Furong Deng

Association of heart rate variability in taxi drivers with marked changes in particulate air pollution in Beijing in 2008.

Background Heart rate variability (HRV), a marker of cardiac autonomic function, has been associated with particulate matter (PM) air pollution, especially in older patients and those with cardiovascular diseases. However, the effect of PM exposure on cardiac autonomic function in young, healthy adults has received less attention. Objectives We evaluated the relationship between exposure to traffic-related PM with an aerodynamic diameter ≤ 2.5 μm (PM2.5) and HRV in a highly exposed panel of taxi drivers. Methods Continuous measurements of personal exposure to PM2.5 and ambulatory electrocardiogram monitoring were conducted on 11 young healthy taxi drivers for a 12-hr work shift during their work time (0900–2100 hr) before, during, and after the Beijing 2008 Olympic Games. Mixed-effects regression models were used to estimate associations between PM2.5 exposure and percent changes in 5-min HRV indices after combining data from the three time periods and controlling for potentially confounding variables. Results Personal exposures of taxi drivers to PM2.5 changed markedly across the three time periods. The standard deviation of normal-to-normal (SDNN) intervals decreased by 2.2% [95% confidence interval (CI), −3.8% to −0.6%] with an interquartile range (IQR; 69.5 μg/m3) increase in the 30-min PM2.5 moving average, whereas the low-frequency and high-frequency powers decreased by 4.2% (95% CI, −9.0% to 0.8%) and 6.2% (95% CI, −10.7% to −1.5%), respectively, in association with an IQR increase in the 2-hr PM2.5 moving average. Conclusions Marked changes in traffic-related PM2.5 exposure were associated with altered cardiac autonomic function in young healthy adults.

Association of cardiopulmonary health effects with source-appointed ambient fine particulate in Beijing, China: a combined analysis from the Healthy Volunteer Natural Relocation (HVNR) study.

Previous studies have associated ambient particulate chemical constituents with adverse cardiopulmonary health effects. However, specific pollution sources behind the cardiopulmonary health effects of ambient particles are uncertain. We examined the cardiopulmonary health effects of fine particles (PM2.5) from different pollution sources in Beijing, China, among a panel of 40 healthy university students. Study subjects were repeatedly examined for a series of cardiopulmonary health indicators during three 2-month-long study periods (suburban period, urban period 1, and urban period 2) in 2010-2011 before and after relocating from a suburban campus to an urban campus with changing air pollution levels and contents. Daily ambient PM2.5 mass samples were collected over the study and measured for 29 chemical constituents in the laboratory. Source appointment for ambient PM2.5 was performed using Positive Matrix Factorization, and mixed-effects models were used to estimate the cardiopulmonary effects associated with source-specific PM2.5 concentrations. Seven PM2.5 sources were identified as traffic emissions (12.0%), coal combustion (22.0%), secondary sulfate/nitrate (30.2%), metallurgical emission (0.4%), dust/soil (12.4%), industry (6.9%), and secondary organic aerosol (9.9%). Ambient PM2.5 in the suburban campus had larger contributions from secondary sulfate/nitrate (41.8% vs. 22.9%-26.0%) and metallurgical emission (0.7% vs. 0.3%) as compared to that in the urban campus), whereas PM2.5 in the urban campus had larger contributions from traffic emissions (13.0%-16.3% vs. 5.1%), coal combustion (21.0%-30.7% vs. 10.7%), and secondary organic aerosol (9.7%-12.0% vs. 8.7%) as compared to that in the suburban campus. Potential key sources were identified for PM2.5 effects on inflammatory biomarkers (secondary sulfate/nitrate and dust/soil), blood pressure (coal combustion and metallurgical emission), and pulmonary function (dust/soil and industry). Analyses using another source appointment tool Unmix yielded a similar pattern of source contributions and associated health effects. In conclusion, ambient PM2.5 in Beijing suburban and urban areas has two distinct patterns of source contributions, and PM2.5 from different sources may play important roles on different aspects of PM2.5-related cardiopulmonary health effects.

