Short‐Term Effects of Particle Size and Constituents on Blood Pressure in Healthy Young Adults in Guangzhou, China
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 (PM2.5), ≤1.0 µm (PM1.0), ≤0.5 µm (PM0.5), ≤0.2 µm (PM0.2), 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 PM2.5 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. PM0.2 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/m3) at lag 0 to 24 hours. For PM2.5 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%]).
Both particle size and constituent exposure are significantly associated with blood pressure in the first 24 hours following exposure in healthy Chinese adults.
diastolic blood pressure
particles with an aerodynamic diameter of ≤0.2 µm
particles with an aerodynamic diameter of ≤0.5 µm
particles with an aerodynamic diameter of ≤1.0 µm
particles with an aerodynamic diameter of ≤2.5 µm
airborne particulates of diameter ≤0.1 μm
systolic blood pressure
What Is New?
Size‐fractionated particulate matter with a wide range of smaller diameters (5 cumulative size fractions with upper limits from 0.1 to 2.5 μm) and various particulate matter 2.5‐μm constituents were measured in a region with high air pollution levels, adding more evidence to the understanding of the association between particulate matter size and constituents and blood pressure.
What Are the Clinical Implications?
Our results could add evidence to the association of particulate matter–related blood pressure in the young population, help us to more deeply understand the physiological mechanisms of the development of hypertension, and also provide healthcare professionals with suggestions or treatments for people to take preventive measures, and ultimately to mitigate the effects of air pollution on hypertension.
Short‐term exposures to ambient particulate air pollution are closely linked to increased risks of morbidity and mortality from cardiovascular diseases1, 2, 3; however, the exact mechanisms underlying these associations remain unclear. High blood pressure (BP) is one of the major risk factors for cardiovascular diseases, and even young adults with elevated BP might have increased risks of cardiovascular events in later life.4 In air pollution epidemiology, high blood pressure is usually hypothesized to be a mediator for the relationships between ambient particulate air pollution and cardiovascular diseases.5 Although numerous epidemiological studies have explored the associations between particulate matter (PM) and blood pressure, the results are still inconsistent.6, 7 For example, while some studies reported that short‐term PM exposures were significantly associated with increased blood pressure,8, 9, 10, 11, 12, 13, 14 others showed a null or inverse association.15, 16, 17, 18, 19, 20
The associations between PM and blood pressure changes could be influenced by many factors. First, PM pollution could differ in different cities because of its spatiotemporal variation and socioeconomic drivers, leading to varying degrees of health effects.21 PM pollution has long been a major public health concern in China, but most previous studies were based on heavily polluted areas in northern China,12, 22, 23 with fewer studies conducted in southern China where particulate air pollution levels are lower compared with northern China. Furthermore, aerodynamic diameter and chemical composition are the main physical characteristics of particles, and different sizes and composition of particles may have different toxicological and physicochemical properties,24, 25 thus leading to the heterogeneous findings of PM health impact. Because most of these studies have been conducted among patients or specific populations,11, 26, 27, 28 evidence from the general population is still scarce.
Therefore, in this study, our objective was to determine the acute effects of size‐fractionated PM as well as chemical composition on blood pressure in healthy young adults in Guangzhou in southern China.
All the data presented in this study are available from the authors upon request.
We carried out a panel study between December 2017 and January 2018 in healthy young adults aged 20 to 26 years. Participants were recruited from the North campus of Sun Yat‐Sen University, which covers only an area of ≈0.39 km2 in Guangzhou, China, and met the following criteria: (1) lived and studied in North campus during the study period; (2) no previous smoking or no alcohol consumption during the study period; (3) no cardiovascular, pulmonary, or other chronic diseases, and (4) free of medications that may influence cardiovascular function. We scheduled 5 weekly visits for each of the study participants during the study period, from December 7, 2017 to January 5, 2018. Finally, 88 students participated in our study. The demographic information of each participant, including name, sex, ethnicity, exercise frequency, and medical history or health status were collected at the first measurement. Height and weight of each participant were also measured, and body mass index was calculated as the weight (kg) divided by the square of the height (meters). All study participants provided written informed consent at the beginning of the study. The Human Studies Committee of the School of Public Health, Sun Yat‐Sen University approved this study (Ethics Approval Number: L2017024).
In order to obtain a BP observer certificate, a qualifying examination was taken for trainees involved in the study, and all investigators were trained according to the guideline of the European Society of Hypertension.29
Before BP measurements, study participants were advised not to exercise for at least 30 minutes, and not to drink coffee or tea on the visit day. With their back and right arm supported, participants sat in a quiet room for at least 5 minutes, feet on the floor and cubital fossa at heart level. The upper right arm brachial artery BP of participants, including systolic blood pressure (SBP) and diastolic blood pressure (DBP), was measured on 3 consecutive occasions using automated oscillometric monitors. The final reported BP value was the average of the 3 BP measurements and was used for analyses. Pulse pressure was calculated as the SBP minus the DBP, and mean arterial pressure (MAP) was calculated as of the DBP plus one third of the pulse pressure.
Five weekly study visits were taken for each participant over the entire study in a school building at the campus. In every repeated measurement on the 88 participants, half of them were measured on Thursday at 6:00 to 10:00 pm to collect their BP information, and the rest of the participants were measured on Friday at the same time and place.
Using standard methods and quality controls, data of real‐time PM mass and number concentration as well as meteorological exposure were measured on the roof of a 10‐story building from December 1, 2017 to January 5, 2018 at the same campus where participants were recruited. A measurement site was established that was clear from any structures that would obstruct the air flow. At the site, minute‐to‐minute mass concentrations of PM with an aerodynamic diameter of ≤2.5 µm (PM2.5), ≤1.0 µm (PM1.0), ≤0.5 µm (PM0.5), and ≤0.2 µm (PM0.2) were measured. In addition, minute‐to‐minute number concentrations of PM with an aerodynamic diameter of ≤0.1 µm (PN0.1) were measured. The measurements used a combination of an Optical Particle Sizer Spectrometer (Model OPS3330; TSI, USA) and a NanoScan Scanning Mobility Particle Sizer (Model 3910; TSI, USA), and the optical diameter was then converted into an aerodynamic diameter through the method suggested by Alas et al.30 A Vaisala Weather Transmitter (Model WXT530; Vaisala, Finland) was used to continuously measure temperature and relative humidity.
