Progress of ambient air pollution and cardiovascular disease research in Asia

Asian countries are with deteriorating air quality accompanying the rapid economic and social development of the past decades, and the potential health impacts of air pollution have been noticed by researchers in the region. We reviewed the scientific literature on air pollution and cardiovascular diseases (CVD) published by Asian researchers in English since the 1980s to determine whether the findings in Europe and North America can be extrapolated to Asia. Epidemiological studies show that short-term particulate matter pollution is a strong predictor for CVD morbidity and mortality and suggestive on cerebrovascular morbidity and mortality in newly developed countries in Asia. Multicountry epidemiological studies are needed to fully appreciate the extent of air pollution on CVD in Asia, especially less developed Asian countries. New cohort studies should be initiated to improve our understanding of particulate matter's toxicological pathways, long-term exposure effects, and gene-environment interaction on CVD among the Asian population.     

Gene-air pollution interaction and cardiovascular disease: a review

Genetic susceptibility is likely to play a role in response to air pollution. Hence, gene-environment interaction studies can be a tool for exploring the mechanisms and the importance of the pathway in the association between air pollution and a cardiovascular outcome.In this article, we present a systematic review of the studies that have examined gene-environment interactions in relation to the cardiovascular health effects of air pollutants.We identified 16 articles meeting our search criteria. Of these studies, most have focused on individual functional polymorphisms or individual candidate genes. Moreover, they were all based on 3 study populations that have been extensively investigated in relation to air pollution effects: the Normative Aging Study, Air Pollution and Inflammatory Response in Myocardial Infarction Survivors: Gene-Environment Interaction in a High Risk Group, and Multiethnic Study of Atherosclerosis.In conclusions, the studies differed substantially in both the cardiovascular outcomes examined and the polymorphisms examined, so there is little confirmation of results across cohorts. Gene-environment interaction studies can help explore the mechanisms and the potential pathway in the association between air pollution and a cardiovascular outcome; replication of findings and studies involving multiple cohorts would be needed to draw stronger conclusions.     

Detrimental correlation between air pollution with skin aging in Taiwan population

Dissecting the complex relationships between skin aging and air pollution has been an ongoing effort. The increased exposure to air pollution over time imposed a negative effect on skin. This study explores the correlation between skin aging in the Asian population and levels of air pollutants to show different relationship between the two. This study was retrospective and included 389 patients, age between 30 and 74, who planned to receive a session of laser treatment for skin disorders in Kaohsiung Medical University Hospital (KMUH) from 2006 to 2019. Preoperative skin condition quantified by VISIA Complexion Analysis System (Canfield Imaging Systems, Fierfield, NJ, US). Eight air pollutants such as carbon monoxide (CO), non-methane hydrocarbon (NMHC), nitrogen oxides (NO, NO₂, and NO_x), particulate matters (PM2.5 and PM10), ozone (O₃), sulfur dioxide (SO₂) and 8 skin condition such as spots, wrinkles, textures, pores, ultraviolet spots (UV spots), brown spots, red area, and porphyrin were analyzed to explore correlation between air pollution and skin aging. Strong correlation was found between NMHC exposure and texture, pores and brown spots formation. A positive correlation between O₃ and better VISIA texture and pores scores was found. Brown spots was found to negatively associate with CO, NMHC, NO₂, NO_x, PM10, PM2.5, and SO₂. The skin condition of population over age 45 affected by CO, NMHC, NO₂, NO_x, PM2.5, PM10, and SO₂. Skin condition of the bottom 10% strongly correlates with exposure to PM10 and SO₂, whereas skin condition of the top 10% was affected by PM10. Air pollutants such as CO, NO₂, NO_x, PM2.5, PM10, SO₂, and NMHC were found to correlate with negative skin quality strongly. In contrast, O₃ exposure is associated with less texture and pores. Future studies are warranted to further appreciate the relationships between air pollutants and skin condition.     

Cool and dry weather enhances the effects of air pollution on emergency IHD hospital admissions

Background

Associations between ambient pollution and cardiovascular morbidity including ischemic heart disease (IHD) have been confirmed. Weather factors such as temperature, season and relative humidity (RH) may modify the effects of pollution. We conducted this study to examine the effects of air pollution on emergency IHD hospital admissions varied across seasons and RH levels, and to explore the possible joint modification of weather factors on pollution effects.

