Health impact assessment of PM2.5 from uncovered coal trains in the San Francisco Bay Area: Implications for global exposures.

Coal generates almost 40% of the world's electricity with 80 countries throughout the world using coal power. An inherent part of this generation is the rail transport of coal in uncovered cars, often up to a mile long. Existing studies document the subsequent increments of PM2.5 to the near-rail populations, which typically include a large number of economically disadvantaged residents and/or people of color. However, to date there is no assessment of the health implications of this stage in the use of coal. The present study quantifies such impacts on a region in the San Francisco Bay Area. The analysis shows important effects on mortality, hospitalization for cardiovascular and respiratory disease, asthma exacerbation, work loss, and days of restricted activity. Several of these outcomes exhibited a one to six percent increase over baseline. As such, it delineates the implications for the global effects of the transport of coal.

The health impacts of Indonesian peatland fires.

BACKGROUND: Indonesian peatlands have been drained for agricultural development for several decades. This development has made a major contribution to economic development. At the same time, peatland drainage is causing significant air pollution resulting from peatland fires. Peatland fires occur every year, even though their extent is much larger in dry (El Niño) years. We examine the health effects of long-term exposure to fine particles (PM2.5) from all types of peatland fires (including the burning of above and below ground biomass) in Sumatra and Kalimantan, where most peatland fires in Indonesia take place. METHODS: We derive PM2.5 concentrations from satellite imagery calibrated and validated with Indonesian Government data on air pollution, and link increases in these concentrations to peatland fires, as observed in satellite imagery. Subsequently, we apply available epidemiological studies to relate PM2.5 exposure to a range of health outcomes. The model utilizes the age distribution and disease prevalence of the impacted population. RESULTS: We find that PM2.5 air pollution from peatland fires, causes, on average, around 33,100 adults and 2900 infants to die prematurely each year from air pollution. In addition, peatland fires cause on average around 4390 additional hospitalizations related to respiratory diseases, 635,000 severe cases of asthma in children, and 8.9 million lost workdays. The majority of these impacts occur in Sumatra because of its much higher population density compared to Kalimantan. A main source of uncertainty is in the Concentration Response Functions (CRFs) that we use, with different CRFs leading to annual premature adult mortality ranging from 19,900 to 64,800 deaths. Currently, the population of both regions is relatively young. With aging of the population over time, vulnerabilities to air pollution and health effects from peatland fires will increase. CONCLUSIONS: Peatland fire health impacts provide a further argument to combat fires in peatlands, and gradually transition to peatland management models that do not require drainage and are therefore not prone to fire risks.

Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter.

Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

Associations of Source-apportioned Fine Particles with Cause-specific Mortality in California.

BACKGROUND: Exposure to ambient fine particulate matter (PM2.5) has been linked with premature mortality, but sources of PM2.5 have been less studied. METHODS: We evaluated associations between source-specific PM2.5 exposures and cause-specific short-term mortality in eight California locations from 2002 to 2011. Speciated PM2.5 measurements were source-apportioned using Positive Matrix Factorization into eight sources and combined with death certificate data. We used time-stratified case-crossover analysis with conditional logistic regression by location and meta-analysis to calculate pooled estimates. RESULTS: Biomass burning was associated with all-cause mortality lagged 2 days after exposure (lag2) (% changelag2 in odds per interquartile range width increase in biomass burning PM2.5 = 0.8, 95% confidence interval [CI] = 0.2, 1.4), cardiovascular (% changelag2 = 1.3, 95% CI = 0.3, 2.4), and ischemic heart disease (% changelag2 = 2.0, 95% CI = 0.6, 3.5). Vehicular emissions were associated with increases in cardiovascular mortality (% changelag0 = 1.4, 95% CI = 0.0, 2.9). Several other sources exhibited positive associations as well. Many findings persisted during the cool season. Warm season biomass burning was associated with respiratory/thoracic cancer mortality (% changelag1 = 5.9, 95% CI = 0.7, 11.3), and warm season traffic was associated with all-cause (% changelag0 = 1.9, 95% CI = 0.1, 3.6) and cardiovascular (% changelag0 = 2.9, 95% CI = 0.1, 5.7) mortality. CONCLUSIONS: Our results suggest that acute exposures to biomass burning and vehicular emissions are linked with cardiovascular mortality, with additional sources (i.e., soil, secondary nitrate, secondary sulfate, aged sea salt, and chlorine sources) showing associations with other specific mortality types.

Assessing the recent estimates of the global burden of disease for ambient air pollution: Methodological changes and implications for low- and middle-income countries.

The Global Burden of Disease (GBD) is a comparative assessment of the health impact of the major and well-established risk factors, including ambient air pollution (AAP) assessed by concentrations of PM2.5 (particles less than 2.5 µm) and ozone. Over the last two decades, major improvements have emerged for two important inputs in the methodology for estimating the impacts of PM2.5: the assessment of global exposure to PM2.5 and the development of integrated exposure risk models (IERs) that relate the entire range of global exposures of PM2.5 to cause-specific mortality. As a result, the estimated annual mortality attributed to AAP increased from less than 1 million in 2000 to roughly 3 million for GBD in years 2010 and 2013, to 4.2 million for GBD 2015. However, the magnitude of the recent change and uncertainty regarding its rationale have resulted, in some cases, in skepticism and reduced confidence in the overall estimates. To understand the underlying reasons for the change in mortality, we examined the estimates for the years 2013 and 2015 to determine the quantitative implications of alternative model input assumptions. We calculated that the year 2013 estimates increased by 8% after applying the updated exposure data used in GBD 2015, and increased by 23% with the application of the updated IERs from GBD 2015. The application of both upgraded methodologies together increased the GBD 2013 estimates by 35%, or about one million deaths. We also quantified the impact of the changes in demographics and the assumed threshold level. Since the global estimates of air pollution-related deaths will continue to change over time, a clear documentation of the modifications in the methodology and their impacts is necessary. In addition, there is need for additional monitoring and epidemiological studies to reduce uncertainties in the estimates for low- and medium-income countries, which contribute to about one-half of the mortality.

Associations of Source-Specific Fine Particulate Matter With Emergency Department Visits in California.

While many studies have investigated the health effects associated with acute exposure to fine particulate matter (particulate matter with an aerodynamic diameter less than or equal to 2.5 µm (PM2.5)), very few have considered the risks of specific sources of PM2.5 We used city-specific source apportionment in 8 major metropolitan areas in California from 2005-2009 to examine the associations of source-specific PM2.5 exposures from vehicular emissions, biomass burning, soil, and secondary nitrate and sulfate sources with emergency department visits (EDVs) for cardiovascular and respiratory diseases, including 7 subclasses. Using a case-crossover analysis, we observed associations of vehicular emissions with all cardiovascular EDVs (excess risk = 1.6%, 95% confidence interval: 0.9, 2.4 for an interquartile-range increment of 2.8 µg/m(3)) and with several subclasses of disease. In addition, vehicular emissions, biomass burning, and soil sources were associated with all respiratory EDVs and with EDVs for asthma. The soil source, which includes resuspended road dust, generated the highest risk estimate for asthma (excess risk = 4.5%, 95% confidence interval: 1.1, 8.0). Overall, our results provide additional evidence of the public health consequences of exposure to specific sources of PM2.5 and indicate that some sources of PM2.5 may pose higher risks than the overall PM2.5 mass.

Long- and Short-term Exposure to Air Pollution and Inflammatory/Hemostatic Markers in Midlife Women.

BACKGROUND: Studies have reported associations between long-term air pollution exposures and cardiovascular mortality. The biological mechanisms connecting them remain uncertain. METHODS: We examined associations of fine particles (PM2.5) and ozone with serum markers of cardiovascular disease risk in a cohort of midlife women. We obtained information from women enrolled at six sites in the multi-ethnic, longitudinal Study of Women's Health Across the Nation, including repeated measurements of high-sensitivity C-reactive protein, fibrinogen, tissue-type plasminogen activator antigen, plasminogen activator inhibitor type 1, and factor VIIc (factor VII coagulant activity). We obtained residence-proximate PM2.5 and ozone monitoring data for a maximum five annual visits, calculating prior year, 6-month, 1-month, and 1-day exposures and their relations to serum markers using longitudinal mixed models. RESULTS: For the 2,086 women studied from 1999 to 2004, PM2.5 exposures were associated with all blood markers except factor VIIc after adjusting for age, race/ethnicity, education, site, body mass index, smoking, and recent alcohol use. Adjusted associations were strongest for prior year exposures for high-sensitivity C-reactive protein (21% increase per 10 µg/m³ PM2.5, 95% confidence interval [CI]: 6.6, 37), tissue-type plasminogen activator antigen (8.6%, 95% CI: 1.8, 16), and plasminogen activator inhibitor (35%, 95% CI: 19, 53). An association was also observed between year prior ozone exposure and factor VIIc (5.7% increase per 10 ppb ozone, 95% CI: 2.9, 8.5). CONCLUSIONS: Our findings suggest that prior year exposures to PM2.5 and ozone are associated with adverse effects on inflammatory and hemostatic pathways for cardiovascular outcomes in midlife women.

