Occupational medicine

Dr. Dalia Abdallah El-Shafei
Lecturer of Community &
Occupational Medicine

 Occupational Health: is defined as the
promotion and maintenance of the highest
degree of physical, mental and social
wellbeing of workers in all occupations
(WHO & ILO, 1950 & revised in 1995).

Occupational Medicine is defined as; a branch of
preventive medicine with some therapeutic
function (Royal College of Physicians, 1978).
It begins as Industrial Medicine then it develops to
Occupational Medicine then to Occupational and
Environmental Medicine.

 Occupational medicine deals with:
1- Health promotion for workers and proper
prevention and treatment.
2- Work environment and its adverse effects on
workers’ health
3-Health problems of workers at any workplace

 More than 2,000,000 people die from
work-related accidents or disease every
year, equivalent to 1 death every 15
seconds.
 Progress in bringing occupational health
to the industrializing countries is
painfully slow. In the poorest countries,
there has been no progress at all.

 What are the differences between
occupational medicine and clinical
medicine?

 It is a disease arising out of or during the
course of employment and its cause present
in the occupation (e.g. silicosis).
Why its diagnosis is very critical?
1. Worker has the right to receive medical care
at the expense of the employer.
2. Worker has the right for paid sick leave.
3. If disability occurs, the worker has the right
for compensation.

Some diseases are not specially caused
by exposures on job, but they are
aggravated by occupational stressors.
 so it can be found in the general
population (e.g. hypertension).
Work-related disease

 Occupational health is concerned with
physical, mental and social conditions of a
worker in relation to his/her work and
working environment as well as his/her
adjustment to work and the adjustment of
work to the worker.

Physician
Hygienist
Ergonomist
Nurse
Safety Engineer
Epidemiologist

Occupational physician:
Is the leader of the team who:
1. Designs and implements the occupational health
program,
2. Conducts medical examination & biological
monitoring,
3. Provides first aid & emergency treatment
4. Supervises the rehabilitative program for disabled
workers.

Occupational nurse:
1-Assists the physician in providing medical services
2- Assists in supervising the work environment
3- Educates workers
4-Keeps medical records.

Demonstrate occupational health
services and occupational health
professionals responsible for
providing these services?

1- Adequate nutrition either by nutrition education and
support as well as prevention and control of parasitic
diseases.
2- Socioeconomic development through:
- Improving workers' income, and proper expending of this
income.
3- Social welfare through:
- Management of family problems.
- Making good social relations at work.
- Encouragement of sport activities.
4- Health education and keeping good medical records.

Good sanitation of work place by:
- Good design of the machines.
- Suitable housekeeping.
- Proper lighting and ventilation.
- Good control for physical hazards as heat,
radiation and noise.
- Supplying work place with washing facilities
and suitable transportation means.

- Pre-employment medical examination: choose the suitable
worker.
- Pre-placement examination: done by the occupational
physician of the plant to put the suitable worker in the
suitable process.
- Periodic medical examination : for early detection of any
health hazards arises from workplace.
Health education about early symptoms and signs of
occupational diseases
Immunization of workers and chemoprophylaxis to combat
any infectious disease.

In Egypt, the law specifies the periodicity of the
examination for workers in each work or job.
It is either every 6 months or every 2 years depending on
the duration of exposure needed to develop the
occupational disease.
the workers may be temporally or permanently removed
from further exposure or may be advised to continue
work.

Through:-
- Mechanization of heavy work process to lighten the
physical strain.
- Enclosure and segregation of hazardous process.
- Good ventilation, lighting and control of other physical
hazards at workplace as heat, noise and radiation.

- Providing good sanitary facilities as washing, changing
clothes.
- Supplying protective equipment as respirators,
protective clothes, and ear muffs or plugs.
- Work environment monitoring for detection and
evaluation of environmental pollutants.
- Ensuring that work legislations are applied and
investigation of workers' absenteeism.

- Pre-placement medical examination which provides
base line data about workers' health status which will
help the occupational physician in detection of any
deviation from these data on subsequent periodic
medical examination.

