BACKGROUND: Telomere length is a biomarker of cellular aging, influenced by various environmental and lifestyle factors. Air pollution is a known environmental stressor that may impact telomere dynamics. This study aimed to investigate the effect of age, lifetime exposure to air pollution, inflammatory parameters and selected lifestyle factors on telomere length. METHODS: The study included 356 participants aged 35-65 living in two regions with varying pollution. Telomere length was measured using qPCR. Individual lifetime exposures to PM10, PM2.5, NO2, benzo(a)pyrene and benzene were calculated based on historical air quality data. Statistical analysis of age, pollution exposure, inflammatory parameters, and lifestyle factors on telomere length was performed using logistic regression and generalized linear models, with odds ratios calculated. RESULTS: Unexpectedly, higher air pollutants lifetime exposures were associated with longer telomeres, particularly for PM10 51-55 μg/m3 (OR = 5.67, p < 0.001), PM2.5 42-45 μg/m3 (OR = 6.56, p < 0.001), B(a)P 6.9-8.3 ng/m3 (OR = 5.25, p = 0.002), NO2 26-27 μg/m3 (OR = 5.22, p = 0.001) and benzene 2.45-2.75 μg/m3 (OR = 6.13, p < 0.001). Age significantly affected telomere length, with older individuals having shorter telomeres. Socioeconomic factors such as college education were positively associated with longer telomeres, while lifestyle factors did not show significant associations. IL-8 was identified as a significant inflammatory marker negatively associated with very long telomeres. CONCLUSION: These baseline findings bring new perspective to the relationship between air pollution and telomere length. Contrary to traditional views, the results suggest potential adaptive responses, highlighting the need for further longitudinal research to explore telomere dynamics over time in conjunction with other factors.

• MeSH
• Benzene analysis   adverse effects   MeSH
• Benzo(a)pyrene analysis   MeSH
• Adult MeSH
• Telomere Homeostasis * MeSH
• Cohort Studies MeSH
• Air Pollutants * analysis   adverse effects   MeSH
• Middle Aged MeSH
• Humans MeSH
• Nitrogen Dioxide analysis   MeSH
• Particulate Matter analysis   adverse effects   MeSH
• Aged MeSH
• Telomere * drug effects   MeSH
• Environmental Exposure * analysis   adverse effects   MeSH
• Life Style MeSH
• Air Pollution * adverse effects   analysis   MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

BACKGROUND: Evidence on the impact of complex neighborhood environment, including air pollution, greenness, and neighborhood socioeconomic deprivation (nSED) on cognitive health in older adults remains scarce. Both cognition and neighborhood environment are associated with physical activity, but little is known about the potential mediating role of physical activity in this association. METHODS: Cross-sectional data of the Czech arm of the HAPIEE cohort study examined 4,178 participants (55.6% women) aged 45-69 years. Global cognitive score was constructed from memory, verbal fluency, and concentration domains. The exposures, assigned to participant's addresses, include 4-year (2000-2003) average concentrations of PM2.5, greenness index calculated from tree crown canopy cover estimation (2000), and census-based nSED characteristics. Physical activity and other covariates were assessed by a questionnaire. Structural equation modelling was used to estimate standardized β coefficients for the relationships between neighborhood environment, physical activity and cognitive performance. RESULTS: After controlling for a range of covariates, global cognitive function was inversely associated with PM2.5 (β = -0.087; 95%CI: 0.122 to -0.052) and nSED (β = -0.147; 95%CI: 0.182 to -0.115), and positively associated with greenness (β = 0.036; 95%CI: 0.001 to 0.069). We identified a weak but statistically significant mediating role of physical activity in the associations of PM2.5 exposures and nSED on global cognitive score. Total mediation proportions ranged from 3.9% to 6.5% for nSED and PM2.5, respectively. CONCLUSIONS: The neighborhood environment was associated with cognitive health in older individuals; the associations were partially mediated by physical activity.

