When we think about environmental causes of cancer, tobacco and sunlight are often the first examples that come to mind. Decades of research have shown that both increase the risk of cancer, yet not everyone who smokes develops lung cancer, and not everyone with years of sun exposure develops skin cancer.

Cancer rarely develops because of a single exposure. Instead, it emerges over time as acquired DNA mutations accumulate throughout life. Environmental exposures increase the likelihood that these mutations occur, but the impact of any one exposure also depends on factors such as age, sex, inherited biology, infections, and even cultural practices.[1]

Some of the greatest advances in our understanding of cancer have come from asking a simple question: Why are certain cancers more common in some populations than others? The answers have revealed that cancer risk often sits at the intersection of our environment, our lifestyle, and our biology.

Table 1: Environmental Factors That Shape Cancer Risk

When Culture Shapes Cancer Risk

One of the most fascinating discoveries in cancer epidemiology is that geography often provides important clues about carcinogenesis.

Take nasopharyngeal carcinoma (NPC). Although relatively uncommon worldwide, NPC occurs much more frequently in Southern Chinese and Southeast Asian populations. Researchers now believe this pattern reflects several interacting factors, including chronic Epstein-Barr virus infection, inherited susceptibility, and traditional dietary practices such as frequent consumption of salt-preserved fish.[2]

A similar story can be found in South Asia, where chewing betel quid, also known as paan, has long been part of cultural and social traditions. The areca nut itself is classified as carcinogenic to humans, and the risk increases further when tobacco is included. Long-term betel quid use is associated with a substantially higher risk of oral cavity and esophageal cancers.[3]

These examples remind us that culture itself is not a cancer risk factor. Rather, certain long-standing dietary habits and lifestyle practices can influence the environmental exposures that accumulate over a lifetime.

Not All Environmental Exposures Are Chemicals

Environmental exposures are not limited to chemicals or radiation. Scientists now estimate that approximately 13% of cancers worldwide are attributable to chronic infections, making them one of the largest preventable causes of cancer.[4]

Human papillomavirus (HPV) is responsible for nearly all cervical cancers and contributes to a growing proportion of oropharyngeal cancers.[5] Chronic hepatitis B and hepatitis C infections increase the risk of liver cancer.[6] Helicobacter pylori infection affects 50% of the world’s population and remains one of the strongest risk factors for gastric cancer.[7]

In parts of sub-Saharan Africa and Southeast Asia, researchers identified another important environmental exposure through unusually high rates of liver cancer. Aflatoxins are naturally occurring toxins produced by fungi that can contaminate improperly stored maize, peanuts, and other grains. On their own, aflatoxins increase liver cancer risk. In people living with chronic hepatitis B infection, the combination is particularly harmful, illustrating how environmental exposures can work together to drive tumorigenesis.[8]

Perhaps the most encouraging aspect of these discoveries is that many infection-associated cancers are preventable through vaccination, food safety, and appropriate screening and treatment of chronic infections.

The Questions We Are Still Answering

While smoking and UV radiation have been studied for decades, many modern environmental exposures are only beginning to be understood.

Long-term exposure to air pollution, particularly fine particulate matter (PM₂.₅), has been associated with an increased risk of lung cancer and is recognized as a Group 1 carcinogen by the International Agency for Research on Cancer.[9]

Researchers are also studying per- and polyfluoroalkyl substances (PFAS), often called "forever chemicals," which have been linked to increased risks of kidney and testicular cancers in highly exposed populations.[10]

Endocrine-disrupting chemicals, including bisphenol A (BPA), phthalates, parabens, and certain pesticides, have received increasing attention because they can interfere with hormone signaling. Laboratory studies have demonstrated plausible biological mechanisms, but evidence from human studies varies considerably depending on the specific chemical, level of exposure, and cancer type being investigated.[11]

For most people, practical measures such as avoiding unnecessary heating of food in plastic containers, washing fruits and vegetables, following local drinking water advisories, and minimizing occupational exposure where appropriate are sensible ways to reduce unnecessary risk.

A More Personal Understanding of Cancer Risk

One person's greatest cancer risk may be smoking. Another's may be chronic hepatitis B infection. Someone else may spend decades working outdoors, while another has inherited characteristics that make UV damage more likely.

Cancer risk is becoming increasingly understood as something personal rather than universal.

This is why the future of cancer screening is also becoming more personalized. Alongside age and family history, factors such as ancestry, biological sex, environmental exposures, lifestyle, and medical history all help build a more complete picture of an individual's cancer risk.

Traditional screening programs remain the foundation of early detection, but they currently cover only a small number of cancers. New multi-cancer early detection (MCED) approaches are designed to complement existing screening by looking for molecular signs of cancer from a single blood draw. As our understanding of cancer continues to evolve, screening is beginning to move beyond a one-size-fits-all approach toward one that better reflects each person's unique risk profile.

References

1. Miya TV, Marima R, Marutha T, et al. Traditional medicine, environmental exposures, and cultural practices in cancer risk: insights from low- and middle-income countries. Front Oncol. 2025;15(1623895):1623895.

2. Chan SM, Paterson IC, Yap LF. Nasopharyngeal carcinoma in Southeast Asia: Current landscape and future priorities. Br J Biomed Sci. 2025;82(15902):15902.

3. Chen PH, Mahmood Q, Mariottini GL, Chiang TA, Lee KW. Adverse health effects of betel quid and the risk of oral and pharyngeal cancers. Biomed Res Int. 2017;2017:3904098.

4. de Martel C, Georges D, Bray F, Ferlay J, Clifford GM. Global burden of cancer attributable to infections in 2018: a worldwide incidence analysis. Lancet Glob Health. 2020;8(2):e180-e190.

5. Saeed M, Faisal SM, Akhtar F, et al. Human Papillomavirus induced cervical and oropharyngeal cancers: From mechanisms to potential immuno-therapeutic strategies. Curr Drug Metab. 2020;21(3):167-177.

6. Bartosch B. Hepatitis B and C viruses and hepatocellular carcinoma. Viruses. 2010;2(8):1504-1509.

7. Duan Y, Xu Y, Dou Y, Xu D. Helicobacter pylori and gastric cancer: mechanisms and new perspectives. J Hematol Oncol. 2025;18(1):10.

8. Nartey Y, Akyea RK, Cox B, Vanderpuye V. Aflatoxin exposure and primary liver cancer in Ghana. BMJ Glob Health. 2025;10(6):e017626.

9. De Guzman R, Schiller J. Air pollution and its impact on cancer incidence, cancer care and cancer outcomes. BMJ Oncol. 2025;4(1):e000535.

10. Seyyedsalehi MS, Boffetta P. Per- and poly-fluoroalkyl substances (PFAS) exposure and risk of kidney, liver, and testicular cancers: A systematic review and meta-analysis. Med Lav. 2023;114(5):e2023040.

11. Modica R, Benevento E, Colao A. Endocrine-disrupting chemicals (EDCs) and cancer: new perspectives on an old relationship. J Endocrinol Invest. 2023;46(4):667-677.