59306 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

DEPARTMENT OF LABOR

Occupational Safety and Health 

Administration 

29 CFR Parts 1910, 1915, 1917, 1918, 

and 1926 

[Docket No. H054A] 

RIN 1218–AB45 

Occupational Exposure to Hexavalent 

Chromium

AGENCY: Occupational Safety and Health 

Administration (OSHA), Department of 

Labor.

ACTION: Proposed rule; request for 

comments and scheduling of informal 

public hearings. 

SUMMARY: The Occupational Safety and 

Health Administration (OSHA) proposes 

to amend its existing standard for 

employee exposure to hexavalent 

chromium (Cr(VI)). The basis for 

issuance of this proposal is a 

preliminary determination by the 

Assistant Secretary that employees 

exposed to Cr(VI) face a significant risk 

to their health at the current permissible 

exposure limit and that promulgating 

this proposed standard will 

substantially reduce that risk. The 

information gathered so far in this 

rulemaking indicates that employees 

exposed to Cr(VI) well below the current 

permissible exposure limit are at 

increased risk of developing lung 

cancer. Occupational exposures to 

Cr(VI) may also result in asthma, and 

damage to the nasal epithelia and skin. 

This document proposes an 8-hour 

time-weighted average permissible 

exposure limit of one microgram of 

Cr(VI) per cubic meter of air (1 mg/m3) 

for all Cr(VI) compounds. OSHA also 

proposes other ancillary provisions for 

employee protection such as preferred 

methods for controlling exposure, 

respiratory protection, protective work 

clothing and equipment, hygiene areas 

and practices, medical surveillance, 

hazard communication, and 

recordkeeping. OSHA is proposing 

separate regulatory texts for general 

industry, construction, and shipyards in 

order to tailor requirements to the 

circumstances found in each of these 

sectors.

DATES: Written comments. The Agency 

invites interested persons to submit 

written comments regarding the 

proposed rule, including comments on 

the information collection 

determination described in Section X of 

the preamble (OMB Review under the 

Paperwork Reduction Act of 1995), by 

mail, facsimile, or electronically. All 

comments, whether submitted by mail, 

facsimile, or electronically through the 

Internet, must be sent by January 3, 

2005.

Informal public hearings. The Agency 

plans to hold an informal public hearing 

in Washington, DC, beginning on 

February 1, 2005. OSHA expects the 

hearing to last from 9:30 a.m. to 5:30 

p.m.; however, the exact daily schedule 

is at the discretion of the presiding 

administrative law judge. 

Notice of intention to appear to 

provide testimony at the informal public 

hearing. Interested persons who intend 

to present testimony at the informal 

public hearing in Washington, DC, must 

notify OSHA of their intention to do so 

no later than December 3, 2004. 

Hearing testimony and documentary 

evidence. Interested persons who 

request more than 10 minutes to present 

their testimony, or who will be 

submitting documentary evidence at the 

hearing, must provide the Agency with 

copies of their full testimony and all 

documentary evidence they plan to 

present by January 3, 2005. See Section 

XVI below for details on the format and 

how to file a notice of intention to 

appear, submit documentary evidence at 

the hearing, and request an appropriate 

amount of time to present testimony.

ADDRESSES: Written comments.

Interested persons may submit three 

copies of written comments to the 

Docket Office, Docket H054A, Room N–

2625, OSHA, U.S. Department of Labor, 

200 Constitution Avenue, NW., 

Washington, DC 20210; telephone (202) 

693–2350. If written comments are 10 

pages or fewer, they may be faxed to the 

OSHA Docket Office, facsimile number 

(202) 693–1648. Comments may also be 

submitted electronically through the 

Internet at http://ecomments.osha.gov.

Supplemental information such as 

studies and journal articles cannot be 

attached to electronic submissions. 

Instead, three copies of each study, 

article, or other supplemental document 

must be sent to the OSHA Docket Office 

at the address above. These materials 

must clearly identify the associated 

electronic comments to which they will 

be attached in the docket by the 

following information: Name of person 

submitting comments; date of comment 

submission; subject of comments; and 

docket number to which comments 

belong. 

Informal public hearings. The 

informal public hearing to be held in 

Washington, DC, will be held in the 

Frances Perkins Building, U.S. 

Department of Labor, 200 Constitution 

Avenue, NW., Washington, DC 20210. 

Notice of intention to appear to 

provide testimony at the informal public 

hearing. Interested persons who intend 

to present testimony at the informal 

public hearing in Washington, DC, may 

submit three copies of their notice of 

intention to appear to the Docket Office, 

Docket H054A, Room N–2625, OSHA, 

U.S. Department of Labor, 200 

Constitution Avenue, NW., Washington, 

DC 20210. Notices may also be 

submitted electronically through the 

Internet at http://ecomments.osha.gov.

OSHA Docket Office and Department of 

Labor hours of operation are 8:15 a.m. 

to 4:45 p.m. 

Hearing testimony and documentary 

evidence. Interested persons who 

request more than 10 minutes in which 

to present their testimony, or who will 

be submitting documentary evidence at 

the informal public hearing must submit 

three copies of the testimony and the 

documentary evidence to the Docket 

Office, Docket H054A, Room N–2625, 

OSHA, U.S. Department of Labor, 200 

Constitution Avenue, NW., Washington, 

DC 20210. Written testimony may also 

be submitted electronically through the 

Internet at http://ecomments.osha.gov.

Please note that security-related 

problems may result in significant 

delays in receiving comments and other 

materials by regular mail. Telephone the 

OSHA Docket Office at (202) 693–2350 

for information regarding security 

procedures concerning delivery of 

materials by express delivery, hand 

delivery, and messenger service. 

All comments and submissions will 

be available for inspection and copying 

in the OSHA Docket Office at the 

address above. Most comments and 

submissions will be posted on OSHA’s 

Web page (http://www.osha.gov). 

Contact the OSHA Docket Office at (202) 

693–2350 for information about 

materials not available on the OSHA 

Web page and for assistance in using 

this Web page to locate docket 

submissions. Because comments sent to 

the docket or to OSHA’s Web page are 

available for public inspection, the 

Agency cautions interested parties 

against including in these comments 

personal information such as social 

security numbers and birth dates.

FOR FURTHER INFORMATION CONTACT: For 

general information and press inquiries, 

contact Mr. George Shaw, Office of 

Communications, Room N–3647, OSHA, 

U.S. Department of Labor, 200 

Constitution Avenue, NW., Washington, 

DC 20210; telephone (202) 693–1999. 

For technical inquiries, contact Ms. 

Amanda Edens, Directorate of Standards 

and Guidance, Room N–3718, OSHA, 

U.S. Department of Labor, 200 

Constitution Avenue, NW., Washington, 

DC 20210; telephone (202) 693–2093 or 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59307

fax (202) 693–1678. For hearing 

information contact Ms. Veneta 

Chatmon, Office of Communications, 

Room N–3647, OSHA, U.S. Department 

of Labor, 200 Constitution Avenue, 

NW., Washington, DC 20210; telephone 

(202) 693–1999.

SUPPLEMENTARY INFORMATION: For 

additional copies of this Federal 

Register document, contact the Office of 

Publications, Room N–3101, OSHA, 

U.S. Department of Labor, 200 

Constitution Avenue, NW., Washington, 

DC 20210; telephone (202) 693–1888. 

Electronic copies of this Federal 

Register, as well as news releases and 

other relevant documents, are available 

at OSHA’s Home page at http://

www.osha.gov.

I. General 

The preamble to the proposed 

standard on occupational exposure to 

chromium (VI) discusses events leading 

to the proposal, health effects of 

exposure, the degree and significance of 

the risk presented, a summary of the 

analysis of technological and economic 

feasibility, regulatory impact, and 

regulatory flexibility, and the rationale 

behind the specific provisions set forth 

in the proposed standard. The 

discussion follows this outline:

I. General 

II. Issues 

III. Pertinent Legal Authority 

IV. Events Leading to the Proposed Standards 

V. Chemical Properties and Industrial Uses 

VI. Health Effects 

VII. Preliminary Quantitative Risk 

Assessment 

VIII. Significance of Risk 

IX. Summary of the Preliminary Economic 

Analysis and Initial Regulatory 

Flexibility Analysis 

X. OMB Review under the Paperwork 

Reduction Act of 1995 

XI. Federalism 

XII. State Plans 

XIII. Unfunded Mandates 

XIV. Protecting Children from Environmental 

Health and Safety Risks

XV. Environmental Impacts 

XVI. Public Participation—Notice of Hearing 

XVII. Summary and Explanation of 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 μg/m3) more consistent 

with concentrations found in the 

workplace today. However, OSHA 

believes the period of follow-up 

observation (median <10 yr), the young 

age (<45 yr at end of follow-up) and the 

low number of observed lung cancers 

(≤15 lung cancers) severely limits these 

cohorts as primary data sets for 

quantitative risk analysis. Other 

limitations to the Alexander study 

include a lack of data on workers who 

were employed between 1940 and 1974, 

but whose employment ended prior to 

1974, and on exposures prior to 1974. 

Are there updated analyses available for 

the Alexander and Pastides cohorts? 

How many years do these cohorts need 

to be followed and how many lung 

cancers need to be observed in order for 

these data sets to provide insight into 

the shape of the exposure-response 

curve at lower levels of Cr(VI) exposure 

(e.g., 0.5 to 5 μg/m3)? In the case of the 

Alexander cohort, is there additional 

information on cohort members’

exposures prior to 1974 or workers who 

left prior to 1974 that could improve the 

analysis? Are there other cohorts 

available to look at low exposures? 

5. OSHA has relied upon a linear 

relative risk model and cumulative 

Cr(VI) exposure for estimating the 

lifetime occupational lung cancer risk 

among Cr(VI)-exposed workers. In 

particular, OSHA has made a 

preliminary determination that a 

threshold model is not appropriate for 

estimating the lung cancer risk 

associated with Cr(VI). However, there 

is some evidence that pathways (e.g., 

extracellular reduction, DNA repair, cell 

apoptosis, etc.) may exist within the 

lung that protect against Cr(VI)-induced 

respiratory carcinogenesis, and may 

potentially introduce non-linearities 

into the Cr(VI) exposure-cancer 

response. Is there convincing scientific 

evidence of a non-linear exposureresponse 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 μg/m3) leads to the same risk 

as an equivalent cumulative exposure 

achieved by longer duration exposure to 

59308 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

lower Cr(VI) exposure (e.g, exposed 45 

years to 1 μg/m3). OSHA preliminarily 

finds this assumed exposure 

equivalency to represent an uncertainty 

in the estimates of risk but does not 

have information that indicates this 

uncertainty introduces serious error in 

its predictions of risk. Does the OSHA 

exposure-response assessment based on 

the higher Cr(VI) air levels and/or 

shorter durations experienced by the 

Gibb and Luippold cohorts lead to a 

serious underprediction or 

overprediction in estimated risks for the 

occupational exposure 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59309

proposal’s requirements be deleted or 

simplified for small entities, while still 

protecting the health of employees? 

Would a longer time allowed for 

compliance for small entities make a 

difference to their ability to comply, and 

if so, why? (Information submitted in 

the SBREFA process is part of the record 

and need not be resubmitted). 

Economic Impacts and Economic 

Feasibility 

20. OSHA, in its Preliminary 

Economic Analysis, has estimated, by 

application group, compliance costs per 

affected entity and the likely impacts on 

revenues and profits under alternative 

market scenarios. OSHA requests that 

affected employers provide comment on 

OSHA’s estimate of revenue, profit, and 

the impacts of costs for their industry or 

application group. Are there special 

circumstances—such as unique cost 

factors, foreign competition, or pricing 

constraints—that OSHA needs to 

consider when evaluating economic 

impacts for particular application 

groups? Comments are requested on 

OSHA’s analysis of economic feasibility 

in the PEA. 

Overlapping and Duplicative 

Regulations 

21. Do any federal regulations 

duplicate, overlap, or conflict with the 

proposed Cr(VI) standard? 

22. In some facilities, adjustments in 

ventilation systems to comply with the 

proposed PEL may require additional 

time and expense to retest these systems 

to ensure compliance with EPA 

requirements or state requirements. 

OSHA requests information and 

comment indicating how frequently 

retesting would be required, and the 

time and costs involved in such 

retesting. 

Environmental Impacts 

23. Submit any data, information, or 

comments pertaining to possible 

environmental impacts of adopting this 

proposal, such as the following: 

a. Any positive or negative 

environmental effects that could result;

b. Any irreversible commitments of 

natural resources which could be 

involved; and 

c. Estimates of the effect of the 

proposed standard on the levels of 

Cr(VI) in the environment. 

In particular, consideration should be 

given to the potential direct or indirect 

impacts of the proposal on water and air 

pollution, energy use, solid waste 

disposal, or land use. 

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

59310 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/m3. The Agency has 

made a preliminary determination that 

this is the lowest level that is both 

technologically and economically 

feasible and is necessary to reduce 

significant risks of material health 

impairment from exposure to Cr(VI). Is 

this PEL appropriate and is it 

adequately supported by the existing 

data? If not, what PEL would be more 

appropriate or would more adequately 

protect employees from Cr(VI)-

associated health risks? Provide 

evidence to support your response. 

34. Should different PELs be 

established for different Cr(VI) 

compounds? If so, how should they be 

established? Where possible, provide 

specific detail about how different PELs 

could be established and how the 

Agency should apply those PELs in 

instances where workers may be 

exposed to more than one Cr(VI) 

compound. 

35. OSHA has proposed an action 

level for Cr(VI) exposure in general 

industry, but not in construction or 

shipyards. Is this an appropriate 

approach? Should OSHA set an action 

level for exposure to Cr(VI) in 

construction and shipyards? Should the 

proposed action level in general 

industry be retained in the final rule? 

36. If an action level is included in 

the final rule, is the proposed action 

level for general industry (0.5 μg/m3) the 

appropriate level for the PEL under 

consideration? If not, at what level 

should the action level be set?

37. If an action level is included in 

the final rule, which provisions should 

be triggered by exposure above the 

action level? Indicate the basis for your 

position and include any supporting 

information. 

38. If no action level is included in 

the final rule, which provisions should 

apply to all Cr(VI)-exposed workers? 

Which provisions should be triggered by 

the PEL? Are there any other 

appropriate triggers for the requirements 

of the standard? 

39. Should OSHA set a short-term 

exposure limit (STEL) or ceiling for 

exposure to Cr(VI)? If so, please specify 

the appropriate air concentration and 

the rationale for its selection. 

40. Do you conduct initial air 

monitoring or do you rely on objective 

data to determine Cr(VI) exposures? 

Describe any other approaches you have 

implemented for assessing an 

employee’s initial exposure to Cr(VI). 

41. Describe any follow-up or 

subsequent exposure assessments that 

you conduct. How often do you conduct 

such follow-up or subsequent exposure 

assessments? Please comment on 

OSHA’s estimate of baseline industry 

practice and the projected costs for 

initial and periodic exposure 

assessment. Are OSHA’s estimates 

consistent with current industry 

practice? 

42. Do shipyard employers presently 

measure their employees’ exposure to 

Cr(VI)? If not, do they use some 

alternative method of identifying which 

employees may be over-exposed to 

Cr(VI)? 

43. OSHA has proposed specific 

requirements for exposure assessment in 

general industry, but has not proposed 

that these requirements apply to 

construction or shipyard employers. 

Should requirements for exposure 

assessment in construction or shipyards 

be included in the final Cr(VI) standard? 

Are there any advantages to requiring 

construction or shipyard employers to 

measure their employees’ exposures to 

Cr(VI)? If so, would the exposure 

assessment requirements proposed for 

general industry be appropriate? Would 

construction or shipyard employers 

encounter situations where monitoring 

would be infeasible if they were 

required to follow the exposure 

assessment requirements proposed for 

employers in general industry? Indicate 

the basis for your position and include 

any supporting information. What types 

of exposure assessment strategies are 

effective for assessing worker exposures 

at construction and shipyard worksites? 

44. Should requirements for exposure 

assessment in general industry be 

included in the final Cr(VI) standard, or 

would the performance-oriented 

requirement proposed for construction 

and shipyards be more appropriate? 

Indicate the basis for your position and 

include any supporting information. 

45. OSHA has proposed that exposure 

monitoring in general industry be 

conducted at least every six months if 

exposures are above the action level but 

below the PEL, and at least every three 

months if exposures are at or above the 

PEL. Are these proposed frequencies 

appropriate? If not, what frequency of 

monitoring would be more appropriate, 

and why?

46. OSHA has proposed that regulated 

areas be established in general industry 

wherever an employee’s exposure to 

airborne concentrations of Cr(VI) is, or 

can reasonably be expected to be, in 

excess of the PEL. OSHA seeks 

comments on this provision and in 

particular: 

a. Describe any work settings where 

establishing regulated areas could be 

problematic or infeasible. If establishing 

regulated areas is problematic, what 

approaches might be used to warn 

employees in such work settings of high 

risk areas (i.e., areas where the airborne 

concentrations of Cr(VI) exceed the 

PEL?). 

b. Should OSHA add hazards from 

eye or skin contact as a trigger for 

establishing regulated areas? Explain the 

basis for your position, and include any 

supporting information. c. Describe any 

methods currently used that have been 

found to be effective in establishing 

regulated areas. 

47. OSHA has not proposed 

requirements for establishment of 

regulated areas in construction or 

shipyards. Should requirements for 

regulated areas for construction or 

shipyards be included in the final Cr(VI) 

standard? If so, would the requirements 

for regulated areas proposed for general 

industry be appropriate? Are there any 

particular problems in construction or 

shipyard settings that make regulated 

areas problematic or infeasible? If 

requirements for regulated areas for 

construction or shipyards are not 

included in the final Cr(VI) standard, 

should OSHA include requirements for 

warning signs or other measures to alert 

employees of the presence of Cr(VI)? If 

so, what practical means could be used 

to determine where and when such 

labeling would be required? What 

potential difficulties might be 

encountered by using such an 

approach? Indicate the basis for your 

position and include any supporting 

information. 

48. Under the proposed standard, 

employers are required to use 

engineering and work practice controls 

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

59312 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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. 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 m3 air in 

the workplace (1 mg/10 m3 CrO3) as a 

ceiling concentration, which 

corresponds to a concentration of 52 μg/

m3 Cr(VI). A separate rule promulgated 

for the construction industry set an 

eight-hour time-weighted-average PEL 

of 1 mg/10 m3 CrO3, also equivalent to 

52 μg/m3 Cr(VI), adopted from the 

American Conference of Governmental 

Industrial Hygienists (ACGIH) 1970 

Threshold Limit Value (TLV) (36 FR 

7340 (4/17/71)).

Following the ANSI standard of 1943, 

other occupational and public health 

organizations evaluated Cr(VI) as a 

workplace and environmental hazard 

and formulated recommendations to 

control exposure. The ACGIH first 

recommended control of workplace 

exposures to chromium in 1946, 

recommending a time-weighted average 

Maximum Allowable Concentration 

(later called a Threshold Limit Value) of 

100 μg/m3 for chromic acid and 

chromates as Cr2O3 (Ex. 5–37), and 

classified certain Cr(VI) compounds as 

class A1 (confirmed human) 

carcinogens in 1974. In 1975, the 

NIOSH Criteria for a Recommended 

Standard recommended that 

occupational exposure to Cr(VI) 

compounds should be limited to a 10-

hour TWA of 1 μg/m3, except for some 

forms of Cr(VI) then believed to be 

noncarcinogenic (Ex. 3–92). The 

National Toxicology Program’s First 

Annual Report on Carcinogens 

identified calcium chromate, chromium 

chromate, strontium chromate, and zinc 

chromate as carcinogens in 1980 (Ex. 

35–157). 

During the 1980s, regulatory and 

standards organizations came to 

recognize Cr(VI) compounds in general 

as carcinogens. The Environmental 

Protection Agency (EPA) Health 

Assessment Document of 1984 stated 

that ‘‘using the IARC [International 

Agency for Research on Cancer] 

classification scheme, the level of 

evidence available for the combined 

animal and human data would place 

hexavalent chromium Cr(VI) 

compounds into Group 1, meaning that 

there is decisive evidence for the 

carcinogenicity of those compounds in 

humans’’ (Ex. 19–1, p. 7–107). In 1988 

IARC evaluated the available evidence 

regarding Cr(VI) carcinogenicity, 

concluding in 1990 that ‘‘There is 

sufficient evidence in humans for the 

carcinogenicity of chromium[VI] 

compounds as encountered in the 

chromate production, chromate pigment 

production and chromium plating 

industries’’, and ‘‘sufficient evidence in 

experimental animals for the 

carcinogenicity of calcium chromate, 

zinc chromates, strontium chromate and 

lead chromates’(Ex. 18–3, p. 213). In 

September 1988, NIOSH advised OSHA 

to consider all Cr(VI) compounds as 

potential occupational carcinogens (Ex. 

31–22–22, p. 8). ACGIH now classifies 

water-insoluble and water-soluble 

Cr(IV) compounds as class A1 

carcinogens (Ex. 35–207). Current 

ACGIH standards include specific 8-

hour time-weighted average TLVs for 

calcium chromate (1 μg/m3), lead 

chromate (12 μg/m3), strontium 

chromate (0.5 μg/m3), and zinc 

chromates (10 μg/m3), and generic TLVs 

for water soluble (50 μg/m3) and 

insoluble (10 μg/m3) forms of hexavalent 

chromium not otherwise classified, all 

measured as chromium (Ex. 35–207). 

In July 1993, OSHA was petitioned for 

an emergency temporary standard to 

reduce occupational exposures to Cr(VI) 

compounds (Ex. 1). The Oil, Chemical, 

and Atomic Workers International 

Union (OCAW) and Public Citizen’s 

Health Research Group (HRG), citing 

evidence that occupational exposure to 

Cr(VI) increases workers’ risk of lung 

cancer, petitioned OSHA to promulgate 

an emergency temporary standard to 

lower the PEL for Cr(VI) compounds to 

0.5 μg/m3 as an eight-hour, timeweighted 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 

59314 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

within the scope of the proposed 

standard (Ex. 35–308, pp. 288–293) and 

that identical PELs should be set for the 

construction, maritime, and general 

industries (Ex. 35–308, pp. 293–297). 

The Committee recommended on May 

18 that the construction industry should 

be included in the current rulemaking, 

and affirmed its earlier recommendation 

regarding portland cement. OSHA 

representatives met with MACOSH in 

March 2004. On March 3, MACOSH 

decided to collect and forward 

additional exposure monitoring data to 

OSHA to help the Agency better 

evaluate exposures to Cr(VI) in 

shipyards (Ex. 310, p. 208). MACOSH 

also recommended a separate Cr(VI) 

standard for the maritime industry, 

arguing that maritime involves different 

exposures and requires different means 

of exposure control than general 

industry and construction (Ex. 310, p. 

227). 

V. Chemical Properties and Industrial 

Uses 

Chromium is a metal that exists in 

several oxidation or valence states, 

ranging from chromium (¥II) to 

chromium (+VI). The elemental valence 

state, chromium (0), does not occur in 

nature. Chromium compounds are very 

stable in the trivalent state and occur 

naturally in this state in ores such as 

ferrochromite, or chromite ore 

(FeCr2O4). The hexavalent, Cr(VI) or 

chromate, is the second most stable 

state. It rarely occurs naturally; most 

Cr(VI) compounds are man made. 

Chromium compounds in higher 

valence states are able to undergo 

‘‘reduction’’ to lower valence states; 

chromium compounds in lower valence 

states are able to undergo ‘‘oxidation’’ to 

higher valence states. Thus, Cr(VI) 

compounds can be reduced to Cr(III) in 

the presence of oxidizable organic 

matter. Chromium can also be reduced 

in the presence of inorganic chemicals 

such as iron. 

Chromium does exist in less stable 

oxidation (valence) states such as Cr(II), 

Cr(IV), and Cr(V). Anhydrous Cr(II) salts 

are relatively stable, but the divalent 

state (II, or chromous) is generally 

relatively unstable and is readily 

oxidized to the trivalent (III or chromic) 

state. Compounds in valence states such 

as (IV) and (V) usually require special 

handling procedures as a result of their 

instability. Cr(IV) oxide (CrO2) is used 

in magnetic recording and storage 

devices, but very few other Cr(IV) 

compounds have industrial use. 

Evidence exists that both Cr(IV) and 

Cr(V) are formed as transient 

intermediates in the reduction of Cr(VI) 

to Cr(III) in the body. 

Chromium (III) is also an essential 

nutrient that plays a role in glucose, fat, 

and protein metabolism by causing the 

action of insulin to be more effective. 

Chromium picolinate, a trivalent form of 

chromium combined with picolinic 

acid, is used as a dietary supplement, 

because it is claimed to speed 

metabolism. 

Elemental chromium and the 

chromium compounds in their different 

valence states have various physical and 

chemical properties, including differing 

solubilities. Most chromium species are 

solid. Elemental chromium is a steel 

gray solid, with high melting and 

boiling points (1857 °C and 2672 °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 °C and 1300 

°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 °C). Chromium (IV) oxide 

is a brown-black solid that decomposes 

at 300 °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 

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

efficiently removed from the air-stream 

in the extrathoracic region (Ex. 35–175). 

Particles greater than 2.5 μm are 

generally deposited in the 

tracheobronchial regions, whereas 

particles less than 2.5 μm are generally 

deposited in the pulmonary region. 

Some larger particles (>2.5 μm) can 

reach the pulmonary region. The 

mucociliary escalator predominantly 

clears particles that deposit in the 

extrathoracic and the tracheobronchial 

region of the lung. Individuals exposed 

to high particulate levels of Cr(VI) may 

also have altered respiratory 

mucociliary clearance. Particulates that 

reach the alveoli can be absorbed into 

the bloodstream cleared by 

phagocytosis. 

2. Absorption of Inhaled Cr(VI) Into the 

Bloodstream 

The absorption of inhaled chromium 

compounds depends on a number of 

factors, including physical and chemical 

properties of the particles (oxidation 

state, size, solubility) and the activity of 

alveolar macrophages (Ex. 35–41). The 

hexavalent chromate anion 

(CrO4)2¥enter cells via facilitated 

diffusion through non-specific anion 

channels (similar to phosphate and 

sulfate anions). Suzuki et al. have 

demonstrated that Cr(VI) is rapidly and 

extensively transported to the 

bloodstream in rats (Ex. 35–97). They 

exposed rats to 7.3–15.9 mg Cr(VI)/m3 as 

potassium dichromate for 2–6 hours. 

Following exposure to Cr(VI), the ratio 

of blood chromium/lung chromium was 

1.44±0.30 at 0.5 hours, 0.81±0.10 at 18 

hours, 0.85±0.20 at 48 hours, and 

0.96±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 51chromiumlabeled compounds (0.38 mg Cr(VI)/kg 

as sodium chromate, 0.36 mg Cr(VI)/kg 

as zinc chromate, or 0.21 mg Cr(VI)/kg 

as lead chromate) intratracheally in rats. 

Peak blood levels of 51chromium were 

reached after 30 minutes for sodium 

chromate (0.35 μg chromium/ml), and 

after 24 hours for zinc chromate (0.60 μg 

chromium/ml) and lead chromate (0.007 

μg chromium/ml). At 30 minutes after 

administration, the lungs contained 36, 

25, and 81% of the respective dose of 

the sodium, zinc, and lead chromate. On 

day six, >80% of the dose of all three 

compounds had been cleared from the 

lungs, during which time the 

disappearance from lungs followed 

linear first-order kinetics. The residual 

amount left in the lungs on day 50 or 

51 was 3.0, 3.9, and 13.9%, respectively. 

From these results authors concluded 

that zinc chromate, which is less soluble 

than sodium chromate, is more slowly 

absorbed from the lungs. Lead chromate 

was more poorly and slowly absorbed, 

as indicated by very low levels in blood 

and greater retention in the lungs. The 

authors also noted that the kinetics of 

sodium and zinc chromates were very 

similar. Zinc chromate, which is less 

soluble than sodium chromate, was 

slowly absorbed from the lung, but the 

maximal blood levels were higher than 

those resulting from an equivalent dose 

of sodium chromate. The authors 

believe that this was probably due to 

irritative properties of the zinc chromate 

used, as it caused hemorrhages in the 

lungs which were macroscopically 

visible as early as 24 hours after 

intratracheal administration. 

