Exposure to flame retardants in electronics recycling sites.

Waste electrical and electronic equipment (WEEE) contains various hazardous substances such as flame retardants (FRs). Inhalation exposures to many FRs simultaneously among WEEE recycling site workers have been little studied previously. The breathing zone airborne concentrations of five brominated FR compounds tetrabromobisphenol-A (TBBP-A), decabromodiphenylethane (DBDPE), hexabromocyclododecane, 1,2-bis(2,4,6-tribromophenoxy)ethane, hexabromobenzene, and one chlorinated FR (Dechlorane Plus®) were measured at four electronics recycling sites in two consecutive years. In addition, concentrations of polybrominated diphenyl ethers (PBDEs) and polybrominated biphenyls were measured. The three most abundant FRs in personal air samples were PBDEs (comprising mostly of deca-BDE), TBBP-A, and DBDPE, with mean concentrations ranging from 21 to 2320 ng m(-)(3), from 8.7 to 430 ng m(-3), and from 3.5 to 360 ng m(-3), respectively. At two of the sites, the emission control actions (such as improvements in ventilation and its maintenance and changes in cleaning habits) proved successful, the mean levels of FRs in personal samples being 10-68 and 14-79% of those from the previous year or alternatively below the limit of quantification. At the two remaining sites, the reductions in FR exposures were less consistent. The concentrations reported may pose a health hazard to the workers, although evaluation of the association between FR exposure and adverse health effects is hampered by lacking occupational exposure limits. Therefore, the exposures should be minimized by adequate control measures and maintaining good occupational hygiene practice.

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.

Handling anticancer drugs: from hazard identification to risk management?

The potential health hazards involved with antineoplastic agents have been known for decades. Many anticancer drugs are recognized as carcinogens and genotoxins in experimental assays. Second cancers have been recorded in follow-up studies with treated patients. The first findings on occupational exposures among hospital personnel administering chemotherapy were reported only in 1979. Since that time a magnitude of studies have been published using various chemical and biological exposure measurements. These findings prompted improvements in the handling practices of personnel working with anticancer drugs. In spite of strict guidelines for the safe handling of cancer chemotherapeutic agents and extensive improvements in the handling facilities in hospitals, also recent studies have revealed detectable, even if generally much decreased, amounts of indicator drugs in air and surface wipe samples, also including biological samples of personnel in hospital pharmacies and cancer therapy wards. Follow-up measurements show that application of strict safety precautions in hospitals decreases the biological exposure and/or effect markers to the level of unexposed referents. Open information and constant tutoring of personnel to avoid the hazards when working with anticancer drugs is absolutely necessary with the increasing use of these important drugs.

Determination of maleic anhydride in occupational atmospheres.

Maleic anhydride has many uses in industry, but workers' exposure to it is poorly known. Our new method allows airborne maleic anhydride to be determined with a limit of quantification of 1 microg/m3 per 12 1 of air, i.e., the concentration of about 0.01 times the occupational exposure standard (0.4 mg/m3). Air samples are collected in Tenax tubes containing sodium sulfate as a drying agent. Maleic anhydride is eluted with methyl tert.-butyl ether containing 5% acetonitrile and 0.1% acetic anhydride, and determined by capillary gas chromatography with electron-capture detection without interference from generic anhydrides. The tested method suits both long-term and short-term measurements.

Dermal exposure to polycyclic aromatic hydrocarbons among road pavers.

