Second-hand smoke (SHS) exposure is one of the most important global public health hazards. There have been extensive convincing studies on the adverse health effects of SHS on both adults and children [
We collected the data via a population-based cross-sectional in-person household health survey of Chinese children aged ≤14 years in Hong Kong during September 2005 to June 2006. The target sample size was set to be approximately 7,500 subjects. Details of the methods are shown in Child Health Survey Report 2005-2006, Department of Health, Hong Kong (accessed via
We obtained information from a parent as proxy respondent when the child was aged under 11, and both directly from the child and from a parent for those aged 11 to 14. We conducted face-to-face interview to obtain household, family and personal characteristics, general health information, prenatal maternal passive smoking and active smoking, and household exposure to ETS at the time of survey. Respondents also completed a Chinese version of International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire [
We used a structured questionnaire [
We selected 5 health incomes of interest which included asthma ever, wheeze ever, current wheeze, allergic rhinitis ever, and eczema ever from the ISAAC questionnaire. They were defined by positive response to the questions “Has your child
We extracted information on participants and their parents’ characteristics, perinatal factors, and personal and family history of atopic illnesses from the structured questionnaire. We chose potential confounders based on previous studies which included socioeconomic status (SES) as defined by the highest education level of either parents (no or primary level, secondary level, tertiary, or above), mode of delivery (vaginal including missing answers versus caesarean section), perinatal problem (presence of any complications in the perinatal period), respondent of interview (father or mother), birthplace (Hong Kong or outside Hong Kong), main child care-giver (father, mother, or other), current parental smoking (yes if either or both parents smoke at the time of survey), and total number of household smokers including the parents (0, 1, ≥2). As there were significant missing responses in questions about gestational age at birth and birth weight, and both could be affected by maternal active and passive smoking [
We used descriptive statistics of proportions and means to describe the sample characteristics. We estimated the associations between baseline characteristics of the participants with foetal exposure to maternal smoking and health outcomes using exact chi-square test and selected those characteristics that were associated with both exposure and outcome with a
Among the 26,373 valid households with domestic household residing, 19,432 (73.3%) were successfully enumerated, 4,570 (17.3%) refused to participate and 2,461 (9.3%) could not be reached despite multiple attempts of contact. For households successfully enumerated, 4975 were found to have children aged ≤14 residing. A total of 7393 children (3839 boys with mean age
The baseline characteristics of the 7393 participants are shown in Table
Baseline characteristics of survey participants (
Number | (%) | |
---|---|---|
Age group, years | ||
0-1 | 548 | 7.41 |
2–5 | 1433 | 19.38 |
6–10 | 2755 | 37.26 |
11–14 | 2657 | 35.94 |
Sex | ||
Female | 3554 | 48.07 |
Male | 3839 | 51.93 |
Highest education level of parents | ||
No and primary | 660 | 9.05 |
Secondary and matriculation | 5344 | 73.29 |
Tertiary | 1288 | 17.66 |
Perinatal and postnatal problem | ||
Yes | 1044 | 14.12 |
No | 6349 | 85.88 |
Current parent smoking | ||
No | 5404 | 73.10 |
Yes | 1989 | 26.90 |
Total no. of household smokers | ||
0 | 5298 | 71.66 |
1 | 1796 | 24.29 |
≥2 | 299 | 4.04 |
Family history of asthma | ||
Yes | 199 | 2.69 |
No | 7194 | 97.31 |
Family history of atopy | ||
Yes | 612 | 8.28 |
No | 6781 | 91.72 |
Respondents | ||
Father | 2127 | 28.77 |
Mother | 5266 | 71.23 |
Birth place | ||
Hong Kong | 6556 | 88.68 |
Non-Hong Kong | 837 | 11.32 |
Mode of delivery | ||
Normal spontaneous delivery + other vaginal | 5869 | 79.39 |
Cesarean delivery | 1390 | 18.80 |
Missing | 134 | 1.81 |
Current primary carer | ||
Father | 523 | 7.07 |
Mother | 5755 | 77.84 |
Other | 1115 | 15.08 |
Five thousand one hundred and nine mothers (69.1%) reported that they never smoked nor were exposed to passive smoking during pregnancy, 2116 (28.6%) reported exposure to passive smoking during pregnancy, and 168 (2.3%) smoked during pregnancy. There were some statistically significant differences when comparing the baseline characteristics across the nonexposure group, the group exposed to maternal passive smoking and the group with maternal active smoking during pregnancy. The proportions of participants with family history of asthma (2.4% versus 2.8% versus 9.5%), parent smoked during time of survey (18.4% versus 43.2% versus 81%), and of age group 0-1 year (7.3% versus 7.1% versus 13%) were significantly the highest in the last group (Table
Baseline characteristics of participants categorized according to level of foetal exposure to maternal smoking during pregnancy.
