3. History
• It is likely that humans have suffered from
occupational lung disease since the change from
hunting to agriculture as a means of providing
food.
• In Roman times it was recorded that mining was
a dangerous trade, fit only for convicts and
slaves.
• The first recorded mention of breathlessness
among handlers of grain was done by Ramazzini,
the father of occupational medicine, in 1713.
Bernardino
Ramazzini
(1633 - 1714)
4. History
• In the eighteenth and early nineteenth centuries, it was thought
that the symptoms from black lung disease were asthma-
related.
• The term "black lung" was coined when medical professionals
discovered the blackening of miners' lungs in post-mortem.
• The first documented case of an asbestos-related death was
reported in 1906 when the autopsy of an asbestos worker
revealed lung fibrosis.
• In the early twentieth century, it was observed that many
asbestos workers were dying unnaturally young.
5. History
• In 1924, Nellie Kershaw, an English textile
worker was the first case of asbestosis to be
described in medical literature.
• Dr William Edmund Cooke testified in
Kershaw's inquest that "mineral particles in
the lungs originated from asbestos and
were, beyond reasonable doubt, the primary
cause of the fibrosis of the lungs and
therefore of death"
• Berylliosis was described first in Germany
in 1933 and in the USA in 1943.
Nellie Kershaw
(1891 –1924)
6. Definitions
• As per International Labour Organization (ILO)
– The term “occupational disease” covers any disease
contracted as a result of an exposure to risk factors arising
from work activity.
• Two main elements are present in the definition of an
occupational disease:
1) The causal relationship between exposure in a specific
working environment or work activity and a specific
disease; and
2) The fact that the disease occurs among a group of exposed
persons with a frequency above the average morbidity of
the rest of the population.
7. Definitions
• The 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 are
conditions such as 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.
8. Definitions
• In other words
– Pneumoconiosis can be defined as the non-neoplastic
reaction of lungs to inhaled minerals or organic dust and
the resultant alteration in their structure excluding asthma,
bronchitis and emphysema. – Textbook of Pulmonary
Medicine , D Behera
9. Pathogenesis
• For clinical pneumoconiosis to develop, 3 essential factors are
required:
– Exposure 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 (1-5μm)
– Exposure for a sufficient length of time (usually around 10
years)
10. Pathogenesis
• From an occupational health point of view, dust is classified by
size into following categories:
• Inhalable Dust: is the one which enters the body, but is trapped
in the nose, throat, and upper respiratory tract. Particle size is
usually 6-25μm.
• Respirable Dust: particles that are small enough to penetrate
the nose and upper respiratory system beyond the body's
natural clearance mechanisms of cilia and mucous and are
more likely to be retained in the lungs. Particle size is usually
1-5μm.
• Particles of <1 μm are exhaled out.
13. types
– Silicosis – from silica dust
– Asbestosis – from asbestos dust
– Coal workers pneumoconiosis (anthracosis) – from coal
dust
– Byssinosis – from cotton dust
– Bagassosis – from sugarcane dust
– Farmer's lung - from hay dust or mold spores or
other agricultural products.
– Berylliosis – from beryllium
14. types
– Siderosis – from iron oxide
– Tanosis – from tin oxide
– Talcosis – from talc (hydrated magnesium silicate)
– Bauxite fibrosis – from bauxite dust
– Mixed dust pneumoconiosis – from a mixture of dusts
– Hard metal pneumoconiosis – from certain metals like
cobalt
– In addition, others dust such as aluminum, barium,
antimony, graphite, kaolin and mica can also cause
pneumoconiosis.
15. types
• Pneumoconiosis is usually divided into three groups:
– Major pneumoconiosis
– Minor pneumoconiosis
– Benign pneumoconiosis
“ Fibrotic Pneumoconiosis”
16. types
• Major Pneumoconiosis: Inhalation of some dusts results
in “major fibrosis” of the lungs, which results in
interference of lung architecture or lung function tests.
• Examples are:
– Silica silicosis
– Asbestos asbestosis
– Coal anthracosis
Healthy lung Silicotic lung
17. types
• Minor Pneumoconiosis: Inhalation of some dusts results in
“minor fibrosis” of the lungs
• There is minimal fibrosis of the lungs without interference of
lung architecture or lung function tests.
