CADMIUM

Cadmium is used to form a variety of alloys, including Lightenberg's, Abel's, Lipowitz', Newton's, and Wood's metal (HSDB , 2000).
Cadmium is a component of dental amalgam, Ni-Cd batteries, welding rods, control rods, television phosphors, artists' pigments, process engraving, rectifiers, semiconductors, solar cells, scintillation counters, dry film lubricants, and automotive paints, among others (ACGIH, 1991) ACGIH, 1996; (Budavari, 1996; Clayton & Clayton, 1994; Hathaway et al, 1996; Sittig, 1991).

FORMS

Cadmium is a soft, ductile, silver-white, somewhat bluish metal (Ashford, 1994; Budavari, 1996; Hathaway et al, 1996).
Cadmium can be purchased as bars, granules, foil, ingots, powder, rod, sheets, single crystals, and wire (Ashford, 1994; Budavari, 1996).
FOOD

The provisional tolerable weekly intake (PTWI) of cadmium (the dietary exposure level that can be ingested weekly over a lifetime without appreciable health risk) - 7 mcg/kg of body weight. This information has been obtained from the Joint FAO/WHO Expert Committee on Food Additives and Contaminants (JECFA), a scientific advisory body of the Codex Committee on Food Additives and Contaminants (CCFAC). This PTWI was established in the 33rd meeting in 1988 and has been maintained at the 61st meeting in 2003(Horiguchi et al, 2004).
In one study, dietary cadmium exposure at close to the current provisional tolerable weekly intake (PTWI) of cadmium, did not affect renal function among female Japanese rice farmers (Horiguchi et al, 2004).
Daily cadmium intake from food averages 10 to 25 mcg/day (Friberg et al, 1985).

Shellfish such as mussels, scallops, and oysters may be a major source of dietary cadmium, and may contain 100 to 1,000 mcg/kg. Shellfish accumulate cadmium from water; it subsequently binds to cadmium-binding peptides in the shellfish (Horiguchi et al, 2004; Klaassen et al, 1986).
Cadmium from polluted water and soil may also accumulate in animal livers, mushrooms, or cereals such as rice and wheat (Horiguchi et al, 2004).

Itai-itai is an endemic disease in Japan, a result of increased dietary intake of cadmium (Murata et al, 1970). These patients experience renal tubular dysfunction, multiple bone fractures due to osteomalacia, and renal anemia (Horiguchi et al, 2004).

Cases of poisoning have followed ingestion of acidic liquid kept in cadmium-plated containers and certain silver polishes.
LEAD ORES: Crude lead and lead ores are often contaminated with cadmium. People working with these ores may be exposed to cadmium vapors (Taylor et al, 1984).
TOBACCO: Smokers usually have twice the body burden of cadmium as non-smokers due to cadmium in cigarettes (up to 30 mcg/pack) producing inhalation of 2 to 4 mcg cadmium/pack smoked (Hallenbeck, 1984).

SOURCES

Cadmium is present in ores containing zinc, lead, and copper. During smelting of these metals, cadmium volatilizes and condenses into particles which are quickly oxidized to a respirable form of cadmium oxide (ATSDR, 1993; HSDB , 2000; NIOSH, 1984; Sittig, 1991).
Cadmium is found in mineral form as greenockite, sphalerite, and hawleyite, among others (Budavari, 1996; HSDB , 2000; Sittig, 1991).
Cadmium is found in air, food, water, soil, rocks, fossil fuels, mineral fertilizers, and cigarette smoke (ATSDR, 1993; Baselt & Cravey, 1995; HSDB , 2000).
Concentrations of cadmium in native soil range from 0.01 to 7.0 ppm typically, with a maximum concentration of 45 ppm (Dragun, 1988).
Cadmium's abundance in the earth's crust is 0.1 to 0.2 ppm (Budavari, 1996).
There are eight stable isotopes (Lewis, 1993; HSDB , 1999). Abundances of the stable isotopes are (Budavari, 1996; HSDB , 1999): 106 (1.21%); 108 (0.88%) 110 (12.39%); 111 (12.75%);112 (24.07%); 113 (12.26%); 114 (28.86%); 116 (7.58%).
Cadmium has two radioisotopes: 109 and 115 (HSDB , 1999).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

SOURCES: Heavy metal used in industrial processes. Primarily found in nickel-cadmium batteries, in electroplating, as an alloy, and in some solders.

TOXICOLOGY: Interferes with cellular function through a variety of mechanisms, including interfering with protein function and calcium homeostasis.

EPIDEMIOLOGY: Uncommon poisoning and primarily an occupational exposure, although environmental exposures have occurred from foods contaminated with cadmium.

WITH POISONING/EXPOSURE

ACUTE INHALATIONAL: Cadmium fume fever (caused by inhalation of fumes generated with welding, soldering, or brazing), characterized by cough, fever, chills, wheezing, headache, pleuritic chest pain, myalgias, and sore throat, typically develops 4 to 12 hours following an acute inhalational exposure and resolves within 1 to 2 days. In severe cadmium inhalation, pneumonitis or acute lung injury may develop 24 hours or longer after exposure and may progress to respiratory failure.
ACUTE INGESTION: Ingestion of large amounts usually produces vomiting, diarrhea (which can be hemorrhagic), and abdominal pain. This can progress to hypotension, renal failure, and death. Large overdoses can result in caustic injury to the gastrointestinal tract. Hepatotoxicity is uncommon.
CHRONIC INHALATIONAL: May cause emphysema or pulmonary fibrosis and is associated with lung cancer. Cadmium is considered an IARC class I carcinogen.
CHRONIC INGESTION: Primarily causes bone disease (often termed itai-itai disease) and renal injury. Cadmium accumulates in bones leading to osteomalacia, osteoporosis, and pathologic fractures. Kidney disease primarily manifests as proteinuria and Fanconi syndrome and less often as nephrolithiasis. Neurotoxicity, including peripheral neuropathy, parkinsonism, and anosmia, has been described.

POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)

TOXIC; inhalation, ingestion or skin contact with material may cause severe injury or death.
Contact with molten substance may cause severe burns to skin and eyes.
Avoid any skin contact.
Effects of contact or inhalation may be delayed.
Fire may produce irritating, corrosive and/or toxic gases.
Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.

ACUTE CLINICAL EFFECTS

Cadmium is intensely irritating with overexposure by inhalation (ACGIH, 1996). It is relatively efficiently absorbed (20 to 50 percent) after inhalation (Baxter et al, 2001; (ILO, 1983). Absorbed cadmium accumulates throughout the body, but is highest in liver and kidney (Zenz, 1994). Tobacco smoking can represent a route of substantial exposure (HSDB , 2001).

Up to several hours after the fumes of heated cadmium are inhaled, the following signs and symptoms may appear: headache, weakness, retrosternal pain, dyspnea, coughing, tracheobronchitis, toxic pneumonitis and pulmonary edema, with a mortality rate of approximately 20 percent (ACGIH, 1996; (Baxter et al, 2000; Budavari, 1996; Hathaway et al, 1996). Symptoms generally resolve within 1 week (Baxter et al, 2000). Survivors of acute poisonings have recovered with no apparent ill effects (ACGIH, 1996).
Most acute intoxications have been caused by inhalation of cadmium fumes at concentrations that did not produce irritation (Hathaway et al, 1996) NIOSH/OSHA). Symptoms may be delayed in onset to by up to 24 hours (ILO, 1983). Inhalation of 4 mg can prove fatal to an adult (Baselt, 2000). Average airborne concentrations causing fatalities have been estimated at 40 to 50 mg/m(3) for 1 hour, or 9 mg/m(3) for 5 hours (ACGIH, 1996).
In one case, an otherwise healthy 53-year-old man died from chemical pneumonitis 19 days after an acute inhalation exposure to cadmium fumes from flame-cutting an alloy for 60 to 75 minutes (Fernandez et al, 1996).
Inhalation of fumes (cadmium oxide) at lower concentrations may result in 'metal fume fever', a flu-like condition involving nausea and vomiting, fever, headache, dizziness, weakness, chills, sweating, aches and pains, irritated and dry nose and throat, cough and difficulty breathing. Symptoms of metal fume fever generally begin within hours after exposure and subside over 24 to 48 hours, but may progress to pulmonary edema, bronchopneumonia and death within 7 to 10 days (ACGIH, 1996; (Harbison, 1998; Hathaway et al, 1996).
Cadmium may exert its toxic effects on the lung by enhancing lipid peroxidation and inflammatory responses. Increases in thiobarbituric acid reactive substances (TBARS, an indicator of lipid peroxidation) and total lung protein (indicative of inflammatory response) were seen in the lungs of rats 24 hours after intraperitoneal injection of cadmium chloride at doses up to 1,000 mcg/kg. There was a linear relationship between the amount of TBARS and lung protein, indicating a direct relationship between the two (Manca et al, 1994).

Soluble cadmium compounds can be very toxic, but their strong emetic activity usually precludes severe poisoning after ingestion (Lewis, 1997). Several hundred milligrams of soluble salt would be a fatal dose by ingestion (Baselt, 2000).

Only about 6 percent of an ingested dose is absorbed (Baxter et al, 2000). Absorption of cadmium from the gastrointestinal tract can be influenced by several factors, including the presence of proteins and calcium (Anon, 1991). Individuals with low iron stores may absorb more cadmium. The small percentage of cadmium absorbed after ingestion is taken up quickly, however (Anon, 1991).
Severe nausea and vomiting, abdominal pain, headache, muscle cramps, vertigo and convulsions can result from ingestion; recovery is generally rapid and complete (Bingham et al, 2001; Budavari, 1996).

Topical application of cadmium results in irritant dermatitis, but percutaneous absorption is negligible (Goldfrank, 1998; Sittig, 1991). Smarting of the eyes and redness and pain can result from exposure to cadmium fumes (Grant & Schuman, 1993; ILO, 1998).

The presence of cadmium initiates synthesis of the metal-binding protein metallothionein. About 80 to 90 percent of the total body burden of cadmium is thought to be bound to this protein, but the extent to which this binding may protect tissues from cadmium toxicity is not known (Barlow & Sullivan, 1982; Goldfrank, 1998; ILO, 1983). Consistent with a model in which metallothionein (MT) protects against cadmium toxicity, MT-null mice lacking the MT gene are approximately ten times more sensitive to the nephrotoxic effects of cadmium (Klaassen et al, 1999).

In rats injected subcutaneously with cadmium (as cadmium chloride) at a dose of 3 mg cadmium/kg/day for 8 days, synthesis of metallothioneins and release of cadmium-bound metallothioneins increased in the liver and plasma. Excess cadmium was bound to cellular membranes in the kidneys, and it was suggested that the membrane-bound cadmium was responsible for the induction of renal injury (Sudo et al, 1996).

The mechanism of cadmium's toxicity may involve its displacement of zinc, whose chemical properties are very similar, from metalloproteins (Meplan et al, 1999a).

CHRONIC CLINICAL EFFECTS

Cadmium is eliminated from the body very slowly, with an estimated half-life of 10 to 30 YEARS in humans; as a result, cadmium accumulates in the body with increasing age and duration of exposure (Baxter et al, 2000). Chronic cadmium poisoning is an insidious disease that takes many years to develop and may continue to progress despite cessation of exposure (ACGIH, 1996; (Friberg et al, 1986).

Signs and symptoms of chronic exposure include gastrointestinal effects, anemia, eosinophilia, rhinitis, nasal septum ulceration, olfactory nerve damage, anosmia, yellow teeth, microfractures, possibly emphysema, and kidney disease (ACGIH, 1996; (Hathaway et al, 1996).

The kidney cortex is the main target organ for long-term cadmium exposure (ACGIH, 1996; (Zenz, 1994). Glomerular damage induced by cadmium is irreversible (Jarup et al, 1995a) 1995b).

The most common abnormality found in cadmium-exposed workers is proteinuria; this is considered the earliest sign of renal tubular dysfunction. Irreversible tubular proteinuria can occur depending on the intensity of the exposure level and the severity of the tubular damage (Bingham et al, 2001).
As kidney function progressively decreases, amino acids, glucose and minerals are also lost in the urine. Increased excretion of calcium and phosphorus may disturb bone metabolism; kidney stones are often found (ILO, 1983).
Approximately 7 percent of US adults have cadmium-induced renal dysfunction (Klaassen et al, 1999).
In a follow-up study of 593 environmentally exposed Belgians with increased cadmium approximately 5 years earlier, blood and urinary cadmium levels as well as prevalence of increased microalbuminuria were all decreased 5 years after intervention. There was no progression of renal damage in this population. This result indicates that environmentally induced renal damage from cadmium can be reversible (Hotz et al, 1999).
Renal tubular damage continued to accumulate over a 12-year period in a cohort of workers who had been occupationally exposed to cadmium-containing solders, even though cadmium exposures during the follow-up period were greatly reduced (Mason et al, 1999).

Possible effects of environmental exposure to cadmium on blood pressure have been less clear. No correlation between cadmium exposure and blood pressure was found in a large cross-sectional study on persons exposed to environmental cadmium in Belgium from 1985 to 1989 (the 'CadmiBel' study) (Staessen et al, 1999).

In a 5-year prospective study follow-up of 692 persons from the CadmiBel study, called the 'PheeCad' study, reductions in blood and urinary cadmium levels did not affect systolic or diastolic blood pressure or hypertension (Staessen et al, 2000).
Residents of Shipham, England, a location with high cadmium levels in the soil, had a borderline increase in mortality from hypertension, cerebrovascular disease, nephritis and nephrosis, for the period 1939 to 1997, compared with a nearby uncontaminated village (Elliott et al, 2000).

Chronic cadmium dust inhalation has been reported to cause pulmonary emphysema and pulmonary fibrosis in workers, although cadmium-induced lung damage has been disputed (Baxter et al, 2000; Bingham et al, 2001).

Cadmium exposure may result in chronic obstructive pulmonary disease through this emphysema. However, lung function studies fail to demonstrate a dose-response relationship (Baxter et al, 2000).
Centrilobular emphysema and bronchitis are the main pulmonary effects of several years of occupational exposure to cadmium oxide fumes or dust, or to cadmium pigment dust (HSDB , 2001). In one epidemiological study, there was increased mortality from respiratory disease, and also an increase in reticuloendothelial tumors (HSDB).
The risk of mortality from chronic non-malignant respiratory diseases was related to cumulative exposure to cadmium in 1,492 cadmium workers followed from 1946 to 1992 (Sorahan et al, 1995).

A painful type of osteomalacia plus renal calcium wasting, called ITAI-ITAI ('ouch-ouch') disease, has occurred in Japan and other areas, resulting from exposure to drinking water and crops contaminated with cadmium, lead and zinc. This disease occurs mainly in postmenopausal women (Baxter et al, 2000; Bingham et al, 2001).

Characteristics of Itai-Itai include osteomalacia, hypercalcuria, Fanconi syndrome, decreased glomerular filtration rate, hypotension, severe leg and back pain, anemia and lymphopenia, plus short stature and a waddling gait (Baselt, 2000; Baxter et al, 2000).
The skeletal deformities of Itai-Itai result from calcium and phosphorous metabolism derangement, a consequence of renal damage or perturbation of vitamin D metabolism (Baselt, 2000; Baxter et al, 2000).
The anemia caused by chronic cadmium exposure in Itai-Itai victims is characterized by low serum erythropoietin and normal serum iron and ferritin levels (Horiguchi et al, 1994).

Decreases in bone density of the forearm correlated with occupational exposure to cadmium, determined by blood cadmium levels, in a group of Swedish workers. Forearm bone density was also lower in workers with tubular proteinuria, compared with those without proteinuria. Urinary cadmium levels also correlated with prevalence of osteoporosis in the same group. It would thus seem that occupational or environmental exposure to cadmium at low levels is a risk factor for osteoporosis (Jarup et al, 1998a).

