Davies v Manildra Flour Mills (Manufacturing) Pty Limited - [2006] NSWDDT 23

No judgment structure available for this case.

Dust Diseases Tribunal

of New South Wales

CITATION: Davies v Manildra Flour Mills (Manufacturing) Pty Limited [2006] NSWDDT 23

PARTIES: Anthony Joseph Davies
Manildra Flour Mills (Manufacturing) Pty Limited

MATTER NUMBER(S): 152 of 2003

JUDGMENT OF: Duck J

CATCHWORDS: Dust Diseases Tribunal :- Dust disease
Occupational asthma
Farmer's lung
Whether a dust which caused asthma might also have caused farmer's lung
Damages

LEGISLATION CITED: Workers' Compensation (Dust Diseases) Act 1942
Workers' Compensation Act 1987, s 4
Workplace Injury Management and Workers Compensation Act 1998

CASES CITED: Britt v Manildra Flour Mills (Manufacturing) Pty Limited (2006) NSW DDT3;
Hampton Court Limited v Crooks (1957) 97 CLR 367 at 371;
CSR Limited v Darcy (1996) 40 NSW LR 721;
Griffiths v Kerkemeyer (1977) 139 CLR 161

DATES OF HEARING: 20 September 2005 and 19, 21, 22 and 23 June 2006

DATE OF JUDGMENT:
07/07/2006

EX TEMPORE JUDGMENT DATE: 07/07/2006

LEGAL REPRESENTATIVES:
Mr A J Bartley, SC with Mr G Sarginson instructed by Higgins and Higgins appeared for the plaintiff
Mr A C Scotting instructed by Moray and Agnew appeared for the defendant

JUDGMENT:

1. The plaintiff was born on 23 April 1964. He is now 42 years old. He has worked for the defendant Manildra Flour Mills (Manufacturing) Pty Limited since 1981 ie from age 17. He worked in the defendant’s flour mill at Manildra. He alleges that in his employment he was negligently exposed to and inhaled dust particles and fibres which have caused the condition known as occupational asthma. He seeks damages.

2. The reason the proceedings are brought in the Dust Diseases Tribunal is that the plaintiff asserts that his occupational asthma comes within the definition “dust disease” set out in the Workers’ Compensation (Dust Diseases) Act 1942. That definition is in the following terms:

Dust Disease means any disease specified in schedule 1, and includes any pathological condition of the lungs, pleura or peritoneum, that is caused by dust that may also cause a disease so specified.

One of the diseases specified is farmer’s lung. It is not suggested that the plaintiff has farmer’s lung. Rather he contends that the dusts which he has ingested have caused the occupational asthma and that they may have also caused farmer’s lung.

3. The defendant’s amended defence admits employment from 14 January 1981 to date. It also admits that it was in breach of a duty owed to the plaintiff and that the breach caused the plaintiff to develop occupational asthma.

4. The defendant disputes that the plaintiff’s occupational asthma comes within the definition of dust disease in the Workers’ Compensation Dust Diseases Act 1942. If the defendant is successful on that issue then it is common ground that the plaintiff has not complied with the modified common law provisions contained in the Workers Compensation Act 1987 and the Workplace Injury Management and Workers Compensation Act 1998.

5. It is helpful in this regard to remember that the definition of injury in the Workers Compensation Act 1987 s 4 is in the following terms:

Injury –

(a) means personal injury arising out of or in the course of employment;

(b) includes –

(i) ………………..

(ii) ………………..

(c) does not include (except in the case of a worker employed in or about a mine to which the Coal Mines Regulation Act 1982 applies) a dust disease, as defined by the Workers’ Compensation (Dust Diseases) Act 1942, or the aggravation, acceleration, exacerbation or deterioration of a dust disease, as so defined.

6. A similar argument was had in a matter of Britt v Manildra Flour Mills (Manufacturing) Pty Limited (2006) NSW DDT 3. Mr Britt was a work mate of the plaintiff’s. In Mr Britt’s case the matter was determined as a preliminary matter pursuant to consent orders made in the Tribunal. The question was resolved in Mr Britt’s favour. The defendant has appealed and the matter is set down for argument in the Court of Appeal some time in September to the best of my knowledge. The evidence in the present case is a little more extensive than was the evidence in Mr Britt’s case.

7. The plaintiff’s first job at the mill was filling hessian bags with flour, weighing them and sowing them up. The flour came down through a chute into the bags. This was associated with some dust (T12).

During the time he was doing that job namely the first two or three years the plaintiff went into other areas in the mill (T12). As time passed, he said, he worked in every part of the mill. (T12)

8. He described how wheat was delivered by truck and rail to the mill. It was dropped into a hopper from which an elevator took it to storage in the wheat silos. The wheat went into tempering bins into which water was introduced. (T13) The purpose of wetting the wheat was to permit it to be milled without shattering. The tempering bins varied in size but they held about 60 to 100 tons of wheat. As later evidence demonstrated in the tempering bins water comprised up to 12.5 per cent by weight of the contents of the bin. The plaintiff said (T13) that condensation ran down the in side of the bins. It took three or four hours to fill a bin. (T14)

9. Before the wheat was milled there was a second tempering. The wheat was moved to the next lot of bins. Further water is added at that stage. (T14) To get the wheat out of the first tempering bin the wheat is released through the bottom of the bin onto conveyors. (T14) The plaintiff said the bins were tall and skinny and perhaps 60 foot high although he wasn’t sure of the height. (T14)

10. Then the wheat apparently goes from the second tempering bin into the first break bin. (T15) Then it is crushed, then it goes through a second break. The by-product from the first break mill is bran. That is the outside of the wheat. After going through the second break mill the wheat is close to flour. Any that is not in the appropriate state is sent back through the mill again. About this aspect of the treatment of the wheat the plaintiff said at T16 lines 14 to 17 “there’s four break rollers which is still breaking the wheat up and after that they call them flour, the rest of it sort of coming up to flour then, and there’s probably a dozen other rolls for it to go through back and forward before it becomes flour.”

