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Standing Committee on Health, Aged Care and Sport
09/08/2018
Biotoxin related illnesses in Australia

BIJLSMA, Mrs Nicole, Vice President, Australasian Society of Building Biologists

DONOHOE, Dr Mark, Private capacity

EDWARDS, Dr Graeme, Fellow and Regional Councillor (Queensland), Faculty of Occupational and Environmental Medicine, Royal Australasian College of Physicians

GREENWAY, Ms Patricia, Consumer Board Member, Australasian Integrative Medicine Association

GUPTA, Dr Sandeep, Board Member, Australian Chronic Infectious and Inflammatory Disease Society

LARK, Mr David, Principal Mycologist, MouldLab

LAW, Dr Tim, Private capacity

RUDD, Mr Caleb, Administrator, Toxic Mould Support Australia

STAMKOS, Mr Jeremy, Private capacity

WILLIAMS, Mrs Jeanette, Building Biologist, Building Biology Sydney

Evidence from Mrs Bijlsma, Mr Lark, Mr Rudd and Mrs Williams was taken via teleconference—

CHAIR: We are now up to roundtable 2, which is focusing on the prevalence, possible diagnosis and treatment of biotoxin related illnesses. We have a slightly diminished number but basically the same cast of characters as previously. Just to save time, we will do opening statements again on this issue if you feel as though there's anything that you want to add at this stage that you haven't already, but don't feel obliged to take up the time unless you want to. If you want to make a further two-minute statement at this stage, feel free. Do you have anything to say about the capacity in which you're appearing?

Mr Stamkos : I am the principal consultant of Eronmor. I am representing myself and also providing advocacy for the restoration industry and the insurance industry.

Dr Donohoe : I am a general practitioner involved in environmental medicine and integrative medicine. I have to admit that I have only a three-year history of understanding anything about biotoxin related illness, so I have limited understanding compared to some of my colleagues.

Dr Gupta : I am representing the Australian Chronic Infectious and Inflammatory Disease Society and the Australian College of Nutritional and Environmental Medicine. I basically have five years of treating biotoxin illness and am certified in the Shoemaker protocol.

Dr Law : I am an architectural scientist, here in a personal capacity.

CHAIR: We might go straight into questions and comments. Dr Gupta, as you specialise in this area, could you just run us through the diagnosis process for a patient and also the treatment options available for biotoxin related illness.

Dr Gupta : Sure. Would it be worth doing a very brief definition? I don't think we've actually defined it.

CHAIR: That's a good starting point.

Dr Gupta : Chronic inflammatory response syndrome is defined as a multisystem, multisymptom illness, which means it's not just limited to one or two body systems. It occurs in genetically susceptible individuals—

CHAIR: Do you also describe it as multifactorial?

Dr Gupta : yes, multifactorial as well—in response to exposure to biotoxins. So the biotoxins can be of various different origins, but the most common is related to water-damaged buildings.

CHAIR: So biological and chemical?

Dr Gupta : That's right. This started appearing in the literature around 2001, so there is about a 15-year history of it appearing. The research group was led by Ritchie Shoemaker and James Ryan, and it actually was accepted by the US patent office last year. It's been patented—

CHAIR: I didn't realise you patented diseases—treatments maybe!

Dr Donohoe : Americans do that a lot!

CHAIR: If you stand still, they'll patent it.

Dr Gupta : The diagnosis process, like anything else we do in medicine, goes back to history and examination, bedside tests and formal investigations. We've already touched on environmental history a little and, like everything, that's probably the most important part of the assessment—

CHAIR: Are there biomarkers for—

Dr Gupta : The biomarkers are the blood-testing markers that are specific for establishing a formal diagnosis.

CHAIR: But there are biomarkers.

Dr Gupta : Yes, and I'll go on to the difficulties in accessing them in a moment. The problem is that we don't have any NATA-accredited labs that are performing those biomarkers at a moment. Briefly, on the history, one of the key things, which was already described by Dr Edwards to some degree, is around simply taking an environmental history of what sort of exposures people have had. It tends to be that a number of different questions need to be asked related to water-damaged buildings and a simple inquiry such as, 'Have you been in a mouldy building?' often doesn't give you the result that you need. There need to be a number of different questions asked around that. For instance: is there any presence of musty smells; has there been a history of water intrusion into the buildings in which that person lives and works; and do they notice a difference in their symptoms on being exposed to that building and being de-exposed for a period of time?

CHAIR: Is a trigger some kinds of moulds and not others?

Dr Gupta : There appear to be some moulds which are more deleterious than others, but we consider it to be the sum total of all of the different constituents of a water-damaged building. It's not just mould; it's mould, bacteria, VOCs, which are like chemicals—and they can be microbial VOCs or chemical VOCs. Parasites have been described as being in water-damaged buildings.

CHAIR: Someone mentioned dust mites before.

Dr Gupta : Dust mites can be another peripheral thing that can be in there. We really talk about water-damaged buildings as being an entirety of different organisms and so on. So, rather than thinking of specific causation, we consider water-damaged buildings to be a group.

Inquiring into exposure to biotoxins is very, very important. Part of the assessment is also working out: does the person truly have a multisystem illness? For instance, if they just say they have some gut related symptoms such as diarrhoea, constipation and bloating, that's not CIRS. If they have that plus some headaches, that's still not CIRS, because that's only two systems involved. However, if they have those plus insomnia, plus anxiety plus muscle pains plus skin rashes, that's clearly multisystem. There are not that many other illnesses that are truly multisystem. There are definitely others, but one of the key parts of the assessment is working out: is it a truly multisystem illness? Has there been exposure to biotoxins? There are also some considerations around timing, which Dr Edwards discussed, and the exposure to the water damage.

CHAIR: So do you see people present with all those symptoms but have no exposure?

Dr Gupta : Absolutely. In some cases, yes. In some cases, there may not be a—

CHAIR: So what would the diagnosis be in that case?

