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      Short‐Term Effects of Particle Size and Constituents on Blood Pressure in Healthy Young Adults in Guangzhou, China

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          Abstract

          Background

          Although several studies have focused on the associations between particle size and constituents and blood pressure, results have been inconsistent.

          Methods and Results

          We conducted a panel study, between December 2017 and January 2018, in 88 healthy university students in Guangzhou, China. Weekly systolic blood pressure and diastolic blood pressure were measured for each participant for 5 consecutive weeks, resulting in a total of 440 visits. Mass concentrations of particles with an aerodynamic diameter of ≤2.5 µm (PM 2.5), ≤1.0 µm (PM 1.0), ≤0.5 µm (PM 0.5), ≤0.2 µm (PM 0.2), and number concentrations of airborne particulates of diameter ≤0.1 μm were measured. Linear mixed‐effect models were used to estimate the associations between blood pressure and particles and PM 2.5 constituents 0 to 48 hours before blood pressure measurement. PM of all the fractions in the 0.2‐ to 2.5‐μm range were positively associated with systolic blood pressure in the first 24 hours, with the percent changes of effect estimates ranging from 3.5% to 8.8% for an interquartile range increment of PM. PM 0.2 was also positively associated with diastolic blood pressure, with an increase of 5.9% (95% CI, 1.0%–11.0%) for an interquartile range increment (5.8 μg/m 3) at lag 0 to 24 hours. For PM 2.5 constituents, we found positive associations between chloride and diastolic blood pressure (1.7% [95% CI, 0.1%–3.3%]), and negative associations between vanadium and diastolic blood pressure (−1.6% [95% CI, −3.0% to −0.1%]).

          Conclusions

          Both particle size and constituent exposure are significantly associated with blood pressure in the first 24 hours following exposure in healthy Chinese adults.

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          Most cited references64

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          Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017

          Summary Background The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 comparative risk assessment (CRA) is a comprehensive approach to risk factor quantification that offers a useful tool for synthesising evidence on risks and risk–outcome associations. With each annual GBD study, we update the GBD CRA to incorporate improved methods, new risks and risk–outcome pairs, and new data on risk exposure levels and risk–outcome associations. Methods We used the CRA framework developed for previous iterations of GBD to estimate levels and trends in exposure, attributable deaths, and attributable disability-adjusted life-years (DALYs), by age group, sex, year, and location for 84 behavioural, environmental and occupational, and metabolic risks or groups of risks from 1990 to 2017. This study included 476 risk–outcome pairs that met the GBD study criteria for convincing or probable evidence of causation. We extracted relative risk and exposure estimates from 46 749 randomised controlled trials, cohort studies, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. Using the counterfactual scenario of theoretical minimum risk exposure level (TMREL), we estimated the portion of deaths and DALYs that could be attributed to a given risk. We explored the relationship between development and risk exposure by modelling the relationship between the Socio-demographic Index (SDI) and risk-weighted exposure prevalence and estimated expected levels of exposure and risk-attributable burden by SDI. Finally, we explored temporal changes in risk-attributable DALYs by decomposing those changes into six main component drivers of change as follows: (1) population growth; (2) changes in population age structures; (3) changes in exposure to environmental and occupational risks; (4) changes in exposure to behavioural risks; (5) changes in exposure to metabolic risks; and (6) changes due to all other factors, approximated as the risk-deleted death and DALY rates, where the risk-deleted rate is the rate that would be observed had we reduced the exposure levels to the TMREL for all risk factors included in GBD 2017. Findings In 2017, 34·1 million (95% uncertainty interval [UI] 33·3–35·0) deaths and 1·21 billion (1·14–1·28) DALYs were attributable to GBD risk factors. Globally, 61·0% (59·6–62·4) of deaths and 48·3% (46·3–50·2) of DALYs were attributed to the GBD 2017 risk factors. When ranked by risk-attributable DALYs, high systolic blood pressure (SBP) was the leading risk factor, accounting for 10·4 million (9·39–11·5) deaths and 218 million (198–237) DALYs, followed by smoking (7·10 million [6·83–7·37] deaths and 182 million [173–193] DALYs), high fasting plasma glucose (6·53 million [5·23–8·23] deaths and 171 million [144–201] DALYs), high body-mass index (BMI; 4·72 million [2·99–6·70] deaths and 148 million [98·6–202] DALYs), and short gestation for birthweight (1·43 million [1·36–1·51] deaths and 139 million [131–147] DALYs). In total, risk-attributable DALYs declined by 4·9% (3·3–6·5) between 2007 and 2017. In the absence of demographic changes (ie, population growth and ageing), changes in risk exposure and risk-deleted DALYs would have led to a 23·5% decline in DALYs during that period. Conversely, in the absence of changes in risk exposure and risk-deleted DALYs, demographic changes would have led to an 18·6% increase in DALYs during that period. The ratios of observed risk exposure levels to exposure levels expected based on SDI (O/E ratios) increased globally for unsafe drinking water and household air pollution between 1990 and 2017. This result suggests that development is occurring more rapidly than are changes in the underlying risk structure in a population. Conversely, nearly universal declines in O/E ratios for smoking and alcohol use indicate that, for a given SDI, exposure to these risks is declining. In 2017, the leading Level 4 risk factor for age-standardised DALY rates was high SBP in four super-regions: central Europe, eastern Europe, and central Asia; north Africa and Middle East; south Asia; and southeast Asia, east Asia, and Oceania. The leading risk factor in the high-income super-region was smoking, in Latin America and Caribbean was high BMI, and in sub-Saharan Africa was unsafe sex. O/E ratios for unsafe sex in sub-Saharan Africa were notably high, and those for alcohol use in north Africa and the Middle East were notably low. Interpretation By quantifying levels and trends in exposures to risk factors and the resulting disease burden, this assessment offers insight into where past policy and programme efforts might have been successful and highlights current priorities for public health action. Decreases in behavioural, environmental, and occupational risks have largely offset the effects of population growth and ageing, in relation to trends in absolute burden. Conversely, the combination of increasing metabolic risks and population ageing will probably continue to drive the increasing trends in non-communicable diseases at the global level, which presents both a public health challenge and opportunity. We see considerable spatiotemporal heterogeneity in levels of risk exposure and risk-attributable burden. Although levels of development underlie some of this heterogeneity, O/E ratios show risks for which countries are overperforming or underperforming relative to their level of development. As such, these ratios provide a benchmarking tool to help to focus local decision making. Our findings reinforce the importance of both risk exposure monitoring and epidemiological research to assess causal connections between risks and health outcomes, and they highlight the usefulness of the GBD study in synthesising data to draw comprehensive and robust conclusions that help to inform good policy and strategic health planning. Funding Bill & Melinda Gates Foundation.
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            Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association.

            In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 microm in diameter (PM(2.5)) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM(2.5) exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM(2.5) exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.
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              Airborne particulate matter and human health: toxicological assessment and importance of size and composition of particles for oxidative damage and carcinogenic mechanisms.

              Air pollution has been considered a hazard to human health. In the past decades, many studies highlighted the role of ambient airborne particulate matter (PM) as an important environmental pollutant for many different cardiopulmonary diseases and lung cancer. Numerous epidemiological studies in the past 30 years found a strong exposure-response relationship between PM for short-term effects (premature mortality, hospital admissions) and long-term or cumulative health effects (morbidity, lung cancer, cardiovascular and cardiopulmonary diseases, etc). Current research on airborne particle-induced health effects investigates the critical characteristics of particulate matter that determine their biological effects. Several independent groups of investigators have shown that the size of the airborne particles and their surface area determine the potential to elicit inflammatory injury, oxidative damage, and other biological effects. These effects are stronger for fine and ultrafine particles because they can penetrate deeper into the airways of the respiratory tract and can reach the alveoli in which 50% are retained in the lung parenchyma. Composition of the PM varies greatly and depends on many factors. The major components of PM are transition metals, ions (sulfate, nitrate), organic compound, quinoid stable radicals of carbonaceous material, minerals, reactive gases, and materials of biologic origin. Results from toxicological research have shown that PM have several mechanisms of adverse cellular effects, such as cytotoxicity through oxidative stress mechanisms, oxygen-free radical-generating activity, DNA oxidative damage, mutagenicity, and stimulation of proinflammatory factors. In this review, the results of the most recent epidemiological and toxicological studies are summarized. In general, the evaluation of most of these studies shows that the smaller the size of PM the higher the toxicity through mechanisms of oxidative stress and inflammation. Some studies showed that the extractable organic compounds (a variety of chemicals with mutagenic and cytotoxic properties) contribute to various mechanisms of cytotoxicity; in addition, the water-soluble faction (mainly transition metals with redox potential) play an important role in the initiation of oxidative DNA damage and membrane lipid peroxidation. Associations between chemical compositions and particle toxicity tend to be stronger for the fine and ultrafine PM size fractions. Vehicular exhaust particles are found to be most responsible for small-sized airborne PM air pollution in urban areas. With these aspects in mind, future research should aim at establishing a cleared picture of the cytotoxic and carcinogenic mechanisms of PM in the lungs, as well as mechanisms of formation during internal engine combustion processes and other sources of airborne fine particles of air pollution.
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                Author and article information

                Contributors
                yangby23@mail.sysu.edu.cn
                donggh5@mail.sysu.edu.cn , donggh512@hotmail.com
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                04 May 2021
                18 May 2021
                : 10
                : 10 ( doiID: 10.1002/jah3.v10.10 )
                : e019063
                Affiliations
                [ 1 ] Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment Department of Occupational and Environmental Health School of Public Health Sun Yat‐sen University Guangzhou China
                [ 2 ] Centre for Air Quality and Health Research and Evaluation Glebe Australia
                [ 3 ] Ingham Institute for Applied Medial Research University of New South Wales Sydney Australia
                [ 4 ] School of Public Health The University of Queensland Herston Queensland Australia
                [ 5 ] Finnish Meteorological Institute Kuopio Finland
                [ 6 ] Department of Applied Physics University of Eastern Finland Kuopio Finland
                [ 7 ] Department of Environmental and Biological Sciences University of Eastern Finland Kuopio Finland
                Author notes
                [*] [* ] Correspondence to: Guang‐Hui Dong, MD, PhD, and Bo‐Yi Yang, MD, PhD, Department of Occupational and Environmental Health, School of Public Health, Sun Yat‐sen University, 74 Zhongshan 2 nd Rd, Yuexiu District, Guangzhou 510080, China. E‐mail: donggh5@ 123456mail.sysu.edu.cn , donggh512@ 123456hotmail.com ; yangby23@ 123456mail.sysu.edu.cn

                [*]

                P. Guo and Z. He contributed equally to this work and are co‐first authors.

                Author information
                https://orcid.org/0000-0001-7664-9621
                https://orcid.org/0000-0003-4308-4534
                https://orcid.org/0000-0002-2578-3369
                Article
                JAH36067
                10.1161/JAHA.120.019063
                8200702
                33942624
                eeb1e3e5-9c84-4732-8aa0-131afa26123d
                © 2021 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 30 October 2020
                : 04 February 2021
                Page count
                Figures: 5, Tables: 2, Pages: 14, Words: 26208
                Funding
                Funded by: National Natural Science Foundation of China , open-funder-registry 10.13039/501100001809;
                Award ID: 81703179
                Award ID: 81950410633
                Award ID: 81972992
                Award ID: 81872582
                Award ID: 81872583
                Funded by: Science and Technology Program of Guangzhou
                Award ID: 201807010032
                Award ID: 201803010054
                Funded by: National Key Research and Development Program of China
                Award ID: 2018YFC1004300
                Award ID: 2018YFE0106900
                Funded by: Guangdong Provincial Natural Science Foundation Team Project
                Award ID: 2018B030312005
                Funded by: Fundamental Research Funds for the Central Universities
                Award ID: 19
                Award ID: ykjc01
                Funded by: Natural Science Foundation of Guangdong Province , open-funder-registry 10.13039/501100003453;
                Award ID: 2020A1515011131
                Award ID: 2019A050510017
                Award ID: 2018B05052007
                Award ID: 2017A090905042
                Categories
                JAHA Spotlight on Air Pollution and Cardiovascular Disease
                JAHA Spotlight on Air Pollution and Cardiovascular Disease
                Original Research
                Custom metadata
                2.0
                May 18, 2021
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.2 mode:remove_FC converted:17.05.2021

                Cardiovascular Medicine
                air pollution,blood pressure,constituents,panel study,particulate matter,high blood pressure

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