Chemical safety

This summary assesses the exposure of children to potentially hazardous chemicals in their food. It focuses on chemicals with the lowest safety margins, namely toxic metals, arsenic and polychlorinated biphenyls (PCBs). In estimating the current situation only the available data have been considered. They mainly address adult populations, as child-specific data are only available for children aged 4–6 years in Germany. The summary also contains information on the environment and health context and the policy relevance and context, and an assessment of the situation in the WHO European Region.

Key message

Only a partial assessment can be made of the extent to which children are exposed to chemical hazards in food in European countries. In many countries, information on exposure to chemical hazards in the diet is collected for the whole population, not specifically for children. When it is collected, it may be incomplete or not comparable with other countries. In order to assess exposures to hazardous chemicals through food, interventions need to be harmonized and data collected regularly that reflect the specific risks to children in the Region.

Figures

Presentation of data

Fig. 1 shows the average intake of heavy metals and arsenic by adult population in various European countries (1).

Fig. 2 depicts the mean values of hazardous metals in the total diet of the Czech Republic’s general population from 1994 to 2001 (note that Fig. 2 is per kg body weight in contrast to Fig. 1). Data are obtained from the Global Environment Monitoring System - Food Contamination Monitoring and Assessment Programme (GEMS/Food) contaminants database, accessed through the WHO Summary of Information on Global Health Trends (SIGHT) (2). Only in the case of cadmium can a consistent downward trend be observed.

Fig. 1. Heavy metal intake through food by adults, selected EU countries, 2004

Note. The intake of mercury (Hg) and cadmium (Cd) is weekly, that for lead (Pb) and arsenic (As) – daily.

Source: European Commission (1).

Fig. 2. Mean level of selected hazardous metals in the total diet of the general population of the Czech Republic, 1994–2001

Source: GEMS/Food contaminants database (2).

Download Excel sheet with Figure data

Rationale

Exposure to hazardous chemicals during growth and development can result in acute long-term effects on the health of children. The strict regulations and measures applied in European countries mean that food is generally safe, but ingestion of contaminated food may still present an important route of exposure to chemical hazards. As their bodies are developing and they generally consume more food on a body weight basis than adults, children are at particular risk of illness from exposure to chemical hazards in food. This indicator focuses on a few contaminants in food, mainly toxic metals. Unacceptably high exposures can be avoided when the levels of hazardous substances in food are monitored.

Health and environment context

Chemical hazards in food are toxic substances that either occur naturally, such as aflatoxins and marine toxins, or are manmade. Manmade toxins can be added to food intentionally, such as antibiotics, preservatives and colorants, or can unintentionally contaminate food, for example, metals, cleaning agents, pesticide residues, animal drugs, other agrochemicals and packaging materials used to keep food safe and fresh. Unintentional contamination may occur through environmental pollution of the water, air and/or soil (3).

Infants and children are especially vulnerable to the acute, sub-acute and chronic effects of ingestion of chemical hazards. Since children consume more food per kilogram of body weight than adults, they are more exposed to chemical hazards in food than are adults. Infants consume twice the amount of food per unit of body weight as adults. Moreover, developing organs and tissues are more susceptible to the toxic effects of certain chemicals. For example, exposure to lead or methylmercury during gestation or early childhood will cause serious damage to the developing brain with consequent loss of intellectual potential, while an adult experiencing the same exposure will suffer no considerable effects to his/her intellectual capacity. With greater exposure and more severe health effects, chemicals in food are more harmful to children than adults (4).

The effects of long-term exposure to chemical hazards in food are of particular concern. Symptoms related to prolonged low-level exposure may not be apparent until later in life and, when they do occur, they may be chronic and irreversible. Serious illness due to long-term exposure to various toxic chemicals may include damage to the immune and nervous systems, impairment of reproductive function and development, congenital anomalies in offspring, cancer and organ-specific damage.

This fact sheet focuses on only a few contaminants (lead, methylmercury, cadmium and arsenic) because, firstly, these are best known for their toxicity and, secondly, the existing data most systematically cover these chemicals. Public concerns about hazards due to chemicals in food are growing due to the increasing number and volume of chemicals produced and used in developed countries, in particular chemicals whose long-term toxicity following chronic exposure has not been yet evaluated (endocrine disruptors, chemicals with toxic effects to reproductive organs, etc). These may or may not be well founded, but better information is necessary.

Lead

Lead is one of the most dangerous chemicals to children. Aside from its acute toxicity, the most important effect of exposure is chronic neurotoxicity, which is particularly severe during the first two to three years of life when early development of the central nervous system occurs. Exposure to lead during this time increases the risk of mild mental retardation, attention deficit hyperactivity disorder and other developmental disabilities (5–7). There are many different ways in which children can be exposed to lead, including through contaminated food and drinking-water, the use of lead-glazed ceramics in cooking and ingestion of paint-chips (especially connected with pica-syndrome typical of poor nutrition) (4). Cumulative exposure from all of these sources should not exceed the provisional tolerable weekly intake (PTWI) of 25 µg/kg body weight/week.

