Chemical pollution is a huge threat to the planet. Bisphenol A, perchlorate, atrazine, phthalates are not just ominous-sounding words—they are part of the group of chemicals that interfere with the human and animal endocrine system, the system that regulates hormones. Endocrine disrupting chemicals (EDCs) are found in plastics, solvents, pharmaceuticals, herbicides, cosmetics and even children’s toys. Exposure to these chemicals can result in various health concerns for humans and the ecosystem.
Biology Professor Vicki Marlatt teaches several environmental toxicology courses at Simon Fraser University (SFU) in one of the few professional environmental toxicology programs in Canada. She has worked in this field within academic, industrial and government settings. Her research and teaching span human and environmental health regulations and governance in North America, Europe and internationally.
Marlatt contributes to the growing body of literature published and applied to these areas. She is a member of the Intersectoral Centre for Endocrine Disruptor Analysis (ICEDA)—a multidisciplinary research network dedicated to inform, assist and serve as a resource for academia, government, non-profit, industry and the Canadian public to identify, recognize and manage EDCs.
Marlatt and several other ICEDA members have compiled their latest work into a Special Issue on EDCs in the Environmental Research Journal to guide the worldwide community on research priorities and regulating actions. The issue includes several articles where Marlatt collaborated, and Impacts of endocrine disrupting chemicals on reproduction in wildlife and humans, which she led.
We talked with Professor Marlatt about her work.
Your research is adding to the understanding of the harms associated with human and wildlife exposure to EDCs. Can you describe some of the health impacts of EDC exposure?
We have strong evidence that EDCs impair reproduction in wildlife based on decades of laboratory and field studies. For example, fish living downstream of sewage treatment plants where numerous chemicals and human hormones such as estrogens and androgens are present, cause altered sex ratios, reduced reproductive rates and ultimately, reduced population sizes. These harmful impacts of EDCs on reproduction are similar across several wildlife species. In humans, evidence from animal studies and human epidemiological studies show similar effects on reproduction, including infertility, but also point to increased risks of breast and prostate cancers and metabolic diseases like diabetes and obesity.
Looking at the molecular mechanisms disrupted by EDCs, can you explain what is happening at the molecular level?
The most well documented molecular mechanisms of EDCs are those that bind to and inhibit or activate estrogen or androgen receptors. These receptors are key in the signaling pathways of sex steroid hormones like estrogens and androgens that regulate reproduction as well as many other physiological processes such as bone growth, metabolism, neuroplasticity, etc. These hormone receptors are present in all vertebrate species, and interactions with these receptors by EDCs causes dysregulation of reproductive processes. Other EDCs can disrupt the synthesis, degradation or transport of hormones, such as estrogen, testosterone, cortisol or thyroid hormone by interacting with various enzymes and transport proteins, causing an imbalance of hormones in important organs or tissues and harmful effects on critical processes that include reproduction, metabolism, growth and development.
Your research has found that EDC exposure can have an impact across multiple generations of fish and birds. Can you describe the findings? Does this suggest that EDCs would affect humans in the same way?
The most well studied EDCs for multi-generation effects after parental exposure interact with estrogen and androgen receptors, so the harmful effects on offspring most often reported tend to be on reproductive organ development and function leading to impaired reproduction. However, other effects such as abnormal growth and stress endocrine axis function have also been reported. Based on the findings from studies in other mammals like rodents and primates, and the historical diethylstilbesterol case study—where a potent estrogenic pharmaceutical administered to pregnant women caused increased genital tract, cervical and breast cancers and infertility in daughters—it is likely that EDCs cause similar multi-generational effects in humans as well.
You note that it is increasingly challenging to keep pace with the testing and assessment needed to regulate harmful chemicals. What needs to happen to get a handle on harmful EDCs?
We need globally harmonized, rapid screening programs to identify and assess the risks of EDCs for the existing 100,000 or so chemicals in commerce and for the 500 to 1000 new chemicals developed annually prior to their registration for use. The Organization for Economic Cooperation and Development has several internationally validated rapid screening assays for estrogen and androgen receptor interactions. More of these mechanistic, rapid screening assays that cover the majority of endocrine modes of action are needed. These types of in vitro screening programs combined with several other new approach methodologies that are revolutionizing toxicology would be rapid and cost-effective. Indeed, some are being implemented in U.S. and European regulatory regimes already to assess the risks of EDCs and manage their use.
Finally, we need industry to fully disclose the quantity and all chemical components of their products in addition to routine and thorough environmental and biota monitoring of EDCs to gain a clearer picture of exposure.