[Federal Register Volume 69, Number 191 (Monday, October 4, 2004)]
[Proposed Rules]
[Pages 59306-59474]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 04-21488]



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Part II





Department of Labor





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Occupational Safety and Health Administration



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29 CFR Parts 1910, 1915, 1917, 1918, and 1926



Occupational Exposure to Hexavalent Chromium; Proposed Rule

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / 
Proposed Rules

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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.

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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/
m<SUP>3</SUP>) 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

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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 the 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/m<SUP>3</SUP>) 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/m<SUP>3</SUP>)? 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/m<SUP>3</SUP>) 
leads to the same risk as an equivalent cumulative exposure achieved by 
longer duration exposure to

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lower Cr(VI) exposure (e.g, exposed 45 years to 1 [mu]g/m<SUP>3</SUP>). 
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 
scenarios 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

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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.
    d. 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 construction 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

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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/
m<SUP>3</SUP>. 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/m<SUP>3</SUP>) 
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 
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 desired.'' 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 m<SUP>3</SUP> air in the 
workplace (1 mg/10 m<SUP>3</SUP> CrO<INF>3</INF>) as a ceiling 
concentration, which corresponds to a concentration of 52 [mu]g/
m<SUP>3</SUP> Cr(VI). A separate rule promulgated for the construction 
industry set an eight-hour time-weighted-average PEL of 1 mg/10 
m<SUP>3</SUP> CrO<INF>3</INF>, also equivalent to 52 [mu]g/
m<SUP>3</SUP> 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/m<SUP>3</SUP> for 
chromic acid and chromates as Cr<INF>2</INF>O<SUP>3</SUP> (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/m<SUP>3</SUP>, 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/
m<SUP>3</SUP>), lead chromate (12 [mu]g/m<SUP>3</SUP>), strontium 
chromate (0.5 [mu]g/m<SUP>3</SUP>), and zinc chromates (10 [mu]g/
m<SUP>3</SUP>), and generic TLVs for water soluble (50 [mu]g/
m<SUP>3</SUP>) and insoluble (10 [mu]g/m<SUP>3</SUP>) 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/m<SUP>3</SUP> 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 
(FeCr<INF>2</INF>O<INF>4</INF>). 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 (CrO<INF>2</INF>) 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

    The studies 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 
(CrO<INF>4</INF>)<SUP>2-</SUP>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)/m<SUP>3</SUP> as potassium 
dichromate for 2-6 hours. Following exposure to Cr(VI), the ratio of 
blood chromium/lung chromium was 1.44<plus-minus>0.30 at 0.5 hours, 
0.81<plus-minus>0.10 at 18 hours, 0.85<plus-minus>0.20 at 48 hours, and 
0.96<plus-minus>0.22 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 <SUP>51</SUP>chromium-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 <SUP>51</SUP>chromium 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)/m<SUP>3</SUP> 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)/m<SUP>3</SUP> 
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 (SrCrO<INF>4</INF>)), water-borne expoxy (30% 
SrCrO<INF>4</INF>) and polyurethane (20% SrCrO<INF>4</INF>) (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 known. 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)/cm<SUP>2</SUP>/hour for a 0.01 molar 
solution, 6.4 [mu]g Cr(VI)/cm<SUP>2</SUP>/hour for a 0.1 molar 
solution, and 10 [mu]g Cr(VI)/cm<SUP>2</SUP>/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 <SUP>51</SUP> 
chromium labeled Cr(VI) compounds (Ex. 35-81). In this study 
radiolabeled sodium chromate solution was dermally applied to guinea 
pigs and <SUP>51</SUP>Cr 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 <SUP>51</SUP>chromium 
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 <SUP>51</SUP>chromium 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 orally 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 excretion 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 (CrO<INF>4</INF>)<SUP>2-</SUP> 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 by 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
                                   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          result of using     chromium exposure
                                                       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-                       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
                                                                           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                       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 mgCrO<INF>3</INF>/m<SUP>3</SUP>-yr; 0.0015-0.0089 
mgCrO<INF>3</INF>/m<SUP>3</SUP>-yr; 0.009-0.0769 mgCrO<INF>3</INF>/
m<SUP>3</SUP>-yr; and 0.077-5.25 mgCrO<INF>3</INF>/m<SUP>3</SUP>-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 workers. 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<5.25 mg CrO<INF>3</INF>/m<SUP>3</SUP>-
years) for both white and nonwhite, based on either the Maryland or the 
Baltimore mortality rates. The authors did not find ``that the 
inclusion of short-term workers had a significant impact on the 
results, especially if Baltimore rates are used in the SMR 
calculations'' (Ex. 31-18-15-1, p. 28).
    Analysis of length of employment and ``peak'' (i.e., highest 
recorded mean annual) exposure level to Cr(VI) was conducted. Exponent 
reported that approximately 50% of the cohort had ``only very low'' 
peak exposure levels (<07.2 [mu]g CrO<INF>3</INF>/m<SUP>3</SUP> or 
approximately 3.6 [mu]g/m<SUP>3</SUP> of Cr(VI)). The ``majority'' of 
the short-term workers had peak exposures of <100 [mu]g 
CrO<INF>3</INF>/m<SUP>3</SUP>. There were five peak Cr(VI) exposure 
levels (<7.2 [mu]g CrO<INF>3</INF>/m<SUP>3</SUP>; 7.2<19.3 [mu]g 
CrO<INF>3</INF>/m<SUP>3</SUP>; 19.3<48.0 [mu]g CrO<INF>3</INF>/
m<SUP>3</SUP>; 48.0<105 [mu]g CrO<INF>3</INF>/m<SUP>3</SUP>; 105<182 
[mu]g CrO<INF>3</INF>/m<SUP>3</SUP>; and 182<806 [mu]g CrO<INF>3</INF>/
m<SUP>3</SUP>) included in the analyses. Overall, the lung cancer SMRs 
for the entire cohort grouped according to the six ``peak'' exposure 
categories were slightly higher using Maryland reference rates compared 
to Baltimore reference rates.
    The Exponent analysis of workers who were ever exposed above the 
current PEL versus those never exposed above the current PEL produced 
slightly higher SMRs for those ever exposed, with the SMRs higher using 
the Maryland standard rather than the Baltimore standard. The only 
statistically significant result was for all lung cancer deaths 
combined.
    Assessment was made of the potential impact of smoking on the lung 
cancer SMRs since Gibb did not adjust the SMRs for smoking. Exponent 
stated that the smoking-adjusted SMRs are more appropriate for use in 
the risk assessment than the unadjusted SMRs. It should be noted that 
smoking adjusted SMRs could not be calculated using Baltimore reference 
rates. As noted by the authors, the smoking adjusted SMRs produced 
using Maryland reference rates are, by exposure, ``reasonably 
consistent with the Baltimore-referenced SMRs'' (Ex. 31-18-15-1, p. 
41).
    Gibb et al. included workers regardless of duration of employment, 
and the cohort was heavily weighted by those individuals who worked 
less than 90 days. In an attempt to clarify this issue, Exponent 
produced analyses of short-term workers, particularly with respect to 
exposures. Exponent redefined short-term workers as those who worked 
less than one year, to be consistent with the definition used in other 
studies of chromate producers. OSHA finds this reanalysis excluding 
short-term workers to be useful. It suggests that including cohort 
workers employed less than one year did not substantively alter the 
conclusions of Gibb et al. with regard to the association between 
Cr(VI) exposure and lung cancer mortality. It should be noted that in 
the Hayes study of the Baltimore plant, the cohort is defined as anyone 
who worked 90 days or more.
    Hayes et al. used Baltimore mortality rates while Gibb et al. used 
U.S. mortality rates to calculate expectations for overall SMRs. To 
calculate

[[Page 59323]]

expectations for the analysis of lung cancer mortality and exposure, 
Gibb et al. used Maryland state mortality rates. The SMR analyses 
provided by Exponent using both Maryland and Baltimore rates are 
useful. The data showed that using Baltimore rates raised the expected 
number lung cancer deaths and, thus, lowered the SMRs. However, there 
remained a statistically significant increase in lung cancer risk among 
the exposed workers and a significant upward trend with cumulative 
Cr(VI) exposure. The comparison group should be as similar as possible 
with respect to all other factors that may be related to the disease 
except the determinant under study. Since the largest portion of the 
cohort (45%) died in the city of Baltimore, and even those whose deaths 
occurred outside of Baltimore (16%) most likely lived in proximity to 
the city, the use of Baltimore mortality rates as an external reference 
population is preferable.
    Gibb's selection of the cut points for the exposure quartiles is 
accomplished by dividing the workers in the cohort into four equal 
groups based on their cumulative exposure at the end of their working 
history. Using the same method but excluding the short-term workers 
would have resulted in slightly different cumulative exposure 
quartiles. Exponent expressed a preference for a six-tiered exposure 
grouping. The impact of using different exposure groupings is further 
discussed in preamble section VII.C of the preliminary quantitative 
risk assessment.
    The exposure matrix of Gibb et al. does utilize a unique set of 
industrial hygiene data. Over 70,000 samples taken to characterize the 
``typical/usual'' working environment is more extensive industrial 
hygiene data then is commonly available for most exposure assessments. 
However, there are several unresolved issues regarding the exposure 
assessment, including the impact of the different industrial hygiene 
sampling techniques used over the sampling time frame, how the use of 
different sampling techniques was taken into account in developing the 
exposure assessment and the use of area vs. personal samples.
    Exponent and the Chrome Coalition also suggested that the SMRs 
should have been adjusted for smoking. According to Exponent, smoking 
adjusted SMRs based upon the Maryland mortality rates produced SMRs 
similar to the SMRs obtained using Baltimore mortality rates (Ex. 31-
18-15-1). The accuracy of the smoking data is still questionable since 
it represents information obtained at the time of hire. Hayes 
abstracted the smoking data from the plant medical records, but ``found 
it not to be of sufficient quality to allow analysis.'' One advantage 
to using the Baltimore mortality data may be to better control for the 
potential confounding of smoking.
    Despite the potential methodological limitations of the Gibb study, 
this is one of the better cohort mortality studies of workers in the 
chromium production industry. The quality of the available industrial 
hygiene data and its characterization as ``typical/usual'' makes the 
Gibb study useful for risk assessment.
    b. Cohort Studies of the Painesville Facility. The Ohio Department 
of Health conducted epidemiological and environmental studies at a 
plant in Painesville that manufactured sodium bichromate from chromite 
ore. Mancuso and Hueper (Ex. 7-12) reported an excess of respiratory 
cancer among chromate workers when compared to the county in which the 
plant was located. Among the 33 deaths in males who had worked at the 
plant for a minimum of one year, 18.2% were from respiratory cancer. In 
contrast, the expected frequency of respiratory cancer among males in 
the county in which the plant was located was 1.2%. Although the 
authors did not include a formal statistical comparison, the lung 
cancer mortality rate among the exposed workers would be significantly 
greater than the county rate.
    Mancuso (Ex. 7-11) updated his 1951 study of 332 chromate 
production workers employed during the period 1931-1937. Age adjusted 
mortality rates were calculated by the direct method using the 
distribution of person years by age group for the total chromate 
population as the standard. Vital status follow-up through 1974 found 
173 deaths. Of the 66 cancer deaths, 41 (62.1%) were lung cancers. A 
cluster of lung cancer deaths was observed in workers with 27-36 years 
since first employment.
    Mancuso used industrial hygiene data collected in 1949 to calculate 
weighted average exposures to water-soluble (presumed to be Cr(VI)), 
insoluble (presumed to be principally Cr(III)) and total chromium (Ex. 
7-98). The age-adjusted lung cancer death rate increased from 144.6 
(based upon two deaths) to 649.6 (based upon 14 deaths) per 100,000 in 
five exposure categories ranging from a low of 0.25-0.49 to a high of 
4.0+ mg/m<SUP>3</SUP>-years for the insoluble Cr(III) exposures. For 
exposure to soluble Cr(VI), the age adjusted lung cancer rates ranged 
from 80.2 (based upon three deaths) to 998.7 (based upon 12 deaths) in 
five exposure categories ranging from <0.25 to 2.0+ mg/m<SUP>3</SUP>-
years. For total chromium, the age-adjusted death rates ranged from 
225.7 (based upon three deaths) to 741.5 (based upon 16 deaths) for 
exposures ranging from 0.50-0.99 mg/m<SUP>3</SUP>-years to 6.0+ mg/
m<SUP>3</SUP>-years.
    Age-adjusted lung cancer death rates also were calculated by 
classifying workers by the levels of insoluble Cr(III) and total 
chromium exposure. From the data presented, it appears that for a fixed 
level of insoluble Cr(III), the lung cancer risk appears to increase as 
the total chromium increases (Ex. 7-11).
    Mancuso (Ex. 23) updated the 1975 study. As of December 31, 1993, 
283 (85%) cohort members had died and 49 could not be found. Of the 102 
cancer deaths, 66 were lung cancers. The age-adjusted lung cancer death 
rate per 100,000 ranged from 187.9 (based upon four deaths) to 1,254.1 
(based upon 15 deaths) for insoluble Cr(III) exposure categories 
ranging from 0.25-0.49 to 4.00-5.00 mg/m<SUP>3</SUP> years. For the 
highest exposure to insoluble Cr(III) (6.00+ mg/m<SUP>3</SUP> years) 
the age-adjusted lung cancer death rate per 100,000 fell slightly to 
1,045.5 based upon seven deaths.
    The age-adjusted lung cancer death rate per 100,000 ranged from 
99.7 (based upon five deaths) to 2,848.3 (based upon two deaths) for 
soluble Cr(VI) exposure categories ranging from <0.25 to 4.00+ mg/
m<SUP>3</SUP> years. For total chromium, the age-adjusted lung cancer 
death rate per 100,000 ranged from 64.7 (based upon two deaths) to 
1,106.7 (based upon 21 deaths) for exposure categories ranging from 
<0.50 to 6.00+ mg/m<SUP>3</SUP> years.
    To investigate whether the increase in the lung cancer death rate 
was due to one form of chromium compound (presumed insoluble Cr(III) or 
soluble Cr(VI)), age-adjusted lung cancer mortality rates were 
calculated by classifying workers by the levels of exposure to 
insoluble Cr(III) and total chromium. For a fixed level of insoluble 
Cr(III), the lung cancer rate appears to increase as the total chromium 
increases for each of the six total chromium exposure categories, 
except for the 1.00-1.99 mg/m<SUP>3</SUP>-years category. For the fixed 
exposure categories for total chromium, increasing exposures to levels 
of insoluble Cr(III) showed an increased age-adjusted death rate from 
lung cancer in three of the six total chromium exposure categories.
    For a fixed level of soluble Cr(VI), the lung cancer death rate 
increased as total chromium categories of exposure increased for three 
of the six gradients of soluble Cr(VI). For the fixed exposure 
categories of total chromium, the increasing exposure to specific 
levels of

[[Page 59324]]

soluble Cr(VI) led to an increase in two of the six total chromium 
exposure categories. Mancuso concluded that the relationship of lung 
cancer is not confined solely to either soluble or insoluble chromium. 
Unfortunately, it is difficult to attribute these findings specifically 
to Cr(III) [as insoluble chromium] and Cr(VI) [as soluble chromium] 
since it is likely that some slightly soluble and insoluble Cr(VI) as 
well as Cr(III) contributed to the insoluble chromium measurement.
    Luippold et al. conducted a retrospective cohort study of 493 
former employees of the chromate production plant in Painesville, Ohio 
(Ex. 31-18-4). This Painesville cohort does not overlap with the 
Mancuso cohort and is defined as employees hired beginning in 1940 who 
worked for a minimum of one year at Painesville and did not work at any 
other facility owned by the same company that used or produced Cr(VI). 
An exception to the last criterion was the inclusion of workers who 
subsequently were employed at a company plant in North Carolina (number 
not provided). Four cohort members were identified as female. The 
cohort was followed for the period January 1, 1941 through December 31, 
1997. Thirty-two percent of the cohort worked for 10 or more years.
    Information on potential confounders was limited. Smoking status 
(yes/no) was available for only 35% of the cohort from surveys 
administered between 1960 and 1965 or from employee medical files. For 
those employees where smoking data were available, 78% were smokers 
(responded yes on at least one survey or were identified as smokers 
from the medical file). Information on race also was limited, the death 
certificate being the primary source of information.
    Results of the vital status follow-up were: 303 deaths; 132 
presumed alive and 47 vital status unknown. Deaths were coded to the 
9th revision of the International Classification of Diseases. Cause of 
death could not be located for two decedents. For five decedents the 
cause of death was only available from data collected by Mancuso and 
was recoded from the 7th to the 9th revision of the ICD. There were no 
lung cancer deaths among the five recoded deaths.
    SMRs were calculated based upon two reference populations: the U.S. 
(white males) and the state of Ohio (white males). Lung cancer SMRs 
stratified by year of hire, duration of exposure, time since first 
employment and cumulative exposure group also were calculated.
    Proctor et al. analyzed airborne Cr(VI) levels throughout the 
facility for the years 1943 to 1971 (the plant closed April 1972) from 
800 area air sampling measurements from 21 industrial hygiene surveys 
(Ex. 35-61). A job exposure matrix (JEM) was constructed for 22 
exposure areas for each month of plant operation. Gaps in the matrix 
were completed by computing the arithmetic mean concentration from area 
sampling data, averaged by exposure area over three time periods (1940-
1949; 1950-1959 and 1960-1971) which coincided with process changes at 
the plant (Ex. 31-18-1).
    The production of water-soluble sodium chromate was the primary 
operation at the Painesville plant. It involved a high lime roasting 
process that produced a water insoluble Cr(VI) residue (calcium 
chromate) as byproduct that was transported in open conveyors and 
likely contributed to worker exposure until the conveyors were covered 
during plant renovations in 1949. The average airborne soluble Cr(VI) 
from industrial hygiene surveys in 1943 and 1948 was 0.72 mg/m \3\ with 
considerable variability among departments. During these surveys, the 
authors believe the reported levels may have underestimated total 
Cr(VI) exposure by 20 percent or less for some workers due to the 
presence of insoluble Cr(VI) dust.
    Reductions in Cr(VI) levels over time coincided with improvements 
in the chromate production process. Industrial hygiene surveys over the 
period from 1957 to 1964 revealed average Cr(VI) levels of 270 [mu]g/
m\3\. Another series of plant renovations in the early 1960s lowered 
average Cr(VI) levels to 39 [mu]g/m\3\ over the period from 1965 to 
1972. The highest Cr(VI) concentrations generally occurred in the 
shipping, lime and ash, and filtering operations while the locker 
rooms, laboratory, maintenance shop and outdoor raw liquor storage 
areas had the lowest Cr(VI) levels.
    The average cumulative Cr(VI) exposure (mg/m \3\-yrs) for the 
cohort was 1.58 mg/m \3\-yrs and ranged from 0.006 to 27.8 mg/m \3\-
yrs. For those who died from lung cancer, the average Cr(VI) exposure 
was 3.28 mg/m \3\-yrs and ranged from 0.06 to 27.8 mg/m \3\-yrs. 
According to the authors, 60% of the cohort accumulated an estimated 
Cr(VI) exposure of 1.00 mg/m \3\-yrs or less.
    Sixty-three per cent of the study cohort was reported as deceased 
at the end of the follow-up period (December 31, 1997). There was a 
statistically significant increase for the all causes of death category 
based on both the national and Ohio state standard mortality rates 
(national: O=303; E=225.6; SMR=134; 95% CI: 120-150; state: O=303; 
E=235; SMR=129; 95% CI: 115-144). Fifty-three of the 90 cancer deaths 
were cancers of the respiratory system with 51 coded as lung cancer. 
The SMR for lung cancer is statistically significant using both 
reference populations (national O=51; E=19; SMR 268; 95% CI: 200-352; 
state O=51; E=21.2; SMR 241; 95% CI: 180-317).
    SMRs also were calculated by year of hire, duration of employment, 
time since first employment and cumulative Cr(VI) exposure, mg/m \3\-
years. The highest lung cancer SMRs were for those hired during the 
earliest time periods. For the period 1940-1949, the lung cancer SMR 
was 326 (O=30; E=9.2; 95% CI: 220-465); for 1950-1959, the lung cancer 
SMR was 275 (O=15; E=5.5; 95% CI: 154-454). For the period 1960-1971, 
the lung cancer SMR was just under 100 based upon six deaths with 6.5 
expected.
    Lung cancer SMRs based upon duration of employment (years) 
increased as duration of employment increased. For those with one to 
four years of employment, the lung cancer SMR was 137 based upon nine 
deaths (E=6.6; 95% CI: 62-260); for five to nine years of employment, 
the lung cancer SMR was 160 (O=8; E=5.0; 95% CI: 69-314). For those 
with 10-19 years of employment, the lung cancer SMR was 169 (O=7; 
E=4.1; 95% CI: 68-349) and for those with 20 or more years of 
employment, the lung cancer SMR was 497 (O=27; E=5.4; 95% CI: 328-723).
    Analyses of cumulative Cr(VI) exposure found the lung cancer SMR 
(based upon the Ohio standard) in the highest exposure group (2.70-
27.80 mg/m \3\-yrs) was 463 (O=20; E=4.3; 95% CI: 183-398). In the 
1.05-2.69 mg/m \3\-yrs cumulative exposure group, the lung cancer SMR 
was 365 based upon 16 deaths (E=4.4; 95% CI: 208-592). For the 
cumulative exposure groups 0.49-1.04, 0.20-0.48 and 0.00-0.19, the lung 
cancer SMRs were 91 (O=4; E=4.4; 95% CI: 25-234; 184 (O=8; E=4.4; 95% 
CI: 79-362) and 67 (O=3; E=4.5; 95% CI: 14-196). A test for trend 
showed a strong relationship between lung cancer mortality and 
cumulative Cr(VI) exposure (p=0.00002). The authors claim that the SMRs 
are also consistent with a threshold effect since there was no 
statistically significant trend for excess lung cancer mortality with 
cumulative Cr(VI) exposures less than about 1 mg/m \3\-yrs. The issue 
of whether the cumulative Cr(VI) exposure-lung cancer response is best 
represented by a threshold effect is discussed further in preamble 
section VII on the preliminary quantitative risk assessment.

[[Page 59325]]

    The Painesville cohort is small (482 employees). Excluded from the 
cohort were six employees who worked at other chromate plants after 
Painesville closed. However, exceptions were made for employees who 
subsequently worked at the company's North Carolina plant (number not 
provided) because exposure data were available from the North Carolina 
plant. Subsequent exposure to Cr(VI) by other terminated employees is 
unknown and not taken into account by the investigators. Therefore, the 
extent of the bias introduced is unknown.
    The 10% lost to follow-up (47 employees) in a cohort of this size 
is striking. Four of the forty-seven had ``substantial'' follow-up that 
ended in 1997 just before the end date of the study. For the remaining 
43, most were lost in the 1950s and 1960s (most is not defined). Since 
person-years are truncated at the time individuals are lost to follow 
up, the potential implication of lost person years could impact the 
width of the confidence intervals.
    The authors used U.S. and Ohio mortality rates for the standards to 
compute the expectations for the SMRs, stating that the use of Ohio 
rates minimizes bias that could occur from regional differences in 
mortality. It is unclear why county rates were not used to address the 
differences in regional mortality.
    c. Other Cohort Studies. The first study of cancer of the 
respiratory system in the U.S. chromate producing industry was reported 
by Machle and Gregorius (Ex. 7-2). The study involved a total of 11,000 
person-years of observation between 1933 and 1947. There were 193 
deaths; 42 were due to cancer of the respiratory system. The proportion 
of respiratory cancer deaths among chromate workers was compared with 
proportions of respiratory cancer deaths among Metropolitan Life 
Insurance industrial policyholders. A non-significant excess 
respiratory cancer among chromate production workers was found. No 
attempt was made to control for confounding factors (e.g., age). While 
some exposure data are presented, the authors state that one cannot 
associate tumor rates with tasks (and hence specific exposures) because 
of ``shifting of personnel'' and the lack of work history records.
    Baetjer reported the results of a case-control study based upon 
records of two Baltimore hospitals (Ex. 7-7). A history of working with 
chromates was determined from these hospital records and the proportion 
of lung cancer cases determined to have been exposed to chromates was 
compared with the proportion of controls exposed. Of the lung cancer 
cases, 3.4% had worked in a chromate manufacturing plant, while none of 
the controls had such a history recorded in the medical record. The 
results were statistically significant and Baetjer concluded that the 
data confirmed the conclusions reached by Machle and Gregorius that 
``the number of deaths due to cancer of the lung and bronchi is greater 
in the chromate-producing industry than would normally be expected'' 
(Ex. 7-7, p. 516).
    As a part of a larger study carried out by the U.S. Public Health 
Service, the morbidity and mortality of male workers in seven U.S. 
chromate manufacturing plants during the period 1940-1950 was reported 
(Exs. 7-1; 7-3). Nearly 29 times as many deaths from respiratory cancer 
(excluding larynx) were found among workers in the chromate industry 
when compared to mortality rates for the total U.S. for the period 
1940-1948. The lung cancer risk was higher at the younger ages (a 40-
fold risk at ages 15-45; a 30-fold risk at ages 45-54 and a 20-fold 
risk at ages 55-74). Analysis of respiratory cancer deaths (excluding 
larynx) by race showed an observed to expected ratio of 14.29 for white 
males and 80 for nonwhite males.
    Taylor conducted a mortality study in a cohort of 1,212 chromate 
workers followed over a 24 year (1937-1960) period (Ex. 7-5). The 
workers were from three chromate plants that included approximately 70% 
of the total population of U.S. chromate workers in 1937. In addition, 
the plants had been in continuous operation for the study period 
(January 1, 1937 to December 31, 1960). The cohort was followed 
utilizing records of Old Age and Survivors Disability Insurance 
(OASDI). Results were reported both in terms of SMRs and conditional 
probabilities of survival to various ages comparing the mortality 
experience of chromate workers to the U.S. civilian male population. No 
measures of chromate exposure were reported although results are 
provided in terms of duration of employment. Taylor concluded that not 
only was there an excess in mortality from respiratory cancer, but from 
other causes as well, especially as duration of employment increased.
    In a reanalysis of Taylor's data, Enterline excluded those workers 
born prior to 1989 and analyzed the data by follow-up period using U.S. 
rates (Ex. 7-4). The SMR for respiratory cancer for all time periods 
showed a nine-fold excess (O=69 deaths; E=7.3). Respiratory cancer 
deaths comprised 28% of all deaths. Two of the respiratory cancer 
deaths were malignant neoplasms of the maxillary sinuses, a number 
according to Enterline, ``greatly in excess of that expected based on 
the experience of the U.S. male population.'' Also slightly elevated 
were cancers of the digestive organs (O=16; E=10.4) and non-malignant 
respiratory disease (O=13; E=8.9).
    Pastides et al. conducted a cohort study of workers at a North 
Carolina chromium chemical production facility (Ex. 7-93). Opened in 
1971, this facility is the largest chromium chemical production 
facility in the United States. Three hundred and ninety eight workers 
employed for a minimum of one year between September 4, 1971 and 
December 31, 1989 comprised the study cohort. A self-administered 
employee questionnaire was administered to collect data concerning 
medical history, smoking, plant work history, previous employment and 
exposure to other potential chemical hazards. Personal air monitoring 
results for Cr(VI) were available from company records for the period 
February 1974 through April 1989 for 352 of the 398 cohort members. A 
job matrix utilizing exposure area and calendar year was devised. The 
exposure means from the matrix were linked to each employee's work 
history to produce the individual exposure estimates by multiplying the 
mean Cr(VI) value from the matrix by the duration (time) in a 
particular exposure area (job). Annual values were summed to estimate 
total cumulative exposure.
    Personal air monitoring indicated that TWA Cr(VI) air 
concentrations were generally very low. Roughly half the samples were 
less than 1 [mu]g/m<SUP>3</SUP>, about 75 percent were below 3 [mu]g/
m<SUP>3</SUP>, and 96 percent were below 25 [mu]g/m<SUP>3</SUP>. The 
average age was 42 years and mean duration of employment was 9.5 years. 
Two thirds of the workers had accumulated less than 0.01mg/
m<SUP>3</SUP>-yr cumulative Cr(VI) exposure. SMRs were computed using 
national, state (not reported) and county mortality rates (eight 
adjoining North Carolina counties, including the county in which the 
plant is located). Two of the 17 recorded deaths in the cohort were 
from lung cancers. The SMRs for lung cancer were 127 (95% CI: 22-398) 
and 97 (95% CI: 17-306) based on U.S. and North Carolina county 
mortality rates, respectively. The North Carolina cohort is still 
relatively young and not enough time has elapsed to reach any 
conclusions regarding lung cancer risk and Cr(VI) exposure.
    A study of four chromate producing facilities in New Jersey was 
reported by Rosenman (Ex. 35-104). A total of 3,408 individuals were 
identified from the four facilities over different time periods (plant 
A from 1951-1954; plant B from

[[Page 59326]]

1951-1971; plant C from 1937-1964 and plant D 1937-1954). No Cr(VI) 
exposure data was collected for this study. Proportionate mortality 
ratios (PMRs) and proportionate cancer mortality ratios (PCMRs), 
adjusted by race, age, and calendar year, were calculated for the three 
companies (plants A and B are owned by one company). Unlike SMRs, PMRs 
are not based on the expected mortality rates in a standardized 
population but, instead, merely represent the proportional distribution 
of deaths in the cohort relative to the general U.S. population. 
Analyses were done evaluating duration of work and latency from first 
employment.
    Significantly elevated PMRs were seen for lung cancer among white 
males (170 deaths, PMR=1.95; 95% CI: 1.67-2.27) and black males (54 
deaths, PMR=1.88; 95% CI: 1.41-2.45). PMRs were also significantly 
elevated (regardless of race) for those who worked 1-10, 11-20 and >20 
years and consistently higher for white and black workers 11-20 years 
and >20 years since first hire. The results were less consistent for 
those with 10 or fewer years since first hire.
    Bidstrup and Case reported the mortality experience of 723 workers 
at three chromate producing factories in Great Britain (Ex. 7-20). Lung 
cancer mortality was 3.6 times that expected (O=12; E=3.3) for England 
and Wales. Alderson et al. conducted a follow-up of workers from the 
three plants in the U.K. (Bolton, Rutherglen and Eaglescliffe) 
originally studied by Bidstrup (Ex. 7-22). Until the late 1950s, all 
three plants operated a ``high-lime'' process. This process potentially 
produced significant quantities of calcium chromate as a by-product as 
well as the intended sodium dichromate. Process changes occurred during 
the 1940s and 1950s. The major change, according to the author, was the 
introduction of the ``no-lime'' process, which eliminated unwanted 
production of calcium chromate. The no-lime process was introduced at 
Eaglescliffe 1957-1959 and by 1961 all production at the plant was by 
this process. Rutherglen operated a low-lime process from 1957/1959 
until it closed in 1967. Bolton never changed to the low-lime process. 
The plant closed in 1966. Subjects were eligible for entry into the 
study if they had received an X-ray examination at work and had been 
employed for a minimum of one year between 1948 and 1977. Of the 3,898 
workers enumerated at the three plants, 2,715 met the cohort entrance 
criteria, (alive: 1,999; deceased: 602; emigrated: 35; and lost to 
follow-up: 79). Those lost to follow-up were not included in the 
analyses. Eaglescliffe contributed the greatest number of subjects to 
the study (1,418). Rutherglen contributed the largest number of total 
deaths (369, or 61%). Lung cancer comprised the majority of cancer 
deaths and was statistically significantly elevated for the entire 
cohort (O=116; E=47.96; SMR= 240; p <0.001). Two deaths from nasal 
cancer were observed, both from Rutherglen.
    SMRs were computed for Eaglescliffe by duration of employment, 
which was defined, based upon plant process updates (those who only 
worked before the plant modification, those who worked both before and 
after the modifications, or those who worked only after the 
modifications were completed). Of the 179 deaths at the Eaglescliffe 
plant, 40 are in the pre-change group; 129 in the pre-/post-change and 
10 in the post-change. A total of 36 lung cancer deaths occurred at the 
plant, in the pre-change group O= 7; E=2.3; SMR=303; in the pre-/post-
change group O=27; E=13; SMR=2.03 and in the post-change group O=2; 
E=1.07; SMR=187.
    In an attempt to address several potential confounders, regression 
analysis examined the contributions of various risk factors to lung 
cancer. Duration of employment, duration of follow-up and working 
before or after plant modification appear to be greater risk factors 
for lung cancer, while age at entry or estimated degree of chromate 
exposure had less influence.
    Davies updated the work of Alderson, et al. concerning lung cancer 
in the U.K. chromate producing industry (Ex. 7-99). The study cohort 
included payroll employees who worked a minimum of one year during the 
period January 1, 1950 and June 30, 1976 at any of the three facilities 
(Bolton, Eaglescliffe or Rutherglen). Contract employees were excluded 
unless they later joined the workforce, in which case their contract 
work was taken into account.
    Based upon the date of hire, the workers were assigned to one of 
three groups. The first, or ``early'' group, consists of workers hired 
prior to January 1945 who are considered long term workers, but do not 
comprise a cohort since those who left or died prior to 1950 are 
excluded. The second group, ``pre-change'' workers, were hired between 
January 1, 1945 to December 31, 1958 at Rutherglen or to December 31, 
1960 at Eaglescliffe. Bolton employees starting from 1945 are also 
termed pre-change. The cohort of pre-change workers is considered 
incomplete since those leaving 1946-1949 could not be included and 
because of gaps in the later records. For those who started after 1953 
and for all men staying 5+ years, this subcohort of pre-change workers 
is considered complete. The third group, ``post-change'' workers, 
started after the process changes at Eaglescliffe and Rutherglen became 
fully effective and are considered a ``complete'' cohort. A ``control'' 
group of workers from a nearby fertilizer facility, who never worked in 
or near the chromate plant, was assembled.
    A total of 2,607 employees met the cohort entrance criteria. As of 
December 31, 1988, 1,477 were alive, 997 dead, 54 emigrated and 79 
could not be traced (total lost to follow-up: 133). SMRs were 
calculated using the mortality rates for England and Wales and the 
mortality rates for Scotland. Causes of death were ascertained for all 
but three decedents and deaths were coded to the revision of the 
International Classification of Diseases in effect at the time of 
death. Lung cancer in this study is defined as those deaths where the 
underlying cause of death is coded as 162 (carcinoma of the lung) or 
239.1 (lung neoplasms of unspecified nature) in the 9th revision of the 
ICD. Two deaths fell into the latter category. The authors attempted to 
adjust the national mortality rates to allow for differences based upon 
area and social class.
    There were 12 lung cancer deaths at Bolton, 117 at Rutherglen, 75 
at Eaglescliffe and one among staff for a total of 205 lung cancer 
deaths. A statistically significant excess of lung cancer deaths (175 
deaths) among early and pre-change workers is seen at Rutherglen and 
Eaglescliffe for both the adjusted and unadjusted SMRs. For Rutherglen, 
for the early period based upon 68 observed deaths, the adjusted SMR 
was 230 while the unadjusted SMR was 347 (for both SMRs p<0.001). For 
the 41 pre-change lung cancer deaths at Rutherglen, the adjusted SMR 
was 160 while the unadjusted SMR was 242 (for both SMRs p<0.001). At 
Eaglescliffe, there were 14 lung cancer deaths in the early period 
resulting in an adjusted SMR of 196 and an unadjusted SMR of 269 (for 
both SMRs p<0.05). For the pre-change period at Eaglescliffe, the 
adjusted SMR was 195 and the unadjusted was 267 (p<0.001 for both 
SMRs). At Bolton there is a non-significant excess among pre-change 
men. There are no apparent excesses in the post-change groups, the 
staff groups or in the non-exposed fertilizer group.
    There is a highly significant overall excess of nasal cancers with 
two cases at Eaglescliffe and two cases at Rutherglen (O=4, 
Eadjusted=0.26; SMR=1538). All four men with nasal

[[Page 59327]]

cancer had more than 20 years of exposure to chromates.
    Aw reported on two case-control studies conducted at the previously 
studies Eaglescliffe plant (Ex. 35-245). In 1960, the plant, converted 
from a ``high-lime'' to a `no-lime' process, reducing the likelihood of 
calcium chromate formation. As of March 1996, 2,672 post-change workers 
had been employed, including 891 office personnel. Of the post-change 
plant personnel, 56% had been employed for more than one year. Eighteen 
lung cancer cases were identified among white male post-change workers 
(13 deceased; five alive). Duration of employment for the cases ranged 
from 1.5 to 25 years with a mean of 14.4. Sixteen of the lung cancer 
cases were smokers.
    In the first case-control study reported, the 15 lung cancer cases 
identified up to September 1991 were matched to controls by age and 
hire date (five controls per case). Cases and controls were compared 
based upon their job categories within the plant. The results showed 
that cases were more likely to have worked in the kiln area than the 
controls. Five of the 15 cases had five or more years in the kiln area 
where Cr(VI) exposure occurred vs. six of the 75 controls. A second 
case-control study utilized the 18 lung cancer cases identified in post 
change workers up to March 1996. Five controls per case were matched by 
age (+/-5 years), gender and hire date. Both cases and controls had a 
minimum of one year of employment. A job exposure matrix was being 
constructed that would allow the investigators to ``estimate exposure 
to hexavalent chromates for each worker in the study for all the jobs 
done since the start of employment at the site until 1980.'' Starting 
in 1970 industrial hygiene sampling was performed to determine exposure 
for all jobs at the plant. Cr(VI) exposure levels for the period 
between 1960 and 1969 were being estimated based on the recall of 
employees regarding past working conditions relative to current 
conditions from a questionnaire. The author stated that preliminary 
analysis suggests that the maximum recorded or estimated level of 
exposure to Cr(VI) for the cases was higher than that of the controls. 
However, specific values for the estimated Cr(VI) exposures were not 
reported.
    Korallus et al. conducted a study of 1,140 active and retired 
workers with a minimum of one year of employment between January 1, 
1948 and March 31, 1979 at two German chromate production plants (Ex. 
7-26). Workers employed prior to January 1, 1948 (either active or 
retired) and still alive at that date were also included in the cohort. 
The primary source for determining cause of death was medical records. 
Death certificates were used only when medical records could not be 
found. Expected deaths were calculated using the male population of 
North Rhineland-Westphalia. Elevated SMRs for cancer of the respiratory 
system (50 lung cancers and one laryngeal cancer) were seen at both 
plants (O=21; E=10.9; SMR=192 and O=30; E=13.4; SMR=224).
    Korallus et al. reported an update of the study. The cohort 
definition was expanded to include workers with one year of employment 
between January 1, 1948 and December 31, 1987 (Ex. 7-91). One thousand 
four hundred and seventeen workers met the cohort entrance criteria and 
were followed through December 31, 1988. While death certificates were 
used, where possible, to obtain cause of death, a majority of the cause 
of death data was obtained from hospital, surgical and general 
practitioner reports and autopsies because of Germany's data protection 
laws. Smoking data for the cohort were incomplete.
    Process modifications at the two plants eliminated the high-lime 
process by January 1, 1958 at one location and January 1, 1964 at the 
second location. In addition, technical measures were introduced which 
led to reductions in the workplace air concentrations of chromate 
dusts. Cohort members were divided into pre- and post-change cohorts, 
with subcohorts in the pre-change group. SMRs were computed with the 
expected number of deaths derived from the regional mortality rates 
(where the plants are located). One plant had 695 workers (279 in the 
pre-change group and 416 in the post change group). The second plant 
had 722 workers (460 in the pre-change group and 262 in the post-change 
group). A total of 489 deaths were ascertained (225 and 264 deaths). Of 
the cohort members, 6.4% were lost to follow-up.
    Lung cancer is defined as deaths coded 162 in the 9th revision of 
the International Classification of Diseases. There were 32 lung cancer 
deaths at one plant and 43 lung cancer deaths at the second plant. Lung 
cancer SMRs by date of entry (which differ slightly by plant) show 
elevated but declining SMRs for each plant, possibly due to lower 
Cr(VI) exposure as a result of improvements in production process. The 
lung cancer SMR for those hired before 1948 at Plant 1 is statistically 
significant (O=13; SMR=225; 95% CI: 122-382). The overall lung cancer 
SMR for Plant 1 is also statistically significantly elevated based upon 
32 deaths (SMR=175; 95% CI: 120-246). At Plant 2, the only lung cancer 
SMR that is not statistically significant is for those hired after 1963 
(based upon 1 death). Lung cancer SMRs for those hired before 1948 
(O=23; SMR=344; 95% CI: 224-508) and for those hired between 1948 and 
1963 (O=19; SMR=196; 95% CI: 1.24-2.98) are statistically significantly 
elevated. The overall lung cancer SMR at Plant 2 based upon 43 deaths 
is 239 (95% CI: 177-317). No nasal cavity neoplasms were found. A 
statistically significant SMR for stomach cancer was observed at Plant 
2 (O=12; SMR=192; 95% CI: 104-324).
    DeMarco et al. conducted a cohort study of chromate production 
workers in northern Italy to assess the existence of excess risk of 
respiratory cancer, specifically lung cancer (Ex. 7-54). The cohort was 
defined as males who worked for a minimum of one year from 1948 to 1985 
and had at least 10 years of follow-up. Five hundred forty workers met 
the cohort definition. Vital status follow-up, carried out through June 
30, 1985, found 427 cohort members alive, 110 dead and three lost to 
follow-up. Analysis utilizing SMRs based on Italian national rates was 
conducted. Of the 110 deaths, 42 were cancer deaths. The statistically 
significant SMR for lung cancer based upon 14 observed deaths with 6.46 
expected was 217 (95% CI: 118-363
    Exposure estimates were based upon the duration of cumulative 
exposure and upon a risk score (low, medium, high and not assessed) 
assigned to the department in which the worker was primarily employed. 
A committee assigned the scores, based upon knowledge of the production 
process or on industrial hygiene surveys taken in 1974, 1982 and 1984. 
The risk score is a surrogate for the workplace concentrations of 
Cr(VI) in the different plant departments. Since no substantial changes 
had been made since World War II, the assumption was made that 
exposures remained relatively stable. Lung cancer SMRs based upon type 
of exposure increased with level of exposure (Low: O=1; E=1.43; SMR=70; 
Medium: O=5; E=202; SMR=2.48; High: O=6; E=1.4; SMR=420; Not Assessed: 
O=2; E=1.6; SMR=126). Only the SMR for those classified as having 
worked in departments characterized as high exposure was statistically 
significant at the p<0.05 level.
    A cohort study of workers at a chromium compounds manufacturing 
plant in Tokyo, Japan by Satoh et al. included males employed between 
1918 and 1975 for a minimum of one year and for whom the necessary data 
were

[[Page 59328]]

available (Ex. 7-27). Date and cause of death data were obtained from 
the death certificate (85%) or from other ``reliable'' written 
testimony (15%). Of the 1,061 workers identified, 165 were excluded 
from the study because information was missing. A total of 896 workers 
met the cohort inclusion criteria and were followed through 1978. The 
causes of 120 deaths were ascertained. SMRs based on age-cause specific 
mortality for Japanese males were calculated for four different time 
periods (1918-1949; 1950-1959; 1960-1969 and 1970-1978) and for the 
entire follow-up period (1918-1978). An elevated SMR for lung cancer is 
seen for the entire follow-up period (O=26; E=2.746; SMR=950). A 
majority of the lung cancer deaths (20) occurred during the 1970-1978 
interval.
    Results from the many studies of chromate production workers from 
different countries indicate a relationship between exposure to 
chromium and malignant respiratory disease. The epidemiologic studies 
done between 1948 and 1952 by Machle and Gregorius (Ex. 7-2), Mancuso 
and Hueper (Ex. 7-12) and Brinton, et al. (Ex. 7-1) suggest a risk for 
respiratory cancer among chromate workers between 15 and 29 times 
expectation. Despite the potential problems with the basis for the 
calculations of the expectations or the particular statistical methods 
employed, the magnitude of the difference between observed and expected 
is powerful enough to overcome these potential biases.
    It is worth noting that the magnitude of difference in the relative 
risks reported in a mortality study among workers in three chromate 
plants in the U.K. (Ex.7-20) were lower than the relative risks 
reported for chromate workers in the U.S. during the 1950s and 1960s. 
The observed difference could be the result of a variety of factors 
including different working conditions in the two countries, a shorter 
follow-up period in the British study, the larger lost-to-follow-up in 
the British study or the different statistical methods employed. While 
the earlier studies established that there was an excess risk for 
respiratory cancer from exposure to chromium, they were unable to 
specify either a specific chromium compound responsible or an exposure 
level associated with the risk. Later studies were able to use superior 
methodologies to estimate standardized lung cancer mortality ratios 
between chromate production cohorts and appropriate reference 
populations (Exs. 7-14; 7-22; 7-26; 7-99; 7-91). These studies 
generally found statistically increased lung cancer risk of around two-
fold. The studies usually found trends with duration of employment, 
year of hire, or some production process change that tended to 
implicate chromium exposure as the causative agent.
    The most recent studies were able to use industrial hygiene data to 
reconstruct historical Cr(VI) exposures and show statistically 
significant associations between cumulative airborne Cr(VI) and lung 
cancer mortality (Exs. 23; 31-22-11; Ex. 31-18-4). Gibb et al. found 
the significant association between Cr(VI) and lung cancer was evident 
in models that accounted for smoking. The exposure'response 
relationship from these chromate production cohorts provide strong 
evidence that occupational exposure to Cr(VI) dust can increase cancer 
in the respiratory tract of workers.
    The Davies, Korallus, and Luippold studies examine mortality 
patterns at chromate producing facilities where one production process 
modification involved conversion from a high-lime to a low-lime or a 
lime-free process (Exs. 7-99; 7-91; 31-18-4). In addition to process 
modification, technical improvements also were implemented that lowered 
Cr(VI) exposure. One of the plants in the Davies study retained the 
high-lime process and is not discussed. The lung cancer SMRs for one 
British plant and both of the German plants declined from early, to 
pre-change to post change time periods. In the remaining British 
plants, the lung cancer SMR is basically identical for the early and 
pre-change period, but does decline in the post-change time period. The 
lung cancer SMR in the Luippold cohort also declined over time as the 
amount of lime was reduced in the roasting process. Other modifications 
at the Painesville plant that reduced airborne Cr(VI) exposure, such as 
installation of covered conveyors and conversion from batch to 
continuous process occurred at the same time (Ex. 35-61). It is not 
clear whether reduced levels of the high-lime byproduct, calcium 
chromate, or the roasting/leaching end product, sodium dichromate that 
resulted from the various process changes is the reason for the 
decrease in lung cancer SMRs in these cohorts. However, it should be 
noted increased lung cancer risk was experienced by workers at the 
Baltimore plant (e.g., Hayes and Gibb cohorts) even though early air 
monitoring studies suggest that a lime-free process was probably used 
at this facility (Ex. 7-17).
2. Evidence From Chromate Pigment Production Workers
    Chromium compounds are used in the manufacture of pigments to 
produce a wide range of vivid colors. Lead and zinc chromates have 
historically been the predominant hexavalent chromium pigments, 
although others such as strontium and barium chromate have also been 
produced. These chromates vary considerably in their water solubility 
with lead and barium chromates being the most water insoluble. All of 
the above chromates are less water-soluble than the highly water-
soluble sodium chromate and dichromate that usually serve as the 
starting material for chromium pigment production. The reaction of 
sodium chromate or dichromate with the appropriate zinc or lead 
compound to form the corresponding lead or zinc chromate takes place in 
solution. The chromate pigment is then precipitated, separated, dried, 
milled, and packaged. Worker exposures to chromate pigments are 
greatest during the milling and packaging stages.
    There have been a number of cohort studies of chromate pigment 
production workers from the United States, the United Kingdom, France, 
Germany, the Netherlands, Norway and Japan. Most of the studies found 
significantly elevated lung cancers in workers exposed to Cr(VI) 
pigments over many years when compared against standardized reference 
populations. In general, the studies of chromate pigment workers lack 
the historical exposure data found in some of the chromate production 
cohorts. The consistently higher lung cancers across several worker 
cohorts exposed to the less water-soluble Cr(VI) compounds complements 
the lung cancer findings from the studies of workers producing highly 
water soluble chromates and adds to the further evidence that 
occupational exposure to Cr(VI) compounds should be regarded as 
carcinogenic. A summary of selected human epidemiologic studies in 
chromate production workers is presented in Table VI-2.

[[Page 59329]]



Table VI-2.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
                                           Chromate Pigment Production
----------------------------------------------------------------------------------------------------------------
                                                           Reference         Chromium (VI)
      Reference/exhibit No.        Study population       population           exposure        Lung cancer risk
----------------------------------------------------------------------------------------------------------------
Langard & Vigander (1983, Ex. 7-  133 Norwegian       Cancer incidence    Lead and zinc       -O/E of 44 for
 36).                              chromium pigment    from Norwegian      chromates with      subcohort of 24
Langard & Vigander (1975, Ex. 7-   production          Cancer Registry     some sodium         workers based on
 33)..                             workers employed    1955-1976.          dichromate as       6 cancer cases.
                                   between 1948 and                        starting           -5 of 6 cases were
                                   1972; 24 workers                        material; Cr(VI)    exposed primarily
                                   with 3+ years                           levels between 10   to zinc chromate.
                                   exposure to                             and 30 [mu]g/m3
                                   chromate dust;                          1975-1980. No
                                   follow up through                       reporting <1975.
                                   1980.
Davies (1984, Ex. 7-42).........  1152 British        Mortality of        Factory A:          --O/E of 2.2
Davies (1979, Ex. 7-41).........   chromate pigment    England and Wales.  chromates--primar   (p<0.05) for high
                                   workers from 3                          ily lead; some      exposed in
                                   plants with a                           zinc; minor         Factory A 1932-
                                   minimum of 1 year                       barium Factory B:   1954; 21 deaths.
                                   employment                              mostly lead and    --O/E of 4.4
                                   between 1930-                           zinc chromates;     (p<0.05) for high
                                   June, 1975;                             minor strontium.    exposed in
                                   follow up through                       Factory C: lead     Factory B 1948-
                                   1981.                                   chromate only No    1967; 11 deaths.
                                                                           Cr(VI) levels      --O/E of 1.1 (NS)
                                                                           reported.           for exposed
                                                                                               Factory C 1946-
                                                                                               1967; 7 deaths.
Hayes et al. (1989, Ex. 7-46)...  1,946 male pigment  U.S. Mortality....  -Primarily lead     --O/E of 1.2 (NS)
Sheffet et al. (1982, Ex. 7-48).   workers from New                        chromate with       for entire cohort
                                   Jersey facility                         some zinc           based on 41
                                   employed for a                          chromate.           deaths.
                                   minimum of one                         -Cr(VI) levels in   --O/E of 1.5
                                   month between                           later years         (p<0.5) for
                                   1940 and 1969;                          reported to be      workers employed
                                   follow up through                       >500 [mu]g/m3 for   >10 yr based on
                                   March, 1982.                            exposed workers..   23 deaths.
                                                                                              --Upward trend
                                                                                               (p<0.01) with
                                                                                               duration of
                                                                                               exposure.
Equitable Environmental Health    574 male chromate   U.S. white male     West Virginia:      --O/E of 1.30 (NS)
 (1983, Ex. 2-D-1).                workers from        mortality rates.    lead chromates.     for West Virginia
Equitable Environmental Health     three plants                           Kentucky:            plant based on 3
 (1976, Ex. 2-D-3).                (West Virginia,                         chromates--mostly   deaths.
                                   New Jersey or                           lead, some zinc,   --O/E of 2.16 (NS)
                                   Kentucky) with a                        minor strontium     for Kentucky
                                   minimum of 6                            and barium..        plant based on 3
                                   months of                              --New Jersey;        deaths.
                                   exposure to lead                        mostly lead and    --O/E of 2.31
                                   chromate prior to                       some zinc           (p<.05) for New
                                   1974.                                   chromate..          Jersey plant
                                                                          --Median Cr(VI) in   based on 9
                                                                           1975 reported to    deaths.
                                                                           equal or exceed
                                                                           52 [mu]g/m3.
Deschamps et al. (1995, 35-234).  294 male pigment    Death rates from    --Mostly lead       --O/E of 3.6
Haguenoer et al. (1981, Ex. 7-     workers from        northern France.    chromate with       (p<0.01) based on
 44).                              French facility                         some zinc           18 deaths.
                                   employed for a                          chromate.          --Upward trend
                                   minimum of six                         --Cr(VI) levels in   (p<0.01) with
                                   months between                          1981 between 2      duration of
                                   1958 and 1987.                          and 180 [mu]g/m3.   exposure.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E).
Relative Risk (RR).
Not Statistically Significant (NS).
Odds Ratio (OR).

    Langard and Vigander updated a cohort study of lung cancer 
incidence in 133 workers employed by a chromium pigment production 
company in Norway (Ex. 7-36). The cohort was originally studied by 
Langard and Norseth (Ex. 7-33). Twenty-four men had more than three 
years of exposure to chromate dust. From 1948, when the company was 
founded, until 1951, only lead chromate pigment was produced. From 1951 
to 1956, both lead chromate and zinc chromate pigments were produced 
and from 1956 to the end of the study period in 1972 only zinc chromate 
was produced. Workers were exposed to chromates both as the pigment and 
its raw material, sodium dichromate.
    The numbers of expected lung cancers in the workers were calculated 
using the age-adjusted incidence rates for lung cancer in the Norwegian 
male population for the period 1955-1976. Follow-up using the Norwegian 
Cancer Registry through December 1980, found the twelve cancers of 
which seven were lung cancers. Six of the seven lung cancers were 
observed in the subcohort of 24 workers who had been employed for more 
than three years before 1973. There was an increased lung cancer 
incidence in the subcohort based on an observed to expected ratio of 44 
(O=6; E=0.135). Except for one case, all lung cancer cases were exposed 
to zinc chromates and only sporadically to other chromates. Five of the 
six cases were known to be smokers or ex-smokers. Although the authors 
did not report any formal statistical comparisons, the extremely high 
age-adjusted standardized incidence ratio suggests that the results 
would likely be statistically significant.
    Davies reported on a cohort study of English chromate pigment 
workers at three factories that produced chromate pigments since the 
1920s or earlier (Ex. 7-41). Two of the factories produced both zinc 
and lead chromate. Both products were made in the same sheds and all 
workers had mixed exposure to both substances. The only product at the 
third factory was lead chromate.
    Cohort members are defined as males with a minimum of one year of 
employment first hired between 1933 and 1967 at plant A; 1948 and 1967 
at plant B and 1946-1961 at plant C. The analysis excludes men who 
entered employment later than 1967 because of the short follow-up 
period. Three hundred and ninety-six (396) men from Factory A, 136 men 
from Factory B and 114 men from Factory C were followed to mid-1977. 
Ninety-four workers with 3-11 months employment during 1932-1945 at 
Factory A were also included. Expectations were based upon calendar 
time period-, gender- and age-specific national cancer death rates for 
England and Wales. The author adjusted the death rates for each factory 
for local differences, but the exact methods of adjustment were not 
explicit.
    Exposure to chromates was assigned as high for those in the dry 
departments where pigments were ground, blended and packed; medium for 
those in the wet departments where precipitates were washed, pressed 
and stove dried and in maintenance or cleaning which required time in 
various departments; or low for those jobs which the author states 
involved ``slight exposure to chromates such as most laboratory jobs, 
boiler stoking, painting and bricklaying'' (Ex. 7-41, p. 159). The high 
and

[[Page 59330]]

medium exposure categories were combined for analytical purposes.
    For those entering employment from 1932 to 1954 at Factory A, there 
were 18 lung cancer deaths in the high/medium exposure group, with 8.2 
deaths expected. The difference is significant at p<. 01. In the low 
exposure group, the number of observed and expected lung cancer deaths 
was equal (two deaths). There were no lung cancer deaths at Factory A 
for those hired between 1955-1960 and 1961-1967.
    For those entering employment between 1948 and 1967 at Factory B, 
there were seven observed lung cancer deaths in the high/medium 
exposure group with 1.4 expected which is statistically significant at 
p<. 001. At Factory C (which manufactured only lead chromate), there 
was one death in the high/medium exposure group and one death in the 
low exposure group for those beginning employment between 1946 and 
1967.
    The author points out that:

    There has been no excess lung cancer mortality amongst workers 
with chromate exposure rated as ``low'', nor among those exposed 
only to lead chromate. High and medium exposure-rated workers who in 
the past had mixed exposure to both lead and zinc chromate have 
experienced a marked excess of lung cancer deaths, even if employed 
for as little as one year'' (Ex. 7-41, p. 157).

It is the author's opinion that the results ``suggest that the 
manufacture of zinc chromate may involve a lung cancer hazard'' (Ex. 7-
41, p. 157).
    Davies updated the lung cancer mortality at the three British 
chromate pigment production factories (Ex. 7-42). The follow-up was 
through December 31, 1981. The cohort was expanded to include all male 
workers completing one year of service by June 30, 1975 but excluded 
office workers.
    Among workers at Factory A with high and medium exposure, mortality 
was statistically significantly elevated over the total follow-up 
period among entrants hired from 1932 to 1945 (O/E=2.22). A similar, 
but not statistically significant, excess was seen among entrants hired 
from 1946 to 1954 (O/E=2.23). The results for Factory B showed 
statistically significantly elevated lung cancer mortality among 
workers classified with medium exposures entering service during the 
period from 1948 to 1960 (O/E=3.73) and from 1961 to 1967 (O/E=5.62). 
There were no lung cancer deaths in the high exposure group in either 
time period. At Factory C, analysis by entry date (early entrant and 
the period 1946-1960) produced no meaningful results since the number 
of deaths was small. When the two periods are combined, the O/E was 
near unity. The author concluded that in light of the apparent absence 
of risk at Factory C, ``it seems reasonable to suggest that the hazard 
affecting workers with mixed exposures at factories A and B * * * is 
attributable to zinc chromates'' (Ex. 7-42, p. 166).
    Davies also studied a subgroup of 57 chromate pigment workers, 
mostly employed between 1930 and 1945, who suffered clinical lead 
poisoning (Ex. 7-43). Followed through 1981, there was a statistically 
significantly elevated SMR for lung cancer based upon four cases (O=4; 
E=2.8; SMR=145).
    Haguenoer studied 251 French zinc and lead chromate pigment workers 
employed for six months or more between January 1, 1958 and December 
31, 1977 (Ex. 7-44). As of December 31, 1977, 50 subjects were 
identified as deceased. Cause of death was obtained for 30 of the 50 
deaths (60%). Lung cancer mortality was significantly elevated based on 
11 fatalities (SMR=461; 95% CI: 270-790). The mean time from first 
employment until detection of cancer was 17 years. The mean duration of 
employment among cases was 15 years.
    The Haguenoer cohort was followed up in a study by Deschamps et al. 
(Ex. 234). Both lead and zinc chromate pigments were produced at the 
plant until zinc chromate production ceased in 1986. The cohort 
consisted of 294 male workers employed for at least six months between 
1958 and 1987. At the end of the follow-up, 182 cohort members were 
alive, 16 were lost to follow-up and 96 were dead. Because of French 
confidentiality rules, the cause of death could not be obtained from 
the death certificate; instead physicians and hospital records were 
utilized. Using cause of death data from sources other than death 
certificates raises the potential for misclassification bias. Cause of 
death could not be obtained for five decedents. Data on smoking habits 
was not available for a number of workers and was not used in the 
analysis.
    Since individual work histories were not available, the authors 
made the assumption that the exposure level was the same for all 
workers during their employment at the plant. Duration of employment 
was used as a surrogate for exposure. Industrial hygiene measurements 
taken in 1981 provide some idea of the exposure levels at the plant. In 
the filtration department, Cr(VI) levels were between 2 and 3 [mu]g/
m\3\; in the grinding department between 6 and 165 [mu]g/m\3\; in the 
drying and sacking department between 6 and 178 [mu]g/m\3\; and in the 
sacks marking department more than 2000 [mu]g/m\3\.
    The expected number of deaths for the SMR analysis was computed 
from age-adjusted death rates in the northern region of France where 
the plant was located. There was a significant increase in lung cancer 
deaths based on 18 fatalities with five expected (SMR=360; 95% CI: 213-
568). Using duration of employment as a surrogate for exposure, 
statistically significant SMRs were seen for the 10-15 years of 
exposure (O=6, SMR=720, 95% CI: 264-1568), 15-20 years (O=4, SMR=481, 
95% CI: 131-1231), and 20+ years (O=6, SMR=377, 95% CI: 1.38-8.21) time 
intervals. There was a significantly elevated SMR for brain cancer 
based upon two deaths (SMR=844, 95% CI: 102-3049). There was a non-
statistically significant increase for digestive tract cancer (O=9, 
SMR=130) consisting of three esophageal cancers, two stomach cancers 
and four colon cancers.
    Equitable Environmental Health, Inc., on behalf of the Dry Color 
Manufacturers Association, undertook a historical prospective mortality 
study of workers involved in the production of lead chromate (Exs. 2-D-
3; 2-D-1). The cohort was defined as male employees who had been 
exposed to lead chromate for a minimum of six months prior to December 
1974 at one of three facilities in West Virginia, Kentucky or New 
Jersey. The New Jersey facility had a unit where zinc chromate was 
produced dating back to 1947 (Ex. 2-D-3). Most workers rotated through 
this unit and were exposed to both lead and zinc chromates. Two men 
were identified at the New Jersey facility with exposure solely to lead 
chromate; no one with exposure only to zinc chromate was identified.
    Subsequent review of the data found that the Kentucky plant also 
produced zinc chromates from the late 1930s to early 1964. During the 
period 1961-1962, zinc chromates accounted for approximately 12% of 
chromate production at the plant. In addition, strontium chromate and 
barium chromate also were produced at the plant.
    The cohort consisted of 574 male employees from all three plants 
(Ex. 2-D-1). Eighty-five deaths were identified with follow up through 
December 1979. Six death certificates were not obtained. SMRs were 
reported based on U.S. white male death rates. There were 53 deaths 
from the New Jersey plant including a statistically significant SMR for 
cancer of the trachea, bronchus and lung based upon nine deaths (E=3.9; 
SMR=231; 95% CI: 106-438). One lung cancer decedent worked solely in 
the

[[Page 59331]]

production of lead chromates. Three of the lung cancer deaths were 
black males. In addition, there were six deaths from digestive system 
cancers, five of which were stomach cancers reported at the New Jersey 
plant. The SMR for stomach cancer was statistically significantly 
elevated (O=5; E=0.63; SMR=792; 99% CI: 171-2243). There were 21 deaths 
from the West Virginia plant, three of which were cancer of the 
trachea, bronchus and lung (E=2.3; SMR=130; 95% CI: 27-381). There were 
11 deaths at the Kentucky plant, two of which were cancer of the 
trachea, bronchus and lung (E=0.9; SMR=216; 95% CI: 26-780).
    Sheffet et al. examined the lung cancer mortality among 1,946 male 
employees in a chromate pigment factory in Newark, New Jersey who were 
exposed to both lead chromate and zinc chromate pigments (Ex. 7-48). 
The men worked for a minimum of one month between January 1, 1940 and 
December 31, 1969. As of March 31, 1979, a total of 321 cohort members 
were identified as deceased (211 white males and 110 non-white males). 
Cause of death could not be ascertained for 37 white males and 12 non-
white males. The proportion of the cohort lost to follow up was high 
(15% of white males and 20% of non-white males).
    Positions at the plant were classified into three categories 
according to intensity of exposure: high (continuous exposure to 
chemical dust), moderate (occasional exposure to chemical dust or to 
dry or wet pigments) and low (infrequent exposure by janitors or office 
workers). Positions were also classified by type of chemical exposure: 
chromates, other inorganic substances, and organics. The authors' state 
that in almost all positions individuals ``who were exposed to any 
chemicals were also exposed to hexavalent chromium in the form of 
airborne lead and zinc chromates (Ex. 7-48, p. 46).'' The proportion of 
lead chromate to zinc chromate was approximately nine to one. 
Calculations, based upon air samples during later years, give an 
estimate for the study period of more than 2000 [mu]g airborne 
chromium/m\3\ for the high exposure category, between 500 and 2000 
[mu]g airborne chromium/m\3\ and less than 100 [mu]g airborne chromium/
m\3\ for the low exposure category. Other suspected carcinogens present 
in the workplace air at much lower levels were nickel sulfate and 
nickel carbonate.
    Because of the large proportion of workers lost to follow-up (15% 
of white males and 20% of non-white males) and the large numbers of 
unknown cause of death (21% of white males and 12% of non-white males), 
the authors calculated three separate mortality ex- pectations based 
upon race-, gender-, age- and time-specific U.S. mortality ratios. The 
first expectation was calculated upon the assumption that those lost to 
follow-up were alive at the end of the study follow-up period. The 
second expectation was calculated on the assumption that those whose 
vital status was unknown were lost to follow-up as of their employment 
termination date. The third expectation was calculated excluding those 
of unknown vital status from the cohort. Deaths with unknown cause were 
distributed in the appropriate proportions among known causes of death 
which served as an adjustment to the observed deaths. The adjusted 
deaths were used in all of the analyses.
    A statistically significant ratio for lung cancer deaths among 
white males (O/E=1.6) was observed when using the assumption that 
either the lost to follow-up were assumed lost as of their termination 
date or were excluded from the cohort (assumptions two and three 
above). The ratio for lung cancer deaths for non-white males results in 
an identical O/E of 1.6 for all three of the above scenarios, none of 
which was statistically significant.
    In addition, the authors also conducted Proportionate Mortality 
Ratio (PMR) and Proportionate Cancer Mortality Ratio (PCMR) analyses. 
For white males, the lung cancer PMR was 200 and the lung cancer PCMR 
was 160 based upon 25.5 adjusted observed deaths (21 actual deaths). 
Both were statistically significantly elevated at the p<.05 level. For 
non-white males, the lung cancer PMR was 200 and the lung cancer PCMR 
was 150 based upon 11.2 adjusted observed deaths (10 actual deaths). 
The lung cancer PMR for non-white males was statistically significantly 
elevated at the p<.05 level. Statistically significantly elevated PMRs 
and PCMRs for stomach cancer in white males were reported (PMR=280; 
PCMR=230) based upon 6.1 adjusted observed deaths (five actual).
    The Sheffet cohort was updated in a study by Hayes et al. (Ex. 7-
46). The follow up was through December 31, 1982. Workers employed as 
process operators or in other jobs which involved direct exposure to 
chromium dusts were classified as having exposure to chromates. 
Airborne chromium concentrations taken in ``later years'' were 
estimated to be >500 [mu]g g/m \3\ for ``exposed'' jobs and >2000 [mu]g 
/m \3\ for ``highly exposed'' jobs.
    The cohort included 1,181 white and 698 non-white males. Of the 453 
deaths identified by the end of the follow-up period, 41 were lung 
cancers. For the entire study group, no statistically significant 
excess was observed for lung cancer (SMR=116) or for cancer at any 
other site. Analysis by duration of employment found a statistically 
significant trend (p=. 04) for lung cancer SMRs (67 for those employed 
< 1 year; 122 for those employed 1-9 years and 151 for those employed 
10+ years).
    Analysis of lung cancer deaths by duration of employment in 
chromate dust associated jobs found no elevation in risk for subjects 
who never worked in these jobs (SMR=92) or for subjects employed less 
than one year in these jobs (SMR=93). For those with cumulative 
employment of 1-9 and 10+ years in jobs with chromate dust exposure, 
the SMRs were 176 (nine deaths) and 194 (eight deaths) respectively.
    Frentzel-Beyme studied the mortality experience of 1,396 men 
employed for more than six months in one of five factories producing 
lead and zinc chromate pigments located in Germany and the Netherlands 
(Ex. 7-45). The observed deaths from the five factories were compared 
with the expected deaths calculated on the basis of mortality figures 
for the region in which the plant was located. Additional analysis was 
conducted on relevant cohorts which included workers with a minimum of 
10 years exposure, complete records for the entire staff, and exclusion 
of foreign nationals. Jobs were assigned into one of three exposure 
categories: high (drying and milling of the filtered pigment paste), 
medium (wet processes including precipitation of the pigment, filtering 
and maintenance, craftsmen and cleaning) and low or trivial exposure 
(storage, dispatch, laboratory personnel and supervisors).
    There were 117 deaths in the entire cohort of which 19 were lung 
cancer deaths (E=9.3). The lung cancer SMRs in the relevant cohort 
analyses were elevated at every plant; however, in only one instance 
was the increased lung cancer SMR statistically significant, based upon 
three deaths (SMR=386, p<0.05). Analysis by type of exposure is not 
meaningful due to the small number of lung cancer death per plant per 
exposure classification.
    Kano et al. conducted a study of five Japanese manufacturers who 
produced lead chromates, zinc chromate, and/or strontium chromate to 
assess if there was an excess risk of lung cancer (Ex. 7-118). The 
cohort consisted of 666 workers employed for a minimum of one year 
between 1950 and 1975. At the end of 1989, 604 subjects were alive, 
five lost to follow-up and 57 dead. Three lung cancer deaths were 
observed

[[Page 59332]]

in the cohort with 2.95 expected (SMR=102; 95% CI: 0.21-2.98). Eight 
stomach cancer deaths were reported with a non-statistically 
significant SMR of 120.
    In response to OSHA's August 2002 Request for Information, the 
Color Pigment Manufacturers Association suggested that OSHA consider 
reviewing the Davies (Ex. 7-43), Cooper [Equitable Environmental 
Health, Inc.] (Ex. 2-D-1) and Kano (Ex. 14-1-B) epidemiologic studies 
with respect to the health effects of lead chromate color pigments. The 
Equitable Environmental Health and the Kano et al. studies each report 
three deaths from lung cancer among chromate pigment production 
workers. The number of lung cancer deaths is too small to be 
meaningful. Even if there were a sufficient number of deaths for 
analysis, no quantitative exposure data are provided. In the case of 
the Davies study, there were seven lung cancer deaths at the one 
manufacturing facility that made only lead chromate pigments. When 
analyzed by period (early, 1946-1967) and high/medium and low exposure 
category, the numbers are too small in any category to be meaningful. 
Studies of lead and zinc chromate pigment worker cohorts that 
experienced a greater number of lung cancer deaths (e.g., >10 deaths) 
consistently found significant elevations in lung cancer risk, 
particularly those workers with the longest latency and durations of 
exposure (Exs. 234; 7-46; 7-42).
3. Evidence From Workers in Chromium Plating
    Chrome plating is the process of depositing chromium metal onto the 
surface of an item using a solution of chromic acid. The items to be 
plated are suspended in a diluted chromic acid bath. A fine chromic 
acid mist is produced when gaseous bubbles, released by the 
dissociation of water, rise to the surface of the plating bath and 
burst. There are two types of chromium electroplating. Decorative or 
``bright'' involves depositing a thin (0.5-1 [mu]m) layer of chromium 
over nickel or nickel-type coatings to provide protective, durable, 
non-tarnishable surface finishes. Decorative chrome plating is used for 
automobile and bicycle parts. Hard chromium plating produces a thicker 
(exceeding 5 [mu]m) coating which makes it resistant and solid where 
friction is usually greater, such as in crusher propellers and in 
camshafts for ship engines. Limited air monitoring indicates that 
Cr(VI) levels are five to ten times higher during hard plating than 
decorative plating (Ex. 35-116).
    There are fewer studies that have examined the lung cancer 
mortality of chrome platers than of soluble chromate production and 
chromate pigment production workers. The largest and best described 
cohort studies investigated chrome plating cohorts in the United 
Kingdom (Exs. 7-49; 7-57; 271; 35-62). They generally found elevated 
lung cancer mortality among the chrome platers, especially those 
engaged in chrome bath work, when compared to various reference 
populations. The studies of British chrome platers are summarized in 
Table VI-3.

Table VI-3.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
                                                Chromium Plating
----------------------------------------------------------------------------------------------------------------
                                                           Reference         Chromium (VI)
      Reference/exhibit No.        Study population       population           exposure        Lung cancer risk
----------------------------------------------------------------------------------------------------------------
Sorahan & Harrington (2000, Ex.   920 male platers    --Mortality rates   --Chromic acid      --O/E of 1.85
 35-62).                           employed in 54      for the general     mist with some      (p=0.001) based
Royle (1975, Ex. 7-49)..........   plants in           population of       nickel and          on 60 deaths and
                                   Yorkshire, UK for   England and Wales.  cadmium co-         general pop.
                                   a minimum of       --Age-, sex-         exposure.          --O/E of 1.39
                                   three months        matched            --Cr(VI) levels in   (p=0.06) based on
                                   between 1969 and    comparison group    1970 reported to    unexposed
                                   1972; follow up     unexposed to        range from <30      comparison group.
                                   through 1997.       CR(VI)..            [mu]g/m\3\ to      --No upward trend
                                                                           >100 [mu]g/m\3\..   w/duration of
                                                                                               exposure.
Sorahan et al. (1998, Ex. 35-     1,762 platers       --Mortality rates   --Chromic acid      --O/E of 1.6
 271).                             employed for a      for the general     mist with nickel    (p<0.01) for male
Sorahan et al. (1987, Ex. 7-57).   minimum of six      population of       co-exposure.        chrome bath
                                   months between      England and Wales. --No reported        workers based on
                                   1946 and 1975                           Cr(VI) exposure     40 deaths.
                                   from a Midlands,                        levels..           --O/E of 0.66 (NS)
                                   UK plant; follow                                            for other chrome
                                   up through 1995.                                            workers based on
                                                                                               9 deaths.
                                                                                              --Upward trend
                                                                                               (p<0.05) with
                                                                                               duration of
                                                                                               chrome bath work.
 
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E).
Relative Risk (RR).
Not Statistically Significant (NS).
Odds Ratio (OR).

    Cohort studies of chrome platers in Italy, the United States, and 
Japan are also discussed in this subsection. Co-exposure to nickel, 
another suspected carcinogen, during plating operations can complicate 
evaluation of an association between Cr(VI) and an increased risk of 
lung cancer in chrome platers. Despite this, the International Agency 
for Research on Cancer concluded that the epidemiological studies 
provide sufficient evidence for carcinogenicity of Cr(VI) as 
encountered in the chromium plating industry; the same conclusion 
reached for chromate production and chromate pigment production (Exs. 
18-1; 35-43). The findings implicate the highly water-soluble chromic 
acid as an occupational carcinogen. This adds to the weight of evidence 
that water-soluble (e.g., sodium chromates, chromic acid) and water-
insoluble forms (e.g., lead and zinc chromates) of Cr(VI) are able to 
cause cancer of the lower respiratory tract.
    Royle reported on a cohort mortality study of 1,238 chromium 
platers employed for a minimum of three consecutive months between 
February 20, 1969 and May 31, 1972 in 54 plating plants in West Riding, 
Yorkshire, England (Ex. 7-49). A control population was enumerated from 
other departments of the larger companies where chromium plating was 
only a portion of the companies' activities and from the former and 
current employees of two industrial companies in York where information 
on past workers was available. Controls were matched for gender, age 
(within two years) and date last known alive. In addition, 229 current 
workers were matched for smoking habits.

[[Page 59333]]

    As of May 1974, there were 142 deaths among the platers (130 males 
and 12 females) and 104 deaths among the controls (96 males and 8 
females). Among the male platers, there were 24 deaths from cancer of 
the lung and pleura compared to 13 deaths in the control group. The 
difference was not statistically significant. There were eight deaths 
from gastrointestinal cancer among male platers versus four deaths in 
the control group. The finding was not statistically significant.
    The Royle cohort was updated by Sorahan and Harrington (Ex. 35-62). 
Chrome plating was the primary activity at all 54 plants, however 49 of 
the plants used nickel and 18 used cadmium. Also used, but in smaller 
quantities according to the authors, were zinc, tin, copper, silver, 
gold, brass or rhodium. Lead was not used at any of the plants. Four 
plants, including one of the largest, only used chromium. Thirty-six 
chrome platers reported asbestos exposure versus 93 comparison workers.
    Industrial hygiene surveys were carried out at 42 plants during 
1969-1970. Area air samples were done at breathing zone height. With 
the exception of two plants, the chromic acid air levels were less than 
30 [mu]g/m<SUP>3</SUP>. The two exceptions were large plants, and in 
both the chromic acid levels exceeded 100 [mu]g/m<SUP>3</SUP>.
    The redefined cohort consisted of 1087 platers (920 men and 167 
women) from 54 plants employed for a minimum of three months between 
February 1969 and May 31, 1972 who were alive on May 31, 1972. 
Mortality data were also available for a comparison group of 1,163 
workers (989 men and 174 women) with no chromium exposure. Both groups 
were followed for vital status through 1997.
    The lung cancer SMR for male platers was statistically significant 
(O=60; E=32.5; SMR=185; 95% CI: 141-238). The lung cancer SMR for the 
comparison group, while elevated, was not statistically significant 
(O=47; E=36.9; SMR=127; 95% CI: 94-169). The only statistically 
significant SMR in the comparison group was for cancer of the pleura 
(O=7; E=0.57; SMR=1235; 95% CI: 497-2545).
    Internal regression analyses were conducted comparing the mortality 
rates of platers directly with those of the comparison workers. For 
these analyses, lung cancers mentioned anywhere on the death 
certificate were considered cases. The redefinition resulted in four 
additional lung cancer cases in the internal analyses. There was a 
statistically significant relative risk of 1.44 (p<0.05) for lung 
cancer mortality among chrome platers that was slightly reduced to 1.39 
after adjustment for smoking habits and employment status. There was no 
clear trend between lung cancer mortality and duration of Cr(VI) 
exposure. However, any positive trend may have been obscured by the 
lack of information on worker employment post-1972 and the large 
variation in chromic acid levels among the different plants.
    Sorahan reported the experience of a cohort of 2,689 nickel/
chromium platers from the Midlands, U.K. employed for a minimum of six 
months between 1946 and 1975 and followed through December 1983 (Ex. 7-
57). There was a statistically significant lung cancer SMR for males 
(O=63; E=40; SMR=158; p<0.001). The lung cancer SMR for women, while 
elevated (O=9; E=8.1; SMR=111), was not statistically significant. 
Other statistically significant cancer SMRs for males included: stomach 
(O=21; E=11.3; SMR=186; p<0.05); liver (O=4; E=0.6; SMR=667; p<0.01); 
and nasal cavities (O=2; E=0.2; SMR=1000; p<0.05). While there were 
several elevated SMRs for women, none were statistically significant. 
There were nine lung cancers and one nasal cancer among the women.
    Analysis by type of first employment (i.e., chrome bath workers vs. 
other chrome work) resulted in a statistically significant SMR for lung 
cancer of 199 (O=46; E=23.1; p<0.001) for chrome bath workers and a SMR 
of 101 for other chrome work. The SMR for cancer of the stomach for 
male chrome bath workers was also statistically significantly elevated 
(O=13; E=6.3; SMR=206; p<0.05); for stomach cancer in males doing other 
chrome work, the SMR was 160 with 8 observed and 5 expected. Both of 
the nasal cancers in males and the one nasal cancer in women were 
chrome bath workers. The nasal cancer SMR for males was statistically 
significantly elevated (O=2; E=0.1; SMR=2000; p<0.05).
    Regression analysis was used to examine evidence of association of 
several types of cancers and Cr(VI) exposure duration among the cohort. 
There was a significant positive association between lung cancer 
mortality and exposure duration as a chrome bath worker controlling for 
gender as well as year and age at the start of employment. There was no 
evidence of an association between other cancer types and duration of 
Cr(VI) exposure. There was no positive association between duration of 
exposure to nickel bath work and cancer of the lung. The two largest 
reported SMRs were for chrome bath workers 10-14 years (O=13; E=3.8; 
SMR=342; p<0.001) and 15-19 years (O=12; E=4.9; SMR=245; p<0.01) after 
starting employment. The positive associations between lung cancer 
mortality and duration of chrome bath work suggests Cr(VI) exposure may 
be responsible for the excess cancer risk.
    Sorahan et al. reported the results of a follow-up to the nickel/
chromium platers study discussed above (Ex. 271). The cohort was 
redefined and excluded employees whose personnel records could not be 
located (650); those who started chrome work prior to 1946 (31) and 
those having no chrome exposure (236). The vital status experience of 
1,762 workers (812 men and 950 women) was followed through 1995. The 
expected number of deaths was based upon the mortality of the general 
population of England and Wales.
    There were 421 deaths among the men and 269 deaths among the women, 
including 52 lung cancers among the men and 17 among the women. SMRs 
were calculated for different categories of chrome work: period from 
first chrome work; year of starting chrome work, and cumulative 
duration of chrome work categories. Poisson regression modeling was 
employed to investigate lung cancer in relation to type of chrome work 
and cumulative duration of work.
    A significantly elevated lung cancer SMR was seen for male workers 
with some period of chrome bath work (O=40; E=25.4; SMR=157; 95% CI: 
113-214, p<0.01) that was not the case for male workers engaged in 
other chrome work away from the chromic acid bath (O=9; E=13.7; SMR=66; 
95% CI: 30-125). Similar lung cancer mortality results were found for 
female chrome bath workers (O=15; E=8.6; SMR=175; 95% CI: 98-285; 
p<0.06). After adjusting for sex, age, calendar year, year starting 
chrome work, period from first chrome work, and employment status, 
regression modeling showed a statistically significant positive trend 
(p<0.05) between duration of chrome bath work and lung cancer mortality 
risk. The relative lung cancer risk for chrome bath workers with more 
than five years of Cr(VI) exposure (i.e., relative to the risk of those 
without any chrome bath work) was 4.25 (95% CI: 1.83-9.37).
    Since the Sorahan cohort consists of nickel/chromium workers, the 
question arises of the potential confounding of nickel. In the earlier 
study, 144 of the 564 employees with some period of chrome bath work 
had either separate or simultaneous periods of nickel bath employment. 
According to the authors, there was no clear association between cancer 
deaths from stomach, liver, respiratory system, nose and larynx, and

[[Page 59334]]

lung and bronchus and the duration of nickel bath employment. In the 
follow-up report, the authors re-iterate this result stating, 
``findings for lung cancer in a cohort of nickel platers (without any 
exposure to chrome plating) from the same factory are unexceptional'' 
(Ex. 271, p. 241).
    Silverstein et al. reported the results of a cohort study of hourly 
employees and retirees with at least 10 years of credited pension 
service in a Midwestern plant manufacturing hardware and trim 
components for use primarily in the automobile industry (Ex. 7-55). Two 
hundred thirty eight deaths occurred between January 1, 1974 and 
December 31, 1978. Proportional Mortality Ratio (PMR) analysis adjusted 
for race, gender, age and year of death was conducted. For white males, 
the PMR for cancer of the lung and pleura was 1.91 (p<0.001) based upon 
28 deaths. For white females, the PMR for cancer of the lung and pleura 
was 3.70 (p<0.001) based upon 10 deaths.
    White males who worked at the plant for less than 15 years had a 
lung cancer PMR of 1.65. Those with 15 or more years at the plant had a 
lung cancer PMR of 2.09 (p<0.001). For white males with less than 22.5 
years between hire and death (latency) the lung cancer PMR was 1.78 
(p<0.05) and for those with 22.5 or more years, the PMR was 2.11 
(p<0.01).
    A case-control analysis was conducted on the Silverstein cohort to 
examine the association of lung cancer risk with work experience. 
Controls were drawn from cardiovascular disease deaths (ICD 390-458, 
8th revision). The 38 lung cancer deaths were matched to controls for 
race and gender. Odds ratios (ORs) were calculated by department 
depending upon the amount of time spent in the department (ever/never; 
more vs. less than one year; and more vs. less than five years). Three 
departments showed increasing odds ratios with duration of work; 
however, the only statistically significant result was for those who 
worked more than five years in department 5 (OR=9.17, p=0.04, Fisher's 
exact test). Department 5 was one of the major die-casting and plating 
areas of the plant prior to 1971.
    Franchini et al. conducted a mortality study of employees and 
retirees from nine chrome plating plants in Parma, Italy (Ex. 7-56). 
Three plants produced hard chrome plating. The remaining six plants 
produced decorative chromium plates. A limited number of airborne 
chromium measurements were available. Out of a total of 10 measurements 
at the hard chrome plating plants, the air concentrations of chromium 
averaged 7 [mu]g/m<SUP>3</SUP> (range of 1-50 [mu]g/m<SUP>3</SUP>) as 
chromic acid near the baths and 3 [mu]g/m<SUP>3</SUP> (range of 0-12 
[mu]g/m<SUP>3</SUP>) in the middle of the room.
    The cohort consisted of 178 males (116 from the hard chromium 
plating plants and 62 from the bright chromium plating plants) who had 
worked for at least one year between January 1, 1951 and December 31, 
1981. In order to allow for a 10 year latency period, only those 
employed before January 1972 were included in further analysis. There 
were three observed lung cancer deaths among workers in the hard chrome 
plating plants, which was significantly greater than expected (O=3; 
E=0.6; p<0.05). There were no lung cancer deaths among decorative 
chrome platers.
    Okubo and Tsuchiya conducted a study of plating firms with five or 
more employees in Tokyo (Exs. 7-51; 7-52). Five hundred and eighty nine 
firms were sent questionnaires to ascertain information regarding 
chromium plating experience. The response rate was 70.5%. Five thousand 
one hundred seventy platers (3,395 males and 1,775 females) met the 
cohort entrance criteria and were followed from April 1, 1970 to 
September 30, 1976. There were 186 deaths among the cohort; 230 people 
were lost to follow-up after retirement. The cohort was divided into 
two groups: chromium platers who worked six months or more and a 
control group with no exposure to chromium (clerical, unskilled 
workers). There were no deaths from lung cancer among the chromium 
platers.
    The Okubo cohort was updated by Takahashi and Okubo (Ex. 265). The 
cohort was redefined to consist of 1,193 male platers employed for a 
minimum of six months between April 1970 and September 1976 in one of 
415 Tokyo chrome plating plants and who were alive and over 35 years of 
age on September 30, 1976. The only statistically significant SMR was 
for lung cancer for all platers combined (O=16; E=8.9; SMR=179; 95% CI: 
102-290). The lung cancer SMR for the chromium plater subcohort was 187 
based upon eight deaths and 172 for the nonchromium plater subcohort, 
also based upon eight deaths. The cohort was followed through 1987. 
Itoh et al. updated the Okubo metal plating cohort through December 
1992 (Ex. 35-163). They reported a lung cancer SMR of 118 (95% CI: 99-
304).
4. Evidence From Stainless Steel Welders
    Welding is a term used to describe the process for joining any 
materials by fusion. The fumes and gases associated with the welding 
process can cause a wide range of respiratory exposures which may lead 
to an increased risk of lung cancer. The major classes of metals most 
often welded include mild steel, stainless and high alloy steels and 
aluminum. The fumes from stainless steel, unlike fumes from mild steel, 
contain nickel and Cr(VI). There are several cohort and case-control 
studies as well as two meta analyses of welders potentially exposed to 
Cr(VI). In general, the studies found an excess number of lung cancer 
deaths among stainless steel welders. However, few of studies found 
clear trends with Cr(VI) exposure duration or cumulative Cr(VI). In 
most studies, the reported excess lung cancer mortality among stainless 
steel welders was no greater than mild steel welders, even though 
Cr(VI) exposure is much greater during stainless steel welding. This 
weak association between lung cancer and indices of exposure limits the 
evidence provided by these studies. Another limitation was the co-
exposures to other potential lung carcinogens, such as nickel, 
asbestos, and cigarette smoke. Nevertheless, these studies add some 
further support to the much stronger link between Cr(VI) and lung 
cancer found in soluble chromate production workers, chromate pigment 
production workers, and chrome platers. The key studies are summarized 
in Table VI-4.

