Could the association between ozone and arterial stiffness be modified by fish oil supplementation?

BACKGROUND: Arterial stiffness (AS) is an important predicting factor for cardiovascular disease. However, no epidemiological studies have ever explored the mediating role of biomarkers in the association between ozone and AS, nor weather fish oil modified such association. METHODS: Study participants were drawn from the UK biobank, and a total of 95,699 middle-aged and older adults were included in this study. Ozone was obtained from Community Multiscale Air Quality (CMAQ) model matched to residential addresses, fish oil from self-reported intake, and arterial stiffness was based on device measurements. First, we applied a double robust approach to explore the association between ozone or fish oil intake and arterial stiffness, adjusting for potential confounders at the individual and regional levels. Then, how triglycerides, apolipoprotein B (Apo B)/apolipoprotein A (ApoA) and non-high-density lipoprotein cholesterol (Non-HDL-C) mediate the relationship between ozone and AS. Last, the modifying role of fish oil was further explored by stratified analysis. RESULTS: The mean age of participants was 55 years; annual average ozone exposure was associated with ASI (beta:0.189 [95%CI: 0.146 to 0.233], P < 0.001), and compared to participants who did not consume fish oil, fish oil users had a lower ASI (beta: 0.061 [95%CI: -0.111 to -0.010], P = 0.016). The relationship between ozone exposure and AS was mediated by triglycerides, ApoB/ApoA, and Non-HDL-C with mediation proportions ranging from 10.90% to 18.30%. Stratified analysis showed lower estimates on the ozone-AS relationship in fish oil users (P = 0.011). CONCLUSION: Ozone exposure was associated with higher levels of arterial stiffness, in contrast to fish oil consumption, which showed a protective association. The association between ozone exposure and arterial stiffness was partially mediated by some biomarkers. In the general population, fish oil consumption might provide protection against ozone-related AS.

Air pollution, greenness and risk of overweight among middle-aged and older adults: A cohort study in China.

BACKGROUND: Exposure to air pollution may increase the risk of obesity, but living in greener space may reduce this risk. Epidemiological evidence, however, is inconsistent. METHODS: Using data from the China Health and Retirement Longitudinal Study (2011-2015), we conducted a nationwide cohort study of 7424 adults. We measured overweight/obesity according to body mass index. We used annual average ground-level air pollutants, including ozone (O3), nitrogen dioxide (NO2), and particulate matter with aerodynamic diameters ≤2.5 µm (PM2.5), to demonstrate air pollution levels. We used the Normalized difference vegetation index (NDVI) to measure greenness exposure. We used time-varying Cox proportional hazard regression models to analyze the connections among air pollution, greenness, and the development of overweight/obesity in middle-aged and older adults in China. We also conducted mediation analyses to examine the mediating effects of air pollution. RESULTS: We found that lower risk of overweight/obesity was associated with more greenness exposure and lower levels of air pollution. We identified that an interquartile increment in NDVI was correlated with a lower hazard ratio (HR) of becoming overweight or obese (HR = 0.806, 95% confidence interval [CI]: 0.754-0.862). Although a 10 µg/m3 increase in PM2.5 and NO2 was correlated with higher risks (HR = 1.049, 95% CI = 1.022-1.075, HR = 1.376, 95% CI = 1.264-1.499). Effects of PM2.5 on being overweight or obese were stronger in men than in women. According to the mediation analysis, PM2.5 and NO2 mediated 8.85% and 19.22% of the association between greenness and being overweight or obese. CONCLUSIONS: An increased risk of being overweight or obese in middle-aged and older adults in China was associated with long-term exposure to higher levels of PM2.5 and NO2. This risk was reduced through NDVI exposure, and the associations were partially mediated by air pollutants. To verify these findings, fine-scale studies are needed.

Does air pollution modify temperature-related mortality? A systematic review and meta-analysis.

INTRODUCTION: There is an increasing interest in understanding whether air pollutants modify the quantitative relationships between temperature and health outcomes. The results of available studies were, however, inconsistent. This study aims to sum up the current evidence and provide a comprehensive understanding of this topic. METHODS: We conducted an electronic search in PubMed (MEDLINE), EMBASE, Web of Science Core Collection, and ProQuest Dissertations and Theses. The modified Navigation Guide was applied to evaluate the quality and strength of evidence. We calculated pooled temperature-related mortality at low and high pollutant levels respectively, using the random-effects model. RESULTS: We identified 22 eligible studies, eleven of which were included in the meta-analysis. Significant effect modification was observed on heat effects for all-cause and non-accidental mortality by particulate matter with an aerodynamic diameter of <10 µm (PM10) and ozone (O3) (p < 0.05). The excess risks (ERs) for all-cause and non-accidental mortality were 5.4% (4.4%, 6.4%) and 6.3% (4.8%, 7.8%) at the low PM10 level, 8.8% (7.5%, 10.1%) and 11.4% (8.7%, 14.2%) at the high PM10 level, respectively. As for O3, the ERs for all-cause and non-accidental mortality were 5.1% (3.9%, 6.3%) and 3.6% (0.1%, 7.2%) at the low O3 level, 7.6% (6.3%, 9.0%) and 12.5% (4.7%, 20.9%) at the high O3 level, respectively. Surprisingly, the heat effects on cardiovascular mortality were found to be lower at high carbon monoxide (CO) levels [ERs = 5.4% (3.9%, 6.9%)] than that at low levels [ERs = 9.4% (7.0%, 11.9%)]. The heterogeneity varied, but the results of sensitivity analyses were generally robust. Significant effect modification by air pollutants was not observed for heatwave or cold effects. CONCLUSIONS: PM10 and O3 modify the heat-related all-cause and non-accidental mortality, indicating that policymakers should consider air pollutants when establishing heat-health warning systems. Future studies with comparable designs and settings are needed.

