Friday, 11 February 2011 04:27


Gunnar Nordberg

Magnesium (Mg) is the lightest structural metal known. It is 40% lighter than aluminium. Metallic magnesium can be rolled and drawn when heated between 300 and 475 ºC, but is brittle below this temperature and is apt to burn if heated much above it. It is soluble in, and forms compounds with, a number of acids, but is not affected by hydrofluoric or chromic acids. Unlike aluminium, it is resistant to alkali corrosion.

Occurrence and Uses

Magnesium does not exist in a pure state in nature, but is generally found in one of the following forms: dolomite (CaCO3·MgCO3), magnesite (MgCO3), brucite (Mg(OH)2), periclase (MgO), carnallite (KClMgCl2·6H2O) or kieserite (MgSO4·H2O). In addition, it is found as a silicate in asbestos and talc. Magnesium is so widely distributed over the earth that facilities for processing and transporting the ore are often the determining factors in selecting a site for mining.

Magnesium is used, mainly in alloy form, for components of aircraft, ships, automobiles, machinery and hand tools for which both lightness and strength are required. It is used in the manufacture of precision instruments and optical mirrors, and in the recovery of titanium. Magnesium is also extensively used in military equipment. Because it burns with such intense light, magnesium is widely used in pyrotechnics, signal flares, incendiary and tracer bullets, and in flash bulbs.

Magnesium oxide has a high melting point (2,500 ºC) and is often incorporated into the linings of refractories. It is also a component of animal feeds, fertilizers, insulation, wallboard, petroleum additives and electrical heating rods. Magnesium oxide is useful in the pulp and paper industry. In addition, it serves as an accelerator in the rubber industry and as a reflector in optical instruments.

Other important compounds include magnesium chloride, magnesium hydroxide, magnesium nitrate and magnesium sulphate. Magnesium chloride is a component of fire extinguishers and ceramics. It is also an agent in fireproofing wood and textile and paper manufacture. Magnesium chloride is a chemical intermediate for magnesium oxychloride, which is used for cement. A mixture of magnesium oxide and magnesium chloride forms a paste which is useful for floors. Magnesium hydroxide is useful for the neutralization of acids in the chemical industry. It is also used in uranium processing and in sugar refining. Magnesium hydroxide serves as a residual fuel-oil additive and an ingredient in toothpaste and antacid stomach powder. Magnesium nitrate is used in pyrotechnics and as a catalyst in the manufacture of petrochemicals. Magnesium sulphate has numerous functions in the textile industry, including weighting cotton and silk, fireproofing fabrics, and dyeing and printing calicos. It also finds use in fertilizers, explosives, matches, mineral water, ceramics and cosmetic lotions, and in the manufacture of mother-of-pearl and frosted papers. Magnesium sulphate increases the bleaching action of chlorinated lime and acts as a water-correcting agent in the brewing industry and a cathartic and analgesic in medicine.

Alloys. When magnesium is alloyed with other metals, such as manganese, aluminium and zinc, it improves their toughness and resistance to strain. In combination with lithium, cerium, thorium and zirconium, alloys are produced which have an enhanced strength-to-weight ratio, along with considerable heat-resisting properties. This renders them invaluable in the aircraft and aerospace industries for the construction of jet engines, rocket launchers and space vehicles. A large number of alloys, all containing over 85% magnesium, are known under the general name of Dow metal.


Biological roles. As an essential ingredient of chlorophyll, the magnesium requirements of the human body are largely supplied by the consumption of green vegetables. The average human body contains about 25 g of magnesium. It is the fourth most abundant cation in the body, after calcium, sodium and potassium. The oxidation of foods releases energy, which is stored in the high-energy phosphate bonds. It is believed that this process of oxidative phosphorylation is carried out in the mitochondria of the cells and that magnesium is necessary for this reaction.

Experimentally produced magnesium deficiency in rats leads to a dilation of the peripheral blood vessels and later to hyperexcitability and convulsions. Tetany similar to that associated with hypocalcaemia occurred in calves fed only milk. Older animals with magnesium deficiency developed “grass staggers”, a condition which appears to be associated with malabsorption rather than with a lack of magnesium in the fodder.

Cases of magnesium tetany resembling those caused by calcium deficiency have been described in humans. In the reported cases, however, a “conditioning factor”, such as an excessive vomiting or fluid loss, has been present, in addition to inadequate dietary intake. Since this tetany clinically resembles that caused by calcium deficiency, a diagnosis can be made only by determining the blood levels of calcium and magnesium. Normal blood levels range from 1.8 to 3 mg per 100 cm3, and it has been found that persons tend to become comatose when the blood concentration approaches 17 mg per cent. “Aeroform tumours” due to the evolution of hydrogen have been produced in animals by introducing finely divided magnesium into the tissues.

Toxicity. Magnesium and alloys containing 85% of the metal may be considered together in their toxicological properties. In industry, their toxicity is regarded as low. The most frequently used compounds, magnesite and dolomite, may irritate the respiratory tract. However, the fumes of magnesium oxide, as those of certain other metals, can cause metal fume fever. Some investigators have reported a higher incidence of digestive disorders in magnesium plant workers and suggest that a relationship may exist between magnesium absorption and gastroduodenal ulcers. In foundry-casting magnesium or high-magnesium alloys, fluoride fluxes and sulphur-containing inhibitors are used in order to separate the molten metal from the air with a layer of sulphur dioxide. This prevents burning during the casting operations, but the fumes of fluorides or of sulphur dioxide could present a greater hazard.

The greatest danger in handling magnesium is that of fire. Small fragments of the metal, such as would result from grinding, polishing or machining, can readily be ignited by a chance spark or flame, and as they burn at a temperature of 1,250ºC, these fragments can cause deep destructive lesions of the skin. Accidents of this type have occurred when a tool was sharpened on a wheel which was previously used to grind magnesium alloy castings. In addition, magnesium reacts with water and acids, forming combustible hydrogen gas.

Slivers of magnesium penetrating the skin or entering deep wounds could cause “aeroform tumours” of the type already mentioned. This would be rather exceptional; however, wounds contaminated with magnesium are very slow to heal. Fine dust from the buffing of magnesium could be irritating to the eyes and respiratory passages, but it is not specifically toxic.

Safety and Health Measures

As with any potentially hazardous industrial process, constant care is needed in handling and working magnesium. Those engaged in casting the metal should wear aprons and hand protection made of leather or some other suitable material to protect them against the “spatter” of small particles. Transparent face shields should also be worn as face protection, especially for the eyes. Where workers are exposed to magnesium dust, contact lenses should not be worn and eyewash facilities should be immediately available. Workers machining or buffing the metal should wear overalls to which small fragments of the metal will not adhere. Sufficient local exhaust ventilation is also essential in areas where magnesium oxide fumes may develop, in addition to good general ventilation. Cutting tools should be sharp, as blunt ones may heat the metal to the point of ignition.

Buildings in which magnesium is cast or machined should be constructed, if possible, of non-flammable materials and without ledges or protuberances on which magnesium dust might accumulate. The accumulation of shavings and “swarf” should be prevented, preferably by wet sweeping. Until final disposal, the scrapings should be collected in small containers and placed apart at safe intervals. The safest method for disposal of magnesium waste is probably wetting and burying.

Since the accidental ignition of magnesium presents a serious fire hazard, fire training and adequate firefighting facilities are essential. Workers should be trained never to use water in fighting such a blaze, because this merely scatters the burning fragments, and may spread the fire. Among the materials which have been suggested for the control of such fires are carbon and sand. Commercially prepared firefighting dusts are also available, one of which consists of powdered polyethylene and sodium borate.



Friday, 11 February 2011 04:24


Gunnar Nordberg

Adapted from ATSDR 1995.

Occurrence and Uses

Lead ores are found in many parts of the world. The richest ore is galena (lead sulphide) and this is the main commercial source of lead. Other lead ores include cerussite (carbonate), anglesite (sulphate), corcoite (chromate), wulfenite (molybdate), pyromorphite (phosphate), mutlockite (chloride) and vanadinite (vanadate). In many cases the lead ores may also contain other toxic metals.

Lead minerals are separated from gangue and other materials in the ore by dry crushing, wet grinding (to produce a slurry), gravity classification and flotation. The liberated lead minerals are smelted by a three-stage process of charge preparation (blending, conditioning, etc.), blast sintering and blast furnace reduction. The blast-furnace bullion is then refined by the removal of copper, tin, arsenic, antimony, zinc, silver and bismuth.

Metallic lead is used in the form of sheeting or pipes where pliability and resistance to corrosion are required, such as in chemical plants and the building industry; it is used also for cable sheathing, as an ingredient in solder and as a filler in the automobile industry. It is a valuable shielding material for ionizing radiations. It is used for metallizing to provide protective coatings, in the manufacture of storage batteries and as a heat treatment bath in wire drawing. Lead is present in a variety of alloys and its compounds are prepared and used in large quantities in many industries.

About 40% of lead is used as a metal, 25% in alloys and 35% in chemical compounds. Lead oxides are used in the plates of electric batteries and accumulators (PbO and Pb3O4), as compounding agents in rubber manufacture (PbO), as paint ingredients (Pb3O4) and as constituents of glazes, enamels and glass.

Lead salts form the basis of many paints and pigments; lead carbonate and lead sulphate are used as white pigments and the lead chromates provide chrome yellow, chrome orange, chrome red and chrome green. Lead arsenate is an insecticide, lead sulphate is used in rubber compounding, lead acetate has important uses in the chemical industry, lead naphthenate is an extensively used dryer and tetraethyllead is an antiknock additive for gasoline, where still permitted by law.

Lead alloys. Other metals such as antimony, arsenic, tin and bismuth may be added to lead to improve its mechanical or chemical properties, and lead itself may be added to alloys such as brass, bronze and steel to obtain certain desirable characteristics.

Inorganic lead compounds. Space is not available to describe the very large number of organic and inorganic lead compounds encountered in industry. However, the common inorganic compounds include lead monoxide (PbO), lead dioxide (PbO2), lead tetroxide (Pb3O4), lead sesquioxide (Pb2O3), lead carbonate, lead sulphate, lead chromates, lead arsenate, lead chloride, lead silicate and lead azide.

The maximum concentration of the organic (alkyl) lead compounds in gasolines is subject to legal prescriptions in many countries, and to limitation by the manufacturers with governmental concurrence in others. Many jurisdictions have simply banned its use.


The prime hazard of lead is its toxicity. Clinical lead poisoning has always been one of the most important occupational diseases. Medico-technical prevention has resulted in a considerable decrease in reported cases and also in less serious clinical manifestations. However, it is now evident that adverse effects occur at exposure levels hitherto regarded as acceptable.

Industrial consumption of lead is increasing and traditional consumers are being supplemented by new users such as the plastics industry. Hazardous exposure to lead, therefore, occurs in many occupations.

In lead mining, a considerable proportion of lead absorption occurs through the alimentary tract and consequently the extent of the hazard in this industry depends, to some extent, on the solubility of ores being worked. The lead sulphide (PbS) in galena is insoluble and absorption from the lung is limited; however, in the stomach, some lead sulphide may be converted to slightly soluble lead chloride which may then be absorbed in moderate quantities.

In lead smelting, the main hazards are the lead dust produced during crushing and dry grinding operations, and lead fumes and lead oxide encountered in sintering, blast-furnace reduction and refining.

Lead sheet and pipe are used principally for the constructon of equipment for storing and handling sulphuric acid. The use of lead for water and town gas pipes is limited nowadays. The hazards of working with lead increase with temperature. If lead is worked at temperatures below 500 °C, as in soldering, the risk of fume exposure is far less than in lead welding, where higher flame temperatures are used and the danger is higher. The spray coating of metals with molten lead is dangerous since it gives rise to dust and fumes at high temperatures.

