Parental smoking and children's respiratory health
Considerable attention has focused recently on the harmful effects of involuntary or “passive” smoking. Many studies have reported adverse effects of prenatal and/or postnatal exposure on children's respiratory health, with much of the literature summarised in a number of reviews.1,2,3,4 Within a broad picture of harmful effects, uncertainties remain, including the relative importance of exposure at different periods in the child's life.
There is some evidence that prevalence of wheeze in childhood is associated more strongly to prenatal (intrauterine) exposure than with current parental smoking.5,6,7,8,9 In the Italian study of Agabiti et al, the effect of current parental smoking on wheeze was evident only in adolescents but not among younger children, while the effect of maternal smoking during pregnancy was greater in children.10 A Polish study found current exposure a stronger predictor than prenatal exposure,11 while a study in Chicago found a protective association with current maternal smoking.12 Similar inconsistencies have been seen for effects of tobacco exposure on child's asthma and other respiratory outcomes.2,4
Several studies have shown protective effects of current parental smoking on atopy, or on atopic‐related conditions such as eczema or hay fever.13,14,15,16 Yet Lam et al found increased risks of hay fever related to passive smoking,15 and passive smoking was also associated with allergic rhinoconjunctivitis and hay fever among Swedish and Turkish schoolchildren.17,18
The Pollution And The Young (PATY) project assembled data on exposures and health for 58 561 children, from cross‐sectional studies carried out in 12 countries with comparable questionnaires. PATY was established primarily to investigate associations between air pollution and respiratory health. Here we use that subset of 53 879 children with information on parental smoking. This pooled analysis, on extensive, original data (with only three of the 12 studies as yet published on this topic),19,20,21 gives a powerful opportunity to examine critical periods of exposure to cigarette smoke, to address the problems of co‐linearity between prenatal and postnatal passive smoking and to assess independent effects of three exposures: maternal smoking during pregnancy, passive smoking during the first two years of the child's life, and current passive smoking. Associations found in this large dataset between prenatal and postnatal passive smoking on children's lung function have already been reported.22
METHODS
Comparable cross‐sectional studies were sought (published or otherwise), which assessed respiratory symptoms and individual risk factors at elementary school age by comparable parent's questionnaires,23 included cough and wheeze as primary outcomes, and (since a primary objective was to assess effects of ambient air pollution) allowed calculation of annual mean particulate matter. To improve comparability further, data were restricted to children aged 6–12 years. Table 1
1
describes the contributing studies, detailed in individual reports.10,19,20,24,25,26,27,28,29
Table 1 Participating studies: geographic units, period of data gathering, and number of children, aged 6–12 years, with information on age, sex, and parental smoking
StudyNumber of study areasData collectionNumber of childrenAge range (years)Austria, Linz Survey8 areas in 1 townJan 1996–Dec 199837766–8Bulgaria, CESAR study4 areas in 3 townsFeb–May 199629737–11Czech Republic, CESAR study4 areas in 1 townFeb–May 199629627–11Germany, Bitterfeldt study3 areas in 3 townsAug 1992–Jul 199319726–12Hungary, CESAR study5 areas in 5 townsFeb–May 199630317–11Italy, Sidria study29 areas in 22 townsOct 1994–Mar 199590736–10Holland, 24 school study24 areas in 19 townsApr 1997–Jul 199819137–12North America, 24 city study24 areas in 24 townsSep–Nov in 1988–90148458–11Poland, CESAR study4 areas in 4 townsFeb–May 199626437–11Russia, 10‐city study13 areas in 10 townsApr–May 199954128–12Slovakia, CESAR study4 areas in 3 townsFeb–May 199625317–11Switzerland, Scarpol study10 areas in 10 townsOct 1992–Mar 199327486–12Total132 areas in 105 towns53879
CESAR, Central European Study on Air pollution and Respiratory health.
All studies collected data on the children's health and individual/household risk factors (including exposure to tobacco smoke) via questionnaires, distributed in schools and filled in by the parents. Care was taken to select or construct variables which were as comparable as possible.23
Eight outcomes were analysed: wheeze in the last 12 months, “woken by wheeze in the last 12 months”, asthma ever, bronchitis in the last 12 months, nocturnal dry cough in the last 12 months, morning cough, “sensitivity to inhaled allergens”, and hay fever ever. Detailed wordings are reported elsewhere.23 Three “parental smoking” measures were defined: mother smoked during pregnancy, child lived with a smoker during the first two years of life (unavailable for Austria and Switzerland, in Germany “first year of life”), and child currently lives with a smoker. The latter included all smokers in the household, in all countries. Passive smoking during the first two years was restricted to parental smoking in Italy, Switzerland and the CESAR (Central European Study on Air pollution and Respiratory health) countries.