Dr Gupta : You can't bring it down to one thing. It could be a whole host of different things. Obviously, there's a differential diagnosis—major depression, fibromyalgia, chronic fatigue syndrome and then autoimmune conditions such as lupus and rheumatoid arthritis. There's a whole group of conditions that is going to be part of the differential diagnosis. That's the first point, to create a proper differential diagnosis. An examination is often to exclude other diagnoses, but there are some signs, on examination, that may suggest CIRS. The presence of a fine tremor has been considered to be one sign that goes along with one of the cytokines, called TGF beta 1, being elevated. There are some other subtle signs that can be seen as well. Sometimes patients have hypermobility, which means that their joints are more mobile than normal.

Dr Donohoe : They always were, though. It's not that the mould has made them—

Dr Gupta : Yes. That's another susceptibility factor—if people are hypermobile. The main bedside test—meaning something that we perform in the clinic—is called a visual contrast sensitivity test. That is like a simple eye test to see how efficient someone's sight is. It gets people to look at circles where there are fine shades of grey. What's observed with patients with chronic inflammatory response syndrome—and this is documented in the literature—is that their vision can be perfectly fine but their ability to notice the differences in fine shades of grey is impaired. That's thought to be due to the effect of inflammatory cytokines or inflammatory compounds on the optic nerve. That's a screening test. It's thought to have around a 90 per cent sensitivity and specificity, which means that 90 per cent of the time it's correct, basically. Any screening test will have some inaccuracy, and we have seen some patients be negative and they do actually have CIRS, and some patients are positive for that and they don't have CIRS. But that's a minority. There is another screening test, which is called antigravity muscle testing, which is a little bit new. It's based on looking at their major muscle groups and, if they have easy fatigability, that is considered to be another screening test for CIRS.

With the three screening tests, we talk about the cluster analysis. The cluster analysis is related to the illness being a multisystem illness. Dr Shoemaker's research team has come up with 13 symptom clusters. So I sit the patient in front of the clusters and say, 'Which of these symptoms do you experience regularly, not just under unusual circumstances?' If even one symptom is present from any particular cluster, we consider that cluster to be positive. The research he found was, if there are eight or more symptom clusters, that's already 95 per cent predictive of CIRS, and, if there are four or fewer clusters, that's 95 per cent predictive that they don't have it. So the screening tests are reasonably effective at being able to rule in or rule out CIRS.

With the formal diagnostic testing, there are around 10 different tests. Of the main ones, the first one is called HLA gene testing. That's a test that can be done with any of the major pathology labs in Australia. It goes under the name of coeliac disease gene testing, because they're the same genes that are looked at. But the Sonic group of laboratories is preferred, because they actually come out with a number rather than just telling you if you have a yes or no to the coeliac disease susceptibility. Based on that, one can work out what the HLA gene type is and assess whether it is considered to be a susceptible gene type or not. That's the first step. Then there are some other tests that can be done in Australia, such as VIP. VIP stands for vasoactive intestinal polypeptide. That's mainly tested in Australia to look for a rare type of tumour in which levels are high. But, in CIRS, levels tend to be low. One of the major treatments of CIRS is to replace levels of VIP via a nasal spray.

Then there are about six tests that we really need to do via the American labs at this point. That's presenting a major logistic difficulty in that, at the moment, the only Australian lab that is willing to forward the blood to America is in the Sunshine Coast, Queensland, which is inaccessible to the majority of people. It was happening in Sydney and Melbourne, but the labs have subsequently said that, logistically, they're not willing to do it anymore. Therefore the vast majority of people are not able to have these blood tests done. They're a considerable expense as well. The full lot of them, I think, is around $1,200 plus $250 collection. So it's very expensive, and there's no Medicare rebate.

CHAIR: We'll come to treatment in a tick. Would anyone else like to comment on diagnosis? Dr Edwards, so you have any thoughts?

Dr Edwards : Only to reinforce the fact that there is no consensus. Just as we saw with the characterisation of the complex regional pain syndromes, over the years we have gone through an evolutionary process to say what the accepted criteria are in order to be entitled to treatment and compensation in relation to complex regional pain syndrome. Likewise, we're on the same production line where at the moment we're still toying with what's in, what's out, what factors do have some form of predictive value, what factors don't, how many characters. Presently, if I draw the analogy with the complex regional pain syndromes, the Budapest criteria defines four symptom categories of what the patient is expressing and four sign categories. For you to get a clinical diagnosis, you need at least three out of four of the symptoms and at least two out of four of the signs at the time of examination, with no other explanation present. So there's a criteria that is set now in terms of what we do in the clinical setting to apply that label.

In the research setting we say you have to have a higher standard to be included in the study group. You have to have four out of four in the symptoms and three out of four in the signs. In some jurisdictions, in order to get access, you actually have to have four out of four in both. So where we're looking in this setting when we're talking about CIRS is how we're starting to see the gelling together of what should be considered and what shouldn't be considered. We're in a very embryonic state of defining what it is. There are still out there in the marketplace people who are naive, and it basically doesn't exist full stop. They resist totally.

Mrs WICKS: I have a question on that and two related subjects. The first is that somebody said we needed a medical debate and also a building debate in the previous session. One of the questions I'd heard from some of the witnesses—or my understanding of what some of the witnesses said—was that there seemed to be a lack of guidelines not just for clinical diagnosis but also to determine which buildings were affected and which were not, which moulds are dangerous and which are not. Do you think that's part of the problem? Is there a need for greater diagnostic tools?

