Characterization of metal(loid)s in indoor and outdoor PM2.5 of an office in winter period

The characterization of indoor (a naturally ventilated office) and outdoor (adjacent courtyard) metals in PM_2.5 during a winter period in Xi'an, China were carried out. The results indicated that the average mass concentrations of PM_2.5 in indoor and outdoor environments all exceeded the daily average limit of 75 µg m^–3 set by the Chinese government. The dominant metals in PM_2.5 were Ca, Al, Zn, Mg, Fe, and Pb in both indoor and outdoor air. Concentration of As was much higher than the standard of 6 ng m^–3 issued by the government. Enrichment factor analysis showed that anthropogenic emissions might be the primary sources of As, Cd, Pb, and Zn, while crust was the main origin of Co. A majority of indoor-to-outdoor concentration ratios of metal were lower than 1 indicating mostly the contribution of outdoor sources rather than indoor ones. As and Cr in both indoor and outdoor air posed the highest noncarcinogenic and carcinogenic risks, respectively. The noncarcinogenic and carcinogenic risks were 2.74 and 2.54 × 10^?4 indoor and 4.04 and 3.87 × 10^?4 outdoor, which suggested that possible adverse health effects should be of concern.     

Long-term air pollution exposure and living close to busy roads are associated with COPD in women

Background

Lung function and exacerbations of chronic obstructive pulmonary disease (COPD) have been associated with short-term exposure to air pollution. However, the effect of long-term exposure to particulate matter from industry and traffic on COPD as defined by lung function has not been evaluated so far. Our study was designed to investigate the influence of long-term exposure to air pollution on respiratory symptoms and pulmonary function in 55-year-old women. We especially focused on COPD as defined by GOLD criteria and additionally compared the effects of air pollution on respiratory symptoms by questionnaire data and by lung function measurements.

Methods

In consecutive cross sectional studies conducted between 1985–1994, we investigated 4757 women living in the Rhine-Ruhr Basin of Germany. NO₂ and PM₁₀ exposure was assessed by measurements done in an 8 km grid, and traffic exposure by distance from the residential address to the nearest major road using Geographic Information System data. Lung function was determined and COPD was defined by using the GOLD criteria. Chronic respiratory symptoms and possible confounders were defined by questionnaire data. Linear and logistic regressions, including random effects were used to account for confounding and clustering on city level.

Results

The prevalence of COPD (GOLD stages 1–4) was 4.5%. COPD and pulmonary function were strongest affected by PM₁₀ and traffic related exposure. A 7 μg/m₃ increase in five year means of PM₁₀ (interquartile range) was associated with a 5.1% (95% CI 2.5%–7.7%) decrease in FEV₁, a 3.7% (95% CI 1.8%–5.5%) decrease in FVC and an odds ratio (OR) of 1.33 (95% CI 1.03–1.72) for COPD. Women living less than 100 m from a busy road also had a significantly decreased lung function and COPD was 1.79 times more likely (95% CI 1.06–3.02) than for those living farther away. Chronic symptoms as based on questionnaire information showed effects in the same direction, but less pronounced.

Conclusion

Chronic exposure to PM₁₀, NO₂ and living near a major road might increase the risk of developing COPD and can have a detrimental effect on lung function.     

Acute Effects of Particulate Air Pollution on the Incidence of Coronary Heart Disease in Shanghai,China

Introduction

Evidence based on ecological studies in China suggests that short-term exposure to particulate matter (PM) is associated with cardiovascular mortality. However, there is less evidence of PM-related morbidity for coronary heart disease (CHD) in China. This study aims to investigate the relationship between acute PM exposure and CHD incidence in people aged above 40 in Shanghai.

Methods

Daily CHD events during 2005–2012 were identified from outpatient and emergency department visits. Daily average concentrations for particulate matter with aerodynamic diameter less than 10 microns (PM₁₀) were collected over the 8-year period. Particulate matter with aerodynamic diameter less than 2.5 microns (PM_2.5) were measured from 2009 to 2012. Analyses were performed using quasi-poisson regression models adjusting for confounders, including long-term trend, seasonality, day of the week, public holiday and meteorological factors. The effects were also examined by gender and age group (41–65 years, and >65 years).

Results

There were 619928 CHD outpatient and emergency department visits. The average concentrations of PM₁₀ and PM_2.5 were 81.7μg/m³ and 38.6μg/m³, respectively. Elevated exposure to PM₁₀ and PM_2.5 was related with increased risk of CHD outpatients and emergency department visits in a short time course. A 10 μg/m³ increase in the 2-day PM₁₀ and PM_2.5 was associated with increase of 0.23% (95% CI: 0.12%, 0.34%) and 0.74% (95% CI: 0.44%, 1.04%) in CHD morbidity, respectively. The associations appeared to be more evident in the male and the elderly.

Conclusion

Short-term exposure to high levels of PM₁₀ and PM_2.5 was associated with increased risk of CHD outpatient and emergency department visits. Season, gender and age were effect modifiers of their association.     

Acute and chronic effects of particles on hospital admissions in New-England

Background

Many studies have reported significant associations between exposure to PM_2.5 and hospital admissions, but all have focused on the effects of short-term exposure. In addition all these studies have relied on a limited number of PM_2.5 monitors in their study regions, which introduces exposure error, and excludes rural and suburban populations from locations in which monitors are not available, reducing generalizability and potentially creating selection bias.

Methods

Using our novel prediction models for exposure combining land use regression with physical measurements (satellite aerosol optical depth) we investigated both the long and short term effects of PM_2.5 exposures on hospital admissions across New-England for all residents aged 65 and older. We performed separate Poisson regression analysis for each admission type: all respiratory, cardiovascular disease (CVD), stroke and diabetes. Daily admission counts in each zip code were regressed against long and short-term PM_2.5 exposure, temperature, socio-economic data and a spline of time to control for seasonal trends in baseline risk.

Results

We observed associations between both short-term and long-term exposure to PM_2.5 and hospitalization for all of the outcomes examined. In example, for respiratory diseases, for every10-µg/m³ increase in short-term PM_2.5 exposure there is a 0.70 percent increase in admissions (CI = 0.35 to 0.52) while concurrently for every10-µg/m³ increase in long-term PM_2.5 exposure there is a 4.22 percent increase in admissions (CI = 1.06 to 4.75).

Conclusions

As with mortality studies, chronic exposure to particles is associated with substantially larger increases in hospital admissions than acute exposure and both can be detected simultaneously using our exposure models.     

The Role of Metal Components in the Cardiovascular Effects of PM2.5

Exposure to ambient fine particulate matter (PM_2.5) increases risks for cardiovascular disorders (CVD). However, the mechanisms and components responsible for the effects are poorly understood. Based on our previous murine exposure studies, a translational pilot study was conducted in female residents of Jinchang and Zhangye, China, to test the hypothesis that specific chemical component of PM_2.5 is responsible for PM_2.5 associated CVD. Daily ambient and personal exposures to PM_2.5 and 35 elements were measured in the two cities. A total of 60 healthy nonsmoking adult women residents were recruited for measurements of inflammation biomarkers. In addition, circulating endothelial progenitor cells (CEPCs) were also measured in 20 subjects. The ambient levels of PM_2.5 were comparable between Jinchang and Zhangye (47.4 and 54.5µg/m³, respectively). However, the levels of nickel, copper, arsenic, and selenium in Jinchang were 82, 26, 12, and 6 fold higher than Zhangye, respectively. The levels of C-reactive protein (3.44±3.46 vs. 1.55±1.13), interleukin-6 (1.65±1.17 vs. 1.09±0.60), and vascular endothelial growth factor (117.6±217.0 vs. 22.7±21.3) were significantly higher in Jinchang. Furthermore, all phenotypes of CEPCs were significantly lower in subjects recruited from Jinchang than those from Zhangye. These results suggest that specific metals may be important components responsible for PM_2.5-induced cardiovascular effects and that the reduced capacity of endothelial repair may play a critical role.     

Chemical speciation and health risks of airborne heavy metals around an industrial community in Nigeria

Abstract

Quantification of PM_2.5 (particulate matter <2.5?µm) bound heavy metals and their potential health risks were carried out around a cement manufacturing company in Ewekoro, Nigeria. The PM_2.5 samples were collected using Environtech gravimetric sampler. A four-staged sequential extraction procedure was used to fractionate PM_2.5 bound chromium (Cr), lead (Pb), aluminum (Al), copper (Cu), and silver (Ag), and further analyzed using inductively coupled plasma mass spectrometry. Chemical speciation results reveal bioavailable levels of Pb (4.05?µg/m³), Cr (10.75?µg/m³), Al (16.47?µg/m³), Cu (4.38E-01?µg/m³), and Ag (1.22E-02?µg/m³) in the airborne particulates. Pb and Cr levels exceeded the World Health Organization allowable limit of 0.5 and 2.5E-05?µg/m³, respectively. The labile phases showed strong indication of the presence of Cr and Cu metal. Excess cancer risks exposure for adults, outdoor workers and children were higher than the acceptable risk target level of 1E-06. Non-carcinogenic health risk estimated using hazard quotients (HQs) and hazard indices (HIs) showed ingestion route within the safe level of HI <1 implying no adverse effect while inhalation route exceeded the safe level for all receptors. Enforcement of pollution control by authorized agencies, and screening of greenbelts as sinks for air pollutants is strongly recommended.     