[[Page 59335]]



Table VI-4.- Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
                                             Stainless Steel Welding
----------------------------------------------------------------------------------------------------------------
                                                           Reference         Chromium (VI)
      Reference/Exhibit No.        Study population       population           exposure        Lung cancer risk
----------------------------------------------------------------------------------------------------------------
Moulin (1997, Ex. 35-285).......  Meta analysis of    Stainless steel     Stainless steel     --RR of 1.50
                                   epidemiological     welding cohort      welders exposed     (p<0.05) for
                                   studies of lung     studies: Simonato   to higher Cr(VI)    stainless steel
                                   cancer risk among   et al., 1991;       than mild steel     welders based on
                                   welders in five     Polednak et al.,    welders.            combined 114
                                   categories          1981 case control                       deaths from five
                                   including           studies: Hull et                        studies
                                   stainless steel     al., 1989; Gerin                       --RR of 1.50
                                   welding and mild    et al., 1984;                           (p<0.05) for mild
                                   steel welding.      Kjuus et al. 1986.                      steel welders
                                                                                               based on combined
                                                                                               137 deaths from
                                                                                               four studies.
Sjogren et al. (1994, Ex. 7-113)  Meta analysis of    Stainless steel     Cr(VI) exposure     RR of 1.94
                                   epidemiological     welding cohort      was not part of     (p<0.05) for
                                   studies of          studies: Moulin     the analysis.       stainless steel
                                   exposure to         et al., 1993;                           welders based on
                                   stainless steel     Sjogren et al.,                         combined 70
                                   welding fumes and   1987 case control                       deaths from five
                                   lung cancer.        studies:                                studies.
                                                       Lauritsen et al.,
                                                       1996; Gerin et
                                                       al., 1984; Kjuus
                                                       et al. 1986.
Simonato et al. (1991, Ex.7-114)  Cohort of 11,092    Age and sex         Avg cumulative      --O/E of 1.23 (NS)
Gerin et al. (1993, Ex. 35-220).   male welders from   specific            Cr(VI) exposures    for primarily
                                   135 companies in    mortality rates     estimated between   stainless steel
                                   nine European       computed using      0.05 to 1.5 mg/     welders based on
                                   countries. Cohort   the WHO mortality   m\3\-yr based on    20 deaths.
                                   entrance criteria   data bank.          job process        --Upward trend
                                   varied by country.                      matrix.             (p<0.05) with
                                                                                               time since first
                                                                                               exposure.
                                                                                              --No trend with
                                                                                               cumulative
                                                                                               exposure
Moulin et al. (1993, Ex. 7-92)..  Cohort of 2,721     6,683 unexposed     --Primarily manual  --O/E of 1.03 (NS)
                                   French male         manual workers      metal arc welding.  for primarily
                                   welders from 13     from 13 factories  --Cr(VI) exposures   stainless steel
                                   factories with a    with a minimum of   not recorded.       welders based on
                                   minimum of one      one year of                             2 deaths.
                                   year of             employment from                        --No trend with
                                   employment from     1975 to 1988.                           exposure
                                   1975 to 1988.                                               duration.
Hansen et al. (1996, Ex. 35-247)  Cohort of 10,059    National cancer     Cr(VI) exposure     --O/E of 2.38 (NS)
                                   male welders and    incidence rates     not recorded.       for stainless
                                   other steel         from the Danish                         steel only
                                   workers from 79     Cancer Registry.                        welders based on
                                   Danish companies                                            5 deaths.
                                   employed for a                                             No trend with
                                   minimum of one                                              exposure
                                   year between 1964                                           duration.
                                   and 1984.
Lauritsen et al. (1996, Ex. 35-   Nested case-        439 eligible        Cr(VI) exposure     --OR of 1.3 (NS)
 291).                             control study of    controls who were   not recorded.       for stainless
                                   94 lung cancer      not cases and did                       steel only
                                   deaths from         not have                                welders.
                                   Hansen study.       respiratory                            --No trend with
                                                       disease or                              exposure
                                                       unknown                                 duration.
                                                       malignancy as
                                                       cause of death.
Sjogren et al. (1987, Ex. 795)..  Cohort of 234 male  Mortality rates     Median Cr level     --O/E of 2.5 (NS)
                                   stainless steel     for Swedish males.  for stainless       for
                                   welders and 208                         steel welding was   stainlesssteel
                                   male railway                            57 [mu]g/m\3\ and   welders based on
                                   track welders.                          for gas shielded    5 deaths.
                                   Minimum                                 welding [railway   --O/E of 0.3 (NS)
                                   employment was 5                        welders] was 5      for railway
                                   years between                           [mu]g/m\3\ in       welders based on
                                   1950 and 1965.                          Sweden during       1 death.
                                   Follow-up through                       1975.
                                   1984.
Kjuus et al. (1986, Ex. 7-72)...  A hospital-based    186 controls        Cr(VI) exposure     --OR of 3.0 (p
                                   case-control        admitted to the     not recorded.       <0.05, adjusted
                                   study of 176 male   same hospitals in                       for smoking) for
                                   incident lung       Norway during                           stainless steel
                                   cancer cases        1979-1983 and                           welding based on
                                   admitted to two     matched to cases                        16 deaths.
                                   hospitals in        for age +/-5                           --Welding not
                                   Norway during       years.                                  significant in
                                   1979-1983.                                                  logistic model
                                                                                               with smoking,
                                                                                               asbestos.
Hull, et al. (1989, Ex. 35-243).  Case-control study  Controls were 74    No direct Cr(VI)    --OR of 0.9 (NS)
                                   of 85 lung cancer   welders with non-   exposure            for stainless
                                   cases in white      pulmonary           measurements        steel welding
                                   male welders        malignancies.       recorded.           based on 34
                                   identified                                                  cases.
                                   through the LA                                             --OR of 1.3 (NS)
                                   County tumor                                                for manual metal
                                   registry (1972-                                             arc welding on
                                   1987).                                                      stainless steel
                                                                                               based on 61
                                                                                               cases.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E)
Relative Risk (RR)
Not Statistically Significant (NS)
Odds Ratio (OR)

    Sjogren et al. reported on the mortality experience in two cohorts 
of welders (Ex. 7-95). The cohort characterized as ``high exposure'' 
consisted of 234 male stainless steel welders with a minimum of five 
years of employment between 1950 and 1965. An additional criterion for 
inclusion in the study was assurance from the employer that asbestos 
had not been used or had been used only occasionally and never in a 
dust-generating way. The cohort characterized as ``low exposure'' 
consisted of 208 male railway track welders working at the Swedish 
State Railways for at least five years between 1950 and 1965. In 1975, 
air pollution in stainless steel welding was surveyed in Sweden. The 
median time weighted average (TWA) value for Cr(VI) was 110 [mu]g 
CrO<INF>3</INF>/m\3\ (57 [mu]g/m\3\ measured as CrVI). The highest 
concentration was 750 [mu]g CrO<INF>3</INF>/m\3\ (390 [mu]g/m\3\ 
measured as CrVI) found in welding involving coated electrodes. For 
gas-shielded welding, the median Cr(VI) concentration was 10 [mu]g 
CrO<INF>3</INF>/m\3\ (5.2 [mu]g/m\3\ measured as CrVI) with the highest 
concentration measured at 440 [mu]g CrO<INF>3</INF>/m\3\ (229 [mu]g/
m\3\ measured as CrVI). Follow-up for both cohorts was through December 
1984. The expected number of deaths was based upon Swedish male death 
rates. Of the 32 deaths in the ``high exposure'' group, five were 
cancers of the trachea, bronchus and lung (E=2.0; SMR=249;

[[Page 59336]]

95% CI: 0.80-5.81). In the low exposure group, 47 deaths occurred, one 
from cancer of the trachea, bronchus and lung.
    Polednak compiled a cohort of 1,340 white male welders who worked 
at the Oak Ridge nuclear facilities from 1943 to 1977 (Ex. 277). One 
thousand fifty-nine cohort members were followed through 1974. The 
cohort was divided into two groups. The first group included 536 
welders at a facility where nickel-alloy pipes were welded; the second 
group included 523 welders of mild steel, stainless steel and aluminum 
materials. Smoking data were available for 33.6% of the total cohort. 
Expectations were calculated based upon U.S. mortality rates for white 
males. There were 17 lung cancer deaths in the total cohort (E=11.37; 
SMR=150; 95% CI: 87-240). Seven of the lung cancer deaths occurred in 
the group which routinely welded nickel-alloy materials (E=5.65; 
SMR=124; 95% CI: 50-255) versus 10 lung cancer deaths in the ``other'' 
welders (E=6.12; SMR=163; 95% CI: 78-300).
    Becker et al. compiled a cohort of 1,213 stainless steel welders 
and 1,688 turners from 25 German metal processing factories who had a 
minimum of six months employment during the period 1950-1970 (Exs. 
227;250;251). The data collected included the primary type of welding 
(e.g., arc welding, gas-shielded welding, etc.) used by each person, 
working conditions, average daily welding time and smoking status. The 
most recent follow-up of the cohort was through 1995. Expected numbers 
were developed using German mortality data. There were 268 deaths among 
the welders and 446 deaths among the turners. An elevated, but non-
statistically significant, lung cancer SMR (O=28; E=23; SMR=121.5; 95% 
CI: 80.7-175.6) was observed among the welders. There were 38 lung 
cancer deaths among the turners with 38.6 expected, resulting in a SMR 
slightly below unity. Seven deaths from cancer of the pleura (all 
mesotheliomas) occurred among the welders with only 0.6 expected 
(SMR=1,179.9; 95% CI: 473.1-2,430.5), compared to only one death from 
cancer of the pleura among the turners, suggesting that the welders had 
exposure to asbestos. Epidemiological studies have shown that asbestos 
exposure is a primary cause of pleural mesotheliomas.
    The International Agency for Research on Cancer (IARC) and the 
World Health Organization (WHO) cosponsored a study on welders. IARC 
and WHO compiled a cohort of 11,092 male welders from 135 companies in 
nine European countries to investigate the relationship between the 
different types of exposure occurring in stainless steel, mild steel 
and shipyard welding and various cancer sites, especially lung cancer 
(Ex. 7-114). Cohort entrance criteria varied by country. The expected 
number of deaths was compiled using national mortality rates from the 
WHO mortality data bank.
    Results indicated the lung cancer deaths were statistically 
significant in the total cohort (116 cases; E=86.81; SMR=134; 95% CI: 
110-160). Cohort members were assigned to one of four subcohorts based 
upon type of welding activity. While the lung cancer SMRs were elevated 
for all of the subcohorts, the only statistically significant SMR was 
for the only mild steel welders (O=40; E=22.42; SMR=178; 95% CI: 127-
243). Results for the other subgroups were: shipyard welders (O=36; 
E=28.62; SMR=126; 95% CI: 88-174); ever stainless steel welders (O=39; 
E=30.52; SMR=128; 95% CI: 91-175); and predominantly stainless steel 
welders (O=20; E=16.25; SMR=123; 95% CI: 75-190). When analyzed by 
subcohort and time since first exposure, the SMRs increased over time 
for every group except shipyard welders. For the predominantly 
stainless steel welder subcohort, the trend to increase with time was 
statistically significant (p <.05).
    An analysis was conducted of lung cancer mortality in two stainless 
steel welder subgroups (predominantly and ever) with a minimum of five 
years of employment. Cumulative Cr(VI) was computed from start of 
exposure until 20 years prior to death. A lung cancer SMR of 170, based 
upon 14 cases, was observed in the stainless steel ever subgroup for 
those welders with >0.5 [mu]g-years/m\3\ Cr(VI) exposure; the lung 
cancer SMR for those in the <0.5 [mu]g-years/m\3\ Cr(VI) exposure group 
was 123 (based upon seven cases). Neither SMR was statistically 
significant. For the predominantly stainless steel welders, which is a 
subset of the stainless steel ever subgroup, the corresponding SMRs are 
167 (>0.5 [mu]g-years/m\3\ Cr(VI) exposure) based upon nine cases and 
191 (<0.5 [mu]g-years/m\3\ Cr(VI) exposure) based upon three cases. 
Neither SMR is statistically significant.
    In conjunction with the IARC/WHO welders study, Gerin et al. 
reported the development of a welding process exposure matrix relating 
13 combinations of welding processes and base metals used to average 
exposure levels for total welding fumes, total chromium, Cr(VI) and 
nickel (Ex. 7-120). Quantitative estimates were derived from the 
literature supplemented by limited monitoring data taken in the 1970s 
from only eight of the 135 companies in the IARC/WHO mortality study. 
An exposure history was constructed which included hire and termination 
dates, the base metal welded (stainless steel or mild steel), the 
welding process used and changes in exposure over time. When a detailed 
welding history was not available for an individual, the average 
company welding practice profile was used. In addition, descriptions of 
activities, work force, welding processes and parameters, base metals 
welded, types of electrodes or rods, types of confinement and presence 
of local exhaust ventilation were obtained from the companies.
    Cumulative dose estimates in mg/m<SUP>3</SUP> years were generated 
for each welder's profile (number of years and proportion of time in 
each welding situation) by applying a welding process exposure matrix 
associating average concentrations of welding fumes (mg/m<SUP>3</SUP>) 
to each welding situation. The corresponding exposure level was 
multiplied by length of employment and summed over the various 
employment periods involving different welding situations. No dose 
response relationship was seen for exposure to Cr(VI) for either those 
who were ``ever stainless steel welders'' or those who were 
``predominantly stainless steel welders''. The authors note that if 
their exposure estimates are correct, the study had the power to detect 
a significant result in the high exposure group for Cr(VI).
    The IARC/WHO multicenter study is the sole attempt to undertake 
even a semi-quantified exposure analysis of stainless steel welders' 
potential exposure to nickel and Cr(VI) for <5 and >=0.5 mg-years/
m<SUP>3</SUP> Cr(VI) exposures. The IARC/WHO investigators noted that 
there was more than a twofold increase in SMRs between the long (>=20 
years since first exposure) and short (<20 years since first exposure) 
observation groups for the predominantly stainless steel welders 
``suggesting a relation of lung cancer mortality with the occupational 
environment for this group'' (Ex. 7-114, p. 152). The authors conclude 
that the increase in lung cancer mortality does not appear to be 
related to either duration of exposure or cumulative exposure to total 
fume, chromium, Cr(VI) or nickel.
    Moulin compiled a cohort of 2,721 French male welders and an 
internal comparison group of 6,683 manual workers employed in 13 
factories (including three shipyards) with a minimum of one year of 
employment from 1975 to 1988 (Ex. 7-92). Three

[[Page 59337]]

controls were selected at random for each welder. Smoking data were 
abstracted from medical records for 86.6% of welders and 86.5% of the 
controls. Smoking data were incorporated in the lung cancer mortality 
analysis using methods suggested by Axelson. Two hundred and three 
deaths were observed in the welders and 527 in the comparison group. A 
non-statistically significant increase was observed in the lung cancer 
SMR (O=19; E=15.33; SMR=124; 95% CI: 0.75-1.94) for the welders. In the 
control group, the lung cancer SMR was in deficit (O=44; E=46.72; 
SMR=94; 95% CI: 0.68-1.26). The resulting relative risk was a non-
significant 1.3. There were three deaths from pleural cancer in the 
comparison group and none in the welders suggesting asbestos exposure 
in the comparison group. The welders were divided into four subgroups 
(shipyard welders, mild steel only welders, ever stainless steel 
welders and stainless steel predominantly Cr(VI) welders). The highest 
lung cancer SMR was for the mild steel welders O=9; SMR of 159). The 
lowest lung cancer SMRs were for ever stainless steel welders (O=3; 
SMR= 92) and for stainless steel predominantly Cr(VI) welders (O=2; 
SMR=103). None of the SMRs are statistically significant.
    Hansen conducted a study of cancer incidence among 10,059 male 
welders, stainless steel grinders and other metal workers from 79 
Danish companies (Ex. 9-129). Cohort entrance criteria included: Alive 
on April 1, 1968; born before January 1, 1965; and employed for at 
least 12 months between April 1, 1964 and December 31, 1984. Vital 
status follow-up found 9,114 subjects alive, 812 dead and 133 had 
emigrated. A questionnaire was sent to subjects and proxies for 
decedents/emigrants in an attempt to obtain information about lifetime 
occupational exposure, smoking and drinking habits. The overall 
response rate was 83%. The authors stated that no major differences in 
smoking habits were found between exposure groups with or without a 
significant excess of lung cancer.
    The expected number of cancers was based on age-adjusted national 
cancer incidence rates from the Danish Cancer Registry. There were 
statistically significantly elevated Standardized Incidence Ratios 
(SIRs) for lung cancer in the welding (any kind) group (O=51; E=36.84; 
SIR=138; 95% CI: 103-181) and in the mild steel only welders (O=28; 
E=17.42; SIR=161; 95% CI: 107-233). The lung cancer SIR for mild steel 
ever welders was 132 (O=46; E=34.75; 95% CI: 97-176); for stainless 
steel ever welders 119 (O=23; E=19.39; 95% CI: 75-179) and for 
stainless steel only welders 238 (O=5; E=2.10; 95% CI: 77-555).
    Laurtitsen reported the results of a nested case-control conducted 
in conjunction with the Hansen cancer incidence study discussed above 
(Exs. 291; 9-129). Cases were defined as the 94 lung cancer deaths. 
Controls were defined as anyone who was not a case, but excluded deaths 
from respiratory diseases other than lung cancer (either as an 
underlying or a contributing cause of death), deaths from ``unknown 
malignancies'' and decedents who were younger than the youngest case. 
There were 439 decedents eligible for use as controls.
    The crude odds ratio (OR) for welding ever (yes/no) was 1.7 (95% 
CI: 1.0-2.8). The crude OR for mild steel welding only was 1.3 (95% CI: 
0.8-2.3) and for stainless steel welding only the crude OR was 1.3 (95% 
CI: 0.3-4.3). When analyzed by number of years exposed, ``ever'' 
stainless steel welding showed no relationship with increasing number 
of years exposed. The highest odds ratio (2.9) was in the lowest 
category (1-5 years) based upon seven deaths; the lowest odds ratio was 
in the highest category (21+ years) based upon three deaths.
    Kjuus et al. conducted a hospital-based case-control study of 176 
male incident lung cancer cases and 186 controls (matched for age, +/-5 
years) admitted to two county hospitals in southeast Norway during 
1979-1983 (Ex. 7-72). Subjects were classified according to exposure 
status of main occupation and number of years in each exposure category 
and assigned into one of three exposure groups according to potential 
exposure to respiratory carcinogens and other contaminants. A 
statistically significantly elevated risk ratio for lung cancer 
(adjusted for smoking) for the exposure factor ``welding, stainless, 
acid proof'' of 3.3 (p<0.05) was observed based upon 16 lung cancer 
deaths. The unadjusted odds ratio is not statistically significant 
(OR=2.8). However, the appropriateness of the analysis is questionable 
since the exposure factors are not discrete (a case or a control may 
appear in multiple exposure factors and therefore is being compared to 
himself). In addition, the authors note that several exposure factors 
were highly correlated and point out specifically that one-half of the 
cases ``exposed to either stainless steel welding fumes or fertilizers 
also reported moderate to heavy asbestos exposure.'' When put into a 
stepwise logistic regression model, exposure to stainless steel fumes, 
which was initially statistically significant, loses its significance 
when smoking and asbestos are first entered into the model.
    Hull et al. conducted a case-control study of lung cancer in white 
male welders aged 20-65 identified through the Los Angeles County tumor 
registry (Southern California Cancer Surveillance Program) for the 
period 1972 to 1987 (Ex. 243). Controls were welders 40 years of age or 
older with non-pulmonary malignancies. Interviews were conducted to 
obtain information about sociodemographic data, smoking history, 
employment history and occupational exposures to specific welding 
processes, metals welded, asbestos and confined space welding. 
Interviews were completed for 90 (70%) of the 128 lung cancer cases and 
116 (66%) of the controls. Analysis was conducted using 85 deceased 
cases and 74 deceased controls after determining that the subject's 
vital status influenced responses to questions concerning occupational 
exposures. The crude odds ratio (ever vs. never exposed) for stainless 
steel welding, based upon 34 cases, was 0.9 (95% CI: 0.3-1.4). For 
manual metal arc welding on stainless steel, the crude odds ratio was 
1.3 (95% CI: 0.6-2.3) based upon 61 cases.
    While the relative risk estimates in both cohort and case-control 
of stainless steel welders are elevated, none are statistically 
significant. However, when combined in two meta-analyses, a small but 
statistically significant increase in lung cancer risk was reported. 
Two meta-analyses of welders have been published. Moulin carried out a 
meta-analysis of epidemiologic studies of lung cancer risk among 
welders, taking into account the role of asbestos and smoking (Ex. 
285). Studies published between 1954 and 1994 were reviewed. The 
inclusion criteria were clearly defined: only the most recent updates 
of cohort studies were used and only the mortality data from mortality/
morbidity studies were included. Studies that did not provide the 
information required by the meta-analysis were excluded.
    Five welding categories were defined (shipyard welding, non-
shipyard welding, mild steel welding, stainless steel welding and all 
or unspecified welding). The studies were assigned to a welding 
category (or categories) based upon the descriptions provided in the 
paper's study design section. The combined relative risks (odds ratios, 
standardized mortality ratios, proportionate mortality ratios and 
standardized incidence ratios) were calculated separately for the 
population-based studies, case-control studies and

[[Page 59338]]

cohort studies and for all the studies combined.
    Three case-control studies (Exs. 243; 7-120; 7-72) and two cohort 
studies (Exs. 7-114; 277) were included in the stainless steel welding 
portion of the meta-analysis. The combined relative risk was 2.00 
(O=87; 95% CI: 1.22-3.28) for the case-control studies and 1.23 (O=27; 
95% CI: 0.82-1.85) for the cohort studies. When all five studies were 
combined, the relative risk was 1.50 (O=114; 95% CI: 1.10-2.05).
    By contrast, the combined risk ratio for the case-control studies 
of mild steel welders was 1.56 (O=58; 95% CI: 0.82-2.99) (Exs. 7-120; 
243). For the cohort studies, the risk ratio was 1.49 (O=79; 95% CI: 
1.15-1.93) (Exs. 270; 7-114). For the four studies combined, the risk 
ratio was 1.50 (O=137; 95% CI: 1.18-191). The results for the stainless 
steel welders and the mild steel welders are basically the same.
    The meta-analysis by Sjogren of exposure to stainless steel welding 
fumes and lung cancer included studies published between 1984 and 1993, 
which took smoking and potential asbestos exposure into account (Ex. 7-
113). Five studies met the author's inclusion criteria and were 
included in the meta-analysis: two cohort studies, Moulin et al. (Ex. 
283) and Sjogren et al. (Ex. 7-95); and three case-control studies, 
Gerin, et al. (Ex. 7-120, Hansen et al. (Ex. 9-129) and Kjuus et al. 
(Ex. 7-72). The calculated pooled relative risk for welders exposed to 
stainless steel welding fumes was 1.94 (95% CI: 1.28-2.93).
5. Evidence From Ferrochromium Workers
    Ferrochromium is produced by the electrothermal reduction of 
chromite ore with coke in the presence of iron in electric furnaces. 
Some of the chromite ore is oxidized into Cr(VI) during the process. 
However, most of the ore is reduced to chrome metal. The manufacture of 
ferroalloys results in a complex mixture of particles, fumes and 
chemicals including nickel, Cr(III) and Cr(VI). Polycyclic aromatic 
hydrocarbons (PAH) are released during the manufacturing process. The 
co-exposure to other potential lung carcinogens combined with the lack 
of a statistically significant elevation in lung cancer mortality among 
ferrochromium workers were limitations in the key studies. 
Nevertheless, the observed increase in the relative risks of lung 
cancer add some further support to the much stronger link between 
Cr(VI) and lung cancer found in soluble chromate production workers, 
chromate pigment production workers, and chrome platers. The key 
studies are summarized in Table VI-5.

Table VI-5.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
                                            Ferrochromium Production
----------------------------------------------------------------------------------------------------------------
                                                           Reference         Chromium (VI)
      Reference/Exhibit No.        Study population       population           exposure        Lung cancer risk
----------------------------------------------------------------------------------------------------------------
Axelsson et al. (1980, Ex. 7-62)  1932 Swedish males  Swedish county      ``Recent'' job-     --O/E of 0.7 (NS)
                                   employed at least   mortality and       specific Cr(VI)     for ferrochromium
                                   one year in a       incidence rates.    levels estimated    workers based on
                                   ferrochromium                           at 10 to 250        5 cases.
                                   between 1930 to                         [mu]g/m3.          --No trend with
                                   1975.                                                       job-specific
                                                                                               Cr(VI).
Langard et al. (1990, Ex. 7-37).  1235 males          --Norwegian Cancer  Avg total Cr        --O/E of 1.5 (NS)
                                   employed at least   Registry.           exposure was 50     for ferrochromium
                                   one year who       --Subcohort of       [mu]g/m3 in 1975    workers based on
                                   started working     ferrosilicon        with 11 to 33%      10 cases.
                                   prior to 1965 in    workers at same     soluble Cr(VI).    --O/E of 0.3 for
                                   a Norway            plant not exposed                       ferrosilicon
                                   ferrochromium       to Cr(VI)..                             workers based on
                                   plant. Follow-up                                            2 cases.
                                   was through 1985.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E).
Relative Risk (RR).
Not Statistically Significant (NS).
Odds Ratio (OR).

    Langard et al. conducted a cohort study of male workers producing 
ferrosilicon and ferrochromium for more than one year between 1928 and 
1977 at a plant located on the west coast of Norway (Exs. 7-34; 7-37). 
The cohort and study findings are summarized in Table VI.5. Excluded 
from the study were workers who died before January 1, 1953 or had an 
unknown date of birth. The cohort was defined in the 1980 study as 976 
male employees who worked for a minimum of one year prior to January 1, 
1960. In the 1990 study, the cohort definition was expanded to include 
those hired up to 1965.
    Production of ferrosilicon at the plant began in 1928 and 
ferrochromium production began in 1932. Job characterizations were 
compiled by combining information from company personnel lists and 
occupational histories contained in medical records and supplemented 
with information obtained via interview with long-term employees. Ten 
occupational categories were defined. Workers were assigned to an 
occupational category based upon the longest time in a given category.
    Industrial hygiene studies of the plant from 1975 indicated that 
both Cr(III) and Cr(VI) were present in the working environment. The 
ferrochromium furnance operators were exposed to measurements of 0.04-
0.29 mg/m<SUP>3</SUP> of total chromium. At the charge floor the mean 
concentration of total chromium was 0.05 mg/m<SUP>3</SUP>, 11-33% of 
which was water soluble. The water soluble chromium was considered to 
be in the hexavalent state.
    Both observed and expected cases of cancer were obtained via the 
Norwegian Cancer Registry. The observation period for cancer incidence 
was January 1, 1953 to December 31, 1985. Seventeen incident lung 
cancers were reported in the 1990 study (E=19.4; SIR=88). A deficit of 
lung cancer incidence was observed in the ferrosilicon group (O=2; 
E=5.8; SIR=35). In the ferrochromium group there were a significant 
excess of lung cancer; 10 observed lung cancers with 6.5 expected 
(SIR=154).
    Axelsson et al. conducted a study of 1,932 ferrochromium workers to 
examine whether exposure in the ferrochromium industry could be 
associated with an increased risk of developing tumors, especially lung 
cancer (Ex. 7-62). The study cohort and findings are summarized in 
Table VI.5. The study cohort was defined as males employed at a 
ferrochromium plant in Sweden for at least one year during the period 
January 1, 1930 to December 31, 1975.
    The different working sites within the industry were classified 
into four groups with respect to exposure to Cr(VI) and Cr(III). 
Exposure was primarily to metallic and trivalent chromium with 
estimated levels ranging from 0-2.5 mg/m<SUP>3</SUP>. Cr(VI) was also 
present in certain operations with estimated levels ranging from 0-0.25 
mg/m<SUP>3</SUP>. The highest exposure to Cr(VI) was in the arc-furnace 
operations. Cr(VI) exposure also

[[Page 59339]]

occurred in a chromate reduction process during chromium alum 
production from 1950-1956. Asbestos-containing materials had been used 
in the plant. Cohort members were classified according to length and 
place of work in the plant.
    Death certificates were obtained and coded to the revision of the 
International Classification of Diseases in effect at the time of 
death. Data on cancer incidence were obtained from the Swedish National 
Cancer Registry. Causes of death in the cohort for the period 1951-1975 
were compared with causes of death for the age-adjusted male population 
in the county in which the plant was located.
    There were seven cases of cancers of the trachea, bronchus and lung 
and the pleura with 5.9 expected (SIR=119) for the period 1958-1975. 
Four of the seven cases in the lung cancer group were maintenance 
workers and two of the four cases were pleural mesotheliomas. In the 
arc furnace group, which was thought to have the highest potential 
exposure to both Cr(III) and Cr(VI), there were two cancers of the 
trachea, bronchus and lung and the pleura. One of the cases was a 
mesothelioma. Of the 380 deaths that occurred during the period 1951-
1975, five were from cancer of the trachea, bronchus and lung and the 
pleura (E=7.2; SMR=70). For the ``highly'' exposed furnace workers, 
there was one death from cancer of the trachea, bronchus and lung and 
the pleura.
    Moulin et al. conducted a cohort mortality study in a French 
ferrochromium/stainless steel plant to determine if exposure to 
chromium compounds, nickel compounds and polycyclic aromatic 
hydrocarbons (PAHs) results in an increased risk of lung cancer (Ex. 
282). The cohort was defined as men employed for at least one year 
between January 1, 1952 and December 31, 1982; 2,269 men met the cohort 
entrance criteria. No quantitative exposure data were available and no 
information on the relative amounts of Cr(VI) and Cr(III) was provided. 
In addition, some workers were also exposed to other carcinogens, such 
as silica and asbestos. The authors estimated that 75.7% of the cohort 
had been exposed to combinations of PAH, nickel and chromium compounds. 
Of the 137 deaths identified, the authors determined 12 were due to 
cancer of the trachea, bronchus and lung (E=8.56; SMR=140; 95% CI: 
0.72-2.45). Eleven of the 12 lung cancers were in workers employed for 
at least one year in the ferrochromium or stainless steel production 
workshops (E=5.4; SMR=204; 95% CI: 1.02-3.64).
    Pokrovskaya and Shabynina conducted a cohort mortality study of 
male and female workers employed ``some time'' between 1955 and 1969 at 
a chromium ferroalloy production plant in the U.S.S.R (Ex. 7-61). 
Workers were exposed to both Cr(III) and Cr(VI) as well as to benzo [a] 
pyrene. Neither the number of workers nor the number of cancer deaths 
by site were provided. Death certificates were obtained and the deaths 
were compared with municipal mortality rates by gender and 10 year age 
groups. The investigators state that they were able to exclude those in 
the comparison group who had chromium exposures in other industries. 
The lung cancer SMR for male chromium ferroalloy workers was 440 in the 
30-39 year old age group and 660 in the 50-59 year old age group 
(p=0.001). There were no lung cancer deaths in the 40-49 and the 60-69 
year old age groups. The data suggest that these ferrochromium workers 
may have been had an excess risk of lung cancer.
    The association between Cr(VI) exposure in ferrochromium workers 
and the incidence of respiratory tract cancer these studies is 
difficult to assess because of co-exposures to other potential 
carcinogens (e.g., asbestos, PAHs, nickel, etc.), absence of a clear 
exposure-response relationship and lack of information on smoking. 
There is suggestive evidence of excess lung cancer mortality among 
Cr(VI)-exposed ferrochromium workers in the Norwegian (Langard) cohort 
when compared to a similar unexposed cohort of ferrosilicon workers. 
However, there is little consistency for this finding in the Swedish 
(Axelsson) or French (Moulin) cohorts.
6. Evidence From Workers in Other Industry Sectors
    There are several other epidemiological studies that do not fit 
into the five industry sectors previously reviewed. These include 
worker cohorts in the aerospace industry, paint manufacture, and 
leather tanning operations, among others. The two cohorts of aircraft 
manufacturing workers are summarized in Table VI-6. All of the cohorts 
had some Cr(VI) exposure but, certain cohorts may have included a 
sizable number of workers with little or no exposure to Cr(VI). This 
creates an additional complexity in assessing whether the study 
findings support a Cr(VI) etiology for cancer of the respiratory 
system.

Table VI-6.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
                                              Aircraft Manufacture
----------------------------------------------------------------------------------------------------------------
                                                           Reference         Chromium (VI)
      Reference/Exhibit No.        Study population       population           exposure        Lung Cancer risk
----------------------------------------------------------------------------------------------------------------
Alexander et al. (1996, Ex. 31-   2429 aerospace      Incidence rates     Painters/sanders    --O/E of 0.8 (NS)
 16-3).                            workers with a      from regional       exposed to zinc     for aerospace
                                   minimum six         cancer              strontium and       cohort based on
                                   months employment   surveillance        lead chromates.     15 deaths.
                                   in Washington       system registry.   Platers/tank        --No clear trend
                                   State from 1974                         tenders exposed     with chromate
                                   to 1994. Median                         primarily to        exposure.
                                   age at end of                           chromic acid
                                   study was 42                            Median cumulative
                                   years with median                       chromate exposure
                                   9 years follow-up.                      between 0.01 and
                                                                           0.18 mg/m\3\-yr
                                                                           based on 1974 to
                                                                           1994 data..
Boice et al. (1999, Ex. 31-16-4)  77,965 workers      Mortality rates     8 percent of        --O/E of 1.02 (NS)
                                   employed for        for white           cohort had          for workers with
                                   minimum of one      population of       potential for       routine Cr(VI)
                                   year in             California and      routine Cr(VI)      exposures based
                                   California          for non-white       exposure as         on 87 deaths.
                                   aircraft            U.S. population.    painters and       --Upward trend
                                   manufacturing                           platers.            (NS) with
                                   plant on or after                      No Cr(VI) exposure   duration of
                                   1960. Follow-up                         levels reported..   exposure.
                                   through 1996.                                              --O/E of 0.71
                                                                                               (p<0.05) for non-
                                                                                               factory workers.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E)
Relative Risk (RR)
Not Statistically Significant (NS)
Odds Ratio (OR)


[[Page 59340]]

    Alexander et al. conducted a cohort study of 2,429 aerospace 
workers with a minimum of six months of cumulative employment in jobs 
involving chromate exposure during the period 1974 through 1994 (Ex. 
31-16-3). Exposure estimates were based on industrial hygiene 
measurements and work history records. Jobs were classified into 
categories of ``high'' (spray painters, decorative painters), 
``moderate'' (sanders/maskers, maintenance painters) and ``low'' 
(chrome platers, surface processors, tank tenders, polishers, paint 
mixers) exposure. Each exposure category was assigned a summary TWA 
exposure based upon the weighted TWAs and information from industrial 
hygienists. The use of respiratory protection was accounted for in 
setting up the job exposure matrix. The index of cumulative total 
chromium exposure (reported as [mu]g/m<SUP>3</SUP> chromate TWA-years) 
was computed by multiplying the years in each job by the summary TWAs 
for each exposure category.
    In addition to cumulative chromate exposure, chromate exposure jobs 
were classified according to the species of chromate. According to the 
authors, in painting operations the exposure is to chromate pigments 
with moderate and low solubility such as zinc chromate, strontium 
chromate and lead chromate; in sanding and polishing operations the 
same chromate pigments exist as dust; while platers and tank tenders 
are exposed to chromium trioxide, which is highly soluble.
    Approximately 26% of the cohort was lost to follow-up. The cohort 
was followed for a relatively short 8.9 years per cohort member. Cases 
were identified through the Cancer Surveillance System (CSS) at the 
Fred Hutchinson Cancer Research Center in Seattle, Washington. CSS 
records primary cancer diagnoses in 13 counties in western Washington. 
Expected numbers were calculated using race-, gender-, age- and 
calendar-specific rates from the Puget Sound reference population for 
1974 through 1994. Fifteen lung cancer cases were identified with an 
overall standardized incidence ratio (SIR) of 80 (95% CI: 0.4-1.3). The 
SIRs for lung cancer by cumulative years of employment in the ``high 
exposure'' painting job category were based upon only three deaths in 
each of the cumulative years categories (<5 and >=5); years of 
employment was inversely related to the risk of lung cancer. For those 
in the ``low exposure'' category, the SIRs were 130 for those who 
worked less than five years in that category (95% CI: 0.2-4.8) and 190 
for those who worked five years or more (95% CI: 0.2-6.9). However, 
there were only two deaths in each category. The SIR for those who 
worked >=5 years was 270 (95% CI: 0.5-7.8), but based only on three 
deaths.
    Boice et al. conducted a cohort mortality study of 77,965 workers 
employed for a minimum of one year on or after January 1960 in aircraft 
manufacturing (Ex. 31-16-4). Routine exposures to Cr(VI) compounds 
occurred primarily while operating plating and coating process 
equipment or when using chromate based primers or paints. According to 
the authors, 3,634 workers, or 8% of the cohort, had the potential for 
routine exposure to chromate and 3,809 workers, or 8.4%, had the 
potential for intermittent exposure to chromate. Estimates of chromate 
exposure were not provided in the study.
    Follow up of the cohort was through 1996. Expectations were 
calculated based on the general population of California for white 
workers, while general population rates for the U.S. were used for non-
white workers. For the 3,634 cohort members who had potential for 
routine exposure to chromates, the lung cancer SMR (race and gender 
combined) was 102 based upon 87 deaths (95% CI: 0.82-1.26). There was a 
slight non-significant positive trend (p value>2.0) for lung cancer 
with duration of potential exposure. The SMR was 108 (95% CI: 0.75-
1.57) for workers exposed to chromate for >=5 years. Among the 
painters, there were 41 deaths from lung cancer yielding a SMR of 111 
(95% CI: 0.80-1.51). For those who worked as a process operator or 
plater the SMR for lung cancer was 103 based upon 38 deaths (95% CI: 
0.73-1.41).
    OSHA believes the Alexander (Ex. 31-16-3) and the Boice et al. (Ex. 
31-16-4) studies have several limitations. The Alexander cohort is 
small and lacks smoking data. In addition, the study's authors cite the 
relatively young age of the population. Considering these three 
factors, the authors note, ``limits the overall power of the study and 
the stability of the risk estimates, especially in exposure-related 
subanalyses'' (Ex. 31-16-3, p. 1256). Another limitation of the study 
is the 26.3% of cohort members lost to follow-up. Boice et al. is a 
well conducted study of workers in the aircraft manufacturing industry, 
but lacks information on Cr(VI) exposure (Ex. 31-16-4).
    Dalager et al. conducted a proportionate mortality study of 977 
white male spray painters potentially exposed to zinc chromate in the 
aircraft maintenance industry who worked at least three months and 
terminated employment within ten years prior to July 31, 1959 (Ex. 7-
64). Follow-up was through 1977. The expected numbers of deaths were 
obtained by applying the cause-specific proportionate mortality of U.S. 
white males to the total numbers of deaths in the study group by five 
year age groups and five year time intervals. Two hundred and two 
deaths were observed. There were 21 deaths from cancer of the 
respiratory system (PMR=184), which was statistically significant. The 
Proportionate Cancer Mortality Ratio for cancer of the respiratory 
system was not statistically significant (PCMR=146). Duration of 
employment as a painter with the military as indicated on the service 
record was used as an estimate of exposure to zinc chromate pigments, 
which were used as a metal primer. The PMRs increased as duration of 
employment increased (<5 years, O=9, E=6.4, PMR=141; 5-9 years, O=6, 
E=3, PMR=200; and 10+ years, O=6, E=2, PMR=300) and was statistically 
significant for those who worked 10 or more years.
    Bertazzi et al. studied the mortality experience of 427 workers 
employed for a minimum of six months between 1946 and 1977 in a plant 
manufacturing paint and coatings (Ex. 7-65). According to the author, 
chromate pigments represented the ``major exposure'' in the plant. The 
mortality follow-up period was 1954-1978. There were eight deaths from 
lung cancer resulting in a SMR of 227 on the local standard (95% CI: 
156-633) and a SMR of 334 on the national standard (95% CI: 106-434). 
The authors were unable to differentiate between exposures to different 
paints and coatings. In addition, asbestos was used in the plant and 
may be a potential confounding exposure.
    Morgan conducted a cohort study of 16,243 men employed after 
January 1, 1946 for at least one year in the manufacture of paint or 
varnish (Ex. 8-4). Analysis was also conducted for seven subcohorts, 
one of which was for work with pigments. Expectations were calculated 
based upon the mortality experience of U.S. white males. The SMR for 
cancer of the trachea, bronchus and lung was below unity based upon 150 
deaths. For the pigment subcohort, the SMR for cancer of the trachea, 
bronchus and lung was 117 based upon 43 deaths. In a follow-up study of 
the subcohorts, case-control analyses were conducted for several causes 
of death including lung cancer (Ex. 286). The details of matching were 
not provided. The authors state that no significant excesses of lung 
cancer risk by job were found. No odds ratios were presented.

[[Page 59341]]

    Pippard et al. conducted a cohort mortality study of 833 British 
male tannery workers employed in 1939 and followed through December 31, 
1982 (Ex. 278). Five hundred and seventy three men worked in tanneries 
making vegetable tanned leathers and 260 men worked in tanneries that 
made chrome tanned leathers. The expected number of deaths was 
calculated using the mortality rates of England and Wales as a whole. 
The lung cancer SMR for the vegetable tanned leather workers was in 
deficit (O=31; E=32.6; 95% CI: 65-135), while the lung cancer SMR for 
the chrome tanned leather workers was slightly elevated but not 
statistically significant (O=13; E=12; SMR=108; 95% CI: 58-185).
    In a different study of two U.S. tanneries, Stern et al. 
investigated mortality in a cohort of all production workers employed 
from January 1, 1940 to June 11, 1979 at tannery A (N=2,807) and from 
January 1, 1940 to May 1, 1980 at tannery B (N=6,558) (Ex. 7-68). Vital 
status was followed through December 31, 1982. There were 1,582 deaths 
among workers from the two tanneries. Analyses were conducted employing 
both U.S. mortality rates and the mortality rates for the state in 
which the plant is located. There were 18 lung/pleura cancer deaths at 
tannery A and 42 lung/pleura cancer deaths at tannery B. The lung 
cancer/pleura SMRs were in deficit on both the national standard and 
the state standard for both tanneries. The authors noted that since the 
1940s most chrome tanneries have switched to the one-bath tanning 
method in which Cr(VI) is reduced to Cr(III).
    Blot et al. reported the results of a cohort study of 51,899 male 
workers of the Pacific Gas & Electric Company alive in January 1971 and 
employed for at least six months before the end of 1986 (Ex. 239). A 
subset of the workers were involved in gas generator plant operations 
where Cr(VI) compounds were used in open and closed systems from the 
1950s to early 1980s. One percent of the workers (513 men) had worked 
in gas generator jobs, with 372 identified from post-1971 listing at 
the company's three gas generator plants and 141 from gas generator job 
codes. Six percent of the cohort members (3,283) had trained at one of 
the gas generator plants (Kettleman).
    SMRs based on national and California rates were computed. Results 
in the paper are based on the California rates, since the overall 
results reportedly did not differ substantially from those using the 
national rates. SMRs were calculated for the entire cohort and for 
subsets defined by potential for gas generator plant exposure. No 
significant cancer excesses were observed and all but one cancer SMR 
was in deficit. There were eight lung cancer deaths in the gas 
generator workers (SMR=81; 95% CI: 0.35-1.60) and three lung cancer 
deaths among the Kettleman trainees (SMR=57; 95% CI: 0.12-1.67). There 
were no deaths from nasal cancer among either the gas generator workers 
or the Kettleman trainees. The risk of lung cancer did not increase 
with length of employment or time since hire.
    Rafnsson and Johannesdottir conducted a study of 450 licensed 
masons (cement finishers) in Iceland born between 1905 and 1945, 
followed from 1951 through 1982 (Ex. 7-73). Stonecutters were excluded. 
Expectations were based on the male population of Iceland. The SMR for 
lung cancer was 314 and is statistically significant based upon nine 
deaths (E=2.87; 95% CI: 1.43-5.95). When a 20 year latency was factored 
into the analysis, the lung cancer SMR remained statistically 
significant (O=8; E=2.19; SMR=365; 95% CI: 1.58-7.20).
    Svensson et al. conducted a cohort mortality study of 1,164 male 
grinding stainless steel workers employed for three months or more 
during the period 1927-1981 (Ex.266). Workers at the facility were 
reportedly exposed to chromium and nickel in the stainless steel 
grinding process. Records provided by the company were used to assign 
each worker to one of three occupational categories: Those considered 
to have high exposure to chromium, nickel as well as total dust, those 
with intermediate exposure, and those with low exposure. Mortality 
rates for males in Blekinge County, Sweden were used as the reference 
population. Vital status follow-up was through December 31, 1983. A 
total of 194 deaths were observed (SMR= 91). No increased risk of lung 
cancer was observed (SMR=92). The SMR for colon/rectum cancer was 2.47, 
but was not statistically significant.
    Cornell and Landis studied the mortality experience of 851 men who 
worked in 26 U.S. nickel/chromium alloy foundries between 1968 and 1979 
(Ex. 7-66). Standardized Proportionate Mortality Ratio (SPMR) analyses 
were done using both an internal comparison group (foundry workers not 
exposed to nickel/chromium) and the mortality experience of U.S. males. 
The SPMR for lung cancer was 105 (O=60; E=56.9). No nasal cancer deaths 
were observed.
    Brinton et al. conducted a case-control study of 160 patients 
diagnosed with primary malignancies of the nasal cavity and sinuses at 
one of four hospitals in North Carolina and Virginia between January 1, 
1970 and December 31, 1980 (Ex. 8-8). For each case determined to be 
alive at the time of interview, two hospital controls were selected 
matched on vital status, hospital, year of admission (+/- 2 years), age 
(+/- 5 years), race and state economic area or county or usual 
residence. Excluded from control selection were malignant neoplasms of 
the buccal cavity and pharynx, esophagus, nasal cavity, middle ear and 
accessory sinuses, larynx, and secondary neoplasms. Also excluded were 
benign neoplasms of the respiratory system, mental disorders, acute 
sinusitis, chronic pharyngitis and nasopharyngitis, chronic sinusitis, 
deflected nasal septum or nasal polyps. For those cases who were 
deceased at the time of interview, two different controls were 
selected. One control series consisted of hospital controls as 
described previously. The second series consisted of decedents 
identified through state vital statistics offices matched for age (+ /- 
5 years), sex, race, county of usual residence and year of death. A 
total of 193 cases were identified and 160 case interviews completed. 
For those exposed to chromates, the relative risk was not significantly 
elevated (OR=5.1) based upon five cases. According to the authors, 
chromate exposure was due to the use of chromate products in the 
building industry and in painting, rather than the manufacture of 
chromates.
    Hernberg et al. reported the results of a case-control study of 167 
living cases of nasal or paranasal sinus cancer diagnosed in Denmark, 
Finland and Sweden between July 1, 1977 and December 31, 1980 (Exs. 8-
7; 7-71). Controls were living patients diagnosed with malignant tumors 
of the colon and rectum matched for country, gender and age at 
diagnosis (+ /- 3 years) with the cases. Both cases and controls were 
interviewed by telephone to obtain occupational histories. Patients 
with work-related exposures during the ten years prior to their illness 
were excluded. Sixteen cases reported exposure to chromium, primarily 
in the ``stainless steel welding'' and ``nickel'' categories, versus 
six controls (OR=2.7l; 95% CI: 1.1-6.6).
7. Evidence From Experimental Animal Studies
    Most of the key animal cancer bioassays for chromium compounds were 
conducted before 1988. These studies have been critically reviewed by 
the IARC in the Monograph Chromium, Nickel, and Welding (Ex. 35-43) and 
by ATSDR in their toxicological profile for chromium (Ex. 35-41). OSHA 
reviewed

[[Page 59342]]

the critical studies from both the IARC Monograph and the ATSDR 
toxicological profile on chromium and conducted its own literature 
search to update and supplement the review.
    In the experimental studies, Cr(VI) compounds were administered by 
various routes including inhalation, intratracheal instillation, 
intrabronchial implantation, and intrapleural injection, as well as 
intramuscular and subcutaneous injection. For assessing human health 
effects from occupational exposure, the most relevant route is 
inhalation. However, as a whole, there were very few inhalation 
studies. In addition to inhalation studies, OSHA is also relying on 
intrabronchial implantation and intratracheal instillation studies for 
hazard identification because these studies examine effects directly 
administered to the respiratory tract, the primary target organ of 
concern, and they give insight into the relative potency of different 
Cr(VI) compounds. In comparison to studies examining inhalation, 
intrabronchial implantation, and intratracheal instillation, studies 
using subcutaneous injection and intramuscular administration of Cr(VI) 
compounds were of lesser significance but were still considered for 
hazard identification.
    In its evaluation, OSHA took into consideration the exposure 
regimen and experimental conditions under which the experiments were 
performed, including the exposure level and duration; route of 
administration; number, species, strain, gender, and age of the 
experimental animals; the inclusion of appropriate control groups; and 
consistency in test results. Some studies were not included if they did 
not contribute to the weight of evidence, lacked adequate 
documentation, were of poor quality, or were less relevant to 
occupational exposure conditions (e.g., some intramuscular injection 
studies).
    The summarized animal studies are organized by Cr(VI) compound in 
order of water solubility (i.e., compounds that are considered highly 
soluble in water, followed by those considered slightly soluble in 
water, and then those considered insoluble in water) since it has been 
suggested that solubility may be an important factor in determining the 
carcinogenic potency of Cr(VI) compounds (Ex 35-47). Solubility 
characteristics described in this section are based on those cited in 
the IARC Monograph (as cited in Ex. 35-43, pages 56-59).
    a. Highly Water Soluble Cr(VI) Compounds. Multiple animal 
carcinogenicity studies have been conducted on highly water soluble 
sodium dichromate and chromic acid. The key studies are summarized in 
Table VI-7.

    Table VI-7.--Summary of Selected Carcinogenicity Studies in Experimental Animals Administered Hexavalent Chromium--Highly Water Soluble Chromates
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                               Sex/species/strain    Dose administered \1\
              Compound                        Route           (<greek-i> in exposed     and observation        Tumor incidence       Reference/exhibit
                                                                     groups)                periods                                      <greek-i>
--------------------------------------------------------------------------------------------------------------------------------------------------------
Chromic acid (Chromium trioxide)...  Inhalation............  Female ICR mice (50     3.6 mg Cr(VI)/m3 for   --Lung tumors: 7/48    Adachi et al. (1986,
                                                              per exposed group.      30 min per day, 2 d/   vs 2/20 for control.   Ex. 35-26-1).
                                                                                      wk up to 12 mo.       --5 benign adenomas
                                                                                      Histopatholoical       and 2
                                                                                      evaluation at          adenocarcinomas..
                                                                                      periods up to 18 mo.
                                     Inhalation............  Female C57BL mice (23   1.8 mg Cr(VI)/m3 120   Nasal papilloma: 6/20  Adachi (1987, Ex. 35-
                                                              examined at 12 mo; 20   min 2 x week for 12    (<0.05) at 18 mo;      219).
                                                              examined at 18 mo).     months;                Lung adenoma: 1/20
                                                                                      Histopatholoical       (NS) at 18 mo.
                                                                                      evaluation at 12 and
                                                                                      18 mo.
                                     Intrabronchial........  Male/female Porton-     1.0 mg Cr(VI) as       Bronchial carcinoma    Levy et al. (1986,
                                                              Wistar rats (50 per     single dose mixed w    (M/F combined): 2/     Ex. 11-2).
                                                              exposed group).         cholesterol in steel   100 (N.S.).
                                                                                      pellet and evaluated
                                                                                      at 2 years.
Sodium dichromate..................  Inhalation............  Male Wistar rats (20    0.025, 0.050 and 0.10  Lung tumors: 0.025 mg/ Glaser et al. (1986,
                                                              per exposed group).     mg Cr(VI)m3 22-23 hr/  m3--0/18; 0.05 mg/     Ex. 10-11).
                                                                                      day, 7 d/wk for 18     m3--0/018; 0.1 mg/
                                                                                      months; evaluated at   m3--3/19(NS).
                                                                                      up to 30 months.
                                     Intrabronchial........  Male/female Porton-     0.8 mg Cr(VI) as a     Bronchial carcinoma    Levy et al. (1986, 11-
                                                              Wistar rats (50 per     single dose mixed w    (M/F combined): 1/     2).
                                                              exposed group).         cholesterol in steel   100 (NS).
                                                                                      pellet and evaluated
                                                                                      at 2 years.
                                     Intratracheal.........  Male/female Sprague     5 x weekly: 0.0034,    Lung tumors (M/F       Steinhoff et al.
                                                              Dawley rats (40 per     0.017, 0.086 mg        combined)-- 5 x        (1986, Ex. 11-7).
                                                              exposed group).         Cr(VI)/kg bw for 30    weekly: 0/80 in all
                                                                                      mo; 1 x weekly:        groups; 1 x weekly:
                                                                                      0.017, 0.086, 0.43     0.017 mg/kg-0/80;
                                                                                      mg Cr(VI)/kg bw for    0.086 mg/kg-1/80;
                                                                                      30 mo.                 0.043 mg/kg-14/80
                                                                                                             (p<0.01).
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Doses calculated and recorded as mg of Cr(VI), rather than specific chromate compound, where possible.
 Not Statistically Significant--NS
 Male/Female M/F.

    Sodium dichromate. Glaser et al. exposed male Wistar rats to 
aerosolized sodium dichromate by inhalation for 22-23 hours per day, 
seven days per week for 18 months (Exs. 10-10; 10-11). The rats were 
held for an additional 12 months at which point the study was 
terminated. Lung tumor incidences among groups exposed to 25, 50, and 
100 [mu]g Cr(VI)/m<SUP>3</SUP> were 0/18, 0/18, and 3/19, respectively, 
vs. 0/37 for the control animals. Histopathology revealed one 
adenocarcinoma and two adenomas in the highest group. The slightly 
elevated tumor incidence at the highest dose was not statistically 
significant. As noted by IARC, a small number of animals (20 per group) 
were used in this study. In addition, the administered doses used in 
this study were fairly low, such that the maximum tolerated dose (i.e., 
the maximum dose level that does not lead to moderate reduction in body 
weight gain) may not have been achieved. Together, these factors limit 
the interpretation of the study.

[[Page 59343]]

    In an analysis prepared by Exponent and submitted by the Chrome 
Coalition in response to OSHA's RFI, Exponent stated that ``inhalation 
studies of Glaser et al. support a position that exposures to soluble 
Cr(VI) at concentrations at least as high as the current PEL (i.e., 52 
[mu]g/m<SUP>3</SUP>) do not cause lung cancer'' (Ex. 31-18-1, page 2). 
However, it should be noted that the Glaser et al. studies found that 
15% (3/19) of the rats exposed to an air concentration just above the 
current PEL developed lung tumors, and that the elevated tumor 
incidence was not statistically significant in the highest dose group 
because the study used a small number of animals. OSHA believes the 
Glaser study lacks the statistical power to state with sufficient 
confidence that Cr(VI) exposure does not cause lung cancer at the 
current PEL, especially when given the elevated incidence of lung 
tumors at the next highest dose level.
    Steinhoff et al. studied the carcinogenicity of sodium dichromate 
in Sprague-Dawley rats (Ex. 11-7). Forty male and 40 female Sprague-
Dawley rats were divided into two sets of treatment groups. In the 
first set, doses of 0.01, 0.05 or 0.25 mg/kg body weight in 0.9% saline 
were instilled intratracheally five times per week. In the second set 
of treatment groups, 0.05, 0.25 or 1.25 mg/kg body weight in 0.9% 
saline doses were instilled intratracheally once per week. Duration of 
exposure in both treatment groups was 30 months. The total cumulative 
dose for the lowest treatment group of animals treated once per week 
was the same as the lowest treatment group treated five times per week. 
Similarly, the medium and high dose groups treated once per week had 
total doses equivalent to the medium and high dose animals treated five 
times per week, respectively. No increased incidence of lung tumors was 
observed in the animals dosed five times weekly. However, in the 
animals dosed once per week, tumor incidences were 0/80 in control 
animals, 0/80 in 0.05 mg/kg exposure group, 1/80 in 0.25 mg/kg exposure 
group and 14/80 in 1.25 mg/kg exposure group (p <0.01). The tumors were 
malignant in 12 of the 14 animals in the 1.25 mg/kg exposure group. The 
authors believe that the results of this study suggest that the dose-
rate for sodium dichromate is a significant factor in its carcinogenic 
potency and that limiting occasional high dose exposures may be 
critical to reducing the risk of carcinogenicity in humans 
occupationally exposed to sodium dichromate.
    In separate but similar studies, Levy et al. and Levy and Venitt 
implanted stainless steel mesh pellets filled with a single dose of 2 
mg sodium dichromate (0.80 mg Cr(VI)) mixed 50:50 with cholesterol in 
the bronchi of male and female Porton-Wistar rats (Exs. 11-2; 11-12). 
Control groups (males and females) received blank pellets or pellets 
loaded with cholesterol. The rats were observed for two years. Levy et 
al. and Levy and Venitt reported a bronchial tumor incidence of 1/100 
and 0/89, respectively, for exposed rats. However, the latter study 
reported a statistically significant increase in squamous metaplasia, a 
lesion believed capable of progressing to carcinoma, among exposed rats 
when compared to unexposed rats. The earlier Levy et al. study did not 
report the incidence of squamous metaplasia. There were no bronchial 
tumors or squamous metaplasia in any of the control animals and no 
significant increases in lung tumors were observed in the two studies.
    In the Hueper study, 26 rats (sex, age, and strain not specified) 
were given intrapleural implantation for 27 months (Ex. 10-4). Dosage 
was not specified. No significant increases in tumor incidence were 
observed in rats exposed to sodium dichromate or in the control group 
(0/26 vs. 0/34 in control).
    Chromic acid (Chromium trioxide). In a study by Adachi et al, ICR/
JcI mice were exposed by inhalation to 3.63 mg/m<SUP>3</SUP> for 30 
minutes per day, two days per week for up to 12 months (Ex. 35-26-1). 
The mice were observed for an additional six months. The authors used a 
miniaturized chromium electroplating system to generate chromic acid 
for the study. The authors found there were elevations in lung adenomas 
at 10-14 months (3/14 vs. 0/10) and lung adenocarcinomas at 15-18 
months (2/19 vs. 0/10), but the results were not statistically 
significant. Statistically significant increases in nasal papillomas 
were observed in another study by Adachi et al., in which 43 C57B1 mice 
were exposed by inhalation to 1.81 mg/m<SUP>3</SUP> chromic acid for 
120 min per day, two days per week for up to 12 months (Ex. 35-26). At 
18 months, the tumor incidence was 6/20 in exposed animals vs. 0/20 in 
the control animals (p<0.05).
    In separate but similar studies, Levy et al. and Levy and Venitt, 
using similar exposure protocol, conducted bronchial implantation 
experiments in which 100 male and female Porton-Wistar rats were dosed 
with single intrabronchial implantations of 2 mg chromic acid (1.04 mg 
Cr(VI)) mixed 50:50 with cholesterol in stainless steel mesh pellets 
(Exs. 11-2; 11-12). The authors found no statistically significant 
increases in lung tumors, although Levy et al. found a bronchial 
carcinoma incidence of 2/100 in exposed rates compared with 0/100 in 
control rats. Levy and Venitt found a bronchial carcinoma incidence of 
1/100 accompanied by a statistically significant increase in squamous 
metaplasia, a lesion believed capable of progressing to carcinoma. 
There was no statistically significant increase in the incidence of 
squamous metaplasia in control rats or rats treated with Cr(III) 
compounds in the same study. This finding suggests that squamous 
metaplasia is specific to Cr(VI) and is not evoked by a non-specific 
stimuli, the implantation procedure itself, or a treatment with Cr(III) 
containing materials. The incidence of squamous metaplasia was not 
investigated in the 1986 Levy et al. study.
    Similar to Levy et al. and Levy and Venitt studies, Laskin et al. 
gave a single intrabronchial implantation of 3-5 mg chromic acid mixed 
50:50 with cholesterol in stainless steel mesh pellets to 100 male and 
female Porton-Wistar rats (Ex. 10-1). The rats were observed for 2 
years. No tumors were identified in the treated or control animals (0/
100 vs. 0/24).
    Potassium chromate. No studies were found that administered this 
compound by way of the respiratory tract. Borneff et al. exposed mice 
to potassium chromate in drinking water for three generations at a dose 
of 9 mg Cr(VI)/kg/day (as cited in ATSDR, Ex. 35-41, Pages 108 and 
345). In treated mice, two of 66 females developed forestomach 
carcinoma and 10/66 females and 1/35 males developed forestomach 
papillomas. The controls also developed forestomach papillomas (2/79 
females, 3/47 males), but no carcinomas were observed. The incidence of 
forestomach tumors was not statistically significant.
    b. Slightly Water Soluble Cr(VI) Compounds. Animal carcinogenicity 
studies have been conducted on slightly water soluble calcium chromate 
and strontium chromate. The key studies are summarized in Table VI-8.

[[Page 59344]]



   Table VI-8: Summary of Selected Carcinogenicity Studies in Experimental Animals Administered Hexavalent Chromium--Slightly Water Soluble Chromates
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                               Sex/species/strain    Dose administered \1\
              Compound                        Route           (<greek-i> in exposed     and observation        Tumor incidence       Reference/exhibit
                                                                     groups)                periods
--------------------------------------------------------------------------------------------------------------------------------------------------------
Calcium chromate...................  Inhalation............  Male/female C57BL/6     4.3 mg Cr(VI)/m3, 5    Lung adenoma (M/F      Nettesheim et al.
                                                              mice (136 per group).   hr/d, 5d/wk over       combined): 14/272 vs   (1971, Ex. 10-8).
                                                                                      animal lifetime.       5/272 for controls.
                                     Intrabronchial........  Male/female Porton-     0.67 mg Cr(VI) as a    Bronchial carcinoma    Levy et al. (1986,
                                                              Wistar rats (100 per    single dose mixed w    (M/F combined): 25/    Ex. 11-2).
                                                              group).                 cholesterol in steel   100 (p<0.01).
                                                                                      pellet and evaluated
                                                                                      at 2 years.
                                     Intratracheal.........  Male/female Sprague     5 x weekly: 0.083 mg   Lung tumors (M/F       Steinhoff et al.
                                                              Dawley rats (40 per     Cr(VI)/kg bw for 30    combined)--5 x         (1986, Ex. 11-7).
                                                              group).                 mo; 1 x weekly:        weekly: 0.083 mg/kg-
                                                                                      0.41.mg Cr(VI)/kg bw   6/80 (p<0.01); 1 x
                                                                                      for 30 mo.             weekly: 0.41 mg/kg-
                                                                                                             13/80 (p<0.01).
                                     Intratracheal.........  Male Sprague Dawley     0.67 mg Cr(VI)/kg bw   Lung tumors: 1/44      Snyder et al. (1997,
                                                              rats (50 per exposed    x 13 installations     (NS).                  Ex. 31-18-12).
                                                              group).                 over 20 wks and
                                                                                      evaluated at 2 to
                                                                                      2.5 yr.
Strontium chromates (two different   Intrabronchial........  Male/female Porton-     0.48 mg Cr(VI) as a    Bronchial carcinoma    Levy et al. (1986,
 compounds).                                                  Wistar rats (50 per     single dose mixed w    (M/F combined): 43/    Ex. 11-2).
                                                              exposed group).         cholesterol in steel   99 & 62/99 (p<0.01).
                                                                                      pellet and evaluated
                                                                                      at 2 years.
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Doses calculated and recorded as mg of Cr(VI), rather than specific chromate compound, where possible.
Not Statistically significant--NS.
Male/Female--M/F.

    Calcium chromate. Nettesheim et al. conducted the only available 
inhalation carcinogenicity study with calcium chromate showing 
borderline statistical significance for increased lung adenomas in 
C57B1/6 mice exposed to 13 mg/m<SUP>3</SUP> for 5 hours per day, 5 days 
per week over the life of the mice. The tumor incidences were 6/136 in 
exposed male mice vs. 3/136 in control male mice and 8/136 in exposed 
female mice vs. 2/136 in control female mice (Ex. 10-8).
    Steinhoff et al. observed a statistically significant increase in 
lung tumors in Sprague-Dawley rats exposed by intratracheal 
instillation to 0.25 mg/kg body weight calcium chromate in 0.9% saline 
five times weekly for 30 months (Ex. 11-7). Tumors were found in 6/80 
exposed animals vs. 0/80 in unexposed controls (p<0.01). Increased 
incidence of lung tumors was also observed in those rats exposed to 
1.25 mg/kg calcium chromate once per week (14/80 vs. 0/80 in controls) 
for 30 months. At the highest dose, the authors observed 11 adenomas, 
one adenocarcinoma, and two squamous carcinomas. The total administered 
doses for both groups of dosed animals (1 x 1.25 mg/kg and 5 x 0.25 mg/
kg) were equal, but the tumor incidence in the rats exposed once per 
week was approximately double the incidence in rats exposed to the same 
weekly dose divided into five smaller doses. The authors suggested that 
the dose-rate for calcium chromate compounds may be important in 
determining carcinogenic potency and that limiting higher single 
exposures may offer greater protection against carcinogenicity than 
reducing the average exposure alone.
    Snyder et al. administered Cr(VI)-contaminated soil of defined 
aerodynamic diameter (2.9 to 3.64 micron) intratracheally to male 
Sprague-Dawley rats (Ex. 31-18-12). For the first six weeks of 
treatment, the rats were instilled with weekly suspensions of 1.25 mg 
of material per kg body weight, followed by 2.5 mg/kg every other week, 
until treatments were terminated after 44 weeks. The investigation 
included four exposure groups: Control animals (50 rats), rats 
administered Cr(VI)-contaminated soil (50 rats), rats administered 
Cr(VI)-contaminated soil supplemented with calcium chromate (100 rats), 
and rats administered calcium chromate alone (100 rats). The total 
Cr(VI) dose for each group was: Control group (0.000002 mg Cr(VI)/kg), 
soil alone group (0.324 mg Cr(VI)/kg), soil plus calcium chromate group 
(7.975 mg Cr(VI)/kg), and calcium chromate alone group (8.700 mg 
Cr(VI)/kg). No primary tumors were observed in the control group or the 
chromium contaminated soil group. Four primary tumors of the lung were 
found in the soil plus calcium chromate group and one primary lung 
tumor was observed in the group treated with calcium chromate alone; 
however, these incidences did not reach statistical significance.
    In the analysis submitted to OSHA by the Chrome Coalition, Exponent 
stated that the ``intratrachael instillation data of Steinhoff et al. 
1986 and Snyder et al. 1997 indicates there is a likely threshold for 
lung cancer'' (Ex. 31-18-1, page 2). OSHA believes the results of the 
Steinhoff et al. 1986 study show that the rate at which Cr(VI) is 
administered may be an important determinant for carcinogenic potency 
and thus useful for hazard identification purposes. However, in 
accordance with the Agency's long standing cancer policy, OSHA believes 
it is inappropriate to establish a threshold or ``no effect'' level of 
exposure to a carcinogen (see 29 CFR 1990.143). Moreover, the Snyder 
1997 study, in particular, used contaminated soil samples and an 
irregular dosing protocol, creating additional complexities in relating 
the results to workplace inhalation exposures.
    Statistically significant increases in the incidence of bronchial 
carcinoma in rats exposed to calcium chromate through intrabronchial 
instillation were reported by Levy et al. (Ex. 11-2) and Levy and 
Venitt (Ex. 11-12). These studies, using a similar protocol, implanted 
a single dose of 2 mg calcium chromate (0.67 mg Cr(VI)) mixed 50:50 
with cholesterol in stainless steel pellets into the bronchi of Porton-
Wistar rats. Levy et al. and Levy and Venitt found bronchial carcinoma 
incidences of 25/100 and 8/84, respectively, following a 24-month 
observation. The increased incidences were statistically significant 
when compared to the control group. Levy and Venitt also reported 
statistically significant increases in squamous metaplasia in the 
calcium chromate-treated rats (Ex. 11-12).
    Laskin et al. observed 8/100 tumors in rats exposed to a single 
dose of 3-5 mg calcium chromate mixed with cholesterol in stainless 
steel mesh

[[Page 59345]]

pellets implanted in the bronchi (Ex. 10-1). Animals were observed for 
a total of 136 weeks. The sex, strain, and species of the rats were not 
specified in the study. Tumor incidence in control animals was 0/24. 
Although tumor incidence did not reach statistical significance in this 
study, OSHA agrees with IARC that the incidences are due to calcium 
chromate itself rather than background variation.
    Strontium chromate. Strontium chromate was tested by intrabronchial 
implantation and intrapleural injection. In a study by Levy et al., two 
strontium chromate compounds mixed 50:50 with cholesterol in stainless 
steel mesh pellets were administered by intrabronchial instillation of 
a 2 mg (0.48 mg Cr(VI)) dose into 100 male and female Porton-Wistar 
rats (Ex. 11-2). Animals were observed for up to 136 weeks. The 
strontium chromate compounds induced bronchial carcinomas in 43/99 (Sr, 
42.2%; CrO<INF>4</INF>, 54.1%) and 62/99 rats (Sr, 43.0%; Cr, 24.3%), 
respectively, compared to 0/100 in the control group. These results 
were statistically significant. The strontium chromates produced the 
strongest carcinogenic response out of the 20 Cr(VI) compounds tested 
by the intrabronchial implantation protocol.
    In the study by Hueper, strontium chromate was administered by 
intrapleural injection (doses unspecified) lasting 27 months (Ex. 10-
4). Local tumors were observed in 17/28 treated rats vs. 0/34 for the 
untreated rats. Although the authors did not examine the statistical 
significance of tumors, the results clearly indicate a statistical 
significance.
    c. Water Insoluble Cr(VI) Compounds. There have been a number of 
animal carcinogenicity studies involving implantation or injection of 
principally water insoluble zinc, lead, and barium chromates. The key 
studies are summarized in Table VI-9.

      Table VI-9.--Summary of Selected Carcinogenicity Studies in Experimental Animals Administered Hexavalent Chromium--Water Insoluble Chromates
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                               Sex/species/strain    Dose administered \1\
              Compound                        Route           (<greek-i> in exposed     and observation        Tumor incidence       Reference/exhibit
                                                                     groups)                periods                                      <greek-i>
--------------------------------------------------------------------------------------------------------------------------------------------------------
Zinc chromates (three different      Intrabronchial........  Male/female Porton-     0.42 to 0.52 mg        Bronchial carcinoma    Levy et al. (1986,
 compounds).                                                  Wistar rats (50 per     Cr(VI) as a single     (M/F combined): 3/61   Ex. 11-2); Levy and
                                                              exposed group).         dose mixed w           (p<0.05), 5/100        Venitt (1986, Ex. 11-
                                                                                      cholesterol in steel   (p<0.05), 3/100        12).
                                                                                      pellet and evaluated   (p=0.07).
                                                                                      at 2 years.
Zinc tetroxychromate...............  Intrabronchial........  Male/female Porton-     0.18 mg Cr(VI) as a    Bronchial carcinoma    Levy et al. (1986,
                                                              Wistar rats (50 per     single dose mixed w    (M/F combined): 1/     Ex. 11-2).
                                                              exposed group).         cholesterol in steel   100 (NS).
                                                                                      pellet and evaluated
                                                                                      at 2 years.
Lead chromates (seven different      Intrabronchial........  Male/female Porton-     0.25 to 0.32 mg        Bronchial carcinoma    Levy et al. (1986,
 compounds).                                                  Wistar rats (50 per     Cr(VI) as single       (M/F combined): 0-1/   Ex. 11-2).
                                                              exposed group).         dose mixed w           100 (N.S.).
                                                                                      cholesterol in steel
                                                                                      pellet and evaluated
                                                                                      at 2 years.
Lead chromates (three different      Subcutaneous..........  Male/female Sprague     1.5 to 4.8 mg Cr(VI)   Sarcomas at injection  Maltoni et al. (1974,
 compounds).                                                  Dawley rats (20 per     as a single dose in    site (M/F combined):   Ex. 8-25); Maltoni
                                                              exposed group).         water and evaluated    26-36/40 vs 0/40 for   (1976, Ex. 5-2).
                                                                                      after 2 years.         controls.
Lead chromate......................  Intramuscular.........  Male/female Fischer     1.29 mg Cr(VI) in      Sarcomas at injection  Furst et al. (1976,
                                                              344 rats (25 per        trioctyanoin 1 x mo    site (M/F combined):   Ex. 10-2).
                                                              exposed group).         for 9 mo and           31/47 vs 0/44 for
                                                                                      evaluated at up to 2   controls.
                                                                                      yr.
                                                             Female NIH-Swiss mice   0.72 mg Cr(VI) in      Sarcomas at injection
                                                              (25 per exposed         trioctyanoin 1 x mo    site: 0/22 (NS).
                                                              group).                 for 4 mo and
                                                                                      evaluated at up to 2
                                                                                      yr.
Barium chromate....................  Intrabronchial........  Male/female Porton-     0.37 mg Cr(VI) as a    Bronchial carcinoma    Levy et al. (1986,
                                                              Wistar rats (50 per     single dose mixed w    (M/F combined): 0/     Ex. 11-2).
                                                              exposed group).         cholesterol in steel   100 (NS).
                                                                                      pellet and evaluated
                                                                                      at 2 years.
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Doses calculated and recorded as mg of Cr(VI), rather than specific chromate compound, where possible.
Not Statistically significant--NS.
Male/Female--M/F.

    Zinc chromate compounds. Animal studies have been conducted to 
examine several zinc chromates that range from water insoluble to 
slightly water soluble compounds depending on the form and composition. 
In separate, but similarly conducted studies, Levy et al. and Levy and 
Venitt studied two water-insoluble compounds (zinc chromate--lW and 
zinc tetroxychromate) and two slightly water-soluble compounds (zinc 
chromate--Norge composition and zinc potassium chromate) (Exs. 11-2; 
11-12). Two milligrams of the compounds were administered by 
intrabronchial implantation to 100 male and female Porton-Wistar rats. 
The slightly water soluble zinc potassium chromate (0.52 mg Cr(VI)) 
produced a bronchial tumor incidence of 3/61 which was statistically 
significant (p<0.05) when compared to a control group (Ex. 11-12). 
There was also a statistically significant increase in bronchial tumors 
in rats receiving water-insoluble zinc chromate--lW (5/100; p=0.04). 
The bronchial tumor incidence with slightly water soluble zinc 
chromate--Norge (3/100; p= 0.068) and water-insoluble zinc 
tetroxychromate (1/100) were not statistically significant when 
compared to a control group. Zinc potassium chromate (slightly water 
soluble) was administered at doses of 0.42 mg Cr(VI), zinc chromate--
Norge (slightly water soluble) was administered at doses of 0.45 mg 
Cr(VI), and zinc tetroxychromate (insoluble in water) was administered 
at doses of 0.18 mg Cr(VI). These studies show that insoluble to 
slightly water soluble zinc chromate compounds may produce 
statistically significant elevated incidences of tumors in rats.
    Basic potassium zinc chromate (slightly water soluble) was 
administered to mice, guinea pigs and rabbits via intratracheal 
instillation (Ex. 35-46). Sixty-two Strain A mice were given six 
injections of 0.03 ml of a 0.2% saline suspension of the zinc chromate 
at six week intervals and observed until death. A statistically 
significant increase in tumor incidence was observed in exposed animals 
when compared to controls (31/62 vs. 7/18). Statistically significant 
effects were not observed

[[Page 59346]]

among guinea pigs or rabbits. Twenty-one guinea pigs (sex and strain 
not given) received six injections of 0.3 ml of a 1% suspension of zinc 
chromate at three monthly intervals and observed until death. Results 
showed pulmonary adenomas in only 1/21 exposed animals vs. 0/18 in 
controls. Seven rabbits (sex and strain not given) showed no increase 
in lung tumors when given 3-5 injections of 1 ml of a saline suspension 
of 10 mg zinc chromate at 3-month intervals. However, as noted by IARC, 
the small numbers of animals used in the guinea pig and rabbit 
experiments (as few as 13 guinea pigs and 7 rabbits per group) limit 
the power of the study to detect increases in cancer incidence.
    Hueper found that intrapleural injection of slightly water soluble 
zinc yellow (doses were unspecified) resulted in statistically 
significant increases in local tumors in rats (sex, strain, and age of 
rat unspecified; dose was unspecified). The incidence of tumors in 
exposed rats was 22/33 vs. 0/34 in controls (Ex. 10-4).
    Maltoni et al. observed increases in the incidence of local tumors 
after subcutaneous injection of slightly water soluble zinc yellow in 
20 male and 20 female Sprague-Dawley rats (statistical significance was 
not evaluated) (Ex. 8-37). Tumor incidences were 6/40 in 20% 
CrO<INF>3</INF> dosed animals at 110 weeks and 17/40 in 40% 
CrO<INF>3</INF> dosed animals at 137 weeks compared to 0/40 in control 
animals.
    Lead chromate and lead chromate pigments. Levy et al. examined the 
carcinogenicity of lead chromate and several lead chromate-derived 
pigments in 100 male and female Porton-Wistar rats after a single 
intrabronchial implantation followed by a two year observation period 
(Ex. 11-12). The rats were dosed with two mg of a lead chromate 
compound and lead chromate pigments, which was mixed 50:50 with 
cholesterol in stainless steel mesh pellets and implanted in the 
bronchi of experimental animals. The lead chromate and lead chromate 
pigment compositions consisted of the following: lead chromate (35.8% 
CrO<INF>4</INF>; 0.32 mg Cr(VI)), primrose chrome yellow (12.6% Cr; 
0.25 mg Cr(VI)), molybdate chrome orange (12.9% Cr; 0.26 mg Cr(VI)), 
light chrome yellow (12.5% Cr; 0.25 mg Cr(VI)), supra LD chrome yellow 
(26.9% CrO<INF>3</INF>; 0.28 mg Cr(VI)), medium chrome yellow (16.3% 
Cr; 0.33 mg Cr(VI)) and silica encapsulated medium chrome yellow (10.5% 
Cr; 0.21 mg Cr(VI)). No statistically significant tumors were observed 
in the lead chromate group compared to controls (1/98 vs. 0/100), 
primrose chrome yellow group (1/100 vs. 0/100), and supra LD chrome 
yellow group (1/100 vs. 0/100). The authors also noted no tumors in the 
molybdate chrome orange group, light chrome yellow group, and silica 
encapsulated medium chrome yellow group.
    Maltoni (Ex. 8-25), Maltoni (Ex. 5-2), and Maltoni et al. (Ex. 8-
37) examined the carcinogenicity of lead chromate, basic lead chromate 
(chromium orange) and molybdenum orange in 20 male and 20 female 
Sprague-Dawley rats by a single subcutaneous administration of the lead 
chromate compound in water. Animals were observed for 117 to 150 weeks. 
After injection of 30 mg lead chromate, local injection site sarcomas 
were observed in 26/40 exposed animals vs. 0/60 and 1/80 in controls. 
Although the authors did not examine the statistical significance of 
sarcomas, the results clearly indicate a statistical significance. 
Animals injected with 30 mg basic lead chromate (chromium orange) were 
found to have an increased incidence of local injection site sarcomas 
(27/40 vs. 0/60 and 1/80 in controls). Animals receiving 30 mg 
molybdenum orange in 1 ml saline were also found to have an increased 
incidence of local injection site sarcomas (36/40 vs. 0/60 controls).
    Carcinogenesis was observed after intramuscular injection in a 
study by Furst et al. (Ex. 10-2). Fifty male and female Fischer 344 
rats were given intramuscular injections of 8 mg lead chromate in 
trioctanoin every month for nine months and observed up to 24 months. 
An increase in local tumors at the injection site (fibrosarcomas and 
rhabdomyosarcomas) was observed (31/47 in treated animals vs. 0/22 in 
controls). These rats also had an increased incidence of renal 
carcinomas (3/23 vs. 0/22 in controls), but IARC noted that the renal 
tumors may be related to the lead content of the compound. In the same 
study, 3 mg lead chromate was administered to 25 female NISH Swiss 
weanling mice via intramuscular injection every 4 months for up to 24 
months. In the exposed group, the authors observed three lung 
alveologenic carcinomas after 24 months of observation and two 
lymphomas after 16 months of observation. Two control groups were used: 
an untreated control group (22 rats) and a vehicle injected control 
group (22 rats). The authors noted one alveologenic carcinoma and one 
lymphoma observed in each control group.
    In response to OSHA's RFI, the Color Pigments Manufacturers 
Association (CPMA) stated that the lack of carcinogenic response in two 
studies (Levy et al. 1986 and Furst et al. 1976) upon exposure to lead 
chromate and lead chromate pigments in animals indicate these Cr(VI) 
compounds are not carcinogenic to workers (Ex. 31-15). As described 
above, the results of the Levy et al. 1986 study showed little tumor 
development (0-1 tumor observed per 100 rats studied in each 
experiment) after receiving a single dose of 2 mg of lead chromate or a 
lead chromate compound by an intrabronchial implantation procedure in 
which the compounds were imbedded in a metal mesh mixed with 
cholesterol (Ex. 11-2). The total administered dose of the Levy et al. 
study was relatively low at 0.67 mg Cr(VI)/kg when administered only 
one time (body weight of the rat was around 0.5 kg). A small, single 
total dose (e.g., 1.6 mg Cr(VI)/kg) of sodium dichromate implanted in 
the lung also did not result in tumors. However, repeated weekly 
intratracheal instillations of a lower dose level (0.43 mg Cr(VI)/kg) 
of sodium dichromate over 30 months for a cumulative total dose of 
about 56 mg Cr(VI)/kg produced a 17.5 percent lung cancer incidence. 
Thus, a greater total dose of lead chromate instilled in the 
respiratory tract may also produce a significant tumor incidence. The 
lack of tumors in the Levy et al. study may also have resulted from the 
inability of water insoluble lead chromate to leach out of the highly 
non-polar cholesterol environment and gain entry into target lung 
cells. OSHA, therefore, does not believe that the findings of this 
study establish that lead chromate and lead chromate pigments are not 
carcinogenic. OSHA does not believe the results of the Furst et al. 
study show a lack of carcinogenic effect. The study found a 66 percent 
tumor incidence at the site of injection after multiple intramuscular 
administrations of lead chromate in rats (Ex. 10-2). Although the route 
of exposure is not comparable to that found in occupational settings, 
the carcinogenic potential of lead chromate is supported by the results 
of several studies showing that pigment workers exposed to lead 
chromate have significantly elevated lung cancer mortality (see section 
V.B.2). Several short-term tests have also linked lead chromate with 
genotoxicity and neoplastic transformation (see section VI.B.8).
    Barium chromate. In the studies reviewed by IARC, barium chromate 
was tested in rats via intrabronchial, intrapleural and intramuscular 
administration. No excess lung or local tumors were observed (Ex. 11-2; 
Ex. 10-4; Ex. 10-6).
    d. Summary. Several Cr(VI) compounds produced tumors in

[[Page 59347]]

laboratory animals under a variety of experimental conditions using 
different routes of administration. The animals were generally given 
the test material(s) by routes other than inhalation (e.g., 
intratracheal administration, intramuscular injection, intrabronchial 
implantation, and subcutaneous injection). Although the route of 
administration may have differed from that found in an occupational 
setting, these studies have value in the identification of potential 
health hazards associated with Cr(VI) and in assessing the relative 
potencies of various Cr(VI) compounds.
    OSHA believes that the results from Adachi et al. (Ex. 35-26-1), 
Adachi et al. (Ex. 35-26), Glaser et al. (Ex. 10-4), Glaser et al. (Ex. 
10-10), Levy et al. (Ex. 11-2), Steinhoff et al. (Ex. 11-7), and Snyder 
et al. (Ex. 31-18-12) studies provide valuable insight on the 
carcinogenic potency of Cr(VI) compounds in laboratory animals. Total 
dose administered, dose rate, amount of dosage, dose per 
administration, number of times administered, exposure duration and the 
type of Cr(VI) compound are major influences on the observed tumor 
incidence in animals. It was found that slightly water soluble calcium, 
strontium, and some zinc chromates showed the highest incidence of lung 
tumors, as indicated in the results of the Steinhoff, Snyder, and Levy 
studies, even when compared to similar doses of the more water soluble 
sodium chromates and chromic acid compounds. The highly insoluble lead 
chromates did not produce lung tumors by the intrabronchial 
implantation procedure but did produce tumors by subcutaneous injection 
and intramuscular injection.
8. Mechanistic Considerations
    Mechanistic information can provide insight into the biologically 
active form(s) of chromium, its interaction with critical molecular 
targets, and the resulting cellular responses that trigger neoplastic 
transformation. There has been considerable scientific study in recent 
years of Cr(VI)-initiated cellular and molecular events believed to 
impact development of respiratory carcinogenesis. Much of the research 
has been generated using in vitro techniques, cell culture systems, and 
animal administrations. The early mechanistic data were reviewed by 
IARC in 1990 (Ex. 35-43). More recent reviews have been done by Singh 
et al. in 1998 (Ex. 35-149), ATSDR in 2000 (Ex. 35-41), and K.S. Crump 
Group in 2000 (Ex. 35-47).
    Recent experimental research has identified several biological 
steps critical to the mode of action by which Cr(VI) transforms normal 
lung cells into a neoplastic phenotype. These are: (a) Cellular uptake 
of Cr(VI) and its extracellular reduction, (b) intracellular Cr(VI) 
reduction to produce biologically active products, (c) damage to DNA, 
and (d) activation of signaling pathways in response to cellular 
stress. Each step will be described in detail below.
    a. Cellular Uptake and Extracellular Reduction. The ability of 
different Cr(VI) particulate forms to be taken up by the 
bronchoalveolar cells of the lung is an essential early step in the 
carcinogenic process. Particle size and solubility are key physical 
factors that influence uptake into these cells. Large particulates (>10 
[mu]m) are generally deposited in the upper nasopharygeal region of the 
respiratory tract and do not reach the bronchoalveolar region of the 
lungs. Smaller Cr(VI) particulates will increasingly reach these lower 
regions and come into contact with target cells.
    Once deposited in the lower respiratory tract, solubility of Cr(VI) 
particulates becomes a major influence on disposition. Aqueous Cr(VI), 
such as sodium chromate and chromic acid, rapidly dissolves in the 
fluids lining the lung epithelia and can be taken up by lung cells via 
facilitated diffusion mediated by sulfate/phosphate anion transport 
channels (Ex. 35-148). This is because Cr(VI) exists in a tetrahedral 
configuration as a chromate oxyanion similar to the physiological 
anions, sulfate and phosphate (Ex. 35-231). Using cultured human 
epithelial cells, Liu et al. showed that soluble Cr(VI) uptake was 
time- and dose-dependant over a range of 1 to 300 [mu]M in the medium 
with 30 percent of the Cr(VI) transported into the cells within two 
hours and 67 percent at 16 hours at the lowest concentration (Ex. 31-
22-18).
    Aqueous insoluble Cr(VI) particulates do not readily dissolve into 
epithelial lining fluids of the bronchoalveolar region. This has led to 
claims that insoluble chromates, such as lead chromate pigments, are 
not bioavailable and, therefore, are unable to cause carcinogenesis 
(Ex. 31-15). However, several scientific studies indicate that 
insoluble Cr(VI) particulates can come in close contact with the 
bronchoalveolar epithelial cell surface, allowing enhanced uptake into 
cells. Wise et al. showed that respirable lead chromate particles 
adhere to the surface of rodent cells in culture causing cell-enhanced 
dissolution of the chromate ion as well as phagocytosis of lead 
chromate particles (Exs. 35-68; 35-67). The intracellular accumulation 
was both time- and dose-dependant. Cellular uptake resulted in damage 
to DNA, apoptosis (i.e., form of programmed cell death), and neoplastic 
transformation (Ex. 35-119). Singh et al. showed that treatment of 
normal human lung epithelial cells with insoluble lead chromate 
particulates (0.4 to 2.0 [mu]g/cm<SUP>2</SUP>) or soluble sodium 
chromate (10 [mu]M) for 24 hours caused Cr(VI) uptake, Cr-DNA adduct 
formation, and apoptosis (Ex. 35-66). The proximate genotoxic agent in 
these cell systems was determined to be the chromate rather than the 
lead ions (Ex. 35-327). Elias et al. reported that cell-enhanced 
particle dissolution and uptake was also responsible for the 
cytotoxicity and neoplastic transformation in Syrian hamster embryo 
cells caused by Cr(VI) pigments, including several complex industrial 
chrome yellow and molybdate orange pigments (Ex. 125).
    Reduction to the poorly permeable Cr(III) in the epithelial lining 
fluid limits cellular uptake of Cr(VI). Ascorbic acid and glutathione 
(GSH) are believed to be the key molecules responsible for the 
extracellular reduction. Cantin et al. reported high levels of GSH in 
human alveolar epithelial lining fluid and Susuki et al. reported 
significant levels of ascorbic acid in rat lung lavage fluids (Exs. 35-
147; 35-143). Susuki and Fukuda studied the kinetics of soluble Cr(VI) 
reduction with ascorbic acid and GSH in vitro and following 
intratracheal instillation (Ex. 35-90). They reported that the 
reduction was pseudo-first order (i.e., rate of Cr(VI) reduction 
appeared to be proportional to metal concentration rather than 
concentration of reductant) with respect to Cr(VI), with a half-life of 
just under one minute to several hours. They found the greatest 
reduction rates with higher levels of reductants. Ascorbic acid was 
more active than GSH. Cr(VI) reduction was slower in vivo than 
predicted from in vitro and principally involved ascorbic acid, not 
GSH. This research indicates that extracellular Cr(VI) reduction to 
Cr(III) is variable depending on the concentration and nature of the 
reductant in the epithelial fluid lining regions of the respiratory 
tract. De Flora et al. determined the amount of soluble Cr(VI) reduced 
in vitro by human bronchiolar alveolar fluid and pulmonary alveolar 
macrophage fractions over a short period and used these specific 
activities to estimate an ``overall reducing capacity'' of 0.9-1.8 mg 
Cr(VI) and 136 mg Cr(VI) per day per individual, respectively (Ex. 35-
140).
    De Flora, Jones, and others have interpreted the extracellular 
reduction data to mean that very high levels of Cr(VI) are required to 
``overwhelm'' the reductive defense mechanism before target cell uptake 
can occur and, as

[[Page 59348]]

such, impart a ``threshold'' character to the exposure-response (Exs. 
35-139; 31-22-7). However, the threshold capacity concept does not 
consider that facilitated lung cell uptake and extracellular reduction 
are dynamic and parallel processes that happen concurrently. If their 
rates are comparable then some cellular uptake of Cr(VI) would be 
expected, even at levels that do not ``overwhelm'' the reductive 
capacity. Based on the in vitro kinetic data, it would appear that such 
situations are plausible, especially when concentrations of ascorbic 
acid are low. Unfortunately, there has been little systematic study of 
the dose-dependence of Cr(VI) uptake in the presence of physiological 
levels of ascorbate and GSH using experimental systems that possess 
active anion transport capability.
    Wise et al. did study uptake of a single concentration of insoluble 
lead chromate particles (0.8 [mu]g/cm<SUP>2</SUP>) and soluble sodium 
chromate (1.3 [mu]M) in Chinese hamster ovary cells co-treated with a 
physiological concentration (1mM) of ascorbate (Ex. 35-68). They found 
that the ascorbate substantially reduced, but did not eliminate, 
chromate ion uptake over a 24 hour period. Interestingly, ascorbate did 
not affect phagocytic uptake of lead chromate particles, although it 
eliminated the Cr(VI)-induced clastogenesis (e.g., DNA strand breakage 
and chromatid exchange) as measured under their experimental 
conditions.
    Singh et al. suggested that cell surface interactions with 
insoluble lead chromate particulates created a concentrated 
microenvironment of chromate ions resulting in higher intracellular 
levels of chromium than would occur from soluble Cr(VI) (Ex. 35-149). 
The evidence for cell membrane mediated uptake of Cr(VI) is consistent 
with the intratracheal and intrabronchial instillation studies in 
rodents that show greater carcingenicity with sparingly soluble (e.g., 
calcium chromate) than insoluble chromate (e.g., lead chromate) 
particulates and soluble chromates (e.g., sodium chromate) (Ex. 11-2).
    Finally, Cr(VI) deposited in the tracheobronchial and alveolar 
regions of the respiratory tract is cleared by the mucocilliary 
escalator (soluble and particulate Cr(VI)) and macrophage phagocytosis 
(particulate Cr(VI) only). In most instances, these clearance processes 
take hours to days to completely clear Cr(VI) from the lung, but it can 
take considerably longer for particulates deposited at certain sites. 
For example, Ishikawa et al. showed that some workers had substantial 
amounts of chromium particulates at the bifurcations of the large 
bronchii for more than two decades after cessation of exposure (Ex. 35-
81). Mancuso reported chromium in the lungs of six chromate production 
workers who died from lung cancer (as cited in Ex. 35-47). The interval 
between last exposure to Cr(VI) until autopsy ranged from 15 months to 
16 years. Using hollow casts of the human tracheobronchial tree and 
comparing particle deposition with reported occurrence of bronchogenic 
tumors, Schlesinger and Lippman were able to show good correlations 
between sites of greatest deposition and increased incidence of 
bronchial tumors (Ex. 35-102).
    b. Intracellular Reduction of Cr(VI). Once inside the cell, the 
hexavalent chromate ion is rapidly reduced to intermediate oxidation 
states, Cr(V) and Cr(IV), and the more chemically stable Cr(III). 
Unlike Cr(VI), these other chromium forms are able to react with DNA 
and protein to generate a variety of adducts and complexes. In 
addition, reactive oxygen species (ROS) are produced during the 
intracellular reduction of Cr(VI) that are also capable of damaging 
DNA. These reactive intermediates, and not Cr(VI) itself, are 
considered to be the ultimate genotoxic agents that initiate the 
carcinogenic process.
    After crossing the cell membrane, Cr(VI) compounds can be non-
enzymatically converted to Cr(III) by several intracellular reducing 
factors (Ex. 35-184). The most plentiful electron donors in the cell 
are GSH, and other thiols, such as cysteine, and ascorbate. Connett and 
Wetterhahn showed that a Cr(VI)-thioester initially forms in the 
presence of GSH (Ex. 35-206). A two-phase reduction then occurs with 
rapid conversion to Cr(V) and glutathionyl radical followed by 
relatively slower reduction to Cr(III) that requires additional 
molecules of GSH. Depletion of cellular GSH and other thiols is 
believed to retard complete reduction of Cr(VI) to Cr(III), allowing 
buildup of intermediates Cr(V) and Cr(IV). The molecular kinetics of 
the Cr(VI) to Cr(III) reduction with ascorbate is less well understood 
but can also involve intermediate formation of Cr(V) and free radicals 
(Ex. 35-184).
    Another important class of intracellular Cr(VI) reductions are 
catalyzed by flavoenzymes, such as GSH reductase, lipoyl dehydrogenase, 
and ferredoxin-NADP oxidoreductase. The most prominent among these is 
GSH reductase that uses NADPH as a cofactor in the presence of 
molecular oxygen (O<INF>2</INF>) to form Cr(V)-NADPH complexes. During 
the reaction, O<INF>2</INF> undergoes one electron reduction to the 
superoxide radical (O<INF>2</INF><SUP>-</SUP>) which produces hydrogen 
peroxide (H<INF>2</INF>O<INF>2</INF>) through the action of the enzyme 
superoxide dismutase. The Cr(V)-NADPH can then react with 
H<INF>2</INF>O<INF>2</INF> to regenerate Cr(VI) giving off hydroxyl 
radicals, a highly reactive oxygen species, by a Fenton-like reaction. 
It is, therefore, possible for a single molecule of Cr(VI) to produce 
many molecules of potentially DNA damaging ROS through a repeated 
reduction/oxidation cycling process. Shi and Dalal used electron spin 
resonance (ESR) to establish formation of Cr(V)-NADPH and hydroxyl 
radical in an in vitro system (Ex. 35-169; 35-171). Sugiyama et al. 
reported Cr(V) formation in cultured Chinese hamster cells treated with 
soluble Cr(VI) (Ex.35-133). Using a low frequency ESR, Liu et al. 
provided evidence of Cr(V) formation in vivo in mice injected with 
soluble Cr(VI) (Ex. 35-141-28). Several studies have documented that 
Cr(VI) can generate Cr(V) and ROS in cultured human lung epithelial 
cells and that this reduction/oxidation pathway leads to DNA damage, 
activation of the p53 tumor suppressor gene and stress-induced 
transcription factor NF-[kappa]B, cell growth arrest, and apptosis 
(Exs. 35-125; 35-142; 31-22-18; 35-135). Leonard et al. used ESR spin 
trapping, catalase, metal chelators, free radical scavengers, and 
O<INF>2</INF>-free atmospheres to show that hydroxyl radical generation 
involves a Fenton-like reaction with soluble potassium dichromate (Ex. 
31-22-17) and insoluble lead chromate (Ex. 35-137) in vitro. Liu et al. 
showed that the Cr(IV)/Cr(V) compounds are also able to generate ROS 
with H<INF>2</INF>O<INF>2</INF> in a Fenton reduction/oxidation cycle 
in vitro (Ex. 35-183).
    Although most intracellular reduction of Cr(VI) is believed to 
occur in the cytoplasm, Cr(VI) reduction can also occur in mitochondria 
and the endoplasmic reticulum. Cr(VI) reduction can occur in the 
mitochondria through the action of the electron transport complex (Ex. 
35-230). The microsomal cytochrome P-450 system in the endoplasmic 
reticulum also enzymatically reduces Cr(VI) to Cr(V), producing ROS 
through reduction/oxidation cycling as described above (Ex. 35-171).
    c. Genotoxicity and Damage to DNA. A large number of studies have 
examined multiple types of genotoxicity in a wide range of experimental 
test systems. Many of the specific investigations have been previously 
reviewed by IARC (Ex. 35-43), Klein (Ex. 35-134), ATSDR (Ex. 35-41), 
and the K.S. Crump Group (Ex. 35-47) and will only be briefly 
summarized here.

