Hongying Wei

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.

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.

Ultrafine carbon black induces glutamate and ATP release by activating connexin and pannexin hemichannels in cultured astrocytes.

Ultrafine particles could enter central nervous system and were associated with brain damage. The underlying mechanisms have not been fully elucidated. Glutamate and ATP are important signaling molecules in brain physiology and pathology. We investigated whether ultrafine carbon black (ufCB) could regulate the release of glutamate and ATP from cultured cortical astrocytes and the involvement of hemichannels in the release mechanism. Our results showed that ufCB dose-dependently increased glutamate and ATP release and activated hemichannels in astrocytes. ufCB-activated hemichannels were attributed to the activation of both connexin 43 (Cx43) and pannexin1 (Panx1) hemichannels, which was based on the finding of increased protein expression and distribution on cell surface of Cx43 and Panx1, and the inhibiting effects of hemichannel inhibitor carbenoxolone, Cx43 hemichannel inhibitor (43)Gap27 and Panx1 hemichannel inhibitor (10)Panx1 on hemichannel activation. Furthermore, ufCB-induced glutamate and ATP release were dependent on Cx43 and Panx1 hemichannels, because carbenoxolone and (43)Gap27 inhibited ufCB-induced glutamate and ATP release, and (10)Panx1 inhibited ufCB-induced ATP release. Taken together, we demonstrated, for the first time, that ufCB could induce glutamate and ATP release by activating Cx43 and Panx1 hemchannels in astrocytes. Our findings suggest a novel mechanism for neurotoxicity caused by ultrafine particles.

Association of chemical constituents and pollution sources of ambient fine particulate air pollution and biomarkers of oxidative stress associated with atherosclerosis: A panel study among young adults in Beijing, China

Ambient particulate air pollution has been associated with increased oxidative stress and atherosclerosis, but the chemical constituents and pollution sources behind the association are unclear. We investigated the associations of various chemical constituents and pollution sources of ambient fine particles (PM2.5) with biomarkers of oxidative stress in a panel of 40 healthy university students. Study participants underwent repeated blood collections for 12 times before and after relocating from a suburban campus to an urban campus with high air pollution levels in Beijing, China. Air pollution data were obtained from central air-monitoring stations, and plasma levels of oxidized low-density lipoprotein (Ox-LDL) and soluble CD36 (sCD36) were determined in the laboratory (n=464). Linear mixed-effects models were used to estimate the changes in biomarkers in association with exposure variables. PM2.5 iron and nickel were positively associated with Ox-LDL (p<0.05). For each interquartile range increase in iron (1-day, 0.51 μg/m(3)) and nickel (2-day, 2.5 ng/m(3)), there were a 1.9% [95% confidence interval (CI): 0.2%, 3.7%] increase and a 1.8% (95% CI: 0.2%, 3.4%) increase in Ox-LDL, respectively. We also found that each interquartile range increase in calcium (1-day, 0.7 μg/m(3)) was associated with a 4.8% (95% CI: 0.7%, 9.1%) increase in sCD36. Among the pollution sources, PM2.5 from traffic emissions and coal combustion were suggestively and positively associated with Ox-LDL. Our findings suggest that a subset of metals in airborne particles may be the major air pollution components that contribute to the increased oxidative stress associated with atherosclerosis.

Chemical constituents and sources of ambient particulate air pollution and biomarkers of endothelial function in a panel of healthy adults in Beijing, China

