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Environment Pathology and Disease

This article explores the various diseases and lesions caused by chemical or physical injuries in the environment. It discusses exposure sources, mechanisms of toxicity, and the absorption and distribution of toxicants. It also covers environmental pollution, industrial exposures, and specific diseases like pneumoconiosis, silicosis, and asbestosis.

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Environment Pathology and Disease

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  1. Environment Pathology and Disease Bethy S Hernowo Faculty Of Medicine UniversitasPadjadjaran

  2. Environmental Disease ٭ Diseases & lesions caused by chemical or physical injuries ٭ Environmental disease : common ٭ ILO (International Labor Organization) estimated : 1.1 million people, work-relate d injuries & illnesses

  3. Sources of Exposure • Environmental • Man-made • Intentional (Hg, Minimata, Japan) • Accidental • methyl isocyanate, Bhopal, India • radiation, Chernobyl • Natural (H2S/CO/CO2, Cameroon) • Occupational (mining, dye, chemical) • Iatrogenic (drugs) • Self-administered (substance abuse, suicide)

  4. Mechanisms of Toxicity • Corrosive, tissue destruction (acids, alkali) • desiccation • protein destruction • denaturation • hydrolysis • fat saponification • Inhibition of enzyme activity cyanide: cytochrome oxidase

  5. ABSORPTION and DISTRIBUTIONS of TOXICANTS

  6. Environmental Pollution Air pollution 1. Outdoor Air Pollution 1.1. Ozone 1.2. Nitrogen dioxide 1.3. Sulfur dioxide 1.4. Carbon monoxide 1.5. Lead 1.6 Particulates

  7. Major Outdoor Air pollutants

  8. Patterns Of Lung injury Related To Air Pollution

  9. Air pollution 2. Indoor Air Pollution 2.1. Tobacco smoke 2.2. Carbon monoxide 2.3. Nitrogen dioxide 2.4. Wood Smoke 2.5. Formaldehyde 2.5. Radon 2.6. Asbestos fibers 2.7. Manufactured mineral fibers 2.8 Bioaerosol

  10. Health Effects Of Indoor Air Pollutans

  11. Toxic And carcinogenic Metals

  12. Heavy Metal Toxic Agents • Mercury (HgCl2 , ATN; org Hg, CNS function) • Lead ( inhibits heme synthesis, CNS function, kidneys, GI) • 2-11% of children in US exceed 10 μg/dL • Arsenic • Iron

  13. Industrial Exposures

  14. Pneumoconiosis ٭ The non-neoplastic lung reaction to inhalation of mineral dust ٭ Agent : coal dust, silica, asbestos, beryllium ٭ Coal Workers’ Pneumoconiosis (CWP) Spectrum of lung finding in coal workers 1. Asymptomatic anthracosis 2. Simple Coal workers pneumoconiosis 3. Progressive massive fibrosis (PMF)

  15. Mineral Dust –Induced Lung Disease

  16. Pathogenesis of Pneumoconiosis

  17. Morphology 1. Pulmonary anthracosis Inhaled carbon pigment is engulfed by alveolar or interstitial macrophage, then accumulate in connective tissue  linear streak & aggregates pigment identify pulmonary lymphatic & mark the pulmonary lymph node 2. Simple CWP Characterized : coal macules & coal nodule. coal macules consist : dust-laden macrophages. The lesion scattered, but uppers lobes & upper zones of the lower lobes more heavily involved

  18. Morphology 3. Caplan syndrome Coexistence of rheumatoid arthritis with a pneumoconiosis  development distinctive nodular develop fairly rapidly The nodular lesions  central necrosis surrounded by palisading fibroblast, palsma cells, macrophages containing coal dust & collagen The syndrome also occur in asbestosis & silicosis

  19. Clinical course CWP • CWP usually benign  produce little decrement in lung function • Minority cases pulmonary dysfunction, hypertension & cor pulmonale • CWP  PMF (progressive massive fibrosis) linked variety factors : coal dust exposure level & total dust burden • PMF  tendency to progress even absence exposure

  20. Silicosis ٭ Caused by inhalation crystalline silica ٭ Occupations associated development silicosis : quarry mining, sandblasting, drilling, tunneling, & stone cutting ٭ Incidence : 1500 cases each year in US ٭ Silica : 1. Crystalline : quartz, cristobalite, tridymite ( most toxic and fibrogenic) 2. Amorphous forms (most commonly implicated in silicosis)

  21. Classification Silicosis • Acute silicosis : exposure very high level of silica & develops quickly • Chronic ( nodular ) silicosis: exposure over prolonged periods  Characteristic fibrotic nodules of silicosis • Complicated ( conglomerate silicosis)  result progression of chronic silicosis • Other pulmonary disease : silicosis associated with TBC

  22. Morphology Gross : Characteristic nodule in early stage: tiny, barely palpable, discrete, pale-to-blackened, nodules in upper zones Microscopically : silicotics nodule demonstrates concentrically arranged hyalinized collagen fibers surrounding an amorphous center.

