Occupational Health
Dr. Anmar Al-Dewachi
Ass. Prof. Of Family Medicine
MD, M.B.Ch.B, MPH,JHSFM
Definitions
Occupational disease → Disease caused by or
resulting from employment
 Occupational environment → sum of external
conditions and influences which exist at work
place and have an effect on the health of
working population.
 The aim of occupational health is to promote and
maintain the highest degree of physical, mental and
social well-being of workers in all occupations.

Occupational Hazards
a)
b)
c)
d)
e)
Physical hazards
Chemical hazards
Biological hazards
Mechanical hazards
Psychological hazards
Occupational diseases:
a)
b)
c)
d)
e)
f)
g)
Diseases due to Physical agents
Diseases due to Chemical agents
Diseases due to Biological agents
Diseases due to Mechanical agents
Occupational cancers
Occupational dermatosis
Diseases due to Psychological origin
Diseases due to Physical agents:



•
•



Heat :either generalized effect as heat hyperpyrexia,
heat exhaustion, heat syncope, heat cramps,or local
effect burns.
Cold :either generalized effect as hypothermia or local
effect as frost bite, chilblains
Light
Dim light → eye strain, occupational cataract, miner's
nystagmus.
High illumination → blurring of vision and lead to
accidents
Ionizing radiation: cancer, aplastic anemia, leukemia,
infertility, anemia.
Ultra violet radiation (arc welding):redness of eyes.
Noise occupational deafness.
Diseases due to Physical agents:
 Pressure:
• Exposure to high pressure in divers (diving deep in
sea) lead to "Caisson disease" and air embolism.
• Exposure to low pressure in high altitudes workers
→ shortness of breath, hypoxia and polycythemia .
 Electricity Burns, disability and death.
Diseases due to chemical agents
GASES → CO, CO2, NH3, N2, HCL, SO2 → GAS
POISONING.
2.
DUSTS
Dust < 5 micron
inhaled into the lung → Pneumoconiosis
1.
I.
o
o
o
o
II.
o
o
o
3.
4.
5.
Inorganic dusts:
Coal dust → Anthracosis (Coal Miner's
Pneumoconiosis)
Silica → Silicosis
Asbestos → Asbestosis
Iron → Siderosis
Organic (vegetable) dusts:
Cotton dust → Byssinosis
Tobacco → Tobacossis
Hay or green dust → Farmers` lung
Metals and their compounds → toxic hazards from
lead, mercury, cadmium, manganese, beryllium,
arsenic, chromium etc.
Chemicals → Acids, alkalies, pesticides.
Solvents → e.g benzene.
c)


d)
e)
f)
g)
Diseases due to Biological agents:
Brucellosis (Malta fever), anthrax, actinomycosis,
hydated cyst ,tetanus, leptospirosis, fungal
infections etc.
Occur in persons working among animals products
(hair, wool) and agricultural workers.
Diseases due to Mechanical agents:
Accidents & fatigue.
Occupational cancers: Cancer of skin, lung,
bladder etc.
Occupational dermatosis: Dermatitis, eczema
Diseases due to Psychological origin: Anxiety,
depression, industrial neurosis etc.
Prevention of occupational diseases
I- Medical measures
1. Pre-placement examination:
◦ It is done at the time of employment and includes:history, thorough physical examination, some
investigations as CXR, ECG, GUE, vision testing and
special tests for endemic disease.
◦ The purpose of pre-placement examination:
 To put the right man in the right job.
 Useful as baseline data for future comparison.
2. Periodical examination:
◦ The frequency (every month, every year) and content
of periodical medical examination will depend upon
the type of occupational exposure
o Routinely workers are examined once a year. But in certain
occupations e.g. lead monthly examinations are indicated.
3. Medical and health care services.
4. Notification of occupational diseases.
5. Supervision of working environment:
Frequent visit done by the physician to the factory to know
various aspects of the working environment as temperature,
lighting, ventilation, humidity, noise, cubic space and air
pollution.
6. Maintenance and analysis of records (worker's health
record).
7. Health education and counseling
II- Engineering measures
1. Design of building
The type of floor, walls, height, ceiling, doors , windows, cubic
space are all important in the original plan of the building.
2. Good housekeeping
It means work environment approximate to house, it cover
good cleanliness, ventilation, lighting, washing …etc.
3. General ventilation
Ventilation opening must be adequate in the rooms, if dust
generated → must be exhaust ventilation system.
4. Mechanization
Machine instead of man e.g. hand mixing replaced by machine →
to prevent dermatitis
5.
6.


