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(c) 2014 Jon L Gelman, All Rights Reserved.

Thursday, August 30, 2007

MD Fed Court Holds a Fighfighter HAS STANDING to bring a private action under the MSP Act

Firefighter brought action against mayor and city council pursuant to private enforcement provision of Medicare Secondary Payer (MSP) statute, alleging that his exposure to asbestos while working caused his pleural malignant mesothelioma. City moved to dismiss.

"...private citizens may collect double damages by bringing claims against primary payers to recover money owed. Id. § 1395y(b)(3)(A). It is under this latter provision that O'Connor asserts the instant suit."

Motion to Dismiss DeniedO'Connor v. Mayor and City Council of Baltimore494 F.Supp.2d 372 D.Md.,2007.July 19, 2007

Jon Gelman
Wayne NJ
http://www.gelmans.com/

Wednesday, August 29, 2007

Asbestos Exposure From Brakes Causes Mesothelioma

Asbestos Exposure Causes Mesothelioma, But Not This Asbestos Exposure: An Amicus Brief to the Michigan Supreme Court†
Chapin v। DaimlerChrysler Corporation et al., Case No. 133178, Supreme Court of Michigan.

LAURA S. WELCH, MD* International Journal of Occupational and Environmental Health 2007; 13:318-३२७

*Dr। Welch is joined by 51 other signers onto this communication; see end of document.

Address correspondence and reprint requests to: Laura S। Welch, MD, Medical Director, Center to Protect Workers Rights, 8484 Georgia Avenue, Silver Spring, MD 20910, U.S.A.

Manufacturers of asbestos brakes, supported by many manufacturing and insurance industry amicus curie, requested the Michigan Supreme Court to dismiss testimony of an expert regarding the ability of asbestos dust from brakes to cause mesothelioma as "junk science." Scientists are concerned with the sweeping and unequivocal claims that any conclusion that asbestos from brakes caused a signature asbestos-related disease in a particular person must be "junk science." The manufacturers' sweeping pronouncements are what veer from accepted, reliable mainstream scientific methods and conclusions. This article outlines the evidence supporting the conclusion that asbestos from brakes can and does cause mesothelioma, and describes the defendants' attempts to fabricate doubt about this conclusion.

Key words: asbestos; brakes; chrysotile; mechanic; occupation; epidemiology; mesothelioma.

Companies that made and sold asbestos-containing brakes asked the Supreme Court of Michigan to effectively rule that it is impossible to contract asbestos-related diseases as a result of exposure to asbestos from asbestos brakes।† As physicians and scientists, we are concerned about the epidemic of asbestos disease that continues to cause the deaths of thousands of workers each year in the United States. The signers of this paper represent hundreds of years of experience researching, diagnosing, and treating asbestos-related diseases in workers and their families. We have published extensively in this field for more than 30 years and have conducted dozens of epidemiologic and other studies into the issues of asbestos and disease. Many of us have testified before legislative and regulatory bodies regarding asbestos and disease and in court proceedings at the request of individuals suffering from mesothelioma and other asbestos-related diseases.

We make no claim to know the "correct" answer to disease causation in the specific case under review in the court। Our concern is with the sweeping and unequivocal claim that any conclusion that asbestos from brakes has caused a signature asbestos-related disease in a particular person must be "junk science." We find that sweeping pronouncement itself is what veers from accepted, reliable mainstream scientific methods and conclusions.

Ample Evidence Supports the Conclusion That Asbestos from Brakes Can and Does Cause मेसोठेलिओमा

Chrysotile causes cancer, including mesothelioma. "There is general agreement among scientists and health agencies . . . [e]xposure to any asbestos type ( i.e., serpentine [chrysotile] or amphibole) can increase the likelihood of lung cancer, mesothelioma, and nonmalignant lung and pleural disorders."१

Many other reviews support this conclusion, such as those from the American Conference of Governmental Industrial Hygienists,2 the American Thoracic Society,3 the Environmental Protection Agency,4 the International Agency for Research on Cancer,5 the National Toxicology Program,6 the Occupational Safety and Health Administration, 7 the Consumer Products Safety Commission (CPSC),8 the World Health Organization,9–11 and the World Trade Organization.12 This scientific consensus is also reflected in the Consensus Report of the 1997 Helsinki Conference,13 and publications from the American Cancer Society14 and the National Cancer Institute of the National Institutes of Health.१५

Thorough scientific inquiry requires consideration of all available information. Accordingly, in reaching the conclusion that chrysotile asbestos causes mesothelioma, scientists properly consider numerous accepted sources of scientific data, including epidemiologic studies of all varieties, case reports and series of case reports, controlled animal experiments, and toxicologic studies.1,16–२३

Asbestos industry arguments to the contrary have not been supported over time. Chrysotile asbestos mining companies and manufacturers have argued for more than 30 years either that their products do not cause disease or that there is insufficient evidence to reach a reliable conclusion. Numerous scientific articles and criticisms have specifically exposed the artificial uncertainty created by the proponents of chrysotile asbestos, and their position has been repeatedly and consistently rejected by the mainstream scientific and regulatory communities.18–20,24–२६

Like many scientists, we are concerned with the development and expansion of "doubt science।"27,28 A centerpiece of the "doubt science" model is the assertion that whatever piece of evidence supports the position of the industry in question (or whatever piece of evidence might be as yet undetermined) is the critical piece of evidence, to the exclusion of all others. While we acknowledge that industry-sponsored research can and does often provide valuable scientific insight and developments, the efforts of the tobacco and asbestos industries to deny their products cause cancer have become a paradigm for "doubt science."

