Environmental health - Addressing patients concerns about PFAS
Jasmine
Welcome to tonight's webinar, Environmental Health, Addressing Patient Concerns About Per- and Poly-fluoroalkyl Substances or PFAS. We are joined tonight by speakers Professor Tim Driscoll and Professor Alison Jones. Our GP facilitator is Dr Kim Loo. My name is Jasmine and I am your RACGP representative for this evening. Before we get started, I would like to make an acknowledgement of country. We recognise the traditional custodians of the land and sea on which we live and work and we pay our respects to Elders past, present and emerging. I would also like to acknowledge any Aboriginal and Torres Strait Islander colleagues that have joined us online this evening. I would like to introduce you to our speakers for this evening. Professor Tim Driscoll is an Occupational Epidemiologist and a specialist in occupational and environmental medicine and public health medicine. Professor Alison Jones is the former director of the UK National Poison Service in London and has advised New South Wales Health on toxicology matters for 14 years. Our GP facilitator for this evening is Dr Kim Loo. Dr Loo is a GP in North West Sydney and is the chair of the Hills Doctors Association and actively advocates for a sustainable future through her work on the RACGP New South Wales Council. I will now pass to Dr Loo to read out the learning outcomes.
Dr Kim Loo
Hello, this will be a great webinar. We can actually understand PFAS and your learning objectives, will try to be clear about it. By the end of this online CPD activity, you should be able to:
One, describe the epidemiology of PFAS exposure in the Australian population.
Two, summarise the current evidence for the potential adverse health effects of PFAS exposure.
Three, implement appropriate counselling with patients on PFAS related concerns such as their risk of adverse health outcomes, the utility of blood tests, side effects of PFAS blood removal methods and patient management.
Four, describe the principles of risk communication in the context of environmental hazards.
Professor Tim Driscoll
Thanks very much, Kim and Jasmine. I am going to get you started on the first half or two thirds of what we are going to cover and then Alison is going to take over from me. First, I just want to spend a little bit of time talking about what is involved in human health risk assessment. We do not have time to go into any detail at all, and some of you may have been involved in this and some of you, might not, but I will just give you a brief overview. Note that little footnote on the bottom. There are a few slides in this presentation that I have stolen or adapted from Nick Buckley with his permission, so you know I did not come up with all these ideas myself. What we are looking to do is to do risk assessment, there are three aspects to that. There are things to do with the hazard. There are things to do with exposure to that hazard, and there are things to do with the vulnerability of the host, the person in this case. If we look at the hazard in terms of where the information typically comes from, often it will come from animal evidence and/or in vitro evidence and/or human evidence, which is nearly always epidemiological evidence, and it is that third one that is clearly the most reliable, although even the epi evidence, and I am speaking as an epidemiologist, that is my specialty area, you have to be careful not to necessarily take things on face value. You have to look at the strengths and limitations of any of the studies, but they are the three usual sources of evidence on the hazard.
In terms of the exposure, the two key things you are looking for are the root of exposure and the level of exposure, and I did not put any detail about the root of exposure here with PFAS, but when we are thinking of PFAS, the primary route of exposure is oral. There is probably some inhalational exposure not thought to be very much dermal exposure. Primarily we are looking at ingestion in some form. In terms of the level of exposure, if we are thinking about PFAS, in so-called contaminated areas, really you are looking at parts per trillion. In terms of biological systems in humans, we are really looking at parts per billion, even in the so-called extremely high blood levels, in Australia, it is maybe up to maybe 50 nanograms per millilitre, and just to keep that in mind that the total body burden then is lot smaller than 1 mg in total. I understand it is going to be a little bit hard for you to interpret without comparing that to a whole lot of other contaminants that we might worry about or so-called poisons we might worry about, but just to show you the total amounts that we are talking about are very small. Just down the bottom to keep in mind, the elimination half-life, there are lots and lots and lots of different types of PFAS. Most of the time I am just going to be talking about PFAS as a group, but I am going to talk about three particular ones that are the most common and seem to have the highest levels, but PFAS as a group, the half-life is on the order of two to 10 years, sometimes more than 10 years. We have done the route of exposure, level of exposure, sources of evidence. In terms of vulnerability, the things that you need to take into account are the severity of the outcome. Is it a trivial thing or is it death, for example? And the probability of getting that outcome. Just to take you back to that first slide, these are the three things we are always thinking about in terms of risk, hazard, exposure, and vulnerability. I am going leave the lesson on risk assessment there and move on specifically to PFAS. In terms of the common sources of PFAS, most of you have probably heard about the aqueous firefighting foams and they certainly have been an important