The studies by Langard et al. and 

Adachi et al. provide further evidence 

of absorption of chromates from the 

lungs (Exs. 35–93; 189). Rats exposed to 

2.1 mg Cr(VI)/m3 as zinc chromate for 6 

hours/day achieved steady state 

concentrations in the blood after 4 days 

of exposure (Ex. 35–93). Adachi et al.

studied rats that were subject to a single 

inhalation exposure to chromic acid 

mist generated from electroplating at a 

concentration of 3.18 mg Cr(VI)/m3 for 

30 minutes which was then rapidly 

absorbed from the lungs (Ex. 189). The 

amount of chromium in the lungs of 

these rats declined from 13.0 mg 

immediately after exposure to 1.1 mg 

after 4 weeks, with an overall half-life 

of five days. 

Several other studies have reported 

absorption of chromium from the lungs 

after intratracheal instillation (Exs. 7–9; 

9–81; Visek et al. 1953 as cited in Ex. 

35–41). These studies indicated that 53–

85% of Cr(VI) compounds (particle size 

<5 μm) were cleared from the lungs by 

absorption into the bloodstream or by 

mucociliary clearance in the pharynx; 

the rest remained in the lungs. 

Absorption of Cr(VI) from the 

respiratory tract of workers has been 

shown in several studies that identified 

chromium in the urine, serum and red 

blood cells following occupational 

exposure (Exs. 5–12; 35–294; 35–84). 

Evidence indicates that even 

chromates that are encapsulated in a 

paint matrix may be released in the 

lungs (Ex. 31–15, p. 2). LaPuma et al.

measured the mass of Cr(VI) released 

from particles into water originating 

from three types of paint particles: 

solvent-borne expoxy (25% strontium 

chromate (SrCrO4)), water-borne expoxy 

(30% SrCrO4) and polyurethane (20% 

SrCrO4) (Ex. 31–2–1). The mean fraction 

of Cr(VI) released into the water after 

one and 24 hours for each primer 

averaged: 70% and 85% (solvent 

epoxy), 74% and 84% (water epoxy), 

and 94% and 95% (polyurethane). 

Correlations between particle size and 

the fraction of Cr(VI) released indicated 

that smaller particles (<5 m) release a 

larger fraction of Cr(VI) versus larger 

particles (>5 μm). 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 

59316 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg 

Cr(VI)/cm2/hour for a 0.01 molar 

solution, 6.4 μg Cr(VI)/cm2/hour for a 

0.1 molar solution, and 10 μg Cr(VI)/

cm2/hour for a 0.2 molar solution. 

Using volunteers, Mali found that 

potassium dichromate penetrates the 

intact epidermis (Exs. 9–49; 35–41). 

Wahlberg and Skog demonstrated the 

presence of chromium in the blood, 

spleen, bone marrow, lymph glands, 

urine and kidneys of guinea pigs 

exposed to 51 chromium labeled Cr(VI) 

compounds (Ex. 35–81). In this study 

radiolabeled sodium chromate solution 

was dermally applied to guinea pigs and 

51Cr was monitored by scintillation 

counting in tissues. These studies 

demonstrate that the absorption of 

Cr(VI) compounds can take place 

through the dermal route. Also, the 

absorption of Cr(VI) can be facilitated by 

organic solvents. 

4. Absorption of Cr(VI) by the Oral 

Route 

Inhaled Cr(VI) can enter the digestive 

tract as a result of mucocilliary 

clearance and swallowing. Studies 

indicate Cr(VI) is absorbed from the 

gastrointestinal tract. The six-day fecal 

and 24-hour urinary excretion patterns 

of radioactivity in groups of six 

volunteers given Cr(VI) as sodium 

chromate labeled with 51chromium 

indicated that at least 2.1% of the Cr(VI) 

was absorbed. After intraduodenal 

administration at least 10% of the Cr(VI) 

compound was absorbed. These studies 

also demonstrated that Cr(VI) 

compounds are reduced to Cr(III) 

compounds in the stomach, thereby 

accounting for the relatively poor 

gastrointestinal absorption of orally 

administered Cr(VI) compounds (Exs. 

35–96; 35–41). 

In the gastrointestinal tract, Cr(VI) can 

be reduced to Cr(III) by gastric juices, 

which is then poorly absorbed 

(Underwood, 1971 as cited in Ex. 19–1; 

Ex. 35–85). The mechanism by which 

Cr(VI) is carried across the intestinal 

wall and the site of absorption are not 

known and may well depend upon the 

efficiency of defense mechanisms 

(Mertz, 1969 as cited in Ex. 19–1). 

Kuykendall et al. studied the 

absorption of Cr(VI) in human 

volunteers after oral administration of 

potassium dichromate (Ex. 35–77). They 

reported the bioavailability based on 14-

day urinary excretion to be 6.9% (range 

1.2–18%) for Cr(VI). Other investigators 

have also reported absorption of Cr(VI) 

compounds after oral administration 

(Exs. 35–76; 31–22–13; 35–91). 

Studies with 51chromium in animals 

also indicate that chromium and its 

compounds are poorly absorbed from 

the gastrointestinal tract after oral 

exposure. When radioactive sodium 

chromate (Cr(VI)) was given 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 

μg/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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 μg 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 μg Cr(VI)/10 6 cells or 14.4 

μg 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 μg/L with a median level 

of 0.4 μg/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 onecompartment 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 halflife 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 μg/

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 physiologicallybased 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, wellVerDate jul<14>2003 19:01 Oct 01, 2004 Jkt 205001 PO 00000 Frm 00013 Fmt 4701 Sfmt 4702 E:\FR\FM\04OCP2.SGM 04OCP2
59318 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 (CrO4)2- enters cells via 

facilitated diffusion through nonspecific 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 bestdocumented 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.

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59319

TABLE VI–1.—SUMMARY OF SELECTED EPIDEMIOLOGIC STUDIES OF LUNG CANCER IN WORKERS EXPOSED TO

HEXAVALENT CHROMIUM—CHROMATE PRODUCTION

Reference/exhibit number Study population Reference population Chromium (VI) exposure Lung Cancer Risk 

Hayes et al. (1979, Ex. 7–14)

Braver et al. (1985, Ex. 7–17). 

1803 male workers initially employed 3 or more months 

1945–1974 at old and new 

Baltimore MD production facility; follow-up through 1977.

Baltimore City mortality ............ Primarily sodium chromate and 

dichromate production. Avg 

Cr(VI) of 21 to 413 μg/m3

and avg duration 1.6 yr to 13 

yr depending on subcohort, 

plant, and year employed.

—O/E of 2.0 (p<0.01) based 

on 59 lung cancer deaths. 

—Increased risk with duration 

of employment. 

Gibb et al. (2000, Ex. 31–22–

11).

2357 male workers initially employed 1950–1974 only at 

new Baltimore MD production facility; follow-up through 

1992.

U.S. mortality ........................... Primarily sodium chromate and 

dichromate. Mean cumulative Cr(VI) of 0.070 mg/m3

¥ yr and work duration of 

3.1 yr.

—O/E of 1.86 (p<0.01) based 

on 71 lung cancer deaths. 

—Significant upward mortality 

trend with cumulative Cr(VI) 

exposure. 

Mancuso (1997, Ex. 23) ..........

Mancuso (1975, Ex. 7–11). 

Mancuso and Heuper (1951, 

Ex. 7–13). 

Bourne and Yee (1950, Ex. 7–

98). 

332 male workers employed at 

Painesville OH facility 1931–

1937; follow-up through 

1993.

Mortality rate directly calculated using the distribution 

of person years by age 

group for the entire exposed 

population as the standard.

Primarily sodium chromate and 

dichromate production with 

some calcium chromate as a 

result of using high lime 

process. Most cumulative 

soluble Cr(VI) between 0.25 

and 4.0 mg/m3 ¥ yr based 

on 1949 survey.

O/E not calculated but significant increase in age-adjusted lung cancer death 

rate with cumulative chromium exposure based on 66 

deaths. 

Luippold et al. (2003, Ex. 31–

18–4).

492 male workers employed 

one year between 1940 and 

1972 at Painesville OH facility; follow-up through 1997.

U.S. and Ohio Mortality Rates Primarily sodium chromate and 

dichromate production with 

minor calcium chromate. 

Mean cumulative soluble 

Cr(VI) of 1.58 mg/m3 ¥ yr.

—O/E of 2.41(p<0.01) based 

on Ohio rates and 51 

deaths. 

—Significant upward mortality 

trend with cumulative Cr(VI) 

exposure 

Davies et al. (1991, Ex. 7–99)

Alderson et al. (1981, Ex. 7–

22). 

Bistrup and Case (1956, Ex. 

7–20). 

2298 male chromate production workers employed for 

one year between 1950 and 

1976 at three different UK 

plants; follow-up through 

1989.

Cancer mortality of England, 

Wales and Scotland and unexposed local workers.

Principally sodium chromate 

and dichromate production 

with some calcium chromate 

before switch from high lime 

to no lime process. Avg 

soluble Cr(VI) in early 1950s 

from 2 to 880 μg/m3 depending on job.

—O/E of 1.97 (p<0.01) preprocess change based on 

175 deaths. 

—SMR of 1.02 (NS) post-process change based on 14 

deaths. 

—Increased risk for high exposed compared with less 

exposed. 

Korallus et al. (1993, Ex. 7–

91)..

Korallus et al. (1982, Ex. 7–

26). 

1417 chromate production 

workers employed for one 

year between 1948 and 

1987 at two different German plants; follow-up 

through 1988.

Mortality rates for North RhineWestphalia region of Germany where plants located.

Principally sodium chromate 

and dichromate production 

with some calcium chromate 

before switch from high lime 

to no lime process. Annual 

mean Cr(VI) between 6.2 

and 38 μg/m3 after 1977. 

Cr(VI) exposure not reported 

before 1977.

—O/E of 2.27 (p<0.01) preprocess change based on 66 

deaths. 

—O/E of 1.25 (NS) post-process change based on 9 

deaths. 

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–

59320 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 shortterm workers initially hired 1945–1949). 

For those characterized as low exposure, 

there was an elevated SMR for the longterm 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 

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

m3. The usual exposure to Cr(VI) was 

estimated to be 218 μg/m3 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 × 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 μg/m3 and 7.3 years at an 

exposure of 218 μg/m3. For the longterm 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 μg/m3-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 airmonitoring zone. The Cr(III):Cr(VI) ratio 

was derived in this manner for each job 

title based on the distribution of time 

spent in exposure zones in 1978. Cr(VI) 

exposures in the JEM were multiplied 

by this ratio to estimate Cr(III) 

exposures. 

A total of 855 observed deaths (472 

white; 323 nonwhite and 60 race 

unknown) were reported. SMRs were 

calculated using U.S. rates for overall 

mortality. Maryland rates (the state in 

which the plant was located) were used 

to analyze lung cancer mortality in 

order to better account for regional 

differences in disease fatality.

A statistically significant lung cancer 

SMR, based on the national rate, was 

found for whites (O=71; SMR=186; 95% 

CI: 145–234); nonwhites (O=47; 

SMR=188; 95% CI: 138–251) and the 

total cohort (O=122; SMR=180; 95% CI: 

149–214). Of the 122 lung cancer cases, 

116 were smokers and four were non 

smokers at the time of hire. Smoking 

status was unknown for two lung cancer 

cases. SMRs were not adjusted for 

smoking. 

The ratio of observed to expected lung 

cancer deaths (O/E) for the entire cohort 

stratified by race and cumulative 

exposure quartile were computed. 

Cumulative exposure was lagged five 

years (only exposure occurring five 

years before a given age was counted). 

The cut point for the quartiles divided 

the cohort into four equal groups based 

upon their cumulative exposure at the 

end of their working history (0–0.00149 

mgCrO3/m3-yr; 0.0015–0.0089 mgCrO3/

m3-yr; 0.009–0.0769 mgCrO3/m3-yr; and 

0.077–5.25 mgCrO3/m3-yr). For whites, 

the relative risk of lung cancer was 

significantly elevated for the second 

through fourth exposure quartiles with 

O/E values of 0.8, 2.1, 2.1 and 1.7 for the 

four quartiles, respectively. For 

nonwhites, the O/E values by exposure 

quartiles were 1.1, 0.9, 1.2 and 2.9, 

respectively. Only the highest exposure 

quartile was significantly elevated. For 

the total cohort, a significant exposureresponse 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 

59322 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 doseresponse at exposures above and below 

the current PEL and calculating 

smoking-adjusted SMRs for use in doseresponse 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 shortterm 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. Shortterm workers in the Gibb study 

comprise 65% of the cohort and 54% of 

the lung cancers. The Coalition also 

suggested that data pertaining to shortterm 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 

CrO3/m3-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 μg CrO3/m3 or approximately 3.6 

μg/m3 of Cr(VI)). The ‘‘majority’’ of the 

short-term workers had peak exposures 

of <100 μg CrO3/m3. There were five 

peak Cr(VI) exposure levels (<7.2 μg 

CrO3/m3; 7.2<19.3 μg CrO3/m3; 

19.3<48.0 μg CrO3/m3; 48.0<105 μg 

CrO3/m3; 105<182 μg CrO3/m3; and 

182<806 μg CrO3/m3) 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 ageadjusted 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/m3¥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/m3¥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/m3¥years to 

6.0+ mg/m3¥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 ageadjusted 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/m3 years. For the highest 

exposure to insoluble Cr(III) (6.00+ mg/

m3 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/m3 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/m3 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/m3¥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 

59324 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/m3. Another series of 

plant renovations in the early 1960s 

lowered average Cr(VI) levels to 39 μg/

m3 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. 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 nonsignificant 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 casecontrol 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 chromateproducing 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 nonmalignant 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 μg/m3, about 

75 percent were below 3 μg/m3, and 96 

percent were below 25 μg/m3. 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/m3-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 

59326 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 ‘‘highlime’’ 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 prechange group; 129 in the pre-/postchange 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-/postchange 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 prechange 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 prechange 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 prechange 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 

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

59328 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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.

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59329

TABLE VI–2.—SUMMARY OF SELECTED EPIDEMIOLOGIC STUDIES OF LUNG CANCER IN WORKERS EXPOSED TO

HEXAVALENT CHROMIUM—CHROMATE PIGMENT PRODUCTION

Reference/exhibit No. Study population Reference population Chromium (VI) exposure Lung cancer risk 

Langard & Vigander (1983, Ex. 

7–36).

Langard & Vigander (1975, Ex. 

7–33). 

133 Norwegian chromium pigment production workers 

employed between 1948 and 

1972; 24 workers with 3+ 

years exposure to chromate 

dust; follow up through 1980.

Cancer incidence from Norwegian Cancer Registry 

1955–1976.

Lead and zinc chromates with 

some sodium dichromate as 

starting material; Cr(VI) levels between 10 and 30 μg/

m3 1975–1980. No reporting 

<1975.

