BACKGROUND: The prevalence of metabolic syndrome (MetS) has increased rapidly, with considerable variation between European countries. The study examined the relationship between air pollutants, greenspace, and MetS and its components in the Czech and Swiss populations. METHODS: Cross-sectional data from the Czech Health, Alcohol and Psychosocial Factors in Eastern Europe (HAPIEE) (n = 4,931) and the Swiss cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) (n = 4,422) cohorts included participants aged 44-73 years. MetS was defined as abdominal obesity plus two additional components (hypertension, diabetes, low high-density lipoprotein cholesterol, and elevated triglycerides). Annual mean concentrations of PM10, PM2.5, NO2, and greenspace (defined as the annual mean of normalized difference vegetation index within 500 m) were assigned to the individual residential level. We estimated odds ratios (OR) using multivariable logistic regressions with cluster-robust standard error, controlling for multiple confounders. RESULTS: The prevalence of MetS was significantly higher in the Czech (51.1%) compared with Swiss (35.8%) population as were the concentration means of PM10 and PM2.5. In HAPIEE, a 5 μg/m3 increase in PM2.5 was associated with 14% higher odds of MetS (OR = 1.14; 95% confidence interval [CI] = 1.01, 1.28). In SAPALDIA, no evidence was found for the associations between air pollutants and MetS (e.g. OR = 1.01; 95% CI = 0.90, 1.13 for PM2.5). No protective effects of normalized difference vegetation index on MetS were observed. Upon inspection of MetS components, PM2.5 and PM10 exposures were associated with higher odds of hypertension and elevated triglycerides in HAPIEE only, while PM2.5, PM10, and NO2 were associated with higher odds of diabetes in SAPALDIA only. CONCLUSION: Individuals with higher exposures to PM2.5 may be at higher risk of MetS. The differential associations with MetS components between the cohorts deserve further investigation.

• Publication type
• Journal Article MeSH

The aim of the study was to analyze the variables that modify the levels of oxidative DNA damage and lipid peroxidation in non-smoking mothers and their newborns from environmentally distinct localities of the Czech Republic: Ceske Budejovice (CB, an agricultural region) and Karvina (an industrial region). Personal, socio-economic and medical data, concentrations of particulate matter of aerodynamic diameter < 2.5 μm (PM2.5) and benzo[a]pyrene (B[a]P) in the ambient air, the activities of antioxidant mechanisms (superoxide dismutase, catalase, glutathione peroxidase) and antioxidant capacity), the levels of pro-inflammatory cytokines, the concentrations of persistent organic pollutants (POPs) in blood plasma/cord blood plasma and urinary levels of polycyclic aromatic hydrocarbons metabolites (OH-PAHs) were investigated as parameters potentially affecting the markers of DNA oxidation (8-oxo-7,8-dihydro-2'-deoxyguanosine, 8-oxodG) and lipid peroxidation (15-F2t-isoprostane, 15-F2t-IsoP). Significantly higher levels of POPs were detected in the plasma of mothers/newborns from CB (p < 0.001), while increased external levels of B[a]P and PM2.5, confirmed by analyzing urinary OH-PAHs, were found in Karvina subjects (p < 0.001). In mothers, multivariate analysis showed no significant difference in oxidative stress markers (15-F2t-IsoP, 8-oxodG) between the two localities. The analysis further revealed that neither in CB nor, unexpectedly, in Karvina, did PAH exposure affect maternal lipid peroxidation. Significant associations between OH-PAHs and 15-F2t-IsoP or 8-oxodG were observed only in newborns. In addition, multivariate analyses revealed a borderline significant association between locality and 8-oxodG in the urine of all newborns (p = 0.05). In conclusion, not only the maternal exposure of PAHs but also some POPs can negatively affect oxidative stress status in the early-life of newborns.

• Publication type
• Journal Article MeSH

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

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

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

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

OBJECTIVES: The purpose of this quantitative study is to assess the impact of fine particles air pollution in major cities of Slovakia. The study aims to estimate number of premature deaths from long-term exposure to fine particles PM2.5 in eight regional capitals of Slovakia in the period 2016-2020. Consequently, the study aims to conduct a comparative analysis using secondary derived indicators. METHODS: For calculations of estimated premature deaths from long-term exposure to fine particles PM2.5 air pollution we used standardized methodology developed by the World Health Organization and the European Environment Agency. RESULTS: The annual average of estimated premature deaths from PM2.5 air pollution in the studied period was in Bratislava 353, Košice 219, Prešov 84, Žilina 90, Banská Bystrica 76, Nitra 73, Trnava 59, and Trenčín 52. In relative terms per 1,000 inhabitants Bratislava had annual average 1.14 of estimated premature deaths, Košice 1.32, Prešov 1.38, Žilina 1.61, Banská Bystrica 1.35, Nitra 1.35, Trnava 1.27, and Trenčín 1.31. Bratislava as the largest city in Slovakia recorded the smallest relative number of estimated premature deaths. The worst results were recorded by the city of Žilina. CONCLUSIONS: The estimated number of premature deaths from long-term exposure to particulate matter air pollution in the regional capitals decreased in the given period. The most of the regional capitals with the exception of Bratislava and Žilina, showed similar levels of estimated premature deaths. However, the current geopolitical situation and rising energy prices threaten return to solid fuel burning which is the largest source of particulate matter air pollution in Slovakia and thus reversing positive trends.