The risks of acute exposure to black carbon in Southern Europe: results from the MED-PARTICLES project.

OBJECTIVES: While several studies have reported associations of daily exposures to PM2.5 (particles less than 2.5 µm) with mortality, few studies have examined the impact of its constituents such as black carbon (BC), which is also a significant contributor to global climate change. METHODS: We assessed the association between daily concentrations of BC and total, cardiovascular and respiratory mortality in two southern Mediterranean cities. Daily averages of BC were collected for 2 years in Barcelona, Spain and Athens, Greece. We used case-crossover analysis and examined single and cumulative lags up to 3 days. RESULTS: We observed associations between BC and all mortality measures. For a 3-day moving average, cardiovascular mortality increased by 4.5% (95% CI 0.7 to 8.5) and 2.0% (95% CI 0 to 4.0) for an interquartile change in BC in Athens and Barcelona, respectively. Considerably higher effects for respiratory mortality and for those above age 65 were observed. In addition, BC exhibited much greater toxicity per microgram than generic PM2.5. CONCLUSIONS: Our findings suggest that BC, derived in western industrialised nations primarily from diesel engines and biomass burning, poses a significant burden to public health, particularly in European cities with high-traffic density.

Short-term effects of particulate matter on mortality during forest fires in Southern Europe: results of the MED-PARTICLES Project.

BACKGROUND: An association between occurrence of wildfires and mortality in the exposed population has been observed in several studies with controversial results for cause-specific mortality. In the Mediterranean area, forest fires usually occur during spring-summer, they overlap with Saharan outbreaks, are associated with increased temperature and their health effects are probably due to an increase in particulate matter. AIM AND METHODS: We analysed the effects of wildfires and particulate matter (PM10) on mortality in 10 southern European cities in Spain, France, Italy and Greece (2003-2010), using satellite data for exposure assessment and Poisson regression models, simulating a case-crossover approach. RESULTS: We found that smoky days were associated with increased cardiovascular mortality (lag 0-5, 6.29%, 95% CIs 1.00 to 11.85). When the effect of PM10 (per 10 µg/m(3)) was evaluated, there was an increase in natural mortality (0.49%), cardiovascular mortality (0.65%) and respiratory mortality (2.13%) on smoke-free days, but PM10-related mortality was higher on smoky days (natural mortality up to 1.10% and respiratory mortality up to 3.90%) with a suggestion of effect modification for cardiovascular mortality (3.42%, p value for effect modification 0.055), controlling for Saharan dust advections. CONCLUSIONS: Smoke is associated with increased cardiovascular mortality in urban residents, and PM10 on smoky days has a larger effect on cardiovascular and respiratory mortality than on other days.

Air pollution and preterm premature rupture of membranes: a spatiotemporal analysis.

Preterm premature rupture of membranes (PROM) is the leading identifiable predisposing factor for preterm birth. Although maternal exposure to air pollution can potentially have an impact on preterm PROM, there is no available evidence on such an impact. In this study, based on 5,555 singleton births occurring in Barcelona, Spain (2002-2005), we investigated the associations of maternal exposure to nitrogen dioxide, nitrogen oxides, and particulate matter with aerodynamic diameters of ≤2.5 µm (PM2.5), 2.5 µm-10 µm, and ≤10 µm and PM2.5 light absorption with preterm PROM and gestational age at the rupture of membranes (ROM). We utilized temporally adjusted land-use regression models to predict pollutant levels at each subject's home address during each week of her pregnancy. We conducted matched (according to the length of exposure) case-control analyses to estimate the preterm PROM risk associated with 1 interquartile-range increase in exposure levels during the entire pregnancy and during the last 3 months prior to ROM. We found an increase in preterm PROM risk of up to 50% (95% confidence interval: 4, 116) and a 1.3-day (95% confidence interval: -1.9, -0.6) reduction in gestational age at ROM associated with PM2.5 absorbance, nitrogen dioxide exposure, and nitrogen oxide exposure during the entire pregnancy and the last 3 months prior to ROM.

Residential proximity to major roads and term low birth weight: the roles of air pollution, heat, noise, and road-adjacent trees.

BACKGROUND: Maternal residential proximity to roads has been associated with adverse pregnancy outcomes. However, there is no study investigating mediators or buffering effects of road-adjacent trees on this association. We investigated the association between mothers' residential proximity to major roads and term low birth weight (LBW), while exploring possible mediating roles of air pollution (PM(2.5), PM(2.5-10), PM(10), PM(2.5) absorbance, nitrogen dioxide, and nitrogen oxides), heat, and noise and buffering effect of road-adjacent trees on this association. METHODS: This cohort study was based on 6438 singleton term births in Barcelona, Spain (2001-2005). Road proximity was measured as both continuous distance to and living within 200 m from a major road. We assessed individual exposures to air pollution, noise, and heat using, respectively, temporally adjusted land-use regression models, annual averages of 24-hour noise levels across 50 m and 250 m, and average of satellite-derived land-surface temperature in a 50-m buffer around each residential address. We used vegetation continuous fields to abstract tree coverage in a 200-m buffer around major roads. RESULTS: Living within 200 m of major roads was associated with a 46% increase in term LBW risk; an interquartile range increase in heat exposure with an 18% increase; and third-trimester exposure to PM(2.5), PM(2.5-10), and PM10 with 24%, 25%, and 26% increases, respectively. Air pollution and heat exposures together explained about one-third of the association between residential proximity to major roads and term LBW. Our observations on the buffering of this association by road-adjacent trees were not consistent between our 2 measures of proximity to major roads. CONCLUSION: An increased risk of term LBW associated with proximity to major roads was partly mediated by air pollution and heat exposures.

Particulate air pollution and preeclampsia: a source-based analysis.

OBJECTIVES: To investigate the association between preeclampsia and maternal exposure to ambient particulate matter (PM) with aerodynamic diameter less than 10 µm (PM10) and 2.5 µm (PM2.5) mass and sources. METHODS: Our analysis was based on a hospital cohort of pregnant women (N=3182) residing in Barcelona, Spain, during 2003-2005. Positive matrix factorisation source apportionment (PMF2) was used to identify sources of PM10 and PM2.5 samples obtained by an urban background monitor, resulting in detection of eight sources. We further combined traffic-related sources (brake dust, vehicle exhaust and secondary nitrate/organics) to generate an indicator of combined traffic sources. Logistic regression models were developed to estimate the association between preeclampsia and exposure to each PM source and mass separately during the entire pregnancy and trimester one, adjusted for relevant covariates. RESULTS: For the exposure during the entire pregnancy, we found a 44% (95% CI 7% to 94%) and a 80% (95% CI 4% to 211%) increase in the risk of preeclampsia associated with one IQR increase in exposure to PM10 brake dust and combined traffic-related sources, respectively. These findings remained consistent after an alternative source apportionment method (Multilinear Engine (ME2)) was used. The results for PM2.5 mass and sources and also exposure during trimester one were inconclusive. CONCLUSIONS: Risk of preeclampsia was associated with exposure to PM10 brake dust and combined traffic-related sources.

Chronic PM2.5 exposure and inflammation: determining sensitive subgroups in mid-life women.

BACKGROUND: Several cohort studies report associations between chronic exposure to ambient fine particles (PM2.5) and cardiovascular mortality. Uncertainty exists about biological mechanisms responsible for this observation, but systemic inflammation has been postulated. In addition, the subgroups susceptible to inflammation have not been fully elucidated. METHODS: We investigated whether certain subgroups are susceptible to the effects of long-term exposure to PM2.5 on C-reactive protein (CRP), a marker of inflammation directly linked to subsequent cardiovascular disease. We used data from the SWAN cohort of 1923 mid-life women with up to five annual repeated measures of CRP. Linear mixed and GEE models accounting for repeated measurements within an individual were used to estimate the effects of prior-year PM2.5 exposure on CRP. We examined CRP as a continuous and as binary outcome for CRP greater than 3mg/l, a level of clinical significance. RESULTS: We found strong associations between PM2.5 and CRP among several subgroups. For example a 10 µg/m(3) increase in annual PM2.5 more than doubled the risk of CRP greater than 3mg/l in older diabetics, smokers and the unmarried. Larger effects were also observed among those with low income, high blood pressure, or who were using hormone therapy, with indications of a protective effects for those using statins or consuming moderate amounts of alcohol. CONCLUSIONS: In this study, we observed significant associations between long-term exposure to PM2.5 and CRP in several susceptible subgroups. This suggests a plausible pathway by which exposure to particulate matter may be associated with increased risk of cardiovascular disease.

