A growing number of extreme climate events are occurring in the setting of ongoing climate change, with an increase in both the intensity and frequency. It has been shown that ambient temperature ...challenges have a direct and highly varied impact on cardiovascular health. With a rapidly growing amount of literature on this issue, we aim to review the recent publications regarding the impact of cold and heat on human populations with regard to cardiovascular disease (CVD) mortality/morbidity while also examining lag effects, vulnerable subgroups, and relevant mechanisms. Although the relative risk of morbidity/mortality associated with extreme temperature varied greatly across different studies, both cold and hot temperatures were associated with a positive mean excess of cardiovascular deaths or hospital admissions. Cause-specific study of CVD morbidity/mortality indicated that the sensitivity to temperature was disease-specific, with different patterns for acute and chronic ischemic heart disease. Vulnerability to temperature-related mortality was associated with some characteristics of the populations, including sex, age, location, socioeconomic condition, and comorbidities such as cardiac diseases, kidney diseases, diabetes, and hypertension. Temperature-induced damage is thought to be related to enhanced sympathetic reactivity followed by activation of the sympathetic nervous system, renin-angiotensin system, as well as dehydration and a systemic inflammatory response. Future research should focus on multidisciplinary adaptation strategies that incorporate epidemiology, climatology, indoor/building environments, energy usage, labor legislative perfection, and human thermal comfort models. Studies on the underlying mechanism by which temperature challenge induces pathophysiological response and CVD await profound and lasting investigation.
Both ozone exposure and extreme temperatures are found to be significantly associated with mortality; however, inconsistent results have been obtained on the modification effects of temperature on ...the ozone–mortality association. In the present study, we conducted a nationwide time-series analysis in 128 counties from 2013–2018 to examine whether temperature modifies the association between short-term ozone exposure with nonaccidental and cause-specific mortality in China. First, we analyzed the effects of ozone exposure on mortality at different temperature levels. Then, we calculated the pooled effects through a meta-analysis across China. We found that high-temperature conditions (>75th percentile in each county) significantly enhanced the effects of ozone on nonaccidental, cardiovascular, and respiratory mortality, with increases of 0.44% (95% confidence interval (CI): 0.36 and 0.51%), 0.42% (95% CI: 0.32 and 0.51%) and 0.50% (95% CI: 0.31 and 0.68%), respectively, for a 10 μg/m3 increase in ozone at high temperatures. Stronger effects on nonaccidental and cardiovascular mortality were observed at high temperatures among elderly individuals aged 65 years and older compared with the younger people. Our findings provide evidence that health damage because of ozone may be influenced by the impacts of increasing temperatures, which point to the importance of mitigating ozone exposure in China under the context of climate change to further reduce the public health burden.
Bioaugmented zeolite-biological aerated filters (Z-BAFs), i.e. adding isolated degrading bacteria into the BAFs with zeolite as fillings, were designed to treat coking wastewater containing high ...concentrations of pyridine and quinoline and to explore the bacterial community of biofilm on the zeolite surface. The investigation was carried out for 91 days of column operation and the treatment of pyridine, quinoline, total organic carbon (TOC), and ammonium was shown to be highly efficient by bioaugmentation and adsorption. Biomass determination and bacterial diversity detection based on 16S rDNA and rRNA techniques supported the treatment data and indicated that bioaugmentation could recover the bacterial richness and diversity from pyridine and quinoline loading shocks. However, bioaugmentation accelerated the shift of the bacterial community structure resulting in a more distinct difference from the starting community. Clone library analysis revealed that pyridine and quinoline were more harmful to Bacterodietes among all ingenious bacteria, and bioaugmentation promoted the growth of Planctomycetes in the biofilm. Moreover, the introduced bacteria did not remain dominant in the bioaugmented biofilm, indicating the indigenous degrading bacteria played the most significant role in the treatment. This bioaugmented Z-BAF method was shown to be an alternative technology for the treatment of wastewater containing pyridine and quinoline or other N-heterocyclic aromatic compounds.
Many multi-center epidemiological studies have robustly examined the acute health effects of exposure to low concentrations of fine particulate matter (PM2.5) on cardiovascular mortality in developed ...counties. However, data limitations have resulted in few related studies being conducted in developing counties with high levels of PM2.5 exposure. In recent years, people in China with a heavy cardiovascular disease burden have been exposed to particularly high levels of PM2.5.
We conducted a multi-county time series study investigating the acute effects of PM2.5 on the increased risk of cardiovascular death across China, and explored subpopulations susceptible to PM2.5 exposure.