[[Page 59349]]

The body of evidence establishes that both soluble and insoluble forms 
of Cr(VI) cause structural DNA damage that can lead to genotoxic events 
such as mutagenisis, inhibition of DNA replication and transcription, 
and altered gene expression, all of which probably play a role in 
neoplastic transformation. The reactive intermediates and products that 
occur from intracellular reduction of Cr(VI) cause a wide variety of 
DNA lesions. At this time, it is not clear which types of DNA damage 
are the most critical to the carcinogenic process.
    Cr(VI) compounds are mutagenic in most bacterial and mammalian test 
systems (Ex. 35-118). In the bacterial Salmonella typhimurium strains, 
soluble Cr(VI) caused base pair substitutions at A-T sites as well as 
frame shift mutations (Ex. 35-161). Nestmann et al. also reported 
forward and frame shift mutations in Salmonella typhimurium with 
insoluble Cr(VI) (Ex. 35-162). Several Cr(VI) compounds have produced 
mutagenic responses at various genetic loci in mammalian cells (Ex. 12-
7). Clastogenic damage, such as sister chromatid exchange and 
chromosomal aberrations, have also been reported for insoluble Cr(VI) 
and soluble Cr(VI) (Exs. 35-132; 35-115). Mammalian cells undergo 
neoplastic transformation following treatment with soluble Cr(VI) or 
insoluble Cr(VI), including a number of zinc and lead chromate pigments 
(Exs. 12-5; 35-186).
    Genotoxicity has been reported from Cr(VI) administration to 
animals in vivo. Soluble Cr(VI) induced micronucleated erythrocytes in 
mice following intraperitoneal (IP) administration (Ex. 35-150). It 
also increased the mutation frequency in liver and bone marrow 
following IP administration to lacZ transgenic mice (Exs. 35-168; 35-
163). Izzotti et al. reported DNA damage in the lungs of rats exposed 
to soluble Cr(VI) by intratracheal instillation (Ex. 35-170). 
Intratracheal instillation of soluble Cr(VI) produced a time- and dose-
dependant elevation in mutant frequency in the lung of Big Blue 
transgenic mice (Ex. 35-174). Oral administration of soluble Cr(VI) in 
animals did not produce genotoxicity in several studies probably due to 
route-specific differences in absorption. OSHA is not aware of 
genotoxicity studies from in vivo administration of insoluble Cr(VI).
    Studies of chromosomal and DNA damage in workers exposed to Cr(VI) 
vary in their findings. Some studies reported higher levels of 
chromosomal aberrations, sister chromatid exchanges, or DNA strand 
breaks in peripheral lymphocytes of stainless steel welders (Exs. 35-
265; 35-160) and electroplaters (Ex. 35-164). Other studies were not 
able to find excess damage in DNA from the blood lymphocytes of workers 
exposed to Cr(VI) (Exs. 35-185; 35-167). These reports are difficult to 
interpret since co-exposure to other genotoxic agents (e.g., other 
metals, cigarette smoke) likely existed and the extent of Cr(VI) 
exposures were not known.
    Because of the consistent positive response across multiple assays 
in a wide range of experimental systems from prokaryotic organisms 
(e.g., bacteria) to human cells in vitro and animals in vivo, OSHA 
regards Cr(VI) as an agent able to induce carcinogenesis through a 
genotoxic mode of action. Both soluble and insoluble forms of Cr(VI) 
are reported to cause mutagenisis, clastogenesis, and neoplastic 
transformation. On the other hand, Cr(III) compounds do not easily 
cause mutations or chromosomal damage in intact cellular systems, 
presumably due to the inability of Cr(III) to penetrate cell membranes 
(Exs. 12-7; 35-186).
    There has been a great deal of research to identify the types of 
damage to DNA caused by Cr(VI), the reactive intermediates that are 
responsible for the damage, and the specific genetic lesions critical 
to carcinogenesis. It was shown that Cr(VI) was inactive in DNA binding 
assays with isolated nuclei or purified DNA (Ex. 35-47). However, 
Cr(III) was able to produce DNA protein cross-links, sister chromatid 
exchanges, and chromosomal aberrations in an acellular system. 
Zhitkovich et al. showed that incubation of Chinese hamster ovary cells 
with soluble Cr(VI) produced ternary complexes of Cr(III) cross-linked 
to cysteine, other amino acids, or glutathione and the DNA phosphate 
backbone (Ex. 312). Utilizing the pSP189 shuttle vector plasmid, they 
showed these DNA-Cr(III)-amino acid cross-links were mutagenic when 
introduced in human fibroblasts (Ex. 35-131).
    Another research group showed that plasmid DNA treated with Cr(III) 
produced intrastrand crosslinks and the production of these lesions 
correlated with DNA polymerase arrest (Ex. 35-126). The same 
intrastrand crosslinks and DNA polymerase arrest could also be induced 
by Cr(VI) in the presence of ascorbate as a reducing agent to form 
Cr(III) (Ex. 35-263). These results were confirmed in a cell system by 
treating human lung fibroblasts with soluble Cr(VI), isolating genomic 
DNA, and demonstrating dose-dependant guanine-specific arrest in a DNA 
polymerase assay (Ex. 35-188). Cr(V) may also form intrastrand 
crosslinks since Cr(V) interacts with DNA in vitro (Ex. 35-178). The 
Cr(V)-DNA crosslinks are probably readily reduced to Cr(III) in cell 
systems. Intrastrand crosslinks have also been implicated in inhibition 
of RNA polymerase and DNA topoisomerase, leading to cell cycle arrest, 
apoptosis and possibly other disturbances in cell growth that 
contribute to the carcinogenic pathway (Ex. 35-149).
    DNA strand breaks and oxidative damage result from the one electron 
reduction/oxidation cycling of Cr(VI), Cr(V), and Cr(IV). Shi et al. 
showed that soluble Cr(VI) in the presence of ascorbate and 
H<INF>2</INF>O<INF>2</INF> caused DNA double strand breaks and 8-
hydroxy deoxyguanine (8-OHdG, a marker for oxidative DNA damage) in 
vitro (Ex. 35-129). Leonard et al. showed that the DNA strand breaks 
were reduced by several experimental conditions including an 
O<INF>2</INF>-free atmosphere, catabolism of H<INF>2</INF>O<INF>2</INF> 
by catalase, ROS depletion by free radical scavangers, and chelation of 
Cr(V). They concluded that the strand breaks and 8-OHdG resulted from 
DNA damage caused by hydroxyl radicals from Cr(VI) reduction/oxidation 
cycling (Ex. 31-22-17). Generation of ROS-dependant DNA damage could 
also be shown with insoluble Cr(VI) (Ex. 35-137). DNA strand breaks and 
related damage caused by soluble Cr(VI) have been reported in Chinese 
hamster cells (Ex. 35-128), human fibroblasts (Ex. 311), and human 
prostate cells (Ex. 35-255). Pretreatment of Chinese hamster cells with 
a metal chelator suppressed Cr(V) formation from Cr(VI) and decreased 
DNA strand breaks (Ex. 35-197). Chinese hamster cells that developed 
resistance to H<INF>2</INF>O<INF>2</INF> damage also had reduced DNA 
strand breaks from Cr(VI) treatment compared to the normal phenotype 
(Ex. 35-176).
    Several researchers have been able to modulate Cr(VI)-induced DNA 
damage using cellular reductants such as ascorbate, GSH and the free 
radical scavenger tocopherol (vitamin E). This has provided insight 
into the relationships between DNA damage, reduced chromium forms and 
ROS. Sugiyama et al. showed that Chinese hamster cells pretreated with 
ascorbate decreased soluble Cr(VI)-induced DNA strand damage (e.g., 
alkali-labile sites), but enhanced DNA-amino acid crosslinks (Ex. 35-
133). Standeven and Wetterhahn reported that elimination of ascorbate 
from rat lung cytosol prior to in vitro incubation with soluble Cr(VI) 
completely inhibited Cr-DNA binding (Ex. 35-180). However, not all 
types of Cr-DNA binding are enhanced by ascorbate. Bridgewater et al. 
found that high ratios of ascorbate to Cr(VI)

[[Page 59350]]

actually decreased intrastrand crosslinks in vitro while low ratios 
induced their formation (Ex. 35-263). This finding is consistent with 
research by Stearns and Watterhahn who showed that excessive ascorbate 
relative to Cr(VI) leads to two-electron reduction of Cr(III) and 
formation of Cr(III)-DNA monoadducts and DNA-Cr(III)-amino acid 
crosslinks (Ex. 35-166). Low amounts of ascorbate primarily cause one-
electron reduction to intermediates Cr(V) and Cr(IV) that form 
crosslinks with DNA and ROS responsible for DNA strand breaks, alkali-
labile sites, and clastogenic damage. This explains the apparent 
paradox that extracellular Cr(VI) reduction by ascorbate to Cr(III) 
reduces Cr(VI)-induced DNA binding but intracellular Cr(VI) reduction 
by ascorbate to Cr(III) enhances Cr-DNA binding. The aforementioned 
studies used soluble forms of Cr(VI), but Blankenship et al. showed 
that ascorbate pretreatment inhibited chromosomal aberrations in 
Chinese hamster ovary cells caused by both insoluble lead chromate 
particles as well as soluble Cr(VI) (Ex. 35-115). Pretreatment with the 
free radical scavenger tocopherol also inhibits chromosomal aberrations 
and alkali-labile sites in Cr(VI)-treated cells (Exs. 35-115; 35-128).
    Studies of the different types of DNA damage caused by Cr(VI) and 
the modulation of that damage inside the cell demonstrate that Cr(VI) 
itself is not biologically active. Cr(VI) must undergo intracellular 
reduction to Cr(V), Cr(IV), and Cr(III) before the damage to DNA can 
occur. The evidence suggests that Cr(III) can cause DNA-Cr-amino acid, 
DNA-Cr-DNA crosslinks and Cr-DNA monoadducts. Cr(V) and possibly Cr(IV) 
contribute to intrastrand crosslinks and perhaps other Cr-DNA binding. 
ROS generated during intracellular reduction of Cr(VI) lead to lesions 
such as chromosomal aberrations, DNA strand breaks, and oxidative DNA 
damage. The specific DNA lesions responsible for neoplastic 
transformation have yet to be firmly established so all forms of DNA 
damage should, at this time, be regarded as potential contributors to 
carcinogenicity.
    d. Cr(VI)-induced Disturbances in the Regulation of Cell 
Replication. Recent research has begun to elucidate how Cr(VI)-induced 
oxidative stress and DNA lesions trigger cell signaling pathways that 
regulate the cell growth cycle. The complex regulation of the cell 
growth cycle by Cr(VI) involves activation of the p53 protein and other 
transcription factors that respond to oxidative stress and DNA damage. 
The cellular response ranges from a temporary pause in the cell cycle 
to terminal growth arrest (i.e., viable cells that have lost the 
ability to replicate) and a programmed form of cell death, known as 
apoptosis. Apoptosis involves alterations in mitochondrial 
permeability, release of cytochrome c and the action of several kinases 
and caspases. Less is known about the molecular basis of terminal 
growth arrest. Terminal growth arrest and apoptosis serve to eliminate 
further growth of cells with unrepaired Cr(VI)-induced genetic damage. 
However, it is believed that cells which escape these protective 
mechanisms and regain replicative competence eventually become 
resistant to normal growth regulation and can transform to a neoplastic 
phenotype (Exs. 35-121; 35-122; 35-120).
    Blankenship et al. first described apoptosis as the primary mode of 
cell death following a two hour treatment of Chinese hamster ovary 
cells with high concentrations (>150 [mu]M) of soluble Cr(VI) (Ex. 35-
144). Apoptosis also occurs in human lung cells following short-term 
treatment with soluble Cr(VI) (Ex. 35-125) as well as longer term 
treatment (e.g., 24 hours) with lower concentrations of soluble Cr(VI) 
(e.g., 10 [mu]M) and insoluble Cr(VI) in the form of lead chromate (Ex. 
35-166). Ye et al. found that the Cr(VI) treatment that caused 
apoptosis also activated expression of p53 protein (Ex. 35-125). This 
apoptotic response was substantially reduced in a p53-deficient cell 
line treated with Cr(VI), suggesting that the p53 activation was 
required for apoptosis. Other studies using p53 null cells from mice 
and humans confirmed that Cr(VI)-induced apoptosis is p53-dependent 
(Ex. 35-225).
    The p53 protein is a transcription factor known to be activated by 
DNA damage, lead to cell cycle arrest, and regulate genes responsible 
for either DNA repair or apoptosis. Therefore, it is likely that the 
p53 activation is a response to the Cr(VI)-induced DNA damage. 
Apoptosis (i.e., programmed cell death) is triggered once the Cr(VI)-
induced DNA damage becomes too extensive to successfully repair. In 
this manner, apoptosis serves to prevent replication of genetically 
damaged cells. Several researchers have gone on to further elucidate 
the molecular pathways involved in Cr(VI)-induced apoptosis. ROS 
produced by intracellular Cr(VI) reduction/oxidation cycling have been 
implicated in the activation of p53 and apoptosis (Exs. 35-255; 35-
122). Using specific inhibitors, Pritchard et al. showed that 
mitochondrial release of cytochrome c is critical to apoptotic death 
from Cr(VI) (Ex. 35-159). Cytochrome c release from mitochondria could 
potentially result from either direct membrane damage caused by Cr(VI)-
induced ROS or indirectly by enhanced expression of the p53-dependent 
apoptotic proteins, Bax and Nova, known to increase mitochondrial 
membrane permeability.
    Cr(VI) causes cell cycle arrest and reduces clonogenic potential 
(i.e., normal cell growth) at very low concentrations (e.g., 1 [mu]M) 
where significant apoptosis is not evident. Xu et al. showed that human 
lung fibroblasts treated with low doses of Cr(VI) caused guanine-
guanine intrastrand crosslinks, guanine-specific polymerase arrest, and 
inhibited cell growth at the G<INF>1</INF>/S phase of the cell cycle 
(Ex. 35-188). Zhang et al. described a dose-dependent increase in 
growth arrest at the G<INF>2</INF>/M phase of the cell cycle in a human 
lung epithelial cell line following 24 hour Cr(VI) treatment over a 
concentration range of 1 to 10 [mu]M (Ex. 35-135). The cell cycle 
arrest could be partially eliminated by reducing production of Cr(VI)-
induced ROS. Apoptosis was not detected in these cells until a 
concentration of 25 [mu]M Cr(VI) had been reached. These data suggest 
that low cellular levels of Cr(VI) are able to cause DNA damage and 
disrupt the normal cell growth cycle.
    Pritchard et al. studied the clonogenicity over two weeks of human 
fibroblasts treated 24 hours with soluble Cr(VI) concentrations from 1 
to 10 [mu]M (Ex. 35-120). They reported a progressive decline in cell 
growth with increasing Cr(VI) concentration. Terminal growth arrest 
(i.e., viable cells that have lost the ability to replicate) was 
primarily responsible for the decrease in clonogenic survival below 4 
[mu]M Cr(VI). At higher Cr(VI) concentrations, apoptosis was 
increasingly responsible for the loss in clonogenicity. Pritichard et 
al. and other research groups have suggested that a subset of cells 
that continue to replicate following Cr(VI) exposure could contain 
unrepaired genetic damage or could have become intrinsically resistant 
to processes (e.g., apoptosis, terminal growth arrest) that normally 
control their growth (Exs. 35-121; 35-122; 35-120). These surviving 
cells would then be more prone to neoplastic progression and have 
greater carcinogenic potential.
    e. Summary. Respirable chromate particulates are taken up by target 
cells in the bronchoalveolar region of the lung, become intracellularly 
reduced to several reactive genotoxic species able to damage DNA, 
disrupt normal regulation of cell division and cause neoplastic 
transformation. Scientific studies indicate that both aqueous

[[Page 59351]]

insoluble and soluble Cr(VI) can be transported into the cell. In fact, 
cell surface interactions with sparingly soluble and some insoluble 
chromates likely create a concentrated microenvironment of chromate ion 
resulting in higher intracellular levels of Cr(VI) than would occur 
from soluble chromates. This is consistent with the studies of 
respiratory tract carcinogenesis in animals that indicate the most 
tumorigenic chromates had low to moderate water solubility. Once inside 
the cell, Cr(VI) is converted to several lower oxidation forms able to 
bind to and crosslink DNA. ROS are produced during intracellular 
reduction/oxidation of Cr(VI) that further damage DNA. This 
genotoxicity is functionally translated into impaired DNA replication, 
mutagenesis, and altered gene expression that ultimately lead to 
neoplastic transformation.
9. Preliminary Conclusions
    OSHA preliminarily concludes that the study data summarized in the 
previous sections support the determination that Cr(VI) compounds 
should be regarded as carcinogenic to workers. The strongest evidence 
comes from the many cohort studies reporting excess lung cancer 
mortality in workers exposed to Cr(VI) during production of chromates 
and chromate pigments. Additional evidence comes from the less 
consistent elevations in lung cancer mortality found in workers exposed 
to Cr(VI) in other occupations, increased tumor incidence in 
experimental animals treated with Cr(VI), and cellular and molecular 
data on mode of action.
    Studies of chromate production workers in several countries have 
consistently found significantly greater mortality from lung cancer 
than expected. In the earliest studies of chromate workers in whom 
Cr(VI) exposures were believed to be highest, the risk for respiratory 
cancer was between 15 and 29 times expectation (Exs. 7-2; 7-13; 7-1). 
Lung cancer risks of this magnitude cannot be explained by potential 
confounders and other biases.
    Later studies that were able to reconstruct exposure histories in 
workers from production plants located in Baltimore, MD and 
Painesville, OH found significant trends between lung cancer mortality 
and both cumulative exposure to Cr(VI) and duration of employment (Exs. 
31-22-11; 33-10). Workers were predominantly exposed to the highly 
water soluble sodium chromate and sodium dichromate at these plants, 
although probable exposure to other chromates also occurred. Gibb et 
al. showed that a significant association between lung cancer and 
Cr(VI) was evident, even in models that accounted for smoking (Ex. 31-
22-11). Other studies documented declines in lung cancer mortality 
rates with reduced Cr(VI) exposures due to improvements in the 
production process (Exs. 7-99; 7-91; 31-18-4). These trends serve to 
strengthen the evidence for causal association between Cr(VI) and lung 
cancer.
    Studies of workers in the chromate pigment production industry also 
consistently show significantly elevated lung cancer mortality. These 
include cohorts from Norway, Great Britain, U.S., and France. The 
workers were principally exposed to zinc and lead chromate pigments, 
but the levels of Cr(VI) exposure were not well characterized. Some 
studies presented data that suggested excess lung cancer was more 
strongly associated with zinc chromate, although workers were exposed 
to several chromium pigments (Exs. 7-41; 7-42).
    Significantly elevated lung cancer mortality was found in two 
British chromium electroplating cohorts (Exs. 35-62; 271). The workers 
were exposed to Cr(VI) in the form of chromic acid mist as well as 
nickel, another potential lung carcinogen. The association between lung 
cancer and Cr(VI) in stainless steel welders and ferrochromium 
production workers are confounded by substantial exposures to other 
potential carcinogens and Cr(III). However, the generally elevated lung 
cancer mortality in these workers supports the stronger evidence from 
the soluble chromate and chromate pigment production cohorts.
    A number of the epidemiological studies cited above were evaluated 
by the IARC in 1990 (Ex. 35-43). IARC found ``sufficient evidence in 
humans for the carcinogenicity of chromium [VI] compounds as 
encountered in chromate production, chromate pigment production and 
chromate plating industries'' (Ex. 35-43, p. 213). IARC gave Cr(VI) 
compounds their highest Group 1 classification for agents considered 
carcinogenic to humans. The EPA and ACGIH have designated Cr(VI) 
compounds as known and confirmed human carcinogens, respectively (Exs. 
35-52; 35-207). NIOSH considers Cr(VI) compounds to be potential 
occupational carcinogens (Ex. 31-22-22, p. 8).
    Experimental animals have generally been administered Cr(VI) 
compounds by routes other than inhalation. A number of studies in which 
Cr(VI) compounds were directly instilled in the respiratory tract of 
rodents produced a significant incidence of lung tumors (Exs. 11-2; 11-
12; 11-7). The findings indicate different tumorigenic potencies among 
Cr(VI) compounds. The less water soluble calcium chromate, strontium 
chromates, and zinc chromates cause higher numbers of lung tumors at 
similar doses than the more water soluble sodium dichromate and chromic 
acid. Experimental research suggests that cellular uptake of the water-
insoluble lead chromate is enhanced by the ability to achieve a high 
local concentration at the lung cell surface that does not occur during 
uptake of soluble chromates (Ex. 35-149). Because of the greater cancer 
potency in animal studies, ACGIH has recommended a lower occupational 
TLV for insoluble Cr(VI) compounds (10 [mu]g/m\3\) than for water-
soluble Cr(VI) compounds (50 [mu]g/m\3\).
    The few available inhalation studies are limited by abbreviated 
exposure durations, low exposure levels, or small number of animals per 
dose group. These studies report slightly elevated lung tumor incidence 
that are not statistically significant (Exs. 10-11; 35-26-1) or 
marginally significant (Exs. 10-8; 35-26). Cr(VI) administered to 
animals by intramuscular, subcutaneous, and other routes of 
administration have consistently produced a high incidence of tumors, 
usually near the site of administration.
    Evidence from in vitro research shows that Cr(VI) enters the cell 
and is rapidly converted to several lower oxidation forms able to bind 
to and crosslink DNA. ROS (reactive oxygen species) are produced during 
intracellular reduction/oxidation of Cr(VI) that can further damage 
DNA. Soluble and insoluble Cr(VI) compounds are reported to cause 
mutagenesis, clastogenesis, and neoplastic transformation across 
multiple assays in a wide range of experimental systems from 
prokaryotic organisms to human cells in vitro and animals in vivo. 
Therefore, OSHA regards all Cr(VI) compounds as agents able to induce 
carcinogenesis through a genotoxic mode of action.
    The rate, as well as the magnitude of the Cr(VI) dose, that reaches 
the lung has been shown to influence carcinogenic outcome in 
experimental animals (Ex. 11-7). Less frequent, but higher dose levels 
of Cr(VI) instilled in the tracheas of rats caused greater tumor 
incidence than the same total amount of Cr(VI) instilled more 
frequently but at lower dose levels. This may result from a 
proliferation of neoplastic cells triggered by lung inflammation at the 
high Cr(VI) dose levels or from overwhelming any of a number of 
molecular pathways that serve to protect against Cr(VI)-induced 
respiratory

[[Page 59352]]

carcinogenesis, including extracellular reduction to poorly absorbed 
Cr(III), intracellular binding of reactive forms to non-critical 
macromolecules, or repair of DNA damage. The existence of dose rate 
effects could potentially introduce non-linearities in the Cr(VI) 
exposure-cancer response. As discussed in the quantitative risk 
assessment section (section VII), OSHA is not aware of reliable data on 
which to confidently predict the range of Cr(VI) air levels at which 
presumed non-linearities might occur or empirical data that 
convincingly establishes the existence of a threshold exposure for 
carcinogenicity.

C. Non-Cancer Respiratory Effects

    The following sections describe the evidence from the literature on 
nasal irritation, nasal ulcerations, nasal perforations, asthma, and 
bronchitis following inhalation exposure to water soluble Cr(VI) 
compounds. The evidence clearly demonstrates that workers can develop 
impairment to the respiratory system (nasal irritation, nasal 
ulceration, nasal perforation, and asthma) after work place exposure by 
inhalation exposure to Cr(VI) compounds below the current PEL.
    It is very clear from the evidence that workers may develop nasal 
irritation, nasal septum ulcerations, and nasal septum perforations at 
occupational exposures level at or below the current PEL of 52 [mu]g/
m<SUP>3</SUP>. However, it is not clear what occupational exposure 
levels lead to the development of occupational asthma or bronchitis.
1. Nasal Irritation, Nasal Septum Ulcerations and Nasal Septum 
Perforations
    Occupational exposure to Cr(VI) can lead to nasal septum 
ulcerations and nasal septum perforations. The nasal septum separates 
the nostrils and is composed of a thin strip of cartilage with an 
overlying mucous membrane known as the mucosa. The initial lesion after 
Cr(VI) exposure is characterized by localized inflammation or a 
reddening of the affected mucosa, which can later lead to atrophy. This 
may progress to an ulceration of the mucosa layer (Ex. 35-1; Ex. 7-3). 
If exposure is discontinued, the ulcer progression will stop and a scar 
may form. However, if exposure continues, the ulcer may break through 
the septum, resulting in a nasal septum perforation sometimes referred 
to chrome hole. Individuals with nasal perforations may experience a 
range of signs and symptoms, such as a whistling sound, bleeding, nasal 
discharge, and infection. Some individuals may experience no noticeable 
effects. It is currently not known precisely what level would trigger 
such nasal problems, but, as stated earlier, it is evident that workers 
are developing nasal problems at levels at or below the current PEL.
    Several cohort and cross-sectional studies have described nasal 
lesions from airborne exposure to Cr(VI) at various electroplating and 
chrome production facilities. Most of these studies have been reviewed 
by the Center for Disease Control's Agency for Toxic Substances and 
Disease Registry (ATSDR) toxicological profile for chromium (Ex. 35-
41). OSHA reviewed the studies summarized in the profile and conducted 
its own literature search to update and supplement the review. In its 
evaluation, OSHA took into consideration the exposure regimen and 
experimental conditions under which the studies were performed, 
including exposure levels, duration of exposure, number, and the 
inclusion of appropriate control groups. Studies were not included if 
they did not contribute to the weight of evidence either because of 
inadequate documentation or because of poor quality. This section only 
covers some of the key studies and reviews. OSHA has also identified 
two case reports demonstrating the development of nasal irritation and 
nasal septum perforations, and these case reports are summarized as 
well. One case report shows how a worker can develop the nasal 
perforations from direct contact (i.e., touching the inner surface of 
the nose with contaminated fingers).
    Lindberg and Hedenstierna examined the respiratory symptoms and 
effects of 104 Swedish electroplaters (Ex. 9-126). Of the 104 
electroplaters, 43 were exposed to chromic acid by inhalation. The 
remaining 61 were exposed to a mixture of chromic acid and nitric acid, 
hydrochloric acid, boric acid, nickel, and copper salts. The workers 
were evaluated for respiratory symptoms, changes in the nasal septum, 
and lung function. All workers were asked to fill out a detailed 
questionnaire on their history of respiratory symptoms and function. 
Physicians performed inspections of the nasal passages of each worker. 
Workers were given a pulmonary function test to assess lung function. 
For those 43 workers exposed exclusively to chromic acid, the median 
exposure time was 2.5 years, ranging from 0.2 to 23.6 years. The 
workers were divided into two groups, a low exposure group (19 workers 
exposed to eight-hour time weighted average levels below 2 [mu]g/m\3\) 
and a high exposure group (24 workers exposed to eight-hour time 
weighted average levels above 2 [mu]g/m\3\). Personal air sampling was 
conducted on 11 workers for an entire week and at stations close to the 
chrome baths to evaluate peak exposures and variations in exposure on 
different days over the week. Nineteen office employees were not 
exposed to Cr(VI) used as controls for nose and throat symptoms, and 
119 auto mechanics (no car painters or welders) whose lung function had 
been evaluated using similar techniques to those used on Cr(VI) exposed 
workers were used as controls for lung function.
    The investigators reported nasal ulcerations and perforations in a 
group of workers exposed at the highest peak exposure levels (ranging 
from 20 [mu]g/m\3\/day to peak levels of 46 [mu]g/m\3\/day) to chromic 
acid as Cr(VI); prevalence of ulceration/perforation was statistically 
higher than the control group. Of the 14 individuals in the 20-46 
[mu]g/m\3\ exposure group, seven developed nasal ulcerations. In 
addition to nasal ulcerations, 2 of the 7 also had progressed to nasal 
perforations. Furthermore, three individuals developed nasal 
perforations only, at the same exposure levels. At average exposure 
levels from 2 [mu]g/m\3\ to 20 [mu]g/m\3\, half of the workers 
complained of ``constantly running nose,'' ``stuffy nose,'' or ``there 
was a lot to blow out.'' (Authors do not provide details of each 
complaint). Atrophy, which is a precursor to ulcerations and 
perforations, was only observed in occupationally exposed workers at 
relatively low peak levels ranging from 2.5 [mu]g/m\3\ to 11 [mu]g/
m\3\. No one exposed to levels below 1 [mu]g/m\3\ (time-weighted 
average, TWA) complained of respiratory symptoms or developed lesions.
    The authors also reported that in the exposed workers, both forced 
vital capacity and forced expiratory volume in one second were reduced 
by 0.2 L, when compared to controls. The forced mid-expiratory flow 
diminished by 0.4 L/second from Monday morning to Thursday afternoon in 
workers exposed to chromic acid as Cr(VI) daily TWA average levels of 2 
[mu]g/m\3\ or higher. The effects were small, not outside the normal 
range and transient (recovery after 2 days). There was no difference 
between the control and exposed group after the weekend. The workers 
exposed to lower levels (2 [mu]g/m\3\ or lower, TWA) showed no 
significant changes.
    Kuo et al. evaluated nasal septum ulcerations and perforations in 
189 electroplaters in 11 electroplating factories (three factories used 
chromic acid, six factories used nickel-chromium, and two factories 
used zinc) in Taiwan (Ex. 35-10). Of the 189 workers, 26 used Cr(VI), 
129 used nickel-chromium, and 34 used zinc. The

[[Page 59353]]

control group consisted of electroplaters who used nickel and zinc. All 
workers were asked to fill out a questionnaire and were given a nasal 
examination including a lung function test by a certified 
otolaryngologist. The authors determined that 30% of the workers (8/26) 
that used chromic acid developed nasal septum perforations and 
ulcerations and 38% (10/26) developed nasal septum ulcers. Using the 
Mantel Extension Test for Trends, the authors also found that chromium 
electroplaters had an increased likelihood of developing nasal ulcers 
and perforations compared to electroplating workers using nickel-
chromium and zinc. Personal sampling of airborne Cr(VI) results 
indicated the highest levels (32 [mu]g/m\3\ <plus-minus> 35 [mu]g/m\3\, 
ranging from 0.1 [mu]g/m\3\ - 119 [mu]g/m\3\) near the electroplating 
tanks of the Cr(VI) electroplating factories (Ex. 35-11). Much lower 
personal sampling levels were reported in the ``other areas in the 
manufacturing area'' and the ``administrative area'' (TWA 0.16 <plus-
minus> 0.10 [mu]g/m\3\) of the Cr(VI) electroplating plant. The 
duration of sampling was not indicated. The results of the lung 
function tests showed significantly lower values among Cr(VI) 
electroplaters compared to the other two exposure groups in regards to 
vital capacity, forced vital capacity, and forced expiratory volume in 
one second.
    Cohen et al. examined respiratory symptoms of 37 electroplaters 
following inhalation exposure to chromic acid (Ex. 9-18). The mean 
length of employment for the 37 electroplaters was 26.9 months (range 
from 0.3 to 132 months). Fifteen workers employed in other parts of the 
plant were randomly chosen for the control group (mean length of 
employment was 26.1 months; range from 0.1 to 96). All workers were 
asked to fill out a questionnaire on their respiratory history, 
including providing details on their symptoms. An otolaryngologist then 
examined each individual's nasal passages and identified ulcerations 
and perforations. Air samples to measure Cr(VI) were collected for 
electroplaters. The air sampling results of chromic acid as Cr(VI) 
concentrations for electroplaters was a mean of 2.9 [mu]g/m\3\ (range 
from non-detectable to 9.1 [mu]g/m\3\). The authors found that 95% of 
the electroplaters developed pathologic changes in nasal mucosa. 
Thirty-five of the 37 workers, who were employed for more than 1 year 
had nasal tissue damage. None of these workers reported any previous 
job experience involving Cr(VI) exposure. Four workers developed nasal 
perforations, 12 workers developed ulcerations and crusting of the 
septal mucosa, 11 workers developed discoloration of the septal mucosa, 
and eight workers developed shallow erosion of septal mucosa. The 
control group consisted of 15 workers who were not exposed to Cr(VI) at 
the plant. All but one had normal nasal mucosa. The one individual with 
abnormal finding was discovered to have a previous Cr(VI) exposure 
while working in a garment manufacturing operation as a fabric dyer for 
three years. In addition to airborne exposure, the authors observed 
employees frequently wiping their faces and picking their noses with 
contaminated hands and fingers. Many did not wear any protective gear, 
such as gloves, glasses, or coveralls.
    Lucas and Kramkowsi conducted a Health Hazard Evaluation (HHE) on 
11 chrome platers in an industrial electroplating facility (Ex. 3-84). 
The electroplaters worked for about 7.5 years on average. Physicians 
evaluated each worker for chrome hole scars, nasal septum ulceration, 
mucosa infection, nasal redness, perforated nasal septum, and wheezing. 
Seventeen air samples for Cr(VI) exposure were collected in the chrome 
area. Cr(VI) air concentrations ranged from 1 to 20 [mu]g/m\3\, with an 
average of 4 [mu]g/m\3\. In addition to airborne exposure, the authors 
observed workers being exposed to Cr(VI) by direct ``hand to nose'' 
contact, such as touching the nose with contaminated hands. Five 
workers had nasal mucosa that became infected, two workers had nasal 
septum ulcerations, two workers had atrophic scarring (author did not 
provide explanation), possibly indicative of presence of past 
ulcerations, and four workers had nasal septum perforations.
    Gomes evaluated 303 employees from 81 electroplating operations in 
Sao Paulo, Brazil (Ex. 9-31). Results showed that more than two-thirds 
of the workers had nasal septum ulcerations and perforations following 
exposure to chromic acid at levels greater than 100 [mu]g/m\3\, but 
less than 600 [mu]g/m\3\ (precise duration of exposure was not stated). 
These effects were observed within one year of employment.
    Lin et al. examined nasal septum perforations and ulcerations in 79 
electroplating workers from seven different chromium electroplating 
factories in Taipei, Taiwan (Ex.35-13). Results showed six cases of 
nasal septum perforations, four having scar formations, and 38 cases of 
nasal septum ulcerations following inhalation exposure to chromic acid. 
Air sampling near the electroplating tanks had the highest range of 
chromic acid as Cr(VI) (mean of 28 [mu]g/m\3\; range from 0.7 to 168.3 
[mu]g/m\3\). In addition to airborne exposures, the authors also 
observed direct ``hand to nose'' contact where workers placed 
contaminated fingers in their nose. The authors attributed the high 
number of cases to poor industrial hygiene practices in the facilities. 
Five of the seven factories did not have adequate ventilation systems 
in place. Workers did not wear any PPE, including respirators.
    Bloomfield and Blum evaluated nasal tissue damage and nasal septum 
perforations in 23 workers employed at six chromium electroplating 
plants (Ex. 9-13). They found that daily exposure to chromic acid as 
Cr(VI) at levels of 52 [mu]g/m\3\ or higher can lead to nasal tissue 
damage. Three workers developed nasal ulcerations, two workers had 
nasal perforations, nine workers had nose bleeds, and nine workers had 
inflamed mucosa.
    Kleinfeld and Rosso found seven cases out of nine of chrome 
electroplaters having nasal septum ulcerations (Ex. 9-41). Workers were 
exposed to chromic acid as Cr(VI) by inhalation at levels ranging from 
93 [mu]g/m\3\ to 728 [mu]g/m\3\. Duration of exposure varied from two 
weeks to one year. Nasal septum ulcerations were noted as early as one 
month of employment in some workers.
    Royle, using questionnaire responses, reported a significant 
increase in the prevalence of nasal ulcerations among 997 British 
electroplaters exposed to chromic acid with an increasing prevalence 
the longer the worker was exposed to chromic acid (e.g., from 14 cases 
with exposure less than one year to 62 cases with exposure over five 
years) (Ex. 7-50). In all but 2 cases, air samples revealed chromic 
acid was at concentrations of 0.03 mg/m\3\ (i.e., 30 [mu]g/m\3\).
    Gibb et al. reported nasal irritations, nasal septum bleeding, 
nasal septum ulcerations and perforations among a cohort of 2,350 
chrome production workers in a Baltimore plant (Ex. 31-22-12). A 
description of the cohort is provided in detail in the cancer health 
effects section V.B. of this preamble. The authors found that more than 
60% of the cohort had experienced nasal ulcerations and irritations, 
and that the workers developed these effects for the first time within 
the first three months of being hired (median). Gibb et al. found the 
median exposure to Cr(VI) during first diagnosis of irritated and/or 
ulcerated nasal septum was 10 [mu]g/m\3\. About 17% of the cohort had 
reported nasal perforations. Based on historical data, the authors 
believe that the nasal findings are attributed to Cr(VI) exposure.

[[Page 59354]]

    Gibb et al. also used a Proportional Hazard Model to evaluate the 
relationship between Cr(VI) exposure and first occurrence of each of 
the clinical findings. Cr(VI) data was entered into the model as a time 
dependent variable. Other explanatory variables were calendar year of 
hire and age of hire. Results of model indicated that airborne Cr(VI) 
exposure was associated with the occurrence of nasal septum ulceration 
(p = 0.0001). The lack of an association of airborne Cr(VI) exposure to 
nasal perforation and bleeding nasal septum may reflect the fact that 
Cr(VI) concentrations used in the model represent annual averages for 
the job, in which the worker was involved in at the time of the 
findings, rather than a short-term average. Annual averages do not 
factor in day-to-day fluctuations or extreme episodic occurrences. 
Also, the author believes poor housekeeping and hygiene practices may 
have contributed to these health effects as well as Cr(VI) airborne 
concentrations.
    Based on their hazard model, Gibb et al. estimated the relative 
risks for nasal septum ulcerations would increase 1.2 for each 52 [mu]g 
of Cr(VI)/m\3\ increase in Cr(VI) air levels. They saw a reduction in 
the incidence of nasal findings in the later years. They found that 
workers from the earlier years who did not wear any PPE had a greater 
risk of developing respiratory problems. They believe that the 
reduction in ulcerations was possibly due to an increased use of 
respirators and protective clothing and improved industrial hygiene 
practices at the facility.
    The U.S. Public Health Service conducted a study of 897 chrome 
production workers in seven chromate-producing plants in the early 
1950s (Ex. 7-3). The findings of this study were used in part as 
justification for the current OSHA PEL. Workers were exposed by 
inhalation to various water soluble chromates and bichromate compounds. 
The total mean exposure to the workers was a TWA of 68 [mu]g/m\3\. Of 
the 897 workers, 57% (or 509 workers) were found to have nasal septum 
perforations. Nasal septum perforations were observed even in workers 
during their first year on the job.
    Case reports provide further evidence that airborne exposure to 
direct ``hand to nose'' contact of Cr(VI) compounds lead to the 
development of nasal irritation and nasal septum perforations.
    For example, a 70-year-old man developed nasal irritation, 
incrustation, and perforation after continuous daily exposure by 
inhalation to chromium trioxide (doses were not specified, but most 
likely quite high given the nature of his duties). This individual 
inhaled chromium trioxide daily by placing his face directly over an 
electroplating vessel. He worked in this capacity from 1934 to 1982. 
His symptoms continued to worsen after he stopped working. By 1991, he 
developed large perforations of the nasal septum and stenosis (or 
constriction) of both nostrils by incrustation (Ex. 35-8).
    Similarly, a 30-year-old female jigger (a worker who prepares the 
items prior to electroplating by attaching the items to be plated onto 
jigs or frames) developed nasal perforation in her septum following 
continuous exposure (doses in this case were not provided) to chromic 
acid mists. She worked adjacent to the automated Cr(VI) electroplating 
shop. She was also exposed to chromic acid from direct contact when she 
placed her contaminated fingers in her nose. Her hands became 
contaminated by handling wet components in the jigging and de-jigging 
processes (Ex. 35-24).
    Evidence of nasal septum perforations has also been demonstrated in 
experimental animals. Adachi exposed 23 C57BL mice to chromic acid by 
inhalation at concentrations of 1.81 mg Cr(VI)/m\3\ for 120 minutes per 
day, twice a week and 3.63 mg Cr(VI)/m\3\ for 30 minutes per day, two 
days per week for up to 12 months (Ex. 35-26). Three of the 23 mice 
developed nasal septum perforations in the 12-month exposure group.
    Adachi et al. also exposed 50 ICR female mice to chromic acid by 
inhalation at concentrations of 3.18 mg Cr(VI)/m\3\ for 30 minutes per 
day, 2 days per week for 18 months (Ex. 35-26-1). The authors used a 
miniaturized chromium electroplating system to mimic electroplating 
processes and exposures similar to working experience. Nasal septum 
perforations were found in six mice that were sacrificed after 10 
months of exposure. Of those mice that were sacrificed after 18 months 
of exposure, nasal septum perforations were found in three mice.
2. Occupational Asthma
    Occupational asthma is considered ``a disease characterized by 
variable airflow limitation and/or airway hyper responsiveness due to 
causes and conditions attributable to a particular occupational 
environment and not to stimuli encountered outside the workplace'' (Ex. 
35-15). Asthma is a serious illness that can damage the lungs and in 
some cases be life threatening. The common symptoms associated with 
asthma include heavy coughing while exercising or when resting after 
exercising, shortness of breath, wheezing sound, and tightness of 
chest. Many workers develop an asthmatic attack. An attack may be 
triggered by particles in the air (Ex. 35-3; Ex. 35-6). It is not clear 
what occupational exposure levels of Cr(VI) compounds would lead to the 
development of occupational asthma.
    The strongest evidence of occupational asthma has been demonstrated 
in four case reports. OSHA chose to focus on these four case reports 
because the data from other occupational studies do not exclusively 
implicate Cr(VI), even though the studies generally show an increased 
prevalence of workers having difficulty breathing and other asthmatic-
related symptoms following inhalation of multiple chemicals. The four 
case reports have the following in common: (1) The worker has a history 
of occupational exposure exclusively to Cr(VI); (2) a physician has 
confirmed a diagnosis that the worker has symptoms consistent with 
occupational asthma; and (3) the worker exhibits functional signs of 
air restriction (e.g., low forced expiratory volume in one second or 
low peak expiratory flow rate) upon bronchial challenge with Cr(VI) 
compounds. These case reports demonstrate, through challenge tests, 
that exposure to Cr(VI) compounds can cause asthmatic responses. The 
other general case reports below did not use challenge tests to confirm 
that Cr(VI) was responsible for the asthma; however, these reports were 
among workers similarly exposed to Cr(VI) such that Cr(VI) is likely to 
have been a contributing factor in the development of their asthmatic 
symptoms.
    DaReave reported the case of a 48-year-old cement floorer who 
developed asthma from inhaling airborne Cr(VI) (Ex. 35-7). This worker 
had been exposed to Cr(VI) as a result of performing cement flooring 
activities for more than 20 years. The worker complained of dyspnea, 
shortness of breath, and wheezing after work, especially after working 
in enclosed spaces. The Cr(VI) content in cement was about 12 ppm. A 
bronchial challenge test with potassium dichromate produced a 50% 
decrease in forced expiratory volume in one second. The occupational 
physician concluded that the worker's asthmatic condition triggered by 
exposure to Cr(VI) caused the worker to develop bronchial constriction.
    LeRoyer reported a case of a 28-year-old roofer who developed 
asthma from breathing dust while sawing material made of corrugated 
fiber cement containing Cr(VI) for nine years (Ex. 35-12). This worker 
demonstrated

[[Page 59355]]

symptoms such as wheezing, shortness of breath, coughing, rhinitis, and 
headaches while working. Skin prick tests were all negative. Several 
inhalation challenges were performed by physicians and immediate 
asthmatic reactions were observed after inhaling nebulization of 
potassium dichromate. A reduction (by 20%) in the forced expiratory 
volume in one second after exposure to fiber cement dust was noted.
    Novey et al. reported a case of a 32-year-old electroplating worker 
who developed asthma from working with chromium sulfate and nickel 
salts (Ex. 35-16). He began experiencing coughs, wheezing, and dyspnea 
within the first week of exposure. Inhalation challenge tests given by 
physicians using chromium sulfate and nickel salts, in separate 
challenges, both resulted in positive reactions. The worker immediately 
had difficulty breathing and started wheezing in both challenges. The 
forced expiratory volume in 1 second decreased by 22% and the forced 
expiratory volume in 1 second/forced vital capacity ratio also 
decreased from 74.5% to 60.4%. The author believes the worker's 
bronchial asthma was induced from inhaling chromium sulfate and nickel 
salts, individually. Similar findings were reported in a different 
individual by Sastre (Ex. 35-20).
    Shirakawa and Morimoto reported a case of a 50-year-old worker who 
developed asthma while working at a metal-electroplating plant (Ex. 35-
21). Bronchial challenge by physicians produced positive results when 
using potassium bichromate, followed by a rapid recovery within 5 
minutes, when given no exposures. The worker's forced expiratory volume 
in 1 second dropped by 37% after inhalation of potassium bichromate. 
The individual immediately began wheezing, coughing with dyspnea, and 
recovered without treatment within five minutes. The author believes 
that the worker developed his asthma from inhaling potassium 
bichromate.
    In addition to the case reports confirming that Cr(VI) is 
responsible for the development of asthma using inhalation challenge 
tests, the following are several other case reports of Cr(VI) exposed 
workers having symptoms consistent with asthma where the symptoms were 
never confirmed by using inhalation challenge tests.
    Lockman reported a case of a 41-year old woman, who was 
occupationally exposed to potassium dichromate during leather tanning 
(Ex. 35-14). The worker developed an occupational allergy to potassium 
dichromate. This allergy involved both contact dermatitis and asthma. 
The physicians considered other challenge tests using potassium 
dichromate as the test agent (i.e., peak expiratory flow rate, forced 
expiratory volume in 1 second and methacholine or bronchodilator 
challenge), but the subject changed jobs before the physicians could 
administer these tests. Once the subject changed jobs, all her symptoms 
disappeared. It was not confirmed whether the occupational exposure to 
Cr(VI) was the cause of the asthma.
    Williams reported a 23-year old textile worker who was 
occupationally exposed to chromic acid. He worked near two tanks of 
chromic acid solutions (Ex. 35-23). He inhaled fumes while frequently 
walking through the room with the tanks. He developed both contact 
dermatitis and asthma. He believes the tank was poorly ventilated and 
was the source of the fumes. He stopped working at the textile firm on 
the advice of his physician. After leaving, his symptoms improved 
greatly. No inhalation bronchial challenge testing was conducted to 
confirm that chromic acid was causing his asthmatic attacks. However, 
as noted above, chromic acid exposure has been shown to lead to 
occupational asthma, and thus, chromic acid was likely to be a 
causative agent in the development of asthma.
    Park et al. reported a case of four workers who worked in various 
occupations involving exposure to either chromium sulfate or potassium 
dichromate (Ex. 35-18). Two worked in a metal electroplating factory, 
one worked at a cement manufacturer, and the other worked in 
construction. All four developed asthma. One individual had a positive 
response to bronchial provocation test (with chromium sulfate as the 
test agent). This individual developed an immediate reaction upon given 
chromium sulfate as the test agent. He experienced wheezing, coughing 
and dyspnea. Peak expiratory flow rate decreased by about 20%. His 
physician determined that exposure to chromium sulfate was contributing 
to his asthma condition. Two had positive reactions to prick skin tests 
with chromium sulfate as the test agent. Two had positive responses to 
patch tests using potassium dichromate as the testing challenge agent. 
Only one out of four underwent inhalation bronchial challenge testing 
(with a positive result to chromium sulfate) in this report.
3. Bronchitis
    In addition to nasal ulcerations, nasal septum perforations, and 
asthma, there is also limited evidence from reports in the literature 
of bronchitis associated with Cr(VI) exposure. It is not clear what 
occupational exposure levels of Cr(VI) compounds would lead to the 
development of bronchitis.
    Royle found that 28% (104/288) of British electroplaters developed 
bronchitis upon inhalation exposure to chromic acid, as compared to 23% 
(90/299) controls (Ex. 7-50). The workers were considered to have 
bronchitis if they had symptoms of persistent coughing and phlegm 
production. In all but two cases of bronchitis, air samples revealed 
chromic acid at levels of 0.03 mg/m<SUP>3</SUP>. Workers were asked to 
fill out questionnaires to assess respiratory problems. Self-reporting 
poses a problem in that the symptoms and respiratory health problems 
identified were not medically confirmed by physicians. Workers in this 
study believe they were developing bronchitis, but it is not clear from 
this study whether the development of bronchitis was confirmed by 
physicians. It is also difficult to assess the bronchitis health 
effects of chromic acid from this study because the study results for 
the exposed (28%) and control groups (23%) were similar.
    Alderson et al. reported 39 deaths of chromate production workers 
related to chronic bronchitis from three chromate producing factories 
(Bolton, Eaglescliffe, and Rutherglen) from 1947 to 1977 (Ex. 35-2). 
The specific Cr(VI) compound, extent, and frequency that the workers 
were exposed to were not specified. However, workers at all three 
factories were exposed to sodium chromate, chromic acid, and calcium 
chromate at one time or another. The authors did not find an excess 
number of number of bronchitis related deaths at the Bolton and 
Eaglescliffe factories. At Rutherglen, there was an excess number of 
deaths (31) from chronic bronchitis with a ratio of observed/expected 
of 1.8 (p<0.001). It is difficult to assess the respiratory health 
effects of Cr(VI) compounds from this study because there are no 
exposure data, there are no data on smoking habits, nor is it clear on 
the extent, duration, and amount of specific Cr(VI) compound the 
workers were exposed to during the study.
    While the evidence for bronchitis is limited, evidence from 
experimental animals demonstrate that Cr(VI) compounds can cause lung 
irritation, inflammation in the lungs, and possibly lung fibrosis at 
various exposure levels. Glaser et al. examined the effects of 
inhalation exposure of chromium (VI) on lung inflammation and alveolar 
macrophage function in rats (Ex. 31-18-9). Twenty, 5-week old male TNO-
W-74 Wistar rats were exposed via

[[Page 59356]]

inhalation to 25-200 [mu]g Cr(VI)/m<SUP>3</SUP> as sodium dichromate 
for 28 days or 90 days for 22 hours per day, 7 days per week in 
inhalation chambers. Twenty, 5-week old male TNO-W-74 Wistar rats also 
served as controls. All rats were killed at the end of the inhalation 
exposure period. The authors found increased lung weight in the 50-200 
[mu]g/m<SUP>3</SUP> groups after the 90-day exposure period. They also 
found that 28-day exposure to levels of 25 and 50 [mu]g/m<SUP>3</SUP> 
resulted in ``activated'' alveolar macrophages with stimulated 
phagocytic activities. A more pronounced effect on the activation of 
alveolar macrophages was seen during the 90-day exposure period of 25 
and 50 [mu]g/m<SUP>3</SUP>.
    Glaser et al. exposed 150 male, 8-week old Wistar rats (10 rats per 
group) continuously by inhalation to aerosols of sodium dichromate at 
concentrations of 50, 100, 200, and 400 [mu]g Cr(VI)/m<SUP>3</SUP> for 
22 hours per day, 7 days a week, for continuous exposure for 30 days or 
90 days in inhalation chambers (Ex. 31-18-11). Increased lung weight 
changes were noticeable even at levels as low as 50 and 100 [mu]g 
Cr(VI)/m<SUP>3</SUP> following both 30 day and 90 day exposures. 
Significant accumulation of alveolar macrophages in the lungs was noted 
in all of the exposure groups. Lung fibrosis occurred in eight rats 
exposed to 100 [mu]g Cr(VI)/m<SUP>3</SUP> or above for 30 days. Most 
lung fibrosis disappeared after the exposure period had ceased. At 50 
[mu]g Cr(VI)/m<SUP>3</SUP> or higher for 30 days, a high incidence of 
hyperplasia was noted, possibly in response to Cr(VI)--induced damage 
to the lung and respiratory tract. The total protein in bronchoalveolar 
lavage (BAL) fluid, albumin in BAL fluid, and lactate dehydrogenase in 
BAL fluid were significant at elevated levels of 200 and 400 [mu]g 
Cr(VI)/m<SUP>3</SUP> in both the 30 day and 90 day exposure groups (as 
compared to the control group). These responses are indicative of 
severe injury in the lungs of animals exposed to these Cr(VI) dose 
levels. At levels of 50 and 100 [mu]g Cr(VI)/m<SUP>3</SUP>, the 
responses are indicative of inflammatory changes in the lungs. The 
authors concluded that these results suggest that the severe 
inflammatory reaction may lead to more chronic and obstructive lesions 
in the lung, and that inflammation is essential for the induction of 
most effects observed following inhalation exposure.
4. Summary
    Overall, there is convincing evidence to indicate that Cr(VI) 
exposed workers can develop nasal irritation, nasal ulcerations, nasal 
perforations, and asthma. There is also some limited evidence that 
bronchitis may occur when exposed to Cr(VI) compounds at high levels. 
Most of the studies involved exposure to water-soluble Cr(VI) 
compounds. It is very clear that workers may develop nasal irritations, 
nasal ulcerations, and nasal perforations at levels below the current 
PEL of 52 [mu]g/m<SUP>3</SUP>. However, it is not clear what 
occupational exposure levels lead to disorders like asthma and 
bronchitis.
    There are numerous studies in the literature showing nasal 
irritations, nasal perforations, and nasal ulcerations resulting from 
Cr(VI) inhalation exposure. It also appears that direct hand-to-nose 
contact (i.e., by touching inner nasal surfaces with contaminated 
fingers) can contribute to the incidence of nasal damage. Additionally, 
some studies show that workers developed these nasal health problems 
because they did not wear any PPE, including respiratory protection. 
Inadequate area ventilation and sanitation conditions (lack of 
cleaning, dusty environment) probably contributed to the adverse nasal 
effects.
    There are numerous well documented case reports in the literature 
describing occupational asthma specifically triggered by Cr(VI) in 
sensitized workers. However, OSHA is not aware of any data from the 
literature to determine a Cr(VI) dose in the work place that leads to 
the asthmatic condition or to determine how many people may be affected 
by such Cr(VI) exposure.
    The evidence that workers breathing Cr(VI) can develop respiratory 
disease that involve inflammation, such as asthma and bronchitis is 
supported by experimental animal studies. The 1985 and 1990 Glaser et 
al. studies show that animals experience irritation and inflammation of 
the lungs following repeated exposure by inhalation to water-soluble 
Cr(VI) at air concentrations near the current PEL.

D. Dermal Effects

    Occupational exposure to Cr(VI) is a well-established cause of 
adverse health effects of the skin. The effects are the result of two 
distinct processes: (1) Irritant reactions, such as skin ulcers and 
irritant contact dermatitis, and (2) delayed hypersensitivity 
(allergic) reactions. Some evidence also indicates that exposure to 
Cr(VI) compounds may cause conjunctivitis.
    The mildest skin reactions consist of erythema (redness), edema 
(swelling), papules (raised spots), vesicles (liquid spots), and 
scaling (Ex. 35-313, p. 295). The lesions are typically found on 
exposed areas of the skin, usually the hands and forearms (Exs. 9-9; 9-
25). These features are common to both irritant and allergic contact 
dermatitis, and it is generally not possible to determine the etiology 
of the condition based on histopathologic findings (Ex. 35-314). 
Allergic contact dermatitis can be diagnosed by other methods, such as 
patch testing (Ex. 35-321, p. 226). Patch testing involves the 
application of a suspected allergen to the skin, diluted in petrolatum 
or some other vehicle. The patch is removed after 48 hours and the skin 
examined at the site of application to determine if a reaction has 
occurred.
    Cr(VI) compounds can also have a corrosive, necrotizing effect on 
living tissue, forming ulcers, or ``chrome holes'' (Ex. 35-315). This 
effect is apparently due to the oxidizing properties of Cr(VI) 
compounds (Ex. 35-318, p. 623). Like dermatitis, chrome ulcers 
generally occur on exposed areas of the body, chiefly on the hands and 
forearms (Ex. 35-316). The lesions are initially painless, and are 
often ignored until the surface ulcerates with a crust which, if 
removed, leaves a crater two to five millimeters in diameter with a 
thickened, hardened border. The ulcers can penetrate deeply into tissue 
and become painful. Chrome ulcers may penetrate joints and cartilage 
(Ex. 35-317, p. 138). The lesions usually heal in several weeks if 
exposure to Cr(VI) ceases, leaving a flat, atrophic scar (Ex. 35-318, 
p.623). If exposure continues, chrome ulcers may persist for months 
(Ex. 7-3).
    It is generally believed that chrome ulcers do not occur on intact 
skin (Exs. 35-317, p. 138; 35-315; 35-25). Rather, they develop readily 
at the site of small cuts, abrasions, insect bites, or other injuries 
(Exs. 35-315; 35-318, p. 138). In experimental work on guinea pigs, 
Samitz and Epstein found that lesions were never produced on undamaged 
skin (Ex. 35-315). The degree of trauma, as well as the frequency and 
concentration of Cr(VI) application, was found to influence the 
severity of chrome ulcers.
    The development of chrome ulcers does not appear to be related to 
the sensitizing properties of Cr(VI). Edmundson provided patch tests to 
determine sensitivity to Cr(VI) in 56 workers who exhibited either 
chrome ulcers or scars (Ex. 9-23). A positive response to the patch 
test was found in only two of the workers examined.
    Parkhurst first identified Cr(VI) as a cause of allergic contact 
dermatitis in 1925 (Ex. 9-55). Cr(VI) has since been confirmed as a 
potent allergen. Kligman (1966) used a maximization test (a skin test 
for screening possible contact allergens) to assess the skin 
sensitizing potential of Cr(VI) compounds (Ex. 35-

[[Page 59357]]

327). Each of the 23 subjects was sensitized to potassium dichromate. 
On a scale of one to five, with five being the most potent allergen, 
Cr(VI) was graded as five (i.e., an extreme sensitizer). This finding 
was supported by a guinea pig maximization test, which assigned a grade 
of four to potassium chromate using the same scale (Ex. 35-328).
1. Prevalence of Dermal Effects
    Adverse skin effects from Cr(VI) exposure have been known since at 
least 1827, when Cumin described ulcers in two dyers and a chromate 
production worker (Ex. 35-317, p. 138). Since then, skin conditions 
resulting from Cr(VI) exposure have been noted in a wide range of 
occupations. Work with cement is regarded as the most common cause of 
Cr(VI)-induced dermatitis (Exs. 35-313, p. 295; 35-319; 35-320). Other 
types of work where Cr(VI)-related skin effects have been reported 
include chromate production, chrome plating, leather tanning, welding, 
motor vehicle assembly, manufacture of televisions and appliances, 
servicing of railroad locomotives, aircraft production, and printing 
(Exs. 31-22-12; 7-50; 9-31; 9-100; 9-63; 9-28; 9-95; 9-54; 35-329; 9-
97; 9-78; 9-9; 35-330). Some of the important studies on Cr(VI)-related 
dermal effects in workers are described below.
    a. Cement Dermatitis. Many workers develop cement dermatitis, 
including masons, tile setters, and cement workers (Ex. 35-318, p. 
624). Cement, the basic ingredient of concrete, may contain several 
possible sources of chromium (Exs. 35-317, p.148; 9-17). Clay, gypsum, 
and chalk that serve as ingredients may contain traces of chromium. 
Ingredients may be crushed using chrome steel grinders that, with wear, 
contribute to the chromium content of the concrete. Refractory bricks 
in the kiln and ash residues from the burning of coal or oil to heat 
the kiln serve as additional sources. Trivalent chromium from these 
sources can be converted to Cr(VI) in the kiln (Ex. 35-317. p. 148).
    Cement dermatitis can be caused by direct irritation of the skin, 
by sensitization to Cr(VI), or both (Ex. 35-317, p. 147). However, 
sensitization is considered to be of greater importance than irritation 
in causing cement dermatitis (Ex. 35-317, p. 147). Burrows (1983) 
combined the results of 16 separate studies to report that, on average, 
over 80% of cement dermatitis cases were found to be sensitized to 
Cr(VI) (Ex. 35-317, p. 148). Cement is alkaline, abrasive, and 
hydroscopic (water-absorbing), and it is likely that the irritant 
effect resulting from these properties interferes with the skin's 
defenses, permitting penetration and sensitization to take place more 
readily (Ex. 35-318, p. 624). Dry cement is considered relatively 
innocuous because it is not as alkaline as wet cement (Exs. 35-317, p. 
147; 9-17). When water is mixed with cement the water liberates calcium 
hydroxide, causing a rise in pH (Ex. 35-317, p. 147).
    Flyvholm et al. (1996) noted a correlation between the Cr(VI) 
concentration in the local cement and the frequency of allergic contact 
dermatitis (Ex. 35-326, p. 278). Because the Cr(VI) content depends 
partially upon the chromium concentration in raw materials, there is a 
great variability in the Cr(VI) content in cement from different 
geographical regions. In locations with low Cr(VI) content, the 
prevalence of Cr(VI)-induced allergic contact dermatitis was reported 
to be approximately one percent, while in regions with higher chromate 
concentrations the prevalence was reported to rise to between 9 to 11% 
of those exposed (Ex. 35-326, p. 278).
    The relationship between Cr(VI) content in cement and the 
prevalence of Cr(VI)-induced allergic contact dermatitis is supported 
by the findings of Avnstorp (1989) in a study of Danish workers who had 
daily contact with wet cement during the manufacture of pre-fabricated 
concrete products (Ex. 9-131). Beginning in September of 1981, low 
concentrations of ferrous sulfate were added to all cement sold in 
Denmark to reduce Cr(VI) to trivalent chromium. Two hundred and twenty 
seven workers were examined in 1987 for Cr(VI)-related skin effects. 
The findings from these examinations were compared to the results from 
190 workers in the same plants who were examined in 1981. The 
prevalence of hand eczema had declined from 11.7% to 4.4%, and the 
prevalence of Cr(VI) sensitization had declined from 10.5% to 2.6%. 
Both of these results were statistically significant. There was no 
significant change in the frequency of skin irritation.
    b. Dermatitis Associated With Cr(VI) From Sources Other Than 
Cement. In 1953 the U.S. Public Health Service reported on hazards 
associated with the chromium-producing industry in the United States 
(Ex. 7-3). Workers were examined for skin effects from Cr(VI) exposure. 
Workers' eyes were also examined for possible effects from splashes of 
Cr(VI)-containing compounds that had been observed in the plants. Of 
the 897 workers examined, 451 had skin ulcers or scars of ulcers. 
Seventeen workers were reported to have skin lesions suggestive of 
chrome dermatitis. The authors noted that most plants provided adequate 
washing facilities, and had facilities for providing clean work 
clothes. A statistically significant increase in congestion of the 
conjunctiva was also reported in Cr(VI)-exposed workers when compared 
with non-exposed workers (38.7% vs. 25.8%).
    In the Baltimore, Maryland chromate production plant examined by 
Gibb et al. (2000), a substantial number of workers were reported to 
have experienced adverse skin effects (Ex. 31-22-12). The authors 
identified a cohort of 2,357 workers first employed at the plant 
between 1950 and 1974. Clinic and first aid records were examined to 
identify findings of skin conditions. These clinical findings were 
identified by a physician as a result of routine examinations or visits 
to the medical clinic by members of the cohort. Percentages of the 
cohort with various clinical findings were as follows:

Irritated skin: 15.1%
Dermatitis: 18.5%
Ulcerated skin: 31.6%
Conjunctivitis: 20.0%

    A number of factors make these results difficult to interpret. The 
reported findings are not specifically related to Cr(VI) exposure. They 
may have been the result of other workplace exposures, or non-workplace 
factors. The report also indicates the percentage of workers who were 
diagnosed with a condition during their tenure at the plant; however, 
no information is presented to indicate the expected incidence of these 
conditions in a population that is not exposed to Cr(VI).
    Measurements of Cr(VI) air concentrations by job title were used to 
estimate worker exposures. Based on these estimates, the authors used a 
proportional hazards model to find a statistically significant 
correlation (p=0.004) between ulcerated skin and airborne Cr(VI) 
exposure. Statistically significant correlations between year of hire 
and findings of ulcerated skin and dermatitis were also reported. 
Exposures to Cr(VI) in the plant had generally dropped over time. 
Median exposure to Cr(VI) at the time of occurrence for most of the 
findings was said to be about 10 [mu]g/m\3\ Cr(VI) (reported as 20 
[mu]g/m\3\ CrO\3\). It is unclear, however, what contribution airborne 
Cr(VI) exposures may have had to dermal effects. Direct dermal contact 
with Cr(VI) compounds in the plant may have been a contributing factor 
in the development of these conditions.
    Mean and median times on the job prior to initial diagnosis were 
also

[[Page 59358]]

reported. The mean time prior to diagnosis of skin or eye effects 
ranged from 373 days for ulcerated skin to 719 days for irritated skin. 
Median times ranged from 110 days for ulcerated skin to 221 days for 
conjunctivitis. These times are notable because many workers in the 
plant stayed for only a short time. Over 40% worked for less than 90 
days. Because these short-term workers did not remain in the workplace 
for the length of time that was typically necessary for these effects 
to occur, the results of this study may underestimate the incidence 
that would occur with a more stable worker population.
    Lee and Goh (1988) examined the skin condition of 37 workers who 
maintained chrome plating baths and compared these workers with a group 
of 37 control subjects who worked in the same factories but were not 
exposed to Cr(VI) (Ex. 35-316). Mean duration of employment as a chrome 
plater was 8.1 (SD<plus-minus>7.9) years. Fourteen (38%) of the chrome 
platers had some occupational skin condition; seven had chrome ulcers, 
six had contact dermatitis and one had both. A further 16 (43%) of the 
platers had scars suggestive of previous chrome ulcers. Among the 
control group, no members had ulcers or scars of ulcers, and three had 
dermatitis.
    Where ulcers or dermatitis were noted, patch tests were 
administered to determine sensitization to Cr(VI) and nickel. Of the 
seven workers with chrome ulcers, one was allergic to Cr(VI). Of the 
six workers with dermatitis, two were allergic to Cr(VI) and one to 
nickel. The worker with ulceration and dermatitis was not sensitized to 
either Cr(VI) or nickel. Although limited by a relatively small study 
population, this report clearly indicates that Cr(VI)-exposed workers 
face an increased risk of adverse skin effects. The fact that the 
majority of workers with dermatitis were not sensitized to Cr(VI) 
indicates that irritant factors play an important role in the 
development of dermatitis in chrome plating operations.
    Royle (1975) also investigated the occurrence of skin conditions 
among workers involved in chrome plating (Ex. 7-50). A questionnaire 
survey completed by 997 chrome platers revealed that 21.8% had 
experienced skin ulcers, and 24.6% had suffered from dermatitis. No 
information was presented to indicate the expected incidence in a 
comparable population that was not exposed to Cr(VI). Of the 54 plants 
involved in the study, 49 used nickel, another recognized cause of 
allergic contact dermatitis.
    The author examined the relationship between the incidence of these 
conditions and length of exposure. The plater population was divided 
into three groups: those with less than one year of Cr(VI) exposure, 
those with one to five years of Cr(VI) exposure, and those with over 
five years of Cr(VI) exposure. A statistically significant trend was 
found between length of Cr(VI) exposure and incidence of skin ulcers. 
The incidence of dermatitis, on the other hand, bore no relationship to 
length of exposure.
    In 1973, researchers from NIOSH reported on the results of a health 
hazard investigation of a chrome plating establishment (Ex. 3-5). In 
the plating area, airborne Cr(VI) concentrations ranged from less than 
0.71 up to 9.12 [mu]g/m\3\ (mean 3.24 [mu]g/m\3\; SD=2.48 [mu]g/m\3\). 
Of the 37 exposed workers who received medical examinations, five were 
reported to have chrome-induced lesions on their hands. Hygiene and 
housekeeping practices in this facility were reportedly deficient, with 
the majority of workers not wearing gloves, not washing their hands 
before eating or leaving the plant, and consuming food and beverages in 
work areas.
    Gomes (1972) examined Cr(VI)-induced skin lesions among 
electroplaters in Sao Paulo, Brazil (Ex. 9-31). A clinical examination 
of 303 workers revealed 88 (28.8%) had skin lesions, while 175 (58.0%) 
had skin and mucus membrane lesions. A substantial number of employers 
(26.6%) also did not provide personal protective equipment to workers. 
The author attributed the high incidence of skin ulcers on the hands 
and arms to inadequate personal protective equipment, and lack of 
training for employees regarding hygiene practices.
    Fleeger and Deng (1990) reported on an outbreak of skin ulcerations 
among workers in a facility where enamel paints containing chromium 
were applied to kitchen range parts (Ex. 9-97). A ground coat of paint 
was applied to the parts, which were then placed on hooks and 
transported through a curing oven. In some cases, small parts were 
places on hooks before paint application. Tiny holes in the oven coils 
apparently resulted in improper curing of the paint, leaving sharp 
edges and a Cr(VI)-containing residue on the hooks. Most of the workers 
who handled the hooks reportedly did not wear gloves, because the 
gloves were said to reduce dexterity and decrease productivity. As a 
result, cuts from the sharp edges allowed the Cr(VI) to penetrate the 
skin, leading to ulcerations (Ex. 9-97).
2. Prognosis of Dermal Effects
    Cr(VI)-related dermatitis tends to become more severe and 
persistent with continuing exposure. Once established, the condition 
may persist even if occupational exposure ceases. Fregert followed up 
on cases of occupational contact dermatitis diagnosed over a 10-year 
period by a dermatology service in Sweden. Based on responses to 
questionnaires completed two to three years after treatment, only 7% of 
women and 10% of men with Cr(VI)-related allergic contact dermatitis 
were reported to be healed (Ex. 35-322). Burrows reviewed the condition 
of patients diagnosed with work-related dermatitis 10-13 years earlier. 
Only two of the 25 cases (8%) caused by exposure to cement had cleared 
(Ex. 35-323).
    Hogan et al. reviewed the literature regarding the prognosis of 
contact dermatitis, and reported that the majority of patients had 
persistent dermatitis (Ex. 35-324). Job changes reportedly did not 
usually lead to a significant improvement for most patients. The 
authors surveyed contact dermatitis experts around the world to explore 
their experience with the prognosis of patients suffering from 
occupational contact dermatitis of the hands. Seventy-eight percent of 
the 51 experts who responded to the survey indicated that chromate was 
one of the allergens associated with the worst possible prognosis.
    Halbert et al. reviewed the experience of 120 patients diagnosed 
with occupational chromate dermatitis over a 10-year period (Ex. 35-
320). The time between initial diagnosis and the review ranged from a 
minimum of six months to a maximum of nine years. Eighty-four (70%) of 
patients were reviewed two or more years after initial diagnosis, and 
40 (33%) after five years or more. In the majority of cases (78, or 
65%), the dermatitis was attributed to work with cement. For the study 
population as a whole, 76% had ongoing dermatitis at the time of the 
review.
    When the review was conducted, 62 (58%) patients were employed in 
the same occupation as when initially diagnosed. Fifty-five (89%) of 
these workers continued to suffer from dermatitis. Fifty-eight patients 
(48%) changed occupations after their initial diagnosis. Each of these 
individuals indicated that they had changed occupations because of 
their dermatitis. In spite of the change, dermatitis persisted in 40 
members of this group (69%).
    Lips et al. found a somewhat more favorable outcome among 88 
construction workers with occupational chromate dermatitis who were 
removed from Cr(VI) exposure (Ex. 35-325). Follow-up one to five years 
after removal indicated that 72% of the patients no longer had 
dermatitis. The

[[Page 59359]]

authors speculated that this result might be due to strict avoidance of 
Cr(VI) contact. Nonetheless, the condition persisted in a substantial 
portion of the affected population.
3. Thresholds for Dermal Effects
    In a response to OSHA's RFI submitted on behalf of the Chrome 
Coalition, Exponent indicated that the findings of Fowler et al. (1999) 
and others provide evidence of a threshold for elicitation of allergic 
contact dermatitis (Ex. 31-18-1, p. 27). Exponent also stated that 
because chrome ulcers did not develop in the Fowler et al. study, 
``more aggressive'' exposures appear to be necessary for the 
development of chrome ulcers.
    The Fowler et al. study involved the dermal exposure of 26 
individuals previously sensitized to Cr(VI) who were exposed to water 
containing 25 to 29 mg/L Cr(VI) as potassium dichromate (pH 9.4) (Ex. 
31-18-5). Subjects immersed one arm in the Cr(VI) solution, while the 
other arm was immersed in an alkaline buffer solution as a control. 
Exposure lasted for 30 minutes and was repeated on three consecutive 
days. Based on examination of the skin, the authors concluded that the 
skin response experienced by subjects was not consistent with either 
irritant or allergic contact dermatitis.
    The exposure scenario in the Fowler et al. study, however, does not 
mimic the occupational experience. While active dermatitis, scratches, 
and skin lesions served as criteria for excluding both initial and 
continuing participation in the study, it is reasonable to expect that 
individuals with these conditions will often continue to work. Cr(VI)-
containing mixtures and compounds used in the workplace may also pose a 
greater challenge to the integrity of the skin than the solution used 
by Fowler et al. Wet cement, for example, may have a pH higher than 
9.4, and may be capable of abrading or otherwise damaging the skin. As 
damaged skin is liable to make exposed workers more susceptible to 
Cr(VI)-induced skin effects, the suggested threshold is likely to be 
invalid. The absence of chrome ulcers in the Fowler et al. study is not 
unexpected, because subjects with ``fissures or lesions'' on the skin 
were excluded from the study (Ex. 31-18-5). As discussed earlier, 
chrome ulcers are not believed to occur on intact skin.
4. Preliminary Conclusions
    OSHA believes that adverse dermal effects from exposure to Cr(VI), 
including irritant contact dermatitis, allergic contact dermatitis, and 
skin ulceration, have been firmly established. The available evidence 
is not sufficient to relate these effects to any given Cr(VI) air 
concentration. Rather, it appears that direct dermal contact with 
Cr(VI) is the most relevant factor in the development of dermatitis and 
ulcers. Based on the findings of Gibb et al. (Ex. 32-22-12) and U.S. 
Public Health Service (Ex. 7-3), OSHA also considers it likely that 
conjunctivitis can result from eye contact with Cr(VI).
    OSHA does not believe that the available evidence is sufficient to 
establish a threshold concentration of Cr(VI) below which dermal 
effects will not occur in the occupational environment. This 
preliminary finding is supported not only by the belief that the 
exposure scenario of Fowler et al. is not consistent with occupational 
exposures, but by experience in the workplace as well. As summarized by 
Flyvholm et al. (1996), numerous reports have indicated that allergic 
contact dermatitis occurs in cement workers exposed to Cr(VI) 
concentrations below the threshold suggested by Fowler et al. (1999). 
OSHA considers the evidence of Cr(VI)-induced allergic contact 
dermatitis in these workers to indicate that the threshold for 
elicitation of response suggested by Fowler et al. (1999) is not 
applicable to the occupational environment.

E. Other Health Effects

    OSHA has examined the possibility of health effect outcomes 
associated with Cr(VI) exposure in addition to such effects as lung 
cancer, nasal ulcerations and perforations, occupational asthma, and 
irritant and allergic contact dermatitis. Unlike the Cr(VI)-induced 
toxicities cited above, the data on other health effects do not 
definitively establish Cr(VI)-related impairments of health from 
occupational exposure at or below the current OSHA PEL.
    There is some positive evidence that workplace inhalation to Cr(VI) 
results in gastritis and gastrointestinal ulcers, especially at high 
exposures (generally over OSHA's current PEL) (Ex. 7-12). This is 
supported by ulcerations in the gastrointestinal tract of mice 
breathing high Cr(VI) concentration for long periods (Ex. 10-8). Other 
studies reported positive effects but significant information was not 
reported or the confounders made it difficult to draw positive 
conclusions (Ex. 3-84; Sassi 1956 as cited in Ex. 35-41). Other studies 
reported negative results (Exs. 7-14; 9-135).
    Likewise, several studies reported increases in renal proteins in 
the urine of chromate production workers and chrome platers (Exs. 35-
107; 5-45; 35-105; 5-57). The Cr(VI) air levels recorded in these 
workers were usually below the current OSHA PEL (Exs. 35-107; 5-45). 
Workers with the highest urinary chromium levels tended to also have 
the largest elevations in renal markers (Ex. 35-107). One study 
reported no relationship between chromium in urine and renal function 
parameters, no relationship with age or with duration of exposure, and 
no relationship between the presence of chromium skin ulcers and 
chromium levels in urine or renal function parameters (Ex. 5-57). In 
most studies, the elevations renal protein levels were restricted to 
only one or two proteins out of several examined per study, generally 
exhibited small increases (Ex. 35-105) and the effects appeared to be 
reversible (Ex. 5-45). It has been stated that low molecular weight 
proteinuria can occur from other reasons and cannot by itself be 
considered evidence of chronic renal disease (Ex. 35-195). Other 
studies reported no changes in renal markers (Exs. 7-27; 35-104) and 
animal inhalation studies did not report kidney damage (Exs. 9-135; 31-
18-11; 10-11; 31-18-10; 10-10). Some studies with Cr(VI) administered 
by drinking water or gavage were positive for increases in renal 
markers, and some cell and tissue damage (Exs. 9-143; 11-10). However, 
it is not clear how to extrapolate such findings to workers exposed to 
Cr(VI) via inhalation. Well designed studies of effects in humans via 
ingestion were not found.
    OSHA did not find information to clearly and sufficiently 
demonstrate that exposures to Cr(VI) result in significant impairment 
to the hepatic system. Two European studies, positive for an excess of 
deaths from cirrhosis of the liver and hepatobiliarity disorders, were 
not able to separate chromium exposures from exposures to the many 
other substances present in the workplace. The authors also could not 
rule out the role of alcohol use as a possible contributor to the 
disorder (Ex. 7-92; Sassi as cited in Ex. 35-41). Other studies did not 
report any hepatic abnormalities (Exs. 7-27; 10-11).
    The reproductive studies showed mixed results. Some positive 
reproductive effects occurred in some welding studies. However, it is 
not clear that Cr(VI) is the causative agent in these studies (Exs. 35-
109; 35-110; 35-108; 35-202; 35-203). Other positive studies were 
seriously lacking in information. Information was not given on 
exposures, the nature of the reproductive complications, or the women's 
tasks (Shmitova 1980, 1978 as cited in Ex. 35-41, p. 52). ATSDR states 
that because these studies were

[[Page 59360]]

generally of poor quality and the results were poorly reported, no 
conclusions can be made on the potential for chromium to produce 
adverse reproductive effects in humans (Ex. 35-41, p.52). In animal 
studies, where Cr(VI) was administered through drinking water or diet, 
positive developmental effects occurred in offspring (Exs. 9-142; 35-
33; 35-34; 35-38). However, the doses administered in drinking water or 
given in the diet were high (i.e., 250, 500, and 750 ppm). Furthermore, 
strong studies showing reproductive or developmental effects in other 
situations where employees were working exclusively with Cr(VI) were 
not found. In fact, the National Toxicology Program (NTP) (Exs. 35-40; 
35-42; 35-44) conducted an extensive multigenerational reproductive 
assessment by continuous breeding where the chromate was administered 
in the diet. The assessment yielded negative results (Exs. 35-40; 35-
42; 35-44). Animal inhalation studies were negative (Exs. 35-199; 9-
135; 10-10; Glaser 1984 as cited in Ex. 31-22-33;). Thus, it cannot be 
concluded that Cr(VI) is a reproductive toxin for normal working 
situations.

VII. Preliminary Quantitative Risk Assessment

A. Introduction

    The Occupational Safety and Health (OSH) Act and some landmark 
court cases have led OSHA to rely on quantitative risk assessment, 
where possible, to support the risk determinations required to set a 
permissible exposure limit (PEL) for a toxic substance in standards 
under the OSH Act. Section 6(b)(5) of the Act states that ``The 
Secretary [of Labor], in promulgating standards dealing with toxic 
materials or harmful agents under this subsection, shall set the 
standard which most adequately assures, to the extent feasible, on the 
basis of the best available evidence, that no employee will suffer 
material impairment of health or functional capacity even if such 
employee has regular exposure to the hazard dealt with by such standard 
for the period of his working life.'' (29 U.S.C. 651 et seq.)
    In a further interpretation of the risk requirements for OSHA 
standard setting, the United States Supreme Court, in the 1980 
``benzene'' decision, (Industrial Union Department, AFL-CIO v. American 
Petroleum Institute, 448 U.S. 607 (1980)) ruled that the OSH Act 
requires that, prior to the issuance of a new standard, a determination 
must be made that there is a significant risk of material impairment of 
health at the existing PEL and that issuance of a new standard will 
significantly reduce or eliminate that risk. The Court stated that 
``before he can promulgate any permanent health or safety standard, the 
Secretary is required to make a threshold finding that a place of 
employment is unsafe in the sense that significant risks are present 
and can be eliminated or lessened by a change in practices' [448 U.S. 
642]. The Court also stated ``that the Act does not limit the 
Secretary's power to require the elimination of significant risks'' 
[488 U.S. 644]. While the Court indicated that the use of quantitative 
risk analysis was an appropriate means to establish significant risk, 
they made clear that ``OSHA is not required to support its finding that 
a significant risk exists with anything approaching scientific 
certainty.''
    Although the Court in the Cotton Dust case, (American Textile 
Manufacturers Institute v. Donovan, 452 U.S. 490 (1981)) rejected the 
use of cost-benefit analysis in setting OSHA standards, it reaffirmed 
its previous position in the ``benzene'' case that a risk assessment is 
not only appropriate but should be used to identify significant health 
risk in workers and to determine if a proposed standard will achieve a 
reduction in that risk. Although the Court did not require OSHA to 
perform a quantitative risk assessment in every case, the Court 
implied, and OSHA as a matter of policy agrees, that assessments should 
be put into quantitative terms to the extent possible.
    The determining factor in the decision to perform a quantitative 
risk assessment is the availability of suitable data for such an 
assessment. As reviewed in section VI.B. on Carcinogenic Effects, there 
are a substantial number of occupational cohort studies that reported 
excess lung cancer mortality in workers exposed to Cr(VI) in several 
industrial operations. Many of these found that workers exposed to 
higher levels of airborne Cr(VI) for a longer period of time had 
greater standardized mortality ratios (SMRs) for lung cancer. OSHA 
believes two recently studied occupational cohorts have the strongest 
data sets on which to quantify lung cancer risk from cumulative Cr(VI) 
exposure (i.e., air concentration x exposure duration). Using a linear 
relative risk model on these data to predict excess lifetime risk, OSHA 
preliminarily estimates that the lung cancer risk from a 45 year 
occupational exposure to Cr(VI) at an 8-hour TWA at the current PEL of 
52 [mu]g/m<SUP>3</SUP> is 106 to 334 excess deaths per 1000. 
Quantitative lifetime risk estimates from a working lifetime exposure 
at several lower alternative PELs under consideration by the Agency are 
also estimated. For example, the projected risk at 0.5 [mu]g/
m<SUP>3</SUP> Cr(VI) is 1.1 to 4.3 per 1000. The sections below discuss 
the selection of the appropriate data sets and risk models, the 
estimation of lung cancer risks based on the selected data sets and 
models, the uncertainty in the risk estimates, the key issues that 
arise as result of the quantitative risk assessment as well as a 
summary describing comments from an expert peer review and the OSHA 
response.
    In contrast to the more extensive occupational cohort data on 
Cr(VI) exposure-response, data from experimental animal studies are 
less suitable for quantitative risk assessment of lung cancer than 
human studies. Besides the obvious species difference, most of the 
animal studies administered Cr(VI) to the respiratory tract by less 
relevant routes, such as instillation or implantation. The few 
available inhalation studies in animals were limited by a combination 
of inadequate exposure levels, abbreviated durations, and small numbers 
of animals per dose group. Despite these limitations, the animal data 
do provide semi-quantitative information with regard to the relative 
carcinogenic potency of different Cr(VI) compounds. A more detailed 
discussion can be found in section VI.B.7.
    The data that relate non-cancer health impairments, such as damage 
to the respiratory tract and skin, to Cr(VI) exposure are also not well 
suited for quantitative assessment. There are some data from cross-
sectional studies and worker surveys that group the prevalence and 
severity of nasal damage by contemporary time-weighted average (TWA) 
Cr(VI) air measurements. However, there are no studies that track 
either incidence or characterize exposure over time. Nasal damage is 
also more likely influenced by shorter-term peak exposures that have 
not been as well characterized. While difficult to quantitate, the data 
indicate that the risk of damage to the nasal mucosa would be 
significantly reduced by lowering the current PEL, discussed further in 
section VIII on Significance of Risk.
    There are even less suitable exposure-response data to assess risk 
for other Cr(VI)-induced impairments (e.g., mild renal damage, 
gastrointestinal ulceration). With the possible exception of 
respiratory tract effects (e.g., nasal damage, occupational asthma), 
the risk of non-cancer adverse effects that result from inhaling Cr(VI) 
are expected to be very low except as a result of long-term regular 
airborne exposure around or above the current PEL (52 [mu]g/
m<SUP>3</SUP>). Since

[[Page 59361]]

the non-cancer effects occur at relatively high Cr(VI) air 
concentrations, OSHA believes that lowering the PEL to reduce the risk 
of developing lung cancer over a working lifetime would also eliminate 
or reduce the risk of developing these other health impairments. As 
discussed in section VI.E., adverse effects to the skin primarily 
result from dermal rather than airborne exposure.

