Adjusted time variant analysis of second-handsmoke ex- posure showed that those reporting increased second- handsmokeexposure had increased risks for the development of doctor-diagnosed asthma, chronic bron- chitis and increased asthma symptom score, reaching con- ventional levels of significance from ECRHS II-III as well as from ECRHS I-III overall (Fig. 2). However, compared to those not exposed on both occasions there was no evi- dence that those reporting exposure on both occasions had an increased risk of asthma or chronic bronchitis. However, asthma score did increase in this group com- pared to the non-exposed. An increased risk of nocturnal dyspnoea was observed only for those reporting increased second-handsmokeexposure between the first and the third survey but not for those exposed at both surveys.
Abstract This survey sought to measure the respiratory health effects and the prevalence of second-handsmokeexposure among school children. A sample of 370 parents selected from primary health care centres in Zarqa governorate, Jordan. International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire was used to gather the data. Descriptive statistics, Person correlation coefficient, and Pearson Chi-Square were used to analyse the data. The prevalence of “at home” exposure was 3.82 hours/day. The main location for exposure was at home (22.1%), with the homes of others (17.3%) and the in vehicle exposure (14.3%) being the next two most commonly cited indoor locations. A significant association was found between exposure to second-handsmoke at home, indoors-other, in vehicles, and in the restaurants and other recreational areas, and asthma and rhinitis symptoms. The number of rooms and people per room, parents’ educational achievement were also associated with respiratory symptoms of children. These results shed light on the importance to protect children from the harm of smoking and to carry out home smoke free policy.
Ending preventable stillbirth in every country by 2030 is one of the targets of sustainable development goals (SDG). 6,7 . Secondhandsmokeexposure is being recognized globally as a threat to intrauterine life. But the impact is less clear than the impact of direct smoking. Most of the evidence on SHS exposure during pregnancy is from developed countries. In many developing countries there are not many well conducted studies to assess the effect on the foetus. In most of the South East Asian countries including India, the prevalence of smoking among women is low, where as smoking among men in high. These women live in environment, home, workplace, public places etc. where they are subjected to high rates of SHS exposure. But evidence from In India is little. Not many well conducted studies are available from India.
In general, the presence of asthma in the family or of respiratory symptoms in the children did not increase parental motivation for participation in the study, neither did the offering of incentives. At the time the PREPASE study started (2010), the Dutch ban on smok- ing in public places was already in effect. Although the reported prevalence of SHS in Dutch children decreased further since the smoking ban, a considerable amount of children were still exposed to SHS, especially in the group of low-social economic status and heavy smokers . The media attention and social pressure since the smoking ban in public places might have motivated par- ents to participate in a study like PREPASE in order to receive support to stop SHS exposure in their children. In contrast, the media attention could have also made parents more reluctant to participate in the study due to perhaps feelings of guilt, shame or fear of being criti- cized. In our experience the last may have played a greater role. Stigmatisation of smokers is a well-known phenomenon in the literature . Some parents reacted very aggressively towards our project team during the telephone contacts regarding SHS in children and others have reported in questionnaires that they were not smokers, yet the questionnaires had the odour of to- bacco. Furthermore, the home was probably for parents who did not want to quit smoking their ‘only safe haven’ , where they were not waiting for outsiders to educate them about smoking in their own house. Probably, this was also the reason why significantly more parents who exposed their children to SHS reported to find an inter- net program effective for parental education and preven- tion of SHS in children, compared to the parents of children without SHS exposure. Moreover, motivational interviewing at home and a group program in the neigh- bourhood were less mentioned as effective measures against SHS in these parents compared to the parents of children without SHS exposure, which may be for the same reason.
