LEAD

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• LEAD
• POISONING

• BENZENE POISONING Bodnar R.Ya.

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PLAN of lecture

• Lead poisoning
• Lead properties.
• Industrial uses.
• Pathogenesis of lead poisoning.
• Clinical picture. Diagnosis.
• Preventive measures.
• Management of lead poisoning.
• Benzene poisoning
• Benzene properties.
• Industrial uses.
• Pathogenesis of benzene poisoning.
• Clinical picture. Diagnosis.
• Management of benzene poisoning.
• Examination of working capacity.

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• LEAD
• POISONING

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INDUSTRIAL USES

• manufacture of storage batteries
• glass manufacture
• ship building
• printing and potteries
• rubber industry
• and several others

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Lead smelterthe starting point of dissemination
of a toxic metal
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Rubber workers in mill room
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Foundry workers may be exposed to a complex
mixture of carcinogenic agents in fumes
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LEAD NON-OCCUPATIONAL SOURCES

• The greatest source of environmental
  (non-occupational) lead is gasoline.
• Thousands of tons of lead every year is exhausted
  from automobiles.
• Lead is one of the few trace metals that is
  abundantly present in the environment.
• Lead exposure may also occur through drinking
  water from lead pipes chewing lead paint on
  window sills or toys in case of children.

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LEADPOISONING
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LEADPOISONING

• (1) INHALATION Most cases of industrial lead
  poisoning is due to inhalation of fumes and dust
  of lead or its compounds.
• (2) INGESTION Poisoning by ingestion is of less
  common occurrence. Small quantities of lead
  trapped in the upper respiratory tract may be
  ingested. Lead may also be ingested in food
  or drink through contaminated hands.
• (3) SKIN Absorption through skin occurs only in
  respect of the organic compounds of lead,
  especially tetraethyl lead Inorganic compounds
  are not absorbed through the skin.

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LEAD DISTRIBUTION IN THE BODY

• 90 of the ingested LEAD is excreted in the
  faeces.
• LEAD absorbed from the gut enters the
  circulation, and 95 enters the ERYTHROCYTES. It
  is then transported to the liver and kidneys and
  finally transported to the bones where it is laid
  down with other minerals.
• LEAD probably exerts its toxic action by
  combining with essential SH-groups of certain
  enzymes, for example some of those involved in
  prophyrin synthesis and carbohydrate metabolism.

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LEAD POISONING
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LEAD POISONING
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CLINICAL PICTURE AFFECTION OF BLOOD SYSTEM

• Syndrome of ANAEMIA (general weakness, fatigue,
  dizziness, paleness of skin) - is the early
  syndrome of chronic lead intoxication.
• ANAEMIA is hypochromic and associated with
  reticulocytosis and erythrocytosis (red blood
  cells with basophilic granularity).

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red blood cells with basophilic granularity
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AFFECTIONOF BLOOD SYSTEM

• EARLY SIGN OF LEAD INTOXICATION
• Affection of porphyrine metabolism which is
  manifested by rise of excretion with urine of
  Aminolevulinic acid and coproporphyrines with
  urine.

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LEAD POISONING
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CLINICAL PICTURE
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AFFECTION OF NERVOUS SYSTEMASTHENIC SYNDROME

• Weakness
• Fatigue
• Disturbance of sleep
• Irritability
• Headache

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AFFECTION OF NERVOUS SYSTEM NEUROPATHY

• Pain in extremities
• Paresis
• Paralysis

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Pathways Leading to Pain in Peripheral
Neuropathy
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AFFECTION OF NERVOUS SYSTEM ENCEPHALOPATHY

• Headache, especially in the back of head,
• Dizziness
• Decline of memory
• Epileptiform attacks
• Mental confusion
• Delirium, etc

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LEAD POISONING
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AFFECTION OF GASTROINTESTINAL SYSTEM

• Dyspeptic syndrome (bitter taste in oral cavity,
  bad appetite, nausea, heartburn, eructation,
  sometimes vomiting)
• Pain syndrome (pain in epigastrium)
• Dyskinetic syndrome (constipation, diarrhea)
• Lead colic

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AFFECTION OF GASTROINTESTINAL SYSTEM
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AFFECTION OF LIVER

• TOXIC HEPATITIS
• Liver is firm, painful, enlarged

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DIAGNOSIS

• HISTORY OF LEAD EXPOSURE
• CLINICAL FEATURES
• -loss of appetite, -intestinal colic,
  -abdominal cramps and constipation, -persistent
  headache, -weakness,
• -joint and muscular pains,
• -BLUE LINE ON GUMS,
• -dermatitis,
• -anaemia, etc.

