‘Bushfire Season’ in Australia: Determinants of Increases in Risk of Acute Coronary Syndromes and Takotsubo Syndrome

BackgroundClimate change has resulted in an increase in ambient temperatures during the summer months as well as an increase in risk of associated air pollution and of potentially disastrous bushfires throughout much of the world. The increasingly frequent combination of elevated summer temperatures and bushfires may be associated with acute increases in risks of cardiovascular events, but this relationship remains unstudied. We evaluated the individual and cumulative impacts of daily fluctuations in temperature, fine particulate matter of less than 2.5 µm (PM_2.5) pollution and presence of bushfires on incidence of acute coronary syndromes and Takotsubo syndrome.MethodsFrom November 1, 2019, to February 28, 2020, all admissions with acute coronary syndromes or Takotsubo syndrome to South Australian tertiary public hospitals were evaluated. Univariate and combined associations were sought among each of 1) maximal daily temperature, 2) PM_2.5 concentrations, and 3) presence of active bushfires within 200 km of the hospitals concerned.ResultsA total of 504 patients with acute coronary syndromes and 35 with Takotsubo syndrome were studied. In isolation, increasing temperature was associated (r_s = 0.26, P = .005) with increased incidence of acute coronary syndromes, while there were similar, but nonsignificant correlations for PM_2.5 and presence of bushfires. Combinations of all these risk factors were also associated with a doubling of risk of acute coronary syndromes. No significant associations were found for Takotsubo syndrome.ConclusionThe combination of high temperatures, presence of bushfires and associated elevation of atmospheric PM_2.5 concentrations represents a substantially increased risk for precipitation of acute coronary syndromes; this risk should be factored into health care planning including public education and acute hospital preparedness.     

Air pollution: The "heart" of the problem

Air pollution exposure is associated with an increased risk of acute and chronic cardiovascular mortality. Recent observations have implicated fine particulate matter (PM_2.5) as one of the most important pollutants. Inhalation of PM_2.5 causes acute pulmonary inflammation and oxidative stress. The subsequent generation of a systemic inflammatory response could link air pollution exposure with the development of cardiovascular disease. Human experiments have demonstrated pro-arrhythmic alterations in cardiac autonomic tone, increased blood pressure, higher serum C-reactive protein levels, and alterations in blood rheology favoring coagulation following controlled pollution exposures or in relation to elevated ambient PM_2.5 levels. Recent studies have also uncovered several harmful impacts on the systemic vasculature, including the triggering of acute vasoconstriction and the enhanced development of atherosclerosis. Many questions, however, remain unanswered and future studies will be required to clarify the relevant biologic mechanisms and to identify the specific constituents responsible for mediating the adverse health impacts.     

Particulate Matter Air Pollution and Atherosclerosis

Particulate matter (PM) air pollution less than 2.5 μm in diameter (PM_2.5), which is now an all-pervading element of modern-day society, is associated with heightened cardiovascular morbidity and mortality. Not only can short-term PM_2.5 exposure trigger acute cardiovascular events, but longer-term exposure over years augments cardiovascular risk to an even greater extent. One biological mechanism capable of explaining this observation is that chronic exposure may promote the progression and vulnerability of atherosclerotic plaques. Indeed, recent epidemiologic studies have demonstrated an association between ambient PM_2.5 exposure and the presence or extent of atherosclerosis in humans. Several animal experiments have provided corroborating evidence that chronic exposures in fact do enhance the progression and perhaps vulnerability of atherosclerotic lesions. Due to the billions of people continually exposed to PM_2.5, the long-term pro-atherosclerotic effects of this ubiquitous air pollutant are likely to be of enormous and growing global public health importance.     

Adverse effects of air pollution‐derived fine particulate matter on cardiovascular homeostasis and disease

Air pollution is a rapidly growing major health concern around the world. Atmospheric particulate matter that has a diameter of less than 2.5 µm (PM_2.5) refers to an air pollutant composed of particles and chemical compounds that originate from various sources. While epidemiological studies have established the association between PM_2.5 exposure and cardiovascular diseases, the precise cellular and molecular mechanisms by which PM_2.5 promotes cardiovascular complications are yet to be fully elucidated. In this review, we summarize the various sources of PM_2.5, its components, and the concentrations of ambient PM_2.5 in various settings. We discuss the experimental findings to date that evaluate the potential adverse effects of PM_2.5 on cardiovascular homeostasis and function, and the possible therapeutic options that may alleviate PM_2.5-driven cardiovascular damage.     

