RESUMEN
Traditionally, environmental authorities make regulatory policies for controlling volatile organic compound (VOC) pollution based on the mitigation of dominant VOC sources. However, the emission from each VOC source has a unique combination of VOC species of different toxicities. Without quantitatively assessing the health risk associated with each source, the effectiveness of the mitigation policy could be undermined. To address this shortcoming, we developed a new health risk-oriented source apportionment method that can provide quantitative health risk assessment and source-specific mitigation strategies for hazardous VOCs. We estimated that the integrated inhalation cancer risk (ICR) of hazardous VOCs was 7.7 × 10-5 in Western Canada, indicating a 100% likelihood of exceeding Health Canada's acceptable risk level (1.0 × 10-5). Anthropogenic sources were responsible for 56.3-73.8% of cancer risks across eight Canadian cities except for the regional background island, where natural sources contributed over 77% to the integrated ICR. Thus, substantial environmental and health cobenefits could be achieved via reducing the ambient levels of benzene and 1,3-butadiene by 39.3-75.7 and 14-69.3%, respectively, and mitigating emissions from fuel combustion (by 31.3-54.1%), traffic source (3.0-36.8%), and other anthropogenic sources (5.3-20.1%) in Western Canada. Our study has significant implications for prioritizing air pollution mitigation policies, especially for quantitative reduction of hazardous air pollutants.
Asunto(s)
Contaminantes Atmosféricos , Ozono , Compuestos Orgánicos Volátiles , Contaminantes Atmosféricos/análisis , Canadá , China , Ciudades , Monitoreo del Ambiente , Ozono/análisis , Emisiones de Vehículos/análisisRESUMEN
Urban areas are increasingly recognized as an important source of methane (CH4), but we have limited seasonally resolved observations of these regions. In this study, we quantify seasonal and annual urban CH4 emissions over the Baltimore, Maryland, and Washington, DC metropolitan regions. We use CH4 atmospheric observations from four tall tower stations and a Lagrangian particle dispersion model to simulate CH4 concentrations at these stations. We directly compare these simulations with observations and use a geostatistical inversion method to determine optimal emissions to match our observations. We use observations spanning four seasons and employ an ensemble approach considering multiple meteorological representations, emission inventories, and upwind CH4 values. Forward simulations in winter, spring, and fall underestimate observed atmospheric CH4 while in summer, simulations overestimate observations because of excess modeled wetland emissions. With ensemble geostatistical inversions, the optimized annual emissions in DC/Baltimore are 39 ± 9 Gg/month (1 δ), 2.0 ± 0.4 times higher than the ensemble mean of bottom-up emission inventories. We find a modest seasonal variability of urban CH4 emissions not captured in current inventories, with optimized summer emissions â¼41% lower than winter, broadly consistent with expectations if emissions are dominated by fugitive natural gas sources that correlate with natural gas usage.
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Metano , Gas Natural , Baltimore , District of Columbia , HumedalesRESUMEN
Crop yields in sub-Saharan Africa remain stagnant at 1 ton ha-1 , and 260 million people lack access to adequate food resources. Order-of-magnitude increases in fertilizer use are seen as a critical step in attaining food security. This increase represents an unprecedented input of nitrogen (N) to African ecosystems and will likely be accompanied by increased soil emissions of nitric oxide (NO). NO is a precursor to tropospheric ozone, an air pollutant and greenhouse gas. Emissions of NO from soils occur primarily during denitrification and nitrification, and N input rates are a key determinant of emission rates. We established experimental maize plots in western Kenya to allow us to quantify the response function relating NO flux to N input rate during the main 2011 and 2012 growing seasons. NO emissions followed a sigmoid response to fertilizer inputs and have emission factors under 1% for the roughly two-month measurement period in each year, although linear and step relationships could not be excluded in 2011. At fertilization rates above 100 kg N ha-1 , NO emissions increased without a concomitant increase in yields. We used the geos-chem chemical transport model to evaluate local impacts of increased NO emissions on tropospheric ozone concentrations. Mean 4-hour afternoon tropospheric ozone concentrations in Western Kenya increased by up to roughly 2.63 ppbv under fertilization rates of 150 kg N ha-1 or higher. Using AOT40, a metric for assessing crop damage from ozone, we find that the increased ozone concentrations result in an increase in AOT40 exposure of approximately 110 ppbh for inputs of 150 kg N ha-1 during the March-April-May crop growing season, compared with unfertilized simulations, with negligible impacts on crop productivity. Our results suggest that it may be possible to manage Kenyan agricultural systems for high yields while avoiding substantial impacts on air quality.
