title: The pathological response and fate in the lung and pleura of chrysotile in combination with fine particles compared to amosite asbestos following short-term inhalation exposure: interim results.
abstract: The pathological response and translocation of a commercial chrysotile product similar to that which was used through the mid-1970s in a joint compound intended for sealing the interface between adjacent wall boards was evaluated in comparison to amosite asbestos. This study was unique in that it presents a combined real-world exposure and was the first study to investigate whether there were differences between chrysotile and amosite asbestos fibers in time course, size distribution, and pathological response in the pleural cavity. Rats were exposed by inhalation 6 h/day for 5 days to either sanded joint compound consisting of both chrysotile fibers and sanded joint compound particles (CSP) or amosite asbestos. Subgroups were examined through 1-year postexposure. No pathological response was observed at any time point in the CSP-exposure group. The long chrysotile fibers (L > 20 microm) cleared rapidly (T(1/2) of 4.5 days) and were not observed in the pleural cavity. In contrast, a rapid inflammatory response occurred in the lung following exposure to amosite resulting in Wagner grade 4 interstitial fibrosis within 28 days. Long amosite fibers had a T(1/2) > 1000 days and were observed in the pleural cavity within 7 days postexposure. By 90 days the long amosite fibers were associated with a marked inflammatory response on the parietal pleural. This study provides support that CSP following inhalation would not initiate an inflammatory response in the lung, and that the chrysotile fibers present do not migrate to, or cause an inflammatory response in the pleural cavity, the site of mesothelioma formation.
authors.affiliation: davidb@itox.ch
authors.forename: D M
authors.initials: DM
authors.lastname: Bernstein
authors.forename: R A
authors.initials: RA
authors.lastname: Rogers
authors.forename: R
authors.initials: R
authors.lastname: Sepulveda
authors.forename: K
authors.initials: K
authors.lastname: Donaldson
authors.forename: D
authors.initials: D
authors.lastname: Schuler
authors.forename: S
authors.initials: S
authors.lastname: Gaering
authors.forename: P
authors.initials: P
authors.lastname: Kunzendorf
authors.forename: J
authors.initials: J
authors.lastname: Chevalier
authors.forename: S E
authors.initials: SE
authors.lastname: Holm
mesh_terms: D000818:Animals; D017639:Asbestos, Amosite / Q000008:administration & dosage* / Q000378:metabolism / Q000633:toxicity; D017632:Asbestos, Serpentine / Q000008:administration & dosage* / Q000378:metabolism / Q000633:toxicity; D019570:Inhalation Exposure / Q000009:adverse effects*; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008297:Male; D052638:Particulate Matter / Q000008:administration & dosage* / Q000633:toxicity; D010865:Pilot Projects; D010994:Pleura / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D013997:Time Factors
chemical_list: D017632:Asbestos, Serpentine; D052638:Particulate Matter; D017639:Asbestos, Amosite