Pesticide, Chemical Exposure in Pregnancy Tied to Higher Breast Cancer Rates
A new lifelong environmental exposure study published in Environment International found exposure to environmental chemicals during the second and third trimesters exacerbates inflammation pathways associated with breast cancer.
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A new study published in Environment International finds novel environmental chemicals (i.e., piperidine insecticide, 2,4-dinitrophenol, benzo[a]carbazole and a benzoate derivative) involved in developing breast cancer through various inflammation pathways.
These new potential factors contribute to breast cancer and highlight the importance of employing epidemiological biomonitoring like exposome (total exposure from birth to death) to discover mechanisms involved in disease development that are otherwise overlooked.
According to the Centers for Disease Control and Prevention, 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.
Several studies and reports, including U.S. Environmental Protection Agency (EPA) data, identify hundreds of chemicals as influential factors (either promoting or initiating) associated with breast cancer risk.
Breast cancer is the most common cancer among women, accounting for 12% of all new annual cancer cases worldwide and causing the second most cancer-related deaths in the U.S. Past studies suggest genetic inheritance factors influence breast cancer occurrence.
However, genetic factors only play a minor role in the incidence of breast cancer, while exposure to external environmental factors (e.g., chemical exposure) appears to play a more notable role.
One in 10 women will receive a breast cancer diagnosis, and genetics can only account for 5 to 10% of cases.
There are grave concerns over exposure to endocrine-disrupting chemicals and pollutants that cause adverse health effects.
Therefore, studies like these highlight the need to investigate how first-generation pesticide exposure can impact future generational health to prevent adverse health outcomes, especially during sensitive developmental periods (i.e., in utero, infancy/childhood).
This study employs omics scale (cell constituents) biomonitoring to determine associations with a disease, also known as “exposome epidemiology.” The goal is to investigate potential new environmental factors influencing breast cancer risk.
Using nontargeted, high-resolution mass spectrometry, researchers test the association between pregnancy cohorts from the Child Health and Development Studies (CHDS) and breast cancer incidence from the California Cancer Registry.
The research evaluates second and third-trimester samples from the CHDS database to analyze environmental chemicals involved in the development of breast cancer among 182 women and 384 randomly selected women who did not develop breast cancer.
Researchers distinguish environmental chemicals using the Toxin and Toxin-Target Database to determine chemical signals with the highest association in breast cancer cases.
Researchers employ the exposome epidemiology analysis to establish a framework that identifies suspected chemicals.
The study results find that exposure to environmental chemicals during the second and third trimesters exacerbates inflammation pathways associated with breast cancer, including linoleate, arachidonic acid and prostaglandins.
These chemicals include an N-substituted piperidine insecticide, 2,4-dinitrophenol, benzo[a]carbazole and a benzoate derivative linked to glycan and amino sugar metabolism.
Inheritance of health issues spanning generations relating to hereditary influence is a familiar phenomenon.
However, this study demonstrates multigenerational/transgenerational health problems from chemical exposure, a non-genetic factor. Epigenetic changes occur through environmental factors that alter gene expression and can impact multiple future generations.
Considering two-thirds of all breast cancer incidences are related to factors outside of heritable gene mutations (e.g., BRCA1 and BRCA2), chemical exposure can explain the increasing rates of breast cancer.
Many studies have long shown that childhood and in-utero exposure to environmental chemicals increases the risk of developing breast cancer later in life.
According to multiple studies, glyphosate exposure has adverse multigenerational effects, causing negligible observable effects on pregnant rodents but severe effects on the two subsequent generations.
Recent research from the Silent Spring Institute links 28 different EPA-registered pesticides with the development of mammary gland tumors in animal studies.
Many of these chemicals are endocrine disruptors and thus have implications for breast cancer risk. Household cleaners, mainly pesticides, contain endocrine-disrupting chemicals that increase breast cancer risk.
Furthermore, long-term exposure to organophosphate pesticides increases adverse health and cancer risk, specifically among women.
Since DDT/DDE residues, current-use pesticides, and other chemical pollutants contaminate the environment, exposure to these chemical mixtures can synergize to increase toxicity and disease effects.
Pregnancy provides the most appropriate timeframe to study potential disease development, especially for the initiation, progression and susceptibility to breast cancer.
Past studies note later age pregnancy is a significant breast cancer risk factor, which is considerable given birth rates have increased six-fold for women ages 35 to 39.
Thus, the study calls for a “more detailed understanding of the respective contributions and interactions must be a priority to learn how to mitigate risk for this population group of higher risk women.”
The exposome epidemiology approach that this study uses is essential as it assumes “chemical exposures which increase cancer risk can occur decades before breast cancer occurrence, that these exposures are detectable and at higher abundance in serum decades before breast cancer detection, and that network analyses of HRM [high-resolution metabolomics] data are sufficient to detect these exposures and link them to biologic responses.”
Considering research over the past 50 years lacks development of a strategy to prevent breast cancer, using the exposome approach can allow analysis to more readily identify chemical carcinogens and the pathways involved in disease development.
Past research demonstrates the mechanism by which cancer can develop after pesticides enter the bloodstream.
In 2013, an experimental study showed that pesticide exposure produces volatile reactive oxygen species that 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.
Accordingly, this study advocates for the integration of omics scale biomonitoring (exposome epidemiology) with these other risk factors to enhance prediction and intervention strategies, subsequently decreasing the disease burden.
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.
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 prevent the problem.
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% of commonly used lawn pesticides and 70% 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 cancer, endocrine disruption and other diseases.
This database supports the need for strategic action to shift away from pesticide dependency.
Moreover, proper prevention practices, like buying, growing 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, preventing pests and generating a higher return than chemical-intensive agriculture.
For more information on how the organic choice is the right choice, see the Beyond Pesticides webpage, Health Benefits of Organic Agriculture.
Originally published by Beyond Pesticides.
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