STUDY DESIGN: This was a cross-sectional comparative study in a Malaysian tertiary obstetric hospital involving 200 non-smoking pregnant women at term, of whom 100 were secondhand smokers and 100 were non-secondhand smokers. Those with multiple pregnancies, with a body mass index (BMI) of more than 30kg/m2or who delivered by Caesarean section were excluded. The participants' basic demographic details, delivery details, neonatal outcome and placental weight were recorded. Umbilical cord blood samples were obtained, and cord blood cotinine levels were measured with a Cotinine ELISA kit. The primary outcomes were baby's birth weight, length, and head circumference, Apgar score at 5min and placental weight. The secondary outcome was difference in cord blood cotinine levels between the two groups and the correlation of these differences with the neonatal outcome.
RESULTS: The secondhand smoker group had significantly lower baby weight (2.94±0.31kg vs 3.05±0.40kg), head circumference (30.87±2.35cm vs 37.13±2.36cm), length (46.58±1.95cm vs 51.53±2.05cm) and placental weight (520±73.5g vs 596±61.3g) and significantly higher cord blood cotinine levels (16.35±12.84ng/mL vs 0.56±0.22ng/mL). Cord blood cotinine levels had significant negative correlations with placental weight (r=-0.461), baby's weight (r=-0.297), baby's head circumference (r=-0.501) and baby's length (r=-0.374).
CONCLUSION: Secondhand smoke increases the incidence of adverse pregnancy outcomes (newborns'anthropometric measurements and placental weight) and causes higher cord blood cotinine levels.
MATERIALS AND METHODS: PM2.5 was measured as a marker of SHS levels in a total of 61 restaurants, entertainment centres, internet cafes and pubs in Kuala Lumpur, Malaysia.
RESULTS: Under the current smoke-free laws smoking was prohibited in 42 of the 61 premises. Active smoking was observed in nearly one-third (n=12) of these. For premises where smoking was prohibited and no active smoking observed, the mean (standard deviation) indoor PM2.5 concentration was 33.4 (23.8) μg/m3 compared to 187.1 (135.1) μg/m3 in premises where smoking was observed The highest mean PM2.5 was observed in pubs [361.5 (199.3) μg/m3].
CONCLUSIONS: This study provides evidence of high levels of SHS across a range of hospitality venues, including about one-third of those where smoking is prohibited, despite 8 years of smoke-free legislation. Compliance with the legislation appeared to be particularly poor in entertainment centres and internet cafes. Workers and non-smoking patrons continue to be exposed to high concentrations of SHS within the hospitality industry in Malaysia and there is an urgent need for increased enforcement of existing legislation and consideration of more comprehensive laws to protect health.
METHOD: This cross-sectional study was carried out to measure salivary cotinine concentrations among 1064 schoolchildren (10-11 years) attending 24 schools in Malaysia following recent partial smoke-free restrictions. Parents completed questionnaires and schoolchildren provided saliva samples for cotinine assay.
RESULTS: The geometric mean (GM) salivary cotinine concentrations for 947 non-smoking schoolchildren stratified by household residents' smoking behaviour were: for children living with non-smoking parents 0.32 ng/ml (95% CI 0.28-0.37) (n = 446); for children living with a smoker father 0.65 ng/ml (95% CI 0.57-0.72) (n = 432); for children living with two smoking parents 1.12 ng/ml (95% CI 0.29-4.40) (n = 3); for children who live with an extended family member who smokes 0.62 ng/ml (95% CI 0.42-0.89) (n = 33) and for children living with two smokers (father and extended family member) 0.71 ng/ml (95% CI 0.40-0.97) (n = 44). Parental-reported SHS exposures showed poor agreement with children's self-reported SHS exposures. Multiple linear regression demonstrated that cotinine levels were positively associated with living with one or more smokers, urban residence, occupation of father (Armed forces), parental-reported exposure to SHS and education of the father (Diploma/Technical certificate).
CONCLUSIONS: This is the first study to characterise exposures to SHS using salivary cotinine concentrations among schoolchildren in Malaysia and also the first study documenting SHS exposure using salivary cotinine as a biomarker in a South-East Asian population of schoolchildren. Compared to other populations of similarly aged schoolchildren, Malaysian children have higher salivary cotinine concentrations. The partial nature of smoke-free restrictions in Malaysia is likely to contribute to these findings. Enforcement of existing legislation to reduce exposure in public place settings and interventions to reduce exposure at home, especially to implement effective home smoking restriction practices are required.
