The Impact of Electronic Cigarettes (e-Cigs) Smoking Habit on Periodontal Status and Salivary pH among Some Passive e-Cigs Smokers Referred to the College of Dentistry Clinics, King Khalid University

Background: Electronic cigarette (e-cigs) smoking is substitutional to traditional cigarette smoking to reduce the dangerous combustion of products. Moreover, passive smoking is involuntarily tobacco smoking due to the exposure to cigarette or tobacco smoke among non-smokers and due to there being little knowledge about the impact of passive e-cigs smoking on periodontal status and salivary pH. Therefore, the present study aimed to evaluate the effect of e-cigs smoking habit on periodontal tissue and salivary pH among some passive e-cigs smokers referred to the college of dentistry clinics, King Khalid University. Material and Methods: Ninety male participants who were referred to the college of dentistry clinics at King Khalid University were included in the study. Age, gender, e-cigs smoking, and general health were recorded. The participants were divided into three equal groups (n = 30) as follows: Group I (Non-passive e-cigs smokers and non-smokers) as the control group, Group II (e-cigs users), and Group III (Passive e-cigs smokers). Salivary pH, plaque control record (PCR), gingival bleeding index (GBI), clinical attachment loss (CAL), percentage of radiographic bone loss (% RBL), periodontal pocket depth (PPD), more than 5 missing teeth due to periodontal diseases (>5 MTDP), tooth mobility (TM), furcation involvement (FI), Bite collapse (BC), and less than 20 remaining teeth (10 Opposing pairs) (L20RT) as well as HbA1c were recorded. ANOVA test was used to the comparison between Groups I, II, and III in the participants’ ages and periodontitis staging clinical findings. The mean of participants’ age groups, the mean of salivary pH values of study groups, and the periodontitis staging complexity and HbA1c were compared between groups with the ANOVA test, Tukey’s test, and the chi-square test. P-value was recorded, and less than 0.5 was considered a statistically significant difference (p Results: The e-cigs users group revealed higher means of PCR, GBI %RBL values, and the participants percentages of >5 MTDP, TM, FI, L20RT, and diabetes mellitus (DM) among participants compared to the passive e-cigs smokers group and control group except for the participants percentage of BC among the participants, which was higher among the control group participants. The differences were not significant in PCR, GBI, %RBL and DM (p > 0.5) and significant in >5 MTDP, TM, FI, L20RT and smoking (p 7% values compared to the e-cigs users group and control group participants. The differences were not significant in CAL and PPD (p > 0.5) and significant in the participants percentages of salivary pH values (p Conclusion: The e-cigs smoking habit was the cause of an increase in periodontal disease severity among the electronic smokers rather than passive e-cigs smokers, although the salivary pH was higher in the latter.

Passive Smoking in China: Contributing Factors and Areas for Future Interventions

Objective To reduce tobacco consumption and exposure to passive smoking in China. Methods Discussion consisting of 80 focus groups and 35 interviews were held in three rural intervention counties of Jiangxi, Henan, and Sichuan Provinces. Participants came from hospitals, schools, rural areas, and urban areas. Results Tobacco use and exposure to passive smoking were widely prevalent in the investigated schools, hospitals, county towns, and rural areas. Knowledge of the risks for passive smoking on health is lacking, especially in rural areas. Barriers to the control of tobacco use in public places include reluctance of administrators to implement tobacco control policies, lack of consistent policies, difficulties with regulations and enforcement, and reluctance of non-smokers to exercise their right to clean air. Conclusion To curb the current tobacco epidemic in China, tobacco control efforts must focus on reducing exposure to passive smoking. A strategy should be formulated to reduce the factors that contribute to tobacco use and exposure to passive smoking.