11. The better quality flour is white. The lesser quality flour is not as white and has small bran particles in it (T16). Bleach and chlorine are added to some of the flour to make sponge flour which is the whitest of the lot. (T16) Whoever does the milling, and this included the plaintiff, the responsibility includes making sure the chemicals are in the chemical mixer and fed out at the desired rate to the flour being milled. (T16)

12. As time passed the plaintiff was rotated around three jobs. They were flour milling, mixing plant operator who worked on the wheat silos, and storeman . (T16)

“I work three weeks on the wheat and three weeks in the mill”

“my job was to test the wheat and unload all the wheat into the appropriate silos.”

“Just a shortness of breath and dry cough and that was the main sort of thing and just a sort of irritation in my chest.”

13. The plaintiff married on 6 May 1989. He was having breathing problems by that time. He had been playing rugby league with the Manildra Rhinos but he stopped playing in the year that he married. He had seen doctors about his breathing by that time. He had also had time off work because of breathing difficulties. (T18)

14. When the wheat was transported from the big silos to the tempering bins there were sometimes blockages of the bins (T19). They had to be unblocked. About the blockages the plaintiff said at T19:

Once the water had been added to the wheat in first temps the wheat wants to hold, it doesn’t want to run naturally because it’s had that water added, it doesn’t want to run through the holes at the bottom.

sort of stars where the wheat comes through into them.

“white and greeny sort of mouldy”

“all you can see is just dust, it’s just full of dust.”

The dust and the mould would be taking your breath away it was just that strong.

Well you’d have to get out and have a spell, you just couldn’t stay in there for any length of time. You’d have to get out and just have a break and get some fresh air before you get back in again.

At the end I could probably stand there 20 minutes and I’d have to get out, just the heat and humidity in there and the dust, you’d just couldn’t stay in there.

The wheat of course is giving off heat at this point?

Yes.

You said at the end you could only stay in there only 20 minutes, before that how long would you be in there each time?

I don’t think you could – no one could stay in there too long, you just couldn’t stay in there.

A. Yes.

A lot of times one would come out and if you couldn’t cope with it then someone else would go and spell you sort of.

Q. Right

A. If you were lucky to have someone around.

15. Sometimes the plaintiff had to get into the silo to clear a blockage using compressed air. In respect of that work he was asked at the foot of T22:

Q. Did it have the same mouldy appearance that you have described, this white and green sort of colour?
A. Not quite as bad as the stuff on the side but yes.

You just couldn’t stay in there sort of too long.

How long would you have to be out before you go back in again

Five or ten minutes till you just got your breath again.

16. Cleaning out the bin to permit new wheat to be introduced for a new product required a similar type of exposure. (T23) Sometimes the plaintiff said the wheat was so mouldy it was just green (T23) and dry and dusty. The mouldy wheat except for the clumpy bits that would not pass through the milling process was milled and turned into flour. When that happened the flour was mouldy. (T24) On occasions export flour has been rejected because it has mould in it. It is then brought back to the mill and reworked and sent to a factory in Nowra to make starch from which ethanol is made.

17. Flour and wheat dust have to be mopped up from the floor every day. (T24) If mouldy wheat is milled then the whole mill reeks of it (T25). The plaintiff was asked about the handling of mouldy wheat. At T26 he said this:

It went into the mill to the point where it couldn’t physically go through the pipes, then they’d have to pull the bottom of the bin off and they just let it go run on the ground.

You’d feel the heat coming off it, it gives off a heat.

Which was dustier three weeks at the wheat end or three weeks in the mill?

Well none of them is real choice you’d have your battle in each department a little bit if you didn’t have to get in silos you’d have a good week but if you’d have to get in silos you didn’t have a real good week.

18. One three week period was worked in the mixing plant. Flours had ingredients added to them in the manner described at T26. This too was dusty work. When asked:

The plaintiff answered:

(T26)

19. Cleaning out machinery was dusty (T27) In this regard the plaintiff said:

You’re lucky it will only happen once, sometimes none but sometimes it would be three times a day depending how many – if your changing from white flour to brown flour you’ve got to totally clean the machinery out and blow it out.

The plaintiff said (T28) that the flour that didn’t make the grade was sent to Nowra for conversion into ethanol.

20. In cross examination the plaintiff confirmed that there was a difference between silos and conditioning bins: the conditioning bins were cylindrical in shape and there were 12 of them on each side of the mill, the A side and the B side. Silos are the biggest receptacle at the mill in which the wheat is stored initially. As far as possible the wheat goes in dry. Tempering bins and conditioning bins are the same thing. It was inside the conditioning bins that the plaintiff experienced the severe exposure he had previously described. Sometimes the cleaning out of silos was not simply a dry dusty job. Sometimes there was mould and wet stuff right up around the silos and right around the rims of the silos. (T75). In the old days before the tempering bins had been built the wheat was tempered in wooden bins which had metal inside them. (T75) The wooden bins were more than 20 feet high. The tempering bins were erected whilst the plaintiff was employed by the defendant.

21. As to the frequency with which the plaintiff had to get into the tempering bins he said:

It all depended on what happened on your shift.

The plaintiff had to get into the tempering bins less frequently than once a week. It could be once every three week period or if you are really unlucky it could be twice (T77). The plaintiff was asked how long he would have to work on the tempering bins, allowing for the fact he had to come out after 20 minutes or so and have a break.

He said (T77.26):

We could be talking about hours like all depending, it could be hours there’s no set thing it all depends how bad it was and how long it took us.

It could have been longer, you know, I can’t give you a definite time, it’s not something you time it’s just a job you’re given.

But it certainly did not take eight hours.

If I said that two hours was a average when it was worst of the worst would that be fair.

(T77.40)

On an average the plaintiff agreed that it was probably for two hours. He was unable to say the longest time he’d spent doing that work. He agreed that from time to time the mould was worse than at other times. (T78)

22. Cross examination at T79 had the thrust of suggesting to the plaintiff that he was exposed to a lot of flour at the mill to which he agreed. He was asked (T79.18)

23. The plaintiff agreed in re-examination that earlier in his career he was able to spend longer than 20 minutes in the tempering bins. The plaintiff said of the comparison between being in the mill generally and being in the tempering bin:

There’s just no comparison between the two – like in the mill I could tolerate it – in the conditioning – I just couldn’t tolerate it, if I didn’t get out I’d probably pass out I’d probably pass out in there. I was that severe at times.

24. I conclude that the plaintiff had significant exposure to wheat dust, flour, and mouldy grain. On occasions the exposure to mouldy grain was severe.