- Periodic medical examination (screening): by which the
occupational disease can be identified in its early stage to
prevent progression of the abnormal physiologic
condition It includes:
a- Survey about history of exposure and any abnormal
symptoms or complains.
b- Clinical examination. c- Laboratory investigations
d- Biologic monitoring for early detection of any
disturbed physiologic function

- Early treatment of the diagnosed occupational diseases.
- First aid treatment of any occupational injuries.

Rehabilitation of disabled workers aims to:
- Minimize or prevent the disability.
- Retraining the disabled worker for a new job suitable
for his new physical and mental capacities.
- Compensation of the disabled workers after evaluation
of the disability resulted from occupational disease or
accident and giving him some privileges.

 To diagnose an occupational disease, the nature of the
worker's occupation and the cause of it must present in
the occupation.
 So, if a worker in a factory of batteries suffered from
exposure to lead toxicity (occupational disease), but he
works as driver away from exposure to lead, he will not
be diagnosed as having an occupational disease as John
Stone reported in his book on occupational health.
 there are 48 occupational diseases in the Egyptian law

33
Occupational
hazards
Physical
Chemical
MechanicalBiological
Socio
phycological

1- Exposure to high or low temperature.
2- Exposure to noise.
3- Exposure to radiation (ionizing and non-
ionizing).
4- Exposure to vibration.
5- Exposure to atmospheric pressure
changes.
6- Exposure to electricity.

1- Exposure to toxic metals.
2- Exposure to dusts and fumes.
3- Exposure to noxious gases.
4- Exposure to toxic organic compounds.

1- Parasites.
2- Bacteria.
3- Viruses.
4- Rickettsia.

 Exposure to work stress - night work shifts -
long working hours .

 Wrong lifting - wrong movements –
 wrong postures - slippery floor or stairs

1- Systemic disorders:
- Heat cramps.
- Heat stroke.
- Heat exhaustion.
2- Skin disorders:
- Prickly heat (heat rash).
3- Psychoneurotic disorders:
- Chronic heat fatigue.
4- Eye affection.
- Cataract on U.V. rays exposure.
5- Heat burn.

Excessive sweating and water intake
without salt replacement causing hyponatremia.
Clinical picture:
- Severe painful cramps in muscles of limbs during work.
- Severe spasm at intestinal smooth muscles
- Headache, dizziness, body temperature may be normal
slightly increased.
Treatment of heat cramps:
-Prevention by adequate salt intake
-Supplementation with salts either oral or intravenous
infusion.
- Control of hot environment to eliminate or minimize heat
hazards.

Disturbance of heat regulating center
at brain causing heat retention in body
causing hyperpyrexia.
Clinical picture:
- Abrupt rise of body temperature (40 - 43°c).
- Flushed hot dry skin.
- Delirium, convulsion: may be coma and death
Treatment:
- Rapid cooling of body by all possible means.
- Removal of patient from the hot environment.
- Treat the symptoms by sedatives or stimulants, I.V. saline
infusion, O2 inhalation, bed rest.

Excessive sweating, salt and water depletion
without replacement causing heamo-concentration
and hypovolemia and circulatory failure.
Clinical picture:
- Headache, weakness and fatigue.
- Anorexia, vomiting and excessive sweating.
- Signs of peripheral circulating failure (pallor - cold
moist skin - hypertension - weak rapid pulse).
Treatment of heat exhaustion:
- Removal of the patient to cool place.
- Water and salt replacement.
- Treatment of shock.

Due to blocking of sweat gland ducts: sweat retention
and inflammatory reactions.
Clinical picture:
- Raised red vesicles on the affected skin.
- Prickling an itchy sensation on exposure to heat.
Treatment of heat rash:
- Removal to cooler environment.
- Skin cleanliness to prevent infections.
- Cool showers.
- Application of mild drying and soothing lotions.

Discuss the health effects resulting
from exposure to high temperature in a
glass factory?

