INTRODUCTION TO OCCUPATIONAL HEALTH

Dr E N Aguwa

Department of Community Medicine

UNTH Enugu

Major contributors to O.H. development Georgius Agricola-He devoted his work on miners. He

wrote a book De Re metallica. He lived between 1494-1555.

PHILIPPUS PARACELSUS, German physician and chemist.

He gave warnings about toxicity due to mercury and sulphur.

GALEN; Most outstanding physician of antiquity after Hippocrates.

He recognised the dangers of acid mist in copper mines. Most renowned for his theory of humors in relation to

disease causation.

Major contributors to O.H.

PLINY THE ELDER (Gius Plinius Secondus) Roman writer and encyclopaedist recognised the danger of zinc and sulphur in mining.

He designed a mask for protection of such workers in mines and in other places involving fumes.

HIPPOCRATES; Greek and greatest physician of antiquity.

Father of scientific medicine. Recognised the danger if lead in mining. His most well known work in environmental

health is the collection titled Waters and Places

Major contributors to O.H. contd.

Bernadino Ramazzini- He was an Italian. He lived between 1633-1714.. He wrote a book De Morbis Artificum Diatriba. He insists that commoners be asked their occupation as part of their clinical history. He is regarded as the father of occupational medicine.

Charles Turner Thackrah- Father of British Industrial Medicine. He broadened the scope of O.H. to also include white collar jobs.

Major contributors to O.H.

Lord Anthony Ashley Cooper-He helped to promote labour laws.

Sir Thomas Legg- He is remembered for his four aphorisms.

George Baker- worked on lead poisoning among lead workers

Percival Pott-Identified soot from chimney as cause of scrotal cancer

George Sofoluwe-First Nigerian Occupational Health Physician.

O.H. development in Nigeria 1941 - Workmen's compensation ordinance introduced, it

was replaced by workmen's compensation decree of 1987. 1942 - Department of labour created 1945 - Labour code ordinance was enacted. This was

replaced by the labour decree ( later Act) of 1974. 1951 - Ministry of labour created. 1952- Mr P. Britnell appointed the chief inspector of

factories in Nigeria on secondment from British labour ministry.

1955- Factory act was enacted. It was amended in 1958 and later replaced by factories decree of 1987.

1958- Various regulations relating to OH and safety in Nigeria introduced.

1964 – A lectureship in OH created at the University of Lagos. Dr G.O.Shofoluwe was in-charge, he later became a professor of OH at University of Benin.

1968 – First international seminar in OH for developing countries organised in Lagos.

O.H. development in Nigeria 1970s – SOHPON was formed, replacing the

previously existing branch of the (British) Association of industrial Medical officer(1977)

Industrial Nurses Association of Nigeria was formed.

Division of occupational and Environmental health created at the FMOH (1976)

Many multinational companies and certain Federal Government parastatals started employing OH specialist specifically for their health services.

WHO/ILO DEFINITION OF O.H.

O.H. 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; the protection of workers in their employment from risks resulting from factors adverse to health; the placing and maintenance of the workers in an occupational environment adapted to his physiological and psychological equipment.

COMPONENTS OF THE WORK ENVIRONMENT

In OH and Safety, components of the work environment are those factors of the work place from which may arise hazards of work to health.

A (health) hazard is a materials substance or a circumstance which pose a danger to human health and well being.

The 5 components of the work environment are;1. Physical environment such as Temperature( excessive heat/cold),

Light ( glare or darkness), Pressure, Humidity, Radiation, Noise and Vibration.

Temperature- ( heat or cold) causes Heat exhaustion, Heat cramps, Heat stroke, Burns and Frost Bite..

Light - Excess leads to Eye stress, Cataract, arc Eye, Poor vision and accident.. Lack of light leads to Eye stress, loss of vision later in life, poor vision and accident.

