Cancer and Environmental Endocrine Disrupting Chemicals

Environmental endocrine disrupting chemicals (EDCs), including pesticides and industrial chemicals, have been and are released into the environment producing deleterious effects on wildlife and humans. The effects observed in animal models after exposure during organogenesis correlate positively with an increased incidence of malformations of the male genital tract and of neoplasms and with the decreased sperm quality observed in European and US populations. Exposure to EDCs generates additional effects, such as alterations in male and female reproduction and changes in neuroendocrinology, behavior, metabolism and obesity, prostate cancer and thyroid and cardiovascular endocrinology. This Review highlights the carcinogenic properties of EDCs, with a special focus on bisphenol A. However, humans and wildlife are exposed to a mixture of EDCs that act contextually. To explain this mindboggling complexity will require the design of novel experimental approaches that integrate the effects of different doses of structurally different chemicals that act at different ages on different target tissues. The key to this complex problem lies in the adoption of mathematical modeling and computer simulations afforded by system biology approaches. Regardless, the data already amassed highlight the need for a public policy to reduce exposure to EDCs.

From press release:

Longtime environmental health researchers at Tufts University School of Medicine describe the carcinogenic effects of endocrine-disrupting chemicals (EDCs), ubiquitous chemicals that have hormone-like effects in the body. In a review article published online May 25 in Nature Reviews Endocrinology, the researchers express the need for more complex strategies for studying how these chemicals affect health but report that ample evidence already supports changing public health and environmental policies to protect the public from exposure to EDCs.

"The strength and breadth of existing research on the negative effects of EDCs, including bisphenol A, warrants immediate action to reduce EDC exposure, particularly among the developing fetus and women of reproductive age," said author Carlos Sonnenschein, MD, professor in the department of anatomy and cellular biology at Tufts University School of Medicine (TUSM).

"Developing embryos 'read' environmental cues as a forecast of the outside world. These cues can affect the way certain genes are expressed and in this way alter the structure and function of organs. Studies in rodents show that EDCs can cause harm at much lower levels if exposure happens during organ formation as opposed to exposures during adulthood," said author Ana Soto, MD, professor in the department of anatomy and cellular biology at TUSM.

"The evidence indicates that exposure to BPA and other EDCs may contribute to diseases that manifest during adult life, such as increased cancer rates in the industrialized world. These chemicals have also been linked to obesity, altered behavior, and infertility," continued Soto.

The researchers drew several key points from the body of observational, epidemiological, and animal research examining EDCs, emphasizing that embryos display an increased sensitivity to the chemicals. In particular, Soto and Sonnenschein focused on bisphenol A (BPA), a chemical they have spent 15 years investigating. BPA, which is found in plastic bottles, reusable food containers, and food cans, is ubiquitous in industrialized nations and is linked to cancer.

"EDCs act additively and their effects are dependent upon exposure and context, making them inherently complex to study. New mathematical modeling tools and computer simulations will provide a more precise understanding of how these chemicals interact with each other and within the body at different stages of life. That said, we already have ample evidence supporting policies that reduce exposure to EDCs, and we recommend rapid action to diminish these harmful environmental exposures," said Sonnenschein.

In previous animal studies, Soto and Sonnenschein observed that exposure to even trace levels of BPA can increase cancer risk in adulthood. The pair also collaborated in proposing the tissue organization field theory of carcinogenesis and metastasis as an alternative to the currently-held somatic mutation theory, arguing that cancer is a tissue-based disease rather than a cell-based disease as proposed by the somatic mutation theory of carcinogenesis. Both authors are also members of the cell, molecular and developmental biology program faculty at the Sackler School of Graduate Biomedical Sciences at Tufts.