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PEDIATRICS Vol. 99 No. 4 April 1997, pp. 639-642
AMERICAN ACADEMY OF PEDIATRICS:
Environmental Tobacco Smoke: A Hazard to Children
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ABSTRACT |
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Results of epidemiologic studies provide strong evidence that exposure of children to environmental tobacco smoke is associated with increased rates of lower respiratory illness and increased rates of middle ear effusion, asthma, and sudden infant death syndrome. Exposure during childhood may also be associated with development of cancer during adulthood. This statement reviews the health effects of environmental tobacco smoke on children and offers pediatricians a strategy for promoting a smoke-free environment.
In 1992, 48 million American adults (26.5%) currently smoked
cigarettes.1 A recent national survey indicated that
43% of children 2 months to 11 years of age live in homes with at
least one smoker.2 Because many young children spend a
large proportion of their time indoors,3 they may have
significant exposure to environmental tobacco smoke.
Environmental tobacco smoke from cigarettes, cigars, and pipes is
composed of more than 3800 different chemical compounds.4 Concentrations of respirable suspended particulate matter (particulates of <2.5 µm) can be two to three times higher in homes with smokers than in homes with no smokers.5 Cigarette smoking is the
most important factor determining the level of suspended particulate matter and respirable sulfates and particles in indoor
air.6,7
Passive smoking has a harmful effect on the respiratory health of
children.4,8,9 This statement reviews the evidence that
children exposed to environmental tobacco smoke have higher rates of
lower respiratory illness during their first year of life, higher rates
of middle ear effusion, and higher rates of sudden infant death
syndrome. In addition, children with asthma whose parents smoke have
more severe symptoms and more frequent exacerbations.
Passive Smoking and Lower Respiratory Illness
The first effect of passive smoking to be documented in children
was an increased rate of illnesses affecting the lower respiratory tract. Cameron10 reported a positive correlation
between the presence of a smoker in the home and the incidence of
perceived disease in children.
Harlap and Davies11 interviewed pregnant women to determine
their smoking habits and then studied hospital admissions for infants
younger than 1 year. The infants whose mothers smoked were 38% more
likely to be admitted to the hospital for bronchitis and pneumonia than
were those whose mothers did not smoke. This increased likelihood was
mainly among infants 6 to 9 months of age; admissions increased with
the number of cigarettes smoked by the infants' mothers.
Rantakallio12 showed that, among children younger
than 1 year, those with mothers who smoked cigarettes were almost four times as likely to be hospitalized as were the infants of nonsmoking mothers, and the number of hospitalizations increased with the number
of cigarettes the mother smoked per day. During the first 5 years of
life, pneumonia and bronchitis were about twice as likely and acute
nasopharyngitis and sinusitis in the upper respiratory tract were about
1.5 times as likely to develop in children whose mothers smoke.
Colley et al13 found a consistent gradient in the incidence
of pneumonia and bronchitis in the child's first year of life in
relation to the parents' smoking habits. Infants with two parents who
smoked were more than twice as likely to have had pneumonia and
bronchitis as were infants with parents who did not smoke.
Fergusson et al14 showed that pneumonia and bronchitis in
an infant's first year of life increased with increasing maternal smoking in an approximately linear manner: increases of five cigarettes a day resulted in an increase of 2.5 to 3.5 incidents of lower respiratory illness per 100 children at risk.
Passive Smoking and Serious Infectious Illnesses
Berg and colleagues15 determined that among
children 3 to 59 months of age, passive smoking was associated with an
almost fourfold risk of a serious infectious illness requiring
hospitalization.
Passive Smoking and Middle Ear Effusions
After a case-control study of risk factors for persistent middle
ear effusions in Seattle, Kraemer and colleagues16
reported that children who lived in households where more than three
packs of cigarettes were smoked per day were more than four times as likely to be admitted to the hospital for tympanostomy tube placement than were children whose parents did not smoke.
Iversen and colleagues17 studied children up to 7 years of
age in Danish day care centers and demonstrated that middle ear effusion as measured by tympanometry was about 60% more likely to
develop in children whose parents smoked. They estimated the overall
fraction of middle ear effusion attributable to passive smoking to be
15%.
