Division of Noncommunicable Diseases
Tobacco Free Initiative
www.who.int/toh
© World Health Organization,
1999
This document is not a
formal publication of the World Health Organization (WHO), and all rights
are reserved by the Organization. The document may, however be freely
reviewed, abstracted, reproduced or translated, in part or in whole, but
not for sale or for use in conjunction with commercial purposes. Contents
III.
Health effects of children's exposure to tobacco smoke
I.
Executive Summary
Responding to the 1997 Declaration on Children's Environmental Health of
the Environment Leaders of the Eight (G8)1 WHO convened an International
Consultation on Environmental Tobacco Smoke (ETS) and Child Health in Geneva,
Switzerland from 11 to 14 January 1999. The Consultation brought
together experts from developed and developing countries to examine the
effects of ETS on child health and to recommend interventions to reduce
these harmful effects and eliminate children's exposure.
The Consultation concluded that ETS is a real and substantial threat to
child health, causing death and suffering throughout the world. ETS exposure
causes a wide variety of adverse health effects in children, including
lower respiratory tract infections such as pneumonia and bronchitis, coughing
and wheezing, worsening of asthma, and middle ear disease. Childrens'
exposure to environmental tobacco smoke may also contribute to cardiovascular
disease in adulthood and to neurobehavioural impairment.
The Consultation also concluded that maternal smoking during pregnancy
is a major cause of sudden infant death syndrome (SIDS) and other well-documented
health effects, including reduced birth weight and decreased lung function.
In addition, the Consultation noted that ETS exposure among nonsmoking
pregnant women can cause a decrease in birth weight and that infant exposure
to ETS may contribute to the risk of SIDS.
The scope of these health effects on children is broad, given that almost
half of the world's children are regularly exposed to ETS. Most have
no choice in the matter. Preventing children's exposure to tobacco
smoke will lead to improved child, adolescent, and ultimately adult health,
resulting in reduced mortality and substantial savings in health care and
other direct costs.
Swift action to highlight the need for strong public policies to protect
children from exposure to tobacco smoke is essential. These policies should
aim to ensure the right of every child to grow up in an environment free
of tobacco smoke. This can be achieved by 2 complementary strategies:
eliminating children's contact with tobacco smoke in utero and in
childhood; and reducing overall consumption of tobacco products.
Effectively implementing these strategies requires combining educational
programmes and legislative interventions aimed particularly at eliminating
tobacco use in settings frequented by children.
In response to the Declaration on Children's Environmental Health, adopted
by the Environment Leaders of the Eight (G8) in May 1997, the World Health
Organization (WHO) convened an International Consultation on Environmental
Tobacco Smoke (ETS) and Child Health in Geneva from 11 to 14 January 1999.
Experts from developing and developed countries gathered to examine the
effects of exposure to tobacco smoke on child health and to develop recommendations
for action to eliminate this exposure.
The adverse health effects of tobacco use among smokers are well described.
Tobacco use generally begins during adolescence and continues through adulthood,
sustained by addiction to nicotine. Smoking causes about four million
deaths annually, mainly attributable to cardiovascular disease, lung cancer
and other cancers, and chronic lung disease. Tobacco smoke is also
an important source of indoor air pollution, contributing to a noxious
environment, eye irritation, and unpleasant odour. Recent evidence
demonstrates that ETS exposure increases risks of lung cancer and ischaemicheart
disease among non-smoking adults.
The vast majority of children exposed to tobacco smoke do not choose to
be exposed. Children's exposure is involuntary, arising from smoking,
mainly by adults, in the places where children live, work and play.
Given that more than a thousand million adults smoke worldwide, WHO estimates
that around 700 million, or almost half of the world's children, breathe
air polluted by tobacco smoke, particularly at home. The large number
of exposed children, coupled with the evidence that ETS causes illness
in children, constitutes a substantial public health threat.
This report concludes that the evidence of this harm to children is consistent
and robust. Even if certain questions still require further research,
there is more than sufficient evidence of harm to demand action to reduce
children's involuntary exposure to tobacco smoke. Furthermore, this
involuntary and harmful exposure can also be seen as a human rights violation,
given the provisions of Articles 6 and 24 of the 1989 United Nations Convention
on the Rights of the Child. These articles create obligations for
signatory governments to guarantee children's right to life, to create
an environment that maximizes the survival and development of children,
and to implement measures ensuring and recognizing children's right to
the highest attainable standard of health. In addition, the Convention's
reporting guidelines include the requirement to identify risks to children
from environmental pollution and report measures taken to reduce these
risks.
The report addresses the threat to child health in three sections.
The first summarizes the health effects of children's exposure to tobacco
smoke. The second addresses measurement issues central to action:
measuring health impacts, children's exposure and the economic burden of
that exposure. The third turns to interventions and includes evidence
of effective policies and programmes to reduce children's exposure to tobacco
smoke along with a framework for designing cost-effective responses to
this threat. It is intended that this report will serve as an impetus
for taking strong and immediate action to ensure that children around the
world can grow up in an environment where their health is not compromised
by being forced to breathe other people's tobacco smoke. III.
Health effects of children's exposure to tobacco smoke
This
section presents evidence of the harmful impact of ETS exposure on children's
health. Table 1 summarizes previous conclusions as to that impact.
The present report specifically addresses respiratory and middle ear disease,
reduced foetal growth, sudden infant death syndrome (SIDS), neurodevelopmental/behavioural
outcomes, cardiovascular effects, and childhood cancer.
Several adverse consequences of involuntary tobacco smoke exposure of children
are well understood and beyond the scope of this report. Specifically,
parental and peer smoking are critical and detrimental influences on future
regular tobacco use. In addition, maternal smoking during pregnancy
causes well-established, demonstrable harm by reducing birth weight and
increasing infant mortality.
For young children, the major source of exposure to tobacco smoke is smoking
by parents and other household members. Maternal smoking is typically
the largest source of a child's exposure because of the cumulative effects
of exposure in utero and close proximity to the mother during early life.
As children grow older, the relative contribution of other exposure sources,
including smoking in public places, increases. Distinguishing between
the effects of maternal smoking during pregnancy and the child's exposure
to both maternal and paternal tobacco smoke after birth can be difficult
because children exposed to the first are usually exposed to the second
as well. While identifying the specific source of tobacco smoke exposure
may improve intervention targeting, cumulative tobacco exposure over a
lifetime, whether in utero, from ETS exposure, or as an active smoker,
causes both acute illness and chronic disease. A.
Respiratory health and middle ear disease
The effects of parental smoking on children's lungs have been extensively
described in the reports listed in Table 1. This report focuses on
lower respiratory tract illness during infancy, asthma, respiratory symptoms,
lung function, and middle ear disease, updating previously published quantitative
syntheses of the evidence on parental smoking and respiratory health of
children. Studying children whose fathers smoke and mothers do not
can help separate postnatal from prenatal effects of tobacco smoke.
Lower
respiratory tract illness
Parental smoking is an important cause of lower respiratory tract illnesses
(e.g. croup, bronchitis, bronchiolitis, pneumonia) during the first years
of life. Of over 40 studies, all but one reported increased risks
among children whose parents smoke. Pooling the studies' results,
children whose mothers smoke are estimated to have a 1.7-fold (95% CI =
1.6-1.9) higher risk of these illnesses than children of nonsmoking mothers.
Paternal smoking alone causes a 1.3-fold (95% CI = 1.2-1.4) increase in
risk. This result is strong evidence for a causal role of ETS exposure,
since it is uncomplicated by maternal smoking during pregnancy. Similar
effects were seen for both wheezing and non-wheezing illnesses, and across
studies done in communities and those done in hospitals. Furthermore,
adjustment for confounding did not change the estimates, and evidence of
exposure-response relationships (i.e. increasing risks of illness with
increasing exposure to tobacco smoke) was frequently observed. Because
lower respiratory tract illness is a common cause of childhood morbidity,
small increases in average individual risk coupled with widespread exposure
imply large population impacts.
Asthma
and respiratory symptoms
Asthma is the most common chronic disease of childhood, and environmental
factors play an important role in determining both onset and severity.
Both asthma and respiratory symptoms (wheeze, cough, breathlessness and
phlegm) are increased among children whose parents smoke, on the basis
of over 60 studies of school-aged children . The pooled relative
risks for either parent smoking range from 1.2 to 1.4. Evidence supporting
a causal role for ETS exposure comes from the small but significant effects
of paternal smoking when the mother does not smoke. As with lower
respiratory tract illness, adjustment for confounding did not significantly
change the results and exposure-response relationships have been described.
Smaller relative risks in school-aged children compared to infants are
consistent with reduced exposure.
Whereas there is clear evidence that tobacco smoke exposure causes non-allergic
wheezing in early life, it probably does not cause the underlying asthmatic
trait. In addition, parental smoking perinatally is not associated
with allergic sensitization. Nevertheless, ETS exposure causes exacerbations
of symptoms in children with asthma. In many countries, this has
led to the standard clinical practice of recommending avoidance of tobacco
smoke for children with asthma.
During childhood, the lung grows as height increases. Damage to the
lung during its development may have lasting effects and reduce the lung's
reserve capacity. Substantial evidence demonstrates that maternal smoking
during pregnancy causes sizeable adverse effects on neonatal lung mechanics.
Maternal smoking is also associated with small deficits in lung function
in school-aged children. However, distinguishing between residual
effects of maternal smoking during pregnancy and childhood ETS exposure
to explain these deficits is difficult.
Early childhood exposure to ETS is also causally associated with a major
child health burden: acute and chronic middle ear disease. Over 40
studies with different designs have investigated effects of parental smoking
across a range of outcomes from acute otitis media to surgery for glue
ear. Pooled relative risks for these outcomes range from 1.2 to 1.4 and
are statistically significant. No single study simultaneously addresses
selection bias, information bias and confounding; where these have been
investigated, however, the associations with parental smoking persist virtually
unchanged. Few studies have compared the effects of maternal and
paternal smoking and none have compared the effects of prenatal and postnatal
exposure. Moreover, prognostic studies, showing improvement when
the child has a smoke-free environment, and consideration of biologic mechanisms
strongly suggest that postnatal ETS causes increased risk of middle ear
disease in children.
