The last training day of 2017 was a real highlight, with the team from the Occupational Lung Disease service at the Royal Brompton Hospital covering a range of topics with characteristic enthusiasm and clinical relevance! Thanks to Jo Szram, Jo Feary and Paul Cullinan for organising the day.
Jo Szram got the day off to a great start. An oft quoted figure is that 10% of adult asthma is attributable to work – but she challenged us to think about what attributable really means? There is an excess of asthma in some jobs/occupations but is this occupation-induced asthma, occupation-exacerbated asthma or something else entirely?
The 10% figure includes IgE mediated occupational asthma (95%), irritant induced occupational asthma (5%) – difficult to prove, and work exacerbated asthma. The term ‘RADS’ (reactive-airways dysfunction syndrome) was used previously but is descriptive rather than diagnosis and is defunct – don’t write RADS on your letters!
In terms of frequency of asthma in working people:
- Most common is asthma unrelated to work.
- Next is work-exacerbated asthma (in someone with pre-existing asthma, symptoms are exacerbated by work).
- Least common is occupational asthma, new asthma, induced at work. Of these, 95% are due to sensitisation after repeated exposure, 5% are due to a high dose of an irritant.
Therefore the number of people we see with true occupational asthma will be small, and we must be very careful about using this term. We were reminded to take a decent occupational history. Retired is not an occupation! Key questions include “does your asthma affect your work?” and “what are your hobbies?”. Security of a diagnosis of occupational asthma is essential, particularly as legal claims are not uncommon. Don’t write ‘occupational asthma’ until it is proven – requires investigation.
As the NICE guidelines state, adult onset asthma is rare – mostly is actually reactivation of childhood asthma OR it could be occupational asthma. Therefore we must pay more attention to occupation in adult onset breathlessness cough and wheeze.
Although people often associate symptoms with exposure to substances that smell strongly, they are not often sensitisers. e.g. spray glue, hairspray, solvents, perfumes, chlorine. These substances are just volatile, which is why they smell. In contrast, all airborne proteins are potentially sensitising agents but often do not smell.
Some workplaces conduct respiratory surveillance, and this data can be very useful. However, it should be interpreted with caution It is not quality assured spirometry and is done by people without respiratory medicine expertise. It is often sporadic and agency workers are not included. there may be documentation of a fall in FEV1 but no action taken. It is important not to be reassured just because someone is under a health surveillance programme. They should still have the same assessment including the usual investigations such as quality assured spirometry.
MSDS – material safety data sheets are required under COSSH. These include risk phrases (R phrases) – e.g. Resp sensitiser R42. Every year 3 or 4 new sensitisers are found so just because there is no sensitiser identified on the label of a substance it is not necessarily off the hook! An example of a substance identified on labels is methacrylate, which are respiratory sensitisers.
The lovely people in Manchester have developed the Asthma Hazard Index. It provides a computer generated probability that a given compound is asthma-genie, based on its chemical structure. NB Polymers don’t cause asthma since they have to be small molecules.
Investigations undertaken in the occupational lung disease clinic include a 2hrly PEFR diary whilst at work, and direct challenge tests. PC20 is recorded – to histamine, to control, and to the active compound. Multiple tests over a number of days are done, proving a reliable asthmatic reaction.
Key facts about occupational asthma:
- Occupational asthma has latency 6-24 months
- Eye/nose symptoms are common in occupational asthma. People often describe as ‘constant cold’, ‘hay fever all year round’, frequent ‘chest infections.’
- If confirm occupational asthma the patient needs to be removed from exposure – otherwise v poor outcomes.
- Compensation is possible – personal injury claim, a civil claim, has a statute of limitations of 3yrs. Legally there has be>50% certainty that the occupation causes asthma. Patients may also be eligible for Industrial Injuries Benefits – have to be 14% ill! (only 1% for pneumoconiosis).
- Whole allergens include flour, alpha-amylase, enzymes, seafood/tea/coffee/egg processing, latex.
- Protein conjugates include: e.g. isocyanates, methacrylate, platinum salts (precious metal processing), persulphate salts (hairdressing).
This website is useful: hse.gov.uk/asthma and includes an official government list of asthmagens – http://www.hse.gov.uk/asthma/asthmagen.pdf
Look out for R42 or H334 on hazard sheets.
Challenge testing to specific agents is conducted at: Brompton, Manchester, Birmingham. This is very helpful for new agents, and when you need a diagnosis. A single-blind challenge series is conducted with FEV1 and PC20 before and after exposure.
RIDDOR – occupational asthma is an ‘accident at work’. This should be reported, which leads to the company getting visited, and can lead to a fine.
SWORD – surveillance of work-related and occupational respiratory disease. Sign up to be an intermittent reporter once you are a Consultant.
Prof Paul Cullinan gave a concise, but comprehensive overview of pneumoconioses, clarifying a number of important points of epidemiology and pathogenesis. Thanks! Pneumoconioses are are group of lung diseases due to inhalation of inorganic dusts. These include: coal, asbestos, silicosis – and many more. Xrays show fine nodular shadowing, which is widespread. Symptoms include breathlessness, dry cough, and weight loss – these are nonspecific. Patients may be asymptomatic despite dramatic X-ray appearances eg Tin-smelters lung (stannosis).
- Inert high radio intensity: tin, iron, talc, fibreglass, titanium, zirconium, barium, antimony
- Inert low radio density: cement, limestone, chalk, marble
- Mixed: coal, kaolin, slate
- Fibrogenic: crystalline silica, asbestos, fibrous clays, zeolite, MMMF
- Granulomatous: beryllium (light metal, hard, used in expensive alloys) looks and behaves like pulmonary sarcoidosis
*beware silica contamination of inert substances
Over the last 40yrs there has been a flat rate of asbestosis causing death (part 1), but increase in mentions on death certificate (part 2) – this is due to the increased use of CT. There has been a sharp rise in compensation claims – due to increased access to lawyers and patients being supported to claim.
Prof Cullinan reminded us of the fact that people we see in clinic may have lived and worked abroad where health and safety legislation may be less consistently applied. He showed an example of some young boys in India who were bike shaft grinding. The grinding wheel is unfortunately made of sandstone, which contains silica. These boys got silicosis. This grinding process has not been allowed in the UK since the 1950s. It has also not been possible to use sand for sandblasting in UK since the 1960s.
Occupations and silicosis:
- Stonemasons: funereal stone masons, kitchen tops, fireplaces, cathedrals and flooring for domestic use (in posh kitchens!)
- Tunnelling – crossrail.
- Cement – mortar (baked limestone) + water + sand = silica. Bricks – 30% silica. Slate for roofing tiles – 50% silica. Use lots of mechanical tools – creates lots of fine dusts when cut. Respirable.
There is a current push to find cases of silicosis – we expect numbers will rocket. People moving here from abroad to work in construction bring their silicosis with them. On imaging we see upper/midzone patchy fibrosis, with raggedy thickening of pleura, and eggshell calcification of hilar nodes. There is no clubbing. Silicosis is increasingly mistaken for sarcoidosis.
Simple (small dots) vs complicated (big lumps = Progressive Massive Fibrosis).
Pathologically whorls of fibrosis are seen. Macrophages eat silica, kills macrophage, induces fibrosis. Once inhaled, even if stop working exposure is there, so fibrosis continues, and progresses.
1/3 lung transplant patients in Israel are due to silicosis!
It is also important to remember that silica exposure predisposes to TB. Patient’s don’t need to have silicosis to be at increased risk, just to have had exposure. The reason is due to a lack of alveolar macrophages – a key line of defence is lost. This is a significant problem in India, China etc.
Alveolar proteinosis is a RARE complication to heavy exposure to silica, classically described as having a ‘crazy-paving’ appearance on CT.
Important conditions to remember that are associated with asbestos exposure:
- Diffuse pleural thickening
- Lung cancer
There are still asbestos mines in the Urals, Canada, Brazil. The asbestos that is mined nowadays is Chrysotile (white, wavy, serpentine).It is less biopersistent than the other forms and therefore is less likely to cause health problems.
The others are Amosite (brown), Crocidolite (blue), Tremolite. These are amphiboles, straight fibres. These are far more toxic, and biopersistent. They are important for pleural disease. In fact, most asbestos is a mixture. Mechanics brake pads are an exception as these used to be pure white asbestos.
Pleural plaques occur on visceral pleura, and are pathognomonic of asbestos exposure. They calcify and are not pre-malignant. There is no compensation or industrial injuries benefit (IIB) available for pleural plaques. However, in Scotland and NI patients can bring a civil case (not in England/Wales) for a personal injury claim (anxiety induced by plaques). Patients do not need much exposure to get plaques.
Diffuse pleural thickening probably follows an asbestos effusion. It results in thickened calcified visceral pleura. A high exposure is needed to get an effusion and thickening. If circumferential patients may get a restrictive lung defect and can therefore claim compensation (IIB).
Asbestosis looks exactly like IPF. It has a basal, subpleural predominance and has a reticular pattern of pulmonary fibrosis.
Mesothelioma is a malignant tumour of the pleura. Barrow in Furness is the hot spot of mesothelioma in the UK. It had a shipyard back in the day. The next highest rates are in Glasgow (Clyde shipyard). We are still seeing the legacy of asbestos use of boilers/pipes on ships. Mesothelioma has a poor prognosis; life expectancy is 11 months, with chemo 14months.
During the 2nd world war Boots (the chemists) employees assembled gas masks. The filters contained crocidolite asbestos (an amphibole). The exposure was only for a short period but 25% died of mesothelioma, with a a latency of 40yrs. Women who worked in the factory in Nottingham sued Boots. This shows how important an occupational history before the age of 30yrs is for this age group. The minimum exposure needed in this cohort was just 3 months. There was probably heavy exposure to pure crocidolite leading to high rates of mesothelioma.
Prof Cullinan showed us some epidemiology of asbestos worldwide. There is an epidemic curve of UK asbestos, and England has the highest rates of mesothelioma in the world (then Scotland, then Dutch). This is likely a combination of factors – we are good at counting it, and we have imported a lot of asbestos! The Empire strikes back!! Despite recognition of the hazards, we continued to import amphiboles for years and years, right into the 1980s. The projected peak is therefore 2020 (3250 cases/yr). Nearly all cases are in men. Now we also see cases from construction worker exposures e.g. carpenters, plumbers, electricians, painter/decorators, other construction.
14% of male and 62% female cases are unexplained which is highly concerning. It prompts the question, was there enough asbestos in urban air previously to induce mesothelioma? Also, 10% peritoneal mesothelioma.
We considered what should be done about asbestos in the public fabric? At present the approach is to leave it there if not damaged and label it so no-one accidentally disturbs it . Removing it puts the building out of action for 6 months as the fibres are disturbed. It is also removed when buildings fall down!
There is no link between smoking and mesothelioma.
Last underground coal mine closed 2yrs ago in the UK, so we think of coal-related pneumoconioses as a historical problem. However, in the US there is still a real problem with coal-workers pneumoconiosis. They have found new ways to mine coal – such as blasting off the top of a mountain then digging the coal out. This is catastrophic environmentally, but unregulated private coal mine proprietors care more about profits that the future of the world.
Don’t forget the healthy worker effect – a key cause of selection bias in cohort studies of occupational exposures! On first glance, it makes it look like a dirty job is good for your life expectancy. But this is only because the only people doing it are young, fit strapping. Anyone sick is stopped working, so they are selected out.
- Li, C-Y., and F-C. Sung. “A review of the healthy worker effect in occupational epidemiology.” Occupational medicine 49.4 (1999): 225-229.
It is pretty well established that coal exposure causes COPD. But how much can COPD in miners be attributed to coal exposure, over and above smoking exposure (as pretty much all miners were regular smokers!)? British Coal Board data was cleverly used to help determine who to give compensation to if they had COPD. The risk of exposure to coal mine dust is independent of smoking exposure. But the risk of COPD more than doubled in those exposed to both. COPD is more likely than not to have come from coal mining – which means compensation is applicable under British law. A more than doubling of risk independent of another risk factor is the key. This legislation was passed in late 90s leading to 1.2million claims!
- Coggon, David, and Anthony Newman Taylor. “Coal mining and chronic obstructive pulmonary disease: a review of the evidence.” Thorax 53.5 (1998): 398-407.
Other occupational lung diseases
Prof Cullinan continued the day with a round up of other occupational lung diseases. Clearly this is a vast subject, filling many a tome in the library, so he concentrated on some key illustrative diseases, and amazingly enthused us all about the fascinating world of welding!
Lots of people weld! And welding is complicated! There are in fact over 90 different ways to weld. Who knew? Electric arc welding is the most common technique. Workers may say that they are TIG (Tungsten Inert Gas) or MIG (Metallic Inert Gas) welders. Impress your friends and patients with this new jargon. Importantly, welding fumes are metal oxides, NO/CO/NO2/CO2/O3. Coating materials are mostly steel.
