Fact Sheet EURO/02 /04

Copenhagen, Rome, Valletta, 25 March 2004

 

 

Hazardous chemicals: main risks to children’s health

 

 

Lead

Lead is still the single most important chemical toxin for children and is probably the best known example of a neurotoxin to which children are particularly vulnerable. Their special vulnerability to lead is related to their exposure (hand–mouth activity, pica, ingestion of paint chips), their absorption (the fraction of absorption in children is 40% compared with 10% in adults) and their susceptibility at a critical period of brain development. Children may be exposed to lead in leaded petrol from car emissions, water contaminated by lead pipes, old paint, emissions from factories, contaminated soil, and food contaminated by environmental sources, including improperly glazed ceramic ware for cooking and food storage.

 

Lead particles can move with water, soil, dust and wind: lead finds its way into the body through inhalation, ingestion and dermal penetration. The neurotoxic effects of lead depend on the exposure level and the stage of central nervous system development at the time of insult. Studies have documented beyond doubt that developmental exposure to lead adversely affects several specific brain functions, resulting in particular in neuro-developmental impairment, learning disabilities, attention deficit, poor motor coordination, visuospatial dysfunction and poor language development, as well as anaemia. The consequences of early lead exposure may increase with time, because the individual is less able to benefit from experience and education. Lead is distributed in blood, soft tissues and bone. Renal elimination is very slow and can take many years (25 days at blood level, 40 days at soft tissue level and 25 years at bone level).

 

Lead can produce a range of acute and chronic toxic effects, but its most important effect is chronic neurotoxicity. Effects are particularly severe during the early development of children’s neuro-developmental system, i.e. in the first 2–3 years, causing impaired cortical functions such as attention deficit disorder and other developmental disabilities. Globally, the estimated annual costs of these effects are US$ 43.4 billion.

 

 

Methylmercury

Environmental methylmercury derives from the methylation of inorganic mercury. Mercury originates mainly from combustion sources such as coal power plants and municipal waste incinerators, is deposited into lakes and rivers and is converted into methylmercury by sediment bacteria. This then accumulates in fish (mostly freshwater trout, pike, bass and saltwater shark and swordfish) and can be introduced into the food chain.

 

Methylmercury is a very dangerous neurotoxin, and can have serious adverse effects on the development and functioning of the human central nervous system. This is especially true when exposure occurs prenatally through maternal diet and in children through direct food intake. At high exposure levels, seizures and spasticity (cerebral palsy) occur. In other cases, methylmercury produces blindness, deafness and mental retardation. At high exposure levels, a dose–response relationship has been established between the levels of mercury in maternal hair during pregnancy and the prevalence of severe psychomotor retardation in children. In some cases, the mother can be unaffected by the toxic exposure that she unwittingly passes on to her child. Postnatal exposure to mercury can come from breast-milk: in a fishing community, the concentration of mercury in a child’s hair has been found to increase with the duration of the breastfeeding period.

 

 

Dioxins, dibenzofurans and polychlorinated biphenyls

Dioxins, dibenzofurans and polychlorinated biphenyls (PCBs) are distributed in the environment mainly through incineration and industrial processes. People are exposed to them from numerous sources, foodstuffs being by far the most important and contributing about 90% of exposure. These compounds are lipid-soluble and poorly eliminated, and therefore accumulate in human adipose tissue. They can pass through the placenta to reach the fetus, and their presence in breast-milk further exposes infants: about 10–12% of total lifetime exposure is likely to occur via nursing. Perhaps the most important, and most disturbing, evidence of the toxicity of these compounds is the neuro-developmental and reproductive effects observed in children; nevertheless, crucial questions remain about the specific causal factors and the detailed dose–response relationship.

 

Since the mid-1980s, the WHO Regional Office for Europe, in collaboration with other international organizations and national institutions, has coordinated a comprehensive programme to investigate the possible health risks of dioxins, dibenzofurans and PCBs, especially in infants from exposure to contaminated breast-milk, and to prevent and control environmental exposure to them. The point of studying the levels of these contaminants in breast-milk is that they reflect the maternal body burden and can thus be used as an indicator for the overall exposure of the general population. Exposure studies have been carried out in three cycles: the declining trend in the levels of compounds indicates the continuous decline in the general population’s exposure, which results from emission reduction measures taken in the past (see Fig. 1). Under the Stockholm Convention on Persistent Organic Pollutants (POPs), the production and emission of dioxins, dibenzofurans and PCBs, as well as other potential endocrine disruptors, are expected to be further reduced and eliminated.

 

Fig. 1. Fall in levels of dioxins and dibenzofurans in breast-milk

 

Pesticides

Pesticides are used extensively worldwide for both agricultural and non-agricultural purposes, and include insecticides, herbicides and fungicides. Currently, over 800 pesticides are registered in the European Union. Harmful pesticide residues can contaminate the environment and accumulate in ecosystems, thus entering the human food chain. Some older pesticides were designed to be persistent and are thus found worldwide in water and soil. Newer pesticides degrade more quickly but are often more acutely toxic. Some of these pesticides may cause cancer or damage the nervous, reproductive or immune systems after short-term high-level exposures.

 

Children and infants are exposed to pesticides daily by three routes, namely ingestion, dermal absorption and inhalation. Children can ingest pesticide residues in food (including baby foods), drinking-water, breast-milk and sometimes in soil. In addition, children can be exposed to pesticides used and/or found on pets and in households, schools, swimming areas, rural environments, parks, etc. The large number of potential sources and pathways of exposure is of particular relevance because it can lead to high cumulative exposure. Because their bodies are still developing, fetuses, infants and children can be more vulnerable to toxic compounds than adults, and their diet and special behaviour patterns often result in greater exposure to pesticides. Pesticide-specific data on prenatal and postnatal developmental toxicity and exposure are lacking for many currently used pesticides.

 

 

Nitrates and nitrites

High concentrations of nitrates in drinking-water and food are of concern because nitrate can be reduced to nitrite, causing methaemoglobinaemia, a condition that reduces the ability of the haem fraction of the blood cell to carry oxygen. The haemoglobin of young children is particularly susceptible to methaemoglobinaemia and this, together with the increased ratio of water consumption to bodyweight, makes infants particularly vulnerable to this disease. Cases have been reported in Hungary, Slovakia and Albania.

 

Benzene

Children have more years of life ahead of them than adults, so they have more time to develop chronic diseases. They may take several decades to appear and may be triggered by early environmental exposure or be determined by continuous exposure. Diseases with long latency periods include benzene-induced leukaemia. Benzene is a product of petrol combustion. Several studies indicate that children living near busy roads have an approximate 50% increased risk of suffering from respiratory diseases. They also suggest an increased risk of childhood leukaemia from exposure to vehicle exhaust, where benzene may be the responsible agent. Benzene is known for its ability to induce leukaemia in occupationally exposed workers, but whether this effect also occurs in children exposed to the lower concentrations typical of the general environment is not known.

 

To assess the effect of road traffic exhaust on the risk of childhood leukaemia, a population-based case–control study was carried out in the Province of Varese, northern Italy, which is covered by a population-based cancer registry. All 120 cases from 1978 to 1997 were included in the study. As an index of exposure to traffic exhaust, the annual mean concentration of benzene outside the home was estimated. The risk of childhood leukaemia was four times higher for children heavily exposed to road traffic emissions (estimated annual average over 10 µg/m³ benzene) compared with children with lower levels of exposure (<0.1 µg/m³). These data, considered with other available evidence, suggest that road traffic emissions may be involved in the etiology of childhood leukaemia.

 

 

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