This document defines occupational lung disorders as diseases of the lung arising from or during employment. It discusses various occupational lung diseases including asbestosis, silicosis, and coal workers' pneumoconiosis. For asbestosis, the document describes the pathology, signs and symptoms, diagnostic tools including chest x-rays and CT scans, management, and complications such as lung cancer and mesothelioma. For silicosis, it discusses the classification including acute, accelerated and chronic forms, associated occupations, determinants, complications including tuberculosis, and management focusing on symptom relief. For coal workers' pneumoconiosis, it outlines the pathology, clinical features, and relationship to chronic bronchitis.

1. Dr. Ashutosh
Date : 12-03-2018

2. DEFINITION
 Occupational lung disorders has been defined as a diseases
of lung arising out of or in course of employment.
OR
Damage to the lungs caused by dusts or fumes or noxious
substances inhaled by the workers in certain specific
occupations is known as “Occupational Lung Diseases”.
 Ramazzini ,the father of occupational medicine who first
described breathlesness among handlers of grains in 1713.

3. Deposition and clearance of particles in lung
 The harmfulness of an inhaled particle depends on its inherent
toxicity, its ability to penetrate to the site at which it can exert
its effects and the amount retained in the lung.
 Penetration depends on the ability of the particle to overcome
the physical forces tending to bring it into contact with the
walls of the airways, namely sedimentation, impaction,
interception, diffusion and electrostatic precipitation.
 The highest rate of alveolar deposition occurs with a particle
size around 0.02–0.06mm (20–60 nm)

4. Once deposited in the respiratory tract, the fate of particle
depends on the body’s clearance mechanisms and on its ability
to resist them
 Larger particles, deposited on the airways, are generally cleared
efficiently within 24 h by the mucociliary mechanism, though
such clearance may be prolonged if the airways are damaged by
cigarette smoke or fume inhalation . Such cleared particles are
either coughed up or swallowed.
 Particles reaching the acinus are beyond the region of cilia and
production of mucus and are cleared much more slowly.
Deposition occurs predominantly at bifurcations of alveolar
ducts . The mechanism of particle removal involves ingestion by
alveolar macrophages or type I alveolar epithelial cells

5. Fractional deposition in different parts of the respiratory
tract of particles of differing aerodynamic diameters

6. PNEUMOCONIOSIS

7. PNEUMOCONIOSIS
 The term ‘Pneumoconiosis’ was coined by Zenker to define a
group of lung diseases caused by inhalation of dust that are
breathed in and then deposited deep in lungs causing damage
 The most common pneumoconioses are Coal-workers’
pneumoconiosis, Silicosis and Asbestosis but many other types
have been described, usually due to inhalation of mixed dusts
containing silicates.

8. ASBESTOS-RELATED DISEASES
 Asbestos is a generic term for several different mineral
silicates, including chrysolite (most widley used), amosite,
anthophyllite, and crocidolite.
 Occupation in the production of asbestos products (mining,
milling, and manufacturing), shipbuilding and construction
trades including pipe fitters
 People are exposed to asbestos anywhere in the chain from the
mine and crusher, the site of production of materials to the
place where the materials are used. Indeed, exposure to waste
asbestos material at dumps is another area of concern
 The major health effects from exposure to asbestos are pleural
and pulmonary fibrosis, cancers of the respiratory tract and
pleural and peritoneal mesothelioma

9. ASBESTOSIS
 Asbestosis is a diffuse interstitial fibrosing disease of the lung
that is directly related to the intensity and duration of exposure
 The disease resembles other forms of diffuse interstitial fibrosis
 Usually, exposure has taken place for at least 10 years before
the disease becomes manifest.

10. Signs and symptoms
 Working either directly with asbestos or adjacent to others working with the
material, usually in very dusty conditions and over a prolonged period.
 Symptoms are exertional dyspnoea and often, dry cough. The dyspnoea
gradually becomes more severe and eventually may be completely
disabling,
 Earliest sign of asbestosis is the presence of repetitive end-inspiratory
crackles, heard at the lung bases posteriorly or in the axillae
 Only at this relatively late stage in the natural history of the disease is
clubbing of the digits
 As the disease reaches its terminal stage, diminished chest wall movements
tachypnoea and evidence of cor pulmonale may be detected, with cyanosis,
tall jugular a waves, right ventricular heave and gallop rhythm. The patient
usually die of hypoxic respiratory failure