Appling a county-specific Poisson regression in 30 Chinese counties, we estimated PM2.5 effects on all-cause mortality and cause-specific mortality of cardiovascular health for 2013–2015. We also considered PM2.5 effects on several subpopulations, including males, females, and three age groups (< 65, 65–74 and > 74 years old). We pooled the county-specific results across China using a random effects meta-analysis by cause and by subpopulation.
We found a 0.13% (95% confidence interval (CI), 0.04–0.22) increase in all-cause mortality, a 0.12% increase (95% CI, 0.001–0.25) increase in cardiovascular disease (CVD), a 0.42% (95% CI, 0.03–0.81) increase in AMI, a 0.17% (95% CI, −0.04–0.40) increase in coronary heart disease, and a 0.13% (95% CI, −0.12–0.33) increase in stroke in association with a 10-μg/m3 increase in PM2.5 concentrations on the same day. The magnitudes of the associations were less than those reported in developed counties with lower PM2.5 levels. A vulnerable effect on all-cause mortality was observed in the elderly population (older than 65 years) and on CVD in males.
This study showed the positive magnitude of PM2.5 effects with high exposure on all natural, CVD, and cause-specific mortality and on the susceptible populations in China. The findings complemented evidence related to exposure-mortality relationships at the higher end of short-term exposure to PM2.5 on a global scale.
•Exploring the association between PM2.5 and cardiovascular mortality in China.•Suggesting that people 65–74 years old and males might be more vulnerable to PM2.5.•Showing the difference of PM2.5 acute effect between developed countries and China.
ObjectiveTo examine cardiovascular disease (CVD) mortality burden attributable to ambient temperature; to estimate effect modification of this burden by gender, age and education level.MethodsWe ...obtained daily data on temperature and CVD mortality from 15 Chinese megacities during 2007–2013, including 1 936 116 CVD deaths. A quasi-Poisson regression combined with a distributed lag non-linear model was used to estimate the temperature-mortality association for each city. Then, a multivariate meta-analysis was used to derive the overall effect estimates of temperature at the national level. Attributable fraction of deaths were calculated for cold and heat (ie, temperature below and above minimum-mortality temperatures, MMTs), respectively. The MMT was defined as the specific temperature associated to the lowest mortality risk.ResultsThe MMT varied from the 70th percentile to the 99th percentile of temperature in 15 cities, centring at 78 at the national level. In total, 17.1% (95% empirical CI 14.4% to 19.1%) of CVD mortality (330 352 deaths) was attributable to ambient temperature, with substantial differences among cities, from 10.1% in Shanghai to 23.7% in Guangzhou. Most of the attributable deaths were due to cold, with a fraction of 15.8% (13.1% to 17.9%) corresponding to 305 902 deaths, compared with 1.3% (1.0% to 1.6%) and 24 450 deaths for heat.ConclusionsThis study emphasises how cold weather is responsible for most part of the temperature-related CVD death burden. Our results may have important implications for the development of policies to reduce CVD mortality from extreme temperatures.
There is increasing evidence suggesting links between exposure to environmental toxins and susceptibility to type 2 diabetes mellitus (DM). In this review, we summarize the experimental evidence to ...support this association that has been noted in many epidemiologic studies. Inflammation in response to particulate matter (PM2.5) exposure in air pollution represents a common mechanism that may interact with other pro-inflammatory influences in diet and life style to modulate susceptibility to cardiometabolic diseases. The role of innate immune cytokines released from macrophages in the lung is well known. In addition, chemokine triggers in response to air-pollution exposure may mediate a cellular response from the bone marrow/spleen through toll-like receptors (TLRs) and Nucleotide Oligomerization Domain receptors (NLRs) pathways to mediate inflammatory response in organs. Emerging data also seem to support a role for PM2.5 exposure in endoplasmic reticulum stress-induced apoptosis and in brown adipose tissue dysfunction. Decreased expression of UCP1 in brown adipose tissue may account for reduced thermogenesis providing another link between PM2.5 and insulin resistance. The implications of an experimental link between air-pollution exposure and type 2 DM are profound as air pollution is a pervasive risk factor throughout the world and even modest alleviation in exposure may provide substantial public health benefits.
Dipeptidyl-peptidase 4 (DPP-4) inhibitors are increasingly used to accomplish glycemic targets in patients with type II diabetes mellitus. Because DPP-4 is expressed in inflammatory cells, we ...hypothesized that its inhibition will exert favorable effects in atherosclerosis.
