short presentation focussing on pneumoconioses

1. Pathology of
environmental
diseases
Dr. Arushi
Agarwal
JR-1

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

3. Causes of environmental
diseases
 Occupational
 Other air pollutants
 Effects of Tobacco, alcohol
 Effects of climate
 Toxic agents
 Therapeutic drugs
 Injury by physical agents

4. Pneumoconiosis
 Diseases induced
by
◦ Organic/inorganic
particulates
◦ Chemical fumes
◦ Vapors

5. Pathogenesis
 Depends on:
◦ Amount of dust retained
◦ Size, shape and
buoyancy of particles
◦ Particle solubility and
physiochemical
reactivity
◦ Additional effect of
other irritants

6. Coal Worker’s
Pneumoconiosis
 Lung 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

7. 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

8. Morphology
 Most innocuous
 Inhaled carbon pigment
 Engulfed by alveolar/interstitial
macrophages
 Accumulates in lymphatics

9. 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

10. 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

11. 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

12.  More common in African-
Americans than Whites
 Occupations related to:
 Repair/demolition of
buildings and roads
 Stone carvers
 Jewelers using chalk
molds
 Sandblasting
 Mining

13. Silica
 Crystalline and amorphous
 Crystalline (quartz, cristobalite, tridymite) more
fibrogenic
 Inhalation phagocytosis inflammosome
activation
inflammatory mediators(IL-1,18)

14. Clinical course
 Chest x-ray: fine nodularity in upper zones
 Pulmonary function normal to moderately
affected
 Associated with increased susceptibility to
tuberculosis
 Onset may be:
 Slow and insidious (10-30yrs)
 Rapid (weeks to months after intense exposure)
 Accelerated (within 10yrs)

15. 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

16.  Further
progression:
◦ Expansion,
coalescence of
lesions
◦ Progressive
massive fibrosis Histologically
◦ Central area of whorled collagen fibres
◦ Peripheral zone of dust-laden macrophages

17. Asbestos-related diseases
 Asbestos:
◦ Family of proinflammatory crystalline hydrated
silicates associated with
 Pulmonary fibrosis
 Carcinoma
 Mesothelioma
 Pleural effusion
 Other carcinomas: laryngeal, ovarian etc.
◦ Tumor initiator and promoter

18. 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

19.  Amphiboles
 Less commonly
used
 More pathogenic
(mesothelioma)
 Stiff, straight
 Aligns in
airstreams
 Goes deeper into
the lungs
Asbestos body revealing typical beading and
knobbed ends

20. Asbestosis
 Begins in the lower lobes
 Diffuse pulmonary
interstitial fibrosis
 Asbestos bodies
 Golden brown
 Fusiform or
 Beaded rods with
translucent centre,
asbestos fibres coated
with iron-containing
proteinaceous material
• Pleural plaques

21. 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

22. 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

23. Tobacco Smoke
 Active smoking
 Passive smoking
 Types of injury
◦ Carcinogens
◦ Cell irritants & damage
◦ Poisons
◦ Drug related
 Diseases
◦ Multiple cancers
◦ Atherosclerosis
◦ Penile dysfunction
◦ Emphysema
◦ Bronchitis

24. 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

27. 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

28. • 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