11. Chest radiography
 The earliest sign of asbestosis is the appearance of short linear shadows
about 1–3 mm thick, predominantly in the lower lung zones.
 Pleural plaques on chest radiographs, which are characterized by either
thickening or calcification along the parietal pleura, particularly along the
lower lung fields, the diaphragm, and the cardiac border.
 “Ground-glass” appearance in the lung fields
 HRCT may show distinct changes of subpleural curvilinear lines 5–10 mm
in length that appear to be parallel to the pleural surface
 HRCT is more sensitive than standard chest films for the detection of early
interstitial fibrosis and nicely demonstrates the peripheral and basal
accentuation of the fibrosis. CT also shows calcified and non-calcified
pleural disease

12. International Labour Office classification
To describe small pneumoconiotic opacities
Rounded
 p: up to 1.5mm diameter
 q: 1.5–3mm diameter
 r: 3–10mm diameter
Irregular
 s: up to 1.5mm in width
 t: 1.5–3mm in width
 u: 3–10mm in width
Large
 A : ≥ 10-50 mm
 B: ≥ 50 – Right upper zone (RUZ)
 C : ≥ RUZ

13. Chest xray shows
bilateral
Calcified pleural
plaques consistent
with asbestos-
related pleural
Disease. Poorly
defined linear and
reticular
abnormalities are
seen in
The lower lobes
bilaterally

14. HRCT thorax shows bilateral, subpleural reticulation (black arrows), representing
fibrotic lung disease due to asbestosis. Calcified pleural plaques representing
asbestos-related pleural disease (white arrows)

15.  Lung function- The functional abnormalities associated with
asbestosis are progressive reduction in carbon monoxide
diffusing capacity, vital capacity and total lung capacity, with
normal residual volume. Compliance is decreased and lung
recoil pressure increased
 Management- No specific therapy is available for asbestosis,
supportive care is the same as that given to any patient with
diffuse interstitial fibrosis of any cause.

16. Asbestos-related diseases
Benign
Pleural diseases
1.Plaques
2.Diffuse pleural thickening
3.Effusion
4.Calcification
Malignancy
1.Malignant mesothelioma
2.Bronchogenic carcinoma
Parenchymal diseases
1.Asbestosis [parenchymal
fibrosis caused by asbestos
inhalation]
2.Rounded atelectasis
3.Benign fibrotic masses
4.Transpulmonary bands

17. LUNG CANCER
 The most common cancer associated with asbestos exposure.
The excess frequency of lung cancer (all histologic types) in
asbestos workers is associated with a minimum latency of 15–
19 years between first exposure and development of the disease

18. MESOTHELIOMAS
 Both pleural and peritoneal, are also associated with asbestos
exposure.
 In contrast to lung cancers, these tumors do not appear to be
associated with smoking. Relatively short term asbestos
exposures of ≤1–2 years, occurring up to 40 years in the past,
have been associated with the development of mesotheliomas
 >80% of mesotheliomas are associated with asbestos exposure,

19. SILICOSIS
 It is a type of pneumoconiosis: condition characterized by
accumulation of silica dust in lung parenchyma & tissue
reaction to it

 Also known as Potter's rot, is a form of occupational lung
disease caused by inhalation of crystalline silica dust & is
marked by inflammation & scarring in forms of nodular lesions
in upper lobes of the lungs
 The name silicosis (from Latin silex or flint) was originally
used in 1870 by Achille Visconti

20.  Silicon dioxide or silica is the most abundant compound in the
earth’s crust, where it is mostly found in the crystalline form
known as quartz.
 Occupations in which exposure to quartz take place are:
 Mining
 Tunnelling
 Quarrying
 Stonemasonry
 Sandblasting
 Fettling and foundry work
 Ceramics
 Brick-making
 Refractory kiln repair
 Silica flour manufacture
 Abrasive manufacture
 Diatomaceous earth manufacture

21. Main determinants of silicosis:
 Silica dust
 Its duration exposure
 Size of particle
 Distribution & respirability of airborne particles
 Their fibrogenic potential

22. Classification of Silicosis
Acute- which develops over months in response to exceedingly
heavy exposures as in sandblasting or dry drilling. It is
characterized by appearances suggestive of pulmonary oedema.
Acute enlargement of the hilar nodes may occur with heavy
exposure to quartz in individuals without prior exposure
Accelerated- associated with heavy exposures over a relatively
short period of a few years, presents radiologically as
progressive irregular upper zone fibrosis, sometimes with
relatively sparse and indistinct nodularity.

23.  Chronic silicosis
 Commonest form
 Occurs after many decades of exposure to relatively low levels
of silica.
 Characterized by gradually progressive dyspnea, dry cough &
evidence of progressive fibrosis of both lungs on chest X-Ray.

