The importance of extinguishing secondhand smoke

Government policies have enormous influence on the health of nations. Arguably, this is illustrated most vividly with tobacco control. However, smoking continues to be a global problem and the major cause of preventable death. The countries with the highest per-capita smoking prevalence rates include (alphabetically) Bangladesh (20.9% of adults), Brazil (16.2% of adults), China (31.4% of adults), Germany (27.2% of adults), India (32.7% of men, 1.4% of women), Indonesia (34.5% of adults), Japan (43.3% of men and 12% of women), the Russian Federation (60.4% of men, 15.5% of women), Turkey (34.6%), and the United States(23.2%).1 Prevalence rates among younger people vary, but in the United States, 18.4% of youths still smoke.

Adverse effects of cigarette smoke on NO bioavailability : role of arginine metabolism and oxidative stress

Endothelial dysfunction is a hallmark of cardiovascular disease, and the l-arginine:NO pathway plays a critical role in determining endothelial function. Recent studies suggest that smoking, a well-recognized risk factor for vascular disease, may interfere with l-arginine and NO metabolism; however, this remains poorly characterized. Accordingly, we performed a series of complementary in vivo and in vitro studies to elucidate the mechanism by which cigarette smoke adversely affects endothelial function. In current smokers, plasma levels of asymmetrical dimethyl-arginine (ADMA) were 80% higher (P=0.01) than nonsmokers, whereas citrulline (17%; P<0.05) and N-hydroxy-l-arginine (34%; P<0.05) were significantly lower. Exposure to 10% cigarette smoke extract (CSE) significantly affected endothelial arginine metabolism with reductions in the intracellular content of citrulline (81%), N-hydroxy-l-arginine (57%), and arginine (23%), while increasing ADMA (129%). CSE significantly inhibited (38%) arginine uptake in conjunction with a 34% reduction in expression of the arginine transporter, CAT1. In conjunction with these studies, CSE significantly reduced the activity of eNOS and NO production by endothelial cells, while stimulating the production of reactive oxygen species. In conclusion, cigarette smoke adversely affects the endothelial l-arginine NO synthase pathway, resulting in reducing NO production and elevated oxidative stress. In conjunction, exposure to cigarette smoke increases ADMA concentration, the latter being a risk factor for cardiovascular disease.

Cigarette smoke-induced changes to alveolar macrophage phenotype and function are improved by treatment with procysteine

Defective efferocytosis may perpetuate inflammation in smokers with or without chronic obstructive pulmonary disease (COPD). Macrophages may phenotypically polarize to classically activated M1 (proinflammatory; regulation of antigen presentation) or alternatively activated M2 (poor antigen presentation; improved efferocytosis) markers. In bronchoalveolar lavage (BAL)–derived macrophages from control subjects and smoker/ex-smoker COPD subjects, we investigated M1 markers (antigen-presenting major histocompatibility complex [MHC] Classes I and II), complement receptors (CRs), the high-affinity Fc receptor involved with immunoglobulin binding for phagocytosis (Fc-gamma receptor, FcγR1), M2 markers (dendritic cell–specific intercellular adhesion molecule-grabbing nonintegrin [DC-SIGN] and arginase), and macrophage function (efferocytosis and proinflammatory cytokine production in response to LPS). The availability of glutathione (GSH) in BAL was assessed, because GSH is essential for both M1 function and efferocytosis. We used a murine model to investigate macrophage phenotype/function further in response to cigarette smoke. In lung tissue (disaggregated) and BAL, we investigated CRs, the available GSH, arginase, and efferocytosis. We further investigated the therapeutic effects of an oral administration of a GSH precursor, cysteine l-2-oxothiazolidine-4-carboxylic acid (procysteine). Significantly decreased efferocytosis, available GSH, and M1 antigen–presenting molecules were evident in both COPD groups, with increased DC-SIGN and production of proinflammatory cytokines. Increased CR-3 was evident in the current-smoker COPD group. In smoke-exposed mice, we found decreased efferocytosis (BAL and tissue) and available GSH, and increased arginase, CR-3, and CR-4. Treatment with procysteine significantly increased GSH, efferocytosis (BAL: control group, 26.2%; smoke-exposed group, 17.66%; procysteine + smoke-exposed group, 27.8%; tissue: control group, 35.9%; smoke-exposed group, 21.6%; procysteine + smoke-exposed group, 34.5%), and decreased CR-4 in lung tissue. Macrophages in COPD are of a mixed phenotype and function. The increased efferocytosis and availability of GSH in response to procysteine indicates that this treatment may be useful as adjunct therapy for improving macrophage function in COPD and in susceptible smokers.

