Asbestos is a naturally occurring mineral that was widely used in a variety of products.?? Asbestos only becomes dangerous when it is broken into small pieces that become airborne.?? When these small pieces of asbestos dust are inhaled they settle into the lungs and can cause life threatening diseases.?? One interesting study is called, "Screening for asbestos-induced diseases in Finland" by Kari Koskinen, MD, Jouko-Pekka Rinne, MD, Anders Zitting, MD, Antti Tossavainen, DTech, Jukka Kivek??s, MD, Kari Reijula, MD, Pekka Roto, MD, MIH, Matti S. Huuskonen, MD, MSc - Finnish Institute of Occupational Health, Helsinki, Finland - American Journal of Industrial Medicine - Volume 30 Issue 3, Pages 241 – 251.?? Here is an excerpt: "Abstract - Screening for asbestos-induced diseases in Finland was carried out in 1990-1992 as a part of the Asbestos Program of the Finnish Institute of Occupational Health. The aim of the present study was to find the workers who had developed an asbestos-induced disease in certain occupations. Examination of active or retired workers included a personal interview on work history and asbestos exposure, and a chest X-ray. The target group for the screening comprised workers under 70 years of age who had worked at least for 10 years in construction, 1 year in a shipyard or in the manufacture of asbestos products. A preliminary questionnaire was sent to 54,409 workers, 18,943 of whom finally participated in the screening examination. The mean age of the workers was 53 years; 95% were employed in construction, 2% in shipyards, and 3% in the asbestos industry. The criteria for a positive screening result were (1) a radiographic finding clearly indicating lung fibrosis (at least ILO category 1/1), (2) a radiographic finding indicating mild lung fibrosis (ILO category I/O) with unilateral or bilateral pleural plaques, (3) marked abnormalities of the visceral pleura (marked adhesions with or without pleural thickening), or (4) bilateral pleural plaques. The positive cases totalled 4,133 (22%) and were sent for further investigation. In addition to the screening, information on the presence of asbestos in the work environment, prevention of asbestos exposure, as well as on the health effects of asbestos exposure and smoking were given to the participating workers. The screening acted as a preliminary survey to prompt further national follow-up of asbestos-induced diseases among the workers who have been exposed to asbestos. This article presents the material, methods, and overall results of the screening. ??
A second study is called, "Clara cell protein (CC-16) and surfactant-associated protein A (SP-A) in asbestos-exposed workers." By Lesur O, Bernard AM, Bégin RO - Unité de Recherche Pulmonaire, Université de Sherbrooke, Québec, Canada.?? Chest. 1996 Feb;109(2):467-74.?? Here is an excerpt: "Abstract - Asbestos-exposed workers (Asb) can sometimes develop lung impairments resembling idiopathic pulmonary fibrosis (IPF). Smoking is often a troubling confounder in the natural history of these lung diseases. Distal airspace epithelial cells, which are also altered in asbestosis, secrete Clara cell protein (CC-16, also designated CC-10) and surfactant-associated protein A (SP-A). By inhibiting phospholipase A2 (PLA2), CC-16 and SP-A are putative candidates for controlling lung inflammatory events. Both were measured with PLA2 activity in alveolar fluids (and sera for CC-16) of smoker and nonsmoker Asb and compared with smoking-matched normal subjects (N). CC-16 (in mg/L) was slightly increased in Asb and affected by smoking: nonsmoker Asb: 3.1 +/- 0.5 vs nonsmoker N: 1.9 +/- 0.2 (p < 0.05), smoker Asb: 1.7 +/- 0.3 vs smoker N: 0.6 +/- 0.1 (p < 0.05). SP-A (in microgram/mL) was enhanced in Asb but not affected by smoking: 5.4 +/- 1.5 in Asb vs 1.6 +/- 0.4 in N (p < 0.05), whereas SP-A to phosphorus ratio was increased in Asb but affected by smoking. CC-16 to albumin and CC-16 in serum to alveolar fluid ratios were altered by cigarette consumption in Asb (p < 0.05 vs N). Secretory PLA2 activity was slightly enhanced in Asb (p < 0.05 vs N). All data were similar between stages of disease. In summary, alveolar CC-16, SP-A, and secretory PLA2 activity were increased in Asb. Smoking affected several parameters. By this habit, Asb might reinforce lung profibrotic factors and increase their risk in developing lung alterations resembling IPF."
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.