25. It is convenient to mention in this regard exhibit PX7, a memo directed to the plaintiff on or about 9 April 1999 in which the Manager, Mr Campbell wrote:

The present condition of hygiene and cleanliness in both mills is atrocious.

Does mould exist in the first tempering bins during the tempering process?

Moulds are likely to be present in the tempering bins.

26. It is not disputed that the plaintiff’s exposure to dusts in the course of his employment by the defendant resulted in him contracting asthma. A central question remaining in dispute is whether the dusts which cause the asthma could also have caused farmer’s lung. The plaintiff relies principally on the evidence of Associate Professor David Bryant which says that it could. Dr Bryant is a specialist physician and for the last 12 or 14 years has been Chairman of the Medical Authority of the Dust Diseases Board. He said in his first report bearing date 17 September 2003 that the plaintiff’s clinical history is indicative of the gradual onset of asthma beginning in 1983. He now has evidence of severe airflow limitation (pg 2). In the last paragraph on pg 4 of the report the following appears:

The disease known as Farmer’s Lung is a disease in which an allergic reaction occurs in the lung tissue to dust particles containing substances to which the worker has become allergic (in the case of Farmer’s Lung mould spores from mouldy hay). The disease Farmer’s Lung can occur in grain dust workers although whether or not this is due to the grain dust itself or fungal, bacterial or storage contamination of the grain has not been clearly established. (Authorities quoted)

27. There is a further report bearing date October 13 2004 following Professor Bryant’s reassessment of the plaintiff. The doctor assessed the plaintiff as having whole person impairment of 40 per cent, all of which is due to his asthma (pg 2).

28. A third report bearing date October 26 2005 was supplied. The third paragraph is in the following terms:

The types of agents implicated in Farmer’s Lung are generally believed to be thermophilic actinomycetes including Saccharopolyspora Rectivirgula (formerly Micropolyspora Faeni) (Rose, page 1783 in Textbook of Respiratory Medicine,Edited by Mason et al, 4th Edition, Vol. 2, Elsevier, Philadelphia, 2005). These bacteria thrive at temperatures between 50 – 55 degrees Centigrade in moist conditions and secrete enzymes that cause decay of vegetable matter. In addition a variety of fungi can germinate producing a diverse range of moulds and yeasts including Aspergillus, Penicillium and other moulds. Immunological responsiveness to these type of agents are widely used to assist in the diagnosis of conditions such as Farmer’s Lung (Rose, 2005, Ibid).

Exposure to moulds from mouldy hay or mouldy grain has been associated with the development of conditions such as Farmer’s Lung (Cormier, page 229 in Occupational Disorders of the Lung, Edited by Hendrick et al, Saunders, London, 2003 ; Selman, page 452 in Interstitial Lung Disease, Schwarz & King, 4th Edition, Decker, Hamilton, 2003; Fink & Zacharisen, page 1373 in Allergy Principles & Practice, 6th Edition, Edited by Franklin Adkinson et al, 2nd Vol., Mosby, Pennsylvania, 2003).

Professor Bryant provided copies of the texts to which he had referred.

Professor Bryant said of the books to which he had referred:

I gave those references because they are all regarded as the outstanding books that would be used by specialists in those areas as their major sources of material and information.

29. Alveolitis is the word used to describe inflammation of that area of the lungs where the small air sacks are, which are called alveoli. This is the part of the lung where gas exchange takes place. The inflammation can be called either alveolitis or pneumonitis, both words mean the same thing. (T94.35-38). Professor Bryant said that: the antigen bacterium faeni rectivirgula.has gone through several name changes over the last 20 years and is now referred to as saccharopolyspora rectivirgula (T94,T95).

30. Hypersensitivity pneumonitis is also known as extrinsic allergic alveolitis.

These antigens encompass a wide variety of organic particles, such as mammalian and avian proteins, fungi, thermophilic bacteria, and certain small-molecular-weight volatile and non-volatile compounds. The disease is characterised by a diffuse and predominantly mononuclear cell inflammation of the small air ways and pulmonary parenchyma.

Hypersensitivity pneumonitis may occur in several clinical forms and may lead to irreversible pulmonary damage that depends on several factors including the amount and duration of exposure to the antigen, the nature of the inhaled dust and the host response. (ibid)

The two most adequately studied and best known forms of HP are farmer’s lung and pigeon breeders disease (PBD).

Disease Antigen Source

Fungal and

bacterial

Farmer’s Lung Faeni rectivirgula Moldy hay, grain, silage

31. At T94.42 the following question and answer appear in Professor Bryant’s evidence:

32. In the Selman article under the heading Pathogenesis the following appears:

The pathogenesis of HP is intricate, and many of the immunopathologic processes – as well as the sequence of events involved in the development of alveolitis – are poorly understood.

At T95 Professor Bryant was asked this question:

Q. If the inhaled antigen is a dust which includes in its composition the saccharopolyspora rectivirgula then is that likely to cause irritation and inflammation throughout the whole of the airways?

A. Yes.

Q. Is there any significant or important difference between the area in the bronchi that becomes inflamed and irritated in asthma and the area where if alveolitis occurs the inflammation is located?

A. Yes. It would result in different symptoms. It would result in ease or difficulty in diagnosis but the nature of response of the body in the two locations is similar.

Q. From a tissue analysis point of view is there any significance between the tissue that becomes irritated and inflamed in asthma and the tissue that becomes irritated and inflamed in alveolitis?

A. Yes. In asthma the area of irritation is the smaller airways and alveolitis in the tissue which becomes irritated is the alveoli.

Q. Are they different from a biological point of view?

A. No. One merges with the other and in these conditions you would invariably have inflammation of both areas but in some patients the inflammation in the alveoli predominates and in other patients the inflammation in the airways predominates. Indeed in a given person over a period of time the major location of the inflammation may vary.

33. Professor Bryant went through the various texts which he had supplied and further illustrated the opinion which he had proffered. There is no need in the present judgment to go to each of them in detail.

34. At pg 229 of the article by Yvon Cormier under the heading Epidemiology the following appears:

The disease is seen worldwide, different regions associating it with different occupational environments and different causal antigens. For example, farmer's lung is frequent in cold humid climates like those of Eastern North America or Northern Europe, pigeon breeder's disease is the most important type in Central and South America, summer-type HP predominates in Japan, and humidifier lung may occur with dramatic prevalence (15 to 70 per cent) without regard to geographic region in small populations working in contaminated offices.

