People cannot always see the pollution they breathe, but a new study suggests that long-term exposure may leave traces inside the blood.
Scientists found changes in normal body chemistry that were linked to air pollution and appeared years before some people developed lung cancer.
The study was carried out by researchers from the American Cancer Society and Emory University’s Rollins School of Public Health. The findings were published in the journal Nature Communications.
Lung cancer causes more cancer deaths in the United States than any other cancer. Cigarettes are responsible for many cases, but smoking does not explain every diagnosis.
Some people who develop lung cancer have never smoked. Others smoked too little or stopped too long ago to qualify for current screening programs, so researchers are increasingly interested in risks that come from the environment.
Air pollution is one of those risks. The air around roads, cities and industrial areas can contain very small particles and other pollutants that enter the lungs every time a person breathes.
Long-term exposure has been linked with lung disease, heart problems and cancer. The World Health Organization’s cancer research agency has classified outdoor air pollution as a cause of cancer in humans.
Knowing that pollution increases risk is only one part of the puzzle. Researchers also want to know what changes inside the body after repeated exposure and how those changes might eventually help a cancer grow.
To investigate this question, the research team examined stored blood samples from 1,357 adults who did not have cancer when the samples were taken. The participants came from long-running American Cancer Society Cancer Prevention Study groups.
Rather than looking only at cholesterol, blood sugar or other familiar medical measurements, the scientists examined a broad collection of small substances created or used by the body. Together, these substances provide a kind of snapshot of the body’s chemical activity.
The researchers then compared these blood measurements with estimates of how much air pollution people had been exposed to over the long term. They found distinct chemical differences associated with greater exposure.
Some of the differences pointed toward inflammation. Inflammation is a normal defense response, but when it continues for a long time it can damage healthy tissue and may create conditions that make cancer more likely to develop.
Other changes were related to oxidative stress, which occurs when harmful unstable molecules overwhelm the body’s defenses. The researchers also saw signs involving energy use and the systems the body uses to process and remove potentially harmful substances.
What made the findings especially interesting was their timing. The pollution-linked changes were present in blood collected several years before lung cancer was diagnosed in some participants.
This does not mean doctors can now use these blood signals to predict who will develop lung cancer. Instead, the findings give scientists possible biological links that can be tested in future research.
That distinction is important because a useful cancer screening marker must work reliably in many different populations. It must also be able to separate people at genuinely high risk from people whose blood chemistry has changed for unrelated reasons.
Current U.S. lung cancer screening mainly uses low-dose CT scans for people with a substantial smoking history who meet age and other requirements. These rules are designed around the strongest established risk factor, but they leave out many people who develop lung cancer.
Donghai Liang of Emory University, one of the study’s senior authors, said understanding risks unrelated to smoking is important for prevention and early detection. He said the newly identified blood changes could eventually help researchers consider whether environmental exposure should play a larger role in assessing risk.
American Cancer Society researcher Ying Wang, another senior author, said epidemiological studies have often found a strong pollution-lung cancer connection among people who have never smoked. Studying changes that can be measured before diagnosis may help scientists understand the mechanisms behind that connection.
The research has several strengths. It used blood collected before cancer appeared, reducing the chance that the tumor itself was responsible for all of the chemical differences, and it drew on participants followed through established long-term research cohorts.
Still, the study cannot prove that air pollution caused each blood change or that those changes caused cancer. Blood chemistry is influenced by many parts of daily life, and estimates of past pollution exposure also have unavoidable uncertainty.
The participants and findings will therefore need to be studied in other populations. Researchers must also determine which signals are most consistent, whether they improve predictions beyond known risk factors, and whether acting on those predictions would actually help patients.
For now, the study should not change an individual person’s screening plan on its own. Its main contribution is showing that long-term air pollution exposure may be connected with detectable biological changes well before a lung cancer diagnosis.
That makes the research promising for two reasons. It may eventually help scientists build better ways to recognize people at risk, while also providing more biological evidence for efforts to reduce harmful air pollution before disease develops.
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Source: American Cancer Society and Emory University
