Examples of occupational diseases with their control and prevention!
Example # 1. Pneumoconiosis:
Dust within the size range 0.5 to 3 microns is a health hazard, producing 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. The hazardous effects of dusts on the lungs depend upon a number of factors such as- (a) chemical composition (b), fineness (c) concentration of dust in the air (d) period of exposure and (e) health’ status of the person exposed.
Therefore, the threshold limit values for different dusts are different. In addition to the toxic effects of the dust on the lung tissues, the super-imposition of infections like tuberculosis may also influence the pattern of pneumoconiosis. The important dust diseases are silicosis, anthracosis, byssinosis, bagassosis, asbestosis and farmer’s lung. As no cure for the pneumoconiosis in known, it is essential to prevent these diseases from arising.
A brief account of these conditions is given in the following pages:
Among the occupational diseases, silicosis is the major cause of permanent disability and mortality. It is caused by inhalation of dust containing free silica or silicon dioxide (SiO2). It was first reported in India from the Kolar Gold Mines (Mysore) in 1947. Ever since, its occurrence has been uncovered in various other industries, e.g., mining industry (coal, mica, gold, silver, lead, zinc, manganese and other metals), pottery and ceramic industry, sand blasting, metal grinding, building and construction work, rock mining, iron and steel industry and several others.
In the mica mines of Bihar, out of 329 miners examined, 34.1 per cent were found suffering from silicosis. In a ceramic and pottery industry, the incidence of silicosis was found to be 15.7 per cent. The incidence of silicosis depends upon the chemical composition of the dust, size of the particles, duration of exposure and individual susceptibility.
The higher the concentration of free silica in the dust, the greater the hazard. Particles between 0.5 to 3 microns are the most dangerous because they reach the interior of the lungs with ease. The longer the duration of exposure, the greater the risk of developing silicosis. It is found that the incubation period may vary from a few months up to 6 years of exposure, depending upon the above factors.
The particles are ingested by the phagocytes which accumulate and block the lymph channels. Pathologically, silicosis is characterized by a dense “nodular” fibrosis, the nodules ranging from 3 to 4 mm in diameter. Clinically the onset of the disease is insidious. Some of the early manifestations are irritant cough, dyspnoea on exertion and pain in the chest. With more advanced disease, impairment of total lung capacity (TLC) is commonly present.
An x-ray of the chest shows “snow-storm” appearance in the lung fields. Silicosis is progressive and what is more important is that silicotics are prone to pulmonary tuberculosis, a condition called “silic, tuberculosis.” In recent years doubts have been raised, whether silico-tuberculotics are really tubercular or purely silicotics.
It is because, sputum in silico-tuberculotics rarely shows” tubercle bacilli; children and women of silico-tuberculotics do not develop tuberculosis; post-mortems on silico-tuberculotics failed to prove the existence of tuberculosis disease, but showed them to be cases of pure silicosis. The radiological evidence in the two conditions is so similar that one is apt to mistake a case of silicotic to be a case of tuberculosis of lungs. The final answer to this question is still awaited.
There is no effective treatment for silicosis. Fibrotic changes that have already taken place cannot be reversed. The only way that silicosis can be controlled (if not altogether eliminated) is by- (a) rigorous dust control measures, e.g., substitution, complete enclosure, isolation, hydro-blasting, good house-keeping, personal protective measures and (b) regular physical examination of workers.
Silicosis was made a notifiable disease under the Factories Act 1948 and the Mines Act 1952.
Previously it was thought that pulmonary “anthracosis”, was inert. Recent studies indicate that there are two general phases in coal miner penumoconiosis- (1) the first phase is labeled simple, pneumoconiosis which is associated with little ventilatory impairment. This phase may require about 12 years of work exposure for its development (2) the second phase is characterised by progressive massive fibrosis (PMF); this causes severe respiratory disability and frequently results in premature death.
Once a background of simple penumoconiosis has been attained in the coal worker, a progressive massive fibrosis may develop out of it without further exposure to it. From the point of view of epidemiology, the risk of death among coal miners has been nearly twice that of the general population. Coal-miners pneumoconiosis has been declared a notifiable disease in the Indian Mines Act of 1952 and also compensable in the Workmen’s Compensation (Amendment) Act of 1959.
