Pesticides linked to prostate cancer incidence, mortality
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Key takeaways:
- Multiple pesticides may be associated with prostate cancer incidence and mortality.
- These pesticides include herbicides, insecticides and fungicides.
Certain pesticides may increase the risk for prostate cancer incidence and mortality, according to results of an environment-wide association study.
Researchers identified more than 20 pesticides that may be linked to prostate cancer development, as well as four that had associations with disease-specific mortality.
“The most important clinical implication is that there are likely to be environmental factors, like exposure to some pesticides, that contribute to people developing prostate cancer,” Simon John Christoph Soerensen, MD, a PhD student in epidemiology and clinical research at Stanford University School of Medicine, told Healio. “This first step should help to guide future epidemiological research, which could in turn inform risk assessments and public health strategies.”
Background and methods
An estimated 299,010 new cases of prostate cancer will be diagnosed in the United States this year, according to an American Cancer Society report released earlier this year. Approximately 35,250 men will die of the disease, according to society statistics.
Prior research has not yielded conclusive evidence about modifiable risk factors. In addition, the impact that exposure to pesticides may have on prostate cancer is “poorly understood,” Soerensen and colleagues wrote.
“Given the high incidence and mortality rates of prostate cancer and its geographic variability, there was a clear need to explore the potential impacts of a wide range of pesticides,” Soerensen told Healio. “This ecological study was crucial as a first step in identifying possible environmental contributors to prostate cancer, which could lead to more targeted future research and, eventually, preventive strategies.”
Soerensen and colleagues evaluated 295 pesticides used in at least 35 contiguous U.S. counties from both 1997 to 2001 and from 2002 to 2006.
Investigators used HHS, CDC and NCI data to analyze prostate cancer incidence and mortality rates from 2011 and 2015 (discovery cohort) and from 2016 and 2020 (replication cohort).
The gap in time periods allowed for the development of prostate cancer.
Researchers observed 953,204 diagnoses and 140,086 deaths in the discovery cohort, and 1,063,671 diagnoses and 156,687 deaths in the replication cohort.
U.S.-wide, county-level age-adjusted prostate cancer incidence served as the primary outcome. Prostate cancer mortality served as a secondary outcome.
Results and next steps
Researchers identified 22 pesticides that had associations with prostate cancer incidence in both cohorts. These included a mix of herbicides, insecticides, fungicides and an all-purpose soil fumigant.
Three of those — 2-4-dichlorophenoxyacetic acid (2,4-D), one of the most common pesticides in the U.S., as well as linuron and carbaryl — previously had been linked to the disease.
Cloransulam‐methyl, diflufenzopyr, thiamethoxam and trifluralin also had associations with prostate cancer mortality in both the discovery and replication groups.
“We were reassured by the consistent associations seen across two separate time periods and multiple cohorts,” Soerensen said. “[Although] it is premature to recommend direct changes to public policy based solely on these results, they provide valuable insights that could lead to more-informed decisions regarding pesticide regulations and their usage to potentially reduce prostate cancer risks.”
Researchers acknowledged study limitations. Because they conducted a county-level analysis, they could not gather individual-level data (eg, people’s residential histories) and determine whether “those diagnosed with prostate cancer had higher pesticide exposures than those who did not develop the disease,” investigators wrote.
“Future research will aim to dissect the biological mechanisms and assess individual-level risk factors associated with pesticide exposure and prostate cancer,” Soerensen said. “It is essential to conduct longitudinal studies to more precisely address individual exposures and control for various confounders with greater rigor.
“These efforts are vital for verifying the findings from our current hypothesis-generating study and for guiding the development of targeted interventions,” Soerensen added. “We are poised to use sophisticated epidemiological methods and advanced computing technologies to enhance the precision and applicability of our findings in the real world.”
This study is “just the beginning of an extensive research process” designed to learn more about these “complex interactions,” he added.
“The associations we identified serve as a foundation for further research, not as definitive conclusions for immediate policy changes,” Soerensen said.
For more information:
Simon John Christoph Soerensen, MD, can be reached at simonjcs@stanford.edu.
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