
Historical
Aspects.
Some of the mental and physical
effects of chronic exposure to mercury are known to us
all, immortalised in Lewis Carroll's Mad Hatter in
'Alice in Wonderland'. Mercury salts were used
historically in the manufacture of felt hats and
absorption of these compounds through the skin gave rise
to body burdens sufficient to cause the symptoms of
madness among this profession. Likewise, the use of
mercury salts in the 19th Century for the treatment of
syphilis gave rise to severe side effects and many
deaths.
Mercury toxicity made headline
news in this country after the release of waste
containing mercuric chloride (a catalyst in the
production of plastics) into the bays of Minemata and
Niigata, Japan in 1953 and 1960. Methylation of the
metal by plankton and its subsequent incorporation into
the food chain caused acute toxicity in victims eating
fish caught in that region. Although immediate
fatalities were apparently limited to 52 persons,
hundreds of children and adults have since developed
degenerative neurological disorders presenting as
paraesthesia, ataxia, dysarthria, hearing and visual
loss. In these regions, cerebral palsy too has persisted
at a high 6% incidence of births.
In 1972, large quantities of
grain treated with methyl mercury fungicide for planting
were accidentally distributed to villagers in Iraq.
Despite official warnings, much of the grain was ground
and made into bread. In the disaster which followed,
6530 people were hospitalised and at least 500 died of
mercury poisoning.
Mercury poisoning used to be
widespread in such industries as mirror making and
cinnabar (mercury ore) mining. In Western countries, the
use of mercury in industrial processes has almost
disappeared. In modern times, exposure, and therefore
toxicity is limited mainly to dentistry; thermometer,
barometer and mercury arc equipment manufacture;
pigment, fungicide, insecticide and dry cell battery
manufacture. Mercury compounds have in the past been
used as diuretics, anti-infectives, laxatives, eye and
skin treatments, but these uses have now been superseded
by more appropriate drugs.
Disposal of mercury-containing
domestic batteries on council dumps poses an enormous
ecological problem; however this does help to put the
dental use of mercury into perspective. It was estimated
in the US in 1989 that discarded household batteries
accounted for 86% of dumped mercury, while dental
amalgam represented just 0.6% and has been declining
steadily in quantity over the past three decades.
Mercury compounds were once used
extensively in the production of paper and Sweden was
found to be dumping enormous quantities of mercury-rich
effluent from its paper industry into the sea. Pressure
from environmentalists has eradicated mercury use in
paper-making for good. Bizarrely, there is also concern
about the risk to health of mercury vapour discharged
from crematoria as a result of incineration of people
with amalgam fillings. Certainly, toxic mercury vapour
is measurable in the the air downwind from crematoria
when this occurs.
There is international concern
at present over the illegal dumping of thousands of
tonnes of mercury every year, used for extraction of
gold from ore, in the Brazilian Amazon area. Many
hundreds of cases of mercury toxicity have been reported
in the area and ecologists are very concerned about
health effects once the water table is contaminated.
More primitive gold extraction techniques involve
boiling off mercury from gold-mercury amalgam in open
pots over a fire.
When you work in an environment
contaminated with mercury, you quickly absorb the toxic
metal. For example, dentists are exposed to mercury
vapour and to mercury-rich amalgam dust; this is the
'fall-out' of aerosols generated during removal of
amalgam restorations. Skin exposure to native mercury
used to be common in dentistry when amalgams were mixed
by hand in a chamois leather, but this practice has
almost ceased.
On occupational exposure to
mercury, absorption is mainly via the lungs; mercury
vapour is absorbed to an extent of between 90 and 100%
by this route. Dust and droplets on the skin and in the
gut are absorbed to a minor extent (about 15%) but doses
to these regions are often high.
Some biotransformation of
inorganic mercury to short-chain alkyl (methyl and
ethyl) forms occurs in micro-organisms in the mouth and
in the gut; absorption of these organic forms is
relatively efficient (80 to 100%); these are the same
chemicals which wreaked so much human devastation in
Minemata. Distribution of absorbed mercury throughout
the body readily occurs via the blood and mercury
partitions reversibly into all organs, including the
brain and nerve tissue, which have a higher affinity for
the organic forms.
Whilst the half-life of mercury
in the blood has been estimated as about 3 days, mercury
in body tissues clears slowly, with a half-life of about
90 days. So cessation of exposure will not therefore
have immediately beneficial results, in the event of
mercury poisoning - benefits of ceasing exposure will
only be seen after about a year - four half-lives.
Both inorganic and organic
mercury compounds have an avid affinity for thiol (-SH)
chemical groups and this is the property which renders
them toxic. Most proteins, and all enzymes, contain
these thiol groups; this explains both the binding of
mercury to all body tissues and many of the biological
effects. Most mercury compounds are potent but
unspecific enzyme inhibitors, affecting membrane
permeability and hence nerve conduction and tissue
respiration. In this respect, the biochemical effects of
mercury resemble those of black widow spider venom.
Disposal of the body's burden of
mercury is via the urine and faeces, although minute
amounts are detectable in expired air. Excretion via the
liver occurs in bile and reabsorption of some of this
mercury does take place. However, the kidney is equipped
with an efficient, energy-dependant mechanism for
disposing of metals such as mercury.
Kidney tissue contains a thiol-rich
protein called metallothionein; exposure to toxic metals
triggers the production of this protein which binds
tightly to the metal, retaining it in the kidney tissue
in a relatively harmless form. As long as the kidney's
capacity for production of metallothionein is not
overwhelmed, mercury excretion can eventually balance
intake, thereby limiting worsening of symptoms. However,
acute high doses of mercury, or an increase in the
chronic dose level can readily precipitate renal
failure, one of the classic symptoms of mercury
poisoning.
A small proportion of total body
mercury is excreted in various forms directly in the
urine without being bound to protein. In low dose,
steady state conditions, such as the dentist who has
worked at a similar exposure level for years, the
urinary output very accurately reflects the total body
burden and this is why urine
monitoring is so important.
Symptoms Characteristic of
Chronic, Low-Dose Exposure