calendar year-, and gender-adjusted rates for the general population of
the State of California (SMR=97). This is not a surprising result
considering more than 90 percent did not work in jobs that routinely
involve Cr(VI) exposure. Factory workers potentially exposed to Cr(VI)
also did not have significantly elevated lung cancer mortality
(SMR=102; 95% CI: 82-126) relative to the California general population
based on 87 observed lung cancer deaths. However, workers engaged in
spray painting/priming operations that likely had the highest potential
for Cr(VI) exposure did experience some excess lung cancer mortality
(SMR=111; 95% CI: 80-151) based on 41 deaths, but the increase was not
statistically significant.
    As commonly encountered in factory work, there was evidence of a
`healthy worker effect' in this aerospace cohort that became
increasingly pronounced in workers with long-term employment. The
healthy worker effect (HWE) refers to the lower rate of disease
relative to the general population sometimes observed in long-term
occupational cohorts. For example, the Boice cohort factory workers
employed for 20 years had statistically significant lower rates of
death than a standardized California reference population for all
causes (SMR=78; 95% CI: 75-81), lung cancer (SMR=70; 95% CI: 61-80),
heart disease (SMR=79; 95% CI: 74-83), cerebrovascular disease (SMR=67;
95% CI: 56-78), non-malignant respiratory disease (SMR=65; 95% CI: 57-
74), and cirrhosis of the liver (SMR=67; 95% CI: 51-88) among other
specific causes (Ex. 31-16-4, Table 5). The study authors note that
``these reductions [in disease mortality] seem in part due to the
initial selection into the workforce and the continued employment of
healthy people [i.e. healthy worker effect] that is often found in
occupational studies'' (Ex. 31-16-4, p. 592). If not properly accounted
for in mortality analysis, HWE can mask evidence of disease risk. Mr.
Robert Park, senior epidemiologist from NIOSH, confirmed this at the
public hearing when addressing implications of HWE for Cr(VI) lung
cancer risk in the Boice cohort.

    This [Boice cohort] is a population where you would expect to
see a very dramatic healthy worker effect * * * so just off the top,
I would say any [relative risk] estimates for lung cancer in the
Boice population based on SMRs, I would want to adjust upwards by
0.9, for example, if the real SMR ought to be around 0.9 due to the
healthy worker effect. So if you do that in their population, they
have classified some workers as [routinely] exposed to chromates,
about 8 percent of the population. They observe a SMR of 1.02 in
that group. If you look at some of the other groupings in that
study, for example, assembly has an SMR of 0.92, fabrication, which
is basically make all the parts, 0.92, maintenance, 0.79. So a lot
of evidence for healthy worker effect in general in that population.
So the chromate group actually is at least 10 or 12 percent higher
in their lung cancer SMR. Now again, the numbers are small, you'd
have to have a very huge study for an SMR of 1.1 or 1.15 to be
statistically significant. So it is not. But it is a hint (Tr. 345-
347).

    OSHA agrees with Mr. Park that the relative risks for lung cancer
in the Boice cohort are likely understated due to HWE. This is also
illustrated in the study analysis of the lung cancer morality patterns
by exposure duration to specific chemicals using internal cohort
comparisons. The internal analysis presumably minimize any biases (e.g.
smoking, HWE) that might exist from comparisons to the general
population. The results for workers potentially exposed to Cr(VI),
trichloroethylene (TCE), and perchloroethylene (PCE) are presented in
Table VI-9.

[GRAPHIC] [TIFF OMITTED] TR28FE06.024

    As shown in the table, there was a statistically significant
decline in relative risk of lung cancer among factory workers with
duration of TCE exposure (p< 0.01) and PCE exposure (p=0.02). This
mirrors the decline with increasing employment duration seen in
comparison with the general California population and strongly suggests
the internal cohort analysis failed to adequately adjust for HWE.
    The table shows that, despite the downward influence of HWE on lung
cancer risk, there was a slight nonsignificant upward trend in excess
lung cancer mortality with duration of exposure to Cr(VI). The result
is that aircraft workers potentially exposed to chromate for five or
more years had 50 to 70 percent greater lung cancer mortality than
coworkers with a similar duration of potential exposure to the
chlorinated solvents. The relative excess is even more noteworthy given
that the subgroups had considerable overlap (e.g., many of the same
workers in the PCE and TCE groups were also in the chromate group).
This implies that a subset of Cr(VI) workers not exposed to chlorinated
solvents, possibly spray painters routinely applying Cr(VI) primers
over many years, may be at greater lung cancer risk than other Cr(VI)-
exposed members of the cohort.
    The AIA and its technical representative, Exponent, objected to
OSHA reliance on the non-statistically significant upward trend in
excess lung cancers with increasing Cr(VI) exposure duration described
above (Exs. 38-215-2; 47-29-2). Exponent stated:

    Statistical tests for trend indicated there is no evidence for a
trend of increasing risk of lung cancer with increasing years
exposed to chromate (P< 0.20). OSHA seems to have `eye-balled' the
estimates and felt confident accepting the slight and non-
significant increases among risk estimates with overlapping
confidence intervals as evidence of a ``slightly positive'' trend.
However, OSHA's interpretation is an overstatement of the finding
and should be corrected in the final rule (Ex. 38-215-2, p. 13).

    OSHA does not agree with these comments and believes it has
objectively interpreted the trend data in a scientifically legitimate
fashion. The fact that an upward trend in lung cancer risk with Cr(VI)
exposure duration fails to meet a statistical confidence of 95 percent
does not mean the relationship does not exist. For example, a trend
with a p-value of 0.2 means random chance will not explain the
relationship 80 percent of the time. The positive trend is all the more
notable given that it occurs in spite of a significant downward trend
in lung cancer mortality with years of employment. In other words,
aerospace workers exposed to Cr(VI) experienced a slightly greater lung
cancer mortality with increasing number of years exposed even while
their co-workers exposed to other chemicals were experiencing a
substantially lower lung cancer mortality with increasing years
exposed.
    In its post-hearing comments, NIOSH calculated the observed excess
lung cancer risk to the Boice spray painters expected to have the
highest Cr(VI) exposures (SMR=1.11) to be 21 percent higher than the
minimally Cr(VI)-exposed assembly workers (SMR=0.92). NIOSH assumed the
painters were exposed to 15 [mu]g CrO3/m3 (i.e.,
the arithmetic mean of Cr(VI) air sampling data in the plant between
1978 to 1991) for 10 years (i.e., the approximate average duration of
employment) to derive an excess risk per mg CrO3/
m3 of 1.4 (Ex. 47-19-1). NIOSH noted that this was very
close to the excess risk per mg CrO3/m3 of 1.44
determined from their risk modeling of the Gibb cohort (Ex. 33-13). In
a related calculation, OSHA derived the expected excess risk ratio from
its linear relative risk model using a dose coefficient consistent with
the Gibb and Luippold data sets. Assuming the Boice spray painters were
exposed to 10 [mu]g Cr(VI)/m3 (90th percentile of plant air
sampling data converted from [mu]g CrO3 to [mu]g Cr(VI)) for
12 years (average employment duration of Boice factory workers), the
model predicts a risk ratio 1.20 which is also very close to the
observed excess risk ratio of 1.21 calculated from the observed SMR
data for spray painters above. These calculations suggest that the
excess lung cancer mortality observed in the Boice subcohort of Cr(VI)-
exposed aerospace workers is consistent with excess risks predicted
from models based on the Gibb and Luippold cohort of chromate
production workers.
    The other cohort studies of aerospace workers cited by AIA were not
informative with regard to the association between Cr(VI) and lung
cancer. A cohort study by Garabrandt et al. of 14,067 persons employed
by an aircraft manufacturing company found significantly reduced excess
lung cancer mortality (SMR=80; 95% CI: 68-95) compared to adjusted
rates in the U.S. and San Diego County populations (Ex. 35-210). The
mean duration of follow-up was only 16 years and the study authors are
careful to state that the study can not rule out excess risk for
diseases, such as lung cancer, that have long latencies of 20 years or
more. The consistently low all-cause and cancer mortalities reported in
the study strongly suggest the presence of a healthy worker effect.
Another cohort study by Blair et al. of 14,457 aircraft maintenance
workers at Hill Air Force base in Utah did not find elevated lung
cancer mortality (SMR=90; 95% CI: 60-130) when compared to the general
population of Utah (Ex. 35-213). However, the study was exclusively
designed to investigate cancer incidence of chlorinated solvents (e.g.
TCE, PCE, methylene chloride) and makes no mention of Cr(VI). This was
also the case for a cohort study by Morgan et al. of 20,508 aerospace
workers employed at a Hughes Aircraft manufacturing

plant, which found no excess lung cancer mortality (SMR=0.96; 95% CI:
87-106) compared to the general U.S. population. However, a detailed
investigation of jobs at a large aircraft manufacturing facility (i.e.
facility studied by Boice et al.) found that only about 8 percent of
employees had potential for routine Cr(VI) exposure (Ex. 47-19-15). If
this is representative of the workforce in the other studies cited
above, it is doubtful whether a Cr(VI)-related increase in lung cancer
from a small proportion of workers would be reflected in the mortality
experience of the entire cohort, most of whom would not have been
exposed to Cr(VI).
    In summary, OSHA does not find convincing evidence from the
aerospace cohort studies that the Agency's quantitative risk assessment
overstates the lung cancer risk to Cr(VI)-exposed workers. An
association between Cr(VI) exposure and lung cancer was never addressed
in most cohorts relied upon by the aerospace industry. Job analysis
shows that only a minor proportion of all aerospace workers are engaged
in workplace activities that routinely lead to Cr(VI) exposure. This
could explain the lack of excess lung cancer mortality found in studies
characterizing the mortality experience of all aerospace workers.
Alexander et al. identified a cohort of Cr(VI) exposed workers, made
individual worker estimates of cumulative Cr(VI) exposures, and found
no exposure-related trend with lung cancer incidence. However, the
absence of exposure-response could be the result of a number of study
limitations including the young age of the cohort (e.g. majority of
workers were under 50 years of age, when lung cancer incidence is
relatively uncommon), the inadequate follow-up period (e.g. majority of
workers followed <  10 years), and the potential for exposure
misclassification (e.g. Cr(VI) exposure levels prior to 1975 were not
monitored). Boice et al. also identified a subcohort of aerospace
workers with potential Cr(VI) exposure but lacked adequate air sampling
to investigate a quantitative relationship between Cr(VI) exposure and
lung cancer response. There was a significant decline in relative lung
cancer risk with length of employment among factory workers as well as
those exposed to chlorinated solvents, indicating a strong healthy
worker survivor effect among this pool of workers. The healthy worker
effect may have masked a significant trend in lung cancer with Cr(VI)
exposure duration. Risk projections based on the OSHA linear model were
found to be statistically consistent with the relative risk ratios
observed in the Boice cohort.
    Cr(VI) Particle Size Distribution During Aerospace Operations.
Differences in the size of Cr(VI) aerosols generated during chromate
production and aerospace operations is another reason representatives
of the aircraft industry believe the OSHA risk estimates overstate risk
to aerospace workers (Exs. 38-106; 38-106-1; 38-215-2; 39-43; 44-33;
47-29-2). The submitted particle size data indicated that spraying
Cr(VI) primers mostly generates large aerosol droplets (e.g.
> 10 [mu]m) not expected to penetrate beyond the very upper portions of
the respiratory tract (e.g. nasal passages, larynx). Some aerospace
commenters also cited research showing that the few respirable primer
particulates that reach the lower regions of the lung contain less
Cr(VI) per particle mass than the larger non-respirable particles (Exs.
44-33; 38-106; 39-43). As a result, aerospace commenters contend that a
very small proportion of Cr(VI) aerosols generated by aircraft primer
operations deposit in the bronchioalveolar regions of the lung where
lung cancer occurs. OSHA agrees that the particle size studies
submitted to the record sufficiently demonstrate that a relatively
small proportion of Cr(VI) reaches the critical regions of the lung as
a result of these aircraft spraying operations. However, the Agency
believes the reduction in lung cancer risk from this lower Cr(VI)
particle burden is likely offset by the greater carcinogenic activity
of the slightly soluble strontium and zinc chromates inhaled during
spray primer application. Evaluation of the study data provided to the
record and the rationale behind the OSHA position are described below.
    The Agency reviewed the information provided by Boeing on the
particle size of paint aerosols from typical spraying equipment used in
aerospace applications. Boeing provided size characterization of paint
aerosol from their in-house testing of spray paint equipment (Ex. 38-
106-1, p. 8-11). They measured droplet size distributions of non-
chromated polyurethane enamels generated by high volume low pressure
(HVLP) and electrostatic air spray guns under typical settings. The
particle size was measured 10 to 12 inches from the nozzle of the gun
using laser diffraction techniques. Boeing found the median volumetric
droplet diameter (Dv50) of the paint particles to be in the range of 17
to 32 [mu]m under the test conditions. Less than 0.5 percent of
droplets in the spray were 5 [mu]m and smaller (e.g. typical of
particles that deposit in the bronchioalveolar region). Boeing
concluded:

    In typical operations and products, the best aerosol size is a
distribution with mass median diameter of about 30-40 microns, and a
relatively monodisperse distribution. As a result, the fraction of
the spray that is < 5 micron is about 1% or less; in overspray
perhaps [ap]2%. Therefore the deposited dose would be far less than
from exposure to an equal concentration of a smaller aerosol size,
and estimates of risk based on studies of other industry sectors are
not relevant to evaluation of risk in aerospace paint spraying (Ex.
38-106-1, p. 16).

Although Boeing used a non-chromated enamel paint in their studies,
they contend that the results would be representative of the particle
size distribution for a Cr(VI) primer using the same equipment under
similar conditions.
    Boeing also submitted recent publications by the UCLA Center for
Occupational and Environmental Health measuring the Cr(VI) particle
size distribution during spray painting operations at an aerospace
manufacturing facility (Ex. 38-106-1). The UCLA group investigated
particle size distributions of Cr(VI) primers sprayed from HVLP
equipment in a lab bench-scale spray booth and in a field study of
spray booths at an aerospace facility (Ex. 38-106-1, attachment 6). The
tested primers contained the slightly soluble strontium chromate. The
study data are presented in two papers by Sabty-Daily et al. The
aerosol particles were collected at different locations several meters
from the spray gun in the bench-scale paint booth using a cascade
impactor. Full shift personal breathing zone samples from workers
spraying primer were also collected with a cascade impactor in the
field studies. The mass median aerodynamic diameter (MMAD) for Cr(VI)
particles in the field study was reported to be 8.5 [mu]m with a
geometric standard deviation of 2.2 [mu]m. On average, 62 percent of
the Cr(VI) mass was associated with non-respirable particles >10 [mu]m.
Taking into account deposition efficiency, it was estimated that less
than five percent of the Cr(VI) would potentially deposit in the lower
regions of the respiratory tract where lung cancer occurs. The bench
scale study gave particle distributions similar to the field studies.
It was shown that particle size decreases slightly as gun atomization
pressure increases. Particles in the direct spray were generally larger
than the overspray. Particle size was shown to decrease with distance
to the target surface due to evaporation of solvent.
    Both Sabty-Daily articles and the Boeing submission made reference
to

another study that measured particle size distribution of a HVLP-
generated paint aerosol in the breathing zone of the worker (Ex. 48-3).
Paint droplets were collected on polycarbonate filters with 0.2 [mu]m
pore size. Aerosol size was measured using a microscopic method that
minimizes bias from solvent evaporation. The breathing zone MMAD in the
overspray was reported to be 15 to 19 [mu]m with a GSD of 1.7 [mu]m. In
another study, LaPuma et al. investigated the Cr(VI) content of primer
particles from an HVLP spray gun using a cascade impactor (Ex. 31-2-2).
They reported that smaller particles (i.e. < 7 [mu]m) contained
disproportionately less Cr(VI) per mass of dry paint than larger
particles.
    Boeing concluded that ``the particle size distribution reported by
Sabty-Daily et al. (2004a) significantly underestimate the size
distribution of paint aerosol'' (Ex. 38-106-1, p. 14). They state that
``in typical [spraying] operations and products the best aerosol size
is a distribution with mass median diameter of about 30-45 microns''
(Ex. 38-106-1, p. 16). This particle size is larger than 15 to 20 [mu]m
reported in independent breathing zone measurements of spray paint
aerosol collected on conventional sampling media (i.e. polycarbonate
filters) (Carlton and Flynn, 1997).
    The Boeing rationale for dismissing the UCLA data was that the
cascade impactor had low collection efficiency for larger particles
relative to the Boeing laser diffraction method, which Boeing believes
is more accurate over the entire size distribution. OSHA notes,
however, that Boeing did not characterize aerosol particles in the
breathing zone of workers spraying Cr(VI) primer. Their study
characterized droplet size from an non-chromated enamel spray directly
out of the spray gun prior to contact with the target surface. While
collection efficiency accounts for some of the particle size
difference, other factors may also have contributed. These factors
include the composition of the spray paint, the sampling location, and
the degree of solvent evaporation. OSHA considers Cr(VI) primer
droplets with an average MMAD of 7 to 20 [mu]m, as measured in
breathing zone studies, to best represent the particle size inhaled by
a worker during spraying operations, since this range was measured in
breathing zone studies. The majority of these droplet particles would
not be expected to penetrate regions of the respiratory tract where
lung cancers occur.
    While aerosol particle size during spray application of Cr(VI)
primers has been measured, AIA acknowledged that the particle size
distribution during sanding procedures has not been well studied (Exs.
38-106; 47-29-2). However, they believe that most of the particles
released as a result of sanding and grinding operations to remove old
paint coatings from aircraft are non-respirable (e.g. >10 [mu]m). OSHA
is not aware of reliable data in the record to support or refute this
claim.
    The Cr(VI) particle size data from spray primer and sanding
applications in aerospace need to be evaluated against Cr(VI) particle
size during chromate production to determine its impact on OSHA risk
estimates. Boeing observed that the high temperature calcination
process that oxidizes chromite ore to sodium chromate would likely lead
to a high proportion of respirable fume (Ex. 38-106). During post-
hearing comments, AIA provided a figure from the 1953 U.S. Public
Health Service survey report that indicated the geometric mean airborne
dust particle size in a chromate production plant was 0.3 to 0.4 m in
size (Ex. 47-29-2, p. 3). The data came from a thermal precipitator
analysis of one-hour dust samples collected from the roasting and
leaching areas of the plant (Ex. 7-3). An independent 1950 industrial
hygiene survey report of the Painesville plant from the Ohio Department
of Health indicates the median size of the in-plant dust was 1.7
microns and the median size of the mist generated during the leaching
operations was 3.8 microns (Ex. 7-98). The measurement method used to
determine this particle size was not clear from the survey report.
    The thermal precipitator used by the U.S. Public Health Service
survey is an older sampling device specifically used to characterize
particles smaller than 5 [mu]m. The thermal precipitator collection
efficiency for particles >5 [mu]m was considered suspect due to
gravitational and inertial effects caused by the very low air flow
rates (e.g. 6 ml/min) necessary to operate the device. The survey
figure shows that 95 percent of collected particles were smaller than 1
[mu]m. However, this is probably an inflated percentage given that the
thermal precipitator is unable to effectively collect particles outside
the fine and ultrafine range (e.g. greater than about 5 [mu]m).
    In their post-hearing brief, AIA introduced an Exponent microscopic
analysis of particles claimed to be landfilled `roast residue'
generated as airborne dust from the Painesville plant `decades' earlier
(Ex. 47-29-2). AIA stated that ``the particle diameters ranged from
0.11 to 9.64 [mu]m and that 82 percent of the particles were less than
2.5 [mu]m (Ex. 47-29-2, p. 3). OSHA was unable to verify the nature of
the landfill dust or determine its relevance from the information
provided by AIA.
    In the same submission, AIA referenced several experimental and
animal studies as evidence that small particles less than 2.5 [mu]m in
diameter cause greater lung toxicity than larger particles (Ex. 47-29-
2). AIA concluded that:

    It is important for OSHA to recognize in the quantitative risk
assessment that the particles to which the featured chromate
production workers were exposed were fine [particle diameters 0.1-
2.5 [mu]m] and ultrafine particles [particle diameters < 0.1 [mu]m]
and that particles of this size range are known to be associated
with greater toxicity than larger particles. Thus, the quantitative
cancer risk estimates based on these studies are very conservative
and likely overestimate risks for Cr(VI) exposures in other
industries, most notably aerospace (Ex. 47-29-2, p. 7).

