China's international trade and air pollution in the United States.
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ABSTRACT:
SUBMITTER: Lin J
PROVIDER: S-EPMC3918792 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Temporal index decomposition analysis and spatial index decomposition analysis were applied to understand the driving forces of the emissions embodied in China's exports and net exports during 2002-2011, respectively. The accumulated emissions embodied in exports accounted for approximately 30% of the total emissions in China; although the contribution of the sectoral total emissions intensity (technique effect) declined, the scale effect was largely responsible for the mounting emissions associated with export, and the composition effect played a largely insignificant role. Calculations of the emissions embodied in net exports suggest that China is generally in an environmentally inferior position compared with its major trade partners. The differences in the economy-wide emission intensities between China and its major trade partners were the biggest contribution to this reality, and the trade balance effect played a less important role. However, a lower degree of specialization in pollution intensive products in exports than in imports helped to reduce slightly the emissions embodied in net exports. The temporal index decomposition analysis results suggest that China should take effective measures to optimize export and supply-side structure and reduce the total emissions intensity. According to spatial index decomposition analysis, it is suggested that a more aggressive import policy was useful for curbing domestic and global emissions, and the transfer of advanced production technologies and emission control technologies from developed to developing countries should be a compulsory global environmental policy option to mitigate the possible leakage of pollution emissions caused by international trade.
| S-EPMC5404823 | biostudies-literature
Project description:PURPOSE:To conduct the first epidemiologic study prospectively examining the association between particulate matter air pollution?<?2.5 µm in diameter (PM2.5) exposure and hepatocellular carcinoma (HCC) risk in the U.S. METHODS:Surveillance, Epidemiology, and End Results (SEER) provided information on HCC cases diagnosed between 2000 and 2014 from 16 population-based cancer registries across the U.S. Ambient PM2.5 exposure was estimated by linking the SEER county with a spatial PM2.5 model using a geographic information system. Poisson regression with robust variance estimation was used to calculate incidence rate ratios and 95% confidence intervals (CIs) for the association between ambient PM2.5 exposure per 10 µg/m3 increase and HCC risk adjusting for individual-level age at diagnosis, sex, race, year of diagnosis, SEER registry, and county-level information on health conditions, lifestyle, demographic, socioeconomic, and environmental factors. RESULTS:Higher levels of ambient PM2.5 exposure were associated with a statistically significant increased risk for HCC (n?=?56,245 cases; adjusted IRR per 10 µg/m3 increase?=?1.26, 95% CI 1.08, 1.47; p?<?0.01). CONCLUSIONS:If confirmed in studies with individual-level PM2.5 exposure and risk factor information, these results suggest that ambient PM2.5 exposure may be a risk factor for HCC in the U.S.
| S-EPMC5940508 | biostudies-literature
Project description:Importance:Ambient fine particulate matter (PM2.5) air pollution is associated with increased risk of several causes of death. However, epidemiologic evidence suggests that current knowledge does not comprehensively capture all causes of death associated with PM2.5 exposure. Objective:To systematically identify causes of death associated with PM2.5 pollution and estimate the burden of death for each cause in the United States. Design, Setting, and Participants:In a cohort study of US veterans followed up between 2006 and 2016, ensemble modeling was used to identify and characterize morphology of the association between PM2.5 and causes of death. Burden of death associated with PM2.5 exposure in the contiguous United States and for each state was then estimated by application of estimated risk functions to county-level PM2.5 estimates from the US Environmental Protection Agency and cause-specific death rate data from the Centers for Disease Control and Prevention. Main Outcomes and Measures:Nonlinear exposure-response functions of the association between PM2.5 and causes of death and burden of death associated with PM2.5. Exposures:Annual mean PM2.5 levels. Results:A cohort of 4?522?160 US veterans (4?243?462 [93.8%] male; median [interquartile range] age, 64.1 [55.7-75.5] years; 3?702?942 [82.0%] white, 667?550 [14.8%] black, and 145?593 [3.2%] other race) was followed up for a median (interquartile range) of 10.0 (6.8-10.2) years. In the contiguous United States, PM2.5 exposure was