Download other pnemumoconioses

PRESENTER: Dr. PRACHETH.R.
CHAIR PERSON: Dr. K.R
PRAVINCHANDRA
 Anthracosis
 Asbestosis
 Byssinosis
 Bagassosis
 Farmer’s
lung
 Coal
mining as occupation historically
important
 First fuel that supported industrial
revolution
 Workers
exposed to a variety of mineral
dusts other than coal
 British

coal mines – in the 19th century
Severe respiratory disease (silicosis)Somerset and South Wales in 1920s:

Simple Coalworker’s Pneumoconiosis
 Complicated
Coalworker’s
Pneumoconiosis
 Progressive massive fibrosis
 Silicosis in coal workers
 Rheumatoid pnemuconiosis
Inhaled coal dust
Terminal bronchioles
Carbon pigment engulfed
by macrophages
Mucocilliary elevator
Expelled in mucus through lymphatics
 In
pneumoconiosis
• Dust laden macrophages accumulate in
alveoli
• Immune response
• Fibroblast secrete reticulin- entrap
macrophages
Macrophages migrate upto lymphatics
Arterioles strangulated
Ischaemic necrosis
 After
high exposure to coal dust over a
period of 20 years
 Accumulation of dust in lung parenchyma
 Tissue reaction to dust
 Early stages: little/ no impairment
 May produce serious respiratory
disability
 Pathology:
Simple coal macules (1-2mm)- dust
laden macrophages
 Larger coal nodules – collagen fibre
 Dilatation of alveoli- centrilobar
emphysema

Chest X- ray:
 Well defined ,discrete pulmonary
nodules
 small rounded opacities scattered
through lung
 HRCT:
 more sensitive

 Simple
pneumoconiosis complicated by
additional pathology.
 Large
masses of solid tissue in
parenchyma
3

main causes:
Coal mine dust itself
 Quartz
 Dust
in coal mines
plus rheumatoid disease
 Develop
even without further exposure
 Mass occurs in lungs:
• Singly or one in each lung
• Others may appear years later
• May be missed for years
• Move towards hilum
• Emphysematous changes
 Not
detectable on physical examination
 Loss of lung function- obstructive
 Loss of lung volume
After many years , masses cavitate
Large quantities of black ink like
material
Necrotic tissue
Aspiration of black material
Death
Cavity may shrink/infected
 Intensely
blackened scars: 2-10 cm
 Centre of lesion necrotic- due to local
ischaemia
 Microscopy: dense collagen pigment
 Formation
of areas of P.M.F
 Lesions occur in mid and upper zones of
lung
 Bilateral, sausage shaped
 Advanced cases: distortion and marked
emphysema
 Attack
 dust
rate influenced by
exposure
 radiographic category of simple
pneumoconiosis
 amount of quartz in dust
 Tuberculosis.
 Exposure
to quartz
 Larger ,rounded opacities in lung fields
 Irregular massive shadows, pleural
thickening
 Egg shell calcification
 When
compared to CWP
 Fibrosis much greater
 Nodules are larger, more discrete,
confluent
 First
noticed by Caplan
 Chest
X-ray:
 Atypical lung shadows
 Round lesions ,1-4 cm diameter
 No change in surrounding lung
 After
5-10 years: cavitation
 Clinical arthritis developed later than
lung lesions
 Prognosis:
 depends on whether rheumatoid
arthritis became inactive
 Usually
benign disease
 Even mild forms of complicated CWP: fail
to demonstrate abnormalities of lung
function
 PMF leads to:
 Pulmonary dysfunction
 Pulmonary hypertension
 Cor pulmonale
Clinical evaluation:
 Detailed occupational history
 Onset and evolving course of symptoms
 Investigations:
 Chest X ray
 Pulmonary function test

 Detection
and treatment of complications
 Fibrosis, emphysema, chronic air flow
obstruction
 Periodic monitoring of spirometry
 Chest X ray to assess progress of disease
 Inhaled and /or oral bronchodilators
 Inhaled steroids
 Broad spectrum antibiotics
 Oxygen
 Cessation of smoking
 Medical
measures
 Engineering
 Legislations
measures
 Medical
measures
Pre-placement medical testing
 Periodic medical examination
 Health education

 Engineering
measures:
 Exposure control:
 Obtain and review the results of air
monitoring
 Miners transferred to a less dusty place
 Dust control
 Respiratory protective equipment
 Legislative
 Notifiable
measures
disease in Indian Miners Act-
1952
 Compensable
in Workmen’s
Compensation
( Amendment) Act1959

Fibrous mineral silicate i.e. silica
combined with oxygen and calcium,
magnesium, iron, sodium or aluminium.
 Uses: asbestos
cements, sheets, pipes,
gaskets, fire proof textiles
 Exposure
occurs in mining, milling,
manufacture of asbestos products
 Serpentine/
chrysolite (white asbestos)hydrated magnesium silicate
 Amphibole type (hydrated silicate of
iron,calcium, sodium)
Amphibole :
 Crocidolite (blue form)- hazardous
 Amosite (brown form)

