Chemistry Reference
In-Depth Information
occurred in hard-metal workers exposed to the dusts of
tungsten and titanium carbides with cobalt used as a
binder. Chronic asthma can occur in workers sensitized
to chromium after the inhalation of chromate dust or
chromic acid fume and also to organic platinum com-
pounds. Once sensitization to platinum has occurred,
the reaction can be triggered by exposure to minute
quantities of the salts of chloroplatinic acid.
with a characteristic neurological syndrome whose
principal features are paresthesia of extremities and
face, ataxia, dysarthria, and concentric constriction of
the fi elds of vision. Pyramidal signs may also occur.
Another characteristic neurological disorder consisting
principally of intention tremor of the hands, tremor of
the eyelids and tongue, and a combination of behavio-
ral and personality changes known as erethism devel-
ops after chronic exposure to mercury vapor.
1.4.4 Effects on the Nervous System
1.4.5 Renal Effects
Peripheral neuropathy may develop in the recovery
stage of acute arsenic intoxication, about 1-3 weeks
after exposure. It is a mixed motor and sensory neu-
ropathy, with a “glove and stocking” distribution.
Neuropathy develops in those who survive the acute
gastrointestinal effects of thallium poisoning, and it
may lead to a later fatal termination. With both these
metals, skin changes occur at a later stage, with the
former metal, arsenical pigmentation results, and with
the latter, hair loss. A motor neuropathy involving
predominantly the upper limbs with wrist drop and
extensor weakness of the fi ngers is seen in chronic lead
poisoning. By contrast, antimony salts of organic acids
give rise to a sensory neuropathy that may involve the
trigeminal nerve. Bismuth and copper have also given
rise to peripheral neuropathy.
Permanent brain damage with cerebral cortical atro-
phy or hydrocephalus may be the sequel to acute lead
encephalopathy. Convulsions may recur over a long
period, and idiocy may develop.
The use of lead paints and leaded gasoline has given
rise to the widespread occurrence of lead in the envi-
ronment. Elevated blood lead levels after long-term
exposure to house dust with decaying fragments of
leaded paint has been shown in epidemiological stud-
ies to affect cognitive development in children (Bell-
inger
et al
., 1992; Needleman
et al
., 1990; Chapter 31).
Degenerative changes in the nerve cells of the basal
ganglia giving rise to a parkinsonian syndrome were
considered to result from the absorption of manganese
after long-term occupational exposure (Mena
et al
.,
1970). Parkinson's disease, a not uncommon disorder, is
characterized by muscular rigidity, akinesia, tremor, and
postural deformities. In a case-control study to deter-
mine whether welding-related parkinsonism differs
from idiopathic Parkinson's disease in welders exposed
to manganese welders had a signifi cantly younger age
of onset of parkinsonism, suggesting welding as a risk
factor for this condition (Racette
et al
., 2001).
Degenerative changes affecting in particular the
granular cells in the cerebellum and neurons in the cal-
carine, precentral, and postcentral cortex, follow the
absorption of alkylmercury compounds and present
Certain chronic renal disorders may also follow
exposure to toxic metals. Proximal renal tubular dys-
function consisting mainly of tubular proteinuria, glu-
cosuria, aminoaciduria, and phosphaturia may develop
after cumulative exposure to cadmium, lead, and ura-
nium compounds. Hypercalciuria has also occurred in
chronic cadmium poisoning as a further manifestation
of renal tubular dysfunction, and this has led to renal
stone formation and to osteomalacia in a few cases
after industrial exposure (Kazantzis, 1979).
Osteomalacia has been observed in a popula-
tion environmentally exposed to cadmium in Japan.
Although the skeletal disorder (Itai-Itai disease) only
occurred in postmenopausal women, evidence of renal
tubular dysfunction was found in the population as
a whole (Friberg
et al
., 1974; 1985).
Progressive impairment in renal function terminat-
ing in uremia and indistinguishable clinically from
chronic nephritis has been observed after childhood
lead poisoning. The wide range of abnormal responses
of the kidney to absorbed metals can be further illus-
trated by reference to the nephrotic syndrome. Heavy
proteinuria, with hypoproteinemia and edema, has
followed exposure to inorganic mercury, organic gold,
and bismuth preparations.
1.4.6 Hemopoietic Effects
Chronic arsenic poisoning is associated with an
anemia caused by decreased red blood cell formation
with increased destruction. The anemia of chronic lead
poisoning also results from decreased hemopoiesis
combined with increased red cell destruction (Goyer
and Rhyne, 1973). By contrast, cobalt has an increased
hemopoietic effect and has given rise to polycythemia,
but not to increased production of other cellular
elements in the blood.
2
DIAGNOSIS OF METAL POISONIN
G
As can be seen from the preceding, metal poisoning
may involve any of the organ systems of the body and
