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MIT study finds children more vulnerable to cancer-causing chemical in water

A common contaminant may quietly pose a far greater cancer risk to children than anyone realized.

Date:

April 29, 2026

Source:

Massachusetts Institute of Technology

Summary:

A troubling new study from MIT reveals that a common environmental contaminant, NDMA—found in polluted water, certain medications, and even processed foods—may pose a far greater cancer risk to children than adults. In experiments with mice, young animals exposed to the chemical developed significantly more DNA damage and cancer, despite experiencing the same initial exposure as adults. The key difference lies in how rapidly children’s cells divide, which turns early DNA damage into dangerous mutations much more easily.

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A widely found contaminant, NDMA, may be much more dangerous for children than adults, according to new MIT research. Faster cell growth in young bodies appears to turn early DNA damage into cancer-driving mutations. Credit: Shutterstock

A new study from MIT indicates that a cancer-causing chemical found in some medications and in drinking water contaminated by industrial activity may pose a much greater risk to children than to adults.

In experiments with mice, researchers discovered that young animals exposed to water containing this compound, called NDMA, developed far more DNA damage and cancer than older mice given the same exposure.

These results may help clarify earlier findings that linked prenatal exposure to NDMA with higher rates of childhood cancer among people living near a contaminated site in Wilmington, Massachusetts. The research also highlights the importance of studying how potential carcinogens affect people at different stages of life.

"We really hope that groups that do safety testing will change their paradigm and start looking at young animals, so that we can catch potential carcinogens before people are exposed," says Bevin Engelward, an MIT professor of biological engineering. "As a solution to cancer, cancer prevention is clearly much better than cancer treatment, so we hope we can spot dangerous chemicals before people are exposed, and therefore prevent extensive cancer risk."

MIT postdoc Lindsay Volk is the lead author of the study, which appears in Nature Communications. Engelward is the senior author.

NDMA Exposure From Water, Drugs, and Food

NDMA (N-Nitrosodimethylamine) forms as a byproduct of various industrial processes. It is also present in cigarette smoke and processed meats. In recent years, it has been detected in certain versions of the drugs valsartan, ranitidine, and metformin. In the 1990s, NDMA was also found in drinking water in Wilmington, Massachusetts, due to pollution from the Olin Chemical site.

A 2021 report from the Massachusetts Department of Health suggested a connection between that contamination and a higher number of childhood cancer cases in the area. Between 1990 and 2000, 22 children in Wilmington were diagnosed with cancer. The affected wells were shut down in 2003.

That same year, Engelward and colleagues published research explaining how NDMA can trigger cancer at the molecular level. In this latest work, the team focused on understanding why younger individuals appear to be more vulnerable than adults.

How NDMA Damages DNA and Triggers Cancer

Most studies of carcinogens rely on adult mice, typically at least 4 to 6 weeks old. In this study, researchers compared two groups: juvenile mice that were 3 weeks old and adult mice that were 6 months old. Both groups drank water containing low levels of NDMA, about five parts per million, over a two week period.

Once inside the body, NDMA is processed by a liver enzyme called CYP2E1. This process creates harmful byproducts that attach small chemical units, known as methyl groups, to DNA. These changes form lesions called adducts.

When scientists examined liver tissue, they found that both young and adult mice developed similar levels of these initial DNA adducts. The difference appeared in how the cells responded afterward. In young mice, the damage led to a buildup of double-stranded DNA breaks, which occur when cells attempt to repair the adducts. These breaks can introduce mutations that eventually lead to liver cancer.

In contrast, adult mice showed almost no double-stranded breaks and far fewer mutations. Their livers also did not develop severe disease or tumors, despite having similar levels of initial DNA damage.

"The initial structural changes to the DNA had very different consequences depending on age," Engelward says. "The double-stranded breaks were exclusively observed in the young."

Rapid Cell Growth Increases Risk in Youth

Further analysis showed that the key factor behind this difference is how quickly cells divide. In young livers, cells are actively growing and dividing, which increases the