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Archived Training Days

Pan London Training Day: Occupational Lung Disease

In November we joined our colleagues from across London at the Hammersmith Hospital, for a day of Occupational Lung Disease. It was hosted by Prof Paul Cullinan and Dr Jo Szram. Their website is here: http://www.lungsatwork.org.uk/ 

hammersmith hospital

Interesting facts about Hammersmith Hospital:

  • Hammersmith Hospital is not in Hammersmith
  • During WW1 Hammersmith Hospital was used as the Military Orthopaedic Hospital
  • The Clinical Imaging Centre, which opened in June 2007, is the largest in Europe

How work works

The day began with an introduction to the subject of occupational lung disease by  Prof Cullinan. Despite his apologies that this was ‘the boring bit’ some important clinical and legal principles were highlighted, creating a sound foundation for the rest of the day.

  • A thorough occupational history is essential if there is any suggestion that work is relevant to a patient’s symptoms. For example, it is not enough to know that someone works in a bakery as the exposures they are at risk from vary widely dependant on the type of work and type of bakery (scratch, plant or craft bakery).
  • Most occupational health services are paid for by companies and sit outside the NHS. Only 20% of workers have occupational health cover.
  • Sickness absence is 6-7 days/yr on average but is very variable. Police and NHS have high sickness rates. The role of a physician seeing a patient with a possible occupation-related condition is not to say whether someone should or should not continue to work, but to provide the information on the condition and its’ prognosis to allow an individual to make this decision themselves.
  • Compensation can be from IIDB (Industrial Injuries Disablement Benefit) which is a ‘no fault’ scheme and includes a statutory list of prescribed conditions for which compensation is available from the state (includes mesothelioma, occupational asthma, primary lung cancer with asbestos). Alternatively a patient can bring a civil claim (usually done on a no win no fee basis) through a lawyer or Union. This is a personal injury claim. If successful any money previously claimed via the IIDB route has to be repaid. Often this is not possible for asbestos claims as the company has gone out of business. There is a three year statute of limitations for claims of three years; this starts from the day that a patient is told that they have a condition AND that it is likely to have been caused by an occupational exposure.
  • For asbestosis the threshold for statutory benefit is only 1% disability, so if there is any evidence of asbestosis it is worth the patient claiming

Occupational asthma

Next Dr Szram introduced us to occupational asthma, highlighting the fact that most referrals come through primary care and occupational health services, in particular occupational health surveillance programmes. Patients with occupational asthma rarely have severe asthma but the consequences for the patient can be very significant. 

  • Respiratory sensitising agents include whole allergens (flour, egg, insects, seafood, tea, coffee, detergent enzymes, latex) and low molecular mass allergens which are hapten and protein conjugates (diocyanate spray painting, methylene from foam manufacturing, woodwork, hairdressing chemicals, dentistry chemicals).  
  • Occupational asthma can present as new, recurrent or deteriorating asthma in an employed person. The latency is usually 6-12 months after starting the job. Often the initial presentation is upper respiratory tract symptoms, progressing to wheeze and then asthma. Patients feel better away from work (eg on holiday).
  • Useful investigations include: peak flow diaries (2hourly PEFR for 28 days on workdays and days off); and bronchial provocation tests (directly observed)
  • All airborne proteins are potentially sensitizing agents. Those that have been identified as causing occupational asthma can be found here: http://www.hse.gov.uk/asthma/substances.htm . On substance labels they are indicated by R42.


We moved on to consider pneumoconioses, in particular asbestosis. We were reminded that there is a disconnect between the radiological and clinical picture, such that a patient can be asymptomatic with a severely affected chest x-ray if the substance is radio-opaque.

Substances may be inert/mixed/fibrogenic and high or low radiodensity.

  • Inert and high radiodensity: tin, iron, fibreglass, titanium, barium
  • Inert and low radiodensity: cement, limestone, chalk, gypsum, marble
  • mixed: coal, kaolin, slate
  • Fibrogenic: crystalline silica, asbestos, fibrous clays, MMF
  • Beryllium is different as it is granulomatous

A list of occupational diseases is available from the Manchester SWORD registry: http://www.population-health.manchester.ac.uk/epidemiology/COEH/research/thor/schemes/sword/ We considered a few specific examples:

  • Silicosis is due to inhalation of sandstone (which is 80% silica) and affects those working in quarries or as masons. The latency is 5-15 years. Silicosis predisposes to TB due to effects on macrophage function, so the Sheffield fork grinders of the 1840s all died before aged 60. Silicosis can easily be confused for sarcoidosis, but the occupational history is telling.
  • Alveolar proteinosis is a rare complication of silica inhalation. It requires a high exposure to fine silicosis and only really occurs in sandblasting. Treatment is with whole lung lavage but even then the prognosis is poor.


Asbestosis was considered in more detail.

Although it is no longer used in the UK, it is still mined in Quebec, Russia, Brazil and Zimbabwe. It continues to be used in significant amounts in industry in India and China. We were reminded of the different types of asbestos fibre:

  • Amosite = brown
  • Crocidolite = blue
  • Chyrysotile = white
  • Tremoolite (not commonly used, but may be contaminant)

We considered the range of effects of asbestos exposure, and their significance.

  • Plaques: benign, a marker of exposure but not directly related to risk of cancer, latency 15-20 years, minimal exposure needed, do not cause pain or breathlessness, no benefits (IIDB). Interesting patients can pursue personal injury claims for anxiety due to plaques in Scotland, but not in the rest of the UK.
  • Diffuse pleural thickening: occurs on visceral pleura, calicification, leads to breathlessness, very slow progression, IIDB benefits available.
  • Asbestosis: an interstitial lung disease, affects basal and subpleural areas of parenchyma, slowly progressive, large exposure required, can get worse due to pulm HTN or lung cancer.
  • Mesothelioma: Barrow-in-Furness has the highest incidence, latency is 35-40years, need short exposure only, high risk occupations were Navy, shipbuilders, railway workers, insulation. Currently 2000 deaths/year – peak soon.
  • Coal workers’ pneumoconiosis: also known as complicated pneumoconiosis, unlikely to see in UK now with closure of the mines in the 1970s. We discussed the way  it was proved that coal exposure is an independent risk factor for COPD, despite most miners being smokers (comparative cohorts), and the “healthy worker effect,” an imporant concept demonstrated well by occupational lung diseases.

Prof highlighted the fact that asbestos-related diseases are something we will all need to deal with as the peak in mortality, particularly for mesothelioma, has not hit yet:

We finished the morning with a medley of interesting cases and facts.

  • IPF and asbestosis may be difficult to distinguish and often it comes down to a balance of probabilities. Helpful clues include: high exposure required for asbestosis; accompanying evidence of asbestos exposure may be seen on CT (ie plaques); honeycombing is uncommon except in advanced asbestosis (but may be present earlier in IPF): folded lung is a helpful finding. A lot of reliance is placed on the exposure history, which helps to indicate whether the minimum exposure of 25f/ml-years is likely to have been reached (Helsinki criteria). In the 1950s a shorter exposure was needed as the intensity was greater as compared to the 1980s.
  • Sarcoidosis and berylliosis may also be difficult to distinguish. In 1946 “Salem sarcoid” was described by Dr Harriet Hardy, a pioneer in occupational medicine. This was due to zinc-beryllium, used in the manufacture of light bulbs. The pattern is largely pulmonary, rather than the classic bilateral hilar lymphadenopathy of sarcoidosis. Latency is 10-15 years.
harriet hardy

Dr Harriet Hardy, who described berylliosis as the cause of “Salem Sarcoid” and established the National Beryllium Registry.

