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Cadmium was discovered in 1817 by Fredrich Stromeyer in Göttingen, Germany as a by-product of the zinc refining process.  It has an atomic number of 48, an atomic volume of 13.1 cm3/mol, an atomic weight of 112.411 gÂ·molâˆ’1.  Cadmium is a soft blue-white metal that is categorized on the periodic table as a transition metal. Cadmium has a heat vaporization of 99.57kJ/mol, a melting point of 320.9Â°C, boiling point of 765Â°C, and specific gravity of 8.65 (20Â°C). 
Cadmium is a naturally occurring element that is found in the earth's crust, oceans, waterways and ambient air; therefore, it is present everywhere in our environment. Greenockite (CdS) is the technical name for the cadmium mineral. Greenockite is frequently associated with weathered sphalerites and wurtzites, but usually only found in microscopic amounts. Discovering cadmium ores are rare; therefore, the trace cadmium mineral is usually recovered from zinc refining, mining, and smelting processes. Cadmium is primarily produced worldwide; however, China, Japan, Korea, Canada and Mexico, are the predominate producers. A small amount is produced in Europe, America and Australia, although these countries are becoming the primary producers of secondary cadmium (recycling cadmium). Since cadmium is polluting the environment and is extremely toxic to humans the supply of secondary cadmium has been increasing. Hopefully, one day, a majority of primary cadmium production will be replaced by secondary cadmium production.
As mentioned above, cadmium occurs naturally in the environment including the air, water, soils and food sources. In addition, cadmium can be found anthropogenically. Anthropogenic cadmium is released into the environment via manufacturing of zinc and products containing cadmium, as well as the use and disposal of products containing cadmium.
Cadmium is natural and is the part of the gradual process of erosion and abrasion of rocks and soils. Cadmium can occur as an impurity in phosphate minerals. In fact, natural phosphate ores contain several hundred parts per million (ppm) of cadmium. In addition, cadmium is released into the atmosphere from naturally occurring events such as forest fires and volcanic eruptions.
1.1.2 Anthropogenic Sources
The most hazardous sources of cadmium are the anthropogenic sources. The primary source of airborne cadmium is smelters. In addition, zinc mine tailings have the potential to transfer cadmium to the environment. Other airborne cadmium sources include burning fuels such as coal and oil, the incineration of municipal waste which contains plastics and nickel-cadmium batteries. In addition, cadmium exposure may occur from the facilities producing iron, steel and plastics.
Cadmium is predominately used in NiCd batteries; however, it is also used in metal plating as an anticorrosion coating, as stabilizers in plastics, in producing pigments, and in nuclear reactors as neutron absorbents. Cadmium may also be produced as a by-products and wastes from the production of zinc products.
2.0 Route of exposure
Since cadmium is present everywhere, cadmium exposure is common. There are two main routes of exposure to cadmium via inhalation and ingestion. Since the United States has implemented stricter action levels for cadmium the workplace exposure has drastically decreased. However, cigarette smoking is still a major source of cadmium inhalation exposure. A minor route is dermal absorption, although this route is rare; a couple studies have revealed that dermal absorption of cadmium is possible.
2.1 Dermal Route
There area two mechanisms that facilitate cadmium absorption into the skin: binding of a free cadmium ion to sulfhydryl radicals of cysteine in epidermal keratins, or an induction and complexing with metallothionein. 
Limited research has been done on dermal absorption of cadmium. However in 1991, Wester et al studied in vitro percutaneous absorption of cadmium from water and soil into human skin.  The experiment was performed on human cadaver skin to determine the reabsorption effect of cadmium-contaminated soil and water. The study demonstrated that 8.8 % of the soil and 12.7% water cadmium solution penetrated into the skin.  It also demonstrated that the plasma uptake from soil was 0.01% and 0.07% from water. 
In addition to Wester et al 1991, studies, Lansdown and Sampson performed studies on the dermal absorption of cadmium on rats. The study consisted of applying a cadmium chloride solution to shaved rat's skin daily for 10 days. After the ten days the rat's skin showed hyperkeratosis and acanthosis with occasional ulcerative change, and an increase of the mitotic index of the skin cells.  Furthermore, the rats showed elevated cadmium concentration in their blood, liver and kidneys indicating percutaneous absorption. 