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DIAGNOSIS

• Positive patch tests to acrylates in a worker
  who glued lead flashing onto window units. She
  had developed an allergic contact dermatitis
  affecting the hands.

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DIAGNOSIS
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TREATMENT

• PRINCIPLES
• To stop contact with a lead
• To get it out of organism
• - complecsons are widely used for lead
  destroying
• - complecsons form steady compounds with a
  lead and are easily extreted by kidneys with
  urine.
• Vitamine therapy (Vit.B1, B6, B12, Vit.C)
• Dezintoxication therapy
• Sedative therapy
• Massage
• Warm bath
• Gymnastics

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TREATMENT

• Tetacin-calcium and Pentacin are used for
  treatment of moderate and severe course of lead
  poisoning
• The use of d-penicillamine has been reported to
  be effective in treatment of mild course of lead
  poisoning

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TREATMENT

• Tetacin-calcium i/v dr. 20 ml 10 in 200 ml 5
  glucose during 3 days (with interruption - 3-4
  days), 2-4 courses.
• You should remember that complecsons excrete
  from an organism different microelements which
  are needed for the vital functions of organism
  (iron, copper, cobalt), thats why we must
  prescribe preparations of iron and vitamin B12,
  which contains cobalt.
• ! Tetacin-calcium may cause exacerbation of
  pathological process in patients with the severe
  disturbance of the nervous system.

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TREATMENT

• More effective is using of Pentacin 5 or 10 20
  ml i/v dr. for 3 days.
• 2-3 courses are conducted with intervals in 5
  days.
• Contraindications to application of pentacini are
  diseases of kidneys, arterial hypertension with
  violation of renal function.

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TREATMENT

• D-penicillamine 150 mg in caps. (450-600mg/ day)
  during 2-4 weeks.

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TREATMENT

• Contraindications for using of complecsones are
• - severe diseases of liver
• - severe diseases of kidneys
• - hemophilia
• - hypocalcemia

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TREATMENT of intestinal colic

• Atropin 0,1 1ml twice/ day
• Novocain blocking
• Sol. Glucose 5 Vit.C 5 i/v
• Warm bath
• Hot-water bag

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PREVENTIVE MEASURES

• (1) Substitution That is, where possible lead
  compounds should be substituted by less toxic
  materials.
• (2) Isolation All processes which give rise to
  harmful concentration of lead dust or fumes
  should be enclosed and segregated.
• (3) Local exhaust ventilation There should be
  adequate local exhaust ventilation system to
  remove fumes and dust promptly
• (4) Personal protection Workers should be
  protected by approved respirators.
• (5) Good housekeeping Good housekeeping is
  essential where lead dust is present. Floors,
  benches, machines should be kept clean by wet
  sweeping.

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PREVENTIVE MEASURES

• (6) Working atmosphere Lead concentration in
  the working atmosphere should be kept below 2.0
  mg per 10 cu. metres of air, which is usually the
  permissible limit or threshold value.
• (7) Periodic examination of workers All
  workers must be given periodical medical
  examination. Laboratory determination of urinary
  lead, blood lead, red cell count, haemoglobin
  estimation and coproporphyrin test of urine
  should be done periodically. Estimation of
  basophylic stippling may also be done.

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PREVENTIVE MEASURES

• (8) Personal hygiene Hand-washing before
  eating is an important measure of personal
  hygiene. There should be adequate washing
  facilities in industry. Prohibition on taking
  food in work places is essential.
• (9) Health education Workers should be educated
  on the risks involved and personal protection
  measures.

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• BENZENE POISONING

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INDUSTRIAL USES

• Amino- and nitrogroups of benzene are
  wide-spread in industry
• for making of organic dyes
• pharmaceutical preparations
• artificial resins
• Insecticides
• blasting matters

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Electron micrograph of benzene
particlesIndividual particles are about 25nm in
diameter
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BENZENE POISONING
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BENZENE POISONING

• Amino- and nitro compounds of benzene, getting to
  the organism, accumulate in a
• -CEREBRUM, -KIDNEYS, -HEART,
• -LIVER.
• Then their redistribution occurs and most of
  matter stay too long in a temporal depot -
  SUBCUTANEOUS-FATTY CELLULOSE and LIVER, that
  causes relapses of intoxication, particular
  after hot procedures and use of alcohol.

