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Background: Intentional poisoning represents a serious health risk for domestic and wild animals, this phenomenon has been widespread in Italy for several years., Aim: Our study aims to examine data on animal poisonings that occurred in the province of Viterbo, Lazio region located in central Italy, from 2003 to 2017. The aim of this study is to provide data on the poisoning of animals in the province of Viterbo., Methods: A total of 1,078 cases of suspected poisoning were analysed during the period under review. Of these, 761 (70.6%) were carcasses, 189 (17.6%) were baits, 107 (9.9%) were gastric contents, and 21 (1.9%) were samples of various origins., Results: A total of 631 cases (58.5%) were confirmed as involving toxic substances. Zinc phosphide (34.7%) was the most prevalent cause of poisoning, followed by metaldehyde (18.7%), a coumarin rodenticide (12.7%), other molecules were also identified with lower percentages. The animal species most frequently involved in poisoning are dogs (66.2%), followed by cats (25.5%), birds (4.9%), while wild animals, ruminants, and fish represent a small percentage of animals involved., Conclusion: This phenomenon represents a significant threat to animals, humans, and the environment. Therefore, it is essential to implement effective measures to combat this issue., Competing Interests: The authors declare no conflict of interest.

Zinc phosphide is a gray to black powder mainly used as a rodenticide. In contact with gastric fluid, it releases phosphine which is the main toxic material of this compound. Phosphine interferes with oxidative respiratory cycle of the cells, but is generally expected to manifest its toxicity with prodromal signs and symptoms including abdominal pain, nausea and vomiting, metabolic acidosis, and increased liver function tests. A 64-year-old man was referred to our center with the history of ingestion of three full table spoons of zinc phosphide powder with only a mild GI discomfort. Abdominal X-ray revealed radiopaque material in epigastric and abdominal right upper quadrant. Despite treatment with polyethylene glycol and completely normal vital signs and lab tests, he experienced sudden cardiac arrest 19 h after admission. Autopsy showed clues of focal myopathy and fibrosis with evidences of ischemia and congestion in cardiac tissue, pulmonary edema, shrunken bilateral kidneys, and nutmeg yellow liver. Toxicology panel confirmed the presence of phosphine and zinc phosphide in the gastric fluid. The patient deteriorated suddenly despite being completely symptom-free during the hours preceding cardiovascular arrest. Since the cardiopulmonary injury is the most rampant cause of early death, checking of the cardiac enzymes and cardiac monitoring could be beneficial for early detection and efficient management of these patients.

Background: Acute pesticide poisoning (APP) is reported to affect community health worldwide but its burden in Tanzania is unknown particularly in women. This study examines APP involving adult females and adolescent girls 10 to 19 years in 3 regions of Tanzania which are famous for coffee and vegetable production., Methods: Over the period of 12 months, health facility-based surveillance for cases of APP was implemented in 10 Tanzanian healthcare facilities in 2006., Results: The study identified 108 APP cases of whom 31 (28.7%) occurred amongst adolescent girls. Suicide was the leading poisoning circumstances (60.2%) and the most vulnerable women were 20-29 years old who comprised 38.4% of all cases with suicide as circumstance. Organophosphates (OPs), zinc phosphide, paraquat and endosulfan were common amongst known reported poisoning agents. The annual APP incidence, mortality and Case Fatality Rate for women were 5.1/100,000, 0.2/100,000 and 3.7/100, respectively., Conclusion: APP amongst women in Tanzania is common and this call for diverse preventive interventions to reduce poisoning incidents.

Background: Aluminum and zinc phosphides are solid fumigants for pest control. Metal phosphide poisoning (PP) is common in suicide and suicide attempts. In Mexico, zinc phosphide is easily available, and is a common agent in poisonings., Objective: To identify mortality in PP, and associated factors in a poison control center., Material and Methods: Prospective cohort study. The starting point was the exposure (PP) and it was made a follow-up on the outcome (mortality and non-mortality). Main factors associated to PP outcome were assessed (e.g.: personal and clinical factors, duration of poisoning, detoxification, and radiographic evidence of poisoning). It was used relative risk (RR) as a risk estimator with 95% CI, as well as chi-squared with Fisher’s exact test, Kaplan-Meier survival curves, and Log- Rank test as a comparative mean., Results: 44 exposed patients, and 88 non-exposed were followed up. Mortality rate in PP was of 16% in acute phase patients; there were no deaths in either subacute or chronic phases. Mortality risk was 14 (95% CI, 2 110). Main factors associated with increased mortality were: time of first medical assistance > 6 hours, RR = 15 (95% CI, 1.7-128); dose of poison ≥ 1 bottle or 1 tablet, RR = 14 (95% CI, 1.8-108); radiographic evidence of poisoning, RR = 10 (95% CI, 1.3 77)., Conclusion: Metal PP has a high mortality rate and is associated to long periods of exposure to the toxic chemical due to ineffective detoxification.

