Pathological changes induced by phosphine poisoning: a study on 8 children

Aluminum phosphide (ALP) has been extensively used as an economical and effective insecticide, rodenticide, and fumigant. The active ingredient of ALP is phosphine (PH 3 ), the use of which can lead to accidental inhalation and mass poisoning with high mortality. Exposure to PH 3 will give rise to global damage in the human body. This study reviewed 4 fatal accidents including 8 children with PH 3 poisoning and aimed to determine the pathological changes that resulted from exposure to PH 3 and, secondly, aimed to determine whether oxidative stress was involved in PH 3 -induced neurotoxicity using histopathological and immunohistochemistry (IHC) methods. After focusing on the pathological changes on the major organs, we found severe damage induced by PH 3 in many systems, especially the neurological system, including neuronal, axonal, and vascular injuries as well as oxidative damage with increased expression of 4-hydroxy-2-trans-nonenal (4HNE), 8-hydroxy-2’-deoxyguanosine (8-OH-dG), and 3-nitrotyrosine (3-NT) in the brain, which indicated that oxidative stress was a crucial mechanism for neuronal death in PH 3 toxicity. Moreover, we observed severe myocardial and hepatocellular fatty degeneration in the tissues of the heart and liver. We considered that these characteristic changes are a suggestive sign of PH 3 poisoning and partly explained the toxic mechanism of PH 3 (inhibition of mitochondrial oxidative phosphorylation). We hope that this research could improve the understanding of the toxicity of PH 3 in both forensic and clinical practice.