Mesothelioma is a deadly disease that has taken thousands of lives in the world. Public awareness about this hazardous material is needed. One interesting research entitled Asbestos and mesothelioma: Worldwide trends by Laurie Kazan-Allen is trying to find a correlation between national asbestos consumption and and the incidence of asbestos disease. Towards the end of the 20th century, governments in many developed countries banned or seriously restricted the use of asbestos. It causes an aggressive marketing campaigns to sell asbestos to developing countries. The consumption of white asbestos is increasing in Asia, Latin America and the Commonwealth of Independent States. It is likely that the lethal asbestos harvest which is occurring in the U.S., the UK and Australia will be reproduced in the developing world.
Another interesting study called, Unsuspected exposure to asbestos and bronchogenic carcinoma by K M Martischnig, D J Newell, W C Barnsley, W K Cowan, E L Feinmann, E Oliver and Br Med J has investigate case of 250 men admitted to a thoracic surgical centre and matched controls were questioned in detail about their occupations after leaving school and their smoking habits. It is reported that 201 of 250 men confirmed bronchial carcinoma 58 gave a history of occupational exposure to asbestos, while the other 29 men matched for age and residential area who were admitted with other diseases gave such a history.
Usually bronchial carcinoma is associated with heavy smoking was observed, but asbestos exposure increased the risk of carcinoma whatever the level of smoking. These results are consistent with the hypothesis that asbestos exposure and the level of smoking act independently in causing bronchial carcinoma. Asbestos regulations have eliminated the risk of exposure to workers in scheduled industries, so asbestos-induced diseases will probably be increasingly found among the many workers who have had incidental exposure to asbestos. It is therefore important to take a full occupational history. More information you can visit asbestoswatchtoowoomba.com.au
A third study worth examining entitled Response of mouse lung to crocidolite asbestos, Minimal fibrotic reaction to short fibres by Dr Ian Y. R. Adamson and Drummond H determined the relationship between the development of pulmonary fibrosis and the size of deposited asbestos, we prepared a pure sample of short crocidolite fibres and instilled 0.5 mg of 0.1 mg to the lungs of mice. Animals were killed up to 20 weeks later with 3H thymidine injected 1 h before death.
There was a rapid transient increase in polymorph neutrophils (PMN) and in glucosaminidase levels by bronchoalveolar lavage; alveolar macrophage (AM) numbers were elevated in the 0.5 mg group for eight weeks. Most fibres were phagocytized by AM, many of which were heavily laden and cleared from the lung over the 20 week period. Some fibres were seen in type 1 epithelial cells, frequently associated with cell injury. From cell kinetic studies, a very brief proliferative response was seen in bronchiolar epithelial and Type 2 alveolar epithelial cells.
A greater response was seen in interstitial fibroblasts which showed increased labelling up to two weeks after 0.5 mg asbestos. However no granulomas were seen and very little fibrosis was found by morphology or by biochemistry at any time after 0.5 mg; no fibrosis was seen after instilling 0.1 mg. The results show that a high dose of exclusively short asbestos fibres produces minimal lung injury and fibrosis in spite of long standing macrophage-fibre interaction in the alveoli.