Abstract
Purpose
The degree of silicosis exposure is closely related to the progress of silicosis. At present, we use animal and human studies to explore whether silicon can be an important exposure marker in the development of silicosis.
Methods
Rats were randomly divided into 2 groups: (1) controls; and (2) silicosis. Rats in the silicosis group were killed at 4, 8, 12, 16, 24 h, 3, 7, 14, 21, and 28 days. Hematoxylin–eosin (HE) and immunohistochemistry (IHC) were performed to observe the histomorphology of lung tissue. The expression levels of CC16 and SP-D were detected using ELISA kits. In addition, we conducted a population study. Workers who have been selected to work in an iron mine for more than 1 year as research objects. The population was divided into four groups: silicosis exposure group (workers exposed to silica dust for more than 1 year in an iron mine were selected); patients group (silicosis patients); observation group (evidence of disease not meeting formal diagnostic criteria) and control group. Both the levels of trace silicon in the urine and blood of rats and human subjects were measured with ICP-MS.
Results
Serum levels of silicon were immediately increased in rats exposed to silicon dust. Similarly, our population study revealed that the silicon level in the silica exposure group and the observing group (exposed but no obvious symptoms) were significantly increased over that of the control group (P < 0.05). In subjects with extended exposure to silica, the serum and urine silicon level in exposed workers appeared to rapidly increase, reaching its peak in 1–5 years, followed by a gradual decline thereafter. Workers exposed to dust for less than 10 years were divided into subgroups by 2-year limit. The levels of serum silicon, urine silicon, TGF-β1, and TNF-α were significantly higher than that of control group.
Conclusion
Changes of the serum levels of silicon occurred earlier than the expression of cytokines such as TNF-α, TGF-β1, CC16, and SP-D. The level of silicon in workers rapidly increased after exposure to silica, and the change occurred before the expression of TGF-β1 and TNF-α. As a whole, the findings suggest that determining the level of silicon in vivo might be an effective exposure marker in the diagnosis and pathogenesis of silicosis.
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Abbreviations
- ICP-MS:
-
Inductively coupled plasma mass spectrometry
- TNF-α:
-
Tumor necrosis factor alpha
- TGF-β1:
-
Transforming growth factor-beta
- CC16:
-
Clara cell protein 16
- SP-D:
-
Surfactant protein D
- BALF:
-
Bronchoalveolar lavage fluid
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Acknowledgements
Prof. Darrell Brann (Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, Augusta, Georgia 30912, USA) helped write and critically reviewed the manuscript and provided intellectual input.
Funding
The work was supported by the National Natural Science Foundation of China (No. 81673119 and No. 81602814), Hebei Province Natural Science Foundation of China (No. H2018209337) and Hebei Provincial Key Research and Development Projects in (No. 192777129D) and Science and Technology Research Project of Colleges and Universities in Hebei Province (No. ZD2016026). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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HW and XH designed the study. JC, LG and RW carried out the experimental work, analyzed the data, and drafted the manuscript. HL participated in the design of the study and critically reviewed the manuscript and provided intellectual input. JZ conceived the study, and participated in coordination, and helped in drafting the manuscript. All authors read and approved the final manuscript.
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This study was approved by the Human Research Ethics Committee of North China University of Science and Technology (Clearance number 2012014). The research objectives and methodology were explained to the subjects and written informed consent was signed by each participant.
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Wang, H., Cui, J., Hao, X. et al. Silicon, an important exposure marker in vivo in silicosis research. Int Arch Occup Environ Health 94, 1513–1522 (2021). https://doi.org/10.1007/s00420-021-01729-4
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DOI: https://doi.org/10.1007/s00420-021-01729-4