This document outlines the sources, modes of exposure, toxicokinetics, mechanisms and symptoms of both acute and chronic arsenic toxicity. It discusses diagnosis and treatment approaches including chelation therapy and removal techniques. Notable cases discussed include a strain of bacteria able to use arsenic instead of phosphorus.
35. SYMPTOMS OF CHRONIC ARSENIC
POISONING
Affected organ Features
Skin Excessive darkening of skin
(hyperpigmentation) in areas that are not
exposed to sunlight
Excessive formation of scaly skin on the
palms and soles (arsenical keratosis)
Exfoliative dermatitis
Arsenic-induced skin cancers (especially
Bowen disease , Squamous cell carcinoma)
Nails Transverse white bands of arsenic deposits
across the bed of the fingernails (Mee's
lines)
36.
37. Hair Arsenic deposits in hair
Nervous system Sensory changes, numbness and
tingling in a “stocking-glove”
distribution (sensory peripheral
neuropathy)
Headache, drowsiness, confusion
Distal weakness of small muscles
e.g. hands and feet
Blood and urine Haemolytic anaemia (moderate)
Leukopaenia (low white cell count)
Proteinuria (protein in urine)
38. Other Inflammation of respiratory mucosa
Peripheral vascular insufficiency
Increased risk of cancer of lung, liver,
bladder, kidney and colon
39. Features of acute arsenic poisoning
Symptoms usually start within 30 minutes to 2 hours.
Acute arsenic ingestion is typically followed by a severe
gastroenteritis, garlic odour and hypersalivation.
There is a characteristic sequence of multi-organ failure,
with: neurological symptoms (within hours) and cardiac
features, succeeded by adult respiratory distress
syndrome and renal/liver dysfunction.
Marrow suppression develops after a few days to weeks in
survivors, as does alopecia and an ascending motor
neuropathy.
40. often present in breath and body
tissues
Hypersalivation, abdominal pain, vomiting,
diarrhoea leading to hypovolaemic shock.
Trivalent arsenic is corrosive - may cause oral
burns, dysphagia and GI bleeding.
Myocardial depression.
Dehydration, hypovolaemia or shock.
ECG changes including ST segment
changes, prolonged QT interval, ventricular
tachycardia, torsades de pointes and ventricular
fibrillation.
Gangrene of extremities.
41. Pulmonary oedema, adult respiratory distress
syndrome and acute respiratory failure.
Inhaled arsenic causes irritation, bronchospasm
and pulmonary oedema
Haematuria or haemoglobinuria (from acute
haemolysis), proteinuria, acute tubular
necrosis with acute renal failure.
Jaundice, hepatomegaly, pancreatitis
CNS depression, encephalopathy and coma.
Seizures.
42. Acute haemolysis.
Bone marrow suppression.
Basophilic stippling and
rouleaux formation may
be seen on a blood film
Rashes
52. 1-Chelation 2-Nutrition 3-Removal
Chemical and synthetic
Supplemental
methods are used to treat
potassium decreases
arsenic poisoning.
the risk of
Dimercaprol and
experiencing a life-threatening
dimercaptosuccinic acid are
heart
chelating agents that
rhythm problem from
sequester the arsenic away
arsenic trioxide.
from blood proteins and are
used in treating acute
arsenic poisoning. The most
important side effect is
hypertension. Dimercaprol
is considerably more toxic
than succimer.[citation
needed]DMSA monoesters,
e.g. MiADMSA, are
promising antidotes for
arsenic poisoning. Calcium
sodium edetate is also
used.
Various techniques have been
evolved for arsenic removal, most
frequently using absorbents such
as activated carbon, aluminium
oxide, co-operative with iron oxide
to form sludges, adsorption onto
iron-oxide-coated polymeric
materials, and electrocoagulation
by nanoparticle. To remove the
stress of heavy and toxic metals,
an environment-friendly approach
must be applied and the use of
naturally occurring microbe must
be emphasized. Bacteria, yeast,
fungi, algae—all of them can be
used for remediation processes
and it is always recommended
that microbe used for
bioremediation must have natural
decontamination process and the
method should be cost-effective.