Women who use biomass as the main source of energy for cooking their food and heating their homes present different biomarkers of pollutants in their bodies such as 1-OHP. They are directly and chronically exposed to pollutants generated during their daily activities and spend a significant amount of time inside their kitchens every day. In this work, all of the samples tested presented values of 1-OHP higher than 0.463 μg/g creatinine, a limit value proposed for a non-occupationally exposed, non-smoking population [13]. We obtained levels almost three times higher (1.09 ± 1.68 μg/L) than Polanska et al., 2014, who reported 0.43 μg 1-OHP/g creatinine [18]. Furthermore, in 2016, Pruneda-Álvarez et al. reported a value of 0.92 ± 0.92 in a study performed in Mexican indigenous and rural communities [19]. Interestingly, in another study in the rural community El Leoncito, San Luis Potosí, the mean value of 1-OHP was 0.56 μg/L for 40 women who cooked on rustic stoves in their homes [20]; the value was similar to the 0.5 μg/L that was established in a German environmental survey for a general population without risk [21]. In both studies, Pruneda and Ruiz included indigenous Mexican women; however, the values were half of those found in the current study. The National Health and Nutrition Examination Survey IV (NHANES IV) reported a geometric mean of 0.074 μg/L for 1-OHP in people aged 20 years and older (n = 1301), a value ten times lower than our results; however, whether they are non-smokers and whether or not they are exposed to either source of PAHs were not specified [22]. Additionally, it should be considered that location, type of house, gender, age and genetic differences could all contribute to 1-OHP concentrations. Pruneda-Álvarez et al., 2012, showed that the levels of 1-OHP in indigenous women exposed either outdoors or indoors were 0.73 ± 0.45 μg/L and 4.81 ± 9.6 μg/L, respectively; the highest levels were in women who had a traditional stove inside their home and spent around 8 h cooking daily [23]. The exposure scenario is similar to our study; however, the mean for 1-OHP μg/L in the Pruneda-Álvarez 2012 report was significantly higher than what is reported here. Exposure to a mixture of PAHs could be an important human health risk factor, and this exposure has been associated with several adverse health effects [22]. The molecular mechanisms related to the health effects include DNA adducts, increased apoptosis, oxidative damage and pro-inflammatory responses [24,25,26,27]. In this regard, we evaluated mRNA levels of TNF-α as a pro-inflammatory biomarker in the women’s samples and our results indicated slight upregulation of mRNA in the high-exposure group, suggesting a probable pro-inflammatory response to PAH exposure. In a recent study performed on 39 taxi drivers potentially exposed to emissions, a positive linear correlation between 1-OHP levels and pro-inflammatory cytokines (IL 1β (r = 0.37, p = 0.007), IL-6 (r = 0.32, p = 0.02) and TNFα (r = 0.33, p = 0.02)) was reported [28], suggesting a weak correlation between PAH exposure and TNFα mRNA and protein expression. The PAHs regulated gene expression at several levels, cell systems and cell-signaling pathways. It was shown that p,p′-Dichlorodiphenyldichloroethylene (DDE) and coplanar 3,3′,4,4′,5-pentachlorobiphenyl (PCBs) compounds were able to enhance AhR transcript expression [24,25]. Recently, enhanced AhR expression has been related to an inflammatory state as a consequence of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), PCBs, DDE and metabolites exposure [6,26,29,30]. Here, we found an augmented expression of AhR in the high-exposure group, suggesting that PAHs promote responses through AhR activation. It has been shown that an increase in TNF-α expression contributes to keeping the activation of the AhR pathway and the chronic inflammatory state producing a positive feedback. AhR is a key regulatory element for some xenobiotic degradation enzymes, notably cytochromes P450 belonging to the CYP1 family. Cytochrome activation is induced by several ligands of AhR, such as TCDD or PAHs such as BaP, as potent inductors of CYP1B1 that could be considered as a biomarker for the activation of AhR [27]. AhR is mainly expressed in liver cells, but it is also present in different types of cells, such as blood cells [29,30,31], suggesting that it could be used as a biomarker for PAH exposure. Recently, epigenetic mechanisms have emerged as an important response to pollutants. PAH exposure can alter epigenetic mechanisms, including miRNAs [32]. miR-125b is a methylation modulator upregulated in cell cultures exposed to BaP and having inflammatory regulation functions [10]. Overexpression of miR-125b induces the expression of TNF-α, IL-6 and IL-1β in plasma from rheumatoid arthritis patients, showing a strong positive correlation between miR-125b and TNF-α [33]. Here, we showed that TNF-α and miR-125b expression were not increased in women from the high PAH exposure group. The difference between the work of Zhang et al. and our results could be attributable to other mechanisms that modulate the expression of TNF-α, including other miRNAs or another epigenetic mechanism, lower sample numbers, a different population and environment, as well as feedback mechanisms activated during inflammatory chronic process. In addition, we analyzed the expression of miR-155, which is a multifunctional microRNA. Recent data indicated that miR-155 has different expression profiles and plays a crucial role in various physiological and pathological processes such as hematopoietic lineage differentiation, immunity, inflammation, cancer and cardiovascular diseases [34]. It has been reported that in human alveolar macrophages, co-culture with miR-155 inhibitors increases TNF-α expression [35], showing similarity to our work, despite the expression of TNF-α and miR-155 not being statistically significant.AhR ligands such as PAHs induce biological effects, including the induction of cytochrome P450 (CYP1B1) and other AhR-regulated genes. Interestingly, it has been reported that other endogenous molecules such as TNF-α have a modulator effect in both cytochrome and AhR expression [26]. In previous studies, it has been shown that AhR ligands induce CYP1B production in cell cultures, and when TNF-α was added, the expression of CYP1B1 was induced. Interestingly, cells co-stimulated with both BaP and TNF-α showed synergized effect, significantly increasing CYP1B1 expression [36,37]. In our results, this association was not found. Interestingly, the AhR expression recorded in response to PAHs is similar in several works; therefore, AhR is an important biomarker for PAH exposure.