Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

CHROMIUM PICOLINATE

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Chromium picolinate or chromium tripicolinate is a bidentate complex of one molecule of trivalent chromium combined with three molecules of picolinic acid through both the pyridine nitrogen and the carboxyl carbon and it is the biologically active form of chromium.
    B) Chromium III chelated to picolinate is not a true herbal product, rather a heavy metal and an isomer of niacin and considered a trace metal and an essential micronutrient.

Specific Substances

    1) Chromium Tripicolinate
    2) Tris (2-pyridinecarboxylato-N(1), O(2)) chromium
    3) Chromium(III) trispicolinate
    4) C(18)H(12)CrN(3)O(6)

Available Forms Sources

    A) FORMS
    1) Chromium picolinate is available in tablet or chewable form and can be found in health or nutritional stores. Additional ingredients in chromium picolinate supplements can include niacin and pyridoxine (Chavez, 1997; Haddad et al, 1998).
    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.
    C) USES
    1) Chromium picolinate is a dietary supplement used for its proposed benefits for improving fasting blood glucose and glycosylated hemoglobin in patients with noninsulin dependent diabetes mellitus, promoting the development of lean body mass, and having beneficial effects on cholesterol profiles (Press & Geller, 1990; Mertz, 1993; Lee & Reasner, 1994; Lukaski et al, 1996).

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 picolinate is a dietary supplement used for its proposed benefits for improving fasting blood glucose and glycosylated hemoglobin in patients with noninsulin dependent diabetes mellitus, promoting the development of lean body mass, and having beneficial effects on cholesterol profiles.
    B) PHARMACOLOGY: Chromium is a naturally occurring pyridine-2-carboxylic acid metabolite of tryptophan. Picolinic acid (a natural ligand that is an isomer of nicotinic acid) improves the bioavailability of chromium and is an effective metal chelator. Trivalent chromium is an essential nutrient that has a role in carbohydrate, lipid, and nucleic acid metabolism by potentiating insulin action. Chromium deficiency has been observed in protein-calorie malnutrition and in patients receiving total parenteral nutrition (TPN) lacking in chromium supplementation.
    C) EPIDEMIOLOGY: Overdose is rare.
    D) WITH THERAPEUTIC USE
    1) Mild gastrointestinal disorders (ie, nausea, loose stools, constipation, and change in appetite) have occurred following nutritional supplementation with chromium picolinate.
    E) WITH POISONING/EXPOSURE
    1) Symptoms of chest pain, erythema/flushing, dizziness, headache, and agitation were reported in a small case series of adults exposed (acute or chronic) to chromium picolinate. Several cases of chronic chromium picolinate exposure in doses exceeding recommended daily allowance have resulted in renal failure, elevated hepatic enzymes, thrombocytopenia, hemolysis, anemia, and alterations in thought process (eg inability to concentrate). Rhabdomyolysis has been reported in one patient following an acute exposure.
    0.2.20) REPRODUCTIVE
    A) Chromium can be detected in breast milk.

Laboratory Monitoring

    A) Monitor vital signs, CBC, liver enzymes, renal function, and serum electrolytes in symptomatic patients following a significant acute exposure or chronic use which exceeds 200 mcg/day.
    B) Monitor serum electrolytes and creatine kinase (CK) in patients with complaints of muscle pain or weakness. Rhabdomyolysis has been reported in one female body builder.
    C) Serum or urine chromium concentrations can confirm exposure but are not useful to guide therapy. Normal serum and urine chromium concentrations are 0.1 to 0.3 mcg/L and less than 40 mcg/L , respectively.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF TOXICITY
    1) Treatment is symptomatic and supportive.
    B) DECONTAMINATION
    1) PREHOSPITAL: Acute toxicity is limited, GI decontamination is generally not necessary.
    2) HOSPITAL: Toxicity has generally only been reported after chronic ingestion. Gastrointestinal decontamination is generally not indicated. Activated charcoal should be considered after very large exposures or when other potentially toxic coingestants are involved.
    C) AIRWAY MANAGEMENT
    1) Airway management is very unlikely to be necessary unless other toxic agents have been administered concurrently.
    D) ANTIDOTE
    1) None.
    E) ENHANCED ELIMINATION PROCEDURE
    1) Chromium is widely distributed throughout the body and can be concentrated in many tissues; hemodialysis is not expected to remove significant amounts of chromium from the body. Hemodialysis has been used to treat acute renal failure associated with chronic excessive doses of chromium picolinate, but it did NOT decrease plasma chromium levels.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    2) OBSERVATION CRITERIA: Patients with deliberate ingestions, eye exposure, or symptoms should be sent to a health care facility for observation until they are clearly improving and clinically stable.
    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.
    G) PITFALLS
    1) Acute toxicity is limited, do not overtreat. Other etiologies for the patients symptoms should be sought. When managing a suspected overdose, the possibility of multiagent involvement should be considered.
    H) DIFFERENTIAL DIAGNOSIS
    1) Includes other agents that can cause renal dysfunction, thrombocytopenia, hemolysis, or rhabdomyolysis.

