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*Information obtained from Sax and Lewis [1987].
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Chemical name | . . . . . . . . . . . . . . . . . . . . | Asphalt |
CAS number | . . . . . . . . . . . . . . . . . . . . | 8052-42-4 |
Synonyms | Asphaltum; asphalt cement; asphalt
emulsion; bitumen; blown asphalt; cutback asphalt; oxidized asphalt;
petroleum asphalt; petroleum bitumen; road asphalt |
Physical state at room temperature Black or
dark-brown solid or viscous liquid
Solubility in water at 20°C Insoluble
Solubility in organ solvents Carbon disulfide
Definition of asphalt -
Asphalt production is dictated by performance
specifications rather than by a specific chemical composition.
To meet those specifications, the residual product of petroleum
distillation may be further processed, usually by air-blowing
or solvent precipitation. The precise chemical composition and
physical properties of the resulting products are influenced by
the composition of the original crude petroleum oil and the manufacturing
processes. The basic chemical components of crude petroleum oil
include paraffinic, naphthenic, and aromatic hydrocarbons as well
as heterocyclic molecules containing sulfur, oxygen, and nitrogen
[AI 1990a]. The proportions of these chemical components may vary
significantly because sources of crude petroleum oil occur in
various locations throughout the world involving different geologic
formations. As a result of these variations, crude oils from different
fields may vary in their chemical composition and sometimes variations
in chemical composition of crude oils can be found among different
locations in the same oil field [Puzinauskas and Corbett 1978].
Therefore, no two asphalts are chemically identical, and chemical
analysis defining the precise structure and size of the individual
molecules found in asphalt is almost impossible.
Asphalt fumes are defined as the cloud of
small particles created by condensation from the gaseous state
after volatilization of asphalt. Fumes from some asphalts have
been analyzed and their chemical compositions are presented in
Table 1
[AI 1975] and
Table 2
[Reinke and Swanson 1993].
Paving asphalts are manufactured principally
by simple atmospheric distillation or by atmospheric distillation
followed by fractionation under vacuum. They may also be manufactured
by solvent precipitation and mild partial air-blowing. Roofing
asphalts are generally produced by atmospheric or vacuum distillation
followed by air-blowing [NAPA 1994].
Most of the asphalt produced in the United
States is used in paving and roofing. Only about 1% is used for
waterproofing, dampproofing, insulation, paints, and other activities
[AI 1990a]. The National Occupational Exposure Survey (NOES) [NIOSH
1983] estimates that during the period 1981-83, more than 473,000
U.S. employees were potentially exposed to asphalt.
Table 3 presents
the 10 industries and the 10 occupations (excluding janitors)
with the most employees potentially exposed to asphalt.
Of the three types of asphalt products used
in the construction of paved surfaces in the United States: asphalt
paving cements (hot-mix asphalt or HMA), cutback asphalts, and
asphalt emulsions, HMA (asphalt mixed with mineral aggregate)
accounts for 85% of the total used. Cutback asphalts and asphalt
emulsions are used for road sealing and maintenance, and account
for 4% and 11% respectively, of the total
used. Currently, about 4,000 HMA facilities and 7,000 paving contractors
employ nearly 300,000 employees in the United States [AI 1990a].
Four types of asphalt (I through IV) are used
in roofing products in the United States. The type of asphalt
used is determined by the grade or slope of the roof. For example,
Type I roofing asphalt, often referred to as "dead level,"
has a low softening point and is used on surfaces with a grade
of 0.5 inch per foot or less. Types II and III roofing asphalt
are typically used on roofs with slopes of 0.5 to 1.5 and 1 to
3 inches per foot, respectively. Type IV roofing asphalt (a hard
asphalt with a high softening point) is used on roofs with a grade
of 2 to 6 inches per foot [ASTM 1992]. In 1990, an estimated 46,000
on-roof employees were exposed to asphalt fumes in the United
States, and about 6,000 to 12,000 employees were exposed in approximately
120 plants manufacturing asphalt roofing shingles and rolls and
modified bitumen2 roofing products [AI 1990a].