To determine risk factors for glue ear (serous otitis media),
Black18 performed a case-control study of 150 children 4 to 9 years old undergoing myringotomy in Oxford, England. Children undergoing myringotomy were about 50% more likely to have lived in
households where someone smoked than were control children.
Hinton19 studied 115 children undergoing ear tube insertion
for otitis media with effusion and a control group of 36 children from
an orthoptic clinic. Children admitted for ear operations were more
likely to have at least one parental smoker at home than the children
in the control group.
Etzel et al20 studied 132 children in a day care
center to determine whether passive smoking was associated with an
increased risk of middle ear effusion during the 18-month period
between 6 and 24 months of age. In this study, the children were
classified as exposed or not exposed to cigarette smoke on the basis of
serum cotinine concentrations at 1 year of age. Middle ear effusion was
diagnosed with the use of pneumatic otoscopy. The 45 children exposed
to environmental tobacco smoke had an average of 7.1 episodes of middle
ear effusion between 6 and 24 months of age, whereas the 87 children
unexposed to environmental tobacco smoke had 5.8 episodes during that
period. The average duration of middle ear effusion was 28 days among
those in the exposed group and 19 days among those in the unexposed
group. An estimated 8% of the middle ear effusions were attributed to
exposure to environmental tobacco smoke.
Strachan et al21 studied the relationship between passive
smoking and middle ear effusion in 736 7-year-old school children in
Edinburgh. In this study, investigators used objective measures of
passive smoking and middle ear effusion, salivary cotinine concentrations, and impedance tympanometry. Children with type B
tympanograms in one or both ears were categorized as having middle ear
effusions. The results of this study indicated that detectable salivary
cotinine was associated with type B tympanograms, even after adjustment
for sex and the type of housing in which the children lived (rented
versus owned). The authors estimated that at least one third of the
cases of middle ear effusion among children in this age group may have
been attributable to passive smoking.
Owen and colleagues22 monitored 435 healthy children by
tympanometry in the home every 2 to 4 weeks until 2 years of age. Of
the children, 41% were exposed to household cigarette smoke. The
authors found a significant association between the number of
cigarettes smoked by household members and the frequency of otitis
media with effusion during the second year of life.
Ey and colleagues23 found that heavy maternal smoking (20 or more cigarettes per day) was a significant risk factor for recurrent
otitis media during the first year of life. No association was found
with paternal smoking.
Passive Smoking and Asthma
Children with asthma whose parents smoke may have more frequent
exacerbations and more severe symptoms.24-35 In one
of the few interventions reported in the literature, Murray and
Morrison30 demonstrated that if parents expose their
children with asthma to less cigarette smoke, the asthmatic symptoms
the children have will be less severe.
Passive Smoking and Sudden Infant Death Syndrome
A growing body of evidence links exposure to environmental tobacco
smoke to sudden infant death syndrome.36-48 This
relationship seems to be independent of birth weight and gestational
age.
Passive Smoking and Lipid Profiles
Passive smoking has also been reported to alter lipid profiles in
adolescents. Feldman et al49 studied 391 nonsmoking
adolescent students and found that those with elevated plasma cotinine
concentrations had an 8.9% greater ratio of total cholesterol to
high-density lipoprotein cholesterol and 6.8% lower high-density
lipoprotein cholesterol than those with lower plasma cotinine
concentrations. This may shed light on the mechanism of increased risk
of coronary heart disease in passive smokers.
Passive Smoking and Cancer
Many studies link passive smoking to lung cancer in nonsmoking
adults living with spouses who smoke.50-57 The US
Environmental Protection Agency9 reviewed this subject and
concluded that environmental tobacco smoke is a group A human
carcinogen, the classification used when sufficient evidence from
epidemiologic studies exists to support a causal association between
exposure and cancer. A small number of studies have examined the
relationship between exposure to environmental tobacco smoke during
childhood and cancer risk. Sandler and colleagues58 found
that the overall cancer risk was greater for individuals with exposures
to environmental tobacco smoke during both childhood and adulthood than
for individuals with exposure during only one period. When specific
cancer sites or types were considered, Sandler et al58
found that leukemia and lymphoma among adults were significantly
related to exposure to maternal passive smoke before 10 years of
age.59
Results of epidemiologic studies provide evidence that exposure of
children to environmental tobacco smoke is associated with increased
rates of lower respiratory illness and increased rates of middle ear
effusion, asthma, and sudden infant death syndrome. Exposure during
childhood to environmental tobacco smoke may also be associated with
development of cancer during adulthood.