associated with excess burden of death due to cardiovascular disease (56?070.1 deaths [95% uncertainty interval {UI}, 51?940.2-60?318.3 deaths]), cerebrovascular disease (40?466.1 deaths [95% UI, 21?770.1-46?487.9 deaths]), chronic kidney disease (7175.2 deaths [95% UI, 5910.2-8371.9 deaths]), chronic obstructive pulmonary disease (645.7 deaths [95% UI, 300.2-2490.9 deaths]), dementia (19?851.5 deaths [95% UI, 14?420.6-31?621.4 deaths]), type 2 diabetes (501.3 deaths [95% UI, 447.5-561.1 deaths]), hypertension (30?696.9 deaths [95% UI, 27?518.1-33?881.9 deaths]), lung cancer (17?545.3 deaths [95% UI, 15?055.3-20?464.5 deaths]), and pneumonia (8854.9 deaths [95% UI, 7696.2-10?710.6 deaths]). Burden exhibited substantial geographic variation. Estimated burden of death due to nonaccidental causes was 197?905.1 deaths (95% UI, 183?463.3-213?644.9 deaths); mean age-standardized death rates (per 100?000) due to nonaccidental causes were higher among black individuals (55.2 [95% UI, 50.5-60.6]) than nonblack individuals (51.0 [95% UI, 46.4-56.1]) and higher among those living in counties with high (65.3 [95% UI, 56.2-75.4]) vs low (46.1 [95% UI, 42.3-50.4]) socioeconomic deprivation; 99.0% of the burden of death due to nonaccidental causes was associated with PM2.5 levels below standards set by the US Environmental Protection Agency. Conclusions and Relevance:In this study, 9 causes of death were associated with PM2.5 exposure. The burden of death associated with PM2.5 was disproportionally borne by black individuals and socioeconomically disadvantaged communities. Effort toward cleaner air might reduce the burden of PM2.5-associated deaths.
| S-EPMC6902821 | biostudies-literature
Project description:This paper examines the impact of Covid-19 lockdowns on exports by Chinese cities. We use city-level export data at a monthly frequency from January 2018 through April 2020. Differences-in-differences estimates suggest cities in lockdown experienced a ceteris paribus 34 percentage points reduction in the year-on-year growth rate of exports. The lockdown impacted the intensive and extensive margin, with higher exit and lower new entry into foreign markets. The drop in exports was smaller in (i) coastal cities; (ii) cities with better-developed ICT infrastructure; and (iii) cities with a larger share of potential teleworkers. Time-sensitive and differentiated goods experienced a more pronounced decline in export growth. Global supply chain characteristics matter, with more upstream products and industries that had accumulated larger inventories experiencing a smaller decline in export growth. Also, products that relied more on imported (domestic) intermediates experienced a sharper (flatter) slowdown in export growth. The rapid recovery in cities' exports after lockdowns were lifted suggests the policy was cost-effective in terms of its effects on trade.
| S-EPMC8447424 | biostudies-literature
Project description:BackgroundSevere ecological and economic impacts caused by some invasive species make it imperative to understand the attributes that permit them to spread. A notorious crop pest across its native range in South America, the monk parakeet (Myiopsitta monachus) has become established on four other continents, including growing populations in the United States. As a critical first step to studying mechanisms of invasion success in this species, here we elucidated the geographical and taxonomic history of the North American invasions of the monk parakeet. Specifically, we conducted a genetic assessment of current monk parakeet taxonomy based on mitochondrial DNA control region sequences from 73 museum specimens. These data supported comparative analyses of mtDNA lineage diversity in the native and naturalized ranges of the monk parakeet and allowed for identification of putative source populations.ResultsThere was no molecular character support for the M. m. calita, M. m. cotorra, and M. m. monachus subspecies, while the Bolivian M. m. luchsi was monophyletic and diagnosably distinct. Three haplotypes sampled in the native range were detected within invasive populations in Florida, Connecticut, New Jersey and Rhode Island, the two most common of which were unique to M. m. monachus samples from eastern Argentina and bordering areas in Brazil and Uruguay.ConclusionThe lack of discrete morphological character differences in tandem with the results presented here suggest that M. m. calita, M. m. cotorra and M. m. monachus are in need of formal taxonomic revision. The genetic distinctiveness of M. m. luchsi is consistent with previous recommendations of allospecies status for this taxon. The geographic origins of haplotypes sampled in the four U.S. populations are concordant with trapping records from the mid-20th century and suggest that propagule pressure exerted by the international pet bird trade contributed to the establishment of invasive populations in the United States.