source in some occupational settings and particularly in terms of contaminating land. These were phased out from the early 2000s. In New South Wales, for example, they ceased to be used from 2007, supposed to be, unless there was some amounts that were around that were not known about, and they were ceased to be obtained from 2007 and they are not being used as far as it is known from like 2022. Sources of PFAS away from firefighting foams. Most stain and water-resistant treatments have PFAS of some sort. Non-stick surfaces, particularly on cooking equipment, and that is clearly an issue if the main source of exposure is ingestion, and food packaging. Fortunately, all of these have been decreasing over time. What I want to move now to, they are the sources, in terms of what we know about the epidemiology of PFAS in Australia, really the main information that we know is from the Australian Bureau of Statistics National Health Measures Survey, which was conducted in 2024. It is publicly available. I put the link in there. It is easy to find, even if you do not use that link, just type in ABS and PFAS and you should find it. It was looking at 11 different types of PFAS and the survey was conducted over 2020 to 2024 but released in 2024. The three main types of PFAS that it provided information on were perfluorooctane sulfonic acid, that is PFOS, perfluorooctanoic acid or sometimes octanoate, it is called PFOA, and perfluorohexane sulfonic acid, and they are the ones I am going to present information on today.
If we are looking at the prevalence of exposure, nothing to do with the level, but the people who are in the survey, had their blood taken, virtually all of those people had PFOS in their blood. Virtually all, just slightly less, had PFOA and nearly all, nearly 90%, had perfluorohexane sulfonic acid. This is a general population survey. Basically, what that are saying is if you take people's blood, you will find PFAS or one or more forms in their blood. What I am showing you now is a series of results from this study. Some of the graphs I have taken straight from the publication, some I have modified a little bit myself. Just notice at the top that these are for people 12 years and over, and on the Y-axis, you have got the proportion as a percentage. We are looking at the proportion of people who had a detectable level of PFOS, and PFOA, and the PFOS is in the light blue, the PFOA is in the dark blue, and on the bottom, we are looking by age. This is not the level, this is just the prevalence, do they have it or not? and what that is showing is really across the age group, you can detect this. Higher prevalence in the older age groups, but over all age groups, the vast majority of people have both PFOS and PFOA. This is instead of the prevalence on the Y-axis, this is the absolute level, ng/ml, and males are in light blue, females are in dark blue, and males and females combined are in the orange. On the Y-axis, you have again got age, and the main things I think you should take away from this is that at most age groups, the levels in males are a bit higher than the levels in females, and that the levels increase with age, and this is geometric mean that it is showing. The reason for increasing levels with increasing age is that the older people have worried around when there were high levels of PFAS in the community, and also that had a longer period of time to be exposed and to absorb it. They have also had long period of time to slowly get rid of it, but the weighing up of those various factors means that levels are higher in older people. This is showing along the Y-axis same thing, the geometric mean, on the X-axis looking at state and territory, and what I am trying to show from here is that the levels are pretty similar in all states and territories. You can see some a higher or lower, but similar-ish. These are the median levels and the 95th percentile to give you a feel about what scatter there is and what the higher levels are for PFAS, PFOA and perfluorohexane sulfonic acid. You are not going to get tested on this, but just to give you a feeling, look, it is around one and a half of PFOS and below one for the other two. Here I am comparing the levels in Australia to the levels in other countries that we have got information for. Again, this is not information I have got independently, this comes from the ABS report. This information in purple is for Australia. I cannot remember why I was looking at this, but I think the only information I had was for younger people, just bear that in mind. For PFOS, the median level was 0.95 in Australia and in Canada, USA and Europe higher. For perfluorohexane sulfonic acid, lower absolute levels in all countries, but lowest in Australia and same for PFOA. That is not to trivialise it, I am just trying to give you a bit of context to show that the levels here are lower than most of our comparators, bearing in mind these are within younger people, children, and adolescents. This is the main summary of what I have just shown you there that I would like you to take away. Firstly, that the sources of exposure are declining in prevalence and also declining in level. PFAS is detectable in the blood of nearly everybody. Levels are somewhat higher in males than females, higher in older people than younger people, similar across the country, probably lower in Australia than comparable industrialised countries. That is the end of the epidemiology, which is sad of course, because I know everybody likes Epi. Now I want to have a look at a little bit on the health effects and the underlying evidence about that. I am not going to go into detail on the evidence. Here I have listed the main associated health effects. I will not read through them. It is the first five and then there is four more. There is some epidemiological