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Fipronil Poisoning Presenting As Sinus Bradycardia - a Rare Case Report
Jemds.com Case Report Fipronil Poisoning Presenting as Sinus Bradycardia - A Rare Case Report Abhijit Wadekar1, Sreekarthik Pratapa2, Maharshi Patel3, Shilpa Gaidhane4, Nazli Khatib5, 1, 2, 3, 4 Department of Medicine, Acharya Vinoba Bhave Rural Hospital, Sawangi, Wardha, Maharashtra, India. 5 Department of Physiology, Acharya Vinoba Bhave Rural Hospital, Sawangi, Wardha, Maharashtra, India. INTRODUCTION Fipronil is an N-phenylpyrazole insecticide, a second-generation insecticide which is Corresponding Author: relatively new and now commonly used in cotton growing community of rural Central Dr. Shilpa Gaidhane, India. Farmer suicide and deliberate self-poisoning is menace to the Vidarbha region Department of Medicine, of rural Central India. There is paucity of research published on fipronil poisoning, Acharya Vinoba Bhave Rural Hospital, Sawangi, Wardha, Maharashtra, India. clinical features, complications and treatment data. It is scarcely documented E-mail: [email protected] worldwide. Agricultural insecticides are common household items in rural areas of DOI: 10.14260/jemds/2021/247 developing countries. Because of their easy availability, insecticides became a major source of deliberate self-poisoning. As per World Health Organization (WHO), around How to Cite This Article: 3 million poisoning cases with around 0.2 million deaths are noted annually in the Wadekar A, Pratapa S, Patel M, et al. world.1 About 99 % of these deaths occur in developing countries. Insecticide Fipronil poisoning presenting as sinus poisoning is an important public issue in India. Around 168,000 deaths occurred from bradycardia - a rare case report. J Evolution Med Dent Sci 2021;10(16):1166-1168, DOI: pesticide self-poisoning which totals to almost 19.7 % of the global suicides.2 The 10.14260/jemds/2021/247 most common cause of self-poisoning in Central India is ingestion of organophosphorus compounds (OPC). -
Mitochondrial Toxicity of Triclosan on Mammalian Cells
Toxicology Reports 2 (2015) 624–637 Contents lists available at ScienceDirect Toxicology Reports j ournal homepage: www.elsevier.com/locate/toxrep Mitochondrial toxicity of triclosan on mammalian cells a,∗,1 a,1 b,1 c Charmaine Ajao , Maria A. Andersson , Vera V. Teplova , Szabolcs Nagy , d e f g Carl G. Gahmberg , Leif C. Andersson , Maria Hautaniemi , Balazs Kakasi , h a Merja Roivainen , Mirja Salkinoja-Salonen a Department of Food and Environmental Sciences, Haartman Institute, University of Helsinki, POB 56, FI-00014, Finland b Institute of Theoretical and Experimental Biophysics, RAS, Puschino, Moscow Region, Russia c Department of Animal Science and Animal Husbandry, University of Pannonia, Georgikon Faculty, Deak F. u.,16, H8360 Keszthely, Hungary d Dept. of Bio- and Environmental Sciences, Haartman Institute, University of Helsinki, FI-00014, Finland e Dept. of Pathology, Haartman Institute, University of Helsinki, FI-00014, Finland f Finnish Food Safety Authority (EVIRA), Research and Laboratory Department, Veterinary Virology Research Unit, Mustialankatu 3, FI 00790 Helsinki, Finland g Institute of Environmental Sciences, University of Pannonia, Egyetem u. 10, H-8200 Veszprem, Hungary h National Institute for Health and Welfare, Department of Virology, Mannerheimintie 166, 00300 Helsinki, Finland a r t a b i c s t l r e i n f o a c t Article history: Effects of triclosan (5-chloro-2 -(2,4-dichlorophenoxy)phenol) on mammalian cells were Received 28 January 2015 investigated using human peripheral blood mono nuclear cells (PBMC), keratinocytes Received in revised form 29 March 2015 (HaCaT), porcine spermatozoa and kidney tubular epithelial cells (PK-15), murine pan- Accepted 30 March 2015 creatic islets (MIN-6) and neuroblastoma cells (MNA) as targets. -
Signs and Symptoms of Pesticide Poisoning