Metal phosphides, particularly zinc and aluminum phosphide, occasionally poison horses and other equids following their use as rodenticides and insecticides. Grain-based aluminum phosphide baits are used to control rodents such as prairie dogs. The clinical course in intoxicated horses is short (<24-48 h), and animals may be found dead. Hepatic lesions caused by phosphine poisoning are not well described. Laboratory confirmation depends on detecting phosphine gas in gastric contents. Eight horses and a mule were exposed to zinc phosphide used to control prairie dogs on a Wyoming ranch. Three of 9 exposed equids developed some combination of sweating, ataxia, anxiety, and colic; 2 died acutely, and 1 recovered. A diagnosis of zinc phosphide was made by detecting phosphine in stomach contents from a horse and a mule. The liver was pale and swollen in the affected horse, which died after a clinical course of ~12 h. Other changes were generalized congestion and edema, pulmonary edema, and acute cerebrocortical edema. There was diffuse hepatocellular microvesicular steatosis. Similar histologic lesions were present in 7 equine livers from 2 previously published episodes of metallic phosphide poisoning. Older lesions (>24 h of clinical signs) had centrilobular hepatic necrosis with congestion and a mixture of microvesicular and macrovesicular steatosis. Phosphine poisoning should be considered in horses that die acutely and are found to have steatosis, either with or without hepatocellular necrosis.

Background: Run Rat® is a rodenticide widely used against small mammals. It comprises of a minimum of 32% zinc phosphide which is highly toxic in acute exposures to humans. It may be consumed accidentally or intentionally. It enters the body via skin, respiratory and gastrointestinal tracts. Zinc phosphide is hydrolyzed by the gastric acid and is transformed into phosphine gas. Phosphine is a respiratory toxin that inhibits cytochrome C oxidase system resulting in renal failure and liver failure., Case Presentation: A 35 year old Sri Lankan female presented following ingestion of 2.5 g of Run Rat®, which is a branded preparation of zinc phosphide, resulting in 61 mg/kg poison load. She developed severe acute kidney injury with acute tubular necrosis, subnephrotic ranged proteinuria and tubulointerstitial nephritis for which she underwent haemodialysis three times along with other measures of resuscitation. She also developed elevated liver enzymes with hyperblirubinaemia, hypoalbuminaemia, acute pancreatitis and mild myocarditis. She improved with supportive therapy over a period of 3 weeks., Conclusion: Run Rat® is a commonly used rodenticide and the toxic effects are mediated through conversion of phosphide to phosphine gas. The majority of the deaths had occurred in the first 12 to 24 h and the main causes identified are refractory hypotension and arrhythmias. The late deaths (beyond 24 h) had been commonly due to adult respiratory distress syndrome, liver and renal failure. The outcome is poorer with delayed presentation, development of coagulopathy, hyperglycaemia and multiorgan failure with elevated liver enzymes. In our patient, Zinc phosphide poisoning caused severe acute kidney injury, abnormal liver profile, pancreatitis and possible myocarditis. The patient improved with repeated haemodialysis. The renal biopsy revealed acute tubulointerstitial nephritis with acute tubular necrosis. In tropical countries, the rural population engaged in agriculture has easier access to the compound, as it is available at a lower cost. Furthermore, the lack of an antidote and advanced resuscitative measures such as inotropic supportive therapy and renal replacement facilities at most of the peripheral hospitals pose a major challenge in providing timely interventions to prevent deaths.

Context: Zinc chloride (ZnCl 2 )-based smoke bombs and screens are in use since the Second World War (1939-1945). Many case descriptions on ZnCl 2 smoke inhalation incidents appeared since 1945., Objective: We provide a comprehensive overview of the clinical symptoms and underlying pathophysiology due to exposure to fumes from ZnCl 2 smoke producing bombs. In addition, we give a historical overview of treatment regimens and their outcomes., Methodology: We performed a literature search on Medline, Scopus and Google Scholar databases using combinations of the following search terms "smoke bomb", "smoke screen", "ZnCl 2 ", "intoxication", "poisoning", "case report", "HE smoke", "hexachloroethane smoke", "smoke inhalation" and "white smoke". We retrieved additional reports based on the primary hits. We collected 30 case reports from the last seven decades encompassing 376 patients, 23 of whom died. Of all the patient descriptions, 31 were of sufficient detail for prudent analysis., Results and Conclusions: Intoxication with clinical signs mainly took place in war situations and in military and fire emergency training sessions in enclosed spaces. Symptoms follow a biphasic course mainly characterised by dyspnoea, coughing and lacrimation, related to irritation of the airways in the first six hours, followed by reappearance of early signs complemented with inflammation related signs and tachycardia from 24 h onwards. Acute respiratory stress syndrome developed in severely affected individuals. Chest radiographs did not always correspond with clinical symptoms. Common therapy comprises corticosteroids, antibiotics and supplemental oxygen or positive pressure ventilation in 64% of the cases. Of the 31 patients included, eight died, three had permanent lung damage and 15 showed complete recovery, whereas in five patients outcome was not reported. Early signs likely relate to caustic reactions in the airway lining, whereas inhaled ZnCl 2 particles may trigger an inflammatory response and associated delayed fibrotic lung damage. Smoke bomb poisoning is a potentially lethal condition that can occur in large cohorts of victims simultaneously.

