Pathology of environmental diseases

Dr. Arushi Agarwal

JR-1Pathology

Environmental diseases are conditions caused by exposure to chemical or physical agents in the ambient, work-place and personal environment

Causes of environmental diseasesOccupational Other air pollutants Effects of Tobacco, alcohol Effects of climateToxic agentsTherapeutic drugs Injury by physical agents

Pneumoconiosis Diseases

induced by

◦Organic/inorganic particulates

◦Chemical fumes◦Vapors

Pathogenesis Depends on:

◦ Amount of dust retained

◦ Size, shape and buoyancy of particles

◦ Particle solubility and physiochemical reactivity

◦ Additional effect of other irritants

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

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

MorphologyMost innocuous

Inhaled carbon pigment

Engulfed by alveolar/interstitial macrophages

Accumulates in lymphatics

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

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

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

More common in African-Americans than Whites

Occupations related to: Repair/demolition of

buildings and roads Stone carvers Jewelers using chalk

molds Sandblasting Mining

Silica Crystalline and amorphousCrystalline (quartz, cristobalite, tridymite)

more fibrogenic Inhalation phagocytosis inflammosome

activation inflammatory mediators(IL-1,18)

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)

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

Further progression:◦ Expansion,

coalescence of lesions

◦ Progressive massive fibrosis

Histologically ◦ Central area of whorled collagen fibres◦ Peripheral zone of dust-laden

macrophages

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

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

Amphiboles Less commonly

used More pathogenic

(mesothelioma) Stiff, straight Aligns in

airstreams Goes deeper into

the lungsAsbestos body revealing typical beading and knobbed ends

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

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

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

Tobacco Smoke

Active smokingPassive smokingTypes of injury

◦ Carcinogens◦ Cell irritants & damage◦ Poisons◦ Drug related

Diseases◦ Multiple cancers◦ Atherosclerosis◦ Penile dysfunction◦ Emphysema◦ Bronchitis

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

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

• 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

Thank you