Study predicts BPA in babies 11 times higher than adults.

Jan 12, 2009

Edginton, A and L Ritter. 2008. Predicting plasma concentrations of Bisphenol A in young children (< two years) following typical feeding schedules using a physiologically-based toxicokinetic model. Environmental Health Perspectives doi:10.1289/ehp.0800073.

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Using a mathematical model based on enzymatic differences between newborns and adults, scientists estimate that the amount of bisphenol A (BPA) circulating in the blood of babies is more than 11 times higher than the amount in adult blood. The striking disparity is most likely due to natural differences in metabolism and body size between babies and adults. This study points to the need for chemical exposure standards to better incorporate differences in vulnerabilities between children and adults.


Bisphenol A (BPA) is used to make polycarbonate plastic, epoxy resins for can linings, and in carbonless paper used for credit card receipts. Recent production estimates approach more than 6 billion pounds each year and that number is growing (vom Saal 2005).

Heat and/or contact with acidic foods (high pH foods such as tomatoes, citric fruits) or basic foods (low pH foods) causes the plastic to break down and release BPA, contaminating food or beverages in contact (vom Saal 2005).

Because of its widespread use, almost all Americans are exposed to this common chemical. BPA levels in adult urine range from 0.4 to 8 parts per billion. Less clear are exposure levels in the most at risk populations -- developing fetuses and newborns.

It is believed that BPA is metabolized and passed through the body rather quickly. But, the widespread use of this synthetic estrogen guarantees a constant, yet low dose, exposure in most Americans.

Hundreds of studies published in the last decade find adverse health effects at low doses. This is especially the case if the exposure occurred at critical developmental periods, such as in the womb or early after birth when babies nurse or drink formula (vom Saal 2005).

The levels found to cause effects with laboratory animals easily fall within the range of adult human exposures. The low doses tested in the animal studies can affect virtually every major organ system of the body. Effects include:

• Early onset of female sexual maturity.
• Increased postnatal growth in both sexes.
• Increased prostate size in male offspring exposed in the womb.
• Decreased sperm production and fertility in males due to developmental exposure.
• Adverse affects on chromosome segregation in eggs.
• Altered immune function.
• Hyperactivity, aggressiveness and impaired learning.

BPA is considered an endocrine disruptor because it interferes with processes that are regulated, at least in part, by estrogen hormones.

However, BPA and natural hormones travel through the body differently; a trait that makes BPA more more potent than would otherwise be predicted. BPA remains unattached to other molecules in the blood stream while the estrogen hormone estradiol is carried by specialized proteins -- called plasma binding proteins -- until it is needed.

Because BPA does not bind to these proteins, it can have a higher relative activity per unit of hormone and is unchecked by normal hormone controls.(vom Saal 2005). BPA can affect endocrine regulated processes by just being near hormone control centers. In contrast, estradiol is controlled (or regulated) by complex hormone system signals that tell the protein when and where to release it for use.

What did they do?

Given the uncertainty about a baby's chemical BPA exposure, the authors set out  to estimate BPA levels and BPA elimination in the very young.

The authors gathered data from published animal and limited human studies to estimate how long BPA might stay in a baby's system. Because little is known about the chemical in children, researchers first gathered and analyzed data from adults. From this, the researchers determined how long BPA stays in an adult body before it is broken apart by liver enzymes and eliminated in the urine.

Based upon assumptions and facts about a baby's development, they then estimated how the rate of BPA elimination might differ in children younger than 2-years-old. They studied several key enzymes known to help dismantle the BPA molecule. Those enzymes, it turns out, have significantly less activity in babies -- particularly very young babies under three months of age -- compared to adults.

Using this knowledge, the scientists devised a mathematical computer model to determine rates of elimination of BPA in babies.

What did they find?

The key liver enzyme that is required to eliminate BPA from the blood and body is lower at birth than it is in a full grown person. It is thought that the enzyme activity gradually increases with age until one year when it is fully mature.

A baby's liver enzyme activity is only 5 percent of an adult's. Assuming that BPA exposure is identical between adults and babies -- an assumption made by the scientists for the purpose of their mathematical model -- then the amount of BPA in a baby's blood is approximately 11 times higher than in an adults.

A young, developing child without a fully matured means to deactivate BPA could be carrying concentrations of the compound that are more than 10-fold higher levels than adults. The results suggest tht children are very likely to be the most severely affected by exposure to BPA and related endocrine disruptors.

The study further emphasizes that traditional toxicology studies that measure only adult  are likely to miss or underestimate exposures and effects in infants. 

The estimates made in this study are most certainly on the conservative side. The researchers assumed that babies ingest equivalent amounts of BPA per their body weight. Because babies feed more often, and consume a larger quantity of food relative to their body weight, it is possible that if their food is contaminated with BPA, they may be eating higher quantities than adults.

However, BPA exposure in children is simply unknown at this point and represents a significant gap in knowledge. Given the range of health effects attributed to developmental exposure to BPA, this is clearly a priority that needs to be addressed.

A second priority is whether babies process and eliminate BPA in the same way as adults. Babies are not simply little adults, and there are previous examples where a compound or drug has unpredictable effects simply because babies detoxification system is not fully developed (Edginton 2006a, 2006b).

Since actual BPA exposures are not known in infants, the conservative estimate that babies have 11 times higher BPA in the blood than adults serves as a caution for current safety standards, which are based on studies performed 20 to 30 years ago.

Regulatory agencies determine whether an agent is safe and/or at what levels. Thresholds are based on high dose experiments that find where half a population succumbs to the agent. The threshold is multiplied by 10 to add a “safety” factor.

If the reported estimates are correct, then a safety factor of 10 likely to be insufficient to protect infants. The authors concede that liver enzymes activity differs among individuals. Some people will be better able to take apart and eliminate BPA than others. Thus, while some babies may have less BPA in the blood, others may have levels that could be 55 times higher than an average adult.

Governments and retailers are addressing BPA's safety -- especially in the young. The US Food and Drug Administration and the National Toxicology Program reviewed research about BPA but came to different conclusions about its safety. Canada has banned the chemical from baby bottles and children's toys, and some large retailers have voluntarily decided not to stock products containing BPA.

While consumers and the public await new safety regulations on BPA, there are measures that can lower exposure risk. Avoid or minimize buying food and drink in plastic containers and aluminum cans, which are lined with a BPA containing resin. Avoid microwaving food in plastic food containers. Use glass or BPA-free baby bottles. (Lunder 2008)


 Edginton, AN, W Schmitt and S Willmann. 2006a. Development and evaluation of a generic physiologically based pharmacokinetic model for children. Clinical Pharmacokinetics. 45(10):1013-34.

 Edginton, AN, N Andrea, W Schmitt, B Voith and S Willmann. 2006b. A mechanistic approach for the scaling of clearance in children. Clinical Pharmacokinetics. 45(7):683-704.

Lunder, S. 2008. Tips to avoid BPA. Environmental Working Group.

 vom Saal, FS and C Hughes. 2005. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Environmental Health Perspectives.  113(8):926-33.



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