Estimating the Inadvertent Decrement in Mortality due to Reduction in Ambient Fine Particulate Concentrations During COVID-19 Lockdown in India
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ABSTRACT:
SUBMITTER: Patra S
PROVIDER: S-EPMC7952262 | biostudies-literature | 2021 Jan
REPOSITORIES: biostudies-literature
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Project description:Air pollution exposure remains a leading public health problem in China. The use of chemical transport models to quantify the impacts of various emission changes on air quality is limited by their large computational demands. Machine learning models can emulate chemical transport models to provide computationally efficient predictions of outputs based on statistical associations with inputs. We developed novel emulators relating emission changes in five key anthropogenic sectors (residential, industry, land transport, agriculture, and power generation) to winter ambient fine particulate matter (PM2.5) concentrations across China. The emulators were optimized based on Gaussian process regressors with Matern kernels. The emulators predicted 99.9% of the variance in PM2.5 concentrations for a given input configuration of emission changes. PM2.5 concentrations are primarily sensitive to residential (51%-94% of first-order sensitivity index), industrial (7%-31%), and agricultural emissions (0%-24%). Sensitivities of PM2.5 concentrations to land transport and power generation emissions are all under 5%, except in South West China where land transport emissions contributed 13%. The largest reduction in winter PM2.5 exposure for changes in the five emission sectors is by 68%-81%, down to 15.3-25.9 μg m-3, remaining above the World Health Organization annual guideline of 10 μg m-3. The greatest reductions in PM2.5 exposure are driven by reducing residential and industrial emissions, emphasizing the importance of emission reductions in these key sectors. We show that the annual National Air Quality Target of 35 μg m-3 is unlikely to be achieved during winter without strong emission reductions from the residential and industrial sectors.
| S-EPMC8095364 | biostudies-literature
Project description:Ambient air pollution of fine particulate matter with diameters less than 2.5 μm (PM2.5) is associated with millions of premature deaths per year, recognized as a leading global health concern. The dose-response relation between ambient PM2.5 exposure and mortality risk is the most fundamental information for assessments of the health effects of PM2.5. The existing dose-response relations were generally developed based on the assumption of equal contribution to toxicity from various sources. However, the sources of PM2.5 may significantly influence health effects. In this study, we conducted an ecological study to investigate the global long-term correlation between source-specific PM2.5 exposure and cause-specific mortality risk (SPECM) based on the regional aggregate data of the publically available official health databases from 528 regions worldwide with a total registered population of 3.2 billion. The results provided preliminary epidemiological evidence for differing chronic health effects across various sources. The relative mortality risks of lung cancer and circulatory diseases were closely correlated with the primary emissions from industrial and residential combustion sources. Chronic lower respiratory diseases were mostly associated with the mass concentration of particulate matter.
| S-EPMC9879273 | biostudies-literature
Project description:Little is known about the effect of air pollution on the gastrointestinal (GI) system. We investigated the association between long-term exposures to outdoor fine particles (PM2.5) and hospitalization for peptic ulcer diseases (PUDs) in a large cohort of Hong Kong Chinese elderly.A total of 66,820 subjects aged ≥65 years who were enrolled in all 18 Government Elderly Health Service centers of Hong Kong participated in the study voluntarily between 1998 and 2001. They were prospectively followed up for more than 10 years. Annual mean exposures to PM2.5 at residence of individuals were estimated by satellite data through linkage with address details including floor level. All hospital admission records of the subjects up to December 31, 2010 were retrieved from the central database of Hospital Authority. We used Cox regression to estimate the hazard ratio (HR) for PUD hospitalization associated with PM2.5 exposure after adjustment for individual and ecological covariates.A total of 60,273 subjects had completed baseline information including medical, socio-demographic, lifestyle, and anthropometric data at recruitment. During the follow-up period, 1991 (3.3%) subjects had been hospitalized for PUD. The adjusted HR for PUD hospitalization per 10 μg/m of PM2.5 was 1.18 (95% confidence interval: 1.02-1.36, P = 0.02). Further analysis showed that the associations with PM2.5 were significant for gastric ulcers (HR 1.29; 1.09-1.53, P = 0.003) but not for duodenal ulcers (HR 0.98; 0.78 to 1.22, P = 0.81).Long-term exposures to PM2.5 were associated with PUD hospitalization in elder population. The mechanism underlying the PM2.5 in the development of gastric ulcers warrants further research.