The major route of occupational exposure to asphalt fumes (e.g., paving, roofing, and asphalt-based paints) is by inhalation; they may also be absorbed through the skin. A summary of representative information on the occurrence of asphalt fumes in the workplace is presented in Table 3 and Table 4.
Dermal exposure to asphalt fumes has been
examined using skin wipes (see
Table 5).
Skin wipe samples were
collected at various worksites (e.g., refineries, HMA facilities,
paving and roofing sites, and roofing manufacturers) and analyzed
for PAHs [AI 1991]. The PAH concentrations determined from postshift
samples ranged from 2.2 to 520 ng/cm2 (see Appendix
A).
The Occupational Safety and Health Administration
(OSHA) currently has no permissible exposure limit (PEL) for asphalt
fumes. In 1989, OSHA announced that it would delay a final decision
to establish a PEL for asphalt fumes because of complex and conflicting
issues submitted to the record [54 Fed. Reg. *2641]. The PEL originally
proposed to reduce the potential carcinogenic risk of occupational
exposure to asphalt fumes was 5 mg/m3 as an 8-hr TWA.
In 1992, OSHA published another proposed rule for asphalt fumes
that included a PEL of 5 mg/m3 (total particulates)
for general industry and for the maritime, construction, and agricultural
industry [57 Fed. Reg. 26182]. Comments are still being received
by OSHA and a final decision is pending.
In a 1977 criteria document, NIOSH established
a recommended exposure limit (REL) of
5 mg/m3 as a 15 min ceiling for
up to a 10-hr work shift, during a 40-hr workweek, to protect
against irritation of the serous membranes
of the conjunctivae and the mucous membranes of the
respiratory tract [NIOSH 1977a]. In 1988,
NIOSH testimony to the Department of Labor and OSHA recommended
that asphalt fumes be considered a potential occupational carcinogen
[NIOSH 1988]. This recommendation was based on information presented
in the 1977 criteria document [NIOSH 1977a] and a study by Niemeier
et al. [1988] showing that exposure to condensates of asphalt
fumes caused skin tumors in two strains of mice.
The American Conference of Governmental Industrial
Hygienists (ACGIH) threshold limit value (TLV®)
is 5 mg/m3 as an 8-hr TWA and was recommended to reduce
the risk of possible carcinogenicity [ACGIH 1991]. Australia,
Belgium, Denmark, and the United Kingdom have also limited occupational
exposures to asphalt fumes to 5 mg/m3 as an 8-hr TWA.
Additionally, the United Kingdom has established a short-term
exposure limit (STEL) of 10 mg/m3. Germany
currently rates asphalt fumes as "suspected
of having a carcinogenic potential [ILO 1991].
The five fractions of laboratory-generated
roofing asphalt fume condensates and unfractionated asphalt fumes
used by Sivak et al [1989] (see description of Sivak study under
Carcinogenic Effects) were examined for their mutagenic potential
in Salmonella. Fractions A through E combined, and fractions B
and C were positive; fractions, A, D, and neat asphalt fumes were
weakly positive; and fraction E was negative [NTP 1990]. Positive
responses required exogenous metabolic activation. The same fractionated
asphalt fume condensates from the Sivak et al.study [1989] were
also tested using a modified Ames assay [ Blackburn and Kriech
1990] and the results were comparable to those of the NTP [1990]
study.
Eight asphalt fume samples collected on teflon
filters at HMA plants as part of an Interagency Agreement with
the Federal Highway Administration (FHA) were tested for mutagenic
activity in a Salmonella mutagenicity assay. Preliminary results
indicate that there was no mutagenic activity in the whole fume
fraction; however, results of 2 of the 8 samples were inconclusive
[Olsen, personal communication].
Two Type III roofing asphalts representing
different crude oil sources , one of which was similar to the
asphalt air-blown using a ferric chloride catalyst and used by
Niemeier et al.[1988] and Sivak et al. [1989]; 18 paving asphalts
(representing 14 crude oil sources and various process
conditions); and Type I coal tar pitch; and
their fume condensates were examined not only
for mutagenic activity in a modified Ames
assay, but also for PAH content [Machado et al. 1993]. The fume
generation temperature of all roofing materials was either 232
or 316°C and that of all paving materials was 163°C (one sample
was heated to 221°C). The results of the modified Ames assay are
presented in Table 6.
