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Accepted Manuscript

Title: Acute and Subacute Chemical-Induced Lung Injuries:

HRCT findings

Author: Masanori Akira Narufumi Suganuma

PII: S0720-048X(14)00224-1

DOI: http://dx.doi.org/doi:10.1016/j.ejrad.2014.04.024

Reference: EURR 6760

To appear in: European Journal of Radiology

Received date: 14-1-2014

Revised date: 8-4-2014Accepted date: 19-4-2014

Please cite this article as: Akira M, Suganuma N, Acute and Subacute Chemical-

Induced Lung Injuries: HRCT findings, European Journal of Radiology (2014),

http://dx.doi.org/10.1016/j.ejrad.2014.04.024

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http://dx.doi.org/doi:10.1016/j.ejrad.2014.04.024



http://dx.doi.org/doi:10.1016/j.ejrad.2014.04.024



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p t Acute and Subacute Chemical-Induced Lung Injuries：HRCT findings

Masanori Akira, M.D.1)

Narufumi Suganuma, M.D.2)

Department of Radiology 1), National Hospital Organization Kinki-Chuo Chest Medical

Center, 1180 Nagasone-cho, Kita-ku, Sakai City, Osaka 591-8555, Japan

Department of Environmental Medicine 2), Kochi Medical School

Corresponding author: Masanori Akira

TEL: +81-072-252-3021 FAX: +81-072-251-1372 E-mail: [email protected]



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Abstract

Lung injury caused by chemicals includes bronchitis, bronchiolitis, chemical pneumonitis,

pulmonary edema, acute respiratory distress syndrome, organizing pneumonia, hypersensitivity

pneumonitis, acute eosinophilic pneumonia, and sarcoid-like granulomatous lung disease. Each

chemical induces variable pathophysiology and the situation resembles to the drug induced lung

disease. The HRCT features are variable and nonspecific, however HRCT may be useful in the

evaluation of the lung injuries and so we should know about HRCT features of lung parenchymal

abnormalities caused by chemicals.


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Introduction

Chemical-induced lung injuries are induced by inhalation. Agrichemicals, such as paraquat,

may cause lung injury following ingestion or dermal absorption. Most commonly, exposure is

accidental and occurs in the workplace, although it may also occur in the home or out in the

community, either by accident or act of terrorism. Household accidents could be underestimated.

Many respiratory diseases are caused by exposure to noxious chemicals. Lung injury caused by

chemicals includes bronchitis, bronchiolitis, chemical pneumonitis, pulmonary edema, acute

respiratory distress syndrome, organizing pneumonia, hypersensitivity pneumonitis, acute

eosinophilic pneumonia, and sarcoid-like granulomatous lung disease. To the best of our

knowledge, HRCT findings of chemical-induced lung injuries have not been well described in the

literature. The HRCT features are variable and nonspecific. When an individual presents acutely

with an abnormal chest radiograph and acute respiratory distress syndrome (ARDS) or acute lung

injury, chemical-induced lung injury must be considered.



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p tlung injury and systemic toxicity (Table 1). The type of injury caused is a function of the toxin or

mix of toxins that constitute the exposure and the physical properties of the toxin, the intensity and

duration of exposure, and the host factor status of the individual. The intensity of exposure to an

inhaled toxin is a major determinant of the severity of ensuing damage. Acute exposure to a high

concentration of toxic fumes causes diffuse alveolar damage, which may result in ARDS [1].

Water solubility plays a significant role in determining the location of the gas or vapor

inhalation injury. A highly soluble gas, such as ammonia or sulfur dioxide, is absorbed in the upper

respiratory tract. However, high-solubility gases are also capable of causing lower tract injury at

sufficiently high doses. A less soluble gas, such as nitrogen dioxide, is not removed in the upper

passages and reaches the more peripheral areas of the respiratory tree. Gases of intermediate

solubility, such as chlorine, may exert irritant effects widely throughout the respiratory tract [2-4].

In addition to water solubility, the particle size of the inhaled substance determines the site and

nature of the injury. All particles with an aerodynamic diameter larger than 10 μm are deposited on

the mucous membranes of the nose and pharynx. Particles between 3 and 10 μm in diameter can be

deposited throughout the tracheobronchial tree, where they initiate reflex bronchial constriction and



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as asthma and COPD, may be more susceptible [2].

