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Occupational poisoning

Occupational poisoning. By: Sotoudeh-manesh MD Occupational medicine specialist. Introduction. Poison: – Any substance that, when administered to a living organism, causes a harmful effect. Poisoning: – The morbid condition produced by a poison. – Systemic effects of toxic materials

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Occupational poisoning

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  1. Occupational poisoning By: Sotoudeh-manesh MD Occupational medicine specialist

  2. Introduction Poison: • – Any substance that, when administered to a living organism, causes a harmful effect. Poisoning: • – The morbid condition produced by a poison. – Systemic effects of toxic materials Toxic: – Term used to describe a chemical that has the ability to cause harmful or fatal effects upon exposure to humans, animals, or plants. • Toxicity: – The capacity of a substance to induce damage to living tissue. Toxicity can be acute, chronic, local, or systemic. (Lewis Dictionary of Occupational and Environmental Safety and Health)

  3. Introduction • Common occupational toxic substances can be divided into 4 groups: • Gases, vapours and particulates • Heavy metals • Pesticides • Organic solvents

  4. Gases, vapours and particulates • Definitions: • • gas is a term usually applied to a substance that is in the gaseous state at room temperature and pressure • • vapour is applied to the gaseous phase of a material that is ordinarily a solid or liquid at room temperature and pressure • • aerosol is applied for a relatively stable suspension of solid particles in air, liquid droplets in air or solid particles dissolved or suspended in liquid droplets in air • • mists and fogs are aerosols of liquid droplets formed by condensation of liquid droplets on particulate nuclei in the air • • fumes are solid particles formed by combustion, sublimation or condensation of vaporised material • • dusts are solid particles in air formed by grinding, milling or blasting • • fibres are solid particles with an increased aspect ratio (the ratio of length to width); they have special properties because of their ability to be suspended in air for longer periods than dusts and other aerosols.

  5. Particulates Classification of particles by size: • 1. Non-inhalable particle • – Larger than 200 μm (0.2mm) • 2. Inhalable particle (nasopharyngeal region) • – Smaller than 200 μm (0.2mm) • – Deposit in nose or trachea • – Dissoluble particles are hazardous (e.g. lead fume) • 3. Respirable particle (alveolar region) • – Smaller than 10 μm (0.01mm) • – Deposition in alveolar area (e.g. pneumoconiosis)

  6. Toxic gas • General consideration • Odors • Asphyxiant • solubility

  7. Factors affecting the dose of inorganic gas delivered to the respiratory system • Physicochemiacal factors • Concentration • Duration of exposure • Minute ventilation

  8. Toxicity of Gases and vapours • • Asphyxiation: • simple asphyxiants • – ability of a gas or vapour to displace oxygen from air by dilution • • Carbon dioxide • • Nitrogen (N2) • • Inert gases such as helium, argon and neon. • toxic asphyxiants • – by interfering with the ability of the body to transport oxygen (). • • Carbon monoxide • • Cyanides • • Hydrogen sulfide • • Irritation to the tissues in respiratory system • – Ammonia • – Chlorine • • Sensitization – asthma

  9. CASE1 • آقاي 26ساله با سردرد يك ماهه در آذرماه مراجعه كرده.دو مرتبه توسط متخصص مربوطه با تشخيص سردرد ناشي از استرس و تشديد در اثر فيومهاي محيط كار بررسي شده است. • PHx :سابقه يك مرتبه سردرد در نوجواني مي دهد.سردرد اخير در حدود4ماه قبل شروع شده كه به تدريج از نظر شدت و تواتر بيشتر شده و بهOTCپاسخ مناسب نمي دهد.سردرد رترواربيتال با انتشار به پشت سرهمراه باحساسيت به نور و سروصدا و گاهي تهوع مي باشد. • OHxشغل نجار و كار بر روي محصولات روكش داربه مدت 6 ماه.10نفر همكار ديگر هم دارد.فضاي کارگاه 25*100 مترمي باشد.در داخل كارگاه يك اتاقك كوچك باز جهت اسپري كردن و استفاده از مواد جلا دهنده با تهويه و يك بخاري گازي وجود دارد.درب كارگاه در فصل زمستان كاملا بسته مي شود. • Task:استفاده از مواد جلا دهنده • MSDS: حدود 70% متيلن كلرايد،تولوئن،متيل اتيل كتون،ايزوپروپيل الكل،اتيل استات

  10. CO poisoning • Colorless, odorless and non irritant • 40000 emergency visit in USA • CoHb:0.5%in nonsmoker adult and 1% in adult that typically exposed in environment