B. Study Selection

    The more than 40 occupational cohort studies reviewed in Section 
VI.B on carcinogenic effects were evaluated to determine the adequacy 
of the exposure-response information for the quantitative assessment of 
lung cancer risk associated with Cr(VI) exposure. The key criteria were 
data that allowed for estimation of input variables, specifically 
levels of exposure and duration of exposure (e.g., cumulative exposure 
in mg/m<SUP>3</SUP>-yr); observed numbers of cancers (deaths or 
incident cases) by exposure category; and expected (background) numbers 
of cancer deaths by exposure category.
    Additional criteria were applied to evaluate the strengths and 
weaknesses of the available epidemiological data sets. Studies needed 
to have well-defined cohorts with identifiable cases. Features such as 
cohort size and length of follow-up affect the ability of the studies 
to detect any possible effect of Cr(VI) exposure. Potential confounding 
of the responses due to other exposures was considered. Study 
evaluation also considered whether disease rates from an appropriate 
reference population were used to derive expected numbers of lung 
cancers. One of the most important factors in study evaluation was the 
ascertainment and use of exposure information (i.e., well-documented 
historical exposure data). Both level and duration of exposure are 
important in determining cumulative dose, and studies are often 
deficient with respect to the availability or use of such information. 
Evidence of exposure-response relationship was also important.
    Two recently studied cohorts of chromate production workers were 
found to be the strongest data sets for quantitative assessment (Exs. 
31-22-11; 33-10). Of the various studies, these two had the most 
extensive and best documented Cr(VI) exposures spanning three or four 
decades. Both cohort studies characterized observed and expected lung 
cancer mortality and reported a statistically significant positive 
association between lung cancer risk and cumulative Cr(VI) exposure. 
Four other cohorts had less satisfactory data for quantitative 
assessments of lung cancer risk (Exs. 7-11; 23; 7-14; 7-120; 31-16-3). 
While the lung cancer response in these cohorts was stratified across 
multiple exposure groups, there were limitations to these data that 
affected the certainty of the risk projections. The cohorts include 
chromate production workers, stainless steel welders, and aerospace 
manufacturing workers. Risk estimates from these lesser cohorts were 
used to examine the robustness of the more precise estimates from the 
Gibb and Luippold cohorts. The strengths and weaknesses of all six 
cohorts in terms of their use in exposure-response analysis are 
discussed in more detail below. Emphasis has been placed on the 
quantitative information available for each cohort.
    Three other cohort studies that were used in the past to develop 
crude risk estimates from worker exposure to Cr(VI) are not being 
relied upon in the present assessment and therefore are not reviewed 
below (Exs. 7-37; 7-62; 7-95). In these cohorts, risk estimates were 
determined from background lung cancer rates and excess lung cancer 
mortality associated with a single, rather than multiple Cr(VI) 
exposure levels. There were also a number of other limitations to the 
study data that required the use of unsupported assumptions and raised 
uncertainties in the risks. The exposure-response data from the three 
studies and the resulting assessments are discussed in the 1995 report 
from the K.S. Crump Division (Ex. 13-5). OSHA believes the recent 
availability of several higher quality cohort studies cited above 
eliminates the need to rely on these more problematic cohorts to assess 
lung cancer risk from occupational Cr(VI) exposure.
1. Gibb Cohort
    The Gibb et al. study was one of the stronger studies for 
quantitative risk assessment, especially in terms of cohort size, 
historical exposure data, and evidence of exposure-response (Exs. 31-
22-11; 33-11). Gibb et al. studied an updated cohort from the same 
Baltimore chromate production plant previously studied by Hayes et al. 
(see section VII.B.4). The cohort consisted of 2357 male workers (white 
and non-white) first employed between 1950 and 1974. Follow-up was 
through the end of 1992 for a total of 70,736 person-years and an 
average length of 30 years per member. Smoking status at the start of 
employment was available for 91% of the cohort members.
    A significant advantage of the Gibb data was the sizable amount of 
personal and area sampling measurements from a variety of locations and 
job titles collected concurrently over the years during which the 
cohort members were exposed (from 1950 to 1985, when the plant closed). 
Using these concentration estimates as the basis, a job exposure matrix 
was constructed giving annual average exposures by job title. Based on 
the job exposure matrix and work histories for the cohort members, Gibb 
et al. computed the person-years of observation, the observed numbers 
of lung cancer deaths, and the expected numbers of lung cancer deaths 
categorized by cumulative Cr(VI) exposure and age of death. They found 
that cumulative Cr(VI) exposure was a significant predictor of lung 
cancer risk over the exposure range of 0 to 2.76 (mean<plus-minus>SD = 
0.70<plus-minus>2.75) mg/m\3\ - yr, even with models that accounted for 
the smoking data at hire. This included a greater than expected number 
of premature lung cancer deaths in some workers. For example, chromate 
production workers between 40 and 50 years of age with mean cumulative 
Cr(VI) exposure of 0.41 mg CrO<INF>3</INF>/m\3\ - yr (equivalent to 
0.21 mg Cr(VI)/m\3\ - yr) were about four times more likely to die of 
lung cancer than a State of Maryland resident of similar age (Ex. 31-
22-11, Table V).
    The detailed reporting of the cumulative exposure, including mean 
values for four categories defined by the quartiles of cumulative 
exposure versus age, was another significant advantage. This level of 
documentation reduced some of the uncertainty associated with the 
estimation of cumulative exposure. Moreover, the cross-classification 
of cumulative exposure with age allowed the application of more 
elaborate models that consider the effect of age on lung cancer risk.
    Since the publication of Gibb et al., the data file containing the 
demographic, exposure, and response data for the individual cohort 
members was made available (Ex. 295). These data have been used in a 
recent reanalysis (see subsection VII.C.1). The advantages of the study 
mentioned above are even greater now that the detailed cohort data can 
be accessed. Among other things, the exposure groups can be defined in 
alternative ways, the effect of considering different reference 
populations can be examined, and additional models can be applied in 
the dose-response analysis.
2. Luippold Cohort
    The other well-documented exposure-response data set comes from a 
second cohort of chromate production workers. Luippold et al. studied a 
cohort of 482 predominantly white, male employees

[[Page 59362]]

who started work between 1940 and 1972 at the same Painesville, Ohio 
plant studied earlier by Mancuso (Ex. 33-10) (see subsection VII.B.3). 
Mortality status was followed through 1997 for a total of 14,048 
person-years and an average length of 30 years. While the Luippold 
cohort was smaller and less racially diverse than the Gibb cohort, the 
workforce contained fewer transient, short-term employees. The Luippold 
cohort consisted entirely of workers employed over one year. Fifty-five 
percent worked for more than five years. In comparison, 65 percent of 
the Gibb cohort worked for less than a year and 15 percent for more 
than five years at the Baltimore plant. There was more limited 
information about the smoking behavior (smoking status available for 
only 35 percent of members) of the Luippold cohort than the Gibb 
cohort.
    One aspect that the Luippold cohort had in common with the Gibb 
cohort was extensive and well-documented air monitoring of Cr(VI). 
Cr(VI) exposures for the Luippold cohort were based on 21 industrial 
hygiene surveys conducted at the plant between 1943 and 1971, yielding 
a total of more than 800 area samples (Ex. 35-61). A job exposure 
matrix was computed for 22 exposure areas for each month starting in 
1940 and, coupled with detailed work histories available for the cohort 
members, cumulative exposures were calculated for each person-year of 
observation. The cumulative Cr(VI) exposures, which ranged from 0.003 
to 23 (mean<plus-minus>SD = 1.58<plus-minus>2.50) mg Cr(VI)/m\3\ - yr, 
were generally higher but overlapped those of the Gibb cohort.
    Luippold et al. found significant dose-related trends for lung 
cancer SMRs as a function of year of hire, duration of employment, and 
cumulative Cr(VI) exposure. The data on exposure-response for this 
cohort are relatively strong. The use of individual work histories to 
define exposure categories and presentation of mean cumulative doses in 
the exposure groups provided a strong basis for a quantitative risk 
assessment. The higher cumulative exposure range and the longer work 
duration of the Luippold cohort serve to complement quantitative data 
available on the Gibb cohort. Risk assessments on the Luippold et al. 
study data performed by Crump et al. had access to the individual data 
and, therefore, had the best basis for analyses of this cohort (Exs. 
31-18-1; 35-205; 35-58).
3. Mancuso Cohort
    Mancuso (Ex. 7-11) studied the lung cancer incidence of an earlier 
cohort of 332 white male employees drawn from the same plant in 
Painesville, Ohio that was evaluated by the Luippold group. The Mancuso 
cohort was first employed at the facility between 1931 and 1937 and 
followed up through 1972, when the plant closed. Mancuso (Ex. 23) later 
extended the follow-up period through 1993, yielding a total of 12,881 
person-years of observation for an average length of 38.8 years and a 
total of 66 lung cancer deaths. Since the Mancuso workers were first 
employed in the 1930s and the Luippold workers were first employed 
after 1940, the cohorts consisted of a completely different set of 
individuals.
    A major limitation of the Mancuso study is the uncertainty of the 
exposure data. Mancuso relied exclusively on the air monitoring 
reported by Bourne and Yee (Ex. 7-98) conducted over a single short 
period of time during 1949. Bourne and Yee presented monitoring data as 
airborne insoluble chromium, airborne soluble chromium, and total 
airborne chromium by production department at the Painesville plant. 
The insoluble chromium was probably Cr(III) compounds with some 
slightly water-soluble and insoluble chromates. The soluble chromium 
was probably highly water-soluble Cr(VI). Mancuso (Exs. 7-11; 23) 
calculated cumulative exposures (mg/m\3\ - yr) for each cohort member 
based on the 1949 mean chromium concentrations, by production 
department, under the assumption that those levels reflect exposures 
during the entire duration of employment for each cohort member, even 
though employment may have begun as early as 1931 and may have extended 
to 1972. Due to the lack of air measurements spanning the full period 
of worker exposure and the lack of adequate methodology to distinguish 
chromium valence states i.e., Cr(VI) vs. Cr(III)), the exposure data 
associated with the Mancuso cohort were not as well characterized as 
data from the Luippold or Gibb cohorts.
    Mancuso presented observed lung cancer deaths and age-adjusted 
death rates stratified by age group and cumulative total, soluble and 
insoluble chromium exposure groups (Ex. 23). However, the study did not 
provide the expected numbers of lung cancers for the exposure 
groupings, making it more difficult to apply appropriate risk models to 
the data. Approaches that attempt to circumvent this limitation are 
discussed in subsection VII.E.1. Mancuso (Ex. 7-11; 23) reported 
cumulative exposure-related increases in age-adjusted lung cancer death 
rates for soluble, insoluble, or total chromium. Within a particular 
range of exposures to insoluble chromium, lung cancer death rates also 
tended to increase with increasing total cumulative chromium. However, 
the study did not report whether these tendencies were statistically 
significant, nor did it report the extent to which exposures to soluble 
and insoluble chromium were correlated. Thus, it is possible that the 
apparent relationship between insoluble chromium e.g., primarily 
Cr(III)) and lung cancer may have arisen because both insoluble 
chromium concentrations and lung cancer death rates were positively 
correlated with Cr(VI) concentrations.
    Although a 1995 risk assessment based on data from the 1975 Mancuso 
study was prepared for OSHA under contract (Ex. 13-5), it has been 
superseded by an updated assessment from the more complete 1997 Mancuso 
data (Ex. 33-15). Specific limitations with respect to quantitative 
risk estimation from the Mancuso cohort are discussed in section 
VII.E.1 on supporting risk assessments.
4. Hayes Cohort
    Hayes et al. (Ex. 7-14) studied a cohort of employees at the same 
chromate production site in Baltimore examined by Gibb et al. The Hayes 
cohort consisted of 2101 male workers who were first hired between 1945 
and 1974, excluding those employed for less than 90 days. The Gibb 
cohort had different date criteria for first employment (1950-1974) and 
no 90-day exclusion.
    Hayes et al. reported SMRs for respiratory tract cancer based on 
workers grouped by time of hire, employment duration, and high or low 
exposure groups. Workers who had ever worked at an older plant facility 
and workers whose location of employment could not be determined were 
considered to have a high or questionable exposure. Workers known to 
have been employed exclusively at a newer renovated facility built in 
1950 and 1951 were considered to have had low exposure. A dose-response 
was observed in the sense that higher SMRs for respiratory cancer were 
observed among long-term workers (workers who had worked for three or 
more years) than among short-term workers. Hayes et al. did not 
quantify occupational exposure to Cr(VI) at the time the cohort was 
studied.
    Later on, Braver et al. (Ex. 7-17) estimated average cumulative 
soluble chromium, (presumed by the authors to be Cr(VI)) exposures for 
four subgroups of the Hayes cohort. The TWA Cr(VI) concentrations were 
determined from a total of 555 midget impinger air measurements that 
were collected at the older plant from 1945 to 1950. The

[[Page 59363]]

cumulative exposure for the subgroups were estimated from the yearly 
average Cr(VI) exposure for the entire plant and their average duration 
of employment rather than job-specific Cr(VI) concentrations and 
individual work histories. Such ``group level'' estimation of 
cumulative exposure is less appropriate than the estimation based on 
individual experiences as was done for the Gibb and Luippold cohorts. 
Another weakness is that exposures attributed to many workers (e.g., 
those hired after 1950) were based on chromium measurements during an 
earlier period (i.e., 1949-1950).
    Braver et al. (Ex. 7-17) discussed a number of other potential 
sources of uncertainty in the Cr(VI) exposure estimates, such as the 
possible conversion to Cr(III) during sample collection, the inability 
to measure insoluble forms of Cr(VI) even though soluble Cr(VI) 
compounds were primarily produced at the plant, and the likelihood that 
samples may have been collected mainly in potential problem areas. 
However, the biggest source of uncertainty was the assumption of rather 
high Cr(VI) air levels in the newly renovated facility at the Baltimore 
site throughout the 1950s based on measurements made 1945 to 1950 in an 
older facility, as explained in section VII.E.2.
5. Gerin Cohort
    Gerin et al. (Ex. 7-120) developed a job exposure matrix that was 
used to quantify cumulative Cr(VI) exposures for male stainless steel 
welders who were part of the International Agency for Research on 
Cancer's (IARC) multi-center historical cohort study (Ex. 7-114). The 
IARC cohort included 11,092 welders for a total of 164,077 person-
years. This resulted in an average of 14.8 person-years of risk for 
each member of the cohort. The number cohort members who were stainless 
steel welders, for which Cr(VI) exposures were estimated, could not be 
determined from their report. Gerin et al. used occupational hygiene 
surveys reported in the published literature to estimate typical eight-
hour TWA Cr(VI) breathing zone concentrations for various combinations 
of welding processes and base metal. The resulting exposure matrix was 
then combined with information about individual work history, 
considering time and length of employment, type of welding, base metal, 
and ventilation status (e.g., confined area, use of local exhaust 
ventilation, etc.) to estimate the cumulative Cr(VI) exposure.
    Unfortunately, the industrial hygiene data used to develop the 
Gerin exposure matrix included measurements in the 1970s from only 8 of 
the 135 companies that employed welders in the cohort. Individual work 
histories were also not available for about 25 percent of the stainless 
steel welders. In these cases, information was assumed based on the 
average distribution of welding practices within the company. The lack 
of specific Cr(VI) air measurements and work practice information for 
this cohort raises questions concerning the accuracy of the exposure 
estimates.
    Gerin et al. reported lung cancer mortality across four cumulative 
Cr(VI) exposure categories for two subcohorts of stainless steel 
welders; each accumulating between 7,000 and 10,000 person-years of 
observation. The welders were also known to be exposed to nickel, 
another potential lung carcinogen. There was no upward trend in lung 
cancer with respect to cumulative Cr(VI) exposure for either subcohort. 
Because of uncertainties in the exposure estimates, the lack of 
exposure-response, and possible confounding co-exposure to nickel, the 
Gerin cohort was not considered a featured data set for exposure-
response assessment.
6. Alexander Cohort
    Alexander et al. (Ex. 31-16-3) conducted a retrospective cohort 
study of 2429 aerospace workers employed in jobs entailing chromate 
exposure (e.g., spray painting, sanding/polishing, chrome plating, 
etc.) between 1974 and 1994. The cohort included workers employed as 
early as 1940. Follow-up averaged a relatively short 8.9 years per 
cohort member.
    Industrial hygiene data collected between 1974 and 1994 were used 
to classify jobs in categories of ``high'' exposure, ``moderate'' 
exposure, or ``low'' exposure to Cr(VI). The use of respiratory 
protection was accounted for when setting up the job exposure matrix. 
These exposure categories were assigned summary TWA concentrations and 
combined with individual job history records to estimate cumulative 
exposures for each person-year of observation. As further discussed in 
section VII.E.4, it was not clear from the study whether exposures are 
expressed in units of Cr(VI) or chromate (CrO<INF>3</INF>). Exposures 
occurring before 1974 were assumed to be at TWA levels assigned to the 
interval from 1974 to 1985. The importance of the exposure assignments 
to the quantitative assessment of risk is further discussed in section 
VII.E.4.
    Alexander et al. presented lung cancer incidence data for four 
cumulative chromate exposure categories based on worker duration and 
the three (high, moderate, low) exposure levels above. Lung cancer 
incidence rates were determined using a local cancer registry, part of 
the National Cancer Institute (NCI) Surveillance Epidemiology and End 
Results (SEER) program. There was no positive trend in lung cancer 
incidence with increasing Cr(VI) exposure. This cohort study was 
limited by the relatively young age of the cohort members, the short 
follow-up time, and lack of information on smoking. The available 
Cr(VI) air measurement data did not span the entire employment period 
of the cohort (e.g., no data for 1940 to 1974) and was heavily grouped 
into a relatively small number of ``summary'' TWA concentrations that 
may not have fully captured individual differences in workplace 
exposures to Cr(VI). For the above reasons, the Alexander cohort was 
not considered as strong a data set for quantitative exposure-response 
analysis as the Gibb and Luippold cohorts.
7. Studies Selected for the Quantitative Risk Assessment
    The epidemiologic database is quite extensive and contains several 
studies that have adequate data suitable for quantitative risk 
assessment. OSHA considers certain studies to be better suited for 
quantitative assessment than others. The Gibb and Luippold cohorts are 
considered the preferred sources for quantitative estimation because 
they have larger cohort sizes, extensive follow-up periods, fairly well 
documented historical Cr(VI) exposure levels, and because analysts have 
had access to the individual job histories and associated exposure 
matrices.
    The Mancuso cohort and the Hayes cohort were derived from workers 
at the same plants as Luippold and Gibb, respectively, but have 
limitations associated with the reporting of quantitative information 
and exposure estimates that make them less suitable for a risk 
assessment. Similarly, the Gerin and Alexander cohorts are less 
suitable either because of the small size of the cohort, the shorter 
follow-up, or limitations with respect to exposure estimation. For 
example, the lung cancer status of the Alexander cohort had only been 
tracked for an average of nine years. This is in contrast to the Gibb, 
Luippold, and Mancuso cohorts that accumulated an average 30 or more 
years of observation. Long-term follow-up of cohort members is 
particularly important for determining the risk of lung cancer, which 
typically has an extended latency period of roughly twenty years. The 
Alexander cohort would need additional 20 years of

[[Page 59364]]

follow-up to achieve the person-years of observation accumulated by the 
Gibb cohort of about the same number of workers. The Guerin cohort is 
also limited by lack of follow-up, since the lung cancer status of the 
stainless steel welders are believed to have only been observed for an 
average of about 15 years.
    Despite the limitations, the lesser studies each provide 
independent estimates of risk, albeit with more uncertainty, that can 
be compared to the estimates derived from the preferred data sets. OSHA 
believes evaluating consistency in risk among several different worker 
cohorts adds to the overall quality of the assessment. In light of the 
extensive worker exposure-response data, there is little additional 
value in deriving quantitative risk estimates from tumor incidence 
results in rodents, especially considering the concerns with regard to 
route of exposure and study design.
    The following sections, describing the quantitative estimates of 
risk, start with the preferred Gibb and Luippold cohorts. The risk 
estimates from the supporting studies and previous risk assessments are 
then discussed. A discussion of remaining issues and uncertainties 
follows the quantitative presentation.

C. Quantitative Risk Assessments Based on the Gibb Cohort

    Quantitative risk assessments have recently been performed on the 
exposure-response data from the Gibb cohort by three groups: Environ 
International (Exs. 33-15; 33-12) under contract with OSHA; the 
National Institute for Occupational Safety and Health (Ex. 33-13); and 
Exponent (Ex. 31-18-15-1) for the Chrome Coalition. All reported 
similar risks for Cr(VI) exposure over a working lifetime despite using 
somewhat different modeling approaches. The exposure-response data, 
risk models, statistical evaluation, and risk estimates reported by 
each group are discussed below.
1. Environ Risk Assessments
    In 2002, Environ International (Environ) prepared a quantitative 
analysis of the association between Cr(VI) exposure and lung cancer 
(Ex. 33-15). The Environ analysis relied on a summary of the person-
years of observation and observed and expected lung cancer deaths 
broken down by age and cumulative exposure (Ex. 31-22-11, Table V). 
These data are presented in Table VII-1. The job exposure matrix was 
the basis for the calculation of individual cumulative exposure 
estimates for all 2357 members of the cohort. The cumulative exposure 
estimates were lagged 5 years (i.e., at any point in time after 
exposure began, an individual's cumulative exposure would equal the 
product of chromate concentration and duration of exposure, summed over 
all jobs held up to five years prior to that point in time). An 
exposure lag is commonly used in the dose-response analysis of lung 
cancer since there is a long latency period between first exposure and 
the development of disease. Gibb et al. found that models using five- 
and ten-year lags provided better fit to the mortality data than lags 
of zero, two and twenty years (Ex. 31-22-11). The cross-classification 
of cumulative exposure with age allowed Environ to evaluate models that 
considered the effect of age on lung cancer risk. A total of 71,994 
person-years summed up from Table V of the Gibb et al. study was 
slightly greater than the reported 70,736 cited in their publication 
(Ex. 31-22-11, p. 119).

  Table VII-1.--Dose-Response Data From Gibb et al. (Ex. 31-22-11): Observed and Expected Number of Lung Cancer
                      Deaths Grouped by Age and Four Cumulative Cr(VI) Exposure Categories
----------------------------------------------------------------------------------------------------------------
                                                                                Age
  Cumulative Cr(VI) exposure                      --------------------------------------------------------------
      ([mu]g/m\3\-years)                            20-29    30-39    40-49    50-59    60-69    70-79     80+
----------------------------------------------------------------------------------------------------------------
0-0.77........................  Observed.........        0        1        0       14        8        2        1
                                Expected.........    0.018     0.39      2.5     7.56    10.79        5     0.88
                                Person-Years.....     5003     7684     6509     5184     3104      865      163
                                Mean Exposure....     0.21     0.21     0.27     0.28     0.26     0.24     0.21
0.78-4.6......................  Observed.........        0        0        2       10       10        4        2
                                Expected.........    0.001     0.18     1.97     6.09     7.85     3.25     0.44
                                Person-Years.....      349     3139     4643     3928     2183      558       79
                                Mean Exposure....      2.2      2.2      2.2      2.2      2.2      2.0      1.9
4.7-40........................  Observed.........        0        0        3       10       11        4        2
                                Expected.........    0.002     0.19     1.93      5.7     7.66     3.26     0.38
                                Person-Years.....      457     3520     4732     3720     2128      559       78
                                Mean Exposure....       16       16       16       16       15       15       14
40-2730.......................  Observed.........        0        0        8        8       18        3        1
                                Expected.........    0.001     0.17     1.82     5.63     6.71     2.48     0.18
                                Person-Years.....      200     2874     4294     3663     1926      423       29
                                Mean Exposure....      110      170      210      270      330      410     450
----------------------------------------------------------------------------------------------------------------
A 5-year lag was used in the calculation of the cumulative exposures. The exposure estimates themselves have
  been converted from those shown in Gibb et al., Table V, by multiplying by 0.52, to convert from chromate
  concentration to hexavalent chromium concentration and by 1000 to convert from mg/m\3\ - years to [mu]g/m\3\-
  years

    A set of ``externally standardized'' models was applied to the data 
in Table VII-1. These are externally standardized because they required 
estimates of expected lung cancer deaths from a standard reference 
population. The 2002 Environ analysis relied on expected lung cancer 
deaths from age-specific Maryland rates, as provided in Gibb et al. The 
observed numbers of cancer cases were assumed to have a Poisson 
distribution, with expected values corresponding to three different 
dose-related models. A Poisson distribution is assumed because it has 
been commonly used in statistics to describe the allocation of rare 
events that occur during a given time period. Regression techniques are 
then used to link explanatory variables (e.g., cumulative exposure) to 
responses of interest (e.g., lung cancer deaths).
    The set of models used was mathematically described as follows:

    E1. N<INF>i</INF> = C<INF>0</INF> * E<INF>i</INF> * 
exp{kt<INF>i</INF>{time}  * (1 + C<INF>1</INF>D<INF>i</INF> + 
C<INF>2</INF>D<INF>i</INF>\2\)
    E2. N<INF>i</INF> = C<INF>0</INF> * E<INF>i</INF> * (1 + 
C<INF>1</INF>D<INF>i</INF> * exp{kt<INF>i</INF>{time} )
    E3. N<INF>i</INF> = C<INF>0</INF> * E<INF>i</INF> + (PY<INF>i</INF> 
* C<INF>1</INF>D<INF>i</INF>)

where N<INF>i</INF> is the predicted number of lung cancers in i\th\ 
group PY<INF>i</INF> is the

[[Page 59365]]

number of person-years for group i; E<INF>i</INF> is the expected 
number of lung cancers in that group, based on the reference 
population; D<INF>i</INF> is the mean cumulative dose for that group; 
and C<INF>0</INF>, C<INF>1</INF>, C<INF>2</INF>, and k are parameters 
to be estimated. In equations E1 and E2, t<INF>i</INF> the mean age for 
group i.
    Models E1 and E2 are relative risk models that differ with respect 
to the effect of age. In model E1, the background rates are adjusted 
for age whereas in E2 the dose coefficient is modified by the age. On 
the other hand, Model E3 is an additive risk model. In the case of 
additive risk models, the exposure-related estimate of risk is the same 
regardless of the age- and race-specific background rate of lung 
cancer. For relative risk models, a dose term is multiplied by the 
appropriate background rate of lung cancer to derive an exposure-
related estimate of risk, so that excess risk is always relative to 
background.
    Estimation of parameters (i.e., C<INF>0</INF>, C<INF>1</INF>, 
C<INF>2</INF>, and k) was accomplished by maximum likelihood 
techniques. For the externally standardized models, likelihood ratio 
tests were used to determine which of the model parameters contributed 
significantly to the fit of the model. Parameters were sequentially 
added to the model, starting with C<INF>1</INF>, when they contributed 
significantly (p >= 0.05) to improving the fit. Parameters that did not 
contribute significantly were excluded from consideration.
    Goodness-of-fit for each model was evaluated by considering the 
deviance, a likelihood-based statistic for which larger p-values 
indicate better model fit. In addition, the fits of different models 
were compared using the Akaike Information Criterion (AIC) value, a 
statistic based on the model's maximized likelihood and the number of 
parameters used. For the quadratic model E1, addition of a dose-squared 
term did not significantly improve the fit of model to the data (i.e., 
C<INF>2</INF> estimated to be zero) relative to a linear model. For 
models E1 and E2, the parameter k was not determined to be different 
from 0, and thus models E1 and E2 defaulted to the same linear relative 
risk model. The deviance-based test of fit suggested an adequate 
correspondence between model predictions and the observations (p >= 
0.13).
    A second set of ``internally standardized'' models, which did not 
require estimation of the expected number of lung cancers, was also fit 
to the data in Table VII-1 (Ex. 33-15). Model parameters were estimated 
by the maximum likelihood procedures described above. The test for 
goodness-of-fit indicated that these models did not fit the data well 
(p <= 0.01). The formulation and a more detailed description of these 
models can be found in the 2002 Environ report (Ex. 33-15).
    Lifetable calculations were made of the number of extra lung 
cancers per 1000 workers exposed to Cr(VI), assuming a constant 
exposure from age 20 through a maximum of age 65. The lifetime 
probability of a lung cancer death was cumulated to age 100, resulting 
in a negligible loss of accuracy since the probability that a person 
will live longer than that is extremely small. Rates of lung cancer and 
other mortality for the lifetable calculations were based, 
respectively, on 1998 U.S. lung cancer and all-cause mortality rates 
for both sexes and all races.
    The lifetable calculation of additional lifetime risk was completed 
for the maximum likelihood parameter estimates for each model. In 
addition, 95% confidence intervals for the additional lifetime risk 
were derived by a likelihood profile method. Details about the 
procedures used to estimate parameters, model fit, lifetable 
calculations, and confidence intervals are described in the 2002 
Environ report (Ex. 33-15, p. 24-26).
    Based on comparison of the models' AIC values, Environ indicated 
that the linear relative risk model (simplified E1/E2) was preferred 
over the E3 additive risk model. The relative risk model is also 
preferred over an additive risk model (fits being adequate in both 
cases) in the case of lung cancer because of its variable background 
rate with age. It may not be appropriate to assume, as an additive 
model does, that increased lung cancer risk at age 25, where background 
risk is relatively low, would be the same (for the same cumulative 
dose) as at age 50, where background rates are much higher.
    The linear relative risk model predicted an excess lifetime risk of 
lung cancer associated with an occupational exposure of 45 years to 1 
[mu]g/m<SUP>3</SUP> Cr(VI) to be 6 per 1000 (95% CI: 0.8 to 14). The 
additive model predicted a slightly lower lifetime risk of 4.4 per 1000 
(95% CI: 0.0 to 11). At the OSHA PEL (52 [mu]g/m<SUP>3</SUP>), the 
maximum likelihood estimate (MLE) using the linear relative risk model 
is 253 per 1000 (95% CI: 39 to 456).
    Since the completion of the 2002 Environ analysis, individual data 
for the 2,357 men in the Gibb et al. cohort have become available. The 
new data included cumulative Cr(VI) exposure estimates, smoking 
information, date of birth, race, date of hire, date of termination, 
cause of death, and date of the end of follow-up for each individual 
(Ex. 35-295). The individual data allowed Environ to do several 
additional analyses that could not be done previously, including 
assessments based on (1) redefined exposure categories, (2) alternate 
background reference rates for lung cancer mortality, and (3) Cox 
proportional hazards modeling (Ex. 33-12). These are discussed below.
    In the 2002 analysis, Environ used the same four-group 
categorization of cumulative exposure reported by Gibb et al. and 
presented in Table VII-1. The individual data allowed Environ to 
investigate alternate groupings of cumulative exposure categories. 
Environ presented two alternate groupings with ten cumulative Cr(VI) 
exposure groups each, six more than reported by Gibb et al. and used in 
the 2002 analysis. One alternative grouping was designed to divide the 
person-years of follow-up and, therefore, the expected numbers of lung 
cancers fairly evenly across groups. The other alternative allocated 
roughly the same number of observed lung cancers to each group. These 
two alternatives were designed to remedy the uneven distribution of 
observed and expected cases in the Gibb et al. categories, which may 
have caused parameter estimation problems due to the small number of 
cases in some groups. The new groupings assigned adequate numbers of 
observed and expected lung cancer cases to all groups and are presented 
in Table VII-2.

[[Page 59366]]



  Table VII-2.--Dose-Response Data From Environ (2003, Ex. 33-12): Observed and Expected Lung Cancer Deaths for
                        Gibb Cohort Grouped by Ten Cumulative Cr(VI) Exposure Categories
----------------------------------------------------------------------------------------------------------------
                                   Cumulative    Mean Cr(VI)                              Expected lung cancers
                                     Cr(VI)        exposure     Person-      Observed  -------------------------
                                 exposure [mu]g/ ([mu]g/m\3\-    years         lung       Maryland    Baltimore
                                   m\3\-years)       yr)                     cancers       rates        rates
----------------------------------------------------------------------------------------------------------------
Alternative 1: Roughly Equal            0-0.151       0.0246        17982           12         10.3        13.37
 Observed Cases per Group......     0.151-0.686        0.395         9314           12         13.0        16.80
                                     0.686-2.08         1.25         8694           12         10.3        13.55
                                      2.08-4.00         2.96         5963           12         7.38         9.42
                                      4.00-8.32         5.89         5102           12         5.63         7.32
                                      8.32-18.2         12.4         5829           13         7.09         9.21
                                        18.2-52         31.1         6679           13         6.83         9.05
                                         52-182          105         6194           12         5.77         7.73
                                        182-572          314         4118           12         5.79         7.66
                                           >572          979          945           12         2.07         2.62
Alternative 2: Roughly Equal            0-0.052      0.00052        14282            4         5.08         6.63
 Number of Person-Years per         0.052-0.273        0.147         6361           11         9.05        11.58
 Group.........................      0.273-0.65        0.455         6278            7         8.71        11.33
                                      0.65-1.43        0.996         6194           11         7.30         9.58
                                      1.43-3.12         2.19         6395           12         8.17        10.52
                                      3.12-6.89         4.59         6207           11         6.90         8.95
                                      6.89-16.1         10.7         6296           17         7.77        10.05
                                      16.1-41.6         25.9         6230           12         6.50         8.57
                                      41.6-1.43         81.5         6287           10         5.56         7.52
                                           >143          384         6289           27         9.17        11.99
                                                --------------
    Total......................  ..............  ...........     70819.38          122         74.2        96.7
----------------------------------------------------------------------------------------------------------------
The lower bounds of the ranges are inclusive; the upper bounds are exclusive.

    The 2003 Environ analysis also derived expected cases using lung 
cancer rates from alternative reference populations. In addition to the 
State of Maryland lung cancer rates that were used by Gibb et al., 
Environ used age- and race-specific rates from the city of Baltimore, 
where the plant was located. Baltimore may represent a more appropriate 
reference population because most of the cohort members resided in 
Baltimore and Baltimore residents may be more similar to the cohort 
members than the Maryland or U.S. populations in their co-exposures and 
lifestyle characteristics, especially smoking habits and urban-related 
risk factors. On the other hand, Baltimore may not be the appropriate 
reference population if the elevated lung cancer rates primarily 
reflect extensive exposure to industrial carcinogens. This could lead 
to an under representation of relative risk attributable to Cr(VI) 
exposure.
    The 2003 analysis used two externally standardized models, a 
quadratic relative risk model (model E1 from above, without the age 
factor) and a quadratic additive risk model (model E3 from above with 
the additional term C<INF>2</INF>D<INF>i</INF><SUP>2</SUP>) defined as 
follows:

E4. N<INF>i</INF> = C<INF>0</INF> * E<INF>i</INF> + PY<INF>i</INF> * 
(C<INF>1</INF>D<INF>i</INF> + C<INF>2</INF>D<INF>i</INF><SUP>2</SUP>).

The age factor was dropped from model E1 because the individual data 
obviated the need to rely on the cross-classifications of cumulative 
exposure. The availability of individual data also allowed a more 
refined approach to internally standardized modeling than employed in 
the 2002 assessment. Two Cox proportional hazards models were fit to 
the individual exposure-response data that incorporated the individual 
ages at death of all the lung cancer cases. The model forms were:

C1. h(t;z;D) = h<INF>0</INF>(t)*exp([bgr]<INF>1</INF>z + 
[bgr]<INF>2</INF>D)
C2. h(t;z;D) = h<INF>0</INF>(t)*[exp([bgr]<INF>1</INF>z)][1 + 
[bgr]<INF>2</INF>D]

where h is the hazard function, which expresses the age-specific rate 
of lung cancer among workers, as estimated by the model. In addition, t 
is age, z is a vector of possible explanatory variables other than 
cumulative dose, D is cumulative dose, h<INF>0</INF>(t) is the baseline 
hazard function (a function of age only), [bgr]<INF>2</INF> is the 
cumulative dose coefficient, and [bgr]<INF>1</INF> is a vector of 
coefficients for other possible explanatory variables (Ex. 35-57). Cox 
modeling is an approach that uses the experience of the cohort to 
estimate an exposure-related effect, irrespective of an external 
reference population or exposure categorization. Cox models can 
sometimes eliminate concerns about choosing an appropriate reference 
population and may be advantageous when the characteristics of the 
cohort under study are not well matched against reference populations 
for which age-related background rates have been tabulated. The two 
forms of the Cox models are consistent with those originally discussed 
by Cox. Model C1 assumes the lung cancer response is nonlinear with 
cumulative Cr(VI) exposure, whereas C2 assumes a linear lung cancer 
response with Cr(VI) exposure.
    All externally standardized models provided a good fit to the data 
(p>=0.40). The choice of exposure grouping had little effect on the 
parameter estimates of either model E1 or E4. However, the choice of 
reference rates had some effect, notably on the ``background'' 
parameter, C<INF>0</INF>, which was included in the models to adjust 
for differences in background lung cancer rates between cohort members 
and the reference population. Such an adjustment was necessary for the 
Maryland reference population (C<INF>0</INF> was significantly 
different from its default value, 1), but not for the Baltimore city 
reference population (C<INF>0</INF> was not significantly different 
from 1). The inclusion of the C<INF>0</INF> parameter allowed the model 
to fit the data and yielded a cumulative dose coefficient that 
reflected the effect of exposure and not the effect of differences in 
background rates. The model results indicated a relatively consistent 
cumulative dose coefficient, regardless of reference population. 
Details about the procedures used to estimate parameters, model fit, 
lifetable calculations, and confidence intervals

[[Page 59367]]

are described in the Environ report (Ex. 33-12, p. 8-9).
    The coefficient for cumulative dose in the model ranged from 2.87 
to 3.48 per mg/m<SUP>3</SUP>-yr for the relative risk model, E1, and 
from 0.0061 to 0.0071 per mg/m<SUP>3</SUP>-person-yr for the additive 
risk model, E4. These coefficients determine the slope of the linear 
cumulative Cr(VI) exposure-lung cancer response relationship. The 
cumulative dose coefficients for the relative risk model (E1) were only 
slightly greater than that obtained from model E1 in the 2002 Environ 
analysis. For the additive risk model (E4), the dose coefficients were 
approximately twice the value obtained from model E3 in the 2002 
analysis (i.e., 0.0033). In no case did the new analysis suggest that a 
quadratic model fit the data better than a linear model.
    For the internally standardized Cox proportional hazards models, C1 
and C2, the other possible explanatory variables considered were 
cigarette smoking status, race, and calendar year of death. For both 
models, addition of a term for smoking status significantly improved 
the fit of the models to the data (p<=0.00001). The experience with 
non-linear model C1 indicated that race (p=0.15) and year of death 
(p=0.4) were not significant contributors when cumulative dose and 
smoking status were included in the model. Based on results for model 
C1, race and year of death were not considered by Environ in the linear 
model C2. The cumulative dose coefficient, [bgr]2, was 1.00 for model 
C1 and 2.68 for model C2. Model C2 provided a slightly better fit to 
the data than did model C1. A more complete description of the models 
and variables can be found in the 2003 Environ analysis (Ex. 33-12, p. 
10).

BILLING CODE 4510-26-P

[[Page 59368]]

[GRAPHIC] [TIFF OMITTED] TP04OC04.000

    Table VII-3 shows each model's predictions of excess lifetime lung 
cancer risk from various occupational exposures. The estimates are very 
consistent regardless of model, exposure grouping, or reference 
population. The model that appears to generate results least similar to 
the others is C1, which yielded one of the higher risk estimates at 52 
[mu]g/m<SUP>3</SUP>, but estimated the lowest risks for exposure levels 
of 10 [mu]g/m<SUP>3</SUP> or lower. The change in magnitude, relative 
to the other models, is a result of the nonlinearity of this model (the 
only nonlinear model among the set being considered). Confidence limits 
for all models, including C1, tend to overlap, suggesting a fair degree 
of consistency.
    The estimates based on the individual data files were slightly 
greater than

[[Page 59369]]

those reported in the previous Environ analysis (Ex. 33-15). For 
example, the 2003 Environ analysis estimated additional lifetime risk 
from 45 years of exposure at the OSHA PEL to be between 290 and 380 per 
1000, whereas the previous analysis estimated 253 per 1000 (Ex. 33-12, 
Table 9). This difference may be partly attributed to the availability 
of individual data, as opposed to data from summary tables, allowing a 
better definition of exposure categories. Some of the difference may be 
attributable to slightly different total person-years of follow-up 
reported by Gibb et al. in their summary table (71,994 from Table V, 
Ex. 31-22-11) and the total person-years accounted for in the 
individual data files (70,819 from Ex. 295). The reason for this 
variation in total person-years is unknown.
2. National Institute for Occupational Safety and Health (NIOSH) Risk 
Assessment
    NIOSH (Ex. 33-13) developed a risk assessment from the Gibb cohort. 
The NIOSH analysis, like the 2003 Environ assessment, used the cohort 
individual data files to compute cumulative Cr(VI) exposure. However, 
NIOSH also explored some other exposure-related assumptions. For 
example, they performed the dose-response analysis with lag times in 
addition to the 5-year lag used by Environ. NIOSH also analyzed dose-
response using as many as 50 exposure categories, although their report 
presents data in five cumulative Cr(VI) exposure groupings.
    NIOSH incorporated information on the cohort smoking behavior in 
their quantitative assessments. They estimated (packs/day)-years of 
cumulative smoking for each individual in the cohort, using information 
from a questionnaire that was administered at the time of each cohort 
member's date of hire. To estimate cumulative smoking, NIOSH assumed 
that the cohort members maintained the level of smoking reported in the 
questionnaire from the age of 18 through the end of follow-up. 
Individuals with unknown smoking status were assigned a value equal to 
the average smoking level among all individuals with known smoking 
levels (presumably including non-smokers). Individuals who were known 
to smoke but for whom the amount was unknown were assigned a smoking 
level equal to the average of all smokers.
    NIOSH considered six different relative risk models, fit to the 
data by Poisson regression methods. They did not consider additive risk 
models. The six relative risk models were externally standardized using 
age- and race-specific U.S. lung cancer rates. Their background 
coefficients, C<INF>0</INF>, explicitly included smoking, race, and age 
terms to adjust for differences between the cohort and the reference 
population. These models are described as follows:

    NIOSH1a: N<INF>i</INF> = C<INF>0</INF> * Ei * 
exp(C<INF>1</INF>D<INF>i</INF>)
    NIOSH1b: N<INF>i</INF> = C<INF>0</INF> * Ei * 
exp(C<INF>1</INF>D<INF>i</INF>\1/2\)
    NIOSH1c: N<INF>i</INF> = C<INF>0</INF> * Ei * exp(1 + 
C<INF>1</INF>D<INF>i</INF> + C<INF>2</INF>D<INF>i</INF><SUP>2</SUP>)
    NIOSH1d: N<INF>i</INF> = C<INF>0</INF> * Ei * (1 + 
D<INF>i</INF>)<SUP>[alpha]</SUP>
    NIOSH1e: N<INF>i</INF> = C<INF>0</INF> * Ei * (1 + 
C<INF>1</INF>D<INF>i</INF>)
    NIOSH1f: N<INF>i</INF> = C<INF>0</INF> * Ei * (1 + 
C<INF>1</INF>D<INF>i</INF><SUP>[alpha]</SUP>)

where the form of the equation has been modified to match the format 
used in the Environ reports. In addition NIOSH fit Cox proportional 
hazard models (not specified) to the lung cancer mortality data using 
the individual cumulative Cr(VI) exposure estimates.
    NIOSH reported that the linear relative risk model 1e generally 
provided a superior fit to the exposure-response data when compared to 
the various log linear models, 1a-d. Allowing some non-linearity (e.g., 
model 1f) did not significantly improve the goodness-of-fit, therefore, 
they considered the linear relative risk model form 1e (analogous to 
the Environ model E1) to be the most appropriate for determining their 
lifetime risk calculations. A similar fit could be achieved with a log-
linear power model (model 1d) using log-transformed cumulative Cr(VI) 
and a piece-wise linear specification for the cumulative smoking term.
    The dose coefficient (C<INF>1</INF>) for the linear relative risk 
model 1e was estimated by NIOSH to be 1.444 per mg CrO<SUP>3</SUP>/
m<SUP>3</SUP>-yr. (Ex. 33-13, Table 4). If the exposures were converted 
to units of mg Cr(VI)/m<SUP>3</SUP>-yr, the estimated cumulative dose 
coefficient would be 2.78 (95% CI: 1.04 to 5.44) per mg/m<SUP>3</SUP>-
yr. This value is very close to the estimates derived in the Environ 
2003 analysis (maximum likelihood estimates ranging from 2.87 to 3.48 
for model E1, depending on the exposure grouping and the reference 
population). Lifetime risk estimates based on the NIOSH-estimated dose 
coefficient and the Environ lifetable method using 2000 U.S. rates for 
lung cancer and all cause mortality are shown in Table VII-4. The 
values are very similar to the estimates predicted by the Environ 2003 
analysis (Table VII-3). The small difference may be due to the NIOSH 
adjustment for smoking in the background coefficient. NIOSH found that 
excess lifetime risks for a 45-year occupational exposure to Cr(VI) 
predicted by the best-fitting power model gave very similar risks to 
the preferred linear relative risk model at TWA Cr(VI) concentrations 
between 0.52 and 52 [mu]g/m<SUP>3</SUP> (Ex. 33-13, Table 5). Although 
NIOSH did not report the results, they stated that Cox modeling 
produced risk estimates similar to the Poisson regression. The 
consistency between Cox and Poisson regression modeling is discussed 
further in section VII.C.4.
[GRAPHIC] [TIFF OMITTED] TP04OC04.001


[[Page 59370]]


    NIOSH reported a significantly higher dose-response coefficient for 
nonwhite workers than for white workers. That is, nonwhite workers in 
the Gibb cohort are estimated to have a higher excess risk of lung 
cancer than white workers, given equal cumulative exposure to Cr(VI). 
In contrast, no significant race difference was found in the Cox 
proportional hazards analysis reported by 2003 Environ.
3. Exponent Risk Assessment
    In response to OSHA's Request For Information, Exponent (Ex. 31-18-
15-1) prepared an analysis of lung cancer mortality from the Gibb 
cohort. Like 2003 Environ and NIOSH, the Exponent analysis relied on 
the individual worker data. Exponent performed their dose-response 
analyses based on three different sets of exposure categories using two 
reference populations and 70,808 person-years of follow-up. A total of 
four analyses were completed, using (1) Maryland reference rates and 
the four Gibb et al. exposure categories; (2) Baltimore reference rates 
and the four Gibb et al. exposure categories; (3) Baltimore reference 
rates and six exposure groups defined by Exponent; and (4) Baltimore 
City reference rates and five exposure categories, obtained by removing 
the highest of the six groups defined by Exponent from the dose-
response analysis. A linear relative risk model without a background 
correction term, C<INF>0</INF>, (as was used by Environ and NIOSH) was 
applied in all of these cases and cumulative exposures were lagged five 
years (as done by Environ and NIOSH). The analyses showed excess 
lifetime risk between 6 and 14 per 1000 for workers exposed to 1 [mu]g/
m<SUP>3</SUP> Cr(VI) for 45 years.
    The analysis using Maryland reference lung cancer rates and the 
Gibb et al. four-category exposure grouping yielded an excess lifetime 
risk of 14 per 1000. This risk, which is higher than the excess 
lifetime risk estimates by Environ and NIOSH for the same occupational 
exposure, probably results from the absence of a background rate 
coefficient in Exponent's model. As reported in the Environ 2002 and 
2003 analyses, the Maryland reference lung cancer rates require a 
background rate coefficient greater than 1 to achieve the best fit to 
the exposure-response data. The unadjusted Maryland rates underestimate 
the cohort's background lung cancer rate, leading to overestimation of 
the risk attributable to cumulative Cr(VI) exposure.
    The two analyses that used Baltimore reference rates and either 
Exponent's six-category exposure grouping or the Gibb et al. four-
category grouping both resulted in an excess lifetime risk of 9 per 
1000 for workers exposed to 1 [mu]g/m<SUP>3</SUP> Cr(VI) for 45 years. 
This risk is close to estimates reported by Environ using their 
relative risk model (E1) and Baltimore reference rates for the same 
occupational exposure (Table VII-3). The Environ analysis showed that, 
unlike the Maryland-standardized model discussed above, the Baltimore-
standardized models had background rate coefficients very close to 1, 
the ``default'' value assumed by the Exponent relative risk model. This 
suggests that the Baltimore reference rates may more accurately 
represent the background lung cancer rate for this cohort.
    The lowest excess lifetime risk for workers exposed to 1 [mu]g/
m<SUP>3</SUP> Cr(VI) for 45 years reported by Exponent, at 6 per 1000, 
was derived from the analysis that excluded the highest of Exponent's 
six exposure groups. While this risk value is close to the Environ and 
NIOSH unit risk estimates, the analysis merits some concern. Exponent 
eliminated the highest exposure group on the basis that most cumulative 
exposures in this group were higher than exposures usually found in 
current workplace conditions. However, eliminating this group could 
exclude possible long-term exposures (e.g., >15 years) below the 
current OSHA PEL (52 [mu]g/m<SUP>3</SUP>) from the risk analysis. 
Moreover, no matter what current exposures might be, data on higher 
cumulative exposures are still relevant for understanding the dose-
response relationships.
    In addition, the Exponent six category cumulative exposure grouping 
may have led to an underestimate of the dose effect. The definition of 
Exponent's six exposure groups was not related to the distribution of 
cumulative exposure associated with individual person-years, but rather 
to the distribution of cumulative exposure among the workers at the end 
of their employment. This division does not result in either a uniform 
distribution of person-years or observed lung cancer cases among 
exposure categories. In fact, the six category exposure groupings of 
both person-years and observed lung cancers were very uneven, with a 
preponderance of both allocated to the lowest exposure group. This 
skewed distribution of person-years and observed cases puts most of the 
power for detecting significant differences from background cancer 
rates at low exposure levels, where these differences are expected to 
be small, and reduces the power to detect any significant differences 
from background at higher exposure concentrations.
    Exponent conducted analyses to further explore the dose-response 
relationship in addition to the assessments described above (Ex. 31-18-
1). Of particular interest was an examination of short-term workers' 
likely impact on the dose-response assessment and an SMR analysis based 
on peak exposure estimates. A substantial proportion of the Gibb cohort 
worked less than one year at the Baltimore plant. Inclusion of these 
workers in the exposure-response assessment could potentially bias the 
results, if, for example, these workers incurred unrecorded Cr(VI) 
exposures at other jobs. In brief, Exponent found that excluding these 
short-term workers would not likely impact the dose-response analysis.
    Exponent reported that SMRs for workers with ``peak'' exposures 
less than 0.18 mg CrO<INF>3</INF>/m<SUP>3</SUP> (0.094 mg Cr(VI)/
m<SUP>3</SUP>) were not significantly elevated and that this exposure 
level may represent a ``threshold'' (i.e., exposure below which the 
probability of cancer is zero), such that workers exposed to 
concentrations below the threshold may not have excess cancer risk (Ex. 
31-18-1). However, the analysis used peak exposure estimates based on 
recorded average annual exposures. True peak exposures were unavailable 
for the Gibb cohort members. The use of the highest recorded average 
annual Cr(VI) air level as an exposure metric ignores any risk 
contribution from the duration of exposure. It assumes the same lung 
cancer risk regardless of whether the worker is exposed at a particular 
Cr(VI) concentration for one month or ten years. This is clearly 
inconsistent with the study results.
    The validity of the ``peak exposure'' analysis also suffers from 
Exponent's problematic definition of exposure categories, which is 
similar to the six-part grouping used in the dose-response assessments. 
As with Exponent's cumulative exposure groups, the peak exposure 
grouping allocates most of the observed cancers and person-years to the 
lowest exposure groups, reducing the power to detect significant 
differences from background at more moderate exposure concentrations 
below 0.094 mg Cr(VI)/m<SUP>3</SUP>. The implication that the data 
indicate a ``threshold'' at 0.094 mg Cr(VI)/m<SUP>3</SUP> is, 
therefore, misleading, and not considered a valid analysis for 
estimating risk of lung cancer to workers exposed to Cr(VI).
4. Summary of Risk Assessments Based on the Gibb Cohort
    OSHA finds remarkable consistency among the risk estimates from the

[[Page 59371]]

various quantitative analyses of the Gibb cohort. The excess lifetime 
risks from cumulative Cr(VI) exposure were similar whether the analyses 
were based on the summary information reported by Gibb et al. or on the 
information provided in the individual data file.
    Both Environ and NIOSH determined that linear relative risk models 
with respect to cumulative exposure generally provided a superior fit 
to the data when compared to other relative risk models. The Environ 
2003 analysis further suggested that a linear additive risk model could 
adequately describe the observed dose-response data. The risk estimates 
for NIOSH and Environ's best-fitting models were statistically 
consistent (compare Tables VI-3 and VI-4).
    The choice of reference population had little impact on the risk 
estimates. NIOSH used the entire U.S. population as the reference, but 
included adjustment terms for smoking, age and race in its models. The 
Environ 2003 analysis used both Maryland and Baltimore lung cancer 
rates, and included a generic background adjustment term. The 
adjustment was significant in the fitted model when Maryland rates were 
used for external standardization, but not when Baltimore rates were 
used. Since no adjustment in the model background term was required to 
better fit the exposure-response data using Baltimore City lung cancer 
rates, they may best represent the cohort's true background lung cancer 
incidence. OSHA considers the inclusion of such adjustment factors, 
whether specific to smoking, race, and age (as defined by NIOSH), or 
generic (as defined by Environ), to be appropriate and contribute to 
accurate risk estimation by helping to correct for confounding risk 
factors. The internally standardized Cox models, especially the linear 
Cox model, which also adjusted for smoking yielded risk estimates that 
were generally consistent with the externally standardized models.
    Finally, the number of exposure categories used in the analysis had 
little impact on the risk estimates. When an appropriate adjustment to 
the background rates was included, the four exposure groups originally 
defined by Gibb et al. and analyzed in the 2002 Environ report, the six 
exposure groups defined by Exponent, the two alternate sets of ten 
exposure categories as defined in the 2003 Environ analysis, and the 
fifty groups defined and aggregated by NIOSH all gave essentially the 
same risk estimates. The robustness of the results to various 
categorizations of cumulative exposure adds to the validity of the risk 
projections.
    Having reviewed the analyses described in this section, OSHA finds 
that the best estimates of excess lung cancer risk to workers exposed 
to the current PEL (52 [mu]g Cr(VI)/m\3\) for a working lifetime are 
about 300 to 400 per thousand based on data from the Gibb cohort. The 
best estimates of excess lung cancer risks to workers exposed to TWA 
exposure concentrations of 1 [mu]g Cr(VI)/m<SUP>3</SUP> for a working 
lifetime range from 7.1 to 9.4 per 1000 with the lowest 95% confidence 
bound being 2.7, and the highest 95% confidence bound being 16 (Table 
VII-3). These estimates are consistent with predictions from Environ, 
NIOSH and Exponent models that applied linear relative and additive 
risk models based on the full range of cumulative Cr(VI) exposures 
experienced by the Gibb cohort and used appropriate adjustment terms 
for the background lung cancer mortality rates.
    It is instructive to examine whether the excess lung cancer risk 
estimated from the mathematical modeling reasonably predicts the risk 
based on the mortality observed in the Gibb et al. study. There were 
855 deaths in the Gibb cohort of which 122 were from cancer of the lung 
(Ex. 31-22-11, Table I). The expected number of lung cancer deaths from 
the age-, gender-, race-, and calendar year-adjusted reference 
population in Baltimore was 96.7 (Table VII-2). Therefore, there were 
about 25 lung cancer deaths (i.e., 122--96.7) presumably attributable 
to Cr(VI) exposure out of the 855 total deaths, or 29 per 1000 workers 
(i.e., 25/855 x 1000). If lung cancer were to continue to occur with 
the same proportionate mortality in this cohort (64 percent of the 
cohort were still living), their excess lifetime lung cancer risk would 
be close to three percent.
    The mean cumulative exposure for the Gibb cohort was 0.134 mg 
CrO<INF>3</INF>/m\3\ - yr with a mean 3.1 years of work (Ex. 31-22-11, 
Table II). An approximate average Cr(VI) air level of 22.5 [mu]g 
Cr(VI)/m\3\ can be calculated after converting from CrO<INF>3</INF> to 
Cr(VI). Using the average Cr(VI) air concentration (22.5 [mu]g/m\3\), 
mean exposure duration (3.1 yr), and mean age of hire of 30 years of 
age (Ex. 31-22-11, Table III), the linear relative risk model E1 (equal 
PYRs per group, Table VII-3) predicts an excess lifetime lung cancer 
risk of 14.8 per 1000 (95% CI: 6.97 to 25.1 per 1000) for workers with 
the mean cumulative exposure of the Gibb cohort. These Cr(VI) levels 
are below the current PEL for considerably shorter than a full working 
lifetime.
    The model-predicted lung cancer risk is about half the risk 
calculated from the observed mortality in the Gibb et al. study. This 
is probably due, in part, to the higher cumulative Cr(VI) exposure for 
the subset of workers who had already died. The mean Cr(VI) exposure of 
the lung cancer cases was slightly over two-fold higher (i.e., 0.294 mg 
CrO<INF>3</INF>/m\3\ - yr) than the cohort as a whole (Ex. 31-22-11, 
Table II). It also seems likely that the workers who already died of 
causes other than lung cancer would be older cohort members that may 
have experienced higher Cr(VI) exposure than the presumably younger 
cohort members hired more recently and still living. If their mean 
cumulative Cr(VI) exposure were more like that of the lung cancer cases 
than the total cohort group, the relative risk model would predict 
risks close to the three percent excess lung cancer risk derived from 
the observed mortality data.

D. Quantitative Risk Assessments Based on the Luippold Cohort

    As discussed earlier, Luippold et al. (Exs. 35-204; 33-10) provided 
information about the cohort of workers employed in a chromate 
production plant in Painesville, Ohio. Follow-up for the 482 members of 
the Luippold cohort started in 1940 and lasted through 1997, with 
accumulation of person-years for any individual starting one year after 
the beginning of his first exposure. There were 14,048 total person-
years of follow-up for the cohort. The person-years were then divided 
into five exposure groups that had approximately equal numbers of 
expected lung cancers in each group. Ohio reference rates were used to 
compute expected numbers of deaths. White male rates were used because 
the number of women was small (4 out of 482) and race was known to be 
white for 241 of 257 members of the cohort who died and for whom death 
certificates were available. The 1960-64 Ohio rates (the earliest 
available) were assumed to hold for the time period from 1940 to 1960. 
Rates from 1990-94 were assumed to hold for the period after 1994. For 
years between 1960 and 1990, rates from the corresponding five-year 
summary were used. There were significant dose-related trends for lung 
cancer SMR as a function of year of hire, duration of employment, and 
cumulative Cr(VI) exposure. Overall, there was significantly increased 
SMR for lung cancer deaths of 241 (95% CI: 180 to 317).

[[Page 59372]]



    Table VII.-5--Dose-Response Data From Luippold Cohort as cited by Environ (2002, Ex. 33-15): Observed and
          Expected Numbers of Lung Cancer Deaths Grouped by Five Cumulative Cr(VI) Exposure Categories
----------------------------------------------------------------------------------------------------------------
                                                              Mean Cr(VI)
                                                                exposure     Observed     Expected     Person-
        Cumulative Cr(VI) exposure (mg/m\3\ - yrs)\a\          (mg/m\3\ -      lung         lung        years
                                                                yrs)\a\      cancers     cancers\b\
----------------------------------------------------------------------------------------------------------------
< 0.20......................................................         0.10            3          4.5         2952
0.20-0.49...................................................         0.36            8          4.4         2369
0.49-1.05...................................................         0.74            4          4.4         3077
1.05-2.70...................................................         1.79           16          4.4         3220
2.70-27.8...................................................         4.81           20          4.3        2482
----------------------------------------------------------------------------------------------------------------
\a\ Note that units mg/m\3\ - yrs is 1000 times greater than [mu]g/m\3\ - yrs in data tables for Gibb cohort.
\b\ Expected lung cancer deaths derived using Ohio state mortality rates.

    Environ conducted a risk assessment based on the cumulative Cr(VI) 
exposure-lung cancer mortality data from Luippold et al. and presented 
in Table VII-5 (Ex. 33-15). Cumulative Cr(VI) exposures were 
categorized into five groups with about four expected lung cancer 
deaths in each group. In the absence of information to the contrary, 
Environ assumed Luippold et al. did not employ any lag time in 
determining the cumulative exposures. The calculated and expected 
numbers of lung cancers were derived from Ohio reference rates. Environ 
applied the relative and additive risk models, E1 and E3, to the data 
in Table VII-5. Model E1 was applied without the 
exp{kt<INF>i</INF>{time}  term, because no categorization by age was 
available. Addition of a quadratic term did not improve the fit over 
that of a linear relative risk model. Model E2 was not applied, because 
without the exp{kt<INF>i</INF>{time}  term model E2 is the same as E1. 
The background rate parameter, C<INF>0</INF>, was assumed to be 1.0 in 
both models since other values did not significantly improve model fit.
    Linear relative and additive risk models fit the Luippold cohort 
data adequately (p>=0.25). The maximum likelihood estimates for the 
Cr(VI) exposure-related parameter, C<INF>1</INF>, of the linear 
relative and additive risk models were 0.88 per mg/m\3\ - yr and 0.0014 
per mg/m\3\ - person-yr, respectively. The C<INF>1</INF> estimates 
based on the Luippold cohort data were about 2.5-fold lower than the 
parameter estimates based on the Gibb cohort data. The excess lifetime 
risk estimate calculated by Environ for a 45-year working-lifetime 
exposure to 1 [mu]g Cr(VI)/m\3\ for both models was 2.2 per 1000 
workers (95% confidence intervals from 1.3 to 3.5 per 1000 for the 
relative risk model and 1.2 to 3.4 per 1000 for the additive risk 
model) using a lifetable analysis with 1998 U.S. mortality reference 
rates. These risks were 2.5 to 3-fold lower than the projected risks 
based on the Gibb data set for equivalent cumulative Cr(VI) exposures.
    Crump et al. (Exs. 33-15; 35-58; 31-18) also performed an exposure-
response analysis from the Painesville data. In a Poisson regression 
analysis, cumulative exposures were grouped into ten exposure 
categories with approximately two expected lung cancer deaths in each 
group. The observed and expected lung cancer deaths by Cr(VI) exposure 
category are shown in Table VII-6. Ohio reference rates were again used 
in calculating the expected lung cancer deaths and cumulative exposures 
were lagged 5 years.

Table VII-6.--Dose-Response Data From Crump et al. (Ex. 35-58): Observed
 and Expected Numbers of Lung Cancer Deaths for Luippold Cohort Grouped
              by Ten Cumulative Cr(VI) Exposure Categories
------------------------------------------------------------------------
                                 Mean
                                Cr(VI)    Observed   Expected
 Cumulative Cr(VI) exposure    exposure     lung       lung     Person-
        (mg/m3-yrs) a          (mg/m3-    cancers    cancer b    years
                                yrs) a
------------------------------------------------------------------------
0-0.06......................     0.0098          0       2.09       3112
0.06-0.18...................       0.11          3       2.19       1546
0.18-0.30...................       0.23          3       2.21       1031
0.30-0.46...................       0.38          5       2.13       1130
0.46-0.67...................       0.56          0       2.22       1257
0.67-1.00...................       0.80          4       2.23       1431
1.00-1.63...................       1.25         12       2.23       1493
1.63-2.60...................       2.10          3       2.18       1291
2.60-4.45...................       3.27         10       2.18       1248
4.45-29.0...................       7.55         11       2.12       904
------------------------------------------------------------------------
The lower bounds of the ranges are inclusive; the upper bounds are
  exclusive.
a Note that units mg/m3-yrs is 1000 times greater than [mu]g/m3-yrs in
  data tables for Gibb cohort.
b Expected lung cancer deaths derived using Ohio state mortality rates.

    The Crump et al. analysis used the same linear relative risk and 
additive risk models as Environ on the individual data categorized into 
the ten cumulative exposure groups (Ex. 35-58). Tests for systematic 
departure from linearity were non-significant for both models (p>= 
0.11). The cumulative dose coefficient determined by the maximum 
likelihood method was 0.79 (95% CI: 0.47 to 1.19) per mg/m<SUP>3</SUP>-
yr for the relative risk model and 0.0016 (95% CI: 0.00098 to 0.0024) 
per mg/m<SUP>3</SUP>--person-yr for the relative and additive risk 
model, respectively. The authors noted that application of the linear 
models to five and seven exposure groups resulted in no significant 
difference in dose coefficients, although the data was not presented. 
The dose coefficients reported by Crump et al. were very

[[Page 59373]]

similar to those obtained by Environ above, even though different 
exposure groups were used and the lag for the cumulative exposure 
calculation was slightly different. The authors noted that the linear 
models did not fit the exposure data grouped into ten categories very 
well (goodness-of-fit p<=0.01) but fit the data much better with seven 
exposure groups (p>0.3) after eliminating the nonmonotonic (i.e., not 
progressively increasing with exposure) scatter contributed by the many 
lower exposure categories where there are few observed and expected 
cancers. This nonmonotonic pattern is avoided by using more stable 
exposure groupings with greater number of cancers. The reduction in 
number of exposure groups did not significantly change the dose 
coefficient estimates.
    The maximum likelihood estimate for the cumulative dose coefficient 
using the linear Cox regression model (i.e., model C2) was 0.66 (90% 
CI: 0.11 to 1.21), which was similar to the linear [Poisson regression] 
relative risk model. When the Cox analysis was restricted to the 197 
workers with known smoking status and a smoking variable in the model, 
the dose coefficient for Cr(VI) was nearly identical to the estimate 
without controlling for smoking. This led the authors to conclude that 
``the available smoking data did not suggest that exposure to Cr(VI) 
was confounded with smoking in this cohort, or that failure to control 
for smoking had an appreciable effect upon the estimated carcinogenic 
potency of Cr(VI)'' (Ex. 35-58, p.1156).
    Crump et al. also presented benchmark dose estimates 
(EC<INF>10</INF>s) of 52 [mu]g/m<SUP>3</SUP> (95 percent lower 
confidence bound, LEC<INF>10</INF>, of 37 [mu]g/m<SUP>3</SUP>) and 49 
[mu]g/m<SUP>3</SUP> (LEC<INF>10</INF> of 35 [mu]g/m<SUP>3</SUP>) for 
the relative risk and additive risk models, respectively. The 
EC<INF>10</INF> is an estimate of the dose associated with a ten 
percent, or 100 in 1000, risk. The EC<INF>10</INF> and its 
LEC<INF>10</INF> are being considered by the U.S. EPA, under certain 
circumstances, as a reasonable point of departure for extrapolation 
modeling below the biologically observable range (Ex. 35-53, p. 3-12 to 
3-15). These results are very consistent with those predicted by 
Environ (Ex. 33-15) for the Luippold et al. cohort (e.g., approximately 
100 lung cancer cases per 1000 workers from estimated working lifetime 
at the OSHA PEL of 52 [mu]g/m<SUP>3</SUP>). There were only minor non-
significant changes in benchmark dose estimates when exposure lags were 
varied from 5 to 20 years using Poisson or Cox linear regression 
models.
    Given the similarity in results, OSHA believes it is reasonable to 
use the dose coefficients reported by Exponent based on their groupings 
of the individual cumulative exposure data to estimate excess lifetime 
risk from the Luippold cohort. Table VII-7 presents the excess risk for 
a working lifetime exposure to various TWA Cr(VI) levels as predicted 
by the relative and additive risk models using a lifetable analysis 
with 2000 U.S. rates for all causes and lung cancer mortality. The 
maximum likelihood estimates and 95 percent confidence limits from the 
Luippold cohort indicate that working lifetime exposures to the current 
Cr(VI) PEL would entail excess lifetime lung cancer risks around 100 
per 1000 and that risks of 1.2 to 3.3 per 1000 would be expected from 
TWA exposures of 1 [mu]g Cr(VI)/m<SUP>3</SUP> for a working lifetime.
[GRAPHIC] [TIFF OMITTED] TP04OC04.002

    The excess lung cancer risk predicted from the mathematical 
modeling can be compared with the risk expected based on the actual 
mortality experience of the Luippold cohort. There were 303 observed 
deaths in the cohort of which 51 were from cancer of the lung (Ex. 33-
10, Table 2). The expected number of lung cancer deaths from the age-, 
gender-, race-, and calendar year-adjusted reference population from 
Ohio was 21.2. Therefore, there were about 30 lung cancer deaths (51-
21.2) presumably attributable to Cr(VI) exposure out of 303 total 
deaths, or 98 per 1000 workers (29.8/303 x 1000). If lung cancer were 
to continue to occur with the same proportionate mortality in this 
cohort (37 percent of the cohort was still living), their excess 
lifetime lung cancer risk would be about ten percent.
    The mean cumulative exposure for the Luippold cohort was 1.58 mg 
Cr(VI)/

[[Page 59374]]

m<SUP>3</SUP>-yr (Ex. 33-10, Table 1), which is about twenty-three 
times the mean exposure for the Gibb cohort (i.e., 0.0697 mg Cr(VI)/
m<SUP>3</SUP>-yr). Although the mean length of employment of the 
Luippold cohort was not reported, a crude distribution of the years 
employed is consistent with an average of about ten years (Ex. 33-10, 
Table 1). If the cohort were exposed an average ten years then their 
average Cr(VI) air level would be roughly 158 [mu]g Cr(VI)/
m<SUP>3</SUP> (1.58 x 10 yr / 1000 [mu]g/mg). Using this Cr(VI) air 
concentration (158 [mu]g/m<SUP>3</SUP>), the estimated mean exposure 
duration (10 yr), and the mean age of hire of 34 years of age (Ex. 33-
10, Table 1), the linear relative risk model E1 predicts an excess 
lifetime lung cancer risk of 74 per 1000 (95% CI: 46 to 110 per 1000). 
This is slightly lower than the 98 per 1000 excess lung cancer deaths 
attributable to Cr(VI) determined from the observed study data. The 
Luippold cohort workers were exposed to mean Cr(VI) levels about three-
fold higher than the current PEL for an average duration that was 
slightly less than a quarter of a full 45 year working lifetime.
    As previously explained, it is not surprising that the relative 
risk model may underpredict the excess risks calculated from study 
mortality data. The risk model predicts the probability of lung cancer 
risk in an individual or set of workers, all with the same cumulative 
Cr(VI) exposure. The excess lung cancer risk calculated from the 
observed mortality data were for a group of workers with a wide range 
of Cr(VI) exposures. Like the Gibb study, the lung cancer cases had a 
mean cumulative Cr(VI) that was twice that of the entire cohort. 
Therefore, their risk may be somewhat higher than predicted for the 
cohort as a whole. Since most of the Luippold cohort had died (i.e., 63 
percent), the model-derived lung cancer risk based on the mean exposure 
of the entire Luippold cohort may better predict the mortality-derived 
excess risk estimate than was the case for the Gibb cohort, which had a 
lower percentage of deaths (i.e., 36 percent).
    Crump et al. reported on tests of trend and of excess lung cancer 
mortality by highest reported monthly TWA Cr(VI) concentration and 
cumulative Cr(VI) exposure for the workers in the Luippold cohort. The 
former analysis examined air concentration irrespective of exposure 
duration, even though there was a significant positive trend for excess 
lung cancer mortality with duration of employment (Ex. 33-10, Table 3). 
They found that a statistically significant excess mortality was not 
observed in workers exposed to less than the current OSHA PEL (i.e., 52 
[mu]g/m<SUP>3</SUP>). An analysis of cumulative Cr(VI) exposure found 
that a statistically significant exposure-related trend in lung cancer 
mortality only occurred if cumulative Cr(VI) exposure estimates above 
1.0 mg/m<SUP>3</SUP>-yr were included. Crump et al. acknowledged that 
their analysis had limited statistical power (i.e., the magnitude of 
excess mortality needed to achieve statistical significance) to detect 
increases in excess mortality at the lower cumulative Cr(VI) exposures 
(Ex. 35-58, p. 1147).
    The lack of statistical significance for the subset of 103 workers 
in the Luippold cohort whose highest monthly TWA exposure was less than 
the OSHA PEL is readily explained by a further examination of the data. 
The highest monthly TWA exposures of those workers averaged 27 [mu]g/
m<SUP>3</SUP> for an average duration of 34 months (Ex. 31-18-3, Table 
8). Using the dose coefficient from the linear relative risk model 
based on cumulative exposure fit to the full Luippold data set in a 
lifetable analysis, where workers were exposed to this Cr(VI) air 
concentration and duration starting at age 34 (the average starting age 
for the Luippold cohort), the additional lifetime risk is predicted to 
be 4.5 per 1000. This means that less than one additional lung cancer 
case would be projected for the Luippold subcohort of approximately 100 
workers whose highest reported eight-hour TWA (i.e., average 27 [mu]g/
m<SUP>3</SUP>) was below the PEL using a linear model without a 
threshold.
    Exponent suggested that the lack of a statistically significant 
increase in lung cancer mortality observed among workers whose reported 
average monthly TWA Cr(VI) was not above the PEL was evidence of an 
absence of increased risk at this level (Ex. 31-18-1). This assertion 
is not supported by the data. As explained above, the Crump et al. 
analysis lacks the statistical power to support this conclusion. Since 
exposure at the highest reported TWA accounts for almost all of the 
cumulative exposure experienced by those workers (Ex. 31-18-3, Table 
8), the lack of an observed increase in the lung cancer SMR is entirely 
consistent with a small, but significant, lung cancer risk as predicted 
by a linear, non-threshold relative risk model.

E. Supporting Quantitative Risk Assessments

    In addition to the preferred data sets analyzed above, there are 
four other cohorts with available data sets for estimation of 
additional lifetime risk of lung cancer. These are the Mancuso cohort, 
the Hayes cohort, the Gerin cohort, and the Alexander cohort. Environ 
(Ex. 33-15) recently did quantitative risk assessments on study data 
for all but the Hayes cohort. Several years earlier, the K.S. Crump 
Division (Ex. 13-5) did quantitative assessments on data from the 
Mancuso and Hayes cohort, under contract with OSHA. The U.S. EPA (Exs. 
19-1; 35-52) developed quantitative risk assessments from the Mancuso 
cohort data for its Integrated Risk Information System (IRIS). The 
California EPA (Ex. 35-54), Public Citizen Health Research Group (Ex. 
1), and the U.S. Air Force Armstrong Laboratory (AFAL) for the 
Department of Defense (Ex. 35-51) performed assessments from the 
Mancuso data using the 1984 U.S. EPA risk estimates as their starting 
point. The U.S. EPA also published a supporting risk assessment based 
on the Hayes cohort data (Ex. 7-102). Until the cohort studies of Gibb 
et al. and Luippold et al. became available, these earlier assessments 
provided the most current projected cancer risks from airborne exposure 
to Cr(VI). While the risk estimates from these data sets are associated 
with a greater degree of uncertainty, it is nevertheless valuable to 
compare them to the risk estimates from the preferred Gibb and Luippold 
cohorts. The cohort data sets and the analyses conducted on them are 
discussed below.
    The Mancuso and Hayes cohorts worked at the Painesville and 
Baltimore chromate production plants, respectively. Even though the 
entry date requirements, other cohort selection criteria, and the 
studied site facilities were different, the lung cancer risk estimated 
from the Hayes data set may not be completely independent from that 
estimated from the Gibb data set. A similar situation exists between 
the Mancuso and Luippold data sets. Unlike the Mancuso and Hayes 
cohorts, the Gerin and Alexander cohorts were not chromate production 
workers and lung cancer mortality did not show a statistically 
significant positive trend with cumulative Cr(VI) exposure. Environ 
performed quantitative assessments on these data sets to determine if 
the predicted lung cancer risks had statistical precision that was 
compatible with those estimated from the preferred Gibb and Luippold 
cohorts.
1. Mancuso Cohort
    As described in subsection VII.B.3, the Mancuso cohort was 
initially defined in 1975 and updated in 1997. The cohort members were 
hired between 1931 and 1937 and worked at the same Painesville facility 
as the Luippold cohort workers. However,

[[Page 59375]]

there was no overlap between the two cohorts since all Luippold cohort 
workers were hired after 1939. The quantitative risk assessment by 
Environ used data reported in the 1997 update (Ex. 23, Table XII) in 
which lung cancer deaths and person-years of follow-up were classified 
into four groups of cumulative exposure to soluble chromium, assumed to 
represent Cr(VI) (Ex. 33-15). The mortality data and person-years were 
further broken down by age of death in five year increments starting 
with age interval 40 to 44 years and going up to >75 years. However, no 
expected numbers of lung cancers were computed, either for the cohort 
as a whole or for specific groups of person-years. Environ used two 
methods for dealing with the lack of expected numbers in order to 
complete the risk assessment based on this cohort.
    In the first method, Environ used the recorded median age and year 
of entry into the cohort to estimate the calendar years that 
corresponded to the middle of the age categories for which expected 
numbers of lung cancers were needed. Data in the Mancuso study 
indicated that the median age at entry into the cohort was somewhere 
between 25 and 29 years and that the median year of entry into the 
cohort was in 1933 or 1934 (Ex. 23). Person-years of observation for 
the 40-44 age category would have been centered around 1948-49 (i.e., 
15 years after 1933-34, where 15 is the difference between the age 
group under consideration and the median age at entry into the cohort, 
equal to 40-25 or 44-29). Similar calculations were made for the other 
age categories. Expected numbers were then derived from the U.S. lung 
cancer mortality rates for years as close to the target years as could 
be obtained.
    The exposure-response data with the resulting expected number of 
lung cancer deaths are reported in Table 3 of the 2002 Environ report 
(Ex. 33-15, p. 39). The mean cumulative exposures to soluble Cr(VI) 
were assumed to be equal to the midpoints of the tabulated ranges. No 
lag was assumed for calculating the cumulative exposures. Environ 
applied three externally standardized models (see models E1-E3 in 
subsection VII.C.1) to these data. Unlike other data sets modeled by 
Environ, the age-related parameter k for the Mancuso data set was 
estimated to be different from 0, so that models E1 and E2 had 
different dose coefficients (Ex. 33-15, Table 6, p. 42). The quadratic 
term (i.e., C<INF>2</INF> in model E1) did not significantly improve 
model fit, so E1 was linear with respect to cumulative exposure.
    Since the expected numbers of lung cancers for the Mancuso cohort 
could only be approximated, Environ also applied a set of internally-
standardized models that did not require estimation of expected number 
of lung cancers to the exposure-response data (Ex. 33-15, p. 24-25). 
While both externally- and internally-standardized models provided 
adequate fit to the data (p>=0.13), the AIC procedure indicated that 
model E2, the linear relative risk model with an age-dependent exposure 
term, provided a superior fit over the other models. The next best 
fitting models, E1 and I2, presented other problems. Model E1 estimated 
risk predictions that were apparent outliers and the confidence 
intervals around risk predictions from model I2 were unusually wide 
(Ex. 33-15, Table 8, p. 43). Further explanation for the inherent 
instability of these models can be found in the 2002 Environ report 
(Ex. 33-15, p. 28-29).
    The excess risk of lung cancer from a working lifetime exposure to 
Cr(VI) at the current OSHA PEL using the preferred model E2 is 293 per 
1000 workers (95% CI: 188 to 403). The maximum likelihood estimate from 
working lifetime exposure to 1.0 [mu]g/m<SUP>3</SUP> Cr(VI) is 7.0 per 
1000 workers (95% CI: 4.1 to 11 per 1000). These estimates are close to 
those predicted from the Gibb cohort but are higher than predicted from 
the Luippold cohort. This result indicates that the non-overlapping 
Painesville worker cohorts (i.e., Mancuso and Luippold cohorts) 
probably generate independent estimates of risk, even though they were 
drawn from the same plant.
    There are uncertainties associated with both the exposure estimates 
and the estimates of expected numbers of lung cancer deaths for the 
1997 Mancuso data set. The estimates of exposure were derived from a 
single set of measurements obtained in 1949 (Ex. 7-98). Although little 
prior air monitoring was available, it is thought that the 1949 air 
levels probably understate the Cr(VI) concentrations in the plant 
during some of the 1930s and much of the 1940s when chromate production 
was high to support the war. The sampling methodology used by Bourne 
and Yee only measured soluble Cr(VI), but it is believed that the 
chromate production process employed at the Painesville plant in these 
early years yielded slightly soluble and insoluble Cr(VI) compounds 
that would not be fully accounted for in the sampling results (Ex. 35-
61). This would imply that risks would be overestimated by use of 
concentration estimates that were biased low. However, it is possible 
that the 1949 measurements may not have underestimated the Cr(VI) air 
levels in the early 1930s prior to the high production years. Some 
older cohort members were also undoubtedly exposed to less Cr(VI) in 
the 1950s than measured in 1949 survey.
    Another uncertainty in the risk assessment for the Mancuso cohort 
is associated with the post-hoc estimation of expected numbers of lung 
cancer deaths. The expected lung cancers were derived based on 
approximate summaries of the ages and assumed start times of the cohort 
members. Several assumptions were dictated by reliance on the published 
groupings of results (e.g., ages at entry, calendar year of entry, age 
at end of follow-up, etc.) as well as by the particular choices for 
reference mortality rates (e.g., U.S. rates, in particular years close 
to the approximated time at which the person-years were accrued). Since 
the validity of these assumptions could not be tested, the estimates of 
expected numbers of lung cancer deaths are uncertain.
    There is also a potential healthy worker survivor effect in the 
Mancuso cohort. The cohort was identified as workers first hired in the 
1930s based on employment records surveyed in the late 1940s (Ex. 2-
16). The historical company files in this time period were believed to 
be sparse and more likely to only identify employees still working at 
the plant in the 1940s (Ex. 33-10). If there was a sizable number of 
unidentified short-term workers who were hired but left the plant in 
the 1930s or who may have died before 1940 prior to systematic death 
registration, then there may have been a selection bias (i.e., healthy 
worker survivor effect) toward longer-term, healthier individuals (Ex. 
35-60). Since the mortality of these long-term ``survivors'' is often 
more strongly represented in the higher cumulative exposures, it can 
negatively confound the exposure-response and lead to an 
underestimation of risk, particularly to shorter-term workers (Ex. 35-
63). This may be an issue with the Mancuso cohort, although the 
magnitude of the potential underestimation is unclear.
    Several earlier quantitative risk assessments were done on cohort 
data presented in the 1975 Mancuso report (Ex. 7-11). These assessments 
did not have access to the 20 additional years of follow-up nor did 
they have age-grouped lung cancer mortality stratified by cumulative 
soluble chromium (presumed Cr(VI)) exposure), which was presented later 
in the 1997 update. Instead, age-grouped lung cancer mortality was 
stratified by cumulative exposure to total chromium that

[[Page 59376]]

included not only carcinogenic Cr(VI) but substantial amounts of non-
carcinogenic Cr(III).
    The 1995 risk analysis by K.S. Crump Division, under contract with 
OSHA, estimated cumulative Cr(VI) exposures by multiplying cumulative 
total chromium exposure by an adjustment factor of 0.4 (Ex. 13-5). This 
factor is roughly the average contribution of soluble chromium to the 
total chromium exposure levels measured across departments in the 
Painesville plant by Bourne and Yee in 1949 (Ex. 7-98). The K.S. Crump 
Division used the lung cancer mortality data cross-classified by the 
eight exposure categories and three age groups reported in Table IX of 
the 1975 Mancuso report (Ex. 7-11). They estimated the expected number 
of lung cancer deaths in a manner similar to the Environ assessments in 
2002. The median age at entry for the cohort was estimated to be 28.5 
years from the 1975 Mancuso study with an estimated median start date 
of 1934. Average values for cumulative exposure in each group were 
estimated by the arithmetic mean of the endpoints defining the group.
    An externally standardized linear relative risk model was used to 
fit the exposure-response data. A sensitivity analysis was used to 
examine the impact of different average cumulative exposure estimates 
to represent the highest exposure group (>3.0 mg-yr/m<SUP>3</SUP>) 
since an arithmetic average could not be calculated for this category. 
The maximum likelihood estimates for the dose coefficient were 
relatively constant over a wide range of assumed average exposures. 
However, the best fit occurred when the high-exposure group was 
excluded from the analysis (p=0.49). This was because the lung cancer 
mortality ratios observed for workers with the highest cumulative 
chromium exposure in the Mancuso data set tended to be lower than 
predicted by linear projections based on the lung cancer mortality data 
from workers exposed to lower cumulative exposures. The excess lung 
cancer risks for a working lifetime at the current OSHA PEL (52 [mu]g/
m<SUP>3</SUP>) for Cr(VI) range from 246 to 342 per 1000 workers using 
the different assumptions about the highest exposure group (Ex. 13-5, 
Table 8). The excess risk estimates from a working lifetime exposures 
to 0.5 [mu]g/m<SUP>3</SUP> Cr(VI) ranged from 2.9 to 4.4 per 1000 
workers. This was similar to the risk estimated by Environ using the 
more updated Mancuso data set.
    Like Environ, the K.S. Crump Division explored another method of 
Poisson regression that internally controlled for age, and which 
consequently alleviated the need to estimate background rates from an 
external control population. The dose coefficients estimated for the 
internally standardized linear relative risk model were similar to 
those from the externally controlled model. However, sensitivity 
analysis indicated that the internally standardized model may lead to 
less stable risk estimates, in that relatively minor changes in average 
exposure assumptions led to bigger changes in the risk estimates.
    The U.S. EPA also used exposure-response data presented in Table IX 
of the 1975 Mancuso report (Ex. 7-11) as the primary data source for 
calculating its unit risk estimate . The unit risk refers to an 
incremental lifetime cancer risk over background occurring in a 
hypothetical population in which all individuals are exposed 
continuously throughout life to a concentration of 1 [mu]g Cr(VI)/
m<SUP>3</SUP> in the air that they breathe. Like the K.S. Crump 
Division, the EPA relied on the observed lung cancer deaths cross-
classified by age group and cumulative exposure to total chromium. 
However, rather than estimate the year of cohort death based on age at 
entry into the study, the EPA chose to determine expected number of 
lung cancers for the entire cohort, regardless of age at death, using 
lung cancer mortality statistics for 1964. They estimated that a large 
proportion of lung cancer deaths in the cohort probably occurred around 
that year.
    The U.S. EPA assessment did not adjust the total cumulative 
chromium exposure estimates of Mancuso for the contribution of Cr(VI). 
While the EPA acknowledged that the resulting overestimation of dose 
would likely lead to an underestimation of risk, they judged that this 
would be potentially balanced by two factors that tend to overestimate 
the risk of lung cancer. One factor was the likelihood that the 
airborne Cr(VI) levels in the 1930s and 1940s were higher than measured 
by Bourne and Yee in 1949, as mentioned previously. EPA also suggested 
the possibility that the Mancuso cohort may have smoked more than the 
general population so that the expected numbers of lung cancer deaths 
associated with Cr(VI) exposure would be low and the relative risk 
overestimated for the cohort.
    The 1984 U.S. EPA assessment employed an exposure-dependent 
multistage model of additive risk to fit the 1975 Mancuso cohort data 
that relied on average chromium exposure, rather than the cumulative 
workplace exposure (Ex. 19-1). In their review of the U.S. EPA 
assessment, the K.S. Crump Division pointed out potential flaws in the 
EPA conversion of cumulative workplace exposure to their ``continuous 
exposure equivalent'' that resulted in high average chromium exposure 
estimates and a correspondingly low unit risk (Ex. 13-5, p. 19-21). The 
U.S. EPA determined that the maximum likelihood estimate of additional 
lung cancer risk associated with continuous lifetime exposure to 1 
[mu]g/m<SUP>3</SUP> of Cr(VI) was 0.012 (i.e., 12 per 1000). More 
recently, the EPA corrected its dose conversion for the Mancuso cohort 
which yielded a higher unit risk estimate of 0.016 per [mu]g Cr(VI)/
m<SUP>3</SUP> (Ex. 35-52).
    In 1985, the California Department of Health Services (CDHS) 
estimated a cancer potency factor for Cr(VI) in support of its Toxic 
Air Contaminants Program (Ex. 35-54, p. 210-215). They estimated the 
relative lung cancer risks and continuous total chromium exposure 
equivalents for the 1975 Mancuso data set using the same assumptions 
and procedures as the 1984 EPA assessment. An average relative risk and 
average total chromium exposure level, weighted by the person-years per 
age and exposure category, were calculated for all groups combined. The 
average total chromium exposure level was multiplied by one-seventh 
(0.142) as an assumed adjustment for the fraction of total chromium 
present as Cr(VI). A linear relative risk model was then used to 
calculate a ``crude'' approximation of the excess risk from continuous 
exposure to 1 [mu]g/m<SUP>3</SUP> of Cr(VI) for a lifetime. The CDHS 
chose the 95 percent upper confidence limit of 0.15 per [mu]g Cr(VI)/
m<SUP>3</SUP> as their cancer potency factor which is about an order of 
magnitude greater than the EPA unit risk estimate.
    The Public Citizen Health Research Group (PCHRG) attempted to 
estimate the magnitude of lung cancer risks associated with 
occupational exposure to Cr(VI) from the 1984 U.S. EPA unit risk for 
continuous lifetime exposure (Ex. 1). They reported that the excess 
lung cancer risk from a working lifetime exposure to Cr(VI) at the OSHA 
PEL (52 [mu]g/m<SUP>3</SUP>) was 220 per 1000 workers. As described in 
the 1995 report by K.S. Crump Division (Ex. 13-5, p. 27-29), there were 
several errors in the PCHRG analysis and the correctly calculated 
excess occupational risk at the OSHA PEL using the EPA unit risk method 
is 80 cases per 1000 workers. This risk is lower than the estimate from 
Environ and the K.S. Crump Division, probably as a result of the EPA 
conversion of occupational cumulative chromium exposure to a continuous 
average Cr(VI) exposure for an individual lifetime.

[[Page 59377]]

    The U.S. Air Force Armstrong Laboratory (AFAL) estimated lung 
cancer risks to U.S. Navy workers from Cr(VI) exposures as a result of 
welding, abrasive blasting, spray painting, and other operations (Ex. 
35-51). They used a cancer potency factor of 41 per mg Cr(VI)/kg-day 
derived from the 1984 EPA unit risk adjusted for an average breathing 
rate of 20 m<SUP>3</SUP>/day and body weight of 70 kg. They also 
reduced their measured airborne Cr(VI) dust concentrations by an 
assumed respirable fraction of 0.23. The estimated excess lifetime risk 
from a 45-year occupational exposure to an eight hour TWA 0.5 [mu]g/
m<SUP>3</SUP> using the AFAL methodology and assumptions is about 0.2 
per 1000 workers. This is lower than the Environ and K.S Crump Group 
estimates due to the lower EPA potency factor and the added adjustment 
for the respirable fraction.
    OSHA believes that the Environ quantitative risk assessment is the 
most credible analysis from the Mancuso cohort. It relied on the 
updated cohort mortality data and cumulative exposure estimates derived 
directly from air measurements of soluble chromium. The other 
assessments used older cohort mortality data with fewer years of 
follow-up and more problematic exposure estimates and calculations.
2. Hayes Cohort
    The K.S. Crump Division (Ex. 13-5) and Gibb et al. (Ex. 7-102) 
assessed risk based on the exposure-response data reported in Table IV 
by Braver et al. (Ex. 7-17) for the cohort studied by Hayes et al. (Ex. 
7-14). The Hayes cohort overlapped with the Gibb cohort. The Hayes 
cohort included 734 members, not part of the Gibb cohort, who worked at 
an older facility from 1945 to 1950 but did not work at the newer 
production facility built in August 1950. The Hayes cohort excluded 990 
members of the Gibb cohort who worked less than 90 days in the new 
production facility after August 1950. As noted in section VII.B.4, 
Braver et al. derived a single cumulative soluble Cr(VI) exposure 
estimate for each of four subcohorts of chromate production workers 
categorized by duration of employment and year of hire by Hayes et al. 
Thus, exposures were not determined for individual workers using a more 
comprehensive job exposure matrix procedure, as was done for the Gibb 
and Luippold cohorts. In addition, the exposures were estimated from 
air monitoring conducted only during the first five of the fifteen 
years the plant was in operation. Unlike the Mancuso cohort, Hayes et 
al. did not stratify the observed lung cancer deaths by age group. The 
expected number of lung cancer deaths for each subcohort was based on 
the mortality statistics from Baltimore.
    The K.S. Crump Division applied the externally standardized linear 
relative risk approach to fit the exposure-response data (Ex. 13-5). 
The maximum likelihood estimate for the dose coefficient (e.g., 
projected linear slope of the Cr(VI) exposure-response curve) was 0.75 
per mg Cr(VI)/m<SUP>3</SUP>-yr with a 90% confidence bound of between 
0.45 and 1.1 per mg Cr(VI)/m<SUP>3</SUP>-yr. These confidence bounds 
are consistent with the dose coefficient estimate obtained from 
modeling the Luippold cohort data (0.83, 95% CI: 0.55 to 1.2) but lower 
than that from the Gibb cohort data (3.5, 95% CI: 1.5 to 6.0). The 
later result indicates that the two Baltimore chromate production 
cohorts (i.e., Hayes and Gibb cohorts) probably generate independent 
estimates of risk, even though they were drawn from facilities at the 
same site for overlapping periods of time. The linear relative risk 
model fit the Hayes cohort data well (p=0.50). The K.S. Crump Division 
predicted the excess risk from occupational exposure to Cr(VI) for a 45 
year working lifetime at the OSHA PEL (52 [mu]g/m<SUP>3</SUP>) to be 88 
lung cancer cases per 1000 workers (95% CI: 61 to 141). For 1 [mu]g/
m<SUP>3</SUP>, about 2 excess lung cancer deaths per 1000 (95% CI: 1.2 
to 3.0) were predicted for the same duration of occupational exposure. 
These estimates are somewhat lower than the corresponding estimates 
based on the Gibb cohort data, probably because of the rather high 
average soluble Cr(VI) level (218 [mu]g/m<SUP>3</SUP>) assumed by 
Braver et al. for plant workers throughout the 1950s. If these assumed 
air levels led to an overestimate of worker exposure, the resulting 
risks would be underestimated.
    Gibb et al. provided a risk assessment for the U.S. EPA of the same 
Braver exposure-response data used by the K.S. Crump Division (Ex. 7-
102). In order to determine the EPA unit risk, the cumulative 
occupational exposures were converted to average lifetime concentration 
(as discussed in section VII.E.2) and an average age of 55 was assumed 
at the end of follow-up for members of the Hayes cohort. Gibb et al. 
used the additive risk model E3 with the default value of 1 for 
C<INF>0</INF>, to fit the data. They reported that the maximum 
likelihood estimate for the dose coefficient was 0.13 per mg/
m<SUP>3</SUP>-yr and it yields a unit risk similar to that derived by 
the EPA from the 1975 Mancuso cohort (Ex. 19-1). Since the excess lung 
cancer risk from lifetime occupational exposure to Cr(VI) at the OSHA 
PEL was 80 cases per 1000 workers based on the EPA unit risk from the 
Mancuso cohort, a similar occupational risk estimate is likely from the 
Gibb et al. unit risk based on the Hayes cohort. This would be 
consistent with the occupational risk (e.g., 88 cases per 1000 workers) 
at the OSHA PEL projected from the assessments of the K.S. Crump 
Division.
3. Gerin Cohort
    Environ (Ex. 33-15) did a quantitative assessment of the observed 
and expected lung cancer deaths in stainless steel welders classified 
into four cumulative Cr(VI) exposure groups reported in Tables 2 and 3 
of Gerin et al. (Ex. 7-120). The lung cancer data come from a large 
combined multi-center welding study in which a statistically 
significant excess lung cancer risk was observed for the whole cohort 
and non-statistically significant elevated lung cancer mortality was 
found for the stainless steel welder subcohorts (Ex. 7-114). A positive 
relationship with time since first exposure was also observed for the 
stainless steel welders (the type of welding with the highest exposure 
to Cr(VI)) but not with duration of employment.
    The exposure-response data from the Gerin study was only presented 
for those stainless steel welders with at least five years employment. 
Workers were divided into ``ever stainless steel welders'' and 
``predominantly stainless steel welders'' groups. The latter group were 
persons known to have had extended time welding stainless steel only or 
to have been employed by a company that predominantly worked stainless 
steel. As mentioned in section VII.B.5, the cumulative exposure 
estimates were not based on Cr(VI) air levels specifically measured in 
the cohort workers, and therefore are subject to greater uncertainty 
than exposure estimates from the chromate production cohort studies. 
Environ restricted their analysis to the ``ever stainless steel 
welders'' since that subcohort had the greater number of eligible 
subjects and person-years of follow-up, especially in the important 
lower cumulative exposure ranges. The person-years, observed numbers of 
lung cancers, and expected numbers of lung cancers were computed 
starting 20 years after the start of employment. Gerin et al. provided 
exposure-response data on welders with individual work histories (about 
two-thirds of the workers) as well as the entire subcohort. Regardless 
of subcohort examined, there was no obvious indication of a Cr(VI) 
exposure-related effect on lung cancer mortality. This may be explained 
by the

[[Page 59378]]

uncertainties in the exposure estimates and presence of co-exposures 
discussed in section VII.B.5.
    Environ used their externally standardized models, E1 to E3, to fit 
the data (Ex. 33-15). They assumed that the cumulative Cr(VI) exposure 
for the workers was at the midpoint of the reported range. A value of 
2.5 mg/m\3\-yr was assumed for the highest exposure group (e.g., >0.5 
mg/m\3\-yr), since Gerin et al. cited it as the mean value for the 
group, which they noted to also include the ``predominantly stainless 
steel welders''. All models fit the data adequately (p>0.28) with dose 
coefficients considerably lower than for the Gibb or Luippold cohorts 
(Ex. 33-15, Table 6). In fact, the maximum likelihood estimates for the 
dose coefficients were not statistically different from 0 at the p=0.05 
significance level, which would be expected when there is no exposure-
related trend.
    Environ chose the linear relative risk model, E2, as the best 
fitting model based on the AIC value. The projected excess risk of lung 
cancer from a working lifetime exposure to Cr(VI) at the current OSHA 
PEL using the preferred model E2 was 46 (95% CI: 0 to 130) cases per 
1000 workers. The maximum likelihood estimates of excess risk from 
working lifetime exposure to 1.0 [mu]g Cr(VI)/m\3\ was 0.9 (95% CI: 0 
to 2.8) cases per 1000 workers, respectively. The rather large 95 
percent confidence interval around the maximum likelihood estimate 
reflects the greater statistical uncertainty associated with risk 
estimates from the Gerin cohort. The confidence interval overlaps that 
for equivalent risk estimates from the Luippold cohort but not the Gibb 
cohort.
4. Alexander Cohort
    Environ (Ex. 33-15) did a quantitative assessment of the observed 
and expected lung cancer incidence in aerospace workers exposed to 
Cr(VI) classified into four cumulative chromate exposure groups, 
reported in Table 4 of Alexander et al. (Ex. 31-16-3). The lung cancer 
data come from a retrospective study with a small number (15) of 
observed lung cancers in a young cohort (median age of 42 years at end 
of follow-up) with a relatively short follow-up period (median nine 
years per member). The authors stated that they derived ``estimates of 
exposure to chromium [VI]'' based on the TWA measurements, but later on 
referred to ``the index of cumulative total chromate exposure (italics 
added) reported as [mu]g/m\3\ chromate TWA-years'' (Ex. 31-16-3, p. 
1254). For their analysis, Environ assumed that the cumulative 
exposures were expressed in [mu]g/m\3\-yr of Cr(VI), rather than 
chromate (CrO<INF>4</INF><SUP>-2</SUP>) or chromic acid 
(CrO<INF>3</INF>).
    Alexander et al. grouped the lung cancer data by cumulative 
exposure with and without a ten year lag period (Ex. 31-16-3). They 
found no statistically significant elevation in lung cancer incidence 
among the chromate-exposed workers or clear trend with cumulative 
chromate exposure. Environ used the externally standardized linear 
relative risk model to fit the unlagged data (Ex. 33-15). The 
additional risk model, E3, could not be applied because no person-years 
of observation were presented by Alexander et al. Environ assumed 
workers were exposed to a cumulative Cr(VI) exposure at the midpoint of 
the reported ranges. For the open-ended high exposure category, Environ 
assumed a cumulative exposure 1.5 times greater than the lower limit of 
0.18 mg/m\3\ - yr. The model did not fit the data particularly well 
(p=0.04) and the dose coefficient was considered to be 0 since positive 
values did not significantly improve the fit. This is not surprising 
considering the lack of a positive trend between lung cancer incidence 
and cumulative Cr(VI) exposure for this cohort. Possible reasons for 
the lack of a positive association between Cr(VI) exposure and lung 
cancer incidence in this cohort were previously discussed in section 
VII.B.6.
    The best estimate of excess risk of lung cancer from the Alexander 
cohort was 0 for all exposures to Cr(VI) based on the default dose 
coefficient. The upper 95 percent confidence bound on the risk was 
estimated to be 212 cases per 1000 workers from a working lifetime 
exposure to Cr(VI) at the current OSHA PEL. The upper 95 percent 
confidence bound on risk from working lifetime exposure to 1.0 mg 
Cr(VI)/m\3\ is 4.8 cases per 1000 workers. The confidence intervals 
around the risk estimates from the Alexander cohort are greater than 
those from the Gerin cohort reflecting greater statistical uncertainty. 
However, the 95 percent confidence intervals for the risk estimates 
from the Alexander cohort overlap those for equivalent risk estimates 
from both the Luippold and Gibb cohorts.
    If the cumulative exposures from Alexander et al. are assumed to be 
cumulative chromate (CrO<INF>4</INF><SUP>-2</SUP>) estimates, then 
exposures in terms of Cr(VI) would be calculated by dividing by 0.45. 
As a result, the upper confidence bound on risk would be higher by 
1/.45 = 2.2-fold, which would also be statistically consistent with the 
risk estimates based on the Gibb and Luippold data sets.

F. Summary of Risk Estimates Based on Gibb, Luippold, and Supporting 
Cohorts

    OSHA believes that the best estimates of excess lifetime lung 
cancer risks are derived from the Gibb and Luippold cohorts. These two 
cohorts have accumulated a substantial number of lung cancer deaths 
that were extensively examined in terms of cumulative Cr(VI) exposure. 
Cohort exposures were reconstructed from air measurements and job 
histories over three or four decades. The linear relative risk model 
adequately fitted the Gibb and Luippold data sets, as well as several 
other supporting data sets. Environ and NIOSH explored a variety of 
nonlinear dose-response forms, but none provided a statistically 
significant improvement over the linear relative risk model.
    The maximum likelihood estimates from a linear relative risk model 
fitted to the Gibb data are three-to five-fold higher than estimates 
based on the Luippold data at equivalent cumulative Cr(VI) exposures 
and the confidence limits around the projected risks from the two data 
sets do not overlap. This indicates that the maximum likelihood 
estimates derived from one data set are unlikely to describe the lung 
cancer mortality observed in the other data set. Despite this 
statistical inconsistency between the risk estimates, the differences 
between them are not unreasonably great given that the cohorts worked 
in different chromate production facilities and the potential 
uncertainties involved in estimating cancer risk from the data (see 
section VII.G). Since the analyses based on these two cohorts are each 
of high quality and their projected risks are reasonably close (e.g., 
well within an order of magnitude), OSHA believes the excess lifetime 
risk of lung cancer from occupational exposure to Cr(VI) is best 
represented by the range of risks that lie between maximum likelihood 
estimates of the Gibb and Luippold data sets.

[[Page 59379]]



    Table VII-8.--OSHA Estimates of Excess Lung Cancer Cases per 1000 Workers\a\ Exposed to Various Eight Hour TWA Cr(VI) With 95 Percent Confidence
                                                             Interval Comparisons by Cohort
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                       95% confidence interval on risk estimates by cohort\c\
                                                                   Best    -----------------------------------------------------------------------------
                     Cr(VI) ([mu]g/m\3\)                        estimates       Featured cohorts                      Supporting cohorts
                                                                of risk\b\ -----------------------------------------------------------------------------
                                                                                Gibb       Luippold     Mancuso       Hayes        Guerin     Alexander
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.25.........................................................     0.52-2.3      1.0-3.9    0.31-0.79      1.0-2.7    0.31-0.75      0.0-0.7      0.0-1.2
0.5..........................................................      1.0-4.6      2.0-7.8     0.62-1.6      2.0-5.4     0.62-1.5      0.0-1.4      0.0-2.4
1.0..........................................................      2.1-9.1       4.0-16      1.2-3.1       4.1-11      1.2-3.0      0.0-2.8      0.0-4.8
2.5..........................................................       5.2-23        10-37      3.1-7.8        10-27      3.1-7.5      0.0-6.9       0.0-12
5.0..........................................................        10-45        20-75       6.2-15        20-52       6.1-15       0.0-14       0.0-24
10...........................................................        21-86       39-142        12-31          n/a        12-30       0.0-29       0.0-50
20...........................................................       41-163       76-256        21-60          n/a        24-51       0.0-54       0.0-91
52...........................................................      101-351      181-493       62-147      188-403       61-141      0.0-130     0.0-212
--------------------------------------------------------------------------------------------------------------------------------------------------------
\a\ The workers are assumed to start work at age 20 and continue to work for 45 years, at a constant exposure level. All estimates were recalculated
  using year 2000 U.S. reference rates, all races, both sexes, for lung cancer and all causes, except for those from Mancuso, for which 1998 rates were
  used.
\b\ OSHA preliminarily finds that the estimates of risk best supported by the scientific evidence are the ranges bounded by the maximum likelihood
  estimates from the linear relative risk models presented in Table VII-3 (Baltimore reference population/exposure grouping with equal person-years) for
  the Gibb cohort and Table VII-7 for the Luippold cohort.
\c\ The confidence intervals for the Gibb and Luippold cohorts are from Tables VII-3 and VII-7. The confidence intervals for the Mancuso, Guerin and
  Alexander cohorts are derived from parameters reported by Environ (2002, Ex. 33-15). All are from the best fitting linear relative risk models and are
  95% confidence intervals. The confidence interval for the Hayes cohort was calculated from the 90 percent confidence interval on the dose coefficient
  for the linear relative risk model reported by the K.S. Crump Division (1995, Ex. 13-5).

    OSHA's best estimates of excess lung cancer cases from a 45-year 
working lifetime exposure to Cr(VI) are presented in Table VII-8. This 
range of projected risks lie between the maximum likelihood estimates 
derived from the Gibb and Luippold data sets. As previously discussed, 
several acceptable assessments of the Gibb data set were performed, 
with similar results. The 2003 Environ model E1, applying the Baltimore 
City reference population and ten exposure categories based on a 
roughly equal number of person-years per group, was selected to 
represent the range of best risk estimates derived from the Gibb 
cohort, in part because this assessment employed an approach most 
consistent with the exposure grouping applied in the Luippold analysis 
(see Table VII-7). To characterize the statistical uncertainty of 
OSHA's risk estimates, Table VII-8 also presents the 95% confidence 
limits associated with the maximum likelihood risk estimates from the 
Gibb cohort and the Luippold cohort. The confidence interval on the 
risk estimates from the Luippold data set is smaller (i.e., just over a 
two-fold range) than those for the Gibb data set (i.e., about a 3.5-
fold range) but the Gibb cohort is larger. Therefore, it appears 
reasonable to consider both analyses jointly in providing estimates of 
lung cancer risk.
    OSHA finds that the most likely lifetime excess risk at the current 
PEL of 52 [mu]g/m\3\ Cr(VI) lies between 101 per 1000 and 351 per 1000, 
as shown in Table VII-8. That is, OSHA predicts that between 101 and 
351 of 1000 workers occupationally exposed for 45 years at the current 
PEL would develop lung cancer as a result of their exposure. The wider 
range of 62 per 1000 (lower 95% confidence bound, Luippold cohort) to 
493 per 1000 (upper 95% confidence bound, Gibb cohort) illustrates the 
range of risks considered statistically plausible, based on these 
cohorts and, thus, represents the statistical uncertainty in the 
estimates of lung cancer risk. This range of risks roughly falls 
proportionally with exposure so that estimates at 5 [mu]g/m\3\ are 
about 10 to 45 cases per 1000 workers and estimates at 0.5 [mu]g/m\3\ 
are about 1 to 4.5 cases per 1000 workers.
    The 95 percent confidence limits on estimates of risk for the four 
supporting cohort data sets are also presented in Table VII-8. As 
discussed previously, the exposure-response data from supporting 
cohorts are not as strong as those from the two featured cohorts. The 
cumulative Cr(VI) exposure reconstructions in these data sets were 
based on more limited air measurements and were frequently not linked 
to cohort workers on an individual basis. Some of the cohort data sets 
were weaker in terms of either number of workers, length of follow-up, 
documented mortality data, and possibility of co-exposures or a healthy 
worker survivor effect. These features may have introduced bias into 
the estimates of risk determined from the studies. However, observed 
lung cancers were grouped across multiple exposure groups in these more 
problematic cohorts that allowed quantitative assessments to be done 
and compared against the stronger Gibb and Luippold cohorts.
    OSHA believes the supplemental assessments support the range of 
projected excess lung cancer risks from the Gibb and Luippold cohorts. 
This is illustrated by the 95 percent confidence intervals shown in 
Table VII-8. The confidence interval encompasses those risk estimates 
that are consistent with the cohort data to a certainty of 95 percent. 
The confidence intervals tend to be smaller for the larger data sets 
and better model fits. OSHA's range of best risk estimates for a given 
occupational Cr(VI) exposure overlap the 95 percent confidence bands 
for each of the four supporting cohorts. This indicates that the range 
of best estimates includes risks with a statistical precision that is 
compatible with all the exposure-response data sets, including the 
smaller Gerin and Alexander cohorts where the lung cancers did not show 
a clear positive trend with cumulative Cr(VI) exposure.
    The 95 percent confidence intervals from the four supporting 
cohorts overlap those of either the Gibb or Luippold cohorts (or both). 
The confidence intervals for estimates of the Mancuso cohort overlap 
with those of the Gibb cohort but are higher than those of the Luippold 
cohort. The risks projected from the Mancuso data set are likely 
overestimated because they depend on air monitoring conducted near the 
end of the study period when exposures were likely lower and because 
the sampling method only captured highly soluble Cr(VI) compounds. The 
Mancuso cohort was also probably exposed to significant

[[Page 59380]]

amounts of the more potent slightly soluble and insoluble chromates 
(e.g., calcium chromate). The relative potency of Cr(VI) compounds is 
further discussed in section VII.G.4. The confidence intervals for 
estimates from the Hayes cohort overlap the Luippold cohort but are 
lower than those of the Gibb cohort. The risks projected from the Hayes 
cohort may be low because the cumulative exposure estimates rely on air 
monitoring near the beginning of the study period when Cr(VI) levels 
were likely higher. The confidence intervals for estimates from the 
Gerin cohort also overlap those from the Luippold but not the Gibb 
cohort. The confidence intervals for estimates from the Alexander 
cohort overlap those from both featured cohorts.
    While there is statistical consistency between the range of best 
risk estimates based on the primary studies and those estimated from 
the supporting data sets, the risk analysis does not account for 
potential bias introduced by the lack of exposure data, inadequate 
follow-up and other limitations in these weaker studies. Unfortunately, 
the magnitude and direction of this potential bias cannot be reasonably 
assessed and, thus, the impacts on the risk estimates are unclear.
    It would be difficult to formally combine the data or the results 
(e.g., parameter estimates) from the six studies considered for 
quantitative analysis. The inclusion criteria (e.g., duration of 
employment required for entry into the cohorts) differed from study to 
study. Moreover, the reported cumulative exposure categories were based 
on different lag periods before accumulation of exposure began. 
Nevertheless, the lung cancer risks derived from all the data sets, as 
a group, support the range of best estimates derived from the two 
featured cohorts.

G. Issues and Uncertainties

    The risk estimates presented in the previous sections include 
confidence limits that reflect statistical uncertainty. This 
statistical uncertainty concerns the limits of precision for 
statistical inference, given assumptions about the input parameters and 
risk models (e.g., exposure estimates, observed lung cancer cases, 
expected lung cancer cases, linear dose-response). However, there are 
uncertainties with regard to the above input and assumptions, not so 
easily quantified, that may impact the degree of confidence in the OSHA 
risk estimates. Some of these uncertainties are discussed below.
1. Uncertainty With Regard to Worker Exposure to Cr(VI)
    The uncertainty that may have the greatest impact on risk estimates 
relates to the assessment of worker exposure. Even for the Gibb cohort, 
whose exposures were estimated from roughly 70,000 air measurements 
over a 35-year period, the calculation of cumulative exposure is 
inherently uncertain. The methods used to measure airborne Cr(VI) did 
not characterize particle size that determines deposition in the 
respiratory tract (see section VI.A.). Workers differ from one another 
with respect to working habits and they may have worked in different 
areas in relation to where samples are taken. Inter-individual (and 
intra-facility) variability in cumulative exposure can only be 
characterized to a limited degree, even with extensive measurement. The 
impact of such variability is likely less for estimates of long-term 
average exposures when there were more extensive measurements in the 
Gibb and Luippold cohorts in the 1960s through 1980s, but could affect 
the reliability of estimates in the 1940s and 1950s when air monitoring 
was done less frequently. Exposure estimates that rely on annual 
average air concentrations are also less likely to reliably 
characterize the Cr(VI) exposure to workers who are employed for short 
periods of time. This may be particularly true for the Gibb cohort in 
which a sizable fraction of cohort members were employed for only a few 
months.
    Like many retrospective cohort studies, the frequency and methods 
used to monitor Cr(VI) concentrations may also be a source of 
uncertainty in reconstructing past exposures to the Gibb and Luippold 
cohorts. Exposures to the Gibb cohort in the Baltimore plant from 1950 
until 1961 were determined based on periodic collection of samples of 
airborne dust using high volume sampling pumps and impingers that were 
held in the breathing zone of the worker for relatively short periods 
of time (e.g., tens of minutes) (Ex. 31-22-11). High volume sampling 
with impingers to collect Cr(VI) samples may have underestimated 
exposure since the accuracy of these devices depended on an air flow 
low enough to ensure efficient Cr(VI) capture, the absence of agents 
capable of reducing Cr(VI) to Cr(III), the proper storage of the 
collected samples, and the ability of short-term collections to 
accurately represent full-shift worker exposures. Further, impingers 
would not adequately capture any insoluble forms of Cr(VI) present, 
although other survey methods indicated minimal levels of insoluble 
Cr(VI) were produced at Baltimore facility (Ex. 13-18-14).
    In the 1960s, the Baltimore plant expanded its Cr(VI) air 
monitoring program beyond periodic high volume sampling to include 
extensive area monitoring in 27 exposure zones around the facility. 
Multiple short-term samples were collected (e.g., twelve one-hour or 
eight three-hour samples) on cellulose tape for an entire 24 hour 
period and analyzed for Cr(VI). Studies have shown that Cr(VI) can be 
reduced to Cr(III) on cellulose filters under certain circumstances so 
there is potential for underestimation of Cr(VI) using this collection 
method. Gibb et al. reported that the full set of monitoring data 
records was not accessible prior to 1971. The area monitoring was 
supplemented by routine full-shift personal monitoring of workers 
starting in 1977. The 24-hour area sampling supplemented with personal 
monitoring was continued until plant closure in 1985.
    The Exponent critique of the Gibb cohort suggested that the tape 
samplers used in the Baltimore plant from the mid-1960s to 1985 
resulted in reduction of Cr(VI) to Cr(III) and that Braver et al. 
excluded these measurements from their analyses because of concerns 
about underestimation of Cr(VI) concentration (Ex. 31-18-14). While 
there may be some potential for Cr(VI) reduction on these tape 
samplers, Gibb et al. reported that the tape measurements did not 
significantly differ from personal breathing zone air measurements 
``for approximately two-thirds of the job titles with sufficient number 
of samples to make the comparison'' (Ex. 31-22-11, p. 118). 
Furthermore, Gibb et al. reported that exposure estimates from the area 
tape sampling system were adjusted to an equivalent personal exposure 
estimate using job-specific ratios of the mean area and personal 
breathing estimates determined during the 1978-1985 time period when 
both were in operation (Ex. 31-22-11, p. 117). Any potential exposure 
underestimation of Cr(VI) by the tape sampling system should be 
minimized by this correction procedure. Braver et al. considered the 
usual post-1960 Cr(VI) exposures of 31 ug/m3 to be ``less credible 
because they were very low'' compared to prior time periods (e.g., pre-
1950s) and, therefore, excluded workers exposed after 1960 from their 
exposure assessment (Ex. 7-17, p. 372). However, this exposure level 
turned out to be very consistent with the more extensive Cr(VI) 
concentrations later reported by Gibb et al. (Ex. 31-22-11) and Proctor 
et al. (Ex. 35-61) for

[[Page 59381]]

chromate production plants in the 1960s and 1970s.
    Some of the same uncertainties exist in reconstructing exposures 
from the Luippold cohort. Exposure monitoring from operations at the 
Painesville plant in the 1940s and early 1950s was sparse and consisted 
of industrial hygiene surveys conducted by various groups (Ex. 35-61). 
The United States Public Health Service (USPHS) conducted two 
industrial hygiene surveys (1943 and 1951), as did the Metropolitan 
Life Insurance Company (1945 and 1948). The Ohio Department of Health 
(ODH) conducted surveys in 1949 and 1950. The most detailed exposure 
information was available in annual surveys conducted by the Diamond 
Alkali Company (DAC) from 1955 to 1971. Exponent chose not to consider 
the ODH data in their analysis since the airborne Cr(VI) concentrations 
reported in these surveys were considerably lower than values measured 
at later dates by DAC. Excluding the ODH survey data in the exposure 
reconstruction process may have led to higher worker exposure estimates 
and lower predicted lung cancer risks.
    There were uncertainties associated with the early Cr(VI) exposure 
estimates for the Painesville cohort. Like the monitoring in the 
Baltimore plant, Cr(VI) exposure levels were determined from periodic 
short-term, high volume sampling with impingers that may have 
underestimated exposures (Ex. 35-61). Since the Painesville plant 
employed a ``high-lime'' roasting process to produce soluble Cr(VI) 
from chromite ore, a significant amount of slightly soluble and 
insoluble Cr(VI) was formed. It was estimated that up to approximately 
20 percent of the airborne Cr(VI) was in the less soluble form in some 
areas of the plant prior to 1950 (Ex. 35-61). The impingers were 
unlikely to have captured this less soluble Cr(VI) so some reported 
Cr(VI) air concentrations may have been slightly underestimated for 
this reason.
    The annual air monitoring program at the Painesville plant was 
upgraded in 1966 in order to evaluate a full 24 hour period (Ex. 35-
61). Unlike the continuous monitoring at the Baltimore plant, twelve 
area air samples from sites throughout the plant were collected for 
only 35 minutes every two hours using two in-series midget impingers 
containing water. The more frequent monitoring using the in-series 
impinger procedure may be an improvement over previous high-volume 
sampling and is believed to be less susceptible to Cr(VI) reduction 
than cellulose filters. While the impinger collection method at the 
Painesville plant may have reduced one source of potential exposure 
uncertainty, another source of potential uncertainty was introduced by 
failure to collect air samples for more than 40 percent of the work 
period. Also, personal monitoring of workers was not conducted at any 
time.
    Another type of uncertainty is associated with extrapolation from 
one exposure pattern to another (e.g., different combinations of 
exposure duration and Cr(VI) air concentrations). Both Gibb et al. and 
Luippold et al. found that lung cancer mortality showed a significant 
trend with cumulative Cr(VI) exposure, which is being employed by OSHA 
as the exposure metric of choice in its quantitative risk assessments. 
However, the Cr(VI) exposure levels experienced by the cohorts were 
higher (e.g., 5 to 10,000 [mu]g/m<SUP>3</SUP>) than for some of the 
lower exposure scenarios (e.g., 0.25 to 2.5 [mu]g/m<SUP>3</SUP>) of 
interest to OSHA. The cohorts were also exposed for a considerably 
shorter duration than a 45-year working lifetime. Uncertainties arise 
when extrapolating risks for Cr(VI) concentrations and exposure 
durations outside the experience of the cohort data, even when 
cumulative exposures are similar.
    There are several examples in which an increasing relative risk of 
chronic disease has been observed to attenuate (e.g., the slope of the 
exposure-response lessens) at high cumulative exposures (Ex. 35-55). A 
variety of reasons can cause this behavior including the healthy worker 
survivor effect previously discussed, a limit on the relative risk that 
can be achieved for diseases with a high background rate (e.g., lung 
cancer), and misclassification of exposure. Since the cumulative 
exposure for a full working lifetime at the current OSHA PEL is higher 
than observed in almost all workers from the Gibb cohort and most of 
the Luippold cohort, it is possible that a linear relative risk model 
might overpredict the excess risk at this exposure if there were a 
significant attenuation in the slope of the exposure-response.
    In order to evaluate the likelihood of an attenuated relative risk 
of lung cancer at high cumulative Cr(VI) exposures, Environ fit the 
Gibb and Luippold data sets to a power model of the form:


Relative Risk = E(1 + bd<SUP>C</SUP>)

where E was the expected number of lung cancer deaths, d is the 
cumulative exposure, and b and c were parameters to be estimated (Ex. 
36-2). The parameter, c, was allowed to be less than 1, which would 
accommodate a decreasing slope in the exposure-response with increasing 
cumulative exposure. Of course, the power model assumes a linear shape, 
if c = 1. The power model fit to the two primary data sets produced 
maximum likelihood estimates of 0.61 and 0.66 for the Gibb and Luippold 
data sets, respectively. However, the power models did not 
significantly improve the fit compared to the linear model (p = 0.41 
and 0.14 for Gibb and Luippold, respectively). This is consistent with 
the conclusions of NIOSH and Exponent who also reported that departure 
from linearity in the exposure-response was not significant for these 
data sets (Exs. 33-13; 33-12). In light of the above analyses, OSHA 
does not find adequate reason to believe a linear relative risk model 
overpredicts the lung cancer risk for a full working lifetime at the 
OSHA PEL. This is especially true since this Cr(VI) exposure is well 
within the range of cumulative exposures experienced by workers in the 
Luippold cohort.
    While the cumulative Cr(VI) exposure estimates determined from the 
Gibb and Luippold cohorts are much more extensive than usually 
available for a cancer cohort, they are still a primary source of 
uncertainty in the assessment of risk. As occurs in many retrospective 
cancer epidemiologic studies, it was difficult to reconstruct worker 
exposure in the 1950s from the limited air monitoring data available 
from the Painesville and Baltimore plants. It appears that the usual 
airborne Cr(VI) exposure levels in some chromate production and 
processing areas at these facilities dropped five to ten-fold from the 
late 1940s to the mid-1960s with little documentation in the 
intervening years. This required more indirect methods to complete the 
job-exposure matrices for these cohorts. The need to reconstruct cohort 
exposure in the absence of extensive air measurements combined with the 
different procedures used to collect air samples at the two plants 
could partially explain the slight but statistically different 
exposure-specific risks between the Gibb and Luippold cohorts. Finally, 
some uncertainty in risk is introduced when extrapolating cohort 
exposures to higher Cr(VI) levels for shorter periods to an equivalent 
cumulative exposure of lower intensity for a longer duration (e.g., 45 
year exposure to 0.25 [mu]g/m<SUP>3</SUP>). Despite the uncertainties, 
the exposure estimates from the Gibb et al. and Luippold et al. studies 
are derived from the best available data and better than is generally 
found in retrospective cohort studies. They are more than adequate to 
assess occupational risk to

[[Page 59382]]

Cr(VI) and OSHA does not believe the potential inaccuracies in the 
exposure assessment for either cohort are large enough to result in 
serious overprediction or underprediction of risk.
2. Model Uncertainty, Exposure Threshold, and Dose Rate Effects
    The models used to fit the observed data may also introduce 
uncertainty into the quantitative predictions of risk. Linear and non-
linear risk models based on a Poisson distribution were applied to the 
exposure-response data sets. Both Environ (Ex. 33-12) and NIOSH (Ex. 
33-13) evaluated nonlinear models among the suite of models fit to the 
Gibb et al. cohort data. These included quadratic, log-linear, log-
square-root, and log-quadratic models as well as models that included 
cumulative dose raised to some power. Cox proportional hazard models 
were also applied to the data. Linear models generally fit the 
exposure-response data better than the nonlinear models. For most data 
sets, there was no indication that any model more elaborate than a 
linear model was necessary to describe the exposure-response patterns 
observed in these cohorts.
    The linear relative risk model was used to estimate excess lung 
cancer risks at cumulative Cr(VI) exposures in the range of 0.01 to 2.3 
mg/m<SUP>3</SUP>-yr (i.e., 0.25-52 [mu]g/m<SUP>3</SUP> for 45 years) 
which, to a large extent, overlap the cumulative exposures experienced 
of workers in either the Gibb or Luippold cohorts. Certainly, 
cumulative exposures above 0.1 mg/m<SUP>3</SUP>-yrs (e.g., 2.5 [mu]g/
m<SUP>3</SUP> for 45 years) are within the exposure range of both 
studies. Since risks were estimated at cumulative exposures generally 
within the range of the data represented in the preferred cohorts, they 
are less susceptible to dose-extrapolation uncertainties and less 
susceptible to model misspecification. Thus, OSHA believes that the use 
of a linear model is a reasonable and appropriate basis on which to 
calculate lung cancer risks at the cumulative occupational exposures of 
interest, especially given the consistency in the results from fitting 
the linear model across most of the studies.
    In their response to the OSHA Request For Information regarding 
occupational exposure to Cr(VI), the Chrome Coalition submitted 
comments, prepared by Exponent, suggesting that a threshold dose-
response model is an appropriate approach to estimate lung cancer risk 
from Cr(VI) exposures (Ex. 31-18-1). Their arguments rely on: (1) The 
lack of a statistically significant increased lung cancer risk for 
workers exposed below a cumulative Cr(VI) exposure of 1.0 mg/
m<SUP>3</SUP>-yr (e.g., roughly equivalent to 20 [mu]g/m<SUP>3</SUP> 
TWA for a 45 year working lifetime) and below ``a highest reported 
eight hour average'' Cr(VI) concentration of 52 [mu]g/m<SUP>3</SUP> 
(i.e., OSHA PEL); (2) the presumed existence of ``an overall reducing 
capacity'' within the lung for extracellular reduction of Cr(VI) to 
Cr(III) that must be exceeded before Cr(VI) can damage cellular DNA, 
and (3) a reported dose rate effect for lung tumor development in rats 
exposed to Cr(VI) by long-term, repeated intratracheal instillations.
    The lack of a statistically significant result for a subset of the 
entire cohort should not be construed to imply a threshold. As pointed 
out in an earlier discussion (section VII.D) and by Crump et al., the 
Luippold data set does not have the statistical power to detect small 
increases in risk that may be associated with the lower cumulative 
exposures in the cohort (Ex. 35-58). In their report, Exponent 
acknowledges that the non-significant increase in lung cancer deaths in 
the Luippold cohort below 1.25 mg Cr(VI)/m<SUP>3</SUP>-yr cumulative 
exposure is consistent with predictions from a linear relative risk 
model (Ex. 31-18-1, p.25).
    The Chrome Coalition characterized the work of De Flora et al. as 
providing convincing support for the existence of a threshold exposure 
(i.e., exposure below which the probability of disease is zero) for 
Cr(VI) carcinogenicity. De Flora et al. determined the amount of 
soluble Cr(VI) reduced to Cr(III) in vitro by human bronchioalveolar 
fluid and pulmonary alveolar macrophage fractions over a short period 
(Ex. 31-18-7). These specific activities were used to estimate an 
``overall reducing capacity'' of 0.9-1.8 mg Cr(VI) and 136 mg Cr(VI) 
per day per individual for the two preparations, respectively. As 
discussed in Health Effects section VI.A., cell membranes are permeable 
to Cr(VI) but not Cr(III), so only Cr(VI) enters cells to any 
appreciable extent. De Flora et al. interpreted these data to mean that 
high levels of Cr(VI) would be required to ``overwhelm'' the reduction 
capacity before significant amounts of Cr(VI) could enter lung cells 
and damage DNA, thus creating a biological threshold to the exposure-
response (Ex. 31-18-8).
    There are several problems with the threshold interpretation of De 
Flora et al. The in vitro reducing capacities were determined in the 
absence of cell uptake. Cr(VI) uptake into lung cells happens 
concurrently and in parallel with its extracellular reduction, so it 
cannot be concluded from the De Flora data that a threshold reduction 
capacity must be exceeded before uptake occurs. The rate of Cr(VI) 
reduction to Cr(III) is critically dependant on the presence of 
adequate amounts of reductant, such as ascorbate or GSH (Ex. 35-65). It 
has not been established that sufficient amounts of these reductants 
are present throughout the thoracic and alveolar regions of the 
respiratory tract to create a biological threshold. Moreover, the in 
vitro activity of Cr(VI) reduction in epithelial lining fluid and 
alveolar macrophages was shown to be highly variable among individuals 
(Ex. 31-18-7, p. 533). It is possible that Cr(VI) is not rapidly 
reduced to Cr(III) in some workers or some areas of the lung. Finally, 
even if there was an exposure threshold created by extracellular 
reduction, the De Flora data do not establish the dose range in which 
the putative threshold would occur. It has already been shown that a 
physiological concentration of ascorbate substantially reduces, but may 
not eliminate, the uptake in cells treated with low M concentrations of 
Cr(VI) for 24 hours (Ex. 35-68). OSHA does not believe that there is 
sufficient scientific evidence to support the Chrome Coalition 
conclusion that the De Flora data ``suggest a linear, non-threshold 
model to predict cancer risk at low exposure levels [at least, those 
being considered by OSHA] is overly conservative and inappropriate'' 
(Ex. 31-18-1, p.2).
    The Chrome Coalition has stated that the intratracheal instillation 
study in rats by Steinhoff et al. ``suggests that there is likely a 
threshold exposure level below which there is no increase in lung 
cancer risk, and that the threshold is compound-specific.'' (Ex. 31-18-
1, p. 2). The Steinhoff study is discussed in detail in section VI.B. 
on carcinogenic effects. Briefly, the study showed that rats 
intratracheally administered 1.25 mg/kg of soluble sodium dichromate or 
slightly soluble calcium chromate once a week for 30 months developed 
significant increases (about 17 percent incidence) in lung tumors (Ex. 
11-7). The same total dose administered more frequently (e.g., five 
times weekly) at a five-fold lower dose level did not increase lung 
tumor incidence in the sodium dichromate-treated rats and significantly 
increased lung tumor incidence (about 7.5 percent) in the calcium 
chromate-treated rats by only about half as much as rats that received 
the greater dose level.
    OSHA does not believe that the accelerated tumor development at the 
high Cr(VI) dose levels in the Steinhoff et al. study ``clearly support 
that there is a threshold for Cr(VI) exposures'' or indicate that 
``peak exposures high enough to overload the reductive capacity of the 
lung may be a better

[[Page 59383]]

predictor of lung cancer risk than lifetime cumulative exposure'' as 
stated by Chrome Coalition (Ex. 31-18-1, p. 31). Rather, OSHA believes 
these findings should be interpreted to suggest that Cr(VI)-induced 
carcinogenesis is influenced not only by the total Cr(VI) dose retained 
in the respiratory tract but also by the rate at which the dose is 
administered. For example, the highest dose level (i.e., 1.25 mg/kg) in 
the study was reported to cause moderate to severe lung damage, 
including inflammation and hyperplasia. It is likely that these effects 
caused a proliferative stimulus that accelerated the neoplastic 
transformation and expansion of initiated (i.e., genetically altered) 
cells. The Steinhoff et al. study also suggests that lung damage is not 
an absolute requirement for Cr(VI)-induced tumorigenesis. This is 
illustrated by the significant, but smaller, increased tumor incidence 
in the animals receiving a lower dose level (i.e., 0.25 mg/kg) of 
Cr(VI), as calcium chromate, that caused relatively minor non-
neoplastic changes in the lungs.
    OSHA believes that the existence of dose rate effects is supported 
by the available scientific evidence and may introduce uncertainty when 
projecting lung cancer risk based on workers exposed to higher Cr(VI) 
concentrations for shorter durations to workers exposed to the same 
cumulative exposure but at substantially lower Cr(VI) concentrations 
for substantially longer periods. However, the Steinhoff et al. study 
instilled the Cr(VI) compounds directly on the trachea rather than 
introduce the test compound by inhalation and was only able to 
characterize a significant dose rate effect at one cumulative dose 
level (e.g., 1.25 mg/kg). For these reasons, OSHA considers the data 
inadequate to reliably determine the human exposures where a dose rate 
effect might occur and to confidently predict its magnitude.
    OSHA solicits comment on the whether the linear relative risk model 
is the most appropriate approach on which to estimate risk associated 
with occupational exposure to Cr(VI). OSHA is particularly interested 
in whether there is convincing scientific evidence of a non-linear 
exposure-response relationship and, if so, whether there are sufficient 
data to develop a non-linear model that would provide more reliable 
risk estimates than the linear approach being used in the preliminary 
assessment.
3. Influence of Smoking, Race, and the Healthy Worker Survivor Effect
    A common confounder in estimating lung cancer risk to workers from 
exposure to a specific agent such as Cr(VI) is the impact of cigarette 
smoking. First, cigarette smoking is known to cause lung cancer. 
Ideally, lung cancer risk attributable to smoking among the Cr(VI)-
exposed cohorts should be controlled or adjusted for in characterizing 
exposure-response. Secondly, cigarette smoking may interact with the 
agent (i.e., Cr(VI)) or its biological target (i.e., susceptible lung 
cells) in a manner that enhances or even reduces the risk of developing 
Cr(VI)-induced lung cancer from occupational exposures, yet is not 
accounted for in the risk model.
    OSHA believes its risk estimates have adequately accounted for the 
potential confounding effects of cigarette smoking in the underlying 
exposure-lung cancer response data, particularly for the Gibb cohort. 
One of the key issues in this regard is whether or not the reference 
population utilized to derive the expected number of lung cancers 
appropriately reflects the smoking behavior of the cohort members. The 
risk analyses of the Gibb cohort by NIOSH and Environ indicate that 
cigarette smoking was properly controlled for in the exposure-response 
modeling. NIOSH applied a smoking-specific correction factor that 
included a cumulative smoking term for individual cohort members 
(Ex.33-13). Environ applied a generic correction factor and used lung 
cancer mortality rates from Baltimore City as a reference population 
that was most similar to the cohort members with respect to smoking 
behavior and other factors that might affect lung cancer rates (Ex. 33-
12). Environ also used internally standardized models that did not 
require use of a reference population and included a smoking-specific 
(yes/no) variable. All these models predicted very similar estimates of 
risk over a wide range of Cr(VI) exposures. There was less information 
about smoking status for the Luippold cohort. However, regression 
modeling that controlled for smoking indicated that it was not a 
significant confounding factor when relating Cr(VI) exposure to the 
lung cancer mortality (Ex. 35-58).
    Smoking has been shown to interact in a synergistic manner (i.e., 
combined effect of two agents are greater than the sum of either agent 
alone) with some lung carcinogens, most notably asbestos (Ex. 35-114). 
NIOSH reported a slightly negative but nonsignificant interaction 
between cumulative Cr(VI) exposure and smoking in a model that had 
separate linear terms for both variables (Ex. 33-13). This means that, 
at any age, the smoking and Cr(VI) contributions to the lung cancer 
risk appeared to be additive, rather than synergistic, given the 
limited smoking information in the Gibb cohort along with the 
cumulative smoking assumptions of the analysis. In their final linear 
relative risk model, NIOSH included smoking as a multiplicative term in 
the background rate in order to estimate lifetime lung cancer risks 
attributable to Cr(VI) independent of smoking. Although this linear 
relative risk model makes no explicit assumptions with regard to an 
interaction between smoking and Cr(VI) exposure, the model does assume 
a multiplicative relationship between the background rate of lung 
cancer in the reference population and Cr(VI) exposure. Therefore, to 
the extent that smoking is a predominant influence on the background 
lung cancer risk, the linear relative risk model implicitly assumes a 
multiplicative (e.g., greater than additive and synergistic, in most 
situations) relationship between cumulative Cr(VI) exposure and 
smoking. Since current lung cancer rates reflect a mixture of smokers 
and non-smokers, it is reasonable to expect that the excess lung cancer 
risks from Cr(VI) exposure predicted by the linear relative risk model 
to overestimate the risks to non-smokers to some unknown extent. By the 
same token, the model may underestimate the risk from Cr(VI) exposure 
to a heavy smoker. Because there were so few non-smokers in the study 
cohorts (e.g., approximately 15 percent of the exposed workers and four 
lung cancer deaths in the Gibb cohort), it was not possible to reliably 
estimate risk for this subpopulation.
    Although OSHA is not aware of any convincing evidence of a specific 
interaction between cigarette smoking and Cr(VI) exposure, prolonged 
cigarette smoking does have profound effects on lung structure and 
function that may indirectly influence lung cancer risk from Cr(VI) 
exposure . Cigarette smoke is known to cause chronic irritation and 
inflammation of the respiratory tract. This leads to decreases in 
airway diameter that could result in an increase in Cr(VI) particulate 
deposition. It also leads to increased mucous volume and decreased 
mucous flow, that could result in reduced Cr(VI) particulate clearance. 
Increased deposition and reduced clearance would mean greater residence 
time of Cr(VI) particulates in the respiratory tract and a potentially 
greater probability of developing bronchogenic cancer. Chronic 
cigarette

[[Page 59384]]

smoking also leads to lung remodeling and changes in the proliferative 
state of lung cells that could influence susceptibility to neoplastic 
transformation. While the above effects are plausible consequences of 
cigarette smoking on Cr(VI)-induced carcinogenesis, the likelihood and 
magnitude of their occurrence have not been firmly established and, 
thus, the impact on risk of lung cancer in workers is uncertain.
    Differences in lung cancer incidence with race may also introduce 
uncertainty in risk estimates. Gibb et al. reported differing patterns 
for the cumulative exposure-lung cancer mortality response between 
whites and non-whites in their cohort of chromate production workers 
(Ex. 31-22-11). In the assessment of risk from the Gibb cohort, NIOSH 
reported a strong interaction between cumulative Cr(VI) exposure and 
race, such that nonwhites had a higher cumulative exposure coefficient 
(i.e., higher lung cancer risk) than whites based on a linear relative 
risk model (Ex. 33-13). If valid, this might explain the slightly lower 
risk estimates in the predominantly white Luippold cohort. However, 
Environ found that including race as an explanatory variable in the Cox 
proportional hazards model C1 did not significantly improve model fit 
(p=0.15) once cumulative Cr(VI) exposure and smoking status had been 
considered (Ex. 33-12).
    NIOSH suggested that exposure or smoking misclassification might 
plausibly account for the Cr(VI) exposure-related differences in lung 
cancer by race seen in the Gibb cohort (Ex. 33-13, p. 15). It is 
possible that such misclassification might have occurred as a result of 
systematic differences between whites and non-whites with respect to 
job-specific Cr(VI) exposures at the Baltimore plant, unrecorded 
exposure to Cr(VI) or other lung carcinogens when not working at the 
plant, or in smoking behavior. Unknown racial differences in biological 
processes critical to Cr(VI)-induced carcinogenesis could also 
plausibly account for an exposure-race interaction. However, OSHA is 
not aware of evidence that convincingly supports any of these possible 
explanations.
    Another source of uncertainty that may impact the risk estimates is 
the healthy worker survivor effect. Studies have consistently shown 
that short-term employed workers have higher mortality rates than 
workers with long-term employment status. This is possibly due to a 
higher proportion of ill individuals and those with a less healthy 
lifestyle (Ex. 35-60). As a result, exposure-response analyses based on 
mortality of long-term healthy workers will tend underestimate the risk 
to short-term workers and vice versa, even when their cumulative 
exposure is similar. This might partially explain the higher risk 
estimates from the Gibb data set relative to the Luippold data set for 
the same cumulative exposures using similar risk models. The Gibb 
cohort contained a higher proportion of workers with short duration of 
employment, lower cumulative Cr(VI) exposure, and is arguably more 
prone to mortality. On the other hand, the Luippold cohort consisted of 
longer-term workers at higher cumulative exposures that may be more 
prone to negative confounding as a result of the survivor effect. The 
healthy worker survivor effect is thought to be less of a factor in 
diseases with a multifactorial causation and long onset, such as 
cancer.
4. Potency Considerations of Different Cr(VI) Compounds
    An issue that needs to be addressed is whether the excess lung 
cancer risks derived from epidemiologic data for chromate production 
workers are representative of the risks for other Cr(VI)-exposed 
workers (e.g., plating, painting, welding operations). Typically, OSHA 
has used epidemiologic studies from one industry to estimate risk for 
other industries. In many cases, this approach is acceptable because it 
is exposure to a common agent of concern that is the primary 
determinant of risk and not some other factor unique to the workplace. 
However, in the case of Cr(VI), workers in different industries are 
exposed to various Cr(VI) compounds that differ in carcinogenic potency 
depending to a large extent on water solubility. The chromate 
production workers in the Gibb and Luippold cohorts were primarily 
exposed to certain highly water-soluble chromates. As more fully 
described in section VI.B. of the Cancer Effects section and summarized 
below, the scientific evidence indicates that the carcinogenic potency 
of the highly water-soluble chromates is likely lower than the potency 
of other less water-soluble Cr(VI) compounds. Therefore, OSHA believes 
that the lung cancer risk of workers in other industries exposed to 
equivalent levels of Cr(VI) will be of similar magnitude, or possibly 
even greater in the case of some workers exposed to certain Cr(VI) 
compounds, than the risks projected from chromate production workers in 
the Gibb and Luippold cohorts.
    The primary operation at the plants in Painesville and Baltimore 
was the production of the water-soluble sodium dichromate from which 
other primarily water-soluble chromates such as sodium chromate, 
potassium dichromate, and chromic acid could be made (Exs. 7-14; 35-
61). Therefore, it is likely that the Gibb and Luippold cohorts were 
principally exposed to water-soluble Cr(VI). The Painesville plant used 
a high-lime process known to form some less water-soluble Cr(VI) 
compounds (Ex. 35-61). Less water-soluble chromates is a designation 
that refers to all chromates not considered to be highly water soluble 
and readily captured by an aqueous impinger sampling device. These 
would include both slightly water-soluble chromates, such as calcium 
and strontium chromate and the more water-insoluble chromates, such as 
zinc and lead chromate. The 1953 USPHS survey confirmed that 
approximately 20 percent of the total Cr(VI) in the roasting residue at 
the Painesville plant consisted of the less water-soluble chromates 
(Ex. 2-14). The Painesville plant subsequently reduced and eliminated 
exposure to Cr(VI) roasting residue through improvements in the 
production process. The high-lime process was not used at the Baltimore 
plant and the 1953 USPHS survey detected minimal levels of less soluble 
Cr(VI) at this facility (Ex. 7-17). Proctor et al. estimated that a 
proportion of the Luippold cohort prior to 1950 were probably exposed 
to the less water-soluble Cr(VI) compounds, but that it would amount to 
less than 20 percent of their total Cr(VI) exposure (Ex. 35-61). A 
small proportion of workers in the Special Products Division of the 
Baltimore plant may also have been exposed to less water-soluble Cr(VI) 
compounds during the occasional production of these compounds over the 
years.
    As discussed in the preamble section VI.B on carcinogenic effects, 
both water-soluble and insoluble forms of Cr(VI) compounds are regarded 
as carcinogenic to the respiratory tract as a result of inhalation. 
This is not only supported by epidemiologic studies of the chromate 
production workers above, but also by studies of chromate pigment 
workers exposed primarily to the insoluble zinc and lead chromates 
(Exs. 7-36; 7-42; 7-49). The standardized lung cancer incidence and 
mortality ratios reported among these pigment workers were relatively 
high and clearly significant. Langard and Vigander found that the lung 
cancer incidence among a cohort of workers exposed primarily to zinc 
chromate, but also lead chromate, at a pigment production plant in

[[Page 59385]]

Norway was 44 times what would be expected from an age- and sex-
adjusted Norwegian population (Ex. 7-36). The Davies study found from 
2.2-(p<0.01) to 5.6-fold (p<0.001) excess lung cancer mortality for 
various cohorts of pigment workers exposed to both zinc and lead 
chromate at two British factories (Ex. 7-42). Workers in jobs judged to 
involve the highest Cr(VI) exposure had the highest risk of lung 
cancer. A cohort study of workers exposed to the highly water-soluble 
chromic acid during electroplating operations also reported excess lung 
cancer mortality (Ex. 35-62). While the lung cancer mortality was 
significantly elevated in pigment and electroplating cohorts, there was 
inadequate exposure information for risk analysis.
    The slightly water-soluble Cr(VI) compounds, calcium and strontium 
chromate, led to significant increases in tumors when instilled in the 
respiratory tract of experimental animals (Exs. 11-7; 11-2). Levy et 
al. reported a bronchial carcinoma incidence of 43 percent (43/99) and 
25 percent (25/100) after a single 2 mg intrabronchial instillation of 
strontium chromate and calcium chromate, respectively (Ex. 11-2). This 
compares with the non-significant bronchial carcinoma incidence of one 
percent (1/100) in rats instilled with 2 mg of highly water-soluble 
sodium dichromate in the same study. Steinhoff et al. reported a 7.5 
percent tumor incidence (6/80, p<0.01) following repeated intratracheal 
instillations of 0.25 mg/kg slightly water-soluble calcium chromate in 
rats (Ex. 11-7). The same dosing of the highly water-soluble sodium 
dichromate produced no tumor incidence (0/80) in the same study. This 
and other evidence led IARC to conclude that there was sufficient 
evidence for carcinogenicity in experimental animals of the less water-
soluble strontium chromate, calcium chromate, zinc chromates, and lead 
chromates but only limited evidence for carcinogencity in experimental 
animals of the highly water-soluble chromic acid and sodium dichromate 
(Ex. 18-1, p. 213). Because the above animal studies either used an 
inadequate number of dose levels (e.g., single dose level) or employed 
a less appropriate route of administration (e.g., tracheal 
instillation), it was not possible to determine a reliable quantitative 
estimate of risk for human workers breathing these chromates during 
occupational exposure. IARC drew the overall conclusion that all Cr(VI) 
compounds are carcinogenic to humans based on the combined results of 
animal studies, human epidemiological evidence and other data relevant 
to the carcinogenic mode of action.
    Other studies reported that insoluble Cr(VI) compounds are retained 
in the lung for longer periods and are considered a more persistent 
source of locally available Cr(VI) for uptake into lung cells than 
water-soluble Cr(VI) compounds. Bragt and Van Dura found that water-
soluble sodium chromate is more rapidly absorbed and cleared from the 
lung than the highly insoluble lead chromate when intratracheally 
instilled in rats (Ex. 35-56). On day 50 after instillation, 13.8 
percent of the initial lead chromate remained in the lungs as opposed 
to only 3.0 percent of the initial sodium chromate. Research at George 
Washington University Medical Center showed that treatment of embryo 
cells in culture with insoluble lead chromate particulates led to cell-
enhanced dissolution and uptake of Cr(VI) resulting in DNA damage and 
neoplastic transformation (Exs. 35-104; 35-69; 35-132). 
Internalization, dissolution, and uptake of lead chromate and the 
resulting damage to DNA were later shown to also occur in normal human 
lung epithelial cells (Exs. 35-66; 35-327). Elias et al. showed that a 
wide range of insoluble lead and zinc chromate pigments could 
morphologically transform normal mammalian cells into neoplastic cells 
(Ex. 12-5). These studies have led the researchers to suggest that the 
less water-soluble Cr(VI) compounds may be more carcinogenic in the 
lung than the highly water-soluble Cr(VI) since these insoluble 
chromate particulates provide a persistent source of high Cr(VI) 
concentration within the immediate microenvironment of the lung cell 
surface (Exs. 35-67; 35-149).
    Experts have evaluated the combined epidemiologic, animal, and 
mechanistic evidence and concluded that the less water-soluble 
chromates are likely more carcinogenic than highly water-soluble Cr(VI) 
compounds (Exs. 17-101; 17-5B). This is reflected in the lower 
recommended ACGIH TLVs for insoluble Cr(VI) compounds (i.e., 10 mg/m3) 
and certain slightly soluble Cr(VI) compounds (e.g., 1 mg/m3 for 
calcium chromate; 0.5 mg/m3 for strontium chromate) than the 
recommended TLV for the water-soluble Cr(VI) compounds (e.g., 50 mg/
m3). For all the reasons cited above, OSHA believes the lung cancer 
risk for workers exposed to equivalent levels of Cr(VI) compounds other 
than sodium chromate and sodium dichromate over a working lifetime is 
likely to be similar in magnitude to the risks projected from the 
chromate production workers in the Gibb and Luippold cohorts, or 
possibly even greater in the case of inhaled slightly water-soluble and 
insoluble Cr(VI) particulates.
    OSHA seeks comment on whether its preliminary assessment of risk 
based on the exposure-response data from the two cohorts of chromate 
production workers is reasonably representative of the risks expected 
from equivalent exposures to different Cr(VI) compounds encountered in 
other industry sectors. Of particular interest is whether there is 
convincing evidence that the preliminary risk estimates from worker 
cohorts primarily engaged in the production of the highly water soluble 
sodium chromate and sodium dichromate would substantially overpredict 
the lung cancer risk for workers exposed at the same level and duration 
to airborne Cr(VI) during welding operations, chromic acid aerosol in 
electroplating operations, the less water soluble Cr(VI) particulates 
encountered during pigment production and painting operations, or 
Cr(VI) exposure in other important industry sectors and job categories.

H. Expert Peer Review of the OSHA Draft Preliminary Quantitative Risk 
Assessment

    OSHA contracted an independent organization known as Toxicology 
Excellence for Risk Assessment (TERA) to organize an external 
scientific peer review of the January 21, 2004 Draft Quantitative Risk 
Assessment (Exs. 36-1-1; 36-1-2). TERA selected three peer reviewers 
based on a high level of competence in occupational epidemiology and/or 
risk assessment. The reviewers were screened to ensure no apparent 
conflict of interest or involvement in the key studies that provided 
the basis for the OSHA assessment. OSHA did not participate in the 
selection process other than to examine reviewer credentials to confirm 
their qualifications. The three peer reviewers selected by TERA were 
Dr. David Gaylor, Dr. Allan Smith, and Dr. Irva Hertz-Picciotto. 
Curriculum Vitae of the three reviewers have been submitted to the 
docket (Ex. 36-1-3).
    TERA provided the peer reviewers with a review package that 
consisted of the draft quantitative risk assessment, copies of the key 
studies, and a set of instructions and questions (Ex. 36-1-1). The 
reviewers were asked to comment on several aspects of the draft OSHA 
risk assessment including the suitability of the different data sets 
for exposure-response analysis, the choice of exposure metric and risk 
models, the appropriateness of the risk estimates, and the 
characterization of key issues and uncertainties. The peer reviewers 
filed written draft reports with TERA

[[Page 59386]]

which then reviewed the comments for completeness before passing the 
reports on to OSHA (Ex. 36-1-4). OSHA requested clarification in 
writing on some of the reviewer responses. These were addressed by the 
peer reviewers in their final peer review reports or answered in an 
attachment (Ex. 36-1-4-3). The clarification process with the reviewers 
was handled by TERA.
    The three peer reviewers agreed that the results from six 
occupational cohorts under review were adequately evaluated as to their 
suitability for exposure-response analysis and concurred that the Gibb 
and Luippold cohorts provided the strongest data sets for quantitative 
assessment. There was general agreement among the peer reviewers that 
the risk models and statistical methodologies used in the OSHA 
assessment were appropriately applied. Dr. Smith remarked that ``there 
is no question in my mind that relative risk models are superior to 
others when conducting quantitative cancer risk assessments on 
epidemiological data'' (Ex. 36-1-4-2) and commended OSHA for supporting 
a relatively straightforward [linear] model widely used in epidemiology 
(Ex. 36-1-4-2). At his suggestion, OSHA expanded on reasons for using a 
linear relative risk model to fit the epidemiological data. The 
selection of the linear relative risk model was not solely based on 
mathematical fit. Relative risk models inherently adjust for age-
related increases in cancer incidence. The linear relative risk model 
has been extensively and successfully used to analyze other cancer 
mortality data sets and is an accepted approach in carcinogen risk 
assessment.
    The peer reviewers were also in general agreement that cumulative 
exposure based on time-weighted average air concentrations by job title 
and employment history was a reasonable exposure metric to use. Dr. 
Hertz-Picciotto stated ``the use of cumulative exposure constructed in 
this way is currently the standard, and the use of individual job 
histories is the best available method at this time (Ex. 36-1-4-4).'' 
She pointed out that the underlying assumption that exposure patterns 
and dose rate differences at equivalent cumulative exposures do not 
influence cancer risk is an uncertainty in the assessment. This is more 
fully explained in section VII.G.1 on uncertainties with regard to 
worker exposure.
    Dr. Smith raised another limitation to the cumulative exposure 
metric as it relates to relative risk. It has been shown, in some 
instances, that relative risk of chronic disease will not continue to 
rise at high cumulative exposure but will tend to stabilize or 
attenuate. In the case of a significant attenuation, the excess risk at 
high Cr(VI) exposures (e.g., working lifetime at the current OSHA PEL) 
could be overestimated by a linear relative risk model. Environ 
examined this possibility by fitting the Gibb and Luippold data sets to 
a power model that requires the exposure-response to rise steeply at 
low exposure and level out at high exposure (Ex. 36-2). The power model 
did not significantly improve the fit compared to the linear relative 
risk model for either data set. This analysis would not support a 
significant attenuation in the relative risk of lung cancer with 
increasing cumulative Cr(VI) exposure. Therefore, OSHA does not find 
adequate reason to believe its linear relative risk model would 
overpredict the lung cancer risk at the OSHA PEL or other cumulative 
exposures in the range of interest. OSHA revised its preliminary 
quantitative risk assessment to fully address this issue in section 
VII.G.1.
    The peer reviewers showed less enthusiasm for the highest reported 
average monthly Cr(VI) air concentration as an appropriate exposure 
metric or for an exposure threshold below which there exists no lung 
cancer risk. Dr. Hertz-Picciotto remarked that ``the newly published 
Crump et al. (2003) uses the monthly maximum [Cr(VI) concentration], 
but fails to take duration into account, and the authors note 
considerable variability was present in duration at the highest monthly 
exposure'' and ``the inadequacy of the attempt to prove a threshold is 
excellently presented [by OSHA]'' (Ex. 36-1-4-4). Dr. Gaylor stated ``a 
threshold concentration or threshold cumulative exposure to Cr(VI) 
below which no excess lung cancer is expected cannot be established 
from the available information (Ex. 36-1-4-1).'' Dr. Smith added ``the 
[OSHA] reasons given for dismissing Exponent's threshold inference are 
valid. I would add [Exponent's] assessment ignores duration of 
exposure. For example, it is unlikely one could detect increased lung 
cancer risks in smokers whose `peak exposure' was a quarter pack per 
day if they only smoked for three years. This would not mean that a 
quarter pack per day is a threshold (Ex. 36-1-4-2).''
    The peer reviewers found the range of excess lifetime risks of lung 
cancer presented by OSHA to be sound and reasonable. These preferred 
risk estimates were those bounded by the maximum likelihood estimates 
determined from the featured Gibb and Luippold data sets. Dr. Gaylor 
wrote ``the confidence limits are tighter for the Luippold study, 
somewhat over a factor of two for the range from the lower to the upper 
95% confidence limit, compared to a range of about 3.5 for the 
confidence limits in the Gibb study. However, the Gibb cohort is larger 
than the Luippold cohort. It appears reasonable to consider the two 
studies jointly to provide estimates of lung cancer risk'' (Ex. 36-1-4-
1). Dr. Gaylor went on to point out that the range of maximum 
likelihood between the featured data sets understates the [statistical] 
uncertainty in the risk estimates. He recommended that the uncertainty 
be expressed as the lower 95% confidence limit from the Luippold data 
set and the 95% upper confidence limit for the Gibb data set. OSHA 
agrees and has revised section VII.F to make clear that while the 
maximum likelihood range represents the most likely estimates of lung 
cancer risk, the 95% confidence bounds are the better representation of 
statistical uncertainty.
    Dr. Gaylor suggested that the OSHA assessment make clear that the 
45-year working lifetime exposure should be regarded as a worst case 
scenario and that the typical worker would be exposed to Cr(VI) for a 
shorter period of time. Dr. Smith also questioned the need to estimate 
risk from a 45-year working lifetime. He suggested that OSHA could 
probably make more confident estimates of risk for shorter exposure 
durations (e.g., ten years) within the range observed in the cohort 
studies. This would avoid the uncertainties of an upward extrapolation. 
OSHA does not disagree with these comments. However, the OSH Act is 
clear on the agency statutory obligation to consider the risk of 
material impairment from regular exposure to the hazardous agent for a 
full working life. The risk of lung cancer from Cr(VI) exposures for 
less than a full working lifetime are discussed in section VIII on 
Significance of Risk and section IX on Benefits Analysis.
    Dr. Hertz-Picciotto felt that OSHA may have overstated the 
consistency in lung cancer risk between the two primary studies and the 
four weaker supporting studies. She pointed out that two of the 
supporting cohorts overlapped the featured cohorts and were not truly 
independent data sets. She indicated that the weaker supporting studies 
had serious bias that rendered the discussion of overlap in confidence 
intervals to be relatively meaningless and, thus, prevented a 
definitive evaluation of consistency. OSHA agrees that the magnitude 
and direction of potential bias introduced by lack of exposure data, 
inadequate follow-up, and other limitations in the

[[Page 59387]]

supporting studies prevents strong statements regarding consistency 
among risks estimates. However, OSHA believes the finding that its risk 
predictions based on the Gibb and Luippold data sets are within a 
statistical precision that is compatible with other exposure-response 
data sets enhances confidence in the estimates. OSHA notes that there 
was no overlap in the Mancuso and Luippold cohorts, even though they 
worked at the same plant, due to vastly different selection criteria 
and exposure estimation based on different industrial hygiene surveys. 
The Hayes and Gibb cohort have some overlap but the cohorts primarily 
worked at different facilities and exposure estimates were, again, 
based on different monitoring surveys. In the case of both cohort 
pairs, statistical comparisons show that the risk estimates from one 
data set would not be consistent with the other data set at the 95% 
confidence level. OSHA believes the risks from the different cohorts 
can be considered independent estimates. OSHA has revised sections 
VII.E and VII.F to clarify the positions discussed above.
    Dr. Smith suggested that OSHA consider presenting risk estimates 
that can be readily calculated from the source data without use of a 
complex mathematical model. He contends that this would allow the 
reader to better understand how the risks relate to measures reported 
in the published studies. He provided some illustrations of simple and 
transparent risk estimations from the Gibb et al. study. OSHA agrees 
there is merit to comparing risk estimates easily calculated from the 
cohort mortality data with the more precise estimates determined from 
the linear relative risk model as a kind of ``reality check''. OSHA has 
included such calculations in sections VII.C.4 for the Gibb data set 
and section VII.D for the Luippold data set.
    OSHA does not agree with assertions by Dr. Smith that ``there is no 
valid basis to conclude that more complex calculations [from 
mathematical models], such as found in the source material and draft 
[OSHA] document, have any greater validity than this estimate [directly 
calculated from the published cohort data]'' and ``there is no gain in 
validity in doing a full life table analysis but there is certainly a 
loss in transparency (Ex. 36-1-4-2).'' OSHA believes excess risk 
estimated from standard, well-supported mathematical model constructs 
that incorporate the entire mortality data set is considerably more 
accurate, more robust, more stable and more statistically rigorous than 
a simple calculation from a single relative risk result determined from 
a small subset of the cohort data as applied by Dr. Smith. The life 
table analysis adjusts for both the increasing probability of 
developing lung cancer with advancing age and the competing risk of 
death from other causes. These age-related factors are not accounted 
for in a simple relative risk calculation and may lead to a less 
accurate risk estimate.
    While the peer reviewers felt that most uncertainties in the risk 
assessment were adequately characterized, they suggested certain topics 
receive more attention. Dr. Hertz-Picciotto suggested that sensitivity 
analyses on plausible alternate exposure assumptions for workers in the 
Gibb and Luippold cohorts during the periods when there was very 
limited air monitoring data ``would add concrete information on the 
magnitude of uncertainty in the risk estimates (Ex. 36-1-4-4).'' 
Environ, while under contract with OSHA, had access to annual exposure 
estimates on individual workers in the Gibb cohort. They explored the 
feasibility of generating plausible alterative exposures using a 
forward and reverse replacement scheme for the air concentrations 
imputed during periods in the Gibb et al. study when air monitoring was 
unavailable (Ex. 36-2). Unfortunately, lack of job title information 
and job-specific monitoring data combined with apparent high job 
transfer and turnover among workers made this approach impracticable 
for estimating plausible exposures that could lead to a meaningful 
analysis. OSHA did not have access to individual exposure data for the 
Luippold cohort.
    Dr. Hertz-Picciotto recommended that OSHA address the potential 
impact on risk of the healthy worker survivor effect. The healthy 
worker survivor effect refers to a common observation that long-term 
workers have been found to have lower mortality than short-term 
workers. As a result, exposure-response analyses based on mortality of 
long-term healthy workers will tend to underestimate the risk to short-
term workers and vice versa. This healthy worker effect may partially 
explain the higher risk estimates for the same cumulative exposures 
from the Gibb cohort, which included a higher proportion of workers 
with short exposure duration, relative to the Luippold cohort of 
longer-term workers. The healthy worker survivor effect may have also 
influenced risks estimated from the Mancuso cohort. OSHA agrees that 
the healthy worker survivor effect contributes to the uncertainty in 
the risk estimates and has included a discussion in section VII.G.3 on 
issues and uncertainties and in the section VII.E.1 on the Mancuso data 
set.
    Dr. Smith thought that some important issues surrounding smoking 
needed to be better addressed in the preliminary risk assessment 
document. He agreed that OSHA adequately discussed the confounding due 
to smoking but suggested that it be made clear that the linear relative 
risk model, in the absence of any explicit interaction term between 
smoking and Cr(VI), implicitly assumes a synergy (i.e., lung cancer 
risk from smoking and Cr(VI) together is greater than the sum of the 
risks from either agent alone) between the two exposures. OSHA believes 
Dr. Smith has a valid point. Although the linear relative risk model 
makes no explicit assumptions with regard to an interaction between 
smoking and Cr(VI) exposure, the model does assume a multiplicative 
relationship between the background rate of lung cancer in the 
reference population and Cr(VI) exposure. Therefore, to the extent that 
smoking is a predominant influence on the background lung cancer risk, 
the linear relative risk model implicitly assumes a multiplicative 
(e.g., greater than additive and synergistic, in most situations) 
relationship between cumulative Cr(VI) exposure and smoking. Since the 
background lung cancer rate reflects a mixture of smokers and non-
smokers, the expectation is that the projected OSHA risks from Cr(VI) 
exposure are overestimated for a non-smoker to some unknown extent. By 
the same token, the model may underestimate the risk from Cr(VI) 
exposure to a heavy smoker. A discussion of this has been included in 
section VII.G.3.
    Finally, the peer reviewers believed that OSHA adequately presented 
its position that workers in the Gibb and Luippold cohorts were 
primarily exposed to the less carcinogenic, highly water-soluble Cr(VI) 
compounds and that the lung cancer risks for workers exposed to 
equivalent levels of other Cr(VI) compounds will be of a similar 
magnitude and possibly greater in the case of certain less water-
soluble Cr(VI). However, the peer reviewers stated that they lacked the 
expertise in toxicology and experimental carcinogenesis to critically 
evaluate its consistency with the existing scientific data. OSHA has 
made it clear in section VII.G.4 that the animal studies demonstrating 
higher carcinogenic potency for sparingly water-soluble Cr(VI), such as 
calcium chromate and strontium chromates, can not provide reliable 
quantitative estimates of human risk. This is because the studies 
employed an inadequate

[[Page 59388]]

number of dose levels or the studies employed routes of administration 
(e.g., intratracheal instillation) less relevant to occupational 
exposure.

I. Preliminary Conclusions

    OSHA believes that the best quantitative estimates of excess 
lifetime lung cancer risks are those derived from the data sets 
described by Gibb et al. and Luippold et al. Both data sets show a 
significant positive trend in lung cancer mortality with increasing 
cumulative Cr(VI) exposure. The exposure assessments for these two 
cohorts were reconstructed from air measurements and job histories over 
three or four decades and were superior to those of other worker 
cohorts. The linear relative risk model generally provided the best fit 
among a variety of different models applied to the Gibb et al. and 
Luippold et al. data sets. It also provided an adequate fit to four 
other supporting data sets. Thus, OSHA believes the linear relative 
risk model is the most appropriate model to estimate excess lifetime 
risk from occupational exposure to Cr(VI). Using the Gibb et al. and 
Luippold et al. data sets and a linear relative risk model, OSHA 
preliminarily concludes that the lifetime lung cancer risk is best 
expressed by the three-to five-fold range of risk projections bounded 
by the maximum likelihood estimates from the two featured data sets. 
This range of projected risks is within the 95 percent confidence 
intervals from all six data sets.
    OSHA does not believe that it is appropriate to employ a threshold 
dose-response approach to estimate cancer risk from a genotoxic 
carcinogen, such as Cr(VI). Federal Agencies, including OSHA, assume an 
exposure threshold for cancer risk assessments to genotoxic agents only 
when there is convincing evidence that such a threshold exists. In 
addition, OSHA does not consider absence of a statistically significant 
effect in an epidemiologic or animal study that lacks power to detect 
such effects to be convincing evidence of a threshold. OSHA also does 
not consider theoretical reduction capacities determined in vitro with 
preparations that do not fully represent physiological conditions 
within the respiratory tract to be convincing evidence of a threshold. 
Finally, as previously discussed, linear (and some non-linear) no-
threshold risk models adequately fit the existing exposure-response 
data.
    The Gibb and Luippold cohorts were predominantly exposed to water-
soluble chromates, particularly sodium dichromate. The scientific 
evidence indicates that the water-soluble Cr(VI) compounds are 
generally less potent carcinogens than slightly-water soluble and 
water-insoluble Cr(VI) compounds. These less water-soluble Cr(VI) 
compounds are retained in the lung for longer periods, are more likely 
to concentrate at the lung cell surface, and are a more persistent 
source of locally available Cr(VI) for uptake into target cells than 
the highly water-soluble Cr(VI) compounds. Risks estimated from 
chromate production workers primarily exposed to water-soluble 
chromates in the Gibb and Luippold cohorts should adequately represent 
risks to workers exposed to other water-soluble Cr(VI) compounds. OSHA 
believes that workers exposed to equivalent levels of the potentially 
more carcinogenic, less water-soluble Cr(VI) compounds may even be at 
greater risk of lung cancer than predicted from the Gibb and Luippold 
cohorts.
    As with any risk assessment, there is some degree of uncertainty in 
the projected risks that result from the data, assumptions, and 
methodology used in the analysis. The exposure estimates in the Gibb et 
al. and Luippold et al. data sets relied, to some extent, on a paucity 
of air measurements using less desirable sampling techniques to 
reconstruct Cr(VI) exposures, particularly in the 1940s and 1950s. 
Additional uncertainty is introduced when extrapolating from the cohort 
exposures to higher Cr(VI) levels for shorter periods to an equivalent 
cumulative exposure of lower intensity and longer duration of interest 
to OSHA. The study cohorts were mostly smokers but detailed information 
on their smoking behavior was unavailable. While the risk assessments 
make some adjustments for the confounding effects of smoking, it is 
unknown whether the assessments fully account for any interactive 
effects that smoking and Cr(VI) exposure may have on the carcinogenic 
action. In any case, OSHA does not have reason to believe the above 
uncertainties would introduce errors that would result in serious 
overprediction or underprediction of risk.
    OSHA s preliminary estimate of lung cancer risk from a 45 year 
occupational exposure to Cr(VI) at an 8-hour TWA at the current PEL of 
52 [mu]g/m<SUP>3</SUP> is 101 to 351 excess deaths per 1000 workers. 
This range, which is defined by maximum likelihood estimates based on 
the Gibb and Luippold epidemiological cohorts, is OSHA's best estimate 
of excess risk; it does not account for uncertainty due to the 
statistical nature of the analyses, or for other potential sources of 
uncertainty or bias. The wider range of 62 to 493 per 1000 represents 
the statistical uncertainty associated with OSHA's excess risk estimate 
at the current PEL, based on lowest and highest 95% confidence bounds 
on the maximum likelihood estimates for the two featured data sets. The 
excess lung cancer risks at alternative 8 hour TWA PELs that were under 
consideration by the Agency are shown in Table VI-8, together with the 
uncertainty bounds for the primary and supporting studies at these 
exposure concentrations. The excess lung cancer risks at alternate 8 
hour TWA PELs under consideration by the Agency are shown in Table VI-
8. For example, OSHA s best estimate of excess risk from 45 years' 
exposure at 1 [mu]g/m<SUP>3</SUP> Cr(VI) is 2.1 to 4.6 per 1000; an 
interval of 1.2- 16 per 1000 represents the statistical uncertainty of 
OSHA s estimate. The 45-year exposure estimates satisfy the Agency s 
statutory obligation to consider the risk of material impairment for an 
employee with regular exposure to the hazardous agent for the period of 
his working life (29 U.S.C. 651 et seq.). Occupational risks from 
Cr(VI) exposure to less than a full working lifetime are considered in 
Section VIII on the Significance of Risk and in Section IX. on the 
Benefits Analysis.

VIII. Significance of Risk

    In promulgating health standards, OSHA uses the best available 
information to evaluate the risk associated with occupational 
exposures, to determine whether this risk is severe enough to warrant 
regulatory action, and to determine whether a new or revised rule will 
substantially reduce this risk. OSHA makes these findings, jointly 
referred to as the ``significant risk determination'', based on the 
requirements of the OSH Act and the Supreme Court's interpretation of 
the Act in the ``benzene'' decision of 1980 (Industrial Union 
Department, AFL-CIO v. American Petroleum Institute, 448 U.S. 607). The 
OSH Act directs the Secretary of Labor to

    set the standard which most adequately assures, to the extent 
feasible, on the basis of the best available evidence, that no 
employee will suffer material impairment of health or functional 
capacity even if such employee has regular exposure to the hazard * 
* * for the period of his working life [6(b)(5)].

OSHA's authority to promulgate regulations for the cause of worker 
protection is limited by the requirement that standards be ``reasonably 
necessary and appropriate to provide safe or healthful employment'' 
[3(8)].
    In the benzene decision, the Supreme Court's interpretation of 
Section 3(8)

[[Page 59389]]

further defined OSHA's regulatory authority. The Court stated:

    By empowering the Secretary to promulgate standards that are 
``reasonably necessary or appropriate to provide safe or healthful 
employment and places of employment,'' the Act implies that, before 
promulgating any standard, the Secretary must make a finding that 
the workplaces in question are not safe (IUD v. API 448 U.S. at 
642).

``But `safe' is not the equivalent of `risk-free' '', the Court 
maintained. ``[T]he Secretary is required to make a threshold finding 
that a place of employment is unsafe--in the sense that significant 
risks are present and can be eliminated or lessened by a change in 
practices'' (IUD v. API 448 U.S. at 642). It has been Agency practice 
to establish this finding by estimating risk to workers using 
quantitative risk assessment, and determining the significance of this 
risk based on judicial guidance, the language of the OSH Act, and 
Agency policy considerations.
    The Agency has considerable latitude in defining significant risk 
and in determining the significance of any particular risk. The Court 
did not stipulate a means to distinguish significant from insignificant 
risks, but rather instructed OSHA to develop a reasonable approach to 
the significant risk determination. The Court stated that ``it is the 
Agency's responsibility to determine in the first instance what it 
considers to be a ``significant'' risk'', and did not express ``any 
opinion on the * * * difficult question of what factual determinations 
would warrant a conclusion that significant risks are present which 
make promulgation of a new standard reasonably necessary or 
appropriate'' (448 U.S. at 659). The Court also stated that, while 
OSHA's significant risk determination should be supported by 
substantial evidence, the Agency ``is not required to support the 
finding that a significant risk exists with anything approaching 
scientific certainty''. Furthermore, ``A reviewing court [is] to give 
OSHA some leeway where its findings must be made on the frontiers of 
scientific knowledge [and] * * * the Agency is free to use conservative 
assumptions in interpreting the data with respect to carcinogens, 
risking error on the side of overprotection rather than 
underprotection'', so long as such assumptions are based in ``a body of 
reputable scientific thought'' (448 U.S. at 655, 656).
    To make the significance of risk determination for a new or 
proposed standard, OSHA uses the best available scientific evidence to 
identify material health impairments associated with potentially 
hazardous occupational exposures, and, when possible, to provide a 
quantitative assessment of exposed workers' risk of these impairments. 
OSHA has reviewed extensive epidemiological and experimental research 
pertaining to adverse health effects of occupational Cr(VI) exposure, 
including lung cancer, and has established preliminary quantitative 
estimates of the excess lung cancer risk associated with currently 
allowable Cr(VI) exposure concentrations and the expected impact of the 
proposed PEL. OSHA has preliminarily determined that long-term exposure 
at the current PEL causes significant risk to workers' health, and that 
adoption of the proposed PEL will significantly reduce this risk.

A. Material Impairment of Health

    As discussed in Section VI of this preamble, inhalation exposure to 
Cr(VI) causes a variety of adverse health effects, including lung 
cancer, nasal septum damage, and asthma. OSHA considers these 
conditions to be material impairments of health, as they are marked by 
significant discomfort and long-lasting adverse effects, can have 
adverse occupational and social consequences, and may in some cases 
have permanent or potentially life-threatening consequences. Based on 
this finding and on the scientific evidence linking Cr(VI) inhalation 
to each of these effects, OSHA concludes that exposure to Cr(VI) causes 
``material impairment of health or functional capacity'' within the 
meaning of the OSH Act.
    OSHA considers lung cancer, an irreversible and frequently fatal 
disease, to be a clear material impairment of health. OSHA's finding 
that inhaled Cr(VI) causes lung cancer is based on the best available 
epidemiological data, reflects substantial evidence from animal and 
mechanistic research, and is consistent with the conclusions of other 
government and public health organizations, including NIOSH, EPA, 
ACGIH, NTP, and IARC (Exs. 35-117; 35-52; 35-158; 17-9-D; 18-3, p. 
213). The Agency's primary evidence comes from two epidemiological 
studies that show significantly increased incidence of lung cancer 
among workers in the chromate production industry (Exs. 25; 33-10). The 
high quality of the data collected in these studies and the analyses 
performed on them has been confirmed by OSHA and by independent peer 
review. Supporting evidence of Cr(VI) carcinogenicity comes from 
occupational cohort studies in chromate production, chromate pigment 
production, and chromium plating, and by cell culture research into the 
processes by which Cr(VI) disrupts normal gene expression and 
replication. Studies demonstrating uptake, metabolism, and genotoxicity 
of a variety of soluble and insoluble Cr(VI) compounds support the 
Agency's position that all Cr(VI) compounds should be regulated as 
occupational carcinogens (Exs. 35-148; 35-68; 35-67; 35-66; 12-5; 35-
149; 35-134).
    While OSHA has relied primarily on the association between Cr(VI) 
inhalation and lung cancer to demonstrate the necessity of the proposed 
standard, the Agency has also determined that several other material 
health impairments can result from exposure to airborne Cr(VI). As 
shown in several cross-sectional and cohort studies, inhalation of 
Cr(VI) can cause nasal passage atrophy, ulceration, and septum 
perforation (Exs. 35-1; 7-3; 9-126; 35-10; 9-18; 3-84; 7-50; 31-22-12). 
Septum ulcerations are often accompanied by swelling and bleeding, heal 
slowly, and in some cases may progress to a permanent perforation that 
can only be repaired surgically. Inhalation of Cr(VI) can also lead to 
occupational asthma, a potentially life-threatening condition in which 
workers become allergic to Cr(VI) compounds and experience symptoms 
such as coughing, wheezing, and difficulty in breathing upon exposure 
to small amounts of airborne Cr(VI). Several case reports have 
documented occupational asthma from Cr(VI) exposure, confirming Cr(VI) 
as the sensitizing agent by bronchial challenge (Exs. 35-7; 35-12; 35-
16; 35-21).

B. Risk Assessment

    When possible, epidemiological or experimental data and statistical 
methods are used to characterize the risk of disease that workers may 
experience under the current PEL, as well as the expected reduction of 
risk that would occur with implementation of the proposed PEL. The 
Agency finds that the available epidemiological data are sufficient to 
support quantitative risk assessment for lung cancer among Cr(VI)-
exposed workers. Using the best available studies, OSHA has 
preliminarily identified a range of expected risk from regular 
occupational exposure at the current PEL (101-351 excess lung cancer 
deaths per 1000 workers) and at the proposed PEL of 1 [mu]g/
m<SUP>3</SUP> (2.1-9.1 per 1000 workers), assuming a working lifetime 
of 45 years' exposure in each case. These values represent the best 
estimates of multiple analysts working with data on two extensively 
studied worker populations,

[[Page 59390]]

and are highly consistent across analyses using a variety of modeling 
techniques and assumptions. While some attempts have been made to 
assess the relationship between Cr(VI) exposure level and noncancer 
adverse health effects, the Agency does not believe that a reliable 
quantitative risk assessment can be performed for noncancer effects at 
this time, and has therefore characterized noncancer risk 
qualitatively.
    For preliminary estimates of lung cancer risk from Cr(VI) exposure, 
OSHA has relied upon data from two cohorts of chromate production 
workers. The Gibb cohort, which originates from a chromate production 
facility in Baltimore, Maryland, includes 2357 workers who began work 
between 1950 and 1974 and were followed up through 1992 (Ex. 25). The 
extensive exposure documentation available for this cohort, the high 
statistical power afforded by the large cohort size, and the 
availability of information on individual workers' race and smoking 
status provide a particularly strong basis for risk analysis. The 
Luippold cohort, from a facility in Painesville, Ohio, includes 482 
workers who began work between 1940 and 1972, worked for at least one 
year at the plant, and were followed up through 1997 (Ex. 33-10). This 
cohort also provides a very strong basis for risk analysis, in that it 
has high-quality documentation of worker Cr(VI) exposure and mortality, 
a long period of followup, and a large proportion of relatively long-
term employees (55% > 5 years).
    Risk assessments were performed on the Gibb cohort data by Environ 
International Corporation (Ex. 33-12), under contract with OSHA; Park 
et al., as part of an ongoing effort by NIOSH (Ex. 33-13); and Exponent 
on behalf of the Chrome Coalition (Ex. 31-18-15-1). A variety of 
statistical models were considered, allowing OSHA to identify the most 
appropriate models and assess the resulting risk estimates' sensitivity 
to alternate modeling approaches. Models were tried with additive and 
relative risk assumptions; various exposure groupings and lag times; 
linear and nonlinear exposure-response functions; external and internal 
standardization; reference lung cancer rates from city-, state-, and 
national-level data; inclusion and exclusion of short-term workers; and 
a variety of ways to control for the effects of smoking. OSHA's 
preferred approach, a relative risk model using Baltimore lung cancer 
reference rates, and NIOSH's preferred approach, a relative risk model 
using detailed smoking information and U.S. lung cancer reference 
rates, are among several models that use reasonable assumptions and 
provide good fits to the data. As discussed in section VII, the 
Environ, Park et al., and linear Exponent models yield similar 
predictions of excess risk from exposure at the current and proposed 
PELs (see Tables VII-3 and VII-4). OSHA's preferred model predicts 
about 350 excess lung cancers per 1000 workers exposed for a working 
lifetime of 45 years at the current PEL (MLE 351, 95% CI 181-493) when 
person-years of exposure are spread evenly across exposure groups (see 
Table VII-3). Implementation of the proposed PEL is expected to reduce 
this risk to about 10 excess lung cancers per 1000 workers (MLE 9.1, 
95% CI 4-16).
    Environ and Crump et al. performed risk assessments on the Luippold 
cohort, exploring additive and relative risk models, linear and 
quadratic exposure-response functions, and several exposure groupings 
(Exs. 35-59; 35-58). Additive and relative risk models by both analyst 
groups fit the data adequately with linear exposure-response. The 
linear models by all of the analyst groups predicted similar excess 
risks, from which OSHA has selected preferred estimates based on the 
Crump et al. analysis of about 100 excess lung cancer deaths per 1000 
workers exposed for 45 years at the current PEL (MLE 101, 95% CI 62-
147), and two excess lung cancer deaths per 1000 workers exposed for 45 
years at the proposed PEL (MLE 2.1, 95% CI 1.2-3.1).
    The risk assessments performed on the Luippold cohort yield 
somewhat lower estimates of lung cancer risk than those performed on 
the Gibb cohort. This discrepancy is probably not due to statistical 
error in the risk estimates, as the confidence intervals for the 
estimates do not overlap. The risk estimates based on the Gibb and 
Luippold cohorts are nonetheless reasonably close. OSHA believes that 
both cohorts support reasonable estimates of lung cancer risk, and 
based on their results has selected a representative range of 101-351 
per 1000 for 45 years' occupational exposure at the current PEL and 
2.1-9.1 per 1000 for 45 years' occupational exposure at the proposed 
PEL for the significant risk determination. OSHA's confidence in these 
risk estimates is further strengthened by the results of the 
independent peer review to which the risk assessment and the primary 
supporting studies were submitted, which generally supported the 
Agency's approach and results.
    Although nasal damage and asthma are well-established effects of 
occupational exposure to airborne Cr(VI), OSHA has preliminarily 
determined that there are no adequate studies to support a quantitative 
risk assessment for these effects. The Agency has nonetheless made 
careful use of the best available scientific information in its 
evaluation of noncancer health risks from occupational Cr(VI) exposure. 
In lieu of a quantitative analysis linking the risk of noncancer health 
effects with specific occupational exposure conditions, the Agency has 
considered information on the extent of these effects and occupational 
factors affecting risk, as discussed below.
    Damage to the nasal mucosa and septum can occur from inhalation of 
airborne Cr(VI) or transfer of Cr(VI) on workers' hands to the interior 
of the nose. Epidemiological studies have found varying, but 
substantial, prevalence of nasal damage among workers exposed to high 
concentrations of airborne Cr(VI). In the cohort of 2357 chromate 
production workers studied by Gibb et al., over 60% experienced nasal 
septum ulcerations at some point during their employment, with half of 
these workers' first ulcerations occurring within 22 days from the date 
they were hired (Ex. 31-22-12). The authors found a statistically 
significant relationship between nasal ulceration and workers' 
contemporaneous exposures, with about half of the workers who developed 
ulcerations first diagnosed with ulcerations while employed in a job 
with average exposure concentrations greater than 20 [mu]g/
m<SUP>3</SUP>. Nasal septum perforations were reported among 17% of the 
Gibb cohort workers, and appeared to develop over relatively long 
periods of exposure (median time 172 days from hire date to diagnosis).
    Another important study, Lindberg and Hedenstierna's 1983 
examination of nasal effects among Swedish chrome platers, 
characterizes the prevalence of nasal irritation, atrophy, ulceration, 
and perforation among workers exposed to various concentrations of 
Cr(VI) (Ex. 9-126). Workers' daily average exposure concentrations were 
measured as 8-hour averages using personal air samplers, and estimates 
of workers' peak exposures were derived from 6-hour average 
concentrations collected with stationary equipment near the chrome 
electroplating baths. Among 43 workers exposed almost exclusively to 
Cr(VI), septum ulceration and perforation were not observed among those 
exposed to peak exposures less than 20 [mu]g/m<SUP>3</SUP> or those 
exposed to 8-hour average concentrations less than 2 [mu]g/
m<SUP>3</SUP>, a result used by the EPA to identify a lowest-observed 
adverse effect level (LOAEL) for their inhalation reference

[[Page 59391]]

concentration (Ex. 35-156). Nasal septum atrophy, a condition that can 
progress to ulceration and perforation, was observed less frequently 
among workers with 8-hour mean exposure concentrations less than 2 
[mu]g/m<SUP>3</SUP> and those with peak exposures less than 20 [mu]g/
m<SUP>3</SUP> than among workers exposed to higher concentrations. It 
is not clear whether workers who had nasal septum atrophy at these 
exposure levels eventually developed ulcerations or perforations. 
Although Lindberg and Hedenstierna's results suggest increasing risk of 
nasal septum damage with increasing exposure concentrations, there are 
considerable uncertainties associated with the cross-sectional study 
design and the possible contribution of hand-to-nose transfer of Cr(VI) 
to the observed nasal effects.

C. Significance of Risk and Risk Reduction

    The Supreme Court's benzene decision of 1980 states that ``before 
he can promulgate any permanent health or safety standard, the 
Secretary [of Labor] is required to make a threshold finding that a 
place of employment is unsafe--in the sense that significant risks are 
present and can be eliminated or lessened by a change in practices'' 
(IUD v. API, 448 U.S. at 642). The Court broadly describes the range of 
risks OSHA might determine to be significant:

    It is the Agency's responsibility to determine in the first 
instance what it considers to be a ``significant'' risk. Some risks 
are plainly acceptable and others are plainly unacceptable. If, for 
example, the odds are one in a billion that a person will die from 
cancer by taking a drink of chlorinated water, the risk clearly 
could not be considered significant. On the other hand, if the odds 
are one in a thousand that regular inhalation of gasoline vapors 
that are 2 percent benzene will be fatal, a reasonable person might 
well consider the risk significant and take the appropriate steps to 
decrease or eliminate it. (IUD v. API,448 U.S. at 655).

The Court further stated, ``The requirement that a `significant' risk 
be identified is not a mathematical straitjacket * * *. Although the 
Agency has no duty to calculate the exact probability of harm, it does 
have an obligation to find that a significant risk is present before it 
can characterize a place of employment as `unsafe' and proceed to 
promulgate a regulation.'' (IUD v. API,448 U.S. at 655).
    Table VIII-1 presents the estimated excess risk of lung cancer 
associated with various levels of Cr(VI) exposure allowed under the 
current rule, based on OSHA's risk assessment and assuming either 20 
years' or 45 years' occupational exposure to Cr(VI) as indicated. The 
purpose of the OSH Act, as stated in Section 6(b), is to ensure ``that 
no employee will suffer material impairment of health or functional 
capacity even if such employee has regular exposure to the hazard * * * 
for the period of his working life.'' 29 U.S.C. 655(b)(5). Taking a 45-
year working life from age 20 to age 65, as OSHA has done in 
significant risk determinations for previous standards, the Agency 
preliminarily finds an excess lung cancer risk of approximately 100 to 
350 per 1000 workers exposed at the current PEL of 52 [mu]g/
m<SUP>3</SUP> Cr(VI). This risk is clearly significant, falling well 
above the level of risk the Supreme Court indicated a reasonable person 
might consider acceptable. Even assuming only a 20-year working life, 
the excess risk of about 50 to 200 per 1000 workers is still clearly 
significant. The proposed PEL of 1 [mu]g/m<SUP>3</SUP> Cr(VI) is 
expected to reduce these risks substantially, to below 10 excess lung 
cancers per 1000 workers. However, even at the proposed PEL, the risk 
posed to workers with a lifetime of regular exposure is still clearly 
significant.

                       Table VIII-1.--Expected Excess Lung Cancer Deaths Per 1000 Workers
----------------------------------------------------------------------------------------------------------------
                                                                 Cr(VI)
                                                              concentratin,        20-year           45-year
                                                                [mu]g/m3          exposure          exposure
----------------------------------------------------------------------------------------------------------------
Current PEL...............................................                52            43-198           101-351
                                                                          20             17-83            41-164
                                                                          10              9-43             21-86
                                                                         5.0            4.3-22             10-45
                                                                         2.5            2.1-11            5.3-23
Proposed PEL..............................................               1.0          0.85-4.4           2.1-9.1
                                                                         0.5          0.43-2.2           1.1-4.6
                                                                        0.25          0.21-1.1          0.53-2.3
----------------------------------------------------------------------------------------------------------------

    Workers exposed to lower concentrations of Cr(VI) and for shorter 
periods of time may also have significant excess cancer risk. OSHA's 
estimates of risk are therefore proportional to concentration for any 
given exposure duration; for example, workers exposed for 20 years to 
10 [mu]g/m<SUP>3</SUP> Cr(VI) have about ten times the risk of workers 
exposed for 20 years to 1 [mu]g/m<SUP>3</SUP> Cr(VI). The Agency's risk 
estimates are also roughly proportional to duration for any given 
exposure concentration, but not exactly proportional due to competing 
mortality effects. The estimated risk to workers exposed at any fixed 
concentration for 10 years is about one-half the risk to workers 
exposed for 20 years; the risk for five years' exposure is about one-
fourth the risk for 20 years. For example, about 11 to 55 out of 1000 
workers exposed at the current PEL for five years are expected to die 
from lung cancer as a result of their exposure. Those exposed to 5 
[mu]g/m<SUP>3</SUP> Cr(VI) for 5 years have an estimated excess risk of 
1-6 lung cancer deaths per 1000 workers. It is thus not only workers 
exposed for many years at high levels who have significant cancer risk 
under the current standard; even workers exposed for shorter periods at 
levels below the current PEL are at substantial risk, and will benefit 
from implementation of the proposed PEL.
    To further demonstrate significant risk, OSHA compares the risk 
from currently permissible Cr(VI) exposures to risks found across a 
broad variety of occupations. The Agency has used similar occupational 
risk comparisons in the significant risk determination for substance-
specific standards promulgated since the benzene decision. This 
approach is supported by evidence in the legislative record that 
Congress intended the Agency to regulate unacceptably severe 
occupational hazards, and not ``to establish a utopia free from any 
hazards''(116 Cong. Rec. 37614 (1970), Leg. Hist 480), or to address 
risks comparable to those that exist in virtually any occupation or 
workplace. It is also consistent with Section 6(g) of the OSH Act, 
which states: ``In

[[Page 59392]]

determining the priority for establishing standards under this section, 
the Secretary shall give due regard to the urgency of the need for 
mandatory safety and health standards for particular industries, 
trades, crafts, occupations, businesses, workplaces or work 
environments.''
    Fatal injury rates for most U.S. industries and occupations may be 
obtained from data collected by the Bureau of Labor Statistics. Table 
VIII-2 shows average annual fatality rates per 1000 employees for 
several industries between 1992 and 2001, as well as projected 
fatalities per 1000 employees for periods of 20 and 45 years based on 
these annual rates (Ex. 35-305). While it is difficult to compare 
aggregate fatality rates meaningfully to the risks estimated in the 
quantitative risk assessment for Cr(VI), which target one specific 
hazard (inhalation exposure to Cr(VI)) and health outcome (lung 
cancer), these rates provide a useful frame of reference for 
considering risk from Cr(VI) inhalation. For example, OSHA's best 
estimate of excess lung cancer deaths per 1000 workers from regular 
occupational exposure to Cr(VI) in the range of 2.5-5 [mu]g/
m<SUP>3</SUP> is roughly comparable to the average number of fatal 
injuries in high-risk occupations such as mining, assuming the same 
duration of employment (see Table VIII-1). Regular exposures at higher 
levels, including the current PEL of 52 [mu]g/m<SUP>3</SUP> Cr(VI), are 
expected to cause substantially more deaths per 1000 workers from lung 
cancer than result from occupational injuries in most private industry. 
At the proposed PEL of 1 [mu]g/m<SUP>3</SUP> Cr(VI) the Agency's 
estimate of excess lung cancer mortality falls much closer to the 
private industry average fatal injury rate, given the same employment 
time, but still exceeds the rates found in lower-risk industries such 
as finance and health services.

                          Table VIII-2.--Fatal Inuries per 1000 Employees, by Industry
----------------------------------------------------------------------------------------------------------------
                                                               Over 1 year      Over 20 years     Over 45 years
----------------------------------------------------------------------------------------------------------------
All Private Industry......................................              0.06               1.1               2.5
Coal Mining...............................................              0.41               8.3              18.6
Mining (General)..........................................              0.27               5.5              12.3
Construction..............................................              0.19               3.9               8.7
Manufacturing.............................................              0.04               0.8               1.8
Wholesale Trade...........................................              0.04               0.8               1.7
Retail Trade..............................................              0.03               0.6               1.4
Finance, Insurance, and Real Estate.......................              0.02               0.3               0.7
Health Services...........................................              0.01               0.2               0.4
----------------------------------------------------------------------------------------------------------------

    Because there is little available information on the incidence of 
occupational cancer, risk from Cr(VI) exposure cannot be compared with 
overall risk from other workplace carcinogens. However, OSHA's previous 
risk assessments provide estimates of risk from exposure to certain 
carcinogens. These risk assessments, like the current assessment for 
Cr(VI), were based on animal or human data of reasonable or high 
quality and used the best information then available. Table VIII-3 
shows the Agency's best estimates of cancer risk from 45 years' 
occupational exposure to several carcinogens, as published in the 
preambles to final rules promulgated since the benzene decision in 
1980.

                  Table VIII-3.--Selected OSHA Risk Estimates (Excess Cancers per 1000 Workers)
----------------------------------------------------------------------------------------------------------------
            Standard                Risk at prior PEL       Risk at current PEL        Federal Register date
----------------------------------------------------------------------------------------------------------------
Ethylene Oxide.................  63-109 per 1000........  1.2-2.3 per 1000.......  June 22, 1984.
Asbestos.......................  64 per 1000............  6.7 per 1000...........  June 20, 1986.
Benzene........................  95 per 1000............  10 per 1000............  September 11, 1987.
Formaldehyde...................  0.4-6.2 per 1000.......  .0056 per 1000.........  December 4, 1987.
Formaldehyde...................  * .0056 per 1000.......  * <.0056 per 1000......  May 27, 1992.
Methylenedianiline.............  ** 6-30 per 1000.......  0.8 per 1000...........  August 10, 1992.
Cadmium........................  58-157 per 1000........  3-15 per 1000..........  September 14, 1992.
1,3-Butadiene..................  11.2-59.4 per 1000.....  1.3-8.1 per 1000.......  November 4, 1996.
Methylene Chloride.............  126 per 1000...........  3.6 per 1000...........  January 10, 1997.
Chromium VI....................  .......................  106-351 per 1000.......  October 2004
----------------------------------------------------------------------------------------------------------------
* From information in December 4, 1987 Federal Register.
** No prior standard; reported risk is based on estimated exposures at the time of the rulemaking.