As mentioned in section 1.0, cadmium is everywhere and has a low volatility; therefore, it tends to exist in the air as a fine particulate matter. The depositions of these fine particles are dependent on their size and the rate of absorption depends on the particles solubility and surface area. Larger particle will be deposited in the upper airways while the smaller particles reach the alveoli region. Once in the lungs, the cadmium is absorbed as cadmium-cysteine into the blood supply via alveolar capillaries. Inhaled cadmium can also be deposited into the gastro-intestinal tract via cadmium particles attached to mucosa of the nasopharynx, trachea or bronchi and then swallowed.
The intake of cadmium through inhalation is generally less than ingestion. However, smokers have a higher level of cadmium intake than non-smokers. This is because tobacco leaves accumulate cadmium.
2.3 Ingestion Route
For non-smokers, ingestion via food (especially plant-based foods) and water is the major route by which cadmium enters the human body. As with all types of exposures, there will be an increase risk of exposure if one is living in a polluted area.
Most ingested cadmium passes through the gastro-intestinal region without being absorbed; however small amounts may remain in this area and are absorbed. Studies have tried to measure the gastro-intestinal absorption of cadmium, but no one has determined an exact amount. This is due to the fact that some cadmium remains in the gastro-intestinal region and is not absorbed; therefore, when the total body cadmium retention is measure it overestimates the cadmium absorption.  In addition, other factors increase the affect of the absorption amount, such as the low intakes of vitamin D, calcium, and trace elements like zinc, iron and copper. 
Once cadmium is ingested it becomes a systemic problem. The absorbed cadmium enters the blood by transporting into cells through calcium channels. The absorbed cadmium usually is in an ion form and binds to proteins, hemoglobin and albumin in the blood. Other factors such as the amount of iron in the blood determine the amount of absorbed cadmium. Thus individuals, such as women of the child bearing years, tend to absorb more cadmium due to their low iron status. Once in the blood cadmium is dispersed to other organs and tissues such as the liver, kidney and bones.
The absorbed cadmium in the blood is first transported to the liver where it activates the synthesis of metallothionein. It is no longer a free ion and is now cadmium-metallothionein. Although some of the cadmium-metallothionein stays in the liver a small amount is released into the plasma via normal cell turnover and transported to the kidneys. In the kidneys, the cadmium is filtered with the primary urine. It is reabsorbed into the proximal tubular cells where lysosomes degrade the metallothionein portion and it becomes a free ion again. The release of free cadmium ions then induces renal metallothionein synthesis. Renal damage occurs when kidneys can no longer produce sufficient metallothionein to bind to the free cadmium ion.
3.0 Acute and Chronic Toxicity
Cadmium is extremely toxic even in low concentrations and tends to bioaccumulate. Cadmium is not an essential mineral found in the human body; but for the most part, the body can tolerate low levels of cadmium without any significant side effects. However, acute exposure or chronic exposure can lead to serious health issues.
3.1 Acute or Chronic Dermal Toxicity
Dermal exposure does not appear to be a significant source of cadmium toxicity and limited studies have been performed on workers who were exposed to cadmium. These studies have not reported any significant negative dermal effects following acute or chronic exposure.
3.2 Acute Toxicity
Acute exposure to cadmium is rare in the United States, since most facilities implement and perform proper industrial hygiene practices. However accidental inhaling of very high levels of cadmium can lead to respiratory problems. The respiratory systems affected by cadmium vary from shortness of breath, lung edema and even death.
