Per Capita Asbestos Consumption Rate and Mesothelioma Incidence

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Who can argue with the facts, exposure to hazardous asbestos can be fatal.  Significant doctors have reached a consensus thanks in big component to the myriad of studies researching Mesothelioma and its causes.  1 interesting study is called, "Ecological Relationship in between Mesothelioma Incidence/Mortality and Asbestos Consumption in Ten Western Countries and Japan" by  Ken TAKAHASHI, et al. Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health – Here is an excerpt: "The objective of the present study was to evaluate the ecological relationship among mesothelioma incidence/mortality and per capita asbestos consumption in ten Western countries and Japan. The two national indices utilized to assess the geographical correlation had been the most recent incidence/mortality rate of mesothelioma for the population over 15 years of age, and the per capita asbestos consumption rate of roughly 10-25 years ago for the population of all ages at that time. Amongst the ten Western countries, a clear linear relationship was shown between the mesothelioma incidence/mortality rate and the preceding per capita asbestos consumption rate with the Spearman correlation coefficient at .70 (p=.03), and R2-value at 66%. Yet, the data-point for Japan was situated apart from the linear relationship due to the lower mesothelioma mortality rate, and when combined with other Western countries, the important relationship diminished. It is probable that the asbestos consumption curve for Japan in past years lagged behind that for the Western countries and the cumulative exposure impact has not yet reached the level that can be expected from other Western countries." (J Occup Well being 1999 41: 8-11)

An additional fascinating study is known as, "Inhibition by phospholipids of haemolytic action of asbestos." – by M C Jaurand, L Magne, J Bignon - Br J Ind Med 197936:113-116.  Here is an excerpt: "Abstract - Haemolysis by asbestos fibres results from an boost in membrane permeability and not from rupture of red blood cells (RBC). The impact of chrysotile asbestos on RBC is at least partly, if not fully, attributable to lipid extraction and adsorption on to the fibres. This was suggested by the hyperbolic relationship between the haemolytic activity of chrysotile and the relative concentration of both chrysotile and RBC. Moreover, it was shown that pre-incubation of chrysotile with lipids, either as RBC membranes or with pure lipids in the form of liposomes, prevents haemolysis."

Another intriguing study is called, "Lung function and exercise performance in smoking and nonsmoking asbestos-exposed workers." By Sue DY, Oren A, Hansen JE, Wasserman K. - Am Rev Respir Dis. 1985 Sep132(3):612-8.  Here is an excerpt: "Abstract - Evaluation of impairment brought on by exposure to an occupational toxin can be complicated by further exposure to other injurious agents. Given that cigarette smoking is frequent and cigarettes are implicated in obstructive lung illness and cardiovascular diseases, we assessed the contribution of smoking to functional abnormalities in a group of asbestos-exposed shipyard workers. Seventy-3 workers who never smoked had been paired with 73 present smokers by age and asbestos exposure. Pulmonary function and performance throughout cycle incremental physical exercise had been compared in between the 2 groups. Nonsmokers had significantly higher VC, FEV1, FEV1/VC, and diffusing capacity for carbon monoxide than did smokers. Only 3 of the 73 nonsmokers but 23 of the 73 smokers had a FEV1/VC below the 95% confidence limit of predicted value. The FEF25-75%, on the other hand, failed to identify additional subjects with obstruction not identified by the FEV1/VC. During exercise, despite no distinction in maximal heart rate, the maximal O2 uptake (VO2max) and oxygen-pulse had been lower amongst smokers. In addition, smokers extra often had abnormal AaPO2 at maximal exercise. Of 33 smokers who had a VO2max less than 80% of predicted, 16 were judged to have cardiac illness, whereas only two appeared to be limited by obstruction. Only 15 of the 73 nonsmokers had a VO2max much less than 80%. We conclude that cigarette smoking was the main contributing factor to the obstructive lung disease observed in asbestos workers, and it also had a strong influence on the occurrence, nature, and magnitude of exercise limitation. The history of cigarette smoking has an necessary impact on the assessment of impairment from asbestos."

We all owe a debt of gratitude to these fine researchers for their essential work.  If you located any of these excerpts valuable, please read the studies in their entirety.