Introduction to occupational health and Occupational hazards - PowerPoint Presentation

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Introduction to occupational health and Occupational hazards

Dr. Urfi

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OCCUPATIONAL HEALTH: DEFINITIONJoint Committee of WHO and ILO, 1950Occupational health should aim at the promotion and maintenance of the highest degree of physical, mental and social well being of workers in all occupations;

The prevention among workers of departures from health caused by their working conditions;

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Protection of workers in their employment from risks resulting from factors adverse to health;

Placing and maintenance of the worker in an occupational environment adapted to his physiological and psychological factors,

And to summarize:

‘The adaptation of work to man and of each man to his job’.

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Occupational Diseases from preventive medicine point of view

Occupational health and preventive medicine have the same aim i.e. prevention of disease and maintenance of well-being

Occupational diseases have a long latent period

Most occupational diseases cannot be treated

All occupational diseases can be prevented

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ERGONOMICS

Ergon meaning work and nomos meaning law

Ergonomics = “the laws of work”

OSHA (Occupational Safety & Health Administration), US,

Deptt

. Of

Labour

defines ergonomics as

“the science of designing the job to fit the worker, instead of forcing the worker to fit the job”

.

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Goals Of Ergonomics

Improve quality of working environment; engineered to the capabilities of the human bodyIncrease efficiency and productivity by reducing fatigue

Prevention of Occupational injury and illness

Work quality improvement

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Occupational environment

Sum of external conditions and influences prevailing at the place of work (apart from domestic environment) have bearing on health of workers

Cannot be considered separate from domestic environment; both complement each other

3 interactions

Man and agents (Physical, Chemical, Biological)

Man and machine

Man and man

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OCCUPATIONAL HEALTH HAZARDS

They are those diseases caused by the exposure to specific hazards at the workplace.Characteristics:-

Occurs mainly among the workers

Exposure to workplace is essential

Notifiable

and compensable

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Depending upon the occupation, an industrial worker

may be exposed to five types of hazards:-Physical HazardsChemical Hazards

Biological Hazards

Mechanical Hazards

Psychosocial Hazards

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1. Diseases due to physical agents

1.

Heat

Prickly heat, syncope,

heat hyperpyrexia, heat exhaustion, cramps

2.

Cold

Hypothermia, frostbite,

trench foot,

chillblains

3. Light

Occupational cataract, miner’s

nystagmus

4. Pressure

Caisson disease,

air embolism, blast

5. Noise

Occupational deafness

6. Radiation

Cancer,

leukaemia

,

aplastic

anemia,

pancytopenia7. Mechanical Injuries, accidents8. ElectricityBurns

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2. Diseases due to chemical agents

1.

Gases

CO

2

, CO, HCN, CS

2

, NH

3

, N

2

, HCL, SO

2

2.

Dusts (Pneumoconiosis)

i

. Inorganic dusts:

a. Coal dust

Anthracosis

b. Silica

Silicosis

c.

Asbestos

Asbestosis, cancer lung d. Iron

Siderosis

ii. Organic (vegetable) dusts: a. Cane fibreBagassosis b. Cotton dustByssinosis c. TobaccoTobaccosis d. Hay or grain dustFarmer’s lung

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2. Diseases due to chemical agents

3.

Metals

Lead, Mercury,

Cadmium, Manganese, Beryllium, Arsenic, Chromium

4. Chemicals

Acids,

alkalies

, pesticides

5. Solvents

Carbon

bisulphide

, benzene, trichloroethylene, chloroform

3. Diseases due to biological agents

Brucellosis,

leptospirosis

, anthrax,

actinomycosis

,

hydatidosis

, psittacosis, tetanus, encephalitis, fungal infections

4. Occupational cancers

Skin, lung, bladder

5. Occupational

dermatosis

Dermatitis, Eczema6. Ds. of

psychological origin

Industrial neurosis, hypertension, peptic ulcer12

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PNEUMOCONIOSIS

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Introduction

Dust within the size range of 0.5 to 3 micron, is a health hazard producing, causes after a variable period of exposure, a lung disease known as pneumoconiosis, which may gradually cripple a man by reducing his working capacity due to lung fibrosis and other complications

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The term coined b

Zenker in 1867The term pneumoconiosis derives its meaning from the Greek words:

pneuma

= air

and

konis

= dust

The International Labour Organization defines pneumoconiosis as

“the accumulation of dust in the lungs and the tissue reactions to its presence”

Not included in the definition of pneumoconiosis

:

Asthma, chronic obstructive pulmonary disease (COPD),

and

hypersensitivity

pneumonitis

,

in which there is no requirement for dust to accumulate in the lungs in the long term

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Hazardous effects of dust on the lung

Depends on following factors: (a) Chemical composition (b) Fineness (3-0.5 µ) (c) Concentration of dust in air (>200 µg/

cu.m

)

(d) Period of exposure

(e) Health status of the person exposed

Therefore, the threshold limit values for different dusts are different

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In addition to the toxic effect of the dust on the lung tissues, the super-imposition of infections like tuberculosis may also influence the pattern of pneumoconiosis

As no cure for the pneumoconiosis is known, it is essential to prevent these diseases from arising

The important disease are

silicosis,

anthracosis

,

byssinosis

,

bagassosis

, asbestosis and farmer’s lung.

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Pathogenesis

For clinical pneumoconiosis to develop, 3 essential factors areExposure to

specific substance

: coal, appear relatively inert and may accumulate in considerable amounts with minimal tissue response; while silica and asbestos, have potent biologic effects

Particles of

appropriate size

to be retained in lung (1-5

μ

m)

Exposure for a

sufficient length of time

(usually 10 years)

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SPECTRUM

Coal dust --- Anthracosis

Silica --- Silicosis

Asbestos --- Asbestosis

Iron ---

Siderosis

Sugar cane ---

Bagassosis

Cotton dust ---

Byssinosis

Tobacco ---

Tobaccosis

Grain dust --- Farmer’s lung

(A) Inorganic Dusts:

(B) Organic Dusts:

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types

Pneumoconiosis is usually divided into three groups:

Major pneumoconiosis

Minor pneumoconiosis

Benign pneumoconiosis

“ Fibrotic Pneumoconiosis”

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Major Pneumoconiosis:

Results in “major fibrosis” of the lungs and interference of lung architecture or lung functions e.g. silicosis, asbestosis, anthracosis

Minor Pneumoconiosis:

Results in “minor fibrosis” of the lungs without interference of lung architecture or lung functions e.g.

Mica and

Koalin

(china clay) pneumoconiosis

Benign Pneumoconiosis:

Dust deposition casts a shadow in x-ray of the lung but there is no fibrosis and no disturbance of lung functions e.g.

siderosis

(Fe),

stannosis

(

Sn

),

chalcosis

(Ca)

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SILICOSIS

Silicon forms 28% of earth’s crustHighly reactive: Combines with oxygen alone to form silicon dioxide (SiO2)

Develops with

repeated

and usually

long-term exposure

to dust containing free silica or silicon dioxide (SiO

2

)

First case reported in India in

Kolar

Gold mines (Mysore) in 1947

Mica mines in Bihar- 34.1%

Ceramic and pottery industry- 15.7%

Incubation period: Few months to 6 years

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exposure to silica dust

Mining

Tunnelling

Quarrying

Sandblasting

Ceramics

Brick-making

Silica flour manufacture

Slate Pencil Industry 

Agate Industry 

Quartz Grinding 

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silicosis

Brick-making

Sand blasting

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PATHOPHYSIOLOGY

Silica inhalationEngulfment by alveolar macrophagesActivation and epithelial injuryRelease of cytokines

CD4 cell & fibroblasts accumulation

Inflammation & fibrosis

Dense nodular fibrosis:

nodules 3-4 mm in diameter and characteristically involve upper lobe of lung

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Early:

Irritant coughDyspnoea on exertionPain in chestAdvanced:

Decrease total lung capacity (TLC)

Chr.

exposure: predispose to TB

X-Ray chest:

“Snow storm” appearance

(Ball of wool appearance)

"Eggshell" calcification

Silicotic

nodule

Symptoms

Diagnosis

Silicotuberculosis

:

Pulmonary tuberculosis occurs in about 25% of patients with acute or classic silicosis

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No specific treatment for the silicosis

Silica exposure has to be stopped to prevent further damage to the lungsSmokers should quit smokingCan be controlled by

