Long-term Particulate Matter Research Articles

A Critical Review on the Effect of Particulate Matter (PM) in Air on Public Health

According to the World Health Organization (WHO), particulate matter (PM) contamination causesaround 800,000 premature deaths per year, ranking 13th in the world in terms of mortality.However, several findings revealed that the correlation is much stronger and more complicated thanpreviously believed. PM is an element of emissions comprised of very small, acidic, organiccompounds, metals, and particulate soil or dust particles or fluid droplets. The most consistent airquality component linked to human illness is PM, which is categorized by size. PM is likely to developcardiovascular and cerebrovascular disorders due to the mechanisms of inflammation, overt andindirect coagulation activation, and direct translocation to the systemic circulation. The evidence onthe cardiovascular system that shows a PM effect is strong. Coronary incidence and mortality ratesin populations prone to long-term PM toxicity were significantly higher. Short-term acute emissionsincrease coronary incidence rates subtly within days of the pollution peak.

Letter to the Editor regarding Wang Y, Liu Y, Yan H. 2020. Effect of long-term particulate matter exposure on Parkinson’s risk

Letter to the Editor regarding Wang Y, Liu Y, Yan H. 2020. Effect of long-term particulate matter exposure on Parkinson’s risk

Socio-economic disparities in exposure to urban restaurant emissions are larger than for traffic

Restaurants and vehicles are important urban sources of particulate matter (PM). Due to the ubiquitous presence of these sources within cities, large variabilities in PM concentrations occur in source-rich environments (e.g. downtown), especially during times of peak activity such as meal times and rush hour. Due to intracity variations in factors such as racial-ethnic composition and economic status, we hypothesized that certain socio-economic groups living closer to sources are exposed to higher PM concentrations. To test this hypothesis, we coupled mobile PM measurements with census data in two midsize US cities: Oakland, CA, and Pittsburgh, PA. A novel aspect of our study is that our measurements are performed at a high (block-level) spatial resolution, which enables us to assess the direct relationship between PM concentrations and socio-economic metrics across different neighborhoods of these two cities. We find that restaurants cause long-term average PM enhancements of 0.1 to 0.3 µg m−3 over length scales between 50 and 450 m. We also find that this PM pollution from restaurants is unevenly distributed amongst different socio-economic groups. On average, areas near restaurant emissions have about 1.5× people of color (African American, Hispanic, Asian, etc), 2.5× poverty, and 0.8× household income, compared to areas far from restaurant emissions. Our findings imply that there are socio-economic disparities in long-term exposure to PM emissions from restaurants. Further, these socio-economic groups also frequently experience acutely high levels of cooking PM (tens to hundreds of µg m−3 in mass concentrations) and co-emitted pollutants. While there are large variations in socio-economic metrics with respect to restaurant proximity, we find that these metrics are spatially invariant with respect to highway proximity. Thus, any socio-economic disparities in exposure to highway emissions are, at most, mild, and certainly small compared to disparities in exposure to restaurant emissions.

Long-term particulate matter 2.5 exposure, insulin resistance and type 2 diabetes risk in Mexican adults: results from GEA study.

Background/Aim. Type two diabetes mellitus (T2DM) is a leading cause of morbidity and mortality in Mexico. The aim of this study was to examine associations between particulate matter 2.5 (PM2.5) exposure and T2DM risk.Methods. This study comprised 1478 individuals belonging to the Genetics of Atherosclerotic Mexican Study (GEA) in Mexico City. Type 2 diabetes mellitus was defined by the American Diabetes Association criteria and insulin resistance (IR) was considered when the HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) values were more than 75 percentile. PM2.5 concentrations for long-term periods (1 to 9 years) were assigned by inverse distance weighted (IDW) of data from air quality monitors. Linear regression models or logistic regression models were employed to assess long-term PM2.5 exposure and continuous variables (HOMA-IR or glycosylated hemoglobin [Hb1Ac]) or binary outcomes (T2DM or IR ), respectively. All models were adjusted for age, sex, body mass index, socioeconomic status, marital status, smoking, physical activity and total calories intake. Results. The prevalence of T2DM was 13.2% and for IR was 57.9%. PM2.5 exposure at year 1, 3, and 5 years before the baseline visit were significantly associated with higher HOMA-IR and IR. Each 10 ug/m3 of PM2.5 at year 1 was associated with 16% (95% CI: 1.01-1.33) higher odds of IR, and year 5 with 20% (95%CI: 1.05-1.36) higher odds of IR. Each 10 ug/m3 PM2.5 increased at year 2 (0.4% [95% CI: 0.04-0.74]) and 7 (0.5% [95% CI: 0.14-0.80]) were associated with increased HbA1c. Finally, no significant associations were observed between PM2.5 exposure at any time point and type 2 diabetes mellitus risk. Conclusions. The association between long-term exposure to PM2.5 and insulin resistance is relevant in the context of high obesity rate and poor glycemic control characteristic of Mexican adults.

