Prevention & Control of Occupational Lung Diseases
What is Occupational Lung Disease?
Lung disorder related to matter inhaled from the occupational environment.
Occupational lung diseases are a broad group of diagnoses caused by the inhalation of dusts, chemicals, or proteins.
Even persons who do not work in the industry can develop occupational disease through indirect exposure.
The effects of an inhaled agent depend on many factors: (1)
- Physical properties
( particle , mist or gas : solubility , shape , density , penetrability , concentration , radioactivity , size )
- Chemical properties
(Acidity, alkalinity, fibrogenicity, antigenicity)
- Susceptibility of the exposed person
(Integrity of body’s defences, immunologic status)
What substances in the workstation can reason for lung disease? (1)
- Dustfrom such things as wood, cotton, coal, asbestos, silica and talc. Dust from cereal grains, coffee, insecticides, drug or enzyme dusts, metals and fiberglass be capable to also injure your lungs.
- Fumesfrom metals that are heated and cooled rapidly. This procedure results in fine, solid particles being carried in the air. Examples of occupations that involve exposure to fumes from metals and other substances that are heated and cooled quickly include welding, melting, furnace work, ceramic making, plastics manufacture and rubber processes.
- Smokefrom fiery organic materials. Smoke can contain a variety of particles, gases and vapours, liable on what substance is being burned. Fire-fighters are at an increased risk.
- Gasessuch as formaldehyde, ammonia, chlorine, sulphur dioxide, ozone and nitrogen oxides. These are linked with jobs where chemical reactions occur and in jobs with high heat actions, such as welding, brazing, smelting, oven drying and furnace work.
- Vapours, which are a form of gas given off by all liquids. Vapours, such as those given off by solvents, usually annoy the nose and throat first, before they affect the lungs.
- Mistsor sprays from paints, lacquers (such as varnish), hair spray, pesticides, cleaning goods, acids, oils and thinners (such as turpentine).
Common Occupational Lung Diseases
- Obstructive Occupational airway
Occupational asthma is the most common form occupational lung disease. Occupational asthma (also known as work-related asthma) is asthma that is caused or made worse by exposures in the workplace. Estimates suggest that 15 to 23 percent of new asthma cases in adults are work related (2).
Occupational asthma refers to the development of asthma following exposure to a known occupational sensitizer (often with evidence of an elevated specific immunoglobulin E [IgE] to the relevant occupational allergen)
Adhesives, Metals (chemical coolants), Resins, Isocyanides, Flour and grain dust, Latex, Animals (shellfish in particular), Aldehydes, Wood dust may act as agents causing occupational asthma (3).
Reactive airways dysfunction syndrome (3)
The term reactive airways dysfunction syndrome (RADS) refers to the development of a persistent asthma-like syndrome for at least three months following inhalation of an airway irritant. The onset of symptoms occurs after a single specific exposure to a gas, smoke, fume, or vapour in very high concentrations. It is sometimes referred to as irritant-induced asthma. The most commonly reported agent causing RADS is Chlorine. Other commonly reported agents include toluene diisocyanate, oxides of nitrogen, acetic acid, Sulphur dioxide, and certain paints.
Occupational chronic obstructive pulmonary Disease (3)
Chronic obstructive pulmonary disease (COPD) is an umbrella term that encompasses several different pathologies, most notably chronic bronchitis, small airways disease and emphysema, and is defined by airflow limitation that is usually progressive. Inhalation of noxious particles or gases encountered in an occupational setting make an important contribution to COPD. Most notably, these include coal dust, cotton textiles, welding vapours, cadmium and silica.
- Pneumoconiosis (4)
The disease is caused by dust particles approximately 2–5μm in diameter that are retained in the small airways and alveoli of the lung. The incidence of the disease is related to total dust exposure, which is highest at the coal face, particularly if ventilation and dust suppression are poor.
Coal-worker’s pneumoconiosis (3), (4)
Coal worker’s pneumoconiosis (CWP) results from the inhalation of particles of coal mine dust, which are engulfed by macrophages which then accumulate to form the coal macule, characteristically located in the centrilobular region. Pneumoconiosis appears on the chest X-ray as small rounded opacities, typically appearing in upper and middle zones. Simple coal worker’s pneumoconiosis is not associated with abnormal clinical signs or significant impairment of lung function. If breathlessness and lung function impairment are present they are likely to be due to associated lung or heart disease. Progressive massive fibrosis (PMF) refers to the coalescence of macules to form irregular masses of fibrous tissue.
Asbestosis is a progressive disease that results from breathing in microscopic fibres of asbestos. These small fibres build up over time and can cause scarring, or fibrosis, in the lungs. This scarring causes the lungs to stiffen and makes it hard to breathe or get enough oxygen into the blood.(5)Asbestosis may not show up until 10 to 40 years after exposure to asbestos fibres.(6)
Silicosis is a disabling, dust-related disease and is one of the oldest occupational lung diseases in the world. Silicosis is caused by exposure to and inhalation of airborne crystalline silica. Silica (SiO2) is the name of a group of minerals that are found in mines, foundries, blasting operations, stone, clay, and glass manufacturing. Dust particles from silica can penetrate the respiratory system and land on alveoli (air sacs).