Characterization and human health risk assessment of trace metal in PM10 in Bac Giang,short-term study in a developing province in Vietnam

Abstract

This study investigated the airborne concentration of PM₁₀ and 20 trace elements (Al, As, Ba, Ca, Cd, Co, Cr, Cu, Fe, K, Mg, Mn, Mo, Na, Ni, Na, Pb, Ti, V, Zn) in residential, industry, traffic road, coal mining, thermal power plant area of Bac Giang province. The average PM₁₀ concentration was highest at coal site, followed by traffic 1 sites, industrial sites and traffic 2 sites, the residential sites, and lowest at the power plant site located in mountain area. While Al, Ca, Fe, K, Mg, Na were the most abundant elements in all sampling sites, accounting for 73–96% of total obtained elements, the concentration of As, Cd, Cr, Cu, Mn, Ni, Pb, V, and Zn occupied from 2.9 to 23.2%. Noticeably, the concentrations of Cd were from 7 to 65 times higher than the concentration limit for Cd (0.1?ng/m³) according the World Health Organization (WHO). Although, the Hazard Index (HI values) of all metals were found to be within the safe level for both children and adults, the Carcinogenic Risk (CR) of Cr and As in all sites were closed to the acceptable levels for children, implying a potential carcinogenic risks of these metals.     

Air Pollution and Stillbirth Risk: Exposure to Airborne Particulate Matter during Pregnancy Is Associated with Fetal Death

Objective

To test the hypothesis that exposure to fine particulate air pollution (PM_2.5) is associated with stillbirth.

Study Design

Geo-spatial population-based cohort study using Ohio birth records (2006-2010) and local measures of PM_2.5, recorded by the EPA (2005-2010) via 57 monitoring stations across Ohio. Geographic coordinates of the mother’s residence for each birth were linked to the nearest PM_2.5 monitoring station and monthly exposure averages calculated. The association between stillbirth and increased PM_2.5 levels was estimated, with adjustment for maternal age, race, education level, quantity of prenatal care, smoking, and season of conception.

Results

There were 349,188 live births and 1,848 stillbirths of non-anomalous singletons (20-42 weeks) with residence ≤10 km of a monitor station in Ohio during the study period. The mean PM_2.5 level in Ohio was 13.3 μg/m³ [±1.8 SD, IQR(Q1: 12.1, Q3: 14.4, IQR: 2.3)], higher than the current EPA standard of 12 μg/m³. High average PM_2.5 exposure through pregnancy was not associated with a significant increase in stillbirth risk, _adjOR 1.21(95% CI 0.96,1.53), nor was it increased with high exposure in the 1^st or 2^nd trimester. However, exposure to high levels of PM_2.5 in the third trimester of pregnancy was associated with 42% increased stillbirth risk, _adjOR 1.42(1.06,1.91).

Conclusions

Exposure to high levels of fine particulate air pollution in the third trimester of pregnancy is associated with increased stillbirth risk. Although the risk increase associated with high PM_2.5 levels is modest, the potential impact on overall stillbirth rates could be robust as all pregnant women are potentially at risk.     

Lacrimal Cytokines Assessment in Subjects Exposed to Different Levels of Ambient Air Pollution in a Large Metropolitan Area

Background

Air pollution is one of the most environmental health concerns in the world and has serious impact on human health, particularly in the mucous membranes of the respiratory tract and eyes. However, ocular hazardous effects to air pollutants are scarcely found in the literature.

Design

Panel study to evaluate the effect of different levels of ambient air pollution on lacrimal film cytokine levels of outdoor workers from a large metropolitan area.

Methods

Thirty healthy male workers, among them nineteen professionals who work on streets (taxi drivers and traffic controllers, high pollutants exposure, Group 1) and eleven workers of a Forest Institute (Group 2, lower pollutants exposure compared to group 1) were evaluated twice, 15 days apart. Exposure to ambient PM_2.5 (particulate matter equal or smaller than 2.5 μm) was 24 hour individually collected and the collection of tears was performed to measure interleukins (IL) 2, 4, 5 and 10 and interferon gamma (IFN-γ) levels. Data from both groups were compared using Student’s t test or Mann- Whitney test for cytokines. Individual PM_2.5 levels were categorized in tertiles (lower, middle and upper) and compared using one-way ANOVA. Relationship between PM_2.5 and cytokine levels was evaluated using generalized estimating equations (GEE).