evidence for all of these, but for all of these, the epi-evidence is not great and/or the evidence that is there of increases or of adverse function, the changes are very small and it is not clear that they are clinically relevant. Again, I am not trying to dismiss it, just saying that the evidence, there really is not good evidence of important clinical effects with the one proviso of cancer, which I will come to, and the problem with that is that the findings have been, with the evidence I mentioned, is the findings have been inconsistent. Generally, the levels of PFAS that have been involved in the populations have been very low, very likely there has been significant selection bias, very likely there has been important measurement bias, very likely there has been problems with confounding and there is definite cause for reverse causation, which I will show you in a moment, and the thing that is, I think, most important from your point of view and in terms of your interaction with the patients and what you might do in response to concerns of patients or lack of concern in patients is to keep in mind that there is no good evidence relating blood levels to clinically meaningful outcomes, which means if you take blood from somebody, and you get a particular PFAS level or a level of a particular PFAS, you do not really know what that means from a clinical point of view, and I will come back to that.
Now, in terms of reverse causation, this is what I am talking about. This is what we often see. People with high PFAS concentrations have high levels of urate, high levels of cholesterol, abnormal kidney function, decreased kidney function, but the interpretation of that is complicated by the fact that if you have decreased kidney function, you will have high PFAS concentrations, high cholesterol and high urate. Cross-sectional studies really do not provide much useful information because you do not know whether the decreased kidney function predated or post-dated the increased PFAS concentrations, and that is a really big concerning a lot of the epidemiological data. Okay, just keep that in mind, but let us move on from that for a moment. In terms of the evidence regarding cancer, the IR, the International Agency for Research on Cancer, is the World Health Organisation body that m looks at various hazards and weighs up the evidence about whether it is likely that these are human carcinogens, and they rate their level of evidence at different levels. If it is a group one, it is seen as a definite human carcinogen, and PFOA was declared a definite human carcinogen by IAC when they last looked at it, which was 2024, I think. It might have been last year, but I think it was 2024, and they labelled PFOS a group 2B carcinogen, and what that means is there is usually some reasonable animal evidence, but very little or no useful human evidence. That is the words they use as a possible human carcinogen. This is for PFOA. It was deemed that there was sufficient animal evidence, that means that PFOA clearly caused cancer in some animals. There was strong mechanistic evidence, that means the way that PFOA seemed to work was consistent with what was understood about the way cancer might occur, but the epidemiological evidence, the human evidence was, what I would call, limited and it is not very strong, and it was for two types of cancers, renal cell cancer and testicular cancer. For PFOS, there was some limited animal evidence, pretty good mechanistic evidence, but virtually no human evidence of a problem. That is why it had a different rating. Now, it is important to keep in mind that IARC looks at hazard, it does not look at risk. It says there is evidence that if people are exposed to PFOA, they have an increased risk of cancer, but there is no mention about what that risk is, and the risk appears to be very low and the evidence as to what cancers are involved and the risk associated with that is pretty poor. Just keep that in mind because as I have said here, the relevant epi studies are not great, and to keep in mind the absolute risk of cancer, and I am to talk about absolute risk in a little while, looks to be low. They are rare cancers and because the PFAS levels in the community are very low, any associated risk is very low, or likely to be very low. I am going to give you just a quick overview about interpreting evidence, just to talk about relative risk and absolute risk, and I appreciate some of you might know this very well, but I suspect some of you might not have done it for a while, just worthwhile keeping in mind. When we are talking about relative risk, it is the comparison of risk in one group compared to another group. For example, if the relative risk of cancer from some exposures five, that means that people who are exposed have five times the risk of cancer compared to people who are not exposed. It is always a comparison. The relative risk is 1.5. Those people have 1.5 times the risk or a 50% higher risk of being diagnosed with cancer compared to unexposed people. Absolute risk does not have that comparison. It is just the risk of getting the outcome, and both of those things are important in terms of interpreting somebody's risk, and as an example, the average risk of lung cancer in one year in Australia in 2021 was approximately 54 per 100,000, that is not a comparison, that is just the absolute risk for the average person. If we look at relative risk and absolute risk, high relative risk is not necessarily worse than lower relative risk because you have got to take into account the underlying risk. Let us say we have got an exposure where the relative risk is 5 and the underlying risk is 1 per 100,000, then the people are exposed, their risk is 5 per 100,000, you are getting four extra cases in a year caused by that exposure, but if the relative