Impacts of Passive Smoking on Learning and Memory Ability of Mouse Offsprings and Intervention by Antioxidants

Objective To determine the impact of passive smoking and the protective effect of antioxidants such as vitamin E and quercetin on learning and memory ability of mouse offsprings. Methods A passive smoking model of pregnant mice was established. Learning and memory ability was evaluated by the water maze test and long term potentiation （LTP）. Nitric oxide （NO）, content, nitric oxide synthase （NOS）, acetylcholinesteras （Ache） activity in brain, vitamin E concentration, and reactive oxygen species （ROS） in serum were determined. The latency period （the time during which the mice swim from the starting position to the ending position） and errors （the number of mice entering the blind end） in control and antioxidant intervention groups were compared with those in the smoke exposure group after 6 days. Results The latency period as well as errors in the air, control diet, tobacco smoke （TS）, and vitamin E diet groups were decreased significantly as compared with the TS and control diet groups （P〈O.05）. LTP was restrained in the TS and control diet groups. LTP in all the antioxidant diet groups was significantly increased compared with the TS and control diet groups. In addition, NOS and acetylcholinesteras （Ache） activitiy was significantly higher in the TS and control diet groups than in the air and control diet group. NO content was not significantly different among the different groups, and significantly lower in the TS and vitamin E diet groups than in the TS group, control diet group, quercetin diet group, and mixture diet group （P〈0.05）. Vitamin E concentration and ROS activity in serum were correlated with the outcome of water maze and LTP. Conclusion Passive smoking reduces LTP formation by disturbing the hippocampus function of mice, by decreasing NOS （especially vitamin E） partially improve the learning and memory smoke during pregnancy. and Ache activity and increasing NO content. Antioxidants ability of offsprings whose mothers are exposed to tobacco

Effect of Bushen Yiqi Huoxue Recipe on Placental Vasculature in Pregnant Rats with Fetal Growth Restriction Induced by Passive Smoking

Interactions of vascular endothelial growth factor （VEGF） with receptors VEGFR1/Fltl and VEGFR2/Flk1, and those of angiopoietins （Ang-1, Ang-2） with receptor Tie2 play important roles in placental angiogenesis. This study investigated vascular morphology and expression of these angiogenic factors in rat placenta on the day 15, 18, 21 of gestation （D 15, D 18 and D21）. The rats were randomly assigned into 3 groups： normal group, model group [fetal growth restriction （FGR） model], and Bushen Tqi Huoxue （BYHR） recipe treatment group （BYHR group, the pregnant rats with FGR were treated with BYHR recipe）. Morphological analysis indicated that during initial villous formation, fetal nucle- ated erythrocytes （FNEs） appeared in maternal blood sinus （MBS）. Subsequently, FNEs were sur- rounded by endothelial cells to form fetal capillary （FC） and then by trophoblast cells to form villi. As pregnancy proceeded, FC density increased progressively with increasing endothelial identification staining （EIS） in normal and BYHR groups. Whereas, villous formation was suppressed, normal in- crease in FC density was impaired and EIS was weakened in model group. Quantitative PCR analysis showed that VEGF and Flkl mRNA increased over gestation in all groups, indicating that VEGF might play a pivotal role in FC growth during late gestation. VEGF mRNA was increased on D15, while de- creased on D21 in model group as compared with normal group and BYHR group. Immunohistochemi- cally, Ang-2 protein was highly expressed in FNEs, gradually disappeared as villi matured, and decreased over gestation in all groups, indicating that Ang-2 might play a pivotal role in villous formation, which was further supported by decreased Ang-2 mRNA and protein expression in model group on D 15. Ang-1 mRNA, Tie2 mRNA and Ang-1/Ang-2 ratio increased from D15 to D18 in all groups as placenta matured. Ang-1 mRNA, Tie2 mRNA and Ang-1/Ang-2 ratio were decreased on D18 in model group as compared with normal and BYHR groups, indicating delayed maturity of FGR placenta. Alterations in angiogenic factors may result in altered placental vasculature and cause placental insufficiency. BYHR recipe could balance the angiogenic factors to promote the formation and maturation of FGR placental vasculature.

Active and passive smoking with breast cancer risk for Chinese females: a systematic review and meta-analysis

