Ruby Injected with Mercury Thallium

[Peter Lemkin]

My training is in Environmental Toxicology and I have lots of reference books on that. While no one book I have has the amalgam of mercury and tallium, each is well known as toxic separately. Here is an entry for tallium....

7.3 Humans
Thallium compounds are extremely toxic. Acute poisoning
is characterized by gastroenteritis, with nausea,
vomiting, diarrhea, and abdominal pain within hours
of absorption. Involvement of the nervous system then
becomes apparent after a few days, with paresthesia,
exquisitely painful and tender extremities, weakness,
mental confusion or delirium, convulsions, with respiratory
and circulatory involvement followed by death.
When the period of survival extends beyond 1 week
or so, a varied neurological picture may develop with
headache, ataxia, tremor, paresthesias, and muscular
atrophy predominating. There may also be cranial nerve
involvement, with ptosis, ophthalmoplegia, retrobulbar
neuritis, or facial paralysis later on in the intoxication.
Tachycardia and hypertension seen in the more severely
affected cases are thought to be due to denervation of
the glossopharyngeal and vagus nerves. The autonomic
neuropathy is a key component of thallium toxicity.
The neurological picture in the subacute case is
characteristically a distal neuropathy that begins with
sensory loss and numbness in the fi ngers and toes that
later spreads proximally. A little while later, there develops
a motor weakness, distal at fi rst, that again spreads
proximally. This neurological pattern of changes may
spread further to involve cranial nerves, respiratory
muscles, and even eye muscle innervation. This steady
proximal spread is reminiscent of Landry’s ascending
paralysis, a condition now not often recognized.
After an interval of 1–3 weeks, alopecia develops,
and the head hair can be readily pulled away; pubic and
axillary hair, and also the medial third hairs of the eyebrows
that do not actively grow, are relatively spared.
Ridges (Mees’s stripes) appear on the fi ngernails.
Recovery may be complete, or neurological defects
may remain for long periods with mental abnormality,
ataxia, and tremor (Bank et al., 1972; Cavanagh et al.,
1974; 1984, personal communication; Clinical Conferences
at the Johns Hopkins Hospital, 1978; Grunfeld
and Hinostroza, 1964; Mathews and Anzarut, 1968;
Reed et al., 1963; Smith and Doherty, 1964).
Three cases, two of which were fatal, were described
in detail by Cavanagh et al. (1974). The more severely
poisoned of these was diagnosed as a case of Guillain-
Barré polyneuritis, and at postmortem, there was little
evidence of neuronal degeneration; but the second
fatal case, who was less acutely poisoned, showed
extensive distal degeneration of all nerves examined,
with chromatolysis of many nerve cells. Neuronal
degeneration was of the distal, dying-back type and
was still actively continuing 3 weeks after the onset
of paresthesia. The more acutely affected of these two
fatal cases was estimated to have ingested 0.93 g Tl as
the acetate in two divided doses, whereas the fatal case
in which symptoms developed less rapidly had taken
the same total amount but in three divided doses.
A survivor had ingested 0.31 g Tl in a single dose. In the
latter, who experienced severe loss of head and beard hair, thallium could not be detected in the serum 7
weeks after exposure but was present in the urine in a
concentration of 3.0 mg/L.
The neuropathy produced by thallium was studied
by Kennedy and Cavanagh (1976) in a further case:
a 32-year-old man who died 1 month after ingesting
thallium sulfate at a calculated dose rate of 33 mg/
kg. The presenting features consisted of distal numbness,
paresthesias, and pains in the limbs followed by
convulsions. The principal clinical fi ndings consisted
of tachycardia, hypertension, peripheral neuropathy,
and cranial nerve involvement. The diagnosis was not
made until the 21st day, when alopecia developed.
Cerebral edema and petechial hemorrhages were the
only abnormalities seen in the cerebral hemispheres,
perhaps related to assisted respiration measures. There
were striking degenerative changes in the dorsal columns
of the spinal cord affecting both major tracts.
Chromatolysis of spinal anterior horn cells was associated
with severe Wallerian degeneration of both motor
and sensory peripheral nerve fi bers.
A symmetrical, mixed peripheral neuropathy is
characteristic, with distal nerves more strongly affected
than proximal nerves (Cavanagh, 1988); another characteristic
feature is an extreme sensitivity of the legs,
followed by the “burning feet” syndrome and paresthesia.
The so-called therapeutic dose for ringworm of the
scalp, recommended to produce hair loss in 2–3 weeks,
was 8 mg Tl/kg. However, Munch (1934) reviewed six
deaths among children given this dose, and found, in
8006 children treated with thallium, 447 cases of poisoning
(5.5%). Altogether he collected reports on 778
cases of thallium poisoning, with a mortality of 6%. The
minimal lethal dose for soluble thallium salts for an
adult is in the order of 1 g Tl (Gettler and Weiss, 1943)
or 10–15 mg/kg. Doses in the order of 1 g Tl are likely
to be fatal within a few days. Doses ranging between
0.5 g and 1 g are likely to give rise to a progressive neurological
defi cit ending in death in 2–3 weeks, whereas
smaller doses will show progression to alopecia and
are more likely to be followed by recovery. There is no
therapeutic dose for thallium salts.
Thallium poisoning has occurred after the unintentional
contamination of food. In one outbreak, barley
containing 1% thallium sulfate for pest control gave rise
to 27 cases of poisoning with 7 deaths (Munch et al.,
1933). Thallium salts have been used for suicide; their
criminal use has been reviewed by Prick et al. (1955).
Industrial thallium poisoning has occurred after
absorption by inhalation of dust or fume, through
ingestion from contaminated hands or food, or as a
result of skin contact. Munch (1934) recorded 12 cases
of industrial poisoning up to 1934. The principal clinical
features in these cases were fatigue, anorexia, pains
in the legs, and loss of hair. There were no deaths, but
one worker lost his sight as a result of optic atrophy. A
worker who, wearing protective clothing, had handled
approximately 6 kg thallium per day for many years,
developed ascending polyneuropathy, visual disturbance,
and fi nally hair loss (Egen, 1955).
No information on exposure levels is available.
Glömme and Sjöström (1955) described four cases in
which absorption was thought to follow skin contact
in the manufacture of rodenticides. Minor degrees of
polyneuropathy and varying degrees of alopecia were
noted, with a maximal urinary thallium excretion of
380 μg/L. Other reports with less specifi c effects after
industrial exposure to thallium are diffi cult to evaluate.
Occupational thallium poisoning has usually followed
long-term, lower level exposure producing a cumulative
effect with a milder clinical course than that
described for acute poisoning, characterized mainly by
subjective symptoms, in some cases with polyneuropathy
and partial alopecia. More data on environmental
and biological levels of thallium are required in such
cases.
As described in Section 6 of this chapter, human
exposures with urinary Tl concentrations <5 μg/L are
unlikely to cause adverse effects. In the range of
5–500 μg/L, risks are uncertain, whereas exposures
with urinary Tl >500 μg/L have been connected with
clinical poisoning.

Mercury, mostly has neural and renal effects on the human. I'd have to do specialized research on the combination's toxic effects. Do you know what its purpose is in the weapons? I see the amalgam is used in special electrical circuits. It is likely a soft solid or liquid at low temperatures, but can be dissolved in some special substances...I'd have to look this all up. Did Ruby loose his hair before he died?! That is one of the most definitive signs of tallium poisoning. Neither are listed as causing cancer quickly. Both could long term. However, the diagnosis of 'cancer' in Ruby is not confirmed and there are other substances known to be used for nefarious purposes which do rapidly induce cancer....