risk is much lower, say 1.5, but the underlying risk is much higher, instead of 1 in this top example here it is 30, then relative risk of 1.5, the risk in the exposed persons would be 45 per 100,000 compared to 30 per 100,000. You have got 15 extra cases in a year. High relative risk is not the only thing you should look at. You should look at underlying risk as well. In terms of PFAS, just to give you a bit of a feel, these are not hard and fast figures, the relative risk of 1.8 for PFAS and renal cancer comes from the paper I have put at the bottom of the page, but there are issues with the studies that this is based on, but let us assume that the relative risk is 1.18, and the lifetime risk in unexposed persons of renal cancer in Australia was 150 on 10,000. If the relative risk is 1.18 and the levels of exposure were the same as the levels of exposure that were in this study up here, then the risk in exposed people would be 177 per 10,000, which would be 27 extra cases for every 10,000 people across their lifetime, which is not trivial, of course, but just gives you some feel of the scale, and it also, need to bear in mind that the 1.18 is not hard and fast because the epi studies on which it is based are not great.
I just want to bring you back to the association versus causation figures that I showed you before, because this often comes up that high PFAS concentrations are associated with these outcomes, and I think probably the best evidence is of increased cholesterol levels with increased PFAS concentrations, not high, but higher, but we always need to keep in mind this problem with reverse causation, and for example, Nick Buckley, when I talked to him about it, he thinks the vast majority of the connections are related to this. The other thing that I think is very important is to keep this in mind, that there is not good evidence relating blood levels to clinically meaningful outcomes, and we will see what Alison thinks about it, but to my mind, it means that in most circumstances, one could even say all circumstances, but certainly I would say in the vast majority of circumstances, blood levels do not give you helpful guidance clinically. Okay, that is it. I will stop sharing now and hand over to Alison.
Professor Alison Jones
Thanks, Tim. That was a real tour de force through very complex literature, and you made it very accessible, and I think represented the literature incredibly well, as I have always heard you do, and you have done again tonight, really clear advice from Tim based on that literature, and now for clinical conversation amongst our colleagues about what are we going to do? Given all that Tim has told us about where the literature sits, how are we going to manage patients who present to us who are concerned about PFAS? And the first thing I would say is, if you hear sneezing in the background, I have to confess I have a beautiful rescue dog and he is sneezing just now. I cannot apologise, but just if you hear some strange noises, I promise that is him rather than anything else.
In assessing patients with PFAS exposures, it is really important to confirm where people may have been exposed from, and then stratifying individual clinical risk with the exception of PFAS levels in blood. What kind of cooking utensils do they use? Have they got fireproofing on the sofa? Have they been in populations where water exposure to PFAS or runoff from firefighting foams has occurred given that there was a cutoff in exposure to the latter two most recently, and then what we would suggest is that you then consider, or I consider when I see patients, targeted screening for any potential associated conditions. Remembering Tim's advice that there are associations, but the associations are not causality, but all of this has to, I think, happen in that context of that broader risk assessment and screening for other age-specific medical conditions, and this is, of course, what general practitioners do fantastically well. It is keeping it in context, I think. When we have identified ongoing exposure sources, it is important to turn off those sources if they seem to be in any way significant, and they can be advised from local authorities around water utilities or consumption of locally sourced foods or drinking water, accepting that most of the drinking water sources are there clear, if not all of the drinking water sources are clear, and certain products like food packaging and household products and firefighting foams which are no longer permitted for use, should not be causing ongoing exposure, but it is worth having a general conversation with patients about what potential ongoing sources could be to turn the exposure tap off if we can. I think it is really important in that concept when I talk about turning taps off, it is not a quick on and off in terms of length of time that these chemicals spend in the human body, recognising that long half-life of the chemicals. PFOA can be 3.1 years, for example, PFOS 3.4 years, can be up to 11 years in some cases, and remembering you need five half-lives to get complete elimination of any substance from the body, and there is a multi-source, therefore multi-year burden of PFASs across the range, which declines slowly after you have got source control, and as we have already articulated, or as Tim has already articulated, renal function is a key determinant of that elimination time, but there are very large inter-individual differences between individuals. Those who were watching very carefully Tim's slides of PFAS blood levels, would notice that women of childbearing age seem to have a lower level, and that is probably secondary to periods and losing blood and therefore reducing the PFAS levels that way as well as the more conventional or the more ubiquitous across all people, renal elimination methods.
