Lung Disease and Work

The Lane Lecture is an annual event hosted by the Centre for Occupational and Environmental Health at the University of Manchester. Named in honour of Ronald Lane, the first ever Professor of Occupational Health at the University.

This year the lecture was delivered by Professor David Fishwick, Chief Medical Officer and Co-Director of the Centre for Workplace Health. His talk was entitled The lungs at work: from cotton mills to composites? One of the key messages is that diseases such as byssinosis and silicosis are not historic issues.

In 1890 there were more cotton mills in Manchester than in the rest of the world. But that is no longer the case – the industry has been transferred overseas, particularly to developing economies. So byssinosis, which is caused by exposure to cotton dust, is no longer a problem in the UK. However, it’s a different matter in those countries where cotton is now produced.

Studies carried out in recent years have shown high incidences of byssinosis in some mills in developing countries. One study in Karachi, Pakistan in 2008 found that among 362 textile workers 35.6% had byssinosis. (Prevalence of Byssinosis in Spinning and Textile Workers of Karachi, Pakistan, Archives of Environmental & Occupational Health, Vol. 63, No. 3, 2008 )

Professor Fishwick also focused on Silicosis, the oldest known occupational lung disease which remains a significant problem across the globe, including the UK. This debilitating disease is caused by exposure to respirable crystalline silica (particles smaller than 10 microns) which can occur in many industries, including mining, quarrying, brick and tile manufacture, stone masonry, glass manufacture, tunnelling, foundries, ceramic manufacturing and construction activities.


The risk is clearly associated with the level of exposure and it only takes a regular exposure to very low concentrations to cause the disease. The US Occupational Safety and Health Administration (OSHA) estimates that 30% of workers with 45 years of exposure to 0.1 mg/m3 respirable crystalline silica dust will develop silicosis (see page 16394 of the “Final Rule”). Yet 0.1mg/m3 (respirable dust) is the current Workplace Exposure Limit for crystalline silica in the UK.

Clearly the current WEL is not a “safe level” and there is a very strong case for reducing it. In the US OSHA has recently announced a reduction in their Permitted Exposure Limit for silica down to 0.05 mg/m3. No change is proposed in the UK. The HSE’s view is that there are difficulties accurately measuring exposures lower than 0.1mg/m3, so it would be difficult to demonstrate compliance, and that, in any case, employers have a duty to not only meet the exposure limit but the apply “principles of good control practice” set out in Schedule 2A of the Control of Substances Hazardous to Health Regulations. Not everyone agrees with them, however.

As well as causing silicosis, respirable crystalline silica is a carcinogen. It’s estimated that in the UK it causes around 600 deaths per year from lung cancer shows  with 450 of these occurring from exposures in the construction sector.

Occupational cancer deaths by cause in Great Britain, 2005 (HSE)

Personally, I’d like to see the WEL reduced and research done to develop better sampling methods which will allow low levels of exposure to be evaluated. I do sympathise, though, with their emphasis on control. Reducing exposure by introducing improved controls is the key to preventing workers from developing industrial disease. Measurement can help us to understand exposure and identify where improved controls are needed. But sometimes the problem is obvious and in those cases it’s better to spend time, effort and money sorting it out, particularly when there are well established solutions available.


Low Toxicity Dusts – Part 1

dust exposure

(Image source: BOHS)

Regulation 2 of COSHH1 states that any dust when present in the workplace at a concentration in air equal to or greater than 10 mg/m3
of inhalable dust or 4 mg/m3 of respirable (as a time-weighted average over an 8-hour period) is considered to be a substance hazardous to health. If the concentration of dust in a workplace exceeds these figures then the requirements of COSHH will apply, including the need to assess the risk to workers and to ensure exposure is prevented or adequately controlled.

The 10 and 4 mg/m3 values are NOT Workplace Exposure Limits (WELs), but, in practice, they are widely used as such by many occupational hygienists for “low toxicity dusts” where a WEL hasn’t been set. This seems like a reasonable thing too do, particularly as these values have been used where WELs have been set for dusts of low toxicity, such as aluminium oxide, barium sulphate and  titanium dioxide.

However, recently, serious doubts have been expressed as to whether this approach is valid and appropriate to protect the health of workers exposed to airborne dust. There is evidence from both animal experiments and industrial experience that relatively low exposure, well below these levels, to “low toxicity” dust (the UK Health and Safety Executive now prefer the term “poorly soluble dusts of limited cytotoxicity”) may cause adverse effects.


At their annual Conference in Cardiff earlier this year, the British Occupational Hygiene Society (BOHS) held a workshop on “low toxicity dusts” to try to advance the debate. The presentations, which summarise the key points made by the speakers can be downloaded from the BOHS website here. The presentations by John Cherrie and Alistair Hay are particularly informative.

Exposure to high concentrations of any dust can overload the normal clearance mechanisms in the lung, leading to inflammation and possible lasting effects. In particular, there is evidence that exposure to many dusts can cause or worsen chronic obstructive pulmonary disease (COPD). According to HSE, 15% of the risk of chronic obstructive pulmonary disease (COPD) is attributable to gases, dusts, vapours, and fumes at work, and 4000 COPD-related deaths in England are due to workplace exposures. High lung burdens of “low toxicity dusts” can also prevent clearance of other, more toxic, particles, leading to a higher risk of other lung diseases.

Too much of any substance will cause harm. The question is, what is “too much”? Unfortunately, for “low toxicity dusts” the evidence is relatively limited.

In 1999 the HSE published a Contract Research Report of work carried out by the Institute of Occupational Medicine (IOM). They developed a mathematical model based on animal experiments  to estimate the no-adverse effect level (the NOAEL) for titanium dioxide, based on avoiding the impairment of dust clearance and the beginning of inflammation. Using the model they derived a human NOAEL of 1.3 mg/m3 .

In his presentation at the BOHS workshop Alastair hay discussed an IOM study on coal-miners, which found that 35 years exposure to 4 mg/m3 respirable could lead to 17% of non-smoking workers experiencing an FEV12 loss of almost a litre, compared with 10% in a non-dust exposed population

The HSE’s Advisory Committee on Toxic Substances (ACTS), considered low toxicity dusts in 2006/7. The outcome was that they decided to take no further action other than to recommend an awareness raising campaign for those exposed to dusts to highlight possible risks to health. A number of independent experts and the Trade Unions were not happy with this decision.

There is also concern about whether the mass concentration is the most appropriate way of evaluating the degree of risk from dust which is probably related to surface area. Exposure to small particles will have a greater effect than the same mass of larger particles of the same dust.

The following charts, extracted from John Cherrie’s presentation at the BOHS Conference show the relationships between pulmonary inflammation and mass (left hand chart) and surface area (right hand chart) for three different dusts


The data was derived from Donaldson K, Brown D, Clouter A, et al. The pulmonary toxicology of ultrafine particles. J Aerosol Med 2002;15:213–220.

The charts show a fairly clear linear relationship between surface area and inflammation, irrespective of the type of dust.

I suspect that the majority of occupational hygienists who attended the workshop came away convinced that applying limits of 10 mg/m3
for inhalable dust and 4 mg/m3  for respirable dust, whether they are “official” or not, is no longer appropriate. So what limit should be applied to these dusts? I’ll return to this in another post.


1 the Control of Substances Hazardous to Health Regulations

2 FEV1 is the “Forced expiratory volume in one second”. This is the amount of air that can forcefully exhaled in one second