At the same time and site of the real‐time PM sampling, daily PM2.5 sampling was also performed for further measurement of PM2.5 constituents. The high‐volume samplers (TH‐1000H; Tianhong Co. Ltd., China) were used with a sampling rate of 1 m3/min and the collection time of each sample was 24 hours. Quartz microfiber filters and Teflon filters were used. After sampling, the filter‐based samples were placed in a desiccator for initial weighing and gravimetric quantification and then stored in a refrigerator (−20°C) for further chemical composition analysis. Using a semicontinuous OC/EC analyzer (Model 4G; Sunset Laboratory, OR) and thermo/optical transmission method, organic carbon (OC), elemental carbon (EC), total carbon, and water‐soluble organic carbon were measured in quartz‐fiber filters. Ten water‐soluble inorganic ions, including ammonium (NH4+), sodium (Na+), potassium (K+), calcium (Ca2+), magnesium (Mg2+), chloride (Cl−), fluoride (F−), sulfate (), nitrite (), and nitrate () were measured by ion chromatography (model ICS‐2000; Dionex Corp., Sunnyvale, CA). Fifteen trace elements, including sodium (Na), potassium (K), calcium (Ca), magnesium (Mg), aluminum (Al), phosphorus (P), vanadium (V), copper (Cu), chromium (Cr), manganese (Mn), iron (Fe), nickel (Ni), zinc (Zn), barium (Ba), and lead (Pb) were measured by inductively coupled plasma mass spectrometry (ICP‐MS; Thermo Scientific, USA).
Because all the outcome variables (SBP, DBP, pulse pressure, and MAP) were not normally distributed, we applied a log transformation. Spearman correlations were used to evaluate the relationship between study pollutants before including them in the regression analyses. Minute‐to‐minute pollutant concentrations, measured 0 to 48 hours before BP measurement every week, were used to calculate the lag concentrations in the following time windows: lag 0 to 6 hours, lag 7 to 12 hours, lag 13 to 24 hours, lag 0 to 24 hours, lag 25 to 48 hours, and lag 0 to 48 hours.
We used linear mixed models to estimate the associations between PM and BP, and random intercept that included each participant was included in each model to adjust for the within‐ participant correlations in repeated measurements. Covariates included as fixed‐effect terms in these models were: age, sex, body mass index, exercise times per week, average temperature, and humidity.31 To adjust for any possible weekly time trends, we also included “week” of BP measurements as an indicator variable. In the weekly repeated measurements, each participant was measured on the same day of week and at the same time of day in the same place, so that potential confounding because of day of week, time of measurement, and site was minimized. In addition, the study was conducted in 1 season with less changing in climate, so that seasonal factors were not considered as confounding factors.
We use 3 models to investigate the effects and robustness of the associations between PM2.5 chemical composition and BP changes.12, 32 First, particles or PM2.5 constituents were incorporated one at a time with adjustment for the above‐mentioned potential confounders. In addition, we built the constituent‐PM2.5 joint model in which PM2.5 total mass was introduced in the single‐constituent model to account for potential confounding by PM2.5 and all other constituents that covary with PM2.5. Furthermore, for the constituent‐residual model, we first created the residual of each constituent by establishing a linear regression model between the constituent and PM2.5 total mass, and then replaced the constituent in the single‐constituent model by its residual. This model could be regarded as a crude measure of the independent contribution of each constituent because the residual of each constituent was uncorrelated with PM2.5 total mass.33, 34, 35
We calculated the percent changes of effect estimates in BP variables for an interquartile range (IQR) increase of particle or a constituent as [10(β×IQR)−1]×100%, and the 95% CIs were [10[IQR×(β±1.96×SE)]−1]×100%, where β and SE were the estimated regression coefficient and its SE, respectively.36
All analyses in this study were conducted in R software (Version 3.6.1, R Foundation for Statistical Computing, Vienna, Austria) and the “lme4” package was used. Statistical significance level was defined as P<0.05 (two sided).
Overall, a total of 88 participants completed all of the 5 weekly control visits, resulting in a total of 440 visits. Characteristics of the study participants are shown in Table 1. The average age of study participants was 21.5±1.1 years old and their average body mass index was 21.4±2.9 kg/m2. Fifty‐four participants were female (n=54), and more than half of the participants exercised at least once a week. During the study period, all participants did not have any disease that would affect the study result and did not take any medication, dietary supplements, or alcoholic beverages. Sex‐stratified descriptive statistics of study participants are shown in Table S1.
|Female (%)||54 (61.4%)|
|Exercise time (%)|
|0 time per wk||41 (46.6%)|
|1 time per wk||19 (21.6%)|
|2 times per wk||20 (22.7%)|
|≥3 times per wk||8 (9.1%)|
Table 2 shows descriptive statistics on BP, average concentrations of air pollutants, weather conditions, and PM2.5 composition during the study period. The mean SBP, DBP, pulse pressure, and MAP were 112.5±14.1 mm Hg, 71.0±8.9 mm Hg, 41.5±11.7 mm Hg, and 84.8±9.4 mm Hg, respectively. On average, daily PM2.5 mass concentration was 72.7±35.1 μg/m3 (mean±SD), and PN0.1 number concentration was 20.2±11.7 (1000 particles/cm3) (mean±SD). Correlations among PM metrics were highest for PM2.5 and PM1.0 (Table S2). Correlations between PM mass or number concentrations and temperature were low (r values between 0.27 and 0.46), and it was the same for relative humidity (r values between −0.14 and 0.16).
|Seated blood pressure|
|SBP, mm Hg||112.5±14.1||86||102||110||121||157||19|
|DBP, mm Hg||71.0±8.9||49||65||71||77||99||12|
|PP, mm Hg||41.5±11.7||18||33||40||48||79||15|
|MAP, mm Hg||84.8±9.4||64.3||77.7||83.7||91.3||112||13.7|
|PM mass concentration|
|PM count concentration|
|PN0.1 (1000 particles/cm3)||20.2±11.7||2.6||12.2||17.3||25.0||133||12.8|
|Relative humidity, %||44.4±13.8||14.6||33.2||44.7||56.2||76.2||23|
The relationship between different lag times of PM exposure and BP are shown in Figures 1 and 2. PM of all the fractions in the 0.2 to 2.5 μm range were positively associated with SBP in the first 24 hours. For an IQR increment of particles between 0.2 and 2.5 μm, this positive effect ranged from 3.5% to 8.8% at different lag times. Furthermore, PM0.2 was also positively associated with DBP and MAP. These associations were first seen at 7 to 12 hours, but were not significant after lag 25 to 48 hours and lag 0 to 48 hours. At lag 0 to 24 hours, an IQR increase in PM2.5 (45.9 μg/m3) was significantly associated with an increase of 8.8% (95% CI, 1.5%–16.6%) in SBP, and an IQR increase in PM0.2 (5.8 μg/m3) was associated with an increase of 5.9% (95% CI, 1.0%–11.0%) in DBP and an increase of 5.1% (95% CI, 1.4%–8.8%) in MAP. The results for PN0.1 were mixed, which had both positive and negative associations in SBP, DBP, and MAP, and was not similar to the results of particles between 0.2 and 2.5 μm. More specifically, for an IQR increase in PN0.1 (12.8 [1000 particles/cm3]), the estimated percent changes showed no statistically significant in PN0.1 and SBP at lag 0 to 24 hours (0.9% [95% CI, −5.2% to 7.5%]), showed negative association with DBP at lag 0 to 6 hours (−5.4% [95% CI, −10.3% to −0.3%]), and showed positive association with DBP at lag 13 to 24 hours (5.4% [95% CI, 0.8%–10.2%]). These results were similar for both the crude and adjusted models.
For PM2.5 constituents, significant positive associations were found between chloride and DBP in all 3 models, and in the single‐constituent model, the increment was 1.7% (95% CI, 0.1%–3.3%) in DBP. In addition, significant negative associations were found between DBP and vanadium, and between MAP and fluoride in all 3 models, with estimated percent changes of −1.6% (95% CI, −3.0% to −0.1%) and −1.5% (95% CI, −2.8% to −0.3%) in the single‐constituent model, respectively. Other constituents, such as OC, EC, and total carbon, were significantly associated with SBP based on single‐constituent models (the estimated percent changes were 4.2% [95% CI, 0.6%–7.9%], 3.2% [95% CI, 0.8%–5.6%], and 4.3% [95% CI, 0.8%–8.0%], respectively), but these associations became nonsignificant in adjusted models (Figures 3, 4, 5).
We measured the effects of size‐fractionated particulate matter (5 cumulative size fractions with upper limits from 0.1 to 2.5 μm) and 29 constituents of PM2.5 (4 carbonaceous components, 10 inorganic ions, and 15 trace elements) on BP in 88 healthy young adults in Guangzhou, China. In the first 24 hours following exposure, positive associations were found between size‐fractionated PM (particles between 0.2 and 2.5 μm) and SBP, and between PM0.2 and DBP and MAP. As for PM2.5 constituent concentrations, positive associations were found between DBP and chloride, and negative associations were found between DBP and vanadium and between MAP and fluoride.
Effect of Particle Size
Several previous studies have observed that short‐term PM exposure may be related to BP changes; however, the results across these studies are inconsistent. In our study, we observed positive association between size‐fractionated PM and SBP; similarly, previous studies have also reported that PM2.5 exposure is related to increased SBP.9, 11, 12, 14, 26, 37, 38 For example, Lin et al found that a 19.1 μg/m3 (IQR) increment of PM2.5 was related to an increase of 1.9 mm Hg (95% CI, 0.7–3.1) in SBP.11 Zhao et al showed in a panel study that an increase in SBP corresponded to size‐fractionated particulate matter among patients with type 2 diabetes mellitus.26 Conversely, other studies have reported inverse or null associations.15, 16, 19, 39 For instance, Scheers et al failed to observe significant associations between PM10, PM2.5 variations, and BP.39
In this panel study, we also found that PM0.2 were positively associated with DBP and MAP. Studies showed that results for PM‐related DBP changes are mixed.10, 11, 12, 14, 37, 38, 40 For instance, Yang et al reported that a 10 μg/m3 increment on 0 to 6‐day mean of PM2.5 was associated with an increase of 0.49 mm Hg (95% CI, 0.45–0.53) in DBP among 6‐ to 17‐year‐old children in Suzhou.14 However, Ibald‐Mulli et al did not find significant positive associations for PM2.5 and DBP among 131 patients with coronary heart disease.17 MAP could be regarded as a strong predictor of cardiovascular events and mortality.41, 42 Consistent with our study, Wang et al found that an IQR increment (26.78 μg/m3) in a 24‐hour mean of PM2.5 was associated with increments of 0.66 mm Hg in DBP and 0.82 mm Hg in MAP.38 Therefore, short‐term exposure to PM may be also related to changes in DBP and MAP, and further studies are still needed to clarify these associations.
Effects of PM2.5 Constituents
Evidence linking PM2.5 chemical composition and cardiovascular outcomes has been growing, and short‐term exposure to various PM2.5 constituents was reported to have an association with BP in several studies.10, 12, 43 For instance, Wu et al found positive associations among zinc, nickel, magnesium, strontium, lead, arsenic, and SBP and DBP, whereas chromium, manganese, and molybdenum had significant inverse associations with SBP or DBP.12 In our study, we found consistent positive associations between chloride and DBP but negative associations between fluoride and MAP in all 3 models. Airborne chloride in urban areas might mainly come from polyvinyl chloride plastic burning in refuse dumps, and pollutants such as fluoride might also come from trash compacting or incineration.44 Consistent with our findings, epidemiologic study found that chloride was slightly but robustly associated with SBP and DBP.11 Previous animal experimental studies have demonstrated that dietary intake of chloride could be associated with increased BP in rats,45 which indicates that chloride might be associated with increased BP. Wu et al found smaller consistent associations between fluoride and DBP.12 Evidence for the association between airborne ions such as chloride and fluoride and BP still requires further investigation.