Association of Ambient Air Pollution with Blood Pressure in Adolescence: A Systematic-review and Meta-analysis

We systematically reviewed the association of ambient air pollution with blood pressure (BP) as a primary outcome in adolescents (10-19 years). Five databases (Ovid Medline, Ovid Embase, Web of Science, The Cochrane Library, and LILACS) were searched for relevant articles published up to August 2022. Meta-analyses were conducted using STATA v17 (Protocol - OSF Registries https://doi.org/10.17605/OSF.IO/96G5Q). Eight studies (5 cohort, 3 cross-sectional) with approximately 15,000 adolescents were included. Data from 6 studies were suitable for inclusion in the meta-analyses. In sub-group analyses, non-significant positive associations were observed for cohort studies assessing long-term exposure to PM₁₀, PM_2.5, and NO₂ on systolic and diastolic BP. At age 12 years old (3702 adolescents), we found significant positive associations for long-term exposure to PM_2.5(β=5.33 (1.56, 9.09) mmHg) and PM₁₀ (β=2.47 (0.10, 4.85) mmHg) on diastolic BP. Significant positive associations were observed (3,592 adolescents) for long-term exposure to PM₁₀(β=0.34 (0.19, 0.50) mmHg) and NO₂ on diastolic BP (β=0.40 (0.09, 0.71) mmHg), and PM₁₀ on systolic BP (β=0.48 (0.19, 0.77) mmHg). The overall quality of evidence analysed was graded as “low/very low.” Insufficient data for short-term exposures to PM₂.₅, PM₁₀, NO₂, CO on BP led to their exclusion from the meta-analysis. Inconsistent associations were reported for gender-stratified results. The evidence, though of low-quality and limited, indicated that ambient air pollution was positively associated with adolescent BP. Future studies need improved measures of air pollutant exposures, consideration of gender and socio-economic circumstances on the observed pollution effects, as well as adjustment for other potential confounding factors.     

Long-term exposure to low concentrations of air pollution and decline in lung function in people with idiopathic pulmonary fibrosis: Evidence from Australia

Background and Objective

Little is known about the association between ambient air pollution and idiopathic pulmonary fibrosis (IPF) in areas with lower levels of exposure. We aimed to investigate the impact of air pollution on lung function and rapid progression of IPF in Australia.

Methods

Participants were recruited from the Australian IPF Registry (n = 570). The impact of air pollution on changes in lung function was assessed using linear mixed models and Cox regression was used to investigate the association with rapid progression.

Results

Median (25th–75th percentiles) annual fine particulate matter (<2.5 μm, PM_2.5) and nitrogen dioxide (NO₂) were 6.8 (5.7, 7.9) μg/m³ and 6.7 (4.9, 8.2) ppb, respectively. Compared to living more than 100 m from a major road, living within 100 m was associated with a 1.3% predicted/year (95% confidence interval [CI] −2.4 to −0.3) faster annual decline in diffusing capacity of the lungs for carbon monoxide (DLco). Each interquartile range (IQR) of 2.2 μg/m³ increase in PM_2.5 was associated with a 0.9% predicted/year (95% CI −1.6 to −0.3) faster annual decline in DLco, while there was no association observed with NO₂. There was also no association between air pollution and rapid progression of IPF.

Conclusion

Living near a major road and increased PM_2.5 were both associated with an increased rate of annual decline in DLco. This study adds to the evidence supporting the negative effects of air pollution on lung function decline in people with IPF living at low-level concentrations of exposure.     

Short-Term Exposure to Ambient Air Pollution and Mortality From Myocardial Infarction

BackgroundShort-term exposure to ambient air pollution has been linked to occurrence of myocardial infarction (MI); however, only a limited number of studies investigated its association with death from MI, and the results remain inconsistent.ObjectivesThis study sought to investigate the association of short-term exposure to air pollution across a wide range of concentrations with MI mortality.MethodsA time-stratified case-crossover study was conducted to investigate 151,608 MI death cases in Hubei province (China) from 2013 to 2018. Based on each case’s home address, exposure to particulate matter with an aerodynamic diameter ≤2.5 μm (PM_2.5), particulate matter with an aerodynamic diameter ≤10 μm (PM₁₀), sulfur dioxide, nitrogen dioxide (NO₂), carbon monoxide, and ozone on each of the case and control days was assessed as the inverse distance–weighted average concentration at neighboring air quality monitoring stations. Conditional logistic regression models were implemented to quantify exposure-response associations.ResultsExposure to PM_2.5, PM₁₀, and NO₂ (mean exposure on the same day of death and 1 day prior) was significantly associated with increased odds of MI mortality. The odds associated with PM_2.5 and PM₁₀ exposures increased steeply before a breakpoint (PM_2.5, 33.3 μg/m³; PM₁₀, 57.3 μg/m³) and flattened out at higher exposure levels, while the association for NO₂ exposure was almost linear. Each 10-μg/m³ increase in exposure to PM_2.5 (<33.3 μg/m³), PM₁₀ (<57.3 μg/m³), and NO₂ was significantly associated with a 4.14% (95% confidence interval [CI]: 1.25% to 7.12%), 2.67% (95% CI: 0.80% to 4.57%), and 1.46% (95% CI: 0.76% to 2.17%) increase in odds of MI mortality, respectively. The association between NO₂ exposure and MI mortality was significantly stronger in older adults.ConclusionsShort-term exposure to PM_2.5, PM₁₀, and NO₂ was associated with increased risk of MI mortality.     

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.     

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.     

Short-term effects of ambient air pollutants on asthma-related emergency department visits in Indianapolis,Indiana, 2007–2011

Objective: We estimate the short-term associations between daily changes in ambient air pollutants and daily asthma-related emergency department (ED) visits in Indianapolis, IN. Methods: We identified asthma-related ED visits among Indianapolis residents aged ≥5 years. We used Poisson regression in a time-series framework to estimate the increased risk for asthma-related ED visits from exposure to ambient SO₂, PM_2.5 and ozone during the warm season (April–September) and SO₂ and PM_2.5 during the cold (October–March) season, from 2007 to 2011. Our models controlled for measured confounders, including weather and respiratory infections, as well as unmeasured confounders using a natural cubic spline to account for long-term seasonal trends. Results: During 2007–2011 in Indianapolis, 165?056 asthma-related ED visits occurred. We found statistically significant positive associations (p?<?0.05) between ambient air pollutants and ED visits during the warm season for persons aged 5–44 years. Interquartile range increases in daily ozone concentrations with same day, 2-day lagged, and 3-day moving average were associated with increased risks for ED visits of 3.2% (95% CI: 0.2%, 6.3%), 4.4% (0.1%, 8.9%) and 4.8% (0.2%, 9.6%), respectively. Interquartile range increases in 3-day moving averages for SO₂ were associated with an increased risk of 3.3% (95% CI: 0.2%, 6.5%). We identified statistically significant associations (p?<?0.05) between increased SO₂ and PM_2.5 levels and decreased ED visits among some age groups, primarily during the cold season, and no significant positive associations between changes in PM_2.5 concentration and asthma-related ED visits. Conclusions: During the warm season, increases in ozone and SO₂ concentrations were associated with increased asthma morbidity in children and young adults in Indianapolis. These results will enable reliable estimation of the health impacts of increases in these pollutants on asthma-related ED visits in Indianapolis and similar communities.     

Relationship Between Particulate Matter (PM2.5) and Hospitalizations and Mortality of Chronic Obstructive Pulmonary Disease Patients: A Meta-Analysis

BackgroundNumerous studies have reported associations between particulate matter with aerodynamic diameters of ≤2.5 μm (PM_2.5) and chronic obstructive pulmonary disease (COPD) hospitalizations and mortality in cities worldwide. Nonetheless, the evidence of an association remains varied and limited.MethodsSystematic searches were conducted in 6 common English and Chinese electronic databases (i.e., PubMed, Web of Science, EMBASE, Ovid, Google Scholar, and China National Knowledge Infrastructure [CNKI]). A meta-analysis was performed to estimate the odds ratio (OR) to evaluate the relationship between PM_2.5 and COPD hospitalizations and mortality. Publication bias and heterogeneity of samples were tested using a funnel plot and the Egger's test. Studies were analyzed using either a random-effect model or a fixed-effect model.ResultsThe search yielded 18 studies suitable for meta-analysis during the period from Jan 1, 2010 to Dec 31, 2018. A 10-μg/m³ increase in PM_2.5 was associated with a 2.5% (95% confidence interval [CI]: 1.8-3.2%) increase in COPD hospitalizations, with an OR of 1.025 (95% CI: 1.018-1.032), and a 1.5% (95% CI: 0.9-2.2%) increase in COPD mortality, with an OR of 1.015 (95% CI: 1.009-1.022). Comparing different age groups, elderly people were more sensitive to the adverse effects. The estimated risk was higher in European countries than Asian countries, and in warm compared cold seasons. Various additional confounding factors also led to different results.ConclusionsPM_2.5 is associated with COPD hospitalizations and mortality. Controlling ambient air pollution would provide benefits to COPD patients.     

Long-Term Exposure to Fine Particulate Matter and Cardiovascular Disease in China

BackgroundEvidence of the effects of long-term fine particulate matter (PM_2.5) exposure on cardiovascular diseases (CVDs) is rare for populations exposed to high levels of PM_2.5 in China and in other countries with similarly high levels.ObjectivesThe aim of this study was to assess the CVD risks associated with long-term exposure to PM_2.5 in China.MethodsA nationwide cohort study, China-PAR (Prediction for Atherosclerotic Cardiovascular Disease Risk in China), was used, with 116,972 adults without CVD in 2000 being included. Participants were followed until 2015. Satellite-based PM_2.5 concentrations at 1-km spatial resolution during the study period were used for exposure assessment. A Cox proportional hazards model with time-varying exposures was used to estimate the CVD risks associated with PM_2.5 exposure, adjusting for individual risk factors.ResultsAnnual mean concentrations of PM_2.5 at the China-PAR sites ranged from 25.5 to 114.0 μg/m³. For each 10 μg/m³ increase in PM_2.5 exposures, the multivariate-adjusted hazard ratio was 1.251 (95% confidence interval: 1.220 to 1.283) for CVD incidence and 1.164 (95% confidence interval: 1.117 to 1.213) for CVD mortality. The slopes of concentration-response functions of PM_2.5 exposure and CVD risks were steeper at high PM_2.5 levels. In addition, older residents, rural residents, and never smokers were more prone to adverse effects of PM_2.5 exposure.ConclusionsThis study provides evidence that elevated long-term PM_2.5 exposures lead to increased CVD risk in China. The effects are more pronounced at higher PM_2.5 levels. These findings expand the current knowledge on adverse health effects of severe air pollution and highlight the potential cardiovascular benefits of air quality improvement in China and other low- and middle-income countries.     

Even low levels of ambient air pollutants are associated with increased emergency department visits for hypertension

Background

Numerous studies have reported associations between air pollution and cardiovascular diseases. While several studies illustrate that exposures to air pollutants can elevate blood pressure, few have evaluated the clinical relevance of this relationship. Hence, we aimed to explore the associations between daily concentrations of several air pollutants and emergency department visits for hypertension.

Methods

Odds ratios (ORs) for emergency department visits for hypertension in Edmonton, Canada, from April 1992 to March 2002 were associated with pollutant levels (CO, NO₂, SO₂, O₃, and particulate matter [PM] < 10 microns [PM₁₀] and < 2.5 microns [PM_2.5] in aerodynamic diameter, respectively) by means of a case-crossover technique with time-stratified strategy to define controls. The analysis was performed for all (N = 5365), male (N = 2069), and female (N = 3296) patients and for six air pollutants lagged by 0 to 9 days. ORs and their 95% confidence intervals (CIs) were reported for an increase in an interquartile range (IQR) for each pollutant.

Results

We observed associations for all patients and levels of NO₂ (IQR = 12.8 parts per billion; OR, 1.06; 95% CI, 1.00-1.12), SO₂ (IQR = 2.3 parts per billion; OR, 1.04; 95% CI, 1.00-1.08), and PM₁₀ (IQR = 15.0 μg/m³; OR, 1.06; 95% CI, 1.01-1.11) for lag day 3, as well as for PM₁₀ (IQR = 15.0 μg/m³; OR, 1.06; 95% CI, 1.01-1.11) and PM_2.5 (IQR = 6.2 μg/m³; OR, 1.07; 95% CI, 1.01-1.11) for lag day 6.

Conclusions

These findings support the contention that ambient pollution can produce clinically meaningful increases in blood pressure.     

Melatonin ameliorates PM2.5‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis

Fine particulate matter (PM_2.5) exposure is correlated with the risk of developing cardiac fibrosis. Melatonin is a major secretory product of the pineal gland that has been reported to prevent fibrosis. However, whether melatonin affects the adverse health effects of PM_2.5 exposure has not been investigated. Thus, this study was aimed to investigate the protective effect of melatonin against PM_2.5‐accelerated cardiac fibrosis. The echocardiography revealed that PM_2.5 had impaired both systolic and diastolic cardiac function in ApoE^?/? mice. Histopathological analysis demonstrated that PM_2.5 induced cardiomyocyte hypertrophy and fibrosis, particularly perivascular fibrosis, while the melatonin administration was effective in alleviating PM_2.5‐induced cardiac dysfunction and fibrosis in mice. Results of electron microscopy and confocal scanning laser microscope confirmed that melatonin had restorative effects against impaired mitochondrial ultrastructure and augmented mitochondrial ROS generation in PM_2.5‐treated group. Further investigation revealed melatonin administration could significantly reverse the PM_2.5‐induced phenotypic modulation of cardiac fibroblasts into myofibroblasts. For the first time, our study found that melatonin effectively alleviates PM_2.5‐induced cardiac dysfunction and fibrosis via inhibiting mitochondrial oxidative injury and regulating SIRT3‐mediated SOD2 deacetylation. Our findings indicate that melatonin could be a therapy medicine for prevention and treatment of air pollution‐associated cardiac diseases.     

Impact of Environmental Particulate Matter and Peritoneal Dialysis-related Infection in Patients Undergoing Peritoneal Dialysis

In patients undergoing peritoneal dialysis (PD), PD-related infection is a major cause of PD failure and hospital admission. Good air quality is required when dialysate exchange or exit site wound care is performed. To our knowledge, investigation of air pollution as a factor for PD-related infection in patients undergoing dialysis is limited. This study aimed to assess the effect of environmental particulate matter (PM) and other important risk factors on 1-year PD-related infection in patients undergoing PD.A total of 175 patients undergoing PD were recruited in this 1-year retrospective observational study. Differences in environmental PMs (PM₁₀ and PM_2.5) were analyzed with respect to the patients’ living areas. The patients undergoing PD were categorized into 2 groups according to PM_2.5 exposure: high (n = 61) and low (n = 114). Demographic, hematological, nutritional, inflammatory, biochemical, and dialysis-related data were analyzed. Multivariate binary logistic and multivariate Cox regression analyses were used to analyze 1-year PD-related infection.A total of 175 patients undergoing PD (50 men and 125 women) were enrolled. Thirty-five patients had PD-related infection within 1 year. Multivariate Cox regression analysis showed that high environmental PM_2.5 exposure (hazard ratio (HR): 2.0, 95% confidence interval [CI] [1.03–3.91]; P = .04) and female sex (HR: 2.77, 95% CI [1.07–7.19]; P = .03) were risk factors for 1-year PD-related infection.Patients undergoing PD with high environmental PM_2.5 exposure had a higher 1-year PD-related infection rate than that in those with low exposure. Therefore, air pollution may be associated with PD-related infection in such patients.     

Acute effects of hourly particulate-matter air pollution on 24 h ambulatory blood pressure in Chinese elderly individuals: a prospective panel study

Background

The association between hourly exposure to air pollution and blood pressure, and its threshold effects, are unclear. We aimed to examine the association between hourly PM_2·5 and PM₁₀ exposure and 24 h ambulatory blood pressure among a panel of Chinese elderly individuals.

Roles of Ambient Temperature and PM2.5 on Childhood Acute Bronchitis and Bronchiolitis from Viral Infection

Studies have associated the human respiratory syncytial virus which causes seasonal childhood acute bronchitis and bronchiolitis (CABs) with climate change and air pollution. We investigated this association using the insurance claims data of 3,965,560 children aged ≤ 12 years from Taiwan from 2006–2016. The monthly average incident CABs increased with increasing PM_2.5 levels and exhibited an inverse association with temperature. The incidence was 1.6-fold greater in January than in July (13.7/100 versus 8.81/100), declined during winter breaks (February) and summer breaks (June–August). The highest incidence was 698 cases/day at <20 °C with PM_2.5 > 37.0 μg/m³, with an adjusted relative risk (aRR) of 1.01 (95% confidence interval [CI] = 0.97–1.04) compared to 568 cases/day at <20 °C with PM_2.5 < 15.0 μg/m³ (reference). The incidence at ≥30 °C decreased to 536 cases/day (aRR = 0.95, 95% CI = 0.85–1.06) with PM_2.5 > 37.0 μg/m³ and decreased further to 392 cases/day (aRR = 0.61, 95% CI = 0.58–0.65) when PM_2.5 was <15.0 μg/m³. In conclusion, CABs infections in children were associated with lowered ambient temperatures and elevated PM_2.5 concentrations, and the high PM_2.5 levels coincided with low temperature levels. The role of temperature should be considered in the studies of association between PM_2.5 and CABs.     

