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CHROMIUM (III)

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Chromium may be found in the environment in two major forms, hexavalent chromium (chromate) and the most abundant form, trivalent chromium. Trivalent (III) form does not enter the body readily and is of a low order of toxicity, but the hexavalent (VI) form does and is known to cause significant damage.
    B) In compounds, chromium demonstrates oxidation numbers (+2 through +6) with trivalent chromium the most stable.
    C) Refer to "CHROMIUM, HEXAVALENT" Poisindex(R) or Meditext(R) managements for further information.
    D) Refer to "CHROMIUM, PICOLINATE" Poisindex(R) management for further information.

Specific Substances

    1) CHROMIC ION
    2) CHROMIUM (3+)
    3) CHROMIUM (III)
    4) CHROMIUM (III) CATION
    5) CHROMIUM (III) ION
    6) CHROMIUM ION (3+)
    7) CHROMIUM ION (Cr3+)
    8) CHROMIUM [TRIVALENT]
    9) Molecular Formula: Cr
    10) CAS 16065-83-1
    11) 16065-83-1 CAS
    1.2.1) MOLECULAR FORMULA
    1) Cr

Available Forms Sources

    A) FORMS
    1) Chromic compounds, Cr (III), are stable and form many commercially used compounds. These include chromic oxide and chromium sulfate (ILO, 1998).
    2) Chromic oxide, a trivalent chromium compound, is the most important chromium compound. It is used as a pigment and is also known as chromic oxide green (Clayton & Clayton, 1994).
    3) Trivalent chromium compounds resemble aluminum (+3) compounds (Clayton & Clayton, 1994).
    4) Trivalent salts can be found in enamel used in the manufacture of kitchen ranges. During the manufacturing process at one plant, the trivalent salts were discovered to convert to hexavalent salts when in contact with the hooks carrying the ranges during the baking process and subsequently caused an outbreak of hand ulceration among workers (Deng et al, 1990).
    B) SOURCES
    1) Chromium can be found in foods. Brewer's yeast, beer, oysters, mushrooms and meats (especially kidney) are good sources of chromium. Some researchers have suggested that low serum levels of chromium may be due to diets high in processed or refined foods.
    2) Trivalent chromium naturally exists in the environment. It is also the most abundant form of chromium in the environment (Clayton & Clayton, 1994).
    3) Normally, trivalent chromium is found as free ionized, protein bound (mainly transferrin), or as a component of the glucose tolerance factor (GTF, Cr-nicotinic acid-amino acid complex) (Leung, 1995).
    C) USES
    1) Trivalent chromium promotes metabolism of glucose, fat, and protein by facilitating the action of insulin in humans and animals. Chromium (III) deficiency can cause impaired glucose metabolism and increased risk of cardiovascular disease (Leung, 1995; Clayton & Clayton, 1994).
    2) Chromium in the +3 oxidation state {Cr(III)} is a trace element that is used by body builders to enhance glucose utilization and increase lean body mass (Katz & Salem, 1993; Ellenhorn et al, 1997).
    3) The National Research Council recommends a daily allowance of 50 to 200 mcg. Men given 200 mcg Cr (III)/day while enlisted in a daily weight training program increased their lean body mass (ATSDR, 1993; (Clayton & Clayton, 1994).
    4) Trivalent chromium compounds are used to make pigments and in the leather tanning process (ATSDR, 1993).
    5) Chromium compounds are used medically in astringents and antiseptics (HSDB , 2001).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Chromium in the +3 oxidation state [Cr(III)] is a trace element that is used by body builders to enhance glucose utilization and increase lean body mass. The National Research Council recommends a daily allowance of 50 to 200 mcg. Trivalent chromium compounds are used to make pigments and in the leather tanning process. Chromium compounds are used medically in astringents and antiseptics.
    B) PHARMACOLOGY: Trivalent chromium is an essential nutrient that promotes metabolism of glucose, fat, and protein by facilitating the action of insulin in humans and animals. Chromium (III) deficiency can cause impaired glucose metabolism and increased risk of cardiovascular disease. Chromium deficiency has been observed in protein-calorie malnutrition and in patients receiving total parenteral nutrition (TPN) lacking in chromium supplementation.
    C) EPIDEMIOLOGY: Exposure is common, but serious toxicity is rare.
    D) WITH POISONING/EXPOSURE
    1) Chromium metal is relatively nontoxic. There is little evidence of substantial toxicity from chromic salts (trivalent chromium), probably because of poor skin and mucous membrane penetration. Trivalent chromium compounds are considered less toxic than hexavalent chromium compounds. It is considered an irritant and contact dermatitis has been reported with exposure. Long-term exposure to chromium may cause chronic bronchitis, sinusitis, rhinitis, asthma, and a type of pneumoconiosis. The sweat-gland lesions that appear after exposure to hexavalent chromium may result from its reduction to trivalent chromium after absorption, and subsequent formation of antigen-antibody complexes. Hexavalent chromium and the supplement chromium picolinate are covered in separate managements. Refer to "CHROMIUM, HEXAVALENT" and "CHROMIUM, PICOLINATE" managements for further information.
    0.2.20) REPRODUCTIVE
    A) Trivalent and hexavalent chromium compounds were embryotoxic and teratogenic in animals.
    0.2.21) CARCINOGENICITY
    A) Chromium III is not classifiable as a human carcinogen (ACGIH, 2002).

