KERACUNAN RAKSA
The growing scarcity of high quality ore
bodies on the earth surface has caused many companies to explore and developed
mines in more extreme condition in a higher, deeper, hotter or colder
environments. Old time gold mining use mercury to extracts gold from host
rocks. Gold in ore dissolved selectively in liquid mercury. When heated, the
liquid mercury evaporates leaving behind the pure gold. This technique of gold
extraction is termed as ‘patio process’ and still continue to be used in the
less developed countries. Small scale miners in Brazil
and Indonesia
use the mercury amalgamation process extensively and have produces millions of
ounces of gold while discharging hundreds of tons of mercury to the
environments every year. Mercury toxicity has been documented extensively in
the small scale gold miners and in humans whom consume fish from the polluted
area (Goldfrank L.R. et al. 1994).
Mercury combines easily with metals such
as silver, gold and tin to form alloy called amalgams. These amalgams are
routinely used in dental fillings. Exposure to the mercury vapor or dust in
dental practice occurs commonly from various sources including instruments that
mix amalgam (mechanical algamators), sterilizing instruments, contaminated with
amalgam, handling, storing, cleaning mercury or amalgam. Elemental mercury is
also used in cantor tubes, thermometers, sphygmomanometers where exposure can
occur following breakage or an incorrectly handled spill or repair (Notani,
S.P. 1980).
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Elemental mercury vapor is readily absorbed into the lung
and transported via red blood cells to the brain and other organs. Mercury is
distributed in the brain gray matter and accumulates in the brainstem nuclei and
in various parts of the cerebellum. Elemental mercury is not absorbed in the
normal gastrointestinal tract and ingestion of elemental contaminated mercury
dust is not a significant route of exposure.
Mercuric salt are used as
tissue fixative in pathology laboratory. Mercuric salt exposures are less
common than elemental mercury exposure in the hospitals. Organic mercury in the
form of methyl mercury or alkyl mercury compounds is encountered mainly in
seafood and may confound attempts at biologic monitoring for elemental mercury
at the workplace. Phenylmercuric acetate was used as one of the most common
biocides (for mold and mildew). It is previously use in interior paints (Lunberg
I. & Hakansson, M. 1985).
For long term mercury
exposure, a person may reveal subtle
personality changes. Tremors, gingivitis, rash or bronchospasm may present. Inhalation
of elemental mercury vapors (quicksilver, Hgº) can initially cause caugh,
chills, fever and shortness of breath and may progress to pulmonary edema,
respiratory failure and death if exposure is substantial. With large inhalational
exposure, acute pulmonary toxicity occurs. An erosive bronchitis or
bronchiolitis with interstitial pneumonitis can result which usually develop
within hours of exposure. Chest X-ray revealed acute interstitial pneumonitis,
along with patchy atelectasis and emphysema (U.S. Department of Health and
Human Services. 1992).
Following low level long
term exposure to environmental mercury or mercuric salts, a range of Central
Nervous System effect may be seen. At lowest levels, syndrome of weakness, fatigue,
anorexia and gastrointestinal disturbances may be manifested which is termed as
micromercurialism. With increasing exposure, there’ll be tremors, initially
occurring in the fingers, eyelids and lips. Progression to generalized tremors
accompanies more extensive Central Nervous System effect, including memory
loss, insomnia, excitability and depression. Subtle and explosive personality
disturbances are classically described. Inadvertent enteral exposure routes of
mercuric salt results in profound gastrointestinal toxicity and renal tubular
dysfunction. Chronic exposure to mercuric salt may leads to sensitization
phenomenon with bronchospasm and dermatitis.
Organic mercury may
adversely affects the CNS and causes tremors, shyness, emotional lability, nervousness,
memory deficit and diminution of psychomotor skills. Contact with
phenylmercuric acetate will cause childhood form of mercury toxicity, i.e.
acrodynia. Symptoms associated with acrodynia include fever, splenomegaly,
irritability, insomnia, personality changes, generalized weakness and
erythematous rashes with peeling on the hands, feet and nose. These symptoms
are somewhat similar to Kawasaki ’s
disease. The differences is the facts that acrodynia has no adverse effecs on
the coronaries arteries while that is the hall mark for Kawasaki’s disease
(Lunberg I. & Hakansson, M. 1985).
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