Dr Edwards : You highlight a very, very, very—and I've used three very deliberately—important feature, and that is the way people are managed at the outset and what we call the outrage factor, which will escalate the level of distress and the sense of grievance if they think something is the cause. When we're talking about these sorts of disorders, the mere thinking that there is a connection escalates the problem, and we call that the outrage factor. If the building manager responds in a very dogmatic way—saying there's no proof, resistant to any sort of intervention—the outrage factor goes skyrocketing and the level of sensitivity and distress that the individual suffers also goes skyrocketing. When we're dealing with statutory obligations, when we're dealing with this sense of responsibility, when we set a standard, we're talking about a standard that will make safe for the majority of the population. Depending on which area, it might be 85 per cent, it might be 95 per cent or it might be 99 per cent, depending upon the consequences. But, in that situation, it's how the entity responds to the minority.

Mrs WICKS: I want to ask a second related question, but I will also throw that question to David Lark from MouldLab. In your view, is there a need for nationally consistent guidelines to mould diagnosis and remediation in buildings, and is that even possible?

Mr Lark : I would have implore that to be of major consideration, most definitely. Is it possible? I believe it is. I believe that certainly, with the knowledge that we have now, that can be achieved in a relatively short time.

Mrs WICKS: Dr Edwards, you mentioned before some other environmental considerations to multisystem illness, as I think you described it, such as multiple chemical sensitivity, EMF frequency et cetera. I wonder whether part of any clinical guidelines ought to be widened to include environmental factors such as that? Could we have a comment or response from you or any other member of the committee?

Dr Edwards : I suspect that, if we get an effective guideline that is applied in the specific setting of CIRS, we're going to have a valuable tool that could be readily replicated or used in these other settings. If we do the groundwork in this setting, it's going to have implication and applicability in other settings.

CHAIR: Does anyone else want to comment on the diagnosis?

Dr Donohoe : I do. One thing you'll notice from both Graeme and Sandeep is that we're talking about a syndrome, not a disease. It's an observational syndrome. I'm aware of this because of the 30 years in chronic fatigue syndrome. And so these are not diagnostic criteria. You diagnose a disease when you have done all the work to say it's a disease rather than a syndrome. These are designed to help doctors. The concepts that Sandeep talked about guide us towards whether this is a case or a non-case when we're dealing with—

CHAIR: Can you go back a step? Can you define a syndrome versus a disease?

Dr Donohoe : A syndrome is an observational gathering of symptoms that are in common between different patients. In chronic fatigue syndrome we have a particular group of people with six months fatigue and five of the eight criteria in addition to it. Do we know cause? No. Do we know treatment? No. There's no one common thing. In medicine and nosology, which is the naming of diseases, medicine owns the term 'disease'. You don't have a disease until the consensus of medicine is that you have a disease, and it moves from syndrome to disease at that point, but that's because you have testing or treatment that is widely accepted to work. So we're dealing with a syndrome—

CHAIR: So is AIDS misnamed then?

Dr Donohoe : AIDS is descriptive. Again, it is acquired immune deficiency syndrome. Once the HIV virus came in, we called it HIV/AIDS, because now we have a virus as a causative factor. So the general thing is you have diagnosis of a disease but you have a contribution to a syndrome. What I'm really saying is there's no diagnostic certainty, because there's no disease certainty yet, and the movement is from syndrome towards disease if we do our job properly. So it's designed to help doctors distinguish case from noncase and is more useful as a starting point.

What Ritchie Shoemaker's provided is a bunch of factors that we believe are associated with something which should move from syndrome to an actual definite diagnosis, and that's a testable hypothesis. What Sandeep pointed out is that those diagnostic criteria involve laboratories which are overseas, inaccessible, and make it extremely hard for us in Australia to tell whether this is or is a case or not a case. So we end up taking a history, doing the minimal test that we can do here and saying probably or probably not.

Again, a part of a consensus at the end of this could be that here is the consensus on what's valuable in the testing based on the literature. Why is it not in Australia? It's not profitable. It's not profitable to bring expensive tests in, but if they are helping with diagnostic certainty that would be a major boon to doctors like myself—to be able to say, 'We can do simple testing and my certainty about what category you fall into goes up.' When it comes to treatment, that's a whole different ballgame.

Dr Edwards : To distinguish between syndrome and disease, the best example I use in clinical practice is Parkinson's disease. Parkinson's disease is a set of symptoms that we know the cause of. Parkinson's syndrome is where you've got the same set of clinical symptoms but the cause isn't there. So there are multiple different causes that might lead to the same set of symptoms that we see manifested in a patient.

CHAIR: I didn't think we knew the cause of Parkinson's.

Dr Edwards : Parkinson's disease we do. Parkinson's syndrome we don't. When we use the term syndrome, we're talking about a much broader heterogenic group of possible explanations. When we're talking about disease, we're talking very specifically about the nature of the pathology that we can test and measure and describe.

CHAIR: I don't mean to divert but I really didn't think we knew the cause of Parkinson's. It's believed to be genetic mutation but we don't know which gene mutations they are.

Dr Edwards : Of Parkinson's disease we have knowledge but of Parkinson's syndrome we don't. There are debates even under the banner of Parkinson's disease, but what I'm trying to highlight here as an example—not to sidetrack today's discussion—is that, when we've got something concrete we can actually hang a hat on, we tend to call that a disease. When we don't have the hat hook, we call it a syndrome.

Mrs WICKS: But if you have patient X with Parkinson's disease and patient Y with Parkinson's syndrome, their symptoms are still very real?

Dr Edwards : They're very real, and we often have to treat them the same. But once we actually drill down to disease, we can be more specific and more effective in our treatments.

CHAIR: But there are no biomarkers for Parkinson's disease yet.

Dr Edwards : There are biomarkers for Parkinson's disease but for Parkinson's syndrome there are not.

CHAIR: We'll have this conversation offline.

Dr Edwards : Yes.

CHAIR: Anything else on the diagnosis before we move on to treatment?

Dr Gupta : I'd just like to add that there is actually a case definition as well. It's gone passed just the fact that there are certain things associated with it. There's a published case definition which was accepted by the Government Accountability Office, or the GAL, in America in 2008. Basically, the case definition was (1) that the condition was a multisystem, multisymptom illness, which we described before, (2) that there is documented exposure to biotoxins, usually in the form of a water damaged building, and (3) that there were at least three abnormal biomarkers. The thing about each of these biomarkers is each one on their own is not very specific. You could have a raised biomarker like C4A, which is one of the important ones. That's actually known to be elevated in a number of different syndromes, like lupus and so on. But when there's a combination of three or more and those other features and then the number four feature of the case definition, which is a response to therapy—the main one being cholestyramine. The combination of those is thought to be very highly accurate for diagnosing CIRS. One could argue that is getting towards the disease side of the spectrum.

Dr Donohoe : Don't tell the rest of the medical profession that! That's within the group who actually takes that on, and it's a smallish section still. Wide acceptance still requires better diagnostic tools. You don't think so, Dr Gupta?

Dr Gupta : You could say that wide acceptance, perhaps, isn't there, but there is documentation that the case definition can very accurately diagnose cases of CIRS and exclude cases that are not CIRS. And therefore, the treatment process—which I know we're going to get on to—is actually very much based on the actual biomarkers and not just symptoms.

Mrs Williams : I will also add to that, going back to Lucy's comment: the Austrian medical association published a document for their general practitioners across the country in relation to the diagnosis and treatment of electromagnetic field sensitivities. That was in 2011. There are countries that are looking at these chronic fatigue-like illnesses and trying to attempt to address this amongst their clinicians.

CHAIR: Does anyone else have any questions on diagnosis? What I'm proposing to do is we will talk about diagnosis and treatment, and then I want to talk about the broader issue of mould management in relation to implications—as a treatment, I suppose—for building standards.

Mr TIM WILSON: I have a quick question, which touches on diagnosis and mould treatment. We've been given a lot of evidence about the process of diagnosing your patients and the conditions and situations. As part of the process of diagnosing a patient, is there any technology that's available to essentially diagnose an environment that can help you to make a decision about whether the environment has an effect so that you can then draw the relationship between that and the diagnosis of a patient?

Dr Gupta : Absolutely, and then there's a range of different tests available for testing and environment. But it also does go down to history, again. For instance, if someone is able to actually detect visible mould and musty smells, one could say that's pretty diagnostic on its own. Would you agree with that?

Mr Stamkos : Yes. The consensus in the wider indoor environmental consulting community is that it's not so much about particular levels of particular moulds; it's in relation to the amount of moisture and dampness in a building. Odours is a big factor. Yes, types of sampling is a very contentious issue, which probably has to be addressed. It's about how people do mould sampling of indoor environments. The odours and the actual amount of moisture in the building are two of the biggest indicators of those causational links.

CHAIR: It's not the amount of mould, but it's the amount of dampness. Is that because the dampness is a conduit to the mould in some way?

Mr Stamkos : The dampness is not just mould. It's bacteria and it's all sorts of other influencing factors. When you have a water damaged building, you have all these other influencing factors coming into it. It's not just the mould. That's why there is no consensus anywhere in the world as to what level of mould exposure for certain individuals is tolerable or allowable.

CHAIR: We'll come back to that when we talk about further regulation.

Mr Edwards : I would express caution in that phrase 'diagnostic' implies that there is a strong connection that is causative. When we have someone reporting the sense of odour, the sense of moisture or whatever it is that they're reporting—the visual or the olfactory sense being stimulated—it raises the level of suspicion but it's not diagnostic. That's the problem. It's because people assert diagnostic connectivity when the evidence isn't there to actually say that that level of mould in that particular premise is causative. It's an implied association. There's an index rather than a specific test that can say, 'That's the end of the story.'

Mrs WICKS: I've heard of things like ERMI tests for water damaged buildings. I'm just wondering if one of the witnesses is able to talk through, for instance, ERMI testing or any of the other diagnostics—

CHAIR: We might get to the building issues as a third element.

Mrs WICKS: I will put that on hold.

CHAIR: How do you treat your patients, Dr Gupta, and how effective is the treatment?

Dr Gupta : There's a 14-step program that has been developed by the Shoemaker research group, which is basically designed to bring the biomarkers back to normal. It has been pretty rigorously tested. The most important step is considered to be de-exposure from the triggering biotoxin. That's the No. 1, and that's the most important thing. That's step 1. If people don't achieve that properly, the effectiveness of the other steps is much reduced. That's also a very heartbreaking and expensive step for people. Some people are in a situation where they simply cannot do anything about that due to financial difficulties or logistical difficulties. Dr Donohoe mentioned that he has had some patients suicide. I don't know what the circumstances were, but I can definitely see that that could be a possibility. That's because it's very, very upsetting to people that they're in a building that could be triggering or causing their illness, but they are unable to do something about it. It's really important. Ideally, having a proper assessment by a building biologist or what we call indoor environmental professionals—like Jeremy, for instance, or Mr Lark, who is on teleconference—is one of the key things for assessing their building and giving advice about what needs to be done to either remediate the building or vacate the building.

CHAIR: That is the most effective treatment?

Dr Gupta : That's the most important.

CHAIR: It stands to reason.

Dr Gupta : That's step 1. Step 2 is giving binder medications to help to remove mycotoxins and other compounds from the system. Mycotoxins are not the mould itself. It's the toxins they're producing that's causing the problem, generally speaking. Colestyramine is actually a very old medication that was used to lower cholesterol. It's also used for various other things. For instance, there's a syndrome called dumping syndrome. A binder is like a powder which binds onto the bile in the small intestine. What has been observed is that mycotoxins are often being excreted in the bile to a certain degree. If you don't give a binder, they get recirculated. That means they get absorbed again. They just keep going round and round in a circle until you give something that binds onto them in these susceptible individuals, which then takes them out of the body. That's another really important step. But if you don't fix the water damaged building, it's like having being in a boat that's leaking: you're throwing the water out, but at the same time it's continuing to leak. You're never going to fix that leak. But if you can stop the exposure to mould and give the colestyramine or another binder, then though even those two steps are a major step forward.

I won't go into the detail of each of the steps, but there's a whole there's a whole range of different steps. The last two are giving VIP nasal spray, which at the moment is not available on Medicare and has to come from a compounding pharmacy. VIP is vasoactive intestinal polypeptide. I would have administered this to about 100 patients with quite good results. The last step is actually similar to what we call graduated exercise therapy. It's considered in general medicine to be one of the effective treatments for chronic fatigue syndrome.

Dr Donohoe : It's overstated.

Dr Gupta : If you try to get a CIRS patient to do graduated exercise therapy from the start, generally you will see that they will get worse or no better. That's because they just don't have the ability to process oxygen properly until their inflammatory markers have been brought down. But once you have done that, then all of a sudden it does seem to work.

CHAIR: Effectively, it's more exercise.

Dr Gupta : Yes, gradually increasing the amount of exercise.

CHAIR: If that treatment regime is followed, obviously including the physical environment, is the recovery pretty universal or do some people still continue to—

Dr Gupta : Some people will still continue to be unwell. I would say that a significant amount do. The most common reason is continued exposure to the water damaged buildings. Step 1 is a big logistic hurdle.

CHAIR: Dr Edwards, is there a consensus on that treatment regime?

Mr Edwards : There is certainly a consensus on the principles of the treatment. There are different levels of experience. In reality, we just haven't had a consensus on these different treatments long enough to be able to know what sort of predictive value they're going to have in terms of the ultimate outcomes. One of the values of what we're doing at the moment, in an international perspective, is that we're compartmentalising the different treatment options and looking at the evidence base to say whether or not it is effective or not across a range of different labelled, multiple and relatively unexplainable symptoms. So we're starting to see in the literature those that are associated with the more predictable, better outcomes. So we can say now that the concept of graduated exercise programs was overstated. It is still a valuable intervention, but it wasn't quite as valuable as some people would purport. It has its role, but where in the process is that role? That's what's being teased out of the marketplace at the moment.

Mrs WICKS: I have a related question to that. We've heard a lot about clinical guidelines. I don't know the answer to this one. What would it take to develop clinical guidelines, given everything that we've heard so far?

Dr Edwards : The only model I've got is what the US Department of Veterans Affairs did in relation to the Gulf War syndrome sufferers that I spoke about it.

CHAIR: Who is responsible for developing clinical guidelines? Is it your society?

Dr Edwards : Basically it's the Department of Health.

CHAIR: Is that federal or does each state do it?

Dr Edwards : It can be a state based activity. It usually is a state activity but coordinated by the federal Department of Health. It's one of those jurisdictional issues. There is transfer of responsibility or buck passing—

CHAIR: No, that would never happen!

Dr Edwards : in the health industry. Cost sharing is not an issue here. At the end of the day, it is a national implication and I would love to see the federal Department of Health take the lead.

Mrs WICKS: In relation to treatment, how much of it is Medicare rebatable? In relation to the principle of access to medical help, how many patients can go to any bulk-billing doctor and have a prescribed treatment that's either on the PBS or reasonably affordable?

Dr Gupta : They're great questions. I guess that leads us to the barriers to effective care in Australia. The basic answer is almost none of it is on Medicare. It is possible to get a PBS prescription for cholestyramine. However, my understanding is it's licensed for high cholesterol. It's not really intended to be used for this syndrome and, therefore, Medicare can come and audit doctors if they're using it under Medicare for these patients. Almost all of the medications are not available under Medicare in the normal way of using them.

There is a major lack of trained medical practitioners in Australia, as you asked about. Certainly coming off the street and just going into a bulk-billed medical centre you couldn't expect that a GP would know about this syndrome or be able to treat you in any significant way. We're really talking about somewhere in the range of 20 practitioners for the whole of Australia who have done some basic training. The advanced training, which is the Shoemaker training, has only been completed by two practitioners in the whole country. So there's a major lack. That's one of the biggest barriers to care. If you live in Western Australia, you're going to have a lot of difficulty. I've had many patients from Western Australia who have had to come to the east coast to see myself or Dr Kim, who's the other Shoemaker certified physician, to get treatment for this condition. So that's a huge expense involved for those people.

Mrs WICKS: Would guidelines, then, enhance the access to treatment? In other words, would more doctors—

Dr Gupta : It needs to be training plus guidelines. There needs to be training as well. The guidelines are not going to be enough on their own. If as a medical practitioner you've never heard of a VCS test, you could have a piece of paper in front of you saying, 'Do a VCS test,' but that's not going to be enough for to know how to utilise those things. They ideally need to attend at least two or three days of training and be familiar with that diagnostic process I've outlined. Then the next bit is having some availability to some of the biomarkers. It would be necessary that they could at least order one or two of the blood tests to find out if a patient likely has CIRS or not.

Mr ZAPPIA: Dr Gupta, do you know if there was any submission made to the government's MBS review with respect to the Medicare payments or the Medicare benefits that might apply to anyone who goes to the doctor for any of the symptoms? There was an MBS review carried out by the government—

CHAIR: It still might be ongoing.

Mr ZAPPIA: Yes, it still might be underway. Given that you said that most of the medicines that might be prescribed are not covered, and I suspect the same might apply with respect to the doctors' MBS payments themselves, was a submission made to the government as part of the review with respect to this syndrome?

Dr Gupta : No, I don't believe so. We're hoping that one of the outcomes of this inquiry is that greater Medicare coverage could be available for patients with the syndrome and greater access to the medications under Medicare. Another thing would be, for instance, if a patient in Western Australia could have access to teleconference consultations under Medicare that would give them the ability to consult with a trained practitioner without having to travel thousands of kilometres. That would be another way of lessening the barriers to patients being able to access diagnosis and treatment.

Ms Greenway : Can I just ask a question of you, if the chair is okay with that?

CHAIR: It's not normal procedure, I have to say! Maybe you could make a contribution that lends itself to a question.

