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Chromium and Compounds

Edouard Bastarache discusses the dangers of chrome in ceramics.

Chromium and Compounds


It is a grey-white metal very resistant to wear. Chromium is produced from chromite, FeO.Cr2O3, by roasting and extraction in the form of chromate which is then reduced to chromium metal.

Green chromium oxide, iron chromite, potassium dichromate and stains are  compounds used by potters.

Chemical and Physical Forms:

Chromium has a molecular weight of 52. Most chromium compounds are solids at room temperature, altough one notable exception is chromyl chloride, a hexavalent chromium compound that is a fuming liquid.

The chemical and toxicologic properties of chromium differ markedly, depending on the valence state of the metal. Chromium  occurs in its metallic state (valence 0), and in valence states 2+ through 6+, but only the trivalent (3+) and hexavalent (6+) are commonly found. Chromium in its 2+ state frequently oxidizes rapidly to 3+ form, and the 4+  and 5+ states are found only as intermediates in the conversion between 3+ and 6+ states.

Some Common Chromium Compounds :

Divalent (Cr2+):

            Chromous chloride                                CrCl2

            Chromous sulfate                                  CrSO4

Trivalent (Cr3+):

            Chromic oxide                                                 Cr2O3

            Chromic sulfate                                   Cr2(SO4)3

            Chromite ore                                        FeO.Cr2O3

Hexavalent (Cr6+):

            Chromium trioxide                               CrO3

            Chromic acid                                       H2CrO4

            Chromic acid anhydrides:

                        Sodium chromate                      Na2CrO4

                        Potassium chromate                  K2CrO4


                        Sodium dichromate                   Na2Cr2O7

                        Potassium dichromate                K2Cr2O7

                        Ammonium dichromate             (NH4)2Cr2O7

Uses and Sources of Exposure :

Chromium is found in:

- the production of chromium metal;

- the production of alloys resistant to corrosion: steel with chromium (ferrochrome);

-electrolytic chromium plating: the metal part to be covered with chromium is placed as   an electrode in a chromic acid solution added with sulphuric acid.

Thick chromium plating (hard type-thickness 5-10µm) can cause significant exposure to chromium whereas thin chromium plating (bright type-thickness 0.5-1µm) does not cause any significant risk of excessive exposure to chromium;

- the manufacture of chromates and dichromates from iron chromate. These have many applications in lithography, textile industry, printing, tannery, dyeing, photography, and the paint industry;

- the manufacture refractory bricks for the furnaces of the metallurgical industry;

- the use of  trivalent derivatives: chromic anhydride used as pesticide in wood preservation;

- welding alloys containing chromium. Welding of stainless steel by the manual metal arc process releases  particles which, after deposition in the respiratory tract, allows the progressive solubilization of chromium. On the other hand, the particles released by welding under inert gas (MIG) are not very soluble.

Chromium dioxichloride (Cl2CrO2) is  a volatile liquid compound of  hexavalent chromium used in a great number of synthesis processes: olefinic hydrocarbon polymerization, hydrocarbon oxidation, production of aldehydes and ketones

Chromium is present in trace amounts in many products (cements, bleach, magnetic tapes....) which can cause skin allergy. Chromium can also be found in tobacco smoke.

Clinical Toxicology:

Chromium is an essential trace element and is present in tissues in its trivalent state.

I-Classification of Chromium and Compounds:

Chromium compounds vary greatly in their toxic and carcinogenic effects. For this reason, ACGIH divides its inorganic compounds into a number of groupings:

A-Chromium metals and alloys: 


-chromium metal;

-stainless steels;

-other chromium-containing alloys.

B-Divalent chromium compounds (Cr2+) (Chromous compounds):


-chromous chloride (CrCl2);

-chromous sulfate (CrSO4);

C-Trivalent chromium compounds (Cr3+) (Chromic compounds):


-chromic sulfate (Cr2(SO4)3);

-chromic oxide (Cr2O3);

-chromic chloride (CrCl3);

-chromic potassium sulfate (KCr(SO4)2);

-chromite ore.

D-Hexavalent chromium compounds (Cr6+):


-chromium trioxide (CrO3);

-the anhydride of chromic acid chromates (e.g Na2CrO4), dichromates,

(e.g., Na2Cr2O7), and polychromates.

Hexavalent salts are regarded as the most hazardous ones.

Trivalent chromium is absorbed poorly by inhalation and throught intact skin, resulting in a low order of systemic toxicity. However, should trivalent chromium gain access to the systemic circulation, toxic effects may develop.