Previous studies suggested that smoking and passive smoking could increase the risk of breast cancer, but the results were inconsistent, especially for Chinese females. Thus, we systematically searched cohort and case-control studies investigating the associations of active and passive smoking with breast cancer risk among Chinese females in four English databases(PubMed, Embase, ScienceDirect, and Wiley) and three Chinese databases(CNKI, WanFang, and VIP). Fifty-one articles(3 cohort studies and 48 casecontrol studies) covering 17 provinces of China were finally included in this systematic review. Among Chinese females, there was significant association between passive smoking and this risk of breast cancer [odds ratio(OR): 1.62; 95% confidence interval(CI): 1.39–1.85; I2 = 75.8%, P < 0.001; n = 26] but no significant association between active smoking and the risk of breast cancer(OR: 1.04; 95% CI: 0.89–1.20; I2 = 13.9%, P = 0.248; n = 31). The OR of exposure to husband's smoking and to smoke in the workplace was 1.27(95% CI: 1.07–1.50) and 1.66(95% CI: 1.07–2.59), respectively. The OR of light and heavy passive smoking was 1.11 and 1.41, respectively, for women exposed to their husband's smoke(< 20 and ≥ 20 cigarettes per day), and 1.07 and 1.87, respectively, for those exposed to smoke in the workplace(< 300 and ≥ 300 min of exposure per day). These results imply that passive smoking is associated with an increased risk of breast cancer, and the risk seems to increase as the level of passive exposure to smoke increases among Chinese females. Women with passive exposure to smoke in the workplace have a higher risk of breast cancer than those exposed to their husband's smoking.

Association between head-and-neck cancers and active and passive cigarette smoking

Although there have been many reports on the toxicity of tobacco smoke, fewer studies have reported the relationship between the smoke and carcinogenesis of head-and-neck cancers. It is assumed that direct stimulations due to tobacco smoke, such as chemical and mechanical stimulations, strongly influence the epithelium of the nasal cavity, paranasal sinuses, pharynx, and larynx. We investigated the influence of active and passive cigarette smoking on head-and-neck cancers. The subjects were 283 head-and-neck cancer patients examined at the otolaryngology department of Showa University Northern Yokohama Hospital in a 9-year and 2-month period from April 2001 to June 2010, in whom the presence or absence of active and passive cigarette smoking could be confirmed in detail. The active and passive smoking rates and the Brinkman index were retrospectively investigated according to the primary cancer site, gender, and histopathological classification. The active and passive smoking rates were high (about 90%) in patients with hypopharyngeal, laryngeal, and cervical esophageal cancers, and the Brinkman index was high in all. Squamous cell carcinoma (SCC) patients accounted for a high ratio of the head-and-neck cancer patients, and the active and passive smoking rates were significantly higher in SCC than in non-squamous cell carcinoma (non-SCC) patients (p < 0.0003). The active and passive smoking rates and the Brinkman index were high in patients with head-and-neck cancers in regions receiving strong direct stimulation from tobacco smoke, and the Brinkman index was also high in these patients, suggesting that carcinogenesis of head-and-neck cancers is strongly influenced by direct tobacco smoke stimulation.

Passive Smoking and Other Principal Risk Factors Associated with Low Birth Weight

Background: Neonatal morbidity and mortality is one of the most public health problems in the world. A lot of neonatal deaths occur in foetus with low birth weight (LBW). Several risk factors of LBW have been described in the literature such as maternal age, chronic and gestational hypertension infection and anémia. Smoking is one of the most important preventable risk factor of LBW in developed and developing countries. Aims: In this study, we evaluated the incidence and the impact of passive smoking and some other principle risk factors of LBW. Material & Methods: This case control study was conducted in the department of obstetrics and gynecology of Marrakesh university hospital in Morocco. During a period of 3 years, all LBW babies were included in the study. Data analysis was performed by SPSS software. The association between LBW and each variable was studied by the chi square test comparing cases and controls groups. Logistic regression analysis was performed after including all variables found to have significant differences on univariate analysis. Results: 288 cases of LBW have been identified representing 2.19% of all births. The study of the categories showed that 84.3% of babies were moderate LBW (1500 - 2500 g), including 49 babies from twin pregnancies. 15.7% were very LBW (<1500 g). Several risk factors have been identified in LBW. Passive smoking was significantly associated with LBW [(OR 1.77;CI: 1.22 - 2.25)]. Conclusion: A number of risk factors are related to low birth weight, which is one of the main predictors of infant mortality. This study shows that passive smoking is one of those risk factors and it is a preventable one.