    The above studies showed that fine/ultrafine particles penetrate
into the alveolar region of the lung, are slowly cleared from
respiratory tract, and can lead to pulmonary inflammation and non-
neoplastic respiratory disease. OSHA agrees that fine/ultrafine
particles can disrupt pulmonary clearance and cause chronic
inflammation if sufficient amounts are inhaled. However, AIA did not
provide data that demonstrated the Gibb and Luippold workers were
routinely exposed to levels of small particles that would trigger
serious lung toxicity.
    AIA also referred to a human epidemiological study that reported
the excess risk of lung cancer mortality from airborne fine/ultrafine
particles (i.e. 8 percent increase per 10 [mu]g/m\3\ in particles) to
be similar to the excess risk of cardiopulmonary disease (i.e. 6
percent increase with each 10 [mu]g/m\3\ in particles). AIA suggested
these results were evidence that the excess lung cancer mortality
attributed to Cr(VI) in chromate production cohorts were, in large
part, due to fine/ultrafine particles. However, the Luippold cohort had
an excess mortality from lung cancer (SMR=239) that was 10.6-fold
higher than the excess mortality of heart disease (SMR=113) (Ex. 33-
10). The Gibb cohort had an excess mortality from lung cancer that was
5.7-fold higher than the excess mortality of arteriosclerotic heart
disease (SMR=114) (Ex. 33-11). These mortality patterns are not
consistent with the small particle study results above and strongly
indicate fine/ultrafine particles are not the primary cause of excess
lung cancer among the chromate production workers in the Luippold and
Gibb cohorts. Given the information provided, OSHA does not have reason
to expect that exposure

to fine/ultrafine particles in the Luippold and Gibb cohorts had a
substantial quantitative impact on its estimates of lung cancer risk
from exposure to Cr(VI).
    Based on the evidence presented, OSHA believes the production of
sodium chromate and dichromate likely generated a greater proportion of
respirable Cr(VI) particles than the aerospace spray priming
operations. The roasting operation that oxidizes trivalent chromite ore
and soda ash to hexavalent sodium chromate salts would be expected to
generate a small particle fume based on information from other high
temperature calcination processes (e.g. beryllium oxide production).
This is supported by a small amount of particle size information from
the 1940s and 1950s (Ex. 7-98). However, there are insufficient data to
reliably determine the median diameter of Cr(VI) particles or otherwise
characterize the particle size distribution generated during sodium
chromate production in the breathing zone of the worker. It should also
be recognized that significant Cr(VI) exposures occurred during other
chromate production operations, such as leaching sodium chromate from
the roast, separating sodium dichromate crystals, and drying/bagging
the final purified sodium dichromate product. There is no information
on particle size for these operations, but it is reasonable to expect
greater proportions of larger particles than generated during the
roasting process. For these reasons, there is some degree of
uncertainty with regard to size distribution of Cr(VI) aerosols inhaled
by chromate production workers.
    OSHA agrees with the aerospace industry that the reduced proportion
of respirable particles from spray primer operations relative to
chromate production will tend to lower the lung cancer risk from
equivalent Cr(VI) exposures. This is because less Cr(VI) will reach the
bronchioalveolar regions of the respiratory tract where lung cancer
occurs. However, the chemical form of Cr(VI) must also be considered.
Spray primer and painting operations expose workers to the slightly
soluble strontium and zinc chromates while chromate production workers
are exposed primarily to highly soluble sodium chromate/dichromate.
    As explained earlier in section V.B.9 on carcinogenic effects,
animal and mechanistic evidence suggest that the slightly soluble
strontium and zinc chromates are more carcinogenic than the highly
soluble Cr(VI) compounds when equivalent doses are delivered to
critical regions of the respiratory tract. Slightly soluble Cr(VI)
compounds produced a higher incidence of bronchogenic tumors than
highly soluble Cr(VI) compounds (e.g. sodium dichromate, chromic acid)
when instilled in the respiratory tract of rats at similar dosing and
other experimental conditions (Ex. 11-2; 11-7). For example,
intrabronchial instillation of strontium chromate produced a 40 to 60-
fold greater tumor incidence than instillation of sodium dichromate in
one study (Ex. 11-2). Unlike the highly soluble Cr(VI) compounds, the
less water soluble Cr(VI) compounds are better able to provide a
persistent source of high Cr(VI) concentration within the immediate
microenvironment of the lung epithelia facilitating cellular uptake of
chromate ion into target cells. The greater carcinogenicity of the
slightly soluble Cr(VI) compounds have led to ACGIH TLVs that are from
5-fold (i.e. zinc chromates) to 100-fold (i.e. strontium chromates)
lower than the TLV for highly water soluble Cr(VI) compounds.
    For these reasons, the risk reductions achieved from the lower
Cr(VI) particle burden that reaches the bronchioalveolar region of the
lung may, to a large extent, be offset by the greater carcinogenic
activity of the Cr(VI) compounds that are inhaled during aircraft spray
painting operations. Since significant lung cancer risk exists at
Cr(VI) air levels well below the new PEL (e.g. 0.5-2.5 [mu]g/m\3\)
based on chromate production cohorts, the risk would also likely be
significant even if the lung cancer risk from similar Cr(VI) exposures
in aerospace operations is slightly lower. Therefore, OSHA believes
that the risk models based on the Gibb and Luippold data sets will
provide reasonable estimates of lung cancer risk for aerospace workers
exposed to equivalent levels of Cr(VI). However, based on the lower
lung burden expected after considering the particle size distribution
evidence submitted to the record, OSHA no longer believes that its risk
projections will underestimate lung cancer risk for aerospace workers
exposed to strontium or zinc chromates, as suggested in the NPRM (69 FR
at 59384).
b. Specialty Steel Industry and Stainless Steel Welding.
    Collier Shannon Scott submitted comments to OSHA on behalf of a
group of steel and superalloy industry trade associations and companies
including the Specialty Steel Industry of North America (SSINA), the
Steel Manufacturers Association (SMA), and the American Iron and Steel
Institute (AISI) as well as various individual companies. They
requested that OSHA ``seriously consider'' the results of the Arena et
al. (1998) study of workers employed in the high nickel alloys industry
(Tr. 661), as well as studies by Huvinen et al. (1996, 2002) and Moulin
et al. (1990) on stainless steel production workers (Exs. 38-233, p.
85; 47-5, p. 10) and by Danielsen et al. (1996) on Norweigen stainless
steel welders (Ex. 47-5, p. 10). On behalf of the SSINA, Ms. Joan
Fessler testified that the Arena et al. study (Ex. 38-233-2), also
referred to as the ``Redmond Study'', found no relationship between
Cr(VI) exposure and lung cancer, and in general `` * * * no strong
epidemiological evidence causally associating occupational exposures
with excess risk'' (Tr. 662). Ms. Fessler concluded that the study
results `` * * * stand in stark contrast to the extrapolated estimates
of cancer risk OSHA has developed from the chromate worker cohorts to
develop the proposed rule'' (Tr. 662) and ``[show] that there is no
significant excess risk of lung cancer for workers in the steel
industry'' (Ex. 40-12-4, p. 2). She cited studies conducted by Huvinen
et al. as additional evidence that workers in the stainless steel
production industry do not have excess risk of lung cancer from Cr(VI)
exposure (Tr. 663).
    OSHA reviewed the Arena et al. (1998) study, which examined
mortality in a cohort of 31,165 workers employed at 13 U.S. high nickel
alloy plants for at least one year between 1956 and 1967 (Ex. 38-233-2,
p. 908). The focus of the study is nickel exposure; it does not report
how many of the cohort members were exposed to Cr(VI) or the levels of
Cr(VI) exposure to which they may have been exposed. Therefore there
does not appear to be any basis for SSINA's conclusion that ``[t]here
was no strong epidemiological evidence causally associating
occupational exposures with excess risk'' in the study and that ``[n]o
dose response relationship was demonstrated * * * '' (Tr. 662). Ms.
Fessler stated, in response to a question by Dr. Lurie of Public
Citizen, that there is no information in the study on Cr(VI) exposures
with which to assess a dose-response relationship between occupational
exposure to Cr(VI) and excess lung cancer risk in the cohort (Tr. 685).
Without any information on the proportion of workers that were exposed
to Cr(VI) or the levels to which they were exposed, one cannot
determine that there is no carcinogenic effect of Cr(VI) exposure, or
that the results of the Arena study contradict OSHA's risk estimates.
    To more meaningfully compare the lung cancer risk predicted by
OSHA's risk model and that observed in the

Arena et al. study, OSHA estimated Cr(VI) exposures for the cohort
members based in part on exposures in the stainless steel industry.
High-nickel alloys that contain chromium are roughly comparable to
stainless steel in terms of chromium content and the temperatures at
which they are melted. This in turn determines the amount of trivalent
chromium that converts to hexavalent chromium in the heating process.
For example, cast stainless steels with high nickel composition (e.g.
Cast 18-38, Cast 12-60, Cast 15-65, and Cast 15-35) have chromium
content ranging from 10-21% and have melting points between 2350 and
2450 degrees Fahrenheit. Other high-nickel alloys with chromium
content, such as Hastelloy alloys C and G, Incoloy, Nimonic, and
Inconel, range from 13 to 22% chromium (except Incoloy 804=29.7% Cr)
with melting points of 2300-2600 degrees Fahrenheit. Stainless steels,
in general, have 12-30% chromium content and melting points between
2350 and 2725 degrees Fahrenheit.
    For this analysis OSHA projected that the proportion of workers in
each production job category is approximately similar in stainless
steel and high-nickel alloy production. For example, OSHA assumed that
the percent of alloy production workers who are furnace operators is,
as in steel production, about 5%. Assuming that both the Cr(VI)
exposures typical of various production jobs and the proportion of
workers employed in each job are roughly similar, workers in the Arena
cohort producing high-nickel stainless steels and alloys containing
chromium are likely to have Cr(VI) exposures comparable to those
generally found in stainless steel production. Workers' exposures were
estimated using the exposure profile shown in Table III-62 of the Final
Economic Analysis section on steel mills (Ex. 49-1).
    Not all workers in the Arena et al. cohort had Cr(VI) exposures
comparable to those in stainless steel facilities. As discussed by Ms.
Fessler at the hearing, exposure to `` * * * [c]hrome was not uniform
in all [industries included in the study] because some of those
industries * * * did only high nickel work or nickel mining or whatever
specific nickel work there was'' (Tr. 683). OSHA assumed that Cr(VI)
exposures of workers producing high-nickel alloys without chromium
content, such as Duranickel, Permanickel, Hastelloy alloys B, D, and G,
and Monel alloys, are similar to those found in carbon steel mills and
other non-stainless facilities, which according to comments submitted
by Collier Shannon Scott:

    * * * may generate Cr(VI) due to trace levels of chromium in
feedstock materials or the inadvertent melting of stainless steel
scrap, as well as during various maintenance and welding operations
(Ex. 38-233, p. 10).

