Occupational Respiratory Diseases
By
Dr.Ashraf Hussain
PhD. Community Medicine
Occupational Respiratory diseases
are broad group of pulmonary disorders that develop from inhalation of specific
particles.
Historically, they have been a major cause of morbidity and mortality before workplace
safety guidelines were rigorously established and enforced.
Although each disease has a slightly unique presentation, they all lead to progressive
deterioration in lung function that can cause severe respiratory compromise if
appropriate measures are not undertaken.
Occupational asthma
airflow limitation and airway hyper-responsiveness caused by specific agents inhaled in
the workplace.
Caused as a direct result of workplace exposure.
It does not include activation of pre-existing asthma or airway hyper-responsiveness
induced by non-toxic irritants or physical stimuli such as cold air.
Two types of occupational asthma are recognised:
v
Immunological asthma appears after a latent period of occupational exposure;
v
Non-immunological occupational asthma develops without a period of latency
and is associated with exposure to high concentrations of irritants also called
(Irritant Induced Occupational Asthma or Reactive Airways Disease).
Irritant Induced Occupational Asthma
Also called reactive airway dysfunction syndrom or reactive airway disease.
Usually develops after a single, very high exposure to an irritant chemical.
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Frequently, individuals complain of a burning sensation in their nose and throat within
minutes of exposure
It is a direct “burn” effect on the airways and is not related to the immune system.
Examples of causal agents include ammonia, chlorine, acids and smoke.
The high levels of exposure required are usually the result of accidents or some major
failure of controls, often in enclosed spaces.
The pa ents nearly always manifest asthma symptoms within 24 hours of the exposure,
that is, there is no latent period.
Symptoms will tend to improve over time and may go away entirely but if symptoms
persist beyond 6 months, persistent problems are possible.
Diagnostic criteria for reactive airways disease syndrome
Individual previously free from respiratory symptoms
History of inhalation of gas, fume, or vapour with irritant properties.
Rapid onset of asthma like symptoms after exposure
Bronchial hyper-responsiveness on methcholine challenge test
Allergic Occupational Asthma
Allergic Occupational Asthma is caused by sensitisation to a specific chemical agent in
the workplace over a period of time.
This is the mechanism for the vast majority (>90%) of cases of occupa onal asthma.
The sensitisation process does not occur after one exposure but develops over time (i.e.,
latency period).
The latency periods are variable and can be as short as several weeks or as long as 30
years.
If exposure is consistent, the period of greatest risk is the first two years of exposure but
the risk does not go away after that but may reduce somewhat.
If exposure to the causative agent ceases completely, the condition will nearly always
improve.
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If this happens within the first two years of the development of the condition then
complete recovery is usual.
The longer exposure however, not only cause the tendency for the condition to get
worse, but the less likely it is that there will be a complete recovery although a cessation
of exposure is nearly always of benefit.
For these reasons identifying a case of occupational asthma as early as possible is of
paramount importance, and hence the reason for health surveillance.
Health surveillance is used to detect the early onset or symptoms of asthma.
It is deemed to be secondary prevention, (by detecting adverse effects early rather than
total prevention)
Health surveillance can take the form of a pre employment medical assessment, an
annual respiratory questionnaire or lung function tests or both depending on the
situation.
This should be carried out by a competent health professional 3 months and 12 months
after job commencement and annually thereafter.
The respiratory questionnaire should be completed again and results compared to pre
employment ones.
If health surveillance indicates that an employee has become sensitized, the employer
should remove the worker from working with the sensitizer and advise him/her to
consult a doctor.
This would also indicate that the existing control measures are inadequate and the Risk
Assessment should be reviewed and any necessary changes should be made.
Byssinosis
v
Hypersensi ve airways and acute reduc on in FEV1 (asthma-like breathing) in
susceptible individuals when they are exposed to dusts of cotton or flax.
v
Also called Monday fever or cotton workers' lung.
v
Acute dyspnoea with cough and chest tightness on the first day of the working
week, then symptoms improve on subsequent working days, despite continued
exposure to the sensitizing agent.
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v
As the disease progresses the symptoms recur on subsequent days of the week,
and eventually even occur at weekends and during holidays.
v
If the workers who develop byssinosis are not removed from further exposure,
they go on to develop long term respiratory impairment and subsequently have
an excess risk of mortality from respiratory disease.
2. Inters al lung diseases (ILDs)
are a heterogeneous group of more than 100 diseases that result in inflamma on
and/or scarring of the lung parenchyma.
Both occupational and non-occupational ILDs have similar pathophysiology(ies),
progressive fibrotic changes, structural abnormalities, and common physiologic
sequelae.
Occupational ILDs have varied latency periods, usually measured in years, and present
predominantly or exclusively with pulmonary manifestations.
Extra pulmonary symptoms and signs rarely occur (eg, cases of beryllium disease, silica-
associated autoimmune disease, or renal disease).
Pneumoconiosis
Pneumoconiosis is the generic term for the inhalation of mineral dust and then the
resultant diffuse, usually fibrotic, reaction in the acinar part of the lung.
