Lead exposure in a battery worker: enzyme inhibition and a microcytic anaemia

Lead inhibits two key enzymes of haem biosynthesis. Delta-aminolevulinic acid dehydratase (also called porphobilinogen synthase) converts two molecules of delta-aminolevulinic acid to porphobilinogen. When it is inhibited, delta-aminolevulinic acid accumulates in blood and urine. Ferrochelatase inserts ferrous iron into protoporphyrin IX to form haem; its inhibition causes protoporphyrin IX to accumulate, and because zinc is inserted instead, zinc protoporphyrin rises. The result is a functional iron block: iron is present in the body but cannot be used for haem synthesis, so haemoglobin production falls and a microcytic anaemia develops. Lead also inhibits pyrimidine 5′-nucleotidase in red cells, causing accumulation of ribosomal RNA, which appears as basophilic stippling. Delta-aminolevulinic acid is neurotoxic and contributes to abdominal colic, peripheral neuropathy and, at higher levels, encephalopathy. The wrist drop and reduced radial sensation fit a lead neuropathy, which is typically motor and affects extensor muscles. The raised zinc protoporphyrin is a useful marker of chronic exposure because it remains elevated after blood lead has fallen.

The anaemia is microcytic because haem synthesis is blocked at ferrochelatase, so erythroid precursors cannot assemble sufficient haemoglobin even though iron stores are adequate. Cell division continues for a time, producing smaller cells with reduced haemoglobin content, and the MCV falls. Normal ferritin makes true iron deficiency unlikely and points to a functional iron block rather than absent iron. Normal B12 and folate exclude a megaloblastic cause, which would usually produce a raised MCV and hypersegmented neutrophils. The reticulocyte count of 3.2% is inappropriately low for the degree of anaemia, suggesting impaired effective erythropoiesis rather than brisk compensation. Basophilic stippling is not specific for lead but is consistent with it, especially with the exposure history. The distinction matters because giving iron would not correct this anaemia and could cause iron overload, while the correct action is to remove the source and consider chelation. A bone marrow examination, if performed, might show ring sideroblasts.

The first step is to remove the patient from further exposure and notify occupational health and public health authorities, because others in the workshop may be affected. Symptomatic adults with blood lead around 70 µg/dL or above, especially with neuropathy or abdominal colic, generally warrant chelation. Options include oral dimercaptosuccinic acid (succimer) for moderate poisoning and intravenous calcium disodium edetate for more severe cases; dimercaprol is reserved for severe encephalopathy. Chelators bind lead and increase urinary excretion, but they do not repair established neurological damage and can cause renal or hepatic toxicity, so renal function, electrolytes and blood counts need monitoring. Exposure control is essential because chelation without source removal leads to rebound as lead redistributes from bone. Supportive care includes treating hypertension, correcting constipation and avoiding further contact. The wrist drop may improve slowly over months. Prevention through workplace ventilation, protective equipment and biological monitoring is more effective than repeated chelation.