severe asthma patient. To make the definition more widely applicable, a global definition was recently published under a World Health Organization (WHO) consultation on severe asthma [10]. It is quite clear that the questions that needed to be answered in the 1990s were as follows. 1) What does the patient with severe asthma look like? 2) Why have these patients developed severe asthma? 3) How should existing treatments be used and what new treatments can be given to control severe asthma? 10 years on and these questions are still unanswered however, there are now important insights from the information that has been obtained from research into severe asthma during this time. Perhaps the most pertinent information is how the disease is heterogeneous, and the challenge for the next 10 years would be to understand the different types of severe asthma. It is also important to determine whether severe asthma represents an altogether different new form of asthma. If one espouses the generally accepted notion that asthma is the result of a complex gene–environment interaction then it could make sense. Certainly, the world has changed more rapidly over the past 25 years than it has in the previous 100 years, in terms of both the environment lived in and lifestyles. It is quite pertinent to ask whether environmental changes could have led to the increase in asthma prevalence and increasing severity of asthma, perhaps through epigenetic changes. Is it a result of disordered immunity to the new challenging environment of allergens, pollutants and infections? Would this drive the inflammatory response that leads to severe asthma? It is important that such questions and other related issues be asked and be answered. The Guest Editors of this Monograph are fortunate to be part of an ongoing ATS/ERS Task Force on severe asthma, through which an eminent group of experts were asked to contribute to the Monograph. The task asked of them was to describe what we have learnt, what are the objectives for the next 10 years, and what milestones can be expected at the end of the next decade. We would like to thank all those who have contributed and we greatly appreciate the time and commitment they spent on this project. We would also like to thank the ERS Publications Office for their enthusiasm and hard work. The burden of severe asthma is substantial and expectations for better treatments are high. We hope this Monograph represents a small step towards achieving these goals. Statement of interest K.F. Chung has been reimbursed for travel expenses to international meetings and received honoraria for speaking at meetings sponsored by GlaxoSmithKline, AstraZeneca and Novartis. K.F. Chung has participated in advisory boards meetings of GlaxoSmithKline, Boehringer Ingelheim and Novartis, and received unrestricted research funding from GlaxoSmithKline and Pfizer and has taken part in clinical trials organised by GlaxoSmithKline, Novartis and Asthmatyx. E.H. Bel has received a fee for speaking from GlaxoSmithKline, has received funds for research from GlaxoSmithKline and Novartis, and has received fees for consulting from MSD and Novartis. S.E. Wenzel’s institute, the University of Pittsburgh, has received money for mulitcenter research studies from MedImmune, GlaxoSmithKline, Amgen, Cephalon and Aerovance. Monies received in each case by the University of Pittsburgh were ,100,000 US$. S.E. Wenzel received consulting funds from GlaxoSmithKline, Merck, Amira, Amgen all ,10,000 US$. References 1. McFadden ER Jr. A century of asthma. Am J Respir Crit Care Med 2004 170: 215–221. 2. Osler W. The Principles and Practice of Medicine. New York, D. Appleton, 1921. 3. Barnes PJ. Drugs for asthma. Br J Pharmacol 2006 147: Suppl. 1, S297–S303. 4. Medical Research Council. Controlled trial of effects of cortisone acetate in chronic asthma. Lancet 1956 798: 167–172. viii INTRODUCTION