Lead serves no useful purpose in the body and can damage the hematopoietic tissues, liver, nervous system, kidneys, gastrointestinal tract, and reproductive system (Table 57–1). Lead is a major environmental hazard because it is present in the air and water throughout the world.
Table 57–1 Important Characteristics of the Toxicology of Arsenic, Iron, Lead, and Mercury. ||Download (.pdf)
Table 57–1 Important Characteristics of the Toxicology of Arsenic, Iron, Lead, and Mercury.
|Metal||Form Entering Body||Route of Absorption||Target Organs for Toxicity||Treatmenta|
Inorganic lead oxides and salts
Gastrointestinal, respiratory, skin (minor)
Skin (major), gastrointestinal
Hematopoietic system, CNS, kidneys
Dimercaprol, EDTA, succimer, unithiol
Inorganic arsenic salts
All mucous surfaces
Capillaries, gastrointestinal tract, hematopoietic system
Dimercaprol, unithiol, succimer, penicillamine
Elemental Inorganic salts
CNS, kidneys Kidneys, gastrointestinal tract
Succimer, unithiol, penicillamine, dimercaprol
|Iron||Ferrous sulfate||Gastrointestinal||Gastrointestinal, CNS, blood||Deferoxamine|
Because of the ban on lead over 20 years ago in gasoline, and because of bans on other industrial products that previously contained lead, acute inorganic lead poisoning is no longer common in the United States. It can occur rarely from industrial exposures (usually via the inhalation of dust) and in children who have ingested large quantities of chips or flakes from surfaces in older houses covered with lead-containing paint. The primary signs of this syndrome are acute abdominal colic and central nervous system (CNS) changes, including, particularly in children, acute encephalopathy. The mortality rate is high in those with lead encephalopathy, and prompt chelation therapy is mandatory.
Chronic inorganic lead poisoning (plumbism) is much more common than the acute form. Signs include peripheral neuropathy (wrist-drop is characteristic), anorexia, anemia, tremor, weight loss, and gastrointestinal symptoms. Treatment involves removal from the source of exposure, and chelation therapy, usually with oral succimer in outpatients and with parenteral agents (eg, EDTA with or without dimercaprol) in more severe cases. Chronic lead poisoning in children presents as growth retardation, neurocognitive deficits, and developmental delay. Succimer is generally used in such children. In workers exposed to lead, prophylaxis with oral chelating agents is contraindicated because some evidence suggests that lead absorption may be enhanced by the presence of chelators. In contrast, high dietary calcium is indicated because it impedes lead absorption.
Now rare, poisoning by organic lead was usually due to tetraethyl lead or tetramethyl lead contained in "antiknock" gasoline additives, which are no longer used. This form of lead is readily absorbed through the skin and lungs. The primary signs of intoxication include hallucinations, headache, irritability, convulsions, and coma. Treatment consists of decontamination and seizure control.
Arsenic is widely used in industrial processes and is also an environmental pollutant released during the burning of coal.
Acute arsenic poisoning results in severe gastrointestinal discomfort, vomiting, "rice-water" stools, and capillary damage with dehydration and shock. A sweet, garlicky odor may be detected in the breath and the stools. Treatment consists of supportive therapy to replace water and electrolytes, and chelation therapy with dimercaprol.
Chronic Arsenic Poisoning
Chronic arsenicintoxication causes skin changes, hair loss, bone marrow depression and anemia, and chronic nausea and gastrointestinal disturbances. Dimercaprol therapy appears to be of value. Arsenic is a known human carcinogen.
Arsine gas (AsH3), an occupational hazard, is formed during the refinement and processing of certain metals and is used in the semiconductor industry. Arsine causes a unique form of toxicity characterized by massive hemolysis. Pigment overload from erythrocyte breakdown can cause renal failure. Treatment is supportive.
The main source of inorganic mercury as a toxic hazard is through the use of mercury-containing materials in dental laboratories and in the manufacture of wood preservatives, insecticides, and batteries. Organic mercury compounds are used as seed dressings (treatments to prevent fungal and bacterial infection of seed and to improve the seed's dispersion and adhesiveness) and fungicides.
Acute mercury poisoning usually occurs through inhalation of inorganic elemental mercury. It causes chest pain, shortness of breath, nausea and vomiting, kidney damage, gastroenteritis, and CNS damage. In addition to intensive supportive care, prompt chelation with oral succimer or with intramuscular dimercaprol is essential. Acute ingestion of mercuric chloride causes a severe, life-threatening hemorrhagic gastroenteritis followed by renal failure.
Chronic Mercury Poisoning
Chronic mercury poisoning may occur with inorganic or organic mercury. Poisoning from inhalation of mercury vapor presents as a diffuse set of symptoms involving the gums and teeth, gastrointestinal disturbances, and neurologic and behavioral changes (erethism). Chronic mercury intoxication has been treated with succimer and unithiol, but their efficacy has not been established. Dimercaprol may redistribute mercury to the CNS and should not be used in chronic exposure to elemental mercury.
Organic Mercury Poisoning
Intoxication with organic mercury compounds was first recognized in connection with an epidemic of neurologic and psychiatric disease in the village of Minamata, Japan, which was first noticed in the 1950s. The outbreak was a result of consumption of fish containing a high content of methylmercury, which was produced by bacteria in seawater from mercury in the effluent of a nearby vinyl plastics-manufacturing plant. Similar epidemics have resulted from the consumption of grain that was intended for use as seed and treated with fungicidal organic mercury compounds. Treatment with chelators has been tried, but the benefits are uncertain.
Acute poisoning from the ingestion of ferrous sulfate tablets occurs frequently in small children, although the incidence of poisonings dropped dramatically in the United States after iron supplements were required to be packed in unit-dose packing. The initial symptoms of iron poisoning include vomiting, gastrointestinal bleeding, lethargy, and gray cyanosis. These can be followed by signs of severe gastrointestinal necrosis, pneumonitis, jaundice, seizures, and coma. Deferoxamine is the chelating agent of choice. Chronic excessive intake of iron can lead to hemosiderosis or hemochromatosis (see Chapter 33).