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EFFECTS OF TOBACCO SMOKE ON CHILDREN
![]()
CONCLUSION
Top
Abstract
Conclusion
Recommendation
References
![]()
RECOMMENDATIONS
Top
Abstract
Conclusion
Recommendation
References
COMMITTEE ON ENVIRONMENTAL HEALTH,
1996 TO 1997
Ruth A. Etzel, MD, PhD, Chairperson
Sophie J. Balk, MD
Cynthia F. Bearer, MD, PhD
Mark D. Miller, MD
Katherine M. Shea, MD, MPH
Peter R. Simon, MD
LIAISON REPRESENTATIVES
Henry Falk, MD
Centers for Disease Control and Prevention
Robert W. Miller, MD
National Cancer Institute
Walter Rogan, MD
National Institute of Environmental Health
Sciences
CONSULTANT
Jim G. Hendrick, MD
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FOOTNOTES |
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The recommendations in this statement do not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate.
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Pediatrics (ISSN 0031 4005). Copyright ©1997 by the American Academy of Pediatrics
Statement of reaffirmation:
-
AAP Publications Reaffirmed and Retired
Pediatrics 2007 120: 683-684.[Extract] [Full Text] [PDF]
The following policy statement is a revision:
- Tobacco Use: A Pediatric Disease
- Committee on Environmental Health, Committee on Substance Abuse, Committee on Adolescence, and Committee on Native American Child Health
Pediatrics 2009 124: 1474-1487.[Abstract] [Full Text] [PDF]
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R. C. Cohn, D. Dodson, A. French, B. Ervin, S. Ciarlariello, and T. N. Wilson Pilot Smoking Cessation on Program Run by Pediatric Respiratory Care Practitioners for Parents Clinical Pediatrics, February 1, 2000; 39(2): 121 - 124. [PDF] |
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K. F. Burnett and P. C. Young Ask, Advise, Assist: Pediatricians and Passive Smoke Exposure Clinical Pediatrics, July 1, 1999; 38(6): 339 - 345. [Abstract] [PDF] |
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K. Piirna Passive smoking among adolescents in Estonia Human and Experimental Toxicology, April 1, 1999; 18(4): 229 - 232. [Abstract] [PDF] |
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L. M. Winn, P. M. Kim, and P. G. Wells Investigation of the Tobacco-Specific Carcinogen 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone for In Vivo and In Vitro Murine Embryopathy and Embryonic ras Mutations J. Pharmacol. Exp. Ther., December 1, 1998; 287(3): 1128 - 1135. [Abstract] [Full Text] |
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A K Hackshaw Lung cancer and passive smoking Statistical Methods in Medical Research, April 1, 1998; 7(2): 119 - 136. [Abstract] [PDF] |
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M. J. Ashley and R. Ferrence Reducing children's exposure to environmental tobacco smoke in homes: issues and strategies Tob. Control, March 1, 1998; 7(1): 61 - 65. [Abstract] [Full Text] |
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N. Setzer The Effect of Tobacco Smoke on Children Undergoing General Anesthesia and Surgery Pediatrics, October 1, 1997; 100(4): 731 - 731. [Full Text] [PDF] |
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A. C. Geller, J. Zapka, K. R. Brooks, C. Dube, C. A. Powers, N. Rigotti, J. O'Donnell, J. Ockene, and for the Prevention and Cessation Education Consort Tobacco Control Competencies for US Medical Students Am J Public Health, June 1, 2005; 95(6): 950 - 955. [Abstract] [Full Text] [PDF] |
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