Range Of Toxicity

    A) TOXICITY: At the time of this review, a toxic dose in humans has not been established. Toxic effects have been reported after ingestion of 1200 to 2400 mcg/day for 4 to 5 months by an adult. A 24-year-old female body builder developed rhabdomyolysis following an ingestion of 1200 mcg of chromium picolinate over a 48-hour period. Of 16 children exposed to chromium picolinate (dose range, 100 to 6000 mcg), 5 were asymptomatic, 9 had minimal symptoms and 2 reported drowsiness which was felt to be unrelated.
    B) ADEQUATE INTAKE (AI): The recommended Adequate Intakes (AI) for chromium (based on average intake of chromium from food): ADULTS: MALE: 19 to 50 years: 35 mcg/day; greater than 50 years: 30 mcg/day. FEMALE: 19 to 50 years: 25 mcg/day; greater than 50 years: 20 mcg/day. PREGNANCY: 14 to 18 years: 29 mcg/day; 19 to 50 years: 30 mcg/day. LACTATION: 14 to 18 years: 44 mcg/day; 19 to 50 years: 45 mcg/day. INFANTS AND CHILDREN: 0 to 6 months: 0.2 mcg/day; 7 to 12 years: 5.5 mcg/day; 1 to 3 years: 11 mcg/day; 4 to 8 years: 15 mcg/day. MALE: 9 to 13 years: 25 mcg/day; 14 to 18 years: 35 mcg/day. FEMALE: 9 to 13 years: 21 mcg/day; 14 to 18 years: 24 mcg/day.

