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ECR 2019 / C-1030
Certificate of Merit
Lungs at Work- Insight into imaging of Occupational Lung Diseases
Congress: ECR 2019
Poster No.: C-1030
Type: Educational Exhibit
Keywords: Lung, Mediastinum, Thorax, Digital radiography, CT-High Resolution, Conventional radiography, Computer Applications-Detection, diagnosis, Statistics, Diagnostic procedure, Occupational / Environmental hazards, Neoplasia, Chronic obstructive airways disease
Authors: G. Ilangovan, S. Ranjan; Chennai, TA/IN
DOI:10.26044/ecr2019/C-1030

Findings and procedure details

Chest radiography is traditionally one of the primary imaging modalities used. However, advent of HRCT offers greater resolution and allows more sensitive, accurate detection and characterization of lung and pleural abnormalities.

 

PNEUMOCONIOSIS

Are caused due to body's reaction to accumulation of dust in the lungs.

 

Silicosis

Grinder's disease/Potter's rot is a fibrotic lung disease caused by inhalation of silica (crystalline silicon-dioxide). Latency period is about 10-30 years, although it can develop faster in workers exposed to high quantities over shorter periods of time, called accelerated silicosis. Occupations at risk include mining, quarrying, drilling and sandblasting.

 

HRCT findings in simple silicosis include small, discrete nodules(~2-5mm), usually in upper and posterior lung zones.

 

Fig. 1: A. Coronal and B. saggital reconstructed CT images showing diffuse centrilobular nodules predominantly in upper lobes and peripheral regions.
References: Ozmen et al; licensee BioMed Central Ltd. 2010

 

Nodules may coalesce to form bigger fibrotic lesions esp. along the pleura forming pseudoplaques. PMF(Progressive massive fibrosis) is characterized by bilateral, often symmetric irregularly shaped masses, mostly in apical and posterior segments of upper and lower lobes, along with peripheral parenchymal distortion. Cavitation occurs due to ischemic necrosis. Differentials for PMF include lung cancer and tuberculosis but PMF tends to have a slower progression on serial imaging.

 

Fig. 2: Fibrotic lung parenchyma with bilateral conglomerated mass lesion indicative of PMF. Associated mediastinal lymphadenopathy and calcification is also seen.
References: 2016 Indian Journal of Occupational and Environmental Medicine

 

Calcification of hilar and mediastinal lymph nodes may be diffuse or peripheral(egg-shell).Other findings may include diffuse interstitial fibrosis, pleural thickening and pleural effusion.

 

HRCT in accelerated silicosis is similar to simple silicosis and may include multiple ill-defined centrilobular nodules, patchy GGO and lung consolidation. Crazy-paving pattern may develop due to deposition of PAS positive proteinaceous material within the alveoli.

 

Silicosis predisposes the individual to pulmonary tuberculosis, chronic interstitial pneumonia(UIP) with subsequent fibrosis. Scleroderma and rheumatoid arthritis and lung cancer have also been linked to silicosis.1

 

 

Coal worker’s pneumoconiosis

CWP results from inhalation of washed coal or mixed dust consisting of coal, kaolin, mica and silica. Exact pathogenesis of CWP remains unclear. Coal macules differ from silicotic macules by their lack of hyalinization and laminated collagen.

 

HRCT is similar to silicosis and includes ill-defined opacities of coal macules with/without dilatation of respiratory bronchioles causing focal emphysema. CWP may also present with PMF. Lung window may present with fine reticular lines or ill-defined centrilobular punctate opacities measuring less than 1.5 mm in type p pneumoconiosis.(Fig 3)

 

Fig. 3: Axial HRCT shows numerous small centrilobular (arrows) and subpleural (arrowheads) nodules in both lungs. The findings overlap in both silicosis and CWP.
References: Satija B, Kumar S, Ojha UC, Gothi D. Spectrum of high-resolution computed tomography imaging in occupational lung disease. Indian J Radiol Imaging 2013;23:287-96

 

Few subpleural micronodules may coalesce form pseudoplaques. Type q and r pneumoconiosis(characterised by opacities measuring 1.5-3mm and 3-10mm respectively) are characterized by sharply demarcated, rounded or contracted nodules.

