Joint effect of heat and air pollution on mortality in 620 cities of 36 countries.
Ontology highlight
ABSTRACT: Background
The epidemiological evidence on the interaction between heat and ambient air pollution on mortality is still inconsistent.Objectives
To investigate the interaction between heat and ambient air pollution on daily mortality in a large dataset of 620 cities from 36 countries.Methods
We used daily data on all-cause mortality, air temperature, particulate matter ≤ 10 μm (PM10), PM ≤ 2.5 μm (PM2.5), nitrogen dioxide (NO2), and ozone (O3) from 620 cities in 36 countries in the period 1995-2020. We restricted the analysis to the six consecutive warmest months in each city. City-specific data were analysed with over-dispersed Poisson regression models, followed by a multilevel random-effects meta-analysis. The joint association between air temperature and air pollutants was modelled with product terms between non-linear functions for air temperature and linear functions for air pollutants.Results
We analyzed 22,630,598 deaths. An increase in mean temperature from the 75th to the 99th percentile of city-specific distributions was associated with an average 8.9 % (95 % confidence interval: 7.1 %, 10.7 %) mortality increment, ranging between 5.3 % (3.8 %, 6.9 %) and 12.8 % (8.7 %, 17.0 %), when daily PM10 was equal to 10 or 90 μg/m3, respectively. Corresponding estimates when daily O3 concentrations were 40 or 160 μg/m3 were 2.9 % (1.1 %, 4.7 %) and 12.5 % (6.9 %, 18.5 %), respectively. Similarly, a 10 μg/m3 increment in PM10 was associated with a 0.54 % (0.10 %, 0.98 %) and 1.21 % (0.69 %, 1.72 %) increase in mortality when daily air temperature was set to the 1st and 99th city-specific percentiles, respectively. Corresponding mortality estimate for O3 across these temperature percentiles were 0.00 % (-0.44 %, 0.44 %) and 0.53 % (0.38 %, 0.68 %). Similar effect modification results, although slightly weaker, were found for PM2.5 and NO2.Conclusions
Suggestive evidence of effect modification between air temperature and air pollutants on mortality during the warm period was found in a global dataset of 620 cities.
SUBMITTER: Stafoggia M
PROVIDER: S-EPMC10702017 | biostudies-literature | 2023 Nov
REPOSITORIES: biostudies-literature
Publications
Joint effect of heat and air pollution on mortality in 620 cities of 36 countries.
Stafoggia Massimo M Michelozzi Paola P Schneider Alexandra A Armstrong Ben B Scortichini Matteo M Rai Masna M Achilleos Souzana S Alahmad Barrak B Analitis Antonis A Åström Christofer C Bell Michelle L ML Calleja Neville N Krage Carlsen Hanne H Carrasco Gabriel G Paul Cauchi John J Dszs Coelho Micheline M Correa Patricia M PM Diaz Magali H MH Entezari Alireza A Forsberg Bertil B Garland Rebecca M RM Leon Guo Yue Y Guo Yuming Y Hashizume Masahiro M Holobaca Iulian H IH Íñiguez Carmen C Jaakkola Jouni J K JJK Kan Haidong H Katsouyanni Klea K Kim Ho H Kyselý Jan J Lavigne Eric E Lee Whanhee W Li Shanshan S Maasikmets Marek M Madureira Joana J Mayvaneh Fatemeh F Fook Sheng Ng Chris C Nunes Baltazar B Orru Hans H V Ortega Nicolás N Osorio Samuel S Palomares Alfonso D L ADL Pan Shih-Chun SC Pascal Mathilde M Ragettli Martina S MS Rao Shilpa S Raz Raanan R Roye Dominic D Ryti Niilo N Hn Saldiva Paulo P Samoli Evangelia E Schwartz Joel J Scovronick Noah N Sera Francesco F Tobias Aurelio A Tong Shilu S Dlc Valencia César C Maria Vicedo-Cabrera Ana A Urban Aleš A Gasparrini Antonio A Breitner Susanne S De' Donato Francesca K FK
Environment international 20231010
<h4>Background</h4>The epidemiological evidence on the interaction between heat and ambient air pollution on mortality is still inconsistent.<h4>Objectives</h4>To investigate the interaction between heat and ambient air pollution on daily mortality in a large dataset of 620 cities from 36 countries.<h4>Methods</h4>We used daily data on all-cause mortality, air temperature, particulate matter ≤ 10 μm (PM<sub>10</sub>), PM ≤ 2.5 μm (PM<sub>2.5</sub>), nitrogen dioxide (NO<sub>2</sub>), and ozone ( ...[more]
Similar Datasets
Project description:Evidence on the health effects of extreme temperatures and air pollution is copious. However few studies focused on their interaction. The aim of this study is to evaluate daily PM10 and ozone as potential effect modifiers of the relationship between temperature and natural mortality in 25 Italian cities. Time-series analysis was run for each city. To evaluate interaction, a tensor product between mean air temperature (lag 0⁻3) and either PM10 or ozone (both lag 0⁻5) was defined and temperature estimates were extrapolated at low, medium, and high levels of pollutants. Heat effects were estimated as percent change in mortality for increases in temperature between 75th and 99th percentiles. Results were pooled by geographical area. Differential temperature-mortality risks by air pollutants were found. For PM10, estimates ranged from 3.9% (low PM10) to 14.1% (high PM10) in the North, from 3.6% to 24.4% in the Center, and from 7.5% to 21.6% in the South. Temperature-related mortality was similarly modified by ozone in northern and central Italy, while no effect modification was observed in the South. This study underlines the synergistic effects of heat and air pollution on mortality. Considering the predicted increase in heat waves and stagnation events in the Mediterranean countries such as Italy, it is time to enclose air pollution within public health heat prevention plans.
