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Heavy Metals
One of 23 chemical elements that has a specific gravity (a measure of density) at least five times that of water.
Common toxic metals
Lead (Pb): Paints, old pipes, contaminated soil/water
Mercury (Hg): Fish (bioaccumulation), industrial processes - hat-making
Arsenic (As): Contaminated water, pesticides
Cadmium (Cd): Batteries, cigarette smoke, industrial pollution
Chromium (Cr), Nickel (Ni): Industrial processes, Jewelry
Mechanisms of metal poisoning
cellular disruption, oxidative stress, enzyme inactivation, accumulation
History of metal poisoning
Has been in use since the middle ages - most common was arsenic poisoning.
Symptoms of poisoning
Can include nausea, vomiting, diarrhea, stomach pain, headache, hair loss, sweating, a metallic taste in the mouth.
impaired cognitive, motor and language ability - neurological damage
some are known carcinogens
Why metals are used as poisons
obtainable without rousing suspicions, toxic in small quantities, colorless, tasteless, odorless, can be hidden in food or drink, have delayed onset of action, be undetectable, be chemically stable, and effects should mimic a natural disease.
Chelation therapy
Treatment for most heavy metal poisoning. chelating agents will bind to metals and facilitate excretion from the body. painful and lengthy process.
Common chelating agents
Calcium disodium edetate, dimercaprol (BAL), and penicillamine.
Detecting metals
in blood, urine, hair and tissue analysis using AAS, ICP, x ray imaging.
blood lead levels above 80ug/L
blood mercury levels above 3.6ug/L
urine mecury levels above 15ug/l
arsenic cleared from blood quickly so urine levels over 50ug/l
Atomic Absorption Spectrometry
Measures absorption of light by vaporised atoms.
graphite furnace atomic absorption spectroscopy: uses heated graphite tube to optimise small samples
ICP Techniques
uses high temperature plasma to excite elements
the high temperatures prevent interference
this allows for analyses of a wide range of elements
Carbon Monoxide (CO)
Odourless, colourless and tasteless gas produced as a result of incomplete combustion of organic compounds.
CO sources
cigarette smoke
exhaust fumes
malfunctioning heating and ventilation systems
fires
CO toxicity mechanism
Carbon monoxide is absorbed into the lungs and rapidly distributes into the blood.
It has a greater affinity to haemoglobin than oxygen.
Haemoglobin takes carbon monoxide around the body instead of oxygen
leading to a shortage of oxygen - anoxia
COHb (%Sat) in non-smokers vs smokers
Ranges from 0 to 3.
3-8 in smokers
Symptoms of acute CO poisoning
Include frontal headache, tremor, nausea, vomiting, blurred vision, seizures, drowsiness, coma, ultimately death.
Postmortem findings for CO poisoning
Cherry pink PM lividity over back indicates suspect CO poisoning.
Treatment of carbon monoxide poisoning
Binding of carbon monoxide to haemoglobin is reversible but it requires the flooding of oxygen. The half life of the carbon monoxide is usually 5 to 6 hours but it is reduced to 30 to 90 minutes in high oxygen environments.
Analysis
GC for the level of CoHb in blood
10-20% - headache, flushed, shortness of breath
30-40% - weakness nausea confusion
>50% Convulsions, loss of reflexes, respiratory paralysis, death