Occupational Lung Diseases Quiz

Cellular Injury III: Disturbance in Pigment Metabolism

• Pigments are colored substances found in most living beings, including humans.
• Pigments are classified into exogenous (outside the body) and endogenous (inside the body).

Exogenous Pigments

• Inhaled pigments
• Ingested pigments
• Injected pigments (tattoos)

Endogenous Pigments

• Melanin
• Hemoprotein-derived pigments (haemosiderin, hemosiderin granules, acid hematin, bilirubin, biliverdin, porphyrins)
• Lipofuscin (wear-and-tear pigment)

Pneumoconiosis

• A non-neoplastic lung reaction to mineral dust inhalation.
• The lungs and lymph nodes accumulate various dust particles.
• Dust particles act as mild irritants, increasing connective tissue build-up (fibrosis) and accumulating macrophages.
• Associated with certain occupations, considered occupational lung diseases.
• The three common mineral dusts causing pneumoconiosis are coal dust, silica, and asbestos.

Anthracosis

• Deposition of carbon or coal dust in the lungs.
• Observed in horses and mules used in coal mines.
• Also seen in dogs living in areas with significant coal dust, soot, and smoke pollution.
• Pulmonary anthracosis is a common exogenous pigment-induced pulmonary lesion in coal miners and smokers.
• Inhaled carbon pigment is engulfed by alveolar macrophages and accumulates in connective tissue, including the pleural lymphatics and lymph nodes.
• Pulmonary anthracosis occurs without noticeable symptoms (asymptomatic).
• Classified into two types:
• Simple coal worker's pneumoconiosis (CWP)- Macrophage accumulations with minimal pulmonary dysfunction.
• Complicated CWP or progressive massive fibrosis- Extensive fibrosis and lung function impairment. Anthracosis can progress into complicated form over years.

Silicosis

• Deposition of fine silica (silicon dioxide) particles in the lungs.
• More prevalent in humans than animals.
• Workers in sandblasting and hard-rock mining are at higher risk.
• A slowly progressing nodular, fibrosing pneumoconiosis (silicotic fibrotic nodules).
• After inhalation, silica particles interact with epithelial cells and macrophages, triggering mediator release (IL-1, TNF, fibronectin, lipid mediators, oxygen-derived free radicals, and fibrogenic cytokines)
• Affected lungs are nodular and firm, with fibrotic lesions in lymph nodes and the pleura.
• The involved tissues exhibit concentric layers of hyalinized center surrounded by inflammatory cells and fibroblasts.

Asbestosis

• A type of exogenous pigment due to asbestos (magnesium silicate) inhalation.
• Characterized by diffuse pulmonary interstitial fibrosis, with presence of characteristic asbestos bodies. These fibers are coated with glycoprotein and hemosiderin, presenting as beaded or dumbbell-shaped structures.
• Asbestos bodies stain positively for Prussian blue reaction.
• Affected lungs are small, gray, and firm, with variable degrees of pulmonary fibrosis (especially in subpleural and basal areas).
• Prolonged asbestos dust exposure can lead to asbestosis, pleural disease, and lung tumors.

Siderosis

• Deposition of iron in the lungs, accompanied by pigmentation and cellular reaction.
• Resulting from iron dust inhalation, seen in horses, mules and dogs working in or around iron mines, smelters, and foundries.
• Initially, iron dust causes focal brown/rusty-red pigmentation due to macrophage accumulation.
• Pigmentation becomes diffuse as dust accumulates.
• Iron is mildly irritating, so only slight fibrosis is noted.
• If silica is present, substantial lung fibrosis results.
• Prussian blue test (iron placed in potassium ferrocyanide solution and hydrochloric acid) yields blue-colored tissue.
• Not usually clinically significant unless iron and/or silicon levels are extreme.

Ingested Pigments

• Chronic ingestion of certain metals can cause pigmentation:
• Argyria (silver compounds) - brownish pigmentation in skin, bowel, and kidneys.
• Chronic lead poisoning (plumbism) - characteristic blue lines on teeth
• Melanosis coli (certain cathartics) -pigmentation of the colon.
• Carotenaemia (carrots) - yellowish-red skin coloration.

Injected Pigments (Tattooing)

• Pigments like India ink, cinnabar, and carbon introduced into dermis; taken up by macrophages and remain permanent in connective tissues.
• Prolonged use of mercury-containing ointments, wound contamination, tattooing by dyes are additional causes of injected pigments.

Hemoprotein-Derived Pigments

• Hematogenous pigments are the most important endogenous pigments derived from hemoglobin, cytochromes, and their breakdown products.
• The average life span of an erythrocyte is approximately 120 days.
• Degradation of red blood cells within phagocytic cells (spleen, liver, bone marrow) releases hemoglobin components: globin, iron, and heme.
• Globin is soluble and removed by blood/lymph.
• Iron is normally stored as ferritin micelles, within cells.
• Ferritin forms hemosiderin granules, which are visible with light microscopy.
• Hemosiderin pigment represents large aggregates of ferritin micelles.

Jaundice (Icterus)

• Bilirubin is a normal non-iron containing pigment found in bile.
• Derived from the porphyrin ring of heme in hemoglobin.
• Normal bilirubin level in blood is less than 1 mg/dL.
• Excess bilirubin, or hyperbilirubinemia, causes jaundice (yellow discoloration of tissues rich in elastin, such as aorta, skin, and sclera).
• Hyperbilirubinemia can be unconjugated or conjugated.
• Prehepatic (hemolytic) causes include excessive red blood cell destruction.
• Hepatic (intrahepatic) causes include liver cell damage.
• Post-hepatic (obstructive) causes include bile duct obstruction.

Lipofuscin (Wear and Tear Pigment)

• Insoluble yellowish-brown granular intracellular pigment (lipofuscin or lipofuscin granules).
• Generally found in atrophied cells of older animals.
• Also observed in various cells during wasting diseases, unrelated to aging, such as hepatocytes, myocardial fibers, Leydig cells in testes and neurons in senile dementia
• Lipofuscin is a product of free radical damage to cell components and accumulation of undigested substances within the cells.

Pathological Calcification

• Abnormal calcium salt deposits in soft tissues other than ossified tissues (such as bone and teeth).
• May be categorized as dystrophic or metastatic:
• Dystrophic calcification: Deposits in dead or degenerating tissues, with normal serum calcium levels
• Metastatic calcification: Deposits in normal tissues, with abnormal calcium metabolism and hypercalcemia.

Gout (Urates & Uric Acids)

• A retrogressive disease characterized by urate and uric acid crystal deposition in various tissues, mainly joints.
• Deposition stems from an increase in uric acid concentration within blood (hyperuricemia).
• Causes can be primary (unknown) and secondary (known cause of hyperuricemia). Possible causes include :Renal dysfunction • High-protein diet or unique type of protein • Vitamin A deficiency due to lack of green food • Insufficient exercise Hereditary predisposition