Methylmercury

Mercury is an environmental contaminant that is present in fish and seafood products largely as methylmercury. Food sources other than fish and seafood products may contain mercury but mostly in the form of inorganic mercury, which is considerably less toxic than methylmercury. Methylmercury is highly toxic, particularly to the nervous system; the developing brain is thought to be the most sensitive target organ for methylmercury toxicity. The Food and Agriculture Organization/World Health Organization Joint Expert Committee on Food Additives (JECFA) has established a PTWI of 1.6 µg/kg body weight. The estimated intakes of mercury in Europe vary by country, depending on the amount and the type of fish consumed. Some population groups may frequently consume large predatory fish (such as swordfish, tuna and pike) which are at the top of the food chain and often have a higher concentration of methylmercury. Methylmercury toxicity has been demonstrated at low exposure levels, and exposure to this compound should therefore be minimized while recognizing that fish constitutes an important part of a balanced diet.

Cadmium

Cadmium is present at very low levels in a wide variety of food, and food products account for more than 90% of human exposure to cadmium, except in the vicinity of cadmium-emitting industries. Nevertheless, poisoning due to cadmium in food is rare. The main food sources are the kidneys of animals, which are generally higher in cadmium than are other foods, as well as contamination of rice, soy beans and seafood with cadmium by local industrial and mining operations. The packaging materials for pre-prepared and fresh foods may contain considerable levels of cadmium that may migrate into food. Intake of highly cadmium-contaminated food causes acute gastrointestinal effects, such as vomiting and diarrhoea (8). The main problem for patients chronically exposed to cadmium is kidney damage (9) with a perturbance of phosphorus and calcium metabolism and a possible higher risk of kidney stones. The amount of cadmium in the kidney tubular cells increases during a person’s lifespan and makes up the major part of the cadmium body burden. Maternal exposure to cadmium is associated with low birth weight and an increase of spontaneous abortion (10,11). The International Agency for Research on Cancer (IARC) classifies cadmium as a human carcinogen group I.

Arsenic

Arsenic is ubiquitous, found in air, water, fuels and marine life. The daily human intake of arsenic contained in food is in the range 0.5–1 mg, with the greatest concentrations coming from fish and crustaceans. Once arsenic is in the body it binds to haemoglobin, plasma proteins and leukocytes and is redistributed to the liver, kidney, lung, spleen and intestines. Most of the arsenic in marine food is in organic form and is excreted more rapidly than inorganic arsenic. Acute arsenic intoxication resulting in fatality is rare. Survivors may have severe disabilities secondary to organ damage. Chronic exposure to arsenic over weeks and months can have severe effects due to its neurotoxicity, cardiovascular and renal toxicity and carcinogenicity.

It is difficult to estimate the true extent of the impact of chemical hazards in food on children’s health due to the long latency periods that may occur between exposure and outcome. When the latency period between an exposure and its health effects is long, it is difficult to prove an association. As a result, knowledge of the effects on health of exposure to hazardous chemicals in the diet is incomplete (12).

Policy relevance and context

Pan-European context

Regional Priority Goal IV of the Children’s Health and Environment Action Plan for Europe aims to reduce the risks of disease and disability arising from exposure to hazardous chemicals (such as heavy metals), physical agents (such as excessive ultraviolet radiation) and biological agents and to hazardous working environments during pregnancy, childhood and adolescence (13).

In the European Region, WHO is helping countries to develop and strengthen their food safety programmes. This includes harmonizing legislation with Codex Alimentarius guidelines (14) and EU policies, strengthening food control services and promoting quality assurance systems. The WHO food safety programme also supports countries in building and updating skills for the safety analysis, monitoring and management of food (15).

EU context

The accession of the EU to the Codex Alimentarius Commission in 2003 strengthened consistency between the standards, guidelines and recommendations adopted under the Codex and binding obligations in the EU and its member states in the area of food standards. The measures taken by the EU with regard to food safety and food frequently invoke the Codex as justification (16).

EU legislation covers the chemical safety of foodstuffs in the following five areas.

1. Additives. Legislation on food additives is based on the principle that only those additives that are explicitly authorized may be used, often in limited quantities in specific foodstuffs.
2. Flavouring. The existing legislation on flavourings sets limits on the presence of undesirable compounds. There is an ongoing safety evaluation programme for chemically defined flavouring substances.
3. Contaminants. The legislation on contaminants is based on scientific advice and the principle that contaminant levels shall be kept as low as can be reasonably achieved by following good working practices. Maximum levels have been set for certain contaminants (for example, mycotoxins, dioxins, heavy metals, nitrates and chloropropanols) in order to protect public health.
4. Residues. Legislation on the residues of veterinary medicinal products used in food-producing animals and on the residues of pesticides has set maximum residue limits. In some cases the use of such substances is prohibited.
5. Contact materials. The legislation on food contact materials provides that these materials shall not transfer their components into food in quantities that could endanger human health or change the composition, taste or texture of food (17).

