Asphalt Fumes Research Articles

Asphalt Fume Exposure Levels in North American Asphalt Production and Roofing Manufacturing Operations

This study extends by 8 years (1998–2005) a previous survey of asphalt fume exposures within North American asphalt processing and roofing product manufacturing workers. It focuses on characterizing personal, full-shift samples and seeks to address several limitations of the previous survey. Five major roofing manufacturers with established occupational health programs submitted workplace asphalt fume sampling results to a central repository for review and analysis. A certified industrial hygienist-led quality assurance team oversaw the data collection, consolidation, and analysis efforts. The analysis dataset consisted of 1261 personal exposure samples analyzed for total particulate (TP) and benzene soluble fraction (BSF) using existing NIOSH methods. For BSF, the survey's arithmetic (0.25 mg/m3, SD = 0.62) and geometric (0.12 mg/m3, GSD = 2.88) means indicate that the industry has sustained the control levels achieved in the late 1980s, early 1990s. Similar results were found for TP. The survey-wide summary statistics are consistent with other post-1990 multi-company exposure studies. Although these findings indicate that currently available controls are capable of achieving substantial (95%) compliance with the current threshold limit value in asphalt processing and inorganic shingle and roll plants, they also show that the majority of plants are not achieving this level of exposure control, and that exposures are significantly higher in plants making other product lines, particularly organic felt products. The current retrospective survey of existing company exposure data, like its predecessor, has several important limitations. These include lack of data on smaller manufacturers and on several commercially important product lines; insufficient information on the prevalence and effectiveness of engineering controls; no standard criteria by which to define and assess exposures in non-routine operations; and a paucity of exposure data collected as part of a random sampling strategy. To improve efforts to characterize exposures and potential health risks in roofing plants, a prospective program is currently being developed and piloted with the aim of building a more complete, higher-quality database based on a common industrial hygiene protocol.

Polycyclic Aromatic Hydrocarbons: Role of Apoptosis in Dermatotoxic and Carcinogenic Effect in Asphalt Road Paving Workers

Asphalt contains a complex mixture of polycyclic aromatic hydrocarbons (PAHs). This work aimed firstly to assess the dermatotoxic and carcinogenic risk associated with chronic PAHs exposure, and secondly to investigate the causal relationship between PAHs exposure and cancer through studying the effect of PAHs on apoptosis. This effect was studied by examining the expression pattern of P53, Bax and Bcl-2 apoptotic proteins in skin specimens from road paving workers. The study was conducted on one hundred and fifty two male subjects classified into 122 asphalt fumes exposed workers (tested group) and 30 non exposed workers (control group); careful skin examination and skin biopsies were obtained from all participants after written consent. Biopsies were examined histopathologically and immunohistochemically. SPSS version 15.0 was used for statistical analysis. Results showed that 71 (58.19%) PAHs exposed workers had erythema, itching, excoriations, chronic dermatitis, chemical keratosis, keratoacanthoma (KA) and nine (7.38%) exposed workers had squamous cell carcinoma (SCC). Imunohistochemically, wild type P53 was significantly higher in epidermal keratinocytes of PAHs exposed normal uninvolved (non lesional) skin (t=0.51, P=0.04) and mutant type P53 was significantly higher in SCC cases (t=4.79, p=0.003) when compared with control. A significant increase in Bax expression was observed in all asphalt exposed workers when compared with the control (t=2.73, P=0.03). A significant decrease in Bcl-2 expression was noted in PAHs exposed un-involved skin (t=2.49, P=0.047) while none of the 9 tested SCC cases were positive for Bcl-2. It could be concluded that chronic exposure to PAHs fumes in asphalt workers may increase the risk for developing dermatotoxic and/ or cancer through disturbing apoptosis. Although PAHs exposure can disturb P53, Bax and Bcl-2 apoptotic protein, more extensive researches on other factors involved in controlling apoptosis as Bcl-xl, Caspase family and Fas are to be undertaken.

