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NIOSH Publication No. 2001-110:

Health Effects of Occupational Exposure to Asphalt

2001

 

Human Health Effects


5.1 Acute Health Effects

In 1977, based on a review of the available scientific literature, NIOSH reported that the acute toxic effects of exposure to asphalt fumes were irritation of the serous membranes of the conjunctivae and the mucous membranes of the respiratory tract [NIOSH 1977a]. Subsequently, a number of noncarcinogenic health effects continued to be reported among workers exposed to asphalt fumes. These effects include eye, nose, throat, skin, and respiratory tissue irritation; fatigue; headaches; dizziness; nausea; stomach discomfort; and insomnia. Hansen [1991] and Maizlish et al. [1988] indicated that nonmalignant lung diseases, such as bronchitis, emphysema, and asthma, were also among the toxic effects of exposure to asphalt fumes. Following is a review of the more pertinent studies concerning the noncarcinogenic health effects (excluding thermal burns) associated with exposure, including studies reported prior to the 1977 NIOSH criteria document. The review is divided into three sections—asphalt paving exposures, roofing industry exposures, and other asphalt exposures—because these categories involve differences in both worker exposures and potential health effects.

5.1.1 Health Effects Associated with Asphalt Exposures during Paving

! Norseth et al. [1991] In a cross-sectional study performed in Norway, Norseth et al. [1991] evaluated the incidence of self-reported symptoms among 333 workers exposed to asphalt and 247 controls. Workers were divided into three groups. Group I consisted of 79 asphalt pavers who underwent personal exposure monitoring during 5 days of paving, group II consisted of 254 asphalt pavers who did not undergo personal exposure monitoring, and group III consisted of 247 maintenance workers with no reported exposure to asphalt. Subjective symptoms for a 1-week period were determined by standardized questionnaires administered to all workers at the end of the week. Asphalt exposure data, weather conditions, and traffic density were monitored for employees in the three groups. Results were calculated separately for (1) smokers and nonsmokers and (2) other background variables, such as age, number of hours worked the previous week, and work experience. Analysis of reported symptoms was based on a symptom sum score that showed significantly increased frequency in the asphalt groups. Calculation of the symptom sum score accounted for the frequency and number of days a symptom was reported.

The response rates for groups I, II, and III were 100%, 57%, and 70%, respectively. Symptoms of fatigue, reduced appetite, eye irritation, and laryngeal-pharyngeal irritation were reported more frequently among workers exposed to asphalt fumes than among unexposed workers. No differences were found for symptoms of headache, dizziness, nausea, abdominal pain, disturbed sleep, skin reactions, or a "smell of sweetness."

Asphalt-exposed workers were found to have a significantly higher symptom sum score than unexposed maintenance workers (P<0.001). These differences could not be explained by smoking, hours worked during the previous week, work experience, traffic density, or weather conditions. In addition, asphalt workers in underground facilities (garages or tunnels) had significantly higher symptom sum scores than other asphalt workers (P<0.05). Even with underground workers excluded, the difference between asphalt workers and unexposed road maintenance workers was still statistically significant (P<0.001).

Symptom sum scores correlated significantly with asphalt temperatures (P<0.01). The most marked increase in scores was recorded when asphalt temperatures reached 146 °C (295 °F) and continued to increase to 175 °C (347 °F). Symptom sum scores also significantly correlated with increasing asphalt fume concentration, which were apparently measured as total organic compounds, but the analytical methods were not clearly defined. The average symptom sum score was 1.3 for employees exposed to asphalt fume concentrations <0.40 mg/m3 and 3.0 (P<0.05) for employees exposed to concentrations >0.40 mg/m3.

Limitations and potential biases of this study include (1) the use of self-administered questionnaires, which may be inaccurate because of recall bias, (2) variations in the response rate among the different groups participating in the study (there may have been a response bias), and (3) lack of control for smoking in all the analyses, although evidence is presented that the unexposed group may have smoked more than the exposed group.

NIOSH-Federal Highway Administration Interagency Agreement Seven health hazard evaluations (HHEs) were completed as part of an interagency agreement between NIOSH and the Federal Highway Administration (FHWA) of the U.S. Department of Transportation. The evaluations were conducted during open-air highway paving operations in Michigan [Hanley and Miller 1996a], Florida [Almaguer et al. 1996], Indiana [Miller and Burr 1996a], Arizona [Miller and Burr 1996b], Massachusetts [Miller and Burr 1998], and two in California—in Sacramento [Hanley and Miller 1996b] and San Diego [Kinnes et al. 1996]. The purpose of the agreement was to evaluate occupational exposures and health effects among workers paving with crumb-rubber-modified (CRM) and conventional (noncrumb-rubber-containing) asphalt. Subjects for each evaluation were the 6 to 10 workers ("pavers") whose various tasks involved direct exposure to asphalt during paving operations. Job titles included the paver, screed, and roller operators; rakers; laborers; and dumpmen. A control group of non-pavers consisted of road workers (i.e., foreman, heavy equipment operators, traffic controllers, road surveyors) employed in the same area who were not exposed to paving operations. Pavers were evaluated during 2 days of paving with asphalt containing CRM and 2 days of paving with conventional asphalt, and nonpavers were evaluated during the corresponding 4-day period. Because of the confounding of health effects associated with CRM asphalt, the only findings presented here involve pavers using conventional asphalt and the nonpavers over the same 2 days.

Asphalt laydown temperatures varied somewhat from day to day and site to site. At five sites, temperatures ranged from 138 to 147 °C (280 to 296 °F). In Indiana, temperatures ranged from 121 to 132 °C (250 to 270 °F), and in Florida, temperatures ranged from 99 to 104 °C (211 to 219 °F). Worker exposures were evaluated during the workshift at each study site and included personal-breathingzone and area measurements (Table 4–2). Each study participant received a one-time general health questionnaire, serial symptom surveys (administered up to five times per day), and serial peak expiratory flow rate (PEFR) tests at the same time as the short symptom surveys. PEFR testing was conducted to evaluate acute changes in lung function.

Forty-four pavers and forty-five nonpavers completed 376 and 389 symptom questionnaires, respectively, over the course of the seven surveys (Table 5–1). While the number of current smokers varied between pavers and nonpavers at individual sites, there was little difference in the overall percentage of current smokers among the groups (i.e., pavers 41%, nonpavers 40%). The number of symptoms reported per completed questionnaire for pavers, as compared to nonpavers, was higher in six of the seven surveys. In Florida, this finding was reversed, and the number of symptoms per completed questionnaire was higher among nonpavers. The number of symptoms for all causes at all seven sites combined was 0.47 among pavers and 0.21 among controls. Pavers reported a higher number of symptoms per completed questionnaire for eye, nose, throat, and skin irritation; shortness of breath; and wheezing as compared to the nonpavers (Table 5–2). The most frequently reported symptoms among pavers, in descending order, were throat irritation, nasal irritation, eye irritation, and coughing. Given the choices of mild, moderate, and severe, over 90% of the symptoms reported by pavers were classified as mild.

One of the 44 pavers (2%) reported symptoms accompanied by increased bronchial lability (i.e., the difference between the minimum and maximum PEFR on at least one survey day exceeded 20% of that day’s maximum PEFR [Scanlon and Hankinson 1996]). This worker was a former smoker with a history of physician-confirmed asthma that had developed after starting work on a road crew. None of the 45 nonpavers experienced increased bronchial lability on any of the survey days.

Table 5–1. Number of symptoms per completed questionnaire among pavers and nonpavers participating in seven NIOSH paving surveys
  Arizona California 1 California 2 Florida Indiana Massachusetts Michigan
Pavers (n=44):              
Total number of workers 6 7 7 4 7 6 7
No. of smokers 2 0 1 3 3 4 5
No. of symptons reported 37 24 70 17 6 16 7
No. of completed questionnaires 60 58 63 35 56 55 49
Rate*,† 0.62 0.41 1.1 0.49 0.11 0.29 0.14
Nonpavers (n=45): Total number of              
Total number of workers 6 7 8 4 7 8 5
No. of smokers 2 2 3 3 2 5 1
No. of symptons reported 19 13 21 24 2 3 0
No. of completed questionaires 55 63 78 33 68 60 32
Rate† 0.35 0.21 0.27 0.73 0.03 0.05 0
*Rates shown are only for periods when pavers were performing conventional asphalt paving and reflect all symptom causes.
†Rate=number of symptoms reported divided by the number of completed questionnaires.

 

Table 5–2. Number of symptoms per completed questionnaire among paversand nonpavers participating in seven NIOSH paving surveys
  Eye irratation Nasal irritation Throat irritation Skin irritation Cough Shortness of breath Wheezing
Pavers (n=44):              
No. of symptoms reported 32 54 45 6 20 13 7
No. of completed questionnaires 376 376 376 376 376 376 376
Rate*,† 0.09 0.14 0.12 0.02 0.05 0.04 0.02
Nonpavers (n=45):              
No. of symptoms reported 10 31 15 1 24 1 0
No. of completed questionnaires 389 389 389 389 389 389 389
Rate*,† 0.03 0.08 0.04 0.003 0.06 0.003 0
*Rates shown are only for periods when pavers were performing conventional asphalt paving and reflect all symptom causes.
†Rate=number of symptoms reported divided by the number of completed questionnaires.

While mean personal exposures to asphalt paving fumes were generally below 1 mg/m3 total particulates calculated as a full-shift TWA (Table 4–2), pavers experienced increased symptom rates for irritation of the eyes, nose, throat, and skin; shortness of breath; and wheezing compared to unexposed road maintenance workers. Pavers did not appear to be at an increased risk for bronchial lability compared to nonpavers under the conventional paving conditions evaluated during these seven surveys (i.e., outdoor paving with highway class pavers).

However, these findings are inconclusive given the small, and possibly unrepresentative, sample groups and the lack of pre- and postshift spirometry with which to evaluate the effects of asphalt exposures on lung function more fully. Also, a possible response bias stemming from differences in worker concerns about the safety of CRM versus conventional asphalt might have influenced symptom reporting. Available sampling technology did not permit continuous short-term, task-based sampling to determine if workers were experiencing peak exposures in association with symptoms or in excess of the NIOSH REL during work. Various exposure-response relationships continue to be analyzed.