A common disease of welders is cadmium-induced pneumonitis (a.k.a. the cadmium blues). This disease occurs when welders inhale an acute amount of cadmium oxide fumes or dust as they work. Cadmium-induced pneumonitis irritates the respiratory tissues and includes flu-like symptoms such as cough, tight chest, pain in chest on coughing, dyspnea, malaise, ache, chilling, sweating, shivering, and muscle aches and destruction of mucous membranes. The problem with cadmium-induced pneumonitis is the symptoms are usually delayed by hours. Sometimes this exposure is not associated with to cadmium fumes exposure due to the delay. Cadmium-induced pneumonitis can last for several days after acute exposure to cadmium fumes. If exposure continues more advanced stages of pulmonary problems can occur, which include severe dyspnea and wheezing, chest pain and pericardial constriction, persistent cough, weakness and malaise, anorexia, nausea, diarrhea, nocturia, abdominal pain, hemoptysis, and complete physical exhaustion. In addition, if acute, high-level exposures of cadmium fumes continue, cadmium-induced pneumonitis can be fatal and death from asphyxia will occur. If death does not occur the symptoms will clear up within a week or so; however severe impaired lung function may occur for years after the initial exposure.
Acute inhalation exposure of cadmium does not appear to have significant effects on the cardiovascular system. In fact some studies, found the death from cardiovascular disease is lower in the cadmium-exposed workers. Although there are reports cadmium increases heart weight, and increases systolic and diastolic blood pressure.  One study demonstrated that hypotension and dysrhythmias have been observed after acute exposure of cadmium fumes and another case, showed inflammatory changes of the myocardium. 
The hematological effects of acute cadmium toxicity following inhalation exposure are conflicting. Studies have shown that hemoglobin concentrations were lower and that decreased packed cell volumes have been observed in some workers. 
There are very limited studies on reproductive, developmental mutagenic and teratgenic effects of inhalation cadmium exposure in worker. However, some studies have found that impaired reproductive function may alter reproductive cycling in females, testicular toxicity, decreased sperm counts and infertility.  In addition, studies have shown that cadmium can cause developmental effects such as fetal death; decreased birth weight; undescended testes; delayed sensory-motor development; altered behavior and skeletal malformations (delayed bone formation, missing or fused limbs, altered facial development). 
Acute cadmium exposure by ingestion is atypical and usually occurs when cadmium contaminated food and water is ingested, or when one uses cadmium-plated cooking utensils, or from acid juice being stored in cadmium containers. Acute ingested toxicity can also be observed in workers exposed to cadmium dust with improper or no hygiene practices. Acute oral toxicity is described by World Health Organization (WHO) as levels cadmium that exceeds 15 mg kg -1 body weight.  Ingesting cadmium at or above this level will cause severe gastro-intestinal symptoms such as vomiting, abdominal cramps and diarrhea. Fatigue, sleep disturbances, sensory and motor function disturbances, anorexia, peripheral neuropathy and headaches may also occur. It has been documented in studies that the ingestion of cadmium at doses at equal or greater than 20-30 mg kg -1 of body weight has caused fatalities. 
Inhaling lower levels of cadmium over long periods of time can results in the presence of excessive protein in the urine, chronic obstructed lung diseases such as chronic bronchitis, emphysema and dyspnoea and cancer. Chronic cadmium toxicity also leads to bone diseases such as osteomalcia and osteoporosis as well as causes anemia, teeth discoloration and loss of smell.
Studies have shown that workers, who are exposed to cadmium long term, are significantly more likely to die from chronic obstructive lung diseases. In addition, shortness of breath, chronic bronchitis and emphysema are all associated with chronic cadmium exposure. Workers, who are chronically exposed to cadmium oxide, may also develop mild to moderate pulmonary fibrosis of the lower airways.
As mention previously, cadmium toxicity increases if you are a smoker. Smoker's absorption of cadmium from cigarettes is dependent on amount of cigarettes they smoke. It has been reported that one cigarette contains about 1 - 2 Âµg of cadmium and that about 10% of that 1 - 2 Âµg is inhaled when the cigarette smoke is inhaled.  It is difficult to conclude that cadmium is the source or cause of the lung diseases associated with smoking, since there is large number of toxic compounds present in cigarette smoke that also contribute to lung diseases. However, there is conclusive evidence that non-smokers have lower total body cadmium and lower risk of chronic obstructed lung diseases.
