Cancer Incidence Among Workers Resulting From Exposure To Asbestos Dust And Fibers
Some occupations are considered more dangerous when it comes to asbestos exposure. For example, people working as pipefitters, plumbers, and electricians suffer from an inordinate rate of mesothelioma disease. This has been the subject of a great deal of research.
One interesting study is called, “Asbestos exposure, smoking habits, and cancer incidence among production and maintenance workers in an electrochemical plant” by Bjorn Hilt, MD, Sverre Langad, MD, MSc, Aage Andersen, Jan Rosenberg, MD – Department of Occupational Medicine, Telemark Sentralsjukehus, Porsgrunn, Norway, Cancer Registry of Norway, Montebello, Oslo, Norway, Health Department, Norsk Hydro A.S., Porsgrunn Fabrikker, Porsgrunn, Norway – American Journal of Industrial Medicine – Volume 8 Issue 6, Pages 565 – 577.
Here is an excerpt:
“Abstract – The incidence of cancer was studied in a cohort of 287 men who were exposed to asbestos at a nitric acid production plant from 1928 onwards. During the observation period from 1953 through 1980 all cancer cases among the cohort members were identified in The Cancer Registry. For the whole cohort 42 cases of cancer were observed versus 30.6 expected. The figures for cancer of the lungs and pleura combined were 17 observed versus 3.7 expected.
The corresponding figures for a heavily exposed subcohort were 11 observed and 1.2 expected. In that group there was also an increased incidence of colon cancer with 3 cases observed against 0.8 cases expected. Within the whole cohort four cases of pleural and one case of peritoneal malignant mesothelioma were found.
There was also an increased incidence of malignant melanoma of the skin with 3 cases observed against 0.6 expected. For cancer cases that were registered as of unknown origin there were 7 cases observed and 1.4 expected. There was no increased rate ratio for cancer at any site before 20 years after the first asbestos exposure.
The smoking habits of all cohort members were recorded and the relative rates for lung cancer were calculated in relation to smoking habits. In common with previous studies the results indicate a multiplicative model for the interaction between asbestos exposure and smoking in regard to lung cancer risk.”
Another interesting study is called, “Tests for effect of asbestos on benzo(a)pyrene carcinogenesis in the respiratory tract” by Miller, L.; Smith, W.E.; Berliner, S.W. Publication Date 1965 Jan 01 – Ann. N.Y. Acad. Sci.; (United States); Journal Volume: 132.
Here is an excerpt:
“Hamsters were given 25 intratracheal injections of 0.5 mg benzopyrene (BaP) in Tween-60 with or without 0.25 mg chrysotile (Chrys) asbestos. 173 to 214 days after start of injections, 4 tumors in 3/5 surviving animals subjected to BaP alone were found whereas 7/7 (15 total) were found in those given BaP plus Chrys. Three of these were larger than 3 mm.
Animals given Chrys or Tween alone or control animals had no tumors. 16 injections of 0.5 mg BaP in Tween-60 with or without 2.5 mg amosite (AM) asbestos were given to hamsters. 29% of group given BaP and 26% of group given BaP plus AM had tracheobronchial tumors when sacrificed at day 240. One form of asbestos synergistically increased carcinogenic activity of BaP. Yield of tumors decreased with time after discontinuation of injections suggesting reversible action.”
Another interesting study is called, “DNA single strand breaks induced by asbestos fibers in human pleural mesothelial cells in vitro” - Environmental and Molecular Mutagenesis Volume 33 Issue 2, Pages 153 – 160.
Here is an excerpt:
“Abstract – The mechanisms of the cellular effects and DNA damage caused by asbestos fibers in human mesothelial cells are not well understood. We exposed transformed human pleural mesothelial cells to 1-4 g/cm2 crocidolite and to 10-100 ng/ml tumor necrosis factor alpha for up to 48 hr and studied the induction of DNA damage using the Comet assay.
As a positive control, 100 M H2O2 was used. The DNA single strand breaks were assessed as the mean tail moments and as distributions of the tail DNA in the cell. The Comet assay showed significant but reversible increases in the mean tail moments, but not in the distribution of Comet tails in the histograms in cells exposed to 1 g/cm2 crocidolite for 6 hr. At higher concentrations of asbestos fibers all the indices in the Comet assay showed significant and irreversible change. All the doses of TNF-caused marginal increase in the mean tail moments.
The mean tail moments were highest in the cells with concurrent treatment to TNF- and crocidolite. In the cells pretreated with inhibitors of antioxidant enzymes (aminotriazole for catalase and buthionine sulfoximine) for (glutamylcysteine synthetase) asbestos fibers slightly increased oxidant-related fluorescence of dichlorofluorescein (DCFH) but did not cause any further increases in the mean tail moments.
This study shows that asbestos fibers cause DNA single strand breaks in human mesothelial cells. Since the inhibition of antioxidant enzymes did not have an effect on the DNA damage caused by the fibers, other mechanisms than free radicals seem to be involved in the induction of DNA damage by mineral fibers.”
If you found any of these excerpts interesting, please read the studies in their entirety.
