Air pollution during New Year's fireworks and daily mortality in the Netherlands.
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ABSTRACT:
SUBMITTER: Greven FE
PROVIDER: S-EPMC6450968 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Anthropogenic disturbances of wildlife, such as noise, human presence, hunting activity, and motor vehicles, are becoming an increasing concern in conservation biology. Fireworks are an important part of celebrations worldwide, and although humans often find fireworks spectacular, fireworks are probably perceived quite differently by wild animals. Behavioral responses to fireworks are difficult to study at night, and little is known about the negative effects fireworks may have on wildlife. Every year, thousands of tons of fireworks are lit by civilians on New Year's Eve in the Netherlands. Using an operational weather radar, we quantified the reaction of birds to fireworks in 3 consecutive years. Thousands of birds took flight shortly after midnight, with high aerial movements lasting at least 45 min and peak densities measured at 500 m altitude. The highest densities were observed over grasslands and wetlands, including nature conservation sites, where thousands of waterfowl rest and feed. The Netherlands is the most important winter staging area for several species of waterfowl in Europe. We estimate that hundreds of thousands of birds in the Netherlands take flight due to fireworks. The spatial and temporal extent of disturbance is substantial, and potential consequences are discussed. Weather radar provides a unique opportunity to study the reaction of birds to fireworks, which has otherwise remained elusive.
| S-EPMC3199162 | biostudies-literature
Project description:BackgroundThe systematic evaluation of the results of time-series studies of air pollution is challenged by differences in model specification and publication bias.MethodsWe evaluated the associations of inhalable particulate matter (PM) with an aerodynamic diameter of 10 ?m or less (PM10) and fine PM with an aerodynamic diameter of 2.5 ?m or less (PM2.5) with daily all-cause, cardiovascular, and respiratory mortality across multiple countries or regions. Daily data on mortality and air pollution were collected from 652 cities in 24 countries or regions. We used overdispersed generalized additive models with random-effects meta-analysis to investigate the associations. Two-pollutant models were fitted to test the robustness of the associations. Concentration-response curves from each city were pooled to allow global estimates to be derived.ResultsOn average, an increase of 10 ?g per cubic meter in the 2-day moving average of PM10 concentration, which represents the average over the current and previous day, was associated with increases of 0.44% (95% confidence interval [CI], 0.39 to 0.50) in daily all-cause mortality, 0.36% (95% CI, 0.30 to 0.43) in daily cardiovascular mortality, and 0.47% (95% CI, 0.35 to 0.58) in daily respiratory mortality. The corresponding increases in daily mortality for the same change in PM2.5 concentration were 0.68% (95% CI, 0.59 to 0.77), 0.55% (95% CI, 0.45 to 0.66), and 0.74% (95% CI, 0.53 to 0.95). These associations remained significant after adjustment for gaseous pollutants. Associations were stronger in locations with lower annual mean PM concentrations and higher annual mean temperatures. The pooled concentration-response curves showed a consistent increase in daily mortality with increasing PM concentration, with steeper slopes at lower PM concentrations.ConclusionsOur data show independent associations between short-term exposure to PM10 and PM2.5 and daily all-cause, cardiovascular, and respiratory mortality in more than 600 cities across the globe. These data reinforce the evidence of a link between mortality and PM concentration established in regional and local studies. (Funded by the National Natural Science Foundation of China and others.).
| S-EPMC7891185 | biostudies-literature
Project description:Epidemiological studies have linked daily concentrations of urban air pollution to mortality, but few have investigated specific traffic sources that can inform abatement policies. We assembled a database of >100 daily, measured and modelled pollutant concentrations characterizing air pollution in London between 2011 and 2012. Based on the analyses of temporal patterns and correlations between the metrics, knowledge of local emission sources and reference to the existing literature, we selected, a priori, markers of traffic pollution: oxides of nitrogen (general traffic); elemental and black carbon (EC/BC) (diesel exhaust); carbon monoxide (petrol exhaust); copper (tyre), zinc (brake) and aluminium (mineral dust). Poisson regression accounting for seasonality and meteorology was used to estimate the percentage change in risk of death associated with an interquartile increment of each pollutant. Associations were generally small with confidence intervals that spanned 0% and tended to be negative for cardiovascular mortality and positive for respiratory mortality. The strongest positive associations were for EC and BC adjusted for particle mass and respiratory mortality, 2.66% (95% confidence interval: 0.11, 5.28) and 2.72% (0.09, 5.42) per 0.8 and 1.0 μg/m(3), respectively. These associations were robust to adjustment for other traffic metrics and regional pollutants, suggesting a degree of specificity with respiratory mortality and diesel exhaust containing EC/BC.
| S-EPMC4756269 | 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:Aiming at improving the air quality and protecting public health, policies such as restricting factories, motor vehicles, and fireworks have been widely implemented. However, fine-grained spatiotemporal analysis of these policies' effectiveness is lacking. This paper collected the hourly meteorological and PM2.5 data for three typical emission scenarios in Hubei, Beijing-Tianjin-Hebei (BTH), and Yangtze River Delta (YRD). Then, this study simulated the PM2.5 concentration under the same meteorological conditions and different emission scenarios based on a reliable hourly spatiotemporal random forest model (R2 exceeded 0.84). Finally, we investigated the fine-grained spatiotemporal impact of restricting factories, vehicles, and fireworks on PM2.5 concentrations from the perspective of hours, days, regions, and land uses, excluding meteorological interference. On average, restricting factories and vehicles reduced the PM2.5 concentration at 02:00, 08:00, 14:00, and 20:00 by 18.57, 16.22, 25.00, and 19.07 ?g/m3, respectively. Spatially, it had the highest and quickest impact on Hubei, with a 27.05 ?g/m3 decrease of PM2.5 concentration and 17 day lag to begin to show significant decline. This was followed by YRD, which experienced a 23.52 ?g/m3 decrease on average and a 23 day lag. BTH was the least susceptible; the PM2.5 concentration decreased by only 8.2 ?g/m3. In addition, influenced by intensive human activities, the cultivated, urban, and rural lands experienced a larger decrease in PM2.5 concentration. These empirical results revealed that restricting factories, vehicles, and fireworks is effective in alleviating air pollution and the effect showed significant spatiotemporal heterogeneity. The policymakers should further investigate influential factors of hourly PM2.5 concentrations, combining with local geographical and social environment, and implement more effective and targeted policies to improve local air quality, especially for BTH and the air quality at morning and night.
| S-EPMC7370000 | 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:BackgroundHeat and air pollution are both associated with increases in mortality. However, the interactive effect of temperature and air pollution on mortality remains unsettled. Similarly, the relationship between air pollution, air temperature, and social deprivation has never been explored.MethodsWe used daily mortality data from 2004 to 2009, daily mean temperature variables and relative humidity, for Paris, France. Estimates of chronic exposure to air pollution and social deprivation at a small spatial scale were calculated and split into three strata. We developed a stratified Poisson regression models to assess daily temperature and mortality associations, and tested the heterogeneity of the regression coefficients of the different strata. Deaths due to ambient temperature were calculated from attributable fractions and mortality rates were estimated.ResultsWe found that chronic air pollution exposure and social deprivation are effect modifiers of the association between daily temperature and mortality. We found a potential interactive effect between social deprivation and chronic exposure with regards to air pollution in the mortality-temperature relationship.ConclusionOur results may have implications in considering chronically polluted areas as vulnerable in heat action plans and in the long-term measures to reduce the burden of heat stress especially in the context of climate change.
| S-EPMC4073194 | biostudies-literature
Project description:Within popular press there has been much coverage of the negative effects associated with firework and horses. The effect of fireworks has been documented in companion animals, yet no studies have investigated the negative effects, or otherwise, of fireworks on horses. This study aims to document horse responses and current management strategies to fireworks via an online survey. Of the total number of horses, 39% (1987/4765) were rated as "anxious", 40% (1816/4765) "very anxious" and only 21% (965/4765) rated as "not anxious" around fireworks. Running (82%, 912/1107) was the most common behaviour reported, with no difference between property type (p > 0.05) or location (p > 0.05). Possibly as a consequence of the high frequency of running, 35% (384/1107) of respondents reported having horses break through fences in response to fireworks and a quarter (26%, 289/1099) reported that their horse(s) had received injuries associated with fireworks. The most common management strategy was moving their horse(s) to a paddock away from the fireworks (77%) and to stable/yard them (55%). However, approximately 30% reported these management strategies to be ineffective. Of the survey participants, 90% (996/1104) were against the sale of fireworks for private use.
| S-EPMC4810048 | biostudies-literature
Project description:Long-term exposure to air pollution is considered a major public health concern and has been related to overall mortality and various diseases such as respiratory and cardiovascular disease. Due to the spatial variability of air pollution concentrations, assessment of individual exposure to air pollution requires spatial datasets at high resolution. Combining detailed air pollution maps with personal mobility and activity patterns allows for an improved exposure assessment. We present high-resolution datasets for the Netherlands providing average ambient air pollution concentration values for the year 2009 for NO2, NOx, PM2.5, PM2.5absorbance and PM10. The raster datasets on 5×5 m grid cover the entire Netherlands and were calculated using the land use regression models originating from the European Study of Cohorts for Air Pollution Effects (ESCAPE) project. Additional datasets with nationwide and regional measurements were used to evaluate the generated concentration maps. The presented datasets allow for spatial aggregations on different scales, nationwide individual exposure assessment, and the integration of activity patterns in the exposure estimation of individuals.
| S-EPMC6413687 | biostudies-literature
Project description:BackgroundAmbient air pollution and tuberculosis (TB) have an impact on public health worldwide, yet associations between the two remain uncertain.ObjectiveWe determined the impact of residential traffic on mortality during treatment of active TB.MethodsFrom 2000-2012, we enrolled 32,875 patients in California with active TB and followed them throughout treatment. We obtained patient data from the California Tuberculosis Registry and calculated traffic volumes and traffic densities in 100- to 400-m radius buffers around residential addresses. We used Cox models to determine mortality hazard ratios, controlling for demographic, socioeconomic, and clinical potential confounders. We categorized traffic exposures as quintiles and determined trends using Wald tests.ResultsParticipants contributed 22,576 person-years at risk. There were 2,305 deaths during treatment for a crude mortality rate of 1,021 deaths per 10,000 person-years. Traffic volumes and traffic densities in all buffers around patient residences were associated with increased mortality during TB treatment, although the findings were not statistically significant in all buffers. As the buffer size decreased, fifth-quintile mortality hazards increased, and trends across quintiles of traffic exposure became more statistically significant. Increasing quintiles of nearest-road traffic volumes in the 100-m buffer were associated with 3%, 14%, 19%, and 28% increased risk of death during TB treatment [first quintile, referent; second quintile hazard ratio (HR)=1.03 [95% confidence interval (CI): 0.86, 1.25]; third quintile HR=1.14 (95% CI: 0.95, 1.37); fourth quintile HR=1.19 (95% CI: 0.99, 1.43); fifth quintile HR=1.28 (95% CI: 1.07, 1.53), respectively; p-trend=0.002].ConclusionsResidential proximity to road traffic volumes and traffic density were associated with increased all-cause mortality in patients undergoing treatment for active tuberculosis even after adjusting for multiple demographic, socioeconomic, and clinical factors, suggesting that TB patients are susceptible to the adverse health effects of traffic-related air pollution. https://doi.org/10.1289/EHP1699.
| S-EPMC5915191 | biostudies-literature