More research needed into potential links between pesticides and prostate cancer

Scientists have observed an “association” between the use of 22 pesticides and prostate cancer incidents in the US, 4 of which were also potentially linked to prostate cancer mortality.

The research is published in the journal Cancer and comes as debate about the safety of the use of the herbicide paraquat heats up in Australia.

However, while the study highlights the need for research into the potential health effects of these specific classes of pesticides, independent expert Oliver Jones, professor of chemistry at RMIT University in Melbourne, says that “more work would be needed to prove any hypothesis” and “no such work has been done in this study.”

The researchers from Stanford University conducted an environment-wide association study (EWAS), which is an exploratory research approach used to identify environmental factors associated with disease outcomes.

To estimate pesticide exposure levels at the county level, they used data on annual estimated total usage (kg per county) for 295 pesticides reported and applied to agricultural crops grown in the US in 1997-2001 and 2002-2006. They then compared these estimated exposure levels to county-level prostate cancer incidence and mortality rates in 2011–2015 and 2016–2020, respectively, to see if there was a statistical association between them.

The lag time of 10–18 years between pesticide use and health outcome data was used to account for the slow-growing nature of most prostate cancers. According to the World Health Organization (WHO), prostate cancer is one of the most common cancers with 1.41 million global cases in 2020.

“I can see this paper being reported in yet another ‘pesticides cause scary disease X’ type way, but to my mind, the evidence in this paper is quite weak for several reasons,” says Jones.

“The authors don’t actually say that pesticides cause prostate cancer, just that they found 22 pesticides that were statistically associated with prostate cancer and that more research is needed.”

This is where phrase “correlation does not imply causation” applies. The study is observational and cannot be used to draw a cause-and-effect relationship between the use of the 22 pesticides and increased prostate cancer cases.

“The work is based on statistics, not direct experiments and the data on pesticide usage and exposure were estimated, not actually measured,” says Jones.

“If we changed the variable under study from pesticide to almost anything else, such as age, sleep, lack of exercise, etc. and ran the same tests using the health records used here for pesticides, we would likely find more associations, but it would not mean there was a connection, just an association.”

The researchers acknowledge further limitations of the study, including the fact that they could not “definitively ascertain whether those diagnosed with prostate cancer had higher pesticide exposures than those who did not develop the disease” and that their “inability to track individual residential histories or to account for potential intercounty and interstate migrations may introduce misclassification bias.”

In addition, they acknowledge that the actual lag time between pesticide exposure and potential cancer development may vary because of numerous factors, including individual susceptibility and exposure levels.

“So, while the work raises interesting research questions, I do not think the evidence or harm is strong if herbicides are used as directed,” concludes Jones.

“The biggest risk factors for prostate cancer are age and genetics, neither of which we can control.”