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Toxic non-metallic.pptx bbbffffffffffffffffffffffffff
- 1. 1 Non-Metallic Environmental Toxicants By: SagniHanbisa B-pharm, MSc in Pharmacology Wallaga University
- 2. 2 Poisoning with organicsolvent 1. Methanol Common industrial solvent as paint remover, varnishes • Routes of poisoning – Inhalation/dermal/oral • Mechanism of poisoning – Produces acidosis (formic acid) • S/S – Blurred vision due to optic nerve damage – headache, vertigo
- 3. 3 • Rx maintainABC dep'ing on need, sympt.therapy, Protect eyes from strong light-b/c optic n is damaged Keep victim warm NaHCO3 to correct acidosis Ethanol(specific antidote) hemodialysis
- 4. 4 2. Ethanol • commonsolvent in many household products, mouthwash, cosmetics and industry • Routes of poisoning – Inhalation/dermal/oral • Mechanism of poisoning – Central depression
- 5. 5 • S/S • Acute –intoxication – Alcohol smell/drunkness – CNS stimulation • Chronic – appetite suppression/malnut.induced complication – hepatitis – ketoacidosis
- 6. 6 • Rx supportivetherapy Symptomatic • Diazepam-for over excit. • caffeine-for over depress. alcohol withdrawal(acute/chronic) alcohol antabuse(chronic)-disulfiram
- 7. 7 3. Isopropanol • Usedas alcohol rub(hosp.,toilet), hand lotion-if no water available-before and after food. • Mechanism of toxicity: – 2 to 3 times more potent CNS depressant than ethanol. • Major metabolite –acetone (CNS depressants) • S/S – Gastritis – Vomiting with aspiration • Rx: – Maintain ABCD,symp.therapy – Hemodialysis(if in circulation provided it recommended) – Gastric lavage(if in GI)
- 8. 8 4. Glycols i. Ethyleneglycol •Used improperly in juice, wines or beer to give flavor • Metabolized to CO2 and formic acid – glyoxal + glyoxylic acid ___ oxalic acid • Routes of exposure – Oral/dermal/inhalation • Mechanism of poisoning – Acidosis (formic acid)and kidney damage (nephrotoxicity)/oxalic acid/
- 9. 9 • S/S –CNS depression(30min-12h), edema(12-48h), acute renal failure (24 –72 h) • Rx –Maintain ABCD,continue symt.therapy –(Diazepam for convulsion, IV Ca for muscle spasm), ethanol (specific antidote), dialysis, emesis
- 10. 10 ii. Propylene glycol –Similar to ethylene glycol – Less toxic • Therefore, Preferred solvent for drugs, cosmetics, lotions, ointments, food materials…than ethyleneglycol.
- 11. 11 Prevention of solventexposure • Avoid indiscriminate use of cosmotics and lotions, ex:if EG avoid it. • Avoid toxic solvents in any preparation such as food, cosmetics, drugs,(i.e, unless they are very crucial.) • Use butane(while cooking)gas carefully- (proper closure) • Handle solvents like benzene carefully
- 12. 12 Poisoning with environmentalpollutants • Enter body predominantly through lungs/inhalation/ • Particles >/=5 um deposited in upper airway • Those deposited in unciliated anterior portion of nose remain till removed by wiping, sneezing, or blowing • Particles < 1 um remain suspended in inhaled air, reach alveoli and absorbed
- 13. 13 • Sources – Transportation(60%) – Industry (18%) – Electric power generation (13%) – Space heating (6%) – Refuse/waste disposal (3%) • Characteristics – Reducing pollutants • SO2 and smoke from incomplete combustion – Oxidizing pollutants • HC, NO2, photochemical oxidants
- 14. 14 • Types – Carbonmonoxide(52%) – Sulfur oxides (18%) – Hydrocarbons (12%) – Particulate matter (10%) – Nitrgen oxide (6%)
- 15. 15 1. CO • Tasteless,colorless, odorless gas produced by incomplete combustion of organic cpds • Obtained from – In nature (90%) through oxidation of methane and terpine, forest fires, etc – Human activity (10%) • Automobile by products • Coal, fuel,wood burning • Tobacco smoking – Human body (0.5%) through Hgb metabolism as carboxy Hgb