Sylvain and Miller [1996]During a NIOSH HHE, industrial hygiene and medical assessments were performed during a single overnight workshift on two separate paving crews (crew 1 and crew 2) working within the Third Harbor Tunnel (Ted Williams Tunnel) in Boston, MA [Sylvain and Miller 1996]. Conventional asphalt was applied at 154 °C (310 °F). Worker exposures were evaluated during the workshift and included personal breathing zone and area measurements (Table 4–4). Nine workers participated in the health assessment, which included a short general health and occupational history questionnaire, serial symptom surveys, and serial peak PEFR testing to evaluate acute changes in lung function. Participants were considered to have increased bronchial lability if the difference between minimum and maximum PEFR on at least one survey day exceeded 20% of that day’s maximum PEFR [Scanlon and Hankinson 1996].

The five workers on crew 1 reported a number of acute health symptoms in association with their work exposures during the survey. However, no acute health symptoms were reported by the four workers on crew 2. The most frequently reported symptoms were eye irritation, coughing, nasal irritation, and shortness of breath. Eighty-four percent of the reported symptoms were rated as mild in severity given choices of mild, moderate, or severe. PEFR measurements indicated three workers (one from crew 1 and two from crew 2) experienced increased bronchial lability during the survey. Only one of the three workers with bronchial lability had a history of smoking.

NIOSH investigators concluded that (1) underground personal exposures (total particulates or benzene solubles) were up to 10 times higher than those found during recent open-air asphalt paving evaluations, but were still below 2.2 mg/m3 calculated as a full-shift TWA (Table 4–5); (2) some workers experienced eye and nasal irritation, coughing, and shortness of breath in association with asphalt paving; and (3) under certain conditions, such as during indoor paving, workers with exposure to asphalt may be at increased risk for bronchial reactivity.

Limitations and potential biases associated with this study are that (1) results are based on a very small, and possibly unrepresentative, sample of pavers, (2) results reflect production and environmental conditions specific to underground paving at this site, and (3) no control group was included.

5.1.2 Health Effects Associated with Asphalt Exposures in the Roofing Industry

Only a few studies are available concerning acute health effects among workers exposed to asphalt fumes within the roofing industry. Further complicating this review is the fact that these studies are limited by their small sample sizes, lack of control groups, and the presence of possible confounding factors, such as coal tar or fiberglass.

Hervin and Emmett [1976] NIOSH researchers evaluated the health of 34 roofers exposed to asphalt, coal-tar pitch, and fiberglass insulation during roofing operations [Hervin and Emmett 1976]. Work involved laying down layers of asphalt applied at approximately 249 °C (480 °F) and fiberglass insulation, and then layers of coal-tar pitch applied at approximately 191 to 204 °C (376 to 399 °F), and felt. During this HHE, workers underwent medical interviews and limited physical exams that focused primarily on the skin and eyes.

Twenty-three (68%) workers complained of skin problems (burning, irritation, blistering), primarily on the face and neck, that were exacerbated by sun exposure. Nineteen roofers (56%) complained of eye irritation, and six (18%) had evidence of conjunctivitis during the survey. Conjunctivitis was significantly correlated with coal-tar-pitch exposures measured as the cyclohexane-soluble portion of total particulate concentrations above 0.2 mg/m3. All air sampling results were less than 40% of the recommended ACGIH TLV® for asphalt fumes (5 mg/m3) and fiberglass (10 mg/m3). For the most part, workers reported that their eye and skin problems were caused by exposures to coal-tar pitch. Aside from thermal burns, none of the workers described eye or skin problems in association with exposure to asphalt fumes. No information was provided to allow researchers to determine if problems other than those related to eyes and skin were occurring in association with asphalt or other exposures. The authors concluded that there was an increase in acute eye and skin disorders that appeared to be related to coal-tar-pitch exposures.

While the findings suggest that exposure to asphalt fumes during roofing does not cause appreciable skin and eye problems, the asphalt fume exposures were quite low and were not evaluated independently of other exposures, such as coal-tar pitch. In addition, these results reflect working conditions specific to this site and are based on a small, and possibly unrepresentative, sample of workers having no comparison group.

Emmett [1986] Emmett [1986] summarized the results from on-site surveys of roofing crews (which included the study by Hervin and Emmett [1976]) during both installation of new roof and tear-off operations. Worker exposures during the roofing operations included coal-tar pitch, asphalt, and fiberglass insulation. The surveys involved over 50 workers and included histories of medical complaints and limited physical examinations in which eyes and skin were emphasized. The largest number of skin and eye complaints were associated with coal-tar-pitch exposures; no complaints were associated with exposure to asphalt fumes. Findings from a survey of 15 roofers asked to rate the environmental causes of their eye and skin problems suggested that asphalt fume exposures were not as irritating as other types of exposures, such as sunlight, summer weather, humidity, and coal-tar pitch. While this suggests that eye and skin problems among roofers are not appreciably related to asphalt fumes, these exposures were not evaluated independently of coal-tar-pitch exposures, nor were exposure-response comparisons described. In addition, no information was given to determine if problems other than those related to eyes and skin were occurring in association with asphalt or other exposures.

Maintz et al. [1987] Maintz et al. [1987] evaluated six roofers who had specialized in the production of asphalt insulating roofs and asphalt insulation of wet rooms for more than 20 years. The insulation process involved laying down a cold coat (asphalt and solvent) followed by several layers of hot asphalt (180 to 200 /C [356 to 392 °F]) or tar paper. All six workers were diagnosed with chronic bronchitis, and five of the workers had a history of obstructive pulmonary function. Five of the six workers had a long-standing history (>20 years) of cigarette smoking. While interesting, this report is of limited value with respect to the pulmonary morbidity of asphalt fume exposure because of the small group size, lack of controls, and the confounding factor of smoking.

5.1.3 Health Effects Associated with Asphalt Exposure among Roofers and Pavers

Nyqvist [1978] Nyqvist [1978] performed a cross-sectional study of 231 asphalt workers (194 road pavers and 37 roofers) and a control group matched by age and smoking habits of workers employed in the building trades who were not normally exposed to smoke, dust, or gas. Participants filled out simple questionnaires concerning symptoms of bronchitis and underwent a one-time spirometry evaluation. The frequency of subjective symptoms of bronchitis increased with increasing time of asphalt exposure, suggesting a dose-related pattern. Compared with controls, asphalt-exposed workers reporting slight symptoms of bronchitis had increased relative risks of 0.67 at <3 years exposure, 1.5 at 3 to 8 years, and 5 at >8 years.

Workers reporting severe symptoms of bronchitis had increased relative risks of 0.33 at <3 years exposure, 1.5 at 3 to 8 years, and 5 at >8 years. Thus relative risks were significant only for symptomatic workers with exposures >8 years as compared to controls. No significant differences in spirometric values were found between exposed workers and controls. While smoking was controlled for between groups, there appeared to be some correlation among bronchitis, smoking, and long-term asphalt exposures.

The author did not provide information concerning group demographics, response rates, and risks by occupation (i.e., pavers versus roofers). The use of self-administered questionnaires for identifying symptoms could result in inaccurate results or recall bias, and the reported years of asphalt exposure might not have accurately reflected actual exposures.

5.1.4 Health Effects Associated with Asphalt Exposures in Other Occupations

Zeglio [1950]Zeglio [1950] published observations on 22 workers who insulated electrical cables and telegraph and telephone lines for a large Italian company. Although only asphalt was reportedly used in the process, the possibility of adulteration of the asphalt with residual coal-tar pitch was raised by the author. Workers exposed to fumes from tanks heated to 120 °C (248 °F) complained of coughing and burning in their throats and chests and frequent hoarseness. Headaches and nasal discharge were also reportedly associated with exposure. Typically, effects were reported to diminish rapidly after workers left work. However, workers with longer lengths of employment tended to experience more instances of chronic nasal, pharyngeal, and pulmonary symptoms. Among the 22 workers evaluated, physical examinations revealed 10 cases of rhinitis, 13 cases of oropharyngitis, 4 cases of laryngitis, and 19 cases of bronchitis.

Limitations and potential biases of the Zeglio study include (1) small and possibly unrepresentative sample group, (2) lack of a comparison group, (3) source and composition of the bitumens not elucidated and the potential for confounding exposure to coal tar, and (4) no measurements of worker exposures.

Baylor and Weaver [1968] Baylor and Weaver [1968] reviewed 841 questionnaires from 462 asphalt workers and 379 controls. The questionnaires were obtained from medical personnel employed by seven petroleum companies that produced asphalt and included information on each worker’s medical history (including a brief physical examination), occupational history, and smoking history. No workers with less than 5 years of work with asphalt were included in the survey; the average duration of employment for both workers and controls was 15.1 years.

Results of the survey indicated no significant differences in cancer, lung disease, and skin disease between asphalt workers and controls. The number of cases of miscellaneous lung disease (such as bronchitis and asthma) were more frequent among asphalt workers (8.6%) compared to controls (4.3%), although excess cigarette use (20 cigarettes a day for >20 years) was similar between asphalt workers (26%) and controls (24%). The vast majority of the cases of miscellaneous lung disease were for chronic bronchitis, while a few cases of asthma and emphysema were noted.

Based on undefined information provided to them by representatives from 31 paving companies, 15 state highway commissions, three roofing manufacturers, and six insurance carriers, the authors also reported that asphalt-exposed workers were not experiencing any notable adverse health effects. While this study is frequently cited in the literature, it is of limited value to the current assessment of health effects because of its lack of information regarding study methods and results (i.e., response rates, selection of participants, content of questionnaires, description of exposures, etc.).

Apol and Okawa [1977] A NIOSH HHE conducted in October 1976 studied 15 workers involved in the production of fibrous glass asphalt roofing shingles [Apol and Okawa 1977]. During the period of the survey, workers had intermittent and variable exposures to mineral dust (slate granules, talc, sand), felt, glue, and asphalt fumes (asphalt heated to approximately 204 °C [399 °F]), depending upon job tasks. No fiberglass was being used at the facility during the portion of the survey discussed here. Participating workers underwent medical interviews and limited physical exams. All were male and had a mean of 7 years employment at the plant.

