This is the third evidence session of our inquiry into perfluoroalkyl and polyfluoroalkyl substances—that is the last time, I hope, that those two words will be used in the conversation this afternoon. Normally we ask people to cash out all the acronyms, but in this case I think we would trip over ourselves. We are talking about PFAS, which are persistent substances or forever chemicals. We are very grateful to Professor Sunderland for joining us from the US and Professor Kirk from Australia, and we have Professor Boobis from the UK here in the room with us. May I ask you all to introduce yourselves and state who you are and what your qualifications are?

Good afternoon. I am Alan Boobis, emeritus professor of toxicology at Imperial College London, where I spent essentially my entire academic career working on the mechanisms of toxicity of chemicals, from environmental contaminants through to human medicines. For the last 30 years or so, I have also been a member of a number of national and international scientific advisory committees providing advice on the safety of chemicals, and until earlier this year I chaired the Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment.

Hello, everyone, and thanks for the invitation to speak to you all this morning. I am Elsie Sunderland; I am the Fred Kavli professor of environmental chemistry at Harvard University, where I am cross-appointed in three different schools: the school of engineering and applied sciences, the department of earth and planetary sciences, and the school of public health. Generally, my group studies how global contaminants distribute in the environment and accumulate in food, different types of food webs including humans, and then their impacts on public health. I have looked at PFAS for a little more than a decade now.

Hi. It is really nice to be joining you. I am envious of Professor Boobis for being able to sit there in the middle of the day; it is 1.30 in the morning here. My name is Martyn Kirk. I am a professor of epidemiology at the Australian National University in Canberra, Australia. I am an infectious disease and environmental epidemiologist. I have spent the last 30 years working on food and waterborne diseases, the first half of my career in government and the second half in the university setting. I have been working on PFAS for about the last decade. We have conducted a range of different studies looking at the health effects of PFAS in some affected communities in Australia, and continue to provide advice to government on health effects.

We are very grateful to you for being with us this afternoon. I wanted to start off by talking about the different international approaches to managing PFAS and the level of consistency that there is, or is not, across the globe. Recently, 20 international scientists produced a letter saying that they wanted to give a strong warning against attempts to narrow the definition of forever chemicals in response to efforts by individuals and groups within the International Union of Pure and Applied Chemistry to narrow the current international definition of PFAS in ways that they felt could be excluding certain chemical sub-groups for, they thought, political or economic reasons rather than scientific reasons. Could you just tell us what the level of global co-ordination is that is needed to effectively manage PFAS? I will start with Professor Sunderland.

I think having a unified definition of PFAS is incredibly important, particularly as we think about managing these chemicals as a class of compounds instead of trying to trace them one by one. Many of you probably know that it is not a single compound; it is a class of many thousands of different structures. That number keeps increasing, and it is a little bit hard to get a substantial handle on. The definition of PFAS really matters as we think about some of these alternative structures that we have not studied as much. Many of you may have heard of PFAS in the context of legacy PFAS and class-based concerns about long-chain PFAS. This definition is important, particularly for the shortest-chain compounds. With that, I talk about the one that has just a single perfluorinated moiety, trifluoroacetic acid, because we see levels of this shortest-chain compound increasing exponentially in many different environmental media globally and fairly high levels in humans emerging in the data. There is another component to this. I realise it is very confusing, because it quickly gets into very technical chemical language, but there are direct uses of these chemicals in commerce, and then there is general production of polymers. When you think about a polymer, you are really thinking about plastics and Teflon and things like that. There is also indirect production of PFAS as side-chain fluoropolymers; I will just flag that as a concern. Do these definitions include the shortest-chain PFAS, side-chain fluoropolymers? Then the other big bucket I would highlight for you would be within certain types of uses of PFAS. For example, in some of our work in the United States, where we are looking in waste water at all the PFAS that are present, the biggest component of that budget ends up being from pharmaceutical uses. There is a lot of organofluorine in pharmaceuticals. Some are defined as PFAS, some are not; it is the same thing for agrichemicals. As we think about class-based definitions and taking a precautionary approach to managing some of the adverse health impacts that we have seen associated generally with chemicals that are as persistent as PFAS, both in the environment and to some extent in organisms, depending on the specific structure, we really need to be careful about those definitions because they can be used to exempt certain classes of uses by industry, so they prevent us from looking at something that might be potentially harmful. They can also be used to change what we consider is the appropriate health-based guidance. For example, this becomes a particularly important concern when we are talking about pharmaceuticals. How do we think about a class-based approach when we are thinking about some regulated compound for a specific therapeutic use? It sounds like a detail, and you might just say, “Of course we don’t need to focus on this definition”, but it is really important. I do agree with my colleagues who have highlighted these concerns.