The Experimental Study on the Road Asphalt Fumes Inhibitors

In order to reduce the road asphalt fumes in the process of construction, the paper proposed to add some substances in asphalt to reduce the yield of asphalt fumes. Firstly, considering the theory of how the asphalt fumes come into being in the process of construction on the pavement, six possible additives to restrain these fumes havd been screened out. And tests of fumes suppression effect had been done to get the results that: SBS has a good effect of fumes suppression. When added by 3%, the asphalt fumes reduced by the rate of 19.2%; PE has an suppressive effect on asphalt fumes. When added by 3%, the asphalt fumes reduced by the rate of 6.5%; Melamine has a good effect of fumes suppression. When added by 3%, the asphalt fumes reduced by the rate of 45.1%; Ammonium molybdophosphate has an abnormal effect of fumes suppression. When added by 1%, the asphalt fumes not only did not reduce but increases. When added by 3%, the asphalt fumes reduced by the rate of 23.3%; nanoCalcium carbonate has an effect of fumes suppression. When added by 3%, the asphalt fumes reduced by the rate of 4.8%; Activated Carbon has a good effect of fumes suppression. When added by 3%, the asphalt fumes reduced by the rate of 41.6%.

Quantitative exposure matrix for asphalt fume, total particulate matter, and respirable crystalline silica among roofing and asphalt manufacturing workers

This paper summarizes available data on worker exposures to asphalt fume (soluble fraction), total particulate matter, and respirable crystalline silica (quartz) [hereinafter RCS] over a 30-year period in Owens Corning’s asphalt production and roofing manufacturing plants. For the period 1977 through 2006, the air-monitoring database contains more than 1,400 personal samples for asphalt fume (soluble fraction), 2,400 personal samples for total particulate, and 1,300 personal samples for RCS. Unique process-job categories were identified for the asphalt production and roofing shingle manufacturing plants. Quantitative exposures were tabulated by agent, process-job, and calendar period to form an exposure matrix for use in subsequent epidemiologic studies of the respiratory health of these workers. Analysis of time trends in exposure data shows substantial and statistically significant exposure reductions for asphalt fume (soluble fraction), total particulate matter, and respirable crystalline silica at Owens Corning plants. Cumulative distribution plots for the most recent sampling period (2001–2006) show that 95% of the asphalt fume (soluble fraction) measurements were less than 0.25 mg/m3; 95% of the total particulate measurements were less than 2.2 mg/m3; and 95% of the RCS measurements were less than 0.05 mg/m3. Several recommendations are offered to improve the design of future monitoring efforts.

Asphalt fume dermal carcinogenicity potential: II. Initiation–promotion assay of Type III built-up roofing asphalt

Clark et al. (accepted for publication) reported that a sample of field-matched fume condensate from a Type III built-up roofing asphalt (BURA) resulted in a carcinogenic response in a mouse skin bioassay, with relatively few tumor-bearing animals, long tumor latency and chronic skin irritation. This mouse skin initiation/promotion study was conducted to assess possible mechanisms, i.e., genotoxic initiation vs. tumor promotion subsequent to repeated skin injury and repair. The same Type III BURA fume condensate sample was evaluated in groups of 30 male Crl:CD1® mice by skin application twice per week (total dose of 50 mg/week) for 2 weeks during the initiation phase and for 26 weeks during the promotion phase. Positive control substances were 7,12-dimethylbenz(a)anthracene (DMBA, 50 μg applied once) as an initiator and 12-O-tetradecanoyl-13-acetate (TPA, 5 μg, applied twice weekly) during the promotion phase. During the 6 months of study with the asphalt fume condensate, eight skin masses were observed when tested for initiation, five of which were confirmed microscopically to be benign squamous cell papillomas. Only two papillomas were observed when tested for promotion. There was no apparent relationship between skin irritation and tumor development in this study. These results are more indicative of genotoxicity rather than a non-genotoxic mode of action.

The Experimental Study on the Road Asphalt Fumes Suppressive Effect of SBS and Nano Calcium Carbonate

In order to study the fume suppressive effect of SBS and nano calcium carbonate， this paper studied the fume suppression laws of SBS and nano calcium carbonate， and carried out ratio test of SBS and nano calcium carbonate, and got the conclusions that: With the increasing adding level of SBS and nano calcium carbonate, the asphalt fume productive rate will reduce gradually and will reach a condition of stability. The adding level of 4% of SBS is a turning point. When less than 4%, the asphalt fume production rate decreased rapidly; and more than 4%, the asphalt fume production rate decreased slowly; when adding nano calcium carbonate at the level of 5%, the asphalt fume won’t decrease. The best ratio of SBS and nano calcium carbonate is 6% of SBS and 6% of nano calcium carbonate, with which asphalt fume reductive rate was up to 30%.

