Fine particulate matter (PM2.5) emitted by wood smoke is a significant environmental pollutant associated with oxidative stress and hypoxia. These conditions can disrupt placental function by altering the expression of key nutrient transporters, such as glucose transporter 1 (GLUT1) and sodium-dependent vitamin C transporter 2 (SVCT2), which are essential for fetal development. This study evaluates the effects of pregestational and gestational exposure to PM2.5 on GLUT1 and SVCT2 expression in the rat placenta. Pregnant Sprague–Dawley rats were exposed to either filtered air (FA) or non-filtered air (NFA) containing PM2.5 from wood combustion in a controlled exposure system. Four experimental groups were established: FA/FA (control), FA/NFA (gestational exposure), NFA/FA (pregestational exposure), and NFA/NFA (continuous exposure). Immunofluorescence and confocal microscopy were used to quantify the expression of GLUT1 and SVCT2 in the placental labyrinth zone. Statistical analyses were performed using Kruskal–Wallis and post hoc Dunn’s test (p < 0.05). Gestational exposure to PM2.5 (FA/NFA) significantly reduced GLUT1 and SVCT2 expression, compromising glucose transport and antioxidant protection in the placenta. Pregestational exposure (NFA/FA) induced a compensatory increase in SVCT2 expression, suggesting an adaptive response to oxidative stress. Continuous exposure (NFA/NFA) resulted in GLUT1 redistribution within the syncytiotrophoblast and decreased membrane localization, potentially impairing glucose uptake. PM2.5 exposure disrupts the expression and localization of GLUT1 and SVCT2 in the placenta, with differential effects depending on the timing of exposure. The gestational phase appears to be particularly vulnerable, as reduced GLUT1 and SVCT2 levels may impair fetal nutrition and antioxidant defense. These findings underscore the need for preventive measures to mitigate air pollution-related risks during pregnancy.

Chronic exposure to fine particulate matter (PM_2.5) derived from wood combustion represents a major environmental health burden, particularly during pregnancy. However, the impact of pregestational and gestational (PM_2.5) exposure on the maternal great vasculature remains largely unexplored. This study evaluates the effects of wood smoke-derived (PM_2.5) on the structural architecture of the maternal aortic arch and associated hemodynamic changes during pregnancy in second-generation Sprague–Dawley rats. Animals were allocated into four groups (n = 12) according to filtered (FA) or non-filtered air (NFA) exposure during pregestational and gestational periods: FA/FA, FA/NFA, NFA/FA, and NFA/NFA. Morphometric analysis revealed significant reductions in tunica media (p = 0.0251) and adventitia thickness (p = 0.0014) in exposed groups, without changes in integrated optical density, suggesting alterations in elastic matrix organization without evidence of net mass loss. Histological analysis supported exposure-dependent structural heterogeneity, including elastic lamellae fragmentation and extracellular matrix disorganization. Each exposed group exhibited a distinct systolic blood pressure trajectory across gestation, with FA/NFA reaching the highest values at day 18 (151.0 ± 17.0 mmHg) and NFA/FA displaying sustained elevations despite gestational low-exposure conditions. Principal component analysis (49.2% explained variance) revealed a structured multivariate distribution of vascular and hemodynamic variables across exposure conditions, consistent with an exposure-window-dependent pattern. These findings suggest that (PM_2.5) exposure is associated with coordinated structural and hemodynamic changes in the aortic arch and support the hypothesis that the pregestational period may represent a window of increased susceptibility.

Maternal exposure to airborne particulate matter smaller than $2.5$ μm (${\mathrm{PM}}_{2.5}$) has been associated with adverse fetal outcomes, although its effects on intramembranous ossification remain poorly understood. This study evaluated the impact of gestational and pregestational exposure to wood-smoke-derived ${\mathrm{PM}}_{2.5}$ on fetal neurocranial ossification in Sprague–Dawley rats. Females were allocated to four exposure conditions combining filtered air (FA) and non-filtered air (NFA): FA/FA, FA/NFA, NFA/FA, and NFA/NFA. Fetuses were collected at gestational day 21 and analyzed using fetal morphometry, radiography, micro-computed tomography, whole-mount alizarin red skeletal staining, histology, and immunohistochemistry for HIF-1$\alpha$, COL-1, BMP-2, FGF-R1, and TGF-$\beta$. Continuous exposure (NFA/NFA) was associated with reduced fetal weight, shorter crown–rump length, impaired craniofacial mineralization, widened cranial sutural regions, and reduced mineral density, particularly in the occipital and interparietal bones. Histologically, exposed fetuses exhibited abundant osteoid, reduced osteocyte incorporation, and diffuse osteoblastic distribution, consistent with delayed osteogenic maturation. Immunohistochemistry showed increased HIF-1$\alpha$ immunoreactivity, altered TGF-$\beta$ regulation, and reduced COL-1 expression in continuously exposed fetuses, whereas BMP-2 and FGF-R1 showed no significant changes. These findings suggest that maternal exposure to wood-smoke-derived PM_2.5 is associated with delayed fetal neurocranial intramembranous ossification, particularly under continuous exposure. The observed immunohistochemical profile, elevated HIF-1$\alpha$, reduced COL-I, and altered TGF-$\beta$, is consistent with a hypoxia-associated imbalance between extracellular matrix deposition and mineral maturation; however, the underlying mechanistic pathway was not directly functionally tested and should be regarded as a biologically plausible inferential model requiring further experimental validation.

Chronic exposure to fine particulate matter (${\mathrm{PM}}_{2.5}$) derived from residential wood combustion is a major environmental health concern in southern Chile and other cold-climate regions. Although ${\mathrm{PM}}_{2.5}$ has been linked to adverse reproductive outcomes, it remains unclear whether sustained exposure induces pregestational uterine alterations that compromise reproductive competence before the first pregnancy. This study evaluated the effects of chronic wood smoke-derived ${\mathrm{PM}}_{2.5}$ exposure on uterine morphology and molecular markers in nulliparous rats. A two-generation exposure model was used to assess cumulative effects. Second-generation (G2) female Sprague Dawley rats continuously exposed from conception were housed in filtered air (FA, control; $n=12$) or ${\mathrm{PM}}_{2.5}$-containing ambient air (NFA; $n=12$) until reproductive maturity (82 days). Uterine horns were analyzed by histology, planimetry, immunohistochemistry, immunofluorescence, and second harmonic generation microscopy. Markers of hypoxia, inflammation, extracellular matrix remodeling, angiogenesis, proliferation, apoptosis, and DNA repair were quantified. Chronic ${\mathrm{PM}}_{2.5}$ exposure increased hypoxia-inducible factor 1$\alpha$, tumor necrosis factor-$\alpha$, vascular endothelial growth factor A, and collagen types I, III, and IV, while transforming growth factor-$\beta$ expression and Ki-67-positive proliferating cells were reduced. Exposed rats showed increased apoptosis and decreased nuclear expression of ${\mathrm{O}}^6$-methylguanine-DNA methyltransferase, indicating impaired DNA repair capacity. Second harmonic generation imaging demonstrated increased collagen deposition with marked fibrillar disorganization. These findings indicate that chronic wood smoke-derived ${\mathrm{PM}}_{2.5}$ exposure induces hypoxia-driven structural and molecular alterations in the uterus of nulliparous rats before first pregnancy, including extracellular matrix remodeling, inflammatory imbalance, angiogenic dysregulation, reduced proliferation, and compromised DNA repair, suggesting early disruption of uterine homeostasis and increased susceptibility to adverse reproductive outcomes.