In this article we will discuss about the major effects of toxic metals on humans and other animals.
1. Effect of Arsenic:
Large doses of arsenic (70-180 mg) ingestion may be fatal. Symptoms of acute illness possibly leading to death consist of fever, hepatomegaly, melanosis, and cardiac arrhythmia. Other features include peripheral neuropathy, gastrointestinal, cardiovascular and hematopoietic effects. Sensory loss in the peripheral nervous system is the most common neurological effect.
Chronic exposure to inorganic arsenic compounds may lead to loss of appetite and weight, diarrhea and neurotoxicity of both the peripheral and central nervous system. Neurotoxicity usually begins with sensory changes, paresthesia, and muscle tenderness followed by weakness. Liver injury is also a characteristic of chronic exposure to arsenic.
Arsenic may induce skin, liver, blood, nasopharyngeal, kidney and bladder cancers in human only but not in any experimental animal. Presence of 0.6-0.8 ppm concentration of arsenic in drinking water in Latin (U.S.A.) caused endemic poisoning and the Black-foot disease (WHO,1972).
Chronic exposure reduces growth of fingerlings of freshwater fishes. Shukla and Pandey (1984, 86, 87) reported impairment in spermatogenesis, oogenesis, nucleic acids (DNA-RNA), and protein metabolism in nature tropical fresh water fishes. Fish liver dysfunctioning at 1-20 mg/1 cone has also been observed. Chronic effects in mammals produce skin damage, liver damage and other pathological effects.
2. Effect of Lead:
The major toxicological effects of lead is its interference with heme synthesis, which leads to haematological damage. Lead inhibits several of the key enzymes involved in the overall process of heme synthesis whereby the metabolic intermediates accumulate as shown in Fig. 13.2.
Since lead interferes with the synthesis of heme, anemia appears to be the first symptom of its chronic poisoning in animals in general and humans in particular.
Chronic exposure to lead causes weight loss, constipation, and loss of teeth.
Lead also damages liver, kidney and central and peripheral nervous system.
Kidney dysfunction occurs due to the impairment of energy metabolism, leading to the expression of Fanconi Syndrome (characterized by an increased loss of amino acids, glucose and phosphate in the urine due to the inability of the damaged tubular cells to resorb these substances). Lead is a renal carcinogen in rodents but whether it is carcinogenic to human kidney is unclear.
An increase in blood pressure is probably the most sensitive adverse health effect from lead exposure occurring in the adult human population.
Lead is also a carcinogen. The most common tumours found in people working in lead industry is of the respiratory and digestive systems, not the kidney.
Lead is now a well-known teratogen leading to embryo toxicity. Due to lead intoxication, the rate of abortions goes up and it may also lead to low birth-rate, brain damage and low reproductive ability. In higher concentration, it tends to accumulate in foetal bone and liver and leads to deformity and physiological malfunctioning. Adverse effects of lead intoxication enhances due to iron deficiency. Cases of lead poisoning have also been noticed in India after the consumption of acidic beverages stored in glazed pottery.
In fishes lead inhibits liver enzymes, causes muscle tremors, and reduces haemoglobin production. Chronic exposure to lead produces renal carcinoma in mammals.
3. Effect of Chromium:
Chromium (III) is considered an essential trace nutrient serving as a component of the “glucose tolerance factor”. No conclusive evidence exists on the toxic effects of chromium in its trivalent state. The adverse effects of chromium are attributed to the hexavalent forms which are highly toxic to humans. Hexavalent chromium is corrosive and causes chronic ulceration and perforation of the nasal septum.
It is because chromium (VI) is a powerful oxidant which can easily penetrate the cell membrane and irritate cells. Chromium (III) is neither irritating nor corrosive. Chromium (VI) is a teratogen and also carcinogenic (inducing bronchogenic cancer).
Studies of chronic exposure on animals to Cr (VI) have not revealed evidence of toxicity.
Fishes as well as mammals are far less susceptible to the toxic effects of chromium.
4. Effect of Cadmium:
Toxic Effects on Human:
The symptoms of acute poisoning in man are vomiting, abdominal cramps and headaches. After inhalation, shortness of breath, general weakness and respiratory insufficiency occurs. Chronic exposure to cadmium results in respiratory disorders, kidney damage, osteoporosis, i.e., decalcification of the skeleton, liver dysfunction, anaemia and hypertension. It has also been found to be highly toxic to the gonads of experimental animals.
Cadmium has recently been accepted as a pulmonary carcinogen in human and rat.
Since the kidney is the principal target organ for cadmium toxicity, the following disorders have been recorded in kidney of human:
ii. Glucosuria – Excretion of blood sugar in the urine.
iii. Hypercalciuria – Excretion of excess calcium in the urine.
iv. Proteinuria – Excretion of proteins in the urine.