MATERIALS AND METHODS: A cross-sectional study was conducted among three secondary schools located in Kudat district, Sabah, Malaysia during the period from June until September 2012. The protocol of this study was approved by ethics committee of Management and Science University, Malaysia. The aims were explained and a consent form was signed by each participant. Respondents were chosen randomly from each school with the help of the headmasters. Self-administrated questionnaires, covering socio-demographic characteristics and general knowledge of lung cancer, were distributed. Once all 150 respondents completed the questionnaire, they passed it to their head master for collecting and recording. All the data were analyzed using Statistical Package for the Social Sciences (SPSS) version 13. ANOVA and t-test were applied for univariate analysis; and multiple linear regression for multivariate analysis.
RESULTS: A total of 150 male secondary school teachers participated in this study. Their mean age was 35.6 ∓ 6.5 (SD); maximum 50 and minimum 23 years old. More than half of the participants were Malay and married (52%, 79%; respectively). Regarding the knowledge about lung cancer, 57.3% of the participants mentioned that only males are affected by lung cancer. Some 70.7% mentioned that lung cancer can be transmitted from one person to another. More than half (56.7%) reported that lung cancer is not the leading cause of death in Malaysian males. As for risk factors, the majority reported that family history of lung cancer is not involved. However, 91.3% were aware that cigarettes are the main risk factor of lung cancer and more than half (52%) believed that second-hand smoking is one of the risk factor of lung cancer. More than half (51.3%) were not aware that asbestos, ionizing radiation and other cancer causing substances are risk factors for lung cancer. Quitting smoking, avoiding second-hand smoking and avoiding unnecessary x-ray image of the chest (53.3%, 96.0%, 87.3%; respectively) are the main preventive measures mentioned by the participants. For the factors that influence the participants knowledge, univariate and multivariate analysis showed that only race was significant.
CONCLUSIONS: Overall, the knowledge of school male teachers about lung cancer was low. However, few items were scored high: cigarettes are the main risk factor; avoiding second-hand smoking; and avoiding x-rays. Interventions to increase lung cancer awareness are needed to improve early detection behavior. Increase the price of pack of cigarettes to RM 20 and banning smoking in public places such as restaurants are highly recommended as primary preventive measures.
AIMS: This study carried out from June 2008 to March 2009 to find the relation between environmental tobacco smoke, stress and miscarriage and preterm births.
METHODS: A total of 33 subjects consisted of multiparous pregnant women that were in their early third trimester were chosen for this investigation. Subjects were divided into test group women with adverse pregnancy outcome, control group women with successful pregnancy. Four ml of unstimulated whole saliva were collected. The concentrations of cotinine and cortisol were evaluated using commercially available ELISA kit.
RESULTS: Pregnancies in which the average standardized cortisol during history of previous miscarriage(s) which occurred within 6th-27th week or/and history of preterm labor which occurred within 28th-36th weeks of gestation, demonstrated higher cortisol level (1.0201 ± 0.1855 ng/ml) compared to control group 0.9757 ± 0.2860 ng/ml (P = 0.323); statistical analysis showed no significant differences. Women of control group were more likely to be environmental tobacco smoke exposed (1.2714 ± 1.7639 ng/ml) than women with miscarriage and preterm births (0.9889 ± 0.5498 ng/ml).
CONCLUSION: The results from this primarily study demonstrated no association between cotinine, cortisol, miscarriage and preterm births.
METHODS: A structured questionnaire was used to collect data on a child's current and previous illnesses, oral health behaviours, dietary habits, parental smoking behaviours and parents' dental history. The intraoral examination recorded dental caries (dmfs), enamel defects, gingival health, melanin pigmentation and soft tissue health. Stimulated saliva was collected. Total sIgA levels were quantified using indirect competitive ELISA with a SalimetricsTM kit.
RESULTS: The 44 children (aged 15-69 months) recruited were divided into two groups: ETS and non-ETS (control). There were 22 children in each: 16 who were exposed to ETS during and after gestation were identified as the ETSB subgroup. Participants exposed to ETS were more likely to have had upper respiratory tract and middle ear infections during the neonatal period and had higher mean dmft, mean dmfs, mean percent of surfaces with demarcated opacities and mean GI than the non-ETS participants. The children exposed to ETS before and after birth had the highest occurrence of enamel opacities showed a higher risk for dental caries even though more children in this group used the recommended fluoride toothpaste (1000 ppm fluoride). Mothers who smoked either never breastfed their children or breastfed their children for less than the recommended period of 6 months. Children exposed to ETS were shown to have higher mean total sIgA (μg/ml) than the children in the control group.
