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The two obstructive airway diseases bronchial asthma and chronic obstructive pulmonary disease (COPD) represent major global causes of disability and death. Whereas COPD research was largely underfunded in the 1980s and 1990s, increased funding activities have been initiated since the year 2000. However, detailed scientometric data on the development of research for asthma and COPD have not been generated so far.The present scientometric study was conducted to establish a database of research quantity and quality in the 20-year period between 1987 and 2006 using the Web of Science information system and the United Kingdom and Germany for comparison of research activities.The information database Web of Science was screened and during the period from 1987 to 2006 a number of 8,874 items related to asthma was published by UK affiliations. Of these, 1,824 were published in cooperation with a total of 86 other countries. This is a ratio of 20.55%. In the same period, 3,341 items were published by German institutions (923 in cooperation with 56 other countries, ratio of 27.63%). Citation analysis demonstrated an average citation of 24.48 per UK article and 17.62 per German article. For COPD, 2,179 items were published by UK affiliations and 689 items by German institutions. Of the UK COPD publications, 570 were published in cooperations with 47 countries (ratio of 22.95 %). By contrast, 218 of the 689 German COPD articles were published with 29 other countries (ratio of 25.49%). When citation analysis was performed, average citation ratios of 18.93 for the UK and 10.61 for German were found.Summarizing this first country-specific comparative benchmarking analysis for obstructive pulmonary diseases it can be concluded that (1) asthma research dominated in the past 20 years; (2) COPD research gained importance in the field since the end of the 1990s; (3) there are large differences present in the research output between the two high-income countries examined.

The effect of prior ozone (O3) exposure on airway hyperresponsiveness and inflammation induced by trimellitic anhydride (TMA) has been investigated in TMA-sensitized guinea pigs. Airway responsiveness was measured as the concentration of acetylcholine needed to increase baseline lung resistance (RL) by 300% (PC300). Ozone (3 ppm for 3 h) caused an increase in -log PC300 at 1 h after exposure, with return of -log PC300 to control levels at 8 h. Ozone also increased baseline RL at 8 h. TMA challenge increase -log PC300 in TMA-sensitized guinea pigs at 8 h after challenge from 3.85 +/- 0.09 to 4.11 +/- 0.09. Ozone exposure prior to TMA challenge prevented the induction of airway hyperresponsiveness with a mean -log PC300 of 3.51 +/- 0.20, which was not different from that of control TMA-sensitized group. Baseline RL was significantly higher in ozone-pretreated animals after TMA challenge when compared to those of either control or challenged with TMA alone. Ozone had no effect on TMA challenge-induced BAL eosinophilia and neutrophilia. We conclude that a single exposure to ozone inhibits the increase in airway responsiveness but increases the bronchoconstrictor response induced by TMA in TMA-sensitized guinea pigs; however, the inflammatory airway response to TMA is unchanged by preexposure to ozone.