Shayesteh Shahriary, Lana McClements, Kristine McGrath
Ultrafine particulate matter (UFPM) is an increasingly important airborne pollutant with distinct physicochemical properties that may enhance its biological reactivity and cardiovascular toxicity. This review provides a critical mechanistic synthesis of current evidence linking UFPM exposure to cardiovascular injury, with particular emphasis on pregnancy-related cardiovascular disorders. Evidence from experimental models, controlled human-exposure studies, and epidemiological investigations indicates that UFPM may contribute to cardiovascular dysfunction through interconnected pathways involving pulmonary and systemic inflammation, oxidative stress, mitochondrial dysfunction, autonomic imbalance, endothelial injury, and altered vascular signalling. During pregnancy, these mechanisms may disrupt maternal cardiovascular adaptation, placental vascular development, and angiogenic balance, thereby contributing to hypertensive disorders of pregnancy, particularly gestational hypertension and preeclampsia. However, the strength of evidence varies substantially across study designs, and UFPM-specific findings are often difficult to distinguish from those relating to PM₂.₅, diesel exhaust particles, engineered nanoparticles, or broader traffic-related air pollution. Important uncertainties also remain regarding particle translocation, exposure metrics, critical gestational windows, long-term maternal effects, and developmental cardiovascular programming in offspring, for which direct UFPM-specific evidence is currently limited largely to animal models. By integrating cardiovascular and placental mechanisms within a unified framework, this review identifies well-supported pathways, distinguishes them from emerging hypotheses, and highlights priorities for mechanistically informed exposure assessment, longitudinal human studies, and future risk-reduction strategies.