Background A significant proportion of children are exposed to environmental tobacco smoke (ETS) throughout the world. This is mainly because of exposure to parental smoking. It is unknown to what extent the negative effects of ETS on respiratory symptoms track from childhood into adulthood. Methods TESAOD (Tucson Epidemiologic Study of Airway Obstructive Disease) is a large population-based prospective study that was initiated in 1972. Participants were followed prospectively with questionnaires and pulmonary function tests (PFTs) completed about every two years in 12 follow-up surveys up to 1996. Skin prick tests and blood samples for IgE measurements were collected at surveys 1, 6, and 11. We identified subjects who entered the study as children (<15 years old) and were followed to adulthood (>18 years) during the study follow-up. Based on questionnaire data, active asthma, wheeze, cough, and chronic cough (cough for three consecutive months) were coded as never (never reported in childhood or adulthood), incident (never reported in childhood, but ≥ one positive report in adulthood), remittent (≥ one positive report in childhood, but not in adulthood), and persistent (≥ one positive report both in childhood and adulthood). PFTs measurements included forced expiratory volume in 1 second, forced vital capacity, and forced expiratory flow at 25-75%. Parent information on smoking status was collected simultaneously at child visits. ETS exposure status was assessed as “ever” or “never” between birth and 15 years. Results Information on parental ETS exposure in childhood and outcomes in adulthood was available for 444 non-Hispanic white participants (51.4% male) with mean age at initial survey of 7.7 years. Total mean follow-up time was 19.0 years (8.8 years in adulthood). Between birth and 15 years, 53.4% of children were exposed to ETS. After adjusting for sex, age at enrollment, years of follow-up, and personal smoking status (assessed at age 15 and above), combined parental ETS exposure in childhood was significantly associated with persistent wheeze (RR(adj) 1.9, p=0.026), persistent cough (RR(adj) 5.9, p<0.001), and persistent (RR(adj) 3.7, p=0.030) and incident chronic cough (RR(adj) 2.3, p=0.040). Paternal ETS exposure in childhood was associated with persistent wheeze (RR(adj) 2.3, p=0.002), persistent cough (RR(adj) 3.9, p<0.001), persistent (RR(adj) 4.8, p=0.004) and incident chronic cough (RR(adj) 2.2, p=0.031), and persistent asthma (RR(adj) 2.3, p=0.016). Maternal ETS exposure was associated with persistent (RR(adj) 1.9, p=0.029) and incident cough (RR(adj) 2.5, p=0.006). Maternal ETS exposure was associated with an increased percent predicted FVC in adulthood (coefficient, 3.75; p=0.019). No other effects on lung function were seen. There were no effects of ETS exposure on total serum IgE or allergic sensitization. ETS exposure was associated with respiratory symptoms in adulthood among both never and current smokers. Conclusions ETS exposure in childhood has long term health effects on lung function and respiratory symptoms. These effects do not appear to be IgE-mediated. ETS exposure, especially paternal ETS exposure, seems to influence the persistence of respiratory symptoms from childhood to adulthood and to affect women more than men. These effects are independent of personal smoking and also seen in never smokers. Both smoking mothers and fathers should be targeted when attempting to reduce ETS exposure among children.

Introduction Although studies have examined the association between childhood asthma and parental smoking and secondhand smoke, little research has explored the moderating role of birth weight and prematurity (BWP) status on this association. We examined the association between secondhand smoke exposure, asthma, and asthma severity in children aged six to 17 as well as the modifying effect of BWP on parental smoking and asthma. Methods We used data from 36,954 children from the National Survey of Children's Health 2017-2018. In addition to univariate analysis, adjusted and unadjusted logistic regression models were used to estimate the effect of secondhand smoke on asthma. The interaction term between parental smoking and BWP was tested. Multinomial regression was used to evaluate the association between secondhand smoke on asthma severity. Results About 15.1 % of children had asthma and 15.4% of parents reported smoking. Odds of asthma were higher in children living with an outdoor (AOR, 1.27; 95% CI, 1.06-1.52) and indoor (AOR, 1.46; 95% CI, 1.01-2.11) smoker in the adjusted model. The association of parental smoking with asthma differed by birth weight and premature status. Normal weight children who are premature had the highest odds ratio (AOR, 2.15; 95% CI, 1.2-3.86). In the multinomial model, low birth weight and premature children had higher odds of mild (AOR, 1.90; 95% CI, 1.40-2.56) and moderate/severe (AOR, 1.81; 95% CI, 1.16-2.84) asthma compared to the no asthma group. Conclusion The Association of parental smoking on asthma was modified by BWP. Focused asthma interventions in children should inquire about BWP status as well as parental smoking and household smoke exposure to reduce asthma morbidity and mortality.

Background: We investigated whether maternal smoking in the first year of life or any current parental smoking is associated with childhood or adolescent body mass index (BMI). Methods: Secondary analysis of data from a multi-centre, multi-country, cross-sectional study (ISAAC Phase Three). Parents/guardians of children aged 6-7 years completed questionnaires about their children's current height and weight, whether their mother smoked in the first year of the child's life and current smoking habits of both parents. Adolescents aged 13-14 years completed questionnaires about their height, weight and current parental smoking habits. A general linear mixed model was used to determine the association between BMI and parental smoking. Results: 77,192 children (18 countries) and 194 727 adolescents (35 countries) were included. The BMI of children exposed to maternal smoking during their first year of life was 0.11 kg/m 2 greater than those who were not (P = 0.0033). The BMI of children of currently smoking parents was greater than those with non-smoking parents (maternal smoking: +0.08 kg/m 2 (P = 0.0131), paternal smoking: +0.10 kg/m 2 (P < 0.0001)). The BMI of female adolescents exposed to maternal or paternal smoking was 0.23 kg/m 2 and 0.09 kg/m 2 greater respectively than those who were not exposed (P < 0.0001). The BMI of male adolescents was greater with maternal smoking exposure, but not paternal smoking (0.19 kg/m 2 , P < 0.0001 and 0.03 kg/m 2 , P = 0.14 respectively). Conclusion: Parental smoking is associated with higher BMI values in children and adolescents. Whether this is due to a direct effect of parental smoking or to confounding cannot be established from this observational study. / This work was supported by Cure Kids New Zealand through a grant to Professor E Mitchell and Dr I Braithwaite. Cure Kids New Zealand had no role or influence in design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. ISAAC Phase Three: / Revisión por pares