Background: Zinc phosphide is a chemical compound that is frequently used as a rodenticide; it is a highly toxic product that is widely used, among other spaces, at home. Given that it is a highly commercialized pesticide and that there is no antidote, it is mandatory to establish favorably the clinical manifestations of the intoxication. The aim was to describe the epidemiological and clinical profile of children intoxicated with zinc phosphide attended in a toxicological center of a tertiary referral hospital., Methods: Cross-sectional, retrospective and observational study based on the medical records of 36 pediatric patients attended from 2005 to 2015 at the Centro de Información y Atención Toxicológica from Hospital General "Dr. Gaudencio González Garza", which belongs to the Instituto Mexicano del Seguro Social., Results: The study didn't show a prevalence of gender; 66% of patients were children between ages 1 and 2. 96% of patients were healthy and three adolescents used the product with suicidal purposes. Zinc phosphide exposure occurred at home. Toxicity was characterized by hypotension, hypoglycemia, metabolic acidosis, abdominal pain, nausea, and vomiting; none of the patients died. In addition, neither required mechanical ventilation nor hemodialysis., Conclusion: The lack of knowledge of the potential toxicity of zinc phosphide and the fact that is easily reached at home allow the exposure to this product; it is an absolutely preventable risk.

Ingestion of large amounts of zinc chloride causes corrosive gastroenteritis with vomiting, abdominal pain, and diarrhea. Some individuals experience shock after ingesting large amounts of zinc chloride, resulting in fatality. Here, we present the results of an administrative autopsy performed on a 70-year-old man who ingested zinc chloride solution and died. After drinking the solution, he developed vomiting, abdominal pain, and diarrhea, and called for an ambulance. Except for tachycardia, his vital signs were stable at presentation. However, he developed hypotension and severe metabolic acidosis and died. The patient's blood zinc concentration on arrival was high at 3030μg/dL. Liver cirrhosis with cloudy yellow ascites was observed, however, there were no clear findings of gastrointestinal perforation. The gastric mucosa was gray-brown, with sclerosis present in all gastric wall layers. Zinc staining was strongly positive in all layers. There was almost no postmortem degeneration of the gastric mucosal epithelium, and hypercontracture of the smooth muscle layer was observed. Measurement of the zinc concentration in the organs revealed the highest concentration in the gastric mucosa, followed by the pancreas and spleen. Clinically, corrosive gastroenteritis was the cause of death. However, although autopsy revealed solidification in the esophagus and gastric mucosa, there were no findings in the small or large intestine. Therefore, metabolic acidosis resulting from organ damage was the direct cause of death., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Brugada syndrome (BrS) is an inherited channelopathy associated with increased incidence of ventricular arrhythmias and has many acquired triggers. Zinc phosphide (ZnP) is a rodenticide and is commonly implicated in suicidal poison ingestion. ZnP poisoning can cause myocardial toxicity and death. We report a case of ZnP poisoning that triggered a type I Brugada pattern and ventricular fibrillation in a 67-year-old male. He had no other features of toxicity and recovered later. As metal phosphide is the commonest toxin involved in suicidal poisoning in India and BrS being endemic here, this case highlights an important clinical problem., (©2015 Wiley Periodicals, Inc.)

Zinc phosphide normally serves as a rodenticide but is occasionally ingested for suicide, potentially causing multiorgan failure. Phosphine gas is commonly in use for fumigation of grain silos and shipping containers.We describe a suicide attempt of a 54 year old female, the clinical symptoms, the treatment, the chemical and biochemical background and we give information on the potential occurrence of zinc phosphide and phosphine gas., (© Georg Thieme Verlag Stuttgart · New York.)

Zinc phosphide (ZnP) containing rodenticide poisoning is a recognized cause of acute liver failure (ALF) in India. When standard conservative measures fail, the sole option is liver transplantation. Records of 41 patients admitted to a single centre with ZnP-induced ALF were reviewed to identify prognostic indicators for requirement of liver transplantation. Patients were analyzed in two groups: group I (n = 22) consisted of patients who either underwent a liver transplant (n = 14) or died without a transplant (n = 8); group II (n = 19) comprised those who survived without liver transplantation. International normalized ratio (INR) in group I was 9 compared to 3 in group II (p < 0.001). Encephalopathy occurred only in group I. Model for End-Stage Liver Disease (MELD) score in group I was 41 compared to 24 in group II (p < 0.001). MELD score of 36 (sensitivity of 86.7 %, specificity of 90 %) or a combination of INR of 6 and encephalopathy (sensitivity of 100 %, specificity of 83 %) were the best indicators of mortality. Such patients should undergo urgent liver transplantation.