Low to moderate environmental exposure to cadmium can also produce skeletal demineralization. A group of 1,014 persons with environmental exposure to cadmium showed skeletal demineralization, manifested as increased risk for fractures in women and loss of height in men, in the prospective 'PheeCad' study. There was a 0.01-g/cm(2) loss of forearm bone density in postmenopausal women for each two-fold increase in urinary cadmium (Staessen et al, 1999).
In results consistent with the effects of chronic cadmium exposure on bone density, high cadmium concentrations in blood or urine correlated with lower concentrations of 5-dihydroxycholecalciferol, a vitamin D(3) metabolite, in 59 smelter workers exposed to both cadmium and lead. Reductions in vitamin D metabolites were more strongly correlated with cadmium than with lead levels, whereas 1-a,25-dihydroxycolecalciferol was somewhat increased with increasing lead levels (Chalkley et al, 1998).

Occupational cadmium exposure was associated with increased prevalence of polyneuropathy in a group of 13 retired workers, compared with 19 age-matched controls (odds ratio = 9.92; P = 0.015) (Viaene et al, 1999).

A group of 42 cadmium-exposed workers performed more poorly on a battery of neurobehavioral tests than did 47 age-matched controls. The exposed group also had more subjective complaints of symptoms consistent with peripheral neuropathy, equilibrium, and ability to concentrate. All of the differences in the exposed group correlated with urinary cadmium levels.
This is the first published study on possible neurologic effects of occupational exposure to cadmium that included a control group (Viaene et al, 2000).

Increased levels of serum IgA and circulating B lymphocytes were found in adults environmentally exposed to cadmium and lead who had urinary cadmium levels greater than 1.5 mcg/g (Sarasua et al, 2000).

Increased deaths from cardiovascular and renal disease were seen in a mortality study of 2,408 residents of the Kakehashi River basin in Japan (heavily polluted with cadmium) from 1974/1975 to 1991 (Nishijo et al, 1995).

Effects of environmental exposure to cadmium on overall mortality have been variable in different studies. An English cohort followed since 1939 has shown lower mortality overall than a comparison group from a nearby village (Elliott et al, 2000). Mortality in residents of the Japanese Kakahashi River basin, however, has shown a dose-related increase with urinary cadmium concentration during a 15-year period (Nishijo et al, 1999).

Liver cadmium concentrations can be high and liver function tests may be abnormal; however, liver damage (necrosis or cirrhosis) is not a principal consequence of cadmium exposure (Baxter et al, 2000).

Cadmium chloride did not inhibit production of immunoglobulin by human lymphocytes in vitro at concentrations consistent with those found in human exposures (Borella & Giardino, 1991).

In an inhalation exposure study in rats, different cadmium salts were retained in the lung to different extents, with cadmium oxide being the most available (Glaser, 1986). Cadmium sulfide was more bioavailable when inhaled than when ingested in rats. Both soluble (cadmium chloride) and insoluble (cadmium sulfide) cadmium compounds had biphasic clearance after inhalation exposure (Klimisch, 1993).

Cadmium sulfate caused ultrastructural deterioration in the thyroid gland in pregnant rats (Yoshizuka et al, 1991). Based on studies in laboratory animals, the thyroid gland seems to be a target organ for cadmium toxicity during pregnancy (Samarawickrama & Webb, 1979).

Lipid peroxidation was increased in the kidney, liver and serum of ascorbic acid-deficient guinea pigs given 1 mg/day of cadmium in the drinking water; however, by 12 weeks the lipid peroxidation in the kidney was lower than it was in controls (Hudecova & Ginter, 1992).

In rats given cadmium chloride intraperitoneally at a dose of 0.228 mg cadmium/kg 3 days per week for 1 year, interstitial fibrosis and inflammatory cell infiltration were seen in the livers, together with degeneration of proximal tubules and inflammatory cell infiltration in the kidneys. Lipid peroxidation was not increased, but glutathione levels were higher (Kamiyama et al, 1995).

Cadmium chloride solutions up to 1.0 percent applied to the shaved skin of rats caused hyperkeratosis, acanthosis and some ulcerative changes in a dose-related way. Blood cadmium levels were increased, indicating percutaneous absorption (Lansdown & Sampson, 1996).

Chelating agents are NOT recommended to lower body burdens of cadmium, because they may exacerbate kidney malfunction (Friberg et al, 1986).

ASCORBIC ACID given in the drinking water at 100 mg/day for 12 weeks reduced the extent of kidney damage induced by cadmium in guinea pigs (Nagyova et al, 1994).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

SUMMARY

Prehospital decontamination (activated charcoal) can be considered for large ingestions in which there will be a delay to definitive health care, but the poison center should be consulted first.

ACTIVATED CHARCOAL

PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION

Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).

In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).

CHARCOAL DOSE

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).

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).

ADVERSE EFFECTS/CONTRAINDICATIONS

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.
Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)

Move victim to fresh air.
Call 911 or emergency medical service.
Give artificial respiration if victim is not breathing.
Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device.
Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes.
In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes.
For minor skin contact, avoid spreading material on unaffected skin.
Keep victim warm and quiet.
Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed.
Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.

FIRST AID

FIRST AID

The following first aid measures are suggested for cadmium DUST or FUME exposure (National Institute for Occupational Safety and Health, 2007):

EYE EXPOSURE: Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles) as defined by the Occupational Safety and Health Administration (OSHA) should be used when working with this chemical. Face shields should only be worn over primary eye protection. Contact lens use is not recommended. If contact lenses are worn, then appropriate eye and face protection devices must be used. OSHA emphasizes that dusty and/or chemical environments may represent an additional hazard to contact lens wearers.
DERMAL EXPOSURE: Immediately wash the contaminated skin with soap and water.
INHALATION EXPOSURE: Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible.
ORAL EXPOSURE: If this chemical has been swallowed, get medical attention immediately.
TARGET ORGANS: Respiratory system, kidneys, prostate and blood [prostatic and lung cancer].

INHALATION EXPOSURE

INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
TREATMENT: Severe pulmonary edema may ensue. Treatment of inhalation toxicity should include recommendations listed in the oral exposure section when appropriate.
ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.

DERMAL EXPOSURE

Significant dermal absorption seldom occurs.
DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

EYE EXPOSURE

DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

ORAL EXPOSURE

Activated charcoal has no proven benefit in cadmium poisoning, but may be considered.
ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
Significant esophageal or gastrointestinal tract irritation or burns may occur following ingestion. The possible benefit of early removal of some ingested material by cautious gastric lavage must be weighed against potential complications of bleeding or perforation.
SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).

Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.

CHELATION

Although not demonstrably efficacious, chelation therapy may be of benefit immediately following ACUTE exposure. Administer CaNa2 EDTA 75 milligrams/kilogram/day deep IM or slow IV infusion given in 3 to 6 divided doses for up to 5 days. May be repeated for a second course after a minimum of two days drug holiday; each course should not exceed a total of 500 milligrams/kilogram body weight. CAUTION - BAL must not be used with cadmium since the complex may be nephrotoxic.
Chelation is not recommended for cases of chronic cadmium poisoning.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

ADULT

INHALATION EXPOSURE

Inhalation of 4 mg of cadmium may be fatal (Baselt & Cravey, 1995).
Workers who inhaled an acutely lethal amount of cadmium fume were found to have 1.5 - 4.1 mg/kg of cadmium in their lungs (Baselt & Cravey, 1995).
Death may result 7-10 days after exposure to air concentrations of 0.5-2.5 mg/m(3). An average concentration of 40-50 mg/m(3) cadmium fume, inhaled over the course of an hour, resulted in death. Under similar circumstances, 9 mg/m(3) for 5 hours and 5 mg/m(3) for 8 hours also resulted in death (ACGIH, 1991) ACGIH, 1996; Hathaway et al., 1996; (Sittig, 1991).
50-111 lung cancer deaths per 1000 workers are expected to result from lifetime (45 years) work exposures to cadmium fume at levels of 100 mcg/m(3) (Zenz, 1994).
Cadmium oxide fume from a furnace cause death when the worker was exposed for 1 hour to an air concentration of 50 mg/m(3). Similarly, a worker died when exposed to 8.6 mg/m(3) for 5 hours. One researcher estimates that exposure to 5 mg/m(3) for 8 hours will result in death (IPCS, 1992).
Inhalation of airborne concentrations of 1-5 mg/m(3) could cause death (ATSDR, 1993).
The lowest published lethal concentration for a human (inhalation route) is 39 mg/m(3)/20M (RTECS , 1999; Lewis, 1996).
Exposure to probably less than 2500 min x mg/m(3) of cadmium oxide fumes or cadmium chloride aerosol is probably fatal (Friberg et al, 1985). 500 min x mg/m(3) is dangerous.
A 20 minute exposure to 39 mg/m(3) aerosolized cadmium resulted in death (NIOSH, 1996).

ORAL EXPOSURE

Ingestion of more than 100 mg of soluble salt may be lethal (Baselt & Cravey, 1995).
Cadmium ingestion of 300 mg, or more, may be fatal (Zenz, 1994).
Two cases of suicide by ingestion of cadmium involved 25 mg/kg and 1500 mg/kg body weight (ATSDR, 1993).
Lethal oral doses have ranged upwards from 150 grams (Bernard & Lauwerys, 1984; Buckler et al, 1986). Following oral ingestion, death results from shock due to fluid loss or acute renal failure, and cardiopulmonary depression.
CASE REPORT: A 23-year-old man intentionally ingested 5 g of cadmium iodide, dissolved in water (approximately 25 mg cadmium/kg of body weight), and, over the next 2 days, developed renal impairment, hypoproteinemia, hypoalbuminemia, metabolic acidosis, and cardiac dysrhythmias. With supportive treatment, including administration of calcium EDTA to increase cadmium excretion, the patient's condition temporarily improved; however, on day 7, he developed hyperthermia, respiratory dysfunction, and ventricular fibrillation progressing to cardiac arrest and death. An autopsy revealed damage to the cardiac muscle, liver, kidneys, and the alimentary tract (Wisniewska-Knypl et al, 1971).

UNKNOWN EXPOSURE

Three people, who succumbed to chronic cadmium poisoning, were found to have an average of 128 mg/kg of cadmium in their livers and 180 mg/kg of cadmium in their kidneys (Baselt & Cravey, 1995).
Four workers who died within 10 years after long periods of cadmium exposure (18-26 years) had liver concentrations of cadmium of 23-145 mg/kg and kidney concentrations of 13-80 mg/kg (Baselt & Cravey, 1995).
The lowest published lethal dose for a man (unknown route) is 15 mg/kg (RTECS , 1999; Lewis, 1996).

MAXIMUM TOLERATED EXPOSURE

ADULT

INHALATION EXPOSURE

Permissible exposure limit (PEL) from the occupational Safety and Health Administration (OSHA) standards for cadmium - 5 mcg/m(3) over an 8-hour TWA (Yassin & Martonik, 2004).
The OSHA action level for airborne levels of cadmium - 2.5 mcg/m(3) over an 8-hour TWA (Yassin & Martonik, 2004).
Lung inflammation has been caused by inhalation of air containing 0.5-2.5 mg/m(3) cadmium dust. Symptoms of this type of exposure occurred within 4-10 hours and included headache, chills, muscle aches, chest pain, diarrhea, nausea, vomiting, difficulty breathing, wheezing, coughing blood, and a dark purple discoloration of the skin (Sittig, 1991).
Inhalation of aerosolized cadmium at concentrations of 0.06-0.68 mg/m(3) over a 4-8 year period may cause sore throat, cough, upset stomach, chest pain, and fatigue. Anemia, lung distention, kidney dysfunction, and protein in urine has resulted from 20 year exposures to cadmium dust and fume in concentrations of 3.0-15.0 mg/m(3) (Sittig, 1991).
Inhalation of cadmium oxide fume, generated by performing hot work on cadmium and its alloys, may result in cough, dyspnoea, retrosternal pain, pulmonary oedema, and symptoms of metal fume fever about 10 hours after exposure. Symptoms generally resolve within a week (Raffle et al., 1994).
A man who worked for 3 days in an environment with 0.5-2.5 mg/m(3) aerosolized cadmium developed pneumonitis. At concentrations below 0.5 mg/m(3), several cases which involved a condition similar to metal fume fever and acute gastroenteritis arose (ACGIH, 1991) ACGIH, 1996).
Inhalation exposures of 0.5 mg/m(3) or less, over a long period of time, cause decreased lung function and emphysema (Hathaway, 1996).
Proteinuria may develop after a worker is exposed to cadmium for 5-10 years at a level of 100 mcg cadmium/m(3) (Hathaway, 1996).
Workers that used cadmium containing solders for 4-24 years were estimated to have been exposed to 0.35-9.9 mg/m(3)year of cadmium. As a result, these workers were found to have slight to pronounced beta-2-microglobulinuria. Workers with an estimated dose of 1 mg/m(3)year rarely developed tubular proteinuria. Workers with an estimated dose >3 mg/m(3)year were more likely to develop slight and pronounced beta-2-microglobulinuria (Clayton & Clayton, 1994).
Workers exposed to >300 mg/m(3)days of cadmium, equivalent to 4.3 years at the current PEL, are more likely to develop multiple tubular abnormalities and raised serum creatinine concentrations (Clayton & Clayton, 1994).
27 male workers, exposed to air concentration of cadmium in a battery factory, were found, on average, to have slightly decreased forced expiratory volume (IPCS, 1992).
Of 96 workers exposed to cadmium oxide fume for up to 27 years, 12 were found to have emphysema. Average air concentrations of cadmium were 40-50 mcg/m(3) (IPCS, 1992).
Seventeen workers exposed for 6 years to cadmium levels commonly near 200 mcg/m(3), were found to have decreased forced vital capacity. Seven, or more, years of exposure to insoluble cadmium compounds at concentrations of 700 mcg/m(3) was associated with emphysema (IPCS, 1992).
Workers using solders containing cadmium were exposed for many years to cadmium concentrations of 0.05-0.5 mg/m(3). Twenty-four of the workers had cadmium related renal tubular dysfunction (IPCS, 1992).
The lowest published toxic concentration for a woman (inhalation route) is 129 mcg/m(3) for a 20-year, continuous exposure (Lewis, 1996).
The lowest published toxic concentration for a man (inhalation route) is 88 mcg/m(3) for an 8.6-year exposure (RTECS , 1999; Lewis, 1996).
In a retrospective study, 311 male workers in an alkaline battery factory were evaluated for cadmium exposure. Workers were exposed to greater than 50 mcg/m(3) for 1 to 35 years. Hypertension (defined by average blood pressure greater than 160/95 over a 5 year period) was noted in 23% of workers over 40 (HSDB , 1999).

ORAL EXPOSURE

Consumption of foods and beverages stored in cadmium-plated containers has resulted in human poisonings (OHM/TADS , 2000).
Ingestion of 15-30 mg of cadmium, or soluble compounds of cadmium, may cause abdominal pain, anemia, choking, diarrhea, increased salivation, vomiting, and constant need to empty the bladder. Symptoms arise 15-30 minutes after exposure and may progress to heart and lung failure (Sittig, 1991).
Complete recovery is expected after an oral dose of cadmium that is less than 300 mg (Zenz, 1994).
Drinking water from a vending machine cooling tank was found to have a cadmium concentration of 16 mg/L, which caused acute illness in consumers. Solder in the tank contained cadmium (IPCS, 1992).
Children who drank soft drinks containing 16 mg/L cadmium, or ate popsicles containing 13 mg/L, developed gastrointestinal symptoms (ATSDR, 1993).
Ingestion of 0.0021 mg/kg/day, corresponding to 2,000 mg of cadmium over a 50 year period, will cause renal damage (ATSDR, 1993).
Long-term daily oral intake of more than 1 mg of cadmium may result in severe bone disease (Friberg et al, 1985).
Cadmium plating of food and beverage containers has resulted in a number of outbreaks of gastroenteritis (food poisoning) (Lewis, 1993).
The provisional tolerable weekly intake (PTWI) of cadmium (the dietary exposure level that can be ingested weekly over a lifetime without appreciable health risk) - 7 mcg/kg of body weight. This information has been obtained from the Joint FAO/WHO Expert Committee on Food Additives and Contaminants (JECFA), a scientific advisory body of the Codex Committee on Food Additives and Contaminants (CCFAC). This PTWI was established in the 33rd meeting in 1988 and has been maintained at the 61st meeting held in 2003 (Horiguchi et al, 2004).

