Abstract
Deposition of particles in the lung is largely controlled by aerodynamic diameter, and fibers greater than a certain diameter cannot reach the alveoli. Coalinga type chrysotiles form long, thick fibers when aerosolized, which are largely nonrespirable and thus have far less potential to produce disease than true long ``non-Coalinga'' chrysotile fibers that are largely thin and mainly respirable. Increased width and reduced respirability, which was first recognized more than 25 years ago, contribute to its lack of biological activity. There is direct qualitative and quantitative evidence to support the enhanced thickness of Coalinga type chrysotiles in an aerosol and indirect evidence by mass concentration measurements. Coalinga chrysotile fibers in aqueous solution, on the other hand, have greatly reduced width distributions, which reflects the fact that their constituent components are weakly bound ultra thin fibrils. Indirect evidence from surface area measurements supports their extremely thin nature. An important consequence is that regulatory counting methods do not discriminate between Coalinga type chrysotiles and truly pathogenic long typical chrysotile fibers. Until regulatory methods are modified accordingly, the risks attributed to Coalinga type chrysotiles will continue to be grossly overestimated.
In litigation, some have claimed that Union Carbide conducted ``secret'' studies that showed Coalinga chrysotile was actually thin and highly respirable in an aerosol. No such studies were ever conducted and these claims were made out of context and are unfounded.
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