Effect of "Jia Wei Fo Shou San" on Erythrocyte Membrane Calcium,Zinc Concentration in Pregnant Rats with Asymmetrical Intrauterine Growth Retardation Induced by Passive Smoking

Using experimental model of pregnant rats with asymmetrical intrauterine fetal growth retardation induced by passive smoking, the effects of natural herb 'Jia Wei Fo Shou San' on erythrocyte membrane calcium, zinc concentration were observed by atomic absorption spectrophotometry. The results showed that the mean fetal birth weight, zinc concentration of erythrocyte membrane were found to be decreased in the model group as compared with the control group (P＜0. 01, P＜0. 01). On the other hand, the element of calcium onto erythrocyte membrane were higher in model group than that in control group(P＜0. 05). These changes were significantly mild in the treated group and were similar to those of the control group (P＜0.05). Furthermore,our findings indicated that the zinc concentration of erythrocyte membrane seems to be positively correlated with the birth weight(P＜0. 01). Calcium composition of red cell membrane showed a significant negative relation to the birth weight (P＜0.05). Our results provided an experimental evidence that normal concentrations of calcium and zinc onto erythrocyte play an important part in fetal growth. One of the mechanisms of 'Jia Wei Fo Shou San' in improving fetal growth may have something to do with modulation of erythrocyte calcium,zinc element,thereby protecting bio-functions of erythrocyte and promoting blood circulation.

Passive Smoking and Children’s Health

Tabagism is one of the greatest public health problems at the present time because this is the most important cause of preventabel deaths worldwide. Due to its impact on the health and welfare of all, the act of smoking causes problems for society, including that children, without being able to enjoy the freedom of choice, eventually become compulsory passive smokers since its conception. This article presents the main damages caused by smoking to human health, especially on children, who, because of their characteristics are more vulnerable to the effects of products derived from cigarette burns, mainly the effects of nicotine, carbon monoxide and more than 4700 substances produced by smoking. Also it highlights the importance that all efforts are directed towards protecting nonsmokers and improving environmental and health conditions for everyone.

Passive Smoking and Infectious Disease: A Serious Hazard for Cardiovascular System

Exposure to passive smoking is usually associated with heavy changes in both function and structure of the cardiovascular system at different levels: coronary circulation, heart metabolism, myocardial muscle. These changes may be transient but may have characteristics of irreversibility. Major determinant of cardiovascular alterations is hypoxia due to tobacco products of the environment although a large number of alterations affect immune t-cells and antibody response. All infectious diseases which involve cardiovascular system, including some tropical patterns, particularly Chagas disease, are adversely influenced as a consequence of a continuous although irregular exposure to passive smoking, which worsens the degree of cardiac muscle alterations at different levels like myocardium, coronary arteries and both these structures. Therefore, exposure to passive smoking must be avoided for those individuals suffering from infectious diseases of the heart whatever factor can be responsible.

Stability Analysis of Chain, Mild and Passive Smoking Model

In this paper, the global stability of free smoking equilibrium point was evaluated and presented graphically. The linear stability of a developed mathematical model illustrates the effect on the population of chain, mild and passive smokers. MATLAB programming was used to simulate the solutions, the reproduction number R0 and the nature of the equilibria.

Impact of baseline smoking status on long-term prognosis of patients with coronary artery disease underwent percutaneous coronary intervention:a large single-center data

Objective This study analyzed a large single-center sample in China to explain the impact of smoking state at baseline on long-term prognosis of coronary artery disease (CAD) patients who received percutaneous coronary intervention (PCI).

Adapting the Stage of Change model to investigate adolescent behavior related to reducing second hand smoke exposure

Aims: Second hand smoke (SHS) exposure is increasingly recognized as a major public health concern. Assessing adolescents’ motivational level to avoid SHS is vital to promote and reinforce reductions in SHS exposure. Methods: A brief measure based on the Stage of Change model was developed to characterize adolescents’ behavior related to reducing SHS exposure and used to identify potential determinants of SHS stage of change. The sample consisted of 1172 adolescents aged 13 to 15 years who participated in an internet-based cohort study of youth in British Columbia, Canada. Results: Sixty-six percent of the adolescents reported they had consistently made efforts to reduce exposure to SHS for more than 6 months, while 19% did not intend to reduce their exposure to SHS in the next 6 months. Adolescents’ SHS stage of change significantly differed by ethnicity, whether they had tried cigarettes, amount of tobacco smoked in their lifetime, parental and peer smoking statuses, past months’ exposure to SHS, frequent smoking in the home, and home smoking restrictions (all p < 0.05). Active smoking and more frequent exposure to SHS were associated with an increased probability of being in the pre-contemplation stage of change with regard to behavior related to reducing SHS exposure. Conclusion: This brief measure based on the Stage of Change model can be used in future studies to characterize adolescents’ behavior around SHS. Adolescents who smoke or have parents and/or friends who smoke appear to be a population that could benefit from stage-matched interventions designed to raise awareness of the risks associated with SHS for smokers and non-smokers, and ultimately reduce SHS exposure.