In this regard, we are cognizant of the fact that the primary articles upon which the asbestos brake manufacturers rely in this matter were paid for by Ford, General Motors, Chrysler and other asbestos brake manufacturers. Publications by Hessel,29 Goodman,30 and Paustenbach31,32 were all expressly funded by Ford, General Motors, and Chrysler. Furthermore, the paper by Hessel et al. appeared in a journal funded by the Ford Motor Company and a subsidiary of General Motors. Wong33 has been reported to have undisclosed origins as an expert witness report for a brake manufacturer. 34 Laden acknowledges funding by a law firm that is "national asbestos counsel" for another asbestos brake manufacturer.35
The Scientific Community is in Consensus that Even Brief and Low-level Exposure to Asbestos Can Cause मेसोठेलिओम.

The mainstream scientific community has long recognized and continues to recognize today that there is no "safe" level of exposure to asbestos।12,13 As noted by NIOSH:

Excessive cancer risks have been demonstrated at all fiber concentrations studied to date। Evaluation of all available human data provides no evidence for a threshold or for a "safe" level of asbestos exposure.36 Attempts to postulate thresholds for exposure have been dismissed as "logical nonsense."37

The lack of a defined "safe" level for exposure to asbestos has been supported by subsequent research. For example, a large French study recently concluded that substantial excess mortality occurs at exposure levels below current regulatory levels.38 A recent study examining the relationship between historical asbestos use and disease rates further supports the conclusion that a linear dose–response relationship exists between exposure to asbestos and disease and that no "safe" level of exposure exists.३९

One of the main studies upon which the asbestos brake manufacturers rely40 similarly concluded that all levels of occupational exposure to asbestos increase the risk of mesothelioma:
Compared to those who never worked or who were never exposed, all levels of probability and intensity [of exposure to asbestos] had an increased significant risk, except subjects with low probability of exposure। For exposure classified as "sure" the OR was 13.2.

Application of this study to the current case under review would result in his placement in the "sure" exposure category, and consequently he would be over 13 times more likely to contract mesothelioma than unexposed individuals. Despite this, the asbestos brake manufacturers assert that the Agudo study proves that no person can ever get mesothelioma from asbestos brakes. That argument is unsound and contrary to the consensus of the scientific community that there is no demonstrable threshold of exposure to asbestos below which adverse health effects do not occur. Accordingly, "an occupational history of brief or low-level exposure should be considered sufficient for mesothelioma to be designated occupationally related" to asbestos exposure.१३

Mesothelioma Is a Signature Malignancy for Asbestos मेसोठेलिओमा

There is no debate that asbestos causes mesothelioma, and that the great majority of mesotheliomas are demonstrably caused by asbestos.41 Some mesotheliomas are never able to be individually linked to asbestos exposure, and the scientific community has defined these cases as "idiopathic" because information regarding asbestos exposure is unavailable.
However, we know that many individuals do not know that they have been exposed to asbestos.42 Many more die before being interviewed regarding potential exposures, forcing researchers to make assumptions about exposure based upon information from next of kin, job titles, or death certificates; these sources often fail to reflect all jobs and exposures.43,44 Many epidemiologic studies assess occupational exposure but not para-occupational or environmental exposure, because only occupational information is available from existing records. The fact that a percentage of mesotheliomas are labeled "idiopathic" does not, however, support the conclusion that there are large numbers of spontaneous ( i.e., non–asbestos-related) mesotheliomas. To the contrary, a large study of numerous sources of information failed to demonstrate evidence for "spontaneous" mesotheliomas,45 and a detailed review of mesothelioma cases in Australia found that over 90% had either a history of exposure or substantial asbestos in lung tissue.४२

The asbestos brake manufacturers attempt, without support, to recast the definition of "idiopathic।" First, in an attempt to undercut the indisputable link between asbestos and mesothelioma, they suggest that "idiopathic" mesotheliomas are not caused by asbestos rather than accepting that these are cases where individual exposure has not been identified. Second, they attempt to place mesotheliomas with demonstrable occupational exposures to asbestos-specifically asbestos from brakes-in the "idiopathic" category. There is no scientific support for either position.

Mesothelioma is a signature tumor for asbestos exposure। Individuals with known occupational exposures to asbestos cannot be recast into the "idiopathic" or "unknown exposure" category. When confronted with an individual who has a demonstrated mesothelioma and demonstrated occupational exposure to asbestos, the mainstream scientific community recognizes that the cause of that mesothelioma is the asbestos exposure of the individual even if that exposure was "brief or low-level."

Because Mesothelioma Is a Signature Malignancy with Essentially One Cause-Asbestos-the Scientific Community Has Long Considered Individual Cases of Mesothelioma to Be Sentinel एवेंट्स

It is not necessary to have an epidemiologic study of a specific occupation to be able to conclude that an individual's exposure to a toxic substance in that occupation can be a cause of disease। To the contrary, as noted by Dr. Lemen,

Specific occupations do not need to be studied nor do epidemiological studies need to be performed to show risk of disease before prevention actions are taken or causal connections concluded. To wait for epidemiology studies of each occupational group is not warranted but has been taken by many in the medico-legal profession as the only way to prove causation by occupation. Such misconceived thinking has been very harmful to the future prevention of asbestos-related diseases.४६

