Lead, Blood

Lead is one of the oldest established poisons. The direct neurotoxic actions of lead include apoptosis leading to neural death, excitotoxicity (neuronal damage and death due to overactivation of receptors), influences on neurotransmitter (acetylcholine, dopamine and amino acid neurotransmitters) storage and release processes, mitochondria, second messengers, cerebrovascular, endothelial cells, and both astroglia and oligodendroglia. Lead’s ability to substitute for calcium, and perhaps zinc, is a factor common to many of its toxic effects. In addition, lead can produce anaemia, both by interfering with haem synthesis and by decreasing iron absorption from the gut.

Effects of chronic long-term exposure to lead include gastrointestinal disturbances, anaemia, insomnia, weight loss, motor weakness, muscle paralysis, and nephropathy. In children, moderately increased lead concentrations have been associated with increased school drop-out rates and increased reading disability. Low levels of lead poisoning can cause anaemia. At high lead concentrations can cause acute encephalopathy, blood brain barrier damage, oedema and possibly brain ischemia. Another indirect effect of lead on the brain is via disruption of thyroid hormone transport into the brain.

2 ml EDTA Whole Blood Room Temperature

< 70 μg/L