Environmental tobacco smoke exposure and lung cancer:A systematic review

AIM： To review evidence relating passive smoking to lung cancer risk in never smokers, considering various major sources of bias.METHODS： Epidemiological prospective or case-control studies were identifed which provide estimates of relative risk （RR） and 95%CI for never smokers for one or more of seven different indices of exposure to environmental tobacco smoke （ETS）： The spouse; household; workplace; childhood; travel; social and other; and total. A wide range of study details were entered into a database, and the RRs for each study, including descriptions of the comparisons made, were entered into a linked database. RRs were derived where necessary. Results were entered, where available, for all lung cancer, and for squamous cell cancer and adenocarcinoma. “Most adjusted” results were entered based on results available, adjusted for the greatest number of potential confounding variables. “Least adjusted” results were also entered, with a preference for results adjusted at least for age for prospective studies. A pre-planned series of fxed-effects and random-effects meta-analyses were conducted. Overall analyses and analyses by continent were run for each exposure index,with results for spousal smoking given by sex, and results for childhood exposure given by source of ETS exposure. For spousal exposure, more extensive analyses provide results by various aspects of study design and defnition of the RR. For smoking by the husband （or nearest equivalent）, additional analyses were carried out both for overall risk, and for risk per 10 cigarettes per day smoked by the husband. These adjusted for uncontrolled confounding by four factors （fruit, vegetable and dietary fat consumption, and education）, and corrected for misclassification of smoking status of the wife. For the confounding adjustment, estimates for never smoking women were derived from publications on the relationship of the four factors to both lung cancer risk and at home ETS exposure, and on the correlations between the factors. The bias due to misclassifcation was calculated on the basis that the proportion of ever smokers denying smoking is 10% in Asian studies and 2.5% elsewhere, and that those who deny smoking have the same risk as those who admit it. This approach, justifed in previous work, balances higher true denial rates and lower risk in deniers compared to non-deniers.RESULTS： One hundred and two studies were identifed for inclusion, published in 1981 onwards, 45 in Asia, 31 in North America, 21 in Europe, and fve elsewhere. Eighty-fve were of case-control design and 17 were prospective. Significant （P 〈 0.05） associations were noted, with random-effects of （RR = 1.22, 95%CI： 1.14-1.31, n = 93） for smoking by the husband （RR = 1.14, 95%CI： 1.01-1.29, n = 45） for smoking by the wife （RR = 1.22, 95%CI： 1.15-1.30, n = 47） for workplace exposure （RR = 1.15, 95%CI： 1.02-1.29, n = 41） for childhood exposure, and （RR = 1.31, 95%CI： 1.19-1.45, n = 48） for total exposure. No signifcant association was seen for ETS exposure in travel （RR = 1.34, 95%CI： 0.94-1.93, n = 8） or in social situations （RR = 1.01, 95%CI： 0.82-1.24, n = 15）. A signifcant negative association （RR = 0.78, 95%CI： 0.64-0.94, n = 8） was seen for ETS exposure in childhood, specifically from the parents. Significant associations were also seen for spousal smoking for both squamous cell carcinoma （RR = 1.44, 95%CI： 1.15-1.80, n = 24） and adenocarcinoma （RR = 1.33,95%CI： 1.17-1.51, n = 30）. Results generally showed marked heterogeneity between studies. For smoking by either the husband or wife, where 119 RR estimates gave an overall estimate of （RR = 1.21, 95%CI： 1.14-1.29）, the heterogeneity was highly significant （P 〈 0.001）, with evidence that the largest RRs were seen in studies published in 1981-89, in small studies （1-49 cases）, and for estimates unadjusted by age. For smoking by the husband, the additional analyses showed that adjustment for the four factors reduced the overall （RR = 1.22, 95%CI： 1.14-1.31） based on 93 estimates to （RR = 1.14, 95%CI： 1.06-1.22）, implying bias due to uncontrolled confounding of 7%. Further correction for misclassification reduced the estimate to a marginally non-signifcant （RR = 1.08, 95%CI： 0.999-1.16）. In the fully adjusted and corrected analyses, there was evidence of an increase in Asia （RR = 1.18, 95%CI： 1.07-1.30, n = 44）, but not in other regions （RR = 0.96, 95%CI： 0.86-1.07, n = 49）. Studies published in the 1980’s, studies providing dose-response data, and studies only providing results unadjusted for age showed elevated RRs, but later published studies, studies not providing dose-response data, and studies adjusting for age did not. The pattern of results for RRs per 10 cigs/d was similar, with no signifcant association in the adjusted and corrected results （RR = 1.03, 95%CI： 0.994-1.07）.CONCLUSION： Most, if not all, of the ETS/lung cancer association can be explained by confounding adjustment and misclassifcation correction. Any causal relationship is not convincingly demonstrated.