II-Routes of Absorption and Exposure:


Inhalation of highly water-soluble hexavalent chromium salts, such as chromic acid, sodium dichromate, and potassium dichromate, may result in substantial systemic absorption.

Less water-soluble salts are unlikely to produce systemic effects but may produce pulmonary effects.

Metallic chromium and chromous or chromic salts (valences 0, +2, +3) are absorbed minimally after inhalation. Local pulmonary deposition of these salts has been reported after exposure but without evidence of adverse systemic effects.


Hexavalent salts are converted by gastric juice to the trivalent form prior to absorption.

Trivalent chromium salts are absorbed after ingestion, but only 1% to 25% of the dose ingested is absorbed.

The extent of absorption varies with the particular salt ingested and the circumstances of ingestion.

C-Dermal Absorption:

Hexavalent salts generally are absorbed well topically through intact skin.

Hexavalent chromium can penetrate the skin and be transformed to trivalent chromium which becomes an hapten  and part of the allergic reaction causing exzematous dermatitis.

Trivalent salts are poorly absorbed through intact skin but, once the dermal barrier is broken, however, absorption may occur.


In industry, workers may be exposed to trivalent and hexavalent chromium compounds whose metabolic handling and toxicity are strikingly different.

Systemic toxicity is mainly due to hexavalent derivatives which, contrary to trivalent ones, may penetrate the body by any possible route including intact skin.

The principal carrier protein for chromium is transferrin; albumin transports chromium to a lesser extent.

Chromium compounds pass through many tissues, including the red blood cell, kidney, liver, spleen, and bone.

Inside cells, hexavalent chromium is reduced to the very reactive pentavalent chromium and the trivalent one.

Only these two forms may alter DNA.


Absorbed chromium is distributed in two compartments:

1-Rapid elimination compartment (half- life of 7 hours).

2-Slow elimination compartment.


Chromium is essentially excreted in the urine and in professionally exposed personnel, its urinary concentration reflects mostly the amount of recently absorbed soluble hexavalent chromium.

However, the presence of a slow elimination compartment explains why those who have been away from exposure, even for many months, have levels of urinary chromium above normal values.

IV-Symptoms and Signs:

A-Acute Toxicity:

After oral or dermal exposure, hexavalent chromium compounds, including chromic acid, the chromates and  dichromates, are potentially the most toxic of the chromium compounds commonly encountered. Ingestion of dichromates has proved fatal in many instances; the oral lethal dose is estimated to be 0.5 to 5 g.


Hexavalent chromium compounds may be absorbed percutaneously, even through intact skin and acute renal failure may occur after a dermal burn of 10% body surface or less.

In a case, 70% total body thermal burn from hot chromic sulfate (trivalent) mixed with sulfuric acid (broken skin barrier) produced chromium poisoning with acute renal failure.

Fumes of chromium dioxichloride are very irritating to the skin.

2-Gastrointestinal System:

Gastric secretions convert hexavalent chromium to trivalent chromium after ingestion.

In this process, the gastric and intestinal mucosa are in grave danger of severe  injury caracterized by massive inflammation and necrosis from the mouth to the jejunum causing:

-abdominal pain;




These rapid onset manifestations may cause death by circulatory collapse (shock).

If the outcome is not rapidly fatal, 12 to 20 hours later, manifestations of hepatic and renal necrosis will appear.

Adult respiratory distress syndrome has been reported after substantial ingestion.

Without treatment, the lethal dose for chromic acid by ingestion is estimated to be between 1 to 3 g.

Even small ingestions of dichromates have resulted in hemorrhagic gastro-enteritis and death.

3-Renal System:

Acute renal failure may occur after large oral ingestions of hexavalent chromium compounds and after dermal exposure.

4-Pulmonary System:

Inhalation of concentrated chromic acid mist has been reported to result in pulmonary edema, which may be delayed up to 72 hours after exposure.

Fumes of chromium dioxichloride are very irritating to the mucous membranes.

Adult respiratory distress syndrome has been reported after substantial ingestion.

5-Hepatic System:

Hepatic necrosis may occur in acute intoxication by ingestion.

B- Chronic Toxicity:

Chronic toxic manifestations are generally due to hexavalent compounds.