 Interaction
of inhaled fibres with lung
macrophages and parenchymal cells
Initial injury in airways, ducts where fibres land , penetrate
Macrophages attempt to ingest and clear fibres
Chemotactic factors
Fibrogenic mediators
chronic deposition and persistent mediator release- interstitial fibrosis
 First
report by a woman factory
inspector-1948
 William
Cooke published a report of
asbestos being associated with disease
 Thomas
Oliver- termed lung condition
asbestosis
 Finger
clubbing
 Breathlessness, chest pain
 Non productive cough
 Weight loss
 Inspiratory crackles
 Other signs: wheeze, pleural rub,
cyanosis, advanced- signs of right heart
failure.
Diffuse pulmonary interstitial fibrosis
 Asbestos bodies:

 Pleural

plaques
Lavage of airway: increased number of
polymorphs, asbestos bodies, fibres
Chest X ray
 Lower lobe involvement with presence of
small irregular opacities
 Advanced disease: parenchymal
abnormalities in all lung zones
 As disease progresses: linear opacities
thicker and obliterate vascular markings,
honey-combing

 Rounded
atelectasis- highly
characteristic
 Diffuse pleural thickening
 Pleural plaques
 Ground glass appearance, shaggy
appearance of heart
 CT scan- Increased diagnostic sensitivity
 HRCT scan –detect parenchymal and
pleural abnormalities
Figure 25-2. Chest X-ray of a patient with asbestosis.
Figure 25-3, Calcified pleural plaques on the superior border of
the diaphragm (arrows) in a patient with asbestosis. Thickening of
the pleural margins also is seen along the lower lateral borders of
the chest. A, Anteroposterior view. B, Lateral view.
 Non
malignant fibrotic parenchymal lung
disease –static/slowly progressive
 Histopathology unavailable in most of
suspected cases: diagnosis based on
clinical features and history of exposure
 When pathological material available:
 asbestos bodies
 Parenchymal fibrosis
History of asbestos exposure
 Latent interval between exposure and
disease (15 years or more)
 Chest X ray: small irregular opacities
 Pulmonary function test: restrictive
pattern
 Diffusion capacity decreased.

Respiratory failure and death
 major cause of death: asbestos related
malignancy :
 lung cancer
 mesothelioma

Bronchodilators or in combination with
ipratropium /inhaled steroid
 Oxygen saturation to be monitored in
severe cases
 Bacterial infections to be treated
 Cessation of smoking
 B-carotene: protective role on loss of
ventilatory function- improvement in
FEV1
•

Medical measures:
 Periodic
medical examinations
 Health education

Engineering measures:
 Use
safer types of asbestos (chrysolite,
amosite)
 Substitution of other insulants: glass fibre,
mineral wool, calcium silicate, plastic
foams
 Eliminate or minimise exposure
 Continuing research
 Respiratory protective equipment
 Legislative

measures:
Notifiable under Factories Act
 Vegetable
fibres used for manufacture of
textile products
 When
vegetable fibres are processedduring early phase (opening, picking,
carding)- more dustier
Non cellulose plant material separated from fibres to obtain plant product
Components of processed plant disseminated into fine dust
Inhalation of this – clinical syndromes in textile workers
First recognised by Ramazzini
 First description of symptomatic pattern:
Mareska and Heyman – 1845
 1860- Greenhow investigated carriers of
excess of pulmonary disease and
described an asthma like condition in
cotton workers

 Acute
response to cotton dust
 Relationship with chronic changes
uncertain
 Mill fever- first exposure to cotton, flax,
hemp
 Fever, non productive cough, malaise,
sneezing, lasts for few hours, resolves
despite continued dust exposure
 Caused by endotoxins from gram
negative bacteria contaminating cotton
 Symptoms
rare in first 5 years of
exposure
 Period of dust exposure- minimum 20
years to produce symptoms
 Smoking
 Bacterial
Endotoxins
 Immunological Mechanisms
 Non immunological histamine release
 Fungal enzyme
 Genetic factors
1.Bacterial endotoxins:
 Predominant species of gram negative
bacteria in cotton dust is Enterobacter
genus- Aerobacter cloace
 Airway
inflammation and immune
responses:
• Neutrophilic bronchitis
• alveolitis
• Alveolar- macrophage activation
• Complement activation
• Mast release of histamine
2.Immunological mechanisms:
 no convincing evidence
 Fungal Antigens: Alternaria tenuis,
A.niger
 Extracts of cotton dust- activate classical
and alternate pathways- biologically
active fragments capable of histamine
release
3.Non immunological histamine release:
 Acute symptoms occurring on first day
back at work
 Amount in work situation too low to
produce airway narrowing
 Can be demonstrated in all pulmonary
responses on bronchial challenge with
histamine
4.Fungal enzyme
5.Genetic factors:
 Endotoxin exposure generate reactive
oxygen species in airways
 Oxidative lung injury and lung function
decline
 Symptoms:
 Chest
 1st
tightness, breathlessness:
day of working week over 2nd half of
working shift
 Tightness subsides in evening
 Well for remainder of week
0- No symptoms
½- Occasional chest tightness on Mondays
or mild symptoms – irritation of
respiratory tract on Mondays
1- Chest tightness and /or breathlessness
on Mondays only
2- Chest tightness and /or breathlessness
on Mondays and other days
3- Grade 2 symptoms +
evidence of permanent respiratory
impairment from reduced ventilatory
capacity