Aim: To evaluate the clinical features of zinc phosphide poisoning and to investigate whether outcome could be prognosticated based on abdominal radiography on presentation., Materials and Methods: All zinc phosphide-poisoned patients who were referred to Loghman-Hakim Hospital between March 2011 and September 2013 were retrospectively reviewed. Data regarding patients' demographic characteristics, characteristics of the poisoning, abdominal radiography results, and patients' outcome were recorded., Results: In 102 patients, the most common presenting signs/symptoms were nausea and vomiting (60%). Four patients died and another seven had developed complications during their hospitalization (metabolic acidosis, liver abnormalities, or acute renal failure). Nineteen patients had radio-opaque abdominal radiographs, nine of whom had died or developed complications (p = 0.001). Plain abdominal radiography had a sensitivity and specificity of 81% and 89% in predicting the patients' death or further development of complications. The positive and negative predictive values were 47% and 97%, respectively., Conclusion: Plain abdominal radiography is a very good tool for prognostication in patients with zinc phosphide poisoning. Immediate abdominal radiography can help stratify patients into high- or low-risk groups and determine treatment strategies., (Copyright © 2014 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.)

Radiography has been proved to be a good diagnostic tool in visualization of many radiopaque xenobiotics in clinical toxicology. Zinc is a potentially radiopaque material which is a constituent of the zinc phosphide (ZN2P3) rodenticide. We report two cases of zinc phosphide poisoning with positive abdominal X-rays in whom the diagnosis was confirmed by abdominal imaging. Positive abdominal imaging was an indication for aggressive management; however, aggressive treatment was not lifesaving in one of them. We aim to emphasize the diagnostic value of abdominal X-rays in zinc phosphide-poisoned patients. We also would like to suggest that zinc phosphide (ZP)-poisoned patients with positive X-rays have more chance to become unstable even if they are symptom free on presentation and should be more aggressively managed.

Epizootic mortality in several geese species, including cackling geese (Branta hutchinsii) and Canada geese (Branta canadensis), has been recognized in the Willamette Valley of Oregon for over a decade. Birds are generally found dead on a body of water or are occasionally observed displaying neurologic clinical signs such as an inability to raise or control the head prior to death. Investigation of these epizootic mortality events has revealed the etiology to be accidental poisoning with the rodenticide zinc phosphide (Zn(3)P(2)). Gross and histologic changes are restricted to acute pulmonary congestion and edema, sometimes accompanied by distension of the upper alimentary tract by fresh grass. Geese are unusually susceptible to this pesticide; when combined with an epidemiologic confluence of depredation of specific agricultural crops by rodents and seasonal avian migration pathways, epizootic toxicosis may occur. Diagnosis requires a high index of suspicion, appropriate sample collection and handling, plus specific test calibration for this toxicant. Interagency cooperation, education of farmers regarding pesticide use, and enforcement of regulations has been successful in greatly decreasing these mortality events since 2009.

Metal phosphides in general and aluminium phosphide in particular are potent insecticides and rodenticides. These are commercially used for protection of crops during storage, as well as during transportation. However, these are highly toxic substances. Their detrimental effects may range from nausea and headache to renal failure and death. It is, therefore, pertinent to ensure their circumspect handling to avoid poisoning episodes. Its poisoning has a high mortality and recent years have seen an increase in the number of poisoning cases and deaths caused by suicidal ingestion. Yet due to their broad spectrum applications, these chemicals cannot be written off. The present communication reviews the various aspects of toxicity associated with metal phosphides., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

No standard protocol exists for the treatment of acute respiratory distress syndrome induced by inhalation of smoke from a smoke bomb. In this case, a 23-year-old man was exposed to smoke from a smoke grenade for approximately 10 to 15 minutes without protective breathing apparatus. Acute respiratory distress syndrome developed subsequently, complicated by bilateral pneumothorax and pneumomediastinum 48 hours after inhalation. Despite mechanical ventilation and bilateral tube thoracostomy, the patient was severely hypoxemic 4 days after hospitalization. His condition improved upon treatment with high-dose corticosteroids, an additional 500-mg dose of methylprednisolone, and the initiation of extracorporeal life support. Arterial oxygenation decreased gradually after abrupt tapering of the corticosteroid dose and discontinuation of the life support. On day 16 of hospitalization, the patient experienced progressive deterioration of arterial oxygenation despite the intensive treatment. The initial treatment regimen (ie, corticosteroids and extracorporeal life support) was resumed, and the patient's arterial oxygenation improved. The patient survived.

