Comparative Forensic Morphology of Pulmonary Changes in Fatal Acute Ethanol Intoxication and Carbon Monoxide (Domestic Gas) Poisoning: A Literature Review

Abstract

Background. Acute fatal ethanol intoxication and domestic-gas (carbon monoxide, CO) poisoning are common causes of toxicological death that regularly confront the forensic pathologist. In both, the lung is a principal target organ, yet the pulmonary changes are largely non-specific, so that morphology alone rarely establishes the cause of death. Understanding the pathogenesis, histological pattern and confirmatory laboratory correlates of each is therefore essential for correct medico-legal interpretation, particularly because the two exposures frequently coexist.

Objective. To review and compare the macroscopic and microscopic pulmonary changes, underlying mechanisms, quantitative autopsy findings and confirmatory tests of fatal acute ethanol intoxication and CO/domestic-gas poisoning, and to define a practical framework for their differential forensic diagnosis.

Methods. A narrative review was performed in PubMed, Scopus and Web of Science, prioritising articles from 2015–2026 and complemented by key earlier and textbook sources. Fifty-two human, experimental and forensic references were analysed and organised by aetiology, level of biological organisation and diagnostic value.

Results. Acute ethanol intoxication produces respiratory-centre depression, microcirculatory disturbance, venous–capillary congestion, red-cell stasis, interstitial and alveolar oedema, alveolo-capillary barrier injury with plasmorrhagia and fibrin, and an aspiration risk from diminished protective reflexes; chronic exposure adds alveolar glutathione depletion (80–90%), surfactant and macrophage dysfunction, and pro-fibrotic remodelling. CO poisoning acts chiefly through carboxyhaemoglobin (COHb) formation and tissue hypoxia with oxidative stress, producing swollen, congested, oedematous, often cherry-red lungs with subpleural petechiae. Pulmonary oedema and congestion are the shared, non-specific endpoints; combined ethanol + CO exposure yields a mosaic microcirculatory picture with mutual aggravation. Confirmation requires blood/vitreous ethanol and blood COHb (cherry-red livor typically >30%, death usually >50–60%).

Conclusion. Pulmonary morphology in these poisonings is corroborative rather than diagnostic. A defensible medico-legal conclusion integrates scene investigation, autopsy, histology and—decisively—toxicology (ethanol concentration and COHb). Awareness of the combined-exposure scenario and of analytical pitfalls is critical to avoid misclassification.

Keywords:

Forensic pathology, acute ethanol intoxication, carbon monoxide poisoning

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