1.
Biomonitoring of humans exposed to arsenic, chromium, nickel, vanadium, and complex mixtures of metals by using the micronucleus test in lymphocytes.
Annangi, B, Bonassi, S, Marcos, R, Hernández, A
Mutation research. Reviews in mutation research. 2016;(Pt A):140-161
Abstract
Various metals have demonstrated genotoxic and carcinogenic potential via different mechanisms. Until now, biomonitoring and epidemiological studies have been carried out to assess the genotoxic risk to exposed human populations. In this sense, the use of the micronucleus assay in peripheral blood lymphocytes has proven to be a useful tool to determine increased levels of DNA damage, as a surrogate biomarker of cancer risk. Here we review those biomonitoring studies focused on people exposed to arsenic, chromium, nickel, vanadium and complex mixtures of metals. Only those studies that used the frequency of micronuclei in binucleated (BNMN) cells have been taken into consideration, although the inclusion of other biomarkers of exposure and genotoxicity are also reflected and discussed. Regarding arsenic, most of the occupational and environmental biomonitoring studies find an increase in BNMN among the exposed individuals. Thus, it seems conclusive that arsenic exposure increases the risk of exposed human populations. However, a lack of correlation between the level of exposure and the increase in BNMN is also common, and a limited number of studies evaluated the genotype as a risk modulator. As for chromium, a BNMN increase in occupationally exposed subjects and a correlation between level of exposure and effect is found consistently in the available literature. However, the quality score of the studies is only medium-low. On the other hand, the studies evaluating nickel and vanadium are scarce and lacks a correct characterization of the individual exposure, which difficult the building of clear conclusions. Finally, several studies with medium-high quality scores evaluated a more realistic scenario of exposure which takes into account a mixture of metals. Among them, those which correctly characterized and measured the exposure were able to find association with the level of BNMN. Also, several genes associated with DNA damage repair such as OGG1 and XRCC1 were found to influence the exposure effect.
2.
Associations of Short-Term and Long-Term Exposure to Ambient Air Pollutants With Hypertension: A Systematic Review and Meta-Analysis.
Cai, Y, Zhang, B, Ke, W, Feng, B, Lin, H, Xiao, J, Zeng, W, Li, X, Tao, J, Yang, Z, et al
Hypertension (Dallas, Tex. : 1979). 2016;(1):62-70
Abstract
Hypertension is a major disease of burden worldwide. Previous studies have indicated that air pollution might be a risk factor for hypertension, but the results were controversial. To fill this gap, we performed a meta-analysis of epidemiological studies to investigate the associations of short-term and long-term exposure to ambient air pollutants with hypertension. We searched all of the studies published before September 1, 2015, on the associations of ozone (O3), carbon monoxide (CO), nitrogen oxide (NO2 and NOX), sulfur dioxide (SO2), and particulate matter (PM10 and PM2.5) with hypertension in the English electronic databases. A pooled odds ratio (OR) for hypertension in association with each 10 μg/m(3) increase in air pollutant was calculated by a random-effects model (for studies with significant heterogeneity) or a fixed-effect model (for studies without significant heterogeneity). A total of 17 studies examining the effects of short-term (n=6) and long-term exposure (n=11) to air pollutants were identified. Short-term exposure to SO2 (OR=1.046, 95% confidence interval [CI]: 1.012-1.081), PM2.5 (OR=1.069, 95% CI: 1.003-1.141), and PM10 (OR=1.024, 95% CI: 1.016-1.032) were significantly associated with hypertension. Long-term exposure (a 10 μg/m(3) increase) to NO2 (OR=1.034, 95% CI: 1.005-1.063) and PM10 (OR=1.054, 95% CI: 1.036-1.072) had significant associations with hypertension. Exposure to other ambient air pollutants (short-term exposure to NO2, O3, and CO and long-term exposure to NOx, PM2.5, and SO2) also had positive relationships with hypertension, but lacked statistical significance. Our results suggest that short-term or long-term exposure to some air pollutants may increase the risk of hypertension.