This causes scar tissue to develop in the lungs and impair the exchange of oxygen and carbon dioxide in the blood.(7)
Though symptoms of silicosis rarely develop in less than five years. Silicosis also makes a person more susceptible to infectious diseases of the lungs, such as tuberculosis.(7)
The symptoms start on the first day back at work after a break (Monday sickness) with improvement as the week progresses. Tightness in the chest, cough and breathlessness occur within the first hour in dusty areas of the mill, particularly in the blowing and carding rooms where raw cotton is cleaned and the fibres are straightened. The most likely aetiology is endotoxins from bacteria present in the raw cotton causing constriction of the airways of the lung.
Beryllium–copper alloy has a high tensile strengthand is resistant to metalfatigue, high temperature and corrosion. It is used in the aerospace industry, in atomic reactors and in many electrical devices. When beryllium is inhaled, it can cause a systemic illness with a clinical picture similar to sarcoidosis. The major chronic problem is that of progressive dyspnoea with pulmonary fibrosis.
- Hypersensitivity pneumonitis
Hypersensitivity pneumonitis (previously called extrinsic allergic alveolitis) refers to an allergic inflammatory pneumonitis following the repeated inhalation of organic material. Workers at risk include those with exposure to mould or fungal spore in agriculture, horticulture, forestry, cultivation of edible fungi or malt working, those handling mould vegetables and those caring for or handling birds. The disease has two patterns: the acute form and chronic form.
- Occupational respiratory cancers
The most notorious occupational cancer in respiratory practice is pleural mesothelioma. Its occurrence almost invariably suggests past asbestos exposure which may have been low level, and even bystander, exposure. The long latency between exposure and presentation suggests that the incidence of mesothelioma will continue to increase. Occupations associated with significantly higher mesothelioma deaths include plumbers, pipefitters, and steamfitters; mechanical engineers; electricians.
- Pleural disease
Asbestos-related pleural disease
Pleural plaques are the most common manifestation of past asbestos exposure. They are discrete circumscribed areas of hyaline fibrosis found on mainly parietal pleura.
Prevention of occupational lung diseases
a. Environmental hazard surveillance
Efforts should be continued to be identify occupations in which workers are likely to have high incidence of occupational lung diseases. Special attention should be given to environmental surveillance and exposure control. Environmental surveillance is the most effective means of identifying problem areas, directing control efforts, and subsequently measuring the impact of prevention strategies.
Occupations where workers are more likely to be at high risk of exposure to asbestos needed to be identified. Special attention should be given to environment surveillance and control of such occupations.
ii. Cotton Dusts
Industries using cotton that contain high levels of endotoxins should be identified and evaluated for possible additional intervention strategies or enactment or enforcement of more stringent dust standard.
Occupations where workers are more likely to be at high risk of exposure to silica needed to be identified. Any work sites (such as coal mines) where silica levels exceed the standard must be enforced by mine safety and health administration.
b. Medical Hazard Observation
Disease surveillance is needed to estimate the prevalence of occupational lung disease. However, because of latency, the lack of treatments, and the progression of some occupational lung diseases after exposure is of limited practical value, and emphasis should be placed on environment surveillance.
Hospitals are potential source of data and should be requested to record work histories and to report occupationally related diseases in their discharge reports. Government reporting systems using local physicians and district health officers are potentially the most effective means of disease surveillance. The primary advantage using local physicians and district health is their familiarity with local industry and the medical community. Involvement of local county health departments would also facilitate follow-up of reported cases. However this surveillance method has several difficulties, the most significant being the unwillingness of physicians and workers to report disease because of the potential for litigation and comebacks.
c. Hazard Removal
For many hazardous substances, control measures are difficult or unavailable. However substitute materials are often available for hazardous substances and should be used.
A rule-making change should be under taken by health authorities to require that a dust control and monitoring plan for all operations with likely asbestos exposure be filed for approval before any work is done in site, Implicit in this requirement would be sound justification for the use of asbestos as opposed to alternative materials. Nonessential uses would not be approved.
ii. Cotton Dusts
Recommended cotton dust level for work places is 0.2mg/m3. Industries in which workers show acute reactions at dust level below 0.2mg/m3 should consider the use of cotton substitutes or lower dust levels.
Because effective controls for silica in abrasive blasting operations have not be demonstrated, silica should be banned as abrasive blasting material. Available silica substitutes that have been shown to be nontoxic should be used.
a. Control Technology
Many exposure control measures are available, such as engineering design and automation, ventilation, substitution, isolation, and changes in work practices.