–O/E of 44 for subcohort of 24 

workers based on 6 cancer 

cases. 

–5 of 6 cases were exposed 

primarily to zinc chromate. 

Davies (1984, Ex. 7–42) ..........

Davies (1979, Ex. 7–41). 

1152 British chromate pigment 

workers from 3 plants with a 

minimum of 1 year employment between 1930–June, 

1975; follow up through 

1981.

Mortality of England and Wales Factory A: chromates—primarily lead; some zinc; 

minor barium Factory B: 

mostly lead and zinc 

chromates; minor strontium. 

Factory C: lead chromate 

only No Cr(VI) levels reported.

—O/E of 2.2 (p<0.05) for high 

exposed in Factory A 1932–

1954; 21 deaths. 

—O/E of 4.4 (p<0.05) for high 

exposed in Factory B 1948–

1967; 11 deaths. 

—O/E of 1.1 (NS) for exposed 

Factory C 1946–1967; 7 

deaths. 

Hayes et al. (1989, Ex. 7–46)

Sheffet et al. (1982, Ex. 7–48). 

1,946 male pigment workers 

from New Jersey facility employed for a minimum of one 

month between 1940 and 

1969; follow up through 

March, 1982.

U.S. Mortality ........................... –Primarily lead chromate with 

some zinc chromate.

–Cr(VI) levels in later years reported to be >500 μg/m3 for 

exposed workers. 

—O/E of 1.2 (NS) for entire cohort based on 41 deaths. 

—O/E of 1.5 (p<0.5) for workers employed >10 yr based 

on 23 deaths. 

—Upward trend (p<0.01) with 

duration of exposure. 

Equitable Environmental 

Health (1983, Ex. 2–D–1).

Equitable Environmental 

Health (1976, Ex. 2–D–3) 

574 male chromate workers 

from three plants (West Virginia, New Jersey or Kentucky) with a minimum of 6 

months of exposure to lead 

chromate prior to 1974.

U.S. white male mortality rates West Virginia: lead chromates

Kentucky: chromates—mostly 

lead, some zinc, minor strontium and barium. 

—New Jersey; mostly lead and 

some zinc chromate. 

—Median Cr(VI) in 1975 reported to equal or exceed 52 

μg/m3

—O/E of 1.30 (NS) for West 

Virginia plant based on 3 

deaths. 

—O/E of 2.16 (NS) for Kentucky plant based on 3 

deaths. 

—O/E of 2.31 (p<.05) for New 

Jersey plant based on 9 

deaths. 

Deschamps et al. (1995, 35–

234).

Haguenoer et al. (1981, Ex. 7–

44) 

294 male pigment workers 

from French facility employed for a minimum of six 

months between 1958 and 

1987.

Death rates from northern 

France.

—Mostly lead chromate with 

some zinc chromate.

—Cr(VI) levels in 1981 between 2 and 180 μg/m3

—O/E of 3.6 (p<0.01) based 

on 18 deaths. 

—Upward trend (p<0.01) with 

duration of 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 exsmokers. Although the authors did not 

report any formal statistical 

comparisons, the extremely high ageadjusted 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 

59330 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/

m3; in the grinding department between 

6 and 165 μg/m3; in the drying and 

sacking department between 6 and 178 

μg/m3; and in the sacks marking 

department more than 2000 μg/m3. 

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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 nonwhite 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 μg airborne chromium/m3 for 

the high exposure category, between 500 

and 2000 μg airborne chromium/m3 and 

less than 100 μg airborne chromium/m3

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 expectations 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 followup 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 nonwhite 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 μg g/m 3 for 

‘‘exposed’’ jobs and >2000 μg /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 

59332 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μm) 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 μm) 

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/exhibit No. Study population Reference population Chromium (VI) exposure Lung cancer risk 

Sorahan & Harrington (2000, 

Ex. 35–62).

Royle (1975, Ex. 7–49) 

920 male platers employed in 

54 plants in Yorkshire, UK 

for a minimum of three 

months between 1969 and 

1972; follow up through 

1997.

—Mortality rates for the general population of England 

and Wales.

—Age-, sex-matched comparison group unexposed to 

CR(VI). 

—Chromic acid mist with some 

nickel and cadmium co-exposure.

—Cr(VI) levels in 1970 reported to range from <30 μg/

m3 to >100 μg/m3. 

—O/E of 1.85 (p=0.001) based 

on 60 deaths and general 

pop. 

—O/E of 1.39 (p=0.06) based 

on unexposed comparison 

group. 

—No upward trend w/duration 

of exposure. 

Sorahan et al. (1998, Ex. 35–

271).

Sorahan et al. (1987, Ex. 7–

57). 

1,762 platers employed for a 

minimum of six months between 1946 and 1975 from a 

Midlands, UK plant; follow 

up through 1995.

—Mortality rates for the general population of England 

and Wales.

—Chromic acid mist with nickel 

co-exposure.

—No reported Cr(VI) exposure 

levels. 

—O/E of 1.6 (p<0.01) for male 

chrome bath workers based 

on 40 deaths. 

—O/E of 0.66 (NS) for other 

chrome 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. Coexposure 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 watersoluble 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. 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 μg/m3. 

The two exceptions were large plants, 

and in both the chromic acid levels 

exceeded 100 μg/m3. 

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 

59334 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

lung and bronchus and the duration of 

nickel bath employment. In the followup 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 μg/m3 (range of 1–

50 μg/m3) as chromic acid near the baths 

and 3 μg/m3 (range of 0–12 μg/m3) 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.

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59335

TABLE VI–4.– SUMMARY OF SELECTED EPIDEMIOLOGIC STUDIES OF LUNG CANCER IN WORKERS EXPOSED TO

HEXAVALENT CHROMIUM—STAINLESS STEEL WELDING

Reference/Exhibit No. Study population Reference population Chromium (VI) exposure Lung cancer risk 

Moulin (1997, Ex. 35–285) ...... Meta analysis of epidemiological studies of lung cancer 

risk among welders in five 

categories including stainless steel welding and mild 

steel welding.

Stainless steel welding cohort 

studies: Simonato et al., 

1991; Polednak et al., 1981 

case control studies: Hull et 

al., 1989; Gerin et al., 1984; 

Kjuus et al. 1986.

Stainless steel welders exposed to higher Cr(VI) than 

mild steel welders.

—RR of 1.50 (p<0.05) for 

stainless steel welders 

based on combined 114 

deaths from five studies 

—RR of 1.50 (p<0.05) for mild 

steel welders based on combined 137 deaths from four 

studies. 

Sjogren et al. (1994, Ex. 7–

113).

Meta analysis of epidemiological studies of exposure to 

stainless steel welding 

fumes and lung cancer.

Stainless steel welding cohort 

studies: Moulin et al., 1993; 

Sjogren et al., 1987 case 

control studies: Lauritsen et 

al., 1996; Gerin et al., 1984; 

Kjuus et al. 1986.

Cr(VI) exposure was not part 

of the analysis.

RR of 1.94 (p<0.05) for stainless steel welders based on 

combined 70 deaths from 

five studies. 

Simonato et al. (1991, Ex.7–

114).

Gerin et al. (1993, Ex. 35–220) 

Cohort of 11,092 male welders 

from 135 companies in nine 

European countries. Cohort 

entrance criteria varied by 

country.

Age and sex specific mortality 

rates computed using the 

WHO mortality data bank.

Avg cumulative Cr(VI) exposures estimated between 

0.05 to 1.5 mg/ m3-yr based 

on job process matrix.

—O/E of 1.23 (NS) for primarily stainless steel welders based on 20 deaths. 

—Upward trend (p<0.05) with 

time since first exposure. 

—No trend with cumulative exposure 

Moulin et al. (1993, Ex. 7–92) Cohort of 2,721 French male 

welders from 13 factories 

with a minimum of one year 

of employment from 1975 to 

1988.

6,683 unexposed manual 

workers from 13 factories 

with a minimum of one year 

of employment from 1975 to 

1988.

—Primarily manual metal arc 

welding.

—Cr(VI) exposures not recorded 

—O/E of 1.03 (NS) for primarily stainless steel welders based on 2 deaths. 

—No trend with exposure duration. 

Hansen et al. (1996, Ex. 35–

247).

Cohort of 10,059 male welders 

and other steel workers from 

79 Danish companies employed for a minimum of one 

year between 1964 and 

1984.

National cancer incidence 

rates from the Danish Cancer Registry.

Cr(VI) exposure not recorded .. —O/E of 2.38 (NS) for stainless steel only welders 

based on 5 deaths. 

No trend with exposure duration. 

Lauritsen et al. (1996, Ex. 35–

291).

Nested case-control study of 

94 lung cancer deaths from 

Hansen study.

439 eligible controls who were 

not cases and did not have 

respiratory disease or unknown malignancy as cause 

of death.

Cr(VI) exposure not recorded .. —OR of 1.3 (NS) for stainless 

steel only welders. 

—No trend with exposure duration. 

Sjogren et al. (1987, Ex. 795) Cohort of 234 male stainless 

steel welders and 208 male 

railway track welders. Minimum employment was 5 

years between 1950 and 

1965. Follow-up through 

1984.

Mortality rates for Swedish 

males.

Median Cr level for stainless 

steel welding was 57 μg/m3

and for gas shielded welding 

[railway welders] was 5 μg/

m3 in Sweden during 1975.

—O/E of 2.5 (NS) for 

stainlesssteel welders based 

on 5 deaths. 

—O/E of 0.3 (NS) for railway 

welders based on 1 death. 

Kjuus et al. (1986, Ex. 7–72) ... A hospital-based case-control 

study of 176 male incident 

lung cancer cases admitted 

to two hospitals in Norway 

during 1979–1983.

186 controls admitted to the 

same hospitals in Norway 

during 1979–1983 and 

matched to cases for age +/-

5 years.

Cr(VI) exposure not recorded .. —OR of 3.0 (p <0.05, adjusted 

for smoking) for stainless 

steel welding based on 16 

deaths. 

—Welding not significant in logistic model with smoking, 

asbestos. 

Hull, et al. (1989, Ex. 35–243) Case-control study of 85 lung 

cancer cases in white male 

welders identified through 

the LA County tumor registry 

(1972–1987).

Controls were 74 welders with 

non-pulmonary malignancies.

No direct Cr(VI) exposure 

measurements recorded.

—OR of 0.9 (NS) for stainless 

steel welding based on 34 

cases. 

—OR of 1.3 (NS) for manual 

metal arc welding on 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 

μg CrO3/m3 (57 μg/m3 measured as 

CrVI). The highest concentration was 

750 μg CrO3/m3 (390 μg/m3 measured as 

CrVI) found in welding involving coated 

electrodes. For gas-shielded welding, 

the median Cr(VI) concentration was 10 

μg CrO3/m3 (5.2 μg/m3 measured as 

CrVI) with the highest concentration 

measured at 440 μg CrO3/m3 (229 μg/m3

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; 

59336 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 fiftynine 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 nonstatistically 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 

μg-years/m3 Cr(VI) exposure; the lung 

cancer SMR for those in the <0.5 μgyears/m3 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 μg-years/m3 Cr(VI) 

exposure) based upon nine cases and 

191 (<0.5 μg-years/m3 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/m3

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/

m3) 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/m3 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 hospitalbased 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 metaanalysis 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 populationbased studies, case-control studies and 

59338 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 coexposure 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/Exhibit No. Study population Reference population Chromium (VI) exposure Lung cancer risk 

Axelsson et al. (1980, Ex. 7–

62).

1932 Swedish males employed 

at least one year in a 

ferrochromium between 

1930 to 1975.

Swedish county mortality and 

incidence rates.

‘‘Recent’’ job-specific Cr(VI) 

levels estimated at 10 to 250 

μg/m3.

—O/E of 0.7 (NS) for 

ferrochromium workers 

based on 5 cases. 

—No trend with job-specific 

Cr(VI). 

Langard et al. (1990, Ex. 7–37) 1235 males employed at least 

one year who started working prior to 1965 in a Norway ferrochromium plant. 

Follow-up was through 1985.

—Norwegian Cancer Registry

—Subcohort of ferrosilicon 

workers at same plant not 

exposed to Cr(VI). 

Avg total Cr exposure was 50 

μg/m3 in 1975 with 11 to 

33% soluble Cr(VI).

—O/E of 1.5 (NS) for 

ferrochromium workers 

based on 10 cases. 

—O/E of 0.3 for ferrosilicon 

workers based on 2 cases. 

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/m3 of 

total chromium. At the charge floor the 

mean concentration of total chromium 

was 0.05 mg/m3, 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/

m3. Cr(VI) was also present in certain 

operations with estimated levels ranging 

from 0–0.25 mg/m3. The highest 

exposure to Cr(VI) was in the arcfurnace operations. Cr(VI) exposure also 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59339

occurred in a chromate reduction 

process during chromium alum 

production from 1950–1956. Asbestoscontaining 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/Exhibit No. Study population Reference population Chromium (VI) exposure Lung Cancer risk 

Alexander et al. (1996, Ex. 31–

16–3).

2429 aerospace workers with a 

minimum six months employment in Washington 

State from 1974 to 1994. 

Median age at end of study 

was 42 years with median 9 

years follow-up.

Incidence rates from regional 

cancer surveillance system 

registry.

Painters/sanders exposed to 

zinc strontium and lead 

chromates.

Platers/tank tenders exposed 

primarily to chromic acid Median cumulative chromate 

exposure between 0.01 and 

0.18 mg/m3-yr based on 

1974 to 1994 data. 

—O/E of 0.8 (NS) for aerospace cohort based on 15 

deaths. 

—No clear trend with chromate 

exposure. 

Boice et al. (1999, Ex. 31–16–

4).

77,965 workers employed for 

minimum of one year in California aircraft manufacturing 

plant on or after 1960. Follow-up through 1996.

Mortality rates for white population of California and for 

non-white U.S. population.

8 percent of cohort had potential for routine Cr(VI) exposure as painters and platers.

No Cr(VI) exposure levels reported. 

—O/E of 1.02 (NS) for workers 

with routine Cr(VI) exposures based on 87 deaths. 

—Upward trend (NS) with duration of exposure. 

—O/E of 0.71 (p<0.05) for nonfactory workers. 

Observed/Expected (O/E) 

Relative Risk (RR) 

Not Statistically Significant (NS) 

Odds Ratio (OR) 

59340 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/m3 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. 