Particulate matter air pollution, neighborhood socio-economic status, and leukocyte telomere length

Background: Telomeres cap and protect chromosomes from degradation and risk factors for telomere attrition include aging and environmental factors. Although exposure to some air pollutants and neighborhood socio-economic factors (nSES) have been associated with telomere length, evidence of associations between exposure to particulate matter (PM) air pollution, nSES, and the interaction between the two in relation to telomere length is limited and inconclusive. Our objective was to examine the associations between exposure to short-, intermediate-, and long-term (1-, 3-, and 12-month) exposure to different size fractions of PM (<2.5 microns [PM2.5], 2.5-10 microns [PM10-2.5], and <10 microns [PM10]) and nSES at blood draw, and leukocyte telomere length.Methods: We used generalized linear regression models to examine the associations between each of the PM exposure metrics, nSES, and z-scores of log-transformed telomere length in 10,212 female participants of the nationwide Nurses’ Health Study, after adjusting for demographics and telomere attrition risk factors. Using participants’ address history, we applied spatio-temporal prediction models to estimate monthly PM exposures.Results: In adjusted models, PM2.5 exposure per 10 μg/m3 increase was not associated with relative telomere length: 1-month exposure: β: 0.01, standard error (SE): 0.01, p: 0.40; 3-month exposure: β: 0.01, SE: 0.01, p: 0.37; 12-month exposure: β: 0.01, SE: 0.01, p: 0.34. Results for exposure to PM10-2.5, and PM10 were similar. nSES at blood draw was also not associated with telomere length: β: -0.001, SE: 0.001, p: 0.28. We observed no multiplicative interactions between 1-, 3-, and 12-month PM exposures and nSES.Conclusions: In this study of U.S. women, short-, intermediate-, and long-term PM exposures were not associated with telomere attrition for any size fraction of PM; nSES was also not associated with telomere length. Additionally, we observed no interactions between PM exposures and nSES in association with telomere length.

Fine Particulate Matter and Dementia in the Adult Changes in Thought Study

Background: Air pollution may be associated with elevated dementia risk, but prior research has limitations that may affect reliability, and no prior studies have evaluated this question in a community-based cohort of men and women in the United States. Methods: We evaluated the association of long-term fine particulate matter (PM2.5) exposure with all-cause dementia during the period 1978-2018 in the Adult Changes in Thought (ACT) study based in Seattle, Washington, USA. PM2.5 exposures linked to participant addresses were obtained from a spatiotemporal model spanning 40 years. Research quality dementia diagnoses were made using standardized diagnosis protocols at biennial follow-ups. We conducted multivariate Cox proportional hazards regression to evaluate the association between time-varying, 10-year average PM2.5 exposure and time to event in a model based on age, stratified by apolipoprotein E (APOE) genotype, and adjusted for sex, education, race, neighborhood median household income, and calendar time. Findings: Mean (standard deviation) 10-year average PM2.5 was 10.0 (2.9) µg/m3, which is below the current national air quality standard. Each 1 µg/m3 increase in the moving average of 10-year PM2.5 was associated with a 16% greater hazard of all-cause dementia (1.16 (1.03, 1.31). Interpretation: In this community-based prospective cohort study with uniquely extensive exposure data and research quality outcome ascertainment, elevated long-term exposure to PM2.5 was associated with an increased hazard of all-cause dementia. These results add to growing evidence on the neurodegenerative effects of air pollution and suggest that reducing exposures across the population could contribute to reducing the burden of dementia. Funding: NIEHS F31ES030972-02, NIEHS T32ES015459, NIA T32AG052354, NIEHS and NIA R01ES026187, U01 AG006781, NIEHS ES026187, NIA AG05136, R01 AG056711 and U01 NS091272, the University of Washington Retirement Association Aging Fellowship, and the Seattle Chapter of the Achievement Rewards for College Scientists (ARCS) Foundation. Declaration of Interests: The authors have no conflicts of interest to disclose. Ethics Approval Statement: ACT participants signed forms indicating their informed consent to enroll in the study. Study procedures were approved by the University of Washington and Kaiser Permanente Institutional Review Boards.

