Evidence map›Paper›PMID 25514459›Full record

Trial reportEnvironmental health perspectives2015

Interaction effects of temperature and ozone on lung function and markers of systemic inflammation, coagulation, and fibrinolysis: a crossover study of healthy young volunteers.

Juliette J Kahle, Lucas M Neas, Robert B Devlin, Martin W Case, Michael T Schmitt, Michael C Madden, David Diaz-Sanchez

Open access · diamondAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Environmental health perspectives, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

50 citing papers in PubMed, 118 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Climate change: a critical time for respiratory health.Respiratory research & clinical practice · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Modifying effects of PMScientific reports · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. The emerging role of fibrin(ogen) in cardiovascular disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Review
  17. Article
  18. The effect modification of PMEnvironmental health and preventive medicine · 2024
    Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Juliette J KahleEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA.
Lucas M Neas
Robert B Devlin
Martin W Case
Michael T Schmitt
Michael C Madden
David Diaz-Sanchez
University of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTrends in climate suggest that extreme weather events such as heat waves will become more common. High levels of the gaseous pollutant ozone are associated with elevated temperatures. Ozone has been associated with respiratory diseases as well as cardiovascular morbidity and mortality and can reduce lung function and alter systemic markers of fibrinolysis. The interaction between ozone and temperature is unclear.

methodsSixteen healthy volunteers were exposed in a randomized crossover study to 0.3 ppm ozone and clean air for 2 hr at moderate (22°C) temperature and again at an elevated temperature (32.5°C). In each case lung function was performed and blood taken before and immediately after exposure and the next morning.

resultsOzone exposure at 22°C resulted in a decrease in markers of fibrinolysis the next day. There was a 51.8% net decrease in PAI-1 (plasminogen activator inhibitor-1), a 12.1% net decrease in plasminogen, and a 17.8% net increase in D-dimer. These significantly differed from the response at 32.5°C, where there was a 44.9% (p = 0.002) and a 27.9% (p = 0.001) increase in PAI-1 and plasminogen, respectively, and a 12.5% (p = 0.042) decrease in D-dimer. In contrast, decrements in lung function following ozone exposure were comparable at both moderate and elevated temperatures (forced expiratory volume in 1 sec, -12.4% vs. -7.5%, p > 0.05). No changes in systemic markers of inflammation were observed for either temperature.

conclusionOzone-induced systemic but not respiratory effects varied according to temperature. Our study suggests that at moderate temperature ozone may activate the fibrinolytic pathway, while at elevated temperature ozone may impair it. These findings provide a biological basis for the interaction between temperature and ozone on mortality observed in some epidemiologic studies.

Indexed as

Blood CoagulationFibrinolysisTemperatureAdultAir PollutantsBiomarkersCross-Over StudiesFemaleFibrin Fibrinogen Degradation ProductsForced Expiratory VolumeHumansInflammationMaleOzoneRespiratory Physiological PhenomenaAir PollutantsBiomarkersFibrin Fibrinogen Degradation Productsfibrin fragment DOzone

Identifiers

PMID25514459
PMCPMC4384199
OpenAlexW2327876745

What OpenQuestion holds

Textmetadata
LicenceCC0
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.