Blood Pressure Changes and Chemical Constituents of Particulate Air Pollution: Results from the Healthy Volunteer Natural Relocation (HVNR) Study

Background: Elevated blood pressure (BP) has been associated with particulate matter (PM) air pollution, but associations with PM chemical constituents are still uncertain. Objectives: We investigated associations of BP with various chemical constituents of fine PM (PM2.5) during 460 repeated visits among a panel of 39 university students. Methods: Resting BP was measured using standardized methods before and after the university students relocated from a suburban campus to an urban campus with different air pollution contents in Beijing, China. Air pollution data were obtained from central monitors close to student residences. We used mixed-effects models to estimate associations of various PM2.5 constituents with systolic BP (SBP), diastolic BP (DBP), and pulse pressure. Results: An interquartile range increase of 51.2 μg/m3 in PM2.5 was associated with a 1.08-mmHg (95% CI: 0.17, 1.99) increase in SBP and a 0.96-mmHg (95% CI: 0.31, 1.61) increase in DBP on the following day. A subset of PM2.5 constituents, including carbonaceous fractions (organic carbon and elemental carbon), ions (chloride and fluoride), and metals/metalloid elements (nickel, zinc, magnesium, lead, and arsenic), were found to have robust positive associations with different BP variables, though robust negative associations of manganese, chromium, and molybdenum with SBP or DBP also were observed. Conclusions: Our results support relationships between specific PM2.5 constituents and BP. These findings have potential implications for the development of pollution abatement strategies that maximize public health benefits.

Chemical constituents of ambient particulate air pollution and biomarkers of inflammation, coagulation and homocysteine in healthy adults: A prospective panel study

BackgroundAmbient air pollution has been associated with activation of systemic inflammation and hypercoagulability and increased plasma homocysteine, but the chemical constituents behind the association are not well understood. We examined the relations of various chemical constituents of fine particles (PM2.5) and biomarkers of inflammation, coagulation and homocysteine in the context of traffic-related air pollution.MethodsA panel of 40 healthy college students underwent biweekly blood collection for 12 times before and after their relocation from a suburban campus to an urban campus with changing air pollution contents in Beijing. Blood samples were measured for circulatory biomarkers of high-sensitivity C reactive protein (hs-CRP), tumor necrosis factor alpha (TNF-α), fibrinogen, plasminogen activator inhibitor type 1 (PAI-1), tissue-type plasminogen activator (t-PA), von Willebrand factor (vWF), soluble platelet selectin (sP-selectin), and total homocysteine (tHcy). Various air pollutants were measured in a central air-monitoring station in each campus and 32 PM2.5 chemical constituents were determined in the laboratory. We used three different mixed-effects models (single-constituent model, constituent-PM2.5 joint model and constituent residual model) controlling for potential confounders to estimate the effects of PM2.5 chemical constituents on circulatory biomarkers.ResultsWe found consistent positive associations between the following biomarkers and PM2.5 chemical constituents across different models: TNF-α with secondary organic carbon, chloride, zinc, molybdenum and stannum; fibrinogen with magnesium, iron, titanium, cobalt and cadmium; PAI-1 with titanium, cobalt and manganese; t-PA with cadmium and selenium; vWF with aluminum. We also found consistent inverse associations of vWF with nitrate, chloride and sodium, and sP-selectin with manganese. Two positive associations of zinc with TNF-α and of cobalt with fibrinogen, and two inverse associations of nitrate with vWF, and of manganese with sP-selectin, were independent of the other constituents in two-constituent models using constituent residual data. We only found weak air pollution effects on hs-CRP and tHcy.ConclusionsOur results provide clues for the potential roles that PM2.5 chemical constituents may play in the biological mechanisms through which air pollution may influence the cardiovascular system.

The impacts of short-term exposure to noise and traffic-related air pollution on heart rate variability in young healthy adults.