• These dusts include:
– Mica pneumoconiosis
– Koalin (china clay) pneumoconiosis
18. types
• Benign Pneumoconiosis: There isn't any reaction in the lungs,
but dust deposition casts a shadow in x-ray of the lung. There
is no fibrosis and no disturbance of lung functions.
• It can result from the inhalation of:
– Iron dust siderosis
– Tin dust stannosis
– Calcium dust chalcosis
• They are characterized by the presence of small rounded dense
opacities on a chest film due to perivascular collections of
dusts.
• The deposits in the lung disappear when exposure is
discontinued.
19. silicosis
• Develops with repeated and usually long-term exposure to
crystalline silica (silica dust)
• The silica dust causes irritation and inflammation of the
airways and lung tissue.
• Scar tissue forms when the inflammation heals, resulting in
fibrosis that gradually overtakes healthy lung tissue.
• The fibrosis continues extending through the lungs even after
exposure ends.
20. silicosis
Occupations with exposure to silica dust
– Mining
– Tunnelling
– Quarrying
– Sandblasting
– Ceramics
– Brick-making
– Silica flour manufacture
– Slate Pencil Industry
– Agate Industry
– Quartz Grinding
22. silicosis
• Three forms of silicosis:
– Acute silicosis: occurs with exposure to fine dust with high
quartz content; very heavy exposure for months, shows
symptoms within weeks to months of exposure,
– Accelerated silicosis: shows rapidly progressive symptoms
after 5 to 10 years of high exposure to fine dust of high
silica content.
– Chronic silicosis: the most common form, results from
long-term exposure (10 to 20 years or longer) to dust
containing less than 30% silica content.
23. silicosis
• Clinical features:
– Chronic cough
– Dyspnea (shortness of breath) that worsens with exertion.
– Fatigue
– Loss of appetite
– Chest pains
– Acute silicosis patients may also have fever and experience
rapid, unintended weight loss.
• Silicotuberculosis:
– Pulmonary tuberculosis occurs in about 25% of patients with
acute or classic silicosis
• "Eggshell" calcification, when present, is strongly suggestive of
silicosis
• On histopathology the hallmark of silicosis is the silicotic nodule
25. silicosis
• According to NIOH (National Institute of Occupational
Health, New Delhi) about 3 million people are occupationally
exposed to free silica dust and are at potential risk of
developing silicosis.
• The various studies carried out by NIOH
– Slate Pencil Industry
– Agate Industry
– Quartz Grinding
– Stone quarries
Source: www.nioh.org
26. silicosis
• Slate Pencil Industry: Study done in Mandsaur, Madhya
Pradesh revealed that
– The air borne free silica dust levels were several times
higher than the limits prescribed under the Factories Act.
– Radiological evidence of silicosis was observed in 54.6%
slate pencil workers.
– About 50% of the workers suffering from silicosis were
below 25 years of age and had worked for less than 7 years.
Source: www.nioh.org
27. silicosis
– Follow up examination of these workers after an interval of
sixteen months revealed rapid progression of the disease.
– 4% of the subjects who had participated in the initial
survey died during the intervening period.
– Their mean age at the time of death was 34.7 (18-55) years
and the mean duration of work was 11.75 (3-20) years.
Source: www.nioh.org
28. silicosis
• Agate Industry:
– Prevalence of silicosis – Male 39.8% Female 34.2%
– Developed silicosis within five years: male 19% , female 22%
– The overall prevalence of tuberculosis: male 37.4% female
40.3%
– Pulmonary function abnormalities were found in about 51%
grinders.
• Stone Quarries:
– Silicosis in 22.4% workers, most of them had worked for >10
years.
– About 32% workers showed evidence of tuberculosis.
Source: www.nioh.org
29. silicosis
• Treatment:
– There is no specific treatment for the silicosis,
– There is no known method of intervention to prevent the
condition's progression.
– Silica exposure has to be stopped to prevent further damage to
the lungs,
– Smokers should quit smoking.
– Tuberculosis positive patients need to be put on anti-tuberculosis
treatment
– The course of progression often extends over decades even after
cessation of exposure.