I am going to talk now about different forms of what I would focus on in terms of my health evaluation in the hope that that framework might be of help to you and that you can adopt or ignore anything that I am talking about this evening and adopt what you feel may be of value to your clinical practice, and this is really a discussion clinically for your consideration. Only your patients well and only you know your practice really well, but sort of things that come to my mind are there is some evidence in association that PFAS exposure can be associated, not causality, with reduced vaccine antibody responses, and what I would do is review vaccine history, ensuring that there is up-to-date immunizations, and if there is a particular high risk thing that you are covering, checking titres to make sure that you have got your seroconversion at the scale that you want to. Lipids, we heard from Tim that cholesterol appears in association to go up as PFAS exposure occurs. I would be, across my patients, assessing their fasting lipids in the normal kind of a way, age specific, blood pressure, glucose, haemoglobin A1c, and manage according to what general practitioners do every day, the ACS and other risk assessment tools to an evidence-based guidelines around managing those results, and nothing about PFAS exposure means that we manage that any differently than we would a cholesterol that is elevated, for example, where there is not a PFAS source known to us. In terms of endocrine or reproductive potential associations, I personally take a history and examine for any thyroid dysfunction. I do anyway in general medical patients and any putative reproductive associations. Again, my index of suspicion is not very high based on the EPI data that Tim has shared with you, but it seems prudent and pragmatic given a weak association data set to at least check through that, and in terms of liver and kidney disease, whether you call it UECs or Chem 20s, checking renal function, dipstick in urine for blood and protein, liver function tests, and then managing those as you would any other patient with abnormalities in liver or renal function tests. In terms of cancer, and this can be very emotive, I am speaking to people who already know this, or speaking with people, colleagues who already know this, but a lot of people have a very understandable cancer fear, and when they link PFAS to associations with cancer, it really does make them concerned, and how can we as health practitioners then accept that concern and deal with that in partnership with our patients. Well, in the same way that we have been trained to do all our lives around taking a really full family history and all likely carcinogen exposures down to workplace type exposures, whether people smoke or full risk of cancer exposure scenario, which may or may not include PFAS. and then undertake normal age specific cancer risk screening. There is association but not causality with endocrine disruption. Do we do specific uterine cancer screening because somebody may be fearing PFAS exposure? No, we do not, but if our normal clinical antenna goes up because of our clinical risk profiling of that patient, then we do the normal investigations around presence, absence and staging if it is the case of any form of cancer, recognising that cancer, as Tim would point out, is a common lifetime disease risk.
Then I thought it would be helpful for us just to have a chat around elimination methods. If you have got a patient who comes in and they have been some private lab, which I would not recommend toxicology wise, and they have got a level, does not really matter in this context what the level is, but they want to know from you, can you get that level down for me? The short answer to that is yes, we probably can. The longer answer to that is, not with that side effects that are probably worse than any potential health risks that we are dealing with and not in a sustainable way moving forward. Various things have been tried and they make intuitive sense. They have face validity. People who have tried cholestyramine are a bile acid binding agent with all of the side effects that we have known and loved with cholestyramine including diarrhoea, malabsorption of the fat-soluble vitamins, etc etc. Venesection, and clearly if PFAS sits in blood, you can remove blood and get a bit levelled down, but of course it re-equilibrates and given the long half-life in blood and fatty tissues anyway, it makes very little overall difference. You can temporarily reduce the blood concentrations, but there is no proven, and there are some studies, not great studies, but small cohort clinical studies, no proven positive health impact, and as I pointed out, the side effects are not acceptable in that risk benefit basis. We currently would not recommend using those for PFAS exposed patients, but we do understand the pressure that you are under, and I have been put under that pressure myself clinically. It is hard, I know. PFAS clinical summary then, I think we do what we are trained to do, which is a risk assessment and risk communication just as we would with every patient in that general context of managing all our risks and all our exposures in an individual patient. I think when a patient comes fearing PFAS exposure clinical effects, it is a wonderful opportunity to provide some precognitive work around alcohol use, around smoking, around other risks that actually are measurable, less of associations actually where there are proven causalities. I would take and I do take the opportunity to get into those conversations, and I think Tim used a wonderful phrase. He does not want to be dismissive, and neither do I want to be dismissive. We understand that these chemicals hang around and understandably people are concerned about their clinical effects, and I think we all acknowledge that together, professionally, and also importantly with our patients, but it is what we do in a meaningful, risk-appropriate way to manage that, that is absolutely core to how we move forward in support of our patients in my view.