This is particularly so when examining mesothelioma। Repeated studies have shown that all levels of exposure increase the risk of mesothelioma.38,40 Moreover, unlike many other cancers, for which there are multiple, well-documented causal factors, mesothelioma is overwhelmingly caused by asbestos. As noted by one of the studies upon which the asbestos brake manufacturers rely:

Mesothelioma is a rare cancer with one major etiologic exposure, therefore surveillance using each case as a sentinel event might seem more reasonable for this disease than for cancers with multifactoral causation।47

In 1983 Rutstein developed a list of sentinel health events (SHE-O) that are occupationally related.48 Mesothelioma as a sentinel disease for asbestos exposure was on the initial list of SHE-O, and all subsequent revisions. In fact, the worldwide acceptance of mesothelioma as an asbestos-related cancer began with the case series published by Wagner in 1960.49
When examining the question of causation of sentinel diseases such as mesothelioma, the scientific community recognizes that case reports and case series reports are useful and valid tools।

Case series are particularly informative in situations where there are identified occurrences of very rare conditions for which there are few, if any, established causal factors. . . . In fact, recognition of even a small number of cases of the "sentinel" diseases-such as liver angiosarcoma and malignant mesothelioma, which is strongly related to asbestos exposure.50
The scientific community has concluded that, for sentinel diseases such as mesothelioma, case series reports can be sufficient by themselves to allow reliable conclusions to be drawn regarding causation। Again, as noted by Checkoway:

Case series reports can be virtually conclusive in their own right when the health outcome is a very rare disease or an uncommon manifestation of a relatively common condition.50
We do not suggest that such conclusions are indisputable or inviolate; scientific knowledge rarely is। The relevant question is whether reliable and scientifically justifiable conclusions can be drawn based upon such information, when considered in connection with all other available evidence. They can. In fact, proper application of the scientific method requires consideration of all forms of available evidence.

Accepted Method for Evaluating Disease Causation in an Individual: Generally and as Applied to Asbestos Exposure and Mesothelioma.

Examining the question of causation of disease in an individual generally involves four questions: 1) was the individual exposed to a toxic agent 2) does the agent cause the disease present in the individual; 3) was the individual exposed to this substance at a level where disease has occurred in other settings; and 4) have other competing explanations for the disease been excluded?
There is no reasonable dispute regarding Question 2-asbestos causes mesothelioma.

Additionally, there are no well-accepted competing explanations regarding mesothelioma that must be excluded, resolving Question 4. As a result, when considering the issue of causation of a mesothelioma, once an occupational or para-occupational exposure to asbestos has been established (Question 1), the sole question remaining for examination is whether the exposure or set of exposures of that individual is similar to exposures that have been documented to cause mesothelioma in others- Question 3.

The mainstream scientific community is in consensus regarding the resolution of Question 3. As discussed above, there is no safe level of exposure to asbestos. Even exposure at current regulatory levels results in excess mesotheliomas.7,38 Accordingly, the consensus of the scientific community is that any occupational or para-occupational exposure to asbestos- even "brief or low-level exposures"-must be considered causal in an individual with a mesothelioma.
The Claim of the Asbestos Brake Manufacturers That the Studies upon Which They Rely Trump All Other Scientific Knowledge Is Scientifically Unsupportable.

The asbestos brake manufacturers cite a number of epidemiologic studies as proof that asbestos from brakes cannot cause mesothelioma. The manufacturers claim the fact that these studies did not detect a statistically significant increased risk of mesothelioma in the occupational groups studied is conclusive proof that no person can ever contract disease from working with asbestos brakes.

That claim is simply not scientifically supportable. We need not examine here the individual shortcomings of the studies relied upon by the asbestos brake manufacturers. Others have done so cogently and in detail.16 ,34 While our rejection of the asbestos brake manufacturers' sweeping claim is supported by these critiques, the fundamental scientific failing of their claim is not based on the obvious limitations of the individual studies. There is a difference between a truly negative result and a non-positive result. A true negative study must be large, sensitive, and contain accurate exposure data. Even then, the study will be negative only with respect to the exposure level studied. Far from proving that no person can ever get sick from asbestos dust released by brakes, the best that can be said for the studies is that they are inconclusive. Instead, such a claim is based on the scientifically unsupportable proposition that one study, or group of studies, trumps all other evidence, no matter how extensive and well-documented that evidence is. Additional discussion of the implication of "negative" epidemiologic studies may be found elsewhere.51–54

As noted above, examination of the question of whether a substance is capable of causing disease requires consideration of all scientific disciplines and all available evidence. This is particularly true when asserting that exposure can not cause an effect.
The conclusion that some exposure is devoid of harmful effect (e.g. a certain chemical is not carcinogenic) must be based on a synthesis of the whole available literature: it can never rely on one single study. Hence, all the scientific evidence ( i.e. theoretical experimental, and epidemiologic) that exists must be combined.55

Substantial insight into this issue is provided by the industry consultants hired by Ford, General Motors, and Chrysler. When hired to represent the auto industry in asbestos-brake litigation, the industry consultants assert that their cited epidemiologic studies trump all other evidence, and conclusively refute the claim that asbestos from brakes can cause mesothelioma.29,30 Conversely, when hired by the power industry to provide testimony regarding epidemiologic studies that were damaging to that industry, Dr. Hessel rejected this same position:
Because of such recognized limitations, epidemiology studies by themselves generally do not provide sufficient basis to support conclusions about causation. That is why the assessment of health risk must rely on data from toxicological studies in animals, studies in human cells and tissues and experimental clinical studies.56

The opportunistic rejection of whatever evidence exists contrary to the position of the industry being defended is a hallmark of "doubt science." We disagree with both extremes. Epidemiologic evidence may, in cases, be sufficient to make reasoned and well-founded judgments regarding causation after consideration of other available evidence, even if evidence from one or more other scientific disciplines is absent. Conversely, consideration of other scientific evidence may allow reasoned conclusions regarding causation in the absence of positive epidemiologic studies regarding a specific population.