A. Rigorous dust control measures

e.g. Substitution, complete enclosure, isolation, good house-keeping, personal protective measures

B. Regular physical examination of workers

Silicosis

notifiable

under The Factories Act 1948 and The Mines Act 1952

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Anthracosis

Coal Worker's Pneumoconiosis or Black lung diseaseFirst documented in Scottish coal miners in 1836Prevalence: Less than 8/1000 miners

Associated with coal mining industry

Accumulation of coal dust in the lungs and the tissue's reaction to its presence

First stage (Simple pneumoconiosis):

Characterized by chronic cough, fever, expectoration and

dyspnoea

on exertion; with little

ventilatory

impairment

Develops after 10-12 years of exposure

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Second stage (Progressive massive fibrosis):

It is irreversible and continues even after cessation of the exposure, prognosis is not good Simple pneumoconiosis may develop into progressive massive fibrosis without further exposureRisk of death among coal miners is nearly twice that of general population

Anthracosis

is

Notifiable

under The Indian Mines Act 1952

Compensable in The Workmen’s Compensation (Amendment) Act of 1959

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Byssinosis

Caused by inhalation of cotton fibre dust

(textile and fibre industries)

Incidence is 7 to 8% in workers

Typically occurring when patients return to work after a weekend or vacation

The chief symptoms are

Chest tightness

Shortness of breath

Cough and

Wheezing

Smoking significantly exacerbates

byssinosis

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B

agassosisInhalation of bagasse

or sugarcane dust

First reported in India in cardboard manufacturing firm in 1955

Exposure:

Sugarcane, paper, cardboard industry

Symptoms:

Breathlessness, Cough,

Haemoptysis

, Fever, Bronchitis, Impairment of Pulmonary functions

If not treated: Diffusion fibrosis, Emphysema,

Bronchiectasis

Diagnosis:

X-Ray “Mottling appearance” (Hazy) in lung fields

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Preventive measures

1. Dust control: Wet process, enclosed apparatus, exhaust ventilation2. Personal protection: Masks/respirators with mechanical filters or oxygen/air supply3. Medical control:

Initial and periodic medical check-ups

4.

Bagasse

control:

Keeping moisture content above 20% and spraying

bagasse

with 2%

propionic

acid (fungicide)

makes

bagasse

safe

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ASBESTOSIS

Diffuse interstitial pulmonary fibrosis that occurs secondary to the inhalation of asbestos fibresAsbestos fibres

1. Serpentine or

chrysolite

(93% of commercial use)

-white asbestos; chemically hydrated magnesium silicate

2. Amphibole (7% of commercial use)

-Hydrated silicates of iron, calcium & sodium

-

Actinolite

,

Amosite

,

Anthophyllite

,

Crocidolite

,

Richterite

,

Tremolite

Exposure:

Cement manufactures, Pipes, Gaskets, Roof tiling, Fire proof textiles, Mining, Milling

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Asbestos: Pulmonary fibrosis leading to respiratory insufficiency and death; Ca bronchus;

mesothelioma of pleura or peritoneum; Ca of GITFibrosis is peri

-bronchial, diffuse in character and basal in location

Symptoms

Average latency period is 5-10 years

Dyspnoea

Cough

Chest pain

In advanced cases, clubbing

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Diagnosis:

1. Sputum: Asbestos bodies (asbestos coated with fibrin)2. X-ray: Ground-glass appearance in the lower 2/3

rd

of lung fields

Prevention:

1. Use of

safer types of asbestos

(

chrysolite

and

amosite

)

2.

Substitution

of other

insulants

: glass

fibre

, mineral wool, calcium silicate, plastic foams

3.

Rigorous dust control

4. Periodic examination of workers

; biological monitoring (clinical, X-ray, lung function)

5.

Continuing research

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Farmer’s lung

Inhalation of mouldy hay or grain dustMouldy

hay or grain dust with moisture content of >30%

Bacteria and fungi

growRise

of temp. to 40-50 deg. C  Growth of

thermophilic

actinomycetes

(

Micropolyspora

faeni

) Farmer’s lung

Acute illness: General and respiratory symptoms and physical signs

Repeated attacks: Pulmonary fibrosis, pulmonary damage and

corpulmonale

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Overall Control of Pneumoconiosis

1. Medical Measures:Application of ergonomicsRegular medical follow upHealth education

Notification of disease & research on it

2. Engineering Measures:

Good ventilation

Isolation of process

Dust control

Substitution if possible

3. Legislation:

Proper laws

Free medical services & leave

Pension of gratuity (Disabled)

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LEAD

POISONING38

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LEAD

Lead is a soft, malleable metalCounted as one of the heavy metalsSometimes found free in nature

Makes up only about 0.0013% of the earth's crust; still not considered as rare element since it is easily mined and refined and widely used

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Why lead is used in industries

Properties of lead which makes it use widespread 1. Low boiling point 2. Mixes with other metals easily to form alloys

3.

Easily oxidized

4. Anticorrosive

All lead compounds are toxic

Lead arsenate, lead oxide, lead carbonate-

Most dangerous

Lead

sulphide

-

Least toxic

More industrial workers are exposed to lead than any other toxic metal

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Industrial Uses Of Lead

Manufacture of storage batteriesGlass manufactureShip building

Printing and potteries

Rubber industry

Jewellery making and cosmetics like

surma

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How can the human be exposed to lead??

1. Occupational exposure: - Main cause of lead poisoning in adults, as in lead miners and smelters,

plumbers, glass manufacturers,

construction workers

2. Paints:

-

Main cause of lead poisoning in children

- Chewing lead paint on window sills

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3. Soil:

- Main cause in the agricultural areas - By eating food grown in contaminated soil or sprayed with insecticides containing lead

4. Water:

-

Lead from the soil or atmosphere

can end up in surface water and

groundwater and in drinking water

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5. Lead containing products:

- Like plastic toys, bottles, cans etc.

6. Hunting:

- Animals which are hunted are at

high risk of exposure because of

the bullets which may contain lead

Breast feeding is also considered as an important route of lead exposure because of the presence of the lead in the affected female’s milk

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Past product exposures-Leaded gasoline

Leaded petrolLead added to petrol for raising octane rating increasing vehicle performance (As Tetra ethyl lead-TEL)

Being heavy metal, not burnt in the engine & comes out in solid form in exhausts from automobiles

Exposure by inhalation of dust & fumes & also by ingestion through contaminated food & water

Ban on leaded petrol came into existence in early 1990s while India banned its use in 2000

Still used in Algeria, Yemen & Iraq

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Mode of absorption

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Body stores of lead

Average adult: 150-400 mgNormal blood level: 25 µg/100 ml

Clinical symptoms: Above 70 µg/100 ml of blood

Normal adult ingest about 0.2 to 0.3 mg of lead per day largely from food and beverages

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Distribution in the body

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lead poisoning

Lead poisoning is a medical condition caused by increased levels of the heavy metal lead in the body, and this can interfere with a variety of body processes and cause toxicity to many organs and tissuesAlso k/a plumbism

,

colica

pictorum

or

saturnism

Most common toxic metal poisoning….

Silent Epidemic

Notifiable

and compensable disease in India since 1924

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Epidemiological features

Occupational inorganic lead poisoning is common among adults & non-occupational organic lead poisoning is common among young childrenChildren suffering from pica are at riskChronic respiratory & intestinal infectionsPregnancy

Alcoholics

Poor personal hygiene, nail biting

Wearing work uniform outside the factory

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Clinical picture of lead poisoning

51Involvement mainly of alimentary system

Can affect almost every system of body

Characteristically involves Central nervous system

INORGANIC LEAD

ORGANIC LEAD

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Clinical Picture Of Lead Poisoning-

Inorganic Lead

A

:

Anaemia

, anorexia,

arthralgia

,

amenorrhoea

B

: Blue-line on the gums

(Burton’s or

Burtonian

line)

due to deposition of lead

sulphide

granules in the gums, 1mm from gingival margin, more in upper jaw, specially over the incisors

C

:

Colicy

abdomen

D

:

Diarrhoea

E

: EncephalopathyF: FatigueG: Giddiness or growth failure among childrenH: Headache52

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I

: Insomnia, irritabilityJ: Joint painK: Kidney damage (Fanconi

syndrome/ chronic nephritis)

L

: Lassitude

M

:

Myalgia

, mental retardation

N

: Nausea, nervousness

O

:

Oliguria

P

: Paralysis (lead palsy), pallor, pica

R

: Restlessness

S

: Stippling of red cells, seizures, sterility

T

: Tremors

V

: Vertigo, vomiting

W

: Wrist drop, weakness53

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Organic Lead

InsomniaHeadacheMental confusionDelirium

Irritability, nervousness, anxiety

Seizures

ComaDeath

Children may also experience hearing loss, delayed growth, drowsiness, clumsiness, or loss of new abilities, especially speech skills

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Complications

System involved

Ill effects

Renal system

Nephropathy,

Fanconi

syndrome

Cardiovascular system

High blood pressure,

Coronary heart disease, Heart rate variability

Reproductive system

Reduction in sperm count, volume

and motility

Nervous system

Degeneration of axons of nerve cells, affect PNS and CNS

Skeletal

system

Bone and teeth decay

Pregnancy

Miscarriage, prematurity, low birth weight

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Diagnosis

1. History of exposure2. Clinical features

3. Laboratory tests

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Laboratory Investigations

Hb percentage: Severity of anaemia

Pallor is out of proportion to

anaemia

Peripheral blood smear:

Microcytic

hypochromia

Basophilic stippling of

rbcs

RBC count:

Decreased

Reticulocyte

count:

Increased

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a. Coproporphyrin in urine (CPU): -useful screening test -in non-exposed persons: < 150 µgm/

litre

-dangerous level : > 250 µgm/

litre

b. Amino

levulinic

acid in urine (ALAU):

-if >5 mg/

litre

 indicates lead absorption

-if >60

mg/

litre

 indicates

dangerous level

c. Lead in blood and urine:

-quantitative indicators of exposure

-

Pb

in urine: >0.8 mg/

litre (normal 0.2 to 0.8 mg) -Pb in blood: >70 µg/100 ml (clinical symptoms)58

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Prevention

In most cases, lead poisoning is preventable

Aim is to prevent the exposure to lead

Prevention strategies can be divided into

-individual measures taken by a family

-identifying the high-risk individuals

-public health measures reducing risk on a population level

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1. Substitution:

Lead compounds by less toxic materials2. Isolation

Enclosure and segregation

3. Good house keeping

Floors, benches, machines should be

cleaned by wet sweeping

4. Periodic examination of workers

-Urinary and blood lead level, RBC count,

Hb

estimation, CPU in urine test,

estimation of basophilic stippling

-Average lead level and no. of subjects

with raised levels

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5. Working atmosphere

Permissible limit: <2 mg per 10 cu. metres of air

6. Personal hygiene

-

Hand washing before eating

-Adequate washing facilities

-Prohibition of food intake at workplaces

7. Health education

-Risks involved

-Personal protection measures

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8. Local exhaust ventilation

To remove fumes and dust promptly

9. Personal protection

Approved respirators

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Management

Prevention of further lead exposure: Early recognition of cases

Prevention of further absorption:

Saline purge: removes unabsorbed lead from gut

Removal of lead from soft tissues:

Decontamination/

Chelation

therapy

Supportive therapy

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Chelation

:Process that lowers the amount of lead stored in the bodyUsed if the blood lead level is very highCause metal-like lead to bind to them and eliminated from the body through urine e.g. EDTA,

DMSA-

Dimercaptosuccinic

acid,

BAL-

Dimercaprol

Penicillamine

-

no

longer recommended

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OCCUPATIONAL CANCER

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Also known as Industrial CancersImportant public health problem as many chemicals employed in industries act as carcinogens

Agents: Chemical carcinogens both organic (lung cancer) & inorganic (skin cancer)Environmental factors: Heat, radiation etc.Influencing factors: Potency of carcinogen, duration of exposure, personal hygiene & availability of preventive measures66

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CHARACTERISTICS OF OCCUPATIONAL CANCER

1. Appear after prolonged exposure2. Period between exposure and development of disease may be as long as 10 to 25 years3. Disease may develop even after the cessation of exposure4. The average age incidence is earlier than that for cancer in general5. More among males than females6. The localization of the tumors is remarkably constant in any one occupation Personal hygiene is very important in the prevention of occupational cancer

