Exposure to Particle Radioactivity and Breast Cancer Risk in the Sister Study: A U.S.-Wide Prospective Cohort

White, Alexandra J.; Gregoire, Allyson M.; Fisher, Jared A.; Medgyesi, Danielle N.; Li, Longxiang; Koutrakis, Petros; Sandler, Dale P.; Jones, Rena R.

doi:10.1289/ehp10288

Cited by 4 publications

(2 citation statements)

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“…Consequently, the gastro-intestinal tract is also an important route by which drugs, chemicals, pesticides, environmental pollutants, and metabolites of other species are absorbed in the human body [ 91 ]. Last but not least, air pollution is known as a human carcinogen, especially by gaseous components, as well as through particulate matter, including fine, inhalable particles that can be vectors for radioactive isotopes [ 92 , 93 ]. Air polluting agents on their way to the bloodstream pass through the lung barriers [ 93 ].…”

Section: Absorption Distribution Metabolism/biotransformation Bioaccu...mentioning

confidence: 99%

“…Air polluting agents on their way to the bloodstream pass through the lung barriers [93]. White et al (2022) showed that higher exposure to ambient particle radioactivity (PR-β) was associated with an elevated risk of ER-BC [92]. Moreover, Smotherman et al (2023) found a positive association of particulate matter with postmenopausal BCR [94].…”

Section: Absorptionmentioning

confidence: 99%

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Breast Cancer Exposomics

Neagu,

Jayaweera,

Corrice

et al. 2024

Life

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We are exposed to a mixture of environmental man-made and natural xenobiotics. We experience a wide spectrum of environmental exposure in our lifetime, including the effects of xenobiotics on gametogenesis and gametes that undergo fertilization as the starting point of individual development and, moreover, in utero exposure, which can itself cause the first somatic or germline mutation necessary for breast cancer (BC) initiation. Most xenobiotics are metabolized or/and bioaccumulate and biomagnify in our tissues and cells, including breast tissues, so the xenobiotic metabolism plays an important role in BC initiation and progression. Many considerations necessitate a more valuable explanation regarding the molecular mechanisms of action of xenobiotics which act as genotoxic and epigenetic carcinogens. Thus, exposomics and the exposome concept are based on the diversity and range of exposures to physical factors, synthetic chemicals, dietary components, and psychosocial stressors, as well as their associated biologic processes and molecular pathways. Existing evidence for BC risk (BCR) suggests that food-borne chemical carcinogens, air pollution, ionizing radiation, and socioeconomic status are closely related to breast carcinogenesis. The aim of this review was to depict the dynamics and kinetics of several xenobiotics involved in BC development, emphasizing the role of new omics fields related to BC exposomics, such as environmental toxicogenomics, epigenomics and interactomics, metagenomics, nutrigenomics, nutriproteomics, and nutrimiRomics. We are mainly focused on food and nutrition, as well as endocrine-disrupting chemicals (EDCs), involved in BC development. Overall, cell and tissue accumulation and xenobiotic metabolism or biotransformation can lead to modifications in breast tissue composition and breast cell morphology, DNA damage and genomic instability, epimutations, RNA-mediated and extracellular vesicle effects, aberrant blood methylation, stimulation of epithelial–mesenchymal transition (EMT), disruption of cell–cell junctions, reorganization of the actin cytoskeleton, metabolic reprogramming, and overexpression of mesenchymal genes. Moreover, the metabolism of xenobiotics into BC cells impacts almost all known carcinogenic pathways. Conversely, in our food, there are many bioactive compounds with anti-cancer potential, exerting pro-apoptotic roles, inhibiting cell cycle progression and proliferation, migration, invasion, DNA damage, and cell stress conditions. We can conclude that exposomics has a high potential to demonstrate how environmental exposure to xenobiotics acts as a double-edged sword, promoting or suppressing tumorigenesis in BC.

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