Citation

Liang Y, Tong F, Huang F, Liu Y, Zhu L, Le Grange JM, He G, Zhou Y. Int. J. Legal Med. 2019; ePub(ePub): ePub.

Affiliation

Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, No. 13 Hangkong Road, Hankou, Wuhan, 430030, People's Republic of China. zhouyiwu@outlook.com.

Copyright

(Copyright © 2019, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s00414-019-02169-z

PMID

31713064

Abstract

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.

Language: en

Keywords

Children; Neurotoxicity; Oxidative stress; Pathology; Phosphine poisoning