Age differences in the pulmonary and vascular pathophysiologic processes after long-term real-time exposure to particulate matter in rats

Existing experimental data do not sufficiently explain which pathophysiologic processes are involved in different age of rats exposed to long-term particulate matter. This study explored the pulmonary and cardiovascular effects of long-term PM2.5 and PM10 exposure in juvenile, adult and senescent rats. Tail cuff plethysmography, whole-body plethysmographic system, myograph, enzyme-linked immunosorbent assay, and inductively coupled plasma-mass spectrometry were used to detect the blood pressure, lung function, endothelium-dependent relaxation, inflammatory cytokines and heavy metals, respectively. The exposure time was from November, 2017 to October, 2018, and the average concentrations of PM2.5 and PM10 were 78.7 and 128.2 μg/m3, respectively. Compared with the filtered air group, the body weight and survival rate in PM2.5 and PM10 exposure group were significantly decreased, and the survival rate of senescent exposed rats was only 30%. PM2.5 and PM10 exposure increased the blood pressure, elevated the levels of serum and bronchoalveolar lavage fluid inflammatory factors, and the senescent exposed rats showed an earlier rising trend in blood pressure and inflammatory factors than those of juvenile and adult exposed rats. Long-term PM2.5 and PM10 exposure could destroy intrapulmonary and small resistance arteries endothelial function, causing vasodilation disorders. PM2.5 and PM10 exposure caused particulate matter to accumulate in the lungs. Additionally, PM2.5 and PM10 exposure could also cause accumulation of cadmium (Cd) and lead in the liver, and chromium and Cd in the kidney. In conclusion, ambient PM2.5 and PM10 exposure induced particulate matter to accumulate in the body, caused severe pulmonary and vascular disorders, and demonstrated age-associated differences.

Association of particulate matter air pollution with leukocyte mitochondrial DNA copy number

BackgroundAmbient particulate matter (PM) has been associated with mitochondrial damage and dysfunction caused by excessive oxidative stress, but the associations between long-term PM exposure and leukocyte mitochondrial DNA copy number (mtDNAcn), a biomarker of mitochondrial dysfunction due to oxidative stress, are less studied. ObjectivesTo investigate the associations between short-, intermediate- and long-term exposure (1-, 3- and 12-months) to different size fractions of PM (PM2.5, PM2.5-10 and PM10) and leukocyte mtDNAcn in a cross-sectional study. MethodsThe associations between each of the PM exposure metrics with z scores of log-transformed mtDNAcn were examined using generalized linear regression models in 2758 female participants from the Nurses’ Health Study (NHS). Monthly exposures to PM were estimated from spatio-temporal prediction models matched to each participants’ address history. Potential effect modification by selected covariates was examined using multiplicative interaction terms and subgroup analyses. ResultsIn single-size fraction models, increases in all size fractions of PM were associated with decreases in mtDNAcn, although only models with longer averages of PM2.5 reached statistical significance. For example, an interquartile range (IQR) increase in 12-month average ambient PM2.5 (5.5 μg/m3) was associated with a 0.07 [95% confidence interval (95% CI): −0.13, −0.01; p-value = 0.02] decrease in mtDNAcn z score in both basic- and multivariable-adjusted models. Associations for PM2.5 were stronger after controlling for PM2.5-10 in two size-fraction models. ConclusionsOur study suggests that long-term exposure to ambient PM2.5 is associated with decreased mtDNAcn in healthy women.

Effect of long-term particulate matter exposure on Parkinson's risk.

