Lung Cancer when Associated with Asbestosis and Mesothelioma is an Occupational Disease

The assertion that asbestosis must be present in order to attribute a lung cancer to asbestos exposure does not meet accepted standards for establishing causation.  One interesting study is called, "Historical perspectives in occupational medicine. Changing attitudes and opinions regarding asbestos and cancer 1934–1965" by Philip E. Enterline PhD - American Journal of Industrial Medicine Volume 20, Issue 5, pages 685–700, 1991.  Here is an excerpt: "Abstract - Literature published in the years 1934–1965 was reviewed to determine attitudes and opinions of scientists as to whether asbestos is a cause of cancer. In Germany, the issue was decided in 1943 when the government decreed that lung cancer, when associated with asbestosis (of any degree), was an occupational disease. In the United States, however, there was no consensus on the issue until 1964. Opinions of scientists over a 22 year period are shown and the contributions of various cultural, social, economic and political factors to these opinions are discussed. A lack of experimental and epidemiological evidence played a major role in delaying a consensus. Other important factors included a rejection of science conducted outside of the U.S. during this period, particularly a rejection of German scientific thought during and after WWII, and a rejection of clinical evidence in favor of epidemiological investigations. Individual writers rarely changed their minds on the subject of asbestos as a cause of cancer."

A second study is called, "Lung cancer and asbestos exposure: Asbestosis is not necessary" - David Egilman MD MPH, Alexander Reinert - American Journal of Industrial Medicine - Volume 30, Issue 4, pages 398–406, October 1996.  Here is an excerpt: "Abstract - Recent commentaries on the issue of asbestos-related lung cancer have raised important points. One major question is whether lung cancer can be attributed to asbestos exposure in the absence of asbestosis. This review attempts to place the debate in the proper context for establishing causation. Relevant epidemiologic and pathologic studies are analyzed, as well as the scientific basis for each position in the debate. The assertion that asbestosis must be present in order to attribute a lung cancer to asbestos exposure does not meet accepted standards for establishing causation. In addition, some evidence has been incorrectly cited in support of this position. This discussion can benefit from clearer definitions of asbestosis, a more thorough evaluation of the available scientific information, and a proper context for determining causation. This review of the available evidence indicates that lung cancers can occur as a result of asbestos exposure, in the absence of clinical or histologic asbestosis. Causation in an individual should be assessed by considering duration of exposure, intensity of exposure, and appropriate latency."

A third study is called, "Induction of micronuclei, hyperdiploidy and chromosomal breakage affecting the centric/pericentric regions of chromosomes 1 and 9 in human amniotic fluid cells after treatment with asbestos and ceramic fibers" by Elke Doppa,  Maik Schuler, Dietmar Schiffmanna and David A. Eastmond - Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 377, Issue 1, 9 June 1997, Pages 77-87.  Here is an excerpt: "Abstract - This article describes the induction of micronuclei, hyperdiploidy and chromosome breakage in human amniotic cells in vitro by amosite, chrysotile and crocidolite asbestos, and ceramic fibers. The response of human (amniotic fluid cells) and rodent (Syrian hamster embryo fibroblasts, SHE) cells to fiber treatment was compared using the micronucleus assay. The data of the rodent studies were taken from a previous investigation (Dopp, E. et al. (1995) Environ. Health Perspect., 103, 268–271). All types of mineral fibers caused a significant increase of micronucleated cells. The kinetochore analysis revealed that all three types of asbestos and ceramic fibers yielded similar effects. Approximately 50% of the induced micronuclei were kinetochore-negative indicating formation through clastogenic events. Human amniotic cells were much less susceptible than SHE cells to the induction of micronuclei by mineral fibers. This again demonstrates that SHE cells are more susceptible to chromosomal changes than human amniotic fluid cells. The application of fluorescence in situ hybridization (FISH) with tandem DNA probes yielded more detailed information about specific structural chromosome aberrations in the 1 (cen–q12) and 9 (cen–q12) regions and about abnormal numbers of chromosomes in interphase human amniotic fluid cells. Using this FISH approach we found a statistically significant increase of chromosomal breakage in the pericentric heterochromatin regions of chromosomes 1 and 9 in interphase human amniotic cells after exposure to asbestos and ceramic fibers compared to control cells. The number of hyperdiploid cells was also significantly increased. Our results show that asbestos fibers as well as ceramic fibers are inducers of structural and numerical chromosomal aberrations in human amniotic fluid cells."

We all owe a debt of gratitude to these fine researchers for their important work.  If you found any of these excerpts helpful, please read the studies in their entirety.