DNA strand breaks, oxidative damage, and 1-OH pyrene in roofers with coal-tar pitch dust and/or asphalt fume exposure.

OBJECTIVE: To determine the potential for asphalt fume exposure to increase DNA damage, we conducted a cross-sectional study of roofers involved in the application of roofing asphalt. METHODS: DNA strand breaks and the ratio of 8-hydroxydeoxyguanosine (8-OHdG) to 2-deoxyguanosine (dG) were measured in peripheral blood leukocytes of roofers. In addition, urinary excretion of 8-OHdG and 8-epi-prostaglandin F2alpha (8-epi-PGF) was also measured. The study population consisted of 26 roofers exposed to roofing asphalt and 15 construction workers not exposed to asphalt during the past 5 years. A subset of asphalt roofers (n = 19) was exposed to coal-tar pitch dust (coal tar) during removal of existing roofs prior to applying hot asphalt. Personal air monitoring was performed for one work-week to measure exposure to total particulates, benzene-soluble fraction of total particulates, and polycyclic aromatic compounds (PACs). Urinary 1-OH-pyrene levels were measured as an internal biomarker of PAC exposure. RESULTS: Full-shift breathing zone measurements for total particulates, benzene-solubles and PACs were significantly higher for coal-tar exposed workers than for roofers not exposed to coal tar. Similarly, urinary 1-OH-pyrene levels were higher in coal-tar exposed roofers than roofers not exposed to coal tar. Total particulates or benzene-soluble fractions were not associated with urinary 1-OH-pyrene, but PAC exposure was highly correlated with urinary 1-OH-pyrene. When stratified by 1-OH-pyrene excretion, DNA strand breaks increased in a dose-dependent manner, and leukocyte 8-OHdG/dG decreased in a dose-dependent manner. Significant changes in DNA damage appeared to be linked to PACs from coal-tar exposure, although asphalt fume alone was associated with a small but significant increase in urinary 1-OH-pyrene and DNA strand breaks. CONCLUSIONS: Results are consistent with previous reports that asphalt or coal-tar exposure can cause DNA damage. Urinary 8-epi-PGF remained relatively constant during the week for virtually all subjects, regardless of exposure indicating that neither asphalt nor coal-tar exposure induces an overt oxidative stress. A small, but statistically significant increase in 8OHdG was evident in end-of-week urine samples compared with start-of-week urine samples in roofers exposed to coal-tar. The increase in urinary 8OHdG coupled with the decrease in leukocyte 8-OHdG/dG, suggests that coal-tar exposure induces protective or repair mechanisms that result in reduced levels of steady-state oxidative-DNA damage.

Environmental sampling and analysis for zeranol.

Due to concern over health effects associated with the use of zeranol, a sampling and analytical method to monitor zeranol in the work environment was developed. The collection strategy included air samples on FHLP filters, area samples on gauze pads, hand/dermal samples on gauze pads and bulk samples. The sampling method evaluation included choice of media, flow rate and duration for air samples, sample preparation, extraction efficiencies and sample stability. Analysis of the samples was accomplished by high performance liquid chromatography with identification and quantification by UV and fluorescence detection. The analytical method evaluation included separation of possible interfering compounds, calibration curves, limits of detection (LOD), limits of quantitation (LOQ), precision and accuracy. The tested analytical range was 0.01 to 150 micrograms/mL with a LOD of 0.007 microgram/mL and a LOQ of 0.02 microgram/mL using UV detection. For the fluorescence detector, the LOD was 0.05 microgram/mL and the LOQ was 0.15 microgram/mL. Peak confirmation was achieved by retention time and comparing the two detector responses. Use of this method provided the sensitivity and specificity to analyze environmental samples for zeranol in the workplace environment.

Development and use of a sampling and analytical method for azodicarbonamide.

Azodicarbonamide is a medium temperature blowing agent used in the production of foamed polymers. Because of worker concern over health effects associated with its use, researchers from the National Institute for Occupational Safety and Health (NIOSH) conducted two health hazard evaluations. This paper describes the health concerns, the sampling and analytical method used, the environments sampled and the results of these surveys. Environmental samples were collected on Teflon filters for total dust and airborne concentration of azodicarbonamide. Analysis was accomplished by high performance liquid chromatography with identification and quantitation by UV detector response ratioing. Use of this method provided the sensitivity and specificity to analyze airborne azodicarbonamide concentrations and allowed evaluation of a workplace environment for a respiratory health hazard.