Substantial benefits to children would arise if parents stopped smoking.
While an important message must be for the mother to stop smoking before
pregnancy, additional important benefits would result from postnatal cessation.
Smoking by the father or other adults may have adverse effects during gestation
and has definite effects after birth including increased relative risks
of lower respiratory tract infection during infancy, and respiratory symptoms,
middle ear disease among older children. Although these increased
risks are modest, these are common health problems around the world.
Thus small increases in risk translate into a substantial burden of disease
for children arising from exposure to ETS.
Further studies might be helpful to distinguish between the effects of
in
utero exposure to tobacco smoke and postnatal exposure. Studies in
settings where women rarely smoke but tobacco smoke exposure from paternal
and other sources is high would be particularly valuable. Where longitudinal
studies are underway, analyses to investigate how changes in exposure are
related to changes in outcome would be a valuable contribution. In
addition, studies demonstrating the reversibility of adverse effects with
reduced exposure to tobacco smoke, particularly in high-risk groups such
as children with asthma and other health conditions exacerbated by tobacco
exposure, would be useful.
The adverse effects of maternal smoking during pregnancy on foetal growth
have been known for some time. Low birth weight (LBW, defined generally
as less than 2500 grams) and intrauterine growth retardation (IUGR) are
important risk factors for childhood morbidity and mortality. Over
30 studies have examined the effects of nonsmoking mothers' exposure to
ETS during pregnancy on foetal growth (e.g. by studying mean birth weight
or LBW/IUGR) or preterm birth. Using mean birth weight as the outcome,
studies from different countries and with different study designs have
consistently found birth weights reduced among the offspring of nonsmoking
women exposed to tobacco smoke during pregnancy. Many of the studies
attempted to control for potential confounding factors. Pooling the
results in a meta-analysis yields a mean reduction in birth weight ranging
from 25 to 40 grams, depending on the subset of studies included.
In addition, pooling estimates for LBW or IUGR yields a relative risk ranging
from 1.2 to1.4. Furthermore, relative risks and mean birth weight
reductions were generally higher in higher exposure groups and in studies
using a biomarker to measure exposure, and thus likely increasing the accuracy
of exposure measurement. These results are supported by animal studies
of sidestream smoke exposure. Thus, the weight of evidence indicates that
ETS exposure in pregnant nonsmokers causes a small reduction in foetal
growth.
At the population level, a small change in average birth weight could affect
large numbers of infants because of the frequency of exposure. Furthermore,
a shift in the birth weight distribution could have profound impacts on
infants already at risk, moving them to a critically low birth weight.
Additional studies of mean birth weight are unlikely to change the pooled
measure of effect to any extent, but studies using a biomarker of exposure
to increase the accuracy of exposure measurement and examine dose levels
may still be warranted. Only a small number of studies have examined
the role of ETS in increasing the risk of preterm birth, and additional
studies would be valuable. In addition, research is needed to examine
potentially more susceptible groups, such as those defined by maternal
age or ethnicity. C.
Sudden infant death syndrome (SIDS)
There is sufficient evidence to conclude that maternal smoking causes a
marked increase in SIDS. Almost 50 studies have examined this relationship
and all indicate an increased risk. Since reductions in the prevalence
of prone sleeping position, eight studies have examined maternal smoking
and SIDS. The pooled unadjusted relative risk from these studies is approximately
5, indicating that infants of mothers who smoke have almost five times
the risk of SIDS compared with infants of mothers who do not smoke. Adjustment
for potential confounders lowers the risk estimate; however, many studies
over-adjust, e.g. by controlling for birth weight, resulting in an inappropriately
low estimate of the risk. Pooling the adjusted results still yields a significantly
increased risk of SIDS from maternal smoking.
With the available data, it is difficult to distinguish the effect of active
maternal smoking during pregnancy from that of postnatal ETS exposure of
the infant from smoking by the mother. While the mechanism for SIDS
is unknown, the predominant effect from maternal smoking is generally attributed
to in utero exposure of the foetus.
However, clear evidence for an ETS effect arises from six studies examining
SIDS and paternal smoking where the mother is a nonsmoker. The pooled unadjusted
relative risk from these studies is 1.4 which, though smaller than the
effect seen for maternal smoking (RR = 4.7), still indicates a significant
risk. Overall, parental smoking, particularly by the mother, appears
to be responsible for between a third and a half of all SIDS cases.
Additional studies are unlikely to influence the pooled estimate of risk
from maternal smoking substantially. Studies of nonsmoking mothers
may clarify to what extent postnatal tobacco smoke exposure contributes
to the risk of SIDS. Given the overwhelming evidence of maternal
smoking's effects in increasing the risk of SIDS, interventions to assist
pregnant women to stop smoking should be given high priority.
When compared to children of nonsmokers, children of smokers perform more
poorly in school. They also have lower scores in cognitive functioning
tests - in particular, language and auditory processing - and have more
behavioural problems, including conduct disorders, hyperactivity, and decreased
attention spans. Cognitive and behavioural deficits in children have lifelong
consequences and result in increased costs for education and social services.