Asphalt fume dermal carcinogenicity potential: I. dermal carcinogenicity evaluation of asphalt (bitumen) fume condensates

Asphalt (bitumen) fume condensates collected from the headspace above paving and Type III built up roofing asphalt (BURA) tanks were evaluated in two-year dermal carcinogenicity assays in male C3H/HeNCrl mice. A third sample was generated from the BURA using a NIOSH laboratory generation method. Similar to earlier NIOSH studies, the BURA fume condensates were applied dermally in mineral oil twice per week; the paving sample was applied 7 days/week for a total weekly dose of 50 mg/wk in both studies. A single benign papilloma was observed in a group of 80 mice exposed to paving fume condensate at the end of the two-year study and only mild skin irritation was observed. The lab generated BURA fume condensate resulted in statistically significant ( P < 0.0001) increases in squamous cell carcinomas (35 animals or 55% of animals at risk). The field-matched BURA condensate showed a weaker but significant ( P = 0.0063) increase (8 carcinomas or 13% of animals) and a longer average latency (90 weeks vs. 76 for the lab fume). Significant irritation was observed in both BURA condensates. It is concluded that the paving fume condensate was not carcinogenic under the test conditions and that the field-matched BURA fume condensate produced a weak tumor response compared to the lab generated sample.

Evaluation of reproductive/developmental and repeated dose (subchronic) toxicity and cytogenetic effects in rats of a roofing asphalt fume condensate by nose-only inhalation

A Type III Built-up Roofing Asphalt (BURA) fume condensate was evaluated for subchronic systemic toxicity and reproductive/developmental toxicity screening in Wistar rats, by OECD protocol 422 and OECD cytogenetic protocol 474. Animals were exposed by nose-only inhalation to target concentrations of 30, 100 and 300mg/m3 total hydrocarbons (actual concentrations, 30.0, 100.1 and 297.3mg/m3). The study was performed to assess potential hazards from asphalt fumes to which humans could be exposed during application. No adverse effects were seen for spermology, reproductive or developmental parameters or early postnatal development of offspring from day 1 to 4 postpartum. BURA fume condensate did not induce any significant increases in micronucleus frequency in polychromatic erythrocytes of rat bone marrow nor was neurobehavioral toxicity observed at any dose. Systemic effects were slight and seen at doses above those measured at work sites. The systemic NOAEC of 100mg/m3 for males was based on decreased body weight gain, food consumption and increased absolute and relative lung wet weight correlated with slight histological changes in the lung, primarily adaptive in nature at 300mg/m3. The female NOAEC of 30mg/m3 was based on a statistically significant increase in relative wet lung weight at higher doses, correlated with slight histopathologic effects in the lungs at the highest dose. However, no increase in relative lung weight was seen in breeding females at 100mg/m3.

Review of mechanistic studies relevant to the potential carcinogenicity of asphalts

Heating of asphalts to facilitate use in paving and roofing applications produces fumes containing polycyclic aromatic compounds (PAC). Regulatory organizations have suggested asphalt fumes of concern to humans due to possible carcinogenic effects but data are inadequate to classify. Two-year rodent inhalation studies and recent European epidemiology research have shown that asphalt fume alone does not pose a carcinogenic risk to humans. Dermal exposure to asphalt fume condensate have produced skin tumors in mouse skin painting studies but no skin cancer studies in humans have been reported occupationally. Mechanistic research explores underlying processes to assess relevance of findings in animals to humans. DNA adducts are useful as biological dosimeters of exposure, but DNA repair processes, lack of correlation with more definitive genotoxic and cancer results in animals and humans limits reliability as a predictor of carcinogenic hazard. Inhibition of gap junction intercellular communication and stimulation of intracellular signaling by asphalt fume condensate can relate to tumor development. Up and down-regulation of expression in genes involved in the metabolism and action of asphalt fume demonstrates intrinsic activity at the cellular level but changes were inconsistent. The relationship of reported effects on the immune system to carcinogenesis is unclear. Overall, results of mechanistic studies provide insights into biological activity from asphalt fume exposure but compositional differences, level of human exposure and detoxification processes must be considered in translating these findings to cancer risk.

