Asbestosis

Background

Pneumoconiosis is the general term for lung disease caused by inhalation and deposition of mineral dust.

Pneumoconiosis caused by asbestos inhalation is called asbestosis. The word asbestos is derived from Greek and means inextinguishable, and asbestos is a group of naturally occurring, heat-resistant fibrous silicates. Asbestos fibers are long and thin (length-to-diameter ratio >3) and may be either curved or straight. The curved fibers are called serpentine (chrysotile is the prime example), and the straight fibers are amphiboles. Several different types of amphiboles (ie, amosite, anthophyllite, tremolite, actinolite, crocidolite) have been recognized. Chrysotile is by far the most common type of asbestos fiber produced in the world and accounts for virtually all asbestos used commercially in the United States.
Production and use of asbestos increased greatly between 1877 and 1967. In the 1930s and 1940s, scientists recognized a causal link between asbestos exposure and asbestosis. In the 1950s and 1960s, researchers established asbestos as a predisposing factor for bronchogenic carcinoma and malignant mesothelioma.

Note the image below.
Asbestos pleural plaques. 

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Causes

In modern times, the risk to persons in the United States occurs mainly through the processing, manufacturing, and end-use of asbestos.
Manufacturers commonly use asbestos in the following products:

• Products containing asbestos cement - Pipes, shingles, clapboards, sheets
• Vinyl-asbestos floor tiles
• Asbestos paper in filtering and insulating products
• Material in brake linings and clutch facings
• Textile products - Yarn, felt, tape, cord, rope
• Spray products used for acoustical, thermal, and fireproofing purposes

Examples of occupations associated with asbestosis include the following:

• Insulation workers
• Boilermakers
• Pipefitters
• Plumbers
• Steamfitters
• Welders
• Janitors
   Imaging
  
  Case 1. Postero-anterior (PA) chest radiograph in a 58-year-old man with a history of occupational exposure to asbestos shows right diaphragmatic pleural plaque calcifications, linear calcification along the left pericardium, and bilateral pleural plaques along upper ribs. 
  
   Case 4. The soft-tissue window setting of this chest computed tomography (CT) scan shows the envelope-like mass along the pleural surface surrounding the lung. This was a mesothelioma.

  Pleural calcification

  On chest radiographs, the prevalence of calcification in pleural plaques is reported to be 10-15%. In profile, calcified plaques appear as opaque lines that lie parallel to the chest wall, mediastinum, pericardium, and diaphragm. Viewed en face, calcified plaques are seen as irregular, heterogeneous densities, the so-called holly leaf. The presence of bilateral, superior diaphragmatic surface calcifications with clear costophrenic angles is virtually pathognomonic for asbestos-related pleural disease. (See the image below.)
  Case 1. Postero-anterior (PA) chest radiograph in a 58-year-old man with a history of occupational exposure to asbestos shows right diaphragmatic pleural plaque calcifications, linear calcification along the left pericardium, and bilateral pleural plaques along upper ribs.
  

  
  

A-a gradient

Alveolar-arterial gradient

Pathophysiology sample values

BMP/ELECTROLYTES:
Na+=140	Cl−=100	BUN=20	/
			Glu=150
K+=4	CO2=22	PCr=1.0	\
ARTERIAL BLOOD GAS:
HCO3-=24	paCO2=40	paO2=95	pH=7.40
ALVEOLAR GAS:
	pACO2=36	pAO2=105	A-a g=10
OTHER:
Ca=9.5	Mg2+=2.0	PO4=1
CK=55	BE=−0.36	AG=16
SERUM OSMOLARITY/RENAL:
PMO = 300	PCO=295	POG=5	BUN:Cr=20
URINALYSIS:
UNa+=80	UCl−=100	UAG=5	FENa=0.95
UK+=25	USG=1.01	UCr=60	UO=800
PROTEIN/GI/LIVER FUNCTION TESTS:
LDH=100	TP=7.6	AST=25	TBIL=0.7
ALP=71	Alb=4.0	ALT=40	BC=0.5
		AST/ALT=0.6	BU=0.2
AF alb=3.0	SAAG=1.0		SOG=60
CSF:
CSF alb=30	CSF glu=60	CSF/S alb=7.5	CSF/S glu=0.4

The Alveolar-arterial gradient (A-a gradient), is a measure of the difference between the alveolar concentration of oxygen and the arterial concentration of oxygen. It is used in diagnosing the source of hypoxemia.^[1]

Equation

A-a gradient = PA_O2 − Pa_O2^[2]

On Room air ( 21 % ) and at sea level, a simplified version of the equation is:
Aa Gradient = (150 - 1.2*(PCO2)) - PaO2

Values and meaning

The A-a gradient is useful in determining the source of hypoxemia. The measurement helps isolate the location of the problem as either intrapulmonary (within the lungs) or extrapulmonary (somewhere else in the body).
A normal A-a gradient for a young adult non-smoker breathing air, is between 5-10 mmHg. Normally, the A-a gradient increases with age. For every decade a person has lived, their A-a gradient is expected to increase by 1 mmHg.
An abnormally increased A-a gradient suggests a defect in diffusion, V/Q (ventilation/perfusion ratio) mismatch, or right-to-left shunt.^[3]
Because A-a gradient is approximated as: (150 - 5/4(P_CO2)) - Pa_O2, the direct mathematical cause of a large value is that the blood has a low P_O2, a low P_CO2, or both. CO2 is very easily exchanged in the lungs and low P_CO2 directly correlates with high minute ventilation; therefore a low arterial P_CO2 indicates that extra respiratory effort being used to oxygenate the blood. A low P_O2 indicates that at the patient's current minute ventilation (whether high or normal) is not enough to allow adequate oxygen diffusion into the blood. Therefore the A-a gradient essentially demonstrates a high respiratory effort (low arterial P_CO2) relative to the achieved level of oxygenation (arterial P_O2). A high A-a gradient could indicate a patient breathing hard to achieve normal oxygenation, a patient breathing normally and attaining low oxygenation, or a patient breathing hard and still failing to achieve normal oxygenation.
If lack of oxygenation is proportional to low respiratory effort, then the A-a gradient is not increased; a healthy person who hypoventillates would have hypoxia, but a normal A-a gradient