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1.
JAMA Netw Open ; 7(7): e2420717, 2024 Jul 01.
Article in English | MEDLINE | ID: mdl-38980674

ABSTRACT

Importance: Air pollution is associated with structural brain changes, disruption of neurogenesis, and neurodevelopmental disorders. The association between prenatal exposure to ambient air pollution and risk of cerebral palsy (CP), which is the most common motor disability in childhood, has not been thoroughly investigated. Objective: To evaluate the associations between prenatal residential exposure to ambient air pollution and risk of CP among children born at term gestation in a population cohort in Ontario, Canada. Design, Setting, and Participants: Population-based cohort study in Ontario, Canada using linked, province-wide health administrative databases. Participants were singleton full term births (≥37 gestational weeks) born in Ontario hospitals between April 1, 2002, and March 31, 2017. Data were analyzed from January to December 2022. Exposures: Weekly average concentrations of ambient fine particulate matter with a diameter 2.5 µm (PM2.5) or smaller, nitrogen dioxide (NO2), and ozone (O3) during pregnancy assigned by maternal residence reported at delivery from satellite-based estimates and ground-level monitoring data. Main outcome and measures: CP cases were ascertained by a single inpatient hospitalization diagnosis or at least 2 outpatient diagnoses for children from birth to age 18 years. Results: The present study included 1 587 935 mother-child pairs who reached term gestation, among whom 3170 (0.2%) children were diagnosed with CP. The study population had a mean (SD) maternal age of 30.1 (5.6) years and 811 745 infants (51.1%) were male. A per IQR increase (2.7 µg/m3) in prenatal ambient PM2.5 concentration was associated with a cumulative hazard ratio (CHR) of 1.12 (95% CI, 1.03-1.21) for CP. The CHR in male infants (1.14; 95% CI, 1.02-1.26) was higher compared with the CHR in female infants (1.08; 95% CI, 0.96-1.22). No specific window of susceptibility was found for prenatal PM2.5 exposure and CP in the study population. No associations or windows of susceptibility were found for prenatal NO2 or O3 exposure and CP risk. Conclusions and relevance: In this large cohort study of singleton full term births in Canada, prenatal ambient PM2.5 exposure was associated with an increased risk of CP in offspring. Further studies are needed to explore this association and its potential biological pathways, which could advance the identification of environmental risk factors of CP in early life.


Subject(s)
Air Pollution , Cerebral Palsy , Particulate Matter , Prenatal Exposure Delayed Effects , Humans , Pregnancy , Female , Cerebral Palsy/epidemiology , Cerebral Palsy/etiology , Prenatal Exposure Delayed Effects/epidemiology , Air Pollution/adverse effects , Air Pollution/analysis , Air Pollution/statistics & numerical data , Male , Ontario/epidemiology , Adult , Particulate Matter/adverse effects , Particulate Matter/analysis , Infant , Child, Preschool , Infant, Newborn , Child , Maternal Exposure/adverse effects , Maternal Exposure/statistics & numerical data , Cohort Studies , Air Pollutants/adverse effects , Air Pollutants/analysis , Adolescent , Nitrogen Dioxide/adverse effects , Nitrogen Dioxide/analysis
2.
Diabetes Care ; 2024 Jul 16.
Article in English | MEDLINE | ID: mdl-39012781

ABSTRACT

OBJECTIVE: To evaluate associations of wildfire fine particulate matter (PM2.5) with diabetes across multiple countries and territories. RESEARCH DESIGN AND METHODS: We collected data on 3,612,135 diabetes hospitalizations from 1,008 locations in Australia, Brazil, Canada, Chile, New Zealand, Thailand, and Taiwan during 2000-2019. Daily wildfire-specific PM2.5 levels were estimated through chemical transport models and machine-learning calibration. Quasi-Poisson regression with distributed lag nonlinear models and random-effects meta-analysis were applied to estimate associations between wildfire-specific PM2.5 and diabetes hospitalization. Subgroup analyses were by age, sex, location income level, and country or territory. Diabetes hospitalizations attributable to wildfire-specific PM2.5 and nonwildfire PM2.5 were compared. RESULTS: Each 10 µg/m3 increase in wildfire-specific PM2.5 levels over the current day and previous 3 days was associated with relative risks (95% CI) of 1.017 (1.011-1.022), 1.023 (1.011-1.035), 1.023 (1.015-1.032), 0.962 (0.823-1.032), 1.033 (1.001-1.066), and 1.013 (1.004-1.022) for all-cause, type 1, type 2, malnutrition-related, other specified, and unspecified diabetes hospitalization, respectively. Stronger associations were observed for all-cause, type 1, and type 2 diabetes in Thailand, Australia, and Brazil; unspecified diabetes in New Zealand; and type 2 diabetes in high-income locations. Relative risks (95% CI) of 0.67% (0.16-1.18%) and 1.02% (0.20-1.81%) for all cause and type 2 diabetes hospitalizations were attributable to wildfire-specific PM2.5. Compared with nonwildfire PM2.5, wildfire-specific PM2.5 posed greater risks of all-cause, type 1, and type 2 diabetes and were responsible for 38.7% of PM2.5-related diabetes hospitalizations. CONCLUSIONS: We show the relatively underappreciated links between diabetes and wildfire air pollution, which can lead to a nonnegligible proportion of PM2.5-related diabetes hospitalizations. Precision prevention and mitigation should be developed for those in advantaged communities and in Thailand, Australia, and Brazil.