The Environmental Protection Agency, the National Institute of Occupational Safety and Health and the American Conference of Governmental Industrial Hygienists have classified cadmium as a probable human carcinogen. While the National Toxicology Program and the World Health Organization's International Agency for Research on Cancer has classified cadmium as a known human carcinogen.
As seen with the organization listed above there is no conclusive evidence that cadmium causes lung and/or prostate cancer. Lung cancer is inconclusive due to the fact scientist are not convinced that the cancer is from cadmium exposure alone or due to the other exposures. As well, cadmium associated with prostatic cancers is inconclusive. There have been a number of more recent studies which showed cadmium exposed workers did not have an increase in expected prostatic cancers; however other studies have demonstrated that workers which were exposed to cadmium have an increased prostate cancer rate in association with their level of exposure. In addition, recent studies have detected prostatic cancers in rodents, following systematic exposure to cadmium. [10, 11]
Chronic ingestion of cadmium usually occurs with the ingestion of food and beverages contaminated with cadmium. Chronic cadmium toxicity was first reported in the 1950s by Japan's consuming contaminated rice plants. These studies showed that subsistence rice farmers had been sickened by ingesting cadmium that had passed from municipal sewage sludge used as fertilizer through the rice crop.  Cadmium is common in edible leaves, fruits and seeds, since cadmium is taken up through the plants roots. Cadmium can also be found in animal's milk and fatty tissues.  In addition, cadmium can be found in seafood, such as clams and lobster, etc.
Numerous studies indicate that the kidneys are the primary target organ of chronic cadmium toxicity. One of the first signs of cadmium-related damage to the kidneys is tubular dysfunction characterized by an increased urinary excretion of low-molecular-weight proteins such as Î²2-microglobulin, Î±1-microglobulin, and retinol binding protein or increased urinary levels of intracellular enzymes such as N-acetyl-Î²-glucosaminidase.  Long-term exposure to cadmium also damages the glomerular membrane of the kidney, leading to the excretion of high molecular weight proteins such as albumin, gamma globulins (IgG and IgA), and alpha2-macroglobulin. 
Liver damage is not usually associated with chronic cadmium exposure, except at chronically high levels of exposure. However, since the liver is a storage region for cadmium (see section 2.3) it can not be excluded as potentially damaging the liver, further studies are need in this area. In addition, the studies that have been done demonstrate that ingestion of a fatal dose of cadmium can cause pronounced liver damage.
Studies have shown that chronic exposure to cadmium can affect the bone directly, by depositing and storaging cadmium. Chronic exposure to cadmium can also indirectly affects the bones by damaging the bones ability to metabolize calcium and Vitamin D. The main bone diseases that cadmium toxicity causes are osteomalacia, osteoporosis, bone fractures, and decreased bone mineral density. These cadmium-related bone diseases generally occur to individuals with nutritional deficiencies, in postmenopausal women and individuals who have high levels of cadmium in their diet.  However, cadmium exposure alone does not explain these diseases, since treatment with Vitamin D, calcium and other supplements has been reported to be effective in relieving some symptoms and strengthening bone.  Nonetheless, recovery is much slower than if the osteomalacia was caused by nutritional deficiency solely.
Chronic exposure to elevated levels of cadmium can lead to hypertension, a dulled sense of smell, yellow discoloration of the teeth, inflammation the mucus membrane of the nose, joint soreness, hair loss, dry scaly skin, loss of appetite and anemia. Studies have shown that chronic dietary exposure to cadmium tends to leave people anemic. This is because cadmium reduces the gastro-intestinal uptake of iron. Cadmium exposure can also weaken the immune system, by causing a decrease production of T lymphotyces.
Cadmium toxicity can cause neurotoxicity which can include decreased activity, tremors, brain weight changes, altered brain dopamine and serotonin levels.  Recently, there have been studies on animals and humans on cadmium's neurological effects. The human studies have not conclusively determined that cadmium is a neurotoxin for several reasons. One of the reason is most people exposed to cadmium have also been exposed to other heavy metals that may be neurotoxins. In addition, many scientists believe that cadmium can not cross the blood-brain barrier; therefore, any toxic effect of cadmium would have to happen at a younger age. Also younger children are less likely to be exposed to cadmium, when the blood-brain barrier is not formed yet. Additional studies are needed to conclusively determine if cadmium is a neurotoxin.
