Association between cadmium exposure and pulmonary function reduction: Potential mediating role of telomere attrition in chronic obstructive pulmonary disease patients
Background: Environmental cadmium (Cd) exposure is linked to pulmonary function injury in the general population. But, the association between blood Cd concentration and pulmonary function has not been investigated thoroughly in chronic obstructive pulmonary disease (COPD) patients, and the potentia...
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| Format: | Article |
| Language: | English |
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Elsevier
2023-02-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651323000520 |
| _version_ | 1828046699816288256 |
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| author | Bian-Bian Lv Chun-Lan Yang Zhu-Xia Tan Ling Zheng Meng-Die Li Ya-Lin Jiang Ling Liu Min-Min Tang Dong-Xu Hua Jin Yang De-Xiang Xu Hui Zhao Lin Fu |
| author_facet | Bian-Bian Lv Chun-Lan Yang Zhu-Xia Tan Ling Zheng Meng-Die Li Ya-Lin Jiang Ling Liu Min-Min Tang Dong-Xu Hua Jin Yang De-Xiang Xu Hui Zhao Lin Fu |
| author_sort | Bian-Bian Lv |
| collection | DOAJ |
| description | Background: Environmental cadmium (Cd) exposure is linked to pulmonary function injury in the general population. But, the association between blood Cd concentration and pulmonary function has not been investigated thoroughly in chronic obstructive pulmonary disease (COPD) patients, and the potential mechanisms are unclear. Methods: All eligible 789 COPD patients were enrolled from Anhui COPD cohort. Blood specimens and clinical information were collected. Pulmonary function test was conducted. The subunit of telomerase, telomerase reverse transcriptase (TERT), was determined through enzyme linked immunosorbent assay (ELISA). Blood Cd was measured via inductively coupled-mass spectrometer (ICP-MS). Results: Blood Cd was negatively and dose-dependently associated with pulmonary function. Each 1-unit increase of blood Cd was associated with 0.861 L decline in FVC, 0.648 L decline in FEV1, 5.938 % decline in FEV1/FVC %, and 22.098 % decline in FEV1 % among COPD patients, respectively. Age, current-smoking, self-cooking and higher smoking amount aggravated Cd-evoked pulmonary function decrease. Additionally, there was an inversely dose-response association between Cd concentration and TERT in COPD patients. Elevated TERT obviously mediated 29.53 %, 37.50 % and 19.48 % of Cd-evoked FVC, FEV1, and FEV1 % declines in COPD patients, respectively. Conclusion: Blood Cd concentration is strongly associated with the decline of pulmonary function and telomerase activity among COPD patients. Telomere attrition partially mediates Cd-induced pulmonary function decline, suggesting an underlying mechanistic role of telomere attrition in pulmonary function decline from Cd exposure in COPD patients. |
| first_indexed | 2024-04-10T18:29:37Z |
| format | Article |
| id | doaj.art-276412510ef94ea6afe13d96b9ccc2b3 |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-04-10T18:29:37Z |
| publishDate | 2023-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-276412510ef94ea6afe13d96b9ccc2b32023-02-02T04:47:04ZengElsevierEcotoxicology and Environmental Safety0147-65132023-02-01251114548Association between cadmium exposure and pulmonary function reduction: Potential mediating role of telomere attrition in chronic obstructive pulmonary disease patientsBian-Bian Lv0Chun-Lan Yang1Zhu-Xia Tan2Ling Zheng3Meng-Die Li4Ya-Lin Jiang5Ling Liu6Min-Min Tang7Dong-Xu Hua8Jin Yang9De-Xiang Xu10Hui Zhao11Lin Fu12Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Institute of Respiratory Diseases, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Department of Toxicology, Anhui Medical University, Hefei, Anhui 230032, ChinaDepartment of Pharmacy, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230032, ChinaDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Institute of Respiratory Diseases, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, ChinaDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Institute of Respiratory Diseases, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, ChinaDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Institute of Respiratory Diseases, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, ChinaDepartment of Respiratory and Critical Care Medicine, Bozhou People's Hospital, Bozhou, Anhui 236800, ChinaDepartment of Respiratory and Critical Care Medicine, People’s Hospital of Yingshang, Fuyang, Anhui 236000, ChinaDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Institute of Respiratory Diseases, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, ChinaDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Institute of Respiratory Diseases, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, ChinaDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Institute of Respiratory Diseases, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, ChinaDepartment of Toxicology, Anhui Medical University, Hefei, Anhui 230032, China; Correspondence to: Anhui Medical University, China.Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Institute of Respiratory Diseases, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Correspondence to: Second Affiliated Hospital of Anhui Medical University, China.Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Institute of Respiratory Diseases, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China; Department of Toxicology, Anhui Medical University, Hefei, Anhui 230032, China; Correspondence to: Second Affiliated Hospital of Anhui Medical University, China.Background: Environmental cadmium (Cd) exposure is linked to pulmonary function injury in the general population. But, the association between blood Cd concentration and pulmonary function has not been investigated thoroughly in chronic obstructive pulmonary disease (COPD) patients, and the potential mechanisms are unclear. Methods: All eligible 789 COPD patients were enrolled from Anhui COPD cohort. Blood specimens and clinical information were collected. Pulmonary function test was conducted. The subunit of telomerase, telomerase reverse transcriptase (TERT), was determined through enzyme linked immunosorbent assay (ELISA). Blood Cd was measured via inductively coupled-mass spectrometer (ICP-MS). Results: Blood Cd was negatively and dose-dependently associated with pulmonary function. Each 1-unit increase of blood Cd was associated with 0.861 L decline in FVC, 0.648 L decline in FEV1, 5.938 % decline in FEV1/FVC %, and 22.098 % decline in FEV1 % among COPD patients, respectively. Age, current-smoking, self-cooking and higher smoking amount aggravated Cd-evoked pulmonary function decrease. Additionally, there was an inversely dose-response association between Cd concentration and TERT in COPD patients. Elevated TERT obviously mediated 29.53 %, 37.50 % and 19.48 % of Cd-evoked FVC, FEV1, and FEV1 % declines in COPD patients, respectively. Conclusion: Blood Cd concentration is strongly associated with the decline of pulmonary function and telomerase activity among COPD patients. Telomere attrition partially mediates Cd-induced pulmonary function decline, suggesting an underlying mechanistic role of telomere attrition in pulmonary function decline from Cd exposure in COPD patients.http://www.sciencedirect.com/science/article/pii/S0147651323000520CadmiumCOPDTelomerasePulmonary functionAssociation |
| spellingShingle | Bian-Bian Lv Chun-Lan Yang Zhu-Xia Tan Ling Zheng Meng-Die Li Ya-Lin Jiang Ling Liu Min-Min Tang Dong-Xu Hua Jin Yang De-Xiang Xu Hui Zhao Lin Fu Association between cadmium exposure and pulmonary function reduction: Potential mediating role of telomere attrition in chronic obstructive pulmonary disease patients Ecotoxicology and Environmental Safety Cadmium COPD Telomerase Pulmonary function Association |
| title | Association between cadmium exposure and pulmonary function reduction: Potential mediating role of telomere attrition in chronic obstructive pulmonary disease patients |
| title_full | Association between cadmium exposure and pulmonary function reduction: Potential mediating role of telomere attrition in chronic obstructive pulmonary disease patients |
| title_fullStr | Association between cadmium exposure and pulmonary function reduction: Potential mediating role of telomere attrition in chronic obstructive pulmonary disease patients |
| title_full_unstemmed | Association between cadmium exposure and pulmonary function reduction: Potential mediating role of telomere attrition in chronic obstructive pulmonary disease patients |
| title_short | Association between cadmium exposure and pulmonary function reduction: Potential mediating role of telomere attrition in chronic obstructive pulmonary disease patients |
| title_sort | association between cadmium exposure and pulmonary function reduction potential mediating role of telomere attrition in chronic obstructive pulmonary disease patients |
| topic | Cadmium COPD Telomerase Pulmonary function Association |
| url | http://www.sciencedirect.com/science/article/pii/S0147651323000520 |
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