• MeSH
• Residence Characteristics * MeSH
• Neighborhood Characteristics MeSH
• Exercise * MeSH
• Cognition * MeSH
• Air Pollutants analysis   MeSH
• Middle Aged MeSH
• Humans MeSH
• Particulate Matter analysis   MeSH
• Cross-Sectional Studies MeSH
• Aged MeSH
• Air Pollution analysis   MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Geographicals
• Czech Republic MeSH

Carbonaceous aerosols (CA), composed of black carbon (BC) and organic matter (OM), significantly impact the climate. Light absorption properties of CA, particularly of BC and brown carbon (BrC), are crucial due to their contribution to global and regional warming. We present the absorption properties of BC (bAbs,BC) and BrC (bAbs,BrC) inferred using Aethalometer data from 44 European sites covering different environments (traffic (TR), urban (UB), suburban (SUB), regional background (RB) and mountain (M)). Absorption coefficients showed a clear relationship with station setting decreasing as follows: TR > UB > SUB > RB > M, with exceptions. The contribution of bAbs,BrC to total absorption (bAbs), i.e. %AbsBrC, was lower at traffic sites (11-20 %), exceeding 30 % at some SUB and RB sites. Low AAE values were observed at TR sites, due to the dominance of internal combustion emissions, and at some remote RB/M sites, likely due to the lack of proximity to BrC sources, insufficient secondary processes generating BrC or the effect of photobleaching during transport. Higher bAbs and AAE were observed in Central/Eastern Europe compared to Western/Northern Europe, due to higher coal and biomass burning emissions in the east. Seasonal analysis showed increased bAbs, bAbs,BC, bAbs,BrC in winter, with stronger %AbsBrC, leading to higher AAE. Diel cycles of bAbs,BC peaked during morning and evening rush hours, whereas bAbs,BrC, %AbsBrC, AAE, and AAEBrC peaked at night when emissions from household activities accumulated. Decade-long trends analyses demonstrated a decrease in bAbs, due to reduction of BC emissions, while bAbs,BrC and AAE increased, suggesting a shift in CA composition, with a relative increase in BrC over BC. This study provides a unique dataset to assess the BrC effects on climate and confirms that BrC can contribute significantly to UV-VIS radiation presenting highly variable absorption properties in Europe.

• MeSH
• Aerosols * analysis   MeSH
• Air Pollutants analysis   MeSH
• Environmental Monitoring MeSH
• Particulate Matter analysis   MeSH
• Light MeSH
• Carbon * analysis   MeSH
• Publication type
• Journal Article MeSH
• Geographicals
• Europe MeSH

Persons living in industrial environments are exposed to levels of air pollution that can affect their health and fertility. The Czech capital city, Prague, and the Ostrava industrial agglomeration differ in their major sources of air pollution. In Prague, heavy traffic produces high levels of nitrogen oxides throughout the year. In the Ostrava region, an iron industry and local heating are sources of particulate matter (PM) and benzo[a]pyrene (B[a]P), especially in the winter. We evaluated the effects of air pollution on human sperm mitochondrial DNA (mtDNA). Using real-time PCR, we analysed sperm mtDNA copy number and deletion rate in Prague city policemen in two seasons (spring and autumn) and compared the results with those from Ostrava. In Prague, the sperm mtDNA deletion rate was significantly higher in autumn than in spring, which is the opposite of the results from Ostrava. The sperm mtDNA copy number did not show any seasonal differences in either of the cities; it was correlated negatively with sperm concentration, motility, and viability, and with sperm chromatin integrity (assessed with the Sperm Chromatin Structure Assay). The comparison between the two cities showed that the sperm mtDNA deletion rate in spring and the sperm mtDNA copy number in autumn were significantly lower in Prague vs. Ostrava. Our study supports the hypothesis that sperm mtDNA deletion rate is affected by the composition of air pollution. Sperm mtDNA abundance is closely associated with chromatin damage and standard semen characteristics.

• MeSH
• Adult MeSH
• Air Pollutants toxicity   adverse effects   MeSH
• Humans MeSH
• DNA, Mitochondrial * genetics   MeSH
• Sperm Motility drug effects   MeSH
• Particulate Matter toxicity   adverse effects   MeSH
• Police MeSH
• Seasons MeSH
• Spermatozoa * drug effects   MeSH
• DNA Copy Number Variations * MeSH
• Air Pollution * adverse effects   MeSH
• Check Tag
• Adult MeSH
• Humans MeSH
• Male MeSH
• Publication type
• Journal Article MeSH
• Comparative Study MeSH
• Geographicals
• Czech Republic MeSH

