Conclusion

The following conclusions concerningpossible health effects caused by exposure to paving and roofing asphalts, raw asphalt, and asphalt-based paint were derived from an evaluation of data from studies in humans and experimental animals that have become available since the 1977 criteria document onasphalt [NIOSH 1977a].

In the 1977 criteria document, NIOSH established a REL of 5 mg/m3 as a 15-min ceiling limit4 for asphalt fumes measured as total particulates. The NIOSH REL was intended to protect workers against acute effects ofexposure to asphalt fumes, including irritation of the serous membranes of the conjunctivae and the mucous membranes of the respiratory tract. In 1988, NIOSH (in testimony to the Department of Labor) recommended thatasphalt fumes should be considered a potential occupational carcinogen [NIOSH 1988].

7.1 Cancer Issues

7.1.1 Characterization of Asphalt Fumes

An analysis of the chemical data indicates that paving and roofing asphalts are qualitatively and quantitatively different; therefore, the vapors and fumes from these asphalt products also may be different. The chemical composition of vapors and fumes from asphalt products is variable and depends on the crude petroleum source, type of asphalt, temperature and extent of mixing during the manufacturing process, and temperature and extent of mixing during laboratory generation or field operation, e.g., paving or roofing. For these reasons, it is possible that asphalt fumes generated in some laboratory experiments may be qualitatively and quantitatively different from fumes workers are exposed to in the workplace.

Although asphalt vapors and fumes are not well characterized, the determination of selected PAHs in asphalt products, vapors, and fumes is of interest. Many studies have been directed to identification of PAHs in asphalt fume samples. PAH identification by HPLC/fluorescence techniques are unreliable and results for asphalt fume samples are considered unreliable. For more information see section 3.5.3. However, asphalt fume PAH data obtained by GC/MS are considered reliable. The most meaningful of these studies used GC/MS for the analysis. Robinson et al. [1984] used GC/MS to analyze several asphalt-based paints for chrysene, benz[a]anthracene, B(a)P, benzo[e]pyrene, and phenanthrene; only trace amounts of phenanthrene (<0.01%) were detected. Also using GC/MS, several other investigators reported on the chemical analysis of paving and roofing asphalt fumes [Niemeier et al. 1988; Lunsford and Cooper 1989; Reinke and Swanson 1993; Hatjian et al. 1995a, 1997].

Low concentrations of carcinogenic PAHs have been detected in laboratory-generated asphalt fumes. Niemeier et al. [1988] measured low concentrations of several carcinogenic PAHs in roofing asphalt fumes generated at both 232 and 316 °C (450 and 601 °F); most were two and three ring. Lunsford and Cooper [1989] reported results similar to those of Niemeier et al. [1988]. Reinke and Swanson [1993] detected chrysene (0.02 µg/m3) in paving asphalt fumes generated in the laboratory at 149 °C (300 °F). Lunsford and Cooper [1989] and Reinke and Swanson [1993] also reported the presence of alkylated PACs in roofing and paving asphalt fumes, which is of concern because these PAHs are structurally similar to known carcinogens.

Few studies have been directed to the identification and measurement of PAHs in asphalt fumes generated at U.S. worksites. Reinke and Swanson [1993] collected paving asphalt fumes at 149 °C (300 °F) from a storage tank at a hot-mix plant, as well as laboratory-generated paving asphalt fumes at 149 and 316 °C (300 and 601 °F) (Table 3–6). Although they detected chrysene in the laboratory-generated asphalt fumes, they did not detect chrysene in the fumes collected from the storage tank. Two- and three-ring PAHs were found in the storage tank fumes, but not four-ring PAHs.

