November 30, 2016
Hormonally Active Pollutants: What Are They,
Where Do They Come From and What Do They Do?
Joan Ruderman
Visiting Senior Biologist and Lecturer,
Princeton Environmental Institute, Princeton University
Hormonally Active Pollutants: What Are They,
Where Do They Come From and What Do They Do?
Joan Ruderman
Visiting Senior Biologist and Lecturer,
Princeton Environmental Institute, Princeton University
Minutes of the 11th Meeting of the 75th Year
President Jock McFarlane called the meeting to order at 10:15 a.m. in the Friend Center of Princeton University. Roland Miller led the invocation and Joan Fleming read the minutes of the previous meeting. David Egger introduced a guest, his wife, Audrey. Attendance was 91. The following 12 individuals, having previously been nominated, were unanimously voted in as members of the Old Guard: Helena J. Bienstock, Barbara J. Felton, John P. Hall Jr., Thomas Harvey, Richard F. Hespos, Susan L. Hockaday, David Long, William Ralph Phillippe, Martin W. Schwartz, Ruth E. Scott, John Silver and David C. Wetherill.
Our speaker, Dr. Joan Ruderman, Visiting Senior Biologist and Lecturer, Princeton Environmental Institute of Princeton University, was introduced by Miquelon Weyeneth. Dr. Ruderman also holds the titles of Nelson Professor of Cell Biology Emeritus at Harvard Medical School, and President and Director Emeritus, Marine Biological Laboratory, Woods Hole, and has received many fellowships and awards. The title of her talk was “Hormonally Active Pollutants: What Are They, Where Do They Come From and What Can They Do?”
With the widespread use of DDT after World War II as an extraordinarily versatile insecticide, a wide variety of effects on wildlife were also seen, in particular, deleterious effects on reproduction in birds.
Surprisingly, although the DDT molecule has only a vague resemblance to estrogens like estradiol and to testosterone, it was found to bind to and activate estrogen receptors in many species, including cancer cells in humans and also interfere with the action of testosterone. We now know of many chemicals that were designed for one purpose and were later found to have the ability to mimic estrogens or interfere with testosterone activity.
Some of these hormonally active compounds, also called endocrine disruptors, interfere with reproduction in many wildlife species and increase cancer risk in lab animals. In birds the action is through interference with eggshell production in the oviduct. In humans, emerging work suggests that early exposure to estrogenic pollutants, even prenatally, can increase the risk of developing breast cancer in later life. Fetuses and newborns are especially sensitive even to small increases in estrogen or chemicals that mimic estrogen.
Another chemical, nonylphenol, was discovered to be an estrogenic endocrine disruptor in a laboratory at Tufts when breast cancer cells in a flask that normally required added estrogen to grow, surprisingly began growing without the added hormone. Scientific detective work revealed that nonylphenol, a chemical impurity in the plastic tubes that the growth medium had been stored in, had leached into it and was the culprit. This compound is found in certain plastics, is a high-volume pollutant in surface waters and can make its presence known by turning male fish embryos into adult females. Again, the chemical structure of this compound is unlike that of familiar estrogens.
Of perhaps greater concern is bisphenol A, a molecule that looks similar to DDT although without the chlorine atoms of DDT. It was investigated as a possibly useful synthetic estrogen in the 1930’s. Though its activity was too weak as an estrogen replacement, it found a new lease on life in the 1960s as a monomer for the production of polycarbonate and other resins, more than 7 billion pounds of which are in current United States production. BPA leaches out of the ubiquitous polycarbonate liners of food cans and into foods. In laboratory animals, it can cause behavioral changes, earlier puberty in females, slightly higher incidence of breast cancer and other adverse effects. Recent studies in women show that high levels of BPA lead to lower levels of fertility.
A final class of worrisome hormonally active pollutants are the phthalates, used as plasticizers in many products, including plastic pipes, auto upholstery, vinyl furniture, food packaging, children’s toys (rubber ducks, teething rings), and in shampoos and perfumes as fragrance binders. Numerous animal studies have shown that prenatal and perinatal exposure to phthalates interferes with male reproductive development and may possibly lead to the recent declines in male fertility.
With a lengthening list of endocrine-disrupting chemicals in the environment, one may ask what is being done to protect people and wildlife from their potentially bad effects. The Toxic Substances Control Act of 1976 provides a federal framework for regulation and includes a register of 83,000 chemicals. But after 40 years, fewer than 3,000 chemicals have been tested and only nine restricted. Some states have taken action themselves. California and Maine, for example, have banned the sale of items for young children containing BPA or phthalates and certain other chemicals. Just this past June President Obama signed the Frank R. Lautenberg Chemical Safety for the 21st Century Act, which will hopefully bring Toxic Substances Control Act into the century of its title.
Respectfully Submitted,
Jerry Berkelhammer
Our speaker, Dr. Joan Ruderman, Visiting Senior Biologist and Lecturer, Princeton Environmental Institute of Princeton University, was introduced by Miquelon Weyeneth. Dr. Ruderman also holds the titles of Nelson Professor of Cell Biology Emeritus at Harvard Medical School, and President and Director Emeritus, Marine Biological Laboratory, Woods Hole, and has received many fellowships and awards. The title of her talk was “Hormonally Active Pollutants: What Are They, Where Do They Come From and What Can They Do?”
With the widespread use of DDT after World War II as an extraordinarily versatile insecticide, a wide variety of effects on wildlife were also seen, in particular, deleterious effects on reproduction in birds.
Surprisingly, although the DDT molecule has only a vague resemblance to estrogens like estradiol and to testosterone, it was found to bind to and activate estrogen receptors in many species, including cancer cells in humans and also interfere with the action of testosterone. We now know of many chemicals that were designed for one purpose and were later found to have the ability to mimic estrogens or interfere with testosterone activity.
Some of these hormonally active compounds, also called endocrine disruptors, interfere with reproduction in many wildlife species and increase cancer risk in lab animals. In birds the action is through interference with eggshell production in the oviduct. In humans, emerging work suggests that early exposure to estrogenic pollutants, even prenatally, can increase the risk of developing breast cancer in later life. Fetuses and newborns are especially sensitive even to small increases in estrogen or chemicals that mimic estrogen.
Another chemical, nonylphenol, was discovered to be an estrogenic endocrine disruptor in a laboratory at Tufts when breast cancer cells in a flask that normally required added estrogen to grow, surprisingly began growing without the added hormone. Scientific detective work revealed that nonylphenol, a chemical impurity in the plastic tubes that the growth medium had been stored in, had leached into it and was the culprit. This compound is found in certain plastics, is a high-volume pollutant in surface waters and can make its presence known by turning male fish embryos into adult females. Again, the chemical structure of this compound is unlike that of familiar estrogens.
Of perhaps greater concern is bisphenol A, a molecule that looks similar to DDT although without the chlorine atoms of DDT. It was investigated as a possibly useful synthetic estrogen in the 1930’s. Though its activity was too weak as an estrogen replacement, it found a new lease on life in the 1960s as a monomer for the production of polycarbonate and other resins, more than 7 billion pounds of which are in current United States production. BPA leaches out of the ubiquitous polycarbonate liners of food cans and into foods. In laboratory animals, it can cause behavioral changes, earlier puberty in females, slightly higher incidence of breast cancer and other adverse effects. Recent studies in women show that high levels of BPA lead to lower levels of fertility.
A final class of worrisome hormonally active pollutants are the phthalates, used as plasticizers in many products, including plastic pipes, auto upholstery, vinyl furniture, food packaging, children’s toys (rubber ducks, teething rings), and in shampoos and perfumes as fragrance binders. Numerous animal studies have shown that prenatal and perinatal exposure to phthalates interferes with male reproductive development and may possibly lead to the recent declines in male fertility.
With a lengthening list of endocrine-disrupting chemicals in the environment, one may ask what is being done to protect people and wildlife from their potentially bad effects. The Toxic Substances Control Act of 1976 provides a federal framework for regulation and includes a register of 83,000 chemicals. But after 40 years, fewer than 3,000 chemicals have been tested and only nine restricted. Some states have taken action themselves. California and Maine, for example, have banned the sale of items for young children containing BPA or phthalates and certain other chemicals. Just this past June President Obama signed the Frank R. Lautenberg Chemical Safety for the 21st Century Act, which will hopefully bring Toxic Substances Control Act into the century of its title.
Respectfully Submitted,
Jerry Berkelhammer