7.
A. II- Engineering measures
Substitution
Replacement of a harmful material by a harmless one,
orlesser toxicity.
Dust control
At the point of origin by water sprays as wet drilling
of rock.
Inclusion of a little moisture in the materials will
make the processes of grinding, sieving and mixing
comparatively dust-free.
Enclosure
Enclosing the harmful materials and processes will
prevent the escape of dust and fumes into the
factory atmosphere e.g. grinding.
8.
9.
10.
II- Engineering measures
Isolation
Isolation of the offensive process in a separate building so
that workers not directly connected with the operation
are not exposed to the hazard (isolation in place or time).
Protective devices
gas masks, ear plugs, safety shoes, gloves, barrier creams …
etc.
Research.
Lead poisoning

Lead poisoning is a medical condition caused by
increased levels of the heavy metal lead in the
body.
Types of lead posisoning:
1. Acute lead poisoning
from intense exposure to lead over short period of
time
2. Chronic lead poisoning
from repeated low-level exposure over long
period of time. Chronic much more common than
acute poisoning.
Lead uses and sources

Industrial uses:
◦ Glass manufacture, ship building
◦ Batteries, printing and potteries
◦ In paints (in the past).
◦ Plastic manufacturers
◦ Rubber product manufacturers

Non-occupational sources:
◦ Gasoline (thousands of tons of tetraethyl lead every year
is exhausted from automobiles).
◦ Drinking water from lead pipes.
◦ Chewing lead paint on toys
Mode of absorption
1.

Inhalation
Most common route 50-70%. Occur due to inhalation of
fumes and dust of lead or its compounds.
2.


Ingestion
Poisoning by ingestion is less common.
Small quantities of lead trapped in upper respiratory
tract may be ingested .Lead may also be ingested in food
or drink through contaminated hands.
Adults absorb about 6 - 10% of ingested lead. Fasting
adults absorb more.
Children absorb much more lead (30-50% if well fed,
and more, if fasting or malnourished).
Increased absorption if low Fe, Ca



3.
Skin
only in case of organic lead compounds (absorption
through skin) Organic lead has greater affinity for CNS
– therefore skin absorption may be SERIOUS.
Lead Storage & Distribution
1 Rapid turnover soft tissue pool:
- T1/2 30-40 days; blood, liver, kidney, CNS
2 Slow turnover skeletal pool:
- T1/2 10-20 years
Distribution of Lead
95% long bones.
 4% brain, liver, kidneys.
 1% blood.
 Crosses placenta

Lead excretion
Renal (90%) and biliary (10%)
• Maximum excretion is ~ 3.5µg/kg/day
• If intake > 3.5 µg/kg/day accumulation will occur
Lead metabolism and nutrition
• Low dietary intake of vitamin D, vitamin C, and iron
enhance absorption and retention of lead in the body.
•
Body stores:



Body stores → 150 – 400 mg in adult.
Blood level → < 10 μg/100ml
Blood level ↑ to 30 - 40 μg/100ml → clinical
symptoms
Health effects of lead exposure
Organs affected by lead
poisoning
 CNS
 Blood
 Renal
 GIT
 Reproductive
 Endocrine (including
Bp)
 Musculoskeletal
Clinical features of lead poisoning
•
•




•
•
•
I. Children
Early symptom are nonspecific (anorexia, irritability,
insomnia……),symptoms slowly intensify over time
Neurological symptoms
Developmental delay and loss of milestone especially
language
Hearing loss
Peripheral neuropathy
Encephalopathy
Hematological → hemolytic anemia
Renal
→ lead nephropathy
GIT
→ lead colic
II. In adults

The manifestations of lead poisoning can vary from
individual to another.

