## 4 Discussion
The expression of XRCC1 increased by just over 10%, but this increase was very mild and, as confirmed by other studies, it can range from mild induction to actual inhibition in response to PM exposure. The ERCC1, XPF, and XPA proteins are involved in the NER process, with XPA (Xeroderma Pigmentosum Group A) recognizing the damage and stabilizing the structure around the lesion. ERCC1 forms a heterodimer with XPF to make a cut at the 5' site of the lesion. The expression of XPA showed a very low average increase, resulting in higher variability, making it not a good marker for damage. Other studies confirmed that PM exposure did not induce a high response for XPA [36], indicating that this protein may not be a sensitive indicator of genomic damage in this condition. XPA and XPF are regulated similarly in expression, as expected, since both operate in the same DNA repair mechanism. A recent study evaluated a causal link between prenatal exposure to pollutants, including PM\({}_{2.5}\), and the methylation of promoters of DNA repair genes, analyzing placental DNA samples. The authors observed a significant association between PM\({}_{2.5}\) exposure and methylation of the XPF promoter, which led to a reduction in expression, while the ERCC1 promoter remained unaffected. The authors suggest that PM\({}_{2.5}\) exposure might have caused a loss of stability in the endonuclease complex, which, although it could still perform the incision at the 5' site of the damage, a task mainly performed by ERCC1, it cannot carry out optimal repair due to the lack of the essential stabilizing action of XPF. This provides a potential mechanism of PM-induced damage, which impairs proper genomic damage repair processes by altering the stability of the complexes that operate in these processes [36]. IL-8 showed the highest and most significant induction in expression, highlighting the elevated inflammatory potential of the analyzed samples. IL-8 is a chemokine that attracts neutrophils and plays a key role in innate defense against bacterial infections, making it an excellent marker of lung inflammation. Elevated levels of IL-8 are associated with the development of chronic obstructive pulmonary diseases, bronchitis, fibrosis, asthma, and allergies [37; 38]. Recently, it has been shown that human lung fibroblasts exposed to various inflammatory stimuli increase IL-8 production and other inflammatory chemokines or cytokines through the overexpression and heightened sensitivity of the TRPA1 receptor (transient receptor potential channel ankyrin 1), normally expressed at the neuronal level, contributing to an allergic/asthmatic phenotype and airway hyperresponsiveness [32]. Additionally, another study found that this receptor is also associated with inflammatory lung damage induced by PM\({}_{2.5}\)[28]. Numerous studies show that PM (particularly PM\({}_{2.5}\) and PM\({}_{0.1}\)) alters normal immune defenses at the lung level through the induction of inflammatory mechanisms, both in vitro and in vivo, with IL-8 being one of the most commonly upregulated chemokines. The production of inflammatory cytokines stimulated by PM may sometimes be the cause of increased severity in pre-existing pulmonary inflammatory diseases. [PERSON] et al. [39] infected human lung fibroblasts exposed to biomass combustion PM extracts and observed significantly increased production of IL-8 compared to unexposed cells, suggesting a potential synergistic mechanism between PM effects and viral infections, leading to exacerbated inflammation through IL-8 production. This aspect is even more relevant from a health perspective in occupational settings, where exposure to potential viral, bacterial, or fungal agents is more frequent, especially in biomass treatment sectors, as shown by numerous cases of infectious diseases (e.g., aspergillosis). Therefore, IL-8 confirms its role as a crucial inflammation marker for exposure to environmental pollutants.