24. Acute silicosis
 The clinical and pathologic features of acute silicosis are
similar to those of pulmonary alveolar proteinosis
 The chest radiograph may show profuse miliary infiltration or
consolidation, and there is a characteristic HRCT pattern
known as “crazy paving”
 The disease may be quite severe and progressive despite the
discontinuation of exposure. Whole-lung lavage may provide
symptomatic relief and slow the progression.

25. Acute silicosis: HRCT scan shows multiple small nodules consistent with silicosis but
also diffuse ground-glass densities with thickened intralobular and interlobular septa
producing polygonal shapes. This has been referred as crazy paving.

26. Chronic silicosis
 Chronic simple : With long-term, less intense exposure, small
rounded opacities in the upper lobes may appear on the chest
radiograph after 15–20 years of exposure, usually without
associated impairment of lung function (simple silicosis)
 Calcification of hilar nodes may occur in as many as 20% of
cases and produces a characteristic “eggshell” pattern. Silicotic
nodules may be identified more readily by HRCT

27. Simple silicosis
HRCT shows numerous
small nodules
diffuse nodular opacities with
relative sparing of the basal lung
zones

28. Complicated silicosis
 The nodular fibrosis may be progressive in the absence of
further exposure, with coalescence and formation of
nonsegmental conglomerates of irregular masses >1 cm in
diameter (complicated silicosis)
 These masses can become quite large, and when this occurs,
the term progressive massive fibrosis (PMF) is applied
 Significant functional impairment with both restrictive and
obstructive components may be associated with PMF.

29. DIAGNOSIS
 There are 3 key elements to diagnosis of silicosis
 Patient history should reveal exposure to sufficient silica dust to
cause this illness.
 Chest X-Ray revealing findings consistent with silicosis.
 There are no underlying illnesses that are more likely to be
causing the abnormalities
 Physical examination is usually unremarkable unless there is
complication. PFT may reveal airflow limitation, restrictive
defects, ↓ diffusion capacity, mixed defects or may be normal
 For uncomplicated silicosis, chest x-ray will confirm presence of
small (<10 mm) nodules in lungs, especially in upper lung zones.

30. Complications
SILICOTUBERCULOSIS
 Patient with silicosis are 3 fold increase risk for TB infection
 silica particles are phagocytosed by alveolar macrophages
leading to death of these macrophages, inhibiting their ability to
kill mycobacteria. Prior to their death macrophages become
activated and secrete IL & TNF-α. These cytokines are
responsible for fibroblast activation & fibrosis. TNF-α also
stimulates neutrophils to release oxidants which produce local
damage. Both humoral & CMI response are inhibited in
silicosis.
 Another hypothesis - Since mycobacteria are dependent on iron
for growth, they use iron stored by the silica particles, even
dormant TB bacilli may be activated.
 Even workers with prolonged silica exposure, but without
silicosis, are at similar risk for TB.

31.  Pulmonary complications of silicosis also include chronic bronchitis &
airflow limitation, fungal lung infections, compensatory emphysema &
pneumothorax.
 There are some data revealing association between silicosis & autoimmune
diseases (Nephritis, Scleroderma & SLE) especially in acute or accelerated
silicosis.
 Esophageal compression
 Atelectasis
 PAH
 Chronic respiratory failure
 Recurrent chest infection
 Lung abscess
 Hydro pneumothorax
 Chronic cor pulmonale
 Lung cancer

32. Management
 Silicosis is an irreversible & progresive condition with no cure.
 Treatment options currently focus on alleviating symptoms &
preventing complications including stopping further exposure
to silica & other lung irritants, including tobacco smoking,
cough suppressants, antibiotics for bacterial lung infection,
ATT for those with active TB, chest physiotherapy to help
bronchial drainage of mucus, O2 administration to treat
hypoxemia, bronchodilators to facilitate breathing.
 Lung transplantation to replace damaged lung tissue is the most
effective treatment.

33. COAL WORKERS PNEUMOCONIOSIS
 Coal miners are exposed to dust that contains mixture of coal,
mica and silica in varying proportions
 Coal-workers’ pneumoconiosis is virtually confined to
underground coal-miners, it may occur in any place where a
worker is exposed to high levels of coal dust in poorly
ventilated conditions. Thus it has been described in coal
trimmers, loading coal in the holds of ships, and in men and
women sorting coal on surface screens.