Bronchitis, bronchiolitis and permeability pulmonary edema without diffuse alveolar damage

(chemical pneumonitis)

Toxic fumes or gasses that, because of their physiochemical characteristics (e.g., small particle

size and low water solubility) or their high inhaled concentration, can reach the peripheral airways

and alveoli will cause injury of the bronchiolar epithelium, alveolar lining cells, vascular

endothelium, and airway macrophages. Consequently, diffuse bronchiolar obstruction from edema

and inflammatory cell infiltration and alveolar and interstitial edema and hemorrhage may develop

[2, 3].

Exposure to a number of irritant substances at high levels may cause bronchiolitis and

pulmonary edema or “chemical pneumonitis”, depending on the solubility and physicochemical

properties of the substance. The site of injury may be limited around the bronchioles, however they

can be more extensive in the lungs. The characteristic thin-section CT findings are bronchial wall

thickening, centrilobular nodular areas of ground-glass attenuation and confluent areas of



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Ammonia

Ammonia is a colorless, highly soluble, extremely irritating alkaline gas with a characteristic

pungent odor. Owing to its high solubility, ammonia causes chemical burns to the eyes, skin,

oropharynx, and upper respiratory tract. After severe exposure, radiographs may reveal a

pulmonary edema pattern (Figure 1). Although most of these patients recover completely, cases of

bronchiectasis, persistent air-flow obstruction, and bronchiolitis obliterans have been reported

following inhalation exposure to ammonia gas [8].

Chlorine gas exposure

Chlorine is a heavy irritating gas with a characteristic odor. Chlorine is intermediate in

solubility and affects the lower respiratory tract more often than does ammonia. Acute exposure of

humans and animals to high concentrations of chlorine gas is known to produce bronchiolar and

alveolar-capillary damage, which is associated with necrotizing bronchiolitis, bronchitis, and

pulmonary edema. Pulmonary function testing typically demonstrates evidence of air-flow

obstruction with air-trapping, although restrictive changes may also be present [9, 10]. Air-flow

obstruction probably reflects injury to the airway mucosa and bronchoconstriction [4]. Chest


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evident in addition to those findings on CT (Fig. 2).

Nitrogen dioxide

NO2 (NO2) is a reddish brown gas that is denser than air, relatively insoluble in water, and has

a characteristic sweet odor. Inhalation of the gases and vapors can be extremely dangerous because

they do not invoke a violent protective cough reflex such as occurs with chlorine and ammonia [12].

Silo filler’s disease is an acute lung injury caused by inhalation of NO2 in or near an agricultural silo.

Symptoms first appear several hours to days after the exposure episode. The injury comprises

diffuse alveolar damage and pulmonary edema [13]. Patients who recover may pass into a latent

period that lasts from 2 to 6 weeks, during which time they continue to improve and the abnormal

clinical and radiographic signs disappear, only to relapse suddenly with a second acute episode

similar to the first without having been re-exposed to the gas (Fig. 3) [10, 14]. It is reported that

the thin-section CT findings of three patients with inhalational lung injury due to NO2 showed

ground-glass attenuation and ill-defined centrilobular nodules distributed predominantly in the inner-

and middle-lung zones (Fig. 4). Two of these three patients showed crazy-paving pattern [15].

Fluorocarbon



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fluorocarbon resin used as ski wax [18] have also been reported (Fig. 5). In a previous study,

fluorocarbon-induced pulmonary edema was correlated to smoking cigarettes (temperature of

approximately 650°C) that were contaminated with the powdered polymer [19].

Acute respiratory distress syndrome associated with diffuse alveolar damage

Irritant gas inhalation is a major cause of ARDS. Some of the patients exposed to these

insults progress ARDS, which may develop gradually over a 24-72-hour period after exposure and

even after a deceptive period of initial improvement in the early symptoms of upper airway

inflammation [1]. Chemical induced ARDS does not differ from ARDS secondary to other causes.

The most striking CT finding in early ARDS is the heterogeneous nature of the lung changes.

These changes may comprise: 1) normal or near-normal lung regions, most frequently located in the

nondependent lung (ventral in the supine position); 2) ground-glass opacification in the middle lung;

and 3) consolidation in the most dependent lung (dorsal in the supine position) [20, 21]. Prone CT

shows that the dependent opacity due to ARDS decreases in degree (Fig. 6), whereas that due to

pneumonia remains unchanged. Consolidation is not invariably confined to the dependent lung.



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injury and that due to extrapulmonary injury do exist and that a typical CT pattern

characterized by more extensive dependent intense parenchymal opacification but less

extensive nondependent consolidation and parenchymal cysts, is more frequently seen

in patients with ARDS due to extrapulmonary injury. Reske et al. [23] found that the most

striking early CT findings in smoke inhalation injury were infiltrations adjacent to the greater

airways in the central and ventral regions of the lungs, in addition to substantial bilateral dorsal

atelectasis.