Aim: We present the case of an adult who ingested soldering fluid containing zinc chloride (ZC) in a suicide attempt. He developed a gastric stricture that was managed successfully by laparoscopic Roux-en-Y gastrojejunostomy. An extensive literature review shows that there are few reports of ZC ingestion. Furthermore, management of corrosive gastrointestinal tract injury is debatable. The evidence is summarized in this case report., Results: ZC is a strong corrosive agent, which, following ingestion, is capable of producing widespread damage locally and systematically with long-lasting morbidity and significant mortality. The mainstay of treatment is supportive. Esophago-gastro-duodenoscopy is the diagnostic procedure of choice in the absence of perforation. Strictures that cannot be dilated endoscopically may require surgery. Emergency surgery is required for patients with evidence of perforation. Early and aggressive surgical resection in patients with high-grade burns may improve mortality and morbidity., Conclusion: Because of the lack of data, it remains debatable as to the optimal management strategies following ZC ingestion. Our patient was managed conservatively throughout the acute phase. However following recognition of the gastric stricture, surgical intervention ensued and he underwent successful laparoscopic Roux-en-Y gastrojejunostomy and was subsequently discharged having made an excellent recovery.

Introduction: Aluminium and zinc phosphides are highly effective insecticides and rodenticides and are used widely to protect grain in stores and during its transportation. Acute poisoning with these compounds may be direct due to ingestion of the salts or indirect from accidental inhalation of phosphine generated during their approved use., Mechanisms of Toxicity: Both forms of poisoning are mediated by phosphine which has been thought to be toxic because it inhibits cytochrome c oxidase. While phosphine does inhibit cytochrome C oxidase in vitro, the inhibition is much less in vivo. It has been shown recently in nematodes that phosphine rapidly perturbs mitochondrial morphology, inhibits oxidative respiration by 70%, and causes a severe drop in mitochondrial membrane potential. This failure of cellular respiration is likely to be due to a mechanism other than inhibition of cytochrome C oxidase. In addition, phosphine and hydrogen peroxide can interact to form the highly reactive hydroxyl radical and phosphine also inhibits catalase and peroxidase; both mechanisms result in hydroxyl radical associated damage such as lipid peroxidation. The major lethal consequence of phosphide ingestion, profound circulatory collapse, is secondary to factors including direct effects on cardiac myocytes, fluid loss, and adrenal gland damage. In addition, phosphine and phosphides have corrosive actions., Clinical Features: There is usually only a short interval between ingestion of phosphides and the appearance of systemic toxicity. Phosphine-induced impairment of myocardial contractility and fluid loss leads to circulatory failure, and critically, pulmonary edema supervenes, though whether this is a cardiogenic or non-cardiogenic is not always clear. Metabolic acidosis, or mixed metabolic acidosis and respiratory alkalosis, and acute renal failure are frequent. Other features include disseminated intravascular coagulation, hepatic necrosis and renal failure. There is conflicting evidence on the occurrence of magnesium disturbances., Management: There is no antidote to phosphine or metal phosphide poisoning and many patients die despite intensive care. Supportive measures are all that can be offered and should be implemented as required.

Zinc as a marker element in the viscera of suspected metal phosphide poisoning has been studied during the present work. Neutron activation analysis (NAA) has been employed to detect and quantify the concentration of zinc in the viscera/stomach portion. The methodology has been developed on simulated and real life viscera samples to quantify the amount of zinc using NAA. The results obtained by NAA for real-life samples have been validated using a complementary analytical technique (viz. differential pulse anodic stripping voltammetry), and the values obtained were in good agreement, within +/- 5-8%. This exercise could be useful in medico-legal field for framing a definitive opinion about zinc phosphide poisoning.

Introduction: The common mixture for smoke bombs contains zinc oxide and a chlorine donor, which allows for the formation of fine particles of zinc chloride. We report a fatal case of exposure to a smoke bomb used for a fire training exercise at a school., Case Report: A 21-year-old student inhaled zinc oxide/hexachloroethane from a smoke bomb during a fire simulation at a school. Fever and tachypnea began six hours after exposure. Radiological evaluation showed a mixed interstitial-alveolar bilateral infiltrates. Despite supportive care, the patient died of multi-organ failure nine days after inhalation., Discussion: ZnCl inhalation is characterized by a lag period between exposure and evidence of respiratory toxicity, ranging from ten to 32 days, depending on the inhaled dose of ZnCl. Subjects inhaling even a small amount of aerosols from a smoke bomb should be carefully managed in a hospital setting where their respiratory function can be closely monitored., Conclusion: This case highlights the risk of serious injury and even death from smoke bombs containing zinc chloride aerosol in schools and suggests that these smoke bombs should not be used for fire simulation or activities where human exposure is suspected, particularly in schools.

