Consumption in the G20 nations causes particulate air pollution resulting in two million premature deaths annually.

Worldwide exposure to ambient PM2.5 causes over 4 million premature deaths annually. As most of these deaths are in developing countries, without internationally coordinated efforts this polarized situation will continue. As yet, however, no studies have quantified nation-to-nation consumer responsibility for global mortality due to both primary and secondary PM2.5 particles. Here we quantify the global footprint of PM2.5-driven premature deaths for the 19 G20 nations in a position to lead such efforts. G20 consumption in 2010 was responsible for 1.983 [95% Confidence Interval: 1.685-2.285] million premature deaths, at an average age of 67, including 78.6 [71.5-84.8] thousand infant deaths, implying that the G20 lifetime consumption of about 28 [24-33] people claims one life. Our results indicate that G20 nations should take responsibility for their footprint rather than focusing solely on transboundary air pollution, as this would expand opportunities for reducing PM2.5-driven premature mortality. Given the infant mortality footprint identified, it would moreover contribute to ensuring infant lives are not unfairly left behind in countries like South Africa, which have a weak relationship with G20 nations.

Environment-lockdown, air pollution and related diseases: could we learn something and make it last?

Although the pandemic has caused substantial losses in economic prosperity and human lives, it has also some positive impacts on the environment. Restricted mobility, complete closure, less traffic and industry have led to improved air quality especially in urban settings. Not only is air pollution an important determinant of chronic diseases, such as heart and lung disorders, but it has also been shown that poor air quality increases the risk of COVID-19. In this article, we review some of the findings on changes in air quality during the pandemic, and its potential effects on health. We need to continue to monitor the effects of change in air quality, due to COVID-19 lockdown or other factors, but also keep all our efforts to improve air quality even faster and more persistent, bringing the pollution levels below what WHO recommends are safe to live with.

Critical supply chains for mitigating PM2.5 emission-related mortalities in India.

Air pollution and its health-related effects are a major concern globally, and many people die from air pollution-related diseases each year. This study employed a structural path analysis combined with a health impact inventory database analysis to estimate the number of consumption-based PM2.5 emission-related deaths attributed to India's power supply sector. We identified critical supply chain paths for direct (production) electricity use and indirect (consumption) use. We also considered both domestic and foreign final demand and its effect on PM2.5 emission-related deaths. Several conclusions could be drawn from our results. First, the effect of indirect electricity usage on PM2.5 emission-related deaths is approximately four times larger than that for direct usage. Second, a large percentage of pollution-related deaths can be attributed to India's domestic final demand usage; however, electricity usage in the intermediate and final demand sectors is inextricably linked. Third, foreign final demand sectors from the Middle East, the USA, and China contribute indirectly toward PM2.5 emission-related deaths, specifically in the rice export supply chain. The results show that the Indian government should implement urgent measures to curb electricity use in rice supply chains in order to reduce the number of PM2.5 emission-related deaths.

Unprecedented reduction in air pollution and corresponding short-term premature mortality associated with COVID-19 lockdown in Delhi, India.

Countries around the world introduced strict restrictions on movement and activities known as 'lockdowns' to restrict the spread of the novel coronavirus disease (COVID-19) from the end of 2019. A sudden improvement in air quality was observed globally as a result of these lockdowns. To provide insight into the changes in air pollution levels in response to the COVID-19 restrictions we have compared surface air quality data in Delhi during four phases of lockdown and the first phase of the restriction easing period (25 March to 30 June 2020) with data from a baseline period (2018-2019). Simultaneously, short-term exposure of PM2.5 and O3 attributed premature mortality were calculated to understand the health benefit of the change in air quality. Ground-level observations in Delhi showed that concentrations of PM10, PM2.5 and NO2 dropped substantially in 2020 during the overall study period compared with the same period in previous years, with average reductions of ~49%, ~39%, and ~39%, respectively. An overall lower reduction in O3 of ~19% was observed for Delhi. A slight increase in O3 was found in Delhi's industrial and traffic regions. The highest peak of the diurnal variation decreased substantially for all the pollutants at every phase. The decrease in PM2.5 and O3 concentrations in 2020, prevented 904 total premature deaths, a 60% improvement when compared to the figures for 2018-2019. The restrictions on human activities during the lockdown have reduced anthropogenic emissions and subsequently improved air quality and human health in one of the most polluted cities in the world.Implications: I am submitting herewith the manuscript entitled "Unprecedented Reduction in Air Pollution and Corresponding Short-term Premature Mortality Associated with COVID-19 Forced Confinement in Delhi, India" for potential publishing in your journal.The novelty of this research lies in: (1) we utilized ground-level air quality data in Delhi during four phases of lockdown and the first phase of unlocking period (25th March to 30th June) for 2020 as well as data from the baseline period (2018-2019) to provide an early insight into the changes in air pollution levels in response to the COVID-19 pandemic, (2) Chatarize the change of diurnal variation of the pollutants and (3) we assess the health risk due to PM2.5 and O3. Results from ground-level observations in Delhi showed that concentrations of PM10, PM2.5 and NO2 substantially dropped in 2020 during the overall study period compared to the similar period in previous years, with an average reduction of ~49%, ~39%, and ~39%, respectively. In the case of O3, the overall reduction was observed as ~19% in Delhi, while a slight increase was found in industrial and traffic regions. And consequently, the highest peak of the diurnal variation decreased substantially for all the pollutants. The health impact assessment of the changes in air quality indicated that 904 short-term premature deaths (~60%) were prevented due to the decline in PM2.5 and O3 concentrations in the study period. The restrictions on human activities during the lockdown have reduced the anthropogenic emissions and subsequently improved air quality and human health in one of the most polluted cities in the world.

Short-term exposure to particulate matters is associated with septic emboli in infective endocarditis.

This survey was to investigate the short-term effect of particulate matters (PMs) exposure on clinical and microbiological variables, especially septic emboli, in infective endocarditis (IE). The study analyzed 138 IE patients in Far Eastern Memorial Hospital from 2005 to 2015 and clinical variables were retrospectively requested. The data of air quality were recorded and collected by a network of 26 monitoring stations spreading in Northern part of Taiwan. We found that IE patients with septic emboli were found to be exposed to a significantly higher level of PM2.5 (32.01 ±â€Š15.89 vs. 21.70 ±â€Š13.05 µg/m, P < .001) and PM10 (54.57 ±â€Š24.43 vs 40.98 ±â€Š24.81 µg/m, P = .002) on lag 0 day when compared to those without. Furthermore, multivariate regression analysis revealed that that ambient exposure to PM2.5 (odds ratio: 3.87, 95% confidence interval: 1.31-8.31; P = .001) and PM10 (odds ratio: 4.58, 95% confidence interval: 2.03-10.32; P < .001) significantly increased risk of septic emboli in IE patients. To our knowledge, this is the first study demonstrating that short-term exposure to PMs was associated with septic emboli in IE.

Carnosine Supplementation Mitigates the Deleterious Effects of Particulate Matter Exposure in Mice.

Background Exposure to fine airborne particulate matter ( PM 2.5) induces quantitative and qualitative defects in bone marrow-derived endothelial progenitor cells of mice, and similar outcomes in humans may contribute to vascular dysfunction and the cardiovascular morbidity and mortality associated with PM 2.5 exposure. Nevertheless, mechanisms underlying the pervasive effects of PM 2.5 are unclear and effective interventional strategies to mitigate against PM 2.5 toxicity are lacking. Furthermore, whether PM 2.5 exposure affects other types of bone marrow stem cells leading to additional hematological or immunological dysfunction is not clear. Methods and Results Mice given normal drinking water or that supplemented with carnosine, a naturally occurring, nucleophilic di-peptide that binds reactive aldehydes, were exposed to filtered air or concentrated ambient particles. Mice drinking normal water and exposed to concentrated ambient particles demonstrated a depletion of bone marrow hematopoietic stem cells but no change in mesenchymal stem cells. However, HSC depletion was significantly attenuated when the mice were placed on drinking water containing carnosine. Carnosine supplementation also increased the levels of carnosine-propanal conjugates in the urine of CAPs-exposed mice and prevented the concentrated ambient particles-induced dysfunction of endothelial progenitor cells as assessed by in vitro and in vivo assays. Conclusions These results suggest that exposure to PM 2.5 has pervasive effects on different bone marrow stem cell populations and that PM 2.5-induced hematopoietic stem cells depletion, endothelial progenitor cell dysfunction, and defects in vascular repair can be mitigated by excess carnosine. Carnosine supplementation may be a viable approach for preventing PM 2.5-induced immune dysfunction and cardiovascular injury in humans.

[Lung cancer deaths attributable to ambient PM(2.5) exposure in 2016 in China].

Objective: To analyze the lung cancer deaths attributable to ambient PM(2.5) exposure in China in 2016. Methods: All data were from the Global Burden of Disease Study 2016 (GBD 2016). Multiple-source data, including satellite observation, ground measurement, chemical migration model simulation, etc., and the data integration model for air quality (DIMAQ) were used to estimate the grid-level exposure to ambient PM(2.5). Data from the vital registry and cancer registry were used to establish statistical model to estimate the lung cancer deaths by province, age and gender. The lung cancer deaths attributable to PM(2.5) were calculated based on the calculation of population attributable fraction (PAF). The GBD world population age structure was adopted to calculate age-standardized rates for comparison among provinces (including 31 provinces, autonomous regions and municipalities directly under the central government, as well as Hong Kong and Macao special administrative regions, excluding Taiwan of China). Results: In 2016, the lung cancer deaths attributable to ambient PM(2.5) exposure in China were 14.56×10(4) (95% uncertainty interval (UI): 9.63×10(4)-19.55×10(4)), accounting for 24.66% (95%UI: 16.38%-33.12%) of total lung cancer deaths. The lung cancer death rate attributable to PM(2.5) increased with age, with the lowest among 25-29 age group (0.25/10(5), 95%UI: 0.17/10(5)-0.34/10(5)), the highest among ≥80 age group (90.70/10(5), 95%UI: 59.85/10(5)-122.20/10(5)). The lung cancer death rate attributable to PM(2.5) among males (14.84/10(5), 95%UI: 9.78/10(5)-19.93/10(5)) was higher than that in females (6.21/10(5), 95%UI: 4.07/10(5)-8.40/10(5)). The age-standardized death rates (ASDR) of lung cancer attributable to PM(2.5) among males and females in China were higher than the global average level. The attributable ASDR of lung cancer varied among provinces, highest in Shandong (13.51/10(5), 95%UI: 9.14/10(5)-18.20/10(5)) and lowest in Tibet (0.85/10(5), 95%UI: 0.44/10(5)-1.51/10(5)). Conclusion: In 2016, the lung cancer deaths attributable to ambient PM(2.5) exposure in China was heavy, and varied in different age groups, genders and provinces.

Occupational exposure to inorganic particles during pregnancy and birth outcomes: a nationwide cohort study in Sweden.

OBJECTIVES: The aim of this study was to investigate if occupational exposure to inorganic particles or welding fumes during pregnancy is associated with negative birth outcomes. DESIGN: A prospective national cohort study. SETTING: All single births from 1994 to 2012 in Sweden. Information on birth weight, preterm birth, small for gestational age, smoking habits, nationality, age, occupation, absence from work and education was obtained from nationwide registers. Exposure to inorganic particles (mg/m3) was assessed from a job exposure matrix. PARTICIPANTS: This study included all single births by occupationally active mothers (995 843). OUTCOME MEASURES: Associations between occupational exposures and negative birth outcomes in the form of low birth weight, preterm birth and small for gestational age. RESULTS: Mothers who had high exposure to inorganic particles and had less than 50 days (median) of absence from work during pregnancy showed an increased risk of preterm birth (OR 1.18; 95% CI 1.07 to 1.30), low birth weight (OR 1.32; 95% CI 1.18 to 1.48) as well as small for gestational age (OR 1.20; 95% CI 1.04 to 1.39). The increased risks were driven by exposure to iron particles. No increased risks were found in association with exposure to stone and concrete particles. High exposure to welding fumes was associated with an increased risk of low birth weight (OR 1.22; 95% CI 1.02 to 1.45) and preterm birth (OR 1.24; 95% CI 1.07 to 1.42). CONCLUSIONS: The results indicate that pregnant women should not be exposed to high levels of iron particles or welding fumes.

[The impact of persistent high ambient fine particulate matters exposures on mortality in the 40 districts/counties of China, 2013-2015].

Objective: To investigate the impact of persistent high ambient fine particulate matters (PM(2.5)) exposures on mortality in the polluted areas of 40 districts/counties in China. Methods: Using a convenient sampling method, we selected 40 districts/counties as research sites from the Beijing-Tianjin-Hebei Metropolitan Region, the Yangtze River Delta, the Pearl River Delta, and Heilongjiang, Shanxi, and Sichuan province. The daily concentrations of PM(2.5), meteorological data and population death data from January 1, 2013 to December 31, 2015 were collected. The six persistent PM(2).5 pollution episode scenarios were defined by the average daily concentration of PM(2.5) (75 µg/m(3), P(75) and P(90) of the average daily concentration of each district/county respectively) and the duration (≥2 days or 3 days). Generalized linear models and meta analyses were used to explore the impact of PM(2.5) pollution episodes on mortality in 40 districts/counties. Results: The mean±SD and P(50) (P(25), P(75)) of average daily temperature, relative humidity and PM(2.5) were (15.26±10.48) ℃, 17.20 (7.50, 23.70) ℃, (67.31±19.26)%, 72.00% (57.00%, 81.00%), (72.81±60.93) µg/m(3) and 55.38 (33.77, 91.45) µg/m(3), respectively in 40 districts/counties during 2013-2015. The average number of non-accidental, cardiovascular and cerebrovascular diseases deaths per day were (12±7), (5±4) and (2±2) in each district/county, respectively. When the daily concentrations of PM(2.5) were ≥75 µg/m(3) (≥2 days), ≥P(75) (≥2 days), ≥P(90) (≥2 days), ≥75 µg/m(3) (≥3 days), and ≥P(75) (≥3 days), the excess risk (95%CI) of the total non-accidental deaths and cardiovascular diseases deaths were 1.77% (0.89%,2.66%), 2.69% (1.06%,4.35%), 1.67% (0.59%,2.76%), 2.31% (0.67%, 3.97%), 0.71% (-0.75%, 2.20%), 1.95% (0.08%, 3.86%), 1.15% (0.12%, 2.18%), 1.85% (0.25%, 3.47%), 1.39% (0.15%, 2.64%), 2.29% (0.39%, 4.23%), respectively. Conclusion: Persistently high PM(2.5) exposures were associated with total non-accidental deaths and cardiovascular disease deaths.

[Multi-site analysis of acute effects of air pollutants combination exposure on mortality in Jiangsu Province, China].

Objective: To explore the acute effect of fine particulate matters (PM(2.5)), O(3), NO(2) on daily non-accidental mortality, cardiovascular disease mortality and respiratory mortality data in thirteen cities of Jiangsu province. Methods: Daily average concentrations of non-accidental mortality, cardiovascular disease mortality, respiratory mortality data and environmental data were collected from January 1, 2015 to December 31, 2017 in thirteen cities of Jiangsu Province. Daily air quality, mortality and meteorology data were collected from the Information System of Air Pollution and Health Impact Monitoring of Chinese Center for Disease Control and Prevention. We used generalized additive model to evaluate the association between daily concentrations of air pollutants and mortality at single-city level and multi-city level, after adjusting the long-term and seasonal trend, as well as meteorological factors and the effect of "days and weeks" . A multivariate Meta-analysis with random effects was applied to estimate dose-response relationship between air pollutants and mortality. Results: At multi-city level, per interquartile range increase of PM(2.5), O(3), NO(2) was associated with an increase of 1.10% (95%CI: 0.66%, 1.54%), 0.59% (95%CI: 0.18%, 1.00%), 2.00% (95%CI: 1.29%, 2.72%) of daily non-accidental mortality respectively; 1.01% (95%CI: 0.63%, 1.38%), 0.66% (95%CI: 0.02%, 1.30%), 1.62% (95%CI: 1.00%, 2.23%) of daily cardiovascular mortality respectively; 1.09% (95%CI: 0.35%, 1.82%), 0.44% (95%CI: -0.29%, 1.16%), 2.75% (95%CI: 1.42%, 4.08%) of daily respiratory mortality respectively. The air pollutants effect varied across different cities. The strongest effect of PM(2.5) was current day (excess risk (ER)=1.10%, 95%CI: 0.66%, 1.54%)), the strongest effect of O(3) was 2-day lag (ER=1.82%, 95%CI: 0.69%, 2.97%) and the strongest effect of NO(2) was 1-day lag (ER=2.09%, 95%CI: 1.34%, 2.83%) of daily non-accidental mortality respectively. Conclusion: The increases of PM(2.5) and NO(2) concentration could result in the increases of daily non-accidental mortality, cardiovascular disease mortality and respiratory mortality. O(3) could result in the increases of daily non-accidental mortality and cardiovascular disease mortality. The acute effects for non-accidental mortality from high to low were NO(2), PM(2.5) and O(3,) and the strongest effect of PM(2.5) was current day. O(3) and NO(2) had lagged effects.

Afghanistan Particulate Matter Enhances Pro-Inflammatory Responses in IL-13-Exposed Human Airway Epithelium via TLR2 Signaling.

Since the start of Afghanistan combat operations in 2001, there has been an increase in complaints of respiratory illnesses in deployed soldiers with no previous history of lung disorders. It is postulated that deployment-related respiratory illnesses are the result of inhalation of desert particulate matter (PM) potentially acting in combination with exposure to other pro-inflammatory compounds. Why some, but not all, soldiers develop respiratory diseases remains unclear. Our goal was to investigate if human airway epithelial cells primed with IL-13, a type 2 inflammatory cytokine, demonstrate stronger pro-inflammatory responses to Afghanistan desert PM (APM). Primary human brushed bronchial epithelial cells from non-deployed, healthy subjects were exposed to APM, both with and without IL-13 pretreatment. APM exposure in conjunction with IL-13 resulted in significantly increased expression of IL-8, a pro-inflammatory cytokine involved in neutrophil recruitment and activation. Furthermore, expression of TLR2 mRNA was increased after combined IL-13 and APM exposure. siRNA-mediated TLR2 knockdown dampened IL-8 production after exposure to APM with IL-13. APM with IL-13 treatment increased IRAK-1 (a downstream signaling molecule of TLR2 signaling) activation, while IRAK-1 knockdown effectively eliminated the IL-8 response to APM and IL-13. Our data suggest that APM exposure may promote neutrophilic inflammation in airways with a type 2 cytokine milieu.

Short communication: Diagnosis of lung cancer increases during the annual southeast Asian haze periods.

There have been few but timely studies examining the role of air pollution in lung cancer and survival. The Southeast Asia haze is a geopolitical problem that has occurred annually since 1997 in countries such as Malaysia, Singapore and Indonesia. To date, there has been no study examining the impact of the annual haze in the presentation of lung cancer. Data on all lung cancers and respiratory admissions to Universiti Kebangsaan Malaysia Medical Centre (UKMMC) from 1st January 2010 to 31th October 2015 were retrospectively collected and categorized as presentation during the haze and non-haze periods defined by the Department of Environment Malaysia. We report a lung cancer incidence rate per week of 4.5 cases during the haze compared to 1.8 cases during the non-haze period (p<0.01). The median survival for subjects presenting during the haze was 5.2 months compared to 8.1 months for the non-haze period (p<0.05). The majority of subjects diagnosed during the haze period initially presented with acute symptoms. Although this study could not suggest a cause and effect relationship of the annual haze with the incidence of lung cancer, this is the first study reporting a local air pollution-related modifiable determinant contributing to the increase in presentation of lung cancer in Southeast Asia.

Impacts and mitigation of excess diesel-related NOx emissions in 11 major vehicle markets.

Vehicle emissions contribute to fine particulate matter (PM2.5) and tropospheric ozone air pollution, affecting human health, crop yields and climate worldwide. On-road diesel vehicles produce approximately 20 per cent of global anthropogenic emissions of nitrogen oxides (NOx), which are key PM2.5 and ozone precursors. Regulated NOx emission limits in leading markets have been progressively tightened, but current diesel vehicles emit far more NOx under real-world operating conditions than during laboratory certification testing. Here we show that across 11 markets, representing approximately 80 per cent of global diesel vehicle sales, nearly one-third of on-road heavy-duty diesel vehicle emissions and over half of on-road light-duty diesel vehicle emissions are in excess of certification limits. These excess emissions (totalling 4.6 million tons) are associated with about 38,000 PM2.5- and ozone-related premature deaths globally in 2015, including about 10 per cent of all ozone-related premature deaths in the 28 European Union member states. Heavy-duty vehicles are the dominant contributor to excess diesel NOx emissions and associated health impacts in almost all regions. Adopting and enforcing next-generation standards (more stringent than Euro 6/VI) could nearly eliminate real-world diesel-related NOx emissions in these markets, avoiding approximately 174,000 global PM2.5- and ozone-related premature deaths in 2040. Most of these benefits can be achieved by implementing Euro VI standards where they have not yet been adopted for heavy-duty vehicles.

Systemic effects of controlled exposure to diesel exhaust: a meta-analysis from randomized controlled trials.

INTRODUCTION: Ambient air pollution is associated with adverse cardiovascular events. This meta-analysis aimed to investigate the short-term association between air pollution and cardiovascular effects on healthy volunteers. METHODS: We searched databases to identify randomized trials with controlled human exposures to either of two models for studying ambient particulate matter: diesel-exhaust or concentrated ambient particles. Estimates of size effect were performed using standardized mean difference (SMD). Heterogeneity was assessed with I2 statistics. Outcomes were vascular function estimated by forearm blood flow (FBF), blood pressure, heart rate, and blood analysis. RESULTS: Database searches yielded 17 articles (n = 342) with sufficient information for meta-analyses. High levels of heterogeneity for the some outcomes were analyzed using random-effects model. The pooled effect estimate showed that short-term exposure to air pollution impaired FBF response from 2.7 to 2.5 mL/100 mL tissue/min (SMD 0.404; p = .006). There was an increase in 5000 platelet/mm3 following pollution exposure (SMD 0.390; p = .050) but no significant differences for other outcomes. CONCLUSION: Controlled human exposures to air pollution are associated with the surrogates of vascular dysfunction and increase in platelet count, which might be related to adverse cardiovascular events. Given the worldwide prevalence of exposure to air pollution, these findings are relevant for public health. KEY MESSAGES Controlled exposure to air pollution impairs vasomotor response, which is a surrogate for adverse cardiovascular events. This is the first meta-analysis from randomized clinical trials showing short-term association between air pollution and cardiovascular effects on healthy volunteers. Given the worldwide prevalence of exposure to air pollution, this finding is important for public health.