Relatively few studies have been reported that relate the effects of involuntary exposure to ETS on the developing fetus The latest studies, however, have indicated that pregnant women who are exposed to ETS are more likely to give birth to infants of lower birth weight than women not so exposed. In one large study of women whose non-smoking status was verified by serum cotinine measurements, there was a statistically significant inverse relationship between levels of serum cotinine measured in the second trimester and the birth weight of the infant. The estimated magnitude of the passive exposure effect has been in the range of about -25 g for a full-term pregnancy vs about -200 g attributed to the effect of direct maternal smoking during pregnancy. An effect as large as -100 g has been suggested by one of these studies.
ACUTE RESPIRATORY ILLNESS MORBIDITY
Community-based, longitudinal, epidemiologic studies that have used a variety of different end points generally have found an increased risk of acute respiratory illness morbidity. Among infants and children aged two years or younger, increased occurrence of episodes of bronchitis/pneumonia (with or without hospitalization, excess risk, 1.4 to 2.6) and increased occurrence of tracheitis and laryngitis have been reported. This effect has been strongest for episodes in the first year of life and more consistently associated with maternal smoking. However, some studies have suggested that the increased risk for hospitalization may extend up to age five years and that paternal smoking may contribute an additional risk. The excess risk appears to be independent of socioeconomic factors, type of feeding (breast vs nonbreast), birth weight, and sex of the infant. In the case of older children, the data are less easily interpreted. Only when morbidity is defined in terms of an acute “respiratory illness” (not further defined) in the year prior to the survey does there appear to be an increase in morbidity. In several of these studies, paternal smoking, in addition to maternal smoking, contributed to the excess risk.
Of particular interest for the clinician have been several studies that have related the occurrence of specific clinical syndromes and maternal smoking. The occurrence of maternal cigarette smoking has been found to be increased among children hospitalized for respiratory syncytial virus (RSV) infection in the first year of life, in the absence of any other underlying pulmonary disease. A similar observation has been made for infants with bronchopulmonary dysplasia who were hospitalized with RSV infection. Increased frequency of tonsillectomy, adenoidectomy, and chronic middle ear effusions also have been attributed to parental smoking. For these latter morbidities, the combined smoking of both parents appeared to contribute to the excess risk.
Taken in aggregate, the data with regard to acute respiratory morbidity show the most consistent increase in risk for children under the age of two years. The specific elements of exposure and biologic susceptibility that define this risk remain unknown. Moreover, the long-term health consequences of this increased risk remain speculative.
CHRONIC RESPIRATORY SYMPTOMS
A large number of epidemiologic studies have reported an increased occurrence of chronic respiratory symptoms (exclusive of asthma) in children between the ages of 5 and 20 years. In the case of a chronic cough, studies have been uniform in their observation of increasing prevalence with an increasing number of parents who smoke. In the case of chronic phlegm production and the occurrence of wheezing (in the absence of a specific diagnosis of asthma), most, but not all, studies demonstrate an increased prevalence with increasing parental smoking. For all of these chronic symptoms, the excess risk associated with two vs 0 smoking parents have been less than two.
In contrast to the studies of acute respiratory morbidity, studies of chronic respiratory symptoms involve age ranges were active smoking by the children themselves could confound the observed results. Although the results of some of the studies may have been influenced by misclassification of smoking adolescents as nonsmokers, the overall conclusions most likely are valid, since similar results have been observed in studies that have controlled for the active smoking status of the children.
ASTHMA, BRONCHIAL RESPONSIVENESS, AND ATOPY
Several lines of evidence suggest that exposure of infants and children to ETS, especially that generated by mothers, plays a role in the occurrence and severity of asthma.
Some epidemiologic studies have demonstrated an increased occurrence of asthma and persistent wheezing in children of smoking mothers. In one such study, 18 to 34 percent of asthma was attributed to maternal smoking. These data have been supported by clinical studies on the role of RSV infection in the occurrence of asthma, which also has demonstrated an increased occurrence of maternal smoking in RSV-infected children, but the extent to which this exposure contributed to the subsequent increased airways reactivity and decreased peak expiratory flow rates observed in the RSV-infected children was not addressed directly.
