BACKGROUND: Exposure to traffic-related air pollutants, including polycyclic aromatic hydrocarbons (PAH) and heavy metals, has been associated with the etiology and prognosis of many illnesses. However, the specific causal agents and underlying mechanisms for different health outcomes remain unclear. The aims of this study were to assess the relations between urinary biomarkers of exposure to PAHs (1-hydroxypyrene-glucuronide, 1-OHPG) and heavy metals (cadmium, Cd; nickel, Ni; arsenic, As; lead, Pb; and copper, Cu) and the effect of their interaction on DNA damage (8-oxo-7,8-dihydro-guanine, 8-oxodG). METHODS: We recruited 91 traffic conductors and 53 indoor office workers between May 2009 and June 2011 in Taipei, Taiwan. Postshift urine samples from 2 consecutive days were analyzed for 1-OHPG, Cd, Ni, As, Pb, Cu, and 8-oxodG. To estimate the effects from PAHs and metals on DNA damage, we constructed a linear mixed model adjusted for confounding variables. RESULTS: We found that urinary 1-OHPG and Cd levels were independent predictors of urinary 8-oxodG levels (β = 0.112; P = 0.015 for 1-OHPG; β = 0.138; P = 0.031 for urinary Cd). The joint effect of urinary 1-OHPG and Cd levels was associated with urinary 8-oxodG levels (P = 0.001). CONCLUSIONS: Co-exposure to environmental PAHs and Cd could cause oxidative DNA damage. IMPACT: These findings suggest that the additive interaction between exposure to environmental PAHs and Cd could enhance the burden of oxidative stress.
BACKGROUND: Exposure to traffic-related air pollutants, including polycyclic aromatic hydrocarbons (PAH) and heavy metals, has been associated with the etiology and prognosis of many illnesses. However, the specific causal agents and underlying mechanisms for different health outcomes remain unclear. The aims of this study were to assess the relations between urinary biomarkers of exposure to PAHs (1-hydroxypyrene-glucuronide, 1-OHPG) and heavy metals (cadmium, Cd; nickel, Ni; arsenic, As; lead, Pb; and copper, Cu) and the effect of their interaction on DNA damage (8-oxo-7,8-dihydro-guanine, 8-oxodG). METHODS: We recruited 91 traffic conductors and 53 indoor office workers between May 2009 and June 2011 in Taipei, Taiwan. Postshift urine samples from 2 consecutive days were analyzed for 1-OHPG, Cd, Ni, As, Pb, Cu, and 8-oxodG. To estimate the effects from PAHs and metals on DNA damage, we constructed a linear mixed model adjusted for confounding variables. RESULTS: We found that urinary 1-OHPG and Cd levels were independent predictors of urinary 8-oxodG levels (β = 0.112; P = 0.015 for 1-OHPG; β = 0.138; P = 0.031 for urinary Cd). The joint effect of urinary 1-OHPG and Cd levels was associated with urinary 8-oxodG levels (P = 0.001). CONCLUSIONS: Co-exposure to environmental PAHs and Cd could cause oxidative DNA damage. IMPACT: These findings suggest that the additive interaction between exposure to environmental PAHs and Cd could enhance the burden of oxidative stress.
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