Environmental exposure to semi-volatile organic compounds and COPD progression: Evidence mapping, exposure assessment and metabolomic insights.
TL;DR
Current evidence supports respiratory relevance of several SVOC classes but is insufficient to establish SVOCs as causal drivers of COPD progression, and future longitudinal COPD cohorts should integrate repeated environmental sampling, human biomonitoring, source attribution, mixture modeling and targeted metabolomics to clarify preventable exposure-progression pathways.
Abstract
INTRODUCTION Chronic obstructive pulmonary disease (COPD) progression may be influenced by non-smoking environmental exposures, especially among never-smokers and environmentally exposed populations. Semi-volatile organic compounds (SVOCs) are relevant because they persist in air, particles, dust, surfaces and biological matrices and can enter the body through inhalation, dust ingestion, diet and dermal uptake. This review aimed to synthesize evidence on SVOC exposure assessment, respiratory and COPD-related outcomes, and candidate metabolomic pathways related to COPD progression.
Methods
We conducted a critical narrative review with structured evidence mapping. PubMed and Web of Science searches identified 4535 records; 3087 remained after DOI- and title-based deduplication, and 1251 unique studies were included in the primary evidence map after screening and manual classification.
Results
Polycyclic aromatic hydrocarbons (PAHs) and phthalates showed the most developed evidence across respiratory and lung-function outcomes and the closest, although still limited, evidence related to COPD progression. Evidence from asthma, airway inflammation, general lung function and cross-sectional COPD occurrence was interpreted as supportive but indirect. Direct progression evidence in diagnosed COPD cohorts remains sparse. Metabolomic evidence suggested candidate pathways involving glycerophospholipid-sphingolipid remodeling, amino-acid metabolism, arginine-nitric oxide signaling, acylcarnitine-tricarboxylic acid cycle activity and redox balance, but these pathways have not been validated as mediators.
Conclusion
Current evidence supports respiratory relevance of several SVOC classes but is insufficient to establish SVOCs as causal drivers of COPD progression. Future longitudinal COPD cohorts should integrate repeated environmental sampling, human biomonitoring, source attribution, mixture modeling and targeted metabolomics to clarify preventable exposure-progression pathways.