The data indicate that all samples tested
exerted mutagenic activity; however, the mutagenic responses of
the asphalt fume condensates were approximately 100-fold less
than the coal tar pitch samples and weak to moderate in potency
[Machado et al. 1993]. Responses for the positive control group
were all within the expected ranges.
Results of analyses for PAH content, measured by HPLC fluorescence, of the roofing and paving asphalts, coal tar pitch, and their fume condensates were as follows [Machado et al. 1993]. Concentrations of individual PAHs in samples of asphalt and asphalt fume condensates were less than 50 parts per million by weight (ppm), while most concentrations of individual PAHs in roofing (232°C or 316°C) and all concentrations in paving (163°C, except for one sample at 221°C) asphalts, whole or fumes, were less than 10 ppm and 2 ppm, respectively. Concentrations of individual PAHs in the coal tar pitch samples were 100- to 1000- fold higher than in the roofing and paving samples. Benzo[a]pyrene (BP) was detected in all samples examined; the maximum concentrations of BP in whole asphalt, whole coal tar pitch, asphalt and coal tar pitch fume condensates were approximately 6 ppm, 18,000 ppm, 0.1 - 2.8 ppm, and 250-480 ppm, respectively.
Although PAH content correlated with mutagenicity
indices for some samples, for others it did not. The investigators
concluded that the data suggest that crude oil source along with
processing conditions had some influence on the PAH content of
the various materials tested
[Machado et al.1993].
Reinke and Swanson [unpublished data 1993]
examined the relationship between field-, 146-157°C (295-314°F),
and laboratory-generated, 149°C (300°F) and 316°C (600°F), asphalt
fume condensates by comparing their chemical content (i.e., PAHs
and sulfur heterocyclics) and mutagenic potential. The asphalt
tested was a straight run, vacuum distilled 85/100 penetration
grade asphalt derived from a blend of Canadian heavy, sour crudes.
The field asphalt fume condensates were collected from the head
space above an asphalt storage tank, stored between 146-157°C (295-314°F),
at a HMA production plant into a cold trap system for about 36
continuous hours. The results of the chemical analyses (GC-MS)
for PAHs and sulfur heterocyclics and the modified Ames assay
are provided in
Table 7
and summarized in Table 8.
The data indicate that field-generated asphalt
fume condensates exerted a MI of >0 and < 1, while fumes
generated in the laboratory at 149°C (300°F) and 316°C (600°F), exerted
MIs of 5.3 and 8.3, respectively.
Condensates of Type I and Type III roofing asphalt fumes generated in the laboratory (same methodology as Sivak et al. 1989) at temperatures (316 ± 10C) similar to actual roofing operations caused a dose-related increase in micronucleus (MN) formation in exponentially growing Chinese hamster lung fibroblasts (V79 cells) [Qian et al. 1995]. The results of immunofluorescent antibody staining showed that both roofing asphalt fume condensates induced mainly kinetochore-positive MN (68-70%). The authors suggested that Type I and Type III roofing asphalt fume condensates are aneuploidogens and possess some clastogenic activities.
Reinke and Swanson [1993] also tested 3 asphalt
fume condensates (field and lab-generated) in a chromosomal aberration
assay and the results were negative. The authors reported that
the absence of positive findings may be explained by the fact
that this assay has not as yet been optimized for petroleum asphalt
fumes.
The five asphalt roofing fume fractions used
by Sivak et al. [1989] were tested for inhibition of intercellular
communication, i.e., one of several proposed mechanisms of tumor
promotion. The inhibition of intercellular communication by a
tumor promoter is believed to isolate an initiated or preneoplastic
cell from the growth regulatory signals of surrounding cells,
leading to the development of neoplasia. All fractions inhibited
intercellular communication in chinese hamster lung fibroblasts
(V79) cells in Toraason et al. [1991]. The greatest activity was
in fraction D and E and the least activity in fraction A.