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

59342 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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

Compound Route Sex/species/strain (# in exposed groups) 

Dose administered 1 and 

observation periods Tumor incidence Reference/exhibit # 

Chromic acid (Chromium 

trioxide).

Inhalation .................. Female ICR mice (50 per 

exposed group.

3.6 mg Cr(VI)/m3 for 30 

min per day, 2 d/wk up 

to 12 mo. 

Histopatholoical evaluation at periods up to 18 

mo.

—Lung tumors: 7/48 vs 2/

20 for control.

—5 benign adenomas and 

2 adenocarcinomas. 

Adachi et al. (1986, 

Ex. 35–26–1). 

Inhalation .................. Female C57BL mice (23 

examined at 12 mo; 20 

examined at 18 mo).

1.8 mg Cr(VI)/m3 120 min 

2 x week for 12 months; 

Histopatholoical evaluation at 12 and 18 mo.

Nasal papilloma: 6/20 

(<0.05) at 18 mo; Lung 

adenoma: 1/20 (NS) at 

18 mo.

Adachi (1987, Ex. 

35–219). 

Intrabronchial ............ Male/female Porton-Wistar 

rats (50 per exposed 

group).

1.0 mg Cr(VI) as single 

dose mixed w cholesterol in steel pellet and 

evaluated at 2 years.

Bronchial carcinoma (M/F 

combined): 2/100 (N.S.).

Levy et al. (1986, Ex. 

11–2). 

Sodium dichromate ............ Inhalation .................. Male Wistar rats (20 per 

exposed group).

0.025, 0.050 and 0.10 mg 

Cr(VI)m3 22–23 hr/day, 7 

d/wk for 18 months; 

evaluated at up to 30 

months.

Lung tumors: 0.025 mg/

m3—0/18; 0.05 mg/m3—

0/018; 0.1 mg/m3—3/

19(NS).

Glaser et al. (1986, 

Ex. 10–11). 

Intrabronchial ............ Male/female Porton-Wistar 

rats (50 per exposed 

group).

0.8 mg Cr(VI) as a single 

dose mixed w cholesterol in steel pellet and 

evaluated at 2 years.

Bronchial carcinoma (M/F 

combined): 1/100 (NS).

Levy et al. (1986, 11–

2). 

Intratracheal .............. Male/female Sprague 

Dawley rats (40 per exposed group).

5 x weekly: 0.0034, 0.017, 

0.086 mg Cr(VI)/kg bw 

for 30 mo; 1 x weekly: 

0.017, 0.086, 0.43 mg 

Cr(VI)/kg bw for 30 mo.

Lung tumors (M/F combined)— 5 x weekly: 0/

80 in all groups; 1 x 

weekly: 0.017 mg/kg–0/

80; 0.086 mg/kg–1/80; 

0.043 mg/kg–14/80 

(p<0.01).

Steinhoff et al. (1986, 

Ex. 11–7). 

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 μg Cr(VI)/m3 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. 

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

μg/m3) 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/

m3 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/

m3 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 PortonWistar 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.

59344 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

TABLE VI–8: SUMMARY OF SELECTED CARCINOGENICITY STUDIES IN EXPERIMENTAL ANIMALS ADMINISTERED HEXAVALENT

CHROMIUM—SLIGHTLY WATER SOLUBLE CHROMATES

Compound Route Sex/species/strain (# in exposed groups) 

Dose administered 1 and 

observation periods Tumor incidence Reference/exhibit 

Calcium chromate .............. Inhalation .................. Male/female C57BL/6 mice 

(136 per group).

4.3 mg Cr(VI)/m3, 5 hr/d, 

5d/wk over animal lifetime.

Lung adenoma (M/F combined): 14/272 vs 5/272 

for controls.

Nettesheim et al.

(1971, Ex. 10–8). 

Intrabronchial ............ Male/female Porton-Wistar 

rats (100 per group).

0.67 mg Cr(VI) as a single 

dose mixed w cholesterol in steel pellet and 

evaluated at 2 years.

Bronchial carcinoma (M/F 

combined): 25/100 

(p<0.01).

Levy et al. (1986, Ex. 

11–2). 

Intratracheal .............. Male/female Sprague 

Dawley rats (40 per 

group).

5 x weekly: 0.083 mg 

Cr(VI)/kg bw for 30 mo; 

1 x weekly: 0.41.mg 

Cr(VI)/kg bw for 30 mo.

Lung tumors (M/F combined)—5 x weekly: 

0.083 mg/kg-6/80 

(p<0.01); 1 x weekly: 

0.41 mg/kg-13/80 

(p<0.01).

Steinhoff et al. (1986, 

Ex. 11–7). 

Intratracheal .............. Male Sprague Dawley rats 

(50 per exposed group).

0.67 mg Cr(VI)/kg bw x 13 

installations over 20 wks 

and evaluated at 2 to 2.5 

yr.

Lung tumors: 1/44 (NS) ..... Snyder et al. (1997, 

Ex. 31–18–12). 

Strontium chromates (two 

different compounds).

Intrabronchial ............ Male/female Porton-Wistar 

rats (50 per exposed 

group).

0.48 mg Cr(VI) as a single 

dose mixed w cholesterol in steel pellet and 

evaluated at 2 years.

Bronchial carcinoma (M/F 

combined): 43/99 & 62/

99 (p<0.01).

Levy et al. (1986, Ex. 

11–2). 

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/m3 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 × 1.25 mg/kg and 5 ×

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 SpragueDawley 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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%; CrO4, 

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

Compound Route Sex/species/strain (# in exposed groups) 

Dose administered 1 and 

observation periods Tumor incidence Reference/exhibit # 

Zinc chromates (three different compounds).Intrabronchial ............ Male/female Porton-Wistar 

rats (50 per exposed 

group).

0.42 to 0.52 mg Cr(VI) as 

a single dose mixed w 

cholesterol in steel pellet 

and evaluated at 2 years.

Bronchial carcinoma (M/F 

combined): 3/61 

(p<0.05), 5/100 (p<0.05), 

3/100 (p=0.07).

Levy et al. (1986, Ex. 

11–2); Levy and 

Venitt (1986, Ex. 

11–12). 

Zinc tetroxychromate ......... Intrabronchial ............ Male/female Porton-Wistar 

rats (50 per exposed 

group).

0.18 mg Cr(VI) as a single 

dose mixed w cholesterol in steel pellet and 

evaluated at 2 years.

Bronchial carcinoma (M/F 

combined): 1/100 (NS).

Levy et al. (1986, Ex. 

11–2). 

Lead chromates (seven different compounds).Intrabronchial ............ Male/female Porton-Wistar 

rats (50 per exposed 

group).

0.25 to 0.32 mg Cr(VI) as 

single dose mixed w 

cholesterol in steel pellet 

and evaluated at 2 years.

Bronchial carcinoma (M/F 

combined): 0–1/100 

(N.S.).

Levy et al. (1986, Ex. 

11–2). 

Lead chromates (three different compounds).Subcutaneous ........... Male/female Sprague 

Dawley rats (20 per exposed group).

1.5 to 4.8 mg Cr(VI) as a 

single dose in water and 

evaluated after 2 years.

Sarcomas at injection site 

(M/F combined): 26–36/

40 vs 0/40 for controls.

Maltoni et al. (1974, 

Ex. 8–25); Maltoni 

(1976, Ex. 5–2). 

Lead chromate ................... Intramuscular ............ Male/female Fischer 344 

rats (25 per exposed 

group).

1.29 mg Cr(VI) in 

trioctyanoin 1 x mo for 9 

mo and evaluated at up 

to 2 yr.

Sarcomas at injection site 

(M/F combined): 31/47 

vs 0/44 for controls.

Furst et al. (1976, Ex. 

10–2). 

Female NIH-Swiss mice 

(25 per exposed group).

0.72 mg Cr(VI) in 

trioctyanoin 1 x mo for 4 

mo and evaluated at up 

to 2 yr.

Sarcomas at injection site: 

0/22 (NS).

Barium chromate ............... Intrabronchial ............ Male/female Porton-Wistar 

rats (50 per exposed 

group).

0.37 mg Cr(VI) as a single 

dose mixed w cholesterol in steel pellet and 

evaluated at 2 years.

Bronchial carcinoma (M/F 

combined): 0/100 (NS).

Levy et al. (1986, Ex. 

11–2). 

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 

59346 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

among guinea pigs or rabbits. Twentyone 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% CrO3 dosed animals at 110 weeks 

and 17/40 in 40% CrO3 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% CrO4; 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% 

CrO3; 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 μm) 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 μM 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 cellenhanced 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 μg/cm2) 

or soluble sodium chromate (10 μM) 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 

59348 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 dosedependence 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 μg/cm2) and 

soluble sodium chromate (1.3 μM) 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 nonenzymatically 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 

(O2) to form Cr(V)-NADPH complexes. 

During the reaction, O2 undergoes one 

electron reduction to the superoxide 

radical (O2

¥) which produces hydrogen 

peroxide (H2O2) through the action of 

the enzyme superoxide dismutase. The 

Cr(V)-NADPH can then react with H2O2

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–kB, 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 

O2-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 H2O2 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. 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 routespecific 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 guaninespecific 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 H2O2 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 O2-free atmosphere, 

catabolism of H2O2 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 H2O2 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) 

59350 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 alkalilabile 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 μM) 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 

μM) 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 μM) 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 G1/S phase of the cell 

cycle (Ex. 35–188). Zhang et al. 

described a dose-dependent increase in 

growth arrest at the G2/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 μM (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 

μM 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 μM 

(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 

μM 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 waterinsoluble 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 μg/m3) than for 

water-soluble Cr(VI) compounds (50

μg/m3). 

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 

59352 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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) exposurecancer 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 μg/m3. 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 

μg/m3) and a high exposure group (24 

workers exposed to eight-hour time 

weighted average levels above 2 μg/m3). 

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 μg/m3/

day to peak levels of 46 μg/m3/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 μg/m3

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 μg/m3 to 20 μg/

m3, 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 μg/m3 to 11 μg/m3. No one exposed 

to levels below 1 μg/m3 (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 μg/m3 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 μg/m3 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 nickelchromium, 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 

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

μg/m3 ± 35 μg/m3, ranging from 0.1 μg/

m3 ¥ 119 μg/m3) 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 ± 0.10 μg/m3) 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 μg/m3 (range from 

non-detectable to 9.1 μg/m3). 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 μg/m3, with an 

average of 4 μg/m3. 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 

μg/m3, but less than 600 μg/m3 (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 μg/m3; range from 0.7 to 

168.3 μg/m3). 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 

μg/m3 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 μg/

m3 to 728 μg/m3. 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/m3 (i.e., 30 

μg/m3). 

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 μg/m3. 

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. 

59354 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg of Cr(VI)/m3 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 chromateproducing 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 μg/m3. 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)/m3 for 120 minutes per day, 

twice a week and 3.63 mg Cr(VI)/m3 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)/m3 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-yearold 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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/m3. 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 

59356 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

inhalation to 25–200 μg Cr(VI)/m3 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 μg/

m3 groups after the 90-day exposure 

period. They also found that 28-day 

exposure to levels of 25 and 50 μg/m3

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 

μg/m3. 

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 μg Cr(VI)/m3 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 μg Cr(VI)/m3 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 μg Cr(VI)/

m3 or above for 30 days. Most lung 

fibrosis disappeared after the exposure 

period had ceased. At 50 μg Cr(VI)/m3

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 μg Cr(VI)/m3 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 μg Cr(VI)/

m3, 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 μg/

m3. 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–

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 prefabricated 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 μg/m3 Cr(VI) 

(reported as 20 μg/m3 CrO3). 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 

59358 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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±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 

μg/m3 (mean 3.24 μg/m3; SD=2.48 μg/

m3). 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 

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

59360 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/

m3 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 μg/m3 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 semiquantitative 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 shorterterm 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 exposureresponse 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 μg/m3). Since 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 exposureresponse 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/m3¥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 welldefined 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., welldocumented 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 exposureresponse 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±SD = 0.70±2.75) mg/m3 - 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 CrO3/m3 - yr 

(equivalent to 0.21 mg Cr(VI)/m3 - 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 exposureresponse data set comes from a second 

cohort of chromate production workers. 

Luippold et al. studied a cohort of 482 

predominantly white, male employees 

59362 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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±SD = 1.58±2.50) mg Cr(VI)/m3

¥ yr, were generally higher but 

overlapped those of the Gibb cohort. 

Luippold et al. found significant doserelated trends for lung cancer SMRs as 

a function of year of hire, duration of 

employment, and cumulative Cr(VI) 

exposure. The data on exposureresponse 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 personyears 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/m3 ¥ 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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) multicenter historical cohort study (Ex. 7–

114). The IARC cohort included 11,092 

welders for a total of 164,077 personyears. 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 (CrO3). 

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 followup 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 

59364 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 exposureresponse 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 exposureresponse 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 tenyear lags provided better fit to the 

mortality data than lags of zero, two and 

twenty years (Ex. 31–22–11). The crossclassification 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

Cumulative Cr(VI) exposure (μg/

m3Øyears)

Age 

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/m3 - years to μg/m3–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 doserelated 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. Ni = C0 * Ei * exp{kti} * (1 + C1Di

+ C2Di

2) 

E2. Ni = C0 * Ei * (1 + C1Di * exp{kti}) 

E3. Ni = C0 * Ei + (PYi * C1Di)

where Ni is the predicted number of 

lung cancers in ith group PYi is the 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59365

number of person-years for group i; Ei is 

the expected number of lung cancers in 

that group, based on the reference 

population; Di is the mean cumulative 

dose for that group; and C0, C1, C2, and 

k are parameters to be estimated. In 

equations E1 and E2, ti 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 racespecific 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., C0, C1, 

C2, 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 C1, 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., C2

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 goodnessof-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 μg/m3 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 μg/

m3), 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.

59366 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 

Cr(VI) exposure μg/m3-

years) 

Mean Cr(VI) 

exposure 

(μg/m3-yr) 

Personyears 

Observed 

lung cancers 

Expected lung cancers 

Maryland 

rates 

Baltimore 

rates 

Alternative 1: Roughly Equal Observed Cases per 

Group ....................................................................... 0–0.151

0.151–0.686

0.686–2.08

2.08–4.00

4.00–8.32 

0.0246

0.395

1.25

2.96

5.89 

17982

9314

8694

5963

5102 

12

12

12

12

12 

10.3

13.0

10.3

7.38

5.63 

13.37

16.80

13.55

9.42

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 Number of PersonYears per Group ..................................................... 0–0.052

0.052–0.273

0.273–0.65

0.65–1.43

1.43–3.12 

0.00052

0.147

0.455

0.996

2.19 

14282

6361

6278

6194

6395 

4

11

7

11

12 

5.08

9.05

8.71

7.30

8.17 

6.63 

11.58

11.33

9.58

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 ageand 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 

C2Di

2) defined as follows:

E4. Ni = C0 * Ei + PYi * (C1Di + C2Di

2).