Clinical Effects

Summary Of Exposure

    A) USES: Chromium picolinate is a dietary supplement used for its proposed benefits for improving fasting blood glucose and glycosylated hemoglobin in patients with noninsulin dependent diabetes mellitus, promoting the development of lean body mass, and having beneficial effects on cholesterol profiles.
    B) PHARMACOLOGY: Chromium is a naturally occurring pyridine-2-carboxylic acid metabolite of tryptophan. Picolinic acid (a natural ligand that is an isomer of nicotinic acid) improves the bioavailability of chromium and is an effective metal chelator. Trivalent chromium is an essential nutrient that has a role in carbohydrate, lipid, and nucleic acid metabolism by potentiating insulin action. Chromium deficiency has been observed in protein-calorie malnutrition and in patients receiving total parenteral nutrition (TPN) lacking in chromium supplementation.
    C) EPIDEMIOLOGY: Overdose is rare.
    D) WITH THERAPEUTIC USE
    1) Mild gastrointestinal disorders (ie, nausea, loose stools, constipation, and change in appetite) have occurred following nutritional supplementation with chromium picolinate.
    E) WITH POISONING/EXPOSURE
    1) Symptoms of chest pain, erythema/flushing, dizziness, headache, and agitation were reported in a small case series of adults exposed (acute or chronic) to chromium picolinate. Several cases of chronic chromium picolinate exposure in doses exceeding recommended daily allowance have resulted in renal failure, elevated hepatic enzymes, thrombocytopenia, hemolysis, anemia, and alterations in thought process (eg inability to concentrate). Rhabdomyolysis has been reported in one patient following an acute exposure.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CHEST PAIN
    1) In a case series of 9 adults exposed (acute and chronic) to chromium picolinate, chest pain was reported in 2 patients (Gorman & Herrington, 1997).
    B) LACK OF INFORMATION
    1) THERAPEUTIC EFFECT
    a) Chromium picolinate supplements have been suggested in the treatment and prevention of hyperlipidemia. Press et al (1990) reported that healthy subjects (initial total cholesterol between 220 to 320 mg/dL) had a decrease in total cholesterol and LDL cholesterol with HDL cholesterol increased following chromium picolinate supplementation.
    b) In a small study of non-insulin dependent diabetes mellitus (NIDDM) subjects, triglyceride levels decreased by 17.4% over a 2 month period of oral chromium supplementation (200 mcg/day) (Lee & Reasner, 1994).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) DIZZINESS
    1) In a case series of 9 adults exposed (acute and chronic) to chromium picolinate, 1 reported dizziness (Gorman & Herrington, 1997).
    B) HEADACHE
    1) One study reported that in a case series of 9 adults ingesting chromium picolinate, 2 reported headache (Gorman & Herrington, 1997).
    C) PSYCHOMOTOR AGITATION
    1) In a case series (n=9), agitation developed in 1 adult following exposure to chromium picolinate (Gorman & Herrington, 1997).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) DRUG-INDUCED GASTROINTESTINAL DISTURBANCE
    1) WITH THERAPEUTIC USE
    a) Mild reports of gastrointestinal disturbances, following chromium picolinate ingestion, have included flatulence, nausea, loose stools, constipation, and an alteration in appetite (Chavez, 1997).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 33-year-old woman ingested 1200 to 2400 micrograms/day (6 to 12 times the maximum RDA) of chromium picolinate for 4 to 5 months to enhance weight loss and developed hepatic dysfunction along with acute renal failure, thrombocytopenia, and hemolysis. Initial AST (International Units/L) 1274, ALT (International Units/L) 992, and alkaline phosphatase (International Units/mL) 131. Supportive care included blood transfusions and hemodialysis with liver function improvement observed about 6 days following hospital admission. She had a history of schizophrenia and an eating disorder and had been treated with paroxetine and monthly fluphenazine injections until 2 weeks prior to admission (Cerulli et al, 1998).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 24-year-old man with a congenital solitary kidney developed acute renal failure (creatinine 4.1 mg/dL, BUN 28 mg/dL) after taking 1 or 2 capsules of a chromium picolinate supplement prior to workouts for 2 weeks. He required hemodialysis for 4 weeks, but renal function ultimately returned to normal. Renal biopsy was consistent with acute tubular necrosis (Wani et al, 2006).
    2) WITH POISONING/EXPOSURE
    a) CASE REPORTS
    1) A 33-year-old woman ingested 1200 to 2400 mcg/day (6 to 12 times the maximum RDA) of chromium picolinate for 4 to 5 months to enhance weight loss and developed acute renal failure along with thrombocytopenia, hemolysis, and hepatic dysfunction. The patient's initial serum creatinine was 5.3 milligrams/deciliter (peaked at 6.1 mg/dL); and BUN 152 milligrams/deciliter. Supportive measures included hemodialysis and blood transfusions. She had a history of schizophrenia and an eating disorder and had been treated with paroxetine and monthly fluphenazine injections until 2 weeks prior to admission (Cerulli et al, 1998).
    2) A 49-year-old woman taking chromium picolinate, 600 mcg daily for 6 weeks (3 times the recommended dietary dose), for weight loss developed chronically elevated renal enzymes (BUN 74 mg/dL, creatinine 5.9 mg/dL). The ingestion occurred 5 months prior to medical evaluation. A renal biopsy showed severe chronic active interstitial nephritis which responded to prednisone therapy; serum creatinine was decreased to 3.8 mg/dL within 2 months. The authors concluded that the effects were consistent with heavy-metal exposure (Wasser et al, 1997).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) THROMBOCYTOPENIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 33-year-old woman ingested 1200 to 2400 mcg/day (6 to 12 times the maximum RDA) of chromium picolinate for 4 to 5 months to enhance weight loss and developed thrombocytopenia and hemolysis along with acute renal failure and hepatic dysfunction. On admission, her hematocrit was 15.3% and platelet count was 15 (10(3)/mm(3)). Packed red blood cells and platelets were given with intravascular hemolysis stabilizing by hospital day 6 (Cerulli et al, 1998).
    B) ANEMIA
    1) WITH POISONING/EXPOSURE
    a) It has been suggested that doses greater that 200 mcg daily of chromium picolinate may lead to anemia (Cowart, 1992).
    b) CASE REPORT: A 33-year-old woman developed hemolytic anemia (hematocrit 15.3% on admission) along with thrombocytopenia, acute renal failure, and hepatic dysfunction following 4 to 5 months of chromium picolinate (1200 to 2400 mcg/day) supplementation (Cerulli et al, 1998).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) In a case series (n=9), erythema and flushing developed in 1 patient following exposure to chromium picolinate (Gorman & Herrington, 1997).
    B) CONTACT DERMATITIS
    1) CASE REPORT: Persistent systemic contact dermatitis was reported in an adult after taking dietary supplements for several weeks which contained chromium picolinate. Patch testing was positive for potassium dichromate at 2, 48, and 96 hours (Fowler, 2000).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 24-year-old woman body builder complained of muscle weakness, pain, and bilateral leg cramping. Approximately 2 days prior to admission, the patient began taking supplements containing chromium picolinate (added to an already complex dietary supplement regimen) and consumed approximately 1200 micrograms (6 to 24 times the recommended daily allowance). Relevant labs included: creatine kinase 22,260 Units/L, LDH 1914 Units/L, alanine aminotransferase (ALT) 158 Units/L, and aspartate aminotransferase (AST) 697 Units/L. Following pain management and intravenous hydration, the patient was asymptomatic and laboratory analysis had improved significantly by hospital day 4 (Martin & Fuller, 1998).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) ABNORMAL GLUCOSE LEVEL
    1) WITH THERAPEUTIC USE
    a) It has been suggested that individuals with noninsulin-dependent diabetes mellitus (NIDDM) may have lower levels of chromium (Chavez, 1997). Based on this theory, chromium supplementation could improve an impaired glucose tolerance (it has no apparent effect on a normal glucose tolerance).
    b) CASE SERIES: Blood glucose levels decreased by 32.6% from a mean of 14.3 mmol/liter (258 milligrams/deciliter) to a mean of 9.3 mmol/liter in 5 Native Americans with NIDDM given 200 mcg daily of chromium picolinate (no change in dietary or exercise habits occurred) for two weeks (Evans, 1991).
    c) CASE SERIES/NO EFFECT: In a small study of NIDDM subjects, Lee & Reasner (1994) reported no difference in fasting blood glucose concentration following a 2 month period of chromium supplementation (200 mcg/day) (Lee & Reasner, 1994).
    d) At the time of this review, it is not thought that blood glucose levels in healthy individuals are affected by the ingestion of chromium picolinate (McCarty, 1993; Chavez, 1997).