| S-EPMC2517076 | biostudies-literature
Project description:We describe spatial patterns in environmental injustice and inequality for residential outdoor nitrogen dioxide (NO2) concentrations in the contiguous United States. Our approach employs Census demographic data and a recently published high-resolution dataset of outdoor NO2 concentrations. Nationally, population-weighted mean NO2 concentrations are 4.6 ppb (38%, p<0.01) higher for nonwhites than for whites. The environmental health implications of that concentration disparity are compelling. For example, we estimate that reducing nonwhites' NO2 concentrations to levels experienced by whites would reduce Ischemic Heart Disease (IHD) mortality by ?7,000 deaths per year, which is equivalent to 16 million people increasing their physical activity level from inactive (0 hours/week of physical activity) to sufficiently active (>2.5 hours/week of physical activity). Inequality for NO2 concentration is greater than inequality for income (Atkinson Index: 0.11 versus 0.08). Low-income nonwhite young children and elderly people are disproportionately exposed to residential outdoor NO2. Our findings establish a national context for previous work that has documented air pollution environmental injustice and inequality within individual US metropolitan areas and regions. Results given here can aid policy-makers in identifying locations with high environmental injustice and inequality. For example, states with both high injustice and high inequality (top quintile) for outdoor residential NO2 include New York, Michigan, and Wisconsin.
| S-EPMC3988057 | biostudies-literature
Project description:Background:The novel human coronavirus disease 2019 (COVID-19) pandemic has claimed more than 240,000 lives worldwide, causing tremendous public health, social, and economic damages. While the risk factors of COVID-19 are still under investigation, environmental factors, such as urban air pollution, may play an important role in increasing population susceptibility to COVID-19 pathogenesis. Methods:We conducted a cross-sectional nationwide study using zero-inflated negative binomial models to estimate the association between long-term (2010-2016) county-level exposures to NO2, PM2.5 and O3 and county-level COVID-19 case-fatality and mortality rates in the US. We used both single and multipollutant models and controlled for spatial trends and a comprehensive set of potential confounders, including state-level test positive rate, county-level healthcare capacity, phase-of-epidemic, population mobility, sociodemographic, socioeconomic status, behavior risk factors, and meteorological factors. Results:1,027,799 COVID-19 cases and 58,489 deaths were reported in 3,122 US counties from January 22, 2020 to April 29, 2020, with an overall observed case-fatality rate of 5.8%. Spatial variations were observed for both COVID-19 death outcomes and long-term ambient air pollutant levels. County-level average NO2 concentrations were positively associated with both COVID-19 case-fatality rate and mortality rate in single-, bi-, and tri-pollutant models (p-values<0.05). Per inter-quartile range (IQR) increase in NO2 (4.6 ppb), COVID-19 case-fatality rate and mortality rate were associated with an increase of 7.1% (95% CI 1.2% to 13.4%) and 11.2% (95% CI 3.4% to 19.5%), respectively. We did not observe significant associations between long-term exposures to PM2.5 or O3 and COVID-19 death outcomes (p-values>0.05), although per IQR increase in PM2.5 (3.4 ug/m3) was marginally associated with 10.8% (95% CI: -1.1% to 24.1%) increase in COVID-19 mortality rate. Discussions and Conclusions:Long-term exposure to NO2, which largely arises from urban combustion sources such as traffic, may enhance susceptibility to severe COVID-19 outcomes, independent of long-term PM2.5 and O3 exposure. The results support targeted public health actions to protect residents from COVID-19 in heavily polluted regions with historically high NO2 levels. Moreover, continuation of current efforts to lower traffic emissions and ambient air pollution levels may be an important component of reducing population-level risk of COVID-19 deaths.
| S-EPMC7273261 | biostudies-literature
Project description:BackgroundThe novel human coronavirus disease 2019 (COVID-19) pandemic has claimed more than 600,000 lives worldwide, causing tremendous public health, social, and economic damages. Although the risk factors of COVID-19 are still under investigation, environmental factors, such as urban air pollution, may play an important role in increasing population susceptibility to COVID-19 pathogenesis.MethodsWe conducted a cross-sectional nationwide study using zero-inflated negative binomial models to estimate the association between long-term (2010-2016) county-level exposures to NO2, PM2.5, and O3 and county-level COVID-19 case-fatality and mortality rates in the United States. We used both single- and multi-pollutant models and controlled for spatial trends and a comprehensive set of potential confounders, including state-level test positive rate, county-level health care capacity, phase of epidemic, population mobility, population density, sociodemographics, socioeconomic status, race and ethnicity, behavioral risk factors, and meteorology.ResultsFrom January 22, 2020, to July 17, 2020, 3,659,828 COVID-19 cases and 138,552 deaths were reported in 3,076 US counties, with an overall observed case-fatality rate of 3.8%. County-level average NO2 concentrations were positively associated with both COVID-19 case-fatality rate and mortality rate in single-, bi-, and tri-pollutant models. When adjusted for co-pollutants, per interquartile-range (IQR) increase in NO2 (4.6 ppb), COVID-19 case-fatality rate and mortality rate were associated with an increase of 11.3% (95% CI 4.9%-18.2%) and 16.2% (95% CI 8.7%-24.0%), respectively. We did not observe significant associations between COVID-19 case-fatality rate and long-term exposure to PM2.5 or O3, although per IQR increase in PM2.5 (2.6 μg/m3) was marginally associated, with a 14.9% (95% CI 0.0%-31.9%) increase in COVID-19 mortality rate when adjusted for co-pollutants.DiscussionLong-term exposure to NO2, which largely arises from urban combustion sources such as traffic, may enhance susceptibility to severe COVID-19 outcomes, independent of long-term PM2.5 and O3 exposure. The results support targeted public health actions to protect residents from COVID-19 in heavily polluted regions with historically high NO2 levels. Continuation of current efforts to lower traffic emissions and ambient air pollution may be an important component of reducing population-level risk of COVID-19 case fatality and mortality.