UNKNOWN EXPOSURE

Battery workers exposed to cadmium at levels of 0.13-1.17 mg/m(3) for 1-12 years were found to have chronic signs of cadmium exposure. Upon radiological examination of the skeletons of 26 battery workers, 7 were found to have proteinuria, 3 had pseudofractures, 13 had sclerotic focii, and 10 had osteoporosis (IPCS, 1992).

Carcinogenicity Ratings for CAS7440-43-9 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A2 ; Listed as: Cadmium

A2 :Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A2 ; Listed as: Cadmium compounds, as Cd

A2 :Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.

EPA (U.S. Environmental Protection Agency, 2011): B1 ; Listed as: Cadmium

B1 : Probable human carcinogen - based on limited evidence of carcinogenicity in humans.

EPA (U.S. Environmental Protection Agency, 2011): B1 ; Listed as: Cadmium

B1 : Probable human carcinogen - based on limited evidence of carcinogenicity in humans.

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): 1 ; Listed as: Cadmium and cadmium compounds

1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.

NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Cadmium dust (as Cd)

Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).

MAK (DFG, 2002): Category 2 ; Listed as: Cadmium and its compounds (as inhalable dusts/aerosols)

Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.

NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): K ; Listed as: Cadmium (See Cadmium and Cadmium Compounds)

K : KNOWN = Known to be a human carcinogen

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS7440-43-9 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor:
RfD: 5x10(-4) mg/kg-day (water) (This represents multiple discrete values for this substance.)

Inhalation:

Unit Risk: 1.8 per mg/m3
RfC:

Drinking Water:

Unit Risk:

Oral:

Slope Factor:
RfD: 1x10(-3) mg/kg-day (food) (This represents multiple discrete values for this substance.)

Inhalation:

Unit Risk:
RfC:

Drinking Water:

Unit Risk:

TOXICITY VALUES

References: Andersen, 1986 Lewis, 1996 OHM/TADS, 2000 RTECS, 2000
- LC50- (ORAL)DOG:
- LC50- (INHALATION)RAT:
- LCLo- (INHALATION)HUMAN:
- LCLo- (INHALATION)MOUSE:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (ORAL)RABBIT:
- LD50- (ORAL)RAT:
- LDLo- (INTRAVENOUS)RABBIT:
- LDLo- (ORAL)RABBIT:
- LDLo- (SUBCUTANEOUS)RABBIT:
- TCLo- (INHALATION)HUMAN:
- TD- (INTRAMUSCULAR)RAT:
- TDLo- (INTRAVENOUS)HAMSTER:
- TDLo- (INTRAPERITONEAL)MOUSE:
- TDLo- (ORAL)MOUSE:
- TDLo- (ORAL)PIG:
- TDLo- (INTRAMUSCULAR)RAT:
- TDLo- (INTRAPERITONEAL)RAT:
- TDLo- (INTRAVENOUS)RAT:
- TDLo- (ORAL)RAT:
- TDLo- (SUBCUTANEOUS)RAT:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS7440-43-9 (American Conference of Governmental Industrial Hygienists, 2010):

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.

Adopted Value

Cadmium

TLV:

TLV-TWA: 0.01 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A2
Codes: BEI
Definitions:

A2: Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.

TLV Basis - Critical Effect(s): Kidney dam
Molecular Weight: 112.4

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Adopted Value

Cadmium compounds, as Cd

TLV:

TLV-TWA: 0.002 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A2
Codes: BEI, R
Definitions:

A2: Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.
R: Respirable fraction; see Appendix C, paragraph C (of TLV booklet).

TLV Basis - Critical Effect(s): Kidney dam
Molecular Weight: Varies

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS7440-43-9 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS7440-43-9 (National Institute for Occupational Safety and Health, 2007):

Listed as: Cadmium dust (as Cd)
REL:

TWA: NIOSH REL*:
STEL:
Ceiling:
Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
Skin Designation: Not Listed
Note(s): See Appendix A; [*Note: The REL applies to all Cadmium compounds (as Cd).]

IDLH:

IDLH: 9 mg Cd/m3 (as Cd)
Note(s): Ca

Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

OSHA PEL Values for CAS7440-43-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Cadmium (as Cd); see 29 CFR 1910.1027
Table Z-1 for Cadmium (as Cd); see 29 CFR 1910.1027:

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3:

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

Table Z-2 for Cadmium fume (Z37.5-1970):

8-hour TWA:1 mg/m(3)
Acceptable Ceiling Concentration: 3 mg/m(3)
Acceptable Maximum Peak above the Ceiling Concentration for an 8-hour Shift:

Concentration:
Maximum Duration:

Notation(s):

(b): This standard applies to any operations or sectors for which the Cadmium standard, 29 CFR 1910.1027, is stayed or otherwise not in effect.

Table Z-2 for Cadmium dust (Z37.5-1970):

8-hour TWA:2 mg/m(3)
Acceptable Ceiling Concentration: 6 mg/m(3)
Acceptable Maximum Peak above the Ceiling Concentration for an 8-hour Shift:

Concentration:
Maximum Duration:

Notation(s):

(b): This standard applies to any operations or sectors for which the Cadmium standard, 29 CFR 1910.1027, is stayed or otherwise not in effect.

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS7440-43-9 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS7440-43-9 (U.S. Environmental Protection Agency, 2010):

Listed as: Cadmium (D006)
Final Reportable Quantity, in pounds (kilograms):

10 (4.54)

Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity
Listed as: Cadmium
Final Reportable Quantity, in pounds (kilograms):

10 (4.54)

Additional Information:
Listed as: Cadmium and compounds

Additional Information:
Listed as: Cadmium compounds

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS7440-43-9 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS7440-43-9 (U.S. Environmental Protection Agency, 2010b):

Not Listed
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS7440-43-9 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS7440-43-9 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Cadmium Compounds: Includes any unique chemical substance that contains cadmium as part of that chemical's infrastructure
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

Listed as: Cadmium
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS7440-43-9 (49 CFR 172.101 - App. B, 2005):

Listed as Cadmium compounds
Severe Marine Pollutant: Yes

EPA TSCA Inventory for CAS7440-43-9 (EPA, 2005):

Listed as: Cadmium

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 2570 (49 CFR 172.101, 2005):

Hazardous materials descriptions and proper shipping name: Cadmium compounds

Symbol(s): Not Listed
Hazard class or Division: 6.1

6.1: Poisonous materials. See 49 CFR section 173.132 for definitions.

Identification Number: UN2570
Packing Group: I

I: Packing Group I - indicates the degree of danger presented by the material is great.

Label(s) required (if not excepted): 6.1

6.1: Poison Inhalation Hazard (inhalation hazard, Zone A or B) or Poison (other than inhalation hazard, Zone A or B; the packing group for a material is indicated in column 5 of the table.).

Special Provisions: IB7, IP1, T6, TP33

IB7: Authorized IBCs: Metal (11A, 11B, 11N, 21A, 21B, 21N, 31A, 31B and 31N); Rigid plastics (11H1, 11H2, 21H1, 21H2, 31H1 and 31H2); Composite (11HZ1, 11HZ2, 21HZ1, 21HZ2, 31HZ1 and 31HZ2); Wooden (11C, 11D and 11F). Additional Requirement: Liners of wooden IBCs must be sift-proof.
IP1: IBCs must be packed in closed freight containers or a closed transport vehicle.
T6: Minimum test pressure (bar): 4; Minimum shell thickness (in mm-reference steel) (See sxn.178.274(d)): sxn.178.274(d)(2); Pressure-relief requirements (See sxn.178.275(g)): Normal; Bottom opening requirements (See sxn.178.275(d)): sxn.178.275(d)(2).
TP33: The portable tank instruction assigned for this substance applies for granular and powdered solids and for solids which are filled and discharged at temperatures above their melting point which are cooled and transported as a solid mass. Solid substances transported or offered for transport above their melting point are authorized for transportation in portable tanks conforming to the provisions of portable tank instruction T4 for solid substances of packing group III or T7 for solid substances of packing group II, unless a tank with more stringent requirements for minimum shell thickness, maximum allowable working pressure, pressure-relief devices or bottom outlets are assigned in which case the more stringent tank instruction and special provisions shall apply. Filling limits must be in accordance with portable tank special provision TP3. Solids meeting the defnintion of an elevated temperature material must be transported in accordance with the applicable requirements of this subchapter.

Packaging Authorizations (refer to 49 CFR 173.***):

Exceptions: None
Non-bulk packaging: 211
Bulk packaging: 242

Quantity Limitations:

Passenger aircraft or railcar: 5 kg
Cargo aircraft only: 50 kg

Vessel Stowage Requirements:

Vessel stowage location: A

A: The material may be stowed "on deck" or "under deck" on a cargo vessel and on a passenger vessel.

Vessel stowage other: Not Listed

Hazardous materials descriptions and proper shipping name: Cadmium compounds

Symbol(s): Not Listed
Hazard class or Division: 6.1

6.1: Poisonous materials. See 49 CFR section 173.132 for definitions.

Identification Number: UN2570
Packing Group: II

II: Packing Group II - indicates the degree of danger presented by the material is medium.

Label(s) required (if not excepted): 6.1

6.1: Poison Inhalation Hazard (inhalation hazard, Zone A or B) or Poison (other than inhalation hazard, Zone A or B; the packing group for a material is indicated in column 5 of the table.).

Special Provisions: IB8, IP2, IP4, T3, TP33

IB8: Authorized IBCs: Metal (11A, 11B, 11N, 21A, 21B, 21N, 31A, 31B and 31N); Rigid plastics (11H1, 11H2, 21H1, 21H2, 31H1 and 31H2); Composite (11HZ1, 11HZ2, 21HZ1, 21HZ2, 31HZ1 and 31HZ2); Fiberboard (11G); Wooden (11C, 11D and 11F); Flexible (13H1, 13H2, 13H3, 13H4, 13H5, 13L1, 13L2, 13L3, 13L4, 13M1 or 13M2).
IP2: When IBCs other than metal or rigid plastics IBCs are used, they must be offered for transportation in a closed freight container or a closed transport vehicle.
IP4: Flexible, fiberboard or wooden IBCs must be sift-proof and water-resistant or be fitted with a sift-proof and water-resistant liner.
T3: Minimum test pressure (bar): 2.65; Minimum shell thickness (in mm-reference steel) (See sxn.178.274(d)): sxn.178.274(d)(2); Pressure-relief requirements (See sxn.178.275(g)): Normal; Bottom opening requirements (See sxn.178.275(d)): sxn.178.275(d)(2).
TP33: The portable tank instruction assigned for this substance applies for granular and powdered solids and for solids which are filled and discharged at temperatures above their melting point which are cooled and transported as a solid mass. Solid substances transported or offered for transport above their melting point are authorized for transportation in portable tanks conforming to the provisions of portable tank instruction T4 for solid substances of packing group III or T7 for solid substances of packing group II, unless a tank with more stringent requirements for minimum shell thickness, maximum allowable working pressure, pressure-relief devices or bottom outlets are assigned in which case the more stringent tank instruction and special provisions shall apply. Filling limits must be in accordance with portable tank special provision TP3. Solids meeting the defnintion of an elevated temperature material must be transported in accordance with the applicable requirements of this subchapter.

Packaging Authorizations (refer to 49 CFR 173.***):

Exceptions: 153
Non-bulk packaging: 212
Bulk packaging: 242

Quantity Limitations:

Passenger aircraft or railcar: 25 kg
Cargo aircraft only: 100 kg

Vessel Stowage Requirements:

Vessel stowage location: A

A: The material may be stowed "on deck" or "under deck" on a cargo vessel and on a passenger vessel.

Vessel stowage other: Not Listed

Hazardous materials descriptions and proper shipping name: Cadmium compounds

Symbol(s): Not Listed
Hazard class or Division: 6.1

6.1: Poisonous materials. See 49 CFR section 173.132 for definitions.

Identification Number: UN2570
Packing Group: III

III: Packing Group III - indicates the degree of danger presented by the material is minor.

Label(s) required (if not excepted): 6.1

6.1: Poison Inhalation Hazard (inhalation hazard, Zone A or B) or Poison (other than inhalation hazard, Zone A or B; the packing group for a material is indicated in column 5 of the table.).

Special Provisions: IB8, IP3, T1, TP33

IB8: Authorized IBCs: Metal (11A, 11B, 11N, 21A, 21B, 21N, 31A, 31B and 31N); Rigid plastics (11H1, 11H2, 21H1, 21H2, 31H1 and 31H2); Composite (11HZ1, 11HZ2, 21HZ1, 21HZ2, 31HZ1 and 31HZ2); Fiberboard (11G); Wooden (11C, 11D and 11F); Flexible (13H1, 13H2, 13H3, 13H4, 13H5, 13L1, 13L2, 13L3, 13L4, 13M1 or 13M2).
IP3: Flexible IBCs must be sift-proof and water-resistant or must be fitted with a sift-proof and water-resistant liner.
T1: Minimum test pressure (bar): 1.5; Minimum shell thickness (in mm-reference steel) (See sxn.178.274(d)): sxn.178.274(d)(2); Pressure-relief requirements (See sxn.178.275(g)): Normal; Bottom opening requirements (See sxn.178.275(d)): sxn.178.275(d)(2).
TP33: The portable tank instruction assigned for this substance applies for granular and powdered solids and for solids which are filled and discharged at temperatures above their melting point which are cooled and transported as a solid mass. Solid substances transported or offered for transport above their melting point are authorized for transportation in portable tanks conforming to the provisions of portable tank instruction T4 for solid substances of packing group III or T7 for solid substances of packing group II, unless a tank with more stringent requirements for minimum shell thickness, maximum allowable working pressure, pressure-relief devices or bottom outlets are assigned in which case the more stringent tank instruction and special provisions shall apply. Filling limits must be in accordance with portable tank special provision TP3. Solids meeting the defnintion of an elevated temperature material must be transported in accordance with the applicable requirements of this subchapter.

Packaging Authorizations (refer to 49 CFR 173.***):

Exceptions: 153
Non-bulk packaging: 213
Bulk packaging: 240

Quantity Limitations:

Passenger aircraft or railcar: 100 kg
Cargo aircraft only: 200 kg

Vessel Stowage Requirements:

Vessel stowage location: A

A: The material may be stowed "on deck" or "under deck" on a cargo vessel and on a passenger vessel.

Vessel stowage other: Not Listed

ICAO International Shipping Name for UN2570 (ICAO, 2002):

Proper Shipping Name: Cadmium compound
UN Number: 2570

LABELS

NFPA

NFPA Hazard Ratings for CAS7440-43-9 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

STORAGE

CONTAINER

Keep containers sealed and away from sources of physical damage (HSDB , 2000).

INCOMPATIBILITIES

Cadmium is incompatible with strong oxidizers (eg. nitric acid, fused ammonium nitrate), selenium, sulfur, and tellurium (HSDB , 2000; Sittig, 1991).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)

Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

RESPIRATORY PROTECTION

Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 7440-43-9.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
- Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes.
- Some are oxidizers and may ignite combustibles (wood, paper, oil, clothing, etc.).
- Contact with metals may evolve flammable hydrogen gas.
- Containers may explode when heated.

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS7440-43-9 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)

Dry chemical, CO2 or water spray.

LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)

Dry chemical, CO2, alcohol-resistant foam or water spray.
Move containers from fire area if you can do it without risk.
Dike fire control water for later disposal; do not scatter the material.

TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)

Fight fire from maximum distance or use unmanned hose holders or monitor nozzles.
Do not get water inside containers.
Cool containers with flooding quantities of water until well after fire is out.
Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from tanks engulfed in fire.

NFPA Extinguishing Methods for CAS7440-43-9 (NFPA, 2002):

Not Listed

Cadmium powder is flammable and produces toxic fumes when burned. A dry chemical extinguisher is recommended; water extinguishers are not recommended (Sittig, 1991).

COMBUSTION TOXICITY

When heated to a high temperature, it emits toxic fumes of cadmium (Lewis, 1996).

EXPLOSION HAZARD

Cadmium dust is explosive when exposed to heat or flame, or by chemical reaction with oxidizing agents, metals, hydrazoic acid (HN3), zinc, selenium and tellurium (Lewis, 1996).

Cadmium explodes on contact with hydrazoic acid. It causes a violent or explosive reaction when heated with ammonium nitrate. It causes a vigorous reaction when heated with nitryl fluoride (Lewis, 1996).

DUST/VAPOR HAZARD

Cadmium is toxic by inhalation of dust or fume (Lewis, 1996).

Fine particles of cadmium metal are pyrophoric (Urben, 1995).

Cadmium powder is flammable in air and becomes explosive when exposed to heat or flame (Lewis, 1996; ITI, 1995).

Cadmium in powder or granular form may explode when mixed with air (ILO, 1998).

Cadmium dust ignites spontaneously in air and is flammable and explosive when exposed to heat or flame, or by chemical reaction with oxidizing agents, metals, hydrazoic acid (HN3), zinc, selenium and tellurium (Lewis, 1996).

REACTIVITY HAZARD

Cadmium reacts with dilute nitric acid, has a slow reaction with hot hydrogen chloride, and does not react with alkalies (Budavari, 1996).

Reaction with acids gives off hydrogen gas (ILO, 1998).

Cadmium dust presents a fire hazard when it is exposed to hydrazoic acid, metals, oxidants, selenium, tellurium, and zinc (HSDB , 2000; ILO, 1998; Lewis, 1996; NFPA, 1997; Pohanish & Greene, 1997).

Cadmium has a rapid reaction with nitryl fluoride when heated (Lewis, 1996).

Cadmium does not react with alkalies, reacts slowly with hot hydrochloric acid (HCl) or sulfuric acid (H2SO4) to produce highly flammable hydrogen gas, and reacts readily with dilute nitric acid (HNO3) (Kirk-Othmer, 1992). Other reactions are similar to those of zinc, but cadmium is not as strongly reactive as zinc (Budavari, 1996; Kirk-Othmer, 1992).

Cadmium explodes on contact with hydrazoic acid. It causes a violent or explosive reaction when heated with ammonium nitrate. It causes a vigorous reaction when heated with nitryl fluoride (Lewis, 1996; Pohanish & Greene, 1997).

When heated to a high temperature, it emits toxic fumes of cadmium (Lewis, 1996).

Cadmium is slowly oxidized by moist air to form cadmium oxide (Budavari, 1996).

Cadmium is a high neutron absorber (Lewis, 1993).

EVACUATION PROCEDURES

SUMMARY

Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.

SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)

If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.

PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)

CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number:

MEXICO:

SETIQ:

01-800-00-214-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5559-1588;
For calls originating elsewhere, call: 011-52-555-559-1588.

CENACOM:

01-800-00-413-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885;
For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.

ARGENTINA:

CIQUIME:

0-800-222-2933 in the Republic of Argentina;
For calls originating elsewhere, call: +54-11-4613-1100.

BRAZIL:

PRÓ-QUÍMICA:

0-800-118270 (Toll-free in Brazil);
For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).

COLUMBIA:

CISPROQUIM:

01-800-091-6012 in Colombia;
For calls originating in Bogotá, Colombia, call: 288-6012;
For calls originating elsewhere, call: 011-57-1-288-6012.

CANADA:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions.
As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.
Keep unauthorized personnel away.
Stay upwind.
Keep out of low areas.
Ventilate enclosed areas.

AIHA ERPG Values for CAS7440-43-9 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS7440-43-9 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Cadmium
TEEL-0 (units = mg/m3): 0.005
TEEL-1 (units = mg/m3): 0.10
TEEL-2 (units = mg/m3): 0.76
TEEL-3 (units = mg/m3): 4.7
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS7440-43-9 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Listed as: Cadmium
Proposed Value:

AEGL-1

10 min exposure:

ppm:
mg/m3: 0.13 mg/m(3)

30 min exposure:

ppm:
mg/m3: 0.13 mg/m(3)

1 hr exposure:

ppm:
mg/m3: 0.1 mg/m(3)

4 hr exposure:

ppm:
mg/m3: 0.063 mg/m(3)

8 hr exposure:

ppm:
mg/m3: 0.041 mg/m(3)

Definitions:

AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.

Listed as: Cadmium
Proposed Value:

AEGL-2

10 min exposure:

ppm:
mg/m3: 1.4 mg/m(3)

30 min exposure:

ppm:
mg/m3: 0.96 mg/m(3)

1 hr exposure:

ppm:
mg/m3: 0.76 mg/m(3)

4 hr exposure:

ppm:
mg/m3: 0.4 mg/m(3)

8 hr exposure:

ppm:
mg/m3: 0.2 mg/m(3)

Definitions:

AEGL-2 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape.

Listed as: Cadmium
Proposed Value:

AEGL-3

10 min exposure:

ppm:
mg/m3: 8.5 mg/m(3)

30 min exposure:

ppm:
mg/m3: 5.9 mg/m(3)

1 hr exposure:

ppm:
mg/m3: 4.7 mg/m(3)

4 hr exposure:

ppm:
mg/m3: 1.9 mg/m(3)

8 hr exposure:

ppm:
mg/m3: 0.93 mg/m(3)

Definitions:

AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.

NIOSH IDLH Values for CAS7440-43-9 (National Institute for Occupational Safety and Health, 2007):

IDLH: 9 mg Cd/m3 (as Cd)
Note(s): Ca

(Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
- ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area).
- Do not touch damaged containers or spilled material unless wearing appropriate protective clothing.
- Stop leak if you can do it without risk.
- Prevent entry into waterways, sewers, basements or confined areas.
- Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers.
- DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 154 (ERG, 2004)
- Wear positive pressure self-contained breathing apparatus (SCBA).
- Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
- Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
Place cadmium in properly labeled box and have it salvaged or sell as scrap metal (HSDB , 2000; ITI, 1995).

WASTE TREATMENT OPTIONS

RECYCLING/RECLAMATION

The maximum allowable level of cadmium in recycled oils to be used as used-oil fuel is 2 mg/kg (Freeman, 1989).
Electrolytic techniques have been used to recover a variety of heavy metals, including cadmium, from process streams or rinsewaters. The recovered metal can either be reused or sold (Freeman, 1989).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

CHEMICAL TREATMENT

Chemical precipitation is applicable to the treatment of aqueous hazardous wastes containing toxic constituents that may be converted to an insoluble form. This includes wastes containing cadmium (Freeman, 1989).
- For certain metals, ie cadmium and lead, carbonate precipitation may produce effluent metal concentrations comparable to those achievable by hydroxide precipitation, with the benefits of lower operating pH and denser, more filterable sludge. A pH of 10 or greater is required for effective precipitation of cadmium and lead hydroxide, but these metals can be precipitated as carbonates at pH of 7.5 to 8.5 (Freeman, 1989).
Resource Conservation and Recovery Act (RCRA) requires that solid waste containing cadmium, which is characterized as hazardous waste when evaluated with the Toxicant Extraction Procedure, must be stored, treated, and disposed of as a hazardous waste (HSDB , 2000).
At the time of this review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices (HSDB , 2000).
Solid waste may not be applied within one meter (three feet) of the surface of land used for the production of food-chain crops, unless in compliance with requirements specified in 40 CFR 257.3-5. These requirements limit cadmium content in the solid waste (HSDB , 2000).

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Cadmium enters the environment from numerous sources. It is released to the atmosphere from fossil fuel combustion, and then to aquatic systems from atmospheric deposition. Other sources of cadmium in the environment are industrial waste discharges such as mining residues, solid wastes, and wastewater; agricultural land surface run-off from its use as a component of fertilizer; use of contaminated irrigation water; or from dredging operations that can release cadmium from river sediments into the river water or to soil if the material is improperly dumped (IPCS, 1992; Muntau & Baudo, 1992).

Smelting and refining of zinc, lead, and copper ores releases cadmium. It is also released when: metal scrap is processed; cadmium metal is melted and poured; cadmium alloys are cast; metal, alloys, and plated steel are fabricated; solders are cast and used; metals are hot dipped or sprayed with cadmium coating; nickel-cadmium batteries are made (HSDB, 2004).

Cadmium can enter the water environment from the plating operations when spent plating solutions are discarded (HSDB , 1994).

Electroplating operations were responsible for 3.2 mg/L of cadmium in groundwater (HSDB , 2000).

Cadmium is used in plastics as a stabilizer and pigment. Incineration of plastics releases cadmium (HSDB, 2004).

Combustion of coal and fossil fuels releases cadmium into the environment (HSDB , 2000).

Volcanoes give off large quantities of aerosols containing cadmium. Mount Etna in Sicily is estimated to emit 10 tons/year of cadmium into the air (HSDB , 2000).

Cadmium is found naturally in groundwater at concentrations below 1 ppb. Natural soil concentration of cadmium typically range between 0.01-7.0 ppm, with peak concentrations reaching up to 45 ppm (Dragun, 1988).

Cigarettes contain 1-2 mcg cadmium (Zenz, 1994).

Side-stream tobacco smoke and environmental tobacco smoke contain 0.72 mcg/cigarette of cadmium (Clayton & Clayton, 1993).

Cadmium in rivers can contaminate land when river water is used for irrigation, when river sediments are dredged and dumped, or when the river floods (IPCS, 1992).

Cadmium levels up to 160 mg/kg have been found in soil near metal processing sources (IPCS, 1992).

Cadmium constitutes 45% of the chemical contaminants found at Superfund hazardous waste sites (Schardein, 1993).

Information from the last 10 years on fate and exposure of cadmium in the environment, ecotoxicological effects, and critical pathways leading to human and environmental exposure in the Community of European Countries was reviewed. Estimates were made on total emission balances for the Netherlands, Denmark, and for the EC as a whole. The balances show that 70-90% of all cadmium circulating in the Community is disposed of as waste in solid waste deposits (Jensen & Bro-Rasmussen, 1992).

Results from various investigations suggest that a loading rate limit of 5 kg cadmium/hectare (equivalent to a soil concentration of about 3.5 mg cadmium/kg) affords adequate protection to the foodchain where sludge is used on agricultural land (Davis, 1986).

ENVIRONMENTAL FATE AND KINETICS

A Yugoslavian air quality monitoring study reported that a 93% reduction in atmospheric cadmium deposits resulted in 17% and 13% decreases in cadmium concentrations in cattle feed and milk, respectively (Vidovic et al, 2005).

WATER

SURFACE WATER
- Cadmium enters surface water from surface run-off and industrial waste discharges. Once in water it may remain suspended or adsorb to sediments and soils (IPCS, 1992).
- Dredging operations releases sediment concentrations of cadmium to the river water (IPCS, 1992).

ABIOTIC DEGRADATION

Cadmium is highly mobile in the aquatic environment and its dissolved species are extremely labile. Cadmium can bioaccumulate in aquatic and terrestrial organisms. Cadmium also can inhibit leaf litter decomposition and nutrient recycling (IPCS, 1992; Muntau & Baudo, 1992).

BIODEGRADATION

Cadmium inhibits leaf litter degradation and decreases recycling of nutrients. This is likely due to smaller populations of the microorganisms responsible for litter decomposition (IPCS, 1992).

BIOACCUMULATION

HUMANS

Half-life of cadmium in the human body, as a whole, is 200 days (OHM/TADS , 2000).

FISH

A survey of heavy metals in marine organisms (teleost and elasmobranch fish species, bivalve and cephalopod mollusc species, crustaceans from the Adriatic and Ionian Seas reported cadmium residue levels in flesh and various organs (Marcotrigiano & Storelli, 2003):
- Fish Muscle: not detected-0.19 (average 0.05) mcg/g wet weight
- Fish Liver: 0.05-1.68 (average 0.28) mcg/g wet weight
- Cephalopod Flesh: 0.04-1.04 (average 0.25) mcg/g wet weight
- Cephalopod Digestive Gland: 1.0-6.92 (average 2.7) mcg/g wet weight
- Bivalve Flesh: 0.01-0.71 (average 0.36) mcg/g wet weight
- Crustacean Flesh: 0.01-0.27 (average 0.11) mcg/g wet weight
A survey of heavy metals in marine organisms (teleost and elasmobranch fish species, bivalve and cephalopod mollusc species, crustaceans from the Adriatic and Ionian Seas reported cadmium residue levels in flesh and various organs (Marcotrigiano & Storelli, 2003): Fish Muscle: not detected-0.19 (average 0.05) mcg/g wet weightFish Liver: 0.05-1.68 (average 0.28) mcg/g wet weightCephalopod Flesh: 0.04-1.04 (average 0.25) mcg/g wet weightCephalopod Digestive Gland: 1.0-6.92 (average 2.7) mcg/g wet weightBivalve Flesh: 0.01-0.71 (average 0.36) mcg/g wet weightCrustacean Flesh: 0.01-0.27 (average 0.11) mcg/g wet weight
- Fish Muscle: not detected-0.19 (average 0.05) mcg/g wet weight
- Fish Liver: 0.05-1.68 (average 0.28) mcg/g wet weight
- Cephalopod Flesh: 0.04-1.04 (average 0.25) mcg/g wet weight
- Cephalopod Digestive Gland: 1.0-6.92 (average 2.7) mcg/g wet weight
- Bivalve Flesh: 0.01-0.71 (average 0.36) mcg/g wet weight
- Crustacean Flesh: 0.01-0.27 (average 0.11) mcg/g wet weight
- Cadmium concentrations in fish liver generally exceeded fish muscle tissue levels.
- Cadmium concentrations in cephalopod digestive glands were notably higher than mean levels in cephalopod flesh.
- Cadmium concentrations in bivalve flesh and crustaceans were relatively low.
Marine fish contain cadmium at levels up to 5.2 mg/kg of whole fish body (IPCS, 1992).
Freshwater fish contain cadmium at levels of 0.01-1.04 mg/kg of whole body (IPCS, 1992).

BIRDS

Marine birds contain cadmium at levels up to 231 mg/kg of kidney (IPCS, 1992).
Terrestrial birds contain cadmium at levels < 0.05-0.24 mg/kg, and up to 7.4 mg/kg of whole body (IPCS, 1992).
Remarkably high concentrations of cadmium (5 to 160 mg/kg) have recently been found in kidneys obtained from penguins living in Antarctica (Elinder, 1992).

