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Written on 25th July 2016 by Laura Magson

Asbestos exposure can cause a multitude of diseases to include pleural plaquespleural thickeningasbestosis, pleural mesothelioma, peritoneal mesothelioma and asbestos induced lung cancer, the latter 3 of which are fatal conditions.

For medical practitioners to confirm a link between asbestos exposure and each of these diseases it is essential to establish exactly how much asbestos a person was exposed to.  This can be determined by conducting air tests in a work place, from witness evidence or by counting fibres of asbestos within a person’s lung.

Air tests

Air tests are (in simple terms) conducted by placing a hoover styled machine in a work place.  The machine is fitted with a filter which catches microscopic asbestos fibres as they are sucked through the machine.

Scientists will then examine the filter in numerous places and will count the microscopic fibres.

The count of the microscopic fibres is then averaged against the number of slides reviewed to calculate the number of fibres in the air.  This is known as a fibre ml count and literally counts the number of fibres present in each millilitre of air in the work place.

Witness evidence

When conducting fibre tests the scientist will also take notes as to the visible dust/fibres present in the air and the practice taking place to produce the visible dust/fibres.

Where fibre ml counts have not been conducted a witness can provide oral evidence as to the workplace practices he was conducting and the visible dust/fibre in the air.

Experts can then compare the witnesses account to scientific notes and previous fibre ml counts to determine how much asbestos was likely to be present in the witnesses vicinity.  Once this task has been conducted it is usual to be able to predict a likely fibre ml count that the person encountered.

Lung sample counts

Lung sample counts are conducted in a similar way to air tests, i.e. microscopic fibres are counted on lung tissue.

So how much asbestos exposure is required to satisfy a diagnosis of asbestos or lung cancer

The Helsinki criteria

In 1997 a group of scientists concerned with asbestos exposure met in Helsinki to discuss asbestos fibres and the effect of the same on a person’s health.  As a result of this conference a fibre ml level of 25 fibre/ml years was deemed to be the level upon which asbestosis or lung cancer could be deemed as being caused by asbestos exposure.  This is now known as “the Helsinki Criteria”.

To satisfy the Helsinki criteria an asbestos victim must show that his exposure was above 25 fibre/ml years.  This level of exposure can be accrued in a number of ways, i.e. 1 years exposure at 25 fibre/ml or 5 years exposure at 5 fibre/ml per year.  In general terms a year of substantial exposure or a longer term of moderate exposure is required to satisfy the criteria.

But is the Helsinki criteria outdated?

The Industrial injuries Advisory Council

In its 2005 paper entitled, “Asbestos-related diseases”, the Industrial Injuries Advisory Council (“IIAC”) considered the criteria by which asbestosis could on the balance of probabilities be attributed to asbestos. The paper at paragraph 60 says this about the Helsinki criteria:

“In 1985, Sir Richard Doll and Julian Peto reviewed the evidence for health hazards associated with asbestos and as far as asbestosis was concerned they concluded that there was a threshold of cumulative exposure below which clinical disease did not occur. They judged that this threshold was about 25 fibres/ml. years (that is an exposure equivalent to 25 years at 1 fibre/ml, 10 years at 2.5 fibres/ml, and so on). It is still believed that the threshold for asbestosis for most people is around this level…

In 1997 the Helsinki workshop proposed that attribution to asbestos should be assumed in cases of lung cancer with 25 fibre years exposure …

There are … problems with the use of 25 fibre years as an exposure criterion”

First, the Council received evidence that the risk of lung cancer varied between different industries at similar levels of cumulative exposure to asbestos; this was in part, but not wholly explained by, exposure to different asbestos fibre types. Using 25 fibre years is unlikely to be valid for all occupations. The Council recognises there are variations in risk from different types of asbestos, but most workers are exposed to mixtures of fibres and for the purposes of the Scheme the common properties must be considered.

Second, calculation of risk based on this formula is not a very satisfactory method for deciding occupational attribution for the purposes of the Scheme. This can be illustrated using another risk formula produced by Doll and Peto in 1988 from which it can be calculated that a doubling of risk of lung cancer would be reached on average only after 100 fibre years asbestos exposure. The level of exposure required to double risk of lung cancer can be calculated as 25 fibre years or 100 fibre years depending on the risk formulae used, demonstrating the difficulty of using this method for deciding attribution….”

This is the current state of scientific opinion on the issue.

The IIAC concluded that:

“We recommend that diagnosis of asbestosis be based on clinical evidence of interstitial pulmonary fibrosis and a history of substantial asbestos exposure. High counts of asbestos bodies or fibres in the lungs may be used to support the diagnosis of asbestosis. However, a lack of asbestos fibres or bodies should not be used to exclude a diagnosis of asbestosis as asbestos bodies may be absent and fibres not increased above background level in clear cut cases (i.e. these counting techniques have a significant false negative rate).”

The IIAC continued:

“42. The Council recommends that:

  1. a) Diagnosis of asbestosis should be based on clinical evidence of interstitial lung fibrosis and a history of substantial occupational exposure to asbestos.
  2. b) The absence or low numbers of asbestos bodies or asbestos fibres in the lungs should not be used to exclude a diagnosis of asbestosis in claimants with a history of substantial occupational asbestos exposure …

Provided IIAC’s new criteria are met, the chance that a patient has asbestosis (rather than idiopathic pulmonary fibrosis) is more than doubled.”

So the new test appears to be one of considering whether a person has suffered “substantial” exposure to asbestos.  But what constitutes substantial exposure?

Case law on the point

In the case of Wallhead v Rushton and Hornsby Ltd. (1973) 14 KIR 285, Bagnall J. considered that “substantial” meant “not negligible”, and this meant a lot of dust when given off, not merely by accumulation over a period.

This approach was accepted by Roger Toulson QC, as he then was, in Bailey v Reed Corrugated Cases Ltd. (1993), where he found that an outsider going in to a factory during an asbestos clean-up would have said that the operation gave rise to clouds of dust or “lots of dust”.

Substantial therefore appears to mean a lot of dust when given off and not necessarily as high a count as 25 fibre/ml years.

The position moving forward

In many cases where asbestos exposure is extremely high the Helsinki criteria may be suitable to confirm that asbestos exposure levels were such to have caused a disease.

In other cases the asbestos exposure levels may not satisfy the Helsinki criteria in precise fibre ml terms, but, if the exposure can be described as “substantial” and “not negligible” then an asbestos victim may be able to prove the link between his asbestos exposure and his disease.

Our view

In most asbestos related disease claims a victim has no other explanation for his condition other than his exposure to asbestos in the workplace.  For a victim to be denied compensation simply because he does not meet a specific fibre ml threshold will often seem unjust, especially where he has suffered substantial asbestos exposure in the past.