ArticleTobacco induced diseases2025
Association between serum copper and COPD: Insights from NHANES 2011-2016 and Mendelian randomization study.
Article in Tobacco induced diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionChronic obstructive pulmonary disease (COPD) affects 390 million people globally, with oxidative stress playing a key pathogenic role. Smoking and other forms of tobacco exposure are major COPD drivers and important sources of systemic oxidative stress, and potentially interact with metal homeostasis. Copper exhibits dual effects in lung homeostasis, as a cofactor for antioxidant enzymes and a potential catalyst for reactive oxygen species. However, the causal relationship between serum copper levels and COPD remains unclear. This study aimed to assess their association using a combination of observational and genetic approaches.
methodsIn stage one, we used multivariate regression to analyze the association between serum copper and COPD in 3166 participants in the National Health and Nutrition Examination Survey (NHANES), 2011-2016. Models adjusted for demographic and clinical covariates including smoking-related variables, and stratified analyses by smoking status. Stage two utilized Mendelian randomization (MR) analysis to explore a potential cause-and-effect link between copper levels in serum determined by genetics and COPD.
resultsObservational analysis showed increased COPD risk in the highest serum copper tertile (T3 vs T1, OR=1.65; 95% CI: 1.09-2.49; p-trend=0.0245). The association remained after adjustment for smoking-related covariates. However, MR analyses using both FinnGen and UK Biobank data suggested no causal effect (FinnGen IVW, OR=1.01; 95% CI: 0.98-1.04, p=0.37; UK Biobank IVW, OR=1.00; 95% CI: 1.00-1.00, p=0.55), with sensitivity analyses confirming result robustness.
conclusionsWhile elevated serum copper is associated with COPD prevalence observationally, the null MR finding suggests it may reflect tobacco-related systemic oxidative stress or reverse causation rather than being a direct causal driver. Therefore, serum copper may be more useful as a biomarker of smoking-induced redox disturbance than as a therapeutic target. These results underscore the importance of integrating tobacco exposure metrics in future studies examining metal biology in COPD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.