Document qaGKJRDOMRw3VMvKqY7z8Z11k
Envimmental Health Prrspcmvcs
v01.84. Pp 185-188. 1989
c
Quantitative Assessment of Lives Lost Due to Delay in the Regulation of Occup-. ational Exposure to Benzene
by William J. Nicholson* and Philip J. Landrigan*
Benzene exposure can cause leukemia. aplastic anemia. and possibly lymphoma. In 1978. on the basis of strong but incomplete data then available on the risk of benzeneinduced leukemia. the U.S. Occupational Safety and Health Administmtion tOSHA) mluced the permissible occup.tid exporumstandud for knmw from 10 ppm to I ppm. Shortly thereafter. t h e Fifth Circuit Court of Appeals stayed this ruling. and in 1980.
the Supreme Court overturned the regulation. citing insufficient evidence of benefit. Thus. from 1978until the standard was again lowered to 1ppmin 1987. .*erica workers were tXpos+d to benzene 8t ltvtia in excess of 1 ppm. An estimated 9600were exposed to levels between 1 and 10 ppm. and a n additional 370 were
exposed a t levels above 10 pprn.
To assess the risk resulting from this delay in rewlation. we have conducted an epidemiologic risk analy-
sis. We merged data on numben of persons t'L38.000b exposed to benzene in seven occupational categoria
~.
exposures to benzene greater man I ppm that occurred betweeiil'978 and 1987. Laths from a p l i t i c anemia and lymphoma will likely add to this toll. These data confirm the risk of regulatory delay. They sup gcst that the courts. in m i e w i n r public health regulations. must bewarc of facile cost-benefit a m r n e n t s and be willing to accept strong evidence of health risk even when such evidence is incomplete.
Introduction
Clinical. epidemiologic. and tosicologc data indicate that occupational esposure to benzene can cause leukemia. The etioiogic asmiation was fmt suggested by case reports originiating more than 50years ago (1-5). Those observations were corroborated by epidemiologic studies among shoe workers (6).chemical workers. and rubber workers (7-11 1. Recently, benzene has been found to be carcinogenic in animal bioassays (12-16). Benzene was formally declared a human carcinogen by the National Institute for Occupational Safety and Health (NIOSH) in 1976 ( 17). by the C.S. Environmental Protection Agency tEP.4) in 1979 (18).and by the International Agency for Research on Cancer tI.4RC) in 1982 (19).
The regulatory history of benzene has been turbulent. Particular controversy has surrounded efforts to regulate ocmpational esposure to benzene a t relatively low levels,
`Division of Envimnmentd and Occupational Medicine. Department of Community Medicine. Mount Sinai School of Medicine. New York. NY 10029.
Address repnnt requests to W. J. Nicholson. Division of Environmental and Occupational Medicine. Department of Community Medicine. Mount S i n i School of Medicine. Yew York. NY 10029.
.-
because until recently only qualitative information \vas available on the risk of leukemia at low levels of exposure
to benzene. In 1958 the Occupational Safety and Health Administration (OSHA)promulgxed an occupational exposure standard reducing permissible workers' esposures by 10-fold, from the previously acceptable 8 hr timeweighted average (TWAO of 10 ppm to 1 ppm (20). This action was based nn infmnatim from case reports and two epidemiologic studies (21).Both of those studies
demonstrated statistically significant excess mortality from leukemia in workers exposed to benzene, but neither presented sufficient data on exposure to permit
examination of quantitative dose-response relationships
(8.9).
On July 2. 1980. in a decision of profound importance
for governmental risk assessment. the US. Supreme Court invalidated the OSHA benzene standard of 1ppm (22).The Court stated that OSHA had failed to provide
substantial evidence of the need for regulation, in that it had not quantified a "significant risk of material health
impairment" a t the previous level of 10ppm and had not established that a new standard would achieve "a substantial reduction in significant risk." As a result of this decision, workers in the United States were allowed to be exposed at levels up to 10 ppm. That situation per-
.,
186 .VICHOLSON AND W.VDRICAS
sisted until December 1987 when. on the basis of new. highly quantitative epidemiologic and toxicologic data.
