- Author:
Gang LI
1
;
Yan Hui JIA
2
;
Yun Shang CUI
3
;
Shao Wei WU
4
;
Tong Yu MA
5
;
Yun Xing JIANG
4
;
Hong Bing XU
6
;
Yu Hui ZHANG
7
;
Mary A FOX
8
Author Information
- Publication Type:Journal Article
- Keywords: Air pollution; Biomarkers; Heart failure; Natriuretic peptides; Troponin; sST2
- MeSH: Heart Failure/epidemiology*; Biomarkers/metabolism*; Humans; Air Pollution/adverse effects*; Air Pollutants/adverse effects*; Particulate Matter/adverse effects*; Environmental Exposure; Natriuretic Peptide, Brain/blood*; Oxidative Stress; Troponin/blood*
- From: Biomedical and Environmental Sciences 2025;38(11):1430-1443
- CountryChina
- Language:English
- Abstract: Ambient air pollution is increasingly being recognized as a risk factor for heart failure; however, its effects on cardiac biomarkers remain unclear. This scoping review assessed the existing evidence on the association between air pollution and cardiac biomarkers in heart failure, described the key concepts, synthesized data, and identified research gaps. Following the PRISMA-ScR guidelines, PubMed, Embase, Web of Science, and CNKI databases were searched for studies on air pollution, heart failure, and biomarkers. A total of 765 records were screened, and 81 full texts were assessed for eligibility, resulting in 15 studies. The results showed that the exposure to particulate matter was associated with elevated N-terminal pro-B-type natriuretic peptide and troponin levels. Several studies have linked particulate matter exposure to a higher cardiovascular risk and heart failure biomarkers. Inflammatory and oxidative stress markers were consistently elevated across studies, supporting the biological relevance of these associations. However, few studies have focused specifically on populations with heart failure or clinically relevant biomarkers, and the evidence for gaseous pollutants remains inconclusive. These findings highlight the need to integrate environmental risk assessment into heart failure care and inform policy efforts to reduce the pollution-related cardiovascular burden. Further research should address these gaps through improved exposure assessments and the integration of mechanistic evidence.

