Coal Worker`s Pneumoconiosis

CoalWorker’s Pneumoconiosis


CoalWorker’s Pneumoconiosis


Coalminers’ pneumoconiosis can be caused by anthracosis andanthrascoliosis. Anthracosis refers to a disease that develops incoal miners when they inhale coal dust that does not have silica(Grossman et al., 2014). Coal workers develop anthrascoliosis whenthey inhale coal dust that has silica. Anthracosis is an asymptomaticcondition in many urban dwellers and tobacco smokers due to theaccumulation of carbon in the lungs. In coal workers, the coal dustaccumulates, overwhelming the immune capacity to eliminate it,leading to coal worker’s pneumoconiosis. Normally, the inhaled coaldust gets to the terminal bronchioles, where the carbon is taken upor engulfed by the alveolar and interstitial macrophages.Phagocytosis of coal particles is followed by their transportation tothe mucociliary elevator by macrophages, to be released into mucus orthrough the lymphatic system (Universityof Maryland Medical Center, 2015).

Thecontinued accumulation of the dust-lade macrophages into this systemas seen in coal workers leads to the overwhelming of the expulsionprocess, leading to an immune reaction. This is because since thedust particles have a small diameter of about 2-5 µm, the lungs mustbe exposed to the dust for a significant length of time for thereaction to occur. During the process, fibroblasts are involved inresponding to the alteration by secreting reticulin, a component thatentraps the macrophages. Lysis of the macrophages causes augmentationof the fibroblastic response causing the release of more reticulinthat is then laid down in the area (University of Maryland MedicalCenter, 2015)

Silicain coal augments lysis of macrophages in a faster way, stimulatingthe more collagen to be added by the fibroblasts in the formation ofa collagen network. The lymphatic tree is contained in the pulmonaryinterstitium contained the lymphatic system, the venous and arterialvessels (Kumar, Abbas &amp Aster, 2012). Partial migration of thesemacrophages up the lymphatic system and to the arterioles can causestrangulation of the arterioles due to the resulting interstitialfibrosis. With continued exposure over a long period, moremacrophages that are dying, fibroblasts, reticulin, and theaccumulating network of collagen that is deposited along the vascularsystem causes a compromise in the architecture of the vessels leadingto fibrosis and ischemic necrosis ensues (Grossman et al., 2014).

Theprogressive massive fibrosis seen in patients with CWP reduces theirdiffusing capacity due to loss of lung volume that causes additionalexcessive obstruction of airflow obstruction. Fibrosis of the lungparenchyma and emphysema can complicate pneumoconiosis. Pulmonaryemphysema causes the destruction of the alveolar leading to anincreased alveolar dead space. Furthermore, fibrosis of the lungcauses a reduction in the lung volume and alveolar membranethickening. This causes an increase in the physiologic shunt becauseof reduced perfusion (Kumar,Abbas &amp Aster, 2012).

Theareas that have coal dust focal deposition with pigment-ladenmacrophages are called coal macules. They are the histologic hallmarkof the condition. The extension of these macules allows them to joinother macules in the vicinity causing widespread interstitialfibrosis. The growth of the extensive network of collagen depositedbecause of the fibrosis leads to distention and restriction of therespiratory bronchioles causing emphysema. Widespread focal emphysemacan cause a significant compromise in respiration, therefore causinga ventilation/perfusion mismatch (University of Maryland MedicalCenter, 2015).

Theprevalence of CWP is related to the length and type of exposure.Therefore, those adversely affected are those exposed to highconcentrations. Disease prevalence varies from one mine to anotherand from state to state. In the US, the areas that have coal minesinclude Kentucky, eastern Pennsylvania, West Virginia, westernMaryland and Virginia. Currently, the overall prevalence of CPW isestimated at 30%, and that of progressive massive fibrosis is 2.5%(CDC, 2011). Center for Disease Control conducted a study on a groupof 3,194 coal workers, which was examined for three years and dataregarding evidence from radiographic studies of coal workers`pneumoconiosis (CWP) was collected. These workers were exposed tounderground bituminous coal. The group also included ex-miners. Theprevalence of the diseases was estimated based on the period ofexposure, the rank of coal and age of the workers. Based on thisdata, medium to low-rank coal miners who worked for about 40 years at2 mg /m3 dust limit, which is the current federal limit, had anestimated 1.4% possibility of developing progressive massive fibrosisafter they retire (CDC, 2011). Less severe forms of pneumoconiosishave a higher prevalence. Miners working in high-rank coal areas havea greater risk of developing severe CWP compared to those working inmedium and low-rank coals. Additionally, the study showed thatex-miners who left their occupation due to health-related problemsdeveloped severe forms of CWP compared to the current workers (CDC,2011). In 2013 alone, the restrictive lung disease due topneumoconiosis resulted in the deaths of 260,000 individuals up from251,000 deaths that were reported in 1990. 46,000 of these deathswere because of silicosis with an additional 24,000 caused byasbestosis and lastly 25,000 due to CWP.