Methods

Daily time series of air pollution concentrations, mean temperature and RH were collected from IHD hospital admissions from 1998 to 2007 in Hong Kong. We used generalized additive Poisson models with interaction term to estimate the pollution effects varied across seasons and RH levels, after adjusting for time trends, weather conditions, and influenza outbreaks.

Results

An increase in the detrimental effects of air pollution in cool season and on low humidity days was observed. In the cool and dry season, a 10 μg/m³ increment of lag₀₃ exposure was associated with an increase of emergency IHD admissions by 1.82% (95% CI: 1.24–2.40%), 3.89% (95% CI: 3.08–4.70%), and 2.19% (95% CI: 1.33–3.06%) for particles with an aerodynamic diameter less than 10 μm (PM₁₀), nitrogen dioxide (NO₂), and ozone (O₃), respectively. The effects of pollutants decreased greatly and lost statistical significance in the warm and humid season.

Conclusions

We found season and RH jointly modified the associations between ambient pollution and IHD admissions, resulting in increased IHD admissions in the cool and dry season and reduced admissions in the warm and humid season.     

Estimated personal soot exposure is associated with acute myocardial infarction onset in a case-crossover study

The current study investigates the association of estimated personal exposure to traffic-related air pollution and acute myocardial infarction (AMI). Cases of AMI were interviewed in the Augsburg KORA Myocardial Infarction Registry from February 1999 through December 2003, and 960 AMI survivors were included in the analyses. The time-varying component of daily personal soot exposure (the temporally variable contribution due to the daily area level of exposure and daily personal activities) was estimated using a linear combination of estimated mean ambient soot concentration, time spent outdoors, and time spent in traffic. The association of soot exposure with AMI onset was estimated in a case-crossover analysis controlling for temperature and day of the week using conditional logistic regression analyses. Estimated personal soot exposure was associated with AMI (relative risk, 1.30 per 1.1 m⁻¹ × 10⁻⁵ [95% confidence interval, 1.09-1.55]). Estimated ambient soot and measured ambient PM_2.5 particulate matter 2.5 µm and smaller in aerodynamic diameter were not significantly associated with AMI onset. Our results suggest that an increase in risk of AMI in association with personal soot exposure may be in great part due to the contribution of personal soot from individual times spent in traffic and individual times spent outdoors. As a consequence, estimates calculated based on measurements at urban background stations may be underestimations. Health effects of traffic-related air pollution may need to be updated, taking into account individual time spent in traffic and outdoors, to adequately protect the public.     

Cholesteryl ester transfer protein genetic polymorphisms, HDL cholesterol, and subclinical cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis

The cholesteryl ester transfer protein (CETP) plays a key role in high-density lipoprotein (HDL) metabolism. Genetic variants that alter CETP activity and concentration may cause significant alterations in HDL-cholesterol (HDL-C) concentration; however, controversies remain about whether these genetic variants are associated with atherosclerosis. We genotyped the CETP R451Q, A373P, −629C/A, Taq1B, and −2505C/A polymorphisms in a cohort of Caucasian, Chinese, African-American, and Hispanic individuals within the Multi-Ethnic Study of Atherosclerosis. Genotypes were examined in relationship to HDL-C, CETP activity, CETP concentration, and three measures of subclinical cardiovascular disease (CVD): coronary artery calcium (CAC) measured by fast CT scanning, carotid intimal-medial thickness (IMT), and carotid artery plaque measured by ultrasonography. Carriers of the 451Q and 373P alleles have a significantly higher CETP concentration (22.4% and 19.5%, respectively; p < 0.001) and activity (13.1% and 9.4%, respectively; p < 0.01) and lower HDL-C (5.6% and 6.0%, respectively; p < 0.05). The minor alleles of the R451Q and A373P polymorphisms are associated with the presence of CAC, even after adjusting for CVD risk factors and HDL-C (p = 0.006 and p = 0.01, respectively). The R451Q polymorphism is also associated with presence of carotid artery plaque (p = 0.036). Polymorphism is associated with neither common nor internal carotid IMT. We confirmed that the −629A, Taq1B B2, and −2505A alleles are significantly associated with lower CETP concentration (20.8%, 25.0%, and 23.7%, respectively; p < 0.001) and activity (14.8%, 19.8%, and 18.4%, respectively; p < 0.001) and higher HDL-C concentration (9.7%, 11.5%, and 10.4%, respectively; p < 0.01). However, we did not find any associations between these non-coding polymorphisms and subclinical CVD.     