study included hospitals, high schools, pubs, and restau- rants. Sampling locations were selected to represent the areas where people frequently work or occupy. Secondhandsmoke was estimated by sampling of vapor-phase nicotine using an air pump (model HB3344-02 Tuff Personal Air Sampling, produced by Casella Cell, Badford, UK) coupled with an impinger (Pyrex glass Midget Impinger, from SKC Ltd, Dorset, UK) filled with 15 mL solvent (usually acetonitrile) for extraction/desolvation of nicotine from pumped air. The pump was set up to pump at a flow of 800 mL/min, for 15 minutes. Each buil- ding selected for this survey was monitored randomly at
We identified all comparative epidemiological studies (case–control, cross-sectional, cohort designs) assessing the association between SHS exposure and the risk of in- vasive meningococcal disease in children (aged < 18 years) through a comprehensive search of three elec- tronic databases (Medline, Embase, and PsychINFO, searched to June 2012), by scanning reference lists of the included studies, and using the CAB Abstracts database (June 2012) to identify relevant conference abstracts. Case reports, case series and grey data were not included. The following search terms were used to iden- tify studies (where ‘mp’ indicates the text was searched for in the abstract, titles, original titles, broad terms, and heading words; ‘/’ indicates MeSH terms, ‘exp’ indicates explosion of MeSH terms): tobacco.mp; cigarette smoke. mp; smoker.mp; smoking.mp; cigar.mp; exp tobacco/; exp tobacco dependence/; exp tobacco smoke/; exp cigarette smoke/; exp cigarette smoking/; exp smoking/; exp smoke/; exp "smoking and smoking related pheno- mena"/; exp adolescent smoking/; exp parental smoking/; exp passive smoking/; exp smoking habit/; exp smoking cessation/; exp Crowding/; exp tobacco smoke pollution/; secondhand smoke.mp; meningitis.mp; septicaemia.mp; meninges.mp; bacterial meningitis.mp; viral meningitis. mp; fungal meningitis.mp; cryptococcal meningitis.mp; exp meningioma/; exp meningism/; exp meningitis/; exp central nervous system infection/; exp meninx disorder/; exp nervous system inflammation/; exp arachnoiditis/; exp aseptic meningitis/; exp bacterial meningitis/; exp epi- demic meningitis/; exp fungal meningitis/; exp group b streptococcal meningitis/; exp haemophilus meningitis/; exp lymphocytic choriomeningitis/; exp meningoence- phalitis/; exp pneumococcal meningitis/; exp primary
Confounding or mediator variables in smoking-related studies are usually controlled by multivariate linear re- gression or logistic regression depending on the object- ive of the study [14, 15]. Mediation analysis is a statistical procedure to examine any possible mediating variables. A mediation effect occurs when a third vari- able carries the influence of a given independent variable on a given dependent variable. We hypothesized that al- cohol drinking acts as a mediator in the relationship be- tween workplace smoking prevalence and SHS exposure. Therefore, we used mediation analysis to clarify the process underlying the relationship between smoking and SHS exposure and the extent to which this relation- ship is mediated by alcohol use.
Because a wide variety of diseases associated with smoking may be classified as age-related, ageing has emerged as in important comparative measure of health outcomes with regards to smoking and SHS exposure. Telomeres are nucleoprotein complexes that localize at the ends of eukaryotic chromosomes and perform functions for chromosomal protection, integration and replication . Due to the end-replication problem, each somatic mitotic division results in the loss of telomeric repeats by 30 to 200 base pairs, leading to gradual telomere shortening . Thus, telomere length can be used as a standard biomarker for cellular aging. Chronic exposure to biological insults such as oxidative stress may result in significantly shortened telomeres which in turn leads to cellular senescence and apoptosis [7, 8].