Oneof the main complications of CWP is an increased risk of developingthe mycobacterial disease, in particular, tuberculosis (Grossman etal., 2014). Mycobacteria tuberculosis infection results from exposureof the lungs and the mucous membrane to aerosols that are infected.The aerosols are 1-5 μm in diameter. A single cough from a personwith an active infection can generate up to 3000 droplets, with only10 bacilli required to initiate active infection (Kumar, Abbas &ampAster, 2012). After inhalation of the droplet nuclei, they aredeposited in the lung’s terminal airspaces. An incubation of 2-12weeks is required before the organisms reach one thousand to tenthousand in number, a number that is enough for an immune reactionsufficient to be detected by the tuberculin skin test to occur.Mycobacteria have a high antigenicity, promoting a rapid and diffuseimmune reaction. The antigenicity is due to multiple constituents onthe mycobacterial cell wall that include phospholipids, glycoproteinsand wax D. All these cause activation of Langerhans cells,polymorphonuclear and leukocytes lymphocytes (Grossman et al., 2014).

Afterinfection, the M. tuberculosis can be cleared by the immune system ofthe host or just suppressed in a latent form called latent TBinfection (LTBI). These individuals cannot spread TB. Lungs are thecommonest site of TB development with 85% of patients complaining ofpulmonary manifestations. This makes the diseases one of thecommonest complications in people who have coal workerspneumoconiosis (Grossman et al., 2014).

TBlesions are typically epithelioid granulomas with a central point ofcaseous necrosis. The alveolar macrophages found in subpleuralregions are the most common sites of TB primary lesions. Ghoncomplexes are formed due to local proliferation and spreading throughthe lymphatic system to the hilar nodes. 0.5- to 3-mm tuberclenodules show three or four cellular zones with central caseationnecrosis, a zone of Langhans giant cells and epithelioid macrophagesmixed with lymphocytes, another cellular zone consisting of plasmacells, lymphocytes, and immature macrophage and lastly a rim offibrosis, which represents lesions that are healing (Kumar, Abbas &ampAster, 2012).


Chronicobstructive pulmonary disease (COPD) is a disease condition due to areduction in the airflow into the pulmonary tree. This conditionrequires time for its development hence, it worsens over time ifappropriate medical intervention is not instituted. Although thecondition is non-reversible, appropriate therapy can reduce itsprogression and the extent of damage (Kumar, Abbas &amp Aster,2012). Patients with this condition are able to inhale normally.However, they have difficulties in exhalation due to changes in thesmall tubular airways because the changes involved in the conditioncause the airways to narrow during exhalation. In many cases of COPD,the small air sacs in the lungs are destroyed, leading to asignificant compromise in gaseous exchangeability. The two majordiseases in this category, which are emphysema and chronicbronchitis, are the major causes of the respiratory compromise(Kumar, Abbass &amp Aster, 2012).

Patientswith chronic obstructive pulmonary disease typically present clinicalmanifestations of emphysema, chronic bronchitis and reactive airwaydisease. These clinical manifestations include a productive coughcharacterized by colorless sputum that worsens in the morning,breathlessness, which is the most significant clinical manifestation.It does not fully manifest until the sixth decade of the patient’slife. Additional clinical manifestations include an acute chestillness and wheezing, which occurs during exacerbations and exertionsin some patients (Grossman et al., 2014). The physical examination isusually specific and sensitive for severe diseases, but poor in mildand moderate forms. These include respiratory distress and tachypneawith simple activity, the Hoover sign (paradoxical lower chest wallindrawing), cyanosis, peripheral edema and an elevated jugular venouspressure (JVP). Additional physical findings on thoracic examinationincluded decreased breath sounds, thoracic hyperinflation causing abarrel chest, hyper-resonance when percussing and prolongedexpiration (Kumar, Abbas &amp Aster, 2012). While patients withchronic bronchitis are usually obese, those with emphysema are thinwith a hyperinflated chest. Additionally, emphysema shows little orno expectoration, unlike chronic bronchitis patients who havesignificant coughing and expectoration. Patients with emphysemausually adopt a tripod sitting position. They also have pursed lipsto facilitate respiration in addition to the use of accessory musclesof respiration. Patients with chronic bronchitis have signs of corpulmonale (Kumar, Abbas &amp Aster, 2012).