Critical Review on Evaporative Loss of Semivolatile Aerosols during Sampling

Semivolatile aerosols exist as vapor and particles at the same time in room temperature and each phase has different intake and uptake mechanisms. This characteristic requires substantial consideration during exposure assessment of semivolatile aerosol. Some sampling methods for solid particles pose high possibility of evaporative loss during sampling. Therefore, when establishing sampling strategy for them, the factors affecting the phase distribution of semivolatile aerosol should be counted including semivolatile aerosol of interest and sampling methods used. Evaluation for phase distributions of semivolatile aerosols is also recommended. Metalworking fluids, pesticides, asphalt fumes, diesel exhaust, and environmental tobacco smoke are common health-related semivolatile aerosols in workplaces.

A Study On Addictives For Fume Reduction In Asphalt Pavement Construction

Abstract In the construction process, asphalt pavement will generate a lot of asphalt fumes, which contain a large number of toxic and hazardous substances that will produce injury to the construction workers and residence around. In order to radically reduce asphalt fumes in the construction process, through self-designed test equipment, we added SBS (Styrene Butadiene Styrene), melamine and activated carbon which may have fumes suppression effect to the asphalt and experimented, obtained: (1) SBS which had fumes suppression effect, could be used as an additive to reduce asphalt fumes; (2) Melamine and activated carbon, which would produced a number of side effects, could not be used as an additive to reduce asphalt fume. At present the research of modified asphalt which produces lower fumes is basically still in a blank state, but the paper will fill the gaps in this aspect and provide a test device and method to study on modified asphalt with low fumes.

Fume Suppression Agents For Environmental-Friendly Asphalt Pavement

Abstract According to the impact of fumes generated by asphalt pavement construction under poor air ventilation conditions on environrnent and operators at pavement construction and mechanism of asphalt fumes generation this article provides the method of addition of addictives in asphalt to suppress fumes due to asphalt pavement construction. Through in house test the variation law of asphalt fames with heating temperature and heating time. The result shows that with an increase of heating time, the yield of asphalt fumes appears increasing tendency. During the initial stage, the smoke yielding rate is fast; in later stage the vaziation slows down; and finally the variation becomes stable. With higher heating temperature, the yield of asphalt fumes is greater. Paztial addictives aze selected for smoke suppression effect test from flame retardant agent, plastic smoke suppression agent, physical adsorbent, polymer modified agent and aging resistant agent. SBS and manometer calcium carbonate compound type m...

Evaluation of indoor air quality by odor units (odor threshold ratio)

Buccal micronucleus cytome (BMCyt) assay monitors genetic damage, cell proliferation and cell death in humans exposed to occupational and environmental agents. BMCyt is used as an indicator of genotoxic exposure, since it is associated with chromosomal instability. There is little research on the occupational exposure among road construction workers for genotoxicity testing. In the present study, we evaluated MN frequencies and other nuclear changes, karyorrhexis (KR), karyolysis (KL), broken egg (BE), binucleate (BN), condensed chromatin cell (CCC), and picnotic cell (PC) in buccal mucosa cells of 40 road construction workers (twenty smokers and twenty non-smokers) and 40 control groups consisting of healthy persons (twenty smokers and twenty non-smokers). Microscopic observation was performed of 2000 cells per individual in both road construction workers and control group. In control and worker groups, for each person repair index (RI) was calculated via formula KR+L/BE+MN. The results showed a statistically significant increase in the frequency of MN in buccal epithelial cells of exposed group compared with control group (p<0.001). There is no significant difference between smokers and non-smokers for incidence of MN or nuclear changes and value of RI in exposed group. In road construction workers, RI is lower than the control group. There is a significant difference between workers and control group (p<0.001) for RI. Our data reveal that asphalt fumes during road paving operations are absorbed by workers and that asphalt fume exposure is able to significantly induce cytogenetic damage in buccal mucosa cells of workers after controlling some possible confounding factors, such as age, sex and smoking habits.In addition to determination of nuclear changes and the micronucleus, the determination of RI value presents a new approach to genotoxic bio-monitoring assessment studies of occupationally exposed population.