  11. CO poisoningExposure setting • Incomplete combustion • Smoking:400ppm(0.04%) • PEL:50 ppm • CoHb:3-8% occasionally up to 15% • Inadequate ventilation • Methylene chloride

  12. CO poisoningEnvironmental measurement • Colorimetric device(in home) • Electronic short testing devices(in home) • CO2 measurement • Indicator tubes

  13. CO poisoningBiologic monitoring • CoHb • COHb=[Co]air*KT • 220 times affinity co for Hb as O2 • Half time=320min

  14. CO poisoningpathophysiology • Reduce the oxygen-carrying • Alter arterial oxygen tension and hemoglobin saturation • Cytochrome effect • Reoxygenation and demyelination

  15. CO poisoningAcute clinical effect • Non-specific =viral infection • COHb 5%:visual perception ,CNS+hypoxia without hyeperventilation • COHb>5%:tissue hypoxia,vasodilation ,…syncope….lactic asidosis and hyperventilation…..seizure,coma,cardiacarrhythmia,MI,Sudden death • Cherry red lips • Retinal hemorrhage • Erythematous lesions with bullae over bony prominences • Sweat gland necrosis • Lab:PaO2,Pulse oximetry,CO oximetry

  16. CO poisoningDelay effects • Incidance:10-30% • 2-40days • Mental deterioration, mood dis,unusual behavior, gait and other movement disturbance, parkinsonian deficit ,focal neurological sings

  17. CO poisoningChronic effects • Erythrocytosis • Angina • Atherosclerosis???

  18. CO Poisoning • Signs and symptoms closely resemble those of other diseases. • Often misdiagnosed as: • Viral illness (e.g., the “flu”) • Acute coronary syndrome • Migraine • Estimated that misdiagnosis may occur in up to 30-50% of CO-exposed patients presenting to the ED. Source: Raub JA, Mathieu-Holt M, Hampson NB, Thom SR. Carbon Monoxide Poisoning: A Public Health Perspective. Toxicology 200;145:1-14

  19. Cherry red skin color is not always present and, when present, is often a late finding. Signs and Symptoms COHb levels do not always correlate with symptoms nor predict sequelae.

  20. CO poisoningClinical evaluation • Clinical suspicion • COHb measurement or CO measurement in exhaled air • Neurology neuropsychology evaluation

  21. CO poisoningManagement • Remove • O2 100% • Mechanical ventilation • Hyperbaric oxygen therapy • any period of unconsciousness • COHb>40% • Pregnancy and COHb>15% • Sign of cardiac ischemia and arrhythmia • PHx of IHD and COHb>20% • Symptom don’t resolved after 4-6h with 100%O2 • RECURRENT SYMPTOM after 3W

  22. case2 • آقاي 40ساله با شرح حال تماس با پودر و مواد جواهرسازی توسط همكاران به اورژانس آورده مي شود.وي داراي يك مغازه طلاسازي و پرداخت كننده طلا مي باشد.در روز حادثه در هنگام كار با مواد صيقل دهنده fanبالاي سرش را روشن مي كند و پودر در داخل مغازه پراكنده مي شود.بلافاصله فرد سريعا دچار تهوع ،استفراغ و احساس سوزش در سراسر بدن مي شود. توسط همكاران به بيمارستان ارجاع مي شود. در هنگام مراجعه فرد هوشيار و اورينته PR=80 و BP=100/60.معاينه شكم و ريه نرمال است.4 مرتبه LOOSE STOOL داشته است .سرگيجه تنگي نفس و خونريزي و تشنج نداشت.بعد از 2 ساعت BPكاهش مي يابد. ABG79= pH 7.30, pO2 50, pCO2 23, HCO3=11.6, SO2 بود. اقدامات ساپرتيو موثر نبود و فرد در نهايت فوت نمود

  23. Hydrogen cyanide is a colorless or pale blue liquid or gas with a faint bitter almond like odor

  24. Cyanide • Hydrogen cyanide is formed during the incomplete combustion of nitrogen- containing polymers, such as certain plastics, polyurethanes, and wool. Hydrogen cyanide is present in cigarette smoke • HUMAN EXPOSURE: Cyanides are well absorbed via the gastrointestinal tract or skin and rapidly absorbed via the respiratory tract. Once absorbed, cyanide is rapidly and ubiquitously distributed throughout the body, although the highest levels are typically found in the liver, lungs, blood, and brain.