– Prevention remains the most effective therapeutic approach.
30. ASBESTOSIS
• Asbestosis is diffuse interstitial pulmonary fibrosis that occurs
secondary to the inhalation of asbestos fibers.
• It is considered separately from other asbestos-related
diseases, such as benign pleural effusion and plaques,
malignant mesothelioma, and bronchogenic carcinoma.
• Asbestos is classified into two groups: serpentine and
amphibole.
31. Serpentine
(93% of commercial use)
Amphibole
(7% of commercial use)
Chrysolite
Actinolite, Amosite, Anthophyllite,
Crocidolite, Richterite, Tremolite
ASBESTOSIS
32. ASBESTOSIS
• Significant occupational exposure to asbestos occurs mainly in
– Asbestos cement factories
– Asbestos textile industry and
– Asbestos mining and milling.
Asbestos cement factories
Asbestos textile industry Asbestos mining
33. ASBESTOSIS
• NIOH (National Institute of Occupational Health, New Delhi)
has carried out studies in Indian Asbestos industries. Its
observations were
• Asbestos Cement Industry:
– Study carried out in 4 (Ahmedabad, Hyderabad,
Coimbatore and Mumbai) of the total 18 asbestos cement
factories in India.
– The prevalence of asbestosis in these factories varied from
3% to 5%.
– The levels of asbestos fibres were found to be higher than
the permissible levels of 2 fibres/ml in two of the factories.
Source: www.nioh.org
34. ASBESTOSIS
• Asbestos Textile Industry:
– The average levels of air borne asbestos fibres varied from
216 to 418 fibres/ ml. The permissible level is 2 fibres/ml.
– The prevalence of asbestosis was 9%. This relatively low
prevalence of asbestosis despite high environmental levels
was attributed to high labour turn over.
– Cases of asbestosis were observed in workers having less
than 10 years exposure in contrast to the reported average
duration of over 20 years.
Source: www.nioh.org
35. ASBESTOSIS
• Asbestos Mining and Milling:
– Done in Cuddapah (Andhra Pradesh) and Devgarh (Rajasthan).
– In asbestos mines at both locations, the air borne fibre levels
were within permissible limits.
– The average fibre levels in milling units varied from 45 fibres/ml
to 244 fibres/ml of air.
– The overall prevalence of asbestosis in mining and milling units
was 3% and 21% respectively.
Source: www.nioh.org
36. ASBESTOSIS
• Symptoms
– Average latency period is 20-30 years
– Dyspnoea
– Cough
– Chest pain
– In advanced cases, clubbing of fingers
• At histopathologic analysis, asbestos bodies, which may
consist of a single asbestos fiber surrounded by a segmented
protein-iron coat, can be identified in intraalveolar
macrophages.
37. ASBESTOSIS
Translucent asbestos fiber (straight
arrow) surrounded by a protein-iron coat
and an alveolar macrophage (curved arrow)
Chest x-ray showing Small, irregular oval
opacities Interstitial fibrosis and “Shaggy
heart sign”
38. ASBESTOSIS
• Treatment Strategy:
– Stopping additional exposure
– Careful monitoring to facilitate early diagnosis
– Smoking cessation
– Regular influenza and pneumococcal vaccines
– Disability assessment
– Pulmonary rehabilitation as needed
– Aggressive treatment of respiratory infections
– Health education to patient
39. Anthracosis
• Anthracosis/ Coal Worker's Pneumoconiosis (CWP) / Black
lung disease:
– Accumulation of coal dust in the lungs and the tissue's
reaction to its presence.
– Associated with coal mining industry
– Takes one or two decades to cause symptoms
– The disease is divided into 2 categories:
• Simple CWP and
• Complicated CWP or
Progressive Massive Fibrosis (PMF).
40. Anthracosis
• Simple Coal Worker's Pneumoconiosis:
– Said to exist in the presence of radiological opacities < 1cm
in diameter.
– Benign disease if no complications.
– Common symptoms: cough, expectoration (black in colour)
and dyspnea.
