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.