Evidence map›Paper›PMID 39151477›Full record

ReviewThe Journal of allergy and clinical immunology2024

The clinical, mechanistic, and social impacts of air pollution on atopic dermatitis.

Jordan Zeldin, Grace Ratley, Nadia Shobnam, Ian A Myles

Abstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Evaluation of Childhood Atopic Dermatitis and Environmental Factors in Turkey with Decision Tree Model.International journal of environmental research and public health · 2025
    Article
  8. Targeting Pollutants in the Treatment and Prevention of Atopic Dermatitis.Immunology and allergy clinics of North America · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. 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

4 authors.

Jordan ZeldinLaboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Md.
Grace RatleyLaboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Md.
Nadia ShobnamLaboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Md.
Ian A MylesLaboratory of Clinical Immunology and Microbiology, Epithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Md. Electronic address: mylesi@niaid.nih.gov.

Funding

Host Immunity Against BacteriaZIAAI001043 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MYLES, IAN · 2009 to 2025
$18.9M
Intramural NIH HHS Z99 AI999999Intramural NIH HHS ZIA AI001043Intramural NIH HHS ZIA AI001205
6 · The paper itself

Abstract

Atopic dermatitis (AD) is a complex disease characterized by dry, pruritic skin and significant atopic and psychological sequelae. Although AD has always been viewed as multifactorial, early research was dominated by overlapping genetic determinist views of either innate barrier defects leading to inflammation or innate inflammation eroding skin barrier function. Since 1970, however, the incidence of AD in the United States has increased at a pace that far exceeds genetic drift, thus suggesting a modern, environmental etiology. Another implicated factor is Staphylococcus aureus; however, a highly contagious microorganism is unlikely to be the primary etiology of a noncommunicable disease. Recently, the roles of the skin and gut microbiomes have received greater attention as potentially targetable drivers of AD. Here too, however, dysbiosis on a population scale would require induction by an environmental factor. In this review, we describe the evidence supporting the environmental hypothesis of AD etiology and detail the molecular mechanisms of each of the AD-relevant toxins. We also outline how a pollution-focused paradigm demands earnest engagement with environmental injustice if the field is to meaningfully address racial and geographic disparities. Identifying specific toxins and their mechanisms can also inform in-home and national mitigation strategies.

Indexed as

Air PollutionDermatitis, AtopicAnimalsEnvironmental ExposureGastrointestinal MicrobiomeHumansSkinStaphylococcus aureusAtopic dermatitiseczemaenvironmental justicemicrobiomepollutionrace science

Identifiers

PMID39151477
PMCPMC11456380

What Socratic 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 Socratic graph.