Evidence map›Paper›PMID 12782502›Full record

ArticleEnvironmental health perspectives2003

World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice.

Stephen H Gavett, Najwa Haykal-Coates, Jerry W Highfill, Allen D Ledbetter, Lung Chi Chen, Mitchell D Cohen, Jack R Harkema, James G Wagner, Daniel L Costa

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
18.1field-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

52 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Article
  3. Myeloid Heterogeneity Mediates Acute Exacerbations of Pulmonary Fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  4. Article
  5. Article
  6. Mutagenicity of the organic fraction of World Trade Center dust.Environmental and molecular mutagenesis · 2023
    Article
  7. Article
  8. Review
  9. Longitudinal Impact of WTC Dust Inhalation on Rat Cardiac Tissue Transcriptomic Profiles.International journal of environmental research and public health · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Stephen H GavettNational Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA. gavett.stephen@epa.gov
Najwa Haykal-Coates
Jerry W Highfill
Allen D Ledbetter
Lung Chi Chen
Mitchell D Cohen
Jack R Harkema
James G Wagner
Daniel L Costa
Environmental Protection Agency · US

Funding

RESEARCH IN ENVIRONMENTAL HEALTH SCIENCES (CENTER GRANT)P30ES000260 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 1985 to 2020
$26.1M
NIEHS NIH HHS ES00260
6 · The paper itself

Abstract

Pollutants originating from the destruction of the World Trade Center (WTC) in New York City on 11 September 2001 have been reported to cause adverse respiratory responses in rescue workers and nearby residents. We examined whether WTC-derived fine particulate matter [particulate matter with a mass median aerodynamic diameter < 2.5 microm (PM2.5)] has detrimental respiratory effects in mice to contribute to the risk assessment of WTC-derived pollutants. Samples of WTC PM2.5 were derived from settled dust collected at several locations around Ground Zero on 12 and 13 September 2001. Aspirated samples of WTC PM2.5 induced mild to moderate degrees of pulmonary inflammation 1 day after exposure but only at a relatively high dose (100 microg). This response was not as great as that caused by 100 microg PM2.5 derived from residual oil fly ash (ROFA) or Washington, DC, ambient air PM [National Institute of Standards and Technology, Standard Reference Material (SRM) 1649a]. However, this same dose of WTC PM2.5 caused airway hyperresponsiveness to methacholine aerosol comparable to that from SRM 1649a and to a greater degree than that from ROFA. Mice exposed to lower doses by aspiration or inhalation exposure did not develop significant inflammation or hyperresponsiveness. These results show that exposure to high levels of WTC PM2.5 can promote mechanisms of airflow obstruction in mice. Airborne concentrations of WTC PM2.5 that would cause comparable doses in people are high (approximately 425 microg/m3 for 8 hr) but conceivable in the aftermath of the collapse of the towers when rescue and salvage efforts were in effect. We conclude that a high-level exposure to WTC PM2.5 could cause pulmonary inflammation and airway hyperresponsiveness in people. The effects of chronic exposures to lower levels of WTC PM2.5, the persistence of any respiratory effects, and the effects of coarser WTC PM are unknown and were not examined in these studies. Degree of exposure and respiratory protection, individual differences in sensitivity to WTC PM2.5, and species differences in responses must be considered in assessing the risks of exposure to WTC PM2.5.

Indexed as

Air PollutantsAnimalsBronchial HyperreactivityBronchoalveolar Lavage FluidDustExplosionsFemaleLungMiceNew York CityNosePlethysmography, Whole BodyTerrorismAir PollutantsDust

Identifiers

PMID12782502
PMCPMC1241535
OpenAlexW1995123015

What OpenQuestion holds

Textmetadata
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.