– Slight decrease in FVC and FEV1/FVC
41. Anthracosis
• Complicated Coal Worker's Pneumoconiosis
– Is diagnosed when large opacity of 1cm or more in
diameter is observed in the CXR
– Pathologically it is characterized by large masses of black
colored fibrous tissue.
– Symptoms are similar but more severe
– Recurrent pulmonary infection
– The large lesions may cavitate as a result of ischemic
necrosis or infection (T.B).
– PFT (Pulmonary function test) reveals decreased FVC,
FEV1/FVC and increased residual volume.
43. Anthracosis
• In a study conducted by National Institute of Occupational
Health in collaboration with the International Development
Research Centre (IDRC), Canada, (5777 underground coal
miners and 1236 surface coal miners)
– revealed that the prevalence of pneumoconiosis (category
1/1 and more) in underground coal miners was 2.84% and
in the surface coal workers it was 2.10%.
– The overall prevalence of functional abnormalities of lung
in underground coal miners and surface coal workers was
45.4% and 42.2% respectively.
Source: www.nioh.org
44. Byssinosis
• Byssinosis:
– Caused by inhalation of cotton fibre dust (textile and fibre
industries)
– The chief symptoms are
• Chest tightness
• Shortness of breath
• Cough and
• Wheezing
– Typically occurring when patients return to work after a
weekend or vacation.
– Smoking significantly exacerbates byssinosis
45. Byssinosis
• When detected in its early stages (acute byssinosis), byssinosis
is reversible by eliminating exposure to the responsible irritant.
• When exposure continues the byssinosis can cause permanent
damage to the lungs (chronic byssinosis)
46. Byssinosis
• Treatment:
– In the acute setting, patients are encouraged to consider alternative
occupations or at least reduce the exposure in the work
environment.
– Smokers should be encouraged to stop smoking.
– In the acute stages, treatment may include :
• Brochodilators for symptomatic relief
• Corticosteroids are best avoided for as long as possible, given
only in severe cases
– Chronic byssinosis: Supportive measures
• Nebulizer use
• Home oxygen therapy
– Physical activity and breathing exercises may help in the
management.
48. • Medical measures:
– Pre-placement examination
– Periodical examination
– Medical and health care services
– Notification
– Maintenance and analysis of records
– Health education and counselling
– Practicing good personal hygiene
Preventive measures
49. • Practicing good personal hygiene:
– Washing hands and face before eating, drinking, going to the
toilet, smoking.
– Do not eat, drink, smoke, or apply cosmetics in areas where
silica is being used.
– Wear protective clothes and respiratory protection (Respirators
must fit tightly.)
– Before leaving work, shower and change into clean clothes.
Leave dusty clothes at work.
Preventive measures
50. • Engineering measures
– Design of building
– Conduct air monitoring to measure the workers’ exposure
to crystalline silica.
– Minimize exposures by controlling the creation of airborne
particles, for example, use wet drilling, local exhaust
ventilation.
– Personal Protective Equipments: Provide workers with
protective clothes, respiratory protection, and facilities for
washing (showers) and changing.
– Enclosure / isolation
– Environmental monitoring
Preventive measures
54. • Other measures:
– Legal measures: Measures to minimize dust emissions and
exposure to dust.
– Law compliance mechanisms, including effective
workplace inspection systems
– Cooperation between management and workers and their
representatives
– A mechanism for the collection and analysis of data on
occupational diseases
– Collaboration with social security schemes covering
occupational injuries and diseases
Preventive measures
55. Preventive measures
• Other measures:
– Training of health professionals in occupational diseases as
majority of medical practitioners lack training in
occupational health and consequently lack the skills to
diagnose and prevent occupational diseases.
56. Recent updates
• 63rd National Conference of Indian Association of
Occupational Health was held in Bengaluru, 22nd – 25th
January, 2013.
• “An International meet on climate, the workplace and the
lungs” 6th -8th December 2012. Main topics discussed were
– Integration of occupational health with primary health care
– Imaging for occupational and environmental respiratory
disorders
• Study of Pneumoconiosis in Thermal Power Station Workers,
– K. D. Garkal, Shete Anjali N. in International Journal of
Recent Trends in Science And Technology, Beed district,
Maharashtra 2012.
