This section summarises the research on the association between exposure to secondhand smoke and the childhood conditions of:
Worldwide, secondhand smoke causes significant morbidity and mortality.1 Children are particularly susceptible to the effects of secondhand smoke due to their higher breathing rates, greater lung surface area,2 and the developmental processes their bodies are undergoing.3 Infants and children are also generally unable to control their environment, and therefore cannot take steps to avoid exposure to secondhand smoke.2 A lower ability to detoxify cancer-causing chemicals from smoke may also make children more susceptible to the effects of secondhand smoke than adults.4
There are several possible routes by which the effects of tobacco smoke may compromise infant and child health. Before birth, there may be damage to sperm from paternal active smoking.3, 5-7 In utero maternal active smoking or maternal secondhand smoke exposure can also cause foetal harm.2, 3 The effects of smoking during pregnancy are discussed further in Section 3.7. Following birth, infants and children may be exposed to parental secondhand smoke in the home,3 to thirdhand smoke in household dust and indoor surfaces,8 and to bacterial or viral infections carried by a parent or carer who smokes.9-11 Both prenatal and postnatal tobacco exposure have been found to contribute to several health conditions.3, 12 Delineating the impact of each route of exposure in the causation of disease can sometimes be difficult, particularly for rare conditions. In many studies, the effects of maternal smoking are considered as a whole, rather than determining the individual effects of pre and post-natal maternal smoking.
Children are most likely to be exposed to secondhand smoke in the home. In Australia, larger household size, rural living, low socioeconomic status and a single-parent household are risk factors for home second-hand smoke exposure.13 Infant exposure to secondhand smoke in Australia (measured by urine cotinine levels) is associated with the smoking status of household members, absence of complete smoking bans in smoking households and having more than one smoker in the home.14 In Australia, the proportion of children who are exposed to secondhand smoke at home is falling—see Section 4.5.
The proportion of mothers who smoke during pregnancy is also falling in Australia. Between 2011 and 2017, the proportion of mothers who reported smoking during the first 20 weeks of pregnancy fell from 13% to 9.5%.15 See Section 1.10.1 for further details.
4.17.1 Infant death
Infant death is defined as the death of a child within the first year of life.15 Exposure to smoking in utero and following birth is associated with several of the major causes of death during infancy, including low birthweight, preterm delivery and sudden infant death syndrome (see Section 4.17.2).3, 12, 16-20 In US prenatal smoking has been associated with preterm-related infant deaths (adjusted OR 1.5) and SIDS deaths (adjusted OR of 2.7). This equated to 5.0% to 7.3% of preterm-related deaths and 23.2% to 33.6% of SIDS deaths attributed to prenatal smoking.21 A study from South-East Asia found that exposure to secondhand smoke increased the odds of under-five child mortality (OR of 1.25), particularly when both parents smoked (OR of 2.6).22
4.17.2 Sudden infant death syndrome (SIDS)
Sudden infant death syndrome (SIDS) is defined as the sudden, unexpected death of an infant under one year of age, occurring during sleep, which remains unexplained after a thorough investigation including performance of a complete autopsy and review of the circumstances of death.23 SIDS is predicted to have a multifactorial cause. The triple risk hypothesis proposes that SIDS occurs when a vulnerable infant is at a critical but unstable developmental period in homeostatic control, and is exposed to an exogenous stressor. Exposure to secondhand smoke during development and after birth can make these infants vulnerable to exogenous stressors, such as sleeping in a prone position.24 The mechanisms behind SIDS are believed to include disrupted cardio‐respiratory control combined with a failure of arousal from sleep.
