Evidence map›Paper›PMID 36600175›Full record

ArticleAnnals of the rheumatic diseases2023

Occupational inhalable agents constitute major risk factors for rheumatoid arthritis, particularly in the context of genetic predisposition and smoking.

Bowen Tang, Qianwen Liu, Anna Ilar, Pernilla Wiebert, Sara Hägg, Leonid Padyukov, Lars Klareskog, Lars Alfredsson, Xia Jiang

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 2% of its field
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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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  15. Alcohol Consumption and Autoimmune Diseases.International journal of molecular sciences · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Bowen TangDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-1391-2522
Qianwen LiuDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Anna IlarDepartment for Knowledge-Based Policy of Health Care, National Board of Health and Welfare, Stockholm, Sweden.
Pernilla WiebertInstitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Sara HäggDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Leonid PadyukovDivision of Rheumatology, Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Lars Klareskog *Division of Rheumatology, Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden lars.alfredsson@ki.se lars.klareskog@ki.se xia.jiang@ki.se.ORCID 0000-0001-9601-6186
Lars Alfredsson *Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden lars.alfredsson@ki.se lars.klareskog@ki.se xia.jiang@ki.se.
Xia Jiang *Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden lars.alfredsson@ki.se lars.klareskog@ki.se xia.jiang@ki.se.
Karolinska Institutet · SEKarolinska University Hospital · SENational Board of Health and Welfare · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo assess the effects of occupational inhalable exposures on rheumatoid arthritis (RA) development and their interactions with smoking and RA-risk genes, stratifying by presence of anticitrullinated protein antibodies (ACPA).

methodsData came from the Swedish Epidemiological Investigation of RA, consisting of 4033 incident RA cases and 6485 matched controls. Occupational histories were retrieved, combining with a Swedish national job-exposure matrix, to estimate exposure to 32 inhalable agents. Genetic data were used to define Genetic Risk Score (GRS) or carrying any copy of human leucocyte antigen class II shared epitope (HLA-SE) alleles. Associations were identified with unconditional logistical regression models. Attributable proportion due to interaction was estimated to evaluate presence of interaction.

resultsExposure to any occupational inhalable agents was associated with increased risk for ACPA-positive RA (OR 1.25, 95% CI 1.12 to 1.38). The risk increased as number of exposed agents increased (P

conclusionsOccupational inhalable agents could act as important environmental triggers in RA development and interact with smoking and RA-risk genes leading to excessive risk for ACPA-positive RA. Future studies are warranted to assess preventive strategies aimed at reducing occupational hazards and smoking, especially among those who are genetically vulnerable.

Indexed as

Arthritis, RheumatoidGenetic Predisposition to DiseaseAutoantibodiesCase-Control StudiesEpitopesHLA AntigensHLA-DRB1 ChainsHumansRisk FactorsSmokingAutoantibodiesEpitopesHLA AntigensHLA-DRB1 ChainsAnti-Citrullinated Protein AntibodiesArthritis, RheumatoidEpidemiologySmoking

Identifiers

PMID36600175
PMCPMC9933179
OpenAlexW4311681685

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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.