I do not have much to add about that. I certainly agree with Professor Sunderland’s comments, except to say that I think it is difficult to understand health effects of the many chemicals that are in the consumer products. I also think that, if these chemicals have been so widely used and it is a tide that we cannot stop, there is a need for greater global governance and management. The big travesty here is the environmental persistence and the fact that many of them do bioaccumulate and they last in the human body for many years, depending on the nature of the chemicals. I do not have much more to add.

What I take from what you have both said is that we should be looking at PFAS as a class and not trying to isolate, because that could be adumbrated infinitely, almost. We should therefore look somewhat askance at any suggestions from businesses that their particular form of PFAS should be allowed and is all right. Is that correct? It is just so that anybody listening understands. You are nodding, but if you could say yes, that would be helpful.

Yes, I would agree with that. One of the things about the legacy PFAS that Professor Sunderland mentioned is that it is really being focused on because we can measure it, and it has been present in higher concentrations. It is the one that we see and can measure easily in humans, and that is part of the reason why we focused on those legacy PFAS. They are still really important, but there are clearly many others that could be important in the future.

The persistence and the accumulation of them, we understand, is of vital importance. Can you give us an overview of the approach to regulating PFAS in your own jurisdictions? I know, Professor Sunderland, that in the US the Environmental Protection Agency has come out with its series of measures earlier this year to address PFAS. Then, perhaps, Professor Kirk, you could outline the same structure in Australia.

Thank you for the question. In the United States, there are two different levels of regulation. There is a federal level of regulation, and then there are also state-based regulations. For brevity, I am just going to focus on the federal landscape. Federally, basically the regulations are co-ordinated and led by the US Environmental Protection Agency. A big step forward, as mentioned, was the establishment of legally enforceable drinking water regulations in 2024. That was for six different PFAS, most of them the legacy PFAS, also including one compound you may have heard of as GenX. This is a compound that is produced widely, particularly in China. PFAS tended to be produced in North America and Europe but, as we have just alluded to, there are these alternative structures as well. So six PFAS were regulated under the Safe Drinking Water Act with legally enforceable levels. For brevity, I will leave it at that, but that was a major accomplishment in the federal landscape in the United States. That has been rolled back and now we are presently seeing a proposal to just have the two oldest, most widely produced PFAS, which have already been fully phased out, PFAS and PFOA, included. For the other four, the regulations are being rolled back, which for somebody like me is quite concerning because, for example, a short-chain PFAS called PFBS—this is one of the replacement PFAS for PFOS—we see in the drinking water of 50 million people in the United States. This is quite concerning. Beyond water, the federal landscape has also looked at the production of new PFAS, and this is done under the TSCA rule, or the Toxic Substance Control Act. There were pretty nice new requirements for reporting on the releases of PFAS. Again, this is a really important step forward for being able to assess the vulnerability of communities for different types of industrial discharges across the country. The definition of PFAS under the TSCA rule and the reporting requirements were quite broad—just going to the earlier context—and included around 1,400 different chemical structures, a little more than 700 that are actively produced in commerce. This was also very nice. Unfortunately, with the current Administration, this is also being rolled back. There are a number of exemptions being issued, and this is not nearly as stringent as the initial proposal moving forward as part of the toxic release inventory in this country. The last major thing is something called the superfund Act, which many of you may have heard of with respect to our most contaminated sites across the country. Again for brevity, the story in the United States is really that many of our most contaminated sites across the country are the result of firefighting foam use at US military bases. They did a lot of training activities historically with those foams, so they are incredibly contaminated sites. They drive a lot of the drinking water problems across the country. There was pretty aggressive action by the Department of Defence to find remediation technology, fund innovation and the destruction technology and remediate those sites, as well as set limits for clean-up targets and other things. I sound like a broken record here, but unfortunately those clean-up targets have also been substantially delayed at this point. There are new announcements quite frequently on delays on clean-ups of those most contaminated sites. There was a movement to phase out the use of firefighting foams, except for particularly hazardous oil-based fires where there was a safety concern, but to really phase out those firefighting foams that were the culprit, that contained PFAS—there are some non-PFAS alternatives—and that has unfortunately also been rolled back. That gives you a sense of the landscape here. There was a PFAS road map produced by the US EPA that was quite aggressive and forward-looking.