Agent source appellation –
Aspergillus fumigatus Vegetable compost – Farmers’ lung

Thermophillic actinomycetes Hay/straw/grain/ Farmers’ lung

(Saccharopolyspora mushroom compost/ Mushroom worker’s lung Rectivirgula) bagasse Bagassosis

35. In Murray and Nadell's textbook of Respiratory Medicine, 4th edition, chapter 62 is entitled "Hypersensitivity Pneumonitis." It is written by Cecile S Rose, MD, M.P.H. At p 1784 the following appears:

Thermophilic actinomycetes, including saccharopolyspora rectivirgula (formerly Micropolyspora faeni) and the Thermoactinomycetes species vulgaris, sachari, viridis, and candidas, are associated causally with the prototypical example of HP, farmer's lung disease, first described by Campbell in 1932. These bacteria thrive at 50 degrees celsius to 55 degrees celsius and in moist condition, and secrete enzymes that cause decay of vegetable matter such as hay (FLD), sugar cane, (bagassosis), and mushroom compost, (“mushroom worker's lung”). ...

Stringent diagnostic criteria may underestimate milder cases of HP in which the chest radiograph is normal or when symptoms are subtle or insidious…… The likelihood that unrecognised HP occurs also is based on several other factors: (1) the signs and symptoms of illness and clinical diagnostic findings are nonspecific and mimic many other diseases, such as asthma, influenza, viral pneumonia, sarcoidosis and idiopathic pulmonary fibrosis (Table 62.4); (2) .....

36. Professor Bryant was asked at T98 what significance he attached to the table 62.4. At T98.47 he said:

It's describing the view that symptoms of asthma are very common in people with a hypersensitivity pneumonitis.

Q. - With the same cause.

A. - Yes.

37. Underneath the table at the foot of the first column and at the top of the second column some material appears about Farmer’s Lung. Professor Bryant was asked at T99.12.

Q. - Is that again describing exactly the same view, or supporting the view that you have, that the same dust that can cause farmer's lung disease, that is the alveolitis, can also cause asthma.

A. - Yes it is.

Thus, although some patients with HP recover completely, permanent sequaelae of the disease include asthma, emphysema, and (sometimes progressive) interstitial fibrosis.

Q. - Do you agree with that statement.

A. - I agree with that statement completely.

Q. - If that statement is correct then the asthma, which is a permanent sequela of the disease has been caused by the same dust that caused the disease itself.

A. - Yes.

38. At the foot of T99 and the top of T100 the plaintiff's working conditions inside the tempering bins were described to Dr Bryant. He was then asked:

Q. - Is that from your knowledge of farmer's lung the type of dust exposure that could well lead to farmer's lung.

A. - Yes, it is, because it is describing intense dust exposure and, in the majority of cases that I have seen, hypersensitivity pneumonitis occurs more commonly in workers who have more intense dust exposure rather than low levels of dust exposure.

Q. - I would like you to assume also that there were some days when that mouldy wheat, containing a combination of fungal and bacterial material, the fungal being either aspergillus or penicillium or both and that the bacterial including significant quantities of the saccharopolysporum bacteria, that there were some days that that wheat was itself put through the mills and turned into flour and that on those days the mill itself smelt of the mouldy wheat being converted into flour and that that flour was itself disseminated as a dust throughout the atmosphere in the middle. Would that flour still contain both the fungal and bacterial material.

A. - Completely. It would be a fine form and so easy to inhale.

39. In cross-examination at T103 Professor Bryant said:

So farmer's lung actually describes the development of a chest condition in farmer's who were using mouldy hay in barns in Europe in winter. Where mouldy hay is being thrown around within enclosed spaces.

Q. - So is what you are talking about in respect of this plaintiff his risk of developing hypersensitivity pneumonitis rather than farmer's lung as it has been classically stated.

A. - Farmer's lung is a blanket term that's used to describe people who develop an inflammatory condition of the lungs in response to the exposure to mouldy cereals or cereal products.

40. At T104 Professor Bryant agreed that thermophilic actinomycetes are widely disseminated but in small amounts. For them to be implicated in a respiratory disease one would expect them to be present in high quantities.

The Professor agreed that those organisms could be present in air conditioning units.

41. Professor Bryant agreed that there have been no epidemiological studies in Australia in respect of farmer's lung. He added the last scientific paper published in Australia on farmer's lung was published by himself back in 1971 and he has not seen a paper published since then on farmer's lung. He was then asked at T105.5:

Q. - Is that not indicative, doctor, that the environmental conditions are not present, that would usually lead to the development of farmer's lung in Australia.

A. - It may be that. It may be that workers developed these conditions and then leave the industry. It may be the condition is not diagnosed. I am not aware, all I can say is, well, I am not aware of any diagnosis.

42. The Professor agreed that dry grain dust can cause respiratory conditions (T105.19). It was possible that this was at the root of the plaintiff's problems. He was asked whether the plaintiff's symptoms could be a reaction to flour. The Professor agreed it could be although he was not aware of that condition occurring with any frequency in wheat silo workers and he added that doctors would generally describe baker's asthma differently insofar as the nature of the agents which cause asthma in bakers is different to the nature of the substances that you become sensitised to or react to if you are a wheat silo worker or if you work in flour mills (T105.25). The Professor was then asked about flour exposure. At T105.44 he said:

A. - All I can say is, well, this man's symptoms suggest to me that he is - has occurred as a consequence of an agent to which he has been exposed to at work and he has been exposed to a number of agents at work and one of those agents may be flour. Other agents would include the various fungal and bacterial products which may have contaminated the flour and because none of the tests that were done of him were successful in demonstrating a reaction either to flour or to other fungal products, we don't really have any scientific basis for being sure about what it was so it may include it all, or some of the substances that I've mentioned.

Q. - What we are presenting in this case, doctor is, it is really a range of possibilities, is it not, and no possibility particularly stands out better than any other, does it.

A. - No.

43. In re-examination the following question was put:

Q. - You were asked, if I may say so, a very standard last question in cross-examination, 'Well, there's a number of possibilities here, are they all possible.' Doctor, do you remain of the view that this man suffers from a condition, namely, asthma, caused by a dust which causes farmer's lung.

