 Endangered professions:

• workers producing batteries

• lead paint
• glass
• ceramics
• tiles
• metallurgy
• printing industry
• electronics
 Metabolism:
• respiratory system ( aerosols, PbO)
• gastrointestinal absorption
• skin (applicable only for organic lead compounds)

• The majority of the metal in the blood is related to low molecular weight
proteins of the erythrocytes, a smaller part with plasma fraction of
albumin or circulates as free ions.

• Pb accumulates in bone / 90% /, kidney, liver and skeletal muscle. In case

of infections, binge drinking, surgical intervantions / crosses back into the
blood. Crosses the placenta and levels in the fetus correlated with maternal
levels. Lead is a cumulative poison.

• Elimination - very slowly and mainly in the urine.

Life Pb - between 5 to 10 years
 PB directly affects the Er:
• violates the structure of erythroblasts and mature forms;
• decrease the viability of the Er
• shortens their lifespan

(basophillic stiplling)
 Acute intoxication:
• abdominal colic
• haemolysis
• encephalopathy
• acute renal failure

 Chronic intoxication:
•  asthenia, arthralgia, myalgia
•  anemia (normochromatic), reticulocytosis, the occurrence of basophil stippled
erythrocytes in the peripheral blood increased free protoporphyrin (at levels of Pb>
40 μg / dl).
• Early impact criteria of lead considerably prior to the decrease in hemoglobin:
inhibiting the activity of DALD-dehidrazata and increased free erythrocyte
protoporphyrin
 Gastrointestinal syndrom:
• changes in the mouth - on the edge of the palatal teeth observed
blue-gray strip of lead sulphide, early and massive destruction of the
teeth.
• dyspepsia - decreased appetite, unpleasant, sweet or metallic taste in
the mouth, epigastric overrides
• Lead colic (a typical and dramatic syndrome) presenting with sudden
severe colicky pain, umbilicus, palpation of the abdomen is painless,
no defense, hypertension, bradycardia, persistent constipation
• DD - acute abdomen
• toxic hepatitis - subikter, hepatomegaly, AST, ALT, GGT,
• DD - viral, drug and chronic hepatitis caused by alcohol.
 Neurological symptoms:
• neurasthenia syndrome - fatigue, headache, dizziness, sleep disturbances,
irritability, sweating
• distal motor neuropathy presenting with "sagging wrist.“
• toxic encephalopathy (prolonged high-exposure) insomnia, confusion, impaired
concentration ability, memory impairment, rarely seizures and coma.

 Endocrinology symptoms:
• men - changes in spermatogenesis, loss of libido and infertility
• women - menstrual disorders and spontaneous abortions
• Lead “ grave’s disease”
 Exposure tests:

PB level:

• blood > 2.88 mol / L

•  urine > 0.53 mol / l;
• DALC over 8,000 nmol/4ch
• Re - more than 15% o
• occurrence of basophil stippled erythrocytes
 Antidote

1. CaNa2EDTA 10% 10 ml in 500 ml of glucose or fiz.serum -1 gr daily

iv for 3 consecutive days

2. CEMET (Succimer)capsules x 0.250-in low-level lead exposure in

10 days x 2.1 grams per day divided in three doses for high lead
absorption takes place 20 days course at the same dosage.
 
3. Cuprenil tablets x 0,250 2 g daily dose divided into 4 portions
Suitable for low-level lead exposure, with high-grade recommended by
ending treatment after administration of CaNa2 EDTA.
 In case of lead colic - antidotal therapy and antispasmodics
 In toxic hepatitis - diet systems Laevulose 5% 500 ml, Carsil (
3x2) and Legalon 140 mg ( 3x1 ) hard capsules containing
Silymarin, Essential phospholipids ( 3x2 ) hard capsules
 In toxic anemia - antidote treatment responds well to anemia
and leads to normalization of porphyrin metabolism. Fe
containing drugs generally are not included , except in case
of low serum iron .
 In lead polyneuritis - vasodilator , NSAIDs , neurotonics ,
vitamins , geritamin.
 In high- lead absorption and excretion after antidotal
treatment courses appropriate medical treatment with water
rich in sulfur
 Risk occupations - production of mercury and
sunlamps, instrumentation and devices, dentists
and dental nurses

 Pathogenesis: affinity to SH groups of cellular

proteins and enzymes
 Inorganic mercury:

• changes in the oral cavity: gingivitis, stomatitis, pharyngitis, dental erosions grey-
violet strip palatal edge
• Atkinson’s syndrome - reddish brown color of the lens of the eye
tremor
• nervousness, emotional lability
• vegetative syndrome - hypersalivation, hyperhidrosis, tachycardia, polyuria
• neuralgia, neuritis, polyneuritis, early myasthenia of extensors of the hand
• nephrosis - proteinuria, renal failure
• psychiatric disorders - hallucinations, dementia
• increase of thyroid gland
• anemia
 Organic compounds of mercury:

• paresthesia
• loss of motor coordination
• atactic gait
• Tremor
• muscle rigidity
• narrowing of the visual field / "tunnel vision" / blindness
• reduction in hearing loss
• mental disorders - depression, memory disturbances, intrusive.
psychosis, schizophrenia
• erythroderma, desquamation, skin rashes
• renal dysfunction / rarely /
 Hg in blood> 0,054 μmol / l;