Emphysemaoccurs when pathologic processes destroy the grape-like air sacsclusters found at the distal bronchioles called the alveoli(Longo,Fauci, Kasper &amp Hauser, 2011). Generally, the disease processincludes inflammation of the walls of alveoli, causing damage. Overtime, they lose their elasticity, making them unable to stretch orshrink in accordance with gaseous exchange requirements. Pockets ofair breathed in stagnate in the air sacs forming bullae in theinjured sacs. The accumulation of the bullae causes an interruptionin the normal function of the lungs, leading to trapping of air inthe air sacs that causes difficulties in breathing out (Longo et al.,2011). The ability to inhale is not interfered. Oxygen and carbondioxide levels remain normal until the advanced stages of thecondition since it takes a long time to develop. Although clarity hasnot been provided on emphysema disease process, it is believed thatinflammatory cells including neutrophils, T lymphocytes and alveolarmacrophages have enzymes released to destroy the air sacs andbronchioles. This causes narrowing of the airways, compromisingbreathing out as the vital air sacs are destroyed with a continuedassault over time (Kumar, Abbas &amp Aster, 2012).

Thesecond condition, chronic bronchitis, refers to coughing andproduction of excess mucus for at least three months, for a period ofnot less than two consecutive years. The bronchial tubes becomeinflamed, followed by excessive mucus production, leading to cloggingof the airways, which consequently making exhalation difficult(Grossman et al., 2014).

Coughingensures expulsion of the excess mucus, however, continued coughingcoupled by the inflammation eventually leads to damage of thebronchioles. This leads to swelling of the tubes, reducing the spacefor airflow, which greatly affects exhalation that inhalation.


Thelungs’ Diffusing capacity (DL) is a measure of gaseous transferfrom the air to the lung, to the reticulocytes and eventually intopulmonary vasculature. Specific components of the Diffusing capacity,such as the DLCOare decreased in certain disease conditions affecting thecardiopulmonary system (Barrett, Barman &amp Boitano, 2010)

Thediffusion capacity is the efficiency with which gases are conductedacross the alveolar-capillary membrane, accounting for the relationbetween some gases with hemoglobin. In this light, Oxygen’sdiffusion capacity (DLO2) refers to the proportionality factorrelated to the rate oxygen is taken up and in the lungs to thegradient of oxygen between the alveoli and blood in the capillaryaccording to Fick`s laws of diffusion (Barret et al., 2010). Thehigher the diffusion capacity of a gas, the higher the gas is takenup by the lungs per unit time for a given diffusion gradient. Carbonmonoxide is bound rapidly and tightly to hemoglobin, therefore makingits partial pressure in the capillaries negligible. For this reason,CO is used to measure the diffusion capacity. Healthy individualshave their diffusion capacity between 75 % and 125% (Hall, 2010).However, variations occur due to age, sex, altitude, heights amongother parameters. An alteration of the volume of blood to the lungs,the CO uptake into the blood and the diffusion gradient across thealveolar capillary membrane affects the diffusion capacity of aperson (Gjedde, 2010).

Diseasesthat destroy the lung parenchyma such as emphysema, those causingscarring of the lungs such as interstitial lung disease, and thosethat cause lung tissue swelling and pulmonary vasculature diseasessuch as pulmonary hypertension and vasculitis reduce the diffusiongradient across the alveolar membrane together with blood volume inthe pulmonary capillaries (Kumar, Abbas &amp Aster, 2012). Clinicalmanifestations of vasculitis include fever, myalgia, weight loss,dyspnea and hemoptysis caused by pulmonary hemorrhage. Pulmonaryhypertension clinical manifestations include syncope, dyspnea,tachycardia, hepatomegaly, edema, increased jugular venous pressure,cyanosis, fatigue and heart murmurs (Kumar, Abbass &amp Aster 2012).Additionally, diseases that increase the diffusion capacity of carbonmonoxide such as Goodpasture’s syndrome, alveolar hemorrhage,polycythemia and asthma also affect the diffusion capacity of thelungs (Longo et al., 2014).

Thediffusion capacity of the lungs reduces during old age due to thecollective reduction in pulmonary function in old age (Barret et al.,2010). Destruction of lung parenchyma coupled with the loss of thesupporting structure to the lung parenchyma are some of the factorsthat contribute to reduced pulmonary function. The oxygen volumetaken up by the lungs (VO2) is reduced. There is another reduction inthe diffusion gradient between the alveoli and the pulmonary artery(due to reduced alveolar oxygen). This also causes a reduction in thealveolar capillary membrane’s (DM)efficiency in facilitating diffusion. Older individuals also haveless hemoglobin, reducing CO uptake into the blood. Destruction oflung parenchyma also reduces the volume of blood in the capillaries(VC)(Hall, 2010)


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