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[Federal Register: October 4, 2004 (Volume 69, Number 191)] [Proposed Rules] [Page 59305-59474] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr04oc04-28] [[Page 59305]] ----------------------------------------------------------------------- Part II Department of Labor ----------------------------------------------------------------------- Occupational Safety and Health Administration ----------------------------------------------------------------------- 29 CFR Parts 1910, 1915, 1917, 1918, and 1926 Occupational Exposure to Hexavalent Chromium; Proposed Rule [[Page 59306]] ----------------------------------------------------------------------- DEPARTMENT OF LABOR Occupational Safety and Health Administration 29 CFR Parts 1910, 1915, 1917, 1918, and 1926 [Docket No. H054A] RIN 1218-AB45 Occupational Exposure to Hexavalent Chromium AGENCY: Occupational Safety and Health Administration (OSHA), Department of Labor. ACTION: Proposed rule; request for comments and scheduling of informal public hearings. ----------------------------------------------------------------------- SUMMARY: The Occupational Safety and Health Administration (OSHA) proposes to amend its existing standard for employee exposure to hexavalent chromium (Cr(VI)). The basis for issuance of this proposal is a preliminary determination by the Assistant Secretary that employees exposed to Cr(VI) face a significant risk to their health at the current permissible exposure limit and that promulgating this proposed standard will substantially reduce that risk. The information gathered so far in this rulemaking indicates that employees exposed to Cr(VI) well below the current permissible exposure limit are at increased risk of developing lung cancer. Occupational exposures to Cr(VI) may also result in asthma, and damage to the nasal epithelia and skin. This document proposes an 8-hour time-weighted average permissible exposure limit of one microgram of Cr(VI) per cubic meter of air (1 mg/ m3) for all Cr(VI) compounds. OSHA also proposes other ancillary provisions for employee protection such as preferred methods for controlling exposure, respiratory protection, protective work clothing and equipment, hygiene areas and practices, medical surveillance, hazard communication, and recordkeeping. OSHA is proposing separate regulatory texts for general industry, construction, and shipyards in order to tailor requirements to the circumstances found in each of these sectors. DATES: Written comments. The Agency invites interested persons to submit written comments regarding the proposed rule, including comments on the information collection determination described in Section X of the preamble (OMB Review under the Paperwork Reduction Act of 1995), by mail, facsimile, or electronically. All comments, whether submitted by mail, facsimile, or electronically through the Internet, must be sent by January 3, 2005. Informal public hearings. The Agency plans to hold an informal public hearing in Washington, DC, beginning on February 1, 2005. OSHA expects the hearing to last from 9:30 a.m. to 5:30 p.m.; however, the exact daily schedule is at the discretion of the presiding administrative law judge. Notice of intention to appear to provide testimony at the informal public hearing. Interested persons who intend to present testimony at the informal public hearing in Washington, DC, must notify OSHA of their intention to do so no later than December 3, 2004. Hearing testimony and documentary evidence. Interested persons who request more than 10 minutes to present their testimony, or who will be submitting documentary evidence at the hearing, must provide the Agency with copies of their full testimony and all documentary evidence they plan to present by January 3, 2005. See Section XVI below for details on the format and how to file a notice of intention to appear, submit documentary evidence at the hearing, and request an appropriate amount of time to present testimony. ADDRESSES: Written comments. Interested persons may submit three copies of written comments to the Docket Office, Docket H054A, Room N-2625, OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW., Washington, DC 20210; telephone (202) 693-2350. If written comments are 10 pages or fewer, they may be faxed to the OSHA Docket Office, facsimile number (202) 693-1648. Comments may also be submitted electronically through the Internet at http://ecomments.osha.gov. Supplemental information such as studies and journal articles cannot be attached to electronic submissions. Instead, three copies of each study, article, or other supplemental document must be sent to the OSHA Docket Office at the address above. These materials must clearly identify the associated electronic comments to which they will be attached in the docket by the following information: Name of person submitting comments; date of comment submission; subject of comments; and docket number to which comments belong. Informal public hearings. The informal public hearing to be held in Washington, DC, will be held in the Frances Perkins Building, U.S. Department of Labor, 200 Constitution Avenue, NW., Washington, DC 20210. Notice of intention to appear to provide testimony at the informal public hearing. Interested persons who intend to present testimony at the informal public hearing in Washington, DC, may submit three copies of their notice of intention to appear to the Docket Office, Docket H054A, Room N-2625, OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW., Washington, DC 20210. Notices may also be submitted electronically through the Internet at http://ecomments.osha.gov. OSHA Docket Office and Department of Labor hours of operation are 8:15 a.m. to 4:45 p.m. Hearing testimony and documentary evidence. Interested persons who request more than 10 minutes in which to present their testimony, or who will be submitting documentary evidence at the informal public hearing must submit three copies of the testimony and the documentary evidence to the Docket Office, Docket H054A, Room N-2625, OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW., Washington, DC 20210. Written testimony may also be submitted electronically through the Internet at http://ecomments.osha.gov. Please note that security-related problems may result in significant delays in receiving comments and other materials by regular mail. Telephone the OSHA Docket Office at (202) 693-2350 for information regarding security procedures concerning delivery of materials by express delivery, hand delivery, and messenger service. All comments and submissions will be available for inspection and copying in the OSHA Docket Office at the address above. Most comments and submissions will be posted on OSHA's Web page (http://www.osha.gov ). Contact the OSHA Docket Office at (202) 693-2350 for information about materials not available on the OSHA Web page and for assistance in using this Web page to locate docket submissions. Because comments sent to the docket or to OSHA's Web page are available for public inspection, the Agency cautions interested parties against including in these comments personal information such as social security numbers and birth dates. FOR FURTHER INFORMATION CONTACT: For general information and press inquiries, contact Mr. George Shaw, Office of Communications, Room N- 3647, OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW., Washington, DC 20210; telephone (202) 693-1999. For technical inquiries, contact Ms. Amanda Edens, Directorate of Standards and Guidance, Room N-3718, OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW., Washington, DC 20210; telephone (202) 693-2093 or [[Page 59307]] fax (202) 693-1678. For hearing information contact Ms. Veneta Chatmon, Office of Communications, Room N-3647, OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW., Washington, DC 20210; telephone (202) 693-1999. SUPPLEMENTARY INFORMATION: For additional copies of this Federal Register document, contact the Office of Publications, Room N-3101, OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW., Washington, DC 20210; telephone (202) 693-1888. Electronic copies of this Federal Register, as well as news releases and other relevant documents, are available at OSHA's Home page at http://www.osha.gov. I. General The preamble to the proposed standard on occupational exposure to chromium (VI) discusses events leading to the proposal, health effects of exposure, the degree and significance of the risk presented, a summary of the analysis of technological and economic feasibility, regulatory impact, and regulatory flexibility, and the rationale behind the specific provisions set forth in the proposed standard. The discussion follows this outline: I. General II. Issues III. Pertinent Legal Authority IV. Events Leading to the Proposed Standards V. Chemical Properties and Industrial Uses VI. Health Effects VII. Preliminary Quantitative Risk Assessment VIII. Significance of Risk IX. Summary of the Preliminary Economic Analysis and Initial Regulatory Flexibility Analysis X. OMB Review under the Paperwork Reduction Act of 1995 XI. Federalism XII. State Plans XIII. Unfunded Mandates XIV. Protecting Children from Environmental Health and Safety Risks XV. Environmental Impacts XVI. Public Participation--Notice of Hearing XVII. Summary and Explanation of Format Factory 4.6.2.0 License Key - Crack Key For U Standards XVIII. Authority and Signature XIX. Proposed Standards II. Issues OSHA requests comment on all relevant issues, including health effects, risk assessment, significance of risk determination, technological and economic feasibility, and the provisions of the proposed regulatory text. OSHA is especially interested in responses, supported by evidence and reasons, to the following questions: Health Effects 1. OSHA has described a variety of studies addressing the major adverse health effects that have been associated with exposure to Cr(VI). Has OSHA adequately identified and documented all critical health impairments associated with occupational exposure to Cr(VI)? Are there any additional studies or other data that would controvert the information discussed or significantly enhance the determination of material health impairment or the assessment of exposure-response relationships? Submit any relevant information, and explain your reasoning for recommending the inclusion of any studies you suggest. 2. Using currently available epidemiologic and experimental studies, OSHA has made a preliminary determination that all Cr(VI) compounds (e.g., water soluble, insoluble and slightly soluble) possess carcinogenic potential and thus present a lung cancer risk to exposed workers. Is this determination correct? Are there additional data OSHA should consider in evaluating the carcinogenicity or relative carcinogenic potencies of different Cr(VI) compounds? Risk Assessment 3. In its preliminary assessment of risk, OSHA has relied primarily on two epidemiologic cohort studies of chromate production workers to estimate the lung cancer risk to workers exposed to Cr(VI) (Exs. 31-22- 11; 33-10). Are there any other studies that you believe are better suited to estimating the risk to exposed workers; if so, please provide the studies and explain why you believe they are better. 4. OSHA is aware of two cohorts (i.e., Alexander cohort, Ex. 31-16- 3, and Pastides cohort, Ex. 35-279) in which a sizable number of workers were probably exposed to low Cr(VI) air levels (e.g., < 10 [mu]g/m3) more consistent with concentrations found in the workplace today. However, OSHA believes the period of follow-up observation (median < 10 yr), the young age (< 45 yr at end of follow-up) and the low number of observed lung cancers (< =15 lung cancers) severely limits these cohorts as primary data sets for quantitative risk analysis. Other limitations to the Alexander study include a lack of data on workers who were employed between 1940 and 1974, but whose employment ended prior to 1974, and on exposures prior to 1974. Are there updated analyses available for the Alexander and Pastides cohorts? How many years do these cohorts need to be followed and how many lung cancers need to be observed in order for these data sets to provide insight into the shape of the exposure-response curve at lower levels of Cr(VI) exposure (e.g., 0.5 to 5 [mu]g/m3)? In the case of the Alexander cohort, is there additional information on cohort members' exposures prior to 1974 or workers who left prior to 1974 that could improve the analysis? Are there other cohorts available to look at low exposures? 5. OSHA has relied upon a linear relative risk model and cumulative Cr(VI) exposure for estimating the lifetime occupational lung cancer risk among Cr(VI)-exposed workers. In particular, OSHA has made a preliminary determination that a threshold model is not appropriate for estimating the lung cancer risk associated with Cr(VI). However, there is some evidence that pathways (e.g., extracellular reduction, DNA repair, cell apoptosis, etc.) may exist within the lung that protect against Cr(VI)-induced respiratory carcinogenesis, and may potentially introduce non-linearities into the Cr(VI) exposure-cancer response. Is there convincing scientific evidence of a non-linear exposure-response relationship in the range of occupational exposures of interest to OSHA? If so, are there sufficient data to define a non-linear approach that would provide more reliable predictions of risk than the linear relative risk model used by OSHA? 6. OSHA's estimates of lung cancer risk are based on workers primarily exposed to highly water-soluble sodium chromate and sodium dichromate. OSHA has preliminarily concluded that the risk for workers exposed to equivalent levels of other Cr(VI) compounds will be of a similar magnitude or, in the case of some Cr(VI) compounds, possibly greater than the risks projected in the OSHA quantitative risk assessment. Is this determination appropriate? Are there sufficient data to reliably quantify the risk from occupational exposure to specific Cr(VI) compounds? If so, explain how the risk could be estimated. 7. The preliminary quantitative risk assessment relies on two (Gibb and Luippold) cohort studies in which most workers were exposed higher Cr(VI) levels than the PEL proposed by OSHA, for shorter durations than a working lifetime exposure. The risks estimated by OSHA for lifetime exposure to the proposed PEL, therefore, carry the assumption that a cumulative exposure achieved by short duration exposure to higher Cr(VI) air levels (e.g., exposed 3 years to 15 [mu]g/m3) leads to the same risk as an equivalent cumulative exposure achieved by longer duration exposure to [[Page 59308]] lower Cr(VI) exposure (e.g, exposed 45 years to 1 [mu]g/m3). OSHA preliminarily finds this assumed exposure equivalency to represent an uncertainty in the estimates of risk but does not have information that indicates this uncertainty introduces serious error in its predictions of risk. Does the OSHA exposure-response assessment based on the higher Cr(VI) air levels and/or shorter durations experienced by the Gibb and Luippold cohorts lead to a serious underprediction or overprediction in estimated risks for the occupational exposure cyberlink powerdvd ultra 19 crack - Activators Patch of interest to OSHA? Please provide any data to support your rationale. 8. OSHA has made a preliminary determination that suitable data are not available for making quantitative risk estimates for the non-cancer adverse health effects associated with exposure to Cr(VI) (e.g., nasal septum ulcerations and perforations, asthma, irritant and allergic contact dermatitis). Are there suitable data for a quantitative estimation of risk for non-cancer adverse effects that OSHA should include in its final quantitative risk assessment? If so, what models or approaches should be used? 9. Are there other factors OSHA should take into consideration in its final quantitative risk assessment to better characterize the risks associated with exposure to Cr(VI)? Technologic and Economic Feasibility 10. In its Preliminary Economic Analysis of the proposed standard, OSHA presents a profile of the affected worker population. In that profile are estimates of the number of affected workers by application group and job category and the distribution of exposures by job category. Are there additional data that will enable the Agency to refine its profile of the worker population exposed to Cr(VI)? If so, how should OSHA use these data in making such revisions? 11. What are the job categories in which employees are potentially exposed to Cr(VI) in your company or industry? For each job category, provide a brief description of the operation and describe the job activities that may lead to Cr(VI) exposure. How many employees are exposed, or have the potential for exposure, to Cr(VI) in each job category in your company or industry? What are the frequency, duration and levels of exposures to Cr(VI) at each job category in your company or industry? Where commenters are able to provide exposure data, OSHA requests that, where possible, exposure data be personal samples with clear descriptions of the length of the sample and analytical method. Exposure data that provide information concerning the controls in place are more valuable than exposure data without such information. 12. Have there been technological changes within your industry that have influenced the magnitude, frequency, or duration of exposure to Cr(VI) or the means by which employers attempt to control exposures? Describe in detail these technological changes and their effects on Cr(VI) exposures and methods of control. 13. Has there been a trend within your industry to eliminate Cr(VI) from production processes, products and services? If so, comments are requested on the success of substitution efforts. Commenters should estimate the percentage reduction in Cr(VI), and the extent to which Cr(VI) is still necessary in their processes within product lines or production activities. OSHA also requests that commenters describe any technical, economic or other deterrents to substitution. 14. Does any job category or employee in your workplace have exposures to Cr(VI) that raw air monitoring data do not adequately portray due to the short duration, intermittent or non-routine nature, or other unique characteristics of the exposure? Please explain your response and indicate peak levels, duration and frequency of exposures for employees in these job categories. 15. OSHA requests the following information regarding engineering and work practice controls in your workplace or industry: a. Describe the operations in which the proposed PEL is being achieved most of the time by means of engineering and work practice controls. b. What engineering and work practice controls have been implemented in these operations? c. For all operations in facilities where Cr(VI) is used, what engineering and work practice controls have been implemented? If you have installed engineering controls or adopted work practices to reduce exposure to Cr(VI), describe the exposure reduction achieved and the cost of these controls. Where current work practices include the use of regulated areas and hygiene facilities, provide data on the implementation of these controls, including data on the costs of installation, operation, and maintenance associated with these controls. d. Describe additional engineering and work practice controls which could be implemented in each operation where exposure levels are currently above the proposed PEL to further reduce exposure levels. e. When these additional controls are implemented, to what levels can exposure be expected to be reduced, or what per cent reduction is expected to be achieved? f. What are the costs and amount of time needed to develop, install and implement these additional controls? Will the added controls affect productivity? g. Are there any processes or operations for which it is not reasonably possible to implement engineering and work practice controls within two years to achieve the proposed PEL? If so, would allowing additional time for employers to implement engineering and work practice controls make compliance possible? How much additional time would be necessary? 16. OSHA requests information on whether there are any limited or unique conditions or job tasks in Cr(VI) manufacture or use where engineering and work practice controls are not available or are not capable of reducing exposure levels to or below the proposed PEL most of the time. Provide data and evidence to support your response. 17. In its Preliminary Economic Analysis, OSHA presents estimated baseline levels of use of personal protective equipment (PPE) and the incremental costs associated with the proposed standard. Are OSHA's estimated compliance rates reasonable? Are OSHA's estimates of PPE costs, and the assumptions underlying these estimates, consistent with current industry practice? Comments are solicited on OSHA's analysis of PPE costs. 18. In its Preliminary Economic Analysis, OSHA presents estimated baseline levels of communication of Cr(VI)-related hazards and the incremental costs associated with the additional requirements for communication in the proposed standard. OSHA requests information on hazard communication programs addressing Cr(VI) that are currently being implemented by employers and any necessary additions to those programs that are anticipated in response to the proposed standard. Are OSHA's baseline estimates and unit costs for training reasonable and consistent with current industry practice? Effects on Small Entities 19. Will difficulties be encountered by small entities when attempting to comply with requirements of the proposed standard? Can any of the [[Page 59309]] proposal's requirements be deleted or simplified for small entities, while still protecting the health of employees? Would a longer time allowed for compliance for small entities make a difference to their ability to comply, and if so, why? (Information submitted in the SBREFA process is part of the record and need not be resubmitted). Economic Impacts and Economic Feasibility 20. OSHA, in its Preliminary Economic Analysis, has estimated, by application group, compliance costs per affected entity and the likely impacts on revenues and profits under alternative market scenarios. OSHA requests that affected employers provide comment on OSHA's estimate of revenue, profit, and the impacts of costs for their industry or application group. Are there special circumstances--such as unique cost factors, foreign competition, or pricing constraints--that OSHA needs to consider when evaluating economic impacts for particular application groups? Comments are requested on OSHA's analysis of economic feasibility in the PEA. Overlapping and Duplicative Regulations 21. Do any federal regulations duplicate, overlap, or conflict with the proposed Cr(VI) standard? 22. In some facilities, adjustments in ventilation systems to comply with the proposed PEL may require additional time and expense to retest these systems to ensure compliance with EPA requirements or state requirements. OSHA requests information and comment indicating how frequently retesting would be required, and the time and costs involved in such retesting. Environmental Impacts 23. Submit any data, information, or comments pertaining to possible environmental impacts of adopting this proposal, such as the following: a. Any positive or negative environmental effects that could result; b. Any irreversible commitments of natural resources which could be involved; and c. Estimates of the effect of the proposed standard on the levels of Cr(VI) in the environment. In particular, consideration should be given to the potential direct or indirect impacts of the proposal on water and air pollution, energy use, solid waste disposal, or land use. iskysoft toolbox for android apk - Activators Patch. Some small entity representatives noted that OSHA PELs are sometimes used to set ``fence line'' standards for air pollutants. OSHA is unable to find evidence of states formally using this procedure, though some states may use such a procedure informally. Do any states or other air pollution authorities base standards on OSHA PELs? What effects might this have on the environment and on environmental compliance? Provisions of the Standard 24. OSHA's safety and health advisory committees for Construction and Maritime advised the Agency to take into consideration the unique nature of their work environments by either settings separate standards or making accommodations for the differences in work environments in construction and maritime. To account for differences in the workplace environment for these different sectors OSHA has proposed separate standards for general industry, construction, and shipyards. Is this approach appropriate? What other approaches should the Agency consider? Please provide a rationale for your response. 25. OSHA has not proposed to cover agriculture, because the Agency is not aware of significant exposures to Cr(VI) in agriculture. Is this determination correct? 26. OSHA has proposed to regulate exposures to all Cr(VI) compounds. As discussed in the health effects section of this preamble, the Agency has made a preliminary determination that the existing data support coverage of all Cr(VI) compounds in the scope of the proposed standard. Is this an appropriate determination or are there additional data that support the exclusion of certain compounds from the scope of the final standard? If so, describe specifically how these data would support a decision to exclude certain compounds from the scope of the final rule. 27. OSHA has made a preliminary determination to exclude Cr(VI) exposures due to work with portland cement from the scope of the construction standard. OSHA believes that guidance efforts by the Agency may be more suitable for addressing the dermal hazards associated with portland cement use in construction settings. OSHA's Advisory Committee for Construction Safety and Health (ACCSH) advised OSHA to include construction cement work under the proposed standard because of the known hazards associated with wet cement and the large number of workers exposed to wet cement in construction work settings. In particular ACCSH advised OSHA that only certain provisions might be necessary for workers exposed to wet cement (e.g., protective work clothing, hygiene areas and practices, medical surveillance for signs and symptoms of adverse health effects only, communication of hazards and recordkeeping for medical surveillance and training). Other provisions, ACCSH advised, might not be necessary (e.g., permissible exposure levels, exposure assessment, methods of compliance and respiratory protection). Should OSHA expand the scope of the construction proposal to include Cr(VI) exposures from portland cement? If so, what would be the best approach for addressing the dermal hazards from Cr(VI) faced by these workers? If Cr(VI) exposure from portland cement work in construction is included in the final standard, should only certain provisions such as those outlined by ACCSH be considered? 28. OSHA has proposed to include exposure to Cr(VI) from portland cement in the scope of the standard for general industry. The Agency believes that the potential for airborne exposure to Cr(VI) in general industry due to work with portland cement, as indicated by the profile of exposed workers presented in Table IX-2 of this preamble, is higher than in the winzip pro price - Free Activators industry. OSHA acknowledges, however, that the exposure profile indicates that no workers are exposed to Cr(VI) at levels over the proposed action level. Given the low level of airborne exposure among cement workers in general industry, should OSHA exclude exposures to Cr(VI) from portland cement from the scope of the general industry standard? OSHA seeks data to help inform this issue, and solicits comments on particular provisions of the general industry and construction standards that may or may not be appropriate for cement workers. 29. OSHA has proposed to exempt from coverage Cr(VI) exposures occurring in the application of pesticides in general industry (such as the treatment of wood with chromium copper arsenate (CCA)) because pesticide application is regulated by EPA, and section 4(b)(1) of the OSH Act precludes OSHA from regulating where other Federal agencies exercise their statutory authority to do so. OSHA has proposed to cover exposures resulting from use of treated materials. Is this approach appropriate? Are there any instances where EPA-regulated pesticide application occurs in construction or shipyard workplaces? 30. Describe any additional industries, processes, or applications that should be exempted from the Cr(VI) standard and provide detailed reasons for any requested exemption. In [[Page 59310]] particular, are the epidemiologic and experimental studies sufficient to support OSHA's the inclusion of various industries or processes under the scope of the proposed standard? Please provide the rationale and supporting data for your response. 31. Can the proposed Cr(VI) standard for the construction industry be modified in any way to better account for the workplace conditions in that industry, while still providing appropriate protection to Cr(VI)-exposed workers in that industry? Would an alternative approach similar to that used in OSHA's asbestos standard, where the application of specified controls in certain situations would be considered adequate to meet the requirements of the standard, be useful? Is there enough information available to define such technology specifications? 32. Can the proposed Cr(VI) standard for shipyards be modified in any way to better account for the workplace conditions in that industry, while still providing appropriate protection to Cr(VI)- exposed workers in that industry? 33. OSHA has proposed a TWA PEL for Cr(VI) of 1.0 [mu]g/ m3. The Agency has made a preliminary determination that this is the lowest level that is both technologically and economically feasible and is necessary to reduce significant risks of material health impairment from exposure to Cr(VI). Is this PEL appropriate and is it adequately supported by the existing data? If not, what PEL would be more appropriate or would more adequately protect employees from Cr(VI)-associated health risks? Provide evidence to support your response. 34. Should different PELs be established for different Cr(VI) compounds? If so, how should they be established? Where possible, provide specific detail about how different PELs could be established and how the Agency should apply those PELs in instances where workers may be exposed to more than one Cr(VI) compound. 35. OSHA has proposed an action level for Cr(VI) exposure in general industry, but not in construction or shipyards. Is this an appropriate approach? Should OSHA set an action level for exposure to Cr(VI) in construction and shipyards? Should the proposed action level in general industry be retained in the final rule? 36. If an action level is included in the final rule, is the proposed action level for general industry (0.5 [mu]g/m3) the appropriate level for the PEL under consideration? If not, at what level should the action level be set? 37. If an action level is included in the final rule, which provisions should be triggered by exposure above the action level? Indicate the basis for your position and include any supporting information. 38. If no action level is included in the final rule, which provisions should apply to all Cr(VI)-exposed workers? Which provisions should be triggered by the PEL? Are there any other appropriate triggers for the requirements of the standard? 39. Should OSHA set a short-term exposure limit (STEL) or ceiling for exposure to Cr(VI)? If so, please specify the appropriate air concentration and the rationale for its selection. 40. Do you conduct initial air monitoring or do you rely on objective data to determine Cr(VI) exposures? Describe any other approaches you have implemented for assessing an employee's initial exposure to Cr(VI). 41. Describe any follow-up or subsequent exposure assessments that you conduct. How often do you conduct such follow-up or subsequent exposure assessments? Please comment on OSHA's estimate of baseline industry practice and the projected costs for initial and periodic exposure assessment. Are OSHA's estimates consistent with current industry practice? 42. Do shipyard employers presently measure their employees' exposure to Cr(VI)? If not, do they use some alternative method of identifying which employees may be over-exposed to Cr(VI)? 43. OSHA has proposed specific requirements for exposure assessment in general industry, but has not proposed that these requirements apply to construction or shipyard employers. Should requirements for exposure assessment in construction or shipyards be included in the final Cr(VI) standard? Are there any advantages to requiring construction or shipyard employers to measure their employees' exposures to Cr(VI)? If so, would the exposure assessment requirements proposed for general industry be appropriate? Would construction or shipyard employers encounter situations where monitoring would be infeasible if they were required to follow the exposure assessment requirements proposed for employers in general industry? Indicate the basis for your position and include any supporting information. What types of exposure assessment strategies are effective for assessing worker exposures at construction and shipyard worksites? 44. Should requirements for exposure assessment in general industry be included in the final Cr(VI) standard, or would the performance- oriented requirement proposed for construction and shipyards be more appropriate? Indicate the basis for your position and include any supporting information. 45. OSHA has proposed that exposure monitoring in general industry be conducted at least every six months if exposures are above the action level but below the PEL, and at least every three months if exposures are at or above the PEL. Are these proposed frequencies appropriate? If not, what frequency of monitoring would be more appropriate, and why? 46. OSHA has proposed that regulated areas be established in general industry wherever an employee's exposure to airborne concentrations of Cr(VI) is, or can reasonably be expected to be, in excess of the PEL. OSHA seeks comments on this provision and in particular: a. Describe any work settings where establishing regulated areas could be problematic or infeasible. If establishing regulated areas is problematic, what approaches might be used to warn employees in such work settings of high risk areas (i.e., areas where the airborne concentrations of Cr(VI) exceed the PEL?). b. Should OSHA add hazards from eye or skin contact as a trigger for establishing regulated areas? Explain the basis for your position, and include any supporting information. c. Describe any methods currently used that have been found to be effective in establishing regulated areas. 47. OSHA has not proposed requirements for establishment of regulated areas in construction or shipyards. Should requirements for regulated areas for construction or shipyards be included in the final Cr(VI) standard? If so, would the requirements for regulated areas proposed for general industry be appropriate? Are there any particular problems in construction or shipyard settings that make regulated areas problematic or infeasible? If requirements for regulated areas for construction or shipyards are not included in the final Cr(VI) standard, should OSHA include requirements for warning signs or other measures to alert employees of the presence of Cr(VI)? If so, what practical means could be used to determine where and when such labeling would be required? What potential difficulties might be encountered by using such an approach? Indicate the basis for your position and include any supporting information. 48. Under the proposed standard, employers are required to use engineering and work practice controls [[Page 59311]] to reduce and maintain employee exposure to Cr(VI) to or below the PEL unless the employer can demonstrate that employees are not exposed above the PEL for 30 or more days per year, or the employer can demonstrate that such controls are not feasible. Is this approach appropriate for Cr(VI)? Indicate the basis for your position and include any supporting information. 49. In OSHA's Cadmium standard (29 CFR 1010.1027), the Agency established separate engineering control air limits (SECALs) for certain processes in selected industries. SECALs were established where compliance with the PEL by means of engineering and work practice controls was infeasible. For these industries, a SECAL was established at the lowest feasible level that could be achieved by engineering and work practice controls. The PEL was set at a lower level, and could be achieved by any allowable combination of controls. SECALs thus allowed OSHA to establish a lower PEL for cadmium than would otherwise have been possible, given technological feasibility constraints. Should OSHA establish SECALs for Cr(VI) in any industries or processes? If so, in what industries or processes, and at what levels? Provide rationale to support your position. 50. The proposed standard prohibits the use of job rotation for the sole purpose of lowering employee exposures to Cr(VI). Are there any circumstances where this practice should be allowed in order to meet the proposed PEL? 51. OSHA is proposing that employers provide appropriate protective clothing and equipment when a hazard is present or is likely to be present from skin or eye contact with Cr(VI). OSHA would expect an employer to exercise common sense and appropriate expertise to determine if a hazard is present or likely to be present. Is this approach appropriate? Are there other approaches that would be better for characterizing eye and skin contact with Cr(VI)? For example, are there methods to measure dermal exposure that could be used to routinely monitor worker exposure to Cr(VI) that OSHA should consider including in the final standard? 52. For employers whose employees are exposed to Cr(VI), what approaches do you currently use to assess potential hazards from eye or skin contact with Cr(VI)? What protective clothing and equipment do you use to protect employees from eye or skin contact with Cr(VI)? What does this protective clothing and equipment cost? Who pays for the protective clothing and equipment? 53. Should OSHA require the use of protective clothing and equipment for those employees who are exposed to airborne concentrations of Cr(VI) in excess of the PEL? If so, what type of protective clothing and equipment might be necessary? 54. OSHA has proposed to require that employers pay for protective clothing and equipment provided to employees. The Agency seeks comment on this provision, in particular: a. Should OSHA refrain from requiring employer payment, and follow the outcome of the rulemaking addressing employer payment for personal protective equipment (64 FR 15401 (3/31/99))? b. Are there circumstances where employers should not be required to pay for clothing and equipment used to protect employees from Cr(VI) hazards, such as situations where it is customary for employees to provide their own protective clothing and equipment (i.e., ``tools of the trade'')? c. OSHA realizes that there is frequent turnover in the construction industry, where employees frequently move from jobsite to jobsite. This is an important factor because an employer with a high- turnover workplace would have to buy protective clothing and equipment for more employees if the protective clothing and equipment could only be used by one employee. The Agency requests comment on whether this proposal's requirement for employer payment for protective clothing and equipment is appropriate in the construction industry. Are there any alternative approaches that would be responsive to the turnover situation and would also be protective of construction workers? Are there any other issues specific to the construction industry that OSHA should be consider in this rulemaking? d. At some ports, employees are hired for jobs in shipyards, longshoring, and marine terminals through a labor pool, and a single employee may work for five different employers in the same week. How do these factors affect who is required to pay for protective clothing and equipment? Are there any other issues specific to shipyards, longshoring, or marine terminals that OSHA should consider in this rulemaking? 55. OSHA is proposing that washing facilities capable of removing Cr(VI) from the skin be provided to affected employees, but does not propose that showers be required. Should OSHA include requirements to provide showers to employees exposed to Cr(VI)? If so, under what circumstances should showers be required? Describe work situations where showers are either unnecessary for employee protection or that present obstacles to their implementation and describe any such obstacles. 56. OSHA has not included housekeeping provisions in the proposed Cr(VI) standard for construction or shipyards. The Agency has made a preliminary determination that the housekeeping requirements proposed for general industry are likely to be difficult to implement in the construction and shipyard environments. Is this an appropriate determination? If not, what practicable housekeeping measures can construction and shipyard employers take to reduce employee exposure to Cr(VI) at the work site? What housekeeping activities are currently being performed? 57. Is medical surveillance being provided to Cr(VI)-exposed employees at your worksite? If so, a. What exposure levels or other factors trigger medical surveillance? b. What tests or evaluations are included in the medical surveillance program? c. What benefits have been achieved from the medical surveillance program? d. What are the costs of the medical surveillance program? How do your current costs compare with OSHA's estimated unit costs for the physical examination and employee time involved in the medical surveillance program? Please comment on OSHA's baseline assumptions and cost estimates for medical surveillance. e. How many employees are included in your medical surveillance program? f. In what North American Industry Classification System (NAICS) code does your workplace fall? 58. OSHA has proposed that medical surveillance be triggered in general industry in the following circumstances: (1) When exposure to Cr(VI) is above the PEL for 30 days or more per year; (2) after an employee experiences signs or symptoms of the adverse health effects associated with Cr(VI) exposure (e.g., dermatitis, asthma); or (3) after exposure in an emergency. OSHA seeks comments as to whether or not these are appropriate triggers for offering medical surveillance and whether there are additional triggers that should be included. Should OSHA require that medical surveillance be triggered in general industry only upon an employee experiencing signs and symptoms of disease or after exposure in an emergency, as in the construction and maritime standards? OSHA also solicits comment on the optimal frequency of medical surveillance. [[Page 59312]] 59. OSHA has proposed that medical surveillance be triggered in construction and shipyards in the following circumstances: (1) after an employee experiences signs or symptoms of the adverse health effects associated with Cr(VI) exposure (e.g., dermatitis, asthma); or (2) after exposure in an emergency. Should medical surveillance in construction or shipyards be triggered by exposure to Cr(VI) above the PEL for 30 days or more per year, as proposed for general industry? OSHA seeks comments as to whether or not the proposed triggers are appropriate for offering medical surveillance and whether there are additional triggers that should be included. 60. OSHA has not included certain biological tests (e.g., blood or urine monitoring, skin patch testing for sensitization, expiratory flow measurements for airway restriction) as a part of the medical evaluations required to be provided to employees offered medical surveillance under the proposed standard. OSHA has preliminarily determined that the general application of these tests is of uncertain value as an early indicator of potential Cr(VI)-related health effects. However, the proposed standard does allow for the provision of any tests (which could include urine or blood tests) that are deemed necessary by the physician or other licensed health care professional. Are there any tests (e.g., urine tests, blood tests, skin patch tests, airway flow measurements, or others) that should be included under the proposed standard's medical surveillance provisions? If there are any that should be included, explain the rationale for their inclusion, including the benefit to worker health they might provide, their utility and ease of use in an occupational health surveillance program, and associated costs. 61. OSHA has not included requirements for medical removal protection (MRP) in the proposed standard. OSHA has made a preliminary determination that there are few instances where temporary worker removal and MRP will be useful. The Agency seeks comment as to whether the final Cr(VI) standard should include provisions for the temporary removal and extension of MRP benefits to employees with certain Cr(VI)- related health conditions. In particular, what endpoints should be considered for temporary removal and for what maximum amount of time should MRP benefits be extended? OSHA also seeks information on whether or not MRP is currently being used by employers with Cr(VI)-exposed workers, and the costs of such programs. 62. OSHA has proposed that employers provide hazard information to employees in accordance with the Agency's Hazard Communication standard (29 CFR 1910.1200), and has also proposed additional requirements regarding signs, labels, and additional training specific to work with Cr(VI). Should OSHA include these additional requirements in the final rule, or are the requirements of the Hazard Communication standard sufficient? 63. OSHA has proposed that bags or containers of laundry contaminated with Cr(VI) bear warning labels. Will this cause you to alter your current laundry practices? Are there laundries in your area that would accept such laundry? Would laundering costs increase? If so, by how much? 64. OSHA requests comment on the time allowed for compliance with the provisions of the proposed standard. Is the time proposed sufficient, or is a longer or shorter phase-in of requirements appropriate? Identify any industries, processes, or operations that have special needs for additional time, the additional time required and the reasons for the request. 65. Some other OSHA health standards have included appendices that address topics such as the hazards associated with the regulated substance, health screening considerations, occupational disease questionnaires, and PLHCP obligations. OSHA has not proposed to include any appendices with the Cr(VI) rule because the Agency has made a preliminary determination that such topics would be best addressed with guidance materials. What would be the advantage of including such appendices in the final rule? If you believe they should be included, what information should be included? What would be the disadvantage of including these appendices in the final rule? III. Pertinent Legal Authority The purpose of the Occupational Safety and Health Act, 29 U.S.C. 651 et seq. (``the Act'') is to ``assure so far as possible every working man and woman in the nation safe and healthful working conditions and to preserve our human resources.'' 29 U.S.C. 651(b). To achieve this goal Congress authorized the Secretary of Labor to promulgate and enforce occupational safety and health standards. 