The age factor was dropped from model 

E1 because the individual data obviated 

the need to rely on the crossclassifications 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) = h0(t)*exp(b1z + b2D) 

C2. h(t;z;D) = h0(t)*[exp(b1z)][1 + b2D]

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, h0(t) is the baseline 

hazard function (a function of age only), 

b2 is the cumulative dose coefficient, 

and b1 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, C0, 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 (C0 was significantly 

different from its default value, 1), but 

not for the Baltimore city reference 

population (C0 was not significantly 

different from 1). The inclusion of the 

C0 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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/m3-yr for the relative risk model, E1, 

and from 0.0061 to 0.0071 per mg/m3-

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, b2, 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

59368 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/m3, but estimated the lowest 

risks for exposure levels of 10 μg/m3 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 


EP04oc04.000</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 racespecific U.S. lung cancer rates. Their 

background coefficients, C0, 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: Ni = C0 * Ei * exp(C1Di) 

NIOSH1b: Ni = C0 * Ei * exp(C1Di

1⁄2) 

NIOSH1c: Ni = C0 * Ei * exp(1 + C1Di

+ C2Di

2) 

NIOSH1d: Ni = C0 * Ei * (1 + Di)a

NIOSH1e: Ni = C0 * Ei * (1 + C1Di) 

NIOSH1f: Ni = C0 * Ei * (1 + C1Dia)

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 exposureresponse 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 (C1) for the linear 

relative risk model 1e was estimated by 

NIOSH to be 1.444 per mg CrO3/m3-yr. 

(Ex. 33–13, Table 4). If the exposures 

were converted to units of mg Cr(VI)/

m3-yr, the estimated cumulative dose 

coefficient would be 2.78 (95% CI: 1.04 

to 5.44) per mg/m3-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 μg/m3 (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.


EP04OC04.001</GPH>
59370 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 doseresponse 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, C0, (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 μg/m3 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 μg/

m3 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 Baltimorestandardized 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 μg/m3 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 μg/m3) from the 

risk analysis. Moreover, no matter what 

current exposures might be, data on 

higher cumulative exposures are still 

relevant for understanding the doseresponse 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 doseresponse analysis. 

Exponent reported that SMRs for 

workers with ‘‘peak’’ exposures less 

than 0.18 mg CrO3/m3 (0.094 mg Cr(VI)/

m3) 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 sixpart 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)/m3. The 

implication that the data indicate a 

‘‘threshold’’ at 0.094 mg Cr(VI)/m3 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 exposureresponse 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 μg Cr(VI)/m3) 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 μg Cr(VI)/m3 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 ×

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 CrO3/m3

- 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 μg Cr(VI)/

m3 can be calculated after converting 

from CrO3 to Cr(VI). Using the average 

Cr(VI) air concentration (22.5 μg/m3), 

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 

CrO3/m3 - 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 personyears 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 doserelated 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).

59372 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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

Cumulative Cr(VI) exposure (mg/m3 ¥ yrs)a

Mean Cr(VI) 

exposure 

(mg/m3 ¥

yrs)a

Observed 

lung cancers 

Expected 

lung cancersb

Personyears 

< 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/m3 ¥ yrs is 1000 times greater than μg/m3 ¥ 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{kti} 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{kti} term model E2 is the same as 

E1. The background rate parameter, C0, 

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, C1, of the 

linear relative and additive risk models 

were 0.88 per mg/m3 ¥ yr and 0.0014 

per mg/m3 ¥ person-yr, respectively. 

The C1 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 μg Cr(VI)/m3 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 exposureresponse 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

Cumulative Cr(VI) exposure (mg/m3-yrs) a

Mean 

Cr(VI) exposure 

(mg/m3-

yrs) a

Observed 

lung cancers 

Expected 

lung cancer b

Personyears 

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 μg/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/m3-yr for the 

relative risk model and 0.0016 (95% CI: 

0.00098 to 0.0024) per mg/m3—personyr 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 (EC10s) of 52 

μg/m3 (95 percent lower confidence 

bound, LEC10, of 37 μg/m3) and 49 μg/

m3 (LEC10 of 35 μg/m3) for the relative 

risk and additive risk models, 

respectively. The EC10 is an estimate of 

the dose associated with a ten percent, 

or 100 in 1000, risk. The EC10 and its 

LEC10 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 μg/m3). 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 μg Cr(VI)/m3 for a 

working lifetime.

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 yearadjusted 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 × 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)/


EP04OC04.002</GPH>
59374 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

m3-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)/m3-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 μg Cr(VI)/m3

(1.58 × 10 yr ÷ 1000 μg/mg). Using this 

Cr(VI) air concentration (158 μg/m3), 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 μg/

m3). 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/m3-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 μg/m3 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 μg/m3) 

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, nonthreshold 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, 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 personyears. 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., C2 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 μg/m3

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 personyears 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 agegrouped 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 

59376 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

included not only carcinogenic Cr(VI) 

but substantial amounts of noncarcinogenic 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/m3) 

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 μg/m3) 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 μg/m3

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 exposureresponse 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 

μg Cr(VI)/m3 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 

μg/m3 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 μg Cr(VI)/m3 (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 personyears per age and exposure category, 

were calculated for all groups 

combined. The average total chromium 

exposure level was multiplied by oneseventh (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 μg/m3 of Cr(VI) for a 

lifetime. The CDHS chose the 95 percent 

upper confidence limit of 0.15 per μg 

Cr(VI)/m3 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 

μg/m3) 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. 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 m3/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 μg/

m3 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 exposureresponse 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)/m3-yr with a 90% 

confidence bound of between 0.45 and 

1.1 per mg Cr(VI)/m3-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 μg/m3) to be 88 

lung cancer cases per 1000 workers 

(95% CI: 61 to 141). For 1 μg/m3, 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 μg/m3) 

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 C0, to fit the data. 

They reported that the maximum 

likelihood estimate for the dose 

coefficient was 0.13 per mg/m3-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 multicenter 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) exposurerelated effect on lung cancer mortality. 

This may be explained by the 

59378 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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/m3-yr 

was assumed for the highest exposure 

group (e.g., >0.5 mg/m3-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 exposurerelated 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 μg Cr(VI)/m3 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 followup) 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 μg/m3

chromate TWA-years’’ (Ex. 31–16–3, p. 

1254). For their analysis, Environ 

assumed that the cumulative exposures 

were expressed in μg/m3-yr of Cr(VI), 

rather than chromate (CrO4

-2) or 

chromic acid (CrO3). 

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 chromateexposed 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/m3 - 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)/m3 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 (CrO4

-2) 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.

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59379

TABLE VII–8.—OSHA ESTIMATES OF EXCESS LUNG CANCER CASES PER 1000 WORKERSa EXPOSED TO VARIOUS EIGHT

HOUR TWA CR(VI) WITH 95 PERCENT CONFIDENCE INTERVAL COMPARISONS BY COHORT

Cr(VI) (μg/m3)

Best estimates of 

riskb

95% confidence interval on risk estimates by cohortc

Featured cohorts Supporting cohorts

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 

aThe 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. bOSHA 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. cThe 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 μg/m3 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 μg/m3 are about 10 

to 45 cases per 1000 workers and 

estimates at 0.5 μg/m3 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 coexposures 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 exposureresponse 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

59380 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 μg/m3) than for some of the 

lower exposure scenarios (e.g., 0.25 to 

2.5 μg/m3) 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 + bdC)

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 exposureresponse 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 exposurespecific 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 μg/m3). 

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 

59382 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 logquadratic 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 exposureresponse 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/m3¥yr (i.e.,

0.25¥52 μg/m3 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/m3¥yrs (e.g., 2.5 μg/m3 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/m3¥yr (e.g., roughly 

equivalent to 20 μg/m3 TWA for a 45 

year working lifetime) and below ‘‘a 

highest reported eight hour average’’

Cr(VI) concentration of 52 μg/m3 (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)/m3¥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 

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

59384 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 nonwhites 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, exposureresponse 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 watersoluble 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 watersoluble 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 watersoluble 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 

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

59386 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 exposureresponse 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 

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

59388 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 doseresponse 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 μg/m3 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 μg/m3

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) 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 ‘riskfree’ ’’, 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 lifethreatening 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 lifethreatening 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 

μg/m3 (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, 

59390 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 nationallevel 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 exposureresponse. 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 

μg/m3. 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 μg/m3 or 

those exposed to 8-hour average 

concentrations less than 2 μg/m3, a 

result used by the EPA to identify a 

lowest-observed adverse effect level 

(LOAEL) for their inhalation reference 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 μg/m3 and 

those with peak exposures less than 20 

μg/m3 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 crosssectional 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 μg/m3 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 μg/m3 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,

μg/m3

20-year

exposure

45-year

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 μg/

m3 Cr(VI) have about ten times the risk 

of workers exposed for 20 years to 1 μg/

m3 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 onefourth 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 μg/m3 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

59392 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/m3 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 μg/m3

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 μg/m3 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 μg/

m3 is expected to significantly reduce 

risks to workers in Cr(VI)-exposed 

occupations. OSHA additionally finds 

that nasal septum ulceration and 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 μg/m3 to 1 μg/m3 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: 

• Identify the establishments and 

industries potentially affected by the 

proposed rule; 

• Estimate current exposures and the 

technologically feasible methods of 

controlling these exposures; 

• 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; 

• Evaluate the costs and economic 

impacts that establishments in the 

regulated community will incur to 

achieve compliance with the proposed 

standard; 

• Assess the economic feasibility of 

the rule for affected industries; and 

• 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 μg/m3 measured as an 8-hour time 

weighted average. OSHA has also 

examined alternative PELs ranging from 

20 μg/m3 to 0.25 μg/m3 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: 

• Monitor the exposure of employees 

(except in shipyards and construction); 

• Establish regulated areas when 

exposures may reasonably be expected 

to exceed the PEL (except in shipyards 

and constructions); 

• Implement engineering and work 

practice controls to reduce employee 

exposures to Cr(VI); 

• 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; 

• Provide other protective clothing 

and equipment as necessary for dermal 

protection; 

• Make industrial hygiene facilities 

(hand washing stations) available in 

some situations; 

• 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); 

• Train workers about the hazards of 

Cr(VI) (including elements already 

required by OSHA’s Hazard 

Communication Standard); and 

• 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 

59394 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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.

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59395


EP04OC04.003</GPH>
59396 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.004</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59397


EP04OC04.005</GPH>
59398 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.006</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59399


EP04OC04.007</GPH>
59400 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.008</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59401


EP04OC04.009</GPH>
59402 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.010</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59403

Various types of welding applications 

account for the greatest number of 

establishments and number of employees affected by the proposed 

standard. 


EP04OC04.011</GPH>
59404 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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.

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59405


EP04OC04.012</GPH>
59406 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 


EP04OC04.013</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 μg/m3, 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 μg/m3 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 μg/m3 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.

59408 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.014</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59409

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 


EP04OC04.015</GPH>
59410 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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.

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59411


EP04OC04.017</GPH>
59412 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.016</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59413

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 


EP04OC04.018</GPH>
59414 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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,

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59415

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.


EP04OC04.019</GPH>
59416 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.020</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59417


EP04OC04.021</GPH>
59418 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.022</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59419

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 


EP04OC04.023</GPH>
59420 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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.

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59421


EP04OC04.024</GPH>
59422 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.025</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59423


EP04OC04.026</GPH>
59424 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.027</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59425


EP04OC04.028</GPH>
59426 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.029</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59427


EP04OC04.030</GPH>
59428 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/m3, 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 (μg/3m) 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 


EP04OC04.031</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 (μg/m3) 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 μg/

m3, 0.5 μg/m3, 1.0 μg/m3, 5.0 μg/m3, 

10.0 μg/m3 and 20.0 μg/m3. 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 μg/m3. 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 μg/m3 and regular short-term 

exposures e.g. an hour or so) were below 

10 μg/m3. Less than 10 percent of 

workers could reasonably be expected to 

experience nasal tissue damage at a 

TWA Cr(VI) below 2 μg/m3 [and shortterm exposures below 10 μg/m3]. It 

appears likely that nasal damage might 

be avoided completely if all Cr(VI) 

[short-term and full shift] exposures 

were kept below 1 μg/m3. 

OSHA estimates that 5,387 nasal 

perforations/ulcerations occur annually 

59430 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

under the current PEL. All of these are 

expected to be prevented under the 

proposed PEL of 1 μg/m3. 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 (μg/m3 ) 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‰10 10‰5 5‰1 1‰0.5 0.5‰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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59431

TABLE IX–12.—INCREMENTAL BENEFITS, COSTS, NET BENEFITS AND COST PER CANCER AVOIDED—Continued

20‰10 10‰5 5‰1 1‰0.5 0.5‰0.25 

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 μg/m3

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 μg/m3 to 20 μg/m3 (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 μg/

m3) 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 μg/m3 to 50 μg/m3). (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.

59432 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 


EP04OC04.032</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59433


EP04OC04.033</GPH>
59434 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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).


EP04OC04.034</GPH>
Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59435

Table IX–14.—Unit Costs Applied in OSHA’s Preliminary Analysis of the Proposed Standard

Cost description Basis Base cost 

Escalation 

factor (October 2003 

basis) 

Index used for 

price escalation Unit cost 

Cost per hour for an outside industrial 

hygiene contractor.

Estimate by In-house CIH .................... $90.00 1 NONE ............... $90.00 

Cost of a personal sampling pump ....... Gilian 3500; Sensidyne, 16333 

Bayvista Drive, Clearwater, FL 

33760.

680.00 1 NONE ............... 680.00 

Variable Cost per sample (e.g., laboratory analysis).Estimate by In-house CIH .................... 60.00 1 NONE ............... 60.00 

Flat Fee For Training Course ................ Estimate by In-house CIH. ................... 400.00 1 NONE ............... 400.00 

Cost of a calibration unit ....................... GILIBRATOR–2; Sensidyne, 16333 

Bayvista Drive, Clearwater, FL 

33760.

1,075.00 1 NONE ............... 1,075.00 

Unit cost of OSHA-regulation warning 

signs with mounting materials.