The most frequently reported problems were nasal irritation (47%), throat irritation (47%), and eye irritation (40%). One worker, a smoker, complained of shortness of breath; otherwise, all the interviewed workers denied past or current breathing problems. Eight workers were noted to have apparent work-related eye irritation during a postshift physical examination. The authors noted that exposure measurements indicated fairly high worker exposures to asphalt fumes and dust during the workshift (one of the 19 asphalt fume samples and seven of the 35 total dust samples exceeded 5.0 mg/m3 of total particulates).

Possible limitations of the study include (1) small and possibly unrepresentative study group, (2) lack of a control group for comparison, and (3) lack of an evaluation of the relationship between specific work exposures and reported health symptoms. No information concerning the asphalt formulation was provided to help determine if other additives or contaminants might have been present.

Chase et al. [1994] Chase et al. [1994] reported complaints of nausea, headache, fatigue, skin rash, and eye, nose, and throat irritation among 27 of 200 employees manufacturing ballast boxes and coils for fluorescent and high-intensity lighting. Symptoms were associated with exposure to fumes from a new asphalt formulation (heated to 270 °C [518 °F]) used to embed and insulate electronic components inside the ballast boxes.

Personal-breathing-zone samples were collected from six of the symptomatic workers and showed asphalt fume levels ranging from 0.50 to 1.30 mg/m3 (mean of 0.83 mg/m3). Headspace analysis of bulk asphalt samples at 180 °C (356 °F) identified volatile thermal decomposition products that included acetaldehyde, acetone, carbon monoxide, and carbonyl sulfide. At 260°C (500 °F), the head-space analysis identified an ether, 1-butanol, butyl Cellosolve®, methanol, carbon disulfide, isobutylene, and ethylene.

Medical assessments of the 27 symptomatic employees included personal interviews, questionnaires, physical examinations, spirometry, and blood tests to screen for hepatic, renal, and hematologic functions. During the initial interviews, all 27 employees reported symptoms relating to the central nervous system, ears, nose, and throat. Other symptoms reported were related to eyes (93%), gastrointestinal (89%), and respiratory (59%) systems, and skin (41%). Physical examinations revealed conjunctivitis (11%), evidence of nose bleeds (52%), throat irritation (59%), and skin rash (15%). Medical tests showed no significant effects on liver, kidneys, or lungs (spirometry results). Hematologic tests showed increased erythrocyte sedimentation rates (48%), increased mean platelet volume values (P = 0.013) (41%), and decreased red blood cell numbers (41%) in comparison with the standard laboratory reference range. Follow-up medical assessments among 15 of the 27 symptomatic employees conducted after workplace modifications had been made (i.e., installation of local exhaust ventilation) showed a significant decline in workers’ acute symptoms and a decrease in mean platelet volume toward normal.

While the findings described in this study are interesting, particularly the hematologic testing, the results are difficult to interpret because of (1) the small and possibly unrepresentative sample group, (2) lack of a comparison group, and (3) confounding exposures to additives likely to have been present in the asphalt formulation.

Tavris et al. [1984] Tavris et al. [1984] investigated an outbreak of health problems related to volatilized asphalt fumes among office workers. Interviews were conducted with 15 of the 19 workers employed in the problem office area. The most frequently reported problems included headaches, eye irritation, sore throat, nasal congestion, nausea, lightheadedness, and itchy skin.

Laboratory analyses of blood specimens (SGOT, BUN, CBCs) of nine of the 15 workers were normal except for a slight eosinophilia (4% to 5%) in five of the workers. Worker symptoms were attributed to volatilized asphalt fumes from a malfunctioning fluorescent light fixture covered with melted asphalt from an overheated light ballast. Workplace measurements for formaldehyde, carbon monoxide, and carbon dioxide were normal; however, no specific measurements for asphalt fumes were made.

Limitations of the study include a small study group and lack of a comparison group. Also, no specific measurements for asphalt fumes were made, and no product information or analysis of the asphalt was provided to help determine if other additives or contaminants might have been present.

5.1.5 Health Effects among Asphalt Workers Reported in Other Studies

A 1990 review of the scientific literature [Fries and Knudson 1990] on asphalt fumes conducted bythe European Asphalt Producers Association cited three European studies that have not been independently reviewed by NIOSH researchers. Short reviews of these studies from the Association report are presented below, without comment, to provide a comprehensive presentation of available literature regarding effects on human health associated with exposure to asphalt fumes. No exposure values or dose-response information were provided in these studies.

(1) Hasle et al. [1977] evaluated 166 Danish pavers. Chronic bronchitis and difficulty in breathing were reported in 25% and 40% of the paving workers, respectively.

(2) Schaffer et al. [1985] conducted clinical, x-ray, and biochemical analyses of 50 bitumen-exposed workers and 15 controls. Among exposed workers, there were increased symptoms of bronchitis, stomach pain, and skin irritation, but no statistical evaluations or conclusions regarding health hazards were reported.

(3) Waage and Nielson [1986] reported significantly higher prevalences of smarting eyes, stomach pains, and skin irritation among Norwegian asphalt pavers. Also, an increased incidence of headaches, dizziness, sleepiness, nausea, reduced appetite, and markedly reduced lung function (PEFR values) was reported.

Exxon [1997] A study by Exxon Biomedical Sciences entitled Shift Study of Pulmonary Function and Symptoms in Workers Exposed to Asphalt Fume [Exxon 1997] was recently completed. In this study, 170 asphalt-exposed workers employed in five segments of the asphalt industry (hot-mix plants [n=11], terminals [n=24], roofing manufacturers [n=43], roofers [n=37], pavers [n=55]) were evaluated to determine whether there was an association between the incidence of symptoms and changes in pulmonary function related to workshift asphalt exposures. Researchers evaluated personal exposures over 2 days for each participant at each worksite. About 288 person-days of observation were completed in different segments of industry as follows: paving, 82 person-days (32.4%); roofing manufacturing, 77 person-days (25.3%); roofing, 62 person-days (21.8%); terminals, 47 person-days (14.1%); and hot-mix plants, 20 person-days (6.5%). Only small differences were noted in mean age, height, and weight among participants from the different industry segments. Smoking varied somewhat by industry segment, i.e., paving, 38%; roofing, 43%; roofing manufacturing, 44%; hot-mix asphalt plants, 54%; and terminals, 17%.

As part of the health assessment, each participant received a standardized respiratory health questionnaire, serial symptom surveys (administered up to five times during a work-shift), and serial PEFR tests performed at the same time as the symptom surveys. Pre- and postshift pulmonary function tests were conducted to evaluate changes in lung function over the workshift and included measures of forced expiratory volume in 1 sec, forced vital capacity, PEFR, and mid-expiratory flow volume (FEF25-75).

All personal-breathing-zone sample results for total particulates and benzene-soluble particulates were measured as 8-hr TWAs (Table 4–12). Results indicated that workers exposed to asphalt were typically symptomatic less than 5% of the time and that most symptoms were reported to be mild. The most commonly reported problems were breathing difficulty, nose irritation, headache, throat irritation, and coughing. Various analyses of individual symptom responses and a developed symptom score (derived from a score for each of the 15 symptoms assessed for each subject) did not reveal any significant associations with workers’ personal-breathing-zone measurements of asphalt exposure. In addition, different analyses (i.e., logistic regression, nonparametric regression, factor analysis) of pulmonary function tests regarding workers’ smoking frequency, reported symptoms, developed symptom score, or measured asphalt exposures did not show any significant associations.

Limitations and potential biases associated with this study include (1) a relatively small and possibly unrepresentative sample from each industry segment, (2) narrow exposure ranges and very little data on higher concentrations, which reduces researchers’ ability to detect significant exposure-response associations and levels of adverse effects (i.e., lowest observable adverse effect level [LOAEL] or no observable adverse effect level [NOAEL]), (3) possible lack of correlation between 8-hr average exposure measurements and assessed acute health effects (which were evaluated every few hours; shortterm peak exposure measurements may be necessary to determine an exposure-response association), and (4) lack of inclusion of an unexposed comparison group (although workers at most study sites who had lesser amounts of exposure were included in the exposure-response analysis).

5.1.6 Conclusions

Studies concerning the acute toxic effects of exposure to asphalt fumes have repeatedly found symptoms of irritation of the serous membranes of the conjunctivae (eye irritation) and the mucous membranes of the upper respiratory tract (nasal and throat irritation) among workers. These health effects have been best described in asphalt road pavers [Norseth et al. 1991; Hanley and Miller 1996a,b; Almaguer et al. 1996; Miller and Burr 1996a,b, 1998; Kinnes et al. 1996; Sylvain and Miller 1996]. They typically appear to be of mild severity and transitory in nature [Hanley and Miller 1996a,b; Almaguer et al. 1996; Miller and Burr 1996a,b, 1998; Kinnes et al. 1996; Exxon 1997]. Similar symptoms have also been reported in workers exposed to asphalt fumes during the manufacture of asphalt roofing shingles [Apol and Okawa 1977] and fluorescent lights [Chase et al. 1994], cable insulating activities [Zeglio 1950], and from a malfunctioning light fixture in an office [Tavris et al. 1984]. The occurrence of mild transitory symptoms (i.e., nasal and throat irritation, headaches, and coughing) was recently reported among workers employed in five segments of the asphalt industry (hot-mix plants, terminals, roofing, roofing manufacturing, and paving), although no significant dose-response associations were found between measured exposures and symptoms [Exxon 1997]. While these acute health effects have been reported in a number of work settings, the specific association, if any, between symptoms and asphalt fume exposure has been difficult to establish because of a lack of research on this topic and various limitations of those studies that have been conducted.

In addition to mucosal irritation, skin irritation, pruritus, and occasionally rashes have been reported [Hanley and Miller 1996a,b; Almaguer et al. 1996; Miller and Burr 1996a,b; Kinnes et al. 1996; Chase et al. 1994; Tavris et al. 1984; Schaffer et al. 1985; Waage and Nielson 1986]. 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. If asphalt-related dermal photosensitization is occurring, such as seen with coal tar, it has not been described in the literature and so needs to be further investigated, as do the other reported skin problems.

Symptoms of nausea, stomach pain, decreased appetite, headaches, and fatigue have also been 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], although no significant dose-response associations were found between measured exposures and symptoms [Exxon 1997]. These nonspecific types of symptoms require further investigation to help clarify and establish the nature of any causal relationships with asphalt fume exposure.