29 PowerDVD 19.0.1515.62 Keygen - Crack Key For U U.S.C. 655(a)(authorizing summary adoption of existing consensus and federal standards within two years of Act's enactment), 655(b)(authorizing promulgation of standards pursuant to notice and comment), 654(b)(requiring employers to comply with OSHA standards). A safety or health standard is a standard ``which requires conditions or the adoption of or use of one or more practices, means, methods, operations or processes, reasonably necessary or appropriate to provide safe or healthful employment or places of employment 29 U.S.C. 652(8). A standard is reasonably necessary or appropriate within the meaning of Section 652(8) if it substantially reduces or eliminates significant risk, and is economically feasible, technologically feasible, cost effective, consistent with prior Agency action or supported by a reasoned justification for departing from prior Agency actions, supported by substantial evidence, and is better able to effectuate the Act's purpose than any national consensus standard it supersedes. See 58 Fed. Reg. 16612-16616 (March 30, 1993). OSHA has generally considered, at minimum, fatality risk of 1/1000 over a 45-year working lifetime to be a significant health risk. See the Benzene standard, Industrial Union Dep't v. American Petroleum Institute, 448 U.S. 607, 646 ((1980); the Asbestos standard, International Union, UAW v. Pendergrass, 878 F.2d 389, 393 (D.C. Cir. 1989). A standard is technologically feasible if the protective measures it requires already exist, can be brought into existence with available technology, or can be created with technology that can reasonably be expected to be developed. American Textile Mfrs. Institute v. OSHA, 452 U.S. 490, 513 (1981)(``ATMI'') American Iron and Steel Institute v. OSHA, 939 F.2d 975, 980 (D.C. Cir. 1991)(``AISI''). A standard is economically feasible if industry can absorb or pass on the costs of compliance without threatening its long-term profitability or competitive structure. See ATMI, 452 U.S. at 530 n. 55; AISI, 939 F. 2d at 980. A standard is cost effective if the protective measures it requires are the least costly of the available alternatives that achieve the same level of protection. ATMI, 453, U.S, at 514 n. 32; International Union, UAW v. OSHA, 37 F.3d 665, 668 (D.C., Cir 1994)(``LOTO III''). All standards must be highly protective. See 58 FR 16614-16615; LOTO III, 37 F. 3d at 669. However, health standards must also meet the ``feasibility mandate'' of Section 6(b)(7) of the Act, 29 U.S.C. 655(b)(5). Section 6(b)(5) requires OSHA to select ``The most protective standard consistent with feasibility'' that is needed to reduce significant risk when regulating health standards. ATMI, 452 U.S. at 509. [[Page 59313]] Section 6(b)(5) also directs OSHA to base health standard on ``the best available evidence,'' including research, demonstrations, and experiments. 29 U.S.C. 655(b)(5). OSHA shall consider ``in addition to the attainment of the highest degree of health and safety protection * * * feasibility and experience gained under this and other health and safety laws.'' Id. Section 6(b)(7) authorizes OSHA to include among a standard's requirements labeling, monitoring, medical testing and other information gathering and transmittal provisions. 29 U.S.C. 655(b)(7). Finally, whenever practical, standards shall ``be expressed in terms of objective criteria and of the performance Audacity 2.3.2 Keygen - Crack Key For U Id. IV. Events Leading to the Proposed Standards OSHA's present standards for workplace exposure to Cr(VI) were adopted in 1971, pursuant to section 6(a) of the OSH Act, from a 1943 American National Standards Institute (ANSI) recommendation originally established to control irritation and damage to nasal tissues (Ex. 20- 3). OSHA's general industry standard set a permissible exposure limit (PEL) of 1 mg chromium trioxide per 10 m3 air in the workplace (1 mg/10 m3 CrO3) as a ceiling concentration, which corresponds to a concentration of 52 [mu]g/ m3 Cr(VI). A separate rule promulgated for the construction industry set an eight-hour time-weighted-average PEL of 1 mg/10 m3 CrO3, also equivalent to 52 [mu]g/ m3 Cr(VI), adopted from the American Conference of Governmental Industrial Hygienists (ACGIH) 1970 Threshold Limit Value (TLV) (36 FR 7340 (4/17/71)). Following the ANSI standard of 1943, other occupational and public health organizations evaluated Cr(VI) as a workplace and environmental hazard and formulated recommendations to control exposure. The ACGIH first recommended control of workplace exposures to chromium in 1946, recommending a time-weighted average Maximum Allowable Concentration (later called a Threshold Limit Value) of 100 [mu]g/m3 for chromic acid and chromates as Cr2O3 (Ex. 5-37), and classified certain Cr(VI) compounds as class A1 (confirmed human) carcinogens in 1974. In 1975, the NIOSH Criteria for a Recommended Standard recommended that occupational exposure to Cr(VI) compounds should be limited to a 10-hour TWA of 1 [mu]g/m3, except for some forms of Cr(VI) then believed to be noncarcinogenic (Ex. 3-92). The National Toxicology Program's First Annual Report on Carcinogens identified calcium chromate, chromium chromate, strontium chromate, and zinc chromate as carcinogens in 1980 (Ex. 35-157). During the 1980s, regulatory and standards organizations came to recognize Cr(VI) compounds in general as carcinogens. The Environmental Protection Agency (EPA) Health Assessment Document of 1984 stated that ``using the IARC [International Agency for Research on Cancer] classification scheme, the level of evidence available for the combined animal and human data would place hexavalent chromium Cr(VI) compounds into Group 1, meaning that there is decisive evidence for the carcinogenicity of those compounds in humans'' (Ex. 19-1, p. 7-107). In 1988 IARC evaluated the available evidence regarding Cr(VI) carcinogenicity, concluding in 1990 that ``There is sufficient evidence in humans for the carcinogenicity of chromium[VI] compounds as encountered in the chromate production, chromate pigment production and chromium plating industries'', and ``sufficient evidence in experimental animals for the carcinogenicity of calcium chromate, zinc chromates, strontium chromate and lead chromates'(Ex. 18-3, p. 213). In September 1988, NIOSH advised OSHA to consider all Cr(VI) compounds as potential occupational carcinogens (Ex. 31-22-22, p. 8). ACGIH now classifies water-insoluble and water-soluble Cr(IV) compounds as class A1 carcinogens (Ex. 35-207). Current ACGIH standards include specific 8-hour time-weighted average TLVs for calcium chromate (1 [mu]g/ m3), lead chromate (12 [mu]g/m3), strontium chromate (0.5 [mu]g/m3), and zinc chromates (10 [mu]g/ m3), and generic TLVs for water soluble (50 [mu]g/ m3) and insoluble (10 [mu]g/m3) forms of hexavalent chromium not otherwise classified, all measured as chromium (Ex. 35-207). In July 1993, OSHA was petitioned for an emergency temporary standard to reduce occupational exposures to Cr(VI) compounds (Ex. 1). The Oil, Chemical, and Atomic Workers International Union (OCAW) and Public Citizen's Health Research Group (HRG), citing evidence that occupational exposure to Cr(VI) increases workers' risk of lung cancer, petitioned OSHA to promulgate an emergency temporary standard to lower the PEL for Cr(VI) compounds to 0.5 [mu]g/m3 as an eight- hour, time-weighted average (TWA). Upon review of the petition, OSHA agreed that there was evidence of increased cancer risk from exposure to Cr(VI) at the existing PEL, but found that the available data did not show the ``grave danger'' required to support an emergency temporary standard (Ex. 1-C). The Agency therefore denied the request for an emergency temporary standard, but initiated section 6(b)(5) rulemaking and began performing preliminary analyses relevant to the rule. In 1997, OSHA was sued by HRG for unreasonable delay in issuing a Cr(VI) standard. The U.S. Court of Appeals for the Third Court ruled in OSHA's favor and the Agency continued its data collection and analytic efforts on Cr(VI) (Ex. 35-208, p. 3). OSHA was sued again in 2002 by HRG for continued unreasonable delay in issuing a Cr(VI) standard (Ex. 31-24-1). In August 2002, OSHA published a Request for Information on Cr(VI) to solicit additional information on key issues related to controlling exposures to Cr(VI)(67 FR 54389 (8/22/02)), and on December 4, 2002 announced its intent to proceed with developing a proposed standard (Ex. 307). The Court ruled in favor of HRG on December 24, 2002, ordering the Agency to proceed expeditiously with a Cr(VI) standard (Ex. 35-208). On April 2, 2003 the Court set deadlines of October 4, 2004 for publication of a proposed standard and January 18, 2006 for publication of a final standard (Ex. 35-306). OSHA initiated Small Business Regulatory Enforcement Act (SBREFA) proceedings in 2003, seeking the advice of small business representatives on the proposed rule. The SBREFA panel, including representatives from OSHA, the Small Business Administration (SBA), and the Office of Management and Budget (OMB), was convened on December 23, 2003. The panel conferred with representatives from small entities in chemical, alloy, and pigment manufacturing, electroplating, welding, aerospace, concrete, shipbuilding, masonry, and construction on March 16-17, 2004, and delivered its final report to OSHA on April 20, 2004. The Panel's report, including comments from the small entity representatives (SERS) and recommendations to OSHA for the proposed rule, is available in the Cr(VI) rulemaking docket (Ex. 34). OSHA provided the Advisory Committee on Construction Safety and Health (ACCSH) and the Maritime Advisory Committee on Occupational Safety and Health (MACOSH) with copies of the draft proposed rule for review in early 2004. OSHA representatives met with ACCSH in February 2004 and May 2004 to discuss the rulemaking and receive their comments and recommendations. On February 13, ACCSH recommended that portland cement should be included [[Page 59314]] within the scope of the proposed standard (Ex. 35-308, pp. 288-293) and that identical PELs should be set for the construction, maritime, and general industries (Ex. 35-308, pp. 293-297). The Committee recommended on May 18 that the construction industry should be included in the current rulemaking, and affirmed its earlier recommendation regarding portland cement. OSHA representatives met with MACOSH in March 2004. On March 3, MACOSH decided to collect and forward additional exposure monitoring data to OSHA to help the Agency better evaluate exposures to Cr(VI) in shipyards (Ex. 310, p. 208). MACOSH also recommended a separate Cr(VI) standard for the maritime industry, arguing that maritime involves different exposures and requires different means of exposure control than general industry and construction (Ex. 310, p. 227). V. Chemical Properties and Industrial Uses Chromium is a metal that exists in several oxidation or valence states, ranging from chromium (-II) to chromium (+VI). The elemental valence state, chromium (0), does not occur in nature. Chromium compounds are very stable in the trivalent state and occur naturally in this state in ores such as ferrochromite, or chromite ore (FeCr2O4). The hexavalent, Cr(VI) or chromate, is the second most stable state. It rarely occurs naturally; most Cr(VI) compounds are man made. Chromium compounds in higher valence states are able to undergo ``reduction'' to lower valence states; chromium compounds in lower valence states are able to undergo ``oxidation'' to higher valence states. Thus, Cr(VI) compounds can be reduced to Cr(III) in the presence of oxidizable organic matter. Chromium can also be reduced in the presence of inorganic chemicals such as iron. Chromium does exist in less stable oxidation (valence) states such as Cr(II), Cr(IV), and Cr(V). Anhydrous Cr(II) salts are relatively stable, but the divalent state (II, or chromous) is generally relatively unstable and is readily oxidized to the trivalent (III or chromic) state. Compounds in valence states such as (IV) and (V) usually require special handling procedures as a result of their instability. Cr(IV) oxide (CrO2) is used in magnetic recording and storage devices, but very few other Cr(IV) compounds have industrial use. Evidence exists that both Cr(IV) and Cr(V) are formed as transient intermediates in the reduction of Cr(VI) to Cr(III) in the body. Chromium (III) is also an essential nutrient that plays a role in glucose, fat, and protein metabolism by causing the action of insulin to be more effective. Chromium picolinate, a trivalent form of chromium combined with picolinic acid, is used as a dietary supplement, because it is claimed to speed metabolism. Elemental chromium and the chromium compounds in their different valence states have various physical and chemical properties, including differing solubilities. Most chromium species are solid. Elemental chromium is a steel gray solid, with high melting and boiling points (1857 [deg]C and 2672 [deg]C, respectively), and is insoluble in water and common organic solvents. Chromium (III) chloride is a violet or purple solid, with high melting and sublimation points (1150 [deg]C and 1300 [deg]C, respectively), and is slightly soluble in hot water and insoluble in common organic solvents. Ferrochromite is a brown-black solid; chromium (III) oxide is a green solid; and chromium (III) sulfate is a violet or red solid, insoluble in water and slightly soluble in ethanol. Chromium (III) picolinate is a ruby red crystal soluble in water (1 part per million at 25 [deg]C). Chromium (IV) oxide is a brown-black solid that decomposes at 300 [deg]C and is insoluble in water. Cr(VI) compounds have mostly lemon yellow to orange to dark red hues. They are typically crystalline, granular, or powdery although one compound (chromyl chloride) exists in liquid form. They range from very soluble to insoluble in water. For example, chromyl chloride is a dark red liquid that decomposes into chromate ion and hydrochloric acid in water. Chromic acids are dark red crystals that are very soluble in water. Other examples of soluble chromates are potassium chromate (lemon yellow crystals), sodium chromate (yellow crystals), and sodium dichromate (reddish to bright orange crystals). Nickel chromate, lead chromate oxide, and zinc chromate are completely insoluble in water. The nickel chromate (black crystals) dissolves in nitric acid and hydrogen peroxide. Lead chromate oxide is a red crystalline powder. The zinc chromate (lemon yellow crystals) decomposes in hot water and is soluble in acids and liquid ammonia. Examples of slightly soluble Cr(VI) compounds are barium (light yellow), calcium (yellow), lead (yellow to orange-yellow), and strontium (yellow) chromates, and zinc chromate hydroxide (yellow). They all exist in solid form as crystals or powder. Potassium zinc chromate hydroxide (greenish-yellow crystals) is also slightly soluble in water. Some major users of chromium are the metallurgical, refractory, and chemical industries. Chromium is used by the metallurgical industry to produce stainless steel, alloy steel, and nonferrous alloys. Chromium is alloyed with other metals and plated on metal and plastic substrates to improve corrosion resistance and provide protective coatings for automotive and equipment accessories. Welders use stainless steel welding rods when joining metal parts. Cr(VI) compounds are widely used in the chemical industry in pigments, metal plating, and chemical synthesis as ingredients and catalysts. Chromates are used as high quality pigments for textile dyes, paints, inks, glass, and plastics. Cr(VI) can be produced during welding operations even if the chromium was originally present in another valence state. While Cr(VI) is not intentionally added to portland cement, it is often present as an impurity. Occupational exposures to Cr(VI) can occur from inhalation of mists (e.g., chrome plating, painting), dusts (e.g., inorganic pigments), or fumes (e.g., stainless steel welding), and from dermal contact (cement workers). There are about thirty major industries and processes where Cr(VI) is used. These include producers of chromates and related chemicals from chromite ore, electroplating, welding, painting, chromate pigment production and use, steel mills, and iron and steel foundries. A detailed discussion of the uses of Cr(VI) in industry is found in Section IX of this preamble. VI. Health Effects iSkysoft DVD Creator Free Download The Format Factory 4.6.2.0 License Key - Crack Key For U of adverse health effects resulting from exposure to hexavalent chromium (Cr(VI)) in humans and experimental animals are summarized in the section below. Section VI includes information on the fate of Cr(VI) in the body and laboratory research that relates to its toxic mode of action. The primary health impairments from workplace exposure to Cr(VI) are lung cancer, asthma, and damage to the nasal epithelia and skin. This chapter on health effects will not attempt to describe every study ever conducted on Cr(VI) toxicity. Instead, only the most important articles and reviews of studies will be evaluated. A. Absorption, Distribution, Metabolic Reduction and Elimination Chromium can exist in a number of valence states from -2 to +6 valence. The most common forms are the elemental metal Cr(0), trivalent Cr(III), and hexavalent Cr(VI). Chromium exists naturally in the environment in [[Page 59315]] chromite ore as Cr(III). Cr(0) and Cr(VI), as well as Cr(III) are produced during industrial processes. Cr(VI) is the form considered to be the greatest health risk. A small amount of Cr(III) is needed for optimal insulin receptor function in human tissues but much larger amounts may be harmful. Much less is known about the toxicity of Cr(0), but it is believed to be converted to Cr(III) in the body and is not considered to be a serious health risk. Cr(VI) enters the body by inhalation, ingestion, or absorption through the skin. For occupational exposure, the airways and skin are the primary routes of uptake. 1. Deposition and Clearance of Inhaled Cr(VI) From the Respiratory Tract Various anatomical, physical and physiological factors determine both the fractional and regional deposition of inhaled particulate matter. Due to the airflow patterns in the lung more particles tend to deposit at certain preferred regions in the lung. Schlesinger and Lippman have shown a high degree of correlation between sites of greatest particle deposition in the tracheobronchial airways and increased incidence of bronchial tumors (Ex. 35-102). It is possible to have a buildup of chromium at certain sites in the bronchial tree that could create areas of very high chromium concentration. This would especially be true for occupational environments that are particularly dusty or contain other irritating aerosols. Large inhaled particles (>5 [mu]m) are efficiently removed from the air-stream in the extrathoracic region (Ex. 35-175). Particles greater than 2.5 [mu]m are generally deposited in the tracheobronchial regions, whereas particles less than 2.5 [mu]m are generally deposited in the pulmonary region. Some larger particles (>2.5 [mu]m) can reach the pulmonary region. The mucociliary escalator predominantly clears particles that deposit in the extrathoracic and the tracheobronchial region of the lung. Individuals exposed to high particulate levels of Cr(VI) may also have altered respiratory mucociliary clearance. Particulates that reach the alveoli can be absorbed into the bloodstream cleared by phagocytosis. 2. Absorption of Inhaled Cr(VI) Into the Bloodstream The absorption of inhaled chromium compounds depends on a number of factors, including physical and chemical properties of the particles (oxidation state, size, solubility) and the activity of alveolar macrophages (Ex. 35-41). The hexavalent chromate anion (CrO4)2-enter cells via facilitated diffusion through non-specific anion channels (similar to phosphate and sulfate anions). Suzuki et al. have demonstrated that Cr(VI) is rapidly and extensively transported to the bloodstream in rats (Ex. 35-97). They exposed rats to 7.3-15.9 mg Cr(VI)/m3 as potassium dichromate for 2-6 hours. Following exposure to Cr(VI), the ratio of blood chromium/lung chromium was 1.440.30 at 0.5 hours, 0.810.10 at 18 hours, 0.850.20 at 48 hours, and 0.960.22 at 168 hours after exposure. Once the Cr(VI) particles reach the alveoli, absorption into the bloodstream is greatly dependent on solubility. Bragt and van Dura demonstrated that more soluble chromates are absorbed faster than less soluble chromates (Ex. 35-56). Insoluble chromates are poorly absorbed and therefore have longer resident time in the lungs. They studied the kinetics of three Cr(VI) compounds: Sodium chromate, zinc chromate and lead chromate. They instilled 51chromium-labeled compounds (0.38 mg Cr(VI)/kg as sodium chromate, 0.36 mg Cr(VI)/kg as zinc chromate, or 0.21 mg Cr(VI)/kg as lead chromate) intratracheally in rats. Peak blood levels of 51chromium were reached after 30 minutes for sodium chromate (0.35 [mu]g chromium/ml), and after 24 hours for zinc chromate (0.60 [mu]g chromium/ml) and lead chromate (0.007 [mu]g chromium/ml). At 30 minutes after administration, the lungs contained 36, 25, and 81% of the respective dose of the sodium, zinc, and lead chromate. On day six, >80% of the dose of all three compounds had been cleared from the lungs, during which time the disappearance from lungs followed linear first-order kinetics. The residual amount left in the lungs on day 50 or 51 was 3.0, 3.9, and 13.9%, respectively. From these results authors concluded that zinc chromate, which is less soluble than sodium chromate, is more slowly absorbed from the lungs. Lead chromate was more poorly and slowly absorbed, as indicated by very low levels in blood and greater retention in the lungs. The authors also noted that the kinetics of sodium and zinc chromates were very similar. Zinc chromate, which is less soluble than sodium chromate, was slowly absorbed from the lung, but the maximal blood levels were higher than those resulting from an equivalent dose of sodium chromate. The authors believe that this was probably due to irritative properties of the zinc chromate used, as it caused hemorrhages in the lungs which were macroscopically visible as early as 24 hours after intratracheal administration. The studies by Langard et al. and Adachi et al. provide further evidence of absorption of chromates from the lungs (Exs. 35-93; 189). Rats exposed to 2.1 mg Cr(VI)/m3 as zinc chromate for 6 hours/day achieved steady state concentrations in the blood after 4 days of exposure (Ex. 35-93). Adachi et al. studied rats that were subject to a single inhalation exposure to chromic acid mist generated from electroplating at a concentration of 3.18 mg Cr(VI)/m3 for 30 minutes which was then rapidly absorbed from the lungs (Ex. 189). The amount of chromium in the lungs of these rats declined from 13.0 mg immediately after exposure to 1.1 mg after 4 weeks, with an overall half-life of five days. Several other studies have reported absorption of chromium from the lungs after intratracheal instillation (Exs. 7-9; 9-81; Visek et al. 1953 as cited in Ex. 35-41). These studies indicated that 53-85% of Cr(VI) compounds (particle size < 5 [mu]m) were cleared from the lungs by absorption into the bloodstream or by mucociliary clearance in the pharynx; the rest remained in the lungs. Absorption of Cr(VI) from the respiratory tract of workers has been shown in several studies that identified chromium in the urine, serum and red blood cells following occupational exposure (Exs. 5-12; 35-294; 35-84). Evidence indicates that even chromates that are encapsulated in a paint matrix may be released in the lungs (Ex. 31-15, p. 2). LaPuma et al. measured the mass of Cr(VI) released from particles into water originating from three types of paint particles: solvent-borne expoxy (25% strontium chromate (SrCrO4)), water-borne expoxy (30% SrCrO4) and polyurethane (20% SrCrO4) (Ex. 31-2- 1). The mean fraction of Cr(VI) released into the water after one and 24 hours for each primer averaged: 70% and 85% (solvent epoxy), 74% and 84% (water epoxy), and 94% and 95% (polyurethane). Correlations between particle size and the fraction of Cr(VI) released indicated that smaller particles (< 5 m) release a larger fraction of Cr(VI) versus larger particles (>5 [mu]m). This study demonstrates that the paint matrix only modestly hinders Cr(VI) release into a fluid, especially with smaller particles. Larger particles, which contain the majority of Cr(VI) due to their size, appear to release proportionally less Cr(VI) (as a percent of total Cr(VI)) than smaller particles. A number of questions remain unanswered regarding encapsulated Cr(VI) and bioavailability from the lung. There is a lack of detailed information on the encapsulation process. The efficiency of encapsulation and whether all of the chromate molecules are [[Page 59316]] encapsulated is not Format Factory 4.6.2.0 License Key - Crack Key For U. The stability of the encapsulated product in physiological and environmental conditions has not been demonstrated. It would be useful to know if any processes can break the encapsulation during its use. Finally, the fate of inhaled encapsulated and unencapsulated Cr(VI) in the respiratory tract as well as the systemic tissues needs to be more thoroughly studied. 