The National Conservation Guild


Indoor Air Quality Issues


Effects Of Environmental Tobacco Smoke
(ETS) on Children.


Excerpts from chapter 1 of the Environmental Protection Agency's report entitled
Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders,
EPA/600/6-90/006F. The report is dated December 1992 and was publicly released on January 7, 1993.


Environmental tobacco smoke (ETS) in the United States presents a
serious and substantial public health impact...

In children:

ETS exposure is causally* associated with an increased risk of lower respiratory tract infections (LRIs) such as bronchitis and pneumonia. This report estimates that 150,000 to 300,000 cases annually in infants and young children up to 18 months of age are attributable to ETS.

ETS exposure is causally associated with increased prevalence of fluid in the middle ear, symptoms of upper respiratory tract irritation, and a small but significant reduction in lung function.

ETS exposure is causally associated with additional episodes and increased severity of symptoms in children with asthma. This report estimates that 200,000 to 1,000,000 asthmatic children have their condition worsened by exposure to ETS.

ETS exposure is a risk factor for new cases of asthma in children who have not previously displayed symptoms.

In 1986, the National Research Council (NRC) and the Surgeon General of the U.S. Public Health Service independently assessed the health effects of exposure to ETS (NRC, 1986;

U.S. DHHS, 1986). Both of the 1986 reports conclude that ETS can cause lung cancer in adult nonsmokers and that children of parents who smoke have increased frequency of respiratory symptoms and acute lower respiratory tract infections, as well as evidence of reduced lung function.

Population estimates of ETS health impacts are also made for certain noncancer respiratory endpoints in children, specifically lower respiratory tract infections (i.e., pneumonia, bronchitis, and bronchiolitis) and episodes and severity of attacks of asthma. Estimates of ETS-attributable cases of LRI in infants and young children are thought to have a high degree of confidence because of the consistent study findings and the appropriateness of parental smoking as a surrogate measure of exposure in very young children...

1. Exposure of children to ETS from parental smoking is causally associated with:

a. increased prevalence of respiratory symptoms of irritation (cough, sputum, and wheeze),

b. increased prevalence of middle ear effusion (a sign of middle ear disease), and

c. a small but statistically significant reduction in lung function as tested by objective measures of lung capacity.

2. ETS exposure of young children and particularly infants from parental (and especially mother's) smoking is causally associated with an increased risk of LRIs (pneumonia, bronchitis, and bronchiolitis). This report estimates that exposure to ETS contributes 150,000 to 300,000 LRIs annually in infants and children less than 18 months of age, resulting in 7,500 to 15,000 hospitalizations. The confidence in the estimates of LRIs is high.

Increased risks for LRIs continue, but are lower in magnitude, for children until about age 3; however, no estimates are derived for children over 18 months...

. a. Exposure to ETS is causally associated with additional episodes and increased severity of asthma in children who already have the disease. This report estimates that ETS exposure exacerbates symptoms in approximately 20% of this country's 2 million to 5 million asthmatic children and is a major aggravating factor in approximately 10%.

b. In addition, the epidemiologic evidence is suggestive but not conclusive that ETS exposure increases the number of new cases of asthma in children who have not previously exhibited symptoms. Based on this evidence and the known ETS effects on both the immune system and lungs (e.g., atopy and airway hyperresponsiveness), this report concludes that ETS is a risk factor for the induction of asthma in previously asymptomatic children. Data suggest that relatively high levels of exposure are required to induce new cases of asthma in children. This report calculates that previously asymptomatic children exposed to ETS from mothers who smoke at least 10
cigarettes per day will exhibit an estimated 8,000 to 26,000 new cases of asthma annually. The confidence in this range is medium and is dependent on the conclusion that ETS is a risk factor for asthma induction.

1.3.2. ETS and Noncancer Respiratory Disorders

Exposure to ETS from parental smoking has been previously linked with increased respiratory disorders in children, particularly in infants. Several studies have confirmed the exposure and uptake of ETS in children by assaying saliva, serum, or urine for cotinine. These cotinine concentrations were highly correlated with smoking (especially by the mother) in the child's presence. Nine to twelve million American children under 5 years of age, or onehalf to two-thirds of all children in this age group, may be exposed to cigarette smoke in the home
(American Academy of Pediatrics, 1986; Overpeck and Moss, 1991).

With regard to the noncancer respiratory effects of passive smoking, this report focuses on epidemiologic evidence appearing since the two major reports of 1986 (NRC and U.S. DHHS) that bears on the potential association of parental smoking with detrimental respiratory effects in their children. These effects include symptoms of respiratory irritation (cough, sputum production, or wheeze); acute diseases of the lower respiratory tract (pneumonia, bronchitis, and bronchiolitis); acute middle ear infections and indications of chronic middle ear infections (predominantly middle ear effusion); reduced lung function (from forced expiratory volume and flow-rate measurements); incidence and prevalence of asthma and exacerbation of symptoms in asthmatics; and acute upper respiratory tract infections (colds and sore throats). The more than 50 recently published studies
reviewed here essentially corroborate the previous conclusions of the 1986 reports of the NRC and Surgeon General regarding respiratory symptoms, respiratory illnesses, and pulmonary function, and they strengthen support for those conclusions by the additional weight of evidence (Chapter 7). For example, new data on middle ear effusion strengthen previous evidence to warrant the stronger conclusion in this report of a causal association with parental smoking. Furthermore, recent studies establish associations between parental smoking and increased incidence of childhood asthma. Additional research also supports the hypotheses that in utero exposure to
mother's smoke and postnatal exposure to ETS alter lung function and structure, increase bronchial
responsiveness, and enhance the process of allergic sensitization, changes that are known to predispose children to early respiratory illness. Early respiratory illness can lead to long-term pulmonary effects (reduced lung function and increased risk of chronic obstructive lung disease).

