UK Government InformationNotes on the Diagnosis of Prescribed Diseases
PRESCRIBED DISEASE C3
Conditions due to Chemical Agents.
DISEASE C3 POISONING BY PHOSPHORUS
or an inorganic compound of phosphorus or poisoning due to
anti-cholinesterase or pseudo anti- cholinesterase action of organic
phosphorus compounds.
SCHEDULED OCCUPATION
Any occupation involving the use of or handling of or exposure to
the fumes dust or vapour of phosphorus or a compound of phosphorus or a substance containing phosphorus.
CAUSATIVE AGENT 1 Elemental phosphorus.
Phosphorus exists in 3 allotropic forms. Black, red and white.
Black phosphorus. Of no industrial importance.
Red phosphorus. The vapour from red phosphorus is identical
to that from the white form. Red phosphorus is less dangerous because
the vapour pressure is much lower. It does not ignite spontaneously.
White phosphorus. A colourless wax-like solid which darkens
when exposed to light and glows in the dark (phosphorescence). It
ignites spontaneously in air and burns with a blue flame. Burning
phosphorus smells something like garlic.
HARMFUL EFFECTS
Full details are not known. It is
suspected that phosphorus causes narrowing or occlusion of the
Haversian canals of bone. The bone, therefore, becomes devitalised and
susceptible to infection. Why the jaw bones should be particularly
affected has not, so far, been explained.
TYPES OF WORK INVOLVED
Red phosphorus
. Matchmaking.
White phosphorus. The production of explosives, chemicals,
rodent poisons, phosphor bronze and fertilizer.
ENVIRONMENTAL LIMITS
Published
occupational exposure limits have been chosen in the expectation that
no-one subjected to them will suffer harm. The limits cannot take into
account individual susceptibility and exposure to permitted levels
does not necessarily rule out a diagnosis of poisoning.
Occupational Exposure Standards (time weighted average) concentrations:
Phosphorus fume
For an 8 hour day/40 hour week 0.1 mgm/m3
For no more than 10 minutes (STEL) 0.3 mgm/m3
DIAGNOSIS - ACUTE
The classical
descriptions of phosphorus poisoning are based on experience dating
from days when environmental exposure limits were either non-existent
of higher than they are now. If exposure to no more than the quoted
levels is expected to have no ill effects a diagnosis of poisoning
implies either that the exposure limit is too high for the particular
claimant or that there has been a failure of environmental control.
HISTORY
Exposure to fume
concentrations perhaps higher than the recommended limits. Accidental
ingestion of phosphorus or one of its compounds.
SYMPTOMS
Blood stained phosphorescent
vomiting with prostration and, later, anuria.
SIGNS
Are those of renal failure,
hepatic failure and anaemia.
INVESTIGATION
Appropriate to the
management of severe, acute poisoning.
DIAGNOSIS - CHRONIC
HISTORY
Exposure to vapour concentrations
at or around the recommended limit with possible intermittent exposure
to higher levels.
SYMPTOMS
These are related to the
progressive devitalisation of bone, particularly the bones of the
mandible and maxilla (Phossy jaw).
SIGNS
In the early stages the signs
may be no more than slightly delayed healing or proneness to infection
after dental procedures or trauma about the mouth.
INVESTIGATION
X-ray appearances of bone
erosion, anaemia, biochemical changes related to kidney and liver
damage.
CAUSATIVE AGENT 2
Phosphine (phosphoretted hydrogen,
phosphorus trihydride, hydrogen phosphide). A colourless gas with an
odour of decaying fish. It ignites spontaneously in air.
HARMFUL EFFECTS An irritant gas.
TYPES OF WORK INVOLVED
1. Fumigation of
grain. 2. Any of the processes which use phosphorus or its
organic compounds. Phosphine is usually liberated accidentally when
acid and metal or alkali react to produce hydrogen. The action of
hydrogen on phosphorus liberates phosphine. (Compare with arsine).
ENVIRONMENTAL LIMITS
Recommended
maximum, time weighted average concentrations.
These are to be reviewed soon by the Advisory Committee on Toxic
Substances.
For an 8 hour day/40 hour week 0.3ppm, 0.4 mgm/m3
For no more than 10 minutes (STEL) 1.0ppm, 1.0 mgm/m3
DIAGNOSIS - ACUTE
HISTORY
Exposure to concentrations of
phosphine which are higher than the recommended limits.
SYMPTOMS
Breathlessness, tremors,
fatigue, slight drowsiness, nausea, vomiting, gastric pain, diarrhoea,
headache, thirst, dizziness, oppression in the chest, burning
substernal pain, dyspnoea and productive cough.
