Shanna H. Swan, PhD is Professor and Vice-Chair for Research and Mentoring Department of Preventive Medicine at Mount Sinai School of Medicine. Dr Swan is known for her work on the impact of environmental exposures on male and female reproductive health and has served on the National Academy of Science's Committee on Hormone-Related Toxicants. She was speaking to EurActiv's editor, Frédéric Simon.
Click here to read a shorter article based on this interview.
You are a well-known scientist in the field of Endocrine Disrupting Chemicals (EDCs), which you have been researching for many years. What were your main findings?
The major findings I have are that certain EDCs – and I’ve looked specifically at pesticides, phthalates and Bisphenol A – are significantly related to human development, more strongly when exposure is foetal but also some adult exposures.
Has exposure tended to increase over time?
There are some studies of old stored samples. That’s the only way we can know about a person’s exposure. So to put this in context, unlike studies of smoking or pharmaceuticals where you can ask the person what their exposure was, you cannot learn anything – or very little – about a person's exposure from EDCs by asking them what they do.
These are chemicals that are hidden – I call them stealth chemicals – and for this reason the only way we can know what the exposure was is to measure it in biological samples, either in urine or blood. Urine is usually easier and for various technical reasons preferable for the non-persistent chemicals.
When older samples are available and have been looked at, they have shown that levels were lower in the past. I can’t unfortunately be more specific but I could point you to some references.
So these go as far back as the 1960s?
There was one study in 1958 called the Collaborative Perinatal Project which had stored urine. There was a Kaiser California study in the early 60s which had stored samples. So these are very rare studies, they are the only ones.
In the most recent years some of the phthalates, for example DEHP, has decreased with the substitution. So we can pick up certain trends in use in these national samples of urinary metabolites.
Do we know precisely what the sources of exposure are?
For that, you have to go chemical by chemical. So if we restrict ourselves to phthalates, you still have to narrow that further because phthalates have different uses. Some phthalates are added to tubing to make it soft, particularly DEHP.
This is in the tubing in hospitals, in the tubing for milking cows, whenever you want a soft, flexible, plastic, you will take DEHP. Whatever is passing through that, particularly if it’s warm, it will absorb that. In this way we get exposure through material that has passed through this.
And also from milk?
It is measurable in milk, yes. So for DEHP, our dominant route of exposure is through food and there’s some in water. But you also get DEHP if you are in a medical department and hooked up to a tube.
Phthalates have been banned in some uses already such as toys, etc. So can we consider the problem solved?
Let me just go back for a second. Phthalate is a chemical class and so it’s important because you ask me if there are many exposures.
If we put cosmetics on our skin, our face – men, women, children, babies – we immediately get another phthalate in our body, which is DEP. And this is very clear. If we put hair spray or put a nail polish, then we inhale that phthalate which is primarily DBP.
So it’s a complicated story because we have many sources and many routes of exposure and also differing toxicity. Now, as for whether the problem is solved – not at all. We’ve only begun to solve the problem.
But there have been bans on some of the uses of phthalates which were of most concern, such as baby bottles…
No, this was Bisphenol A, it's another chemical class. Think of it this way. Phthalates makes plastic soft, BPA makes plastic hard. So if you have one of these sports water bottles, those were made with BPA. Hard baby bottles, that's BPA. Lining of tin cans, that's also BPA. But Phthalates are on the soft side of the equation although they are both plasticisers.
Ok, so why do I say the problem is not solved? The primary elimination of phthalates has been from children’s toys. Certainly this is important but it does not protect the most sensitive organism, and that is the developing foetus.
So a toy is something you play with after birth, the pregnant mother is getting an exposure which is for the foetus much more potent than what the child will get with a toy.
By eliminating these phthalates from children's toys – I think it is important, excellent, I certainly support it – but I would not do that at the expense of eliminating phthalates in products to which pregnant women are exposed. Because that is the most critical target for phthalates.
There has been a lot of controversy for many years over the health risks of low-dose exposure to chemicals such as phthalates. Looking at the science, is there any evidence to support this?