It was in 2021, yes?

Yes. What we are seeing right now is, unfortunately, a shift backward from some of those aggressive regulatory targets. I had looked at those and thought, “This is great as a first step.” We still have much to do, and I think that is what you are all thinking about. Unfortunately, right now the landscape in this country is fighting for the ground that we had already made in trying to uphold those protections.

Thank you—that was very comprehensive. Can I push you for a brief answer? How much did litigation by communities affected here drive the superfund Act, which I believe involves a levy on the chemicals industry as a whole?

That is a very specific question. I would say that, with respect, the specific Act is in place. I would say that the community action and litigation in this country is essential for almost all environmental action and for upholding regulatory deadlines. So your point is right on. The community outreach and work on their own has been essential for pushing this move forward.

Thank you. Professor Kirk?

We are similar in Australia in that we have a federated system of government with states, and we have six states and two territories that have responsibility for public health and environmental management. They are the ones that are making Acts and regulations regarding PFAS and implementing them. However, there is a lot of federal regulation and involvement in PFAS in Australia. Often federal government in Australia will set standards and guidelines that will be called into power in the jurisdictions. We have a national environmental management plan, which specifically references PFAS and sets guideline limits for waters, soil and biota. We also have a national chemical regulator, which specifically covers PFAS and related chemicals. One thing that has happened recently in Australia is that we have had new drinking water guidelines brought into being, which has led to a significant reduction. Australia had relatively high drinking water guidelines prior to this year; they have come in and they are not as low as the US EPA’s guidance. They use different health endpoints to derive them, but they are still very low. Most water authorities around the country that have been doing testing have not found exceedances to these water guidelines, although there have been a couple that have generated quite a bit of community concern. There are also contaminated sites and response protocols, which have been driven largely by defence force sites, as Professor Sunderland just mentioned. We have about 27 defence force sites around the country that have used some form of PFAS in aqueous film-forming foams. That has led to contamination of the surrounding environment, which has meant that federal government has had to be very strongly involved, particularly through the Department of Defence. As a consequence, there has been a huge amount of community engagement in some communities in particular, and that has led to numerous committees like the one that you are conducting at the moment. The most recent one has just handed down its report. It was a Senate Select Committee looking at PFAS management in Australia. Despite all our efforts—and there have been a lot of efforts from governments at state and federal level—they still came up with about 47 recommendations, many of which are quite difficult to implement, but the Government have not brought out their response yet. I think the situation in Australia is relatively similar, in a sense, to that in the US. We are still grappling with the problems of the legacy PFAS. We have seen about a tenfold reduction in PFAS in blood serum over the last 20 years, as have many countries around the world, so there has obviously already been a change in consumer products and the sources of exposure, irrespective of regulation. We have seen that consistently.

Thank you. Very, very briefly, because I am afraid we are now really pushing against time: how important is the consistency of PFAS definitions in regulating PFAS across jurisdictions? It is really a yes or no question, if you can just briefly respond to that.

Certainly, in Australia, yes, there is a need for consistency and a higher degree of co-operation between states and territories and federal government.

Just building on what Professor Kirk said—sorry, this is not yes or no. My answer is, yes, it is important; no, it is not being considered right now, because we are still focusing on that largely from a regulatory perspective, the one-by-one regulatory approach for PFAS. As Professor Kirk has alluded to a number of times already, the new production is not those compounds. The thing that we are looking forward and concerned about is not on the regulatory landscape yet, which is why we need this PFAS class-based approach.

Thank you very much.

