Urinary metals are considered measures of long-term exposures of metals, such as cadmium (Cd). Some studies indicate reduced renal function may affect the urinary excretion of several metals in general population making assessments difficult. To examine whether reduced renal function is associated with reduced urinary excretion of 12 metals or their metabolites and, in turn, an underestimated measure of Cd in general population. We conducted analyses using data from the National Health and Nutrition Examination Survey (NHANES) 2003-2012. Multiple linear regression models were used to examine the associations between urinary metal levels and estimated glomerular filtration rate (eGFR). Restricted cubic spline regression models were used to evaluate the nonlinearity. Urinary metal levels significantly increased (p < 0.001) with increasing eGFR, except for antimony (p = 0.172). Urinary levels of arsenic, dimethylarsonic acid, cobalt, molybdenum and tungsten increased linearly with eGFR, while Cd, lead, mercury, barium, cesium and thallium increased nonlinearly (p < 0.001) with eGFR. Based on a restricted cubic spline regression model, we found, corresponding to a fixed blood Cd adverse cutpoint of 5 μg/L, predicted urinary Cd cutpoints substantially varied from 0.78-1.21 μg/g for urinary Cd between those aged <40 years and who had chronic kidney disease and those aged 60 years or over with normal renal function, respectively. Reduced renal function is associated with reduced urinary metals; and associations are also observed across the eGFR range not just in the reduced range. Urinary abnormal cutpoints of metals are likely dependent on eGFR and age. The associations between urinary exposure of metals and disease risk are likely underestimated without considering the modifying effect of renal function.

Objectives: To investigate the occupational and genetic risk factors inducing lumbar disc degeneration in a Chinese population, and to explore their synergistic interactions. Methods: A case-control study involving 178 low back pain patients with lumbar disc degeneration and 284 controls was carried out. Five types of work-related factors were investigated using questionnaires. Polymerase chain reaction and restriction fragments length polymorphism was used to detect the polymorphisms of MMP-3 (matrix metalloproteinase-3)(rs731236), VDR-Taq (vitamin D receptor-Taq) and VDR-Apa (vitamin D receptor-Apa)(rs35068180). Rothman's synergy index was used to measure the synergistic interactions between gene polymorphisms and occupational risk factors. Results: Family history of lumbar disc diseases, back injury history, whole-body vibration, bending/twisting, heavy physical workload, age, mutation alleles 5A of MMP-3 and A of VDR-Apa were significantly associated with lumbar disc degeneration (OR=12.70, 11.79, 8.96, 5.46, 1.05, 1.96 and 1.70, respectively, p<0.05). Synergistic interactions existed between the mutation allele 5A of MMP-3 and whole-body vibration exposure, the mutation allele 5A of MMP-3 and bending/twisting, and the mutation allele A of VDR-Apa and bending/twisting (SI=13.27, 2.91, 2.35, respectively, p<0.05). Conclusions: The results of this study suggest that gene-occupation interaction might play a certain role in exaggerating lumbar disc degeneration. There is a possibility that subjects who carry mutation alleles 5A of MMP-3 and/or A of VDR-Apa are more vulnerable to lumbar disc degeneration when they are exposed to whole-body vibration and/or bending/twisting under ergonomic loads.

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death globally and ozone exposure is a main cause of its disease burden. However, studies on COPD hospitalizations from short-term ambient level ozone exposure have not generated consensus results. To address the knowledge gap, comprehensive and systematic searches in several databases were conducted using specific keywords for publications up to February 14, 2020. Random-effect models were used to derive overall excess risk estimates between short-term ambient-level ozone exposure and COPD hospitalizations. The influence analyses were used to test the robustness of the results. Both meta-regression and subgroup analyses were used to explore the sources of heterogeneity and potential modifying factors. Based on the results from 26 eligible studies, the random-effect model analyses show that a 10 µg/m³ increase in maximum 8-h ozone concentration was associated with 0.84% (95% CI: 0.09%, 1.59%) higher COPD hospitalizations. The estimates were higher for warm season and multiple-day lag but lower for old populations. Results from subgroup analyses also indicate a multiple-day lag trend and bigger significant health effects during longer day intervals. Although characteristics of individual studies added modest heterogeneity to the overall estimates, the results remained robust during further analyses and exhibited no evidence of publication bias. Our systematic review and meta-analysis indicate that short-term ambient level ozone exposure was associated with increased risk of COPD hospitalizations. The significant association with multiple-day lag trend indicates that a multiple-day exposure metric should be considered for establishing ambient ozone quality and exposure standards for improvement of population health. Future investigations and meta-analysis studies should include clinical studies as well as more careful lag selection protocol.

It is widely accepted that the cytotoxicity and genotoxicity of benzene results from the action of reactive metabolites. Therefore, genetic variation in metabolic enzyme genes may contribute to susceptibility to chronic benzene poisoning (CBP) in the exposed population. Using a case–control study that included 268 benzene-poisoned patients and 268 workers occupationally exposed to benzene in South China, we aimed to investigate the association between single-nucleotide polymorphisms in genes with phase I and II of metabolism and risk of CBP. The TaqMan technique was used to detect polymorphisms of CYP1A1 , CYP1A2 , CYP1B1 , ADH1B , EPHX1 , EPHX2 , NQO1 , MPO , GSTP1 and UGT1A6 genes. We also explored potential interactions of these polymorphisms with lifestyle factors such as cigarette smoking and alcohol consumption. A weak positive association was found between glutathione S -transferase pi-1 ( GSTP1 ) rs1695 polymorphism and the risk of CBP ( P = 0.046), but this association was not statistically significant ( P = 0.117) after adjustment for potential confounders. Further analysis showed that the risk of CBP increased in the subjects with EPHX1 GGAC/GAGT diplotype ( P = 0.00057) or AGAC/GAGT diplotype ( P = 0.00086). In addition, we found that alcohol drinkers with the EPHX1 rs3738047 GA + AA genotypes and non-alcohol drinkers with the GSTP1 rs1695 AA genotype tended to be more susceptible to benzene toxicity. Our results suggest that genetic polymorphisms in EPHX1 may contribute to risk of CBP in a Chinese occupational population.