The European Food Safety Authority (EFSA) was established in 2002 (Regulation (EC) 178/2002) to ensure common principles and responsibilities regarding food, scientific quality and efficient procedures for decision-making in matters of food safety (18). It is responsible for collecting data on food contaminants. The regulation was based on the White Paper on Food Safety, which proposed a radical revision of the EU’s food hygiene rules (19). Surveys show that the levels of hazardous chemicals in food are generally below the maximum amounts permitted by health authorities. The Scientific Cooperation on Questions Related to Food (SCOOP) project, coordinated by EFSA, aims to retrieve pooled data from across the EU on particular issues of concern regarding food safety. These data are used to assist the Commission in developing EU legislation to increase the protection of consumers (20).

Global context

In order to ensure adequate standards of food safety and quality, the Food and Agricultural Organization (FAO) and WHO developed the Codex Alimentarius (14). The Codex was created in 1963 and includes a collection of standards for food labelling, additives, contaminants, food hygiene, methods of analysis and sampling and for residues of veterinary drugs and pesticides in foods. In 1985, the United Nations recommended national governments to adopt food safety standards from the Codex Alimentarius (14). At present, food standards apply to individual contaminants in various foods in terms of total intake from all food sources. WHO’s Global Environment Monitoring System/Food Contamination Monitoring and Assessment Programme (GEMS/Food) encourages all countries, in particular developing countries, to undertake total diet studies (21).

Assessment

Chemical hazards that give most concern with regard to children’s health due to the lower safety margins in children’s food are toxic metals (lead, methylmercury, cadmium, arsenic) and some persistent organic pollutants (POPs), notably dioxin-like compounds.

SCOOP data from 2004 on average intake levels of lead, mercury, cadmium and arsenic in adults’ diet is available for 13 European countries (Belgium, Denmark, Finland, France, Germany, Greece, Ireland, Italy, the Netherlands, Norway, Portugal, Sweden and the United Kingdom). In most European countries adult intake levels have been 10–30% of PTWI levels, sometimes higher. The data on intake among children are very patchy. The total intake seems to be lower than in adults, but per kg body weight the intake is higher (1).

Monitoring of chemical contaminants in food in the Czech Republic through total diet studies is an established practice and recent, nationally representative data on the levels of chemical hazards in food are available. The observed amount of all metals in the total diet of the general population between 1994 and 2001 was far below the PTWI values (Table 1).

Table 1. Tolerable intake values of selected toxic metals for adults

Note. These values are not isolated dietary intake values. A full risk assessment of dietary intake of metals should also take into account other sources of exposure (such as dermal and inhalation exposures).

The total diet studies in the Czech Republic estimate levels of contaminants in the diet of the general population. Due to the fact that young children tend to eat different types of food and a different amount per kilogram body weight than adults, these values are not directly applicable to children under three years old who are particularly vulnerable to the neurotoxic effects of chemical hazards.

In summary, due to the scarcity of child-specific data on food consumption, the extent of the exposure of children to chemical hazards in food is still patchy. For many countries, data on contamination of and exposure through food are not collected or may be incomplete or collected in a way that makes it difficult to make intercountry comparisons.

National authorities have the responsibility and obligation to ensure that toxic chemicals such as pesticides, metals, environmental contaminants and naturally occurring toxins are not present in food at levels that may adversely affect the health of their citizens. To assess the risk to children’s health arising from the presence of hazardous chemicals in food, the actual dietary intake of chemicals should be estimated and compared with their corresponding toxicological reference intakes, such as PTWI. Estimation of the actual dietary intake of chemical hazards is essential for risk assessment and can be used in determining whether there may be a relationship between the observed adverse effects in humans and exposure to a particular contaminant. Standardizing the methods of data collection across the Region will strengthen such risk and health impact assessments.

Any assessment of the exposure of children to chemical hazards in food should address their unique biological characteristics and exposure patterns. The different exposures (according to different types of food consumed) and outcomes (susceptibility to neurotoxic effects) among children of different ages should be considered. In adults, 200 chemicals are known to cause clinical neurotoxic effects. Despite an absence of systematic testing, many additional chemicals have been shown to be neurotoxic in laboratory models. The toxic effects of such chemicals in the developing human brain are not known and they are not regulated to protect children. When assessing risks from chemicals in food, additional safety factors for infants and children need to be applied. Available information on aggregate exposure from single chemicals should be considered, including exposure through dietary and drinking-water sources and other exposures. Available information on the cumulative effects of chemicals with common toxicity mechanisms should be considered.