Excess mortality in Europe following a future Laki-style Icelandic eruption.

Historical records show that the A.D. 1783-1784 Laki eruption in Iceland caused severe environmental stress and posed a health hazard far beyond the borders of Iceland. Given the reasonable likelihood of such an event recurring, it is important to assess the scale on which a future eruption could impact society. We quantify the potential health effects caused by an increase in air pollution during a future Laki-style eruption using a global aerosol model together with concentration-response functions derived from current epidemiological studies. The concentration of particulate matter with diameters smaller than 2.5 µm is predicted to double across central, western, and northern Europe during the first 3 mo of the eruption. Over land areas of Europe, the current World Health Organization 24-h air quality guideline for particulate matter with diameters smaller than 2.5 µm is exceeded an additional 36 d on average over the course of the eruption. Based on the changes in particulate air pollution, we estimate that approximately 142,000 additional cardiopulmonary fatalities (with a 95% confidence interval of 52,000-228,000) could occur in Europe. In terms of air pollution, such a volcanic eruption would therefore be a severe health hazard, increasing excess mortality in Europe on a scale that likely exceeds excess mortality due to seasonal influenza.

Health cobenefits and transportation-related reductions in greenhouse gas emissions in the San Francisco Bay area.

OBJECTIVES: We quantified health benefits of transportation strategies to reduce greenhouse gas emissions (GHGE). METHODS: Statistics on travel patterns and injuries, physical activity, fine particulate matter, and GHGE in the San Francisco Bay Area, California, were input to a model that calculated the health impacts of walking and bicycling short distances usually traveled by car or driving low-emission automobiles. We measured the change in disease burden in disability-adjusted life years (DALYs) based on dose-response relationships and the distributions of physical activity, particulate matter, and traffic injuries. RESULTS: Increasing median daily walking and bicycling from 4 to 22 minutes reduced the burden of cardiovascular disease and diabetes by 14% (32,466 DALYs), increased the traffic injury burden by 39% (5907 DALYS), and decreased GHGE by 14%. Low-carbon driving reduced GHGE by 33.5% and cardiorespiratory disease burden by less than 1%. CONCLUSIONS: Increased physical activity associated with active transport could generate a large net improvement in population health. Measures would be needed to minimize pedestrian and bicyclist injuries. Together, active transport and low-carbon driving could achieve GHGE reductions sufficient for California to meet legislative mandates.

Long-term air pollution exposure and cardio- respiratory mortality: a review.

Current day concentrations of ambient air pollution have been associated with a range of adverse health effects, particularly mortality and morbidity due to cardiovascular and respiratory diseases. In this review, we summarize the evidence from epidemiological studies on long-term exposure to fine and coarse particles, nitrogen dioxide (NO2) and elemental carbon on mortality from all-causes, cardiovascular disease and respiratory disease. We also summarize the findings on potentially susceptible subgroups across studies. We identified studies through a search in the databases Medline and Scopus and previous reviews until January 2013 and performed a meta-analysis if more than five studies were available for the same exposure metric.

The impact of coal trains on PM2.5 in the San Francisco Bay area.

Exposure to fine particulate matter (PM2.5) is associated with adverse health effects, including mortality, even at low concentrations. Rail conveyance of coal, accounting for one-third of American rail freight tonnage, is a source of PM2.5. However, there are limited studies of its contribution to PM2.5, especially in urban settings where residents experience higher exposure and vulnerability to air pollution. We developed a novel artificial intelligence-driven monitoring system to quantify average and maximum PM2.5 concentrations of full and empty (unloaded) coal trains compared to freight and passenger trains. The monitor was close to the train tracks in Richmond, California, a city with a racially diverse population of 115,000 and high rates of asthma and heart disease. We used multiple linear regression models controlling for diurnal patterns and meteorology. The results indicate coal trains add on average 8.32 µg/m3 (95% CI = 6.37, 10.28; p < 0.01) to ambient PM2.5, while sensitivity analysis produced midpoints ranging from 5 to 12 µg/m3. Coal trains contributed 2 to 3 µg/m3 more of PM2.5 than freight trains, and 7 µg/m3 more under calm wind conditions, suggesting our study underestimates emissions and subsequent concentrations of coal train dust. Empty coal cars tended to add 2 µg/m3. Regarding peak concentrations of PM2.5, our models suggest an increase of 17.4 µg/m3 (95% CI = 6.2, 28.5; p < 0.01) from coal trains, about 3 µg/m3 more than freight trains. Given rail shipment of coal occurs globally, including in populous areas, it is likely to have adverse effects on health and environmental justice.