1-Skin symptoms:

On contact with skin, hexavalent chromium compounds act as both irritants and sensitizers.

a-Exzematous Dermatitis (Allergic Contact Dermatitis) :

This clinical entity is characterized by erythematous, or vesico-papular, wet, pruriginous lesions localised especially on the forearms (chromium bracelets).

It is very frequent among individuals in contact with cement.

In practice, only chromium hexavalent compounds are sensitizers.

Hexavalent chromium can penetrate the skin where it is reduced to trivalent chromium which plays the role of an hapten; when fixed on a protein, it becomes a complete antigen.

Chromate sensivity has proved fairly persistent once developed. In one study, 92% of the study patients with dichromate sensivity induced by exposure to Portland cement continued to display contact dermatitis 10 years after initially developed symptoms.

Once induced, chromate sensivity may produce difficulty in multiple settings.

Contact with textiles colored with chromate-based pigments can be sufficient to exacerbate the dermatitis. The wearing of leather shoes tanned with chromates can produce dermatitis of the feet if these are allowed to remain sweaty. « Housewife exzema » may be largely a chromate sensitivity phenomenon, as detergents and bleaches in some areas contain more than trace amounts of chromate salts

In sensitized individuals, the absorption of chromium by pulmonary and/or oral way could cause an exzematous reaction.

Trivalent chromium only penetrates with much difficulty into the skin and the risk of sensitizing is thus weak. Chromium metal is not in theory an allergen

The allergy to chromium is confirmed by skin patch testing.

Some authors claim that the measurement of urinary chromium allows to confirm the occupational origin of dermatitis in tanners.

b-Chrome ulcers:

After cutaneous exposure to chromic acid, erosions of the skin may occur. These « chrome holes » initially appear as papular lesions, either singly  or grouped, with central ulceration. They occur chiefly on the hands and forearms where there has been a break in the epidermis; they are believed to be due to a direct necrotizing effect of the chromate ion. These ulcers are from 5 to 10 mm in diameter, painless, with sharp edges, sometimes itchy and have the possibility of extending into joints; they heal slowly and produce a characteristic depressed scar.

These ulcers are observed mainly among workers of the electrolytic chromium plating industry.

c-Teeth and Skin:

Yellowish discoloration of the tongue and teeth is a sign of chronic intoxication.

2-Irritation of mucous membranes:

Atrophy of the nasal mucous membrane followed by ulceration and perforation may occur. It is generally painless and is found at medical examination. It may be found in nearly 50 % of workers exposed to chromates and may be associated to anosmia.

Nasal septal ulcerations were observed after only 2 weeks of exposure to 1mg/m3 of zinc chromate whilst 18 months of exposure to 0.02-0.1 mg/m3 did not cause any perforation or ulceration. These ulcerations were obseved mainly among electrolytic chromium plating workers

In one study of chromic acid workers, the incidence and severity of nasal injury was related both to lenght of exposure and the laxity of industrial hygiene practiced by individual workers.

Let us remember that perforation of the nasal septum is also associated with exposure to many other industrial toxicants:


-mercury fulminate;


-cement dust;

-potassium salts (potash mines).

Symptoms of rhinitis, conjonctivitis, shortness of breath and pruritus are more frequent among electolytic chromium plating workers. Workers of the same type of industry, excreting more than 15 µg / g of creatinine of chromium, have impairments of spirometric measurements, for instance a reduction of FEV1.0. Therefore, it is logical to conclude that chronic exposure to chromic acid fumes may cause chronic obstructive pulmonary disease.

Exposure to chromic acid (hexavalent) may cause chronic pharyngitis and laryngitis.

Oesophagitis, gastritis and stomach ulcers have been described among workers exposed to hexavalent chromium salts.

3-Respiratory Tract:

Occupational asthma has occurred among workers exposed to chromic acid fumes, to hexavalent chromium compounds present in bauxite used in the production of aluminium, and from hexavalent chromium in welding fumes.

The bronchospastic reaction may be of the delayed type and accompanied by an anaphylactoid reaction including urticaria, skin swelling and an increase in serum histamine.

Inhalation of trivalent chromium salts can also cause occupational asthma (chromium sulfate).

Pneumoconiosis has been observed also after exposure to chromite ore dust.


Certain hexavalent chromium compounds have been demonstrated to be carcinogenic on the basis of epidemiologic investigations of workers and of experimental studies with animals.