Lower respiratory tract symptoms (coughing, wheezing, shortness of breath) [Hanley and Miller 1996a,b; Almaguer et al. 1996; Miller and Burr 1996a,b; 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] have been described among workers exposed to asphalt fumes. Results from recent studies [Exxon 1997; Hanley and Miller 1996a,b; Almaguer et al. 1996; Miller and Burr 1996a,b; Kinnes et al. 1996] showed that some workers experienced lower respiratory tract problems or changes in pulmonary function when exposure to asphalt fumes was relatively low, such as during open-air highway paving. The NIOSH studies [Kinnes et al. 1996; Sylvain and Miller 1996] indicated significant changes in pulmonary function in one of 44 workers engaged in open-air asphalt paving and three of nine workers engaged in underground asphalt paving. The Exxon study [1997] found no significant association between pulmonary function measurements and asphalt exposures among workers employed in five segments of the asphalt industry. Some limited evidence suggests that personal health factors (i.e., preexisting asthma) or exposures to greater amounts of asphalt fumes, such as those found during underground paving, may increase workers risk for lower respiratory tract symptoms or changes in pulmonary function [Norseth et al. 1991; Sylvain and Miller 1996]. However, the current data are insufficient to determine the relationship between asphalt fume exposures and these health effects.

While asphalt fume concentrations associated with the health effects noted above have not been well characterized, symptoms of irritation were noted during open-air paving among workers whose average personal exposures were 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 [Norseth et al. 1991; Hanley and Miller 1996a,b; Almaguer et al. 1996; Miller and Burr 1996a,b, 1998; Kinnes et al. 1996; Sylvain and Miller 1996; Exxon 1997]. Presently, none of these studies have established a clear exposure-response relationship between exposures and health effects. However, health effect findings from research on underground asphalt paving, where exposures are greater, suggest that a dose-response relationship may exist [Norseth et al. 1991; Sylvain and Miller 1996]. Improved research studies, such as those involving larger groups of participants and controls, evaluation of workers with higher levels of exposure, and enhanced measurement of exposures (i.e., real-time peak concentrations) in relation to health responses may be necessary to elucidate any exposure-response relationships, if present.

In addition, bronchitis possibly related to chronic lower respiratory tract irritation has been reported among asphalt workers in several studies [Hansen 1991; Maizlish et al. 1988; Maintz et al. 1987; Nyqvist 1978; Zeglio 1950; Baylor and Weaver 1968; Hasle et al. 1977]. Unfortunately, the limited data preclude making any determinations concerning asphalt-exposure-related chronic pulmonary morbidity. Until additional data have been gathered to clarify the health risks associated with occupational exposure to asphalt, it would be prudent to be cautious when working with these materials and to limit worker exposures to the extent feasible.

5.2 Chronic Health Effects

The 1977 NIOSH Criteria for a Recommended Standard: Occupational Exposure to Asphalt Fumes contains discussions of the pertinent epidemiologic data published through 1976 on workers exposed to roofing or paving asphalt fumes. These earlier studies relating asphalt fume exposure to cancer mortality were judged to be inconclusive because of methodological problems, such as incomplete exposure data, discrepancies in terminology, insufficient latency periods, and confounding variables (e.g., smoking and exposure to other potential carcinogens, such as coal-tar products) [NIOSH 1977a]. These problems made it impossible to determine the cause of observed excesses of cancer incidence in employees exposed to asphalt fumes during roofing and paving operations.

Since the release of the NIOSH criteria document, additional epidemiologic studies have been conducted to evaluate the possible association between asphalt fume exposure and cancer risk [Hansen 1989 a,b, 1991; Engholm et al. 1991; Wilson 1984; Maizlish et al. 1988; Bender et al. 1989; Mommsen et al. 1983; Risch et al. 1988; Bonassi et al. 1989]. These studies are reviewed below under the headings of "Road Workers," "Pavers," "Roofers," and "Others" because the nature of exposures to asphalt fumes is different and because exposures to other carcinogenic hazards may confound interpretations of the data.

The results of the studies are summarized in Tables 5–3 through 5–8.

5.2.1 Pavers
5.2.1.1 Cohort Studies

Hansen [1989a, 1991] In a retrospective cancer incidence study by Hansen [1989a], the causes of death of 679 male Danish mastic asphalt employees were compared with causes of death in the total Danish male population over the same period. Mastic asphalt, which is a mixture of fine sand, stone powder, finely divided limestone, and 12% to 17% asphalt, is used in paving and flooring operations in Denmark. The mix is emptied into buckets at worksites, and workers apply the mastic asphalt by pouring out a given amount and leveling or smoothing it with a wooden trowel.

The same workers perform both flooring and paving activities. To determine asphalt fume concentrations, the Danish National Institute of Occupational Health collected 35 personalbreathing- zone samples during flooring operations, representing a third of the total work hours of the cohort, and two samples during paving operations, representing the remaining two-thirds of the total work hours. The 35 samples collected during flooring operations ranged from 0.5 to 260 mg/m3 of asphalt fume condensate, with a median of 19.7 mg/m3, and the two samples collected during paving operations were 3.5 and 4.3 mg/m3 of asphalt fume condensate. On the basis of these results, occupational exposure to asphalt fumes was estimated to be almost the equivalent of a continuous work-time exposure at the current Danish TWA standard of 5 mg/m3.

Hansen identified the employees through files covering the time period 1959-1980 and followed them through January 1, 1985. As of January 1, 1985, 524 employees were living, 149 were deceased, and 6 had emigrated. The standardized incidence ratio (SIR) for all malignant neoplasms was 1.95 (75 cases, with a confidence interval [CI] of 95%=1.53-2.44). As a group, mastic asphalt employees 40 years or older when diagnosed (n=547) had statistically significant increases in SIRs for cancers of the lung (SIR=3.44; 95% CI=2.27-5.01), mouth (SIR=11.11; 95% CI=1.35-40.14), esophagus (SIR=6.98; 95% CI=1.44-20.39), and rectum (SIR=3.18; 95% CI=1.28-6.56). Hansen divided the cohort into three birth-year subcohorts (18931919, 1920-1929, and 1930-1960). Lung cancer was elevated in all three subcohorts, but was highest among workers born in the period between 1930 and 1960 (SIR=8.57, 95% CI=1.77-25.05). These workers were believed to be the least likely to have been exposed to coal-tar pitch.

Histories for tobacco consumption were not available for the cohort. However, Hansen cited a 1976 survey of smoking habits of Danish mastic asphalt employees that found that 22% were nonsmokers and 78% were smokers. Hansen also cited another survey of the Danish male population done in 1982 that found fewer smokers among men the same ages as the cohort (39% nonsmokers and 61% smokers).

