Abstract
ABSTRACT
Fatal opioid toxicity is proximally mediated by respiratory depression, but whether an opioid exposure becomes lethal depends on opioid identity, dose, potency, route, tolerance, co‐intoxicants, naloxone availability, and the response environment. Interruption of opioid agonist treatment (OAT) may alter several of these conditions through medication‐uncovered time, withdrawal‐driven re‐exposure, tolerance change, and loss of clinical contact. We position treatment continuity as an additional time‐varying exposure for overdose investigation, not as a substitute for or presumed priority over recent release from custody, treatment cessation, polydrug use, use in isolation, or lack of naloxone. We hypothesize that adding a time‐resolved OAT continuity timeline to established person‐, agent‐, and environment‐level variables will improve identification of modifiable pathways to fatal and nonfatal opioid toxicity. Its contribution is expected to vary by OAT medication and dose, treatment phase, supervised or take‐home delivery, accessibility, and accompanying interventions. We propose triangulation across postmortem or clinical toxicology, longitudinal treatment and dispensing records, health and correctional data, and structured event review. A Haddon matrix organizes determinants across pre‐event, event, and postevent phases. Core measures include documented OAT coverage‐gap days, time to reassessment and relinkage, dose and delivery conditions, transition context, co‐intoxicants, naloxone coverage, and rescue timing. Taiwan is presented as an instructive access setting rather than a universal delivery model. The hypothesis is testable through linked time‐updated cohorts, within‐person analyses, policy evaluations, and structured mortality and near‐fatal‐event review.