- 16. 16 • Most victimsdie from acute poisoning/ i.e,smoke/than from burns • Efficient natural ways of removal – Reaction of CO with ambient OH-to form CO2 – Upper atmosphere as a sink – Soil as a sink
- 17. 17 • Route ofexposure – Inhalational • Mechanism of poisoning – Interact with Hgb-depriving oxygen • S/S – Hypoxia, Rp, syncope, headache, blurred vision, ↓ acidosis • Rx – Artificial Rp (maintain B) and stabilize,take specimen – Correction of acidosis and Rp (symptomatic ↓ therapy) – Transferring to fresh air – Oxygen administration (specific antidote)
- 18. 18 2. Ozone (O3) •Oxidant found in highest conc. in polluted air • Several miles above earth’s surface, sufficient UV to convert O2 to O3 by direct absorption • Of major pollutants, NO2 is most efficient in absorbing UV light as follow: • NO2 UV NO + O • O + O2___ O3 • O3 +NO ____ NO2+ O2
- 19. 19 • O reactswith HC in atmosphere to produce oxidized cpds and free radicals that react with NO to produce more NO2 and O3 while NO is depleted → • Routes of exposure – inhalation • Mechanism of poisoning – Irritation of lungs/brochi – Sensitizes lungs to autacoids,ex:histamine:H1 rec in bronchi=bronchoconstriction/spasm.
- 20. 20 3. Sulfur dioxide •Obtained from burned fossil fuels that contain sulfur • Causes bronchoconstriction (0.25ppm) • 5 ppm of sulfurdioxide increases resistance to flow of air within 10 minutes, i.e, obstruction of breathing • RX – art.Rp – no antidote
- 21. 21 4. Nitrogen dioxide •Lung irritant pulmonary complication → • Risky to farmers as it can be released from silage 5. Particulate matters – Inhalation of dust silcosis → – Asbestosis results from inhalation of asbestos dust – usually affects the URT - removed by sneezing,coughing or whiping.
- 22. 22 Hydrocarbons • Organ cpdsthat contain H and C atoms only • Most are extracted from petroleum distillation, e.g., terpentin distilled from pine woods • Sources – Lighter fluid, kerosine, naphta, lubricating oils, asphalt, benzene • Routes of exposure: inhalation (abuse), oral
- 23. 23 • Classes-based onvolatility – High volatile: methane, buthane –CNS symptoms ex:comma – Intermediate volatile: gasoline, terpentine, naphtha-aspiration – Low volatile: kerosine (cooking), petrolium spirit-pulmonary complication – Minimal volatile: lubricating oil(semisolid), asphalt(solid)-nontoxic
- 24. 24 • Pathology – Pulmonarycomplications: pneumonitis – CNS toxicity – CNS depression – Cardiac manifestations: arrhythmias – Cutaneous injury: wound – GI effects: irritation – Kidney damage • S/S: – aspiration, nausea/vomiting/D, dizziness , erythema(skin)
- 25. 25 • Rx: – Nospecific antidotes – Supportive-maintain ABCD/symptomatic Rx • Positive airway pressure • Cloth removal – Correction of fluid/electrolytes imbalance N.B. no gastric emptying-b/c of aspiration and no gastric charcoal-active. charcoal doesn't bind
- 26. 26 Poisoning with foodcontaminants • Over 3000 different substances added to food • Primary purpose of additives – Color – Texture – Flavor – Preservative • Include
- 27. 27 i. Nitrites – Fromuse of fertilizers-plant if consumed. – Toxicity manifested in form of methemoglobinemia ii. Mercury – From use as antifungal agent(spray)on seeds-if consumed – in sea water/fish/- if consumed iii. Lead – From use of Pb pots(to cook food some of them enter), shellfish, air born iv. Hepatotoxins – From plants like castor oil
- 28. 28 V. Goiterogens – Fromplants like cabbage – Toxicity manifested in form of methemoglobinemia vi. saponins – From plants like soybeans (hemolyse RBC) vii. neurotoxins – From fish viii. Fungal toxins – Aflatoxin - contaminate milk,beans,meat, ergots(alkaloids-cont.rice) ix. Mushrooms – From plants