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Skin cancer

Nearly 75% of occupational cancers are skin cancer1775: Cancer of scrotum in chimney sweepersOccupational hazard in: Gas workers, coke oven workers, tar distillers, oil refiners, dye-stuff makers, farmers, shepherds, road makers and in industries using mineral oil, pitch, tar etc.Agents: Coal tar, X-rays, certain oils and dyes

68

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Lung cancer

Hazard in gas industry, asbestos industry, nickel and chromium work, arsenic roasting plants, mining of radio-active substances (e.g. uranium), carpentersProven carcinogens: Nickel, chromates, asbestos, coal tar (3-4 benzpyrene), radioactive substances, cigarette-smoke, wood dustSuspected carcinogens: Arsenic, beryllium, isopropyl oil More than nine-tenths of lung cancer



Tobacco smoking, air pollution and occupational exposure

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CANCER BLADDER

First noted in aniline industry in 1895Caused due to aromatic amines which are metabolized in body and excreted in the urineOccupations: Dye-stuffs and dyeing industry, rubber, gas and electric cable industriesBladder carcinogens: Beta-naphthylamines, benzidine

,

para

-amino-diphenyl, auramine and magenta

70

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LEUKAEMIA

Exposure to benzol, roentgen rays and radio-active substancesBenzol: Chemical used as solvent in industriesLeukaemia may appear long after exposure has ceasedExposure noted in radiology department, atomic energy research station

71

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PREVENTION OF INDUSTRIAL CANCER

1. Health Promotion:Pre-placement examination: ErgonomicsSanitation in working environment: Good housekeeping, ventilation & Personal hygiene measuresHealth EducationControl of Dust in asbestos industry2. Specific protection:Elimination or avoidance of industrial carcinogensPersonal protective devices:

Masks, gloves, spectacles, barrier creams

Safety of worker

by wearing ‘Pocket dosimeter’ for personal monitoring of radiation72

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3. Early diagnosis & treatment:Periodic medical examinations of at risk groups; to be continued even after cessation of exposure

Treatment depending upon the type of cancer4. Disability limitation:By giving intensive treatment when the patient comes in advanced stage5. Rehabilitation:Physical/ social/ psychological/ vocational73

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OCCUPATIONAL HAZARDS OF AGRICULTURAL WORKERS

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Agricultural occupation differs from other

Workers work in open fieldsExposed to vagaries of the nature, like sun’s heat, rainfall, winterNo labour laws in practiceRemotely dispersed in rural areas such that the health services may not reach themActivities: Ploughing the soil, growing crops, harvesting, processing of crops, breeding, raising and caring for animals including poultry and tending gardens and nurseries, handling of machines, tools, insecticides, pesticides

75

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Accidents

in industry77

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Accidents are common in industries: Coal and mining industries, quarries, construction work; 0.14 per 1000 workers per year

Impact of accidents in India: Nearly 3 million Mondays are lost yearly; 2-3% fatal What an accident do?To the worker: Loss of wages, human sufferingsTo the industry: Compensation costs, medical care, lowered morale, lowered production and damage to machinery and goods

To the nation:

Lost production

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CAUSES OF ACCIDENTS

A. Human factors: More important than environmental factors; responsible for 85% of all accidents 1. Physical factors:Physical capabilities of the worker may not meet the job requirementsVisual and hearing ability 2. Physiological factors:

a. Sex:

Doing comparative jobs women have less

accidents; 5 times lower rate than males

79

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b. Age: Younger ages and very old are prone to accidents

c. Time: Minimum at the beginning of the day and increase gradually as fatigue sets ind. Experience: First 6 months of employment: 50% of accidentsNext 6 months: 23%Thereafter: Only 3%e. Working hours: Increase in accidents with increase in daily or weekly working hours

80

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3. Psychological factors:

Carelessness, inattentiveness, overconfidence, slow cerebration, ignorance, inexperience, emotional stress and accident pronenessAccident proneness: 75% of all industrial accidents occur to the same 25% of the workersB. Environmental factors:Temperature, poor illumination, humidity, noise, and unsafe machinesUnsafe machines: Account for 10-20 percent of all accidents

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PREVENTION

98% of accidents are preventablePrinciples of accident prevention 1. Adequate preplacement examination 2. Adequate job training 3. Continuing education

4. Ensuring safe working environment

5. Establishing a safety department in the organization under a competent safety engineer

6. Careful reporting, maintenance of records and publicity

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Thank

you83