Only the exposures relate to different periods of the child's life. Health questionnaires were administered only once per child.
Statistical analyses
Analyses were done using STATA v8. A two‐stage approach was used. In stage 1, study‐specific parental smoking effects were estimated using logistic regression (on individual level records). Three models were used: The first (“confounder adjusted”) controlled for potential confounders (listed below), but not for the other smoking variables. The second and third models additionally adjusted for one and then both other smoking variables. In stage 2, the study specific results were entered into a meta‐analysis, to obtain forest plots of the estimates, a mean estimate (a weighted mean of the study specific estimates), and a measure and Cochran χ2 test of between‐study heterogeneity. Study specific estimates were assumed to follow a random distribution about a mean, and the estimation of this mean and its confidence interval took into account both variation among study‐specific estimates and uncertainty (due to sampling variability) related to each study‐specific estimate.30
We controlled for age, sex, maternal education, paternal education, nationality, household crowding, gas for cooking, unvented gas/oil/kerosene heater, mould, birth order, “ever had a pet”, and study area. Adjusting for study area accounts for risk factors such as ambient air pollution, climate, and neighbourhood socioeconomic differences.
Meta‐regressions assessed associations between study‐specific estimates and study‐characteristics. These potential sources of heterogeneity between estimates were: season of data collection; study period; proportion of younger children (6–8 years old); response rate (above/below 80%); Western or former “Eastern Block” countries.
We tested robustness of results to controlling for parental illness (a potentially problematic variable, since parental smoking may cause both parent's and child's illness), attendance at kindergarten, and breastfeeding. We also assessed effect modification by age (6–8 v 9–12), breastfeeding, household crowding and, since a recent study found that associations between maternal smoking during pregnancy and asthma were restricted to girls,31 for effect modification by the child's sex.
RESULTS
Table 2
2
shows study characteristics, frequency of exposure to passive smoking, and prevalences of respiratory and allergic disorders. Bronchitis was reported most frequently, prevalences exceeding 30% in four of the studies. Hay fever and “woken by wheeze in the last 12 months” were reported least frequently, with prevalences under 10% in most studies.
Table 2 Study characteristics, prevalences of children's passive smoking and respiratory symptoms
AustriaBulgariaCzechGermanyHungaryItalyHollandN AmericaPolandRussiaSlovakiaSwitzEast/West (E or W)WEEEEWWWEEEW2/3 questionnaires in spring. 1 = yes, 0 = no011010001010Post 1995 study. 1 = yes, 0 = no111010101110Response rate <0.8. 1 = yes, 0 = no001010101011% of children in age range 6–8 years98443432306133537173455Frequencies of exposures (%):Maternal smoking during pregnancy17.5%6.4%8.9%4.9%12.7%17.2%28.7%26.6%25.3%4.4%6.0%17.0%Smoking during first 2 years of life–70.1%62.0%18.7%62.9%57.6%60.7%63.4%74.8%46.3%54.9%–Current smoker in household62.5%70.9%57.4%45.8%55.9%58.2%58.1%50.4%64.9%46.1%48.4%48.2%Prevalences of symptoms (%): Wheeze in last 12 months13.6716.4119.7610.219.926.769.4519.4011.8413.299.3710.32 Asthma ever8.4916.509.728.5222.358.998.069.6910.211.866.889.00 Bronchitis in the last 12 months–23.6941.12–32.5712.407.826.1934.6014.7130.9418.26 Nocturnal dry cough10.405.3518.5418.579.4215.6621.74–13.55–12.8321.57 Morning cough5.2816.0225.6113.826.17––6.0245.7111.3514.4011.83 Sensitivity to inhaled allergens12.8512.3716.67–14.0210.9215.1721.0013.906.4414.6513.70 Hay fever ever5.32––4.55–7.787.1914.34–1.20–10.10 Woken by wheeze in the last 12 months–7.0714.78–8.371.874.925.188.624.258.584.59
Numbers living with a reported current smoker ranged from 45.8% in Germany to 70.9% in Bulgaria. Passive smoking during the first two years of life ranged from 18.7% in Germany (first year of life only), then from 46.3% in Russia, to 74.8% in Poland. Reported prenatal exposure tended to be rarer in Eastern countries and ranged from 4.4% in Russia to 28.7% in Holland.
The exposures were correlated, as anticipated. Coefficients of correlation (r) between current exposure and exposure during the first two years ranged from 0.22 in Germany to 0.75 in the Czech Republic. Between prenatal exposure and exposure in the first two years, r ranged from 0.16 in Bulgaria to 0.42 in North America and the Netherlands, and between current and prenatal exposure, r ranged from 0.14 in Bulgaria to 0.42 in North America.