OSHA reimposed a 1-ppm standard (3).
We have undertaken a quantitative assessment of the number of excess deaths from leukemia that ultimately mill result from this lo-year delay in regulation. This anal-
vsis merges inforrr5tion developed by OSHA on numbers
bf workers exposed to benzene at various concentrations in seven industrial categories with quantitative data from epidemiologic studies on risk of benzene-induced leukemia. This analysis provides a basis for reconsideration of the premises underlying the 1980 Supreme Court decision on benzene.
Methods
Populations Exposed to Benzene
In its final benzene rule, OSHA provided estimates of
the numbers of workers exposed to various concentra-
tions of benzene in the U.S. in seven different occupa-
tional categories (23).Overall in 1987. 238.0oO workers were occupationally exposed to benzene: approximately 1O.OOO wokers were exposed to timeweighted concentrations in excess of the 1-ppm standard promulgated by
OSHA in 1978(Table 1). Earlier estimates by OSH.4 had
suggested a .greater population esposure: the proposed ivle ( 3h)ad indicated that 274.OOO were esposed. 27.500 to concentrations in excess of 1 ppm.
Epidemiologic Risk Assessments
Between 1982and 1988. at least seven quantitative risk itssessments were published evaluating the risk oi leukemia in persons esposed to benzene. IARC (19)estimated that 140 to 170 excess leukemia deaths would occur per loo0 workers exposed to benzene for a 45-year working lifetime a t levels of 10 to 100 ppm (10)and that 72excess cleaths per lo00 workers would occur from exposures of the same duration at levels between 1and 30 ppm (9).Using geometric means to estimate average exposures. these data suggest that 44 to 132 excess deaths from leukemia will occur per 10oOworkers exposed a t 10ppm benzene for a 15-year working lifetime.
OSHA staff members published a risk assessment
which estimated that lito 152 escess leukemia deaths will occur per loo0 workers for the same exposure conditions (25).Another risk assessment commissioned by
OSHA for their review of the standard in 1984indicated
the best estimate of risk to be 95 excess leukemia deaths per 1OOO workers at benzene exposures of 10 ppm for a
working lifetime (3)Th.is estimate was based on an analysis of data from three exposed populations. A 1979 EP.4
assessment. although methodologically imprecise. was in approximate agreement with the above analyses (18).
Those risk assessments used slightly different methodologiesand considered different models for the dose- and timecourse of benzene-related leukemias. Nevertheless. the results were in remarkable agreement. The results
of all of the analyses fall within the range of the OSHA
estimate of U to 152 excess leukemia deaths per 10oO workers esposed to benzene for 45 years at concentrations of 10 ppm. All of the above analyses were based upon estimates of group exposure.
More recently. research has been published by Rinsky et al. (11)on the risk of leukemia related to the benzene exposures of individual subjects. The results indicate, that the above assessments based on group exposure may
actually underestimate the risk of benzeneinduced leuke mia. Tdble 2 shows observed and expected deaths from leukemia according to cumulative individual esposure. .A weighted least-squaresregression line through an SMR of 100 at zero exposure yields the relationship:
SMR = 100 + 0.035 x ppm.
The standard error on the coefficient of cumulative esposure in this equation is 0.024 to 0.045.
Rinsky et al. performed a matched case-control analysis of their data using conditional logistic regression. The
odds ratio (OR)for leukemia in relation to cumulative
benzene esposure was determined to be
OR = exp(0.0126 x ppm-yearsi.
Because of the exponential relationship. risks predicted by this model are extremely high for cumulative esposures in excess of 300 ppm-years.
We have estimated the excess leukemia mortality from this exposure-response relationship using a life-table analpis. with the risk lagged by 5 years. The results for a 45-year exposure. brining at age 25.suggest that 71 to 132 of loo0 workers initially exposed to benzene a t 10
ppm will die of benzene-related leukemia. X dose-
response relationship determined from a case-control analysis of the data from this study suggests an even higher mortality.