It is unscientific for the asbestos brake manufacturers to assert that their chosen epidemiologic studies trump all other evidence, just as it was unscientific for the tobacco industry to claim that lack of understanding of the mechanism by which tobacco causes cancer made it impossible to conclude that cigarettes cause cancer. Proper application of the scientific method requires that all available evidence be considered when examining issues of causation.

Evidence Supporting the Conclusion That Asbestos from Brakes Can and Does Cause Disease, Including Mesothelioma

The danger of asbestos in brakes has been recognized for decades. The hazard from exposure to asbestos in friction products has been known and accepted for over 70 years. In 1948, General Motors' chief industrial hygienist published regarding the hazards created when manipulating asbestos brake materials in the factory.57 By 1958, the danger of exposure to asbestos dust from brakes was sufficiently well documented that it was included in the American Industrial Hygiene Association's Hygienic Guide series.58 Additionally, mesotheliomas have been documented repeatedly in workers at friction-product factories.34,59–62

Today, the asbestos brake manufacturers assert that this danger is confined to the friction-product manufacturing facility. However, there is no scientific justification for asserting that dust from an asbestos brake can cause disease when the brake is ground in a factory but cannot cause disease when that same brake is ground in a garage.

Mechanics who work with asbestos brakes without dust-control measures are exposed to asbestos. Numerous studies have demonstrated that mechanics who worked with asbestoscontaining brakes without dust-control measures were exposed to asbestos dust. This is particularly true when the mechanic grinds, files, or sands the new asbestos brake and uses compressed air or dry brushing to clean out wear dust from old asbestos brakes.63–66 Both the EPA and OSHA have issued guidance to reduce the risk of disease from asbestos exposure during brake work.7,67,68 OSHA requires the use of dust controls when employees work with asbestos-containing brakes and clutches (for specific details see appendix F of the standard).7 The EPA has adopted these standards for municipal employees in jurisdictions not governed by state asbestos-control plans.67 Other regulatory agencies have similarly issued guidance to mechanics to reduce exposures to asbestos from brakes and clutches.69–72

Equally important, it has been proven that use of effective dust-control measures can lower exposure levels during work with asbestos brakes.73,74 Accordingly, to provide a reliable basis for the conclusion that asbestos from brakes can never cause disease, a study of brake mechanics would ascertain whether individuals considered "exposed" to asbestos brakes used dust-control practices. None of the studies relied upon by the asbestos brake manufacturers contains such information.

Studies have shown increased incidences of non-malignant asbestos-related diseases among mechanics known to have performed work with asbestos-containing brakes. Excessive nonmalignant disease in mechanics occurs in individuals known to have worked with asbestos-containing brakes.65,75 It is universally accepted that the amount of asbestos exposure needed to cause asbestosis is greater than the amount needed to cause mesothelioma. Accordingly, studies demonstrating excess asbestosis in asbestos brake-repair workers demonstrate that these workers were historically exposed to quantities of asbestos far in excess of that needed to cause mesothelioma.

Proper scientific inquiry cannot ignore the hundreds of reported cases of mesothelioma in mechanics. We reject the contention of the asbestos brake manufacturers that the scientist must close his or her eyes and refuse to consider case reports or case series of mesothelioma in mechanics, irrespective of how many cases are reported. This contention flies in the face of sound scientific reasoning, which requires thoughtful consideration of all available evidence.
As discussed above, the consideration of case reports is even more critical when examining rare, sentinel diseases such as mesothelioma because of the great difficulty in conducting epidemiologic studies with sufficient power to reliably detect increases in disease.53,54 Hundreds of cases of mesothelioma in mechanics have been reported in the medical literature, including dozens of cases in the studies relied upon by the asbestos brake manufacturers.16
The precise number of cases is not important for purposes of our discussion, nor is the possibility that some cases may have involved exposures to asbestos from sources other than brakes. The important point is that proper scientific inquiry not only can consider these reports, but, in fact, must consider them. Contrary to the suggestion of the asbestos brake manufacturers, these cases cannot be cavalierly dismissed as "unscientific" or "insufficient to support conclusions regarding causation." When considering the important question of whether working with asbestos-containing brakes can cause incurable, inevitably terminal diseases, such as mesothelioma, case series must be considered and evaluated, along with all other available evidence.

There is nothing novel regarding the use of Sir Austin Bradford Hill's viewpoints to arrive at the conclusion that asbestos from brakes can cause disease. Application of his viewpoints has been an accepted and valid method for examination of questions of causation for decades and remains so today.76 His own wise words are worth repeating:

Here then are nine different viewpoints from all of which we should study association before we cry causation. What I do not believe-and this has been suggested-that we can usefully lay down some hard-and-fast rules of evidence that must be obeyed before we can accept cause and effect. None of my nine viewpoints can bring indisputable evidence for or against the cause-and-effect hypothesis and none can be required as a sine qua non. What they can do, with greater or less strength, is to help us make up our minds on the fundamental question-is there any other way of explaining the set of facts before us, is there any other answer equally, or more, likely than cause and effect?

Contrary to the all-or-nothing position of the asbestos brake manufacturers, there is no single scientific discipline or type of study that takes precedence over others. Thoughtful scientific inquiry requires consideration of all evidence when making determinations regarding causation.

CONCLUSION
Asbestos causes mesothelioma. Mechanics are exposed to asbestos dust during the servicing and replacement of brakes. While the asbestos brake manufacturers claim that the average amount of asbestos released from brake repair work is comparatively low, there is no reasonable dispute that exposure levels were higher when mechanics routinely ground, filed, and sanded brakes and used compressed air to blow out brake wear debris, and did this work without dust control. It is those historic higher exposures that caused disease appearing now. The scientific community is in consensus that brief and lowlevel exposures to asbestos can cause mesothelioma. The scientific literature contains hundreds of cases of mesothelioma among brake mechanics; and epidemiologic studies of mechanics known to have performed repair work on asbestos-containing brakes have demonstrated increased levels of nonmalignant diseases.
This combination of evidence, and the vast amount of additional scientific information regarding asbestos and mesothelioma, provides more than sufficient evidence to allow someone to conclude within a reasonable degree of scientific certainty that a mesothelioma in a mechanic who worked with asbestos-containing brakes was caused by that asbestos exposure.
Since 2000, Ford, General Motors, and Chrysler have paid over $30,000,000 to hire consultants for the purpose of generating the very papers they rely upon, and for testifying regarding those papers in Courts.† One of the main industry experts has acknowledged that the papers were conceived and authored for the purpose of buttressing testimony in court cases involving mechanics suffering from mesothelioma.‡