A. - Yes.

44. Related to the opinions of Professor Bryant are the opinions provided by Dr Hocking. She is a senior principal research scientist with the CSIRO. She describes herself as a food mycologist.

45. Mycology is the study of fungi or moulds, fungi and mould being interchangeable. (T107) Mycotoxins are metabolites produced by moulds that are toxic to animals, humans or other biological systems. Mycology is a subset of microbiology. Dr Hocking was the lead author of an article published in the International Journal of Food and Microbiology 85 (2003) 137 to 149 entitled "Microbiology of Wheat and Flour Milling in Australia." In her first report of 18 November 2005 Dr Hocking dealt with the moulds most commonly associated with stored wheat. She said that they fell into two categories: those that are already on the wheat when it is harvested (field fungi) and those that may develop during storage (storage fungi). In the category of storage fungi the most common fungi are species belonging in the genera aspergillus and penicillium. If grain becomes moist during storage these fungi may develop to high levels causing clumping and caking of grain. There are too many species from these genera to list individually those that may be found in grain that has gone mouldy during storage.

Wheat is wetted ("or conditioned") immediately prior to milling to ensure that the grain has become pliable enough to be milled into flour without shattering. Conditioning may be as short as 8 hours, or, if left over the weekend as long as 48 hours. During conditioning, the moisture content of the grain is generally not sufficiently high, and the time frame of this increase moisture level is insufficiently long to allow substantial growth of fungi. However, the higher moisture content can contribute to growth of moulds in dust and residues on the walls of silos. The moulds most commonly associated with this residue are Aspergillus and Penicillium species.

... there is

some

bacterial growth, during conditioning with slight increases in counts of Bacillus, coliforms and other common bacteria that can be found on the grain surface.

The report goes on:

However, during the conditioning process moisture, grain dust and grains themselves will adhere to the sides of the silo or bin. It is in this residue that most microbial growth occurs, as this residue remains behind after the conditioned grain is emptied from the bin or silo. Microbial colonisation of stored grains, and residues adhering to the walls of grain storage bins, occurs in a succession which is determined by the available moisture and the temperature of the grain bulk or residue. This process is known as microbial succession. A pioneer species such as aspergillus penicillioides, which is able to grow at low moisture content, becomes established and starts to grow slowly. As it grows some metabolic moisture is generated which in turn raises the moisture content immediately surrounding the established mould colony, and the spores of other types of moulds, which require high moisture content, are then able to germinate and grow. This process continues, with more moisture being produced and more types of moulds growing. This increased metabolic activity also generates heat. As the moisture level and heat generation increase, some moulds die off, as the conditions become less suitable for them. Eventually at temperatures above 50 C most of the moulds are unable to grow. By this stage, the moisture level is high, and the bacteria, particularly thermophilic actinobacteria (eg Saccharopolyspora rectivirgula) are able to proliferate. Even though the moulds die off their spores and hyphae remain as part of the mass of material adhering to the silo walls.

At T110.38 the doctor was asked:

Q. - Then once water was introduced and assuming the wheat is left long enough so that it at times up to 48 hours, and it is able to cake up to a foot thick on the sides of the bin, so assuming that is the case, then has that pioneer species advanced in terms of how many spores will be present.

A. - It certainly would have, or it may even have been replaced by other species that prefer a more moist environment because the conditions that you are describing to me with grain a foot thick on the silo walls, that to me would take longer than 48 hours to occur.

Q. - Let us just take the 48 hours first. These pioneer species which are all a form of fungi or mould, do they include others other than aspergillus penicillioides.

A. - Yes, there are a number of species that are closely related to aspergillus penicillioides and some other aspergillus species that are known as eurotium. These have an aspergillus state - it starts getting complicated now. But they are also xerophiles and they also are the early colonisers of grain that is slightly above moisture content that is safe.

Q. - As they continue this process of colonisation, these fungi, do they produce an environmental effect in the area where they are proliferating.

A. - They certainly do. The metabolic activities of this fungi are such that they are breaking down the starch to sugars and then the sugars to carbon dioxide and water. This is an exothermic reaction so they're producing both moisture and heath while they're growing.

Q. - Are they able to survive in heat up to a certain level.

A. - Up to a certain level, but as the conditions change the organisms that find those conditions suitable will also change, and so as you get the moisture increasing and the temperature increasing that's what we call microbial succession. The species that started off at the beginning will sort of be overgrown or left behind or even die out and other species that prefer the conditions of slightly higher moisture and temperature will take over.

Q. - So if the process starts at the ambient temperature, whatever that may be, and it does not matter much at the moment, then as the colonisation by the fungi proceeds then the temperature within that area, that is the caked on material, will increase.

A. - It will increase, yes.

Q. - As the temperature is increasing will the proliferation of thermophilic actino bacteria increase.

A. - Yes.

Q. - But the thermophilic actino bacteria including saccharopolyspora rectivirgula thrive.

A. - Yes.

Q. - What is it about the storage process, leave aside for the moment moisture, the storage process itself that causes them to become identifiable (ie the storage fungi).

A. - Well, partly because the field fungi have died off so there's less competition when you are looking at what's actually present on the grain. But also in the storage environment such as silos and transport also, trucks and things, the dust and adhering grain particles will contaminate the incoming grain with the spores of the aspergillus and penicillium. So that in the storage environment and they just sort of wait there until they can grow.

46. The clagging of the wheat on the side of a bin happens not infrequently (T112.42). Dr Hocking added that it usually does not get to as thick as a foot. At T113.44 the following appears:

Q. - Did you ever visit a mill where the mouldy wheat was being sent through and that whilst that was being done the whole mill reeked of moulds and the stale smell of stale wheat.

A. - No. I've never seen a mill in that condition. I'd be horrified to see those sorts of conditions.

47. At T113.47 the following appears:

Q. - Just one last assumption that I would like you to make, that is that these tempering bins, when filled, held between 60 and 100 tons and that by the time the person had to go in there to clean out the clagged on material, there would actually be condensation running down the sides of the bins. Does that suggest anything, from your point of view, as to how advanced the process was of the moulds producing water and heat.

A. - Certainly you wouldn't expect to see moisture running down the sides of the bins, unless there was significantly more moisture and heat generating the steam, the gases then condense on the sides of the bins and run down.

