Genetic risk modifies the effect of long-term fine particulate matter exposure on coronary artery disease.

BACKGROUND: Although both environmental and genetic factors were linked to coronary artery disease (CAD), the extent to which the association of air pollution exposure with CAD can be influenced by genetic risk was not well understood. METHODS: A total of 41,149 participants recruited from the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR) were included. Genetic risk scores of CAD were constructed based on 540 genetic variants. Long-term PM2.5 exposures were assessed by adopting satellite-based PM2.5 estimations at 1-km resolution. We used stratified Cox proportional hazards regression model to examine the impact of PM2.5 exposure and genetic risk on CAD risk, and further analyzed modification effect of genetic predisposition on association between PM2.5 exposure and CAD risk. RESULTS: During a median of 13.01 years of follow-up, 1,373 incident CAD events were observed. Long-term PM2.5 exposure significantly increased CAD risk, and the hazard ratios (HRs) [95% confidence intervals (CIs)] were 1.27 (1.05-1.54) and 1.95 (1.57-2.42) among intermediate and high PM2.5 exposure groups compared to low PM2.5 exposure group. The relative risks of CAD were 40% (HR: 1.40, 95%CI: 1.18-1.66) and 133% (HR: 2.33, 95%CI: 1.94-2.79) higher among individuals at intermediate and high genetic risk than those at low genetic risk. Compared with individuals with both low genetic risk and low PM2.5 exposure, those with high genetic risk and high PM2.5 exposure had highest CAD risk, with HR of 4.37 (95%CI: 3.13-6.11). We observed significant multiplicative (P < 0.001) and additive interaction [relative excess risk due to interaction (95%CI): 2.75 (1.32-4.20); attributable proportion due to interaction (95%CI): 0.56 (0.42-0.70)] between genetic risk and PM2.5 exposure on CAD. CONCLUSION: This study provided evidence that long-term PM2.5 exposure might increase CAD risk, especially among people at high genetic risk. Our findings highlighted the importance of taking strategies on air quality improvement to cardiovascular disease prevention.

Characteristics of the source apportionment of primary and secondary inorganic PM2.5 in the Pearl River Delta region during 2015 by numerical modeling.

Fine particulate matter (PM2.5) contains both primary and secondary components, and their source apportionment characteristics in the Pearl River Delta (PRD) region during 2015 were compared by applying an air quality model coupled with an on-line tracer-tagged module. The results of contributions from different source regions to primary PM2.5 (PPM2.5) and secondary inorganic PM2.5 (SIPM2.5) in four selected cities show that the effect of regional transport on the SIPM2.5 level is stronger than that on the PPM2.5 level in the PRD region. For both Guangzhou city and the average of the entire PRD region, the industrial (25-40%) and transportation (20-25%) sectors are major sources of PPM2.5 and SIPM2.5. However, the residential sector contributes approximately 25% to the PPM2.5 level, mainly from residential biomass burning, but accounts for only approximately 10% of the SIPM2.5 level. The relative importance of each sector to the contributions from local and regional transport indicates that industrial emissions appear to lead to regional air pollution, while the transportation emissions seem to mainly affect the local and surrounding areas. Considering the impact of regional contributions to air quality, efforts made to reduce emissions in each city could not only improve the local air quality but also benefit downstream regions. To further decrease the PM2.5 level, the local government of each city in the PRD region should not only continue to strengthen the control of local emissions, such as those from transportation and residential biomass burning, but also increase their focus on regional joint prevention and control strategies with upstream area (such as northern Guangdong Province, and Jiangxi, Fujian and Hunan provinces).

Modeling study of ozone source apportionment over the Pearl River Delta in 2015.

In recent years, the concentration of fine particulate matter has decreased gradually in the Pearl River Delta (PRD) region, but the ozone (O3) concentration remains high and has become the primary air pollutant. In this study, using a three-dimensional numerical model [nested air quality prediction modeling system (NAQPMS)] coupled with an on-line source apportionment module, the contribution of different source regions and source categories to the O3 concentration in the PRD region was quantified. A comparison with observation data confirmed that the NAQPMS adequately reproduced surface O3 concentrations in different seasons. Compared with biogenic emissions, anthropogenic precursors play a dominant role in O3 production. In Guangzhou city, among different source categories, mobile emission is the largest contributor (accounting for approximately 40%), followed by industry emissions (20%-24%). Regional control measures for solvent use and mobile emissions are effective for reducing O3 concentration. In the PRD region, self-contribution is more significant in daytime (∼40%) than in nighttime (∼10%) on average. Among the source regions outside PRD, the northern part of Guangdong province, Jiangxi province, and Fujian province are important contributors. Within the PRD region, the self-contribution of each city increases by 12%-32% during O3 episodes (>80 ppbv) compared with the annual mean contribution. The contribution of the entire PRD region and the entire Guangdong province is 46%-63% and 63%-74% in PRD cities during O3 episodes. These results indicate that regional collaboration on emission control within PRD or Guangdong province is effective for reducing O3 episodes in the PRD region. In addition, because long-range transport from regions outside Guangdong province played an important role in the O3 concentration in the PRD region, long-term emission control measures throughout China in subsequent years should be propitious to further reduce the annual O3 level and improve air quality in the PRD region.

Neuroprotective effects of Rhizoma Dioscoreae polysaccharides against neuronal apoptosis induced by in vitro hypoxia.

Rhizoma Dioscoreae polysaccharides (RDPS) are the primary active ingredient of Rhizoma Dioscoreae, which is a traditional Chinese medicine. RDPS have previously been shown to scavenge reactive oxygen species, and protect against D-galactose-induced mimetic aging. The present study aimed to investigate the neuroprotective effects of RDPS against hypoxia-induced neuronal cell apoptosis. Neuronal cells harvested from pregnant Sprague-Dawley rats were divided into groups, as follows: i) Normal control group; ii) hypoxia-induced apoptosis neuronal cell model; iii) 0.025 g/l RDPS-treated group; iv) 0.05 g/l RDPS-treated group; v) 0.1 g/l RDPS-treated group; and vi) 0.25 g/l RDPS treated group. Neuronal cell viability was investigated using an MTT assay, and neuronal cell apoptosis was analyzed using Annexin V-fluorescein isothiocyanate/propidium iodide double-staining, Hoechst 33342 fluorescent staining, Rhodamine 123 staining, polymerase chain reaction and immunocytochemical staining. The RDPS-treated neuronal cells exhibited improved viability, and decreased hypoxia-induced mitochondrial injury and apoptosis. In addition, the mRNA and protein expression levels of caspase-3 and B-cell lymphoma (Bcl)-2-associated X protein (Bax) were significantly downregulated, whereas the mRNA and protein expression levels of Bcl-2 were significantly upregulated, in the RDPS-treated hypoxic neurons, as compared with the apoptosis model (P<0.05). Furthermore, the ratio of Bcl-2 expression:Bax expression significantly increased following RDPS treatment, as compared with the apoptosis model (P<0.05). The results of the present study suggested that RDPS may attenuate hypoxia-induced neuronal cell apoptosis by altering the expression levels of key apoptosis-regulating proteins in hypoxic neurons.