Table 5-3. Epidemiologic studies on asphalt exposure: cohort studies, pavers
Author, country, and occupation No. of study subjects Dates of case ascertainme at Type or site of condition No. of deaths or cases Risk ratio 95% CI or P value
Hansen 1989a, Denmark, mastic asphalt workers 679 1959-1986 All cancers 74 SIR 1.95* 1.53-2.44
      Lung CAncer 27 SIR 3.44† 2.27-5.01
      Mouth 2 SIR 11.11† 1.35-40.14
      Esophagus 3 SIR 6.98† 1.44-20.39
      Rectum 7 SIR 3.18† 1.28-6.56
Hansen 1991, Denmark, mastic asphalt workers 679 1959-1986 All causes 148 SMR 1.57† 1.34-1.85
      All cancers 62 SMR 2.29† 1.75-2.93
      Lung Cancer 25 SMR 2.90† 1.88-4.29
      Nonlung Cancer 37 SMR 2.00† 1.41-2.76
      Bronchitis, emphysema, asthma 9 SMR 2.07† 0.95-3.93
      Liver cirrhosis 7 SMR 4.67† 1.88-9.62
Engholm et al. 1991, Sweden, pavers 2572 1971-1985 All causes 96 SMR 0.69 NR
      All cancers 47 SIR 0.86 NR
      Stomach cancer 5 SMR 2.01 NR
      Stomach cancer 6 SIR 2.07 NR
      Lung cancer 7 SMR 1.10 NR
      Lung cancer 8 SIR 1.24 NR
Maizlish et al. 1988, United States, highway maintenance workers (n=307) 1570 1970-1983 Emphysema 8 PMR 2.50 1.80-4.92
      Digestive system cancer 25 PMR 1.51 0.97-2.33
      Stomach cancer 6 PMR 2.27 0.83-4.95
      Skin cancer 2 PMR 1.22 0.12-4.93
      Prostate cancer 7 PMR 2.26 0.91-4.66
      Brain cancer 4 PMR 1.60 0.40-4.10
      Lymphopoietic cancer 8 PMR 1.15 0.50-2.26
Bender et al. 1989, United States, highway maintenance workers 4849 1945-1984 All causes 1530 SMR 0.9 0.86-0.96
      All cancers 274 SMR 0.83 0.73-0.94
      Lung cancer 57 SMR 0.69 0.52-0.90
      Mouth, pharyngeal cancer 2‡ SMR 11.10 1.30-40.10
      Gastrointestinal cancer SMR 5.82 1.20-17.00
      Prostate cancer 11** SMR 2.98 P<0.01
      Kidney, bladder, other urinary organ cancers 7†† SMR 2.92 1.17–6.02
      Leukemia 8‡‡ SMR 4.49 1.94–8.84
Partanen et al. 1997, Finland, road pavers (males only)     Lung cancer NR SMR 1.5 1.2–1.9
        NR SIR 1.4§§ 0.9–1.9
Milham 1997, United States, road graders, pavers, machine operators, excavators, operating
engineers
7,266 1950-1989 Respiratory system 614 PMR 1.1 P<0.01
      Bronchus, trachea, lung cancer (ICD 162) 558 PMR 1.20 P<0.01
operating engineers, only     Respiratory system cancer 136 PMR 1.21 P<0.05
      Bronchus, trachea, lung (ICD 162) 122 PMR 1.21 P<0.05
      Bronchus, lung (ICD 162.1, 163) 76 PMR 1.42 P<0.01
      Asthma 5 PMR 1.60 NS
      Lymphatic, hematopoietic cancer 43 PMR 1.42 P<0.05
      Reticulosarcoma 7 PMR 1.37 NS
      Lymphosarcoma 6 PMR 1.88 NS
      Hodgkins disease 4 PMR 1.58 NS
      Other lymphomas 10 PMR 2.00 P<0.05
      Motor vehicle accidents 47 PMR 1.59 P<0.01
road graders, pavers, machine     Bronchus, lung cancer (ICD 162.1, 163) 288 PMR 1.24 P<0.01
operators, and excavators     Motor vehicle accidents 249 PMR 1.39 P<0.01
Hammond et al. 1976, United States, Roofer, waterproofer 5939 1960-1971 Lung cancer 99 SMR 1.58* 1.29-1.94
      Lung cancer 24 SMR 2.0† 1.28-4.32
      Respiratory disease‡ 71 SMR 1.67  
Menck and Henderson 1976, United States, Roofer 2000 1963-1970 Lung cancer 3 SMR 8.78 P<0.01
        2 incident cases    
Engholm et al. 1991, Sweden, Roofer 704 1971-1985 Lung cancer 3 deaths SMR 2.79  
        4 cases SIR 3.62  
        3 cases OR 6.0§  
      Stomach cancer 5 deaths SMR 2.01  
        1 case SIR 1.98  
      Lymphatic, hematopoietic cancer 2 deaths SMR 2.68  
      Leukemia 1 case SIR 2.26  
Hrubec et al. 1992, United States, Roofer, slater 52 1954-1980 Lung cancer 4 deaths RR 3.0 1.30-6.75**
Pukkala 1995, Finland, Asphalt roofer 47000 1970-1985 Lung cancer 18 cases SIR 3.25 †† 1.92–5.13
Milham 1997, United States, Washington State, Roofers and slaters 1057 1950-1989 Buccal cavity, pharynx cancer 9 PMR 1.67 NS
      Respiratory cancer 105 PMR 1.53 P<0.01
      Larynx cancer 6 PMR 2.59 P<0.05
      Bronchus, trachea, lung cancer (ICD 162) 86 PMR 1.44 P<0.01
      Bronchus, lung cancer (ICD 162.1, 163) 53 PMR 1.60 P<0.01
      Asthma 7 PMR 2.86 P<0.01
      Diseases of circulatory system 364 PMR .88 P<0.05
      Diseases of respiratory system 76 PMR 1.20 NS
      Chronic bronchitis 4 PMR 1.99 NS
      Bronchitis with emphysema 4 PMR 2.16 NS
      Other diseases of respiratory system (ICD 510-527) 52 PMR 1.43 P<0.05
      Other diseases of lung, pleural cavity 46 PMR 1.49 P<0.01
      Emphysema without bronchitis 28 PMR 1.63 P<0.01
      Cirrhosis of liver with alcoholism 17 PMR 2.84 P<0.01
      Cirrhosis of liver without alcoholism 23 PMR 1.49 NS
      Falls from elevation 17 PMR 4.00 P<0.01
      Psychosis 5 PMR 2.23 NS
Abbreviations: CI=confidence interval; ICD=International Classification of Diseases; NS=not statistically significant; OR=odds ratio; PMR=proportionate mortality ratio; RR=relative risk; SIR=standardized incidenceratio; SMR=standardized mortality ratio.
*> 20 years since joining union.
†>40 years since joining union.
‡Pneumonia, TB, influenza excluded.
§Adjusted for smoking, relative risk. xx90% confidence interval.
††Adjusted for age, calendar time, and soclal class.
Table 5-4. Epidemiologic studies on asphalt exposure: cohort studies, roofers
Author, country, and occupation No. of study subjects Dates of case ascertainme at Type or site of condition No. of deaths or cases Risk ratio 95% CI or P value
Hammond et al. 1976, United States, Roofer, waterproofer 5939 1960-1971 Lung cancer 99 SMR 1.58* 1.29-1.94
      Lung cancer 24 SMR 2.0† 1.28-4.32
      Respiratory disease‡ 71 SMR 1.67  
Menck and Henderson 1976, United States, Roofer 2000 1968-1970 Lung cancer 3 SMR 8.78 P>0.01
        2 incident cases    
Engholm et al. 1991, Sweden, Roofer 704 1971-1985 Lung cancer 3 deaths SMR 2.79  
        4 cases SIR 3.62  
        3 cases OR 6.0§  
      Stomach cancer 5 deaths SMR 2.01  
        1 case SIR 1.98  
      Lymphatic, hematopoietic cancer 2 deaths SMR 2.68  
      Leukemia 1 case SIR 2.26  
Hrubec et al. 1992, United States, Roofer, slater 52 1954-1980 Lung cancer 4 deaths RR 3.0 1.30-6.75**
Pukkala 1995, Finland, Asphalt roofer 47000 1971-1985 Lung cancer 18 cases SIR 3.25†† 1.92-5.13
Milham 1997, United States, Washington State, Roofers and slaters 1057 1950-1989 Buccal cavity, pharynx cancer 9 PMR 1.67 NS
      Respiratory cancer 105 PMR 1.53 P<0.01
      Larynx cancer 6 PMR 2.59 P<0.05
      Bronchus, trachea, lung cancer (ICD 162) 86 PMR 1.44 P<0.01
      Bronchus, lung cancer (ICD 162.1, 163) 53 PMR 1.60 P<0.01
      Asthma 7 PMR 2.86 P<0.01
      Diseases of circulatory system 364 PMR 0.88 P<0.05
      Diseases of respiratory system 76 PMR 1.20 NS
      Chronic bronchitis 4 PMR 1.99 NS
      Bronchitis with emphysema 4 PMR 2.16 NS
      Other diseases of respiratory system (ICD 510-527) 52 PMR 1.43 P<0.05
      Other diseases of lung, pleural cavity 46 PMR 1.49 P<0.01
      Emphysema without bronchitis 28 PMR 1.63 P<0.01
      Cirrhosis of liver with alcoholism 17 PMR 2.84 P<0.01
      Cirrhosis of liver without alcoholism 23 PMR 1.49 NS
      Falls from elevation 17 PMR 4.00 P<0.01
      Psychosis 5 PMR 2.23 NS
Abbreviations: CI=confidence interval; ICD=International Classification of Diseases; NS=not statistically significant; OR=odds ratio; PMR=proportionate mortality ratio; RR=relative risk; SIR=standardized incidenceratio; SMR=standardized mortality ratio.
*> 20 years since joining union.
†>40 years since joining union.
‡Pneumonia, TB, influenza excluded.
§Adjusted for smoking, relative risk.
**90% confidence interval.
††Adjusted for age, calendar time, and soclal class.
Table 5-5. Epidemiologic studies on asphalt exposure: case-control studies of roofers
    Number of study subjects Number of subjects with lung cancer    
Author, country, and occupation Dates of case ascertainment Cases Controls Cases Controls Odds ratio* 95% CI
Zahm et al. 1989, United States Roofer 1980-1985 4,431 11,326 6 7 2.1 0.6-8.2
Schoenberg et al. 1987, United States Roofer, slater 1967-1976 763 900 13 8 1.7 0.7-4.4
Morabia et al. 1992, United States Roofer, slater 1980-1985 1,793 3,228 7 6 2.1 0.7-6.2
Abbreviations: CI=confidence interval.
*Adjusted for smoking


Table 5-6. Epidemiologic studies of asphalt exposure: case control studies of bladder, pelvis, and ureter cancer
      Number of study subjects Number of subjects with lung cancer    
Author, country, and exposure or occupations Dates of case ascertainment Site Cases Controls Cases Controls Risk ratio* 95% CI
Mommsen et al. 1983, Denmark Petroleum or asphalt Not given Bladder 212 259 2 3 RR 2.36 NS
Risch et al. 1988, Canada Asphalt or tar 1979-1982 Bladder 739 781 739 781 OR 1.44* 0.78-2.74
              OR 3.11† 1.19-9.68
              OR 2.02† 1.08-4.97
Bonassi et al. 1989, United States Road menders Not given Bladder 121 342 2 6 OR 1.40 0.27-7.28
Jensen et al. 1988, Denmark Asphalt or tar 1979-1982 Renal pelvis, ureter 96 294 9 6 RR 5.5 1.6-19.6
Abbreviations: CI=confidence interval; NS=not statistically significant; OR=odds ratio; RR=relative risk.
*Ever exposed to "tar and asphalts" (n = 46). †Exposed during full-time job of at least 6 months 8 to 28 years before diagnosis (n = 23).
‡Trend with duration. Odds ratio for trend at 10 years duration.


Table 5–7. Epidemiologic cohort study of asphalt exposure during manufacture
Number of study subjects Type of condition No. of deaths or cases SMR 95% CI
1,320 exposed All cases 29 1.59* 1.06-2.28
43,024 unexposed Digestive cancer 6 1.57 0.58-3.43
  Respiratory cancer 11 1.52 0.76-2.71
  Bladder cancer 3 2.91 0.60-8.51
  Brain cancer 3 5.00 1.03-14.61
  Ischemic heart disease 29 1.31 0.88-1.89
Abbreviations: CI=confidence interval; SMR=standardized mortality ratio.
*Workers >45 years of age between 1975-1980.
NOTE: Case ascertainment was for 1970-1980.


Table 5-8. Epidemiologic studies on asphalt exposure: case control studies of respiratory cancer and other diseases
      Number of study subjects Number of subjects with lung cancer    
Author, country, and exposure or occupations Dates of case ascertainment Site Cases Controls Cases Controls Risk ratio* 95% CI
Vineis et al. 1988, United States Roofers, asphalt workers 1974-1981 Lung cancer 2,973 3,210 45 37 1.4 0.9-2.3
Zahm et al. 1989, United States Pavers, surfacers, materials-moving equipment operators. 1980-1985 Lung cancer 4,431 11,326 32 64 0.9 0.6-1.5
Roofers         6 7 2.1 0.6-8.2
Chiazze et al. 1993, United States* Not given Lung cancer Nonmalignant respiratory 144 260 111 251 0.96 0.65-1.42
Austin et al. 1987, United States† Not given Hepatocellular carcinoma 80 146 7 5 3.2 0.9-11
Siemiatycki 1991, Canada Not given Colon cancer 3,730 533‡ 22 1.6 1.1-2.5
Abbreviations: CI=confidence interval.
*Exposed to asphalt fumes of >0.01 mg/m3 cumulative exposure concentration.
†Exposed to asphalt.
‡Number of controls exposed not available.

