2. Lung diseases caused by
inhalation of dust, mostly at
work (pneumo = lung; conis =
dust in Greek)
Diseases are, also called ‘dust
diseases’ or ‘occupational lung
diseases’.
3. The Pneumoconiosis are a group of lung diseases caused by
the lung’s reaction inhaling certain dusts. The main cause of
the pneumoconiosis is work-place exposure. Environmental
exposures have rarely been related to these diseases.
Type of lung disease varies according to the nature of inhaled
dust.
Some dusts are inert, cause no reaction, no damage, others
cause immunologic damage and predispose to tuberculosis or
to neoplasia.
4. Factors which determine the extent of damage caused by inhaled
dusts are:
Size and shape of the particles;
Solubility and physicochemical composition;
Amount of dust retained in lungs;
Additional effect of other irritants such as tobacco smoke
Host factors such as efficiency of clearance mechanism and immune
status of the host.
Inhaled dust particles larger than 5 μm reach the terminal airways
where they are ingested by alveolar macrophages.
Most of these too are eliminated by expectoration but the remaining
accumulate in alveolar tissue
5. The primary pneumoconiosis are:
• Asbestosis – caused by inhaling Asbestos Fibers
• Silicosis – caused by inhaling Silica Dust
• Coal workers’ pneumoconiosis (commonly referred
to as CWP or black lung) – caused by inhaling coal
mine dust
These three diseases typically take many years to
develop. However, rapidly progressive forms of
silicosis can occur after short periods of intense
exposure. When severe, the diseases often lead to
lung impairment, disability, and premature death.
6. Other forms of pneumoconiosis can be caused by inhaling dusts
containing:
• Aluminum
• Antimony
• Barium
• Graphite
• Iron
• Kaolin
• Mica
• Talc
Byssinosis, caused by exposure to cotton dust, is sometimes included
among the pneumoconiosis
7. Asbestosis is a progressive pulmonary
disease.
Asbestosis is long-term inflammation and
scarring of the lungs due to asbestos
fibers
While avoiding asbestos exposure can
prevent the condition from worsening, it
cannot reverse the damage that has
already been done
8. Once inhaled into the lungs, these fibers cannot be
destroyed or expelled by the body.
They remain embedded in the lung tissue and cause
chronic irritation and inflammation.
Over time, as this irritation continues, scar tissue
develops and replaces healthy lung tissue. Scar
tissue is inflexible and cannot contract and expand,
which leads to symptoms of asbestosis.
9. Shortness of breath
Coughing
Pain when breathing
Finger Clubbing
Inability to do physical labor
Most people do not realize that chest pain and coughing is a
symptom of asbestosis because it can be attributed to other
conditions, such as a common cold or heartburn. As the symptoms
intensify, it becomes difficult to breathe and impossible to do
physical labor.
10. When such fibers reach the alveoli (air sacs) in
the lung, where oxygen is transferred into the
blood, the foreign bodies (asbestos fibers) cause
the activation of the lungs' local immune system
and provoke an inflammatory reaction
dominated by lung macrophages that respond to
chemotactic factors activated by the fibers.
This inflammatory reaction can be described as
chronic rather than acute, with a slow ongoing
progression of the immune system attempting
to eliminate the foreign fibers.
Macrophages phagocytose (ingest) the fibers
and stimulate fibroblasts to deposit connective
tissue.
11. Due to the asbestos fibers'
natural resistance to digestion,
some macrophages are killed and
others release inflammatory
chemical signals, attracting
further lung macrophages and
fibroblastic cells that synthesize
fibrous scar tissue, which
eventually becomes diffuse and
can progress in heavily exposed
individuals.
12. Computerized tomography (CT) scan combine a
series of X-ray views taken from many different
angles to produce cross-sectional images of the
bones and soft tissues inside your body. These
scans generally provide greater detail and
might help detect asbestosis in its early stages,
even before it shows up on a chest X-ray.
Imaging tests:
• Chest X-ray- Advanced asbestosis appears
as excessive whiteness in the lung tissue. If
the asbestosis is severe, the tissue in both
lungs might be affected, giving them a
honeycomb appearance.
13. There is no cure for asbestosis, and no treatments
that can reverse the lung damage caused by
exposure to asbestos
Treatments for asbestosis are split into three main
categories: surgical treatments, drugs, and
alternative treatments.
14. Lung disease resulting from inhalation
of coal dust particles, in coal-miners
engaged in handling soft bituminous
coal for a number of years, often 20 to
30 years.
Coal worker’s pneumoconiosis, or black
lung, is one of over 200 types of
pulmonary fibrosis and is classified as
an interstitial lung disease.
15. 2 types:
Milder form of the disease called simple coal
workers’ Pneumoconiosis
Advanced form termed progressive massive
fibrosis (complicated coal-miners’
pneumoconiosis)
Anthracosis, is not a lung disease in true
sense, is common, benign and asymptomatic
accumulation of carbon dust in lungs of most
urban dwellers due to atmospheric pollution
and cigarette smoke.
16. In the early stage of the illness, there may be
no immediate symptoms. However, the latter
stages of the disease, known as Progressive
Massive Fibrosis or PMF, will cause shortness
of breath, coughing and pain during
breathing. PMF may result in permanent
disability and early death
Most chronic pulmonary symptoms in coal
miners are caused by other conditions, such
as industrial bronchitis due to coal dust or
coincident emphysema due to smoking
Regressive massive fibrosis causes
progressive dyspnoea. Occasionally, patients
cough up black sputum (melanoptysis), which
occurs when progressive massive fibrosis
lesions rupture into the airways
17. Coal dust that enters the lungs can neither be
destroyed nor removed by the body. The particles
are engulfed by resident alveolar or interstitial
macrophages and remain in the lungs, residing in
the connective tissue or pulmonary lymph nodes.