PM2.5 Air Pollution and Cardiovascular Disease-Associated Disability among Middle-Aged and Older Adults

Background:Increasing evidence regards the role of ambient particles on morbidity and mortality caused by cardiovascular diseases (CVDs). However, there was no evidence about the association between ambient particles and CVD-associated disability. This study used large national representative data to investigate the relationship between long-term exposure to an aerodynamic diameter less than or equal to 2.5 µm (PM_2.5) and CVD-associated disability among Chinese adults aged 45 years old and above and estimated the burden of CVD-associated disability attributed to PM_2.5.Methods:Using data from the Second National Sample Survey on Disability, this study used a combination of self-reports or family members’ reports and on-site medical diagnosis by experienced specialists to ascertain CVD-associated disability in 852,742 adults aged 45 years old and above. Logistic regression models and spline regression models were used to examine the association between PM_2.5 long-term exposure and CVD-associated disability, and the population attributable risk was calculated to assess the burden of CVD-associated disability contributed to PM_2.5.Results:Every increase of 10 μg/m³ in PM_2.5 was associated with an 8% (OR = 1.08, 95% CI: 1.05, 1.10) increase the odds of CVD-associated disability. Stratified analyses by demographic factors suggested that this association was robust. There were 1.05 (0.74,1.35) million -3.53 (3.29,3.75) million CVD-associated disabilities attributed to high PM_2.5 concentration exposure (≥35 µg/m³) among middle-aged and older adults in 2006. A reduction in PM_2.5 concentrations to 35 µg/m³ corresponded to a decrease of 13.59% (9.55%, 17.46%)–23.98% (17.17%, 30.25%) in CVD-associated disability by age group, respectively, and this magnitude increased in areas with a high prevalence of CVD-related disability.Conclusions:This study suggests that reducing PM_2.5 concentrations may contribute to preventing CVD-associated disability and decreasing air pollution-related medical expenditures and rehabilitation fees.     

Exposure to Elevated Nitrogen Dioxide Concentrations and Cardiac Remodeling in Patients With Dilated Cardiomyopathy

BackgroundEmpirical evidence suggests a strong link between exposure to air pollution and heart failure incidence, hospitalizations, and mortality, but the biological basis of this remains unclear. We sought to determine the relationship between differential air pollution levels and changes in cardiac structure and function in patients with dilated cardiomyopathy.Methods and ResultsWe undertook a prospective longitudinal observational cohort study of patients in England with dilated cardiomyopathy (enrollment 2009–2015, n = 716, 66% male, 85% Caucasian) and conducted cross sectional analysis at the time of study enrollment. Annual average air pollution exposure estimates for nitrogen dioxide (NO₂) and particulate matter with diameter of 2.5 µm or less (PM_2.5) at enrolment were assigned to each residential postcode (on average 12 households). The relationship between air pollution and cardiac morphology was assessed using linear regression modelling. Greater ambient exposure to NO₂ was associated with higher indexed left ventricular (LV) mass (4.3 g/m² increase per interquartile range increase in NO₂, 95% confidence interval 1.9–7.0 g/m²) and lower LV ejection fraction (–1.5% decrease per interquartile range increase in NO₂, 95% confidence interval –2.7% to –0.2%), independent of age, sex, socioeconomic status, and clinical covariates. The associations were robust to adjustment for smoking status and geographical clustering by postcode area. The effect of air pollution on LV mass was greatest in women. These effects were specific to NO₂ exposure.ConclusionsExposure to air pollution is associated with raised LV mass and lower LV ejection fraction, with the strongest effect in women. Although epidemiological associations between air pollution and heart failure have been established and supported by preclinical studies, our findings provide novel empirical evidence of cardiac remodeling and exposure to air pollution with important clinical and public health implications.     

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.