Confounder adjusted results
Wheeze and nocturnal cough were associated with all three smoking measures, with harmful effects seen in nearly all studies (fig 1
1).
). Mean odds ratios for wheeze ranged from 1.17 (95% confidence interval (CI) 1.02 to 1.33) for the effect of smoking during the first two years, to 1.25 (95% CI 1.14 to 1.37) for smoking during pregnancy (table 3
3).
).
Figure 1 Forest plots of study‐specific odds ratios, and mean odds ratios, for effects of “current smoker” (top row), “smoking during pregnancy” (middle row) and “smoking during first two years of life” (bottom row), on wheeze, nocturnal cough, asthma, and woken by wheeze. Odds ratios are not mutually adjusted, but adjusted for all other potential confounders listed above. Vertical line indicates null position (odds ratio of 1). Horizontal lines represent 95% confidence intervals. Diamond shapes indicates the positions, and confidence intervals, of the mean estimates. Extreme confidence intervals are truncated at 0.25 and 3.0.
Table 3 Mean odds ratios (95% confidence intervals) for associations between smoking exposures and each outcome
OutcomeExposure to:Current smokingSmoking in pregnancySmoking in first 2 yearsConfounder adjustedFully adjustedConfounder adjustedFully adjustedConfounder adjustedFully adjustedWheeze1.20 (1.06 to 1.35)H **1.12 (0.98 to 1.27)H1.25 (1.14 to 1.37)**1.12 (1.04 to 1.22)**1.17 (1.02 to 1.33)H*1.06 (0.95 to 1.19)Asthma1.09 (1.01 to 1.19)*1.03 (0.95 to 1.12)1.18 (1.08 to 1.28)**1.17 (1.04 to 1.31)*1.10 (1.00 to 1.21)*1.04 (0.95 to 1.14)Bronchitis1.11 (1.05 to 1.18)**1.10 (1.03 to 1.19)**1.03 (0.92 to 1.16)H0.98 (0.86 to 1.11)H1.08 (1.02 to 1.14)*1.03 (0.94 to 1.12)Nocturnal dry cough1.11 (1.03 to 1.19)**1.05 (0.94 to 1.17)1.13 (1.03 to 1.24)**1.15 (1.00 to 1.32)1.11 (1.03 to 1.21)**1.05 (0.94 to 1.18)Morning cough1.07 (0.98 to 1.16)1.04 (0.95 to 1.13)1.12 (0.97 to 1.30)H1.14 (0.94 to 1.39)H1.12 (0.99 to 1.27)H1.09 (0.96 to 1.25)HSensitivity to inhaled allergens0.96 (0.91 to 1.02)0.96 (0.88 to 1.04)0.98 (0.91 to 1.05)0.98 (0.91 to 1.07)1.02 (0.94 to 1.12)H1.06 (0.94 to 1.20)HHay fever0.92 (0.81 to 1.04)0.99 (0.81 to 1.20)H0.87 (0.79 to 0.96)**0.89 (0.80 to 1.00)*0.91 (0.83 to 0.98)*0.97 (0.87 to 1.07)Woken by wheeze1.12 (0.99 to 1.25)1.16 (1.03 to 1.30)**1.15 (0.93 to 1.43)H1.13 (0.88 to 1.45)H1.04 (0.91 to 1.20)H0.98 (0.85 to 1.12)
*p<0.05 **p<0.01.
Differences between estimates from the two models may include the loss of up to two studies when adjusting for smoking during the first two years of life.
HHeterogeneity between study specific results (p<0.10).
Odds ratios are from confounder adjusted models, and from fully adjusted (for previous covariates plus both other smoking variables).
There was evidence of heterogeneity (within a strong predominance of positive results) among results for both current smoking and smoking during the first two years. Mean odds of nocturnal cough were raised by around 12% for all three smoking variables, with no evidence of heterogeneity.
Asthma was clearly related to smoking during pregnancy, with a mean odds ratio of 1.18 (95% CI 1.08 to 1.28). Odds ratios for the other periods of exposure were also above one in nine of the 12 countries, with no evidence of heterogeneity.
Associations between current smoking and “woken by wheeze” were predominantly positive, with a mean odds ratio of 1.12 (95% CI 0.99 to 1.25). For the other two smoking measures results were less clear—mean associations were positive, but with considerable heterogeneity.
Bronchitis was related to current smoking, and to smoking during the first two years, with mean odds ratios of about 1.10 (fig 2
2).
). Associations of bronchitis with smoking during pregnancy were heterogeneous, within no clear pattern.
Figure 2 Forest plots of study‐specific odds ratios, and mean odds ratios, for the effects of “current smoker” (top row), “smoking during pregnancy” (middle row), and “smoking during first two years of life” (bottom row), on bronchitis, hay fever, sensitivity to inhaled allergens, and morning cough.