Artificial light at night, MRI-based measures of brain iron deposition and incidence of multiple mental disorders.

BACKGROUND: Epidemiologic evidence on whether iron accumulation in brain modified the association between artificial light at night (ALAN) and incident mental disorders is lacking. The authors aims to investigate modification of brain iron deposition on the associations of ALAN with multiple mental disorders in the middle-aged and older adults. METHODS: This prospective study used data from the UK Biobank. ALAN was drawn from satellite datasets. Susceptibility-weighted magnetic resonance imaging was used to ascertain iron content of each brain region. T2* signal loss was used as indices of iron deposition. The main outcomes are impacts of ALAN exposure on onset of wide spectrum of physician-diagnosed mental disorders, which was estimated by time-varying Cox proportional hazard model. The authors further conducted stratified analyses by levels of iron brain deposition to examine the potential modifying effects. RESULTS: Among 298,283 participants followed for a median of 10.91 years, higher ALAN exposure was associated with increased risk of mental disorders. An IQR (11.37 nW/cm2/sr) increase in annual levels of ALAN was associated with an HR of 1.050 (95 % CI: 1.034,1.066) for any mental disorder, 1.076 (95 % CI: 1.053,1.099) for substance use disorder, and 1.036 (95 % CI: 1.004,1.069) for depression disorder in fully adjusted models. The exposure-response curves showed steeper trends at lower ALAN levels and a plateau at higher exposures. The associations were stronger in participants with high iron deposition in left hippocampus, left accumbens and left pallidum. CONCLUSIONS: ALAN was associated with multiple mental disorders in the middle-aged and older adults, and the findings indicated stricter standards of ALAN is needed and targeted preventive measures are warranted, especially with high brain iron deposition.

The Improvement of Air Quality and Associated Mortality during the COVID-19 Lockdown in One Megacity of China: An Empirical Strategy.

Although the lockdown policy implemented during the COVID-19 pandemic indeed improved the air quality and reduced the related health risks, the real effects of the lockdown and its resulting health risks remain unclear considering the effects of unobserved confounders and the longstanding efforts of the government regarding air pollution. We compared air pollution between the lockdown period and the period before the lockdown using a difference-in-differences (DID) model and estimated the mortality burden caused by the number of deaths related to air pollution changes. The NO2 and CO concentrations during the lockdown period (17 days) declined by 8.94 µg/m3 (relative change: 16.94%; 95% CI: 3.71, 14.16) and 0.20 mg/m3 (relative change: 16.95%; 95% CI: 0.04, 0.35) on an average day, respectively, and O3 increased by 8.41 µg/m3 (relative change: 32.80%; 95% CI: 4.39, 12.43); no meaningful impacts of the lockdown policy on the PM2.5, PM10, SO2, or the AQI values were observed. Based on the three clearly changed air pollutants, the lockdown policy prevented 8.22 (95% CI: 3.97, 12.49) all-cause deaths. Our findings suggest that the overall excess deaths caused by air pollution during the lockdown period declined. It is beneficial for human health when strict control measures, such as upgrading industry structure and promoting green transportation, are taken to reduce emissions, especially in cities with serious air pollution in China, such as Shijiazhuang.

Suppression of miR-451a accelerates osteogenic differentiation and inhibits bone loss via Bmp6 signaling during osteoporosis.

Bone homeostasis is known as a dynamic balance, including bone formation through osteoblasts and bone resorption by osteoclasts. MicroRNAs (miRs) play a critical role in regulating bone formation and homeostasis. In the study, the effects of miR-451a on bone homeostasis were investigated. The results indicated that the primary osteoblasts and mesenchymal stem cells (MSCs), as the main source of osteoblasts, isolated from miR-451a-knockout (KO) mice showed promoted osteogenesis. in vivo, an ovariectomized (OVX) animal model was used to further explore the effect of miR-451a on osteoporosis. Micro-computed tomography (µCT) indicated a promoted bone volume in miR-451a-KO mice compared to wild-type (WT) mice after OVX operation, demonstrating a redundant bone formation after the knockout of miR-451a. Importantly, we for the first time found that bone morphogenetic protein 6 (Bmp6) was a direct target of miR-451a, elevating bone formation through regulating SMAD1/5/8 expression. In conclusion, reducing miR-451a expression levels could enhance bone formation during the progression of osteoporosis, which might be at least partly via the meditation of Bmp6 expression.

The SWI/SNF subunit SWI3B regulates IAMT1 expression via chromatin remodeling in Arabidopsis leaf development.

The SWI/SNF complex is crucial to chromatin remodeling in various biological processes in different species, but the distinct functions of its components in plant development remain unclear. Here we uncovered the role of SWI3B, a subunit of the Arabidopsis thaliana SWI/SNF complex, via RNA interference. Knockdown of SWI3B resulted in an upward-curling leaf phenotype. Further investigation showed that the RNA level of IAA carboxyl methyltransferase 1 (IAMT1), encoding an enzyme involved in auxin metabolism, was dramatically elevated in the knockdown (SWI3B-RNAi) plants. In addition, activation of IAMT1 produced a leaf-curling phenotype similar to that of the SWI3B-RNAi lines. Database analysis suggested that the last intron of IAMT contains a site of polymerase V (Pol V) stabilized nucleosome, which may be associated with SWI3B. Data from a micrococcal nuclease (MNase) digestion assay showed that nucleosome occupancy around this site was downregulated in the leaves of SWI3B-RNAi plants. In addition, knockdown of IAMT1 in the SWI3B-RNAi background repressed the abnormal leaf development. Thus, SWI3B-mediated chromatin remodeling is critical in regulating the expression of IAMT1 in leaf development.