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.

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.

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

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.

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.

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.

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.

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.

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.

Family lifestyle factors related to children's congenital heart defects in China:a case-control study

Objective To explore the multiple risk factors for family lifestyle of children with congenital heart defects(CHDs)in Shaanxi Province,China.Methods A 1∶1 case-control study was carried out to investigate 60 pairs of children and their parents.The univariate and multivariable logistic regression models were used to analyze the influence of risk factors related to parents’ lifestyle on CHDs.Results Several possible risk factors were found for CHDs,including fever(OR=4.465,P=0.017),pesticides contact(OR=2.234,P=0.083),passive smoking during pregnancy(OR=20.529,P=0.007)and father’s smoking(OR=3.342,P=0.005);fever(OR=2.428,P=0.012)and passive smoking during pregnancy(OR=1.201,P=0.037)were also correlated with ventricular sepal defect(VSD).Conclusion Fever,pesticides contact and passive smoking are associated with CHDs during pregnancy.We should focus our attention on health care during pregnancy to avoid the above-mentioned risk factors and call on parents to hold on to a good healthy lifestyle.

Passive cigarette smoking induces inflammatory injury in human arterial walls

Background Epidemiological studies have shown that both active and passive cigarette smoking increase the risk of atherosclerosis. But very little is known about the biological processes induced by passive cigarette smoking that contribute to atherosclerosis. We observe the expression of a few of biological and inflammatory markers in human arterial walls in vitro which were treated with the second-hand smoke solution （sidestream whole, SSW）, and discuss the possible mechanism of inflammatory injury induced by second-hand smoke. Methods The biological markers （platelet endothelial cell adhesion molecule-I, PECAM-1; a-smooth muscle actin, a-SMA; collagen IV, Col IV） and inflammatory markers （vascular cell adhesion molecule-1, VCAM-1; monocyte chemoattractant protein-1, MCP-1 ; interleukin-8, IL-8） of human aortat wall were tested by immunofluorescence staining. The levels of MCP-1 and IL-8 mRNA expression were detected by reverse transcription-polymerase chain reaction （RT-PCR）. Results No distinct difference was observed between SSW and the control group on the expression of biological markers as assessed by the light microscope. But the inflammatory markers VCAM-1, MCP-1 and IL-8 on the subendothelial layer and smooth muscle cell layers, which are near the endothelium of arterial wall, were strongly stained in the SSW group compared with the control group. Their fluorescence intensities in the 1：40 SSW group （VCAM-1： 0.35±0.04, MCP-1： 0.34±0.05, IL-8： 0.37±0.05） and the 1：20 SSW group （VCAM-I： 0.40±0.04, MCP-1： 0.52±0.09, IL-8： 0.51±0.07） were significantly stronger than the control group （VCAM-1： 0.12±0.04, MCP-1： 0.06±0.02, IL-8： 0.24±0.03） by semi-quantitative analysis of immunofluorescence （P 〈0.001 vs control）. MCP-1 mRNA expression in the 1：40 SSW （0.15±0.04） and the 1：20 SSW （0.19±0.06） group was significantly higher than in the control group （0.09±0.03） （P 〈0.05, P 〈0.01 vs control）; IL-8 mRNA expression in the 1：40 SSW （0.64±0.12） and 1：20 SSW （0.72±0.13） groups was also significantly higher than that in the control group （0.49±0.13） （P 〈0.05, P 〈0.01 vs control） by RT-PCR. Conclusions It is implied that a second-hand smoke solution induces the inflammatory reaction of the arterial wall by release of inflammatory factors even though there is no distinct structural change on the arterial walls under light microscope, indicating that passive cigarette smoking is related to inflammatory injury in human arterial wall and could be closely related to the early inflammatory stage of atherosclerosis.

Prevalence of active and passive tobacco smoking among Beijing residents in 2011

Objectives: This study was aimed to investigate the prevalence of active and passive tobacco smoking among Beijing residents in 2011. Methods: A cross-sectional survey was conducted, using a stratified multistage cluster random sampling method to select a representative sample of 20,242, among Beijing residents aged 18-79 years. Active and passive tobacco smoking information was collected by a standardized and validated questionnaire in a face-to-face interview. All estimates of prevalence and numbers were weighted by the 2010 Beijing Population Census data and the sampling scheme. Results: Among Beijing residents aged 18-79 years, the overall prevalence of ever smokers and current smokers were 33.13%and 30.18%, respectively. The prevalence in males was much higher than that in females (60.75%vs. 3.75%for ever smokers, and 55.53% vs. 3.21% for current smokers, respectively). For overall current smokers, 14.12 cigarettes were consumed per day. However, only 8.91%of ever smokers quitted smoking at the time of the survey, and 2.44%of ever smokers quitted smoking in recent two years. Furthermore, 44.74%of overall nonsmokers and former smokers, with 47.03%of males and 43.63%of females, reported exposure to secondhand smoke for at least 15 minutes per day and at least one day per week. Conclusions: Tobacco smoking prevalence is still extremely high in Beijing. Nonsmokers do still suffer from secondhand smoke critically. Further urgent efforts for tobacco control are warranted in Beijing.