Endocrine disruptors and fertility
So far we’ve looked at male and female factors that can influence fertility, and we’ve touched on how the environment might be involved. One way it might play a role is if we encounter chemicals that can mimic some of the hormones used in our bodies to control reproductive processes. These are called “endocrine disruptors” and Chris Smith spoke with Paul Fowler from the University of Aberdeen who researches them...
Paul - Well they fall into a lot of categories. So things like organic pesticides, products of combustion so dioxins, polycyclic aromatic hydrocarbons, phthalates - which are softeners, things like parabens, which is used in a lot of body care products. Bisphenols, including the controversial Bisphenol A. Cigarette smoke contains a lot of endocrine disruptors as Bill mentioned. Non-stick coatings PFOA and PFOS, which are very, very persistent in the environment. Food contact materials, so again, Bisphenol A as a tin liner, for instance. So a wide range of compounds.
Chris - How can a compound that lines a tin can, or something in a cigarette, end up behaving the same way in the body as a hormone?
Paul - Hormones typically act on one or a few receptors. A lot of these receptors have evolved over time from structures that detected the environment, and they now detect these chemical signals sent around the body. And it is possible, if the shape of the molecule, or the binding part of the molecule to the receptor, for a non hormone to act on the hormone system. But it can also do that by other means - if it interferes with the production of the hormone or the breakdown of the hormone or the secretion of the hormone, it can seriously inbalance the endocrine system. Hormones frequently act in concert, so you have a cascade of hormones and an endocrine disruptor may affect a different element from the one you end up looking at.
Chris - So they're basically chemicals with the capacity to throw a spanner in our hormonal works and disrupt very delicately orchestrated signalling pathways in the body, which could have a knock-on effect for things like fertility. Is there actually evidence though that this is happening?
Paul - Well, there's a lot of animal data and quite a lot of that data is of good quality, not all of it. And that supports the effects of some of these compounds, for instance Bisphenol A and phthalates, for endocrine disrupting effects that lead to impaired fertility.
Chris - This is exposing animals to these chemicals does actually translate into a change in their fertility?
Paul - Yes, it depends on which chemical and what dose.
Chris - Sure - but does that happen naturally? As in, have we got evidence that rather than doing this in a laboratory situation where we effectively expose animals to high levels of these things, are they picking up enough of the stuff in the environment, in the same way as we're kind of speculating humans might, for this effect to be manifest?
Paul - Yes, we are. So in terms of wildlife, so non experimental animals, there's been cases of male fish in UK waters and elsewhere producing female egg proteins. And this is due to, amongst others, products from contraceptive pills getting into the water system. There've been plenty of observations of impaired masculinisation in wildlife. A lot of that data has come from areas that are relatively polluted, like Lake Apopka in Florida.
Chris - Okay there's reasonable evidence for that, but it's a different thing to say that humans are susceptible in the same way. So is there evidence that it's impacting us?
Paul - Well, there's associative evidence - and I think all three of your speakers before me alluded to that - that there are studies that associate people with say a higher level of a particular compound with an increased risk of something. If you take the woman, an increased risk of endometriosis with certain compounds, or reduced birth weight of offspring, and that's been linked to a PFOS, for instance, so women with higher levels of PFOS. And in terms of lab evidence that's difficult.
Chris - I was going to follow up Paul by saying, do we know whether this is a comprehensive effect across all aspects of reproduction in both men and women, or whether it's hitting chiefly one aspect of reproduction? Do we know?
Paul - We don't.
Chris - Could there be a legacy effect here? In the sense that, say a child is exposed as it's developing inside its mum to something, could that have an impact, even though the baby hasn't been exposed directly, could that have an effect on the fertility of her unborn child?
Paul - Yes, that's potential. And an example would be some small studies conducted a while back that looked at the chance of a woman having a baby was lower if her mother's mother had smoked while pregnant.
Chris - Goodness. So we're storing up potentially quite a problem for ourselves. And could it be then that what we see now as a decline in fertility could be an even bigger issue in the next generation?
Paul - Well, that's possible. One thing to bear in mind is that the profile of chemicals we're exposed to is continuously changing. If you take sewage sludge, for instance, processed human sewage used as a fertiliser on fields, the processing of sewage changes over time as new ways and better ways are found to make it safer. At the same time manufacturers are changing what's coming into the food chain. So all the pressure to ban Bisphenol A has led to some manufacturers switching to Bisphenol S and Bisphenol F about which we know much less.