3. Dermal Absorption of Cr(VI) Both human and animal studies demonstrate that Cr(VI) compounds are absorbed after dermal exposure. Dermal absorption depends on the oxidation state of chromium, the vehicle and the integrity of the skin. Cr(VI) readily traverses the epidermis to the dermis (Exs. 9-49; 309). The histological distribution of Cr(VI) within intact human skin was studied by Liden and Lundberg (Ex. 35-80). They applied test solutions of potassium dichromate in petrolatum or in water as occluded circular patches of filter paper to the skin. Results with potassium dichromate in water revealed that Cr(VI) penetrated beyond the dermis and penetration reached steady state with resorption by the lymph and blood vessels by 5 hours. About 10 times more chromium penetrated when potassium dichromate was applied in petrolatum than when applied in water, indicating that organic solvents facilitate the absorption of Cr(VI) from the skin. Baranowska-Dutkiewicz also demonstrated that the absorption rates of sodium chromate solutions from the occluded forearm skin of volunteers increase with increasing concentration (Ex. 35-75). The rates were 1.1 [mu]g Cr(VI)/cm2/hour for a 0.01 molar solution, 6.4 [mu]g Cr(VI)/cm2/hour for a 0.1 molar solution, and 10 [mu]g Cr(VI)/cm2/hour for a 0.2 molar solution. Using volunteers, Mali found that potassium dichromate penetrates the intact epidermis (Exs. 9-49; 35-41). Wahlberg and Skog demonstrated the presence of chromium in the blood, spleen, bone marrow, lymph glands, urine and kidneys of guinea pigs exposed to 51 chromium labeled Cr(VI) compounds (Ex. 35-81). In this study radiolabeled sodium chromate solution was dermally applied to guinea pigs and 51Cr was monitored by scintillation counting in tissues. These studies demonstrate that the absorption of Cr(VI) compounds can take place through the dermal route. Also, the absorption of Cr(VI) can be facilitated by organic solvents. 4. Absorption of Cr(VI) by the Oral Route Inhaled Cr(VI) can enter the digestive tract as a result of mucocilliary clearance and swallowing. Studies indicate Cr(VI) is absorbed from the gastrointestinal tract. The six-day fecal and 24-hour urinary excretion patterns of radioactivity in groups of six volunteers given Cr(VI) as sodium chromate labeled with 51chromium indicated that at least 2.1% of the Cr(VI) was absorbed. After intraduodenal administration at least 10% of the Cr(VI) compound was absorbed. These studies also demonstrated that Cr(VI) compounds are reduced to Cr(III) compounds in the stomach, thereby accounting for the relatively poor gastrointestinal absorption of orally administered Cr(VI) compounds (Exs. 35-96; 35-41). In the gastrointestinal tract, Cr(VI) can be reduced to Cr(III) by gastric juices, which is then poorly absorbed (Underwood, 1971 as cited in Ex. 19-1; Ex. 35-85). The mechanism by which Cr(VI) is carried across the intestinal wall and the site of absorption are not known and may well depend upon the efficiency of defense mechanisms (Mertz, 1969 as cited in Ex. 19-1). Kuykendall et al. studied the absorption of Cr(VI) in human volunteers after oral administration of potassium dichromate (Ex. 35- 77). They reported the bioavailability based on 14-day urinary excretion to be 6.9% (range 1.2-18%) for Cr(VI). Other investigators have also reported absorption of Cr(VI) compounds after oral administration (Exs. 35-76; 31-22-13; 35-91). Studies with 51chromium in animals also indicate that chromium and its compounds are poorly absorbed from the gastrointestinal tract after oral exposure. When radioactive sodium chromate (Cr(VI)) was given Nero Burning ROM 23.5.1010 Crack Product Key Free Download 2021 to rats, the amount of chromium in the feces was greater than that found when sodium chromate was injected directly into the small intestine. These results are consistent with evidence that the gastric environment has a capacity to reduce Cr(VI) to Cr(III) and therefore decrease the amount of Cr(VI) absorbed from the GI tract. Treatment of rats by gavage with an unencapsulated lead chromate pigment or with a silica-encapsulated lead chromate pigment resulted in no measurable blood levels of chromium (measured as Cr(III), detection limit=10 [mu]g/L) after two or four weeks of treatment or after a two- week recovery period. However, kidney levels of chromium (measured as Cr(III)) were significantly higher in the rats that received the unencapsulated pigment when compared to the rats that received the encapsulated pigment, indicating that silica encapsulation may reduce the gastrointestinal bioavailability of chromium from lead chromate pigments (Ex. 11-5). This study does not address the bioavailability of encapsulated chromate pigments from the lung where residence time could be different. 5. Distribution of Cr(VI) in the Body Once in the bloodstream, Cr(VI) is taken up into erythrocytes, where it is reduced to lower oxidation states and forms chromium protein complexes during reduction (Ex. 35-41). Once complexed with protein, chromium cannot leave the cell. The binding of chromium compounds by proteins in the blood has been studied in some detail (Exs. 5-24; 35-41; 35-52). It was found that intravenously injected anionic Cr(VI) passes through the membrane of red blood cells and binds to the globin fraction of hemoglobin. It has been hypothesized that before Cr(VI) is bound by hemoglobin, it is reduced to Cr(III) by an enzymatic reaction within red blood cells. Once inside the blood cell, chromium ions are unable to repenetrate the membrane and move back into the plasma (Exs. 7-6; 7-7; 19-1; 35-41; 35-52). According to Aaseth et al., the intracellular Cr(VI) reduction depletes Cr(VI) concentration in the red blood cell (Ex. 35-89). This serves to enhance diffusion of Cr(VI) from the plasma into the erythrocyte resulting in very low plasma levels of Cr(VI). It is also believed that the rate of uptake of Cr(VI) by red blood cells may not exceed the rate at which they reduce Cr(VI) to Cr(III) (Ex. 35-99). The higher tissue levels of chromium after administration of Cr(VI) than after administration of Cr(III) reflect the greater tendency of Cr(VI) to traverse plasma membranes and bind to intracellular proteins in the various tissues, which may explain the greater degree of toxicity associated with Cr(VI) (MacKenzie et al. 1958 as cited in 35-52; Maruyama 1982 as cited in 35- 41; Ex. 35-71). Examination of autopsy tissues from chromate workers who were occupationally exposed to Cr(VI) showed that the highest chromium levels were in the lungs. The liver, bladder, and bone also had chromium levels above background. Mancuso examined tissues from three individuals with lung cancer who were exposed to chromium in the workplace (Ex. 124). One was employed for 15 years as a welder, the second and third worked for 10.2 years and 31.8 years, respectively, in ore milling and preparations and boiler operations. The cumulative [[Page 59317]] chromium exposures for the three workers were estimated to be 3.45, 4.59, and 11.38 mg/m \3\-years, respectively. Tissues from the first worker were analyzed 3.5 years after last exposure, the second worker 18 years after last exposure, and the third worker 0.6 years after last exposure. All tissues from the three workers had elevated levels of chromium, with the possible exception of neural tissues. Levels were orders of magnitude higher in the lungs when compared to other tissues. The highest lung level reported was 456 mg/10 g tissue in the first worker, 178 in the second worker, and 1,920 for the third worker. There were significant chromium levels in the tissue of the second worker even though he had not been exposed to chromium for 18 years. Similar results were also reported in autopsy studies of people who may have been exposed to chromium in the workplace as well as chrome platers and chromate refining workers (Exs. 35-92; 21-1; 35-74; 35-88). Animal studies have shown similar distribution patterns after inhalation exposure. The distribution of Cr(VI) compared with Cr(III) was investigated in guinea pigs after intratracheal instillation of potassium dichromate or chromium trichloride (Ex. 7-8). At 24 hours after instillation, 11% of the original dose of chromium from potassium dichromate remained in the lungs, 8% in the erythrocytes, 1% in plasma, 3% in the kidney, and 4% in the liver. The muscle, skin, and adrenal glands contained only a trace. All tissue concentrations of chromium declined to low or nondetectable levels in 140 days, with the exception of the lungs and spleen. After chromium trichloride instillation, 69% of the dose remained in the lungs at 20 minutes, while only 4% was found in the blood and other tissues, with the remaining 27% cleared from the lungs and swallowed. The only tissue that contained a significant amount of chromium two days after instillation of chromium trichloride was the spleen. After 30 and 60 days, 30 and 12%, respectively, of the Cr(III) was retained in the lungs, while only 2.6 and 1.6%, respectively, of the Cr(VI) dose was retained in the lungs. 6. Metabolic Reduction of Cr(VI) Cr(VI) is reduced to Cr(III) in the lungs by a variety of reducing agents. This serves to limit uptake into lung cells and absorption into the bloodstream. Cr(V) and Cr(IV) are transient intermediates in this process. The genotoxic effects produced by the Cr(VI) are related to the reduction process and are further discussed in the section on Mechanistic Considerations. In vivo and in vitro experiments in rats indicated that, in the lungs, Cr(VI) can be reduced to Cr(III) by ascorbate and glutathione. The reduction of Cr(VI) by glutathione is slower than the reduction by ascorbate (Ex. 35-65). Other studies have reported the reduction of Cr(VI) to Cr(III) by epithelial lining fluid (ELF) obtained from the lungs of 15 individuals by bronchial lavage. The average overall reduction capacity was 0.6 [mu]g Cr(VI)/mg of ELF protein. In addition, cell extracts made from pulmonary alveolar macrophages derived from five healthy male volunteers were able to reduce an average of 4.8 [mu]g Cr(VI)/10 \6\ cells or 14.4 [mu]g Cr(VI)/mg protein (Ex. 35-83). Postmitochondrial (S12) preparations of human lung cells (peripheral lung parenchyma and bronchial preparations) were also able to reduce Cr(VI) to Cr(III) (De Flora et al. 1984 as cited in Ex. 35-41). As discussed earlier, Cr(VI) is also reduced to Cr(III) in the gastric environment by the gastric juice (Ex. 35-85) and ascorbate after oral exposure (Ex. 35-82). 7. Elimination of Cr(VI) From the Body Excretion of chromium from Cr(VI) compounds is predominantly in the urine, although there is some biliary excretion into the feces. In both urine and feces, the chromium is present as low molecular weight Cr(III) complexes. Absorbed chromium is excreted from the body in a rapid phase representing clearance from the blood and at least two slower phases representing clearance from tissues. Urinary excretion accounts for over 50% of eliminated chromium (Ex. 35-41). Although chromium is excreted in urine and feces, the intestine plays only a minor part in chromium elimination, representing only about 5% of elimination from the blood (Ex. 19-1). Normal urinary levels of chromium in humans have been reported to range from 0.24-1.8 [mu]g/L with a median level of 0.4 [mu]g/L (Ex. 35-79). Humans exposed to 0.05- 1.7 mg Cr(III)/m \3\ as chromium sulfate and 0.01-0.1 mg Cr(VI)/m \3\ as potassium dichromate (8-hour time-weighted average) had urinary excretion levels from 0.0247 to 0.037 mg Cr(III)/L. Workers exposed mainly to Cr(VI) compounds had higher urinary chromium levels than workers exposed primarily to Cr(III) compounds. An analysis of the urine did not detect Cr(VI), indicating that Cr(VI) was rapidly reduced before excretion (Exs. 35-294; 5-48). A half-life of 15-41 hours has been estimated for chromium in urine for four welders using a linear one-compartment kinetic model (Exs. 35- 73; 5-52; 5-53). Limited work on modeling the absorption and deposition of chromium indicates that adipose and muscle tissue retain chromium at a moderate level for about two weeks, while the liver and spleen store chromium for up to 12 months. The estimated half-life for whole body chromium retention is 22 days for Cr(VI) and 92 days for Cr(III) (Ex. 19-1). The half-life of chromium in the human lung is 616 days, which is similar to the half-life in rats (Ex. 7-5). Elimination of chromium was shown to be very slow in rats exposed to 2.1 mg Cr(VI)/m \3\ as zinc chromate six hours/day for four days. Urinary levels of chromium remained almost constant for four days after exposure and then decreased (Ex. 35-93). After intratracheal administration of sodium dichromate to rats, peak urinary chromium concentrations were observed at six hours, after which the urinary concentrations declined rapidly (Ex. 35-94). The more prolonged elimination of the less soluble zinc chromate as compared to the more soluble sodium dichromate is consistent with the influence of Cr(VI) solubility on absorption from the respiratory tract discussed earlier. Information regarding the excretion of chromium in humans after dermal exposure to chromium or its compounds is limited. Fourteen days after application of a salve containing potassium chromate, which resulted in skin necrosis and sloughing at the application site, chromium was found at 8 mg/L in the urine and 0.61 mg/100 g in the feces of one individual (Brieger 1920 as cited in Ex. 19-1). A slight increase over background levels of urinary chromium was observed in four subjects submersed in a tub of chlorinated water containing 22 mg Cr(VI)/L as potassium dichromate for three hours (Ex. 31-22-6). For three of the four subjects, the increase in urinary chromium excretion was less than 1 [mu]g/day over the five-day collection period. Chromium was detected in the urine of guinea pigs after radiolabeled sodium chromate solution was applied to the skin (Ex. 35-81). 8. Physiologically-based Pharmacokinetic Modeling O'Flaherty developed physiologically-based pharmacokinetic (PBPK) models that simulate absorption, distribution, metabolism, and excretion of Cr(VI) and Cr(III) compounds in humans (Ex. 35-95) and rats (Exs. 35-86; 35-70). The original model (Ex. 35-86) evolved from a similar model for lead, and contained compartments for the lung, GI tract, skin, blood, liver, kidney, bone, well- [[Page 59318]] perfused tissues, and slowly perfused tissues. The model was refined to include two lung subcompartments for chromium, one of which allowed inhaled chromium to enter the blood and GI tract and the other only allowed chromium to enter the GI tract (Ex. 35-70). Reduction of Cr(VI) to Cr(III) was considered to occur in every tissue compartment except bone. The model was developed from several data sets in which rats were dosed with Cr(VI) or Cr(III) intravenously, orally or by intratracheal instillation, because different distribution and Format Factory 4.6.2.0 License Key - Crack Key For U patterns occur depending on the route of administration. In most cases, the model parameters (e.g., tissue partitioning, absorption, reduction rates) were estimated by fitting model simulations to experimental data. The optimized rat model was validated against the 1978 Langard inhalation study (Ex. 35-93). Chromium blood levels were overpredicted during the four-day inhalation exposure period, but blood levels during the post-exposure period were well predicted by the model. The model- predicted levels of liver chromium were high, but other tissue levels were closely estimated. A human PBPK model recently developed by O'Flaherty et al. is able to predict tissue levels from ingestion of Cr(VI) (Ex. 35-95). The model incorporates differential oral absorption of Cr(VI) and Cr(III), rapid reduction of Cr(VI) to Cr(III) in major body fluids and tissues, and concentration-dependent urinary clearance. The model does not include a physiologic lung compartment, but can be used to estimate an upper limit on pulmonary absorption of inhaled chromium. The model was calibrated against blood and urine chromium concentration data from a group of controlled studies in which adult human volunteers drank solutions of soluble Cr(III) or Cr(VI). PBPK models are increasingly used in risk assessments, primarily to predict the concentration of a potentially toxic chemical that will be delivered to any given target tissue following various combinations of route, dose level, and test species. Further development of the respiratory tract portion of the model, specific Cr(VI) rate data on extracellular reduction and uptake into lung cells, and more precise understanding of critical pathways inside target cells would improve the model value for risk assessment purposes. 9. Summary Based on the studies presented above, evidence exists in the literature that shows Cr(VI) can be systemically absorbed by the respiratory tract. The absorption of inhaled chromium compounds depends on a number of factors, including physical and chemical properties of the particles (oxidation state, size, and solubility), the reduction capacity of the ELF and alveolar macrophages and clearance by the mucocliary escalator and phagocytosis. Soluble Cr(VI) compounds enter the bloodstream more readily than highly insoluble Cr(VI) compounds. However, insoluble compounds may have longer residence time in lung. Absorption of Cr(VI) can also take place after oral and dermal exposure, particularly if the exposures are high. The chromate (CrO4)2- enters cells via facilitated diffusion through non-specific anion channels (similar to phosphate and sulfate anions). Following absorption of Cr(VI) compounds from various exposure routes, chromium is taken up by the blood cells and is widely distributed in tissues as Cr(VI). Inside blood cells and tissues, Cr(VI) is rapidly reduced to lower oxidation states and bound to macromolecules which may result in genotoxic or cytotoxic effects. However, in the blood a substantial proportion of Cr(VI) is taken up into erythrocytes, where it is reduced to Cr(III) and becomes bound to hemoglobin and other proteins. Inhaled Cr(VI) is reduced to Cr(III) in vivo by a variety of reducing agents. Ascorbate and glutathione in the ELF and macrophages have been shown to reduce Cr(VI) to Cr(III) in the lungs. After oral exposure, gastric juices are also responsible for reducing Cr(VI) to Cr(III). This serves to limit the amount of Cr(VI) systemically absorbed. Absorbed chromium is excreted from the body in a rapid phase representing clearance from the blood and at least two slower phases representing clearance from tissues. Urinary excretion is the primary route of elimination, accounting for over 50% of eliminated chromium. Although chromium is excreted in urine and feces, the intestine plays only a minor part in chromium elimination representing only about 5% of elimination from the blood. B. Carcinogenic Effects There has been extensive study on the potential for Cr(VI) to cause carcinogenic effects, particularly cancer of the lung. OSHA reviewed epidemiologic data from several industry sectors including chromate production, chromate pigment production, chromium plating, stainless steel welding, and ferrochromium production. Supporting evidence from animal studies and mechanistic considerations are also evaluated in this section. 1. Evidence from Chromate Production Workers The epidemiologic literature of workers in the chromate production industry represents the earliest and best-documented relationship between exposure to chromium and lung cancer. The earliest study of chromate production workers in the United States was reported by Machle and Gregorius in 1948 (Ex.7-2). In the United States, two chromate production plants, one in Baltimore, Maryland and one in Painesville, Ohio have been the subject of multiple studies. Both plants were included in the 1948 Machle and Gregorius study and again in the study conducted Format Factory 4.6.2.0 License Key - Crack Key For U the Public Health Service and published in 1953 (Ex. 7-3). Both of these studies reported the results in aggregate. The Baltimore chromate production plant was studied by Hayes et al. (Ex. 7-14) and more recently by Gibb et al. (Ex. 31-22-11). The chromate production plant in Painesville, Ohio has been followed since the 1950s by Mancuso with his most recent follow-up published in 1997. The most recent study of the Painesville plant was published by Luippold et al. (Ex. 31-18- 4). The studies by Gibb and Luippold present historical exposure data for the time periods covered by their respective studies. The Gibb exposure data are especially interesting since the industrial hygiene data were collected on a routine basis and not for compliance purposes. These routine air measurements may be more representative of those typically encountered by the exposed workers. In Great Britain, three plants have been studied repeatedly, with reports published between 1952 and 1991. Other studies of cohorts in the United States, Germany, Italy and Japan are also reported. The consistently elevated lung cancer mortality reported in these cohorts and the significant upward trends with duration of employment and cumulative exposure provide some of the strongest evidence that Cr(VI) be regarded as carcinogenic to workers. A summary of selected human epidemiologic studies in chromate production workers is presented in Table VI-1. [[Page 59319]] Table VI-1.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium-- Chromate Production ---------------------------------------------------------------------------------------------------------------- Reference Chromium (VI) Reference/exhibit number Study population population exposure Lung Cancer Risk ---------------------------------------------------------------------------------------------------------------- Hayes et al. (1979, Ex. 7-14). 1803 male workers Baltimore City Primarily sodium --O/E of 2.0 Braver et al. (1985, Ex. 7-17). initially mortality. chromate and (p< 0.01) based on employed 3 or dichromate 59 lung cancer more months 1945- production. Avg deaths. 1974 at old and Cr(VI) of 21 to --Increased risk new Baltimore MD 413 [mu]g/m\3\ with duration of production and avg duration employment. facility; follow- 1.6 yr to 13 yr up through 1977. depending on subcohort, plant, and year employed. Gibb et al. (2000, Ex. 31-22-11) 2357 male workers U.S. mortality. Primarily sodium --O/E of 1.86 initially chromate and (p< 0.01) based on employed 1950- dichromate. Mean 71 lung cancer 1974 only at new cumulative Cr(VI) deaths. Baltimore MD of 0.070 mg/m\3\ - --Significant production yr and work upward mortality facility; follow- duration of 3.1 trend with vuescan full version crack download - Crack Key For U up through 1992. yr. cumulative Cr(VI) exposure. Mancuso (1997, Ex. 23). 332 male workers Mortality rate Primarily sodium O/E not calculated Mancuso (1975, Ex. 7-11). employed at directly chromate and but significant Mancuso and Heuper (1951, Ex. 7- Painesville OH calculated using dichromate increase in age- 13). facility 1931- the distribution production with adjusted lung Bourne and Yee (1950, Ex. 7-98). 1937; follow-up of person years some calcium cancer death rate through 1993. by age group for chromate as a with cumulative the entire Format Factory 4.6.2.0 License Key - Crack Key For U result of using chromium exposure photopad 5.39 registration code exposed high lime based on 66 population as the process. Most deaths. standard. cumulative soluble Cr(VI) between 0.25 and 4.0 mg/m\3\ - yr based on 1949 survey. Luippold et al. (2003, Ex. 31-18- 492 male workers U.S. and Ohio Primarily sodium --O/E of 4). employed one year Mortality Rates. chromate and 2.41(p< 0.01) between 1940 and dichromate based on Ohio 1972 at production with rates and 51 Painesville OH minor calcium deaths. facility; follow- advanced installer architect 15.1 - Crack Key For U chromate. Mean --Significant up through 1997. cumulative upward mortality soluble Cr(VI) of trend with 1.58 mg/m\3\ - yr. cumulative Cr(VI) exposure Davies et al. (1991, Ex. 7-99). 