Seventeen studies have addressed the effects of ETS exposure on child development
and behaviour. Most have controlled for sociodemographic characteristics
and some have demonstrated dose-response relationships, with greater deficits
among children with higher exposures. In some studies, children's
postnatal ETS exposure and ETS exposure of nonsmoking mothers during pregnancy
have been independently associated with subtle changes, albeit statistically
significant, in child development and behaviour. Adverse effects
resulting from children's postnatal exposure to tobacco smoke are biologically
plausible in light of evidence of altered brain development in animal models.
Taken as whole, however, these studies are difficult to interpret, in part
due to the possible influence of uncontrolled confounding factors.
Thus, the effects of prenatal and postnatal ETS exposure on cognition and
behaviour remain unclear.
Future studies need to focus on specific effects or outcomes associated
with different periods of exposure. Particular attention should be
given to controlling for essential explanatory variables such as maternal
intelligence, social class, and home environment.
In adults, active and passive smoking cause cardiovascular disease.
In children, adolescents, and young adults, there is some evidence that
ETS exposure may accelerate the evolution of cardiovascular disease.
These studies document deleterious effects on oxygen transport, high-density
lipoprotein (HDL) cholesterol, and possibly endothelial function.
In addition, the adverse effects of tobacco smoke exposure in adults in
thrombosis, endothelial function, and low-density lipoprotein (LDL) oxidation
can be plausibly inferred to occur in children. Studies of atherosclerosis
in young adults indicate that exposure to tobacco smoke during childhood
may also accelerate the progressive development of atherosclerosis.
Evidence from animal models supports this initiation. However, the
magnitude and clinical significance of these changes with respect to disease
during adulthood are at present unknown. Neither the relationship
of tobacco smoke exposure to vascular events during childhood nor the reversibility
of these adverse effects has been assessed.
Due to the limited number of studies in this area, further work on the
evolution of atherosclerosis during youth and into young adulthood, with
particular attention to tobacco smoke exposure, would be valuable.
In addition, measurable cardiovascular endpoints of tobacco smoke exposure
occurring in children and youth need to be developed. Such endpoints
would also aid in evaluating reversibility of effects when exposure is
discontinued. Focusing on studies of children, adolescents, and young
adults with other major cardiovascular risk factors to examine whether
tobacco smoke exposure enhances the effect of other risk factors would
also add substantially to current knowledge.
Tobacco smoke, whether voluntarily or involuntarily inhaled, includes numerous
carcinogens. Among adults, active smoking has been causally linked
to cancers at a number of sites and exposure to ETS is an established cause
of lung cancer among nonsmokers.
On the issue of childhood neoplasms, the pooled estimate of the relative
risk of any childhood neoplasm from exposure to maternal smoking is 1.11
(95% CI = 1.00-1.23, based on 11 studies), and that for leukaemia is 1.14
(95% CI = 0.97-1.33, based on 8 studies). While fewer studies are
available on paternal smoke exposure, associations are suggested for brain
tumours and lymphomas. No consistent pattern of dose-response relationship
has been found with either maternal or paternal smoking in the limited
set of studies addressing this issue. Although known risk factors
for childhood cancer do not appear to confound the observed associations,
the small increases in risk might be the result of confounding by unknown
factors. In most available studies, no distinction is made between
preconceptional, in utero and postnatal exposure to parental smoke,
making it difficult to assess the separate contribution of these periods
of exposure. In conclusion, there is suggestive evidence linking
exposure to tobacco smoke and childhood cancer.
Future studies on exposure to tobacco smoke and childhood cancer should
be based on large series of cases and should address the contribution of
exposure preconceptionally, in utero, and postnatally. IV.
Measurement: health impact, exposure and economic impact
Estimating the public health impact of ETS exposure in children, the extent
of that exposure, and the economic costs associated with it are essential
to provide the information necessary for action to reduce the public health
consequences of ETS on child health.
Health impact can be measured using attributable risk methods. These combine
information on the extent to which disease outcomes are increased among
children exposed to tobacco smoke with data on the number of children who
are exposed in order to estimate the proportion of disease caused by tobacco
smoke. For many of tobacco smoke's effects on children, epidemiological
evidence is sufficiently strong to estimate the attributable risk of disease.
From a public health perspective, even if individual risks are only slightly
increased, exposure to tobacco smoke nevertheless has a major health impact
because almost half of the world's children are exposed.
Measures of impact are needed to motivate and guide policy development
and interventions to protect children from tobacco smoke exposure.
Given limited resources, intervention priorities would ideally be established
on the basis of measures of impact. Some tools are already available
for this purpose but further development is encouraged, particularly of
generally applicable models. At the most basic level, surveys of
tobacco use including questions to assess children's household exposure
to tobacco smoke are needed.
Children's involuntary exposure to tobacco smoke can be measured in several
ways: air sampling, uses of biomarkers, and application of survey instruments.
Air sampling involves measuring concentrations of such markers as respirable
suspended particulates or nicotine in the air. Biomarkers involve
measuring concentrations of smoke components in biological materials, most
commonly cotinine in saliva or urine. Both cotinine measurement and
air sampling are limited to describing current exposure. Biomarkers
may also be valuable to validate questionnaire responses.
Numerous studies have established that young children's exposure to tobacco
smoke comes mainly from smoking within the home, especially by parents.