Exposure levels for Arena cohort workers producing these alloys were
estimated using the carbon steel exposure profile shown in Table III-64
of the Final Economic Analysis section on steel mills (Ex. 49-1).
    Table VI-10 below shows the risk ratios (ratio of excess plus
background cancers to background only cancers) predicted by OSHA's
model for workers producing high-nickel alloys with and without
chromium content. The percentage of workers with 8-hour TWA exposures
in each range shown below are calculated for Ni-Cr alloys and non-Cr
alloys using profiles developed for the Final Economic Analysis
sections on stainless steel and carbon steel industries, respectively
(Ex. 49-1). An average exposure duration of 20 years was assumed. While
it was not clear how long workers were exposed on average, the reported
length of follow-up in the study indicates that the duration of
exposure was probably less than 20 years for most workers. Risk ratios
were calculated assuming that workers were followed through age 70. The
average age at end of follow-up was not clear from the Arena et al.
publication. Over half of the original cohort was under 30 as of 1978,
and follow-up ended in 1988 (Ex. 38-233-2, p. 908). Follow-up through
age 70 may therefore lead OSHA's model to overestimate risk in this
population, but would probably not lead to underestimation of risk.
[GRAPHIC] [TIFF OMITTED] TR28FE06.025

    The Arena et al. study reported lung cancer rates among white males
(who comprised the majority of the cohort) about 2%-13% higher than
background depending on the reference population used. The table above
illustrates that with reasonable assumptions about exposures in the
Arena cohort, OSHA's risk model predicts excess risks as low as those
reported by Arena et al. OSHA's model predicts the highest risks (1-6%
higher than background) among workers producing alloy mixtures similar
to stainless steel in chromium content. Unfortunately, it is not clear
from the Arena et al. publication how many of the workers were involved
in production of chromium-containing alloys. If an even split is
assumed between workers producing alloys with and without chromium
content in the Arena et al. cohort, OSHA's model predicts a lung cancer
rate between 0.8% and 3.8% higher than background.
    More precise information about the level or duration of cohort
members' exposures might increase or decrease OSHA's model predictions
somewhat. For example, some workers in the historical alloy industry
would have had higher exposures than their modern-day counterparts, so
that better exposure information may lead to somewhat higher model
predictions. On the other hand, better information on the duration of
exposure and workers' age at the end of follow-up would lower the model
predictions, because this analysis made assumptions likely to
overestimate both. The analysis presented here should be interpreted
cautiously in light of the considerable uncertainty about the actual
exposures to the Arena cohort members, and the fact that OSHA's model
predictions are based on a lifetable using year 2000 U.S. all-cause
mortality data (rather than data from the time period during which the
cohort was followed). This analysis is not intended to provide a
precise estimate of risk from exposure to Cr(VI) in the Arena cohort,
but rather to demonstrate that the relatively low excess risk seen in
the cohort is reasonably consistent with the excess risk that OSHA's
model would predict at low exposures. It illustrates that OSHA's risk
model does not predict far higher risk than was observed in this
cohort. Rather, the majority of workers in alloy production would be
predicted to have relatively low risk of occupational lung cancer based
on their relatively low exposure to Cr(VI).
    Regarding the Huvinen et al. (1996, 2002) studies, the comments
submitted by Collier Shannon Scott state that ``there was not a
significant increase in the incidence of any disease, including lung
cancer, as compared to the control population'' (Ex. 38-233, p. 85).
However, the authors also noted that risk of cancer could not be
excluded because the follow-up time was short and the exposed group was
young and small (Ex. 38-233-3, p. 747).
    In addition to the small size (109 workers) and young age (mean
43.3 years) of the Cr(VI)-exposed group in the Huvinen et al. study
population, the design of this study limits its relevance to the issue
of lung cancer risk among stainless steel workers. The subjects were
all employed by the company at the time of the study. Individuals with
lung cancer would be expected to leave active employment, and would not
have been surveyed in the study. The authors made only a limited
attempt to track former workers: Those who met the study criteria of 8
years' employment in a single production department were surveyed by
mailed questionnaire (Ex. 38-233-3, p. 743), and no follow-up on
nonrespondents was reported. A second study conducted on the original
study group five years later was again limited to employed workers, as
those who had left the company `` * * * could not be contacted'' (Ex.
38-233-3, p. 204). Due to the short follow-up period and the
restriction to living workers (still employed or survey respondents),
these studies are not well suited to identify lung cancer cases.
    Post-hearing comments stated that `` * * * OSHA has failed to even
consider specific epidemiological studies performed on stainless steel
production workers and welders that would be far more relevant than the
chromate production studies OSHA relied upon for its analysis'' (Ex.
47-5, p. 10). In particular, they suggest that OSHA should consider a
study by Danielsen et al. (1996) on Norweigian boiler welders and a
study by Moulin et al. (1990) on French stainless steel production
workers (Ex. 47-5, p. 10). However, the Moulin et al. study (Ex. 35-
282), was discussed in the Preamble to the Proposed Rule (69 FR at
59339). OSHA concluded that the association between Cr(VI) and
respiratory tract cancer in this and similar studies is difficult to
assess because of co-exposures to other potential carcinogens such as
asbestos, polycyclic aromatic hydrocarbons, nickel, and the lack of
information on smoking (69 FR at 59339).
    The Danielsen et al. study was not evaluated in the NPRM, but is
similar to other studies of welders evaluated by OSHA in which excess
risk of lung cancer did not appear to be associated with stainless
steel welding. In Danielsen et al., as in most other welding studies,
no quantitative information on Cr(VI) exposure was available, there was
potential confounding by smoking and asbestos exposure, and there
appeared to be an overall healthy worker effect in the study (625
deaths vs. 659 expected). Therefore, OSHA does not believe that
Danielsen et al. contributes significant information beyond that in the
studies that are reviewed in Section V.B.4 of this preamble. OSHA's
interpretation and conclusions regarding the general findings of
welding cohort studies, discussed below in the context of comments
submitted by the Electric Power Research Institute, apply to the
results of Danielsen et al. as well.
    The Electric Power Research Institute (EPRI), Exponent, and others
submitted comments to OSHA that questioned whether the Agency's
exposure-response model, based on the Gibb and Luippold chromate
production industry cohorts, should be used to estimate lung cancer
risks to welders exposed to Cr(VI) (Exs. 38-8; 38-233-4; 39-25, pp. 2-
3). EPRI stated that:

    OSHA's review of the toxicology, epidemiology, and mechanistic
data associated with health effects among welders was thorough and
accurate. We concur with the selection of the two focus cohorts
(Luippold et al. 2003 and Gibb et al. 2000) as the best data
available upon which to base an estimate of the exposure-response
relationship between occupational exposure to Cr(VI) and an
increased lung cancer risk''; however * * * it may be questionable
whether that relationship should be used for stainless steel welders
given that a positive relationship between exposure to Cr(VI) and
lung cancer risk was not observed in most studies of welder cohorts
(Ex. 38-8, pp. 6-7).

EPRI's concerns, like other comments submitted to OSHA on risk to
welders, are based primarily on the results of the Gerin et al. (1993)
study and on several studies comparing stainless steel and mild steel
welders.
    As discussed above in Section V., Gerin et al. (1993) is the only
available study that attempts to relate estimated cumulative Cr(VI)
exposure and lung cancer risk among welders. While excess lung cancer
risks were found among stainless steel welders, there was no clear
relationship observed between the estimated amount of Cr(VI) exposure
and lung cancer (Ex. 38-8, p. 8). This led the authors to suggest that
the elevated risks might be `` * * * related to other exposures such as
cigarette smoking, background asbestos exposure at work or other
occupational or environmental risks * * * '' rather than to Cr(VI)
exposure. On the other hand, Gerin et al. stated that `` * * * the
welding fume exposures in these

populations may be too low to demonstrate a gradient of risk'', or
misclassification of exposure might obscure the dose-response
relationship (Ex. 7-120, pp. S25-S26), a point with which EPRI
expressed agreement (Ex. 38-8, p. 8).
    OSHA agrees with Gerin et al. that co-exposures to carcinogens such
as nickel, asbestos, and cigarette smoke may have contributed to the
elevated lung cancer risks among welders. OSHA also agrees with the
authors that exposure misclassification may explain the absence of a
clear relationship between Cr(VI) and lung cancer in this study. Gerin
et al. derived their exposure data primarily from literature on welding
fume, as well as from a limited number of industrial hygiene
measurements taken in the mid 1970s in eight of the 135 companies
participating in the study (Ex. 7-120, p. S24, p. S27). Their exposure
estimates took account of the welding process used and the base metal
welded by individuals in the cohort, but they apparently had no
information on other important items, such as the size of the work
piece and weld time, which were identified by EPRI as factors affecting
the level of Cr(VI) exposure from welding (Ex. 38-8, p. 5).
    EPRI also identified ventilation as a particularly important
determinant of exposure (Ex. 38-8, p. 5). Gerin et al. did not appear
to have individual information on ventilation use for their exposure
estimates, relying instead on ``information on the history of welding
practice * * * obtained from each company on the basis of an ad hoc
questionnaire'' that described for each company the average percent of
time that welders used local ventilation, operated in confined or open
areas, and worked indoors or outdoors (Ex. 7-120, p. S23). The use of
local ventilation, time spent welding in confined areas, and time spent
welding outdoors may have varied considerably from worker to worker
within any single company. In this case exposure estimates based on
company average information would tend to overestimate exposure for
some workers and underestimate it for others, thus weakening the
appearance of an exposure-response relationship in the cohort.
    Gerin et al. also stated that the average exposure values they
estimated do not account for a number of factors which affect welders'
exposure levels, including `` * * * type of activity (e.g. maintenance,
various types of production), special processes, arcing time, voltage
and current characteristics, welder position, use of special electrodes
or rods, presence of primer paints and background fumes coming from
other activities'' (Ex. 7-120, p. S25). They noted that the resulting
difficulty in the construction of individual exposure estimates is
exacerbated by aggregation of data across small cohorts from many
different companies that may have different exposure conditions (Ex. 7-
120, p. S25). According to Gerin et al., exposure misclassification of
this sort may have obscured a dose-response relationship in this cohort
(Ex. 7-120, p. S25). The authors suggest that their estimates should be
checked or corrected `` * * * with data coming from well-documented
industrial hygiene studies or industrial hygiene data banks including
information on the major relevant factors'' (Ex. 7-120, p. S26). OSHA
believes that there is insufficient information to determine why a
clear relationship between Cr(VI) exposure and lung cancer is not
observed in the Gerin et al. study, but agrees with the authors that
exposure misclassification and the influence of background exposures
may explain this result.
    EPRI noted the apparent lack of a relationship between exposure
duration and lung cancer risk in the Gerin et al. cohort (Ex. 38-8, p.
10). Duration of exposure is expected to show a relationship with
cancer risk if duration serves as a reasonable proxy for a measure of
exposure (e.g. cumulative exposure) that is related to risk. Since
cumulative exposure is equal to exposure duration multiplied by average
exposure level, duration of exposure may correlate reasonably well with
cumulative exposure if average exposure levels are similar across
workers, or if workers with longer employment tend to have higher
average exposure levels. In a cohort where exposure duration is
believed to correlate well with cumulative exposure, the absence of a
relationship between exposure duration and disease risk could be
interpreted as evidence against a relationship between cumulative
exposure and risk.
    High variation in average exposures among workers, unrelated to the
duration of their employment, would tend to reduce the correlation
between exposure duration and cumulative exposure. If, as EPRI states,
Cr(VI) exposure depends strongly on process, base metal, and other work
conditions that vary from workplace to workplace, then duration of
exposure may not correlate well with cumulative exposure across the 135
companies included in the Gerin et al. study. The lack of a positive
relationship between exposure duration and lung cancer in the Gerin et
al. cohort may therefore signify that duration of exposure is not a
good proxy for the amount of exposure accumulated by workers, and
should not be interpreted as evidence against an exposure-response
relationship.
    In post-hearing comments Mr. Robert Park of NIOSH discussed other
issues related to exposure duration in the Gerin et al. and other
welding cohorts:

    Several factors may impact the interpretation of [the Gerin et
al. (1993) and Simonato et al. (1991) welder cohort studies] and are
consistent with an underlying risk associated with duration * * *.
The healthy worker survivor effect is a form of confounding in which
workers with long employment durations systematically diverge from
the overall worker population on risk factors for mortality. For
example, because smoking is a risk factor for disease, disability
and death, long duration workers would tend to have a lower smoking
prevalence, and hence lower expected rates of diseases that are
smoking related, like lung cancer. Not taking this into account
among welders might result in long duration welders appearing to
have diminished excess risk when, in fact, excess risk continues to
increase with time (Ex. 47-19-1, p. 6).