CONCLUSIONS: Associations between ETS exposure before and after gestation and oral health, including salivary changes in young children were shown in the present study. Dental health professionals should include a question about household smoking in children's dental histories, which would allow opportunities to discuss the impact of smoking on child oral health. Longitudinal oral health studies should include a history of maternal smoking during pregnancy and afterwards.
METHODS: At a regional meeting of the Asia Pacific Child and Family Health Alliance for Tobacco Control, members reviewed existing good practices of child-focused tobacco control approaches using health promotion strategies. These interventions were implemented nationally in Malaysia, the Philippines and Singapore.
RESULTS: Three good practice national examples were identified that focused on creating supportive tobacco-free environments and upgrading cessation skills among paediatricians. These country examples highlight strategic areas to protect children and families from the harms of tobacco, as part of NCD prevention and control. Training paediatricians in brief cessation advice has enabled them to address tobacco-using parents. Fully enforcing smoke-free public areas has led to an increase in smoke-free homes. The Tobacco Free Generation is a tobacco control 'endgame' strategy that taps into a social movement to deglamorize tobacco use and empower youth born in and after year 2000 to reject tobacco and nicotine addiction.
CONCLUSION: Tobacco control is pivotal in the fight against NCDs; health promotion strategies to protect children and youth from tobacco have a critical role to play in NCD prevention and control. Frontline health workers, including primary care paediatricians, need to step up and actively advocate for full implementation of the WHO Framework Convention on Tobacco Control, including tobacco tax increases and smoke-free areas, while monitoring patients and their parents for tobacco use and second-hand smoke exposure, preventing adolescent smoking uptake, and offering cessation support. A life-course approach incorporating child-focused efforts to prevent initiation of smoking and second-hand smoke exposure with measures promoting cessation among parents will offer the greatest chance of overcoming future tobacco-related NCD burden.
METHODS: A multistage sampling was performed across rural primary schools in Kuala Krai, Kelantan, Malaysia. Data were collected using self-administered questionnaires and the children aged 10-11 years (n=312) were subjected to cognitive tests including digit span, letter-number sequencing, coding, and symbol search. Cognitive performance was tested using subscales derived from the Wechsler Intelligence Scale for Children.
RESULTS: The prevalence of SHS exposure at home was 55.8%, where 11.9% of children lived with one smoker, while 43.9% of children lived with ≥2 smokers. There was a significant difference in the mean score of the combined cognitive tests between SHS-exposed and non-exposed children after adjustment for sex, parental educational level, family income and academic performance [Pillai's Trace=0.084, F statistic (df)=6.803 (4302), p<0.001].
CONCLUSIONS: More than half of the primary school children in rural Kuala Krai were exposed to SHS from at least one smoker at home. There was a significant association between SHS exposure at home and cognitive performance.
METHODS: A total of 715 incident PD cases were ascertained in a cohort of 220 494 individuals from NeuroEPIC4PD, a prospective European population-based cohort study including 13 centres in eight countries. Smoking habits were recorded at recruitment. We analysed smoking status, duration, and intensity and exposure to passive smoking in relation to PD onset.
RESULTS: Former smokers had a 20% decreased risk and current smokers a halved risk of developing PD compared with never smokers. Strong dose-response relationships with smoking intensity and duration were found. Hazard ratios (HRs) for smoking <20 years were 0.84 [95% confidence interval (CI) 0.67-1.07], 20-29 years 0.73 (95% CI 0.56-0.96) and >30 years 0.54 (95% CI 0.43-0.36) compared with never smokers. The proportional hazard assumption was verified, showing no change of risk over time, arguing against a delaying effect. Reverse causality was disproved by the consistency of dose-response relationships among former and current smokers. The inverse association between passive smoking and PD, HR 0.70 (95% CI 0.49-0.99) ruled out the effect of unmeasured confounding.
CONCLUSIONS: These results are highly suggestive of a true causal link between smoking and PD, although it is not clear which is the chemical compound in cigarette smoking responsible for the biological effect.