Evidence map›Paper›PMID 38888597›Full record

ArticleJournal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine2024

Nasal resistance and inflammation: mechanisms for obstructive sleep apnea from chronic rhinosinusitis.

Indu Ayappa, Robert Laumbach, Kathleen Black, Michael Weintraub, Priya Agarwala, Akosua Twumasi, Haley Sanders, Iris Udasin, Denise Harrison, Rafael E de la Hoz and 7 more

Abstract read
In one paragraph

Article in Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

17 authors.

Indu AyappaDivision of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Robert LaumbachSchool of Public Health, Rutgers Biomedical and Health Sciences, Piscataway, New Jersey.
Kathleen BlackEnvironmental and Occupational Health Sciences Institute, Rutgers Biomedical and Health Sciences, Piscataway, New Jersey.
Michael WeintraubDivision of Endocrinology, Department of Medicine, New York University Grossman School of Medicine, New York, New York.
Priya AgarwalaDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, New York University Grossman School of Medicine, New York, New York.
Akosua TwumasiDivision of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Haley SandersDivision of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Iris UdasinEnvironmental and Occupational Health Sciences Institute, Rutgers Biomedical and Health Sciences, Piscataway, New Jersey.
Denise HarrisonDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, New York University Grossman School of Medicine, New York, New York.
Rafael E de la HozDivision of Occupational and Environmental Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Yingfeng ChenSchool of Public Health, Rutgers Biomedical and Health Sciences, Piscataway, New Jersey.
Nishay ChitkaraDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, New York University Grossman School of Medicine, New York, New York.
Anna E MullinsDivision of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Horacio Romero CastilloDivision of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
David M RapoportDivision of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Shou-En LuSchool of Public Health, Rutgers Biomedical and Health Sciences, Piscataway, New Jersey.
Jag SunderramDivision of Pulmonary and Critical Care Medicine, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, New Jersey.

Funding

Project-005UL1TR001445 · NCATS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BREDELLA, MIRIAM ANTOINETTE, HOCHMAN, JUDITH S · 2015 to 2025
$103.5M
Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Jose Guillermo Cedeno Laurent · 1988 to 2026
$47.4M
Obstructive Sleep Apnea in WTC Responders: Role of Nasal PathologyU01OH010415 · OH · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI AYAPPA, INDU A, SUNDERRAM, JAG · 2012 to 2015
$4.0M
Mentoring Research in the Physiology of Sleep Disordered BreathingK24HL109156 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI AYAPPA, INDU A · 2013 to 2023
$1.0M
NCATS NIH HHS UL1 TR001445NHLBI NIH HHS K24 HL109156NIEHS NIH HHS P30 ES005022NIOSH CDC HHS U01 OH010415
6 · The paper itself

Abstract

STUDY

objectivesWe have previously estimated that the prevalence of obstructive sleep apnea (OSA) among World Trade Center rescue and recovery workers is 75% and identified that having symptoms of chronic rhinosinusitis (CRS) is an independent risk factor for OSA in this population. Nasal inflammation and/or elevated awake nasal resistance that carried over into sleep could explain this association. To understand the mechanism(s) for the elevated risk of OSA observed in World Trade Center responders with CRS symptoms we examined if elevated awake supine nasal resistance was associated with OSA, CRS and/or nasal inflammatory biomarkers.

methodsA total of 601 individuals (83% male, average age 53 years, body mass index = 29.9 ± 5.5 kg/m

resultsAwake supine nasal resistance was not associated with OSA; 74.8% and 74.4% of the participants with low and high nasal resistance respectively, had OSA. Patients with CRS had elevated nasal inflammatory markers (interleukin 6, interleukin 8, eosinophilic cationic protein, and neutrophil) but did not have high nasal resistance. Nasal inflammatory markers were not correlated with nasal resistance.

conclusionsAs awake nasal resistance did not explain the relationship of CRS to OSA in this large and well characterized dataset, our findings suggest that either "sleep" nasal resistance or other factors such as increased supraglottic inflammation, perhaps through impairing upper airway reflex mechanisms, or systemic inflammation are involved in the pathophysiology of OSA in the World Trade Center population. CITATION: Ayappa I, Laumbach R, Black K, et al. Nasal resistance and inflammation: mechanisms for obstructive sleep apnea from chronic rhinosinusitis.

Indexed as

InflammationRhinitisSinusitisSleep Apnea, ObstructiveAdultAirway ResistanceBiomarkersChronic DiseaseFemaleHumansMaleMiddle AgedRhinomanometryRhinosinusitisSeptember 11 Terrorist AttacksBiomarkerschronic rhinosinusitisnasal inflammationnasal resistanceobstructive sleep apneaWTC dust exposure

Identifiers

PMID38888597
PMCPMC11446130

What OpenQuestion holds

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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.