PFOA is a persistent organic chemical that is used in industrial and consumer goods including nonstick cookware and stain- and water-resistant coatings for carpets and fabrics. The study revealed that people with higher concentrations of PFOA in their blood have higher rates of thyroid disease. The researchers analysed samples from 3966 adults aged 20 and older from the US Centers for Disease Control and Prevention’s nationally representative National Health and Nutrition Examination Survey (NHANES). The researchers found that the individuals with the highest 25% of PFOA concentrations were more than twice as likely to report current thyroid disease than individuals with the lowest 50% of PFOA concentrations. The main source of human exposure to PFOA and PFOS remains uncertain but is believed to be through diet. However, people may also be exposed through consumer goods such as textiles, footwear, furniture, and carpets, which can contaminate indoor air and dust.

A fact sheet developed by the UK Science Media Centre on PFOA is provided below

Feel free to use the quotes below in your stories. Any further comments will be posted here. If you would like to speak to an expert, please don’t hesitate to contact us on (08) 7120 8666 or by email.

Professor Chris Winder is Professor of toxicology and occupational health at the University of New South Wales

“Plastics made of PFOA (this time Teflon) have been around since the 1940s. We already know that it is found in the blood of people (usually at low levels) and we know about the toxic and carcinogenic effects of PFOA. It is also environmentally persistent.

This paper raises another flag about yet another plastics monomer that was considered safe if polymerised into a plastic and may now be associated with adverse health problems in people.

Thyroid disease is fairly common and a small increase may not be significant. However, it points to another health problem of plastics that requires close study, and possible reconsideration of the use of this chemical in plastics manufacture.”

Professor Brian Priestly is Director of the Australian Centre for Human Health Risk Assessment (ACHHRA) at Monash University

“PFOA & PFOS measurements were obtained from random samples from three waves of a large US survey (the NHAMES study). The authors used standard statistical methods to assess the relationship between serum PFOA & PFOS and self-reported thyroid disease in the cohorts. It was not possible to determine the nature of the thyroid disease, which can include either increased to decreased thyroid function associated with quite different mechanisms, nor was it possible to relate the PFOA/PFOS or disease data to serum thyroid hormone levels. The increased risk comparison between the highest and lowest quartiles of the PFOA & PFOS serum measurements was highest in women, where the incidence of thyroid disease is roughly five times higher than in men, although similar trends for increased risk associated with PFOA (and to a lesser extent PFOS) could be seen across both genders. When the data were adjusted for factors also shown to influence PFOA/PFOS exposure patterns (e.g. smoking, age, drinking patterns, educational status) the strength of the association with thyroid disease appeared to become stronger.

To date, there has been no confirmation of an increased thyroid disease risk in workers manufacturing PFOA/PFOS, despite reports that serum levels in these workers are orders of magnitude higher than the subjects in the NHAMES samples. While there is some confirmatory evidence that high PFOA doses in animals can alter thyroid function, the mechanisms (including hormone carrier protein and/or receptor displacement and altered thyroid hormone metabolism) are complex and likely to be relevant only at exposure levels well above those in the human population. The authors concede that the findings in their study simply point to an association between PFOA (but not PFOS) serum levels (measured on a single sample) and thyroid disease. While the findings merit further study, including further exploration of biologically plausible mechanisms, they do not definitively prove that PFOA/PFOS exposures cause thyroid disease in humans.”

Professor Jack Ng is a certified toxicologist who holds the Professorial Research Fellow position at the National Research Centre for Environmental Toxicology, University of Queensland and is the Program Manager for Metals and Metalloids Research. He is also a Program Leader for Risk Assessment for the CRCCARE.

“This research studied a reasonable cohort of samples and the association is ‘obviously’ statistically valid. The authors also acknowledged other negative studies, as well as other parameters which might have influenced the significant observation. However the causal relationship between these chemicals and thyroid disease is yet to be demonstrated and in a dose response manner. The authors also didn’t measure thyroid hormones and didn’t measure iodine status in the studied subjects.”

Dr Stuart Khan is a Senior Research Fellow at the UNSW Water Research Centre, University of New South Wales

“Perfluorochemicals such as perfluorooctanoic acid (PFOA) and perflluorooctane sulfonate (PFOS) are persistent and toxic chemicals.

“Recent reports from the USA and Europe indicate that these chemicals are often found in drinking water supplies. This includes drinking water supplies that are not known to be directly impacted by discharge from a facility that manufactures them. As a result, Australian drinking water suppliers and regulators have begun to focus attention on these chemicals as new potential drinking water contaminants of concern.

“The Australian Drinking Water Guidelines do not specifically address perfluorochemicals and there is currently insufficient information to determine safe concentrations or guideline values. Furthermore, no systematic studies have been undertaken to determine concentrations in Australian drinking waters, so we are generally unaware of the significance of drinking water as an exposure source to these chemicals in Australia.

“Since perfluorochemicals are very water-soluble, most conventional drinking water treatment processes are not effective for removing them. However, recent research* undertaken at the University of Queensland has shown that advanced water recycling treatment processes are very effective. In particular, treatment by reverse osmosis was shown to almost completely remove any measurable trace of these chemicals from water. A consequence of this research is that it demonstrates that recycled water is potentially a much lesser source of these toxic chemicals than many conventional water supplies.”

*Reference: J. Thompson, G. Eaglesham, M. Lawrence, Y. Poussade, J. Keller, J.F. Mueller (2009). Fate of Perfluorochemicals (PFCs) in an Advanced Water Treatment Plant (AWTP). Presented at 7th IWA World Congress on Water Reclamation and Reuse; 20-25 September 2009; Brisbane, Australia.

The comments below were gathered by our colleagues at the UK Science Media Centre

Prof Ashley Grossman, Professor of Neuroendocrinology, Queen Mary, University of London, said:
“In this study, researchers looked a large number of people and found an association between a commonly used chemical and thyroid disease. However, studies like this cannot tell us that the two things are definitely linked. What’s more, the paper doesn’t tell us what sort of thyroid disease people were suffering with.

“We also don’t know whether this chemical is directly affecting the thyroid. Thyroid disease is often caused by the body’s own immune system attacking the thyroid gland so perhaps this chemical is having some effect on the immune system, rather than directly on the thyroid.

“We’d need to do a lot more research to verify this link and to understand how the two are linked. In the meantime, it’s important to remember that thyroid disease can be successfully treated.”

Prof Ieuan Hughes, Prof of Paediatrics and Head of Department of Paediatrics, University of Cambridge and Chair of the Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment, said:
“I am surprised that the paper is generating so much interest. Yes, these compounds are ubiquitous and can be detected readily in humans. The problem with this study is the evidence for a direct link with thyroid effects from PFOS is at best tenuous. There has been some clever statistical analysis to suggest that self-report of a ‘thyroid problem’ is associated with higher levels of exposure (but based on just one serum sample) to these chemicals AND, corrected for a number of possible confounders. One must also recognise that thyroid disease is very common and those with a so-called ‘thyroid problem’ must be even more common. The authors recognise the blindingly obvious…that more work needs to be done to prove any association. That would at least mean data collected to analyse exposure in relation to actual thyroid data, i.e. thyroid hormone levels: TSH, FT4, FT3, thyroglobulin, TBG (these chemicals appear to preferentially bind to proteins). If nuclear receptors are invoked, then the TRs would need to be studied.”

Dr Diane Benford, Head of Toxicology of Food, UK Food Standards Agency, said:
“This type of study investigates associations and cannot establish causality. It is important to look at the consistency of the data with the results of other studies, and with what is known about the toxicity of PFOA and PFOS, which differ. Studies of workers with higher exposure to these compounds have not shown consistent evidence of increased risk of thyroid disease, which would be expected if effects are occurring in the general population. A very large number of analyses have been conducted with the NHANEs samples, and statistically it would be expected that some will show associations due to chance alone. More research is needed to establish whether this association is causal.”

Prof Alan Boobis, Toxicologist, Division of Investigative Science, Imperial College London, said:
“It is not possible to establish causation only from association in a cross-sectional epidemiological study. The considerations outlined by Bradford Hill would be of value here, looking at factors such as exposure gradient, biological plausibility, experimental evidence, etc. If these do not exist, it strongly suggests that the case is not proven. At best, the study would be hypothesis generating, for further more directed studies. PFOA and PFOS have somewhat different toxicological profiles, so I am not sure it is sensible to combine them. There are data from occupational cohorts to these compounds. I do not recollect any evidence for effects on thyroid in humans. The experimental studies suggest that any effect on thyroid is indirect and seen only with PFOS. Other more direct, effects should be apparent at lower exposures, if indeed the thyroid is affected by these compounds.”

Science Media Centre Fact Sheet

PFOA/PFOS

General information

Perfluorooctanoic acid (PFOA) and perfluoroctane sulphonate (PFOS) are two man-made chemicals used in a range of industrial and commercial applications, including the manufacturing of non-stick cookware

Both are examples of perfluorinated chemicals (PFCs) – or perfluorochemicals – a class of manmade chemicals that consist of variable-length chains of carbon atoms to which fluorine atoms are bonded (this arrangement is also given the name ‘perfluorocarbon’).

PFCs are characterised by their stability, heat resistance, and water/oil repelling properties. They are also highly resistant to degradation, meaning that they tend to persist in the environment.

They are widely manufactured on an industrial scale and are used in the production of a range of heat- and chemical-resistant materials, including clothing, upholstery and carpets.

Characteristics and applications

PFOA is a highly stable compound that is very good at repelling water, oil, grease, stains and heat. Because of these properties it is used as a component in the production of fluoropolymers, a class of perfluorocarbons (see above for explanation) which have a range of similarly useful properties, including high stability, strength, water repellency and resistance to oil and heat.

Fluoropolymers have a great many applications in manufacturing and industry including the production of non-stick cookware, heat-resistant materials (including as a component of Teflon) and materials used in waterproof and protective clothing (such as Gore-Tex). They are also used in the production of electrical components such as wire coatings.

PFOS is a similarly stable compound that also has strong water-repelling properties. It was formerly used in the production of the fabric protector Scotchguard and other surface treatment products. It was also a component of some chemical products including insecticides and fire extinguisher foam, although is use has been steadily reduced since the late 1990s due to concerns over its persistence in the environment.

Health impacts

PFOA/PFOS are the subject of ongoing research as to their potential health impacts, due to concerns raised about their persistence in the body and in the environment. They can get into the environment during the production process or as a result of the use of PFOA/PFOS-containing products by companies or individuals.

They have been detected at low levels in human blood, and high concentrations have been linked to organ damage in rats and mice. There has been no evidence of harmful effects in humans (based on studies of employees involved in the manufacturing process), although this area has not yet been widely studied (see links below for further information).

A few notes on thyroid disease

The thyroid gland, located in the neck, is responsible for controlling the body’s rate of metabolism through the release of thyroid hormones, including thyroxine. It also controls the rate of protein production and the body’s sensitivity to other hormones. The thyroid gland is controlled by the hypothalamus and pituitary, in the brain.

Conditions affecting the thyroid gland are hyperthyroidism – in which the gland becomes overactive, causing symptoms like restlessness, anxiety, weight loss and goitre (swelling of the neck) – or hypothyroidism, in which the gland is underactive, causing tiredness, weight gain, constipation and sleep problems.

Most cases of hyper- and hypothyroidism are caused by autoimmune reactions. However there are other causes which are not always clear. Causes of hypothyroidism can include iodine deficiency, inflammation of the thyroid, side effects of some medicines (such as lithium) or, in rare cases, a condition affecting the pituitary gland. In addition, some children are born with an underactive thyroid gland. Hyperthyroidism can be caused by Graves’ disease (an autoimmune condition) or, less commonly, a growth or nodule on the thyroid gland itself. It can also be caused (rarely) by a reaction to some medicines.

Sources / further information

Australia’sNational Industrial Chemicals Notification and Assessment Scheme
http://www.nicnas.gov.au/Publications/NICNAS_Alerts/EC_Alert6.pdf

UK Health Protection Agency:
http://www.hpa.org.uk/HPA/Topics/ChemicalsAndPoisons/CompendiumOfChemicalHazards/1219302574442/

US Environmental Protection Agency
http://www.epa.gov/oppt/pfoa/

Lancaster Environment Centre for Chemicals Management
http://www.lec.lancs.ac.uk/ccm/research/perfluorinated/index.htm

Ohio Department of Health
http://www.odh.ohio.gov/ASSETS/9E109AB669EB4589864F1D59F48806EC/PFC.pdf

Society of the Plastics Industry site on PFOA
http://www.pfoa-facts.com/

Info from HPA on levels of PFOS/PFOA in drinking water:
http://www.hpa.org.uk/web/HPAweb&HPAwebStandard/HPAweb_C/1195733828490

On thyroid disease:
BBC Health page:
http://www.bbc.co.uk/health/conditions/thyroid1.shtml#what_is_thyroid_illness?_

Patient UK pages:
http://www.patient.co.uk/health/Hypothyroidism-Underactive-Thyroid.htm
http://www.patient.co.uk/showdoc/23068880/
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This is a fact sheet issued by the UK Science Media Centre to provide background information on science topics relevant to breaking news stories. This is not intended as the ‘last word’ on a subject, but rather a summary of the basics and a pointer towards sources of more detailed information. These can be read as supplements to our ‘round-up’ press releases.

BPA is used in plastics in many products including plastic packaging for food. There have been previous studies linking bisphenol A to adverse effects in animals and this has created concern over low-level chronic exposure in humans. This is the first study of associations with BPA levels in a large population, and it explores “normal” levels of BPA exposure.

Feel free to use these quotes in your stories. Any further comments will be posted here. If you would like to speak to an expert, please don’t hesitate to contact us on (08) 8207 7415 or by email.

Bisphenol A fact sheet produced with advice from Dr Alan Scarlett, School of Biosciences, University of Exeter, UK and Dr Iain Lang, Research Fellow in Epidemiology and Public Health at the Peninsula Medical School, UK – two of the authors of this paper.

Professor Michael Moore is the Director of the National Research Centre for Environmental Toxicology, University of Queensland

“This is a very interesting finding. The changes is liver enzymes are not surprising as there is a known mechanism for how bisphenol A might cause these changes and the results fit with previous animal work. But there is no mechanism we know of to explain the cardiovascular disease. The question we now need to answer is are these associations actually caused by bisphenol A or is it a surrogate for something else that is present in the environment. This study has done a good job in ruling out other potential causes but we have no mechanism to explain the cardiovascular effects so the reason for the association remains a mystery. The main thing is that bisphenol A is widely used and so people should be asking questions about whether this is safe.

One of the most important points to make is that bisphenol A is very water soluble and is rapidly metabolised, so for any untoward effects to occur you would need continuous exposure. This is not impossible as there is sufficient use of bisphenol A in the environment that body concentrations could remain relatively high. But all we have here is a single point measurement in urine. This tells us how much bisphenol A has been cleared from the body but it does not tell you what the concentration remaining in the body is over the long term which is really the crucial factor in proving a dose response relationship.”

Professor Ian Rae is an Honorary Professorial fellow at the University of Melbourne, President of the Royal Australian Chemical Institute, and an expert on the assessment of chemical hazards.

“The findings of Lang and his co-workers will increase pressure on industry to avoid the use of bisphenol-A (BPA) in food and beverage application, or find ways to prevent its release. Bisphenol A is used to react with other components to form polymers like polycarbonate and epoxy resins.A very small proportion of bisphenol-A does not get bound up in the polymerand can leach out into foods and beverages that are in contact with the polymers.

Last month, the US EPA determined that levels of bisphenol-A found in foods and beverages were too low to cause health effects in humans. Although welcomed by industry, that finding has been challenged by environment groups. The US EPA will holda public forum in mid-September to discuss competing claims, and the Laing paper will no doubt be presented there.

The levels of bisphenol-A found in the urine of some 1400 Americans are low, and the increases reported in clinical symptoms are likewise, modest. However, many people believe that any body-burden of a synthetic chemical (a xenobiotic) is of concern. Epidemiology, the traditional tool for investigating environmental toxicity, doesn’t work well with such low-level effects. The present article takes notice of diagnostic information provided by participants, but also usesenzyme assays to probe more deeply.

The authors draw attention to the possibility that ‘exposure to BPA also might be an indicator of exposure to multiple xenobiotics’,and they searched without success for links to other possibly chemicals. Nonetheless, there remains the possibility that bisphenol-A is not the real villain, but that the observed effectsare caused by other things altogether, such as lifestyle and infections.There is even very faint possibility thatbisphenol-A might not be acting alone, given the suite of other xenobiotics that we carry around in our bodies and the prevalence of the other factors.

There are some internal clues in the data reported by Laing and his colleaguesthat the situation might be more complicated than simple toxicology. For example, the urinary concentration is much lower in those with college education than those who did not finish high school. It also drops sharply with increasing income but increases with the incidence of smoking. These are well-known factors that correlate with a wide range of disease conditions, although specific causes are seldom identified and exposure to xenobiotics may be just one cause among many.

A Japanese study from the 1990s linked urinary concentration to consumption of canned beverages, and that could be thesocio-economic link found by the Americans. The statistical analyses performed by the researchers are supposed to have taken these things into account,but it’s hard to believe that they are not important factors.”

Associate Professor Peter Dingle is an environmental toxicologist at Murdoch University in WA.

“Traditionally we’ve associated bisphenol A (BPA) with endocrine disruption, i.e. at very low levels, in the parts per trillion, it’s able to influence reproductive and oestrogen-related effects on the body. What this paper shows is that there is another impact that was unknown to us – it is effecting protein enzymes which suggests the chemical is having an effect on the DNA. When you start altering the DNA you can actually have almost anything occurring. So we can see that there is a potential mechanism.

There is also research that shows that people who have higher blood levels of the chlorinated pesticides like DDT and heptachlor have higher rates of obesity and diabetes, similar to this recent study. But the current research also looked at the enzymes, suggesting a mechanism by altering our DNA. This touches on the new field of epigenetics where chemicals can alter or influence the way our genes are expressed.

The biggest problem with BPA is that it is one of the most prevalent chemicals and is thus very hard to regulate. I would recommend that people reduce their exposure to this chemical by not microwaving their food and beverages in plastic, including microwave safe plastics. Any form of heating of plastic will cause more of these chemicals to leach out into food and drinks. I would also recommend that people don’t store oily foods and liquids in plastic for any length of time. Where possible it is better to store fatty foods and liquids in Pyrex, glass or stainless steel.”

Comments from the UK Science Media Centre

Prof Richard Sharpe, MRC Human Reproductive Sciences Unit, University of Edinburgh, UK

“Cardiovascular diseases and diabetes are ‘Western’ diseases that are becoming ever more common. We have all presumed that this is due to what and how much we eat, and under-exercising, but this study raises a new possibility by showing an association with exposure to bisphenol A. As the authors stress, this study does not show that bisphenol A causes or contributes to these diseases, as such information would require more detailed studies that followed individuals over time (what is called a ‘longitudinal’ study).

It is all too common today for the media to jump to the obvious scary conclusion that a common environmental chemical (bisphenol A) causes increasingly common, and important, human diseases. However, as the authors acknowledge to an extent, there may be an altogether more commonsense (although still scary) explanation for the observations in this study. That is, that if you drink lots of high sugar canned drinks you will over time increase your risk of cardiovascular diseases and diabetes (I think we already suspect this), and incidentally you will be exposed to more bisphenol A (from the can lining). The fact that the younger age groups in this study had the highest bisphenol A exposures would certainly fit with this. Our present understanding, and this study, do not allow us to choose between these two explanations, but in the interests of health protection it is obviously a priority that we design studies to provide this information before we label bisphenol A as the prime suspect and possibly end up ‘putting the wrong person in jail’.”

Prof David Coggon, Professor Of Occupational And Environmental Medicine, University of Southampton, UK

“These are preliminary but potentially important findings. As the researchers indicate, there is now a need to establish whether the association of BPA with heart disease and diabetes can be independently replicated, and if so, whether BPA is a cause of the disorders or is linked to them in some other way. If low-level BPA were confirmed to cause disease, there would be a need to review controls on sources of exposure to the chemical.”