Proportionate mortality among unionized roofers and waterproofers

Stern, Frank; Ruder, Avima M.; Chen, Guang

doi:10.1002/(sici)1097-0274(200005)37:5<478::aid-ajim4>3.0.co;2-8

Cited by 60 publications

(32 citation statements)

References 23 publications

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“…(11) CONCLUSIONS I n a recent mortality study, the authors stated the need to control airborne exposures to hazardous substances within the roofing industry. (1) The data presented here suggest that dermal exposure should be controlled as well, particularly during the removal of old coal tar pitch roofs. In the absence of coal tar pitch, asphalt-related dermal exposures were comparable to those observed among asphalt paving workers.…”

Section: Urinary 1-ohpmentioning

confidence: 84%

“…(1) Accordingly, roofers are exposed to complex mixtures of polycyclic aromatic compounds (PACs) that include unsubstituted polycyclic aromatic hydrocarbons (PAHs), substituted PAHs, and PAH heterocyclic derivatives. (2) The United States National Toxicology Program lists 15 of these compounds as reasonably anticipated to be human carcinogens (NTP, 1998), including benzo(a)pyrene (BAP).…”

Section: Introductionmentioning

confidence: 99%

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Dermal Exposure and Urinary 1-Hydroxypyrene among Asphalt Roofing Workers

McClean

Rinehart

Sapkota

et al. 2007

Journal of Occupational and Environmental Hygiene

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The primary objective of this study was to identify significant determinants of dermal exposure to polycyclic aromatic compounds (PACs) among asphalt roofing workers and use urinary 1-hydroxyprene (1-OHP) measurements to evaluate the effect of dermal exposure on total absorbed dose. The study population included 26 asphalt roofing workers who performed three primary tasks: tearing off old roofs (tear-off), putting down new roofs (put-down), and operating the kettle at ground level (kettle). During multiple consecutive work shifts (90 workerdays), dermal patch samples were collected from the underside of each worker's wrists and were analyzed for PACs, pyrene, and benzo(a)pyrene (BAP). During the same work week, urine samples were collected at pre-shift, post-shift, and bedtime each day and were analyzed for 1-OHP (205 urine samples). Linear mixed effects models were used to evaluate the dermal measurements for the purpose of identifying important determinants of exposure, and to evaluate urinary 1-OHP measurements for the purpose of identifying important determinants of total absorbed dose. Dermal exposures to PAC, pyrene, and BAP were found to vary significantly by roofing task (tear-off > put-down > kettle) and by the presence of an old coal tar pitch roof (pitch > no pitch). For each of the three analytes, the adjusted mean dermal exposures associated with tear-off (812 ng PAC/cm2, 14.9 ng pyrene/cm2, 4.5 ng BAP/cm2) were approximately four times higher than exposures associated with operating the kettle (181 ng PAC/cm2, 4.1 ng pyrene/cm2, 1.1 ng BAP/cm2). Exposure to coal tar pitch was associated with a 6-fold increase in PAC exposure (p = 0.0005), an 8-fold increase in pyrene exposure (p < 0.0001), and a 35-fold increase in BAP exposure (p < 0.0001). Similarly, urinary 1-OHP levels were found to be significantly higher on days when an old pitch roof was removed, accounting for a 3.7-fold difference at pre-shift (p = 0.01), a 5.0-fold difference at post-shift (p = 0.004), and a 7.2-fold difference at bedtime (p = 0.002). The pyrene measurements obtained during the work shift were found to be strongly correlated with urinary 1-OHP measurements obtained at the end of that shift (r = 0.8, p < 0.001) as well as at bedtime (r = 0.7, p < 0.001). Ultimately, the results of a distributed lag model indicated that dermal exposure during the preceding 40 hours had a statistically significant effect on urinary 1-OHP. The presence of coal tar pitch was the primary determinant of dermal exposure, particularly for exposure to BAP. However, the task-based differences that were observed while controlling for pitch suggest that exposure to asphalt also contributes to dermal exposures. We found that dermal exposure was a significant determinant of total absorbed dose, suggesting that control strategies aimed at reducing occupational exposure to PACs should include an effort to minimize dermal exposure.

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Section: Urinary 1-ohpmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Dermal Exposure and Urinary 1-Hydroxypyrene among Asphalt Roofing Workers

McClean

Rinehart

Sapkota

et al. 2007

Journal of Occupational and Environmental Hygiene

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“…(1−3) Several potential confounding exposures, however, prevent identification and quantification of a clear relationship due to concomitant exposure to smoke, diesel, asbestos, and coaltar. (3,4) For this reason differentiation of the true long term effects of occupational exposure to bitumen fumes from other environmental and lifestyle factors remains difficult. Notably, the molecular effects of bitumen fumes on human health are, at best, only minimally understood.…”

Section: Introductionmentioning

confidence: 99%

Importance of DNA-Adduct Formation and Gene Expression Profiling of Disease Candidate Genes in Rats Exposed to Bitumen Fumes

Halter

Hansen

Seidel

et al. 2007

Journal of Occupational and Environmental Hygiene

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The equivocal experimental and epidemiological evidence of bitumen fumes and the possible mechanisms of toxicity remain uncertain. This study therefore aimed at investigating the genotoxicity of bitumen fumes, the biotransformation and urinary excretion of PAHs, and altered expression of a selected number of genes in lung, nasal epithelium, and white blood cells of rats. Animals were exposed to three different concentrations (low: 4 mg/m 3 ; medium: 20 mg/m 3 ; high: 100 mg/m 3 ) of bitumen fume condensate for 5 days, 30 days, and 12 months (6 hours per day) or ambient air. Notably, no dose-related signs of intolerance were observed throughout the inhalation period but dose dependent uptake of bitumen fumes was observed based on urinary excretion of PAHs and metabolites. At best, measurements of naphthols enabled an estimate of dose-dependent body burden. Excretion of 1-hydroxy-and 2-hydroxyphenanthrene was dose dependent and their production is catalyzed by the CYP1A1 monooxygenase which we found to be strongly induced upon exposure to bitumen fumes. Furthermore, pyrene, a minor component in bitumen fumes, produced hydroxypyrene levels close to the detection limit in rat urine. We additionally determined DNA adduct formation by the 32 P-postlabelling assay and observed a dose and time dependent increase of 3 to 4 stable DNA adducts in lung, nasal, and alveolar epithelium. DNA adduct levels were highest in nasal epithelium, the relative adduct level (RAL) being 450 adducts per 10 9 nucleotides. For lung and alveolar epithelium the RAL was 114 and 76 adducts per 10 9 nucleotides, respectively. However, we did not observe micronucleated red blood cells of the peripheral blood or with polychromatic erythrocytes of the bone marrow (after 12 months). It is important to note that erythrocyte cell count in bone marrow smears was reduced in four out of six animals after 12 months of exposure, clearly demonstrating that components of bitumen fume had reached the bone marrow. Finally, we investigated by reverse transcription polymerase chain reaction regulation of genes with known functions in inflammation, asthma and other pulmonary diseases. Gene expression changed during the time of exposure. With the monooxygenases CYP1A1 and CYP2G1 we observed dose dependent regulation in nasal and lung tissue. We also observed significant, but dose independent, regulation of cathepsin K and D, cadherin 22, platelet activating factor acetylhydrolase isoform 1b alpha subunit and the regulator of G-protein signalling in nasal epithelium of male rats after exposure to bitumen fumes. We found bitumen fumes to be genotoxic in target tissue of exposure and observed altered regulation of genes involved in the metabolic activation of polycyclic aromatic hydrocarbons and cellular inflammatory processes. These findings are consistent with the histopathology observed in the respiratory tract of rats chronically exposed to bitumen fume. An understanding of the regulation of suspected disease candidate genes in target tissues of exposure will be a...

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“…(2) Three commercially popular roofing products or systems are asphalt shingles and roll roofing, built-up roofing (BUR) systems, and modified bitumen systems. (3) A more detailed description of the roofing industry and materials used is provided elsewhere.…”

Section: Introductionmentioning

confidence: 99%

An Assessment of the Possible Extent of Confounding in Epidemiological Studies of Lung Cancer Risk Among Roofers

Mundt

Wijngaarden

Mundt

2007

Journal of Occupational and Environmental Hygiene

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industry employs about 200,000 workers and estimates indicate about 50,000 on-roof workers are exposed to asphalt fumes during approximately 40% of their working hours. Numerous epidemiological studies have been conducted to evaluate cancer outcomes among roofers, including exposure to asphalt/bitumen fume. However, most studies relied on job title as a surrogate for exposure to asphalt or asphalt fumes because individual exposure data were not available. Therefore, it is unclear whether reported results of an increased risk of lung cancer reflect the direct impact of asphalt exposure on employee health, or if findings are due to bias, such as the presence of other risk factors for lung cancer (i.e., "confounding" exposures) or the use of comparison populations that are inherently different with respect to lung cancer risk. We evaluated the likelihood and extent to which the observed increased risk of lung cancer may be due to confounding (a mixing of effects of multiple exposures) by co-exposure to other potential carcinogens present in roofing or to lifestyle variables. We conducted a review of the epidemiological and industrial hygiene literature of asphalt-exposed workers. Peer-reviewed epidemiological studies of asphalt fumes, related occupational exposures, and confounding factors were identified from MEDLINE (1966-early 2004). Industrial hygiene studies of asphalt workers were identified through MEDLINE, publicly available government documents, and asphalt industry documents. Using wellestablished statistical methods, we quantified the extent to which lung cancer relative risk estimates among roofers reflect confounding from other exposures, using different prevalence and risk scenarios. The relative risk of lung cancer varied from 1.2 to 5.0 in 13 epidemiological studies of roofers; most studies reported a relative risk between 1.2 and 1.4. Smoking, asbestos and coal tar were the most likely confounders, but the prevalence of these factors varied over time. For example, smoking prevalence declined more steadily in the general population than among roofers, and coal tar and asbestos exposures among roofers have declined over the past 50 years. Depending on prevalence estimates used, the relative risk due to confounding ranged from 1.17 to 1.52 (current smoking); 1.36 to 1.78 (asbestos); and 1.04 to 2.32 (coal tar). The results of the study indicate that much of the observed risk reported in epidemiological studies of cancer among roofers is well within the range of what may have resulted from confounding by reasonable and expected levels of smoking, asbestos or coal tar. This may be particularly true for those studies that did not adjust for these confounders and where the exposure was defined as employment in the roofing industry. In addition to poorly defined asphalt exposure, uncontrolled confounding cannot reliably be ruled out in studies of lung cancer among asphalt-exposed roofers. Therefore, it is not possible to conclude whether roofers are at increased risk of lung cancer due to asphalt exposure....

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Proportionate mortality among unionized roofers and waterproofers

Cited by 60 publications

References 23 publications

Dermal Exposure and Urinary 1-Hydroxypyrene among Asphalt Roofing Workers

Dermal Exposure and Urinary 1-Hydroxypyrene among Asphalt Roofing Workers

Importance of DNA-Adduct Formation and Gene Expression Profiling of Disease Candidate Genes in Rats Exposed to Bitumen Fumes

An Assessment of the Possible Extent of Confounding in Epidemiological Studies of Lung Cancer Risk Among Roofers

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