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American Journal of Respiratory Cell and Molecular Biology. Vol. 32, pp. 167, 2005
© 2005 American Thoracic Society
DOI: 10.1165/rcmb.F288


Correspondence

Effects of Cigarette Smoke on Pulmonary Homeostasis

K. Fan Chung, M.D., D.Sc.a and David A. Groneberg, M.D.b

a Imperial College London, United Kingdom
b Free University and Humboldt-University Berlin, Germany

To the Editor:

We read with great interest the article of Kim and colleagues (1) and the ensuing discussion about analyzing cigarette smoke effects (24). We agree with the opinion that it is difficult to extrapolate the experimental findings to the effects on the human pulmonary homeostasis caused by long-term inhalation by smokers of low concentrations of cigarette smoke. We would like to point out that current approaches to dissect detrimental effects of airborne pollutants such as cigarette smoke, allergens, or gases in cell cultures or animal models are not only biased by the artificial background of high concentrations and short-term exposure, but also by a lack of standardizations and agreement amongst the research community about "acceptable"/"relevant" levels and duration of exposure. There are numerous approaches to exposure, varying from different components (e.g., cigarette smoke extract versus single substances) to different exposure protocols. Whereas all these studies may provide new and important details into pathomechanisms, the heterogeneity of exposure protocols leads to a situation in which most studies cannot easily be compared with each other due to major differences in exposure modes and protocols. There is a need for some agreement amongst researchers in the field on exposure protocols for all major exposure agents including i.e., smoke, allergen, SO2, NO2, fiber particles, etc. These agreements could encompass, for example, not only the length of exposure (acute and chronic exposure models should be described) but also the concentration, etc., and should be made for relevant species. Definition of optimized protocols for murine models of asthma already exist (5), but should be extended. We believe that the uniformity of exposure protocols would drastically improve the comparison between individual studies and could allow for extrapolation of data, thus leading to real progress. Uniformity of models would also provide an improved peer reviewing process because technical concerns about exposure protocols could be eliminated.

Footnotes

Conflict of Interest Statement: K.F.C. has no declared conflicts of interest; D.A.G. has no declared conflicts of interest.

References

  1. Kim H, Liu X, Kobayashi T, Conner H, Kohyama T, Wen FQ, Fang Q, Abe S., Bitterman P, Rennard SI. Reversible cigarette smoke extract–induced DNA damage in human lung fibroblasts. Am J Respir Cell Mol Biol 2004;31:483–490.[Abstract/Free Full Text]
  2. Shapiro SD. Smoke gets in your cells. Am J Respir Cell Mol Biol 2004;31:481–482.[Free Full Text]
  3. Rennard SI. Cigarette smoke in research. Am J Respir Cell Mol Biol 2004;31:479–480.[Free Full Text]
  4. Shapiro SD. The search for biological truth using imperfect models in an imperfect world. Am J Respir Cell Mol Biol 2004;31:479.
  5. Kips JC, Anderson GP, Fredberg JJ, Herz U, Inman MD, Jordana M, Kemeny DM, Lotvall J, Pauwels RA, Plopper CG, et al. Murine models of asthma. Eur Respir J 2003;22:374–382.[Abstract/Free Full Text]




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Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2005 American Thoracic Society.