Hansen estimated that differences in smoking rates between mastic asphalt workers and the general population would increase the incidence of lung cancer in mastic asphalt workers by about 20%, which would not account for the threefold increase in cancer in the mastic asphalt cohort.

Hansen also considered the potential for confounding by urbanization. Urban areas of Denmark were reported to have higher incidences of cancer than rural areas. Hansen suggested that nearly all of the asphalt workers in her study were urban dwellers, as compared to only 40% of the referent population, and that this potential bias may have underestimated the expected cancer incidence in the study population by 35%. However, again, this would not account for the observed threefold excess of respiratory cancer among workers exposed to asphalt fumes.

In 1991, Hansen conducted a retrospective mortality study of the original cohort in whichthe study population was followed to June 10, 1986 [Hansen 1991]. As of that date, 504 employees were living, 169 were deceased, and the vital status of six workers could not be determined. The overall mortality of the cohort was significantly elevated compared to the general population (standardized mortality ratio [SMR] =1.63; 95% CI=1.41-1.90). SMRs for all cancers (SMR=2.29; 95% CI=1.75-2.93), lung cancer (SMR=2.90; 95% CI=1.88-4.29), and all nonlung cancers (SMR=2.00; 95% CI=1.41-2.76) were significantly elevated among workers aged 40 to 89. Increased mortality was also reported for nonmalignant respiratory diseases (emphysema, bronchitis, and asthma) (SMR=2.07; 95% CI=0.95-3.93) and liver cirrhosis (SMR=4.67; 95% CI=1.88-9.62). As she did in the 1989 cancer incidence study, Hansen considered the potentially confounding effects of smoking and urbanization on lung cancer. For urbanization, Hansen used an adjustment factor of 10% to increase the expected number of lung cancers, whereas in the 1989 study, she used an adjustment factor of 35%. The 10% adjustment factor appears to be based on reported differences in urban and rural lung cancer mortality rates. For smoking, Hansen used an upward adjustment factor of 18% for the expected number of lung cancers, which is similar to the 20% factor she used in her 1989 study [Hansen 1989a]. Based on these adjustment factors, Hansen estimated that among mastic asphalt employees 40 years or older, the SMR for lung cancer mortality was 2.46 (95% CI=1.59-3.63) when adjusted for smoking, 2.64 (95% CI=1.71-3.90) when adjusted for urbanization, and 2.24 (95% CI=1.45-3.30) when adjusted for both smoking and urbanization. Hansen then concluded that the increase in lung cancer mortality observed in the 1991 study could not be explained by differences in either smoking habits or degree of urbanization.

The validity of several aspects of the design and analysis of Hansen’s incidence and mortality studies has been debated. Wong et al. [1992] critiqued both studies, and Hansen [1992] subsequently published a reply. The major criticisms were the lack of control for confounding by smoking and urbanization, possible confounding by coal tar, biases in the selection of the cohort, and inadequate data on work and exposure histories. The issue of confounding by coal tar and other materials remains unresolved and limits and complicates overall interpretation of the studies.

Engholm et al. [1991] The Swedish Construction Industry's Organization for Working Environment, Safety and Health conducted a study of cancer mortalityand incidence among Swedish construction workers [Engholm et al. 1991]. Male workers (n=226,000) who received medical examinations between 1971 and 1979 were followed for mortality to 1985 and for cancer incidence until December 1984. National mortality and incidence rates were used as reference rates to estimate age and calendar-year-adjusted SMRs and SIRs. Of the original cohort, 2,572 construction workers were road pavers exposed to asphalt. The results for 704 roofers in this cohort are described in section 5.2.2. The average length of the follow-up period for mortality was 11.5 years, and median age during the follow-up was 42 years. This implies that the study cohort was very young at the beginning of the study. The long latency period required for most cancers to become detectable would make it difficult to find any increased risk of occupationally related cancer during such a short follow-up period.

The overall SMR for all causes of death was 0.69 (96 cases), and the SIR for all cancer sites was 0.86 (47 cases). Excess mortality from and incidences of stomach cancer were observed among pavers (SMR=2.01; SIR=2.07), although the number of cases was small and was reported by the authors not to be statistically significant. Lung cancer among pavers was not statistically significantly elevated in the analyses of mortality (SMR=1.10; 95% CI=0.44-2.23) or incidence (SIR=1.24; 95% CI=0.53-2.44). A case-control study of lung cancer was conducted to control for cigarette smoking using data collected during examinations of the employees. Among pavers, there were seven incident cases of lung cancer. The odds ratio (OR) for lung cancer was approximately 2 before adjusting for smoking and population density and approximately3 after adjusting for smoking.

Significant limitations of this study include a short latency period (11.5 years) and lack of quantitative information about exposures.

Maizlish et al. [1988] Maizlish et al. [1988] conducted a proportional mortality study of 27,162 employees who left employment with the California Department of Transportation between 1970 and 1983. Of the 1,570 deaths during that time, 307 occurred among highway maintenance employees considered most likely to have been exposed to asphalt fumes. The authors found that these employees had a statistically significant increase in mortality from emphysema (proportional mortalityratio [PMR]=2.50; 95% CI=1.08-4.92) and a statistically nonsignificant excess of deaths from cancer of the lymphopoietic system, digestive organs, skin, stomach, prostate, and brain. However, the study did not find an excess of deaths from lung cancer.

As the authors clearly state, proportionate mortality studies are inherently limited by the lack of independence among causes of death. Furthermore, no exposure measurements were available for asphalt fumes or other chemicals used by highway maintenance employees, and no data were available on tobacco consumption.

Bender et al. [1989] Bender et al. [1989] conducted a retrospective mortality study of a cohort of 4,849 men who each had at least 1 year of experience as a Minnesota highway maintenance employee and who had worked at least 1 day between January 1, 1945, and December 31, 1984. During the study period, 1,530 deaths occurred among these 4,849 men with 96,596 person years at risk. The male population of Minnesota was used as the reference group. The highway maintenance employee cohort and the reference group were divided into urban and rural categories to evaluate the effects of differences in mortality rates between urban and rural populations.

Mortality from all causes (SMR=0.91; 95% CI=0.86-0.96) and all cancers (overall SMR= 0.83; 95% CI=0.73-0.94; P<0.01) was statistically significantly lower than expected. Mortality from lung and respiratory cancers was also significantly less than expected (overall SMR=0.69; 95% CI=0.52-0.90; P<0.05) based on 57 deaths (82.6 were expected) regardless of latency or whether the employee worked in an urban or a rural environment. No deaths resulted from melanoma or soft tissue cancers (2.9 and 1.4, respectively, were expected). Bender et al. attributed these decreases in mortality to the healthy worker effect, which may be particularly applicable to highway maintenance employees who have physically demanding jobs.

Statistically significant excesses of cancer mortality rates at industrial sites were reported in the investigation of subgroups, particularly among workers employed for a long time or with long latency (time since first exposure). Statistically significant (P<0.05) excesses of mortality were reported for (1) cancer of the mouth and pharynx (SMR=11.10; 95% CI=1.3040.10) among men who were employed for 40 or more years (two deaths), (2) gastrointestinal cancer among urban workers with 40 to 49 years of latency (SMR=5.82; 95% CI=1.20-17.00) (three deaths), (3) prostatic cancer among workers who started work between 1955 and 1964 (SMR=2.98, P<0.01), (4) cancers of the kidneys, bladder and other urinary organs among workers employed for 40 to 49 years (overall SMR=2.92; 95% CI=1.17-6.02), and (5) leukemia among workers employed for 30 to 39 years (overall SMR=4.25; 95% CI=1.71-8.76). The Minnesota Department of Health [1993] concluded that it was unlikely that the excess leukemia mortality observed among the highway maintenance employees was job related.

Interpretation of the study is limited by two considerations. (1) Employees could have been exposed to a variety of confounding factors. (2) The category of "highway maintenance employee" covers a wide range of jobs, including paving, sign painting, mowing, landscaping, and garage and office work.

Analysis of personal-breathing-zone samples and bulk samples of asphalts, oils, and tack coats failed to detect pyrene, B(a)P, or chrysene in any of the substances in use at the time of this study. It is also important to note that highway maintenance work in Minnesota has not involved application of coal-tar products in highway repairs for more than 50 years, thus minimizing risks of exposure to this potential confounder.

Partanen et al. [1997] Partanen et al. [1997] recently reported findings from a retrospective cohort study of 9,643 Finnish workers employed for at least 3 months between 1969 and 1984 by one of six companies involved in road paving. This study is a part of a larger ongoing study by the International Agency for Research on Cancer (IARC) on cancer risk in European asphalt workers in seven countries. The cohort was followed for both mortality and cancer incidence through 1994. Relative to the general Finnish population, a statistically significant excess of deaths from lung cancer (SMR=1.5; 95% CI=1.4-1.7) was observed in the entire cohort. However, the excess of lung cancer was evident in both workers exposed to asphalt (SMR=1.4) and workers not exposed to asphalt (construction, SMR=1.4; excavation, SMR=1.8). Associations were also observed for incidences of lung cancer and exposure to asphalt (SIR=1.4; 95% CI=0.9-1.9), as well as exposure to silica, diesel exhaust, gasoline exhaust, and inorganic dusts. The authors did not attempt to separate the possible effects of asphalt, diesel exhaust, and silica. This report was an abstract from conference proceedings, and thus a thorough evaluation of the study is not possible at this time.

Milham [1997] Milham [1997] analyzed occupational and cause-of-death information on 588,090 Washington State males between 1950 and 1989 and 88,071 females between 1974 and 1989 compared to deaths in the general population of the state using an age and year-of-death standardized PMR program. Occupation was abstracted from the “Usual Occupation” field on each death certificate. Ninety-seven percent of all death certificates of males contained information on usual occupation. Based on interviews with next-of-kin, the accuracy of the Usual Occupation field was greater than 75%. Occupations reported included 7,266 deaths among "road graders, pavers, machine operators, and excavators" and 1,437 deaths among "operating engineers." These two groups are believed to have had the greatest likelihood of being exposed to asphalt.