Pressure- Decompression sickness (caison dx) Eardrum disorder. Humidity. – Potentates the effect of Temp. by sweating leading to

exhaustion..Radiation. – Radiation sickness, Burns and Cancer .Noise – Distraction, Lack of concentration, Fatigue and Hearing Loss. Vibration - Arthritis and Vibration white finger.

COMPONENTS OF THE WORK ENVIRONMENTChemical Environment – Most rapidly and increasingly

expanding component of the work environment. It is one of the least understood or least to be fully known

component. Some chemicals in the work place with their known

health problems are;1. Lead. Anaemia, Intestinal Colic, Nervous and Mental

Disorder.2. Mercury. Nervous and Mental Disorders, Nephrosis and

Mecurialentis.3. Nickel.- Nasal Carcinoma.4. Benzene. Leukaemia.5. Asbestos. Asbestosis, Mesotelioma, Pleural Plaques and

Lung cancer.

COMPONENTS OF THE WORK ENVIRONMENTBiological Environment. Consist of all living organisms, plants and animals

in the work environment. These are Viruses , Fungi, Bacteria, Protozoa and

plants. Some of these can cause diseases e.g. . Hookworm in farmers, Rabies in Veterinarians

and wild life keepers, Leptospirosis in sewer workers.

COMPONENTS OF THE WORK ENVIRONMENTMechanical Environment; Referred to as the man machine interphase. Consist of all the implements/machines of the

work places which because of their pointed edges, sharp edges, high powered force, misbalance with human anthropometry provide a stress which can harm human health.

Control lies in modification of these tools to guard or eliminate their hazardous components.

COMPONENTS OF THE WORK ENVIRONMENTSocial Environment. This is the man- man interphase in the work place. It is

very important in OH. It is one of the least remembered, least well known and

least able to be manipulated component. It involves worker – worker relationships, worker-

management group relationship and (boss-subordinate) line management relationship.

It contributes and determine a lot of the job satisfaction in the place of work

An alcoholic who is a manager is a social hazard to the rest of the work force.

COMPONENTS OF THE WORK ENVIRONMENT

Ergonomic Environment This is man – machine interphase. It deals on the principle that machine/tools

should be made to fit the anthropometric measures of man.

This will prevent some chronic diseases like arthritis

SPECIALIST PROFESSIONAL GROUP IN OH.Specialist training required in the field of OH for maximal functioning are; Occupational Physicians; Their training span the entire field and all levels of OH practise and services. Occupational Nurses;Lower level of expertise to occupational physician. Occupational Hygienist (including toxicologist);Concerned mainly with the chemical and physical components of the work

environment, their monitoring and control. Ergonomist/Safety Engineer:Involved with the mechanical aspect of the work environment.Usually mechanical engineers concerned with the safe performance and

modification of tools and machines to fit mans make up in the work situation. Occupational Psychologist:Involved with the man-man interphase at work and especially with the

behavioural modifications, better individual and group occupational health and safety relationships. E.g. conditions of service, and social services at work

INTERACTION BETWEEN MAN AND WORK

Positive effect of work on man: -occupies time constructively -provides source of income -results in satisfaction Negative effect of work on man -are many and can be discussed under the different work environment Positive effect of man on work -improves quality and quantity -improves creativity Improved strength to work Negative effect of man to work -spoils tools easily -is a danger to others -reduced work output.

Functions of occupational health physicians

Pre-employment medical examination: Gives a baseline medical record of the employee. The workplace has no identifiable health hazard e.g. lecturer.

Pre-placement medical examination: This is done for those who are going to engage in known hazardous jobs.

Periodic medical examination: This is done routinely to detect health problem early enough. It is not a regulated interval examination at all times and professions. Certain reasons may make one do the periodic medical exam before the required time.

Functions of Occ. Health Physician contd.

Primary medical care: Provision of first aid and treatment of minor ailments e.g. cuts. Immunization is also given when necessary.

Mandatory medical examination: This may be done as compensational medical exam.

Functions of Occ. Health Physician contd. Environmental safety and monitoring: This is by

occupational hygienists. They measure gases, dust levels, etc to make sure they fall within acceptable values. These values are called Threshold Limit Values (TLV). TLV is the average daily working air concentration 8hrs a day, 5days a week without calendar restriction, of a chemical which will cause no adverse effect in nearly all work people. TLV is not a dividing line between what is safe or unsafe because symptoms may arise below the TLV except when the TLV is qualified with a “c” meaning ceiling level. C limits are often for substances that are fast acting. TLV may also be with “skin” notation meaning that it can also be absorbed through the skin. Hence when used alone, TLV assumes no skin absorption has occurred.

Functions of Occ. Health Physician contd.

Other environmental safety measurements: -Time Weighted Average: TWA is the

value you don’t exceed on average in an 8hrs daily working.

-Maximum Allowable Concentration: This is for substances, the level of which must never exceed a particular value.

Functions of Occ. Health Physician Contd.

Control of effluents or waste for industries: Effluents or waste are treated to make them less harmful before being dispersed into the environment.

Health education: O.H. has 2main interest groups- owner of labor and the workers.

Maintenance of records and periodic surveillance. Social services: school for children, 1toilet for 25men

and 1toilet for 20men. Planning function for factory development. Provides rehabilitation for workers: occupational

therapists. Counseling services to both employers and

employees.

SCOPE OF OCCUPATIONAL HEALTH– This depends on the scale of the occupational

practice– -small scale industries-employing 50workers or

less.– medium scale industries-employing 51 to

1000workers.– Large scale industries- employing more than

1000workers.– Large scale industries often have their private

occupational health practice while small and medium scale often have group occupational health practice like “Area type” and “Estate type”.

INDUSTRIAL LEGISLATION IN NIGERIA

Before Independence: workman’s ordinance of 1941; labour code ordinance of 1945 and Factories act of 1955 revised in 1958. These were modeled after the colonial masters and did not take into consideration our poor level of industrial development

After Independence: workman’s compensation decree of 1987; labour law and factory decree of 1987. Some changes were made due to inadequacies of previous legislations.

Factory Act It stipulates some requirements for work situations

and provides for factory inspectorates to police industry and ensure compliance to the stipulated requirements.

Factory decree (1987): factory was defined as a place employing 10 or more persons. Present definition-Any premises in which or within which one person is, or more persons are, employed in any process for or incidental to any of the following purposes, namely;

1. the making of any article or part of any article; or

2.the altering, repairing, ornamenting, finishing, cleaning or washing or the breaking up or demolition of any article or

3. the adapting for sale of any article.

The following areas are covered by this decree:

cleanliness, overcrowding, ventilation, lighting, drainage of floors, sanitary accommodation (conveniences).

Workman compensation Decree(1987)

Every factory is expected to register with the workman compensation board before registration

The employer is liable for death or incapacity resulting from accident (not deliberate) which incapacitates the worker for a period of 3 consecutive days.

Usually 3 types of claims for damages can be made against the employer. These are

1. injury benefit 2. disablement benefit 3. death benefit

Labour Law: This identifies the minimum age of

employment, provision for leave (maternity, sick, annual, research, study, etc)

It makes labour pensionable and contractual

DISEASE NOTIFICATION

It is mandatory for a factory owner to notify the factory inspectorate of any occupationally related disease condition that results in loss of life or disability for 3 or more consecutive days.

Occupationally notifiable diseases in Nigeria include: lead poisoning; phosphorus poisoning; mercury poisoning; manganese poisoning; arsenic poisoning; aniline poisoning; carbon bisulphide poisoning; benzene poisoning.

Disease notification contd.

Others are chrome ulceration due to chromic acid or bichromate of potassium, sodium or ammonium; anthrax; silicosis; asbestosis; compressed air illness (cassion disease); toxic anaemia; poisoning by halogen derivatives of hydrocarbons of the aliphatic series; toxic jaundice due to tetrachloroethane or amido derivatives of benzene or other poisonous substances; pathological manifestation due to radium or other radio-active substances or x-rays; primary epitheliomatous ulceration of the skin, due to the handling or use of tar, pitch, bitumen, mineral oil, paraffin, or the compounds, products or residues of these substances.

