Evidence map›Paper›PMID 39780163›Full record

ArticleRespiratory research2025

Interaction study of the effects of environmental exposure and gene polymorphisms of inflammatory and immune-active factors on chronic obstructive pulmonary disease.

Rui Wang, Yuanyuan Li, Yuting Jiang, Xiaona Liu, Hongqi Feng, Zhe Jiao, Bingyun Li, Chang Liu, Yuncheng Shen, Fang Chu and 3 more

Abstract read
In one paragraph

Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Rui Wang *Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Yuanyuan Li *Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Yuting Jiang *Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Xiaona LiuCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Hongqi FengCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Zhe JiaoCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Bingyun LiCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Chang LiuCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Yuncheng ShenCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Fang ChuCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Chenpeng ZhuCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Dianjun SunCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China. hrbmusdj@163.com.
Wei ZhangCenter for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China. zwhxd@126.com.

Funding

the Heilongjiang Academy of Medical Sciences CR201801
6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) is a heterogeneous disease, influenced by both environmental and genetic factors. Single nucleotide polymorphism (SNP) in the human genome may influence the risk of developing COPD and the response to treatment. We assessed the effects of gene polymorphism of inflammatory and immune-active factors and gene-environment interaction on risk of COPD in middle-aged and older Chinese individuals.

methodsIn this community-based case-control study, 471 patients with COPD and 485 controls aged 40-76 years in Heilongjiang Province, China were included. Face-to-face interviews, lung function tests, and multiplex polymerase chain reaction were used to obtain data. Logistic regression model, generalized multifactor dimensionality reduction and crossover analysis were used to analyse the effects of SNPs, gene-gene interactions, and gene-environment interactions on COPD.

resultsCRP gene[rs1130864-A allele (OR, 1.77; 95% CI 1.11-2.81); G/A + A/A genotype (OR, 1.75; 95% CI 1.07-2.84)], FCAR gene[rs4806606-G (OR, 0.72; 95% CI 0.53-0.98); rs8112766-G (OR, 0.79; 95% CI 0.64-0.98)] and FCGR2A gene[rs4656308-C (OR, 0.74; 95% CI 0.55-1.00); rs4656309-T (OR, 0.81; 95% CI 0.66-0.99)] are independent influential factors for COPD. Rs1205 [RERI: 0.15 (0.07-1.00)] and rs1130864 [RERI: 2.45 (0.73-4.18)] of CRP gene, rs11084376 [OR: 0.54 (0.29-0.97)] of FCAR gene, rs844 of FCGR2B [SI: 0.30 (0.11-0.77); OR: 0.46 (0.24-0.90)] gene, rs4656308-rs4656309-rs2165088 haplotype [SI: 0.48 (0.26-0.89)] of FCGR2A gene and exposure to smoking index > 200, indoor coal/wood/straw use, and outdoor straw burning play synergistic or antagonistic roles in the development of COPD.

conclusionsAlleles and genotypes of the CRP/FCAR/FCGR2A gene can increase the susceptibility to COPD in the northern Chinese population. For the first time, environmental exposure to the CRP/FCAR/FCGR2A/FCGR2B genes has been shown to have synergistic or antagonistic effects on COPD susceptibility on genotypes or haplotypes.

Indexed as

Environmental ExposureGene-Environment InteractionGenetic Predisposition to DiseasePolymorphism, Single NucleotidePulmonary Disease, Chronic ObstructiveAdultAgedCase-Control StudiesChinaC-Reactive ProteinFemaleHumansInflammation MediatorsMaleMiddle AgedReceptors, IgGC-Reactive ProteinInflammation MediatorsReceptors, IgGChronic obstructive pulmonary diseaseEnvironmental exposureHaplotypeInteractionsSingle nucleotide polymorphism

Identifiers

PMID39780163
PMCPMC11707857

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Registered trials

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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.