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Question:
I have a 16 month old son who has lived in Moscow since he was six weeks old. After reading an article concerning lead poisoning in a parenting magazine I have been wondering if he should be tested. What would you recommend? Have you run into cases of expat kids in Moscow with high lead levels?
MK
Answer:
Thank you for your inquiry. This gets technical... Lead is a common element. It is not toxic in levels found naturally; it was only the addition of lead salts to paints as coloring agents and stabilizers that caused the largest epidemic of lead poisoning in history, that of childhood lead poisoning. Despite efforts to the contrary (see below), as of 1993 as many as 12 million preschool children in the United States were said to still be affected annually by this syndrome, caused by ingestion of lead from paint, soil, household dust, and infrequently, drinking water. Evidence of permanent damage to the nervous system of those exposed - even to levels of lead previously thought to be safe - raised fears of possible damage to the fetus and newborn as well. In many countries this resulted in prohibition against the addition of organic lead salts to petrol as well as extensive prohibitions against the use of lead in consumer products. In the US these efforts reduced the mean blood lead level from 0.8 umol/L (16 ug/dL) in 1978 to less than 0.3 umol/L (6 ug/dL) in 1990. (In the late 90s, the US CDC updated screening guidelines, believing universal screening is no longer necessary since most children's blood levels are low unless exposed to residential lead-based paint). LEAD METABOLISM Inorganic lead salts are absorbed through ingestion or inhalation; organic lead salts also may be absorbed through the skin. Generally, gastrointestinal absorption is about 10 percent of an ingested dose, but in children it may be as high as 50 percent; and it is enhanced by deficiencies in iron, calcium, and zinc. Adults may take in up to 0.5 umol/day of lead from normal exposure to food and drinking water. Positive lead balance (i.e. accumulation of lead in the body over time) may occur at these levels, since renal excretion normally does not exceed 0.4 umol/d (80 ug/d). But in children no more than 0.02 umol/kg (5 ug/kg) of body weight can be tolerated without increasing the body lead burden. Infants in the developing world and elsewhere are a particular risk through consumption of formula reconstituted with contaminated tap water. Childhood lead poisoning may present as abdominal pain and anemia, but the central nervous system effects are most important; excessive lead affects developing tissues more than tissues with slow turnover. Background or "subtle" lead poisoning is most dangerous to children because its effects emerge without associated symptoms that bring the victim to medical attention. More acute presentations of lead poisoning - seen in developed countries usually by younger children gnawing lead-based paint flakes off cribs and bedroom furniture, and in children whose homes are being renovated with lead-based paints being sanded off - reflect the direct effect of high concentrations of lead [i.e., blood lead greater than 4 umol/L (80 ug/dL)] usually involved. Signs and symptoms include abdominal pain and irritability, followed by lethargy, anorexia, pallor (anemia), ataxia, and slurred speech. In more severe cases, convulsions, coma, and death are usually due to severe generalized cerebral edema and renal failure. The history of "high-dose" exposure to lead (usually paint chips), pica (the ingestion of nonfood substances), and malnutrition (iron, calcium, and zinc deficiency) almost always is associated with this syndrome. The subclinical form of childhood lead poisoning is associated with elevated blood lead exceeding 1.5 umol/L (30 ug/dL). However, no symptoms are usually detected. The syndrome is widespread, and its effects on the developing central nervous system are largely irreversible. These include mental retardation and selective deficits in language, cognitive functions, and behavior, depending on the age and duration of exposure. These latter factors are more important than the height of the lead level. Elevated lead levels at or about 2 years of age are predictive of neurodevelopmental outcome. ASSESSMENT OF ENVIRONMENTAL RISK The environmental risk in the absence of such obvious causes such as flaking or sanding lead-based paint in the child's home environment (an in older houses with painted corrugated iron roofs, where if the paint is lead-based lead can leach into water collected for drinking) is difficult to assess without checking the child's blood lead levels. In many countries where there is not the risk from the child's immediate environment, the likelihood of lead poisoning from environmental exposure - other than that from vehicle exhausts - is less than that in many developed countries: Because few people rely on the (possibly contaminated) ground water supply for drinking, mostly using bottled water instead because of the architectural styles and habits current locally - not using lead based paints - not power-sanding walls - not carrying out renovations while still living in the house - buying safe (new) nursery furniture - having tiled rather than painted corrugated iron roofs on houses The likelihood of exposure to car exhaust fumes causing clinically significant lead poisoning in inhabitants of Moscow is overall lower than may be feared. On the one hand there is no doubt (from studies of traffic policemen, most recently in Thailand) that appreciable and clinically significant lead levels can be found in adults exposed to pollution from motor vehicle exhausts for 8 or more hours a day (this is also likely to be the case in the children, teenagers and adults seen selling items at traffic lights around Moscow). On the other hand, there is a wide difference in exposure between such cases and those of an adult or child who lives / works in a relatively lead-free environment and spends 1 hour a day in traffic in an air-conditioned car, commuting to and from school or work. Any measurement of the actual lead level in air would therefore not be relevant to assessing an individual's risk of lead poisoning. As above, the best - and only reliable - way to determine an individual's level of exposure to lead is to measure it in blood. To the best of our knowledge, this has not been carried out on any significant scale for inhabitants of Moscow, nor has sending blood for testing been a request we have encountered. In the absence of such testing it is not possible to say what the individual level of risk is; and the level of risk for the population could only be estimated after a representative sample has been so tested.
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