AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) -v- PATRICIA MARGARET HANNELL as Executor of the Estate of DAVID RICHARD HANNELL (Dec) [2007] WASCA 158 (2 August 2007)

AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) -v- PATRICIA MARGARET HANNELL as Executor of the Estate of DAVID RICHARD HANNELL (Dec) [2007] WASCA 158 (2 August 2007) - WASCA 2007 case summary — Zoe

[15]

"The plaintiff suffers pleural mesothelioma. The pleura is a membrane lining the lungs and separating the lungs from other organs of the chest. Mesothelioma was first reported in 1960 in relation to the inhalation of asbestos. Knowledge as to the nature of mesothelioma has accumulated gradually over the years since 1960.

In Australia, mesothelioma is associated with the inhalation of asbestos. Generally speaking, there are three major issues relating to the connection between mesothelioma and the inhalation of asbestos: the dose issue, the fibre type issues and the lag time issue.

The risk of contracting mesothelioma is related to the dose of the asbestos inhaled. An asbestos fibre must be very small before it can be inhaled and retained in the fine airways of the lung. These tiny fibres are called respirable fibres. A dose may be calculated by counting the concentration of respirable fibres in an atmosphere. This is often expressed in terms of the number of fibres in a millilitre of air and abbreviated to the number of 'fibres/ml'. Calculations of the cumulative dose of asbestos likely to have been inhaled by an individual may be made by multiplying the concentration of asbestos fibres in an atmosphere by the time that an individual was exposed to that atmosphere. The cumulative dose may then be expressed in terms of the numbers of fibres in a millilitre of air over so many years and abbreviated to the number of 'fibres/ml years'.

The risk of contracting mesothelioma is directly related to the type of asbestos fibre which was inhaled by the individual. Studies have demonstrated that each fibre type has a different propensity to induce mesothelioma. Crocidolite or blue asbestos, is the most potent. Amosite or brown asbestos, is the median in terms of potency. Chrysotile or white asbestos is the least potent.

The risk of contracting mesothelioma is greatly increased by the expiry of time since the exposure - the lag time. Mesothelioma has a long latency period. Asbestos inhaled within 10 years of the contraction of mesothelioma is considered by relevant experts to be causally irrelevant to the contraction of the disease.

Medical science cannot explain precisely how asbestos causes mesothelioma. There are different theories. Dr James Leigh, an occupational physician, explained one theory, involving multi-stage carcinogenesis through initiation followed by promotion. Professor Bruce Robinson, a chest physician, considered this theory to be unhelpful and outdated. Professor Robinson advanced an alternative theory based upon a prolonged period of irritation and inflammation arising from the inhaled asbestos fibres. Once an asbestos fibre or fibres have initiated the carcinogenesis it is not known whether the inhalation of additional fibres has any role in the development of mesothelioma."

[205]

"(a) that the cause and effect relationship between asbestos and mesothelioma is one of the strongest associations known to medical science. This powerful association is supported by the growth in mesothelioma paralleling the growth in the use of asbestos last century, the incidence in exposed cohorts and the fact that if you implant asbestos fibres into mice you get mesothelioma;

(b) no threshold dose below which no risk of mesothelioma exists has been demonstrated. Consequently all asbestos inhalation increases the risk of mesothelioma. If a mesothelioma occurs after a period of latency after inhalation then the exposure must be presumed to have had significance in the aetiology of the disease. And each exposure contributing to the cumulative total dose will have significance.

(c) low risks calculated from comparatively low doses of asbestos may state the chance of a particular individual contracting mesothelioma, but once the mesothelioma occurs the risk is realised and the chance means nothing. It is like having tickets in a lottery; a Wittenoom worker exposed to millions of fibres has millions of tickets and a high chance; someone such as Mr Hannell or Mr Moss may only have tens of thousands of tickets and a relatively low chance of the ticket coming up; but there are a lot of people with the same number of tickets and inevitably some will win, or in the case of mesothelioma, lose. Or as in the case of uv and melanoma, another cause and effect with a strong association, everyone will get sunburnt, but only some people will be unfortunate to contract a melanoma.

(d) 'background risk' of asbestos disease other than the 1 in a million incidence in non asbestos-exposed populations is something of a misnomer. Nearly everyone in Australia has had some significant level of exposure and each time they are further exposed the total cumulative dose increases, increasing their chance of mesothelioma; of 'winning the lottery'. We are seeing more cases of so-called low dose exposure such as these cases. It may just be that the ability to identify relevant causative exposure is getting better, and our understanding of the effects of such exposures is better, so that the percentage of 'background' or 'no known exposures' will continue to lessen.

(e) In these cases we have a clear history of asbestos exposure and a subsequent mesothelioma after a sufficient, albeit short latency. The exposure is the likely cause of the disease in each case.

(f) Although the latency periods from first exposure are short in each case (about 20 years in Mr Hannell's case and about 15-17 years in the case of Mr Moss) each is a sufficient period of latency. I have seen a clear history of an 11 year latency described and I have had four patients who developed mesothelioma in their 20's; one a Wittenoom child, one who did an apprenticeship at the Midland Railway workshops, one a fitter-and-turner with no identifiable exposure and one a student at Belmont High School, one of the schools identified as having asbestos hazards. Other latencies less than 20 years are described in the literature. In my opinion these cases cannot be excluded as having been caused by the exposures described on the basis of the periods of latency."

[208]

'Whilst it's not absolutely certain, I can tell you, ... current concepts of what is most likely. The types of asbestos that cause mesothelioma or are most likely to cause it are shaped like a spear, are long and narrow, and when they're inhaled they work their way through the lungs and find themselves on the outside of the lungs where they irritate the sac in which the lung sits known as the pleura ... It is thought that over a period of time the damage caused by that fibre, which is probably made worse by breathing - if you can imagine the lung rubbing up against the pleura every time you take a breath and you've got fibres sticking out, it's always scratching the pleura causing damage and it's those repeated cycles over many years of damage and repair, damage and repair and production of molecules like oxidants that damage the DNA that allow pleura mesothelial cells to accumulate DNA damage. Now, most of the time damage does not cause mesothelioma but it is thought that in everybody that has been exposed to asbestos there is probably some DNA damage. How much DNA damage do you need to get mesothelioma? Well, the answer is every cancer cell probably has tens of thousands of mutations but most of them occur in non-dangerous genes. It's when you get a set, may be two, three, four, five, six genes, that cause cancer in that, let's say 15,000 or 11,000 mutations - call it 11,000. You need 11,000 and you get six maybe that are the dangerous ones. They are the ones that unfortunately trigger the mesothelioma but it takes a long time to accumulate that much DNA damage. When the cancer is finally triggered, it has disordered growth. Cells of course normally grow. That's how we grow from childhood to adulthood and that's how when we have a wound the skin will grow and cover it over. So growth is normal but cancer is when that growth has lost its controls. I guess like a mob out of control. That happens because of a number of reasons but the simplest way to think about it is that the cell growth is driven by an accelerator, which are growth factors and by brakes which stop growth, so that when your skin has healed from a wound the body realises that and the skin stops growing. So there's an accelerator and a brake and cancer is when there's too much accelerator and no brake. The things that are accelerators are ... things called oncogenes and the things that are the brakes are things called tumour suppressor genes and mesothelioma clearly has disorders in both of those two things. So it grows. It takes a while to kick off but once it has kicked off it grows relentlessly unfortunately ...'

[244]

"Given Mr Hannell's development of pleural mesothelioma with a relatively short latency interval and only light asbestos exposure (and provided that he did not sustain any exposure to asbestos apart from those exposures recorded in your letter of 07 April), there appears to be a reasonable likelihood that he has an underlying innate/acquired susceptibility to carcinogenesis - specifically mesothelioma induction - by asbestos. Even so, it would be highly unlikely that any such predisposition to the carcinogenicity of asbestos would find expression as mesothelioma, in the absence of the asbestos exposure (in other words, if no exposure, then no mesothelioma, at a good order of probability).

Therefore, although Mr Hannell's first 'handyman'-type exposure in 1983 was apparently chrysotile-only exposure, it is worth pointing out that the risk of mesothelioma from chrysotile only exposure although substantially less on a fibre-for-fibre basis than for the amphibole forms of asbestos, it is not a zero risk. Therefore, it is my assessment at a reasonable order of confidence and a level of reasonable medical certainty that Mr Hannell's pleural malignant mesothelioma is attributable by way of causal-contributory relationship to his total cumulative 'handyman'-type asbestos exposures sustained in 1983, 1985 and 1990 as set forth in your letter of 07 April 2006. I suspect that the 1990 exposure may have made a somewhat (but unquantifiably) greater causal contribution towards the development of Mr Hannell's mesothelioma than the earlier 1983 chrysotile-only exposure, but the effect of the lower potency of chrysotile-only exposure for mesothelioma induction is offset to some degree in this case by the earlier timing of that 1983 chrysotile-only exposure. The point is that it is my assessment that the combined and cumulative effects of the 1983 + 1985 + 1990 exposures was significant for causation of Mr Hannell's mesothelioma.

It is also my assessment that the causal relationship between Mr Hannell's 1983 + 1985 + 1990 exposure took the form of a causal-contributory relationship, whereby his total cumulative 'handyman'-type exposure imposed a significant increase in the risk of developing mesothelioma, by way of an incremental risk on top of any underlying background risk of mesothelioma in Mr Hannell's case." (not my emphasis)

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AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) -v- PATRICIA MARGARET HANNELL as Executor of the Estate of DAVID RICHARD HANNELL (Dec) [2007] WASCA 158 (2 August 2007)

Cases Cited (33)