Reproductive

    3.20.1) SUMMARY
    A) Chromium can be detected in breast milk.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Chromium can be detected in breast milk (Anderson et al, 1993). The authors observed that breast milk chromium content was independent of dietary chromium intake and serum or urinary chromium values.

Carcinogenicity

    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) In vitro studies indicate that trivalent chromium induces DNA damage. Based on this data, the International Agency for Research on Cancer has categorized chromium(III) as "not classifiable as to carcinogenic potential" (Stearns et al, 1995). At the time of this review, further data is required to determine if trivalent chromium is a carcinogen.
    2) Chromium(III) has been found to accumulate in the body which has been supported by numerous animal and human studies (Stearns et al, 1995).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, CBC, liver enzymes, renal function, and serum electrolytes in symptomatic patients following a significant acute exposure or chronic use which exceeds 200 mcg/day.
    B) Monitor serum electrolytes and creatine kinase (CK) in patients with complaints of muscle pain or weakness. Rhabdomyolysis has been reported in one female body builder.
    C) Serum or urine chromium concentrations can confirm exposure but are not useful to guide therapy. Normal serum and urine chromium concentrations are 0.1 to 0.3 mcg/L and less than 40 mcg/L , respectively.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor renal function and hepatic enzymes in symptomatic patients following acute exposure or significant long-term chromium picolinate (doses above 200 micrograms/day) supplementation.
    2) Obtain CBC in symptomatic patients following significant exposure or chronic use which exceeds 200 micrograms/day.
    3) Serum chromium concentrations can confirm exposure but are not useful to guide therapy. Normal serum chromium concentrations are 0.1 to 0.3 mcg/L (Lee & Reasner, 1994).
    4) Monitor serum electrolytes and creatine kinase (CK) in patients with complaints of muscle pain or weakness. Rhabdomyolysis has been reported in one female body builder.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Urine chromium concentrations can confirm exposure but are not useful to guide therapy. Normal urinary chromium concentration should be less than 40 mcg/L (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) Lee & Reasner (1994) described a method to obtain serum chromium concentrations using flameless atomic absorption spectrometry. Normal serum concentrations are 0.1 to 0.3 microgram/liter (Lee & Reasner, 1994).

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 an 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 deliberate ingestions, eye exposure, or symptoms should be sent to a health care facility for observation until they are clearly improving and clinically stable.

Monitoring

    A) Monitor vital signs, CBC, liver enzymes, renal function, and serum electrolytes in symptomatic patients following a significant acute exposure or chronic use which exceeds 200 mcg/day.
    B) Monitor serum electrolytes and creatine kinase (CK) in patients with complaints of muscle pain or weakness. Rhabdomyolysis has been reported in one female body builder.
    C) Serum or urine chromium concentrations can confirm exposure but are not useful to guide therapy. Normal serum and urine chromium concentrations are 0.1 to 0.3 mcg/L and less than 40 mcg/L , respectively.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Acute toxicity is limited, GI decontamination is generally not necessary.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Most cases of toxicity reported have involved chronic ingestion of chromium picolinate. Gastrointestinal decontamination is generally not indicated. Activated charcoal should be considered after very large exposures or when other potentially toxic coingestants 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) Treatment is symptomatic and supportive.
    B) MONITORING OF PATIENT
    1) Monitor vital signs, CBC, liver enzymes, renal function, and serum electrolytes in symptomatic patients following a significant acute exposure or chronic use which exceeds 200 mcg/day.
    2) Monitor serum electrolytes and creatine kinase (CK) in patients with complaints of muscle pain or weakness. Rhabdomyolysis has been reported in one female body builder.
    3) Serum and urine chromium concentrations can confirm exposure but are not useful to guide therapy. Normal serum concentrations are 0.1 to 0.3 mcg/L. Urinary chromium concentration should be less than 40 mcg/L.

Enhanced Elimination

    A) HEMODIALYSIS
    1) SUMMARY: Chromium is widely distributed throughout the body and can be concentrated in many tissues (Haddad et al, 1998); hemodialysis is not expected to remove significant amounts of chromium from the body.
    2) CASE REPORT: Hemodialysis has been used to treat acute renal failure associated with chronic excessive doses of chromium picolinate, but it did NOT decrease plasma chromium levels. Serum creatinine was 5.3 mg/dL and plasma chromium concentration was 4.6 mcg/mL (normal 0.1 to 2.1) on admission. Hemodialysis was conducted on 8 different days during the patients 26 day hospital course with a discharge creatinine of 1.3 mg/dL. The patient's chromium level rose on the third day of dialysis to 6.5 mcg/mL and the authors suggested that this effect was due to redistribution of chromium (creating a concentration gradient) from the tissues into the blood. Chromium dialysance was not determined (Cerulli et al, 1998).

Range Of Toxicity

Summary

    A) TOXICITY: At the time of this review, a toxic dose in humans has not been established. Toxic effects have been reported after ingestion of 1200 to 2400 mcg/day for 4 to 5 months by an adult. A 24-year-old female body builder developed rhabdomyolysis following an ingestion of 1200 mcg of chromium picolinate over a 48-hour period. Of 16 children exposed to chromium picolinate (dose range, 100 to 6000 mcg), 5 were asymptomatic, 9 had minimal symptoms and 2 reported drowsiness which was felt to be unrelated.
    B) ADEQUATE INTAKE (AI): The recommended Adequate Intakes (AI) for chromium (based on average intake of chromium from food): ADULTS: MALE: 19 to 50 years: 35 mcg/day; greater than 50 years: 30 mcg/day. FEMALE: 19 to 50 years: 25 mcg/day; greater than 50 years: 20 mcg/day. PREGNANCY: 14 to 18 years: 29 mcg/day; 19 to 50 years: 30 mcg/day. LACTATION: 14 to 18 years: 44 mcg/day; 19 to 50 years: 45 mcg/day. INFANTS AND CHILDREN: 0 to 6 months: 0.2 mcg/day; 7 to 12 years: 5.5 mcg/day; 1 to 3 years: 11 mcg/day; 4 to 8 years: 15 mcg/day. MALE: 9 to 13 years: 25 mcg/day; 14 to 18 years: 35 mcg/day. FEMALE: 9 to 13 years: 21 mcg/day; 14 to 18 years: 24 mcg/day.

