Concurrently, research fi ndings provide a clearer understanding of the hazards children face and of the links
between environmental degradation and health. Since 19, concern for the environment and health in Europe
has united the Member States in the WHO European Region, intergovernmental organizations, civil-society
organizations and the European Commission in a common commitment to improve our environment and our
health.
In 2002, Margot Wallström,1 then European Commissioner for the Environment, stressed that children’s
health and environment needed to be high on the political agenda. Political attention to environmental and
health matters culminated in the Fourth Ministerial Conference on Environment and Health, held in Budapest,
Hungary in June 2004. Here, the Children’s Environment and Health Action Plan for Europe was agreed at the
highest political level, setting the scene for national action and implementation.
The political momentum from the still tangible enthusiasm of the Conference should not be lost. To be effective,
the Action Plan, with its commitments packed concisely into less than a dozen pages, needs to be adapted
to particular national settings. This publication provides the tools for countries effectively to do just that.
Today, collaboration between WHO and the European Commission continues to strengthen, with the support
of our Member States. We are all committed to channelling our efforts towards a common goal – that of
providing a healthier future for our children.
Children’s vulnerability to
biological and social factors in the
physical environment
Biological, economic and social factors greatly infl uence children’s vulnerability to environmental risk factors
in their different developmental stages, from conception to adolescence. Environment and health policies
aimed at protecting children (and women of reproductive age) need to account for these factors and their interactions.
Biological factors
Critical windows of susceptibility during growth and development
Developing organisms are fragile and – due to their rapid growth and development – exceptionally
susceptible
to various chemical and physical agents. Developing organs and systems typically go through periods of high
vulnerability or critical windows of susceptibility. For example, in the embryo, cell growth is particularly rapid
and primary differentiation occurs, providing more opportunity for toxicants to cause mutations and congenital
anomalies (Selevan, Kimmel & Mendola, 2000). During the prenatal and postnatal periods, structures are
developed and vital connections are established. For example, during the fi rst years of life, most of the nervous
system develops. The nervous system has a limited capacity to repair any structural damage; the destruction of
brain cells by chemicals such as lead and mercury, or failure to establish vital connections between nerve cells,
may therefore result in permanent and irreversible dysfunction (Rice & Barone, 2000).
This is why exposure to many external agents during growth and development may produce adverse effects
on health, such as birth defects and neurodevelopmental damage, that have no counterpart in adult life. The
concept of windows of susceptibility is particularly important since it emphasizes that both the dose and the
timing of the exposure may be crucial in determining the nature and amount of the effect. Immature metabolism
Children’s metabolic pathways, especially in the fi rst 6–12 months after birth, are immature and may therefore
be less capable of detoxifying and excreting chemicals than those in adults, which is why lower doses per kg of
weight and longer intervals are recommended for most drugs prescribed for infants during the fi rst weeks and
months of life (Chemtob, 1991). In some instances, however, metabolic immaturity may be benefi cial with respect
to toxicity. Children may actually be less sensitive than adults to some compounds, because the metabolic
pathways that activate their toxic metabolites are not yet developed. In many other instances, infants are more
susceptible, because they do not have the capacity to metabolize (and thus detoxify) toxic compounds (Crom
et al., 1987; Bruckner, 2000; Scheuplein, Charnley & Dourson, 2002). The whole sequence of absorption, distribution,
biotransformation and excretion of xenobiotics in children differs from that of adults, particularly in
the fi rst months of life, and the overall result of these toxicity differences is typically substance specifi c (Bearer,
1995; Faustman et al., 2000; Scheuplein, Charnley & Dourson, 2002).
Greater exposure
Children may be more heavily exposed, per unit of body weight or body surface, to environmental risk factors
than are adults. There are a number of reasons for this. First, infants and young children drink more water, eat
more food and breathe more air than adults in relation to their body weight (Table 1).
Second, the absorption of many chemicals in the intestines is also increased in children. For example, infants absorb as much as 50% of the lead present in food, while adults have an uptake of only 10% (Royce, 1992). Overview of environmental risk factors and their effects on children’s health Introduction
Some of the environmental risk factors to which children are exposed act in a very specifi c way and contribute
to specifi c effects on health. Most of the effects, however, as outlined in Chapter 2, are the combined result of
many environmental factors and their interactions with social and economic factors. Understanding the hazards
prevalent in the various settings for children’s lives is a very important foundation for setting-based interventions.
Also, understanding the role of each factor and its contribution to specifi c adverse outcomes on children’s
health would be very useful in identifying courses of protective action.