Byssinosis is due to inhalation of cotton fibre dust over long periods of time. The symptoms are chronic cough and progressive dyspnoea, ending in chronic bronchitis and emphysema. India has a large textile industry employing nearly 35 per cent of the factory workers. Incidence of byssinosis is reported to be 7 to 8 percent in three independent surveys carried out in Bombay, Ahmedabad and Delhi.
Bagassosis is the name given to an occupational disease of the lung caused by inhalation of bagasse or sugar-cane dust. It was first reported in India by Ganguli and Pal in 1955 in a cardboard manufacturing firm near Calcutta. India has a large sector of cane-sugar industry. The cane-sugar fibre which until recently went to waste is now utilized in the manufacture of paper, cardboard and rayon.
Bagassosis has been shown to be due to a thermophilic actinomycete for which the name Thermoactinomyces sacchari was suggested. The symptoms consist of breathlessness, cough, haemoptysis and slight fever. Initially there is acute diffuse bronchiolitis. Skiagram may show mottling in lungs or shadow. There is impairment of pulmonary function. If treated early, there is resolution of the acute inflammatory condition of the lung. If left untreated, there is diffuse fibrosis, emphysema and bronchiolitis.
(1) Dust Control:
Measures for the prevention and suppression of dust such as, wet process, enclosed apparatus, exhaust ventilation etc., should be used.
(2) Personal Protection:
Personal protective equipment (masks or respirators with mechanical filters or with oxygen or air supply) may be necessary.
(3) Medical Control:
Initial medical examination and periodical medical checkups of workers are indicated.
(4) Bagasse Control:
By keeping the moisture content below 20 per cent and spraying the bagasse with 2 per cent propionic acid, a widely used fungicide, bagasse can be rendered safe for manufacturing use.
Asbestos is the commercial name given to certain types of fibrous materials. They are silicates of varying composition; the silica is combined with such bases as magnesium, iron, calcium, sodium and aluminium. Asbestos is of two types – serpentine or chrysolite variety and the amphibole type. Ninety per cent of the world’s production of asbestos is of the serpentine variety, which is hydrated magnesium silicate, the amphibole type contains little magnesium.
The amphibole type occurs in different varieties, e.g., crocidolite (blue), amosite (brown), and anthrophyllite (white). Asbestos fibres are usually from 20 to 500 p in length and 0.5 to 50 u in diameter. Asbestos is used in the manufacture of asbestos cement, fire-proof textiles, roof tiling, brake lining, gaskets and several other items. Asbestos is mined in Andhra Pradesh (Cudappah), Bihar, Karnataka, and Rajasthan – but most of it is imported from USSR. Canada, US and South Africa.
Asbestos enters the body by inhalation, and fine dust may be deposited in the alveoli. The fibres are insoluble. The dust deposited in the lungs causes pulmonary fibrosis leading to respiratory insufficiency and death; carcinoma of the bronchus; mesothelioma of the pleura or peritoneum; and cancer of the gastro-intestinal tract.
In Great Britain, an association was reported between mesothelioma and living within a half-mile (1 km) of an asbestos factory. The risk of bronchial cancer is reported to be high if occupational exposure to asbestos is combined with cigarette smoking. Mesothelioma, a rare form of cancer of the pleura and peritoneum, has been shown to have a strong association with the crocidolite variety of asbestos.
The disease does not usually appear until after 5 to 10 years of exposure. The fibrosis in asbestosis is due to mechanical irritation, and is peribronchial, diffuse in character, and basal in location in contrast to silicosis in which the fibrosis is nodular to character and present in the upper part of the lungs. Clinically the disease is characterised by dyspnoea which is frequently out of proportion to the clinical signs in the lungs.
In advanced cases, there may be clubbing of fingers, cardiac distress and cyanosis. The sputum shows “asbestos bodies” which are asbestos fibres coated with fibrin. An x-ray of the chest shows a ground-glass appearance in the lower two thirds of the lung fields. Once established, the disease is progressive even after removal of the worker from contact.
