Transcript of Q&A session

Our speakers discussed endocrine disrupting chemicals and how they can affect your thyroid health at our 'Meet the Experts' webinar in April 2024. This is a transcript of the patient questions answered live by our experts and chaired by Professor Marian Ludgate. 

ML - Prof Marian Ludgate 

EP - Prof Elizabeth Pearce 

JL - Prof John Lazurus 

You stated it would not be possible to measure endocrine disrupting chemicals (EDCs) as a routine part of managing an individual who comes into your practice but have there been any studies to measure these EDCs in people? You commented on the huge amount of exposure that we get but do we know that they are in our systems?  

We do. In the US where I practice and study, the National Health and Nutrition Examination Survey (NHANES), which is a nationally representative survey, has blood and urine data for a lot of these exposures and it’s shocking how many of them are truly ubiquitous. Exposure to many of these EDCs is seen in virtually everybody who is studied. So yes, they definitely get into humans. It’s possible to measure them for epidemiologic studies. What we don’t really have right now is a panel of endocrine disrupting tests that have clinical application in most settings. They’re either not available or not paid for by health insurance systems. (EP)

Do we have any idea of how long these EDCs can actually stay in our system or is it just that they’re being replaced constantly so they’re always there?

It depends on which disruptor we’re talking about. Some of these, including Polyfluoroalkyl substances (PFAs) and Polychlorinated biphenyls substances (PCBs) for example, are known as ‘forever chemicals’. Meaning once they get into the environment, they are very stable and they are going to be there indefinitely if nothing is done to mitigate them. In the body some of these disruptors will tend to accumulate over time. So, the longer you live the more they can accumulate in the body. Some of these are more transient to exposures so it depends a little bit on which of these disruptors we are talking about.  (EP)

Are there any specific chemical names that people can look out for so that they know where they are, such as in foods, beauty and cleaning products etc. Things that can heighten our awareness so that we know to try and avoid them or is it impossible to avoid them?  

It’s probably impossible to avoid everything, no matter how vigilant you are by policing what you are buying and bringing into the household. I think avoiding things that have added fragrances, some cosmetic type products containing ingredients like phthalates, parabens and triclosan. However, I am not a chemist. Reading labels of some cosmetics is not for the faint of heart and it’s not for most of us who aren’t experts in the field. So it can be hard to decipher what’s really in them.  (EP)

Would water in glass bottles be more beneficial than water filters?  

Possibly, yes and for the environment in general, by reducing plastic waste.  (EP)

In the map that you showed of the UK, the areas with high concentrations of PFAs in the drinking water, are often those associated with cities which is what you would expect where you have large numbers of people. I was then reflecting that much of our water storage and collection happens out in the countryside so it’s slightly surprising that, or even more worrying if you like, that our water supplies are so compromised when you think where they are collected. (ML)

Again, these are forever chemicals so that once they get into the soil and get into the groundwater they’re going to be there in the aquifer and maybe over wide territories. I’m not an environmental scientist so I’m not an expert on how this gets into the environment, but I think probably this is becoming widespread in water supplies. The map shows the ones where we know there is exposure but certainly there may be places where we don’t have any measurements yet. (EP)

One of our participants states they don’t have a thyroid so how are EDCs going to affect their thyroid? I know you’ve touched on this a little bit but is there anything specific that would be applicable to someone who’s had a thyroidectomy in the context of endocrine disruptors?  (ML)

I guess the good news about having a thyroidectomy is that your thyroid is no longer susceptible to or influenced by endocrine disruptors. You might still be susceptible to changes in protein binding in the circulation of thyroid hormone which could necessitate increases or decreases in dosing of your thyroid hormone replacement. You could be susceptible to endocrine disruptors that increase thyroid hormone metabolism, which again might necessitate increasing doses to keep levels stable. A pregnant person who doesn’t have a thyroid is going to give birth to a foetus who does and who still could have some susceptibility once the foetal thyroid is working in the second half of pregnancy. So there is some protection but perhaps not complete protection against these effects.