    At 106-351 excess lung cancer deaths per 1000 workers, the 
estimated risk from lifetime occupational exposure to Cr(VI) at the 
current PEL is much higher than the estimated risk from permissible 
exposures to other workplace carcinogens for which OSHA has performed 
risk assessments (Table VIII-3, ``Risk at Current PEL''). The Cr(VI) 
risk estimate is also higher than many risks the Agency has found to be 
significant in previous rules (Table VIII-3, ``Risk at Prior PEL''). 
The estimated risk from lifetime occupational exposure to Cr(VI) at the 
proposed PEL is 2.2-9.1 excess lung cancer deaths per 1000 workers, a 
range comparable to the risks from other carcinogenic exposures 
remaining under recent rules (Table VIII-3, ``Risk at Current PEL'').
    Based on the results of the quantitative risk assessment, the 
Supreme Court's guidance on acceptable risk, comparison with rates of 
occupational fatality in various industries, and comparison with cancer 
risk estimates developed in previous rules, OSHA preliminarily finds 
that the risk of lung cancer posed to workers under currently 
permissible levels of occupational Cr(VI) exposure is significant. The 
proposed PEL of 1 [mu]g/m<SUP>3</SUP> is expected to significantly 
reduce risks to workers in Cr(VI)-exposed occupations. OSHA 
additionally finds that nasal septum ulceration and

[[Page 59393]]

perforation can occur with significant frequency and seriousness in 
exposure conditions allowed by the current rule. The proposed reduction 
of the Cr(VI) PEL from 52 [mu]g/m<SUP>3</SUP> to 1 [mu]g/m<SUP>3</SUP> 
is expected to substantially reduce or eliminate workers' risk of these 
adverse health effects.

IX. Summary of the Preliminary Economic Analysis and Initial Regulatory 
Flexibility Analysis

A. Introduction

    OSHA's Preliminary Economic and Initial Regulatory Flexibility 
Analysis (PEA) addresses issues related to the costs, benefits, 
technological and economic feasibility, and the economic impacts 
(including small business impacts) of the Agency's Occupational 
Exposure to Hexavalent Chromium rule. The full Preliminary Economic and 
Regulatory Flexibility Analysis has been placed in the docket as Ex. 
35-391. The analysis also evaluates regulatory alternatives to the 
proposed rule. This rule is an economically significant rule under 
3(f)(1) of Executive Order 12866 and has been reviewed by the Office of 
Information and Regulatory Affairs in the Office of Management and 
Budget, as required by executive order.
    The purpose of this Preliminary Economic and Regulatory Flexibility 
Analysis is to:
    <bullet> Identify the establishments and industries potentially 
affected by the proposed rule;
    <bullet> Estimate current exposures and the technologically 
feasible methods of controlling these exposures;
    <bullet> Estimate the benefits of the rule in terms of the 
reduction in lung cancer and dermatoses employers will achieve by 
coming into compliance with the standard;
    <bullet> Evaluate the costs and economic impacts that 
establishments in the regulated community will incur to achieve 
compliance with the proposed standard;
    <bullet> Assess the economic feasibility of the rule for affected 
industries; and
    <bullet> Evaluate the principal regulatory alternatives to the 
proposed rule that OSHA has considered.
    The Full Preliminary Economic Analysis contains the following 
chapters:

Chapter I. Introduction
Chapter II. Industrial Profile
Chapter III.Technological Feasibility
Chapter IV. Costs of Compliance
Chapter V. Economic Impacts
Chapter VI. Benefits and Net Benefits
Chapter VII. Regulatory Flexibility Analysis
Chapter VIII. Environmental Impacts
Chapter IX. Non Regulatory Alternatives.

    These chapters are summarized in sections B to G of this Preamble 
summary.

B. Introduction and Industrial Profile (Chapters I and II)

    The proposed standard for occupational exposure to hexavalent 
chromium was developed by OSHA in response to evidence that 
occupational exposure to Cr(VI) poses a significant risk of lung 
cancer, nasal septum ulcerations and perforations and dermatoses. 
Exposure to Cr(VI) can also lead to asthma. To protect exposed workers 
from these effects, OSHA has set a Permissible Exposure Limit (PEL) of 
1 [mu]g/m<SUP>3</SUP> measured as an 8-hour time weighted average. OSHA 
has also examined alternative PELs ranging from 20 [mu]g/m<SUP>3</SUP> 
to 0.25 [mu]g/m<SUP>3</SUP> measured as 8-hour time weighted averages.
    OSHA's proposed standards for occupational exposure to Cr(VI) are 
similar in format and content to other OSHA health standards 
promulgated under Section 6(b)(5) of the Act. In addition to setting 
PELS, the proposal requires employers to:
    <bullet> Monitor the exposure of employees (except in shipyards and 
construction);
    <bullet> Establish regulated areas when exposures may reasonably be 
expected to exceed the PEL (except in shipyards and constructions);
    <bullet> Implement engineering and work practice controls to reduce 
employee exposures to Cr(VI);
    <bullet> Provide respiratory protection to supplement engineering 
and work practice controls where they are not feasible, where such 
controls are insufficient to meet the PELS, or in emergencies;
    <bullet> Provide other protective clothing and equipment as 
necessary for dermal protection;
    <bullet> Make industrial hygiene facilities (hand washing stations) 
available in some situations;
    <bullet> Provide medical surveillance when employees are exposed 
above the PEL in general industry (In the shipyard and construction 
sectors, medical exposure is only required for signs or symptoms of 
Cr(VI) related disease);
    <bullet> Train workers about the hazards of Cr(VI) (including 
elements already required by OSHA's Hazard Communication Standard); and
    <bullet> Keep records related to the standard.
    The contents of the standards, and the reasons for proposing the 
separate standards for general industry, construction and shipyard 
employment, are more fully discussed the Summary and Explanation 
Section of this Preamble.
    Chapter II of the full PEA describes the uses of Cr(VI) and the 
industries in which such uses occur. Employee exposures are defined in 
terms of ``application groups,'' i.e., groups of firms where employees 
are exposed to Cr(VI) when performing a particular function. This 
methodology is appropriate to exposure to Cr(VI) where a widely used 
chemical like chromium may lead to exposures in many kinds of firms in 
many industries, but the processes used, exposures generated, and 
controls needed to achieve compliance may be the same. For example, 
because a given type of welding produces Cr(VI) exposures that are 
essentially the same regardless of whether the welding occurs in a 
ship, on a construction site, as part of a manufacturing process, or as 
part of a repair process, it is appropriate to analyze such processes 
as a group. However, OSHA's analysis of costs and economic feasibility 
reflect the fact that baseline controls, ease of implementing ancillary 
provisions, and the economic situation of the employer may differ 
within different industries in an application group. One complication 
with the use of the application group concept is that some firms may 
have exposures in two or more different application groups. For 
example, a large transportation equipment company may engage in 
chromium electroplating, painting with paints that use chromium 
pigments, and welding of metal containing chromium.
    The most common reasons to encounter occupational exposure to 
Cr(VI), in addition to the production and use of chromium metal and 
chromium metal alloys, are chromium electroplating; welding of metals 
containing chromium, such as stainless steel or other high chromium 
steels, or with chromium coatings; the production and use of Cr(VI) 
containing compounds, particularly Cr(VI) pigments, but also Cr(VI) 
catalysts, chromic acid, and the production of chromium-containing 
pesticides.
    Some industries are seeing sharp declines in chromium use. However, 
many of the industries that are seeing a sharp decline have either a 
small number of employees or have low exposure levels (e.g., Wood 
Working, Printing Ink Manufacturers, and Printing). In the case of lead 
chromate in Pigment Production, OSHA's sources indicate that there is 
no longer domestic output containing lead chromates. Therefore, this 
trend has been recognized in the PEA. Painting activities in General 
Industry primarily

[[Page 59394]]

involve the application of strontium chromate coatings to aerospace 
parts; these exposures are likely to continue into the foreseeable 
future. Similarly, removal of lead chromate in Construction and 
Maritime is likely to present occupational risks for many years.
    In application groups where exposures are particularly significant, 
both in terms of workforce size and exposure levels--notably in 
electroplating and welding--OSHA anticipates very little decline in 
exposures to hexavalent chromium due to the low potential for 
substitution in the foreseeable future.
    Table IX-1 shows the application groups analyzed in OSHA's PEA, as 
well as the principle industries in each application group, and for 
each provides the number of establishments affected, the number of 
employees working in those establishments, the number of entities 
(firms or governments) fitting SBA's small business criteria for the 
industry, and the number of employees in those firms. (The table shows 
data for both establishments, and entities-defined as firms or 
governments. An entity may own more than one establishment.) The table 
also shows the revenues of affected establishment and entities. (This 
table provides the latest available data at the time this analysis was 
produced. However, since the analysis was produced, there have been 
changes to some of the affected industries. OSHA will continue to 
incorporate more recent data as it becomes available.) As shown in the 
table, there are a total of 38,000 to 55,000 establishments, depending 
on the degree of overlap between application groups in some industries, 
affected by the proposed standard.

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[[Page 59403]]


[GRAPHIC] [TIFF OMITTED] TP04OC04.011

    Various types of welding applications account for the greatest 
number of establishments and number of employees affected by the 
proposed standard.

[[Page 59404]]

    Table IX-2 shows the current exposures to Cr(VI) by application 
group. The exposure data relied on by OSHA in developing the exposure 
profile and evaluating technological feasibility was compiled in a 
database of exposures taken from OSHA compliance officers, Site visits 
by OSHA contractors and the National Institute for Occupational Safety 
and Health (NIOSH), the U.S. Navy, published literature, and interested 
parties.
    In all sectors OSHA has used the best available information to 
determine baseline exposures and technological feasibility. In a few 
sectors this information has been difficult to obtain and OSHA has had 
to rely on limited data in the industry or used analogous operations 
from similar processes. In these cases OSHA (or its contractor) 
discussed issues with industry experts and used their professional 
judgment to determine technological feasibility. The sectors that fall 
into the above categories are steel mills, welding in construction, 
woodworking and catalyst users.
    Data obtained for steel mills included several sources such as 
NIOSH HHEs, IMIS exposure data and a site visit from IT Corporation, an 
OSHA contractor. OSHA's contractor could only obtain permission to 
conduct a site visit at a steel mill that used the teeming and primary 
rolling method versus continuous casting which is now used in 
approximately 95% of the steel mills. OSHA acknowledges this and uses 
exposures from analogous operations with additional information from 
industry experts. OSHA requests worker exposure information from steel 
mills using the continuous casting process. Exposure information was 
also limited for welding at construction sites. OSHA could use 
analogous operations from welding in maritime in open spaces. This 
could give a more detailed distribution for the baseline exposure 
profile. OSHA requests comments on the use of the Maritime data as an 
analogous operation for welding at construction sites.
    In several sectors, such as woodworking and catalyst use, OSHA 
anticipates that airborne exposures will be low. In these cases 
exposure monitoring has been performed infrequently. OSHA then used 
professional judgment or has calculated exposure using total dust 
exposure to estimate employees' exposures to Cr(VI).
    OSHA's analysis of technological feasibility analyzes employee 
exposures at the operation or task level to the extent that such data 
are available. There are a total of 380,000 workers exposed to Cr(VI), 
of which 84,000 are exposed above the proposed PEL of 1 microgram per 
cubic meter.

[[Page 59405]]

[GRAPHIC] [TIFF OMITTED] TP04OC04.012


[[Page 59406]]


[GRAPHIC] [TIFF OMITTED] TP04OC04.013

C. Technological Feasibility

    In Chapter II of OSHA's PEA, OSHA also assesses the technological 
feasibility of the proposed standard across a range of potential PELs 
in all affected industry sectors.
    Many employers, and some entire application groups already have 
nearly all exposures below the proposed PEL. However, OSHA recognizes 
that some employers in some application groups may not be able to 
achieve the proposed PEL with engineering controls and work practices 
for all job categories and may need to use respirators.
    In general, OSHA considered the following kinds of possible 
controls that could reduce employee exposures to Cr(VI): Local exhaust 
ventilation (LEV) which could include the maintenance or upgrade of the 
current LEV or installation of additional LEV; process enclosures that 
would isolate the worker

[[Page 59407]]

from the exposure; process modifications that would reduce the 
generation of Cr(VI) dust or fume in the work place; improved 
housekeeping; improved work practices; and the supplemental use of 
respiratory protection if engineering controls are not sufficient to 
meet the proposed PEL. The technologies used in this analysis are 
commonly known, readily available and are currently used to some extent 
in the affected industries and processes. OSHA's assessment of feasible 
controls and what PELs they can achieve is based on information 
collected by Shaw Environmental, Inc., consultant to OSHA, on current 
exposure levels and associated existing controls, on the availability 
of additional controls needed to reduce employee exposures and on other 
evidence presented in the docket.
    OSHA has determined that the primary controls most likely to be 
effective in reducing employee exposure to Cr(VI) are LEV, process 
enclosure and process modification, or substitution. In some cases, 
firms need not improve their local exhaust systems, but instead must 
spend more effort insuring that the exhaust system is working according 
to design specification throughout the process. In other cases, 
employers will need to upgrade or install new LEV. This includes 
installing duct work, a type of hood and/or a collection system. 
Examples of processes that would need to improve, maintain, or install 
LEV include hard chrome plating and welding processes that generate 
large volumes of fume such as shielded metal arc welding (SMAW) and gas 
metal arc welding (GMAW). (LEV is defined to include portable LEV 
systems such as fume extraction guns (FEG).) Other sectors where new or 
better maintained LEV may be needed are: painting and abrasive 
blasting, chromate production, the production of pigments, catalyst, 
dyes and plastic colorants.
    OSHA estimates that process enclosures will be needed for difficult 
to control operations such as dusty operations. These enclosures would 
isolate the employees from high exposure processes and reduce the need 
for respirators. For example, the packaging of chromic acid in small 
bags is totally enclosed and therefore, employees only need to enter 
the room during product upset or planned changes. This technology could 
also be applied to other packaging operations involving similar sized 
bags in other industries such as pigment manufacturing, catalyst 
production and plastic colorants. Process modifications can also be 
effective in reducing exposures in some industries. For example, 
employers can significantly reduce employee exposure through the use of 
automation in catalyst production, the use of fume suppressants in 
electroplating and significant reduction of welding fume emission, by 
up to 80 percent, is attainable using the pulsed arc GMAW welding 
process as compared to the conventional short arc GMAW process.
    OSHA recognizes that there are certain instances where the 
supplemental use of respirators may be needed because engineering and 
work practices are not sufficient to reduce airborne exposures below 
the proposed PEL. For example, this is the case for hard chrome 
electroplating in some circumstances. There are many factors that are 
involved in the generation of Cr(VI) including the size of the part and 
the thickness of the coating needed. In some worst case conditions, 
respirators will be needed to supplement engineering controls. Welding 
also includes many factors that contribute to Cr(VI) exposures; these 
include type of welding, the base metal, the consumable, as well as the 
environment in which the welding is being conducted. As a result, 
engineering controls and work practices may not be sufficient in the 
most severe conditions and therefore the supplemental use of 
respirators will be needed. Table IX-3 shows OSHA's estimate of 
respirator use by industry for each of the proposed PELs.
    Table IX-3 identifies sectors where respirators will be needed for 
some workers. Even at a PEL of 1 [mu]g/m\3\, a majority of exposed 
workers in the chromium catalyst user application group will need 
respirators, but this use is largely intermittent. As a result, workers 
will not need to wear respirators on a daily basis.
    PELs lower than 1 [mu]g/m<SUP>3</SUP> could not be achieved by 
means of engineering controls and work practices alone for some types 
of welding (particularly GMAW and SMAW) and in hard chromium plating. 
Based on this finding, OSHA has preliminarily determined that a PEL of 
1 [mu]g/m<SUP>3</SUP> is the lowest technologically feasible level.
    For a complete analysis of technical feasibility please see the 
Preliminary Economic Analysis, Chapter III, where feasibility is 
reviewed for each industry/process by job category.

[[Page 59408]]

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[[Page 59409]]


[GRAPHIC] [TIFF OMITTED] TP04OC04.015

D. Costs

    The costs employers are expected to incur to comply with the 
proposed standard are $223 million per year. In addition, OSHA 
estimates that employers will incur $67 million per year to comply with 
the personal protective equipment and hygiene requirements already 
present in existing generic standards. The proposed requirements to 
provide protective clothing and equipment and hygiene

[[Page 59410]]

areas are closely aligned with the requirements of OSHA's current 
generic PPE and Sanitation standards (e.g. 1910.132 and 1926.95 for PPE 
and 1910.142 and 1926.51 for the hygiene requirements). Therefore, OSHA 
estimates that the marginal cost of complying with the new PPE and 
sanitation requirements of the Cr(VI) standard were lower for firms 
currently subject to and in compliance with existing generic standards. 
OSHA's research on these current standards, however, uncovered some 
noncompliance. The baseline chosen for the Cr(VI) regulatory impact 
analysis reflects this non-compliance with current requirements. 
Although OSHA estimates that employers would need to spend an 
additional $67 million per year to bring themselves into compliance 
with the personal protective equipment and hygiene requirements already 
prescribed in existing generic standards, this additional expenditure 
is not attributable to the Cr(VI) rulemaking. However, by incurring the 
obligation and expense of providing PPE to their employees, employers 
are essentially transferring a benefit to employees $24 million per 
year.
    All costs are measured in 2003 dollars. Any one-time costs are 
annualized over a ten year period, and all costs are annualized at a 
discount rate of 7 percent. (A sensitivity analysis using a discount 
rate of 3 percent is presented in the discussion of net benefits.) The 
derivation of these costs is presented in Chapter III of the full PEA. 
Table IX-4 provides the annualized costs by provision and by industry. 
Engineering control costs represent 45 percent of the costs of the new 
provisions of the proposed standard, and respiratory protection costs 
represent 19 percent of the costs of the new provisions of the proposed 
standard.

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[[Page 59413]]


[GRAPHIC] [TIFF OMITTED] TP04OC04.018

    Costs for the new provisions for General Industry are $179 million 
per year, costs for constructions $35 million per year, and costs for 
the shipyard sector and $9 million per year. (In developing the costs 
for construction, OSHA assumed that all work by construction firms 
would be covered by the construction standard. However, in practice 
some work by construction firms takes the form of maintenance 
operations that would be covered by the

[[Page 59414]]

general industry standard. OSHA seeks comment on the extent to which 
welding, painting, and wood working done by construction firms might be 
covered by the general industry standard.) Table IX-4 also shows the 
costs by application group. The various types of welding represent the 
most expensive application group, accounting for 47 percent of the 
total costs.
    OSHA also presents the distribution of compliance costs according 
at the time they are imposed in Table IX-5. Because firms will have the 
choice of whether to finance expenditures in order to spread out, for 
example, startup costs over several years, OSHA considers it unlikely 
that a firm would be impacted in an amount equal to the entire startup 
cost in the year that the initial requirements are imposed. On the 
other hand, capital markets are not perfectly liquid and particular 
firms may face additional lending constraints, therefore OSHA believes 
that identifying startup costs and the time distribution of imposed 
costs, in addition to the annualized costs, is relevant when exploring 
the question of economic feasibility and the overall impact of this 
rulemaking.

E. Economic Impacts

    To determine whether the proposed rule's projected costs of 
compliance would raise issues of economic feasibility for employers in 
affected industries, i.e., would adversely alter the competitive 
structure of the industry,

[[Page 59415]]

[GRAPHIC] [TIFF OMITTED] TP04OC04.019

    OSHA developed quantitative estimates of the economic impact of the 
proposed rule on the affected establishments. In this analysis, 
compliance costs are compared with industry revenues and profits.
    To assess the potential economic impacts of the proposed standard, 
OSHA compared the anticipated costs of achieving compliance against 
revenues and profits of entities affected by the rule. OSHA compared 
the baseline financial data (from Table IX-1) with total annualized 
costs of compliance by computing compliance costs as a percentage of 
revenues. This impact assessment is presented in Table IX-6. This table 
is considered a screening analysis because it measures costs as a 
percentage of pre-tax profits and revenues but does not predict impacts 
on pre-tax profits and sales.

[[Page 59416]]

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[[Page 59417]]


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[[Page 59418]]


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[[Page 59419]]


[GRAPHIC] [TIFF OMITTED] TP04OC04.023

    This screening analysis is used to determine whether the compliance 
costs potentially associated with the standard would lead to 
significant impacts on establishments in the affected industries. The 
actual impact of the standard on the viability of establishments in a 
given industry will depend on the price elasticity of demand for the 
services sold by establishments in that industry.
    Price elasticity refers to the relationship between the price 
charged for a service and the demand for that service; that is, the 
more elastic the relationship, the less able an establishment is to 
pass the costs of compliance through to its customers in the form of a 
price increase and the more it will have to absorb the costs of 
compliance from its profits. When demand is inelastic, establishments 
can recover most of the costs of compliance simply by raising the 
prices they charge for that service; under this scenario, profit rates 
are largely unchanged and the industry remains viable. On the other 
hand, when demand is elastic, establishments cannot recover all the 
costs simply by passing the cost increase through in the form of a 
price increase; instead, they must absorb some of the increase from 
their profits. Commonly, this will mean both reductions in the quantity 
of goods and services produced and in profits. In general, ``when an 
industry is subject to a higher cost, it does not simply swallow it, it 
raises its price and reduces its output, and in this way shifts a part 
of the cost to its consumers and a part to its suppliers,'' in the 
words of the court in American Dental Association v. Secretary of Labor 
(984 F.2d 823, 829 (Seventh Cir. 1993)).
    Specifically if demand is completely inelastic (i.e., price 
elasticity is 0), then the impact of compliance costs that amount to 1 
percent of revenues would be a 1 percent increase in the price of the 
product or service, with no decline in demand or in profits. Such a 
situation is rare but might be approximately correct in situations in 
which there are few, if any, substitutes for the product or service 
offered by the affected sector or if the products or services of the 
affected sector account for only a small portion of the income of its 
consumers. If the demand is perfectly elastic (i.e., the price 
elasticity is infinitely large), then no increase in price is possible, 
and before-tax profits would be reduced by an amount equal to the costs 
of compliance (minus any savings resulting from improved worker health) 
if the industry attempted to keep producing the same amount of goods 
and services as previously. Under this scenario, if the costs of 
compliance represent a large percentage of the sector's profits, some 
establishments might be forced to close. This scenario is highly 
unlikely to occur, however, because it can only arise when there are 
other goods and services that are, in the eye of the consumer, perfect 
substitutes for the goods and services the affected establishments 
produce or provide.
    A common intermediate case would be a price elasticity of one. In 
this situation, if the costs of compliance amount to 1 percent of 
revenues, then production would decline by 1 percent and prices would 
rise by 1 percent. In this case, the industry revenues would stay the 
same, with somewhat lower production but similar profit rates. 
Consumers would, however, get less of the product or the service for 
their expenditures, and producers would collect lower total profits; 
this, as the court described in ADA v. Secretary of Labor, is the more 
typical case.
    Table IX-6 provides costs as percentage of revenues and profits for 
all affected establishments. OSHA believes that this is the best way to 
examine its statutory responsibility to determine whether the standard 
affects the viability of an industry as a whole. There is only one 
industry where costs exceed one percent of revenues (chromium catalyst 
production), and none in which costs exceed 1.5 percent of revenues. In 
only four industries (electroplating, construction welding, chromium 
catalyst production and chromium catalyst service) do compliance costs 
exceed 10 percent of profits.
    In the case of construction, such cost changes are unlikely to 
significantly alter the demand for construction welding services which 
are essential for many projects and not subject to foreign competition. 
Independent electroplating shops have also been subject to annual 
changes larger in magnitude than the

[[Page 59420]]

costs of hexavalent chromium. The required price increase to fully 
restore profits of 0.93 percent is significantly less than the average 
annual increase in price of electroplating services. While such an 
additional price change might cause some small drop in the demand for 
services, the historical data clearly show that such price changes can 
be incurred without affecting the viability of the industry. Chromium 
catalyst production and service companies are also unlikely to be 
affected by costs of the relative magnitude found here. While there may 
be a small long term shift from the use of chromium catalysts as a 
result of the regulation, most companies are locked into the use of 
specific catalyst without major new investments. As a result, while 
there may be some long term shift away from the use of chromium 
catalysts, a price change of one percent are unlikely to immediately 
prompt such a change. This also means that the market for the services 
of chrome catalyst services is likely to be maintained. Further, faced 
with a new regulation, companies are more rather than less likely to 
turn to a service company to handle chromium products. Based on these 
considerations, OSHA preliminarily determines that the proposed 
standard is economically feasible.
    Table IX-7 shows costs as percentage of profits and revenues for 
firms classified as small by the Small Business Administration and 
Table IX-8 shows costs as a percentage of revenues and profits for 
establishments with less than 20 employees. These Tables show greater 
potential impacts, especially for small electroplating establishments. 
Based on these results, OSHA has prepared an Initial Regulatory 
Flexibility Analysis to examine the impacts on small businesses and how 
they can be alleviated.

[[Page 59421]]

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[[Page 59428]]


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F. Benefits and Net Benefits

    OSHA estimated the benefits associated with alternative PELs for 
Cr(VI) by applying the dose-response relationship developed in the risk 
assessment to current exposure levels. OSHA determined current exposure 
levels by first developing an exposure profile for industries with 
Cr(VI) exposures using OSHA inspection and site visit data, and then 
applying this profile to the current worker population. The industry by 
industry exposure profile was given in Table IX-2 above.
    By applying the dose-response relationship to estimates of current 
exposure levels across industries, it is possible to project the number 
of lung cancers expected to occur in the worker population given 
current exposures (the ``baseline''), and the number of these cases 
that would be avoided under alternative, lower PELs. OSHA assumed that 
exposures below the limit of detection (LOD) are equivalent to no 
exposure to Cr(VI), thus assigning no baseline or avoided lung cancers 
(and hence, no benefits) to these exposures. For exposures above the 
current PEL and for purposes of determining the benefit of reducing the 
PEL, OSHA assumed exposure at exactly the PEL. Consequently, the 
benefits computed below are attributable only to a change in the PEL. 
No benefits are assigned to the effect of a new standard increasing 
compliance with the current PEL. OSHA estimates that between 2,247 and 
8,708 lung cancers attributable to Cr(VI) exposure will occur during 
the working lifetime of the current worker population. Table IX-9 shows 
the number of avoided lung cancers by PEL. At the proposed PEL of 1 
[mu]g/m<SUP>3</SUP>, and estimated 1,970 to 7,500 lung cancers would be 
prevented over the working lifetime of the current worker population.

                                                   Table IX-9.--Avoided Lung Cancers Estimates by PEL
--------------------------------------------------------------------------------------------------------------------------------------------------------
                    PEL ([mu]g/\3\m)                           0.25             0.5              1               5              10              20
--------------------------------------------------------------------------------------------------------------------------------------------------------
Avoided Cancers (Total).................................     2,147-8,270     2,078-7,968     1,970-7,500     1,440-5,233     1,052-3,649       585-1,864
Avoided Cancers (Annual)................................          48-184          46-177          44-167          32-116           23-81           13-41
--------------------------------------------------------------------------------------------------------------------------------------------------------

    Note that the Agency based these estimates on a worker that is 
employed in a Cr(VI) exposed occupation for his entire working life, 
from age 20 to 65. The calculation also does not allow workers to enter 
or exit Cr(VI) jobs, or switch to other exposure groups during their 
working lives. While the assumptions of 45 years of exposure and no 
mobility among exposure groups may seem restrictive, these assumptions 
actually are likely to yield somewhat conservative estimates of the 
number of avoided cancers, given the nature of the risk assessment 
model. For example, consider the case of job covered by five workers, 
each working nine years rather than one worker for 45 years. The former 
situation will likely yield a slightly higher rate of lung cancers, 
since more workers are exposed to the carcinogen (albeit for a shorter 
period of time) and that the average age of the workers exposed is 
likely to decrease. This is due to: (1) The linearity of the estimated 
dose-response relationship, and (2) once an individual accumulates a 
dose, the increase in relative risk persists for the remainder of his 
lifetime. For example, a worker exposed from age 20 to 30 will have a 
constant increased relative risk for about 50 or so years (from age 30 
on, assuming no lag between exposure and increased risk and death at 
age 80), whereas a person exposed from age 40 to 50 will have only 
about 30 years of increased risk (again assuming no lag and death at 
age 80). The persistence of the increased relative risk for a lifetime 
follows directly from the risk assessment, and is typical of life table 
analysis. OSHA intends to investigate the implications of alternative 
exposure scenarios in the

[[Page 59429]]

course of further developing its economic benefits assessment.
    For informational purposes only, OSHA has estimated the monetary 
value of the benefits associated with the draft proposed rule. These 
estimates are informational because OSHA cannot use benefit-cost 
analysis as a basis for determining the PEL for a health standard. In 
order to estimate monetary values for the benefits associated with the 
proposed rule, OSHA reviewed the approaches taken by other regulatory 
agencies for similar regulatory actions. OSHA found that occupational 
illnesses are analogous to the types of illnesses targeted by EPA 
regulations and has thus used them in this analysis.
    OSHA is adopting EPA's approach, applying a value of $6.8 million 
to each premature fatality avoided. The $6.8 million value represents 
individuals' willingness-to-pay (WTP) to reduce the risk of premature 
death.
    Nonfatal cases of lung cancer can be valued using a cost of illness 
(COI) approach, using data on associated medical costs. The EPA Cost of 
Illness Handbook (Ex.35-333) reports that the medical costs for a 
nonfatal case of lung cancer are, on average, $136,460. Updating the 
EPA figure to 2003 dollars yields the value of $160,030 Including 
values for lost productivity, the total COI which is applied to the 
OSHA estimate of nonfatal cases of lung cancer is $188,502.
    An important limitation of the COI approach is that it does not 
measure individuals' WTP to avoid the risk of contracting nonfatal 
cancers or illnesses. As an alternative approach, nonfatal cancer 
benefits may be estimated by adjusting the value of lives saved 
estimates. In its Stage 2 Disinfection and Disinfection Byproducts 
water rule, EPA used studies on the WTP to avoid nonfatal lymphoma and 
chronic bronchitis as a basis for valuing nonfatal cancers. In sum, EPA 
valued nonfatal cancers at 58.3% of the value of a fatal cancer. Using 
WTP information would yield a higher estimate of the benefits 
associated with the reduction in nonfatal lung cancers, as the nonfatal 
cancers would be valued at $4 million rather than $188,502 per case. 
These values represent the upper bound values for nonfatal cases of 
lung cancer avoided.
    Using these assumptions, and latency periods of 10, 20 and 35 years 
and possible increases in the value of life over time, OSHA estimated 
the total annual benefits of the standard at various PELS in Table IX-
10, considering both the benefits from preventing fatal and non-fatal 
cases of lung cancer.

                                                     Table IX-10.--Total Annual Lung Cancer Benefits
                                                               [Millions of 2003 Dollars]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                    PEL ([mu]g/m\3\)                           0.25             0.5              1               5              10              20
--------------------------------------------------------------------------------------------------------------------------------------------------------
Undiscounted............................................      $287-1,189      $278-1,145      $263-1,078        $192-753        $141-525         $78-269
Discount Rate = 3%......................................       102-1,131        99-1,090        94-1,026          69-716          50-500          28-256
Discount Rate = 7%......................................          27-773          26-745          25-701          18-490          14-342           8-175
--------------------------------------------------------------------------------------------------------------------------------------------------------

    Occupational exposure to Cr(VI) has also been linked to a multitude 
of other health effects, including irritated and perforated nasal 
septum, skin ulceration, asthma, and dermatitis. Current data on Cr(VI) 
exposure and health effects are insufficient to quantify the precise 
extent to which many of these ailments occur. However, it is possible 
to provide an upperbound estimate of the number of cases of dermatitis 
that occur annually and an upper estimate of the number that will be 
prevented by a standard. This estimate is an upperbound because it uses 
data on incidence of dermatitis among cement workers, where dermatitis 
is more common than it would be for other exposures to Cr(VI). It is 
important to note that if OSHA were able to quantify all Cr(VI)-related 
health effects, the quantified benefits would be somewhat higher than 
the benefits presented in this analysis.
    Using National Institute for Occupational Safety and Health (NIOSH) 
data, Ruttenberg and Associates (Ex. XXXX) estimate that the incidence 
of dermatitis among concrete workers is between 0.2 and 1 percent. 
Applying the 0.2 percent-1 percent incidence rate indicates that there 
are presently 418-2,089 cases of dermatitis occurring annually. This 
approach represents an overestimate for cases of dermatitis in other 
application groups, since some dermatitis among cement workers is 
caused by other known factors, such as the high alkalinity of cement. 
If the measures in this draft proposed standard are 50 percent 
effective in preventing dermatitis, then there would be an estimated 
209-1,045 cases of Cr(VI) dermatitis avoided annually.
    To assign values to the cases of avoided dermatitis OSHA applied 
the COI approach. Ruttenberg and Associates computed that, on average, 
the medical costs associated with a case of dermatitis are $119 (in 
2003 dollars) and the indirect and lost productivity costs are $1,239. 
These estimates were based on an analysis of BLS data on lost time 
associated with cases of dermatitis, updated to current dollars. Based 
on the Ruttenberg values, OSHA estimates that a Cr(VI) standard will 
yield $0.3 million to $1.4 million in annual benefits due to reduced 
incidence of dermatitis. (These benefits associated with dermatitis are 
not included in the net benefits analysis, as these benefits largely 
result from full compliance with existing requirements for PPE and 
hygiene areas.)
    Occupational exposure to Cr(VI) can lead to nasal septum 
ulcerations and nasal septum perforations. As for cases of dermatitis, 
the data were insufficient to conduct a formal quantitative risk 
assessment to relate exposures and incidence. However, previous studies 
provide a basis for developing an approximate estimate of the number of 
nasal perforations expected under the current PEL as well as PELs of 
0.25 [mu]g/m\3\, 0.5 [mu]g/m\3\, 1.0 [mu]g/m\3\, 5.0 [mu]g/m\3\, 10.0 
[mu]g/m\3\ and 20.0 [mu]g/m\3\. Cases of nasal perforations were 
computed only for workers in electroplating and chrome production. The 
percentage of workers with nasal tissue damage is expected to be over 
50 percent for those regularly exposed above approximately 20 [mu]g/
m\3\. Less than 25 percent of workers could reasonably be expected to 
experience nasal tissue damage if Cr(VI) exposure was kept below an 8-
hour TWA of 5 [mu]g/m\3\ and regular short-term exposures e.g. an hour 
or so) were below 10 [mu]g/m\3\. Less than 10 percent of workers could 
reasonably be expected to experience nasal tissue damage at a TWA 
Cr(VI) below 2 [mu]g/m\3\ [and short-term exposures below 10 [mu]g/
m\3\]. It appears likely that nasal damage might be avoided completely 
if all Cr(VI) [short-term and full shift] exposures were kept below 1 
[mu]g/m\3\.
    OSHA estimates that 5,387 nasal perforations/ulcerations occur 
annually

[[Page 59430]]

under the current PEL. All of these are expected to be prevented under 
the proposed PEL of 1 [mu]g/m\3\. Due to insufficient data, it was not 
possible to monetize the benefits. Thus, the benefits associated with a 
reduction in nasal perforations/ulcerations are excluded from the net 
benefits analysis presented below.
    Finally, for informational purposes, OSHA examined the net benefits 
of the standard, based on the benefits and costs presented above, and 
the costs per case of cancer avoided as shown in Table IX-11.

                                          Table IX-11.--Annual Net Benefits and Cost Per Cancer Avoided by PEL
                                                               [Millions of 2003 Dollars]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                 PEL ([mu]g/m\3\ )                        0.25             0.5               1                5                10               20
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                   Discount Rate = 3%
                                                            Costs (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Total Annual......................................           $524             $381             $212             $119              $91              $81
---------------------------------------------------
                                                         Net Benefits (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Minimum...........................................           -422             -282             -119              -51              -41              -53
Maximum...........................................            606              708              813              596              408              174
Midpoint..........................................             92              213              347              273              183               60
---------------------------------------------------
                                                   Cost Per Cancer Avoided (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Minimum...........................................              2.9              2.2              1.3              1.0              1.1              2.0
Maximum...........................................             11.0              8.3              4.8              3.7              3.9              6.2
Midpoint..........................................              6.9              5.2              3.1              2.4              2.5              4.1
---------------------------------------------------
                                                                   Discount Rate = 7%
                                                            Costs (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Total Annual......................................            548              402              223              125               95               84
---------------------------------------------------
                                                         Net Benefits (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Minimum...........................................           -521             -376             -198             -107              -82              -77
Maximum...........................................            224              342              477              363              246               90
Midpoint..........................................           -149              -17              139              128               82                7
---------------------------------------------------
                                                   Cost Per Cancer Avoided (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Minimum...........................................              3.0              2.3              1.3              1.1              1.2              2.0
Maximum...........................................             11.5              8.7              5.1              3.9              4.1              6.5
Midpoint..........................................              7.2              5.5              3.2              2.5              2.6              4.2
--------------------------------------------------------------------------------------------------------------------------------------------------------

    In addition to examining alternative PELs, OSHA also examined 
alternatives to other provisions of the standard. These alternatives 
are discussed in the Initial Regulatory Flexibility Analysis in the 
next section.
    As noted above, the OSH Act requires OSHA to set standards based on 
eliminating risk to the extent feasible. Eliminating risk to the extent 
feasible does not necessarily have anything to do with the results of a 
benefit cost analysis. Thus, these analyses of net benefits cannot be 
used as the basis for a decision concerning the choice of a PEL for a 
Cr(VI) standard.
    Incremental costs and benefits are those that are associated with 
increasing stringency of the standard. Comparison of incremental 
benefits and costs provides and indication of the relative efficiency 
of the various PELs. OSHA cannot use this information in selecting a 
PEL, but it has conducted these calculations for informational 
purposes. Incremental costs, benefits, net benefits and cost per cancer 
avoided are presented in Table IX-12. Note that dermal benefits are 
excluded since they do not vary with the PEL and hence, do not affect 
the calculations.

               Table IX-12.--Incremental Benefits, Costs, Net Benefits and Cost Per Cancer Avoided
----------------------------------------------------------------------------------------------------------------
                                 20<r-arrow>10   10<r-arrow>5     5<r-arrow>1    1<r-arrow>0.5  0.5<r-arrow>0.25
----------------------------------------------------------------------------------------------------------------
                                               Discount Rate = 3%
----------------------------------------------------------------------------------------------------------------
Benefits......................          $133.0          $117.4          $167.4           $34.5            $22.3
Costs.........................           -10.0           -28.0           -93.0          -169.0           -143.0
Net Benefits..................           123.0            89.4            74.4           134.5            120.7
Cost Per Cancer Avoided.......             1.6             0.1            -0.7            -2.3             -1.7
-------------------------------
                                               Discount Rate = 7%
----------------------------------------------------------------------------------------------------------------
Benefits......................            86.2            76.4           109.1            22.5             14.5
Costs.........................           -11.0           -30.0           -98.0           179.0           -146.0

[[Page 59431]]

 
Net Benefits..................            75.2            46.4            11.1           156.5            131.5
Cost Per Cancer Avoided.......             1.6             0.1            -0.7            -2.3             -1.7
----------------------------------------------------------------------------------------------------------------

G. Initial Regulatory Flexibility Analysis

Reasons Why Action by the Agency Is Being Considered
    Several well-conducted scientific investigations have found 
increased lung cancer mortality among workers breathing Cr(VI) dusts 
and mists in the workplace. The high rate of lung cancer mortality has 
been documented in workers from several countries across multiple 
industries that use a broad spectrum of Cr(VI) compounds. Many of the 
studies found that the rate of lung cancer was greatest among workers 
in jobs where Cr(VI) exposure was highest and in workers employed in 
those jobs for the longest periods of time. These exposure-related 
trends implicate Cr(VI) as a likely causative agent and suggest that 
other known lung carcinogens to which the workers may be exposed, such 
as cigarette smoke, are unlikely to account for the increased lung 
cancers observed in the studies. The International Agency for Research 
on Cancer, the U.S. Environmental Protection Agency, and the American 
Conference of Governmental Industrial Hygienists have evaluated the 
human, animal, and other experimental evidence and concluded that 
Cr(VI) compounds are ``known'' or ``confirmed'' human carcinogens.
    Two independent epidemiologic studies of workers from chromate 
production plants in Baltimore, Maryland (Gibb et al., Ex. 31-22-11) 
and Painesville, Ohio (Luippold et al., Ex. 33-10) were considered to 
present the strongest data sets for quantitative risk assessment. 
OSHA's analysis found that a linear, relative risk model provided the 
best fit to the data (Ex. 33-15; Ex. 33-12). The Agency preliminarily 
estimates that the excess lifetime lung cancer risk for workers exposed 
at the current Permissible Exposure Limit (PEL) of 52 [mu]g/m\3\ 
Cr(VI), as an eight-hour time-weighted average for a 45-year working 
lifetime, ranges from 106 to 351 excess lung cancers per thousand 
workers exposed. OSHA applied the linear relative risk model to 
preliminarily estimate excess lifetime lung cancer risks from 45-year 
exposure at alternative PELs ranging from 0.25 [mu]g/m<SUP>3</SUP> to 
20 [mu]g/m<SUP>3</SUP> (the range considered for the draft proposed 
standard). The projected risks at these alternate PELs are between 
four- and 200-fold lower than risks estimated at the current PEL. NIOSH 
and the Exponent group have reported similar lung cancer risks based on 
the Gibb (Ex. 33-13; Ex. 31-18-15-1) and the Luippold (Ex. 31-18-3) 
data sets and a relative risk model. The risk estimates at the very 
lowest Cr(VI) exposure levels under consideration (e.g., 0.25 to 2.5 
[mu]g/m<SUP>3</SUP>) are considered to be somewhat more uncertain than 
those projected at the higher Cr(VI) levels because they involve risk 
model extrapolations below the range of exposures experienced by the 
Gibb and Luippold worker cohorts.
    Exposure to airborne Cr(VI) can cause other adverse effects to the 
respiratory tract and the skin. Occupational surveys and medical 
examinations have found nasal septum ulcerations and perforations (i.e. 
``chrome holes'') among chromium production workers and chrome 
electroplaters exposed repeatedly to relatively high levels of Cr(VI) 
(e.g., 20 [mu]g/m\3\ to 50 [mu]g/m\3\). (Exs. 31-22-11; 9-126). Several 
case reports have also documented occupational asthma triggered by 
breathing Cr(VI) compounds in the workplace. Workers can also develop 
an allergic reaction of the skin known as allergic contact dermatitis 
as a result of repeated direct dermal contact with Cr(VI) solutions or 
other Cr(VI)-containing materials. Allergic contact dermatitis is most 
common on the hands and arms of workers who mix and use wet Cr(VI)-
containing cement. Dermal contact with Cr(VI) can also cause an 
irritant dermatitis and ulceration of the skin called ``chrome 
ulcers''. This type of dermatitis is not an allergic condition and 
requires contact with a fairly concentrated form of Cr(VI). It has been 
reported primarily in chromate production plants and chrome 
electroplating facilities with poor industrial hygiene (work) 
practices.
    A full discussion of the health effects and risk assessment that 
support the reasons why this action is being considered are given in 
Section VI of the Preamble, Health Effects, and Section VII, 
Quantitative Risk Assessment.
Objective of and Legal Basis for the Proposed Rule
    The objective of the proposed rule is to reduce the numbers of 
fatalities and illnesses occurring among employees exposed to Cr(VI) in 
general industry, construction, and shipyard sectors. This objective 
will be achieved by requiring employers to install engineering controls 
where appropriate and to provide employees with the equipment, 
respirators, training, medical surveillance, and other protective 
measures to perform their jobs safely.
    The legal basis for the rule is the responsibility given the U.S. 
Department of Labor through the Occupational Safety and Health Act of 
1970 (OSH Act). The OSH Act authorizes the Secretary of Labor to 
promulgate occupational safety and health standards as necessary ``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). The legal authority can also be cited as 
29 U.S.C. 655(b).
    In addition to the statutory basis for a possible standard, the 
legal basis for the action also involves litigation on the need for and 
timetable for a Cr(VI) standard. See the Preamble Section III, for a 
fuller discussion.
Description and Estimate of Affected Small Entities
    Table IX-1 above provides an overview of the number of small 
entities affected by the standard, by sector. Additional detail is 
provided in the Full Preliminary Economic Analysis and Initial 
Regulatory Flexibility Analysis (Ex. 35-391).
Summary of Reporting, Recordkeeping, and Other Compliance Requirements
    Table IX-13 shows the costs of the proposed standard for entities 
classified as small businesses by the SBA.

[[Page 59432]]

[GRAPHIC] [TIFF OMITTED] TP04OC04.032


[[Page 59433]]


[GRAPHIC] [TIFF OMITTED] TP04OC04.033


[[Page 59434]]


[GRAPHIC] [TIFF OMITTED] TP04OC04.034

    Table IX-14 shows the unit costs these estimates are based on. (For 
a full discussion of the engineering control costs, and of the basis 
for the unit costs, see Chapter 3 of the Preliminary Economic Analysis 
and Initial Regulatory Flexibility Analysis).

[[Page 59435]]



            Table IX-14.--Unit Costs Applied in OSHA's Preliminary Analysis of the Proposed Standard
----------------------------------------------------------------------------------------------------------------
                                                                 Escalation
                                                                   factor     Index used for price
       Cost description               Basis         Base cost     (October         escalation         Unit cost
                                                                2003 basis)
----------------------------------------------------------------------------------------------------------------
Cost per hour for an outside    Estimate by In-         $90.00            1  NONE..................       $90.00
 industrial hygiene contractor.  house CIH.
Cost of a personal sampling     Gilian 3500;            680.00            1  NONE..................       680.00
 pump.                           Sensidyne, 16333
                                 Bayvista Drive,
                                 Clearwater, FL
                                 33760.
Variable Cost per sample        Estimate by In-          60.00            1  NONE..................        60.00
 (e.g., laboratory analysis).    house CIH.
Flat Fee For Training Course..  Estimate by In-         400.00            1  NONE..................       400.00
                                 house CIH..
Cost of a calibration unit....  GILIBRATOR-2;         1,075.00            1  NONE..................     1,075.00
                                 Sensidyne, 16333
                                 Bayvista Drive,
                                 Clearwater, FL
                                 33760.
Unit cost of OSHA-regulation    July 1993 EMMED           3.03       1.2702  CPI--All items........         3.84
 warning signs with mounting     Co, Inc. Catalog.
 materials.
Cost of materials per           Banana Oil Fit            0.07            1  NONE..................         0.07
 qualitative fit-testing.        Test Kit; Lab
                                 Safety Supply
                                 Catalog 2003, PO
                                 Box 1368,
                                 Janesville, WI
                                 53547-1368.
Unit cost per worker for an     Allegro One-          1,473.33            1  NONE..................     1,473.33
 air-supplied respirator.        Worker Full Face
                                 Kit; Lab Safety
                                 Supply Catalog
                                 2003, PO Box
                                 1368,
                                 Janesville, WI
                                 53547-1368.
Unit cost per employee for a    MSA Ultra Twin          243.00            1  NONE..................       243.00
 full-face respirator.           Full Face
                                 Respirator; Lab
                                 Safety Supply
                                 Catalog 2003, PO
                                 Box 1368,
                                 Janesville, WI
                                 53547-1368.
Unit cost per employee for a    MSA Comfro               35.30            1  NONE..................        35.30
 half-mask respirator.           Classic Half-
                                 Mask Respirator;
                                 Lab Safety
                                 Supply Catalog
                                 2003, PO Box
                                 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of replacement cartridges  MSA P100 Filter          13.74            1  NONE..................        13.74
 cartridges per mask).           (2 Cartridge:
                                 Lab Safety
                                 Supply Catalog
                                 2003, PO Box
                                 1368,
                                 Janesville, WI
                                 53547-1369.
Unit cost per employee for a    Allegro Three         1,164.00            1  NONE..................     1,164.00
 blasting helmet air-supplied    Person Air Pump,
 respirator.                     Bullard 1/2''
                                 Hose, 100'L,
                                 Bullard Helmet w/
                                  constant air
                                 flow; Lab Safety
                                 Supply Catalog
                                 2003, PO Box
                                 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of materials to clean one  Respirator                1.86            1  NONE..................         1.86
 respirator.                     Cleaning/Storage
                                 Kit; Lab Safety
                                 Supply Catalog
                                 2003, PO Box
                                 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of PE coated Tyvek         KAPPLER Poly-Coat         6.60            1  NONE..................         6.60
 coveralls.                      Coveralls; Lab
                                 Safety Supply
                                 Catalog 2003, PO
                                 Box 1368,
                                 Janesville, WI
                                 53547- 1368.
Cost of Saranex coveralls.....  Tychem QC                32.85            1  NONE..................        32.85
                                 Coveralls; Lab
                                 Safety Supply
                                 Catalog 2003, PO
                                 Box 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of Tyvek coveralls.......  Tyvek Protective          4.50            1  NONE..................         4.50
                                 Wear Coveralls;
                                 Lab Safety
                                 Supply Catalog
                                 2003, PO Box
                                 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of bib aprons............  Polypropylene Bib         0.58            1  NONE..................         0.58
                                 Apron; Lab
                                 Safety Supply
                                 Catalog 2003, PO
                                 Box 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of laundering uniforms     Aramark                   5.50            1  NONE..................         5.50
 for one employee per week.      Cincinnati
                                 Representative.
Cost of laundering uniforms     Aramark                   3.75            1  NONE..................         3.75
 for one employee per week.      Cincinnati
                                 Representative.
Cost of clear indirect vent     Lab Supply                6.00            1  NONE..................         6.00
 goggles.                        Catalog 2003, PO
                                 Box 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of clear lens safety       Lab Supply                5.00            1  NONE..................         5.00
 glasses.                        Catalog 2003, PO
                                 Box 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of grey lens safety        Lab Supply                5.00            1  NONE..................         5.00
 glasses.                        Catalog 2003, PO
                                 Box 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of lined nitrile gloves..  Ansell Sol-Vex            2.50            1  NONE..................         2.50
                                 Flock Lined
                                 Nitrile Gloves;
                                 Lab Safety
                                 Supply Catalog
                                 2003, PO Box
                                 1368,
                                 Janesville, WI
                                 53547-1368.
Cost of powder surgical         N-Dex 4-mil               0.24            1  NONE..................         0.24
 nitrile gloves.                 powdered
                                 disposable
                                 Nitrile Lab
                                 Gloves; Lab
                                 Safety Supply
                                 Catalog 2003, PO
                                 Box 1368,
                                 Janesville, WI
                                 53547-1368.

[[Page 59436]]

 
Cost of rough PVC gloves......  BEST Super Flex           4.10            1  NONE..................         4.10
                                 PVC-gloves
                                 Coated Gloves;
                                 Lab Safety
                                 Supply Catalog
                                 2003, PO Box
                                 1368,
                                 Janesville, WI
                                 53547-1368.
Unit cost of change rooms per   Based upon Means        856.00       1.4742  CPI--All items........     1,261.92
 employee.                       Square Foot
                                 Costs, 1989.
Cost per shower head..........  Based upon Means      3,590.00       1.4742  CPI--All items........     5,292.39
                                 Square Foot
                                 Costs, 1989.
Cost per hand washing facility  Glacier Bay 4 in        500.00            1  NONE..................       500.00
                                 Chrome Two
                                 Handle Bar
                                 Faucet, 40 in x
                                 24In. White
                                 Double Bowl
                                 Utility Tub, 505
                                 E. Kemper Rd.,
                                 Cincinnati, OH
                                 45246--Estimated
                                 Installation
                                 Cost.
Variable cost per shower        Estimate.........         0.50            1  NONE..................         0.50
 (soap, clean towel, water,
 etc.).
Variable cost per hand washing  Kimberly-Clark            0.06            1  NONE..................         0.06
 facility (roll paper towels,    OnePak
 liquid soap, water).            Dispenser,
                                 WINDSOFT
                                 Bleached White
                                 Paper Roll
                                 Towels; The
                                 Betty Mills
                                 Company, 60 East
                                 3rd Ave, Ste
                                 201, San Mateo,
                                 CA 94401 (2003).
Unit cost of HEPA vacuums.....  CONSAD (1993)         1,580.00       1.4742  CPI--All items........     2,329.24
                                 base price is
                                 1991.
Unit cost of HEPA vacuum        CONSAD (1993)           212.00       1.4742  CPI--All items........       312.53
 replacement filters.            base price is
                                 1991.
Unit cost of garbage bags and   Estimate--Includi       500.00            1  NONE..................       500.00
 disposal.                       ng RCRA disposal.
Full cost of a comprehensive    1994 Quote from         282.00       1.4211  CPI--Medical Care            400.76
 medical exam.                   two hospitals.                               Services.
                                 Bethesda Care,
                                 Cincinnati, OH
                                 and Abington
                                 Memorial
                                 Hospital, Willow
                                 Grove, PA.
Full cost of a limited medical  2003 cost of            125.00            1  NONE..................       125.00
 exam.                           physical exams
                                 in Maryland (as
                                 directed by
                                 OSHA)..
Cost of additional medical      Estimated to be         150.00       1.4211  CPI--Medical Care            213.17
 testing after exam results      equal to cost of                             Services.
 are abnormal.                   limited medical
                                 exam.
Cost of a partial               1994 Quote from         141.00       1.4211  CPI--Medical Care            200.38
 comprehensive medical exam.     two hospitals.                               Services.
                                 Bethesda Care,
                                 Cincinnati, OH
                                 and Abington
                                 Memorial
                                 Hospital, Willow
                                 Grove, PA--
                                 Estimated half
                                 of comprehensive
                                 and/or limited
                                 exam cost.
Cost of a partial medical exam  1994 Quote from          75.00       1.4211  CPI--Medical Care            106.59
                                 two hospitals.                               Services.
                                 Bethesda Care,
                                 Cincinnati, OH
                                 and Abington
                                 Memorial
                                 Hospital, Willow
                                 Grove, PA--
                                 Estimated half
                                 of comprehensive
                                 and/or limited
                                 exam cost.
Cost per employee for training  Estimate.........         2.00            1  NONE..................         2.00
 aids and materials.
Cost per employee for computer  Estimate.........         1.00            1  NONE..................         1.00
 file space.
Cost of Medical History         OSHA. Preliminary           25       1.4211  CPI--Medical Care             35.53
 Questionnaire.                  Regulatory                                   Services.
                                 Impact and
                                 Regulatory
                                 Flexibility
                                 Analysis of the
                                 Proposed
                                 Respiratory
                                 Protection
                                 Standard, 1994.
Cost of Medical Exam for        OSHA. Preliminary           75       1.4211  CPI--Medical Care            106.58
 Respirator Use.                 Regulatory                                   Services.
                                 Impact and
                                 Regulatory
                                 Flexibility
                                 Analysis of the
                                 Proposed
                                 Respiratory
                                 Protection
                                 Standard. 1994.
Cost of Mop and Bucket........  The Home Depot.          62.92            1  NONE..................        62.92
                                 Contico, 35qt
                                 Mop Bucket and
                                 Wringer. Wilen,
                                 16oz Cotton Cut-
                                 End Mop.
Cost of Mop...................  The Home Depot.          62.92            1  NONE..................        62.92
                                 Wilen, 16oz
                                 Cotton Cut-End
                                 Mop.
Cost of Mobile Shower Unit      Ameri-can               42,960            1  NONE..................       42,960
 (construction).                 Engineering.
                                 Basic 828
                                 Decontamination
                                 Trailer. 2003.
                                 15886 Michigan
                                 Road. Argos, IN
                                 46501.
Cost of Change Area per         Estimate.........          720            1  NONE..................         300
 employee (construction).
----------------------------------------------------------------------------------------------------------------
Source: U.S. Dept. of Labor, OSHA, Office of Regulatory Analysis, based on IT, 2004, Ex. 35-390.


[[Page 59437]]

Federal Rules That May Duplicate, Overlap, or Conflict With the 
Proposed Rules
    OSHA's SBREFA panel for this rule suggested that OSHA address a 
number of possible overlapping or conflicting rules: EPA's Maximum 
Achievable Control Technology (MACT) standard for chromium 
electroplaters; EPA's standards under the Federal Insecticide, 
Fungicide, and Rodenticide Act (FIFRA) for Chromium Copper Arsenate 
(CCA) applicators; and state use of OSHA PELs for setting fenceline air 
quality standards. The Panel was also concerned that, in some cases 
other OSHA standards might overlap and be sufficient to assure that a 
new proposed standard would not be needed, or that some of the proposed 
standard's provisions might not be needed.
    OSHA has discussed EPA's MACT standard with EPA. The standards are 
not duplicative or conflicting. The rules are not duplicative because 
they have different goals--environmental protection and protection 
against occupation exposure. It is quite possible, as many 
electroplaters are now doing, to achieve environmental protection goals 
without achieving occupational protection goals. The regulations are 
not conflicting because there exist controls that can achieve both 
goals without interfering with one another. However, it is possible 
that meeting the proposed OSHA standard would cause someone to incur 
additional costs for the MACT standard. If an employer has to make 
major changes to install LEV, this could result in significant expenses 
to meet EPA requirements not accounted for in OSHA's cost analysis. 
OSHA believes that chromium electroplaters can generally meet a PEL of 
1 [mu]g/m<SUP>3</SUP> without such major changes, and has not included 
costs. This issue is discussed in detail in Chapter 2 of the full PEA. 
However, OSHA welcomes comment on this issue.
    OSHA examined the potential problem of overlapping jurisdiction for 
CCA applicators, and found that there would indeed be overlapping 
jurisdiction. For this proposed rule, OSHA had excluded CCA applicators 
from the scope of the coverage of the proposed rule. OSHA has been 
unable to find a case where a state, as a matter of law, bases 
fenceline standards on OSHA PELs. OSHA notes that the OSHA PEL is 
designed to addresses the risks associated with life long occupational 
exposure only. OSHA welcomes comment on this issue.
    OSHA has also examined other OSHA standards, and where standards 
are overlapping, referred to them by reference in the proposed 
standard. Existing OSHA standards that may duplicate the proposed 
provisions in some respect include the standards addressing respiratory 
protection (29 CFR 1910.134); hazard communication (29 CFR 1910.1200); 
access to medical and exposure records (29 CFR 1910.1020); general 
requirements for personal protective equipment in general industry (29 
CFR 1910.132), construction (29 CFR 1926.95), and shipyards (29 CFR 
1915.152); and sanitation in general industry (29 CFR 1910.141), 
construction (29 CFR 1926.51), and shipyards (29 CFR 1915.97).
Regulatory Alternatives
    This section discusses various alternatives to the proposed 
standard that OSHA is considering, with an emphasis on the those 
suggested by the SBREFA Panel as potentially alleviating impacts on 
small firms. (A discussion on the costs of some if these alternatives 
to OSHA's proposed regulatory requirements for the hexavalent chromium 
standard can be found in Section III.2 Costs of Regulatory Alternatives 
in the final report by OSHA's contractor, IT (IT, 2004). In the IT 
report, Tables III.42-III.51, costs are analyzed by regulatory 
alternative and major industry sector at discount rates of 7 percent 
and 3 percent).
    Scope: The proposed standard covers exposure to all types of Cr(VI) 
compounds in general industry, construction, and shipyard. Cement work 
in construction is excluded.
    OSHA considered the Panel recommendation that sectors where there 
is little or no known exposure to Cr(VI) be excluded from the scope of 
the standard. OSHA has preliminarily decided against this option. The 
costs for such sectors are relatively small--probably even smaller than 
OSHA has estimated because OSHA did not assume that any industry would 
use objective data to demonstrate that initial assessment was not 
needed. However, it is possible that changes in technology and 
production processes could change the exposure of employees in what are 
currently low exposure industries. If this happens, OSHA would need to 
issue a new standard to address the situation. As a result, OSHA is 
reluctant to exempt industries from the scope of the standard.
    As stated above, the proposed standard does not cover cement work 
in construction. OSHA's preliminary assessment of the data indicates 
that the primary exposure to cement workers is dermal contact that can 
lead to irritant or contact allergic dermatitis. Current information 
indicates that the exposures in wet cement work in construction are 
well below 0.25 [mu]g/<SUP>3</SUP>. Moreover, unlike other exposures in 
construction, general industry or shipyards, exposures from cement work 
are most likely to be solely from dermal contact. There is little 
potential for airborne exposures and unlikely to be any in the future, 
as Cr(VI) appears in wet cement in only minute quantities naturally. 
Cement work also is found in the general industry setting, however the 
data there indicate that, because of the volume of cement involved and 
the nature of the work, airborne exposures are likely to be slightly 
higher, with 3-5% of the exposures being greater than 0.25 [mu]g/
m<SUP>3</SUP>. Given these factors, the proposed standard excludes 
cement work in construction. OSHA has made a preliminary determination 
that addressing the dermal hazards from these exposures to Cr(VI) 
through guidance materials and enforcement of existing personal 
protective equipment and hygiene standards may be a more effective 
approach. Such guidance materials would include recommendations for 
specific work practices and personal protective equipment for cement 
work in construction.
    OSHA's analysis suggests that there are 2,093 to 10,463 cases of 
dermatitis among cement workers annually. Using a cost of illness (COI) 
approach, avoiding 95 percent of these dermatoses would be valued at 
$2.5 to $12.6 million annually, and avoiding 50 percent of these 
dermatoses would be valued $1.3 million to $6.6 million annually.
    The costs of including wet cement would depend on what requirements 
were applied to wet cement workers. OSHA estimates that adding wet 
cement to the scope of the standard would have costs of $33 million per 
year. The cost of addressing the problem through existing standards 
could range from $80 to $300 million per year. OSHA considered the 
SBREFA Panel recommendation that sectors where there is little or no 
known exposure to Cr(VI) be excluded from the scope of the standard. 
OSHA has preliminarily decided against this option. The costs for such 
sectors are relatively small--probably even smaller than OSHA has 
estimated because OSHA did not assume that any industry would use 
objective data to demonstrate that initial assessment was not needed. 
Beyond the initial exposure assessment (required only in general 
industry), very little would be required in workplaces where Cr(VI) 
exposures are below the PEL and no hazard is present from skin or eye

[[Page 59438]]

contact with Cr(VI). Additional requirements would generally be limited 
to housekeeping (in general industry) and hazard communication (warning 
labels on containers of Cr(VI)-contaminated materials that are 
consigned for disposal, training regarding the Cr(VI) standard). Where 
exposures in general industry exceed the Action Level, periodic 
monitoring would also be required. However, it is possible that changes 
in technology and production processes could change the exposure of 
employees in what are currently low exposure industries. If this 
happens, OSHA would need to issue a new standard to address the 
situation. As a result, OSHA is reluctant to exempt industries from the 
scope of the standard.
    PELS: Section F of this preamble summary presented data on the 
costs and benefits of alternative PELS for all industries. The full PEA 
contains detailed data on the impacts of small firms at each level of 
PEL.
    The SBREFA Panel also suggested alternatives to a uniform PEL 
across all industries and exposures. The Panel recommended that OSHA 
consider alternative approaches to industries that are intermittent 
users of Cr(VI). OSHA has preliminarily adopted the concept of 
permitting employers with intermittent exposures to meet the 
requirements of the standard using respirators rather than engineering 
controls. This approach has been used in other standards and does not 
require workers to routinely wear respirators.
    The SBREFA Panel also recommended considering Separate Engineering 
Control Airborne Limits (SECALs). OSHA has preliminarily not adopted 
this approach because OSHA does not believe it would serve workers or 
small businesses well. If an approach which requires a significant 
number of workers to wear respirators on a regular basis were to be 
adopted, that approach would result in many workers wearing respirators 
with the associated risks, and in setting a lower PEL in accord with 
the QRA's estimate that there is significant risk at PELS lower than 
one.
    The SBREFA Panel also suggested that OSHA consider different PELs 
for different Cr(VI) compounds leading to exposure to Cr(VI). This 
issue is fully discussed in the QRA. Here, it will only be noted that 
this would suggest lower PELs than OSHA is setting in at least some 
industries, and thus potentially increase impacts on small businesses.
    Special Approaches to the Shipyard and Construction Industries: The 
SBREFA Panel was concerned that changing work conditions in the 
shipyard and construction industry would make it difficult to apply 
some of the provisions that OSHA suggested at the time of the Panel. 
OSHA has preliminarily decided to change its approach in these sectors. 
OSHA is proposing 3 separate standards, one for general industry, one 
for construction, and one for shipyards. In shipyard and construction, 
OSHA will not require exposure monitoring of any kind; will not have an 
action level; will require medical surveillance only for persons with 
signs and symptoms; and will not require regulated areas. However, 
employers must still meet the PEL with engineering controls and work 
practices where feasible.
    This approach reduces the specification oriented aspects of the 
standard in these sectors, but may make it difficult for employers to 
determine how to comply with the standard. OSHA is considering a more 
specification oriented approach, similar to that used in the asbestos 
in construction standard, and in ``control banding'' approaches used 
abroad. Such an approach would require OSHA to specify what controls 
would need to be used in various circumstances, and employers using 
such controls would be considered to be in compliance with the 
standard. OSHA does not have the information at this time to develop or 
cost such an approach. OSHA welcomes comments on how it might develop 
such an approach.
    Timing of the Standard: The SBREFA Panel also recommended 
considering a multi-year phase in of the standard. OSHA is examining 
and soliciting comment on this issue. Such a phase-in would have 
several advantages from a viewpoint of impacts on small businesses. 
First, it would reduce the one time initial costs of the standard by 
spreading them out over time. This would be particularly useful for 
small businesses that have trouble borrowing large amounts of capital 
in a single year. A phase-in would also be useful in the electroplating 
sector by allowing employers to coordinate their environmental and 
occupational safety and health control strategies to minimize potential 
costs. A differential phase-in for smaller firms would also aid very 
small firms by allowing them to gain from the control experience of 
larger firms. However a phase-in would also postpone the benefits of 
the standard.
SBREFA Panel
    Table IX-15 lists all of the SBREFA Panel recommendations and notes 
OSHA responses to these recommendations.

      Table IX-15.--SBREFA Panel Recommendations and OSHA Responses
------------------------------------------------------------------------
      SBREFA panel recommendation                 OSHA response
------------------------------------------------------------------------
The Panel recommends that, as time       OSHA has extensively reviewed
 permits, OSHA revise its economic and    its costs estimates, and
 regulatory flexibility analyses as       changed many of them in
 appropriate to reflect the SERs'         response to SER comments and
 comments on underestimation of costs     solicits comments on these
 and that the Agency compare the OSHA     revised cost estimates. A few
 revised estimates to alternative         examples of OSHA's cost
 estimates provided and methodologies     changes are given in the
 suggested by the SERs. For those SER     responses to specific issues,
 estimates and methodological             below (e.g., medical exams,
 suggestions that OSHA does not adopt,    training and familiarization).
 the Panel recommends that OSHA explain
 its reasons for preferring an
 alternative estimate and solicit
 comment on the issue.
The Panel recommends that, to the        The PEA reflects OSHA's
 extent time permits, OSHA should         judgment on technological
 carefully consider the ability of each   feasibility and includes
 potentially affected industry to meet    responses to specific issues
 any proposed PEL for CR(VI) and          raised by the Panel and SERs.
 solicit comment on the costs and         OSHA will solicit comment on
 technological feasibility of the PEL.    the accuracy and
                                          reasonableness of these
                                          judgments.
The Panel recommends that OSHA           OSHA has increased the
 carefully review the basis for its       estimated time for a limited
 estimated medical surveillance           medical exam from 1.5 hours to
 compliance costs, consider these         3 hours and solicits comment
 concerns raised by the SERs, and         on all other cost projections
 ensure that its estimates are revised,   for medical surveillance. See
 as appropriate and time permits, to      Chapter IV OF THE PEA; COSTS
 fully reflect the costs likely to be     OF COMPLIANCE, COSTS BY
 incurred by potentially affected         PROVISION--Medical
 establishments.                          Surveillance, for details of
                                          OSHA's unit costs for medical
                                          surveillance.

[[Page 59439]]

 
The Panel recommends that, as time       OSHA revised the standard to
 permits, OSHA consider alternatives      relieve Construction and
 that would alleviate the need for        Shipyards from requirements
 extensive monitoring on construction     for exposure assessment; for
 sites, and solicit comment on this       General Industry, OSHA
 issue. If OSHA does not adopt such       believes that its unit cost
 alternatives, then OSHA should           estimates are realistic but
 consider increasing the estimated        will raise that as an issue.
 costs of such monitoring in              See  CHAPTER IV OF THE PEA:
 construction, and solicit comment on     COSTS OF COMPLIANCE, COSTS BY
 the costs of monitoring.                 PROVISION--Exposure Monitoring
                                          (Initial and Periodic), for
                                          details of OSHA's unit costs
                                          for exposure monitoring in
                                          general industry.
The Panel recommends that OSHA           OSHA's proposed standard will
 carefully review the basis for its       permit hand washing as a
 estimated hygiene compliance costs,      hygiene option; OSHA's
 consider the concerns raised by the      analysis will also reflect,
 SERs, and, to the extent time permits,   where data confirm, any cost
 ensure that its estimates are revised,   premium related to handling
 as appropriate, to fully reflect the     contaminated waste water or
 costs likely to be incurred by           laundry, or where uncertainty
 potentially affected establishments.     exists, the issue will be
                                          raised.
The Panel recommends that OSHA examine   OSHA has recognized costs for
 and solicit comment on this issue        training and familiarization
 [possible understates in the costs of    to cover a better
 regulated areas].                        understanding of the costs of
                                          regulated areas, and solicit
                                          comment on the issue. See
                                          CHAPTER IV OF THE PEA; COSTS
                                          OF COMPLIANCE, COSTS BY
                                          PROVISION--Communication of
                                          Hazards to Employees--Training
                                          and Familiarization, for
                                          details of OSHA's unit costs
                                          for this provision.
The Panel recommends that OSHA examine   OSHA has examined and solicits
 and solicit comment on these issues      comment on this issue and the
 [costs of laundering PPE].               cost OSHA has estimated. See
                                          CHAPTER IV OF THE PEA; COSTS
                                          OF COMPLIANCE, COSTS BY
                                          PROVISION--Housekeeping,
                                          Protective Work Clothing and
                                          Equipments, and Table IV-8 for
                                          details of OSHA's unit costs
                                          for laundering PPE and other
                                          related costs.
The Panel recommends that OSHA examine   OSHA's analysis assumes that
 whether its cost estimates reflect the   employers will need time for
 full costs of complying with the         familiarization with the
 hazard communication standard.           standard, training on the
                                          standard, and increased
                                          initial supervision.
The Panel recommends that OSHA           OSHA has reviewed and revised
 thoroughly review the economic impacts   many of its revenue and profit
 of compliance with a proposed Cr(VI)     estimates in the light of
 standard and develop more detailed       specific SER comments.
 feasibility analyses where               Examples of application groups
 appropriate. The Panel also recommends   with revised revenue and
 that OSHA, to the extent permitted by    profit estimates include Group
 time and the availability of economic    4, Chromate Production; Group
 data, reexamine its estimates of         5, Chromate Pigment Producers;
 profits and revenues in light of SER     and Group 17, Chromium Dye
 comments, and update economic data to    Producers. However, OSHA has
 better reflect recent changes in the     not updated revenue and profit
 economic status of the affected          impacts across the board--OSHA
 industries, consistent with its          estimates of costs, revenues,
 statutory mandate. The Panel also        and profits require consistent
 recommends that OSHA examine, to the     data sets which are not yet
 extent feasible with the time            available for more recent
 available, the possibility that users    years. OSHA's continues to
 will substitute non-Cr(VI) products      examine, and will solicit
 for Cr(VI) products. The Panel           comment on this issue.
 recommends that OSHA solicit comment
 on the extent to which foreign
 competition may or may not impact what
 is feasible for the industries
 affected by this rule.
The Panel recommends that OSHA consider  OSHA is reluctant to exempt
 and solicit comments on selective        industries where exposures are
 exemption of some industries from the    minimal because changes in
 proposed standard, especially those      technology could change
 industries whose inclusion is not        exposures in the future.
 supported by the industry-specific       However, OSHA is seeking
 data or in which inhalation exposure     comment on the issue of the
 to Cr(VI) is minimal.                    scope of the standard and data
                                          that would support not
                                          covering certain sectors.
The Panel recommends that OSHA exempt    OSHA has decided to exempt
 applicators of CCA given that they are   applicators of CCA in this
 already regulated by EPA as pesticide    proposal.
 applicators under FIFRA. In addition,
 OSHA should clarify and seek comment
 as to why users of CCA-treated wood
 should be covered under the Cr(VI)
 proposal given that the use of CCA-
 treated wood was previously excluded
 by OSHA in its standard for inorganic
 arsenic.
The Panel recommends that OSHA clearly   The Quantitative Risk
 explain the way that Cr(VI) exposure     Assessment section of the
 and risk for the worker cohort studies   Preamble addresses this issue
 used in the quantitative risk            in detail, and OSHA is seeking
 assessment were calculated, and should   comments on this issue.
 consider and seek comment as to
 whether the major assumptions used in
 these calculations are reasonable.
The Panel recommends that OSHA consider  The Quantitative Risk
 the available information on reduction   Assessment of this Preamble
 of inhaled Cr(VI) to Cr(III) in the      addresses the issue of
 body, to determine whether exposures     possible threshold effects and
 below a threshold concentration can be   OSHA is seeking comments on
 shown not to cause the genetic           the issue.
 alterations that are believed to cause
 cancer. In addition, OSHA should
 review epidemiological analyses
 relevant to the question of threshold
 dose, to determine whether such a dose
 is identifiable from the available
 human data. OSHA should further
 consider and seek comment on these
 findings in relation to the risk
 assessment and the proposed PEL,
 allowing for a higher PEL than those
 presented in the draft standard if the
 risk assessment so indicates.

[[Page 59440]]

 
The Panel recommends that OSHA should    OSHA is required by law to set
 clarify the meaning of the projected     health standards so that they
 lung cancer risk estimates used to       avoid significant risk over a
 support the proposed standard. In        working lifetime. Both in the
 particular, OSHA should explain these    QRA and in the Benefits
 estimates, which are based on a          Chapter of the PEA, OSHA has
 working lifetime of 45 years' exposure   examined alternative exposure
 at the highest allowable Cr(VI)          scenarios. See VII.
 concentration, and, where appropriate,   Preliminary Quantitative Risk
 note projected excess cancers that may   Assessment in the Preamble and
 result from shorter periods of           CHAPTER VI of the PEA;
 occupational Cr(VI) exposure.            BENEFITS and NET BENEFITS,
                                          Lung Cancers Avoided in this
                                          PEA.
The Panel recommends that OSHA solicit   OSHA has added information
 information to better characterize the   provided by firms in the
 exposure patterns and Cr(VI) compounds   shipyard industry since the
 encountered in the maritime              Panel meeting. (See Chapter II
 environment, and should encourage        of the PEA; PROFILE OF
 input from marine chemists at            AFFECTED INDUSTRIES,
 appropriate points in the rulemaking.    PROCESSES, AND APPLICATIONS
                                          GROUPS, AFFECTED INDUSTRIES--
                                          Welding and Painting and
                                          Chapter III: Technological
                                          Feasibility, Welding and
                                          Painting). OSHA is soliciting
                                          comment on shipyard issues and
                                          from maritime chemists.
The Panel recommends that OSHA consider  OSHA considered this
 the appropriateness of separate PELs     possibility and preliminarily
 for specific Cr(VI) compounds, with      decided against it, in part,
 attention to the weight and extent of    because it would require lower
 the best available scientific evidence   PELs with many persons in
 regarding their relative carcinogenic    respirators. OSHA is
 potency.                                 soliciting comment on this
                                          issue.
The Panel recommends that OSHA solicit   OSHA has eliminated the
 information to better define             requirement for monitoring in
 construction activities likely to be     the construction industry.
 above and below the PEL (for initial     OSHA has considered a control
 exposure monitoring purposes) to         banding approach to
 minimize the amount of respiratory       construction, but lacks the
 protection that would need to be used    data to fully implement this
 for compliance.                          approach, and solicits comment
                                          on the issue.
The Panel recommends that OSHA provide   OSHA has removed the
 a better explanation of how to           requirement for exposure
 implement an exposure assessment         monitoring in construction and
 program for construction activities.     shipyards. The monitoring-
 Also, OSHA should provide further        related topics are further
 explanation on monitoring-related        discussed in the Preamble,
 topics like the selection of sampling    XVII. Summary and Explanation
 and analytical methods, the selection    of the Standard.
 of plus-or-minus 25% as a confidence
 interval, and the use of objective
 data in lieu of monitoring.
The Panel recommends that OSHA consider  OSHA has preliminarily left the
 less frequent monitoring for exposures   monitoring frequency
 above the PEL, especially in             unchanged, but has solicited
 situations where the employer has        comment on the issue.
 already engineered down to the lowest
 feasible level and is not able to
 maintain levels below the PEL.
The Panel recommends that OSHA review    OSHA has reviewed its
 the technologies used to reduce Cr(VI)   technological feasibility
 exposure to ensure to ensure that they   analysis and solicited comment
 are available or reasonably              on it.
 anticipated to be available in the
 future.
The Panel recommends that OSHA clarify   The Summary and Explanation of
 the purpose of the prohibition on the    the Preamble explains further
 use of employee rotation to meet the     the prohibition on employee
 PEL and take into account the needs      rotation and the methods of
 expressed by the SERs on the issue.      compliance.
The Panel recommends that OSHA clarify   ...............................
 the methods of compliance section.
The Panel recommends that OSHA clarify   OSHA has eliminated the
 how to implement the use of regulated    requirement for regulated
 areas particularly for construction      areas in construction and
 activities. OSHA should better explain   shipyards. The Summary and
 how employers would delineate            Explanation section of the
 boundaries for regulated areas and       Preamble explains the
 should better clarify the use of         regulated area requirements in
 respiratory protection, personal         General Industry.
 protective clothing and equipment, and
 hygiene facilities and practices in
 regulated areas.
The Panel recommends that OSHA provide   These issues are addressed in
 a clearer explanation of why it is       the Summary and Explanation
 necessary to remove Cr(VI)-              Section of the Preamble.
 contaminated protective clothing and
 wash hands prior to entering non-
 Cr(VI) work areas and eating, drinking
 or smoking and take into account lost
 time and costs associated with
 conducting such activities.
The Panel recommends that OSHA clarify   ...............................
 its definition of contaminated
 clothing or waste, provide evidence
 supporting the view that
 ``contaminated'' clothing presents a
 hazard, and better explain the special
 treatment of such items and why the
 treatment is necessary.
The Panel recommends that OSHA clarify   OSHA has changed the rule from
 its definition of reasonably             SBREFA draft in order to
 anticipated skin and eye contact.        clarify when PPE is required
The Panel recommends that OSHA clarify    and to assure that it is not
 the circumstances under which the        required except where a dermal
 proposed rule would require the use of   hazard exists.
 personal protective equipment to
 prevent dermal exposures to solutions
 containing Cr(VI). In particular, OSHA
 should reconsider the requirements for
 the use of dermal protection when the
 PEL is exceeded; consider alternatives
 that are more clearly risk based; and
 determine whether the use of very
 dilute Cr(VI) solutions, as used in
 some laboratories, requires the use of
 personal protective equipment..

[[Page 59441]]

 
The Panel recommends that OSHA provide   OSHA has preliminarily dropped
 a clearer explanation of the benefits    routine medical surveillance
 and the need for its proposed medical    in the shipyard and
 surveillance provisions.                 construction industries. The
The Panel recommends that OSHA provide    Preamble Summary and
 a clearer guidance as to which           Explanation clarify what is
 employees are intended to be covered     required of medical
 under the medical surveillance           surveillance, and the extent
 provisions and, in particular, how the   to which the same medical
 standard is intended to cover            examination can be used to
 employees who work for several           meet the requirements of
 different employers during the course    different standards.
 of a year.
The Panel recommends that OSHA clarify
 the qualifications necessary to
 provide a medical examination
 (including what knowledge of Cr(VI) is
 necessary) and what the elements of
 such a medical examination should be.
The Panel recommends that OSHA design
 the medical surveillance provisions to
 be consistent with existing OSHA
 standards (e.g., lead and arsenic)
 wherever possible, in order to
 minimize the need for duplicative
 medical examinations. The Panel also
 recommends that OSHA clarify that
 differences in medical surveillance
 requirements that may be unavoidable
 across OSHA standards nevertheless
 often will not require completely
 separate medical examinations.
With respect to the EPA electroplating   OSHA discusses the impact of
 standards, the Panel recommends that     EPA's electroplating standard
 OSHA examine whether important costs     in the PEA, (See Chapter II:
 have been omitted, seek to develop       Technological Feasibility,
 alternatives that minimize these         Electroplating and Chapter
 costs, and seek comment on the issue.    VIII: Environmental Impacts)
                                          and seeks comments on this
                                          issue.
With respect to possible dual            OSHA preliminarily has decided
 jurisdiction with FIFRA, the Panel       to exclude CCA applicators
 recommends that OSHA consider dropping   from the scope of the
 CCA applicators from the scope of the    standard.
 rule, and seek comment on this issue.
With respect to the issue of using OSHA  OSHA solicits comment on the
 PELs as a basis for fenceline            ``fence line'' standard issue.
 standards, the Panel recommends that
 OSHA make clear the purpose of its
 PELs, and explain that they are not
 developed or examined in terms of
 their validity as a basis for air
 quality standards.
The Panel recommends that OSHA examine   OSHA has preliminarily
 whether existing standards are           determined that, except for
 adequate to cover occupational           CCA applicators and wet cement
 exposure to Cr(VI), and, if not,         workers, other standards
 develop the Cr(VI) standard in such a    cannot provide the worker
 way as to eliminate duplicative and      protection needed, but has
 overlapping efforts on the part of       sought to avoid duplication of
 employers.                               effort between standards.
The Panel recommends that OSHA consider  OSHA has included an analysis
 the scientific evidence in favor of a    of the costs and benefits of a
 higher PEL, analyze the costs and        PEL of 20 in this Preamble
 economic impacts of a PEL of 20 or       summary, and has a full
 greater, and solicit comment on this     analysis of this option in the
 option.                                  PEA.
The Panel recommends that OSHA           OSHA preliminarily determined
 carefully examine the entire issue of    that intermittent users need
 intermittent exposures, consider         not use engineering controls
 options that can alleviate the burden    to assure compliance with the
 on such firms while meeting the          PEL.
 requirements of the OSH Act, and
 solicit comment on such options.
Some SERs argued that some Cr(VI)        OSHA has preliminarily
 compounds offer lesser risks of cancer   determined that all Cr(VI)
 than others, and should be subject to    compounds should have the same
 different PELs. The Panel recommends     PEL, but seeks comment on the
 that OSHA consider these arguments and   issue.
 seek comment on the issue.
The Panel recommends that OSHA continue  OSHA has preliminarily
 to exempt wet cement from the scope of   determined to exempt wet
 the standard, and that if OSHA seeks     cement from the scope of the
 comment on this option, OSHA should      standard, but has sought
 note the Panel's recommendation and      comment on the issue.
 the reasons for the recommendation.     OSHA has made a number of
 The Panel also recommends that OSHA      changes to the construction
 seek ways of adapting the standard       standard in this proposal,
 better to the dynamic working            including eliminating the
 conditions of the construction           exposure assessment
 industry, examine the extent to which    requirements, the regulated
 Cr(VI) exposures are already covered     area requirement, and the
 by other standards, and seek comment     action level. OSHA seeks
 on these issues. The Panel also          comment on its new approach.
 recommends that OSHA consider the
 alternative of developing a
 construction standard in a separate
 rulemaking.
The Panel recommends that OSHA           OSHA has made a number of
 consider, and solicit comment on,        changes to the shipyard
 approaches to their special problems;    standard in this proposal,
 that OSHA consider the possibility of    including eliminating the
 making the maritime proposed standard    exposure assessment
 more similar to the construction draft   requirements, the regulated
 standard, or consider the alternative    area requirement, and the
 of developing a maritime standard in a   action level. OSHA has sought
 separate rulemaking.                     comment on its new approach.
The Panel recommends that OSHA consider  This option is discussed in the
 and seek comment on multi-year phase-    regulatory alternatives
 in alternatives.                         section of the PEA, and OSHA
                                          is seeking comments on this
                                          alternative.
The Panel recommends that OSHA better    OSHA has eliminated the action
 explain the action level, including      level in the construction and
 its role in ensuring workers are         shipyard standards, and
 protected.                               explains its role in the
                                          General Industry in the
                                          Summary and Explanation of the
                                          Preamble.
The Panel recommends that OSHA consider  OSHA has preliminarily
 the use of SECALs and solicit comment    determined not to use SECALs,
 on whether and in what industries they   but solicits comments on this
 are appropriate using the Cadmium        issue.
 standard as a model.
------------------------------------------------------------------------


[[Page 59442]]

X. OMB Review Under the Paperwork Reduction Act of 1995

    The proposed standard for chromium (VI) contains collections of 
information (paperwork) that are subject to review by the Office of 
Management and Budget (OMB) under the Paperwork Reduction Act of 1995 
(PRA95), 44 U.S.C. 3501 et seq, and its regulation at 5 CFR Part 1320. 
PRA 95 defines collection of information to mean, ``the obtaining, 
causing to be obtained, soliciting, or requiring the disclosure to 
third parties or the public of facts or opinions by or for an agency 
regardless of form or format'' [44 U.S.C. Sec.  3502(3)(A)].
    The title, description of the need for and proposed use of the 
information, summary of the collections of information, description of 
respondents, and frequency of response of the information collection 
are described below with an estimate of the annual cost and reporting 
burden has required by Sec.  1320.5(a) (1)(iv) and Sec.  1320.8(d)(2). 
The reporting burden includes the time for reviewing instructions, 
gathering and maintaining the data needed, and completing and reviewing 
the collection of information.
    OSHA invites comments on whether each proposed collection of 
information:
    (1) Ensures that the collection of information is necessary for the 
proper performance of the functions of the agency, including whether 
the information will have practical utility;
    (2) Estimates the projected burden accurately, including the 
validity of the methodology and assumptions used;
    (3) Enhances the quality, utility, and clarity of the information 
to be collected; and
    (4) Minimizes the burden of the collection of information on those 
who are to respond, including through the use of appropriate automated, 
electronic, mechanical, or other technological collection techniques or 
other forms of information technology, e.g., permitting electronic 
submissions of responses.
    Title: Chromium (VI) Standard for General Industry (Sec.  
1910.1026), Shipyards (Sec.  1915.1026); and Construction (Sec.  
1926.1126)
    Description: The proposed Cr(VI) standard is an occupational safety 
and health standard's information collection requirements are essential 
components that will assist both employers and their employees in 
identifying exposures as well as identifying means to take to reduce or 
eliminate Cr(VI) overexposures.
    Summary of the Collections of Information:

<bullet> 1910.1026(d)--Exposure Assessment

    Paragraph (d)(5) of this section requires the employer to notify 
employees of their exposure monitoring results within 15 working days 
after the receipt for the exposure monitoring performed in this section 
(Sec.  1910.1026(d)(2) Initial Exposure Monitoring, Sec.  
1910.1026(d)(3) Periodic Monitoring, and Sec.  1910.1026 (d)(4) 
Additional Monitoring).
    Employers may notify each affected employee individually in writing 
of the results or by posting the exposure-monitoring results in an 
appropriate location that is accessible to all affected employees. If 
the exposure monitoring results indicate that employee exposure is 
above the PEL, the employer must include in the written notification 
the corrective action being taken to reduce employee exposure to or 
below the PEL.

<bullet> 1910.1026(g), 1915.1026(e), 1926.1126(e)--Respiratory 
Protection

    Paragraph (g)(2) in the general industry section, and paragraph 
(e)(2) in the shipyards and construction sections require the employer 
to institute a respiratory protection program in accordance with 29 CFR 
1910.134. The Respiratory Protection Standard's (Sec.  1910.134) 
information collection requirements require employers to: Develop a 
written respirator program; conduct employee medical evaluations and 
provide follow-up medical evaluations to determine the employee's 
ability to use a respirator; provide the physician or other licensed 
health care professional with information about the employee's 
respirator and the conditions under which the employee will use the 
respirator; and administer fit-tests for employees who will use 
negative or positive-pressure, tight-fitting facepieces.

<bullet> 1910.1026(h), 1915.1026(f), 1926.1126(f)--Protective Work 
Clothing and Equipment

    Paragraph (h)(3)(iii) in the general industry section and 
(f)(3)(iii) in the shipyards and construction sections require the 
employer to inform any person who launders or cleans protective 
clothing or equipment contaminated with chromium (VI) of the 
potentially harmful effects of exposure to chromium (VI) and that the 
clothing and equipment should be laundered or cleaned in a manner that 
minimizes skin or eye contact with chromium (VI) and effectively 
prevents the release of airborne chromium (VI) in excess of the PEL.

<bullet> 1910.1026(k), 1915.1026(h), and 1926.1126(h)--Medical 
Surveillance

    Paragraphs (k)(4) in the general industry section and (h)(4) in the 
shipyards and construction sections require the employer to provide the 
examining PLHCP with a copy of the standard. In addition, for each 
employee receiving a medical examination, the employer must provide the 
following information:
    1. A description of the affected employee's former, current, and 
anticipated duties as they relate to the employee's occupational 
exposure to chromium (VI);
    2. The employee's former, current and anticipated levels of 
occupational exposure to chromium;
    3. A description of any personal protective equipment used or to be 
used by the employee, including when and for how long the employee has 
used that equipment; and,
    4. Information from records of employment-related medical 
examinations previously provided to the affected employee currently 
within the control of the employer.
    Paragraphs (k)(5) in the general industry section, and (h)(5) in 
shipyards and construction sections require the employer to obtain a 
written medical opinion from the PLHCP, within 30 days for each medical 
examination performed on each employee. The employer must provide the 
employee with a copy the PLHCPs written medical opinion within two 
weeks of receipt. This written opinion must contain the following 
information:
    1. The PLHCP's opinion as to whether the employee has any detected 
medical condition(s) that would place the employee at increased risk of 
material impairment to health from further exposure to chromium (VI);
    2. Any recommended limitations upon the employee's exposure to 
chromium (VI) or upon the use of personal protective equipment such as 
respirators;
    3. A statement that the PLHCP has explained to the employee the 
results of the medical examination, including any medical conditions 
related to chromium (VI) exposure that require further evaluation or 
treatment, and any special provisions for use of protective clothing or 
equipment.

<bullet> 1910.1026(l), 1915.1026(i), and 1926.1126(i)--Communication of 
Chromium (VI) Hazards to Employees

    Paragraph (l)(4) of the general industry section, and (i)(3) of the 
shipyards and construction sections require that the employer provide

[[Page 59443]]

training for all employees who are exposed to airborne chromium (VI), 
or who have skin or eye contact with chromium (VI). Employers must 
maintain a record of the training provided. Also employers must provide 
initial training prior to or at the time of initial assignment to a job 
involving potential exposure to chromium (VI). However, employers do 
not need to provide training to a new employee, if they can demonstrate 
that a new employee has received training within the last 12 months 
that addresses the elements specified in the paragraph and that the 
employee can demonstrate knowledge of those elements. Employers must 
provide training that is understandable to the employee and must ensure 
that each employee can demonstrate knowledge of at least the following:
    1. The health hazards associated with chromium (VI) exposure;
    2. The location, manner of use, and release of chromium (VI) in the 
workplace and the specific nature of operations that could result in 
exposure to chromium (VI), especially above the PEL;
    3. The engineering controls and work practices associated with the 
employee's job assignment;
    4. The purpose, proper selection, fitting, proper use, and 
limitations of respirators and protective clothing;
    5. Emergency procedures;
    6. Measures employees can take to protect themselves from exposure 
to chromium (VI), including modification of personal hygiene and habits 
such as smoking;
    7. The purpose and a description of the medical surveillance 
program required by paragraph (k) of the general industry section and 
paragraph (h) of shipyards and construction sections;
    8. The contents of the standard; and
    9. The employee s rights of access to records under 29 CFR 
1910.1020(g).

