Long-term exposure to air pollution and severe COVID-19 in Catalonia: a population-based cohort study.

The association between long-term exposure to ambient air pollutants and severe COVID-19 is uncertain. We followed 4,660,502 adults from the general population in 2020 in Catalonia, Spain. Cox proportional models were fit to evaluate the association between annual averages of PM2.5, NO2, BC, and O3 at each participant's residential address and severe COVID-19. Higher exposure to PM2.5, NO2, and BC was associated with an increased risk of COVID-19 hospitalization, ICU admission, death, and hospital length of stay. An increase of 3.2 µg/m3 of PM2.5 was associated with a 19% (95% CI, 16-21) increase in hospitalizations. An increase of 16.1 µg/m3 of NO2 was associated with a 42% (95% CI, 30-55) increase in ICU admissions. An increase of 0.7 µg/m3 of BC was associated with a 6% (95% CI, 0-13) increase in deaths. O3 was positively associated with severe outcomes when adjusted by NO2. Our study contributes robust evidence that long-term exposure to air pollutants is associated with severe COVID-19.

Critical air pollutant assessments and health effects attributed to PM2.5 during and after COVID-19 lockdowns in Iran: application of AirQ+ models.

Objectives: The aim of this study was to evaluate changes in air quality index (AQI) values before, during, and after lockdown, as well as to evaluate the number of hospitalizations due to respiratory and cardiovascular diseases attributed to atmospheric PM2.5 pollution in Semnan, Iran in the period from 2019 to 2021 during the COVID-19 pandemic. Methods: Daily air quality records were obtained from the global air quality index project and the US Environmental Protection Administration (EPA). In this research, the AirQ+ model was used to quantify health consequences attributed to particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5). Results: The results of this study showed positive correlations between air pollution levels and reductions in pollutant levels during and after the lockdown. PM2.5 was the critical pollutant for most days of the year, as its AQI was the highest among the four investigated pollutants on most days. Mortality rates from chronic obstructive pulmonary disease (COPD) attributed to PM2.5 in 2019-2021 were 25.18% in 2019, 22.55% in 2020, and 22.12% in 2021. Mortality rates and hospital admissions due to cardiovascular and respiratory diseases decreased during the lockdown. The results showed a significant decrease in the percentage of days with unhealthy air quality in short-term lockdowns in Semnan, Iran with moderate air pollution. Natural mortality (due to all-natural causes) and other mortalities related to COPD, ischemic heart disease (IHD), lung cancer (LC), and stroke attributed to PM2.5 in 2019-2021 decreased. Conclusion: Our results support the general finding that anthropogenic activities cause significant health threats, which were paradoxically revealed during a global health crisis/challenge.

[Long-term exposure to ambient air pollution and the incidence of SARS-CoV-2 infections in Italy: The EpiCovAir study]. / Esposizione a lungo termine a inquinamento dell'aria ambiente e incidenza di infezioni di SARS-CoV-2 in Italia: lo studio EpiCovAir.