PLANTS

AQUATIC
- Cadmium readily accumulates in laboratory-exposed alligator weed. The bioaccumulation factor (BF) for cadmium in alligator weed plants is 16.6 (Naqvi et al, 1993).
- Marine algae contain cadmium at levels < 1-16 mg/kg (IPCS, 1992).
- Plants accumulate and translocate cadmium. Cadmium causes reduced plant growth, but over long periods of time plants may develop a tolerance. Fresh water plants were reported to contain cadmium at levels of 0.5-1.8 mg/kg of whole plant, and up to 6.7 mg/kg of roots(IPCS, 1992).
TERRESTRIAL
- Rice, beans, and wheat accumulate high concentrations of cadmium when grown in cadmium contaminated soils (Hathaway, 1996; (Zenz, 1994).
- Accumulation and translocation of cadmium occurs in plants. Terrestrial plants contained cadmium at levels up to 27.1 mg/kg of whole plant, and up to 257 mg/kg of grain. Cadmium causes reduced plant growth, but over long periods of time plants may develop a tolerance. (IPCS, 1992).
- The critical levels of metal uptake by wheat and rice plants after metal oxides were applied to soil (cadmium oxide, zinc oxide, and lead oxide) were determined. The highest concentration obtained for wheat grain was 141 mcg/g cadmium at 10,000 ppm cadmium in soil. Also, concentrations of more than 1.0 mcg/g cadmium in wheat were observed at 5 ppm cadmium, while similar concentrations for rice plants were observed at 30 ppm cadmium in soil (Muramoto et al, 1990).
- Radish, spinach and lettuce were grown in the field on (109)cadmium-labelled soil. Efficient transfer to the plant was observed with concentration factors (cadmium concentration in plant (dry weight) divided by cadmium concentration in soil (dry wt) of between 0.30 and 2.00. Soil uptake of cadmium accounted for only 64% to 69% of cadmium in the plants, the remainder arising from atmospheric deposition (Harrison & Chirgawi, 1989).
- The accumulation of cadmium by four crops (cabbage, carrot, lettuce and radish) grown on soils contaminated from a variety of sources was investigated in greenhouse pot experiments. Stepwise multiple regression analyses of the data revealed that, out of the 23 soil variables determined, only eight were significantly related to cadmium accumulation in the edible plant tissues. The most frequently occurring soil parameter was total cadmium, which was inversely related to plant cadmium accumulation. This implies that, for the heterogeneous group of soils used, as the concentration of cadmium in the soil increases the proportion available to the plant decreases. This may be due to the presence of metallic ore particles and/or the high sorptive capacity of the most contaminated soils (Alloway et al, 1990).

MAMMALS

The liver and kidneys of mammals accumulate cadmium (Zenz, 1994).
Mammals were reported to contain cadmium at levels up to 8.1 mg/kg of kidney (IPCS, 1992).
In mammals and birds, cadmium accumulates in livers and kidneys at concentrations of 0.1 to 2 mg/kg and 1 to 10 mg/kg wet weight, respectively. Animals with long life spans, such as horses, have very high concentrations of cadmium in their organs, In renal cortex samples obtained from old horses, concentrations of nearly 200 mg/kg have been found (Elinder, 1992).
Median cadmium concentrations were significantly higher for liver (0.154 mg/kg-wet wt) and kidneys (1.521 mg/kg-wet wt) of adult brown hares (Lepus europaeus) compared to juvenile liver (0.048 mg/kg-wet wt) and kidney (0.582 mg/kg-wet wt). Results from a 1-year study conducted in a West Slovakian lowland showed(Massanyi et al, 2003):
- Adult female kidneys had significantly higher cadmium levels (1.464 mg/kg-wet wt) than adult male kidneys (1.384 mg/kg-wet wt).
- Seasonal differences in cadmium tissue concentrations were not significant.
- Cadmium, mercury, and lead levels in kidneys were significantly correlated.

OTHER

INVERTEBRATES
- A study of cadmium and lead residues in field-collected red swamp crayfish (Procambarus clarkii) and uptake by alligator weed (Alternanthera philoxiroides) was conducted in Louisiana, USA. The bioaccumulation factors (BFs) for cadmium and lead in crayfish tissues were determined to be 5.1 and 1.7, respectively. BFs for alligator weed plants for cadmium and lead were 16.6 and 14.8, respectively. Data from the study suggest that although there is no biomagnification of cadmium and lead from alligator weed to crayfish, both metals readily accumulate in field-collected crayfish and laboratory-exposed alligator weed (Naqvi et al, 1993).
- In a study of the effects of metals on the isopod Porcellio scaber and the implication of metal pollution for the functioning of isopods in soil decomposition processes, it was concluded that the bioavailability of cadmium in laboratory tests is often higher than the bioavailability in the field at the same total concentrations (Van Wensem et al, 1992).

BIOCONCENTRATION FACTOR

In a review of information from the latest 10 years concerning fate and exposure of cadmium in the environment, ecotoxicological effects, and critical pathways leading to human and environmental exposure in the Community of European Countries, it was found that aquatic organisms could be classified in order of decreasing accumulation: algae greater than mollusks, greater than crustaceans, greater than fish. There was no evidence of biomagnification of cadmium within marine or fresh water food webs (Jensen & Bro-Rasmussen, 1992).
- Biomagnification in terrestrial food chains was also not observed. The uptake into plants is plant specific. Within plants, significant variations were seen, with concentrations generally decreasing in the order: roots greater than leaves, greater than fruiting parts, greater than seeds (Jensen & Bro-Rasmussen, 1992).

ENVIRONMENTAL TOXICITY

ECOTOXICITY VALUES

AMPHIBIANS

Adrenotoxicity of cadmium (as CdCl2) (Goulet & Hontela, 2003):

EC50 - AFRICAN CLAWED FROG (Xenopus larvis): 127 mcM of CdCl2 for 1H in vitro steroidogenic cells -- endocrine toxicity, impaired ACTH-stimulated corticosterone secretion (Goulet & Hontela, 2003)
EC50 - BULLFROG (Rana catesbeiana): 22 mcM of CdCl2 for 1H in vitro steroidogenic cells -- endocrine toxicity, impaired ACTH-stimulated corticosterone secretion (Goulet & Hontela, 2003)
LC50 - AFRICAN CLAWED FROG (Xenopus larvis): 3,312 mcM of CdCl2 for 1H in vitro steroidogenic cells -- adrenal cytoxicity (Goulet & Hontela, 2003)
LC50 - BULLFROG (Rana catesbeiana): 907 mcM of CdCl2 for 1H in vitro steroidogenic cells -- adrenal cytoxicity (Goulet & Hontela, 2003)

FRESHWATER TOXICITY (OHM/TADS , 2000)

IL50 ROOT WEIGHT - EURASION WATERMILFOIL: 7.4 ppm
IL50 STEM LENGTH - EURASION WATERMILFOIL: 80.9 ppm
IL50 STEM WEIGHT - EURASION WATERMILFOIL: 14.6 ppm
IL50 ROOT LENGTH - EURASION WATERMILFOIL: 20.8 ppm
LC - DAPHNIA MAGNA: 0.1 ppm
LC0 - BLUEGILL: 0.08 ppm for 6 MONTHS
LC0 - LARGEMOUTH BASS: 0.001 ppm for 6 MONTHS
LC0 - STRIPED BASS FINGERLING: 0.001 ppm for 24-96H
LC0 - STRIPED BASS LARVAE: 0.001 ppm for 24H and 48H
LC0 - STRIPED BASS LARVAE: <0.001 ppm for 72H and 96H
LC50 - ACRONEURIA: 32 ppm for 332H
LC50 - EPHEMERELLA: 2 ppm for 96H
LC50 - HYDROPSYCHE: 32 ppm for 240H
LC50 - RAINBOW TROUT: 0.007 ppm for 96H
LC50 - RAINBOW TROUT: 0.007 ppm for 240H
LC50 - STEELHEAD TROUT, ADULT: 2.9-4.95 ppb for 17D
LC50 - STEELHEAD TROUT, ADULT: 2.9-4.95 ppb for 17D
LC50 - STEELHEAD TROUT: 9.5x10(-4) ppm for 96H
LC50 - STRIPED BASS FINGERLING: 0.002 ppm for 24-96H
LC50 - STRIPED BASS LARVAE: 0.003 ppm for 24H
LC50 - STRIPED BASS LARVAE: 0.002 ppm for 48H
LC50 - STRIPED BASS LARVAE: 0.001 ppm for 72H and 96H
LC50 - STRIPED BASS LARVAE: 0.005 ppm for 24H
LC50 - TETRAHYMENA PYRIFORMIS: 1.67 ppm for 96H
LC100 - STRIPED BASS FINGERLING: 0.003 ppm for 24-96H
LC100 - STRIPED BASS LARVAE: 0.003 ppm for 48-96H
LD50 - ASPERGILLUS NIGER: 6.8 ppm for 40H
MEDIAN SURVIVAL - RAINBOW TROUT: 0.1 ppm for 64H
NO EFFECT - BLUEGILL: 0.031 ppm for 11 MONTHS
TL50 - FATHEAD MINNOW: 7.2 ppm for 96H
TLM - RAINBOW TROUT: 0.008-0.01 ppm for 168H
TLM - RAINBOW TROUT: 0.1 ppm for 168H
TLM - RAINBOW TROUT: 30 ppm for 24H

SALTWATER TOXICITY (OHM/TADS , 2000)

LC50 - CRANGDON SEPTEMSPINOSA: 0.32 ppm for 96H
LC50 - CYPRINODON VARIEGATUS: 50 ppm for 96H
LC50 - FUNDULUS MUGALIS: 21 ppm for 96H
LC50 - MUMMICHOG: 55 ppm for 96H
LC50 - MYA ARENARIA: 2.2 ppm for 96H
LC50 - MYTILUS EDULIS: 25 ppm for 96H
LC50 - NASSARIUS OBSOLETUS: 10.5 ppm for 96H
LC50 - NEREIS VIRIENS: 11 ppm for 96H
LC50 - PAGARUS LONGICARPUS: 0.32 ppm for 96H
LC50 - PALAEMONETES VULGARIS: 0.42 ppm for 96H
LC50 - SHORE CRAB: 4.1 ppm for 96H
LC50 - SHRIMP: 3-10 ppm for 48H
LC50 - STARFISH: 0.82 ppm for 96H
LC50 - UROSAIPINX CINEREA: 6.6 ppm for 96H
TLM - EASTERN OYSTER: 0.2 ppm for 1344H
TLM - EASTERN OYSTER: 0.1 ppm for 2520H

SOIL MICROORGANISMS (Dragun, 1988)

10 ppm of cadmium in pH 5, loamy sand caused a 17% decrease in microorganisms performing respiration.
100 ppm of cadmium in pH 5, loamy sand caused an 11% decrease in microorganisms performing respiration.
100 ppm of cadmium in pH 6.75, silt loam caused significant retardation of microorganisms performing denitrification.500 ppm of cadmium in pH 4.8, sandy loam caused retardation of microorganisms performing nitrification.
1000 ppm of cadmium in pH 4.8, sandy loam had no effect on microorganisms performing ammonification.
1000 ppm of cadmium in pH 4.8, sandy loam caused retardation of microorganisms performing nitrification.

ECOTOXICITY STUDIES -- AQUATIC

Previous studies suggest apotosis could be key mediator of cadmium toxicity. Exposure to 100 mcM cadmium (as CdCl2) induced ectopic apotosis at 28 hours post fertilization (hpf) in embryos of zebrafish (Danio rerio). No effects on apotosis were found at earlier embryo stages (13, 16, 19 hpf) using same TUNEL assay. No effects were reported for embryo cell cycle arrest (Chan & Cheng, 2003).
Common carp embryos were incubated in water containing trace amounts of cadmium (0.001 to 0.05 ppm). This resulted in delayed hatching, decreased swelling of the eggs, and reduced embryo survival rates. Ninety-six hour LC50 values were: 0.002 ppm cadmium for fish under 10 days; 0.005 ppm cadmium for fish 10 to 20 days; and, 0.007 ppm cadmium for fish over 20 days (Witeska et al, 1995).
Acute (96 hour) LC50 tests of cadmium toxicity under four different water chemistry conditions were conducted on the mangrove-dwelling fish, Rivulus marmoratus. The four different water chemistry conditions represented fresh water (low (Ca+Mg) and low (Na+K)), 14 ppt sea water simulated with Cl salts (high (Ca+Mg) and high (Na+K)) and two artificial conditions (high (Ca+Mg), low (Na+K) and low (Ca+Mg), high (Na+K)). The mean LC50's (as mg total Cd/L) were 2.96 (fresh water), 21.12 (high (Ca+Mg), high (Na+K)), 17.86 (high (Ca+Mg), low (Na+K)) and 12.67 (low (Ca+Mg), high (Na+K)) (Lin & Dunson, 1993).
In order to evaluate ecological consequences of the long-term presence of metals in aquatic ecosystems, the filtration rate and survival of zebra mussels (Dreissena polymorpha) during chronic exposure to cadmium was investigated. The chronic LC50 for cadmium was 130 mcg/L. The LC50 for cadmium decreased markedly from 388 mcg/L to 27 mcg/L when the exposure time was lengthened from 48 hours to 10 weeks (Kraak et al, 1992).
Chronic effects of cadmium on the growth and reproduction of the guppy (Poecilia reticulata) were studied using a food chain model, midge larvae as prey and guppy as predator. Cumulative numbers of fry produced by the guppy fed cadmium-accumulated midge larvae (210 mcg/g) for 2 months decreased to approximately 80% of the control. Guppies had been fed the cadmium-accumulated midges from 30 days old for 7 months. Cumulative numbers of fry produced by the guppy fed cadmium-accumulated midge larvae (500, 800, and 1,300 mcg cadmium/g) for 6 months decreased to 79%, 65%, and 55% of the control, respectively (Hatakeyama & Yasuno, 1987).
In a long-term exposure study (16 weeks) of the American eel, Anguilla rostrata, to an environmentally realistic concentration of cadmium (150 mcg/L), a chronic elevation of plasma cortisol was noted in the fish. The study concluded that moderate cadmium pollution of the eel's habitat suffices to cause chronic stimulation of the eel's adrenocortical axis and the resulting continued hypercortisolemia must seriously affect the eel's metabolism, immunosystem, gonadal maturation, and ability to migrate to its spawning grounds (Gill et al, 1993).
A steady-state microbial food chain consisting of the green alga Chlamydomonas reinhardii and the ciliated protozoan Tetrahymena vorax was established in a two-stage, nitrogen-limited chemostat. The lowest concentration of cadmium which produced a toxic effect at the population level was between 7.5 and 10 mcg/L. The algal population acclimated to the presence of cadmium up to 40 mcg/L added in increments over time, but demonstrated lowered cell numbers and reduced cell weights. Protozoan populations acclimated to 40 mcg/L cadmium added incrementally if the rate of dilution was lowered. Abrupt elevation of the cadmium concentration to 40 mg/L resulted in extreme fluctuations in the specific growth rates of both populations and the incipient loss of all cells from the system (washout) (Lawrence et al, 1989).

ECOTOXICITY STUDIES -- TERRESTRIAL

A field study on Great tit (Parus major) nestlings examined possible toxic effects from heavy metals exposure on bird condition and health. Sampling occurred along a pollution gradient (0-4000 m) near a large non-ferrous smelter in Belgium over three consecutive breeding seasons. Nestlings' excrement from nest sites closest to the smelter had significantly higher arsenic, cadmium, lead, silver and mercury concentrations (Janssens et al, 2003).

Nestlings from the most contaminated nest site showed significant reduction in body mass and condition.
Nestlings' legs in three nests near the smelter had growth abnormalities.
Measures of other toxic endpoints (tarsus length, wing length, haematocrit values) were not significantly different among nest sites.
Mean cadmium fecal levels (9.4 mcg/g-dry wt) were significantly higher at closest site vs. farthest site (2.9 mcg/g-dry wt).

To minimize phytotoxicity to crops, soil water should not exceed 0.1 ppm cadmium and soil 2.5 ppm cadmium. Maximum concentrations above 8 ppm in the top 12 inches of soil may lead to toxic levels in product crops (OHM/TADS , 2000).

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

112.41 (ATOMIC WEIGHT)

DESCRIPTION/PHYSICAL STATE

ATOMIC NUMBER: 48

Cadmium is an odorless, soft, ductile, silver-white, somewhat bluish metal (Ashford, 1994; Budavari, 1996) Hathaway et al., 1996; (HSDB , 2000).

Cadmium becomes brittle at 80 degrees and tarnishes in moist air. Its corrosion resistance is poor in industrial atmospheres (Lewis, 1993).