My questions relate to the research about the impact on health, particularly human health, of PFAS. We were recently on a field trip to France to find out more about the legislation that they are bringing in there on PFAS. When we asked questions there about the actual data points, the research on the human health impacts, we were maybe a little surprised that there did not seem to be as strong an evidential link as we were expecting. Clearly, forever chemicals that accumulate in the environment and in our bodies intuitively does not sound like a good thing, so I would be curious. What evidence do we have linking PFAS exposure to health issues in humans particularly? Perhaps we can start with Professor Boobis on that.

That is one of the biggest areas of uncertainty, I would say, for many reasons. I am not an epidemiologist, but I have looked at the data as part of the committee work. It is a problem we have with many, let us say, low-level contaminants, that the human exposures are mixed, so it is very difficult to find a population with a clearly defined level of exposure to just the PFAS, because they are being exposed to other things. It would appear that any impact in humans is relatively low and that the relative risks are not as striking. They are not easy to detect by cohort studies. The studies we are doing are largely cross-sectional. We are looking at existing populations, and we are not following them through in time. There are some cohorts, but not many. All that adds to the uncertainty.[1] Then the effects we are seeing that are associated with PFAS exposure are of, let us say, questionable impact on human health. The one that EFSA and some other authorities have used has been a reduction in the response to some vaccines, notably the diphtheria vaccine, but linking that change to an actual health outcome is actually quite difficult. The data on which it is based is not as robust as some of us would like to see. I think that that is part of the complication of trying to pin down an actual human health impact of a PFAS. I would just add to what my colleagues have said that the problem is that we tend to look at the things we measure, which is like six or eight out of a total of several thousand PFAS, so we just do not know what is going on in the background with all those others.

That makes sense. Can I come to Professor Sunderland next with the same question? What evidence do we have about the link between PFAS and health outcomes?

Respectfully to my colleague, I do disagree with that assessment. I think we have a large body of evidence that grows every day, and this is common for a new class of chemicals. When we start studying them, as he alluded to, we have to set up studies to have the statistical power to see those effects. As he discussed, it is really difficult. We have to set up longitudinal studies and follow people over time to really be able to tease out the impacts of PFAS exposure on health, and we have a number of those studies globally. We see a large range of health impacts of these chemicals, with a much greater diversity than we have seen for other classes of compounds, which makes them incredibly concerning. I like to quote the former director of the National Institute of Environmental Health Sciences, Dr Linda Birnbaum, who was overseeing all the epidemiological research and funding those portfolios across the United States. She stood up at a PFAS-focused topic area meeting with a group of scientists about five years ago and said, “Hey, everyone—if you are an environmental health scientist, these are the chemicals for you to study, because we have now got a statistical association with every major organ system in the human body.” We do not just have those epidemiological associations; we also have animal data. With animal data, we are able to get to this idea of teasing out causal mechanisms. I think where the gap is in this field is jumping between those longitudinal data on outcomes and really understanding causally what is going on. How, for example, is the immune system responding to these chemicals in the field of epidemiology? We ask because if it is a statistical correlation between an exposure and a health outcome, where if the study is done well you correct for other confounding factors, statistically there is a whole field known as causal inference that Professor Kirk can probably speak to better than I can. The evidence is built by replication. So, for example, the immune impact, I think, has been replicated across a number of different studies now and is the most sensitive impact that we are seeing. There are other things. I will just point you to an article in the proceedings of the National Academy of Sciences in the United States that came out last week on drinking water-exposed communities in New Hampshire, where you see a higher rate of infant mortality. We see studies like that coming out in the literature all the time. I think the question for you as a Committee when you see this evidence is: is that enough, because it is not a causal mechanism? Do you need to go beyond that to study the impacts and understand the causal mechanisms for the next decade or so, or should you protect people now? My opinion is very strongly that we have enough health information; we have a very robust and growing field of data. It is not all causal, but it is more than enough to tell us that these chemicals are terrible for the communities that are highly exposed, and our understanding is growing and growing. I will stop there to give Professor Kirk a chance, but I think this is a really important question, so thank you for asking.

Thank you very much. Maybe we can get hold of the links to some of those research papers from you. Professor Kirk, the same question to you, please.

