Lead

Contamination of food with lead (Pb) appears to be inevitable. Lead originates from natural sources as well as from human activities (see Part 1). The majority of organic lead in the environment is accounted for by the anti-knock gasoline additive tetraethyllead. Since the introduction of lead-free gasoline, the concentration of air-borne Pb and the lead content of food are decreasing. Contamination of food of vegetable origin with lead is rather high. In food of animal origin, the lead content is very low, if not nil. For example, the milk from cows grazing on grass with 100 times the normal lead level contained only 4 times more lead than the milk from cows grazing on uncontaminated grass. Increases in the lead level of foods are mostly due to indirect contamination from packaging material and handling.

Lead is absorbed more easily by children (about 40%) than by adults (about 10%). The distribution of lead can be described by a three-compartment model, including bone tissue (95%), blood (2%), and soft tissues (3%). Lead blood levels (PbB) parallel the concentrations in soft tissues. Therefore, the effects of Pb are usually related to the PbB level. A clinical manifestation of lead poisoning is anemia due to a decreased lifespan of the erythrocytes and interaction with several enzyme systems in heme synthesis (Figure 10.3).

The most sensitive indicator of hematologicalchangesafterexposuretoleadisinhibi-tion of the enzyme 5-aminolevulinic acid (5-ALA) dehydratase. ALA blood levels increase at PbB levels of 40 to 80|g/l. However, the toxicological significance of the inhibition of this enzyme (i.e., change in hemoglobin levels) is not yet fully understood. Anemia clinically manifests itself at higher PbB levels. The WHO (1987) has set the lowest-observed-adverse-effect level (LOAEL) (see Chapter 21, Section 21.4.4.3) at 200 |g/l blood. Recent findings have shown that exposure to low lead levels may lead to neurological disorders which used to go unnoticed, in particular in the developing brains of children. Prenatal exposure to lead is also of great concern, as Pb passes the placenta, and the blood-brain barrier of the fetus.

enzymatic steps inhibited by lead

1 Pb

2 Pb

7 Pb normal pathways

Porphyrin formation

Porphyrin formation

5 - Aminolevulinic acid (ALA)-ALAD

5 - Aminolevulinic acid (ALA)-ALAD

Porphobilinogen (PBG)

Uroporphyrinogen III urogenase

Coproporphyrinogen III

Iron utilization metabolites and abnormal products accumulated in human lead poisoning

Fe transferrin (serum)

into serum Fe reticulocytes may be increased

ALA in serum, urine

CP in RBC, urine

Uroporphyrinogen III urogenase

Coproporphyrinogen III

PP in RBC

► Ferritin, Fe micelles in RBC

► Damaged mitochondria and immature RBC fragments (basophilic stippled cells)

Hemoglobin

Figure 10.3 Lead interferes with the biosynthesis of heme at several enzymatic steps (Source: Goodman et al., 1990).

PP in RBC

► Ferritin, Fe micelles in RBC

► Damaged mitochondria and immature RBC fragments (basophilic stippled cells)

Hemoglobin

Figure 10.3 Lead interferes with the biosynthesis of heme at several enzymatic steps (Source: Goodman et al., 1990).

The absorption of Pb is higher in children than in adults. Generally, children are exposed to higher lead levels from the environment (dust, pica). Furthermore, children are particularly sensitive. Today's concern about lead intake has drawn the attention to neu-rotoxicity at prenatal lead blood levels and to the effect of lead on the development of the child after birth. For babies, the lead intake from milk powder and dust is estimated at ±35 |g and ±40 |g per week respectively. The lead intake by babies from drinking water with a lead content of 50 |g/l is estimated at ±25 |g per day. However, the lead intake by sucklings should not exceed 25 |g/kg per week according the WHO standardization. This means that the average lead level in drinking water is probably too high for babies.

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