oyal Society and the MRC Human Genetics Unit. DNA extraction was performed at the Wellcome Trust Clinical Research Facility in Edinburgh. Genotyping was funded by the European Union Framework Programme 6 EUROSPAN project. SHIP: SHIP is part of the Community Medicine Research net of the University of Greifswald, Germany, which is funded by the Federal Ministry of Education and Research, the German Asthma and COPD Network, the Ministry of Cultural Affairs as well as the Social Ministry of the Federal State of Mecklenburg-West Pomerania. Genome-wide data have been supported by the Federal Ministry 17785458 of Education and Research and a joint grant from Siemens Healthcare, Erlangen, Germany and the Federal State of MecklenburgWest Pomerania. The University of Greifswald is a member of the `Center of Knowledge RO4929097 site Interchange’ program of the Siemens AG. TwinsUK: TwinsUK is funded by the Wellcome Trust; the Arthritis Research Campaign; European Community’s Seventh Framework Programme /grant agreement HEALTH-F22008-201865-GEFOS and Seventh Framework Programme, ENGAGE project grant agreement HEALTH-F4-2007-201413 and the European Union FP-5 GenomEUtwin Project. The study also receives support from the National Institute for Health Research comprehensive Biomedical Research Centre award to Guy’s & St Thomas’ NHS Foundation Trust in partnership with King’s College London. TDS is an NIHR senior Investigator. The project also received support from a Biotechnology and biological Sciences Research Council project grant. Vis: The Vis study was funded by grants from the Medical Research Council, European Commission Framework 6 project EUROSPAN and Republic of Croatia Ministry of Science, Education and Sports research grants to I.R.. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist. E-mail: [email protected]; [email protected] 2 May 2011 | Volume 6 | Issue 5 | e19382 Candidate Genes Evaluation in SpiroMeta Introduction Pulmonary function is usually assessed by measurement of forced expiratory volume in one second, forced vital capacity, and the ratio of FEV1 to FVC. The measurements are integral to the diagnosis of chronic obstructive pulmonary disease, and also are important long term predictors of population morbidity and mortality. Reduced FEV1/FVC defines airways obstruction; whereas reduced FEV1 grades the severity of obstruction. Pulmonary function is determined by both environmental and genetic factors. Tobacco smoking is the major environmental risk factor for the development of COPD. A genetic contribution to pulmonary function is well established with heritability estimates reaching 77 percent for FEV1. Linkage analyses within families have previously identified multiple genomic regions associated with spirometry measures and respiratory diseases. In addition, candidate gene studies have identified more than 100 genes which have been suggested to contribute to variability in lung function. The majority have been studied because of their potential pathophysiological role in the development of COPD. Some genes have been examined for association with lung function measurements in individuals with other specific respiratory diseases, or to a lesser extent, in the general population. With the 
exception of SERPINA1, which is the best documented genetic risk factor to influence the development of COPD,