I think I am in between Professor Sunderland and Professor Boobis here. There have been thousands of studies conducted on the health effects of PFAS. Many of them are quite confusing. When you go and have a look at them, you will find studies that find an association and then the next one does not. We do have good evidence for some health effects, particularly things like elevated cholesterol, the vaccine immune response that we have just been talking about—there is good evidence for that—and possibly birth weight as well. There is another range of health effects where you have more moderate evidence and/or low evidence, and I would include some of the cancers in that. I think the real challenge here is that because exposure to these chemicals is so ubiquitous in society, you find that everyone has been exposed to these chemicals. You can find it in the blood of most populations around the globe, so that makes it difficult to compare groups of people who have had no exposure with people who have had high levels of exposure. I think we get the best evidence from studies conducted in highly exposed communities like Ronneby or the C8 study or Veneto in Italy. That is where we are likely to get the best information, but it is important not to look at a single study and make a decision based on that. It comes back down to what the weight of evidence is from a range of different studies and looking for other contributing factors like is there a gradient of health outcome with higher exposure? For many health effects where people claim that there is a link with PFAS, that is not actually really present. We do not see dose response very commonly. It is a very confusing area. However, I definitely think we should be acting to reduce exposure to PFAS. That is what I would say. It is about the difficulty of not knowing. There is a lot of uncertainty around the health effects.

It certainly seems that the precautionary principle would be the best way to go here. I am conscious of the passing of time, so maybe we can go for relatively short answers to my next question. What approach does the jurisdiction in your country take to assess the toxicity of individual PFAS? Does it use that to inform the health guidance? We will come to Professor Sunderland first, please.

It is difficult to give a brief answer, so I will do my best. Professor Kirk can wave or something if I go on too long.

Perhaps write to us if you cannot say everything that you want to say.

Yes, I will—I promise. It is generally a risk-based approach, as I alluded to a moment ago, and there is a health endpoint considered. Right now, it is generally the immune impact, because it is looking at the most sensitive population, where the attempt is to regulate for the most sensitive population. However, there is variability across different regulations. It is single chemical by single chemical right now, I think, which is the important point. There is an attempt, as I have just alluded to, to trace the causal mechanism as opposed to just associating an effect, so there is a weight of evidence that is being established. I will just say that I think it is impossible to get a handle on this problem for a class of chemicals this large, going single chemical by single chemical. Again, it brings up this idea of a class-based approach because going one chemical at a time will simply take too long. I will stop there.

Professor Kirk?

Yes, Australia has been taking a chemical-by-chemical approach. They take a risk-based approach to setting guidance around limits. Another thing is that it is important to recognise that communities have a big stake in this, so it has been intense scrutiny for the regulators. The amount of interest from communities is quite staggering.

I have a slightly different question now for Professor Boobis: in your view, what approaches could the UK adopt to ensure that any regulations we bring in here are appropriately robust?

We would use a risk-based approach as well. I do not think that there is any fundamental difference across most authorities in the principle we apply. We look at the most sensitive relevant endpoint using a weight of evidence approach, then apply appropriate factors to derive a human health-based guidance value. We would want to group the PFAS together rather than singly. I think we would also like to think about the possibility of not including all 7,000 in a single group, because there are very marked differences in their potency and in their persistence in the body, so perhaps some broad sub-groups would be the way to go, using in vitro and computational approaches to subdivide them. There is work ongoing on that already.

Very briefly, we have a question from Carla Denyer.

This is a follow-up question to you, Professor Kirk. You listed immune response, cholesterol and birth rates as three examples of where the evidence is fairly strong. With the caveat that I do not have a medical background, those seem three fairly unrelated things. Do you have any insight about why it seems to be affecting three fairly unrelated areas?

It is a good question for the toxicologists as well. These chemicals are largely inert but are endocrine-disrupting, meaning that they interact with hormones, and that is largely what we are seeing here. I think they are interacting with biomarkers; they stay labile in the blood and blood-rich organs. I think that is the main reason. However, again I think we have good evidence for those health effects; we see them consistently. However, coming to a place of cause is another thing altogether. I think the mechanisms are probably reasonably well supported for some of those in animal models. Given that we have a lot of uncertainty in the epidemiology and the epidemiological studies, using animal models and some of the mechanistic work that happens in laboratories is important as well. The list of things that have been associated with PFAS is large, but the evidence body is confusing for many of them.