  25. Cyanide • Usage • Insecticides & rodenticide • Electroplating • Nylon • Metal cleaning • PEL:10PPM, • IDHI:50PPM

  26. Cyanidemeasurement • Difficult • BM:thiocyanate level in blood or urine

  27. Cyanidepathophysiology • Cytochrome oxidase enzyme

  28. Cyanideclinical features • Mild: bitter almond taste, irritation of mucous membrane, dyspnea,headache, dizziness, nausea and vomiting, agitation • Severe:hypotention ,arrhythmias, cardiogenic and non-cardiogenic pulmonary edema,lacticacidosis,seizure,coma, • Cherry red skin color • Acute cyanidexp :hyperpnea,respiratory arrest • Delay effect :leukoencephalopathy

  29. Cyanidechronic clinical effects • Skin and MM irritation and ulcer • Thyroid gland enlargement • Rash, bitter almond ,headache • Smokers amblyopia

  30. Cyanidemanagement • Sodium nitrate: 10ml of 30%solution(300 mg) over 5-20 min • Amyl nitrate:0.3ml ampoule crushed every minute inhalation • Sodium thiosulfate:50ml 25%solution(12.5g)IV over 10 minute • Hydroxycobalamine:10ml of 40% solution(4g) iv over 20 min

  31. Case3 • آقاي 27 ساله –كارگر دامپروري -به منظور تميز كردن پمپ داخل گودالي از كود به عمق 6 متر مي شود.پس از پايين رفتن در حدود 3 متر داخل گودال سقوط مي كند.همكار فرد داخل گودال مي شود تا وي را نجات دهد كه او نيز به داخل گودال سقوط مي كند.20دقيقه بعد نيروي امداد مي رسد و با كمك آپارات هردو را خارج مي كند ولي هردو نفر در مسير بيمارستان فوت مي كنند

  32. Hydrogen sulfidegeneral consideration • Irritant • Asphyxiant in cellular level and inactive cytochrome oxidase • Odor threshold: 5ppm :rotten eggs • Irritant threshold: 10ppm • >100ppm: toxic effect on the olfactory nerve

  33. Hydrogen sulfideexposure • Decay of organic sulfur-containing material: sewer gas • Petroleum process • Underground coal mines • Livestock raising • Nuclear reactors • Sour gas • TLV:20PPM • IDHL:100PPM

  34. Hydrogen sulfideacute clinical effects • CNS abnormality :rapid loss of consciousness“knockdown” • Respiratory paralysis • Tachycardia and hyperpenea,cv collapse • Irritation effects: from MM to pulmonary edema

  35. Hydrogen sulfidechronic clinical effects • Irritation • Loss of odor sensation • Cognitive and personality

  36. H2S Awareness

  37. Hydrogen sulfideclinical evaluation • Awareness of the circumstances: patients breath , clothing • Urinary thiosulfate??

  38. Hydrogen sulfidemanagement • O2 100% • Sodium nitrate 300mg,iv for2-4min

  39. Ozone’s Effects on Health:A Story of Good and Bad Where Healthcare Meets Policy

  40. We Must First Understand Ozone to Understand the Effects It Has on Our Health Ozone: Discovered in a lab in the mid 1800sFrom the Greek ozein – “to smell” A pungent blue gas, detectable in small amounts Chemical Formula: O3 Highly reactive with many chemicals Source: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: http://www.epa.gov/ozone/science/unepSciQandA.pdf. Accessed February 9, 2005.

  41. What Are the Differences Between Ozone in the Stratosphere and the Troposphere? Stratospheric Ozone • 90% of all ozone exists in “ozone layer” • Naturally forms during chemical reactions between UV sunlight and O2 • 12,000 ozone molecules per billion air molecules • Shields humans from harmful UV rays/stabilizes weather Tropospheric Ozone • 20–100 ozone molecules per billion air molecules • It’s the result of human pollution • Irritates the heart and lungs and traps heat (global warming) Sources: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: http://www.epa.gov/ozone/science/unepSciQandA.pdf. Accessed February 9, 2005. Bell ML, McDermott A, Zeger SL, Samet JM, Dominici F. Ozone and short-term mortality in 95 US urban communities, 1987-2000. JAMA. 2004;292:2372-2378.

  42. Some Human-Produced Chemicals Can Destroy Stratospheric Ozone Refrigerants Air conditioning Foam blowing Industrial cleaning UV protection Weather stabilization Chlorofluorocarbons (CFCs) (Stable in troposphere) Deplete ozone Release chlorine Bromine-containing compounds are even more destructive StratosphereCFCs Broken Down by UV Rays Sources: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: http://www.epa.gov/ozone/science/unepSciQandA.pdf. Accessed February 9, 2005. US Environmental Protection Agency. Ozone Depletion Glossary. Available at: http://www.epa.gov/Ozone/defns.html. Accessed February 9, 2005.

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