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PATHOGENESIS

• During acute intoxication central NERVOUS SYSTEM
  and PERIPHERAL BLOOD are mainly affected
  (formation of methaemoglobin and development of
  hemolysis of erythrocytes occur).
• During chronic intoxication LIVER, URINARY
  TRACTS, VISION ORGAN AND NERVOUS SYSTEM are
  affected .

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BENZENE POISONING

• Intoxication by compounds of methaemoglobin
  causes development of irreversible degenerative
  changes in erythrocytes with formation of the
  rounded dark-blue inclusions on periphery -
  Gaints corpuscles. In the severe case the amount
  of methaemoglobin is increased to 60-70 , Gaints
  corpuscles - to 8 .

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Erythro-cytes with Gaints corpuscles
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CLINICAL PICTURE Cerebral manifestations

• Acute headache, severe fatigue, nausea, vomiting,
  disorders of equilibrium (balance).
• Patients are disposed to syncope, depression.
• Cramps occur, tendon reflexes disappear.
• The loss of consciousness and comma appear.
• Patients may die from the paralysis of
  respiratory centre, heart failure.
• In the first days after the comma patient
  complains on intensive headache, weakness,
  dizziness.

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CLINICAL PICTURE

• One of the most characteristic signs of acute
  intoxication of amino- and nitrocompounds is
  discoloration of skin.
• During examination grey-dark blue colouring of
  mucus and skin, cyanosis are revealed, dyspnoea
  is absent.
• Blood is of chocolate-brown colour its colour
  depends on the quantity of formed methaemoglobin
  and sulfhaemoglobin.

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CLINICAL PICTURE

• Amino- and nitrocompounds of benzene cause the
  irritation of mucus of respiratory tract that is
  accompanied by the sneeze, cough.
• Burns of nose mucus, nose-bleeding may occur.

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CLINICAL PICTURE

• Urinary tracts are affected. Dysuric changes
  occur. In some cases ,,haemolitic kidney and
  acute renal failure.
• Acute toxic hepatitis. In some cases acute or
  subacute atrophy of liver occur and it is
  accompanied by the severe haemorrhagic syndrome
  and hepatic comma.

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Results of blood investigations

• ?methaemoglobin level
• ? conjugated bilirubin
• Geynts bodies
• Anizocytosis, Poycilocytosis, Erythrocytes with a
  basophilic stippling
• Reticulocytosis
• Blood viscosity rises.
• ?ESR decreases.

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BENZENE POISONING
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BENZENE POISONINGMILD STAGE

• Patients complain on the headache, dizziness,
  weakness, sleepiness.
• At the objective examination cyanosis of mucus
  and skin of fingers, auricles, and uncertain
  step, rise of tendinous reflexes, tachycardia are
  revealed.
• Pathological changes of internal organs are
  absent.

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BENZENE POISONINGMILD STAGE

• Results of blood investigations
• content of methaemoglobin in blood does not
  exceed 15-20 ,
• single Geynts bodies.
• In a few hours after intoxication all these
  complaints pass, methaemoglobin level decreases,
  a work capacity recovers.
• Duration of intoxication does not exceed 2-4
  days.

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BENZENE POISONINGMODERATE STAGE

• neurological symptoms acute headache, dizziness,
  nausea, vomiting, severe muscles weakness,
  clouded consciousness. The patient orientation is
  broken, there is uncertain step. In these stage
  syncope may occur.
• At the objective examination more expressed
  cyanosis of skin and mucus, pulse is labile, rise
  of tendinous reflexes, insignificant dyspnoea,
  poor reaction on light, insignificant expansion
  of heart, quit heart sounds, tahycardia.
• Sometimes liver is enlarged.
• Neurological status nervous trunks are painful.

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BENZENE POISONINGMODERATE STAGE

• Results of blood investigations
• ?methaemoglobin level (to 30-40),
• ? little Geynts bodies (to 15).
• Blood viscosity rises.
• ?ESR decreases.
• Sometimes moderate leucocytosis.
• ?content of oxygen in an arterial blood.
• The clinical-laboratory symptoms of intoxication
  are observed during 5-7 days, although reverse
  development of basic manifestations of illness
  begins in 1-2 days.

