Occupational health: Promotion & Maintenance of the highest degree of physical, mental & social wellbeing of workers in all occupations (WHO & ILO, 1950 & revised in 1995). Occupational medicine: A branch of preventive medicine with some therapeutic function (Royal College of Physicians, 1978).

1. Dr. Dalia El-Shafei
Assist.Prof., Community Medicine Department, Zagazig University
http://www.slideshare.net/daliaelshafei

2. 1) To define occupational health, occupational medicine, occupational
disease, and work-related disease.
2) To demonstrate the difference between occupational medicine and
clinical medicine.
3) To demonstrate occupational health services and the duties of
occupational health professionals.
4) To enumerate and identify occupational hazards.
5) To recognize and diagnose different occupational diseases.

3. Promotion & Maintenance of the highest degree of physical,
mental & social wellbeing of workers in all occupations
(WHO & ILO, 1950 & revised in 1995).

4. A branch of preventive medicine with some therapeutic
function (Royal College of Physicians, 1978).
Industrial Medicine Occupational Medicine
Occupational &
Environmental
Medicine

5. Health
promotion for
workers &
proper
prevention &
ttt.
Work
environment &
its adverse
effects on
workers’ health
Health
problems of
workers at any
workplace

6. 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.

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

9. 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. HPN).
Work-related disease

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

11. Physician
Hygienist
Ergonomist
Nurse
Safety Engineer
Epidemiologist

12. Occupational physician
Designs & implements
OH program
Conducts medical exam.
& biological monitoring
Provides 1st aid &
emergency ttt.
Supervises the
rehabilitative program
for disabled workers
Team leader

13. Assists the physician in
providing medical
services
Assists in supervising the
work environment
Educates workers Keeps medical records

14. Occupational
Health Program

15. Health
Promotion
Improvement of
the health &
working capacity
of workers
Improvement of
work
environment
Hazard
Prevention
Medical
Engineering
Hygienic
Hazard
Control
Medical
examinations
“pre-placement
& periodic”
ttt
1st aid
Rehabilitation
&
Compensation

17. Adequate
nutrition
• Nutrition
education &
support
• Prevention &
control of
parasitic
diseases.
Socioeconomic
development
• Improving
workers' income
• Proper expending
of this income.
Social welfare
• Management of
family problems.
• Making good
social relations at
work.
• Encouragement
of sport
activities.
Health
education &
keeping good
medical
records

18. Good design
of the
machines
Suitable
housekeeping
Proper
lighting &
ventilation
Good control
for physical
hazards
Washing
facilities &
suitable
transportation
means

20. Pre-employment medical
exam. “PEME”
Pre-placement exam.
Periodic medical exam.
“PME”
Health education
Immunization &
chemoprophylaxis
• Choose suitable worker.
• Put the suitable worker in the
suitable process.
• Early detection of any health
hazards arises from workplace.
• Early symptoms & signs of
occup. diseases
• To combat any infectious
disease.

21. Law specifies the periodicity of the PME for workers in each work or job “48
Occupational diseases”.
It is either every 6 Ms or every 2 Ys depending on duration of exposure needed to
develop the occupational disease.
Workers may be temporally or permanently removed from further exposure or may
be advised to continue work.

22. Mechanization of heavy
work process to lighten
the physical strain.
Enclosure & segregation
of hazardous process.
Good ventilation, lighting
& control of other
physical hazards at
workplace.