Large opacities may cavitate due to mycobacterial infection. Interstitial lung fibrosis and lung carcinoma may develop.

 

 

Asbestos-related disorders

Asbestos fiber is a mineral with an aspect ratio of at least 3:1(length:diameter) in contrast to silica and coal dust which are particulates. Asbestos is found in brake linings, construction, mining and processing, insulation and textile manufacturing, shipbuilding, tiles, bricks, and linings of furnaces and ovens. Asbestos fibers can be serpentine eg.chrysotile or more fibrogenic and carcinogenic amphibole eg.crocidolite.

 

Inhalation may cause asbestosis, pleural plaques, diffuse pleural thickening, round atelectasis, lung cancer, and mesothelioma- all take at least 20 years to manifest, except for benign pleural effusion which is earliest manifestation.

 

HRCT shows pleural plaques which serve as a biomarker for asbestos exposure without causing any functional impairment. They are usually found bilaterally along antero/postero-lateral chest wall between 6th-9th rib spaces and along the dome of diaphragm on parietal pleura. They may calcify over time.(Fig 4)

 

Fig. 4: HRCT shows multiple calcified pleural plaques (arrows), indicating prior asbestos exposure.
References: Copyright St Vincent's University Hospital Radiology Department 2019

 

Diffuse pleural thickening results from prior asbestos-related exudative effusions and chronic pleural inflammation. It is less specific for asbestos exposure than pleural plaques and can develop as a consequence of hemothorax, empyema, or instrumentation.

 

On HRCT, Lynch and colleagues defined diffuse pleural thickening as a continuous sheet of pleural thickening >5 cm wide, >8 cm in craniocaudal extent, and >3 mm thick.2

 

Rounded atelectasis occurs due to buckling of thickened visceral pleura into the adjacent lung, resulting in tethering and subsequent atelectasis of underlying lung.  On HRCT a lentiform or wedge-shaped outline, spiraling of bronchovascular structures into a peripheral lung mass (comet tail sign) located adjacent to thickened pleura in association with volume loss in the affected lobe is characteristic.(Fig 5)

 

Fig. 5: Axial CECT shows a nodular-area of increased density (blue arrow), associated with pleural thickening and pleural plaques (yellow arrows) consistent with asbestos- related pleural disease. Red arrow point to "comet tail" density that surrounds rounded atelectasis
References: http://learningradiology.com/notes/chestnotes/roundatelectasispage.htm

 

HRCT findings of asbestosis include interstitial lines (intralobular interstitial thickening and interlobular septal thickening), subpleural curvilinear lines (peribronchiolar fibrotic thickening combined with flattening and collapse of the alveoli caused by fibrosis), subpleural dot like opacities, pleura-based nodular irregularities, parenchymal bands, patchy areas of ground-glass attenuation, traction bronchiectasis, and honeycombing.(Fig 6)

 

Fig. 6: HRCT shows interlobular septal thickening with subpleural lines and centriacinar nodules with peribronchial fibrosis, ground glass opacities and honeycombing.
References: http://www.chestx-ray.com/HRCT/HRCTpicker/infopages/infopage99.htm

 

Asbestos is a known carcinogen and is associated with increased risk of lung carcinoma and mesothelioma. Malignant pleural mesothelioma manifests as circumferential pleural thickening measuring >1cm with mediastinal and fissural pleural involvement, and invasion of mediastinal structures, chest wall, or diaphragm often accompanied by unilateral pleural effusion/ diffuse pleural thickening or both.(Fig 7)

 

Fig. 7: Diffuse irregular and nodular pleural thickening with involved mediastinal pleura and mediastinal lymphadenopathy- Malignant mesithelioma
References: Bakhshayesh Karam M, Karimi S, Mosadegh L, Chaibakhsh S. Malignant Mesothelioma Versus Metastatic Carcinoma of the Pleura: A CT Challenge, Iran J Radiol. 2016 ; 13(1):e10949

 

 

Talcosis

Occupational talc exposure occurs through inhalation of talc dust(hydrated magnesium silicate) used in manufacture of leather, rubber, paper, textiles, plastic and ceramic tiles. Talcosis can also occur through illicit intravenous drug abuse.

