Our population-based epidemiologic study showed the harmful effects of fetal and current exposure to tobacco smoke products. Prenatal exposure due to maternal smoking had the strongest effects on respiratory symptoms. Current household ETS exposure also showed significant adverse effects, but past-only ETS exposure was not associated with any respiratory outcome. In addition, the number of current household cigarettes smoked, the percentage of ETS exposure during lifetime, and the number of current smokers at home showed increasing trends in risks of respiratory symptoms.
Age, sex, active smoking habits, parental atopic history, and parental education might contribute to asthma and wheeze in childhood [3
]. We minimized interference from these confounders by recruiting lifelong non-smokers of similar age at study entry, and adjusting potential confounders by regression models. Although maternal smoking was, as expected, a strong determinant of preterm delivery and low birth weight, and these adverse pregnancy outcomes were strong predictors of respiratory problems, only gestational age showed an effect in our study. Adjustment for indoor residential factors resulted in only small changes in the effect estimates, and these covariates were not included in the final models.
In our population, 197 (3.9%) children were reported to have had in utero
ETS exposure (Table ). The prevalence is much lower than other Western studies [11
]. In utero
exposure to maternal smoking showed significant adverse effects on respiratory health, with an adjusted OR of 3.21 (95% CI 1.95-5.29) for current wheeze. In contrast, current exposure to ETS showed a smaller effect, with an adjusted OR of 1.30 (95% CI 0.96-1.78) for current wheeze (Table and Table ). Our findings on the stronger effect of prenatal exposure compared with current ETS exposure are consistent with the results in the 24 Cities Study [25
]. Other studies of Californian[11
] and Russian[32
] children also provided evidence of the relative importance of prenatal exposure on respiratory outcomes.
These associations of in utero
exposure with respiratory outcomes are consistent with the evidence that in utero
exposure adversely affects postnatal pulmonary function and increases the occurrence of respiratory symptoms [19
]. Furthermore, in utero
exposure may also affect the development and maturation of the pulmonary immune system [35
]. Inappropriate persistence of a Th2
-dominant response appears to increase allergic sensitization upon sufficient exposure to a variety of common antigens that underlie the pathogenesis of asthma [36
]. Our result is in agreement with the biological plausibility that in utero
exposure to maternal smoking, through mechanisms of decreasing pulmonary function and increasing bronchial hyper-responsiveness (BHR), induces asthma occurrence, especially during the first five years of life (Table ).
Exposure at home by parental smoking is likely the most common source of ETS exposure in children. Exposure to household ETS among children has been reported to vary from 27.6% to 77.8% [8
]. Our prevalence of 49.0% for lifetime ETS exposure and 44.9% for current ETS exposure are similar to many Western countries, but are far lower than the prevalence of 80.0% reported in a recent study in a Chinese population [22
]. While a review of epidemiologic studies on allergies has been inconclusive [16
], murine model and human experimental studies may explain the findings of the present investigation. In our results, current household cigarettes smoked, percent of ETS exposure during lifetime, and the number of current smokers at home all showed increasing trends in the risks of respiratory outcomes, consistent with the dose-response relationship of household ETS in many recent studies [34
]. In a recent meta-analysis of the effects of household ETS on asthma and wheeze, Vork et al reported a summary relative risk for asthma of 1.21 (95% CI 1.17-1.26) that is consistent with our estimate of 1.15 (95% CI 0.92-1.44). Our estimate for the association between household ETS and active asthma (1.39, 95% CI 1.00-1.93) is slightly higher than that from the meta-analysis (1.25, 95% CI 1.21-1.30), but the confidence intervals show considerable overlap [39
]. The literature on the relationship between household ETS exposure and respiratory symptoms gives conflicting results with regard to sex differences in susceptibility [40
]. We found almost all respiratory outcomes showed non-significant interaction between household ETS exposure and sex in health outcomes (Table S4 in Additional file 1
), consistent with the findings from a recent study in Singapore [38
The prevalence of maternal and paternal smoking in this study was 3.4% and 36.0%, respectively, which is comparable to an earlier survey in Singapore [41
]. The prevalence of maternal smoking in Taiwan is much lower than the 13% reported in Sweden [42
], 23.8% in USA [43
], and 32% in Austria [44
]. Studies using cotinine as a biomarker show that the strength of the association between maternal smoking and respiratory outcomes is in part due to larger ETS doses from maternal smoking than from other sources [24
]. In our study, maternal ETS conferred a higher risk of respiratory symptoms compared with paternal ETS (Table and Table ). Several reasons could explain this phenomenon: mothers have more direct contact with their children at home compared with fathers; women who smoke during pregnancy are likely to continue smoking after delivery. In Taiwan, the ratio of current smoker/ex-smoker rates in adulthood is close to 7 [15
], far higher than the ratio near to one in the United States [45
] and indicating a particularly low rate of smoking cessation in Taiwanese adults. Depending on which symptom is considered, our results show the higher risk for ETS from both parents when compared with just maternal or just paternal ETS exposure (Table ). The reasons for this are not clear and could be partly attributed to the behavior of the parents [23
We found that in utero
exposure to maternal smoking had larger effects on early-onset asthma than those asthmatics diagnosed after 5 years of age (Table ). Previous studies showed a stronger risk for incident asthma or wheezing illness among younger children compared with older children [21
]. These investigators suggested that the stronger relationship might be attributed to exacerbation of intercurrent infection among young children, resulting in transient wheeze that would tend to diminish with age and increasing airway caliber. The proposed mechanism would suggest that household ETS may not be the sole primary cause of early childhood asthma.
Our study has some limitations. Because of cross-sectional data, the factors we studied may have affected outcome prevalence through effects on disease duration rather than disease incidence. Biases could also be introduced if parents or children change their time-activity patterns to avoid ETS exposure. However, we note that the prevalence of past-only ETS exposure is very low, suggesting that adult smoking patterns would not differentially change over time. Differential participation by children with respiratory outcomes who had different ETS exposure histories is unlikely to have been significant enough to produce substantial bias, as participation rates in each classroom were high. Retrospective recall of tobacco smoking by questionnaire is likely to have produced some misclassification of exposure. However, the validity of ETS exposure estimates based on questionnaire responses have been investigated and found to provide reasonably valid data [46
]. It can be expected that more parents would not want to be seen as flouting the law and thus report that they are smoking within the privacy of their homes. Under these conditions, it can be anticipated that the proportions of exposure misclassification are likely to be non-differential for symptomatic children as for the healthy children.
In summary, our results showed that prenatal and current household ETS exposure in Taiwan had significant adverse effects on respiratory health in children. Eliminating household ETS exposure may offer the most promising opportunity for reducing morbidity, because this risk factor is potentially modifiable. Public health policy for reducing the burden of respiratory symptoms may require a stronger focus on smoking cessation in the home, where children could gain significant health benefits.