34. Pathology of CWP
 The coal macule is the primary lesion of simple CWP- Macule consists of a
focal collection of coal dust in pigment-laden macrophages around the
respiratory bronchioles and tapering off toward the alveolar duct.
 Centriacinar emphysema part of the simple lesion of CWP - enlargement of
the airspaces immediately adjacent to the dust macule. Severity of the
emphysema increases with increasing lung dust retention.
 Essential mechanism of simple pneumoconiosis is likely to be dust mediated
damage to macrophages, release of cytokines accompanied by recruitment
of polymorphonuclear cells, resulting in activation of fibroblasts and also
local initiation of emphysema by Elastolysis
 Muscular thickening of pulmonary arteries in conjunction with hypertrophy
of the right ventricle can be observed with both simple and complicated
cwp
 Pathological changes in the airways consistent with chronic bronchitis,
including enlargement of mucous gland

35.  With increasing dust exposure, due to the normal clearance mechanisms
being overwhelmed, the lung lesions increase in size and number. These
larger fibrotic lesions are called coal nodules
 Progressive enlargement and aggregation of quartz-induced lesions leads
diffuse fibrosing and necrotic process with marked vasculitis
 With considerable accumulation of dust -- local impairment of clearance,
lymphatic blockage, lymph node destruction occurs
 Severe destruction of hilar nodes is almost universal in miners with PMF
and progressive silicosis
 Blockage of this escape route for the dust is relevant to its accumulation in
the lung and provocation of a chronic progressive inflammatory reaction
there

36. A coal macule, microscopic section

37. Clinical Features of CWP
 Chronic cough and sputum production are more common with
increasing dust-exposure, regardless of the presence or absence
of simple pneumoconiosis.
 Some miners with simple pneumoconiosis may have no related
symptoms or physical signs, but with severe airflow
obstruction or advanced pneumoconiosis, dyspnea, cough, and
sputum production are frequent. Edema of the lower
extremities, and findings consistent with corpulmonale may
occur.
 Melanoptysis (expectoration of black sputum) occasionally
results from excavation of a PMF lesion

38.  Atypical cases included crackles, finger clubbing, restrictive impairment,
diffusion block, and neutrophilic bronchoalveolar lavage (BAL)
 CWP has not been associated with increased risk for development of
coexisting mycobacterial infection,
Simple CWP
 With prolonged exposure to coal dust for 15 to 20 years, small rounded
opacities develop usually not associated with pulmonary impairment
• Asymptomatic & is often a radiographic diagnosis
• When exposure is terminated the simple type will not progress
Complicated CWP
 Appearance of nodules > 1cm in diameter on chest radiography usually
confined to upper half of the lungs .
 progresses to PMF, that is accompanied by severe lung deficits causing
chronic bronchitis and COPD .

39. Chest radiography
 Earliest sign of CWP is nodular shadowing on the chest radiograph.
 These appearances are classified according to ILO standard
 They are usually more profuse in the upper and middle zones
 The early nodular lesions are frequently accompanied by kerley B lines.
 This condition presents as a larger shadow, equal to or greater than 1cm in
maximum diameter, often initially in the right upper zone. The lesion
gradually grows, becomes more radiodense and causes distortion of
adjacent lung and bronchi often with bullous emphysema.
 Ultimately it is completely replaced by PMF and emphysema, with resultant
cor pulmonale
 HRCT may reveal parenchymal nodules and emphysema when standard
radiographs are normal. In atypical cases, CT scans may show ground-glass
 Opacities and honeycombing, at times without nodular findings typical of
CWP.

40. Multiple rounded lesions of Caplan’s
syndrome in coal-miner with RA.
Coal-workers’ pneumoconiosis: extensive
simple pneumoconiosis with early massive
fibrosis in right upper zone

41. Caplan’s syndrome
 A few miners, especially those with rheumatoid arthritis or with
rheumatoid factor in their blood, develop well defined rounded
lesions that grow to about 2–3cm in diameter or rarely somewhat
larger
 They are usually multiple and have a marked tendency to cavitate.
 They often occur on a background of no simple pneumoconiosis and
in miners with a relatively low dust exposure.
 They are called Caplan’s lesions and their combination with
rheumatoid disease
 They do not have an ominous prognosis and cause no significant
functional impairment, being unassociated with emphysema

42. CHRONIC BERYLLIUM DISEASE
 Beryllium is extracted from Beryllium ore (beryl or beryllium
aluminium silicate) by heating and treatment with sulphuric
acid or fluoride and is used as an alloy in the manufacture of
components in X-ray equipment, atomic reactors, the aerospace
industry, armaments and heat-resistant ceramics
 Exposure to high concentrations of beryllium fume may cause
an acute toxic pneumonitis with oedema of mucous membranes
from pharynx to small airways together with pulmonary
oedema. The radiograph shows evidence of the pulmonary
oedema and the clinical signs are tachypnoea cyanosis and
diffuse inspiratory crackles