Paraquat

Paraquat is an herbicide that is used widely in agricultural industries around the world.

Respiratory failure from ARDS is a prominent outcome of paraquat ingestion. Paraquat

accumulates rapidly in the lungs, and the consequent lung damage is linked to oxygen radicals that

destroy the cell membranes [24]. A characteristic time course for the CT findings of the lung

related to paraquat poisoning has been described [25, 26]. The predominant finding within the first

7 days is areas of ground-glass attenuation. The initial areas of ground-glass attenuation are

subsequently transformed into areas of consolidation associated with bronchiectasis and irregular



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Organizing pneumonia

Organizing pneumonia is a pathologic finding characterized by histological evidence of

intraluminal polyps of the connective tissue in the distal pulmonary air-spaces, contrasting with

minor interstitial fibrosis, together with distinctive clinical and radiographic features. The

idiopathic form is called cryptogenic organizing pneumonia (COP) and the predominant finding is

organizing pneumonia with minimal or absent bronchiolitis obliterans [27]. In inhalation lung

injury, different proportions of bronchiolitis obliterans and organizing pneumonia can be found.

Organizing pneumonia has been reported to result from occupational exposure to aerosolized paint

in the textile industry [28-30]. Most of these cases occurred in the Ardystil plant in Alcoy, Spain,

so the disease has been named Ardystil syndrome [31]. Acramin FWN, which is a

polyamide-amine, is considered to be a causative agent. The prognosis was variable and a sizable

proportion of the patients developed chronic lung fibrosis. The lack of response to steroids or

cyclophosphamide in these cases contrasts with COP.

Very few cases of authentic OP have been related to airborne agents, i.e., single massive



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Eosinophilic pneumonia

An identifiable chemical or drug exposure has rarely been associated with acute eosinophilic

pneumonia. Cases of acute eosinophilic pneumonia induced by inhaled crack cocaine [32],

inhalation of heroin [33], cigarette smoking [34, 35], and smoke from fireworks [36] have been

described. As nickel-associated respiratory disorders, induction of asthma is relatively well known,

in addition to pulmonary infiltrates with eosinophilia syndrome [37].

The predominant patterns of acute eosinophilic pneumonia seen at HRCT are bilateral patchy

areas of ground-glass opacity, frequently accompanied by interlobular septal thickening and

sometimes by consolidation or poorly defined nodules (Fig. 9) [38]. The radiologic features of EP

due to chemical exposure are sometimes different from those of idiopathic etiology. We

experienced air-space consolidation which is concentrated in the posterior portion of the lower lung

(Fig. 10). In part, the predominant distribution of posterior portion may be due to regional

differences in lymphatic function. Lymph flows centripetally in the center of the lung and

centrifugally in the periphery of the lung; en route to the hilum and clearance of particles is poorest



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Cobalt, titanium, aluminum, copper, talc, and glass fibers have been reported to cause

granulomatous pneumonitis with sarcoid-like granuloma [40-42]. Organic isocyanates, such as

toluene diisocyanate and diphenylmethane diisocyanate, have been associated with hypersensitivity

pneumonitis [43]. The characteristic HRCT features of hypersensitivity pneumonitis are

centrilobular nodules, ground-glass opacities, and mosaic perfusion pattern [44]. Subacute

hypersensitivity pneumonitis is one of the most common diseases that manifest

centrilobular ground-glass nodules without associated tree-in-bud opacities. In the

prominent symptomatic period, airspace consolidation and ground-glass opacities are prominent and

micronodules are fine and ambiguous on CT (Fig. 11).

Diffuse pulmonary hemorrhage

Trimellitic anhydride (TMA)-induced pulmonary hemosiderosis is the most firmly established

occupationally related diffuse pulmonary hemorrhage syndrome [45-48]. This syndrome is

correlated with high levels of antibodies against trimellityl-human serum albumin (TM-HAS) after

exposure to trimellitic anhydride (TMA) sprayed on a hot metal in poorly ventilated areas. A



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Conclusion

Lung injury caused by chemicals covers a wide spectrum of diseases, including bronchiolitis,

pulmonary edema, ARDS, sarcoid-like granulomatous lung disease, hypersensitivity pneumonitis,

BOOP, AEP, and so on. CT detects abnormalities following exposure, even when the chest

radiography does not, and CT helps to define the range of severity of the inhalation injury. HRCT

demonstrates a more characteristic pattern and distribution of parenchymal opacities. In

chemical-induced lung injury, rapid deterioration may occur during the course of the illness, so

careful follow-up is crucial for these patients. We should know about HRCT features of lung

parenchymal abnormalities caused by chemicals.