We also found that increased BP is associated with OC, EC, and total carbon in single‐constituent models, but the result became inconsistent in adjusted models. Studies have demonstrated that carbonaceous particles (such as OC and EC) might come from traffic emissions.44 Lin et al found that ambient OC and EC exposure had significant associations with increased risk of cardiovascular disease mortality in Guangzhou,46 and another panel study in Shanghai found that OC and EC had associations with BP increment among people with chronic obstructive pulmonary disease.11
However, we also found negative associations between vanadium and DBP, in which vanadium can be generated from oil combustion.47, 48 Similarly, Jacobs et al found negative associations between DBP and vanadium,10 and Sorensen et al found that vanadium was associated with oxidative stress,49 which may have influenced BP.
Plausible Biological Mechanisms
We found consistent associations among PM2.5, PM1.0, PM0.5, PM0.2, and BP except for PN0.1. PM2.5 and PM1.0 were highly correlated in our study, which was consistent with a previous study showing that that PM1.0 is the major component of PM2.5 in China.50 Associations between PM2.5 and PN0.1 were inconsistent, and one possible biological mechanism for this result could be the weak correlation between PM2.5 and PN0.1 (r=0.18). Similarly, Rich et al found that ultrafine particles and PM2.5 were weakly correlated (r=0.11),51 and some studies have found that ultrafine particles and PM2.5 have a weak inverse correlation (r=−0.18).52 De Jesus et al found that particle number concentration and PM2.5 measurements show little correlation, and they are not representative of each other.53 That may be because particles sized smaller than 0.1 µm do not contribute very much to PM2.5 because the ultrafine particles mass is low compared with those of the larger fractions. Gong et al found that PM‐induced pathophysiological pathways affected by the fine and ultrafine size fraction of PM2.5 might be independently.52 Therefore, although some studies have found that PM‐related health effects may be greater with smaller‐sized PM,26 other studies have shown that fine and coarse particles, instead of ultrafine particles, might be responsible for the associations between PM and health.54, 55 The differences in health effects between size‐fractionated particles might reflect differences in clearance, deposition, and translocation after inhalation.24, 52
Possible mechanistic explanations for the observed association include autonomic nervous system imbalance, systemic inflammation and oxidative stress, and the increase in plasma endothelin‐1.10 Sympathovagal balance of cardiovascular regulation is regarded as the major determinant of BP variability.56 Inhaled particles stimulate the nerve endings and receptors in the airways, resulting in an imbalance of the autonomic nervous system57 and vasoconstriction.58, 59 This may help explain the rapid changes of BP in response to short‐term exposure to PM in our study. Second, systemic inflammation and oxidative stress induced by PM may enhance vasoconstriction and play a vital role in the cardiovascular diseases pathophysiologic process such as hypertension.60 Short‐term exposure to PM can lead to measurable systemic inflammation and oxidative stress in adults.61, 62 Third, short‐term PM exposure may be associated with acute endothelial response and artery vasoconstriction.63
Strengths and Limitations
Our study has several strengths. First, we recruited nonsmoking, healthy college students rather than a susceptible population, that is, our participants had good compliance, were free of any cardiovascular disease, and did not take antihypertensive medication. Compared with the elderly, young people are less likely to be chronically exposed to various environmental confounders that may have cumulative effects on health. Second, size‐fractionated PM with a wide range of smaller diameters (5 cumulative size fractions with upper limits from 0.1 to 2.5 μm) and various PM2.5 constituents were measured in a region where air pollution levels are much higher than those in developed countries, adding more evidence to the understanding of the relationship between PM size and constituents and BP.
There are also several limitations to our study. First, PM measurement data were obtained on the rooftop of the school building rather than personal exposure measurements; thus a potential exposure measurement error cannot be fully excluded in this study. However, the measurement site was at the same campus where participants were recruited and the campus only covers an area of ≈0.39 km2, so that the exposure misclassification may be quite low. Second, ambient gaseous pollutants and noise, both of which may contribute to the BP, were not monitored in this study, and their effect on BP should not be ignored. Third, the strong correlations among different particle‐size fractions meant that we were not able to identify the independent effects of the different‐sized PM. Fourth, we assessed the associations between 5 individual PMs with 6 different lag times and 4 BP outcomes, leading to a large number of statistical tests that might have inflated the amount of type I errors, leading to false‐positive results, or results by chance. However, we did not correct for multiple testing in order to maximize our ability to detect and confirm modest effects of PM exposures by future investigations. Fifth, because study participants are young and nonhypertensive, there are limits to applying this result to other populations such as older or hypertensive adults. Finally, other information, such as dietary intake and detailed daily activities, which may have an influence on BP, were unfortunately not collected in this study and therefore we were not able to account for them.
In summary, this study suggests that short‐term PM exposure is positively associated with SBP, DBP, and MAP in the first 24 hours following exposure and some PM2.5 constituents also seem to be related to BP in China. The observed PM–BP associations should not only focus on PM2.5, but also on smaller particles as well as PM2.5 constituents. It should be noted that the prevalence of hypertension in younger adults is steadily rising,64 and young adults with elevated BP may have an increased risk of cardiovascular events later in life.4 Our results could add evidence to the association of PM‐related BP in the young population, help us more deeply understand the physiological mechanisms of the development of hypertension, and also provide healthcare professionals with suggestions or treatments for people to take preventive measures, and ultimately to mitigate the effects of air pollution on hypertension. Further studies will help to clarify the role of particle size and chemical composition on BP.
Sources of Funding
This work was supported by the National Natural Science Foundation of China (81703179, 81950410633, 81972992, 81872582, 81872583), the Science and Technology Program of Guangzhou (201807010032, 201803010054), National Key Research and Development Program of China (2018YFC1004300, 2018YFE0106900), Guangdong Provincial Natural Science Foundation Team Project (2018B030312005), Fundamental Research Funds for the Central Universities (19ykjc01), and Natural Science Foundation of Guangdong Province (2020A1515011131, 2019A050510017, 2018B05052007, 2017A090905042).
We thank the principals, teachers, students, and participants in the Sun Yat‐Sen University for their cooperation.
Supplementary Material for this article is available at https://www.ahajournals.org/doi/suppl/10.1161/JAHA.120.019063
For Sources of Funding and Disclosures, see page 12.
- 1 Martinelli N, Olivieri O, Girelli D. Air particulate matter and cardiovascular disease: a narrative review. Eur J Intern Med. 2013; 24:295–302. DOI: 10.1016/j.ejim.2013.04.001.CrossrefMedlineGoogle Scholar
- 2 Brook RD, Rajagopalan S, Pope CA, Brook JR, Bhatnagar A, Diez‐Roux AV, Holguin F, Hong Y, Luepker RV, Mittleman MA, et al. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation. 2010; 121:2331–2378. DOI: 10.1161/CIR.0b013e3181dbece1.LinkGoogle Scholar
- 3 Chen R, Yin P, Meng X, Liu C, Wang L, Xu X, Ross JA, Tse LA, Zhao Z, Kan H, et al. Fine particulate air pollution and daily mortality: a nationwide analysis in 272 Chinese cities. Am J Respir Crit Care Med. 2017; 196:73–81. DOI: 10.1164/rccm.201609‐1862OC.CrossrefMedlineGoogle Scholar
- 4 Luo D, Cheng Y, Zhang H, Ba M, Chen P, Li H, Chen K, Sha W, Zhang C, Chen H. Association between high blood pressure and long term cardiovascular events in young adults: systematic review and meta‐analysis. BMJ. 2020; 370:m3222. DOI: 10.1136/bmj.m3222.CrossrefMedlineGoogle Scholar
- 5 Stanaway JD, Afshin A, Gakidou E, Lim SS; Collaborators GBDRF . 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. Lancet. 2018; 392:1923–1994. DOI: 10.1016/S0140‐6736(18)32225‐6.MedlineGoogle Scholar
- 6 Yang BY, Qian Z, Howard SW, Vaughn MG, Fan SJ, Liu KK, Dong GH. Global association between ambient air pollution and blood pressure: a systematic review and meta‐analysis. Environ Pollut. 2018; 235:576–588. DOI: 10.1016/j.envpol.2018.01.001.CrossrefMedlineGoogle Scholar
- 7 Magalhaes S, Baumgartner J, Weichenthal S. Impacts of exposure to black carbon, elemental carbon, and ultrafine particles from indoor and outdoor sources on blood pressure in adults: a review of epidemiological evidence. Environ Res. 2018; 161:345–353. DOI: 10.1016/j.envres.2017.11.030.CrossrefMedlineGoogle Scholar
- 8 Chang L, Chuang K, Yang W, Wang V, Chuang H, Bao B, Liu C, Chang T. Short‐term exposure to noise, fine particulate matter and nitrogen oxides on ambulatory blood pressure: a repeated‐measure study. Environ Res. 2015; 140:634–640. DOI: 10.1016/j.envres.2015.06.004.CrossrefMedlineGoogle Scholar
- 9 Hoffmann B, Luttmann‐Gibson H, Cohen A, Zanobetti A, de Souza C, Foley C, Suh HH, Coull BA, Schwartz J, Mittleman M, et al. Opposing effects of particle pollution, ozone, and ambient temperature on arterial blood pressure. Environ Health Perspect. 2012; 120:241–246. DOI: 10.1289/ehp.1103647.CrossrefMedlineGoogle Scholar
- 10 Jacobs L, Buczynska A, Walgraeve C, Delcloo A, Potgieter‐Vermaak S, Van Grieken R, Demeestere K, Dewulf JO, Van Langenhove H, De Backer H, et al. Acute changes in pulse pressure in relation to constituents of particulate air pollution in elderly persons. Environ Res. 2012; 117:60–67. DOI: 10.1016/j.envres.2012.05.003.CrossrefMedlineGoogle Scholar
- 11 Lin Z, Niu Y, Chen R, Xu W, Li H, Liu C, Cai J, Zhao Z, Kan H, Qiao L. Fine particulate matter constituents and blood pressure in patients with chronic obstructive pulmonary disease: a panel study in Shanghai, China. Environ Res. 2017; 159:291–296. DOI: 10.1016/j.envres.2017.08.024.CrossrefMedlineGoogle Scholar
- 12 Wu S, Deng F, Huang J, Wang H, Shima M, Wang X, Qin YU, Zheng C, Wei H, Hao YU, et al. Blood pressure changes and chemical constituents of particulate air pollution: results from the Healthy Volunteer Natural Relocation (HVNR) study. Environ Health Perspect. 2013; 121:66–72. DOI: 10.1289/ehp.1104812.CrossrefMedlineGoogle Scholar
- 13 Tan YQ, Rashid SKA, Pan W, Chen Y, Yu LE, Seow WJ. Association between microenvironment air quality and cardiovascular health outcomes. Sci Total Environ. 2020; 716:137027. DOI: 10.1016/j.scitotenv.2020.137027.CrossrefMedlineGoogle Scholar
- 14 Yang H, Teng C, Hu J, Zhu X, Wang Y, Wu J, Xiao Q, Yang W, Shen H, Liu F. Short‐term effects of ambient particulate matter on blood pressure among children and adolescents: a cross‐sectional study in a city of Yangtze River delta, China. Chemosphere. 2019; 237:124510. DOI: 10.1016/j.chemosphere.2019.124510.CrossrefMedlineGoogle Scholar
- 15 Ren M, Zhang H, Benmarhnia T, Jalaludin B, Dong H, Wu K, Wang Q, Huang C. Short‐term effects of real‐time personal PM2.5 exposure on ambulatory blood pressure: a panel study in young adults. Sci Total Environ2019; 697:134079. DOI: 10.1016/j.scitotenv.2019.134079.CrossrefMedlineGoogle Scholar
