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COVID-19 in Chemical Lung Injury Cases

Published online by Cambridge University Press:  08 January 2021

Ramezan Jafari
Affiliation:
Department of Radiology, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran Chemical Injuries Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
Amin Saburi*
Affiliation:
Chemical Injuries Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
Mostafa Ghanei
Affiliation:
Chemical Injuries Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
*
Corresponding author: Amin Saburi, Email: aminsaburi@yahoo.com.
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Abstract

Type
Letter to the Editor
Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
© Society for Disaster Medicine and Public Health, Inc. 2021

The journal recently published a hypothesis review titled, “Are Iranian Sulfur Mustard Gas-Exposed Survivors More Vulnerable to SARS-CoV-2? Some Similarity in Their Pathogenesis.” In this article, possible coronavirus disease (COVID-19) complications in chemical lung injured cases were assessed. Farnoosh et al. aimed to investigate about “the different pathologic aspects of lung injury caused by mustard gas and also the relationship between this damage and the increased susceptibility of Iranian mustard gas exposed survivors to COVID-19.” Reference Farnoosh, Ghanei and Khorramdelazad1

The authors first discussed pulmonary complications of sulfur mustard (SM) in clinic and radiologic studies and then pathogenesis of mustard lung, pathogenesis of COVID-19, and the risk of COVID-19 for SM injured cases was discussed. Finally, in conclusion, they predicted that the respiratory and pulmonary clinical manifestations of COVID-19 will be more severe in SM-exposed patients; therefore, COVID-19 is more lethal in SM-exposed individuals.

This review presented compact data from chemically injured lung secondary to SM, which previously presented as mustard lung, and it can be a research model for other industrial and inhalation chemical injuries. There are 2 main pathogenic hypotheses in survivors who inhaled SM: chronic inflammatory process with fluctuation in severity, and oxidative stress-antioxidant imbalance. Reference Saber, Saburi and Ghanei2 Evidence for both hypotheses is interesting and acceptable, with most cases presenting a suitable response to anti-inflammatory or anti-oxidative medications, Reference Shohrati, Karimzadeh and Saburi3 but it seems that antioxidant imbalance may be the main basic pathogenesis that triggers the long-term chronic inflammatory process in the lung. Reference Saburi and Ghanei4

Each mechanism of pathogenesis increases host susceptibility to pulmonary infections like COVID-19 (and virus SARS-CoV-2 that causes COVID-19) infections. Although there is no original research on COVID-19 in SM-injured cases, due to the similarity with chronic obstructive pulmonary disease (COPD) and bronchiolitis obliterans (BO), as the main possible lung pathology in SM injury, we can temporally rely on the COPD case findings. A recent meta-analysis declared that “underlying respiratory diseases, specifically COPD, and smoking were associated with severe COVID-19 outcomes.” Reference Sanchez-Ramirez and Mackey5 Therefore, the conclusions reached by Farnoosh et al. can be closer to the fact. Here, CT scans of 4 SM pulmonary injury survivors who were affected by COVID-19 will be presented. A CT scan provides the most useful and reliable evidence for the diagnosis of pulmonary COVID-19. Bilateral ground glass opacities and patchy consolidation as the most frequent findings in pulmonary SARS-CoV-2 were observed in these 4 cases and pneumomediastinum was present in 1 case. Two of 4 presented cases were expired due to severity of the diseases (Figure 1, A-B: Cases 1 and 2). Finally, when we carefully looked at the SM lung injuries from pathogenesis to bedside, as well as the pathogenesis of COVID-19, which includes coagulation of proteins and fibrin in combination with debris, infiltration of fibroblasts and other inflammatory cells at interstitium and alveoli, and injury to capillary endothelial cells and also over coagulation process, we concluded that, in these 2 diseases, an intersection/overlap occurs in the accompaniment and type of pulmonary involvement, including the alveoli and small airways (bronchioles), which is likely to exacerbate the disease. Recently, organizing pneumonia (OP) was presented as one of the main possible pathogenesis mechanisms of COVID-19 lung involvement. Reference Nicholson, Osborn, Devaraj and Wells6,Reference Saburi, Schoepf and Ulversoy7 Therefore, SM-injured case-patients who were previously affected by BO can overlap with new small airway disorders, such as a type of OP, or BOOP. Furthermore, SM-injured survivors are more susceptible for coronary artery disease, Reference Mohammadzadeh Shabestari, Alizadeh and Moshiri8 which in itself predisposes the patients to more mortality in SARS-CoV-2 disease.

Figure 1A–D. Four cases of SM-injured survivors who were affected with PCR proved COVID-19.

In all cases, patchy ground glass opacities and evolving opacities to consolidation were seen, as well as the usual feature of COVID-19 in healthy individuals. Pneumomediastinum as one of the complications of severe cough was observed in the first case (A).

This feature can accelerate the deterioration and severe phase of the illness and impair the oxygenation cycle. A cohort study on SM-lung-injured survivors, along with healthy controls, is needed to finally prove this vulnerability.

Conflict(s) of Interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this paper.

References

Farnoosh, G, Ghanei, M, Khorramdelazad, H, et al. Are Iranian sulfur mustard gas-exposed survivors more vulnerable to SARS-CoV-2? Some similarity in their pathogenesis. Disaster Med Public Health Prep. 2020. doi: 10.1017/dmp.2020.156 CrossRefGoogle ScholarPubMed
Saber, H, Saburi, A, Ghanei, M. Clinical and paraclinical guidelines for management of sulfur mustard induced bronchiolitis obliterans; from bench to bedside. Inhal Toxicol. 2012;24(13):900906.CrossRefGoogle ScholarPubMed
Shohrati, M, Karimzadeh, I, Saburi, A, et al. The role of N-acetylcysteine in the management of acute and chronic pulmonary complications of sulfur mustard: a literature review. Inhal Toxicol. 2014;26(9):507523.Google ScholarPubMed
Saburi, A, Ghanei, M. Comments on “sulfur mustard and respiratory diseases,” Tang & Loke (2012) and a prepared integrated mechanism for chronic pulmonary disease from exposure to sulfur mustard. Crit Rev Toxicol. 2013;43(3):275276. doi: 10.3109/10408444.2013.764842 CrossRefGoogle Scholar
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Saburi, A, Schoepf, UJ, Ulversoy, KA, et al. From radiological manifestations to pulmonary pathogenesis of COVID-19: a bench to bedside review. Radiol Res Pract. 2020;epub, doi: 10.1155/2020/8825761 CrossRefGoogle ScholarPubMed
Mohammadzadeh Shabestari, M, Alizadeh, L, Moshiri, M, et al. Late cardiac complications of sulfur mustard poisoning in 38 Iranian veterans. Cardiovasc Toxicol. 2019;19(3):220228.Google ScholarPubMed
Figure 0

Figure 1A–D. Four cases of SM-injured survivors who were affected with PCR proved COVID-19.In all cases, patchy ground glass opacities and evolving opacities to consolidation were seen, as well as the usual feature of COVID-19 in healthy individuals. Pneumomediastinum as one of the complications of severe cough was observed in the first case (A).