4.0 Dose/Response Relationships
A dose-response relationship was demonstrated between urinary cadmium and urinary Î²2-microglobulin. Î²2-microglobulin is a low molecular weight protein that is useful as a biomarker in cadmium to tubular effects. The levels of cadmium in the urine provide an estimate of the total amount of cadmium in the body. Therefore the amount of Î²2-microglobulin in the urine can accurately indicate changes in kidney function.
Î²2-microglobulin is a protein which is normally found in the blood as it is being filtered in the kidney, and the kidney reabsorbs or returns almost all of the Î²2-microglobulin to the blood. A very small amount of Î²2-microglobulin is not reabsorbed into the blood, but is released in the urine. Cadmium damaged kidneys, increase the amount of Î²2-microglobulin in the urine. This is because the kidney cells are unable to reabsorb the Î²2-microglobulin normally. If Î²2-microglobulin greater than 1000 micrograms per gram of creatinine one has a much greater chance of developing other kidney diseases. 
5.0 Factors Influencing Toxicity
The toxicity of cadmium is influenced by a number of factors such as, the route of exposure, the dosage one is exposed to and for how long, and the chemical form of the metal. One of the major influencing factors is cadmium's accumulative properties. Cadmium is a non essential mineral that accumulate in the body over time. Therefore newborns have zero total body cadmium and increases with age. This increase is due to the fact cadmium has long half-life (approximately 38 years  and eliminates from the body very slowly (approximately 0.001% of cadmium is excreted per day ).
Another influencing factor is an individual's health status. Many factors such as the one's daily diet, one's essential mineral deficiency, their age, their gender (cadmium absorption is also increased during pregnancy) and other physiological factors. In addition to one's health status, cadmium is influenced by one's job or hobby such as jewelry making. All these things can increase one's toxicity.
Another factor, which is related to one's health status, is if the person is a smoker or not. Every time a smokers inhales, they inhale particles of cadmium which are concentrated in the tobacco leaves. Tests have shown that the average cigarette contains 2 Î¼g of cadmium; 2-10% of that dose is transferred by primary cigarette smoke.  Of that, 10% to 50% of cadmium in cigarette smoke is absorbed by the lungs.  Therefore, the average smoker is exposed to twice the amount of cadmium and accumulates two times the amount in their bodies than non-smokers. 
6.0 Affected Organ(s)
The primary organs affected by cadmium are the kidneys and bones. However, the lungs can also be a target organ for cadmium exposure, especially the inhalation of cadmium oxide fumes and tobacco smoke. Cadmium also has been linked the liver, prostate, testes and blood. Studies on laboratory animal which are exposed to cadmium have developed malignant and benign tumors of the testes, prostate, liver and adrenal gland as well as leukemia, lymphomas and sarcoma.
The biotransformation of cadmium involves cadmium binding to small cellular proteins called metallothionein. Metallothioneins are intracellular, low molecular weight; cysteine-rich proteins that are involved in normal homeostatis of essential metals. Metallothioneins also form complexes with nonessential heavy metal ions and bind to xenobiotic heavy metals such as cadmium.
After absorption cadmium is transported in plasma bound to proteins, hemoglobin and albumin. From there it goes to the liver where metallothionein is initiated. Metallothionein binds to the free cadmium ion to prevent its toxic effects. The cadmium-metallothionein leaves the liver in the blood and is transported to the kidneys. The cadmium-metallothionein is filtered through the glomeruli into the primary urine. Since cadmium-metallothionein is a low molecular weight protein it is reabsorbed from the primary urine into the proximal tubular cells. Here enzymes digest and degrade the proteins into small peptides and amino acids. Since the metallothionein is degraded, free cadmium ions are released in the cells and a new synthesis of metallothionein begins again to protect the cells from the free cadmium ion. This process continues until the tubular cells can no longer keep up the production of metallothionein. Kidneys are damaged at this point when the toxicity of the free cadmium ions is no longer protected by the metallothionein.