Results

PM_2.5 levels in the three categories differed significantly (lower: ≤22 μg/m³; middle: 23–37.5 μg/m³; upper: >37.5 μg/m³; p<0.001). The subjects from the two groups were distributed unevenly in the lower category (Group 1 = 8%; Group 2 = 92%), the middle category (Group 1 = 89%; Group 2 = 11%) and the upper category (Group 1 = 100%). A significant relationship was found between IL-5 and IL-10 and PM_2.5 levels of the group 1, with an average decrease of 1.65 pg/mL of IL-5 level and of 0.78 pg/mL of IL-10 level in tear samples for each increment of 50 μg/m3 of PM_2.5 (p = 0.01 and p = 0.003, respectively).

Conclusion

High levels of PM_2.5 exposure is associated with decrease of IL-5 and IL-10 levels suggesting a possible modulatory action of ambient air pollution on ocular surface immune response.     

Prenatal Air Pollution Exposure and Early Cardiovascular Phenotypes in Young Adults

Exposure to ambient air pollutants increases risk for adverse cardiovascular health outcomes in adults. We aimed to evaluate the contribution of prenatal air pollutant exposure to cardiovascular health, which has not been thoroughly evaluated. The Testing Responses on Youth (TROY) study consists of 768 college students recruited from the University of Southern California in 2007–2009. Participants attended one study visit during which blood pressure, heart rate and carotid artery arterial stiffness (CAS) and carotid artery intima-media thickness (CIMT) were assessed. Prenatal residential addresses were geocoded and used to assign prenatal and postnatal air pollutant exposure estimates using the U.S. Environmental Protection Agency’s Air Quality System (AQS) database. The associations between CAS, CIMT and air pollutants were assessed using linear regression analysis. Prenatal PM₁₀ and PM_2.5 exposures were associated with increased CAS. For example, a 2 SD increase in prenatal PM_2.5 was associated with CAS indices, including a 5% increase (β = 1.05, 95% CI 1.00–1.10) in carotid stiffness index beta, a 5% increase (β = 1.05, 95% CI 1.01–1.10) in Young’s elastic modulus and a 5% decrease (β = 0.95, 95% CI 0.91–0.99) in distensibility. Mutually adjusted models of pre- and postnatal PM_2.5 further suggested the prenatal exposure was most relevant exposure period for CAS. No associations were observed for CIMT. In conclusion, prenatal exposure to elevated air pollutants may increase carotid arterial stiffness in a young adult population of college students. Efforts aimed at limiting prenatal exposures are important public health goals.     

Effects of air pollution and habitual exercise on the risk of death: a longitudinal cohort study

Background:Exercise may exacerbate the adverse health effects of air pollution by increasing the inhalation of air pollutants. We investigated the combined effects of long-term exposure to fine particle matter (PM_2.5) and habitual exercise on deaths from natural causes in Taiwan.Methods:We recruited 384 130 adults (aged ≥ 18 yr) with 842 394 medical examination records between 2001 and 2016, and followed all participants until May 31, 2019. We obtained vital data from the National Death Registry of Taiwan. We estimated PM_2.5 exposure using a satellite-based spatiotemporal model, and collected information on exercise habits using a standard self-administered questionnaire. We analyzed the data using a Cox regression model with time-dependent covariates.Results:A higher level of habitual exercise was associated with a lower risk of death from natural causes, compared with inactivity (hazard ratio [HR] 0.84, 95% confidence interval [CI] 0.80–0.88 for the moderate exercise group; HR 0.65, 95% CI 0.62–0.68 for the high exercise groups), whereas a higher PM_2.5 exposure was associated with a higher risk of death from natural causes compared with lower exposure (HR 1.02, 95% CI 0.98–1.07, and HR 1.15, 95% CI 1.10–1.20, for the moderate and high PM_2.5 exposure groups, respectively). Compared with inactive adults with high PM_2.5 exposure, adults with high levels of habitual exercise and low PM_2.5 exposure had a substantially lower risk of death from natural causes. We found a minor, but statistically significant, interaction effect between exercise and PM_2.5 exposure on risk of death (HR 1.03 95% CI 1.01–1.06). Subgroup analyses, stratified by PM_2.5 categories, suggested that moderate and high levels of exercise were associated with a lower risk of death in each PM_2.5 stratum, compared with inactivity.Interpretation:Increased levels of exercise and reduced PM_2.5 exposure are associated with a lower risk of death from natural causes. Habitual exercise can reduce risk regardless of the levels of PM_2.5 exposure. Our results suggest that exercise is a safe health improvement strategy, even for people residing in relatively polluted regions.