Definition: Noise is any unwanted or undesirable sound.
Auditory field lies between 20-20000 hertz (Hz) or cycles
per second. If noise is below the lower level of normal
hearing (below 20 Hz) it is called infra sound but if the noise
above the upper limit of normal hearing (above 20 kHz) it is
called ultrasound.
Exposure to noise occurs in the following occupations:
- Weaving.
- Hammering of metals.
- Military exposure due to explosions and shooting.
- Building and construction.
- Aviation and submarines.

1- The duration of exposure.
2- The intensity of the sound.
3- The frequency of sound waves.
4- The type of noise either continuous
noise or impact noise which is more
dangerous.
5- Personal susceptibility.

Effects of noise:
A) Auditory effect: hearing loss.
B) Non auditory effects:
1- The heart rate: either increased or decreased
depending in the type of noise.
2- The respiratory rate: often increased.
3- Performance of psycho-motor tasks either
adversely or beneficially.
4- Deafness is associated with significantly higher
rates of mental illness in the community.

There are many components to a hearing
conservation program including:
1- Reduction of noise at source.
2- Limit exposure with or without ear protectors.
3- Routine monitoring of the place for noise level
and the population at work for hearing ability.

Radiation is the straight line transport of energy
through space or matter.
Classification of radiation:
1- Ionizing radiation: any electromagnetic or
particulate radiation capable of producing ions, directly
or indirectly when passing through matter.
2- Non ionizing radiation: electromagnetic radiation
with a wave length not sufficient for ionization.

OH
.
(hydroxyl radical)
H
.
Radiation Damage
water molecule
-ray
2 OH
.
 H2O2
What happens
when the water
molecule is
struck by the
gamma ray?

Alpha Particles
Stopped by a sheet of paper
Beta Particles
Stopped by a layer of clothing
or less than an inch of a substance
(e.g. plastic)
Gamma Rays
Stopped by inches to feet of concrete
or less than an inch of lead
Radiation
Source
Neutrons
Stopped by a few feet of concrete

Mechanism of action:
a) Ionization: is to ripe electrons away from atoms and
molecules.
b) Excitation of molecules.
Type:
A) Electromagnetic radiation as: X- ray ,Gama ray
B) Corpuscular radiation as:
* Alpha particles with low power of penetration and
great power of ionization.
* Beta particles with greater power of penetration.
* Neutrons * Protons * Electrons.

1- Uranium miners and atomic millers.
2- Nuclear reactors and atomic energy plant.
3- Radiologist.
4- Scientists using radioactive materials.

A) Acute effect:
1- Whole body irradiation: if exposure to doses > 1Gy,
acute radiation syndrome will result. It is characterized by
prodromal symptoms (nausea, vomiting) and bone
marrow depression (leukaemia, anaemia,
thrombocytopenia).
2- Local irradiation: producing skin reactions according to
the dose from mild erythema to tissue necrosis and
ulceration.

B) Chronic effect:
1- Chronic radiation sickness.
2- Chronic radio-dermatitis: disturbed sensation, focal
hyperkeratosis, congestive hyperaemia, painful cracks and
ulceration with malignant changes.
3- Eye cataract: cataract starts at posterior people of lens
capsule.
4- Carcinogenic and hereditary harm.

1- Those working in compressed air that
is too rapidly decompressed. (caisson
disease)
2- Divers who surface too rapidly from
depths greater than about 10 meters.
3- Crew or paratroopers in aircraft who
ascend too rapidly from sea level to
heights greater than 5487 meters.

The manifestations of decompression
sickness are due to the formation of
nitrogen bubbles in the body fluids and
in the tissues.
The symptoms produced depend upon
the site in which the bubbles are formed
whilst size and rate of growth of the
bubbles determines the severity of the
symptoms.

A) Acute symptoms that is divided into:
1- Type I: - Mild or severe limb pain.
- Skin mottling or skin irritation.
2- Type II: - Paralysis or weakness of the limbs
- Tingling or numbness of the limbs.
- Vertigo. - Headache.
- Dyspnea, chest pain. - Hypotension, coma.
B) Chronic symptoms:
- Aseptic necrosis of the bones.
- Neurological or psychological symptoms.