Table 1. ?lumber of worken ex& to benzene and c u m n t exposure levels by industry divisions (23).
Industv Petrochenucll planu
Petmleum refineries Coke and coal chemicals
Tire manufmurers
Bulk temunals Bulk planu Transponauon wa tank VU&
Totals
Exposure category by &hr time-weiehted averqe benzene concentrations. pprn
-Il.o-o.1
30,715 00
34.710 15.661 26.197 32s 139.841
0.11-05
3208
12410
372 24375 8.887
14.866 10.996 75.113
0.51-1.0
-
2.187 261
4.095
1.436
2402 2.523 12.904
1.1-5.0
989 1.a07 260 1.820 1.003 1,677 1380 8.936
51-10
103 238
42
-
81 136 48 647
10,
0 190 12
-
27 45 95 370
T~~ numbr of workers
4.300 47.37
947
8.ooo
n.095 45.323 47.600 ma12
.'
B E S Z E S E A.VD OSHA RECl'WTI0.V
187
An analysis by Crump and Allen (26).which used the same data base as that used by Rinsky et al. (11).and which employed a relative risk model. found an escess risk of death from leukemia of 72 per, loo0 workers esposed to 10 ppm for a 45-year working lifetime.
An additional analysis of the data of Rinsky et al. was undertaken by Austin et al. (23using the risk assessment methodolog propmed by Enterline et al. (28).This analysis estimated that 125 escess leukemia deaths could result per 1MMworkers esposed for ii 45-year working lifetime to 10pprn benzene. A further itnalysis by Austin et
d.. based on the Dow Chemical Company cohort (9). found that ti9 excess leukemia deaths would result per lo00 iwrkers esposed over a 45-year working lifetime to 10 ppm benzene.
Results
From these risk assessments. we have estimated the
number of lives of American workers that ultimately will
be lost because of exposure to unnecessarily high concen-
trations of benzene between 19'78and 198i. We used data
on the sizes of the esposed population from Table 1. We
used the estimate from OSHA (25)that Ut o 152 escess
leukemia deaths per lo00 workers will result from 13
years of occupational esposure to benzene at 10 ppm and
that shorter and lower esposures will result in propor-
tionally fewer deaths ti.e.. that risk is linearly related tci
cumuiative esposure,. W e calculate. on the basis of those
estimates.
to 103 premature leukemia deaths will
eventually Be caused by benzene e?tposures resulting from
the delay in implementing a 1-ppm standard between
F e b r u a r y 1978 a n d September 1987. In addition
to the leukemia deaths. deaths from aplastic anemia and
lymphomas will likely add to this toll. If. on the other
hand. the earlier population esposure estimates of OSH-4
( 2 ; ~are used. the escess leukemia death toll will range
fromJ-lt? to -1% If one use:: the dose-response r'elation-
>hip u i Rinsky et al. and the population estimate:: ofT;i-
ble 1. depending on assumptions made about esposures
prior to 1978. the number of escess deaths will range
from $0 to lo00 o r more.
The above mortality estimates were calculated using the relationship
Total deaths = P, x (E,- E,) A R x (9.6/43)
Here P, is the population (in thousands, in one of the three highest esposure categories of Table 1: E, is the category
average benzene exposure in ppm: E, is the residual ex-
posure under a 1-ppm standard: R is the risk for a &year esposure to 1 ppm. either 4.4lIOOU or 13.2'1000 and (9.6/'45is)the fraction of 45 years that the 1-ppmstandard
was delayed. The average exposures used in these calc'ulations were geometric means. 2.2 ppm and 7.1 ppm for the esposure ranges 1.1 to 5.0 ppm and 5.1 to 10 ppm. respectively, and 30 ppm for the 10- ppm category. We assumed that the residual average exposure for in-
dividuals in these categories under a 1-ppm PEL stan-
dard would be 0.3 ppm. Q p i d l y . average exposures cannot exceed one-third of the PEL if compliance with the standard is to be maintained.
