Evidence map›Paper›PMID 17607002›Full record

ReviewProceedings of the American Thoracic Society2007

Gene-air pollution interactions in asthma.

Stephanie J London

Abstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

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

  1. Pooled it
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  14. Early-life air pollution and asthma risk in minority children. The GALA II and SAGE II studies.American journal of respiratory and critical care medicine · 2013
    Article
  15. Article
  16. Article
  17. Article
  18. Role of GSTM1 in resistance to lung inflammation.Free radical biology & medicine · 2012
    Review
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  20. Review
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.

Stephanie J LondonEpidemiology Branch and Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA. London2@niehs.nih.gov

Funding

Genetic Analyses For Epidemiologic Studies Of Respiratory DiseaseZIAES025045 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI LONDON, STEPHANIE · 2009 to 2025
$7.3M
Genetic And Environmental Factors In Childhood Respiratory HealthZIAES049019 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI LONDON, STEPHANIE · 2009 to 2025
$6.8M
GENETIC AND ENVIRONMENTAL FACTORS IN CHILDHOOD RESPIRATORY HEALTHZ01ES049019 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI LONDON, STEPHANIE JOAN · 1996 to 2008
$537k
Genetic Analyses For Epidemioloy Of Respiratory DiseaseZ01ES025045 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI LONDON, STEPHANIE JOAN · 2000 to 2008
$238k
Intramural NIH HHS
6 · The paper itself

Abstract

Genetic and environmental factors interact to cause asthma. However, genetic studies have generally ignored environmental factors and environmental studies have generally ignored genetics. Thus, there are few examples from the literature of specific gene-environment interactions in relation to asthma. The clearest examples of genetic interactions for inhaled pollutants exist for endotoxin, environmental tobacco smoke, and ozone. Endotoxin-genetic interactions in asthma are the focus of two other manuscripts from this conference, so this review focuses on environmental tobacco smoke and ozone. In the sparse literature, there is evidence for the role of specific genes involved in oxidative stress, notably GSTM1 and TNF, in the respiratory responses to ozone and environmental tobacco smoke. There are few data on genes involved in innate immune pathways, which are crucial in response to endotoxin and may play a role in response to ozone and environmental tobacco smoke. Genes involved in oxidative stress may interact with both air pollutants and diet in relation to asthma phenotypes. Future directions to advance the field include whole genome association studies, better assessment of exposure and phenotypes, and consideration of joint interactions with diet and other co-factors that influence individual susceptibility.

Indexed as

AsthmaGenetic Predisposition to DiseaseGenotypeGlutathione S-Transferase piGlutathione TransferaseHumansOzonePhenotypePolymorphism, GeneticTobacco Smoke PollutionTumor Necrosis Factor-alphaGlutathione S-Transferase piGlutathione TransferaseGSTP1 protein, humanOzoneTobacco Smoke PollutionTumor Necrosis Factor-alpha

Identifiers

PMID17607002
PMCPMC2647621

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.