†Ford, General Motors, and Chrysler have admitted in litigation that, since 2000, they have paid over $30,000,000 to these experts.See, Ford and General Motors, Answers to Interrogatories, Unden v. General Motors, Case No. 05:6311, Circuit Court for Hillsborough County, Florida, and Chrysler IRS Form 1099s produced in litigation.
‡Deposition of Dennis Paustenbach, July 1, 2005, Mallia v. BennettAuto et al., Case Number 04-16236 CA 42, CIrcuit Court in and for Dade County, Florida.
The same expert also acknowledged that this business model is a pattern he has also followed with dioxin, benzene, hexavalent chromium, beryllium, formaldehyde, and glycol ethers. Recent revelations regarding undisclosed involvement of the employer of these experts in connection with publication of a paper favorable to the chromium industry have been well publicized and led to the retraction of that paper.77,78 It is in no way surprising that the experts and papers financed by these manufacturers conclude that asbestos in brakes can never cause mesothelioma. To the contrary, the exoneration of the sponsoring industry is the expected conclusion of doubt science. Despite the best efforts of the asbestos brake manufacturers and their hired experts to fabricate scientific uncertainty where none exists, the mainstream scientific community and regulatory communities have considered the available evidence and concluded that the danger to mechanics from asbestos in brakes is real.
Apparently, the asbestos brake manufacturers hope that these arguments can be used to sway the Supreme Court of Michigan and other courts. As scientists who have devoted substantial portions of our professional lives working to research, prevent, and treat asbestosrelated diseases, we reject these attempts to fabricate uncertainty where none exists. Instead, we request that these courts attend to the work of thousands of experts from around the world who have concluded that asbestos, in any form, and through any occupational exposure, can and does cause disease.
LAURA S. WELCH, MD Medical Director, Center to Protect Workers Rights, Silver Spring, MDProfessorial LecturerGeorge Washington University School of Public Health and Health Sciences
HENRY A. ANDERSON, MD Chief Medical OfficerWisconsin Division of Public HealthMadison, Wisconsin
JOHN C. BAILAR III, MD, PHDProfessor EmeritusUniversity of ChicagoChicago, IllinoisPresently: Washington, DC
JOHN R. BALMES, MDProfessor of MedicineUniversity of California, San FranciscoProfessor of Environmental Health SciencesSchool of Public HealthUniversity of California, BerkeleyDirector, Northern California Center for Occupational and Environmental HealthUC Berkeley–UC Davis–UCSF
LUNDY BRAUN, PHDAssociate ProfessorDepartments of Pathology and Laboratory Medicine and AfricanaStudiesBrown UniversityProvidence, Rhode Island
ARNOLD BRODY, PHDProfessor, Department of Molecular and Biomedical SciencesNorth Carolina State UniversityRaleigh, North Carolina
BARRY CASTLEMAN, SCDKensington, Maryland
DAVID C. CHRISTIANI, MD, MPH, MS Professor, Harvard School of Public HealthProfessor, Harvard Medical SchoolCambridge, MassachusettsPhysician, Massachusetts General HospitalBoston, Massachusetts
DEVRA DAVIS, PHDDirector, Center for Environmental Oncology University of Pittsburgh Cancer InstituteProfessor, Department of Epidemiology,University of Pittsburgh Graduate School of Public HealthPittsburgh, Pennsylvania
JOHN M. DEMENT, PHD, CIHProfessor, Division of Occupational and Environmental Medicine Department of Community & Family MedicineDuke University Medical CenterDurham, North Carolina
RONALD F. DODSON, PHDPresident, Dodson Environmental Consulting, Inc.Tyler, Texas
ANDERS ENGLUND, MD Former Director Medical and Social AffairsSwedish Work Environment AuthorityFormer Director UICCStockholm, Sweden
BRADLEY EVANOFF, MD, MPHAssociate Professor of MedicineWashington University School of Medicine St. Louis, Missouri
ARTHUR FRANK, MD, PHDProfessor, Chair, Department of Environmental and Occupational HealthDrexel School of Public HealthPhiladelphia, Pennsylvania
FERNANDA GIANNASISafety and Health Engineer Labour Inspector at the Brazilian Labor Inspectorate in Sao Paulo StateManager of Asbestos Replacement ProjectWork and Employment Department in Sao Paulo StateCoordinator of the Virtual-Citizen Ban Asbestos Network for Latin America Founder of the ABREA-Brazilian Asbestos Victims AssociationSao Paulo, Brazil
MICHAEL GOCHFELD, MD, PHDEnvironmental and Occupational Health Sciences InstituteRobert Wood Johnson Medical SchoolPiscataway, New Jersey
BERNARD D. GOLDSTEIN, MDProfessor, Environmental and Occupational HealthGraduate School of Public HealthUniversity of PittsburghPittsburgh, Pennsylvania
JULIETTA RODRÍGUEZ GUZMÁN, MDGraduate Occupational Health Program Universidad El BosqueColombia
DOUGLAS HENDERSON, MDAssociate Professor of PathologyHead, Department of HistopathologyFlinders Medical CenterAdelaide, South Australia
ROBIN HERBERT, MD Associate Professor, Department of Community and Preventive MedicineCo-Division DirectorMount Sinai Center for Occupational and Environmental MedicineDirector, World Trade Center Monitoringand Treatment Program Data and Coordination Center Mount Sinai School of MedicineNew York, New York
JAMES HUFF, PHDAssociate Director for Chemical CarcinogenesisNational Institute of Environmental Health SciencesNational Institutes for HealthResearch Triangle Park, North Carolina
PETER F. INFANTE, DRPHProfessorial Lecturer, Environmental and Occupational HealthSchool of Public Health and Health ServicesThe George Washington UniversityWashington, DC Former Director Office of Standards ReviewHealth Standards ProgramsOccupational Safety and Health AdministrationWashington, DC
TUSHAR KANT JOSHI, MBBS, MS, MSCCentre for Occupational and Environmental Health Lok Nayak HospitalNew Delhi, India
DAVID KREIBEL, SCDProfessor of EpidemiologySchool of Health and EnvironmentUniversity of Massachusetts LowellLowell, Massachusetts
JOSEPH LADOU, MS, MD Director, International Center for Occupational MedicineUniversity of California School of MedicineSan Francisco, California
PHILIP J. LANDRIGAN, MD, MSCProfessor and ChairmanDepartment of Community and Preventive Medicine Professor of PediatricsMount Sinai School of MedicineNew York, New YorkPresident, Collegium Ramazzini
JAMES LEIGH, MB, MD, PHD, MA, MSC, BLEGSSenior Lecturer and DirectorCentre for Occupational and Environmental Health School of Public HealthUniversity of SydneyNew South Wales, Australia
STEPHEN M. LEVIN, MDAssociate Professor, Department of Community and Preventive MedicineMount Sinai School of MedicineMedical Director Mount Sinai-IJ Selikoff Center for Occupational and Environmental MedicineNew York, New York
EUGENE J. MARK, MDProfessor of PathologyHarvard Medical SchoolMassachusetts General HospitalBoston, Massachusetts
ARTHUR MCIVOR, PHDProfessor of Social HistoryDirector, Scottish Oral History CentreHistory DepartmentUniversity of StrathclydeGlasgow, Scotland
DAVID MICHAELS, PHD, MPHDirector, The Project on Scientific Knowledge and Public Policy Research Professor and Acting ChairmanDepartment of Environmental and Occupational HealthThe George Washington University School of Public Health and Health ServicesWashington, DC
KAREN B. MULLOY, DO, MSCH Associate Professor, Department of Preventive Medicine and BiometricsUniversity of Colorado School of MedicineDirector, Occupational Health and Safety Denver HealthDenver, Colorado
L. CHRISTINE OLIVER, MD Assistant Clinical Professor of MedicineHarvard School of Public HealthCambridge, Massachusetts
RORY O'NEILLEditor, Hazards MagazineSheffield, England
DOMYUNG PAEK, MD, MSC, SCD Professor, Occupational and Environmental Medicine School of Public HealthSeoul National UniversitySeoul, Korea
LEWIS PEPPER, MD, MPHAssistant Professor, Environmental HealthBoston University School of Public Health Boston, Massachusetts
BERNARDO REYESDirector, Institute of Political EcologySantiago, Chile
CECILE ROSE, MD, MPHActing Head, Division of Environmental and Occupational Health SciencesNational Jewish Medical and Research Center Denver, Colorado
KENNETH D. ROSENMAN, MDProfessor of MedicineChief, Division of Occupational and Environmental MedicineMichigan State UniversityDepartment of MedicineEast Lansing, Michigan
BRIAN S. SCHWARTZ, MD, MSProfessor of Environmental Health Sciences, Epidemiology, and MedicineJohns Hopkins UniversityBloomberg School of Public HealthBaltimore, Maryland
MICHAEL SILVERSTEIN, MD, MPH Clinical Professor of Environmental and Occupational Health SciencesUniversity of Washington School of Public Health and CommunityMedicineSeattle, Washington
ROSEMARY K. SOKAS, MD, MOHDirector, Division of Environmental and Occupational Health Sciences School of Public HealthUniversity of Illinois at ChicagoChicago, Illinois
NANCY L. SPRINCE, MD, MPHProfessor, Department of Occupational and Environmental HealthUniversity of Iowa College of Public Health Iowa City, Iowa
KEN TAKAHASHI, MD, MPH, PHDActing Director of WHOCC in Occupational HealthProfessor of Environmental EpidemiologyUniversity of Occupational and Environmental HealthKitakyushu City, Japan
TIM K. TAKARO, MD, MPH, MSAssociate ProfessorFaculty of Health Sciences Simon Fraser UniversityBurnaby, British Columbia
DANIEL THAU TEITELBAUM, MDAdjunct Professor of Environmental Sciences The Colorado School of MinesGolden, ColoradoAssociate Clinical Professor of Preventive MedicineThe University of Colorado Health Sciences Center at DenverDenver, Colorado.
KAY TESCHKE, PHDProfessor and Chair Division of Public, Environmental and Occupational HealthDepartment of Health Care and EpidemiologyThe University of British ColumbiaVancouver, BC, Canada
LORENZO TOMATIS, MDFormer DirectorInternational Agency for Research on Cancer (IARC) Trieste, Italy
IVANCICA TROSIC, PHDInstitute for Medical Research and Occupational HealthUniversity of ZagrebZagreb, Croatia
ROBERT VOJAKOVIC, AM, JPPresident of the Asbestos Diseases Society of Australia, Inc. Osborn Park, Australia
ANDREW WATTERSON, PHD, CSHPProfessor of HealthDirector, Occupational and Environmental Health Research GroupUniversity of Stirling,Stirling, Scotland
DAVID H. WEGMAN, MD, MSC Dean and Professor of Work EnvironmentSchool of Health and EnvironmentUniversity of Massachusetts LowellLowell, Massachusetts
The views expressed in this paper are those of the individuals signing it. The affiliations listed with those signers are for identification purposes only, and the views expressed herein are not necessarily the views of those affiliate entities. References
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Thursday, August 23, 2007