Doesn’t consider irritant effects of dust
exposure or lung function changes which
may occur even in asymptomatic workers
Classification
Symptoms
Grade 0
No symptoms
Byssinosis
Grade B1
Chest tightness and /or short of
breath on most of first days back at
work
Grade B2
Chest tightness and/or short of
breath on first and other days of
working week
Respiratory tract irritation
Grade RT1
Cough associated with dust
exposure
Grade RT2
Persistent phlegm (i.e on most days
during 3 months of year) initiated or
exacerbated by dust exposure
Grade RT3
Persistent phlegm initiated or made
worse by dust exposure either with
exacerbations of chest illness or
persisting for 2 years or more
Lung function
1. Acute changes
No effect
Consistent decline in FEV1 of less
than 5% or increase in FEV1 during
work shift
Mild effect
Consistent decline of between 5 and
10% in FEV1 during work shift
Moderate effect
Consistent decline of between 10
and 20% in FEV1 during work shift
Severe effect
A decline of 20% or more in FEV1
during work shift
2. Chronic changes
No effect
FEV1- 80% of predicted value
Mild to moderate effect
FEV1- 60-79% of predicted value
Severe effect
FEV1- less than 60% of predicted
value
 Non
specific
 Signs of chest hyperinflation, prolonged
expiration
 Expiratory wheeze
 Decline
in FEV1 across working shift in
Grades 1 and 2
 Maximum
decline – first day of working
week; doesn’t imply overall level of
airway obstruction improves in
remainder of week





No specific abnormality
Macroscopically: heavy black
pigmentation
Emphysema
Smooth muscle hypertrophy
Mucus gland hyperplasia
 Antihistamines, bronchodilators:
decrease or prevent fall in FEV 1
 Aerosolized steroids
 Cessation of smoking

Medical measures:
 Pre-employment
screening to identify
those with airway hyperactivity or
allergic condition
 Periodic Medical Testing

•
•
•
•
Engineering measures
Dust abatement
Treatment of raw cotton to eliminate toxic
factors
Move the worker to less dusty area
Respiratory protective equipment
 Legislative
measures
Bagasse
 Fibrous cellulose residue of sugarcane
remains after sugar extracted
 Uses: paper, cardboard, rayon
 Storage with water content above 27%:
 moulding
 Heat generation
 Growth of Thermactinomycetes sacchari

Exposure to T.sacchari
 removing, opening, milling of stored
bagasse

History:
 First reported in India by Ganguly and
Pal in 1955 at a cardboard manufacturing
firm, Kolkata.

Breathlessness
 Cough, haemoptysis, slight fever
 Initially- acute diffuse bronchiolitis
 Impairment of pulmonary function
 If treated early: resolution
 If untreated- diffuse fibrosis,
emphysema, bronchiectasis


Mottling in lungs or shadow
 Symptomatic
 Preventive
, supportive treatment
measures:
 Medical measures
 Medical examination, periodic check up


Engineering measures




Dust control measures:
wet process
enclosed apparatus
exhaust ventilation




Bagasse control:
Keep moisture content below 20%
2% propionic acid – prevent moulding
Personal protective equipment
Usually due to allergic response to
thermophillic actinomycetes which cause
vegetable matter to mould during
storage
 Thermophillic actinomycetes:
 S.rectivirguala (formerly M. faeni)
 T. vulgaris
 Saccharomonospora viridis
 T.sacchari

Inhalation of spores and mycelial
fragments occurs when mouldy hay, straw
or grain handled in enclosed and poorly
ventilated buildings
 Harvested damp and stored with high
water content- Moulding
 Permits growth of T. actinomycetes

prevalence more in:
 more rainfall
 no drying of crops before storage or
prevention of wetting during storage


Similar to bronchial asthma

First acute attacks noticed

Pulmonary fibrosis, cor pulmonale

X-ray chest: fine nodular opacity
Symptomatic treatment
 Prevention:
 Drying crops before storage, preventing
their becoming damp, good ventilation
during storage
 Store hay with water content less than
20%
 Substitution of silage for hay
 Respiratory protective equipment

 Textbook
of clinical occupational and
environmental medicine, 2nd edition –
Linda Rosenstock, Mark R Cullen, Carl A
Brooke, Carrie A Redlich.
 Hunter’s diseases of occupation, 10th
edition.
 International
occupational
and
environmental medicine – Herzstein,
Bunn, Fleming, Harrington, Jeyratnam,
Gardner.
 Oxford
textbook of public health, 5th edition.
 Harrison’s principles of internal medicine, 18th
edition.
 Robin’s textbook of Pathology
 Park’s textbook of preventive and social
medicine, 21st edition – K Park.
 Textbook of public health and community
medicine, 2009.
 Community medicine with recent advances, 2nd
edition – AH Suryakantha