Copper rates, and carcass dressing percentages. Chronic copper toxicity does not normally occur in humans because of transport systems that regulate absorption and excretion. Autosomal recessive mutations in copper transport proteins can disable these systems, leading to Wilson's disease with copper accumulation and cirrhosis of the liver in persons who have inherited two defective genes. Elevated copper levels have also been linked to worsening symptoms of Alzheimer's disease. In the US, the Occupational Safety and Health Administration (OSHA) has designated a permissible exposure limit (PEL) for copper dust and fumes in the workplace as a time-weighted average (TWA) of 1 mg/m.
Lead poisoning; low levels cause increased susceptibility. Lead can cause severe damage to the brain and kidneys and, ultimately, death. By mimicking calcium, lead can cross the blood–brain barrier. It degrades the myelin sheaths of neurons, reduces their numbers, interferes with neurotransmission routes, and decreases neuronal growth. In the human body, lead inhibits porphobilinogen synthase and ferrochelatase, preventing both porphobilinogen formation and the incorporation of iron into protoporphyrin IX, the final step in heme synthesis. This causes ineffective heme synthesis and microcytic anemia. Symptoms of lead poisoning include nephropathy, colic-like abdominal pains, and possibly weakness in the fingers, wrists, or ankles.