University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Historical Materials from University of Nebraska-Lincoln Extension Extension 1997 EC97-2505 Signs and Symptoms of Pesticide Poisoning Larry D. Schulze University of Nebraska - Lincoln, [email protected] Clyde Ogg University of Nebraska - Lincoln, [email protected] Edward F. Vitzthum University of Nebraska - Lincoln, [email protected] Follow this and additional works at: https://digitalcommons.unl.edu/extensionhist Part of the Agriculture Commons, and the Curriculum and Instruction Commons Schulze, Larry D.; Ogg, Clyde; and Vitzthum, Edward F., "EC97-2505 Signs and Symptoms of Pesticide Poisoning" (1997). Historical Materials from University of Nebraska-Lincoln Extension. 1225. https://digitalcommons.unl.edu/extensionhist/1225 This Article is brought to you for free and open access by the Extension at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Historical Materials from University of Nebraska-Lincoln Extension by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. University of Nebraska Cooperative Extension EC97-2505-A Signs and Symptoms of Pesticide Poisoning Larry D. Schulze, Extension Pesticide Coordinator Clyde L. Ogg, Extension Assistant, Pesticide Training Edward F. Vitzthum, Coordinator, Environmental Programs z Manage Your Risk z Signal Words z Read the pesticide Label z Routes of Exposure z Pesticide Toxicity z Recognizing Signs and Symptoms of Poisoning z Recognizing Common pesticide Poisonings { Organophosphate and Carbamate Insecticides { Organochlorine Insecticides { Synthetic Pyrethroid Insecticides { Plant-derived Insecticides { Inorganic Insecticides { Microbial Insecticides { DEET Repellent { Bipyridyl Herbicides { Chlorophenoxy Herbicides { Arsenical Herbicides { Wood Preservatives { Fumigants { Rodenticides { Fungicides z What To Do When Pesticide Poisoning Occurs z References z Pesticide Safety Telephone Numbers Accidental exposure or overexposure to pesticides can have serious implications. -
Sound Management of Pesticides and Diagnosis and Treatment Of
* Revision of the“IPCS - Multilevel Course on the Safe Use of Pesticides and on the Diagnosis and Treatment of Presticide Poisoning, 1994” © World Health Organization 2006 All rights reserved. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters. All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either expressed or implied. The responsibility for the interpretation and use of the material lies with the reader. In no event shall the World Health Organization be liable for damages arising from its use. CONTENTS Preface Acknowledgement Part I. Overview 1. Introduction 1.1 Background 1.2 Objectives 2. Overview of the resource tool 2.1 Moduledescription 2.2 Training levels 2.3 Visual aids 2.4 Informationsources 3. Using the resource tool 3.1 Introduction 3.2 Training trainers 3.2.1 Organizational aspects 3.2.2 Coordinator’s preparation 3.2.3 Selection of participants 3.2.4 Before training trainers 3.2.5 Specimen module 3.3 Trainers 3.3.1 Trainer preparation 3.3.2 Selection of participants 3.3.3 Organizational aspects 3.3.4 Before a course 4. -
Aluminium Phosphide Poisoning: a Case Report
International Journal of Medical Toxicology and Forensic Medicine. 2014;4(4): 149-53. Aluminium Phosphide Poisoning: a Case Report 1 1 Vaghefi SS *, Emamhadi MA 1 Department of Forensic Medicine and Toxicology, Loghman Hakim Poison Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran A R T I C L E I N F O A B S T R A C T Article Type: Background: Aluminum phosphide as pesticide commonly Case Report used to protect crops from pests. Despite the limited number of cases of poisoning with this substance, it is Article History: important due to the high risk of being fatal. The major Received: 9 April 2014 cause of the poisoning is suicide attempt. Due to the lack of Revised: 14 April 2014 specific treatment in poisoning, taking more than 500 mg is Accepted: 9 May 2014 fatal. Case Report: The patient was a 16-year-old woman who Keywords: attempted suicide by consuming some 4.5gram aluminum Aluminum Phosphide phosphide tablets. Within half an hour after consumption Poisoning she had vomiting and nausea then smoking cigar, followed Hearing Loss closely by smoking in her mouth flames around his mouth is created which will burn (grade II). Subsequently she had argument with her husband and injured her right ear. During the admission she was alert, 2nd degree burn were observed on the upper lip and around the mouth and nose and ears areas. Physical examination was normal, when she arrived she had severe hypotension and her oxygen saturation was 69% with tachycardia. The patient was immediately intubated and received mechanical ventilation. -