The aim of this study was to investigate the relationship between source-specific ambient particulate air pollution concentrations and the incidence of dementia. The study encompassed 70,057 participants from the Västerbotten intervention program cohort in Northern Sweden with a median age of 40 years at baseline. High-resolution dispersion models were employed to estimate source-specific particulate matter (PM) concentrations, such as PM10 and PM2.5 from traffic, exhaust, and biomass (mainly wood) burning, at the residential addresses of each participant. Cox regression models, adjusted for potential confounding factors, were used for the assessment. Over 884,847 person-years of follow-up, 409 incident dementia cases, identified through national registers, were observed. The study population's average exposure to annual mean total PM10 and PM2.5 lag 1-5 years was 9.50 μg/m3 and 5.61 μg/m3, respectively. Increased risks were identified for PM10-Traffic (35% [95% CI 0-82%]) and PM2.5-Exhaust (33% [95% CI - 2 to 79%]) in the second exposure tertile for lag 1-5 years, although no such risks were observed in the third tertile. Interestingly, a negative association was observed between PM2.5-Wood burning and the risk of dementia. In summary, this register-based study did not conclusively establish a strong association between air pollution exposure and the incidence of dementia. While some evidence indicated elevated risks for PM10-Traffic and PM2.5-Exhaust, and conversely, a negative association for PM2.5-Wood burning, no clear exposure-response relationships were evident.

• MeSH
• Dementia * epidemiology   etiology   MeSH
• Adult MeSH
• Incidence MeSH
• Cohort Studies MeSH
• Air Pollutants analysis   adverse effects   MeSH
• Middle Aged MeSH
• Humans MeSH
• Particulate Matter * analysis   adverse effects   MeSH
• Aged MeSH
• Environmental Exposure * adverse effects   MeSH
• Air Pollution * adverse effects   analysis   MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Geographicals
• Sweden MeSH

The article assesses differences in lifetime losses caused by premature deaths from cardiopulmonary disease in populations living in areas with different environmental burdens. The results provide different perspectives on data on total years lost and lifetime losses attributable to air pollution. Such lifetime losses in the industrial area related to cardiovascular causes of death are 7.6 or 5.1 years per male or female deceased, representing an average lifetime loss of 0.01907 years (i.e. 7 days) per 1 male or 0.01273 years (i.e. 4.6 days) per 1 female in the entire population. Losses related to cerebrovascular or respiratory causes of death are about 5.4 or 5.9 years per 1 deceased male or 3.9 or 5 years per 1 deceased female, respectively, which represents a loss of 0.00481 (1.8 days), or 0.00148 years (0.5 days) per 1 male or 0.00466 (1.7 days), or 0.00058 years (0.2 days) per 1 female.

• MeSH
• Cardiovascular Diseases * chemically induced   epidemiology   MeSH
• Air Pollutants * toxicity   analysis   MeSH
• Humans MeSH
• Respiratory Tract Diseases * chemically induced   epidemiology   MeSH
• Particulate Matter analysis   MeSH
• Mortality, Premature MeSH
• Environmental Exposure adverse effects   analysis   MeSH
• Air Pollution * adverse effects   analysis   MeSH
• Check Tag
• Humans MeSH
• Male MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

BACKGROUND: Model-estimated air pollution exposure products have been widely used in epidemiological studies to assess the health risks of particulate matter with diameters of ≤2.5 μm (PM2.5). However, few studies have assessed the disparities in health effects between model-estimated and station-observed PM2.5 exposures. METHODS: We collected daily all-cause, respiratory and cardiovascular mortality data in 347 cities across 15 countries and regions worldwide based on the Multi-City Multi-Country collaborative research network. The station-observed PM2.5 data were obtained from official monitoring stations. The model-estimated global PM2.5 product was developed using a machine-learning approach. The associations between daily exposure to PM2.5 and mortality were evaluated using a two-stage analytical approach. RESULTS: We included 15.8 million all-cause, 1.5 million respiratory and 4.5 million cardiovascular deaths from 2000 to 2018. Short-term exposure to PM2.5 was associated with a relative risk increase (RRI) of mortality from both station-observed and model-estimated exposures. Every 10-μg/m3 increase in the 2-day moving average PM2.5 was associated with overall RRIs of 0.67% (95% CI: 0.49 to 0.85), 0.68% (95% CI: -0.03 to 1.39) and 0.45% (95% CI: 0.08 to 0.82) for all-cause, respiratory, and cardiovascular mortality based on station-observed PM2.5 and RRIs of 0.87% (95% CI: 0.68 to 1.06), 0.81% (95% CI: 0.08 to 1.55) and 0.71% (95% CI: 0.32 to 1.09) based on model-estimated exposure, respectively. CONCLUSIONS: Mortality risks associated with daily PM2.5 exposure were consistent for both station-observed and model-estimated exposures, suggesting the reliability and potential applicability of the global PM2.5 product in epidemiological studies.