细颗粒物暴露与心血管疾病队列研究进展

细颗粒物(PM2.5)的暴露与心血管疾病具有较强的相关性,是心血管疾病发生和加重过程中可控的危险因素。PM2.5来源广泛,组成成分复杂,可通过多种生物学机制引起心血管疾病的发生、发展。本文主要综述国内外基于人群的队列研究,评价PM2.5对心血管疾病的慢性效应,并总结了PM2.5健康危害的干预研究,并提出了我国探索PM2.5对心血管疾病慢性效应研究的局限性,为心血管疾病防治提供一些参考和依据。     

PM2.5激活内质网应激诱导肺组织细胞凋亡对慢性阻塞性肺疾病大鼠的影响

目的：探讨PM2.5的暴露是否激活内质网应激诱导肺组织细胞凋亡及其对 COPD大鼠的影响。方法将40只健康的雄性 SD 大鼠[体质量为(200±20)g]按随机数字表法分为对照组(N组)、PM2.5组(P组)、COPD模型组(C组)、COPD+PM2.5组(C+P 组)。采取熏烟联合两次气管内注入脂多糖(LPS)(200μg/100μl)法建造 COPD大鼠模型,C+P 组在构建 COPD模型基础上给予气管内注入PM2.5混悬液(5 mg/kg,体积0.25 ml/kg),P 组大鼠给予气管内注入等量PM2.5混悬液,N组给予气管内滴注相同体积生理盐水。模型建立结束后,检测各组大鼠的肺功能;行 HE染色,观察各组肺组织病理学改变;TUNEL法测定肺结构细胞的凋亡程度;免疫组织化学检测肺组织中 GRP78、ATF6和CHOP蛋白的表达;Real-time RT-PCR检测CHOP mRNA表达水平。结果①肺功能：C+P组 FEV0.3/FVC (%)、呼气峰流速均较其余3组显著降低(P<0.05),C组与 P 组及 N 组比较明显下降(P <0.05),而 P 组与 N 组比较结果尚不能认为差异有统计学意义(P >0.05)。②HE染色：N组大鼠肺组织结构正常;P 组肺组织结构基本比较完整,肺泡间隔破坏不明显,与 N组比较,支气管管壁周围有明显的炎性细胞浸润;C 组肺组织结构不完整,破坏明显,肺泡壁变薄、断裂,肺泡腔扩大,有的融合成肺大疱,支气管黏膜上皮细胞坏死、部分脱落,管壁周围有大量的炎性细胞浸润;C+P 组肺组织结构破坏程度较 C 组更加严重。③肺组织细胞凋亡：P 组、C组、C+P组细胞凋亡率均较 N 组升高(P <0.05),其中 C 组凋亡率明显高于 P 组(P <0.05), C+P组较C组进一步升高(P<0.05)。④免疫组织化学：GRP78、ATF6和CHOP均主要表达于支气管上皮细胞、肺泡上皮细胞及血管内皮细胞,而前两者主要表达于胞浆内,后者主要表达于胞核内。N组肺组织中 GRP78、ATF6和CHOP蛋白均无明显表达或极少量表达,而在 P 组、C组及 C+P组这三种蛋白的表达均较 N组升高(P<0.05),其中 C组较 P 组均显著升高(P <0.05),C+P组较C组均进一步升高(P <0.05)。⑤Real-time RT-PCR 结果：P 组、C 组及 C+P 组 CHOP mRNA表达含量均较 N组增高(P<0.05),其中C组较P组明显增高(P<0.05),C+P组较C组则进一步增高(P<0.05)。结论 PM2.5暴露可激活内质网应激途径诱导肺组织细胞凋亡,从而促进COPD加重和发展。     

The association between air pollution level and breast cancer risk in Taiwan

Breast cancer has the highest incidence of cancer among women in Taiwan, and air pollutants have been documented to have multiple adverse effects on human health. There is no relevant data, there has been no research in Taiwan to discuss the relevance of air pollutants to breast cancer, and evidence is sparse and inconclusive.Air quality data used in this study was collected from the 78 air quality monitoring stations situated in 74 municipalities in Taiwan during 2000 to 2011. The daily measurements taken at each monitoring station represented the level of exposure for each participant residing in that zone. The air pollution concentration is partitioned based on the concentration level in Quartile. We calculate the annual average air pollutants concentration (CO, NO, NO₂, PM_2.5, THC, and CH₄) and the long-term average exposure levels of these pollutants until diagnosis of breast cancer, ending the study period for each individual.Patients who were living in areas with the highest air pollutants concentration (Quartile 4) had the most people diagnosed with breast cancer (CO:1.47%, NO:1.41%, NO₂:1.63%, PM_2.5:0.91%, THC:1.53%, CH₄:2.33%). The patients who were exposed to Quartile 1 level of CO, NO, and NO₂ concentration were the oldest, and other patients who were exposed to Quartile 4 level of CO, NO, and NO₂ concentration were living in the areas of highest urbanization. Participants exposed to Quartile 4 level concentrations of air pollutants were associated with highest hazards ratios for breast cancer incidences.Most participants who were exposed to the high concentration of air pollutants (CO, THC and CH₄) had a significantly higher risk of breast cancer. If we can improve air pollution in the environment, we can reduce the incidence of breast cancer and save precious medical resources.     

Exposure to ambient air particulate matter and non-alcoholic fatty liver disease

The present study was designed to alert the public opinion and policy makers on the supposed enhancing effects of exposure to ambient air particulate matter with aerodynamic diameters < 2.5 mm (PM 2.5 ) on non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease in Western countries. For far too long literature data have been fixated on pulmonary diseases and/or cardiovascular disease, as consequence of particulate exposure, ignoring the link between the explosion of obesity with related syndromes such as NAFLD and air pollution, the worst characteristics of nowadays civilization. In order to delineate a clear picture of this major health problem, further studies should investigate whether and at what extent cigarette smoking and exposure to ambient air PM 2.5 impact the natural history of patients with obesity-related NAFLD,i.e. , development of non alcoholic steatohepatitis, disease characterized by a worse prognosis due its progression towards fibrosis and hepatocarcinoma.     

Air pollution interacts with genetic risk to influence cortical networks implicated in depression

Air pollution is a reversible cause of significant global mortality and morbidity. Epidemiological evidence suggests associations between air pollution exposure and impaired cognition and increased risk for major depressive disorders. However, the neural bases of these associations have been unclear. Here, in healthy human subjects exposed to relatively high air pollution and controlling for socioeconomic, genomic, and other confounders, we examine across multiple levels of brain network function the extent to which particulate matter (PM_2.5) exposure influences putative genetic risk mechanisms associated with depression. Increased ambient PM_2.5 exposure was associated with poorer reasoning and problem solving and higher-trait anxiety/depression. Working memory and stress-related information transfer (effective connectivity) across cortical and subcortical brain networks were influenced by PM_2.5 exposure to differing extents depending on the polygenic risk for depression in gene-by-environment interactions. Effective connectivity patterns from individuals with higher polygenic risk for depression and higher exposures with PM_2.5, but not from those with lower genetic risk or lower exposures, correlated spatially with the coexpression of depression-associated genes across corresponding brain regions in the Allen Brain Atlas. These converging data suggest that PM_2.5 exposure affects brain network functions implicated in the genetic mechanisms of depression.

More than 90% of the world’s population live in places with atmospheric exposures exceeding World Health Organization air quality guidelines (1). Ambient air pollution is a major but potentially reversible cause of global morbidity and mortality (2). Empirical evidence suggests there may also be neurotoxic effects of air pollution, especially fine particulate matter (e.g., PM_2.5) (3) that, over exposure periods of several months or more, is associated with increased risk for major depressive disorders (4, 5). These exposures have also been observed to affect cognition (6). Moreover, gene-by-environment interactions are implicated in air pollution and genetic risk for neurodegenerative disorders, potentially involving inflammatory processes (7, 8). Air pollution and inflammation may both affect mood regulation in major depression (9, 10), and indeed, inflammatory processes are implicated in putative risk genes associated with depression (11). These observations raise the possibility that air pollution may interact with depression-associated genes in influencing stress-related brain network function. While these associations at multiple levels of in vivo brain network function have yet to be reported, familial vulnerability to depression may be influenced by genetic interactions with environmental stressors (12, 13).In this study, we examine the putative effects of recent months of relatively high air pollution exposures on cognitive (14) and emotional risk factors (trait anxiety/depression) of depressive illness (15–17) and, subsequently, pollution effects on underlying cognitive and stress-related brain network function in relation to genetic risk for major depression (11). In the latter, we focus on cognition during emotional stress as a paradigm to engage frontal and cortical–subcortical networks, which have been shown to be sensitive to disruption by stress and are also implicated in depressive disorders (18). Of note, the dysfunction of prefrontal and parietal cortex circuitry during working memory (WM) occurs in patients with depression and in healthy individuals with high polygenic risk for depression (14, 18, 19). Here, we aim to further define how exposure to recent months of air pollution may affect WM, social stress, and associated brain connectivity in the context of polygenic risk for depression.We examine the behavioral risk factors for depression and associated brain networks engaged during WM under varying social stress levels in a community sample from Beijing, who were exposed to relatively high levels of air pollution (e.g., PM_2.5). These exposures varied across the study period, during which pollution levels were moderated some 33% by policy interventions on industrial emissions (20), thus providing a unique opportunity to examine demographically and genomically well-matched individuals living in similar communities with varying (but still relatively high) pollution exposures. As poorer cognition was previously associated with higher levels of air pollution exposures over 3 mo to 3 y in an independent East Asian study (6) and adverse environments over recent months may affect emotional traits associated with depression (21) and indeed air pollution exposures over similar time periods have been associated with depression (4, 5), we examined the effects of recent 6 mo PM_2.5 exposure on these behavioral characteristics, the effects of exposure on brain connectivity networks, and their interaction with polygenic risk for depression (11). We then leveraged recent developments linking live functional brain network data with postmortem gene expression data across the same brain regions (22, 23), made possible by the unique Allen Brain Atlas resource that has densely sampled genome-wide expression at multiple brain regions. Here, we surveyed spatial coexpression of depression-related genes across the human brain in the Allen Brain Atlas and the extent to which the spatial correlation of coexpression with cognitive and stress-related connectivity may differ in individuals based on levels of depression genetic risk and PM_2.5 exposure.     

The Impact of Neighborhoods on CV Risk

Cardiovascular disease (CVD) continues to be the leading cause of death and a major source of health disparities in the Unites States and globally. Efforts to reduce CVD risk and eliminate cardiovascular health disparities have increasingly emphasized the importance of the social determinants of health. Neighborhood environments have emerged as a possible target for prevention and policy efforts. Hence there is a need to better understand the role of neighborhood environments in shaping cardiovascular risk. The MESA (Multi-Ethnic Study of Atherosclerosis) Neighborhood Study provided a unique opportunity to build a comprehensive place-based resource for investigations of associations between specific features of neighborhood physical and social environments and cardiovascular risk factors and outcomes. This review summarizes the approaches used to characterize residential neighborhood environments in the MESA cohort, provides an overview of key findings to date, and discusses challenges and opportunities in neighborhood health effects research. Results to date suggest that neighborhood physical and social environments are related to behavioral and biomedical risk factors for CVD and that cardiovascular prevention efforts may benefit from taking neighborhood context into account.     

Diagnosis of fatty liver by computed tomography coronary artery calcium score

Nonalcoholic fatty liver disease may range from simple steatosis to fibrosis and cirrhosis. It is associated with the development of coronary artery calcification and appears to be an independent predictor of future adverse cardiovascular events. As the presence of a fatty liver appears to portray an independent increased risk, it may be beneficial to note this on coronary artery calcium scoring reports. Determination of fatty liver is relatively easy to perform. We discuss the method used by the Multi‐Ethnic Study of Atherosclerosis (MESA) study for determination of fatty liver from CT coronary artery calcium scoring acquisitions, which may be implemented in clinical analysis.     

The effect of pollutional haze on pulmonary function

Detrimental health effects of atmospheric exposure to ambient particulate matter (PM) have been investigated in numerous studies. Exposure to pollutional haze, the carrier of air pollutants such as PM and nitrogen dioxide (NO₂) has been linked to lung and cardiovascular disease, resulting increases in both hospital admissions and mortality. This review focuses on the constituents of pollutional haze and its effects on pulmonary function. The article presents the available information and seeks to correlate pollutional haze and pulmonary function.     

Why physicians who treat hypertension should know more about air pollution

Exposure to ambient levels of particulate matter (PM) air pollution increases the risk of a host of cardiovascular diseases and events. One potential mechanism explaining this association is that acute exposure to PM at high concentrations is capable of raising blood pressure within hours to days. Epidemiologic studies confirm that even commonly encountered levels of airborne pollutants can result in a prohypertensive response in humans. Several biologic pathways may be involved, including autonomic nervous system imbalance and arterial vascular dysfunction/vasoconstriction due to systemic oxidative stress/inflammation triggered by PM inhalation. The clinical importance of this vasopressor response and its relative role in promoting cardiovascular events associated with PM remain unclear. Because air pollution exposure is ubiquitous throughout the world, however, all health care providers and especially those who treat hypertension should be aware of this emerging and important biologic relationship.     

Whole grain intake and cardiovascular disease: a meta-analysis

Background and aimsWhole grain food sources have been associated with lowered risk of cardiovascular disease (CVD). Studies in recent years have strengthened this observation and elucidated potential mechanisms for this association. This study sought to quantitate the available observational evidence on whole grain intake and clinical cardiovascular events.Methods and resultsSeven prospective cohort studies with quantitative measures of dietary whole grains and clinical cardiovascular outcomes were identified from MEDLINE searches and a review of the literature. Based on event estimates adjusted for cardiovascular risk factors, greater whole grain intake (pooled average 2.5 servings/d vs. 0.2 servings/d) was associated with a 21% lower risk of CVD events [OR 0.79 (95% CI: 0.73–0.85)]. Similar estimates were noted for different CVD outcomes (heart disease, stroke, fatal CVD) and in sex-specific analyses. Conversely, refined grain intake was not associated with incident CVD events [1.07 (0.94–1.22)].ConclusionsThere is a consistent, inverse association between dietary whole grains and incident cardiovascular disease in epidemiological cohort studies. In light of this evidence, policy-makers, scientists, and clinicians should redouble efforts to incorporate clear messages on the beneficial effects of whole grains into public health and clinical practice endeavors.     

Wildfire smoke impacts on indoor air quality assessed using crowdsourced data in California

Wildfires have become an important source of particulate matter (PM_2.5 < 2.5-µm diameter), leading to unhealthy air quality index occurrences in the western United States. Since people mainly shelter indoors during wildfire smoke events, the infiltration of wildfire PM_2.5 into indoor environments is a key determinant of human exposure and is potentially controllable with appropriate awareness, infrastructure investment, and public education. Using time-resolved observations outside and inside more than 1,400 buildings from the crowdsourced PurpleAir sensor network in California, we found that the geometric mean infiltration ratios (indoor PM_2.5 of outdoor origin/outdoor PM_2.5) were reduced from 0.4 during non-fire days to 0.2 during wildfire days. Even with reduced infiltration, the mean indoor concentration of PM_2.5 nearly tripled during wildfire events, with a lower infiltration in newer buildings and those utilizing air conditioning or filtration.

Fine particulate matter (PM_2.5) air pollution is the single largest environmental risk factor for human health and death in the United States (1). Wildfires are a major source of PM_2.5 and are documented to cause adverse respiratory health effects and increased mortality (2). Toxicological and epidemiological studies suggest that PM_2.5 from wildfires is more harmful to the respiratory system than equal doses of non-wildfire PM_2.5 (3, 4). The number and magnitude of wildfires in the western United States has increased in recent decades due to climate change and land management (5–7). Although the annual mean level of PM_2.5 has substantially declined over this period following the implementation of extensive air quality policies to reduce emissions from controllable sources, the frequency and severity of smoke episodes with PM_2.5 exceedances has increased sharply due to wildfires in the Pacific Northwest and California (8, 9). The annual mean PM_2.5 in Northern California has increased since 2015 (SI Appendix, Fig. S1) due to massive seasonal fire events, and these events have become the dominant cause of PM_2.5 exceedances.People in the United States spend 87% of their time indoors (10). However, the protection against air pollutants of outdoor origin provided by buildings is commonly overlooked in air quality, epidemiologic, and risk assessment studies (11). To accurately characterize and reduce population exposures to wildfire PM_2.5, it is necessary to understand how buildings are used by their occupants to mitigate exposure. Previous estimations of indoor particles of outdoor origin typically relied on measurements from a limited number of buildings and extrapolation of these measurements to other buildings based on the empirical infiltration and removal parameters (12, 13). However, such extrapolation is not applicable to wildfire events because it does not take into account the distribution of protection provided by buildings (including natural and mechanical ventilation) due to lack of data measuring infiltration under representative conditions. The infiltration of outdoor particles is dependent on people’s behavior (11, 14, 15), which changes during wildfires (and in 2020 during the COVID-19 pandemic). Pollution levels during wildfire events, and knowledge of those pollution levels through available air quality data, directly impact human responses aimed at controlling the infiltration of outdoor PM_2.5 including reducing ventilation, using air conditioning, and using active filtration. Statistically robust observations of the variability of PM_2.5 infiltration during actual wildfire events across a broad cross-section of normally occupied residences provides the opportunity to understand the distribution of real infiltration rates affecting human exposure and the factors controlling them, potentially informing guidance toward improvement.Here, we exploit a recent trend in air quality sensing—public data from a network of ubiquitous crowdsourced low-cost PM_2.5 sensors—to characterize how indoor air quality during wildfire episodes is affected by buildings and their occupants. We demonstrate that buildings provide substantial protection against wildfire PM_2.5 and that behavioral responses of building occupants contribute to effective mitigation of wildfire smoke exposure. Real-time PM_2.5 sensors based on aerosol light scattering have proliferated as easy to use and low-cost consumer devices in recent years, providing a novel opportunity to explore the indoor intrusion of wildfire PM_2.5. Among various networks of devices, the crowdsourced PurpleAir network is the most extensive public-facing network currently available. As of June 2, 2021, there are 15,885 publicly accessible active PurpleAir sensors reporting data from across the earth; 76% are outdoor (12,088), and 24% are indoor (3,797). Of these PurpleAir sensors, 57% are installed in California (9,072), split into 69% outdoor (6,273) and 31% indoor (2,799). As shown in Fig. 1, California accounts for 74% of all indoor PurpleAir sensors in the United States, with adoption increasing most rapidly following individual wildfire episodes as noted by prior work (16). We focus here on analyzing the data from these sensors deployed across the metropolitan regions of San Francisco and Los Angeles, California, where the public adoption of indoor and outdoor PurpleAir sensors is especially high, at least partially in response to the high frequency of recent wildfire events. Analyses are presented for the wildfire season in the San Francisco Bay Area of Northern California (NC) during August to September 2020 (denoted NC 2020) and November 2018 (NC 2018) and for the Los Angeles area of Southern California (SC) in August to September 2020 (SC 2020). Maps of the measurement regions are provided in SI Appendix, Figs. S2 and S3. We analyzed the data from over 1,400 indoor sensors and their outdoor counterparts to characterize levels of and dynamics of indoor PM_2.5 and the fraction of outdoor PM_2.5 that entered buildings, comparing wildfire and non-fire periods. The vast majority (>87%) of sensors in our dataset are in buildings that are unambiguously identified as residential. We mainly focus on residential buildings, which is facilitated by linking individual PurpleAir sensor locations with a dataset of detailed home property characteristics (Zillow).Open in a separate windowFig. 1.Number of publicly accessible indoor PurpleAir sensors in the United States and California. The shadings show major wildfire periods (start date to containment date of fires with >50,000 total acres burned) in California. Wildfire periods are from the Cal Fire website (https://www.fire.ca.gov/incidents/).     

