期刊
CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
卷 14, 期 5, 页码 1340-1343出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1055-9965.EPI-04-0899
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Ambient particulate matter (PM) has been associated with increased risk of lung cancer. One proposed mechanism is that PM induces oxidative stress mediated by transition metals contained within this mixture. We examined the relationship between the personal exposure to water-soluble transition metals in PM2.5 and oxidative DNA damage. In 49 students from central Copenhagen, we determined PM2.5 exposure by personal sampling twice in I year, and measured in these PM2.5 samples the concentration of the soluble transition metals vanadium, chromium, iron, nickel, copper, and platinum. Collected lymphocytes and 24-hour urine samples were analyzed for DNA damage in terms of 7-hydro-8-oxo-2'-deoxyguanosine (8-oxodG). We found that the 8-oxodG concentration in lymphocytes was significantly associated with the vanadium and chromium concentrations with a 1.9% increase in 8-oxodG per 1 mu g/L increase in the vanadium concentration and a 2.2% increase in 8-oxodG per 1 mu g/L increase in the chromium concentration. We have previously reported that in this study population the personal exposure to PM2.5 was associated with an increase in 8-oxodG in lymphocytes. However, vanadium and chromium were associated with the 8-oxodG concentration in lymphocytes independently of the PM2.5 mass concentration. The four other transition metals were not associated with 8-oxodG in lymphocytes and none of the transition metals was significantly associated with 8-oxodG in urine. Our results could indicate that vanadium and chromium present in PM2.5 have an effect on oxidative DNA damage that is independent of particle mass and/or other possible toxic compounds contained within this particulate mixture.
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