Color in water: generally colorless (OHM/TADS , 2000)

VAPOR PRESSURE

1 mmHg (at 394 degrees C) (OHM/TADS , 2000)

0.095 torr (at 320.9 degrees C) (ACGIH, 1996)

1.4 mmHg (at 400 degrees C); 16 mmHg (at 500 degrees C) (Zenz, 1994)

0 mmHg (approximately) (NIOSH , 2000)

SPECIFIC GRAVITY

NORMAL TEMPERATURE AND PRESSURE

(25 degrees C; 77 degrees F and 760 mmHg)
8.65 (at 25 degrees C) (Budavari, 1996)

DENSITY

NORMAL TEMPERATURE AND PRESSURE

(25 degrees C; 77 degrees F and 760 mmHg)
8.65 g/cm(3) (Ashford, 1994; Budavari, 1996)

BOILING POINT

765 degrees C (ACGIH, 1991; Budavari, 1996)

767 degrees C (ITI, 1995; Lewis, 1997)

770 degrees C (Ashford, 1994)

AUTOIGNITION TEMPERATURE

250 degrees C for a layer of cadmium metal dust (HSDB , 2000)

SOLUBILITY

IN WATER

Insoluble in water (HSDB , 2000; OHM/TADS , 2000; Sittig, 1991)

OTHER

Dissolved by ammonium nitrate and acids, especially nitric acid (ACGIH, 1996; (HSDB , 2000; Lewis, 1997)
Soluble in hot sulfuric acid (H2SO4) (Clayton & Clayton, 1994; HSDB , 2000)
Cadmium is soluble in acids (HSDB , 2000; Sittig, 1991).

OTHER/PHYSICAL

INDEX OF REFRACTION

1.13 (Lewis, 1997; ITI, 1995)
INDEX OF REFRACTION: 1.8 (at 578 nm, 20 degrees C/D) (HSDB , 2000)

-REFERENCES

GENERAL BIBLIOGRAPHY

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.

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.

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.

49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.

62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.

65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.

67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.

68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.

69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.

ACGIH: 1996 Supplements to the Sixth Edition of the ACGIH Documentation of Threshold Limit Values and Biological Exposure Indices, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1996a.

ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, Vol 1, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991, pp 190-194.

AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.

AMA: Effects of Toxic Chemicals on the Reproductive System, American Medical Association, Council on Scientific Affairs, Chicago, IL, 1985.

ATSDR: ToxFAQs - Cadmium. U.S, Agency for Toxic Substances and Disease Registry, US Dept of Health and Human Services, Atlanta, GA, 1993.

Achanzar WE, Achanzar KB, & Lewis JG: Cadmium induces c-myc, p53, and c-jun expression in normal human prostate epithelial cells as a prelude to apoptosis. Toxicol Appl Pharmacol 2000; 164:291-300.

Al-Bader A, Omu AE, & Dashti H: Chronic cadmium toxicity to sperm of heavy cigarette smokers: immunomodulation by zinc. Arch Androl 1999; 43:135-140.

Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.

Alessio L, Apostoli P, & Forni A: Biological monitoring of cadmium exposure -- an Italian experience. Scand J Work Environ Health 1993; 19(Suppl 1):27-33.

Alloway BJ, Jackson AP, & Morgan H: The accumulation of cadmium by vegetables grown on soils contaminated from a variety of sources. Sci Total Environ 1990; 91:223-36.

American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.

Andersen O, Nielsen JB, & Svendsen P: Oral cadmium toxicology. ACTA Pharmacol Toxicol 1986; 59(Suppl 7):44-47.

Andersen O: Chelation of cadmium. Environ Health Perspect 1984; 54:249-266.

Angle CR, Thomas DJ, & Swanson SA: Cadmium and bone toxicity: protective effect of 1,25(OH)2 vitamin D3 (Abstract). Vet Human Toxicol 1989; 31:351.

Anon: Reproductive Toxicology Newsletter, 3, Reproductive Toxicology Center, Inc, Washington, DC, 1986.

Anon: Toxicology 1991; 70:39-79.

Armstrong BG & Kazantzis G: Prostatic cancer and chronic respiratory and renal disease in British cadmium workers. Br J Ind Med 1985; 42:540-545.

Artigas A, Bernard GR, Carlet J, et al: The American-European consensus conference on ARDS, part 2: ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling.. Am J Respir Crit Care Med 1998; 157:1332-1347.

Ashford RD: Ashford's Dictionary of Industrial Chemicals, Wavelength Publications, London, United Kingdom, 1994.

Bar-Sela S, Levy M, & Westin JB: Medical findings in nickel-cadmium battery workers. Israel J Med Sci 1992; 28:578-583.

Baranski B: Effect of maternal cadmium exposure on postnatal development and tissue cadmium, copper and zinc concentrations in rats. Arch Toxicol 1986; 58:255-260.

Barlow SM & Sullivan FM: Reproductive Hazards of Industrial Chemicals, Academic Press, London, UK, 1982.

Barnhart S & Rosenstock L: Cadmium chemical pneumonitis. Chest 1984; 86:789-791.

Baselt RC & Cravey RH: Disposition of Toxic Drugs and Chemicals in Man, 4th ed, Year Book Medical Publishers, Chicago, IL, 1995, pp 105-107.

Baselt RC: Biological Monitoring Methods for Industrial Chemicals, 3rd ed, PSG Publishing Company, Littleton, MA, 1997.

Baselt RC: Disposition of Toxic Drugs and Chemicals in Man, 5th ed, Chemical Toxiology Institute, Foster City, CA, 2000.

Baxter PJ, Adams PH, & Aw TC: Hunter's Diseases of Occupations, 9th ed, Oxford University Press Inc, New York, NY, 2000.

Bernard A & Lauwerys R: Cadmium in human population. Experientia 1984; 40:143-152.

Bernard A, Roels H & Buchet JP et al: Cadmium and Health: The Belgian Experience, IARC Scientific Publications No. 118. International Agency for Research On Cancer, 1992.

Beton DC, Andrews GS, & Davies HJ: Acute cadmium fume poisoning. Five cases with one death from renal necrosis. Br J Ind Med 1966; 23:292-301.

Bigardi AS, Pigatto PD, & Moroni P: Occupational Skin Granulomas. Clin Dermatol 1992; 10:219-223.

Bingham E, Cohrssen B, & Powell CH: Patty's Toxicology, Vol 2. 5th ed, John Wiley & Sons, New York, NY, 2001.

Blaha K, Nerudova J, & Jehlicova H: In vivo and in vitro efficacy of a new carbodithioate for the mobilization of cadmium. J Toxicol Environ Health 1995; 44:87-100.

Blumenthal S, Lewand D, & Sochanik A: Inhibition of Na(+)-glucose cotransport in kidney cortical cells by cadmium and copper: protection by zinc. Toxicol Appl Pharmacol 1994; 129:177-187.

Borella P & Giardino A: Lead and cadmium at very low doses affect in vitro immune response of human lymphocytes. Environ Res 1991; 55:165-177.

Braunwald E, Isselbacher KJ, & Petersdorf RG: Harrison's Principles of Internal Medicine, 11th ed, McGraw-Hill Book Company, New York, NY, 1987.

Britt A, Burkhart KK, & Petrini G: Treatment of a child intoxicated with cadmium using succimer: a case report (Abstract), North Am Cong Clini Toxicol, Salt Lake City, UT, 1994.

Brower RG, Matthay AM, & Morris A: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301-1308.

Buckler HM, Smith WDF, & Rees WDW: Self poisoning with oral cadmium chloride. Br Med J 1986; 292:1559-1560.

Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996, pp 265.

Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.

Caravati EM, Knight HH, & Linscott MS: Esophageal laceration and charcoal mediastinum complicating gastric lavage. J Emerg Med 2001; 20:273-276.

Cataletto M: Respiratory Distress Syndrome, Acute(ARDS). In: Domino FJ, ed. The 5-Minute Clinical Consult 2012, 20th ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2012.

Chalkley SR, Richmond J, & Barltrop D: Measurement of vitamin D3 metabolites in smelter workers exposed to lead and cadmium. Occup Environ Med 1998; 55:446-452.

Chan P & Cheng S: Cadmium-induced ectopic apoptosis in zebrafish embryos. Arch Toxicol 2003; 77:69-79.

Chia SE, Xu B, & Ong CN: Effect of cadmium and cigarette smoking on human semen quality. Internat J Fertil Menopausal Stud 1994; 39:292-298.

Choi JH & Rhee SJ: Effects of vitamin E on renal dysfunction in chronic cadmium-poisoned rats. J Medicinal Food 2003; 6(3):209-215.

Christoffersson JO, Welinder H, & Spang G: Cadmium concentration in the kidney cortex of occupationally exposed workers measured in vivo using x-ray fluorescence analysis. Environ Res 1987; 42:489-499.

Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.

Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Volume 2A, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1993.

Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Volume 2C, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1994, pp 1954-1967.

Coogan TP, Shiraishi N, & Waalkes MP: Apparent quiescence of the metallothionein gene in the rat ventral prostate: association with cadmium-induced prostate tumors in rats. Environ Health Perspect 1994; 102:137-139.

Cosma GN, Currie D, & Squibb KS: Detection of cadmium exposure in rats by induction of lymphocyte metallothionein gene expression. J Toxicol Environ Health 1991; 34:39-49.

DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.

Dabeka RW, Karpinski KF, & McKenzie AD: Survey of lead, cadmium and fluoride in human milk and correlation of levels with environmental and food factors. Food Chem Toxicol 1986; 9:913-921.

Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.

Dalton T, Fu K, & Enders GC: Analysis of the effects of overexpression of metallothionein-I in transgenic mice on the reproductive toxicology of cadmium. Environ Health Persp 1996; 104:68-76.

Davis RD: Cadmium in sludges used as fertilizer. Experientia 1986; 50:55-65.

Davison AG, Newman Taylor AJ, & Darbyshire J: Cadmium fume inhalation and emphysema. Lancet 1988; 1:663-667.

Dawson EB, Ritter S, & Harris WA: Comparison of sperm viability with seminal plasma metal levels. Biol Trace Elem Res 1998; 64:215-219.

Dragun J: The Soil Chemistry of Hazardous Materials, The Hazardous Materials Control Research Institute, Silver Spring, MD, 1988.

EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.

ERG: Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident, U.S. Department of Transportation, Research and Special Programs Administration, Washington, DC, 2004.

Edling C, Elinder CG, & Raudma E: Lung function in workers using cadmium containing solders. Br J Ind Med 1986; 43:657-662.

El Azzouzi B, Tsangaris G, & Pellegrini O: Cadmium induces apoptosis in a human T cell line. Toxicology 1994; 88:127-139.

Elinder CG, Elling C, & Lindberg E: Beta2-microglobulinuria among workers previously exposed to cadmium: follow-up and dose-response analysis. Am J Ind Med 1985; 8:553-564.

Elinder CG: Cadmium as an environmental hazard. IARC Sci Publ 1992; 118:123-32.

Elinder CG: Health hazards from environmental or occupational exposure to cadmium. Arch Pharmacol Toxicol 1986; 59(Suppl 7):24-30.

Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.

Elliott P, Arnold R, & Cockings S: Risk of mortality, cancer incidence, and stroke in a population potentially exposed to cadmium. Occup Environ Med 2000; 57:94-97.

Eriksen KT, Halkjaer J, Sorensen M, et al: Dietary cadmium intake and risk of breast, endometrial and ovarian cancer in Danish postmenopausal women: a prospective cohort study. PLoS One 2014; 9(6):e100815.

FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.

Fernandez MA, Sanz P, & Palomar M: Fatal chemical pneumonitis due to cadmium fumes. Occup Med (Oxford) 1996; 46:372-374.

Fouad AA, Eldin NAS, & Eweda MH: Protective effects of desferroxamine on cadmium induced testicular toxicity in rats (Abstract). J Toxicol - Clin Toxicol 1995; 33:539.

Fournier L, Thomas G, & Garnier R: 2,3-dimercaptosuccinic acid treatment of heavy metal poisoning in humans. Med Toxicol 1988; 3:499-504.

Freeman HM: Standard Handbook of Hazardous Waste Treatment and Disposal, McGraw-Hill Book Company, New York, NY, 1989.

Frery N, Nessmann C, & Girard F: Environmental exposure to cadmium and human birthweight. Toxicology 1993; 79:109-118.

Friberg L, Norberg GF, & Vouk V: Handbook on the Toxicology of Metals, 2nd ed, Elsevier Science Publishers, New York, NY, 1986.

Fuortes L, Leo A, & Ellerback PG: Acute respiratory fatality associated with exposure to sheet metal and cadmium fumes. Clin Toxicol 1991; 29:279-283.

Furst A & Fan AM: Carcinogenic action of nickel and cadmium powders in the same rat. Biol Tr Elem Res 1993; 36:243-249.

Gerhardsson L, Borjesson J, & Mattsson S: Cadmium in kidney cortex in exposed workers (abstract), Fifth COMTOX Symposium on Toxicology and Clinical Chemistry of Metals, Vancouver, BC, 1995.

Gill TS, Leitner G, & Porta S: Response of plasma cortisol to environmental cadmium in the eel, Anguilla rostrata LeSueur. Comp Biochem Physiol 1993; 104:489-95.

Giovannucci E: Epidemiologic characteristics of prostate cancer. Cancer 1995; 75(7 Suppl S):1766-1777.

Glaser U: Ecotoxicol Environ Saf 1986; 11:261-271.

Goldfrank LR: Goldfrank's Toxicological Emergencies, 6th ed, McGraw-Hill, New York, NY, 1998.

Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.

Gorman RL, Khin-Maung-Gyi MT, & Klein-Schwartz W: Initial symptoms as predictors of esophageal injury in alkaline corrosive ingestions. Am J Emerg Med 1992; 10:89-94.

Gosselin RE, Smith RP, & Hodge HC: Clinical Toxicology of Commercial Products, 5th ed, Williams & Wilkins, Baltimore, MD, 1984.

Goulet BN & Hontela A: Toxicity of cadmium, endosulfan, and atrazine in adrenal steroidogenic cells of two amphibian species, Xenopus laevis and Rana catesbeiana. Environ Toxicol Chem 2003; 22, No. 9:2106-2113.

Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.

Grant WM & Schuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993.

Gray JA, Nicholson JK, & Timbrell JA: Creatinuria as an early indicator of cadmium-induced testicular damage. Human Toxicol 1986; 5:402-403.

Guenther Skokan E, Junkins EP, & Corneli HM: Taste test: children rate flavoring agents used with activated charcoal. Arch Pediatr Adolesc Med 2001; 155:683-686.

HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1994; provided by Truven Health Analytics Inc., Greenwood Village, CO.

HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1999; provided by Truven Health Analytics Inc., Greenwood Village, CO.

HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.

HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.

HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2004; provided by Truven Health Analytics Inc., Greenwood Village, CO.

Haas CF: Mechanical ventilation with lung protective strategies: what works?. Crit Care Clin 2011; 27(3):469-486.

Hallenbeck WH: Human health effects of exposure to cadmium. Experientia 1984; 40:136-142.

Harbison RM: Hamilton and Hardy's Industrial Toxicology, 5th ed, Mosby, St Louis, MO, 1998.

Harding JJ: Cigarettes and cataract: cadmium or a lack of vitamin C?. Br J Ophthalmol 1995; 79:199-200.

Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.

Harrison RM & Chirgawi MB: The assessment of air and soil as contributors of some trace metals to vegetable plants. II. Translocation of atmospheric and laboratory-generated cadmium aerosols to and within vegetable plants. Sci Total Environ 1989; 83:35-45.

Hartwig A, Schlepegrell R, & Dally H: Interaction of carcinogenic metal compounds with deoxyribonucleic acid repair processes. Ann Clin Lab Sci 1996; 26:31-38.

Hartwig A: Role of DNA repair inhibition in lead- and cadmium-induced genotoxicity: a review. Environ Health Perspect 1994; 102(Suppl 3):45-50.

Hatakeyama S & Yasuno M: Chronic effects of Cd on the reproduction of the guppy (Poecilia reticulata) through Cd-accumulated midge larvae (Chironomus yoshimatsui). Ecotoxicol Environ Safety 1987; 14:191-207.

