Op de website www.veiligengezondwerken.nl vindt u een interactieve digitale kennisbank over tal van aspecten in de bouw die met Veiligheid, gezondheid en de (arbo) regelgeving daarover te maken hebben. U vindt er o.a. twee brochures over asbestgerelateerde veiligheids- en gezondheidsaspecten in de bouw. Bron: Arbouw.nl/CNV 20 april 2005.
Meer http://www.arbouw.nl/page.aspx?p=/content/nieuws/artikelen/veiligengezondwerken.xml
Toezichthouders asbestsloop (DTA’ers) komen soms in de knel door de druk van aannemers om het werk sneller af te maken. Dat gaat volgens een rapport van de Inspectie Werk en Inkomen (IWI) ten koste van de veiligheid van werknemers en omgeving.
Bron: Persbericht Inspectie Werk en Inkomen, 3 mei
Alpha-TOS, een soort vitamine E, heeft in experimenten met muizen mesothelioomkankercellen gedood en de groei van tumoren tegengehouden, zegt de Australische celbioloog Dr. Neuzil. Hij hoopt dat het middel over ongeveer 2 jaar bij mensen kan worden getest.
Bron: The Courier Mail, Daily Telegraph, 23 mei 2005.
The Courier Mail (Queensland, Australia)
May 23, 2005 Monday
HEADLINE: Vitamin cancer treatment hope
BODY:
A VITAMIN E-related compound may kill deadly cancer cells caused by asbestos exposure, says an Australian cell biologist who has already established its success in trials using mice.
Gold Coast-based Griffith University researcher Jiri Neuzil said alpha-TOS, which is closely related to vitamin E, killed mesothelioma cancer cells in experiments with mice.
Most victims of mesothelioma, an aggressive cancer that destroys a protective membrane covering internal organs including the lungs, have inhaled asbestos particles.
Dr Neuzil said alpha-TOS also halted growth of mesothelioma tumours, for which there is currently no cure, under a five-year study involving researchers from Australia, Italy and the Czech Republic.
He said the compound had also showed hints of suppressing breast cancer, melanoma, lung cancer and colon cancer tumours in animal experiments. Dr Neuzil said alpha-TOS would ultimately be put to the test in human trials, which he hoped to begin within two years.
Alpha-TOS was selective because it pursued mesothelioma cancer cells but caused only minor damage, if any, to normal cells in mice, he said.
Dr Neuzil said he stumbled on the compound’s promising qualities “by mistake five years ago.
In de West-australische plaats Wittenoom werd van 1943 tot 1966 het gevaarlijke blauwe asbest gewonnen (crocidoliet). In 2002 werden 1885 inwoners, waarvan 1042 (ex-)werknemers onderzocht op asbestose (stoflongen) en bepaalde vitamine-niveaus in het bloed (retinol, caroteen en vitamine E). De onderzoekers vonden een relatie tussen chronisch lagere vitamine-niveaus en een grotere kans om aan asbestose te overlijden. Van de onderzoeksgroep overleden 76 personen aan asbestose, een te kleine groep om causaliteit te kunnen bepalen. Meer onderzoek is nodig.
Bron: Alfonso, H.S. et al. (2005). Plasma Concentrations of Retinol, Carotene, and Vitamin E and Mortality in Subjects With Asbestosis in a Cohort Exposed to Crocidolite in Wittenoom, Western Australia. Journal of occupational and environmental medicine. vol. 47, afl. 6, pag. 573-579 (7)
Alfonso, Helman S.. Fritschi, Lin. de Klerk, Nicholas H.. Ambrosini, Gina. Beilby, John. Olsen, Nola. Musk, A William (2005). Plasma Concentrations of Retinol, Carotene, and Vitamin E and Mortality in Subjects With Asbestosis in a Cohort Exposed to Crocidolite in Wittenoom, Western Australia. Journal of occupational and environmental medicine. vol. 47, afl. 6, pag. 573-579 (7).
Abstract
Objective:We sought to examine the relationships between plasma concentrations of retinol, carotene, and vitamin E and mortality associated with asbestosis in people previously exposed to crocidolite.
Methods:Cox regression modeling was applied to examine these relationships at the first measurement of each vitamin, at the measurement at each visit, and with the rate of change of each vitamin during the follow-up.
Results:There were 76 deaths of people with asbestosis during the follow-up period and 1885 subjects censored. Mortality in subjects with asbestosis was inversely related to plasma levels of retinol and Vitamin E concentrations and to their rate of increase during the follow-up. Carotene concentrations at first visit were associated with lower mortality but not during the follow up period.
Conclusions:Chronically low levels of these vitamins are associated with an increased risk of dying with asbestosis.
Asbest bestaat uit microscopisch kleine vezels. Er zijn verschillende soorten, onderverdeeld in serpentijnen en amfibolen. Serpentijnen hebben gekrulde vezels, de vezels van amfibolen hebben de vorm van staafjes en zijn gevaarlijker. Een groep ratten werd gedurende 5 dagen herhaaldelijk blootgesteld aan een groot aanta calidria chrysotiel vezels (serpentijn), een andere groep aan een aantal tremolietvezels (amfibool). Tot één jaar na de proef werd bij de ratten die aan chrysotiel waren blootgesteld geen ontstekingsreactie gezien. Dit in tegenstelling tot de aan tremoliet blootgestelde ratten die sterk reageerden, ondanks blootstelling aan 16 x minder vezels dan de aan chrysotiel blootgestelde ratten. Bernstein, D. et. al., (2005). Comparison of Calidria Chrysotile Asbestos to Pure Tremolite : Final Results of the Inhalation Biopersistence and Histopathology Examination Following Short-Term Exposure. Inhalation toxicology. vol. 17, afl. 9, pag. 427-450 (24).
Bernstein, David. Chevalier, Jörg. Smith, Paul (2005). Comparison of Calidria Chrysotile Asbestos to Pure Tremolite : Final Results of the Inhalation Biopersistence and Histopathology Examination Following Short-Term Exposure. Inhalation toxicology. vol. 17, afl. 9, pag. 427-450 (24).
Abstract:
Calidria chrysotile asbestos, which is a serpentine mineral, has been shown to be considerably less biopersistent than the durable amphibole mineral tremolite asbestos, which persists once deposited in the lung. The initial results of this inhalation biopersistence study in rats that demonstrates this difference were reported in Bernstein et al. (2003). This article presents the full results through 1 yr after cessation of the 5-day exposure. This study was based upon the recommendations of the European Commission (EC) Interim Protocol for the Inhalation Biopersistence of synthetic mineral fibers (Bernstein & Riego-Sintes, 1999). In addition, the histopathological response in the lung was evaluated following exposure. In order to quantify the dynamics and rate by which these fibers are removed from the lung, the biopersistence of a sample of commercial-grade chrysotile from the Coalinga mine in New Idria, CA, of the type Calidria RG144 and that of a long-fiber tremolite were studied. For synthetic vitreous fibers, the biopersistence of the fibers longer than 20 µm has been found to be directly related to their potential to cause disease. This study was designed to determine lung clearance (biopersistence) and the histopathological response. As the long fibers have been shown to have the greatest potential for pathogenicity, the aerosol generation technique was designed to maximize the number of long respirable fibers. The chrysotile samples were specifically chosen to have 200 fibers/cm 3 longer than 20 µm in length present in the exposure aerosol. These longer fibers were found to be largely composed of multiple shorter fibrils. The tremolite samples were chosen to have 100 fibers/cm 3 longer than 20 µm in length present in the exposure aerosol. Calidria chrysotile has been found to be one of the most rapidly cleared mineral fibers from the lung. The fibers longer than 20 µm in length are cleared with a half-time of 7 h. By 2 days postexposure all long fibers have dissolved/disintegrated into shorter pieces. The fibers between 5 and 20µm in length were cleared with a half-time of 7 days. This length range represents a transition zone between those fibers that can be fully phagocytosed and cleared as particles and the longer fibers that cannot be fully engulfed by the macrophage. The fibers/objects shorter than 5 µm in length were cleared with a half-time of 64 days, which is faster than that reported for insoluble nuisance dusts such as TiO 2 . By 12 months postexposure, 99.92% of all the remaining chrysotile was less than 5 µm in length. Following the 5 days of repeated exposure to more than 48,000 chrysotile fibers/cm 3 (190 fibers L > 20 µm), histopathological examination revealed no evidence of any inflammatory reaction either after the cessation of the last exposure or at any time during the subsequent 12-mo period. This is in marked contrast to the amphibole tremolite, which was also investigated using the same inhalation biopersistence protocol. The long tremolite fibers, once deposited in the lung, remain over the rat’s lifetime with essentially an infinite half-time. Even the shorter fibers, following early clearance, also remain with no dissolution or further removal. At 365 days postexposure, there was a mean lung burden was of 0.5 million fibers L > 20 µm and 7 million fibers 5-20 µm in length with a total mean lung burden of 19.6 million fibers. The tremolite exposed rats, even with exposure to 16 times fewer total fibers than chrysotile, showed a pronounced inflammatory response with the rapid development of granulomas as seen at day 1 postexposure, followed by the development of fibrosis characterized by collagen deposition within these granulomas and by 90 days even mild interstitial fibrosis. With the short exposure, this study was not designed specifically to evaluate pathological response. however, it is quite interesting that even so there was such a marked response with tremolite. These findings provide an important basis for substantiating both kinetically and pathologically the differences between chrysotile and the amphibole tremolite. As Calidria chrysotile has been certified to have no tremolite fiber, the results of the current study together with the results from toxicological and epidemiological studies indicate that this fiber is not associated with lung disease.
Nog steeds is niet helemaal duidelijk hoe asbest kanker veroorzaakt. Men denkt dat ijzer daarbij een rol speelt. De meest gevaarlijke asbestsoorten hebben een relatief hoog ijzergehalte. Baldys en Aust onderzochten de werking van asbestvezels en ijzer op de Epidermale Groei Factor Receptor (EGFR) in menselijke epitheel en mesotheelcellen uit long en longvlies. Zij gebruikten drie soorten asbest, t.w. crocidoliet, amosiet en chrysotiel met respectievelijk 27, 27 en 2% ijzer. Zij vonden dat ingekapselde crocidoliet asbestvezels de EGFR receptor inactiveerden en daarmee indirect de celdeling kunnen ontregelen. IJzer lijkt daarbij een mediërende werking te hebben. Baldys, A. & Aust, A.E. (2005). Role of Iron in Inactivation of Epidermal Growth Factor Receptor after Asbestos Treatment of Human Lung and Pleural Target Cells. American journal of respiratory cell and molecular biology. vol. 32, afl. 5, pag. 436-442 (7).
American Journal of Respiratory Cell and Molecular Biology. Vol. 32, pp. 436-442, 2005
Role of Iron in Inactivation of Epidermal Growth Factor Receptor after Asbestos Treatment of Human Lung and Pleural Target Cells. Aleksander Baldys and Ann E. Aust
Department of Chemistry and Biochemistry, Utah State University, Logan, Utah
Abstract
Although the mechanism by which asbestos causes cancer remains unknown, iron associated with asbestos is thought to play a role in the pathogenic effects of fibers. Here, we examined the effects of asbestos on the epidermal growth factor receptor (EGFR) in human lung epithelial (A549) cells, human pleural mesothelial (MET5A) cells, and normal human small airway epithelial (SAEC) cells. Treatment of A549, MET5A, and SAEC cells with asbestos caused a significant reduction of EGFR tyrosine phosphorylation. This was both time- (15 min to 24 h) and concentration-dependent (1.5, 3, and 6 µg/cm2) in A549 cells. Also, treatment with 6 µg/cm2 crocidolite for 24 h diminished the phosphorylation levels of human EGFR 2 (HER2). Exposure of A549 cells to 6 µg/cm2 crocidolite for 3–24 h resulted in no detectable Y1045 phosphorylation and no apparent degradation of the EGFR. Inhibition of fiber endocytosis resulted in a considerable inhibition of EGFR dephosphorylation. Removal of iron from asbestos by desferrioxamine B or phytic acid inhibited asbestos-induced decreases in EGFR phosphorylation. The effects of crocidolite, amosite, and chrysotile on the EGFR phosphorylation state appeared to be directly related to the amount of iron mobilized from these fibers. These results strongly suggest that iron plays an important role in asbestos-induced inactivation of EGFR.
De vraag of longkanker door asbest is veroorzaakt terwijl er geen sprake is van asbestose, blijft controversieel. Dit concluderen Engelse onderzoekers na analyse van 9 epidemiologische artikelen. De momenteel beschikbare technische middelen bieden niet voldoende mogelijkheden om dit te onderzoeken. Waarschijnlijk is het type asbestvezel van belang, concluderen Engelse en Amerikaanse onderzoekers.
Bron: Thorax. vol. 60 (2005), afl. 5, pag. 433-436 (4)
Asbestos, asbestosis, and lung cancer : a critical assessment of the epidemiological evidence
Hessel, P.A.. Gamble, J.F.. Mcdonald, J.C. / In: Thorax. vol. 60 (2005), afl. 5, pag. 433-436 (4)
The question of whether lung cancer can be attributed to asbestos exposure in the absence of asbestosis remains controversial. Nine key epidemiological papers are reviewed in a point/counterpoint format, giving the main strengths and limitations of the evidence presented. Of the nine papers, two concluded that asbestosis was necessary and seven that it was not. However, the study design, nature and circumstances of exposure and method of analysis of the studies differed considerably, and none was considered definitive. It is concluded that, because of the relative insensitivity of chest radiography and the uncertain specificity of findings from histological examinations or computed tomography, it is unlikely that epidemiology alone can put either the strict scientific or practical medicolegal questions beyond doubt. It is probable that the issue may depend critically on asbestos fibre type, an aspect not so far addressed.
In Woodstock werd in 1985 asbestvervuiling ontdekt in het drinkwater. Dit kwam door asbestcementpijpen die half jaren 50 waren geïnstalleerd. De kankerstatistieken van Woodstock werden over de periode 1980-1998 vergeleken met nationale gegevens. Er werd geen relatie met asbest gevonden.
Bron: Browne, M. L. et al. (2005). Environmental research. vol. 98 (2005), afl. 2, pag. 224-232 (9)
Cancer incidence and asbestos in drinking water, Town of Woodstock, New York, 1980#x0201.1998
Browne, Marilyn L.. Varadarajulu, Deepa. Lewis-Michl, Elizabeth L.. Fitzgerald, Edward F. / In: Environmental research. vol. 98 (2005), afl. 2, pag. 224-232 (9) / 2005
Abstract
Late in 1985, asbestos contamination was discovered in the public water supply of the Town of Woodstock, Ulster County, New York. Contamination resulted from asbestos’cement pipes installed in the town water system in the mid to late 1950s and the corrosiveness of the local water. The New York State (NYS) Department of Health established the Woodstock Asbestos Exposure Registry (WAER) in 1986 to monitor rates of cancer among individuals who lived on the water supply between 1960 and 1985. Demographic, health, and residential information were collected on 2936 registrants. The follow-up period for observation of cancer was 1980-1998, consistent with the expected lag of 20-30+ years for development of asbestos-related cancers. The NYS Cancer Registry was used to ascertain cancer diagnoses. Standardized incidence ratios (SIRs) for gastrointestinal, respiratory, and total cancers were all approximately 1.00 or less and all 95% confidence intervals (CIs) included 1.00. For individual types of the gastrointestinal cancers, only the SIR for pancreatic cancer was marginally statistically significant at 2.19 (95% CI=1.00-4.16), based on a total of nine observed cases. The excess in pancreatic cancer occurred primarily among men (SIR=3.08. 95% CI=1.13-6.70) and was only slightly elevated among women (SIR=1.39. 95% CI=0.29-4.06). This association may be related to factors other than asbestos exposure such as occupation and lifestyle or to chance. No cases of mesothelioma were observed among WAER participants. There was no increase in incidence by latency or duration of residence on the water supply, but the ability to detect these trends is limited by small numbers and unknown dates of initial exposure. The general pattern of results did not demonstrate a likely link between exposure to asbestos in drinking water and cancer occurrence among participants in the WAER.
Op 28 april, Workers Memorial Day, werd in Brazilië, Canada en het Verenigd Koninkrijk een herdenking gehouden voor asbestslachtoffers en werd opgeroepen tot een wereldwijd verbod op asbest en recht voor alle asbestslachtoffers.
Bron: International Ban Asbestos Secretariat, 12 mei 2005.
Meer http://www.ibas.btinternet.co.uk
Dit artikel beschrijft hoe claims ten gevolge van blootstelling aan asbest in de VS tot een crisis in het juridische systeem hebben geleid. Bedrijven gaan failliet door: rechters die dubieus medisch bewijs van blootstelling aan asbest accepteren, door het grote aantal schadevergoedingen aan mensen die wel met asbest hebben gewerkt, maar niet ziek zijn. En door de hoge juridische kosten. De echt zieke slachtoffers zijn daarvan de dupe. Bron: Brickman, L. & Shapiro, H.D (2005). Asbestos kills. National Review, 31 januari, 39-41.
Asbestos kills
And more than just people: jobs, ethics, and elementary justice
L E S T E R B R I C K M A N & H A RV E Y D. S H A P I RO
IT�S become a familiar scenario across the U.S.: A jovial air pervades this parking lot adjacent to a union hall that belies the serious purpose that has brought together a group of middle-aged men. For much of the afternoon they�ve been sipping coffee and waiting their turn to enter the trailer parked at one end of the parking lot. The trailer contains X-ray equipment, and they�re about to have their lungs checked for asbestos-related diseases. They�re here in response to postcards saying things like, �You Might Have Million Dollar Lungs!�
They know they�re entering a lottery, one in which a tiny few may find they have cancer but many more will find themselves perfectly healthy yet entitled to receive checks from 20 or 30 different companies totaling as much as $60,000�of course, that�s after their lawyers have deducted their 40 percent cut. For decades, scenes like this have been played out in the parking lots of hundreds of union halls, motels, and strip malls across America. For most Americans, asbestos litigation, like asbestos itself, is now a dimly remembered artifact of an earlier age. But despite 30 years of sweeping efforts to remove every trace of asbestos from American life, more than 100,000 new claims of asbestos-related diseases were filed in 2003�the most ever in a single year. While there was a sharp fall-off in nonmalignant claims filed in 2004, many experts anticipate that hundreds of thousands of additional claims will yet be brought, joining the 850,000 that have already come forward.
GONE BUT NOT FORGOTTEN
After years of asbestos-removal programs, prominent medical researchers Kevin Browne, Edward A. Gaensler, and Andrew Churg have called asbestosis a �disappearing disease,� and a condition that is �exceedingly rare.� So how is it that thousands and thousands of claims continue to be filed? This is a question the new Congress is likely to be asking, because of the increased power of Republican critics of trial lawyers. Asbestos could become the poster child for tort reform. As one leading medical expert on asbestos-related diseases, Dr. James Crapo, has said, claimants are being compensated �for illnesses that, according to the clear weight of medical evidence, either are not caused by asbestos or do not result in a significant impairment�i.e., are not generally regarded by the medical profession as an illness.� Yet asbestos lawyers continue their vigorous pursuit of potential claimants�not just through labor unions, but also through radio and TV ads and the Internet. So far, employers and their insurers have paid out over $70 billion�with more than half of that sum going to those who have either no injury or no proof that asbestos caused their injury. (That, of course, leaves far less to be paid to those who are truly suffering as a result of terrible asbestos-related injuries.) An additional $150 billion is likely to be required before the asbestos gods have been satiated. So far, some 8,400 companies have been sued. more than 70 have filed for bankruptcy. as a result of this financial drain, an estimated 500,000 jobs have been eliminated or not created. For a millennium, asbestos was �the magic mineral� because of its resistance to heat. In World War II, it was declared a �strategic and critical material� because of its value as insulation. After 9/11, experts said the World Trade Center would have burned more slowly, perhaps permitting more people to survive, had its asbestos insulation not been removed. And the O-rings in the doomed Challenger spacecraft would not have failed had they continued to contain asbestos.
But exposure to asbestos can cause cancer or asbestosis, a scarring of lung tissue. Between 1960 and 2003, some 75,000 people died of mesothelioma (tumors of the lung), and another 35,000 are likely to succumb before 2050. Knowledge of the hazards of asbestos dates back a century, and documents from the 1930s and 1940s revealed that two leading asbestos manufacturers had conspired to conceal the serious health threat posed to their workers. During World War II, naval officials ignored the consequences to 4.5 million shipyard workers�a cover-up that reached the highest levels of government. In the 1960s, Dr. Irving Selikoff of the Mount Sinai School of Medicine published research showing alarming rates of lung cancer and asbestosis among insulation workers, and a series of New Yorker articles by Paul Brodeur in the early 1970s helped focus public attention on asbestos. As awareness of the dangers grew, there was a sweeping campaign to remove asbestos wherever it had been used. Meanwhile, the growing awareness of the risks�and the cover-up�led to a spate of lawsuits, beginning in 1973 when the Fifth Circuit Court of Appeals allowed workers injured by exposure to asbestos to file a product-liability suit (in which juries determine the size of the award) rather than a workers�-compensation case (in which claims are paid according to a formula).
Much of the initial litigation targeted the Johns Manville Corporation, which had long been the nation�s principal miner and fabricator of materials containing asbestos. In 1982, after some 16,000 suits were filed, Manville declared bankruptcy. It emerged from bankruptcy in 1988 under an innovative plan in which almost $2 billion of cash and most of the company�s stock were transferred to the Manville Personal Injury Trust, and all asbestos claims were to be directed to the Trust. Claimants who submitted only minimal proof of exposure to a Manville product and asserted that they had an asbestos-related medical condition were paid according to a schedule of benefits. This set off a feeding frenzy: The Manville Trust quickly became insolvent after distributing nearly $680 million, including approximately $266 million to plaintiffs� lawyers. After this second Manville bankruptcy,
lawyers turned their attention to smaller asbestos producers and to construction firms that used asbestos products. Several critical legal principles fanned the flames of litigation. The principle of joint and several liability meant that a worker could sue several dozen companies, and any one of them could end up being held responsible for 100 percent of the claim, no matter how minor its involvement. Another key principle involved insurance coverage. Asbestos-related diseases take years to manifest themselves, so which liability insurers should pay the claims? Should it be the insurers at the time when the worker was exposed? Or the insurers when the disease was found? Or the insurers in the intervening 15 to 40 years, when initial exposures were slowly injuring a worker�s lungs? In 1988, a court held that all three sets of insurers would be liable. Originally, most asbestos litigation involved seriously injured claimants�those stricken with mesothelioma, asbestosis, or lung cancer. But since the Manville Trust and insurance companies were paying claims without demanding much in the way of proof, plaintiffs� lawyers began to seek compensation based on decidedly modest evidence of injuries and product exposure. For example, they obtained statements from doctors that an individual�s lung conditions were �consistent with asbestosis��even though anything from old age and obesity to smoking can account for the same lung condition.
READING THE B-READERS
The asbestos lawyers have created an entrepreneurial model to seek out potential claimants and send them to screening enterprises. The X-rays taken by the screeners are then sent for analysis to �B-readers,� specialized radiologists retained by plaintiffs� lawyers. The comparative handful of B-readers regularly selected by plaintiffs� lawyers consistently diagnose 60 to 80 percent of those screened with mild asbestosis. But in a Johns Hopkins study, approximately 500 X-rays in which plaintiffs� lawyers� Breaders had found signs of asbestosis were reread by other radiologists who did not know who was hiring them. These B-readers found that, at most, 4.5 percent of the X-rays indicated lung conditions consistent with mild asbestosis. Only about 5 percent of potential B-readers are used by plaintiffs� lawyers, and they have earned substantial fees for their services.
They also seem to have made convenient shifts in their diagnoses. Until the mid-1990s, most asbestos claimants were diagnosed as having �pleural plaques,� which are deposits of collagen fibers on the lining of the lungs. This typically produces no symptoms and does not increase the likelihood of contracting an asbestos-related disease, so many states do not allow suits based on pleural plaques. (In states that do allow such suits, however, juries have awarded damages as high as $1 million.) After a putative mega-settlement of asbestos issues proposed in 1993 placed no value on future pleural-plaques claims, the doctors hired by plaintiffs� lawyers almost immediately stopped diagnosing the newly screened as having pleural plaques. instead they found mild asbestosis.
In another very suggestive shift, on several occasions in which companies were entering bankruptcy, and their ability to pay claims dwindling, a number of witnesses suddenly recalled that the products they had handled were from companies that had not filed for bankruptcy. For example, in a deposition taken in October 1981, when Johns Manville was the premier target for plaintiffs� attorneys, one long-time New York Shipyard employee estimated that Johns Manville had supplied between 75 and 80 percent of the products containing asbestos. But when another witness was deposed in December 1982�several months after the Manville bankruptcy�that figure had shrunk to 25 percent and other companies were implicated instead.
�PRE-PACKED��AND STACKED
Faced with this movable feast of claims, some 70 companies have followed Johns Manville into bankruptcy, with more to come. Many follow the Manville model and transfer assets to a trust which is to pay future claims. Thus, claimants need a viable company to emerge from bankruptcy and generate revenues for the trust. To help facilitate this, Congress in 1994 created statutory authority to channel all asbestos claims to these trusts, not to the companies. But one of the provisions of the legislation increased the proportion of tort claimants who had to agree before the �channeling� function of the trust could become effective. This created perverse incentives for lawyers to recruit more claimants�regardless of the merits of their claims�because that gave the lawyers more leverage over the bankruptcy process (not to mention additional legal fees).
Recently, companies facing insolvency because of asbestos claims have turned to �pre-packaged� bankruptcies in which attorneys for the asbestos claimants and the company agree on a plan of reorganization and then present it to the bankruptcy court for approval. In other settings, �pre-packs� can minimize litigation costs, expedite claims payments, and give the company a better chance of surviving. In an asbestos pre-pack, the company typically negotiates an agreement in which it settles a large number of pending asbestos cases for highly inflated values�to be paid by its insurance company�and in return, the plaintiffs� lawyers let the company retain a substantial portion of its assets when it emerges from bankruptcy.
Claimants whose lawyers are part of the pre-pack negotiations Legislation created perverse incentives for lawyers to recruit more claimants�regardless of the merits of their claims�because that gave the lawyers more leverage over the bankruptcy process.
often receive highly favorable treatment in pre-packs. In December, the Third Circuit Court of Appeals turned down the proposed settlement in the Combustion Engineering bankruptcy, in which a pool of unimpaired claimants was supposed to get 95 cents out of every dollar they would have received in a pre-bankruptcy payment�while real cancer victims would get what was left: about 20 cents for every dollar of a pre-bankruptcy settlement. Moreover, the lawyer for the claimants was to get a $20 million fee from the company for putting together this deal. After lower courts approved this plan, 291 cancer victims appealed to the Third Circuit, which found that it did not meet the standards of fair treatment for all creditors required in a bankruptcy proceeding. Most judges, however, have been content to approve whatever is negotiated in a pre-pack. There is little doubt that after 30 years of lawsuits, the biggest beneficiary of the asbestos mess has been the plaintiffs� bar�to the tune of $20 billion in fees so far, and counting. This has come at the expense of those who are seriously ill, as well as companies that had only a peripheral involvement in the asbestos industry. The process is also burdening the property and casualty insurance industry. The 205-year-old Providence Washington Insurance Co., once the third-oldest insurer in the U.S., succumbed to asbestos liability, as has the Kemper Insurance Co. No skin off your back? Insurers recoup their losses by raising their rates. Higher insurance costs will inevitably be reflected in higher product prices.
There have recently been some signs that the plaintiffs� bar has gone a step too far. The Ohio legislature passed a law limitingasbestos claims to persons who can demonstrate actual illness. Courts in Mississippi have demanded more rigorous proof of injury in asbestos cases. And the conflictsof interest of several advisers retained by one judge in several asbestos bankruptcies
led the Third Circuit Court of Appeals to the highly unusual step of removing that judge from presiding over these bankruptcies.
After resigning from the bench in response, that judge went to work for one of those advisers.
A CHANCE FOR FAIRNESS
Over the years, parties to the litigation have entered into periodic and always
unsuccessful negotiations to settle the whole asbestos issue once and for all.
Intermittent congressional efforts have
been equally inconclusive. Last year, for
example, the proposed Fairness in Asbestos
Injury Resolution Act (FAIR) would have
set up a $140 billion industry-funded trust
fund to pay off all asbestos claims, including
those of the non-sick, and put an end
to further litigation. But trial lawyers and
labor unions decided it wasn�t enough and
blocked the measure.
The November elections have not only
brought additional advocates of tort reform
Bron: Brickman, L. & Shapiro, H.D (2005). Asbestos kills. National Review, 31 januari, 39-41.
