Autism Spectrum Disorder (ASD) is a complex neurodevelopmental disorder characterized by deficits in social interaction, communication challenges, and repetitive behaviors. Its etiology is multifactorial, involving interactions among genetic, epigenetic, and environmental factors. Recent studies have revealed that environmental pollutants, immune dysregulation, mitochondrial dysfunction, oxidative stress, and epigenetic alterations play significant roles in the development of ASD. Exposure to environmental toxins such as heavy metals and air pollutants has been linked to an increased risk of ASD, primarily by inducing oxidative stress, neuroinflammation, and neurotoxicity. Immune dysregulation, marked by abnormal immune responses, may also contribute to neurodevelopmental alterations observed in ASD. Mitochondrial dysfunction, resulting in impaired energy metabolism and elevated oxidative stress, is frequently reported in individuals with ASD. In addition, epigenetic mechanisms—such as DNA methylation and histone modifications—are crucial for regulating gene expression and can be influenced by environmental exposures. Abnormal epigenetic patterns have been identified in individuals with ASD, suggesting that the environment can affect gene function without altering the genetic code itself. The higher prevalence of ASD in males indicates potential sex-specific susceptibilities and points to a complex gene–environment interaction. While genetic predisposition is a major factor, environmental influences may intensify or reduce the risk. Understanding these interconnected mechanisms is vital for developing improved diagnostic tools, early interventions, and effective therapies. Future research should aim to identify specific biomarkers and molecular targets, enabling personalized approaches to ASD management. A deeper understanding of these mechanisms offers promising pathways for prevention, early detection, and treatment of ASD.