The demolition of steel structures such as bridges and ships that have been painted with lead-based paints frequently gives rise to cases of lead poisoning. When metallic lead is heated to 550 °C, lead vapour will be evolved and will become oxidized. This is a condition that is liable to be present in metal refining, the melting of bronze and brass, the spraying of metallic lead, lead burning, chemical plant plumbing, ship breaking and the burning, cutting and welding of steel structures coated with paints containing lead tetroxide.

Routes of entry

The main route of entry in industry is the respiratory tract. A certain amount may be absorbed in the air passages, but the main portion is taken up by the pulmonary bloodstream. The degree of absorption depends on the proportion of the dust accounted for by particles less than 5 microns in size and the exposed worker’s respiratory minute volume. Increased workload therefore results in higher lead absorption. Although the respiratory tract is the main route of entry, poor work hygiene, smoking during work (pollution of tobacco, polluted fingers while smoking) and poor personal hygiene may considerably increase total exposure mainly by the oral route. This is one of the reasons why the correlation between the concentration of lead in workroom air and lead in blood levels often is very poor, certainly on an individual basis.

Another important factor is the level of energy expenditure: the product of concentration in air and of respiratory minute volume determines lead uptake. The effect of working overtime is to increase exposure time and reduce recovery time. Total exposure time is also much more complicated than official personnel records indicate. Only time analysis in the workplace can yield relevant data. The worker may move around the department or the factory; a job with frequent changes in posture (e.g., turning and bending) results in exposure to a great range of concentrations. A representative measure of lead intake is almost impossible to obtain without the use of a personal sampler applied for many hours and for many days.

Particle size. Since the most important route of lead absorption is by the lungs, the particle size of industrial lead dust is of considerable significance and this depends on the nature of the operation giving rise to the dust. Fine dust of respirable particle size is produced by processes such as the pulverizing and blending of lead colours, the abrasive working of lead-based fillers in automobile bodies and the dry rubbing-down of lead paint. The exhaust gases of gasoline engines yield lead chloride and lead bromide particles of 1 micron diameter. The larger particles, however, may be ingested and be absorbed via the stomach. A more informative picture of the hazard associated with a sample of lead dust might be given by including a size distribution as well as a total lead determination. But this information is probably more important for the research investigator than for the field hygienist.

Biological fate

In the human body, inorganic lead is not metabolized but is directly absorbed, distributed and excreted. The rate at which lead is absorbed depends on its chemical and physical form and on the physiological characteristics of the exposed person (e.g., nutritional status and age). Inhaled lead deposited in the lower respiratory tract is completely absorbed. The amount of lead absorbed from the gastrointestinal tract of adults is typically 10 to 15% of the ingested quantity; for pregnant women and children, the amount absorbed can increase to as much as 50%. The quantity absorbed increases significantly under fasting conditions and with iron or calcium deficiency.

Once in the blood, lead is distributed primarily among three compartments—blood, soft tissue (kidney, bone marrow, liver, and brain), and mineralizing tissue (bones and teeth). Mineralizing tissue contains about 95% of the total body burden of lead in adults.

The lead in mineralizing tissues accumulates in subcompartments that differ in the rate at which lead is resorbed. In bone, there is both a labile component, which readily exchanges lead with the blood, and an inert pool. The lead in the inert pool poses a special risk because it is a potential endogenous source of lead. When the body is under physiological stress such as pregnancy, lactation or chronic disease, this normally inert lead can be mobilized, increasing the lead level in blood. Because of these mobile lead stores, significant drops in a person’s blood lead level can take several months or sometimes years, even after complete removal from the source of lead exposure.

Of the lead in the blood, 99% is associated with erythrocytes; the remaining 1% is in the plasma, where it is available for transport to the tissues. The blood lead not retained is either excreted by the kidneys or through biliary clearance into the gastrointestinal tract. In single-exposure studies with adults, lead has a half-life, in blood, of approximately 25 days; in soft tissue, about 40 days; and in the non-labile portion of bone, more than 25 years. Consequently, after a single exposure a person’s blood lead level may begin to return to normal; the total body burden, however, may still be elevated.

For lead poisoning to develop, major acute exposures to lead need not occur. The body accumulates this metal over a lifetime and releases it slowly, so even small doses, over time, can cause lead poisoning. It is the total body burden of lead that is related to the risk of adverse effects.

Physiological effects

Whether lead enters the body through inhalation or ingestion, the biologic effects are the same; there is interference with normal cell function and with a number of physiological processes.

Neurological effects. The most sensitive target of lead poisoning is the nervous system. In children, neurological deficits have been documented at exposure levels once thought to cause no harmful effects. In addition to the lack of a precise threshold, childhood lead toxicity may have permanent effects. One study showed that damage to the central nervous system (CNS) that occurred as a result of lead exposure at age 2 resulted in continued deficits in neurological development, such as lower IQ scores and cognitive deficits, at age 5. In another study that measured total body burden, primary school children with high tooth lead levels but with no known history of lead poisoning had larger deficits in psychometric intelligence scores, speech and language processing, attention and classroom performance than children with lower levels of lead. A 1990 follow-up report of children with elevated lead levels in their teeth noted a sevenfold increase in the odds of failure to graduate from high school, lower class standing, greater absenteeism, more reading disabilities and deficits in vocabulary, fine motor skills, reaction time and hand-eye coordination 11 years later. The reported effects are more likely caused by the enduring toxicity of lead than by recent excessive exposures because the blood lead levels found in the young adults were low (less than 10 micrograms per deciliter (μg/dL)).

Hearing acuity, particularly at higher frequencies, has been found to decrease with increasing blood lead levels. Hearing loss may contribute to the apparent learning disabilities or poor classroom behavior exhibited by children with lead intoxication.

Adults also experience CNS effects at relatively low blood lead levels, manifested by subtle behavioural changes, fatigue and impaired concentration. Peripheral nervous system damage, primarily motor, is seen mainly in adults. Peripheral neuropathy with mild slowing of nerve conduction velocity has been reported in asymptomatic lead workers. Lead neuropathy is believed to be a motor neuron, anterior horn cell disease with peripheral dying-back of the axons. Frank wrist drop occurs only as a late sign of lead intoxication.

Haematological effects. Lead inhibits the body’s ability to make hemoglobin by interfering with several enzymatic steps in the heme pathway. Ferrochelatase, which catalyzes the insertion of iron into protoporphyrin IX, is quite sensitive to lead. A decrease in the activity of this enzyme results in an increase of the substrate, erythrocyte protoporphyrin (EP), in the red blood cells. Recent data indicate that the EP level, which has been used to screen for lead toxicity in the past, is not sufficiently sensitive at lower levels of blood lead and is therefore not as useful a screening test for lead poisoning as previously thought.

Lead can induce two types of anaemia. Acute high-level lead poisoning has been associated with hemolytic anaemia. In chronic lead poisoning, lead induces anemia by both interfering with erythropoiesis and by diminishing red blood cell survival. It should be emphasized, however, that anemia is not an early manifestation of lead poisoning and is evident only when the blood lead level is significantly elevated for prolonged periods.

Endocrine effects. A strong inverse correlation exists between blood lead levels and levels of vitamin D. Because the vitamin D-endocrine system is responsible in large part for the maintenance of extra- and intra-cellular calcium homeostasis, it is likely that lead impairs cell growth and maturation and tooth and bone development.

Renal effects. A direct effect on the kidney of long-term lead exposure is nephropathy. Impairment of proximal tubular function manifests in aminoaciduria, glycosuria and hyperphosphaturia (a Fanconi-like syndrome). There is also evidence of an association between lead exposure and hypertension, an effect that may be mediated through renal mechanisms. Gout may develop as a result of lead-induced hyperuricemia, with selective decreases in the fractional excretion of uric acid before a decline in creatinine clearance. Renal failure accounts for 10% of deaths in patients with gout.

Reproductive and developmental effects. Maternal lead stores readily cross the placenta, placing the foetus at risk. An increased frequency of miscarriages and stillbirths among women working in the lead trades was reported as early as the end of the 19th century. Although the data concerning exposure levels are incomplete, these effects were probably a result of far greater exposures than are currently found in lead industries. Reliable dose-effect data for reproductive effects in women are still lacking today.

Increasing evidence indicates that lead not only affects the viability of the foetus, but development as well. Developmental consequences of prenatal exposure to low levels of lead include reduced birth weight and premature birth. Lead is an animal teratogen; however, most studies in humans have failed to show a relationship between lead levels and congenital malformations.

The effects of lead on the male reproductive system in humans have not been well characterized. The available data support a tentative conclusion that testicular effects, including reduced sperm counts and motility, may result from chronic exposure to lead.

Carcinogenic effects. Inorganic lead and inorganic lead compounds have been classified as Group 2B, possible human carcinogens, by the International Agency for Research on Cancer (IARC). Case reports have implicated lead as a potential renal carcinogen in humans, but the association remains uncertain. Soluble salts, such as lead acetate and lead phosphate, have been reported to cause kidney tumors in rats.

Continuum of signs and symptoms associated with lead toxicity

Mild toxicity associated with lead exposure includes the following:

  • myalgia or paresthesia
  • mild fatigue
  • irritability
  • lethargy
  • occasional abdominal discomfort.


The signs and symptoms associated with moderate toxicity include:

  • arthralgia
  • general fatigue
  • difficulty concentrating
  • muscular exhaustibility
  • tremor
  • headache
  • diffuse abdominal pain
  • vomiting
  • weight loss
  • constipation.


The signs and symptoms of severe toxicity include:

  • paresis or paralysis
  • encephalopathy, which may abruptly lead to seizures, changes in consciousness, coma and death
  • lead line (blue-black) on gingival tissue
  • colic (intermittent, severe abdominal cramps).


Some of the haematological signs of lead poisoning mimic other diseases or conditions. In the differential diagnosis of microcytic anaemia, lead poisoning can usually be ruled out by obtaining a venous blood lead concentration; if the blood lead level is less than 25 μg/dL, the anaemia usually reflects iron deficiency or haemoglobinopathy. Two rare diseases, acute intermittent porphyria and coproporphyria, also result in haeme abnormalities similar to those of lead poisoning.

Other effects of lead poisoning can be misleading. Patients exhibiting neurological signs due to lead poisoning have been treated only for peripheral neuropathy or carpal tunnel syndrome, delaying treatment for lead intoxication. Failure to correctly diagnose lead induced gastrointestinal distress has led to inappropriate abdominal surgery.

Laboratory evaluation

If pica or accidental ingestion of lead-containing objects (such as curtain weights or fishing sinkers) is suspected, an abdominal radiograph should be taken. Hair analysis is not usually an appropriate assay for lead toxicity because no correlation has been found between the amount of lead in the hair and the exposure level.

The probability of environmental lead contamination of a laboratory specimen and inconsistent sample preparation make the results of hair analysis difficult to interpret. Suggested laboratory tests to evaluate lead intoxication include the following:

  • CBC with peripheral smear
  • blood lead level
  • erythrocyte protoporphyrin level
  • BUN and creatinine level
  • urinalysis.


CBC with peripheral smear. In a lead-poisoned patient, the haematocrit and haemoglobin values may be slightly to moderately low. The differential and total white count may appear normal. The peripheral smear may be either normochromic and normocytic or hypochromic and microcytic. Basophilic stippling is usually seen only in patients who have been significantly poisoned for a prolonged period. Eosinophilia may appear in patients with lead toxicity but does not show a clear dose-response effect.