Poisoning is an important health hazard and one of the leading causes of morbidity and mortality worldwide. Poisoning is one of the preferred means of committing suicide among males and females in India. A five year retrospective study from January 2000 to December 2004 was conducted at the Department of Forensic Medicine & Toxicology, Kasturba Medical College, Manipal, to understand the magnitude and pattern of suicidal poisoning deaths among males and females in Southern India. During this period, a total of 137 cases of suicidal poisoning related deaths were autopsied. Males were predominantly affected (male:female 2.8:1). Maximum victims of suicidal poisoning mortalities were in their 3rd decade. Mean age for males and females was 40.5 years and 34.4 years, respectively. 27.8% of females and 10.9% males were suffering from depression. Preference for organophosphates was relatively more in males when compared to females, who preferred zinc phosphide, carbamates and medicinal agents. Suicidal poisoning was commonly encountered during afternoon hours in females. Males usually consumed poison during evening and late night hours. Maximum male mortalities were noted during second quarter of the year in contrast to first quarter in females. This paper examines the difference in pattern of suicidal poisoning among males and females to identify population at risk, and understand the problem status among both genders.

An analysis of all poisoning cases admitted in medical and pediatric wards of Patan Hospital for one year (1st Jan to 31st Dec 2004) was carried out. A total of 154 cases were admitted which was 0.8% of total hospital admissions. Females outnumbered males and almost two-thirds patients were young adults (15-34 years). Seasonal variation in poisoning was observed with more cases in the summer months. Organophosphorus compounds (42%), drugs (25%), and zinc phosphide (6.5%) were common poisonings in total and in adult populations, whereas kerosene was the most frequent poisoning in pediatric age group. Paracetamol, benzodiazepines, and tricyclic antidepressants were the most frequently used drugs. The circumstances of poisoning were intentional (75%) and accidental (20%); most of the childhood poisonings were accidental in nature. The mean hospital stay for all type of poisoning was 7.5 days; whereas it was 10.2 days for organophosphorus, 2.5 days for paracetamol, and 1.5 days each for zinc phosphide and kerosene ingestion. Intensive care unit (ICU) service was required in 17% of patients; and almost 25% developed complications. Aspiration pneumonia and respiratory failure were the most frequently observed complications. Ninety four percent of admitted patients recovered completely; leaving a mortality rate of 5%.

Study Objectives: Zinc chloride smoke inhalation injury (ZCSII) is uncommon and has been rarely described in previous studies. We hypothesized that structural changes of the lung might correlate with pulmonary function. To answer this question, we correlated findings from high-resolution CT (HRCT) scan and the results of pulmonary function tests (PFTs) in patients with ZCSII., Design: Retrospective cohort study., Setting: University hospital., Patients: Twenty patients who had been hospitalized with ZCSII-related conditions., Measurements: The study included HRCT scan scores (0 to 100), static and dynamic lung volumes, and diffusing capacity of the lung for carbon monoxide (D(LCO))., Results: HRCT scans and PFTs were performed initially after injury (range, 3 to 21 days) in all patients and during the follow-up period (range, 27 to 66 days) in 10 patients. The predominant CT scan findings were patchy or diffuse ground-glass opacities with or without consolidation. The majority of patients showed a significant reduction of FVC, FEV1, total lung capacity, and D(LCO), but normal FEV1/FVC ratio values. Changes of functional parameters correlated well with HRCT scan scores. Substantial improvements in CT scan abnormalities and pulmonary function were observed at follow-up., Conclusions: The majority of our patients with ZCSII presented with a predominant parenchymal injury of the lung that was consistent with a restrictive type of functional impairment and a reduction in Dlco rather than with obstructive disease. Our results suggest that HRCT scanning and pulmonary function testing may reliably predict the severity of ZCSII.

Approximately 200 chickens were found dead after the flooring of a slat-and-litter house was breached. No clinical signs of illness were observed in the surviving birds. During necropsy, rolled oats were found in the chickens' crops and gizzards, and the contents had a petroleum-like odor. Histopathologic examination revealed severe pulmonary edema and congestion of the chickens' lungs, hearts, livers, and kidneys. Based on the history and necropsy findings, zinc phosphide exposure was suspected. Diagnosis of zinc phosphide poisoning has previously been based on history of exposure, identification of the bait material in the gastrointestinal tract, and chemical detection of phosphine gas. However, currently available diagnostic methods are nonconfirmatory, and may produce false positive results. The objective of this case report was to determine whether the sudden death described in these chickens was caused by the ingestion of zinc phosphide, by developing a sensitive and highly specific gas chromatography/mass spectrometry (GC/MS) methodology for analysis of the gastrointestinal samples submitted to the laboratory. It was also found that the determination of zinc concentrations in liver or kidney tissue or stomach contents is not a reliable indicator of zinc phosphide poisoning.

Zinc phosphide (Zn3P2) is a rodenticide used to control a variety of small mammal species. It is available over-the-counter or as a restricted-use pesticide depending on how it is to be applied. The toxicity of Zn3P2 is dependent on the species exposed, whether the animal is able to vomit or not, and whether it is ingested on a full or empty stomach. Nontarget species can be exposed through inadvertent or intentional product misapplication. In this article we describe four mortality events in which wild turkeys (Meleagris gallopavo) were believed to have been intoxicated following the ingestion of baits containing Zn3P2.

One of the most sensitive measures of health state depending on for example social conditions of the society and family as well as the degree of environmental pollution is somatic development of children. Changes in the somatic and descriptive values, which have been observed for the decades, are known as secular trend that is tendency for changes over centuries. One of its parts is enlargement of parameters of somatic development that is acceleration. Numerous studies on the development of children living in Silesia, the area of great economic potential, however, highly polluted, show the deterioration of developmental parameters of children in Silesia in comparison with their peers from other parts of Poland. The aim of the study is to evaluate the acceleration of somatic development of children living nearby zinc plant. Studies on the somatic development of children at the age between 7-15 years attending the same primary school were carried out in Miasteczko Slaskie at interval of 15 years (1983-1998). Miasteczko Slaskie is the town known for its zinc plant that emits the highest levels of pollution of all steelworks in Poland. This is related to metallurgy of non-ferrous metals. The results were compared with the results of body measurement of the peers from one of the schools in Tarnowskie Góry carried out in the years 1988 and 1998. It was shown that boys and girls from both communities presented lower body mass and height in all periods of study than the standards of The Institute of Mother and Child showed in 1983. No acceleration of somatic development was present among children in Tarnowskie Góry, which may be explained by deterioration of social conditions of these children. However, this acceleration is present in the population of children in Miasteczko Slaskie. This fact may be explained by significantly decreased emission of pollution by the zinc plant and intense care for children shown by the plant managers as well as the foundation for children "Miasteczko Slaskie". They improve life conditions of children in this area and health awareness of their families.

Toxicosis from pesticides rarely occurs in horses and is usually the result of inappropriate pesticide use or handling by humans. Organophosphorus and carbamate insecticides inhibit acetylcholinesterase and are the insecticide class most frequently associated with toxicosis in domestic animals. Metaldehyde is a molluscicide, and zinc phosphide is a rodenticide, both of which have caused toxicosis in horses. All three of these pesticides affect the nervous system of horses and can be fatal if not treated promptly.

Zinc chloride smoke inhalation is a rare cause of slowly progressive and often fatal acute respiratory distress syndrome (ARDS). The conventional treatment includes intravenous N-acetylcysteine, L-3, 4-dehydroproline, methylene blue, and respiratory support according to the lung protective strategy. This report presents the cases of three patients with serious zinc chloride inhalation and ARDS, the last of whom survived after prolonged intensive care, videothoracoscopic excision of emphysema bullae, and recurrent chemical pleurodesis.

Introduction: In April 1996, in Aswan Governorate, Egypt, an outbreak of vomiting without diarrhea, abdominal and leg pain was reported., Methods: A case-control study was conducted to determine the cause of the outbreak. 25 cases who had vomiting without diarrhea, abdominal and leg pain. Controls were randomly chosen from adjacent houses to cases and another village., Results: No occupational exposure was associated with the disease, 84% of cases lived in households where chemical rodenticide had been used for rat infestations compared to 22% of controls. Laboratory analysis and field investigation identified zinc phosphide intoxication as the probable cause of this outbreak.

Twenty cases of zinc phosphide (Zn3P2) ingestion (self-poisoning) were seen during the last 5 years (January 1992-December 1996). Poisoning was rare before 1986. Profuse vomiting (100%), pain in abdomen (100%), palpitation and sweating (80%), dyspnea and tachypnea (75%), metabolic acidosis (60%), shock (40%), and hypotension (40%) were the most common presenting features. Five patients (25%) died. The toxic effects were due to liberation of toxic phosphine (PH3) gas which was detected by qualitative silver nitrate paper test in majority of cases.

"Kela" is a commercial rodenticide bait commonly used in Israel, made of wheat grains, which, according to its label, contains chlorophacinone. This product was involved in the death case of a man in which the victim's female companion was accused of assisting in this suicide and was subsequently convicted. Analysis of the wheat grains revealed zinc phosphide, whose use is restricted to authorized exterminators only, instead of chlorophacinone. Zinc phosphide was identified using microscopic examination, scanning electron microscopy/energy dispersive X-ray spectroscopy (SEM/EDX) and X-ray powder diffraction (XRD).

Zinc chloride is a powerful corrosive agent. Reports of zinc chloride ingestion are uncommon, and there is little information about its toxicity and management. The authors report the clinical course of a 10-year-old girl who accidentally ingested an acid soldering flux solution (pH, 3.0; zinc chloride, 30% to < 60%). Systemic effects after the ingestion were unremarkable except for lethargy. Thus, chelation therapy was not considered. Severe gastric corrosion was caused by local caustic action. An antral stricture of the stomach approximately 3 weeks after the ingestion developed, and she underwent a modified Heineke-Mikulicz antropyloroplasty. Postoperatively, she made an uneventful recovery. On follow-up, although she was tolerating a normal diet, results of a barium meal showed her stomach to be totally aperistaltic. Results of a nuclear medicine study showed moderately delayed gastric emptying. Careful long-term follow-up is necessary, because there is potential risk for malignancy in the damaged stomach.

