Asbestos exposure determined 357 days after death through autopsy: a report of a multidisciplinary approach

Abstract

Asbestosis is an interstitial lung disease caused by the inhalation of asbestos fibers and poses a significant risk to individuals working in construction, shipping, mining, and related industries. In a forensic context, postmortem investigations are crucial for accurate diagnosis, for which the gold standard is the histopathological examination. This case report describes the autopsy and related investigations conducted on an 84-year-old man, nearly one year (357 days) after his death. After a post-mortem CT scan, an autoptic investigation was performed, followed by histopathological, immunohistochemical, and scanning electron microscopy examinations. The integration of the evidence from these examinations with previously available personal and clinical information conclusively confirmed the diagnosis of asbestosis. We demonstrated the efficacy and reliability of our diagnostic protocol in detecting asbestosis and asbestos fibers and excluding mesothelioma even in decomposed tissues. According to our findings autopsy remains the diagnostic gold standard in cases of suspected asbestosis within a forensic context, even 1 year after death, therefore it is always highly recommended, even in cases where the body has decomposed.

Keywords: Asbestos fibers; Asbestosis; Autopsy; Exhumation; Multidisciplinary approach; Post-mortem CT (PMCT); Scanning electron microscopy.

Fig. 1

Coronal reconstruction (bone window), showingevidence of various pleural plaques, with signs of calcification (blue arrows)

Fig. 2

Coronal reconstruction (mediastinal window), showing evidence of various pleural plaques (parietal and diaphragmatic pleura) (blue arrows)

Fig. 3

Macroscopic examination of the ribcage: A, B, C, D: evidence of multiple fibrotic adhesions along the right and left ribs, all covered in vegetative neoformations (blue arrows)

Fig. 4

Macroscopic examination of thoracic organs bloc district: A, B evidence of pleural plaques (forceps) at both lungs’ bases

Fig. 5

Macroscopic examination of left (A) and right (B) hemicostates after formalin fixation: evidence of multiple, gray and irregular vegetative neoformations strictly adhered to the hemicostates (pleural plaques)

Fig. 6

Parietal pleura (A, H&E, 10X; B, H&E, 20X): fibrotic plaques with acellular hyalin collagen fibers in a reticular pattern, including areas with calcium salt deposits

Fig. 7

Visceral pleura: A thickening caused by fibrotic phenomena (Masson’s trichrome, 2.5X); B pleural thickness = 1.5 mm (yellow line) (H&E, 20X)

Fig. 8

A Fibrosis of respiratory bronchiole walls (H&E, 20X), extending (B) to alveolar ducts and adjacent alveoli (Masson trichrome, 20X)

Fig. 9

A Fibrosis of respiratory bronchiole wall (Van Gieson trichrome, 20X); B fibrosis of alveolar ducts and alveoli walls (Masson trichrome, 20X)

Fig. 10

A Fibrosis of alveolar ducts and alveoli walls (Masson trichrome, 20X); B fibrotic thickening of the inter-alveolar septa between two or more contiguous respiratory bronchioles (Van Gieson’ trichrome, 20X)

Fig. 11

Amorphous fusiform structure compatible with asbestos fiber (yellow arrow), located in thealveolar space with fibrotic thickening of the wall. (Masson trichrome, 100X)

Fig. 12

Image of an asbestos fiber (yellow arrow) detected during the analysis (magnification 12000X)