Mr. Park also emphasized the special importance of detailed information
for individual workers in multi-employer studies with exposure
conditions that vary widely across employers. He notes that high worker
turnover in highly exposed jobs `` * * * could result in long duration
welding employment appearing to have lower risk than some shorter
duration [welding] employment when it does not'' (Ex. 47-19-1, p. 6).
    EPRI compared the risk of lung cancer among a subset of workers in
the Gerin cohort exposed to high cumulative levels of Cr(VI) to the
risk found among chromate production workers in the Gibb et al. and
Luippold et al. studies. ``Focusing on the highest exposure group, SMRs
for the cohorts of stainless steel workers studied by Gerin et al
(1993) * * * range from 133 to 148 for exposures >1.5 mg-yrs/m\3\ * *
*. By comparison, the SMR from the Luippold et al. (2003) cohort is 365
for cumulative exposures of 1.0 to 2.69 mg-yrs/m\3\'', a difference
that EPRI argues `` * * * draws into question whether the exposure-
specific risk estimates from the chromate production industry can be
extrapolated to welders'' (Ex. 38-8, p. 25). It is not clear why EPRI
chose to focus on the high exposure group, which had a minimum of 1.5
mg/m\3\-years cumulative Cr(VI) exposure, a mean of 2.5 mg/m\3\-years,
and no defined upper limit. Compared to the other exposure groups
described by Gerin et al., this group is likely to have had more
heterogenous exposure levels; may be expected to have a stronger

healthy worker effect due to the association between high cumulative
exposure and long employment history; and is the least comparable to
either workers exposed for a working lifetime at the proposed PEL (1
[mu]g/m\3\ * 45 years = 0.045 mg/m\3\-years cumulative exposure) or
welders in modern-day working conditions, who according to an IARC
review cited in EPRI's comments typically have exposure levels less
than 10 [mu]g/m\3\ (<  0.45 mg/m\3\-years cumulative exposure over 45
years) (Ex. 38-8, p. 4). In addition, the majority of the observation
time in the Luippold et al. cohort and the vast majority in the Gibb et
al. cohort is associated with exposure estimates lower than 1.5 mg/
m\3\-years Cr(VI) (Ex. 33-10, p. 455, Table 3; 25, p. 122, Table VI).
    It should be noted that the levels of excess lung cancer risk
observed among welders in the Gerin et al. cohort and chromate
production workers in the Gibb and Luippold cohorts are quite similar
at lower cumulative exposure ranges that are more typical of Cr(VI)
exposures experienced in the cohorts. For example, the group of welders
with estimated cumulative exposures ranging from 50 to 500 [mu]g-yrs/
m\3\ has an SMR of 230. Chromate production workers from the Gibb and
Luippold cohorts with cumulative exposures within this range have
comparable SMRs, ranging from 184 to 234, as shown in Table VI-11
below. For reference, 45 years of occupational exposure at
approximately 1.1 [mu]g/m\3\ Cr(VI) would result in a cumulative
exposure of 50 [mu]g-yrs/m\3\; 45 years of occupational exposure at
approximately 11.1 [mu]g/m\3\ Cr(VI) would result in a cumulative
exposure of 500 [mu]g-yrs/m\3\.
[GRAPHIC] [TIFF OMITTED] TR28FE06.026

    OSHA performed an analysis comparing the risks predicted by OSHA's
models, based on the Gibb and Luippold data collected on chromate
production workers, with the lung cancer deaths reported for the
welders in the Gerin et al. study. Gerin et al. presented observed and
expected lung cancer deaths for four categories of cumulative exposure:
< 50 [mu]g-yrs/m\3\, 50-500 [mu]g-yrs/m\3\, 500-1500 [mu]g-yrs/m\3\, and
1500+ [mu]g-yrs/m\3\. The great majority of the Gerin et al. data on
stainless steel welders (98% of person-years) are in the highest three
categories, while the lowest category is extremely small (< 300 person-
years of observation). OSHA's preferred risk models (based on the Gibb
and Luippold cohorts) were used to predict lung cancer risk for each of
the three larger exposure categories. The OSHA predictions were derived
using the mean values from each exposure range, except for the open-
ended highest category, for which Gerin et al. reported a mean exposure
level of 2500 [mu]g-yrs/m\3\ (Ex. 7-120, p. S26). The ratio of
predicted to background lung cancer deaths, which approximately
characterizes the expected SMRs for these exposure groups, was
calculated for each group.
    The OSHA model predictions were calculated assuming that workers
were first exposed to Cr(VI) at age 29, the average age at the start of
employment reported by Gerin et al. (Ex. 7-120, p. S26). The SMRs
reported by Gerin et al. were calculated for welders with at least five
years of employment and at least 20 years of follow-up. However, the
average duration of employment and follow-up was not evident from the
publication. The OSHA model predictions were therefore calculated using
a range of reasonable assumptions about the duration of employment over
which workers were exposed (5, 10, 15, and 20 years) and the length of
follow-up (30, 40, and 50 years).
    Table VI-12 below presents the SMRs reported by Gerin et al. for
stainless steel welders in the three highest exposure categories,
together with the ratio of predicted to background lung cancer deaths
from OSHA's risk models. It should be noted that the ratio was
calculated using year 2000 U.S. lung cancer mortality rates, while the
SMRs reported by Gerin et al. were calculated using national lung
cancer mortality rates for the nine European countries represented in
the study (Ex. 7-114).

[GRAPHIC] [TIFF OMITTED] TR28FE06.027

    Table VI-12 shows that the range of risk ratios predicted by OSHA's
model is higher than the ratios reported for the highest exposure group
in the Gerin et al. cohort, consistent with EPRI's observations (Ex.
38-8, p. 25). However, the risk ratios predicted by OSHA's model are
consistent with the Gerin SMRs for the 500-1500 [mu]g-yrs/m\3\
cumulative exposure range. For the 50-500 [mu]g-yrs/m\3\ cumulative
exposure range, the OSHA prediction falls slightly below the lung
cancer mortality ratio observed for the Gerin et al. cohort. The OSHA
predictions for each group overlap with the 95% confidence intervals of
the Gerin et al. SMRs, suggesting that sampling error may partly
account for the discrepancies between the observed and predicted risk
ratios in the lowest and highest exposure groups.
    As previously discussed, OSHA believes that the lack of a clear
exposure-response trend in the Gerin et al. study may be partly
explained by exposure misclassification. As shown in Table VI-12, the
highest exposure group has lower risk than might be expected based on
OSHA's preferred risk models, while the lowest exposure group appears
to have higher risk than OSHA's models would predict. This overall
pattern of generally elevated but non-increasing SMRs across the three
larger exposure groups in the Gerin study is consistent with
potentially severe exposure misclassification. The higher-than-
predicted risks among welders in the lowest exposure group could
similarly reflect misclassification. However, it is not possible to
determine with certainty that exposure misclassification is the cause
of the differences between the risk predicted by OSHA's model and that
observed in the Gerin cohort.
    Finally, EPRI cites the generally similar relative risks found
among stainless steel and mild steel welders as further evidence that
exposure to Cr(VI) may not carry the same risk of lung cancer in
welding operations as it does in the chromate production industry. EPRI
states:

    [I]t is reasonable to expect that if Cr(VI) were a relevant risk
factor for welders in the development of lung cancer, and certain
types of welding involve Cr(VI) more than other types, then
subgroups of welders who are more exposed to Cr(VI) by virtue of the
type of welding they do should have higher rates of lung cancer than
welders not exposed to Cr(VI) in their welding occupation;

in particular, `` * * *stainless steel welders should have a higher
risk of lung cancer than welders of mild steel'' (Ex. 38-8, p. 13).
OSHA believes that EPRI's point would be correct if the subgroups in
question are similar in terms of other important risk factors for lung
cancer, such as smoking, co-exposures, and overall population health.
However, no analysis comparing stainless steel welders with mild steel
welders has properly controlled for these factors, and in fact there
have been indications that mild steel welders may be at greater risk of
lung cancer than stainless steel welders from non-occupational causes.
As discussed by EPRI, ``[r]esults from cohort studies of stainless
steel welders with SMRs much less than 100 support an argument that the
healthy worker effect might be more marked among stainless steel
workers compared to mild steel welders'; also `` * * *stainless steel
welders are generally more qualified and paid more than other welders''
(Ex. 38-8, p. 16), a socioeconomic factor that suggests possible
differences in lung cancer risk due to smoking, community exposures, or
occupational exposures from employment other than welding.
    Comments submitted by Exponent (Ex. 38-233-4) and EPRI (Ex. 38-8)
compare the Cr(VI) compounds found in welding fumes and those found in
the chromate production environments of the Gibb and Luippold cohorts.
Exponent stated that ``[t]he forms of Cr(VI) to which chromate
production workers were historically exposed are primarily the soluble
potassium and sodium chromates'' found in stainless steel welding
fumes. Less soluble forms of Cr(VI) are also found in stainless steel
welding fumes in limited amounts, as discussed in the 1990 IARC
monograph on welding (Ex. 35-242, p. 460), and are believed to have
been present in limited amounts at the plants where the Gibb and
Luippold workers were employed (Ex. 38-233-4, p. 4). Exponent concludes
that, while it is difficult to compare the exposures of welders to
chromate production workers, `` * * *there is no obvious difference * *
* in solubility * * * '' that would lead to a significantly lesser risk
from Cr(VI) exposure in welding as compared to the Gibb and Luippold
cohort exposures (Ex. 38-233-4, p. 3, p. 11). OSHA believes that the
similarity in the solubility of Cr(VI) exposures to welders and
chromate production workers supports the Agency's use of its risk model
to describe Cr(VI)-related risks to welders.
    Exponent and others (Exs. 38-8; 39-25) commented on the possibility
that the bioavailability of Cr(VI) may nevertheless differ between
welders and chromate production workers, stating that `` * * *
bioavailability of Cr(VI)-containing particles from welding fumes may
not be specifically related to solubility of the Cr(VI) chemical
species in the fume'' (Ex. 38-233-4, p. 11). In this case, Exponent
argues,

delivered doses of Cr(VI) to the lung could be quite dissimilar
among welders as compared to chromate production industry workers
exposed to the same Cr(VI) chemical species at the same Cr(VI)
airborne concentrations (Ex. 38-233-4, p. 11).