Maternal smoking has a greater impact on children's measured cotinine levels
than paternal smoking. Smoking by other household members and child
care personnel accounts for a smaller proportion of children's total exposure.
From a survey design perspective, this point is critical, because children's
exposure can be measured with a few simple questions about parental smoking.
Three kinds of surveys are generally used for this purpose: household,
school-based and general surveys. In household surveys, both parental
smoking and the presence of children can be directly measured. In
school-based surveys, children can accurately report whether or not their
parents smoke but are less able to give valid reports of parental cigarette
consumption. Surveys of smoking in the general adult population may
also be useful, as smoking prevalence among all adults between the ages
of 20 and 50 years is similar to that among parents with children.
In most countries, particularly those where people are generally not aware
of tobacco smoke's harmful effects on children's health, parental smoking
status will reflect children's exposure, as smoking parents are unlikely
to minimize their children's exposure by not smoking in their presence.
However, in countries where concerns about children's exposure are growing,
more parents, including smokers, are initiating smoking policies in the
home and reporting that they generally restrict smoking to outdoors.
In the future, therefore, parental smoking status by itself may become
a less valid indicator and information regarding self-reported behaviours
to protect children will be needed. Moreover, these self-reports
will need to be validated by biomarkers of children's actual exposure to
offset socially desirable but inaccurate questionnaire responses.
Estimating the public health burden of children's exposure to tobacco smoke
requires accurate data on the number of children exposed, on a country-by-country
basis. Based on present estimates of global cigarette smoking prevalence,
WHO estimates that almost half of all children worldwide live in a home
with at least one smoker. However, accurate country-level estimates
are lacking, and few countries have data tracking the proportion of children
living in smoking households over time.
WHO has already developed standardized questionnaires to measure adult
smoking prevalence. Modifying them to include items enquiring specifically
about household smoking and any rules adopted to protect children would
be a potentially cost-effective way of gathering this crucial information.
In addition to questionnaire-based surveys, cross-national surveys, incorporating
a biomarker such as cotinine, in as many cultures, climates and regions
as possible would quantify the extent of exposure worldwide and determine
the significance of parental smoking as a predictor of dose across countries
and cultures. If repeated over time, such a series would establish
trends within and across countries in children's actual exposure to tobacco
smoke, taking into account both changes in cigarette smoking prevalence
and the effects of measures adopted to protect children from exposure.
Estimating costs of children's exposure to tobacco smoke is important in
evaluating tax and fiscal policy, managing public and private health care
costs, and evaluating programmes to induce smokers to stop smoking or reduce
the amount they smoke. Governments can use economic impact estimates
as they consider policy and programme choices, since cost-benefit analyses
may contribute to decision-making. Economic impact estimates are
also useful from a health services perspective, because they highlight
the savings if adults stop smoking or otherwise reduce exposure of children
to tobacco smoke.
Costs arise from the established adverse health effects of children's exposure
to tobacco smoke. Tobacco smoke exposure contributes to morbidity
in children, increasing short-term direct health costs. These costs
are largely preventable, because the behaviour of adults who are exposing
infants and children to tobacco smoke can be altered, yielding direct savings
for those who pay for health care services, whether government, insurers,
or individuals.
Morbidity costs accrue from direct outlays for health care for children
experiencing middle ear infections, lower respiratory tract illness and
asthma, all of which are increased among children exposed to tobacco smoke.
Children with these conditions will require more services from physicians,
more prescription drugs and more hospitalizations. Their families
may well suffer indirect costs in the form of time spent seeking care.
Indirect costs also arise from the additional mortality of children exposed
to tobacco smoke. Economists typically estimate these costs in terms
of the value of life lost. Specifically, maternal smoking during
pregnancy or exposure of the infant to smokers causes additional deaths
from sudden infant death syndrome (SIDS). Although the predominant tobacco
exposure of an infant dying of SIDS occurs in utero as a result
of maternal smoking during pregnancy, risk of death appears to be elevated
by exposure to tobacco smoke after birth, and death as an infant entails
a substantial loss of years of life.
Using mortality and morbidity rates, together with estimates of the increased
rates attributable to tobacco smoke, researchers have measured the costs
of children's exposure to tobacco smoke, mostly in developed countries.
These studies have generally estimated the extra costs associated with
health care services related to the childhood conditions discussed in section
III of this report. While these studies are limited in number and
the cost estimates vary, annual health care costs attributable to children's
involuntary exposure to tobacco smoke in the United States alone are estimated
at approximately US$ 1 000 million (1997 dollars). If the effects
of active maternal smoking in reducing birth weight are included, this
figure more than doubles. Furthermore, the long-term costs of special educational
or other services for those with developmental impairments secondary to
low birth weight are not included in this estimate. Considering indirect
costs would further increase the estimated costs. D.
Extrapolating to developing countries
The majority of studies measuring costs of children's exposure to tobacco
smoke have been in developed countries. For developing countries,
these costs, while likely to be significant, may be affected by country-specific
conditions. The magnitude of costs in any country depends not only
on the levels of children's exposure and rates of disease, but also on
the monetary values placed on health care and other resources. If
a country lacks a well developed health care system, costs will appear
artificially low as individuals cannot have access to care. As less developed
countries develop and their health systems evolve, costs will become more
real and are likely to grow from their current levels as smoking prevalence
rises in these countries, more children are affected, and services become
available to offer them treatment for the illnesses in which tobacco smoke
is implicated.
The epidemiological evidence indicates that the effects of children's exposure
to tobacco smoke are significant. Measuring these exposures in developing
countries and monitoring the health effects of tobacco smoke in all countries
continues to be a priority. While developing countries may not at
first seek to precisely estimate the costs of children's exposure to tobacco
smoke, they will need to monitor levels of children's exposure over time.
In this manner they will have an indication of the direction of change
in adverse health effects and health care costs borne by their citizens. V.
Interventions to eliminate children's exposure to environmental tobacco
smoke
In view of the significant health risks posed to children by ETS, public
health policies are needed to protect this vulnerable population.
The aim of such policies is to ensure the right of every child to grow
up in an environment free of tobacco smoke, in accordance with the United
Nations Convention on the Rights of the Child.
The tobacco industry has deliberately misrepresented the extent of the
harms of passive smoking, and has undertaken a campaign to discredit the
scientific findings and confuse the public. Yet the evidence brought
together in this report demonstrates an overwhelming scientific consensus
about the health risks to children from involuntary exposure to tobacco
smoke. These risks are avoidable and can often be addressed simply
and without great expense. This section recommends a range of interventions
and outlines the policy tools needed to eliminate childhood exposure to
tobacco smoke. B.
Strategies for Reducing Children's Exposure to Tobacco Smoke
Strategies to prevent children's involuntary exposure to tobacco smoke
fall into two general groups: a primary focus on eliminating children's
contact with the tobacco smoke of others, and secondary benefits from reducing
the prevalence and consumption of tobacco products. Protecting children
from tobacco smoke is essential to comprehensive tobacco control, which
includes preventing the initiation of smoking, eliminating involuntary
exposure to tobacco smoke, and supporting smoking cessation. The
following key points should be considered in any intervention programme: VI.
Conclusions and recommendations Table
1. Summary of conclusions from earlier health
agency reports on environmental tobacco smoke and child health Australian National
Health and Medical Research Council. The Health Effects of Passive
Smoking (1997) ISBN 0-642-27270-0
World Health Organization,
Division of Noncommunicable Diseases, Tobacco Free Initiative
Synthesis: The
Health Effects of Tobacco Smoke Exposure on Children. J. Samet, Department
of Epidemiology School of Hygiene and Public Health Johns Hopkins University,
Baltimore, MD, USA
Association of
in
utero or Postnatal Environmental Tobacco Smoke Exposure and Neurodevelopmental
and Behavioral Problems in Children.
B. Eskenazi, School of Public Health, University of California, Berkeley;
R. Castorina, School of Public Health, University of California, Berkeley.
Effects of Maternal
and Paternal Smoking on Children's Respiratory Health. D. Cook,
Department of Public Health Sciences St. Georges Hospital Medical School,
London and D. Strachan.
Effects of Passive
Smoking on the Cardiovascular System in Children and Adolescents.
S.S. Gidding, Pediatrics and Preventive Medicine, Northwestern University
Medical School; Attending Cardiologist, Children's Memorial Hospital, Chicago,
Il.
Parental Tobacco
Smoke and Childhood Cancer. P. Boffetta, International Agency
for Research, Lyon, France; J. Trédaniel, Saint Louis Hospital,
Paris, France; A. Greco, University of Lyon, France.
Prenatal Exposure
to Environmental Tobacco Smoke and Fetal Health. G.C. Windham,
Reproductive Epidemiology Section, Division of Environmental and Occupational
Disease Control, Department of Health Services, Oakland, CA.
Smoking and Sudden
Infant Death Syndrome. E.A Mitchell, University of Auckland, Auckland,
New Zealand; Milerad, Department of Women and Child Health, A. Lindgren,
Children Hospital at Karolinska Institute, Stockholm, Sweden
Exposure
to ETS and Public Health Impact
Children's Exposure
to Passive Smoking: Survey Methodology and Monitoring Trends.
M.J Jarvis, Health Behaviour Unit, Department of Epidemiology and Public
Health, University of College, London.
Magnitude of Smoking
Attributable Costs. K. Adams, Rollins School of Public Health,
Emory University, Atlanta, GA.
Properties of Environmental
Tobacco Smoke. W. Rickert, President, Labstat Inc., Kitchner,
Ontario, Canada.
Environmental Tobacco
Smoke Public Policies and Interventions: Using Communication and Outreach
to Reduce Childhood Exposure to ETS. W. Long, Environmental Protection
Specialists, Office of Air and Radiation, US Environmental Protection Agency,
Washington, D.C.
Risk Communication,
Children's Health, and Environmental Tobacco Smoke.
V.T. Covello, Director, Center for Risk Communication, New York, New York
Risk Perception
and Communication: Environmental Tobacco Smoke and Child Health. W.
Leiss, Eco-Research Chair in Enironmental Policy, School of Policy Studies,
Queen's University, Kingston, Ontario, Canada.
Theories of Behavior
Change in Relation to Environmental Tobacco Smoke Control to Protect Children.
R. Borland, Centre for Behavioural Research in Cancer, Anti Cancer Council
of Victoria. Victoria, Australia. Extracts of the
1997 Declaration of the Environment Leaders Miami, May 1997
"Environmental Tobacco
Smoke: Children exposed to environmental tobacco smoke are more likely
to suffer from reduced lung function, lower respiratory tract infections
and respiratory irritations. Asthmatic children are especially at
risk. Many of these symptoms lead to increased hospitalizations of
children.
We affirm that environmental
tobacco smoke is a significant public health risk to young children and
that parents need to know about the risks of smoking in the home around
their young children. We agree to cooperate on education and public
awareness efforts aimed at reducing children's exposure to environmental
tobacco smoke."
Implementation
Actions on Protecting Children's Health and Environment which the Environment
Leaders of the Eight have agreed to promote within their governments and
countries:
"Environmental Tobacco
Smoke: Convene a scientific conference, through WHO or another appropriate
scientific organization, to synthesize and share the latest scientific
information on risks to infants and children from environmental tobacco
smoke and compile information on the most effective education strategies
concerning exposure to children."
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A.
Respiratory health and middle ear disease
Research
directions
IV.
Measurement: health impact, exposure and economic impact
B.
Foetal Growth
C.
Sudden infant death syndrome (SIDS)
D.
Neurodevelopmental effects
E.
Cardiovascular effectsA.
Measuring health impact
V.
Interventions to eliminate children's exposure to environmental tobacco
smoke
VI.
Conclusions and recommendations
VII.
Additional Sources and Links
VIII.
Annex 1 G-8 Declaration
B.
Measuring exposure
C.
Measuring economic impact
D.
Extrapolating to developing countries
1.
Canada, France, Germany, Italy, Japan, Russian Federation, United Kingdom
of Great Britain and Northern Ireland, United States of America
Because
many of these adverse health effects are common ailments and ETS exposure
is very widespread, even small increases in average individual risk result
in large population risks. In other words, a large number of cases
of these illnesses can be attributed to ETS exposure. Furthermore,
there may be susceptible subgroups of children that are at even higher
individual risk, although this issue has not been well studied. Finally,
while the effects may be difficult to measure, it is plausible that children's
exposure to ETS and consequent health effects may increase risks of further
adverse health effects in adulthood.
ETS exposure is causally associated with increased
risks of lower respiratory tract illnesses, including bronchitis and pneumonia,
in the first years of life.
ETS exposure is a cause of chronic respiratory
symptoms in school-aged children.
ETS exposure increases the severity and frequency
of symptoms in children with asthma.
ETS exposure is causally associated with increased
risk of acute and chronic middle ear disease.
Maternal smoking is a cause of small reductions
in lung function. The predominant effect may be from smoking during pregnancy.
ETS exposure of nonsmoking women during pregnancy
is a cause of small reductions in average birth weight.
Maternal smoking is a major cause of SIDS.
The predominant effect is believed to be from in utero exposure.
There is also some evidence that postnatal ETS exposure contributes to
the risk of SIDS.
Parental smoking is associated with learning
difficulties, behavioural problems, and language impairment. There is some
evidence that both ETS exposure to nonsmoking women during pregnancy and
children's postnatal ETS exposure may contribute to small impairments.
ETS exposure is associated with physiological
changes in children that may increase the risk of cardiovascular disease.
There is suggestive evidence that parental
smoking may increase the risk of some childhood cancers. However, the potential
roles of preconceptional, in utero, and postnatal exposures are
unknown.
Successfully eliminating children's involuntary
exposure to tobacco smoke requires a comprehensive health promotion effort
with two main thrusts: legislation and education.
Legislation encompasses all regulatory approaches
to controlling where and when people can smoke. Education includes public
information, debate, and advocacy, all designed to encourage behaviour
change. These two approaches are complementary, and the appropriate mix
of education and legislation will depend on the culture of the particular
country or region.
Governments have a responsibility to legislate
to control exposure to tobacco smoke in public spaces. Legislation to ban
smoking in places children frequent is an important first step. These include
schools, child care and health care facilities, and places where young
people gather, including sports clubs, restaurants (especially fast food
outlets), shopping centres and public transport. Smoking restrictions in
the workplace are important to protect pregnant women and minors.
Legislation is of limited value in reducing
exposure in private homes. Educational strategies, including education
about the risks to children from ETS exposure and steps to eliminate exposure,
are likely to be more effective in these settings. Educational programmes
must strategically target household decision-makers, either directly or
indirectly, such as through other family members. Similar strategies are
needed to protect children from ETS exposure in cars.
Effective education may ease implementation
of legislation but does not do away with the need for enforcement of legislation.
Health warnings on cigarette packages advising
smokers that their tobacco smoke is injurious to children and others should
be included in the range of required messages.
Health care workers are an important component
of any education strategy as they can counsel children about avoiding smoke
and adults about the importance of smoke-free air for children. This role
is particularly critical when young patients are already suffering from
a ETS-induced illness. Training for physicians and other health professionals
should include adequate attention to issues of ETS.
Skilful use of mass media, based on principles
of communication science, coupled with advocacy that links government public
health policy with efforts by health professionals and grassroots groups,
is essential to the success of any educational campaign.