3.
Lancet Planet Health ; 8(7): e452-e462, 2024 Jul.
Article in English | MEDLINE | ID: mdl-38969473

ABSTRACT

BACKGROUND: Wildfire activity is an important source of tropospheric ozone (O3) pollution. However, no study to date has systematically examined the associations of wildfire-related O3 exposure with mortality globally. METHODS: We did a multicountry two-stage time series analysis. From the Multi-City Multi-Country (MCC) Collaborative Research Network, data on daily all-cause, cardiovascular, and respiratory deaths were obtained from 749 locations in 43 countries or areas, representing overlapping periods from Jan 1, 2000, to Dec 31, 2016. We estimated the daily concentration of wildfire-related O3 in study locations using a chemical transport model, and then calibrated and downscaled O3 estimates to a resolution of 0·25°â€ˆ× 0·25° (approximately 28 km2 at the equator). Using a random-effects meta-analysis, we examined the associations of short-term wildfire-related O3 exposure (lag period of 0-2 days) with daily mortality, first at the location level and then pooled at the country, regional, and global levels. Annual excess mortality fraction in each location attributable to wildfire-related O3 was calculated with pooled effect estimates and used to obtain excess mortality fractions at country, regional, and global levels. FINDINGS: Between 2000 and 2016, the highest maximum daily wildfire-related O3 concentrations (≥30 µg/m3) were observed in locations in South America, central America, and southeastern Asia, and the country of South Africa. Across all locations, an increase of 1 µg/m3 in the mean daily concentration of wildfire-related O3 during lag 0-2 days was associated with increases of 0·55% (95% CI 0·29 to 0·80) in daily all-cause mortality, 0·44% (-0·10 to 0·99) in daily cardiovascular mortality, and 0·82% (0·18 to 1·47) in daily respiratory mortality. The associations of daily mortality rates with wildfire-related O3 exposure showed substantial geographical heterogeneity at the country and regional levels. Across all locations, estimated annual excess mortality fractions of 0·58% (95% CI 0·31 to 0·85; 31 606 deaths [95% CI 17 038 to 46 027]) for all-cause mortality, 0·41% (-0·10 to 0·91; 5249 [-1244 to 11 620]) for cardiovascular mortality, and 0·86% (0·18 to 1·51; 4657 [999 to 8206]) for respiratory mortality were attributable to short-term exposure to wildfire-related O3. INTERPRETATION: In this study, we observed an increase in all-cause and respiratory mortality associated with short-term wildfire-related O3 exposure. Effective risk and smoke management strategies should be implemented to protect the public from the impacts of wildfires. FUNDING: Australian Research Council and the Australian National Health and Medical Research Council.


Subject(s)
Air Pollutants , Cardiovascular Diseases , Ozone , Respiratory Tract Diseases , Wildfires , Ozone/adverse effects , Ozone/analysis , Humans , Cardiovascular Diseases/mortality , Air Pollutants/adverse effects , Air Pollutants/analysis , Respiratory Tract Diseases/mortality , Environmental Exposure/adverse effects , Global Health , Air Pollution/adverse effects , Air Pollution/analysis
4.
Cancer Epidemiol ; 92: 102606, 2024 Jul 09.
Article in English | MEDLINE | ID: mdl-38986354