Is there another slide or I think we might be moving on to our case studies. Thank you very much everyone.
Jasmine
I will just get Kim to come back and we can go through that case study.
Dr Kim Loo
I think the next thing we might do before the case studies is to actually go through the questions that are in the Q&A and we will ask our wonderful speakers have done such a great job with explaining complex stuff because it is really a risk. It is one of those things we have to understand. All the epidemiological stuff is so important to grasp. Let us go through the questions. Now the first one is from Dr Gomes. Half-life of 2 to 10 years or more in the environment of once in the host, I am reading the question specifically, but is that clear? Tim and Alison?
Professor Tim Driscoll
Yeah, I might jump in, but then I suspect Alison might be able to answer it even better than me. Look, the way I am interpreting that, and Bernadine, if you have got another, if you want to add some more, let me know, but I was interpreting to say, well, if you had a one-off exposure or a big exposure, is that what the half-life is? The half-life's independent of the source and the level of exposure, and as Alison was saying, you need four or five half-lives to get pretty much get rid of everything. My initial response, and I do not know whether I am answering that question in terms of what Bernadine was interested in, but that half-life is constant regardless of whether it is one or four long-term exposures, but if you continue to have exposure, well then of course your elimination is going to go further down the track as well, it is going to take longer.
Professor Alison Jones
That is perfect Tim, absolutely agree. The half-life just to be as my med students would call me, anally retentive, is the time taken to go from an initial blood concentration to half of that value, and that remains constant appropriate to the renal elimination. If my EGFR remains the same, then pretty much my half-life for PFASs will remain the same, but as I age or I develop some nephropathy, then that elimination of half-life might change on that basis.
Dr Kim Loo
Okay, thank you much. Next question is from Dr Freeman and says here, my 78-year-old mid-low bath patient has had 30 years of exposure, had renal functions decline for no other reason for creatinine of 70 to approximately 190, and she cannot afford a PFAS test.
Professor Alison Jones
Well, I have some good news there because I genuinely do not believe a PFAS test would be of value to that patient, and recognising, of course, that there is very good evidence that after the age of 60, our glomerular filtration rate significantly, on average, reduces. Anno Domini, age over time, renal function may deteriorate, but just as we were talking about risk assessment before clinically, I want to know with this patient that they are not diabetic. I will dipstick their urine for blood and protein, asking about any autoimmune diseases, looking for any other cause of nephropathy that is a reversible cause or could explain the change in renal function, but I would be very surprised in the extreme if PFAS were the cause of renal dysfunction per se, it is probably that the renal dysfunction has occurred, and then if you did measure a PFAS level, it will still be reducing, but reduce at a slower rate than it otherwise might have. I hope that is helpful.
Dr Kim Loo
Yeah, that is super helpful actually, because there are many causes for renal decline as well, and even dehydration, can get a major drop in your eGFR. Okay, the next question is from Dr Punhella and it says, non-stick cookware, is it best to avoid all? How reliable are these labels? I heard there is no strict regulation in industry.
Professor Tim Driscoll
I might jump in there. Basically, I do not know the answer about the labelling. In terms of the non-stick cookware, I am definitely not an expert on this, but my understanding is that there is much less involvement of various PFASs now in non-stick cookware, but I do not think it is zero, and if people are concerned about it, then sure, trying to avoid it is the best approach. As I said, I do not know about the labels. It is worthwhile keeping in mind that the blood levels in Australia are definitely decreasing considerably over time, which is good evidence to say that whatever the sources of exposure have been, and it is not just non-stick cookware, but whatever the sources have been, they are definitely significantly declined or declining.