Traffic-related air pollution and noise are associated with cardiovascular diseases, and alternation of heart rate variability (HRV), which reflects cardiac autonomic function, is one of the mechanisms. However, few studies considered the impacts of noise when exploring associations between air pollution and HRV. We explored whether noise modifies associations between short-term exposure to traffic-related air pollution and HRV in young healthy adults. In this randomized, crossover study, 40 young healthy adults stayed for 2 h in a traffic center and, on a separate occasion, in a park. Personal exposure to traffic-related air pollutants and noise were measured and ambulatory electrocardiogram was performed. Effects were estimated using mixed-effects regression models. Traffic-related air pollution and noise were both associated with HRV, and effects of air pollutants were amplified at high noise level (>65.6 A-weighted decibels (dB[A])) compared with low noise level (≤65.6 dB[A]). High frequency (HF) decreased by −4.61% (95% confidence interval, −6.75% to−2.42%) per 10 μg/m3 increment in fine particle (PM2.5) at 5-min moving average, but effects became insignificant at low noise level (P>0.05). Similar effects modification was observed for black carbon (BC) and carbon monoxide (CO). We conclude that noise is an important factor influencing the effects of air pollution on HRV.

Fine particulate matter, temperature, and lung function in healthy adults: Findings from the HVNR study

Both ambient particulate air pollution and temperature alterations have been associated with adverse human health effects, but the interactive effect of ambient particulate and temperature on human health remains uncertain. The present study investigated the effects of ambient particulate matter with an aerodynamic diameter⩽2.5 μm (PM2.5) and temperature on human lung function simultaneously in a panel of 21 healthy university students from the Healthy Volunteer Natural Relocation (HVNR) study in the context of suburban/urban air pollution in Beijing, China. Each study subject used an electronic diary meter to record peak expiratory flow (PEF) and forced expiratory volume in 1s (FEV1) twice a day for 6 months in three periods before and after relocating from a suburban area to an urban area with changing ambient PM2.5 and temperature levels in Beijing. Hourly-averaged environmental data were obtained from central air-monitoring sites. Exposure effects were estimated using generalized linear mixed models controlling for potential confounders. Study subjects provided 6494 daily measurements on PEF and 6460 daily measurements on FEV1 over the study. PM2.5 was associated with reductions in evening PEF and morning/evening FEV1 whereas temperature was associated with reductions in morning PEF. The estimated PM2.5 effects on evening PEF and morning/evening FEV1 in the presence of high temperature were generally stronger than those in the presence of low temperature, and the estimated temperature effects on morning/evening PEF and morning FEV1 in the presence of high PM2.5 were also generally stronger than those in the presence of low PM2.5. For example, there were a 2.47% (95% confidence interval: -4.24, -0.69) reduction and a 0.78% (95% confidence interval: -1.59, 0.03) reduction in evening PEF associated with an interquartile range increase (78.7 μg/m(3)) in PM2.5 at 4-d moving average in the presence of high temperature (⩾21.6 °C) and low temperature (<21.6 °C), respectively. Our findings suggest that ambient particulate and temperature may interact synergistically to cause adverse respiratory health effects.

Chemical constituents of fine particulate air pollution and pulmonary function in healthy adults: the Healthy Volunteer Natural Relocation study.

The study examined the associations of 32 chemical constituents of particulate matter with an aerodynamic diameter ≤2.5 μm (PM₂.₅) with pulmonary function in a panel of 21 college students. Study subjects relocated from a suburban area to an urban area with changing ambient air pollution levels and contents in Beijing, China, and provided daily morning/evening peak expiratory flow (PEF) and forced expiratory volume in 1s (FEV₂₁) measurements over 6 months in three study periods. There were significant reductions in evening PEF and morning/evening FEV₂₁ associated with various air pollutants and PM₂.₅ constituents. Four PM₂.₅ constituents (copper, cadmium, arsenic and stannum) were found to be most consistently associated with the reductions in these pulmonary function measures. These findings provide clues for the respiratory effects of specific particulate chemical constituents in the context of urban air pollution.

Short-term exposure to high ambient air pollution increases airway inflammation and respiratory symptoms in chronic obstructive pulmonary disease patients in Beijing, China