1- Gradual decompression according to
the well known standards
2- Use of pressurized airplanes.
3- Inhalation of helium/oxygen mixture
instead of air by divers to avoid nitrogen
narcosis.
4- Pre-employment medical
examination: Those with chronic
sinusitis, otitis media, lung cysts or
emphysema must not be employed.
5- Periodic medical examination.

6- Treatment of decompression sickness:
recompressing the patient and reducing the
pressure in accordance with a protocol laid
down in set of tables.

Definition: Pneumoconiosis or dusty lung = dust
collection in the lung and the lung reaction to its
presence.
Types of pneumoconiosis:
1- Collagenous: - There is fibrosis.
- Permanent destruction of the normal alveolar
architecture as: silicosis, asbestosis, coal workers
pneumoconiosis and Talcosis.
2- Non collagenous (benign pneumoconiosis): -
Minimal reticular reaction.
- Alveolar architecture intact.
Such as: Iron oxide: siderosis Tin: stannosis
Barium: baritosis Titanium: titanosis

1- Occupational history.
2- Clinical picture:
a- Symptoms:
-The most important is progressive dyspnea.
-Melanoptysis in CWP.
b- Signs:
- Cyanosis
- Clubbing
- Crepitations.

(a) Chest X- ray: shows lung opacities,
ILO classification of lung opacities
include:
* Small opacities: < 1cm
Rounded Irregular
P
Q
R
Up to 1.5mm
From 1.5 – 3mm
From 3- 10mm
S
T
U
Fine opacities
Medium sized opacities
Coarse opacities

* Large opacities > 1cm
A: area of opacity from 1-5 cm2
B: combined area of opacity < area of the right upper
lobe.
C: combined area of opacity > area of the right upper
lobe.
(b) Pulmonary function: restrictive or obstructive or
mixed pattern.
(c) Autopsy or biopsy:
- Nature of the dust.
- The pathological reaction in the lung.

Definition: it is fibrotic lung disease due to
inhalation of dust containing crystalline silicon
dioxide (free silica).
Workers at risk for silicosis:
1- Miners or workers in tunnels.
2- Sand blasters.
3- Quarry workers.
4- Glass workers.
5- Ceramic workers.

1- Acute silicosis: due to inhaled high level of recently
fractured quartz causing immediate damage of the
alveoli with acute alveolitis then fibrosis.
2- Chronic classic silicosis: due to repeated exposure
of low level of silica for more than 20 years.
- Lung: Discrete fibrotic nodules of 2-3mm, mainly in
upper lobes with whorled pattern. These nodules may
coalesce together to form massive fibrosis, which may
show central ischemic necrosis with cavitation.
- Pleura: thickening, fixed, hard with fibrotic nodules.
3- Accelerated silicosis: As classic but progress more
rapidly.

1- Chronic or classic silicosis: It needs 20 years to
develop:
- Early stages asymptomatic discovered accidentally
on doing chest X-ray.
- Progressive dyspnea.
- Cough and sputum due to bronchitis.
2- Accelerated: As chronic silicosis but progress within
shorter period.
3- Acute silicosis: It is fatal. It develops in few weeks
and progress in 1-3 years only. There is:
- Progressive dyspnea.
- Massive proteinuria with renal failure.
- Respiratory failure and death.

1- History of exposure. 2- clinical picture.
3- X- ray is the clue diagnostic tool.
a) Chronic silicosis:
Small rounded opacities in the upper lung zones.
In massive fibrosis: bilateral opacities and there may
be cavitation if TB infection occurred.
Egg shell calcification when hilar and mediastinal
lymph nodes are enlarged and calcified.
Bilateral pleural thickening adjacent to pulmonary
fibrotic nodules.
b) Accelerated: As chronic silicosis but progress more
rapidly.
c) Acute silicosis: ground glass appearance.
1- Pulmonary function tests: (restrictive pattern).

Complications:
1- Tuberculosis “silicotuberculosis”.
2- Respiratory failure.
3- Emphysema, bronchitis.
Management:
1- Removal from exposure.
2- Corticosteroid.
3- Anti-tuberculosis drugs.
4- Treatment of complications.

1- Medical measures:
- Pre-employment & Periodic medical examination.
2- Engineering measures:
- Enclosure of dusty processes.
- Substitution of silica by safer material.
- Proper ventilation of the work place.
3- Hygienic measures:
- Work place monitoring for keeping the dust level at
its threshold limit value (TLV).
- Use of respiratory protective devices.
- Avoid smoking.

Asbestos ore
Naturally occurring fibrous minerals
Good tensile strength
Flexible
Heat resistant
Electrical resistance
Good insulation
Chemical resistant
Because of these unique properties, asbestos
was used extensively in variety of products.
Asbestos fibers

- Chrysotile - “White asbestos”
- Amosite - “Brown asbestos”
- Crocidolite - “Blue asbestos”
Most
commonly
used:
Others:
Tremolite
(sometimes found in vermiculite)
Actinolite
Anthophyllite

 Pipe insulation
 Surfacing insulating materials
 Reinforcement of materials
 Fireproofing
 Acoustic and decorative plaster
 Textiles
Asbestos insulated pipe
Asbestos insulated boiler
Greatly increased during and after
World War II in ship insulation
Use has greatly declined since the late 1970’s

1- Asbestosis.
2- Hyaline plaques in parietal pleura.
3- Malignant mesothelioma of pleura &
peritoneum.
4- Bronchogenic carcinoma.
5- Asbestos warts.
6- Cancer larynx.

Joe Darabant, 1949,
covered with
chrysotile asbestos
fibers. Worked for
30+ years at the
Johns-Manville Plant
in New Jersey, cutting
asbestos shingles and
making asbestos
block and pipe-
covering materials.
Joe, 1989. Forced
to retire in 1974 at
age 50 from poor
health; he died
from asbestosis in
1990 at age 66.
Photos © RAVANESI@2000
Asbestosis is a serious chronic, progressive disease that can eventually lead to
disability or death in people exposed to high amounts of asbestos over a long
period. Asbestos fibers cause the lung tissues to scar; when the scarring spreads,
it becomes harder and harder to breathe. Symptoms include shortness of breath, a
dry crackling sound in the lungs while inhaling, coughing, and chest pain. This
condition is permanent and there is no effective treatment.

Definition: diffuse interstitial
pulmonary fibrosis which is
usually accompanied by pleural
fibrosis and thickening.
Pathogenesis:

Clinical picture:
Symptoms: progressive dyspnea.
Signs:
- Clubbing.
- Cyanosis.
- Limitation of the movement of the lower chest
wall.
- Bilateral basal crepitations.
Diagnosis:
1- History of exposure.
2- Clinical picture.

Digital
Clubbing
Figure 2-46. Digital clubbing.

Figure 25-2. Chest X-ray of a patient with asbestosis.

Complications:
1- Cancer lung.
2- Respiratory failure due to pulmonary hypertension
and core pulmonale.
Treatment:
1- Corticosteroid may relieve dyspnea.
2- Treatment respiratory failure.
2- Stop smoking.

- Developed after 10 years.
- Not malignant.
- Bilateral yellowish well demarcated raised areas of
hyaline fibrosis.
- X-ray: bilateral linear opacities parallel to ribs.

- Latent period about 40years.
- Most commonly affecting pleura but peritoneum is also
affected.
- Crocidolite is the most important type involved in this
disease.

Photo © RAVANESI@2000
Mesothelioma is a rare form of cancer
of the pleura, the thin membrane
lining the lungs. About 200 cases are
diagnosed each year in the U.S.
Virtually all cases are linked with
asbestos exposure.
The cancer is very invasive and
spreads quickly, eventually crushing
the lungs so that the patient cannot
breathe. It is painful and always fatal.
It can be caused by very low exposure
and is not directly related to the
amount inhaled. This cancer may take
30-40 years to develop.
Richard Pankowski, 1986. Diagnosed
in 1985 with pleural mesothelioma;
died 5 months later at age 36. In
college, he worked for less than a year
at the Manville Plant in N.J. Father
also worked at the plant 30+ years and
died from asbestosis. Richard’s
exposure may have begun when he
was a child.
Tumors protruding
through the right
rib cage.

- It is dose dependent.
- Smoking is risk factor.
- Long thin fibers (crocidolite).
- adenocarcinoma type.
Preventive measures:
1- Engineering:
Enclosure, substitution, ventilation, keeping asbestos dust
concentration in work place below TLV.
2- Hygienic: Personal protective devices. Avoid smoking.
3- Medical measures:
- Pre-placement examination.
- Periodic medical examination.

Lung Cancer
Lung cancer causes the largest number of deaths from asbestos exposure.
The risk greatly increases in workers who smoke.

Definition:
Chronic respiratory disease affecting proportion of workers
involved in the manufacture of cotton, flax, hemp, jute & sisal.

Mechanism:
1- Mechanical irritation theory:
Mechanical irritation of airway epithelial surface by
short cotton fibers causes reflex narrowing of airways.
2- Pharmacological agent theories:
a) Cotton plant contains histamine that cause
bronchoconstriction.
b) Inhalation of cotton dust will liberate histamine
from platelets.
c) Release of bronchoconstrictor mediators from
polymorph nuclear leucocytes such as:
- Slow reacting substance of anaphylaxis.
- Leukotriens. - Platelet activation factors.

3- Immunologic mechanism:
Massoud & Taylor found that the byssinotic
manifestations are due to type III immune complex
hypersensitivity reaction.
4- Chemotactic theory: chemotaxis of P.N.L.
5- Endotoxin activity theory.
6- Fungus enzymes.
Pathology: No specific abnormalities in lung and
bronchi have been described with byssinosis.

- Byssinosis usually requires 20-25 years to develop.
- Symptoms of Byssinosis appear on the first day back
to work by chest tightness and breathlessness.
- Grading according to severity of symptoms:
0: No symptoms.
1/2: Occasional chest tightness on the first day of the
working week.
1: Chest tightness + breathlessness in the first day.
2: Chest tightness + breathlessness in the first day and
other days.
3: As grade 2 + permanent respiratory disability.

1- History of exposure to cotton, flax, hemp.
2- Typical manifestations.
3- Lung function:
- Decline in forced vital capacity in 1st second
FEV1(between 5- 10%) during shift.
- Decreased forced vital capacity (FVC).
- Decreased FEF 25-75%.
- Decreased PEFR.
- Decreased FEV1/FVC%

1- Continuous dust conc. measurements in
work place.
2- Pre-placement examinations: recording
history of chest troubles and base line lung
function evaluation.
3- Periodic medical examination: by measuring
FVC and FEV1.
4- Treatment of cotton before processing
(washing, steaming, treatment with alkali).

Toxic gases can be classified into:
1- Simple asphyxiants: the most important gases are
nitrogen, methane and carbon dioxide.
2- Chemical ashyxiants: the most important gases are:
A- Carbon monoxide (Co).
B- Hydrogen cyanide (HCN).
C- Hydrogen sulphide (H2S).
3- Systemically active gases:
The most important gases are:
A) Arsine (which is a powerful hemolytic agent).
B) Stibene (also is a hemolytic agent).
C) Phosphine (which is respiratory irritant and neurotoxic).

4- Irritant gases:
A) Upper respiratory irritants:
They are highly soluble in water so they dissolved in
the upper respiratory tract causing irritation.
-Ammonia (NH3) and Sulpher dioxide.
B) Lung tissue irritants:
They are less soluble in water so they penetrate deep
to lung tissue.
- chlorine – phosgene - fluorine - nitrogen oxides -
ozone

When you smell an odorless gas,
it is probably carbon monoxide.

Sources of incomplete combustion:
• Furnaces, boilers
• Internal combustion engine
(warehouses, auto plants)
Hazards increased in COLD
weather with closed doors &
windows

 Fire fighters
 Garage mechanics
 Aircraft refuelers
 Truck Drivers
 Kiln & furnace operators
 Forklift operators
 Janitorial staff
 Disaster relief workers
 Miners
 Parking garage
attendants
 Agricultural workers

Chronic exposure to CO
NYC bridge & tunnel officers

Acute toxicity: depends on concentration of
carboxyhemoglobin in blood.
Chronic toxicity:
- Sleep disturbance, headache, memory loss.
- Arrythmia, myocarditis.
- Impaired autonomic nervous system.
<10% No symptoms
At 10% Headache
10-20% Headache, tinnitus, dyspnea
20-30% As above + nausea, vomiting
30-45% As above + confusion, coma
> 50% Respiratory center depression and death

Recommendation limits:
TLV of CO in respirable air is 50 ppm and TLV of
carboxyhemoglobin in blood must not exceed 5g/100g Hb.
Prevention and control:
- Continuous environmental assessment and keep the
concentration below the recommended limit.
- Personal protective devices.
- Smoking cessation program.
Treatment:
- Removal from exposure.
- 100% O2 using a face mask.
- Hyperbaric O2.
- Blood transfusion.

Uses:
1- Fumigant (rodenticide, insecticide).
2- Extraction of silver and gold.
Mechanism of action:
- HCN absorbed through the lung.
- Excreted in urine and feces as thiocyanates.
- It inhibits cytochrome oxidase enzymes.

Toxicity:
- Acute: Headache, confusion, nausea, vomiting, rapid
weak respiration, convulsions, coma and death.
- Chronic: Neurathenia, Psychic alterations, Allergic
dermatosis.
Treatment: Removal from exposure.
- Amyle or Na nitrite inhalation.
- Na thiosulfate intravenously infusion.
- Recently, Di cobalt EDTA (600 mg intravenously)
and Na thiosulfate.

Uses:
- Manufacture pipes, sheet metals and foil.
- In paints, enamels and glazes.
Inlet to the body:
Through inhalation of dust and fumes. Also,
ingestion and absorption through the skin (by organic
compounds) may occur.

A- Distribution in the body:
- Bound to RBCs, membranes.
- Precipitate in bone, teeth.
- Exist in the plasma.
B- Excretion:
- Almost via the kidney.
- Small amount excreted through bile.
- Sweat and milk.

* G.I.T:
- Vomiting, diarrhea. - Abdominal colic. -
- Constipation.
* Nervous system:
- Headache. - Psychiatric disturbances.
- Tremors. - Mania, loss of weight.
* Blood:
Disturbance in haemosynthesis.
Anemia is due to:
- Direct effect on RBCs.
- Decreased life span of RBCs.

Prevention: By the triad of:
a) Engineering control measures.
b) Good industrial hygiene.
c) Regular clinical examination and investigation.
Treatment of lead poisoning:
a) Identification of source of lead poisoning.
b) Removal from exposure.
c) Chelation therapy for symptomatic patient with
blood lead level more than 100 microgram/ dl.
d) Chelation is performed under strict medical
supervision by giving the patient injections of calcium
ethylene dianine tetra acetic acid (Ca EDTA) and/ or
oral penicillamine.

The term "ergonomics" is derived from two Greek
words: "ergo", meaning work and "nomi", meaning
natural laws. Ergonomists study human capabilities
in relationship to work demands. It is the application
of knowledge as regards human abilities and
limitations to the design of tools, machines, tasks etc.

ergonomic principles regarding posture:
1- All work activities should permit the worker to
adopt several different, but equally healthy and safe
postures.
2- Where muscular force has to be exerted it should be
done by the largest appropriate muscle groups
available.
3- Work activities should be performed with the
joints at about mid-point of their range of
movement. This applies particularly to the head,
trunk, and upper limbs.

In order to derive the benefits of ergonomic
research, we must learn how to observe our
bodies in a new way. Any attempt to
improve workplace conditions can have only
limited success if this issue is ignored.

1- Repeated exertions
2- Lack of balance between rest and
activities
3- Awkward and extreme postures
4- Psychosocial stressors
5- Mechanical stressors
6- Extreme temperature

The following symptoms may be found:
• Tingling
• Swelling in the joints
• Decreased ability to move
• Decreased grip strength
• Pain from movement, pressure, or exposure to cold
or vibration
These symptoms may not appear immediately
because they develop over weeks, months, or years. By
then, the damage may be serious.

Occupational medicine

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