In general, these compounds tend to be of low solubility in water and, thus, are subdivided into two sub-groups by ACGIH :

a-Water-soluble hexavalent chromium compounds:

1-chromic acid;

2-chromic acid anhydrides;

3-monochromates and dichromates of:







b-Water-insoluble hexavalent chromium compounds:

    1-zinc chromate,

    2-calcium chromate,

    3-lead chromate,

    4-barium chromate,

    5-strontium chromate,

    6-sintered chromium trioxide.

Chronic inhalation of hexavalent chromium compounds presents an increased risk of lung cancer, with the degree of risk depending on the particular salts and their solubility under biological conditions, on the circumstances of exposure, and on such concomitant risk factors as cigarette smoking.

Epidemiologic studies conducted in the USA 40 years ago, demonstrated a 10 to 30 fold- increased risk of lung cancer among workers of the chromate industry compared to the general population. Many studies have confirmed the carcinogenic risk among workers employed in the manufacture of chromates and the use of chromium-based pigments.

Among individuals who have been severely exposed, the increased risk of lung cancer is still detectable 20 years after cessation of exposure. In most studies, a positive correlation between duration of exposure and lung cancer death was found.

In the electrolytic chromium plating industry, mainly of the « hard type », the cancer (mainly lung cancer) risk is quite lower than in the chromate industry; this is explained by the fact that soluble hexavalent chromium is used in the former while rather insoluble compounds are used in the latter.

The cancer risk among stainless steel welders, exposed to soluble hexavalent chromium compounds has not been precised.

In the production of ferrochrome, workers are exposed mainly to metallic and trivalent chromium and lightly to hexavalent compounds, under these circumstances an increased lung cancer risk does not seem to exist.

Exposure to chromates would also favor cancers of other sites such as nasal cavities, larynx and stomach.

Zinc chromate is the most potent carcinogen among chromates commonly found in industrial settings; calcium chromate and lead chromate pose a lesser risk.

According to Levy et al., chromic acid (a very soluble compound) would be a weak carcinogen.

The risk of lung cancer appears non-existent among tanners using mainly trivalent chromium compounds.

Trivalent chromium compounds and metallic chromium generally are considered to be very weak carcinogens or noncarcinogenic.


Hexavalent chromium compounds have been consistently genotoxic, inducing a wide variety of effects, including DNA damage, gene mutation, sister chromatid exchange, chromosomal aberrations, cell transformation, and dominant lethal mutations.

Hexavalent chromium compounds have caused developmental effects in rodents in the absence of maternal toxicity following oral administration.

As in the case of chromium exzematous dermatitis, it appears that the genotoxic substance is pentavalent chromium or trivalent chromium produced from the intracellular reduction of hexavalent chromium after penetration into the cell. According to Molyneux and Davies, it is the re-oxidation of pentavalent chromium by hydrogen peroxide, or eventually by other peroxides, that would cause the production of hydroxyl radicals responsible for DNA alterations induced by chromium.

Trivalent chromium per se is not genotoxic as demonstrated in epidemiologic studies among which one conducted among exposed tannery workers.

Management of Acute Toxicity:

Treatment is symptomatic.

I-Clinical Management:

No matter the route of exposure, the initial approach to an affected individual includes a brief assessement of his clinical status followed by support of basic cardiopulmonary functions.

Once the airway has been stabilized and cardiopulmonary support has been instituted as indicated, further measures can be considered.



Emesis generally should not be induced in the patient exposed to chromium via ingestion, owing to the potential corrosive effect of the chromium compound and the potential for rapid deterioration of the patient.

Usually ascorbic acid should be administered orally or nasogastrically, if the patient still has chromium in his stomach. Ascorbic acid has been shown to ameliorate the effects of topical human exposure to chromates. Ascorbic acid acts chemically by reducing Cr6+ to Cr3+, the form less toxic to the gastric and intestinal mucosa.. The ascorbic acic dosage for treatment of hexavalent chromium ingestion varies with the salt ingested.

Dilution of the ingested agent may be appropriate if dilution can be accomplished within minutes after ingestion, particularly if the ingested material’s pH is fairly low (e.g. chromic acid) or fairly high (e.g. ammonium dichromate).

Dilution may be accomplished with water or with fluids that also serve as demulcents, such as milk. The use of demulcent compounds (e.g. antacids, corn starch, or milk) in addition to those used for dilution has been recommneded and seems reasonable but have not been studied formally.

Gastric lavage to reduce the ingested dose may be desirable if chromium is likely to be present in the stomach. But, there is a risk of perforation of the injuried oesophagus and stomach; if the decision to proceed to lavage is made,  a soft tube is preferable.