Adults with severe lead poisoning (with blood lead
levels generally above 80 μg/100ml ) can present
with the following:
 Abdominal
pain ("lead colic"), constipation, joint
pains, muscle aches, headache, hypertension
anorexia, decreased libido, difficulty concentrating
and deficits in short-term memory, anemia,
nephropathy.
 A "lead line," a bluish
pigmentation seen at the
gum-tooth line, is not a very
sensitive finding, and is the
result of a reaction of lead
with dental plaque
A peripheral neuropathy that frequently manifests
with extensor weakness or "wrist/ankle drop“
 Nephrotoxicity can occur in chronic poisoning

Diagnosis:
History of lead exposure
 Clinical examination
 LAB test
1. Blood lead level (BLL)The main tool in diagnosing and
assessing the severity of lead poisoning .
2. The Free Erythrocyte Protoporphyrin (FEP)
 EP increased when the amount of lead in the blood is high,
with a delay of a few weeks .
 EP levels in conjunction with blood lead levels can suggest
the time period of exposure; if blood lead levels are high
but EP is still normal, this finding suggests exposure was
recent.

EP level alone is not sensitive enough to identify elevated blood
lead levels below 35 μg/dL.Due to this and the fact that EP levels
also increase in iron deficiency, use of this method for detecting
lead exposure has decreased.
CBC :
 basophilic stippling
 Microcytic hypochromic
blood picture
3.
4.
Renal function test (urea
& creatinine )
Radiology (in children)
 Radio-opaque lead flecks in
the intestinal tract
suggesting recent ingestion


Lead lines at the end of
growing long bones (seen at
end of metaphysis of long
bones) in children.
Managment
Reduction or removal from lead exposure is the key
first step in treating lead toxicity.
2.
Chelation therapy

In most cases, removal from exposure is the only
therapy needed.

Chelation is recommended for individuals with BLL
>80 μg/100ml and those with levels between 60 -80
μg/100ml if they have lead-related symptoms.
 Chelating agents :
Promote lead excretion with urine
• Ca-EDTA (Ca ethylene- diamine tetra- acetic acid)
• DMSA (2,3-dimercaptosuccinic acid)
• D-penicillamine.
1.
3.
Prevention of recurrence
Preventive measures
1.
2.
3.
4.
5.
6.
Periodic examination of the workers
Substitution
Isolation
Local exhaust ventilation
Personal protection and personal hygiene
Health education.
Occupational Lung Diseases
Occupational lung diseases (OLD) are caused by the
inhalation of dusts, fumes, gases or vapors.
Four main categories of OLD can be identified
3.
Occupational asthma.
Chemical pnemonitis.
Pneumoconiosis [fibrotic and non-fibrotic].
4.
Granulomata.
1.
2.
Occupational asthma



Occupational asthma (OA) is
characterized by airflow
obstruction, airway
hyperresponsiveness, and airway
inflammation that results from a
workplace stimulus.
Occupational asthma is one of the most common
occupational lung diseases in developed countries.
5 - 10% of adult-onset asthma is due to occupational
exposure.
Occupations at risk






Animal handlers and
veterinarians (animal proteins)
Bakers and millers (cereal
grains)
Carpet makers (gums)
Cleaning staff (e.g. detergents ,
bleach)
Electronics workers
(soldering resin)
Carpenters (wood dust)





Pharmaceutical workers
(drugs, enzymes)
Seafood processors
Spray painters
Hair dressers
Health care workers
(latex and chemicals)
Characteristics of Occupational Asthma
1.
2.
3.
4.
5.
6.
A workplace substance is aerosolized or
vaporized
Patient has symptoms of asthma, but cough is
the most common symptom.
Affects only some of those exposed
Onset often after symptom-free period of
months to years
Improvement after removal from work early
in course
Recurrence of symptoms on re-exposure
Clinical features

The latency period between exposure to stimuli and
development of symptom varies among different stimuli.

