Breast Cancer Rates Higher Among African American Women from Disproportionate Chemical Exposure
(Beyond Pesticides, February 25, 2021) A University of Michigan study finds a link between elevated rates of breast cancer incidents and chemical exposure from pesticides among African American women. Breast cancer is the most common cancer among women, causing the second most cancer-related deaths in the United States. However, breast cancer outcomes differ significantly among women of various races/ethnicities, with African American women being 40 per cent more likely to die from breast cancer than women of any other race. Furthermore, incidences of triple-negative breast cancer (TNBC)—an aggressive breast cancer subtype lacking remediation—is approximately three-fold higher in non-Hispanic Black women (NHBW) compared to non-Hispanic White women (NHWW). 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.
This study highlights the significance of understanding how chemical exposure drives disease outcomes and increases disease risk, especially for more virulent diseases that disproportionately (unequally) impact specific communities. Prior research infers differences in chemical exposure may explain racial disparities for several illnesses, and growing evidence suggests common chemical exposure patterns influence the risk of breast cancer. Therefore, advocates point to the need for national policies to assess exposure hazards’ involvement in disease development and diagnosis. The researchers in the study note, “[…]African American women are disproportionately exposed to chemicals with breast cancer-associated biological activity at doses relevant to human exposure. Future studies should aim to analyze pathways and genes identified as active at biologically relevant concentrations as more (EPA) ToxCast assay data becomes available. […]These experiments will help to inform whether [the] integration of exposure data from NHANES (National Health and Nutrition Examination Survey) with biological activity data from Toxcast is a relevant methodology to identify hazardous chemicals that may be involved in the development and prognosis of breast cancer.”
The study identifies 44 chemicals with considerable exposure inequalities, by race, that have biological activity concerning breast cancer. Aggressive cancer subtypes, including triple-negative breast cancer and others—all of which African American women are more likely to die—have stem-cell-like properties that allow pesticides to dysregulated hormonal pathways. The very chemicals this study finds racial disparities in biomarker concentrations also target specific stem cell-related genes, including AHR, SOX1, GLI1, and HIF-1A, responsible for normal bodily regulation and function.
Furthermore, this research highlights the faults of environmental pesticide monitoring as it fails to account for unequal exposure and specific disease outcomes in communities of colour. The study authors conclude, “Advancing methods to screen candidate chemicals for associations with specific disease outcomes is critical for prioritizing chemicals for further experimental and epidemiological investigation, as well as to design interventions in highly exposed populations.”
People of colour and low-income populations are at higher exposure risk of environmental contaminants (i.e., pesticides) exposure that can catalyze adverse health and birth effects, especially in urban areas. Although Black women endure higher disease burdens than other U.S. populations, there remains a lack of research surrounding how chemical exposure may perpetuate these patterns of racial disparities in disease outcomes.
To identify chemical exposures which may cause racial disparities in breast cancer outcomes, researchers assessed chemical biomonitoring data from the National Health and Nutrition Examination Survey (NHANES), an ongoing population-based health study. The data included toxicological reports of chemicals present in U.S. Non-Hispanic Black women at higher biomarker (indicators of exposure to a chemical) concentrations. Using the U.S. Environmental Protection Agency’s (EPA) ToxCast assay (test), researchers measured active concentrations of these chemicals and assessed efficacy and potency effects. Lastly, researchers conducted a literature search to identify genes responsible for breast cancer development. They analyzed the biological activity (high, moderate, low) of the selected chemicals on genes at human-relevant exposure doses.
The results of the study found 44 chemicals at considerably higher biomarker concentrations in NHBW: the fungicide thiram, pesticide metabolites (2,5-dichlorophenol, 1,4-dichlorobenzene, p, pp DDE), chemicals in personal care products (methylparaben, propylparaben, monoethyl phthalate), and heavy metals (mercury and lead). The assay finds that active concentrations of these chemicals are comparable to biomarker concentrations in Black women. In addition to disproportionate chemical exposure among Black women, human-exposure relevant doses of all 44 chemicals have high to moderate breast cancer-associated biological activity.
