Evidence map›Paper›PMID 19304273›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2009

Asbestos-induced lung diseases: an update.

David W Kamp

Open access · greenAbstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 2 pooled it
16.0field-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

85 citing papers in PubMed, 2 syntheses or guidelines pooled it, 248 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Global burden of lung cancer attributable to occupational asbestos exposure: 1990 to 2021.Environmental health : a global access science source · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Environmental Causes of Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Lung cancer risk in never-smokers: An overview of environmental and genetic factors.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2021
    Article
  20. Long Noncoding RNAInternational journal of molecular sciences · 2021
    Article

25 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

David W KampDepartment of Medicine, Northwestern University Feinberg School of Medicine and Jesse Brown VA Medical Center, Chicago, Ill 60611-3010, USA. d-kamp@northwestern.edu
Jesse Brown VA Medical Center · US

Funding

Respiratory and Metabolic Adaptation to HypoxiaR01HL035440 · NHLBI · UNIVERSITY OF CHICAGO · PI SCHUMACKER, PAUL T · 1986 to 2018
$5.0M
Signaling in the lung induced by particulate matter air pollutionR01ES013995 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BUDINGER, GR SCOTT · 2006 to 2015
$3.3M
NHLBI NIH HHS R01 HL035440NIEHS NIH HHS R01 ES013995
6 · The paper itself

Abstract

Asbestos causes asbestosis (pulmonary fibrosis caused by asbestos inhalation) and malignancies (bronchogenic carcinoma and mesothelioma) by mechanisms that are not fully elucidated. Despite a dramatic reduction in asbestos use worldwide, asbestos-induced lung diseases remain a substantial health concern primarily because of the vast amounts of fibers that have been mined, processed, and used during the 20th century combined with the long latency period of up to 40 years between exposure and disease presentation. This review summarizes the important new epidemiologic and pathogenic information that has emerged over the past several years. Whereas the development of asbestosis is directly associated with the magnitude and duration of asbestos exposure, the development of a malignant clone of cells can occur in the setting of low-level asbestos exposure. Emphasis is placed on the recent epidemiologic investigations that explore the malignancy risk that occurs from nonoccupational, environmental asbestos exposure. Accumulating studies are shedding light on novel mechanistic pathways by which asbestos damages the lung. Attention is focused on the importance of alveolar epithelial cell (AEC) injury and repair, the role of iron-derived reactive oxygen species (ROS), and apoptosis by the p53- and mitochondria-regulated death pathways. Furthermore, recent evidence underscores crucial roles for specific cellular signaling pathways that regulate the production of cytokines and growth factors. An evolving role for epithelial-mesenchymal transition (EMT) is also reviewed. The translational significance of these studies is evident in providing the molecular basis for developing novel therapeutic strategies for asbestos-related lung diseases and, importantly, other pulmonary diseases, such as interstitial pulmonary fibrosis and lung cancer.

Indexed as

AsbestosHumansLung DiseasesAsbestos

Identifiers

PMID19304273
PMCPMC3544481
OpenAlexW2115450306

What OpenQuestion 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 OpenQuestion graph.