A study by the US University of Rochester Medical Centre study challenges common assumptions about the chemical bisphenol A (BPA), by showing that in some people, surprisingly high levels remain in the body even after fasting for as long as 24 hours.
The finding suggests that BPA exposure may come from non-food sources, or that BPA is not rapidly metabolised, or both.
Controversy around BPA is mounting. In December the US Food and Drug Administration (FDA) agreed to reconsider the health risks of the chemical, which is used to make plastic baby bottles, water bottles and many other consumer products.
Scientific studies suggest that BPA may harm the brain and prostate glands in developing foetuses and infants; adults with higher BPA levels in their urine were linked to higher risks for heart disease and diabetes, according to a study published last September in the Journal of the American Medical Association.
The latest finding from Rochester is important because, until now, scientists believed that BPA was excreted quickly and that people were exposed to BPA primarily through food. Indeed, the FDA and the European Food Safety Authority have declared BPA safe based, in part, on those assumptions.
"Our results simply do not fit that picture," said lead author Richard W Stahlhut, of the University of Rochester's Environmental Health Sciences Centre. "The research community has clues that could help explain some of these results but to date the importance of the clues have been underestimated. We must chase them much more vigorously now."
Manufacturers use BPA to harden plastics in many types of products. In addition to plastic bottles, BPA is used in PVC water pipes and food storage containers. BPA also coats the inside of metal food cans, and is used in dental sealants.
Stahlhut and colleagues obtained data for a sample of 1469 American adults through the Centre for Disease Control's National Health and Nutrition Examination Survey (NHANES). The researchers sought to explore the link between BPA urine concentration and the length of time a person had been fasting.
Accepting the widely held assumption that food is the most common route of exposure to BPA, Stahlhut expected to see a relationship between the last food ingested, fasting time, and BPA levels. People who had fasted longest (15 to 24 hours), for example, should have had much lower BPA levels than people who had eaten more recently, Stahlhut said.
Instead, those who fasted had levels that were only moderately lower than people who had just eaten. This is significant because scientists expected BPA levels to decrease by about half every five hours.
"In our data, BPA levels appear to drop about eight times more slowly than expected - so slowly, in fact, that race and sex together have as big an influence on BPA levels as fasting time," Stahlhut said.
According to the authors, two possible explanations may exist for the higher-than-expected levels of BPA in people who fasted. One is that exposure to BPA might come through other means, such as house dust or tap water.
In addition, Stahlhut theorises that BPA may seep into fat tissues, where it would be released more slowly. However, further study is needed to evaluate the effects of BPA on adipose tissue hormones and function, Stahlhut said, as well as more studies to compare BPA levels in fat versus blood and urine.
The Centre for Disease Control estimates that 93 per cent of Americans have detectable levels of BPA in their urine. The latest data also supports the idea that individuals might be re-exposed throughout the course of a day, Stahlhut said.
In 2000 another research group found that BPA can migrate from PVC pipes or hoses into room temperature water, producing another potential route of exposure.
The Rochester work builds on a set of six environmental research studies published in October 2008 by Environmental Research. These find that exposure to BPA, phthalates and flame retardants (PBDEs) are strongly associated with adverse health effects on humans and laboratory animals.
Two articles report very similar changes in male reproductive organs in rats and humans related to foetal exposure to phthalates. Two articles show that foetal exposure to BPA or PBDEs disrupts normal development of the brain and behaviour in rats and mice. Two other articles provide data that these chemicals are massively contaminating the oceans and causing harm to aquatic wildlife.
The other studies integrate new laboratory research with a broader view reflecting exposures to a variety of chemicals in plastic. These ubiquitous chemicals found in many plastics act independently and together to adversely affect human, animal and environmental health.
The articles show amongst others the massive contamination of the Pacific Ocean with plastic, and the amount of contamination has increased dramatically in recent years; animal brain structure, brain chemistry and behavioural effects from exposure to BPA and 'phthalate syndrome' in rats' male offspring.
And DBT too
Meanwhile an international team of researchers at the University of California, San Diego School of Medicine and the University of Basel in Switzerland have issued a report on the mechanism of toxicity of a chemical compound called dibutyltin (DBT).
DBT is part of a class of high toxic and widely distributed chemical compounds called organotins, DBT is most commonly used as an anti-fouling agent in paint, for example in the fishing and shipbuilding industries. It is also used in the production of polyvinyl chloride (PVC) plastic tubes and bottles.
According to co-lead investigators Michael E Baker, researcher in UC San Diego's Department of Medicine, Division of Nephrology-Hypertension, and Alex Odermatt at the University of Basel, DBT is closely related to tributyltin (TBT), another well-known pollutant. Concern about the side effects of TBT led the United Nations' International Maritime Organisation to organise a global ban on its use.
"TBT is metabolised by the body's liver into DBT," the scientists explained. "Humans are also exposed to DBT by drinking water from PVC pipes. Because it is poorly broken down, DBT remains in the environment and it appears that its toxic effects are more rapid and more pronounced than those of TBT."
Symptoms of organotin exposure can include irritated skin, dizziness, difficulty breathing, and flu-like symptoms. Although long-terms effects in humans are uncertain, large doses of certain organotins have been shown to damage the reproductive and central nervous systems, bone structure, the liver and immune system in mammals.
Combining studies of the effect in cell culture of DBT on the function of a key class of steroid hormone, glucocorticoids, with computer-based analyses of the molecular interaction of DBT and the glucocorticoid receptor (GR), the US and Swiss scientists explained the mechanism by which DBT inhibits transcriptional activity of the GR.
The GR is expressed in almost every cell in the body. Besides important functions in energy metabolism, the GR helps to regulate genes that control the body's immune system. The researchers propose that by blocking GR activation, DBT disrupts the appropriate response of the immune system during inflammation, providing an explanation for some of the toxic effects of this organotin