The preventive measures consist of:
(1) Use of safer types of asbestos (chrysolite and amosite);
(2) Substitution of other insulants- glass fibre, mineral wool, calcium silicate, plastic foams, etc.;
(3) Rigorous dust control;
(4) Periodic examination of workers; biological monitoring (clinical, x-ray, lung function), and
(5) Continuing research.
Farmers lung, is due to the inhalation of mouldy hay or grain dust. In grain dust or hay with a moisture content of over 30 per cent bacteria and fungi grow rapidly, causing a rise of temperature to 40 to 50° C. This heat encourages the growth of thermophilic atinomycetes, of which Micropolyspora faeni is the main cause of farmer’s lung.
The acute illness is characterised by general and respiratory symptoms and physical signs. Repeated attacks cause pulmonary fibrosis and inevitable pulmonary damage and corpulmonale. It is quite possible that this condition might be widespread in India considering the bulk of the population engaged in agricultural work.
Example # 2. Lead Poisoning (Plumbism):
More industrial workers are exposed to lead than to any other toxic metal. Lead is used widely in a variety of industries because of its properties- (1) low boiling point (2) mixes with other metals easily to form alloys (3) easily oxidised and (4) anticorrosive. All lead compounds are toxic – lead arsenate, lead oxide and lead carbonate are the most dangerous; lead sulphide is the least toxic.
Over 200 industries are counted where lead is used – manufacture of storage batteries; glass manufacture; ship building; printing and potteries; rubber industry and several others.
The greatest source of environmental (non-occupational) lead is gasoline. Thousands of tons of lead every year is exhausted from automobiles. Lead is one of the few trace metals that is abundantly present in the environment. Lead exposure may also occur through drinking water from lead pipes chewing lead paint on window sills or toys in case of children.
Mode of Absorption:
Lead poisoning may occur in three ways:
Most cases of Industrial lead poisoning is due to inhalation of fumes and dust of lead or its compounds.
Poisoning by ingestion is of less common occurrence. Small quantities of lead trapped in the upper respiratory tract may be ingested. Lead may also be ingested in food or drink through contaminated hands.
Absorption through skin occurs only in respect of the organic compounds of lead, especially tetraethyl lead. Inorganic compounds are not absorbed through the skin.
The body store of lead in the average adult population is about 150 to 400 mg and blood levels average about 25 μg/100 ml. An increase to 70 μg/100 ml blood is generally associated with clinical symptoms. Normal adults ingest about 0.2 to 0.3 mg of lead per day largely from food and beverages.
Distribution in the Body:
Ninety per cent of the ingested lead is excreted in the faeces. Lead absorbed from the gut enters the circulation, and 95 per cent enters the erythrbcytes. It is then transported to the liver and kidneys and finally transported to the bones where it is laid down with other minerals. Although bone lead is thought to be ‘metabolically inactive’, it may be released to the soft tissues again under conditions of bone resumption.
Lead probably exerts its toxic action by combining with essential SH-groups of certain enzymes, for example some of those involved in porphyrin synthesis and carbohydrate metabolism. Lead has an effect on membrane permeability and potassium leakage, has been demonstrated from erythrocytes exposed to lead.
The clinical picture of lead poisoning or plumbism is different in the inorganic and organic lead exposures. The toxic effects of inorganic lead exposure are abdominal colic, obstinate constipation, loss of appetite, blue-line on the gums, stippling of red cells, anaemia, wrist drop and foot drop. The toxic effects of organic lead compounds are mostly on the central nervous system – insomnia, headache; mental confusion, delirium, etc.