Similarly, Wey et al. [1992] examined the effect of these fractions on intercellular communication in human epidermal keratinocytes. All asphalt roofing fume fractions inhibited intercellular concentrations in a concentration dependent fashion.
Since publication of the NIOSH criteria document
[NIOSH 1977a], there have been reports of carcinogenicity following
dermal applications of laboratory-generated asphalt roofing fume
condensates [Niemeier et al. 1988; Sivak et al. 1989] and raw
roofing asphalt [Sivak et al. 1989]. Additional data from these
studies are summarized in detail in Appendix B.
Niemeier et al. [1988] investigated the tumorigenicity
of fume condensates generated at 232°C (450°F) and 316°C (601°F) from
Types I and III roofing asphalt and Types I and III coal-tar
pitch through topical applications to the
skin of male CD-1 and C3H/HeJ mice. A total of 48 groups of 50
mice each (1 strain) received applications of cryogenically collected
fume condensates singly and in combination (Type III asphalt and
Type I coal-tar pitch, both generated at 316°C [601°F]) biweekly
for 78 weeks (18 months). Half of each group was exposed to simulated
sunlight to determine whether photochemical reactions might alter
the carcinogenic activity. Analysis of the skin painting solutions
by GC/MS revealed that the solutions containing coal-tar pitch
fume condensates had higher concentrations of select PAHs than
the solutions containing asphalt fume condensates. The authors
report that analysis by nuclear magnetic resonance (NMR) indicated
that the asphalt fume condensate was <1% aromatic and >99%
aliphatic, whereas the coal-tar pitch condensate was >90% aromatic.
BaP was selected as a marker compound based on correlations of
BaP concentrations and carcinogenicity.
Tumors were produced by fume condensates of both types of asphalt (see Tables 9 and 10) and both types of coal-tar pitch. The majority of benign tumors were papillomas; the majority of malignant tumors were squamous cell carcinomas. The fume condensates from the coal-tar pitches had slightly greater carcinogenic activity than the fume condensates from the asphalts, but the total amount of select PAHs or BaP needed to produce a 50% tumor incidence was much smaller for the asphalt fume condensates (PAHs, 0.58 to 2.63 mg; BaP, less than or equal to 13.6 mg) than for the coal-tar pitch fume condensates (PAHs, >24.5 to >57.4 mg; BaP, 354 to 405 mg). Tumor response to the coal-tar pitch fume condensates was comparable with that of the BaP controls, based on the total dosage of BaP administered. Both strains of mice exposed to asphalt fumes had significantly (P=0.01) more tumors than the control groups, although the C3H/HeJ mice demonstrated a greater tumorigenic and carcinogenic response to both asphalt and coal-tar pitch fume solutions than did the CD-1 mice. The C3H/HeJ mice showed a significant increase (P=0.01; Fisher-Irwin exact test) in tumorigenic response for both types of condensed asphalt fumes generated at 316°C (601°F) compared with those generated at 232°C (450°F); a similar increase was noted only for Type III coal-tar pitch fumes. Overall, simulated sunlight inhibited tumorigenic responses. The authors speculated that this inhibition may have resulted from the photo-oxidation or photodestruction of the carcinogenic components of the test materials. Niemeier et al. [1988] concluded that the enhanced carcinogenic activity of the asphalt fume condensates may have been due to their high concentration of aliphatic hydrocarbons, which have cocarcinogenic effects. They also concluded that higher generation temperatures may have further increased that hazard. Finally, Niemeier et al. [1988] concluded that the carcinogenic activity of the coal-tar pitch fume condensates (but not that of the asphalt fume condensates) could be explained by their BaP (or PAH) contents.
