Onderzoek van Wang geeft aanwijzingen dat asbest en tabaksrook elk een eigen onafhankelijke schadelijke invloed hebben op de longfunctie. Asbest heeft vooral negatief effect op de longcapaciteit en tabaksrook op het vermogen lucht op te nemen. Nymark en collega’s zagen verschillen in genetische patronen tussen twee groepen longkankerpatiënten (totaal 28 personen), waarvan één groep intensief aan asbest blootgesteld was geweest. Ook zagen zij dat tabaksrook de cellen op genetisch niveau meer kwetsbaar maakt voor de schadelijke effecten van asbest. Voor dit onderzoek werd de array-CGH moluculair genethische techniek gebruikt. Bron: Nymark P. et al. (2006). Identification of specific gene copy number changes in asbestos-related lung cancer. Cancer Research Jun 1.66(11):5737-43.
Wang X, Yano E, Wang Z, Wang M, Christiani DC. (2006). Adverse effects of asbestos exposure and smoking on lung function. American Journal of Industrial Medicine May.49(5):337-42.
BACKGROUND: Exposure to asbestos is a well-recognized cause of both malignant and nonmalignant diseases of lung parenchyma and pleura. This study was conducted to determine the adverse effects of exposure to asbestos and smoking on pulmonary function.
METHODS: Four hundred and sixty-eight workers who were occupationally exposed to asbestos for an average of 13 years were selected from an asbestos-product factory in China. Of them, 85 workers were diagnosed with asbestosis. Additionally, 282 workers who had no experience of exposure to industrial dust were included as a control group. A questionnaire was administered during a face-to-face interview and spirometric maneuvers and single-breath CO diffusing capacity (DL(CO)) were performed.
RESULTS: Multivariate regression analysis showed that exposure to asbestos was more strongly associated with decreased forced vital capacity (FVC) and DL(CO), and asbestosis more strongly associated with decreased FVC, while smoking was a major contributing factor to reduced FEV1/FVC. The results were confirmed by a further analysis where the subjects were grouped exclusively by smoking, asbestos exposure, and chest radiographic changes. No interaction or joint effect was observed between asbestos exposure and smoking.
CONCLUSIONS: This analysis suggested that asbestos and smoking might play independent roles, in which asbestos caused mainly a restrictive impairment, and smoking was a major causal factor for airway obstruction in the workers who were intensively exposed to asbestos.
Nymark P, Wikman H, Ruosaari S, Hollmen J, Vanhala E, Karjalainen A, Anttila S, Knuutila S., (2006). Identification of specific gene copy number changes in asbestos-related lung cancer. Cancer Research Jun 1.66(11):5737-43.
Abstract
Asbestos is a well-known lung cancer-causing mineral fiber. In vitro and in vivo experiments have shown that asbestos can cause chromosomal damage and aberrations. Lung tumors, in general, have several recurrently amplified and deleted chromosomal regions. To investigate whether a distinct chromosomal aberration profile could be detected in the lung tumors of heavily asbestos-exposed patients, we analyzed the copy number profiles of 14 lung tumors from highly asbestos-exposed patients and 14 matched tumors from nonexposed patients using classic comparative genomic hybridization (CGH). A specific profile could lead to identification of the underlying genes that may act as mediators of tumor formation and progression. In addition, array CGH analyses on cDNA microarrays (13,000 clones) were carried out on 20 of the same patients. Classic CGH showed, on average, more aberrations in asbestos-exposed than in nonexposed patients, and an altered region in chromosome 2 seemed to occur more frequently in the asbestos-exposed patients. Array CGH revealed aberrations in 18 regions that were significantly associated with either of the two groups. The most significant regions were 2p21-p16.3, 5q35.3, 9q33.3-q34.11, 9q34.13-q34.3, 11p15.5, 14q11.2, and 19p13.1-p13.3 (P < 0.005). Furthermore, 11 fragile sites coincided with the 18 asbestos-associated regions (P = 0.08), which may imply preferentially caused DNA damage at these sites. Our findings are the first evidence, indicating that asbestos exposure may produce a specific DNA damage profile.