At the same time, the highest risks in food for children are not contaminants or added chemicals, but unhealthy food choices including snack foods with too much fat, sugar and salt. These may affect children’s health even decades later as risk factors for obesity, diabetes, hypertension, cardiovascular diseases and cancer. It is important to emphasize the health value of vegetables, fruit, berries and fish regardless of contaminants that may be present.

The potential impacts on health of consuming contaminated food can be greatly reduced by preventing exposure through improved production, processing and handling of food and educating people to avoid high-risk foods. Sound management of chemicals, particularly metals, pesticides and POPs, is vital to the protection of children’s health. In view of the seriousness of their impact on children, the initial focus for action should be placed on chemicals that are toxic to the developing human brain: lead, mercury and PCBs. Chemicals of particular concern are those that tend to accumulate in the body, such as cadmium and POPs, and to which chronic exposure at even low levels may cause serious health problems (21).

Metadata

Name: Exposure of children to chemical hazards in food

Definition: Dietary exposure to potentially hazardous chemicals in children’s food.

Code: RPG4_Food_Ex1

Data source

The data used for this indicator were collected from the SCOOP reports by EFSA (23) and from the GEMS/Food database by the United Nations Environment Programme (2).

Description of data

SCOOP projects are specific projects launched in the EU for the estimation of dietary intake of contaminants, carried out before EFSA was set up. Data from member states were collected but the methods and techniques were not harmonized, so the quality of data and the results may vary between countries.

The GEMS/Food total diet study database contains information from 1972 to 2003 on contaminants in the diets of 15 countries throughout Europe. Information is submitted to the database by participating institutions, which use standardized methods for measuring contaminants and submitting data. The database contains information from total diet studies, which provide the most accurate estimate of dietary intakes of contaminants. By explicitly taking into account the kitchen preparation of foods, total diet studies assess the levels of contaminants in food as it is consumed.

Method for indicator calculation

The exposure is estimated by average intake of selected chemicals. This includes data on the presence of a chemical in individual foods and diets, including its fate during the processes within the food production chain, and data on the consumption patterns of the individual foods containing the relevant chemicals.

Geographical coverage

For SCOOP data: Belgium, Denmark, Finland, France, Germany, Greece, Ireland, Italy, the Netherlands, Norway, Portugal, Sweden and the United Kingdom

For GEMS/FOOD data: Czech Republic.

Period of coverage

2004 for SCOOP. 1994–2001 for GEMS/FOOD.

Frequency of update

For SCOOP data, the measures were not repeated in time. GEMS/FOOD data were updated on a yearly basis.

Data quality

Data from both sources refer mostly to the adult population. Specific data on the exposure of children are not available.

The SCOOP data are collected from different countries, with no harmonized methods and techniques so that the quality of data from different countries may vary. They only reflect the situation at one point in time. There are no updates for time trend estimation.

The GEMS/Food data from Czech Republic are one order of magnitude lower than SCOOP data and it was not possible to clarify this difference. The data are, therefore, only valuable to show trends in food contamination in time.

To assess the exposure of children to hazardous chemicals in food, their actual dietary intake should be estimated. In order to compare exposure across all the European Region Member States, a standard methodology should be employed. In particular, attention should be paid to collecting data on representative samples of the child population. Standardizing the methods of data collection across the Region can strengthen common efforts for the development of policies and action to reduce hazardous exposures and their effects on health.

For more information on meta data and calculation of this indicator, please refer to the methodology .