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 like kidney cancer nephroblastoma (Wilms’ tumour). Although the link between agricultural practices and pesticide-related illnesses is stark, over 63 per cent of commonly used lawn pesticides and 70 per cent of commonly used school pesticides have links to cancer. 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, tumours, and endocrine disruption. For breast cancer, one and ten women will receive a diagnosis, and genetics can only account for five to ten per cent of cases. Therefore, it is essential to understand how external stimuli—like environmental pollution from pesticides—can drive breast cancer development.
The connection between cancer and pesticides is of specific concern to communities of colour, as etiological studies often attribute cancer to genetics or environmental contamination without considering the disproportionate risk of exposure to contaminants. Many people of colour communities or members of low-socioeconomic backgrounds experience unequal amounts of chemical exposure from various sources. Placement of toxic waste plants, garbage dumps, industrial factories, farms, and other hazardous pollution sources lowers the quality of life for minority populations. Such high levels of chemical exposure can cause these communities to suffer from health outcomes that affect their ability at work and in schools. Women of colour are especially vulnerable to chemical exposure as a 2020 study comparing women of different ethnicities in the U.S. finds these women have higher levels of pesticides and their metabolites, including toxic DDE and 2,4-D. The presence of pesticides in the body has implications for women’s health. Studies suggest women are more susceptible than men to certain types of cancers (i.e., breast cancer) as several pesticides produce endocrine-disrupting effects. Endocrine disruption promotes the development of hormone-related cancers that affect women more than men.
Current pesticide laws lack adequate policies that protect workers and minority communities from pesticide exposure. Risk assessments that calculate “acceptable” risks across population groups fail to disclose the disproportionate effects pesticide use has on people of colour communities. Although EPA’s Food Quality Protection Act (FQPA) establishes safety standards that use a “health-based” standard for pesticide regulation, there is an inherent assumption that if a pesticide meets a highly questionable “acceptable” risk threshold, it has value or benefit. However, this flawed assumption allows the use of unnecessary toxic pesticide products without regard for either the health effects of chemical interactions or the availability of safer, non-toxic practices and products. These standards ignore the disproportionate risk, for example, to African American children whose asthmatic conditions are caused or triggered by the exact pesticide products that meet health-based standards. Furthermore, federal pesticide laws that aim to categorize disproportionate harm allow elevated risk to workers, particularly farmers and landscapers who are predominantly people of colour, who experience aggregate effects of pesticide exposure from multiple sources.
EPA’s failure to address the long-standing effects of chemical exposure differences among various communities is only the tip of the iceberg. As has been previously stated: “[Beyond Pesticides] has long been critical of EPA’s risk assessment process, which fails to look at chemical mixtures—including inert ingredients—and synergistic effects in common pesticide products. Additionally, lack of awareness on specific health endpoints (such as endocrine disruption), disproportionate effects to vulnerable population groups, and regular non-compliance with product label directions hinder accurate risk assessments. These deficiencies contribute to its severe limitations in defining real-world poisoning, as captured by epidemiologic studies in Beyond Pesticides’ Pesticide-Induced Diseases Database.”
The evidence, associating disproportionate chemical exposure to pesticides and cancer, in this study and others like it, highlights the need for better long-term risk assessment of pesticide use on human health, as current evaluations fail to capture chronic (long-term) risks fully.
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.
Global leaders must have a full understanding of the cause of pesticide-induced diseases before the chemicals enter the environment. Policy reform and the adoption of practices that eliminate toxic pesticide use can end the uncertainty surrounding harm. With far too many diseases in the U.S. associated with pesticide exposure, reducing pesticide use is a critically important aspect of safeguarding public health and addressing cost burdens for local communities, particularly minority and underserved. Beyond Pesticides’ Pesticide-Induced Diseases Database is a great 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, pesticides can cause, see PIDD pages on breast cancer, endocrine disruption, and other diseases.
Proper prevention practices, like buying, growing, and supporting organics, can eliminate exposure to toxic pesticides. Organic agriculture has many health and environmental benefits, which 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 organic 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: University of Michigan/*54745756836*/