An Evaluation of Cotinine as an Index of Exposure to Tabacco Smoke in Children with Recurrent Respiratory Tract Infections Using HPLC Method

The authors evaluated the frequency of exposure to tobacco smoke among children suffering from respiratory tract infections. The investigations comprised 141 children aged from 2 months to 6 years that were treated in the 2nd Department of Pediatric and Allergology of Polish Mother’s Memorial Hospital Research Institute in ?ód? (Poland). 69 of them were exposed to tobacco smoke in their home environment. The remaining 72 children came from non-smoking families. 26 (37.7%) individuals among the passive smokers and 15 (20.83%) among the children from non-smoking families suffered from recurrent respiratory tract infections. Cotinine concentrations were evaluated in the group of 69 children using the HPLC-UV method. The determined average cotinine/creatinine index expressed as median was higher in passive smokers with recurrent respiratory infections than among passive smokers with non-recurrent respiratory infections. Moreover, it was stated that the exposure to cigarette smoke was more often among children of younger and less well educated parents as well as living in poor housing conditions. These studies clearly indicate that there is a need for extensive education on the harmful effects of passive smoking and the recurrence of infections.

Misclassification of smoking habits:An updated review of the literature

BACKGROUND Misclassification of smoking habits leads to underestimation of true relationships between diseases and active smoking, and overestimation of true relationships with passive smoking. Information on misclassification rates can be obtained from studies using cotinine as a marker.AIM To estimate overall misclassification rates based on a review and meta-analysis of the available evidence, and to investigate how misclassification rates depend on other factors.METHODS We searched for studies using cotinine as a marker which involved at least 200 participants and which provided information on high cotinine levels in selfreported non-, never, or ex-smokers or on low levels in self-reported smokers. We estimated overall misclassification rates weighted on sample size and investigated heterogeneity by various study characteristics. Misclassification rates were calculated for two cotinine cut points to distinguish smokers and nonsmokers, the higher cut point intended to distinguish regular smoking.RESULTS After avoiding double counting, 226 reports provided 294 results from 205 studies. A total of 115 results were from North America, 128 from Europe, 25 from Asia and 26 from other countries. A study on 6.2 million life insurance applicants was considered separately. Based on the lower cut point, true current smokers represented 4.96%(95% CI 4.32-5.60%) of reported non-smokers, 3.00%(2.45-3.54%) of reported never smokers, and 10.92%(9.23-12.61%) of reported exsmokers. As percentages of true current smokers, non-, never and ex-smokers formed, respectively, 14.50%(12.36-16.65%), 5.70%(3.20-8.20%), and 8.93%(6.57-11.29%). Reported current smokers represented 3.65%(2.84-4.45%) of true non-smokers. There was considerable heterogeneity between misclassification rates.Rates of claiming never smoking were very high in Asian women smokers, the individual studies reporting rates of 12.5%, 22.4%, 33.3%, 54.2% and 66.3%. False claims of quitting were relatively high in pregnant women, in diseased individuals who may recently have been advised to quit, and in studies considering cigarette smoking rather than any smoking. False claims of smoking were higher in younger populations. Misclassification rates were higher in more recently published studies. There was no clear evidence that rates varied by the body fluid used for the cotinine analysis, the assay method used, or whether the respondent was aware their statements would be validated by cotinine-though here many studies did not provide relevant information. There was only limited evidence that rates were lower in studies classified as being of good quality,based on the extent to which other sources of nicotine were accounted for.CONCLUSION It is important for epidemiologists to consider the possibility of bias due to misclassification of smoking habits, especially in circumstances where rates are likely to be high. The evidence of higher rates in more recent studies suggests that the extent of misclassification bias in studies relating passive smoking to smoking-related disease may have been underestimated.