Rhinitis and conjunctivitis may proceed or accompany
asthma symptoms.

Cough, dyspnea ,chest tightness , wheezes.

The patient report increased symptoms while at work or
within several hours of the completion of a shift, and
definite improvement on weekends or during vacations.
Diagnosis
1.
2.


History and examination
Investigations
Pulmonary function test PFT
Skin test
Managements:
1.
2.
3.
4.
Stop exposure
Treatment of occupational asthma is the same as for
non-occupational asthma
The prognosis depends upon rapid diagnosis and
prompt removal of the worker from further exposure
Most patients show incomplete resolution of asthma,
even many years following cessation of exposure
Pneumoconiosis

The term “Pneumoconiosis” group of lung disorders
which result from inhalation of dusts. (dust size 0.5 –
3 micron)

Many of these dusts give raise to fibrotic reaction in
the lung with clinical symptoms.

Other group of dusts causes opacities on CXR, but
no symptoms. These radiographic changes called
Benign Pneumoconiosis
Classification








Benign pneumoconiosis
Siderosis (iron oxide lung)
Stannosis
Other Benign Pneumoconiosis
Fibrotic pneumoconiosis
Silicosis
Asbestosis
Coal Miner’s Pneumoconiosis
(anthracosis)
Benign pneumoconiosis
Siderosis (iron oxide lung)


The most common benign pneumoconiosis.
Result from inhalation of iron dust as iron oxide fume in
iron and steel foundries during mining and during grinding
and welding operation.
Stannosis

Caused by deposition of tin in the lungs and it is less
common than siderosis. The opacities are much denser with
hilar L.N due to deposition of tin within them .
Other Benign Pneumoconiosis:

Calcium, Barium (baritosis), Chromate, Zirconium and
Cerium.
Fibrotic pneumoconiosis
Silicosis
Disease produced due to inhalation of free silica or silicon
dioxide (SiO2).
 Occupational exposure:
 works in mining (coal, gold, copper, silver , and lead)
 Tunneling, stone cutting
 Pottery and ceramic industry
 Rock mining and metal grinding
 The incidence of silicosis depends upon the chemical
composition of the dust, size of the particles, duration of
exposure and individual susceptibility.


The incubation period vary from few months up to 6
years, depending upon the above factors.
Clinical features:
Insidious onset, they are divided into arbitrary 3 stages
which merge into one another.
 1st stage: irritant cough, dyspnea on exertion and chest
pain. His working capacity is little affected or not affected.
 2nd stage: dyspnea with impaired ability to work.
 3rd stage: patient is totally incapacitated (signs of RHF).
 Silicosis is associated with increased risk of Lung cancer
&T.B
Prevention
Control of dust:
◦ Substitution of the substance if possible.
◦ Complete enclosure.
◦ Isolation.
◦ Wet procedure.
◦ Regular cleaning (use of vacuum).
◦ Personal protective measures.
2.
Regular physical examination of the workers.
1.
Asbestosis



Asbestosis specifically refers to the pneumoconiosis
caused by inhalation of asbestos fibers.
The disease is characterized by slowly progressive,
diffuse pulmonary fibrosis.
The spectrum of pulmonary disorders associated with
asbestos exposure includes :
Asbestosis
2. Pleural disease (focal and diffuse benign pleural
plaques)
3. Malignancies (non-small cell and small cell carcinoma
of the lung as well as malignant mesothelioma)
1.
Source of exposure

Mining and milling of the fibers

Industrial sources of asbestos (eg, work with
textiles, cement, insulation, shipbuilding)

Non-occupational exposure to airborne
asbestos (eg, regular exposure to soiled work
clothes brought home by an asbestos worker,
environmental exposure in the neighborhood of
industrial sources….)
Clinical features