• MeSH
• Air Pollutants * MeSH
• Humans MeSH
• Particulate Matter MeSH
• Mortality, Premature MeSH
• Environmental Exposure adverse effects   MeSH
• Air Pollution * adverse effects   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Geographicals
• Slovakia MeSH

BACKGROUND: Evidence on the potential interactive effects of heat and ambient air pollution on cause-specific mortality is inconclusive and limited to selected locations. OBJECTIVES: We investigated the effects of heat on cardiovascular and respiratory mortality and its modification by air pollution during summer months (six consecutive hottest months) in 482 locations across 24 countries. METHODS: Location-specific daily death counts and exposure data (e.g., particulate matter with diameters ≤ 2.5 μm [PM2.5]) were obtained from 2000 to 2018. We used location-specific confounder-adjusted Quasi-Poisson regression with a tensor product between air temperature and the air pollutant. We extracted heat effects at low, medium, and high levels of pollutants, defined as the 5th, 50th, and 95th percentile of the location-specific pollutant concentrations. Country-specific and overall estimates were derived using a random-effects multilevel meta-analytical model. RESULTS: Heat was associated with increased cardiorespiratory mortality. Moreover, the heat effects were modified by elevated levels of all air pollutants in most locations, with stronger effects for respiratory than cardiovascular mortality. For example, the percent increase in respiratory mortality per increase in the 2-day average summer temperature from the 75th to the 99th percentile was 7.7% (95% Confidence Interval [CI] 7.6-7.7), 11.3% (95%CI 11.2-11.3), and 14.3% (95% CI 14.1-14.5) at low, medium, and high levels of PM2.5, respectively. Similarly, cardiovascular mortality increased by 1.6 (95%CI 1.5-1.6), 5.1 (95%CI 5.1-5.2), and 8.7 (95%CI 8.7-8.8) at low, medium, and high levels of O3, respectively. DISCUSSION: We observed considerable modification of the heat effects on cardiovascular and respiratory mortality by elevated levels of air pollutants. Therefore, mitigation measures following the new WHO Air Quality Guidelines are crucial to enhance better health and promote sustainable development.

• MeSH
• Cardiovascular Diseases * MeSH
• Air Pollutants * toxicity   analysis   MeSH
• Environmental Pollutants * MeSH
• Humans MeSH
• Mortality MeSH
• Respiratory Tract Diseases * MeSH
• Particulate Matter adverse effects   analysis   MeSH
• Cities MeSH
• Hot Temperature MeSH
• Environmental Exposure adverse effects   analysis   MeSH
• Air Pollution * adverse effects   analysis   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Geographicals
• Cities MeSH

BACKGROUND: The impact of the urban environment on human health is a contemporary subject of environmental research. Air pollution is often considered a leading environmental driver. However, a plethora of other factors within the urban exposome may be involved. At the same time, the resolution of spatial data is also an important facet to consider. Generally, systematic tools for accurate health risk assessment in the urban environment are missing or are not implemented. METHODS: The long-term impact of air quality (PM10, PM2.5, NO2, benzene, and SO2) on respiratory and cardiovascular health was assessed with a log-linear model. We used the most accurate health data in high city scale spatial resolution over the period 2010 to 2018. Selected external exposome parameters were also included in the analysis. RESULTS: Statistically significant associations between air pollution and the health of the urban population were found. The strongest association was between benzene and the incidence of bronchitis in the adult population [RR 1.552 95% CI (1.415-1.704) per 0.5 μg/m3 change in benzene concentration]. A similar relation was observed between NO2 and the same health condition [RR 1.483 95% CI (1.227-1.792) per 8.9 μg/m3 of change in NO2]. Other weaker associations were also found between asthma in children and PMs, NO2, or benzene. Cardiovascular-related hospitalizations in the general population were linked with NO2 [RR 1.218 95% CI (1.119-1.325) per 9.7 μg/m3 change in NO2]. The remaining pollutants were slightly less but still significantly associated with cardiovascular-related hospitalizations. CONCLUSION: Our findings are mostly highly statistically significant (p ≤ 0.001) and are in line with current literature on the adverse effects of air pollution on the human population. The results highlight the need for continual improvements in air quality. We propose the implementation of this approach as a systematic tool for the investigation of possible health risks over a long period of time. However, further research involving other variables is an essential step toward understanding the complex urban exposome and its implications for human health. An increase in data spatial resolution is especially important in this respect as well as for improving city health risk management.

• MeSH
• Benzene analysis   MeSH
• Child MeSH
• Adult MeSH
• Air Pollutants * adverse effects   analysis   MeSH
• Humans MeSH
• Nitrogen Dioxide analysis   MeSH
• Cities epidemiology   MeSH
• Air Pollution * adverse effects   analysis   MeSH
• Check Tag
• Child MeSH
• Adult MeSH
• Humans MeSH
• Publication type
• Journal Article MeSH
• Geographicals
• Cities epidemiology   MeSH