Heavy metals toxicity

1. HEAVY METALS TOXICITY
Ishita Gupta,
M.V.Sc Scholar,
Veterinary Public Health & Epidemiology,
ICAR-IVRI,Bareilly,(UP).

2. INTRODUCTION
 Heavy metal refers to any metallic chemical element that has a
relatively high density and is toxic or poisonous at low
concentrations.
 According to the WHO, 2011 the common toxic ‘heavy metals’
that can be of public health concerns are beryllium (Be),
aluminium (Al), chromium(Cr), manganese (Mn), iron (Fe), cobalt
(Co), nickel (Ni), copper (Cu), zinc (Zn), arsenic (As),selenium (Se),
molybdenum (Mo), silver (Ag), cadmium (Ca), tin (Sn), antimony
(Sb), barium (Ba),mercury (Hg), thallium (Tl) and lead (Pb).
 Heavy metals are natural components of the earth's crust.
 Heavy metals are non-biodegradable, so they bio accumulate in
tissues and are biomagnified along with the trophic levels.
 As trace elements, some heavy metals (e.g. copper , selenium ,
zinc) are essential to maintain the metabolism of the human
body. However, at higher concentrations they can lead to
poisoning.

3. Major sources of heavy metal pollution:
 Mining & processing of ores: operations of ore processing, smelting , refining can cause
deposition of large quantities of heavy metals into drainage or in aquatic environments.
 Domestic waste water effluents: Significant quantities of trace metals are present in domestic
wastewater effluents due to metabolic waste products, corrosion of water pipes - copper (Cu),
lead (Pb), zinc (Zn), and cadmium (Cd), and household products - manganese (Mn), chromium
(Cr), nickel (Ni), cobalt (Co), zinc (Zn), boron (B), and arsenic (As). Wastewater treatment usually
eliminates less than half of the metal content of the effluent, leaving a large metal load in the
effluent.
 Industrial effluents: Heavy metal concentrations in industrial effluents are generally far higher
than their allowable limits , necessitating immediate treatment of metal-containing effluents
prior to discharge into aquatic bodies.
 Agricultural run off: Animal and plant residues, fertilisers, herbicides and fungicides all
contribute to the heavy metal pollution
 Combustion of fossil fuels: The burning of fossil fuels is a significant cause of airborne metal
pollution on of fossil fuels:
 Food sources: vegetables, dairy, meat & its products.

4. Sources of heavy metals in food:

5. Heavy metal contamination from diverse sources in global food crops
No. Food crops (cereals, fruits,
vegetables, etc.)
Country where
investigated
Sources of heavy
metal contaminants
affecting food chains
Metal
concentrations
recorded in food
crops (dry weight)
References
1.
Brassica sp., Chenopodium sp.,
leafy and root,vegetables,
grains
India
Sewage effluent
(inadequately treated)
Cu 1.7–12.9 mg/kg
Pb 0.13 mg/kg
Zn 7.25–24.6 mg/kg
Cr 0.08–0.38 mg/kg
Pb 0.02–0.013 mg/kg
Cu 0.16–0.85 mg/kg
Zn
Rattan et al. (2005)
2. Spinach India
Sewage wastewater
(inadequately
treated)
Cu 0.09 mg/kg
Cr 2.9 mg/kg
Pb 3.1 mg/kg
Zn 10 mg/kg
Ni 3.2 mg/kg
Chary et al. (2008)
3. Radish India
Diverse contamination
sources
Cu 5.96 mg/kg
Cr nil
Pb nil
Cd nil
Zn 22.5 mg/kg
Ni nil
Arora et al. (2008)

6. Lead toxicity:
Synonyms: Plumbism, Painter’s colic, Colica, Saturnism
 Sources of exposure:
• Drinking water pipes : from plumbing and fixtures that are either made of
lead or have lead solder. Since acidic water breaks down lead in plumbing
more readily (Plumbosolvency) chemicals can be added to municipal water
to increase the ph.
• Paints, Cosmetics, toys.
• Occupational exposure: miners , smelters, plumbers, battery recycling
workers.
• Soil by breakdown of lead paint, gasoline residues containing lead
• Food sources: Food grown rich in lead content in soil.
• Globally 800 million children & IN INDIA, OVER 275 MILLION CHILDREN
suffers from mild to severe effects of lead toxicity having level >5ug/dl of
blood ( UNICEF).