Environmental pollution is a critical predisposing factor underlying neurodegenerative diseases, but the association between particulate matter (PM) exposure and Parkinson's disease (PD) remains unclear. This study aimed to evaluate the association between long-term PM2.5/PM10 exposure and PD risk. We searched the PubMed, Ovid Medline, EMBASE, Cochrane Library, and Web of Science citation databases to select studies about the relationship between long-term PM exposure and PD risk. The association was assessed using meta-analysis, and subgroup analysis was carried out on the basis of the types of PM (PM2.5 and PM10). Among the 611 articles identified from the databases, we selected six articles, including three cohort studies and three case-control studies, which collectively involved 10,077,029 participants. With every 10μg/m3 increment, the relative risks (RRs) and 95% confidence intervals (CIs) were 1.03 (0.98, 1.07), 1.21 (0.95, 1.54), and 1.01 (0.97, 1.05) for the total PM, PM2.5, and PM10, respectively. In the current study, no statistically substantial association was observed between long-term PM2.5/PM10 exposure and PD incidence. However, further large-scale prospective studies are needed to determine the association.

Long-term particulate matter exposure increases the mortality risk of patients with end-stage renal disease

Long-term particulate matter exposure increases the mortality risk of patients with end-stage renal disease

Particulate matter air pollution and blood glucose in children and adolescents: A cross-sectional study in China.

The health effects of particulate matter (PM) air pollution on glucose metabolism have been rarely examined in children and adolescents. We aimed to investigate the associations between long-term PM exposure and blood glucose and prevalence of impaired fasting glucose in a large population of Chinese children and adolescents. In 2013, a total of 11,814 children and adolescents aged 7 to 18 years were recruited from seven provinces/municipalities in China. Fasting blood sample was taken for the measurement of blood glucose. Satellite-based spatial-temporal models were used to estimate exposure to ambient submicrometer particles (PM1), fine particles (PM2.5) and thoracic particles (PM10). Cross-sectional analyses were performed using mixed-effects multivariable linear and logistic regression models. After adjustment for a range of covariates, every 10 μg/m3 increment in PM1, PM2.5 and PM10 concentrations was associated with 0.160 [95% confidence interval (CI): 0.039, 0.280], 0.150 (95% CI: 0.044, 0.256) and 0.079 (95% CI: -0.009, 0.167) mmol/L higher blood glucose levels, respectively. PM exposure was also associated with higher prevalence of impaired fasting glucose, but the associations did not reach statistical significance [odds ratio per 10 μg/m3 increment in PM1, PM2.5 and PM10: 1.30 (95% CI: 0.86,1.96), 1.20 (95% CI: 0.85,1.69) and 1.08 (95% CI: 0.83,1.41)]. We found that long-term exposure to PM air pollution was associated with increased levels of blood glucose in children and adolescents. The associations were more evident for PM1 and PM2.5.

Personal exposure to particulate matter in peri-urban India: predictors and association with ambient concentration at residence.

Scalable exposure assessment approaches that capture personal exposure to particles for purposes of epidemiology are currently limited, but valuable, particularly in low-/middle-income countries where sources of personal exposure are often distinct from those of ambient concentrations. We measured 2 × 24-h integrated personal exposure to PM2.5 and black carbon in two seasons in 402 participants living in peri-urban South India. Means (sd) of PM2.5 personal exposure were 55.1(82.8) µg/m3 for men and 58.5(58.8) µg/m3 for women; corresponding figures for black carbon were 4.6(7.0) µg/m3 and 6.1(9.6) µg/m3. Most variability in personal exposure was within participant (intra-class correlation ~20%). Personal exposure measurements were not correlated (Rspearman < 0.2) with annual ambient concentration at residence modeled by land-use regression; no subgroup with moderate or good agreement could be identified (weighted kappa ≤ 0.3 in all subgroups). We developed models to predict personal exposure in men and women separately, based on time-invariant characteristics collected at baseline (individual, household, and general time-activity) using forward stepwise model building with mixed models. Models for women included cooking activities and household socio-economic position, while models for men included smoking and occupation. Models performed moderately in terms of between-participant variance explained (38-53%) and correlations between predictions and measurements (Rspearman: 0.30-0.50). More detailed, time-varying time-activity data did not substantially improve the performance of the models. Our results demonstrate the feasibility of predicting personal exposure in support of epidemiological studies investigating long-term particulate matter exposure in settings characterized by solid fuel use and high occupational exposure to particles.

Long-Term Particulate Matter Exposure and Onset of Depression in Middle-Aged Men and Women.