43.  Chronic Berylliosis was first described in 1946 . It is different
from other mineral pneumoconioses in that it is a systemic
hypersensitivity disease, with principal effects on the lung and
skin.
 Unless one inquires specifically about occupational exposures
to beryllium in the manufacture of alloys, ceramics or high-
technology electronics in a patient with sarcoidosis, one may
miss entirely the etiology

45.  Patients presents with cough and breathlessness
 The radiographic changes -- Initially diffuse fine granularity
that evolves into a reticulonodular pattern and finally irregular
fibrosis, often of a coarse generalized type as in chronic
sarcoidosis.
 Bilateral hilar adenopathy may occur but only when there is
also evidence of interstitial lung infiltration. reduced Dlco and
progressive reduction in lung volumes and compliance as
fibrosis increases

46. Chronic berylliosis
showing diffuse
irregular
pulmonary fibrosis.

47. OTHER PNEUMOCONIOSES
ALUMINIUM
 A diffuse interstitial fibrosis has been described in workers
manufacturing alumina abrasives (corundum) composed of
bauxit
 The disease, characterized by honeycombing and a high risk of
pneumothorax, has been called shaver’s disease after one of the
physicians who first described it in 1947
 Pulmonary fibrosis and progressive encephalopathy is of
interest in view of the association of aluminium with the
plaques in the brains of people dying with alzheimer’s disease

48. CARBON
 Workers exposed to dust from graphite and carbon pigment
may develop a form of pneumoconiosis indistinguishable from
that afflicting miners of high-rank coal
 Simple nodular changes and PMF have been described and
there is also evidence of some impairment of lung function in
relation to exposure to carbon black

49. BARIUM
 Barium is mined mostly as barytes, barium sulphate, and may
be used in the production of paints, rubber and glass, and as a
drilling mud in the oil industry
 Workers grinding barium salts develop strikingly dense
micronodular radiological shadows without any functional
abnormalities. This benign, non-fibrosing pneumoconiosis is
called baritosis

50. SIDEROSIS
 Pure siderosis is due to deposition of iron oxides in the lung,
where they are taken up by macrophages in both the alveoli and
interstitial tissue
 Occurs in arc welders and oxyacetylene cutters due to the
presence of iron oxides in the fume from the heated metal
 No fibrous reaction occurs
 Chest radiograph shows multiple radiodense nodules due to
the presence of the iron

51.  Siderosis also occurs in silver polishers, who use iron oxide
(jeweller’s rouge) to polish the metal
 The radiological changes of siderosis tend to regress after
exposure ceases and the condition in its pure form is not
associated with abnormality of lung function
 There has been debate about the possible carcinogenicity of
inhaled iron, However iron itself is not carcinogenic and it is
probably due to concomitant exposure to other carcinogens in
either cigarettes or the occupational environment

52. Welders’ siderosis
showing diffuse
pin-point opacities.
The peripheral
lesion in
the right mid zone

53. ORGANIC DUST DISEASES

54. BYSSINOSIS
 Byssinosis is a term applied to a complex of symptoms
associated with the manufacture of cotton, flax, jute dust and
hemp
 Up to one-third of people exposed to cotton dust for the first
time develop an acute airway reaction with often substantial
fall in FEV1
 This is more likely to occur in atopic subjects and people with
asthma and is associated with increased bronchial reactivity
 A sensation of oppression in the chest or difficulty in breathing
on the first day of the working week. A slight rise in
temperature with cough and wheeze. The symptoms usually
occur after about 2–4h of exposure and clear some time after
going home

55. For epidemiological purposes symptoms have been
used in the following classification of the disease
 Grade 0: no byssinosis.
 Grade 0.5: occasional chest tightness on the first day of the
working week.
 Grade 1: chest tightness on the first day of every working
week.
 Grade 2: chest tightness on the first and following days of
every working week.
 Grade 3: grade 2 symptoms accompanied by evidence of
permanent incapacity from diminished exercise tolerance
and/or reduced ventilatory capacity.

