Population studies have consistently linked residential pesticide exposure to an elevated risk of developing childhood leukemia, emphasizing both in utero and postnatal exposures [6,34,35,36]. Like other leukemogenic agents, such as etoposide, benzene metabolites, and lack of bioflavonoids, certain pesticides exert toxicity through oxidative stress and mitochondrial dysfunction. These processes can induce DNA breaks, potentially leading to chromosomal rearrangements (duplications, deletions, and translocations) if not properly repaired [37]. The initial impact often occurs in utero, giving rise to oncogenic fusion proteins. Subsequent insults, determining disease latency, occur post-birth and may involve genetic, epigenetic, or immune factors (e.g., delayed infection-mediated immune deregulation) [2]. Studies suggest that pesticides like organophosphates, carbamates, and pyrethroids—commonly present in insecticides and herbicides—can impair leukocyte function by inducing apoptosis, arresting the cell cycle, and disrupting immune cell functions [38]. Distinct patterns in chromosomal aberrations, cytologic features, and peripheral blood and bone marrow indices (similar to those found in patients with secondary leukemia typically induced by radiation or chemotherapy) have been documented in adult patients with acute myeloblastic leukemia who have been exposed to pesticides (n = 21) vs. those not exposed (n = 40) [39]. The authors suggested that pesticide exposure may worsen leukemia prognosis and survival by triggering harder-to-treat cytogenetic and clinical subtypes. Overall, epidemiological and biological data support the role of certain pesticides in both the development and prognosis of leukemias.