 Hg in urine> 0,118 μmol / l;

 Hg in saliva> 0,15 μmol / l

 Antidote:
 Unithiol 5% 5 ml x1 amp. i.m. daily for 5 days.
 Succimer 0,350 capsules, 2,1 g daily dose for 5 days.
 Na thiosulfuricum-10-20% - 10 ml, 5 days.
 Symptomatic: antidepressants, hepatoprotective drugs,
vasodilators.
 Vitamins- vit.B1, B6, C
 Spa treatment with lead sulfide waters.
CADMIUM

 Risk groups/contingent:
workers in the manufacturing of
• Cd-Ni batteries
• cadmium lamps
• alloys
• galvano-technicians
• metallurgists.
 CADMIUM
 Metabolism
• Inhaling cadmium dust or fumes of cadmium oxide.
Resorption in the lungs – depending on the size and
chemical composition of particulate matter (20–30 %,
smokers 50 %)

• Gastrointestinal resorption – 2 to 6 % (in case of

↓ Fe and poor in Ca, Zn and protein food > 20 %
absorption)

• Skin resorption – slight

CADMIUM
• After the absorption through the lungs and
gastrointestinal tract Cd is transported to the liver where
it is combined with low molecular weight protein, rich in
sulfhydryl groups – metallothionein (90 % of the total
quantity).

• Depots of Cd in the body – liver and kidneys.

• Elimination – very slowly. Biological half-life – 7–30

years!
CADMIUM

 Pathogenesis:
• violates the metabolism of Ca and P
• reduces the alpha antitrypsin activity in the
pulmonary mucosa
• binds the sulfhydryl groups of cellular enzymes
and proteins
• has a direct irritant effect on mucous membranes.
 CADMIUM - Clinics

 Acute poisoning:
 Upon inhalation:
• Mild – metal fever - sore throat, nausea, metallic taste in mouth, headache,
myalgias
• Medium – pneumonia - cough, chest tightness, dyspnea, chills
• Severe – pulmocardiac syndrome (pulmonary edema and cardiac
decompensation) and toxic hepatitis
 In case of ingestion
• gastrointestinal disturbances (nausea, vomiting, stomachache, diarrhea)
• toxic hepatitis
• toxic nephropathy
• hepatorenal syndrome
• acute renal failure
 CADMIUM - Clinics

 Chronic poisoning:
• anosmia, rhinopharingitis, yellowing of tooth necks;
• emphysema, bronchitis, diffuse interstitial fibrosis (> 10 years
of exposure);
• renal syndrome – tubulopathy with proteinuria (lysozyme, В2
microglobulin, ribonuclease);
• Fanconi syndrome – aminoaciduria, glycosuria, calcium- and
phosphaturia;
• osteomalacia, osteoporosis, spontaneous fractures (> 20 years
of exposure).
CADMIUM

 Remote consequences:

Ca of lungs and prostate !!!

CADMIUM

 Laboratory tests:
Cd bl >0,03µmol/l

Cd ur>0,01 µmol/l;

В2 microglobulin

lysozyme in urine
 CADMIUM
 Treatment:
• Antidotal – CaNa2 EDTA 10 % 10 ml to 500 ml of 5 % serum
glucose iv – 6 days

• Symptomatic – depending on the type and severity of organ

damage.
• Preventive: Vit. D-amp. – 600 000 ME i.m. once monthly
• Calcium C – 2x1 tabl.; Calcium phospho C – 3x1 tabl.
MANGANESE

 Risk groups

mining and processing of manganese ores

production of ferroalloys, steel, electrolytic

alloys for non-ferrous metals

MANGANESE

 Pathogenesis
• affinity to thiol groups by forming complex
compounds with methionine, cysteine, cystine

• direct damage to extrapyramidal structures

(palidum, substantia nigra, corpus striatum)

• disorder in the metabolism of adrenergic

neuromediators
 MANGANESE - Clinics

 Acute poisoning (MnO; manganese carbonyl) –

metal fever, dyspnoea

 Chronic poisoning:
• fatigue, headache, apathy;
• changes in behavior to psychosis;
• Parkinson's syndrome – slow monotone speech,
mask-like face, tremor, bradi- to akinesia,
micrography, increased muscle tone;
• pneumofibrosis (at extraction of manganese ore).
MANGANESE

 Laboratory tests:
Mnbl > 3 μmol / l
Mnu > 1 μmol / l

Mn levels are increased in exposed workers,

but do not correlate with its toxic effects!
 MANGANESE
 Treatment:
I. Antidote:
CaNa2 EDTA 10 % 10 ml 1 x daily in 5% 500 ml of glucose i.v.
d- Penicilamin (Cuprenil) 0,250 g; 4x2 tabl., 5 days