 

HRCT findings in pulmonary talcosis include small centrilobular & subpleural nodules, heterogenous appearing coalesced masses containing focal areas of high attenuation (talc deposition), septal/subpleural lines, ground-glass opacities, and lareas of low attenuation. Pleural plaques and lymphadenopathy with focal areas of high attenuation may seen.(Fig 8)

 

Fig. 8: Small centrilobular & subpleural nodules,coalesced masses of high attenuation dur to talc deposition,ground-glass opacities, and lobular areas of low attenuation in a case of pulmonary talcosis.
References: Pereira Faria, H. et al. Clinical Radiology , Volume 69 , Issue 3 , e136 - e139

 

HRCT in intravenous drug abuse patients includes diffuse small nodules, perihilar conglomerate masses with areas of high attenuation, patchy GGO, and basal predominant paracicatricial, panacinar emphysema.3(Fig 9)

 

Fig. 9: HRCT in an IV drug abuser shows conglomerated masses (arrows) in left lower lobe, lingula,and superior segment of right lower lobe with panacinar emphysema in both lower lobes and lingula.
References: AJR 2000;174:789–793

 

 

Mixed-dust pneumoconiosis

Its caused by simultaneous exposure to silica and less fibrogenic dusts (iron, silicates, carbon) as seen with metal miners, quarry workers, foundry workers, pottery/ceramics workers, and stonemasons.  As the share of inhaled silica increases, the number of silicotic nodules also increase in proportion to the mixed-dust nodules.

 

HRCT findings include a mixture of small rounded and irregular opacities of mixed dust fibrotic nodules and silicotic nodules. Honeycombing and emphysematous areas may be seen.

 

 

Aluminium pneumoconiosis

Inhalation of aluminium/alumina/pot-room fumes from aluminium welding has been associated with diffuse (upper lobe predominant) interstitial fibrosis,desquamative interstitial pneumonia, granulomatous lung reaction, and pulmonary alveolar proteinosis.

 

HRCT may mimic silicosis, sarcoidosis, NSIP, and UIP. It includes bilateral diffuse well-defined nodules (2-5 mm), or ill-defined centrilobular nodules, reticular pattern as in UIP occasionally with honeycombing, and upper-lung fibrosis patterns. Conglomeration with shrinkage in both upper lungs, ground-glass opacities with traction bronchiectasis mimicking NSIP may be seen. Increased density of mediastinal lymphnodes may also be seen.(Fig 10)

 

Fig. 10: HRCT in aluminium pneumoconiosis- diffuse small, ill-defined,centrilobular opacities with few subpleural curvilinear lines.
References: Kraus, T., Schaller, K., Angerer, J. et al. Int Arch Occup Environ Health (2000) 73: 61. https://doi.org/10.1007/PL00007939

 

 

Arc Welder’s lung/Pneumosiderosis

Exposure to welding fumes(iron-oxide) which accumulate in alveolar macrophages causes chronic respiratory disorders such as pneumoconiosis, chronic bronchitis and lung cancer.

 

HRCT shows diffuse ill-defined centrilobular micronodules with fine reticulations mimicking HP, peribronchiolar fibrosis and paracicatricial emphysema. Honeycombing and patchy GGO are less common.(Fig 11)

 

Fig. 11: HRCT in a welder shows presence of small, round opacities in bilateral upper lobes with patchy areas of ground glass attenuation.
References: Satija, Bhawna & Ojha, Uc & Kumar, Sanyal & Gupta, Rajiv & Gothi, Dipti & S Pal, R. (2013). Spectrum of High Resolution Computed Tomography Findings

 

Silicosiderosis occurs on exposure to both iron oxide and silica as in foundry work, iron and steel mills, mining and processing of iron ore and is associated with pulmonary fibrosis.

 

 

IMMUNE MEDIATED OCCUPATIONAL LUNG DISEASES (IMOLD)

Occupational exposure to dusts/antigens leads to complex immune response in lungs. Hypersensitivity pneumonitis is the most common IMOLD and is associated with a growing list of inciting antigens. Others include berylliosis and hard metal pneumoconiosis.

 

 

Hypersensitivity pneumonitis

Exposure to antigens causes an immune-mediated diffuse granulomatous interstitial pneumonia in susceptible individuals.

 

Entity of HP encompasses organic as well as inorganic inciting agents. Organic inciting agents like hay dust and mould spores cause farmer’s lung. Inhalation of avian proteins present in bird droppings causes bird fancier’s lung. Aspergillus and thermophilic Actinomyces are the most common inciting agents related to agriculture. Other industrial antigens include isocynates in paint sprays, plastic vapours in packing plants, and nontuberculous Mycobacteria in metal working fluids and water sources such as showerheads and hot tubs (hot-tub lung).4

 

HRCT in acute HP shows patchy or diffuse ground-glass opacities, reticulations, lower lobe predominant small, poorly-defined nodules and airspace consolidation.

HRCT in subacute HP shows diffuse or patchy ground-glass opacity, small(<5mm), poorly defined centrilobular nodules, and lobular areas of decreased attenuation(air trapping) giving mosaic pattern. Few scattered thin walled cysts and mediastinal lymphadenopathy may be seen.(Fig 12)

 

Fig. 12: HRCT in subacute HP shows geographical ground-glass opacity with interlobular septal thickening (crazy-paving pattern)(asterisk) with some lucent lobules(arrows).
References: American Journal of Roentgenology. 2010;194: W20-W26. 10.2214/AJR.09.2593

 

Chronic HP(CHP) may show features similar to those of subacute HP along with irregular fibrotic opacities, traction bronchiectasis, and upper lobe predominant subpleural honeycombing. Pulmonary fibrosis manifesting as upper and mid zone reticulation, traction bronchiectasis, and volume loss may be present.

 

 

Berylliosis

Beryllium(dust/fume/aerosol) inhalation occurs in nuclear power plants, nuclear weapons manufacturing, aerospace, ceramics, dentistry, and metal manufacturing. Amount/length of exposure do not correlate with the occurrence/severity. Exposure may cause acute chemical pneumonitis(acute berylliosis) or chronic granulomatous disease (CBD) which may involve extrathoracic sites.

 

HRCT appearance of CBD is similar to sarcoidosis and includes parenchymal nodules along bronchovascular bundles or interlobular septa, peri lymphatic micronodules in mid and upper lung zones, smooth/nodular septal thickening, GGO and bronchial wall thickening. Advanced disease presents with honeycombing and conglomerate masses. Mediastinal and hilar lymphadenopathy may be seen.(Fig 13)

 

Fig. 13: HRCT in CBD shows multiple small nodules (arrowheads), predominantly subpleural conglomerate masses (asterisk) associated with interlobular septal thickening (open arrows), marked distortion and dilation of segmental bronchi.
References: American Journal of Roentgenology. 2010;194: W20-W26. 10.2214/AJR.09.2593

 

 

Hard-metal Pneumoconiosis

Aka giant cell interstitial pneumonia is a rare OLD resulting from exposure to cobalt(mainly), diamond dust, titanium, nickel, chromium, niobium, vanadium and molybdenum produced in hard-metal cutting, polishing, and drilling industries.

 

Exposure may lead to occupational asthma, bronchiolitis, HP or alveolitis, pulmonary fibrosis, constrictive bronchiolitis, and giant cell interstitial pneumonia (GIP).

 

HRCT varies and may mimic sarcoidosis, NSIP, and UIP. Findings consist of parenchymal distortion in the form of bilateral GGO or consolidation in panlobular or multilobular form, extensive reticular opacities, micronodules and traction bronchiectasis- all having lower lobe predominance. Honeycombing is peripheral and basal predominant.

 

 

CHEMICAL PNEUMONITIS

Exposure and absorption of toxic fumes of sulphur-dioxide, ammonia, chlorine, phosgene, nitrogen oxides and ozone from respiratory tract causes chemical pneumonitis. Effects may range from laryngeal oedema causing death to pulmonary oedema without any pulmonary sequelae. Bronchiolitis obliterans or bronchiectasis may develop in survivors. An asthma like condition can arise after a single inhalation of miscellaneous irritant agent, so-called reactive airways dysfunction syndrome.5

Silo filler’s disease is an acute lung injury caused by inhalation of nitrogen-dioxide in an agricultural silo.

 

 

Thesaurosis

Chronic absorption/inhalation of chemicals in cosmetics and hairsprays leads to upper and lower airway inflammation called thesaurosis.

Hairdressers are mostly affected where PFTs are altered and suggest obstructive pulmonary disease.6 HRCT may show GGO but is nonspecific and not well documented.

 

 

NEWER OCCUPATIONAL LUNG DISEASES

 

Flavor worker’s lung

Occurs after exposure to diacetyl(2,3-butanedione), a ketone used in butter flavouring of microwave popcorn. Popcorn production plant workers and other workers in food manufacturing are affected. First described in 2000 in 8 workers who developed progressive dyspnoea and obstructive lung disease.7

It is characterized by constrictive bronchiolitis causing progressive dyspnoea and air flow obstruction. Advanced lesions may lack any perceptible airway lumen.

 

HRCT resembles other forms of obliterative bronchiolitis with mosaic attenuation and air-trapping on expiratory imaging. Mild cylindrical bronchiectasis and bronchial wall thickening may be present.8

 

 

Flock worker’s lung

It is related to inhalation of tiny nylon fibres, and is characterized by GGO and centrilobular nodularities.9

                                          

 

Calcicosis

Inhalation of limestone dust(calcium-carbonate,magnesium-oxide,silica-dioxide,aluminum-oxide) causes calcinosis.

HRCT findings have not been well established although widespread small nodules have been described.10 (Fig14)

 

Fig. 14: HRCT in calcinosis shows small diffuse nodules (arrows), some subpleural compounding pseudoplaques (arrowheads).
References: American Journal of Roentgenology. 2010;194: W20-W26. 10.2214/AJR.09.2593

 

Thus its diagnosis relies on an accurate histology and occupational history.

 

 

Ardystil Syndrome

First described in 1992 when an outbreak of organizing pneumonia occurred among textile printing sprayers in factories in Spain. Epidemiologic investigation proposed that the disease was due to aerosol of Acramin-FWN (a polyamidoamine that is applied with a brush or sponge for textile printing).11 The organizing pneumonia evolves into progressive interstitial fibrosis despite the use of corticosteroids.

 

HRCT findings show two different patterns: patchy areas of air-space consolidation with subpleural distribution, similar to idiopathic forms of organizing pneumonia and multiple small nodular opacities.11 (Fig 15)

 

Fig. 15: HRCT in a case of Ardystil syndrome shows small diffuse centrilobular nodules. Transbronchial biopsy showed changes of organizing pneumonia.
References: American Journal of Roentgenology. 2010;194: W20-W26. 10.2214/AJR.09.2593

 

In patients with progressive course,added coarse reticular pattern, more consistent with chronic interstitial pneumonia, was observed later.11

 

 

Carbon Black Pneumoconiosis

Burning of natural gas produces carbon black which is used as a filler in rubber, plastics, phonograph records, inks and in carbon paper and carbon electrode manufacturing.

A 1993 survery in workers with chest radiographs, revealed reticulonodular abnormalities in 25% of cases.12

The likelihood of identifying these abnormalities was related to total cumulative dust exposure. However, exposure to pure carbon black was reported to induce little if any clinical or functional impairment.

 

 

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