Hathaway GJ, Proctor NH, & Hughes JP: Chemical Hazards of the Workplace, 4th ed, Van Nostrand Reinhold Company, New York, NY, 1996, pp 100-106.

Hochi Y, Kido T, & Nogawa K: Dose-response relationship between total cadmium intake and prevalence of renal dysfunction using general linear models. J Appl Toxicol 1995; 15:109-116.

Hoffmann K, Becker K, & Friedrich C: The German Environmental Survey 1990/1992 (GerES II): cadmium in blood, urine and hair of adults and children. J Exp Anal Environ Epidemiol 2000; 10:126-135.

Holt DH & Webb M: Arch Toxicol 1986; 58:249-254.

Horiguchi H, Oguma E, Sasaki S, et al: Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Environ Res 2004; 95:20-31.

Horiguchi H, Teranishi H, & Niiya K: Hypoproduction of erythropoietin contributes to anemia in chronic cadmium intoxication: clinical study of Itai-Itai disease in Japan. Arch Toxicol 1994; 68:632-636.

Hotz P, Buchet JP, Bernard A, et al: Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Lancet 1999; 354(9189):1508-1513.

Hudecova A & Ginter E: The influence of ascorbic acid on lipid peroxidation in guinea pigs intoxicated with cadmium. Food Chem Toxicol 1992; 30:1011-1013.

Hung YM & Chung HM: Acute self-poisoning by ingestion of cadmium and barium. Nephrol Dial Transplant 2004; 19:1308-1309.

IARC : Monographs on the Evaluation of the Carcinogenicity of Chemicals to Humans. Cadmium, CAS No. 7440-43-9. International Agency for Research on Cancer. 58. International Agency for Research on Cancer, World Health Organization. Geneva, Switzerland. 1997. Available from URL: http://www.iarc.fr. As accessed Accessed 5 Oct 01.

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.

IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.

ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.

ILO: Encyclopaedia of Occupational Health and Safety, 3rd ed, Vols 1 & 2, International Labour Organization, Geneva, Switzerland, 1983.

ILO: Encyclopaedia of Occupational Health and Safety, 4th ed, Vols 1-4. Stellman JM (Ed), International Labour Organization, Geneva, Switzerland, 1998.

IPCS: Environmental Health Criteria 134, Cadmium, World Health Organization, Geneva, Switzerland, 1992.

ITI: Toxic and Hazardous Industrial Chemicals Safety Manual, The International Technical Information Institute, Tokyo, Japan, 1995.

International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.

International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.

Iwata K, Saito H, & Moriyam M: Follow up study of renal tubular dysfunction and mortality in residents of an area polluted with cadmium. Br J Ind Med 1992; 49:736-737.

Jagetia GC & Adiga SK: Cadmium chloride induces dose-dependent increases in the frequency of micronuclei in mouse bone marrow. Mutat Res 1994; 306:85-90.

Janssens E, Dauwe T, Pinxten R, et al: Effects of heavy metal exposure on the condition and health of nestlings of the great tit (Parus major), a small songbird species. Environ Pollut 2003; 126:267-274 .

Jarup L & Elinder CG: Incidence of renal stones among cadmium exposed battery workers. Br J Ind Med 1993; 50:598-602.

Jarup L, Alfven T, & Persson B: Cadmium may be a risk factor for osteoporosis. Occup Environ Med 1998a; 55:435-439.

Jarup L, Carlsson MD, & Elinder CG: Enzymuria in a population living near a cadmium battery plant. Occup Environ Med 1995a; 52:818-822.

Jarup L, Persson B, & Elinder CG: Decreased glomerular filtration rate in cadmium exposed solderers (Abstract), Fifth COMTOX Symposium on Toxicology and Clinical Chemistry of Metals, Vancouver, BC, 1995a.

Jarup L, Persson B, & Elinder CG: Decreased glomerular filtration rate in solderers exposed to cadmium. Occup Environ Med 1995; 52(12):818-822.

Jensen A & Bro-Rasmussen F: Environmental cadmium in Europe. Rev Environ Contam Toxicol 1992; 125:101-181.

Jin T, Nordberg G, Ye Tingting, et al: Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Environ Research 2004; 96:353-359.

Jung K, Pergande M, & Graubaum HJ: Urinary proteins and enzymes as early indicators of renal dysfunction in chronic exposure to cadmium. Clin Chem 1993; 39:757-765.

Kamiyama T, Miyakawa H, & Li JP: Effects of one-year cadmium exposure on livers and kidneys and their relation to glutathione levels. Res Comm Mol Pathol Pharmacol 1995; 88:177-186.

Karakaya A, Yucesoy B, & Sardas OS: An immunological study on workers occupationally exposed to cadmium. Human Exp Toxicol 1994; 13:73-75.

Keck C, Bramkamp G, & Behre HM: Lack of correlation between cadmium in seminal plasma and fertility status of nonexposed individuals and two cadmium-exposed patients. Reprod Toxicol 1995; 9:35-40.

Kido K, Nogawa K, & Honda R: The association between renal dysfunction and osteopenia in environmental cadmium-exposed subjects. Environ Res 1990; 51:71-82.

Kirk-Othmer: Encyclopedia of Chemical Technology, Vol 4, 4th ed, John Wiley & Sons, New York, NY, 1992.

Kirshenbaum LA, Mathews SC, & Sitar DS: Whole-bowel irrigation versus activated charcoal in sorbitol for the ingestion of modified-release pharmaceuticals. Clin Pharmacol Ther 1989; 46:264-271.

Klaassen CD, Amdur MO, & Doull J: Casarett and Doull's Toxicology, 3rd ed, Macmillan Publishing Co, New York, NY, 1986.

Klaassen CD, Liu J, & Choudhuri S: Metallothionein: an intracellular protein to protect against cadmium toxicity. Ann Rev Pharmacol Toxicol 1999; 39:267-294.

Klaassen CD, Waalkes MP, & Catilena LR: Alteration of tissue disposition of cadmium by chelating agents. Environ Health Perspect 1984; 54:233-242.

Klaassen CD: Heavy metals and heavy-metal antagonists, in: Gilman AG, Rall TW, Niew AS et al (Eds), Goodman and Gilman's the Pharmacological Basis of Therapeutics, 3rd ed, Pergamon Press, New York, NY, 1990, pp 1605-1606.

Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.

Klimisch HJ: Lung deposition, lung clearance and renal accumulation of inhaled cadmium chloride and cadmium sulphide in rats. Toxicology 1993; 84:103-124.

Kollef MH & Schuster DP: The acute respiratory distress syndrome. N Engl J Med 1995; 332:27-37.

Kosnett MJ: Medical surveillance for renal endpoints. Occup Med State of the Art Rev 1990; 5:531-546.

Kowal NE, Johnson DE, & Kraemer DF: Normal levels of cadmium in diet, urine, blood, and tissues of inhabitants of the United States. J Toxicol Environ Health 1979; 5:995-1014.

Kraak MH, Lavy D, & Peeters WH: Chronic ecotoxicity of copper and cadmium to the zebra mussel Dreissena polymorpha. Arch Environ Contam Toxicol 1992; 23:363-9.

Kreis IA, Dedoes M, & Hoekstra JA: Effects of cadmium on reproduction, an epizootologic study. Teratology 1993; 48:189-196.

Krzystyniak K, Fournier M, & Trottier B: Immunosuppression in mice after inhalation of cadmium aerosol. Toxicol Lett 1987; 38:1-12.

Kuntzelman DR & Angle CR: Abnormal liver function in childhood lead poisoning unaffected by DMSA (Abstract). Vet Hum Toxicol 1992; 34:355.

Lafuente A & Esquifino AI: Cadmium effects on hypothalamic activity and pituitary hormone secretion in the male. Toxicol Lett 1999; 110:209-218.

Lansdown ABG & Sampson B: Dermal toxicity and percutaneous absorption of cadmium in rats and mice. Lab Animal Sci 1996; 46:549-554.

Laudanski T, Sipowicz M, & Modzelewski P: Influence of high lead and cadmium soil content on human reproductive outcome. Internat J Gynecol Obste 1991; 36:309-315.

Lawrence SG, Holoka MH, & Hamilton RD: Effects of cadmium on a microbial food chain, Chlamydomonas reinhardii and Tetrahymena vorax. Sci Total Environ 1989; 87-88:381-395.

Leduc D, de Francquen P, & Jacobovitz D: Association of cadmium exposure with rapidly progressive emphysema in a smoker. Thorax 1993; 48:570-571.

Lewis RA: Lewis' Dictionary of Toxicology, Lewis Publishers, Boca Raton, FL, 1998.

Lewis RJ: Hawley's Condensed Chemical Dictionary, 12th ed, Van Nostrand Reinhold Company, New York, NY, 1993.

Lewis RJ: Hawley's Condensed Chemical Dictionary, 13th ed, John Wiley & Sons, Inc, New York, NY, 1997.

Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 9th ed, Van Nostrand Reinhold Company, New York, NY, 1996.

Lin HC & Dunson WA: The effect of salinity on the acute toxicity of cadmium to the tropical, estuarine, hermaphroditic fish, Rivulus marmoratus: a comparison of Cd, Cu, and Zn tolerance with Fundulus heteroclitus. Arch Environ Contam Toxicol 1993; 25:41-7.

Liu YP, Liu J, & Iszard MB: Transgenic mice that overexpress metallothionein-I are protected from cadmium lethality and hepatotoxicity. Toxicol Appl Pharmacol 1995; 135:222-228.

Loiacono NJ, Graziano JH, & Kline JK: Placental cadmium and birthweight in women living near a lead smelter. Arch Environ Health 1992; 47:250-255.

Luckett BG, Su LJ, Rood JC, et al: Cadmium exposure and pancreatic cancer in south Louisiana. J Environ Public Health 2012; 2012:180186-.

Manahan SE: Toxicological Chemistry, Lewis Publishers, Inc, Chelsea, MI, 1991.

Manca D, Ricard AC, & Vantra H: Relation between lipid peroxidation and inflammation in the pulmonary toxicity of cadmium. Arch Toxicol 1994; 68:364-369.

Mandel JS, Mclaughlin JK, & Schlehofer B: International renal-cell cancer study. 4. occupation. Internat J Cancer 1995; 61:601-605.

Marcotrigiano GO & Storelli MM: Heavy metal, polychlorinated biphenyl and organochlorine pesticide residues in marine organisms: risk evaluation for consumers. Vet Res Commun 2003; 27 Suppl 1:183-195.

Marcus S, Okose P, & Jennis T: Untoward effects of oral dimercaptosuccinic acid in the treatment for lead poisoning (Abstract). Vet Hum Toxicol 1991; 33:376.

Mascagni P, Consonni D, Bregante G, et al: Olfactory function in workers exposed to moderate airborne cadmium levels. NeuroToxicol 2003; 24:717-724.

Mason HJ, Williams N, & Armitage S: Follow up of workers previously exposed to silver solder containing cadmium. Occup Environ Med 1999; 56:553-558.

Massanyi P, Tataruch F, Slameka J, et al: Accumulation of lead, cadmium, and mercury in liver and kidney of the brown hare (Lepus europaeus) in relation to the season, age, and sex in the west Slovakian lowland. J Environ Sci Health A 2003; A38/7:1299-1309.

Meplan C, Mann K, & Hainaut P: Cadmium induces conformational modifications of wild-type p53 and suppresses p53 response to DNA damage in cultured cells. J Biol Chem 1999a; 274:31663-31670.

Meplan C, Verhaugh G, & Richard M-J: Metal ions as regulators of the conformation and function of the tunour suppressor protein p53: implications for carcionogenesis. Proc Nutr Soc 1999b; 58:565-571.

Metwalley HE & Melies AE: Protective effects of desferroxamine on cadmium induced liver and kidney toxicity in rats (Abstract). J Toxicol - Clin Toxicol 1995; 33:541.

Moazam F, Talbert JL, & Miller D: Caustic ingestion and its sequelae in children. South Med J 1987; 80:187-188.

Mokhtar G, Hossny E, El-Awady M, et al: In Utero exposure to cadmium pollution in Cairo and Giza governorates of Egypt. La Revue de Sante de la Mediterranee orientale 2002; 8(2/3):254-260.

Moon C-S, Zhang Z-W, & Shimbo S: Evaluation of urinary cadmium and lead as markers of background exposure of middle-aged women in Korea: dietary intake as an influential factor. Toxicol Lett 1999; 108:173-178.

Morgan WD: New ways of measuring cadmium in man. Nature 1979; 282:673-674.

Moriguchi J, Ezaki T, Tsukahara T, et al: Alpha(1)-microglobulin as a promising marker of cadmium-induced tubular dysfunction, possibly better than beta(2)-microglobulin. Toxicol Let 2004; 148:11-20.

Mueller PW, Price RG, & Finn WF: New approaches for detecting thresholds of human nephrotoxicity using cadmium as an example. Environ Health Perspect 1998; 106:227-230.

Mueller PW, Smith SJ, & Steinberg KK: Chronic renal tubular effects in relationship to urine cadmium levels. Nephron 1989; 52:45-54.

Muller T, Schuckelt R, & Jaenicke L: Evidence for radical species as intermediates in cadmium zinc-metallothionein-dependent DNA damage in vitro. Environ Health Perspect 1994; 102(Suppl 3):27-29.

Muntau H & Baudo R: Sources of cadmium, its distribution and turnover in the freshwater environment. IARC Sci Publ 1992; 118:133-48.

Muramoto S, Nishizaki H, & Aoyama I: The critical levels and the maximum metal uptake for wheat and rice plants when applying metal oxides to soil. J Environ Sci Health [B] 1990; 25:273-80.

Murata I, Hirono T, & Saeki Y: Cadmium enteropathy, renal osteomalacia (Itai Itai disease in Japan). Bull Soc Internat la Soc Internatn de Chir 1970; 1:34-42.

NFPA: Fire Protection Guide to Hazardous Materials, 12th ed, National Fire Protection Association, Quincy, MA, 1997.

NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.

NHLBI ARDS Network: Mechanical ventilation protocol summary. Massachusetts General Hospital. Boston, MA. 2008. Available from URL: http://www.ardsnet.org/system/files/6mlcardsmall_2008update_final_JULY2008.pdf. As accessed 2013-08-07.

NIOSH : Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.

NIOSH: Current Intelligence Bulletin 42, Cadmium, National Institute for Occupational Safety and Health, Cincinnati, OH, 1984.

NIOSH: IDLH Documentation - Cadmium Compounds (as Cd), National Institute for Occupational Safety and Health, Cincinnati, OH, 1996.

NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.

NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.

NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.

NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.

Nagyova A, Galbavy S, & Ginter E: Histopathological evidence of vitamin C protection against Cd-nephrotoxicity in guinea pigs. Exp Toxicol Pathol 1994; 46:11-14.

Naqvi SM, Howell RD, & Sholas M: Cadmium and lead residues in field-collected red swamp crayfish (Procambarus clarkii) and uptake by alligator weed, Alternanthera philoxiroides. J Environ Sci Health B 1993; 28:473-85.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.

National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.

National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.

National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.

National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.

National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.

Nicholson G, Flynn J, & Coroneos N: Cadmium poisoning in a crematorium worker. Anaesth Intens Care 1997; 25:163-165.

Nielsen JB, Andersen O, & Svendsen P: Effect of DDC on acute oral Cd toxicity. Acta Pharmacol Toxicol 1986; 59(Suppl 7):490-493.

Nilsson U, Schutz A, & Skerfving S: Cadmium in kidneys in Swedes measured in vivo using x-ray fluorescence analysis. Int Arch Occup Environ Health 1995; 405-411.

Nishijo M, Nakagawa H, & Morikawa M: Relationship between urinary cadmium and mortality among inhabitants living in a cadmium polluted area in Japan. Toxicol Lett 1999; 108:321-327.

