In the late 1960s, doctors in Boston encountered seven teenage girls with an extraordinarily rare vaginal cancer, a disease almost exclusively seen in older patients. The cancer was traced back to a medication their mothers had been prescribed during pregnancy — a synthetic form of estrogen called DES. The daughters were an early-warning sign that cancer risk may begin in the womb.
Most cancer diagnoses occur later in life. Yet a growing number of people today are developing the disease in their 20s, 30s, and 40s, suggesting that something is not right.
In recent decades, global rates of early-onset cancers have risen by nearly 80 percent and are projected to rise another 31 percent over the next decade, driven in large part by rising rates of colorectal cancer, thyroid cancer, and breast cancer.
Women are disproportionately affected. Two-thirds of people diagnosed with early-onset cancer are women, most with breast cancer. Breast cancer is now the most common cancer in young adults, with rates nearly three times higher than thyroid cancer, the second most common early-onset cancer. Most of these diagnoses occur before routine screening recommendations even kick in.
The subject has captured the public’s attention for good reason. These cancers are striking people during one of the busiest stages of life — a time when they are building their careers, caring for loved ones, or starting families of their own. The ripple effects are felt through households, communities, workplaces, and the economy.
The usual explanations — obesity, alcohol use, or women having fewer children — don’t fully hold up. Nor can we point the finger at inherited genes, the most common reason people think of.
In older adults, cancer typically develops as genetic mutations arise over time rather than being inherited, gradually building up over the person’s lifetime through exposure to carcinogens and from aging. Cancers in young adults, by contrast, have historically been more closely linked to inherited mutations passed down through families. But genetics alone can’t explain the sharp rise in early-onset cancers because our genes do not change that quickly.
Something else is going on. Our environment has changed dramatically.
Forty-four percent of the U.S. population lives in areas with unsafe levels of air pollution. About 200 million people are exposed to toxic PFAS chemicals in their drinking water. More than 5,000 tons of toxic chemicals are released from consumer products every year inside homes and workplaces. And every day, people are exposed to dozens of potentially harmful chemicals in cosmetics and personal care products, most of which have not been fully tested for long-term health effects.
The evidence linking these exposures with cancer is growing. A study by Silent Spring Institute identified 921 chemicals that could increase breast cancer risk, the vast majority of which people encounter in everyday life—in consumer products, food and drink, pesticides, and medications. More than half are known to disrupt hormones in ways that could lead to breast cancer, and 414 are used in plastics.
Studies in people are now revealing the imprint these exposures leave behind. We are beginning to see the ways the environment leaves its mark on our genes, on our cells, and on our tissues and organs. We can start connecting the dots.
These imprints happen early in life, during critical windows of development in the womb, childhood, and adolescence, when the body is changing rapidly and is especially sensitive to chemical exposures.
For example, we have found that women who were exposed to the pesticide DDT in the womb and early infancy had an increased risk of early-onset breast cancer and greater breast density, a known risk factor for the disease. We’ve seen a similar pattern with air pollution, where exposure to high levels indoor air pollutants early in life has been linked to increased breast density in adolescence.
The implications extend beyond breast cancer. Many of the same chemicals involved in the development of breast cancer are also implicated in other cancers. And what we learn from this research will help us understand the influence of the environment on cancers in older adults as well, where the effects of aging can obscure the long-term effects of chemical exposures — where it can be hard to see the signal in the noise.
We are at a critical juncture. For the first time, researchers have the tools and scientific foundation to uncover the environmental drivers of early-onset cancer with far greater precision. Rather than focusing on a handful of chemicals at a time, we can now measure hundreds of chemicals — in our air, in our water, our bodies—that better reflect what the average person is exposed to daily.
Investment in prevention research is essential, not only to pinpoint the most dangerous exposures, but to accelerate prevention strategies, guide health policy, reduce cancer rates, and ultimately save lives.
Imagine a future in which people can better understand and manage their cancer risk not only through genetic screening, but also through a personal environmental health assessment that describes their unique chemical exposures and how to reduce them. That is the future of prevention — one in which tools for reducing environmental exposures are integrated alongside programs for reducing tobacco and alcohol use, expanding use of cancer vaccines, and increasing physical activity.
At the end of the day, whether you’re talking about treatments or prevention, research saves lives. But if we invest in prevention with the same urgency that we invest in treatments, we could reduce incidence rates and save countless more lives.
Rachel Carson once asked, “Why should we tolerate a diet of weak poisons, a home in insipid surroundings? Who would want to live in a world which is just not quite fatal?”
She was right. Even when chemical exposures are not immediately deadly, they can still erode human health over time. The damage often happens slowly, subtly, and cumulatively, until it becomes impossible to ignore.
Dr. Mary Beth Terry is a cancer epidemiologist with more than 26 years of experience studying breast cancer risk factors. She leads an international study on the drivers of early-onset breast cancer, looking at the influence of environmental exposures during key windows of susceptibility. Dr. Terry is a professor of epidemiology at Columbia University and the executive director of Silent Spring Institute. Learn more at silentspring.org.
