toxic element

1.  Presented by :Pavan Barot
 Group:218
 Subject:Ecological Physiology

2. INTRODUCTION
Encountered in earth’s crust combined with chlorine (CdCl2),
oxygen (CdO),sulphur (CdS)
Exists as small particles in air, result of smelting, soldering
or other high temp. industrial processes
By-product of smelting of zinc, lead, copper ores .
Used mainly in metal plating, producing pigments,
batteries, plastics and as a neutron absorbent in nuclear
reactors

3. CADMIUM POISONING
 Caused by excessive exposure to cadmium
 No constructive purpose in the human
body.
 Extremely toxic even in low
concentrations, and will bioaccumulation
in organisms and ecosystems

4. EXPOSURE SOURCES
 Tobacco smoke (a one pack a day smoker
absorbs roughly 5 to 10 times the amount
absorbed from the average daily diet)
 Tobacco smoke is an important source of
cadmium exposure
 Cadmium a component of chuifong tokwan ,
sold illegally as a miracle herb in china.
 Low levels are found in grains, cereals, leafy
vegetables, and other basic foodstuffs

5. Toxicity
 Primary effects on kidneys
 Emphysema, Kidney, Calcium metabolism, Possible kidney
carcinogen.
 Secondary effects on urinary system
 Mechanisms
 Binds to sulfhydryl groups, displacing other metals from
metalloenzymes, disrupting those enzymes
 competing with calcium for binding sites (calmodulin)
 Kidney toxicity
 Free Cd binds to kidney glomerulus
 Proximal tubule dysfunction

6. Effects
kidney toxicity:
 Edema and Emphysema by killing macrophages
Skeletal effects:
 Osteoporosis and osteomalacia (pseudofractures)
 Cancer:
 Carcinogenic in animal studies
 Approx.8% of lung cancers may be attributable to Cd

7. Inhibition of DNA repair
Cell damage
Oxidative stress
Enhancement of DNA
damage
Decrease of Antioxidants
Activation of cellular
signals
Inhibition of DNA
Methylation
E-cadherin dysfunction
DNA
damage
Induction of Proto-
Oncogenes
Disruption Cell Adhesion
Induction of Apoptosis
Gene
Mutation
Promotion of
proliferation
Malignant
Cancer
Preneoplastic
lesion
Cd+2
A Model: Major mechanism involved in Cd+2 Carcinogenesis

8. Cadmium epidemics
Japan (1950s) “Itai-Itai” is Japanese for “ouch-
ouch”-refers to bone pain related to calcium loss
Renal failure,Anemia, severe muscle pain
River polluted with waste from factory, water
used on rice fields for many years
Rice accumulated high level of Cd Community
was poor (and therefore malnourished with
respect to calcium)

9. Metabolism, storage and excretion of cadmium in
human body
Journal of Occupational Medicine and Toxicology 2006

10. Mechanism
 Two mechanisms are involved in cadmium mutagenicity,
 Induction of reactive oxygen species and
 Inhibition of DNA repair
 Cystein is a precursor to the anti-oxidant protein glutathione and
is also required for metallothionein which is a protein that binds
to cadmium specifically
 Intracellular, cadmium binds to metallothionein
 Cadmium is released into the plasma after haemolysis or when
the erythrocytes lifetime has expired
 Cadmium is transported in blood plasma initially bound to
albumin
 Cadmium bound to albumin is preferentially taken up by the liver

11. Contd..
 In the liver, cadmium induces the synthesis of
metallothionein
 After a few days exposure metallothionein-bound
cadmium appears in the blood plasma
 Plasma metallothionein play an important role in
transport of cadmium
 Bound to sulfhydryl groups of cystein residues
 After chronic exposure, cadmium accumulates in the
liver then redistributed slowly to the kidney

12. Mechanism responsible for the selective accumulation of cadmium in proximal tubular cells
Mechanism

13. Proposed pathways for ROS in Cd toxicology and carcinogenesis
following acute and chronic exposures

14. EFFECTS OF POISONING:

15. SYMPTOMS
 Food poisoning (ingestion)
 Bronchitis (inhalation)
 Interstitial pneumonitis (inhalation)
 Pulmonary edema (inhalation)
MEDICAL CONDITIONS
 Osteoporosis
 Osteomalacia
 Hyperuricemia
 Hypophosphatemia
 Itai-itai disease
 Renal failure

16. DIAGNOSIS
DIRECT EVALUATION
 24 hour urine cadmium – reflects exposure over time Blood
cadmium-estimated
INDIRECT EVALUATION
 Urinary ß 2 -microglobulin – evaluate urine levels > 300 g/g
creatinine
 Urinary retinol-binding protein(RBP)Urinary
 Metallothionein (MT)
 Critical levels:
 blood cadmium: 10 micrograms/l
 Urinary cadmium: 10 micrograms/g creatinine
 Urinary beta 2-microglobulin: 2000 micrograms/g creatinine
 Urinary retinol-binding protein: 200 micrograms/g creatinine

17.  Elements like calcium and selenium are shown to
have protective effect against cadmium-induced
toxicity
 Adequate levels of zinc in the body helps to
displace cadmium from the tissues
 Potent antioxidants like Vitamin C, E,glutathione,
methionine, glycine, cysteine has great protective
efficiency.
TREATMENT

18. TREATMENT:
 Smoking should be avoided and do check
your house products for compounds which
contain cadmium
 Render gastric lavage or make the infected
person vomit within an hour if the person has
consumed cadmium salts
 Chelation therapy

19. Reference
• Wikipedia (heavy metal toxicity)
• Google(toxicity of cadmium)
• @Web search :effects of cadmium on kidney
@ Thank you @