Oxidative Dna Damage In Diesel Bus Mechanics
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Rationale:
Diesel exposure has been associated with adverse health effects, including susceptibility to asthma, allergy and cancer. Previous epidemiological studies demonstrated increased cancer incidence among workers exposed to diesel. This is likely due to oxidative DNA damage in response to diesel exhaust particulates (DEP) that contain polycyclic aromatic hydrocarbons (PAH) and many other known carcinogens.
Objective:
To determine the relationship between occupational diesel exposure and oxidative DNA damage in diesel bus mechanics.
Methods:
A short-term, prospective study of diesel bus mechanics from 6 work sites was performed. Mechanics from each work site were monitored over 5 consecutive workdays. Self-administered questionnaires were used to collect information on medical, smoking, and occupational history. Pre- and post-shift urine samples (N=10/subject) were collected and analyzed for 8-hydroxy-2'-deoxyguanosine by ELISA (8-OH-dG; a particular DNA modification in response to oxidative injury) and cross-week mononuclear cells were examined for the presence of PAH-DNA adducts by ELISA. Generalized estimating equations (GEE) were used to investigate the association of the 8-OH-dG level with the explanatory variables. Results: The mean age for all subjects (N=36; 35 male, 1 female) was 42 years (range 21-53 years); 36% of the subjects were current smokers. 8-OH-dG levels (corrected for creatinine) were determined for 355 urine samples; PAH-DNA adducts were determined for 70 blood samples. Multivariate GEE analysis suggested there was no difference in 8-OH-dG levels across the 8-hour workshift in workers. However, the mean cross-week increase in 8-OH-dG levels was 70.0% (SE=18.3%, p=0.01) and in PAH-DNA adduct staining was 69.8% (SE=10.9%, p<0.05).
Conclusions:
This study suggests that diesel bus mechanics develop cumulative oxidative DNA damage in response to occupational DEP exposure.
NIH grant CA94715
Diesel exposure has been associated with adverse health effects, including susceptibility to asthma, allergy and cancer. Previous epidemiological studies demonstrated increased cancer incidence among workers exposed to diesel. This is likely due to oxidative DNA damage in response to diesel exhaust particulates (DEP) that contain polycyclic aromatic hydrocarbons (PAH) and many other known carcinogens.
Objective:
To determine the relationship between occupational diesel exposure and oxidative DNA damage in diesel bus mechanics.
Methods:
A short-term, prospective study of diesel bus mechanics from 6 work sites was performed. Mechanics from each work site were monitored over 5 consecutive workdays. Self-administered questionnaires were used to collect information on medical, smoking, and occupational history. Pre- and post-shift urine samples (N=10/subject) were collected and analyzed for 8-hydroxy-2'-deoxyguanosine by ELISA (8-OH-dG; a particular DNA modification in response to oxidative injury) and cross-week mononuclear cells were examined for the presence of PAH-DNA adducts by ELISA. Generalized estimating equations (GEE) were used to investigate the association of the 8-OH-dG level with the explanatory variables. Results: The mean age for all subjects (N=36; 35 male, 1 female) was 42 years (range 21-53 years); 36% of the subjects were current smokers. 8-OH-dG levels (corrected for creatinine) were determined for 355 urine samples; PAH-DNA adducts were determined for 70 blood samples. Multivariate GEE analysis suggested there was no difference in 8-OH-dG levels across the 8-hour workshift in workers. However, the mean cross-week increase in 8-OH-dG levels was 70.0% (SE=18.3%, p=0.01) and in PAH-DNA adduct staining was 69.8% (SE=10.9%, p<0.05).
Conclusions:
This study suggests that diesel bus mechanics develop cumulative oxidative DNA damage in response to occupational DEP exposure.
NIH grant CA94715