Laboratory Monitoring

    A) No routine laboratory studies are needed unless otherwise clinically indicated.
    B) If respiratory tract irritation is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) Obtain serum and urine chromium levels in symptomatic patients. However, serum and urine concentrations are not readily available or clinically useful in the management of overdose.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Minimal toxicity is expected after an acute ingestion. Treatment is symptomatic and supportive.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Significant toxicity is not expected.
    C) DECONTAMINATION
    1) PREHOSPITAL: Prehospital gastrointestinal decontamination is generally not necessary.
    2) HOSPITAL: Severe toxicity is not expected. Gastrointestinal decontamination is generally not necessary. Consider activated charcoal only after very large ingestions or if coingestants with significant toxicity are involved.
    D) AIRWAY MANAGEMENT
    1) Airway management is very unlikely to be necessary unless other toxic agents have been administered concurrently. Ensure adequate ventilation and perform endotracheal intubation early in patients with severe respiratory distress.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION
    1) Hemodialysis is not recommended given the low toxicity of this drug.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: A patient with a small inadvertent exposure, that remains asymptomatic, can be managed at home.
    2) OBSERVATION CRITERIA: Patients with a deliberate overdose, and those who are symptomatic, should be sent to a healthcare facility for evaluation.
    3) ADMISSION CRITERIA: Patients who remain symptomatic despite treatment should be admitted.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    H) PITFALLS
    1) Failure to obtain a complete history of other possible ingestions or etiologies for the patient's symptoms. History of exposure may be difficult to obtain in some settings.
    I) DIFFERENTIAL DIAGNOSIS
    1) Includes other agents that may cause contact dermatitis or respiratory distress.

Range Of Toxicity

    A) TOXICITY: At the time of this review, a toxic dose in humans has not been established. It has been estimated that hexavalent chromium compounds are 10 to 100 times more toxic than trivalent compounds by the oral route.

Clinical Effects

Summary Of Exposure

    A) USES: Chromium in the +3 oxidation state [Cr(III)] is a trace element that is used by body builders to enhance glucose utilization and increase lean body mass. The National Research Council recommends a daily allowance of 50 to 200 mcg. Trivalent chromium compounds are used to make pigments and in the leather tanning process. Chromium compounds are used medically in astringents and antiseptics.
    B) PHARMACOLOGY: Trivalent chromium is an essential nutrient that promotes metabolism of glucose, fat, and protein by facilitating the action of insulin in humans and animals. Chromium (III) deficiency can cause impaired glucose metabolism and increased risk of cardiovascular disease. Chromium deficiency has been observed in protein-calorie malnutrition and in patients receiving total parenteral nutrition (TPN) lacking in chromium supplementation.
    C) EPIDEMIOLOGY: Exposure is common, but serious toxicity is rare.
    D) WITH POISONING/EXPOSURE
    1) Chromium metal is relatively nontoxic. There is little evidence of substantial toxicity from chromic salts (trivalent chromium), probably because of poor skin and mucous membrane penetration. Trivalent chromium compounds are considered less toxic than hexavalent chromium compounds. It is considered an irritant and contact dermatitis has been reported with exposure. Long-term exposure to chromium may cause chronic bronchitis, sinusitis, rhinitis, asthma, and a type of pneumoconiosis. The sweat-gland lesions that appear after exposure to hexavalent chromium may result from its reduction to trivalent chromium after absorption, and subsequent formation of antigen-antibody complexes. Hexavalent chromium and the supplement chromium picolinate are covered in separate managements. Refer to "CHROMIUM, HEXAVALENT" and "CHROMIUM, PICOLINATE" managements for further information.