Sivak et al. [1989] heated Type III roofing
asphalt at 316°C, generated fume condensates, and separated them
by high-performance liquid chromatography [Belinky et al.]. The
chemical composition of the fractions (A through E) is provided
in Table 11. Raw asphalt, neat asphalt (whole or unfractionated
condensate) fume, the reconstituted asphalt fume, and the asphalt
fractions, individually and in various combinations, were then
tested for their carcinogenic and tumor-promoting activity. Fractions
A through E were dissolved in a 1:1 solution of cyclohexane and
acetone to yield concentrations proportional to their presence
in the neat asphalt fume condensate, i.e., 64.1%, 8.3%, 10.5%,
11.5% and 5.6%, respectively, and were applied biweekly to 40
groups of male C3H/HeJ mice and 2 groups of Sencar
mice (30 male mice per group) for 104 weeks (2 years).
A single initial treatment of BaP followed
by individual treatments with fractions A, D, and E was used to
test the tumor-promoting activity of the asphalt fume condensate.
The cocarcinogenicity of fractions A, D, and E was tested with
three different doses of BaP. Fractions A, D, and E were used
because they were the fractions Sivak et al. [1989] deemed most
likely to exhibit cocarcinogenic or tumor-promoting activity based
on their chemical compositions, i.e., primarily long chain alkanes
and phenol compounds. Two groups of male Sencar mice were included
to allow for possible genetic variation and sensitivity to tumor
promotion. One of the two groups of Sencar mice was treated with
neat asphalt fume (whole
condensate), and the other was used as an
unexposed solvent control. The negative control group
was treated with cyclohexane and acetone,
and the positive control groups were treated with three different
concentrations of BaP.
Table
12 presents only the treatment groups which induced histopathologically
confirmed carcinomas (malignant tumors), the number of carcinomas
per group, the number of mice with histologically confirmed carcinomas,
and the average time (in weeks) to carcinoma development. The
raw asphalt and neat asphalt fume induced carcinomas (local skin
cancers) in 3 of 30 and 20 of 30 C3H/HeJ mice, respectively.
Fractions B and C induced carcinomas in 10 of 30 and 17 of 30
C3H/HeJ mice, respectively, while fractions A, D, and
E failed to induce any carcinomas when applied singly. All the
combinations of the fractions induced tumors only if they included
B or C; combinations A and D; A and E; and A, D, and E failed
to induce any tumors. Furthermore, fractions A, D, and E failed
to act as either tumor promoters or cocarcinogens. Fourteen of
the 30 Sencar mice treated with the asphalt fume condensate developed
carcinomas.
As noted previously, only fractions B and
C applied singly and in combinations elicited tumor responses.
Fractions containing B and C PACs including PAHs, S-PACs, and
O-PACs such as alkylated aryl thiophenes, alkylated phenanthrenes,
alkylated acetophenones, and alkylated dihydrofuranones. Fraction
B contained most of the S-PACs, and only a few were carried over
to fraction C. Fraction C contained a small amount of 4-ring PACs
(refer to previous Table). Sivak et al. [1989] stated the
need for additional cocarcinogenesis and tumor-promotion experiments
using a wider range of experimental variables, further chemical
separation of fractions B and C, more short-term genotoxicity
assays, and additional carcinogenicity assays to identify biologically
active materials in the roofing asphalt fume condensates.
Table 10 lists the positive tumor responses
among the groups of mice studied. The raw asphalt (diluted with
a 1:1 solution of cyclohexane and acetone to a final concentration
of 0.5 g/ml) produced carcinomas in 3 of 30 C3H/HeJ mice. The
neat asphalt fume (diluted with a 1:1 solution of cyclohexane
and acetone to a final concentration of 0.5 g/ml) produced carcinomas
in 20 of 30 C3H/HeJ mice. Fraction B produced local skin cancers
(carcinomas) in 10 of 30 male C3H/HeJ mice, and fraction C produced
local skin cancers (carcinomas) in 17 of 30 male C3H/HeJ mice.
