One interesting study is called, “Malignant and non-malignant
asbestos-related pleural and lung disease: 10-yearfollow-up study.” By Slavica
Cvitanovi, Ljubo Znaor, Toni Konsa, Zeljko Ivancevi, Irena Peri, Marijan Erceg,
Mirjana Vujovi, Jonatan Vukovi, Zlata Beg-Zec - Croat Med J 2003; 44(5):618-625.
Here is an excerpt: “AIM: To examine the presence of radiologically visible
lung and pleuralchanges in patients who were exposed to the asbestos dust, and
to correlate the progression of thesechanges with the duration and intensity of
exposure and smoking. We also evaluated possible correlationbetween
non-malignant asbestos-related pleural abnormalities and the occurrence of
malignant pleuralmesothelioma. METHODS: Among 7,300 patients who visited our
department between 1991 and 2000 due to non-specificrespiratory symptoms, we
selected 2,420 with chest X-rays indicating the possible existence of
non-malignantasbestos-related diseases. The selected group was followed-up for
progression of radiological changesand the development of malignant pleural
mesothelioma, and the changes were correlated with the intensityand duration of
exposure to asbestos dust and smoking. RESULTS: Radiological changes
characteristic fo rnon-malignant asbestos-related pleural disease or lung
asbestosis were identified in 340 (14%) out of2,420 examined patients, of whom
77 (22.6%) developed malignant pleural mesothelioma, as compared with 13
patients out of 2,080 (0.6%) without radiological signs of asbestosis or
pleural changes. Twenty-three(29.9%) patients who presented with a progression
of pleural disease and lung asbestosis had a very significantincidence of
malignant pleural Mesothelioma.”
Another interesting study is called, “Cytokine regulation of
lung fibroblast proliferation. Pulmonary and systemic changes in asbestos-induced
pulmonary fibrosis.” By Lemaire, I Beaudoin, H Dubois, C - American Journal of
Respiratory and Critical Care Medicine [AM. REV. RESPIR. DIS.]. Vol. 134, no.
4, pp. 653-658. 1986. Here is an excerpt: “A complex series of interactions
between immunocompetent cells and fibroblasts exists. Because pulmonary
fibrosis may result from an increased number of collagen-producing fibroblasts,
the authors studied the production of fibroblast growth factors derived from
alveolar macrophages (AM) and peripheral blood mononuclear leukocytes (PBML)
during the development of asbestos-induced fibrosis. One month after asbestos
exposure, when fibrotic lesions were apparent, AM production of fibroblast
growth factor was significantly enhanced, and such increase persisted for as
long as 6 months.”
Another study is called, “Sister chromatid exchange frequency
in asbestos workers.”Rom WN, Livingston GK, Casey KR, Wood SD, Egger MJ, Chiu
GL, Jerominski L - J Natl Cancer Inst. 1983 Jan;70(1):45-8. Here is an excerpt:
“Abstract - In vitro cytogenetic studies of amosite, chrysotile, and
crocidolite asbestos have shown that these fibers may induce chromosome
abnormalities and an elevated sister chromatid exchange (SCE) rate in mammalian
cells. Twenty-five asbestos insulators (6 with radiographic asbestosis) were
compared to 14 controls frequency matched for age and were found to have a
marginally increased SCE rate in circulating lymphocytes with increasing years
of exposure (P= 0.057). There was a significant association between SCE rate
and smoking (P=0.002) after controlling for years of asbestos exposure and age.
Smoking asbestos insulators had the highest SCE rate. Sister chromatid
exchanges in chromosomes of group A, i.e., the group with the longest
chromosomes, were significantly associated with asbestos exposure and cigarette
smoking, with an interaction between the two.”
Another study is called, “Pathologic changes in the small
airways of the guinea pig after amosite asbestos exposure.” By D. Filipenko, J.
L. Wright, and A. Churg - Am J Pathol. 1985 May; 119(2): 273–278. Here is an
excerpt: “Abstract - To determine whether asbestos dust produces pathologic
changes in the small airways, and to determine where the anatomic lesions of
asbestosis commence, the authors examined lungs from guinea pigs exposed to 10
or 30 mg of amosite asbestos by intratracheal instillation and sacrificed 6
months later. Measurement of airway wall thickness revealed that membranous and
respiratory bronchioles of all sizes in exposed animals were significantly
thicker than those of controls. Amosite fibers were found embedded in the walls
of bronchi and in membranous and respiratory bronchioles; where these fibers
penetrated the airway walls, an interstitial inflammatory and fibrotic reaction
(asbestosis) occurred. It is concluded that :
1) Amosite asbestos
produces diffuse abnormalities throughout the noncartilagenous airways and
possibly the cartilagenous airways as well;
2) This effect is independent of interstitial
fibrosis of the parenchyma (classical asbestosis);
3) Asbestosis, at
least that induced by amosite, commences at any site in the parenchyma to which
the asbestos fibers can gain access, either by deposition in alveoli and
alveolar ducts or by direct passage of fibers through the walls of all types
and sizes of small airways.”
If you found any of these excerpts interesting, please read
the studies in their entirety. We all owe a debt of gratitude to these fine
researchers.
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