“You can’t just look at the dose, you must also look at the timing of exposure.”
– Vincent Cogliano
When researchers began collecting the occupational histories of cancer patients in Essex County, Ontar io during the mid-1990s they hypothesized they would find higher rates of the disease among male industrialized workers.
What they found shocked them.
A disproportionate number of breast cancer patients were women who came from a farm background.
“Our cases were three times more likely to have grown up or worked on a farm,” said Dr. Jim Brophy, now an adjunct professor with the University of Windsor.
What’s more, it was their work on the farm as young children that seemed to predispose these women to developing breast cancer later in life. “When we asked women ‘what was your first job?’ they said they had worked on the farm. They started working on the farm when they were nine, 10, 11 years old. They all worked as kids,” Brophy said in an interview.
Brophy’s team has continued research with patients, non-pat ients and focus groups with farmers in the region to better understand farming practices that might have influenced the disease’s development. While the correlation between farm work as a young person and breast cancer held up through increasingly more in-depth studies, researchers have yet to find an explanation or a causal link.
He was in the audience earlier this month at the conference sponsored by the Canadian Cancer Society, exploring the connection between pesticides and cancer, and hoping to learn more about how pesticides may act as “endocrine disrupters” or triggers for cancer.
His current theory is that these women were exposed to something when their bodies were developing that caused a change that put them on a path towards cancer later in life. But because they were children at the time of exposure, they don’t know the names of the products in use on the farm at that time or to what extent they might have been exposed.
“We know chemicals that mimic hormones; we also know that with carcinogens that might be associated with breast cancer that if you get exposed at a certain moment – what they call a window of vulnerability – it can have a very profound effect,” Brophy said.
It may all be a moot point. He readily concedes that even if the cancers could be directly linked to specific products, most of the products widely used on farms in the 1940s to 1950s, such as DDT, have long since been pulled from the market.
But Brophy isn’t alone in questioning whether the rigorous scrutiny new pesticide products undergo before being registered for commercial use does an adequate job of assessing the long-term risks they pose to vulnerable populations such as children.
While testing protocols to determine the level of carcinogenity in new products involve feeding the active ingredient to live rodents for extended periods to determine whether they develop tumours, those tests are conducted on rats or mice that are mature.
Vincent Cogliano, a scientist with the International Agency for Research on Cancer, said there are several flaws in the methodology which may cloak a more sinister impact of chemicals.
The testing protocols measure only the impact of the active ingredient when ingested in food, not for multiple exposures in drinking water, ambient dust in the air or direct exposure.
“A safe level for exposure from food alone may not be safe when there is exposure through other pathways,” Cogliano said.
As well, he said it is important to consider the synergistic effects of exposure to multiple active ingredients or even inert ingredients in a product that alone may not be toxic – something current testing protocols do not do. “If you look at one chemical at a time, they may all be safe, but is exposure to a group of chemicals safe?” he said.
Cogliano said the testing protocols also do not factor in the timing of exposure or the fact that people may be exposed in different ways. For example, studies involving rats and mice result in very different outcomes depending on the dose and how old the animal is when exposed.
Fully mature rodents are capable of absorbing much higher doses for prolonged periods, compared to immature rodents. Short bursts of exposure early in life may be more damaging than longer periods of exposure later. “Early life exposure could lead to cancer risk later in life,” he said. “There is a different capacity to metabolize and clear chemicals,” he said.
“You can’t just look at the dose, you must also look at the timing of exposure,” he said.
Rats and people
Other conference participants noted the rodents used in laboratory tests are genetically similar; they eat the same things and lead a standardized lifestyle. Humans come from a broad genetic base and they lead vastly different lifestyles, which may cause toxins to interfere differently with their systems.
Connie Moase, a senior scientist with Health Canada’s Pest Management Regulatory Agency, said Canada’s testing procedures build in a buffer when setting maximum residue limits (MRLs) to compensate for potential differences between the rodent trials and human effects.
MRLs for most products are set at least 100 times lower than the non-toxic dose established in animal trials and up to 1,000 times lower for children, she said.