56. Pathogenesis
 The prevalence of byssinosis varies from mill to mill, although
the condition occurs in many different countries
 The common factor seems to be the raw Fibres always being
contaminated by fungi and Gram-negative bacteria
 Inhalation of cotton dust has been shown to lead to a neutrophil
response in airways, probably due to a lipid fraction of
bacterial cell walls, and it may be that release of leukotrienes
and platelet activating factor by these cells plays a part in
causing the disease

58.  Lung function studies have shown declines in FEV1 both throughout a shift
and throughout the week, the change over a shift being greatest on the first
day
 Lung function changes
 Acute changes
 No effect A consistent decline of <5% (or an increase) in FEV1 over
a work shift
 Mild effect- A consistent decline of 5–10% over the work shift
 Moderate effect – A consistent decline of 10–20% over the work shift
 Severe effect- A decline of 20% or more over the work shift
 Chronic changes
 No effect FEV1 at least 80% of predicted
 Mild to moderate FEV1 60–79% of predicted
 Severe FEV1 <60% of predicted

59. Treatment and Prevention
 The most important treatment for byssinosis is removal of the
individual from the offending work environment.
 Dust exposure can be reduced by the use of exhaust hoods,
general increases in ventilation, and wetting procedures, but
respiratory protective equipment may be required during
certain operations
 Screening pulmonary function testing at the workplace is
important to identify susceptible individuals who exhibit
airflow abnormalities.
 Once the condition has developed, some symptomatic relief
may be obtained by the use of inhaled bronchodilators and
steroids if removal from the workplace proves impracticable.

60. GRAIN DUST−INDUCED INDUSTRIAL
BRONCHITIS
 Exposure to grain dust can also result in the development of chronic
bronchitis between 4 and 11 percent of grain workers
 Show a reduction in FEV1 of 10 percent or greater over the work
shift. This reduction in flow rates is directly related to the amount of
dust in the air
 Grain dust extract, possibly its endotoxin contaminant can activate
complement and this may be a mechanism by which grain dust
induces inflammation in bronchi

61.  Grain dust also tends to produce skin abnormalities in affected
individuals, in contrast to cotton dust, which generally does not
cause skin reactions
 The presentation of obstructive airway disease in grain dust–
exposed workers is virtually identical to the characteristic
findings in cigarette smokers, i.e. persistent cough, mucus
hypersecretion, wheeze and dyspnea on exertion, and reduced
FEV1 and FEV1/FVC ratio

62. HYPERSENSITIVITY PNEUMONITIS (HP)
 Also referred to as extrinsic allergic alveolitis
 Pulmonary disease that occurs due to inhalational exposure to a
variety of antigens leading to an inflammatory response of the
alveoli and small airways.
 Systemic manifestations such as fever and fatigue can
accompany respiratory symptoms.
 Sensitization to an inhaled antigen as manifested by specific
circulating IgG antibodies is necessary for development of HP
 Causes of HP include farmer’s lung, bagassosis, mushroom
workers lung, Air conditioner and humidifier lung,
woodworkers lung….

63. FARMER’S LUNG
 Caused by inhalation of spores of thermophilic actinomycetes,
higher bacteria of a filamentous appearance that grow in hay or
other organic matter that has been stored in a damp condition
 Spores of Thermophilic actinomycetes produce a
hypersensitivity pneumonitis
 A patient with acute farmer’s lung presents 4–8 h after
exposure with fever, chills, malaise, cough and dyspnea
without wheezing.

64.  The history of exposure is obviously essential to distinguish
this disease from influenza or pneumonia with similar
symptoms.
 In the chronic form of the disease, the history of repeated
attacks after similar exposure is important in differentiating this
syndrome from other causes of patchy fibrosis
(like- Sarcoidosis)
 For patients who present with hypersensitivity pneumonitis,
specific and careful inquiry about occupations, hobbies and
other environmental exposures is necessary to uncover the
source of the etiologic agent.

65. Management
 Acute episodes of allergic alveolitis may require hospitalization
and oxygen therapy to help the patient during the reaction;
occasionally hypoxaemia may be so severe and the lungs so
stiff as to necessitate assisted ventilation
 Corticosteroids in a dose of 40mg prednisolone daily until lung
function and Po2 have improved to clinically adequate levels
 Proper drying of damp hay and use of a respirator when
exposure cannot be prevented are the principles of management

66. MUSHROOM WORKER’S LUNG
 Mushrooms are grown commercially on compost, often made
of straw and horse droppings that is allowed to ferment, which
is then heated in moist air to just below 60°C
 While these conditions suit the mushroom mycelia with which
it is seeded, they are also ideal for the growth of thermophilic
actinomycetes
 Workers may be exposed to spores when compost and mycelia
are mechanically mixed or when the sheds are being cleaned.
 The manifestations of the disease are clinically
indistinguishable from those of farmer’s lung

67. BAGASSOSIS
 Bagasse is the residue after sugar is extracted from cane. It is a
fibrous material used in the manufacture of paper, boards and
building materials
 Typically it becomes contaminated with thermophilic
actinomycetes when lying in the hot and humid conditions
where sugar cane is processed.
 Although the disease commonly affects workers handling the
bagasse it may also occur wherever mouldy material is
imported
 The disease is a variant of farmer’s lung.