The term excludes asthma, neoplasia, and emphysema.
Hundreds of types of pneumoconioses have been identified, but only three are common
: asbestosis, silicosis, and coal workers’ pneumoconiosis.
In these conditions, the radiologic findings were resulting from the accumulation of
inflammatory and fibrotic responses triggered by dust deposition.
Coal Worker’s Pneumoconiosis (CWP
Also known as black lung disease
Inters al lung disease result from long term exposure (usually more than 20 years) to
high levels of Coal dust.
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Simple CWP is largely only an abnormality on the chest radiograph; there are small spots
in the upper lung zones that reflect inhalation of coal dust, but nothing more.
Symptoms include shortness of breath, cough may be chronic and problematic in
patients even after they leave the workplace and lowered pulmonary function.
However, it can develop into complicated CWP, which is also called progressive massive
fibrosis in which the smaller shadows coalesce into large nodules, 1 to 2 cen meters in
diameter.
These lesions can distort and destroy normal lung architecture and result in severe
shortness of breath, disability and can lead to death.
CWP is diagnosed based on chest X-ray or CT findings, and a history of work in coal
mines.
There is no cure for coal worker’s pneumoconiosis.
Caplan Syndrome
Exposure to coal dust has been found to result in airflow obstruction and chronic
bronchitis and is also associated with the development of rheumatoid arthritis, which
when combined with CWP is known as Caplan syndrome
Asbestosis
What is asbestos ?
Asbestos is a set of six naturally occurring silicate minerals , which is called by that name
due to asbestiform habbit :
long thin fibrous crystals, and each visible fiber composed of millions of microscopic
"fibrils" that can be released by abrasion and other processes
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Characteristics of asbestos ?
Asbestos fibers are:
•
Very strong
•
Highly flexible
•
Resistant
to
breakdown
by
acid,
alkali,
water, heat, and flame
•
Non-biodegradable
•
Environmentally persistent
Uses of Asbestos
Automotive Parts: Brake pads, clutches, gaskets and valves.
1. Tiles: Flooring, ceiling and roofing tiles were commonly made with asbestos. The
adhesive used to lay down flooring tiles has also been a source of exposure.
2. Cement: Asbestos-containing cement was used in building materials because the
fibers provided strength without adding much weight.
3. Its insulating and fire-resistant properties also made the mineral an ideal
substance to add to cement.
4. Textiles: Asbestos was used in the production of cloths and garments for its
resistance to heat and corrosive elements. Some of the most common textiles
included blankets, fireman suits and rope.
Asbestos exposure is a concern for the following workplaces and processes:
1. Mining of asbestos occurring from natural mineral deposits
2. Processing of asbestos minerals (millers)
3. Manufacture of asbestos-containing products
4. Construction industry - disturbing asbestos-containing materials during building
renovations or demolitions
5. Mechanics - vehicle brake and clutch repairs
6. Marinas - renovating or demolishing ships constructed with asbestos-containing
materials
7. Insulation workers and heating trades
8. Sheet metal workers, plumbers and pipe fitters
9. Workers responsible for disposing of asbestos waste, and waste workers
10. Cement workers
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11. Custodial workers - contact with deteriorating asbestos-containing materials in
buildings
Pathophysiology and health effects
Diseases ?
Respiratory :
q
Parenchymal asbestosis : Diffuse interstitial fibrosis
q
Asbestos-related pleural abnormalities
Pleura plaques
Benign asbestos pleural effusions
Diffuse pleural thickening
Pleural mesothelioma
q
Lung carcinoma
It depends on:
o
Nature and extent of exposure
o
Concentration of asbestos fibers
o
Duration of exposure
o
Frequency of exposure
o
Cigarette smoking
Silicosis
•
occupational lung disease caused by inhalation of crystalline silica dust
•
marked by inflammation and scarring in the form of nodular lesions in the upper
lobes of the lungs.
Silicosis is caused by inhalation of unbound (free) crystalline silica dust
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Characterized by nodular pulmonary fibrosis.
Chronic silicosis initially causes no symptoms or only mild dyspnea.
But over years can advance to involve most of the lung and cause dyspnea,
hypoxemia, pulmonary hypertension, and respiratory impairment.
Diagnosis is based on history and chest x-ray findings.
No effective treatment exists except supportive care and, for severe cases, lung
transplantation.
Workers at greatest risk are those who move or blast rock and sand (miners, quarry
workers, stonecutters) or who use silica-containing rock or sand abrasives (sand
blasters; glass makers; foundry, gemstone, and ceramic workers; potters).
Coal miners are at risk of mixed silicosis and coal workers’ pneumoconiosis
Factors that influence the likelihood of development of silicosis include
1. Duration and intensity of exposure
2. Form of silica
3. Surface characteristics (exposure to the uncoated form poses greater risk than
the coated form)
4. Rapidity of inhalation after the dust is fractured and becomes airborne (exposure
immediately after fracturing poses greater risk than delayed exposure)
It is found in many rocks, such as granite, sandstone, gneiss and slate, and in some
metallic ores.