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Figure legends

Figure 1. Images in a 63-year-old man with ammonia gas exposure (high water-solubility).

(a) Chest radiograph obtained on the day of exposure shows consolidation with a central distribution

and sparing of the lung cortex.

(b) Transverse HRCT scan shows ground-glass opacity with a central distribution and sparing of the

lung cortex. Smooth thickening of interlobular septae (open arrows) and bronchial wall thickening

(arrowheads) are seen.

Figure 2. Images in a 31-year-old man with chlorine gas exposure (moderate water-solubility).

(a) Chest radiograph obtained on the day of exposure shows patchy areas of ground-glass opacity in

both lungs.

(b) Transverse HRCT scan shows centrilobular nodular areas of ground-glass attenuation, confluent

ground-glass opacity in peribronchiolar distribution and bronchial wall thickening (a solid black

arrow). Multi-panlobular low attenuation areas are also seen in the subpleural region, suggesting

air-trapping (arrows).



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(a) Chest radiograph taken 8 hours after exposure to nitrogen dioxide shows consolidation in the

central zone of the right lung.

(b) Transverse CT scan reveals consolidation in the central zone of the right lung and right pleural

effusion. Consolidation is also seen in the central zone of the left lung.

(c) Chest radiograph taken 3 weeks after exposure shows ill-defined nodules and patchy

consolidation throughout the lung.

(d) Transverse HRCT scan shows centrilobular nodules (open arrows), interlobular septal

thickening, patchy areas of ground-glass attenuation, and irregular consolidation. Pleural effusion

and interlobar pleural effusion are evident.

Figure 4. Images in a 49-year-old man with inhalation of nitrogen dioxide (low water-solubility).

(a) Chest radiograph shows patchy areas of consolidation in both middle lungs.

(b) Chest radiograph taken a few hours later shows increased consolidation in both middle lungs.

(c) Transverse HRCT scan shows centrilobular opacities diffusely distributed throughout the lung.

Figure 5. Images in a 20-year-old man with inhalation of a fluorocarbon used as a waterproofing

spray.



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Figure 6. Supine (A) and prone (B) HRCT images in a 64-year-old woman with ARDS. The

supine HRCT image shows extensive consolidation in the dorsal lung and consolidation along with

bronchovascular bundles. The prone HRCT image shows a prominent decrease in consolidation in

the gravity-dependent portion.

Figure 7. Post-mortem low-kilovoltage radiograph (a) and HRCT (b) of the inflated and fixed right

lung obtained from a patient who died within 1 week of ingesting paraquat. Consolidation,

ground-glass opacity, and nodular opacities are evident. Traction bronchiectasis is present (white

arrows). Lung abscess presenting as a cavitary lesion is seen in the right middle lobe (arrowhead).

Figure 8. Post-mortem low-kilovoltage radiograph (a) and HRCT (b) of the inflated and fixed right

lung of a patient who died 1 month after ingesting paraquat. Posterior consolidation, reticulation, and

cyst formation are evident.

Figure 9. Images in a 40-year-old man with acute eosinophilic pneumonia induced by cigarette

smoking.

(a) Chest radiograph shows bilateral pleural effusion and consolidation in the peripheral lungs.

(b) Transverse HRCT scan shows smooth thickening of interlobular septae in the anterior portion of





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Table 1. Representative Substances of Each Type of Injury

・Diffuse alveolar damage: irritant gas, heated polymers, paraquat, zinc chloride

・ Non-cardiogenic pulmonary edema: irritant gas, heated polymers, metal fume

・ Necrotizing bronchitis and bronchiolitis: irritant gas, zinc chloride, petroleum

・Organizing pneumonia: acramin FWN, NO2, chlorine, cocaine, cadmium

・Eosinophilic pneumonia: firework smoke, cigarette smoke, cocaine, heroin, scotchguard, nickel,

acetylene

・Granulomatous pneumonitis and extrinsic allergic alveolitis: cobalt, titanium, aluminum, copper,

talc, glass fibers, toluene diisocyanate, diphenylmethane diisocyanate

・Diffuse pulmonary hemorrhage: trimellitic anhydride, isocyanates



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All authors do not have any financial and personal relationships with other people or

organizations that could inappropriately influence (bias) our work.

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