pathology of environmental diseases
TRANSCRIPT
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Pathology of environmental diseases
Dr. Arushi Agarwal
JR-1Pathology
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Environmental diseases are conditions caused by exposure to chemical or physical agents in the ambient, work-place and personal environment
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Causes of environmental diseasesOccupational Other air pollutants Effects of Tobacco, alcohol Effects of climateToxic agentsTherapeutic drugs Injury by physical agents
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Pneumoconiosis Diseases
induced by
◦Organic/inorganic particulates
◦Chemical fumes◦Vapors
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Pathogenesis Depends on:
◦ Amount of dust retained
◦ Size, shape and buoyancy of particles
◦ Particle solubility and physiochemical reactivity
◦ Additional effect of other irritants
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Coal Worker’s PneumoconiosisLung disease Caused by inhalation of
◦ coal particles◦ Other admixed forms of dust
Coal dust contaminated with silica: progressive disease
Coal workers may also develop emphysema, chronic bronchitis
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Clinical features Usually benign; causing little
decrement in lung function Leads to increased pulmonary
dysfunction, pulmonary hypertension and cor pulmonale in <10% cases
May continue to worsen even if further exposure is prevented
Use of ‘smoky coal’ associated with increased risk of lung cancer
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MorphologyMost innocuous
Inhaled carbon pigment
Engulfed by alveolar/interstitial macrophages
Accumulates in lymphatics
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Coal workers pneumoconiosis
Simple
• Coal macules (1-2mm in dia)• Nodules• Scattered throughout the lung• Upper lobes/upper zones of
lower lobes more common• Adjacent to respiratory
bronchioles• May give rise to centrilobular
emphysema
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Complicated/ progressive massive fibrosis
• Occurs on background of simple disease• Requires many years to
develop• Multiple, intense blackened
scars >1cm, • Lesions consists of dense
collagen and pigment• Necrotic centre due to local
ischaemia
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Silicosis Lung disease caused by:
Proinflammatory crystalline silicon dioxide
(silica)
Presents after years of exposure as Slowly progressing Nodular Fibrosing pneumoconiosis
Acute silicosis Heavy exposure over months –few years Accumulation of abundant lipoproteinaceous material within
alveoli
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More common in African-Americans than Whites
Occupations related to: Repair/demolition of
buildings and roads Stone carvers Jewelers using chalk
molds Sandblasting Mining
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Silica Crystalline and amorphousCrystalline (quartz, cristobalite, tridymite)
more fibrogenic Inhalation phagocytosis inflammosome
activation inflammatory mediators(IL-1,18)
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Clinical courseChest x-ray: fine nodularity in upper zonesPulmonary function normal to moderately
affectedAssociated with increased susceptibility to
tuberculosisOnset may be:
Slow and insidious (10-30yrs) Rapid (weeks to months after intense exposure) Accelerated (within 10yrs)
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Morphology In early stages:
◦ Tiny, barely palpable, discrete, pale-black nodules
◦ In hilar lymph nodes and upper zones of lungs
As disease progresses:◦ Nodules may undergo central
softening, cavitation◦ Fibrotic lesion in hilar lymph nodes
and pleura◦ Eggshell calcification
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Further progression:◦ Expansion,
coalescence of lesions
◦ Progressive massive fibrosis
Histologically ◦ Central area of whorled collagen fibres◦ Peripheral zone of dust-laden
macrophages
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Asbestos-related diseasesAsbestos:
◦ Family of proinflammatory crystalline hydrated silicates associated with Pulmonary fibrosis Carcinoma Mesothelioma Pleural effusion Other carcinomas: laryngeal, ovarian etc.
◦ Tumor initiator and promoter
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Pathogenesis Disease causing capabilities depend
on Concentration, size, shape, solubility
Serpentine chrysolite : More commonly used Less pathogenic Flexible and curled Gets impacted in respiratory tracts Removed by mucociliary elevators
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Amphiboles Less commonly
used More pathogenic
(mesothelioma) Stiff, straight Aligns in
airstreams Goes deeper into
the lungsAsbestos body revealing typical beading and knobbed ends
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Asbestosis Begins in the lower lobesDiffuse pulmonary
interstitial fibrosisAsbestos bodies
Golden brown Fusiform or Beaded rods with
translucent centre, asbestos fibres coated with iron-containing proteinaceous material
• Pleural plaques
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Other air pollutants Carbon monoxide (CO) Nonirritating, colorless, tasteless, odorless gas Product of imperfect oxidation Affinity of CO to Hb is 200x higher, than that of O2 -
carboxyhemoglobin - systemic hypoxia Acute intoxication - cherry red skin, liquid blood (no post-
mortal coagulation) Hb saturated with CO
◦ 20-30% = systemic hypoxia◦ 60-70% =unconsciousness, death
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Indoor air pollutants Wood-smoke contains oxides of nitrogen, may
predispose to lung infections Bio-aerosols may cause legionnaires disease, viral
pneumonia, eye irritation, allergies etc. Radon: radioactive gas may cause lung cancer Formaldehyde may cause breathing difficulties, eye
irritation etc. Sick-building syndrome
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Tobacco Smoke
Active smokingPassive smokingTypes of injury
◦ Carcinogens◦ Cell irritants & damage◦ Poisons◦ Drug related
Diseases◦ Multiple cancers◦ Atherosclerosis◦ Penile dysfunction◦ Emphysema◦ Bronchitis
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Tobacco
• Cigarette smoking facts– Causes 90% of lung cancers
– Can cause lung cancer in non-smokers as “secondhand
smoke”
– Causes more than 5 million deaths annually from:• Cardiovascular disease
• Cancer
• Chronic respiratory problems
– Of people alive today, 500 million will likely die of
smoking-related causes
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Lung cancer– Polycyclic hydrocarbon and nitrosamine metabolites
cause mutations in oncogenes and tumor suppressor genes
Emphysema and bronchitis– Leukocyte recruitment to lung
– Increased elastase production
– Chronic tissue damage
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• Myocardial infarction and stroke
– Increased platelet aggregation
– Decreased myocardial oxygen supply
• Lung disease
• Smoking while pregnant increases the risk of:
– Preterm birth– Intrauterine growth restriction– Spontaneous abortion
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Thank you