Effect of Second-hand Smoke on Children

The symptomatic response to SHS, and its severity, depends not only on the child but also on the duration of exposure. Prenatal exposure due to maternal smoking has a long-term effect on the child’s respiratory health. The evidence linking asthma with maternal smoking during pregnancy is clearly established, and postnatal exposure to parental smoking is associated with respiratory symptoms such as wheeze, bronchitis, cough, nocturnal cough, hay fever and sensitivity to inhaled allergens.1

Second-hand tobacco smoke (SHS) is a major pollutant of indoor air. Because children spend a large part of eachday indoors, they tend to have the greatest exposure to SHS. And since their bodies are developing, they are more vulnerable to its effects. Further, the size of their airways makes them distinctly susceptible to irritants.

Maternal exposure to tobacco smoke affects the fetus. It results in

  • an increased risk of low birth weight
  • a 23% risk of a still birth2 or SIDS3
  • reduced lung function (an FEV1 reduced on average by 20%)4
  • recurrent wheeze and increased incidence of asthma in infants5,6
  • increased risk of nocturnal cough, respiratory infections and otitis media during the first year of life.4
  • a 13% increase in risk of congenital malformations that included an increased risk of the following2

    –  anencephaly (OR 2.10) (defect in brain development)
    –  conotruncal heart defects (OR 1.30)
    –  clubfoot and other similar deformities of the feet (OR 1.80)
    –  craniosynostosis (OR 1.30) (premature fusing of the skull)
    –  cryptorchidism (OR 1.55) (failure of one or both testes to move into the male scrotum)
    –  neural tube defects (OR 1.20)
    –  orofacial clefts (OR 1.09)
    –  spina bifida (OR 1.90) (defect of the spine where part of the cord is exposed)

Another study7 of interest looked at parental smoking and its effect in infancy. This was a systematic review and meta-analysis of 60 studies that linked passive smoking and lower respiratory tract infections (LRI) with diagnostic subcategories of bronchitis and bronchiolitis in infants aged 2 and under. It found that in infants under the age of 2, exposure to smoking increased the odds for LRI by:

  • 1.54 if any household member smoked
  • 1.22 for paternal smoking
  • 1.58 for maternal smoking
  • 1.62 if both parents smoked, and
  • bronchiolitis by 2.51 if any household member smoked

Researchers concluded that exposure to all types of passive smoke (and particularly maternal smoking) resulted in a statistically significant increase in the risk that infants under the age of 2 would develop lower respiratory tract infections. This study identifies bronchiolitis, which often results in severe morbidity and mortality, as a consequence of passive exposure to tobacco smoke. Further it showed that post-natal exposure to tobacco is the most likely reason for lower respiratory tract infections in children under the age of two.7-9

Tobacco smoke is know to affect bystanders, particularly children. In children, SHS is known to affect blood pressure and induce respiratory symptoms. Even newborn children, exposed to tobacco smoke in the womb, show symptoms of cardiovascular stress hyperreactivity.10

Children appear to be particularly affected. SHS exposure is associated with

  • longer sleep-onset delay
  • sleep-disordered breathing
  • parasomnias
  • daytime sleepiness
  • overall sleep disturbance11

Tobacco smoke has also been linked to recurrent ear infections in children aged 12 to 17 years where someone smoked inside the home.12 In children under 12 years, SHS has also been associated with neurobehavioural disorders such as attention deficit, hyperactivity, conduct disorders and learning disabilities.13 Both pre- and post-natal exposure to SHS has been associated with problems that further include irritability and oppositional defiant behaviour in children. SHS is associated with multiple problems in children’s neurodevelopment and behaviour.14

The effect of SHS on asthma morbidity in children has been well documented. It increases the risk of childhood asthma and has an impact on the child’s response to treatment. Cohen and others evaluated the effect of prenatal smoke exposure on children. Those children who had been exposed in utero were more likely to have corticosteroid-resistant asthma than children who had not been exposed. The effects of corticosteroid treatment were attenuated in children exposed to SHS.15

Children with asthma, whenexposed to SHS, exhibit increased symptoms and reduced levels of asthma control.16 To quantify the risk, a study led by the Mayo Clinic Research Center found that for children with asthma, exposure to SHS doubled the risk of hospitalization. Researchers reviewed 25 studies involving over 434,000 children and analyzed asthma-related outcomes such as hospitalization, emergency or urgent care visits, symptoms, acute exacerbations, pulmonary function, and medication use including oral steroids. For children with asthma exposed to SHS17 the odds ratio was

  • 1.32 for symptoms
  • 1.66 for emergency or urgent care visit
  • 1.85 for hospitalization
  •  – 3.34 for lower FEV1 /FVC ratios

The children affected also had more frequent exacerbations and were deemed to be more likely to have lower pulmonary function tests.

A study (part of the Greater Cincinnati Asthma Risks Study) involving 619 children between the ages of 1 and 16 found that while there was no correlation between caregiver reports on tobacco exposure and actual SHS exposure (done through cotinine measured in blood and saliva), children who were exposed had more than twice the risk of being readmitted to hospital than children who were not.18 Sociodemographics were closely linked – black children had higher rates of serum and salivary cotinine (61.1% and 86.8%) compared with while children (50% and 68.7% respectively).

When Pyle and others19 did a retrospective study that looked at children with asthma and their co-morbidities in comparison with children who did not have asthma, they noted that children with asthma exposed to SHS had significant higher body mass (OR 1.64). These children were also more likely to be obese, have more severe asthma and less health care usage, and less likely to receive an influenza vaccination (OR 0.61)

It has been known that SHS exposure is also connected to increased hospitalizations for asthma. A recent epidemiological study in Scotland seconded the benefits of smoke-free legislation, because one of the results of such legislation was a decrease in rates of asthma-related hospitalization from a previous mean rate increase of 5.2% a year to a mean reduction of 18.2% per year for both preschool and school-age children.20 A similar study in Canada found that ear infections declined significantly across the country.21

The future of children exposed to SHS is also clouded. A study in Maryland, of 624 individuals with lung cancer and 348 healthy control individuals, evaluated their exposure to SHS using interviews. DNA samples were also collected. Researchers found that among those individuals who had never smoked but had been exposed to SHS in childhood, the odds for lung cancer was 2.25. DNA tests also showed increased activity of a gene related to an increased risk of cancer.22

The scientific evidence is clear. SHS is detrimental to the current and future health and well-being of individuals but particularly of children. Asthma educators must encourage parents and caregivers to stop smoking not only for their own good but for the health of their children. Since children of smokers respond less well to asthma medications, there is also a financial incentive to be considered. Any reason would be a good reason if it stopped exposure to SHS.

FEV1      forced expiratory volume in one second
FVC       forced vital capacity
SHS       second hand smoke
LRI        lower respiratory tract infection
OR        odds ratio


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