Hatjian et al. [1995a, 1997] reported on a GC/MS analysis for selected PAHs in asphalt paving and roofing fumes collected at several worksites. These investigators found that naphthalene accounted for 60% to 90% of the measured PAH exposure for the asphalt workers studied. Also, two- and three-ring PAHs accounted for 99% of the measured PAH exposure for asphalt pavers and 84% to 94% for asphalt roofers. B(a)P was detected in less than 6% of the personal-breathing-zone air samples of asphalt road pavers and manual laborers who had no occupational exposure to PAHs; B(a)P was detected in 28% and 25% of the personal-breathing zone samples from the two roofing groups R1 and R2, respectively.

In a NIOSH study, researchers detected PAHs in environmental samples from paving operations, but made no attempt to determine individual car c i n o g enic PAHs [Hanley and Miller 1996 a,b; Miller and Burr 1996 a,b, 1998; Kinnes et al. 1996; Almaguer et al. 1996].

While the data regarding the presence of carcinogens in asphalt fumes generated at U.S. worksites are limited, the occasional detection of B(a)P at worksites and the more frequent detection of B(a)P and other carcinogenic PACs in laboratory-generated asphalt fumes indicate that, under some conditions, known carcinogens are likely to be present. Moreover, asphalt fumes generated at high temperatures are more likely to generate carcinogenic PAHs and therefore are potentially more hazardous than fumes generated at lower temperatures.

7.1.2 Paving Asphalt

7.1.2.1 Short-Term Assays

Several laboratory-generated paving asphalt fume condensates were mutagenic in an Ames Salmonella mutagenicity assay [Machado et al. 1993; Reinke and Swanson 1993; De Méo et al. 1996a], while samples of field-generated fumes were nonmutagenic [Reinke and Swanson 1993]. Fumes generated in the laboratory from two paving asphalts induced in vitro and in vivo DNA-adduct formation [De Méo et al. 1996a; Genevois et al. 1996]. No other experimental animal studies have been conducted to determine the carcinogenic potential of either field- or laboratory-generated paving asphalt fume condensates.

7.1.2.2 Human Studies

Epidemiology

Epidemiologic studies of pavers and highway workers exposed to asphalt were examined to determine the carcinogenic potential of paving asphalt fumes. An analysis of these studies indicates that although some studies reported an elevated risk for lung cancer among pavers [Hansen 1989a; Engholm et al. 1991; Partanen et al. 1997; Milham 1997], others did not [Maizlish et al. 1988; Bender et al. 1989]. Design limitations of both positive and negative studies restrict their interpretation. Partanen and Boffetta [1994] recently conducted a metaanalysis of studies involving pavers and highway workers exposed to asphalt. Their assessment did not find overall evidence for lung cancer risk among pavers. Overall, the epidemiologic evidence for an association between lung cancer and exposure to asphalt in paving is inconclusive at this time.

Biomarkers

Reported urinary 1-hydroxypyrene data suggest that asphalt road pavers are at increased risk of exposure to PAHs in asphalt fume. Of the seven reports [Jongeneelen et al. 1988; Burgaz et al. 1992; Levin et al. 1995; Hatjian et al. 1995 a,b, 1997; Zhou 1997] in which the use of urinary 1-hydroxypyrene was described, three [Burgaz et al. 1992; Levin et al. 1995; Zhou 1997] noted statistically significant, increased postshift levels compared with reference populations, and one [Hatjian et al. 1997] noted a significant increase in one of two paving groups over a 3-day period. Four studies in which urinary thioethers were analyzed [Lafuente and Mallol 1987; Burgaz et al. 1988, 1992; Pasquini et al. 1989; Hatjian et al. 1995b] and two studies in which urinary D-glucaric acid was analyzed [Pasquini et al. 1989; Hatjian et al. 1995b] found no significant elevations in these biomarkers for asphalt-exposed workers relative to the reference populations. However, Burgaz et al. [1992] found significantly elevated urinary thioethers when only nonsmokers wereevaluated.