7.  Since lead in the soil can settle on or be absorbed by plants grown for fruits or vegetables or plants used
as ingredients in food, like dietary supplements, lead can reach our food supply.
 Washing or other food processing measures can not fully eliminate lead that has entered into or on
plants.Lead found in plants or water can be consumed and absorbed by the animals we feed, and then
passed on to us.
 Manufacturing processes may introduce lead inadvertently. Plumbing containing lead , can contaminate
water used for food production.
S.
No.
Sources of lead Place where
investigated in
India
Levels References
1. Spices
( Chilli & turmeric powder)
West Bengal Chilli powder: 0.8-7.6μg/g
Turmeric powder: 2.9-9.2μg/g
FAQ/WHO recommendation: 0.3μg/g
I. Mazumdar,& K.
Goswami,2014
2. Agricultural crops Source:
irrigation from glass industry
effluents
Uttarakhand Hordeum vulgare- 0.29 mg/kg
Triticum aestivum- 0.25 mg/kg
MPL- O.2 mg/kg
Vinod Kumar, AK
Chopra,2015
3. Children: Lead level in blood Metro cities of
India
47% children in India have >10μg/dL Pb
levels in blood.
Normal blood levels: 5μg/dL
Chaudhary et
al,2018

8. Mechanism of toxicity :
 Lead interferes with the activity of an essential enzyme called delta-aminolevulinic acid
dehydratase, or ALAD, which is important in the biosynthesis of heme, the cofactor found
in haemoglobin (Patrick et al., 2006) .Due to inhibition of this enzyme,anemia occurs.
 It also inhibits Pyrimidine 5- Nucleotidase enzyme that is responsible for Basophilic
Stippling.
 Lead disrupts the maintenance of the cell membrane, red blood cells with a damaged
membrane become more fragile, which results in anaemia (White et al., 2007). Lead is
also speculated to alter the permeability of blood vessels and collagen synthesis
(Needlemann , 2004).
 The primary target of lead toxicity is the central nervous system.
 Lead also interferes with the enzymes that help in the synthesis of vitamin D & interferes
with DNA transcription.

9. Clinical manifestation in humans:
 Acute poisoning: Nervous signs, numbness, tingling , haemolysis.
 Blood lead levels from 25 and 60 μg/dL give rise to neuropsychiatric effects such as delayed
reaction times, irritability, and difficulty in concentrating, as well as slowed down motor nerve
conduction and headache (Merill et al., 2007).
 Anaemia may appear at blood lead levels higher than 50 μg/dL (Merill et al., 2007),
haemolysis.
 Abdominal colic, involving paroxysms of pain, may appear at blood lead levels higher than 80
μg/dL (Kosnett, 2005).
 High blood lead levels which exceed 100 μg/dL cause very severe manifestations, like signs of
encephalopathy .
 Chronic toxicity : blue line along the gums with bluish black edging to the teeth, known as
a Burton lines, is an indication of chronic lead poisoning.
• Lead lines in radiograph.
• Decreased sperm count in men.

10. Lead lines in radiograph
Burton lines in
gums
Basophilic stippling

11. Diagnosis & Prevention :
 Diagnosis: Clinical signs , history with inquiry into possible routes of exposure,
 Blood smear examination: Reveals Basophilic stillpling.
 Radiography : Lead lines in bones ( chronic exposure).
 Blood lead level estimation. Normal levels:
 Adults : < 10 micrograms/dl of blood
 Children: < 5 micrograms/dl of blood (CDC)
 Prevention: prevention strategies can be divided into
 individual (measures taken by a family).
 preventive medicine (identifying and intervening with high-risk individuals)
 public health (reducing risk on a population level).
 Reducing the blood lead levels of children include increasing their frequency of hand washing and
their intake of calcium and iron.
 Screening may be an important method of prevention for those who are at higher risk, such as those
who live near lead-related industries.