Thrombogenicity and cardiovascular effects of ambient air pollution

Exposure to air pollution is associated with adverse effects on health. In particular, a strong epidemiologic association is observed between acute and chronic exposures to particulate matter and the occurrence of cardiovascular events, coronary artery disease, cerebrovascular disease and venous thromboembolism, especially among older people and people with diabetes and previous cardiovascular conditions. Multiple mechanisms have been postulated to cause the increase in atherothrombotic and thromboembolic events, including the activation by particulate matter of inflammatory pathways and hemostasis factors, production of reactive oxygen species through the oxidative stress pathway, alterations in vascular tone, and decreased heart rate variability (a marker of cardiac autonomic dysfunction and a predictor of sudden cardiac death and arrhythmias). Current knowledge on the biologic mechanisms and the clinical effect of short- and long-term exposure to particulate air pollutants is discussed, emphasizing that life expectancy improved significantly in sites where air pollutants were controlled.     

Atherosclerotic plaque biomarkers: beyond the horizon of the vulnerable plaque

Cardiovascular disease (CVD) is the number one cause of death globally, and the majority of CVD is caused by atherosclerosis. Atherosclerosis is a systemic inflammatory disease that leads to myocardial infarction, stroke and lower limb ischemia. Pathological studies have given insight to development of atherosclerosis and the importance of local plaque vulnerability, leading to thrombus formation and cardiovascular events. Due to the burden of cardiovascular disease, identification of patients at risk for cardiovascular events and treatment stratification is needed. The predictive power of classical risk factors is limited, especially in patients with manifest atherosclerosis. Imaging modalities have focused on the characteristics of the vulnerable plaque. However, it has become evident that not all so-called vulnerable plaques lead to rupture and subsequent thrombosis. The latter obviously limits the positive predictive value for imaging assessment of plaques and patients at risk. Serum biomarkers have also been studied extensively, but have very limited application in a clinical setting for risk stratification. In line with the important relation between vulnerable plaques and cardiovascular events, plaque biomarker studies have been initiated. These longitudinal studies are based on the concept, that a vulnerable plaque contains predictive information for future cardiovascular events, also in other territories of the vascular tree. Results look promising and plaque markers can be used to develop imaging modalities to identify patients at risk, or to monitor treatment effect. Plaque biomarker studies do not challenge the definition of the vulnerable plaque, but use its concept in favor of prediction improvement for vascular patients.     

Limited benefit of haemoglobin glycation index as risk factor for cardiovascular disease in type 2 diabetes patients

BackgroundThe haemoglobin glycation index (HGI) has been proposed as a marker of interindividual differences in haemoglobin glycosylation. Previous studies have shown a relationship between high HGI and risk of cardiovascular disease (CVD) in patients with diabetes. However, no studies have investigated the role of previous CVD in this association.MethodsThe study cohort comprised patients with type 2 diabetes mellitus (T2DM; n = 1910) included in the Second Manifestations of Arterial Disease (SMART) study. The relationship between either HGI or HbA_1c and a composite of cardiovascular events as the primary outcome, and mortality, cardiovascular mortality, myocardial infarction and stroke as secondary outcomes, was investigated using Cox proportional-hazards models. Similar analyses were performed after stratification according to previous CVD.ResultsA 1-unit higher HGI was associated with a 29% greater risk of a composite of cardiovascular events (HR: 1.29, 95% CI: 1.06–1.57) in patients without previous CVD, whereas no such relationship was seen in patients with previous CVD (HR: 0.96, 95% CI: 0.86–1.08). The direction and magnitude of the hazard ratios (HRs) of HGI and HbA_1c in relation to outcomes were similar. Additional adjustment for HbA_1c in the association between HGI and outcomes lowered the HRs.ConclusionSimilar to HbA_1c, higher HGI is related to higher risk of cardiovascular events in patients with T2DM without CVD. As HbA_1c has proved to be a comparable risk factor, and obtaining and interpreting the HGI is complicated, any additional benefit of applying the HGI in clinical settings is likely to be limited.