It is important to note that these chemicals cross the placenta and sadly, also, they get into breast milk. (EP)

We have another question related to this idea of the impact on fertility. You mentioned differences in sex ratio, numbers of offspring, foetal size, etc. Could you give us a little bit more information about those specific effects in the pregnant woman and in her foetus? (ML)

Here’s where I am limited by the fact that I’m a thyroid endocrinologist, not a reproductive endocrinologist. So I don’t know the ramifications of, for example, the sex ratio very well. Certainly, thyroid hormone levels in pregnancy are linked to alterations in child birth weight, so they can increase the likelihood of both large- and small-for-birth weight babies depending on what the perturbation is in the system. Also, thyroid hormone has been linked to higher rates of pregnancy-induced hypertension. Those are just some downstream effects specific to thyroid disruption. 

It’s hard to study fertility; it’s hard to study something which is sometimes called fecundability, which is the likelihood of getting pregnant when you’re trying, because you need to enroll large groups of people who aren’t pregnant yet and those are hard people to enrol in studies. There’s some evidence that perhaps some of these disruptors are associated with reduced fecundability. Some of that could be related to thyroidal disruption because you need optimal thyroid function for optimal fecundability. But some of it also probably relates to reproductive hormone disruption and again because these factors can all be affected in so many different ways the problem gets a little bit complex. (EP) 

Staying with the neonate, a little bit closer to the thyroid now: Congenital hypothyroidism (CHT). I’m sure many of the people listening will be aware that this is one of the conditions that we test for in the UK, and indeed in many, many countries worldwide. and it’s the little heel prick test that children have. I know from experience, and from talking with other people, that we really know very little about the genes responsible for CHT. Do you think that the missing cases could be due to epigenetic modification because of these disruptors?  (ML)

It’s certainly possible. Certainly, we know the genetics of some CHT but we can’t identify a genetic cause in all cases and we’re still learning more about the genetics of that disorder. It might also be worth noting that throughout life there may be genetic differences that will alter the effects that these chemicals will have on us. Thus some of us may be relatively protected, or relatively more at risk, due to our underlying genetics. An example is that 10 or 12% of the population probably have mutations in the gene for the deiodinases that convert the precursor hormone T4 to the active hormone T3 and there’s a suggestion that perhaps those individuals might be those that feel less well with thyroid hormone replacement. There's also a suggestion that those individuals might be particularly susceptible to some of these environmental disruptors if there’s less ability to activate hormones. Some of these environmental disruptors are known to alter those deiodinases systems and perhaps some individuals with these mutations might be more susceptible to that kind of disruption. (EP)

I was very interested in the comments you made about attention deficit hyperactivity disorder (ADHD). I think that globally there has been quite an increase in the number of people of all ages being diagnosed with ADHD. One of our participants would like a little bit more information, if you have any more you can tell us, about EDCs and cognitive problems. (ML)

There are a lot of epidemiologic studies that have linked EDCs to higher rates of ADHD, PFAS are among those and this is again probably complicated because there are probably a lot of different impacts on the developing brain that can increase the susceptibility. Some of the epidemiology is tricky because we are probably diagnosing this more because we have better tools and more knowledge about the need to diagnose than we did decades ago.  So it’s hard to really gauge what are true trends in increasing incidence of this disorder over time and what is just our better ability to diagnose and identify it. Certainly within the thyroid realm, iodine deficiency has been linked to ADHD and possibly also to higher rates for autism spectrum disorder. And we know that the developing brain has an enormous number of inputs which makes it hard to study: nutrition and environmental disruption and genetics and all kinds of environmental inputs that could increase or decrease risks for these things. So the studies are, by definition, hard to really narrow down on cause and effect. But I showed you the slide that ADHD/ lower IQ seems to be the biggest financial hit from these EDCs in most analyses and it probably is substantial.