Epidemiologic studies have demonstrated that bronchial responsiveness to carbachol or cold air is increased in children with smoking parents (mothers only in one study) and that this observation is due largely to a greater degree of responsiveness in asthmatic patients with smoking mothers vs those with nonsmoking mothers. In one of these studies, virtually no maternal smoking occurred during pregnancy, which suggests that postpartum exposure to ETS has a direct role in the observed effects of ETS on bronchial responsiveness. Responsiveness to isoproterenol also has been associated with parental smoking.
A clinical study has observed that bronchial responsiveness is greater and levels of and FEF25-75 are lower in asthmatic subjects with smoking mothers vs those without. In that same study, these differences were shown to be most striking during the times of the year when homes were least likely to be well ventilated and when exposure to ETS might be expected to be greatest. A large study of inner-city asthmatic children showed that asthmatic subjects with smoking parents appear to have more emergency room visits for asthma, even after adjustment for asthma severity and asthma self-management practices.
Some insight into the possible mechanisms by which ETS might influence the occurrence and/or severity of asthma comes from recent data on the possible effects of cigarette smoke on the immune system. Cigarette smoking has been shown to increase levels of IgE and to enhance the occurrence of a specific IgE response to aeroallergens. Increased frequency of response to skin tests has been observed in the children of smoking parents/mothers, particularly in male children in one study. Postnatal exposure to ETS has been associated with raised levels of total IgE, and cord blood IgE levels have been found to be increased in infants whose mothers smoked during pregnancy. Infants of these latter mothers were found to have a four-fold excess risk of developing a clinically manifest allergic disease state. Even the study that failed to document an increased allergic sensitization in the children of smoking mothers did find that maternal smoking was significantly more common in children with clinically recognizable allergic disease. Thus, exposure to ETS may function as an environmental agent that enhances biologic mechanisms that relate to bronchial responsiveness and asthma. The association of ETS with acute respiratory illness morbidity, as discussed previously, and the observed association of increased early life respiratory illness morbidity in skin test positive children that has been observed in at least one study also suggests that ETS may play an important role in the hypothesized relationship between infant lower respiratory illness (especially RVS-associated) and the subsequent occurrence of asthma.
A large number of studies have investigated the relationship between involuntary exposure to ETS and pulmonary function in children. While not all of these studies have been uniform in their demonstration of an effect, the vast majority of both longitudinal and cross-sectional epidemiologic studies have observed an effect of such exposure. The most consistent effects have been observed for maternal smoking, but a number of studies have observed a supplemental effect of paternal smoking or an effect confined to paternal smoking.
Deficits in the level have been observed for FEF25-75, Vmax25, Vmax50, and Vmax75 as have deficits in the rate of growth and change in the level of and FEF25-75 in adolescents and children. Estimates of the cumulative effect on of childhood exposure to maternally generated ETS have been in the range of about 3 to 5 percent by age 20 years.
The sex of the child appears to relate to the observed effect of maternal ETS. Overall, most studies have found that female children are more likely to be affected than male children. The middle portion of the maximum expiratory flow-volume or time-volume curves is most consistently affected in females, although deficits in the proximal portions of these curves have been reported. When an effect has been observed for males, the portion of the curves affected has been less consistent.
The explanation for the predominance of the maternal smoking effect remains speculative. The explanation most often given relates to the time mothers spend with their children relative to that of fathers. Another explanation for which there is some supporting data relates to the possibility that maternal smoking during pregnancy produces effects on the lung that parallel the general growth-retarding effects of smoking on the fetus. Several studies have produced results that are compatible with this possibility. A similar interpretation has been given to the effect of maternal smoking on reduced height in their exposed children. Data from experimental animal systems also are compatible with this explanation.
The major unanswered question relates to the long-term consequences of the observed small deficits in pulmonary function that have been attributed to ETS exposure. Most studies of the effect of involuntary exposure to ETS on the pulmonary function of adults offer little insight since they generally have not evaluated childhood exposures. One investigation that sought specifically to evaluate a semiquantitative measure of lifetime exposure to ETS on the pulmonary function of subjects aged 15 to 35 years did find that exposure to maternal smoking and exposure to ETS during childhood had a significant effect on FEF25-75 in males. Effects in females in this study only related to exposure in the work environment. Thus, the matter remains unresolved.