Study design

In their epidemiological study, Trasande and co-workers used statistical analysis to identify whether increased levels of BPA were more likely to be detected in 6 to 19 year old persons that were overweight or obese. The data came from the NHANES study, a US government initiative where health and nutrition status is assessed in a representative sub-sample of the US population [link to NHANES, link to CDC Report 2009]. During this survey urine samples were also collected. BPA was measured in these urine samples by government laboratories. The New York scientists divided their data into four groups, depending on the level of BPA: a low level, two intermediate levels and a high level. They then looked at body mass index (BMI, height divided by weight square) levels and analyzed whether the risk of being obese (defined as BMI >30) was increased in the groups with intermediate or high BPA levels, compared to the low level group.


The result of this statistical analysis was that all three intermediate and high dose BPA groups had an increased risk (odds ratio) for being obese. This means, that higher levels of urinary BPA in children and adolescents are statistically associated with an increased risk for being obese.


Higher levels of BPA are associated with an increased risk for being obese in children and adolescents. The study design does not permit conclusions on the causality of this association, i.e. does BPA cause obesity. The reverse may be true: BPA is a fat-soluble molecule, and higher urinary levels may be associated with a higher BPA body level due to fatty tissue acting as a reservoir. Other factors, like life style and calorie consumption, may also be responsible for the association, though the authors observed no statistical influence.

The association has also been observed in adults, using data from the same NHANES study. Such associations need to be questioned with biological plausibility – i.e. is there an underlying biological explanation how BPA may lead to obesity? Two recently published studies offer a possible explanation for this. Cells that are destined to become fat storing cells (so called adipocytes) were triggered to differentiate into adipocytes by BPA. And a study in mice showed that BPA induced genes involved in the production of fat molecules and led to a higher level of fat in the liver.

More research is needed to understand the plausibility of BPA associations with obesity, to understand what the underlying biological mechanisms are and whether there are sensitive windows of development (prenatal, early childhood, puberty, etc.).


BPA is a chemical that has many different uses. People’s exposure occurs mainly via food, because BPA can be used to make coatings that are approved for direct contact with food. This application is increasingly being questioned, because of numerous studies showing an association between BPA levels in people and health effects, like cardiovascular disease (; ; and diabetes ( Many different studies have also shown that BPA is an endocrine disrupting chemical (EDC) and can cause health effects in lab studies [reviewed in this abstract].

In 2009 the Endocrine Society published a scientific statement on EDCs, highlighting the need for public health measures. Several producing industry funded associations oppose this view and argue that BPA is not an EDC [ ; ;]. A large government funded research project on the toxicity of BPA at low doses is currently ongoing in the US.

The European Food Safety Authority (EFSA), responsible for risk assessment of BPA in food packaging, is currently reviewing its scientific opinion and will publish it in 2013. Previous EFSA scientific opinions have assured the safety of BPA in food packaging at current exposure levels [2007 opinion2010 opinion].

The European Commission manages the risk of food packaging substances and banned the use of BPA in the manufacture of plastic baby bottles, starting from June 2011more…

In July 2012, the Federal Drug Administration (FDA), announced a ban for BPA in baby bottles