Male LDLR(-/-) mice (6 weeks) were fed a high-fat diet or normal chow diet for 4 weeks and then randomized to vehicle or alogliptin, a high-affinity DPP-4 inhibitor (40 mg · kg(-1) · d(-1)), for 12 weeks. Metabolic parameters, blood pressure, vascular function, atherosclerosis burden, and indexes of inflammation were obtained in target tissues, including the vasculature, adipose, and bone marrow, with assessment of global and cell-specific inflammatory pathways. In vitro and in vivo assays of DPP-4 inhibition (DPP-4i) on monocyte activation/migration were conducted in both human and murine cells and in a short-term ApoE(-/-) mouse model. DPP-4i improved markers of insulin resistance and reduced blood pressure. DPP-4i reduced visceral adipose tissue macrophage content (adipose tissue macrophages; CD11b(+), CD11c(+), Ly6C(hi)) concomitant with upregulation of CD163. DPP-4 was highly expressed in bone marrow-derived CD11b(+) cells, with DPP-4i downregulating proinflammatory genes in these cells. DPP-4i decreased aortic plaque with a striking reduction in plaque macrophages. DPP-4i prevented monocyte migration and actin polymerization in in vitro assays via Rac-dependent mechanisms and prevented in vivo migration of labeled monocytes to the aorta in response to exogenous tumor necrosis factor-α and DPP-4.
DPP-4i exerts antiatherosclerotic effects and reduces inflammation via inhibition of monocyte activation/chemotaxis. These findings have important implications for the use of this class of drugs in atherosclerosis.
Background & Aims Air pollution is a global challenge to public health. Epidemiological studies have linked exposure to ambient particulate matter with aerodynamic diameters <2.5 μm (PM2.5 ) to the ...development of metabolic diseases. In this study, we investigated the effect of PM2.5 exposure on liver pathogenesis and the mechanism by which ambient PM2.5 modulates hepatic pathways and glucose homeostasis. Methods Using “Ohio’s Air Pollution Exposure System for the Interrogation of Systemic Effects (OASIS)-1”, we performed whole-body exposure of mice to concentrated ambient PM2.5 for 3 or 10 weeks. Histological analyses, metabolic studies, as well as gene expression and molecular signal transduction analyses were performed to determine the effects and mechanisms by which PM2.5 exposure promotes liver pathogenesis. Results Mice exposed to PM2.5 for 10 weeks developed a non-alcoholic steatohepatitis (NASH)-like phenotype, characterized by hepatic steatosis, inflammation, and fibrosis. After PM2.5 exposure, mice displayed impaired hepatic glycogen storage, glucose intolerance, and insulin resistance. Further investigation revealed that exposure to PM2.5 led to activation of inflammatory response pathways mediated through c-Jun N-terminal kinase (JNK), nuclear factor kappa B (NF-κB), and Toll-like receptor 4 (TLR4), but suppression of the insulin receptor substrate 1 (IRS1)-mediated signaling. Moreover, PM2.5 exposure repressed expression of the peroxisome proliferator-activated receptor (PPAR)γ and PPARα in the liver. Conclusions Our study suggests that PM2.5 exposure represents a significant “hit” that triggers a NASH-like phenotype and impairs hepatic glucose metabolism. The information from this work has important implications in our understanding of air pollution-associated metabolic disorders.
Although existing studies have linked high temperature to mortality in a small number of regions, less evidence is available on the variation in the associations between high temperature exposure and ...cause-specific mortality of multiple regions in China. Our study focused on the use of time series analysis to quantify the association between high temperature and different cause-specific mortalities for susceptible populations for 43 counties in China. Two-stage analyses adopting a distributed lag non-linear model (DLNM) and a meta-analysis allowed us to obtain county-specific estimates and national-scale pooled estimates of the nonlinear temperature-mortality relationship. We also considered different populations stratified by age and sex, causes of death, absolute and relative temperature patterns, and potential confounding from air pollutants. All of the observed cause-specific mortalities are significantly associated with higher temperature. The estimated effects of high temperature on mortality varied by spatial distribution and temperature patterns. Compared with the 90th percentile temperature, the overall relative risk (RR) at the 99th percentile temperature for non-accidental mortality is 1.105 (95%CI: 1.089, 1.122), for circulatory disease is 1.107 (95%CI: 1.081, 1.133), for respiratory disease is 1.095 (95%CI: 1.050, 1.142), for coronary heart disease is 1.073 (95%CI: 1.047, 1.099), for acute myocardial infarction is 1.072 (95%CI: 1.042, 1.104), and for stroke is 1.095 (95%CI: 1.052, 1.138). Based on our findings, we believe that heat-related health effect in China is a significant issue that requires more attention and allocation of existing resources.
•Heat effects for cause-specific mortality in 43 Chinese counties are estimated.•The first evidence of heat effects for six different causes of mortality in multi-center studies.•We examine how heat effects vary across diverse climates patterns.
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