Urinary BPA Concentrations and Chronic Diseases

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Urinary Bisphenol A Concentration

IFC Comments on a Recent Study that Finds Association with Urinary Bisphenol A Concentration and Chronic Diseases

A study published in the September 17, 2008 edition of the Journal of the American Medical Association (JAMA) showed a relationship between increasing urinary bisphenol A (BPA) concentration and the prevalence of self-reported chronic disease, including diabetes and cardiovascular disease.  The study examined data from a cross-sectional survey, the 2003-2004 US National Health and Nutrition Examination Survey (NHANES). 

The authors reported that a 1-standard deviation increase in urinary BPA excretion was associated with an adjusted odds ratio of 1.39 for diabetes and also for cardiovascular disease.   This finding was statistically significant.  However, this type of data, as the authors note, cannot show causation, only associations.  Great care should be exercised in the interpretation of odds ratios from epidemiological studies.  Consideration must be given to the magnitude of the odds ratio’s departure from the “no-association” value of 1.00, the width of the 95% confidence intervals, and the ability of the research group to account for as many confounders as possible.  As described in the next paragraph, there are other confounders that could have altered the results.  When an odds ratio is already fairly close to 1.00 and there is the strong likelihood of unrecognized confounders, there is much less confidence in this statistical association.  Finally, the diseases examined were self-reported and the number of study participants who were clinically diagnosed with these diseases is unknown. 

A critical limitation of this study is that findings are based on a single urine sample.  The day- to-day variability in urinary BPA in this population, how long the people in this study might have had this level of BPA in the urine, and if repeat urine samples obtained days, weeks, or months later would have shown the same results, is unknown.  BPA is quickly and efficiently eliminated from the body through urine; therefore, one measure of urinary BPA is not sufficient evidence to confirm that BPA consumption is linked to complex diseases such as diabetes and cardiovascular disease.

Another important weakness of this study is that the authors did not attempt to control for dietary factors.  The authors comment that “canned beverages constitute a major dietary source” of BPA.  Thus, it is likely that BPA consumption is highly correlated with soft drink intake, which also may be correlated with diabetes and cardiovascular disease.  The authors did adjust for obesity, smoking, and some other potential confounders.  However, they did not adjust for various dietary confounders, such as a high intake of highly sweetened beverages, including soft drinks, and high sodium and high fat canned foods.  It is likely that these foods, and not BPA, caused the observed relationships.  Because the authors did not control for these dietary factors, despite having access to this type of information, it is reasonable to question whether BPA alone can be attributed to the development of these diseases.  Higher urinary BPA levels could be linked with a poorer overall diet, including a high consumption of processed foods and little consumption of fresh fruits and vegetables, which have been shown to help protect against these diseases.   

There are numerous internal inconsistencies in the study as well.  For example, C-reactive protein, a measure of inflammation in the body, was not elevated in the group with increased urinary BPA concentrations.  Neither were LDL-cholesterol and triglycerides increased, even though these are major risk factors for heart disease.  Fasting blood sugar and insulin levels, typical measures of diabetes, also were not elevated.  Even if BPA consumption was shown to cause these diseases, it might be expected that well-known risk factors for these diseases would be affected by BPA.  It is interesting that the authors cited extensive metabolic studies demonstrating the rapid detoxification (glucuronidation) and elimination of BPA from the body and yet still reported these statistical associations with chronic disease.  It seems logical to question how BPA could be having the proposed toxic effects given its relatively quick passage, in a detoxified form, through the body.

Due to the many serious limitations of this study, further research is needed to make any conclusion about BPA consumption and chronic diseases such as diabetes and cardiovascular disease.