• MeSH
• Adult MeSH
• Cardiovascular Diseases * mortality   MeSH
• Air Pollutants * adverse effects   analysis   MeSH
• Middle Aged MeSH
• Humans MeSH
• Environmental Monitoring methods   MeSH
• Mortality trends   MeSH
• Respiratory Tract Diseases mortality   MeSH
• Particulate Matter * adverse effects   analysis   MeSH
• Aged MeSH
• Machine Learning MeSH
• Cities * epidemiology   MeSH
• Environmental Exposure * adverse effects   MeSH
• Air Pollution * adverse effects   analysis   MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Research Support, N.I.H., Extramural MeSH
• Comparative Study MeSH
• Geographicals
• Cities * epidemiology   MeSH

Environmental exposure is associated with increased incidence of respiratory and cardiovascular diseases and reduced fertility. Exposure to air pollution can influence gene expression through epigenetic mechanisms. In this study, we analysed gene-specific CpG methylation in spermatozoa of city policemen occupationally exposed to air pollution in two Czech cities differing by sources and composition of the air pollution. In Prague, the pollution is mainly formed by NO2 from heavy traffic. Ostrava is a hotspot of industrial air pollution with high concentrations of particular matter (PM) and benzo[a]pyrene (B[a]P). We performed genome-wide methylation sequencing using the SureSelectXT Human Methyl-Seq system (Agilent Technologies) and next-generation sequencing to reveal differentially methylated CpG sites and regions. We identified differential methylation in the region chr5:662169 - 663376 annotated to genes CEP72 and TPPP. The region was then analysed in sperm DNA from 117 policemen using targeted methylation sequencing, which proved its hypermethylation in sperm of Ostrava policemen.

• MeSH
• Adult MeSH
• Air Pollutants * analysis   toxicity   MeSH
• Middle Aged MeSH
• Humans MeSH
• DNA Methylation * drug effects   MeSH
• Particulate Matter analysis   toxicity   MeSH
• Police MeSH
• Occupational Exposure MeSH
• Spermatozoa * drug effects   MeSH
• Air Pollution * adverse effects   analysis   MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Publication type
• Journal Article MeSH
• Geographicals
• Czech Republic MeSH

Air pollution is the leading cause of lung cancer after tobacco smoking, contributing to 20% of all lung cancer deaths. Increased risk associated with living near trafficked roads, occupational exposure to diesel exhaust, indoor coal combustion and cigarette smoking, suggest that combustion components in ambient fine particulate matter (PM2.5), such as polycyclic aromatic hydrocarbons (PAHs), may be central drivers of lung cancer. Activation of the aryl hydrocarbon receptor (AhR) induces expression of xenobiotic-metabolizing enzymes (XMEs) and increase PAH metabolism, formation of reactive metabolites, oxidative stress, DNA damage and mutagenesis. Lung cancer tissues from smokers and workers exposed to high combustion PM levels contain mutagenic signatures derived from PAHs. However, recent findings suggest that ambient air PM2.5 exposure primarily induces lung cancer development through tumor promotion of cells harboring naturally acquired oncogenic mutations, thus lacking typical PAH-induced mutations. On this background, we discuss the role of AhR and PAHs in lung cancer development caused by air pollution focusing on the tumor promoting properties including metabolism, immune system, cell proliferation and survival, tumor microenvironment, cell-to-cell communication, tumor growth and metastasis. We suggest that the dichotomy in lung cancer patterns observed between smoking and outdoor air PM2.5 represent the two ends of a dose-response continuum of combustion PM exposure, where tumor promotion in the peripheral lung appears to be the driving factor at the relatively low-dose exposures from ambient air PM2.5, whereas genotoxicity in the central airways becomes increasingly more important at the higher combustion PM levels encountered through smoking and occupational exposure.

• MeSH
• Air Pollutants * toxicity   MeSH
• Humans MeSH
• Environmental Monitoring MeSH
• Tumor Microenvironment MeSH
• Lung Neoplasms * chemically induced   genetics   MeSH
• Particulate Matter toxicity   MeSH
• Polycyclic Aromatic Hydrocarbons * toxicity   MeSH
• Receptors, Aryl Hydrocarbon genetics   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Research Support, N.I.H., Extramural MeSH

• MeSH
• Diabetes Mellitus * epidemiology   MeSH
• Hypertension * epidemiology   MeSH
• Air Pollutants * analysis   MeSH
• Humans MeSH
• Nitrogen Dioxide analysis   MeSH
• Particulate Matter analysis   MeSH
• Prevalence MeSH
• Environmental Exposure analysis   MeSH
• Life Style MeSH
• Air Pollution * analysis   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH