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Brief research report pesticide occupational exposure leads to significant inflammatory changes in normal mammary
Ruan Gabriel Soares da Silva1, Mariane Okamoto Ferreira1, Isabella Mitsu Suo Komori1
1Laboratory of Tumor Biology, State University of West Paraná, Unioeste, Francisco Beltrão, Paraná, Brazil.
Abstract:
Studies have documented the high occurrence of several tumors, including female breast cancer, in populations occupationally exposed to pesticides worldwide. It is believed that in addition to direct DNA damage, other molecular alterations that indicate genomic instability are associated, such as epigenetic modifications and the production of inflammation mediators. The present study characterized the profile of inflammatory changes in the breast tissue of women without cancer occupationally exposed to pesticides. In samples of normal breast tissue collected during biopsy and evaluated as negative for cancer by a pathologist, oxidative stress levels were assessed as inflammatory markers through measurements of lipoperoxides and total antioxidant capacity of the sample (TRAP) by high-sensitivity chemiluminescence, as well as levels of nitric oxide (NOx) metabolites. The levels of inflammation-modulating transcription factors PPAR-γ (peroxisome proliferator-activated receptor gamma) and NF-κB (nuclear factor kappa B) were also quantified, in addition to the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukin 12 (IL-12). The levels of lipoperoxides, TRAP, and NOx were significantly lower in the exposed group. On the other hand, PPAR-γ levels were increased in the breast tissue of exposed women, with no variation in NF-κB. There was also a rise of TNF-α in exposed women samples without significant variations in IL-12 levels. These findings suggest an inflammatory signature of the breast tissue associated with pesticide exposure, which may trigger mechanisms related to mutations and breast carcinogenesis.
Insights
Occupational pesticide exposure in women is linked to specific inflammatory changes in breast tissue, potentially increasing breast cancer risk. This study identified an inflammatory signature associated with pesticide exposure in healthy women.
Area of Science:
- Environmental Health
- Molecular Biology
- Oncology
Background:
- Pesticide exposure is globally linked to increased cancer incidence, including breast cancer.
- Genomic instability, epigenetic modifications, and inflammation mediators are implicated in pesticide-induced carcinogenesis.
- Understanding the inflammatory profile in breast tissue of occupationally exposed individuals is crucial.
Purpose of the Study:
- To characterize the inflammatory changes in normal breast tissue of women occupationally exposed to pesticides.
- To assess oxidative stress markers and key inflammation-modulating factors.
Main Methods:
- Analysis of normal breast tissue samples from women with and without occupational pesticide exposure.
- Quantification of oxidative stress markers: lipoperoxides, total radical-trapping antioxidant capacity (TRAP), and nitric oxide metabolites (NOx).
- Measurement of inflammation-modulating transcription factors: peroxisome proliferator-activated receptor gamma (PPAR-γ) and nuclear factor kappa B (NF-κB).
- Assessment of pro-inflammatory cytokines: tumor necrosis factor-alpha (TNF-α) and interleukin 12 (IL-12).
Main Results:
- Significantly lower levels of lipoperoxides, TRAP, and NOx were observed in the pesticide-exposed group.
- Increased levels of PPAR-γ were found in the breast tissue of exposed women, with no change in NF-κB.
- Elevated TNF-α levels were detected in exposed women, while IL-12 levels remained unchanged.
Conclusions:
- Occupational pesticide exposure is associated with a distinct inflammatory signature in breast tissue.
- This inflammatory profile, characterized by altered oxidative stress and specific cytokine levels, may contribute to breast carcinogenesis.
- Further research is warranted to elucidate the mechanisms linking pesticide-induced inflammation to breast cancer development.