OBJECTIVES: Dermal exposure to polycyclic aromatic hydrocarbons (PAHs) and the role of an industrial by-product, coal fly ash, on workers' PAH exposure were investigated during stone mastic asphalt (SMA) paving and remixing. METHODS: PAH exposure was measured at eight sites during the laying of SMA containing coal fly ash or limestone (conventional SMA) as the filler. Six of the surveys were carried out during SMA paving and two during remixing of SMA (hot recycling at the paving site). Dermal PAH exposure was measured by hand washing (using sunflower oil and wiping with Kleenex tissues) before and after the work shift, and by placing exposure pads on the workers' wrists during the work shift. The analyses included 15 native PAHs from the hand-washing samples determined using high-performance liquid chromatography equipped with a two-channel fluorescence detector and 16 native PAHs and four methylated PAHs from the exposure pads using gas chromatography with mass-selective detection. RESULTS: The PAH results obtained using the pad and hand-washing methods (concentrations after the work shift) were equivalent and showed a strong correlation (r = 0.757, P < 0.001, N = 23 for total PAHs). There was a statistically significant difference between pre- and post-shift samples as measured by hand washing. The skin contamination by PAHs was significantly higher (P < 0.01) during remixing than during SMA paving. The variation in PAH contamination on the skin explained more of the variation in the excretion of urinary 1-hydroxypyrene and phenanthrols than the variation in the respiratory PAH concentrations. CONCLUSIONS: The industrial by-product investigated in asphalt, coal fly ash, had no statistically significant effect on the workers' dermal PAH exposure. The dermal exposure of paving workers to PAHs was higher during remixing than during SMA paving.

Exposure to cyclic anhydrides in welding: a new allergen-chlorendic anhydride.

Respiratory effects associated with welding fumes have been manifested in welders as occupational asthma. Previous studies have concerned mainly the effects of metal fume exposure, although it has also been suggested that asthma may develop as a result of exposure to contaminants generated from painted metals. To determine whether welding fumes contain irritating and sensitizing anhydrides, air samples were collected during the repair welding of forest harvesters, which were painted with chlorinated polyester paint. Samples were collected with an assembly of a spiral glass trap inserted between a filter holder with a Teflon filter and a Tenax sampling tube. Sample analyses were with GC-MS and GC-ECD. Sensitizing anhydrides released from the paint into the air were primarily chlorendic anhydride (<2-44 microg/m(3)) and phthalic anhydride (11-21 microg/m(3)). Hydrogen chloride (HCl) and hexachlorocyclopentadiene were also found. Airborne HCl was measured with Dräger tubes. Since paint films are electrical insulators, the film around the welding seam was removed before arc welding. Removal of paint with an abrasive wheel caused the least exposure to HCl (<0.5 ppm) in contrast to burning with a gas fuel torch, (HCl approximately 5 ppm). HCl exposure was the highest (<0.5-20 ppm) during welding. It is recommended that dry paint coating be removed from an area around the seam with an abrasive wheel, not by burning, before welding.

Exposure to methylhexahydrophthalic anhydride (MHHPA) in two workplaces of the electric industry.

Methylhexahydrophthalic anhydride (MHHPA) is a hardener for hot-cured epoxy resins employed as insulators in the electric industry. MHHPA has only been measured as an ingredient with other alicyclic anhydrides, albeit there are also large processes which use only MHHPA. We collected MHHPA vapour in a set of devices: Teflon filter, glass spiral, TenaxTA tube connected consecutively together. Elution was performed with a solvent mixture of methyl-tert-butyl ether (70%), acetonitrile (30%), and acetic anhydride (0.5%). By capillary GC-ECD, the regression was linear (0.9994) in the practical low concentration range of 0.04-1 microg ml(-1) being equal to 0.001-0.035 mg m(-3) in 30 l of air. The exposure was measured in two factories manufacturing electric appliances. The assembled objects were first impregnated with a liquid epoxy/hardener mixture, and then the resin hardened at elevated temperature. In condenser manufacturing, the operators' 8 h exposure ranged from 0.068 to 0.118 mg m(-3), and the short-term exposure was during operation at ovens mean 1.90 mg m(-3). The impregnation of coiled resistors and transfer of them to ovens caused the worst exposures, short-term mean 3.846 mg m(-3) and long-term mean 2.191 mg m(-3). During the 'baking', the ovens were closed and evacuated, but when the hot objects were moved out of the ovens, they continued during chilling to emit MHHPA, mean 0.366 mg m(-3). In the adjacent areas, assembling, control rooms, offices, the exposure was still significant, 0.017-0.043 mg m(3), due to leaks from the high exposure areas. Mechanical general ventilation and local exhausts were functioning. Respirators were available for short supervising of the hot equipment.