II. Antiparkinsonian drugs

Dopaminergic: Levodopa, Sinemet, Madopar, Izicom – scheduled

III. Symptomatic

IV. Vitamin therapy - В1 ; В6 ; В 12; Geritamin

NICKEL

 Use:
 for preparing alloys with Fe, Cr, Cu
 for anticorrosion coatings
 for alkaline batteries
 for chemical equipment
 chemical reactions catalyst
 in the reactive technique
 in nuclear reactors
NICKEL

 Absorption pathways

by inhalation of vapor and dust – nickel and

its compounds

through the skin – nickel carbonyl

NICKEL

 Pathogenesis:

• general toxic action – on NS and disorder of

metabolism

• allergenicity – on the skin and lungs

• carcinogenic effect – Са of the lungs

 NICKEL - Clinics
Acute poisoning (rarely)

• in case of ingestion – profuse vomiting, cramping

abdominal pain, loose watery stools;

• when inhaled – catarrh of the upper respiratory tract,

headache, fatigue;

• when contacted – eczema and ulcers on the fingers.

 NICKEL
 Chronic poisoning
• rhinitis, sinusitis, anosmia, nasal septum perforation
• metal fever
• allergic contact dermatitis, "nickel eczema" ("nickel
itch")
• bronchial asthma
• toxic pneumosclerosis (> 10 years of exposure to metal
aerosols)
• lung cancer (at Ni refining)
• vascular dystonia
allergic contact dermatitis, "nickel eczema"
allergic contact dermatitis, "nickel eczema"
allergic contact dermatitis, "nickel eczema"
NICKEL

 Treatment:
• corticosteroids
• Ca preparations
• intravenous infusion of water-saline and glucose
solutions
• Dimercaprol i.m.– 3 mg / kg every 6 hours.
 CHROME
 Risk groups
workers employed in the manufacture of:
 steel
 synthetic rubber
 grinding pastes
 paints for glass and ceramics
 chromium catalysts
 furriery and textile industry
 CHROME
 PATHOGENESIS

 Denaturates proteins in plasma with subsequent

irritative and corrosive changes of the mucous
membranes and skin

 Stimulates the synthesis of cholesterol

 Allergic effect

 Carcinogenic effect
 CHROME - CLINICS

 Acute poisoning

● when inhaled – tracheobronchitis, pneumonia,

pulmonary edema;

● when swallowed – gastrointestinal and

hepatorenal syndrome, uremia;

● when contacted – allergic and irritant dermatitis,

ulcers of "bird’s eye" type
CHROME - CLINICS

 Chronic poisoning:
● conjunctivitis, keratitis
● atrophic rino-faringo-laringita
● perforation of the nasal septum
● tracheobronchitis, emphysema, pneumosclerosis
● bronchial asthma
● bronchogenic carcinoma of the lungs
● chronic gastritis, perforations of ulcers in the gastrointestinal tract
● allergic dermatitis, ulcers of "bird's eye" type
● toxic hepatitis
● toxic nephritis
● anemia
 CHROME
 TREATMENT

 In case of chromium compounds ingestion – gastric lavage

with activated charcoal, intravenous infusions of water-salt
and glucose solutions, glucocorticoids, antibiotics

 Locally – cleaning the affected areas with 5 % solution of

sodium bicarbonate and dressings, containing fish oil and
CaNa2 EDTA

 In case of chronic injuries – symptomatic treatment and

vitamins
ARSENIC

 Risk groups:
manufacturing and use of

pesticides containing arsenic

aniline, acetylene

 arsenic dyes

in metallurgy
ARSENIC

 Pathogenesis:

thiol poison with an affinity to SH groups of

several enzyme systems, disturbing cellular
metabolism.

As belongs to I group of elements

carcinogenic to humans according to IARC !
 ARSENIC - Clinics

 Acute poisoning:
 oral – acute gastroenterocolitis with symptoms similar
to cholera, toxic cardiopathy, hepatorenal syndrome,
impaired consciousness, epileptiform convulsions,
coma;

 when inhaled – catarrh of the upper respiratory tract,

pharyngitis, laryngitis.
ARSENIC
 Chronic poisoning:
Mild – rinofaringolaringitis, perforation of the nasal septum,
chron. gastritis and gastroduodenites, neurasthenia,
poliglobulia and increased haemoglobin
Medium: toxic polyneuropathy – ascending, vegeto-sensor with
pronounced pain syndrome
toxic hepatitis, toxic nephropathy, contact dermatitis, ulcers,
hyperkeratize, melanosis, alopecia.
Severe: hepatorenal syndrome, sensorimotor polyneuropathy,
mielopolyneuritis with signs of severe ataxia, "pseudotabes";
toxic anemia; cardiomyopathy with rhythm and conduction
disturbances; carcinoma of the lungs and skin.
ARSENIC

 Paraclinics

As urine
 ARSENIC
 Treatment:
Antidote
 BAL or Unithiol 5 % 5 ml x 1 amp. i.m. daily for 5 days.
 Succimer capsules 0,350; dayly dose 2,1 g for 5 days.
 CaNa2 EDTA 10 % 10 ml 500 ml phys. serum or glucose
– 1 g daily i.v. for 3 consecutive days
 Na thiosulfuricum – 10–20 % – 10 ml i.v., 5 days.

Symptomatic – organ protectors and antioxidants