2298 male chromate Cancer mortality Principally sodium --O/E of 1.97 Alderson et al. (1981, Ex. 7- production of England, Wales chromate and (p< 0.01) pre- 22). workers employed and Scotland and dichromate process change Bistrup and Case (1956, Ex. 7- for one year unexposed local production with based on 175 20). between 1950 and workers. some calcium deaths. 1976 at three chromate before --SMR of 1.02 (NS) different UK switch from high post-process plants; follow-up lime to no lime change based on through 1989. process. Avg 14 deaths. soluble Cr(VI) in --Increased risk early 1950s from for high exposed 2 to 880 [mu]g/ compared with Format Factory 4.6.2.0 License Key - Crack Key For U m\3\ depending on less exposed. job. Korallus et al. (1993, Ex. 7- 1417 chromate Mortality rates Principally sodium --O/E of 2.27 91). production for North Rhine- chromate and (p< 0.01) pre- Korallus et al. (1982, Ex. 7- workers employed Westphalia region dichromate process change 26). for one year of Germany where production with based on 66 between 1948 and plants located. some calcium deaths. 1987 at two chromate before --O/E of 1.25 (NS) different German switch from high post-process plants; follow-up Format Factory 4.6.2.0 License Key - Crack Key For U lime to no lime change based on 9 through 1988. process. Annual deaths. mean Cr(VI) between 6.2 and 38 [mu]g/m\3\ after 1977. Cr(VI) exposure not reported before 1977. ---------------------------------------------------------------------------------------------------------------- Observed/Expected (O/E) Relative Risk (RR) Not Statistically Significant (NS) Odds Ratio (OR) The basic hexavalent chromate production process involves milling and mixing trivalent chromite ore with soda ash, sometimes in the presence of lime (Exs. 7-103; 35-61). The mixture is ``roasted'' at a high temperature, which oxidizes much of the chromite to hexavalent sodium chromate. Depending on the lime content used in the process, the roast also contains other chromate species, especially calcium chromate under high lime conditions. The highly water-soluble sodium chromate is water-extracted from the water-insoluble trivalent chromite and the less water-soluble chromates (e.g., calcium chromate) in the ``leaching'' process. The sodium chromate leachate is reacted with sulfuric acid and sodium bisulfate to form sodium dichromate. The sodium dichromate is prepared and packaged as a crystalline powder to be sold as final product or sometimes used as the starting material to make other chromates such as chromic acid and potassium dichromate. a. Cohort Studies of the Baltimore Facility. The Hayes et al. study of the Baltimore, Maryland chromate production plant was designed to determine whether changes in the industrial process at one chromium chemical production facility were associated with a decreased risk of cancer, particularly cancer of the respiratory system (Ex. 7-14). Four thousand two hundred and seventeen (4,217) employees were identified as newly employed between January 1, 1945 and December 31, 1974. Excluded from this initial enumeration were employees who: (1) were working as of 1945, but had been hired prior to 1945 and (2) had been hired since 1945 but who had previously been employed at the plant. Excluded from the final cohort were those employed less than 90 days; women; those with unknown length of employment; those with no work history; and those of unknown age. The final cohort included 2,101 employees (1,803 hourly and 298 salaried). Hayes divided the production process into three departments: (1) The mill and roast or ``dry end'' department which consists of grinding, roasting and leaching processes; (2) the bichromate department which consists of the acidification and crystallization processes; and (3) the special products department which produces secondary products including chromic acid. The bichromate and special products departments are referred to as the ``wet end''. The construction of a new mill and roast and bichromate plant that opened during 1950 and 1951 and a new chromic acid and special products plant that opened in 1960 were cited by Hayes as ``notable production changes'' (Ex. 7- [[Page 59320]] 14). The new facilities were designed to ``obtain improvements in process technique and in environmental control of exposure to chromium bearing dusts * * *'' (Ex. 7-14). Plant-related work and health histories were abstracted for each employee from plant records. Each job on the employee's work history was characterized according to whether the job exposure occurred in (1) a newly constructed facility, (2) an old facility, or (3) could not be classified as having occurred in the new or the old facility. Those who ever worked in an old facility or whose work location(s) could not be distinguished based upon job title were considered as having a high or questionable exposure. Only those who worked exclusively in the new facility were defined for study purposes as ``low exposure''. Data on cigarette smoking was abstracted from plant records, but was not utilized in any analyses since the investigators thought it ``not to be of sufficient quality to allow analysis.'' One thousand one hundred and sixty nine (1,169) cohort members were identified as alive, 494 not individually identified as alive and 438 as deceased. Death certificates could not be located for 35 reported decedents. Deaths were coded to the 8th revision of the International Classification of Diseases. Mortality analysis was limited to the 1,803 hourly employees calculating the standardized mortality ratios (SMRs) for specific causes of death. The SMR is a ratio of the number of deaths observed in the study population to the number that would be expected if that study population had the same specific mortality rate as a standard reference population (e.g., age- gender- calendar year adjusted U.S. population). The SMR is typically multiplied by 100, so a SMR greater than 100 represents an elevated mortality in the study cohort relative to the reference group. In the Hayes study, the expected number of deaths was based upon Baltimore, Maryland male mortality rates standardized for age, race and time period. For those where race was unknown, the expected numbers were derived from mortality rates for whites. Cancer of the trachea, bronchus and lung accounted for 69% of the 86 cancer deaths identified and was statistically significantly elevated (O = 59; E = 29.16; SMR = 202; 95% CI: 155-263). Analysis of lung cancer deaths among hourly workers by year of initial employment (1945-1949; 1950-1959 and 1960-1974), exposure category (low exposure or questionable/high exposure) and duration of employment (short term defined as 90 days-2 years; long term defined as 3 years +) was also conducted. For those workers characterized as having questionable/high exposure, the SMRs were significantly elevated for the 1945-1949 and the 1950-1959 hire periods and for both short- and long-term workers (not statistically significant for the short-term workers initially hired 1945-1949). For those characterized as low exposure, there was an elevated SMR for the long-term workers hired between 1950 and 1959, but based only on three deaths (not statistically significant). No lung cancer cases were observed for workers hired 1960-1974. Case-control analyses of (1) a history of ever having been employed in selected jobs or combinations of jobs or (2) a history of specified morbid conditions and combinations of conditions reported on plant medical records were conducted. Cases were defined as decedents (both hourly and salaried were included in the analyses) whose underlying or contributing cause of death was lung cancer. Controls were defined as deaths from causes other than malignant or benign tumors. Cases and controls were matched on race (white/non-white), year of initial employment (+/-3 years), age at time of initial employment (+/-5 years) and total duration of employment (90 days-2 years; 3-4 years and 5 years +). An odds ratio (OR) was determined where the ratio is the odds of employment in a job involving Cr(VI) exposure for the cases relative to the controls. Based upon matched pairs, analysis by job position showed significantly elevated odds ratios for special products (OR = 2.6) and bichromate and special products (OR = 3.3). The relative risk for bichromate alone was also elevated (OR = 2.1, not statistically significant). The possible association of lung cancer and three health conditions (skin ulcers, nasal perforation and dermatitis) as recorded in the plant medical records was also assessed. Of the three medical conditions, only the odds ratio for dermatitis was statistically significant (OR = 3.0). When various combinations of the three conditions were examined, the odds ratio for having all three conditions was statistically significantly elevated (OR = 6.0). Braver et al. used data from the Hayes study discussed above and the results of 555 air samples taken during the period 1945-1950 by the Baltimore City Health Department, the U.S. Public Health Service, and the companies that owned the plant, in an attempt to examine the relationship between exposure to Cr(VI) and the occurrence of lung cancer (Ex. 7-17). According to the authors, methods for determining the air concentrations of Cr(VI) have changed since the industrial hygiene data were collected at the Baltimore plant between 1945 and 1959. The authors asked the National Institute for Occupational Safety and Health (NIOSH) and the Occupational Safety and Health Administration (OSHA) to review the available documents on the methods of collecting air samples, stability of Cr(VI) in the sampling media after collection and the methods of analyzing Cr(VI) that were used to collect the samples during that period. Air samples were collected by both midget impingers and high volume samplers. According to the NIOSH/OSHA review, high volume samplers could have led to a ``significant'' loss of Cr(VI) due to the reduction of Cr(VI) to Cr(III) by glass or cellulose ester filters, acid extraction of the chromate from the filter, or improper storage of samples. The midget impinger was ``less subject'' to loss of Cr(VI) according to the panel since neither filters nor acid extraction from filters was employed. However, if iron was present or if the samples were stored for too long, conversion from Cr(VI) to Cr(III) may have occurred. The midget impinger can only detect water soluble Cr(VI). The authors noted that, according to a 1949 industrial hygiene survey by the U.S. Public Health Service, very little water insoluble Cr(VI) was found at the Baltimore plant. One NIOSH/OSHA panel member characterized midget impinger results as ``reproducible'' and ``accuracy * * * fairly solid unless substantial reducing agents (e.g., iron) are present'' (Ex. 7-17, p. 370). Based upon the panel's recommendations, the authors used the midget impinger results to develop their exposure estimates even though the panel concluded that the midget impinger methods ``tend toward underestimation'' of Cr(VI). The authors also cite other factors related to the industrial hygiene data that could have potentially influenced the accuracy of their exposure estimates (either overestimating or underestimating the exposure). These include: measurements may have been taken primarily in ``problem'' areas of the plant; the plants may have been cleaned or certain processes shut down prior to industrial hygiene monitoring by outside groups; respirator use; and periodic high exposures (due to infrequent maintenance operations or failure of exposure control equipment) which were not measured and therefore not reflected in the available data. The authors estimated exposure indices for cohorts rather than for specific individuals using hire period (1945-1949 or 1950-1959) and duration [[Page 59321]] of exposure, defined as short (at least 90 days but less than three years) and long (three years or more). The usual exposure to Cr(VI) for both the short- and long-term workers hired 1945-1949 was calculated as the average of the mean annual air concentration for 1945-1947 and 1949 (data were missing for 1948). This was estimated to be 413 [mu]g/m\3\. The usual exposure to Cr(VI) was estimated to be 218 [mu]g/m\3\ for the short and long employees hired between 1950 and 1959 based on air measurements in the older facility in the early 1950s. Cumulative exposure was calculated as the usual exposure level x average duration. Short-term workers, regardless of length of employment, were assumed to have received 1.6 years of exposure regardless of hire period. For long-term workers, the average length of exposure was 12.3 years. Those hired 1945-1949 were assigned five years at an exposure of 413 [mu]g/m\3\ and 7.3 years at an exposure of 218 [mu]g/m\3\. For the long-term workers hired 1950-1959, the average length of exposure was estimated to be 13.4 years. The authors estimated that the cumulative exposures at which ``significant increases in lung cancer mortality'' were observed in the Hayes study were 0.35, 0.67, 2.93 and 3.65 [mu]g/m\3\-years. The association seen by the authors appears more likely to be the result of duration of employment rather than the magnitude of exposure since the variation in the latter was small. Gibb et al. relied upon the Hayes study to investigate mortality in a second cohort of the Baltimore plant (Ex. 31-22-11). The Hayes cohort was composed of 1,803 hourly and 298 salaried workers newly employed between January 1, 1945 and December 31, 1974. Gibb excluded 734 workers who began work prior to August 1, 1950 and included 990 workers employed after August 1, 1950 who worked less than 90 days, resulting in a cohort of 2,357 males followed for the period August 1, 1950 through December 31, 1992. Fifty-one percent (1,205) of the cohort was white; 36% (848) nonwhite. Race was unknown for 13% (304) of the cohort. The plant closed in 1985. Deaths were coded according to the 8th revision of the International Classification of Diseases. Person years of observation were calculated from the beginning of employment until death or December 31, 1992, whichever came earlier. Smoking data (yes/no) were available for 2,137 (93.3%) of the cohort from company records. Between 1950 and 1985, approximately 70,000 measurements of airborne Cr(VI) were collected utilizing several different sampling methods. The program of routine air sampling for Cr(VI) was initiated to ``characterize `typical/usual exposures' of workers'' (Ex. 31-22-11, p.117). Area samples were collected during the earlier time periods, while both area and personal samples were collected starting in 1977. Exposure estimates were derived from the area sampling systems and were adjusted to ``an equivalent personal exposure estimate using job- specific ratios of the mean area and personal sampling exposure estimates for the period 1978-1985 * * *.'' (Ex. 31-22-11, p.117). According to the author, comparison of the area and personal samples showed ``no significant differences'' for about two-thirds of the job titles. For several job titles with a ``significant point source of contamination'' the area sampling methods ``significantly underestimated'' personal exposure estimates and were adjusted ``by the ratio of the two'' (Ex. 31-22-11, p.118). A job exposure matrix (JEM) was constructed, where air sampling data were available, containing annual average exposure for each job title. Data could not be located for the periods 1950-1956 and 1960- 1961. Exposures were modeled for the missing data using the ratio of the measured exposure for a job title to the average of all measured job titles in the same department. For the time periods where ``extensive'' data were missing, a simple straight line interpolation between years with known exposures was employed. In an attempt to estimate airborne Cr(III) concentrations, 72 composite dust samples were collected at or near the fixed site air monitoring stations about three years after the facility closed. The dust samples were analyzed for Cr(VI) content using ion chromatography. Cr(III) content was determined through inductively coupled plasma spectroscopic analysis of the residue. The Cr(III):Cr(VI) ratio was calculated for each area corresponding to the air sampling zones and the measured Cr(VI) air concentration adjusted based on this ratio. Worker exposures were calculated for each job title and weighted by the fraction of time spent in each air-monitoring zone. The Cr(III):Cr(VI) ratio was derived in this manner for each job title based on the distribution of time spent in exposure zones in 1978. Cr(VI) exposures in the JEM were multiplied by this ratio to estimate Cr(III) exposures. A total of 855 observed deaths (472 white; 323 nonwhite and 60 race unknown) were reported. SMRs were calculated using U.S. rates for overall mortality. Maryland rates (the state in which the plant was located) were used to analyze lung cancer mortality in order to better account for regional differences in disease fatality. A statistically significant lung cancer SMR, based on the national rate, was found for whites (O=71; SMR=186; 95% CI: 145-234); nonwhites (O=47; SMR=188; 95% CI: 138-251) and the total cohort (O=122; SMR=180; 95% CI: 149-214). Of the 122 lung cancer cases, 116 were smokers and four were non smokers at the time of hire. Smoking status was unknown for two lung cancer cases. SMRs were not adjusted for smoking. The ratio of observed to expected lung cancer deaths (O/E) for the entire cohort stratified by race and cumulative exposure quartile were computed. Cumulative exposure was lagged five years (only exposure occurring five years before a given age was counted). The cut point for the quartiles divided the cohort into four equal groups based upon their cumulative exposure at the end of their working history (0- 0.00149 mgCrO3/m3-yr; 0.0015-0.0089 mgCrO3/m3-yr; 0.009-0.0769 mgCrO3/ m3-yr; and 0.077-5.25 mgCrO3/m3-yr). For whites, the relative risk of lung cancer was significantly elevated for the second through fourth exposure quartiles with O/E values of 0.8, 2.1, 2.1 and 1.7 for the four quartiles, respectively. For nonwhites, the O/E values by exposure quartiles were 1.1, 0.9, 1.2 and 2.9, respectively. Only the highest exposure quartile was significantly elevated. For the total cohort, a significant exposure-response trend was observed such that lung cancer mortality increased with increasing cumulative Cr(VI) exposure. Proportional hazards models were used to assess the relationship between chromium exposure and the risk of lung cancer. The lowest exposure quartile was used as the reference group. The median exposure in each quartile was used as the measure of cumulative Cr(VI) exposure. When smoking status was included in the model, relative lung cancer risks of 1.83, 2.48 and 3.32 for the second, third and fourth exposure quartiles respectively were estimated. Smoking, Cr(III) exposure, and work duration were also significant predictors of lung cancer risk in the model. The analysis attempted to separate the effects into two multivariate proportionate hazards models (one model incorporated the log of cumulative Cr(VI) exposure, the log of cumulative Cr(III) exposure and smoking; the second incorporated the log of cumulative Cr(VI), work duration and smoking). In either regression model, lung cancer mortality remained significantly associated (p < .05) with [[Page 59322]] cumulative Cr(VI) exposure even after controlling for the combination of smoking and Cr(III) exposure or the combination of smoking and work duration. On the other hand, lung cancer mortality was not significantly associated with cumulative Cr(III) or work duration in the multivariate analysis indicating lung cancer risk was more strongly correlated with cumulative Cr(VI) exposure than the other variables. Exponent, as part of a larger submission from the Chrome Coalition, submitted comments on the Gibb paper asking that OSHA review methodological issues believed by Exponent to impact upon the usefulness of the Gibb data in a risk assessment analysis. While Exponent states that the Gibb study offers data that ``are substantially better for cancer risk than the Mancuso study* * *'' they believe that further scrutiny of some of the methods and analytical procedures are necessary (Ex. 31-18-15-1, p. 5). The issues raised by Exponent and the Chrome Coalition (Ex. 31-18- 14) concerning the Gibb paper are: selection of the appropriate reference population for compilation of expected numbers for use in the SMR analysis; inclusion of short term workers (< 1 year); expansion of the number of exposure groupings to evaluate dose response trends; analyzing dose response by peak JEM exposure levels; analyzing dose- response at exposures above and below the current PEL and calculating smoking-adjusted SMRs for use in dose-response assessments. Exponent obtained the original data from the Gibb study. The data were reanalyzed to address the issues cited above. Exponent's findings are presented in Exhibit 31-18-15-1 and are discussed below. Exponent suggests that Gibb's use of U.S. and Maryland mortality rates for developing expectations for the SMR analysis was inappropriate and suggested that Baltimore city mortality rates would have been the appropriate standard to select since those mortality rates would more accurately reflect the mortality experience of those who worked at the plant. Exponent reran the SMR analysis to compare the SMR values reported by Gibb (U.S. mortality rates for SMR analysis) with the results of an SMR analysis using Maryland mortality rates and Baltimore mortality rates. Gibb reported a lung cancer SMR of 1.86 (95% CI: 1.45-2.34) for white males based upon 71 lung cancer deaths using U.S. mortality rates. Reanalysis of the data produced a lung cancer SMR of 1.85 (95% CI: 1.44-2.33) for white males based on U.S. mortality rates, roughly the same value obtained by Gibb. When Maryland and Baltimore rates are used, the SMR drops to 1.70 and 1.25 respectively. Exponent suggested conducting sensitivity analysis that excludes short-term workers (defined as those with one year of employment) since the epidemiologic literature suggests that the mortality of short-term workers is different than long-term helium music management. Short-term workers in the Gibb study comprise 65% of the cohort and 54% of the lung cancers. The Coalition also suggested that data pertaining to short-term employee's information are of ``questionable usefulness for assessing the increased cancer risk from chronic occupational exposure to Cr(VI)'' (Ex. 31-18-15-1, p. 5). Lung cancer SMRs were calculated for those who worked < 1 year and for those who worked one year or more. Exponent defined short-term workers as those who worked a minimum of one year ``because it is consistent with the inclusion criteria used by others studying chromate chemical production worker cohorts'' (Ex. 31-18-15-1, p. 12). Exponent also suggested that Gibb's breakdown of exposure by quartile was not the most ``appropriate'' way of assessing dose-response since cumulative Cr(VI) exposures remained near zero until the 50th to 60th percentile, ``so there was no real distinction between the first two quartiles * * *'' (Ex. 31-18-15-1, p. 24). They also suggested that combining ``all workers together at the 75th quartile * * * does not properly account for the heterogeneity of exposure in this group'' (Ex. 31-18-15-1, p. 24). The Exponent reanalysis used six cumulative exposure levels of Cr(VI) compared with the four cumulative exposure levels of Cr(VI) in the Gibb analysis. The lower levels of exposure were combined and ``more homogeneous'' categories were developed for the higher exposure levels. Using these re-groupings and excluding workers with less than one year of employment, Exponent reported that the highest SMRs are seen in the highest exposure group (1.5
Источник: https://www.osha.gov/laws-regs/federalregister/2004-10-04