Fractions A, D, and E failed to produce any carcinomas when applied
singly. Of the other combinations of fractions, all produced tumors
except the following: A and D; A and E; and A, D, and E. None
of the groups of mice with the initiating dose of 200 mg of
BaP developed tumors, but 7 of the 9 groups tested for cocarcinogenicity
developed carcinomas (see Table 10). Fourteen of the 30 Sencar
mice treated with neat asphalt fumes (whole condensate) produced
carcinomas, and 1 mouse in the Sencar solvent control group produced
1 tumor (sarcoma). Mice in the C3H/HeJ solvent control group failed
to develop tumors, whereas the C3H/HeJ mice in two BaP control
groups developed skin tumors (see 0.01% and 0.001% BaP groups
in Table 10).
Sivak
et al. [1989] observed no tumor responses with the three roofing
asphalt fractions (A, D, and E) they considered most likely to
exhibit cocarcinogenic or tumor-promoting activities based on
their aliphatic hydrocarbon, alcohol, and phenol contents. Treatment
with the combined fractions did not produce any synergistic effects.
However, tumor responses were elicited by other fractions (B and
C) that contained PACs including PAHs, S-PACs, N-PACs, and O-PACs
such as alkylated aryl thiophenes, alkylated phenanthrenes, alkylated
phenylethanones, and alkylated dihydrofuranones. Fraction B contained
most of the S-PACs, and only a few were carried over to fraction
C, which contained mainly O-PACs. Because the O-PACs may result
from the air-blowing/oxidation refining process common among roofing
asphalts, they may be present only in roofing asphalt. If such
is the case, the refining process could be altered to eliminate
the O-PACs and possibly the carcinogenicity of fraction C. Sivak
et al. [1989] stated
the need for additional cocarcinogenesis and
tumor-promotion experiments using a wider range of experimental
variables, further chemical separation of fractions B and C, more
short-term genotoxicity assays, and additional carcinogenicity
assays to identify biologically active materials in the roofing
asphalt fume condensates.
ACUTE
Asphalt fumes are irritants to the mucous
membranes of the eyes and respiratory tract; hot asphalt can also
cause burns of the skin [NIOSH 1977]. It has been reported that
irritant effects on the respiratory tract can possibly progress
to such nonmalignant lung diseases as bronchitis, emphysema, and
asthma [Hansen, 1991; Maizlish et al. 1988]. Workers engaged in
road repair and construction reported symptoms of abnormal fatigue,
reduced appetite, eye irritation, and
laryngeal/pharyngeal irritation [Norseth et
al. 1991].
CHRONIC
Considerable data from epidemiological studies
on workers exposed to asphalt fumes during paving and roofing
operations, and during the production of asphalt, have become
available since the publication of the NIOSH criteria document
on asphalt [NIOSH 1977]. The mortality experience of Danish mastic
asphalt workers [Hansen 1989a; Hansen 1991] and Swedish asphalt
road pavers [Engholm 1991] was investigated (see
Table 13). Hansen
[1989a] reported that the mastic asphalt workers, when compared
with the total male Danish population , experienced significantly
increased mortality from cancers of the digestive and respiratory
systems, with standardized incidence rates (SIR) of 227 (95% confidence
interval of 142-344) and 195 ( 95% confidence interval of 236-493),
respectively. The SIR for all malignant neoplasms was 195
(95% confidence interval of 153-244). Overall,
Hansen [1989a] reported that she observed a three-fold increase
in the expected number of lung cancers in the mastic asphalt workers
compared with the general Danish population. For an assessment
of the induction of primary lung cancer Hansen divided the cohort
into subcohorts based on birth year because it was necessary to
determine the number of employees potentially exposed to coal
tar pitch, which had been added to mastic asphalt during World
War II. The SIRs for primary lung cancer were then determined
to range from 632 (for employees aged 40 to 54) to about 300(for
employees aged 64 to 89). Although smoking histories of the cohort
were unknown, an inquiry was made in 1976 into the smoking habits
of mastic asphalt workers and a pattern emerged. Based on the
approximate rates that were calculated, Hansen suggested that
smoking could not account for the three-fold increase she had
observed.