However, Exponent provided no data or plausible rationale that would
support a Cr(VI) bioavailability difference between chromate production
and welding. The low proportion of respirable Cr(VI) particles that
apparently limits bioavailability of inhaled Cr(VI) during aircraft
spray priming operations described previously is not an issue with
welding. High temperature welding generates fumes of small

respirable-size Cr(VI) particles able to penetrate the bronchoalveolar
region of the lung. OSHA finds no evidence indicating that Cr(VI) from
welding is less bioavailable than Cr(VI) from soluble chromate
production.
    In summary, OSHA agrees with EPRI and other commenters that
evidence of an exposure-response relationship is not as strong in
studies of Cr(VI)-exposed welders compared to studies of chromate
production workers. OSHA believes that the available welding studies
are less able to detect an exposure-response relationship, due to the
potentially severe exposure misclassification, occupational exposure to
other cancer causing agents, and the general lack of information with
which to control for any differences in background lung cancer risk
between Cr(VI)-exposed and unexposed welders. In contrast, the two
featured cohorts had sufficient information on workers' Cr(VI)
exposures and potential confounding exposures to support a reliable
exposure-response assessment. These are the primary factors that led
OSHA to determine (like EPRI and Exponent) that the Luippold and Gibb
cohorts are the best data available on which to base a model of
exposure-response between Cr(VI) and lung cancer (Exs. 38-8, p. 6; 38-
233-4, p. 1). Moreover, EPRI admitted that examination of `` * * * the
forms of Cr(VI) to which welders are exposed, exposure concentrations,
and other considerations such as particle size * * * '' identified `` *
* * no specific basis * * * '' for a difference in Cr(VI)-related lung
cancer risk among welders and the Gibb and Luippold chromate production
cohorts (Ex. 38-8, p. 7). OSHA concludes that it is reasonable and
prudent to estimate welders' risk using the exposure-response model
developed on the basis of the Gibb et al. and Luippold et al. datasets.

H. 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 three
additional data sets (Mancuso, Hayes et al., and Gerin et al.). 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. datasets and a linear
relative risk model, OSHA 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 five data sets.
    OSHA does not believe that it is appropriate to employ a threshold
dose-response approach to estimate cancer risk from a genotoxic
carcinogen, such as Cr(VI). Federal agencies, including OSHA, assume an
exposure threshold for cancer risk assessments to genotoxic agents only
when there is convincing evidence that such a threshold exists (see
e.g. EPA, Guidelines for Carcinogen Risk Assessment, March 2005, pp. 3-
21). 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 or
other non-linearity. 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. While physiological defense
mechanisms (e.g. extracellular reduction, DNA repair, apoptosis) can
potentially introduce dose transitions, there is no evidence of a
significantly non-linear Cr(VI) dose-lung cancer response in the
exposures of interest to OSHA. Finally, as previously discussed, linear
no-threshold risk models adequately fit the existing exposure-response
data.
    The slightly soluble Cr(VI) compounds produced a higher incidence
of respiratory tract tumors than highly water soluble or highly water
insoluble Cr(VI) compounds in animal studies that tested Cr(VI)
compounds under similar experimental conditions. This likely reflects
the greater tendency for chromates of intermediate water solubility to
provide a persistent high local concentration of solubilized Cr(VI) in
close proximity to the target cell. Highly soluble chromates rapidly
dissolve and diffuse in the aqueous fluid lining the epithelia of the
lung and are more quickly cleared from the respiratory tract. Thus,
these chromates are less able to achieve the higher and more persistent
local concentrations within close proximity of the lung cell surface
than the slightly water soluble chromates. Water insoluble Cr(VI)
particulates are also able to come in close contact with the lung cell
surface but do not release readily absorbed chromate ions into the
biological environment as rapidly. OSHA concludes that slightly soluble
Cr(VI) compounds are likely to exhibit a greater degree of
carcinogenicity than highly water soluble or water insoluble Cr(VI)
when the same dose is delivered to critical target cells in the
respiratory tract of the exposed worker. OSHA also believes it
reasonable to regard water insoluble Cr(VI) to be of similar
carcinogenic potency to highly water soluble Cr(VI) compounds in the
absence of convincing scientific evidence to indicate otherwise.
    The Gibb and Luippold cohorts were predominantly exposed to highly
water-soluble chromates, particularly sodium chromate and dichromate.
After evaluating lung cancer rates in other occupational cohort studies
with respect to the forms of Cr(VI) in the workplace, reliability in
the Cr(VI) exposure data, and the presence of potentially confounding
influences (e.g. smoking) and bias (e.g. healthy worker survivor bias)
as well as information on solubility, particle size, cell uptake, and
other factors influencing delivery of Cr(VI) to lung cells, OSHA finds
the risks estimated from the Gibb and Luippold cohorts adequately
represent risks to workers exposed to equivalent levels of Cr(VI)
compounds in other industries.
    As with any risk assessment, there is some degree of uncertainty in
the projection of risks that results 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, which usually involved exposures to higher Cr(VI) levels for
shorter periods of time to an equivalent cumulative exposure involving
a lower level of exposure for a working lifetime. The study cohorts
consisted mostly of 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

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 estimate of lung cancer risk from a 45 year occupational
exposure to Cr(VI) at the previous PEL of 52 [mu]g/m\3\ 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 statistical uncertainty, or for other potential sources of
uncertainty or bias. The wider range of 62 to 493 excess deaths per
1000 represents the statistical uncertainty associated with OSHA's
excess risk estimate at the previous 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 were previously
shown in Table VI-7, together with the uncertainty bounds for the
primary and supplemental studies at these exposure concentrations. 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 VII on the
Significance of Risk and in Section VIII on the Benefits Analysis.

VII. 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, 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 to protect workers 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) further defined OSHA's regulatory authority. The Court
stated:

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

    ``But `safe' is not the equivalent of `risk-free' '', the Court
maintained. ``[T]he Secretary is required to make a threshold finding
that a place of employment is unsafe-in the sense that significant
risks are present and can be eliminated or lessened by a change in
practices'' (IUD v. API, 448 U.S. at 642). It has been Agency practice
in regulating health hazards 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 it 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 must be supported by substantial
evidence, the Agency ``is not required to support the finding that a
significant risk exists with anything approaching scientific
certainty'' (448 U.S. at 656). 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 on] 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 quantitative estimates of
the excess lung cancer risk associated with previously allowable Cr(VI)
exposure concentrations and the expected impact of the new PEL. OSHA
has determined that long-term exposure at the previous PEL would pose a
significant risk to workers' health, and that adoption of the new PEL
and other provisions of the final rule will substantially reduce this
risk.

A. Material Impairment of Health

    As discussed in Section V of this preamble, there is convincing
evidence that exposure to Cr(VI) may cause a variety of adverse health
effects, including lung cancer, nasal tissue damage, asthma, and
dermatitis. OSHA considers these conditions to be material impairments
of health, as they are marked by significant discomfort and long-
lasting adverse effects, can have adverse occupational and social
consequences, and may in some cases have permanent or potentially life-
threatening consequences. Based on this finding and on the scientific
evidence linking occupational Cr(VI) 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.
1. Lung Cancer
    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).
2. Non-Cancer Impairments
    While OSHA has relied primarily on the association between Cr(VI)
inhalation and lung cancer to demonstrate the necessity of the
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 ulceration of the nasal passages and perforation of
the nasal septum (Exs. 35-1; 7-3; 9-126; 35-10; 9-18; 3-84; 7-50; 31-
22-12). Nasal tissue ulcerations are often accompanied by swelling and
bleeding, heal slowly, and in some cases may progress to a permanent
perforation of the nasal septum that can only be repaired surgically.
Inhalation of Cr(VI) may also lead to asthma, a potentially life-
threatening condition in which workers become allergic to Cr(VI)
compounds and experience symptoms such as coughing, wheezing, and
difficulty in breathing upon exposure to small amounts of airborne
Cr(VI). Several case reports have documented asthma from Cr(VI)
exposure in the workplace, supporting Cr(VI) as the sensitizing agent
by bronchial challenge (Exs. 35-7; 35-12; 35-16; 35-21).
    During the comment period, NIOSH requested that OSHA consider
allergic contact dermatitis (ACD) as a material impairment of health
due to occupational exposure to Cr(VI). NIOSH reasoned:

    Dermal exposure to Cr(VI) through skin contact * * * may lead to
sensitization or allergic contact dermatitis. This condition, while
not life-threatening, is debilitating and marked by significant
discomfort and long-lasting adverse effects; it can have adverse
occupational and social consequences and should be a material
impairment to the health of affected workers * * * Including
allergic contact dermatitis in OSHA's determination of material
impairment of health draws attention to the fact that Cr(VI) is both
a dermal exposure hazard and an inhalation hazard, and alerts
employers that they should seek to minimize exposure to both routes
(Ex. 40-10-2, p. 3)

    OSHA fully agrees with the NIOSH comment. There is strong evidence
that unprotected skin contact with Cr(VI)-containing materials and
solutions can cause ACD as well as irritant dermatitis and skin
ulceration (see section V.D). ACD is a delayed hypersensitivity
response. The worker initially becomes sensitized to Cr(VI) following
dermal exposure. Once a worker becomes sensitized, brief exposures to
small amounts of Cr(VI) can trigger symptoms such as redness, swelling,
itching, and scaling. ACD is characterized by the initial appearance of
small raised papules that can later develop into blisters and dry
thickened, cracked skin. The allergic condition is persistent, causing
some workers to leave their jobs (Ex. 35-320). Symptoms of ACD
frequently continue long after occupational exposure to Cr(VI) ends,
since sensitized individuals can react to contact with Cr(VI) in
consumer products and other non-occupational sources.
    Skin exposure to Cr(VI) compounds can also cause a non-allergic
form of dermatitis. This skin impairment results from direct contact
with Cr(VI) doses that damage or irritate the skin, but do not involve
immune sensitization. This form of dermatitis can range from mild
redness to severe burns and ulcers, known as ``chrome holes'', that
penetrate deep into tissues. Once the worker is removed from exposure,
the skin ulcers heal slowly, often with scarring.