Ms Greenway : Something like that. The chronic illness packages under Medicare whereby people get longer consultations and a series of programs—do you envisage that this might fit that bill once there's a bit more consensus developed? Because that's a starting point, isn't it? People are talking about exposure history taking quite a deal of time. Do you think it would fit the six-week chronic illness plans that they have?

Dr Gupta : Yes, it would. It's a chronic illness with very high care needs and so on. My understanding of that program is it's designed to help with care needs for people with chronic illness.

Dr Donohoe : Just to be clear, the MBS payments are made to doctors for seeing a person presenting with an illness in Australia. The guideline of Medicare is exactly that. So there's no failure to pay. On the PBS side, the colestyramine referred to can be used off label; it's not a restricted medication. It is a general low-cost medication that was used for cholesterol and is now commonly used for other things as well. But it's not illegal, immoral or damaging to be using that. PBS do not pursue anybody for that particular use. So it's not that nothing is paid; it's that this is complicated. You need to raise doctors' awareness that this could be a problem. The primary treatment is avoidance, which isn't a Medicare item at all. From that point going on, I can understand what Sandeep was saying—the more specialised you get in this area, the higher the costs that arise for people that have to go down that path. They're already sick and disadvantaged, and then they run into problems of American testing rather than Australian testing, and there's no opportunity for payment of those. So I see the patients that are affected, and the costs escalate, and it's a never-ending battle to reach even reasonable diagnostic certainty. On every step of the way the costs escalate for those people, and the hardship increases if you go down that path.

CHAIR: There are item numbers—

Dr Donohoe : For everything. But, as you would know with Medicare, and as I have felt many times over the years, you spend hours with a person and that's not exactly what Medicare funds; they're always a bit suspicious and will come visiting to say, 'Maybe this isn't that complex; maybe it's an easier illness.' That's been a problem for lots of doctors; they're having complex consultations and Medicare sees it a different way.

Mr ZAPPIA: What are the shortfalls in the Medicare system?

Dr Donohoe : The one that has been put up by the chronic fatigue syndrome group over and over to inquiries is the lack of appropriate funding for prolonged consultations. If you spend two hours with a person, you cannot go billing Medicare for those people without them visiting and making life fairly miserable for you. So one barrier is that complex illnesses are not well covered by a quick disease-care system that works efficiently with rapid throughput. It's not conducive to do six consultations where one would have done had you taken a proper history. That's one Medicare lack. The other ones apply to where you draw the line with testing. Diagnostic testing is not cheap, so Medicare is never over thrilled about something which would escalate diagnostic testing. There may be special considerations for specialists. It's easy—all of theirs are paid for by Medicare, whereas for GPs only the most expensive three tests are paid for by Medicare. So it adds cost to the person very significantly if you do any more testing than three items for a GP. For specialists, I think, whatever you order can be bulk-billed. Is that not correct?

Dr Edwards : No.

Dr Donohoe : There's no payment?

Dr Edwards : There are there are major deficiencies in the MBS system and the PBS system when it comes to this area. Formally, there have been no submissions because, basically, historically—

CHAIR: To MBS or to PBAC?

Dr Edwards : Both. Because it's been put in the too-hard basket multiple times in the past—for decades, not just the current government. First of all I'm a specialist in occupational and environmental medicine. If I don't get a referral from a GP, and someone comes in to see me because they've found me through the network, I get paid at a non-VR rate, even though I'm a specialist, because it's an unreferred consultation. The item numbers that apply to my speciality—item numbers 385 and 386—do not apply. They only apply under the constraints of the MBS to those when we're talking about return to work and occupational fitness for duty issues. When I'm talking about the general health and wellbeing of an individual and trying to understand what's going on in their home, I can't actually charge MBS. That's at the specialist level.

What I would like to go back to, if I may, is that we've highlighted the importance of de-exposure. We're talking about stuff that is ubiquitous in our environment. You cannot get no exposure—in most situations. So we're actually having to look at how we minimise, not remove or abstain from, exposure. As we've highlighted previously, if you maintain living in an environment where there is predictable high exposure, you're not going to get better. But if you can restructure your environment so that you can minimise the exposure, then you've got a chance to optimise the outcome. They're still going to have the sensitivity phenomenon, and they're still going to have the long-term implications for their health and wellbeing, but at least they may have a level of functioning in our society.

CHAIR: Can I suggest, if you're happy to, Dr Edwards, in relation to the schedule, you could provide the committee some advice of the clear deficiencies in the current schedule in terms of item numbers et cetera, and Dr Gupta, you could provide some advice on those medications you referred to that are unsubsidised and the testing costs as well. That would be helpful—in some specificity.

Dr Gupta : Yes.

CHAIR: Are you able to do that?

Dr Edwards : I'll take that on notice.

CHAIR: Thank you very much. I did want to talk about the issue of mould management in buildings—I suppose it comes to treatment. I know that Mr Stamkos might have some views on this, but also some of our witnesses on the teleconference.

You're talking about a very unregulated sector, but you're also talking about a sector where people may be unnecessarily being told to fear mould—it's like full body scans—and it's work generating, because you've got to have a mould-free house whether you need it or not. Firstly, would anyone like to comment—just as a factual thing—on the best way of eliminating mould from an existing built environment? Secondly, what type of regulatory system do we need in place to ensure that consumers are actually getting cost-effective and effective treatment to their buildings and homes?

Mrs Bijlsma : The key here is moisture and dampness, which we've already alluded to quite a few times. Moisture is the key because, of course, a healthy home should be dry and stable like a Mediterranean-like climate, but, when we add moisture, microbes are naturally going to utilise the substrates, which is pretty much all our materials and furnishings. It's the perfect food. When moisture hits the surface and it sits there for 48 hours or so, the microbes are going to start producing toxins to outcompete and kill each other off to take over the site, because that's what nature does. It's dampness. The external sources, the internal sources and sources created during the construction phase of a building are key to preventing all of these problems. It was commented on that we're all exposed. In a damp environment, something unique happens. We have Gram-positive bacteria that don't have lipopolysaccharides in their cell walls going to Gram-negative bacteria, which stimulate the innate immune response. It's a very different environment when we add moisture to that particular environment. There are myriad sources of external water that can impact a home: hot, high-humidity climates, for example, where the relative humidity regularly exceeds 70 per cent; natural events from storms and floods; water damage after a fire; farming related issues. In fact, an insurance study showed that, in Australia, 20 per cent of the water damage claims were because of the splitting of braided water hoses, especially if they were imported from Asian countries. That is a huge contributing factor to water damage.

We also know that the switch from sheet based waterproof membranes to acrylic has result in a significant reduction in the service life of these waterproof membranes. Most of these acrylic membranes have a service life of five to seven years, which covers the building warranty, but, after seven years, who can afford to completely do a new bathroom or laundry because the waterproof membranes are breaking down and the moisture is getting through the grout? The use of cleaning products with deliminine is actually significantly compromising waterproof membrane, so it could be two years before the new renovation of a bathroom starts showing water damage that could result in hidden mould in walls. We also have internal sources arising from plumbing issues and, as Tim mentioned, who's an expert in the field, condensation in new homes because the movement of water vapour through the building envelope being compromised. We've got occupants contributing because of their behaviour: loads of washing inside in wintertime in small rooms; the use of humidifiers; cultural bathing issues. I've talked in New South Wales about looking at cultural building problems. A lot of older Asian people bathe outside of the shower cubicle, on the tiles, and that water runs into neighbouring rooms that are closely associated with it. Heating, ventilation and air conditioning systems that are not properly maintained are frequently a source of biotoxins, especially in commercial buildings et cetera. It's such a huge problem that involves so many different industries, so we need education across multiple industries, including building and construction, especially in relation to the renovation of homes that could expose people to the invisible mould, which I've mentioned a few times. Real estate agents need to be mindful and give people duty of care if they've got asthma or allergies by saying, 'This has water damage history,' and give them informed choice before they even move into these environments. What I'd like to see is a move from not talking about mould. We're not talking about fungi. The literature is very clear that dampness and a multitude of antigens in a damp environment appears to correlate with some of these adverse health effects.

CHAIR: I will ask the obvious question. Forty per cent of the world's population lives in the tropics, in exceptionally damp and humid environments. Why don't we see significant problems in those parts of the world?

Mrs Bijlsma : I'm only giving you my hypothesis on this, but a lot of the building materials we're using have changed significantly. For example, in Australia we've got very different types of building materials to what we see in poor countries, in Third World countries. The substrate that fungi can feed off can determine the types of toxins that are emitted into that indoor air.

CHAIR: It does seem curious, though, that such a large part of the world does live in exceptionally damp conditions.

Dr Law : Could I offer a few insights into this. If we're looking in high-density areas, typically they're built out of reinforced concrete, so naturally you have material that is fairly resistant. The difference in Australian construction is that we are building timber-framed buildings. A lot of our timber products are engineered timber products, meaning we use wood glues, and wood glues have starches and that feeds the mould. We clad our buildings or reline them with gypsum boards, and that has a paper face on that, and that is mould food as well. So if you look at the construction practices, they're quite different. The other area that's quite different also is that, in tropical areas, you tend to cope with thermal comfort by naturally ventilating the buildings, so that keeps the humidity levels compensated for, whereas when you tend to start air-conditioning buildings, that's where you start seeing problems as well. So it's not that tropical countries don't have the problems. They are found more in air-conditioned buildings and especially timber-framed air-conditioned buildings.

Dr Edwards : The short answer is we don't see it in those other countries because the burden of disease in those conditions is different. They're there. It's just that the dominant burden of disease is different, and it reflects the culture and the built environment as well as the behaviour of the communities.

CHAIR: And I suppose also diagnosis as well.

Dr Edwards : As well.

CHAIR: So in terms of regulation of the building sector particularly in relation to those offering their services, there do seem to be a lot of businesses that are keen to capitalise. Firstly, is there a degree of concern about mould for someone who is not susceptible to mould related illness in the community?

Dr Gupta : There are going to be levels that are likely to be deleterious to anyone. In relation to the levels you were talking about where the ceiling of a building is barely visible due to the amount of mould, it's highly likely that there's going to be a direct toxic effect that anyone will experience if there's enough water damage and enough mould. However, what we're talking about with CIRS is smaller levels in highly susceptible individuals, so there are almost two different scenarios. You could say the standards of mould cleanliness that are needed for CIRS patients are very different to those needed for someone who's not a CIRS-susceptible patient. Therefore, it's very important that building biologists and indoor environmental professionals work with doctors and that it's clear what the needs of the patient are. If a patient has been fully diagnosed with CIRS, then one would think that it's perfectly legitimate for an indoor environmental professional or building biologist to be trying to offer solutions to reduce the water damage to the levels that have been shown in peer-reviewed studies to be necessary. However, to be offering that to someone who's not diagnosed would be inappropriate, and a much more broad level of cleanliness is needed just for the general population. Does that makes sense?

CHAIR: Yes, thank you.

Mrs WICKS: I do have some questions on this, with all of the reading I've done and my own crazy experience over the last couple of years. It seems to me that you get diagnoses from different businesses. One option is that they come in and say, 'Don't worry, we'll whack a coat of paint over that.' Somebody else may say, 'No, you need an ERMI test, and it's going to cost this much. You need to do this; you need to do that.' On the Chair's point, is there a need for a nationally consistent approach such that there's a level of consumer certainty and probably a level of confidence from the medical profession as well that there's some form of diagnostic approach that can give you a reasonable certainty that perhaps that is causing it? This goes to your point, Dr Edwards, about making sure that there's not an overdiagnosis. You were saying that people are getting scared. You called it the outrage syndrome, so that it actually does become normalised to whatever degree that is.

CHAIR: Mr Lark, do you have any comments on this issue?

Mr Lark : Maybe I should declare that we're the only laboratory in Australia, to my knowledge, that actually offers an ERMI test and/or it's derivative, the HERTSMI-2 test, which is done on five organisms as opposed to the 36 that are covered by the ERMI test. This has been now used exclusively by the CIRS community and the surviving mould community in America, where we also have a laboratory doing the same sort of testing. While one test is never going to replace an IEP or a trained mould assessor from going in and doing it, it is a very good starting point. And, as Ms Wicks said, it is expensive. It's about $400 have this test done but, by traditional mould testing, as a mycologist of 50 years' experience, I would have to build 10 times that to give me the same amount of information. I declare I have a pecuniary interest in declaring this but it's a great place to start.

Mr Stamkos : Can I also add the importance of assessing buildings. You mentioned about how there's no uniform approach, which is a huge problem in the restoration industry, as you know, and in the insurance industry. The insurance industry gets fed all sorts of different stories from different organisations, different individuals. Consumers will pay several thousands of dollars to have an indoor environmental professional, building biologist or people who are self-proclaimed experts in mould investigations, come in and give very different results, from the way they do their sampling to giving different scope of works. They provide incorrect advice on building from saying that they either don't have contamination issues where they clearly have mould growing on walls or out of carpets and significant water damage to other people going in and over analysing a building and giving misinformation about the levels of contamination saying the whole building has to be condemned because of certain types of mould present. So there is no uniform approach.

In the property industry, especially the remediation restoration industry, remember, tens of thousands of homes, if not hundreds of thousands of homes, have water leaks every year. In the property insurance industry, water-damage claims and flooding-risk claims are the biggest costs to the insurance industry so they're always looking to short circuit and reduce costs on claims. Unfortunately, people with some magic spray can come in and paint over mould or cover up the mould, not dry buildings properly, so they have prolonged water ingress and prolonged moisture issues. We're not dealing with that initial exposure of the water-damaged building and the subsequent mould contamination so there is a huge need for standards training, a uniform approach to how we deal with rectifying these water-damaged buildings and moisture-damaged buildings. Unfortunately, in this space, we do have Australian standards for air conditioning systems, and some of the other witnesses have spoken about our heating, ventilation and air-conditioning systems. We have hospitals and schools, and daycare centres that are rife with mould. These are our most sensitive populations.

In some of the states and territories, some of these standards are actually legislated but they're not regulated. So people are getting sick, children are being exposed in hospitals and people are dying because of hospital acquired infections. They are very limited and very rare but it does happen. And they are avoidable if the existing Australian standards were actually regulated. So there is a huge need for standards, training, certification and a uniform approach to actually prevent a lot of these avoidable illnesses.

Dr Donohoe : Just from a historical perspective, from the advantage of 30 years as a GP, we went through something like this with volatile organic chemicals in indoor paint; there was outrage over the whole idea of volatile organics causing harm. Paints were high in VOCS. People routinely painted their baby's room just before they came home and it contributed to harm. There was a lot of testing that went on, massive amounts of testing. In the same way that we see now, as the outrage grew, there was always someone there to meet the needs. What happened in that industry was the products changed in response to the consumers. Low VOC paint started to become the norm and now we're at the point where nobody would use high-volatile organics in their home or in their businesses because there are better alternatives. But until it was driven by the paranoia somewhat there was no need to change as far as industry was concerned. The doctors would scream and nothing would happen. Then when the outrage factor went high enough it did something to change the industry to say, 'Consumers would prefer something else. There may or may not be a problem, but let's move on and solve the problem.'

The same can be done with mould. Solving the problem in the home is not as hard as it sounds. It's just laziness that allows us to say, 'Mould is really a problem. If consumer outrage is high enough there'll be people who will always fit that need, and there'll be homes that are built better in the future.' What we can do is progress that to better homes, better schools, better workplaces and treat the people who are most severely affected. The medical side is not treat everybody but those who fall off the edge, who are the most sensitive, and get the buildings right, get the biologists doing their job to make the industry behave in a better way.

Mr ZAPPIA: Are there any pre-existing medical conditions that make a person more prone to a biotoxin-related illness?

Dr Gupta : The number one, which I think Dr Edwards mentioned, is what we call immunosuppression. That's where someone has a deficiency of their immune system. HIV was mentioned. There is a whole host of other conditions which can cause that. In those cases, people who have immunosuppression, there is a risk of life-threatening mould infection. Just be clear, that is different to CIRS. That's like aspergillosis or other types of bloodstream infection with fungi. That's the sort of condition which is often treated in an intensive care unit. That would be the number one thing that would predispose a person to more severe illness due to mould. Over and above that, when we're talking about CIRS, it's the fact that they have genetic predisposition, which is usually predicted by their HLA type. Hypermobility, as I mentioned before, can also be a type of predisposition. There has been some research on that. Then it appears that often some kind of viral infection or some kind of infection will prime their genes to start activating or being expressed. That's what the immunology theory has shown. That's the pre-existing medical situation often of a patient who then goes on to have CIRS. Of course, having any other pre-existing medical problem, such as diabetes or thyroid, will add to their disease burden, but it's not specific to CIRS.

Dr Donohoe : I also see allergy. There are a lot of people with severe, prolonged allergy where there may already be some sensitisation of the airways. Maybe that's a good group to look at as, if they've already started down that path, could a second insult be the kind of thing that makes them worse?

CHAIR: Thank you all very much for attending today. It's been a very helpful start to our inquiry. My knowledge base has gone up by about 1,000 per cent. To those of you who offered to provide additional information to the committee, or anyone who wants to make a supplementary submission, could you please do so to our committee secretariat by 23 August. You will be provided with a Hansard transcript of today's proceedings, and if there are any corrections to that please let the secretariat know as soon as possible.

Proceedings suspended from 12:49 to 13:51