Air concentrations and urinary metabolites of polycyclic aromatic hydrocarbons among paving and remixing workers.

The exposure of paving workers to polycyclic aromatic hydrocarbons (PAH) during stone mastic asphalt (SMA) paving and remixing was evaluated. The effects on the workers' PAH exposure were also evaluated during the use of an industrial by-product, coal fly ash (CFA), instead of limestone as the filler in the SMA. The PAH exposure was measured by personal air sampling and by analysing the levels of urinary naphthols, phenanthrols and 1-hydroxypyrene (1-OHP) in the workers' pre- and post-shift urine samples. The respiratory PAH exposure of the paving workers (geometric mean (GM) 5.7 microg m(-3)) was about ten-fold that of the traffic controllers (GM 0.43 microg m(-3)). The levels of PAH metabolites were significantly higher (p < 0.05) in the post-shift urine samples than in the pre-shift urine samples, and the levels of metabolites in the post-shift urine of paving workers were significantly higher than in that of the controls (p < 0.01). Urinary 1-naphthol correlated well with the airborne concentrations of the two- to three-ring PAHs (r = 0.544, p = 0.003) and naphthalene (r = 0.655, p < 0.001), when non-smoking paving workers were tested. A good correlation was observed between urinary 1-OHP and the airborne concentrations of the four- to six-ring PAHs (r = 0.524, p = 0.003) as well as total PAHs (r = 0.575, p = 0.001). The concentrations of 1-OHP and phenanthrols in the urine of the pavers were significantly higher (p < 0.01) during remixing than during SMA paving. The CFA in the asphalt had no effect on the airborne PAH exposure or on the concentrations of the PAH metabolites in the paving workers' urine.

Occupational exposure to bitumen during road paving.

The exposure of road pavers to total particulates, bitumen fumes, semivolatile organic compounds (SVOCs), polycyclic aromatic hydrocarbons (PAHs), low-molecular-weight amines, styrene, and 1,3-butadiene was studied at 13 paving sites where 11 different asphalt mixtures were laid. Researchers analyzed 1-hydroxypyrene in the workers' pre- and postshift urine samples. The arithmetic mean concentrations of total particulates, bitumen fumes, SVOCs, and PAHs in the breathing zone of road pavers were 0.6 mg/m3, 0.29 mg/m3, 5.6 mg/m3, and 5.03 microg/m3, respectively. The highest bitumen fume concentrations (2.65 mg/m3) were measured in manual mastic laying, that is, when the paving temperature was highest. More than 90% of air impurities measured were in the vapor phase. Workers laying surface dressing were exposed to the highest SVOC concentrations (27.8 mg/m3). The paving temperature and the concentrations of bitumen fume correlated positively, but the weather conditions significantly affected the workers' exposure; for example, increased wind velocity resulted in lower concentrations of SVOCs and PAHs. Job title was not found to be a significant determinant of exposure, but exposure to bitumen fume and greater than or equal to four-ring PAHs among manual mastic pavers, and that to SVOCs and total PAHs among surface dressing workers, were significantly higher than among other pavers. Exposure during road paving operations was, on average, more than 10-fold higher to PAHs than was the exposure of a traffic controller (0.34 microg/m3) caused by automobile exhausts from background traffic. The PAHs were comprised mainly of two- and three-ring compounds. The concentrations of amines, and impurities from polymer modified bitumens, styrene, and 1,3-butadiene were below detection limits. Urinary 1-hydroxypyrene concentrations were higher among road pavers than among office workers serving as referents.