Dr Kim Loo
Okay, and it is Dr Freeman again, how does PFAS exposure actually reduce vaccine-induced or native immune function?
Professor Alison Jones
Good question. Nobody in the world knows the answer to that. It is a postulated association, could be lipid mechanics, could be some immune direct suppression. We genuinely do not know, and it is more of an observed association mechanistically we are in our infancy with that one. I do not know whether Tim can add.
Professor Tim Driscoll
No, nothing useful.
Dr Kim Loo
What is considered high risk for PFAS exposure? Does living in certain numbers of years in Europe or US count?
Professor Tim Driscoll
I think the answer is look, it is not clear. I do not think that you get any agreement as to what would be considered high risk for PFAS exposure in terms of, I presume, meaning what blood level would be seen as being bad as opposed to less bad. I do not think there is an answer for that, and I would go back to the one of my closing points was there really is not good. In fact, there is bad correlation between blood levels and meaningful clinical findings or implications. I do not think really it is helpful to think this is high risk, this blood level is high risk and this blood level is not high risk. I think if people are concerned, then it is helpful, as Alison was saying, to guide them as to how they could decrease their exposure, and to help them understand that the risks are likely to be of anything clinically meaningful, are likely to be very low, even really regardless of what the blood level is, but certainly any blood level that people are likely to have in Australia, and I noticed what Freeman has written a bit further below about higher levels in the Blue Mountains and I am not saying that is not the case but I am not aware of any evidence that one would then say well therefore those people need to be worried about having an adverse clinical outcome as a result of that. Alison I am not sure what you think. I guess that is where I sit on it.
Professor Alison Jones
No, I will sit with you absolutely, Tim. The only people that I think about as potentially being of higher risk than, if I can call it, the rest of us, might be occupational exposure. If you worked in a particular proofing area, but there again, in an occupational environment, there are so many rules to reduce human exposure, and mechanisms to prevent inhalation or ingestion exposure or contamination, that even that is probably not a high risk either, but there are some studies, and Tim knows these very well indeed, from Washington DC, I will not name the company, but where they produced firefighting type foams, and some of the original cohort studies were done there, but even with those studies, there is really no causality and the amount of association is still so minimal that I cannot see anyone can claim. I cannot see that as being a bona fide high risk.
Professor Tim Driscoll
Kim, would you mind if I just jump in there to add something because Alison brought up the occupational setting and I should have commented on that given my occupational background. It reminded me of an important thing. There is a lot of concern about aqueous firefighting foam and clearly the people who have the highest exposure to that are maybe the manufacturing workers, but then the firefighters, but in terms of the risks that firefighters should worry about, there is much better evidence of concerns about the things that they would be exposed to in part of their job as firefighters, there is much stronger evidence of higher risk from other exposures than there is for PFAS, and again, that is not to trivialise people's concern, but I just think it is useful in that setting and also useful in you talking with your patients that if people are concerned about ways of improving their health, most people have other areas for which there is much stronger evidence and for which the associated risks are much higher and for which a lot of them, there is good evidence about what can be done to either control any further increase in risk, to decrease the risk, or to put in place some appropriate screening program in some situations, as Alison was mentioning. Again, I know it is tricky to handle in the clinical setting, but just think in the long run, you will be doing your patients more of a service in a way, not to trivialise their concerns, but to help them understand the different risks and the different levels of evidence and the different abilities to do something useful about them, about other exposures apart from PFAS. Not everybody will agree with what I just said, but I am pretty confident that is useful approach.
Dr Kim Loo
I mean, all the particulates and aerosols that firefighters breathe in are really more significant because of the risk of lung cancer and everything else. Now, Dr Harrison, I had a patient who was a past firefighter had a brain tumour with liability accepted by WorkCover due to his past exposure. Is this likely related to the PFAS or something else, and Dr Sam Dennis says she would like to answer this one. Sam?
