Kim YD, et al. J Korean Med Sci. 2016 Apr;31(4):489-496. https://doi.org/10.3346/jkms.2016.31.4.489

Eom SY, et al. J Korean Med Sci. 2017 Nov;33(2):e9. https://doi.org/10.3346/jkms.2018.33.e9

Purpose: This cross-sectional study aimed to assess the effect of environmental cadmium (Cd) exposure and essential metal imbalance on renal tubular damage and oxidative stress in 979 adults living in a Cd-polluted area near an abandoned copper (Cu) refinery. Methods: We analyzed urinary Cd concentrations, renal tubular damage and oxidative stress markers, such as beta-2 microglobulin (β2-MG) and N-acetyl-β-d-glucosaminidase (NAG) activity and urine malondialdehyde (MDA) levels. The serum copper-to-zinc ratio (CZR) was used as an essential metal imbalance indicator. We divided the subjects into two Cd exposure groups based on the reference level of urinary Cd for renal dysfunction (2 μg/g creatinine). Results: The geometric mean concentration of urinary Cd in all subjects was 2.25 μg/g creatinine. In both low and high Cd exposure groups, urinary Cd levels were positively correlated with urinary NAG activity, but not with serum CZR. After multivariate adjustment, serum CZR was strongly associated with urinary β2-MG levels in the low Cd exposure group (β = 1.360, P = 0.019) and was significantly associated with urinary MDA levels, regardless of Cd exposure level. In addition, the risk of renal tubular damage was significantly associated with urinary Cd level, particularly in the lowest or highest CZR tertile groups. Conclusions: Essential metal imbalance may be a determinant of oxidative stress and renal tubular damage in a chronically Cd-exposed population, and proper zinc supplementation will be effective in preventing adverse health effects due to Cd exposure.

In our study, we estimated formaldehyde exposure levels of Korean medical students during their cadaver dissection practice hours. In addition, we examined the prevalence rates of formaldehyde-specific immunoglobulin E or immunoglobulin G antibodies and compared the results with the symptoms the students experienced as a result of formaldehyde exposure. There were 167 Korean medical students (i.e., subjects) aged 23.8 ± 2.5 y (mean ± standard deviation) and a control group of 67 premedical students aged 20.1 ± 2.8 y (mean ± standard deviation). Concentrations of formaldehyde in the cadaver dissection practice laboratory ranged from 0.194 to 11.245 mg/m³ (3.736 ± 3.478 mg/m³ [mean ±standard deviation]). Students reported by self-administered questionnaires that eye soreness (92.8%) and lacrimation (74.9%) were the most common symptoms they experienced during the laboratory sessions. One (0.6%) of the 167 medical students had a history of wheezing during dissection. Fourteen (8.4%) had specific immunoglobulin G antibody, but none had specific immunoglobulin E antibody. These results suggest that (a) Korean medical students are exposed to formaldehyde at a relatively high levels in their dissection practice hours, (b) specific immunoglobulin G is not related to adverse eye or respiratory symptoms, and (c) specific immunoglobulin E is rarely induced as a result of exposure to formaldehyde.

A major constituent of urban air pollution is diesel exhaust, a complex mixture of gases, chemicals, and particles. Recent evidence suggests that exposure to air pollution can increase the risk of a fatal stroke, cause cerebrovascular damage, and induce neuroinflammation and oxidative stress that may trigger neurodegenerative diseases, such as Parkinson's disease. The specific aim of this study was to determine whether ultrafine diesel exhaust particles (DEPs), the particle component of exhaust from diesel engines, can induce oxidative stress and effect dopamine metabolism in PC-12 cells. After 24 h exposure to DEPs of 200 nm or smaller, cell viability, ROS and nitric oxide (NO(2)) generation, and levels of dopamine (DA) and its metabolites, (dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)), were evaluated. Results indicated cell viability was not significantly changed by DEP exposure. However, ROS showed dramatic dose-dependent changes after DEP exposure (2.4 fold increase compared to control at 200 μg/mL). NO(2) levels were also dose-dependently increased after DEP exposure. Although not in a dose-dependent manner, upon DEP exposure, intracellular DA levels were increased while DOPAC and HVA levels decreased when compared to control. Results suggest that ultrafine DEPs lead to dopamine accumulation in the cytoplasm of PC-12 cells, possibly contributing to ROS formation. Further studies are warranted to elucidate this mechanism.