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Dietary copper intake may be associated with cognitive decline and dementia. We used data from 10,269 participants of the Atherosclerosis Risks in Communities Study to study the associations of dietary copper intake with 20-year cognitive decline and incident dementia. Dietary copper intake from food and supplements was quantified using food frequency questionnaires. Cognition was assessed using 3 cognitive tests at study visits; dementia was ascertained at study visits and via surveillance. Multiple imputation by chained equations was applied to account for the missing information of cognitive function during follow-up. Survival analysis with parametric models and mixed-effect models were used to estimate the associations for incident dementia and cognitive decline, respectively. During 20 years of follow-up (1996–1998 to 2016–2017), 1,862 incident cases of dementia occurred. Higher intake of dietary copper from food was associated with higher risk of incident dementia among those with high intake of saturated fat (hazard ratio = 1.49, 95% confidence interval: 1.04, 1.95). Higher intake of dietary copper from food was associated with greater decline in language overall (beta = −0.12, 95% confidence interval: −0.23, −0.02). Therefore, a diet high in copper, particularly when combined with a diet high in saturated fat, may increase the risk of cognitive impairment. [ABSTRACT FROM AUTHOR]

BACKGROUND: Practical approaches to protect individuals from ambient particulate matter (PM) are urgently needed in developing countries. Evidence on the health benefits of wearing particulate-filtering respirators is limited. OBJECTIVES: We evaluated the short-term cardiovascular health effects of wearing respirators in China. METHODS: A randomized crossover trial was performed in 24 healthy young adults in Shanghai, China in 2014. The subjects were randomized into two groups and wore particulate-filtering respirators for 48 hr alternating with a 3-week washout interval. Heart rate variability (HRV) and ambulatory blood pressure (BP) were continuously monitored during the 2nd 24 hr in each intervention. Circulating biomarkers were measured at the end of each intervention. Linear mixed-effect models were applied to evaluate the effects of wearing respirators on health outcomes. RESULTS: During the intervention periods, the mean daily average concentration of PM with an aerodynamic diameter < 2.5 μm (PM2.5) was 74.2 μg/m3. Compared with the absence of respirators, wearing respirators was associated with a decrease of 2.7 mmHg [95% confidence interval (CI): 0.1, 5.2 mmHg] in systolic BP and increases of HRV parameters, including 12.5% (95% CI: 3.8%, 21.2%) in high frequency (HF) power, 10.9% (95% CI: 1.8%, 20.0%) in the root mean square of the successive differences, and 22.1% (95% CI: 3.6%, 40.7%) in the percentage of normal RR intervals with duration > 50 msec different from the previous normal RR interval (pNN50). The presence of respirators was also associated with a decrease of 7.8% (95% CI: 3.5%, 12.1%) in the ratio of low frequency (LF)/HF power. CONCLUSIONS: Short-term wearing of particulate-filtering respirators may produce cardiovascular benefits by improving autonomic nervous function and reducing BP. CITATION: Shi J, Lin Z, Chen R, Wang C, Yang C, Cai J, Lin J, Xu X, Ross JA, Zhao Z, Kan H. 2017. Cardiovascular benefits of wearing particulate-filtering respirators: a randomized crossover trial. Environ Health Perspect 125:175-180; http://dx.doi.org/10.1289/EHP73 [ABSTRACT FROM AUTHOR]

