Authors' response
- Susan Peters1,
- Hans Kromhout1,
- Ann Olsson2,
- Kurt Straif2,
- Roel Vermeulen1,3 on behalf of all authors
- 1Environmental Epidemiology Division, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
- 2International Agency for Research on Cancer, Lyon, France
- 3Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, The Netherlands
- Correspondence to Susan Peters, Environmental Epidemiology Division, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands; s.peters{at}uu.nl
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Contributors The letter was prepared by SP, HK, AO, KS and RV on behalf of all authors of the original article.
- Accepted 29 November 2011
- Published Online First 26 January 2012
- Lung cancer
- occupational lung disease
- tobacco and the lung
- asthma epidemiology
- COPD epidemiology
- asbestos induced lung disease
- non-small cell lung cancer
In their letter,1 Mastrangelo and colleagues argue that our analyses on occupational organic dust exposure and its specific constituents (eg, endotoxin) suffered from inadequacies that hampered their interpretation. They argue that, given that the effect of endotoxin might diminish after cessation of exposure, analyses of ever versus never exposed to endotoxin might fail to identify the protective effect of endotoxin. Furthermore, they argue that the failure to differentiate between livestock/dairy and crop/orchard farmers may have obscured the protective effect as some papers have argued that the effect is contained (largely) to livestock/dairy farmers only.
The main aim of our paper was to study …