Diagnosis of lead poisoning is based on- (1) History- a history of lead exposure (2) Clinical features- such as loss of appetite, intestinal colic, persistent headache, weakness, abdominal cramps and constipation, joint and muscular pains, blue line on gums, anemia, etc. (3) Laboratory tests- (a) Coproporphyrin in urine (CPU)- Measurement of CPU is a useful screening test. In non-exposed persons, it is less than 150 micrograms/litre. (b) Amino levulinic acid in urine (ALAU)- If it exceeds 5 mg/litre, it indicates clearly lead absorption, (c) Lead in blood and urine- Measurement of lead in blood or urine requires refined laboratory techniques. They provide quantitative indicators of exposure. Lead in urine of over 0.8 mg/litre (normal is 0.2 to 0.8 mg) indicates lead exposure and lead absorption. A blood level 70 μg/1 00 ml is associated with clinical symptoms, (d) Basophilic stipling of RBC- It is a sensitive parameter of the hematological response.
(1) Substitution- That is, where possible lead compounds should by substituted by less toxic materials.
(2) Isolation- All processes which’ give rise to harmful concentration of lead dust or fumes should be enclosed and segregated.
(3) Local exhaust ventilation- There should be adequate local exhaust ventilation system to remove fumes and dust promptly
(4) Personal protection- Workers should be protected by approved respirators.
(5) Good housekeeping- Good housekeeping is essential where lead dust is present. Floors, benches, machines should be kept clean by wet sweeping.
(6) Working atmosphere- Lead concentration in the working atmosphere should be kept below 2.0 mg per 10c.metres of air, which is usually the permissible limit or threshold value.
(7) Periodic examination of workers- All workers must be given periodical medical – examination. Laboratory determination of urinary lead, blood lead, red cell count, hemoglobin estimation and coproporphyrin test of urine should be- done periodically. Estimation of basophilic stippling may also be done. An Expert Committee of WHO states that in the case of exposure to lead, it is not the average level of lead in the blood that is important, but the number of subjects whose blood level exceeds a certain value (e.g., 70 p μg/ml or whose ALA in the urine exceeds 10 mg/ litre,
(8) Personal hygiene- Hand washing before eating is an important measure of personal hygiene. There should be adequate washing facilities in industry, prohibition on taking food in work places is essential.
(9) Health education- Workers should be educated on the risks involved and personal protection measures.
The major objectives in management of lead poisoning are the prevention of further absorption, the removal of lead from soft tissues and prevention of recurrence. Early recognition of cases will help in removing them from further exposure. A saline purge will remove unabsorbed lead from the gut. The use of d-penicillamine has been reported to be effective. Like Ca-EDTA, it is a chelating agent and works by promoting lead excretion in urine, Lead poisoning is a notifiable and compensable disease in India since 1924.
Example # 3. Occupational Cancer:
Occupational cancer is an important problem in Industry. The sites of the body most commonly affected are skin, lungs, bladder and blood-forming organs.
i. Skin Cancer:
Percival Pott was first to draw attention to cancer of scrotum in chimney sweeps in 1775. It was subsequently found that cancer of the scrotum and of the skin in other parts of the body was caused by coal tar, x-rays, certain oils and dyes. Statistics now show that nearly 75 per cent of occupational cancers are skin cancer.
Skin cancers are an occupational hazard among gas workers, coke oven workers, tar distillers, oil refiners, dye-stuff makers, road makers and in industries associated with the use of mineral oil, pitch, tar and related compounds.
ii. Lung Cancer:
Lung cancer is a hazard in gas industry, asbestos industry, nickel and chromium work, arsenic roasting plants and in the mining of radio-active substances (e.g., uranium). Nickel, chromates, asbestos, coal tar (presumably 3.4 benzpyrene), radioactive substances and cigarette-smoking are proved carcinogens for the lung. Arsenic, beryllium and isopropyl oil are suspected carcinogens. More than nine-tenths of lung cancer are attributed to tobacco smoking, air pollution and occupational exposure.
iii. Bladder Cancer:
Cancer bladder was first noted in man in aniline industry in 1895. In more recent years, it was noted in the rubber industry. It is now known that bladder cancer is caused by aromatic amines, which are metabolised in the body and excreted in the urine.
The industries associated with bladder cancer are the dye-stuffs and dyeing industry, rubber, gas and the electric cable industries. The following have been mentioned as possible bladder carcinogens- beta-naphthylamines, benzidine, paraamino- diphenyl, auramine and magenta.