Therapeutic Dose

    7.2.1) ADULT
    A) ADEQUATE INTAKE (AI): The recommended Adequate Intakes (AI) for chromium, which is based on average intake of chromium from food, are listed below (Office of Dietary Supplements, 2005):
    1) MALE: 19 to 50 years: 35 mcg/day; greater than 50 years: 30 mcg/day
    2) FEMALE: 19 to 50 years: 25 mcg/day; greater than 50 years: 20 mcg/day
    3) PREGNANCY: 14 to 18 years: 29 mcg/day; 19 to 50 years: 30 mcg/day
    4) LACTATION: 14 to 18 years: 44 mcg/day; 19 to 50 years: 45 mcg/day
    7.2.2) PEDIATRIC
    A) ADEQUATE INTAKE (AI): The recommended Adequate Intakes (AI) for chromium, which is based on average intake of chromium from food, are listed below (Office of Dietary Supplements, 2005):
    1) INFANTS AND CHILDREN: 0 to 6 months: 0.2 mcg/day; 7 to 12 years: 5.5 mcg/day; 1 to 3 years: 11 mcg/day; 4 to 8 years: 15 mcg/day
    2) MALE: 9 to 13 years: 25 mcg/day; 14 to 18 years: 35 mcg/day
    3) FEMALE: 9 to 13 years: 21 mcg/day; 14 to 18 years: 24 mcg/day

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) CHRONIC
    a) A 49-year-old woman ingested 600 mcg/day of over-the-counter (OTC) chromium picolinate for 6 weeks for weight reduction and developed chronic renal failure (Wasser et al, 1997).
    b) A 33-year-old woman ingested 1200 to 2400 mcg/day of OTC chromium picolinate tablets for 4 to 5 months for weight reduction and developed thrombocytopenia, hemolysis, hepatic dysfunction, and acute renal failure (Cerulli et al, 1998).
    2) PEDIATRIC
    a) Of 16 children exposed to chromium picolinate (dose range 100 to 6000 mcg), 5 were asymptomatic, 9 had minimal symptoms and 2 reported drowsiness which was felt to be unrelated (Gorman & Herrington, 1997).
    3) ADULT
    a) A 24-year-old female body builder developed rhabdomyolysis following an ingestion of 1200 micrograms of chromium picolinate over a 48 hour period. Initial creatine kinase was 22,260 Units/L which improved with intravenous hydration and supportive care (Martin & Fuller, 1998).

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).
    2) CHRONIC
    a) Following a 4 to 5 month exposure of daily chromium picolinate (between 1200 to 2400 micrograms/day) a 33-year-old female developed thrombocytopenia, hepatic dysfunction, and acute renal failure and was hospitalized with a chromium concentration of 4.6 micrograms/milliliter (normal 0.1. to 2.1 micrograms/milliliter) (Cerulli et al, 1998).

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Chromium is a naturally occurring pyridine-2-carboxylic acid metabolite of tryptophan (Chavez, 1997). Picolinic acid (a natural ligand that is an isomer of nicotinic acid) improves the bioavailability of chromium and is an effective metal chelator (Press & Geller, 1990; Chavez, 1997).
    B) 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).
    C) Chromium picolinate has been evaluated in limited studies in patients with non-insulin-dependent diabetes mellitus (NIDDM) as a possible adjunct to therapy to improve glucose tolerance (Evans, 1991; Chavez, 1997).
    D) Athletes have used chromium picolinate to aid in glucose utilization and to increase lean body mass (Ellenhorn et al, 1997).