It is important to note that basophilic stippling is not always seen in lead poisoned patients.

Blood lead level. A blood lead level is the most useful screening and diagnostic test for lead exposure. A blood lead level reflects lead’s dynamic equilibrium between absorption, excretion and deposition in soft- and hard-tissue compartments. For chronic exposures, blood lead levels often underrepresent the total body burden; nevertheless, it is the most widely accepted and commonly used measure of lead exposure. Blood lead levels srespond relatively rapidly to abrupt or intermittent changes in lead intake (e.g., ingestion of lead paint chips by children) and, within a limited range, bear a linear relationship to those intake levels.

Today, the average blood lead level in the US population, for example, is below 10 μg/dL, down from an average of 16 μg/dL (in the 1970s), the level before the legislated removal of lead from gasoline. A blood lead level of 10 μg/dL is about three times higher than the average level found in some remote populations.

The levels defining lead poisoning have been progressively declining. Taken together, effects occur over a wide range of blood lead concentrations, with no indication of a threshold. No safe level has yet been found for children. Even in adults, effects are being discovered at lower and lower levels as more sensitive analyses and measures are developed.

Erythrocyte protoporhyrin level. Until recently, the test of choice for screening asymptomatic populations at risk was erythrocyte protoporphyrin (EP), commonly assayed as zinc protoporphyrin (ZPP). An elevated level of protoporphyrin in the blood is a result of accumulation secondary to enzyme dysfunction in the erythrocytes. It reaches a steady state in the blood only after the entire population of circulating erythrocyles has turned over, about 120 days. Consequently, it lags behind blood lead levels and is an indirect measure of long-term lead exposure.

The major disadvantage of using EP (ZPP) testing as a method for lead screening is that it is not sensitive at the lower levels of lead poisoning. Data from the second US National Health and Nutrition Examination Survey (NHANES II) indicate that 58% of 118 children with blood lead levels above 30 μg/dL had EP levels within normal limits. This finding shows that a significant number of children with lead toxicity would be missed by reliance on EP (ZPP) testing alone as the screening tool. An EP (ZPP) level is still useful in screening patients for iron deficiency anaemia.

Normal values of ZPP are usually below 35 μg/dL. Hyperbilirubinaemia (jaundice) will cause falsely elevated readings when the haematofluorometer is used. EP is elevated in iron deficiency anaemia and in sickle cell and other haemolytic anaemias. In erythropoietic protoporphyria, an extremely rare disease, EP is markedly elevated (usually above 300 μg/dL).

BUN, creatinine and urinalysis. These parameters may reveal only late, significant effects of lead on renal function. Renal function in adults can also be assessed by measuring the fractional excretion of uric acid (normal range 5 to 10%; less than 5% in saturnine gout; greater than 10% in Fanconi syndrome).

Organic lead intoxication

The absorption of a sufficient quantity of tetraethyllead, whether briefly at a high rate or for prolonged periods at a lower rate, induces acute intoxication of the CNS. The milder manifestations are those of insomnia, lassitude and nervous excitation which reveals itself in lurid dreams and dream-like waking states of anxiety, in association with tremor, hyper-reflexia, spasmodic muscular contractions, bradycardia, vascular hypotension and hypothermia. The more severe responses include recurrent (sometimes nearly continuous) episodes of complete disorientation with hallucinations, facial contortions and intense general somatic muscular activity with resistance to physical restraint. Such episodes may be converted abruptly into maniacal or violent convulsive seizures which may terminate in coma and death.

Illness may persist for days or weeks, with intervals of quietude readily triggered into over-activity by any type of disturbance. In these less acute cases, fall in blood pressure and loss of body weight are common. When the onset of such symptomatology follows promptly (within a few hours) after brief, severe exposure to tetraethyllead, and when the symptomatology develops rapidly, an early fatal outcome is to be feared. When, however, the interval between the termination of brief or prolonged exposure and the onset of symptoms is delayed (by up to 8 days), the prognosis is guardedly hopeful, although partial or recurrent disorientation and depressed circulatory function may persist for weeks.

The initial diagnosis is suggested by a valid history of significant exposure to tetraethyllead, or by the clinical pattern of the presenting illness. It may be supported by the further development of the illness, and confirmed by evidence of a significant degree of absorption of tetraethyllead, provided by analyses of urine and blood which reveal typical findings (i.e., a striking elevation of the rate of excretion of lead in the urine) and a concurrently negligible or slight elevation of the concentration of lead in the blood.

Lead Control in the Working Environment

Clinical lead poisoning has historically been one of the most important occupational diseases, and it remains a major risk today. The considerable body of scientific knowledge concerning the toxic effects of lead has been enriched since the 1980s by significant new knowledge regarding the more subtle subclinical effects. Similarly, in a number of countries it was felt necessary to redraft or modernize work protective measures enacted over the last half-century and more.

Thus, in November 1979, in the US, the Final Standard on Occupational Exposure to Lead was issued by the Occupational Safety and Health Administration (OSHA) and in November 1980 a comprehensive Approved Code of Practice was issued in the United Kingdom regarding the control of lead at work.

The main features of the legislation, regulations and codes of practice emerging in the 1970s concerning the protection of the health of workers at work involved establishing comprehensive systems covering all work circumstances where lead is present and giving equal importance to hygiene measures, ambient monitoring and health surveillance (including biological monitoring).

Most codes of practice include the following aspects:

  • assessment of work which exposes persons to lead
  • information, instruction and training
  • control measures for materials, plant and processes
  • use and maintenance of control measures
  • respiratory protective equipment and protective clothing
  • washing and changing facilities and cleaning
  • separate eating, drinking and smoking areas
  • duty to avoid spread of contamination by lead
  • air monitoring
  • medical surveillance and biological tests
  • keeping of records.


Some regulation, such as the OSHA lead standard, specifies the permissible exposure limit (PEL) of lead in the workplace, the frequency and extent of medical monitoring, and other responsibilities of the employer. As of this writing, if blood monitoring reveals a blood lead level greater than 40 μg/dL, the worker must be notified in writing and provided with medical examination. If a worker’s blood lead level reaches 60 μg/dL (or averages 50 μg/dL or more), the employer is obligated to remove the employee from excessive exposure, with maintenance of seniority and pay, until the employee’s blood lead level falls below 40 μg/dL (29 CFR 91 O.1025) (medical removal protection benefits).

Safety and Health Measures

The object of precautions is first to prevent the inhalation of lead and secondly to prevent its ingestion. These objects are most effectively achieved by the substitution of a less toxic substance for the lead compound. The use of lead polysilicates in the potteries is one example. The avoidance of lead carbonate paints for the painting of the interiors of buildings has proved very effective in reducing painters’ colic; effective substitutes for lead for this purpose have become so readily available that it has been considered reasonable in some countries to prohibit the use of lead paint for the interiors of buildings.

Even if it is not possible to avoid the use of lead itself, it is still possible to avoid dust. Water sprays may be used in large quantities to prevent the formation of dust and to prevent it from becoming airborne. In lead smelting, the ore and the scrap may be treated in this way and the floors on which it has been lying may be kept wet. Unfortunately, there is always a potential source of dust in these circumstances if the treated material or floors are ever allowed to become dry. In some instances, arrangements are made to ensure that the dust will be coarse rather than fine. Other specific engineering precautions are discussed elsewhere in this Encyclopaedia.

Workers who are exposed to lead in any of its forms should be provided with personal protective equipment (PPE), which should be washed or renewed regularly. Protective clothing made of certain man-made fibres retains much less dust than cotton overalls and should be used where the conditions of work render it possible; turn-ups, pleats and pockets in which lead dust may collect should be avoided.

Cloakroom accommodation should be provided for this PPE, with separate accommodation for clothing taken off during working hours. Washing accommodation, including bathing accommodation with warm water, should be provided and used. Time should be allowed for washing before eating. Arrangements should be made to prohibit eating and smoking in the vicinity of lead processes and suitable eating facilities should be provided.

It is essential that the rooms and the plant associated with lead processes should be kept clean by continuous cleaning either by a wet process or by vacuum cleaners. Where, in spite of these precautions, workers may still be exposed to lead, respiratory protective equipment should be provided and properly maintained. Supervision should ensure that this equipment is maintained in a clean and efficient condition and that it is used when necessary.

Organic lead

Both the toxic properties of organic lead compounds, and their ease of absorption, require that contact of the skin of workers with these compounds, alone or in concentrated mixtures in commercial formulations or in gasoline or other organic solvents, must be scrupulously avoided. Both technological and management control are essential, and appropriate training of workers in safe work practices and the use of PPE is required. It is essential that atmospheric concentrations of alkyl lead compounds in the workplace air should be maintained at extremely low levels. Personnel should not be allowed to eat, smoke or keep unsealed food or beverages at the workplace. Good sanitary facilities, including showers, should be provided and workers should be encouraged to practise good personal hygiene, especially by showering or washing after the work shift. Separate lockers should be supplied for working and private clothes.



Friday, 11 February 2011 04:23


Gunnar Nordberg

Iridium (Ir) belongs to the platinum family. Its name derives from the colours of its salt, which are reminiscent of a rainbow (iris). Although it is very hard and the most corrosion-resistant metal known, it is attacked by some salts.

Occurrence and Uses

Iridium occurs in nature in the metallic state, usually alloyed with osmium (osmiridium), platinum or gold, and it is produced from these minerals. The metal is used to manufacture crucibles for chemical laboratories and to harden platinum. Recent in vitro studies indicate the possible effects of iridium on Leishmania donovani and the trypanocidal activity of iridium against Trypanosoma brucei. Ir is used in industrial radiology and is a gamma emitter (0.31 MeV at 82.7%) and beta emitter (0.67 MeV at 47.2%). 192Ir is a radioisotope which has also been used for clinical treatment, particularly cancer therapy. It is one of the most frequently used isotopes in interstitial brain irradiation.


Very little is known about the toxicity of iridium and its compounds. There has been little opportunity to note any adverse human effects since it is used only in small amounts. All radioisotopes are potentially harmful and must be treated with appropriate safeguards required for handling radioactive sources. Soluble iridium compounds such as iridium tribromide and tetrabromide and iridium trichloride could present both toxic effects of the iridium or the halogen, but data as to its chronic toxicity are unavailable. Iridium trichloride has been reported to be a mild irritant to the skin and is positive in eye irritation test. Inhaled aerosol of metallic iridium is deposited in the upper respiratory ways of rats; the metal is then quickly removed via the gastrointestinal tract, and approximately 95% can be found in the faeces. In humans the only reports are those concerning radiation injuries due to accidental exposure to 192Ir.

Safety and Health Measures

A radiation safety and medical surveillance programme should be in place for persons responsible for nursing care during interstitial brachytherapy. Radiation safety principles include exposure reduction by time, distance and shielding. Nurses who care for brachytherapy patients must wear radiation monitoring devices to record the amount of exposure. To avoid industrial radiography accidents, only trained industrial radiographers should be allowed to handle radionuclides.



Friday, 11 February 2011 04:10


Gunnar Nordberg

Occurrence and Uses

In nature, Indium (In) is widely distributed and occurs most frequently together with zinc minerals (sphalerite, marmatite, christophite), its chief commercial source. It is also found in the ores of tin, manganese, tungsten, copper, iron, lead, cobalt and bismuth, but generally in amounts of less than 0.1%.

Indium is generally used in industry for surface protection or in alloys. A thin coat of indium increases the resistance of metals to corrosion and wear. It prolongs the life of moving parts in bearings and finds wide use in the aircraft and automobile industries. It is used in dental alloys, and its “wettability” makes it ideal for plating glass. Because of its resistance to corrosion, indium is utilized extensively in making motion picture screens, cathode ray oscilloscopes and mirrors. When joined with antimony and germanium in an extremely pure combination, it is widely used in the manufacture of transistors and other sensitive electronic components. Radioisotopes of indium in compounds such as indium trichloride and colloidal indium hydroxide are used in organic scanning and in the treatment of tumours.

