BPA: How Your Genes Influence BPA Detoxification

Key takeaways:
~ BPA is an endocrine disruptor similar to estrogen.
~ We are all exposed to it.
~ Individuals differ in how they break down and get rid of BPA.

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BPA: It’s everywhere…

BPA, a chemical found in some plastics, has been linked to a variety of effects on people, including obesity, insulin resistance, and epigenetic effects on babies.

BPA is everywhere in our food supply. In fact, a CDC report showed that 93% of people have BPA in their urine.[ref]

This article explains the peer-reviewed research and the links to genetic variants involved in getting rid of BPA.

Two questions that I wanted answers to about BPA:

    1. Is BPA really a problem?
    2. Does BPA affect everyone the same way —or do genetic variants play a role?

I’m diving into the research on the topic, looking past the hyped-up ‘sky is falling’ type of headlines to see if there really is a reason for concern.

What is BPA:

  • Bisphenol-A is a component of some plastics (recycling symbols 3, 6, and 7).
  • It is considered to be an endocrine disruptor because of the similarity of the molecules to estrogen.
  • It is now ubiquitous in the environment, and >90% of people have detectable levels in their blood.

How are we exposed to BPA:

While we often think of BPA as something to avoid in plastic water bottles, our routes of exposure are much greater than just in plastic containers.

For example, BPA can be found in

  • teabags that contain plastic[ref]
  • thermal printed receipts (somel)[ref], especially when combined with hand sanitizer[ref]
  • food and beverage contact paper – e.g. wrappers, paper plates, cardboard food boxes[ref]
  • canned foods often have BPA in the can liner[ref]
  • pantyhose[ref]
  • composite dental resins and sealants[ref] as well as brackets for bonding braces[ref]
  • most food – whether through plastic contamination or through the BPA in the soil[ref][ref]
  • hot beverages, such as coffee from a plastic cup[ref]

What do studies show about BPA?

Ok, so BPA is everywhere and may act similarly to estrogen.

Animal studies clearly show that BPA can cause weight gain, alter hormone levels, disrupt reproduction, affect offspring, etc.[ref]

While animal studies are important and have their place, I’m going to focus here on recent human studies that take into account current human levels of exposure.

Changes to insulin:
A study published in the Journal of the Endocrine Society looked at the effect of BPA on insulin secretion and glucose levels. The researchers gave an oral dose of BPA at 50 ug/kg body weight, which is the daily limit set by the EPA as being safe daily exposure over a lifetime. They found that this BPA dose increased initial insulin release (oral glucose tolerance) but then showed no statistical difference with the later phase blood glucose response. This is an important study because they used the EPA guidelines for an amount of BPA that was not supposed to elicit a response.[ref] I found it interesting that there was a large variation between individuals in their BPA levels over time after ingestion — individual rates of BPA metabolism varied a lot!

Exposure starts before birth:
Another recent study looked at BPA and PFOAs in over 6,000 newborns to determine if there was an effect on birth size. Researchers found that over 90% of the infants had detectable levels of BPA in their blood, and over 99% had detectable PFOA and PFOS. The study did find that average BPA levels were higher in twins born with lower birth weight, possibly because higher BPA levels also correlated with a greater number being born before 37 weeks of age.[ref] Most remarkable to me is that 90% of babies were born with BPA in their blood. The infants in the study were born between 2008-2010 in NY.

Male fertility:
BPA was shown in a recent study (and several previous studies) to reduce sperm motility in men.[ref]

Previous studies also showed decreased testosterone levels in male teenagers with higher levels of BPA.[ref]

Linked to obesity:
A small study published in Sept 2018 found that children and teens with higher BPA exposure (the top third of the group) had a 12x risk of obesity.[ref] This is likely an overestimate of the impact of obesity since the study group was only 138 people. Nonetheless, this is one more study in a long line of human studies that show that higher BPA exposure increases weight.[ref][ref][ref][ref][ref][ref]

A study from August 2018 found that BPA at normal exposure levels alters insulin response in a way that is independent of adipogenesis (fat creation).  The study found that BPA causes a low-level inflammatory response.[ref] This is in line with previous epidemiological studies that tie higher BPA levels to insulin resistance in men, women, and children.[ref][ref][ref]

BPA Genotype Report:

Not everyone is affected by BPA in the same way. Genetic variants impact how quickly you clear it out of your body.

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Oxidative Stress:

BPA exposure increases oxidative stress and mitochondrial dysfunction. A study that looked at BPA exposure in children with autism found that all children (with and without autism) had an increase in oxidative stress and mitochondrial dysfunction when exposed to BPA.[ref] Another study found increased oxidative stress biomarkers in pregnant women based on BPA exposure.[ref]

COX2 gene:
COX2 is an enzyme that acts as part of the body’s inflammatory response

Check your genetic data for rs5277 (23andMe v4; AncestryDNA):

  • C/C: increase in risk for liver dysfunction with BPA exposure[ref]
  • C/G: lower risk for liver dysfunction with BPA exposure
  • G/G: low risk for liver dysfunction with BPA exposure

Members: Your genotype for rs5277 is .

CAT gene:
atalase is an enzyme involved in cellular detoxification

Check your genetic data for rs769217 (23andme v4, v5; AncestryDNA):

  • C/C: typical risk
  • C/T: increased risk of liver dysfunction in the elderly with BPA exposure[ref], lower catalase activity
  • T/T: no data was given in the study on BPA, but lower catalase activity[ref]

Members: Your genotype for rs769217 is .

SOD2 gene:
The SOD2 gene codes for a mitochondrial enzyme that converts superoxide into hydrogen peroxide and oxygen. It is important in detoxification.

Check your genetic data for rs4880 (23andMe v4, v5; AncestryDNA):

  • A/A: increased risk of liver dysfunction with BPA exposure[ref]
  • A/G: no increase in the risk of liver dysfunction with BPA
  • G/G: no increase in the risk of liver dysfunction with BPA

Members: Your genotype for rs4880 is .

The study results here showed that the more common variant of rs4880 (A/A) was associated with an increased risk of liver dysfunction. This seems contradictory, but a new cell study on vitamin D levels, SOD, and BPA help to clear up the confusion. The study showed that “BPA administration elevated Mn-superoxide dismutase (MnSOD) expression but negatively regulated total SOD activity”. The researchers go on to explain: “Our results suggest that 1,25D3 attenuates BPA-induced decreases in 17β-estradiol and that treatment with 1,25D3 plus BPA regulates granulosa cell mitochondria by elevating mitochondrial biogenesis-related protein levels.”[ref]

Metabolism of BPA:

UGT2B15 metabolizes BPA (through glucuronidation)[ref]; “the polymorphic alleles of UGT2B15 are closely associated with variations in the metabolism and toxicity of BPA.”[ref] A study looked at the expression of UGT2B15 during the third trimester and in infants (3 – 15 weeks). UGT2B15 levels varied (by 31 fold) among the group due in part to gender and UGT2B15 polymorphisms.[ref] Another study found that UGT2B15 metabolizes up to 80% of BPA when concentrations are low but that another enzyme (UGT1A9) becomes more important at higher BPA levels.[ref]

Check your genetic data for rs1902023 ( 23andMe v4 ; AncestryDNA):

  • A/A: causes decreased enzyme activity[ref], possibly impairs BPA detoxification
  • A/C: probably normal BPA detoxification
  • C/C: typical

Members: Your genotype for rs1902023 is .

UGT1A: Glucuronidation of BPA through UGT1A[ref]

Check your genetic data for rs34983651 (23andMe v4 only):

  • II: lower liver clearance of BPA with UG/T1A1*28[ref], lower clearance in breast tissue[ref]
  • ID: lower clearance of BPA
  • DD: typical

Members: Your genotype for rs34983651 is .


The BPA that isn’t metabolized through glucuronidation usually gets taken care of through SULT1A1. Mouse studies show that obese livers are less able to sulfate BPA than lean mice. “Taken together these findings establish a profoundly reduced capacity of BPA elimination via sulfonation in obese or diabetic individuals and in those with fatty or cirrhotic livers versus individuals with healthy livers.”[ref][ref]

Check your genetic data for rs9282861 or i6018900 (23andMe v4):

  • T/T: low activity of the enzyme[ref][ref]
  • C/T: lower enzyme activity
  • C/C: typical

Members: Your genotype for rs9282861 is or for i6018900 is .

Caffeine induces the SULT1A1 enzyme[ref][ref]

Lifehacks for getting rid of BPA:

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About the Author:
Debbie Moon is the founder of Genetic Lifehacks. Fascinated by the connections between genes, diet, and health, her goal is to help you understand how to apply genetics to your diet and lifestyle decisions. Debbie has a BS in engineering and also an MSc in biological sciences from Clemson University. Debbie combines an engineering mindset with a biological systems approach to help you understand how genetic differences impact your optimal health.

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