Background:Long-term exposure to particulate matter (PM) air pollution is associated with all-cause mortality and adverse cognitive outcomes, but the association with developing depression remains inconsistent.Objective:Our goal was to evaluate the prospective association between PM air pollution and developing depression assessed using the Center for Epidemiological Studies Depression (CES-D) scale.Methods:Subjects were drawn from a prospective cohort study of 123,045 men and women free of depressive symptoms at baseline who attended regular screening exams in Seoul and Suwon, South Korea, from 2011 to 2015. Exposure to PM with an aerodynamic diameter of ( and , respectively) was estimated using a land-use regression model based on each subject’s residential postal code. Incident depression was defined as a CES-D score during follow-up. As a sensitivity analyses, we defined incident depression using self-reports of doctor’s diagnoses or use of antidepressant medications during follow-up.Results:The mean baseline 12-month concentrations of and were 50.6 (4.5) and , respectively. The hazard ratios (HRs) and 95% confidence intervals (CIs) for developing depression associated with a increase in 12- and 60-month exposure were 1.11 (95% CI: 1.06, 1.16) and 1.06 (95% CI: 1.01, 1.11), respectively. The corresponding HRs for 12-month exposure was 0.96 (95% CI: 0.64, 1.43). Similar results were obtained when incident depression was identified using self-reports of doctor’s diagnoses or the use of antidepressant medications.Conclusion:In this large cohort study, we found a positive association between long-term exposure to outdoor air pollution and the developing depression. We did not find an association for outdoor air pollution; however, we had a much shorter follow-up for subjects’ exposure to . https://doi.org/10.1289/EHP4094

Spatio-Temporal Variation in the Concentration of Inhalable Particulate Matter (PM10) in Uganda.

Long-term particulate matter (PM10) measurements were conducted during the period January 2016 to September 2017 at three sites in Uganda (Mbarara, Kyebando, and Rubindi) representing a wide range of urbanization. Spatial, temporal and diurnal variations are assessed in this paper. Particulate matter (PM10) samples were collected for 24-h periods on PTFE filters using a calibrated pump and analyzed gravimetrically to determine the average density. Particulate levels were monitored simultaneously using a light scattering instrument to acquire real time data from which diurnal variations were assessed. The PM10 levels averaged over the sampling period at Mbarara, Kyebando, and Rubindi were 5.8, 8.4, and 6.5 times higher than the WHO annual air quality guideline of 20 µg·m−3, and values exceeded the 24-h mean PM10 guideline of 50 µg·m−3 on 83, 100, and 86% of the sampling days. Higher concentrations were observed during dry seasons at all sites. Seasonal differences were statistically significant at Rubindi and Kyebando. Bimodal peaks were observed in the diurnal analysis with higher morning peaks at Mbarara and Kyebando, which points to the impact of traffic sources, while the higher evening peak at Rubindi points to the influence of dust suspension, roadside cooking and open-air waste burning. Long-term measurement showed unhealthy ambient air in all three locations tested in Uganda, with significant spatial and seasonal differences.

Air pollution by particulate matter as the risk factor for the cardiovascular diseases

In the review there highlighted contemporary concepts about the relation between the air pollution by the particulate matter (PM) and human morbidity and mortality rate due to cardiovascular diseases. There are considered results of the short- and long-term PM impact on the human cardiovascular system in the dependence on size, origin, chemical composition, and concentration in the air. Authors performed the formalized description of the action and possible effects of PM on vascular endothelium presented as an example of systemization. Summarizing data respective knowledge collected in the literature were used in the article as an example.

Monitoring Impacts of Urbanisation and Industrialisation on Air Quality in the Anthropocene Using Urban Pond Sediments

The release of toxic atmospheric pollutants since the Industrial Revolution is a major global challenge, driving climate change and damaging human health. Spatial health inequalities highlight the need to explore air pollution in different localities throughout the Anthropocene. Air quality monitoring programmes are spatially and temporally limited. We show how suitable urban sediment archives provide site specific records of long-term particulate matter (PM) releases, in cities and urban landscapes, that are or have been subjected to high pollution levels. High-resolution PM records spanning from the mid-20th century were reconstructed from an urban pond in Chongqing, southwest China, one of the fastest growing Chinese urban centres in the late 20th century. Temporal variations in pollution proxies including geomagnetic, geochemical and spheroidal carbonaceous particle trends correspond to key phases of industrial and urban developments, that are representative of the locality. Observed increases in air pollution proxies post-1960 coincide with the location of military-related industries to Chongqing and industrial intensification. Post-1997 pollution mirrors rapid urbanisation that occurred following the designation of Chongqing as a government-controlled municipality at this time and reveals a steadily increasing pollution trend to present day (2015). In comparison to Chongqing, an atmospheric depositional history was constructed from an urban pond in the Merseyside region of northwest England that has experienced a legacy of contamination since the early 19th century. In northwest England, changing characteristics of pollution are related to the establishment of localised, modern industries, power generation, urban sprawl, increased combustion-derived pollution post-1990 and effective pollution legislations. Whereas a reduction in air pollution has occurred post-2000 in Merseyside, in Chongqing, however, air pollution has continued to increase in spite of national efforts in pollution control. These urban sediments reveal the changing nature of air pollution in different urban landscapes, allowing us to assess air quality impacts of progressive industrial activity, increased road and air travel, urban expansion and the efficacy of pollution controls. It appears that air pollution remains an inevitable consequence of global industrialisation. It is therefore crucial to understand pollution histories in densely populated urban regions to determine environmental burdens of pollution on health over generational timescales.