Long-term exposure to air pollution and cardiorespiratory disease in the California teachers study cohort.

RATIONALE: Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease. OBJECTIVES: To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction and stroke, as well as all-cause and cause specific mortality. METHODS: We estimated long-term residential air pollution exposure for more than 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals.We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident myocardial infarction and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models. MEASUREMENTS AND MAIN RESULTS: We found elevated hazard ratios linking long-term exposure to particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5), scaled to an increment of 10 µg/m3 with mortality from ischemic heart disease (IHD) (1.20; 95% confidence interval [CI], 1.02-1.41) and, particularly among postmenopausal women, incident stroke (1.19; 95% CI, 1.02-1.38). Long-term exposure to particulate matter less than 10 µm in aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06; 95% CI, 0.99-1.14) and incident stroke (1.06; 95% CI, 1.00-1.13), while exposure to nitrogen oxides was associated with elevated risks for IHD and all cardiovascular mortality. CONCLUSIONS: This study provides evidence linking long-term exposure to PM2.5 and PM10 with increased risks of incident stroke as well as IHD mortality; exposure to nitrogen oxides was also related to death from cardiovascular diseases.

The impact of future summer temperature on public health in Barcelona and Catalonia, Spain.

Several epidemiological studies have reported associations between increases in summer temperatures and risks of premature mortality. The quantitative implications of predicted future increases in summer temperature, however, have not been extensively characterized. We have quantified these effects for the four main cities in Catalonia, Spain (Barcelona, Tarragona, Lleida, Girona). We first used case-crossover analysis to estimate the association between temperature and mortality for each of these cities for the period 1983 to 2006. These exposure-response (ER) functions were then combined with local measures of current and projected changes in population, mortality and temperature for the years 2025 and 2050. Predicted daily mean temperatures were based on the A1B greenhouse gas emission, "business-as-usual" scenario simulations derived from the ENSEMBLES project. Several different ER functions were examined and significant associations between temperature and mortality were observed for all four cities. For these four cities, the age-specific piecewise linear model predicts 520 (95%CI 340, 720) additional annual deaths attributable to the change in temperature in 2025 relative to the average from the baseline period of 1960-1990. For 2050, the estimate increases to 1,610 deaths per year during the warm season. For Catalonia as a whole, the point estimates for those two years are 720 and 2,330 deaths per year, respectively, or about 2 and 3% of the warm season. In comparing these predicted impacts with current causes of mortality, they clearly represent significant burdens to public health in Catalonia.

Heat waves and cause-specific mortality at all ages.

BACKGROUND: Mortality has been shown to increase with extremely hot ambient temperatures. Details on the specific cause of mortality can be useful for improving preventive policies. Infants are often identified as a population that is vulnerable to extreme heat conditions; however, information on heat and infant mortality is scarce, with no studies reporting on cause-specific mortality. METHODS: The study includes all deaths in the Catalonia region of Spain during the warm seasons of 1983-2006 (503,389 deaths). We used the case-crossover design to evaluate the association between the occurrence of extremely hot days (days with maximum temperature above the 95th percentile) and mortality. Total mortality and infant mortality were stratified into 66 and 8 causes of death, respectively. RESULTS: Three consecutive hot days increased total daily mortality by 19%. We calculated that 1.6% of all deaths were attributable to heat. About 40% of attributable deaths did not occur during heat-wave periods. The causes of death that were increased included cardiovascular and respiratory diseases, mental and nervous system disorders, infectious and digestive system diseases, diabetes, and some external causes such as suicide. In infants, the effect of heat was observed on the same day and was detected only for conditions originating in the perinatal period (relative risk = 1.53 [95% confidence interval = 1.16-2.02]). Within the perinatal causes, cardiovascular, respiratory, digestive system, and hemorrhagic and hematologic disorders were the causes of death with stronger effects. CONCLUSIONS: Heat contributes to an increase in mortality from several causes. In infants, the first week of life is the most critical window of vulnerability.