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 currently allowable exposure conditions, as well
as the expected reduction in risk that would occur with implementation
of the new 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 identified a range of expected risk from regular occupational
exposure at the previous PEL (101-351 excess lung cancer deaths per
1000 workers) and at the new PEL of 5 [mu]g/m\3\ (10-45 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 from two extensively studied worker populations, 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 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. 33-11). 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
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 strong basis for
risk analysis, in that it has high-quality documentation of worker
Cr(VI) exposure and mortality, a long period of follow-up, and a large
proportion of relatively long-term employees (55% were employed for
longer than 5 years).
1. Lung Cancer Risk Based on the Gibb Cohort
    Risk assessments were performed on the Gibb cohort data by Environ
International Corporation (Ex. 33-12), under contract with OSHA; Park
et al., as part of an ongoing effort by NIOSH (Ex. 33-13); and Exponent
on behalf of the Chrome Coalition (Ex. 31-18-15-1). A variety of
statistical models were considered, allowing OSHA to identify the most
appropriate models and assess the resulting risk estimates' sensitivity
to alternate modeling approaches. Models were tried with additive and
relative risk assumptions; various exposure groupings and lag times;
linear and nonlinear exposure-response functions; external and internal

standardization; reference lung cancer rates from city-, state-, and
national-level data; inclusion and exclusion of short-term workers; and
a variety of ways to control for the effects of smoking. OSHA's
preferred approach, a relative risk model using Baltimore lung cancer
reference rates, and NIOSH's preferred approach, a relative risk model
using detailed smoking information and U.S. lung cancer reference
rates, are among several models that use reasonable assumptions and
provide good fits to the data. As discussed in section VI, the Environ,
Park et al., and linear Exponent models yield similar predictions of
excess risk from exposure at the previous PEL and the new PEL (see
Tables VI-2 and VI-3). OSHA's preferred models (from the Gibb data set)
predict about 300-350 excess lung cancers per 1000 workers exposed for
a working lifetime of 45 years at the previous PEL and about 35-45
excess lung cancers per 1000 workers at the new PEL of 5 [mu]g/m\3\.
    Environ and Crump et al. performed risk assessments on the Luippold
cohort, exploring additive and relative risk models, linear and
quadratic exposure-response functions, and several exposure groupings
(Exs. 35-59; 35-58). Additive and relative risk models by both analyst
groups fit the data adequately with linear exposure-response. All
linear models 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 previous PEL, and ten excess lung cancer deaths per 1000
workers at the new PEL.
2. Lung Cancer Risk Based on the Luippold Cohort
    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 previous PEL and
10-45 per 1000 for 45 years' occupational exposure at the new 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 was submitted, which supported
the Agency's approach and results. OSHA also received several comments
in support of its risk estimates (Exs. 44-7, 38-222; 39-73-1). A full
analysis of major comments on the results of OSHA's quantitative risk
assessment can be found in section VI.F.
3. Risk of Non-Cancer Impairments
    Although nasal damage and asthma may be associated with
occupational exposure to airborne Cr(VI), OSHA has determined that
there are insufficient data to support a formal quantitative risk
assessment for these effects. Available occupational studies of Cr(VI)-
induced nasal damage are either of cross-sectional study design, do not
provide adequate data on short-term airborne Cr(VI) exposure over an
entire employment period, or do not account for possible contribution
from hand-to-nose transfer of Cr(VI) (Exs. 31-22-12; 9-126; 35-10; 9-
18). Occupational asthma caused by Cr(VI) has been documented in
clinical case reports but asthma occurrence has not been linked to
specific Cr(VI) exposures in a well-conducted epidemiological
investigation. 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, such as damage
to nasal tissue, with specific occupational exposure conditions, the
Agency has qualitatively 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
tissue ulceration 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 while employed in a job with average
exposure concentrations greater than 20 [mu]g/m3. Nasal
septum perforations were reported among 17% of the Gibb cohort workers,
and developed over relatively long periods of exposure (median time 172
days from hire date to diagnosis).
    A high prevalence of nasal damage was also found in a study of
Swedish chrome platers (Ex. 9-126). Platers exposed to average 8-hour
Cr(VI) concentrations above 2 [mu]g/m3 with short-term
excursions above 20 [mu]g/m3 from work near the chrome bath
had a nearly 50 percent prevalence (i.e. 11 out of 24 workers) of nasal
ulcerations and septum perforations. These data, along with that from
the Gibb cohort, suggest a substantial and clearly significant risk of
nasal tissue damage from regular short-term exposures above 20 [mu]g/
m3. More than half of the platers (i.e. 8 of 12 subjects)
with short-term excursions to somewhat lower Cr(VI) concentrations
between 2.5 and 11 [mu]g/m3 had atrophied nasal mucosa (i.e.
cellular deterioration of the nasal passages) but not ulcerations or
perforations. This high occurrence of nasal atrophy was substantially
greater than found among the workers with mean Cr(VI) levels less than
2 [mu]g/m3 (4 out of 19 subjects) and short-term Cr(VI)
exposures less than 1 [mu]g/m3 (1 of 10 subjects) or among
the office workers not exposed to Cr(VI) (0 of 19 subjects). This
result is consistent with a concentration-dependant gradation in
response from relatively mild nasal tissue atrophy to the more serious
nasal tissue ulceration with short-term exposures to Cr(VI) levels
above about 10 [mu]g/m3. For this reason, OSHA believes
short-term Cr(VI) exposures regularly exceeding about 10 [mu]g/
m3 may still result in a considerable risk of nasal
impairment. However, the available data do not allow a precise
quantitative estimation of this risk.
    While dermal exposure to Cr(VI) can cause material impairment to
the skin, a credible quantitative assessment of the risk is not
possible because few occupational studies have measured the amounts of
Cr(VI) that contact the skin during job activities; studies rarely
distinguish dermatitis due to Cr(VI) from other occupational and non-
occupational sources of dermatitis; and immune hypersensitivity
responses, such as ACD, have an exceedingly complex dose-response.

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 VII-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 always done in
significant risk determinations for previous standards, the Agency
finds an excess lung cancer risk of approximately 100 to 350 per 1000
workers exposed at the previous PEL of 52 [mu]g/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
new PEL of 5 [mu]g/m3 Cr(VI) is expected to reduce these
risks substantially, to below 50 excess lung cancers per 1000 workers.
However, even at the new PEL, the risk posed to workers with a lifetime
of regular exposure is still clearly significant.
[GRAPHIC] [TIFF OMITTED] TR28FE06.028

    Workers exposed to concentrations of Cr(VI) lower than the new PEL
and for shorter periods of time may also have significant excess cancer
risk. The Agency's risk estimates are roughly proportional to duration
for any given exposure concentration. The estimated risk to workers
exposed at any fixed concentration for 10 years is about one-half the
risk to workers exposed for 20 years; the risk for five years' exposure
is about one-fourth the risk for 20 years. For example, about 11 to 55
out of 1000 workers exposed at the previous PEL for five years are
expected to develop lung cancer as a result of their exposure. Those
exposed to 10 [mu]g/m3 Cr(VI) for 5 years have an estimated
excess risk of about 2-12 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 old standard; even workers exposed
for shorter periods at levels below the previous PEL are at substantial
risk, and will benefit from implementation of the new 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 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
VII-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. Regular exposures at high
levels, including the previous PEL of 52 [mu]g/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 new PEL of 5 [mu]g/m3 Cr(VI) the Agency's
estimated range of excess lung cancer mortality overlaps the fatality
risk for

mining and approaches that for construction, but still clearly exceeds
the risk in lower-risk industries such as manufacturing.
[GRAPHIC] [TIFF OMITTED] TR28FE06.029

    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 VII-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.
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    The Cr(VI) risk estimate at the previous PEL is higher than many
risks the Agency has found to be significant in previous rules (Table
VII-3, ``Risk at Previous PEL''). The estimated risk from lifetime
occupational exposure to Cr(VI) at the new PEL is 10-45 excess lung
cancer deaths per 1000 workers, a range which overlaps the estimated
risks from exposure at the current PELs for benzene and cadmium (Table
VII-3, ``Risk at new 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 finds that the risk of
lung cancer posed to workers under the previous permissible level of
occupational Cr(VI) exposure is significant. The new PEL of 5 is
expected to reduce risks to workers in Cr(VI)-exposed occupations
substantially (by about 8- to 10-fold). OSHA additionally finds that
nasal tissue ulceration and septum perforation can occur under exposure
conditions allowed by the previous PEL leading to an additional health
risk beyond the significant lung cancer risk present. The reduction of
the Cr(VI) PEL from 52 [mu]g/m3 to 5 [mu]g/m3 is
expected to substantially reduce workers' risk of nasal tissue damage.
With regard to dermal effects from Cr(VI) exposure, OSHA believes that
provision of appropriate protective clothing and adherence to
prescribed hygiene practices will serve to protect workers from the
risk of Cr(VI)-induced skin impairment.

VIII. Summary of the Final Economic and Regulatory Flexibility Analysis

A. Introduction

    OSHA's Final Economic and Regulatory Flexibility Analysis (FEA)
addresses issues related to the costs, benefits, technological and
economic feasibility, and economic impacts (including small business
impacts) of the Agency's Occupational Exposure to Hexavalent Chromium
rule. The full Final Economic and Regulatory Flexibility Analysis has
been placed in the docket as Ex. 49. The analysis also evaluates
alternatives that were

considered by the agency before adopting the final rule. This rule is
an economically significant rule under Section 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 Final Economic and Regulatory
Flexibility Analysis is to:
     Identify the establishments and industries potentially
affected by the final 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 final standard;
     Assess the economic feasibility of the rule for affected
industries; and
     Evaluate the principal regulatory alternatives to the
final rule that OSHA has considered.
    The full Final 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. Final Regulatory Flexibility Analysis
Chapter VIII. Environmental Impacts
Chapter IX. Assessing the Need for Regulation.

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

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

    The final 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)
may also lead to asthma. To protect exposed workers from these effects,
OSHA has set a Permissible Exposure Limit (PEL) of 5 [mu]g/m\3\
measured as an 8-hour time weighted average. OSHA also examined
alternative PELs ranging from 20 [mu]g/m\3\ to 0.25 [mu]g/m\3\ measured
as 8-hour time weighted averages.
    OSHA's final 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 final rule requires employers to:
     Monitor the exposure of employees (though allowing a
performance-oriented approach to monitoring);
     Establish regulated areas when exposures may reasonably be
expected to exceed the PEL (except in shipyards and construction);
     Implement engineering and work practice controls to reduce
employee exposures to Cr(VI);
     Provide respiratory protection to supplement engineering
and work practice controls where those controls are not feasible, where
such controls are insufficient to meet the PEL, 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 action level for 30 days or more;
     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 issuing separate
standards for general industry, construction and shipyard employment,
are more fully discussed in the Summary and Explanation section of this
Preamble.
    Chapter II of the full FEA 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 analyses 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.
    The most common sources of 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, particularly stainless steel or other high-chromium steels,
or with chromium coatings; and 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 a sharp decline 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 FEA. Painting activities in general
industry primarily 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 paints
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.
    OSHA has made a number of changes to the industrial profile of the
application groups as a result of comments on the proposed rule. Among
the most important are:
     Additions to the electroplating application group to
include such processes as chrome conversion, which were not considered
at the time of the proposal;
     Additions to the painting application group to cover
downstream users, particularly automobile repair shops and construction
traffic painting;
     Additions to glass manufacturing to cover fiberglass, flat
glass, and container glass industries;
     Addition of the forging industry;
     Addition of the ready mixed concrete industry;