References

1. Assessment of the dietary exposure to arsenic, cadmium, lead and mercury of the population of the EU member states. Brussels, Commission of the European Communities, Directorate-General of Health and Consumer Protection, 2004 (SCOOP task 3.2.11; http://ec.europa.eu/food/food/chemicalsafety/contaminants/scoop_3-2-11_heavy_metals_report_en.pdf).
2. Global Environment Monitoring System – Food Contamination Monitoring and Assessment Programme (GEMS/Food) Contaminants Database [online database] (http://www.who.int/foodsafety/chem/gems/en/index.html). Accessed through WHO Summary of Information on Global Health Trends (SIGHT) [web site]. Geneva, World Health Organization, 2007 (http://sight.who.int/, accessed 24 March 2007).
3. Etzel RA ed. Pediatric environmental health, 2nd ed. Elk Grove Village, IL, American Academy of Pediatrics, 2003:165–180.
4. Pronczuk de Garbino J, ed. Children’s health and the environment: a global perspective. Geneva, World Health Organization, 2004 (http://whqlibdoc.who.int/publications/2005/9241562927_eng.pdf, accessed 29 March 2007).
5. Lidsky TI, Schneider JS. Lead neurotoxicity in children: basic mechanisms and clinical correlates. Brain, 2003, 126:5–19.
6. Needleman HL, Gatsonis CA. Low-level lead exposure and the IQ of children. A meta-analysis of modern studies. Journal of the American Medical Association, 1990, 263:673–678.
7. Needleman HL et al. The long-term effects of exposure to low doses of lead in childhood. An 11-year follow-up report. New England Journal of Medicine, 1990, 322:83–88.
8. Nordberg GF. Cadmium and health in the 21st century – historical remarks and trends for the future. Biometals, 2004, 17:485–489.
9. Frery N et al. Environmental exposure to cadmium and human birthweight. Toxicology, 1993, 79:109–118.
10. Shiverick KT, Salafia C. Cigarette smoking and pregnancy I: ovarian, uterine and placental effects. Placenta, 1999, 20:265–272.
11. Barbier O et al. Effect of heavy metals on, and handling by, the kidney. Nephron Physiology, 2005, 99:105–110.
12. Children’s Environmental Health [web site]. Chemical hazards. Geneva, World Health Organization, 2007 (http://www.who.int/ceh/risks/cehchemicals/en/, accessed 29 March 2007).
13. Children’s Environment and Health Action Plan for Europe. Declaration. Fourth Ministerial Conference on Environment and Health, Budapest, 23–25 June 2004 (EUR/04/5046267/6; http://www.euro.who.int/document/e83335.pdf, accessed 16 March 2007).
14. FAO/WHO. Codex Alimentarius [web site]. Rome, Food and Agricultural Organization and Geneva, World Health Organization, 2006 (http://www.codexalimentarius.net/web/index_en.jsp, accessed 29 March 2007).
15. Food Safety. Country support [web site]. Copenhagen, WHO Regional Office for Europe, 2007 (http://www.euro.who.int/foodsafety/assistance/20020418_1, accessed 6 April 2007).
16. Council Decision 2003/822/EC of 17 November 2003 on the accession of the European Community to the Codex Alimentarius Commission. Official Journal of the European Union, 26.11.2003, L309(46):14 (http://europa.eu/scadplus/leg/en/lvb/f84006.htm, accessed 29 March 2007).
17. Food Safety – From the farm to the fork. Chemical safety of food [web site]. Brussels, European Commission, 2007 (http://ec.europa.eu/food/food/chemicalsafety/index_en.htm and http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=CELEX:32002R0178:EN:HTML, accessed 6 April 2007).
18. Regulation (EC) No 178/2002 of the European Parliament and of the Council of 28 January 2002 laying down the general principles and requirements of food law, establishing the European Food Safety Authority and laying down procedures in matters of food safety. Official Journal of the European Union, 1.2.2002, L031:1–24 (http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=CELEX:32002R0178:EN:HTML, accessed 29 March 2007).
19. White paper on food safety. Brussels, European Commission, 2000 (COM (1999) 719 final; http://ec.europa.eu/dgs/health_consumer/library/pub/pub06_en.pdf, accessed 29 March 2007).
20. Council Directive 93/5/EEC of February 1993 on assistance to the Commission and cooperation by the Member States in the scientific examination of questions relating to food. Official Journal of the European Union, 4.3.1993, L 52:18–21 (http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=CELEX:31993L0005:EN:HTML, accessed 29 March 2007).
21. GEMS Food. Total diet studies: A recipe for safer food. Geneva, World Health Organization, 2005 (http://www.who.int/foodsafety/publications/chem/recipe/en/index.html, accessed 29 March 2007).
22. Food and health in Europe: a new basis for action. Copenhagen, WHO Regional Office for Europe, 2004 (WHO Regional Publications European Series, No. 96; http://www.euro.who.int/document/E82161.pdf, accessed 29 March 2007).
23. SCOOP [web site]. Brussels, Commission of the European Communities, Directorate-General for Health and Consumer Protection, 2007 (http://ec.europa.eu/food/fs/scoop/index_en.html, accessed 4 April 2007).

Authors: Pia Vracko, National Institute of Public Health, Ljubljana, Slovenia; Jouko Tuomisto, National Public Health Institute, Kuopio, Finland; Jennifer Grad, WHO European Centre for Environment and Health, Bonn, Germany; Eva Kunseler, National Public Health Institute, Kuopio, Finland.

This summary is based on data on the mean blood lead levels in children of various age groups in a number of European countries between 1991 and 2006. It also contains information on the environment and health context and the policy relevance and context, and an assessment of the situation in the WHO European Region. Suggestions for improving the data quality and biomonitoring are provided as well.

Key message

The phasing out of lead from petrol, first in western Europe and later in central and eastern Europe, has resulted in a significant decrease in blood lead levels in children during the last two decades. Industrial emissions are still important local sources of lead exposure in some countries. Since lead was phased out from petrol, other sources of exposure to lead that had previously been ignored have become increasingly significant. It is still necessary to reduce the levels of lead in the blood further because there is no known safe level in children.