Extracellular vesicle-enriched microRNAs interact in the association between long-term particulate matter and blood pressure in elderly men

BackgroundSeveral studies have shown that exposure to particulate matter (PM) may lead to increased systemic blood pressure, but the underlying biological mechanisms remain unknown. Emerging evidence shows that extracellular vesicle-enriched miRNAs (evmiRNAs) are associated with PM exposure and cardiovascular risk. In this study, we investigated the role of evmiRNAs in the association between PM and blood pressure, as well as their epigenetic regulation by DNA methylation. MethodsParticipants (n = 22, men) were randomly selected from the Veterans Affairs Normative Aging Study (NAS). Long-term (1-year and 6-month average) PM2.5 exposure was estimated at 1 × 1-km resolution using spatio-temporal prediction models and BC was estimated using validated time varying land use regression models. We analyzed 31 evmiRNAs detected in ≥ 90% of all individuals and for statistical analysis, we used mixed effects models with random intercept adjusted for age, body mass index, smoking, C-reactive protein, platelets, and white blood cells. ResultsWe found that per each 2-standard deviations increase in 6-month PM2.5 ambient levels, there was an increase in 0.19 mm Hg (95% Confidence Interval [95%CI]: 0.11, 0.28 mmHg; p < 0.001) in systolic blood pressure (SBP). Per each 2-standard deviations increase in 1-year PM2.5 levels, there was an increase in 0.11 mm Hg (95% Confidence Interval [95% CI]: 0.03, 0.19 mmHg; p = 0.012) in SBP in older male individuals. We also found that both miR-199a/b (β = 6.13 mmHg; 95% CI: 0.87, 11.39; pinteraction = 0.07) and miR-223–3p (β = 30.17 mmHg; 95% CI: 11.96, 48.39 mmHg; pinteraction = 0.01) modified the association between 1-year PM2.5 and SBP. When exploring DNA methylation as a potential mechanism that could epigenetically regulate expression of evmiRNAs, we found that PM2.5 ambient levels were negatively associated with DNA methylation levels at CpG (cg23972892) near the enhancer region of miR-199a/b (β = −13.11; 95% CI: −17.70, −8.52; pBonferroni< 0.01), but not miR-223-3p. ConclusionsOur findings suggest that expression of evmiRNAs may be regulated by DNA methylation in response to long-term PM2.5 ambient levels and modify the magnitude of association between PM2.5 and systolic blood pressure in older individuals.

Spatial and temporal (short and long-term) variability of submicron, fine and sub-10 μm particulate matter (PM1, PM2.5, PM10) in Cyprus

Long-term particulate matter (PM) mass concentration measurements have been performed in Cyprus at three major cities, one industrial area and two remote stations covering the entire southern part of the island in an effort to assess; i) the spatial and temporal variability of sub-10 μm (PM10), fine (PM2.5) and submicron (PM1) particulate matter in the eastern Mediterranean, ii) the main source areas contributing to their levels and iii) the relative contribution of regional and local anthropogenic and natural sources to PM levels. It was found that dust is responsible for the 33.6 ± 5.2% or about 10 μg m−3 of the annual PM10 levels reported in background stations; the latter underlines the significant contribution of natural sources on the ambient PM10 amounts in the eastern Mediterranean region. A significant (p < 0.001) decreasing trend of 0.7 ± 0.1 μg m−3 y−1 was observed when both PM10 and PM2.5 annual values are considered, indicating contribution from both natural and anthropogenic sources to this tendency. By considering the PMx (with x = 1, 2.5 and 10) mass concentrations obtained at the background station of Agia Marina as representative of the regional influence, the local influence of the urban and industrial sites on the measured PMx levels can be estimated. On average, 36–44% of the observed PM10 levels at the urban and industrial locations is estimated to originate from local anthropogenic and/or natural emissions including vehicle, biomass-burning, shipping emissions (in Limassol), airport related emissions (in Larnaca), resuspension of dust and sea-salt (in coastal locations). These local emissions are almost equally distributed in the fine and coarse fractions as 40–50% of the local PM10 amounts are due to fine particles emissions. The above results highlight significant emissions from both fine mode (e.g. residential heating and traffic) and coarse mode urban emissions (e.g. dust resuspension, wear and tear in brakes and tires, respectively) in urban and industrial locations in Cyprus.

