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    Previously unstudied chemical in common plastics found to have carcinogenic effects

    Data on terephthalic acid suggests the need for a new model of testing potentially harmful polyesters

    December 11, 2014 (San Francisco, CA)

    Researchers at California Pacific Medical Center Research Institute (CPMCRI) have found new evidence of potentially carcinogenic effects of a chemical found in commonly used plastics, called terephthalic acid (TPA).

    Their findings were published online today in Carcinogenesis, as a follow-up to preliminary results presented last year at the San Antonio Breast Cancer Symposium.

    By expanding the measures typically investigated in safety studies on industrial chemicals, the results also validate the importance of wider testing of materials used to package a variety of foods and beverages.

    “The biological effects of TPA are much more complex than those of other common chemical compounds such as bisphenol A (BPA),” said Gloria Luciani-Torres, Ph.D., a researcher at CPMCRI and first author of the study. “TPA causes some of the same deleterious cellular effects as BPA, but in addition activates the cells’ DNA damage response. The damaged cells were not targeted for elimination—as occurs in healthy tissues—allowing cells harboring DNA damage from TPA to proliferate and increase the potential for tumor development.”

    “Relying entirely on current testing models, TPA might be classified as a safe chemical without recognizing its potential to induce the DNA damage that underlies common cancer pathways,” added William Goodson, M.D., CPMC scientist and breast surgeon, and co-author of the study. “We believe these findings suggest it is critical to ascertain the safety of long-term, cumulative exposure to this chemical.”

    Previous studies have shown that food and beverage packaging materials leach chemicals that disrupt cells’ normal functioning in humans and mammals. Some of the chemicals are known as “endocrine disruptors” because they interfere with the body’s endocrine (glands and hormones) system and produce adverse developmental, reproductive, neurological, and immune effects. Traditionally, safety testing on plastics is conducted by ascertaining any unusual cell growth after chemical exposure, and determining how the chemicals bind estrogen receptors in the cells. Harmful chemicals can ”pose” as estrogen, binding with protein receptors in the cell membrane, and initiating a cascade of harmful cellular effects, leading to cancer.

    To investigate the effects of TPA on cells from non-cancerous human breast tissue, the researchers exposed the cells in vitro to the chemical at a range of concentrations that would be reached after ingestion via food or beverage packaging (e.g., plastic drinking bottles). After exposure to the chemical, the cells’ proteins were isolated so that specific cellular cycle changes could be observed and genetic material analyzed.

    After seven days of exposure, TPA was shown to increase estrogen-receptor levels in the cells. (About 75 percent of all breast cancers are estrogen-receptor positive and grow in response to the hormone estrogen.) The chemical also activated DNA-damage response pathways in the estrogen-receptor positive cells, and compromised the natural defense mechanism, which eliminates damaged cells. DNA changes characteristic of cancerous growth persisted even after the TPA was removed from the cell samples.

    “The findings call into question the way current chemical testing is conducted,” said Dr. Goodson.
    “We consistently observed molecular changes in breast tissue cells indicative of the hallmarks of cancer, suggesting that determining safe levels of TPA exposure must be considered a high priority.”

    The present study builds upon previous findings of this research group led by CPMCRI Principal Investigator Shanaz Dairkee, Ph.D., that BPA causes normal cells to behave like aggressive cancer cells—which was the first evidence pointing to BPA's harmful effects in limiting the efficacy of a commonly used chemoprevention drug.

    The study was funded by The Cancer League, the Clarence E. Heller Charitable Foundation, and the California Breast Cancer Research Program.


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