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) Long-term exposure to chromium may cause chronic bronchitis, sinusitis, rhinitis, asthma, and a type of pneumoconiosis (Nadig, 1998).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Leather products may cause chromium dermatitis. Although only chromium III is used for tanning, small amounts of chromium hexavalent may be found in the final leather product due to oxidation of chromium III during the tanning process. Therefore, both chromium hexavalent and chromium III can cause dermatitis at low levels in the leather user (Hansen et al, 2003).
    a) Two workers developed work-related allergic contact dermatitis of the hands, arms, and legs from trivalent chromium in leather tanning (Estlander et al, 2000).
    2) The majority of occupational dermatitis occurs secondary to exposure to hexavalent chromium. It is believed that the sweat-gland lesions that appear after exposure to hexavalent chromium may result from its reduction to trivalent chromium after absorption, and subsequent formation of antigen-antibody complexes (Milner, 1980).
    3) A high incidence of chromium sensitivity (contact dermatitis) has been reported in Israeli women following exposure to detergents and bleaches. Testing showed that the chromium concentration was greater than 5 ppm in 56% of the consumer products tested and between 1 and 5 ppm in 32% of the consumer products tested (Ingber et al, 1998).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Leather products may cause chromium dermatitis. Although only chromium III is used for tanning, small amounts of chromium hexavalent may be found in the final leather product due to oxidation of chromium III during the tanning process. Therefore, both chromium hexavalent and chromium III can cause dermatitis at low levels in the leather user (Hansen et al, 2003).
    b) Two workers developed work-related allergic contact dermatitis of the hands, arms, and legs from trivalent chromium in leather tanning (Estlander et al, 2000).
    c) Chromium III compounds do not cause allergic sensitization as frequently as hexavalent chromium compounds, probably due to their low solubility (Nadig, 1998).

Reproductive

    3.20.1) SUMMARY
    A) Trivalent and hexavalent chromium compounds were embryotoxic and teratogenic in animals.
    3.20.2) TERATOGENICITY
    A) EMBRYOTOXICITY
    1) ANIMAL STUDY - Trivalent and hexavalent chromium compounds were embryotoxic and teratogenic in animals (Elbetieha & Al-Hamood, 1997).
    2) Animal studies have shown that the long-term exposure of male and female mice to trivalent and hexavalent chromium compounds would cause adverse effects on fertility and reproduction (e.g., reduced fertility, reduced implantation sites, increased number of resorptions and dead fetuses) (Elbetieha & Al-Hamood, 1997).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS16065-83-1 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Chromium III compounds
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.2) SUMMARY/HUMAN
    A) Chromium III is not classifiable as a human carcinogen (ACGIH, 2002).
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) Increased incidence of LUNG CANCER among workers in the manufacture of chrome pigments has been reported in Germany, Norway, Canada, and the United States (ACGIH, 1996a; HSDB , 2001). Exposures were generally mixed, involving both trivalent and hexavalent chromium compounds. Relative risk for lung cancer has been in the range of 3- to 50-fold, with a latent period of as much as 36 years (Clayton & Clayton, 1994).

Genotoxicity

    A) DNA adduct was noted in mouse ascites tumor and E coli at 5 micromol/L.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No routine laboratory studies are needed unless otherwise clinically indicated.
    B) If respiratory tract irritation is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) Obtain serum and urine chromium levels in symptomatic patients. However, serum and urine concentrations are not readily available or clinically useful in the management of overdose.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor serum chromium levels in symptomatic patients. Normal serum concentrations are 0.1 to 0.3 mcg/L (Lee & Reasner, 1994).
    B) ARTERIAL BLOOD GASES
    1) If respiratory tract irritation is evident, monitor pulse oximetry and/or arterial blood gases, chest x-ray, and pulmonary function tests.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Monitor urine chromium levels in symptomatic patients. Urinary chromium concentration should be less than 40 micrograms/liter (Haddad et al, 1998). Absorbed chromium is excreted primarily in the urine; therefore, urinary chromium excretion can be used as a fairly accurate estimation of the amount of chromium absorbed (Anderson & Kozlovsky, 1985; Anderson et al, 1983).