Technology transfer and implementation goals should be established, so that both workers and management are familiar with control technology and its application.
b. Regulatory Enforcement
Regulatory enforcement is the most effective element in the strategy to prevent occupational lung disease. Many acts (such as Mine Safety and Health Act and Occupational Safety and Health Act) place the responsibility for providing a safe and healthful work place directly on the shoulders of employer. Other measures of enforcement include sampling requirements for operators, an inspector audit programme, pre-operational filling hazard control plans and the right for inspectors to unsafe operations onsite.
Evidence indicates that the current asbestos standard provides only partial protection from asbestos-related diseases. Particularly cancer. The present permissible exposure limit (PEL) should be reduced to recommended concentration of 100,000 fibres/m3 since that is the lowest level of exposure that can be accurately measured using currently available analytical techniques.
Once silica exposure is recognized, control could be accomplished in particularly every instance. The most effective measure for silicosis is preventing hazardous exposure, through strict enforcement of an appropriate exposure standard. Present federal standard based on percent silica range from allowable exposure of 33μg/m3 to 98 μg/m3 free silica. These levels should be unified to a single standard that provide protecting against silicosis over working lifetime.
iii. Coal Dust
Most effective prevention strategy for Coal-worker’s pneumoconiosis is declining coal dust level to 2mg/m3. In addition efforts should be made to increase the awareness of dust control techniques among small-scale operations.
c. Education and Training
An education program must be targeted to future engineers and managers to increase the appropriate use of control techniques. Involvement should be directed toward schools of engineering, public health, business, and vocational education. The occupational health professional must also trained and actively involved as a ‘change agent’ in trying to improve working environments and developing informed worker and management groups.
The educational program of occupational health professionals should include special emphasis on epidemiology, biostatistics, industrial sanitation and safety, toxicology, and occupational health. Professionals need to learn what the work environment is, how to assess the work exposure, and how to control them. Proper use of engineering controls and professional protective devices is necessary component of such education.
Government and local health departments can offer a ready source of expertise such as physicians, nurses, sanitarians, epidemiologists. These departments and primary care physicians should be used to identify small and local plant problems. Primary care physicians should be taught to recognize work related diseases as part as of their medical training.
d. Incentive Systems
Although workers’ compensation lows do provide some financial relief for disabled workers, they are essentially applied only after existing prevention system have failed and when physical therapies are non-existent. For this reason, and because the individual state compensation lows are diverse, significant modifications to present system will not be achievable as part of prevention strategy.
Economic incentives, such as lower insurance premiums, should be explored as a means for industry to implement new controls.
Respirators and other personal protective devices should not be considered a primary control mechanism because they depend on human intervention.
a. Health Promotion and Smoking
Smoking is strongly associated with many lung diseases, including chronic bronchitis, emphysema, and lung cancer. Moreover, smoking has an additive effect on risk for chronic bronchitis in workers exposed to coal mine and other dusts, and it acts synergistically with asbestos to increase the risk of lung cancer. So that management and workers should work together to develop appropriate non-smoking policies such as; prohibit smoking at work places with sufficient disincentives for those who do not comply, Distribute information on health promotion and the harmful effects of smoking and etc.
b. Worker Knowledge of Exposure and Control Measures
Workers should be specifically informed of the hazards to which they are exposed and the control measures available. This should be accomplished by employers distribution information to employees and by public education at school level. Workers right to know lows should be enacted to ensure that workers exposed to hazardous substances, such as silica and asbestos, are informed and aware of the importance of control measures.
c. Disease Surveillance
Disease surveillance oriented toward the worker is design to discover those workers who may be at increased risk if exposure continues. This increased risk may result from pre-existing condition, early development of disease, or hyper susceptibility to a particular agent. When these workers are identified some form of intervention is warranted, usually involving a reduction of further exposure.
Control Occupational Lung Diseases
For some diseases there is no treatment other than improving the patient’s current health and preventing further exposure.
Early detection of occupational lung disease is often difficult, in part because in many cases, the latent period is long (eg, 15years for chronic silicosis and over 30 years for some asbestos related cancers). In addition, symptoms are often nonspecific and may not appear till disease well advanced.
01. Management of occupational asthma
Approximately two-thirds of patients don’t achieve full symptomatic healing and approximately three-quarters have persistent non-specific bronchial hyper responsiveness. After the diagnosis nearly one third of the patients with OA are unemployed up to few years.
02. Management of Mesothelioma
The therapy is focused towards relieving of symptoms. Highly selected patients can be prepared for radical surgery. Also the chemotherapy gives a small survival benefit of nearly three months. Pleural effusions can be managed with drain age and pleurodesis.
03. Management of Silicosis
All the patients who suffer from silicosis should be screened for active or latent tuberculosis infection. They are also evaluated for other tuberculosis risk factors. (Eg: HIV infection). There was no drug has been found to stop the progression of disease.
04. Management of hypersensitivity pneumonitis
Treatments include be away from source of the exposure and eradication of any residual antigens to prevent re-exposure. Self-limited exposure or if the exposure is short term complete recovery can be expected from most of the patents. But the patients with long –term exposure will suffer from permanent damage to the lungs.
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