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tremor - pentachlorophenol


Here goes another one - PCP:

WT

<<<<<< Attached TEXT file named "Commercial Products" follows >>>>>>
Commercial Products

PCP, Penta, Penchlorol, Santophen, Chlorophen, Pentacon, Penwar, Sinituho.
The sodium salt is sodium pentachlorophenate.

In various products, pentachlorophenol has been used as an herbicide,
algacide, defoliant, wood preservative, germicide, fungicide, and
molluscicide. As a wood preservative, it is commonly applied as a 0.1%
solution in mineral spirits, No. 2 fuel oil, or kerosene. It is used in
pressure treatment of lumber at 5% concentration. Weed killers contain
higher concentrations. PCP is no longer available for over-the-counter sale
in the United States.

Pentachlorophenol volatilizes from treated wood and fabric. It is virtually
odorless. Excessively treated interior surfaces may be a source of exposure
sufficient to cause irritation to eyes, nose, and throat.

Technical PCP contains lower chlorinated phenols (4-12%) plus traces of
chlorobenzodioxins, chloro-benzofurans, and chlorobenzenes.



<<<<<< Attached TEXT file named "Symptoms and Signs of Poisoning" follows
>>>>>>
Symptoms and Signs of Poisoning

IRRITATION of the nose, throat, and eyes is the most common symptom of
airborne PCP, causing stuffy nose, scratchy throat, and tearing. Dermal
exposure may lead to contact dermatitis, or more rarely, diffuse urticaria
or chloracne.

Commonly reported symptoms of systemic poisoning by PCP are profuse
SWEATING, weakness, dizziness, anorexia, nausea and - in workers exposed
over long periods - weight loss. Indications of severe acute poisoning are
HYPERTHERMIA, muscle spasms, tremor, labored breathing, a sense of
constriction in the chest, abdominal pain and vomiting, restlessness,
excitement, and mental confusion. Tachycardia and increased respiratory
rate are usually apparent. Intense THIRST is characteristic.



<<<<<< Attached TEXT file named "Toxicology" follows >>>>>>
Toxicology

PCP is efficiently absorbed across the skin, the lung, and the
gastro-intestinal lining. It is rapidly excreted, mainly in the urine as
unchanged PCP and as PCP glucuronide. In the blood, a large fraction of
absorbed PCP is protein-bound.

The residence half-life of PCP in humans is about 27-36 hours. Because
minute amounts of PCP are consistently detectable in the blood and urine of
the general population, a continuing low-level intake (micrograms per day)
of PCP by virtually everyone is implied.

In adequate concentration, PCP is irritating to mucous membranes and skin.
Contact dermatitis occurs commonly in workers having contact with PCP.

Internally, large doses are toxic to the liver, kidneys, and nervous
system. An important mechanism of toxic action is increased cellular
oxidative metabolism resulting from the uncoupling of oxidative
phosphorylation. This leads to increased heat production (hyperthermia).

Severe poisoning and death have occurred as a result of intensive PCP
exposure. Dermal absorption has been the basis of virtually all
occupational poisonings. Most adult fatalities have occurred in persons
working in hot environments where hyperthermia is poorly tolerated. Several
infant deaths have occurred in a nursery where a PCP-containing diaper
rinse had been used. Chloracne has occurred in production workers, possibly
due to chlorodioxin contaminants. Individual cases of exfoliative
dermatitis of the hands and diffuse urticaria and angioedema of the hands
have been reported in intensively exposed workers. Cases of aplastic
anemia, peripheral neuropathy, and leukemia have been reported which were
associated temporally with PCP exposure. Causal relationships in these
cases were not established.

Albuminuria, glycosuria, and aminoaciduria, and elevated BUN reflect renal
injury. Liver enlargement, anemia and leukopenia have been reported in some
intensively exposed workers. Elevated serum alkaline phosphatase, GOT, and
LDH enzymes indicate significant insult to the liver, including both
cellular damage and some degree of biliary obstruction.


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