Table 2.

The physical, chemical, and clinical properties of heavy metals included in the review.

Physical/chemical/clinical properties	Heavy metals
	Arsenic (As)	Lead (Pb)	Cadmium (Cd)	Mercury (Hg)
Absorption	GI inorganic: trivalent and pentavalent salts >90%; organic: also bound as tri- and pentavalent >90%; inhalation: uptake is dependent upon particle size	Skin: alkyl lead compounds, because of lipid solubility (methyl and tetraethyl lead); inhalation: up to 90% depending upon particle size; GI: adults 5 to 10%, children 40%	Inhalation 10 to 40%; GI 1.5 to 5%	GI: inorganic salts may be absorbed and may be converted to organic mercury in the gut by bacteria; inhalation: elemental Hg completely absorbed
Distribution	Accumulates in lung, heart, kidney, liver, muscle, and neural tissue; concentrates in skin, nails, and hair	Initially carried in red cells and distributed to soft tissues (kidney and liver); bone, teeth, and hair mostly as a phosphate salt	Initially bound to albumin and blood cells, subsequently to metallothionene in liver and kidney	Elemental Hg (vapor) crosses membranes well and rapidly moves from lung to CNS. Organic salts (lipid soluble) are evenly distributed, intestinal (intracellular)-fecal elimination. Inorganic salts concentrate in blood, plasma, and kidney (renal elimination)
Half-life	7 to 10 h	Blood: 30–60 days; bone: 20–30 years	10 to 20 years	60 to 70 days
Sources of exposure	GI: well water, food. Environmental: by-product of smelting ore, as Ga in semiconductors, herbicides, and pesticides; inhalation: fumes and dust from smelting	GI: paint, pottery, moonshine; inhalation: metal fumes skin: tetraethyl lead in gasoline	GI: pigments, polishes, antique toys; environmental: Electroplating, galvanization, plastics, batteries; inhalation: industrial, metal fumes, tobacco	Environmental: electronics and plastic industry; seed fungicide treatment; dentistry
Mechanism of toxicity	Membranes: protein damage of capillary endothelium increased vascular permeability leading to vasodilation and vascular collapse; inhibition of sulfhydryl group containing enzymes; inhibition of anaerobic and oxidative phosphorylation (substitutes for inorganic phosphate in synthesis of high-energy phosphates)	Inhibition of heme biosynthesis; heme is the essential structural component of hemoglobin, myoglobin, and cytochromes. Binds to sulfhydryl groups (-SH groups) of proteins	Inhalation: lung, local irritation, and inhibition of alpha1-antitrypsin associated with emphysema; oral: kidney: proximal tubular injury, (proteinuria) associated with beta2-acroglobulin	Dissociation of salts precipitates proteins and destroys mucosal membranes; necrosis of proximal tubular epithelium; inhibition of sulfhydryl (-SH) group containing enzymes
Diagnosis	History of exposure; blood and urinary levels (acute); hair or fingernail (chronic)	History of exposure, whole blood level (children >25 ug/dL and adults >50 ug/dL), protoporphyrin levels in RBCs >40 ug/dL, urinary lead >80 μg/dL	History of exposure, whole blood Cd level >80 μg/dL	History of exposure; blood mercury
Symptoms	Acute-damage to mucosa, sloughing, hypovolemic shock, fever, GI discomfort/pain, anorexia; chronic weakness, GI, hepatomegaly (jaundice > cirrhosis), melanosis, arrhythmias, peripheral neuropathy, peripheral vascular disease (blackfoot disease); carcinogenicity: epidemiologic evidence; liver angiosarcoma and skin and lung cancer	Acute: nausea, vomiting, thirst, diarrhea/constipation, abdominal pain, hemoglobinuria, and oliguria leading to hypovolemic shock Chronic: GI: lead colic (nausea, vomiting, abdominal pain) NMJ: lead palsy (fatigue, wrist drop) CNS: lead encephalopathy (headache, vertigo, irritation, insomnia, CNS edema)	Acute: oral: vomiting, diarrhea, abdominal cramps, inhalation: chest pains, nausea, dizziness, diarrhea, pulmonary edema, Chronic: oral: nephrotoxicity, inhalation: emphysema-like syndrome and nephrotoxicity	Acute: (a) inorganic salts degradation of mucosa-GI pain, vomiting, diuresis, anemia, hypovolemic shock, renal toxicity; (b) organic CNS involvement: vision, depression, irritability, blushing, intention tremors, insomnia, fatigue, diuresis. Chronic: CNS symptoms similar to acute organic poisoning with gingivitis, tachycardia, goiter, increased urinary Hg.
Treatments	Removal from exposure Acute: supportive therapy: fluid, electrolyte replacement, blood pressure support (dopamine); chronic: penicillamine w/o dialysis arsine gas (AsH3) acts as a hemolytic agent with secondary to renal failure. Supportive therapy: transfusion; chelators have not been shown to be beneficial	Removal from exposure, treatment with chelators like CaNa2EDTA, BAL, dimercaprol, D-penicillamine	Removal from exposure, chelation therapy with CaNa2EDTA, BAL but BAL-Cd complex is extremely toxic, so it is not used	Removal from exposure; Hg and Hg salts >4 μg/dL: 2,3-dimercaptopropanol (BAL), β, β-dimethyl cysteine (penicillamine), most effective is N-acetyl-β, β-dimethyl cysteine (N-acetyl-penicillamine); methyl Hg-supportive treatment (nonabsorbable thiol resins can be given orally to reduce methyl Hg level in gut)
Minimal permissible dose for humans	10–50  μ gkg −1   (EPA reference)	5  μ gkg −1 day −1   (EPA reference)	0.5–1  μ gkg −1 day −1  (EPA reference)	0.1–2  μ gkg −1 day −1    (EPA reference)