Chemical injuries
Jan de Boer, Marcel Dubouloz in Handbook of Disaster Medicine, 2020
Organophosphate compounds are commonly used as pesticides but can also be used as chemical warfare agents. The toxicity seen with these agents is due to inhibition of acetylcholinesterase, which causes accumulations of acetylcholine at cholinergic synapses, accounting for a cholinergic crisis with a variety of central and peripheral neurologic manifestations. Increased muscarinic activity produces activation of all the exocrine glands causing lacrimation, salivation, perspiration and excessive secretion by the bronchial and intestinal glands and stimulation of the pancreas, bronchospasm, sinus bradycardia, miosis and involuntary contractions of the muscles of the gastrointestinal tract causing abdominal cramps, vomiting, diarrhea and involuntary urination. Pulmonary symptoms are most marked after an inhalation exposure. Nicotine effects include those involving the skeletal muscles, including the muscles of the respiratory system as reflected by fasciculations and fibrillation and weakness followed by paralysis but also hypertension and tachycardia. Central nervous system effects are confusion, anxiety, restlessness, agitation, insomnia, ataxia, drowsiness, convulsions, coma and paralysis of respiratory centres10,13,21,23. Both central respiratory depression and the ventilatory compromise produced by bronchospasm, hypersecretion and respiratory muscle weakness are the most life-threatening manifestations13,21,23.
The Gulf War's Troubling Legacy
Peggy Munson in Stricken, 2014
More and more truths are being acknowledged about the Gulf War syndrome picture, and one of the most important is that our troops were exposed not just to a single toxin, but to a whole variety. So we can't lose sight of the power of synergy. That is, when two or more relatively weak illness-causing factors are combined, they can be quite harmful. This was underscored by a January 1997 paper by researchers who had studied both experimental animals and Gulf War vets at the University of Texas Southwestern Medical Center in Dallas. Their findings: Harmless levels of two or more chemicals can combine to cause precisely the symptoms reported by Gulf War syndrome sufferers. These symptoms appear to be a type of organophosphate poisoning, report the researchers. What's more, they note that the subtle nerve damage caused by organophosphate poisoning can be missed by physicians unfamiliar with the phenomenon.15
The Safe and Healthy Autopsy
Julian L Burton, Guy Rutty in The Hospital Autopsy, 2010
To the writer’s knowledge there have been no reported cases of secondary toxicity due to organophosphates among autopsy staff, but there is a theoretical risk (e.g. deaths following industrial accidents or terrorist attacks). Organophosphates such as malathion and parathion may be consumed as part of a suicide attempt and pose a hazard when the stomach is opened (Sharma and Reader, 2005). Occupationally acquired organophosphate toxicity has been reported among healthcare workers who failed to take appropriare precautions when treating organophosphate poisoning (Geller et al., 2002). Organophosphates that may be encountered as a result of terrorist attacks include sarin and tabun (Sharma and Reader, 2005). Organophosphates are readily absorbed through the skin. Healthcare workers handling the bodies of those contaminated by organophosphates should use chemical barrier protection (latex gloves and aprons afford little protection) and the body should be thoroughly washed with water or 5% hypochlorite solution prior to the examination (Geller et al., 2002; Burton, 2003; Sharma and Reader, 2005).
Transient receptor potential ankyrin 1 (TRPA1)-mediated toxicity: friend or foe?
Published in Toxicology Mechanisms and Methods, 2020
Mohaddeseh Sadat Alavi, Ali Shamsizadeh, Gholamreza Karimi, Ali Roohbakhsh
Organophosphates are commonly used as insecticides in many countries (Balali-Mood et al. 2012). The organophosphate-mediated delayed neuropathy (OPIDN) often leads to ataxia, paresthesia, and paralysis that occurs in the late stages of acute poisoning or after repeated exposures to organophosphates such as malathion, phoxim, chlorpyrifos, and fenthion (Jamal et al. 2002). Malathion, in an experimental model of OPIDN, induced nerve injuries and ataxia similar to tri-ortho-cresyl phosphate (TOCP). Both compounds also activated TRPA1. TRPA1 gene ablation or treatment with HC030031, as a selective TRPA1 antagonist, reduced the damages that were induced by malathion or TOCP (Ding et al. 2017). Duloxetine and ketotifen, which have apparent TRPA1 inhibitory activity, showed neuroprotective effects against OPIDN as well. The researchers suggested that TRPA1 was the major mediator of OPIDN (Ding et al. 2017).
Polyneuropathy following acute fenitrothion poisoning
Published in Clinical Toxicology, 2018
Jung Taek Park, Kyoung Ho Choi
Organophosphate poisoning commonly leads to various degrees of cholinergic symptoms, intermediate syndrome (IMS), and OP-induced delayed polyneuropathy (OPIDP) [4]. Given that delayed respiratory failure caused by IMS is closely related with high morbidity and mortality, early prediction of poor prognosis following OP poisoning is one of the most important clinical issues [2,3]. Characteristic electrophysiological features after RNS closely parallel clinical severity during clinical progression following OP poisoning, however, these features are not always observed during recovery [2]. Electrophysiological study in our patient resembled early or intermediate recovering IMS patterns, but was not absolutely consistent with such patterns [1]. Our patient showed sensory neuropathy of upper extremities and motor neuropathy of upper and lower extremities. OPIDP or critical illness polyneuropathy and myopathy (CIPNM) have these patterns of neuropathy in common [4,5]. However, results from electrophysiological studies are different. In OPIDN, an increased distal latency is noted with reduced amplitude of action potential; however, the velocity is not reduced or only slightly reduced. In addition, motor neurons are more affected than sensory neurons. In CIPNM, decreased amplitude of sensory and motor action potential of upper and lower extremities occurs, as shown in our case [4,5]. Although not confirmed, clinical and electrophysiological features in our patient were suggestive of CIPNM or a combination of CIPNM with recovering IMS, but not OPIDN (Table 1) [2,5,6].
Vitamin B6 prevents isocarbophos-induced vascular dementia in rats through N-methyl-D-aspartate receptor signaling
Published in Clinical and Experimental Hypertension, 2018
Peng Li, Mo-Li Zhu, Guo-Pin Pan, Jun-Xiu Lu, Fan-Rong Zhao, Xu Jian, Li-Ying Liu, Guang-Rui Wan, Yuan Chen, Song Ping, Shuang-Xi Wang, Chang-Ping Hu
Mechanically, we discovered that NR2B, PSD50, and CaMK-II were possibly involved in the protective effects of vitamin B6 on isocarbophos-induced VD. Organophosphates are highly toxic compounds that cause cholinergic neuronal toxicity and dysfunction by the irreversible inhibition of AChE, resulting in delayed brain damage (36,37). Chronic exposure of organophosphates also produces delayed secondary neuronal destruction, which arises primarily in the cholinergic areas of the brain that contain the dense accumulations of cholinergic neurons and the majority of cholinergic projection, and could be largely responsible for the persistent profound neuropsychiatric and neurological impairments, such as AD (38). Here, we observed that vitamin B6 upregulated the protein levels of NR2B, PSD50, and CaMK-II in PSDs, which were key molecules for the memory, cognitive, and learning functions of the hippocampus. Of course, whether these alterations induced by vitamin B6 are related to AChE inhibition needs further investigations.
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