68. AIR CONDITIONER AND HUMIDIFIER LUNG
 Many workers exposed to ‘conditioned’ air (air in which the humidity and
temperature have been controlled to produce comfortable conditions) suffer
mild general malaise known as humidifier fever, particularly on the first day
of the week
 Some develop a true allergic alveolitis.
 Various organisms have been incriminated - thermophilic actinomycetes , in
some aspergillus spp., In others penicillium spp. And thermotolerant
bacteria resembling bacillus cereus , while in some the cause has not been
identified.
 In general, humidifier fever, in which the predominant antigen source is
naegleria gruberi or other amoebae, is not associated with evidence of
interstitial lung disease
 Results from exposure to droplets from humidifying systems in which the
water is sprayed into a moving stream of air.

69. Management of HP
 The mainstay of treatment for HP is antigen avoidance.
 A careful exposure history must be obtained to attempt to identify the potential
offending antigen and to identify the location where a patient is exposed.
 Once a potential antigen and location are identified, efforts should be made to
modify the environment to minimize patient exposure.
 This may be accomplished with measures such as removal of birds, removal of
molds, and improved ventilation.
 Personal protective equipment including respirators and ventilated helmets can be
used but may not provide adequate protection for sensitized individuals.
 In some cases, fully avoiding specific environments may be necessary, although
such a recommendation must be balanced against the effects to an individual’s
lifestyle or occupation.
 It is not uncommon for patients with HP due to exposure to household birds to be
unwilling to remove them from the home.

70. TOXIC GASES AND FUMES

71. TOXIC GASES AND FUMES
 The lungs and airways are in constant contact with the outside
world and thus are especially vulnerable to toxic substances
present in the environment.
 Within seconds of exposure to an inhaled toxin, pathological
events occur that may cause immediate distress, systemic
illness lasting days or even lead to the development of chronic
lung disease

72. Factors that determine the pathological results of a
toxic inhalation
 Size of inhaled particles
 Solubility of the inhaled substance in water
 Concentration of the inhalant in ambient air
 Duration of exposure
 Presence or absence of ventilation
 Host factors - age, smoking, co-morbid diseases, use of
respiratory protection, and perhaps even genetic susceptibility
Physical properties mainly particle size and water
solubility are of fundamental importance in determining the site
and severity of pulmonar injury.

73. Toxic fumes and gases

74. ASPHYXIANT GASES
Asphyxiation may occur as a result of exclusion of oxygen
from the air by physiologically relatively inert gases or by
interference with oxygen transport within the body by
inhalation of metabolic poisons
Simple asphyxiants - carbon dioxide, nitrogen and methane
Toxic asphyxiants - carbon monoxide, phosphine, cyanides
and hydrogen sulphide

75. Simple Asphyxiants
 Carbon dioxide causes hyperventilation, sweating, headache and
vasodilatation, with loss of consciousness
 Unconsciousness occurs rapidly and often unexpectedly when
breathing nitrogen, as the oxygen concentration falls to about 10%.
 Methane has a similar effect. It is an important problem in mines,
where it may accumulate as a result of decaying vegetable matter and
is released spontaneously from the coal seam
 Management of asphyxiation depends on removal of the victim and
administration of oxygen, Self-contained breathing apparatus should
be available to all workers at risk of such accident

76. Toxic Asphyxiants
Carbon monoxide, Phosphine, Cyanides and Hydrogen sulphide
Carbon monoxide
 CO is a product of incomplete combustion and is encountered
classically in fires. It combines not only with haemoglobin
(with an affinity some 200 times that of oxygen) but also with
myoglobin and cytochrome oxidase resulting in impairment
oxygen uptake into mitochondria.
 The first symptom of carbon monoxide poisoning is usually
headache and general malaise, which occurs with
carboxyhaemoglobin concentrations around 10%.

77.  Higher concentrations lead to dizziness, nausea, weakness in the limbs and
at 30% clouding of consciousness occurs. Death in fit people occurs at
carboxyhaemoglobin concentrations of about 50%, though lower levels may
be fatal in people with coronary artery disease or if oxygen demands are
higher as during exercise
 Longterm sequelae may include myocardial and cerebral infarction; in about
10% of survivors, a neuropsychiatric syndrome occurs that may include
extrapyramidal signs due to damage to basal ganglia, amnesia and psychotic
 Symptoms Management of CO poisoning depends upon removal of the
victim and administration of 100% oxygen. Use of a hyperbaric chamber is
desirable if one is available and is advisable if the patient has been
unconscious, even if recovery has occurred, in order to prevent the
neurological complications

