Evidence map›Paper›PMID 38637696›Full record

ArticleCommunications medicine2024

Spatial modeling connecting childhood atopic dermatitis prevalence with household exposure to pollutants.

Grace Ratley, Jordan Zeldin, Ashleigh A Sun, Manoj Yadav, Prem Prashant Chaudhary, Ian A Myles

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Targeting Pollutants in the Treatment and Prevention of Atopic Dermatitis.Immunology and allergy clinics of North America · 2025
    Review
  3. Review
  4. Article
  5. 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

6 authors at 1 institution in 1 country.

Grace Ratley *Laboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-3940-3993
Jordan Zeldin *Laboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, USA.
Ashleigh A SunLaboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, USA.
Manoj YadavLaboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, USA.
Prem Prashant ChaudharyLaboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, USA.
Ian A MylesLaboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, USA. mylesi@niaid.nih.gov.ORCID http://orcid.org/0000-0001-9316-3703
National Institutes of Health · US

Funding

Host Immunity Against BacteriaZIAAI001043 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MYLES, IAN · 2009 to 2025
$18.9M
U.S. Department of Health & Human Services | National Institutes of Health (NIH) Intramural
6 · The paper itself

Abstract

backgroundAtopic dermatitis (AD) is a chronic, inflammatory disease characterized by dry, pruritic skin. In the U.S., the prevalence of AD has increased over three-fold since the 1970s. We previously reported a geographic association between isocyanate-containing air pollution and AD as well as mechanistic data demonstrating that isocyanates induce skin dysbiosis and activate the host itch receptor TRPA1. However, non-spatial models are susceptible to spatial confounding and may overlook other meaningful associations.

methodsWe added spatial analysis to our prior model, contrasting pollution data with clinical visits. In addition, we conducted a retrospective case-control survey of childhood exposure to BTEX-related products. Finally, we assessed implicated compounds, in pure form and as part of synthetic fabric, for their effect on the growth and metabolism of skin commensal bacteria.

resultsSpatial analysis implicate benzene, toluene, ethylbenzene, and, most significantly, xylene (BTEX) compounds. Survey odds ratios for AD were significant for xylene-derived polyester bed sheets (OR = 9.5; CI 2.2-40.1) and diisocyanate-containing wallpaper adhesive (OR = 6.5; CI 1.5-27.8). Staphylococcus aureus lives longer on synthetic textiles compared to natural textiles. Meanwhile, synthetic fabric exposure shifts the lipid metabolism of health-associated commensals (Roseomonas mucosa and S. epidermidis) away from therapeutic pathways.

conclusionsWe propose that BTEX chemicals in their raw forms and in synthetic products represent a unifying hypothesis for environmentally induced AD flares through their ability to create dysbiosis in the skin microbiota and directly activate TRPA1. Unequal distribution of these pollutants may also influence racial disparities in AD rates.

Identifiers

PMID38637696
PMCPMC11026442
OpenAlexW4394931371

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.