BACKGROUND Few studies have investigated the short-term respiratory effects of ambient air pollution in chronic obstructive pulmonary disease (COPD) patients in the context of high pollution levels in Asian cities. METHODS A panel of 23 stable COPD patients was repeatedly measured for biomarkers of airway inflammation including exhaled nitric oxide (FeNO) and exhaled hydrogen sulfide (FeH2S) (215 measurements) and recorded for daily respiratory symptoms (794person-days) in two study periods in Beijing, China in January-September 2014. Daily ambient air pollution data were obtained from nearby central air-monitoring stations. Mixed-effects models were used to estimate the associations between exposures and health measurements with adjustment for potential confounders including temperature and relative humidity. RESULTS Increasing levels of air pollutants were associated with significant increases in both FeNO and FeH2S. Interquartile range (IQR) increases in PM2.5 (76.5μg/m(3), 5-day), PM10 (75.0μg/m(3), 5-day) and SO2 (45.7μg/m(3), 6-day) were associated with maximum increases in FeNO of 13.6% (95% CI: 4.8%, 23.2%), 9.2% (95% CI: 2.1%, 16.8%) and 34.2% (95% CI: 17.3%, 53.4%), respectively; and the same IQR increases in PM2.5 (6-day), PM10 (6-day) and SO2 (7-day) were associated with maximum increases in FeH2S of 11.4% (95% CI: 4.6%, 18.6%), 7.8% (95% CI: 2.3%, 13.7%) and 18.1% (95% CI: 5.5%, 32.2%), respectively. Increasing levels of air pollutants were also associated with increased odds ratios of sore throat, cough, sputum, wheeze and dyspnea. CONCLUSIONS FeH2S may serve as a novel biomarker to detect adverse respiratory effects of air pollution. Our results provide potential important public health implications that ambient air pollution may pose risk to respiratory health in the context of high pollution levels in densely-populated cities in the developing world.

The relationship between traffic-related air pollutants and cardiac autonomic function in a panel of healthy adults: a further analysis with existing data.

Context: Epidemiological studies have linked particulate matter (PM) and carbon monoxide (CO) exposures with alterations in cardiac autonomic function as measured by heart rate variability (HRV) in populations. Recently, we reported association of several HRV indices with marked changes in particulate air pollution around the Beijing 2008 Olympic Games in a panel of healthy adults. Objective: We further investigated the cardiac effects of traffic-related air pollutants over wide exposure ranges with expanded data set in this panel of healthy adults. Methods: We obtained real-time data on nine taxi drivers’ in-car exposures to PM ≤2.5 µm in aerodynamic diameter (PM2.5) and CO and on multiple HRV indices during a separate daily work shift in four study periods with dramatically changing air pollution levels around the Beijing 2008 Olympic Games. Mixed effect models and a loess smoother method were used to investigate the associations of exposures with HRV indices. Results: Results showed overall negative associations of traffic-related air pollutants with HRV indices across periods, as well as differences in period-specific and individual associations. After stratifying the individuals into two different response groups (positive/negative), cardiac effects of air pollutants became stronger within each group. Exposure–response modeling identified changed curvilinear relationships between air pollution exposures and HRV indices with threshold effects. Discussion and conclusion: Our results support the association of exposure to traffic-related air pollution with altered cardiac autonomic function in young healthy adults free of cardiovascular compromises. These results suggest a complicated mechanism that traffic-related air pollutants influence the cardiovascular system of healthy adults.

Acute effect of ambient ozone on heart rate variability in healthy elderly subjects

Acute ambient ozone (O3) exposure is associated with the increased mortality and morbidity of cardiovascular diseases. The dysfunction of cardiac autonomic nervous system (ANS), indicated by the disturbed heart rate variability (HRV), may be the most important underlying mechanism. Previous studies reported the heterogeneous associations between O3 within several hours’ exposure and HRV on general elderly subjects, in which poor surrogate of exposure evaluation and different health status of the subjects may be responsible for the heterogeneous associations. No studies were found focusing on the O3-mediated HRV effects within several minutes’ exposure on healthy older subjects until recently. We measured the real-time 5-min ambient O3 concentration and HRV frequency indices in 20 healthy elderly subjects in two surveys, with the 1st and 2nd survey in summer and winter, respectively. Mixed-linear model was used to evaluate the associations between the ambient 5-min average O3 and concurrent 5-min HRV frequency indices measured during the outdoor period. After adjusting the co-pollutants (ambient PM2.5 and nitrogen oxides concentrations) and subject characteristics, high frequency (HF) changed –4.87% (95% CI –8.62 to –0.97%) per 10 ppb increment of O3, whereas decreased low frequency (LF) and increased LFHFR were found to be marginally associated with the elevated O3 (P values were 0.092 and 0.069). We concluded that the ambient O3 exert transient decrease effects on HRV, which may induce acute cardiac events.