OBJECTIVE: Workers in various industries can be exposed to polycyclic aromatic hydrocarbons (PAHs). The relationship between biomarkers of genotoxic risk, PAH compounds in air (ambient monitoring) and PAH metabolites in urine (internal exposure) were studied in 17 workers exposed to PAHs in a fireproof-material producing plant before and 3 months after the PAH profile was altered in the binding pitch.

METHODS: Two biomarkers of exposure, specific DNA adducts of (+/-)-r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE) and non-specific DNA adduct of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) were determined in white blood cells (WBCs). In addition, DNA strand breaks were analysed in lymphocytes by single-cell gel electrophoresis in a genotoxic risk assessment. Sixteen PAH compounds in air were determined by personal air sampling, and hydroxylated metabolites of phenanthrene, pyrene and naphthalene were determined in urine.

RESULTS: After substitution of the binding pitch the concentrations of benzo[a]pyrene in air decreased (P<0.01). No changes could be observed for pyrene, while levels of phenanthrene (P=0.0013) and naphthalene (P=0.0346) in air increased. Consequently, median DNA adduct rates of anti-BPDE decreased after alteration of the production material (from 0.9 to <0.5 adducts/10(8) nucleotides). No changes in the excretion of 1-hydroxypyrene in urine could be determined, whereas increased levels of 1-, 2+9-, 3- and 4-hydroxyphenanthrene (P<0.0001) and 1-naphthol and 2-naphthol (P=0.0072) were found in urine. In addition, a statistically significant increase in DNA strand break frequencies (P<0.01) and elevated 8-oxodGuo adduct levels (P=0.7819, not statistically significant) were found in the WBCs of exposed workers 3 months after the PAH profile in the binding pitch had been altered.

CONCLUSION: The results presented here show that the increased concentration of naphthalene and/or phenanthrene in the air at the work place could induce the formation of DNA strand breaks and alkali-labile sites in WBCs of exposed workers.

[Untagged]
━ Inclusion
━ ━ Human
━ ━ Animal
━ Exclusion
━ ━ TIAB
━ ━ Full text
━ ━ ━ Not relevant to PECO
━ ━ ━ Unable to obtain full-text
━ Supplemental material
━ ━ Mechanistic
━ ━ ━ Cell signaling/function
━ ━ ━ Structure-activity
━ ━ ━ Enzyme activity
━ ━ ━ Oxidative stress
━ ━ ━ Cytotoxicity
━ ━ ━ Epigenetics
━ ━ ━ Receptor binding/activity
━ ━ ━ Genotoxicity
━ ━ ━ Immune
━ ━ ADME/TK
━ ━ PBPK model
━ ━ Non-inhalation/non-oral route of administration
━ ━ Non-mammalian models
━ ━ Exposure
━ ━ Mixture
━ ━ Case reports or case series
━ ━ No original data
━ ━ Conference abstracts
━ ━ Unnamed reports

References (1600 found)