Maternal Smoking During Pregnancy and Sudden Infant Death Using the National Maternal and Infant Health Survey: A Case-Case Study

We utilized data from the National Maternal and Infant Health Survey (NMHIS) to analyze the risk of SIDS and other infant deaths among women who smoke during pregnancy adjusting for potentially modifiable risk factors such as secondhand smoke exposure and breastfeeding. The following variables were assessed with respect to risk for SIDS and other infant deaths: smoking exposure, level of education, infant and maternal age, infant and maternal birthweight, maternal BMI, gender, secondhand smoke exposure, breast feeding, prenatal vitamins, WIC, multiple gestation, sleep apnea monitor prescription, sleep apnea incidents and maternal alcohol use. Univariate analysis and multivariate logistic regression were performed to identify variables significantly associated with the odds of mortality from SIDS. Analysis utilized weighted estimates using SUDAAN 9.0.0 to adjust for design effects. A p-value <0.01 was considered statistically significant. Women who smoked during pregnancy were 1.83 times more likely to give birth to an infant that died from SIDS versus some other cause of death, OR (95%) = 1.83(1.33, 2.51). Other Race infants and Black infants were more likely to suffer SIDS mortality than White infants, but the result was not significant in the final model. Other modifiable risk factors, such as secondhand smoke exposure and breast feeding, were not significant predictors of SIDS mortality. Independent of sociodemographic variables and other potential risk factors for SIDS death, maternal smoking was associated with an increased risk of SIDS death versus other death. This study highlights the importance of screening all pregnant women for tobacco use and emphasizes the importance of smoking cessation to decrease the risk of infant death from SIDS.

Application of an amphipathic molecule at the NiO_(x)/perovskite interface for improving the efficiency and long-term stability of the inverted perovskite solar cells

The presence of defects and detrimental reactions at NiO_(x)/perovskite interface extremely limit the efficiency performance and long-term stability of the perovskite solar cells(PSCs) based on NiO_(x).Herein,an amphipathic molecule Triton X100(Triton) is modified on the NiO_(x)surface.The hydrophilic chain of Triton as a Lewis base additive can coordinate with the Ni3+on the NiO_(x)surface which can passivate the interfacial defects and hinder the detrimental reactions at the NiO_(x)/perovskite interface.Additionally,the hydrophobic chain of Triton protrudes from the NiO_(x)surface to prevent moisture from penetrating into the NiO_(x)/perovskite interface.Consequently,the NiO_(x)/Triton-based devices(MAPbI3as absorbing layer) show superior moisture and thermal stability,retaining 88.4% and 64.3% of the initial power conversion efficiency after storage in air(40%-50% relative humidity(RH)) at 25 ℃ for 1070 h and in N2at 85℃ for 800 h,respectively.Moreover,the efficiency increases from 17.59% to 19.89% because of the passivation defect and enhanced hole-extraction capability.Besides,the NiO_(x)/Triton-based PSCs with Cs_(0.05)(MA_(0.15)FA_(0.85))_(0.95)Pb(I_(0.85)Br_(0.15))3perovskite as the light-absorbing layer also exhibits better moisture and thermal stability compared to the control devices,indicating the viability of our strategies.Of particular note,a champion PCE of 22.35% and 20.46% was achieved for small-area(0.1 cm^(2)) and large-area(1.2 cm^(2)) NiO_(x)/Triton-based devices,respectively.