BACKGROUND Exposure to ambient air pollution has been associated with endothelial dysfunction as reflected by short-term alterations in circulating biomarkers, but the chemical constituents and pollution sources behind the association has been unclear. METHODS We investigated the associations between various ambient air pollutants including gases and 31 chemical constituents and seven sources of fine particles (PM2.5) and biomarkers of endothelial function, including endothelin-1 (ET-1), E-selectin, soluble intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), based on 462 repeated measurements in a panel of 40 college students who were followed for three study periods before and after relocating from a suburban area to an urban area in Beijing, China in 2010-2011. Air pollution data were obtained from central air-monitoring stations. Linear mixed-effects models were used to estimate the changes in biomarkers associated with exposures. RESULTS Total PM2.5 mass showed few appreciable associations with examined biomarkers. However, several PM2.5 constituents and related sources showed significant associations with examined biomarkers. PM2.5 from dust/soil and several crustal and transition metals, including strontium, iron, titanium, cobalt and magnesium, were significantly associated with increases in ET-1 at 1-day average; manganese and potassium were significantly associated with increases in ICAM-1 at 2-day average; and PM2.5 from industry and metal cadmium were significantly associated with decreases in VCAM-1 at 1-day average. In addition, carbon monoxide was significantly associated with increasing ICAM-1 at 1-day and 2-day averages, whereas nitric oxide was significantly associated with decreasing ICAM-1 at 1-day and 3-day averages. CONCLUSIONS Our results suggest that certain PM2.5 metal constituents were more closely associated with circulating biomarkers of endothelial function than PM2.5, and therefore highlight the research necessity to examine pollution chemical constituents in future studies.

Does ambient temperature interact with air pollution to alter blood pressure? A repeated-measure study in healthy adults.

Objectives: Both low temperature and high air pollution have been associated with an increased risk of cardiovascular events, which could be predicted by increased arterial blood pressure (BP) within short periods. However, whether exposures to temperature and air pollution simultaneously may have interactive effects on BP has been unknown. We investigated this potential interaction during 460 repeated visits in 39 healthy university students in the context of traffic-related air pollution. Methods: Study participants in the Healthy Volunteer Natural Relocation study underwent repeated BP measurements for 12 occasions under three exposure scenarios in Beijing, China, in 2010–2011. We used generalized linear mixed-effects models to estimate exposure effects. Results: Decreasing temperature was associated with significant increases in BP. There were significant interactions between temperature and traffic-related air pollutants (particulate matter with an aerodynamic diameter ⩽2.5 &mgr;m, organic carbon, elemental carbon and nitrogen dioxide) on BP (P < 0.05 for all interaction tests). The estimated increases in SBP and DBP were 4.9 mmHg [95% confidence interval (CI) 2.9–6.8] and 3.7 mmHg (95% CI 2.3–5.1) at high elemental carbon level (≥median), and were −1.3 mmHg (95% CI −6.3 to 3.6) and 0.7 mmHg (95% CI −2.8 to 4.2) at low elemental carbon level (<median) per 10°C decrease in daily minimum temperature. We also found stronger air pollution effects on BP at low temperature levels (<median) than at high temperature levels (≥median). Conclusion: Low temperature and high air pollution may act synergistically to increase BP in healthy adults. Our findings may have potential implications for prevention of cardiovascular events associated with increased BP among high-risk individuals.

Silver nanoparticles increase connexin43-mediated gap junctional intercellular communication in HaCaT cells through activation of reactive oxygen species and mitogen-activated protein kinase signal pathway: Silver nanoparticles and GJIC

Silver nanoparticles (AgNPs) are widely used in health and consumer products that routinely contact skin. However, the biological effects and possible mechanisms of AgNPs on skin remain unclear. Gap junctional intercellular communication (GJIC) plays a critical role in multicellular organisms to maintain tissue homeostasis. The aim of this study is to examine if non‐coated AgNPs affect GJIC in human keratinocytes (HaCaT cells), and to identify the possible molecular mechanisms responsible for the effects. GJIC, connexin (Cx)43 protein and mRNA expression, and the effect of siRNA‐mediated knockdown of Cx43 on GJIC were assessed. HaCaT cells exposed to non‐coated AgNPs at different doses after a 24 hour exposure. To explore further the underlying mechanism, reactive oxygen species and mitogen‐activated protein kinase pathway were evaluated after 2, 6, 12 and 24 hours. Our results revealed that non‐coated AgNP exposure at subcytotoxic doses increase GJIC partially via Cx43 upregulation. Reactive oxygen species and extracellular signal‐regulated kinase and activation of c‐Jun N‐terminal kinase were involved in the AgNP‐induced upregulation of Cx43. This study provides new insight into the potential mechanism of AgNP biological activity.