Four studies were RCTs [22–25] and two were before- and-after studies without a control group [17, 26]. Two studies were from high income countries [22, 24]. The sample size ranged from 45 to 758. Only one study in- cluded non-smoking pregnant women . All studies recruited the study participants from antenatal clinics (ANC). One study included non-pregnant women at- tending paediatric clinics (only data for pregnant women were included in this review) . Two studies used the Health Belief Model (HBM) [17, 23], two used the Transtheoretical Model (TTM) [24, 26], one used an In- tegrated Behavioural Intervention  and one used the Theory of Reasoned Action (TRA) . The interven- tions were in a variety of formats ranging from advice from doctors, a telephone hot-line, one-to-one consult- ation, motivational interviews, video, role play, informa- tion booklet and accessory articles such bibs and hangers with reminder messages about the harms of SHS. In one study, the intervention was delivered at home , the others were delivered in hospital clinics. Two studies [22, 26] reported objective measures for SHS exposure, but only El-Mohandes  used these data in the analyses. Karatay et al.  used this
Professional nurses could bene ﬁ t from the ﬁ ndings of the current study. Nurses can increase the patient`s awareness of the harmful effects of exposure to SHS on their health. Increasing awareness of the community will encourage them to prohibit smoking in their houses and to avoid it in other places. Moreover, one of the nursing roles is to implement a recurrent assessment of exposure to SHS in each visit. The AHA (2019) also recommended that clin- icians should advise patients to avoid SHS exposure in homes, vehicles, public places, and workplaces. 24 In light of the current study, it is essential to include SHS exposure in the nursing curriculum for university students, as guide- lines for health promotion and primary prevention. Practical training should be provided too, to present a proper assessment, counseling, and health education. Also, the policymakers should activate community-based comprehensive policies, to prohibit exposure to SHS and to maintain a smoke-free environment. This could be achieved by applying smoking penalties in all public places, and continuous monitoring to ensure the imple- mentation and compliance of smoking bans. A Literature review paper concluded that the toxic elements of SHS are responsible for signi ﬁ cant cardiovascular morbidity and mortality. Consequently, the vital goal at a societal level must be zero SHS exposure through legislative efforts resulting in 100% smoke-free policies in workplaces and public spaces. Informed individuals and groups can further encourage these efforts in their own settings by eliminat- ing all forms of SHS exposure. 25
The perceived inability to recruit smoking parents was unexpected since our previous experience was that many clients who were invited to take part and who attended the centres were regular smokers. Better-funded statutory bodies or recruiting participants directly may ameliorate these issues. The challenge in recruiting community “champions” is an important message for future studies and suggests that specific staff dedicated to smoke-free homes interventions are required rather than seeing this as an ‘add-on’ to the already high workload of support staff or support workers dealing with parents in deprived settings. Contacting potential partner organisations further in advance than the timeline of this study permitted, or providing them with financial compensation for engaging in the intervention programme, may improve participation rates.
Birth weight is the most important determinant for the survival, health, growth and development of an infant. Low birth weight (LBW) is associated with fetal and neonatal mortality and morbidity, inhibited growth and cognitive development, and risk of chronic diseases in later life (6). There are many factors related to LBW, including socio-demographic factors, genetic and constitutional factors, nutrition, maternal morbidity, toxic exposures, obstetric factors and prenatal care. Smoke is considered a toxic agent to the fetus during pregnancy and an established, important and independent risk factor for LBW. Although the level of tobacco smokeexposure is lower in SHS exposure than in active smoking, the potential for biologic action is expected to be similar (7). The risk estimates for SHS exposure and LBW have generally been small, which is consistent with the expectation that exposure to SHS produces a smaller effect than exposure to active smoking. Most studies have shown a reduction in the mean birth weight and an increased risk for LBW among infants whose mothers were exposed to SHS (8,9). The mean birth weight of babies born to mothers exposed to SHS was 138 grams less than that of babies in non-exposed groups. Exposed women also had a significantly higher risk of having babies that were small for their gestational age (10). Furthermore, SHS also has adverse effects on other pregnancy outcomes such as spontaneous abortion, pre- term delivery, and small-for-gestation infant (10). Although an association between SHS exposure and birth weight has been established, most of the evidence was drawn from studies conducted in western and developed countries. In developing countries such as Malaysia, with higher smoking rates and poorer environmental conditions, particularly housing ventilation, the health effects of SHS exposure may be more pronounced. Many women are involuntarily exposed to SHS because the majority of smokers in Malaysia are males and the subsequent health implications apply not only to fetuses but also to women themselves. Furthermore, exposure to SHS can be prevented. Findings from this study should help increase awareness among physicians and patients about the importance of avoiding SHS exposure, particularly to those who are already at higher risk of poorer pregnancy outcomes.