12. Regulations:
 FDA Regulations and Guidance to Industry to Limit Lead in Food
 Bottled Water: The FDA restricts levels of lead (and other contaminants) in bottled water by defining
allowable levels in the quality standard for bottled water under its regulatory authority under the Federal
Food, Drug, and Cosmetic Act. This level is set at 5 ppb for lead.
 Juice and Candy: The FDA has released proposed recommendations to industry on specific foods and
beverages that are more likely to be ingested by small children, such as restricting lead in candy to a
maximum of 0.1 ppm and in juice to a maximum of 50 ppb.
 Tablewares:The FDA sets permissible amounts in glazed ceramic pottery (for use in serving and storing
food) to reduce the amount of lead that may leach into foods from tableware. These ceramic wares must
contain a specific label identifying the danger of using it with food.
 The Ministry of Environment, Forest and Climate Change (MOEFCC), Government of India has passed a
notification in November 2016 as “Regulation on Lead contents in Household and Decorative Paints
Rules, 2016" and has prohibited manufacture, trade, import & export of household and decorative paints
containing lead or its compounds in excess of 90 parts per million .

13. Arsenic poisoning:
 King of poisons & poison of Kings.
 Form: Inorganic Arsenic i.e. Arsinites are more toxic than Arsinates due to more
solubility.
 Sources : Food: rice & infant cereals. Fish, shellfish, meat, poultry, dairy products, rice
and cereals can also be dietary sources of arsenic, although exposure from these foods is
generally much lower compared to exposure through contaminated groundwater
 Occupational : Mining, Smelting.
 Insecticide ( Paris green).
 Incineration of preserved wood products, pressure treated with chromate copper
arsenate was found to be a source of environmental arsenic contamination.
 Herbicide or preservative for wood due to its germicidal power and resistance to rotting
and decay.
 Drinking water & food sources: Ground water is a major source of Inorganic As.
 Arsine gas & As Trioxide used for making silicone computer chips.
 Arsenic is also used in the pharmaceutical and glass industries in the manufacturing of
alloy.
 Sheep dips, leather preservatives, arsenic-containing pigments and poison baits.

15. Arsenic toxicity in India:
 Water sources of As: Arsenic contamination of ground water in West Bengal
 In India, As contamination is maximum in the states of West Bengal & Bihar.In West Bengal, around 26 million
people are at risk of drinking As contaminated water.Ganga Brahmaputra region is one of the most contaminated
regions in the world.Drainage pattern of Ganga Brahmaputra is responsible for sedimentation. Source of As can
be from coal mines. ( Santra et al,2017).
 It is a serious problem since 1980s.Around 20% population of West Bengal in 9 districts is affected by As
problem.( Santra et al ,2017).
 According to a recent study conducted on ground water samples in 38 districts of Bihar, 16% of the samples
(n=273) were having Arsenic conc. More than recommended by WHO in water i.e. >10μg/L. ( Richards et
al,2020.)
 Furthermore, in Bihar, 22 out of 38 districts were having ground water arsenic level >10 μg/L. (Chakraborti et
al,2018).
 Food sources of As: Rice accumulates more As as compared to other crops. It is the largest source of most toxic
form of As i.e. inorganic As.In Bihar, high levels of As in potato & rice were found.
 In FDA report, samples of rice from India showed that fully cooked basmati contained up to 0.9 units of inorganic
arsenic per serving, boiled variety had 2.3 units, aged variety had up to 3.9 units, white variety had up to 3.9
units and the brown variety had up to 6 units of As present.

16. Mechanism of toxicity & Clinical
manifestations:
 Mechanism of toxicity: Trivalent arsenic (As 3+ ) has a great affinity for
sulfhydryl groups of enzymes & inhibits them. It effects capillary integrity,
causes GI tract dilation , exudation of plasma fluids & diarrhoea.
 Arsine gas causes haemolysis.
 Pentavalent arsenate is uncoupler of oxidative phosphorylation, also
causes Arsenolysis.Inhibits ATP synthesis by replacement of phosphate
group.
 In chronic poisoning, As is found in in keratin containing tissues [skin,
hair, nails] for years. Attaches itself to –SH groups which are abundant in
keratin.
 Acute : shock , cholera like symptoms : vomiting, abdominal pain , gastro
enteritis, diarrhoea( rice watery).
 Chronic Arsenic Poisoning: Peripheral neuropathy ( tingling, numbness).
 Known carcinogen : causes Hepato cellular carcinoma, skin cancer.
 Black foot disease: it is the severe form of peripheral vascular disease in
which blood vessels of lower limbs are damaged resulting in gangrene.
Black foot disease