An efficient surveillance system, using comparable methods of blood sampling, analysis and data presentation to monitor lead levels in children’s blood, is urgently required for the identification and elimination of the remaining sources of exposure to lead and monitoring of the effectiveness of preventive action.

Figures

Presentation of data

Fig. 1 shows average levels of lead in children’s blood in 11 countries (Bulgaria, the Czech Republic, France, Germany, Hungary, Israel, Poland, Romania, the Russian Federation, Sweden and The former Yugoslav Republic of Macedonia) at different times between 1990 and 2006. This array of data was used due to the paucity of recent data, to allow data from many countries to be considered and to provide some indication of trends.

Where possible, average blood lead levels are given as the geometric mean as the distribution of blood lead levels is generally log-normal.

Fig. 1. Mean blood lead levels (PbB) of children measured in selected European countries, 1991–2006 (age ranges in years)

Note. TFYR Macedonia = The former Yugoslav Republic of Macedonia.

Bulgaria 1999−2003: data represent industry

Bulgaria 2003: data represent traffic

The former Yugoslav Republic of Macedonia 2001−2003 and 2004: data represent industry (see Assessment section below, third paragraph)

Data for Bulgaria (2003), the Czech Republic and The former Yugoslav Republic of Macedonia are arithmetic means.

Source: Country case studies (4–15).

Rationale

Lead is one of the best known toxic heavy metals. The level of lead in the blood is a highly reliable biological marker of recent exposure to lead. Elevated blood lead level (10 μg/dl or above) has been associated with toxicity in the developing brain and nervous system of young children, leading to lower intelligence quotient (IQ) (1). According to recent evidence, however, loss of IQ was observed in children with blood lead levels below 10 μg/dl, so prevention activities should be initiated to bring down the levels of lead in the blood to the lowest possible level.

Health and environment context

Lead in the environment has multiple sources (e.g. petrol, industrial processes, paint, solder in canned foods, water pipes) and reaches people via a number of pathways (such as air, household dust, street dirt, soil, water, food). As a consequence, evaluation of the relative contribution of different sources is complex and is likely to differ between areas and population groups. Lead-containing petrol remains the most important source of atmospheric lead and is a significant contributor to the lead burden in the body in the countries where it is still used. Industrial emissions are also important sources of lead contamination of the soil and ambient air. Lead from atmospheric air or flaked paint deposited in soil and dust may be ingested by children and may substantially raise their blood lead levels. In addition, food and water may also be important media of baseline exposure to lead (2).

In children, the potential for adverse effects of exposure to lead is increased because (i) the intake of lead per unit of body weight is higher for children than for adults; (ii) young children often place objects in their mouths, resulting in ingestion of dust and soil and, possibly, increased intake of lead; (iii) physiological uptake rates of lead in children are higher than in adults; and (iv) young children are undergoing rapid development, their systems are not fully developed and consequently they are more vulnerable than adults to the toxic effects of lead.

Epidemiological studies show that exposure to lead during the early stages of children’s development is linked to, among other things, deficits in later neurobehavioral performance. Studies suggest that for each 10μg/dl of blood lead, IQ is reduced by 1–3 points. At the individual level, this drop may seem small and reasonably inconsequential, but at the population level, small effects on many individuals may be a significant burden to society, with reduced overall intellectual performance and resulting economic losses. This has been studied by researchers in the United States, who have calculated the financial earnings that could be achieved if the level of lead in children’s blood were to be reduced. Cognitive ability affects school performance, educational attainment and success in the labour market, and is thus positively associated with earnings. Improvements in cognitive ability benefit society by raising economic productivity, including profits and tax revenues, and by reducing crime and other behaviour which has a negative impact on other people (2,3).

The following public health measures may be used to reduce the exposure of children to lead in the environment and thus to lower the level of lead in their blood (2):

• phasing out lead additives in fuels and removing lead from petrol;
• reducing and phasing out the use of lead-based paints;
• eliminating the use of lead in food containers;
• identifying, reducing and eliminating lead used in traditional medicines and cosmetics;
• minimizing the dissolving of lead in water treatment and water distribution systems;
• improving identification of populations at high risk of exposure on the basis of monitoring systems;
• improving the promotion of understanding and awareness of exposure to lead;
• placing greater emphasis on adequate nutrition, health care and attention to socioeconomic conditions that may enhance the effects of lead.

Policy relevance and context

International conventions and action programmes as well as European Union (EU) directives and resolutions have acknowledged the importance of exposure to lead as a key public health issue.

