Pleural Thickening and Profusion Resulting From Asbestos Exposure

Pleural Thickening and Profusion Resulting From Asbestos Exposure

Asbestos exposure is a known cause of cancer.  A plethora of research has been done in the past to establish causation.  One interesting study is called, “Asbestos exposure and asbestos-related pleural and parenchymal disease associations with immune imbalance” by Sprince NL, Oliver LC, McLoud TC, Eisen EA, Christiani DC, Ginns LC – Am Rev Respir Dis. 1991 Apr;143(4 Pt 1):822-8. Medical Services Pulmonary and Critical Care Unit, Massachusetts General Hospital, Boston, Massachusetts.  Here is an excerpt: “Abstract – The study hypothesis was that asbestos exposure and asbestos-related pleural plaques and interstitial disease are associated with (1) immune imbalances favoring helper-inducer T-cell subsets in blood and bronchoalveolar lavage (BAL) and (2) T-lymphocyte accumulation in BAL. One hundred twenty-two asbestos-exposed subsets (AES), including 27 nonsmokers (NS), were evaluated and compared with 10 unexposed normal subjects. Data were collected on medical, smoking, and occupational histories, physical examination, spirometry, lung volumes, single-breath DLCO, chest films read by a “B” reader, and T-lymphocyte characterization in blood and BAL using flow cytometry analysis of monoclonal-antibody-treated cells. On average, AES were 47 yr of age and had 23 yr of asbestos exposure. Fifty-eight (48%) had pleural thickening, and seven (6%) had profusion greater than or equal to 1/0. In blood, asbestos-exposed NS had lower total and percent CD8 and lower total CD3 than did normal subjects. In BAL, asbestos-exposed NS had higher total CD3 than did normal subjects. Among AES, increased asbestos exposure was associated with increased percent CD8 in BAL and decreases in both percent lymphocytes and total CD8 in blood. Increase in CD4/CD8 ratio in BAL were associated with pleural thickening. In those seven with profusion greater than or equal to 1/0, there was increased percent CD4 in blood and decreased percent CD8 in BAL. These results suggest immune imbalance favoring helper-inducer T-cell subsets in association with asbestos exposure systemically and with pleural plaques in BAL.”

A second study is called, “Changing attitudes and opinions regarding asbestos and cancer 1934-1965″ by Enterline PE.  Department of Biostatistics, Graduate School of Public Health, University of Pittsburgh, PA 15261.  Am J Ind Med. 1991;20(5):685-700.  Here is an excerpt: “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.”

If you found any of these studies interesting, please read them in their entirety.  We all owe a great deal of thanks to the people who are researching these important issues.

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