Exposures and idiopathic lung disease

Varsha Taskar, David Coultas

Research output: Contribution to journalReview articlepeer-review

57 Scopus citations

Abstract

Of the idiopathic lung diseases, idiopathic pulmonary fibrosis (IPF) and sarcoidosis have been the focus of a growing number of epidemiological investigations on the risk of environmental and occupational exposures. To date, the consistency of epidemiological evidence is suggestive of a causal relationship between several environmental exposures and IPF, with the strongest evidence for cigarette smoking and metal dust. Current knowledge about pathogenesis provides further support for a causal link. However, scant epidemiological evidence for dose-response and temporality weaken the case for making causal inferences. In contrast to IPF, the quantity of epidemiological evidence for environmental exposures and sarcoidosis is smaller. Two studies provide consistent evidence for exposures to agricultural dust and musty odor/mold/mildew, and studies among military personnel and firefighters suggest mixed dust and fume exposures as risk factors for sarcoidosis. Although studies of the pathogenesis of sarcoidosis also provide evidence supporting environmental causation, more epidemiological studies are needed to establish consistency of associations, dose-response, and temporality. Future investigations, of gene-environment interaction offer the potential for strengthening the evidence of causation between several environmental and occupational exposures and idiopathic lung diseases.

Original languageEnglish (US)
Pages (from-to)670-679
Number of pages10
JournalSeminars in Respiratory and Critical Care Medicine
Volume29
Issue number6
DOIs
StatePublished - Dec 2008
Externally publishedYes

Keywords

  • Causation
  • Epidemiology
  • Exposures
  • Idiopathic pulmonary fibrosis
  • Sarcoidosis

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

Fingerprint

Dive into the research topics of 'Exposures and idiopathic lung disease'. Together they form a unique fingerprint.

Cite this