2-Elimination Enhancement:

Existing evidence does not allow the conclusion that exchange transfusion generally should be employed.

Hemodialysis and charcoal hemoperfusion do not substantially enhance chromium removal from the body if renal function remains normal. However, if renal failure ensues, hemodialysis may be necessary for management of the renal failure itself.


Fluid balance must be maintained. Affected patients should be monitored carefully for evidence of gastrointestinal bleeding, methemoglobinemia, hemolysis, coagulopathy, seizures, or pulmonary dysfunction. Appropriate supportive measures should be employed as indicated.


Alkaline diuresis may be indicated to reduce the possibility of further renal injury.


It should be treated with methylene blue if the methemoglobin level exceeds 30% or if signs or symptoms of methemoglobinemia are present.


The use of the chelating agent  dimercaptopropane sulfonate has been proposed.


After inhalation of hexavalent or trivalent chromium compounds, patients should be removed from further exposure and assessed carefully.

If respiratory distress or cyanosis is noted, oxygen should be administered. Bronchospasm should be treated with bronchodilatators.

If the inhaled agent was chromic acid, continued observation and assessement should be considered, to note any developement of pulmonary edema up to 72 hours after exposure.

Similar precautions after the inhalation of other concentrated hexavalent, highly soluble compounds are prudent.

C-Dermal Absorption:

In cases of dermal absorption, the skin should be irrigated copiously with water. The affected area should be evaluated for the presence of chemical or thermal burns, and treatment should be provided as indicated.

The topical application of a freshly made 10% ascorbic acid solution or of a barrier cream containing 2% glycine and 1% tartaric acid has proved beneficial in some industrial settings in reducing  the consequences of topical exposure to hexavalent chromium compounds.

D-Laboratory Studies:

Specific measurements of chromate levels after exposure have not been shown to have prognostic or therapeutic value. However, it may allow further documentation of exposure and assessement of the efficacy of measures to enhance elimination.

Medical Measures:

A-Pre-employment examination:

It is recommended that before work assignments, where hexavalent chromium exposure is likely, that the following measures should be taken.

1-      History:

A detailed personal medical and work history should be reviewed by a physician familiar with the potential health risks of exposure to the specific chromium compounds.

2-      Physical examination:

A thorough general physical examination should be done, with a special attention to the skin, mucous membranes, and lungs. Those with skin lesions  and  chronic bronchitis should be discarded.

3-Chest X-ray:

A base line standard chest x-ray film should be obtained and retained indefinitely for future comparison.


Spirometry should be obtained to minimally include FVC, FEV1 and the FEV1/FVC, chiefly for base-line information.

5-Blood tests:

Blood tests to assure normal kidney and liver function should be performed.


Urinalysis should be obtained for the same reasons as in 5.

B-Periodical examination:

Once medically approved for hexavalent chromium compounds  exposure, items 1, 2 4, 5, 6 should be repeated annually. Also, beginning with the tenth year of exposure to carcinogenic chromium compounds, a standard chest x-ray and sputum cytology may also be helpful to verify that lung cancer has not developed.

If it is known with absolute certainty that the worker has never been exposed above the maximum allowable concentration, is a non-smoker, and has meticulous work habits, this precaution may be eliminated.

A special attention should be paid to the skin and nasal septum.

C-Biological Monitoring:

In persons non-occupationally exposed to chromium, the concentration of chromium in serum or plasma and in urine usually does not exceed 0.05µg/100ml and 5µg/ g creatinine, respectively.

The values reported by WHO (1988) and based on the data of the U.S. EPA (1978) range from 0.02 to 7 µg/100 ml in serum and plasma, and 0.5µg to 5.4µg/100 ml in red blood cells.

1-Biological exposure index (BEI):

ACGIH has determined two (2) biological exposure index (BEI) measures for hexavalent chromium compounds as a water-soluble fume.

a-BEI (#1):

Monitors the increase in total chromium in urine during a work shift, with an upper limit of 10µg per g of creatinine.

b-BEI (#2):

Samples the total urinary chromium at the end of the shift at the end of the work week, with an upper limit of 30 µg per g of creatinine.

Studies show that the predominant form of chromium recovered in blood and tissues, even after exposure to hexavalent chromium, is trivalent chromium because the hexavalent form is reduced to the trivalent form in tissues in biological media.  Reduction of Cr6+ to Cr3+ decreases the entry of chromium into cells and lessens intracellular and DNA damage.

