Co toxicity by rishav
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Carbon monoxide is a colorless, odorless, and tasteless gas that is slightly less dense than air. It consists of one carbon atom and one oxygen atom connected by a triple bond. As the second most common molecule in the interstellar medium after hydrogen, it is also a primary air pollutant and part of the chemical reactions that form photochemical smog. Carbon monoxide poisoning can cause bizarre behavior, declining intellect, memory disturbances, and symptoms that are often misdiagnosed as other conditions. Key steps to prevent carbon monoxide poisoning include installing detectors, opening garage doors before starting cars, keeping fuel burning appliances and engines properly vented, and using caution with solvents.
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Smoke inhalation injuries can cause both local pulmonary damage and systemic toxicity from inhaled chemicals. Thermal injuries damage mucous membranes while chemical injuries depend on particle size and solubility. Systemic toxins include carbon monoxide, which binds hemoglobin, and cyanide, which inhibits ATP production. Initial management focuses on airway support, 100% oxygen, and observation. Hyperbaric oxygen may benefit patients with significant carbon monoxide exposure. Burn depth depends on extent of skin layer damage. Minor burns are cleaned and covered while major burns require fluid resuscitation and potential transfer to facilities with specialized burn care resources.
Toxicity of Pesticides
This document discusses toxicity from pesticides, specifically organophosphates and paraquat. It provides information on:
1) Organophosphates are commonly found in household and agricultural pesticides as well as some medical treatments. They work by inhibiting cholinesterase enzymes, leading to excess acetylcholine and symptoms like muscle fasciculations, weakness, and seizures.
2) Paraquat is a herbicide that is toxic when ingested, with a lethal dose between 1-4 grams. It causes lung damage through redox cycling and production of reactive oxygen species.
3) Clinical manifestations of organophosphate toxicity include muscarinic effects like increased salivation as well as nicotinic effects
Oxidative stress and the eye
Every component of the eye is vulnerable to damage from ROI, particularly retina. There are several reasons for the vulnerability of the retina, including high concentrations of polyunsaturated fatty acid (PUFA), constant exposure to visible light, high consumption of oxygen, an abundance of photosensitisers in the neurosensory retina and the RPE, the process of phagocytosis by the RPE which is known to generate hydrogen peroxide.
Occupational poisonings and toxicity
The document discusses occupational poisonings from toxic substances like heavy metals, pesticides, and organic solvents. It describes the health effects of various heavy metals including arsenic, cadmium, chromium, lead, mercury, and nickel. Signs and symptoms of acute poisoning from organophosphate pesticides are also outlined, which develop rapidly from inhalation or skin exposure and involve excessive sweating, vomiting, and seizures.
Chronic Obstructive Pulmonary Disease (COPD) 1.pptx
Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by persistent respiratory symptoms and airflow limitation. The main symptoms include dyspnea, cough, and sputum production. COPD is caused by exposure to inhaled irritants, most often cigarette smoke, leading to chronic inflammation and structural changes in the lungs.
The predominant form of COPD is chronic bronchitis, which involves chronic cough and sputum production for at least 3 months per year for 2 consecutive years. This is associated with inflammation and eventual thickening of the bronchial tubes. Emphysema is another form of COPD characterized by permanent enlargement of airspaces and destruction of lung parenchyma.
The airflow limitation in COPD is due to a combination of parenchymal destruction (emphysema) and small airways disease (chronic bronchitis). The obstruction is generally progressive and irreversible. Diagnosis is based on symptoms, exposure history, and spirometry showing irreversible airflow limitation.
COPD treatment aims to reduce symptoms, improve exercise tolerance, prevent exacerbations, and slow disease progression. Smoking cessation is essential. Medications used include bronchodilators and inhaled steroids. Supplemental oxygen may be required in advanced disease. Exacerbations are treated with antibiotics, oral steroids, and other supportive therapies. Patients often have decreased quality of life and COPD is a leading cause of mortality worldwide.
Carbon monoxide
This document discusses carbon monoxide (CO), an odorless and colorless gas that is a toxic air pollutant produced by incomplete combustion of carbon-containing fuels. It summarizes that CO is released through natural sources like volcanoes and forest fires as well as human sources such as vehicles, stoves, heaters, and industry. Exposure to high levels of CO can cause nausea, headaches, dizziness and even death in humans. It also presents examples of CO poisoning incidents that resulted in deaths and hospitalizations. The document concludes by emphasizing the importance of inspecting fuel-burning appliances and using CO detectors to help manage the risks from this toxic gas.
Chemical based hazards
This document discusses various chemical hazards. It begins by defining chemical hazards as chemicals that have the potential to cause harm to life or health. The actual risk depends on factors like exposure amount, use, and typical exposure from a product. Sources of chemical hazards include agricultural chemicals, cleaning chemicals, equipment components, maintenance chemicals, and packaging materials. Common types of chemical hazards are irritants, sensitizers, toxics, asphyxiates, anesthetics/narcotics, and systemic poisons. Organic synthesis presents hazards from active agents used, intermediate compounds formed, and final products introduced. Specific examples like mepacrine, acriflavine, nicotinic acid, chloroform, ethylene dichloride,
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Chronic Obstructive Pulmonary Disease (COPD) 1.pptx
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Co toxicity by rishav
- 1. PRESENTED BY, RISHAV RAY, MSc II SEM-3rd, DEPARTMENT OF ENVIRONMENTAL STUDIES, VISVA BHARATI, SANTINIKETAN
- 2. •It is a colorless, odorless, and tasteless flammable gas that is slightly less dense than air. • Consists of one carbon atom and one oxygen atom, connected by a triple bond containing 2 covalent bonds & 1 dative covalent bond •Along with aldehydes, part of the series of chemical reactions that form photochemical smog •It is the second-most common molecule in the interstellar medium, after hydrogen. •Primary air pollutant
- 9. • Bizarre behaviour abnormalities • Declining intellect • Memory disturbances • Chronic cough • Diarrhoea • Patients may occasionally present with polycythemia or increased hematocrit • Condition often misguided as chronic fatigue symptoms,viral,bacterial,pulmonary,GIT infections or immunodeficiency .
- 10. •INSTALLING CARBON MONOXIDE DETECTORS •OPEN THE GARAGE DOOR BEFORE STARTING YOUR CAR •USE GAS APPLAINCES AS RECOMMENDED •KEEP YOUR FUEL BURNING APPLIANCES AND ENGINES PROPERLY VENTED •KEEP VENTS AND CHIMNEYS UNBLOCKED DURING REMODELLING •USE CAUTION WHEN WORKING WITH SOLVENTS IN A CLOSED AREA
- 11. • Health, National Center for Environmental (30 December 2015). "Carbon Monoxide Poisoning – Frequently Asked QuestionS". www.cdc.gov.from the original on 5 July 2017. Retrieved 2 July 2017. • Penney, David G. (2007). Carbon Monoxide Poisoning. CRC Press. p. 569. ISBN 978-0849384189. Archived from the original on 10 September 2017. Retrieved 2 July 2017. • Omaye ST (Nov 2002). "Metabolic modulation of carbon monoxide toxicity". Toxicology. 180 (2): 139–50. • Kao LW, Nañagas KA (March 2006). "Toxicity associated with carbon monoxide". Clinics in Laboratory Medicine. 26 (1): 99– 125. doi:10.1016/j.cll.2006.01.005. PMID 16567227 • Ducasse JL, Celsis P, Marc-Vergnes JP (March 1995). "Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation