Perfluorooctanoic Acid (PFOA) is in the news this week with two recently released studies. As you may remember from one of my previous articles, PFOA is persistent organic pollutant which can accumulate in the environment (including food, although most people are exposed to PFOA from drinking water). As well, it is quite long lived, and has the potential to reach levels which can affect our health.
The first paper (Perfluorooctanoic Acid and Cardiovascular Disease in US Adults) adds further information about the potential effects POFA on the heart and blood vessels. Previous animal and indirect studies have suggested that PFOA exposure may harm the heart and blood vessels.
The results of this cross sectional study suggest that adults with the highest levels of PFOA in their blood are more likely to have cardiovascular disease than those with the lowest levels.
However, there are a number of limitations which make interpretation of these results difficult. A cross-sectional study looks at the relationship between a disease and other variables (such as PFOA concentration in the blood) in a defined population at a single point (or short period) in time.
In this case the measurement of blood PFOA levels were done once either in 1999-2000 or 2003-2004 and the actual long term exposure to PFOA may be very different from that suggested by a single measurement. We know for example that blood levels for PFOA were falling during the study due to regulation of this chemical.
Also, the incidence of cardiovascular disease was self reported, which is subject to bias. The objective measure of blood vessel function had a much weaker association with PFOA. Unusually, the association disappeared in smokers and people with Body Mass Index’s less than 30.
As well, there were significant differences in lifestyle, education and background between the people with the lowest levels of PFOA and those with the highest. PFOA may simply be a marker for low socioeconomic status, which itself is known to be correlated with risk of cardiovascular disease.
Finally, studies of people who have been chronically exposed to significant levels of PFOA have not show statistically significant increases in cardiovascular disease for those exposed to PFOA.
The current study is suggestive, but is a long way from showing that exposure to the background levels of PFOA in our environment harms our heart and blood vessels. It requires follow up with studies that track exposure to PFOA to better understand the possible role of PFOA in cardiovascular disease.
The next paper is Maternal Concentrations of Polyfluoroalkyl Compounds during Pregnancy and Fetal and Postnatal Growth in British Girls. Here girls with higher prenatal exposure to polyfluroinated chemicals were smaller at birth than those with lower exposure.
However, it suffers from the same limitations as the previous study (a single measurement of the chemicals may not reflect the real exposure, and it is difficult to full correct for other environmental factors that may have a role).
As well, there were only 17 low birth weight girls in the sample, the result could well be by chance alone.
We should keep an eye on levels of pefluorinated compounds, and try to minimise our exposure to them as a matter of course, but there is currently no good evidence that the levels mots of us are exposed to are harmful.
Certainly more research is needed, but the current guidelines on minimising risk for cardiovascular disease and increasing baby health (including increasing consumption of fresh fruit and vegetables) are those that minimise exposure to these chemicals in the first place.