Cancer occurs when genetic changes disrupt normal cell functions. These genetic mutations can be inherited; they can happen spontaneously when cells make copies of themselves; or they can be caused by environmental carcinogens—chemicals capable of causing cancer.
While we can avoid some environmental carcinogens, like cigarette smoke and excessive sun exposure, it's much harder to avoid pollutants in the air and contaminants in our drinking water. As a result, it is crucial to understand which environmental factors are associated with cancer, where they are found, and how they contribute to cancer development. This understanding requires taking reliable measurements of environmental factors, gathering data from disproportionately affected populations, and devising experimental approaches to investigate their biological impact.
Researchers at the University of Chicago are helping lead this effort, leveraging large datasets, cutting-edge technologies and advanced methodologies to unravel the complex relationship between cancer and the environment.
Analyzing disparities through an environmental lens
Brisa Aschebrook-Kilfoy, Associate Professor of Family Medicine at UChicago, is an expert in conducting environmental exposure assessments. She is actively leading efforts to build resources to study the impact of the urban “exposome”—the measure of everything an individual is exposed to in their lifetime—on human health, particularly cancer risk.
Earlier this year, her team published a paper detailing their first-of-its-kind analysis of air pollution data from the National Institute of Health All of Us research program, which has enrolled over 500,000 individuals representing diverse racial and ethnic backgrounds. They explored the association between the concentration of air pollutants in a person’s environment and their cancer risk.
The study found a significant association between higher levels of airborne pollutant particles in a person’s ZIP code and increased risk of several types of cancer (breast, ovarian, blood and endometrial). The researchers also found that risks differed by race and ethnicity. For instance, they observed an increased risk of blood cancers among non-Hispanic Black and Asian people, and increased risks of bone, breast and endometrial cancers among Hispanic people.
“Our hope is this work supports further consideration of the role of the environment on cancer disparities both in Chicago and nationally,” Aschebrook-Kilfoy said.
Anand A. Patel, a medical oncologist and researcher at UChicago Medicine, also studies the impact of environmental factors on cancer. His research centers on studying novel therapies and improving the standard of care for patients with blood cancers, with a special interest in the impact of air pollutants in the Chicago area.
In a prior study, Patel and colleagues demonstrated poorer leukemia-related outcomes among non-Hispanic Black and Hispanic patients compared to non-Hispanic white patients with acute myeloid leukemia. The disparity was largely attributed to structural racism; however, individual components that contribute are not fully known.
In a new study, Patel and colleagues investigated the impact of air pollutant exposure on disease characteristics and survival outcomes. They found that in a Chicagoland cohort of patients with acute myeloid leukemia, non-Hispanic Black and Hispanic patients were exposed to higher levels of pollutants associated with leukemia when compared to non-Hispanic white patients.
They also found that increased exposure to polycyclic aromatic hydrocarbons and polycyclic organic matter in the air was associated with higher-risk disease features.
The cellular and genetic impact of environmental carcinogens
To further understand how environmental factors might contribute to disease mechanisms, researchers are exploring those factors’ cellular and genetic impact. Yu-Ying He, Professor of Medicine, and Muhammed Kibriya, Research Associate Professor at the Institute for Population and Precision Health, are applying a range of molecular genomic approaches to study the impact of environmental carcinogens.
He's group is studying the interaction between environmental carcinogens and the epitranscriptome — chemical modifications that regulate gene expression without altering the DNA sequence. The team has developed sophisticated cell and mouse model systems that allow them to precisely dissect the effects of various carcinogens, including arsenic exposure.
“Genetics and epigenetics are known to play critical roles in gene-environment interactions in health and diseases. Now epitranscriptomics is introducing a new layer of mechanisms in environment-associated diseases, including cancer,” He said.
"In the future, identifying the specific profiles of epitranscriptome-environment interactions can not only help us understand how environmental exposure increases cancer risk, but also may identify new targets and pathways for evidence-based cancer prevention, interception and therapy,” He continued.
Similarly, Kibriya has investigated the effects of arsenic exposure in Bangladesh for several years. In the past, some of his research has aimed to provide insights into the genetic and environmental factors that influence an individual’s susceptibility to arsenic toxicity.
—Prof. Jacqueline Stewart