ABSTRACT

BACKGROUND: Air pollution has been classified as a human carcinogen based largely on findings for respiratory cancers. Emerging, but limited, evidence suggests that it increases the risk of breast cancer, particularly among younger women. We characterized associations between residential exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and breast cancer. Analyses were performed using data collected in the Ontario Environmental Health Study (OEHS). METHODS: The OEHS, a population-based case-control study, identified incident cases of breast cancer in Ontario, Canada among women aged 18-45 between 2013 and 2015. A total of 465 pathologically confirmed primary breast cancer cases were identified from the Ontario Cancer Registry, while 242 population-based controls were recruited using random-digit dialing. Self-reported questionnaires were used to collect risk factor data and residential histories. Land-use regression and remote-sensing estimates of NO2 and PM2.5, respectively, were assigned to the residential addresses at interview, five years earlier, and at menarche. Logistic regression was used to estimate odds ratios (OR) and their 95 % confidence intervals (CI) in relation to an interquartile range (IQR) increase in air pollution, adjusting for possible confounders. RESULTS: PM2.5 and NO2 were positively correlated with each other (r = 0.57). An IQR increase of PM2.5 (1.9 µg/m3) and NO2 (6.6 ppb) at interview residence were associated with higher odds of breast cancer and the adjusted ORs and 95 % CIs were 1.37 (95 % CI = 0.98-1.91) and 2.33 (95 % CI = 1.53-3.53), respectively. An increased odds of breast cancer was observed with an IQR increase in NO2 at residence five years earlier (OR = 2.16, 95 % CI: 1.41-3.31), while no association was observed with PM2.5 (OR = 0.96, 95 % CI 0.64-1.42). CONCLUSIONS: Our findings support the hypothesis that exposure to ambient air pollution, especially those from traffic sources (i.e., NO2), increases the risk of breast cancer in young women.

5.
Environ Res ; 261: 119706, 2024 Jul 30.
Article in English | MEDLINE | ID: mdl-39084506

ABSTRACT

The direction and magnitude of association between maternal exposure to ambient air pollutants across gestational windows and offspring risk of autism spectrum disorders (ASD) remains unclear. We sought to evaluate the time-varying effects of prenatal air pollutant exposure on ASD. We conducted a matched case-control study of singleton term children born in Ontario, Canada from 1-Apr-2012 to 31-Dec-2016. Provincial birth registry data were linked with applied behavioural analysis services and ambient air pollutant datasets to ascertain prenatal exposure to nitrogen dioxide (NO2), ground-level ozone (O3), fine particulate matter (PM2.5), and ASD diagnoses. Covariate balance between cases and controls was established using coarsened exact matching. Conditional logistic regression was used to assess the association between prenatal air pollutant exposure and ASD. Distributed lag non-linear models (DLNM) were used to examine the effects of single-pollutant exposure by prenatal week. Sensitivity analyses were conducted to assess the impact of exposure period on the observed findings. The final sample included 1589 ASD cases and 7563 controls. Compared to controls, cases were more likely to be born to mothers living in urban areas, delivered by Caesarean section, and assigned male sex at birth. NO2 was a consistent and significant contributor to ASD risk after accounting for co-exposure to O3, PM2.5 and covariates. The odds ratio per interquartile range increase was 2.1 (95%CI 1.8-2.3) pre-conception, 2.2 (2.0-2.5) for the 1st trimester, 2.2 (1.9-2.5) for the 2nd trimester, and 2.1 (1.9-2.4) for the 3rd trimester. In contrast, findings for O3 and PM2.5 with ASD were inconsistent. Findings from DLNM and sensitivity analyses were similar. Exposure to NO2 before and during pregnancy was significantly associated with ASD in offspring. The relationship between prenatal O3 and PM2.5 exposure and ASD remains unclear. Further investigation into the combined effects of multi-pollutant exposure on child neurodevelopment is warranted.

6.
Environ Epidemiol ; 8(4): e323, 2024 Aug.
Article in English | MEDLINE | ID: mdl-39045485

ABSTRACT

Background: Epidemiological evidence suggests that long-term exposure to outdoor ultrafine particles (UFPs, <0.1 µm) may have important human health impacts. However, less is known about the acute health impacts of these pollutants as few models are available to estimate daily within-city spatiotemporal variations in outdoor UFPs. Methods: Several machine learning approaches (i.e., generalized additive models, random forest models, and extreme gradient boosting) were used to predict daily spatiotemporal variations in outdoor UFPs (number concentration and size) across Montreal and Toronto, Canada using a large database of mobile monitoring measurements. Separate models were developed for each city and all models were evaluated using a 10-fold cross-validation procedure. Results: In total, our models were based on measurements from 12,705 road segments in Montreal and 10,929 road segments in Toronto. Daily median outdoor UFP number concentrations varied substantially across both cities with 1st-99th percentiles ranging from 1389 to 181,672 in Montreal and 2472 to 118,544 in Toronto. Outdoor UFP size tended to be smaller in Montreal (mean [SD]: 34 nm [15]) than in Toronto (mean [SD]: 44 nm [25]). Extreme gradient boosting models performed best and explained the majority of spatiotemporal variations in outdoor UFP number concentrations (Montreal, R 2: 0.727; Toronto, R 2: 0.723) and UFP size (Montreal, R 2: 0.823; Toronto, R 2: 0.898) with slopes close to one and intercepts close to zero for relationships between measured and predicted values. Conclusion: These new models will be applied in future epidemiological studies examining the acute health impacts of outdoor UFPs in Canada's two largest cities.