Fabrication of superhydrophobic surfaces by smoke deposition and application in oil-water separation

 Utilizing the smoke emitted by discarded silicone combustion, a simple method of smoke deposition is presented for fabricating a superhydrophobic surface with outstanding water repellence, which exhibited a water contact angle of 164 ± 0.8° and a sliding angle of lower than 1°. In addition, the as-prepared surface possesses favourable heat, water impact and water immersion stabilities. Oil leakages seriously endanger both the environment and the social economy. By this simple smoke deposition method, a selective-wettability copper mesh has been fabricated to separate oil-water mixtures. The smoke-deposited mesh achieved a high separation efficiency of over 93% for various oils, and showed excellent reusability, maintaining a high separation efficiency over 10 cycles. The water repellence of the used mesh can be refreshed by recoating with silicone and smoke deposition. This work provides a new strategy to utilize discarded silicone to fabricate superhydrophobic surfaces and oil-water separation meshes.

Effects of exercise on the desire to smoke and physiological responses to temporary smoking abstinence: a crossover trial

RATIONALE: Exercise has been shown to attenuate cigarette cravings during temporary smoking abstinence; however, the mechanisms of action are not clearly understood. OBJECTIVES: The objectives of the study were to compare the effects of three exercise intensities on desire to smoke and explore potential neurobiological mediators of desire to smoke. METHODS: Following overnight abstinence, 40 participants (25 males, 18-59 years) completed three 15 min sessions of light-, moderate-, or vigorous-intensity exercise on a cycle ergometer in a randomized crossover design. Ratings of desire to smoke were self-reported pre- and post-exercise and heart rate variability was measured throughout. Saliva and blood were analyzed for cortisol and noradrenaline in a sub-sample. RESULTS: Exercise influenced desire to smoke (F [2, 91] = 7.94, p < 0.01), with reductions greatest immediately after vigorous exercise. There were also significant time x exercise intensity interaction effects for heart rate variability and plasma noradrenaline (F [8, 72] = 2.23, p = 0.03), with a bias in noradrenaline occurring between light and vigorous conditions (adjusted mean difference [SE] = 2850 ng/ml [592], p < 0.01) at 5 min post-exercise. There was no interaction of time x exercise intensity for plasma and salivary cortisol levels. CONCLUSIONS: These findings support the use of vigorous exercise to reduce cigarette cravings, showing potential alterations in a noradrenergic marker.

This continent of smoke

Another fire season looms, and chances are it will be severe. As it has been before. And probably will be again. This country’s relationship with fire is long and complex, but still little understood.

Family and carer smoking control programmes for reducing children's exposure to environmental tobacco smoke