Evaluation of Biorational and Natural Products for Vegetable Crop Management in Commercial Market Gardens and Home Gardens
Report to the Ohio IPM Program on a Vegetable Team Project funded by the Ohio IPM Block Grant Program, 2005 Title: Evaluation of biorational and natural products for vegetable crop management in commercial market gardens and home gardens Investigators: Celeste Welty (entomologist), Sally Miller (plant pathologist), Doug Doohan (weed scientist); Mark Bennett, Matt Kleinhenz, Bob Precheur (horticulturists). Background: The insect pests and diseases that affect vegetable crops are the same whether grown on large farms for commercial production or on small diversified farms or home gardens, but the management tactics preferred by growers are often different for the different scale operations. Many market gardeners prefer to avoid using conventional pesticides because of concern about human safety and environmental contamination. During the past few years, many biorational crop protection products have become available. While it is known that biorational products are safer to humans than conventional pesticides, it is not known whether they are effective in controlling the target pests that they claim to control. In addition to products for insect and disease control, there are many products that promote plant growth, such as microbial soil inoculants. There is little to no unbiased data available on efficacy of these products. This deficit is a limiting factor in formulating up-to-date extension recommendations for market gardens and home gardens. This project was an important first step in the development of a set of recommended garden IPM tactics that will include cultural controls to prevent or delay pest problems, along with biological controls and selective chemical controls. Objective: To evaluate efficacy of biorational products that are available for vegetable crop management, in comparison with standard conventional materials. -
Effect of Triclosan on the Functioning of Liver Mitochondria And
The Journal of Membrane Biology https://doi.org/10.1007/s00232-019-00099-w Efect of Triclosan on the Functioning of Liver Mitochondria and Permeability of Erythrocyte Membranes of Marsh Frog (Pelophylax ridibundus (Pallas, 1771)) Mikhail V. Dubinin1 · Kirill S. Tenkov1 · Anton O. Svinin1 · Victor N. Samartsev1 · Konstantin N. Belosludtsev1,2 Received: 28 June 2019 / Accepted: 24 September 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract The paper examines the efects of the antimicrobial agent triclosan on the functioning of the liver mitochondria of marsh frog (Pelophylax ridibundus (Pallas, 1771)). It was established that triclosan inhibits DNP-stimulated respiration of mito- chondria and decreases respiratory control ratio. In addition, triclosan causes the collapse of the mitochondrial membrane potential on both types of substrates. Such an action of triclosan can be mediated by both a protonophore efect and suppres- sion of the activity of complex II and combined activity of complexes II + III (and, to a lesser degree, the combined activity of complexes I + III) of the mitochondrial respiratory chain. It is shown that high concentrations of triclosan enhance the production of hydrogen peroxide during the oxidation of substrates of the complex I by mitochondria, and decrease it in the case of succinate oxidation. It is found that triclosan is able to induce nonspecifc permeability of the liver mitochondria of these amphibians, as well as the plasma membrane of erythrocytes. The possible mechanisms of triclosan efect on marsh frog liver mitochondria and red blood cells are discussed. Graphic Abstract Keywords Triclosan · Toxicology · Mitochondria · Pelophylax ridibundus · Erythrocytes · Membrane permeability Abbreviations TCS Triclosan CsA Cyclosporine * Mikhail V. -
Gas-Phase Chemical Reduction (GPCR)
Gas-Phase Chemical Reduction (GPCR) Name of Process: Status: Gas-Phase Chemical Reduction (GPCR) A Commercial system operated in Australia for more than 5 years, treating Vendor: more than 2,500 tons of PCB’s, DDT and other POPs. In 1999 a full-scale test ELI Eco Logic International Inc. on HCB was conducted using the commercial plant. Web site: http://www.ecologic.ca Eco Logic’s partners in Japan have recently built a semi-mobile GPCR plant for Applicable Pesticides and related the treatment of PCB wastes, which will be operational in 2003. POPs wastes: Pesticides such as Hexachlorobenzene, In combination with Foster Wheeler and Kvaerner the company is DDT, Aldrin, Dieldrin, HCB’s, DDT, PCB’s, participating at present in the ACWA (Army Chemical Weapons Assessment) dioxins and furans and other POPs. Program for the destruction of chemical warfare agents. Eco Logic has partnered with Torftech Inc. for the treatment of soils and sediments at rates of up to 20 tons per hour. Eco Logic has also been selected by UNIDO for a pilot project for treatment of 1000 tons of PCB wastes in Slovakia. Additional approvals received: -for PCB and dioxin waste in Japan -for PCB’s TSCA permit in USA -for PCB’s and other toxic compounds in the Province of Ontario (Canada) Technology description: Eco Logic’s GPCR technology involves the gas-phase chemical reduction of organic compounds by hydrogen at a temperature of 850°C or higher. Chlorinated hydrocarbons, such as HCB, polychlorinated dibenzo-p-dioxins (dioxins) and other POPs, are chemically reduced to methane and hydrogen chloride (HCl). -
Vol 3 No 2 Mar Apr 2003 Online.P65
School Pesticide Monitor A Bi-monthly Bulletin on Pesticides and Alternatives Vol. 3 No. 2 March/April 2003 Beyond Pesticides / National Coalition Against the Misuse of Pesticides 701 E Street, SE, Suite 200 Washington, DC 20003 202-543-5450 [email protected] www.beyondpesticides.org Three New Reports Reveal Children’s Chemical Exposure Evidence Continues to Mount for School Pesticide Reform U.S. EPA released their second edi-tion of tion letters to students and teachers. bicides, pest repellents and disinfectants. America’s Children and the Environment: The Environmental Working Group (EWG), Measures of Contaminants, Body Burdens, The Centers for Disease Control and Preven- in partnership with Mt. Sinai School of Com- and Illnesses (www.epa.gov/envirohealth/ tion (CDC) released the second National Re- munity Medicine and Commonweal, released children) in February. Included in the report port on Human Exposure to Environmental a similar study, Body Burden: The Pollution are the results of a Minnesota study of pes- Chemicals (www.cdc.gov/exposurereport), In People (www.ewg.org/reports/ ticides in schools, which found that some which measured blood and urine samples for bodyburden/index.php). Published in the pesticides have been detected at indoor con- 116 chemicals that found their way into the peer-reviewed journal Public Health Reports, centrations potentially hazardous to chil- human population through pollution or con- the study offers an up-close and personal dren weeks and months after application. sumer products. look at nine individuals whose bodies were tested for 210 chemicals. Subjects contained Forty percent of the responding custodians The report found positive results for 89 an average of 91 compounds, most of which reported that their schools provided no no- chemicals in the volunteers tested, including did not exist 75 years ago. -
A Review of Aluminium Phosphide Poisoning and a Flowchart to Treat It Arh Hig Rada Toksikol 2016;67:183-193 183
Hashemi-Domeneh, et al. A review of aluminium phosphide poisoning and a flowchart to treat it Arh Hig Rada Toksikol 2016;67:183-193 183 Review DOI: 10.1515/aiht-2016-67-2784 A review of aluminium phosphide poisoning and a flowchart to treat it Behrooz Hashemi-Domeneh1,2, Nasim Zamani1,2, Hossein Hassanian-Moghaddam1,2, Mitra Rahimi1,2, Shahin Shadnia1,2, Peyman Erfantalab1,2, and Ali Ostadi1,2 Toxicological Research Center, Department of Clinical Toxicology, Loghman-Hakim Hospital, Shahid Beheshti University of Medical Sciences1, Excellence Center of Clinical Toxicology, Iranian Ministry of Health2, Tehran, Iran [Received in February 2016; CrossChecked in February 2016; Accepted in September 2016] The use of pesticides such as aluminium phosphide (AlP) has increased in the recent years and improved the quantity and quality of agricultural products in a number of developing countries. The downside is that AlP causes severe chronic and acute health effects that have reached major proportions in countries such as India, Iran, Bangladesh, and Jordan. Nearly 300,000 people die due to pesticide poisoning in the world every year. Poisoning with AlP accounts for many of these deaths. Unfortunately, at the same time, there is no standard treatment for it. The aim of this article is to give a brief review of AlP poisoning and propose a treatment flowchart based on the knowledge gained so far. For this purpose we reviewed all articles on the management of AlP poisoning published from 2000 till now. Using a modified Delphi design, we have designed a handy flowchart that could be used as a guide for AlP poisoning management of patients in emergency centres. -