Among workers classified as road graders, pavers, machine operators, and excavators, mortality was statistically significantly increased (P<0.05) for cancers of the respiratory system (PMR=1.17, based on 614 deaths) and bronchus, trachea, and lungs (PMR=1.20, based on 558 deaths). Mortality was also increased because of motor vehicle accidents (PMR=1.39, based on 249 deaths).

Among individuals classified as operating engineers, mortality was statistically significantly increased for cancers of the respiratory system (PMR=1.21, based on 136 deaths) and bronchus, trachea, and lungs (PMR=1.21, based on 76 deaths). The PMRs for the categories of all malignancies of the lymphatic and hematopoietic system (PMR=1.42, based on 42 deaths) and other lymphomas (PMR=2.00, based on 10 deaths) were statistically significantly increased (P<0.05). Deaths from motor vehicle accidents were also significantly higher (PMR=1.59, based on 47 deaths).

The results of this study are limited by the limitations of proportionate mortality studies, e.g., interdependence of cause-specific PMRs, inaccuracies resulting from obtaining usual occupations from death certificates, and lack of detailed information on exposures and confounders, particularly smoking.

5.2.1.2 Case-Control Studies

Zahm et al. [1989] compiled information from the Missouri Cancer Registry on 4,431 histologically confirmed lung cancer cases and 11,326 cancer controls diagnosed in white males between 1980 and 1985. Occupational history was obtained from medical records and coded according to the U.S. Bureau of Census’ 1980 Alphabetical Index of Industries and Occupation. Sufficient occupational data to perform an analysis were contained in the medical records of only 52% of the cases and 45% of the controls. After adjusting the analyses for age and cigarette smoking, 32 cases and 64 controls were identified among workers classified as pavers, surfacers, and materialsmoving- equipment operators. The OR for working in these occupations was below 1.00 (OR=0.9; 95% CI=0.6-1.5).

5.2.2 Roofers
5.2.2.1 Cohort Studies

There have been several cohort mortality studies of roofers exposed to asphalt fumes. These studies share a common limitation, i.e., the potential for confounding because of exposure to coal tar and asbestos. Coal tar is a well-recognized human lung carcinogen.

Hammond et al. [1976] Many studies use the "Usual Occupation" field from death certificates or interviews as surrogates for exposure information. The earliest epidemiologic study was done by Hammond et al. in 1976 in a retrospective mortality study of members of the United Slate, Tile and Composition Roofers, Damp and Waterproof Workers’ Association. Local unions involved only in the tile and slate industries were excluded. Workers included were those involved primarily in applying hot pitch or asphalt to roofs or waterproofing materials to basements. According to the authors, “In former years pitch was used more frequently than asphalt, but today asphalt is more commonly used.” Hence workers in this study were exposed to both asphalt and coal tar. The study included 5,939 active, probational, and retired workers who had been in the union for at least 9 years when the studybegan on January 1, 1960. Vital status, primarily from union life insurance records, was established as of December 31, 1970, for 97.5% of this cohort.

Lung cancer mortality was observed to increase with time since a worker first joined the union (a surrogate for length of exposure). A statistically significant excess of lung cancer was observed among workers who had first joined the union more than 20 years earlier (SMR=1.58; 95% CI=1.29-1.94) and also among workers with more than 40 years of work (SMR=2.0; 95% CI=1.28-4.32). A statistically significant excess of upper respiratory cancers (buccal cavity, pharynx, larynx, and esophagus) was also reported (SMR=1.59; 95% CI=1.32-2.76). Although the authors suggested their findings might be explained by exposure to B(a)P, it is impossible to rule out exposure to asphalt or other substances, or smoking, as contributing to the observed excesses of respiratory cancer.

Menck and Henderson [1976] Menck and Henderson [1976] conducted an investigation of lung cancer mortality and incidence rates in Los Angeles. A total of 2,161 deaths and 1,777 lung cancer incidents were identified among white males aged 20 to 64 during 1968 and 1970. The subjects’ last known occupations and industry affiliations were coded from death certificates or from medical records. Age-, industry-, and occupation-specific estimates of the population at risk were derived from the 1970 census for Los Angeles. A statistically significant excess of lung cancer (mortality and incidence combined) was observed for the occupational category of roofers (SMR=8.78; P<0.01).

In addition to possible confounding by coal tar, this study is limited in that the analysis was based on the "Usual Occupation" field on the death certificate, which may not accurately reflect lifetime work histories of individuals. Moreover, the authors were unable to analyze the data by level of exposure, duration of exposure, or latency.

Engholm et al. [1991] The Swedish Construction Industry's Organization for Working Environment, Safety and Health [Engholm et al. 1991] conducted a study of cancer mortality and incidence among Swedish construction workers (described earlier in section 5.2.1), who included 704 roofers. Increased mortality and/or incidence were observed among roofers for cancers of the lung (SMR=2.79, three deaths; SIR=3.62, four cases) and stomach (SMR=2.01, five deaths; SIR=1.98, one case); lymphatic and hematopoietic tumors (SMR=2.68, two deaths); and leukemia (SIR=2.26, one case).

As noted, these findings were all based on a relatively small number of cases and are therefore statistically unstable. After controlling for smoking, an OR of 6, based on three cases, was derived for lung cancer among roofers in a nested case-control analysis of incidents.

Hrubec et al. [1992] Hrubec et al. [1992] conducted a mortality study of approximately 300,000 veterans who served in the U.S. Armed Forces between 1917 and 1940. Information on occupation, industry of employment, and smoking history was obtained from a questionnaire mailed to veterans in 1954 and a follow-up questionnaire mailed to nonrespondents in 1957. The 284,046 respondents to this questionnaire were followed for vital status ascertainment as of 1980. Poisson regression models were used to estimate rate ratios for each occupation and industry while controlling for smoking habits. An elevated risk of respiratory cancer was observed among the job category "roofers and slaters" (rate ratio=3.0; 90% CI=1.30-6.75).

One strength of this study is that the analyses were adjusted for smoking. Weaknesses are that information on work histories was obtained at one point in time only and that it was obtained from a self-administered questionnaire.

Pukkala [1995] Pukkala [1995] reported findings from a study in which the entire 1970 population of Finland was followed from 1971 to 1985 to track cancer incidence. An analysis of the relationship between cancer incidence and occupation was performed among individuals between the ages of 25 to 64 in 1970. The analysis controlled for possible confounding by social class, age, and calendar time; smoking was not considered in the analysis. The SIR for cancers of the lung, bronchus, and trachea among men coded as "asphalt roofers" in the 1970 census was 3.25 (95% CI=1.92-5.13).

Milham [1997] In Washington State, 1,057 deaths among male residents classified as “roofers and slaters” were recorded for the years 1950 through 1989 [Milham 1997]. For this occupational classification, statistically significant (P<0.01) PMRs were observed for cancers of the respiratory system (PMR=1.53, based on 105 deaths); larynx (PMR=2.59, based on six deaths, P<0.05); and bronchus, trachea, and lungs (PMR=1.44, based on 86 deaths); as well as asthma (PMR=2.86, based on seven deaths); emphysema without bronchitis (PMR=1.63, based on 28 deaths); and cirrhosis of the liver with alcoholism (PMR=1.49, based on 17 deaths). Of note is that PMRs from these causes were elevated despite a significant increase in deaths from falls from heights (PMR=4.00, based on 17 deaths). Not statistically significant increased PMRs were noted for cancers of the buccal cavity and pharynx (PMR=1.67, based on nine deaths), diseases of the respiratory system, chronic bronchitis with and without emphysema, cirrhosis of the liver without alcoholism, and psychosis. In contrast, mortality from diseases of the circulatory system was statistically significantly decreased (PMR=0.88, based on 364 deaths).

The results of this study are limited by the interdependence of cause-specific PMRs, the accuracy of the "Usual Occupation" field on death certificates, and lack of detailed information on exposures and confounders, particularly smoking.

5.2.2.2 Case-Control Studies

Three case-control studies examined the relationship between lung cancer and occupation as a roofer [Zahm et al. 1989] or as a roofer and slater [Schoenberg et al. 1987; Morabia et al. 1992]. Each of the studies included only histologically confirmed lung cancer cases among males. All studies adjusted the risk measures for smoking and found elevated ORs that were not statistically significant. Only Zahm et al. evaluated roofers as a separate occupation, while Morabia et al. and Schoenberg et al. analyzed roofers and slaters as a single occupational group. Inclusion of slaters in these analyses could dilute the effects of relationships between exposure to asphalt roofing products and lung cancer.

In the study by Zahm et al. [1989], six cases and seven controls were coded as roofers (Bureau of the Census code 595). There was a twofold increase in lung cancer among roofers that was not statistically significant (OR=2.1; 95% CI=0.6-8.2).

Schoenberg et al. [1987] conducted a hospital-based study of 763 lung cancer cases and 900 controls among white males in New Jersey. New cases diagnosed between September 1980 and October 1981 and reported to the New Jersey State Department of Health were included in the study. Occupational history was obtained by interviewing the patient or the patient’s next-of-kin. Thirteen cases and 8 controls were identified as roofers or slaters. The OR was not statistically significant, although it was greater than 1 (OR=1.7; 95% CI=0.7-4.4).

Morabia et al. [1992] interviewed 1,793 cases and 3,228 controls (one cancer control and one noncancer control per case), matched for age, race, geographical area, questionnaire version, and history of smoking, from 24 hospitals in nine metropolitan areas in the United States between 1980 and 1989. Seven cases and six controls were identified as roofers and slaters. The ORs for roofers and slaters were not statistically significant (OR=2.1; 95% CI=0.7-6.2). Neither Morabia et al. nor Schoenberg et al. identified the number of individuals who were exposed to hot asphalt roofing products. Indeed, it is not clear that either the cases or the controls had significant occupational exposure.