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

25. Provides base line data about
workers' health status
Detection of any deviation from these
data on subsequent PME.

26. OD can be identified in its early stage to prevent progression of the abnormal
physiologic condition It includes:
Survey “history
of exposure &
any abnormal
symptoms or
complains”.
Clinical
examination.
Laboratory
investigations
Biologic
monitoring for
early detection of
any disturbed
physiologic
function

27. Early ttt of diagnosed
occupational diseases.
1st aid ttt of any occupational
injuries.

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

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

32. Occupational
hazards
Physical
Chemical
MechanicalBiological
Psycho-
social

33. Physical
Temperature
Radiation
Noise
Vibration
Atmospheric
pressure
Electricity
Chemical
Metals
Solvents
Dusts &
fumes
Gases
Pesticides
Biological
Bacteria
Viruses
Parasites
Rickettsia
Psychosocial
Stress &
PTSD
Violence
Long
working
hours
Mechanical
Wrong
lifting
Wrong
movements
Wrong
postures
Slippery
floor or
stairs

36. Systemic
Heat
cramps
Heat
exhaustion
Heat
stroke
Skin
Rash
Burn
Psychoneurotic
Chronic
heat
fatigue
Eye
Cataract
“U.V
rays”

38. Excessive sweating & water intake without salt replacement causing
hyponatremia.
C/P:
ttt:
- Prevention by adequate salt intake
- Supplementation with salts “oral or I.V. infusion”.
- Control of hot environment to eliminate or minimize heat hazards.
Severe painful cramps
in muscles of limbs
during work.
Severe spasm at
intestinal smooth
muscles
Headache, dizziness
Body temperature
“normal or slightly ↑”.

40. Excessive sweating, salt & water depletion without replacement causing heamo-
concentration & hypovolemia & circulatory failure.
C/P:
ttt:
- Removal of the patient to cool place.
- Water & salt replacement.
- ttt of shock.
Headache, weakness,
fatigue.
Anorexia, vomiting.
↑ body temperature (<40
°C) & excessive
sweating.
Peripheral circulatory
failure (Pallor, Cold
moist skin, HPN, Weak
rapid pulse).

41. Disturbance of heat regulating center at brain → heat retention → hyperpyrexia.
C/P:
ttt:
- Rapid cooling of body by all possible means.
- Removal of patient from the hot environment.
- Symptomatic “sedatives or stimulants, I.V. saline, O2 inhalation, bed rest”
Abrupt ↑ of body
temperature (≥40°C).
Flushed hot dry skin.
Delirium, convulsion Coma & death

45. Blocking of sweat gland ducts → sweat retention & inflammatory reactions.
C/P:
ttt:
- Removal to cooler environment.
- Skin cleanliness to prevent infections.
- Cool showers.
- Mild drying & soothing lotions.
Raised red vesicles
on the affected skin.
Prickling & itchy
sensation on
exposure to heat.

47. Noise is any unwanted or undesirable sound.
Auditory field lies between 20-20000 hertz (Hz) or cycles/second. If noise is below
the lower level of normal hearing (<20Hz) it is called infra sound but if the noise
above the upper limit of normal hearing (>20kHz) it is called ultrasound.

48. Weaving Hammering of
metals
Military
exposure due
to explosions
& shooting
Building &
construction
Aviation &
submarines

49. Duration of
exposure
Intensity of the
sound
Frequency of
sound waves
Type of noise
“continuous or
impact which
is more
dangerous”
Personal
susceptibility

51. NIHL
Auditory effect
• HR: ↑ or ↓ “type of noise”.
• RR: often ↑.
• Performance of psycho-motor
tasks “↓or ↑”.
• ↑ community mental illness.
Non-auditory effects

52. Reduction of noise at
source.
Limit exposure with or
without ear protectors.
Routine monitoring of the
place for noise level &
the population at work for
hearing ability “PME”.

54. Radiation is the straight line transport of energy through space or matter
Electromagnetic or particulate
radiation capable of producing ions,
directly or indirectly when passing
through matter.
Ionizing radiation
“IR”
Electromagnetic radiation with a
wave length not sufficient for
ionization.
Non ionizing radiation
“NIR”

56. Mechanism of action:
a) Ionization: is to ripe electrons away from atoms & molecules.
b) Excitation of molecules.
Electromagnetic radiation
“EMR”
• X- ray
• Gama “γ”ray
Corpuscular radiation
• Alpha “α” particles “low power
of penetration & great power of
ionization”.
• Beta “β” particles “greater
power of penetration”.
• Neutrons
• Protons
• Electrons.

57. 
or X-rayNeutron

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

59. 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::
1:100:10,000

60. Uranium miners
& atomic
millers
Nuclear reactors
& atomic energy
plant
Radiologist Scientists using
radioactive
materials

62. Whole body irradiation
Exposure to doses > 1Gy →
acute radiation syndrome
“Prodromal symptoms (nausea,
vomiting) & bone marrow
depression (leukaemia,
anaemia, thrombocytopenia)”.
Local irradiation
Skin reactions according to the
dose “mild erythema → tissue
necrosis & ulceration”.

65. Chronic radiation
sickness.
Chronic radio-
dermatitis: disturbed
sensation, focal
hyperkeratosis,
congestive
hyperaemia, painful
cracks & ulceration
with malignant
changes.
Eye cataract: starts at
posterior pole of lens
capsule.
Carcinogenic &
hereditary harm.
Chronic effect

71. Working in compressed
air that is too rapidly
decompressed (Caisson
disease).
Divers who surface too
rapidly from depths >10
m.
Crew or paratroopers in
aircraft who ascend too
rapidly from sea level to
heights >5487 m.

73. Manifestations of DSI are due to formation of nitrogen bubbles in body
fluids & tissues.
Site in which bubbles are
formed
• Site of symptoms
Size & Rate of growth of
bubbles
• Severity of symptoms

74. Type I
• Mild or severe limb pain.
• Skin mottling or skin irritation.
Type II
• Paralysis or weakness, Tingling or
numbness of the limbs,
• Vertigo, Headache, coma
• Dyspnea, chest pain, Hypotension.

75. Aseptic necrosis of the bones
“dysbaric osteonecrosis”.
Neurological or psychological
symptoms.

76. Gradual
decompression
according to the
well known
standards
Use of
pressurized
airplanes.
Inhalation of
helium/oxygen
mixture instead
of air by divers
to avoid
nitrogen
narcosis.
PEME:
“exclude
chronic
sinusitis, otitis
media, lung
cysts or
emphysema”.
PME

77. ttt: recompressing the patient & reducing pressure in accordance
with a protocol laid down in set of tables.

81. Pneumoconiosis or dusty lung = dust collection in the lung &
the lung reaction to its presence.

82. Collagenous
Non-collagenous
(benign
pneumoconiosis)
• Fibrosis.
• Permanent destruction of normal
alveolar architecture
• Silicosis
• Asbestosis
• Coal workers pneumoconiosis
• Talcosis
• Minimal reticular reaction.
• Alveolar architecture intact.
• Iron oxide: siderosis
• Tin: stannosis
• Barium: baritosis
• Titanium: titanosis
Types of pneumoconiosis

85. Investigations
X-ray
PFTs
Autopsy
& Biopsy
C/P
Symptoms
”D”
Signs
“3C”
Occupational
History

86. 1- Occupational history.
2- Clinical picture:
a- Symptoms:
-The most important is progressive dyspnea.
-Melanoptysis in CWP.
b- Signs:
Cyanosis Clubbing Crepitations

87. (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

88. * Large opacities > 1cm
A: area of opacity from 1-5 cm2
B: combined area of opacity < area of Rt. upper lobe.
C: combined area of opacity > area of Rt. 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.

91. Fibrotic lung disease due to inhalation of dust containing crystalline silicon
dioxide (free silica)
Miners or
workers in
tunnels
Sand blasters Quarry
workers
Glass
workers
Ceramic
workers

92. • Repeated exposure of low level of silica for >20 years.
• Lung: Discrete fibrotic nodules of 2-3mm, mainly in upper lobes with whorled
pattern. These nodules may coalesce together → Progressive massive fibrosis
“PMF” → central ischemic necrosis with cavitation.
• Pleura: thickening, fixed, hard with fibrotic nodules.
Chronic classic silicosis
• As classic but progress more rapidly.
Accelerated silicosis
• Inhaled high level of recently fractured quartz → immediate damage of the
alveoli → acute alveolitis → fibrosis.
Acute silicosis

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

96. History C/P X-ray PFTs

97. X- ray is the clue diagnostic tool.
Pulmonary function tests: (restrictive pattern).
• Small rounded opacities in the upper lung zones.
• In massive fibrosis: bilateral opacities “cavitation if TB infection occurred”.
• Egg shell calcification: Hilar & mediastinal LNs are enlarged & calcified.
• Bilateral pleural thickening adjacent to pulmonary fibrotic nodules.
Chronic silicosis
• As chronic silicosis but progress more rapidly.
Accelerated
• Ground glass appearance.
Acute silicosis

101. Complications
Management
TB
“silicotuberculosis”
Respiratory failure Emphysema Bronchitis
Removal from
exposure
Corticosteroid
Anti-TB
drugs
ttt of
complications

103. Medical measures
• PEME & PME.
Engineering measures
•Substitution of silica by
safer material.
•Enclosure of dusty
processes.
•Proper ventilation of the
work place.
Hygienic measures
• Work place monitoring
for keeping dust level ˂
threshold limit value
(TLV).
• Use of respiratory
protective devices.
• Avoid smoking.

106. Asbestos ore Asbestos fibers
Naturally
occurring
fibrous minerals
Good tensile
strength
Flexible Good insulation
Heat resistant
Electrical
resistance
Chemical
resistant

107. - Chrysotile - “White asbestos”
- Amosite - “Brown asbestos”
- Crocidolite - “Blue asbestos”
Most
commonly
used

108. Greatly ↑ during & after World War II in ship insulation.
Use has greatly declined since the late 1970’s
Pipe insulation Surfacing
insulating
materials
Reinforcement
of materials
Fireproofing Acoustic &
decorative
plaster
Textiles

110. Asbestosis Hyaline
plaques in
parietal pleura
Asbestos warts Cancer: Pleura
“Malignant
mesothelioma”,
Lung, larynx

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

113. Clinical picture:
Symptoms: progressive Dyspnea.
Signs:
Diagnosis:
1- History of exposure.
2- Clinical picture.
Clubbing Cyanosis
Crepitations
“Bilateral basal”
Limitation of the
movement of the
lower chest wall

115. Chest X-ray of a patient with asbestosis.

116. Complications
Treatment
Cancer lung Respiratory failure
PH+ & core
pulmonale
Corticosteroid
“relieve dyspnea”
ttt of respiratory
failure
Stop smoking

117. Developed after 10
years.
Non-malignant Bilateral yellowish
well demarcated
raised areas of
hyaline fibrosis.
X-ray: bilateral
linear opacities
parallel to ribs.

118. Latent period about 40
years.
Most commonly
affecting pleura >
peritoneum
Crocidolite “most
involved type”.

119. Dose dependent Smoking is risk
factor
Long thin fibers
(crocidolite)
Adenocarcinoma
type

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

121. Engineering
Hygienic
Medical
• Substitution
• Enclosure
• Ventilation
• Keeping asbestos dust concentration
in work place below TLV.
• PPE & Avoid smoking.
• PEME & PME.

123. Chronic respiratory disease affecting proportion of workers involved in the
manufacture of
Cotton Flax Hemp
Jute Sisal

125. Mechanical
irritation
• Short cotton
fibers
→Mechanic
al irritation
of airway
epithelial
surface →
BC.
Pharmacolog
ical agents
• Histamine in
Cotton → BC.
• Cotton dust
inhalation→
liberate histamine.
• Release of BC
mediators from
PNL “Slow
reacting substance
of anaphylaxis,
Leukotriene,
Platelet activation
factors”.
Immunologic
mechanism
“Massoud &
Taylor”
• Type III
immune
complex
hypersensiti
vity
reaction.
Chemotactic
• Chemotaxis
of P.N.L.
Endotoxin
activity
Fungus
enzymes

126. No specific abnormalities in lung & bronchi.

127. - Byssinosis usually requires 20-25 years to develop.
- Symptoms appear on the 1st day back to work by chest tightness &
breathlessness.