It is a very good question. I have to say that when we have conducted epidemiological studies, we have been surprised that we have not seen more consistency among health effects. From my perspective, I think these chemicals have been used because they are useful for being anti-stain and anti-stick and withstanding high temperatures; they are fantastic firefighting properties, so that has driven their use. They have been ubiquitous in consumer products. The key thing is to deal first with that problem and make sure that we are eradicating them from the consumer supply chain as much as we can and not using them unless absolutely necessary. Then, if we are talking about setting limits, I think we have to choose health endpoints that are reasonable. Personally, I think some of the water limits are possibly too low because they are around the limits of detection of much of the analytical chemistry, but that is probably where we need to go. They have been relying on their health endpoints of vaccine antibody response. We have used different health endpoints in Australia and they have not been based on epidemiological studies, but more on animal data and other mechanistic evidence. It is very challenging for regulators; I acknowledge that.

I would just add a couple of things. One is that as a mechanistic toxicologist I very much like a defined model and to get at the actual mechanism involved. The difficulty with the PFAS and using animal models is that we know that they affect hormonal receptors and other receptors, which tend to have rodent-selective effects because we know that other compounds that act on those receptors are used in human medicines and do not have the same effects in humans. It makes it quite difficult to translate some of those experimental results into humans. That is one of the reasons we tend to rely very heavily on the epidemiology. As my colleagues have said, some of those effects are associations, so we are driven to the situation of saying that there is going to be uncertainty and asking how we balance that against the need to reduce something that is very persistent and very bioaccumulative. Maybe we have to use caution or precaution and accept that it is going to be uncertain, but we will have to introduce regulations accordingly. As I say, that is beyond my sphere of expertise, because I am a scientist, not a regulator.

The main reason is that you have people who have not much exposure and some who have had a lot of exposure. If there is disease associated with it, you would expect to see it more clearly. A huge array of studies are conducted in the background population of many countries, where they have tested people’s blood and looked at health outcomes. You do not have very much contrast in the exposure that they have had, so the blood test results do not vary much. When you do get these—I would call them natural experiments; it is not a very kind thing to communities—but where a community has been impacted, I should also say that the psychological impacts of living in these communities and the financial impacts are immense. When there is recognised contamination, it is difficult and challenging for those communities, but that is where we will get the best information and where we have the best opportunity. People have made use of that, but where we have that, we have an obligation to collect good information. Then, when we can put all those studies together, we get much more reliable information on potential health effects and we get closer to a situation where we could talk about cause.

I can give a quick answer on this one, because I think that the weight of evidence right now on these chemicals is strong enough to proceed with regulation. Emphasising the scientific uncertainty can go on forever. In many cases, you see null findings in epidemiological studies that you are describing as uncertain or conflicting, where it simply reflects the statistical power of the study designed to see effects. So it is constraining the magnitude of the effect, but it is not saying that that is necessarily a contradiction. It can be a feature of the design of the study or the population and the levels of exposure that have been examined. In this case, we can talk about uncertainty forever. From my perspective, having studied a number of different classes of chemicals across my career and looking at them, PFAS are incredibly bad in general in terms of the diversity of health impacts that we see in the body of work that is emerging. Typically, when we start to study a new class of chemicals, it takes many years to fully discover their potential impact. What you need to think about is whether you want to wait to see that and wait for that uncertainty to be resolved, or whether you want to take a precautionary approach—I would not even call it a particularly precautionary approach right now. I think that the evidence is already there and is sufficient for regulation, and the precautionary approach applies to the structures that we have not studied. Again, that links to the class-based approach. Thank you for the question.

I agree. The environmental persistence and the bioaccumulative nature, from my perspective, send alarm bells regardless of the difficulty showing causal health effects. If I were talking about epidemiological studies that I would focus on, possibly it would be on looking at health effects in children. Again, you need situations where there are reasonably high levels of exposure. Some questions that are relatively easy to solve are things like immune response and susceptibility to infection, because children get six to eight respiratory infections every year. That is an area where you could look at whether PFAS is associated with it. You can also do trials of vaccine response, which is what we do all the time when we are introducing new vaccines. It is relatively simple to incorporate PFAS into some of that. That is where I would focus attention: on the health of children. Again, it is not worth doing studies unless you have a population that has a reasonable level of exposure to PFAS.