Air pollution and physical inactivity are both major public health challenges worldwide.¹ Air pollution was the fifth leading cause of disability related to health and accounted for 4.9 million deaths worldwide in 2017.² More than 91% of the global population lives in areas where air quality does not meet the World Health Organization (WHO) guidelines.³ In addition, physical inactivity was the fourth leading risk factor for death globally, accounting for 5.3 million deaths worldwide in 2012.⁴ The WHO has challenged its member states to reduce physical inactivity by 15% by 2030.⁵As people exercise, their ventilation rate increases, which increases the volume of air pollutants they inhale. This may exacerbate the adverse health effects of air pollutants. Thus, the risk–benefit relation between air pollution and exercise needs to be assessed to understand whether it is safe to exercise regularly in polluted regions. Indeed, some studies have shown that acute exposure to air pollution when exercising may override the benefits of exercise.^6,7 It is possible that the effects of long-term exposure to air pollution may be irreversible and cause a much larger disease burden than short-term exposure. Limited information exists on the combined effects of long-term exposure to air pollution and habitual exercise on human health, and findings have been inconsistent depending on health outcome. Three cohort studies have explored the relation between air pollution, physical activity and risk of death in Hong Kong,⁸ Denmark and the United States,⁹ with relatively small sample sizes.¹⁰ Therefore, we sought to investigate the combined effects of habitual exercise and long-term exposure to fine particle matter (PM_2.5) on the risk of death from natural causes (i.e., deaths not attributable to accident, suicide or homicide) using a longitudinal cohort of adults in Taiwan, where the annual PM_2.5 concentrations are 1.6 times higher than the WHO-recommended limit. We hypothesized that the beneficial effects of habitual exercise on risk of death may outweigh the risk of high levels of air pollutants inhaled during exercise.     

Modeling of Human Exposure to In-Vehicle PM2.5 from Environmental Tobacco Smoke

Environmental tobacco smoke (ETS) is estimated to be a significant contributor to in-vehicle human exposure to fine particulate matter of 2.5 μm or smaller (PM_2.5). A critical assessment was conducted of a mass balance model for estimating PM_2.5 concentration with smoking in a motor vehicle. Recommendations for the range of inputs to the mass-balance model are given based on literature review. Sensitivity analysis was used to determine which inputs should be prioritized for data collection. Air exchange rate (ACH) and the deposition rate have wider relative ranges of variation than other inputs, representing inter-individual variability in operations, and inter-vehicle variability in performance, respectively. Cigarette smoking and emission rates and vehicle interior volume are also key inputs. The in-vehicle ETS mass balance model was incorporated into the Stochastic Human Exposure and Dose Simulation for Particulate Matter (SHEDS-PM) model to quantify the potential magnitude and variability of in-vehicle exposures to ETS. The in-vehicle exposure also takes into account near-road incremental PM_2.5 concentration from on-road emissions. Results of probabilistic study indicate that ETS is a key contributor to the in-vehicle average and high-end exposure. Factors that mitigate in-vehicle ambient PM_2.5 exposure lead to higher in-vehicle ETS exposure, and vice versa.     

Association of EGF Receptor and NLRs signaling with Cardiac Inflammation and Fibrosis in Mice Exposed to Fine Particulate Matter

?Ambient fine particulate matter (PM_2.5) could induce cardiovascular diseases (CVD), but the mechanism remains unknown. To investigate the roles of epidermal growth factor receptor (EGFR) and NOD‐like receptors (NLRs) in PM_2.5‐induced cardiac injury, we set up a BALB/c mice model of PM_2.5‐induced cardiac inflammation and fibrosis with intratracheal instillation of PM_2.5 suspension (4.0 mg/kg b.w.) for 5 consecutive days (once per day). After exposure, we found that mRNA levels of CXCL1, interleukin (IL)‐6, and IL‐18 were elevated, but interestingly, mRNA level of NLRP12 was significant decreased in heart tissue from PM_2.5‐induced mice compared with those of saline‐treated mice using real‐time PCR. Protein levels of phospho‐EGFR (Tyr1068), phospho‐Akt (Thr308), NLRP3, NF‐κB‐p52/p100, and NF‐κB‐p65 in heart tissue of PM_2.5‐exposed mice were all significantly increased using immunohistochemistry or Western blotting. Therefore, PM_2.5 exposure could induce cardiac inflammatory injury in mice, which may be involved with EGFR/Akt signaling, NLRP3, and NLRP12.     

Obesity and the relation between joint exposure to ambient air pollutants and incident type 2 diabetes: A cohort study in UK Biobank

BackgroundAir pollution has been related to incidence of type 2 diabetes (T2D). We assessed the joint association of various air pollutants with the risk of T2D and examined potential modification by obesity status and genetic susceptibility on the relationship.Methods and findingsA total of 449,006 participants from UK Biobank free of T2D at baseline were included. Of all the study population, 90.9% were white and 45.7% were male. The participants had a mean age of 56.6 (SD 8.1) years old and a mean body mass index (BMI) of 27.4 (SD 4.8) kg/m². Ambient air pollutants, including particulate matter (PM) with diameters ≤2.5 μm (PM_2.5), between 2.5 μm and 10 μm (PM_2.5–10), nitrogen dioxide (NO₂), and nitric oxide (NO) were measured. An air pollution score was created to assess the joint exposure to the 4 air pollutants. During a median of 11 years follow-up, we documented 18,239 incident T2D cases. The air pollution score was significantly associated with a higher risk of T2D. Compared to the lowest quintile of air pollution score, the hazard ratio (HR) (95% confidence interval [CI]) for T2D was 1.05 (0.99 to 1.10, p = 0.11), 1.06 (1.00 to 1.11, p = 0.051), 1.09 (1.03 to 1.15, p = 0.002), and 1.12 (1.06 to 1.19, p < 0.001) for the second to fifth quintile, respectively, after adjustment for sociodemographic characteristics, lifestyle factors, genetic factors, and other covariates. In addition, we found a significant interaction between the air pollution score and obesity status on the risk of T2D (p-interaction < 0.001). The observed association was more pronounced among overweight and obese participants than in the normal-weight people. Genetic risk score (GRS) for T2D or obesity did not modify the relationship between air pollution and risk of T2D. Key study limitations include unavailable data on other potential T2D-related air pollutants and single-time measurement on air pollutants.ConclusionsWe found that various air pollutants PM_2.5, PM_2.5–10, NO_2, and NO, individually or jointly, were associated with an increased risk of T2D in the population. The stratified analyses indicate that such associations were more strongly associated with T2D risk among those with higher adiposity.

Xiang Li and co-workers study the potential influence of obesity on associations between air pollutants and incidence of type 2 diabetes.     

Air Pollution and the microvasculature: a cross-sectional assessment of in vivo retinal images in the population-based multi-ethnic study of atherosclerosis (MESA)

Background

Long- and short-term exposures to air pollution, especially fine particulate matter (PM_2.5), have been linked to cardiovascular morbidity and mortality. One hypothesized mechanism for these associations involves microvascular effects. Retinal photography provides a novel, in vivo approach to examine the association of air pollution with changes in the human microvasculature.

Methods and Findings

Chronic and acute associations between residential air pollution concentrations and retinal vessel diameters, expressed as central retinal arteriolar equivalents (CRAE) and central retinal venular equivalents (CRVE), were examined using digital retinal images taken in Multi-Ethnic Study of Atherosclerosis (MESA) participants between 2002 and 2003. Study participants (46 to 87 years of age) were without clinical cardiovascular disease at the baseline examination (2000–2002). Long-term outdoor concentrations of PM_2.5 were estimated at each participant''s home for the 2 years preceding the clinical exam using a spatio-temporal model. Short-term concentrations were assigned using outdoor measurements on the day preceding the clinical exam. Residential proximity to roadways was also used as an indicator of long-term traffic exposures. All associations were examined using linear regression models adjusted for subject-specific age, sex, race/ethnicity, education, income, smoking status, alcohol use, physical activity, body mass index, family history of cardiovascular disease, diabetes status, serum cholesterol, glucose, blood pressure, emphysema, C-reactive protein, medication use, and fellow vessel diameter. Short-term associations were further controlled for weather and seasonality. Among the 4,607 participants with complete data, CRAE were found to be narrower among persons residing in regions with increased long- and short-term levels of PM_2.5. These relationships were observed in a joint exposure model with −0.8 µm (95% confidence interval [CI] −1.1 to −0.5) and −0.4 µm (95% CI −0.8 to 0.1) decreases in CRAE per interquartile increases in long- (3 µg/m³) and short-term (9 µg/m³) PM_2.5 levels, respectively. These reductions in CRAE are equivalent to 7- and 3-year increases in age in the same cohort. Similarly, living near a major road was also associated with a −0.7 µm decrease (95% CI −1.4 to 0.1) in CRAE. Although the chronic association with CRAE was largely influenced by differences in exposure between cities, this relationship was generally robust to control for city-level covariates and no significant differences were observed between cities. Wider CRVE were associated with living in areas of higher PM_2.5 concentrations, but these findings were less robust and not supported by the presence of consistent acute associations with PM_2.5.