In addition to the metal, the most common industrial compounds of indium are the trichloride, used in electroplating; the sesquioxide, used in glass manufacture; the sulphate; and the antimonide and the arsenide used as semiconductor material.


No cases have been reported of systemic effects in humans exposed to indium. Probably the greatest current potential hazard comes from the use of indium together with arsenic, antimony and germanium in the electronics industry. This is due primarily to the fumes given off during welding and soldering processes in the manufacture of electronic components. Any hazard arising from the purification of indium is probably attributable to the presence of other metals, such as lead, or chemicals, such as cyanide, used in the electroplating process. Exposure of the skin to indium does not seem to present a serious hazard. The tissue distribution of indium in various chemical forms has been studied by administration to laboratory animals.

The sites of highest concentration were kidney, spleen, liver and salivary glands. After inhalation, widespread lung changes were observed, such as interstitial and desquamative pneumonitis with consequent respiratory insufficiency.

The results of animal studies showed that the more soluble salts of indium were very toxic, with lethality occurring after administration of less than 5 mg/kg by way of parenteral routes of injection. However, after gavage, indium was poorly absorbed and essentially non-toxic. Histophathological studies indicated that death was due primarily to degenerative lesions in the liver and kidney. Minor changes in the blood have also been noted. In chronic poisoning by indium chloride the main change is a chronic interstitial nephritis with proteinuria. The toxicity from the more insoluble form, indium sesquioxide, was only moderate to slight, requiring up to several hundred mg/kg for lethal effect. After administration of indium arsenide to hamsters, the uptake in various organs differed from the distribution of ionic indium or arsenic compounds.

Safety and Health Measures

Preventing the inhalation of indium fumes by the use of correct ventilation appears to be the most practical safety measure. When handling indium arsenide, safety precautions such as those applied for arsenic should be observed. In the field of nuclear medicine, correct radiation safety measures must be followed when handling radioactive indium isotopes. Intoxication in rats from indium-induced hepatic necrosis has been reduced considerably by administration of ferric dextran, the action of which is apparently very specific. The use of ferric dextran as a prophylactic treatment in humans has not been possible owing to a lack of serious cases of industrial exposures to indium.



Friday, 11 February 2011 04:09


Gunnar Nordberg

Occurrence and Uses

Germanium (Ge) is always found in combination with other elements and never in the free state. Among the most common germanium-bearing minerals are argyrodite (Ag8GeS6), containing 5.7% germanium, and germanite (CuS·FeS·GeS2), containing up to 10% Ge. Extensive deposits of germanium minerals are rare, but the element is widely distributed within the structure of other minerals, especially in sulphides (most commonly in zinc sulphide and in silicates). Small quantities are also found in different types of coal.

The largest end use of germanium is the production of infrared sensing and identification systems. Its use in fibre-optical systems has increased, while consumption for semiconductors has continued to decline due to advances in silicon semiconductor technology. Germanium is also used in electroplating and in the production of alloys, one of which, germanium-bronze, is characterized by high corrosion resistance. Germanium tetrachloride (GeCl4) is an intermediate in the preparation of germanium dioxide and organogermanium compounds. Germanium dioxide (GeO2) is used in the manufacture of optical glass and in cathodes.


Occupational health problems may arise from the dispersion of dust during the loading of germanium concentrate, breaking up and loading of the dioxide for reduction to metallic germanium, and loading of powdered germanium for melting into ingots. In the process of producing metal, during chlorination of the concentrate, distillation, rectification and hydrolysis of germanium tetrachloride, the fumes of germanium tetrachloride, chlorine and germanium chloride pyrolysis products may also present a health hazard. Other sources of health hazards are the production of radiant heat from tube furnaces for GeO2 reduction and during melting of germanium powder into ingots, and the formation of carbon monoxide during GeO2 reduction with carbon.

The production of single crystals of germanium for the manufacture of semiconductors brings about high air temperatures (up to 45 ºC), electromagnetic radiation with field strengths of more than 100 V/m and magnetic radiation of more than 25 A/m, and pollution of the workplace air with metal hydrides. When alloying germanium with arsenic, arsine may form in the air (1 to 3 mg/m3), and when alloying it with antimony, stibine or antimonous hydride may be present (1.5 to 3.5 mg/m3). Germanium hydride, which is used for the production of high-purity germanium, may also be a pollutant of the workplace air. The frequently required cleaning of the vertical furnaces causes the formation of dust, which contains, apart from germanium, silicon dioxide, antimony and other substances.

Machining and grinding of germanium crystals also give rise to dust. Concentrations of up to 5 mg/m3 have been measured during dry machining.

Absorbed germanium is rapidly excreted, mainly in urine. There is little information on the toxicity of inorganic germanium compounds to humans. Germanium tetrachloride may produce skin irritation. In clinical trials and other long-term oral exposures to cumulative doses exceeding 16 g of spirogermanium, an organogermanium antitumour agent or other germanium compounds have been shown to be neurotoxic and nephrotoxic. Such doses are not usually absorbed in the occupational setting. Animal experiments on the effects of germanium and its compounds have shown that dust of metallic germanium and germanium dioxide causes general health impairment (inhibition of body weight increase) when inhaled in high concentrations. The lungs of the animals presented morphological changes of the type of proliferative reactions, such as thickening of the alveolar partitions and hyperplasia of the lymphatic vessels around the bronchi and blood vessels. Germanium dioxide does not irritate the skin, but if it comes into contact with the moist conjunctiva it forms germanic acid, which acts as an eye irritant. Prolonged intra-abdominal administration in doses of 10 mg/kg leads to peripheral blood changes.

The effects of germanium concentrate dust are not due to germanium, but to a number of other dust constituents, in particular silica (SiO2). The concentrate dust exerts a pronounced fibrogenic effect resulting in the development of connective tissue and formation of nodules in the lungs similar to those observed in silicosis.

The most harmful germanium compounds are germanium hydride (GeH4) and germanium chloride. The hydride may provoke acute poisoning. Morphological examinations of organs of animals which died during the acute phase revealed circulatory disorders and degenerative cell changes in the parenchymatous organs. Thus the hydride appears to be a multi-system poison that may affect the nervous functions and peripheral blood.

Germanium tetrachloride is a strong irritant of the respiratory system, skin and eyes. Its threshold of irritation is 13 mg/m3. In this concentration it depresses the pulmonary cell reaction in experimental animals. In stronger concentrations it leads to irritation of the upper airways and conjunctivitis, and to changes in respiratory rate and rhythm. Animals which survive acute poisoning develop catarrhal-desquamative bronchitis and interstitial pneumonia a few days later. Germanium chloride also exerts general toxic effects. Morphological changes have been observed in the liver, kidneys and other organs of the animals.

Safety and Health Measures

Basic measures during the manufacture and use of germanium should be aimed at preventing the contamination of the air by dust or fumes. In the production of metal, continuity of the process and enclosure of the apparatus is advisable. Adequate exhaust ventilation should be provided in areas where the dust of metallic germanium, the dioxide or the concentrate is dispersed. Local exhaust ventilation should be provided near the melting furnaces during the manufacture of semiconductors, for example on zone-refining furnaces, and during the cleaning of the furnaces. The process of manufacturing and alloying monocrystals of germanium should be carried out in a vacuum, followed by the evacuation of the formed compounds under reduced pressure. Local exhaust ventilation is essential in operations such as dry cutting and grinding of germanium crystals. Exhaust ventilation is also important in premises for the chlorination, rectification and hydrolysis of germanium tetrachloride. Appliances, connections and fittings in these premises should be made of corrosion-proof material. The workers should wear acid-proof clothing and footwear. Respirators should be worn during the cleaning of appliances.

Workers exposed to dust, concentrated hydrochloric acid, germanium hydride and germanium chloride and its hydrolysis products should undergo regular medical examinations.



Friday, 11 February 2011 04:07


Gunnar Nordberg

Chemically, gallium (Ga) is similar to aluminium. It is not attacked by air and does not react with water. When cold, gallium reacts with chlorine and bromine, and when heated, with iodine, oxygen and sulphur. There are 12 known artificial radioactive isotopes, with atomic weights between 64 and 74 and half-lives between 2.6 minutes and 77.9 hours. When gallium is dissolved in inorganic acids, salts are formed, which change into insoluble hydroxide Ga(OH)3 with amphoteric properties (i.e., both acidic and basic) when the pH is higher than 3. The three oxides of gallium are GaO, Ga2O and Ga2O3.

Occurrence and Uses

The richest source of gallium is the mineral germanite, a copper sulphide ore which may contain 0.5 to 0.7% gallium and is found in southwest Africa. It is also widely distributed in small amounts together with zinc blendes, in aluminium clays, feldspars, coal and in the ores of iron, manganese and chromium. On a relatively small scale, the metal, alloys, oxides and salts are used in industries such as machine construction (coatings, lubricants), instrument making (solders, washers, fillers), electronics and electrical equipment production (diodes, transistors, lasers, conductor coverings), and in vacuum technology.

In the chemical industries gallium and its compounds are used as catalysts. Gallium arsenide has been widely used for semiconductor applications including transistors, solar cells, lasers and microwave generation. Gallium arsenide is used in the production of optoelectronic devices and integrated circuits. Other applications include the use of 72Ga for the study of gallium interactions in the organism and 67Ga as a tumour-scanning agent. Because of the high affinity of macrophages of the lymphoreticular tissues for 67Ga, it can be used in the diagnosis of Hodgkin’s disease, Boeck’s sarcoid and lymphatic tuberculosis. Gallium scintography is a pulmonary imaging technique which can be used in conjunction with an initial chest radiograph to evaluate workers at risk of developing occupational lung disease.


Workers in the electronics industry using gallium arsenide may be exposed to hazardous substances such as arsenic and arsine. Inhalation exposures of dusts are possible during the production of the oxides and powdered salts (Ga2(SO4)3, Ga3Cl) and in the production and processing of monocrystals of semiconductor compounds. The splashing or spilling of the solutions of the metal and its salts may act on the skin or mucous membranes of workers. Grinding of gallium phosphide in water gives rise to considerable quantities of phosphine, requiring preventive measures. Gallium compounds may be ingested via soiled hands and by eating, drinking and smoking in workplaces.

Occupational diseases from gallium have not been described, except for a case report of a petechial rash followed by a radial neuritis after a short exposure to a small amount of fumes containing gallium fluoride. The biological action of the metal and its compounds has been studied experimentally. The toxicity of gallium and compounds depends upon the mode of entry into the body. When administered orally in rabbits over a long period of time (4 to 5 months), its action was insignificant and included disturbances in protein reactions and reduced enzyme activity. The low toxicity in this case is explained by the relatively inactive absorption of gallium in the digestive tract. In the stomach and intestines, compounds are formed which are either insoluble or difficult to absorb, such as metal gallates and hydroxides. The dust of the oxide, nitride and arsenide of gallium was generally toxic when introduced into the respiratory system (intratracheal injections in white rats), causing dystrophy of the liver and kidneys. In the lungs it caused inflammatory and sclerotic changes. One study concludes that exposing rats to gallium oxide particles at concentrations near the threshold limit value induces progressive lung damage that is similar to that induced by quartz. Gallium nitrate has a powerful caustic effect on the conjunctivae, cornea and skin. The high toxicity of the acetate, citrate and chloride of gallium was demonstrated by intraperitoneal injection, leading to death of animals from paralysis of the respiratory centre.