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BENZENE POISONINGSEVERE STAGE

• Severe changes of the central nervous system
  Consciousness is cloded, often absent, cramps,
  dilation of pupils, disappearance of reaction on
  light, absence of tendon reflexes.
• In a acute period prostration is determined, it
  changes by acute excitement, involuntary
  urination and act of defecation.
• At the objective examination severe cyanosis of
  skin and mucus, caused by connsiderable met- and
  sulfhaemoglobinemia and vein congestion. Skin
  hemorrhages, ulcer of mucus are revealed. Heart
  is delateted, heart sounds are decreased,
  tachycardia, decreasing of arterial pressure.
  Liver is enlarged and painful.

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BENZENE POISONINGSEVERE STAGE

• Results of blood investigations
• ?conjugated bilirubin in blood
• A blood is thick, chocolate-brown coloured,
  contains 60-70 methaemoglobin, a lot of Geynts
  corpuscles,
• anizocytosis, reticulocytosis, a lot of
  normoblasts and megaloblasts,
• leucocytosis may appear,
• ESR slows down.

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CHRONIC BENZENE POISONING

• develops as a result of the protracted influence
  of small doses of poison that have cumulative
  action.
• Hot bath action, alcohol, the carried infection
  may cause exacerbation of chronic intoxication.

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CHRONIC BENZENE POISONINGCLINICAL PICTURE

• weakness, headache, dizziness, disturbance of
  sleep, rapid fatigue, dyspeptic symptoms, pain in
  right hypohondrium.
• Skin is pale, with cyanosis, colour of the eyes
  is icteric, pulse is labile, AP has a tendency to
  hypotonic. Heart sounds are decreased, chronic
  gastritis (frequently with decreased secretion),
  toxic hepatitis with moderate disturbance of
  liver function occur. The function of pancreas is
  affected.
• Disturbance of the urinary system occurs
  chronic inflammation of mucus of urinary bladder,
  appearance of pappiloms of urinary bladder,
  malignant formations.
• Some benzene compounds cause occupational
  cataract.

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BENZENE POISONING Occupational Cataract
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ACUTE BENZENE POISONING DIAGNOSIS

• Diagnosis is made in case of contact of the
  patient with high concentrations of aromatic
  amino- and nitrocompounds (occupational
  anamnesis),
• characteristic clinical-laboratory symptoms
  grey-dark-blue colour of skin and mucus,
• increased level of blood methaemoglobin and
  sulfhaemoglobin, appearance of Geynts corpuscles,
  erythrocytes with a basophilic stippling,
  reticulocytosis.

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CHRONIC BENZENE POISONING DIAGNOSIS

• Diagnosis is based on a presence of complex of
  the exposed violations of blood, liver, nervous
  system, protracted contact with the indicated
  compounds.

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BENZENE POISONING TREATMENT

• At acute intoxications patient should be taken
  out of the gassed atmosphere.
• At the getting of poison to skin it is necessary
  to wash soil area by water.
• Hot baths or showers are contraindicated.
• According to indications cardiac medicines are
  prescribed camphora, coffein, cordiamin,
  corglycon.
• Desintoxication, vitamin and symptomatic therapy
  is recommended.
• At deppression of the central nervous system
  cytiton, lobelin are given.
• Oxygen therapy is the basic method of medical
  treatment.

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BENZENE POISONING TREATMENT

• For reduction of blood viscosity - Glucose 40
  20-30 ml i/v Vit.C 5.
• Glucose is a good demethaemoglobinisation mean.
• Use of vitamin B12 is also recommended.
• In case of renal failure hemodialysis is
  conducted.
• During chronic intoxication medical treatment is
  conducted taking into account the clinical
  picture of disease.

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EXAMINATION OF WORKING CAPACITY

• is made taking into account severity of the
  carried intoxication.
• At mild form after complete renewal of working
  capacity workers can go back to previous work.
• In the case of development of severe forms of
  intoxication after medical treatment, work out
  of contact with the toxic substances is
  recommended to the patient for the temporal time.
• At presence of the steady remaining pathological
  changes of different organs and systems, the work
  in contact with the toxic substances is stopped.

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