Trivalent chromium is excreted mostly in the urine.

2-Erythrocyte Chromium:

Some researchers maintain that hexavalent chromium determination in erythrocytes is a more useful estimation of the body burden of hexavalent chromium after exposure.

When low chromium levels are found in the erythrocytes along with high urine chromium concentrations, extracellular reduction of hexavalent chromium is assumed to be sufficient for detoxification.

Technical Measures:

I-General Hygiene :

 - to conduct all dangerous operations (crushing of chromites, etc) in closed  containement;

- to carry out aspiration of fumes and dusts above the vats of electrolysis or to prevent the release of chromic acid mist by covering the bath of electrolysis by a liquid or solid screen . Suppressors of mist over the vats of chromium plating are currently used. They act either by reducing the surface tension of the liquid or by forming a thick foam barrier.

- to mechanically place and withdraw parts to be chromium plated;

- to add 0.1 to 0.2% ferrous sulphate to Portland cement to reduce the hexavalent chromium it contains. It was shown that this measure had a beneficial effect on exzematous contact dermatitis in Denmark.

- to add 1% zinc in welding wire, which causes a significant reduction in hexavalent chromium in welding fumes.

II-Personal Hygiene:

Depending on the type of compounds used, type and severity of exposure, it may be necessary to wear:

-special clothing: gloves, aprons;

- a hand cream or solution based on 10% ascorbic acid, or on sodium dithionite (Na2SO4), or on an ion exchange resin and or tartaric acid.

60% of the subjects sensitized to chromium can be protected completely or partially by the following formulation: silicone 10%, lactate of glycerol 2%, glycine 2%, tartaric acid 1%, excipient ad 100% .These preventive cutaneous treatments would be indicated in subjects allergic to chromium and who cannot, for various reasons, avoid any contact with chromium.

A zinc oxide or 10 % ascorbic acid ointment is also recommended to protect the nasal mucous membrane.
- an air adduction respiratory tract protection apparatus  when there are cancerogenic derivatives.

Exposure limits :

A-Quebec's exposure limits :

VEMP: Valeur d’Exposition Moyenne Pondérée:

Chromium compound



Chromium (metal)

0.5 mg/m3


Chromium II, compounds,

as Cr.

0.5 mg/m3


Chromium III, compounds,

as Cr. 

0.5 mg/m3


Chromium VI, certain water- insoluble compounds,

as Cr.  

0.05 mg/m3

C1, RP, EM

Chromium VI, water- soluble compounds,

as Cr.

0.05 mg/m3


C1 = Confirmed carcinogen to humans

RP =  Substance whose recirculation is prohibited in accordance with the law

EM = Substance that should be kept at the lowest practicable level

B-NIOSH’s IDLH (Immediately Dangerous to Life and Health):

Chromium compound

Air Concentration

Metallic chromium

250 mg Cr/m3

Insoluble chromium salts

500 mg Cr/m3

Soluble divalent salts


250 mg Cr/m3

Soluble trivalent salts

25 mg Cr/m3

Hexavalent chromium compounds and chromic acid

15 mg CrO3/m3


Chromium toxicity varies with particular chromium compounds.

Metallic chromium, divalent, and trivalent chromium compounds generally are less toxic than hexavalent compounds.

Trivalent compounds, such as green chromium oxide used by potters, do not appear to cause other effects associated with the hexavalent chromium compounds, such as chrome ulcers (hands and forearms), nasal septal perforation, lung cancer, etc.
Hexavalent chromium compounds are dangerous after acute substantial exposure.

Certain hexavalent chromium compounds have been demonstrated to be carcinogenic.

The optimal treatment for chromium toxicity lies in its prevention, with the use of good industrial hygiene practices, proper workplace industrial controls and good personal hygiene measures.

Edouard Bastarache M.D. (Occupational & Environmental Medicine)

Author of Substitutions for raw ceramic materials




1-Occupational Medicine,Carl Zenz, last edition.
2-Clinical Environmental Health and Toxic Exposures, Sullivan & Krieger; last edition.
3-Sax’s Dangerous Properties of Industrial Materials, Lewis C., last edition.

4-Toxicologie Industrielle et Intoxications Professionnelles, Lauwerys R. last edition.

5-Chemical Hazards of the Workplace, Proctor & Hughes, 4th edition.


Many thanks to Edouard Bastarache for this and previous contributions.

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Ceramic Toxic Materials
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