I didn’t learn about environmental health disparities in a classroom. I saw them growing up in San Pedro Sula, Honduras. I remember neighborhoods built from scrap materials, homes close to industrial waste, and families who seemed to face illness more often than chance alone could explain. At the time, I didn’t question it. Now, as I prepare for a career in medicine, I find myself revisiting those memories with a different perspective.
We often talk about cancer in terms of genetics and lifestyle. We ask patients about smoking, diet, and family history. But we rarely ask about the environments they come from. And yet, those environments may be shaping disease risk long before a patient ever steps foot in a clinic.
Research has consistently shown that environmental exposures play a meaningful role in carcinogenesis. Heavy metals such as arsenic and lead can persist in soil and contaminate water and food sources. Chronic arsenic exposure, for example, has been linked to increased risks of skin, bladder, and lung cancers.
What has struck me most is how ordinary these exposures can be. Patients are not only affected by industrial accidents or extreme conditions. They are exposed through daily routines. Produce grown in contaminated soil can carry trace amounts of heavy metals. Repeated contact with treated landscapes, such as agricultural fields or even golf courses, can increase exposure to pesticides. Long-term exposure to certain pesticides has been associated with cancers such as non-Hodgkin lymphoma.
Air pollution follows a similar pattern. Fine particulate matter, or PM2.5, consists of particles small enough to be inhaled deep into the lungs and enter the bloodstream. It is produced by vehicle emissions, industrial activity, and combustion. The International Agency for Research on Cancer has classified outdoor air pollution as carcinogenic, and even small increases in PM2.5 exposure have been linked to increased lung cancer risk.
At the cellular level, these exposures are not subtle. They contribute to oxidative stress, DNA damage, and disruptions in normal cell regulation, all of which are central to tumor development. These processes often unfold gradually, which makes them easy to overlook in clinical conversations.
What is harder to ignore is how unevenly these risks are distributed. Communities with fewer resources are more likely to live near polluted environments and have fewer protections in place. This means that by the time we see patients, their risk has already been shaped by factors beyond their control.
This is where I think we, as future clinicians, have an opportunity to shift our approach. We may not be able to change a patient’s environment overnight. But we can start by acknowledging it. Asking where patients live, what they are exposed to, and how their surroundings may affect their health can open conversations that are often left unexplored. It also allows us to advocate more effectively, both within and beyond the clinic.
For me, this topic is personal. The environments I grew up in are no longer just memories; they are part of a larger pattern supported by scientific evidence. Understanding this has changed how I think about medicine. It is not only about diagnosing disease, but about recognizing the conditions that make disease more likely in the first place.
If we want to move toward more effective prevention, we have to expand what we consider relevant to patient care. Sometimes, that starts with something as simple as asking a different question.
Natalia Perez is an undergraduate student.