Second-handsmoke is associated with morbidity and mortality for both adults and children. A 2004 global study with data from 192 countries revealed that more than 600,000 deaths which represent 1% of worldwide mortality, and more than ten million disability-adjusted life-years worldwide were due to second-handsmokeexposure (Oberg, Jaakkola, Woodward, Peruga, & Pruss-Ustun, 2011). There is a secular trend of increasing smoke-free homes. From 1992 to 2003 in the United States of America even children living with at least one smoker are increasingly likely to live in smoke-free homes (Anon, 2007) with an increase from 10% to 32% among households with at least one smoker and from 57% to 83% among households with no smoker. In Scotland the smoke-free legislation reduced second-handsmokeexposure in children (P. Akhtar, Currie, Currie, & Haw, 2007) despite responses that it did not affect smoking in the home
induced incidence or prevalence of diseases, has the ad- vantage that impacts can easily be aggregated across dif- ferent diseases. To indicate an impact from exposure to tobacco smoking, healthcare costs have to differ signifi- cantly, which is a more conservative approach than relying on a diagnostic label alone. Given that active smoking significantly increases the risk of age-related diseases such as heart and cardiovascular disease or can- cer, one cannot expect comparable cost impacts of second-handsmoke on children with a mean age of 10 years. As the correlation between health problems and secondhandsmokeexposure in childhood is not trivial and still not completely understood, the excess cost approach is a possibility to capture all the diffe- rences between the analysed groups, but it does not allow for interpretation of causal pathways. The excess cost approach used in this study is aimed at identifying all excess healthcare utilisation due to either the condi- tion under research itself (in this case smokeexposure) or any other disorder related to this condition, i.e. its consequences on health status. Thus, estimating the ex- cess costs of exposure to secondhand tobacco smoke in a data set comprising current utilisation of health care could potentially permit one to assess the total impact of this exposure on costs of care.
Additionally, a significant increase in HIF-1α levels is observed in 1-day-SHS exposed mice compared to 1-day room air control (p < 0.05). Moreover, after 14 days of SHS exposure, there is even more significant (p < 0.05) change in HIF-1α as compared to 14-day room air con- trols. Data suggests that HIF-1α may be elevated to con- trol the acute response to SHS exposure. Previous studies have shown that HIF-1α is degraded via the ubiquitin-proteasome system . We also observed a significant increase in HIF1-α levels in Beas2b cells upon proteasome inhibition using MG-132, which was re- stored by treatment with an autophagy-inducing drug, cysteamine (Fig. 2a, b, p < 0.05), indicating that HIF-1α levels could be modulated by proteostasis/autophagy im- pairment. Overall, these findings suggest that even acute exposure to SHS during pregnancy (14 days; day 1
Results: Untreated new patients with a histologically confirmed diagnosis of first primary SCC of the UADT (defined as cancer of the oral cavity, the oropharynx, the hypopharynx, and the larynx) were recruited. Patients seen at The University of Texas Medical Branch (UTMB) Head and Neck oncology clinic from 1988 to 1996 were considered as cases in this study. One hundred and thirty-five patients were enrolled in the study. The median follow-up time for the sample was 54 months (3.92 years). Complete records were achieved for 92% of patients, thus 124 patients were included in the final analysis. SHS significantly correlated with recurrence and recurrence-free survival. The rate of recurrence was 46% in the group exposed to SHS and 22% in the non-exposed group. Based on multivariate binary logistic regression analysis, SHS exposure was detected as a significant independent predictor for recurrence (HR = 3.00 [95% CI 1.18 – 7.63]). Kaplan-Meier analysis demonstrated that patients who were not exposed to SHS had a statistically significant longer recurrence-free survival (log-rank P = 0.029). The mean survival for non SHS-exposed patients was 76 [63 – 89] months versus 54 [45 – 63] months for those exposed to SHS.