48. When cross-examined this question was put to Dr Hocking (T114.17):

Q. - You do not tell his Honour that you can be sure from your study that there would be any actino bacteria present in conditioned wheat silos at any particular point in time.

A. - No, I can't be sure from our actual studies but I can infer from my general knowledge of microbial physiology and ecosystems of grain that it is highly likely that if the grain conditions were suitable, ie high moisture and high temperature, then there would be growth of thermophilic actino bacteria.

Q. - We are talking about a temperature of at least 45 degrees celsius.

A. - At least.

49. Questions were put to the doctor saying that no tests had been made, and she agreed that that was so. In re-examination at T116.8:

Q. it ( an extract of a report found by Dr Hocking) states:

- Saccharopolyspora rectivirgula is one of the major agents responsible for farmer's lung disease, a form of hypersensitivity pneumonitis. Is that right.

A. - Yes.

Q. - We do not know the range of the study, do we.
A. No, if you really wanted to know more you'd have to find
the full paper.

50. Professor Bryant's evidence provides a firm foundation for saying that the dusts which caused the plaintiff's asthma could also cause farmer's lung. Dr Brooking's evidence proves that on the balance of probabilities the wheat dust in the conditioning bins and the mould associated therewith contained the fungi and microbes classically associated with the contracting of farmer's lung.

51. I should add that Professor Bryant's evidence was given in a straightforward careful manner and was compelling in its effect.

52. What then militates against such a finding? Broadly there are two matters to be considered: firstly, the evidence of Dr Julian Lee, given in the matter of Britt, and secondly, the submissions of learned counsel for the defendant.

53. Dr Lee's evidence in Britt was tendered in this case because Dr Lee is very unwell and is unable to attend court. His illness is a matter of great regret. I had considered that evidence when giving judgment in Britt and for the reasons therein set out did not accept the broad thrust of it. There seems to be no point in repeating what was there said.

54. Learned counsel for the defendant submitted that in the definition of dust disease the word "may" must mean something more than a tentative risk. It must have some medically recognised causative capacity. It must be something more than a slight illusory risk. In developing the submission it was pointed out that the environmental conditions favourable for the development of farmer's lung are not present in Australia, they are common in Europe. Further, there has been no study published in Australia about a person suffering from farmer's lung since 1971. That was a case resulting from exposure to mouldy hay. The last case of farmer's lung compensated by the Dust Board was in 1968. The submission was developed by saying that the law does not compensate for risk. The disease is not regularly recognised and not epidemiologically studied. Therefore it is difficult to say when in fact the risk materialises. The submission was varied slightly by saying that the risk is hypothetical i.e. in Australia. I think that there are two responses which may be made reasonably to the submissions. Firstly, the words parliament has chosen to use are ordinary English words and should be given their ordinary meaning. Secondly, while it may be true that the disease is uncommon in Australia the thrust of Professor Bryant's evidence is that nonetheless the inhalation of mouldy grain dusts in particular can cause both asthma and farmer's lung.

55. A further submission was made to the following effect: the risk of contracting farmer's lung depends on a high concentration of antigens. The plaintiff bears the onus in this regard. A simple test would have shown (i) the state in which the bins were from time to time, and (ii) what bacteria were present in high concentrations. It is true that no tests were carried out but the evidence of Dr Hocking seems to me to go straight to this submission, in particular that evidence appearing at T114.19 to .22. Further, as was submitted by Mr Sarginson, learned junior counsel for the plaintiff, the facts were peculiarly in the knowledge of the defendant. The evidence adduced by the plaintiff must be weighed in accordance with his power to adduce it. (Hampton Court Limited v Crooks 1957 97 CLR 367 at 371).

56. Further, the report of Dr Breslin bearing date 28 October 2002, part of PX4 states:

Dusts cause the asthma but do not cause any of the listed conditions. Some moulds that may be experienced in stored cereal may lead to farmer's lung or a similar condition, but as I understand it this man did not have farmer's lung .... Farmer's lung may be due to the inhalation of fungi in stored grain and accordingly it is possible that work at the Manildra Flour Mill may lead to one of the scheduled diseases, but I understand this man has asthma ...

This opinion, which was obtained by the defendant's solicitors seems to be strongly confirmatory of Professor Bryant's opinion.

57. A further submission was made relating to the definition of dust disease and the word "may" in it. It was submitted that the Court should look at the whole of the legislative scheme to glean parliament's intention. "May" should be construed as "must" otherwise the Act opens itself up to a large number of claims. I believe the response that might properly be made to that submission is: if parliament wanted to say "must" it could have done so.

58. A submission was made that having regard to all the facts it was more probable that flour was the cause of the asthma rather than the other dusts. The plaintiff had to breathe a mixture of dusts at different times, some of those dusts could cause both asthma and farmer's lung. Uncontaminated flour alone has not been shown to have that capacity. Having regard to the intensity of exposure in the conditioning bins and the exposure to mould in the mill generally, and the well documented ability of the moulds to cause irritation to lung tissue, it seems to me unlikely that the blame for the plaintiff's asthma can be placed solely on his exposure to uncontaminated flour in the mill. Further when the proposition was put to Professor Bryant at T105 he gave the answer described at para 42.

59. I find that as a result of the plaintiff's exposure to dusts in the course of his employment by the defendant he suffers from a pathological condition of the lungs, namely, asthma, which has been caused by those dusts, and that they may also cause farmer's lung; that is I find that the plaintiff suffers from a dust disease.

Having regard to the matters admitted on the pleadings the plaintiff is entitled to a verdict.

60. I turn to the assessment of damages. Firstly, as regards general damages it may be noted that the plaintiff has suffered from symptoms of asthma since 1983 i.e. he has been suffering for 23 years already. There is nothing in the evidence to suggest that his life is likely to be shortened by reason of his physical problems. That suggests that he may have another 32 years within which to put up with his symptoms. (See Australian Life Tables 1980 to 1982 published in the 3rd edition of Luntz assessment of damages).

The extent of the disability from asthma is said by Professor Bryant to amount to a whole person impairment of 40 per cent and by Dr Julian Lee, who saw him for the defendant, to amount to a whole person impairment of 50 per cent (report 24 August 2005 part of DX4).

61. As Dr Lee reports, the prospect of significant improvement in ventilatory function is remote.

He cannot participate in active sport or tasks requiring sustained physical exertion. The plaintiff suffers from shortness of breath about which he said (T50):

It's a terrible feeling just trying to get your breath back, just trying to slow yourself down trying to get it back, and sometimes it's very hard.

Q. - How does that make you feel.

A. - I have a form of claustrophobia, I can't sleep without a window or door open and panic attacks, I'm prone to, you know, make a little bit worse sometimes when I can't get breath I sort of panic a bit.
Q. - How often do you have panic attacks about your
breathing.

A. - Probably every time I get really bad if I push myself a bit too far and lose my breath pretty bad.

Mostly always of a night, sleeping of a night, it's always very hard.

Q. - Do you cough at night.

A. - Yes.

The more I talk the more irritation and I'll start coughing the more I talk. [T49]

62. He has a nebulizer at home. He no longer goes to clubs or pubs.

Perfume can cause him to have breathing difficulties. If he goes to church and incense is used for a funeral or something like that he has to leave the church.(T50).

Exercise causes the plaintiff shortness of breath and to do any proper exercise is very hard. He has put on a stone and a half and he believes that that is increasing.

His physical problems have created a stressful environment for his family. (T51).

Sexual relations with his wife have been adversely affected by his condition. (T51).

The plaintiff attempts to exercise by walking around the block but has to stop for a break in the course of that activity. Hills and stairs present difficulty for him. The fact that the plaintiff gets "pretty crook" upsets his wife and his family. The plaintiff’s ability to provide domestic and gardening services for his family is reduced.

When asked to explain what he meant by the use of the word "depression" the plaintiff said (T41):

Depression to me is that you just can't see an end to your problems. You've got problems and you just can't see an end to them or don't think there's ever going to be an end to them I suppose.

63. The plaintiff's wife says of him that he has depression and he is just a changed man. He had been a very easygoing person but is now very moody and shuts down and is just very depressed. (T83). She says:

we can't go on walks any more.

Q. - Have you seen your husband when he has had asthma attacks.

A. - I have.

Q. - How often does it happen.

A. - I just feel like it's just constant, he can't -

Q. - What happens when he has an attack.

A. - He loses his breath and just sweating and just scary.

Q. - Are you able to help him. Has it put a strain on your marriage.

A. - It has.

64. The evidence suggests that the plaintiff is significantly disabled by his asthma. As regards the extent of whole person impairment, having regard to the opinions expressed by the two experts who have ventured an opinion, I find that the plaintiff suffers whole person impairment of 45 per cent.

65. It seems to me that the appropriate award for general damages is one of $130,000.

66. I notionally apportion the award for general damages so that $60,000 relates to the past.

Interest on $60,000 at 2 per cent over 17 years amounts to $20,400. That amount should be included in the verdict.

67. As regards pre-trial earning loss the plaintiff identified Mr Thornbury as an employee, although less senior to himself, who was on the same level. (T36). PX8 is a schedule of comparable wages. The approach of the parties at address has been the difference between the plaintiff and Mr Thornbury is reasonably to be explained by his asthma. The plaintiff had increasing difficulties and went off work finally in 2001. The defendant has kept him employed and made available to him work in a house near the company's old piggery. Wages have continued to be paid as demonstrated in the schedule PX8. In fact there is very little work for the plaintiff to do and in the months between the first hearing day and the second he spent much of his time reading science fiction novels. Nonetheless in terms of assessing pre-trial economic loss it is not disputed that the payments shown in the schedule have in fact been made to him.

Fox v Wood

68. As regards loss of earning capacity the plaintiff's earning capacity has obviously been significantly impaired. He has been maintained in a make-weight position by the defendant for a number of years. This is both unsatisfactory for the defendant commercially and for the plaintiff emotionally. Having regard to these facts and to the content of the letter PX1 bearing date 25 August 2005 the penultimate paragraph of which threatens termination of employment if he is unable to return to normal duties, it seems to me more probable than not that the present state of affairs is not likely to continue for long after the court case has been concluded.

69. On the balance of probabilities I think the plaintiff retains some earning capacity. He has been for years earning at a rate considerably above average weekly earnings for New South Wales. He is an experienced millhand. While that form of activity is now denied him because of the problems it occasions to his health, he is demonstrably more capable than a simple labourer. Nonetheless he remains seriously handicapped by his breathing troubles and restricted as to the types of employment he can hope to look for.

70. I accept that Mr Thornbury's earnings provide a reasonable guide to the plaintiff's capacity to earn but for injury. I think it reasonable to allow him six months within which to try to find some alternative occupation. It is more probable than not that some new employment will be in a place other than Manildra, probably in Orange or a neighbouring town. I say so because in Manildra there is little employment to be had other than at the mill. Molong is a relatively small town. Orange is a thriving country centre. Parkes is a smaller town which might provide an alternative source of work. The plaintiff has worked nowhere but Manildra since he was seventeen years old. At age forty-two it is going to take him a little time to locate and obtain new employment. It seems reasonable to allow him six months to do that. I allow 26 weeks at $975 ie $25,337.

71. As for his capacity to earn Mr Stinson, whose report is DX3, identifies a number of employments which he believes the plaintiff might undertake. (See p 12). The plaintiff has never done clerical duties. I think it is unlikely that he would obtain work in such a position. He may obtain work as a forklift driver after tuition and obtaining the necessary licence provided that the atmosphere in which it had to work did not aggravate his asthma. It seems a little far fetched to think that a man who, so far as the evidence goes, has never driven heavy vehicles can suddenly become a bus driver. He may perhaps manage the job of delivery driver. Or messenger. He may perhaps work as a sales assistant, for example in a hardware store or something similar. It is unlikely that he would work as a check out operator or as a cleaner. As to the latter the solvents and cleaning aids are likely to aggravate his asthma. As regards a hand packer the evidence does not describe what that entails and the parties have not addressed it. The suggested range of employments carries a range of salaries for those 30 to 34 (that being the last statistic available in the exhibit) from $601 to $725. It seems not unreasonable to conclude that he has the capacity to earn something of the order of $670 gross = $546 nett in some such employment, subject to the matters which follow immediately hereafter.