An acute zinc chloride poisoning due to ingestion is a rare event. Symptoms include: corrosive pharyngeal lesions, vomiting and lethargy. Laboratory findings may include hyperglycaemia, hyperamylasaemia, exocrine pancreatic insufficiency and renal insufficiency. This case report describes an accidental zinc chloride poisoning in a child, with lethargy as the most pronounced clinical sign. Clinical evaluation and chelator therapy are discussed.

Thirteen patients were exposed to accidental zinc chloride inhalation during an army exercise. Smoke bombs were released in open air. The exposure was modest ranging from "taking a few inhalations" to "5-10 minutes in a house with smoke drifting in through unshuttered windows". Initial symptoms were scanty. All patients received inhalation steroid on admittance followed by i.v. bolus of hydrocortisone. Four patients continued systemic steroid treatment (prednisolone 40 mg with stepwise reduction to zero over four weeks) because exposure was judged significant (> 1 minute of unprotected inhalation). No respiratory symptoms developed within an eight week observation period. However, a gradual decline in pulmonary CO diffusion capacity (to 85% (76-99 of initial capacity) was observed within the first four weeks. It is concluded that a very modest inhalation of zinc chloride smoke may induce prolonged impairment of pulmonary function.

Eighty-six workers exposed to zinc phosphide (Zn3P2) pesticide were studied for evidence of neuropsychiatric manifestations. They were evaluated clinically, by electroencephalography (EEG), and, in some cases, by electromyography (EMG). All were males (mean age, 35.8 years; mean duration of exposure to zinc phosphide, 11.3 years). Most presented with one (or more) neuropsychiatric symptom(s), including fear of poisoning, anxiety, impotence, and easy fatigue. About half showed evidence of neuropsychiatric signs, including hyperreflexia, polyneuropathy, lumber radiculopathy, and cervical myelopathy, as well as anxious mood, impaired attention, and psychomotor stimulation. EEG recordings showed abnormal findings in 17.4% of the subjects. The mean age in that group was 39.1 years; mean duration of exposure to Zn3P2 was 15.1 years. EMG studies showed evidence of partial denervation of the anterior tibial group of muscles and flexor digiti minimi in 2 of the 30 workers (6.7%) who underwent EMG examination. Serum levels of zinc (Zn) and cadmium (Ca) were significantly higher in exposed workers than in controls (P < 0.005). Serum copper (Cu), iron (Fe), phosphorus (P), and magnesium (Mg) were significantly lower in exposed workers than in controls. Electrophoretic pattern of globulin showed that gammaglobulin fraction was significantly increased (P < 0.005); alpha2 and beta-globulin were decreased (P < 0.005) in exposed workers. Lipoprotein pattern showed that the total lipids, B-lipoprotein, and B/alpha ratio were significantly increased (P < 0.005) in exposed workers; the alpha1 lipoprotein was decreased. Triglycerides and cholesterol were significantly increased (P < 0.001), and phospholipids and phospholipid/cholesterol ratio were significantly decreased (P < 0.005) in exposed workers compared to controls. The study findings indicated that exposure to Zn3P2 not only caused mild acute and subacute liver cell damage, but also affected renal function and perhaps B-cells of the pancreas. A total of 68.6% of the exposed workers had chest symptoms; only 24.4% presented with chest or cardiac signs. Ventilatory functions were abnormal in 70% of the exposed workers; abnormal ECG findings were present in 12.8%., (Copyright 1997 Academic Press.)

The case of a young woman is described who suffered from acute pancreatitis related to the ingestion of zinc phosphide. This unusual complication was successfully managed with conservative treatment.

A prospective study of 559 cases of acute poisoning who came to this hospital over a period of 14 months. 91.4% cases were of self poisoning (suicidal), 8.1% accidental and only 0.5% homicidal. Majority of patients were young (mean age 27 years), males twice the number of females. Almost 3/4th of the total patients belonged to lower socio-economic group (rural more than urban). The common causative factors which led to self poisoning were marital disharmony, economic hardships and scolding/disagreement with other family members. Aluminium phosphide (ALP) was the most commonly abused substance followed by organophosphates and zinc phosphide in 67.8, 13.9 and 4.3% cases respectively. The overall mortality rate in the series was 33.82%, but true mortality rate in patients who consumed ALP was as high as 67.6%. Most of these cases (94.9%) were not given any preliminary treatment in the village primary health centre (PHC) nearest to the site of mishap and they were brought/referred to this hospital straight and thus most valuable time crucial for effective treatment was lost. Easy availability of a highly toxic substance like ALP at peak moments of frustration has added fuel to the fire and pushed up the incidence of self-poisoning. Suggested preventive measures include caging of tablets in plastic packs, stringent restrictions on free supply of ALP and education of medical/paramedical personnel involved in health care delivery at grass root level.