It is not ceizain which of these estimates is Colrect. The lowest is very likely an underestimate. because the p p u -
lation estimated in the OSHA final rule were derived
principally from esposure concenti-dtions measuret1after 1985: higher esposure values tvoultl likely have esistetl in earlier years. The highest estimate may be an overeirimate. because of uncertainties in the close-response relationship cstemminrr from the small of c;ises).particularly
Discussion
The data presented in this analysis show that a courtimposed l0-year delay in the regulation of occupational t-sposure to benzene resulted in substantial unnecessary r . ~ c e sms onality from leukemia 129).The C.S. Supreme C'ourt. in its 19N d i n g . established it new criterion that
must henceforth be met by OSHX in the promulpdcion of
\\-trrkplacehealth s~a~~tliirttIlistn.Iely. :hiit it "::igiiticant" risk must be shown to esist under present conditions and that this risk will be significiintly reduced by ii new s u n (lard. This approach to regulation breaks precedent with
Table 2.Obscn.d and cxpcctd deaths from leukemia in rubber workers exposed to benzene between 1940 and 1965 by cumulative exposure and years of latency t I I ) .
Latency. years e5
0.00140 Z'O. 10
5- 10 10-15 15-20 3-25 5-30
>30 Totals'
Standardized monality ratio Confidence interval
010.16 0lO.E 010.27 010.32 010.37 0/0.40 91.83 109 12-394
'The numbers of expected deaths have been rounded.
40-LW
ti. n.p?
01 0.05
1:o.o; 110.09
010.10
OIO.I:! 010.16
2'0.62 3.z 36-1.165
Exposure. pprn-year
-L W 4 0 0
0~0.01
110.02 110.03
010.03 010.04 1/0.04 20.17 1,186 133-4.BS
>-100
-
-
0/0.00 2'0.01
1;0.01 wo.01 wo.01 30.04 6.637
1.a19.-393
Totals'
20.12
th0.2.2
90.31 :u0.39
Y0.46 0lO.S U0.Q 912.66 Si 154441
188
long-standing tradition in public health. The tradition
urges in the interest of disease prevention that public
health regulations be set early. even on the basis of in-
complete evidence. That approach embodies a conscious
clecision to err on the side of prevention in regulatory de
cision making (30).In the decade of regulatory inaction
that followed the Supreme Court decision. additional
epidemiologic anftoxicologic data were developed on
benzene. These data confirmed and strengthened the
luuults of earlier analyses and documented the esistence
of esposurerelated risk. However. as we have shown.
this additional certainty was gained a t a cost (31).
Importantly. the Supreme Court did not require that
OSHA conduct a cost-benefit analysis. the basis on which
the Fifth Circuit Court of .Appeals initially vacated the
1978 standard. Also. the Supreme Court provided some
guidance as to what mipht constitute a * ' s g n E & h & L
-eEsk. . suggestmp.that a risk ofhieatb pr lMUamq-
mKDOS
' The residual risk from
a x y e a r esposure to 1 ppm of L n z e n e vapor is est.-
lrorn 4 to 15 deaths per loo0 espod.
has finally made progress in reducing
what was clearly a significant risk in the case of benzene,
several aspects of the Supreme Court decision continue
to have disturbing ramifkxtions. First. this decision im-
plies that less than significant risks need not be regu-
lated. even though such regulation might be economically
feasible and of public health benefit. Second. individual
risk was the only criterion listed for consider;lrion: no
mention was made of considering the number of in-
dividuais exposed to a given risk. Is a risk to 500 workers
to be considered the same as a risk t o 5 million workers
in terms of significance? Finally. the Supreme Court de-
cision may turn future regulatory hearings into forums
arguing such nebulous questions as what risk is "signif-
cant"'or what benefit is "substantial." rather than'focus-
ing on such basic scientific issues as identification of
health effects definition of dose-response relationships
and design of control measures
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