     Additions to the welding application group to include
welding on low-chromium steel and increase the estimated number of
exposed workers in the maritime sector; and
     More careful division of the many different industries in
which electroplating, welding and painting may appear as applications.
    Table VIII-1 shows the application groups analyzed in OSHA's FEA,
as well as the 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, updated to reflect
2002 data. (This table provides the latest available data at the time
this analysis was produced.) As shown in the table, there are a total
of 52,000 establishments affected by the final standard.
    Various types of welding applications account for the greatest
number of establishments and number of employees affected by the final
standard.
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    Table VIII-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 were 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, commenters on the proposed rule and other interested
parties.
    It is also important to note that Table VIII-2 and OSHA's cost and
feasibility analyses reflect the full range of exposures occurring in
each application group, not the median exposures. Some commenters
(e.g., Ex. 47-27-1) misunderstood this and believed OSHA determined
that only employers with median exposures above the PEL would incur
costs for engineering and work practice controls. OSHA did not use
exposure medians to assign compliance costs in this rulemaking. OSHA
made limited use of exposure medians for only a few purposes. The first
was in the analysis of baseline controls, described in the
technological feasibility discussion below. Where both exposure data
and information on the controls in place were available, OSHA used the
median exposure level experienced in the presence of a specific type of
control to assign an effectiveness level to the control. Second, to
determine whether to assume baseline controls were already in place in
cases where OSHA only had exposure data available, it compared median
exposure levels to the median exposure levels previously assigned to
baseline controls.
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    In all sectors OSHA has used the best available information to
determine baseline exposures and technological feasibility. Throughout
the rulemaking process OSHA requested industry-specific information.
These requests included site visits, discussions with industry experts
and trade associations, the 2002 Request for Information (RFI), and the
SBREFA process. These requests continued through the proposal and the
public hearing process where OSHA continued to request information.
OSHA reviewed all the data submitted to the record and where
appropriate updated the exposure profile. For exposure information to
be useful in the profile, only individual personal exposures
representing a full shift were used.
    As noted earlier, OSHA used a variety of sources to obtain
information about exposures in each application group. These sources
include: NIOSH Health Hazard Evaluations (HHEs), OSHA's Integrated
Management Information System (IMIS) exposure data, data from other
government agencies, published literature, OSHA/NIOSH site visits,
discussions with industry experts and trade associations, and data
submitted to the OSHA record. In some instances OSHA's contractor had
difficulty obtaining permission to perform site visits in a specific
application group. For instance, OSHA's contractor could obtain
permission to conduct a site visit only at a steel mill that used the
teeming and primary rolling method--in contrast to continuous casting,
now used in approximately 95 percent of steel mills. In these few
cases, OSHA acknowledged these potential problems and OSHA (or its
contractor) discussed its concerns with industry experts and used their
professional judgment to determine technological feasibility.
    In response to the exposure data submitted to the record OSHA has
made the following major changes to the exposure profile:
     Electroplating--Revised the exposure distribution for hard
chrome electroplating to use only the more-detailed exposure data from
site visits and other NIOSH reports.
     Welding--In construction, OSHA used exposure data from the
maritime sector for analogous operations to supplement the exposure
profile. Added additional exposure data to the profile as provided to
the record.
     Painting--Revised the exposure profile to reflect the
additional aerospace exposure data submitted to the record.
     Steel Mills--Revised the exposure profile to reflect
additional exposure data supplied to the record; welders were added
directly to this application group.
     Chromium Catalyst Users--Revised the exposure profile
based on additional exposure data from a NIOSH HHE.
     Wood working--Added information from the record.
     Construction--Revised the exposure profile to reflect the
additional exposure information submitted to the record.
    Detailed information on the changes made in the exposure profile
for each application group can be found in Chapter III of the Final
Economic Analysis.
    OSHA's analysis of technological feasibility examined employee
exposures at the operation or task level to the extent that such data
were available. There are approximately 558,000 workers exposed to
Cr(VI), of which 352,000 are exposed above 0.25 micrograms per cubic
meter and 68,000 above the PEL of 5 micrograms per cubic meter.

C. Technological Feasibility

    In Chapter III of OSHA's FEA, OSHA assesses the current exposures
and the technological feasibility of the final standard in all affected
industry sectors. The analysis presented in this chapter is organized
by application group and analyzes employee exposures at the operation
or task level to the extent that such data are available. Accordingly,
OSHA collected exposure data at the operation or task level to identify
the Cr(VI)-exposed workers or job operations that need to improve their
process controls to achieve exposures at or below the PEL. In the few
instances where there were insufficient exposure data, OSHA used
analogous operations to characterize these operations.
    In general, OSHA considered the following kinds of controls that
could reduce employee exposures to Cr(VI): local exhaust ventilation
(LEV), which could include maintenance or upgrade of the current local
exhaust ventilation or installation of additional LEV; process
enclosures that would isolate the worker from the exposure; process
modifications that would reduce the generation of Cr(VI) dust or fume
in the work place; improved general dilution ventilation including
assuring that adequate make-up air is supplied to the work place;
improved housekeeping; improved work practices; and the supplemental
use of respiratory protection if engineering and work practice controls
were not sufficient to meet the 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
the exposure levels they can achieve is based on information collected
by Shaw Environmental, Inc. (Ex. 50), a consultant to OSHA, on the
current exposure levels associated with existing controls, on the
availability of additional controls needed to reduce employee
exposures, and on other evidence presented in the docket.
    Through the above analysis, OSHA finds that a PEL of 5 [mu]g/m\3\
is technologically feasible for most operations in all affected
industries through the use of engineering and work practice controls.
As discussed further below, the final rule requires that when painting
of aircraft or large aircraft parts is performed in the aerospace
industry, the employer is only required to use engineering and work
practice controls to reduce employee exposures to Cr(VI) to or below 25
[mu]g/m\3\. The employer must then use respiratory protection to
achieve the PEL. Apart from this limited exception, all other
industries can achieve the PEL with only minimal reliance on
respiratory protection. Table VIII-3 shows OSHA's estimate of
respirator use by industry for each of the PELs that OSHA considered.
At the final PEL of 5 [mu]g/m\3\, only 3.5 percent of exposed employees
will be required to use respirators.
    In only three sectors will respirator use be required for more than
5 percent of exposed employees. In two of these sectors, chromate
pigment producers and chromium dye producers, use of respirators will
be intermittent. The third sector, stainless steel welding, presents
technological challenges in certain environments such as confined
spaces. OSHA has concluded that, with a few limited exceptions which
are discussed below, employers will be able to reduce exposures to the
PEL through the use of engineering and work practice controls.
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    In determining technological feasibility OSHA has used the median
to describe the exposure data. Since the median is a statistical term
indicating the central point of a sequence of numbers (50 percent below
and 50 percent above) it best describes exposures for most people. The
median is also a good substitute for the geometric mean for a log
normal distribution which often describes exposure data. As described
by the Color Pigments Manufacturers Association, Inc. (CPMA) in an
economic impact study by IES Engineers:

    The exposure distribution (assuming it is log normal) can be
characterized by the geometric mean and standard deviation. The
median (not the average) is a reasonable estimate of the geometric
mean (Ex. 47-3, p. 54).

    In contrast, the use of an arithmetic mean (or average) may tend to
misrepresent the exposure of most people. For example, if there are a
few workers with very high exposures due to poor engineering or work
practice controls, the arithmetic mean will be artificially high, not
representing realistic exposures for the workers.
    The technological feasibility chapter of the FEA is broken down
into five main parts: Introduction, Exposure Profile, Baseline
Controls, Additional Controls and Substitution. The first part is an
introduction to the application group, which outlines the major changes
in the analysis between the Preliminary Economic Analysis and the Final
Economic Analysis and addresses comments specific to the application
group.
    The next part of the technological feasibility analysis is the
exposure profile. The exposure profile describes the prevailing
exposures in each application group on a job-by-job basis. The exposure
profile represents exposure situations that may be well controlled or
poorly controlled. The data used to determine the current exposures
were obtained from any of the following sources: OSHA site visits; the
OSHA compliance database, Integrated Management Information System
(IMIS); NIOSH site visits; NIOSH control technology or health hazard
evaluation reports (HHE); information from the U.S. Navy; published
literature; submissions by individual companies or associations; or, in
a few cases, by consideration of analogous operations. While the
exposure profile was developed from current exposures and is not
intended to demonstrate feasibility, there were a few instances where
the exposure profile was used as ancillary support for technological
feasibility if there were a significant number of facilities already
meeting the PEL. An example of this case can be seen in the production
of colored glass, where over 90 percent of the exposure data were below
0.25 [mu]g/m3.
    In the cases where analogous operations were used to determine
exposures, OSHA used data from industries or operations where materials
and exposure routes are similar. OSHA also tended to be conservative
(over-estimating exposures). For example, exposure data for the bagging
of pigments were used to estimate exposures for the bagging of plastic
colorants. In both cases the operation consists of bagging a pigmented
powder. However, exposures would tend to be higher for bagging pigments
due to the fact that in pigments there is a higher percentage of Cr(VI)
and the pigments tend to consist of finer particles than those in
plastic colorants where the Cr(VI) particles are diluted with other
ingredients. As Mr. Jeff Cox from Dominion Colour Corporation stated:

    Exposure of packers in the pigment industry, who are making a
fine powder, is very much higher than packers in the plastics
colorants industry, who are basically packing pellets of
encapsulated product which are a few millimeters in diameter (Tr.
1710).

    The use of operations that are more difficult to control to
estimate analogous operations would result in an overestimate of
exposures, subsequently resulting in an overestimate of the controls
needed to reduce the exposures to Cr(VI) in those analogous operations.
    The next section of OSHA's analysis of technological feasibility in
the FEA describes the baseline controls. OSHA determined controls to be
``baseline'' if OSHA believed that such controls are commonly used in
the application group. This should not be interpreted to mean that OSHA
believes that all firms use these controls, but rather that the
controls are common and widely

available in the industry. Information on the controls used in each
specific application group was obtained from several different sources
such as: site visits, NIOSH HHEs, industry experts, industry
associations, published literature, submissions to the docket, and
published reports from other federal agencies. OSHA used the median to
estimate the exposure level associated with the baseline controls. For
the majority of the operations, the median was calculated using the
exposures directly associated with the baseline controls. However,
there were a few cases where the median was calculated from the
exposure profile and OSHA determined these exposures reflected the
baseline controls (e.g., fiberglass production).
    The fourth section of the technological feasibility analysis
determined the need for additional controls. If the median exposure was
above the PEL with the use of baseline controls, OSHA would recommend
additional engineering or work practice controls that would reduce
exposures to or below the PEL. The final rule does not require an
employer to use these specific controls. The engineering controls or
work practices are, however, OSHA's suggestions for possible ways to
achieve the PEL. Through this process a few situations could arise when
the exposures with baseline exposures are above the PEL:
     Engineering and work practice controls alone: OSHA
determined that additional controls would reduce worker's exposure
below the PEL if: 1) the proposed additional controls were already in
use at other facilities in the same application group and exposures
there were below the PEL, or 2) the additional controls were used in
analogous industries or operations and they were effective.
     Respiratory protection required to meet the PEL: There
were a few instances where workers' exposures would remain above the
PEL even with the installation of additional controls. In these cases
OSHA indicated that the supplemental use of respirators may be needed
(e.g. enclosed spray-painting operations in aerospace).
     Intermittent respiratory protection: There were instances
where a worker performs specific job-related activities that could
result in higher exposures above the PEL for limited periods of time.
In these cases OSHA noted that the supplemental use of respirators
during these activities may be necessary. For example, an employee who
works in pigment production generally, may need to use a respirator
only when entering the enclosure where the bagging operations take
place because the enclosure is the engineering control in this
operation.
    The final component of the technological feasibility section in the
FEA is a discussion of substitution. Here, OSHA describes the options
available for eliminating or reducing the use of ingredients that