We are in a situation now in which it is difficult to think of a strategy whereby we could do epidemiology studies that would resolve the problem to everybody’s satisfaction. My view is that there is uncertainty and we are not sure of the relationship between PFAS and some of the health outcomes, but there are sufficient studies to suggest that there may well be something going on. They are persistent and accumulative and therefore we will probably have to move forward, accepting there is uncertainty, and do something. Where I would focus my research is on thinking about whether there is a way to divide up the world of PFAS better than just treating them as a single class of 7,000 chemicals.

I suspect that we will need to think about targeted funding to ensure that that is done effectively and efficiently, yes.

We know that the EU is considering a class-wide restriction on PFAS and allowing only essential uses. How should essential use be defined? You have already answered whether or not this approach might be more effective than regulating one substance at a time, but how preventative action on PFAS is implemented will also draw questions about disproportionate disruption of essential sectors. Do you have thoughts about what essential use should be and what essential sectors should be, given that we have spoken about things like pharmaceuticals and heavy industry, as well as things like cosmetics?

. That is a great question. When you start to think about regulating these chemicals and what is essential, there is a defining paper by Professor Ian Cousins and colleagues in the Royal Society of Chemistry that defines this and talks about the practical implementation of some of these concepts. That might be helpful to you all. To summarise, basically there are three bins: non-essential, substitutable and essential. You want to start to think about what falls in each bin. The central question is whether these chemicals are necessary for the health, safety and functioning of society. There are definitely uses that are non-essential. Those include things like food packaging and a variety of textile additives. A lot of times, the PFAS are added at the end of the production stream for those products, so they are relatively easy to take out. We hear that. We have had it with many companies in the United States, and some bans on food packaging—aggressive action that can happen quickly and with minimal disruption. That is the low-hanging category. The second category is where could you substitute a more benign alternative. Things in that category include cleaning products and outdoor textiles. With a lot of those relatively low-hanging things, industry can innovate pretty easily without disrupting its production cycles particularly dramatically, and there is a potential market for green alternatives. The difficult one, as you say, is essential use and defining what is essential. That ends up including things like certain firefighting foam applications where there is an immediate hazard. There is a lot of discussion in the US about electronics and particularly semiconductor use. Again, in those categories you can have innovation to try to phase out over a longer period the use of these chemicals. Then there is a whole grouping of medical devices, military uses and medical applications. To summarise: start with the low-hanging things, and that can be very effective and very fast.

I do not have a lot to add to that excellent response from Professor Sunderland, except to say that consumer sentiment often drives industrial innovation in a way that regulators cannot. We see that through retailers in the supermarket chains. They can really drive what farmers do, for instance. That is not necessarily around PFAS, but thinking about more than regulation is important if you want to change the way products are used.

I have very little to add, except to say that I do not know to what extent the proposed regulation applies to those compounds that are converted into low-molecular-weight PFAS like trifluoroacetic acid, which is a common breakdown product of a number of other chemicals that are used widely and have significant economic advantages. That is not to say that they should not be replaced, but the regulators need to think about how broadly they cast the net.

That leads to my next question. How should Governments balance the environmental protection with the economic and societal needs of PFAS? Where would you draw the line?

It is one of the most difficult questions that advanced societies face today, that we depend so heavily on a technologically driven society for all the interconnecting parts, for example food security, the electronics industry and communications. What do we consider we could do without to balance against the potential health risk? I cannot answer that question; I just know that this is the balancing that needs to be done. Then we have to superimpose a socioeconomic impact on that.

I will move on with the other panellists. We have heard from some industries that have difficulties with changing their products to not include PFAS, which might be challenging in certain industries. Looking forward, what lessons can be learned, in terms of regulatory approach, about any new classes of chemicals that are developed, so that we do not end up in a similar situation in 50 years’ time when we are talking about—I do not know what they would be called—any new classes? Is there anything that we should learn from the situation we are in now, in terms of regulatory approach? Professor Kirk, do you want to come in first on that one?

