In: Smoking17 Aug 2015
The detrimental effects of smoking on adult pulmonary function has led to concern that passive smoking (the exposure to smoke from others cigarettes) may be harmful, especially to young children. The major studies that have examined the relation between parental smoking and childhood symptoms and pulmonary function are summarized in Table 3. Of these studies, all but four are cross-sectional analytic surveys. In such studies, childrens’ symptoms and/or pulmonary function are examined at a single point in time and related to parental smoking habits. Inference from cross-sectional analytic surveys is limited by the fact that predisposition to decreased pulmonary function may have preceded the exposure to smoke. It is known, for example, that smokers have smaller babies (not only because of smoking, but probably because of other factors associated with smoking). It is possible that lung development, or predisposition to pulmonary infection, may differ in these smaller babies. In addition, analytic surveys tell us about symptoms only over a relatively short period of time. Thus, while cough or respiratory infections might not be different in ten-year-olds depending on parental smoking, differences may have been apparent earlier in life, or develop later.
Although prospective cohort studies provide stronger evidence about the effects of smoking on childrens health, they share with analytic surveys a large number of potential confounders. Obviously, when measuring pulmonary function, one needs to take into account a childs height, weight, age, and ethnic background. However, parental smoking is associated with a large number of other variables that may also effect childhood symptoms and pulmonary function. These include socioeconomic status, the use of gas stoves for cooking, parental symptoms of cough and sputum, the childs birth weight, number of siblings, and the childs tendency to smoke. Some of these are such strong confounders that failure to take them into account can completely invalidate the results of a study. For example, in two independent studies an apparent association between parental smoking and childhood symptoms disappeared completely when parental respiratory symptoms were taken into account. This finding severely limits the usefulness of any study of childhood symptoms in which parental symptoms were not considered. An equally powerful confounder in studies of children over ten years of age is the child s own smoking, known to be associated with parental habits. When childhood and parental smoking have been examined together, the child’s own smoking (as one might expect) has proved a far more important factor. Studies which include adolescents and do not take the child’s smoking into account are of limited use. To know more about smoking in children, their passive participation and influence on them and some other interesting facts about medicine are represented here healthcaremall4you.com Canadian Health&Care Mall.
Most of the above problems would tend to bias the studies in favor of finding an association when there is no true causal relation. There are other features which may attenuate a true relationship. For example, obtaining precise and accurate measures of both parental smoking and childhood symptoms is difficult. To whatever extent assessment of exposure and outcome is subject to random measurement error, a misleadingly low estimate of the relationship between the two will result.
Even in the studies in which parental smoking has been associated with childhood symptoms and decreased pulmonary function, the relationship has not been strong. The greatest effect on pulmonary function was seen in a study by Tager and colleagues who estimated an adverse effect of maternal smoking on forced expired volume in one second (FEV,) of 100 ml over five years. The study design was strong in that 1,156 children were followed-up over six years in a prospective cohort design; childhood smoking habits were ascertained in an interview when parents were not present and then taken into account in the analysis. However, this study dealt largely with adolescents, and one might expect an underreporting of smoking even with parents absent, an effect which would bias the results toward an apparent effect of parental smoking. In addition, there was a great deal of missing data in this study, and the precision of the authors’ statistical model is questionable. As far as symptoms are concerned, the biggest effects have been an approximately twofold increase in cough or respiratory infections seen in a number of studies.
Results have not been consistent. A number of workers have failed to find any relation between symptoms and parental smoking. However, it is worthwhile to examine the effects of parental smoking on children of different ages. The three best studies in the literature, all using prospective cohort designs taking into consideration a large number of confounding factors, found approximately twofold increases in lower respiratory tract infections in smokers’ children in the first year of life. Two of these studies followed children beyond the first year of life; in both, the relationship disappeared in subsequent years. There have not been any studies focusing on the first year that have failed to find an effect of maternal smoking.
As far as pulmonary function is concerned, Tager s prospective study found an effect of maternal smoking on pulmonary function, but Dodges did not. Among the analytic surveys, the results have been equally inconsistent.
Temporality can be rigorously assessed only in the prospective studies. However, it is implausible that childhood symptoms or decreases in pulmonary function would precede or lead to increases in parental smoking.
A dose-response gradient (the more the parents smoked, the worse the child’s health) has been consistently found in the three prospective cohort studies which examined lower respiratory infections in the first year of life. However, even among the studies which showed a relationship between parental smoking and older childrens symptoms or pulmonary function, a dose-response gradient has not always been present.
Finally, there is the issue of biologic plausibility. It is established that smoking can decrease pulmonary function in adults, and causes inflammatory changes in the lung. Therefore, one might suspect that childrens lungs, perhaps more vulnerable to insult, could be damaged by lower concentrations of irritants than those to which the active smoker is exposed.
In summary, three studies using powerful designs have demonstrated a consistent (though only moderately strong) relation between maternal smoking and lower respiratory infections in the first year of life. These studies also satisfy criteria of temporality and the presence of a dose-response gradient, and the hypothesis is biologically plausible. The case for a causal role of smoking in this context is thus quite strong. However, the relationship of symptoms or pulmonary function to parental smoking in older children is weak, inconsistent, and does not always demonstrate a dose-response gradient. A deleterious effect of passive smoking in older children is unproven.