| S-EPMC6122066 | 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 μm or less (PM10) and fine PM with an aerodynamic diameter of 2.5 μm 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 μg 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:PurposeThe association between air pollutant (PM2.5, PM10, NO2, and O3) concentrations and daily number of COVID-19 confirmed cases and related deaths were evaluated in three major Iranian cities (Tehran, Mashhad, and Tabriz).MethodsHourly concentrations of air pollutants and daily number of PCR-confirmed cases and deaths of COVID-19 were acquired (February 20th, 2020 to January 4th, 2021). A generalized additive model (GAM) assuming a quasi-Poisson distribution was used to model the associations in each city up to lag-day 7 (for mortality) and 14 (for morbidity). Then, the city-specific estimates were meta-analyzed using a fixed effect model to obtain the overall relative risks (RRs).ResultsA total of 114,964 confirmed cases and 21,549 deaths were recorded in these cities. For confirmed cases, exposure to PM2.5, NO2, and O3 for several lag-days showed significant associations. In case of mortality, meta-analysis estimated that the RRs for PM2.5, PM10, NO2, and O3 concentrations were 1.06 (95% CI: 0.99, 1.13), 1.06 (95% CI: 0.93, 1.19), 1.15 (95% CI: 0.93, 1.38), and 1.07 (95% CI: 0.84, 1.31), respectively. Despite several positive associations with all air pollutants over multiple lag-days, COVID-19 mortality was only significantly associated with NO2 on lag-days 0-1 and 1 with the RRs of 1.35 (95% CI: 1.04, 1.67) and 1.16 (95% CI: 1.02, 1.31), respectively.ConclusionThis study showed that air pollution can be a factor exacerbating COVID-19 infection and clinical outcomes. Actions should be taken to reduce the exposure of the public and particularly patients to ambient air pollutants.Supplementary informationThe online version contains supplementary material available at 10.1007/s40201-021-00736-4.
| S-EPMC8553398 | biostudies-literature
Project description:Recent studies have identified inequality in the distribution of air pollution attributable health impacts, but to our knowledge this has not been examined in Canadian cities. We evaluated the extent and sources of inequality in air pollution attributable mortality at the census tract (CT) level in seven of Canada's largest cities. We first regressed fine particulate matter (PM2.5) and nitrogen dioxide (NO2) attributable mortality against the neighborhood (CT) level prevalence of age 65 and older, low income, low educational attainment, and identification as an Indigenous (First Nations, Métis, Inuit) or Black person, accounting for spatial autocorrelation. We next examined the distribution of baseline mortality rates, PM2.5 and NO2 concentrations, and attributable mortality by neighborhood (CT) level prevalence of these characteristics, calculating the concentration index, Atkinson index, and Gini coefficient. Finally, we conducted a counterfactual analysis of the impact of reducing baseline mortality rates and air pollution concentrations on inequality in air pollution attributable mortality. Regression results indicated that CTs with a higher prevalence of low income and Indigenous identity had significantly higher air pollution attributable mortality. Concentration index, Atkinson index, and Gini coefficient values revealed different degrees of inequality among the cities. Counterfactual analysis indicated that inequality in air pollution attributable mortality tended to be driven more by baseline mortality inequalities than exposure inequalities. Reducing inequality in air pollution attributable mortality requires reducing disparities in both baseline mortality and air pollution exposure.
| S-EPMC10465848 | biostudies-literature
Project description:Studying weekend-weekday variation in ground-level ozone (O3) allows one to better understand O3 formation conditions, with a potential for developing effective strategies for O3 control. Reducing inappropriately the O3 precursors emissions can either produce no reduction or increase surface O3 concentrations. This paper analyzes the weekend-weekday differences of O3 at 300 rural and 808 urban background stations worldwide from 2005 to 2014, in order to investigate the O3 weekend effect over time and assess the effectiveness of the precursors emissions control policies for reducing O3 levels. Data were analyzed with the non-parametric Mann-Kendall test and Theil-Sen estimator. Rural sites typically did not experience a weekend-weekday effect. In all urban stations, the mean O3 concentration on the weekend was 12% higher than on weekdays. Between 2005 and 2014, the annual mean of daily O3 concentrations increased at 74% of urban sites worldwide (+ 0.41 ppb year-1) and decreased in the United Kingdom (- 0.18 ppb year-1). Over this time period, emissions of O3 precursors declined significantly. However, a greater decline in nitrogen oxides (NOx) emissions caused an increase in Volatile Organic Compounds (VOCs) to NOx ratios leading to O3 formation. In France, South Korea and the United Kingdom, most urban stations showed a significant upward trend (+ 1.15% per year) for O3 weekend effect. Conversely, in Canada, Germany, Japan, Italy and the United States, the O3 weekend effect showed a significant downward trend (- 0.26% per year). Further or inappropriate control of anthropogenic emissions in Canada, Southern Europe, Japan, South Korea and the United States might result in increased daily O3 levels in urban areas.
| S-EPMC7483290 | biostudies-literature
Project description:Objectives To estimate the short term effect of particulate air pollution (particle diameter <10 μm, or PM10) on mortality and explore the heterogeneity of particulate air pollution effects in major cities in China.Design Generalised linear models with different lag structures using time series data.Setting 38 of the largest cities in 27 provinces of China (combined population >200 million).Participants 350 638 deaths (200 912 in males, 149 726 in females) recorded in 38 city districts by the Disease Surveillance Point System of the Chinese Center for Disease Control and Prevention from 1 January 2010 to 29 June 2013.Main outcome measure Daily numbers of deaths from all causes, cardiorespiratory diseases, and non-cardiorespiratory diseases and among different demographic groups were used to estimate the associations between particulate air pollution and mortality.Results A 10 µg/m3 change in concurrent day PM10 concentrations was associated with a 0.44% (95% confidence interval 0.30% to 0.58%) increase in daily number of deaths. Previous day and two day lagged PM10 levels decreased in magnitude by one third and two thirds but remained statistically significantly associated with increased mortality. The estimate for the effect of PM10 on deaths from cardiorespiratory diseases was 0.62% (0.43% to 0.81%) per 10 µg/m3 compared with 0.26% (0.09% to 0.42%) for other cause mortality. Exposure to PM10 had a greater impact on females than on males. Adults aged 60 and over were more vulnerable to particulate air pollution at high levels than those aged less than 60. The PM10 effect varied across different cities and marginally decreased in cities with higher PM10 concentrations.Conclusion Particulate air pollution has a greater impact on deaths from cardiorespiratory diseases than it does on other cause mortality. People aged 60 or more have a higher risk of death from particulate air pollution than people aged less than 60. The estimates of the effect varied across cities and covered a wide range of domain.
| S-EPMC6287590 | biostudies-literature
Project description:BackgroundThe evidence for acute effects of air pollution on mortality in India is scarce, despite the extreme concentrations of air pollution observed. This is the first multi-city study in India that examines the association between short-term exposure to PM2·5 and daily mortality using causal methods that highlight the importance of locally generated air pollution.MethodsWe applied a time-series analysis to ten cities in India between 2008 and 2019. We assessed city-wide daily PM2·5 concentrations using a novel hybrid nationwide spatiotemporal model and estimated city-specific effects of PM2·5 using a generalised additive Poisson regression model. City-specific results were then meta-analysed. We applied an instrumental variable causal approach (including planetary boundary layer height, wind speed, and atmospheric pressure) to evaluate the causal effect of locally generated air pollution on mortality. We obtained an integrated exposure-response curve through a multivariate meta-regression of the city-specific exposure-response curve and calculated the fraction of deaths attributable to air pollution concentrations exceeding the current WHO 24 h ambient PM2·5 guideline of 15 μg/m3. To explore the shape of the exposure-response curve at lower exposures, we further limited the analyses to days with concentrations lower than the current Indian standard (60 μg/m3).FindingsWe observed that a 10 μg/m3 increase in 2-day moving average of PM2·5 was associated with 1·4% (95% CI 0·7-2·2) higher daily mortality. In our causal instrumental variable analyses representing the effect of locally generated air pollution, we observed a stronger association with daily mortality (3·6% [2·1-5·0]) than our overall estimate. Our integrated exposure-response curve suggested steeper slopes at lower levels of exposure and an attenuation of the slope at high exposure levels. We observed two times higher risk of death per 10 μg/m3 increase when restricting our analyses to observations below the Indian air quality standard (2·7% [1·7-3·6]). Using the integrated exposure-response curve, we observed that 7·2% (4·2%-10·1%) of all daily deaths were attributed to PM2·5 concentrations higher than the WHO guidelines.InterpretationShort-term PM2·5 exposure was associated with a high risk of death in India, even at concentrations well below the current Indian PM2·5 standard. These associations were stronger for locally generated air pollutants quantified through causal modelling methods than conventional time-series analysis, further supporting a plausible causal link.FundingSwedish Research Council for Sustainable Development.
| S-EPMC11774940 | biostudies-literature
Project description:RationaleA large body of epidemiologic literature has found an association of increased fine particulate air pollution (PM2.5) with acute and chronic mortality. The effect of improvements in particle exposure is less clear.ObjectivesEarlier analysis of the Harvard Six Cities adult cohort study showed an association between long-term ambient PM2.5 and mortality between enrollment in the mid-1970s and follow-up until 1990. We extended mortality follow-up for 8 yr in a period of reduced air pollution concentrations.MethodsAnnual city-specific PM2.5 concentrations were measured between 1979 and 1988, and estimated for later years from publicly available data. Exposure was defined as (1) city-specific mean PM2.5 during the two follow-up periods, (2) mean PM2.5 in the first period and change between these periods, (3) overall mean PM2.5 across the entire follow-up, and (4) year-specific mean PM2.5. Mortality rate ratios were estimated with Cox proportional hazards regression controlling for individual risk factors.Measurements and main resultsWe found an increase in overall mortality associated with each 10 microg/m3 increase in PM2.5 modeled either as the overall mean (rate ratio [RR], 1.16; 95% confidence interval [CI], 1.07-1.26) or as exposure in the year of death (RR, 1.14; 95% CI, 1.06-1.22). PM2.5 exposure was associated with lung cancer (RR, 1.27; 95% CI, 0.96-1.69) and cardiovascular deaths (RR, 1.28; 95% CI, 1.13-1.44). Improved overall mortality was associated with decreased mean PM2.5 (10 microg/m3) between periods (RR, 0.73; 95% CI, 0.57-0.95).ConclusionTotal, cardiovascular, and lung cancer mortality were each positively associated with ambient PM2.5 concentrations. Reduced PM2.5 concentrations were associated with reduced mortality risk.
| S-EPMC2662950 | 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:BackgroundCoarse particulate matter with aerodynamic diameter between 2.5 and [Formula: see text] ([Formula: see text]) air pollution is a severe environmental problem in developing countries, but its challenges to public health were rarely evaluated.ObjectiveWe aimed to investigate the associations between day-to-day changes in [Formula: see text] and cause-specific mortality in China.MethodsWe conducted a nationwide daily time-series analysis in 272 main Chinese cities from 2013 to 2015. The associations between [Formula: see text] concentrations and mortality were analyzed in each city using overdispersed generalized additive models. Two-stage Bayesian hierarchical models were used to estimate national and regional average associations, and random-effect models were used to pool city-specific concentration-response curves. Two-pollutant models were adjusted for fine particles with aerodynamic diameter [Formula: see text] ([Formula: see text]) or gaseous pollutants.ResultsOverall, we observed positive and approximately linear concentration-response associations between [Formula: see text] and daily mortality. A [Formula: see text] increase in [Formula: see text] was associated with higher mortality due to nonaccidental causes [0.23%; 95% posterior interval (PI): 0.13, 0.33], cardiovascular diseases (CVDs; 0.25%; 95% PI: 0.13, 0.37), coronary heart disease (CHD; 0.21%; 95% PI: 0.05, 0.36), stroke (0.21%; 95% PI: 0.08, 0.35), respiratory diseases (0.26%; 95% PI: 0.07, 0.46), and chronic obstructive pulmonary disease (COPD; 0.34%; 95% PI: 0.12, 0.57). Associations were stronger for cities in southern vs. northern China, with significant differences for total and cardiovascular mortality. Associations with [Formula: see text] were of similar magnitude to those for [Formula: see text] in both single- and two-pollutant models with mutual adjustment. Associations were robust to adjustment for gaseous pollutants other than nitrogen dioxide and sulfur dioxide. Meta-regression indicated that a larger positive correlation between [Formula: see text] and [Formula: see text] predicted stronger city-specific associations between [Formula: see text] and total mortality.ConclusionsThis analysis showed significant associations between short-term [Formula: see text] exposure and daily nonaccidental and cardiopulmonary mortality based on data from 272 cities located throughout China. Associations appeared to be independent of exposure to [Formula: see text], carbon monoxide, and ozone. https://doi.org/10.1289/EHP2711.
| S-EPMC6378682 | biostudies-literature