SIGNS
Commensurate with the symptoms.
INVESTIGATION As appropriate.
DIAGNOSIS - CHRONIC
HISTORY
Exposure to phosphine gas at or
about the recommended limit.
Possible short term exposures above the recommended limit.
SYMPTOMS
Cough, gastro-intestinal
disturbances. Disturbances of vision, speech and movement.
SIGNS
Anaemia, bronchitis.
Neurological signs commensurate with the symptoms.
INVESTIGATION As appropriate.
CAUSATIVE AGENT 3
Inorganic compounds of
phosphorus other than phosphine.
HARMFUL EFFECTS
These compounds tend to
be less toxic than phosphineitself. Their ability to produce poisoning
depends upon their tendency to release phosphorus vapour or phosphine
gas. In many cases the toxicity is related to that part of the
compound which is not phosphorus eg, chlorine, bromine fluorine.
ENVIRONMENTAL LIMITS
Depend on the
particular compound involved. Please consult the appropriate
specialist publications and/or HSE.
DIAGNOSIS - ACUTE
As for phosphorus
and phosphine.
DIAGNOSIS CHRONIC
As for phosphorus and
phosphine.
CAUSATIVE AGENT 4 Organo-phosphorus
pesticides, one or more of a large group.
HARMFUL EFFECTS
Irreversible
inhibition of acetyl cholinesterase. At high doses the action of other
enzymes may also be impaired. Organic phosphorus compounds may be
ingested, inhaled or absorbed through the skin. Absorption through
the skin is rapid. Repeated absorption of small doses is cumulative to
a point where a slight additional uptake is sufficient to cause an
attack of poisoning.
TYPES OF WORK INVOLVED
The
production or use of pesticides.
ENVIRONMENTAL LIMITS
This varies with
the type of pesticide. Detailed information, including the name of the
manufacturer, should be given on the product label.
If the information supplied with the claim is not adequate for
diagnosis purposes please ask for more.
BIOLOGICAL MONITORING
Red cell
anti-cholinesterase activity can be monitored.
The level should be no higher than 70% above the baseline which has
been established for any particular worker. The test is non specific
and can be difficult to interpret but the presence of raised levels
may be used to confirm that there has been exposure.
DIAGNOSIS ACUTE
HISTORY
Exposure to organophosphorus
pesticides. This may be as a single high dose or repeated low dose
exposures.
SYMPTOMS
Early. Headaches, giddiness,
nausea, fatigue, blurred vision.
Late. (2-8 hours) abdominal pain, cramp, vomiting, diarrhoea,
sweating, sphincter paralysis leading to urinary and faecal
incontinence.
SIGNS
Hot dry skin, constricted
pupils, tachycardia, pulmonary oedema, muscular fibrillation.
INVESTIGATION
The demonstration of
reduced cholinesterase activity in red blood cells, plasma or whole
blood.
DIAGNOSIS - CHRONIC
HISTORY
Exposure to toxic doses of
organo-phosphorus pesticides. Normally recovery after acute poisoning
is complete but in some cases there are late onset neuropathic and
neuro-behavioural disorders. They are not inevitable and they seem not
to occur without previous cholinesterase inhibition.
SYMPTOMS
Symptoms may be delayed by up to
4 weeks. There may be tingling and burning in the extremities,
weakness of the legs and ataxia followed by progressive paralysis of
the legs and arms. Neuro behavioural disorders are manifest as
gastro-intestinal symptoms, headaches and nervousness.
SIGNS
Flaccid followed by spastic
paralysis.
INVESTIGATION
Peripheral nerves may
show axonal degeneration with secondary myelin loss.
DUE TO THE NATURE OF
When a Prescribed
Disease is diagnosed in a worker who is:
a. currently employed in or;
b. within a month of having left the relevant scheduled occupation,
the disease should be presumed to be due to the nature of the
occupation unless there is evidence to the contrary. Such evidence
might be, for example, that the claimant was a gardener who used
organo-phosphorus pesticides on his or her garden at home. Outside
those time limits each case should be considered on its merits and
the evidence weighed before expressing an opinion as to whether or
not the condition was due to the nature of the claimant's work.
SPECIAL POINTS
The neuro behavioural
symptoms of late organo-phosphorus poisoning are common in the
unpoisoned population. Careful attention should be paid to any
evidence of prior acute poisoning before, in any particular case,
such as symptoms are attributed to exposure to organo-phosphates.
The full paper ISBN 1 85197 770 8 may be difficult to obtain.
It has been officially confirmed that the Act which recognises Poisoning by OP pesticides as depicted in this paper became law in the UK in 1958.
Dated 16/9/2000 Updated 1/8/2001
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