Number of participants | Unexposed (mother did not smoke and mother not exposed to SHS during pregnancy) | Mother did not smoke but exposed to SHS during pregnancy | Mother smoked with/without exposure to SHS during pregnancy |
|
|
---|---|---|---|---|---|
|
|
|
|||
Family history of asthma | |||||
Yes | 199 | 123 (2.4%) | 60 (2.8%) | 16 (9.5%) | <0.0001 |
Current parent smoking | |||||
Yes | 1989 | 940 (18.4%) | 913 (43.2%) | 136 (81.0%) | <0.0001 |
Perinatal and postnatal problem | |||||
Yes | 1044 | 649 (12.7%) | 370 (17.5%) | 25 (14.9%) | <0.0001 |
Highest education level of parents | <0.0001 | ||||
No and primary | 660 | 451 (8.8%) | 200 (9.5%) | 9 (5.4%) | |
Secondary and |
5445 | 3709 (72.6%) | 1587 (75.0%) | 149 (88.7%) | |
Teritiary | 1288 | 949 (18.6%) | 329 (15.6%) | 10 (6.0%) | |
Age group, year | 0.0003 | ||||
0-1 | 548 | 375 (7.3%) | 151 (7.1%) | 22 (13.0%) | |
2–5 | 1433 | 952 (18.6%) | 436 (20.6%) | 45 (26.8%) | |
6–10 | 2755 | 1891 (37.0%) | 804 (38.0%) | 60 (37.1%) | |
11–14 | 2657 | 1891 (37.0%) | 725 (34.3%) | 41 (24.4%) | |
Sex | 0.47 | ||||
Female | 3554 | 2470 (48.4%) | 998 (47.2%) | 86 (51.2%) | |
Male | 3839 | 2639 (51.7%) | 1118 (52.8%) | 82 (48.8%) |
Association between baseline characteristics selected for logistic regression analysis and the 5 health outcomes.
Numbers of participants | Asthma ever |
Wheeze ever |
Current wheeze |
Allergic rhinitis ever |
Eczema ever |
|
---|---|---|---|---|---|---|
Family history of asthma | ||||||
No | 7194 | Reference | Reference | Reference | Reference | Reference |
Yes | 199 | 10.43 (7.41–14.67) | 5.29 (3.47–8.07) | 6.26 (3.86–10.16) | 2.20 (1.65–2.94) | 2.87 (2.08–3.97) |
Current parent smoking | ||||||
No | 5404 | Reference | Reference | Reference | Reference | Reference |
Yes | 1989 | 1.25 (0.97–1.61) | 1.42 (1.08–1.86) | 1.44 (1.03–2.01) | 0.94 (0.83–1.06) | 1.01 (0.86–1.18) |
Perinatal and postnatal problem | ||||||
No | 6349 | Reference | Reference | Reference | Reference | Reference |
Yes | 1044 | 1.64 (1.22–2.19) | 2.00 (1.48–2.70) | 2.18 (1.51–3.14) | 1.77 (1.53–2.04) | 2.00 (1.67–2.38) |
Highest education level of parents | ||||||
No and primary | 660 | Reference | Reference | Reference | Reference | Reference |
Secondary and matriculation | 5445 | 1.50 (0.91–2.48) | 2.29 (1.16–4.49) | 4.39 (1.39–13.86) | 1.18 (0.96–1.44) | 1.28 (0.96–1.70) |
Teritiary | 1288 | 1.95 (1.13–3.35) | 4.03 (2.00–8.13) | 7.74 (2.40–25.03) | 1.67 (1.33–2.10) | 2.27 (1.66–3.10) |
Age group, years | ||||||
0-1 | 548 | Reference | Reference | Reference | Reference | Reference |
2–5 | 1433 | 3.52 (1.39–8.92) | 1.37 (0.76–2.44) | 1.44 (0.73–2.82) | 2.81 (1.98–4.00) | 0.85 (0.64–1.13) |
6–10 | 2755 | 4.77 (1.94–11.74) | 1.04 (0.59–1.81) | 0.88 (0.46–1.71) | 4.71 (3.36–6.59) | 0.73 (0.56–0.95) |
11–14 | 2657 | 5.22 (2.13–12.84) | 1.36 (0.78–2.36) | 0.99 (0.52–1.92) | 4.79 (3.42–6.70) | 0.64 (0.49–0.84) |
Sex | ||||||
Female | 3554 | Reference | Reference | Reference | Reference | Reference |
Male | 3839 | 1.29 (1.02–1.64) | 1.87 (1.43–2.44) | 2.01 (1.43–2.83) | 1.55 (1.39–1.73) | 1.00 (0.86–1.15) |
Table
Associations between foetal exposure to maternal smoking and 5 health outcomes including asthma ever, wheeze ever, current wheeze, allergic rhinitis ever, and eczema ever.