Managing Pesticide Poisoning Risk and Understanding the Signs and Symptoms Clyde L
EC2505 Revised June 2018 Managing Pesticide Poisoning Risk and Understanding the Signs and Symptoms Clyde L. Ogg, Extension Educator Jan R. Hygnstrom, Project Manager Cheryl A. Alberts, Project Coordinator Erin C. Bauer, Entomology Lecturer The potential for accidents with pesticides is real. Ac- cidental exposure or overexposure to pesticides can have seri- ous consequences. While most pesticides can be used with relatively little risk when label directions are followed, some are extremely toxic and require special precautions. The Poison Control Centers receive about 90,000 calls each year related to pesticide exposures. Pesticides are re- sponsible for about 3 percent of all accidental exposures to children 5 years and younger and about 4 percent for adults. In addition, pesticides are the cause of about 3 percent of children’s deaths reported to the Poison Control Centers. Routes of Exposure Pesticides can enter the human body three ways: 1) der- mal exposure, by absorption through the skin or eyes; 2) oral exposure, through the mouth; and 3) through inhalation or respiratory exposure, by inhaling into the lungs. Some classify exposure through the eyes as ocular exposure. Dermal exposure results in absorption immediately after Figure 1. Absorption rates of different a pesticide contacts the skin or eyes. Absorption will contin- parts of the body based on the absorption ue as long as the pesticide remains in contact with the skin or of parathion into the forearm over 24 eyes. The rate at which dermal absorption occurs is different hours. for each part of the body (Figure 1). Maiback and Feldman (1974) measured the amount of the pesticide parathion absorbed by different parts of the human body over 24 hours. -
Mitochondrial Complex I Inhibition Depletes Plasma Testosterone in the Rotenone Model of Parkinson’S Disease
Physiology & Behavior 83 (2004) 395–400 Mitochondrial complex I inhibition depletes plasma testosterone in the rotenone model of Parkinson’s disease M. Alam, W.J Schmidt* Zoological Institute, Department of Neuropharmacology, Morgenstelle 28E, University of Tuebingen, 72076 Tuebingen, Germany Received 5 April 2004; received in revised form 29 July 2004; accepted 11 August 2004 Abstract Age-related depletion of testosterone may increase the brain’s vulnerability to parkinsonian- or Alzheimer’s-like neurodegenerative disorders. In rats, rotenone, a mitochondrial complex I inhibitor, causes specific nigral dopaminergic neurodegeneration producing parkinsonian symptoms. In this study, rotenone was administered on a daily basis (2 mg/kg i.p.) to two groups of rats, over a period of 30 and 60 days, respectively. In order to contribute towards the validation of the rotenone rat model, the changing level of the peripheral sex steroid hormone, testosterone, which would also mimic those found in Parkinson’s disease (PD) patients, was evaluated. Parallel to this, prolactin, luteinizing hormone (LH), the nonsexual steroid thyroid-stimulating hormone, and the corticosterone hormone levels in the peripheral blood plasma were measured to show whether other hormones have also been affected by complex I inhibition. The rotenone treatment caused a decrease of testosterone level in the peripheral blood plasma. There were no differences in the thyroid hormone and prolactin but increases in leutinizing hormone and corticosterone were observed. Data from this study indicate that rotenone depleted the sex steroid hormone which is preferentially produced in the periphery, e.g., adrenal gland and testis. In conclusion, because a decrease in testosterone levels is also one of the comorbidities which are found in male PD patients, our results indicate that the rotenone model mimics PD symptoms not only on a neuronal and behavioral level, but also on the testosterone levels.