Occupational Pulmonary Disease Flashcards
(27 cards)
Tell me about lung structure
- Airways of the lung derive from the trachea downwards, by progressive division into two, or more, branches
- Airways beyond the trachea that contain cartilage are referred to as bronchi
- Airways beyond the bronchi, that lack cartilage, are called bronchioles
- Bronchioles terminate in hollow spaces called alveoli, which have a diameter of ~0.1mm
- There are approximately 300 million alveoli in the lung, with a total surface area of 140m2
- The conducting airways are lined by cells with cilia - small, motile surface projections - interspersed with mucous secreting cells
- Secreted mucous spreads out over the cilia, which direct the mucous upwards to the larger airways via rhythmic, undulating movements, thus helping to clear deposited dusts
What is Pneumoconiosis?
Pneumoconioses are a group of chronic lung diseases caused by long-term exposure to respirable particles (<5 um diameter) of mineral dust.
Two important pneumoconioses are coal workers pneumoconiosis and silicosis.
Mineral pneumoconiosis can also be caused by beryllium, talc, kaolin and mica exposure.
N.B. Pneumoconioses excludes diseases mainly of the airways such as asthma, bronchitis and emphysema
What are the classical features of pneumoconioses?
1) Deposition of mineral dust in the alveoli
2) The mineral dust particles are phagocytosed by alveolar macrophages
3) This causes a localised inflammatory reaction, which leads to long term histological changes in the lung
- Fibrotic reaction in the surrounding parenchyma, with reticulin formation and collagen deposition
- Necrosis and cavitation of fibrotic nodules in the later stages
- Progression of the disease can lead to coalescence of fibrotic areas into large parenchymal masses (progressive massive fibrosis)
4) Gas diffusion is affect, leading to a reduced transfer factor
5) Lung volumes are reduced (FEV1 and FVC), with classically a restrictive pattern
What are some radiological features of pneumoconioses?
- Chest X-ray shows small nodular opacities in the lung parenchyma
- Distribution depends on the specific disease, but tends to affect the upper lobes first
- Progressive massive fibrosis is associated with large areas of confluent shadowing, with upper lobe predominance
What is Coal-Workers Pneumoconiosis?
- Coal workers pneumoconiosis is a pneumoconiosis caused by inhalation of coal dust
- It is characterised pathologically by collections of coal-laden macrophages in the lung parenchyma, surrounded by fibrosis and localized emphysema
- It is more prevalent in underground workers exposed to higher concentrations of dust than in surface workers
- It causes damage to the lung via fibrosis and emphysema
- Onset of CWP generally lags behind exposure by > 10 years, so incidence generally reflect past exposures / working conditions
Prevention and surveillance strategies for Coal Workers Pneumoconiosis?
- Exposure controls in the mining industry, including ventilation, dust-reduction measures and use of PPE
- Miners must undergo regular CXRs at 4-yearly intervals
- Those in whom early signs of CWP are detected should be removed from exposure (early signs may include nodular opacities, with upper lobe predominance)
What is Silicosis?
Silicosis is a pneumoconiosis caused by inhalation of quartz (or other crystalline forms of Silicon Dioxide):
- Quartz / other crystalline forms of silicon dioxide are lethal to macrophages, that ingest it causing release of their contained enzymes
- In its early stages, Silicosis is similar to Coal Workers Pneumoconiosis, but the resulting nodules in the lung tend to be denser
- There is a long latent period between exposure to silica and onset of the disease
- Silicosis is a serious, progressive disease
Clinical and radiographic features of Silicosis?
There are three types of silicosis:
1) Acute: early onset of dyspnoea and dry cough within a few months of heavy exposure to fine dusts (e.g. sand-blasting). CXR shows patchy small airway consolidation. Progression over 1 - 2 years, with respiratory failure
2) Subacute: gradual onset of dyspnoea and dry cough over years after moderate exposure. CXR shows upper and mid-zone nodular fibrosis with ‘egg-shell’ calcification of the hilar lymph nodes. Progressive massive fibrosis can occur, with coalescnnce of fibrotic nodules. Restrictive pattern of impaired lung function
3) Chronic: slow development of nodules on CXR over many years after low level exposure
Silicosis is associated with larger nodules on CXR, and more rapid progression than coal workers pneumoconiosis. With the exception of ‘egg’shell’ calcification, it can be difficult to distringuish from CWP clinically and radiologically
What is mixed dust fibrosis?
- This is the pulmonary disorder caused by inhalation of silica dust simultaneously with another non-fibrogenic dust
What is asbestosis?
Asbestosis is characterized by chronic pulmonary interstitial fibrosis resulting from exposure to asbestos.
- Develops after a long latent period (25 - 40 yrs) following exposure
- Clear dose-response relationship. Asbestosis tends to occur in those exposed heavily
Asbestosis is a serious and incurable condition, which can result in death at an early age.
Treatment and prognosis in Asbestosis?
- There are no specific interventions that can halt the disease
- Supportive treatment can be offered in the later stages
- Patients should be advised to stop smoking (smoking is associated with increased severity and rate of deterioration)
- There is an increased risk of lung cancer in asbestosis patients
What are clinical features of Asbestosis?
- Gradual onset of dyspnoea and cough
- Basal crepitations on auscultation
- Finger clubbing in 40% of cases
Clinical assessment and diagnosis of asbestosis?