Certainly, over recent decades we have had increasing exposure to these chemicals at the same time that we have seen increasing rates of ADHD, which again may have multiple reasons. But I think there is good evidence from epidemiologic studies that environmental disruption may increase that risk and the exact mechanisms I think we don’t really know.  (EP)

What should we all be doing to try and encourage our governments to take these issues a lot more seriously.

I think just having a voice that all of us as individual constituents can have can be powerful. So when people in government hear that this is an issue that we all care about, that drives it to the top of agendas and drives legislation and regulation and measuring and all the things that are really ultimately going to have to happen at a pretty high level to protect all of us from these exposures.  (EP)

This is very much the case. You commented that PFAs have been very much in the news recently in the US and also here. I know when we were chatting a couple of weeks ago I made the comment that another thing that we hear a lot about is microplastics and nanoplastics and from what I can see it seems as if these may be a medium for introducing some of these endocrine disruptors into our systems as well. Do you have any further insight or any other comment about microparticles? Things like the wipes that we use to take makeup off, for example, contain large amounts of them so they are also just everywhere.  (ML)

I think it’s another potentially somewhat ubiquitous exposure. I don’t think there’s a lot of data yet specifically looking at thyroidal disruption but I think there’s data looking at disruption of other hormone systems related to some of those exposures. Something I alluded to briefly is the microparticles in the air, so air pollution. It’s sort of astonishing, I wouldn’t have predicted this but this is also clearly an endocrine disruptor, a thyroidal disruptor among others. So routes of inhalation to these tiny, tiny particles in water, in food, in things we are applying to our skin, in the air we breathe, it’s kind of everywhere. (EP)

We have a question which is not specifically about endocrine disruptors but does relate to something that you commented on and it’s possible that John might also have some comment. Individuals who are on thyroid hormone replacement sometimes find that the messaging around iodine can be a little bit confusing. So could you both explain if you have no thyroid or if you have an underactive thyroid and you’re taking levothyroxine, what you should and shouldn’t do about iodine. (ML)

The only known use of iodine in the body is in making thyroid hormone. It’s an important use but that’s all it does. If you don’t have a thyroid anymore to make thyroid hormone, if you have had a thyroidectomy, it probably doesn’t really matter how much iodine you are ingesting because you are not making your own thyroid hormone anyway.  If you are a pregnant individual who has had a thyroidectomy, and again the foetus has a thyroid that needs its own iodine supply in the second half of pregnancy, there is iodine that gets metabolised from the thyroid hormone that’s ingested so I’m not sure it’s really critically important in most cases for pregnant individuals specifically who are taking full thyroid hormone replacement to necessarily get that iodine in the diet. Altering iodine intakes will shift thyroid function. People with some underlying thyroid compromise can be particularly susceptible to developing either iodine-induced hyperthyroidism or iodine-induced hypothyroidism, particularly with high iodine doses, which probably should be largely avoided. So the amount of iodine that’s really required for thyroid hormone production is in the microgram range. 150 mcg a day if you’re a non-pregnant adult and maybe 250 mcg a day if you are pregnant. Exceeding that by a large factor actually increases the risk for thyroid dysfunction. John you want to maybe chime in and add to that. (EP)

Only that people should be aware that they should try and look carefully at the amount of iodine they are taking in because the information is not obvious in many cases. So if they’ve got any problem they should act on that and try and get some more information. As you point out it’s a hugely complex business but people should perhaps consider that under any circumstances too much or too little may be a problem.  (JL)

As per most nutrients, too little is not a good thing and it’s probably still the world’s leading cause of preventable brain damage, but too much is not a good thing either so there’s a sweet spot in the middle. (EP)

And I know John has been working very hard to try and get the salt in the UK iodised at a sensible level but that has been an uphill battle sometimes won and sometimes less so, so still some work to be done there.  (ML)