72. It will be difficult for him to find employment with his disability. A man with his degree of whole body impairment will not be an attractive employee for some employers. If for some reason he loses his position he may take some time to get another. Notwithstanding the best efforts of the rehabilitation providers Interact Injury Management, who have had the care of his rehabilitation for several years, he has been able to work only for five and a half hours per day in the very light duties made available to him by the defendant. This is probably a fair measure of his capacity for lighter duties, notwithstanding the opinion of Dr Jones that he could do it for eight hours per day. (T61.38-40, T62.4-5) In this regard it is pertinent to remember that at present he goes home for a couple of hours a day in the middle of the day and that he has a nebuliser at home which he uses when necessary.

73. Furthermore to exercise such earning capacity as he has will probably require that he drive to Orange or a neighbouring town away from Manildra. If he has to drive 70 kilometres a day or 350 kilometres a week it is likely that petrol alone will cost him (12 litres per 100 kilometres equals 42 litres of fuel per week @ $1.40 per litre) something approximating $60 a week. When one adds the cost of oil, tyres and wear and tear on his car it seems to me not unreasonable to say that it will cost him $70 per week to exercise his capacity to earn.

74. If a worker working seven and a half hours per day can earn say $546 per week a worker working for five and a half hours per day might hope to earn (mathematically) $400 per week or thereabouts. If one deducts the cost of travelling to exercise earning capacity of $70 per week the resulting figure is $351 per week. In attempting to make some allowance for the insecurity of employment and the risk that he might lose it because of ill health some further reduction is required. Acknowledging that the exercise is incapable of precise calculation I find that the plaintiff on the balance of probabilities has the capacity to earn something of the order of $330 per week.

75. Mr Thornbury's current weekly earnings are of the order of $975 per week net after tax. That leaves a net weekly loss of $645.

The capitalised value of that sum over 23 years (multiplier 870.8) equals $561,666. Discounted by 15 per cent for vicissitudes the amount thrown up is $477,416.

CSR Limited v Darcy

76. In the course of addresses counsel suggested that if the Tribunal made the necessary findings of fact, because of the complexity of the calculations required a reasonable means of approaching this aspect of the matter would be to stand the matter over while counsel could attend to the calculations and thereafter, presumably, bring in short minutes. I propose to adopt that course.

77. Similarly, an allowance for lost superannuation needs to be calculated. That calculation needs to be undertaken by reference to gross weekly earnings rather than net. Counsel might also undertake that calculation.

78. Finally, the issue of past and future medical expenses needs to be dealt with. Although counsel undertook to submit a schedule of future medical expenses, whatever the schedule contains, those expenses which will be paid for by the Dust Board will not be recoverable as damages. At the time of delivering these reasons no schedule of figures had been provided.

79. I propose therefore to publish these reasons and to request counsel, in the light of them, to bring in short minutes of order to give effect to them. By way of summary then the plaintiff is entitled to the following damages. General damages $130,000. Interest on past general damages $20,400. Pre-trial earning loss $31,554. Damages for loss of earning capacity: $25,337 plus $448,375 less the capitalised benefit of payments which the plaintiff is entitled to receive from the Dust Diseases Board. The loss of superannuation benefits (counsel to calculate). Past and future medical expenses (counsel to agree or to submit schedules setting out their submissions).

80. There is one further item of claim to which reference should be made. That is, the cost of care for the plaintiff (Griffiths v Kerkemeyer (1977) 139 CLR 161). The evidence of Dr Prendergast suggests that the plaintiff needs help with heavier household maintenance tasks such as mowing, gardening and cleaning the gutters (report 14 June 2005 part of PX4). It seems to me that these activities reflect partly a need in the plaintiff and partly a loss of ability to provide services for others. The opinion is couched in terms of the help needed in an average suburban cottage. In fact the plaintiff lives on three-quarters of an acre at Manildra (see report of Shirley Wruck 31 July 2005 part PX4). Insofar as there is heavier housework to be done such as vacuuming and cleaning the bathroom, these are probably things which in the ordinary course of events would be done by his wife rather than by the plaintiff. The cleaning of gutters is something that the plaintiff might be expected to do from time to time. It seems to me to be reasonable to allow one hour per week at $21.68 per hour until the plaintiff turns 60. Thereafter he is likely to make other arrangements in any event. The allowance to be made therefore is $21.68 per week for 18 years (multiplier 728.4) ie $15,788.07. This should be discounted by 15 per cent for vicissitudes, to, $13,420. That sum should also be allowed by way of damages.

81. I stand the matter over for further mention on Thursday, 13 July 2006 and request Counsel to bring in short minutes on that day to give effect to these findings.

Mr A J Bartley, SC with Mr G Sarginson instructed by Higgins and Higgins appeared for the plaintiff

Mr A C Scotting instructed by Moray and Agnew appeared for the defendant

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Citations

Davies v Manildra Flour Mills (Manufacturing) Pty Limited [2006] NSWDDT 23

Cases Citing This Decision

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Cases Cited

3

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Griffiths v Kerkemeyer [1977] HCA 45

Russo v Aiello [2003] HCA 53

CITATION:	Davies v Manildra Flour Mills (Manufacturing) Pty Limited [2006] NSWDDT 23
PARTIES:	Anthony Joseph Davies Manildra Flour Mills (Manufacturing) Pty Limited
MATTER NUMBER(S):	152 of 2003
JUDGMENT OF:	Duck J
CATCHWORDS:	Dust Diseases Tribunal :- Dust disease Occupational asthma Farmer's lung Whether a dust which caused asthma might also have caused farmer's lung Damages
LEGISLATION CITED:	Workers' Compensation (Dust Diseases) Act 1942 Workers' Compensation Act 1987, s 4 Workplace Injury Management and Workers Compensation Act 1998
CASES CITED:	Britt v Manildra Flour Mills (Manufacturing) Pty Limited (2006) NSW DDT3; Hampton Court Limited v Crooks (1957) 97 CLR 367 at 371; CSR Limited v Darcy (1996) 40 NSW LR 721; Griffiths v Kerkemeyer (1977) 139 CLR 161
DATES OF HEARING:	20 September 2005 and 19, 21, 22 and 23 June 2006
DATE OF JUDGMENT:	07/07/2006
EX TEMPORE JUDGMENT DATE:	07/07/2006
LEGAL REPRESENTATIVES:	Mr A J Bartley, SC with Mr G Sarginson instructed by Higgins and Higgins appeared for the plaintiff Mr A C Scotting instructed by Moray and Agnew appeared for the defendant