Bisphenol A exposure linked to brain tumor diagnosis.

Jun 26, 2012

Duan, B, X Hu, H Zhao, J Qin and J Luo. 2012. The relationship between urinary bisphenol A levels and meningioma in Chinese adults. International Journal of Clinical Oncology

Exposure to bisphenol A may be a risk factor for a common type of brain tumor called meningioma, reports a study from China. This is the first study to suggest a link between brain cancer and the chemical, which is widely used in consumer products.
Those with the highest urine BPA levels were about 1.6 times more likely to be diagnosed with meningioma compared to those with lower concentrations.
This link was observed even after accounting for other factors associated with meningioma. More research is needed to confirm the findings.


Meningioma is a type of brain tumor that develops from the meninges, the membrane that surrounds the brain and spinal cord.

About 90 percent of diagnosed meningiomas are benign. That is, they are non-cancerous, slow-growing tumors. The other 10 percent are malignant. However, benign tumors can cause illness and death as they grow and press against the brain and spinal cord.

Meningioma affects six in 100,000 people in the United States. It is more common in women than in men (Bondy et al. 1996) and in those older than 40. Radiation, genetic disorders and hormone replacement therapy (HRT) (Blitshteyn et al. 2008) are potential risk factors. Tumors may also be related to previous head injury and viral infections, although more research is needed to confirm this.

Meningioma is a hormone-sensitive cancer – the tumor thrives and grows in the presence of hormones. Because of this, there are concerns that endocrine disruptors – compounds known to mimic or block hormones in the body – may play a role in the development of cancers like meningioma.

Bisphenol A (BPA) is a widely used chemical that can behave like estrogen. It is used in the manufacture of polycarbonate plastics and epoxy resins. BPA is in many consumer products, including the lining of food and beverage cans, plastic food packaging, dental sealants, paper receipts and water pipes. Exposure in people is widespread and occurs mainly through eating or drinking contaminated food and beverages.

Animal and human studies have linked BPA to hormone-sensitive cancers, including breast and prostate cancers. The relationship between BPA exposure and meningioma is unclear.

What did they do?

Researchers examined the relationship between BPA exposure and the diagnosis of meningioma. They followed 247 patients with the brain cancer and 258 patients with no history of cancer who were getting medical exams at the Union Hospital in Wuhan, China.

Meningioma was confirmed with a brain scan or a biopsy – a tissue sample. BPA concentrations were measured in participants' urine samples.

Researchers used questionnaires and medical records to collect the patients medical history and information on factors potentially related to meningioma – for example, age, gender, use of hormone replacement therapy (HRT), body mass index (BMI) and family history of cancer.

Participants were placed into one of four exposure groups based on the BPA concentrations in their urine: less than 0.53 nanograms per milliliter (ng/mL), 0.54 - 0.91 ng/mL, 0.92 - 1.69 ng/mL and greater than 1.69 ng/ml. They assessed whether the odds of being diagnosed with meningioma increased with increasing BPA concentrations in urine.

Several factors potentially associated with meningioma – age, gender, race, BMI, family history of cancer, HRT use –also were considered in their analysis.

What did they find?

There was a positive association between BPA concentrations in urine and diagnosis of meningioma.

The patients with higher concentrations of BPA in their urine – the three groups with greater than 0.53 ng/ml – were more likely to have the brain cancer compared to those with the lower concentrations – less than 0.53 ng/mL. Specifically, those with higher concentrations were 1.4 to 1.6 times more likely to be diagnosed than patients in the group with the lowest urine concentrations.

The results also support what other studies have shown. The personal factors of gender, BMI and use of HRT influence the risk of the disease. However, when considering the link with BPA, the personal factors did not alter the results.

This means the association was consistent regardless of BMI status. There was a positive association between BPA levels in urine and meningioma among normal weight, overweight and obese participants.

Similar results were observed for patients with or without HRT use. Among HRT users, those with urine BPA concentrations above 0.92 ng/mL had 1.4 to 1.5 times the risk of being diagnosed with meningioma compared to those with lower concentrations. Non-HRT users had 1.5 to 1.7 times the risk of a positive diagnosis.

What does it mean?

Exposure to BPA may be a risk factor for the hormone-related brain cancer meningioma. The preliminary study found the higher the levels of BPA measured in urine samples, the higher the chance of a positive tumor diagnosis.

This is the first study to show a link between BPA exposure and diagnosis of meningioma.

Previous studies in animals have observed an association between BPA and other hormone-sensitive cancers like breast and prostate cancer. This study adds to that because, according to the authors, it "demonstrated emerging evidence of the role of environmental exposure to BPA on estrogen-sensitive tumors in humans."

The study findings are also consistent with prior studies that report hormone replacement therapy raises the risk of the disease.

Importantly, the association between BPA exposure and meningioma diagnosis was present even when they included other known risk factors for the disease. This is important because it indicates that BPA is a risk factor by itself – regardless of body mass or HRT use.

Results also confirm findings from previous research regarding the risk factors. Gender, HRT, and BMI were associated with the cancer.

There are several study limitations. For one, researchers measured only one urine sample to establish exposure to BPA but a one-time, current sample is a fairly weak indicator of the long-term exposure presumably required to cause or promote tumors. In part, this is because BPA exposure varies greatly from day to day (Ye et al. 2001). BPA is rapidly excreted from the body (Stahlhut et al. 2009) so one sample may not adequately reflect long-term exposure. This is a particular concern for a disease like meningioma, which can take years to develop. Additionally, a one-time, current sample cannot confirm that BPA exposure preceded and led to the tumors.

Additionally, while one previous study (Stahlhut et al. 2009) suggests that BPA might linger in the body and not be rapidly eliminated, the prevailing view is that BPA is rapidly cleared and excreted (Völkel et al., 2002). If the latter is true, then using one urine sample to assess long-term exposure is a particular concern for a disease like meningioma, which can take years to develop. (Correction 6/26/12)

Also, researchers did not report or statistically account for the type of urine samples collected. Samples collected in the morning may be more concentrated than spot samples randomly collected throughout the day.

Because researchers also failed to report average BPA concentrations observed in the participants’ urine, the results cannot be compared to other populations.

Larger, more in-depth studies that address these study limitations are needed. Even with these caveats, the authors suggest that "until then, however, clinicians and patients should be aware of the risk of those products that contain BPA."


Bisphenol A (BPA). National Institute of Environmental Health.

Blitshteyn, S, JE Crook and KA Jaeckle. 2008. Is there an association between meningioma and hormone replacement therapy? Journal of Clinical Oncology 26(2):279-82.

Bondy, M, and B Lee Ligon. 1996. Epidemiology and etiology of intracranial meningiomas: A review. Journal of Neuro-Oncology. 29(3):197-205.

Meningiomas. Bringham and Women's Hospital.

Stahlhut, RW, WV Welshons and WH Swan. 2009. Bisphenol A data in NHANES suggest longer than expected half-life, substantial nonfood exposure or both. Environmental Health Perspectives 117: 784-789.

Völkel, W, T Colnot, GA Csanády, JG Filser and W Dekant. 2002. Metabolism and kinetics of bisphenol a in humans at low doses following oral administration. Chemical Research in Toxicology 15(10):1281-7.

Ye, X, LY Wong, AM Bishop and AM Calafat. 2011. Variability of urinary concentrations of bisphenol A in spot samples, first morning voids, and 24-hour collections. Environmental Health Perspectives 119(7):983-8.



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