EasyWorship (2009) V2.4 for Win10 Crack [UPDATE 2019]

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pass: MaRk15

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-EW2009b2.4 Patch

-EW2009b2.4 Crack

- Instructions.txt

Or  Mirror {UPDATE WORK 100%}


EasyWorship (2009) V2.4
EasyWorship (2009) V1.4
Pass: abbysoft.com 

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Extract the downloaded file then follow the instructions (instructions actually already given in the file)


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if you have not yet, follow this link: 

EasyWorship (2009) + 1.9 Build Patch by MaRk15

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1. Open "Patch" then Folder
         Double click "EasyWorship2009_2_4_PatchForWindows10.exe"
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3. Lastly, open "Crack" folder then
         -Run "Easyworship.2009. (Build.2.4) .patch.by.mark15.exe"
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Источник: https://soft-apk-free.blogspot.com/2017/12/easyworship-2009-v24-for-win10-crack-by.html
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port Indirect-Fast Path Interface : MII0

TD-W8970 v1.0

The TD-W8970 v1 is a 450Mbps Wireless N Gigabit ADSL2+ / VDSL2 Modem Router, wrongly advertised as a 300Mbps and only ADSL2+ capable product. The Router is based on a SoC.

The TD-W8970 v3 is a Broadcom router which is not supported by OpenWrt.

The TD-W8970 v1 is very similar to the TD-W8980 and TD-W9980.

(for OEM firmware version 1.2)

partition address space name filesystem function
mtd0 0x00000000-0x00020000 boot n/a U-Boot v2.0.40
mtd1 0x00020000-0x00160000 kernel RAM executable kernel 2.6.32
mtd2 0x00160000-0x007c0000 rootfs squashfs root
mtd3 0x007c0000-0x007d0000 config XML string user configuration
mtd4 0x007d0000-0x007e0000 romfile n/a ???
mtd5 0x007e0000-0x007f0000 rom n/a ???
mtd6 0x007f0000-0x00800000 radio n/a radio settings

There are two viable ways to install OpenWrt; the “classic” method using serial access, or the “web interface hack” which allows to flash the firmware without opening the case!

Once a serial console has been established (see Serial for further details):

  1. Download the openwrt-lantiq-xrx200-TDW8970-uImage-sysupgrade.image (in OpenWRT 19.07.2, this is named openwrt-19.07.2-lantiq-xrx200-tplink_tdw8970-squashfs-sysupgrade.bin)

  2. Switch on the device and press 't' on the serial console until you get a prompt, then run commands similar to these:

  3. Set the device's IPif you don't want the default 192.168.1.1: (so you don't have to move your TFTPserver onto a different subnet)setenv ipaddr 192.168.1.1
  4. Set the address of your TFTPserver:setenv serverip 192.168.1.2
  5. Set the board type (not sure if this is necessary):setenv bootargs 'board=WD8970'
  6. Download the image into RAM (*not* flash):tftpboot 0x81000000 openwrt-lantiq-xrx200-TDW8970-sysupgrade.image
  7. Erase the rootfs flash area:sf erase 0x20000 0x7a0000
  8. Write image to flash:sf write 0x81000000 0x20000 0x$(filesize)
  9. Reboot into OpenWrt:reset

Starting with FW build 12.10.2013, the TP-Link webinterface accepts only RSA signed firmware images with the v3 header. Therefore flashing firmware via webinterface is not so easy anymore.

SSID Config Injection

Newer versions of TP-Link firmwares do besides encryption furthermore compression of config files. Without knowledge of the compression algorithm it's not that easy to inject shell commands (like in the StatPost approach). But there is a much easier approach. It seems the whole config gets executed / evaluated through ash somehow. Therefor you can inject commands anywhere in this config file or it attributes. To get shell access we use the SSID of wifi:

  1. Login to the router web ui at 192.168.1.1. T

  2. Set Wifi (2.4 or 5GHz) SSID to `telnetd -p 1023 -l login`

  3. telnet 192.168.1.1 1023 (User: admin Password: 1234)

This procedure seems not to work with TD-W8970B V1, at least not with following firmware builds: 141008,150526 and 160808. Instead you have to manipulate the router settings as described in the following section:

StatPost

Steps to access the linux shell using telnet, without opening the router physically:

  1. Login to the router web ui at 192.168.1.1.

  2. Take backup of the router configuration conf.bin (Keep one copy safely in case you screw up things!)

  3. Change the config file:

    1. either by Java tool:

      1. Download tplink configuration encrypter/decrypter Java tool from the following link. http://ejs1920.users.sourceforge.net/StatPOSTer-20160306.jar (Thanks ejs1920 for making this tool)

      2. Launch the program StatPOSTer-20160306.jar (java -jar StatPOSTer-20160306.jar)

        1. Note:In Java version > 10 some needed classes were removed. You have to install “lib-jaxb-api-java” and “lib-jaxb-java” package and start the tool in a special way (Thanks Christoph Müller to find out):$ java -cp /usr/share/java/javax.activation.jar:/usr/share/java/jaxb-api.jar:/usr/share/java/jaxb-impl.jar:/usr/share/java/jaxb-core.jar:StatPOSTer-20160306.jar StatPOSTer
      3. Select the router as TD-w8970v1 and click on decrypt button in the program and select the conf.bin file you saved via the router web ui.

      4. Save the decrypted conf.xml

      5. Open the the decrypted conf.xml with a texteditor (e.g. gedit,notepad)

      6. Add the xml tag after the xml node SerialNumber and save it.

      7. Click the encrypt button, select the modified conf.xml, save as conf_modified.bin

    2. or by Python tool:

      1. Download tplink configuration encrypter/decrypter Python tool from the following link. https://github.com/sta-c0000/tpconf_bin_xml (Thanks sta-c0000 for making this tool)

      2. Decrypt config file: $ python3 tpconf_bin_xml.py conf.bin conf.xml
      3. Open the the decrypted conf.xml with a texteditor (e.g. gedit,notepad)

      4. Add the xml tag after the xml node SerialNumber and save it.

      5. Encrypt modified config file: $ python3 tpconf_bin_xml.py conf.xml conf_modified.bin
  4. Login to the router web ui at 192.168.1.1 and upload the new conf_modified.bin. Let the router reboot.

  5. Router will reboot and have at the top, this is expected (but not always the case).

  6. Telnet to 192.168.1.1 at port 1023 otherwise you will only reach the standard CLI daemon. For example: telnet 192.168.1.1 1023 on linux.

  7. Enter the username/login: admin and password: 1234. The login credentials are defined in the orginal firmware image. But without a listening ssh/telnet daemon you cannot use them.

  8. Now you have access to the linux root shell on the device and have to flash the firmware via CLI. https://forum.archive.openwrt.org/viewtopic.php?id=42380&p=13#p340785Note: You have to use OpenWRT 15.05 release for the procedure, 19.07 did not work (for me).

How does it work: probably by injecting the command telnetd -p 1023 -l login

Reported TP-Link FW Builds this approach has been used successfully:

TD-W8970 V1: 140613
TD-W8970B V1: 141008,160808

Maybe other FW revisions also.

Also confirmed working:

Openwrt Performance

This video might give you a glimpse about td8970 openwrt performance. Its about 25MBps=400mbps on gigabit lan and 5MBps=40mbps on wireless

For testing purpose only ;-) wrote this from my notes it should work.

Once a serial console has been established (see Serial for further details):

  1. Obtain your Image, you need to care about you model type TD-W8970 or TD-W8970B both images work but the modem part is different. You might need to strip the header off with for newer FW like or flash an older one directly like

  2. Switch on the device and press 't' on the serial console until you get a prompt, then run commands similar to these:

    1. Set the device's IPif you don't want the default 192.168.1.1: (so you don't have to move your TFTPserver onto a different subnet)setenv ipaddr 192.168.1.1
    2. Set the address of your TFTPserver:setenv serverip 192.168.1.2
    3. Set the board type (not sure if this is necessary might be also WD8970B):setenv bootargs 'board=WD8970'
    4. Download the image into RAM (*not* flash):tftpboot 0x81000000 TD-W8970v1_0.6.0_2.1_up(130415).bin
    5. Erase the rootfs flash area:sf erase 0x20000 0x7a0000
    6. Write image to flash:sf write 0x81000000 0x20000 0x7a0000
  3. the rootfs area is 0x7c0000, erase command is to 0x7a000 and write is also 0x7a000 you can see the image size in after the tftpboot command

  4. be careful when erasing/writing the flash the radio is required for WLAN and should not be overwritten or erased. A backup is nice to have if something went wrong, it stores also the MAC address for your WLAN (ART Partition).

If you don't have a GUI (LuCI) available, you can alternatively upgrade via the command line. There are two command line methods for upgrading:

Note: It is important that you put the firmware image into the ramdisk (/tmp) before you start flashing.

sysupgrade

cd /tmp wget http://downloads.openwrt.org/snapshots/trunk/XXX/xxx.abc sysupgrade /tmp/xxx.abc

mtd

If does not support this router, use.

cd /tmp wget http://downloads.openwrt.org/snapshots/trunk/XXX/xxx.abc mtd write /tmp/xxx.abc firmware && reboot

→ generic.debrick

Quoting **joseba_g**:

(…)
As programmer I use buspirate, however its easy to use other things, like a raspberry, or even computer motherboard. only need point flashrom to the programmer.

First make a flash copy

tp# flashrom -p buspirate_spi:dev=/dev/ttyUSB0,pullups=on,spispeed=1M -r tplink.bin


I have old backup with atheros caldata (art) but you can extract from extracted tplink.bin

dd if=tplink.bin of=caldata.bin bs=1 skip=8323072


the numbers are total flash 8 MiB converted to decimal bit 8388608
Art partition last 64 kib in dec 65536
dd takes a file, ignores first 8323072 bit and writes the rest 65536 to caldata.bin. I am really bad changing those numbers, I use a calculator and change from hex to dec.

With clear copy of a working flash you can use any hexeditor and change de last 64 kib with your caldata, or flash directly and write from OpenWrt command line, I use old working copy, so I flash it (as root)

# flashrom -p buspirate_spi:dev=/dev/ttyUSB0,pullups=on,spispeed=1M -w tplinkgood.bin


Several comments, flashrom tries to write at maximum speed, (8M for my flash) and fails, I'm unsure why, maybe something in circuit can't work at this speed, or the use of large wires broke com, I don't know.

Slowering spispeed parameter works for me. I only connect 6 pins (the soic have 8) take a look to this spi programing post when I'm writing flash one of the led Format Factory 4.6.2.0 License Key - Crack Key For U on. however, everything goes OK. maybe in other devices de-soldering is a must, but give a try to a clip programming, is easy and fast.

Use RaspberryPI SPI programming header with POMONA clip-in programmer following Debricking Guide. BusPirate is currently not working, Pickit2 has not been tried, Olimex is not-working.

→ failsafe_and_factory_reset

Currently LED's are non-showing factory reset mode/failsafe nide, so when router is not accessible due bad config, you can enter factory reset mode/failsafe via following workaround:

:!: Not needed in trunk

Chaos Calmer and earlier need firmware for the DSL system installed in /lib/firmware. As of 2017, the default install URL no longer works, so you need to find the file some other way. To further complicate matters, this firmware only seems to work for Barrier Breaker and not with Chaos Calmer on some devices. Thus the recommended course of action is to skip Chaos Calmer and go straight to Designated Driver (trunk as of March 2017), or use the LEDE firmware instead. The rest of this section applies to Chaos Calmer and earlier. [Tip: save your settings when upgrading to trunk so the router comes back up properly configured. SSH in and run “opkg update && opkg install luci” to get the web interface back.]

A whole Point for this? yes there is much trouble with this. But the Devs made it very simple, you only need to know. There is a command for obtaining the vdsl.bin and put it to an separate partition that is mounted in the right place, so it does not eat up your free space. But the Telekom removed the Image they chose to obtain the bin because of stability issues with their HW. The replacement for this is V1.21 and is available on their server. You can either get a newer “vdsl_fw_install” (this is the command) or modify it to work again. edit the comand with vi:

vi /sbin/vdsl_fw_install.sh

edit line URL to:

URL="http://hilfe.telekom.de/dlp/eki/downloads/Speedport/Speedport%20W%20921V/Firmware_Speedport_W921V_1.21.000.bin"

edit line MD5 to:

MD5_FW="0a099d08dbf091c74d685b532cbb1390"

This file isn't hosted anymore on the Deutsche Telekoms servers due to newer versions. As of November 2017 the most current firmware is:

URL="https://www.telekom.de/hilfe/downloads/firmware-speedport-w921v-1.44.000.bin" MD5_FW="cefbeb7073e02e0fa4ddb6b31ecb3d1e"

I was still able to cut the annex-b firmware by using the “w921v_fw_cutter” tool.

and run it:

vdsl_fw_install.sh

It is fixed in trunk already, you can also obtain other working bins, to play around, they should only meet your Annex Type.

You might need to obtain the files via internet, so you need to setup the device as a client first. To do so temporary you need to set the nameserver and maybe th IP. to set the IP:

udhcp -i br-lan

to set the NS:

echo "nameserver 192.168.1.254" > /tmp/resolv.conf

mine is 192.168.1.254

It seems the TCOM server only offers https but wget does not wget-ssl-certs you can either specify another Webserver after the command or download it to /tmp on the device and run it.

UPDATE for CC and Changes

:!: As of March 2017 this site is down. Find the firmware file and place in /tmp, then run vdsl_fw_install.sh.

Telekom changed to SSL so we need wget with ssl (wget from ox is not working) and “–no-check-certificate” the following commands are the fastest way to get the firmware when you have a dhcp-server and internet.

udhcpc -i br-lan echo "nameserver 192.168.1.254" > /tmp/resolv.conf opkg update opkg install wget sed -i 's/wget/wget --no-check-certificate/g' /sbin/vdsl_fw_install.sh vdsl_fw_install.sh opkg remove wget libpcre libopenssl zlib

librt is an essential package that needs to be forced removed, firmware is stored in mtd4 now

Update for LEDE trunk

As the time of writing c18bf14 the 2 packages needed for annex a and b are available at compile time in section.

Once the image is flashed they are present in directory as and which you can later choose instead of searching for a workingsee UCI networking options cheatsheet section DSL/VDSL

depending on you Country/ISP you need to modify your DSL config settings, ATM or PTM and Annex A or B the following is the default:

config vdsl 'dsl' option annex 'a' option firmware '/lib/firmware/vdsl.bin' option tone 'av' option xfer_mode 'atm'

to set it for Annex B issue the next 2 commands and with PTM the next 3 (you need to install the Kernel Module with the fourth)

uci set network.dsl.annex=b uci set network.dsl.tone=bv uci set network.dsl.xfer_mode=ptm opkg install kmod-ltq-ptm-vr9

Similar to TD-W9980. Numbers 0-3 are Ports 1-4 as labeled on the unit, number 4 is the Internet (WAN) on the unit, 6 is the internal connection to the router itself.

vlan0 = eth0.0, vlan1 = eth0.1 and so on.

Port Switch port
LAN 1 5
LAN 2 0
LAN 3 2
LAN 4 /WAN 4
GMII 6 (marked as CPU)

→ hardware.button on howto use and configure the hardware button(s). FIXME Here, we merely name the buttons, so we can use them in the above Howto.

Chaos Calmer

OpenWrt Chaos Calmer 15.05.1 does not support the status LED on this router, so boot status and failsafe will not be indicated visually. Support is being added in 15.05.2.

If you want to have a LED switch on after boot is completed, you can append this to your /etc/config/system file:

config led 'led_system' option name 'System' option sysfs 'wps' option default '1'

Trunk

In trunk, the WPS LED is used as status LED on this router, as in other TP-LINK routers which do not have a dedicated status LED.

However, the behaviour of the status LED has changed since r48041, only for this router: it will switch off after boot is completed, instead of staying on.

If you want to have the LED stay on after boot is completed, you can append this to your /etc/config/system file:

config led 'led_system' option name 'System' option sysfs 'tdw89x0:green:wps' option default '1'
Instruction set:MIPS
Vendor:Lantiq
bootloader:U-Boot 2010.06-LANTIQ-v-2.0.40-svn2583
(press t to enter U-Boot console on OEM firmware)
System-On-Chip:XWAY VRX268 (VR9 Family)
CPU/Speed: MIPS34Kc @ 500 MHz
Flash Chip:cFeon Q64-104HIP other Winbond 25Q64FVSIG
Flash Specs: 8 MiB SPI
RAM Chip:Hynix H5PS5162GFR-Y5C other Winbond W9751G6KB or Zentel A3R12E40CBF
RAM Specs: 64 MiB DDR2 @ 250 MHz (3-5-5-5)
Wireless: AR9381 2.4 GHz (3×3) 802.11bgn
Ethernet: 4x 10/100/1000 BASE-TX Ethernet Interface
(2x XWAY VR9 GPHY 11G & 2x XWAY PEF7071 via RGMII)
Switch:Internal configurable (Infineon)
xDSL:Lantiq XWAY VRX208
ADSL1/2/2+ (G.992.1/3/5) Annexes A, B, I, J, M, L,
VDSL1 (G.993.1, T1.424, TS 101 270),
VDSL2 (G.993.2),
ITU-T G 998.2 Bonding,
EFM (IEEE 802.3ah)
USB: 2 x USB 2.0
GPIO Buttons: WPS button, WiFi toggle switch, Reset button
GPIO LEDs: ADSL, Internet, WPS, USB Port 1, USB Port 2
Power: External 12V 1.5A
Serial:Yes
JTAG: Yes
Item Consumption @ 12.0V (Lab PSU)
Bootup 0.21 A
Idle 0.43 A
Idle + Wifi 0.44 A
100% CPU-load + Wifi 0.50 A
Idle + Wifi + DSL ? A

Front:
FIXMEInsert photo of front of the casing

Back:
FIXMEInsert photo of back of the casing

Backside label:
FIXMEInsert photo of backside label

Note: This will void your warranty!

orlohct.jpg

Main PCB:

→ port.serial general information about the serial port, serial port cable, etc.

How to connect to the Serial Port of this specific device:
**PCB with markings for serial port**

Serial connection parameters
for TP-Link TD-W8970 v1.x
115200, 8N1
Connector J7
Pins (from top to bottom) VCC (3.3V), GND, Rx, Tx

(Hint: If you are soldering headers to the board, the GND point can be quite tricky because it is not drilled all the way through. There is, however, a via marked “GND3” closeby you can alternatively use.)

Press on the console to interrupt U-Boot autobooting.
Logon through serial by pressing and using: admin/1234.

UART Boot

Temporarily connect the left side of R225 to GND, to get into UART mode.
Be careful, if you connect too long you can stuck in this mode and your device is really hard bricked!
You should see a message similar to this:

ROM VER: 1.1.4 CFG 04 EEPROM Data OK UART

Upload the U-Boot Image via:

cat u-boot.asc > /dev/ttyUSB0

Now you can for example install OpenWrt 15 if you have working tftp server at address 192.168.1.2 :
(Newer versions won´t work, at least not 18 and 19, but you can upgrade in a next step)

VR9 # tftp 0x80800000 openwrt-15.05.1-lantiq-xrx200-TDW8970-sysupgrade.image VR9 # sf erase 0x20000 0x7a0000 VR9 # sf write 0x80800000 0x20000 0x400004

Or reflash even the bootloader with the newest stock firmware:

VR9 # tftp 0x80800000 TD-W8970Bv1_0.6.0_2.8_up_boot(140930)_2014-09-30_14.44.25.bin VR9 # sf erase 0x00000 0x7a0000 VR9 # sf write 0x80800000 0x00000 0x7c0000

But before you have to strip off the 512 Byte header of the Orginal Firmware using a Hex Editor or dd.

→ port.jtag general information about the JTAG port, JTAG cable, etc.

How to connect to the JTAG Port of this specific device:
FIXMEInsert photo of PCB with markings for JTAG port

:!: Tested only on Lantiq (Rev 1), this MOD could damage your device.

This procedure allows you to replace the SPI flash with a bigger one, this mod requires the a different version of u-boot, you also must have a backup of the calibration partition. It also requires good skills in soldering and desoldering SMD components.

You will need:

Steps to replace the rom:

  1. Remove the flash chip, use the clamp or the socket to extract data if not done previously

  2. Clean the pads

  3. Use the clamp or the socket to write the modified u-boot on address 0x0, caldata partition on address 0xFD0000. You can also boot from serial the modified uboot and flash from there.

  4. Solder the new flash, be sure on pin orientation. Clean the pads. and check for continuity.

  5. Power on the router, you should be able to see the full flash.

  6. At this point you can install a standard OpenWrt image, but note that the calibration partition has been moved so you need a modified version of OpenWrt or LEDE to be able to use the full flash size and to make the wireless card works propely.

TP-Link W8970 16MB Flash MODTP-Link W8970 16MB Flash MOD

New Flash layout
partition address space name filesystem function
mtd0 0x00000000-0x00020000 boot n/a U-Boot
mtd1 0x00020000-0x00160000 kernel RAM executable Kernel
mtd2 0x00160000-0x00FCE000 rootfs squashfs root
mtd3 0x00FCE000-0x00FD0000 uboot-env n/a U-Boot Env (Right now it is unused)
mtd4 0x00FD0000-0x01000000 boardconfig n/a radio settings

:!: If you want to keep using the firmware for the 8MB flash, you must write the boardconfig partition to address 0x007F0000, note that the modified U-Boot is still needed.

:!: Flash addresses 0x00FE0000 - 0x00FEFFFF are used by U-Boot to store ddr_settings, on original U-Boot the address range were 0x007E0000 - 0x007EFFFF.