This report also summarizes the evidence for an association between parental smoking and SIDS, which was not addressed in the 1986 reports of the NRC or Surgeon General. SIDS is the most common cause of death in infants ages 1 month to 1 year. The cause (or causes) of SIDS is unknown; however, it is widely believed that some form of respiratory pathogenesis is generally involved. The current evidence strongly suggests that infants
whose mothers smoke are at an increased risk of dying of SIDS, independent of other known risk factors for SIDS, including low birthweight and low gestational age, which are specifically associated with active smoking during pregnancy. However, available studies do not allow this report to conclude whether that increased risk is related to in utero versus postnatal exposure to tobacco smoke products, or to both.

The 1986 reports of the NRC and Surgeon General conclude that both the prevalence of respiratory symptoms of irritation and the incidence of lower respiratory tract infections are higher in children of smoking parents. In the 18 studies of respiratory symptoms subsequent to the 2 reports, increased symptoms (cough, phlegm production, and wheezing) were observed in a range of ages from birth to midteens, particularly in infants and preschool children. In addition to the studies on symptoms of respiratory irritation, 10 new studies have addressed the topic of parental smoking and acute lower respiratory tract illness in children, and 9 have reported statistically significant associations. The cumulative evidence is conclusive that parental smoking, especially the mother's,
causes an increased incidence of respiratory illnesses from birth up to the first 18 months to 3 years of life, particularly for bronchitis, bronchiolitis, and pneumonia. Overall, the evidence confirms and strengthens the previous conclusions of the NRC and Surgeon General.

Recent studies also solidify the evidence for the conclusion of a causal association between parental smoking and increased middle ear effusion in young children. Middle ear effusion is the most common reason for hospitalization of young children for an operation.

Regarding the effects of passive smoking on lung function in children, the 1986 NRC and Surgeon General reports both conclude that children of parents who smoke have small decreases in tests of pulmonary output function of both the larger and smaller air passages when compared with the children of nonsmokers. As noted in the NRC report, if ETS exposure is the cause of the observed decrease in lung function, the effect could be due to the direct action of agents in ETS or an indirect consequence of increased occurrence of acute respiratory illness related to ETS.

Results from eight studies on ETS and lung function in children that have appeared since those reports add some additional confirmatory evidence suggesting a causal rather than an indirect relationship. For the population as a whole, the reductions are small relative to the interindividual variability of each lung function parameter.

However, groups of particularly susceptible or heavily exposed children have shown larger decrements. The studies reviewed suggest that a continuum of exposures to tobacco products starting in fetal life may contribute to the decrements in lung function found in older children. Exposure to tobacco smoke products inhaled by the mother during pregnancy may contribute significantly to these changes, but there is strong evidence indicating that postnatal exposure to ETS is an important part of the causal pathway.

For diseases for which ETS has been either causally associated (LRIs) or indicated as a risk factor (asthma cases in previously asymptomatic children), estimates of population-attributable risk can be calculated. A population risk assessment (Chapter 8) provides a probable range of estimates that 8,000 to 26,000 cases of childhood asthma per year are attributable to ETS exposure from mothers who smoke 10 or more cigarettes per day. The confidence in this range of estimates is medium and is dependent on the suggestive evidence of the database. While the data show an effect only for children of these heavily smoking mothers, additional cases due to lesser ETS exposure also are a possibility. If the effect of this lesser exposure is considered, the range of estimates of new cases
presented above increases to 13,000 to 60,000. Furthermore, this report estimates that the additional public health impact of ETS on asthmatic children includes more than 200,000 children whose symptoms are significantly aggravated and as many as 1,000,000 children who are affected to some degree.

This report estimates that ETS exposure contributes 150,000 to 300,000 cases annually of lower respiratory tract illness in infants and children younger than 18 months of age and that 7,500 to 15,000 of these will require hospitalization. The strong evidence linking ETS exposure to increased incidence of bronchitis, bronchiolitis, and pneumonia in young children gives these estimates a high degree of confidence. There is also evidence suggesting a smaller ETS effect on children between the ages of 18 months and 3 years, but no additional estimates have been
computed for this age group. Whether or not these illnesses result in death has not been addressed here.

In the United States, more than 5,000 infants die of SIDS annually. It is the major cause of death in infants between the ages of 1 month and 1 year, and the linkage with maternal smoking is well established. The Surgeon General and the World Health Organization estimate that more than 700 U.S. infant deaths per year from SIDS are attributable to maternal smoking (CDC, 1991a, 1992b). However, this report concludes that at present there is not enough direct evidence supporting the contribution of ETS exposure to declare it a risk factor or to estimate its
population impact on SIDS.

* Definition:
caus*al (kô-zõl) adj.
1. Of, involving, or constituting a cause.
2. Indicative of or expressing a cause.

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