BackgroundChildren's exposure to other people's cigarette smoke (environmental tobacco smoke, or ETS) is associated with a range of adverse health outcomes for children. Parental smoking is a common source of children's exposure to ETS. Older children are also at risk of exposure to ETS in child care or educational settings. Preventing exposure to cigarette smoke in infancy and childhood has significant potential to improve children's health worldwide.ObjectivesTo determine the effectiveness of interventions aiming to reduce exposure of children to ETS.Search methodsWe searched the Cochrane Tobacco Addiction Group Specialized Register and conducted additional searches of the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, PsycINFO, EMBASE, CINAHL, ERIC, and The Social Science Citation Index & Science Citation Index (Web of Knowledge). Date of the most recent search: September 2013.Selection criteriaControlled trials with or without random allocation. Interventions must have addressed participants (parents and other family members, child care workers and teachers) involved with the care and education of infants and young children (aged 0 to 12 years). All mechanisms for reduction of children's ETS exposure, and smoking prevention, cessation, and control programmes were included. These include health promotion, social-behavioural therapies, technology, education, and clinical interventions.Data collection and analysisTwo authors independently assessed studies and extracted data. Due to heterogeneity of methodologies and outcome measures, no summary measures were possible and results were synthesised narratively.Main resultsFifty-seven studies met the inclusion criteria. Seven studies were judged to be at low risk of bias, 27 studies were judged to have unclear overall risk of bias and 23 studies were judged to have high risk of bias. Seven interventions were targeted at populations or community settings, 23 studies were conducted in the 'well child' healthcare setting and 24 in the 'ill child' healthcare setting. Two further studies conducted in paediatric clinics did not make clear whether the visits were to well or ill children, and another included both well and ill child visits. Thirty-six studies were from North America, 14 were in other high income countries and seven studies were from low- or middle-income countries. In only 14 of the 57 studies was there a statistically significant intervention effect for child ETS exposure reduction. Of these 14 studies, six used objective measures of children's ETS exposure. Eight of the studies had a high risk of bias, four had unclear risk of bias and two had a low risk of bias. The studies showing a significant effect used a range of interventions: seven used intensive counselling or motivational interviewing; a further study used telephone counselling; one used a school-based strategy; one used picture books; two used educational home visits; one used brief intervention and one study did not describe the intervention. Of the 42 studies that did not show a significant reduction in child ETS exposure, 14 used more intensive counselling or motivational interviewing, nine used brief advice or counselling, six used feedback of a biological measure of children's ETS exposure, one used feedback of maternal cotinine, two used telephone smoking cessation advice or support, eight used educational home visits, one used group sessions, one used an information kit and letter, one used a booklet and no smoking sign, and one used a school-based policy and health promotion. In 32 of the 57 studies, there was reduction of ETS exposure for children in the study irrespective of assignment to intervention and comparison groups. One study did not aim to reduce children's tobacco smoke exposure, but rather aimed to reduce symptoms of asthma, and found a significant reduction in symptoms in the group exposed to motivational interviewing. We found little evidence of difference in effectiveness of interventions between the well infant, child respiratory illness, and other child illness settings as contexts for parental smoking cessation interventions.Authors' conclusionsWhile brief counselling interventions have been identified as successful for adults when delivered by physicians, this cannot be extrapolated to adults as parents in child health settings. Although several interventions, including parental education and counselling programmes, have been used to try to reduce children's tobacco smoke exposure, their effectiveness has not been clearly demonstrated. The review was unable to determine if any one intervention reduced parental smoking and child exposure more effectively than others, although seven studies were identified that reported motivational interviewing or intensive counselling provided in clinical settings was effective.

Preventing tobacco use and harm: what is evidence based policy?

The majority of tobacco users commence in early to mid-adolescence. Tobacco smoking can be characterised as a chronic, relapsing disorder. While risk increases with amount smoked, there is no safe level of use (i.e., all use is risky). Duration of use is the most important predictor of premature death with the majority of excess morbidity and mortality avoidable if people quit before middle age. Investment in initiatives that reduce smoking among pregnant women and those at risk of cardiovascular disease provide quickest returns -in reduced health care episodes and expenditure.  Measures that successfully reduce smoking among parents probably reduce smoking uptake by children, and high levels of smoking among both children and parents appear to be associated with higher levels of illicit drug use.
The evidence base for pharmcotherapies in the treatment of tobacco dependence is very strong. Population-level initiatives such as tax increases, mass media-led campaigns and smoke-free policies are all highly cost-effective in reducing population-smoking levels, including among children and young people.
Australian tobacco control initiatives have been based on "social ecology" conceptualisations of the problem, which acknowledge the pivotal role of the media in shaping social values, and public and political opinion.
Broad social change, as well as more focused prevention and cessation initiatives, has drawn heavily on research findings from the behavioural sciences. Considerable effort (mainly, in Australian, in the NGO sector) has gone into documenting policy inputs and monitoring impact and outcome measures.
This chapter discusses why conceptualising tobacco-related harm from legal, economic and social policy perspectives should also help build support for tobacco control policy among academic and practising economists and lawyers, and in the business, welfare and government sectors.

The narrative of evaluations: medically supervised injecting centers

Medically supervised injecting centers, or drug consumption rooms are officially sanctioned places where people can inject or smoke illegal drugs in hygienic conditions and under supervision. Their ostensible purposes are to protect the health of drug users and contain the nuisance potential of open drug markets. This article argues that the debates and arguments supporting the establishment and existence of medically supervised injecting centers follow four interweaving narratives. These narratives can be characterized as (1) Caring and humanitarian (2) Elimination of public nuisance (3) Governance of the drug-using subject (4) Neo-liberal, utilitarian, and bureaucratic. These narratives alternatively combine and oppose each other. This means that the analysis of the benefits and problems with such initiatives depends on the perspective of the actors involved and the claims made for their effectiveness.