Safety and Health Measures

In order to avoid contamination of the atmosphere of workplaces by the dusts of gallium dioxide, nitride and semiconductor compounds, precautionary measures should include enclosure of dust-producing equipment and effective local exhaust ventilation (LEV). Personal protective measures during the production of gallium should prevent ingestion and contact of gallium compounds with the skin. Consequently, good personal hygiene and the use of personal protective equipment (PPE) are important. The US National Institute for Occupational Safety and Health (NIOSH) recommends control of worker exposure to gallium-arsenide by observing the recommended exposure limit for inorganic arsenic, and advises that concentration of gallium arsenide in air should be estimated by determining arsenic. Workers should be educated in possible hazards, and proper engineering controls should be installed during production of microelectronic devices where exposure to gallium arsenide is likely. In view of the toxicity of gallium and its compounds, as shown by experiments, all persons involved in work with these substances should undergo periodic medical examinations, during which special attention should be paid to the condition of the liver, kidneys, respiratory organs and skin.



Friday, 11 February 2011 04:04


Gunnar Nordberg

Occurrence and Uses

Iron is second in abundance amongst the metals and is fourth amongst the elements, surpassed only by oxygen, silicon and aluminium. The most common iron ores are: haematite, or red iron ore (Fe2O3), which is 70% iron; limonite, or brown iron ore (FeO(OH)·nH2O), containing 42% iron; magnetite, or magnetic iron ore (Fe3O4), which has a high iron content; siderite, or spathic iron ore (FeCO3); pyrite (FeS2), the most common sulphide mineral; and pyrrhotite, or magnetic pyrite (FeS). Iron is used in the manufacture of iron and steel castings, and it is alloyed with other metals to form steels. Iron is also used to increase the density of oil-well drilling fluids.

Alloys and Compounds

Iron itself is not particularly strong, but its strength is greatly increased when it is alloyed with carbon and rapidly cooled to produce steel. Its presence in steel accounts for its importance as an industrial metal. Certain characteristics of steel—that is, whether it is soft, mild, medium or hard—are largely determined by the carbon content, which may vary from 0.10 to 1.15%. About 20 other elements are used in varied combinations and proportions in the production of steel alloys with many different qualities—hardness, ductility, corrosion resistance and so on. The most important of these are manganese (ferromanganese and spiegeleisen), silicon (ferrosilicon) and chromium, which is discussed below.

The most important industrial iron compounds are the oxides and the carbonate, which constitute the principal ores from which the metal is obtained. Of lesser industrial importance are cyanides, nitrides, nitrates, phosphides, phosphates and iron carbonyl.


Industrial dangers are present during the mining, transportation and preparation of the ores, during the production and use of the metal and alloys in iron and steel works and in foundries, and during the manufacture and use of certain compounds. Inhalation of iron dust or fumes occurs in iron-ore mining; arc welding; metal grinding, polishing and working; and in boiler scaling. If inhaled, iron is a local irritant to the lung and gastrointestinal tract. Reports indicate that long-term exposure to a mixture of iron and other metallic dusts may impair pulmonary function.

Accidents are liable to occur during the mining, transportation and preparation of the ores because of the heavy cutting, conveying, crushing and sieving machinery that is used for this purpose. Injuries may also arise from the handling of explosives used in the mining operations.

Inhaling dust containing silica or iron oxide can lead to pneumoconiosis, but there are no definite conclusions as to the role of iron oxide particles in the development of lung cancer in humans. Based on animal experiments, it is suspected that iron oxide dust may serve as a “co-carcinogenic” substance, thus enhancing the development of cancer when combined simultaneously with exposure to carcinogenic substances.

Mortality studies of haematite miners have shown an increased risk of lung cancer, generally among smokers, in several mining areas such as Cumberland, Lorraine, Kiruna and Krivoi Rog. Epidemiological studies of iron and steel foundry workers have typically noted risks of lung cancer elevated by 1.5- to 2.5-fold. The International Agency for Research on Cancer (IARC) classifies iron and steel founding as a carcinogenic process for humans. The specific chemical agents involved (e.g., polynuclear aromatic hydrocarbons, silica, metal fumes) have not been identified. An increased incidence of lung cancer has also been reported, but less significantly, among metal grinders. The conclusions for lung cancer among welders are controversial.

In experimental studies, ferric oxide has not been found to be carcinogenic; however, the experiments were not carried out with haematite. The presence of radon in the atmosphere of haematite mines has been suggested to be an important carcinogenic factor.

Serious accidents can occur in iron processing. Burns can occur in the course of work with molten metal, as described elsewhere in this Encyclopaedia. Finely divided freshly reduced iron powder is pyrophoric and ignites on exposure to air at normal temperatures. Fires and dust explosions have occurred in ducts and separators of dust-extraction plants, associated with grinding and polishing wheels and finishing belts, when sparks from the grinding operation have ignited the fine steel dust in the extraction plant.

The dangerous properties of the remaining iron compounds are usually due to the radical with which the iron is associated. Thus ferric arsenate (FeAsO4) and ferric arsenite (FeAsO3·Fe2O3) possess the poisonous properties of arsenical compounds. Iron carbonyl (FeCO5) is one of the more dangerous of the metal carbonyls, having both toxic and flammable properties. Carbonyls are discussed in more detail elsewhere in this chapter.

Ferrous sulphide (FeS), in addition to its natural occurrence as pyrite, is occasionally formed unintentionally when materials containing sulphur are treated in iron and steel vessels, such as in petroleum refineries. If the plant is opened and the deposit of ferrous sulphide is exposed to the air, its exothermic oxidation may raise the temperature of the deposit to the ignition temperature of gases and vapours in the vicinity. A fine water spray should be directed on such deposits until flammable vapours have been removed by purging. Similar problems may occur in pyrite mines, where the air temperature is increased by a continuous slow oxidation of the ore.

Safety and health measures

The precautions for the prevention of mechanical accidents include the fencing and remote control of machinery, the design of plant (which, in modern steel-making, includes computerized control) and the safety training of workers.

The danger arising from toxic and flammable gases, vapours and dusts is countered by local exhaust and general ventilation coupled with the various forms of remote control. Protective clothing and eye protection should be provided to safeguard the worker from the effects of hot and corrosive substances, and heat.

It is especially important that the ducting at grinding and polishing machines and at finishing belts be maintained at regular intervals to keep up the efficiency of the exhaust ventilation as well as to reduce the risk of explosion.


A ferroalloy is an alloy of iron with an element other than carbon. These metallic mixtures are used as a vehicle for introducing specific elements into the manufacture of steel in order to produce steels with specific properties. The element may alloy with the steel by solution or it may neutralize harmful impurities.

Alloys have unique properties dependent on the concentration of their elements. These properties vary directly in relation to the concentration of the individual components and depend, in part, on the presence of trace quantities of other elements. Although the biological effect of each element in the alloy may be used as a guide, there is sufficient evidence for the modification of action by the mixture of elements to warrant extreme caution in making critical decisions based on extrapolation of effect from the single element.

The ferroalloys constitute a wide and diverse list of alloys with many different mixtures within each class of alloy. The trade generally limits the number of types of ferroalloy available in any one class but metallurgical developments can result in frequent additions or changes. Some of the more common ferroalloys are as follows:

  • ferroboron—16.2% boron
  • ferrochromium—60 to 70% chromium, that may also contain silicon and manganese
  • ferromanganese—78 to 90% manganese; 1.25 to 7% silicon
  • ferromolybdenum—55 to 75% molybdenum; 1.5% silicon
  • ferrophosphorus—18 to 25% phosphorus
  • ferrosilicon—5 to 90% silica
  • ferrotitanium—14 to 45% titanium; 4 to 13% silicon
  • ferrotungsten—70 to 80% tungsten
  • ferrovanadium—30 to 40% vanadium; 13% silicon; 1.5% aluminium.



Although certain ferroalloys do have non-metallurgical uses, the main sources of hazardous exposure are encountered in the manufacture of these alloys and in their use during steel production. Some ferroalloys are produced and used in fine particulate form; airborne dust constitutes a potential toxicity hazard as well as a fire and explosion hazard. In addition, occupational exposure to the fumes of certain alloys has been associated with serious health problems.

Ferroboron. Airborne dust produced during the cleaning of this alloy may cause irritation of the nose and throat, which is due, possibly, to the presence of a boron oxide film on the alloy surface. Some animal studies (dogs exposed to atmospheric ferroboron concentrations of 57 mg/m3 for 23 weeks) found no adverse effects.

Ferrochromium. One study in Norway on the overall mortality and the incidence of cancer in workers producing ferrochromium has shown an increased incidence of lung cancer in causal relationship with the exposure to hexavalent chromium around the furnaces. Perforation of the nasal septum was also found in a few workers. Another study concludes that excess mortality due to lung cancer in steel-manufacturing workers is associated with exposure to polycyclic aromatic hydrocarbons (PAHs) during ferrochromium production. Yet another study investigating the association between occupational exposure to fumes and lung cancer found that ferrochromium workers demonstrated excess cases of both lung and prostate cancer.

Ferromanganese may be produced by reducing manganese ores in an electric furnace with coke and adding dolomite and limestone as flux. Transportation, storage, sorting and crushing of the ores produce managanese dust in concentrations which can be hazardous. The pathological effects resulting from exposure to dust, from both the ore and the alloy, are virtually indistinguishable from those described in the article “Manganese” in this chapter. Both acute and chronic intoxications have been observed. Ferromanganese alloys containing very high proportions of manganese will react with moisture to produce manganese carbide, which, when combined with moisture, releases hydrogen, creating a fire and explosion hazard.

Ferrosilicon production can result in both aerosols and dusts of ferrosilicon. Animal studies indicate that ferrosilicon dust can cause thickening of the alveolar walls with the occasional disappearance of the alveolar structure. The raw materials used in alloy production may also contain free silica, although in relatively low concentrations. There is some disagreement as to whether classical silicosis may be a potential hazard in ferrosilicon production. There is no doubt, however, that chronic pulmonary disease, whatever its classification, can result from excessive exposure to the dust or aerosols encountered in ferrosilicon plants.

Ferrovanadium. Atmospheric contamination with dust and fumes is also a hazard in ferrovanadium production. Under normal conditions, the aerosols will not produce acute intoxication but may cause bronchitis and a pulmonary interstitial proliferative process. The vanadium in the ferrovanadium alloy has been reported to be appreciably more toxic than free vanadium as a result of its greater solubility in biological fluids.

Leaded steel is used for automobile sheet steel in order to increase malleability. It contains approximately 0.35% lead. Whenever the leaded steel is subject to high temperature, as in welding, there is always the danger of generating lead fumes.

Safety and health measures

Control of fumes, dust and aerosols during the manufacture and use of ferroalloys is essential. Good dust control is required in the transport and handling of the ores and alloys. Ore piles should be wetted down to reduce dust formation. In addition to these basic dust-control measures, special precautions are needed in the handling of specific ferroalloys.

Ferrosilicon reacts with moisture to produce phosphine and arsine; consequently this material should not be loaded in damp weather, and special precautions should be taken to ensure that it remains dry during storage and transport. Whenever ferrosilicon is being shipped or handled in quantities of any importance, notices should be posted warning workers of the hazard, and detection and analysis procedures should be implemented at frequent intervals to check for the presence of phosphine and arsine in the air. Good dust and aerosol control is required for respiratory protection. Suitable respiratory protective equipment should be available for emergencies.

Workers engaged in the production and use of ferroalloys should receive careful medical supervision. Their working environment should be monitored continuously or periodically, depending on the degree of risk. The toxic effects of the various ferroalloys are sufficiently divergent from those of the pure metals to warrant a more intense level of medical supervision until more data have been obtained. Where ferroalloys give rise to dust, fumes and aerosols, workers should receive periodic chest x-ray examinations for early detection of respiratory changes. Lung function testing and monitoring of metal concentrations in the blood and/or urine of exposed workers may also be required.



Friday, 11 February 2011 03:54


Gunnar Nordberg

Copper (Cu) is malleable and ductile, conducts heat and electricity exceedingly well and is very little altered in its functional capacity by exposure to dry air. In a moist atmosphere containing carbon dioxide it becomes coated with a green carbonate. Copper is an essential element in human metabolism.

Occurrence and Uses

Copper occurs principally as mineral compounds in which 63Cu constitutes 69.1% and 65Cu, 30.9% of the element. Copper is widely distributed in all continents and is present in most living organisms. Although some natural deposits of metallic copper have been found, it is generally mined either as sulphide ores, including covellite (CuS), chalcocite (Cu2S), chalcopyrite (CuFeS2) and bornite (Cu3FeS3); or as oxides, including malachite (Cu2CO3(OH)2); chrysocolla
(CuSiO3·2H2O) and chalcanthite (CuSO4·5H2O).

Because of its electrical properties, more than 75% of copper output is used in the electrical industries. Other applications for copper include water piping, roofing material, kitchenware, chemical and pharmaceutical equipment, and the production of copper alloys. Copper metal is also used as a pigment, and as a precipitant of selenium.

Alloys and Compounds

The most widely used non-ferrous copper alloys are those of copper and zinc (brass), tin (bronze), nickel (monel metal), aluminium, gold, lead, cadmium, chromium, beryllium, silicon or phosphorus.

Copper sulphate is used as an algicide and molluscicide in water; with lime, as a plant fungicide; as a mordant; in electroplating; as a froth flotation agent for the separation of zinc sulphide ore; and as an agent for leather tanning and hide preservation. Copper sulphate neutralized with hydrated lime, known as Bordeaux mixture, is used for the prevention of mildew in vineyards.

Cupric oxide has been used as a component of paint for ship bottoms and as a pigment in glass, ceramics, enamels, porcelain glazes and artificial gems. It is also used in the manufacture of rayon and other copper compounds, and as an optical glass polishing agent and a solvent for chromic iron ores. Cupric oxide is a component of flux in copper metallurgy, pyrotechnic compositions, welding fluxes for bronze and agricultural products such as insecticides and fungicides. Black cupric oxide is used for correcting copper-deficient soils and as a feed supplement.

Copper chromates are pigments, catalysts for liquid-phase hydrogenation and potato fungicides. A solution of cupric hydroxide in excess ammonia is a solvent for cellulose used in the manufacture of rayon (viscose). Cupric hydroxide is used in the manufacture of battery electrodes and for treating and staining paper. It is also a pigment, a feed additive, a mordant in dyeing and an ingredient in fungicides and insecticides.


Amine complexes of cupric chlorate, cupric dithionate, cupric azide and cuprous acetylide are explosive but are of no industrial or public health importance. Copper acetylide was found to be the cause of explosions in acetylene plants and has caused the abandonment of the use of copper in the construction of such plants. Fragments of metallic copper or copper alloys that lodge in the eye, a condition known as chalcosis, may lead to uveitis, abscess and loss of the eye. Workers who spray vineyards with Bordeaux mixture may suffer from pulmonary lesions (sometimes called “vineyard sprayer’s lung”) and copper-laden hepatic granulomas.

Accidental ingestion of soluble copper salts is generally innocuous since the vomiting induced rids the patient of much of the copper. The possibility of copper-induced toxicity may occur in the following situations:

  • The oral administration of copper salts is occasionally employed for therapeutic purposes, particularly in India.
  • Copper dissolved from the wire used in certain intra-uterine contraceptive devices has been shown to be absorbed systemically.
  • An appreciable fraction of the copper dissolved from the tubing commonly used in haemodialysis equipment may be retained by the patient and can produce significant increases in hepatic copper.
  • Copper, not uncommonly added to feed for livestock and poultry, concentrates in the liver of these animals and can greatly increase the intake of the element when these livers are eaten. Copper is also added, in large amounts relative to the normal human dietary intake, to a number of pet animal foods that are occasionally consumed by people. Manure from animals with copper-supplemented diets can result in an excessive amount of copper in vegetables and feed grains grown on soil dressed with this manure.


Acute toxicity

Although some chemical reference works contain statements to the effect that soluble salts of copper are poisonous, in practical terms this is true only if such solutions are used with misguided or suicidal intent, or as topical treatment of extensively burned areas. When copper sulphate, known as bluestone or blue vitriol, is ingested in gram quantities, it induces nausea, vomiting, diarrhoea, sweating, intravascular haemolysis and possible kidney failure; rarely, convulsions, coma and death may result. Drinking of carbonated water or citrus fruit juices which have been in contact with copper vessels, pipes, tubing or valves can cause gastrointestinal irritation, which is seldom serious. Such beverages are acidic enough to dissolve irritating levels of copper. There is a report of corneal ulcers and skin irritation, but little other toxicity, in a copper-mine worker who fell into an electrolytic bath, but the acidity, rather than the copper, may have been the cause. In some instances where copper salts have been used in the treatment of burns, high concentrations of serum copper and toxic manifestations have ensued.

The inhalation of dusts, fumes and mists of copper salts can cause congestion of the nasal and mucous membranes and ulceration with perforation of the nasal septum. Fumes from the heating of metallic copper can cause metal fume fever, nausea, gastric pain and diarrhoea.

Chronic toxicity

Chronic toxic effects in human beings attributable to copper appears only to be found in individuals who have inherited a particular pair of abnormal autosomal recessive genes and in whom, as a consequence, hepatolenticular degeneration (Wilson’s disease) develops. This is a rare occurrence. Most daily human diets contain 2 to 5 mg of copper, almost none of which is retained. The adult human body copper content is quite constant at about 100 to 150 mg. In normal individuals (without Wilson’s disease), almost all of the copper is present as an integral and functional moiety of one of perhaps a dozen proteins and enzyme systems including, for example, cytochrome oxidase, dopa-oxidase and serum ceruloplasmin.

Tenfold, or more, increases in the daily intake of copper can occur in individuals who eat large quantities of oysters (and other shellfish), liver, mushrooms, nuts and chocolate—all rich in copper; or in miners who may work and eat meals, for 20 years or more, in an atmosphere laden with 1 to 2% copper ores dusts. Yet evidence of primary chronic copper toxicity (well defined from observations of patients with inherited chronic copper toxicosis—Wilson’s disease—as dysfunction of and structural damage to the liver, central nervous system, kidney, bones and eyes) has never been found in any individuals except those with Wilson’s disease. However, the excessive copper deposits that are found in the livers of patients with primary biliary cirrhosis, cholestasis and Indian childhood cirrhosis may be one contributing factor to the severity of the hepatic disease that is characteristic of these conditions.

Safety and Health Measures

Workers exposed to copper dusts or mists should be provided with adequate protective clothing to prevent repeated or prolonged skin contact. Where dust conditions cannot be sufficiently controlled, appropriate respirators and eye protection are necessary. Housekeeping and the provision of adequate sanitary facilities is essential since eating, drinking and smoking should be prohibited at the worksite. In mines where there are water-soluble ores such as chalcanthite, workers should be particularly careful to wash their hands with water before eating.

The prevention of metal fume fever is a matter of keeping exposure below the level of concentration currently accepted as satisfactory for working with copper in industry. The employment of local exhaust ventilation (LEV) is a necessary measure to collect copper fumes at the source.

People with Wilson’s disease should avoid employment in copper industries. The serum concentration of ceruloplasmin is a screen for this condition, since unaffected individuals have levels which range from 20 to 50 mg/100 cm3 of this copper protein whereas 97% of patients with Wilson’s disease have less than 20 mg/100 cm3. This is a relatively expensive procedure for broad-based screening programmes.



Friday, 11 February 2011 03:52


Gunnar Nordberg

Occurrence and Uses

Elemental chromium (Cr) is not found free in nature, and the only ore of any importance is the spinel ore, chromite or chrome iron stone, which is ferrous chromite (FeOCr2O3), widely distributed over the earth’s surface. In addition to chromic acid, this ore contains variable quantities of other substances. Only ores or concentrates containing more than 40% chromic oxide (Cr2O3) are used commercially, and countries having the most suitable deposits are the Russian Federation, South Africa, Zimbabwe, Turkey, the Philippines and India. The prime consumers of chromites are the United States, the Russian Federation, Germany, Japan, France and the United Kingdom.

Chromite may be obtained from both underground and open cast mines. The ore is crusted and, if necessary, concentrated.

The most significant usage of pure chromium is for electroplating of a wide range of equipment, such as automobile parts and electric equipment. Chromium is used extensively for alloying with iron and nickel to form stainless steel, and with nickel, titanium, niobium, cobalt, copper and other metals to form special-purpose alloys.

Chromium Compounds

Chromium forms a number of compounds in various oxidation states. Those of II (chromous), III (chromic) and VI (chromate) states are most important; the II state is basic, the III state is amphoteric and the VI state is acidic. Commercial applications mainly concern compounds in the VI state, with some interest in III state chromium compounds.

The chromous state (CrII) is unstable and is readily oxidized to the chromic state (CrIII). This instability limits the use of chromous compounds. The chromic compounds are very stable and form many compounds which have commercial use, the principal of which are chromic oxide and basic chromium sulphate.

Chromium in the +6 oxidation state (CrVI) has its greatest industrial application as a consequence of its acidic and oxidant properties, as well as its ability to form strongly coloured and insoluble salts. The most important compounds containing chromium in the CrVI state are sodium dichromate, potassium dichromate and chromium trioxide. Most other chromate compounds are produced industrially using dichromate as the source of CrVI.


Sodium mono- and dichromate are the starting materials from which most of the chromium compounds are manufactured. Sodium chromate and dichromate are prepared directly from chrome ore. Chrome ore is crushed, dried and ground; soda ash is added and lime or leached calcine may also be added. After thorough mixing the mixture is roasted in a rotary furnace at an optimum temperature of about 1,100°C; an oxidizing atmosphere is essential to convert the chromium to the CrVI state. The melt from the furnace is cooled and leached and the sodium chromate or dichromate is isolated by conventional processes from the solution.

ChromiumIII compounds

Technically, chromium oxide (Cr2O3, or chromic oxide), is made by reducing sodium dichromate either with charcoal or with sulphur. Reduction with sulphur is usually employed when the chromic oxide is to be used as a pigment. For metallurgical purposes carbon reduction is normally employed.

The commercial material is normally basic chromic sulphate [Cr(OH)(H2O)5]SO4, which is prepared from sodium dichromate by reduction with carbohydrate in the presence of sulphuric acid; the reaction is vigorously exothermic. Alternatively, sulphur dioxide reduction of a solution of sodium dichromate will yield basic chromic sulphurate. It is used in the tanning of leather, and the material is sold on the basis of Cr2O3 content, which ranges from 20.5 to 25%.

ChromiumVI compounds

Sodium dichromate can be converted into the anhydrous salt. It is the starting point for preparation of chromium compounds.

Chromium trioxide or chromium anhydride (sometimes referred to as “chromic acid”, although true chromic acid cannot be isolated from solution) is formed by treating a concentrated solution of a dichromate with strong sulphuric acid excess. It is a violent oxidizing agent, and the solution is the principal constituent of chromium plating.

Insoluble chromates

Chromates of weak bases are of limited solubility and more deeply coloured than the oxides; hence their use as pigments. These are not always distinct compounds and may contain mixtures of other materials to provide the right pigment colour. They are prepared by the addition of sodium or potassium dichromate to a solution of the appropriate salt.

Lead chromate is trimorphic; the stable monoclinic form is orange-yellow, “chrome yellow”, and the unstable orthombic form is yellow, isomorphous with lead sulphate and stabilized by it. An orange-red tetragonal form is similar and isomorphous with lead molybdate (VI) PbMoO4 and stabilized by it. On these properties depends the versatility of lead chromate as a pigment in producing a variety of yellow-orange pigments.


Compounds containing CrVI are used in many industrial operations. The manufacture of important inorganic pigments such as lead chromes (which are themselves used to prepare chrome greens), molybdate-oranges, zinc chromate and chromium-oxide green; wood preservation; corrosion inhibition; and coloured glasses and glazes. Basic chromic sulphates are widely used for tanning.

The dyeing of textiles, the preparation of many important catalysts containing chromic oxide and the production of light-sensitive dichromated colloids for use in lithography are also well-known industrial uses of chromium-containing chemicals.

Chromic acid is used not only for “decorative” chromium plating but also for “hard” chromium plating, where it is deposited in much thicker layers to give an extremely hard surface with a low coefficient of friction.

Because of the strong oxidizing action of chromates in acid solution, there are many industrial applications particularly involving organic materials, such as the oxidation of trinitrotoluene (TNT) to give phloroglucinol and the oxidation of picoline to give nicotine acid.

Chromium oxide is also used for the production of pure chromium metal that is suitable for incorporation in creep-resistant, high-temperature alloys, and as a refractory oxide. It may be included in a number of refractory compositions with advantage—for example, in magnetite and magnetite-chromate mixtures.


Compounds with CrIII oxidation states are considerably less hazardous than are CrVI compounds. Compounds of CrIII are poorly absorbed from the digestive system. These CrIII compounds may also combine with proteins in the superficial layers of the skin to form stable complexes. Compounds of CrIII do not cause chrome ulcerations and do not generally initiate allergic dermatitis without prior sensitization by CrVI compounds.

In the CrVI oxidation state, chromium compounds are readily absorbed after ingestion as well as during inhalation. The uptake through intact skin is less well elucidated. The irritant and corrosive effects caused by CrVI occur readily after uptake through mucous membranes, where they are readily absorbed. Work-related exposure to CrVI compounds may induce skin and mucous membrane irritation or corrosion, allergic skin reactions or skin ulcerations.

The untoward effects of chromium compounds generally occur among workers in workplaces where CrVI is encountered, in particular during manufacture or use. The effects frequently involve the skin or respiratory system. Typical industrial hazards are inhalation of the dust or fumes arising during the manufacture of dichromate from chromite ore and the manufacture of lead and zinc chromates, inhalation of chromic acid mists during electroplating or surface treatment of metals, and skin contact with CrVI compounds in manufacture or use. Exposure to CrVI-containing fumes may also occur during welding of stainless steels.

Chrome ulcerations. Such lesions used to be common after work-related exposure to CrVI compounds. The ulcers result from the corrosive action of CrVI, which penetrates the skin through cuts or abrasions. The lesion usually begins as a painless papule, commonly on the hands, forearms or feet, resulting in ulcerations. The ulcer may penetrate deeply into soft tissue and may reach underlying bone. Healing is slow unless the ulcer is treated at an early stage, and atrophic scars remain. There are no reports about skin cancer following such ulcers.

Dermatitis. The CrVI compounds may cause both primary skin irritation and sensitization. In chromate-producing industries, some workers may develop skin irritation, particularly at the neck or wrist, soon after starting work with chromates. In the majority of cases, this clears rapidly and does not recur. However, sometimes it may be necessary to recommend a change of work.

Numerous sources of exposure to CrVI have been listed (e.g., contact with cement, plaster, leather, graphic work, work in match factories, work in tanneries and various sources of metal work). Workers employed in wet sandpapering of car bodies have also been reported with allergy. Affected subjects react positively to patch testing with 0.5% dichromate. Some affected subjects had only erythema or scattered papules, and in others the lesions resembled dyshidriotic pompholyx; nummular eczema may lead to misdiagnosis of genuine cases of occupational dermatitis.

It has been shown that CrVI penetrates the skin through the sweat glands and is reduced to CrIII in the corium. It is shown that the CrIII then reacts with protein to form the antigen-antibody complex. This explains the localization of lesions around sweat glands and why very small amounts of dichromate can cause sensitization. The chronic character of the dermatitis may be due to the fact that the antigen-antibody complex is removed more slowly than would be the case if the reaction occurred in the epidermis.

Acute respiratory effects. Inhalation of dust or mist containing CrVI is irritating to mucous membranes. At high concentrations of such dust, sneezing, rhinorrhoea, lesions of the nasal septum and redness of the throat are documented effects. Sensitization has also been reported, resulting in typical asthmatic attacks, which may recur on subsequent exposure. At exposure for several days to chromic acid mist at concentrations of about 20 to 30 mg/m3, cough, headache, dyspnoea and substernal pain have also been reported after exposure. The occurrence of bronchospasm in a person working with chromates should suggest chemical irritation of the lungs. Treatment is only symptomatic.

Ulcerations of the nasal septum. In previous years, when the exposure levels to CrVI compounds could be high, ulcerations of the nasal septum were frequently seen among exposed workers. This untoward effect results from deposition of CrVI-containing particulates or mist droplets on the nasal septum, resulting in ulceration of the cartilaginous portion followed, in many cases, by perforation at the site of ulceration. Frequent nose-picking may enhance the formation of perforation. The mucosa covering the lower anterior part of the septum, known as the Kiesselbach’s and Little’s area, is relatively avascular and closely adherent to the underlying cartilage. Crusts containing necrotic debris from the cartilage of the septum continue to form, and within a week or two the septum becomes perforated. The periphery of the ulceration remains active for up to several months, during which time the perforation may increase in size. It heals by the formation of vascular scar tissue. Sense of smell is almost never impaired. During the active phase, rhinorrhoea and nose-bleeding may be troublesome symptoms. When soundly healed, symptoms are rare and many persons are unaware that the septum is perforated.

Effects in other organs. Necrosis of the kidneys has been reported, starting with tubular necrosis, leaving the glomeruli undamaged. Diffuse necrosis of the liver and subsequent loss of architecture has also been reported. Soon after the turn of the century there were a number of reports on human ingestion of CrVI compounds resulting in major gastro-intestinal bleeding from ulcerations of the intestinal mucosa. Sometimes such bleedings resulted in cardiovascular shock as a possible complication. If the patient survived, tubular necrosis of the kidneys or liver necrosis could occur.

Carcinogenic effects. Increased incidence of lung cancer among workers in manufacture and use of CrVI compounds has been reported in a great number of studies from France, Germany, Italy, Japan, Norway, the United States and the United Kingdom. Chromates of zinc and calcium appear to be among the most potent carcinogenic chromates, as well as among the most potent human carcinogens. Elevated incidence of lung cancer has also been reported among subjects exposed to lead chromates, and to fumes of chromium trioxides. Heavy exposures to CrVI compounds have resulted in very high incidence of lung cancer in exposed workers 15 or more years after first exposure, as reported in both cohort studies and case reports.

Thus, it is well established that an increase in the incidence of lung cancer of workers employed in the manufacture of zinc chromate and the manufacture of mono- and dichromates from chromite ore is a long-term effect of work-related heavy exposure to CrVI compounds. Some of the cohort studies have reported measurements of exposure levels among the exposed cohorts. Also, a small number of studies have indicated that exposure to fumes generated from welding on Cr-alloyed steel may result in elevated incidence of lung cancer among these welders.

There is no firmly established “safe” level of exposure. However, most of the reports on association between CrVI exposure and cancer of the respiratory organs and exposure levels report on air levels exceeding 50 mg CrVI/m3 air.

The symptoms, signs, course, x-ray appearance, method of diagnosis and prognosis of lung cancers resulting from exposure to chromates differ in no way from those of cancer of the lung due to other causes. It has been found that the tumours often originate in the periphery of the bronchial tree. The tumours may be of all histological types, but a majority of the tumours seem to be anaplastic oat-celled tumours. Water-soluble, acid soluble and water insoluble chromium is found in the lung tissues of chromate workers in varying amounts.

Although it has not been firmly established, some studies have indicated that exposure to chromates may result in increased risk of cancer in the nasal sinuses and the alimentary tract. The studies that indicate excess cancer of the alimentary tract are case reports from the 1930s or cohort studies that reflect exposure at high levels than generally encountered today.

Safety and Health Measures

On the technical side, avoidance of exposure to chromium depends on appropriate design of processes, including adequate exhaust ventilation and the suppression of dust or mist containing chromium in the hexavalent state. Built-in control measures are also necessary, requiring the least possible action by either process operators or maintenance staff.

Wet methods of cleaning should be used where possible; at other sites, the only acceptable alternative is vacuum cleaning. Spill of liquids or solids must be removed to prevent dispersion as airborne dust. The concentration in the work environment of chromium-containing dust and fumes should preferably be measured at regular intervals by individual and area sampling. Where unacceptable concentration levels are found by either method, the sources of dust or fumes should be identified and controlled. Dust masks, preferably with an efficiency of more than 99% in retaining particles of 0.5 µm size, should be worn in situations above non-hazardous levels, and it may be necessary to provide air-supplied respiratory protective equipment for jobs considered to be hazardous. Management should ensure that dust deposits and other surface contaminants should be removed by washing down or suction before work of this type begins. Providing laundering overalls daily may help in avoiding skin contamination. Hand and eye protection is generally recommended, as is repair and replacement of all personal protective equipment (PPE).

The medical surveillance of workers on processes in which CrVI compounds may be encountered should include education in toxic and the carcinogenic properties of both CrVI and CrIII compounds, as well as on the differences between the two groups of compounds. The nature of the exposure hazards and subsequent risks of various diseases (e.g., lung cancer) should be given at job entry as well as at regular intervals during employment. The need to observe a high standard of personal hygiene should be emphasized.

All untoward effects of exposure to chromium can be avoided. Chrome ulcers of the skin can be prevented by eliminating sources of contact and by preventing injury to the skin. Skin cuts and abrasions, however slight, should be cleaned immediately and treated with 10% sodium EDTA ointment. Together with the use of a frequently renewed impervious dressing, this will enhance rapid healing for any ulcer that may develop. Although EDTA does not chelate CrVI compounds at room temperature, it reduces the CrVI to CrIII rapidly, and the excess EDTA chelates CrIII. Both the direct irritant and corrosive action of CrVI compounds and the formation of protein/CrIII complexes are thus prevented. After accidental ingestion of CrVI compounds, immediate swallowing of ascorbic acid may also quickly reduce the CrVI.

Careful washing of the skin after contact and care to avoid friction and sweating are important in the prevention and the control of primary irritation due to chromates. In previous years an ointment containing 10% sodium EDTA was applied regularly to the nasal septum before exposure. This preventive treatment could assist in keeping the septum intact. Soreness of the nose and early ulceration were also treated by regular application of this ointment, and healing could be achieved without perforation.

Results from research indicate that workers exposed to high air concentrations of CrVI could be monitored successfully by monitoring the excretion of chromium in the urine. Such results, however, bear no relation to the hazard of skin allergy. As of today, with the very long latent period of CrVI-related lung cancer, hardly anything can be said regarding the cancer hazard on the basis of urinary levels of Cr.