Drop in California Spending Lowers U.S. Workers' Compensation Benefits and Costs

August 22, 2007

WASHINGTON, DC—U.S. workers’ compensation payments for medical care and cash benefits for workers disabled by workplace injuries or diseases declined in 2005, according to a study released today by the National Academy of Social Insurance (NASI).

The drop in payments in 2005 (the most recent year with data) reflects large declines in California payments, as reforms enacted in 2003 and 2004 took effect. Nationally, workers’ compensation payments for injured workers fell by 1.4 percent to $55.3 billion in 2005. The payments include $26.2 billion to providers of medical care and $29.1 billion in cash wage replacement benefits for injured workers. California payments fell by 12.2 percent; a change made up of a 16.0 percent decline in medical payments and an 8.6 percent decline in cash payments. “The reduced spending for benefits and medical care reflects the initial stages of cost containment measures that were put in place in 2003 and 2004 reforms to the California system,” according to NASI member Christine Baker, who directs the California Commission on Health and Safety and Workers’ Compensation, a nonpartisan labor-management group that advises state policymakers.

Because it is a large state – accounting for nearly 20 percent of national benefit payments in 2005 –California altered national trends. Outside California, total workers’ compensation payments rose by 1.7 percent, an increase driven by a 4.1 percent increase in payments to medical providers. Cash payments to injured workers outside California showed a small decline (0.3 percent).

The costs to employers for workers’ compensation are what they pay each year. For employers who buy insurance, costs are premiums they pay to insurance companies plus benefits they pay under deductible arrangements in their insurance policies. For employers who insure their own workers, costs are the benefits they pay plus administrative costs. In 2005, employers paid a total of $88.8 billion nationwide for workers’ compensation. A sharp drop in California employers’ costs (of 9.8 percent) held down the national increase in employer costs to 2.3 percent. Outside California, employer costs for workers’ compensation rose by 6.5 percent.

The new report tracks trends since 1989 in workers’ compensation benefits and employer costs relative to total wages of workers covered by the program. Relative to wages, cash benefits in 2005 were the lowest in 17 years ($0.56 per $100 of wages). Nationally, total benefits (cash plus medical) and employer costs fell relative to wages in 2005. Cash and medical benefits combined were $1.06 per $100 of covered wages in 2005, a drop of $0.07 from 2004, while employer costs were $1.70 per $100 of wages in 2005, down $0.05 from 2004.

Outside California, benefits per $100 of wages fell by a smaller amount ($0.03) and employer costs per $100 of wages rose slightly (by $0.02). According to John F. Burton, Jr., chair of the panel that oversees the study, “The relative stability of benefits outside the Golden State reflects a rough balance between the declining frequency of workplace injuries and higher expenditures for medical benefits.”

The new report, Workers’ Compensation: Benefits, Coverage and Costs, 2005, is the tenth in a NASI series that provides the only comprehensive national data that covers all types of employers. The study provides estimates of workers’ compensation cash and medical payments for each state, the District of Colombia, and federal programs.

To download the full report, click here.
To download a PDF of this release, click here.