129. 1- History of exposure to cotton, flax, hemp.
2- Typical manifestations.
3- PFTs “Obstructive”:
Forced vital capacity in 1st sec. (FEV1)
Forced vital capacity (FVC).
Forced expiratory flow (FEF) 25-75%.
Peak expiratory flow rate (PEFR).
FEV1/FVC%

130. Continuous dust conc.
measurements
PEME & PME: PFTs Cotton ttt before
processing (washing,
steaming, ttt with alkali)

132. Simple
asphyxiants
Nitrogen
Methane
CO2
Chemical
ashyxiants
Carbon monoxide
(Co)
Hydrogen cyanide
(HCN)
Hydrogen sulphide
(H2S)
Systemically
active gases
Arsine (Powerful
hemolytic agent).
Stibene (Hemolytic
agent).
Phosphine
(Respiratory irritant
& neurotoxic).
Irritant
gases
Upper respiratory
irritants: Highly
soluble in water →
dissolved in URT →
irritation
”Ammonia (NH3) &
SO2”
Lung tissue
irritants: Less
soluble in water →
penetrate deep to
lung tissue
“Chlorine –
Phosgene - Fluorine
- NOx- O3

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

138. Firefighters Kiln &
furnace
operators
Garage
mechanics
Aircraft
refuelers
Truck Drivers Forklift
operators
Janitorial staff Disaster relief
workers
Miners Parking garage
attendants
Agricultural
workers

139. Chronic exposure to CO
NYC bridge & tunnel officers

141. Acute toxicity: depends on concentration of COHb in blood.
Chronic toxicity:
<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 & death
Sleep disturbance,
headache, memory loss.
Arrhythmias
Myocarditis
Impaired ANS

144. Prevention & control
Treatment
Continuous
environmental
assessment
PPE
Smoking cessation
program
Removal from
exposure
O2 “100% or
Hyperbaric”
Blood transfusion
Recommendation limits:
TLV: CO in respirable air is 50 ppm & COHb in blood is 5g/100g Hb.

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

149. Toxicity
.
Headache, Confusion, Nausea,
Vomiting, Rapid weak
respiration, Convulsions, Coma
& Death.
Acute
Neurathenia
Psychic alterations
Allergic dermatosis
Chronic

150. Treatment
Removal from exposure
Amyle or Na nitrite
inhalation
Na thiosulfate IV infusion
Di cobalt EDTA (600 mg IV)
& Na thiosulfate

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

158. 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 & milk.

159. What are the Normal levels of lead??
 Adults:
<20 micrograms/dL of lead in the blood
 Children:
<5 micrograms/dL of lead in the blood

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

163. Prevention:
Engineering control
measures
Good industrial
hygiene
Regular clinical
examination &
investigation

164. Treatment of lead poisoning:
Identification of source
of lead poisoning.
Removal from exposure Chelation therapy
• Symptomatic patient with
BLL >100 µg/dl.
• Ca EDTA and/ or oral
penicillamine.

168. The term "ergonomics" is derived from 2 Greek words: "ergo
= work" & "nomi = natural laws”.
Ergonomists study human capabilities in relationship to work
demands.
It is the application of knowledge as regards human abilities &
limitations to the design of tools, machines, tasks etc.

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

171. Repeated exertions
Lack of balance
between rest &
activities
Awkward &
extreme postures
Psychosocial
stressors
Mechanical
stressors
Extreme
temperature

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