Conclusions

Residing in regions with higher air pollution concentrations and experiencing daily increases in air pollution were each associated with narrower retinal arteriolar diameters in older individuals. These findings support the hypothesis that important vascular phenomena are associated with small increases in short-term or long-term air pollution exposures, even at current exposure levels, and further corroborate reported associations between air pollution and the development and exacerbation of clinical cardiovascular disease. Please see later in the article for the Editors'' Summary     

Polybrominated Diphenyl Ethers (PBDEs) in PM2.5, PM10, TSP and Gas Phase in Office Environment in Shanghai,China: Occurrence and Human Exposure

To evaluate risk via inhalation exposure of polybrominated diphenyl ethers (PBDEs) in office environment, thirty-six pairs air samples including PM_2.5 (particles with aerodynamic diameter less than 2.5 μm), PM₁₀ (particles with aerodynamic diameter less than 10 μm), total suspended particles (TSP) with matching gas phase were collected in office environment in Shanghai, China. The average concentrations of PM_2.5, PM₁₀ and TSP were 20.4, 27.2 and 50.3 μg/m₃, respectively. Σ₁₅PBDEs mean concentrations in PM_2.5, PM₁₀, TSP and gas phase were 51.8, 110.7, 148 and 59.6 pg/m³, respectively. Much more PBDEs distributed in fine fractions than coarse ones. PBDEs congener profiles found in PM_2.5, PM₁₀ and TSP (dominated by BDE-209) were different from that in gas phase (dominated by the tri- to penta-BDEs). Approximately 3.20 pg/kg/d PM_2.5 bound PBDEs can be inhaled into the lung; 3.62 pg/kg/d PM₁₀-PM_2.5(particles with aerodynamic diameter of 2.5-10 μm) bound PBDEs tended to be deposited in the upper part of respiratory system, and the intake of PBDEs via gas-phase was 2.74 pg/kg/d. The exposure of PBDEs was far below the minimal risk levels (MRLs), indicating lower risk from PBDEs via inhalation in the studied office in Shanghai.     

Oxidative stress-mediated epidermal growth factor receptor activation regulates PM2.5-induced over-secretion of pro-inflammatory mediators from human bronchial epithelial cells

BackgroundExposure to PM_2.5 has been associated with increased morbidity and mortality of lung diseases although the underlying mechanisms have not been fully uncovered. Airway inflammation is a critical event in the pathogenesis of lung diseases. This study aimed to examine the role of oxidative stress and epidermal growth factor receptor (EGFR) in PM_2.5-induced pro-inflammatory response in a human bronchial epithelial cell line, BEAS-2B.MethodsBEAS-2B cells were exposed to 0, 20, 50, 100 and 150 μg/ml of PM_2.5. Secretion of pro-inflammatory mediators including interleukin-6 (IL-6), IL-8 and IL-1β was determined using enzyme linked immunosorbent assay. Levels of intracellular reactive oxygen species (ROS) were determined using flow cytometry. Phosphorylation of the EGFR was examined with immunoblotting.ResultsPM_2.5 exposure increased the secretion of IL-6, IL-8, and IL-1β in a concentration-dependent fashion. Moreover, exposure to PM_2.5 elevated intracellular levels of ROS, and phosphorylation of the EGFR (Y1068). Pretreatment of BEAS-2B cells with either an antioxidant or a specific EGFR inhibitor significantly reduced PM_2.5-induced IL-6, IL-8 and IL-1β secretion, implying that both oxidative stress and EGFR activation were involved in PM_2.5-induced pro-inflammatory response. Furthermore, pre-treatment of BEAS-2B cells with an antioxidant significantly blunted PM_2.5-induced EGFR activation, suggesting that oxidative stress was required for PM_2.5-induced EGFR activation.ConclusionPM_2.5 exposure induces pro-inflammatory response in human bronchial epithelial cells through oxidative stress-mediated EGFR activation.     

DDAH1 plays dual roles in PM2.5 induced cell death in A549 cells

BackgroundDimethylarginine dimethylaminohydrolase 1 (DDAH1) is an enzyme that can degrade asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor. Emerging evidence suggests that alterations in the ADMA–DDAH1 pathway are involved in environmental pollution induced airway inflammation. However, the role of DDAH1 in protection against cytotoxicity of ambient airborne particulate matter is unclear.MethodsWe examined the influence of DDAH1 expression on oxidative stress and cell apoptosis in human type II alveolar epithelial A549 cells exposed to PM_2.5 (particulate matter with an aerodynamic diameter less than 2.5 μM).ResultsWe found that PM_2.5 exposure for 48 h significantly decreased DDAH1 expression. However, knockdown of DDAH1 prior to PM_2.5 exposure actually attenuated the cytotoxicity of PM_2.5. Cytoprotection in DDAH1 deficient cells was due to increased reactive oxygen species, activation of PI3K–AKT and mitogen-activated protein kinase (MAPK) pathways, subsequent activation of nuclear factor erythroid-2-related factor 2 (Nrf2) and this caused a subsequent reduction in PM_2.5 induced oxidative stress relative to control. DDAH1 depletion also repressed the induction of inducible NOS (iNOS) in PM_2.5-exposed cells and knockdown of iNOS protected cells against PM_2.5 induced cell death. Interestingly, overexpression of DDAH1 also exerted a protective effect against the cytotoxicity of PM_2.5 and this was associated with a reduction in oxidative stress and upregulation of the anti-apoptotic protein Bcl-2.ConclusionsOur data indicate that DDAH1 plays dual roles in protection against cytotoxicity of PM_2.5 exposure, apparently by limiting PM_2.5 induced oxidative stress.General significanceOur findings reveal new insights into the role(s) of the DDAH1/ADMA in pulmonary protection against airborne pollutants. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.     