  • It is thought that there is misdiagnosed berylliosis within some cohorts of sarcoidosis: Muller-Quernheim et al: ERJ, 2006. There is a specific test for beryllium: BeLPT (Beryllium Lymphocyte Proliferation Test), available at only 1 UK lab – the Hammersmith! Fresh blood is needed to run this test, so don’t just send a sample in the post. Beryllium is in use in several industries as it makes a good alloy. Dental technicians, those working in the nuclear industry, and in microelectronics are at risk.

Hyperbaric Medicine

A guest speaker, Dr Mark Glover, Navy officer and Occupational Medicine Consultant, provided an overview of diving medicine. Some in the audience did question when we might put this knowledge into practice in central London, but the scuba-enthusiasts asked some interesting questions.

  •  Immersion in water has several physiological effects: VC is decreased due to diaphragm splinting; extrathoracic pressure is increased by 100kPa for every 10m descended; the gravitational pooling of blood is neutralised so blood redistributes to the thorax, R heart filling in increased and there is an immersion diuresis.
  • Many of the side effects of diving can be understood by revising the effects on alveolar gases, which dissolve in greater quantity on the blood at depth. Inert gases (N, He) accumulate until each tissue is saturated.
  • Decompression illness occurs when bubbles are generated on resurfacing. The lungs act as a bubble filter so gas emboli are usually prevented from getting to the L side of the heart. However, if there are shunts (eg PFO, pulm AV shunt) systemic embolisation can occur. In autopsy studies 30% of people have PFOs, with 1.3% >10mm (clinically significant) so this possibility is worth considering in unwell divers. Both extravascular and intravascular bubbles can occur. Complications include neurological signs and symptoms, limb pain, cutaneous and cardiopulmonary complications. Treatment is basic life support, oxygen, restorative normovolaemia and recompression.
  • The world record for free-diving (without oxygen) is 214m, held by Alexey Molchanov of Greece. The rules are that if you lose consciousness before you reach the surface, the dive doesn’t count……Fun fact: actress and model, Jessica Alba is an accomplished free diver and did many of her own stunts in the film “Into the Blue.”
  • Barotrauma and lung rupture are additional complications (pneumothorax, pneumomediastinum, cerebral or coronary gas embolism).
  • BTS guidelines on diving can be found here: Fitness for Diving, Thorax, 2003


Simon Levene, of Temple Bar, who “sues doctors for fun” rounded off the day with some medicolegal aspects of occupational medicine.

  • Negligence is common law and requires: a duty of care, a breach of that duty and resulting harm. Most legal work related to occupational lung disease is related to asbestos exposure.
  • Asbestosis, pleural thickening and lung cancer all attract compensation and may interest lawyers. Lung cancer as a result of asbestos exposure is a divisable condition so blame can be divided between multiple employers. Smoking is felt to have a contributory effect in law and may be calculated to have 15% of the negligence.
  • Marvel comic characters include  The Asbestos Lady, who first appeared in the Captain America series in 1948. She robbed banks by setting fires to hold back the police, and her arch nemesis was the Human Torch: she created  bullets to puncture his defenses. The Asbestos Lady is, sadly, believed to have died of cancer related to asbestos exposure around 1990.
  • Not only is it possible to sue for personal asbestos exposure, wives of asbestos workers have successfully sued. In addition environmental exposure from living close to factories has been successful in Leeds and County Durham.

Key messages from the day were not to go outside your remit, or your expertise, in this area, and not to be afraid to say “I don’t know”. Giving advice that you think is helpful may not be, and may land you in legal trouble. If in doubt about whether a disease is occupation-related, or what to advise a patient about work, get specialist advice. The team at the Hammersmith welcome your referrals. 

Watch out Toto, that snow contains asbestos!

Watch out Toto, that snow contains asbestos!

The next training event will be the BTS Winter Meeting. We hope to see you there!  

The training programme for the next year is currently being constructed. If you have suggestions for titles/topics or activities you would like to see or that your centre could offer please get in touch.


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