Agricultural practices expose women to a wide range of chemical, physical, and environmental hazards, which may adversely affect reproductive outcomes, particularly spontaneous abortion. This review synthesizes recent evidence (2020–2025) linking agricultural exposures—including organophosphate pesticides, herbicides, fertilizers, heavy metals, persistent organic pollutants, and occupational stressors—to miscarriage. Epidemiological studies consistently demonstrate that maternal exposure to these hazards, especially during the peri-conceptional period and first trimester, is associated with increased miscarriage risk. Mechanistic insights reveal multiple pathways by which agricultural toxins disrupt early pregnancy, including endocrine disruption, oxidative stress, placental toxicity, and immune dysregulation. Molecular genetic factors, such as polymorphisms in detoxification enzymes (e.g., PON1, GSTs), and epigenetic alterations, including DNA methylation, histone modification, and microRNA dysregulation, further modulate susceptibility and mechanistically link environmental exposures to adverse outcomes. Immunological mechanisms, including T helper cell imbalance, reduced regulatory T cells, and pro-inflammatory cytokine induction, contribute to compromised maternal–fetal tolerance. Fertilizer-related nitrate and heavy metal exposures additionally induce oxidative and epigenetic stress, highlighting the importance of cumulative and mixture effects. Overall, these findings underscore the complex interplay between environmental exposures, genetic susceptibility, and immune-epigenetic mechanisms in the etiology of miscarriage. Enhanced occupational safety, reduction of chemical exposures, and early biomarker-based risk assessment are essential to mitigate the burden of spontaneous abortion in agricultural populations. This review consolidates epidemiological, mechanistic, and molecular evidence, providing a comprehensive framework for understanding the impact of agricultural hazards on reproductive health