Methods

    A) SPECTROMETRY
    1) Lee & Reasner (1994) described a method to determine serum chromium concentrations using flameless atomic absorption spectrometry. Normal serum concentrations are 0.1 to 0.3 microgram/liter (Lee & Reasner, 1994).
    2) Although chromium concentrations can be measured in the blood and urine, measurements of blood or red blood cell chromium is difficult due to contamination during collection and analysis (Goldfrank et al, 1998).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients who remain symptomatic despite treatment should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) A patient with a small inadvertent exposure, that remains asymptomatic, can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with a deliberate overdose, and those who are symptomatic, should be sent to a healthcare facility for evaluation.

Monitoring

    A) No routine laboratory studies are needed unless otherwise clinically indicated.
    B) If respiratory tract irritation is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) Obtain serum and urine chromium levels in symptomatic patients. However, serum and urine concentrations are not readily available or clinically useful in the management of overdose.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Minimal toxicity is expected after an acute ingestion. Prehospital gastrointestinal decontamination is generally not necessary.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Severe toxicity is not expected. Gastrointestinal decontamination is generally not necessary. Consider activated charcoal only after very large ingestions or if coingestants with significant toxicity are involved.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Minimal toxicity is expected after an acute ingestion. Treatment is symptomatic and supportive.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Significant toxicity is not expected.
    B) MONITORING OF PATIENT
    1) No routine laboratory studies are needed unless otherwise clinically indicated.
    2) If respiratory tract irritation is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    3) Obtain serum and urine chromium levels in symptomatic patients. However, serum and urine concentrations are not readily available or clinically useful in the management of overdose.

Dermal Exposure

    6.9.2) TREATMENT
    A) DECONTAMINATION
    1) Wash the exposed area with water for 15 minutes. A physician may need to examine the exposed area if irritation or pain persists. Some authors have recommended dermal irrigation for 15 minutes with a 10% ascorbic acid solution for hexavalent chromium decontamination. Ascorbic acid will reduce the more toxic chromium (VI) to the less toxic chromium (III) ion (Bradberry & Vale, 1999; Milner, 1980; Korallus et al, 1984). Unless a mixed exposure, there is no proven benefit to the use of ascorbic acid for chromium (III) compound decontamination.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis is not recommended given the low toxicity of this drug.

Range Of Toxicity

Summary

    A) TOXICITY: At the time of this review, a toxic dose in humans has not been established. It has been estimated that hexavalent chromium compounds are 10 to 100 times more toxic than trivalent compounds by the oral route.

Therapeutic Dose

    7.2.1) ADULT
    A) ROUTE OF ADMINISTRATION
    1) ORAL - At the time of this review the National Research Council has recommended a daily chromium intake of 50 to 200 micrograms, based on an average intake of 50 micrograms/day and resulting in no signs of deficiency (Clayton & Clayton, 1994) Ellenhorn, 1997). The minimum suggested safe and adequate chromium intake is 50 micrograms/day as recommended by the US National Academy of Sciences (Anderson et al, 1991).

Maximum Tolerated Exposure

    A) SUMMARY
    1) Exposure to trivalent chromium appears to be less toxic than hexavalent chromium (Katz & Salem, 1993; Haddad et al, 1998).
    2) It has been estimated that hexavalent chromium compounds are 10 to 100 times more toxic than trivalent compounds by the oral route (Katz & Salem, 1993).
    B) ADULT
    1) 236 ferrochromite workers exposed to an average concentration of 0.075 mg Cr (III)/ m(3) were not found to have any renal impairment (ATSDR, 1993).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) NORMAL VALUES - The mean serum chromium level in healthy individuals is between 0.1 mcg/L to 0.3 mcg/L (Chavez, 1997).