Problems resulting from welding include:
- Metal fume fever (known as other things such as the ‘zinc shakes’ and ‘monday morning fever’) is due to inhalation of zinc oxide. This is common using ‘galvanised’ steel. It is unpleasant but benign and feels like the flu.
- Pneumonia – lobar most commonly. Pneumococcal pneumonia. There is a question as to whether all welders should be vaccinated. The mechanism of increased risk is unclear.
- Asthma (stainless steel). Due to chromium oxide exposure.
There are many, many causes, of HP most of which are organic, in particular fungi. However, there are also a few chemical/non-organic causes. Metal worker’s lung is a new and very important epidemic. It is pretty common and is increasing. It far outstrips farmers lung, bird fanciers lung etc.
HP in this context is due to inhalation of aerosolised coolant (metal working fluid). The sump gets contaminated with Pseudomonas / fungi / NTM contaminate which then puts the worker at risk. It is very frequently missed by Respiratory physicians as signs, symptoms are non-specific. Don’t miss it!
Workers at risk are ‘Tool setters’, who may call themselves machinists, lathe setters, tool grinders, drillers, millers, CNC operators (Computer Numeric Control). They are exposed to aerosolised metal working fluid/coolant/suds. Make sure you work out what someone’s job actually is, rather than just the term they use to describe their role!
Acute HP: 6-12hrs after exposure the worker feels unwell, often with SOB and wheeze, in addition to systemic symptoms. It is self-limiting, and responds to Prednisolone and avoidance of exposure. Sp IgG can be detected, and BAL will be lymphocytic
Chronic HP: gradual onset of SOB/cough, weight loss, crackles (squawks) +/- fibrotic radiology. Sp IgG can again be detected, but cause is often unknown (50%). Indoor moulds, outdoor moulds, feather duvets and who knows what else!
Interestingly smoking is protective against HP (bit still not recommended!).
Jo Feary rounded off the day by equipping us to be useful physicians come the apocalyse, revolution, or war….
Inhalation injuries are an acute exposure to a potentially toxic agent that can cause respiratory illness. They are gases / vapours / aerosols / fumes.
Key questions to ask about exposure:
- Duration of exposure
- Agent (if known)
- Latency of symptoms
- Previous exposure(s)
- Number affected
The important determinants of inhalation injury are agent, environment, and host.
The solubility of the agent is very important. An example of a highly soluble agent is ammonia which is used in fertilisers and crystal meth production. Also, chloride, and sulphur dioxide (used in dried fruit preparation).
Zinc oxides, in contrast are low solubility agents. These are used in smoke bombs in army. These inhalation injuries occur distal in airways and come on up to 48hrs after exposure so need to monitor rather than discharge. Density of gas is also importnat (ww1 trenches, displacement of O2 if lighter than air). And of course the environment in which the exposure occurs is highly relevant – poorly ventilated or enclosed areas lead to greater injurues.
Acute management is supportive. In an ideal world get spirometry done as soon as possible after exposure and track progress. There is a danger of airway oedema, but no evidence for steroids acutely, although they are usually given. ICS, and bronchodilators are both useful in the short term but avoid prolonged polypharmacy without objective ongoing assessment. Generally there are no longterm adverse outcomes.
A minority develop complications, but there is little data available. All of the following have been reported:
- upper airway symptoms eg VCD/ILO
- airflow obstruction
- small airways disease
Inhalation injuries are a result of a single massive exposure to an irritant. Patients will have a positive nonspecific BHR test but often a normal CXR. There is no hypersensitivity so they can tolerate exposure to the same agent at a later date (in contrast to occupational asthma). Recall bias is a problem. And it is important to consider the impact of psychological factors. Someone may associate confined spaces or certain smells with a memory of exposure and develop symptoms again, but this does not mean there is a physical/immunological process occurring in the airways. DO not underestimate the power of the mind and the relevance of PTSD.
- 1. establish disease
- consider attribution (can be difficult – consider exposure, biological plausibility, and prior experience).
Investigations include: lung function tests, measure of BHR, CT, CPET, nasendoscopy (dynamic), physio (breathing pattern disorder).
What a great training day! Thanks again to the team from the OcLD service at The Brompton.
Don’t forget that you need to spend some time in an occupational lung disease service pre-CCT (see FAQs). Contact Julie Cannon, clinical nurse specialist who will confirm dates with you. Interested in research? Contact Paul Cullinan or Jo Szram for a chat.
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