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 (PH3), the use of which can lead to accidental inhalation and mass poisoning with high mortality. Exposure to PH3 will give rise to global damage in the human body. This study reviewed 4 fatal accidents including 8 children with PH3 poisoning and aimed to determine the pathological changes that resulted from exposure to PH3 and, secondly, aimed to determine whether oxidative stress was involved in PH3-induced neurotoxicity using histopathological and immunohistochemistry (IHC) methods. After focusing on the pathological changes on the major organs, we found severe damage induced by PH3 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 PH3 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 PH3 poisoning and partly explained the toxic mechanism of PH3 (inhibition of mitochondrial oxidative phosphorylation). We hope that this research could improve the understanding of the toxicity of PH3 in both forensic and clinical practice.