Asunto(s)
Agricultura , Contaminación del Aire , Óxido Nítrico/química , Ozono , Monitoreo del Ambiente , Fertilizantes , Kenia , SueloRESUMEN
Epidemiological studies have shown that long-term exposure to toxic volatile organic compounds, such as benzene, toluene, ethylbenzene, and xylene (BTEX), is associated with preterm births (PTB). However, global PTB attributable to long-term BTEX exposure has not been reported in the literature yet. In this study, we employed a global chemical transport model, GEOS-Chem (Goddard Earth Observing System coupled with chemistry), in conjunction with an epidemiological model, to quantify the global country-specific PTB associated with long-term BTEX exposure at the horizontal resolution of 1 km × 1 km for the year 2015. Model simulated surface annual mean BTEX concentrations in GEOS-Chem have been thoroughly evaluated against global in-situ observations, which demonstrated that model simulated BTEX concentrations fairly agreed with observations but tended to be underestimated in India. Our study found that the global annual total PTB attributable to BTEX was 2.01 million [95% confidence interval (95CI): 1.16-2.70 million] in 2015, with largest contributions from India (28.3%), followed by China (27.5%), Pakistan (6.2%), Indonesia (4.2%), Bangladesh (3.7%) and United States (2.3%). The global annual total PTB due to BTEX exposure accounted for 19.6% (95CI: 11.3-26.4%) relative to the global annual total all-cause PTB (10.24 million) in 2015. Our study has significant implications on air pollution mitigation policy associated with country-specific anthropogenic BTEX emission reductions to achieve the benefit of human health.
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Contaminantes Atmosféricos , Nacimiento Prematuro , Contaminantes Atmosféricos/análisis , Benceno/análisis , Derivados del Benceno/análisis , Monitoreo del Ambiente , Femenino , Humanos , Recién Nacido , Nacimiento Prematuro/inducido químicamente , Nacimiento Prematuro/epidemiología , Tolueno/análisis , Xilenos/análisisRESUMEN
Accumulating data suggest that air pollution increases the risk of internalizing psychopathology, including anxiety and depressive disorders. Moreover, the link between air pollution and poor mental health may relate to neurostructural and neurofunctional changes. We systematically reviewed the MEDLINE database in September 2021 for original articles reporting effects of air pollution on 1) internalizing symptoms and behaviors (anxiety or depression) and 2) frontolimbic brain regions (i.e., hippocampus, amygdala, prefrontal cortex). One hundred and eleven articles on mental health (76% human, 24% animals) and 92 on brain structure and function (11% human, 86% animals) were identified. For literature search 1, the most common pollutants examined were PM2.5 (64.9%), NO2 (37.8%), and PM10 (33.3%). For literature search 2, the most common pollutants examined were PM2.5 (32.6%), O3 (26.1%) and Diesel Exhaust Particles (DEP) (26.1%). The majority of studies (73%) reported higher internalizing symptoms and behaviors with higher air pollution exposure. Air pollution was consistently associated (95% of articles reported significant findings) with neurostructural and neurofunctional effects (e.g., increased inflammation and oxidative stress, changes to neurotransmitters and neuromodulators and their metabolites) within multiple brain regions (24% of articles), or within the hippocampus (66%), PFC (7%), and amygdala (1%). For both literature searches, the most studied exposure time frames were adulthood (48% and 59% for literature searches 1 and 2, respectively) and the prenatal period (26% and 27% for literature searches 1 and 2, respectively). Forty-three percent and 29% of studies assessed more than one exposure window in literature search 1 and 2, respectively. The extant literature suggests that air pollution is associated with increased depressive and anxiety symptoms and behaviors, and alterations in brain regions implicated in risk of psychopathology. However, there are several gaps in the literature, including: limited studies examining the neural consequences of air pollution in humans. Further, a comprehensive developmental approach is needed to examine windows of susceptibility to exposure and track the emergence of psychopathology following air pollution exposure.
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Contaminantes Atmosféricos , Contaminación del Aire , Embarazo , Femenino , Humanos , Adulto , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Exposición a Riesgos Ambientales/efectos adversos , Contaminación del Aire/efectos adversos , Trastornos de Ansiedad/epidemiología , Trastornos de Ansiedad/etiología , Encéfalo , Material Particulado/toxicidad , Material Particulado/análisisRESUMEN
With urban air quality being a pressing public health concern, community members are becoming increasingly engaged in determining the links between air quality and human health. Although new measurement tools such as low-cost sensors make local data more accessible, a better understanding of gaps in regional datasets is needed to develop effective metropolitan-scale solutions. Using scoping review methodology, we compiled 214 published journal articles and grey literature reports of air quality data from the Detroit, Michigan area from 1952 through 2020. This critical scoping review focuses on air quality datasets, but related topics such as health studies and community-based participatory science studies were examined from the included articles. Most of these publications were peer-reviewed journal articles published after 2001. Particulate matter, nitrous oxides, and sulfur dioxide were the most commonly studied air pollutants, and asthma was the most frequently associated health outcome paired with air pollution datasets. Few publications reported methods for community-based participatory science. This critical scoping review establishes a foundation of historical air quality data for the Detroit metropolitan area and a set of evaluation criteria that can be replicated in other urban centers. This foundation enables future detailed analysis of air quality datasets and showcases strategies for implementing effective community science programs and monitoring efforts.
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Contaminantes Atmosféricos , Contaminación del Aire , Contaminantes Atmosféricos/análisis , Contaminación del Aire/análisis , Monitoreo del Ambiente , Humanos , Michigan , Material Particulado/análisis , Dióxido de Azufre/análisisRESUMEN
Global solid biofuel stove emissions strongly impact air quality, climate change, and human health. However, investigations of the impacts of global solid biofuel stove emissions on human health associated with PM2.5 (particulate matter with aerodynamic diameter ≤2.5 µm) and ozone (O3) are limited. Here, we quantify the impacts of global solid biofuel stove emissions on ambient PM2.5 and O3 air quality and the associated human health effects for the year 2010, using the Community Atmosphere Model coupled with Chemistry version 5.3. Annual mean surface PM2.5 concentrations from global solid biofuel stove emissions averaged over 2006-2010 are up to 23.1 µg m-3, with large impacts found over China, India, sub-Saharan Africa, and eastern and central Europe. For surface O3 impacts, we find that global solid biofuel stove emissions lead to increases in surface O3 concentrations by up to 5.7 ppbv for China, India, and sub-Saharan Africa, and negligible impacts or reductions of up to 0.5 ppbv for the US, Europe, and parts of South America. Global solid biofuel stove emissions for the year 2010 contribute to 382,000 [95% confidence interval (95CI): 349,000-409,000] annual premature deaths associated with PM2.5 and O3 exposure, with the corresponding years of life lost as 8.10 million years (95CI: 7.38-8.70 million years). Our study highlights air quality and human health benefits of mitigating emissions from the global solid biofuel stove sector, especially over populous regions of low-income and middle-income countries, through promoting clean household energy programs for the residential energy supply.
RESUMEN
The global gasoline and diesel fuel vehicle fleets impose substantial impacts on air quality, human health, and climate change. Here we quantify the global radiative forcing and human health impacts of the global gasoline and diesel sectors using the NCAR CESM global chemistry-climate model for year 2015 emissions from the IIASA GAINS inventory. Net global radiative effects of short-lived climate forcers (including aerosols, ozone, and methane) from the gasoline and diesel sectors are +13.6 and +9.4 mW m-2, respectively. The annual mean net aerosol contributions to the net radiative effects of gasoline and diesel are -9.6 ± 2.0 and +8.8 ± 5.8 mW m-2. Aerosol indirect effects for the gasoline and diesel road vehicle sectors are -16.6 ± 2.1 and -40.6 ± 4.0 mW m-2. The fractional contributions of short-lived climate forcers to the total global climate impact including carbon dioxide on the 20-year time scale are similar, 14.9% and 14.4% for gasoline and diesel, respectively. Global annual total PM2.5- and ozone-induced premature deaths for gasoline and diesel sectors approach 115,000 (95% CI: 69,000-153,600) and 122,100 (95% CI: 78,500-157,500), with corresponding years of life lost of 2.10 (95% CI: 1.23-2.66) and 2.21 (95% CI: 1.47-2.85) million years. Substantial regional variability of premature death rates is found for the diesel sector when the regional health effects are normalized by the annual total regional vehicle distance traveled. Regional premature death rates for the gasoline and diesel sectors, respectively, vary by a factor of eight and two orders of magnitude, with India showing the highest for both gasoline and diesel sectors.