Document N2XvwxE5mGn9BY8pnVrbebR8Q

106 - within the general population with a higher frequency than In workers popula tion, subjects with an Increased susceptibility may occur. However, this hypothesis can neither be confirmed, nor rcjected> no specific study has been undertaken on this topic. This demands an extra safety factor. On the other hand, taking Into account thc^long latency period of asbestos related cancers, one should realise that 20 to 40 years ago many workers entered employment without any medical selection procedure. Nevertheless, If one wants to evaluate the public health risk, one has to base oneself on the available data of dose-rcspon6c relationship, however in sufficient they may be, and one has to extrapolate from occupational health to public health. There apparently exist qualitative dose-response relationships: concen tration in air end/or duration of exposure determine the relative number of subjects affected end also the diagnosis. However, very few quantitative data exist. Sturm (1975) quotes bohlig in stating that necessary previous intensity of asbestos exposure is decreasing in the following order: asbestosi s * bronchial carcinoma, plcurehyalir.osis - mesothol i c-.a; the duration of development of disease (exposure 4 latency) decreases os follows: mesothelioma - bronchial carcinoma plcurahyel 1 nosis asbestosis. In heavy mixed asbes tos exposure there docs seem to be some inverse relationship between asbestosis end mesothel ioroa. Very heavy exposures perhaps kill'by asbestos] s and/or bronchial cancers before mesotheliomas arise, or in some way may modify the ability of fibres to reach the periphery of the lung. It may also be that those who develop asbostosis, bronchial cancers or mesothel3ome have something in common, and which one develops depends on the dose: this might fit as the dosc-rcsponsc relationship is less clear for the r-cscthel Sernas. In a cohort r-tudy in a O.K. factory with mixed rrvs.i'o there was a .meso thelioma incidence rate per 300,000 subject years ranging from > (10-1S year exposure) to 210 (30- year)# and front 3) (<2 year ensure slight to moderate) to 195 (>? year, severe exposure) in r.alee {?: wJv.vse it al l/5), i.c. a clear dependence on duration ar.d sev* rity of exposure. . N Enterlinc et al (1912) cv.lcu1ut*d 'he cumulative dua* ^yvosure in m.\.pef* * - i.jjipcf nil lion particles per cubic foot. -years and i from asbcsti was used as <]2S wnpeffor non-mal cancers of mmpef-yr fc malignant c significant had higher: respirator) exposure t carcinoma of nor.-sal same dosag a si.gni fit di r. cancers* suggest 1! nay occur hicjh >;;t*? or true" more reoC ct al c-xper'-re tent. 3 c-vj.c; ure Of f>.pC.v :.>ut LiCU) cf l-.-t^s ir:-rn9 tiyrtem . ,Vn. v:..ti-cr.d v.-i: in r.OOi 0799 PRODUCED BY FORD