Smoking is a cause of SIDS, from smoking by the parents during pregnancy and by exposure to secondhand smoke after birth.2, 3 Estimating individual risks from maternal smoking during pregnancy and secondhand smoke after birth can be challenging, as the two are closely associated.25 According to Australian estimates, infants exposed to maternal secondhand smoke after birth have nearly 2.5 times the risk of dying from SIDS compared with unexposed infants.26 International reviews estimate that secondhand smoke exposure during infancy doubles the risk of SIDS.2, 3, 27 When the mother is a non‐smoker, parental smoking has an estimated risk of 1.5 times that of non-smoking parents.25 A dose–dependent effect is predicted, where the risk of SIDS increases with the number of cigarettes smoked by the parents. Infants who die from SIDS have been found to have a higher concentration of nicotine in their lungs than infants who have died from other causes.3, 20 These findings make secondhand smoke exposure an important preventable risk factor for SIDS.3 In recent years, increasing numbers of parents have striven to protect their children from secondhand smoke by forgoing smoking within their homes, which is likely to have contributed to a substantial reduction in deaths from SIDS.26
The exact mechanisms by which secondhand smoke is causing SIDS are under investigation. Research in humans and from animal studies have uncovered numerous possibilities. The relative contributions of prenatal and post-natal secondhand smoke exposure to these mechanisms is difficult to determine, as most studies in humans involved parents that smoked before as well as after birth. Studies of human preterm infants show that exposure to cigarette smoke is associated with impaired recovery from hypoxia —a drop in oxygen supply to the body, such as from a breathing pause.20, 28 Human infants whose mothers smoke had less progression from sub-cortical activation to cortical arousal compared to unexposed infants.29 There was a significant dose-dependent association between cortical activation and urinary cotinine levels, a biomarker for nicotine.29 Animal studies are better able to separate the two exposures. Animals studies of secondhand, but not prenatal, smoke exposure have demonstrated changes to brain development that may contribute to SIDS. Some of these changes are known to affect cardio-respiratory function.3
4.17.3 Childhood asthma and other chronic respiratory conditions
Exposure to secondhand smoke causes a range of respiratory symptoms, such as cough, phlegm production, breathlessness and wheezing in children of primary school age.3 These symptoms are common in childhood, and may restrict the activities of those who experience them.3, 30
Asthma is a significant issue for the health of primary school children in Australia. Among all children aged 5–14, asthma was the leading cause of disease burden in 2015.15 The National Health and Medical Research Council (1997)31 and the California Environmental Protection Agency (2005)2 have both concluded that secondhand smoke causes asthma as well as exacerbates asthma in children. The US Surgeon General’s 2006 report states that secondhand smoke exposure is a cause of asthma in childhood and makes asthma more severe.3 A later meta-analysis supported the association of prenatal and postnatal secondhand smoking exposure and occurrence of childhood asthma (OR of 1.24), asthma-like syndrome, and wheezing.32 Worldwide data from 2004 showed that children (0 to 14 years) had a higher chance of having asthma if at least one parent smoked (OR 1.32 (1.24–1.41)).1 The prevalence of asthma is greater among children living in households with smokers and the risk of developing asthma increases in proportion with the number of smokers in the home.3 Among children with asthma, those exposed to secondhand smoke are nearly twice as likely to be hospitalised with an acute asthma episode and have poorer pulmonary function test results.30 In 2004–05, 11% of Australian children with asthma were living in homes where smoking took place indoors.33 It is estimated that 2% of asthma deaths in Australian children under 15 years in that year were attributable to secondhand smoke.34
The evidence is unclear on whether there is an association between secondhand smoke exposure and allergic sensitisation (initiation of allergic responses due to exposure to an allergen).2, 3, 35-37 However, some studies suggest there may be a synergy between hereditary risk for allergies and secondhand smoke exposure.3, 38, 39 Children exposed to secondhand smoke may be more likely to snore40-42 or suffer sleep-related breathing problems.43, 44 One large study has reported that respiratory symptoms such as chronic dry cough and production of phlegm may persist into adulthood among children who live with a smoker, independent of later exposure to secondhand smoke.45
In an African study, children exposed to secondhand smoke had a 3-fold higher chance of catching tuberculosis than unexposed children.46
4.17.4 Acute respiratory tract infections in infancy and childhood
Children exposed to secondhand smoke in the home have a greater risk of contracting acute chest infections, including bronchitis, bronchiolitis and pneumonia.3, 47, 48 The effect is most pronounced in children aged under two.2, 3 Infants exposed to secondhand smoke in the home have a 50% higher chance of developing lower respiratory illness than unexposed children.27, 47 This risk is even greater for those children living in households in which the mother smokes (about 60%).3, 27, 47 In infants up to 2 years of age, there was an increased chance of admission to hospital for lower respiratory tract infection if either parent smoked (OR of 1.55).1, 49 Exposure to secondhand smoke is also associated with chronic rhinosinusitis in children (inflammation of the nose and the paranasal sinuses).50 More research is necessary to determine whether these associations are causative.
Implementation of comprehensive smoke-free legislation can result in a significant reduction in hospital admissions for childhood lower respiratory tract infections.51-53
4.17.5 Decreased lung function
The lungs continue to grow and develop throughout childhood and adolescence. The period between birth and four years of age is a particularly vulnerable time for lung growth and development, when the number of alveoli in the lungs is increasing. Secondhand smoke causes decreased lung function during childhood, leading to a reduced maximum level in adolescence and early adulthood.3, 54, 55 This impairment may potentially increase vulnerability to other lung damage, including damage caused by active smoking, secondhand smoke exposure later in life, and exposure to air pollution and occupational irritants.2, 3
Maternal smoking increases the risk of below-average lifetime lung function trajectories that increase the risk of chronic obstructive pulmonary disease in later life, according to results from the Tasmanian Longitudinal Health Study.56
4.17.6 Middle ear disease
Middle ear disease (otitis media) occurs when the eustachian tube, which connects the middle ear to the back of the throat, becomes blocked or swollen, causing fluid to build up in the middle ear. This fluid can become infected, usually by bacteria.2, 57 Exposure to secondhand smoke causes middle ear disease, including acute and recurrent otitis media and chronic middle ear effusion (fluid build-up without infection, also known as ‘glue ear’).3 Children exposed to secondhand smoke in the home have a 30% to 40% increased risk for middle ear disease,1, 58, 59 and a 46% increased risk if their mother smokes.27 Moreover, ear disease in children of smokers appears less likely to resolve spontaneously than among children of non-smokers.3 This has important implications for child health. Episodes of glue ear in early life are associated with hearing loss and may lead to long-term problems with speech, and a range of developmental, behavioural and social consequences.60
4.17.7 Reduced sense of smell
Children exposed to secondhand smoke in the home may have impaired olfactory function, but the research in this field is limited. One small study has shown that children living with a parent who smoked a packet of cigarettes a day were more likely to mis-identify aromas compared with a control group of children not living with a smoker.61, 62
4.17.8 Longer-term developmental effects
There is evidence suggesting an association between exposure to secondhand smoke and an impact on cognition and behaviour, including higher likelihood of childhood conduct problems and learning difficulties.2, 3, 63-72 Smoking by either parent was associated with a slower language development in their children.73 Postnatal exposure to secondhand smoke in children increased the risk of attention deficit hyperactivity disorder in one study, with an odds ratio of 1.60.74 Children up to the age of eight years with smoking mothers were more likely to be shorter and weigh less than their unexposed peers, indicating a negative effect on development.75 For all these potential developmental effects of secondhand smoke, more research is necessary to determine whether these associations are causal.
4.17.9 Childhood cancers
There is a growing body of evidence suggesting an association between parental smoking (during the preconception, prenatal and postnatal periods) and brain tumours, lymphomas and acute lymphocytic leukaemia in children.2, 3, 76, 77 However, not all studies have found a positive relationship between secondhand smoke exposure and childhood cancers.78 The 2009 review by the International Agency for Research in Cancer (IARC) concluded that children born of parents who smoke (father, mother or both, including in the preconception period and pregnancy) are at a significantly higher risk of hepatoblastoma, a rare childhood cancer of the liver.77 Possible mechanisms include damage to sperm DNA and damage to the foetal liver from carcinogens in the blood of the pregnant mother, either from active smoking or secondhand smoke.79, 80 The 2009 IARC review also stated there was limited evidence to suggest that paternal smoking before pregnancy was associated with childhood leukaemia.7, 77 Since this report, a longitudinal study has shown that maternal smoking during pregnancy and postnatally is associated with lower overall survival for children with acute lymphoblastic leukaemia.81 The relationship between secondhand smoke and childhood cancers requires further research to investigate causality.
4.17.10 Perioperative complications
A strong association has been observed between the incidence of respiratory complications in children undergoing general anaesthesia and a history of exposure to secondhand smoke.82-84 There is also evidence that children exposed to secondhand smoke have a different metabolic response to drugs administered during surgery.85
4.17.11 Other conditions in childhood
Limited research suggests an association between exposure to secondhand smoke and dental problems in children, such as delayed dental development,86 tooth decay87, 88 and poorer attachment of the teeth to the gum and supporting structures.2, 89-92
Some studies indicate an association between exposure to secondhand smoke and gastrointestinal problems in children, such as diarrhoea and gastroenteritis.93-95
There is some research suggesting that secondhand smoke exposure in utero or during childhood may be associated with an increased risk of obesity and central obesity.96-99
For children of parents who smoke, there is some evidence of impaired bone health as adults.100 Eye defects may also be associated with childhood exposure to secondhand smoke, although the affected children were more likely to have lower socioeconomic status.101
For all these conditions, further research is necessary to determine whether these associations with secondhand smoke exposure are causal.
Relevant news and research
For recent news items and research on this topic, click here. ( Last updated January 2021)
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