Physicochemical

Molecular Weight

    A) 418.31 (Budavari, 1996)

References

General Bibliography

    1) Anderson RA & Kozlovsky AS: Chromium intake, absorption and excretion of subjects consuming self-selected diets. Am J Clin Nutr 1985; 41:1177-1183.
    2) Anderson RA, Bryden NA, & Patterson KY: Breast milk chromium and its association with chromium intake, chromium excretion, and serum chromium. Am J Clin Nutr 1993; 57:519-523.
    3) Anderson RA, Polansky MM, & Bryden NA: Effects of chromium supplementation on urinary Cr excretion of human subjects an correlation of Cr excretion with selected clinical parameters. J Nutr 1983; 113:276-281.
    4) Budavari S: The Merck Index, (12th ed), Merck & Co, Inc, Whitehouse Station, NJ, 1996.
    5) Cerulli J, Grabe DW, & Gauthier I: Chromium picolinate toxicity. Ann of Pharmacotherapy 1998; 32:428-430.
    6) Chavez ML: Chromium picolinate. Hospital Pharmacy 1997; 32:1466-1478.
    7) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    8) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology (4th Ed). Part C Toxicology, II, John Wiley & Sons Inc, New York, NY, 1994.
    9) Cowart VS: Sizing up a few supplements. Phys & Sportsmed 1992; 20:190-191.
    10) Ellenhorn MJ, Schonwald S, & Ordog G: Ellenhorn's Medical Toxicology: Diagnosis & treatment of human poisoning, 2nd ed, Williams & Wilkins, Baltimore, MD, 1997.
    11) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    12) Evans GW: An inexpensive, convenient adjunct for the treatment of diabetes (letter). West J Med 1991; 155:549.
    13) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    14) Fowler JF: Systemic contact dermatitis caused by oral chromium picolinate. Cutis 2000; 65:116.
    15) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    16) Gorman SE & Herrington LF: Chromium picolinate: The (nontoxic?) wonder mineral! (abstract). J Tox - Clin Tox 1997; 35:546.
    17) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    18) Haddad LM, Shannon MW, & Winchester JF: Clinical Management of Poisoning and Drug Overdose, 3rd ed, WB Saunders Company, Philadelphia, PA, 1998.
    19) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    20) Huszonek J: Over-the-counter chromium picolinate (letter). Am J Psych 1993; 150:1560-1561.
    21) Katz SA & Salem H: The toxicology of chromium with respect to its chemical speciation: a review. J Appl Toxicol 1993; 13:217-224.
    22) Lee NA & Reasner CA: Beneficial effect of chromium supplementation on serum triglyceride levels in NIDDM. Diabetes Care 1994; 17:1449-1452.
    23) Lukaski HC, Bolonchuk WW, & Siders WA: Chromium supplementation and resistance training: effects on body composition, strength, and trace element status of men. Am J Clin Nutr 1996; 63:954-965.
    24) Martin WR & Fuller RE: Suspected chromium picolinate-induced rhabdomyolysis. Pharmacotherapy 1998; 18:860-862.
    25) McCarty MF: Homologuous physiological effects on phenformin and chromium picolinate. Med Hypotheses 1993; 41:316-324.
    26) Mertz W: Chromium in human nutrition: a review. J Nutr 1993; 123:626-633.
    27) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    28) Office of Dietary Supplements: Dietary Supplement Fact Sheet: Chromium. National Institutes of Health. Bethesda, MD. 2005. Available from URL: http://ods.od.nih.gov/factsheets/Chromium-HealthProfessional/. As accessed 2013-10-01.
    29) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    30) Press RI & Geller J: The effect of chromium picolinate on serum cholesterol and apolipoprotein fractions in human subjects. West J Med 1990; 152:41-45.
    31) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    32) Stearns DM, Belbruno JJ, & Wetterhahn K: A prediction of chromium(III) accumulation in humans from chromium dietary supplements. FASEB J 1995; 9:1650-1657.
    33) Wani S, Weskamp C, Marple J, et al: Acute tubular necrosis associated with chromium picolinate-containing dietary supplement. Ann Pharmacother 2006; 40(3):563-566.
    34) Wasser WG, Feldman NS, & D'Agati VD: Chronic renal failure after ingestion of over-the-counter chromium picolinate. Ann Intern Med 1997; 126(5):410-.