ABSTRACT
Mesothelioma is a "new" malignant disease strongly associated with exposure to amphibole asbestos exposure (amosite and crocidolite) environmentally and in the work place. Nonetheless, in recent years, we have learned that many cases of mesothelioma are idiopathic, while some are caused by therapeutic irradiation or chronic inflammation in body cavities. This paper reviews the key epidemiological features of the malignancy in the context of the biological and mineralogical factors that influence mesothelioma development. These tumors challenge the diagnostic pathologist's acumen, the epidemiologist's skill in devising meaningful and definitive studies, the industrial hygienist's knowledge of environmental hazards in diverse occupational settings, and the clinician's skill in managing an intrepid and uniformly fatal malignancy.
Subject(s)
Asbestos, Amosite/toxicity , Asbestos, Amphibole/toxicity , Asbestos, Crocidolite/toxicity , Mesothelioma/epidemiology , Asbestos, Amosite/history , Asbestos, Amphibole/history , Asbestos, Crocidolite/history , Asbestos, Serpentine/history , Asbestos, Serpentine/toxicity , Female , History, 20th Century , Humans , Lung Neoplasms/epidemiology , Lung Neoplasms/etiology , Male , Mesothelioma/history , Mining , Occupational Diseases/epidemiology , Occupational Diseases/etiologyABSTRACT
The exposure of Libby MT residents to amphibole-contaminated vermiculite is well known. To explore the gene-environment interactions in the development of asbestos-related diseases (ARD), a mouse model of asbestos exposure using Six-mix (a combination of amphibole fibers gathered from six sites at the Libby vermiculite mine), crocidolite asbestos, or saline as a negative control was used to determine both gene expression responses by using mouse 10,000 oligonucleotide array and to visualize these changes histologically. Mice were sacrificed and whole lungs harvested for histology and microarray analysis six months following exposure via intratracheal instillation. Using an arbitrary cutoff of 1.25-fold change, genes whose RNA expression levels were specifically altered in response to the different amphibole exposures were grouped into categories by a gene ontology analysis program, GoMiner. Our hypothesis was that assessment of asbestos-responsive genes would provide a better understanding of response mechanisms. These experiments have provided new candidates for genes involved in the asbestos response pathways.
Subject(s)
Aluminum Silicates/toxicity , Asbestos, Amphibole/toxicity , Asbestosis/immunology , Disease Models, Animal , Environmental Exposure/adverse effects , Gene Expression Regulation/drug effects , Aluminum Silicates/history , Animals , Asbestos, Amphibole/history , Asbestosis/genetics , Electronic Data Processing , Environmental Exposure/history , Gene Expression Profiling , Gene Expression Regulation/genetics , Gene Expression Regulation/immunology , History, 20th Century , Humans , Mice , Mining/history , Montana , Oligonucleotide Array Sequence Analysis , Software , Time FactorsABSTRACT
In the first half of the twentieth century, asbestos was a controversial mineral because of its association with asbestosis and asbestos-related lung cancer. It has proved no less so since the 1960s, when another asbestos cancer, mesothelioma, was identified. Mesothelioma appeared to be more strongly linked with blue asbestos (crocidolite) than with the other asbestos varieties, brown (amosite) and white (chrysotile). This finding triggered a fierce debate between "chrysophiles" (those who declared chrysotile innocuous) and "chrysophobes" (those who believed it was a mortal hazard). This essay attempts the first history of the chrysotile controversy, which shows that a scientific consensus on the safety of white asbestos was very slow to emerge. This was only partly due to the complexities of scientific research. Political, economic, and social factors have militated against a speedy resolution of the debate, facilitating the continued production and use of asbestos in the developing world.