- 16 Mirowsky JE, Peltier RE, Lippmann M, Thurston G, Chen LC, Neas L, Diaz‐Sanchez D, Laumbach R, Carter JD, Gordon T. Repeated measures of inflammation, blood pressure, and heart rate variability associated with traffic exposures in healthy adults. Environ Health. 2015; 14:66. DOI: 10.1186/s12940‐015‐0049‐0.CrossrefMedlineGoogle Scholar
- 17 Ibald‐Mulli A, Timonen KL, Peters A, Heinrich J, Wölke G, Lanki T, Buzorius G, Kreyling WG, de Hartog J, Hoek G, et al. Effects of particulate air pollution on blood pressure and heart rate in subjects with cardiovascular disease: a multicenter approach. Environ Health Perspect. 2004; 112:369–377. DOI: 10.1289/ehp.6523.CrossrefMedlineGoogle Scholar
- 18 Smargiassi A, Goldberg MS, Wheeler AJ, Plante C, Valois M‐F, Mallach G, Kauri LM, Shutt R, Bartlett S, Raphoz M, et al. Associations between personal exposure to air pollutants and lung function tests and cardiovascular indices among children with asthma living near an industrial complex and petroleum refineries. Environ Res. 2014; 132:38–45. DOI: 10.1016/j.envres.2014.03.030.CrossrefMedlineGoogle Scholar
- 19 Hu L‐W, Qian Z, Bloom MS, Nelson EJ, Liu E, Han B, Zhang N, Liu Y, Ma H, Chen D‐H, et al. A panel study of airborne particulate matter concentration and impaired cardiopulmonary function in young adults by two different exposure measurement. Atmos Environ. 2018; 180:103–109. DOI: 10.1016/j.atmosenv.2018.03.001.CrossrefGoogle Scholar
- 20 Stanković A, Bogdanović D, Nikolić M, Anđelković AM. Does short‐term air pollution exposure have effects on blood pressure and heart rate in healthy women in the city of Niš, Serbia?Cent Eur J Public Health. 2018; 26:310–315. DOI: 10.21101/cejph.a5104.CrossrefMedlineGoogle Scholar
- 21 Xu W, Sun J, Liu Y, Xiao Y, Tian Y, Zhao B, Zhang X. Spatiotemporal variation and socioeconomic drivers of air pollution in China during 2005–2016. J Environ Manage. 2019; 245:66–75. DOI: 10.1016/j.jenvman.2019.05.041.CrossrefMedlineGoogle Scholar
- 22 Zhang J, Zhu T, Kipen H, Wang G, Huang W, Rich D, Zhu P, Wang Y, Lu S‐E, Ohman‐Strickland P, et al. Cardiorespiratory biomarker responses in healthy young adults to drastic air quality changes surrounding the 2008 Beijing Olympics. Res Rep Health Eff Inst. 2008; 2013:5–174.Google Scholar
- 23 Huang W, Wang LU, Li J, Liu M, Xu H, Liu S, Chen J, Zhang YI, Morishita M, Bard RL, et al. Short‐term blood pressure responses to ambient fine particulate matter exposures at the extremes of global air pollution concentrations. Am J Hypertens. 2018; 31:590–599. DOI: 10.1093/ajh/hpx216.CrossrefMedlineGoogle Scholar
- 24 Valavanidis A, Fiotakis K, Vlachogianni T. Airborne particulate matter and human health: toxicological assessment and importance of size and composition of particles for oxidative damage and carcinogenic mechanisms. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2008; 26:339–362. DOI: 10.1080/10590500802494538.CrossrefMedlineGoogle Scholar
- 25 Organization WH. WHO's global air‐quality guidelines. Lancet. 2006; 368:1302. DOI: 10.1016/S0140‐6736(06)69530‐5.CrossrefGoogle Scholar
- 26 Zhao A, Chen R, Wang C, Zhao Z, Yang C, Lu J, Chen X, Kan H. Associations between size‐fractionated particulate air pollution and blood pressure in a panel of type II diabetes mellitus patients. Environ Int. 2015; 80:19–25. DOI: 10.1016/j.envint.2015.03.003.CrossrefMedlineGoogle Scholar
- 27 Stieb DM, Shutt R, Kauri LM, Roth G, Szyszkowicz M, Dobbin NA, Chen LI, Rigden M, Van Ryswyk K, Kulka R, et al. Cardiorespiratory effects of air pollution in a panel study of winter outdoor physical activity in older adults. J Occup Environ Med. 2018; 60:673–682. DOI: 10.1097/JOM.0000000000001334.CrossrefMedlineGoogle Scholar
- 28 Santos UP, Ferreira Braga AL, Bueno Garcia ML, Amador Pereira LA, Lin CA, Chiarelli PS, Saldiva de André CD, Afonso de André P, Singer JM, Nascimento Saldiva PH. Exposure to fine particles increases blood pressure of hypertensive outdoor workers: a panel study. Environ Res. 2019; 174:88–94. DOI: 10.1016/j.envres.2019.04.021.CrossrefMedlineGoogle Scholar
- 29 Parati G, Stergiou GS, Asmar R, Bilo G, de Leeuw P, Imai Y, Kario K, Lurbe E, Manolis A, Mengden T, et al. European Society of Hypertension guidelines for blood pressure monitoring at home: a summary report of the Second International Consensus Conference on Home Blood Pressure Monitoring. J Hypertens. 2008; 26:1505–1526. DOI: 10.1097/HJH.0b013e328308da66.CrossrefMedlineGoogle Scholar
- 30 Alas HDC, Weinhold K, Costabile F, Di Ianni A, Müller T, Pfeifer S, Di Liberto L, Turner JR, Wiedensohler A. Methodology for high‐quality mobile measurement with focus on black carbon and particle mass concentrations. Atmos Meas Tech. 2019; 12:4697–4712. DOI: 10.5194/amt‐12‐4697‐2019.CrossrefGoogle Scholar
- 31 Sinharay R, Gong J, Barratt B, Ohman‐Strickland P, Ernst S, Kelly FJ, Zhang JJ, Collins P, Cullinan P, Chung KF. Respiratory and cardiovascular responses to walking down a traffic‐polluted road compared with walking in a traffic‐free area in participants aged 60 years and older with chronic lung or heart disease and age‐matched healthy controls: a randomised, crossover study. Lancet. 2018; 391:339–349. DOI: 10.1016/S0140‐6736(17)32643‐0.MedlineGoogle Scholar
- 32 Zhang Q, Niu Y, Xia Y, Lei X, Wang W, Huo J, Zhao Q, Zhang Y, Duan Y, Cai J, et al. The acute effects of fine particulate matter constituents on circulating inflammatory biomarkers in healthy adults. Sci Total Environ. 2019; 707:135989. DOI: 10.1016/j.scitotenv.2019.135989.CrossrefMedlineGoogle Scholar
- 33 Zhang Q, Wang W, Niu Y, Xia Y, Lei X, Huo J, Zhao Q, Zhang Y, Duan Y, Cai J, et al. The effects of fine particulate matter constituents on exhaled nitric oxide and DNA methylation in the arginase‐nitric oxide synthase pathway. Environ Int. 2019; 131:105019. DOI: 10.1016/j.envint.2019.105019.CrossrefMedlineGoogle Scholar
- 34 Chen R, Qiao L, Li H, Zhao Y, Zhang Y, Xu W, Wang C, Wang H, Zhao Z, Xu X, et al. Fine particulate matter constituents, nitric oxide synthase DNA methylation and exhaled nitric oxide. Environ Sci Technol. 2015; 49:11859–11865. DOI: 10.1021/acs.est.5b02527.CrossrefMedlineGoogle Scholar
- 35 Cavallari JM, Eisen EA, Fang SC, Schwartz J, Hauser R, Herrick RF, Christiani DC. PM2.5 metal exposures and nocturnal heart rate variability: a panel study of boilermaker construction workers. Environ Health. 2008; 7:36. DOI: 10.1186/1476‐069X‐7‐36.CrossrefMedlineGoogle Scholar
- 36 Dong W, Pan L, Li H, Miller MR, Loh M, Wu S, Xu J, Yang X, Shan J, Chen Y, et al. Association of size‐fractionated indoor particulate matter and black carbon with heart rate variability in healthy elderly women in Beijing. Indoor Air. 2018; 28:373–382. DOI: 10.1111/ina.12449.CrossrefMedlineGoogle Scholar
- 37 Xu WX, Chen RJ, Kan HD. The impact of ambient fine particulate matter on the blood pressure of an urban population in Shanghai, China: a panel study. Zhonghua Yu Fang Yi Xue Za Zhi. 2016; 50:716–720.MedlineGoogle Scholar
- 38 Wang C, Chen R, Cai J, Shi J, Yang C, Tse LA, Li H, Lin Z, Meng X, Liu C, et al. Personal exposure to fine particulate matter and blood pressure: a role of angiotensin converting enzyme and its DNA methylation. Environ Int. 2016; 94:661–666. DOI: 10.1016/j.envint.2016.07.001.CrossrefMedlineGoogle Scholar
- 39 Scheers H, Nawrot TS, Nemery B, Casas L. Changing places to study short‐term effects of air pollution on cardiovascular health: a panel study. Environ Health. 2018; 17:80. DOI: 10.1186/s12940‐018‐0425‐7.CrossrefMedlineGoogle Scholar
- 40 Auchincloss AH, Diez Roux AV, Dvonch JT, Brown PL, Barr RG, Daviglus ML, Goff DC, Kaufman JD, O'Neill MS. Associations between recent exposure to ambient fine particulate matter and blood pressure in the Multi‐ethnic Study of Atherosclerosis (MESA). Environ Health Perspect. 2008; 116:486–491. DOI: 10.1289/ehp.10899.CrossrefMedlineGoogle Scholar
- 41 Sesso HD, Stampfer MJ, Rosner B, Hennekens CH, Gaziano JM, Manson JE, Glynn RJ. Systolic and diastolic blood pressure, pulse pressure, and mean arterial pressure as predictors of cardiovascular disease risk in men. Hypertension. 2000; 36:801–807. DOI: 10.1161/01.HYP.36.5.801.CrossrefMedlineGoogle Scholar
- 42 Xie X, Lv D, Zheng H, Zhang X, Han F, Chen J. The associations of blood pressure parameters with all‐cause and cardiovascular mortality in peritoneal dialysis patients: a cohort study in China. J Hypertens. 2020; 38:2252–2260. DOI: 10.1097/HJH.0000000000002526.CrossrefMedlineGoogle Scholar
- 43 Delfino RJ, Tjoa T, Gillen DL, Staimer N, Polidori A, Arhami M, Jamner L, Sioutas C, Longhurst J. Traffic‐related air pollution and blood pressure in elderly subjects with coronary artery disease. Epidemiology. 2010; 21:396–404. DOI: 10.1097/EDE.0b013e3181d5e19b.CrossrefMedlineGoogle Scholar
- 44 Sun Y, Zhuang G, Wang Y, Han L, Guo J, Dan M, Zhang W, Wang Z, Hao Z. The air‐borne particulate pollution in Beijing—concentration, composition, distribution and sources. Atmos Environ. 2004; 38:5991–6004. DOI: 10.1016/j.atmosenv.2004.07.009.CrossrefGoogle Scholar
- 45 Ziomber A, Machnik A, Dahlmann A, Dietsch P, Beck FX, Wagner H, Hilgers KF, Luft FC, Eckardt KU, Titze J. Sodium‐, potassium‐, chloride‐, and bicarbonate‐related effects on blood pressure and electrolyte homeostasis in deoxycorticosterone acetate‐treated rats. Am J Physiol Renal Physiol. 2008; 295:F1752–F1763. DOI: 10.1152/ajprenal.00531.2007.CrossrefMedlineGoogle Scholar
- 46 Lin H, Tao J, Du Y, Liu T, Qian Z, Tian L, Di Q, Rutherford S, Guo L, Zeng W, et al. Particle size and chemical constituents of ambient particulate pollution associated with cardiovascular mortality in Guangzhou, China. Environ Pollut. 2016; 208:758–766. DOI: 10.1016/j.envpol.2015.10.056.CrossrefMedlineGoogle Scholar
- 47 Buzcu‐Guven B, Brown SG, Frankel A, Hafner HR, Roberts PT. Analysis and apportionment of organic carbon and fine particulate matter sources at multiple sites in the midwestern United States. J Air Waste Manag Assoc. 2007; 57:606–619. DOI: 10.3155/1047‐3222.214.171.1246.CrossrefMedlineGoogle Scholar
- 48 Thomaidis NS, Bakeas EB, Siskos PA. Characterization of lead, cadmium, arsenic and nickel in PM2.5 particles in the Athens atmosphere, Greece. Chemosphere. 2003; 52:959–966. DOI: 10.1016/S0045‐6535(03)00295‐9.CrossrefMedlineGoogle Scholar
- 49 Sorensen M, Schins RP, Hertel O, Loft S. Transition metals in personal samples of PM2.5 and oxidative stress in human volunteers. Cancer Epidemiol Biomarkers Prev. 2005; 14:1340–1343. DOI: 10.1158/1055‐9965.EPI‐04‐0899.CrossrefMedlineGoogle Scholar
- 50 Yang B‐Y, Guo Y, Bloom MS, Xiao X, Qian Z, Liu E, Howard SW, Zhao T, Wang S‐Q, Li S, et al. Ambient PM1 air pollution, blood pressure, and hypertension: insights from the 33 Communities Chinese Health Study. Environ Res. 2019; 170:252–259. DOI: 10.1016/j.envres.2018.12.047.CrossrefMedlineGoogle Scholar
- 51 Rich DQ, Zareba W, Beckett W, Hopke PK, Oakes D, Frampton MW, Bisognano J, Chalupa D, Bausch J, O’Shea K, et al. Are ambient ultrafine, accumulation mode, and fine particles associated with adverse cardiac responses in patients undergoing cardiac rehabilitation?Environ Health Perspect. 2012; 120:1162–1169. DOI: 10.1289/ehp.1104262.CrossrefMedlineGoogle Scholar
- 52 Gong J, Zhu T, Kipen H, Wang G, Hu M, Guo Q, Ohman‐Strickland P, Lu S‐E, Wang Y, Zhu P, et al. Comparisons of ultrafine and fine particles in their associations with biomarkers reflecting physiological pathways. Environ Sci Technol. 2014; 48:5264–5273. DOI: 10.1021/es5006016.CrossrefMedlineGoogle Scholar
- 53 de Jesus AL, Rahman MM, Mazaheri M, Thompson H, Knibbs LD, Jeong C, Evans G, Nei W, Ding A, Qiao L, et al. Ultrafine particles and PM(2.5) in the air of cities around the world: are they representative of each other?Environ Int. 2019; 129:118–135.CrossrefMedlineGoogle Scholar
- 54 Iskandar A, Andersen ZJ, Bønnelykke K, Ellermann T, Andersen KK, Bisgaard H. Coarse and fine particles but not ultrafine particles in urban air trigger hospital admission for asthma in children. Thorax. 2012; 67:252. DOI: 10.1136/thoraxjnl‐2011‐200324.CrossrefMedlineGoogle Scholar
- 55 Chang LT, Tang CS, Pan YZ, Chan CC. Association of heart rate variability of the elderly with personal exposure to PM 1, PM 1‐2.5, and PM 2.5‐10. Bull Environ Contam Toxicol. 2007; 79:552–556. DOI: 10.1007/s00128‐007‐9233‐4.CrossrefMedlineGoogle Scholar
- 56 Laitinen T, Hartikainen J, Niskanen L, Geelen G, Länsimies E. Sympathovagal balance is major determinant of short‐term blood pressure variability in healthy subjects. Am J Physiol Heart Circ Physiol. 1999; 276:H1245–H1252. DOI: 10.1152/ajpheart.1999.276.4.H1245.CrossrefMedlineGoogle Scholar
- 57 Widdicombe J, Lee LY. Airway reflexes, autonomic function, and cardiovascular responses. Environ Health Perspect. 2001; 109:579–584.CrossrefMedlineGoogle Scholar
- 58 Tsimikas S, Mallat Z, Talmud PJ, Kastelein JJP, Wareham NJ, Sandhu MS, Miller ER, Benessiano J, Tedgui A, Witztum JL, et al. Oxidation‐specific biomarkers, lipoprotein(a), and risk of fatal and nonfatal coronary events. J Am Coll Cardiol. 2010; 56:946–955. DOI: 10.1016/j.jacc.2010.04.048.CrossrefMedlineGoogle Scholar
- 59 Brook RD, Rajagopalan S. Particulate matter, air pollution, and blood pressure. J Am Soc Hypertens. 2009; 3:332–350. DOI: 10.1016/j.jash.2009.08.005.CrossrefMedlineGoogle Scholar
- 60 Lassègue B, Griendling KK. Reactive oxygen species in hypertension: an update. Am J Hypertens. 2004; 17:852–860.CrossrefMedlineGoogle Scholar
- 61 Zhang Y, Chu M, Zhang J, Duan J, Hu D, Zhang W, Yang X, Jia X, Deng F, Sun Z. Urine metabolites associated with cardiovascular effects from exposure of size‐fractioned particulate matter in a subway environment: a randomized crossover study. Environ Int. 2019; 130:104920. DOI: 10.1016/j.envint.2019.104920.CrossrefMedlineGoogle Scholar
- 62 Tsai D‐H, Riediker M, Berchet A, Paccaud F, Waeber G, Vollenweider P, Bochud M. Effects of short‐ and long‐term exposures to particulate matter on inflammatory marker levels in the general population. Environ Sci Pollut Res Int. 2019; 26:19697–19704. DOI: 10.1007/s11356‐019‐05194‐y.CrossrefMedlineGoogle Scholar
- 63 Peretz A, Sullivan Jeffrey H, Leotta Daniel F, Trenga Carol A, Sands Fiona N, Allen J, Carlsten C, Wilkinson Charles W, Gill Edward A, Kaufman JD. Diesel exhaust inhalation elicits acute vasoconstriction in vivo. Environ Health Perspect. 2008; 116:937–942.CrossrefMedlineGoogle Scholar
- 64 De Venecia T, Lu M, Figueredo VM. Hypertension in young adults. Postgrad Med. 2016; 128:201–207. DOI: 10.1080/00325481.2016.1147927.CrossrefMedlineGoogle Scholar