Evidence map›Paper›PMID 41350531›Full record

ArticleNPJ primary care respiratory medicine2025

Air pollution exposure modes, smoking and genetic risk with chronic respiratory diseases: a prospective study.

Ting Wang, Linfang Lyu, Ru Yuan, Lei Lei, Fanqing Meng, Meng Zhu, Weiwei Duan

Abstract read
In one paragraph

Article in NPJ primary care respiratory medicine, 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. Article
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

7 authors.

Ting Wang *Department of Pathology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China.
Linfang Lyu *Department of Bioinformatics, School of Biomedical Engineering and Informatics, Nanjing Medical University, Nanjing, China.
Ru YuanDepartment of Emergency and Rescue Medicine, Second Clinical Medical College, Xuzhou Medical University, Xuzhou, China.
Lei LeiDepartment of Pathology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China.
Fanqing MengDepartment of Pathology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China.
Meng ZhuDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China. zhmnjmu@njmu.edu.cn.
Weiwei DuanDepartment of Bioinformatics, School of Biomedical Engineering and Informatics, Nanjing Medical University, Nanjing, China. passion@njmu.edu.cn.

Funding

Clinical Trials from the Affiliated Drum Tower Hospital, Medical School of Nanjing University 2024-LCYJ-DBZ-02Key Project supported by Medical Science and technology development Foundation Nanjing Department of Health YKK24069National Natural Science Foundation of China 81602813National Natural Science Foundation of China 81903409National Natural Science Foundation of China 82302950Natural Science Research of Jiangsu Higher Education Institutions of China 24KJB310010
6 · The paper itself

Abstract

Previous studies often focused on single pollutant source, failing to replicate real-world exposure scenarios for chronic respiratory disease (CRD) risk. We aimed to explore the mixed exposure patterns of CRD risk factors and investigate interactions with smoking and genetic risk. We identified air pollution exposure modes using latent class analysis (LCA) in the UK Biobank. Cox model assessed associations between exposure modes and lung cancer (LC), idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and asthma. Interactions among exposure modes, smoking and genetic risk were analyzed. LCA divided participants into five groups, and hazard ratios (HRs) for "High air pollution" group were 1.28 for LC (95% CI: 1.08-1.52), 1.23 for IPF (95% CI: 1.03-1.48), 1.28 for COPD (95% CI: 1.17-1.39) and 1.09 for asthma (95% CI: 1.01-1.18). Significant additive interactions between high air pollution and smoking were observed for LC and COPD. Individuals with high genetic risk exposed to both smoking and high air pollution showed the relative excess risk due to interaction (RERI) of 2.74 for LC, 3.93 for IPF, and 1.68 for COPD. Smoking and air pollution together accounted for over 40% of LC, IPF and COPD cases. Our findings highlight the complex interplay between environmental air pollution, smoking, and genetic risk in CRD development in real-world exposure scenarios.

Indexed as

Air PollutionEnvironmental ExposureSmokingAdultAgedAsthmaChronic DiseaseFemaleGenetic Predisposition to DiseaseHumansIdiopathic Pulmonary FibrosisLung NeoplasmsMaleMiddle AgedProportional Hazards ModelsProspective Studies

Identifiers

PMID41350531
PMCPMC12800334

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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.