Bootlog

Customized U-Boot and Lede:

ROM VER: 1.1.4 CFG 05 DDR autotuning Rev 0.3d DDR size from 0xa0000000 - 0xa3ffffff DDR check ok. start booting. U-Boot 2010.06-LANTIQ-v-2.0.40-00026-g22bd014-dirty (Jan 13 2017 - 17:24:09) CLOCK CPU 500M RAM 250M DRAM: 64 MiB Using default environment In: serial Out: serial Err: serial Net: Internal phy(GE) firmware version: 0x841d vr9 Switch16384 KiB W25Q128 at 0:3 is now current device Type "run flash_nfs" to mount root filesystem over NFS Hit any key to stop autoboot: 0 16384 KiB W25Q128 at 0:3 is now current device 16384 KiB W25Q128 at 0:3 is now current device Uncompressing . Starting kernel . [ 0.000000] Linux version 4.4.40 ([email protected]) (gcc version 5.4.0 (LEDE GCC 5.4.0 r2952-4de56ee) ) #0 Fri Jan 13 16:46:12 2017 [ 0.000000] SoC: xRX200 rev 1.2 [ 0.000000] bootconsole [early0] enabled [ 0.000000] CPU0 revision is: 00019556 (MIPS 34Kc) [ 0.000000] MIPS: machine is TDW8970 - TP-LINK TD-W8970 [ 0.000000] Determined physical RAM map: [ 0.000000] memory: 04000000 @ 00000000 (usable) [ 0.000000] Initrd not found or empty - disabling initrd [ 0.000000] Zone ranges: [ 0.000000] Normal [mem 0x0000000000000000-0x0000000003ffffff] [ 0.000000] Movable zone start for each node [ 0.000000] Early memory node ranges [ 0.000000] node FxSound Enhancer Premium Keygen [mem 0x0000000000000000-0x0000000003ffffff] [ 0.000000] Initmem setup node 0 [mem 0x0000000000000000-0x0000000003ffffff] [ 0.000000] Primary instruction cache 32kB, VIPT, 4-way, linesize 32 bytes. [ 0.000000] Primary data cache 32kB, 4-way, VIPT, cache aliases, linesize 32 bytes [ 0.000000] Built 1 zonelists in Zone order, mobility grouping on. Total pages: 16256 [ 0.000000] Kernel command line: console=ttyLTQ0,115200 [ 0.000000] PID hash table entries: 256 (order: -2, 1024 bytes) [ 0.000000] Dentry cache hash table entries: 8192 (order: 3, 32768 bytes) [ 0.000000] Inode-cache hash table entries: 4096 (order: 2, 16384 bytes) [ 0.000000] Writing ErrCtl register=000405b0 [ 0.000000] Readback ErrCtl register=000405b0 [ 0.000000] Memory: 58240K/65536K available (3819K kernel code, 161K rwdata, 1160K rodata, 1244K init, 212K bss, 7296K reserved, 0K cma-reserved) [ 0.000000] SLUB: HWalign=32, Order=0-3, MinObjects=0, CPUs=1, Nodes=1 [ 0.000000] NR_IRQS:256 [ 0.000000] Setting up vectored interrupts [ 0.000000] CPU Clock: 500MHz [ 0.000000] clocksource: MIPS: mask: 0xffffffff max_cycles: 0xffffffff, max_idle_ns: 7645041786 ns [ 0.000010] sched_clock: 32 bits at 250MHz, resolution 4ns, wraps every 8589934590ns [ 0.007856] Calibrating delay loop. 332.54 BogoMIPS (lpj=665088) [ 0.042314] pid_max: default: 32768 minimum: 301 [ 0.047153] Mount-cache hash table entries: 1024 (order: 0, 4096 bytes) [ 0.053721] Mountpoint-cache hash table entries: 1024 (order: 0, 4096 bytes) [ 0.066955] clocksource: jiffies: mask: 0xffffffff max_cycles: 0xffffffff, max_idle_ns: 7645041785100000 ns [ 0.076760] pinctrl core: initialized pinctrl subsystem [ 0.082629] NET: Registered protocol family 16 [ 0.091921] pinctrl-xway 1e100b10.pinmux: Init done [ 0.097480] dma-xway 1e104100.dma: Init done - hw rev: 7, ports: 7, channels: 28 [ 0.207727] dcdc-xrx200 1f106a00.dcdc: Core Voltage : 1016 mV [ 0.333861] PCI host bridge /[email protected]/[email protected] ranges: [ 0.354962] usbcore: registered new interface driver usbfs [ 0.360460] usbcore: registered new interface driver hub [ 0.365815] usbcore: registered new device driver usb [ 0.371335] PCI host bridge to bus 0000:00 [ 0.375334] pci_bus 0000:00: root bus resource [mem 0x1c000000-0x1cffffff] [ 0.382242] pci_bus 0000:00: root bus resource [io 0x1d800000-0x1d8fffff] [ 0.389185] pci_bus 0000:00: root bus resource [??? 0x00000000 flags 0x0] [ 0.396040] pci_bus 0000:00: No busn resource found for root bus, will use [bus 00-ff] [ 0.404107] ifx_pcie_rc_class_early_fixup: fixed pcie host bridge to pci-pci bridge [ 0.423077] pci 0000:00:00.0: BAR 8: assigned [mem 0x1c000000-0x1c0fffff] [ 0.429760] pci 0000:00:00.0: BAR 9: assigned [mem 0x1c100000-0x1c1fffff pref] [ 0.437031] pci 0000:01:00.0: BAR 0: assigned [mem 0x1c000000-0x1c01ffff 64bit] [ 0.444426] pci 0000:01:00.0: BAR 6: assigned [mem 0x1c100000-0x1c10ffff pref] [ 0.451692] pci 0000:00:00.0: PCI bridge to [bus 01] [ 0.456725] pci 0000:00:00.0: bridge window [mem 0x1c000000-0x1c0fffff] [ 0.463582] pci 0000:00:00.0: bridge window [mem 0x1c100000-0x1c1fffff pref] [ 0.470890] ifx_pcie_bios_map_irq port 0 dev 0000:00:00.0 slot 0 pin 1 [ 0.477544] ifx_pcie_bios_map_irq dev 0000:00:00.0 irq 144 assigned [ 0.483896] ifx_pcie_bios_map_irq port 0 dev 0000:01:00.0 slot 0 pin 1 [ 0.490563] ifx_pcie_bios_map_irq dev 0000:01:00.0 irq 144 assigned [ 0.497936] clocksource: Switched to clocksource MIPS [ 0.504580] NET: Registered protocol family 2 [ 0.509778] TCP established hash table entries: 1024 (order: 0, 4096 bytes) [ 0.516673] TCP bind hash table entries: 1024 (order: 0, 4096 bytes) [ 0.523048] TCP: Hash tables configured (established 1024 bind 1024) [ 0.529564] UDP hash table entries: 256 (order: 0, 4096 bytes) [ 0.535402] UDP-Lite hash table entries: 256 (order: 0, 4096 bytes) [ 0.542079] NET: Registered protocol family 1 [ 0.553465] gptu: totally 6 16-bit timers/counters [ 0.558332] gptu: misc_register on minor 63 [ 0.562404] gptu: succeeded to request irq 126 [ 0.566889] gptu: succeeded to request irq 127 [ 0.571402] gptu: succeeded to request irq 128 [ 0.575916] gptu: succeeded to request irq 129 [ 0.580430] gptu: succeeded to request irq 130 [ 0.584943] gptu: succeeded to request irq 131 [ 0.589822] phy-xrx200 gphy-xrx200: requesting lantiq/vr9_phy11g_a2x.bin [ 0.597194] phy-xrx200 gphy-xrx200: booting GPHY0 firmware at 3980000 [ 0.603528] phy-xrx200 gphy-xrx200: booting GPHY1 firmware at 3980000 [ 0.710263] No VPEs reserved for AP/SP, not initialize VPE loader [ 0.710263] Pass maxvpes=<n> argument as kernel argument [ 0.721632] No TCs reserved for AP/SP, not initializing RTLX. [ 0.721632] Pass maxtcs=<n> argument as kernel argument [ 0.733611] futex hash table entries: 256 (order: -1, 3072 bytes) [ 0.739710] Crashlog allocated RAM at address 0x3f00000 [ 0.765107] squashfs: version 4.0 (2009/01/31) Phillip Lougher [ 0.770858] jffs2: version 2.2 (NAND) (SUMMARY) (LZMA) (RTIME) (CMODE_PRIORITY) (c) 2001-2006 Red Hat, Inc. [ 0.785042] io scheduler noop registered [ 0.788869] io scheduler deadline registered (default) [ 0.794736] 1e100c00.serial: ttyLTQ0 at MMIO 0x1e100c00 (irq = 112, base_baud = 0) is a lantiq,asc [ 0.803633] console [ttyLTQ0] enabled [ 0.803633] console [ttyLTQ0] enabled [ 0.810955] bootconsole [early0] disabled [ 0.810955] bootconsole [early0] disabled [ 0.824383] m25p80 spi0.4: w25q128 (16384 Kbytes) [ 0.827718] 4 ofpart partitions found on MTD device spi0.4 [ 0.833136] Creating 4 MTD partitions on "spi0.4": [ 0.837944] 0x000000000000-0x000000020000 : "u-boot" [ 0.844872] 0x000000020000-0x000000fce000 : "firmware" [ 0.970694] random: nonblocking pool is initialized [ 1.178538] 2 tplink-fw partitions found on MTD device firmware [ 1.183052] 0x000000020000-0x0000001bb9c4 : "kernel" [ 1.189750] 0x0000001bb9c4-0x000000fce000 : "rootfs" [ 1.195537] mtd: device 3 (rootfs) set to be root filesystem [ 1.200393] 1 squashfs-split partitions found on MTD device rootfs [ 1.205991] 0x0000008b0000-0x000000fc0000 : "rootfs_data" [ 1.213176] 0x000000fce000-0x000000fd0000 : "uboot-env" [ 1.219243] 0x000000fd0000-0x000001000000 : "boardconfig" [ 1.225352] spi-lantiq 1e100800.spi: Lantiq SPI controller (TXFS 8, RXFS 8, DMA 32) [ 1.334775] libphy: lantiq,xrx200-mdio: probed [ 1.410669] eth0: attached PHY [Lantiq XWAY PEF7071] (phy_addr=0:00, irq=-1) [ 1.478644] eth0: attached PHY [Lantiq XWAY PEF7071] (phy_addr=0:05, irq=-1) [ 1.546637] eth0: attached PHY [Lantiq XWAY VR9 GPHY 11G v1.4] (phy_addr=0:11, irq=-1) [ 1.614627] eth0: attached PHY [Lantiq XWAY VR9 GPHY 11G v1.4] (phy_addr=0:13, irq=-1) [ 1.722999] ltq-cputemp [email protected]: Current CPU die temperature: 41.5 °C [ 1.728579] wdt 1f8803f0.watchdog: Init done [ 1.735541] NET: Registered protocol family 10 [ 1.744563] NET: Registered protocol family 17 [ 1.747720] bridge: automatic filtering via arp/ip/ip6tables has been deprecated. Update your scripts to load br_netfilter if you need this. [ 1.760231] 8021q: 802.1Q VLAN Support v1.8 [ 1.774879] VFS: Mounted root (squashfs filesystem) readonly on device 31:3. [ 1.784709] Freeing unused kernel memory: 1244K (80509000 - 80640000) [ 2.965544] init: Console is alive [ 2.967839] init: - watchdog - [ 4.671507] eth0: port 4 got link [ 5.295478] exFAT: Version 1.2.9 [ 5.338028] SCSI subsystem initialized [ 5.349238] dwc2 1e101000.ifxhcd: requested GPIO 495 [ 6.210150] dwc2 1e101000.ifxhcd: DWC OTG Controller [ 6.213728] dwc2 1e101000.ifxhcd: new USB bus registered, assigned bus number 1 [ 6.221076] dwc2 1e101000.ifxhcd: irq 62, io mem 0x00000000 [ 6.226598] dwc2 1e101000.ifxhcd: Hardware does not support descriptor DMA mode - [ 6.234028] dwc2 1e101000.ifxhcd: falling back to buffer DMA mode. [ 6.241534] hub 1-0:1.0: USB hub found [ 6.244458] hub 1-0:1.0: 1 port detected [ 7.106134] dwc2 1e106000.ifxhcd: DWC OTG Controller [ 7.109727] dwc2 1e106000.ifxhcd: new USB bus registered, assigned bus number 2 [ 7.117040] dwc2 1e106000.ifxhcd: irq 91, io mem 0x00000000 [ 7.122567] dwc2 1e106000.ifxhcd: Hardware does not support descriptor DMA mode - [ 7.130010] dwc2 1e106000.ifxhcd: falling back to buffer DMA mode. [ 7.137473] hub 2-0:1.0: USB hub found [ 7.140486] hub 2-0:1.0: 1 port detected [ 7.149237] usbcore: registered new interface driver usb-storage [ 7.156951] init: - preinit - Press the [f] key and hit [enter] to enter failsafe mode Press the [1], [2], [3] or [4] key and hit [enter] Format Factory 4.6.2.0 License Key - Crack Key For U select the debug level [ 11.227079] mount_root: loading kmods from internal overlay [ 12.279330] jffs2: notice: (413) jffs2_build_xattr_subsystem: complete building xattr subsystem, 0 of xdatum (0 unchecked, 0 orphan) and 0 of xref (0 dead, 0 orphan) found. [ 12.294238] block: attempting to load /tmp/jffs_cfg/upper/etc/config/fstab [ 12.308511] block: extroot: not configured [ 12.365829] jffs2: notice: (410) jffs2_build_xattr_subsystem: complete building xattr subsystem, 0 of xdatum (0 unchecked, 0 orphan) and 0 of xref (0 dead, 0 orphan) found. [ 12.382213] mount_root: loading kmods from internal overlay [ 12.907141] block: attempting to load /tmp/jffs_cfg/upper/etc/config/fstab [ 12.918439] block: extroot: not configured [ 12.922679] mount_root: switching to jffs2 overlay [ 13.214386] urandom-seed: Seeding with /etc/urandom.seed [ 13.346180] procd: - early - [ 13.347790] procd: - watchdog - [ 13.794064] eth0: port 4 lost link [ 14.105905] procd: - ubus - [ 14.500141] procd: - init - Please press Enter to activate this console. [ 15.157376] IFXOS, Version 1.5.19 (c) Copyright 2009, Lantiq Deutschland GmbH [ 15.173169] NET: Registered protocol family 8 [ 15.176141] NET: Registered protocol family 20 [ 15.190824] ntfs: driver 2.1.32 [Flags: R/O MODULE]. [ 15.223126] PPP generic driver version 2.4.2 [ 15.247702] ip6_tables: (C) 2000-2006 Netfilter Core Team [ 15.271659] Netfilter messages via NETLINK v0.30. [ 15.289063] ip_set: protocol 6 [ 15.402405] Lantiq (VRX) DSL CPE MEI driver, version 1.5.17.6, (c) 2007-2015 Lantiq Beteiligungs-GmbH & Co. KG Lantiq CPE API Driver version: DSL CPE API V4.17.18.6 [ 15.466800] [ 15.466800] Predefined debug level: 3 [ 15.486582] u32 classifier [ 15.487836] input device check on [ 15.491534] Actions configured [ 15.498130] Mirror/redirect action on [ 15.553055] Loading modules backported from Linux version wt-2016-10-03-1-g6fcb1a6 [ 15.559248] Backport generated by backports.git backports-20160324-9-g0e38f5c [ 15.586095] ip_tables: (C) 2000-2006 Netfilter Core Team [ 15.614503] Infineon Technologies DEU driver version 2.0.0 [ 15.642588] IFX DEU DES initialized (multiblock). [ 15.646967] IFX DEU AES initialized (multiblock). [ 15.651040] IFX DEU ARC4 initialized (multiblock). [ 15.655652] IFX DEU SHA1 initialized. [ 15.659246] IFX DEU MD5 initialized. [ 15.662880] IFX DEU SHA1_HMAC initialized. [ 15.666908] IFX DEU MD5_HMAC initialized. [ 15.683098] nf_conntrack version 0.5.0 (929 buckets, 3716 max) [ 15.715825] NET: Registered protocol family 24 [ 15.731408] usbcore: registered new interface driver usbserial [ 15.736022] usbcore: registered new interface driver usbserial_generic [ 15.742543] usbserial: USB Serial support registered for generic [ 15.797786] xt_time: kernel timezone is -0000 [ 15.803656] usbcore: registered new interface driver cdc_ether [ 15.841077] usbcore: registered new interface driver ftdi_sio [ 15.845630] usbserial: USB Serial support registered for FTDI USB Serial Device [ 15.914213] usbcore: registered new interface driver rndis_host [ 15.969406] PCI: Enabling device 0000:00:00.0 (0000 -> 0002) [ 15.973762] PCI: Enabling device 0000:01:00.0 (0000 -> 0002) [ 15.989482] ath: phy0: disabling 5GHz band [ 16.009156] ieee80211 phy0: Atheros AR9300 Rev:3 mem=0xbc000000, irq=144 [ 23.316546] PTM 1.0.27 PTM (E1) firmware version 0.30 [ 23.320482] ifxmips_ptm: PTM init succeed [ 29.828934] IPv6: ADDRCONF(NETDEV_UP): eth0: link is not ready [ 29.860143] device eth0.1 entered promiscuous mode [ 29.863569] device eth0 entered promiscuous mode [ 29.879400] IPv6: ADDRCONF(NETDEV_UP): br-lan: link is not ready [ 30.001503] IPv6: ADDRCONF(NETDEV_UP): ptm0: link is not ready [ 30.114214] eth0: port 4 got link [ 30.116284] IPv6: ADDRCONF(NETDEV_CHANGE): eth0: link becomes ready [ 30.146180] br-lan: port 1(eth0.1) entered forwarding state [ 30.150451] br-lan: port 1(eth0.1) entered forwarding state [ 30.218093] IPv6: ADDRCONF(NETDEV_CHANGE): br-lan: link becomes ready [ 32.153972] br-lan: port 1(eth0.1) entered forwarding state

Work-in-progress

The XWAY VRX286 SoC features an internal configurable Infineon Gigabit Ethernet switch that connects all the physical Ethernet ports together.

As of yet (trunk: 38701) no support for this switch exists on OpenWrt.

However a GPL source code exists for the switch under the name “” for the kernel module and “” for the user-space configuration tool. The code can be found from links below:

On the OEM firmware the driver initialization looks like this:

IFX SWITCH API, Version 1.1.7.2 SWAPI: Registered character device [switch_api] with major no [81] Switch API: PCE MicroCode loaded !! Init IFX_ETHSW_Switch_API_procModule successfully.

And the Aiseesoft FoneLab Crack tool can be found at:

~ # switch_utility Switch Utility Version : v1.1.7.

OEM Default settings

These are the switch_utility settings on the OEM firmware right after booting up.

~ # brctl show bridge name bridge id STP enabled interfaces br0 8000.f81a67d8b108 no eth0.2 eth0.3 waterfox 32 bit - Free Activators eth0.4 eth0.5 ath0 nas0_1 ~ # switch_utility CfgGet MAC_Table Age Timer = 3 VLAN_Aware = 1 Max Packet Len = 1536 Max Packet Len = 0 Pause MAC Mode = 0 Pause MAC Src = 00:d0:8f:00:01:00 ~ # switch_utility PortCfgGet 4 Port Id = 4 Port Enable = 1 Unicast Unkown Drop = 0 Multicast Unkown Drop = 0 Reserved Packet Drop = 0 Broadcast Packet Drop = 0 Aging = 0 Learning Mac Port Lock = 0 Learning Limit = 255 Port Monitor = 0 Flow Control = 0 ~ # switch_utility PortLinkCfgGet 4 Port Id = 4 Force Port Duplex Mode. = 0 Port Duplex Status. = 0 Force Link Speed. = 0 Port link speed status = 1000 Force Link = 0 Force link status = 0 Selected interface mode = 0 Select if MAC or PHY mode = 1 Interface clock Mode = 0 ~ # switch_utility PortRedirectGet 4 Port Id = 4 Port Redirect Egress = 0 Port Redirect Ingress = 0 ~ # switch_utility MAC_TableEntryRead ERROR: (VID does not exists) drivers/net/ifxmips_switch_api/ifx_ethsw_flow_api.c:IFX_FLOW_VLAN_IdGet:1711 -------------------------------------------------------------- MAC Address Format Factory 4.6.2.0 License Key  - Crack Key For U

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