| S-EPMC4863781 | biostudies-literature
Project description:BackgroundAmbient fine particulate matter [PM ≤2.5μm in aerodynamic diameter (PM2.5)] is a major health risk for children, particularly in South Asia, which currently experiences the highest PM2.5 levels globally. Nevertheless, there is comparatively little epidemiological evidence from this region to quantify the effects of PM2.5 on child survival.ObjectivesWe estimated the association between PM2.5 exposure and child survival in India.MethodsWe constructed a large, retrospective, and nationally representative cohort of children <5 years of age, born between 2009-2016, from the publicly available, cross-sectional 2015-2016 Demographic Health Surveys in India. In utero and post-delivery lifetime average ambient PM2.5 exposures were estimated with data from satellite remote sensing, meteorology, and land use information (model R2= 0.82). We used Cox proportional hazards regression to estimate the association between both average in utero and post-delivery lifetime PM2.5 and all-cause child mortality, controlling for individual- and household-level covariates, seasonality, location, and meteorology.ResultsOver 7,447,724 child-months of follow-up, there were 11,559 deaths at <5 years of age reported by the children's mothers. The mean concentrations of 9-month in utero and post-delivery lifetime average ambient PM2.5 exposure were 71.1 μg/m3 (range: 20.9-153.5 μg/m3) and 73.7 μg/m3 (range: 14.0-247.3 μg/m3), respectively. Estimated child mortality adjusted hazard ratios were 1.023 [95% confidence interval (CI): 1.008, 1.038] and 1.013 (95% CI: 1.001, 1.026) per 10-μg/m3 increase of in utero and post-delivery lifetime PM2.5, with both exposures in the model.DiscussionThis study adds to the growing body of evidence about the adverse health effects of PM2.5 by demonstrating the association between exposure, both in utero and post-delivery, on child survival at the national level in India. Strategies to reduce ambient air pollution levels, including steps to minimize in utero and early life exposures, are urgently needed in India and other countries where exposures are above recommended guideline values. https://doi.org/10.1289/EHP8910.
| S-EPMC8791069 | biostudies-literature
Project description:BackgroundEstimating the burden of disease attributable to long-term exposure to fine particulate matter (PM2.5) in ambient air requires knowledge of both the shape and magnitude of the relative risk (RR) function. However, adequate direct evidence to identify the shape of the mortality RR functions at the high ambient concentrations observed in many places in the world is lacking.ObjectiveWe developed RR functions over the entire global exposure range for causes of mortality in adults: ischemic heart disease (IHD), cerebrovascular disease (stroke), chronic obstructive pulmonary disease (COPD), and lung cancer (LC). We also developed RR functions for the incidence of acute lower respiratory infection (ALRI) that can be used to estimate mortality and lost-years of healthy life in children < 5 years of age.MethodsWe fit an integrated exposure-response (IER) model by integrating available RR information from studies of ambient air pollution (AAP), second hand tobacco smoke, household solid cooking fuel, and active smoking (AS). AS exposures were converted to estimated annual PM2.5 exposure equivalents using inhaled doses of particle mass. We derived population attributable fractions (PAFs) for every country based on estimated worldwide ambient PM2.5 concentrations.ResultsThe IER model was a superior predictor of RR compared with seven other forms previously used in burden assessments. The percent PAF attributable to AAP exposure varied among countries from 2 to 41 for IHD, 1 to 43 for stroke, < 1 to 21 for COPD, < 1 to 25 for LC, and < 1 to 38 for ALRI.ConclusionsWe developed a fine particulate mass-based RR model that covered the global range of exposure by integrating RR information from different combustion types that generate emissions of particulate matter. The model can be updated as new RR information becomes available.