<bullet> 1910.1026(m), 1915.1026(j), and 1926.1126(j)--Recordkeeping

    Paragraph (m)(1) of the general industry section requires that 
employers maintain an accurate record of all employee exposure-
monitoring records required in paragraph (d) of this section. The 
record must include at least the following information:
    1. The date of measurement for each sample taken;
    2. The operation involving exposure to chromium (VI) that is being 
monitored;
    3. Sampling and analytical methods used and evidence of their 
accuracy;
    4. Number, duration, and the results of samples taken;
    5. Type of personal protective equipment, such as respirators worn; 
and,
    6. The name, social security number, and job classification of all 
employees represented by the monitoring, indicating which employees 
were actually monitored.
    Employers must maintain and make available employee exposure 
monitoring records in accordance with 29 CFR 1910.1020.
    Paragraph (m)(2) of the general industry section requires employers 
who rely on historical monitoring data to maintain a record of 
historical data. The record must include information that reflects the 
following conditions:
    1. The data were collected using methods that meet the accuracy 
requirements of paragraph (d)(6) of the general industry section;
    2. The processes and work practices that were in use when the 
historical monitoring data were obtained are essentially the same as 
those to be used during the job for which initial monitoring will not 
be performed;
    3. The characteristics of the chromium (IV) containing material 
being handled when the historical monitoring data were obtained are the 
same as those on the job for which initial monitoring will not be 
performed;
    4. Environmental conditions prevailing when the historical 
monitoring data were obtained are the same as those on the job for 
which initial monitoring will not be performed; and
    5. Other data relevant to the operations, materials, processing, or 
employee exposures covered by the exception.
    This record must be maintained and must be made available in 
accordance with 29 CFR 1910.1020.
    Paragraph (m)(3) of the general industry section requires employers 
who rely on objective data to satisfy initial monitoring requirements 
to establish and maintain an accurate record of the objective data 
relied upon. The record must include at least the following 
information:
    1. The chromium (VI)-containing material in question;
    2. The source of the objective data;
    3. The testing protocol and results of testing, or analysis of the 
material for the release of chromium (VI);
    4. A description of the operation exempted from initial monitoring 
and how the data support the exemption; and
    5. Other data relevant to the operations, materials, processing or 
employee exposures covered by the exemption.
    Employers must maintain this record for the duration of the 
employer's reliance upon such objective data and must make such records 
available in accordance with 29 CFR 1910.1020.
    Paragraph (m)(4) of the general industry section, and paragraph 
(j)(1) of the shipyard and construction sections, require employers to 
establish and maintain an accurate record for each employee covered by 
medical surveillance under paragraph (k) of the general industry 
section, or paragraph (h) of the shipyard and construction sections. 
This record must include the following information about the employee:
    1. Name and social security number;
    2. A copy of the PLHCP's written opinions as required by paragraph 
(k)(5) of the general industry section, or paragraph (h)(5) for the 
shipyard and construction sections;
    3. A copy of the information provided to the PLHCP as required by 
paragraph (k)(4) of the general industry section, or (h)(4) in the 
shipyards and construction sections; Employers must ensure that medical 
records are maintained and made available in accordance with 29 CFR 
1910.1020.
    Paragraph (m)(5) of the general industry section and paragraph 
(j)(2) of the shipyards and construction sections require employers to 
prepare a record at the completion of training that indicates the 
identity of the individuals trained and the date the training was 
completed. This record must be maintained for three years after the 
completion of training. The employer must provide to the Assistant 
Secretary or the Director, upon request, all materials relating to 
employee information and training.
    Respondents: Employers in general industry, shipyards or 
construction whose employees work in jobs where there is a potential 
for chromium (VI) exposure (38,391 businesses).
    Frequency of Response: Frequency of response varies depending on 
the specific collection of information.
    Average Time Per Response: Varies from 5 minutes (.08 hour) for the 
employer to provide a copy of the written physician's opinion to the 
employee, to 12 hours to conduct exposure monitoring.
    Total burden hours: 696,659.
    Costs: (purchase of capital/startup costs): $30,793,697.
    The Agency has submitted a copy of the information collection 
request to OMB for its review and approval. Interested persons may 
submit comments regarding the burden

[[Page 59444]]

estimates or other aspects of the information collection request to the 
OSHA Docket Office, Docket No. H054A, Occupational Safety and Health 
Administration, Room N-2625, 200 Constitution Avenue, NW., Washington, 
DC 20210, and to the Office of Information and Regulatory Affairs, 
Office of Management and Budget, New Executive Office Building, Room 
10235, 725 17th Street, NW., Washington, DC 20503 (Attn: OSHA Desk 
Officer (RIN 1218-AB45)). Comments submitted in response to this notice 
will be summarized and/or included in the request for OMB approval of 
the final information collection request, and they will also become a 
matter of public record.
    Copies of the referenced information collection request are 
available for inspection and copying in the OSHA Docket Office and will 
be provided to persons who request copies by telephoning Todd Owen at 
(202) 693-1941. For electronic copies of the chromium (VI) information 
collection request, contact the OSHA Web page on the Internet at http://www.osha.gov/.

XI. Federalism

    The Agency reviewed the proposed Cr(VI) standard according to the 
most recent Executive Order on Federalism (Executive Order 13132, 64 FR 
43225, August 10, 1999). This Executive Order requires that federal 
agencies, to the extent possible, refrain from limiting state policy 
options, consult with states before taking actions that restrict their 
policy options, and take such actions only when clear constitutional 
authority exists and the problem is of national scope. The Executive 
Order allows federal agencies to preempt state law only with the 
expressed consent of Congress; in such cases, federal agencies must 
limit preemption of state law to the extent possible. Under section 18 
of the Occupational Safety and Health Act (the ``Act'' or ``OSH Act''), 
Congress expressly provides that OSHA preempt state occupational safety 
and health standards to the extent that the Agency promulgates a 
federal standard under section 6 of the Act. Accordingly, under section 
18 of the Act OSHA preempts state promulgation and enforcement of 
requirements dealing with occupational safety and health issues covered 
by OSHA standards unless the state has an OSHA-approved occupational 
safety and health plan (i.e., is a state-plan state) [see Gade v. 
National Solid Wastes Management Association, 112 S. Ct. 2374 (1992)]. 
Therefore, with respect to states that do not have OSHA-approved plans, 
the Agency concludes that this proposal falls under the preemption 
provisions of the Act. Additionally, section 18 of the Act prohibits 
states without approved plans from issuing citations for violations of 
OSHA standards; the Agency finds that this proposed rulemaking does not 
expand this limitation. OSHA has authority under Executive Order 13132 
to propose a Cr(VI) standard because the problems addressed by these 
requirements are national in scope.
    As explained in section VIII of this preamble, employees face a 
significant risk from exposure to Cr(VI) in the workplace. These 
employees are exposed to Cr(VI) in general industry, construction, and 
shipyards. Accordingly, the proposal would establish requirements for 
employers in every state to protect their employees from the risks of 
exposure to Cr(VI). However, section 18(c)(2) of the Act permits state-
plan states to develop their own requirements to deal with any special 
workplace problems or conditions, provided these requirements are at 
least as effective as the final requirements that result from this 
proposal.

XII. State Plans

    The 26 states and territories with their own OSHA-approved 
occupational safety and health plans must adopt comparable provisions 
within six months after the Agency publishes the final hexavalent 
chromium standard. These states and territories are: Alaska, Arizona, 
California, Hawaii, Indiana, Iowa, Kentucky, Maryland, Michigan, 
Minnesota, Nevada, New Mexico, North Carolina, Oregon, Puerto Rico, 
South Carolina, Tennessee, Utah, Vermont, Virginia, Virgin Islands, 
Washington, and Wyoming. Connecticut, New Jersey and New York have 
OSHA-approved State Plans that apply to state and local government 
employees only. Until a state-plan state promulgates its own comparable 
provisions, Federal OSHA will provide the state with interim 
enforcement assistance, as appropriate.

XIII. Unfunded Mandates

    The Agency reviewed the proposed Cr(VI) standard according to the 
Unfunded Mandates Reform Act of 1995 (UMRA)(2 U.S.C. 1501 et seq.) and 
Executive Order 12875. As discussed in section IX of this preamble, 
OSHA estimates that compliance with this proposal would require 
private-sector employers to expend about $223 each year. However, while 
this proposal establishes a federal mandate in the private sector, it 
is not a significant regulatory action within the meaning of section 
202 of the UMRA (2 U.S.C. 1532). OSHA standards do not apply to state 
and local governments, except in states that have voluntarily elected 
to adopt an OSHA-approved state occupational safety and health plan. 
Consequently, the proposed provisions do not meet the definition of a 
``Federal intergovernmental mandate'' [see section 421(5) of the UMRA 
(2 U.S.C. 658(5)]. Therefore, based on a review of the rulemaking 
record to date, the Agency believes that few, if any, of the employers 
affected by the proposal are state, local, and tribal governments. 
Therefore, the proposed Cr(VI) requirements do not impose unfunded 
mandates on state, local, and tribal governments.

XIV. Protecting Children From Environmental Health and Safety Risks

    Executive Order 13045 requires that Federal agencies submitting 
covered regulatory actions to OMB's Office of Information and 
Regulatory Affairs (OIRA) for review pursuant to Executive Order 12866 
must provide OIRA with (1) an evaluation of the environmental health or 
safety effects that the planned regulation may have on children, and 
(2) an explanation of why the planned regulation is preferable to other 
potentially effective and reasonably feasible alternatives considered 
by the agency. Executive Order 13045 defines ``covered regulatory 
actions'' as rules that may (1) be economically significant under 
Executive Order 12866 (i.e., a rulemaking that has an annual effect on 
the economy of $100 million or more, or would adversely effect in a 
material way the economy, a sector of the economy, productivity, 
competition, jobs, the environment, public health or safety, or state, 
local, or tribal governments or communities), and (2) concern an 
environmental health risk or safety risk that an agency has reason to 
believe may disproportionately affect children. In this context, the 
term ``environmental health risks and safety risks'' means risks to 
health or safety that are attributable to products or substances that 
children are likely to come in contact with or ingest (e.g., through 
air, food, water, soil, product use). The proposed Cr(VI) standard is 
economically significant under Executive Order 12866 (see section IX of 
this preamble). However, after reviewing the proposed Cr(VI) standard, 
OSHA has determined that the standard would not impose environmental 
health or safety risks to children as set forth in Executive Order 
13045. The proposed standard would require employers to limit employee 
exposure to Cr(VI) and take other precautions to protect employees from 
adverse health effects associated with exposure to Cr(VI). To

[[Page 59445]]

the best of OSHA's knowledge, no employees under 18 years of age work 
under conditions that involve exposure to Cr(VI). However, if such 
conditions exist, children who are exposed to Cr(VI) in the workplace 
would be better protected from exposure to Cr(VI) under the proposed 
rule than they are currently. Based on this preliminary determination, 
OSHA believes that the proposed Cr(VI) standard does not constitute a 
covered regulatory action as defined by Executive Order 13045.

XV. Environmental Impacts

    The Agency reviewed the proposed Cr(VI) standard according to the 
National Environmental Policy Act (NEPA) of 1969 (42 U.S.C. 4321 et 
seq.), the regulations of the Council on Environmental Quality (40 CFR 
part 1500), and the Department of Labor's NEPA procedures (29 CFR part 
11).
    As a result of this review, OSHA has made a preliminary 
determination that the proposed Cr(VI) standard will have no impact on 
air, water, or soil quality; plant or animal life; the use of land or 
aspects of the external environment. Therefore, OSHA concludes that the 
proposed Cr(VI) standard would have no significant environmental 
impacts.

XVI. Public Participation--Notice of Hearing

    OSHA encourages members of the public to participate in this 
rulemaking by submitting comments on the proposal, and by providing 
oral testimony and documentary evidence at the informal public hearing 
that the Agency will convene after the comment period ends. The Agency 
invites interested persons having knowledge of, or experience with, 
occupational exposure to Cr(VI) to participate in this process, and 
welcomes any pertinent data and cost information that will provide it 
with the best available evidence on which to develop the final 
regulatory requirements. This section describes the procedures the 
public must use to submit their comments to the docket in a timely 
manner, and to schedule an opportunity to deliver oral testimony and 
provide documentary evidence at informal public hearings on the 
proposal. Comments, notices of intention to appear, hearing testimony, 
and documentary evidence will be available for inspection and copying 
at the OSHA Docket Office. You also should read the sections above 
titled DATES and ADDRESSES for additional information on submitting 
comments, documents, and requests to the Agency for consideration in 
this rulemaking.
    Written Comments. OSHA invites interested persons to submit written 
data, views, and arguments concerning this proposal. In particular, 
OSHA encourages interested persons to comment on the issues raised in 
section II of this preamble. When submitting comments, parties must 
follow the procedures specified above in the sections titled DATES and 
ADDRESSES. The comments must clearly identify the provision of the 
proposal you are addressing, the position taken with respect to each 
issue, and the basis for that position. Comments, along with supporting 
data and references, received by the end of the specified comment 
period will become part of the record, and will be available for public 
inspection and copying at the OSHA Docket Office.
    Informal Public Hearing. Pursuant to section 6(b)(3) of the Act, 
members of the public will have an opportunity to provide oral 
testimony concerning the issues raised in this proposal at informal 
public hearings. The hearings will commence at 9:30 a.m. on February 1, 
2005. At that time, the presiding administrative law judge (ALJ) will 
resolve any procedural matters relating to the proceeding. The 
legislative history of section 6 of the OSH Act, as well as OSHA's 
regulation governing public hearings (29 CFR 1911.15), establish the 
purpose and procedures of informal public hearings.
    Although the presiding officer at such hearings is an ALJ, and 
questioning by interested persons is allowed on crucial issues, the 
proceeding is informal and legislative in purpose. Therefore, the 
hearing provides interested persons with an opportunity to make 
effective and expeditious oral presentations in the absence of 
procedural restraints or rigid procedures that could impede or protract 
the rulemaking process. The hearing is an informal administrative 
proceeding, rather than adjudicative one in which the technical rules 
of evidence would apply; its primary purpose is to gather and clarify 
information. The regulations that govern public hearings, and the pre-
hearing guidelines issued for this hearing, will ensure participants 
fairness and due process, and also will facilitate the development of a 
clear, accurate, and complete record. Accordingly, application of these 
rules and guidelines will be such that questions of relevance, 
procedure, and participation generally will favor development of the 
record. Conduct of the hearing will conform to the provisions of 29 CFR 
part 1911, ``Rules of Procedure for Promulgating, Modifying, or 
Revoking Occupational Safety and Health Standards.''
    Although the ALJs who preside over these hearings make no decision 
or recommendation on the merits of OSHA's proposal, they do have the 
responsibility and authority to ensure that the hearing progresses at a 
reasonable pace and in an orderly manner. To ensure that interested 
persons receive a full and fair informal hearing as specified by 29 CFR 
part 1911, the ALJ has the authority and power to: Regulate the course 
of the proceedings; dispose of procedural requests, objections, and 
comparable matters; confine the presentations to matters pertinent to 
the issues raised; use appropriate means to regulate the conduct of the 
parties who are present at the hearing; question witnesses, and permit 
others to question witnesses; and limit the time for such questioning.
    At the close of the hearing, the ALJ will establish a post-hearing 
comment period for parties who participated in the hearing. During the 
first part of this period, the participants may submit additional data 
and information to OSHA, while during the second part of this period, 
they may submit briefs, arguments, and summations.
    Notice of Intention to Appear to Provide Testimony at the Informal 
Public Hearing. Interested persons who intend to provide oral testimony 
at the informal public hearing must file a notice of intention to 
appear by using the procedures specified above in the sections titled 
DATES and ADDRESSES. This notice must provide the: Name, address, and 
telephone number of each individual who will provide testimony; 
capacity (e.g., name of the organization the individual is 
representing; the individual's title and position) in which each 
individual will testify; approximate amount of time required for each 
individual's testimony; specific issues each individual will address, 
including a brief statement of the position that the individual will 
take with respect to each of these issues; and any documentary evidence 
the individual will present, including a brief summary of the evidence. 
The hearings are open to the public, and all interested persons are 
welcome to attend. However, only a person who files a proper notice of 
intention to appear may ask questions and participate fully in the 
proceedings. While a person who did not file a notice of intention to 
appear may be allowed to testify at the hearing if time permits, this 
determination is at the discretion of the presiding ALJ.
    Hearing Testimony and Documentary Evidence. Any person requesting 
more than 10 minutes to testify at the informal public hearing, or who 
intends to submit documentary evidence at the hearing, must provide the 
complete text

[[Page 59446]]

of the testimony and the documentary evidence as specified above in the 
DATES and ADDRESSES sections. The Agency will review each submission 
and determine if the information it contains warrants the amount of 
time requested. If OSHA believes the requested time is excessive, it 
will allocate an appropriate amount of time to the presentation, and 
will notify the participant of this action, and the reasons for the 
action, prior to the hearing. The Agency may limit to 10 minutes the 
presentation of any participant who fails to comply substantially with 
these procedural requirements; in such instances, OSHA may request that 
the participant return for questioning at a later time.
    Certification of the Record and Final Determination After the 
Informal Public Hearing. Following the close of the hearing and post-
hearing comment period, the presiding ALJ will certify the record to 
the Assistant Secretary of Labor for Occupational Safety and Health; 
the record will consist of all of the written comments, oral testimony, 
and documentary evidence received during the proceeding. OSHA will 
review the proposed Cr(VI) standard in light of all the evidence 
received as part of the record, and will make its decisions based on 
substantial evidence in the record as a whole.

XVII. Summary and Explanation of the Standards

    OSHA believes that, based on currently available information, the 
proposed requirements set forth in this notice are necessary and 
appropriate to provide adequate protection to employees exposed to 
Cr(VI). OSHA has considered responses to the RFI as well as numerous 
reference works, journal articles, and other data obtained by the 
Agency in the development of this proposed standard.
    The language of the standards and the order of the various 
provisions are generally consistent with drafting in other recent OSHA 
health standards, such as the methylene chloride, formaldehyde, and 
cadmium standards. OSHA believes that a similar style should be 
followed from standard to standard when possible in order to facilitate 
uniformity of interpretation of similar provisions. This approach is 
also consistent with Section 6(b)(5) of the OSH Act, which states that 
health standards shall consider ``experience gained under this and 
other health and safety laws.''

(a) Scope and Application

    OSHA is proposing to issue separate standards addressing hexavalent 
chromium exposure in general industry, construction, and shipyards. The 
standard for shipyards would also apply to marine terminals and 
longshoring. The standards are intended to provide equivalent 
protection for all workers, while accounting for the different work 
activities, anticipated exposures, and other conditions in these 
sectors. The proposed standards for construction and shipyards are very 
similar to each other, but differ in some respects from the proposed 
standard for general industry. This summary and explanation will 
describe the proposed standard for general industry and will note 
differences between it and the proposed standards for construction and 
shipyards.
    Based on the record developed to date, OSHA believes that certain 
activities in construction and shipyards are different enough to 
warrant requirements that are somewhat modified from those proposed for 
general industry. This preliminary determination is consistent with the 
recommendation of the Maritime Advisory Committee on Occupational 
Safety and Health (MACOSH), which has recommended that a separate 
standard be developed for maritime. The proposed standards do not cover 
the agricultural sector. OSHA is not aware of significant exposures to 
Cr(VI) in agriculture. The Agency is interested in any evidence 
indicating that significant exposures to Cr(VI) occur in sectors not 
covered under the proposed standards. Accordingly, the subject has been 
raised in the ``Issues'' section of this proposal.
    The proposed standard applies to occupational exposures to 
hexavalent chromium (also referred to as chromium (VI) or Cr(VI)), that 
is, any chromium species with a valence of positive six, regardless of 
form or compound. Examples of Cr(VI) compounds include chromium oxide 
(CrO<INF>2</INF>), ammonium dichromate 
((NH<INF>4</INF>)<INF>2</INF>Cr<INF>2</INF>O<INF>7</INF>), calcium 
chromate (CaCrO<INF>4</INF>), chromium trioxide (CrO<INF>3</INF>), lead 
chromate (PbCrO<INF>4</INF>), potassium chromate 
(K<INF>2</INF>CrO<INF>4</INF>), potassium dichromate 
(K<INF>2</INF>Cr<INF>2</INF>O<INF>7</INF>), sodium chromate 
(Na<INF>2</INF>CrO<INF>4</INF>), strontium chromate 
(SrCrO<INF>4</INF>), and zinc chromate (ZnCrO<INF>4</INF>).
    Some stakeholders have argued that specific Cr(VI) compounds should 
be excluded from this rulemaking and addressed in a separate standard. 
Notably, after OSHA was initially petitioned to issue a Cr(VI) 
standard, the Color Pigments Manufacturers Association (CPMA) submitted 
a cross-petition calling for a separate standard for lead chromate 
pigments (Ex. 2). CPMA argued that differences in the bioavailability 
and toxicity of lead chromate when compared to other Cr(VI) compounds 
warranted a separate standard (Ex. 2, p. 5). CPMA stated:

    Simply put, there are no studies which show a link between lead 
chromate pigments in a finished form and cancer caused by exposure 
to Chromium VI. To the contrary, studies of lead chromate workers in 
the manufacture of lead chromate pigments alone do not show any 
increased risk of cancer (Ex. 2, p. 5).

Because CPMA deemed that lead chromate pigments posed little threat to 
employee health, and because of concern about adverse economic impacts 
associated with regulation, the Association considered that ``* * * no 
good purpose would be served by additional restrictions on lead 
chromate pigments'' (Ex. 2, p. 6). This position was reiterated in 
CPMA's response to the RFI (Ex. 31-15, p. 6).
    In its response to the RFI, the Boeing Company also expressed the 
view that OSHA should consider the bioavailability of different Cr(VI) 
compounds (Ex. 31-16, p. 8). Boeing indicated that exposures to 
strontium chromate and zinc chromate used in aerospace manufacturing 
are not equivalent to Cr(VI) exposures in other industries. The 
findings of two epidemiological studies of Cr(VI)-exposed aerospace 
workers were said to support this conclusion.
    OSHA has proposed a rule that covers all Cr(VI) compounds because 
the Agency believes the evidence supports this approach. As discussed 
in Section VI.A of this preamble, absorption of Cr(VI) from the lung 
into the bloodstream is greatly dependent on the solubility of the 
Cr(VI) compound. Insoluble chromates are poorly absorbed and as a 
result remain in the lungs for a longer period of time (Ex. 35-87). 
While in the lungs, insoluble Cr(VI) particulates can come into contact 
with the epithelial cell surface, resulting in uptake into cells (Exs. 
35-68; 35-67). Cellular uptake leads to DNA damage, apoptosis, and 
neoplastic transformation (Ex. 35-119). Less water-soluble chromates 
(e.g., lead chromate) appear to be more potent carcinogens than more 
soluble chromates (e.g., sodium chromate). (For a detailed discussion, 
see Section VI.B.8 of this preamble.)
    Experimental studies involving Syrian hamster embryo cells support 
the belief that cytotoxicity and neoplastic transformation occur when 
exposures involve lead chromate pigments (Ex. 12-5). Evidence indicates 
that even chromates that are encapsulated in a paint matrix may be 
released in the lungs (Ex. 31-15, p. 2). OSHA therefore sees no reason 
to exempt these

[[Page 59447]]

compounds from the current Cr(VI) rulemaking.
    OSHA believes this view is consistent with the epidemiological 
studies involving chromate pigment production workers and aerospace 
workers. While co-exposures to other Cr(VI) compounds do not allow for 
specific findings related to lead chromate exposure, OSHA has found 
that epidemiological studies of workers in the chromate pigment 
production industry have consistently shown excess risks for lung 
cancer (see Section VI.B.2 of this preamble). The studies of aerospace 
workers did not find an increased risk of lung cancer. However, this is 
not convincing evidence that aerospace workers are not at risk from 
Cr(VI) exposure. The small cohort size, lack of smoking data, 
relatively young age of the population, and number of members lost to 
follow-up in the study reported by Alexander et al. (Ex. 31-16-3) and 
the lack of exposure information in the report of Boice et al. (Ex. 31-
16-4) do not allow for any broad conclusions regarding aerospace 
workers to be reached on the basis of these two studies. OSHA's 
preliminary conclusion that Cr(VI) compounds should be addressed 
collectively under a single standard is consistent with the findings of 
IARC, NTP, and NIOSH. These organizations have each found Cr(VI) 
compounds to be carcinogenic, without exception. Although ACGIH has 
issued different TLVs for soluble and insoluble Cr(VI) compounds, and 
for certain specific compounds, the TLV for insoluble Cr(VI) compounds 
is five-fold lower than the TLV for soluble Cr(VI) compounds. This is 
consistent with OSHA's preliminary finding that less soluble Cr(VI) 
compounds, to the extent that they differ from more soluble Cr(VI) 
compounds, are more potent carcinogens and pose a greater risk to the 
health of workers.
    The proposed standard applies to occupational exposure in which 
Cr(VI), in any quantity, is present in an occupationally related 
context. Exposure of employees to the ambient environment, which may 
contain small concentrations of Cr(VI) unrelated to the job, is not 
subject to this standard.
    The proposed standard for construction does not cover exposure to 
Cr(VI) in portland cement. Cement ingredients (clay, gypsum, and 
chalk), chrome steel grinders used to crush ingredients, refractory 
bricks lining the cement kiln, and ash may serve as sources of chromium 
that may be converted to Cr(VI) during kiln heating, leaving trace 
amounts of Cr(VI) in the finished product (Ex. 35-317, p. 148).
    The amount of Cr(VI) in American cement is generally less than 20 
[mu]g/g (Ex. 9-57). While the Cr(VI) in cement may represent a dermal 
hazard, the evidence obtained by OSHA thus far indicates that the 
Cr(VI) concentration is generally so low that the proposed PEL could 
not be reached without exceeding OSHA's current PEL for Particulates 
Not Otherwise Regulated (PNOR). The PEL for PNOR (15 [mu]g/
m<SUP>3</SUP> for total dust) thus is at least as protective as the 
proposed Cr(VI) PEL in limiting the Cr(VI) inhalation exposure of 
cement workers. OSHA's preliminary exposure profile indicates that no 
employees are exposed to levels of Cr(VI) above 0.25 [mu]g/
m<SUP>3</SUP> as an 8-hour TWA during cement work in construction. 
Because airborne exposures to Cr(VI) during cement work in construction 
are expected to be minimal, and because of the economic burden of 
applying the ancillary provisions of the proposed standard to workers 
exposed to portland cement in the construction environment, OSHA has 
preliminarily concluded that exposures to Cr(VI) from portland cement 
are best addressed by providing guidance to employers rather than 
including portland cement in the construction rule.
    OSHA has proposed to cover exposures to Cr(VI) in portland cement 
in general industry. The Agency's preliminary exposure profile 
indicates that some employees in general industry are exposed to 
airborne Cr(VI) levels associated with a significant risk of lung 
cancer as a result of work with portland cement. OSHA's preliminary 
findings show that nearly 2500 workers in general industry are exposed 
to Cr(VI) levels between 0.25 [mu]g/m<SUP>3</SUP> and 0.5 [mu]g/
m<SUP>3</SUP> as an 8-hour TWA. Because of the evidence of higher 
airborne Cr(VI) exposures in general industry than in construction, and 
because lower burdens are anticipated in the more stable work 
environments found in general industry, the Agency believes it is 
appropriate to cover Cr(VI) exposures from portland cement under the 
general industry proposed standard. OSHA is interested in comments and 
information regarding this preliminary determination, and has included 
this topic in the ``Issues'' section of this preamble.
    This proposal does not cover exposures to Cr(VI) that occur in the 
application of pesticides. Some Cr(VI)-containing chemicals, such as 
chromated copper arsenate (CCA) and acid copper chromate (ACC), are 
used for wood treatment and are regulated by EPA as pesticides. Section 
4(b)(1) of the OSH Act precludes OSHA from regulating working 
conditions of employees where other Federal agencies exercise statutory 
authority to prescribe or enforce standards or regulations affecting 
occupational safety or health. Therefore, OSHA proposes to specifically 
exclude those exposures regulated by EPA from coverage under the 
standard.
    The manufacture of pesticides containing Cr(VI) is not considered 
pesticide application, and is covered under this proposed standard. The 
use of wood treated with pesticides containing Cr(VI) is also covered. 
In this respect, the proposed Cr(VI) standard differs from OSHA's 
Inorganic Arsenic standard (29 CFR 1910.1018). The Inorganic Arsenic 
standard explicitly exempts the use of wood treated with arsenic. When 
the Inorganic Arsenic standard was issued in 1978, OSHA found that the 
evidence in the record indicated ``the arsenic in the preserved wood is 
bound tightly to the wood sugars, exhibits substantial chemical 
differences from other pentavalent arsenicals after reaction, and 
appears not to leach out in substantial amounts'' (43 FR 19584, 19613 
(5/5/78)). Based on the record in that rulemaking, OSHA did not 
consider it appropriate to regulate the use of preserved wood. The 
record in this rulemaking indicates that work with wood treated with 
pesticides containing Cr(VI) can involve significant Cr(VI) exposures. 
OSHA's exposure profile for woodworking indicates that over 30% of 
current employee Cr(VI) exposures exceed the proposed PEL. OSHA 
therefore believes it appropriate to include these activities under the 
scope of the proposed standard.

(b) Definitions

    ``Action level'' is defined as an airborne concentration of Cr(VI) 
of 0.5 micrograms per cubic meter of air (0.5 [mu]g/m<SUP>3</SUP>) 
calculated as an eight-hour time-weighted average (TWA). The action 
level triggers requirements for exposure monitoring and medical 
surveillance in general industry workplaces. In this proposal, as in 
other standards, the action level has been set at one-half of the PEL.
    Because of the variable nature of employee exposures to airborne 
concentrations of Cr(VI), maintaining exposures below the action level 
provides reasonable assurance that employees will not be exposed to 
Cr(VI) at levels above the PEL on days when no exposure measurements 
are made. Even when all measurements on a given day may fall below the 
PEL (but are above the action level), there is some chance that on 
another day, when exposures are not measured, the employee's actual 
exposure may exceed

[[Page 59448]]

the PEL. When exposure measurements are above the action level, the 
employer cannot be reasonably confident that employees may not be 
exposed to Cr(VI) concentrations in excess of the PEL during at least 
some part of the work week. Therefore, requiring periodic exposure 
measurements when the action level is exceeded provides the employer 
with a reasonable degree of confidence in the results of the exposure 
monitoring.
    The action level is also intended to encourage employers to lower 
exposure levels in order to avoid the costs associated with the 
exposure monitoring and medical surveillance provisions. Some employers 
would be able to reduce exposures below the action level in all work 
areas, and other employers in some work areas. As exposures are 
lowered, the risk of adverse health effects among workers decreases.
    OSHA s preliminary risk assessment indicates that significant risk 
remains at the proposed PEL of 1.0 [mu]g/m<SUP>3</SUP>. Where there is 
continuing significant risk, the decision in the Asbestos case 
(Building and Construction Trades Department, AFL-CIO v. Brock, 838 F. 
2d 1258, (D.C. Cir 1988)) indicated that OSHA should use its legal 
authority to impose additional requirements on employers to further 
reduce risk when those requirements will result in a greater than de 
minimus incremental benefit to workers' health. OSHA's preliminary 
conclusion is that the action level will result in a very real and 
necessary, but non-quantifiable, further reduction in risk beyond that 
provided by the PEL alone. OSHA's choice of proposing an action level 
of one-half of the PEL is based on the Agency's successful experience 
with other standards, including those for inorganic arsenic (29 CFR 
1910.1018), ethylene oxide (29 CFR 1910.1047), benzene (29 CFR 
1910.1028), and methylene chloride (29 CFR 1910.1052).
    As discussed under the requirements for exposure monitoring, OSHA 
has not proposed an action level for construction and shipyards. This 
definition is therefore not included in the proposed standards for 
construction and shipyards.
    ``Chromium (VI) [hexavalent chromium or Cr(VI)]'' means chromium 
with a valence of positive six, in any form or chemical compound in 
which it occurs. This term includes Cr(VI) in all states of matter, in 
any solution or other mixture, even if encapsulated by another or 
several other substances. The term also includes Cr(VI) when created by 
an industrial process, such as when welding of stainless steel 
generates Cr(VI) fume.
    For regulatory purposes, OSHA is treating Cr(VI) generically, 
instead of addressing specific compounds individually. This is based on 
OSHA's preliminary determination that the toxicological effect on the 
human body is similar from Cr(VI) in any of the substances covered 
under the scope of this standard, regardless of the form or compound in 
which it occurs. As discussed in Section VI of this preamble, some 
variation in potency may result due to differences in the solubility of 
compounds. Other factors, such as encapsulation, may have some effect 
on the bioavailability of Cr(VI). However, OSHA believes that these 
factors do not result in differences that merit separate provisions for 
different Cr(VI) compounds. OSHA considers it appropriate to apply the 
requirements of the proposed standard uniformly to all Cr(VI) 
compounds.
    ``Emergency'' means any occurrence that results, or is likely to 
result, in an uncontrolled release of Cr(VI), such as, but not limited 
to, equipment failure, rupture of containers, or failure of control 
equipment. Every spill or leak is not necessarily an emergency. The 
exposure to Cr(VI) must be unexpected and significant.
    If an incidental release of Cr(VI) may be safely cleaned up by 
employees at the time of release, it is not considered to be an 
emergency situation for the purposes of this section. The particular 
circumstances of the release itself, such as the quantity involved, 
confined space considerations, and the adequacy of ventilation will 
have an impact on employee safety. In addition, factors such as the 
knowledge of employees in the immediate work area, the personal 
protective equipment available, pre-established standard operating 
procedures for responding to releases, and engineering controls that 
employees can activate to assist them in controlling and stopping the 
release are all factors that must be considered in determining whether 
a release is incidental or an emergency. Those instances that 
constitute an emergency trigger certain requirements in this proposed 
standard (e.g., medical surveillance) that are discussed later in this 
section.
    ``Employee exposure'' means exposure to airborne Cr(VI) that would 
occur if the employee were not using a respirator. This definition is 
included to clarify the fact that employee exposure is measured outside 
any respiratory protection worn. It is consistent with OSHA's previous 
use of the term in other standards.
    ``Physician or other licensed health care professional (PLHCP)'' 
refers to an individual who is legally permitted to provide some or all 
of the health care services required by this section. This definition 
is included because the proposed standard requires that all medical 
examinations and procedures be performed by or under the supervision of 
a PLHCP.
    Any professional may perform the medical examinations and 
procedures provided under the standard when they are licensed by state 
law to do so. The Agency recognizes that this means that the personnel 
qualified to provide the required medical examinations and procedures 
may vary from state to state, depending on state licensing laws. This 
provision grants the employer the flexibility to retain the services of 
a variety of qualified licensed health care professionals, provided 
that these individuals are licensed to perform the specified service. 
OSHA believes that this flexibility will reduce cost and compliance 
burdens for employers and increase convenience for employees. The 
approach taken in this proposed standard is consistent with the 
approach OSHA has taken in other recent standards, such as those for 
methylene chloride (29 CFR 1910.1052), bloodborne pathogens (29 CFR 
1910.1030), and respiratory protection (29 CFR 1910.134).
    ``Regulated area'' means an area, demarcated by the employer, where 
an employee's exposure to airborne concentrations of Cr(VI) exceeds, or 
can reasonably be expected to exceed the PEL. This definition is 
consistent with the use of the term in other standards, including those 
for cadmium (29 CFR 1910.1027), butadiene (29 CFR 1910.1051), and 
methylene chloride (29 CFR 1910.1052).
    OSHA has not proposed a requirement for regulated areas in 
construction and shipyards. This definition is therefore not included 
in the proposed standards for construction and shipyards.
    The definitions for ``Assistant Secretary'', ``Director'', ``High-
efficiency particulate air [HEPA] filter'', and ``This section'' are 
consistent with OSHA's previous use of these terms found in other 
health standards.

(c) Permissible Exposure Limit (PEL)

    OSHA proposes to set an 8-hour time-weighted average (TWA) exposure 
limit of 1 microgram of Cr(VI) per cubic meter of air (1 [mu]g/
m<SUP>3</SUP>). This limit means that over the course of any 8-hour 
work shift, the average exposure to Cr(VI) cannot exceed 1 [mu]g/
m<SUP>3</SUP>. The proposed limit applies to Cr(VI), as opposed to the 
current PEL which is measured as CrO<INF>3</INF>. The current PEL of 1 
milligram per 10 cubic meters of air (1 [mu]g/10 m<SUP>3</SUP>, or 100

[[Page 59449]]

[mu]g/m<SUP>3</SUP>) reported as CrO<INF>3</INF> is equivalent to a 
limit of 52 [mu]g/m<SUP>3</SUP> as Cr(VI). The current PEL is enforced 
as a TWA in construction and as a ceiling (a level not to be exceeded 
at any time) in general industry.
    OSHA proposes a new PEL of 1 [mu]g/m<SUP>3</SUP> because the Agency 
has preliminarily determined that occupational exposure to Cr(VI) at 
the current PEL results in a significant risk of lung cancer among 
exposed workers, and that compliance with the proposed standard will 
substantially reduce that risk. OSHA's preliminary risk assessment, 
presented in Section VII of this preamble, indicates that the most 
reliable lifetime estimate of risk from a 45 year exposure to Cr(VI) at 
the current PEL is 101 to 351 excess deaths from lung cancer per 1000 
workers. As discussed in Section VIII of this preamble, this clearly 
represents a risk of material impairment of health that is significant 
within the context of the Benzene decision. OSHA believes that lowering 
the PEL to 1 [mu]g/m<SUP>3</SUP> would reduce the lifetime excess risk 
of death from lung cancer to between 2.1 and 9.1 per 1000 workers.
    OSHA considers the level of risk remaining at the proposed PEL to 
be significant. However, as discussed in Section IX of this preamble, 
the proposed PEL is set at the lowest level that the Agency believes to 
be feasible in all affected industry sectors. As guided by the 1988 
Asbestos decision, OSHA is proposing additional requirements to further 
reduce the remaining risk. OSHA anticipates that the ancillary 
provisions in the proposed standard will further reduce the risk beyond 
the reduction that would be achieved by the proposed PEL alone.
    OSHA believes that it is appropriate to establish a single PEL that 
applies to all Cr(VI) compounds. OSHA's preferred estimates of risk 
supporting the proposed PEL are derived from worker cohorts that were 
predominantly exposed to soluble sodium chromate. The evidence reviewed 
by OSHA indicates that similar doses of less soluble chromates result 
in higher numbers of lung tumors when compared to more soluble 
compounds such as sodium chromate (see Section VI of this preamble). 
Thus, any variation in toxicological effect due to solubility is 
expected to result in a higher level of risk than is indicated by 
OSHA's preliminary risk estimates. OSHA consequently believes that the 
Agency's findings regarding significance of risk are valid regardless 
of the solubility of the Cr(VI) compound. However, the available 
evidence is not sufficient to make quantitative estimates of risk for 
each individual Cr(VI) compound. OSHA is therefore proposing a single 
PEL for all Cr(VI) compounds. The Agency seeks comment on whether 
different PELs for different Cr(VI) compounds should be set and how 
such determinations should be made, and has included this topic in the 
``Issues'' section of the preamble.

(d) Exposure Monitoring

    The proposed general industry standard imposes monitoring 
requirements pursuant to Section 6(b)(7) of the OSH Act (29 U.S.C. 655) 
which mandates that any standard promulgated under section 6(b) shall, 
where appropriate, ``provide for monitoring or measuring of employee 
exposure at such locations and intervals, and in such manner as may be 
necessary for the protection of employees.''
    The purpose of requiring assessment of employee exposures to Cr(VI) 
include: determination of the extent and degree of exposure at the 
worksite; identification and prevention of employee overexposure; 
identification of the sources of exposure to Cr(VI); collection of 
exposure data so that the employer can select the proper control 
methods to be used; and evaluation of the effectiveness of those 
selected methods. Assessment enables employers to meet their legal 
obligation to ensure that their employees are not exposed to Cr(VI) in 
excess of the permissible exposure level and to notify employees of 
their exposure levels, as required by section 8(c)(3) of the Act. In 
addition, the availability of exposure data enables the PLHCP 
performing medical examinations to be informed of the extent of 
occupational exposures.
    Paragraph (d)(1) contains proposed general requirements for 
exposure monitoring. Monitoring to determine employee exposures must 
represent the employee's time-weighted average exposure to airborne 
Cr(VI) over an eight-hour workday. Samples must be taken within the 
employee's breathing zone (i.e., ``personal breathing zone samples'' or 
``personal samples''), and must represent the employee's exposure 
without regard to the use of respiratory protection.
    Employers must accurately characterize the exposure of each 
employee to Cr(VI). In some cases, this will entail monitoring all 
exposed employees. In other cases, monitoring of ``representative'' 
employees is sufficient. Representative exposure sampling is permitted 
when a number of employees perform essentially the same job under the 
same conditions. For such situations, it may be sufficient to monitor a 
fraction of these employees in order to obtain data that are 
``representative'' of the remaining employees. Representative personal 
sampling for employees engaged in similar work with Cr(VI) exposure of 
similar duration and magnitude can be achieved by monitoring the 
employee(s) reasonably expected to have the highest Cr(VI) exposures. 
For example, this may involve monitoring the Cr(VI) exposure of the 
employee closest to an exposure source. This exposure result may then 
be attributed to the remaining employees in the group.
    Exposure monitoring should include, at a minimum, one full-shift 
sample taken for each job function in each job classification, in each 
work area, for each shift. These samples must consist of at least one 
sample characteristic of the entire shift or consecutive representative 
samples taken over the length of the shift. Where employees are not 
performing the same job under the same conditions, representative 
sampling will not adequately characterize actual exposures, and 
individual monitoring is necessary.
    OSHA proposes that employers who have workplaces covered by the 
general industry standard determine if any of their employees are 
exposed to Cr(VI) at or above the action level. Further obligations 
under the standard would be based on the results of this assessment. 
These may include obligations for periodic monitoring, establishment of 
regulated areas, implementation of control measures, and provision of 
medical surveillance.
    Initial monitoring need not be conducted under two circumstances. 
First, where the employer has previously monitored for Cr(VI) in the 
past 12 months and the data were obtained during work operations 
conducted under workplace conditions closely resembling the processes, 
types of material, control methods, work practices, and environmental 
conditions used and prevailing in the employer's current operations, 
and where that monitoring satisfies all other requirements of this 
section, including the accuracy and confidence requirements, the 
employer may rely on such earlier monitoring results to satisfy the 
initial monitoring requirements of this section. This provision is 
designed to make it clear that OSHA does not intend to require 
employers who have recently performed appropriate employee monitoring 
to conduct ``initial'' monitoring. OSHA anticipates that this provision 
will reduce the compliance burden on employers, since monitoring for 
tasks that involve essentially the same exposures would

[[Page 59450]]

not be required. The Agency believes allowing the use of 12 month old 
data is appropriate; samples taken earlier than 12 months previously 
may not adequately represent current workplace conditions. The 12 month 
limit is consistent with the Methylene Chloride standard (29 CFR 
1910.1052).
    Second, where the employer has objective data demonstrating that a 
particular product or material containing Cr(VI) or a specific process, 
operation, or activity involving Cr(VI) cannot release dust, fumes, or 
mist in concentrations at or above the action level under any expected 
conditions of use, the employer may rely upon such data to satisfy 
initial monitoring requirements. The data must reflect workplace 
conditions closely resembling the processes, types of material, control 
methods, work practices, and environmental conditions in the employers' 
current operations.
    Objective data demonstrate that the work operation or the product 
may not reasonably be foreseen to release Cr(VI) in airborne 
concentrations at or above the action level under the expected 
conditions of use that will cause the greatest possible release, or in 
any plausible accident. The objective data may include monitoring data, 
or mathematical modeling or calculations based on the chemical and 
physical properties of a material. For example, data collected by a 
trade association from its members that meet the definition of 
objective data may be used. When using the term ``objective data'', 
OSHA is referring to employers' reliance on manufacturers' worst case 
studies, laboratory studies, and other research that demonstrates, 
usually by means of exposure data, that meaningful exposures cannot 
occur. OSHA has allowed employers to use objective data in other 
standards such as those for formaldehyde (29 CFR 1910.1048) and 
asbestos (29 CFR 1910.1001) in lieu of initial monitoring and hence, 
from most of the provisions of these standards.
    Paragraph (d)(3) contains requirements for periodic monitoring. The 
requirement for continued monitoring depends on the results of initial 
monitoring. If the initial monitoring indicates that employee exposures 
are below the action level, no further monitoring would be required 
unless changes in the workplace result in new or additional exposures. 
If the initial determination reveals employee exposures to be at or 
above the action level but below the PEL, the employer must perform 
periodic monitoring at least every six months. If the initial 
monitoring reveals employee exposures to be above the PEL, the employer 
must repeat monitoring at least every three months.
    The proposed rule also includes provisions to adjust the frequency 
of periodic monitoring based on monitoring results. If periodic 
monitoring results indicate that employee exposures have fallen below 
the action level, and those results are confirmed by consecutive 
measurements taken at least seven days later, the employer may 
discontinue monitoring for those employees whose exposures are 
represented by such monitoring. Similarly, if periodic monitoring 
measurements indicate that exposures are below the PEL but above the 
action level, and those results are confirmed by consecutive 
measurements taken at least seven days later, the employer may reduce 
the frequency of the monitoring to at least every six months.
    OSHA recognizes that exposures in the workplace may fluctuate. 
Periodic monitoring provides the employer with assurance that employees 
are not experiencing higher exposures that may require the use of 
additional control measures. In addition, periodic monitoring reminds 
employees and employers of the continued need to protect against the 
hazards associated with exposure to Cr(VI).
    Because of the fluctuation in exposures, OSHA believes that when 
initial monitoring results exceed the action level but are below the 
PEL, employers should continue to monitor employees to ensure that 
exposures remain below the PEL. Likewise, when initial monitoring 
results exceed the PEL, periodic monitoring allows the employer to 
maintain an accurate profile of employee exposures. If the employer 
installs or upgrades controls, periodic monitoring will demonstrate 
whether or not controls are working properly. Selection of appropriate 
respiratory protection also depends on adequate knowledge of employee 
exposures.
    In general, the more frequently periodic monitoring is performed, 
the more accurate the employee exposure profile. Selecting an 
appropriate interval between measurements is a matter of judgment. OSHA 
believes that the proposed frequency of six months for subsequent 
periodic monitoring for exposures above the action level but below the 
PEL, and three months for exposures above the PEL, provides intervals 
that are both practical for employers and protective for employees. 
This belief is supported by OSHA's experience with comparable 
monitoring intervals in other standards, including those for cadmium 
(29 CFR 1910.1027), methylenedianiline (29 CFR 1910.1050), methylene 
chloride (29 CFR 1910.1052), and formaldehyde (29 CFR 1910.1048). The 
proposed requirement for periodic monitoring is also consistent with 
OSHA's Standards Improvement Project (SIPs) proposal for monitoring 
frequency (67 FR 66494, 66504 (8/31/02)).
    OSHA recognizes that monitoring can be a time-consuming, expensive 
endeavor and therefore offers employers the incentive of discontinuing 
monitoring for employees whose sampling results indicate exposures are 
below the action level. The Agency does not believe that periodic 
monitoring is generally necessary when monitoring results show that 
exposures are below the action level because there is a low probability 
that the results of future samples would exceed the PEL. The Agency 
intends for this provision to encourage employers to control their 
employees' exposures to Cr(VI) below the action level, thus maximizing 
the protection of employees' health.
    Under paragraph (d)(4), employers are to perform additional 
monitoring when there is a change in production process, raw materials, 
equipment, personnel, work practices, or control methods, that may 
result in new or additional exposures to Cr(VI). In addition, there may 
be other situations which can result in new or additional exposures to 
Cr(VI) which are unique to an employer's work situation. In order to 
cover those special situations, OSHA requires the employer to perform 
additional monitoring whenever the employer has any reason to believe 
that a change has occurred which may result in new or additional 
exposures. This additional monitoring is necessary to ensure that 
monitoring results accurately represent existing exposure conditions. 
This is necessary so that the employer can take appropriate action to 
protect exposed employees, such as instituting additional engineering 
controls or providing appropriate respiratory protection.
    Under paragraph (d)(5) of the general industry standard, employers 
are to notify each affected employee of their monitoring results within 
15 working days after the receipt of the results. The employer shall 
either notify each affected employee in writing or post the monitoring 
results in an appropriate location accessible to all affected 
employees. In addition, whenever the PEL has been exceeded, the written 
notification must contain a description of the corrective action(s) 
being taken by the employer to reduce the employee's exposure to or 
below the PEL. The requirement to inform employees of the

[[Page 59451]]

corrective actions the employer is taking to reduce the exposure level 
to or below the PEL is necessary to assure employees that the employer 
is making efforts to furnish them with a safe and healthful work 
environment, and is required under section 8(c)(3) of the Act.
    The proposal would require that all affected employees be notified 
of the monitoring results. When using the term ``affected employees'' 
in this context, OSHA is not referring only to the employee(s) actually 
subject to personal monitoring. Affected employees include all 
employees represented by the employee(s) sampled.
    Individual notification in writing or posting would be acceptable 
under the proposed rule. This is consistent with other OSHA standards 
such as those for methylenedianiline (29 CFR 1910.1050), butadiene (29 
CFR 1910.1051), and methylene chloride (29 CFR 1910.1052). In addition, 
the SIPs proposal (67 FR 66494, 66508 (10/31/02)) allows for employer 
choice of notification method. The Cr(VI) proposal is also consistent 
with SIPs in that SIPs specifies 15 working days after the receipt of 
monitoring results as the appropriate time to notify employees in 
general industry (67 FR 66494, 66508 (10/31/03)).
    Under paragraph (d)(6), the employer would be required to use 
monitoring and analytical methods that can measure airborne levels of 
Cr(VI) to within an accuracy of plus or minus 25% (+/-25%) and can 
produce accurate measurements to within a statistical confidence level 
of 95% percent for airborne concentrations at or above the action 
level. Many laboratories presently have methods to measure Cr(VI) at 
the proposed action level with at least the required degree of 
accuracy. One example of an acceptable method of monitoring and 
analysis is OSHA method ID215. Rather than specifying a particular 
method that must be used, OSHA proposes to take a performance approach 
and instead allows the employer to use any method as long as the chosen 
method meets the accuracy specifications.
    Paragraph (d)(7) requires the employer to provide affected 
employees or their designated representatives an opportunity to observe 
any monitoring of employee exposure to Cr(VI). When observation of 
monitoring requires entry into an area where the use of protective 
clothing or equipment is required, the employer must provide the 
observer with that protective clothing or equipment, and assure that 
the observer uses such clothing or equipment and complies with all 
other applicable safety and health procedures.
    The requirement for employers to provide employees or their 
representatives the opportunity to observe monitoring is consistent 
with the OSH Act. Section 8(c)(3) of the OSH Act mandates that 
regulations developed under Section 6 provide employees or their 
representatives with the opportunity to observe monitoring or 
measurements. Also, Section 6(b)(7) of the OSH Act states that where 
appropriate, OSHA standards are to prescribe suitable protective 
equipment to be used in dealing with hazards. The provision for 
observation of monitoring and protection of the observers is also 
consistent with OSHA's other substance-specific health standards such 
as those for cadmium (29 CFR 1910.1027) and methylene chloride (29 CFR 
1910.1052).
    The proposed construction and shipyard standards for Cr(VI) do not 
include provisions for exposure monitoring. OSHA recognizes that in 
these sectors in many instances the results of exposure monitoring 
required under this proposed standard would not be available until 
after operations involving Cr(VI) exposure have been completed. For 
example, a welding task may be finished in a single day. If air 
monitoring is performed, the task would be completed before the 
employer is informed of the monitoring results. Therefore, the employer 
would not be in a position to make use of the monitoring results to 
determine appropriate control measures for that task. In other cases, 
the workplace conditions in construction and shipyard worksites may 
vary to such a great extent that it may be difficult to accurately 
characterize employee exposure from one day to the next. For example, a 
stainless steel welder may work outdoors on a windy day one day and in 
an enclosed environment the next day. Personal monitoring for Cr(VI) 
exposure on a given day may not accurately reflect these changing 
conditions. OSHA has therefore proposed a performance-oriented 
requirement for construction and shipyard employers. Rather than 
include specific requirements for exposure monitoring for these 
employers, OSHA proposes to allow construction and shipyard employers 
the flexibility to assess Cr(VI) exposures in any manner they choose. 
Thus, construction and shipyard employers could use historical data, 
objective data, or employee monitoring to determine employee exposures. 
Because the obligation to comply with the PEL would remain, whatever 
method the employer chooses would have to be sufficient to ensure that 
no employee is exposed to an airborne concentration of Cr(VI) in excess 
of the PEL.
    In some cases, the employer may choose not to perform any 
monitoring. For example, certain tasks (e.g., abrasive blasting of 
materials coated with Cr(VI); welding, cutting, or torch burning of 
stainless steel or of materials coated with Cr(VI); or spray 
application of Cr(VI) containing paints or coatings) frequently entail 
exposures to Cr(VI) above the proposed PEL. OSHA estimates that 
approximately 43% of the exposures in construction welding and 17.9% of 
the exposures in shipyard welding are greater than the proposed PEL of 
1 [mu]g/m<SUP>3</SUP>. A construction or shipyard employer has the 
option of assuming the employee is exposed above the PEL and providing 
appropriate protective measures as prescribed by the standard.
    Similarly, an employer may not find it necessary to perform 
exposure monitoring where exposures are well below the PEL. For 
example, there are several construction application groups (e.g., 
industrial rehabilitation and maintenance, hazardous waste site work, 
and refractory restoration and maintenance) where a large percentage of 
exposures are either below 0.25 [mu]g/m<SUP>3</SUP> or below the limit 
of detection for Cr(VI). In these situations, employers may be 
relatively assured that employees' exposure are well below the PEL and 
would therefore not need to conduct exposure monitoring.
    This approach is consistent with OSHA's standard for air 
contaminants (29 CFR 1910.1000), which establishes PELs for over 400 
substances, but does not include specific requirements for exposure 
monitoring. The Agency seeks comment as to whether this performance-
oriented approach to exposure monitoring is appropriate in construction 
and shipyard workplaces, and has included this topic in the ``Issues'' 
section of this preamble.

(e) Regulated Areas

    Under paragraph (e), general industry employers must establish 
regulated areas wherever an employee's exposure to airborne 
concentrations of Cr(VI) is, or can reasonably be expected to be, in 
excess of the PEL. Regulated areas are to be demarcated from the rest 
of the workplace in a manner that adequately establishes and alerts 
employees to the boundaries of these areas, and would be required to 
include the warning signs specified in paragraph (l)(2) of the proposed 
standard. Access to regulated areas is limited to persons authorized by 
the employer and required by work

[[Page 59452]]

duties to be present in the regulated area; any person entering the 
regulated area to observe monitoring procedures; or any person 
authorized by the OSH Act or regulations issued under it to be in a 
regulated area.
    The purpose of a regulated area is to ensure that the employer 
makes employees aware of the presence of Cr(VI) at levels above the 
PEL, and to limit Cr(VI) exposure to as few employees as possible. The 
establishment of a regulated area is an effective means of limiting the 
risk of exposure to substances known to have carcinogenic effects. 
Because of the potentially serious results of exposure and the need for 
persons entering the area to be properly protected, the number of 
persons given access to the area should be limited to those employees 
needed to perform the job. Limiting access to regulated areas also has 
the benefit of reducing the employer's obligation to implement 
provisions of this proposal to as few employees as possible.
    In keeping with the performance orientation of this proposed 
standard, OSHA has not specified how employers are to demarcate 
regulated areas. The demarcation should effectively warn employees not 
to enter the area unless they are authorized, and then only if they are 
using the proper personal protective equipment. The demarcation must 
include display of warning signs at all approaches to the regulated 
areas, consistent with the requirements of paragraph (l)(2) of this 
proposed standard. In many cases these warning signs alone will be 
sufficient to identify the boundaries of the regulated area.
    Access to the regulated area is restricted to ``authorized 
persons''. For the purposes of this proposed standard, these are 
persons required by their job duties to be present in the area, as 
authorized by the employer. In addition, persons exercising the right 
to observe monitoring procedures are also allowed to enter regulated 
areas. Employees in some workplaces may designate a union 
representative to observe monitoring; this person would be allowed to 
enter the regulated area. Persons authorized under the OSH Act, such as 
OSHA compliance officers, are also allowed access to regulated areas.
    OSHA has not included a requirement for regulated areas in 
construction and shipyard workplaces, due to the expected difficulties 
in establishing regulated areas in construction and shipyard 
workplaces. For example, several small entity representatives (SERs) 
from the construction and shipyard industries who participated in the 
SBREFA review noted that in their work settings regulated areas would 
be particularly problematic and might require that the entire worksite 
be designated as a regulated area. They also noted that due to the 
changing nature of the work site (namely construction sites) the 
demarcation of the regulated area would have to be changed each day as 
the work progressed (e.g., Exs. 34-6, 34-14). The same rationale 
applies to shipyards. The Agency seeks comment as to whether a 
requirement for the establishment of regulated areas would be 
appropriate for construction or shipyard workplaces and how such areas 
could be established, and has included this topic in the ``Issues'' 
section of this preamble.

(f) Methods of Compliance

    The proposed standard requires employers to institute effective 
engineering and work practice controls as the primary means to reduce 
and maintain employee exposures to Cr(VI) to levels that are at or 
below the PEL, unless the employer can demonstrate that such controls 
are not feasible, or if employees are not exposed above the PEL for 30 
or more days per year. Employers would be required to institute 
engineering controls and work practices to reduce exposure to the 
lowest feasible level even if these measures alone would not reduce the 
concentration of airborne Cr(VI) to or below the PEL. The employer 
would then be required to supplement these controls with respirators to 
ensure that employees are not exposed to Cr(VI) above the PEL.
    Primary reliance on engineering controls and work practices is 
consistent with good industrial hygiene practice and with OSHA's 
traditional adherence to a hierarchy of preferred controls. Engineering 
controls are reliable, provide consistent levels of protection to a 
large number of workers, can be monitored continually and 
inexpensively, allow for predictable performance levels, and can 
efficiently remove toxic substances from the workplace. Once removed, 
the toxic substance no longer poses a threat to employees. The 
effectiveness of engineering controls does not generally depend to any 
substantial degree on human behavior, and the operation of equipment is 
not as vulnerable to human error as is personal protective equipment. 
For these reasons, engineering controls are preferred by OSHA.
    Engineering controls can be grouped into three main categories: (1) 
Substitution; (2) isolation; and (3) ventilation, both general and 
localized. Quite often a combination of these controls can be applied 
to an industrial hygiene control problem to achieve satisfactory air 
quality. It may not be necessary to apply all these measures to any 
specific potential hazard.
    Substitution can be an ideal control measure. One of the best ways 
to prevent workers from being exposed to a toxic substance is to stop 
using it entirely. Although substitution is not always possible, 
replacement of a toxic material with a less hazardous alternative 
should always be considered.
    In those cases where substitution of a less toxic material is not 
possible, substituting one type of process for another process may 
provide effective control of an air contaminant. For example, process 
changes from batch operations to continuous operations will usually 
reduce exposures. This is true primarily because the frequency and 
duration of workers' potential contact with process materials is 
reduced in continuous operations. Similarly, automation of a process 
can further reduce the potential hazard.
    In addition to substitution, isolation should be considered as an 
option for controlling employee exposures to Cr(VI). Isolation can 
involve containment of the source of a hazard, thereby separating it 
from most workers. Workers can be isolated from Cr(VI) by working in a 
clean room or booth, or by placing some other type of barrier between 
the source of exposure and the employee. Employees can also be 
protected by being placed at a greater distance from the source of 
Cr(VI) emissions.
    Frequently, isolation enhances the benefits of other control 
methods. For example, Cr(VI) compounds may be used in the formulation 
of certain paints. If the mixing operation is conducted in a small, 
enclosed room the airborne Cr(VI) potentially generated by the 
operation could be confined to a small area. By ensuring containment, 
local exhaust ventilation is more effective.
    Ventilation is a method of controlling airborne concentrations of a 
contaminant by supplying or exhausting air. A local exhaust system is 
used to remove an air contaminant by capturing the contaminant at or 
near its source before it spreads throughout the workplace. General 
ventilation (dilution ventilation), on the other hand, allows the 
contaminant to spread throughout the work area but dilutes it by 
circulating large quantities of air into and out of the area. A local 
exhaust system is generally preferred to dilution ventilation because 
it provides a cleaner and healthier work environment.

[[Page 59453]]

    Work practices controls involve adjustments in the way a task is 
performed. In many cases, work practice controls complement engineering 
controls in providing worker protection. For example, periodic 
inspection and maintenance of process equipment and control equipment 
such as ventilation systems is an important work practice control. 
Frequently, equipment which is in disrepair or near failure will not 
perform normally. Regular inspections can detect abnormal conditions so 
that timely maintenance can then be performed. If equipment is 
routinely inspected, maintained, and repaired or replaced before 
failure is likely, there is less chance that hazardous exposures will 
occur.
    Workers must know the proper way to perform their job tasks in 
order to minimize their exposure to Cr(VI) and to maximize the 
effectiveness of control measures. For example, if an exhaust hood is 
designed to provide local ventilation and a worker performs a task that 
generates a contaminant away from the exhaust hood, the control measure 
will be of no use. Workers can be informed of proper operating 
procedures through information and training. Good supervision provides 
further support for ensuring that proper work practices are carried out 
by workers. By persuading a worker to follow proper procedures, such as 
positioning the exhaust hood in the correct location to capture the 
contaminant, a supervisor can do much to minimize unnecessary exposure.
    Employees' exposures can also be controlled by scheduling 
operations with the highest exposures at a time when the fewest 
employees are present. For example, routine clean-up operations that 
involve Cr(VI) releases might be performed at night or at times when 
the usual production staff is not present.
    OSHA has traditionally relied less on respiratory protection in the 
hierarchy of controls because the use and efficacy of respirators 
depends to a great extent on human behavior. Often work is strenuous, 
and the increased breathing resistance of the respirator reduces its 
acceptability to employees. Respirators can limit an employee's vision 
and ability to communicate. In some difficult and dangerous jobs, 
effective vision or communication is vital to a safe, efficient 
operation. Voice communication when using a respirator can be difficult 
and fatiguing. In any event, movement of the jaw in speaking can cause 
a temporary breaking of the face-to-facepiece seal, thereby reducing 
the efficiency of the respirator and decreasing the employee's 
protection. Skin irritation can result from wearing a respirator in 
hot, humid conditions. Such irritation can cause considerable distress 
to workers and may disrupt work schedules. To be used effectively, 
respirators must be individually selected; fitted and periodically 
refitted; conscientiously and properly worn; regularly maintained, 
including filter changes; and replaced as necessary. In some 
workplaces, these preconditions for effective respirator use can be 
difficult to achieve. It is more difficult to assure that each employee 
is wearing a respirator correctly than to ascertain that engineering 
controls are operational. Thus, OSHA has concluded that reliance upon 
respirators should be minimized when engineering and work practice 
controls are found to be effective.
    OSHA has proposed an exception to the general requirement for 
primary reliance on engineering and work practice controls for those 
employers who do not have employee exposures above the PEL for 30 or 
more days per year (12 consecutive months) from a particular process or 
task. Thus, if an employee is exposed to Cr(VI) on only 29 days during 
any 12 consecutive months from a particular process or task, even if 
the exposure is above the PEL on all of these days, the employer would 
not be required by this proposed standard to implement engineering and 
work practice controls to control exposures to the PEL. The burden 
would be on the employer to show that exposures do not exceed the PEL 
on 30 or more days per year. OSHA believes this provision would provide 
needed flexibility to employers, while still protecting workers.
    Under the proposed exception, the employer's obligation to 
implement engineering and work practice controls to comply with the PEL 
would not be triggered until an employee in a process or task is 
exposed above the PEL on 30 or more working days during a year. Where 
the exposure is for fewer than 30 working days, the employer could use 
any combination of controls to prevent employees from being exposed 
above the PEL, including respirators alone. The employer may use this 
exception if he or she has a reasonable basis for believing that 
employees in a process or task will not be exposed above the PEL for 30 
or more days per year (12 consecutive months). OSHA intends for this 
exception to be process- or task-based, i.e., it is specific to a 
process where engineering controls might be implemented to reduce 
exposures below the PEL. For example, an employer might have two 
processes, A and B, where A involved an ongoing process in the facility 
with exposures above the PEL for more than 30 days and another process, 
B, only resulted in exposures above the PEL between 10 and 29 days. The 
fact that the employer had employees exposed above the PEL for more 
than 30 days in process A would not be used to determine that 
engineering and work practice controls had to be used for process B. 
OSHA intends this exception to be similarly applied by process or task 
in the construction and shipyard environments where employees may move 
from one work site to another.
    OSHA has proposed this exception because the Agency realizes that 
in some industries (e.g., color pigment manufacturing), exposure to 
Cr(VI) is typically infrequent (i.e., fewer than 30 days, over 12 
consecutive months). For example, certain Cr(VI) processes may occur 
only several days a year when production of a particular product is 
needed. Under such conditions of exposure, it may not be economically 
feasible or cost effective to invest the monies needed to install 
engineering controls or to institute work practices to control Cr(VI) 
to the PEL. Without such an exception, employers would be required to 
implement feasible engineering controls or work practice controls 
wherever employees are exposed to Cr(VI) above the PEL, even if they 
are only exposed on one or several days a year. OSHA believes that the 
expense of implementing engineering and work practice controls in such 
circumstances may not be justified. Consequently, incorporating an 
exception is a reasonable way to lessen the burden on employers while 
still protecting employees. OSHA's proposed exception for fewer than 30 
working days per year is consistent with the standards for lead (29 CFR 
1910.1025) and cadmium (29 CFR 1910.1027), both of which incorporate 
similar provisions.
    In proposing this exception, OSHA intends to provide relief 
exclusively to employers whose employees are exposed to Cr(VI) only for 
short periods (in terms of days and weeks) and otherwise are not 
exposed to Cr(VI) above the PEL. Where the employee has other exposures 
above the PEL, the employer would be obligated to achieve the PEL by 
means of engineering and work practice controls. The Agency believes 
the proposed 30-working-day exclusion would make the standard more 
flexible in workplaces where exposure days are extremely limited.
    In order for this exception to apply, the proposed standard states 
that the employer must have a ``reasonable basis for believing that no 
employees in a

[[Page 59454]]

process or task will be exposed above the PEL for 30 or more days''. 
Historical data, objective data, or exposure monitoring data may all 
provide a reasonable basis for believing that employees will not be 
exposed above the PEL for 30 or more days per year. Other information, 
such as production orders showing that processes involving Cr(VI) 
exposures are conducted on fewer than 30 days per year, may also serve 
as a reasonable basis for believing that employees will not be exposed 
above the PEL for 30 or more days per year.
    In order to take advantage of the proposed exception, the employer 
would have the burden to demonstrate that his or her employees in a 
process or task will not be exposed above the PEL for more than 30 days 
per year. The burden of proof is placed on the employer because the 
employer has access to needed information about employee exposure 
levels and processes and tasks at the worksite. Where existing 
information is inadequate, the employer is also in the best position to 
develop the necessary information. The obligation to demonstrate that a 
reasonable basis exists for believing that employees in a process or 
task will not be exposed above the PEL for more than 30 days per year 
is the same for general industry, construction, and shipyard employers.
    Paragraph (f)(2) of the proposed rule (paragraph (d)(2) of the 
construction and shipyard proposals) would prohibit the employer from 
using employee rotation as a means of compliance with the PEL. Worker 
rotation reduces the exposures to individual employees, but increases 
the number of employees exposed. Since OSHA has made a preliminary 
determination that Cr(VI) is carcinogenic, the Agency considers it 
inappropriate to place more workers at risk. Since no threshold has 
been established for the carcinogenic effects of Cr(VI), it is prudent 
to limit the number of workers exposed at any concentration. This 
provision does not, however, prohibit worker rotation when it is 
conducted for reasons other than compliance with the PEL. For example, 
an employer may rotate workers in order to provide cross-training on 
different tasks, or to allow workers to alternate physically demanding 
tasks with less strenuous activities. OSHA does not intend for this 
provision to be interpreted as a general prohibition on employee 
rotation where workers are exposed to Cr(VI). This proposed provision 
is consistent with other OSHA standards such as those for butadiene (29 
CFR 1910.1051), methylene chloride (29 CFR 1910.1052), and cadmium (29 
CFR 1910.1027).

(g) Respiratory Protection

    When engineering controls and work practices cannot reduce employee 
exposure to Cr(VI) to within the PEL, OSHA proposes that the employer 
must protect employees' health through the use of respirators. 
Specifically, respirators would be required as supplementary protection 
to reduce employee exposure during the installation and implementation 
of engineering and work practice controls; during work operations where 
engineering and work practice controls are not feasible; when all 
feasible engineering and work practice controls have been implemented, 
but are not sufficient to reduce exposure to or below the PEL; during 
work operations where employees are exposed above the PEL for fewer 
than 30 days per year, and the employer has elected not to implement 
engineering and work practice controls to achieve the PEL; and during 
emergencies.
    These limitations on the required use of respirators are generally 
consistent with other OSHA health standards, such as those for 
butadiene (29 CFR 1910.1051) and methylene chloride (29 CFR 1910.1052). 
They reflect the Agency's determination, discussed in the section on 
methods of compliance, that respirators are inherently less reliable 
than engineering and work practice controls. OSHA has therefore 
proposed to allow reliance on respirators only in certain designated 
situations.
    In those circumstances where engineering and work practice controls 
cannot be used to achieve the PEL (e.g., in emergencies, or during 
periods when equipment is being installed), or where engineering 
controls may not be reasonably necessary (e.g., where employees are 
exposed above the PEL for fewer than 30 days per year), OSHA recognizes 
that respirators may be essential to reduce worker exposure, and 
provision is made for their use as primary controls. In other 
circumstances, where feasible work practices and engineering controls 
alone cannot reduce exposure levels to the PEL, respirators also may be 
used for supplemental protection. In these situations, the burden of 
proof is placed on the employer to demonstrate that engineering and 
work practice controls are not feasible.
    OSHA anticipates that engineering and work practice controls will 
be in place by the effective dates specified in paragraph (n) of this 
proposal (paragraph (k) for construction and shipyards). The Agency 
realizes that in some cases employers may commence operations that 
involve employee Cr(VI) exposures after that date, may install new or 
modified equipment, or make other workplace changes that result in new 
or additional exposures to Cr(VI). In these cases, a reasonable amount 
of time may be needed before appropriate engineering controls can be 
installed and proper work practices implemented. When employee 
exposures exceed the PEL in these situations, employers are expected to 
provide respiratory protection to protect workers.
    Respiratory protection is also required during work operations 
where engineering and work practice controls are not feasible. OSHA 
anticipates that there will be very few situations where no engineering 
and work practice controls are feasible to limit employee exposure to 
Cr(VI). In other cases, some engineering and work practice controls may 
be feasible, but these controls may not be capable of lowering employee 
exposures to or below the PEL. For example, tasks such as stainless 
steel welding or abrasive blasting may present certain difficulties 
when performed in confined spaces. In these cases, the employer would 
be required to provide respiratory protection. In any event, the 
employer must always install engineering controls and implement work 
practice controls when such controls are feasible to reduce exposures, 
even if these controls cannot reduce exposures below the PEL.
    The requirement to provide respiratory protection when feasible 
engineering controls are not sufficient to reduce exposures to within 
the PEL would also apply in instances where effective engineering 
controls have been installed and are being maintained or repaired. In 
these situations, controls may not be effective while maintenance or 
repair is underway. Where exposures exceed the PEL, the employer would 
be required to provide respirators.
    As discussed earlier with regard to methods of compliance, OSHA is 
proposing an exemption from the general requirement for use of 
engineering and work practice controls where employee exposures do not 
exceed the PEL on 30 or more days per year. Where this exception 
applies, the employer would then be required to provide respiratory 
protection to achieve the PEL. OSHA also believes that emergencies are 
situations where respirators must be used to protect employees. Since 
an emergency, by definition, involves or is likely to involve an 
uncontrolled release of Cr(VI), it is important to protect

[[Page 59455]]

employees from the significant exposures that may occur.
    Whenever respirators are used to comply with the requirements of 
the standard, OSHA proposes that the employer implement a comprehensive 
respiratory protection program in accordance with the Agency's 
Respiratory Protection standard (29 CFR 1910.134). The respiratory 
protection program is designed to ensure that respirators are properly 
used in the workplace, and are effective in protecting workers. The 
program must include procedures for selecting respirators for use in 
the workplace; medical evaluation of employees required to use 
respirators; fit testing procedures for tight-fitting respirators; 
procedures for proper use of respirators in routine and reasonably 
foreseeable emergency situations; procedures and schedules for 
maintaining respirators; procedures to ensure adequate quality, 
quantity, and flow of breathing air for atmosphere-supplying 
respirators; training of employees in the proper use of respirators; 
and procedures for evaluating the effectiveness of the program. In 
addition, this provision will serve as a reminder to employers covered 
by the Cr(VI) rule that they must also comply with the Respiratory 
Protection standard when respirators are provided to employees.
    OSHA has proposed to revise the Respiratory Protection standard to 
include assigned protection factors (68 FR 34036 (6/6/03)). The 
proposed revision includes a table which indicates the level of 
respiratory protection that a given respirator or class of respirators 
is expected to provide, and will apply to employers whose employees use 
respirators for protection against Cr(VI) when it becomes a final rule 
(68 FR 34036, 34115 (6/6/03)).

(h) Protective Work Clothing and Equipment

    The proposed standard would require that the employer provide 
protective clothing and equipment at no cost to employees where a 
hazard is present or is likely to be present from skin or eye contact 
with Cr(VI). The employer would also be required to ensure that 
employees use the clothing and equipment provided. The intent of this 
provision is to prevent the adverse health effects associated with 
dermal exposure to Cr(VI) (described in Section VI.D of this preamble) 
and the potential for inhalation of Cr(VI) that may be deposited on 
employees' street clothing. The proposed requirements for protective 
clothing and equipment are similar to those in other OSHA health 
standards such as those for cadmium (29 CFR 1910.1027) and 
methylenedianiline (29 CFR 1910.1050), and are based upon widely 
accepted principles and conventional practices of industrial hygiene. 
The proposed requirements are also consistent with Section 6(b)(7) of 
the OSH Act which states that, where appropriate, standards shall 
prescribe suitable protective equipment to be used in connection with 
hazards.
    OSHA has proposed a standard that will cover payment for personal 
protective equipment in all workplaces (64 FR 15401 (3/31/99)). The 
Agency is incorporating the record of that rulemaking into the Cr(VI) 
rulemaking and will give due consideration to all relevant comments.
    Criteria for determining when a hazard is present or is likely to 
be present from skin or eye contact with Cr(VI) are not specified. When 
evaluating the potential for hazardous eye or skin contact with Cr(VI), 
OSHA anticipates that the employer will assess the workplace in a 
manner consistent with the current requirements of the Agency's 
standards for use of personal protective equipment in general industry 
(29 CFR 1910.132) and shipyards (29 CFR 1915.152). These standards 
require the employer to assess the workplace to determine if hazards 
(including hazards associated with eye and skin contact with chemicals) 
are present, or are likely to be present.
    As described in the non-mandatory appendices providing guidance on 
hazard assessment for these standards (29 CFR 1910 Subpart I Appendix 
B; 29 CFR 1915 Subpart I Appendix A), the employer should ``exercise 
common sense and appropriate expertise'' in assessing hazards. The 
recommended approach involves a walk-through survey to identify sources 
of hazards to workers. Review of injury/accident data is also 
recommended. Information obtained during this process provides a basis 
for the evaluation of potential hazards.
    Based on the results of this assessment, the employer must 
determine what clothing and equipment is necessary to protect employees 
from Cr(VI) hazards. The proposed requirement is performance-oriented, 
and is designed to allow the employer flexibility in selecting the 
clothing and equipment most suitable for his or her particular 
workplace. The type of protective clothing and equipment needed to 
protect employees from Cr(VI) hazards will depend on the potential for 
exposure and the conditions of use in the workplace. Examples of 
protective clothing and equipment include, but are not limited to 
gloves, aprons, coveralls, foot coverings, and goggles. Ordinary street 
clothing and work uniforms or other accessories that do not serve to 
protect workers from Cr(VI) hazards are not considered protective 
clothing and equipment under this proposed standard.
    The employer must exercise reasonable judgment in selecting the 
appropriate clothing and equipment to protect employees from Cr(VI) 
hazards. This provision is consistent with OSHA's current standards for 
provision of personal protective equipment (e.g., 29 CFR 1910.132, 29 
CFR 1915.152, 29 CFR 1926.95). For example, a worker who is 
constructing a home foundation using wood treated with chromated copper 
arsenate, leather gloves may be all that is necessary to prevent 
hazardous Cr(VI) exposure. In other situations, such as when a worker 
is performing abrasive blasting on a structure covered with Cr(VI)-
containing paint, more extensive measures such as coveralls, head 
coverings, and goggles may be needed. Where exposures to Cr(VI) are 
minute, no protective clothing or equipment may be necessary. Many 
Cr(VI) compounds are acidic or alkaline (e.g., chromic acid, portland 
cement), and these characteristics may also influence the choice of 
protective clothing and equipment. For example, a chrome plater may 
require an apron, gloves, and goggles to protect against possible 
splashes of chromic acid that could result in both Cr(VI) exposure and 
chemical burns.
    OSHA has not proposed a threshold concentration of Cr(VI) for 
determining when a substance would be covered under the rule. In some 
OSHA standards an exemption from certain requirements based on 
percentage composition has been included. For example, the standard for 
formaldehyde requires that the employer prevent eye and skin contact 
with liquids containing one percent or more formaldehyde (29 CFR 
1910.1048(h)(1)(i)). Contact with liquids containing less than one 
percent formaldehyde is exempt from this provision. Such exemptions 
have been included so that coverage would not be extended to trivial 
exposures that were not associated with adverse health effects.
    A similar exemption has not been included in this proposed standard 
because adverse health effects have been shown to occur as a result of 
dermal contact to relatively low concentrations of Cr(VI). For example, 
exposures to portland cement have been associated with allergic contact 
dermatitis, even though Cr(VI) concentrations in the cement were 
reported to be below 10 [mu]g/

[[Page 59456]]

g (i.e., 0.001%) (Ex. 35-326). OSHA is not aware of any evidence that 
would allow establishment of a threshold concentration of Cr(VI) below 
which adverse dermal effects would not occur.
    Paragraph (h)(2) (paragraph (f)(2) of the proposals for 
construction and shipyards) contains proposed requirements for removal 
and storage of protective clothing and equipment. The employer must 
ensure that all protective clothing and equipment contaminated with 
Cr(VI) is removed at the completion of the work shift or at the 
completion of tasks involving Cr(VI) exposure. Where employees must 
change their clothes (i.e., take off their street clothes), removal of 
protective clothing and equipment must occur in change rooms provided 
in accordance with paragraph (i) of this section (paragraph (g) of the 
construction and shipyard proposals). This provision is intended to 
reduce Cr(VI) contamination of the workplace, and limit Cr(VI) 
exposures outside the workplace. Wearing contaminated clothing outside 
the work area could lengthen the duration of exposure, and could carry 
Cr(VI) from regulated areas to other areas of the workplace. In 
addition, contamination of personal clothing could result in Cr(VI) 
being carried to employees' cars and homes, increasing the worker's 
exposure as well as exposing other individuals to Cr(VI) hazards.
    Contaminated protective clothing and equipment must be removed at 
the end of the work shift or at the completion of tasks involving 
Cr(VI) exposure, whichever comes first. This language is intended to 
convey that protective clothing contaminated with Cr(VI) must generally 
not be worn when tasks involving Cr(VI) exposure have been completed 
for the day. For example, if employees perform work tasks involving 
Cr(VI) exposure for the first two hours of a work shift, and then 
perform tasks that do not involve Cr(VI) exposure, they must remove 
their protective clothing after the exposure period to avoid the 
possibility of increasing the duration of exposure and contamination of 
the work area from Cr(VI) residues on the protective clothing. If, 
however, employees are performing tasks involving Cr(VI) exposure 
intermittently throughout the day, or if employees are exposed to other 
contaminants where their protective clothing and equipment is needed, 
this provision does not prevent them from wearing the clothing and 
equipment until the completion of their shift.
    To limit exposures outside the workplace, OSHA proposes that the 
employer ensure that Cr(VI)-contaminated protective clothing and 
equipment be removed from the workplace only by those employees whose 
job it is to launder, clean, maintain, or dispose of such clothing or 
equipment. Furthermore, the proposed standard would require that 
clothing and equipment that is to be laundered, cleaned, maintained, or 
disposed of be placed in closed, impermeable containers. This provision 
is intended to assure that contamination of the change room is 
minimized and that employees who later handle these items are 
protected. Those cleaning the Cr(VI)-contaminated clothing and 
equipment will be further protected by the requirement that warning 
labels be placed on containers to inform them of the potential hazards 
of exposure to Cr(VI).
    The proposed standard requires that the employer clean, launder, 
repair and replace protective clothing as needed to ensure that the 
effectiveness of the clothing and equipment is maintained. This 
provision is necessary to ensure that clothing and equipment continue 
to serve their intended purpose of protecting workers. This would also 
prevent unnecessary exposures outside the workplace from employees 
taking contaminated clothing and equipment home for cleaning.
    In keeping with the performance-orientation of the proposed rule, 
OSHA does not specify how often clothing and equipment should be 
cleaned, repaired or replaced. The Agency believes that appropriate 
time intervals may vary widely based on the types of clothing and 
equipment used, Cr(VI) exposures, and other circumstances in the 
workplace. The obligation of the employer, as always, is to keep the 
clothing and equipment in the condition necessary to perform its 
protective functions.
    Removal of Cr(VI) from protective clothing and equipment by 
blowing, shaking, or any other means which disperses Cr(VI) in the air 
would be prohibited. Such actions would result in unnecessary exposure 
to airborne Cr(VI) as well as possible dermal contact.
    The proposal would require that the employer inform any person who 
launders or cleans protective clothing or equipment contaminated with 
Cr(VI) of the potentially harmful effects of exposure to Cr(VI), and 
the need to launder or clean contaminated clothing and equipment in a 
manner that effectively prevents skin or eye contact with Cr(VI) or the 
release of airborne Cr(VI) in excess of the PEL. This provision is 
intended to ensure that persons who clean or launder Cr(VI)-
contaminated items are aware of the associated hazards, and can then 
take appropriate protective measures.
    The proposed standard would require employers to provide protective 
clothing and equipment at no cost to employees. The Agency believes 
that the employer is generally in the best position to select and 
obtain the proper type of protective clothing and equipment. OSHA also 
believes that by providing and owning protective clothing and 
equipment, the employer will be in a better position to maintain 
control over the inventory of protective clothing and equipment, 
conduct periodic inspections, and, when necessary, repair or replace it 
to maintain its effectiveness. The protective clothing and equipment at 
issue is designed and intended for work use. As discussed above, 
employees must remove contaminated clothing and equipment at the end of 
the work shift or the completion of tasks involving Cr(VI) exposure, 
whichever comes first. Employees may not remove contaminated clothing 
and equipment from the worksite, except for the employees whose job it 
is to launder, clean, maintain, or dispose of such clothing or 
equipment. The employer is responsible for cleaning or disposing of the 
protective clothing and equipment and retains complete control over it. 
The Agency is seeking comment on the proposed provision, and has 
included this topic in the ``Issues'' section of this preamble.

(i) Hygiene Areas and Practices

    The proposed standard would require employers to provide hygiene 
facilities and to assure employee compliance with basic hygiene 
practices that serve to minimize exposure to Cr(VI). The proposal 
includes requirements for change rooms and washing facilities, ensuring 
that Cr(VI) exposure in eating and drinking areas is minimized, and a 
prohibition on certain practices that may contribute to Cr(VI) 
exposure. OSHA believes that strict compliance with these provisions 
would substantially reduce employee exposure to Cr(VI).
    Several of these provisions are presently required under other OSHA 
standards. For example, OSHA's current standard addressing sanitation 
in general industry (29 CFR 1910.141) requires that whenever employees 
are required by a particular standard to wear protective clothing 
because of the possibility of contamination with toxic materials, 
change rooms equipped with storage facilities for street clothes and 
separate storage facilities for protective clothing shall be provided. 
The sanitation standard also includes

[[Page 59457]]

provisions for washing facilities, and prohibits storage or consumption 
of food or beverages in any area exposed to a toxic material. Similar 
provisions are in place for construction (29 CFR 1926.51). The hygiene 
provisions of this paragraph are intended to augment the requirements 
established under other standards with additional provisions applicable 
specifically to Cr(VI) exposure.
    In workplaces where employees must change their clothes to use 
protective clothing and equipment, OSHA believes it is essential to 
have change rooms with separate storage facilities for street and work 
clothing to prevent contamination of employees' street clothes. This 
provision will minimize employee exposure to Cr(VI) after the work 
shift ends, because it reduces the duration of time they may be exposed 
to contaminated work clothes. Potential exposure resulting from 
contamination of the homes or cars of employees is also avoided. Change 
rooms also provide employees with privacy while changing their clothes. 
OSHA intends the proposed requirement for change rooms to apply to all 
covered workplaces where employees must change their clothes (i.e., 
take off their street clothes) to use protective clothing and 
equipment. In those situations where removal of street clothes would 
not be necessary (e.g., in a workplace where only gloves are used as 
protective clothing), change rooms would not be required.
    Paragraph (i)(3) (paragraph (g)(3) of the proposals for 
construction and shipyards) contains proposed requirements for washing 
facilities. The employer is to provide readily accessible washing 
facilities capable of removing Cr(VI) from the skin and is to ensure 
that affected employees use these facilities when necessary. Also, the 
employer is to ensure that employees who have skin contact with Cr(VI) 
wash their hands and faces at the end of the work shift and prior to 
eating, drinking, smoking, chewing tobacco or gum, applying cosmetics, 
or using the toilet.
    Washing reduces exposure by diminishing the period of time that 
Cr(VI) is in contact with the skin. Although engineering and work 
practice controls and protective clothing and equipment are designed to 
prevent hazardous skin and eye contact from occurring, OSHA realizes 
that in some circumstances these exposures will occur. For example, a 
worker who wears gloves to protect against hand contact with Cr(VI) may 
inadvertently touch his face with the contaminated glove during the 
course of the day. The intent of this provision is to have employees 
wash in order to mitigate the adverse effects when skin and eye contact 
does occur. At a minimum, employees are to wash their hands and faces 
at the end of the shift because washing is needed to remove any 
residual Cr(VI) contamination. Likewise, washing prior to eating, 
drinking, smoking, chewing tobacco or gum, applying cosmetics or using 
the toilet also protects against further Cr(VI) exposure.
    OSHA has made a preliminary determination that washing facilities 
would be sufficient to allow employees to remove significant levels of 
Cr(VI) contamination that may occur under the proposed standard. A 
requirement for provision and use of showers has not been included in 
the proposal. Some other health standards, such as the standards for 
cadmium (29 CFR 1910.1027) and lead (29 CFR 1910.1025), have included 
requirements for showers. OSHA requests information and comment as to 
whether provisions for showers should be included in a final Cr(VI) 
standard, and has included this topic in the ``Issues'' section of this 
preamble.
    To minimize the possibility of food contamination and to reduce the 
likelihood of additional exposure to Cr(VI) through inhalation or 
ingestion, OSHA believes it is imperative that employees have a clean 
place to eat. Where the employer chooses to allow employees to eat at 
the facility, the proposal would require the employer to ensure that 
eating and drinking areas and surfaces are maintained as free as 
practicable of Cr(VI). Employers would also be required to assure that 
employees do not enter eating or drinking areas wearing protective 
clothing, unless properly cleaned beforehand. This is to further 
minimize the possibility of contamination and reduce the likelihood of 
additional Cr(VI) exposure from contaminated food or beverages. 
Employers are given discretion to choose any method for removing 
surface Cr(VI) from clothing and equipment that does not disperse the 
dust into the air or onto the employee's body. For example, if a worker 
is wearing coveralls for protection against Cr(VI) exposure, thorough 
HEPA vacuuming of the coveralls could be performed prior to entry into 
a lunchroom.
    The employer is not required to provide eating and drinking 
facilities to employees. Employees may consume food or beverages off 
the worksite. However, where the employer chooses to allow employees to 
consume food or beverages at a worksite where Cr(VI) is present, OSHA 
intends to ensure that employees are protected from Cr(VI) exposures in 
these areas.
    Proposed paragraph (i)(5) (paragraph (g)(5) in the construction and 
shipyard proposals) specifies certain activities that would be 
prohibited. These activities would include eating, drinking, smoking, 
chewing tobacco or gum, or applying cosmetics in regulated areas, or in 
areas where skin or eye contact occurs. Products associated with these 
activities, such as food and beverages, could not be carried or stored 
in these areas. This provision is intended to protect employees from 
additional sources of exposure to Cr(VI). Because the construction and 
shipyard proposals do not include requirements for regulated areas, 
reference to regulated areas is omitted in the proposed regulatory text 
for these standards.

(j) Housekeeping

    The proposed standard includes housekeeping provisions that would 
require the employer to maintain surfaces as free as practicable of 
Cr(VI), promptly clean Cr(VI) spills and leaks, use appropriate 
cleaning methods, and properly dispose of Cr(VI)-contaminated waste. 
These provisions are exceptionally important because they minimize 
additional sources of exposure that engineering controls generally are 
not designed to address. Good housekeeping is a cost effective way to 
control employee exposures by removing accumulated Cr(VI) that can 
become entrained by physical disturbances or air currents and carried 
into an employee's breathing zone, thereby increasing employee 
exposure. Contact with contaminated surfaces may also result in dermal 
exposure to Cr(VI). The proposed provisions are consistent with 
housekeeping requirements in other OSHA standards, such as those for 
cadmium (29 CFR 1910.1027) and lead (29 CFR 1910.1025).
    Cr(VI) deposited on ledges, equipment, floors, and other surfaces 
should be removed as soon as practicable, to prevent it from becoming 
airborne and to minimize the likelihood that skin contact will occur. 
When Cr(VI) is released into the workplace as a result of a leak or 
spill, the proposal would require the employer to promptly clean up the 
spill. Measures for clean-up of liquids should provide for the rapid 
containment of the leak or spill to minimize potential exposures. 
Clean-up procedures for dusts must not disperse the dust into the 
workplace air. These work practices aid in minimizing the number of 
employees exposed, as well as the extent of any potential Cr(VI) 
exposure.

[[Page 59458]]

    The proposed standard would require that, where possible, surfaces 
contaminated with Cr(VI) be cleaned by vacuuming or other methods that 
minimize the likelihood of Cr(VI) exposure. OSHA believes vacuuming to 
be the most reliable method of cleaning surfaces on which dust 
accumulates, but equally effective methods may be used. Shoveling, dry 
or wet sweeping, and brushing would be permitted only if the employer 
shows that vacuuming or other methods that are usually as efficient as 
vacuuming are not effective under the particular circumstances found in 
the workplace. The proposal would also require that vacuum cleaners be 
equipped with HEPA filters to prevent the dispersal of Cr(VI) into the 
workplace. The use of compressed air for cleaning would only be allowed 
when used in conjunction with a ventilation system designed to capture 
the dust cloud created by the compressed air. This provision is also 
intended to prevent the dispersal of Cr(VI) into the workplace.
    Cleaning equipment is to be handled in a manner that minimizes the 
reentry of Cr(VI) into the workplace. For example, cleaning and 
maintenance of HEPA-filtered vacuum equipment should be done carefully 
to avoid exposures to Cr(VI). Filters need to be changed and the 
contents of bags disposed of properly to avoid unnecessary Cr(VI) 
exposures.
    The proposal would also require that items contaminated with Cr(VI) 
and consigned for disposal be collected and disposed of in sealed 
impermeable bags or other closed impermeable containers. These 
containers would include warning labels to inform individuals who 
handle these items of the potential hazards. By alerting employers and 
employees who are involved in disposal to the potential hazards of 
Cr(VI) exposure, they will be better able to implement protective 
measures.
    No housekeeping provision has been included in the proposals 
covering construction or shipyards. OSHA has made a preliminary 
determination that a specific housekeeping provision is not appropriate 
because of the difficulties of performing housekeeping related to 
Cr(VI) exposure in the construction and shipyard environments. For 
example, in shipyard and particularly in construction work environments 
the generally dusty nature of outdoor work settings is likely to make 
it difficult to distinguish Cr(VI)--contaminated dusts from other dirt 
and dusts commonly found at the work site. The same control measures 
that apply to general industry are likely to be more difficult to 
implement and burdensome in these environments.
    This preliminary determination differs from OSHA's determination in 
the standards for lead in construction (29 CFR 1926.62) and cadmium in 
construction (29 CFR 1926.1127), where the Agency included housekeeping 
provisions. In these rulemakings, OSHA did not find housekeeping 
provisions to present the difficulties anticipated with Cr(VI). The 
Agency believes that Cr(VI)-contaminated dusts will not generally be as 
easily identified as lead- or cadmium-contaminated dusts. Welding, in 
particular, could result in deposition of minute quantities of Cr(VI) 
that would be difficult for a construction or shipyard employer to 
identify. OSHA seeks comment on this preliminary finding, and has 
included this topic in the ``Issues'' section of this preamble.
    Construction and shipyard employers would still need to comply with 
the general housekeeping requirements found at 29 CFR 1926.25 (for 
construction) or 29 CFR 1915.91 (for shipyards). These standards 
include general provisions for keeping workplaces clear of debris, but 
do not contain the more specific requirements found in the proposed 
Cr(VI) standard for general industry (such as those addressing cleaning 
methods) that are designed to limit Cr(VI) contamination of the 
workplace.