MONITORING POLYCYCLIC AROMATIC COMPOUNDS IN ENVIRONMENTAL AND WORKPLACE SAMPLES USING CONVENTIONAL METHODS AND THE AMES MUTAGENICITY ASSAY OF THEIR NITRATED DERIVATIVES

The development of sensitive methods for monitoring polycyclic aromatic compounds (PACs) has been a central focus of industrial hygiene studies in those industries where workers are exposed to petroleum oils, bitumen fumes or fuel combustion products. The work reported here focuses on one aspect of that effort—workplace monitoring of airborne PAC levels in the hot-mix asphalt paving industry. During the manufacture, transport, and roadway application of hot-mix asphalt (HMA), workers are exposed to low levels of bitumen fumes emanating from the hot product. Over the last twenty-five years, concerns about the health effects of these exposures have prompted numerous studies of the airborne levels of asphalt fumes in the workplace. By and large, these studies have shown that PAC exposures are extremely low—often below the detection limits of standard analytical techniques. For the present study, we have used standard industrial hygiene methods, together with a newer, biologically based assay called the Nitration Assay to measure relative ambient levels of fumes and/or PACs in various paving workplace settings. The latter assay was also used to test bitumen fumes generated in the laboratory by a new “microfuming” technique and to determine specific activities of the 16 PAHs designated by the US EPA as priority pollutants. The Nitration Assay takes advantage of two properties of 3–7-ring PACs: the ease with which they can be chemically nitrated and the high mutagenic potency of the nitrated products in the Ames Salmonella mutagenicity assay. Measurements of fumes and nitratable PAC levels on seven different hot-mix paving jobs showed reasonable correlations between the various methods, as well as patterns of exposure consistent with proximity to fume source.

Exposure to Ultrafine Particles in Asphalt Work

An epidemiologic study has demonstrated that asphalt workers show increased loss of lung function and an increase of biomarkers of inflammation over the asphalt paving season. The aim of this study was to investigate which possible agent(s) causes the inflammatory reaction, with emphasis on ultrafine particles. The workers' exposure to total dust, polycyclic aromatic hydrocarbons, and NO 2 was determined by personal sampling. Exposure to ultrafine particles was measured by means of particle counters and scanning mobility particle sizer mounted on a van following the paving machine. The fractions of organic and elemental carbon were determined. Asphalt paving workers were exposed to ultrafine particles with medium concentration of about 3.4 × 104/cm3. Ultrafine particles at the paving site originated mainly from asphalt paving activities and traffic exhaust; most seemed to originate from asphalt fumes. Oil mist exceeded occupational limits on some occasions. Diesel particulate matter was measured as elemental carbon, which was low, around 3 μg/m3. NO2 and total dust did not exceed limits. Asphalt pavers were exposed to relatively high concentrations of ultrafine particles throughout their working day, with possible adverse health effects.

Built Environment: New Default for Asphalt?

Built Environment: New Default for Asphalt?

Genotoxic effects of fumes from asphalt modified with waste plastic and tall oil pitch

As the use of recycled materials and industrial by-products in asphalt mixtures is increasing, we investigated if recycled additives modify the genotoxicity of fumes emitted from asphalt. Fumes were generated in the laboratory at paving temperature from stone-mastic asphalt (SMA) and from SMA modified with waste plastic (90% polyethylene, 10% polypropylene) and tall oil pitch (SMA–WPT). In addition, fumes from SMA, SMA–WPT, asphalt concrete (AC), and AC modified with waste plastic and tall oil pitch (AC–WPT) were collected at paving sites. The genotoxicity of the fumes was studied by analysis of DNA damage (measured in the comet assay) and micronucleus formation in human bronchial epithelial BEAS 2B cells in vitro and by counting mutations in Salmonella typhimurium strains TA98 and YG1024. DNA damage was also assessed in buccal leukocytes from road pavers before and after working with SMA, SMA–WPT, AC, and AC–WPT. The chemical composition of the emissions was analysed by gas chromatography/mass spectrometry. The SMA–WPT fume generated in the laboratory induced a clear increase in DNA damage in BEAS 2B cells without metabolic activation. The laboratory-generated SMA fume increased the frequency of micronucleated BEAS 2B cells without metabolic activation. None of the asphalt fumes collected at the paving sites produced DNA damage with or without metabolic activation. Fumes from SMA and SMA–WPT from the paving sites increased micronucleus frequency without metabolic activation. None of the asphalt fumes studied showed mutagenic activity in Salmonella. No statistically significant differences in DNA damage in buccal leukocytes were detected between the pre- and post-shift samples collected from the road pavers. However, a positive correlation was found between DNA damage and the urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) after work shift, which suggested an association between occupational exposures during road paving and genotoxic effects. Our results indicate that fumes from SMA and SMA–WPT contain direct-acting genotoxic components.