Particular attention should be given to interventions
to assist pregnant women to stop smoking. Preventing them from relapsing
and inducing their partners to stop smoking will increase the likelihood
of a smoke-free environment for children. Training for health professionals
who work with pregnant women is crucial.
A secondary benefit of reduced tobacco consumption
is reduced exposure of children to tobacco smoke. WHO and other international
and intergovernmental bodies recommend measures such as: 1) banning all
advertising and promotion of tobacco products, 2) increasing prices beyond
inflation, 3) regulating tobacco products, and 4) prohibiting sales to
minors as steps towards reducing overall consumption.
Interventions should be monitored and evaluated
from the perspective of both efficacy and cost-effectiveness.
Almost half of the world's children are involuntarily
exposed to tobacco smoke.
Exposure to environmental tobacco smoke causes
increased risks of several illnesses in children and may increase the risk
of death from sudden infant death syndrome (SIDS). Exposure of nonsmoking
women to environmental tobacco smoke during pregnancy also causes reductions
in fetal growth.
Children do not choose this exposure. Their
right to grow up in an environment free from tobacco smoke must be safeguarded
through actions by national and local governments, voluntary bodies, community
leaders, health workers, educators and parents.
Reducing children's exposure to tobacco smoke
requires a two-pronged strategy: reducing smoking in spaces where children
live, play and learn, and reducing overall tobacco consumption.
Effective public policy is important to protect
this vulnerable group.
To maximize impact, policies to protect children
from tobacco smoke exposure should be implemented as part of comprehensive
tobacco control programmes.
Legislated restrictions on smoking in public
places and the workplace will protect nonsmokers in general and vulnerable
groups such as children and pregnant women in particular.
Young children's greatest exposure to tobacco
smoke occurs at home. Increasing the percentage of tobacco-free homes is
generally not amenable to legislation but can be achieved by a combination
of mass media campaigns and smoking restrictions in public places and the
workplace.
Programmes to raise awareness and motivate
behaviour change among pregnant women and their partners are needed to
reduce the harmful effects of prenatal and postnatal exposure to tobacco
smoke.
Interventions through legislation and education
need to be culturally specific.
Surveys, using biomarkers where possible, will
be necessary to plot changes in children's involuntary exposure and monitor
the effectiveness of interventions.
Report 1
Lower respiratory tract infections
2
Middle ear disease
Chronic respiratory symptoms
Asthma
Lung function
Sudden infant death syndrome
(SIDS)
United States Surgeon General
(1986)
More frequent in children whose parents smoke
Suggestive evidence that middle ear effusion3
is more common in children whose parents smoke
More frequent in children whose parents smoke
Not reviewed
Small decrements in children whose parents smoke
Not reviewed
United States Environmental
Protection Agency (1992)
ETS is causally associated with increased risk
ETS is causally associated with increased prevalence
of middle ear effusion
ETS is causally associated with increased prevalence
ETS is causally associated with additional episodes
and increased severity of symptoms in asthmatic children; suggestive evidence
that ETS causes new cases of asthma
ETS is causally associated with small reductions
Strong evidence that maternal smoking increases
the risk of SIDS. Data inadequate to assess specific role of ETS
California Environmental Protection
Agency (1997)4
ETS is causally associated
ETS is causally associated
ETS is causally associated
ETS is causally associated with asthma exacerbation
and induction
Suggestive evidence of causal association with
ETS
ETS is causally associated
Australian National Health
and Medical Research Council (1997)5
ETS has cause-and-effect relationship
Causal link between ETS and middle ear effusion
Not reviewed
Causal relationship between ETS and asthma
Association with ETS exposure
Causal association with ETS
United Kingdom Scientific
Committee on Tobacco and Health (1998)
ETS is a cause
Parental smoking causes acute and chronic middle
ear disease
Convincing evidence that parental smoking increases
risk
ETS is a cause of asthma attacks
Not reviewed
ETS has cause-and-effect association
VII.
Additional Sources and Links
Further details and
full text available at:
California Environmental
Protection Agency Office of Environmental Health Hazard Assessment.
Health Effects of Exposure to Environmental Tobacco Smoke. (1997)
www.health.gov.au/nhmrc/advice/nhmrc/foreword.htmFurther details and
full text available at:
Report of the Scientific
Committee on Tobacco and Health. Department of Health, UK (1998)
www.oehha.org/archive/tobacco_smoke.htmlFurther details at:
United States Environmental
Protection Agency. EPA Office of Research and Development, "Respiratory
Health Effects of Passive Smoking: Lung Cancer and Other Disorders", EPA/600/6-
90/006F, December 1992.
www.official-documents.co.uk/document/doh/tobacco/contents.htmFurther details of
this and other EPA work on ETS at:
US Department of Health
and Human Services. The health consequences of involuntary smoking:
a report of the Surgeon General. Washington DC: US Government Printing
Office, 1986. (DHSS Pub No. (PHS) 87-8398).
www.epa.gov/ncea/smoking.html
www.epa.gov/iaq/ets.html
Further details on:
B.
Background Papers prepared for the Consultation
www.who.int/toh
of the Eight on
Children's Environmental Health
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