Friday, 11 February 2011 03:51


Gunnar Nordberg

Occurrence and Uses

Cadmium (Cd) has many chemical and physical similarities to zinc and occurs together with zinc in nature. In minerals and ores, cadmium and zinc generally have a ratio of 1:100 to 1:1,000.

Cadmium is highly resistant to corrosion and has been widely used for electroplating of other metals, mainly steel and iron. Screws, screw nuts, locks and various parts for aircraft and motor vehicles are frequently treated with cadmium in order to withstand corrosion. Nowadays, however, only 8% of all refined cadmium is used for platings and coatings. Cadmium compounds (30% of the use in developed countries) are used as pigments and stabilizers in plastics, and cadmium is also used in certain alloys (3%). Rechargeable, small portable cadmium-containing batteries, used, for example, in mobile telephones, comprise a rapidly increasing usage of cadmium (55% of all cadmium in industrialized countries in 1994 was used in batteries).

Cadmium occurs in various inorganic salts. The most important is cadmium stearate, which is used as a heat stabilizer in polyvinyl chloride (PVC) plastics. Cadmium sulphide and cadmium sulphoselenide are used as yellow and red pigments in plastics and colours. Cadmium sulphide is also used in photo- and solar cells. Cadmium chloride acts as a fungicide, an ingredient in elecroplating baths, a colourant for pyrotechnics, an additive to tinning solution and a mordant in dyeing and printing textiles. It is also used in the production of certain photographic films and in the manufacture of special mirrors and coatings for electronic vacuum tubes. Cadmium oxide is an elecroplating agent, a starting material for PVC heat stabilizers and a component of silver alloys, phosphors, semiconductors and glass and ceramic glazes.

Cadmium can represent an environmental hazard, and many countries have introduced legislative actions aimed towards decreasing the use and subsequent environmental spread of cadmium.

Metabolism and accumulation

Gastrointestinal absorption of ingested cadmium is about 2 to 6% under normal conditions. Individuals with low body iron stores, reflected by low concentrations of serum ferritin, may have considerably higher absorption of cadmium, up to 20% of a given dose of cadmium. Significant amounts of cadmium may also be absorbed via the lung from the inhalation of tobacco smoke or from occupational exposure to atmospheric cadmium dust. Pulmonary absorption of inhaled respirable cadmium dust is estimated at 20 to 50%. After absorption via the gastrointestinal tract or the lung, cadmium is transported to the liver, where production of a cadmium-binding low-molecular-weight protein, metallothionein, is initiated.

About 80 to 90% of the total amount of cadmium in the body is considered to be bound to metallothionein. This prevents the free cadmium ions from exerting their toxic effects. It is likely that small amounts of metallothionein-bound cadmium are constantly leaving the liver and being transported to the kidney via the blood. The metallothionein with the cadmium bound to it is filtered through the glomeruli into the primary urine. Like other low-molecular-weight proteins and amino acids, the metallothionein-cadmium complex is subsequently reabsorbed from the primary urine into the proximal tubular cells, where digestive enzymes degrade the engulfed proteins into smaller peptides and amino acids. Free cadmium ions in the cells result from degradation of metallothionein and initiate a new synthesis of metallothionein, binding the cadmium, and thus protecting the cell from the highly toxic free cadmium ions. Kidney dysfunction is considered to occur when the metallothionein-producing capacity of the tubular cells is exceeded.

The kidney and liver have the highest concentrations of cadmium, together containing about 50% of the body burden of cadmium. The cadmium concentration in the kidney cortex, before cadmium-induced kidney damage occurs, is generally about 15 times the concentration in liver. Elimination of cadmium is very slow. As a result of this, cadmium accumulates in the body, the concentrations increasing with age and length of exposure. Based on organ concentration at different ages the biological half-life of cadmium in humans has been estimated in the range of 7 to 30 years.

Acute toxicity

Inhalation of cadmium compounds at concentrations above 1 mg Cd/m3 in air for 8 hours, or at higher concentrations for shorter periods, may lead to chemical pneumonitis, and in severe cases pulmonary oedema. Symptoms generally occur within 1 to 8 hours after exposure. They are influenza-like and similar to those in metal fume fever. The more severe symptoms of chemical pneumonitis and pulmonary oedema may have a latency period up to 24 hours. Death may occur after 4 to 7 days. Exposure to cadmium in the air at concentrations exceeding 5 mg Cd/m3 is most likely to occur where cadmium alloys are smelted, welded or soldered. Ingestion of drinks contaminated with cadmium at concentrations exceeding 15 mg Cd/l gives rise to symptoms of food poisoning. Symptoms are nausea, vomiting, abdominal pains and sometimes diarrhoea. Sources of food contamination may be pots and pans with cadmium-containing glazing and cadmium solderings used in vending machines for hot and cold drinks. In animals parenteral administration of cadmium at doses exceeding 2 mg Cd/kg body weight causes necrosis of the testis. No such effect has been reported in humans.

Chronic toxicity

Chronic cadmium poisoning has been reported after prolonged occupational exposure to cadmium oxide fumes, cadmium oxide dust and cadmium stearates. Changes associated with chronic cadmium poisoning may be local, in which case they involve the respiratory tract, or they may be systemic, resulting from absorption of cadmium. Systemic changes include kidney damage with proteinuria and anaemia. Lung disease in the form of emphysema is the main symptom at heavy exposure to cadmium in air, whereas kidney dysfunction and damage are the most prominent findings after long-term exposure to lower levels of cadmium in workroom air or via cadmium-contaminated food. Mild hypochromic anaemia is frequently found among workers exposed to high levels of cadmium. This may be due to both increased destruction of red blood cells and to iron deficiency. Yellow discolouration of the necks of teeth and loss of sense of smell (anosmia) may also be seen in cases of exposure to very high cadmium concentrations.

Pulmonary emphysema is considered a possible effect of prolonged exposure to cadmium in air at concentrations exceeding 0.1 mg Cd/m3. It has been reported that exposure to concentrations of about 0.02 mg Cd/m3 for more than 20 years can cause certain pulmonary effects. Cadmium-induced pulmonary emphysema can reduce working capacity and may be the cause of invalidity and life shortening. With long-term low-level cadmium exposure the kidney is the critical organ (i.e., the organ first affected). Cadmium accumulates in renal cortex. Concentrations exceeding 200 µg Cd/g wet weight have previously been estimated to cause tubular dysfunction with decreased reabsorption of proteins from the urine. This causes tubular proteinuria with increased excretion of low-molecular-weight proteins such as
α,α-1-microglobulin (protein HC), β-2-microglobulin and retinol binding protein (RTB). Recent research suggests, however, that tubular damage may occur at lower levels of cadmium in kidney cortex. As the kidney dysfunction progresses, amino acids, glucose and minerals, such as calcium and phosphorus, are also lost into the urine. Increased excretion of calcium and phosphorous may disturb bone metabolism, and kidney stones are frequently reported by cadmium workers. After long-term medium-to-high levels of exposure to cadmium, the kidney’s glomeruli may also be affected, leading to a decreased glomerular filtration rate. In severe cases uraemia may develop. Recent studies have shown the glomerular dysfunction to be irreversible and dose dependent. Osteomalacia has been reported in cases of severe chronic cadmium poisoning.

In order to prevent kidney dysfunction, as manifested by β-2-microglobulinuria, particularly if the occupational exposure to cadmium fumes and dust is likely to last for 25 years (at 8 hours workday and 225 workdays/year), it is recommended that the average workroom concentration of respirable cadmium should be kept below 0.01 mg/m3.

Excessive cadmium exposure has occurred in the general population through ingestion of contaminated rice and other foodstuffs, and possibly drinking water. The itai-itai disease, a painful type of osteomalacia, with multiple fractures appearing together with kidney dysfunction, has occurred in Japan in areas with high cadmium exposure. Though the pathogenesis of itai-itai disease is still under dispute, it is generally accepted that cadmium is a necessary aetiological factor. It should be stressed that cadmium-induced kidney damage is irreversible and may grow worse even after exposure has ceased.

Cadmium and cancer

There is strong evidence of dose-response relationships and an increased mortality from lung cancer in several epidemiological studies on cadmium-exposed workers. The interpretation is complicated by concurrent exposures to other metals which are known or suspected carcinogens. Continuing observations of cadmium-exposed workers have, however, failed to yield evidence of increased mortality from prostatic cancer, as initially suspected. The IARC in 1993 assessed the risk of cancer from exposure to cadmium and concluded that it should be regarded as a human carcinogen. Since then additional epidemiological evidence has come forth with somewhat contradictory results, and the possible carcinogenicity of cadmium thus remains unclear. It is nevertheless clear that cadmium possesses strong carcinogenic properties in animal experiments.

Safety and Health Measures

The kidney cortex is the critical organ with long-term cadmium exposure via air or food. The critical concentration is estimated at about 200 µg Cd/g wet weight, but may be lower, as stated above. In order to keep the kidney cortex concentration below this level even after lifelong exposure, the average cadmium concentration in workroom air (8 hours per day) should not exceed 0.01 mg Cd/m3.

Work processes and operations which may release cadmium fumes or dust into the atmosphere should be designed to keep concentration levels to a minimum and, if practicable, be enclosed and fitted with exhaust ventilation. When adequate ventilation is impossible to maintain (e.g., during welding and cutting), respirators should be carried and air should be sampled to determine the cadmium concentration. In areas with hazards of flying particles, chemical splashes, radiant heat and so on (e.g., near electroplating tanks and furnaces), workers should wear appropriate safety equipment, such as eye, face, hand and arm protection and impermeable clothing. Adequate sanitary facilities should be supplied, and workers should be encouraged to wash before meals and to wash thoroughly and change clothes before leaving work. Smoking, eating and drinking in work areas should be prohibited. Tobacco contaminated with cadmium dust from workrooms can be an important exposure route. Cigarettes and pipe tobacco should not be carried in the workroom. Contaminated exhaust air should be filtered, and persons in charge of dust collectors and filters should wear respirators while working on the equipment.

To ensure that excessive accumulation of cadmium in the kidney does not occur, cadmium levels in blood and in urine should be checked regularly. Cadmium levels in blood are mainly an indication of the last few months exposure, but can be used to assess body burden a few years after exposure has ceased. A value of 100 nmol Cd/l whole blood is an approximate critical level if exposure is regular for long periods. Cadmium values in urine can be used to estimate the cadmium body burden, providing kidney damage has not occurred. It has been estimated by the WHO that 10 nmol/mmol creatinine is the concentration below which kidney dysfunction should not occur. Recent research has, however, shown that kidney dysfunction may occur already at around 5 nmol/mmol creatinine.

Since the mentioned blood and urinary levels are levels at which action of cadmium on kidney has been observed, it is recommended that control measures be applied whenever the individual concentrations of cadmium in urine and/or in blood exceed 50 nmol/l whole blood or
3 nmol/mmol creatinine respectively. Pre-employment medical examinations should be given to workers who will be exposed to cadmium dust or fumes. Persons with respiratory or kidney disorders should avoid such work. Medical examination of cadmium-exposed workers should be carried out at least once every year. In workers exposed to cadmium for longer periods, quantitative measurements of ß-2-microglobulin or other relevant low-molecular-weight proteins in urine should be made regularly. Concentrations of ß-2-microglobulin in urine should normally not exceed 34 µg/mmol creatinine.

Treatment of cadmium poisoning

Persons who have ingested cadmium salts should be made to vomit or given gastric lavage; persons exposed to acute inhalation should be removed from exposure and given oxygen therapy if necessary. No specific treatment for chronic cadmium poisoning is available, and symptomatic treatment has to be relied upon. As a rule the administration of chelating agents such as BAL and EDTA is contraindicated since they are nephrotoxic in combination with cadmium.



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