Background: Ambient air pollution has been linked to the development of gestational diabetes mellitus (GDM). However, evidence of the association is very limited, and no study has estimated the effects of ozone. Objective: Our aim was to determine the association of prenatal exposures to particulate matter ≤ 2.5 μm (PM2.5) and ozone (O3) with GDM. Methods: We used Florida birth vital statistics records to investigate the association between the risk of GDM and two air pollutants (PM2.5 and O3) among 410,267 women who gave birth in Florida between 2004 and 2005. Individual air pollution exposure was assessed at the woman's home address at time of delivery using the hierarchical Bayesian space–time statistical model. We further estimated associations between air pollution exposures during different trimesters and GDM. Results: After controlling for nine covariates, we observed increased odds of GDM with per 5-μg/m3 increase in PM2.5 (ORTrimester1 = 1.16; 95% CI: 1.11, 1.21; ORTrimester2 = 1.15; 95% CI: 1.10, 1.20; ORPregnancy = 1.20; 95% CI: 1.13, 1.26) and per 5-ppb increase in O3 (ORTrimester1 = 1.09; 95% CI: 1.07, 1.11; ORTrimester2 = 1.12; 95% CI: 1.10, 1.14; ORPregnancy = 1.18; 95% CI: 1.15, 1.21) during both the first trimester and second trimester as well as the full pregnancy in single-pollutant models. Compared with the single-pollutant model, the ORs for O3 were almost identical in the co-pollutant model. However, the ORs for PM2.5 during the first trimester and the full pregnancy were attenuated, and no association was observed for PM2.5 during the second trimester in the co-pollutant model (OR = 1.02; 95% CI: 0.98, 1.07). Conclusion: This population-based study suggests that exposure to air pollution during pregnancy is associated with increased risk of GDM in Florida, USA. [ABSTRACT FROM AUTHOR]

The association between glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1) null polymorphisms and oral cancer is not consistent across studies, and data on their interaction with smoking in oral cancer are lacking. The authors systematically searched PubMed and SciVerse Scopus for case-control studies examining the association between null genotypes of the GSTM1 and GSTT1 genes and oral cancer. Twenty-eight case-control studies published in English were identified. Summary odds ratios were derived via random-effects models. The summary odds ratio for the GSTM1 null genotype was 1.43 in Asians (95% confidence interval (CI): 1.14, 1.78; P < 0.01, I 2 = 73%) and 0.98 in Caucasians (95% CI: 0.76, 1.28; P = 0.91, I 2 = 0%). Case-only analysis of 6 studies (552 cases) showed an inverse multiplicative interaction between GSTM1 null polymorphisms and smoking (ever/high levels of smoking vs. never/low levels) (odds ratio (OR) = 0.51, 95% CI: 0.32, 0.82; P = 0.01, I 2 = 34%). The GSTT1 null genotype was not significantly associated with oral cancer in Asians (OR = 1.07, 95% CI: 0.82, 1.38; P = 0.63, I 2 = 65%) or Caucasians (OR = 1.04, 95% CI: 0.41, 2.65; P = 0.93, I 2 = 55%). In conclusion, the GSTM1 null genotype may be associated with a higher risk of oral cancer in Asians but not in Caucasians, and this effect may be modified by smoking status. The GSTT1 null genotype may not be associated with oral cancer. [ABSTRACT FROM PUBLISHER]

Abstract: Background Studies show that active smoking may be associated with cognitive decline. However, the consequence of secondhand smoke on cognitive and physical performance remains unclear. The purpose of this study was to assess the association of secondhand smoke with cognitive performance and physical function using a population-based sample. Methods: Data of 2,542 non-smoking participants from the 1999–2002 National Health and Nutrition Examination Survey were analyzed. Secondhand smoke exposure level was estimated using blood cotinine concentrations. Cognitive performance was assessed with the Digit Symbol Substitution Test and self-reported confusion/memory problems. Physical performance was analyzed using visual gait speed (m/s) and self-reported physical function. Multivariate linear and logistic regression models were used to assess the association. Results: In never smokers, cognitive performance score decreased by 2.03 points (95% confidence interval (CI): −3.00, –1.05) per one unit increase in log-transformed blood cotinine level. After adjusting for potential confounders, including diabetes, hypertension, body mass index, alcohol, and blood lead level, change in cognitive performance score was still statistically significant (−1.17 95% CI: −2.32, –0.02). Similar trends were observed in former smokers. Gait speed decreased by 0.02m/s for one unit increase in log-transformed blood cotinine level. This was evident in both never and former smokers. The relationship remained significant after adjusting for potential confounders in former smokers. Conclusions: Our study suggests that secondhand smoke may contribute to cognitive decline in never and former smokers. Considering the cross-sectional design and the limitations of this study, the relationship warrants further assessment. [Copyright &y& Elsevier]