To definitively establish the role of passive smoking in childhood health would require an RCT of an effective anti-smoking intervention for pre-term smoking mothers. Such a trial has been conducted, and demonstrated an increased birth weight in the experimental group whose smoking was reduced. The investigators, however, have not taken the next required step: following the infants in the two groups with serial measures of respiratory symptoms and pulmonary function. If such a trial were conducted, it may be desirable to stratify the two groups according to other variables shown or suspected to be related to childhood respiratory health, including socioeconomic status, the use of gas stoves for cooking, parental symptoms of cough and sputum, and the number of siblings. Complete or nearly complete followup would be necessary for the results to be valid. This would suggest conducting the study on a geographically stable population, and building in resources for followup visits in patients’ homes. Finally, attempts to improve measurement of exposure to tobacco smoke should be undertaken; urinary excretion of nicotine metabolites may be useful in this regard.
In conclusion, we have presented a method for assessing questions of causation and applied it to two ongoing controversies. Awareness of the relative merit of various research designs, and of the criteria for determining causation, can provide a framework for assessing new evidence regarding the causal connection between smoking and adverse health outcomes.
Table 3—Studies of Parental Smoking and Childrens Respiratory Health
|Seniorauthor||Studydesign||Number of subjects||Age (years)||Percent eligible compl. study||Sources of data||Confounding considered in analysis||Outcomes||Result||Dose-responsegradient|
|Ferguson||prospectiveCohort||1.165||birth to age 3||90||interviewparents:hospitals||maternal age, education, family size, birth weight, gestational age, sex||bronchitis/pneumonia,respiratory|
symptoms2 x incidence of bronchitis & pneumonia with maternal smoking in first, but not subsequent, yearsyesBland*cross-sectionalcohortanalytic5,835secondaryschool79questionnaire to childrenchild’ssmokingcough and morning coughIncrease cough Boys: NS 2.3,* S 3.6t Girls: NS 0.9,S 2.2noBonham®cross-sectionalcohortanalytic37,000households0-16 questionnaire to parentsnumber of childrenrestricted activity days9.1 days in NS 10.2 in SyesCameron*cross-sectionalcohortanalytic6950-16>90phone interview with parentsNonerespiratory and total illnesstotal S 8.8 NS 5.6 respiratory S 5.9 NS 3.1yesColleycross-sectionalcohortanalytic2,6006-1493questionnairesocial class, family size, parental symptomscoughno effect of S when parental symptoms considerednoDodgeprospectivecohort5258-10, followed for 3 yrs<75questionnaire to parents, spirometer childarea of residence, gas cooking, height, agepulmonaryfunction,coughno difference in rate of increase in lung function; cough increasednoEkwoMcross-sectionalcohortanalytic1,3556-12<60questionnaire to parentsgas cooking, dx of bronchitis andemphysemasymptoms,pulmonaryfunctionno difference in any variablenoHarlapprospectivecohort10,672first year interviewmothersbirth weight, social classhospitalizations for bronchitis andemphysemaNS 9.5/100/yr S 13. l/10Q/yryesHasselbladt**cross-sectionalcohortanalytic16,6895-13<50questionnaire to parentsheight, age, sex,community,education,
seasonpulmonaryfunctiondecreased spirometry with maternal of variance explainedyesLebowitz*cross-sectionalcohortanalytic1,655households0-14 questionnaire to parentsage, social status, family size, parental symptomscoughapparent effect disappeared when parental symptoms considerednoSchillingcross-sectionalcohortanalytic8167-18 questionnaire to parents and childrenheight, weight, age, SESpulmonaryfunction,coughno effectnoSpeizer*cross-sectionalcohortanalytic8,1206-10>95questionnaire to parentsgas cooking, height, weight, city, social classpulmonary function, respiratory disease before age 2S related to respiratory disease before age 2; no other effectnoTager”cross-sectionalcohortanalytic4445-950interviews with parentschild’s smoldng, Sibship size, age, sex, height, previous respiratory illnesspulmonary’function,respiratory
illness‘flow rates in S; no relation to respiratory illnessyeslager”prospectivecohort1,1565-9 at start, followed 6 years interviews with parents of children under 10; interviews with children age 10 or moreage, sex, initial height, change in height, child’s smokingpulmonaryfunctionmother’s smoking = estimated loss of 100 ml in FEV, over 5 years Tashkincross-sectionalcohortanalytic9717-17-80interviews with parents and childrenage, height,geographicarea, sex
symptomsno difference in symptoms; 3.5% decrease in FEV, in males, 1.3% in femalesnoCharlton*2cross-sectionalcohortanalytic15,1268-1996questionnaire to childrenchildrens smoking, age, sexcougheffect of smoking yesstrongest inchildren under 11
Boys: NS 35%, OS 42%,t BS 54%f
Girls: NS 32%, OS 40%, BS 52%
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