Exposure to benzol, roentgen rays and radio-active substances give rise to leukemia. Benzol is a dangerous chemical and is used as a solvent in many industries. Leukaemia may appear long after exposure has ceased.
The characteristics of occupational cancer are- (1) they appear after prolonged exposure, (2) the period between exposure and development of the disease may be as long as 10 to 25 years, (3) the disease may develop even after the cessation of exposure, (4) the average age incidence is earlier than that for cancer in general, (5) the localisation of the tumours is remarkably constant in anyone occupation. Personal hygiene is very important in -the prevention of occupational cancer.
v. Control of Industrial Cancer:
The control measures comprise the following- (1) elimination or control of industrial carcinogens. Technical measures like exclusion of the carcinogen from the industry, well-designed building or machinery, closed system of production, etc., (2) medical examinations, (3) inspection of factories, (4) notification (5) licensing of establishments, (6) personal hygiene measures, (7) education of workers and management, and (8) research.
Example # 4. Occupational Dermatitis:
Occupational dermatitis is a big health problem in many industries. The causes may be, Physical – heat, cold, moisture, friction, pressure, x – rays and other rays; Chemical- acids, alkalies, dyes, solvents, grease, tar, pitch, chlorinated phenols etc. Biologic-living agents such as viruses, bacteria, fungi and other parasites; Plant products – leaves, vegetables, fruits, flowers, vegetable dust, etc.
The dermatitis – producing agents are further classified into- (1) primary irritants and (2) sensitizing substances. Primary irritants (e.g. acids, alkalies, dyes, solvents, etc.) cause dermatitis in workers exposed in sufficient concentration and for a long period of time. On the other hand, allergic dermatitis occurs only in small percentage of cases, due to sensitization of the skin.
Occupational dermatitis is largely preventable if proper control measures are adopted:
The workers should be medically examined before employment, and those with an established or suspected dermatitis or who have a known pre-disposition to skin disease should be kept away from jobs involving a skin hazard.
The worker should be given adequate protection against direct contact by protective clothing, long leather gloves, aprons and boots. The protective clothing should be frequently washed and kept in good order. There are also, what are known as barrier creams which must be used regularly and correctly. There is no barrier cream so far invented which will prevent dermatitis in all occupations.
(3) Personal Hygiene:
There should be available a plentiful supply of warm water, soap and towels. The worker should be encouraged and educated to make frequent use of these facilities. Adequate washing facilities in industry are a statutory obligation under the Factories Act.
(4) Periodic Inspection:
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 risk. The worker should be educated to report any skin irritation, no matter how mild or insignificant.
Example # 5. Radiation Hazards:
A number of industries use radium and other radio-active substances, e.g., painting of luminous dials for watches; and other instruments, manufacture of radio-active paints. Exposure to radium also occurs in mining of radio-active ores, monazite sand workers and handling of their products. X-rays are used both in medicine and industry.
Exposure to ultraviolet rays occurs in arc and other electric welding processes. Infrared rays are produced in welding, glass blowing, foundry work and other processes where metal and glass are heated to the molten state and in heating and drying of painted and lacquered objects.
Occupational hazards due to ionizing radiation may be acute burns, dermatitis and blood dyscrasias; chronic exposure may cause malignancies and genetic effects. Lung cancer may develop in miners working in uranium mines due to inhalation of radioactive dust.
(1) Inhalation, swallowing or direct contact with the skin should be avoided,
(2) In case of X-rays, shielding should be used of such thickness and of such material as to reduce the exposure below allowable exposures,
(3) The employees should be monitored at intervals not exceeding 6 months by use of the film badge or pocket electrometer devices,
(4) Suitable protective clothing to prevent contact with harmful material should be used,
(5) Adequate ventilation of work-place is necessary to prevent inhalation of harmful gases and dusts,
(6) Replacement and periodic examination of workers should be done every 2 months. If harmful effects are found, the employees should be transferred to work not involving exposure to radiation,
(7) Pregnant women should not be allowed to work in places where there is continuous exposure.