GENERAL METHODS OF DETECTING OCCUPATIONAL DISEASES Biological monitoring: *pre-employment and periodic- medical exam laboratory radiological Epidemiological: *For detecting occupational and non occupational

diseases *Aims at studying the distribution, determinants and

deterrents of diseases and ailments among segments of the labour force

Environmental measurements: *To detect presence of harmful agents in the environment

e.g. dust sampling

SICKNESS ABSENCE

Definition-absence from work attributed to incapacity.

Doctor grants and issues the sick leave paper.

This is presented to management who are obliged to approve it.

A record of the sick leave is kept at the hospital.

CLASSIFICATION OF SICKNESS ABSENCE

Occupational-includes occupational illnesses and accidents at work

Medical-includes medical causes such as pneumonia, malaria, diarrhoel diseases, etc.

Psychosocial-includes sickness of family members, bereavement, etc.

CLASSIFICATION OF HARZARDS

Physical hazards: noise, radiation, vibration, extremes of temperature, etc.

Biological hazards: viruses, bacteria, fungi, etc. Chemical hazards: solids, liquids, gases, e.g.

pesticides, acids, alkali. Mechanical hazards: accidents; cuts and

bruises. Psychosocial hazards: long stay in work place,

poor work condition, etc. Ergonomic hazards: poor design of tools.

ROUTE OF ENTRY

Respiratory route: is the commonest route. Respirable dusts, fumes, etc.

Absorption through the skin. Inoculation through the skin. Ingestion: more common in hand to mouth

activities in work place e.g. smoking, chewing gum.

METHODS OF DETECTION OF O.H. Every occupation carries with it some form of health

hazard and hazards which are unrecognized will always remain uncontrolled.

Have a high index of suspicion. Observe the work environment while the workers are

at work. Listen to workers’ complaints Monitor increasing incidence of disease or accidents

or presence of rare disease. There should be frequent analysis of the records.

DETECTION OF HAZARDS Contd.

Biological monitoring: medical examination (pre-placement and periodic medical exam) and occupational history (Ramazzini).

Occupational history has 5major sequences: -description of all the patient’s pertinent jobs,

both past and present. Ask about the tasks involved or performed.

-review the exposures faced on the job. Ask about the chemicals used, etc.

-Timing of symptoms in relation to work.

Detection of hazards contd.

-Find out if co-workers have similar problems -Obtain more information on non-work factors

e.g. smoking, hobbies, etc. Epidemiological methods: this is by studying the

distribution and determinants of diseases among the work force. The start point is from the sickness or medical records analysis to determine the distribution etc. of disease.

Environmental monitoring: this is concerned with measurement of the dose of hazardous agents in the work environment e.g. dust measurement in coal mines, asbestos industries, etc.

CONTROL OF OCCUPATIONAL HAZARDS

Elimination by substitution; e.g. asbestos to polyvinyl alcohol, white phosphorus to phosphorus sesquisulphide in matches manufacturing to prevent phossy jaw, benzene to xylene or toluene, coal to electric train.

Total enclosure: e.g. lead shield in radiation industries. Automated procedures can be used to prevent human contact.

Locally applied exhaust ventilation: this is for dust particles. The exhaust ventilator is placed close to the source of contamination. The suction pressure must be greater than the force with which the particle are released into the surrounding.

Control of occupational hazards contd.

Suppression by wetting e.g. in coal mining. Prevents most of the dusts from being airborne.

Segregation of hazardous process Limitation of time of exposure Cleanliness of workplace. “good house keeping”.

The floor should be cleaned regularly especially at the end of the day’s work.

Adequate ventilation Personal cleanliness Personal protective measures

OCCUPATIONAL DISEASES OF THE LUNGS

Respirable dusts: <5microns Some substances e.g. gases like chlorine,

ammonia, hydrogen sulphide, nitrous fumes, etc can be noticed when inhaled. This may be due to their irritant properties or smell.

Those that are not very soluble e.g. sulphure dioxide will cause bronchospasm while the more soluble ones will cause pulmonary oedema.

Lung pathologies Acute: occur within first 6months of exposure 1. occupational rhinitis: involves inflammation of the nasal

membrane. Has 2 types; (a) allergic o.r. Latency period=2months-18years. (b) irritant or non-allergic o.r. may occur immediately following exposure.

There is reduction in lung function. Nasal mucociliary function is impaired.

Symptoms may include: sneezing, rhynorrhoea, obstruction of of the nasal passages, conjunctival, nasal and pharyngeal itching and lacrimation all occurring in temporal relationship to the allergen.

The ability of allergens to cause rhinitis may be attributable to their size (10 to 100micrometer).

Example of agent is wood dust e.g. Iroko.

2. Occupational asthma Similar to allergenic rhinitis. Allergen may cause any of the

following: -formation of a specific antibody IgE. The cause is

immunologic and could result in immediate, late or dual reactions.

-direct liberation of bronchoconstrictor substances. -direct or reflex stimulation of the airways of individuals with

either latent or frank asthma. Symptoms include: breathlessness, chest tightness, wheezing

which gets worse by the day following exposure but gets better the next day following withdrawal from exposure.

To know whether an asthma is occupationally related you do a vitellogram (using a spirometer) before after work. If you able to elicit a decrease of more than 10% in FEV(1) then it is most likely occupational.

Effects of o.a. on LFT

It is an obstructive lung disease. FVC, FEV(1) and Peak flow rates are reduced.

FEV(1) is much more reduced. FEV(1)/FVC is much reduced. RV/TLC% is increased. Agents: wood dust (mahogany); tobacco

leaves; tea plantation workers; sea food handling; nickel (jewelries manufacturing); gum plantation; drugs (penicillin, methyldopa); epoxy resins; isocyanates.

C. Hypersensitivity pneumonitis

Response is in lung parenchyma. Allergen is usually a protein which has bacteria and/or fungal components. Symptoms: dry cough, breathlessness and fever with chills. No wheezing. It

is not an infective condition. Chronic condition may show dyspnoea, weight loss, lethargy and finger clubbing

It produces inflammatory reaction It also results in restrictive lung disease Physical exam. Fine basal crepitations. CXR varies from patchy infilterates to widespread nodular shadows LFT are all reduced Agents: 1. bird’s droppings causing bird fancier’s disease. Observed in those

who keep birds. 2. Farmer’s lung: spores of actinomycetes (fungal spores). Occurs in

temperate zones and produces fever and cough.

D. Bagasossis: It occurs in sugar cane farmers. Pathogenesis is unclear It involves fungal growth in bagasse E. Bysinossis: Disease of cotton farmers Pathogenesis is still poorly understood but it is believed not to be

immunogenic but as a direct toxic effect to the airways Produces an obstructive lung pathology and affects the bronchi. FEV(1)

is reduced but the CXR is mostly normal Mild bysinossis is reversible as long as exposure seizes but if prolonged

it becomes irreversible. Cigarette smokers are at increased risk of having the irreversible form Also called Monday tightness: condition is worst on Mondays but gets

better as the day progressed.

PNEUMOCONIOSES

Accumulation of dust (mineral/inorganic) in the lungs & the tissue reaction to its presence.

Examples: silicosis (silica), coal worker’s pneumoconiosis (coal), asbestosis (asbestos), stannosis (tin oxide), barytosis (barium sulphate), arsenic dust, chromic dust.

PATHOLOGICAL TYPES Non-collagenous pnuemoconiosis:

-Intact alveolar architecture-minimal stromal rxn consisting mainly of reticular fibres.-potentially reversible dust rxn. e.g. stannosis and barytosis.