(k) Medical Surveillance

    OSHA proposes to require that each employer covered by this rule 
make medical surveillance available at no cost, and at a reasonable 
time and place, for all employees who are experiencing signs or 
symptoms of the adverse health effects associated with Cr(VI) exposure, 
or who are exposed in an emergency. In addition, general industry 
employers would be required to provide medical surveillance for all 
employees exposed to Cr(VI) at or above the PEL for 30 or more days a 
year. The required medical surveillance must be performed by or under 
the supervision of a physician or other licensed health care 
professional.
    The purpose of medical surveillance for Cr(VI) is, where reasonably 
possible, to determine if an individual can be exposed to the Cr(VI) 
present in his or her workplace without experiencing adverse health 
effects; to identify Cr(VI)-related adverse health effects so that 
appropriate intervention measures can be taken; and to determine the 
employee's fitness to use personal protective equipment such as 
respirators. The proposal is consistent with Section 6(b)(7) of the OSH 
Act which requires that, where appropriate, medical surveillance 
programs be included in OSHA health standards to aid in determining 
whether the health of workers is adversely affected by exposure to 
toxic substances. Other OSHA health standards have also included 
medical surveillance requirements.
    The proposed standard is intended to encourage participation by 
requiring that medical examinations be provided by the employer without 
cost to employees (also required by section 6(b)(7) of the Act), and at 
a reasonable time and place. If participation requires travel away from 
the worksite, the employer would be required to bear the cost. 
Employees would have to be paid for time spent taking medical 
examinations, including travel time. OSHA is proposing that medical 
surveillance be provided to employees in general industry exposed at or 
above the PEL for 30 or more days a year in order to focus on those 
workers at greatest risk. Employees exposed below the PEL, or exposed 
for only a few days in a year, will be at lower risk of developing 
Cr(VI)-related disease. OSHA believes that these cutoffs, based both on 
exposure level and on the number of days an employee is exposed to 
Cr(VI), are a reasonable and administratively convenient basis for 
providing medical surveillance benefits to Cr(VI)-exposed workers. In 
past health standards, OSHA has used 30 days above the action level for 
triggering medical surveillance. Because of the large reduction in the 
PEL down to 1 [mu]g/m<SUP>3</SUP> OSHA believes that 30 days above the 
PEL may be more reasonable since exposures above the PEL are more 
likely to result in adverse health effects that might benefit from 
medical surveillance. OSHA is seeking comment on the appropriateness of 
this trigger for medical surveillance, and whether the Agency should 
consider a trigger at the action level or an alternative trigger.
    OSHA has not included exposure above the PEL for 30 or more days 
per year as a trigger for medical surveillance in the construction or 
shipyard Cr(VI) proposals. As discussed earlier, OSHA has not proposed 
to require exposure monitoring for construction or shipyard employment 
because of the difficulties in conducting such monitoring in these work 
settings. While OSHA assumes that some monitoring will be conducted in 
order for employers to know when or if they are above the PEL, OSHA 
also assumes that certain employers will not conduct exposure 
monitoring and may choose to presume that certain work processes or 
practices are above the PEL or rely on historical or objective data to 
show exposure levels. However, if medical surveillance for individual

[[Page 59459]]

employees is triggered by exposures above the PEL for 30 days or more, 
these employers would be forced to do monitoring in order to determine 
which employees are exposed above the PEL for 30 days or more. This 
would have the effect of re-introducing an exposure monitoring burden 
that the Agency is attempting to relieve.
    Some employees may exhibit signs and symptoms of the adverse health 
effects associated with Cr(VI) exposure even when not exposed above the 
PEL for 30 or more days per year. These employees could be especially 
sensitive, may have been unknowingly exposed, or may have been exposed 
to greater amounts than the exposure assessment suggests. OSHA has 
therefore proposed that employees who experience signs or symptoms of 
the adverse health effects associated with Cr(VI) exposure be subject 
to medical surveillance. Signs and symptoms that may warrant 
surveillance include dermatitis, chrome holes, and nasal septum ulcers 
or perforations. Thus, the proposal would protect all employees exposed 
to Cr(VI) in unusual circumstances even if they fall outside the 
criteria for routine medical surveillance.
    Appropriate surveillance would be required to be made available for 
employees exposed in an emergency regardless of the airborne 
concentrations of Cr(VI) normally found in the workplace. Emergency 
situations involve uncontrolled releases of Cr(VI), and the significant 
exposures that occur in these situations justify a requirement for 
medical surveillance. The proposed requirement for medical examinations 
after exposure in an emergency is consistent with the provisions of 
several other OSHA health standards, including the standards for 
methylenedianiline (29 CFR 1910.1050), butadiene (29 CFR 1910.1051), 
and methylene chloride (29 CFR 1910.1052).
    OSHA has made a preliminary determination not to include eye or 
skin contact as a basis for medical surveillance. OSHA believes that 
compliance with the proposed provisions for protective work clothing 
and equipment, hygiene areas and practices, and other protective 
measures will minimize the potential for adverse eye and skin effects. 
When such health effects occur, OSHA believes that trained employees 
will be able to detect these conditions, report them to their employer, 
and obtain medical assistance. In such situations, affected employees 
would be provided medical surveillance on the basis that they are 
experiencing signs or symptoms of Cr(VI)-related health effects.
    OSHA has proposed that the medical examinations provided under the 
rule be performed by or under the supervision of a physician or other 
licensed health care professional (PLHCP). The Agency considers it 
appropriate to allow any professional to perform medical examinations 
and procedures provided under the standard when they are licensed by 
state law to do so. This provision provides flexibility to the 
employer, and would reduce cost and compliance burdens. The proposed 
requirement is consistent with the approach of other recent OSHA 
standards, such as those for methylene chloride (29 CFR 1910.1052), 
bloodborne pathogens (29 CFR 1910.1030), and respiratory protection (29 
CFR 1910.134).
    The proposed standard also specifies how frequently medical 
examinations are to be offered to those employees covered by the 
medical surveillance program. Employers would be required to provide 
all covered employees with medical examinations whenever an employee 
shows signs or symptoms of Cr(VI) exposure; within 30 days after an 
emergency resulting in an uncontrolled release of Cr(VI); and within 30 
days after a PLHCP's written medical opinion recommends an additional 
examination. In addition, employers in general industry would be 
required to provide covered employees with examinations within 30 days 
after initial assignment unless the employee has received a medical 
examination provided in accordance with the standard within the past 12 
months; annually; and at the termination of employment, unless an 
examination has been given less than six months prior to the date of 
termination.
    Signs or symptoms may indicate that adverse health effects 
attributable to Cr(VI) exposure are occurring. In such situations OSHA 
believes it would be appropriate to evaluate the employee's condition 
to determine if exposure to Cr(VI) is the cause of the condition, and 
to determine if protective measures are necessary. Emergency situations 
may involve high or unknown exposures, and OSHA believes that a medical 
examination is necessary to evaluate the possible adverse effects of 
these exposures.
    In addition to medical evaluations after exposures in an emergency 
or when signs or symptoms occur, OSHA is proposing that additional 
examinations be offered following a PLHCP's recommendation that 
additional exams are necessary. A PLHCP may recommend additional 
evaluations in order to follow developments in a worker's condition, or 
to allow for specialized evaluation. For example, if nasal ulceration 
is identified in a Cr(VI)-exposed worker, a PLHCP may recommend follow-
up examinations to ensure that treatment and workplace interventions 
are successful in addressing the condition, or a worker who exhibits 
dermatitis may be referred to a dermatologist for testing to determine 
if they are sensitized to Cr(VI).
    The proposed requirement for general industry that a medical 
examination be offered at the time of initial assignment is intended to 
achieve the objective of determining if an individual will be able to 
work in the job involving Cr(VI) exposure without adverse effects. It 
also serves the useful function of establishing a health baseline for 
future reference. Where an examination that complies with the 
requirements of the standard has been provided in the past 12 months, 
that previous examination would serve these purposes, and an additional 
examination would not be needed.
    OSHA believes that the provision of medical surveillance on an 
annual basis in general industry is an appropriate frequency for 
screening employees for Cr(VI)-related diseases. The main goal of 
periodic medical surveillance for workers is to detect adverse health 
effects at an early and potentially reversible stage. The proposed 
requirement for annual examinations is consistent with other OSHA 
health standards, including those for cadmium (29 CFR 1910.1027), 
formaldehyde (29 CFR 1910.1048), and methylene chloride (29 CFR 
1910.1052). Based on the Agency's experience, OSHA believes that annual 
surveillance would strike a reasonable balance between the need to 
diagnose health effects at an early stage, and the limited number of 
cases likely to be identified through surveillance. The proposed 
requirement for general industry that the employer offer a medical 
examination at the termination of employment is intended to assure that 
no employee terminates employment while carrying an active, but 
undiagnosed, disease.
    The examination to be provided by the PLHCP is to consist of a 
medical and work history; a physical examination of the skin and 
respiratory tract; and any additional tests considered appropriate by 
the PLHCP. Special emphasis is placed on the portions of the medical 
and work history focusing on Cr(VI) exposure, health effects associated 
with Cr(VI) exposure, and smoking. The physical exam focuses on organs 
and systems known to be susceptible to Cr(VI) toxicity. The information 
obtained will allow the PLHCP to assess

[[Page 59460]]

the employee's health status, identify adverse health effects related 
to Cr(VI) exposures, and determine if limitations should be placed on 
the employee's exposure to Cr(VI).
    The proposal does not indicate specific tests that must be included 
in the medical examination. OSHA does not believe that any particular 
tests are generally applicable to all employees covered by the medical 
surveillance requirements, and the Agency proposes to give the 
examining PLHCP the flexibility to determine any appropriate tests to 
be selected for a given employee. For example, tests for dermal 
sensitization exist, but they are not recommended as a screening tool 
because they are capable of sensitizing persons who had not been 
affected previously. These tests should be considered by the PLHCP if a 
medical history indicating probable sensitization exists or if the 
employee experiences signs or symptoms indicative of sensitization. 
Radiological examinations and pulmonary function tests may also be 
useful in evaluating possible effects of Cr(VI). OSHA believes that the 
PLHCP is in the best position to decide which medical tests are 
necessary for each individual examined. Where specific tests are deemed 
appropriate by the PLHCP, the proposed standard would require that they 
be provided.
    OSHA is aware that certain methods are available for evaluating 
Cr(VI) exposures based on analysis of chromium in urine or blood. 
However, the Agency is not aware of evidence indicating that these 
methods adequately characterize Cr(VI) exposures in most occupational 
environments. OSHA has also found no medical justification for routine 
urine or blood analysis for the detection of Cr(VI)-related health 
effects. Therefore, no requirement for such analysis is proposed.
    The proposed standard would require the employer to ensure the 
PLHCP has a copy of the standard, and to provide the following 
information: a description of the affected employee's former and 
current duties as they relate to Cr(VI) exposure; the employee's 
former, current, and anticipated exposure level; a description of any 
personal protective equipment used or to be used by the employee, 
including when and for how long the employee has used that equipment; 
and information from records of employment-related medical examinations 
previously provided to the affected employee, currently within the 
control of the employer. Making this information available to the PLHCP 
will aid in the evaluation of the employee's health in relation to 
assigned duties and fitness to use personal protective equipment, when 
necessary.
    The results of exposure monitoring are part of the information that 
would be supplied to the PLHCP responsible for medical surveillance. 
These results contribute valuable information to assist the PLHCP in 
determining if an employee is likely to be at risk of harmful effects 
from Cr(VI) exposure. A well-documented exposure history would also 
assist the PLHCP in determining if a condition (e.g., dermatitis) may 
be related to Cr(VI) exposure.
    The proposed rule would require employers to obtain from the 
examining PLHCP a written opinion containing the results of the medical 
examination with regard to Cr(VI) exposure, the PLHCP's opinion as to 
whether the employee would be placed at increased risk of material 
health impairment as a result of exposure to Cr(VI), and any 
recommended limitations on the employee's exposure or use of personal 
protective equipment. The PLHCP would also need to state in the written 
opinion that these findings were explained to the employee. The purpose 
of requiring the PLHCP to supply a written opinion to the employer is 
to provide the employer with a medical basis to aid in the 
determination of placement of employees and to assess the employee's 
ability to use protective clothing and equipment. The employer must 
obtain the written opinion within 30 days of the examination; OSHA 
believes this will provide the PLHCP sufficient time to receive and 
consider the results of any tests included in the examination, and 
allow the employer to take any necessary protective measures in a 
timely manner. The proposed requirement that the opinion be in written 
form is intended to ensure that employers and employees have the 
benefit of this information.
    The PLHCP would not be allowed to include findings or diagnoses 
which are unrelated to Cr(VI) exposure in the written opinion provided 
to the employer. OSHA has proposed this provision to reassure employees 
participating in medical surveillance that they will not be penalized 
or embarrassed by the employer's obtaining information about them not 
directly pertinent to Cr(VI) exposure. The employee would be informed 
directly by the PLHCP of all results of his or her medical examination, 
including conditions of non-occupational origin. The employer would 
also be required to provide a copy of the PLHCP's written opinion to 
the employee within two weeks after receiving it, to ensure that the 
employee has been informed of the result of the examination in a timely 
manner.
    In some OSHA health standards, a provision for medical removal 
protection (MRP) has been included. MRP typically requires that the 
employer temporarily remove an employee from exposure when such an 
action is recommended in a written medical opinion. During the time of 
removal, the employer is required to maintain the total normal 
earnings, as well as all other employee rights and benefits. However, 
MRP is not intended to serve as a worker's compensation system. The 
primary reason MRP has been included in these previous standards has 
been to encourage employee participation in medical surveillance. By 
protecting employees who are removed on a temporary basis from economic 
loss, this potential disincentive to participating in medical 
surveillance is alleviated.
    The proposed rule does not include a provision for MRP, because 
OSHA has made a preliminary determination that MRP is not reasonably 
necessary or appropriate for Cr(VI)-related health effects. The Agency 
believes that Cr(VI)-related health effects generally fall into one of 
two categories: Either they are chronic conditions that temporary 
removal from exposure will not remedy (e.g., lung cancer, respiratory 
or dermal sensitization), or they are conditions that can be addressed 
through proper application of control measures and do not require 
removal from exposure (e.g., irritant dermatitis). Since situations 
where temporary removal would be appropriate are not anticipated to 
occur, OSHA does not believe that MRP is necessary. The Agency seeks 
comment on this preliminary determination, and has included this topic 
in the ``Issues'' section of this preamble.

(1) Communication of Hazards to Employees

    The proposed standard includes requirements intended to ensure that 
the dangers of Cr(VI) exposure are communicated to employees by means 
of signs, labels, and employee information and training. These proposed 
requirements would parallel the existing requirements of OSHA's Hazard 
Communication standard (29 CFR 1910.1200). The hazard communication 
requirements of the proposed rule are designed to be substantively as 
consistent as possible with the Hazard Communication standard, while 
including additional specific requirements needed to protect employees 
exposed to Cr(VI).
    The proposed standard would require that all approaches to 
regulated areas be

[[Page 59461]]

posted with legible and readily visible warning signs stating: Danger; 
Chromium (VI); Cancer Hazard; Can Damage Skin, Eyes, Nasal Passages, 
and Lungs; Authorized Personnel Only; Respirators Required in this 
Area. Such warning signs would be required wherever a regulated area 
exists, that is, wherever the PEL is exceeded in general industry. 
Because the construction and shipyard proposals do not include 
requirements for regulated areas, no provision is included for warning 
signs in the proposed regulatory text for the construction and shipyard 
standards.
    The signs are intended to serve as a warning to employees who 
otherwise may not be aware that they are entering a regulated area, and 
to remind employees of the hazards of Cr(VI) so that they take 
necessary protective steps before entering the area. These signs are 
intended to supplement the training that employees receive regarding 
the hazards of Cr(VI), since even trained employees need to be reminded 
of the locations of regulated areas and of the precautions necessary 
before entering these dangerous areas.
    In some instances, regulated areas are permanent, because the 
employer is unable to reduce Cr(VI) exposures in that area below the 
PEL with engineering controls. In those cases, the signs serve to warn 
employees not to enter the area unless they are authorized and are 
wearing respirators. In other cases, such as emergency situations and 
maintenance operations, regulated areas may be established temporarily. 
The use of warning signs is particularly important in these situations 
to make employees who are regularly scheduled to work at these sites 
aware of the hazards. Access is limited to authorized personnel to 
ensure that those entering the area are adequately trained and 
equipped, and to limit exposure to only those whose presence is 
absolutely necessary.
    The proposed standard specifies the wording of the warning signs 
for regulated areas in order to ensure that the proper warning is given 
to employees. OSHA believes that the use of the word ``Danger'' is 
appropriate, based on the evidence of the toxicity and carcinogenicity 
of Cr(VI). ``Danger'' is used to attract the attention of workers in 
order to alert them to the fact that they are entering an area where 
the PEL may be exceeded and to emphasize the importance of the message 
that follows. The use of the word ``Danger'' is also consistent with 
other OSHA health standards dealing with carcinogens such as cadmium 
(29 CFR 1910.1027), methylenedianiline (29 CFR 1910.1050), asbestos (29 
CFR 1910.1001), and benzene (29 CFR 1910.1028).
    The proposed standard would also require that the sign indicate 
that respirators are required in the area. Regulated areas are areas 
demarcated by the employer where the employee's exposure to airborne 
concentrations of chromium (VI) exceeds, or can reasonably be expected 
to exceed the PEL (definition of a regulated area). The employer has 
made the determination that such areas are regulated on the basis of 
his/her own exposure assessments of the employees in the area. Since 
the employer has determined that such areas are not able to be reduced 
below the PEL, respirators are required as a means of control to 
protect the employees in those areas. The sign also serves as a means 
to warn other employees not in the regulated area not to enter, or if 
those other employees enter the area, they need to protect themselves 
in situations where excessive exposures can occur.
    The proposal would require that warning labels be affixed to all 
bags or containers of contaminated clothing and equipment that are to 
be removed from the workplace for laundering, cleaning, or maintenance. 
Containers of waste, scrap, debris, and any other materials 
contaminated with Cr(VI) that are consigned for disposal would also 
need to be labeled. The labels must state: Danger; Contains Chromium 
(VI); Cancer Hazard; Can Damage Skin, Eyes, Nasal Passages, and Lungs. 
The purpose of this requirement is to ensure that all affected 
employees, not only those of a particular employer, are apprised of the 
hazardous nature of Cr(VI) exposure. These proposed requirements are 
consistent with the mandate of Section (6)(b)(7) of the OSH Act, which 
requires that OSHA health standards prescribe the use of labels or 
other appropriate forms of warning to apprise employees of the hazards 
to which they are exposed. Because the construction and shipyard 
proposals do not include disposal requirements, no provision is 
included in the construction and shipyard proposals for placing warning 
labels on containers of waste, scrap, debris, and other materials 
contaminated with Cr(VI).
    Information and training is essential to inform employees of the 
hazards to which they are exposed and to provide employees with the 
necessary understanding of the degree to which they themselves can 
minimize potential health hazards. As part of an overall hazard 
communication program, training serves to explain and reinforce the 
information presented on labels and in material safety data sheets. 
These written forms of communication will be successful and relevant 
only when employees understand the information presented and are aware 
of the actions to be taken to avoid or minimize exposures, thereby 
reducing the possibility of experiencing adverse health effects.
    OSHA proposes that employers provide training for all employees who 
are exposed to airborne Cr(VI) or who have skin or eye contact with 
Cr(VI), ensure that employees participate in the training, and maintain 
a record of the training provided. Training would be provided to all 
employees exposed to Cr(VI), and would not be limited to only those 
exposed above the PEL or action level. This proposed requirement is 
consistent with the Hazard Communication standard (29 CFR 1910.1200), 
which requires training for all employees exposed to hazardous 
chemicals and defines this to include potential (e.g., accidental or 
possible) exposure. This training would allow employees to make efforts 
to avoid exposures altogether or mitigate those exposures that do 
occur.
    The employer is to provide initial training prior to or at the time 
of initial assignment to a job involving potential exposure to Cr(VI). 
An employer who is able to demonstrate that a new employee has received 
training within the last 12 months is allowed to use that training for 
purposes of initial training required by the standard, provided the 
previous training has addressed the elements specified in the training 
provisions of the proposal, and the employee is able to demonstrate 
knowledge of those elements. In cases where understanding of some 
elements is lacking or inadequate, the employer would be required to 
provide training only in those elements. This allowance for prior 
training is intended to ensure that employees receive sufficient 
training, without requiring unnecessary repetition of that training.
    The training requirements in this standard are performance-
oriented. The proposed standard lists the subjects that must be 
addressed in training, but not the specific ways that this is to be 
accomplished. Hands-on training, videotapes, slide presentations, 
classroom instruction, informal discussions during safety meetings, 
written materials, or any combination of these methods may be 
appropriate. Such performance-oriented requirements are intended to 
encourage employers to tailor training to the needs of their 
workplaces, thereby resulting in the most effective training program in 
each specific workplace.

[[Page 59462]]

    OSHA believes that the employer is in the best position to 
determine how the training can most effectively be accomplished. The 
Agency has therefore laid out the objectives to be met to ensure that 
employees are made aware of the hazards associated with Cr(VI) in their 
workplace and how they can help to protect themselves. The specifics 
regarding how this is to be achieved are left up to the employer.
    In order for the training to be effective, the employer must ensure 
that it is provided in a manner that the employee is able to 
understand. Employees have varying educational levels, literacy, and 
language skills, and the training must be presented in a language and 
at a level of understanding that accounts for these differences in 
order to meet the proposed requirement that individuals being trained 
understand the specified elements. This may mean, for example, 
providing materials, instruction, or assistance in Spanish rather than 
English if the workers being trained are Spanish-speaking and do not 
understand English. The employer would not be required to provide 
training in the employee's preferred language if the employee 
understood both languages; as long as the employee is able to 
understand the language used, the intent of the proposed standard would 
be met.
    In order to ensure that employees comprehend the material presented 
during training, it is critical that trainees have the opportunity to 
ask questions and receive answers if they do not fully understand the 
material that is presented to them. When videotape presentations or 
computer-based programs are used, this requirement may be met by having 
a qualified trainer available to address questions after the 
presentation, or providing a telephone hotline so that trainees will 
have direct access to a qualified trainer.
    Under the proposal, the employer would be required to ensure that 
each employee can demonstrate knowledge of the specified elements. This 
could be determined through methods such as discussion of the required 
training subjects, written tests, or oral quizzes.
    The frequency of training under the proposed standard would be 
determined by the needs of the workplace. Individuals would need to be 
trained sufficiently to understand the specified elements. Additional 
training is needed periodically to refresh and reinforce the memories 
of individuals who have previously been trained, and to ensure that 
these individuals are informed of new developments in the workplace 
that may result in new or additional exposures to Cr(VI). For example, 
training after new control measures are implemented would generally be 
necessary in order to ensure that employees are able to properly use 
the new controls that are introduced. Employees would likely be 
unfamiliar with new work practices undertaken, with the operation of 
new engineering controls, or the use of new personal protective 
equipment; training would rectify this lack of understanding. 
Additional training would ensure that employees are able to actively 
participate in protecting themselves under the conditions found in the 
workplace, even if those conditions change.

(m) Recordkeeping

    The proposed standard for general industry would require employers 
to maintain exposure monitoring, medical surveillance, and training 
records. Because the proposed construction and shipyard standards do 
not include requirements for exposure monitoring, no provision for 
retention of exposure monitoring records is included in the proposed 
regulatory texts for construction and shipyards. However, the record 
retention requirements of OSHA's standard on access to medical and 
exposure records (29 CFR 1910.1020) apply to any exposure records that 
construction and shipyard employers produce.
    The recordkeeping requirements are proposed in accordance with 
section 8(c) of the OSH Act, which authorizes OSHA to require employers 
to keep and make available records as necessary or appropriate for the 
enforcement of the Act or for developing information regarding the 
causes and prevention of occupational injuries and illnesses. The 
proposed recordkeeping provisions are also consistent with the OSHA's 
standard addressing access to employee exposure and medical records (29 
CFR 1910.1020).
    The proposal would require that records be kept of environmental 
monitoring results that identify the monitored employee and accurately 
reflect the employee's exposure. The employer would be required to keep 
records for each exposure measurement taken. Specifically, records must 
include the following information: The date of measurement for each 
sample taken; the operation involving exposure to Cr(VI) that was 
monitored; sampling and analytical methods used and evidence of their 
accuracy; the number, duration, and results of samples taken; the type 
of personal protective equipment used; and the name, social security 
number, and job classification of all employees represented by the 
monitoring, indicating which employees were actually monitored.
    Most of OSHA's substance-specific standards require that exposure 
monitoring and medical surveillance records include the employee's 
social security number. OSHA has included this requirement in the past 
because social security numbers are particularly useful in identifying 
employees, since each number is unique to an individual for a lifetime 
and does not change when an employee changes employers. When employees 
have identical or similar names, identifying employees solely by name 
makes it difficult to determine to which employee a particular record 
pertains. However, based on privacy concerns, OSHA is examining 
alternatives to requiring social security numbers for employee 
identification. In its Standards Improvement Project proposal, the 
Agency requested public comment on the necessity, usefulness, and 
effectiveness of social security numbers as a means of identifying 
employee records, and any privacy concerns or issues raised by this 
requirement, as well as the availability of other effective methods of 
identifying employees for OSHA recordkeeping purposes (67 FR 66493 (19/
31/02)). OSHA intends for the requirements of the Cr(VI) standard to 
conform with any final determination made through the Standards 
Improvement Project.
    The proposal would allow the employer to rely on Cr(VI) monitoring 
results obtained in the past 12 months when the data were obtained 
during operations conducted under workplace conditions closely 
resembling the employer's current operations. Where historical 
monitoring data are used, the proposal would require that records of 
these data be maintained. The records of historical data must 
demonstrate that exposures on a particular job will be below the action 
level by showing that the work being performed, Cr(VI)-containing 
material being handled, and environmental conditions at the time the 
historical data were obtained are the same as those on the job for 
which monitoring was not performed. The records must also demonstrate 
that the data were obtained using a method sufficiently accurate to be 
allowed under the standard. Other data relevant to operations, 
materials, processing, or employee exposures must also be included in 
records.
    A provision allowing the use of objective data in place of initial 
monitoring is included in this proposed standard. Objective data are 
information demonstrating that a particular product or material cannot 
release Cr(VI) in

[[Page 59463]]

concentrations at or above the action level under any expected 
conditions of use, even under conditions of worst-case release. Where 
objective data are used to satisfy initial monitoring requirements, the 
proposal would require employers to establish and maintain accurate 
records of the objective data relied upon. Since the use of objective 
data exempts the employer from requirements for conducting periodic 
monitoring and certain other provisions of the proposal due to the low 
level of potential exposure, it is critical that this determination be 
carefully documented. The record would be required to include 
identification of the Cr(VI)-containing material in question; the 
source of the objective data; the testing protocol and results of 
testing, or analysis of the material for the release of Cr(VI); a 
description of the operation exempted from initial monitoring and how 
the data support the exemption; and any other data relevant to the 
operations, materials, processing or employee exposures covered by the 
exemption.
    Compliance with the requirement to maintain a record of objective 
data protects the employer at later dates from the contention that 
initial monitoring was not conducted in an appropriate manner. The 
record would also be available to employees so that they can examine 
the determination made by the employer. The employer would be required 
to maintain the record for the duration of the employer's reliance upon 
the objective data.
    In addition to records relating to employee exposures to Cr(VI), 
the proposal would require the employer to establish and maintain an 
accurate medical surveillance record for each employee subject to the 
medical surveillance requirements of the standard. OSHA believes that 
medical records, like exposure records, are necessary and appropriate 
both to the enforcement of the standard and to the development of 
information regarding the causes and prevention of occupational 
illnesses. Good medical records, including the record of the 
examination at termination of employment itself, can be useful to the 
Agency and others in enumerating illnesses and deaths attributable to 
Cr(VI), in evaluating compliance programs, and in assessing the 
accuracy of the Agency's risk estimates. Furthermore, medical records 
are necessary for the proper evaluation of the employee's health.
    The medical surveillance records would be required to include the 
following information: The name, social security number, and job 
classification of the employee; a copy of the PLHCP's written opinions; 
and a copy of the information provided to the PLHCP. This information 
includes the employee's duties as they relate to Cr(VI) exposure, 
Cr(VI) exposure levels, and descriptions of personal protective 
equipment used by the employee.
    The employer would be required under the proposal to maintain 
records of employees' Cr(VI)-related training. At the completion of 
training, the employer would be required to prepare a record that 
indicates the identity of the individuals trained and the date the 
training was completed. The record would need to be maintained for 
three years after the completion of training. In addition, the employer 
would need to provide materials relating to employee information and 
training to OSHA or NIOSH, if requested.
    OSHA believes that a three year retention period for training 
records is reasonable. Since OSHA is not proposing specific intervals 
for periodic retraining, but is making retraining contingent upon the 
need to maintain employee understanding of safe use and handling of 
Cr(VI) and workplace changes which result in significant increases in 
employee exposures to Cr(VI), it is appropriate to have records of 
training to allow employers to determine when and how employees have 
been trained. The proposed requirement to provide training materials 
upon request is necessary to allow for evaluation of training programs, 
and is consistent with the other OSHA standards such as those for 
bloodborne pathogens (29 CFR 1910.1030) methylene chloride (29 CFR 
1910.1052), butadiene (29 CFR 1910.1051), and methylenedianiline (29 
CFR 1910.1050).
    All medical and exposure records developed under the Cr(VI) rule 
would be made available to employees and their designated 
representatives in accordance with OSHA's standard on access to records 
(29 CFR 1910.1020). The medical and exposure records standard requires 
that exposure records be kept for at least 30 years and that medical 
records be kept for the duration of employment plus thirty years. It is 
necessary to keep these records for extended periods because of the 
long latency period commonly associated with cancer. Cancer often 
cannot be detected until 20 or more years after first exposure. The 
extended record retention period is therefore needed because diagnosis 
of disease in employees is assisted by, and in some cases can only be 
made by, having present and past exposure data as well as the results 
of present and past medical examinations.

(n) Dates

    OSHA proposes that the final Cr(VI) rule become effective 60 days 
after its publication in the Federal Register. This period is intended 
to allow affected employers the opportunity to familiarize themselves 
with the standard. Employer obligations to comply with most 
requirements of the final rule would begin 90 days after the effective 
date (150 days after publication of the final rule). This is designed 
to allow employers sufficient time to complete initial exposure 
assessments, establish regulated areas, obtain appropriate work 
clothing and equipment, and comply with other provisions of the rule.
    Additional time would be allowed for the employer to establish 
change rooms and to implement engineering controls. Change rooms would 
be required no later than one year after the effective date of the 
standard, and engineering controls would need to be in place within two 
years after the effective date. This is to allow affected employers 
sufficient time to design and construct change rooms (where necessary), 
and to design, obtain, and install the necessary control equipment. 
OSHA solicits comment on the adequacy of these proposed start-up dates. 
In particular, the Agency is aware that in some cases employers may be 
required to reevaluate modified ventilation systems for compliance with 
regulations governing discharges of Cr(VI) to the environment. OSHA 
would like to ensure that employers are provided sufficient time to 
complete this process, and has included this topic in the ``Issues'' 
section of this preamble.

XVIII. Authority and Signature

    This document was prepared under the direction of John L. Henshaw, 
Assistant Secretary of Labor for Occupational Safety and Health, U.S. 
Department of Labor, 200 Constitution Avenue, NW., Washington, DC 
20210.
    The Agency issues the proposed sections under the following 
authorities: Sections 4, 6(b), 8(c), and 8(g) of the Occupational 
Safety and Health Act of 1970 (29 U.S.C. 653, 655, 657); section 107 of 
the Contract Work Hours and Safety Standards Act (the Construction 
Safety Act) (40 U.S.C. 333); section 41, the Longshore and Harbor 
Worker's Compensation Act (33 U.S.C. 941); Secretary of Labor's Order 
No. 5-2002 (67 FR 65008); and 29 CFR Part 1911.

[[Page 59464]]

List of Subjects in 29 CFR Parts 1910, 1915, 1917, 1918, and 1926

    Cancer, Chemicals, Hazardous substances, Health, Occupational 
safety and health, Reporting and recordkeeping requirements.

    Signed at Washington, DC, this 21st day of September, 2004.
John L. Henshaw,
Assistant Secretary of Labor.

XIX. Proposed Standards

    Chapter XVII of Title 29 of the Code of Federal Regulation is 
proposed to be amended as follows:

PART 1910--[AMENDED]

Subpart Z--[Amended]

    1. The authority citation for Subpart Z of Part 1910 is revised to 
read as follows:

    Authority: Secs. 4, 6, 8 of the Occupational Safety and Health 
Act of 1970 (29 U.S.C. 653, 655, 657: Secretary of Labor's Order No. 
12-71 (36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736), 1-90 (55 
FR 9033), 6-96 (62 FR 111), 3-2000 (65 FR 50017), or 5-2002 (67 FR 
65008), as applicable; and 29 CFR part 1911.
    All of subpart Z issued under section 6(b) of the Occupational 
Safety and Health Act, --except those substances that have exposure 
limits listed in Tables Z-1, Z-2, and Z-3 of 29 CFR 1910.1000. The 
latter were issued under Sec. 6(a) (29 U.S.C. 655(a)).
    Section 1910.1000, Tables Z-1, Z-2 and Z-3 also issued under 5 
U.S.C. 553, Section 1910.1000 Tables Z-1, Z-2, and Z-3 not issued 
under 29 CFR part 1911 except for the arsenic (organic compounds), 
benzene, and cotton dust listings.
    Section 1910.1001 also issued under Sec. 107 of the Contract 
Work Hours and Safety Standards Act (40 U.S.C. 3704) and 5 U.S.C. 
553.
    Section 1910.1002 also issued under 5 U.S.C. 553 but not under 
29 U.S.C. 655 or 29 CFR part 1911.
    Sections 1910.1018, 1910.1029 and 1910.1200 also issued under 29 
U.S.C. 653.
    Section 1910.1030 also issued under Pub. L. 106-430, 114 Stat. 
1901.


Sec.  1910.1000  [Amended]

    2. In Sec.  1910.1000, Table Z-2, the entry for Chromic acid and 
chromates 1.0 mg/10 m<SUP>3</SUP> is removed and the following entry 
added in its place:


Sec.  1910.1000  Air contaminants.

* * * * *

                                                    Table Z-2
----------------------------------------------------------------------------------------------------------------
                                                                             Acceptable maximum peak above the
                                                                                acceptable ceiling average
            Substance                 8-hour time     Acceptable ceiling      concentration for an 8-hr shift
                                   weighted average      concentration   ---------------------------------------
                                                                             Concentration     Maximum duration
----------------------------------------------------------------------------------------------------------------
 
                                                  * * * * * * *
Chromium (VI) compounds (as Cr);
 see 1910.1026.
 
                                                  * * * * * * *
----------------------------------------------------------------------------------------------------------------

* * * * *
    3. A new Sec.  1910.1026 is added to read as follows:


Sec.  1910.1026  Chromium (VI).

    (a) Scope. This standard applies to occupational exposures to 
chromium (VI) in all forms and compounds in general industry, except 
exposures that occur in the application of pesticides (e.g., the 
treatment of wood with preservatives).
    (b) Definitions. For the purposes of this section the following 
definitions apply:
    Action level means a concentration of airborne chromium (VI) of 0.5 
microgram per cubic meter of air (0.5 [mu]g/m<SUP>3</SUP>) calculated 
as an 8-hour time-weighted average (TWA).
    Assistant Secretary means the Assistant Secretary of Labor for 
Occupational Safety and Health, U.S. Department of Labor, or designee.
    Chromium (VI) [hexavalent chromium or Cr(VI)] means chromium with a 
valence of positive six, in any form and in any compound.
    Director means the Director of the National Institute for 
Occupational Safety and Health (NIOSH), U.S. Department of Health and 
Human Services, or designee.
    Emergency means any occurrence that results, or is likely to 
result, in an uncontrolled release of chromium (VI). If an incidental 
release of chromium (VI) can be controlled at the time of release by 
employees in the immediate release area, or by maintenance personnel, 
it is not an emergency.
    Employee exposure means the exposure to airborne chromium (VI) that 
would occur if the employee were not using a respirator.
    High-efficiency particulate air [HEPA] filter means a filter that 
is at least 99.97 percent efficient in removing mono-dispersed 
particles of 0.3 micrometers in diameter or larger.
    Physician or other licensed health care professional [PLHCP] is an 
individual whose legally permitted scope of practice (i.e., license, 
registration, or certification) allows him or her to independently 
provide or be delegated the responsibility to provide some or all of 
the particular health care services required by paragraph (k) of this 
section.
    Regulated area means an area, demarcated by the employer, where an 
employee's exposure to airborne concentrations of chromium (VI) 
exceeds, or can reasonably be expected to exceed, the PEL.
    This section means this chromium (VI) standard.
    (c) Permissible exposure limit (PEL). The employer shall ensure 
that no employee is exposed to an airborne concentration of chromium 
(VI) in excess of 1 microgram per cubic meter of air (1 [mu]g/m\3\), 
calculated as an 8-hour time-weighted average (TWA).
    (d) Exposure assessment. (1) General. The employer shall determine 
the 8-hour TWA exposure for each employee on the basis of a sufficient 
number of personal breathing zone air samples to accurately 
characterize full shift exposure on each shift, for each job 
classification, in each work area. Where an employer does 
representative sampling instead of sampling all employees in order to 
meet this requirement, the employer shall sample the employee(s) 
expected to have the highest chromium (VI) exposures.
    (2) Initial exposure monitoring. (i) Except as provided for in 
paragraphs (d)(2)(ii) and (d)(2)(iii) of this section, each employer 
who has a workplace or work operation covered by this section shall 
determine if any employee may be

[[Page 59465]]

exposed to chromium (VI) at or above the action level.
    (ii) Where the employer has monitored for chromium (VI) in the past 
12 months, and the data were obtained during work operations conducted 
under workplace conditions closely resembling the processes, types of 
material, control methods, work practices, and environmental conditions 
used and prevailing in the employer's current operations, and where 
that monitoring satisfies all other requirements of this section, 
including the accuracy and confidence levels of paragraph (d)(6) of 
this section, the employer may rely on such earlier monitoring results 
to satisfy the requirements for initial monitoring.
    (iii) Where the employer has objective data demonstrating that a 
material containing chromium (VI) or a specific process, operation, or 
activity involving chromium (VI) cannot release dust, fumes, or mist of 
chromium (VI) in concentrations at or above the action level under any 
expected conditions of use, the employer may rely upon such data to 
satisfy initial monitoring requirements. The data must reflect 
workplace conditions closely resembling the processes, types of 
material, control methods, work practices, and environmental conditions 
in the employer's current operations.
    (3) Periodic monitoring. (i) If initial monitoring or periodic 
monitoring indicates that employee exposures are below the action 
level, the employer may discontinue monitoring for those employees 
whose exposures are represented by such monitoring.
    (ii) If initial monitoring or periodic monitoring reveals employee 
exposures to be at or above the action level, the employer shall 
perform periodic monitoring at least every six months.
    (iii) If initial monitoring reveals employee exposures to be at or 
above the PEL, the employer shall perform periodic monitoring at least 
every three months.
    (iv) If periodic monitoring indicates that employee exposures are 
below the action level, and the result is confirmed by the result of 
another monitoring taken at least seven days later, the employer may 
discontinue the monitoring for those employees whose exposures are 
represented by such monitoring.
    (4) Additional monitoring. The employer shall perform additional 
monitoring when there has been any change in the production process, 
raw materials, equipment, personnel, work practices, or control methods 
that may result in new or additional exposures to chromium (VI), or 
when the employer has any reason to believe that new or additional 
exposures have occurred.
    (5) Employee notification of monitoring results. (i) Within 15 
working days after the receipt of the results of any monitoring 
performed under this section, the employer shall either notify each 
affected employee individually in writing of the results or shall post 
the results of the exposure monitoring in an appropriate location that 
is accessible to all affected employees.
    (ii) Whenever monitoring results indicate that employee exposure is 
above the PEL, the employer shall describe in the written notification 
the corrective action being taken to reduce employee exposure to or 
below the PEL.
    (6) Accuracy of measurement. The employer shall use a method of 
monitoring and analysis that can measure chromium (VI) to within an 
accuracy of plus or minus 25 percent (+/- 25%) and can produce accurate 
measurements to within a statistical confidence level of 95 percent for 
airborne concentrations at or above the action level.
    (7) Observation of monitoring. (i) The employer shall provide 
affected employees or their designated representatives an opportunity 
to observe any monitoring of employee exposure to chromium (VI).
    (ii) When observation of monitoring requires entry into an area 
where the use of protective clothing or equipment is required, the 
employer shall provide the observer with clothing and equipment and 
shall assure that the observer uses such clothing and equipment and 
complies with all other applicable safety and health procedures.
    (e) Regulated areas. (1) Establishment. The employer shall 
establish a regulated area wherever an employee's exposure to airborne 
concentrations of chromium (VI) is, or can reasonably be expected to 
be, in excess of the PEL.
    (2) Demarcation. The employer shall ensure that regulated areas are 
demarcated from the rest of the workplace in a manner that adequately 
establishes and alerts employees of the boundaries of the regulated 
area, and shall include the warning signs required under paragraph 
(l)(2) of this section.
    (3) Access. The employer shall limit access to regulated areas to:
    (i) Persons authorized by the employer and required by work duties 
to be present in the regulated area;
    (ii) Any person entering such an area as a designated 
representative of employees for the purpose of exercising the right to 
observe monitoring procedures under paragraph (d) of this section; or
    (iii) Any person authorized by the Occupational Safety and Health 
Act or regulations issued under it to be in a regulated area.
    (f) Methods of compliance. (1) Engineering and work practice 
controls. (i) Except as permitted in paragraph (f)(1)(ii) of this 
section, the employer shall use engineering and work practice controls 
to reduce and maintain employee exposure to chromium (VI) to or below 
the PEL unless the employer can demonstrate that such controls are not 
feasible. Wherever feasible engineering and work practice controls are 
not sufficient to reduce employee exposure to or below the PEL, the 
employer shall use them to reduce employee exposure to the lowest 
levels achievable, and shall supplement them by the use of respiratory 
protection that complies with the requirements of paragraph (g) of this 
section.
    (ii) Where the employer has a reasonable basis for believing that 
no employee in a process or task will be exposed above the PEL for 30 
or more days per year (12 consecutive months), the requirement to 
implement engineering and work practice controls to achieve the PEL 
does not apply to that process or task.
    (2) Prohibition of rotation. The employer shall not rotate 
employees to different jobs to achieve compliance with the PEL.
    (g) Respiratory protection. (1) General. The employer shall provide 
respiratory protection for employees during:
    (i) Periods necessary to install or implement feasible engineering 
and work practice controls;
    (ii) Work operations, such as maintenance and repair activities, 
for which engineering and work practice controls are not feasible;
    (iii) Work operations for which an employer has implemented all 
feasible engineering and work practice controls and such controls are 
not sufficient to reduce exposures to or below the PEL;
    (iv) Work operations where employees are exposed above the PEL for 
fewer than 30 days per year, and the employer has elected not to 
implement engineering and work practice controls to achieve the PEL; or
    (v) Emergencies.
    (2) Respiratory protection program. Where respirator use is 
required by this section, the employer shall institute a respiratory 
protection program in accordance with 29 CFR 1910.134.
    (h) Protective work clothing and equipment. (1) Provision and use. 
Where a hazard is present or is likely to be present from skin or eye 
contact with chromium (VI), the employer shall provide appropriate 
personal protective

[[Page 59466]]

clothing and equipment at no cost to employees, and shall ensure that 
employees use such clothing and equipment.
    (2) Removal and storage. (i) The employer shall ensure that 
employees remove all protective clothing and equipment contaminated 
with chromium (VI) at the end of the work shift or at the completion of 
their tasks involving chromium (VI) exposure, whichever comes first.
    (ii) The employer shall ensure that no employee removes chromium 
(VI)-contaminated protective clothing or equipment from the workplace, 
except for those employees whose job it is to launder, clean, maintain, 
or dispose of such clothing or equipment.
    (iii) When contaminated protective clothing or equipment is removed 
for laundering, cleaning, maintenance, or disposal, the employer shall 
ensure that it is stored and transported in sealed, impermeable bags or 
other closed, impermeable containers.
    (iv) Bags or containers of contaminated protective clothing or 
equipment that are removed from change rooms for laundering, cleaning, 
maintenance, or disposal shall be labeled in accordance with paragraph 
(l) of this section.
    (3) Cleaning and replacement. (i) The employer shall clean, 
launder, repair and replace all protective clothing and equipment 
required by this section as needed to maintain its effectiveness.
    (ii) The employer shall prohibit the removal of chromium (VI) from 
protective clothing and equipment by blowing, shaking, or any other 
means that disperses chromium (VI) into the air or onto an employee's 
body.
    (iii) The employer shall inform any person who launders or cleans 
protective clothing or equipment contaminated with chromium (VI) of the 
potentially harmful effects of exposure to chromium (VI) and that the 
clothing and equipment should be laundered or cleaned in a manner that 
minimizes skin or eye contact with chromium (VI) and effectively 
prevents the release of airborne chromium (VI) in excess of the PEL.
    (i) Hygiene areas and practices. (1) General. Where protective 
clothing and equipment is required, the employer shall provide change 
rooms in conformance with 29 CFR 1910.141. Where skin contact with 
chromium (VI) occurs, the employer shall provide washing facilities in 
conformance with 29 CFR 1910.141. Eating and drinking areas provided by 
the employer shall also be in conformance with Sec.  1910.141.
    (2) Change rooms. The employer shall assure that change rooms are 
equipped with separate storage facilities for protective clothing and 
equipment and for street clothes, and that these facilities prevent 
cross-contamination.
    (3) Washing facilities. (i) The employer shall provide readily 
accessible washing facilities capable of removing chromium (VI) from 
the skin, and shall ensure that affected employees use these facilities 
when necessary.
    (ii) The employer shall ensure that employees who have skin contact 
with chromium (VI) wash their hands and faces at the end of the work 
shift and prior to eating, drinking, smoking, chewing tobacco or gum, 
applying cosmetics, or using the toilet.
    (4) Eating and drinking areas. (i) Whenever the employer allows 
employees to consume food or beverages at a worksite where chromium 
(VI) is present, the employer shall ensure that eating and drinking 
areas and surfaces are maintained as free as practicable of chromium 
(VI).
    (ii) The employer shall ensure that employees do not enter eating 
and drinking areas with protective work clothing or equipment unless 
surface chromium (VI) has been removed from the clothing and equipment 
by methods that do not disperse chromium (VI) into the air or onto an 
employee's body.
    (5) Prohibited activities. The employer shall ensure that employees 
do not eat, drink, smoke, chew tobacco or gum, or apply cosmetics in 
regulated areas, or in areas where skin or eye contact with chromium 
(VI) occurs; or carry the products associated with these activities, or 
store such products in these areas.
    (j) Housekeeping. (1) General. The employer shall ensure that:
    (i) All surfaces are maintained as free as practicable of 
accumulations of chromium (VI).
    (ii) All spills and releases of chromium (VI) containing material 
are cleaned up promptly.
    (2) Cleaning methods. (i) The employer shall ensure that surfaces 
contaminated with chromium (VI) are cleaned by HEPA-filter vacuuming or 
other methods that minimize the likelihood of exposure to chromium 
(VI).
    (ii) Shoveling, sweeping, and brushing may be used only where HEPA-
filtered vacuuming or other methods that minimize the likelihood of 
exposure to chromium (VI) have been tried and found not to be 
effective.
    (iii) The employer shall not allow compressed air to be used to 
remove chromium (VI) from any surface unless the compressed air is used 
in conjunction with a ventilation system designed to capture the dust 
cloud created by the compressed air.
    (iv) The employer shall ensure that cleaning equipment is handled 
in a manner that minimizes the reentry of chromium (VI) into the 
workplace.
    (3) Disposal. The employer shall ensure that:
    (i) Waste, scrap, debris, and any other materials contaminated with 
chromium (VI) and consigned for disposal are collected and disposed of 
in sealed, impermeable bags or other closed, impermeable containers.
    (ii) Bags or containers of waste, scrap, debris, and any other 
materials contaminated with chromium (VI) that are consigned for 
disposal are labeled in accordance with paragraph (l) of this section.
    (k) Medical surveillance. (1) General. (i) The employer shall make 
medical surveillance available at no cost to the employee, and at a 
reasonable time and place, for all employees:
    (A) Who are or may be occupationally exposed to chromium (VI) above 
the PEL for 30 or more days a year;
    (B) Experiencing signs or symptoms of the adverse health effects 
associated with chromium (VI) exposure; or
    (C) Exposed in an emergency.
    (ii) The employer shall assure that all medical examinations and 
procedures required by this section are performed by or under the 
supervision of a PLHCP.
    (2) Frequency. The employer shall provide a medical examination:
    (i) Within 30 days after initial assignment, unless the employee 
has received a chromium (VI) related medical examination, provided in 
accordance with this standard, within the last twelve months;
    (ii) Annually;
    (iii) Within 30 days after a PLHCP's written medical opinion 
recommends an additional examination;
    (iv) Whenever an employee shows signs or symptoms of the adverse 
health effects associated with chromium (VI) exposure;
    (v) Within 30 days after exposure during an emergency which results 
in an uncontrolled release of chromium (VI); or
    (vi) At the termination of employment, unless the last examination 
that satisfied the requirements of paragraph (k) of this section was 
less than six months prior to the date of termination.
    (3) Contents of examination. A medical examination consists of:
    (i) A medical and work history, with emphasis on: past, present, 
and anticipated future exposure to chromium (VI); any history of 
respiratory system dysfunction; any

[[Page 59467]]

history of asthma, dermatitis, skin ulceration, or nasal septum 
perforation; and smoking status and history;
    (ii) A physical examination of the skin and respiratory tract; and
    (iii) Any additional tests deemed appropriate by the examining 
PLHCP.
    (4) Information provided to the PLHCP. The employer shall ensure 
that the examining PLHCP has a copy of this standard, and shall provide 
the following information:
    (i) A description of the affected employee's former, current, and 
anticipated duties as they relate to the employee's occupational 
exposure to chromium (VI);
    (ii) The employee's former, current, and anticipated levels of 
occupational exposure to chromium (VI);
    (iii) A description of any personal protective equipment used or to 
be used by the employee, including when and for how long the employee 
has used that equipment; and
    (iv) Information from records of employment-related medical 
examinations previously provided to the affected employee, currently 
within the control of the employer.
    (5) PLHCP's written medical opinion. (i) The employer shall obtain 
a written medical opinion from the PLHCP, within 30 days for each 
medical examination performed on each employee, which contains:
    (A) The PLHCP's opinion as to whether the employee has any detected 
medical condition(s) that would place the employee at increased risk of 
material impairment to health from further exposure to chromium (VI);
    (B) Any recommended limitations upon the employee's exposure to 
chromium (VI) or upon the use of personal protective equipment such as 
respirators;
    (C) A statement that the PLHCP has explained to the employee the 
results of the medical examination, including any medical conditions 
related to chromium (VI) exposure that require further evaluation or 
treatment, and any special provisions for use of protective clothing or 
equipment.
    (ii) The PLHCP shall not reveal to the employer specific findings 
or diagnoses unrelated to occupational exposure to chromium (VI).
    (iii) The employer shall provide a copy of the PLHCP's written 
medical opinion to the examined employee within two weeks after 
receiving it.
    (l) Communication of chromium (VI) hazards to employees.
    (1) General. In addition to the requirements of the Hazard 
Communication Standard, 29 CFR 1910.1200, for labels, material safety 
data sheets, and training, employers shall comply with the following 
requirements.
    (2) Warning signs. (i) The employer shall ensure that legible and 
readily visible warning signs are displayed at all approaches to 
regulated areas so that an employee may read the signs and take 
necessary protective steps before entering the area.
    (ii) Warning signs required by paragraph (l)(2)(i) of this section 
shall include at least the following information:

                                 DANGER
                              CHROMIUM (VI)
                              CANCER HAZARD
            CAN DAMAGE SKIN, EYES, NASAL PASSAGES, AND LUNGS
                        AUTHORIZED PERSONNEL ONLY
                    RESPIRATORS REQUIRED IN THIS AREA
 

    (3) Warning labels. The employer shall ensure that bags or 
containers of contaminated clothing and equipment to be removed for 
laundering, cleaning, or maintenance, and containers of waste, scrap, 
debris, and any other materials contaminated with chromium (VI) that 
are consigned for disposal, bear appropriate warning labels that 
include at least the following information:

                                 DANGER
                         CONTAINS CHROMIUM (VI)
                              CANCER HAZARD
            CAN DAMAGE SKIN, EYES, NASAL PASSAGES, AND LUNGS
 

    (4) Employee information and training. (i) For all employees who 
are exposed to airborne chromium (VI), or who have skin or eye contact 
with chromium (VI), the employer shall provide training, ensure 
employee participation in training, and maintain a record of training 
provided.
    (ii) The employer shall provide initial training prior to or at the 
time of initial assignment to a job involving potential exposure to 
chromium (VI). An employer who is able to demonstrate that a new 
employee has received training within the last 12 months that addresses 
the elements specified in paragraph (l)(4)(iii) of this section is not 
required to repeat such training provided that the employee can 
demonstrate knowledge of those elements.
    (iii) The employer shall provide training that is understandable to 
the employee and shall ensure that each employee can demonstrate 
knowledge of at least the following:
    (A) The health hazards associated with chromium (VI) exposure;
    (B) The location, manner of use, and release of chromium (VI) in 
the workplace and the specific nature of operations that could result 
in exposure to chromium (VI), especially exposure above the PEL;
    (C) The engineering controls and work practices associated with the 
employee's job assignment;
    (D) The purpose, proper selection, fitting, proper use, and 
limitations of respirators and protective clothing;
    (E) Emergency procedures;
    (F) Measures employees can take to protect themselves from exposure 
to chromium (VI), including modification of personal hygiene and habits 
such as smoking;
    (G) The purpose and a description of the medical surveillance 
program required by paragraph (k) of this section;
    (H) The contents of this section; and
    (I) The employee's rights of access to records under 29 CFR 
1910.1020(g).
    (iv) The employer shall provide additional training when:
    (A) Training is necessary to ensure that each employee maintains an 
understanding of the safe use and handling of chromium (VI) in the 
workplace.
    (B) Workplace changes (such as modification of equipment, tasks, or 
procedures) result in an increase in employee exposures to chromium 
(VI), and those exposures exceed or can reasonably be expected to 
exceed the action level or result in a hazard from skin or eye contact 
with chromium (VI).
    (v) The employer shall make a copy of this section and its 
appendices readily available without cost to all affected employees.
    (m) Recordkeeping. (1) Exposure measurements. (i) The employer 
shall maintain an accurate record of all measurements taken to monitor 
employee exposure to chromium (VI) as prescribed in paragraph (d) of 
this section.
    (ii) This record shall include at least the following information:
    (A) The date of measurement for each sample taken;
    (B) The operation involving exposure to chromium (VI) that is being 
monitored;
    (C) Sampling and analytical methods used and evidence of their 
accuracy;
    (D) Number, duration, and the results of samples taken;
    (E) Type of personal protective equipment, such as respirators 
worn; and
    (F) Name, social security number, and job classification of all 
employees represented by the monitoring, indicating which employees 
were actually monitored.
    (iii) The employer shall ensure that exposure records are 
maintained and made available in accordance with 29 CFR 1910.1020.

[[Page 59468]]

    (2) Historical monitoring data. (i) Where the employer has 
monitored for chromium (VI) in the past 12 months, and has relied on 
this historical monitoring data to demonstrate that exposures on a 
particular job will be below the action level, the employer shall 
establish and maintain an accurate record of the historical monitoring 
data relied upon.
    (ii) The record shall include information that reflects the 
following conditions:
    (A) The data were collected using methods that meet the accuracy 
requirements of paragraph (d)(6) of this section;
    (B) The processes and work practices that were in use when the 
historical monitoring data were obtained are essentially the same as 
those to be used during the job for which initial monitoring will not 
be performed;
    (C) The characteristics of the chromium (VI) containing material 
being handled when the historical monitoring data were obtained are the 
same as those on the job for which initial monitoring will not be 
performed;
    (D) Environmental conditions prevailing when the historical 
monitoring data were obtained are the same as those on the job for 
which initial monitoring will not be performed; and
    (E) Other data relevant to the operations, materials, processing, 
or employee exposures covered by the exception.
    (iii) The employer shall ensure that historical exposure records 
are maintained and made available in accordance with 29 CFR 1910.1020.
    (3) Objective data. (i) Where an employer uses objective data to 
satisfy initial monitoring requirements, the employer shall establish 
and maintain an accurate record of the objective data relied upon.
    (ii) This record shall include at least the following information:
    (A) The chromium (VI)-containing material in question;
    (B) The source of the objective data;
    (C) The testing protocol and results of testing, or analysis of the 
material for the release of chromium (VI);
    (D) A description of the operation exempted from initial monitoring 
and how the data support the exemption; and
    (E) Other data relevant to the operations, materials, processing or 
employee exposures covered by the exemption.
    (iii) The employer shall maintain this record for the duration of 
the employer's reliance upon such objective data and shall make such 
records available in accordance with 29 CFR 1910.1020.
    (4) Medical surveillance. (i) The employer shall establish and 
maintain an accurate record for each employee covered by medical 
surveillance under paragraph (k) of this section.
    (ii) The record shall include the following information about the 
employee:
    (A) Name and social security number;
    (B) A copy of the PLHCP's written opinions;
    (C) A copy of the information provided to the PLHCP as required by 
paragraph (k)(4) of this section.
    (iii) The employer shall ensure that medical records are maintained 
and made available in accordance with 29 CFR 1910.1020.
    (5) Training. (i) At the completion of training, the employer shall 
prepare a record that indicates the identity of the individuals trained 
and the date the training was completed. This record shall be 
maintained for three years after the completion of training.
    (ii) The employer shall provide to the Assistant Secretary or the 
Director, upon request, all materials relating to employee information 
and training.
    (n) Dates. (1) Effective date. This section shall become effective 
[60 days after publication of the final rule in the Federal Register].
    (2) Start-up dates. All obligations of this section commence 90 
days after the effective date except as follows:
    (i) Change rooms required by paragraph (i) of this section shall be 
provided no later than one year after the effective date.
    (ii) Engineering controls required by paragraph (f) of this section 
shall be implemented no later than two years after the effective date.

PART 1915--[AMENDED]

    4. The authority citation for 29 CFR part 1915 is revised to read 
as follows:

    Authority: Sec. 41, Longshore and Harbor Workers' Compensation 
Act (33 U.S.C. 941); secs. 4, 6, 8, Occupational Safety and Health 
Act of 1970 (29 U.S.C. 653, 655, 657); Secretary of Labor's Order 
No. 12-71 (36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736), 1-90 
(55 FR 9033), 6-96 (62 FR 111), 3-2000 (65 FR 50017) or 5-2002 (67 
FR 65008), as applicable.
    Sections 1915.120, 1915.152 and 1915.1026 also issued under 29 
CFR part 1911.

    5. In Sec.  1915.1000, Table Z, the entry for ``Chromic acid and 
chromates (as CrO(3)) 0.1'' is removed and the following entry added in 
its place:


Sec.  1915.1000  Air contaminants.

* * * * *

                                               TABLE Z--SHIPYARDS
----------------------------------------------------------------------------------------------------------------
            Substance                  CAS No.d             ppm a *           mg/m 3 b *       Skin designation
----------------------------------------------------------------------------------------------------------------
 
                                                  * * * * * * *
Chromium (VI) compounds (as Cr);
 see 1915.1026.
 
                                                 * * * * * * *
----------------------------------------------------------------------------------------------------------------
* * * * * * *
3 Use Asbestos Limit Sec.   1915.1001.
* * * * * * *
* The PELS are 8-hour TWAs unless otherwise noted; a (C) designation denotes a ceiling limit. They are to be
  determined from breathing-zone air samples.
a Parts of vapor or gas per million parts of contaminated air by volume at 25[deg] C and 760 torr.
b Milligrams of substance per cubic meter of air. When entry is in this column only, the value is exact; when
  listed with a ppm entry, it is approximate.
* * * * * * *
d The CAS number is for information only. Enforcement is based on the substance name. For an entry covering more
  than one metal compound, measured as the metal, the CAS number for the metal is given--not CAS numbers for the
  individual compounds.


[[Page 59469]]

* * * * *
    6. A new Sec.  1915.1026 is added, to read as follows:


Sec.  1915.1026  Chromium (VI).

    (a) Scope. This standard applies to occupational exposures to 
chromium (VI) in all forms and compounds in shipyards, marine 
terminals, and longshoring.
    (b) Definitions. For the purposes of this section the following 
definitions apply:
    Assistant Secretary means the Assistant Secretary of Labor for 
Occupational Safety and Health, U.S. Department of Labor, or designee.
    Chromium (VI) [hexavalent chromium or Cr(VI)] means chromium with a 
valence of positive six, in any form and in any compound.
    Director means the Director of the National Institute for 
Occupational Safety and Health (NIOSH), U.S. Department of Health and 
Human Services, or designee.
    Emergency means any occurrence that results, or is likely to 
result, in an uncontrolled release of chromium (VI). If an incidental 
release of chromium (VI) can be controlled at the time of release by 
employees in the immediate release area, or by maintenance personnel, 
it is not an emergency.
    Employee exposure means the exposure to airborne chromium (VI) that 
would occur if the employee were not using a respirator.
    High-efficiency particulate air [HEPA] filter means a filter that 
is at least 99.97 percent efficient in removing mono-dispersed 
particles of 0.3 micrometers in diameter or larger.
    Physician or other licensed health care professional [PLHCP] is an 
individual whose legally permitted scope of practice (i.e., license, 
registration, or certification) allows him or her to independently 
provide or be delegated the responsibility to provide some or all of 
the particular health care services required by paragraph (h) of this 
section.
    This section means this chromium (VI) standard.
    (c) Permissible exposure limit (PEL). The employer shall ensure 
that no employee is exposed to an airborne concentration of chromium 
(VI) in excess of 1 microgram per cubic meter of air (1 [mu]g/m\3\), 
calculated as an 8-hour time-weighted average (TWA).
    (d) Methods of compliance. (1) Engineering and work practice 
controls. (i) Except as permitted in paragraph (d)(1)(ii) of this 
section, the employer shall use engineering and work practice controls 
to reduce and maintain employee exposure to chromium (VI) to or below 
the PEL unless the employer can demonstrate that such controls are not 
feasible. Wherever feasible engineering and work practice controls are 
not sufficient to reduce employee exposure to or below the PEL, the 
employer shall use them to reduce employee exposure to the lowest 
levels achievable, and shall supplement them by the use of respiratory 
protection that complies with the requirements of paragraph (e) of this 
section.
    (ii) Where the employer has a reasonable basis for believing that 
no employee in a process or task will be exposed above the PEL for 30 
or more days per year (12 consecutive months), the requirement to 
implement engineering and work practice controls to achieve the PEL 
does not apply to that process or task.
    (2) Prohibition of rotation. The employer shall not rotate 
employees to different jobs to achieve compliance with the PEL.
    (e) Respiratory protection. (1) General. The employer shall provide 
respiratory protection for employees during:
    (i) Periods necessary to install or implement feasible engineering 
and work practice controls;
    (ii) Work operations, such as maintenance and repair activities, 
for which engineering and work practice controls are not feasible;
    (iii) Work operations for which an employer has implemented all 
feasible engineering and work practice controls and such controls are 
not sufficient to reduce exposures to or below the PEL;
    (iv) Work operations where employees are exposed above the PEL for 
fewer than 30 days per year, and the employer has elected not to 
implement engineering and work practice controls to achieve the PEL; or
    (v) Emergencies.
    (2) Respiratory protection program. Where respirator use is 
required by this section, the employer shall institute a respiratory 
protection program in accordance with 29 CFR 1910.134.
    (f) Protective work clothing and equipment. (1) Provision and use. 
Where a hazard is present or is likely to be present from skin or eye 
contact with chromium (VI), the employer shall provide appropriate 
personal protective clothing and equipment at no cost to employees, and 
shall ensure that employees use such clothing and equipment.
    (2) Removal and storage. (i) The employer shall ensure that 
employees remove all protective clothing and equipment contaminated 
with chromium (VI) at the end of the work shift or at the completion of 
their tasks involving chromium (VI) exposure, whichever comes first.
    (ii) The employer shall ensure that no employee removes chromium 
(VI)-contaminated protective clothing or equipment from the workplace, 
except for those employees whose job it is to launder, clean, maintain, 
or dispose of such clothing or equipment.
    (iii) When contaminated protective clothing or equipment is removed 
for laundering, cleaning, maintenance, or disposal, the employer shall 
ensure that it is stored and transported in sealed, impermeable bags or 
other closed, impermeable containers.
    (iv) Bags or containers of contaminated protective clothing or 
equipment that are removed from change rooms for laundering, cleaning, 
maintenance, or disposal shall be labeled in accordance with paragraph 
(i) of this section.
    (3) Cleaning and replacement. (i) The employer shall clean, 
launder, repair and replace all protective clothing and equipment 
required by this section as needed to maintain its effectiveness.
    (ii) The employer shall prohibit the removal of chromium (VI) from 
protective clothing and equipment by blowing, shaking, or any other 
means that disperses chromium (VI) into the air or onto an employee's 
body.
    (iii) The employer shall inform any person who launders or cleans 
protective clothing or equipment contaminated with chromium (VI) of the 
potentially harmful effects of exposure to chromium (VI) and that the 
clothing and equipment should be laundered or cleaned in a manner that 
minimizes skin or eye contact with chromium (VI) and effectively 
prevents the release of airborne chromium (VI) in excess of the PEL.
    (g) Hygiene areas and practices. (1) General. Where protective 
clothing and equipment is required, the employer shall provide change 
rooms in conformance with 29 CFR 1910.141. Where skin contact with 
chromium (VI) occurs, the employer shall provide washing facilities in 
conformance with 29 CFR 1915.97. Eating and drinking areas provided by 
the employer shall also be in conformance with Sec.  1915.97.
    (2) Change rooms. The employer shall assure that change rooms are 
equipped with separate storage facilities for protective clothing and 
equipment and for street clothes, and that these facilities prevent 
cross-contamination.
    (3) Washing facilities. (i) The employer shall provide readily 
accessible washing facilities capable of removing chromium (VI) from 
the skin, and shall ensure that affected employees use these facilities 
when necessary.

[[Page 59470]]

    (ii) The employer shall ensure that employees who have skin contact 
with chromium (VI) wash their hands and faces at the end of the work 
shift and prior to eating, drinking, smoking, chewing tobacco or gum, 
applying cosmetics, or using the toilet.
    (4) Eating and drinking areas. (i) Whenever the employer allows 
employees to consume food or beverages at a worksite where chromium 
(VI) is present, the employer shall ensure that eating and drinking 
areas and surfaces are maintained as free as practicable of chromium 
(VI).
    (ii) The employer shall ensure that employees do not enter eating 
and drinking areas with protective work clothing or equipment unless 
surface chromium (VI) has been removed from the clothing and equipment 
by methods that do not disperse chromium (VI) into the air or onto an 
employee's body.
    (5) Prohibited activities. The employer shall ensure that employees 
do not eat, drink, smoke, chew tobacco or gum, or apply cosmetics in 
areas where skin or eye contact with chromium (VI) occurs; or carry the 
products associated with these activities, or store such products in 
these areas.
    (h) Medical surveillance. (1) General. (i) The employer shall make 
medical surveillance available at no cost to the employee, and at a 
reasonable time and place, for all employees:
    (A) Experiencing signs or symptoms of the adverse health effects 
associated with chromium (VI) exposure; or
    (B) Exposed in an emergency.
    (ii) The employer shall assure that all medical examinations and 
procedures required by this section are performed by or under the 
supervision of a PLHCP.
    (2) Frequency. The employer shall provide a medical examination:
    (i) Whenever an employee shows signs or symptoms of the adverse 
health effects associated with chromium (VI) exposure;
    (ii) Within 30 days after exposure during an emergency which 
results in an uncontrolled release of chromium (VI); or
    (iii) Within 30 days after a PLHCP's written medical opinion 
recommends an additional examination.
    (3) Contents of examination. A medical examination consists of:
    (i) A medical and work history, with emphasis on: Past, present, 
and anticipated future exposure to chromium (VI); any history of 
respiratory system dysfunction; any history of asthma, dermatitis, skin 
ulceration, or nasal septum perforation; and smoking status and 
history;
    (ii) A physical examination of the skin and respiratory tract; and
    (iii) Any additional tests deemed appropriate by the examining 
PLHCP.
    (4) Information provided to the PLHCP. The employer shall ensure 
that the examining PLHCP has a copy of this standard, and shall provide 
the following information:
    (i) A description of the affected employee's former, current, and 
anticipated duties as they relate to the employee's occupational 
exposure to chromium (VI);
    (ii) The employee's former, current, and anticipated levels of 
occupational exposure to chromium (VI);
    (iii) A description of any personal protective equipment used or to 
be used by the employee, including when and for how long the employee 
has used that equipment; and
    (iv) Information from records of employment-related medical 
examinations previously provided to the affected employee, currently 
within the control of the employer.
    (5) PLHCP's written medical opinion. (i) The employer shall obtain 
a written medical opinion from the PLHCP, within 30 days for each 
medical examination performed on each employee, which contains:
    (A) The PLHCP's opinion as to whether the employee has any detected 
medical condition(s) that would place the employee at increased risk of 
material impairment to health from further exposure to chromium (VI);
    (B) Any recommended limitations upon the employee's exposure to 
chromium (VI) or upon the use of personal protective equipment such as 
respirators;
    (C) A statement that the PLHCP has explained to the employee the 
results of the medical examination, including any medical conditions 
related to chromium (VI) exposure that require further evaluation or 
treatment, and any special provisions for use of protective clothing or 
equipment.
    (ii) The PLHCP shall not reveal to the employer specific findings 
or diagnoses unrelated to occupational exposure to chromium (VI).
    (iii) The employer shall provide a copy of the PLHCP's written 
medical opinion to the examined employee within two weeks after 
receiving it.
    (i) Communication of chromium (VI) hazards to employees.
    (1) General. In addition to the requirements of the Hazard 
Communication Standard, 29 CFR 1910.1200, for labels, material safety 
data sheets, and training, employers shall comply with the following 
requirements.
    (2) Warning labels. The employer shall ensure that bags or 
containers of contaminated clothing and equipment to be removed for 
laundering, cleaning, or maintenance, bear appropriate warning labels 
that include at least the following information:

                                 DANGER
                         CONTAINS CHROMIUM (VI)
                              CANCER HAZARD
            CAN DAMAGE SKIN, EYES, NASAL PASSAGES, AND LUNGS
 

    (3) Employee information and training. (i) The employer shall 
provide training for all employees who are potentially exposed to 
chromium (VI), ensure employee participation in training, and maintain 
a record of training provided.
    (ii) The employer shall provide initial training prior to or at the 
time of initial assignment to a job involving potential exposure to 
chromium (VI). An employer who is able to demonstrate that a new 
employee has received training within the last 12 months that addresses 
the elements specified in paragraph (l)(4)(iii) of this section is not 
required to repeat such training provided that the employee can 
demonstrate knowledge of those elements.
    (iii) The employer shall provide training that is understandable to 
the employee and shall ensure that each employee can demonstrate 
knowledge of at least the following:
    (A) The health hazards associated with chromium (VI) exposure;
    (B) The location, manner of use, and release of chromium (VI) in 
the workplace and the specific nature of operations that could result 
in exposure to chromium (VI), especially exposure above the PEL;
    (C) The engineering controls and work practices associated with the 
employee's job assignment;
    (D) The purpose, proper selection, fitting, proper use, and 
limitations of respirators and protective clothing;
    (E) Emergency procedures;
    (F) Measures employees can take to protect themselves from exposure 
to chromium (VI), including modification of personal hygiene and habits 
such as smoking;
    (G) The purpose and a description of the medical surveillance 
program required by paragraph (h) of this section;
    (H) The contents of this section; and
    (I) The employee's rights of access to records under 29 CFR 
1910.1020(g).
    (iv) The employer shall provide additional training when:
    (A) Training is necessary to ensure that each employee maintains an 
understanding of the safe use and handling of chromium (VI) in the 
workplace.

[[Page 59471]]

    (B) Workplace changes (such as modification of equipment, tasks, or 
procedures) result in an increase in employee exposures to chromium 
(VI), and those exposures exceed or can reasonably be expected to 
exceed the PEL or result in a hazard from skin or eye contact with 
chromium (VI).
    (v) The employer shall make a copy of this section and its 
appendices readily available without cost to all affected employees.
    (j) Recordkeeping. (1) Medical surveillance. (i) The employer shall 
establish and maintain an accurate record for each employee covered by 
medical surveillance under paragraph (h) of this section.
    (ii) The record shall include the following information about the 
employee:
    (A) Name and social security number;
    (B) A copy of the PLHCP's written opinions;
    (C) A copy of the information provided to the PLHCP as required by 
paragraph (h)(4) of this section.
    (iii) The employer shall ensure that medical records are maintained 
and made available in accordance with Sec. 1910.1020.
    (2) Training. (i) At the completion of training, the employer shall 
prepare a record that indicates the identity of the individuals trained 
and the date the training was completed. This record shall be 
maintained for three years after the completion of training.
    (ii) The employer shall provide to the Assistant Secretary or the 
Director, upon request, all materials relating to employee information 
and training.
    (k) Dates. (1) Effective date. This section shall become effective 
[60 days after publication of the final rule in the Federal Register].
    (2) Start-up dates. All obligations of this section commence 90 
days after the effective date except as follows:
    (i) Change rooms required by paragraph (g) of this section shall be 
provided no later than one year after the effective date.
    (ii) Engineering controls required by paragraph (d) of this section 
shall be implemented no later than two years after the effective date.

PART 1917--[AMENDED]

    7. The authority citation for 29 CFR Part 1917 is revised to read 
as follows:

    Authority: Sec. 41, Longshore and Harbor Workers' Compensation 
Act (33 U.S.C. 941); secs. 4, 6, 8, Occupational Safety and Health 
Act of 1970 (29 U.S.C. 653, 655, 657); Secretary of Labor's Order 
Nos. 12-71 (36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736), 6-
96 (62 FR 111), or 5-2002 (67 FR 65008), as applicable; 29 CFR part 
1911.
    Section 1917.28 also issued under 5 U.S.C. 553.

    8. New paragraphs (a)(2)(xiii)(E) and (b) are added to Sec.  
1917.1, to read as follows:


Sec.  1917.1  Scope and applicability.

* * * * *
    (a) * * *
    (2) * * *
    (xiii) * * *
    (E) Hexavalent chromium Sec.  1910.1026 (See Sec.  1915.1026)
* * * * *
    (b) Section 1915.1026 applies to any occupational exposures to 
hexavalent chromium in workplaces covered by this part.

PART 1918--[AMENDED]

    9. The authority citation for 29 CFR Part 1918 is revised to read 
as follows:

    Authority: Secs. 4, 6, 8, Occupational Safety and Health Act of 
1970, 29 U.S.C. 653, 655, 657; Walsh-Healey Act, 41 U.S.C. 35 et 
seq.; Service Contract Act of 1965, 41 U.S.C. 351 et seq,; Sec. 107, 
Contract Work Hours and Safety Standards Act (Construction Safety 
Act), 40 U.S.C. 333; Sec. 41, Longshore and Harbor Workers' 
Compensation Act, 33 U.S.C. 941; National Foundation of Arts and 
Humanities Act, 20 U.S.C. 951 et seq.; Secretary of Labor's Order 
Nos. 6-96 (62 FR 111) or 5-2002 (67 FR 65008), as applicable; and 29 
CFR part 1911.
    10. New paragraphs (b)(9)(v) and (c) are added to Sec.  1918.1 to 
read as follows:


Sec.  1918.1  Scope and application.

* * * * *
    (b) * * *
    (9) * * *
    (v) Hexavalent chromium Sec.  1910.1026 (See Sec.  1915.1026)
* * * * *
    (c) Section 1915.1026 applies to any occupational exposures to 
hexavalent chromium in workplaces covered by this part.

PART 1926--[AMENDED]

Subpart D--[Amended]

    11. The authority citation for subpart D of 29 CFR Part 1926 is 
revised to read as follows:

    Authority: Sec. 107, Contract Work Hours and Safety Standards 
Act (40 U.S.C. 333); secs. 4, 6, 8, Occupational Safety and Health 
Act of 1970 (29 U.S.C. 653, 655, 657); Secretary of Labor's Order 
Nos. 12-71 (36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736), 6-
96 (62 FR 111), or 5-2002 (67 FR 65008), as applicable; and 29 CFR 
part 1911.


Sec.  1926.55  [Amended]

    12. In Appendix A to Sec.  1926.55, the entry for ``Chromic acid 
and chromates (as CrO<INF>3</INF>) 0.1'' is removed and the following 
entry added in its place:


Sec.  1926.55  Gases, vapors, fumes, dusts, and mists.

* * * * *

                        Threshold Limit Values of Airborne Contaminants for Construction
----------------------------------------------------------------------------------------------------------------
            Substance                 CAS No.\d\            ppm \a\          mg/m \3\ \b\      Skin Designation
----------------------------------------------------------------------------------------------------------------
 
                                                  * * * * * * *
Chromium (VI) compounds (as Cr);
 see 1926.1126.
 
                                                 * * * * * * *
----------------------------------------------------------------------------------------------------------------
3 Use Asbestos LimitSec.   1915.1001
* * * * * * *
a Parts of vapor or gas per million parts of contaminated air by volume at 25 [deg] C and 760 torr.
3b Milligrams of substance per cubic meter of air. When entry is in this column only, the value is exact; when
  listed with a ppm entry, it is approxiate
* * * * * * *
d The CAS number is for information only. Enforcement is based on the substance name. For an entry covering more
  than one metal compound, measured as the metal, the CAS number for the metal is given--not CAS numbers for the
  individual compounds.


[[Page 59472]]

* * * * *

Subpart Z--[Amended]

    13. The authority citation for subpart Z of 29 CFR Part 1926 is 
revised to read as follows:

    Authority: Sec. 107, Contract Work Hours and Safety Standards 
Act (40 U.S.C. 333); secs. 4, 6, 8, Occupational Safety and Health 
Act of 1970 (29 U.S.C. 653, 655, 657); Secretary of Labor's Order 
Nos. 12-71 (36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736), 1-
90 (55 FR 9033), 6-96 (62 FR 111), or 5-2002 (67 FR 65008), as 
applicable; and 29 CFR part 1911.
    Section 1926.1102 not issued under 29 U.S.C. 655 or 29 CFR part 
1911; also issued under 5 U.S.C. 553.

    14. A new Sec.  1926.1126 is added to subpart Z of 29 CFR Part 1926 
to read as follows:


Sec.  1926.1126  Chromium (VI).

    (a) Scope. This standard applies to occupational exposures to 
chromium (VI) in all forms and compounds in construction, except for 
exposures to portland cement.
    (b) Definitions. For the purposes of this section the following 
definitions apply:
    Assistant Secretary means the Assistant Secretary of Labor for 
Occupational Safety and Health, U.S. Department of Labor, or designee.
    Chromium (VI) [hexavalent chromium or Cr(VI)] means chromium with a 
valence of positive six, in any form and in any compound.
    Director means the Director of the National Institute for 
Occupational Safety and Health (NIOSH), U.S. Department of Health and 
Human Services, or designee.
    Emergency means any occurrence that results, or is likely to 
result, in an uncontrolled release of chromium (VI). If an incidental 
release of chromium (VI) can be controlled at the time of release by 
employees in the immediate release area, or by maintenance personnel, 
it is not an emergency.
    Employee exposure means the exposure to airborne chromium (VI) that 
would occur if the employee were not using a respirator.
    High-efficiency particulate air [HEPA] filter means a filter that 
is at least 99.97 percent efficient in removing mono-dispersed 
particles of 0.3 micrometers in diameter or larger.
    Physician or other licensed health care professional [PLHCP] is an 
individual whose legally permitted scope of practice (i.e., license, 
registration, or certification) allows him or her to independently 
provide or be delegated the responsibility to provide some or all of 
the particular health care services required by paragraph (h) of this 
section.
    This section means this chromium (VI) standard.
    (c) Permissible exposure limit (PEL). The employer shall ensure 
that no employee is exposed to an airborne concentration of chromium 
(VI) in excess of 1 microgram per cubic meter of air (1 [mu]g/
m<SUP>3</SUP>), calculated as an 8-hour time-weighted average (TWA).
    (d) Methods of compliance. (1) Engineering and work practice 
controls. (i) Except as permitted in paragraph (d)(1)(ii) of this 
section, the employer shall use engineering and work practice controls 
to reduce and maintain employee exposure to chromium (VI) to or below 
the PEL unless the employer can demonstrate that such controls are not 
feasible. Wherever feasible engineering and work practice controls are 
not sufficient to reduce employee exposure to or below the PEL, the 
employer shall use them to reduce employee exposure to the lowest 
levels achievable, and shall supplement them by the use of respiratory 
protection that complies with the requirements of paragraph (e) of this 
section.
    (ii) Where the employer has a reasonable basis for believing that 
no employee in a process or task will be exposed above the PEL for 30 
or more days per year (12 consecutive months), the requirement to 
implement engineering and work practice controls to achieve the PEL 
does not apply to that process or task.
    (2) Prohibition of Rotation. The employer shall not rotate 
employees to different jobs to achieve compliance with the PEL.
    (e) Respiratory Protection. (1) General. The employer shall provide 
respiratory protection for employees during:
    (i) Periods necessary to install or implement feasible engineering 
and work practice controls;
    (ii) Work operations, such as maintenance and repair activities, 
for which engineering and work practice controls are not feasible;
    (iii) Work operations for which an employer has implemented all 
feasible engineering and work practice controls and such controls are 
not sufficient to reduce exposures to or below the PEL;
    (iv) Work operations where employees are exposed above the PEL for 
fewer than 30 days per year, and the employer has elected not to 
implement engineering and work practice controls to achieve the PEL; or
    (v) Emergencies.
    (2) Respiratory protection program. Where respirator use is 
required by this section, the employer shall institute a respiratory 
protection program in accordance with 29 CFR 1910.134.
    (f) Protective work clothing and equipment. (1) Provision and use. 
Where a hazard is present or is likely to be present from skin or eye 
contact with chromium (VI), the employer shall provide appropriate 
personal protective clothing and equipment at no cost to employees, and 
shall ensure that employees use such clothing and equipment.
    (2) Removal and storage. (i) The employer shall ensure that 
employees remove all protective clothing and equipment contaminated 
with chromium (VI) at the end of the work shift or at the completion of 
their tasks involving chromium (VI) exposure, whichever comes first.
    (ii) The employer shall ensure that no employee removes chromium 
(VI)-contaminated protective clothing or equipment from the workplace, 
except for those employees whose job it is to launder, clean, maintain, 
or dispose of such clothing or equipment.
    (iii) When contaminated protective clothing or equipment is removed 
for laundering, cleaning, maintenance, or disposal, the employer shall 
ensure that it is stored and transported in sealed, impermeable bags or 
other closed, impermeable containers.
    (iv) Bags or containers of contaminated protective clothing or 
equipment that are removed from change rooms for laundering, cleaning, 
maintenance, or disposal shall be labeled in accordance with paragraph 
(i) of this section.
    (3) Cleaning and replacement. (i) The employer shall clean, 
launder, repair and replace all protective clothing and equipment 
required by this section as needed to maintain its effectiveness.
    (ii) The employer shall prohibit the removal of chromium (VI) from 
protective clothing and equipment by blowing, shaking, or any other 
means that disperses chromium (VI) into the air or onto an employee's 
body.
    (iii) The employer shall inform any person who launders or cleans 
protective clothing or equipment contaminated with chromium (VI) of the 
potentially harmful effects of exposure to chromium (VI) and that the 
clothing and equipment should be laundered or cleaned in a manner that 
minimizes skin or eye contact with chromium (VI) and effectively 
prevents the release of airborne chromium (VI) in excess of the PEL.
    (g) Hygiene areas and practices. (1) General. Where protective 
clothing and equipment is required, the employer shall provide change 
rooms in conformance with 29 CFR 1926.51.

[[Page 59473]]

Where skin contact with chromium (VI) occurs, the employer shall 
provide washing facilities in conformance with 29 CFR 1926.51. Eating 
and drinking areas provided by the employer shall also be in 
conformance with Sec.  1926.51.
    (2) Change rooms. The employer shall assure that change rooms are 
equipped with separate storage facilities for protective clothing and 
equipment and for street clothes, and that these facilities prevent 
cross-contamination.
    (3) Washing facilities. (i) The employer shall provide readily 
accessible washing facilities capable of removing chromium (VI) from 
the skin, and shall ensure that affected employees use these facilities 
when necessary.
    (ii) The employer shall ensure that employees who have skin contact 
with chromium (VI) wash their hands and faces at the end of the work 
shift and prior to eating, drinking, smoking, chewing tobacco or gum, 
applying cosmetics, or using the toilet.
    (4) Eating and drinking areas. (i) Whenever the employer allows 
employees to consume food or beverages at a worksite where chromium 
(VI) is present, the employer shall ensure that eating and drinking 
areas and surfaces are maintained as free as practicable of chromium 
(VI).
    (ii) The employer shall ensure that employees do not enter eating 
and drinking areas with protective work clothing or equipment unless 
surface chromium (VI) has been removed from the clothing and equipment 
by methods that do not disperse chromium (VI) into the air or onto an 
employee's body.
    (5) Prohibited activities. The employer shall ensure that employees 
do not eat, drink, smoke, chew tobacco or gum, or apply cosmetics in 
areas where skin or eye contact with chromium (VI) occurs; or carry the 
products associated with these activities, or store such products in 
these areas.
    (h) Medical Surveillance. (1) General. (i) The employer shall make 
medical surveillance available at no cost to the employee, and at a 
reasonable time and place, for all employees:
    (A) Experiencing signs or symptoms of the adverse health effects 
associated with chromium (VI) exposure; or
    (B) Exposed in an emergency.
    (ii) The employer shall assure that all medical examinations and 
procedures required by this section are performed by or under the 
supervision of a PLHCP.
    (2) Frequency. The employer shall provide a medical examination:
    (i) Whenever an employee shows signs or symptoms of the adverse 
health effects associated with chromium (VI) exposure;
    (ii) Within 30 days after exposure during an emergency which 
results in an uncontrolled release of chromium (VI); or
    (iii) Within 30 days after a PLHCP's written medical opinion 
recommends an additional examination.
    (3) Contents of examination. A medical examination consists of:
    (i) A medical and work history, with emphasis on: Past, present, 
and anticipated future exposure to chromium (VI); any history of 
respiratory system dysfunction; any history of asthma, dermatitis, skin 
ulceration, or nasal septum perforation; and smoking status and 
history;
    (ii) A physical examination of the skin and respiratory tract; and
    (iii) Any additional tests deemed appropriate by the examining 
PLHCP.
    (4) Information provided to the PLHCP. The employer shall ensure 
that the examining PLHCP has a copy of this standard, and shall provide 
the following information:
    (i) A description of the affected employee's former, current, and 
anticipated duties as they relate to the employee's occupational 
exposure to chromium (VI);
    (ii) The employee's former, current, and anticipated levels of 
occupational exposure to chromium (VI);
    (iii) A description of any personal protective equipment used or to 
be used by the employee, including when and for how long the employee 
has used that equipment; and
    (iv) Information from records of employment-related medical 
examinations previously provided to the affected employee, currently 
within the control of the employer.
    (5) PLHCP's Written Medical Opinion. (i) The employer shall obtain 
a written medical opinion from the PLHCP, within 30 days for each 
medical examination performed on each employee, which contains:
    (A) The PLHCP's opinion as to whether the employee has any detected 
medical condition(s) that would place the employee at increased risk of 
material impairment to health from further exposure to chromium (VI);
    (B) Any recommended limitations upon the employee's exposure to 
chromium (VI) or upon the use of personal protective equipment such as 
respirators;
    (C) A statement that the PLHCP has explained to the employee the 
results of the medical examination, including any medical conditions 
related to chromium (VI) exposure that require further evaluation or 
treatment, and any special provisions for use of protective clothing or 
equipment.
    (ii) The PLHCP shall not reveal to the employer specific findings 
or diagnoses unrelated to occupational exposure to chromium (VI).
    (iii) The employer shall provide a copy of the PLHCP's written 
medical opinion to the examined employee within two weeks after 
receiving it.
    (i) Communication of chromium (VI) hazards to employees. (1) 
General. In addition to the requirements of the Hazard Communication 
Standard, 29 CFR 1910.1200, for labels, material safety data sheets, 
and training, employers shall comply with the following requirements.
    (2) Warning labels. The employer shall ensure that bags or 
containers of contaminated clothing and equipment to be removed for 
laundering, cleaning, or maintenance, bear appropriate warning labels 
that include at least the following information:

                                 DANGER
                         CONTAINS CHROMIUM (VI)
                              CANCER HAZARD
            CAN DAMAGE SKIN, EYES, NASAL PASSAGES, AND LUNGS
 

    (3) Employee information and training. (i) The employer shall 
provide training for all employees who are potentially exposed to 
chromium (VI), ensure employee participation in training, and maintain 
a record of training provided.
    (ii) The employer shall provide initial training prior to or at the 
time of initial assignment to a job involving potential exposure to 
chromium (VI). An employer who is able to demonstrate that a new 
employee has received training within the last 12 months that addresses 
the elements specified in paragraph (l)(4)(iii) of this section is not 
required to repeat such training provided that the employee can 
demonstrate knowledge of those elements.
    (iii) The employer shall provide training that is understandable to 
the employee and shall ensure that each employee can demonstrate 
knowledge of at least the following:
    (A) The health hazards associated with chromium (VI) exposure;
    (B) The location, manner of use, and release of chromium (VI) in 
the workplace and the specific nature of operations that could result 
in exposure to chromium (VI), especially exposure above the PEL;
    (C) The engineering controls and work practices associated with the 
employee's job assignment;
    (D) The purpose, proper selection, fitting, proper use, and 
limitations of respirators and protective clothing;
    (E) Emergency procedures;

[[Page 59474]]

    (F) Measures employees can take to protect themselves from exposure 
to chromium (VI), including modification of personal hygiene and habits 
such as smoking;
    (G) The purpose and a description of the medical surveillance 
program required by paragraph (h) of this section;
    (H) The contents of this section; and
    (I) The employee's rights of access to records under 29 CFR 
1910.1020(g).
    (iv) The employer shall provide additional training when:
    (A) Training is necessary to ensure that each employee maintains an 
understanding of the safe use and handling of chromium (VI) in the 
workplace.
    (B) Workplace changes (such as modification of equipment, tasks, or 
procedures) result in an increase in employee exposures to chromium 
(VI), and those exposures exceed or can reasonably be expected to 
exceed the PEL or result in a hazard from skin or eye contact with 
chromium (VI).
    (v) The employer shall make a copy of this section and its 
appendices readily available without cost to all affected employees.
    (j) Recordkeeping. (1) Medical surveillance. (i) The employer shall 
establish and maintain an accurate record for each employee covered by 
medical surveillance under paragraph (h) of this section.
    (ii) The record shall include the following information about the 
employee:
    (A) Name and social security number;
    (B) A copy of the PLHCP's written opinions;
    (C) A copy of the information provided to the PLHCP as required by 
paragraph (h)(4) of this section.
    (iii) The employer shall ensure that medical records are maintained 
and made available in accordance with Sec. 1910.1020.
    (2) Training. (i) At the completion of training, the employer shall 
prepare a record that indicates the identity of the individuals trained 
and the date the training was completed. This record shall be 
maintained for three years after the completion of training.
    (ii) The employer shall provide to the Assistant Secretary or the 
Director, upon request, all materials relating to employee information 
and training.
    (k) Dates. (1) Effective date. This section shall become effective 
[60 days after publication of the final rule in the Federal Register].
    (2) Start-up dates. All obligations of this section commence 90 
days after the effective date except as follows:
    (i) Change rooms required by paragraph (g) of this section shall be 
provided no later than one year after the effective date.
    (ii) Engineering controls required by paragraph (d) of this section 
shall be implemented no later than two years after the effective date.

[FR Doc. 04-21488 Filed 10-1-04; 8:45 am]
BILLING CODE 4510-26-P