78. Cyanides
 Act by blocking the cytochrome oxidase enzyme system, preventing
access of oxygen to the tricarboxylic acid cycle.
 Encountered in industry as hydrogen cyanide gas or as inorganic
cyanates in metal refining, plating, laboratories and fumigation. In
addition, vinyl cyanide (acrylonitrile) is a gas used in the production of
synthetic rubbers.
 Exposure to these gases causes rapid onset of dizziness, nausea and
tachypnoea, these symptoms usually serve as a warning so that the
worker can escape, but if ignored unconsciousness and death ensue very
rapidly.
 Treatment should be available in any sites where exposure may occur
the traditional kit consists of amyl nitrite for immediate inhalation and
sodium nitrite with sodium thiosulphate for intravenous injection.

79.  The nitrites combine with haemoglobin to form methaemoglobin, which in
turn reacts with cyanide to form cyanmethaemoglobin, this then combines
with thiosulphate to form harmless thiocyanate. This reaction reduces the
oxygen-carrying power of the blood because of the formation of
methaemoglobin and is also less effective for treatment of vinyl cyanide
poisoning.
 Thus the preferred treatment is usually to neutralize the cyanide by
intravenous injection of dicobalt edetate, 150 mg of which contains
sufficient cobalt to deal with 40% of an LD50 of cyanide. Up to 600mg may
be given slowly, each 300mg being followed by 50mLof 50% dextrose to
reduce risks of the anaphylactoid side-effects of the cobalt. Clearly the
patients should be removed from exposure by rescuers wearing self-
contained breathing apparatus and given oxygen in high concentrations.

80. Hydrogen sulphide
 Inhibitor of the cytochrome oxidase system and is as rapidly fatal as
cyanides.
 Smell of rotten eggs, although olfactory accommodation occurs rapidly so
that high concentrations may not be noticed.
 Fatal exposures have occurred in tanning, fish processing, chemical waste
disposal and natural gas production industries
 Survivors may develop pulmonary oedema several days after exposure.
 Low level exposures are associated with conjunctivitis and keratitis and
various neurological syndromes.
 Treatment of hydrogen sulphide poisoning requires removal from exposure,
administration of oxygen and of amyl nitrite and intravenous sodium nitrite,
which combine with sulphide to form sulphmethaemoglobin. Ventilatory
support may be necessary for delayed pulmonary oedema and hyperbaric
oxygen may help to prevent long-term neurological sequelae.

81. Phosphine (PH3)
 Is a gas used mainly in the fumigation of grain, it is introduced into cargoes
in the form of tablets of aluminium phosphide, which react with water to
produce the gas. Accidental poisoning of workers, particularly grain
inspectors, has been described as a result of entering the holds of ships or
rail freighters holding fumigated grain
 The gas poisons intracellular oxygen transport mechanisms and manifests
effects particularly on heart and liver. Cardiac failure and dysrhythmias are
common complications of poisoning. There is no antidote, treatment being
symptomatic

82. IRRITANT GASES AND FUMES
 Irritant gases injure the respiratory tract by causing acute inflammation
when inhaled in high concentration.
 The main site of injury depends on the solubility of the gas, the more
soluble gases exerting maximal effects more proximally.
 It is probable that the consequences of inhalation of irritant gases are non-
specific to the particular chemical and that any one or more of a spectrum of
adverse effects may follow exposure to any such gas when inhaled in
sufficient concentration. Short-term reactions include cough, wheeze, acute
bronchoconstriction, tracheobronchitis and laryngeal or pulmonary oedema.
These may be followed by temporary or persistent bronchial hyperreactivity
with a syndrome indistinguishable from bronchial asthma, often called the
reactive airways dysfunction syndrome
 In some subjects, airways obstruction is much less reversible and resistant to
antiasthma treatment, suggesting the development of obliterative
bronchiolitis.

84. RADS-Reactive Airways Dysfunction Syndrome
Bronchiolitis obliterans organizing pneumonia (BOOP)

85. Management
 Removal of the victim from site of exposure
 Maintenance of oxygenation for the 2–3 days until laryngeal
oedema settles; this may require tracheostomy
 Management is that of non-cardiogenic pulmonary oedema;
 There is anecdotal evidence that early use of corticosteroids
may be of benefit both in the acute stage and in preventing
bronchiolitis obliterans

86. REFERENCES
Harrison’s Principles of Internal Medicine 19th e
Fishman’s Pulmonary Diseases and Disorders 5th e
Crofton and Douglas’s Respiratory diseases 5th e
Thank You