July 1993 EMMED Co, Inc. Catalog .... 3.03 1.2702 CPI—All items .. 3.84 

Cost of materials per qualitative fit-testing.Banana Oil Fit Test Kit; Lab Safety 

Supply Catalog 2003, PO Box 1368, 

Janesville, WI 53547–1368.

0.07 1 NONE ............... 0.07 

Unit cost per worker for an air-supplied 

respirator.

Allegro One-Worker Full Face Kit; Lab 

Safety Supply Catalog 2003, PO Box 

1368, Janesville, WI 53547–1368.

1,473.33 1 NONE ............... 1,473.33 

Unit cost per employee for a full-face 

respirator.

MSA Ultra Twin Full Face Respirator; 

Lab Safety Supply Catalog 2003, PO 

Box 1368, Janesville, WI 53547–

1368.

243.00 1 NONE ............... 243.00 

Unit cost per employee for a half-mask 

respirator.

MSA Comfro Classic Half-Mask Respirator; Lab Safety Supply Catalog 

2003, PO Box 1368, Janesville, WI 

53547–1368.

35.30 1 NONE ............... 35.30 

Cost of replacement cartridges cartridges per mask).MSA P100 Filter (2 Cartridge: Lab 

Safety Supply Catalog 2003, PO Box 

1368, Janesville, WI 53547–1369.

13.74 1 NONE ............... 13.74 

Unit cost per employee for a blasting 

helmet air-supplied respirator.

Allegro Three Person Air Pump, 

Bullard 1/2′′ Hose, 100′L, Bullard 

Helmet w/ constant air flow; Lab 

Safety Supply Catalog 2003, PO Box 

1368, Janesville, WI 53547–1368.

1,164.00 1 NONE ............... 1,164.00 

Cost of materials to clean one respirator.Respirator Cleaning/Storage Kit; Lab 

Safety Supply Catalog 2003, PO Box 

1368, Janesville, WI 53547–1368.

1.86 1 NONE ............... 1.86 

Cost of PE coated Tyvek coveralls ....... KAPPLER Poly-Coat Coveralls; Lab 

Safety Supply Catalog 2003, PO Box 

1368, Janesville, WI 53547– 1368.

6.60 1 NONE ............... 6.60 

Cost of Saranex coveralls ..................... Tychem QC Coveralls; Lab Safety 

Supply Catalog 2003, PO Box 1368, 

Janesville, WI 53547–1368.

32.85 1 NONE ............... 32.85 

Cost of Tyvek coveralls ......................... Tyvek Protective Wear Coveralls; Lab 

Safety Supply Catalog 2003, PO Box 

1368, Janesville, WI 53547–1368.

4.50 1 NONE ............... 4.50 

Cost of bib aprons ................................. Polypropylene Bib Apron; Lab Safety 

Supply Catalog 2003, PO Box 1368, 

Janesville, WI 53547–1368.

0.58 1 NONE ............... 0.58 

Cost of laundering uniforms for one 

employee per week.

Aramark Cincinnati Representative ...... 5.50 1 NONE ............... 5.50 

Cost of laundering uniforms for one 

employee per week.

Aramark Cincinnati Representative ...... 3.75 1 NONE ............... 3.75 

Cost of clear indirect vent goggles ........ Lab Supply Catalog 2003, PO Box 

1368, Janesville, WI 53547–1368.

6.00 1 NONE ............... 6.00 

Cost of clear lens safety glasses .......... Lab Supply Catalog 2003, PO Box 

1368, Janesville, WI 53547–1368.

5.00 1 NONE ............... 5.00 

Cost of grey lens safety glasses ........... Lab Supply Catalog 2003, PO Box 

1368, Janesville, WI 53547–1368.

5.00 1 NONE ............... 5.00 

Cost of lined nitrile gloves ..................... Ansell Sol-Vex Flock Lined Nitrile 

Gloves; Lab Safety Supply Catalog 

2003, PO Box 1368, Janesville, WI 

53547–1368.

2.50 1 NONE ............... 2.50 

Cost of powder surgical nitrile gloves ... N-Dex 4-mil powdered disposable 

Nitrile Lab Gloves; Lab Safety Supply Catalog 2003, PO Box 1368, 

Janesville, WI 53547–1368.

0.24 1 NONE ............... 0.24 

59436 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

Table IX–14.—Unit Costs Applied in OSHA’s Preliminary Analysis of the Proposed Standard—Continued

Cost description Basis Base cost 

Escalation 

factor (October 2003 

basis) 

Index used for 

price escalation Unit cost 

Cost of rough PVC gloves ..................... BEST Super Flex PVC-gloves Coated 

Gloves; Lab Safety Supply Catalog 

2003, PO Box 1368, Janesville, WI 

53547–1368.

4.10 1 NONE ............... 4.10 

Unit cost of change rooms per employee.Based upon Means Square Foot 

Costs, 1989.

856.00 1.4742 CPI—All items .. 1,261.92 

Cost per shower head ........................... Based upon Means Square Foot 

Costs, 1989.

3,590.00 1.4742 CPI—All items .. 5,292.39 

Cost per hand washing facility .............. Glacier Bay 4 in Chrome Two Handle 

Bar Faucet, 40 in x 24In. White Double Bowl Utility Tub, 505 E. Kemper 

Rd., Cincinnati, OH 45246—Estimated Installation Cost.

500.00 1 NONE ............... 500.00 

Variable cost per shower (soap, clean 

towel, water, etc.).

Estimate ................................................ 0.50 1 NONE ............... 0.50 

Variable cost per hand washing facility 

(roll paper towels, liquid soap, water).

Kimberly-Clark OnePak Dispenser, 

WINDSOFT Bleached White Paper 

Roll Towels; The Betty Mills Company, 60 East 3rd Ave, Ste 201, San 

Mateo, CA 94401 (2003).

0.06 1 NONE ............... 0.06 

Unit cost of HEPA vacuums .................. CONSAD (1993) base price is 1991 .... 1,580.00 1.4742 CPI—All items .. 2,329.24 

Unit cost of HEPA vacuum replacement 

filters.

CONSAD (1993) base price is 1991 .... 212.00 1.4742 CPI—All items .. 312.53 

Unit cost of garbage bags and disposal Estimate—Including RCRA disposal .... 500.00 1 NONE ............... 500.00 

Full cost of a comprehensive medical 

exam.

1994 Quote from two hospitals. Bethesda Care, Cincinnati, OH and Abington Memorial Hospital, Willow 

Grove, PA.

282.00 1.4211 CPI—Medical 

Care Services.

400.76 

Full cost of a limited medical exam ....... 2003 cost of physical exams in Maryland (as directed by OSHA)..125.00 1 NONE ............... 125.00 

Cost of additional medical testing after 

exam results are abnormal.

Estimated to be equal to cost of limited 

medical exam.

150.00 1.4211 CPI—Medical 

Care Services.

213.17 

Cost of a partial comprehensive medical exam.1994 Quote from two hospitals. Bethesda Care, Cincinnati, OH and Abington Memorial Hospital, Willow 

Grove, PA—Estimated half of comprehensive and/or limited exam cost.

141.00 1.4211 CPI—Medical 

Care Services.

200.38 

Cost of a partial medical exam ............. 1994 Quote from two hospitals. Bethesda Care, Cincinnati, OH and Abington Memorial Hospital, Willow 

Grove, PA—Estimated half of comprehensive and/or limited exam cost.

75.00 1.4211 CPI—Medical 

Care Services.

106.59 

Cost per employee for training aids and 

materials.

Estimate ................................................ 2.00 1 NONE ............... 2.00 

Cost per employee for computer file 

space.

Estimate ................................................ 1.00 1 NONE ............... 1.00 

Cost of Medical History Questionnaire .. OSHA. Preliminary Regulatory Impact 

and Regulatory Flexibility Analysis of 

the Proposed Respiratory Protection 

Standard, 1994. 

25 1.4211 CPI—Medical 

Care Services.

35.53 

Cost of Medical Exam for Respirator 

Use.

OSHA. Preliminary Regulatory Impact 

and Regulatory Flexibility Analysis of 

the Proposed Respiratory Protection 

Standard. 1994. 

75 1.4211 CPI—Medical 

Care Services.

106.58 

Cost of Mop and Bucket ........................ The Home Depot. Contico, 35qt Mop 

Bucket and Wringer. Wilen, 16oz 

Cotton Cut-End Mop.

62.92 1 NONE ............... 62.92 

Cost of Mop ........................................... The Home Depot. Wilen, 16oz Cotton 

Cut-End Mop.

62.92 1 NONE ............... 62.92 

Cost of Mobile Shower Unit (construction).Ameri-can Engineering. Basic 828 Decontamination Trailer. 2003. 15886 

Michigan Road. Argos, IN 46501.

42,960 1 NONE ............... 42,960 

Cost of Change Area per employee 

(construction).

Estimate ................................................ 720 1 NONE ............... 300 

Source: U.S. Dept. of Labor, OSHA, Office of Regulatory Analysis, based on IT, 2004, Ex. 35–390. 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 μg/m3 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 μg/3. 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 μg/m3. 

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 

59438 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 permits, OSHA revise its economic and regulatory flexibility analyses as appropriate to reflect the 

SERs’ comments on underestimation of costs and that the Agency 

compare the OSHA revised estimates to alternative estimates provided and methodologies suggested by the SERs. For those SER 

estimates and methodological suggestions that OSHA does not 

adopt, the Panel recommends that OSHA explain its reasons for preferring an alternative estimate and solicit comment on the issue.

OSHA has extensively reviewed its costs estimates, and changed 

many of them in response to SER comments and solicits comments 

on these revised cost estimates. A few examples of OSHA’s cost 

changes are given in the responses to specific issues, below (e.g., 

medical exams, training and familiarization). 

The Panel recommends that, to the extent time permits, OSHA should 

carefully consider the ability of each potentially affected industry to 

meet any proposed PEL for CR(VI) and solicit comment on the costs 

and technological feasibility of the PEL.

The PEA reflects OSHA’s judgment on technological feasibility and includes responses to specific issues raised by the Panel and SERs. 

OSHA will solicit comment on the accuracy and reasonableness of 

these judgments. 

The Panel recommends that OSHA carefully review the basis for its estimated medical surveillance compliance costs, consider these concerns raised by the SERs, and ensure that its estimates are revised, 

as appropriate and time permits, to fully reflect the costs likely to be 

incurred by potentially affected establishments.

OSHA has increased the estimated time for a limited medical exam 

from 1.5 hours to 3 hours and solicits comment on all other cost projections for medical surveillance. See Chapter IV OF THE PEA; 

COSTS OF COMPLIANCE, COSTS BY PROVISION—Medical Surveillance, for details of OSHA’s unit costs for medical surveillance. 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59439

TABLE IX–15.—SBREFA PANEL RECOMMENDATIONS AND OSHA RESPONSES—Continued

SBREFA panel recommendation OSHA response

The Panel recommends that, as time permits, OSHA consider alternatives that would alleviate the need for extensive monitoring on 

construction sites, and solicit comment on this issue. If OSHA does 

not adopt such alternatives, then OSHA should consider increasing 

the estimated costs of such monitoring in construction, and solicit 

comment on the costs of monitoring.

OSHA revised the standard to relieve Construction and Shipyards from 

requirements for exposure assessment; for General Industry, OSHA 

believes that its unit cost estimates are realistic but will raise that as 

an issue. See CHAPTER IV OF THE PEA: COSTS OF COMPLIANCE, COSTS BY PROVISION—Exposure Monitoring (Initial and 

Periodic), for details of OSHA’s unit costs for exposure monitoring in 

general industry. 

The Panel recommends that OSHA carefully review the basis for its estimated hygiene compliance costs, consider the concerns raised by 

the SERs, and, to the extent time permits, ensure that its estimates 

are revised, as appropriate, to fully reflect the costs likely to be incurred by potentially affected establishments.

OSHA’s proposed standard will permit hand washing as a hygiene option; OSHA’s analysis will also reflect, where data confirm, any cost 

premium related to handling contaminated waste water or laundry, or 

where uncertainty exists, the issue will be raised. 

The Panel recommends that OSHA examine and solicit comment on 

this issue [possible understates in the costs of regulated areas].

OSHA has recognized costs for training and familiarization to cover a 

better 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 and solicit comment on 

these issues [costs of laundering PPE].

OSHA has examined and solicits comment on this issue and the 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 whether its cost estimates 

reflect the full costs of complying with the hazard communication 

standard.

OSHA’s analysis assumes that employers will need time for familiarization with the standard, training on the standard, and increased initial 

supervision. 

The Panel recommends that OSHA thoroughly review the economic 

impacts of compliance with a proposed Cr(VI) standard and develop 

more detailed feasibility analyses where appropriate. The Panel also 

recommends that OSHA, to the extent permitted by time and the 

availability of economic data, reexamine its estimates of profits and 

revenues in light of SER comments, and update economic data to 

better reflect recent changes in the economic status of the affected 

industries, consistent with its statutory mandate. The Panel also recommends that OSHA examine, to the extent feasible with the time 

available, the possibility that users will substitute non-Cr(VI) products 

for Cr(VI) products. The Panel 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.

OSHA has reviewed and revised many of its revenue and profit estimates in the light of specific SER comments. Examples of application groups with revised revenue and profit estimates include Group 

4, Chromate Production; Group 5, Chromate Pigment Producers; 

and Group 17, Chromium Dye Producers. However, OSHA has not 

updated revenue and profit impacts across the board—OSHA estimates of costs, revenues, and profits require consistent data sets 

which are not yet available for more recent years. OSHA’s continues 

to examine, and will solicit comment on this issue. 

The Panel recommends that OSHA consider and solicit comments on 

selective exemption of some industries from the proposed standard, 

especially those industries whose inclusion is not supported by the 

industry-specific data or in which inhalation exposure to Cr(VI) is 

minimal.

OSHA is reluctant to exempt industries where exposures are minimal 

because changes in technology could change exposures in the future. However, OSHA is seeking comment on the issue of the scope 

of the standard and data that would support not covering certain sectors. 

The Panel recommends that OSHA exempt applicators of CCA given 

that they are already regulated by EPA as pesticide 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.

OSHA has decided to exempt applicators of CCA in this proposal. 

The Panel recommends that OSHA clearly explain the way that Cr(VI) 

exposure and risk for the worker cohort studies used in the quantitative risk assessment were calculated, and should consider and 

seek comment as to whether the major assumptions used in these 

calculations are reasonable.

