In the past 50 years, we have seen declining sperm counts, earlier puberty in girls worldwide, and genital malformations in people and animals.
At the same time, the annual global production of plastics, which contain endocrine-disrupting chemicals (EDCs), has grown from 50 million tons to 300 million since the 1970s and continues to increase. Science is now seeing the connection between these major changes.
In some ways, it’s not surprising that EDCs cause unfortunate consequences. For instance, since human reproductive processes are similar to those of other species, many pest-control chemicals designed to harm pest reproductive systems also damage people’s reproductive systems.
Hormones are critical to reproduction. They include the sex hormones estrogen in women, androgens (testosterone) in men, and hormones secreted by the pituitary gland and hypothalamus in both genders.
EDCs block connections between these hormones and their receptors, or they mimic hormonal activity, thereby tricking a hormone receptor into action. Either way, EDCs interfere with the normal function of hormonal systems.
For example, estrogenic EDCs (chemicals that act bind to and activate estrogen receptors) are the best studied endocrine disruptors. Girls exposed in the womb to DES—a medication similar to natural estrogen hormones—often developed reproductive tract malformations and had a higher risk of rare cancers. That’s why the US Food and Drug Administration urged doctors to stop prescribing DES in 1971, but only after as many as 10 million women had used it in the mistaken belief that it could prevent miscarriages. DES was banned completely in 2000. Other studies have shown how EDCs interfere with testosterone, progesterone, and other hormones.
Healthy fertility rates depend on viable eggs in women and plentiful sperm in men. Research studies have linked EDCs to negative impacts on both.
For example, BPA changes the neuroendocrine pathways fundamentally in reproductive health. Other culprits include PBDEs, used in products from flame retardants to electronics, and phthalates, which are commonly used to increase the flexibility of plastic and vinyl. There’s also evidence that EDCs induce changes to “germ cells,” the precursors to sperm and egg cells.
BPA exposure during a woman’s reproductive years has been shown to compromise embryo implantation. In Denmark, women under 40 working in the plastics industry were more likely to have sought fertility assistance than unexposed women of the same age.
For men, sperm counts in certain regions of the world including the United States have declined by as much as 50 percent over the last half century.
EDCs can also affect the duration of fertility. In girls, early life exposure to DDT may contribute to an earlier onset of puberty; once they become adults, this exposure may also lengthen menstrual cycles and accelerate menopause.
Lead, another reproductive toxicant, may shorten a woman’s reproductive lifespan. Even at low levels, lead changes reproductive hormones in pre-pubescent girls and healthy premenopausal women.
A recent study linked prenatal exposure to EDCs used in hydraulic fracturing (fracking) to adverse reproductive and developmental outcomes in female mice.
Exposure to EDCs has been linked to structural and functional impairments of reproductive systems. In wild American alligators in Florida, exposure to a DDT-like pesticide caused genital and reproductive malformations—a phenomenon that was later seen in a variety of animal species.
In people, EDCs have been linked to undescended testicles and urethra defects in men and endometriosis and fibroids in women. Ovarian cysts have been associated with higher amounts of chemicals such as BPA in the body.
Knowing the effects of EDCs is an important first step. Here are a few resources to learn more:
