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Daily News Blog

27
Oct

Breast Cancer Month: Neonicotinoid Insecticides and Breast Cancer Risk (Triple Negative Breast Cancer)

(Beyond Pesticides, October 27, 2022) A study published in Environment International adds to the growing body of research evaluating the association between neonicotinoid insecticides (neonics/NIs) and breast cancer. Past studies suggest neonics act as endocrine disruptors, affecting the development and regulation of estrogen hormones that promote breast cancer. However, this study is one of the few to evaluate the toxicological and molecular mechanisms involved in initiating breast cancer events. According to the Centers for Disease Control and Prevention (CDC), breast cancer is a disease that causes breast cells to grow out of control, with the type of breast cancer depending on the cells themselves. Most common forms of breast cancer have receptors on the cell surface that can increase cancer growth when activated by estrogen, progesterone, or too much of the protein called HER2. One in ten women will receive a breast cancer diagnosis, and genetics can only account for five to ten percent of cases.

When a cancer cell lacks receptors for these molecules, G protein-coupled estrogen receptors (GPERs) are an essential biological target of estrogen and plays a role in hormone-dependent cancer development. GPERs regulate estrogen through non-genetic cellular pathways, forgoing attachment to standard molecular receptors, leading to triple-negative breast cancer (TNBC). Although past studies suggest genetic and environmental factors interact to produce these differences in breast cancer outcomes, genetic factors only play a minor role, while disparities (differences) in external factors (i.e., chemical exposure) may play a more notable role.

Studies like this highlight the significance of understanding how chemical exposure drives disease outcomes and increases disease risk, especially when disease biomarkers are not genetic. The study notes, “[…]NIs could promote breast cancer progression at human-related exposure levels, which was owing to the activation and up-regulation of GPER. We found a novel estrogenic disruption molecular mechanism of NIs and revealed NIs’ potential female adverse effects via GPER pathway, which are expected to provide a new theoretical basis for the health risk assessment and safe usage of NIs.”

The researchers suggest upregulation of GPER is a biomarker for breast cancer, specifically triple-negative breast cancer (TNBC), which has a higher rate of recurrence and worse clinical outcomes than other breast cancers. External estrogen and synthetic compounds sources can stimulate GPER up-regulation and activation in cancer cells. However, the cells in TNBC lack receptors for estrogen or progesterone hormones, as well as limited HER2 protein occurrence. Therefore, TNBC does not respond to hormonal therapy medicines or medicines that target the HER2 protein.

The study evaluates the activity of seven neonics on the GPER pathway using a calcium mobilization assay. The seven neonics include thiamethoxam, imidacloprid, nitenpyram, thiacloprid, clothianidin, acetamiprid, and dinotefuran. Of the seven neonics, clothianidin, acetamiprid, and dinotefuran bind most strongly and activate GPER, thus indicating these chemicals induce breast cancer cell migration. Thus, GPER is a potential molecular target for the estrogenic disruption of neonicotinoids. Overall, the study demonstrates that neonics promote breast cancer progression through the GPER pathway at human-related exposure levels.

Over the past 20 years, neonicotinoids have replaced four major chemical classes of insecticides in the global market (organophosphates, carbamates, phenyl-pyrazoles, and pyrethroids). These systemic agricultural pesticides are highly toxic, resembling nicotine and affect the central nervous system of insects, resulting in paralysis and death, even at low doses. Like other pesticides, neonics readily contaminate water and food resources as traditional water waste treatments typically fail to remove the chemical from tap water, and the systemic nature of neonics allows the chemical to accumulate within the product rather than externally. According to the Centers for Disease Control and Prevention (CDC), nearly half the U.S. population encounters at least one type of neonic daily, with children ages three to five having the highest exposure risk. Health impacts of exposure to neonics can include neurotoxicityreproductive anomalies, hepatic and renal damage, and an increase in gene expression linked to hormone-dependent breast cancer. Additionally, researchers identified the role some neonicotinoids play in enzyme (aromatase) production that stimulates excess estrogen production, a known event in hormone-dependent cancer development.

Beyond its link to human health effects, neonicotinoids are infamous for their well-documented role in driving mass pollinator declines. However, pollinators are far from the only victims of ubiquitous neonicotinoid contamination. In a recent avian risk assessment, EPA scientists found that neonicotinoids present in treated seeds exceeds the agency’s level of concern for certain birds by as much as 200-fold. A 2017 study by researchers at the University of Saskatchewan confirmed that tiny amounts of neonicotinoids – the equivalent of just four treated canola seeds, for example – are enough to cause migrating songbirds to lose their sense of direction and become emaciated. Recent research uncovered the endocrine-disrupting health impacts of imidacloprid on white-tailed deer, adding to the concern of the same effect in humans.

Several studies link pesticide use and residue to various cancers, from more prevalent forms like breast cancer to rare like kidney cancer nephroblastoma (Wilms’ tumor). Although the connection between pesticides and associated cancer risks is nothing new, this study is one of the first to report GPER upregulation in cancer cells (4T1-Luc) associated with breast cancer development. The researchers consider these cancer cells ideal models to study the upregulation of GPER function, especially for TNBC. Past research demonstrates the mechanism by which cancer can develop after pesticides enter the bloodstream. In 2013, an experimental study showed that exposure to pesticides produces reactive oxygen species (ROS), which are highly unstable and cause potential DNA and cell damage that propagates cancer development. Additionally, pesticides can increase cancer risk through alternate mechanisms, including genotoxicity (gene damage), epigenetics (gene expression), immunotoxicity, tumors, and endocrine disruption. Therefore, it is essential to understand how external stimuli—like environmental pollution from pesticides—can drive breast cancer development, as female health risks need urgent concerns.

Cancer is a leading cause of death worldwide. Much pesticide use and exposure are associated with cancer effects. Studies concerning pesticides and cancer help future epidemiological research understand the underlying mechanisms that cause cancer. Although the link between agricultural practices and pesticide-related illnesses is stark, over 63 percent of commonly used lawn pesticides and 70 percent of commonly used school pesticides have links to cancer. Advocates argue that global leaders must fully understand the cause of pesticide-induced diseases before the chemicals enter the environment. Policy reform and practices that eliminate toxic pesticide use can end the uncertainty surrounding potential harm. For more information on the multiple health effects associated with pesticides, see Beyond Pesticides’ Pesticide-Induced Diseases Database pages on breast cancerendocrine disruption, and other diseases. This database supports the need for strategic action to shift away from pesticide dependency.

Prevention of the causes of breast cancer, not just awareness, is critical to solving this disease. In 1985, Imperial Chemical Industries and the American Cancer Society declared October “Breast Cancer Awareness Month” as part of a campaign to promote mammograms for the early detection of breast cancer. Unfortunately, most people are all too aware of breast cancer. Detection and treatment of cancers do not solve the problem. Tell EPA to evaluate and ban endocrine-disrupting pesticides, and make organic food production and land management the standard that legally establishes toxic pesticide use as “unreasonable.”

Moreover, proper prevention practices, like buyinggrowing, and supporting organics, can eliminate exposure to toxic pesticides. Organic agriculture has many health and environmental benefits that curtail the need for chemical-intensive agricultural practices. Regenerative organic agriculture nurtures soil health through organic carbon sequestration while preventing pests and generating a higher return than chemical-intensive agriculture. For more information on how the organic choice is the right choice, see Beyond Pesticides webpage, Health Benefits of Organic Agriculture

All unattributed positions and opinions in this piece are those of Beyond Pesticides.

Source: Environment International

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