Collagenous pneumoconiosis:-permanent scaring of the lung-permanent alteration or destruction of alveolar structure.-moderate to maximal collagenous stromal rxn.

ASBESTOSIS 3 types; chrysotile (white), amosite (brown) and

crocidolite (blue). Occupations exposed: mining, fire insulators,

brake pads, pipes, motor gaskets, floor tiles, roofing sheets,etc.

Route: inhalation. Pathology: Diffuse interstitial fibrosis esp. lower

lobe; pleural plaques; lung cancer; mesothelioma of the pleura and peritoneum.

Symptoms: breathlessness, cough, weight loss, cyanosis, finger clubbing, basal crepitations.

Radiology

Non specific, pleural thickening, pleural effusion, basal fibre-like opacities.Lung Function Test: Restrictive defect- decreased TLC, VC, RV, FEV(1). Increased RV/TLC%. FEV(1)/FVC normal or raised.

Diagnosis: based on history, signs, symptoms, radiology, LFT.

Treatment: No treatment is effective. Withdraw from further exposure.

COAL MINER’S PNEUMOCONIOSIS

Exposure to silica and coal Sources: coal miners Route: inhalation Pathological types: (1) Simple CMP & (2) Complicated

CMP associated with progressive massive fibrosis Symptoms: In SCMP there may be no symptom or mild

breathlessness may appear. In CCMP – weight loss, fever, breathlessness, cough and signs of cardiac failure. TB is often associated with CCMP.

LFT: decreased TLC, FEV(1)/FVC, gas transfer. Increased RV.

Withdrawal does not improve condition.

Caplan’s syndrome & Anthracosis

Caplan’s syndrome-reported in coal workers, asbestos workers & foundry men. Nodular shadows seen on CXR and presence of rheumatoid arthritis. Cavitation & calcification may occur.

Anthracosis: benign, harmless form of pneumoconiosis caused by inhalation of soot or carbon smoke lacking in free silica. Common in city dwellers due to smoke.

SILICOSIS

Inhalation of silica dust. Sources: mining, quarrying, foundry, sand blasting. Pathology: Fibrosis, emphysema. May be

complicated by TB or lung cancer. No cyanosis. No finger clubbing.

CXR: Pinhead nodules seen all over the lung fields. LFT: FEV(1)/FVC is normal or slightly reduced.

Peak flow rate is normal. Treatment: Non.

Control of pneumoconiosis Elimination by substitution e.g. PVA Total enclosure of process Locally applied exhaust ventilation and suppression of

dust generation by wetting Segregation of hazardous process Limitation of exposure time Adequate ventilation Cleanliness of the workplace Personal hygiene Self protection e.g. wearing dust masks, respirators,etc.

Other control measures include

Pre- employment medical exam Periodic medical exam e.g. 3yearly CXR

for coal workers Pre- placement medical exam Environmental dust sampling Disease Notification

LEAD WORKERS

Commonest industrial poisoning 2 types of lead: Inorganic & organic Inorganic: Lead acid battery makers, battery

chargers, painters, solderers, plumbers, welders Route: Inhalation of dust & fumes; ingestion Symptoms: colicky abdominal pain, decreased

appetite, constipation, greyish pigmentation of the gum (lead line). Others are anemia, decreased hand grip, encephalopathy, renal failure.

Exposure to inorganic Lead contd.

Diagnosis: Blood lead estimation; urinary corporphyrin & alpha-laevulinic acid (both are precursors of haem)

Treatment: remove from further exposure, high milk intake & haematinics

Organic Lead poisoning Oily liquid in form of tetra-ethyl & tetra-methyl lead Source: petroleum industry & storage tank cleaners. Route: skin & lungs Symptoms: Insomnia, headache, anxiety, irritability,

metallic taste in mouth, encephalopathy with delirium, mania and schizophrenia.

Control: health education, routine monitoring, personal protection, cleaning of workplace, personal cleanliness.

AGRICULTURAL WORKERS Definition of Agriculture: all forms of activities connected

with growing, harvesting and primary processing of all types of crops with the breeding, raising and caring of animals and with tendering gardens and nurseries.

Definition of agricultural worker: any person engaged either permanently or temporarily, irrespective of his legal status, in activities related to agriculture as defined above.

Forms of Agriculture:

Peasant (subsistent) farming;

Small scale organized farming;

Large scale organized farming.

Health Problems of Agricultural Workers General: malnutrition, malaria, TB, RTI, gastroenteritis,

dracontiasis, leishmaniasis (kalar azar), trachoma, CSM. Specific:

(1) Biologic – (a) Zoonoses e.g. Bovine TB, Antrax, Brucellosis, etc. (b)Parasitic e.g.Bilharziasis, Ancylostomiasis, Leptospirosis, etc. © Others e.g. Tetanus, snake bite, scorpion bite, bee sting, etc.(2) Chemical - Poisoning from insecticides e.g. chlorinated hydrocarbons (DDT, BHC, Dieldrin); organophosphates (paration, malation, abate); carbamates (propoxsure, carbaryl); others (fungicides, herbicides, rodenticides, etc.).

Health problems contd. (3)Physical hazards: Heat – heat fatigue, heat cramps, heat

syncope, heat exhaustion and heat stroke; Noise – from machinery; Dust and Fumes.

(4) Mechanical: Cuts from machetes and hoes ; injuries from falling off tractors and felling of trees.

(5) Ergonomics: Joint pains from working with poorly fitting tools.

(6) Allergic diseases: Farmer’s Lung (dust containing fungi); Byssinosis from cotton; Allergic conjuctivitis (from latex of rubber); URTI (rhinitis) and dermatitis from wood dust.

Control measures: Health education Improve nutrition Improve hygiene Regular de-worming Working when the weather is less hostile Shades or resting areas should be constructed near

the working site. Early identification and treatment of cases Provision of referral services Personal protection e.g. hats, gloves,boots, etc.

OCCUPATIONAL CANCERS

Delayed toxicity

About 2-8% of all human cancers are occupational in origin

Long and latent period

from 1 year- skin cancer

4-5years – haematological cancers

8-26 years – lung cancers

up to 40 years-bladder cancer

Hx Percival Pott 1775

Scrotal Ca among chimney

Sweeps. Soot – 3,4 benzpyrenes

Stages of carcinogenesis Initiation – irreversible DNA

damage – mutation Promotion – agent increases response to a carcinogen

previously administered

-initiated cells develop and multiply to form a focal

collection of cells

Progression – proliferation of cells – malignant tumour

These 3 stages make up the latent period

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER-IARC LISTING OF CARCINOGENS

Group 1 –carcinogenic to humans Group 2 – probably/possibly carcinogenic but

insufficient evidence Group 3- unclassified Group 4 –not carcinogenic ie evidence of lack

of carcinogenicity

Common occupational cancers and aetiological agents

Lungs asbestos arsenic radon in uranium mining nickel

chromiumNose(nasal sinus) leather dust wood dust nickel Skin polychlorinated aromatic hydrocarbons eg,coal tar,

soot, diesel exhaust ionizing radiation

arsenic

Common occupational cancers and aetiological agents

Leukaemia benzene ionizing radiation

Bladder napthylamines shistosomiasis

Liver vinyl chloride monomers (refrigerant used in plastic industries), hepatitis B & C

Stomach and large intestine- asbestos

Prostate cadmium

Carcinogenicity testing Animal expts. 2 doses

2 strains 2 sexes at least 50 in each group Exposure for 2-4 years before results

In vitro AMES TEST Non tryptophan producing salmonella typhimurium. Grows in a culture medium only after mutation that

enables it to produce tryptophan.

Control Identify carcinogens in the workplace Alert physician Epid studies Carcinogenicity testing Elimination/substitution Legislation e.g for asbestos

Enclosure e.g radiation

Protective equipment Screening