Cadmium (Cd)

Courtney Gagnon
Biol 464 Presentation
May 5, 2011
Discovered in 1817 in Germany as an impurity in
zinc carbonate
Atomic number: 48
Melting point: 609.93° F
Chemically similar to zinc and mercury
Natural Abundances: Earth’s crust: 15x10-6 %
Oceans: 5x10-9 % Humans: 7x10-5 %
Semiconductor as cadmium sulfide that becomes
more conductive when exposed to light
Classic paint pigment popularly used by
impressionist painters like Monet
Anticorrosive plating (most popular use)
Thin foil used in nuclear research facilities for
use as radiation shielding.
Ni-Cd batteries and Li-Cd batteries
Present in P fertilizers used for crop production
Solar panels
Runoff during storm events
◦ Rain is slightly acidic from dissolved CO2 and leeches cadmium
from metals
◦ Washed from crops treated with Cd-P fertilizers
Release of wastewaters generated by anthropogenic
Settlement of air particles on water that are polluted by
cigarette smoke, road dust, burning plastics and wood.
Accumulates in mud and microalgae
Cadmium does not react with water
Instead, it accumulates over time in bottom
Natural Radioisotopes
Half life = 7.7x1015 years
116Cd: Half life = 2.9x1019 years
Contamination starts at the level of microalgae , which
bioaccumulates and biomagnifies at higher trophic
The surface of microalgal cells is negatively charged
and provides binding sites for metal cations
Algae bioabsorb and bioconcentrate heavy metals from
the aquatic environment:
Cd2+ > Hg2+ > Cr6+ > Pb2+ > As5+
Cd concentrations were shown to cause 90% cell
inhibition of microalgae at 5 mg/L. Lower
concentrations caused a slow decline in biomass
Cadmium concentration in fish (also meat and fruit):
0.005- 0.01 μg/g of dry weight. Shellfish contain
higher concentrations.
Dissolution of Cd-P in fertilizers increases with
decreasing soil pH
Half life in blood 75-128 days (fast component) to 716 years (slow component), in bone is 30 years, and in
the kidney is 6-38 years.
Accumulates in humans by contaminated food, coffee,
and water, inhalation of contaminated air and cigarette
smoke (20 μg/pack)
The EPA calculated an inhalation unit risk estimate of
1.8x10-3 (μg/m3 )
The estimated lowest observed adverse effect level for
a single oral dose is 19.5 μg/lb body weight
Cadmium, once in the body, stays, probably for life, in
the kidneys, the liver, bone and the blood vessels.
As little as 2 μg daily absorbed and retained results in
a body burden of 30 mg in 40 years
Chronic intake of Cd over a long period of time most
commonly cause kidney damage and weak bones
The lungs and gastrointestinal tract are the two main routes
of Cd to cause toxicity. Skin does not easily absorb
Cd is absorbed from the gastrointestinal tract by a
transporter, DMT1 in the duodenum.
Cd absorbed into circulation is taken up by the liver and
bound to metallothionein (MT) where it is filtered in the
kidney and almost completely reabsorbed in renal tubules.
Only a small amount is absorbed into the body from the gut
10%, most of which is excreted in the urine.
About half of Cd inhaled is retained, which is absorbed from
the lungs.
The kidney is the main organ affected by chronic
Cd exposure and toxicity
Cd2+ induces an increase in lipid peroxidation
which can damage organs such as the liver, kidney,
and testis.
Cd directly inhibits Na-K channels
Cd-MT is degraded in endosomes and
lysosomes, which releases Cd2+ into the cytosol.
Cd2+ accumulates in the mitochondria and
inhibits the respiratory chain (by electron
Results in production of reactive oxygen species
(ROS) and mitochondrial disruption with the
release of cytochrome c, causing cell death by
apoptosis and necrosis
Classified as a carcinogen, but it is hard to
determine if due to high Cd concentrations, or
from other toxins present in cigarettes
Cd can induce autoantibodies to MT, which may
interfere with Cd detoxification.
Plants and algaes use the phytohormone, gibberellic
acid (GA3 ) to metabolize Cd; however, it does not
withstand strong toxic dosage (10-4 M).
Exposure significantly decreases the cytochrome P450
side chain cleavage complex which catalyzes the
biosynthesis of steroids
Cd2+ induces oxidative stress by binding to sulfyhydryl
groups of proteins and by depleting glutathione.
Lipoic acid and selenium have been proven to reverse
damage caused by Cd2+ on antioxidant defense
Cd exposure up-regulates MT production in the
liver as a protective response, but once the MTproducing capacity is exhausted, tubular cells are
Urinary cadmium excretion is slow; however, it
constitutes the major mechanism of elimination
Hair has proven to be a vehicle of detoxification of
substances from the human body because metal
cations bind to the sulphur of keratin.
Concentrations were up to 10 fold higher than
levels found in blood and urine samples
Bharavi, K., Reddy, A.G., Rao, G.S., Kumar, P.R., Prasadini, P.P. 2011.
Prevention of cadmium bioaccumulation by herbal adaptogens. Indian J.
Pharmacol. 43: 45-49. Available from:
Falkowshka, M., Pietryczuk, A., Piotrowska, A., Bajguz, A., Grygoruk, A.,
Czerpak, R. 2011. The effect of gibberellic acid (GA3 ) on growth, metal
biosorption and metabolism of the green algae Chlorella vulgaris
(Chlorophyceae) Beijerinck exposed to cadmium and lead stress. Polish J.
of Environ. Stud. 20(1): 53-59.
Gel, F., Hernandez, A.F., Marquez, C., Femia, P., Olmedo, P., LopezGuarnido, O., Pla, A. 2011. Biomonitorization of cadmium, chromium,
manganese, nickel and lead in whole blood, urine, axillary hair and saliva
in an occupationally exposed population. Science of the Total
Environment 409: 1172-1180.
Johri, N., and Jacquillet, G., Heavy metal poisoning: the effects of cadmium
on the kidney. Biometals 23: 783-792.
Monteiro, C.M., Fonseca, S.C., Castro, P.M.L., Melcata, F.X. 2011. Toxicity
of cadmium and zinc on two microalgae, Scenedesmus obliquus and
Desmodesmus pleiomorphus, from Northern Portugal. J. Appl. Phycol 23:
Schroeder, M.D., Henry. 1974. The Poisons Around Us, Toxic metals in
food, air and water. Found on:
Illinois Dept. of Public Health

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