Environmental tobacco smoke exposure and heart disease:A systematic review

AIM To review evidence relating passive smoking to heart disease risk in never smokers. METHODS Epidemiological studies were identified providing estimates of relative risk(RR) of ischaemic heart disease and 95%CI for never smokers for various indices of exposure to environmental tobacco smoke(ETS). "Never smokers" could include those with a minimal smoking experience. The database set up included the RRs and other study details. Unadjusted and confounderadjusted RRs were entered, derived where necessary using standard methods. The fixed-effect and randomeffects meta-analyses conducted for each exposure index included tests for heterogeneity and publication bias. For the main index(ever smoking by the spouse or nearest equivalent, and preferring adjusted to unadjusted data), analyses investigated variation in the RR by sex, continent, period of publication, number of cases, study design, extent of confounder adjustment, availability of dose-response results and biomarkerdata, use of proxy respondents, definitions of exposure and of never smoker, and aspects of disease definition. Sensitivity analyses were also run, preferring current to ever smoking, or unadjusted to adjusted estimates, or excluding certain studies.RESULTS Fifty-eight studies were identified, 20 in North America, 19 in Europe, 11 in Asia, seven in other countries, and one in 52 countries. Twenty-six were prospective, 22 case-control and 10 cross-sectional. Thirteen included 100 cases or fewer, and 11 more than 1000. For the main index, 75 heterogeneous(P < 0.001) RR estimates gave a combined random-effects RR of 1.18(95%CI: 1.12-1.24), which was little affected by preferring unadjusted to adjusted RRs, or RRs for current ETS exposure to those for ever exposure. Estimates for each level of each factor considered consistently exceeded 1.00. However, univariate analyses revealed significant(P < 0.001) variation for some factors. Thus RRs were lower for males, and in North American, larger and prospective studies, and also where the RR was for spousal smoking, fatal cases, or specifically for IHD. For case-control studies RRs were lower if hospital/diseased controls were used. RRs were higher when diagnosis was based on medical data rather than death certificates or self-report, and where the never smoker definition allowed subjects to smoke products other than cigarettes or have a limited smoking history. The association with spousal smoking specifically(1.06, 1.01-1.12, n = 34) was less clear in analyses restricted to married subjects(1.03, 0.99-1.07, n = 23). In stepwise regression analyses only those associations with source of diagnosis, study size, and whether the spouse was the index, were independently predictive(at P < 0.05) of heart disease risk. A significant association was also evident with household exposure(1.19, 1.13-1.25, n = 37). For those 23 studies providing dose-response results for spouse or household exposure, 11 showed a significant(P < 0.05) positive trend including the unexposed group, and two excluding it. Based on fewer studies, a positive, but non-significant(P > 0.05) association was found for workplace exposure(RR = 1.08, 95%CI: 0.99-1.19), childhood exposure(1.12, 0.95-1.31), and biomarker based exposure indices(1.15, 0.94-1.40). However, there was a significant association with total exposure(1.23, 1.12-1.35). Some significant positive dose-response trends were also seen for these exposure indices, particularly total exposure, with no significant negative trends seen. The evidence suffers from various weaknesses and biases. Publication bias may explain the large RR(1.66, 1.30-2.11) for the main exposure index for smaller studies(1-99 cases), while recall bias may explain the higher RRs seen in casecontrol and cross-sectional than in prospective studies. Some bias may also derive from including occasional smokers among the "never smokers", and from misreporting smoking status. Errors in determining ETS exposure, and failing to update exposure data in long term prospective studies, also contribute to the uncertainty. The tendency for RRs to increase as more factors are adjusted for,argues against the association being due to uncontrolled confounding.CONCLUSION The increased risk and dose-response for various exposure indices suggests ETS slightly increases heart disease risk. However heterogeneity, study limitations and possible biases preclude definitive conclusions.

尼古丁在被动吸烟大鼠口腔硬组织中的分布及其对牙周膜干细胞的影响

目的探究被动吸烟及戒除被动吸烟后大鼠血液及口腔硬组织中的尼古丁分布情况和变化规律,并通过体外尼古丁对牙周膜干细胞(PDLSCs)增殖及成骨能力的影响,间接证实口腔组织中尼古丁沉积的危害。方法建立被动吸烟大鼠模型,采用液相色谱-串联质谱法检测大鼠血液、牙齿和牙槽骨中尼古丁分布情况。体外尼古丁刺激PDLSCs,通过CCK-8、茜素红染色、Western Blot检测尼古丁对PDLSCs增殖能力和成骨能力的影响。结果在为期3个月的被动吸烟中,大鼠血液、牙槽骨,牙齿中的尼古丁浓度分别在2月、1月、2月达到峰值,随后逐渐降低;戒除被动吸烟后,尼古丁仍维持一定浓度水平。体外尼古丁刺激PDLSCs后,细胞增殖受到抑制,矿化结节显著减少,ALP、Runx2、OPG等蛋白表达均下调。结论尼古丁在被动吸烟大鼠血液、牙齿和牙槽骨中的分布情况具有时间相关性,戒除被动吸烟后,尼古丁可长期蓄积于体内,对牙周膜干细胞的增殖和成骨分化产生不利影响。