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Prevention and Control of Viral Hemorrhagic Fevers
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
The methods to be utilized clearly must be determined by the species and habits of the rodents concerned, seasonal fluctuations in population density, and the interrelationship between the animal and the virus. For example, the arenaviruses tend to be excreted especially into the urine and this continues for life. The reservoir host of Lassa fever, Mastomys coucha (formerly known as M. natalensis3), almost invariably urinates when frightened.4 Any control measure which frightens the animal, such as trapping, therefore has the potential to promote rather than discourage virus transmission. Rodenticides may be preferred, taking due cognizance of patterns of behavior, such as feeding, breeding, and nesting habits, as well as home range and reproductive capacity of the locally prevailing species. Wild rodents which tend to shun human habitation are, because of their wide dispersion, less amenable to control than domestic or semidomestic species which are associated with the human habitat. However, greater care needs to be taken with the choice of rodenticide in order to avoid harm to children, dogs, poultry, and livestock. Zinc phosphide, a reliable acute poison, has been widely used. Fumigation with hydrocyanic acid in powder form or with carbon monoxide is especially useful for burrowing rodents, but the potential dangers require it to be practiced by trained and experienced personnel.5
Rodenticides
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Phosphine gas is generated when solid rodenticides, such as zinc or aluminum phosphides, contact oxidizing agents or weak acids. The liberation and inhalation of the gas imparts a characteristic “fish odor” breath, especially when the powder mixes with stomach acid. Exposure produces signs and symptoms similar to those of pulmonary irritants and toxic products of combustion (see Chapter 25). Inhalation of phosphine vapors and fumes induces upper and lower respiratory tract injury (URT and LRT, respectively). Upper airway and ophthalmic injury is distinguished by local inflammation and irritation of ocular, oral, and nasal mucous membranes, including conjunctivitis, lacrimation, rhinitis, and pharyngitis. LRT symptoms include cough, wheezing, and tightness of chest with painful breathing. Early symptoms include nausea, fatigue, tremors, dizziness, and hypotension, followed by pulmonary edema, cardiogenic shock, central nervous system depression, convulsions, and coma.
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Inhaled phosphine gas (PH3, a grain fumigant) and ingested metal phosphides cause pulmonary edema, CNS depression, toxic myocarditis, and circulatory collapse. Victims who survive these immediate reactions suffer liver injury (fatty degeneration and necrosis) and acute renal tubular necrosis. Unlike its analog arsine, phosphine is not hemolytic. Enzymatic mechanisms of toxicity are not known. Ingested metal phosphide (from which phosphine is generated) causes intense GI irritation followed by degenerative and necrotizing lesions of the liver, kidney, and heart. Death is often due either to cariogenic shock or pulmonary edema.
Refractory cardiogenic shock caused by zinc phosphide toxicity
Published in Baylor University Medical Center Proceedings, 2023
Nitish Mittal, Mohamed Elmassry, Mostafa Abohelwa
No antidote for zinc phosphide toxicity has proven effective, and management is usually supportive treatment.1 Activated charcoal can be given orally, after gastric lavage, within an hour of ingestion to decrease symptom severity.13 Hypotension is a very common finding in phosphine toxicity, so fluid resuscitation followed by vasopressors, such as norepinephrine or dobutamine, should be started appropriately.14 Another study showed that minocycline reversed electrocardiographic abnormalities and heart failure signs due to its ability to improve mitochondrial function and inhibit apoptosis.15 Thus, further studies are needed to assess the role of potential treatments for the management of phosphide toxicity.
Intentional pesticide poisoning and pesticide suicides in Nepal
Published in Clinical Toxicology, 2022
Rakesh Ghimire, Leah Utyasheva, Manisha Pokhrel, Neshan Rai, Birendra Chaudhary, Pratap Narayan Prasad, Sangha Ratna Bajracharya, Bhupendra Basnet, Krishna Deo Das, Nandu Kumar Pathak, Madan Prasad Baral, Rajan Pande, Pramod Paudel, Sanu Krishna Shrestha, Sumana Bajracharya, Ritesh Chaudhary, Gyanendra Bahadur Malla, Dilli Ram Sharma, Buddha Basnyat, Mahesh Kumar Maskey, Michael Eddleston
A total of 2535 pesticide suicide poisoning cases were identified from the two forensic laboratories − 1463 (57.7%) were due to ingestion of OP insecticides and 653 (25.7%) due to exposure to phosphine gas after ingesting aluminum or zinc phosphide. Pyrethroids, carbamate and OP and pyrethroid combinations insecticides were responsible for 95, 83, and 31 deaths respectively. The most important OP identified was dichlorvos (273, 60.6%) followed by unidentified OP insecticides (210, 31.8%) (Table 4 and Figure 2). Aluminum phosphide was identified in 299/891, 33.5% of cases from CPFSL.
Exploring research gaps and trends in the management of acute phosphide poisoning: a systematic review
Published in Critical Reviews in Toxicology, 2023
Zahraa Khalifa Sobh, Marwa Kholief, Eman Khalifa Sobh, Manal Ibrahim Fathy Balah
Phosphine (PH3) gas is the toxic ingredient of metal phosphides. It has a low molecular weight that enables rapid diffusion and deep penetration into stored grains or packed materials. PH3 is odorless in its pure state; however, a foul odor is often associated with the evolution of PH3 from various commercial products because of impurities (Alzahrani and Ebert 2023).