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John Wiley Jones Distinguished Lecture
March 22, 2013 1:00 pm CAR 1125 reception to follow
From Silent Spring To Silent Night: A Tale of Toads and Men
The herbicide, atrazine is a potent endocrine disrupter that chemically castrates and feminizes exposed male amphibians. Further, atrazine exposure results in neural damage and hyperactivity and induces a hormonal stress response that leads to retarded growth and development, and immune suppression. The immune suppression results in increased disease rates and mortality. Though many factors likely contribute to amphibian declines, pesticides (such as atrazine) likely play an important role even in populations that appear to decline for other reasons, such as disease. Pesticides like atrazine are ubiquitous, persistent contaminants and, though more pronounced in amphibians, the effects described above occur in all vertebrate classes (fish, amphibians, reptiles, and mammals) examined, via common mechanisms. These observations demonstrate the critical impact that pesticides have on environmental health. Furthermore, reproductive cancers and birth defects associated with exposure to many of these same chemicals (e.g. atrazine) via identical mechanisms demonstrate that the impact on environmental health is an indicator of a negative impact on public health. Many of these mechanisms are being revealed only now in the scientific literature and agencies are just now beginning to deal with this emergent science and translate it efficiently into health-protective policies. In particular, ethnic minorities and lower socio-economic communities are at risk: More likely to live in contaminated communities, work in occupations that increase hazard exposure and less likely to have educational and healthcare access. Given the importance of this science and relevance to public health, there is a strong need to translate this information and provide public access to this knowledge. Command of the science and active involvement by the public in policy decisions is vital.
Tyrone B. Hayes, Ph.D.
Department of Integrative Biology
University of California, Berkeley
My research focuses on the role of steroid hormones in amphibian development and I conduct both laboratory and field studies in the U.S. and Africa. The two main areas of interest are metamorphosis and sex differentiation, but I am also interested in growth (larval and adult) and hormonal regulation of reproductive behavior. My work addresses problems on several levels including ecological, organismal, and molecular questions. My main goal is to synthesize ecological/evolutionary, organismal/physiological, and biochemical/molecular studies to learn how an animal translates changes in its external environment to internal changes, how these internal changes are coordinated, what molecular mechanisms are involved, and in turn, how changes at the molecular level affect an animal's ability to adapt to the changes in its external environment. Most recently, my studies have been used as models to develop laboratory and field techniques to examine the effects of endocrine disrupting chemical contaminants on amphibian development. My research now focuses on the effects of pesticides on larval development and the potential role of pesticides in amphibian declines.
I was born and raised in Columbia, South Carolina. Encouraged by my parents (Romeo and Susie Hayes) and inspired by the wildlife around me, hiking in Congaree Swamp, reading National Geographic Magazine, and watching the television show “Wild Kingdom”, I developed an interest in biology very early in my childhood. In particular, I was fascinated by amphibians and the influences that environmental changes have on their development, growth, and reproduction. After graduating from Dreher High School in 1985, I attended Harvard University. I graduated in 1989 after writing an honor’s thesis on the influence of temperature on larval growth, development, metamorphosis and sex differentiation in woodfrogs. I then entered the Department of Integrative Biology at the University of California, Berkeley to obtain my PhD. For my doctoral dissertation, I examined the role of hormones in mediating developmental responses to environmental changes in amphibians. I completed my doctoral work in 1993 and began post-doctoral studies at the National Institute of Child Health and Human Development, National Institutes of Health and the Cancer Research Laboratories, UC Berkeley (funded by the National Science Foundation), where I examined molecular mechanisms of hormone action in amphibians. In 1994, I joined the faculty at Berkeley as an Assistant Professor. Through my research, I began to realize that the most important environmental factors affecting amphibian development were synthetic chemicals (such as pesticides) that interact with hormones in a variety of ways to alter developmental responses. In 1998, I was appointed Associate Professor with tenure at Berkeley. By this time, my work focused on the effects of endocrine disrupting pesticides on amphibian growth, development, reproduction and immune function. In that same year, I began consulting with and conducting research for the chemical company, Novartis (which eventually became the agri-chemical giant, Syngenta Crop Protection). My laboratory showed that the herbicide atrazine (the number one selling product for Syngenta) is a potent endocrine disruptor that chemically castrates and feminizes exposed male amphibians at low ecologically relevant concentrations. The company and their contracted consultants at Ecorisk Inc. were not enthusiastic about my findings and prevented me from presenting these data at scientific meetings, publishing the data, and hindered progress to replicate/validate the data. In 2000, I resigned my consulting position with the company and published my work and further supportive findings with independent funding. Despite controversy generated by the industry giant (attempts to finance me and keep my work under the control of the corporation and to discredit me and my work), I was promoted to full professor in 2003. Presently, my work continues to focus on the effects of pesticides on amphibians and the role of this threat in amphibian declines. Furthermore, it has become clear that the adverse effects of atrazine extend beyond amphibians. Through endocrine-disrupting mechanisms identical to those acting in amphibians, atrazine produces effects in other animals, including prostate and breast cancer and decreased fertility in laboratory rodents. These same effects are associated with atrazine exposure in humans. In addition to the scientific interests, this issue is one of environmental justice. Citizens in lower socio-economic classes and, in particular, ethnic minorities are less likely to have access to this information, more likely to be employed and live in areas where they are exposed to pesticides, less likely to have access to appropriate health care, and more likely to die from what are already the number one cancers in men in women (prostate and breast cancer, respectively), with cancer now being the number one cause of death in the US. Industry has increased efforts to discredit my work, but my laboratory continues to examine the impacts of atrazine and other pesticides on environmental and public health. My decision to stand up and face the industry giant was not a heroic one. My parents taught me, “Do not do the right thing because you seek reward… and do not avoid the wrong thing because you fear punishment. Do the right thing, because it is the right thing.” If I want to raise my own children with the same philosophy, then I have to live my life in accordance with the way that I direct theirs. There was only one choice.
“What you want and what you say should be the same…
Neither future nor past can exist alone.”
Tao Te Ching, Chapter 2