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A study published in Ecotoxicology and Environmental Safety finds that the commonly used herbicide, atrazine, promotes breast cancer development through suppression of immune cell stimulation, and thus function, and upregulation of enzymes mediating tumor development.
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.
Breast cancer is the most common cancer among women, causing the second most cancer-related deaths in the U.S. Past studies suggest genetic inheritance factors influence breast cancer occurrence.
One in 10 women will receive a breast cancer diagnosis, and genetics can only account for 5-10% of cases. There are grave concerns over exposure to endocrine (hormone) disrupting chemicals and pollutants that cause adverse health effects.
Therefore, advocates point to the need for national policies to reassess hazards associated with disease development from exposure to chemical pollutants.
The study notes:
“This study demonstrated that atrazine accelerated the cell cycle and encouraged the proliferation and invasion of breast cancer tumor cells. Furthermore, atrazine can reduce anti-tumor immunity by decreasing lymphocyte infiltration and modulating cytokine production inside the tumor microenvironment, thereby promoting tumor immune escape and breast cancer progression. To fully understand the mechanism underlying atrazine’s immunosuppression of breast cancers, further research is needed.”
Beyond cancer, atrazine is a notoriously toxic herbicide known to cause different health issues, including skin and respiratory diseases, cancer and kidney/liver damage.
Therefore, it is essential to understand how external stimuli — like environmental pollution from pesticides — can drive breast cancer development.
The researchers examine how exposure to atrazine impacts 4T1 breast cancer cell development, facilitating tumor metastasis (spread from the primary site of origin into different parts of the body) and angiogenesis (the formation of new blood vessels to support tissue growth).
Exposure to atrazine significantly increases breast cancer cell spread, tumor size and the expression/upregulation of MMPs (matrix metalloproteinases) enzymes, mediating precursor tumors to breast cancer.
The percentage of lymphocytes in the thymus and spleen responsible for coordinating the immune response by stimulating other immune cells (CD4 + and CD3) are lower in atrazine exposure cohorts, with the CD4 + CD8 + immune cell ratio lower than control groups.
The abundance of CD4 + and CD8 + lymphocytes that infiltrate tumors decreases, suggesting atrazine’s suppression of the local and systemic immune function on tumors and upregulation of tumor growth promotes breast cancer development.
The connection between pesticides and associated cancer risks is nothing new. Several studies link pesticide use and residue to various cancers, from more prevalent forms like breast cancer to rare forms like kidney cancer nephroblastoma (Wilms’ tumor).
Past research demonstrates the mechanism by which cancer can develop after pesticides enter the bloodstream.
An experimental study showed that pesticide exposure produces reactive oxygen species, 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 (hormone) disruption.
Research demonstrates that endocrine disruption is prevalent among many pesticide products like herbicides, fungicides, insecticides and pesticide manufacturing by-products or contaminants like dioxin.
Regarding atrazine, EPA registers the pesticide as a restricted-use, and only certified pesticide applicators can use the chemical because of its effects on health and ecology.
However, encountering pesticides can happen at any point during the pesticide’s production, transportation, storage, or application.
The general population mainly encounters atrazine through drinking water, as reports of atrazine contamination demonstrate the chemical’s widespread contamination of waterways (e.g., rivers, streams, surface/groundwater).
However, licensed pesticide applicators may also encounter atrazine via inhalation during crop treatments. Furthermore, atrazine can volatilize into the atmosphere by up to 14% of the applied volume during treatments.
Hormone-related cancers have ties to endocrine disruption and immune disruption. The endocrine and immune systems transmit signals to one another as multiple immune processes are involved in endocrine diseases.
Thus, hormones generated by the endocrine system greatly influence breast cancer and other hormonal cancer (e.g., prostate, thyroid, etc.) incidents among humans.
Although most types of breast cancers are hormonally responsive and thus dependent on the synthesis of either estrogen, progesterone, or too much of the protein called HER2, G protein-coupled estrogen receptors (GPERs) regulate estrogen through non-genetic cellular pathways, forgoing attachment to standard molecular receptors, leading to triple-negative breast cancer (TNBC).
Triple-negative breast cancer has a higher rate of recurrence and worse clinical outcomes than other breast cancers.
Xenoestrogens, like atrazine (external estrogen and synthetic compounds sources), can stimulate GPER upregulation and activation in cancer cells.
However, although the connection between pesticides and associated cancer risks is nothing new, this study demonstrates the upregulation of MMP enzymes in cancer cells (4T1-Luc) associated with breast cancer development.
The researchers consider these cancer cells ideal models to study the immune mechanisms, especially for TNBC, as the cells in TNBC lack receptors for estrogen or progesterone hormones, as well as limited HER2 protein occurrence, and TNBC does not respond to hormonal therapy medicines or medicines that target the HER2 protein.
Cancer is a leading cause of death worldwide. Hence, studies concerning pesticides and cancer help future epidemiologic research understand the underlying mechanisms that cause cancer.
With far too many diseases in the U.S. associated with pesticide exposure, eliminating pesticide use is critically important to the safeguarding of public health and addressing cost burdens for local communities.
Beyond Pesticides’ Pesticide-Induced Diseases Database (PIDD) is a vital resource for additional scientific literature that documents elevated cancer rates and other chronic diseases and illnesses among people exposed to pesticides.
This database supports the clear need for strategic action to shift away from pesticide dependency. For more information on the multiple harms of pesticide exposure, see PIDD pages on breast cancer, endocrine disruption and other diseases.
For more information on how organic is the right choice for farmers and consumers, see the Beyond Pesticides webpage, Health Benefits of Organic Agriculture.
Originally published by Beyond Pesticides.