Workplace Standards

    A) ACGIH TLV Values for CAS16065-83-1 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Chromite ore processing (Chromate), as Cr
    a) TLV:
    1) TLV-TWA: 0.05 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A1
    2) Codes: Not Listed
    3) Definitions:
    a) A1: Confirmed Human Carcinogen: The agent is carcinogenic to humans based on the weight of evidence from epidemiologic studies.
    c) TLV Basis - Critical Effect(s): Lung cancer
    d) Molecular Weight:
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS16065-83-1 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Chromium(III) compounds (as Cr)
    2) REL:
    a) TWA: 0.5 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix C
    3) IDLH:
    a) IDLH: 25 mg Cr(III)/m3 [as Cr(III)]
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS16065-83-1 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A1 ; Listed as: Chromite ore processing (Chromate), as Cr
    a) A1 :Confirmed Human Carcinogen: The agent is carcinogenic to humans based on the weight of evidence from epidemiologic studies.
    2) EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Chromium(III), insoluble salts
    a) D : Not classifiable as to human carcinogenicity.
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Chromium III compounds
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Chromium(III) compounds (as Cr)
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS16065-83-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: (ATSDR, 1993; NIOSH, 1996
    1) LD50- (ORAL)MOUSE:
    a) 110 mg Cr (III)/kg (NIOSH, 1996)
    2) LD50- (ORAL)RAT:
    a) Female, 183 mg Cr (III)/kg/day for 1 D
    b) Male, 200 mg Cr (III)/kg/day for 1 D
    c) 2365 mg Cr (III)/kg/day for 1 D
    d) 1870 mg Cr (III)/kg (NIOSH, 1996)
    e) 3250 mg Cr (III)/kg (NIOSH, 1996)
    7.7.2) RISK ASSESSMENT VALUES
    A) References: (ATSDR, 1993; NIOSH, 1996. Values are from ATSDR, 1993, unless otherwise noted.
    1) LOAEL- (INHALATION)HUMAN:
    a) 0.25 mg insoluble Cr (III)/m(3) - occupational exposure for 1 to 7 years; outcome measured was cancer effect level for the lungs.
    2) NOAEL- (UNASSIGNED)HUMAN:
    a) 0.075 mg Cr (III)/m(3) for 2-12 Y -- no damage to renal system as a result of occupational exposure.
    b) 1.99 mg Cr (III)/m(3) -- no damage to respiratory or hematological systems as a result of occupational exposure
    3) NOAEL- (ORAL)RAT:
    a) 1806 mg Cr (III)/kg/day for 90 D, 5 D/W -- no damage to the respiratory, cardiovascular, gastrointestinal, hematological, hepatic, renal, or reproductive systems; healthy offspring produced.
    b) 2.7 mg Cr (III)/kg/day for 7 D/W for 1 Y -- no damage to the hematological, hepatic, or renal systems
    c) 3.5 mg Cr (III)/kg/day for 7 D/W for 1 Y -- no damage to the hematological, hepatic, or renal systems
    d) 0.46 mg Cr (III)/kg/day for 7 D/W for 2-3 Y -- no damage to the cardiovascular, hepatic, or renal systems
    e) 2040 mg Cr (III)/kg/day for 5 D/W for 2 Y-- no damage to the respiratory, cardiovascular, gastrointestinal, hepatic, or renal systems

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Trivalent chromium is an essential nutrient that has a role in carbohydrate, lipid, and nucleic acid metabolism by potentiating insulin action (Clayton & Clayton, 1994; Katz & Salem, 1993). Chromium deficiency has been observed in protein-calorie malnutrition and in patients receiving total parenteral nutrition (TPN) lacking in chromium supplementation (Katz & Salem, 1993).
    B) Picolinic acid (a natural ligand that is an isomer of nicotinic acid) improves the bioavailability of chromium and is an effective metal chelator (Press et al, 1990; (Chavez, 1997).

Physicochemical

Physical Characteristics

    A) Trivalent chromium compounds are amphoteric (Clayton & Clayton, 1994). The majority of trivalent chromium compounds are insoluble in water. Exceptions include acetate, nitrate, and chromium (III) chloride-hexahydrate salts (ATSDR, 1993).

Molecular Weight

    A) 52.00 (RTECS , 2000)

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
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