5.2.3 Meta-analysis of Asphalt Workers and Roofers

Partanen and Boffetta [1994] Partanen and Boffetta [1994] conducted a comprehensive review and meta-analysis of 20 epidemiologic studies of asphalt workers and roofers. The “most relevant” relative risk (RR) estimates (OR, SMR or SIR) were extracted from the reports for the meta-analysis. The authors defined the most relevant RR estimates to be those that (1) best approximated exposure to asphalt, (2) were adjusted to the extent possible for potential confounders, and (3) used an appropriate induction-latency period. Summary RRs were estimated from the individual study findings for (1) all asphalt workers and roofers, (2) road pavers and highway maintenance workers, (3) roofers, and (4) "miscellaneous or unspecified" asphalt and bitumen workers. The summary RR for lung cancer was increased among roofers (RR=1.78; 95% CI=1.50-2.10) and miscellaneous or unspecified workers (RR=1.49; 95% CI=1.22-1.80), but not among pavers and highway maintenance workers (RR=0.9; 95% CI=0.8-1.0). Statistically significant increased RRs were also observed for stomach cancer among roofers (RR=1.7; 95% CI=1.1-2.5) and for nonmelanotic skin cancer among pavers and highway maintenance workers (RR=2.2; 95% CI=1.2-3.7). Similar results for lung cancer were found when the analysis was restricted to studies that controlled for cigarette smoking. The authors appropriately suggest that the available studies (and hence their meta-analysis) were "poorly focused" to address the question of whether asphalt exposure is carcinogenic because of numerous limitations in the design of these studies, many of which are discussed in previous sections.

5.2.4 Other Studies of Asphalt Exposure
5.2.4.1 Cohort Studies

Hansen [1989b] In a retrospective cohort mortality study, Hansen [1989b] compared the mortality rates of 1,320 Danish workers employed in the asphalt industry at asphalt plants, roofing felt plants, and one tar plant with those of 43,024 unskilled Danish employees employed in other industries. The cohort was selected from the November 9, 1970, Danish census conducted bythe Danish National Bureau of Statistics and was traced until November 9, 1980. There were 113 deaths among the 1,320 asphalt employees and 3,811 deaths among the 43,024 unskilled employees.

During the last 5 years of the 10-year follow-up study, asphalt employees aged 45 or older had a statistically significant SMR for all malignant neoplasms (SMR=1.59; 95% CI=1.06-2.28) and brain cancers (SMR=5.00; 95% CI=1.03-14.61) and elevated SMRs for digestive cancer (SMR=1.57; 95% CI=0.583.43), respiratory cancer (SMR=1.52; 95% CI=0.76-2.71), and bladder cancer (SMR=2.91; 95% CI=0.60-8.51). Limitations of the study include lack of information about the length of employment in the asphalt industry and the extent of exposure.

5.2.4.2 Case-Control Studies

Three case-control studies [Mommsen et al. 1983; Risch et al. 1988; Bonassi et al. 1989] examined the relationship between bladder cancer and a variety of occupational exposures, including exposures to asphalt. Broad categories of jobs or industries were included that were not specific to asphalt, limiting the use of these studies in assessing risks of asphalt exposures.

Mommsen et al. [1983] Mommsen et al. [1983] reported findings of a study of 212 bladder cancer cases (165 men and 47 women) admitted to the Department of Oncology and Radiotherapy in Aarhas, Denmark. Information on male cases was collected from 1977 to 1979 and on female cases from 1977 to 1980. The 259 controls were matched for age, sex, geographic area, and degree of urbanization. Information on smoking and occupational history was also collected from each studyparticipant by questionnaire. An approximately 2½-fold increase in risk of bladder cancer was reported for occupational exposure to "petroleum or asphalt."

Risch et al. [1988] Risch et al. [1988] studied 781 controls and 739 patients with bladder cancer diagnosed between 1979 and 1982 in Edmonton and Calgary, AB, and Toronto and Kingston, ON, Canada. Information on occupation, tobacco use, and other factors likely to be related to bladder cancer was collected during interviews. Histologic verification of all tumors was obtained. However, only 67% of the eligible cases and 53% of the eligible controls participated in the study. A statistically significant association (OR=3.11; 95% CI=1.19-9.68) was observed among workers exposed to "tar and asphalts" during a full-time job of at least 6 months duration and at least 8 years of latency.

Bonassi et al. [1989] Bonassi et al. [1989] examined the relationship between bladder cancer and potential lifetime occupational exposure to PAHs in 121 cases and 342 controls. Cases were histologically confirmed, and smoking history was obtained. Eleven occupational categories were selected on the basis of their potential for exposing workers to PAHs, and subjects were classified into these categories if they had worked in one for a year or more. A statistically nonsignificant association (OR=1.4; 95% CI=0.27-7.28) was observed between bladder cancer and employment as a "road mender" based on two cases and six controls.

Jensen et al. [1988] Jensen et al. [1988] investigated the relationship between occupational exposure and incidence of renal pelvis and ureter cancer among Danish residents. Occupational history and demographic data were obtained by interviewing 96 cases and 294 hospital controls; cases and controls were matched by age (within 5 years), hospital, and sex. Of the male study subjects, nine cases and six controls reported exposure to asphalt or tar. Smoking-adjusted RRs for exposure to asphalt or tar were statistically significantly elevated (RR=5.5; 95% CI=1.6-19.6).

Vineis et al. [1988] One case-control study evaluated the relationship between lung cancer and occupation or occupational exposure to well-known and suspected lung carcinogens. Vineis et al. [1988] combined 2,973 male cases and 3,210 controls from five studies conducted throughout the United States and adjusted them for age, birth cohort, and cigarette use. Forty-five cases and 37 controls were classified into the category of “roofers and asphalt workers.” Risk of lung cancer for the combined group of “roofers and asphalt workers” was not statistically significant [OR=1.4; 95% CI=0.9-2.3)].

Chiazze et al. [1993] Chiazze et al. [1993] conducted a case-control study of malignant and nonmalignant respiratory disease in workers employed in a fiberglass insulation production facility. The maximum number available for a matched analysis of interview data was 144 lung cancer cases with 260 controls and 101 nonmalignant respiratory disease cases with 183 controls. Quantitative estimates of lifetime exposure to asbestos, talc, asphalt fumes, formaldehyde, and silica were calculated. Asphalt exposure was dichotomized in "never-exposed" versus “exposures $0.01-mg/m3" days. ORs were calculated using conditional logistic regression adjusted for age, smoking, and occupational exposure to respirable fibers, asbestos, talc, formaldehyde, silica, and total particulates. Asphalt exposure was not related to either lung cancer (OR=0.96; 95% CI=0.65-1.4) or nonmalignant respiratory disease (OR=1.3; 95% CI=0.82-2.2) for workers in the higher exposure group.

Siemiatycki [1991] Siemiatycki [1991] obtained occupational history and exposure information from interviews with 3,730 hospital-based cancer cases and 533 population-based controls residing in the province of Quebec, Canada. ORs were calculated for 23 cancer sites adjusted for confounding variables, including smoking. Statistically significant increased ORs for any exposure to asphalt were observed for colon cancer (OR=1.6; 95% CI=1.1-2.5, based on 22 cases), while ORs for cancers of the esophagus, stomach, pancreas, lungs, prostate, and non-Hodgkins lymphoma were approximately 1 and not statistically significant.

Austin et al. [1987] Austin et al. [1987] conducted a hospital-based case-control study to examine the role of occupation and other factors in the etiology of hepatocellular carcinoma. Cases and controls were patients at one of five participating hospitals. Each case was matched to two controls by age, sex, race, and study hospital. Occupational or recreational exposures to 26 substances, including asphalt, were obtained from each of the 80 cases and 146 matched controls. Seven cases and five controls reported exposure to asphalt for at least 3 hr/wk for at least 6 months at some time during their lives (RR=3.2; 95% CI=0.9-11). Of these cases and controls, one case and one control had worked for more than 10 years in road building, and one other case had worked as a laborer in an asphalt manufacturing company.

5.2.5 Conclusions
5.2.5.1 Lung Cancer among Pavers

Epidemiologic studies of lung cancer among pavers exposed to asphalt fumes have yielded contradictory results. That is, while some studies have reported an elevated risk of lung cancer, design limitations of these studies preclude drawing any strong conclusions [Hansen 1989a; Engholm et al. 1991; Partanen et al. 1997; Milham 1997]. Of particular concern is the possibility of confounding from coexposures to coal tar and other potential lung carcinogens (e.g., diesel exhaust, silica, and asbestos) [Hansen 1989a]. Failure to control adequately for smoking is also an issue in several studies [Engholm et al. 1991; Milham 1997]. Several studies of pavers or highway workers have failed to demonstrate an excess of lung cancer [Maizlish et al. 1988; Bender et al. 1989]. A meta-analysis of all these studies failed to find overall evidence for a lung cancer risk among pavers exposed to asphalt [Partanen and Bofetta 1994]. Hence, the epidemiologic evidence for an association between lung cancer and exposure to asphalt in paving is inconclusive at this time.

5.2.5.2 Lung Cancer among Roofers

In contrast to pavers, epidemiologic studies of roofers have generally demonstrated an excess number of lung cancer cases [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]. The metaanalysis by Partanen and Boffetta [1994] has also revealed an overall excess of lung cancer among roofers. However, it is uncertain to what extent these findings may be attributable to asphalt exposures. In the past, roofers have been exposed to coal tar and asbestos, which are known human lung carcinogens, as well as asphalt. Hence, while strong epidemiologic evidence of an association between lung cancer and working as a roofer exists, it is uncertain whether asphalt or other substances are responsible for these findings.

5.2.5.3 Cancers at Other Sites

A few studies have reported an association between cancers at sites other than lungs and occupations having the potential for exposures to asphalt [Mommsen et al. 1983; Risch et al. 1988; Bonassi et al. 1989; Jensen et al. 1988]. Of particular interest is an association reported in several case-control studies between bladder and renal cancers and occupations having exposures to asphalt. Isolated studies have reported associations between occupations with asphalt exposure and cancers of the brain, liver, and other digestive organs [Hansen 1989b; Austin et al. 1987; Siemiatycki 1991]. Interpretation of the findings of these studies is limited by a lack of consistency among studies and issues of the confounding effects of other substances. Furthermore, many of these findings are from population-based, case-control studies organized by broad job classifications that are prone to errors in defining asphalt exposures [Mommsen et al. 1983; Risch et al. 1988; Bonassi et al. 1989; Jensen et al. 1988; Siemiatycki 1991]. Thus, the evidence for an association between exposure to asphalt and nonrespiratory cancers is weak and requires further confirmation by studies with better control of confounding variables and better identification of asphalt exposures.

 

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Exposure
Experimental Studies