17. Chronic arsenic exposure illness :
when levels in drinking water are
>50 μg /L causes “Arsenicosis”.
Skin lesions :
 Chronic toxicity.
 Hyperkeratosis, melanosis.
 Typical dew drop like appearance.
Mees lines : In finger nails

18. Diagnosis & treatment:
 Classical symptoms in chronic poisoning : dermatitis, mees lines on nails.
 The concentration of total As in urine has often been used as an indicator of recent As
exposure because urine is the main route of excretion of most As species.
 Blood arsenic level.
 Hair is a potential bioindicator for arsenic exposure due to its ability to store trace
elements from blood.
 Treatment :
 Chelation therapy: DMSA (meso - 2,3- dimercaptosuccinc acid, Succimer) DMPS , D-
Penicillamine, Thioptic, lipoic acid sequesters the arsenic away from blood proteins and
are used in treating acute arsenic poisoning.

19. Prevention :
 The current recommended limit of arsenic in according to WHO :
Drinking-water - 10 μg /L.
Tolerable intake level : 3μg /kg BW/day
• Substitute high-arsenic sources, such as groundwater, with low-arsenic, microbiologically safe
sources such as rain water and treated surface water.
• Low-arsenic water can be used for drinking, cooking and irrigation purposes, whereas high-arsenic
water can be used for other purposes such as bathing and washing clothes.
• Discriminate between high-arsenic and low-arsenic sources. For example, test water for arsenic
levels and paint tube wells or hand pumps different colours. This can be an effective and low-cost
means to rapidly reduce exposure to arsenic when accompanied by effective education.
• Public awareness. Project Far Ganga is examining the sources of this arsenic pollution and
forecasting how its extent might change in the coming decades. Future Secular Changes &
Remediation of Groundwater Arsenic in the Ganga River Basin (FAR-GANGA).
• Regular water testing.

20. Mercury poisoning:
Synonyms: Acrodynia, Pink disease.
 Minamata bay disease/ Chisso-Minamata disease is a neurological disease caused
by severe Hg poisoning.
 Signs and symptoms include ataxia, numbness in the hands and feet,
general muscle weakness, and damage to hearing & speech. In extreme cases,
paralysis ,coma and death can occur within weeks of the onset of symptoms.
 Minamata disease was first discovered in the city of Minamata, Japan, in 1956. It
was caused by the release of Methyl mercury in the industrial wastewater from a
chemical factory owned by the Chisso corporation.
 This highly toxic chemical bioaccumulated and biomagnified in shellfish and fish
in Minamata Bay, which was eaten by the local population, resulted in mercury
poisoning.
 A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965.

21. Forms & Sources:
 According to WHO, maximum human exposure to mercury is caused by
outgassing of mercury from dental amalgam, ingestion of
contaminated fish, or occupational exposure.
 Iraq grain disaster:In 1971-72, a large outbreak of poisoning caused by
the consumption of seed dressed with organic mercury compound
occurred in Iraq.
 Elemental mercury: Liquid metal.
• Volatize at room temperature.
• Inhalation of vapors is toxic.
• Crosses BBB.
• Sources : Batteries, dental amalgams, thermometers.
 Organic mercury:
• Most toxic form of Hg.
• E.g. Methyl mercury.
• Crosses placenta & is secreted in breast milk.
• Sources: Fungicides, seed preservatives , fish & shellfish consumption.

