The following are the important toxic metals of global concern: 1. Arsenic 2. Lead 3. Mercury 4. Chromium 5. Cadmium 6. Copper 7. Zinc 8. Aluminium 9. Manganese.
Arsenic is particularly difficult to characterize as a single element because its chemistry is so complex and there are many different arsenic compounds. It may be trivalent or pentavalent and is widely distributed in nature. The most common inorganic trivalent arsenic compounds are arsenic trioxide, sodium arsenite, and arsenic trichloride. Pentavalent inorganic compounds are arsenic pentoxide, arsenic acid, and arsenates, such as lead arsenate and calcium arsenate.
Organic compounds may also be trivalent or pentavalent, such as arsanilic acid, or may even occur in methylated forms as a consequence of biomethylation by organisms in soil, fresh water, and sea water. Arsenic trioxide (As2O3) is known as white arsenic. It constitutes about 97% of all arsenic produced and used in end-product manufacturing. Arsenic has been known to mankind from ancient times.
Already in the 8th century its compounds were known to Arabian chemists, while in the 9th century Avicenna described arsenous anhydride in his works. T. Paracelsus (1493-1541) was the first to use arsenic compounds for medical purposes. Arsenic and its compounds in small doses are valuable drugs having a tonic effect on an organism. They improve the state of an organism and increase metabolism. A solution of potassium arsenite, KAsO2, called Fowler’s Solution, is used in medicine.
Mine wastes and land erosion.
Inorganic arsenic is released into the environment from a number of anthropogenic sources which include primary copper, zinc, and lead smelters, glass manufacturers that add arsenic to raw materials, and chemical manufacturers.
The arsenical compounds are used as:
(i) Pesticides- Lead arsenate; sodium arsenite; calcium arsenite etc.
(ii) Herbicides- NaAsO2.
(iii) Wood Preservatives- Monosodium arsenite; Dimethyl arsenic compounds like fluorochrome arsenate phenol (FCAP) and chromated copper arsenate (CCA).
(iv) Chemotherapic Agents- Methylated Arsenic acid (CH3AsO (OH)2 and cocydylic acid (CH3)2AsOOH.
(v) Lead and copper based alloys to increase hardness and heat resistance.
(vi) Warfare- Lewistios (CH3CH = CH As Cl2).
Researchers reported release of arsenic as its trioxide from HPC Tower of Urea manufacturing plants.
Sequential methylation of arsenic by certain soil microbes (fungi and bacteria) releasing dimethyl and trimethyl arsine has been reported.
Actually arsenic is a metalloid and not a metal. The toxicity of arsenic in trivalent state is greater than pentavalent state. It is because the arsenites bind strongly with the -SH-groups of proteins resulting in enzyme inhibition, whereas the arsenates neither bind to-SH-groups nor inhibit enzyme systems. However arsenates inhibit ATP synthesis by oxidative uncoupling of certain reaction. To sum up, As (III) is most potent, followed by As (v), monomethylarsenate, and dimethyl- arsenate.
In fact, ingested arsenite gets oxidized to arsenate and the latter is reduced to arsenite again. Both these inorganic forms are partly methylated to form monomethyl arsenic acid and dimethyl arsenic acid (also called cacodylic acid). The formation of methylated forms is regarded as a detoxication mechanism, as far as arsenic toxicity is concerned.
Excretion of absorbed arsenic is mainly via urine. The biological half-life of ingested inorganic arsenic is about 10 hours and 50 to 80% is excreted in about 3 days. The biological half-time to methylated arsenic is about 30 hours.
When low chronic doses of arsenic are ingested, it tends to accumulate in lipid-rich tissues. It also concentrates in nails, hair and skin. Arsenic in nails produces Mee’s lines (transverse white bands across finger nails). Human milk contains about 3 μg/liter of arsenic. Inhaled arsenic may retain in the lung tissue for relatively long periods of time.
Arsenic crosses placental membranes and is a known animal teratogen. It induces skin lesions and may lead to skin cancer. Inorganic arsenicals are known lung carcinogens in humans.
Trivalent arsenic exerts its toxic action by attacking -SH-groups of an enzyme, thereby inhibiting enzyme action:
The enzymes which generate cellular energy in the TCA cycle are adversely affected. The inhibitory action is based on bioactivation of pyruvate dehydrogenase by complexation with As (III), whereby the generation of ATP is presented.
As (III) compounds at high concentrations coagulate proteins, possibly by attacking the sulphur bonds, maintaining the secondary and tertiary structures of proteins.
Arsenic affects mitochondrial enzymes and impairs tissue respiration, which seems to be related to the cellular toxicity of arsenic.
Arsenic compounds are inducers of metallothionein in vivo. Potency depends on the chemical form of arsenic.
Lead is the most ancient industrial toxicant known to man. Earth contains about 0.00002% of lead by weight. It occurs in nature as its sulphide (galena), cerrusite (lead carbonate), and anglesite (lead sulphate). The average lead content of mined ores ranges from 3-8%. Lead smelting and refining are probably the most hazardous operation in regard to exposure to lead with recorded mean concentration of lead in air of 80-4,000 μg/m3.
Lead occurs in two valence states i.e., +2 and +4. Lead in inorganic formulations normally exists in the divalent (+2) state; but in the +4 form occurs in lead acetate and tetra alkyl lead (R4Pb) compounds.
Lead is extensively used in printing, manufacture of paints, water pipes, storage, battery manufacture, pottery and soldering operations, etc. Besides, it is used as an antiknock agent in gasoline. Lead in gasoline, accounting for 20% of lead used by mankind, is responsible for about 96-98% of the pollution problems caused by lead. Lead arsenate is used as pesticide.
Air-borne lead of small particle size is readily absorbed through the lungs. About 50% of inhaled particle lead (size < 0.9 μm) is absorbed; as much as 90% may be absorbed when the size is still smaller (< 0.1 μm). About 90% of lead particles in ambient air that are deposited in the lungs are small enough to be retained. Absorption of retained lead through alveoli is relatively efficient and complete.
Net absorption of lead in the alimentary tract is very low (5-15%) because of its low solubility. More than 90% of the lead in blood is in R.B.C. Lead in bone may contribute as much as 50% of blood lead. Mobilization of lead from maternal bone is of particular concern during pregnancy and lactation and may be mobilized in later years in persons with osteoporosis. The total lifetime accumulation of lead may be as much as 200 mg to over 500 mg for a worker with heavy occupational exposure.
Most of the lead intake by a typical city dweller is from diet (about 200-300 μg/day), air and water adding a further 10-15 /μg/day each. Of this total intake, 200 μg of lead is excreted while 25 μg is stored in the bones each day. Renal excretion of lead is usually with glomerular filtrate with some renal tubular resorption. Lead also crosses the placenta. Possibility of lead poisoning in Indian women who apply sindoor (red lead) to the scalp (hair parting) and forehead has also been reported.
Mercury is a well-known toxic metal which came to the limelight after the incidence of “Minamata Disease” in 1953-1960 in Japan. No other metal better illustrates the diversity of effects caused by various chemical species than does mercury. On the basis of chemical speciation, there are three forms of mercury- (i) elemental (ii) inorganic, and (iii) organic compounds, each of which has characteristic toxicokinetics and health effects as shown in Table 13.1.
In the environment, mercury occurs as metallic mercury and as HgS and HgCl2 in the earth’s crust. Anthropogenic sources consist of mining, smelting, paper pulp, paints, batteries, lamps, switches, caustic soda, medicine and instruments. Twenty five percent of the total production of mercury is consumed by the chlor-alkali plants, rest is used in electrical equipments, paints, in measurement and control like thermometers, sphygmomanometers, in dental practice and in agriculture.
Methyl and ethyl mercury have been extensively used in seed dressings. Mercury is released into the environment during its production and by human activities like combustion of fossil fuels, waste disposal and industrial activities. Annual production of mercury in the world is estimated to be about 9,000 tons. About 50% of which is estimated to be lost into the environment. As per WHO (1971) standards, the maximum permissible limits of mercury in drinking water should not be more than 0.001 ppm.
Inorganic mercury released into the environment is converted into more toxic methyl mercury compounds by the action of certain anaerobic bacteria present in the sediments and bottom muds of waterways. The major source of exposure to methyl mercury for people in general population is from the consumption of fish.
Metallic or elemental mercury volatizes to mercury vapour at ambient air temperatures, and most human exposure is by inhalation. Mercury vapour readily diffuses across the alveolar membrane and is fat soluble so that it has an affinity for R.B.C. and the central nervous system. Metallic mercury is very slowly absorbed by the alimentary tract (0.01%).
Inorganic mercury salts may be divalent (mercuric) or monovalent (mercurous). Kidneys contain the maximum concentrations of mercury following exposure to inorganic salts of mercury and mercury vapour, whereas organic mercury has greater affinity for the brain, especially the posterior cortex. All forms of mercury cross the placenta to the fetus in experimental animals.
Elemental or metallic mercury is oxidized to divalent mercury after absorption which is mediated by catalases. Also inhaled mercury vapour absorbed into R.B.C. is transformed into divalent mercury. Methyl mercury may undergo biotransformation to divalent mercury compounds in tissues by cleavage of the CHg bond. Formation of any organic form of mercury, however, in mammalian tissues has not yet been reported.
Within cells, mercury may bind to a variety of enzyme system producing non-specific cell injury or cell death.
Chromium is generally an abundant element at about 100 ppm levels in the earth’s crust and occurs in oxidation states ranging from Cr2+ to Cr6+ as shown in Table 13.2, but only trivalent and hexavalent forms are of biological significance.
Uses and Pollution Sources:
Chromium is extensively used in electroplating, polishing, paint-pigment industry. Chromium in ambient air originates from industrial sources, particularly ferrochrome production, ore refining, chemical and refractory processing, and combustion of fossil fuels. Cement-producing plants are another potential sources of atmospheric chromium. The potential sources of chromium in aquatic environment are effluents from tanneries and textile mills.
Tannery wastes contain 10-50 ppm of chromium. Its permissible limit in drinking water is 0.05 ppm.
Chromium (+3) is the most common form found in nature and in biological components. Now report is available that trivalent chromium is converted into hexavalent forms in biological systems. However, hexavalent chromium readily crosses cell membranes and is reduced intracellularly to trivalent chromium. Trivalent chromium compounds are considerably less toxic than the hexavalent chromium compounds.
The excretion of chromium increases with the duration of exposure.
Cadmium is a toxic heavy metal belonging to the same family as zinc and mercury from toxicology view point. It is relatively rare but toxic to all systems and functions of animals and humans at high levels of exposure.
The occurrence of free metallic cadmium in nature is rare but it exists in close association with other metallic ores. It occurs mainly with zinc (in the ratio of 1 Cd: 200 Zn in zinc sulphide ores) and is obtained as a byproduct from the refining of zinc, copper and lead.
Cadmium has been used in a number of industrial processes, as in electroplating, in the manufacture of pigments and paints, as a stabilizer in plastics and in welding electrodes. As copper- cadmium alloy, it is used in automobile radiators and cadmium may serve as an electrode component in alkaline accumulators.
It is of interest to note that an extremely wide range of cadmium concentration have been reported in foodstuffs from many parts of the world. In water, cadmium is found mainly in the bottom sediments and suspended particles. Pollution of drinking water with cadmium can occur as a result of leaching from solders containing the metal in fittings of water heaters, coolers and taps. Cadmium in the ambient air occurs mostly in the particulate form.
Smoking tobacco may be an important route of exposure for the general population. Both water-borne and air-borne cadmium can cause an increased concentration of cadmium in soil. The use of cadmium containing sewage sludge and superphosphate fertilizers lead to contamination of the soil.
Cadmium present in the soil is taken up by plants. It has been observed that more than 50 percent of the soil samples from Punjab and Haryana were sandy with low organic matter, low pH and were deficient in zinc; these conditions are favourable to promote cadmium uptake by the plants.
Fertilizers like superphosphate, rock phosphate, diammonium phosphate etc. used in Punjab contained cadmium. Sea water from Bhavnagar, Gogna and Mandapam used for preparation of salt contained cadmium more than the recommended permissible limits. Studies carried out on fly ash produced by casal burning power plants during electricity generation shows that the dust contains high contents of cadmium.
Respiratory absorption of cadmium is about 15 to 30 percent. Workplace exposure to cadmium is particularly hazardous where there are cadmium fumes or airborne cadmium. Most airborne cadmium is respirable. A major non-occupational source of respirable cadmium is cigarettes. One cigarette contains 1 to 2 μg cadmium, and 10 percent of the cadmium in a cigarette is inhaled (0.1 to 0.2μg). Smoking one or more packs of cigarettes a day may double the daily absorbed burden of cadmium.
Of various heavy metals present in the aquatic environment, cadmium pollution is especially a problem because it is not only highly toxic to the organisms but its toxicity is also cumulative.
Alimental absorption is less than respiratory absorption and is about 5 to 8 percent. Absorption is actually enhanced by dietary deficiencies of calcium and iron and by low protein diets. Low dietary calcium stimulates synthesis of calcium- binding protein, which enhances cadmium absorption. Women with low serum ferritin levels have been shown to have twice the normal absorption of cadmium. Zinc decreases cadmium absorption, probably by stimulating production of metallotheionein.
Cadmium is transported in blood by binding to erythrocytes i.e., red blood cells and large- molecular-weight proteins in plasma, especially albumin. A small fraction of blood cadmium may be transported by metallotheionein. Blood cadmium levels in adults without excessive exposure is usually less than 1 μg/dL. Newborns have a low body content of cadmium, usually less than 1 mg total body burden.
The placenta synthesizes metallotheionein and may serve as a barrier to maternal cadmium, but the fetus may be exposed with increased maternal exposure. Human breast and cow’s milk are low in cadmium, with less than 1 μg/kg of milk. About 50 to 75 percent of the body burden of cadmium is in the liver and kidneys; its half-life in the body is not exactly known, but it is many years and may be as long as 30 years.
With continued retention, there is progressive accumulation in the soft tissues, particularly in the kidneys, through ages 50 to 60, when the cadmium burden in soft tissues begins to decline slowly. Because of the potential for accumulation in the kidneys, there is considerable concern about the levels of dietary cadmium intake for the general population. However, presence of higher concentrations of zinc in water may reduce cadmium toxicity.
Once absorbed into the body, cadmium has a strong affinity for the imidazole moiety of histidine, phosphates, sulfhydryl groups and inhibits a number of enzymes. About a third of the cadmium absorbed is stored in the kidney, which constitutes the principal target organ. Also lung is the major target organ effected by air-borne Cd. The symptoms are the development of severe tracheobronchitis, pneumonitis, emphysema and pulmonary edema. Sampson et al (1984) reported development of pulmonary fibrosis. Cadmium is proved immunosuppressive as indicated by IgG mediated rosette formation.
Copper (Cu) is an essential element and is widely distributed in nature. Substantial copper deposits in India are known to occur in Rajasthan. It occurs primarily as its oxide or sulphide ores. Copper deficiency is characterized by hypochromic microcytic anemia resulting from defective hemoglobin synthesis. Oxidative enzymes viz., peroxidase, catalase, cytochrome oxidase and others also require copper.
Next to iron and aluminium, copper is the third most important metal used in the industries. It is second to silver in its thermal and electrical conductivities, hence it finds use as a conductor in many alloys. It is also used in paints and ceramics. Copper sulphate is used medicinally as an emetic and also as an anthelmintic. Copper sulphate mixed with lime has been used as a fungicide.
The environmental contamination with copper primarily results from its discharge from the industrial plants producing non-ferrous metals. Additional sources comprise wood combustion and steel production. Copper mining and metallurgical operations contribute to contaminations of aquatic environment.
Some of the copper salts are used as algicides and fungicides. Apart from these, copper is also used as antifouling agents in paints. Most of the paints contain 100-200 g copper oxide/liter. Fertilizer production and disposal of industrial/municipal sewage wastes represent minor sources of copper in the environment.
Alimental absorption of copper is generally regulated by body stores. It is transported in serum bound initially to albumin and later more firmly bound to ceruloplasmin, where it is exchanged in the cupric form. The normal serum level of copper is 120 to 145 μg per liter. The bile is the normal excretory pathway and plays an initial role in copper homeostasis. Most copper is stored in liver and bone marrow where it may be bound to metallothionein.
The amount of copper in milk is not enough to maintain adequate copper levels in the liver, lungs, and spleen of the newborn. Tissue levels gradually decline up to about ten years of age, remaining relatively constant thereafter. Brain levels, on the other hand, tend to almost double from infancy to adulthood.
The ratio of newborn to adult liver copper levels shows considerable species difference- human, 15: 4; rat, 6: 4, and rabbit, 1: 6. Since urinary copper levels may be increased by soft water, under these conditions concentrations of approximately 60 μg per liter are not uncommon.
Copper is an essential component for various enzymes, including tyrosinase, involved in the formation of melanin pigments, cytochrome oxidase, superoxide dismutase, amine oxidase (involved in the formation of two proteins — elastin and collagens) and uricase. It is essential for the utilization of iron. Iron deficiency anemia in infancy is sometimes accompanied by copper deficiency. Molybdenum also influences tissue levels of copper.
The recommended daily intake of copper ranges from 2-3 mg/day. The impairment of the ability to absorb copper resulting in its deficiency is called Menke’s Disease whereas Wilson’s disease is its opposite (i.e., excessive accumulation of copper).
Zinc is a nutritionally essential trace metal to all organisms, as it is necessary for the normal functioning of various enzymes. More than 200 metalloenzymes require zinc as a cofactor.
Zinc is ubiquitous in the environment so that it is present in most foodstuffs, water and air. The important ores of zinc are- Willemite (Zn2SiO4), Zincite (ZnO), Zinc Blends (ZnS), Smithsmite (ZnCO3), etc. Zinc forms about 40 mg/kg of the earth’s crust. Atmospheric zinc levels are higher in industrial areas.
Zinc is used in dry batteries, construction materials, pigments and printing processes. It is also used for protective coatings on iron, steel, brass and alloys.
Smelting of ores contributes appreciably to the atmospheric levels of zinc. Municipal refuse and automobiles serve as additional pollutional sources. Agricultural use of ZnSO4 — containing pesticides and fungicides, for example — Manozeb (16% Mn and 2% Zn), Zineb and Ziram (1-18% Zn) may be yet another source of Zinc in the environment.
Approximately 20-30% of ingested zinc is absorbed. Its absorption is generally influenced by prostaglandins E2 and F2 and is chelated by tryptophan derivatives like picolinic acid. Zinc concentration in tissues varies widely. The liver receives up to about 40% zinc. It is bound there to metallotheionin. The greatest concentration of zinc in the body is in the prostate, probably related to the rich content of zinc-containing enzyme and phosphatase.
It is interesting to note that Zinc is necessary for the normal functioning of the cell, viz., protein synthesis, carbohydrate metabolism, cell division and growth. Recommended daily dietary allowances of zinc are at 15 mg for adults and 10 mg for children over a year old. The average dietary intake of zinc in India is about 12-15 mg, mostly from food.
Aluminium (Al) is one of the most ubiquitous elements in the environment. It is the third most abundant element in the earth’s crust (about 8-15%). In industrial societies it is the second most important metal. Bauxite, the principal ore source of aluminium, is widely distributed in India. The most important deposits are found in Bihar, M.P. and Maharashtra.
Aluminium is a non-ferrous metal, chiefly extracted from bauxite. It is extensively used for canning, food packaging, and as foil for covering and preserving foodstuff. Beverage cans and cooking utensils constructed of Al are extensively used around the world.
Contamination of the total environment with Al may result from the indiscriminate disposal of Al-containing products and wastes. Workers in the mining and manufacturing industries may be exposed to aluminium particles. Human exposure to Al comes from foods and drinking water as well as pharmaceuticals.
Average daily intake of Al by human has been reported to be 18-20 mg/day through foods and drinking water. In plasma 80-90% of Al binds to transferrin, an iron-transport protein for which there are receptors in many body tissues.
Aluminium at higher levels of exposure interferes with phosphate metabolism. It reduces the bioavailability of ATP and casein, and inhibits certain active enzymes by complexing them.
Bone and lung have the highest concentration of aluminium. Actually bone may be a “sink” for aluminium. It does not normally accumulate in blood to any great extent.
Aluminium compounds may affect absorption of other elements in the alimentary tract and alter its motility by inhibition of acetylcholine-induced contractions. Aluminium has been found to inhibit fluoride absorption and may decrease the absorption of calcium and iron compounds. Al may cross the placental barrier. Al in its dissolved form in water is much more toxic than suspended form.
Manganese (Mn) is an essential trace element and is a cofactor for a number of enzymatic reaction, particularly those involved in phosphorylation, fatty acid and cholesterol synthesis. It is toxic at higher concentrations. The most important commercial source of manganese is Pyrolusite (MnO2) containing 60-63% manganese. India ranks third in the production of manganese. About 75% of Mn is produced in Orissa, Karnataka, M.P. and Maharashtra.
Besides export, indigenous demand for this metal is constantly increasing with the growth of the steel industry. Manganese is also used for the manufacture of ferromanganese alloys and in non- ferrous industries. MnO2 is utilized in dry cell batteries as a polarizer; metallic manganese is coated in the electrodes in welding rods and fluxes for iron and steel.
Manganese is also used in the production of zinc by electrolysis, manufacturing pigments, paints, and ceramics, in photographic material, as a wood- preservative and in fertilizers. Organic manganese compounds are used as additives in gasoline, fuel oil and diesel.
Burning of fossil fuels (coal, oil) is the principal source of Mn in the environment. Industrial processes of battery, glass and steel manufacture provide additional input of Mn into the environment. The use of Mn in some fertilizers contributes further to air and water pollution.
Manganese can exist in seven possible oxidation states – O, +1, +2, +3, +4, +6 and +7. Of these, only two valence states, +2 and +4, are encountered commonly from toxicological view-point.
Mn is present in all living organisms. Vegetables, the germinal portions of grains, fruits, nuts, tea, and some spices are rich in manganese. A daily allowance of 2.5-9.0 mg of Mn is recommended for humans. But when exposed to higher levels of Mn, approximately 1-4% of it is absorbed, retained, and accumulated — chiefly in kidney, liver, and bones.
Gastrointestinal absorption is less than 3-4%. Mn concentrates in mitochondria so that tissues rich in these organelles have the maximum concentration of Mn, including the pancreas, liver, kidneys and intestines. Biological half-life of the manganese in the body is 37 days. It readily crosses the blood- brain barrier and its half-time in the brain is longer than in the whole body. The principal route of its excretion is with feces.