Nishijo M, Nakagawa H, & Morikawa Y: Mortality of inhabitants in an area polluted by cadmium -- 15 year follow up. Occup Environ Med 1995; 52:181-184.

Noackfuller G, Debeer C, & Seibert H: Cadmium, lead, selenium, and zinc in semen of occupationally unexposed men. Andrologia 1993; 25:7-12.

Nogawa K: Environ Res 1986; 40:251-260.

None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.

Nuutinen M, Uhari M, & Karvali T: Consequences of caustic ingestions in children. Acta Paediatr 1994; 83:1200-1205.

OHM/TADS : Oil and Hazardous Materials/Technical Assistance Data System. US Environmental Protection Agency. Washington, DC (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.

Oberdorster G, Cherian MG, & Baggs RB: Importance of species differences in experimental pulmonary carcinogenicity of inhaled cadmium for extrapolation to humans. Toxicol Lett 1994; 72:339-343.

Okuda B, Iwamoto Y, & Tachibana H: Parkinsonism after acute cadmium poisoning. Clin Neurol Neurosurg 1997; 99:263-265.

Oldereid NB, Thomassen Y, & Attramadal A: Concentrations of lead, cadmium and zinc in the tissues of reproductive organs of men. J Reprod Fertil 1993; 99:421-425.

Ostapczuk P: Direct determination of cadmium and lead in whole blood by potentiometric stripping analysis. Clin Chem 1992; 38:1995-2001.

Panemangalore M: Interaction among zinc, copper, and cadmium in rats -- effects of low zinc and copper diets and oral cadmium exposure. J Trace Elem Exp Med 1993; 6:125-139.

Paschal DC, Burt V, & Caudill SP: Exposure of the US population aged 6 years and older to cadmium: 1988-1994. Arch Environ Contam Toxicol 2000; 38:377-383.

Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.

Piasek M & Laskey JW: Acute cadmium exposure and ovarian steroidogenesis in cycling and pregnant rats. Reprod Toxicol 1994; 8:495-507.

Pless-Mulloli T, Boettcher M, & Steiner M: alpha-1-Microglobulin: epidemiological indicator for tubular dysfunction induced by cadmium?. Occup Environ Med 1998; 55:440-445.

Pohanish RP & Greene SA: Rapid Guide to Chemical Incompatibilities, Van Nostrand Reinhold, New York, NY, 1997.

Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.

Previtera C, Giusti F, & Gugliemi M: Predictive value of visible lesions (cheeks, lips, oropharynx) in suspected caustic ingestion: may endoscopy reasonably be omitted in completely negative pediatric patients?. Pediatr Emerg Care 1990; 6:176-178.

Product Information: CHEMET(R) oral capsules, succimer oral capsules. Ovation Pharmaceuticals,Inc, Deerfield, IL, 2005.

Product Information: CHEMET(R) oral capsules, succimer oral capsules. Lundbeck Inc. (per Manufacturer), Deerfield, IL, 2011.

Product Information: Pentetate Calcium Trisodium Injection, Pentetate calcium trisodium injection. Hameln Pharmaceuticals, Hameln, Germany, 2004.

Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.

Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.

Provias JP, Ackerley CA, & Smith C: Cadmium encephalopathy: a report with elemental analysis and pathological findings. Acta Neuropathol 1994; 88:583-586.

RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1994; provided by Truven Health Analytics Inc., Greenwood Village, CO.

RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1999; provided by Truven Health Analytics Inc., Greenwood Village, CO.

RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.

Ramakrishnan S, Sulochana KN, & Selvaraj T: Smoking of beedies and cataract: cadmium and vitamin C in the lens and blood. Br J Opthalmol 1995; 79:202-206.

Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.

Roels HA, Lauwerys RR, & Bernard AM: Assessment of the filtration reserve capacity of the kidney in workers exposed to cadmium. Br J Ind Med 1991; 48:365-374.

Roels HA, Lauwerys RR, & Buchet JP: Health significance of cadmium-induced renal dysfunction: a five year followup. Br J Ind Med 1989; 46:755-764.

Rose CS, Heywood PG, & Costanzo RM: Olfactory impairment after chronic occupational cadmium exposure. J Occup Med 1992; 34:600-605.

Samarawickrama GP & Webb M: Acute effects of cadmium on the pregnant rat and embryo-fetal development. Environ Health Perspect 1979; 28:245-249.

Sarasua SM, Vogt RF, & Henderson LO: Serum immunoglobulins and lymphocyte subset distributions in children and adults living in communities assessed for lead and cadmium exposure. J Toxicol Environ Health Part A 2000; 60:1-15.

Saric MM, Blanusa M, Juresa D, et al: Combined early treatment with chelating agents DMSA and CaDTPA in acute oral cadmium exposure. Basic Clin PHarmacol Toxicol 2004; 94:119-123.

Schardein JL: Chemically Induced Birth Defects, 2nd ed, Marcel Dekker, Inc, New York, NY, 1993.

Schild JA: Caustic ingestion in adult patients. Laryngoscope 1985; 95:1199-1201.

Schwartz GG & Reis IM: Is cadmium a cause of human pancreatic cancer?. Cancer Epidemiol Biomarkers Prev 2000; 9:139-145.

Seidal K, Jorgensen N, & Elinder C: Fatal cadmium-induced pneumonitis. Scand J Work Environ Health 1993; 19:429-431.

Shaham J, Ashkenazi R, & Meltzer A: Immunotoxicity of cadmium and nickel due to chronic exposure, National Institute of Occupational and Environmental Health, Raanana, Israel, 1995.

Shaham J, Rosenboim J, & Ophire D: The correlation between blood and urine level of cadmium and nasal and paranasal sinuses disorders. Int Arch Occup Environ Health 1993; 65:S91-S93.

Shaikh ZA, Ellis KJ, & Subramanian KS: Biological monitoring for occupational cadmium exposure: the urinary metallothionein. Toxicology 1990; 63:53-62.

Sherief LM, Abdelkhalek ER, Gharieb AF, et al: Cadmium status among pediatric cancer patients in Egypt. Medicine (Baltimore) 2015; 94(20):e740.

Sikorski R, Radomanski T, & Paszkowski T: Smoking during pregnancy and the perinatal cadmium burden. J Perinat Med 1988; 16:225-231.

Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, Vols 1-2, 3rd ed, Noyes Publications, Park Ridge, NJ, 1991.

Smith SW, Ling LJ, & Halstenson CE: Whole-bowel irrigation as a treatment for acute lithium overdose. Ann Emerg Med 1991; 20:536-539.

Sorahan T & Waterhouse JAH: Cancer of prostate among nickel-cadmium battery workers (Letter). Lancet 1985; 1:459-460.

Sorahan T, Lister A, & Gilthorpe MS: Mortality of copper cadmium alloy workers with special reference to lung cancer and non-malignant diseases of the respiratory system, 1946-92. Occup Environ Med 1995; 52:804-812.

Spiller HA & Rogers GC: Evaluation of administration of activated charcoal in the home. Pediatrics 2002; 108:E100.

Staessen JA, Kuznetsova T, & Roels HA: Exposure to cadmium and conventional and ambulatory blood pressures in a prospective population study. Am J Hyperten 2000; 13:146-156.

Staessen JA, Roels HA, & Emelianov D: Environmental exposure to cadmium, forearm bone density, and risk of fractures: prospective population study. Lancet 1999; 353:1140-1144.

Stolbach A & Hoffman RS: Respiratory Principles. In: Nelson LS, Hoffman RS, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies, 9th ed. McGraw Hill Medical, New York, NY, 2011.

Sudo J, Hayashi T, & Kimura S: Mechanism of nephrotoxicity induced by repeated administration of cadmium chloride in rats. J Toxicol Environ Health 1996; 48:333-348.

Sugawa C & Lucas CE: Caustic injury of the upper gastrointestinal tract in adults: a clinical and endoscopic study. Surgery 1989; 106:802-807.

Tabacova S, Little RE, & Balabaeva L: Complications of pregnancy in relation to maternal lipid peroxides, glutathione, and exposure to metals. Reprod Toxicol 1994; 8:217-224.

Takebayashi S, Harada T, & Kamura S: Cadmium-induced osteopathy: clinical and autopsy findings of four patients. Bone Pathol Appl Pathol 1987; 5:190-197.

Tanaka M, Yanagi M, & Shirota K: Effect of cadmium in the zinc-deficient rat. Vet Human Toxicol 1995; 37:203-208.

Tandon SK, Flora SJS, & Behari JR: Vitamin B complex in treatment of cadmium intoxication. Ann Clin Lab Sci 1984; 14:487-492.

Taylor A, Jackson MA, & Patil D: Poisoning with cadmium fumes after smelting lead. Br Med J 1984; 288:1270-1271.

Telisman S, Cvitkovic P, & Jurasovic J: Semen quality and reproductive endocrine function in relation to biomarkers of lead, cadmium, zinc and copper in men. Environ Health Perspect 2000; 108:45-53.

Tenenbein M, Cohen S, & Sitar DS: Whole bowel irrigation as a decontamination procedure after acute drug overdose. Arch Int Med 1987; 147:905-907.

Tennant CJ: Potential contribution of dietary sources to urinary cadmium and beta2-microglobulin excretion of occupationally exposed workers. J Occup Med 1992; 33:1175-1179.

Thakore S & Murphy N: The potential role of prehospital administration of activated charcoal. Emerg Med J 2002; 19:63-65.

Thun MJ, Elinder CG, & Friberg L: Scientific basis for an occupational standard for cadmium. Am J Ind Med 1991; 20:629-642.

Tibbits PA & Milroy WC: Pulmonary edema induced by exposure to cadmium oxide fume: case report. Milit Med 1980; 145:435-437.

Trevisan A, Nicoletto G, & Maso S: Biological monitoring of cadmium exposure: reliability of spot urine samples. Int Arch Occup Environ Health 1994; 65:373-375.

Tsuritani I, Honda R, & Ishizaki M: Impairment of vitamin-D metabolism due to environmental cadmium exposure, and possible relevance to sex-related differences in vulnerability to the bone damage. J Toxicol Environ Health 1992; 37:519-533.

Tsuritani I, Honda R, & Ishizaki M: Serum bone-type alkaline phosphatase activity in women living in a cadmium-polluted area. Toxicol Lett 1994; 71:209-216.

U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.

U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.

U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.

U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.

U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.

U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.

U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.

U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.

U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.

United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

Vahter M, Berglund M, & Lind B: Personal monitoring of lead and cadmium exposure - a Swedish study with special reference to methodological aspects. Scand J Work Environ Health 1991; 17:65-74.

Vainio H, Heseltine E, & Partensky C: Meeting of the IARC working group on beryllium, cadmium, mercury and exposures in the glass manufacturing industry. Scand J Work Environ Health 1993; 19:360-363.

Vale JA, Kulig K, American Academy of Clinical Toxicology, et al: Position paper: Gastric lavage. J Toxicol Clin Toxicol 2004; 42:933-943.

Vale JA: Position Statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997; 35:711-719.

Van Wensem J, Krijgsman M, & Postma JF: A comparison of test systems for assessing effects of metals on isopod ecological functions. Ecotoxicol Environ Safety 1992; 24:203-16.

Vergauwen P, Moulin D, & Buts JP: Caustic burns of the upper digestive and respiratory tracts. Eur J Pediatr 1991; 150:700-703.

Verschoor M, Herber R, & van Hemmen J: Renal function of workers with low-level cadmium exposure. Scand J Work Environ Health 1987; 13:232-238.

Vestergaard P & Shaikh ZA: The nephrotoxicity of intravenously administered cadmium metallothionein: effect of dose, mode of administration and preexisting renal cadmium burden. Toxicol Appl Pharmacol 1994; 126:240-247.

Viaene MK, Masschelein R, Leenders J, et al: Neurobehavioral effects of occupational exposure to cadmium: a cross sectional epidemiological study. Occup Environ Med 2000; 57:19-27.

Viaene MK, Roels HA, Leenders J, et al: Cadmium: a possible etiological factor in peripheral polyneuropathy. Neurotoxicology 1999; 20(1):7-16.

Vidovic M, Sadibasic A, Cupic S, et al: Cd and Zn in atmospheric deposit, soil, wheat, and milk. Environ Res 2005; 97(1):26-31.

Vonzglinicki T, Edwall C, & Ostlund E: Very low cadmium concentrations stimulate DNA synthesis and cell growth. J Cell Sci 1992; 103:1073-1081.

Waalkes MP & Rehm S: Chronic toxic and carcinogenic effects of cadmium chloride in male DBA/2NCr and NFS/NCr mice: strain-dependent association with tumors of the hematopoietic system, injection site, liver, and lung. Fundam Appl Toxicol 1994; 23:21-31.

Waalkes MP, Diwan BA, & Weghorst CM: Further evidence of the tumor-suppressive effects of cadmium in the b6c3f1 mouse liver and lung -- late stage vulnerability of tumors to cadmium and the role of metallothionein. J Pharmacol Exp Ther 1993; 266:1656-1663.

Wahba ZZ, Coogan TP, & Rhodes SW: Protective effects of selenium on cadmium toxicity in rats: Role of altered toxicokinetics and metallothionein. J Toxicol Environ Health 1993; 38:171-182.

Wang C, Brown S, & Bhattacharyya MH: Effect of cadmium on bone calcium and (45)Ca in mouse dams on a calcium-deficient diet: evidence of Itai-Itai-like syndrome. Toxicol Appl Pharmacol 1994; 127:320-330.

Willson DF, Truwit JD, Conaway MR, et al: The adult calfactant in acute respiratory distress syndrome (CARDS) trial. Chest 2015; 148(2):356-364.

Wilson DF, Thomas NJ, Markovitz BP, et al: Effect of exogenous surfactant (calfactant) in pediatric acute lung injury. A randomized controlled trial. JAMA 2005; 293:470-476.

Wisniewska-Knypl J, Jablonska J, & Myslak Z: Binding of cadmium on metallothionein in man: an analysis of a fatal poisoning by cadmium iodide. Arch Toxikol 1971; 28(1):46-55.

Witeska M, Jezierska B, & Chaber J: The influence of cadmium on common carp embryos and larvae. Aquaculture 1995; 129:129-132.

Xu B, Chia S-E, & Ong C-N: Concentrations of cadmium, lead, selenium, and zinc in human blood and seminal plasma. Biol Tr Elem Res 1994; 40:49-57.

Xu B, Chia SE, & Tsakok M: Trace elements in blood and seminal plasma and their relationship to sperm quality. Reprod Toxicol 1993; 7:613-618.

Yang JL, Chao JI, & Lin JG: Reactive oxygen species may participate in the mutagenicity and mutational spectrum of cadmium in Chinese hamster ovary-K1 cells. Chem Res Toxicol 1996; 9:1360-1367.

Yassin AS & Martonik JF: Urinary cadmium levels in the US working population, 1988-1994. J Occupat Environ Hygiene 2004; 1:324-333.

Yasuda M, Miwa A, & Kitagawa M: Morphometric studies of renal lesions in Itai-itai disease: chronic cadmium nephropathy. Nephron 1995; 69:14-19.

Yoshizuka M, Mori N, & Hamasaki K: Cadmium toxicity in the thyroid gland of pregnant rats. Exp Mol Pathol 1991; 55:97-104.

Zargar SA, Kochhar R, & Mehta S: The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc 1991; 37:165-169.

Zenz C: Occupational Medicine, 3rd ed, Mosby - Year Book, Inc, St. Louis, MO, 1994.

Zhao JY, Foulkes EC, & Jones M: Delayed nephrotoxic effects of cadmium and their reversibility by chelation. Toxicology 1990; 64:235-243.

dell'Omo M, Muzi G, & Piccinini R: Blood cadmium concentrations in the general population of Umbria, Central Italy. Sci Total Environ 1999; 226:57-64.

FeedBack

CADMIUM

Classification | Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents