Effects of air pollution on the potential transmission and mortality of COVID-19: A preliminary case-study in Tarragona Province (Catalonia, Spain)
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ABSTRACT:
SUBMITTER: Marques M
PROVIDER: S-EPMC7550102 | biostudies-literature | 2020 Oct
REPOSITORIES: biostudies-literature
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Project description:Restaurant meal consumption has increased substantially, but the ability of restaurants to adhere to guidelines for the Mediterranean diet, healthiness and food allergen management is a challenge. This cross-sectional study aims to assess the Mediterranean diet adherence, healthiness, nutritional quality and food allergen management of meals at restaurants in the Tarragona province (Catalonia, Spain). Primary outcomes included adherence to criteria for the Mediterranean diet (AMed) and gluten management (SMAP), nutritional quality of dishes indicated by a green traffic light rating, meal nutrient content and allergen-free options. Secondary outcomes included restaurant staff knowledge about the Mediterranean diet and food allergens. Forty-four restaurants and 297 dishes were analysed. The restaurants fulfilled an average (mean ± SD) of 5.1 ± 1.6 of 9 compulsory AMed criteria and 12.9 ± 2.8 of 18 SMAP criteria. Dishes were mainly rated green for sugar (n = 178/297; 59.9%) but not for energy (n = 23/297; 7.7%) or total fat (n = 18/297; 6.1%). Waiters and cooks received passing scores for food allergen knowledge (5.8 ± 1.7 and 5.5 ± 1.5 out of 10 points, respectively). Restaurants partially met the AMed and SMAP criteria. Increasing fibre and decreasing saturated fat content are necessary to improve consumers' adherence to healthy diets. For restaurant staff, training courses should be considered to improve their food allergen management.
| S-EPMC8308532 | biostudies-literature
Project description:The Beijing-Tianjin-Hebei (BTH) air pollution transmission channel and its surrounding areas are of importance to air pollution control in China. Based on daily data of air quality index (AQI) and air pollutants (PM2.5, PM10, SO2, NO2, CO, and O3) from 2015 to 2016, this study analyzed the spatial and temporal characteristics of air pollution and influencing factors in Henan Province, a key region of the BTH air pollution transmission channel. The result showed that non-attainment days and NAQI were slightly improved at the provincial scale during the study period, whereas that in Hebi, Puyang, and Anyang became worse. PM2.5 was the largest contributor to the air pollution in all cities based on the number of non-attainment days, but its mean frequency decreased by 21.62%, with the mean occurrence of O3 doubled. The spatial distribution of NAQI presented a spatial agglomeration pattern, with high-high agglomeration area varying from Jiaozuo, Xinxiang, and Zhengzhou to Anyang and Hebi. In addition, the NAQI was negatively correlated with sunshine duration, temperature, relative humidity, wind speed, and positively to atmospheric pressure and relative humidity in all four clusters, whereas relationships between socioeconomic factors and NAQI differed among them. These findings highlight the need to establish and adjust regional joint prevention and control of air pollution as well as suggest that it is crucially important for implementing effective strategies for O3 pollution control.
| S-EPMC7084533 | biostudies-literature
Project description:The health, economic, and social impact of COVID-19 has been significant across the world. Our objective was to evaluate the association between air pollution (through NO2 and PM2.5 levels) and COVID-19 mortality in Spanish provinces from February 3, 2020, to July 14, 2020, adjusting for climatic parameters. An observational and ecological study was conducted with information extracted from Datadista repository (Datadista, 2020). Air pollutants (NO2 and PM2.5 levels) were analyzed as potential determinants of COVID-19 mortality. Multilevel Poisson regression models were used to analyze the risk of mortality after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Models were adjusted by four climatic variables (hours of solar radiation, precipitation, daily temperature and wind speed) and population size. The mean levels of PM2.5 and NO2 across all provinces and time in Spain were 8.7 μg/m3 (SD 9.7) and 8.7 μg/m3 (SD 6.2), respectively. High levels of PM2.5 (IRR = 1.016, 95% CI: 1.007-1.026), NO2 (IRR = 1.066, 95% CI: 1.058-1.075) and precipitation (IRRNO2 = 0.989, 95% CI: 0.981-0.997) were positively associated with COVID-19 mortality, whereas temperature (IRRPM2.5 = 0.988, 95% CI: 0.976-1.000; and IRRNO2 = 0.771, 95% CI: 0.761-0.782, respectively) and wind speed (IRRNO2 = 1.095, 95% CI: 1.061-1.131) were negatively associated with COVID-19 mortality. Air pollution can be a key factor to understand the mortality rate for COVID-19 in Spain. Furthermore, climatic variables could be influencing COVID-19 progression. Thus, air pollution and climatology ought to be taken into consideration in order to control the pandemic.Supplementary informationThe online version contains supplementary material available at 10.1007/s11869-021-01062-2.
| S-EPMC8310774 | biostudies-literature
Project description:BackgroundTraffic-related air pollution is emerging as a risk factor for Alzheimer's disease (AD) and impaired brain development. Individual differences in vulnerability to air pollution may involve the ε4 allele of Apolipoprotein E (APOE) gene, the primary genetic risk factor for AD.ObjectiveWe analyzed whether the association between traffic air pollution and neurodevelopmental outcomes is modified by APOEε4 status in children.MethodsData on parent-reported behavior problems (total difficulties scores, Strengths and Difficulties Questionnaire), teacher-reported attention-deficit hyperactivity disorder (ADHD) symptom scores, cognitive performance trajectories (computerized tests of inattentiveness and working memory repeated 2-4 times during January 2012-March 2013), and APOE genotypes were obtained for 1,667 children age 7-11 y attending 39 schools in or near Barcelona. Basal ganglia volume (putamen, caudate, and globus pallidum) was measured in 163 of the children by MRI (October 2012-April 2014.) Average annual outdoor polycyclic aromatic hydrocarbons (PAHs), elemental carbon (EC), and nitrogen dioxide (NO2) concentrations were estimated based on measurements at each school (two 1-wk campaigns conducted 6 months apart in 2012).ResultsAPOEε4 allele carriers had significantly higher behavior problem scores than noncarriers, and adverse associations with PAHs and NO2 were stronger or limited to ε4 carriers for behavior problem scores (P-interaction 0.03 and 0.04), caudate volume (P-interaction 0.04 and 0.03), and inattentiveness trajectories (P-interaction 0.15 and 0.08, respectively). Patterns of associations with the same outcomes were similar for EC.ConclusionPAHs, EC, and NO2 were associated with higher behavior problem scores, smaller reductions in inattentiveness over time, and smaller caudate volume in APOEε4 allele carriers in our study population, and corresponding associations were weak or absent among ε4 noncarriers. These findings support a potential role of APOE in biological mechanisms that may contribute to associations between air pollution and neurobehavioral outcomes in children. https://doi.org/10.1289/EHP2246.
| S-EPMC6108838 | biostudies-literature
Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Experiment Overall Design: Group 1 received Saline to serve as a control. Group 2 received Mount St. Helenâs ash, which does not contain any water-soluble zinc or other metals such that we can delineate any cardiac effect secondary to pulmonary deposition of these particles as these fine mode particles themselves are not likely to translocate to the heart. Group 3 received whole saline suspension of the same fugitive oil combustion particle sample used in the previous study, which contained insoluble components plus water-soluble zinc (Kodavanti et al., 2003; 14.5 ug/mg zinc) and also a small amount of water-soluble nickel (3.0 µg/mg). Elemental composition of this PM is comparable to Ottawa urban PM (Kodavanti et al., 2003). Group 4 also received same particle sample but at half the dose than group 3. Group 5 received saline-soluble or leachable fraction of PM-HD devoid of any solid material but contained soluble components including zinc and nickel. And, group 6 received zinc sulfate at concentration that was present in groups 3 or 5. This design allowed us to test if cardiac injury in rats was due to leached of zinc or solid particles. There were 4 replicates per treatment group.
2008-06-14 | E-GEOD-6541 | biostudies-arrayexpress
Project description:Burn injuries are one of the leading causes of morbidity worldwide. Although the overall incidence of burns and burn-related mortality is declining, these factors have not been analysed in our population for 25 years. The aim of this study has been to determine whether the epidemiological profile of patients hospitalized for burns has changed over the past 25 years. We performed a retrospective cohort study of patients hospitalised between 1 January 2011 and 31 December 2018 with a primary diagnosis of burns. The incidence of burns in our setting was 3.68/105 population. Most patients admitted for burns were men (61%), aged between 35 and 45 years (16.8%), followed by children aged between 0 and 4 years (12.4%). Scalding was the most prevalent mechanism of injury, and the region most frequently affected was the hands. The mean burned total body surface (TBSA) area was 8.3%, and the proportion of severely burned patients was 9.7%. Obesity was the most prevalent comorbidity (39.5%). The median length of stay was 1.8 days. The most frequent in-hospital complications were sepsis (16.6%), acute kidney injury (7.9%), and cardiovascular complications (5.9%). Risk factors for mortality were advanced age, high abbreviated burn severity index score, smoke inhalation, existing cardiovascular disease full-thickness burn, and high percentage of burned TBSA. Overall mortality was 4.3%. Multi-organ failure was the most frequent cause of death, with an incidence of 49.5%. The population has aged over the 25 years since the previous study, and the number of comorbidities has increased. The incidence and severity of burns, and the percentage of burned TBSA have all decreased, with scalding being the most prevalent mechanism of injury. The clinical presentation and evolution of burns differs between children and adults. Risk factors for mortality were advanced age, smoke inhalation, existing cardiovascular disease, full-thickness burn, and high percentage of burned TBSA.
| S-EPMC10474035 | biostudies-literature
Project description:ObjectiveTo estimate the attributable and targeted avoidable deaths (ADs; TADs) of outdoor air pollution by ambient particulate matter (PM10), PM2.5 and O3 according to specific WHO methodology.DesignHealth impact assessment.SettingCity of Valladolid, Spain (around 300 000 residents).Data sourcesDemographics; mortality; pollutant concentrations collected 1999-2008.Main outcome measuresAttributable fractions; ADs and TADs per year for 1999-2008.ResultsHigher TADs estimates (shown here) were obtained when assuming as 'target' concentrations WHO Air Quality Guidelines instead of Directive 2008/50/EC. ADs are considered relative to pollutant background levels. All-cause mortality associated to PM10 (all ages): 52 ADs (95% CI 39 to 64); 31 TADs (95% CI 24 to 39).All-cause mortality associated to PM10 (<5 years): 0 ADs (95% CI 0 to 1); 0 TADs (95% CI 0 to 1). All-cause mortality associated to PM2.5 (>30 years): 326 ADs (95% CI 217 to 422); 231 TADs (95% CI 153 to 301). Cardiopulmonary and lung cancer mortality associated to PM2.5 (>30 years): Cardiopulmonary: 186 ADs (95% CI 74 to 280); 94 TADs (95% CI 36 to 148). Lung cancer : 51 ADs (95% CI 21 to 73); 27 TADs (95% CI 10 to 41).All-cause, respiratory and cardiovascular mortality associated to O3 (all ages): All-cause: 52ADs (95% CI 25 to 77) ; 31 TADs (95% CI 15 to 45). Respiratory: 5ADs (95% CI -2 to 13) ; 3 TADs (95% CI -1 to 8). Cardiovascular: 30 ADs (95% CI 8 to 51) ; 17 TADs (95% CI 5 to 30). Negative estimates which should be read as zero were obtained when pollutant concentrations were below counterfactuals or assumed risk coefficients were below one.ConclusionsOur estimates suggest a not negligible negative impact on mortality of outdoor air pollution. The implementation of WHO methodology provides critical information to distinguish an improvement range in air pollution control.
| S-EPMC4202014 | biostudies-literature
Project description:BackgroundEmerging evidence links ambient air pollution with coronavirus 2019 (COVID-19) disease, an association that is methodologically challenging to investigate.ObjectivesWe examined the association between long-term exposure to air pollution with SARS-CoV-2 infection measured through antibody response, level of antibody response among those infected, and COVID-19 disease.MethodsWe contacted 9,605 adult participants from a population-based cohort study in Catalonia between June and November 2020; most participants were between 40 and 65 years of age. We drew blood samples from 4,103 participants and measured immunoglobulin M (IgM), IgA, and IgG antibodies against five viral target antigens to establish infection to the virus and levels of antibody response among those infected. We defined COVID-19 disease using self-reported hospital admission, prior positive diagnostic test, or more than three self-reported COVID-19 symptoms after contact with a COVID-19 case. We estimated prepandemic (2018-2019) exposure to fine particulate matter [PM with an aerodynamic diameter of ≤2.5μm (PM2.5)], nitrogen dioxide (NO2), black carbon (BC), and ozone (O3) at the residential address using hybrid land-use regression models. We calculated log-binomial risk ratios (RRs), adjusting for individual- and area-level covariates.ResultsAmong those tested for SARS-CoV-2 antibodies, 743 (18.1%) were seropositive. Air pollution levels were not statistically significantly associated with SARS-CoV-2 infection: Adjusted RRs per interquartile range were 1.07 (95% CI: 0.97, 1.18) for NO2, 1.04 (95% CI: 0.94, 1.14) for PM2.5, 1.00 (95% CI: 0.92, 1.09) for BC, and 0.97 (95% CI: 0.89, 1.06) for O3. Among infected participants, exposure to NO2 and PM2.5 were positively associated with IgG levels for all viral target antigens. Among all participants, 481 (5.0%) had COVID-19 disease. Air pollution levels were associated with COVID-19 disease: adjusted RRs=1.14 (95% CI: 1.00, 1.29) for NO2 and 1.17 (95% CI: 1.03, 1.32) for PM2.5. Exposure to O3 was associated with a slightly decreased risk (RR=0.92; 95% CI: 0.83, 1.03). Associations of air pollution with COVID-19 disease were more pronounced for severe COVID-19, with RRs=1.26 (95% CI: 0.89, 1.79) for NO2 and 1.51 (95% CI: 1.06, 2.16) for PM2.5.DiscussionExposure to air pollution was associated with a higher risk of COVID-19 disease and level of antibody response among infected but not with SARS-CoV-2 infection. https://doi.org/10.1289/EHP9726.
| S-EPMC8597405 | biostudies-literature
Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Keywords: Pulmonary exposure, Cardiac gene expression
2007-11-15 | GSE6541 | GEO
Project description: Not available
| S-EPMC7906723 | biostudies-literature