Of three studies of possible genetic damage, none reported that exposure to asphalt fumes led to a substantial elevation of biomarkers of genetic damage. Pasquini et al. [1989] found significantly increased urinary mutagenicity, but only for nonsmokers; therefore, smoking status was a more important factor than was asphalt fume exposure. Fuchs et al. [1996] found no significant end-of-workweek elevation of DNA strand breaks. An observed elevation in sister chromatid exchange [Hatjian et al. 1995b] was confounded by smoking status and other exposures to PAHs.

7.1.3 Roofing Asphalt

7.1.3.1 Animal Studies

Data from experimental studies in animals and cultured mammalian cells indicate that laboratory-generated roofing asphalt fume condensates are genotoxic [NTP 1990; AI 1990a; Machado et al. 1993; Qian et al. 1996;Toraason et al. 1991; Wey et al. 1992] and cause skin tumors in mice when applied dermally [Niemeier et al. 1988; Sivak et al. 1989, 1997]. The absence of data to indicate that laboratory-generated roofing asphalt fume condensates are representative of field-generated fumes limits the usefulness of these data for determining the genotoxicity and potential carcinogenicity of field-generated roofing asphalt fume condensates.

7.1.3.2 Human Studies

Epidemiology

Epidemiologic studies of roofers have generally demonstrated an excess of lung cancer in these workers [Hammond et al. 1976; Menck and Henderson 1976; Engholm et al. 1991; Hrubec et al. 1992; Pukkala 1995; Milham 1997; Zahm et al. 1989; Schoenberg et al. 1987; Morabia et al. 1992] (see sections 5.2.3 and 5.2.4). A meta-analysis of these studies conducted by Partanen and Boffetta [1994] also indicated an overall excess of lung cancer among roofers. However, it is unclear to what extent these cancers may be attributable to asphalt exposures during roofing operations, since in the past, roofers have been exposed to coal tar and asbestos, which are known human lung carcinogens. Although strong epidemiologic evidence exists of an association between lung cancer and working as a roofer, it is uncertain whether exposure to asphalt is related to this association.

Biomarkers

Biomarker concentrations provided no clear insight about hazards from exposure to asphalt fumes. In a study by Hatjian et al. [1995a, 1997], one of two groups of roofers may have had elevated urinary 1-hydroxypyrene. Both groups had significantly elevated levels of SCE but no elevated level of urinary thioethers or urinary D-glucaric acid. In two other studies, Herbert et al. [1990] found slightly elevated levels of DNA adducts, and Fuchs et al. [1996] found elevated levels of DNA strand breaks in end-of-workweek samples. However, in these studies, prior exposure to aged coal-tar pitch from roofing tear-off operations might have occurred. Currently, the available data indicate that roofers may be at risk for carcinogenic and genotoxic effects. However, it is uncertain whether exposure to roofing asphalt fumes is associated with this risk.

7.1.4 Exposures to Other Asphalt Products

7.1.4.1 Animal Studies—Raw Asphalt and Asphalt-Based Paint

The results are conflicting as to the carcinogenicity of raw roofing asphalt considering one experimental study reported a weakcarcinogenic response in mice [Sivak et al. 1989, 1997], while another study reported no carcinogenic response [Emmett et al. 1981]. Similarly, the available data indicate that while not all asphalt-based paint formulations may exert genotoxicity and carcinogenicity, some are genotoxic [Robinson et al. 1984; Schoket et al. 1988 a,b] and carcinogenic [Robinson et al. 1984; Bull et al. 1985]. Although no published data exist that examine the carcinogenic potential of asphalt-based paints in humans, NIOSH concludes that asphalt-based paints are potential occupational carcinogens.

7.1.4.2 Human Studies

Epidemiology

No epidemiologic studies of worker exposure to asphalt or asphalt-based paints have been reported.

Biomarkers

Three reported studies provide no evidence for an exposure risk. In one study, a group of workers who loaded asphalt tankers and another group involved in the manufacture of asphalt showed no elevation of urinary 1-hydroxypyrene [Boogard and van Sittert 1995]. Burgaz et al. [1988] reported that workers in an asphalt hot-mix plant showed no elevation in urinary thioethers, and Fuchs et al. [1996] reported that asphalt painters showed no elevated levels of DNA strand breaks.

7.2 Noncarcinogenic Health Effects

A relatively small number of studies on the acute health effects associated with exposure to asphalt fumes have been published since the NIOSH criteria document on asphalt was published in 1977. Although the results from these studies are of limited value because of limitations in design and inadequate characterization of workers’ exposures, certain acute health effects can reasonably be ascribed to asphalt fume exposure on the basis of the consistency of findings among studies.

Studies of workers exposed to asphalt fumes have repeatedly found irritation of the serous membranes of the conjunctivae (eye irritation) and the mucous membranes of the upper respiratory tract (nasal and throat irritation). These health effects, which have been best described in asphalt road pavers [Norseth et al. 1991; Hanley and Miller 1996 a,b; Almaguer et al. 1996; Miller and Burr 1996 a,b, 1998; Kinnes et al. 1996; Sylvain and Miller 1996], typically appear to be mild and transitory. In studies of open-air paving, irritant symptoms occurred among workers exposed to asphalt fumes at geometric mean concentrations generally below 1.0 mg/m3 total particulates and 0.3 mg/m3 benzene- or carbon disulfide-soluble particulates calculated as a full-shift TWA [Almaguer et al. 1996; Hanley andMiller 1996 a,b; Miller and Burr 1996 a,b, 1998; Kinnes et al. 1996; Exxon 1997;Norseth et al. 1991]. Similar symptoms were reported in workers exposed to asphalt fumes during the manufacture of asphalt roofingshingles [Apol and Okawa 1977] andfluorescent lights [Chase et al. 1994], during insulation of cable [Zeglio 1950], and from a malfunctioning light fixture in an office[Tavris et al. 1984]. Exxon [1997] reported the occurrence of mild transitory symptoms of nasal and throat irritation, headaches, andcoughing among workers employed in five segments of the asphalt industry (hot-mixplants, terminals, roofing application, roofing product manufacturing, and paving), although no significant dose-response associations were found between measured exposures andsymptoms.

In addition to mucosal irritation, reports of skin irritation, pruritus, and occasionallyrashes have been described in workers with occupational exposures to asphalt fumes[Hanley and Miller 1996 a,b; Almaguer et al. 1996; Miller and Burr 1996 a,b, 1998; Kinnes et al. 1996; Chase et al. 1994; Tavris et al. 1984; Schaffer et al. 1985; Waage and Nielson 1986]. In a recent survey of 50 roofers and 101 road pavers [Riala et al. 1998], work-induced skin irritation was reported in 44% of the roofers and 31% of the pavers. Dermatitis, predominately of the face, hands and arms, and lower extremities, occurred more often among road pavers (22%) than among roofers (15%). It was not determined if the dermatitis was irritant or allergic in nature, or if dermal photosensitization similar to that seen with coal tar, was occurring. Given the presence of confounding co-exposures (i.e., diesel fuel, coal tar, fiberglass) and environmental conditions (wind, heat and humidity, UV radiation), the extent to which asphalt fumes may be associated with these skin problems is unclear and should be studied further.

Symptoms of nausea, stomach pain, decreased appetite, headaches, and fatigue have been commonly reported among workers exposed to asphalt [Norseth et al. 1991; Chase et al. 1994; Tavris et al. 1984; Schaffer et al. 1985; Waage and Nielson 1986; Exxon 1997]. These nonspecific symptoms also require further investigation to clarify and establish the nature of any causal relationships with asphalt fume exposure.

Reports of acute lower respiratory tract symptoms (i.e., coughing, wheezing, shortness of breath) [Hanley and Miller 1996 a,b; Almaguer et al. 1996; Miller and Burr 1996 a,b, 1998; Kinnes et al. 1996; Sylvain and Miller 1996; Nyqvist 1978; Zeglio 1950]) and changes in pulmonary function (e.g., bronchial lability) [Sylvain and Miller 1996; Waage and Nielson 1986] among exposed workers are of particular concern. Results from recent studies [Exxon 1997; Hanley and Miller 1996 a,b; Almaguer et al. 1996; Miller and Burr 1996 a,b, 1998; Kinnes et al. 1996] indicated that some workers experienced lower respiratory tract symptoms (and in one case, significant changes in pulmonary function) during relatively low exposures to asphalt fumes, such as those found during open-air highway paving (0.075 to 0.48 mg/m3 total particulates and 0.07 to 0.24 mg/m3 benzene-soluble particulates, mean range exposures). Present data are insufficient to determine the causal relationship between asphalt fume exposures and lower respiratory symptoms or changes in pulmonary function; however, personal health factors (i.e., pre-existing asthma) or higher exposures to asphalt fumes, such as those found during underground paving, might increase risks to workers [Norseth et al. 1991; Sylvain and Miller 1996].

Bronchitis, possibly related to chronic lower respiratory tract irritation, was reported among workers exposed to asphalt in several studies [Hansen 1991; Maizlish et al. 1988; Nyqvist 1978; Zeglio 1950; Baylor and Weaver 1968; Hasle et al. 1977]. Reports from Hueper and Payne [1960] and Simmers [1964] in IARC [1985] indicated that patchy distributions of emphysema, bronchiolar dilatation, pneumonitis, and severe localized bronchitis were observed in guinea pigs, rats, and mice chronically exposed to bitumens during inhalation studies. Findings of measurable decrements in pulmonary function and reports of bronchitis among asphalt-exposed workers suggest that chronic exposure to asphalt fumes may pose similar risks for humans. Unfortunately, the limited data preclude making any determinations concerning asphalt exposure-related chronic pulmonary morbidity at this time.

7.3 Overall Conclusions

In this hazard review, NIOSH has evaluated the scientific evidence concerning the potential health effects of occupational exposure toasphalt. On the basis of available data from studies in animals and humans, NIOSHconcludes the following about the acute health effects of asphalt exposure:

• The findings of this hazard review continue to support the assessment of the 1977 NIOSH criteria document on asphalt fumes, which associated exposure to asphalt fumes from roofing, paving, and other uses of asphalt with irritation of the eyes, nose, and throat. Furthermore, in studies conducted since the publication of the 1977 criteria document, these symptoms have also been noted among workers exposed to asphalt fumes at geometric mean concentrations generally below 1 mg/m3 total particulates and 0.3 mg/m3 benzene-soluble or carbon disulfide-soluble particulates, calculated as a full-shift TWA. Recent studies also report evidence of acute lower respiratory tract symptoms among workers exposed to asphalt fumes. These data are currently being further analyzed to assess the relationship between lower respiratory tract symptoms and asphalt fume exposure. The available data on chronic pulmonary effects (such as bronchitis) are insufficient to support an association with asphalt fume exposures.

In 1988, NIOSH recommended to OSHA that asphalt fumes be considered a potential occupational carcinogen based on the results of an animal study in which laboratory-generated roofing asphalt fume condensates induced malignant skin tumors in mice. Since then, investigators have described differences in chemical composition, physical characteristics, and biological activity between asphalt fumes collected in the field and those generated in the laboratory. The relevance of these differences in ascribing adverse health effects in humans is unknown. Data from studies in humans indicate that some workers exposed to asphalt fumes are at an elevated risk of lung cancer; however, it is uncertain whether this excess is related to asphalt and/or other carcinogens in the workplace. Although carcinogenic PAHs have been identified in asphalt fumes atvarious work sites, the measured concentrations and the frequency of their occurrence have been low. In addition, data from studies using HPLC analysis to identify PAHs were not considered because of the limitations of this method (e.g., compound resolution).

Based on evaluation of these data, thefollowing conclusions were drawn regarding the carcinogenicity of asphalt under several conditions of use:

• Data regarding the potential carcinogenicity of paving asphalt fumes in humans are limited. Only one study identifiedB(a)P in field fumes, but it was unclear whether paving asphalt fumes were the source of the B(a)P. Chrysene has been identified only in laboratory-generatedpaving asphalt fumes. The available data from studies in humans have not provided consistent evidence of carcinogenic effects in workers exposed to asphalt fumes during paving operations. No animal studies have examined the carcinogenic potential of either field- or laboratory-generatedsamples of paving asphalt fume condensates. Although genotoxicity assays (but no carcinogenicity assays) using laboratory-generated and field-generated (storage tank paving asphalt) fumes have beenconducted, only the laboratory-generated fumes were genotoxic. Therefore, NIOSH concludes that the collective data currently available from studies on paving asphalt provide insufficient evidence for an association between lung cancer and exposure to asphalt fumes during paving. The available data, however, do not preclude a carcinogenic risk from asphalt fumesgenerated during paving operations.
• The results from epidemiologic studiesindicate that roofers are at an increased risk of lung cancer, but it is uncertain whether this increase can be attributed to asphalt and/or to other exposures such as coal tar or asbestos. Data from experimental studies in animals and cultured mammalian cells indicate that laboratory-generatedroofing asphalt fume condensates are genotoxic and cause skin tumors in mice when applied dermally. Furthermore, a known carcinogen, B(a)P, was detected in field-generated roofing fumes. The collective health and exposure data provide sufficient evidence for NIOSH to conclude that roofing asphalt fumes are a potential occupational carcinogen.
• The available data indicate that although not all asphalt-based paint formulations may exert genotoxicity, some are genotoxic and carcinogenic in animals. No published data examine the carcinogenic potential of asphalt-based paints in humans, but NIOSH concludes that asphalt-based paints are potential occupational carcinogens.

7.4 Recommendations

In 1977, NIOSH recommended a REL of 5 mg/m3 (15-min sample5) for asphalt fumes to minimize the risk of acute respiratory and eye irritation. Because there were insufficient data to ascribe the chemical fume components responsible for the irritant effects, the REL was based on a total particulate sample, which was determined to be an appropriate surrogate for exposure.

Recent epidemiologic studies of workers exposed to asphalt fumes indicate that irritant effects and acute respiratory symptoms (e.g., coughing, shortness of breath) are still occurring. In addition, exposure assessment studies demonstrate the complexity of monitoring and evaluating the many components that may be present in asphalt, asphalt-based paints, and asphalt fumes and vapors. The complexity occurs because the quantities of these components vary depending on use conditions.

Current data are considered insufficient for quantifying the acute and chronic health risks of exposure to asphalt, asphalt-based paint, or asphalt fumes and vapors. However, data from at least two studies of acute effects are currently being evaluated to determine their usefulness in deriving an REL. Additional studies of workers exposed to asphalt fumes, vapors, and aerosols (e.g., during paving, roofing, and painting operations) are needed to better characterize exposures and to evaluate the risk of chronic disease, including lung cancer. Also required are experimental animal studies that use laboratory generation methods to produce fumes and vapors representative of asphalt roofing and paving operations. Until the results of these studies become available, NIOSH recommends minimizing possible acute or chronic health effects from exposure to asphalt, asphalt fumes and vapors, and asphalt-based paints by adhering to the current NIOSH REL of 5 mg/m3 (15-min sample) and by implementing the following practices:

• Prevent dermal exposure.
• Keep the application temperature of heated asphalt as low as possible.
• Use engineering controls and good work practices at all work sites to minimize worker exposure to asphalt fumes and asphalt-based paint aerosols.
• Use appropriate respiratory protection (see Appendix C).