BPA linked to cell damage in post-menopausal women but not men, younger women.

Jul 13, 2009

 Yang YJ, YC Hong, SY Oh, MS Park, H Kim, JH Leem, and EH Ha. 2009. Bisphenol A exposure is associated with oxidative stress and inflammation in postmenopausal women. Environmental Research http://dx.doi.org/10.1016/j.envres.2009.04.014.

mylissa, Flickr.
Women in menopause are more prone to the BPA-associated health effects of inflammation and oxidative stress than either men or women who are still menstruating, finds this study of Korean adults. This is the first time BPA has been linked to these conditions in people and suggests older women may be more susceptible to the chemical's estrogen-like manner that drives these particular types of cell damage. Oxidative stress can be involved with aging, cancer and other disease states.


Bisphenol A (BPA) is a chemical used in polycarbonate plastics and epoxy resins. It is found in a variety of consumer products. Plastic bottles, compact disks, thermal store receipts, dental sealants and the lining of food cans are just some of the products that contain the chemical.

Exposure to BPA is widespread. More than 90 percent of Americans have measurable levels of BPA in their urine (Calafat et al. 2008).

BPA is linked to several types of human health effects. Urine levels of BPA in US adults have been associated with type 2 diabetes, heart disease and heart attacks.

BPA's health effects are due in part to its ability to mimic estrogens – hormones that are important in female development, fertility, menopause, cardiovascular disease and breast cancer. Estrogens are the dominant female hormones, but they are also important for men.

Estrogen levels vary during a women's lifetime. The hormone kicks in during puberty to guide reproductive development, peaks during childbearing years and decreases in post-menopausal women. 

Aging occurs in part because of cell damage due to an overactive immune system. Two responses – inflammation and its contributing partner oxidative stress – are tied to, and can increase with, age.

Exercise and metabolism burn fat to create energy. The process – called oxidation – contributes to “oxidative stress.” Oxidative stress occurs when there are too many highly reactive chemicals – called oxidants – in the body that readily react – or oxidize – with other substances. These reactions damage cells and are thought to contribute to aging, cancer and other changes. Antioxidants – such as vitamins A, C and E – can sop up the oxidants and render them harmless, thus helping defray the damaging effects on cells.

Prior studies show BPA can induce oxidative stress by altering liver functions in rodents. These changes can affect male reproduction and organ development in mice (Chitra et al. 2003, Kabuto et al. 2004). Whether this occurs in people is not known.

Oxidative stress and inflammation are both linked to diabetes, cardiovascular disease and even to the spread of cancer. Because inflammation can lead to poor health, doctors monitor inflammation by measuring C reactive protein.

What did they do?

The authors evaluated inflammation and oxidative stress markers in the blood of adult Koreans and then compared them to BPA measured in their urine. They examined the measurements in three groups: men, premenopausal women and postmenopausal women.

The urine and blood samples were collected from the participants at the same time. Two markers of oxidative stress – malondialdehyde and 8-hydroxydeoxyguanosine – and two markers of inflammation – white blood cells and C-reactive protein – were measured.

Questionnaires were administered to gather medical, lifestyle, exposure and demographic information.

Scientists know that inflammation and oxidative stress increase with age. The authors statistically controlled for age so they could see BPA effects independent of age. They also controlled for body mass and possible factors identified elsewhere that could influence oxidative stress.

The study included 259 men, 92 premenopausal women and 134 post-menopausal women.

What did they find?

BPA was found in the urine of 76 percent of the Korean adults in this study. Concentrations were similar among groups for all levels except those with the highest measured amounts, where men had three times the levels of premenopausal women (26.5 versus 7.72 micrograms/gram) and about 50% more than postmenopausal women (17.90 microg/g).

Urine levels of bisphenol A were higher in older adults.

Associations between BPA levels and both oxidative stress and inflammation only occurred in postmenopausal women. Oxidative stress levels were higher in older women who also had higher levels of BPA. Further, levels of the inflammation-marker C- reactive protein was increased in the women with higher levels of BPA.

Bisphenol A exposure in men and premenopausal women did not correlate to any of the markers of inflammation or oxidative stress.

What does it mean?

The effects of BPA varied between men and women and also by age – and thus by menopausal stutus and estrogen levels during this time. The chemical "was clearly associated with oxidative stress and inflammatory markers in postmenopausal women, but not in premenopausal women and adult men."

This is the first study that attempts to determine if BPA contributes to inflammation and oxidative stress in people.

BPA's effects may be stronger in postmenopausal women because of a paucity of estrogen, with levels far below those of menstruating women and lower than men's levels. Lower levels of the natural hormones may allow BPA to affect estrogen signaling channels that would then trigger the cell responses associated with oxidative stress, leading to inflammation.

The increased oxidative stress and inflammation seen in the older, Korean women with higher levels of BPA suggests that BPA might increase both conditions. However, because BPA, inflammation and oxidative stress were measured at the same time, it is not certain that BPA caused the observed increases.

One marker of oxidative stress, 8-hydroxydeoxyguanosine, represents oxidation of DNA. This type of DNA damage has been linked to cancer in other studies and could help explain why animals are more prone to breast- and prostate- cancers when exposed to BPA.

The adults in this study were less exposed to BPA than prior reports of adults in the US and Japan. The levels of BPA found in the Koreans studied here are lower than levels seen in US adults and Japanese women. Also, fewer Koreans had measurable BPA in their urine than those persons studied in the United States and Japan.

If bisphenol A is responsible for the higher levels of inflammation and oxidative stress seen in the Koreans, it is possible that adults in the United States and Japan are at greater risk of these two conditions due to their higher exposures.

The authors did not take into account whether or not the study participants took anti-inflammatory medicine or ate foods rich in antioxidants. Aspirin, acetaminophen and other mild pain relievers relieve pain by changing – decreasing – inflammation. Many older adults use these medicines frequently, and this use could alter the inflammation results of the study. Likewise, antioxidants – which are believed to counteract oxidative stress – are in a wide variety of foods, yet it was not reported if the study participants ate the foods.


Antioxidants and oxidative stress. 2007. NetDoctor.com.

Bisphenol A overview. Environment California.

Calafat, AM, X Ye, LY Wong, JA Reidy and LL Needham. 2008. Exposure of the US
population to bisphenol A and 4-tertiary-octylphenol:2003–2004
. Environmental
Health Perspectives 116:39–44

Chitra, KC, C Latchoumycandane and PP Mathur. 2003. Induction of oxidative stress
by bisphenol A in the epididymal sperm of rats

Is your plastic safe? Natural Resources Defense Fund.

Kabuto, H., M Amakawa and T Shishibori. 2004. Exposure to bisphenol A during embryonic/fetal life and infancy increases oxidative injury and causes under-development of the brain and testis in mice. Life Science 74:2931–2940.

What is menopause? The Hormone Foundation.



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