Silica can be a main component of sand. It can also be in soil, mortar, plaster, and
shingles.
The cutting, breaking, crushing, drilling, grinding, or abrasive blasting of these materials
may produce fine to ultra fine airborne silica dust.
Pathophysiology
When silica dust particles are inhaled → embed deeply into the tiny alveolar sacs and
ducts in the lungs.
There, the lungs cannot clear out the dust by mucous or coughing.
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crystalline silica dust deposited in the lungs→ macrophages ingest the dust particles
→inflammation response →produce collagen around the silica particle → fibrosis and
the formation of the nodular lesions.
There is only abnormal chest X-ray in the beginning and then slowly develop a cough
and breathing difficulty.
More than a third of people with silicosis have phlegm production and cough
Chronic bronchitis-like symptoms may occur, and the lungs have additional sounds
called wheezes and crackles.
Compensatory emphysema may develop also.
Classification of silicosis
1. Chronic simple silicosis : long-term exposure (10 years or more) + low
concentrations of silica dust → appearing 10–30 years a er first exposure.
Often asymptomatic, but many patients eventually develop dyspnea during exertion
that progresses to dyspnea at rest.
Productive cough, when present, may be due to silicosis, coexisting chronic occupational
(industrial) bronchitis, or smoking.
Breath sounds diminish as the disorder progresses, and pulmonary consolidation,
pulmonary hypertension, and respiratory failure with or without right ventricular failure
may develop in advanced disease.
2. Accelerated silicosis : Patients often experience the same symptoms as those
with chronic silicosis, but symptoms develop over a shorter period.
develops 5–10 years a er first exposure to higher concentra ons of silica dust
2. Acute silicosis :
-develops a few weeks to 5 years a er exposure to high concentra ons of silica dust
- Patients experience rapid progression of dyspnea, weight loss, and fatigue with
diffuse bilateral crackles.
-Respiratory failure o en develops within 2 yr.
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4. Complicated silicosis : complicated by
1. progressive Massive fibrosis
Also patients with silicosis are at risk of other disorders:
1. Progressive systemic sclerosis
2. Tuberculosis
3. Nocardiosis
4. Lung cancer
5. Chronic kidney disease
6. Possibly rheumatoid arthritis
Prevention
The most effective preventive interventions for silicosis occur at an industrial rather
than clinical level and include
dust suppression, process isolation, ventilation, and use of non–silica-containing
abrasives.
Respiratory masks provide imperfect protection and, although helpful, are not an
adequate solution.
Surveillance of exposed workers with respiratory questionnaires, spirometry, and chest
x-rays is recommended.
Other preventive measures include smoking cessation and pneumococcal and influenza
vaccination.
2. Hypersensi vity pneumoni s (HP),
also known as extrinsic allergic alveolitis,
Granulomatous inflammatory reaction caused by an immunological response to certain
inhaled organic dusts and some low molecular weight chemicals.
Farmer’s lung (an immune response to spores of thermophilic actinomycete bacteria)
and bird fancier’s lung remain the most prevalent forms of the disease.
Others including humidifier lung, and mushroom picker's disease.
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Hypersensitivity pneumonitis (Cont.),
Diagnosis based on history, physical examination, and radiographic findings.
Pa ents may report fever, chills, malaise, cough, dyspnea, and headaches 4-6 hours
after heavy exposure to an inciting agent in acute HP.
Chronic extrinsic allergic alveolitis is caused either by chronic exposure to low doses of
the causative antigen, or as a consequence of repeated attacks of acute alveolitis over
many years.
Characterized by cough, progressive dyspnea, fatigue, anorexia, and weight loss.
On examination, patients may present with fever, tachypnea, and diffuse fine basilar
crackles; with muscle wasting, clubbing, and respiratory distress in severe cases.
Chest radiographs may show micronodular or reticular opacities in acute or subacute HP
and progressive fibrosis with lung volume loss in chronic HP.
Bagassosis: This is a form of Hypersensitivity Pneumonitis which is caused as a result of
exposure to sugarcane fiber waste.
Bird Fancier's Lung caused as a result of dust present in the feathers of birds.
Farmers Lung: induced by the inhalation of biologic dusts coming from hay dust
or mold spores or any other agricultural products
Lung Cancer
A number of occupations or occupational exposures are established or suspected risk
factors for lung cancer.
The International Agency for Research on Cancer has identified some occupational
exposure factors as being carcinogenic to the human lung (aluminum production,
arsenic, asbestos, beryllium, cadmium, hexavalent chromium and coal gasification
fumes, crystalline silica, nickel, radon, and soot)
Depending on the agent, additive or multiplicative modes of interaction have been
shown to operate with cigarette smoking.
The majority of these cancers are caused by asbestos, followed by radon, silica,
chromium.
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Cigarette smoke and asbestos interact strongly in causing bronchogenic carcinomas, and
the risk of carcinoma is greater in persons with the interstitial fibrosis of asbestosis.
Lung infections:
contact with other people who are ill
infected from a source at work, such as a contaminated humidifier.
Influenza and other infections such as tuberculosis or legionella can be occupational
infections.
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