Friday, August 17, 2007

U.S. Department of Labor's OSHA proposes $2.78 million fine against Cintas Corp. following Tulsa, Okla., employee death in industrial dryer

U.S. Department of Labor's OSHA proposes $2.78 million fine against Cintas Corp. following Tulsa, Okla., employee death in industrial dryer Alabama, Arkansas, Ohio and Washington facilities also inspected

U.S. Department of Labor press releaseAugust 17, 2007

http://www.osha.gov/pls/oshaweb/owasrch.search_form?p_doc_type=NEWS_RELEASES&p_toc_level=1&p_keyvalue=200708&p_status=CURRENT

WASHINGTON – The U.S. Department of Labor's Occupational Safety and Health Administration (OSHA) today proposed $2.78 million in penalties against Ohio-based Cintas Corp. following an inspection into the March 2007 employee death at the Cintas laundry facility in Tulsa, Okla. The employee was killed when he fell into an operating industrial dryer while clearing a jam of wet laundry on a conveyor that carries the laundry from the washer into the dryer.
Cintas is the largest uniform supplier in North America, with more than 400 facilities employing more than 34,000 people. The facility in Tulsa has 160 employees.
"Plant management at the Cintas Tulsa laundry facility ignored safety and health rules that could have prevented the death of this employee," said Assistant Secretary of Labor for OSHA Edwin G. Foulke Jr.
Forty-two willful, instance-by-instance citations allege violations of the OSHA lockout/tagout standard for the failures to shut down and to lock out power to the equipment before clearing jams, and to train four employees responsible to clear jams that lockout/tagout applies and how to perform the operations. One repeat citation alleges the failure to protect employees from being struck or pinned by the conveyor. Three serious citations allege the failures to protect employees from falls, to have a qualified person inspect the lockout/tagout procedures and to certify the procedures as required.
In a separate case, OSHA today issued five repeat and two serious citations with penalties totaling $117,500 for violations of the lockout/tagout and machine guarding standards found at the Cintas Columbus, Ohio, facility. OSHA also has opened investigations in Arkansas and Alabama. Washington, an OSHA State Plan state, has issued four citations with proposed fines totaling $13,650, alleging violations for similar hazards at the Yakima Cintas facility.
A willful violation is one committed with intentional disregard of the requirements of the Occupational Safety and Health Act or plain indifference to employee safety or health. A serious violation is one that could cause death or serious physical harm to employees, and the employer knew or should have known of the hazard.
Cintas has 15 working days from receipt of the citations to contest the citations and the proposed penalties before the independent Occupational Safety and Health Review Commission.

Saturday, August 11, 2007

NJ Permits Intentional Tort Claim Against Former Employer- PVC Exposure

While denying class action certification for a medical monitoringclass and a punitive damage class, the NJ App Div permitted an INTENTIONAL TORT action against the employer to go forward in a common law civil claim.

This case involved exposure to poly vinyl chloride at a Pantasote, a Paterson NJ plant, causing disease to former workers which is characteristic of Raynaud's phenomenon ( fingers blanch and numbnessand discomfort are experienced upon exposure to the cold), changes inthe bones at the bones at the end of the fingers [Known asacro-osteolysis (AOL)], joint and muscle pain, and scleroderma-likeskin changes (thickening of the skin, deceased elasticity and slightedema).

Inhaled vinyl chloride has been shown to increase the risk of a rareform of liver cancer (angiosarcoma of the liver) in humans. It is classified by the Environmental Protection Agency (EPA) as a Group A, human carcinogen.

Plaintiffs represented by: Jon Gelman (NJ), Ron Simon (DC), Herschel Hobson (TX) and Mark Cuker (PA)

Decision- Buynie v. Airco Co, NJ App Div 2007, Decided August 10, 2007

See related articles:
Misleading Statements Made By Vinyl Chloride Companies Held Valid Basis for Suit

Workplace Poison

Vinyl Chloride Conspiracy Documents: Part 4 (Jun 1974 - Dec 1974)

Vinyl Chloride Plants in New Jersey

Thursday, August 9, 2007

National Census of Fatal Occupational Injuries 2005

A total of 5,702 fatal work injuries were recorded in the United States in 2005, down

about 1 percent from the revised total of 5,764 fatal work injuries recorded in 2004. The rate at

which fatal work injuries occurred in 2005 was 4.0 per 100,000 workers, down slightly from a

rate of 4.1 per 100,000 in 2004.

The Census of Fatal Occupational Injuries has been conducted each year since 1992. The

numbers reported in this release are preliminary and will be updated in April 2007.

Press Release: Aug 10, 2007 - National Census of Fatal Occupational Injuries in 2005
http://www.bls.gov/news.release/pdf/cfoi.pdf

Additional Information:
Census of Fatal Occupational Injuries Summary, 2005

Text version of entire news release

Monday, August 6, 2007

Insurance Industry Again Offers MSP Legislation That Would Discourage Workers' Compensation Periodic Payments

After a failed attempt in the last Congress, the Insurance Industry has again offered similar legislation to encourage "lump sum" settlements in Workers' Compensation hearings, H.R.2549, and circumvent reimbursement of the ailing Medicare program. This legislation failed to gain acceptance in the last Congress as it did not receive the support of interest groups involved in preserving the Medicare system and Labor who continues to support a periodic benenfit system in Workers' Compensation. The proposal would encourage the dismantling of the current Workers' Compensation system in favor of lump sum benenfits. Leading commentators also oppose such legislation.

"In some jurisdictions, the excessive and indiscriminate use of the lump-summing device has reached a point at which it threatens to undermine the real purposes of the compensation system. Since compensation is a segment of a total income insurance system, it ordinarily does its share of the job only if it can be depended on to supply periodic income benefits replacing a portion of lost earnings. If a partially or totally disabled worker gives up these reliable periodic payments in exchange for a large sum of cash immediately in hand, experience has shown that in many cases the lump sum is soon dissipated and the worker is right back where he or she would have been if workers' compensation had never existed."
[8 Larson's Workers' Compensation Law, § 132.07[1] at 132-17 (2006).]

See: http://thomas.loc.gov/cgi-bin/bdquery/z?d110:h.r.02549: