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.
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 26 pre-schools in Seremban, Malaysia were randomly selected using the probability proportional to size sampling. Dental examination was performed by a dentist to record the number of decayed teeth (dt). Weight and height of the pre-schoolers were measured. The mother-administered questionnaire was used to gather information pertaining to the sociodemographic characteristics and second-hand smoke exposure. Total sugar exposure was calculated from a 3-day food record.
RESULTS: Among the 396 participating pre-schoolers, 63.4% of them had at least one untreated caries, with a mean ± SD dt score of 3.56 ± 4.57. Negative binomial regression analysis revealed that being a boy (adjusted mean ratio = 1.42, 95% CI = 0.005-0.698, p = 0.047), exposed to second-hand smoke (adjusted mean ratio = 1.67, 95% CI = 0.168-0.857, p = 0.004) and those who had more than 6 times of daily total sugar exposure (adjusted mean ratio = 1.93, 95% CI = 0.138-0.857, p = 0.013) were significantly associated with dental caries among pre-schoolers.
CONCLUSION: A high prevalence of dental caries was reported in this study. This study highlights the need to reduce exposure to second-hand smoke and practice healthy eating behaviours in reducing the risk of dental caries among pre-schoolers.
Methods: This is a prospective, non-interventional, comparative study of 59 male (27 smokers and 32 non-smokers) undergraduates of a public university. Tear film stability was evaluated using non-invasive tear break-up time and fluorescein tear break-up time. Corneal staining was determined using Efron grading scale. MDEQ and OSDI Questionnaires were used to assess dry eye symptoms. Data were obtained from the right eye only and analyzed using descriptive and correlation analysis.
Results: The age range of the participants was between 19 and 25 years. The mean age for smokers and non-smokers was 22.19 ± 2.20 and 21.22 ± 1.83 years, respectively (P = 0.07). The smoker group had statistically significant lower tear film stability than the non-smoker group (P < 0.0001). Corneal staining was statistically significant higher at the nasal and temporal parts of the cornea in smokers (P < 0.05). There was a moderate correlation between tear film stability and scores of MDEQ and OSDI.
Conclusions: Tobacco smoke has a significant effect on the tear film stability, seen in reduced tear stability values among smokers. Corneal staining was found to be more extensive in the smokers. These findings would be useful to eye-care providers in the management of their dry eye patients related to smoking.
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.
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 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.