Symptoms are insidious with variable latent period.
Dyspnea is the first symptom, which is frequently out
of proportion to the clinical signs in the lungs
In advanced cases, there may be clubbing of fingers,
cardiac distress , cyanosis , respiratory insufficiency
and death.
The sputum shows “asbestos bodies” which are
asbestos fibers coated with fibrin give rise to golden
yellow or brown color
Prognosis → once established; the disease is
progressive even after removal of worker from contact.
Prevention
1.
2.
3.
4.
5.
6.
Use of safer types of asbestos.
Substitution.
Rigorous dust control.
Regular physical examination of the workers (clinical
,CXR, lung function).
Health education and stop smoking.
Continuing research
Occupational skin diseases
Occupational skin diseases are very common, it
responsible for 70% of occupational diseases.
Classification of agents causing occupational
skin diseases:
1.
2.
3.
4.
5.
Mechanical agents : friction, pressure and trauma.
Physical agents : Heat, cold, humidity, light, ionizing
radiation.
Chemical agents : both organic and inorganic
chemicals.
Biological agents: Viral, bacterial and parasitic agents.
Plants and their products: leaves, fruits, dust, and other.
Mechanical agents



In the form of cuts,
abrasions, repeated
trauma → Calluses and
blisters.
Callus is thickening of the
skin in response to
repeated trauma, friction
or irritation.
Blisters result from acute
trauma to the skin
Physical agents
1. Heat :Intertrigo.,Erythema ab igne and burns
2. Cold → frost bite, chilblains.
3. Radiation → burns, dermatitis
and cancer (BCC, SCC, melanoma).
4. Electricity → Burns.
Erythema ab igne:


Occurred in those exposed to furnaces, as cooks,
glassblowers and kiln operators and long term exposure
to a heating pad.
Pathogenesis:
Long term exposure to radiant heat to the same area
over time produces persistent vasodilatation of the
dermal-subcutaneous blood vessels which leads to
clinical changes.
Clinical Feature

The early stage is an
asymptomatic
reticulated pattern of the
cutaneous blood
vessels, which proceed
to reticulated
pigmentation called
poikiloderma.

Areas of poikiloderma
are prone to SCC and
other types of skin
cancers.
Cold induced skin injuries
1.
2.
3.

Frostnip : The mildest cold-induced injury,
characterized by localized paresthesia that resolve
with rewarming. There is no permanent tissue
damage.
Chilblain (Pernio) : is characterized by localized
inflammatory lesions that result from acute or repetitive
exposure to cold above the freezing point. Lesions are
edematous, red, and may be very painful or pruritic.
Trench foot (immersion foot)
Involves the sympathetic nerves and vasculature of the
feet. It resulted from prolonged exposure of the feet to
the combination of dampness and cold.

Feet were red, edematous, numb or extremely painful,
and often covered with hemorrhagic bullae.
4. Frostbite :
 The most severe form of the localized cold-induced
injuries. Frostbite results from the freezing of tissue.
 The tissue destruction of frostbite is due to both
immediate cold-induced cell death and the more
gradual development of localized inflammatory
processes and tissue ischemia
Chemical agents
Contact Dermatitis:
1. Primary irritants contact dermatitis:
Irritants can produce lesions by direct contact to the skin,
and this depend on the concentration of substance and
the duration of exposure. [e.g. acids, alkaline, dyes,
solvents].
2. Allergic contact dermatitis:
Cause cell-mediated hypersensitivity reaction → Dermatitis.
Chemical agents
◦ Occupational acne
is caused by several different groups of industrial
compounds, including coal tar derivatives, insoluble oils,
and chlorinated hydrocarbons
◦ Disorder of pigment
hyperpigmentation
hypopigmentation
Hyperpigmentation happened in exposure to heavy metals,
organic nitrogen compounds and dyes.
Pathological mechanisms of hyperpigmentations:
Exogenous pigment deposition
Deposition in skin systemically (silver tattoos in
silver worker)
Photoeruptions
Post inflammatory hyperpigmentation
Pathological mechanisms of hypopigmentations:
Post inflammatory hypopigmentation
Chemical leukoderma (vetiligo)
Vetiligo
• Depigmentation of skin
without evidence of
autoimmune disorder as
in true condition.
• It caused by handling of
P-Tri-Butyl Phenol (PTBP)
which is used in car
industry.
• stop exposure and give Bcomplex and steroids →
get improvement
4.
Biological Agents
Infectious
Agent
Bacillus
anthracis
Skin Manifestation
Workers Exposed
Ulcerated nodular lesion
(malignant pustule)
workers with animal
skin or hair (wool)
Furuncles
Staph. aureus
Furuncles (boils)
Military and athletes
Candidiasis
C. albicans
Intertrigo, paronychia
Tinea species
T. pedis (athletes foot)
and T. corporis
Diseases
Bacterial
Anthrax
Fungal Dermatophyte
(Ringworm)
Herpes
simplex
infection
Viral
Parasitic
Herpes H. simplex inf. of fingers
simplex-1
(herpetic whitlow)
Warts
Human
papillo v-7
AIDS
HIV
Cutaneous
L. species
Leishmaniasis
Military, athletes, and
agriculture workers
Health-care workers
Warts in hands
Meat handlers
(Butcher’s warts)
Different skin lesions
Health-care workers
and Kaposi sarcoma
Muco-cutaneous ulcer
Military, farmers and
(Baghdad or Delhi boil) tropical forest workers
Control and prevention
Pre-selection
 The workers should be medically examined before
employment.
 Those with an established or suspected dermatitis or
liable for skin disease should be kept away from jobs
involving a skin hazard
2. Protection
 Protective clothing when using chemical
sprays (insecticides, etc.).
 Long leather gloves and boots.
 Barrier creams which must be used regularly
and correctly.
I.
3. Personal Hygiene:

There should be available a plentiful supply of
worm water; soap and towels.

The workers should be encouraged and educated
to make frequently use of these facilities.
4. There should be a periodic medical check-up of all
workers for early detection and treatment of
occupational dermatitis &If necessary, the affected
worker may have to be transferred to a job not
exposing him to irritation.
Occupational cancer




Occupational cancer is a serious problem in industry.
The sites of body most commonly affected are skin, lung,
bladder, and blood forming organs.
The risk of exposure is considerably increased in smokers.
Occupational cancers are usually reported to account for 1 5 % of all human cancers.
Characteristics of Occupational Cancer
1.
2.
3.
They appear after long exposure.
The period between exposure and development of the
disease may be as long as 10 - 25 years.
The disease may develop even after cessation of
exposure.
4.
5.
The average age incidence is earlier than that for cancer in
general.
The localization of the tumors is remarkably constant in any
occupation.
Lung cancer:




Occupational lung cancer has been reported in selected
workplace situations.
Asbestos, nickel, arsenic, polycyclic aromatic hydrocarbons
(PAHs) and radioactive substances as uranium and radon are
proved to be lung carcinogens.
Whereas, cadmium, beryllium ,glass fibers and ceramic fibers are
suspected to be lung carcinogens
Prevention is the key to future work-related lung cancers
Skin cancer
Nearly 75% of occupational cancers are skin cancer.
 Skin cancers are an occupational hazard among gas worker,
coke oven workers, tar distiller (road makers ), oil refiners.
 Chronic Arsenic compounds exposure
 BCC, SCC, Bowen's disease.

Leukemia
Exposure to benzene, cytotoxic drugs and ionizing radiation
give rise to leukemia.
 Benzene is a dangerous chemical and is used as a solvent in
many industries. Leukemia may appear long after exposure
has ceased.

Bladder cancer
Cancer bladder was first noted in man in aniline industry
in 1895.
 In more recent years, it was noticed in the rubber
industry.
 It is now known that cancer bladder is caused by aromatic
amines, which are metabolized in the body and excreted
in the urine.
 The following has been mentioned as possible bladder
carcinogens:
 Beta-naphthylamines
 Benzidine
 Paraamino-diphenyl
 auramine and magenta.

Prevention and control






Elimination or control of industrial carcinogens
Periodic medical examination
Notification
Licensing of establishments
Personal hygiene measures
Education of workers