7.
Article in English | MEDLINE | ID: mdl-38924496

ABSTRACT

RATIONALE: Outdoor fine particulate air pollution (PM2.5) contributes to millions of deaths around the world each year, but much less is known about the long-term health impacts of other particulate air pollutants including ultrafine particles (a.k.a. nanoparticles) which are in the nanometer size range (<100 nm), widespread in urban environments, and not currently regulated. OBJECTIVES: Estimate the associations between long-term exposure to outdoor ultrafine particles and mortality. METHODS: Outdoor air pollution levels were linked to the residential addresses of a large, population-based cohort from 2001 - 2016. Associations between long-term exposure to outdoor ultrafine particles and nonaccidental and cause-specific mortality were estimated using Cox proportional hazards models. MEASUREMENTS: An increase in long-term exposure to outdoor ultrafine particles was associated with an increased risk of nonaccidental mortality (Hazard Ratio = 1. 073, 95% Confidence Interval = 1. 061, 1. 085) and cause-specific mortality, the strongest of which was respiratory mortality (Hazard Ratio = 1.174, 95% Confidence Interval = 1.130, 1.220). MAIN RESULTS: Long-term exposure to outdoor ultrafine particles was associated with increased risk of mortality. We estimated the mortality burden for outdoor ultrafine particles in Montreal and Toronto, Canada to be approximately 1100 additional nonaccidental deaths every year. Furthermore, we observed possible confounding by particle size which suggests that previous studies may have underestimated or missed important health risks associated with ultrafine particles. CONCLUSIONS: As outdoor ultrafine particles are not currently regulated, there is great potential for future regulatory interventions to improve population health by targeting these common outdoor air pollutants.

8.
Pediatr Obes ; 19(8): e13117, 2024 Aug.
Article in English | MEDLINE | ID: mdl-38872449

ABSTRACT

BACKGROUND: Whilst single chemical exposures are suspected to be obesogenic, the combined role of chemical mixtures in paediatric obesity is not well understood. OBJECTIVES: We aimed to evaluate the potential associations between chemical mixtures and obesity in a population-based sample of Canadian children. METHODS: We ascertained biomonitoring and health data for children aged 3-11 from the cross-sectional Canadian Health Measures Survey from 2007 to 2019. Several chemicals of interest were measured in blood or urine and paediatric obesity was defined based on measured anthropometrics. Using quantile-based G computational analysis, we quantified the effects of three chemical mixtures selected a priori. Models were adjusted for sociodemographic and environmental factors identified through a directed acyclic graph. Results are presented through adjusted relative risks (RR) with 95% confidence intervals (95% CI). RESULTS: We included 9147 children. Of these, 24.1% were overweight or obese. Exposure to the mixture of bisphenol A, acrylamide, glycidamide, metals, parabens and arsenic increased the risk of childhood overweight or obesity by 45% (95% CI 1.09, 1.93), obesity by 109% (95% CI 1.27, 3.42) and central obesity by 82% (95% CI 1.30, 2.56). CONCLUSIONS: Our findings support the role of early childhood chemical exposures in paediatric obesity and the potential combined effects of chemicals.


Subject(s)
Environmental Exposure , Pediatric Obesity , Humans , Child , Cross-Sectional Studies , Canada/epidemiology , Female , Pediatric Obesity/epidemiology , Male , Environmental Exposure/adverse effects , Child, Preschool , Benzhydryl Compounds , Environmental Pollutants/adverse effects , Phenols , Risk Factors , Arsenic
9.
Environ Res ; 257: 119347, 2024 Sep 15.
Article in English | MEDLINE | ID: mdl-38844034

ABSTRACT

BACKGROUND: As climate change increases the frequency and intensity of extreme heat events, there is an urgent need to quantify the heat-related health burden. However, most past studies have focussed on a single health outcome (mainly mortality) or on specific heatwaves, thus providing limited knowledge of the total pressure heat exerts on health services. OBJECTIVES: This study aims to quantify the heat-related mortality and morbidity burden for five different health outcomes including all-cause mortality, hospitalizations, emergency department (ED) visits, ambulance transports and calls to a health hotline, using the province of Quebec (Canada) as a case study. METHODS: A two-step statistical analysis was employed to estimate regional heat-health relationships using Distributed Lag Non-Linear Models (DLNM) and pooled estimates using a multivariate meta-regression. Heat burden was quantified by attributable fraction (AF) and attributable number (AN) for two temperature ranges: all heat (above the minimum mortality/morbidity temperature) and extreme heat (above the 95th percentile of temperature). RESULTS: Higher temperatures were associated with greater risk ratios for all health outcomes studied, but at different levels. Significant AF ranging from 2 to 3% for the all heat effect and 0.4-1.0% for extreme heat were found for all health outcomes, except for hospitalizations that had an AF of 0.1% for both heat exposures. The estimated burden of all heat (and extreme heat) every summer across the province was 470 (200) deaths, 225 (170) hospitalizations, 36 000 (6 200) ED visits, 7 200 (1 500) ambulance transports and 15 000 (3 300) calls to a health hotline, all figures significant. DISCUSSION: This new knowledge on the total heat load will help public health authorities to target appropriate actions to reduce its burden now and in the future. The proposed state-of-the-art framework can easily be applied to other regions also experiencing the adverse effects of extreme heat.


Subject(s)
Hospitalization , Hot Temperature , Quebec/epidemiology , Humans , Hospitalization/statistics & numerical data , Hot Temperature/adverse effects , Emergency Service, Hospital/statistics & numerical data , Heat Stress Disorders/mortality , Heat Stress Disorders/epidemiology , Morbidity , Extreme Heat/adverse effects , Mortality/trends , Aged
10.
Commun Earth Environ ; 5(1): 310, 2024.
Article in English | MEDLINE | ID: mdl-38873360

ABSTRACT

Cities concentrate problems that affect human well-being and biodiversity. Exploring the link between mental health and biodiversity can inform more holistic public health and urban planning. Here we examined associations between bird and tree species diversity estimates from eBird community science datasets and national forest inventories with self-rated mental health metrics from the Canadian Community Health Survey. We linked data across 36 Canadian Metropolitan Areas from 2007-2022 at a postal code level. After controlling for covariates, we found that bird and tree species diversity were significantly positively related to good self-reported mental health. Living in a postal code with bird diversity one standard deviation higher than the mean increased reporting of good mental health by 6.64%. Postal codes with tree species richness one standard deviation more than the mean increased reporting of good mental health by 5.36%. Our results suggest that supporting healthy urban ecosystems may also benefit human well-being.

11.
Environ Pollut ; 356: 124353, 2024 Sep 01.
Article in English | MEDLINE | ID: mdl-38866318

ABSTRACT

The development of high-resolution spatial and spatiotemporal models of air pollutants is essential for exposure science and epidemiological applications. While fixed-site sampling has conventionally provided input data for statistical predictive models, the evolving mobile monitoring method offers improved spatial resolution, ideal for measuring pollutants with high spatial variability such as ultrafine particles (UFP). The Quebec Air Pollution Exposure and Epidemiology (QAPEE) study measured and modelled the spatial and spatiotemporal distributions of understudied pollutants, such as UFPs, black carbon (BC), and brown carbon (BrC), along with fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) in Quebec City, Canada. We conducted a combined fixed-site (NO2 and O3) and mobile monitoring (PM2.5, BC, BrC, and UFPs) campaign over 10-months. Mobile monitoring routes were monitored on a weekly basis between 8am-10am and designed using location/allocation modelling. Seasonal fixed-site sampling campaigns captured continuous 24-h measurements over two-week periods. Generalized Additive Models (GAMs), which combined data on pollution concentrations with spatial, temporal, and spatiotemporal predictor variables were used to model and predict concentration surfaces. Annual models for PM2.5, NO2, O3 as well as seven of the smallest size fractions in the UFP range, had high out of sample predictive accuracy (range r2: 0.54-0.86). Varying spatial patterns were observed across UFP size ranges measured as Particle Number Counts (PNC). The monthly spatiotemporal models for PM2.5 (r2 = 0.49), BC (r2 = 0.27), BrC (r2 = 0.29), and PNC (r2 = 0.49) had moderate or moderate-low out of sample predictive accuracy. We conducted a sensitivity analysis and found that the minimum number of 'n visits' (mobile monitoring sessions) required to model annually representative air pollution concentrations was between 24 and 32 visits dependent on the pollutant. This study provides a single source of exposure models for a comprehensive set of air pollutants in Quebec City, Canada. These exposure models will feed into epidemiological research on the health impacts of ambient UFPs and other pollutants.


Subject(s)
Air Pollutants , Air Pollution , Cities , Environmental Monitoring , Ozone , Particulate Matter , Environmental Monitoring/methods , Air Pollutants/analysis , Air Pollution/statistics & numerical data , Particulate Matter/analysis , Quebec , Ozone/analysis , Spatio-Temporal Analysis , Nitrogen Dioxide/analysis
12.
Environ Int ; 187: 108712, 2024 May.
Article in English | MEDLINE | ID: mdl-38714028

ABSTRACT

BACKGROUND: Temperature variability (TV) is associated with increased mortality risk. However, it is still unknown whether intra-day or inter-day TV has different effects. OBJECTIVES: We aimed to assess the association of intra-day TV and inter-day TV with all-cause, cardiovascular, and respiratory mortality. METHODS: We collected data on total, cardiovascular, and respiratory mortality and meteorology from 758 locations in 47 countries or regions from 1972 to 2020. We defined inter-day TV as the standard deviation (SD) of daily mean temperatures across the lag interval, and intra-day TV as the average SD of minimum and maximum temperatures on each day. In the first stage, inter-day and intra-day TVs were modelled simultaneously in the quasi-Poisson time-series model for each location. In the second stage, a multi-level analysis was used to pool the location-specific estimates. RESULTS: Overall, the mortality risk due to each interquartile range [IQR] increase was higher for intra-day TV than for inter-day TV. The risk increased by 0.59% (95% confidence interval [CI]: 0.53, 0.65) for all-cause mortality, 0.64% (95% CI: 0.56, 0.73) for cardiovascular mortality, and 0.65% (95% CI: 0.49, 0.80) for respiratory mortality per IQR increase in intra-day TV0-7 (0.9 °C). An IQR increase in inter-day TV0-7 (1.6 °C) was associated with 0.22% (95% CI: 0.18, 0.26) increase in all-cause mortality, 0.44% (95% CI: 0.37, 0.50) increase in cardiovascular mortality, and 0.31% (95% CI: 0.21, 0.41) increase in respiratory mortality. The proportion of all-cause deaths attributable to intra-day TV0-7 and inter-day TV0-7 was 1.45% and 0.35%, respectively. The mortality risks varied by lag interval, climate area, season, and climate type. CONCLUSIONS: Our results indicated that intra-day TV may explain the main part of the mortality risk related to TV and suggested that comprehensive evaluations should be proposed in more countries to help protect human health.


Subject(s)
Cardiovascular Diseases , Temperature , Humans , Cardiovascular Diseases/mortality , Mortality , Respiratory Tract Diseases/mortality , Seasons
13.
Environ Int ; 187: 108691, 2024 May.
Article in English | MEDLINE | ID: mdl-38718673

ABSTRACT

Assessing the association between temperature frequency and mortality can provide insights into human adaptation to local ambient temperatures. We collected daily time-series data on mortality and temperature from 757 locations in 47 countries/regions during 1979-2020. We used a two-stage time series design to assess the association between temperature frequency and all-cause mortality. The results were pooled at the national, regional, and global levels. We observed a consistent decrease in the risk of mortality as the normalized frequency of temperature increases across the globe. The average increase in mortality risk comparing the 10th to 100th percentile of normalized frequency was 13.03% (95% CI: 12.17-13.91), with substantial regional differences (from 4.56% in Australia and New Zealand to 33.06% in South Europe). The highest increase in mortality was observed for high-income countries (13.58%, 95% CI: 12.56-14.61), followed by lower-middle-income countries (12.34%, 95% CI: 9.27-15.51). This study observed a declining risk of mortality associated with higher temperature frequency. Our findings suggest that populations can adapt to their local climate with frequent exposure, with the adapting ability varying geographically due to differences in climatic and socioeconomic characteristics.


Subject(s)
Mortality , Humans , Mortality/trends , Temperature , Acclimatization/physiology , Climate Change , Australia , New Zealand , Hot Temperature/adverse effects , Climate
14.
PLoS Med ; 21(5): e1004364, 2024 May.
Article in English | MEDLINE | ID: mdl-38743771

ABSTRACT

BACKGROUND: The regional disparity of heatwave-related mortality over a long period has not been sufficiently assessed across the globe, impeding the localisation of adaptation planning and risk management towards climate change. We quantified the global mortality burden associated with heatwaves at a spatial resolution of 0.5°×0.5° and the temporal change from 1990 to 2019. METHODS AND FINDINGS: We collected data on daily deaths and temperature from 750 locations of 43 countries or regions, and 5 meta-predictors in 0.5°×0.5° resolution across the world. Heatwaves were defined as location-specific daily mean temperature ≥95th percentiles of year-round temperature range with duration ≥2 days. We first estimated the location-specific heatwave-mortality association. Secondly, a multivariate meta-regression was fitted between location-specific associations and 5 meta-predictors, which was in the third stage used with grid cell-specific meta-predictors to predict grid cell-specific association. Heatwave-related excess deaths were calculated for each grid and aggregated. During 1990 to 2019, 0.94% (95% CI: 0.68-1.19) of deaths [i.e., 153,078 cases (95% eCI: 109,950-194,227)] per warm season were estimated to be from heatwaves, accounting for 236 (95% eCI: 170-300) deaths per 10 million residents. The ratio between heatwave-related excess deaths and all premature deaths per warm season remained relatively unchanged over the 30 years, while the number of heatwave-related excess deaths per 10 million residents per warm season declined by 7.2% per decade in comparison to the 30-year average. Locations with the highest heatwave-related death ratio and rate were in Southern and Eastern Europe or areas had polar and alpine climates, and/or their residents had high incomes. The temporal change of heatwave-related mortality burden showed geographic disparities, such that locations with tropical climate or low incomes were observed with the greatest decline. The main limitation of this study was the lack of data from certain regions, e.g., Arabian Peninsula and South Asia. CONCLUSIONS: Heatwaves were associated with substantial mortality burden that varied spatiotemporally over the globe in the past 30 years. The findings indicate the potential benefit of governmental actions to enhance health sector adaptation and resilience, accounting for inequalities across communities.


Subject(s)
Climate Change , Extreme Heat , Humans , Extreme Heat/adverse effects , Global Health/trends , Hot Temperature/adverse effects , Mortality/trends , Seasons
15.
Stroke ; 55(7): 1847-1856, 2024 Jul.
Article in English | MEDLINE | ID: mdl-38776169

ABSTRACT

BACKGROUND: Extreme temperatures contribute significantly to global mortality. While previous studies on temperature and stroke-specific outcomes presented conflicting results, these studies were predominantly limited to single-city or single-country analyses. Their findings are difficult to synthesize due to variations in methodologies and exposure definitions. METHODS: Within the Multi-Country Multi-City Network, we built a new mortality database for ischemic and hemorrhagic stroke. Applying a unified analysis protocol, we conducted a multinational case-crossover study on the relationship between extreme temperatures and stroke. In the first stage, we fitted a conditional quasi-Poisson regression for daily mortality counts with distributed lag nonlinear models for temperature exposure separately for each city. In the second stage, the cumulative risk from each city was pooled using mixed-effect meta-analyses, accounting for clustering of cities with similar features. We compared temperature-stroke associations across country-level gross domestic product per capita. We computed excess deaths in each city that are attributable to the 2.5% hottest and coldest of days based on each city's temperature distribution. RESULTS: We collected data for a total of 3 443 969 ischemic strokes and 2 454 267 hemorrhagic stroke deaths from 522 cities in 25 countries. For every 1000 ischemic stroke deaths, we found that extreme cold and hot days contributed 9.1 (95% empirical CI, 8.6-9.4) and 2.2 (95% empirical CI, 1.9-2.4) excess deaths, respectively. For every 1000 hemorrhagic stroke deaths, extreme cold and hot days contributed 11.2 (95% empirical CI, 10.9-11.4) and 0.7 (95% empirical CI, 0.5-0.8) excess deaths, respectively. We found that countries with low gross domestic product per capita were at higher risk of heat-related hemorrhagic stroke mortality than countries with high gross domestic product per capita (P=0.02). CONCLUSIONS: Both extreme cold and hot temperatures are associated with an increased risk of dying from ischemic and hemorrhagic strokes. As climate change continues to exacerbate these extreme temperatures, interventional strategies are needed to mitigate impacts on stroke mortality, particularly in low-income countries.


Subject(s)
Stroke , Humans , Stroke/mortality , Male , Female , Aged , Cross-Over Studies , Hemorrhagic Stroke/mortality , Ischemic Stroke/mortality , Middle Aged , Hot Temperature/adverse effects , Extreme Heat/adverse effects
17.
Environ Res ; 252(Pt 2): 118828, 2024 Jul 01.
Article in English | MEDLINE | ID: mdl-38583657

ABSTRACT

BACKGROUND: Increasing evidence links early life residential exposure to natural urban environmental attributes and positive health outcomes in children. However, few studies have focused on their protective effects on the risk of autism spectrum disorder (ASD). The aim of this study was to investigate the associations of neighborhood greenspace, and active living environments during pregnancy with ASD in young children (≤6 years). METHODS: We conducted a population-based matched case-control study of singleton term births in Ontario, Canada for 2012-2016. The ASD and environmental data was generated using the Ontario Autism Spectrum Profile, the Better Outcomes Registry & Network Ontario, and Canadian Urban Environmental Health Research Consortium. We employed conditional logistic regressions to estimate the odds ratio (OR) between ASD and environmental factors characterizing selected greenspace metrics and neighborhoods conducive to active living (i.e., green view index (GVI), normalized difference vegetation index (NDVI), tree canopy, park proximity and active living environments index (ALE)). RESULTS: We linked 8643 mother-child pairs, including 1554 cases (18%). NDVI (OR 1.034, 0.944-1.024, per Inter Quartile Range [IQR] = 0.08), GVI (OR 1.025, 95% CI 0.953-1.087, per IQR = 9.45%), tree canopy (OR 0.992, 95% CI 0.903-1.089, per IQR = 6.24%) and the different categories of ALE were not associated with ASD in adjusted models for air pollution. In contrast, living closer to a park was protective (OR 0.888, 0.833-0.948, per 0.06 increase in park proximity index), when adjusted for air pollution. CONCLUSIONS: This study reported mixed findings showing both null and beneficial effects of green spaces and active living environments on ASD. Further investigations are warranted to elucidate the role of exposure to greenspaces and active living environments on the development of ASD.


Subject(s)
Autism Spectrum Disorder , Humans , Autism Spectrum Disorder/epidemiology , Case-Control Studies , Ontario/epidemiology , Female , Male , Child, Preschool , Adult , Residence Characteristics/statistics & numerical data , Pregnancy , Infant , Neighborhood Characteristics , Child , Parks, Recreational/statistics & numerical data , Infant, Newborn
18.
Lancet Planet Health ; 8(3): e146-e155, 2024 03.
Article in English | MEDLINE | ID: mdl-38453380

ABSTRACT

BACKGROUND: The acute health effects of short-term (hours to days) exposure to fine particulate matter (PM2·5) have been well documented; however, the global mortality burden attributable to this exposure has not been estimated. We aimed to estimate the global, regional, and urban mortality burden associated with short-term exposure to PM2·5 and the spatiotemporal variations in this burden from 2000 to 2019. METHODS: We combined estimated global daily PM2·5 concentrations, annual population counts, country-level mortality rates, and epidemiologically derived exposure-response functions to estimate the mortality attributable to short-term PM2·5 exposure from 2000 to 2019, in the continental regions and in 13 189 urban centres worldwide at a spatial resolution of 0·1°â€ˆ× 0·1°. We tested the robustness of our mortality estimates with different theoretical minimum risk exposure levels, lag effects, and exposure-response functions. FINDINGS: Approximately 1 million (95% CI 690 000-1·3 million) premature deaths per year from 2000 to 2019 were attributable to short-term PM2·5 exposure, representing 2·08% (1·41-2·75) of total global deaths or 17 (11-22) premature deaths per 100 000 population. Annually, 0·23 million (0·15 million-0·30 million) deaths attributable to short-term PM2·5 exposure were in urban areas, constituting 22·74% of the total global deaths attributable to this cause and accounting for 2·30% (1·56-3·05) of total global deaths in urban areas. The sensitivity analyses showed that our worldwide estimates of mortality attributed to short-term PM2·5 exposure were robust. INTERPRETATION: Short-term exposure to PM2·5 contributes a substantial global mortality burden, particularly in Asia and Africa, as well as in global urban areas. Our results highlight the importance of mitigation strategies to reduce short-term exposure to air pollution and its adverse effects on human health. FUNDING: Australian Research Council and the Australian National Health and Medical Research Council.


Subject(s)
Air Pollution , Particulate Matter , Humans , Particulate Matter/analysis , Australia , Air Pollution/adverse effects , Air Pollution/analysis , Mortality, Premature , Asia
19.
Nat Commun ; 15(1): 1796, 2024 Feb 27.
Article in English | MEDLINE | ID: mdl-38413648

ABSTRACT

Older adults are generally amongst the most vulnerable to heat and cold. While temperature-related health impacts are projected to increase with global warming, the influence of population aging on these trends remains unclear. Here we show that at 1.5 °C, 2 °C, and 3 °C of global warming, heat-related mortality in 800 locations across 50 countries/areas will increase by 0.5%, 1.0%, and 2.5%, respectively; among which 1 in 5 to 1 in 4 heat-related deaths can be attributed to population aging. Despite a projected decrease in cold-related mortality due to progressive warming alone, population aging will mostly counteract this trend, leading to a net increase in cold-related mortality by 0.1%-0.4% at 1.5-3 °C global warming. Our findings indicate that population aging constitutes a crucial driver for future heat- and cold-related deaths, with increasing mortality burden for both heat and cold due to the aging population.


Subject(s)
Climate Change , Global Warming , Temperature , Cold Temperature , Hot Temperature , Mortality
20.
One Earth ; 7(2): 325-335, 2024 Feb 16.
Article in English | MEDLINE | ID: mdl-38420618

ABSTRACT

Short-term exposure to ground-level ozone in cities is associated with increased mortality and is expected to worsen with climate and emission changes. However, no study has yet comprehensively assessed future ozone-related acute mortality across diverse geographic areas, various climate scenarios, and using CMIP6 multi-model ensembles, limiting our knowledge on future changes in global ozone-related acute mortality and our ability to design targeted health policies. Here, we combine CMIP6 simulations and epidemiological data from 406 cities in 20 countries or regions. We find that ozone-related deaths in 406 cities will increase by 45 to 6,200 deaths/year between 2010 and 2014 and between 2050 and 2054, with attributable fractions increasing in all climate scenarios (from 0.17% to 0.22% total deaths), except the single scenario consistent with the Paris Climate Agreement (declines from 0.17% to 0.15% total deaths). These findings stress the need for more stringent air quality regulations, as current standards in many countries are inadequate.

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