Coal dust provides a sufficient stimulus for the
macrophage to release various products, including
enzymes, cytokines, oxygen radicals, and fibroblast
growth factors, which are important in the
inflammation and fibrosis of CWP
These aggregations can cause inflammation and
fibrosis, as well as the formation of nodular lesions
within the lungs
18. In patients with Coal workers’ Pneumoconiosis, chest
x-ray or CT reveals diffuse, small, rounded opacities
or nodules.
Chest CT is more sensitive and specific than chest x-
ray for detecting coalescing nodules, early
progressive massive fibrosis, and cavitation
Pulmonary function tests are nondiagnostic but are
useful for characterizing lung function in patients in
whom obstructive, restrictive, or mixed defects may
develop
Because patients with coal workers' pneumoconiosis
often have had exposure to both silica dust and coal
dust, surveillance for tuberculosis (TB) is usually
done
19. There is no cure or discovered treatments for pneumoconiosis.
Some patients are given oxygen to help with their breathing and are advised to
stop smoking to prevent further decline in lung function
Pulmonary rehabilitation.
Treatment is rarely necessary in simple coal workers' pneumoconiosis, although
smoking cessation and TB surveillance are recommended.
20. Some of the ways to prevent this disease include: not smoking,
wearing ventilated masks when coming in contact with potentially
dangerous airborne particles, regular pulmonary exams, and
becoming educated about the risks of lung diseases in your work
environment
21. Caused by prolonged inhalation of silicon dioxide, commonly called silica.
Persons at increased risk: • Miners (e.g. of granite, sandstone, slate, coal, gold, tin
and copper), quarry workers, tunnellers, sandblasters, grinders, ceramic workers,
foundry workers and those involved in the manufacture of abrasives containing
silica
22. Dyspnea (shortness of breath) exacerbated by exertion
Cough, often persistent and sometimes severe
Fatigue
Tachypnea (rapid breathing) which is often labored,
Loss of appetite and weight loss
Chest pain
Fever
Gradual darkening of skin (blue skin)
In advanced cases, the following may also occur:
Cyanosis, pallor along upper parts of body (blue skin)
Cor pulmonale (right ventricle heart disease)
Respiratory insufficiency
23. Silica particles between 0.5 to 5 μm size on
reaching alveoli taken by the macrophages
which undergo necrosis. • 2. Some silica-laden
macrophages carried to respiratory bronchioles,
alveoli and in interstitial tissue. Some silica dust
transported to subpleural and interlobar
lymphatics and into regional lymph nodes
Silica is cytotoxic and kills the macrophages
which engulf it. Released silica dust activates
viable macrophages leading to secretion of
macrophage derived growth factors as
interleukin-1 that favour fibroblast proliferation
and collagen synthesis
24. The patient history should reveal exposure to sufficient silica dust to
cause this illness.
Chest imaging (usually chest x-ray) that reveals findings consistent
with silicosis.
Pulmonary function testing may reveal airflow limitation, restrictive
defects, reduced diffusion capacity.
Sputum test: Collecting coughed up mucus for evaluation
Bronchoscopy-will pass a bronchoscope (small flexible tube with a
video camera attached at its end) either through your nose or mouth
and into your windpipe and lung. This tool can be used to collect
tissue samples from your lung for further testing.
25. There is no cure for silicosis and once the damage is done
it cannot be reversed
Treatment plan may include : Using a bronchodilator to
help relax your air tubes and decrease inflammation.
Oxygen therapy- prescribed to help get more air into
your lungs when needed. Though you may need it only
while exercising at the beginning, as the disease
progresses you may need it at all times.
Pulmonary rehabilitation
Cough suppressants.
Antibiotics for bacterial lung infection.
26. Prevent silicosis is to avoid worker exposure to dust containing
respirable crystalline silica.
Quitting smoking as soon as possible. Smoking can increase the
damage done by silica and speed up the progression of the disease.
27. ‘Caplan's syndrome, also referred to as RP, is
defined as the combination of multiple well-
defined pulmonary nodules predominantly in the
lung periphery and inorganic dust exposure in
patients with Rheumatoid arthritis.
Caplan syndrome occurs only in patients with
both RA and pneumoconiosis related to mining
dust (coal, asbestos, silica). The condition occurs in
miners (especially those working in anthracite
coal-mines), asbestosis, silicosis and other
pneumoconiosis.
28. Caplan syndrome presents with cough and shortness of breath in conjunction with
features of rheumatoid arthritis, such as painful joints and morning stiffness.
Examination should reveal tender, swollen metacarpophalangeal joints and
rheumatoid nodules; auscultation of the chest may reveal diffuse crackles that do
not disappear on coughing or taking a deep breath.
29. The presence of rheumatoid arthritis alters how a person's immune system
responds to foreign materials, such as dust from a coal mine.
When a person with rheumatoid arthritis is exposed to such offensive materials,
they are at an increased risk of developing pneumoconiosis.
30. Chest radiology shows multiple, round, well
defined nodules, usually 0.5-2.0 cm in
diameter, which may cavitate and resemble
tuberculosis.
Lung function tests may reveal a mixed
restrictive and obstructive ventilatory
defect with a loss of lung volume. There
may also be irreversible airflow limitation
and a reduced DLCO.
Rheumatoid factor, antinuclear antibodies,
and non-organ specific antibodies may be
present in the serum.
31. There is no specific treatment for Caplan syndrome
but all exposure to coal dust must be stopped,
smoking cessation should be done.
