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.
Toraason
M
M
National Institute for Occupational Safety and Health, Cincinnati, OH 45226, USA.
Hayden
C
C
Marlow
D
D
Rinehart
R
R
Mathias
P
P
Werren
D
D
Olsen
L D
LD
Neumeister
C E
CE
Mathews
E S
ES
Cheever
K L
KL
Marlow
K L
KL
DeBord
D G
DG
Reid
T M
TM
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D003252:Construction Materials / Q000009:adverse effects*; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives* / Q000097:blood / Q000652:urine; D015237:Dinoprost / Q000652:urine; D004391:Dust; D006801:Humans; D006838:Hydrocarbons / Q000009:adverse effects*; D007962:Leukocytes / Q000378:metabolism; D008875:Middle Aged; D016273:Occupational Exposure / Q000009:adverse effects*; D018384:Oxidative Stress; D011721:Pyrenes / Q000009:adverse effects*; D012907:Smoking; D014481:United States
D004391:Dust; D006838:Hydrocarbons; D011721:Pyrenes; C006647:asphalt; D000080242:8-Hydroxy-2'-Deoxyguanosine; D015237:Dinoprost; D003849:Deoxyguanosine; C033146:1-hydroxypyrene