22. Mercury toxicity in India:
 Major contributors of Hg toxicity in India: Chlor alkali industries, coal mines, thermometers,
CFLs,dental amalgams.
 Kodaikanal mercury poisoning : Occurred in 2001 at hill station of Kodaikanal, originated at thermometer
factory which was owned by Hindustan Unilever, when company disposed off waste without following
proper protocols & affected hundred of its workers following exposure to toxic Hg vapours. Around 290
tonnes of dumped waste was collected from the shola forest & was sent back to US in 2003 for recycling.
 Even after 4 years of stoppage of emission of Hg, a lake in Kodaikanal showed elevated levels of Hg in
samples of fish, sediment, water.( Karunasagar et al,2005)
 India ranks 2nd for the emission of Hg in the environment globally with an estimated emission of 144
tonnes Hg/year. ( UNEP,2013). Top contributor is coal burning industries (89.4 tonnes/year), next to it is
chlor alkali sector which contributes to about 79 tonnes/year.
 Mercury pollution in UP: Sonbhadra region is one of the largest reservoir of coal in India. Mercury blood
levels in people of this area was 34.3ppb which is above the safe limits of 5.8 ppb as prescribed by USEPA.
( Sahu et al,2014)
 High levels of Hg in fish is found around costal areas of Mumbai, Kolkata. Mercury levels in fish in Mumbai
were 0.03-0.82 mg total Hg/kg Dry Weight as compared to permissible limits i.e. 0.5 mg/kg.
 Minamata convention: is an environmental agreement whose aim is to protect human health &
environment from anthropogenic release of mercury & its compounds. To limit India’s contribution to
global Hg pollution, Minamata Convention was signed in 2014.

23. Food sources of human exposure:
 Ingestion of methyl, dimethyl, and ethyl mercury from contaminated fish is a major source of
human mercury toxicity. Fish and shellfish, especially top predatory fish like swordfish and
marlin, are the most common dietary sources of methyl mercury exposure.
 As a result of industrial releases of inorganic mercury into marine ecosystems, followed by
ingestion by marine microorganisms, which then transform the less toxic inorganic mercury
into the more toxic methyl mercury. Due to the low rate of breakdown, this accumulates across
the food chain, reaching potentially toxic levels in organisms at the top of the food chain, such
as swordfish and marlin, which then forms part of the human diet.
 The amount of methyl mercury in fish and shellfish is related to a variety of factors, including
the fish's size and age, the species, and the mercury level in the waters where they live. Larger,
older predatory fish like shark, marlin, swordfish, and new tuna have higher levels than other
marine fish.
 Methyl mercury deposited in muscle tissue is rapidly absorbed by fish. This involves mercury
bioaccumulation in the adipose tissues of successive trophic levels in the food chain, such as
zooplankton, small nekton, larger fish, and so on.

24. Mercury cycle

25. Mechanism of toxicity:
 The toxicity of mercury sources depend on its nature, i.e., salts, organomercury compounds or
elemental mercury.
 Elemental/ metallic Hg: Approximately 80% of metallic mercury vapour is absorbed through inhalation.
 Mercury vapor has great affinity for sulfhydryl groups and binds to sulphur-containing amino acids
throughout the body.
 Organic Hg: Methyl mercury bio accumulates in fish and shellfish. Ingestion of fish is the most
common way to be exposed to methyl mercury.
 Although, gastrointestinal tract is the main route of absorption, the skin and lungs are minor routes of
absorption.
 Methyl mercury once absorbed into the bloodstream, enters RBCs,where More than 90% Hg is found
bound to Hb. About 10% methyl Hg is found in the brain where it gradually undergoes demethylation,
resulting in an inorganic Hg form. Methyl mercury easily passes the placenta and reaches the foetus,
where the deposition takes place in the developing fetal brain.
 Methyl mercury potentially interferes with the function of any cellular or subcellular structure.
Mercury is believed to interfere with DNA transcription and protein synthesis.
 Methyl mercury has been associated with reduction in Natural Killer cell activity , as well as an
imbalance in Th2 : Th1 ratios favouring autoimmunity .

26. Signs & Symptoms:
 Acute exposure: Elemental Hg : Inhalation : Fever, chills, shortness
of breath, pleuritic chest pain and a metallic taste. Nervous signs:
Ataxia,Paresis,Delirium.
 Inorganic Hg: Occurs due to oral ingestion. Ashen grey mucous
membrane due to precipitation of inorganic salts, hematochezia,
severe abdominal pain. Systemic effects include gingival irritation,
teeth loosening, renal tubular necrosis leading to anuria.
 Chronic exposure: classical manifestations like
gingivitis,temors,erethism which includes neuropsychiatric
findings like insomnia, memory loss, shyness, emotional instability,
visual disturbances.
 Pink foot / Acrodynia: mercury allergy ,generalized rashes over
the body, results from chronic exposure to mercury in any forms.
Erythematous, eczematous (watery and weeping) type of skin
lesion is produced.
 Mostly, the hands and feet are affected accompanied by
thickening of skin.
Acrodynia

27. Diagnosis & treatment:
 The mercury concentration in whole blood is usually lower than 10 μg/L in normal concentrations.
 When urinary excretion of mercury is > 50 µg/L suggestive of significant exposure.(WHO) When the
urine mercury concentration exceeds 100 μg/L, neurological symptoms can develop, and the level
of 800 μg/L or above can be fatal.
 Hair mercury concentration is also found to be proportionate to blood mercury concentration.
 After exposure to methylmercury, total mercury levels in hair and blood are used as biomarkers of
mercury intoxication. The hair-to-blood mercury concentration ratios set by the U.S. Food and Drug
Administration (FDA) and the World Health Organization (WHO) is 250:1 and 250–300: 1 ,
respectively.
 Chelating agents that can be used for acute inorganic mercury (Hg0 or Hg++) poisoning include
dimercaprol (British Anti-Lewisite, BAL), D-penicillamine (DPCN), dimercaptopropane sulfonate
(DMPS), and succimer (dimercaptosuccinic acid, DMSA).

28. Prevention:
 Reducing human exposure from mercury sources.
 Non-essential mercury-containing goods should be phased out, and the
remaining mercury-containing products should be handled, used, and disposed
off safely.
 Food and Drug Administration has recommended methyl mercury levels in
seafood, the maximum allowable concentration is 1ppm.
 The overall contaminant amount of inorganic Hg in drinking water is 2ppb.
 Because of the greater effect of mercury toxicity on the population, the EPA
created the "Fish Kids" awareness campaign for children and young adults.
 In 2005, the United Nations Environment Programme drafted a global treaty to
limit mercury production and prohibit the export of mercury between
countries.

29. Cadmium toxicity:
 Itai-Itai disease/ ouch ouch disease.: Itai-itai disease is the most severe form of chronic cadmium
intoxication. It was Ist recognized in Jinzu river, Toyama Prefecture, Japan around 1912. Cd was released
into rivers by mining companies.
 The Japanese government had officially acknowledged 187 cases of itai-itai disease (184 women and 3 men)
between 1967 and 2003, but only four of them were still alive. The majority of the victims were middle-aged
women who were calcium deficient as a result of multiple pregnancies, postmenopausal calcium loss, and had
lived in this community for over 30 years. Skeletal deformities are among the clinical symptoms. Fractures are
caused by a decrease in bone density. Osteoporotic fractures, which can cause disability, are most common
among postmenopausal women.
 Sources: Water : anthropogenic sources cause release in water e.g. industrial effluents, Ni-Cd batteries,
discarded electronic products released into water.
 In a recent study of groundwater contamination of Cd in India in 4 districts of western UP regions revealed
higher Cd conc. in drinking water i.e.. 0.07 mg/L as compared to limit set by WHO ( 0.003mg/L). ( Idres et
al,2018).
 Occupational exposure: Zn smelting, battery production, e waste, jewellery, industries,fuel combustion.
 Occupational exposure among jewellery workers in India caused oxidative stress & increased RBCs fragility.
( Moitra et al,2014).

30. Cadmium cycle:

31. Toxicity mechanism:
 Primary effects on lungs & kidneys.
• Acute exposure to cadmium fumes may cause flu-like symptoms including chills, fever, and muscle
ache sometimes referred to as "the cadmium blues." Symptoms may resolve after a week if there is
no respiratory damage. More severe exposures can lead to tracheobronchitis, pneumonitis.
• Effects on skeletal system : Exposure to cadmium causes skeletal demineralization, whereby it may
directly interact with bone cells, diminish mineralization, also inhibit procollagen C-proteinases and
collagen production.
• Clinical findings are associated with osteoporosis include pain, physical impairment and decreased
quality of life.
• Mechanism: Binds to sulfhydryl groups, displacing other metals from metalloenzymes competing
with calcium for binding sites (calmodulin).
• Renal toxicity: Primary organ of toxicity : Kidney. Severe cadmium toxicity may induce nephrotoxicity
with complications such as; glucosuria, hypercalciuria, polyuria and kidney stones. Free Cd binds to
kidney glomerulus causes proximal tubule dysfunction.
• Cadmium is mainly stored in the kidneys and has a biological half-life of 10–35 years in humans.
There is evidence that cadmium is carcinogenic when inhaled, and the International Agency for
Research on Cancer has listed cadmium and cadmium compounds as carcinogens,Group 2A (possibly
human carcinogenic).

32.  The US EPA has established a Maximum Contaminant Level (MCL) of 0.005 milligrams per liter
(mg/L) for Cadmium in drinking water.
Skeletal deformities : Cadmium toxicity

33. Diagnosis & treatment :
 Biomarkers of excessive exposure :Increased concentrations of urinary beta-2 microglobulin can be an
early indicator of kidney dysfunction in persons chronically exposed to low levels of environmental
cadmium. The urinary beta-2 microglobulin test is an indirect method of measuring cadmium exposure.
 Blood: The limit of detection for blood cadmium concentration is 0.3 µg/L . Blood Cadmium is measured
by two techniques; either by atomic- absorption spectrophotometry or the inductively coupled plasma
mass spectrometry.
 Urine: Kidneys are the main organ to be affected by cadmium in long term exposure. Urinary cadmium
concentration equal or greater than 0.5 µg/g creatinine is associated with renal damage.
 Treatment : Chelation therapy.
 Interventions to reduce global environmental cadmium releases and occupational and environmental
exposure include:
• Increasing recycling of Cadmium in a safe and efficient manner.
• Minimizing pollution and discharges from mining and waste disposal activities.
• Promoting safe working conditions for cadmium-containing product handlers.
• Promoting the removal of cadmium from items like toys, jewellery, and plastics.

34. Other heavy metals toxicity:
 Chromium toxicity: Major sources in India: Leather tanning
industries, steel production, dyes & pigment industries,
mining of Chromite ore( Alka et al,2017).
 Hexavalent form of Cr is toxic even in low doses than trivalent
forms.
 Health effects in humans: allergic reactions, by breathing
hexavalent form can cause nose bleeding, irritation of
pharynx, asthmatic bronchitis.
 Copper toxicity : cookware, drinking water.
 Health effects in humans:
 Chronic toxicity: Wilson’s disease: characterized by Cu
deposition in the cornea, brown ring at the edge of cornea is
formed called as Kayser Fleischer Ring other symptoms are
liver cirrhosis, demyelination & brain damage.
Wilson disease along with ring
formation at periphery of
cornea.(arrow)

35.  Central Water Commission report on river contamination with
heavy metals in India (August,2019)
 Major findings:
 Two-thirds of water quality stations along India's major rivers are polluted
with one or more heavy metals, exceeding the Bureau of Indian Standards
safe limits.
 Iron has emerged to become the most common contaminant.
 Arsenic and zinc are two toxic metals whose concentrations are within
regulatory limits. Lead, nickel, chromium, cadmium, and copper were
among the other significant pollutants discovered in the samples.
 The prevalence of pollutants at water sites varies depending on the season,
various seasons have different levels of pollution.
 Non-Monsoon Period includes metals include lead, cadmium, nickel,
chromium, and copper.
 Monsoon Period: During this time, iron, lead, chromium, and copper levels
frequently exceeded ‘tolerance limits.‘
 Mining, milling, plating industries are the primary sources of heavy metal
waste, since they release a range of toxic metals into the atmosphere.
 Contamination of surface water is also caused by population growth and an
increase in agricultural and industrial activities.

36. Preventive measures to reduce heavy metals
contamination of environment:
 Remediation technologies : these should be environmentally friendly, rapid, and cost-effective. The
remediation of heavy metals in soil can be conducted through physical, biological, ecological, and
chemical approaches.
 Bioremediation is a strategy for removing and recovering heavy metal ions from contaminated
environments. It involves using living organisms like algae,fungus,bacteria to minimise and recycle
heavy metal compounds into less toxic types.
 Heavy metals have been removed from polluted wastewaters and soils using this method.
Microorganisms play an important role in heavy metal remediation, and this approach is an
attractive alternative to physical and chemical techniques. Similarly, using microorganisms to
remediate contaminated habitats is long-term and aids in the restoration of the polluted
environment's natural state.
 Source reduction: Reducing the sources of heavy metals is an effective strategy for improving
human welfare. Avoiding inadequately treated effluent and sewage sludge could significantly reduce
the heavy metal accumulation in food crops.
 Air-quality management could result in less PM deposition in the soil and reduce the contamination
of food crops.

37. Phytoremediation:
 Phytoremediation is the process of using plants and associated soil
microbes to minimise the concentrations of pollutants in the
atmosphere & their toxic effects. This contains the following:
 Phytoextraction is the uptake/absorption and translocation of
pollutants through plant roots into the above-ground parts of plants
(shoots) that can be collected and burned for energy and metal
recycling.
 Phytostabilization is the use of specific plant species to immobilise
pollutants in soil and groundwater by absorbing them and
accumulating them in plant tissues.
 Phytovolatilization is the process of a plant absorbing and transpiring
a contaminant, followed by the release of the contaminant or a
changed form of the contaminant into the atmosphere. It happens
when water and chemicals are taken up by rising trees and other
plants. At relatively low concentrations, some of these pollutants will
move through the plants to the leaves and volatilize into the
atmosphere.
 Plants like (Brassica carinata, Brassica juncea, Helianthus
annuus L., Glycine max L. Merr, Zea mays L., Sorghum
bicolor, Medicago sativa L.) has shown that the most efficient hyper
accumulator of cadmium, lead, copper, nickel, chromium, arsenic.

38. References:
 www.who.org
 www.ncbi.nlm.nih.gov
 www.epa.gov
 www.cdc.gov.
 Lead: A Silent Menace in Household Spices of India I. Mazumdar & K. Goswami,2014.
 Distribution and Geochemical Controls of Arsenic and Uranium in Groundwater-Derived Drinking Water in Bihar,
India, Laura a Richards, Arun Kumar.
 Groundwater Arsenic Contamination in the Ganga River Basin: A Future Health Danger Dipankar
Chakraborti,2018.
 Arsenic Contamination of Groundwater in West Bengal: Awareness for Health and Social Problems Bidyut Kumar
Santra,2017.
 Heavy metals toxicity and the environment; Paul B Tchounwou, Clement G Yedjou, Anita K Patlolla & Dwayne J
Sutton,2014.
 Heavy Metals Accumulation in Soil and Agricultural Crops Grown in the Province of Asahi India Glass Ltd.,
Haridwar (Uttarakhand), India.; Vinod Kumar, AK Chopra,2015.
 Toxicity, mechanism and health effects of some heavy metals; Monisha Jaishankar, Tenzin Tseten, Naresh
Anbalagan, Krishnamurthy N Beeregowda, 2014.
 Phytoremediation of heavy metals—Concepts and applications ;Hajrat AlEzzat Khan, Muhammad Anwar Sajad,
2013.

39.  Studies of mercury pollution in a lake due to a thermometer factory situated in a tourist resort:
Kodaikkanal, India ;D. Karunasagar , M.V. Balarama Krishna a , Y. Anjaneyulu b , J.
Arunachalam,2005.
 Groundwater contamination with cadmium concentrations in some West U.P Regions, India
;NidaIdreesB.Tabassum,Elsayed Fathi Abd Allah AbeerHashem,RobeenaSarah Mohammad Hashim,
2018.
 Occupational cadmium exposure-associated oxidative stress and erythrocyte fragility among
jewellery workers in India ;Subhabrata Moitra, Bill B Brashier, Subhashis Sahu,2014.
 Status of trace & toxic metals in Indian rivers, Dept. of Water Resources, River Development and
Ganga Rejuvenation Central Water Commission August, 2019.
 A review of hexavalent chromium contamination in India; Banchor Alka, Pandey
Madhurima,Pandey Piyush Kant,2017.