Air pollution-induced placental epigenetic alterations in early life: a candidate miRNA approach

Particulate matter (PM) exposure during in utero life may entail adverse health outcomes in later-life. Air pollution's adverse effects are known to alter gene expression profiles, which can be regulated by microRNAs (miRNAs). We investigate the potential influence of air pollution exposure in prenatal life on placental miRNA expression. Within the framework of the ENVIRONAGE birth cohort, we measured the expression of six candidate miRNAs in placental tissue from 210 mother-newborn pairs by qRT-PCR. Trimester-specific PM_2.5 exposure levels were estimated for each mother's home address using a spatiotemporal model. Multiple regression models were used to study miRNA expression and in utero exposure to PM_2.5 over various time windows during pregnancy. The placental expression of miR-21 (?33.7%, 95% CI: ?53.2 to ?6.2, P = 0.022), miR-146a (?30.9%, 95% CI: ?48.0 to ?8.1, P = 0.012) and miR-222 (?25.4%, 95% CI: ?43.0 to ?2.4, P = 0.034) was inversely associated with PM_2.5 exposure during the 2nd trimester of pregnancy, while placental expression of miR-20a and miR-21 was positively associated with 1st trimester exposure. Tumor suppressor phosphatase and tensin homolog (PTEN) was identified as a common target of the miRNAs significantly associated with PM exposure. Placental PTEN expression was strongly and positively associated (+59.6% per 5 µg/m³ increment, 95% CI: 26.9 to 100.7, P < 0.0001) with 3rd trimester PM_2.5 exposure. Further research is required to establish the role these early miRNA and mRNA expression changes might play in PM-induced health effects. We provide molecular evidence showing that in utero PM_2.5 exposure affects miRNAs expression as well as its downstream target PTEN.     

Fine Particulate Air Pollution and the Progression of Carotid Intima-Medial Thickness: A Prospective Cohort Study from the Multi-Ethnic Study of Atherosclerosis and Air Pollution

Background

Fine particulate matter (PM_2.5) has been linked to cardiovascular disease, possibly via accelerated atherosclerosis. We examined associations between the progression of the intima-medial thickness (IMT) of the common carotid artery, as an indicator of atherosclerosis, and long-term PM_2.5 concentrations in participants from the Multi-Ethnic Study of Atherosclerosis (MESA).

Methods and Results

MESA, a prospective cohort study, enrolled 6,814 participants at the baseline exam (2000–2002), with 5,660 (83%) of those participants completing two ultrasound examinations between 2000 and 2005 (mean follow-up: 2.5 years). PM_2.5 was estimated over the year preceding baseline and between ultrasounds using a spatio-temporal model. Cross-sectional and longitudinal associations were examined using mixed models adjusted for confounders including age, sex, race/ethnicity, smoking, and socio-economic indicators. Among 5,362 participants (5% of participants had missing data) with a mean annual progression of 14 µm/y, 2.5 µg/m³ higher levels of residential PM_2.5 during the follow-up period were associated with 5.0 µm/y (95% CI 2.6 to 7.4 µm/y) greater IMT progressions among persons in the same metropolitan area. Although significant associations were not found with IMT progression without adjustment for metropolitan area (0.4 µm/y [95% CI −0.4 to 1.2 µm/y] per 2.5 µg/m³), all of the six areas showed positive associations. Greater reductions in PM_2.5 over follow-up for a fixed baseline PM_2.5 were also associated with slowed IMT progression (−2.8 µm/y [95% CI −1.6 to −3.9 µm/y] per 1 µg/m³ reduction). Study limitations include the use of a surrogate measure of atherosclerosis, some loss to follow-up, and the lack of estimates for air pollution concentrations prior to 1999.

Conclusions

This early analysis from MESA suggests that higher long-term PM_2.5 concentrations are associated with increased IMT progression and that greater reductions in PM_2.5 are related to slower IMT progression. These findings, even over a relatively short follow-up period, add to the limited literature on air pollution and the progression of atherosclerotic processes in humans. If confirmed by future analyses of the full 10 years of follow-up in this cohort, these findings will help to explain associations between long-term PM_2.5 concentrations and clinical cardiovascular events. Please see later in the article for the Editors'' Summary