  23. Microscopically: Silicosis

  24. Clinical course ≈ Chronic silicosis  detected routine chest radiographs (asymptomatic) ≈ Radiographs : fine nodularity in the upper zones  function : normal/ moderately affected ≈ Most patients do not develop shortness of breath until late in the course ≈ The disease  slow to kill

  25. Asbestosis » Asbestos  family of crystalline hydrated silicates » Occupotional exposure to asbestos, linked to: • Parenchymal interstitial fibrosis (asbestosis) • Bronchogenic carcinoma • Pleural effusions • Localized fibrous plaque, rarely diffuse fibrous plaque • Malignant pleural & peritoneal mesothelioma • Laryngeal carcinoma

  26. Pathogenesis Asbestosis ٭ Dictate : concentration, size, shape & solubility of different forms asbestos ٭ Two forms asbestos: 1. Serpentine (fiber is curly & flexible) : Chrysotile 2. Amphibole (fiber is straight, stiff,& brittle)  more pathogenic ٭ The greater pathogenicity amphiboles related: 1. Chrysotiles impacted respiratory  removed mucociliary  trapped gradually leached from tissue 2. Amphiboles  align themselvesairstream  deliver deeper  penetrate epithelial cells  reach interstitium

  27. Morphology Gross: diffuse pulmonary interstitial fibrosis Microscopically : Characteristic  asbestos bodies : golden brown, fusiform or beaded rods with a translucent center. They consist of asbestos fibers coated with an iron containing proteinaceous material. Pleural plaque : well-circumscribes plaque of dense collagens

  28. Asbestos Body

  29. Clinical course ≈ Indistinguishable from other diffuse interstitial lung disease ≈ Typically, progressively worsening dyspnea appears 10-20 years after exposure ≈ The disease may static or progress to congestive heart failure, cor pulmonale and death.

  30. Tobacco Smoking • 400,000 deaths/yr (21% of all deaths in US) • 50 Million smokers in US • Smoke composition • carcinogens (polycyclic HC, b-naphthylamine, nitrosamines) • Irritants and toxins • ammonia, formaldehyde, oxides of nitrogen • CO • Nicotine

  31. Relative Disease RisksAssociated with Smoking Male Female Lung Ca death 22 12 Mouth Ca 27 6 Larynx Ca 10 18 Esophogus Ca 8 10 CAD >35 yo 3 2 Cerebro VD >35 yo 4 5 COPD 10 10 Ill health effects of smoking partially reversible

  32. Tobacco smoke

  33. Adverse effects of smoking

  34. Injury By Chemical Agents Mechanisms of chemical injury: • Dose • Requirement for metabolic conversion • Sites of absorption, accumulation, or excretion • Individual variation • The capacity of the chemical to induce an immune response • Unintentional transmission of infections

  35. Injury by Therapeutic Agents (adverse Drug Reactions)

  36. Exogenous Estrogens And Oral Contraceptives • Exogenous Estrogens ( alone & usually natural estrogen) Adverse effects of estrogen therapy : » Endometrial carcinoma » Breat carcinoma » Thromboembolism » Cardiovascular disease

  37. 2. Oral contraseptives Adverse effects of oral contraseptives ( contain synthetic estrogens & always with progestin) 1.Breast carcinoma 6.Hypertension 2.Endometrial cancer 7. Hepatic adenoma 3.Cervical cancer 8. Gallbladder disease 4.Ovarian cancer 9. Cadiovascular 5.Thromboembolism disease

  38. Acetaminophen ≈ When taken very large doses  hepatic necrosis ≈ The window therapeutic dose : 0,5 gr ≈ Toxic dose : 15-25 gr ≈ Toxicity begins : nausea, vomiting, diarrhea, sometimes shock and jaundice ≈ Serious overdose : liver failure, renal and myocardial damage

  39. Aspirin (Acetylsalicylic Acid) ≈ Overdose ( 2-4 gr) : accidental ingestion of large number table  young children ≈ Suicidal ( 10-30 gr)  adult ≈ Effects : at first : respiratory alkalosis  metabolic acidosis death ≈ Chronic : take > 3 gr daily  headache, dizziness, tinnitus, difficulty hearing, mental confusion, nausea, vomiting and diarrhea

  40. Injury by Non therapeutic Toxic Agents 1. Lead poisoning 2. Carbon monoxide 3. Alcohol and drug abuse

  41. Clinical And Pathologic Features Of Lead Poisoning

  42. Lead Lines

  43. Lead causes injury by its multiple metabolic effects: • High affinity for sulfhydryl groups & interferes with enzymes • Competes with calcium • Interferes with membrane-associated enzymes • Interferes with nerve transmission and brain • Membrane effects damage the kidneys

  44. Morphology Major target of Lead toxicity : blood, CNS, GIT and kidneys • Blood changes  characteristic  result lead accumulation occur fairly early. • Brain damage is prone to occur in children • GIT : colic, extremely severe • Kidney : proximal tubular damage with intranuclear lead inclusions.

  45. Normal Kidney

  46. Acute Tubular Necrosis

  47. Carbon Monoxide ٭ Nonirritating, colorless, tasteless, odorless  imperfect oxidation of carboneceous materials  continues to be cause accidental & suicidal death ٭ CO kills by inducing CNS depression ٭ CO act as a systemic asphyxiant carboxyhemoglobin incapable carrying oxygen ٭Acute Poisoning: generalized cherry-red color skin & mucous membrane ٭chronic poisoning : evoke widespread ischemic changes in the CNS

  48. Classification Of Drugs Of Abuse

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