Heavy metal toxicity can cause chronic, degenerative conditions. General symptoms include: headache, short-term memory loss, mental confusion, sense of unreality, distorted perception, pain in muscles and joints, and gastro-intestinal upsets, food intolerances, allergies, vision problems, chronic fatigue, fungal infections etc. Sometimes the symptoms are vague and difficult to diagnose.
Absorption of Lead (Pb) from different sources is dependent on the amount of Pb presented to portals per unit time and the physical and chemical state in which Pb is presented. It is also influenced by factors such as age and physiological status. In adults, almost 20-30% and in children almost 50% lead is absorbed through the GI track. Depending on the particle size, lead can enter through lungs. While organic lead is well absorbed through the skin, inorganic lead is not. Since lead is chemically similar to calcium, body handles it like calcium. In the body lead is distributed throughoutbone, teeth, liver, lung, brain and spleen; bone being the major accumulator. Lead can cross blood brain barrier as well as placental barrier. Excretion occurs through urine and faeces. Dose and duration dependent genotoxic effects have been observed.
Nutritional iron deficiency enhances Pb toxicity, raising concern that pregnant women and young children in whom iron deficiency anaemia is high, may be more susceptible to Pb toxicity8. Pb absorption is increased considerably with fasting or in persons whose diet is deficient in calcium, iron, phosphorous or zinc. In children the blood lead level (BLL) above 10 μg/dl is labelled as poisoning. Recent studies from Hyderabad also show abnormal cognitive functions in children at levels > 10 μg/dl. A study done in Hyderabad showed high blood lead levels in neonates and mothers in general population.
In general Pb is excreted very slowly from the body. Its biological half-life estimated at 10 years, facilitates accumulation in the body. Almost 90% lead is bound to red blood cells. Lead has high affinity for SH groups and hence it impairs the activity of zinc-dependent enzymes like δ-aminolevulinic acid dehydratase (ALAD) which is involved in haem synthesis. As low as 10 μg/dL BLL is known to inhibit the ALAD activity. Apart from haemoglobin, cytochrome synthesis, steroid metabolism, membrane integrity, synthesis of active metabolite of vitamin D in renal tubular cells (conversion of 1-hydroxyvitamin D to 1,25-hydroxyvitamin D) are also affected.
Absorption of Lead (Pb) from different sources is dependent on the amount of Pb presented to portals per unit time and the physical and chemical state in which Pb is presented. It is also influenced by factors such as age and physiological status. In adults, almost 20-30% and in children almost 50% lead is absorbed through the GI track. Depending on the particle size, lead can enter through lungs. While organic lead is well absorbed through the skin, inorganic lead is not. Since lead is chemically similar to calcium, body handles it like calcium. In the body lead is distributed throughoutbone, teeth, liver, lung, brain and spleen; bone being the major accumulator. Lead can cross blood brain barrier as well as placental barrier. Excretion occurs through urine and faeces. Dose and duration dependent genotoxic effects have been observed.
Nutritional iron deficiency enhances Pb toxicity, raising concern that pregnant women and young children in whom iron deficiency anaemia is high, may be more susceptible to Pb toxicity8. Pb absorption is increased considerably with fasting or in persons whose diet is deficient in calcium, iron, phosphorous or zinc. In children the blood lead level (BLL) above 10 μg/dl is labelled as poisoning. Recent studies from Hyderabad also show abnormal cognitive functions in children at levels > 10 μg/dl. A study done in Hyderabad showed high blood lead levels in neonates and mothers in general population.
In general Pb is excreted very slowly from the body. Its biological half-life estimated at 10 years, facilitates accumulation in the body. Almost 90% lead is bound to red blood cells. Lead has high affinity for SH groups and hence it impairs the activity of zinc-dependent enzymes like δ-aminolevulinic acid dehydratase (ALAD) which is involved in haem synthesis. As low as 10 μg/dL BLL is known to inhibit the ALAD activity. Apart from haemoglobin, cytochrome synthesis, steroid metabolism, membrane integrity, synthesis of active metabolite of vitamin D in renal tubular cells (conversion of 1-hydroxyvitamin D to 1,25-hydroxyvitamin D) are also affected.
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