Outcomes are more reliable if they are objective. Most studies in this review used self-reported smoking behav- iours and knowledge as outcomes. Without an objective measure, it is not possible to know if changes in know- ledge and husbands/partners ’ smoking behaviour actually reduce SHS exposure and improve pregnancy outcomes. For example, SHS exposure from other family members and visitors may persist. Only one study  reported objective outcome measures, such as cotinine levels in urine and saliva or health outcomes. The review by Tong et al. also reported a paucity of literature with objectively measure outcomes and recommended using the bio- chemical measures to reduce the biases . However, whilst biochemical markers are more robust measure of recent smoking behaviour, they are expensive to assess. More research is required to evaluate the feasibility and effectiveness of the biochemical markers.
Beyond the scientific arguments, there are also conceptual justifications for legislative banning of smoking in public places mainly related with public policy issue. For instance, Chapman, Borland, Scollo, Brownson, Dominello & Wood- ward (1999) argued that reducing exposure to second-hand tobacco smoke ben- efits health in many ways, such as by significantly reducing tobacco consump- tion and by reducing the likelihood that young people will progress to estab- lished smoking. Thus, legislative restriction of smoking at public places are justi- fied to save vulnerable children who simply follow smokers at their environment and to reduce the frequency of smokers enabling them quitting smoking for good (Ibid). As the public supports attempts to reduce adolescent smoking and exposure to SHS, children are vulnerable groups of society who always attempt to replicate what they perceive at their compound. Among children exposed SHS tobacco smoke, there is a 50% - 100% higher risk of acute respiratory illness, higher incidence of ear infections and an increased likelihood of developmental disabilities and behavioral problems (WHO Report, 2009). Globally, over 165,000 children die every year from lower respiratory infections, middle ear infections, and asthma caused by SHS (Ibid). To be sure, a question of banning smoking in public places is not hardly challenged in terms of schools, day care centers, and transportation facilities who mostly host the vulnerable groups of society.
function we observed in male mice, we conducted RNA sequencing on lung tissue. This analysis was conducted only on male mice to identify the expression of key genes dysregulated by the in utero SHS exposure, since only male mice exhibited both structural and functional changes. Figure 4 shows that in utero SHS exposure in male mice dysregulated the expression of 33 lung genes, with 21 genes being down-regulated and 12 genes up-regulated. Nine of those genes were associated with three functional clusters: 1) a fibronectin type III (FN3) cluster [fibronectin type 3 and SPRY domain containing protein (Fsd1l), obscurin-like 1 (Obsl1), and tripartite motif-containing 46 (Trim46)]; 2) a kin- ase cluster [MAP-kinase activating death domain (Madd), Moloney sarcoma oncogene (Mos), and mitogen-activated protein kinase 7 (Mapk7)]; and 3) a transcription regulation cluster [DNA methyltransfer- ase 3a (Dnmt3a), PHD finger protein 17 (Phf1), and mediator of RNA polymerase II transcription subunit 12 homolog (yeast)-like (Med12l)]. In addition, the gene Serpina1a, the mouse ortholog of the human gene α1-antitrypsin (A1AT), was down-regulated 7.3- fold in the SM mice compared with the AM controls. The Western blots (Fig. 5) confirmed the RNA sequencing results and were obtained for both male and female mice. Expression of both DNMT3A and SERPINA1A were down-regulated, while MAPK7 and PHF1 were up-regulated in male mice exposed in utero to SHS. Similar trends were found in female mice exposed in utero to SHS, with the exception of the DNMT3A protein which was up-regulated 5.5 fold compared with the air controls.
Youth defined as having asthma have been found to be two to four times more likely to start smoking than non-susceptible youth [17, 18, 19]. Consequently, smoking has a negative impact on the economy and affects policy effectiveness in many areas. The present study showed that asthma is a major factor in smoking, and this understanding can help to formulate a variety of initiatives to reduce smoking and exposure to second-handsmoke. Addressing smoking in these environments can prevent a wide range of exposure .