Professor Tim Driscoll
I think Sam just said she was going to put that down, not because she wanted to answer it, but because she wanted us to answer, and I would not mind jumping in there, Kim, because I was on the IARC working group that dealt with cancers, and we have not got a lot of time to talk about this. Firstly, I would say no, this is very unlikely to be related to PFAS. There is no evidence as far as I am aware of a relationship between, I mean, even more than a smidgen of suggestion of a relationship between PFAS and brain cancer. Secondly, there is very little evidence of a connection between work as a firefighter and an increased risk of brain cancer, and the reason that someone in New South Wales or elsewhere receives compensation for a whole range of cancers is about 20, is not because of the level of epidemiological evidence about it, except for mesothelioma and bladder cancer. They are the only two IOC having looked at it, they are the only two for which there seemed to be sufficient evidence. There is another three or four for which the evidence is pretty suggestive, but there are still concerns about the methodology of the studies, but for a whole range of other cancers, including brain cancer, for which firefighters do receive liability acceptance, it is because they are on the list of deemed diseases for firefighters, and we do not have time to talk about that now, but that list is not based on epidemiological evidence or strong epidemiological evidence anyway. There are other reasons why that liability is accepted, but in terms of today's topic, no, that it is very, very unlikely that is related to PCOS.
Jasmine
I feel like we may have lost Kim there, but I think there is one more question in here. Can certain water filtration methods reduce exposure from water sources?
Professor Alison Jones
Do I take that one, Tim? Yes, different filtration devices. There are many different filtration devices, and they all remove different things from water. Some are very good at removing particulates. Some are more active at removing different types of chemicals. You could ask me what a toxicologist uses at home, and it is just a simple water filter that you just put in a jug and then the jug goes in the fridge and I think those simple filters that probably many of us use at home are potentially helpful if you want to be extra certain in what you are taking and making sure you are not getting the insides of your tap directly into your drinking vessels, but in sheer scientific terms, there is no evidence that people should be protecting themselves with either big water filter that is at a house level or little filters from within the home. People may choose to, and it is largely, I think, around the taste of drinking water and improving that appetite for drinking water, and making sure that we get a bit more of it into us as a substitute for much less healthy drinks of Coke or Diet Coke, whatever, that we really want to be avoiding. For palatability, yes, why not? It is not going to cause any harm.
Jasmine
Okay, I think we have gotten through all of the questions. that is fantastic. If we have got time, I might just quickly run through that case study, Alison and Tim, if you are happy to do that. This has got an example, patient is 65-year-old female, presents with concerns regarding her PFAS levels. She obtained private blood testing for PFAS and advises you her total PFAS level is 22 ng/mL. She has hypercholesterolemia for several years, wants to know if her high cholesterol is due to PFAS. She has got some past medical history here, fatty liver disease, knee osteoarthritis, hypercholesterolaemia, cholesterol is 5.9, LDL is 4. Her BP and BMI are currently in the normal range. We have just got some results there as well. How would you counsel this patient?
Professor Alison Jones
I think I would begin by acknowledging the patient's likely concern because they have gone out and they have got a private blood test, acknowledging the emotion and acknowledging the concern and going through Tim's kind of presentation about where the PFAS data sits with the Epidemiological Association and no causality, and importantly reminding or stating that the blood levels are really not helpful, and I say to people, even though I have done clinical toxicology for many years, I cannot interpret these levels either. They do not make any sense to me and I would not be trying to interpret them for this patient. However, she does have a cholesterol that is higher than I would like and an LDL that is also higher than I would like. In the same way that I articulated previously, we would risk assessor for the hypercholesterolaemia and then do all the diet lifestyle factors, plus or minus statins, the coronary artery scan, all of the usual ACS assessments that GPs are fantastically good at. Would I do anything about the PFAS, only talking about it and trying to explain the data as I understand it and explaining that anything that we would actively do to get the levels down, would cause more harm than good in my view.
Jasmine
I think that covers the extra questions that we have got in there, like with the further blood tests and the extra straining that should occur.
Professor Alison Jones
It is a wonderful opportunity to do the lifestyle intervention pieces. You come to me worried that you got PFAS and I think Tim's got a wonderful phrase of, I do not want to trivialise it. I do want to accept that that is a genuine concern that you have, but if your concern is that about PFAS, there are many other higher risk drivers here that are modifiable, that we have really good evidence alters outcome when we do something about those. Let us go for the ones that we know with modification result in better clinical outcomes from a cardiovascular, cerebrovascular point of view and others, and the fatty liver will be dealt with that as well.