- 29. 29 Poisoning with householdproducts • Most common household products include – Bleaches • Include oxalic acid, hypochlorate • Commercial liquid bleaches cause esophageal damage • Granular bleaches-more toxic – Cosmetics • perfumes/colognes/,aftershave lotions, oral hygiene products ,shampoo–mainly dependent on their concentration of alcohol • deoderants composed of Al and Zn -low toxicity • for accidental,homicide or sucide
- 30. 30 – Hair products •Dyes/bleaches (hydrogen peroxide-low toxicity) • Hair straightening/hair waving (contains NaOH, ammonium hydroxide, potassium carbonate, potassium bicarbonate-corrosive) – Detergent and soaps • Soaps-salts of fatty acid –low toxicity (nausea, vomiting, diarrhea) • Detergents –non-soap (granular, liquid or spray) – Contain surfactants »Nonionic »Ionic -cationic (ammonium quaternary compounds) -amphoteric
- 31. 31 – Plants – Hydrocarbons:kerosin – Insecticides: organophosphates – Art supplies: magic markers – Paints/varnishes
- 32. 32 Prevention of householdproducts poisoning – Advocating child resistant containers – Keeping products in their original containers – Storing food and chemicals separately – Purchasing least toxic chemicals/check exp.date and small chem ingredient/ – Purchasing smallest possible amount – Not giving medicines in presence of children – Keeping chemicals out of sight or reach of children – Keeping a bottle of emetic
- 33. 33 General management ofdetergent poisoning – for eye/skin exposure-irrigation with water for 15 min – For ingestion -dilution with water/milk immediately (gastric emptying/charcoal) not recommended) – Neutralization not recommended – Esophagoscopy in case of bloody vomiting/oral ulcer – Antimicrobials not routinely recommended
- 34. 34 Acids and alkalipoisoning • Sources for acids – Household products • Automobile battery (sufuric acid) • Toilet bowel cleaner (HCl) • Metal cleaners/antirusts (phosphoric acid, oxalic acid, HCl, sulfuric acid, chromic acid)
- 35. 35 – Industrial uses •Acetic acid (printing, dying, disinfection) • Carbolic acid (dying, disinfection) • Chromic acid (leather tanning, photography, cement) • Formic acid (glue manufacturing, tanning) • HCl (dye, bleaching, plumbing) • Nitric acid (leather tanning, chemical manufacturing) • Phosphoric acid (metal cleaning, disinfection)
- 36. 36 • Sources foralkalis – Household bleaches (Na hypochlorite) – Detergents (Na tripolyphosphate) – Drain cleaners (NaOH) – Cement (CaO, silca, aluminium Oxide) – Ammonium compounds (ammonium hydroxide) – drugs-antacid
- 37. 37 • Mechanisms – Acids:coagulation necrosis acid penetration →↓ superficial damage → – Alkalis: liquification necrosis (fat/protein saponification) deep tissue damage further → → injury through thrombosis
- 38. 38 • Factors affectingdegree of injury – Concentration (pH) – Volume – Contact time – Pre-existing stomach state • Empty stomach-damages 2/3 sparing only fundus • Full stomach-damages only pylorus and lower curvature
- 39. 39 • Time courseof injury – Inflammatory stage:0-4 days-tissue necrosis – Granulation stage: 4-7 days-mucus sloughing – Perforation stage: 7-21 days-peritonitis, sepsis – Cicatrization (dense fibrous tissue) stage: > 21 days –scar, esophageal obstruction • Location of injury – Acid-stomach pylorus – Alkali-esophagus
- 40. 40 • S/S – Pharengealpain – Erythema edema-skin – Hypotension-bv dilated – Rp depression • Rx – Stabilization (airway support)-intensive care – IV line establishment immediately – Maintain ABCD, specimen to analysis – Vital sign monitoring (symptomatic therapy) – Fluid/electrolytes (symptomatic therapy),i.e, • parentral food+Glucose+fluid+electrolyte are given along the IV line never give orally b/c the GI is damaged.
- 41. 41 • Treatment ofpoison-if confirmed-no antidote – Dilutional therapy: 1 or 2 glass of milk/water. C/I in shock – Neutralization contraindicated-b/c heat is generated w/c totally damage the GI – Gastric lavage – Perforation requires surgery – Parenteral nutrition – ICU admission
- 42.