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Environmental noise is a ubiquitous physical exposure and a biologically active non-auditory stressor, yet its relevance to autism has received substantially less attention compared to chemical components of the urban exposome. Two questions are often conflated: whether prenatal or early-life noise contributes to autism-related neurodevelopmental susceptibility and whether adverse auditory environments increase functional burden after autistic characteristics are present. In this structured narrative review, we integrate environmental epidemiology, developmental and auditory neuroscience, sleep and stress research, and environmental acoustics within a two-pathway life-course framework. PubMed/MEDLINE and the Web of Science Core Collection were searched from inception through 4 September 2026, supplemented by targeted Google Scholar searching. We included English-language peer-reviewed primary studies, systematic reviews and meta-analyses, and authoritative guidance or standards documents and excluded conference abstracts, dissertations, and preprints. Evidence was prioritized by directness to the autism question, study design, exposure characterization, outcome validity, precision, and recency; the evidence matrix is intentionally selective. Direct human evidence that quantified environmental noise independently increasing the risk of autism diagnosis or persistently worsening autistic traits is sparse and inconsistent, and current data do not support a causal claim. A more direct functional evidence stream—studies conducted on autistic participants that experimentally manipulate auditory conditions and/or measure real-world functional outcomes—indicates that some autistic individuals show altered auditory responsivity, reduced or delayed habituation, speech-in-noise and selective-attention difficulties, and greater burden in noisy or unpredictable settings. We conceptualize this pathway as a person–environment interaction in which acoustic structure, sensory phenotype, task demand, and predictability or control jointly shape functioning. Standard metrics such as LAeq, Lden, and Lnight remain necessary for comparability and policy and are supplemented, not replaced, by multidimensional characterization. Event peaks and temporal fluctuation receive empirical support from studies on child neurodevelopment, whereas spectral content, reverberation, source multiplicity, predictability, controllability, and personal time–activity patterns remain framework-generated hypotheses requiring direct autism-specific testing. This framework separates etiologic inference from phenotypic modification and identifies testable priorities for early-life research and co-designed acoustic accessibility.
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Gao et al. (2026) studied this question.
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