The Humoral Immune Response of Mice Exposed to Simulated Road Paving-Like Asphalt Fumes

Asphalt is a complex mixture of organic molecules, including polycyclic aromatic hydrocarbons (PAH), which have been reported to cause serious adverse health effects in humans. Workers in manufacturing and construction trades exposed to asphalt are potentially at risk for being exposed to asphalt fumes and PAHs. Epidemiological investigations have collected mounting evidence that chemicals found in asphalt fumes present carcinogenic and possibly immunotoxic hazards. Studies evaluating the immunotoxic effects of asphalt fume are limited due to the large number of variables associated with asphalt fume exposures. This work investigates the immuno-toxic effects of road paving-like asphalt fume by analyzing the in vivo IgM response to a T-dependent antigen after exposure to whole, vapor, and particulate phase road paving-like asphalt fumes and asphalt fume condensate. Systemic exposures via intraperitoneal injection of asphalt fume condensate (at 0.625 mg/kg) and the particulate phase (at 5 mg/kg) resulted in significant reductions in the specific spleen IgM response to SRBC. Pharyngeal aspiration of the asphalt fume condensate (at 5 mg/kg) also resulted in significant suppression of the IgM response to SRBC. A significant reduction in the specific spleen IgM activity was observed after inhalation exposure to whole asphalt fumes (35 mg/m3) and the vapor components (11 mg/m3). Dermal exposures to the asphalt fume condensate resulted in significant reductions in the total (at 50 mg/kg) and specific (at 250 mg/kg) spleen IgM response to SRBC. These results demonstrate that exposure to road paving-like asphalt fumes is immunosuppressive through systemic, respiratory, and dermal routes of exposure in a murine model and raise concerns regarding the potential for adverse immunological effects.

Characterization of asphalt fume composition by GC/MS and effect of temperature

The aim of this work is to identify the volatile organic compounds (VOC) from asphalt by developing a process at atmospheric pressure under air flow in order to qualify and quantify the asphalt emissions by a standard analytical protocol with gas chromatography coupled to mass spectrometry. VOC formation depends on various parameters such as the asphalt temperature, the asphalt oxidation, and the humidity of air. This research contributes to improve knowledge of asphalt emissions. A decrease in VOC is mainly correlated with the asphalt temperature.

Ultrastructure observation for petroleum asphalt fume induced impairment of liver and kidney in mice

目的 观察石油沥青烟对小鼠肝、肾组织损伤的超微结构改变.方法 按染毒时间2、4、8周将120只小鼠雌雄各半随机分为3组,每组40只,每组再按染毒浓度的不同随机分为低浓度组(平均为41 mg/m3)、中浓度组(平均为82 mg/m3)、高浓度组(平均为165 mg/m3)和阴性对照组.取肝肾组织分别以光学显微镜和电子显微镜观察肝肾组织的形态学改变.结果 光学显微镜下染毒4、8周时各剂量组肝脏组织可见细胞核的固缩、碎裂;电子显微镜下观察,在染毒2周时高剂量组和染毒4、8周时各剂量组中肝组织和染毒4、8周时各剂量组肾组织均可见线粒体肿胀、染色质边集、核固缩等超微结构改变.结论 石油沥青烟可致小鼠肝肾组织线粒体肿胀、染色质边集、核固缩等超微结构改变。