Rice, as in India, is the staple food in most of the regions of Japan. Normally, people living in uncontaminated parts of the globe ingest about 25- 60 μg of cadmium daily. However, the reports reveal that the people living along the banks of juntsu river in northern Japan were ingesting 100- 1,000 μg of cadmium every day. It was because of the fact that the rice they consumed were grown with such irrigation water supplies (effluent from zinc smelter) that contained 0.35-3.5 ppm of cadmium.
It caused about one hundred deaths until the end of 1965. As a result of the analyses carried out by Jun Kobayashi at Okayama University, it became apparent that cadmium intake was the causative factor. The victims accumulated 500 mg of cadmium in their body over the lifetime. This disorder was termed ‘Itai-ltai’ (literally meaning “ouch-ouch”) characterized by renal malfunction (reduced ability to resorb water), drop in the phosphate level of blood serum, loss of minerals from the bone and osteomalacia, a ricket-like condition characterized by pathological bone fracture and intense pain.
Actually the onset of symptoms occurs only several years after the consumption of cadmium. Nogawa (1987) reported that serum 1, 25 (OH)2 Vit. D levels were lower in Itai-ltai diseased patients.
In fishes, Cd accumulates in muscle, liver, gills and bones where it produces toxicity. Cadmium chloride can produce acute but reversible effects on ovarian tissue in sexually immature rats. The ovarian stimulation induced by CdCl2 was manifested as follicular maturation and corpora lutea formation but did not seem to lead to the production of sex hormones. A single intraovarian injection of this salt (1 to 3 mg/kg) sterilized adult goats, all the germinal elements and corpora lutea were destroyed.
The stromal tissue with vasculatures was also damaged. Similar changes have also been observed in other species of animals. The change commenced with damage to the vascular structure indicating the primary role of vascular injury in producing acute degeneration of the tissue.
5. Effect of Copper:
Acute poisoning resulting from ingestion of excessive amounts of oral copper salts may produce death. The ingestion of 15-75 mg of copper causes gastrointestinal disturbances. Further increase in amount may cause hemolysis, hepatotoxic and nephrotoxic effects.
Inhalation of air born copper causes irritation of the respiratory tract and metal fume fever and ultimately lung cancer after chronic exposure.
Reduces growth, survival and rate of reproduction. It also causes necrosis of kidney cells and brain haemorrhage.
6. Effect of Zinc:
Zinc at concentration over 15 mg/m3 in air may produce metal fume fever. Large doses of zinc salts (220-440 mg of zinc as ZnSO4) cause gastrointestinal disorders including vomiting and diarrhea. There is no evidence of zinc being teratogenic or mutagenic. Zn shows no hematological, hepatic or renal toxicity.
In fish zinc causes decrease in O2 consumption. It also damages gills, decreases growth and fecundity.
7. Effect of Aluminium:
Generally, human beings are least affected by aluminium; however, inhalations with aerosol produce pneumonia. In general, Al binds with bone and causes osteomalacia. Al competes with or alters calcium metabolism in several organ systems including the brain. Calcium rises in brain tissue following Al exposure and disrupts neurotubular integrity and transport.
In fishes, Al causes gill hyperplasia and mortality.
8. Effect of Manganese:
Evidence of occupational Mn poisoning was reported for the first time as early as 1837 in France in a few workers engaged in the grinding of manganese ores.
A definite relationship was established only in 1919. Since then several cases of chronic manganese poisoning have been detected in miners, steel plant and foundry workers, welders, workers employed in dry cell battery manufacturing industries and in families consuming water with high manganese contents.
Industrial toxicity from inhalation exposure, generally to manganese dioxide, in mining or manufacturing, is of two types – The first, manganese pneumonitis, is the result of acute exposure. Men working in plants with high concentrations of manganese dust show an incidence of respiratory disease 30 times greater than normal. Pathological changes include epithelial necrosis followed by mononuclear proliferation.
The second and more serious type of disease resulting from chronic inhalation exposure to manganese dioxide, generally over a period of more than 2 years, involved the central nervous system.
Chronic manganese poisoning (manganism) produced a neuropsychiatric disorder characterized by irritability, difficulty in walking, speech disturbances, and compulsive behaviour that may include running, fighting and singing. If the condition persists a masklike face, retropulsion or propulsion, and a Parkinson’s Disease-like syndrome develops.
To sum up, the symptoms of neurological syndrome of manganese poisoning are usually insidious and progressive. An initial phase of psychomotor excitement is followed by asthenia, somnolence, imbalance while walking, slurred speech, difficulty in fine movements, impotence, etc.
Established cases show tremors, paresthesia, memory loss, difficulty in walking and swallowing. Bradykinesia, impaired postural stability, diminished associated movements, gait disorder described as “Cock-walk”, retropulsion and masked faces are also observed.
Victims of chronic manganese poisoning tend to recover slowly, even when removed from the excessive exposure. The oral absorption of Mn is increased by iron deficiency.
Mn is neuro- and pancreotoxic to fishes and mammals.