Unfortunately, the epidemiological and toxicological studies intended to unravel associations between environmental
risk factors and specifi c conditions have several limitations. These are both external (such as insuffi
cient resources and available information for potentially important studies) and internal (such as inherent or
unavoidable limitations in design). An awareness of these limitations might help in understanding the varying
strength of the evidence on specifi c associations. Given these limitations, this chapter provides an overview of
the current knowledge of the main environmental risk factors and the main effects on health that result from
exposure in childhood, from before conception to adolescence. Current estimates of the burden of disease in
children, expressed in deaths and DALYs associated with some of the main environmental factors in the European
Region, are also provided. Valent et al. (2004a) describe WHO’s methods in estimating the burden of
disease attributable to each factor.
Poor indoor air quality
Burning coal or biomass at home for cooking and heating creates smoke emissions. Such smoke contains carbon
monoxide, nitrogen oxides, sulfur oxides, benzene, formaldehyde, polyaromatic compounds, and suspended
particulate matter (PM). Indoor sources of air pollution are likely to produce very high levels of exposure
(Bruce, Perez-Padilla & Albalak, 2000; Ezzati & Kammen, 2001), and the highest levels of indoor air pollution
(up to 2000 μg/m3 PM10 – PM with an aerodynamic diameter smaller than or equal to 10 μm) are produced
by use of biomass solid fuel. Since children spend most of their time indoors, they are likely to receive high
levels of exposure, even for pollutants with relatively low concentrations in air. Exposure levels are higher in
conditions of poor ventilation.
On a global basis, solid fuel use represents the largest source of indoor air pollution. It is still widespread in
many countries in the European Region. In eastern Europe and central Asia, an estimated 22.8–41.5% of households
still rely on biomass fuel (wood and coal) combustion for heating and cooking (World Bank, 2003).
High levels of indoor air pollution lead to an increased risk of lower respiratory infection in children, resulting
in increased morbidity and mortality (Bruce, Perez-Padilla & Albalak, 2000; Ezzati & Kammen, 2001;
Black, Morris & Bryce, 2003). In Eur-B and -C, it has been estimated that 1.1–6.6% of deaths and 0.7–5.0%
of DALYs in children aged 0–4 years, as well as 3.7–11.5% of the total asthma burden in children aged
5–14 years, are attributable to indoor air pollution due to solid fuel use (Valent et al., 2004b).
Morbidity linked to poor indoor air is observed even in the most developed areas, owing to exposure to ETS,
chemicals in furnishing and construction materials, and such biological agents as moulds. Maternal smoking is associated with adverse outcomes of pregnancy, such as miscarriage premature
birth, low birth weight and some congenital anomalies, and with increased risk of respiratory diseases and developmental delay in the early years of life (DiFranza & Lew, 1995, 1996). Also, exposure to ETS after birth
is associated with increased incidence of respiratory infections and wheezing and is likely to cause an increase
in chronic respiratory disease and cancer later in life (DiFranza & Lew, 1996; Ji et al., 1997; Strachan & Cook,
1998; Courage, 2002). Environmental health indicators
In recent years, the WHO Regional Offi ce for Europe, working with several Member States, EEA and the
EC Directorate-General for Health and Consumer Protection, has made substantial progress towards creating
a harmonized environment and health information system based on common indicators. The environmental
health indicators that have been developed and pilot tested use solid scientifi c evidence about the links between
health effects and environmental exposures to foster policy development. The work resulted in: • methodological guidance for generating and analysing key environmental health indicators and using them
in policy-oriented reporting;
• after a check of the indicators for compatibility with EU legislation, the proposal of a core set of 17 to become
part of the EC health indicators (WHO Regional Offi ce for Europe, 2003a, 2004b); and
• World-Wide-Web-based tools bringing together the data necessary to construct selected indicators from
different information sources and to facilitate access to information.
Demonstration products applying the environmental health indicator methodology were prepared for the Budapest
Conference: a pilot report (WHO Regional Offi ce for Europe, 2004c) and a prototype Web portal (WHO
European Centre for Environment and Health, 2004).
Along with the CEHAPE, the Budapest Conference participants
References
American Academy of Pediatrics (2003). Handbook on children’s environmental health, 2nd ed. Elk Grove
Village, IL, American Academy of Pediatrics. ATSDR (1988). The nature and extent of lead poisoning children in the United States: a report to Congress.
Atlanta, GA, Agency for Toxic Substances and Disease Registry.
ATSDR (1995). Study of effect of residential proximity to waste incinerators on lower respiratory illness in
children. Atlanta, GA, US Department of Health and Human Services, Agency for Toxic Substances and Disease Registry.
Autier P, Doré JF (1998). Infl uence of sun exposures during childhood and during adulthood on melanoma risk.
EPIMEL and EORTC Melanoma Cooperative Group. European Organisation for Research and Treatment
of Cancer. International Journal of Cancer, 77(4):533–537.
Barker DJP (1998). Mothers, babies, and health in later life. Edinburgh, Churchill Livingstone. Bearer CF (1995). How are children different from adults? Environmental Health Perspectives, 103(Suppl. 6):7–12.
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