• Clinical epidemiology
• drug induced lung disease
• interstitial fibrosis
• occupational lung disease
• histology/cytology
• COPD pathology
• asthma epidemiology
• COPD epidemiology
• allergic alveolitis
• allergic lung disease
• asthma
• sarcoidosis

We thank Drs Barber and Fishwick for their interest in our paper and would like to briefly respond to their comments.1 Our paper describes a pragmatic epidemiological study with individuals who had an underlying diagnosis of idiopathic pulmonary fibrosis clinical syndrome (IPF-CS).2 The aim was to investigate recent temporal trends in incidence and survival and not to consider environmental exposures that may have an aetiological link. Hence, although this increase may be linked to occupational or other environmental exposures, our data do not permit firm conclusions to be drawn. It is also possible that the rapid increase in incidence reported is due to an increasing tendency to investigate patients in the UK.

We agree that there is a possibility that a proportion of our cases may have been exposed to asbestos. However, 39% of registered deaths from IPF-CS (from the Office of National Statistics dataset) and 37% of cases in primary care (from The Health Improvement Network dataset) were women, who are unlikely to have had a substantial direct exposure to asbestos. We believe that factors other than occupational exposure to asbestos are important in explaining our data and until firm aetiological links are established, similar cases of pulmonary fibrosis should be considered idiopathic.