| S-EPMC7505160 | biostudies-literature
Project description:BACKGROUND:Few studies have investigated air pollution exposure disparities by race/ethnicity and income across criteria air pollutants, locations, or time. OBJECTIVE:The objective of this study was to quantify exposure disparities by race/ethnicity and income throughout the contiguous United States for six criteria air pollutants, during the period 1990 to 2010. METHODS:We quantified exposure disparities among racial/ethnic groups (non-Hispanic White, non-Hispanic Black, Hispanic (any race), non-Hispanic Asian) and by income for multiple spatial units (contiguous United States, states, urban vs. rural areas) and years (1990, 2000, 2010) for carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), particulate matter with aerodynamic diameter ≤2.5μm (PM2.5; excluding year-1990), particulate matter with aerodynamic diameter ≤10μm (PM10), and sulfur dioxide (SO2). We used census data for demographic information and a national empirical model for ambient air pollution levels. RESULTS:For all years and pollutants, the racial/ethnic group with the highest national average exposure was a racial/ethnic minority group. In 2010, the disparity between the racial/ethnic group with the highest vs. lowest national-average exposure was largest for NO2 [54% (4.6 ppb)], smallest for O3 [3.6% (1.6 ppb)], and intermediate for the remaining pollutants (13%-19%). The disparities varied by U.S. state; for example, for PM2.5 in 2010, exposures were at least 5% higher than average in 63% of states for non-Hispanic Black populations; in 33% and 26% of states for Hispanic and for non-Hispanic Asian populations, respectively; and in no states for non-Hispanic White populations. Absolute exposure disparities were larger among racial/ethnic groups than among income categories (range among pollutants: between 1.1 and 21 times larger). Over the period studied, national absolute racial/ethnic exposure disparities declined by between 35% (0.66μg/m3; PM2.5) and 88% (0.35 ppm; CO); relative disparities declined to between 0.99× (PM2.5; i.e., nearly zero change) and 0.71× (CO; i.e., a ∼29% reduction). DISCUSSION:As air pollution concentrations declined during the period 1990 to 2010, absolute (and to a lesser extent, relative) racial/ethnic exposure disparities also declined. However, in 2010, racial/ethnic exposure disparities remained across income levels, in urban and rural areas, and in all states, for multiple pollutants. https://doi.org/10.1289/EHP8584.
| S-EPMC8672803 | biostudies-literature
Project description:Ambient air pollution is a well-known risk factor of various asthma-related outcomes, however, past research has often focused on acute exacerbations rather than asthma development. This study draws on a population-based, multigenerational panel dataset from the United States to assess the association of childhood asthma risk with census block-level, annual-average air pollution exposure measured during the prenatal and early postnatal periods, as well as effect modification by neighborhood poverty. Findings suggest that early-life exposures to nitrogen dioxide (NO₂), a marker of traffic-related pollution, and fine particulate matter (PM2.5), a mixture of industrial and other pollutants, are positively associated with subsequent childhood asthma diagnosis (OR = 1.25, 95% CI = 1.10⁻1.41 and OR = 1.25, 95% CI = 1.06⁻1.46, respectively, per interquartile range (IQR) increase in each pollutant (NO₂ IQR = 8.51 ppb and PM2.5 IQR = 4.43 µ/m³)). These effects are modified by early-life neighborhood poverty exposure, with no or weaker effects in moderate- and low- (versus high-) poverty areas. This work underscores the importance of a holistic, developmental approach to elucidating the interplay of social and environmental contexts that may create conditions for racial-ethnic and socioeconomic disparities in childhood asthma risk.
| S-EPMC6025399 | biostudies-literature