- Lung function generally shows reduced FEV1 and FVC, with a restrictive pattern (though obstructive and mixed patterns can occur)
- CXR shows fine nodular shadowing, predominantly in the lower zones. There may also be pleural plaques
- HRCT is often used for diagnosis, as CXR is relatively insensitive
- Lung biopsy (gold standard) shows interstitial fibrosis and asbestos bodies
What is Byssinosis
Byssinosis is a now rare disease associated with exposure to cotton dust. It is caused by an endotoxin, produced by the bacteria in raw cotton.
It causes symptoms including wheezing and chest tightness.
There are no specific radiological abnormalities associated with the disease and it is normally diagnosed from clinical history and decline in FEV1. It is treated with bronchodilators and antihistamines .
It may be seen in workers in the textile or rope-making industries, who handle raw cotton, flax or hemp. Usually symptoms are associated with exposure > 20 years.
Tell me about Mesothelioma?
Mesothelioma is a diffuse, malignant tumour arising in the pleural, peritoneal and (rarely) pericardial lining.
Asbestos exposure is the single major cause (in 90% of cases).
Any kind of asbestos can cause the disease, and risk is highest with amphibole fibres.
There is a long latency between exposure and disease (mean 40 years).
There is no dose-response relationship, and no threshold below which there is no risk (although risk is very small in low exposure levels).
Mesothelioma is typically fatal within 1 - 2 years. Surgical intervention with pleurectomy may be offered in some cases, in addition to palliative treatments with pleurodesis or draining of effusions.
What are the clinical features of mesothelioma?
- Mesothelioma generally presents with a pleural effusion
- Patient may complain of chest wall pain and dyspnoea
- Occasionally, can present with ascites, pericardial effusion or encasement syndromes
- CXR/CT may show pleural effusion, pleural mass or thickening, local invasion into the chest wall, heart or mediastinum, concomitant pleural plaques or pulmonary fibrosis
What are occupational asthma and rhinitis?
Occupational asthma and rhinitis are caused by immunological sensitisation to agents in the workplace. This causes inflammation of the lining of the airways and intermittent spasm of the underlying smooth muscle.
Up to 15% of cases of asthma in adults of working age is occupational.
Following sensitisation, symptoms can occur with very low level exposure.
Symptoms generally resolve after removal from the exposure.
What are the clinical features of Occupational Asthma + rhinitis?
Asthma:
- Wheeze
- Chest tightness
- Dyspnoea
Typically, symptoms are work at work / soon after work and improve at the weekends / holidays.
Rhinitis / Conjunctivitis:
- Rhinorrhoea
- Nasal congestion
- Itching of eyes / nose
- Sneezing
Often associated with asthma, and may precede chest symptoms.
Clinical assessment and diagnosis of Occupational Asthma?
- Lung function tests (including FEV1 + FVC + peak flow). Generally show reversible airway obstruction
- Serial peak flow recording and bronchial provocation challenge tests (in specialist centres only)
- Specific IgE, skin prick testing
- Pattern of exposure to specific allergens and relationship to symptoms
Health Surveillance for Occupational Asthma / Rhinitis?
Individuals who are exposed to respiratory sensitisers must undergo health surveillance as per COSHH + Management of Health and Safety at Work regulations.
Surveillance depends on likelihood of sensitisation.
What are some causal industries and exposures in Occupational Asthma + Rhinitis?
- Car Body Shops: isocyanates
- Bakeries / Agriculture: flour, grain dust
- Electronics / Soldering: Rosin flux
- Manufacture of washing powders: proteolytic enzymes
- Pharma manufacturing: ispaghula, antibiotics, cimetidine
- Healthcare: latex
- Construction / Forrestry: wood dust
- Hairdressing: henna, persulphate salts
- Food industry: fish proteins, soya bean, tea dust
- Manufacturing: metal-working fluids, acid anhydrites
What is Extrinsic Allergic Alveolitis?
Extrinsic Allergic Alveolitis is also known as Hypersensitivity Pneumonitis.
It is an inflammatory disorder of the lower respiratory system resulting from allergic sensitisation and immunological reaction to allergens in organic dusts.
It causes a lymphocytic interstitial pneumonitis.
It likely results from a type II immune complex or type IV cell-mediated immune reaction, and is not a IgE mediated type I allergic condition.
It tends to mainly affect the respiratory units of the lung, as opposed to the conducting airways.
Tell me about different forms of Extrinsic Allergic Alveolitis?
- Farmers Lung: actinomycetes + aspergillus species in mouldy hay, grain or straw
- Bird Fanciers Lung: avian proteins in bird excreta + bloom
- Mushroom workers lung: aspergillus in mushroom compost
- Bagassosis: thermoactinomyces in fibrous residue of sugar cane
- Malt Workers lung: aspergillus clavatus in mouldy barley / whiskey distilling
- ventilation Pneumonitis: thermophilic actinomycetes in water reservoirs / air conditioning systems
Clinical Assessment of Extrinsic Allergic Alveolitis?
- Causal exposure e.g. agricultural worker, forestry worker, mushroom workers, bird handlers, sugar cane processors, distillery workers
- Raised ESR and neutrophil count
- Restrictive pattern of lung function tests (FEV1 + FVC)
- Impaired gas transfer, hypoxia may occur
- Chest XR: in acute may show diffuse pulmonary infiltrates, in chronic cases upper and mid-zone interstitial fibrosis
- Serum Precipitins to causal allergens