Particulate Matter Triggers Depressive-Like Response Associated With Modulation of Inflammatory Cytokine Homeostasis and Brain-Derived Neurotrophic Factor Signaling Pathway in Mice

Particulate matter (PM) exposure may contribute to depressive-like response in mice. However, few studies have evaluated the adaptive impacts of long-term PM exposure on depressive-like response associated with systemic inflammation and brain-derived neurotrophic factor (BDNF) signaling pathway. We studied the association among depressive-like behaviors, mRNA levels of pro and anti-inflammatory cytokines, and the expression of BDNF signaling pathway in mice by long-term PM exposure. C57BL/6 male mice were exposed to ambient air alongside control mice breathing air filtered through a high-efficiency air PM (HEPA) filter. Depressive-like behaviors were assessed together with proinflammatory, anti-inflammatory cytokine mRNA levels and the modulation of BDNF pathway in hippocampus and olfactory-bulb of mice exposed to PM for 4, 8, and 12 weeks. Exposure to HEPA-filtered air for 4 weeks may exert antidepressant like effects in mice. Proinflammatory cytokines were up-regulated while the expression of BDNF, its high-affinity receptor tropomyosin-related kinase B (TrkB), and the transcription factor (cyclic adenosine monophosphate)-response element-binding protein (CREB) were down-regulated in ambient air mice. However, after 8 weeks, there was no significant difference in the rate of depressive-like behaviors between the 2 groups. After 12 weeks, mice exposed to ambient air again had a higher rate of depressive-like behaviors, significant up-regulation of proinflammatory cytokines, down-regulation of interleukin-10, BDNF, TrkB, and CREB than HEPA mice. Ultrafine PM in brain tissues of mice exposed to ambient air was observed. Our results suggest continuous high-level PM exposure alters the depressive-like response in mice and induces a damage-repair-imbalance reaction.

The Association of Long-Term Exposure to Particulate Matter Air Pollution with Brain MRI Findings: The ARIC Study.

Background:Increasing evidence links higher particulate matter (PM) air pollution exposure to late-life cognitive impairment. However, few studies have considered associations between direct estimates of long-term past exposures and brain MRI findings indicative of neurodegeneration or cerebrovascular disease.Objective:Our objective was to quantify the association between brain MRI findings and PM exposures approximately 5 to 20 y prior to MRI in the Atherosclerosis Risk in Communities (ARIC) study.Methods:ARIC is based in four U.S. sites: Washington County, Maryland; Minneapolis suburbs, Minnesota; Forsyth County, North Carolina; and Jackson, Mississippi. A subset of ARIC participants underwent 3T brain MRI in 2011–2013 (). We estimated mean exposures to PM with an aerodynamic diameter less than 10 or ( and ) in 1990–1998, 1999–2007, and 1990–2007 at the residential addresses of eligible participants with MRI data. We estimated site-specific associations between PM and brain MRI findings and used random-effect, inverse variance–weighted meta-analysis to combine them.Results:In pooled analyses, higher mean and exposure in all time periods were associated with smaller deep-gray brain volumes, but not other MRI markers. Higher exposures were consistently associated with smaller total and regional brain volumes in Minnesota, but not elsewhere.Conclusions:Long-term past PM exposure in was not associated with markers of cerebrovascular disease. Higher long-term past PM exposures were associated with smaller deep-gray volumes overall, and higher exposures were associated with smaller brain volumes in the Minnesota site. Further work is needed to understand the sources of heterogeneity across sites. https://doi.org/10.1289/EHP2152