A systematic review and meta-analysis of human population studies on the association between exposure to toxic environmental chemicals and left ventricular dysfunction (LVD).

Cardiovascular diseases Chemical pollution Epidemiological evidence Heart failure LVD Meta-analysis Regulatory policy Systematic review

Journal

Environmental research
ISSN: 1096-0953
Titre abrégé: Environ Res
Pays: Netherlands
ID NLM: 0147621

Informations de publication

Date de publication:
12 Feb 2024
Historique:
received: 24 08 2023
revised: 08 11 2023
accepted: 04 02 2024
medline: 15 2 2024
pubmed: 15 2 2024
entrez: 14 2 2024
Statut: aheadofprint

Résumé

Exposure to environmental chemicals has been linked to an increased risk of heart failure, but the impact on left ventricular dysfunction (LVD) markers remains uncertain. To establish a foundation of evidence regarding early HF markers and their association with environmental pollutants, a systematic review and meta-analysis was conducted. The search, conducted on October 13th, 2023, encompassed PubMed, Embase, and Web of Science without filters, focusing on observational studies reporting myocardial geometrical, structural, or functional alterations in individuals without a history of heart disease. This included the general adult population, workers, young people, and the elderly. The risk of bias was assessed using the ROBINS-I tool at both study and item levels. The systematic review included 17 studies involving 43.358 individuals exposed to air pollution and 2038 exposed to heavy metals. Approximately 41% of the effect measures of associations reported significant abnormalities in myocardial structure or function. The metanalyses by pollutants categories indicated positive associations between LV systolic and diastolic abnormalities and exposure to PM2.5 [-0.069 (-0.104, -0.033); -0.044 (-0.062, -0.025)] and PM10 [-0.055 (-0.087, -0.022); -0.030 (-0.050, -0.010)] and NO2 [-0.042 (-0.071, -0.013); -0.021 (-0.037, -0.004)], as well as positive associations between lead exposure and LV systolic abnormalities [-0.033 (-0.051, -0.016)]. To strengthen confidence in the findings and improve the attribution of baseline exposures, the authors recommend conducting more longitudinal and case-control studies. These studies should consider co-exposures, account for vulnerable groups, and identify cardiotoxic compounds that may require regulation. When examining the link between myocardial abnormalities and environmental exposure, it is also advisable to explore the supportive use of Adverse Outcome Pathway (AOP) approaches to confirm a causal relationship.

Sections du résumé

BACKGROUND BACKGROUND
Exposure to environmental chemicals has been linked to an increased risk of heart failure, but the impact on left ventricular dysfunction (LVD) markers remains uncertain.
OBJECTIVE OBJECTIVE
To establish a foundation of evidence regarding early HF markers and their association with environmental pollutants, a systematic review and meta-analysis was conducted.
METHODS METHODS
The search, conducted on October 13th, 2023, encompassed PubMed, Embase, and Web of Science without filters, focusing on observational studies reporting myocardial geometrical, structural, or functional alterations in individuals without a history of heart disease. This included the general adult population, workers, young people, and the elderly. The risk of bias was assessed using the ROBINS-I tool at both study and item levels.
RESULTS RESULTS
The systematic review included 17 studies involving 43.358 individuals exposed to air pollution and 2038 exposed to heavy metals. Approximately 41% of the effect measures of associations reported significant abnormalities in myocardial structure or function. The metanalyses by pollutants categories indicated positive associations between LV systolic and diastolic abnormalities and exposure to PM2.5 [-0.069 (-0.104, -0.033); -0.044 (-0.062, -0.025)] and PM10 [-0.055 (-0.087, -0.022); -0.030 (-0.050, -0.010)] and NO2 [-0.042 (-0.071, -0.013); -0.021 (-0.037, -0.004)], as well as positive associations between lead exposure and LV systolic abnormalities [-0.033 (-0.051, -0.016)].
CONCLUSIONS CONCLUSIONS
To strengthen confidence in the findings and improve the attribution of baseline exposures, the authors recommend conducting more longitudinal and case-control studies. These studies should consider co-exposures, account for vulnerable groups, and identify cardiotoxic compounds that may require regulation. When examining the link between myocardial abnormalities and environmental exposure, it is also advisable to explore the supportive use of Adverse Outcome Pathway (AOP) approaches to confirm a causal relationship.

Identifiants

pubmed: 38354889
pii: S0013-9351(24)00333-5
doi: 10.1016/j.envres.2024.118429
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

118429

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

G Donzelli (G)

Institute of Clinical Physiology of the National Research Council (CNR-IFC), Pisa, Italy. Electronic address: gabriele.donzelli@ifc.cnr.it.

F Sera (F)

Department of Statistics, Computer Science and Applications "G. Parenti", University of Florence, Florence, Italy. Electronic address: francesco.sera@unifi.it.

M A Morales (MA)

Institute of Clinical Physiology of the National Research Council (CNR-IFC), Pisa, Italy. Electronic address: morales@ifc.cnr.it.

F Vozzi (F)

Institute of Clinical Physiology of the National Research Council (CNR-IFC), Pisa, Italy. Electronic address: vozzi@ifc.cnr.it.

T Roos (T)

Department of Population Health Sciences, Institute for Risk Assessment Sciences (IRAS), Faculty of Veterinary Medicine, Utrecht University, Utrecht, the Netherlands. Electronic address: t.s.roos@uu.nl.

A Schaffert (A)

Institute of Medical Biochemistry, Medical University Innsbruck, Innsbruck, Austria. Electronic address: alexandra.schaffert@i-med.ac.at.

M Paparella (M)

Institute of Medical Biochemistry, Medical University Innsbruck, Innsbruck, Austria. Electronic address: martin.paparella@i-med.ac.at.

S Murugadoss (S)

Scientific Direction of Chemical and Physical Health Risks, Sciensano, Brussels, Belgium. Electronic address: sivakumar.murugadoss@sciensano.be.

B Mertens (B)

Scientific Direction of Chemical and Physical Health Risks, Sciensano, Brussels, Belgium. Electronic address: Birgit.Mertens@sciensano.be.

R Gehring (R)

Department of Population Health Sciences, Institute for Risk Assessment Sciences (IRAS), Faculty of Veterinary Medicine, Utrecht University, Utrecht, the Netherlands. Electronic address: r.gehring@uu.nl.

N Linzalone (N)

Institute of Clinical Physiology of the National Research Council (CNR-IFC), Pisa, Italy. Electronic address: linunzia@ifc.cnr.it.

Classifications MeSH