I do not have a lot to say on this, but what is important to recognise is the globalisation of trade and the fact that it is impossible to resolve everything through regulation. You cannot monitor everything and test everything, all the cosmetics and food packaging, so it is a very vexed question, and I do not have a good answer for that one.

Across chemical classes we have been playing this game of chemical whack-a-mole where we regulate one and produce another. When we produce another, we as an academic community or as chemists cannot detect the new compound. Then there is a lag of decades or more before we understand the impacts. It is the cycle of regrettable substitution that we need to end. That is why I continue to advocate for this class-based approach. PFAS themselves are a microcosm of the global chemical manufacturing industry, which continuously innovates with chemical structures to literally produce large quantities of compounds in our water and in our food that we cannot detect until a chemist goes out and searches for it with very advanced mass spectrometry tools and reports back in communities. There is a cycle that repeats itself and has repeated itself since many of these chemicals were invented after military applications in the second world war. It is an excellent question, and the question for you all is: do you want to continue to play chemical whack-a-mole and risk people’s health and risk the health of people in these highly exposed communities? I always think back to our former EPA administrator, Gina McCarthy, when she was speaking to one of my classes. She looked at all the young, bright minds and she said, “Hey, everyone—I personally believe that if you take care of yourself and sleep and eat good food and exercise, you have a right to a healthy life.” That is the question that you are all contemplating right now, and it is a really important question.

“Regrettable substitution” is a great phrase, and so is “whack-a-mole”.

For me, it is not replacing one PFAS with another; it is replacing what we are currently using a PFAS for with something that has a similar functional characteristic but is a completely different chemical structure. Your question is an excellent question, because that comes under what we require under REACH or its equivalent in the UK.[2] What is the pre-release package of information that we need to assure the acceptability of this chemical? We need to look at the effects that were associated with PFAS and related chemicals and think about whether we are getting enough information before we release these into common use to judge the safety. Some of the effects that we think PFAS are associated with would not be detected by the package that we currently require. We think about how we re-engineer that, going forward, with new approaches—not legacy animal tests, but new approaches that allow us to predict better what a novel structure will do. That is why I think that mechanistic toxicology is important for that purpose.

We have made up some of the time that we lost at the beginning, but not all. If we could move swiftly in response to Martin Rhodes’s questions, that would be helpful.

This is a question to Professor Sunderland and Professor Kirk. From your experiences with the US Environmental Protection Agency, health departments and so on in Australia, what do you see as the main regulatory barriers to managing PFAS?

The main barrier right now is a political will to regulate and a political set of policy priorities.

Australia has done a pretty good job of regulating PFAS. What we are dealing with is contamination that occurred some time ago. It has been a huge issue for governments to manage that. I cannot say that we have been thinking too far into other forms of PFAS and other substitute compounds that have been used in place of PFAS. The main barriers are getting the community messages right and engaging with communities. We have to make it a place where we do privilege the voices of communities and listen to them. We have seen huge issues where we have had contamination events. Trying to actually work on them without properly engaging communities is terrible for regulators.

Sticking in the space of regulation but looking more specifically at the UK’s: Professor Boobis, do you think a national database of PFAS contamination across water, soil and air would improve transparency, public awareness and regulatory decision making?

It would be helpful to have more national information centralised so that we have that holistic picture of what is happening across the country. We are certainly missing it at the moment. I think that that could be really helpful.

Who do you think should lead on that?

It probably should be the Health and Safety Executive that has overall responsibility for that.

I thank our first panel for their time, with apologies for the technical problems at the beginning. What we have heard from you, in terms of the recommendations that we might wish to take away, is that we should perhaps look at treating PFAS as a class and not regulate them individually, but with a few sub-groups to that class. A definition of PFAS should be consistent internationally, and more research studies on association and cause are required. In the meantime, bioaccumulation plus persistence means that we should recommend a precautionary approach; regulation can be for non-essential, essential and replaceable; and we should always consult with the affected communities as a priority. Thank you very much for the evidence that you have supplied to the Committee.     [1] Witness has added for clarity ‘observational studies’ rather than ‘cohort studies’   [2] Witness added for clarification the question is what ‘comes under what we should under Reach’ instead of require.