| S-EPMC3984213 | biostudies-literature
Project description:BACKGROUND:Fine particulate matter (PM2.5) air pollution is a leading cause of global cardiovascular mortality. A key mechanism may be PM2.5-induced blood pressure (BP) elevations. Whether consistent prohypertensive responses persist across the breadth of worldwide pollution concentrations has never been investigated. METHODS:We evaluated the hemodynamic impact of short-term exposures to ambient PM2.5 in harmonized studies of healthy normotensive adults (4 BP measurements per participant) living in both a highly polluted (Beijing) and clean (Michigan) location. RESULTS:Prior 7-day outdoor-ambient and 24-hour personal-level PM2.5 concentration averages were much higher in Beijing (86.7 ± 52.1 and 52.4 ± 79.2 µg/m3) compared to Michigan (9.1 ± 1.8 and 12.2 ± 17.0 µg/m3). In Beijing (n = 73), increased outdoor-ambient exposures (per 10 µg/m3) during the prior 1-7 days were associated with significant elevations in diastolic BP (0.15-0.17 mm Hg). In overweight adults (body mass index ≥25 kg/m2), significant increases in both systolic (0.34-0.44 mm Hg) and diastolic (0.22-0.66 mm Hg) BP levels were observed. Prior 24-hour personal-level exposures also significantly increased BP (0.41/0.61 mm Hg) in overweight participants. Conversely, low PM2.5 concentrations in Michigan (n = 50), on average within Air Quality Guidelines, were not associated with BP elevations. CONCLUSIONS:Our findings demonstrate that short-term exposures to ambient PM2.5 in a highly polluted environment can promote elevations in BP even among healthy adults. The fact that no adverse hemodynamic responses were observed in a clean location supports the key public health importance of international efforts to improve air quality as part of the global battle against hypertension.
| S-EPMC5905592 | biostudies-literature
Project description:The COVID-19 pandemic elicited a global response to limit associated mortality, with social distancing and lockdowns being imposed. In India, human activities were restricted from late March 2020. This 'anthropogenic emissions switch-off' presented an opportunity to investigate impacts of COVID-19 mitigation measures on ambient air quality in five Indian cities (Chennai, Delhi, Hyderabad, Kolkata, and Mumbai), using in-situ measurements from 2015 to 2020. For each year, we isolated, analysed and compared fine particulate matter (PM2.5) concentration data from 25 March to 11 May, to elucidate the effects of the lockdown. Like other global cities, we observed substantial reductions in PM2.5 concentrations, from 19 to 43% (Chennai), 41-53% (Delhi), 26-54% (Hyderabad), 24-36% (Kolkata), and 10-39% (Mumbai). Generally, cities with larger traffic volumes showed greater reductions. Aerosol loading decreased by 29% (Chennai), 11% (Delhi), 4% (Kolkata), and 1% (Mumbai) against 2019 data. Health and related economic impact assessments indicated 630 prevented premature deaths during lockdown across all five cities, valued at 0.69 billion USD. Improvements in air quality may be considered a temporary lockdown benefit as revitalising the economy could reverse this trend. Regulatory bodies must closely monitor air quality levels, which currently offer a baseline for future mitigation plans.
| S-EPMC7357527 | biostudies-literature
Project description:Short-term elevations in fine particulate matter air pollution (PM2.5) are associated with increased risk of acute cerebrovascular events. Evidence from the peripheral circulation suggests that vascular dysfunction may be a central mechanism. However, the effects of PM2.5 on cerebrovascular function and hemodynamics are unknown.We used transcranial Doppler ultrasound to measure beat-to-beat blood flow velocity in the middle cerebral artery at rest and in response to changes in end-tidal CO2 (cerebral vasoreactivity) and arterial blood pressure (cerebral autoregulation) in 482 participants from the Maintenance of Balance, Independent Living, Intellect, and Zest in the Elderly (MOBILIZE) of Boston study. We used linear mixed effects models with random subject intercepts to evaluate the association between cerebrovascular hemodynamic parameters and mean PM2.5 levels 1 to 28 days earlier adjusting for age, race, medical history, meteorologic covariates, day of week, temporal trends, and season.An interquartile range increase (3.0 µg/m(3)) in mean PM2.5 levels during the previous 28 days was associated with an 8.6% (95% confidence interval, 3.7%-13.8%; P<0.001) higher cerebral vascular resistance and a 7.5% (95% confidence interval, 4.2%-10.6%; P<0.001) lower blood flow velocity at rest. Measures of cerebral vasoreactivity and autoregulation were not associated with PM2.5 levels.In this cohort of community-dwelling seniors, exposure to PM2.5 was associated with higher resting cerebrovascular resistance and lower cerebral blood flow velocity. If replicated, these findings suggest that alterations in cerebrovascular hemodynamics may underlie the increased risk of particle-related acute cerebrovascular events.
| S-EPMC3722046 | biostudies-literature
Project description:BackgroundEpidemiological observations have demonstrated that ambient fine particulate matter with dp < 2.5 μm (PM2.5) as the major factor responsible for the increasing incidence of lung cancer in never-smokers. However, there are very limited experimental data to support the association of PM2.5 with lung carcinogenesis and to compare PM2.5 with smoking carcinogens.MethodsTo study whether PM2.5 can contribute to lung tumorigenesis in a way similar to smoking carcinogen 4-methylnitrosamino-l-3-pyridyl-butanone (NNK) via 15-lipoxygenases (15-LOXs) reduction, normal lung epithelial cells and cancer cells were treated with NNK or PM2.5 and then epigenetically and post-translationally examined the cellular and molecular profiles of the cells. The data were verified in lung cancer samples and a mouse lung tumor model.ResultsWe found that similar to smoking carcinogen NNK, PM2.5 significantly enhanced cell proliferation, migration and invasion, but reduced the levels of 15-lipoxygenases-1 (15-LOX1) and 15-lipoxygenases-2 (15-LOX2), both of which were also obviously decreased in lung cancer tissues. 15-LOX1/15-LOX2 overexpression inhibited the oncogenic cell functions induced by PM2.5/NNK. The tumor formation and growth were significantly higher/faster in mice implanted with PM2.5- or NNK-treated NCI-H23 cells, accompanied with a reduction of 15-LOX1/15-LOX2. Moreover, 15-LOX1 expression was epigenetically regulated at methylation level by PM2.5/NNK, while both 15-LOX1 and 15-LOX2 could be significantly inhibited by a set of PM2.5/NNK-mediated microRNAs.ConclusionCollectively, PM2.5 can function as the smoking carcinogen NNK to induce lung tumorigenesis by inhibiting 15-LOX1/15-LOX2.
| S-EPMC6697918 | biostudies-literature
Project description:Epidemiologic and health impact studies are inhibited by the paucity of global, long-term measurements of the chemical composition of fine particulate matter. We inferred PM2.5 chemical composition at 0.1° × 0.1° spatial resolution for 2004-2008 by combining aerosol optical depth retrieved from the MODIS and MISR satellite instruments, with coincident profile and composition information from the GEOS-Chem global chemical transport model. Evaluation of the satellite-model PM2.5 composition data set with North American in situ measurements indicated significant spatial agreement for secondary inorganic aerosol, particulate organic mass, black carbon, mineral dust, and sea salt. We found that global population-weighted PM2.5 concentrations were dominated by particulate organic mass (11.9 ± 7.3 ?g/m(3)), secondary inorganic aerosol (11.1 ± 5.0 ?g/m(3)), and mineral dust (11.1 ± 7.9 ?g/m(3)). Secondary inorganic PM2.5 concentrations exceeded 30 ?g/m(3) over East China. Sensitivity simulations suggested that population-weighted ambient PM2.5 from biofuel burning (11 ?g/m(3)) could be almost as large as from fossil fuel combustion sources (17 ?g/m(3)). These estimates offer information about global population exposure to the chemical components and sources of PM2.5.
| S-EPMC4238642 | biostudies-literature