When Hansen [1991] updated her cohort and
adjusted for smoking and urbanization, she reported that the statistically
significant (P<0.01) increase in cancer mortality among mastic
asphalt workers remained. The SIR for lung cancer mortality was
224 (95% CI, 145-330). Criticisms by Wong et al. [1992] and Kreich
et al.] 1991] of the Hansen studies [1989a; 1991] are provided
in the comments section of Table 13 and include the following:
possible exposure to coal tar pitch and inadequate adjustment
for smoking and urbanization.
Engholm et al. reported [1991] the occurrence
of lung (SIR of 207) and stomach cancers (SIR of 207) in Swedish
asphalt road pavers (see Appendix C). Data on previous and current
smoking histories had been collected and were used in determining
the relative risk (RR) for lung cancer. The RR for lung cancer
was on the order of 2 before adjustment for smoking, and it was
on the order of 3 after adjustment for smoking. Despite the short
follow-up period ( an average of 11.5 years) and the very young
age (42 years) of the cohort, the authors concluded that this
cohort exhibited a slight excess of lung cancer. However, in a
later submission to NIOSH [Engholm and Englund 1993], the results
of an update based on the inclusion of three additional years
of follow-up were reported. Engholm [1993] indicated that: 1)
with the additional follow-up, all measures of any cancer risk
were not statistically signigicant; 2) the study results may reflect
some selection bias; 3) exposure of the cohort is in doubt.
Results of a proportionate mortality study
of California highway maintenance workers [Maizlish et al. 1988]
and a long-term mortality study of Minnesota highway maintenance
workers [Bender et al. 1989] are also presented in Table 13. Maizlish
et al.[1988] determined that the increased mortality from all
malignant neoplasms for their cohort was not statistically significant.
Additionally, exposure measurements and data on tobacco or alcohol
consumption of the cohort were unavailable.
Bender et al. [1989] reported that workers
with 30 to 39 years of work experience had a statistically significant
(P<0.01) SMR of 425 (95% CI, 170-870) for leukemia deaths.
The authors concluded, however, that they were unable to relate
these findings to asphalt exposure. After additional study of
this cohort (case-control studies, cytogenetic studies, updated
chhort mortality, and personal air monitoring effort, the Minnesota
Department of Health [1993] concluded that it was unlikely that
the excess leukemia mortality observed among the highway maintenance
workers was job-related.
Only one study is available regarding the mortality experience of roofers [Engholm et al. 1991].
During their investigation of asphalt road
pavers in Sweden, these investigators also examined a cohort of
roofers (see Appendix C). After adjustment for smoking, the RR
for lung cancer in roofers was on the order of 6. The data indicated
that though the number of cases was small, there was a lung cancer
excess among roofers [Engholm et al. 1991]. Even though the authors
acknowledged that the short follow-up period (11.5 years) and
the young age (42 years) of the cohort were too short for the
normal latency period of a potential carcinogen, they concluded
that an excess of lung cancer existed among roofers. In 1993 Engholm
and Englund presented to NIOSH information based on their three-year
follow-up of Enghom et al. 1991. They concluded that results of
the follow-up study " did not permit any final conclusions"
regarding health risks of the respective cohorts.
Partanen and Boffetta [1994] conducted a review
and meta-analysis of the epidemiologic studies regarding cancer
risk in asphalt workers and roofers. They concluded that existing
data are insufficient to make a judgment with regard to asphalt.
Most epidemiologic studies for lung carcinogenicity (as well as
other cancer sites ) are either too non-specific for exposure
(e.g., highway maintenance workers , census occupational data),
or confounded by coal tar exposure.
In 1987, the International Agency for Research
on Cancer (IARC) evaluated the available studies involving asphalt
fumes [IARC 1987] and concluded that the carcinogenicity of bitumens
(shich include asphalt ) is unclassifiable in humans.
NIOSH investigators (Kyle Steenland) agree with the review of Partanen and Bofetta [1994]. In addition to the studies' deficiencies already enumerated, insufficient latency for workers exposed to asphalt is also noted. Deficiencies of the Hansen [1989, 1991] studies include the unresolved controversy concerning possible exposure to coal tar, possible selection biases, and the appropriate beginning of person-time at risk.
APPENDIX B
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