Let me say three things.
First of all, there is absolutely no doubt that tiny, tiny doses of hormones can permanently alter the development of the foetus – at the right time. You cannot look at the dose alone, you must look at the dose in a particular time window, because otherwise you don’t have the toxicity captured because that’s really a product of two things: Not just the dose but the timing as well.
The next thing is a story that isn’t obviously about chemicals but just to point out that we know from some human and many animal studies that when a rodent is in utero (in the mother’s womb), each one of those is hooked up in the uterine horn and they will be located between two other pups.
So if you look at a male between two males, and a male between two females, you can measure how much testosterone is in those two males. And the difference is significant and measurable and very, very small. It’s about a drop in an Olympic-size swimming pool. That’s how small it is. It’s an extremely low dose, one part per trillion.
And what is the consequence of exposure to this?
The consequence is that the rodent that is a male between two males grows to be more aggressive, more masculine in behaviour and in his general development. He will have a stronger sperm count; he will be more fertile. And there’s no question about that, it has been shown in a number of species. And there are a number of supporting human studies. I only mention this as proof of principle that a very small amount of hormonal substance at the right time alters development.
Now let’s just go to the human situation. When people say, 'Well the doses are too low,' I say two things. One is, 'Maybe so, but we are seeing effects'. So whatever dose it is, it seems to be doing something. There are probably close to 30 studies that find associations between phthalates and a variety of human health end points.
The counter-argument could be that these effects could be coming from something completely different.
Exactly. Not the counter argument, but a relevant, additional point is that, we are never exposed to one chemical. In fact a recent study found 200 chemicals on average in babies at birth.
That means that in utero the babies had 200 chemicals circulating in their bodies affecting their development, on average. The maximum in that study sample of ten was 287. So we are unquestionably exposed, and the foetuses as well.
So yes, there are many chemicals and statistically you can ask what are the associations with just DEHP metabolites, just DBP metabolites. But it's not the most efficient way to do it. Better is to ask what about co-exposure to all of those? What about the cocktail effect?
Now, we cannot reasonably, with the sample sizes we have available, yet look at the 200 all together. But we could look at and do look at multiple exposures. So the fact that they may be quite low individually, we know that these doses add up, and so if you have several of these, you already add up to a much higher dose.
Do we know specific combinations that are particularly harmful?
Yes, among the DEHP metabolites, there are many of them, we currently look at four or five of them and can assess the sum of them. That’s one example but there are others.
This sounds quite scary. How should consumers behave or react? If my wife was pregnant what should I be telling her?
I get this question all the time. It’s a frustrating question because I can only give you a partial answer. On a simple side, I would tell her she could limit her exposure to harmful personal care products.
And the reason we can give this advice is that they have been looked at quite carefully by a number of NGOs, and specifically I point you to the Environmental Working Group website called 'Not Too Pretty', where they actually go through product by product and talk about the chemicals in them. That’s a nice tool for consumers.
You can also say, just a blanket precaution: Do not use air fresheners, do not spray things in your house, products and so on.
Where it gets more problematic is that even when we tell people all these things, only in rare situations can we remove these chemicals from their body. And one of the major reasons is that they are so deeply hidden, you can check the label on the lotion but you can’t check the label on your spaghetti sauce or on your bottle of milk and so on.
So we need to give consumers the tools to make informed choices. And at this point we don’t have those tools.
You mean labelling?
Labelling, yes, and also advice about behaviour – for example not to store in plastic, not to microwave in plastic.
What I tell people if you want to do the best you can, buy local produce, buy it unprocessed, buy it organic. There is a population in New York that does this, and that is the Old Order Mennonites [an anti-technology religious group similar to the Amish]. They’re quite severe, they grow everything themselves, they don’t drive in cars, they don’t use sprays… and they have very low levels of environmental chemicals.
And that has been scientifically measured?
Yes, we measured how many phthalates and phenols were in their urine and they had almost none. And it’s interesting because a couple of women did have peaks. One was a woman who used a hairspray. And you could see this because we asked what did you do before you came here and gave your urine? And this woman said, 'Well, I was not supposed to but I used hairspray because I was going out.' And there we see the peak for MBP in her urine.
And then another woman rode in a car even though they don’t do this normally and you see another peak. So in an extreme situation – which to most consumers is quite radical action – you can eliminate.
Another population was given regular food and then they fasted. Their urine was tested under the normal diet and after 48 hours of fasting and they had no DEHP in their urine at all.
Of course we can’t all fast! So I think we have to make it much easier for consumers to avoid these products.
In terms of chemical presence in food, there have been measures taken at EU level to reduce the use of pesticides. In France for example there is an objective of halving the use of pesticides by 2018, and there have been bans on aerial spraying and things like that. Are these steps sufficient to reduce the risk of contamination in food?
Well, removing pesticides certainly removes one source of exposure to EDCs – and a very important one, and I think this is great.
By the way, aside from phthalates, we found a number of pesticides and herbicides in the Midwest where they were associated with a lower sperm count. So these are acting as well. Also I should point out that phthalates are actually in pesticides – they are put in there to increase absorption.
So these measures to reduce pesticide use are certainly a good thing to do but it won’t do the whole job. As long as the food is processed in contact with phthalates or Bisphenol A, canned, shipped in plastic, stored in plastic or cooked in Teflon, there are just a lot of occasions along the way to pick endocrine-disrupting chemicals.
And pesticide removal is certainly a very important first step but then we have to worry about what happens to the food after it is picked and along the rest of the chain from farm to fork.
In Europe, we have minimum residue levels for pesticides in food below which ingestion is not considered to pose any risk for human health. Are you saying these should be lowered further?
I cannot comment on permissible level of pesticides. But I can comment on the question of a threshold. We have many examples in environmental science – the best I think is lead – that no matter how we keep dropping the permissible level, we see adverse effects still at a lower level.
And I think that what we have to keep in mind is that to some particular sensitive populations and particularly sensitive periods, perhaps the level has to be reduced further. But there will have to be some practical level – obviously we can't remove everything entirely.
You may be aware that in Europe we have this REACH regulation on chemicals which is undergoing a review this year. Are you encouraging policymakers to tighten REACH even further?
For me the most important thing about REACH it that it alters the burden of proof. Of the 80,000 chemicals in commerce in the world, 62,000 were just blessed and assumed to be safe in the United States.
That is actually the default assumption still in the United States: That until a chemical is proven harmful it is assumed to be safe. This of course places the burden of proof on the consumer, to prove harm, which is not where the burden should be in my opinion. So generally shifting the burden of proof I think is extremely important and should be implemented in US policies as well.
The US must actually follow REACH if they are going to export to Europe. What has been the impact on the US industry the way you see it?
I can’t tell you that. I do know that that is not the default assumption in regulation. So whether they do something different to send things to Europe, I’m sure they have to, and I’m sure they do, but it is not what they accept as their burden to prove safety before a product is marketed.
As far as whether the regulation should be tightened, that is a very broad question. And what I have an opinion about is that I feel that endocrine disruption is a category deserving its own regulation. It’s different enough from reproductive toxicity and carcinogenicity. The risk assessment for endocrine disruption is different. The scientific issues are different enough that it would protect public health much further if we could deal with this as a class of chemicals. So that’s where I see maybe tightening up.
For you as a scientist, the link between endocrine-disrupting chemicals, the ones you have been studying, and lower fertility has been proven and is scientifically watertight? Can it be argued against?
Watertight? This is never the case, of course. There are still people here who argue cigarettes don’t cause lung cancer. Of course it will always be argued against.
I think we have now a lot of data that environmental chemicals can and do lower sperm count, impact time to conception, increase foetal loss in early pregnancy, affect pregnancy outcomes. Do we need more studies? Of course we do. But do we have enough information to act on these studies that we have? I say that we do.