BACKGROUND: after the outbreak of the SARS-CoV-2 pandemic in 2020, several waves of pandemic cases have occurred in Italy. The role of air pollution has been hypothesized and investigated in several studies. However, to date, the role of chronic exposure to air pollutants in increasing incidence of SARS-CoV-2 infections is still debated. OBJECTIVES: to investigate the association between long-term exposure to air pollutants and the incidence of SARS-CoV-2 infections in Italy. DESIGN: a satellite-based air pollution exposure model with 1-km2 spatial resolution for entire Italy was applied and 2016-2019 mean population-weighted concentrations of particulate matter < 10 micron (PM10), PM <2.5 micron (PM2.5), and nitrogen dioxide (NO2) was calculated to each municipality as estimates of chronic exposures. A principal component analysis (PCA) approach was applied to 50+ area-level covariates (geography and topography, population density, mobility, population health, socioeconomic status) to account for the major determinants of the spatial distribution of incidence rates of SARS-CoV-2 infection. Detailed information was further used on intra- and inter-municipal mobility during the pandemic period. Finally, a mixed longitudinal ecological design with the study units consisting of individual municipalities in Italy was applied. Generalized negative binomial models controlling for age, gender, province, month, PCA variables, and population density were estimated. SETTING AND PARTICIPANTS: individual records of diagnosed SARS-2-CoV-2 infections in Italy from February 2020 to June 2021 reported to the Italian Integrated Surveillance of COVID-19 were used. MAIN OUTCOME MEASURES: percentage increases in incidence rate (%IR) and corresponding 95% confidence intervals (95% CI) per unit increase in exposure. RESULTS: 3,995,202 COVID-19 cases in 7,800 municipalities were analysed (total population: 59,589,357 inhabitants). It was found that long-term exposure to PM2.5, PM10, and NO2 was significantly associated with the incidence rates of SARS-CoV-2 infection. In particular, incidence of COVID-19 increased by 0.3% (95%CI 0.1%-0.4%), 0.3% (0.2%-0.4%), and 0.9% (0.8%-1.0%) per 1 µg/m3 increment in PM2.5, PM10 and NO2, respectively. Associations were higher among elderly subjects and during the second pandemic wave (September 2020-December 2020). Several sensitivity analyses confirmed the main results. The results for NO2 were especially robust to multiple sensitivity analyses. CONCLUSIONS: evidence of an association between long-term exposure to ambient air pollutants and the incidence of SARS-CoV-2 infections in Italy was found.

PM10 promotes an inflammatory cytokine response that may impact SARS-CoV-2 replication in vitro.

Introduction: In the last decades, a decrease in air quality has been observed, mainly associated with anthropogenic activities. Air pollutants, including particulate matter (PM), have been associated with adverse effects on human health, such as exacerbation of respiratory diseases and infections. High levels of PM in the air have recently been associated with increased morbidity and mortality of COVID-19 in some regions of the world. Objective: To evaluate the effect of coarse particulate matter (PM10) on the inflammatory response and viral replication triggered by SARS-CoV-2 using in vitro models. Methods: Peripheral blood mononuclear cells (PBMC) from healthy donors were treated with PM10 and subsequently exposed to SARS-CoV-2 (D614G strain, MOI 0.1). The production of pro-inflammatory cytokines and antiviral factors was quantified by qPCR and ELISA. In addition, using the A549 cell line, previously exposed to PM, the viral replication was evaluated by qPCR and plaque assay. Results: SARS-CoV-2 stimulation increased the production of pro-inflammatory cytokines in PBMC, such as IL-1ß, IL-6 and IL-8, but not antiviral factors. Likewise, PM10 induced significant production of IL-6 in PBMCs stimulated with SARS-CoV-2 and decreased the expression of OAS and PKR. Additionally, PM10 induces the release of IL-1ß in PBMC exposed to SARS-CoV-2 as well as in a co-culture of epithelial cells and PBMCs. Finally, increased viral replication of SARS-CoV-2 was shown in response to PM10. Conclusion: Exposure to coarse particulate matter increases the production of pro-inflammatory cytokines, such as IL-1ß and IL-6, and may alter the expression of antiviral factors, which are relevant for the immune response to SARS-CoV-2. These results suggest that pre-exposure to air particulate matter could have a modest role in the higher production of cytokines and viral replication during COVID-19, which eventually could contribute to severe clinical outcomes.

Particulate matter air pollution and COVID-19 infection, severity, and mortality: A systematic review and meta-analysis.

Ecological evidence links ambient particulate matter ≤2.5 mm (PM2.5) and the rate of COVID-19 infections, severity, and deaths. However, such studies are unable to account for individual-level differences in major confounders like socioeconomic status and often rely on imprecise measures of PM2.5. We conducted a systematic review of case-control and cohort studies, which rely on individual-level data, searching Medline, Embase, and the WHO COVID-19 database up to 30 June 2022. Study quality was evaluated using the Newcastle-Ottawa Scale. Results were pooled with a random effects meta-analysis, with Egger's regression, funnel plots, and leave-one-out/trim-and-fill sensitivity analyses to account for publication bias. N = 18 studies met inclusion criteria. A 10 µg/m3 increase in PM2.5 was associated with 66 % (95 % CI: 1.31-2.11) greater odds of COVID-19 infection (N = 7) and 127 % (95 % CI: 1.41-3.66) odds of severe illness (hospitalisation, ICU admission, or requiring respiratory support) (N = 6). Pooled mortality results (N = 5) indicated increased deaths due to PM2.5 but were non-significant (OR 1.40; 0.94 to 2.10). Most studies were rated "good" quality (14/18 studies), though there were numerous methodological issues; few used individual-level data to adjust for socioeconomic status (4/18 studies), instead using area-based indicators (11/18 studies) or no such adjustments (3/18 studies). Most severity (9/10 studies) and mortality studies (5/6 studies) were based on people already diagnosed COVID-19, potentially introducing collider bias. There was evidence of publication bias in studies of infection (p = 0.012) but not severity (p = 0.132) or mortality (p = 0.100). While methodological limits and evidence of bias require cautious interpretation of the findings, we found compelling evidence that PM2.5 increases the risk of COVID-19 infection and severe disease, and weaker evidence of an increase in mortality risk.

A Literature Review of the Effects of Air Pollution on COVID-19 Health Outcomes Worldwide: Statistical Challenges and Data Visualization.

Several peer-reviewed papers and reviews have examined the relationship between exposure to air pollution and COVID-19 spread and severity. However, many of the existing reviews on this topic do not extensively present the statistical challenges associated with this field, do not provide comprehensive guidelines for future researchers, and review only the results of a relatively small number of papers. We reviewed 139 papers, 127 of which reported a statistically significant positive association between air pollution and adverse COVID-19 health outcomes. Here, we summarize the evidence, describe the statistical challenges, and make recommendations for future research. To summarize the 139 papers with data from geographical locations around the world, we also present anopen-source data visualization tool that summarizes these studies and allows the research community to contribute evidence as new research papers are published.

Impact of air pollution on ischemic heart disease: Evidence, mechanisms, clinical perspectives.

Ambient air pollution, and especially particulate matter (PM) air pollution <2.5 µm in diameter (PM2.5), has clearly emerged as an important yet often overlooked risk factor for atherosclerosis and ischemic heart disease (IHD). In this review, we examine the available evidence demonstrating how acute and chronic PM2.5 exposure clinically translates into a heightened coronary atherosclerotic burden and an increased risk of acute ischemic coronary events. Moreover, we provide insights into the pathophysiologic mechanisms underlying PM2.5-mediated atherosclerosis, focusing on the specific biological mechanism through which PM2.5 exerts its detrimental effects. Further, we discuss about the possible mechanisms that explain the recent findings reporting a strong association between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, increased PM2.5 exposure, and morbidity and mortality from IHD. We also address the possible mitigation strategies that should be implemented to reduce the impact of PM2.5 on cardiovascular morbidity and mortality, and underscoring the strong need of clinical trials demonstrating the efficacy of specific interventions (including both PM2.5 reduction and/or specific drugs) in reducing the incidence of IHD. Finally, we introduce the emerging concept of the exposome, highlighting the close relationship between PM2.5 and other environmental exposures (i.e.: traffic noise and climate change) in terms of common underlying pathophysiologic mechanisms and possible mitigation strategies.

Avoidable mortality due to long-term exposure to PM2.5 in Colombia 2014-2019.

OBJECTIVE: To compare estimates of spatiotemporal variations of surface PM2.5 concentrations in Colombia from 2014 to 2019 derived from two global air quality models, as well as to quantify the avoidable deaths attributable to the long-term exposure to concentrations above the current and projected Colombian standard for PM2.5 annual mean at municipality level. METHODS: We retrieved PM2.5 concentrations at the surface level from the ACAG and CAMSRA global air quality models for all 1,122 municipalities, and compare 28 of them with available concentrations from monitor stations. Annual mortality data 2014-2019 by municipality of residence and pooled effect measures for total, natural and specific causes of mortality were used to calculate the number of annual avoidable deaths and years of potential life lost (YPLL) related to the excess of PM2.5 concentration over the current mean annual national standard of 25 µg/m3 and projected standard of 15 µg/m3. RESULTS: Compared to surface data from 28 municipalities with monitoring stations in 2019, ACAG and CAMSRA models under or overestimated annual mean PM2.5 concentrations. Estimations from ACAG model had a mean bias 1,7 µg/m3 compared to a mean bias of 4,7 µg/m3 from CAMSRA model. Using ACAG model, estimations of total nationally attributable deaths to PM2.5 exposure over 25 and 15 µg/m3 were 142 and 34,341, respectively. Cardiopulmonary diseases accounted for most of the attributable deaths due to PM2.5 excess of exposure (38%). Estimates of YPLL due to all-cause mortality for exceeding the national standard of 25 µg/m3 were 2,381 years. CONCLUSION: Comparison of two global air quality models for estimating surface PM2.5 concentrations during 2014-2019 at municipality scale in Colombia showed important differences. Avoidable deaths estimations represent the total number of deaths that could be avoided if the current and projected national standard for PM2.5 annual mean have been met, and show the health-benefit of the implementation of more restrictive air quality standards.

Association between long-term air pollution exposure and COVID-19 mortality in Latin America.

Recent studies have shown a relationship between air pollution and increased vulnerability and mortality due to COVID-19. Most of these studies have looked at developed countries. This study examines the relationship between long-term exposure to air pollution and COVID-19-related deaths in four countries of Latin America that have been highly affected by the pandemic: Brazil, Chile, Colombia, and Mexico. Our results suggest that an increase in long-term exposure of 1 µg/m3 of fine particles is associated with a 2.7 percent increase in the COVID-19 mortality rate. This relationship is found primarily in municipalities of metropolitan areas, where urban air pollution sources dominate, and air quality guidelines are usually exceeded. By focusing the analysis on Latin America, we provide a first glimpse on the role of air pollution as a risk factor for COVID-19 mortality within a context characterized by weak environmental institutions, limited health care capacity and high levels of inequality.

Public health in Global South: effect of environmental pollutant PM2.5 on the incidence and mortality of SARS-CoV-2 in Karachi, Lahore, and Islamabad.

OBJECTIVE: Environmental pollution has undoubtedly been established as a planetary, intergenerational, and existential threat to global human health and safety. Environmental pollution is adversely affecting the world, mainly the countries where human health is not a priority aspect, and this has been exacerbated due to the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), and pandemic is known as "COVID pandemic". This study investigates the association of environmental pollutants, particulate matter (PM2.5), with SARS-CoV-2 daily cases and deaths in Karachi, Lahore, and Islamabad, Pakistan, presenting the perspectives from the Global South. MATERIALS AND METHODS: The day-to-day PM2.5 levels were recorded from the metrological website, Real-Time Air Quality Index-AQI. The corresponding data on the COVID cases and deaths in Karachi, Lahore, and Islamabad were obtained from August 1, 2020, to September 30, 2021, from the Health Ministry and National Command Operations Centre Pakistan. RESULTS: The mean values for PM2.5 in Karachi were 110.4±46.2; in Lahore 174.0±83.2; and in Islamabad 107.1±40.0. The COVID-19 mean daily cases in Karachi were 538.9±446.6; Lahore 398.3±403.1; and Islamabad 212.2±187.6; and mean daily deaths in Karachi were 9.2±8.3; Lahore 9.3±9.7; and Islamabad 1.8±1.8. The results further depicted that the SARS-CoV-2 cases were 2.86 times higher in Karachi and 1.4 times higher in Lahore than in Islamabad. Similarly, the SARS-CoV-2 deaths were 3.6 and 2.8 times higher in Karachi and Lahore, respectively, compared to Islamabad. CONCLUSIONS: The findings claim that cases and deaths augmented significantly along with PM2.5 levels. These empirical estimates demonstrate an association between PM2.5 and SARS-CoV-2 daily cases and deaths in the cities of the Global South. These findings can contribute to policy-making decisions about addressing air pollutants and climate concerns in developing countries and create an urgency to develop a strategy for minimizing environmental pollution. This study can also steer the actions needed to address the environmental problems in developing countries to improve public health and safety.

Co-exposure to urban particulate matter and aircraft noise adversely impacts the cerebro-pulmonary-cardiovascular axis in mice.

Worldwide, up to 8.8 million excess deaths/year have been attributed to air pollution, mainly due to the exposure to fine particulate matter (PM). Traffic-related noise is an additional contributor to global mortality and morbidity. Both health risk factors substantially contribute to cardiovascular, metabolic and neuropsychiatric sequelae. Studies on the combined exposure are rare and urgently needed because of frequent co-occurrence of both risk factors in urban and industrial settings. To study the synergistic effects of PM and noise, we used an exposure system equipped with aerosol generator and loud-speakers, where C57BL/6 mice were acutely exposed for 3d to either ambient PM (NIST particles) and/or noise (aircraft landing and take-off events). The combination of both stressors caused endothelial dysfunction, increased blood pressure, oxidative stress and inflammation. An additive impairment of endothelial function was observed in isolated aortic rings and even more pronounced in cerebral and retinal arterioles. The increase in oxidative stress and inflammation markers together with RNA sequencing data indicate that noise particularly affects the brain and PM the lungs. The combination of both stressors has additive adverse effects on the cardiovascular system that are based on PM-induced systemic inflammation and noise-triggered stress hormone signaling. We demonstrate an additive upregulation of ACE-2 in the lung, suggesting that there may be an increased vulnerability to COVID-19 infection. The data warrant further mechanistic studies to characterize the propagation of primary target tissue damage (lung, brain) to remote organs such as aorta and heart by combined noise and PM exposure.

Air pollution and meteorology as risk factors for COVID-19 death in a cohort from Southern California.

BACKGROUND: Recent evidence links ambient air pollution to COVID-19 incidence, severity, and death, but few studies have analyzed individual-level mortality data with high quality exposure models. METHODS: We sought to assess whether higher air pollution exposures led to greater risk of death during or after hospitalization in confirmed COVID-19 cases among patients who were members of the Kaiser Permanente Southern California (KPSC) healthcare system (N=21,415 between 06-01-2020 and 01-31-2022 of whom 99.85 % were unvaccinated during the study period). We used 1 km resolution chemical transport models to estimate ambient concentrations of several common air pollutants, including ozone, nitrogen dioxide, and fine particle matter (PM2.5). We also derived estimates of pollutant exposures from ultra-fine particulate matter (PM0.1), PM chemical species, and PM sources. We employed Cox proportional hazards models to assess associations between air pollution exposures and death from COVID-19 among hospitalized patients. FINDINGS: We found significant associations between COVID-19 death and several air pollution exposures, including: PM2.5 mass, PM0.1 mass, PM2.5 nitrates, PM2.5 elemental carbon, PM2.5 on-road diesel, and PM2.5 on-road gasoline. Based on the interquartile (IQR) exposure increment, effect sizes ranged from hazard ratios (HR) = 1.12 for PM2.5 mass and PM2.5 nitrate to HR âˆ¼ 1.06-1.07 for other species or source markers. Humidity and temperature in the month of diagnosis were also significant negative predictors of COVID-19 death and negative modifiers of the air pollution effects. INTERPRETATION: Air pollution exposures and meteorology were associated the risk of COVID-19 death in a cohort of patients from Southern California. These findings have implications for prevention of death from COVID-19 and for future pandemics.

Environmental Impacts on COVID-19: Mechanisms of Increased Susceptibility.

Background: Since 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in >554M cases and >6.3M deaths worldwide. The disease caused by SARS-CoV-2, COVID-19, has resulted in a broad range of clinical symptoms differing in severity. Initially, the elderly were identified as particularly susceptible to severe COVID-19, with children experiencing less severe disease. However, as new variants arise, the epidemiology of SARS-CoV-2 infection is changing, and the disease severity in children is increasing. While environmental impacts on COVID-19 have been described, the underlying mechanisms are poorly described. Objective: The Pacific Basin Consortium for Environment and Health (PBC) held meeting on September 16, 2021, to explore environmental impacts on infectious diseases, including COVID-19. Methods: The PBC is an international group of environmental scientists and those interested in health outcomes. The PBC met to present preliminary data and discuss the role of exposures to airborne pollutants in enhancing susceptibility to and severity of respiratory tract viral infections, including COVID-19. Findings: Analysis of the literature and data presented identified age as an important factor in vulnerability to air pollution and enhanced COVID-19 susceptibility and severity. Mechanisms involved in increasing severity of COVID-19 were discussed, and gaps in knowledge were identified. Conclusions: Exposure to particulate matter (PM) pollution enhanced morbidity and mortality to COVID-19 in a pediatric population associated with induction of oxidative stress. In addition, free radicals present on PM can induce rapid changes in the viral genome that can lead to vaccine escape, altered host susceptibility, and viral pathogenicity. Nutritional antioxidant supplements have been shown to reduce the severity of viral infections, inhibit the inflammatory cytokine storm, and boost host immunity and may be of benefit in combating COVID-19.

Effects of Air Pollution on Chemosensory Dysfunction in COVID-19 Patients.

BACKGROUND: In some patients, coronavirus disease 2019 (COVID-19) is accompanied by loss of smell and taste, and this has been reportedly associated with exposure to air pollutants. This study investigated the relationship between the occurrence of chemosensory dysfunction in COVID-19 patients and air pollutant concentrations in Korea. METHODS: Information on the clinical symptom of chemosensory dysfunction, the date of diagnosis, residential area, age, and sex of 60,194 confirmed COVID-19 cases reported to the Korea Disease Control and Prevention Agency from January 20 to December 31, 2020 was collected. In addition, the daily average concentration of air pollutants for a week in the patients' residential area was collected from the Ministry of Environment based on the date of diagnosis of COVID-19. A binomial logistic regression model, using age and gender, standardized smoking rate, number of outpatient visits, 24-hour mean temperature and relative humidity at the regional level as covariates, was used to determine the effect of air pollution on chemosensory dysfunction. RESULTS: Symptoms of chemosensory dysfunction were most frequent among patients in their 20s and 30s, and occurred more frequently in large cities. The logistic analysis showed that the concentration of particulate matter 10 (PM10) and 2.5 (PM2.5) up to 2 days before the diagnosis of COVID-19 and the concentration of sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) at least 7 days before the diagnosis of COVID-19 affected the development of chemosensory dysfunction. In the logistic regression model adjusted for age, sex, standardized smoking rate, number of outpatient visits, and daily average temperature and relative humidity, it was found that an increase in the interquartile range of PM10, PM2.5, SO2, NO2, and CO on the day of diagnosis increased the incidence of chemosensory dysfunction 1.10, 1.10, 1.17, 1.31, and 1.19-fold, respectively. In contrast, the O3 concentration had a negative association with chemosensory dysfunction. CONCLUSION: High concentrations of air pollutants such as PM10, PM2.5, SO2, NO2, and CO on the day of diagnosis increased the risk of developing chemosensory dysfunction from COVID-19 infection. This result underscores the need to actively prevent exposure to air pollution and prevent COVID-19 infection. In addition, policies that regulate activities and products that create high amounts of harmful environmental wastes may help in promoting better health for all during COVID-19 pandemic.

Air pollution exposure induces a decrease in type II interferon response: A paired cohort study.

BACKGROUND: While air pollution is a major issue due to its harmful effects on human health, few studies focus on its impact on the immune system and vulnerability to viral infections. The lockdown declared following the COVID-19 pandemic represents a unique opportunity to study the large-scale impact of variations in air pollutants in real life. We hypothesized that variations in air pollutants modify Th1 response represented by interferon (IFN) γ production. METHODS: We conducted a single center paired pilot cohort study of 58 participants, and a confirmation cohort of 320 participants in Nice (France), with for each cohort two samplings at six months intervals. We correlated the variations in the production of IFNγ after non-specific stimulation of participants' immune cells with variations in key regulated pollutants: NO2, O3, PM2.5, and PM10 and climate variables. Using linear regression, we studied the effects of variations of each pollutant on the immune response. FINDINGS: In the pilot cohort, IFNγ production significantly decreased by 25.7% post-lockdown compared to during lockdown, while NO2 increased significantly by 46.0%. After the adjustment for climate variations during the study period (sunshine and temperature), we observed a significant effect of NO2 variation on IFNγ production (P=0.03). In the confirmation cohort IFNγ decreased significantly by 47.8% and after adjustment for environmental factors and intrinsic characteristics we observed a significant effect of environmental factors: NO2, PM10, O3, climatic conditions (sunshine exposure, relative humidity) on variation in IFNγ production (P=0.005, P<0.001, P=0.001, P=0.002 and P<0.001 respectively) but not independently from the BMI at inclusion and the workplace P=0.007 and P<0.001 respectively). INTERPRETATION: We show a weakening of the antiviral cellular response in correlation with an increase of pollutants exposition. FUNDING: Agence Nationale de la Recherche, Conseil Départemental des Alpes-Maritimes and Region Sud.

The Impact of Meteorological Factors and Air Pollutants on Acute Coronary Syndrome.

PURPOSE OF REVIEW: Several studies have found that air pollution and climate change can have an impact on acute coronary syndromes (ACS), the leading cause of death worldwide. We synthesized the latest information about the impact of air pollution and climate change on ACS, the latest data about the pathophysiological mechanisms of meteorological factors and atmospheric pollutants on atherosclerotic disease, and an overall image of air pollution and coronary heart disease in the context of the COVID-19 pandemic. RECENT FINDINGS: The variation of meteorological factors in different seasons increased the risk of ACS. Both the increase and the decrease in apparent temperature were found to be risk factors for ACS admissions. It was also demonstrated that exposure to high concentrations of air pollutants, especially particulate matter, increased cardiovascular morbidity and mortality. Climate change as well as increased emissions of air pollutants have a major impact on ACS. The industrialization era and the growing population cause a constant increase in air pollution worldwide. Thus, the number of ACS favored by air pollution and the variations in meteorological factors is expected to increase dramatically in the next few years.

Assessing the impact of long-term exposure to nine outdoor air pollutants on COVID-19 spatial spread and related mortality in 107 Italian provinces.

This paper investigates the air quality in 107 Italian provinces in the period 2014-2019 and the association between exposure to nine outdoor air pollutants and the COVID-19 spread and related mortality in the same areas. The methods used were negative binomial (NB) regression, ordinary least squares (OLS) model, and spatial autoregressive (SAR) model. The results showed that (i) common air pollutants-nitrogen dioxide (NO2), ozone (O3), and particulate matter (PM2.5 and PM10)-were highly and positively correlated with large firms, energy and gas consumption, public transports, and livestock sector; (ii) long-term exposure to NO2, PM2.5, PM10, benzene, benzo[a]pyrene (BaP), and cadmium (Cd) was positively and significantly correlated with the spread of COVID-19; and (iii) long-term exposure to NO2, O3, PM2.5, PM10, and arsenic (As) was positively and significantly correlated with COVID-19 related mortality. Specifically, particulate matter and Cd showed the most adverse effect on COVID-19 prevalence; while particulate matter and As showed the largest dangerous impact on excess mortality rate. The results were confirmed even after controlling for eighteen covariates and spatial effects. This outcome seems of interest because benzene, BaP, and heavy metals (As and Cd) have not been considered at all in recent literature. It also suggests the need for a national strategy to drive down air pollutant concentrations to cope better with potential future pandemics.