Level of exposure | Numbers of participants | Asthma ever# ( |
Wheeze ever## ( |
Current wheeze## ( |
Allergic rhinitis ever# ( |
Eczema ever## ( |
||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Unadjusted | Model 1 | Model 2 | Unadjusted | Model 1 | Model 2 | Unadjusted | Model 1 | Model 2 | Unadjusted | Model 1 | Model 2 | Unadjusted | Model 1 | Model 2 | ||
Un-exposed (mother did not smoke and mother did not expose to ETS during pregnancy) | 5109 | Reference | Reference | Reference | Reference | Reference | Reference | Reference | Reference | Reference | Reference | Reference | Reference | Reference | Reference | Reference |
Mother did not smoke but exposed to ETS during pregnancy | 2116 | 1.28 |
1.27 |
1.29 |
2.05 |
2.04 |
2.00 |
2.06 |
2.01 |
2.03 |
1.22 |
1.22 |
1.23 |
1.61 |
1.59 |
1.60 |
Mother smoked with/without exposed to ETS during pregnancy | 168 | 2.10 |
1.75 |
2.32 |
2.46 |
2.34 |
2.61 |
2.74 |
2.36 |
2.72 |
1.01 |
1.14 |
1.14 |
1.38 |
1.31 |
1.32 |
Values are shown as OR (95% CI) *
Unadjusted Cochrane-Mantel-Haenszel test for trend #
Model 1: adjusted for age group, gender, highest education level of parents, perinatal and postnatal problem, and family history of asthma.
Model 2: adjusted for age group and gender only.
Our study shows a significant relationship between foetal exposure to tobacco smoke via maternal passive smoking and wheeze ever, current wheeze, allergic rhinitis, and eczema. The odds ratio of the associations between the prevalence of wheeze ever and current wheeze with exposure via maternal active smoking is greater than that with exposure via maternal passive smoking suggesting a possible dose response relationship, but further studies are warranted to ascertain it. To the best of our knowledge, our study is the first one to show foetal exposure to tobacco smoke via maternal passive smoking with allergic rhinitis and wheeze ever.
Maternal smoking is one of the important risk factors associated with adverse respiratory health in children. The effect of SHS exposure during pregnancy in nonsmoking women did not receive too much attention despite sufficient evidence to infer a causal relationship between maternal exposure to SHS during pregnancy and a small reduction in birth weight [
Unlike many cross-sectional studies, the difficulty in ascertaining temporal relationship between exposure and disease outcome is not a major issue in our study. Exposure in our subjects occurred before birth and health outcomes occurred after birth. The dose response relationship between wheeze ever and current wheeze with increasing exposure, from no exposure to maternal passive smoking and then to maternal active smoking, further supports causality. Nevertheless, the association between foetal exposure to maternal passive smoking and asthma ever was only marginally significant, unlike that with wheeze ever. We speculate that the adverse effect of maternal passive smoking or maternal active smoking on foetuses is operated via effects on lung function resulting in wheezing in early childhood, while further progression to asthma will depend on whether there are any other triggers after birth. Further study is warranted to elucidate the underlying mechanisms of maternal passive smoking and maternal active smoking on foetuses although evidence of biological plausibility exists. It is now well understood that the immature detoxification system and immature immune system make a foetus more vulnerable to any environmental toxins. Maternal active smoking during pregnancy lowers uterine blood flow and increases placental vascular resistance. Foetal haemoglobin has a greater affinity for carbon monoxide than adult haemoglobin. The resultant foetal hypoxia and transplacental delivery of many other toxic substances due to maternal smoking may have differential effect on immune and respiratory system during critical periods of in-utero development, leading to different manifestations of allergic diseases, modified further by postnatal environmental effects. More direct evidence supports the hypothesis that maternal SHS exposure, specifically to nicotine, may lead to low birth weight through a pathway of fetal hypoxia [
The effect of foetal exposure to maternal active smoking on allergic rhinitis and eczema is more controversial when compared to that on asthma and wheezing. While some studies did not find any effect of prenatal passive nor active maternal smoking with development of atopy, eczema, or hay fever [
The prevalence of self-reported maternal active smoking during pregnancy in our study was much lower than Western countries [
We hereby address the limitations of our study. Firstly, there is potential information bias inherent in a cross-sectional design. It was not likely since our Child Health Survey aimed to explore a much broader scope including general, physical, and psychosocial health status of our children population. Secondly, only a questionnaire was employed to assess exposure and outcome. Large-scale population study and the long latency period between exposure and health outcome of interest precluded the use of personal monitoring or stationary measurement of air nicotine or the use of biomarkers for exposure assessment in our study. Previous studies [
To conclude, our study shows the significant association of foetal exposure to maternal passive smoking with wheezing, allergic rhinitis, and eczema. This adds to the list of adverse effects of prenatal ETS through nonsmoking mothers to their foetuses. While most of the aggressive antismoking campaigns during pregnancy are addressed to smoking women [
Child Health Survey
Confidence interval
Census and Statistics Department
Hong Kong
International Study of Asthma and Allergies in Childhood
Odds ratio
Socioeconomic status
Second-hand smoke.
All authors declare that they have no conflict of interests to declare.
S. L. Lee, and T. H. Lam contributed equally to the paper.
The authors thank the Department of Health, Hong Kong for commissioning of the Child Health Survey; all the participants and their parents; our research nurse, Ms. Winnie Lau, for her assistance; Ms. Rita So for her secretarial support. They are grateful to The Doris Zimmern Charitable Foundation for supporting their Community Child Health Programme.