8.0 Storage, Secretion, Excretion
Because excretion of cadmium is low, it accumulates in the body especially in the liver, kidneys and testes. The biologic half-life of cadmium in the liver is between 4 and 19 years while the half life in the kidneys is estimated to be between 6 to 38 years.  The body is able to tolerate most of the cadmium is stored in the body. This is because cadmium is not being stored as harmful free ions, but as cadmium-metallothionein which is not harmful. But if the kidneys stores too much cadmium the production of metallothionein breaks down and free cadmium ions are released into the kidneys causing health problems.
As in nature, cadmium and zinc are found together in the body since they have similar structures. When cadmium accumulates in the liver and kidneys, it replaces the storage of essential zinc, increasing the cadmium levels and leaving the zinc deficient. This zinc-cadmium relationship is very important, because cadmium toxicity and storage increase when zinc is deficient. Healthy levels of zinc can protect against tissue cadmium damage.
Limited knowledge is known about cadmium secretion. Although a small amount of cadmium is secreted into human milk. Bovine milk contains a slightly large amount of cadium. However this may be due to cross contamination of the equipment used in the processing plant.
Absorbed cadmium is eliminated from the body primarily in the urine and in the feces. The rate of excretion is low, approximately 0.001%.  This excretion is low because cadmium remains tightly bound to metallothionein, which is almost completely reabsorbed in the renal tubules. Almost all fecal cadmium is material that was not absorbed from the gastro-intestinal tract. The absorbed cadmium is excreted very slowly, equally through urinary and fecal excretion. Cadmium is excreted into hair and breast milk; however, these excretion routes are extremely low and not significant.
9.0 Treatment or Therapy
Blood, urine, and hair tests are used to confirm cadmium poisoning. Blood test are used to shows the amount of cadmium in your body from a recent exposure. Since blood test only shows recent acute exposure, it should not be used as the only test to determine cadmium exposure.
Urine testing is performed to show both your recent and your past exposure. In addition, to a urine test often additional tests such as a complete blood count, to determine if one is anemic, and a liver function test are performed. Initial urine tests should include the following:
blood urine nitrogen,
cadmium in blood and urine,
serum and urinary creatinine,
serum creatinine (and/or calculated creatinine clearance),
serum electrolytes, and
urinary protein (low-molecular-weight proteins such as Î²2-microglobulin and RBP and urinary metallothionein). 
Î²2-microglobulin has been found in workers who have been chronically exposed to cadmium. However, an increased level of this protein alone does not confirm cadmium exposure, since other renal diseases can also increase Î²2-microglobulin excretion. In addition, RBP in the urine is just a general finding that the kidney's tubular reabsorption is decreasing. This test also could indicate other renal problems. Therefore, all of these tests should be run to positively confirm cadmium poisoning. Urinary metallothionein levels have a direct correlation with urinary cadmium levels and can accurately reflect the body's total cadmium; however, elevated levels will be shown in this test once the kidney is already damaged.
OSHA requires hair testing to workers occupationally exposed to high cadmium levels to screen for renal damage. To date there is no positive association with cadmium levels in the hair and levels in the body, and this test should only be used as biomarkers to indicate early toxic effects on the kidney.
There is no effective treatment for cadmium poisoning. Generally cadmium poisoning is treated symptomatically. An example of symptomatic treatment is the administration of vitamin B1, B12, D, and calcium, when diagnosed with cadmium-induced osteomalacia. Vitamin B1, B12, D, and calcium does remove the cadmium in the bone, however the symptoms are alleviated by this treatment.
There is a basic treatment standard for acute inhalation exposure, which includes:
supplemental oxygen, and
mechanical ventilation. 
For accidental ingestion, vomiting or gastric lavage may be beneficial immediately after exposure. In addition, chelation and dimercaprol should not be used since they can increase renal toxicity.
Hemodialysis with ethylenediamine tetraacetic acid added to the dialysate can also be used to remove circulating cadmium from the blood; however, there is not enough studies on its effectiveness.
The best treatment for cadmium poisoning is preventive measures with good industrial hygiene engineering, work practice, and administrative controls set in the workplace. Some of these controls are listed below:
ventilate when working with cadmium;
install a mechanical ventilation system; and
maintaining a clean work area free of dust;
showering and changing clothes immediately and dispose of contaminated clothing;
no smoking in the work area;
no eating or drinking in the work area;
washing hands well before smoking, eating, or drinking after work or during breaks; and
wearing proper personal protective equipment such as respiratory protection, protective clothing, eye protection, and gloves when necessary. 
In addition, workers should be educated on the prevention and early detection of cadmium toxicity. Good record keeping and yearly physicals should also be administered.
10.0 High Risk Groups
Cadmium toxicity occurs to everyone as a result of eating foods contaminated with cadmium or being exposed to cadmium at the workplace; however certain groups are more likely to be exposed to cadmium. Below is a list of factors that will increase your chances of being exposed to cadmium:
Living near hazardous waste sites or industrial factories that are contaminated with cadmium;
Working in a metal smelting and/or refining plant;
Working in a plant that produces or recycles cadmium products (e.g., batteries, coatings, plastics, pigments, computers);
And finally having a deficiency in calcium, iron, protein, and/or zinc especially if you have one of the above factors in addition.
11.0 Regulatory Efforts
Many health agencies have set exposure standards to protect the general public from excess cadmium exposure. These regulatory standards include air, soil, drinking water and/or food.
11.1 Environmental Protection Agency (EPA)
EPA classifies cadmium as a probable human carcinogen (Group B1). 
Drinking water - maximum contaminant level for cadmium in drinking water is 0.005 mg/L. 
Air - Cadmium is on the EPA National Emission Standards for Hazardous Air Pollutants (NESHAP) list of 189 hazardous air pollutants. Cadmium is listed as one of 33 hazardous air pollutants that present the greatest threat to public health in urban areas. 
Soil - EPA biosolids rule states that the ceiling for the amount of cadmium that can be applied to land is 85 mg/kg fill material. 
Food - Reference dose is 1 x 10-3 mg/kg/day. 
Water - Reference dose for human exposure is 5 x 10-4 mg/kg/day. 
Reference dose (Rfd) is an estimate of a daily exposure to the general population (including sensitive subgroups) that is likely to be without appreciable risk of deleterious effects during a lifetime. 
11.2 U.S. Food and Drug Administration (FDA)
Maximum limit of cadmium in bottled water: 0.005 mg/L. 
11.3 Occupational Health and Safety Administration (OHSA)
OSHA regulates cadmium under 29 CFR 1910.1027 for general industry and 29 CFR 1926.1127 for construction. The OSHA limit is:
Permissible Exposure Limit- TWA (PEL): 5 Âµg/m3 (fumes).
11.4 National Institute of Occupational Safety and Health (NIOSH)
Listed as a potential occupational carcinogen (cadmium dust & fume)
Immediately Dangerous to Life and Health level (IDLH) which is 9 mg/m3. 
11.5 Agency for Toxic Substances and Disease Registry (ATSDR)
Chronic durational oral minimal risk level (MRL) of 0.0002 mg/kg/day of cadmium based on its renal effects. 
This MRL standard states how much cadmium can be taken in orally chronically without risk of adverse health effects. 
11.6 National Toxicology Program (NTP)
The National Toxicology Program (NTP) has characterized cadmium as known to be a human carcinogen. 
11.7 American Conference of Governmental Industrial Hygienists (ACGIH)
American Conference of Governmental Industrial Hygienists (ACGIH) considers cadmium a suspected human carcinogen.
Threshold Limit Values (TLVs) for cadmium are 10 Âµg/m3 [8 hour Time-Weighted Average (TWA)] 
2 Âµg/m3 [8 hour TWA] for respirable fraction. 
11.8 World Health Organization (WHO)
The World Health Organization's (WHO) International Agency for Research on Cancer (IRAC) classifies cadmium as a known human carcinogen.
Tolerable weekly intake for cadmium at 7Î¼g/kg/body weight/week.