The Quantitative Risk Assessment section of the Preamble addresses 

this issue in detail, and OSHA is seeking comments on this issue. 

The Panel recommends that OSHA consider the available information 

on reduction of inhaled Cr(VI) to Cr(III) in the body, to determine 

whether exposures below a threshold concentration can be shown 

not to cause the genetic 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.

The Quantitative Risk Assessment of this Preamble addresses the 

issue of possible threshold effects and OSHA is seeking comments 

on the issue. 

59440 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

TABLE IX–15.—SBREFA PANEL RECOMMENDATIONS AND OSHA RESPONSES—Continued

SBREFA panel recommendation OSHA response

The Panel recommends that OSHA should clarify the meaning of the 

projected lung cancer risk estimates used to support the proposed 

standard. In particular, OSHA should explain these estimates, which 

are based on a working lifetime of 45 years’ exposure at the highest 

allowable Cr(VI) concentration, and, where appropriate, note projected excess cancers that may result from shorter periods of occupational Cr(VI) exposure.

OSHA is required by law to set health standards so that they avoid significant risk over a working lifetime. Both in the QRA and in the Benefits Chapter of the PEA, OSHA has examined alternative exposure 

scenarios. See VII. Preliminary Quantitative Risk Assessment in 

the Preamble and CHAPTER VI of the PEA; BENEFITS and NET 

BENEFITS, Lung Cancers Avoided in this PEA. 

The Panel recommends that OSHA solicit information to better characterize the exposure patterns and Cr(VI) compounds encountered in 

the maritime environment, and should encourage input from marine 

chemists at appropriate points in the rulemaking.

OSHA has added information provided by firms in the shipyard industry 

since the Panel meeting. (See Chapter II of the PEA; PROFILE OF 

AFFECTED INDUSTRIES, 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 the appropriateness of 

separate PELs for specific Cr(VI) compounds, with attention to the 

weight and extent of the best available scientific evidence regarding 

their relative carcinogenic potency.

OSHA considered this possibility and preliminarily decided against it, in 

part, because it would require lower PELs with many persons in respirators. OSHA is soliciting comment on this issue. 

The Panel recommends that OSHA solicit information to better define 

construction activities likely to be above and below the PEL (for initial 

exposure monitoring purposes) to minimize the amount of respiratory 

protection that would need to be used for compliance.

OSHA has eliminated the requirement for monitoring in the construction industry. OSHA has considered a control banding approach to 

construction, but lacks the data to fully implement this approach, and 

solicits comment on the issue. 

The Panel recommends that OSHA provide a better explanation of how 

to implement an exposure assessment program for construction activities. Also, OSHA should provide further explanation on monitoringrelated topics like the selection of sampling and analytical methods, 

the selection of plus-or-minus 25% as a confidence interval, and the 

use of objective data in lieu of monitoring.

OSHA has removed the requirement for exposure monitoring in construction and shipyards. The monitoring-related topics are further discussed in the Preamble, XVII. Summary and Explanation of the 

Standard.

The Panel recommends that OSHA consider less frequent monitoring 

for exposures above the PEL, especially in situations where the employer has already engineered down to the lowest feasible level and 

is not able to maintain levels below the PEL.

OSHA has preliminarily left the monitoring frequency unchanged, but 

has solicited comment on the issue. 

The Panel recommends that OSHA review the technologies used to reduce Cr(VI) exposure to ensure to ensure that they are available or 

reasonably anticipated to be available in the future.

OSHA has reviewed its technological feasibility analysis and solicited 

comment on it. 

The Panel recommends that OSHA clarify the purpose of the prohibition on the use of employee rotation to meet the PEL and take into 

account the needs expressed by the SERs on the issue.

The Summary and Explanation of the Preamble explains further the 

prohibition on employee rotation and the methods of compliance. 

The Panel recommends that OSHA clarify the methods of compliance 

section.

The Panel recommends that OSHA clarify how to implement the use of 

regulated areas particularly for construction activities. OSHA should 

better explain how employers would delineate boundaries for regulated areas and should better clarify the use of respiratory protection, 

personal protective clothing and equipment, and hygiene facilities 

and practices in regulated areas.

OSHA has eliminated the requirement for regulated areas in construction and shipyards. The Summary and Explanation section of the 

Preamble explains the regulated area requirements in General Industry. 

The Panel recommends that OSHA provide a clearer explanation of 

why it is necessary to remove Cr(VI)-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.

These issues are addressed in the Summary and Explanation Section 

of the Preamble. 

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 its definition of reasonably 

anticipated skin and eye contact. 

The Panel recommends that OSHA clarify the circumstances under 

which the proposed rule would require the use of 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..

OSHA has changed the rule from SBREFA draft in order to clarify 

when PPE is required and to assure that it is not required except 

where a dermal hazard exists. 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59441

TABLE IX–15.—SBREFA PANEL RECOMMENDATIONS AND OSHA RESPONSES—Continued

SBREFA panel recommendation OSHA response

The Panel recommends that OSHA provide a clearer explanation of the 

benefits and the need for its proposed medical surveillance provisions.

The Panel recommends that OSHA provide a clearer guidance as to 

which employees are intended to be covered under the medical surveillance provisions and, in particular, how the standard is intended 

to cover employees who work for several different employers during 

the course of a year.

OSHA has preliminarily dropped routine medical surveillance in the 

shipyard and construction industries. The Preamble Summary and 

Explanation clarify what is required of medical surveillance, and the 

extent to which the same medical examination can be used to meet 

the requirements of different standards. 

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 standards, the Panel recommends that OSHA examine whether important costs have been 

omitted, seek to develop alternatives that minimize these costs, and 

seek comment on the issue.

OSHA discusses the impact of EPA’s electroplating standard in the 

PEA, (See Chapter II: Technological Feasibility, Electroplating

and Chapter VIII: Environmental Impacts) and seeks comments on 

this issue. 

With respect to possible dual jurisdiction with FIFRA, the Panel recommends that OSHA consider dropping CCA applicators from the 

scope of the rule, and seek comment on this issue.

OSHA preliminarily has decided to exclude CCA applicators from the 

scope of the standard. 

With respect to the issue of using OSHA PELs as a basis for fenceline 

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.

OSHA solicits comment on the ‘‘fence line’’ standard issue. 

The Panel recommends that OSHA examine whether existing standards are adequate to cover occupational exposure to Cr(VI), and, if 

not, develop the Cr(VI) standard in such a way as to eliminate duplicative and overlapping efforts on the part of employers.

OSHA has preliminarily determined that, except for CCA applicators 

and wet cement workers, other standards cannot provide the worker 

protection needed, but has sought to avoid duplication of effort between standards. 

The Panel recommends that OSHA consider the scientific evidence in 

favor of a higher PEL, analyze the costs and economic impacts of a 

PEL of 20 or greater, and solicit comment on this option.

OSHA has included an analysis of the costs and benefits of a PEL of 

20 in this Preamble summary, and has a full analysis of this option in 

the PEA. 

The Panel recommends that OSHA carefully examine the entire issue 

of intermittent exposures, consider options that can alleviate the burden on such firms while meeting the requirements of the OSH Act, 

and solicit comment on such options.

OSHA preliminarily determined that intermittent users need not use engineering controls to assure compliance with the PEL. 

Some SERs argued that some Cr(VI) compounds offer lesser risks of 

cancer than others, and should be subject to different PELs. The 

Panel recommends that OSHA consider these arguments and seek 

comment on the issue.

OSHA has preliminarily determined that all Cr(VI) compounds should 

have the same PEL, but seeks comment on the issue. 

The Panel recommends that OSHA continue to exempt wet cement 

from the scope of the standard, and that if OSHA seeks comment on 

this option, OSHA should note the Panel’s recommendation and the 

reasons for the recommendation. The Panel also recommends that 

OSHA seek ways of adapting the standard better to the dynamic 

working conditions of the construction industry, examine the extent to 

which Cr(VI) exposures are already covered by other standards, and 

seek comment on these issues. The Panel also recommends that 

OSHA consider the alternative of developing a construction standard 

in a separate rulemaking.

OSHA has preliminarily determined to exempt wet cement from the 

scope of the standard, but has sought comment on the issue. 

OSHA has made a number of changes to the construction standard in 

this proposal, including eliminating the exposure assessment requirements, the regulated area requirement, and the action level. OSHA 

seeks comment on its new approach. 

The Panel recommends that OSHA consider, and solicit comment on, 

approaches to their special problems; that OSHA consider the possibility of making the maritime proposed standard more similar to the 

construction draft standard, or consider the alternative of developing 

a maritime standard in a separate rulemaking.

OSHA has made a number of changes to the shipyard standard in this 

proposal, including eliminating the exposure assessment requirements, the regulated area requirement, and the action level. OSHA 

has sought comment on its new approach. 

The Panel recommends that OSHA consider and seek comment on 

multi-year phase-in alternatives.

This option is discussed in the regulatory alternatives section of the 

PEA, and OSHA is seeking comments on this alternative. 

The Panel recommends that OSHA better explain the action level, including its role in ensuring workers are protected.OSHA has eliminated the action level in the construction and shipyard 

standards, and explains its role in the General Industry in the Summary and Explanation of the Preamble. 

The Panel recommends that OSHA consider the use of SECALs and 

solicit comment on whether and in what industries they are appropriate using the Cadmium standard as a model.

OSHA has preliminarily determined not to use SECALs, but solicits 

comments on this issue. 

59442 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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. 

§ 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 § 1320.5(a) (1)(iv) and § 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 (§ 1910.1026), 

Shipyards (§ 1915.1026); and 

Construction (§ 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:

• 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 

(§ 1910.1026(d)(2) Initial Exposure 

Monitoring, § 1910.1026(d)(3) Periodic 

Monitoring, and § 1910.1026 (d)(4) 

Additional Monitoring). 

Employers may notify each affected 

employee individually in writing of the 

results or by posting the exposuremonitoring 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. 

• 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 

(§ 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, tightfitting facepieces. 

• 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. 

• 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.

• 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 

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

• 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 

59444 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 OSHAapproved 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 

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

59446 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 (CrO2), ammonium 

dichromate ((NH4)2Cr2O7), calcium 

chromate (CaCrO4), chromium trioxide 

(CrO3), lead chromate (PbCrO4), 

potassium chromate (K2CrO4), 

potassium dichromate (K2Cr2O7), 

sodium chromate (Na2CrO4), strontium 

chromate (SrCrO4), and zinc chromate 

(ZnCrO4). 

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 crosspetition 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 watersoluble 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 followup 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 μg/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 μg/m3 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 μg/m3 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 μg/m3 and 0.5 μg/

m3 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 

μg/m3) calculated as an eight-hour timeweighted 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 

59448 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/m3. 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, preestablished 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 timeweighted average (TWA) exposure limit 

of 1 microgram of Cr(VI) per cubic meter 

of air (1 μg/m3). This limit means that 

over the course of any 8-hour work shift, 

the average exposure to Cr(VI) cannot 

exceed 1 μg/m3. The proposed limit 

applies to Cr(VI), as opposed to the 

current PEL which is measured as CrO3. 

The current PEL of 1 milligram per 10 

cubic meters of air (1 μg/10 m3, or 100 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59449

μg/m3) reported as CrO3 is equivalent to 

a limit of 52 μg/m3 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 μg/

m3 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 μg/m3 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 

59450 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 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 μg/m3. 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 μg/

m3 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 

59452 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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. 

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

59454 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 

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

59456 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 performanceorientation 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 

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

59458 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 μg/

m3 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 

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

59460 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 nonoccupational 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 

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

59462 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 Spanishspeaking 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 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59463

concentrations at or above the action 

level under any expected conditions of 

use, even under conditions of worstcase 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.

59464 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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.

§ 1910.1000 [Amended] 

2. In § 1910.1000, Table Z–2, the entry 

for Chromic acid and chromates 1.0 mg/

10 m3 is removed and the following 

entry added in its place:

§ 1910.1000 Air contaminants.

* * * * *

TABLE Z–2 

Substance 8-hour time weighted average 

Acceptable ceiling concentration 

Acceptable maximum peak above the acceptable ceiling average concentration for an 8-hr shift 

Concentration Maximum duration 

* * * * * * * 

Chromium (VI) compounds 

(as Cr); see 1910.1026.

* * * * * * * 

* * * * *

3. A new § 1910.1026 is added to read 

as follows:

§ 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 

μg/m3) calculated as an 8-hour timeweighted 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 monodispersed 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 μg/m3), 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 

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

59466 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

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 § 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 

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

59468 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

(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 § 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:

§ 1915.1000 Air contaminants.

* * * * *

TABLE Z—SHIPYARDS 

Substance CAS No.d ppm a * mg/m 3b* Skin designation 

* * * * * * * 

Chromium (VI) compounds 

(as Cr); see 1915.1026.

* * * * * * * 

* * * * * * * 

3 Use Asbestos Limit § 1915.1001. 

* * * * * * * 

* The PELS are 8-hour TWAs unless otherwise noted; a (C) designation denotes a ceiling limit. They are to be determined from breathingzone air samples. a Parts of vapor or gas per million parts of contaminated air by volume at 25° 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. 

Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 59469

* * * * *

6. A new § 1915.1026 is added, to 

read as follows:

§ 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 monodispersed 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 μg/m3), 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 § 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. 

59470 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

(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. 

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

§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 § 1917.1, to read as 

follows:

§ 1917.1 Scope and applicability.

* * * * *

(a) * * * 

(2) * * * 

(xiii) * * * 

(E) Hexavalent chromium § 1910.1026 

(See § 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 § 1918.1 to read as follows:

§ 1918.1 Scope and application.

* * * * *

(b) * * * 

(9) * * * 

(v) Hexavalent chromium § 1910.1026 

(See § 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.

§ 1926.55 [Amended] 

12. In Appendix A to § 1926.55, the 

entry for ‘‘Chromic acid and chromates 

(as CrO3) 0.1’’ is removed and the 

following entry added in its place:

§ 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 Limit§ 1915.1001

* * * * * * * 

aParts of vapor or gas per million parts of contaminated air by volume at 25 ° 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 

* * * * * * * 

dThe 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. 

59472 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

* * * * *

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 § 1926.1126 is added to 

subpart Z of 29 CFR Part 1926 to read 

as follows:

§ 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 monodispersed 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 μg/m3), 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. 

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

59474 Federal Register / Vol. 69, No. 191 / Monday, October 4, 2004 / Proposed Rules 

(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 

§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