteroid use, potentially reaching nonsmoker levels after 10 to 20 years.
An increasing number of US states and localities have implemented comprehensive policies prohibiting tobacco smoking in all indoor areas of public places and worksites. However, private settings such as homes and vehicles remain a major source of exposure to secondhand smoke (SHS) for many people. This study assessed the prevalence and correlates of voluntary smoke-free rules and SHS exposure in homes and vehicles among US adults.