Global and pan-European context

The Convention on the Rights of the Child (United Nations General Assembly resolution 44/25 of 20 November 1989) and Agenda 21 (adopted by more than 178 governments at the United Nations Conference on Environment and Development held in Rio de Janeiro, Brazil, in 1992) form the general framework to protect children’s health from hazardous environmental exposures (16,17).

The 1979 Convention on Long-Range Transboundary Air Pollution on Heavy Metals and the Basel Convention on the Control of Transboundary Movements of Hazardous Wastes and their Disposal recognize the need for international cooperation in reducing exposure to toxic heavy metals (18,19). The Rotterdam Convention promotes the exchange of information as well as shared responsibility and cooperative efforts among the parties in the international trade of certain hazardous chemicals (20).

The recently adopted strategic approach to international chemicals management goes a step further in committing the parties to ensuring that chemicals are produced and used in ways that minimize significant adverse impacts on the environment and on human health (21).

In addition, international commitments are made that specifically address the exposure of children to lead. In February 1996, the environment ministers of the Organisation for Economic Co-operation and Development (OECD) issued a Declaration on Lead Risk Reduction seeking voluntarily to develop and strengthen national and cooperative efforts considered necessary to reduce the risks from exposure to lead. Their goals include efforts to phase out leaded gasoline and eliminate the exposure of children to lead (22).

The 1997 Declaration of the Environment Leaders of the Eight on Children’s Environmental Health commits the G8 countries to fulfil and promote internationally the OECD Declaration on Lead Risk Reduction. They specifically called for further action to reduce the levels of lead in children’s blood to below 10 µg/dl. When this level is exceeded, further action is required. They agreed to conduct public awareness campaigns on the risks to children from exposure to lead and to develop scientific protocols and programmes to monitor the levels of lead in children’s blood to track progress in this important area (23).

In September 2006, the Intergovernmental Forum on Chemical Safety was the setting for the Budapest Statement on Mercury, Lead and Cadmium, which recognizes that the risks from these three substances need to be addressed by further global, regional, national and local action, as appropriate (24). In the same context, the Declaration of Brescia on Prevention of the Neurotoxicity of Metals supported the revision of lead exposure standards and promoted an immediate reduction of the level of lead in children’s blood to a concentration of 5 μg/dl worldwide (25). This level is proposed as a temporary measure that may need to be revised further downwards in future years as new evidence accumulates on toxicity at still lower levels of lead in the blood.

In 2004, the Fourth Ministerial Conference on Environment and Health adopted the Children’s Health and Environment Action Plan for Europe (CEHAPE), which includes four regional priority goals to reduce the burden of environment-related diseases in children. One of the goals (RPG IV) aims to reduce the risks of disease and disability arising from exposure to hazardous chemicals (such as heavy metals), physical agents (such as excessive ultraviolet radiation) and biological agents and to hazardous working environments during pregnancy, childhood and adolescence. In CEHAPE RPG IV specific action is set out to reduce the exposure of children to lead, such as the enactment of legislation on the content of lead in petrol and building materials, to develop and enforce regulations to minimize the risks from hazardous building materials (such as lead) and to carry out biomonitoring of lead in infants and mothers at risk (26).

EU context

The Seventh Research Framework Programme (2006–2013) of the EU emphasizes the development of a coherent approach to human biomonitoring, which is necessary to assure appropriate risk assessment and management for chemicals that influence human health (27).

In 1977, Council Directive on Biological Screening of the Population for Lead (77/312/EEC) committed the EU member states to apply a common procedure for biological screening in order to assess the exposure of the population to lead outside the working environment (28). Several European policy initiatives on reducing the amount of leaded petrol (the main source of elevated levels of lead in children’s blood) are in place in the member states. The Fourth Ministerial Conference “Environment for Europe” in June 1998 endorsed the United Nations Economic Commission for Europe’s Declaration on the Phase-out of Added Lead in Petrol for general use by road vehicles as early as possible, and not later than 1 January 2005. Thirty governments signed this declaration, including most central and eastern European countries; this can be seen as an important step to reducing airborne lead pollution (29). Resolution No. 99/6 on phasing out lead in petrol by the Council of Ministers of Transport, meeting in Warsaw on 18 and 19 May 1999, reiterated the recommendation that where they have not already done so, governments should encourage the more rapid and widespread introduction of unleaded fuel by measures including the use of fiscal incentives and information campaigns (30).

Assessment

In general terms, levels of lead in the blood started to decline earlier in the western European and Scandinavian countries than in eastern Europe, largely because the gradual introduction of unleaded petrol began earlier in the western and northern countries. In the mid-1980s, a collaborative study between WHO and the Commission of the European Communities on levels of lead in children’s blood found levels of 18.2–18.9 μg/dl in Bulgaria, Hungary and Romania, compared to 11.0 μg/dl in Italy and 7.4 μg/dl in Germany (31). This difference was still evident in the 1990s, with considerably lower levels in France, Germany, Israel and Sweden than in Hungary, Poland and the Russian Federation. The beneficial effects of a switch to unleaded petrol are shown by a series of measurements of levels of lead in the blood of children living in an urban environment in Sweden: the geometric mean lead level was 5.8 μg/dl in 1978–1982, 3.4 μg/dl in 1989 and 2.3 μg/dl in 1993.

Data suggest that following the phase-out of leaded petrol, the rate of decline of lead in the continued, albeit more slowly. For instance, the mean level of lead in children’s blood in Germany has fallen by more than 50% over the past 12–14 years. The evidence of reduced levels is positive, but many children still have levels that may harm their health. For example, in France there has been a significant fall in the amount of lead in the blood over the past eight years, but the level in about 10% of children is still above 5.0 μg/dl. This may affect their neurobehavioral performance.

Besides car exhausts, industrial emissions are important sources of exposure to lead. Data from industrial areas in Bulgaria, Poland and The former Yugoslav Republic of Macedonia show the significant impact of lead emitted by nearby plants on the level of lead in children’s blood (Fig. 1). In The former Yugoslav Republic of Macedonia, Fig. 1 shows two measurements made in the same community: one during the time a lead and zinc smelter plant was active (up to 2003), the second after the plant had closed in the second half of 2003 (2004). In Poland, the geometric mean of lead levels in the blood of children living in the vicinity of zinc and copper mills ranged between 7.4 μg/dl and 11.4 μg/dl, in contrast to 3.0–6.3 μg/dl among children living in five towns with no industrial lead emitters (32).

The questionnaires that accompanied the surveys of lead levels in the blood identified other determinants of higher levels in children, including tap water, the age of the dwelling, poor housing conditions, environmental tobacco smoke, breastfeeding by mothers exposed to lead, the use of painted ceramic dishes and cosmetic kohl, low milk intake and poor socioeconomic status. These findings indicate the importance of public education and risk communication. Regularly conducted harmonized assessments of the levels of lead in children’s blood are needed to identify and eliminate existing sources of environmental exposure to lead and to monitor the effectiveness of preventive action. This monitoring would be preferable in pre-school age children, as young children tend to have high levels of lead in their blood due to their tendency to put things into their mouths, and lead levels may affect their school performance.

Metadata

Name: Levels of lead in children’s blood

Definition: The level of lead in the blood of children in a community, a region or a country is expressed as the geometric mean of individual blood lead concentrations in micrograms per decilitre (μg/dl).

Code: RPG4_Chem_Ex1

Data source

Data were kindly provided by: the National Centre for Public Health Protection, Bulgaria; Centre of Environmental Health, National Institute of Public Health, Czech Republic; National Institute of Public Health Sruveillance, France; Landesinstitut für den Öffentlichen Gesundheitsdienst NRW, Germany; National Institute of Environmental Health, Hungary; Hebrew University-Hadassah International School of Public Health and Community Medicine, Israel; Institute of Occupational Medicine and Environmental Health, Poland; Institute of Public Health, Romania; National Board of Health and Welfare, Sweden and Institute for Health Protection, The former Yugoslav Republic of Macedonia. Data for the Russian Federation were taken from reference (4).

Description of data

The levels of lead in children’s blood were determined mostly from venous blood samples using atomic absorption spectrometry or ICP-MS. Three countries reported the use of capillary samples and blood test kits (based on electro-chemistry). According to the comparison tests performed in each case, these data were claimed to be comparable with the results produced by the above-mentioned methods (4,10,11,13). Levels of lead in the blood were provided in the form of arithmetic mean and/or geometric mean. One country presented only the percentages of lead in children’s blood.

Method for indicator calculation

As the data were provided in various forms and for various time periods and age groups, it was not possible to do a meta-analysis. In the case of Romania, geometric mean was estimated on the basis of frequency distribution among blood lead level categories.

Geographical coverage

Bulgaria, the Czech Republic, France, Germany, Hungary, Israel, Poland, Romania, Russian Federation, Sweden and The former Yugoslav Republic of Macedonia.

Period of coverage

1991–2006.

Frequency of update

None.

Data quality

The accuracy and precision are high for measurements of lead in the blood reported by the countries, regardless of different methods of analysis. All samples were analysed by laboratories participating in international proficiency programmes. Only the report from Germany for 2003–2006 was based on representative samples of the population in one part of the country. Other data presented in this fact-sheet are specific to the areas, time of the study and the given age groups. Comparison of the data over time and between countries should, therefore, be made with extra caution. Harmonized methods of blood sampling, analysis and data presentation with improved comparability are needed in the future for monitoring the level of lead in children’s blood.

For more information on meta data and calculation of this indicator, please refer to the methodology .

References

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Author: Dr Peter Rudnai, National Institute of Environmental Health, Budapest, Hungary.