Evidence map›Paper›PMID 35143075›Full record

ReviewJournal of internal medicine2022

The role of environmental exposures and gene-environment interactions in the etiology of systemic lupus erythematous.

Jennifer M P Woo, Christine G Parks, Søren Jacobsen, Karen H Costenbader, Sasha Bernatsky

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of internal medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
17.7field-weighted citation impact, top 1% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

  1. Pooled it
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  16. Lupus nephritis.Nature reviews. Disease primers · 2025
    Review
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  20. Article

4 more citing papers are in PubMed but not listed here.

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

5 authors at 4 institutions in 3 countries.

Jennifer M P WooEpidemiology Branch, National Institutes of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Christine G ParksEpidemiology Branch, National Institutes of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Søren JacobsenCopenhagen Lupus and Vasculitis Clinic, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
Karen H CostenbaderDivision of Rheumatology, Inflammation and Immunity, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Sasha BernatskyCentre for Outcomes Research and Evaluation, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada.ORCID 0000-0002-9515-2802
National Institutes of Health · USBrigham and Women's Hospital · USCopenhagen University Hospital · DKMcGill University Health Centre · CA

Funding

Environmental Exposures And Risk For Cancer and Chronic Diseases In AdultsZIAES049028 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SANDLER, DALE P · 2009 to 2024
$1.6M
Intramural NIH HHS Z99 ES999999NIH, National Institute of Environmental Health Sciences
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a complex, chronic autoimmune disease, whose etiology includes both genetic and environmental factors. Individual genetic risk factors likely only account for about one-third of observed heritability among individuals with a family history of SLE. A large portion of the remaining risk may be attributable to environmental exposures and gene-environment interactions. This review focuses on SLE risk associated with environmental factors, ranging from chemical and physical environmental exposures to lifestyle behaviors, with the weight of evidence supporting positive associations between SLE and occupational exposure to crystalline silica, current smoking, and exogenous estrogens (e.g., oral contraceptives and postmenopausal hormones). Other risk factors may include lifestyle behaviors (e.g., dietary intake and sleep) and other exposures (e.g., ultraviolet [UV] radiation, air pollution, solvents, pesticides, vaccines and medications, and infections). Alcohol use may be associated with decreased SLE risk. We also describe the more limited body of knowledge on gene-environment interactions and SLE risk, including IL-10, ESR1, IL-33, ITGAM, and NAT2 and observed interactions with smoking, UV exposure, and alcohol. Understanding genetic and environmental risk factors for SLE, and how they may interact, can help to elucidate SLE pathogenesis and its clinical heterogeneity. Ultimately, this knowledge may facilitate the development of preventive interventions that address modifiable risk factors in susceptible individuals and vulnerable populations.

Indexed as

Arylamine N-AcetyltransferaseLupus Erythematosus, SystemicOccupational ExposurePesticidesEnvironmental ExposureGene-Environment InteractionHumansRisk FactorsArylamine N-AcetyltransferaseNAT2 protein, humanPesticidesenvironmentgene-environment interactionsgeneticsrisk factorsSLEsystemic lupus erythematosus

Identifiers

PMID35143075
PMCPMC12369280
OpenAlexW4211051788

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.