Mean Annual Exposure Research Articles

Air Pollution and Parkinson Disease in a Population-Based Study

The role of air pollution in risk and progression of Parkinson disease (PD) is unclear. To assess whether air pollution is associated with increased risk of PD and clinical characteristics of PD. This population-based case-control study included patients with PD and matched controls from the Rochester Epidemiology Project from 1998 to 2015. Data were analyzed from January to June 2024. Mean annual exposure to particulate matter with a diameter of 2.5 µm or less (PM2.5) from 1998 to 2015 and mean annual exposure to nitrogen dioxide (NO2) from 2000 to 2014. Outcomes of interest were PD risk, all-cause mortality, presence of tremor-predominant vs akinetic rigid PD, and development of dyskinesia. Models were adjusted for age, sex, race and ethnicity, year of index, and urban vs rural residence. A total of 346 patients with PD (median [IQR] age 72 [65-80] years; 216 [62.4%] male) were identified and matched on age and sex with 4813 controls (median [IQR] age, 72 [65-79] years, 2946 [61.2%] male). Greater PM2.5 exposure was associated with increased PD risk, and this risk was greatest after restricting to populations within metropolitan cores (odds ratio [OR], 1.23; 95% CI, 1.11-1.35) for the top quintile of PM2.5 exposure compared with the bottom quintile. Greater NO2 exposure was also associated with increased PD risk when comparing the top quintile with the bottom quintile (OR, 1.13; 95% CI, 1.07-1.19). Air pollution was associated with a 36% increased risk of akinetic rigid presentation (OR per each 1-μg/m3 increase in PM2.5, 1.36; 95% CI, 1.02-1.80). In analyses among patients with PD only, higher PM2.5 exposure was associated with greater risk for developing dyskinesia (HR per 1-μg/m3 increase in PM2.5, 1.42; 95% CI, 1.17-1.73), as was increased NO2 exposure (HR per 1 μg/m3 increase in NO2, 1.13; 95% CI, 1.06-1.19). There was no association between PM2.5 and all-cause mortality among patients with PD. In this case-control study of air pollution and PD, higher levels of PM2.5 and NO2 exposure were associated with increased risk of PD; also, higher levels of PM2.5 exposure were associated with increased risk of developing akinetic rigid PD and dyskinesia compared with patients with PD exposed to lower levels. These findings suggest that reducing air pollution may reduce risk of PD, modify the PD phenotype, and reduce risk of dyskinesia.

Association between residential air pollution exposure and cardiovascular risk factors in adults living in northern France.

Air pollution is associated with elevated cardiovascular mortality and an increase in cardiovascular risk factors. However, the literature data on associations between air pollution and cardiovascular risk factors are contradictory. To explore the relationship between residential exposure to atmospheric pollutants and cardiovascular risk factors (lipid biomarker and blood pressure levels). We studied a sample of 2339 adult participants in the ELISABET study from the Dunkirk and Lille urban areas of France. The mean annual exposure to atmospheric pollutants (PM10, NO2 and SO2) at the home address was estimated via an air dispersion model. The associations were probed in multivariate linear regression models. The mean NO2 level was 26.05 μg/m3 in Lille and 19.96 µg/m3 in Dunkirk. The mean PM10 level was 27.02 μg/m3 in Lille and 26.53 μg/m3 in Dunkirk. We detected a significant association between exposure to air pollutants and the high-density lipoprotein (HDL) (which is a protective factor against cardiovascular diseases) level: for a 2 µg/m3 increment in PM10, the HDL level decreased by 1.72% (p = 0.0037). None of the associations with other lipid variables or with blood pressure were significant. We didn't find evidence significant associations for most of the risk factors but, long-term exposure of adults to moderate levels of ambient air pollution was associated with a decrement in HDL.

#506 Long-term exposure to air pollution and CKD-associated mortality: results from the pooled cohort of the European multicentre ELAPSE-study

Abstract Background and Aims Air pollution has been shown to be associated with cause-specific mortality. However, mortality due to chronic kidney disease (CKD) is understudied in this context, with no European data available so far. We investigated the relation between long-term exposure to air pollution and CKD-associated mortality in the Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE). Method Data of five population-based cohorts from four European countries from the pooled ELAPSE cohort were linked to data from local mortality registries. CKD-associated mortality was defined using ICD10 codes N18-N19 or corresponding ICD9 codes. Mean annual exposure at home address was determined with Europe-wide hybrid land use regression models for nitrogen dioxide (NO2), black carbon (BC), ozone (O3), particulate matter ≤2.5 µm (PM2.5) and several elemental constituents of PM2.5 with a spatial resolution of 100 m x 100 m. Cox regression models were adjusted for age (time-axis), cohort and sex (both as strata), calendar year of recruitment, smoking status, marital status, employment status and neighborhood mean income. Results Over a mean follow-up time of 20.4 years, 313 of 289,564 persons died from CKD. Associations were observed for all pollutants, positive for PM2.5 (hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03-1.66) per 5 µg/m3 increase), BC (1.26 (1.03-1.53) per 0.5 × 10− 5/m), NO2 (1.13 (0.93-1.38) per 10 µg/m3) and negative for O3 (0.71 (0.54-0.93) per 10 µg/m3). Results were robust when additionally adjusting for smoking intensity and duration, BMI, education or residential greenness, but susceptible to cohort selection. Findings are mainly based on the large Austrian cohort, that contributed 226 cases. Among the elemental constituents, Cu, Fe, K, Ni, S and Zn, representing different PM2.5 sources including traffic, industry, biomass and oil burning and long-range transport, were associated with CKD-related mortality. Conclusion In conclusion, our results suggest a possible association between air pollution from different sources with CKD-related mortality. Our results indicate that measures to improve air quality and decrease air pollution might also be beneficial from a renal perspective.

Sex-specific associations between air pollutants and asthma prevalence in Japanese adults: a population-based study

ABSTRACT This study investigated the association between air pollutants and asthma prevalence in male and female Japanese adults. In this retrospective cross-sectional analysis, annual mean exposure levels of air pollutants, specifically nitrogen dioxide (NO2) and particulate matter with a median aerodynamic diameter ≤2.5 μm (PM2.5), were assessed at a local monitoring site. Multivariable logistic regression models, adjusted for genetic and/or lifestyle factors, were used to explore the association between air pollutants and asthma, with stratification by sex. A total of 1,497 participants aged ≥40 years were included. Their mean age was 65.9 ± 12.4 years, with 847 being women. Overall, 91 participants were diagnosed with asthma. In the multivariable model, ambient exposure levels of NO2 and PM2.5 were significantly associated with asthma in women but not in men. This study highlights sex as a significant determinant of the link between air pollutants and asthma exacerbation, particularly among female Japanese adults.

Long-term exposure to air pollution and chronic kidney disease-associated mortality–Results from the pooled cohort of the European multicentre ELAPSE-study

Despite the known link between air pollution and cause-specific mortality, its relation to chronic kidney disease (CKD)-associated mortality is understudied. Therefore, we investigated the association between long-term exposure to air pollution and CKD-related mortality in a large multicentre population-based European cohort.Cohort data were linked to local mortality registry data. CKD-death was defined as ICD10 codes N18–N19 or corresponding ICD9 codes. Mean annual exposure at participant's home address was determined with fine spatial resolution exposure models for nitrogen dioxide (NO2), black carbon (BC), ozone (O3), particulate matter ≤2.5 μm (PM2.5) and several elemental constituents of PM2.5. Cox regression models were adjusted for age, sex, cohort, calendar year of recruitment, smoking status, marital status, employment status and neighbourhood mean income.Over a mean follow-up time of 20.4 years, 313 of 289,564 persons died from CKD. Associations were positive for PM2.5 (hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03–1.66) per 5 μg/m3, BC (1.26 (1.03–1.53) per 0.5 × 10− 5/m), NO2 (1.13 (0.93–1.38) per 10 μg/m3) and inverse for O3 (0.71 (0.54–0.93) per 10 μg/m3). Results were robust to further covariate adjustment. Exclusion of the largest sub-cohort contributing 226 cases, led to null associations. Among the elemental constituents, Cu, Fe, K, Ni, S and Zn, representing different sources including traffic, biomass and oil burning and secondary pollutants, were associated with CKD-related mortality.In conclusion, our results suggest an association between air pollution from different sources and CKD-related mortality.

Longitudinal associations between ambient PM2.5 exposure and lipid levels in two Indian cities.

Exposure to ambient PM2.5 is known to affect lipid metabolism through systemic inflammation and oxidative stress. Evidence from developing countries, such as India with high levels of ambient PM2.5 and distinct lipid profiles, is sparse. Longitudinal nonlinear mixed-effects analysis was conducted on >10,000 participants of Centre for cArdiometabolic Risk Reduction in South Asia (CARRS) cohort in Chennai and Delhi, India. We examined associations between 1-month and 1-year average ambient PM2.5 exposure derived from the spatiotemporal model and lipid levels (total cholesterol [TC], triglycerides [TRIG], high-density lipoprotein cholesterol [HDL-C], and low-density lipoprotein cholesterol [LDL-C]) measured longitudinally, adjusting for residential and neighborhood-level confounders. The mean annual exposure in Chennai and Delhi was 40 and 102 μg/m3 respectively. Elevated ambient PM2.5 levels were associated with an increase in LDL-C and TC at levels up to 100 µg/m3 in both cities and beyond 125 µg/m3 in Delhi. TRIG levels in Chennai increased until 40 µg/m3 for both short- and long-term exposures, then stabilized or declined, while in Delhi, there was a consistent rise with increasing annual exposures. HDL-C showed an increase in both cities against monthly average exposure. HDL-C decreased slightly in Chennai with an increase in long-term exposure, whereas it decreased beyond 130 µg/m3 in Delhi. These findings demonstrate diverse associations between a wide range of ambient PM2.5 and lipid levels in an understudied South Asian population. Further research is needed to establish causality and develop targeted interventions to mitigate the impact of air pollution on lipid metabolism and cardiovascular health.

Exposure of U.S. adults to microplastics from commonly-consumed proteins

We investigated microplastic (MP) contamination in 16 commonly-consumed protein products (seafoods, terrestrial meats, and plant-based proteins) purchased in the United States (U.S.) with different levels of processing (unprocessed, minimally-processed, and highly-processed), brands (1 – 4 per product type, depending on availability) and store types (conventional supermarket and grocer featuring mostly natural/organic products). Mean (±stdev) MP contamination per serving among the products was 74 ± 220 particles (ranging from 2 ± 2 particles in chicken breast to 370 ± 580 in breaded shrimp). Concentrations (MPs/g tissue) differed between processing levels, with highly-processed products containing significantly more MPs than minimally-processed products (p = 0.0049). There were no significant differences among the same product from different brands or store types. Integrating these results with protein consumption data from the American public, we estimate that the mean annual exposure of adults to MPs in these proteins is 11,000 ± 29,000 particles, with a maximum estimated exposure of 3.8 million MPs/year. These findings further inform estimations of human exposure to MPs, particularly from proteins which are important dietary staples in the U.S. Subsequent research should investigate additional drivers of MPs in the human diet, including other understudied food groups sourced from both within and outside the U.S.

Evaluation of outdoor radon levels and its dependence on the radium content in soil in the environs of Belagavi India

The paper presents the seasonal variation of outdoor radon levels and the measured lung dose to the population of the Belagavi region of India. The outdoor radon levels were measured in different seasons using LR-115 (type II) films fixed in a pin-hole cup detector. The outdoor radon levels in this work were found to be high in summer with values ranging from 11.8 to 27.3 Bq m−3 with a mean value of 20.0 Bq m−3. Lower radon levels were observed in monsoon season and the values range from 3.8 to 15.8 Bq m−3, with a mean value of 10.0 Bq m−3. The potential alpha energy concentration was maximum in summer with a mean value of 3.3 mWLM. The mean annual exposure was found to be 1.4 mWLM and the mean annual inhalation dose was 0.2 mSv y−1. The activity of 226Ra in soils was measured using a NaI (Tl) detector based on gamma ray spectrometer. The 226Ra activity of the study area was in the range of 16.5 to 70.4 Bq kg−1 with a mean value of 32.4 Bq kg−1. The correlation coefficient between the radium content in soil and outdoor radon levels was studied. The present study shows a significant correlation of 0.7, between outdoor radon levels and the radium content in the soil.

Wood heater smoke and mortality in the Australian Capital Territory: a rapid health impact assessment.

To estimate the number of deaths and the cost of deaths attributable to wood heater smoke in the Australian Capital Territory. Rapid health impact assessment, based on fine particulate matter (PM2.5 ) data from three outdoor air pollution monitors and published exposure-response functions for natural cause mortality attributed to PM2.5 exposure. Australian Capital Territory (population, 2021: 454 000), 2016-2018, 2021, and 2022 (2019 and 2020 excluded because of the impact of extreme bushfires on air quality). Proportion of PM2.5 exposure attributable to wood heaters; numbers of deaths and associated cost of deaths (based on the value of statistical life: $5.3 million) attributable to wood heater smoke. Wood heater emissions contributed an estimated 1.16-1.73 μg/m3 to the annual mean PM2.5 concentration during the three colder years (2017, 2018, 2021), or 17-25% of annual mean exposure, and 0.72 μg/m3 (15%) or 0.89 μg/m3 (13%) during the two milder years (2016, 2022). Using the most conservative exposure-response function, the estimated annual number of deaths attributable to wood heater smoke was 17-26 during the colder three years and 11-15 deaths during the milder two years. Using the least conservative exposure-response function, an estimated 43-63 deaths per year (colder years) and 26-36 deaths per year (milder years) were attributable to wood heater smoke. The estimated annual equivalent cost of deaths was $57-136 million (most conservative exposure-response function) and $140-333 million (least conservative exposure-response function). The estimated annual number of deaths in the ACT attributable to wood heater PM2.5 pollution is similar to that attributed to the extreme smoke of the 2019-20 Black Summer bushfires. The number of wood heaters should be reduced by banning new installations and phasing out existing units in urban and suburban areas.

Linking Air Pollution Exposure to Blood-Based Metabolic Features in a Community-Based Aging Cohort with and without Dementia.

Long-term exposure to air pollution has been associated with changes in levels of metabolites measured in the peripheral blood. However, most research has been conducted in ethnically homogenous, young or middle-aged populations. To study the relationship between the plasma metabolome and long-term exposure to three air pollutants: particulate matter (PM) less than 2.5μm in aerodynamic diameter (PM2.5), PM less than 10μm in aerodynamic diameter (PM10), and nitrogen dioxide (NO2) in an ethnically diverse, older population. Plasma metabolomic profiles of 107 participants of the Washington Heights and Inwood Community Aging Project in New York City, collected from 1995-2015, including non-Hispanic white, Caribbean Hispanic, and non-Hispanic Black older adults were used. We estimated the association between each metabolic feature and predicted annual mean exposure to the air pollutants using three approaches: 1) A metabolome wide association study framework; 2) Feature selection using elastic net regression; and 3) A multivariate approach using partial-least squares discriminant analysis. 79 features associated with exposure to PM2.5 but none associated with PM10 or NO2. PM2.5 exposure was associated with altered amino acid metabolism, energy production, and oxidative stress response, pathways also associated with Alzheimer's disease. Three metabolites were associated with PM2.5 exposure through all three approaches: cysteinylglycine disulfide, a diglyceride, and a dicarboxylic acid. The relationship between several features and PM2.5 exposure was modified by diet and metabolic diseases. These relationships uncover the mechanisms through which PM2.5 exposure can lead to altered metabolic outcomes in an older population.

Long-term exposure to air pollution and prevalent nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is a disease characterized by lipid accumulation within hepatocytes, ranging from simple steatosis to steatohepatitis, in the absence of secondary causes of hepatic fat accumulation. Although air pollution (AP) has been associated with several conditions related to NAFLD (e.g., metabolic syndrome, type 2 diabetes mellitus), few studies have explored an association between AP and NAFLD. The aim of the study was to investigate whether exposure to AP is associated with NAFLD prevalence. We used baseline cross-sectional data (2000-2003) of the Heinz-Nixdorf-Recall cohort study in Germany (baseline n = 4,814), a prospective population-based cohort study in the urbanized Ruhr Area. Mean annual exposure to size-fractioned particulate matter (PM10, PM2.5, PMcoarse, and PM2.5abs), nitrogen dioxide, and particle number was assessed using two different exposure models: a chemistry transport dispersion model, which captures urban background AP exposure on a 1 km2 grid at participant's residential addresses, and a land use regression model, which captures point-specific AP exposure at participant's residential addresses. NAFLD was assessed with the fatty liver index (n = 4,065), with NAFLD defined as fatty liver index ≥60. We estimated ORs of NAFLD per interquartile range of exposure using logistic regression, adjusted for socio-demographic and lifestyle variables. We observed a NAFLD prevalence of 31.7% (n = 1,288). All air pollutants were positively associated with NAFLD prevalence, with an OR per interquartile range for PM2.5 of 1.11 (95% confidence interval [CI] = 1.00, 1.24) using chemistry transport model, and 1.06 (95% CI = 0.94, 1.19) using the land use regression model, respectively. There was a positive association between long-term AP exposure and NAFLD.

Fine particulate matter air pollution and the mortality of children under five: a multilevel analysis of the Ethiopian Demographic and Health Survey of 2016.

Every year, polluted air is costing the globe 543,000 deaths of children under five. The particulate matter below 2.5 μm diameter (PM2.5) is a part of air pollution that has adverse effects on children's health. In Ethiopia, the effect of ambient PM2.5 is least explored. This study aimed to assess the association between PM2.5 and under-five mortality in Ethiopia. The study used the data from the Ethiopian Demographic Health Surveys conducted in 2016, collected between January 18 and June 27. All children under five who had data on child mortality and location coordinates were included in the study. Exposure to ambient PM2.5 concentration was a satellite-based estimate by the Atmospheric Composition Analysis Group at Washington and Dalhousie University, in the United States and Canada, respectively. Annual mean pollution levels and mortality datasets were matched by children's geographical location and dates of birth, death, and interview. The relationship between ambient PM2.5 and under-five mortality was determined by a multilevel multivariable logistic regression on R software. The statistical analyses were two-sided at a 95% confidence interval. The study addressed 10,452 children with the proportion of under-five mortality being 5.4% (95% CI 5.0-6.8%). The estimated lifetime annual mean exposure of ambient total PM2.5 was 20.1 ± 3.3 μgm-3. A 10-unit increase in the lifetime annual mean ambient total PM2.5 was associated with 2.29 [95% CI 1.44, 3.65] times more odds of under-five mortality after adjusting for other variables. Children under five are exposed to higher levels of ambient PM2.5 concentration, exceeding the limit set by the World Health Organization. Ambient PM2.5 is significantly associated with under-five mortality, adjusting for other variables. Strong measures need to be taken to reduce air pollution.

Spatial distribution of radon contamination in hot springs water and its cancer and non-cancer risks in the Hunza-Nagar valley, Pakistan.

Radon (222Rn) is a ubiquitous radioactive gas and could threaten human life due to its potential for cancer and non-cancer risks. This study examined the measurement of 222Rn concentration and associated health risks in the hot springs of Hunza-Nagar valley. For this purpose, the hot springs water of Hunza and Nagar districts and the background sites were analyzed for 222Rn concentration using the RAD7 detector (Durridge Company, USA). The average concentrations of 222Rn were 46.1 ± 0.94, 65.3 ± 0.45, and 5.47 ± 0.25Bq/L in the Hunza district, Nagar district, and background sites, respectively. Results showed that 222Rn concentrations of hot springs water were multifold higher than the background sites. 222Rn concentrations for hot springs water in Hunza-Nagar valley had surpassed the maximum contamination level set by the US environmental protection agency (USEPA). Humans' annual mean exposure dose rates of various age groups were calculated for the estimated lifetime cancer risk (ELCR) and non-cancer risks. The total annual mean exposure doses from 222Rn in water (EwTotal) values were (187 ± 3.80, 265 ± 1.84, and 22.2 ± 1.02μSv/a) for infants (143 ± 2.92, 203 ± 1.40, and 17.0 ± 0.78μSv/a) children, and (138 ± 2.80, 196 ± 1.35, and 16.4 ± 0.76μSv/a) adults in the Hunza district, Nagar district, and background, respectively. Among the age groups of humans, infants showed a higher risk than others. Results showed that hot springs water consumption surpassed the world health organization threshold of 100μSv/y for chronic or non-cancer and USEPA 0.1 × 10-3 for ELCR risks.The concentration of 222Rn showed a positive correlation (> 0.68) with hot springs' water temperature and pH suggesting a common origin.

The relationship between residential exposure to atmospheric pollution and circulating miRNA in adults living in an urban area in northern France

IntroductionMicroRNAs are epigenetic regulatory factors capable of silencing the expression of target genes and might mediate the effects of air pollution on health. The objective of the present population-based study was to investigate the association between microRNA expression and long-term, residential exposure to atmospheric PM10 and NO2. MethodWe included 998 non-smoking adult participants from the cross-sectional ELISABET survey (2010–2014) in the Lille urban area of France. The mean residential annual pollution levels were estimated with an atmospheric dispersion modelling system. Ten microRNAs were selected on the basis of the literature data, together with two housekeeping microRNAs (miR-93-5p and miR-191-5p) and were quantified with RT-qPCRs. Multivariate linear regression models were used to study the association between microRNAs and air pollution. The threshold for statistical significance (after correction for the FDR) was set to p < 0.1. ResultsThe mean annual exposure between 2011 and the year of inclusion was 26.4 ± 2.0 µg/m3 for PM10 and 24.7 ± 5.1 µg/m3 for NO2. Each 2 µg/m3 increment in PM10 exposure was associated with an 8.6% increment (95%CI [3.1; 14.3]; pFDR = 0.019) in miR-451a expression.A 5 µg/m3 increment in NO2 exposure was associated with a 5.3% increment ([0.7; 10]; pFDR = 0.056) in miR451a expression, a 3.6% decrement (95%CI [-6.1; −1.1]; pFDR = 0.052) in miR-223-3p expression, a 3.8% decrement (95%CI[-6.8; −0.7]; pFDR = 0.079) in miR-28-3p expression, a 4.3% decrement (95%CI [-7.7; −0.8]; pFDR = 0.055) in miR-146a-5p expression, and a 4.0% decrement (95% CI[−7.4; −0.4]; pFDR = 0.059) in miR-23a-5p expression. The difference between the two housekeeping microRNAs miR-93-5p and miR-191-5p was also associated with PM10 and NO2 exposure. ConclusionOur results suggest that circulating miRNAs are potentially valuable biomarkers of the effects of air pollution.

Greening the GDP——Exploration of the Relationship between Economy and Environment

GDP has always been regarded as a significant indicator to measure the overall economic volume of a country. However, blindly pursuing high economic growth may cause waste of natural resources and damage to the ecological environment, which is not conducive to the long-term and sustainable economic development of the country. This paper aims to explore the deep relationship between economy and resources and environment through the study of Green GDP. Using CoalProducts, Fossil fuels (% equivalent primary energy), PM2.5 air pollution, mean annual exposure (micrograms per cubic meter) and other effective indicators, we developed a TOPSIS model based on The System of Environmental Economic Accounting (SEEA) to assess impacts on climate mitigation. It collects data from reliable sources, including around 42 countries and 18 statistical indicators. In addition, through the forecast of future resource consumption, population and GDP changes, it is further concluded that it is worthwhile to choose Green GDP as an indicator to measure the economy. This study takes China as an example, and the empirical results show that using Green GDP instead of GDP to calculate the national economy can effectively mitigate the negaitve impact of climate, which has certain reference value for the sustainable development and green economy construction of countries around the world.

Association between long-term air pollution exposure and insulin resistance independent of abdominal adiposity in Korean adults

Significant associations between air pollution (AP) and insulin resistance (IR) have been reported in limited populations or certain patient groups, but few studies have addressed this association in the general population, especially in Asians. Although abdominal fat is a major contributor to IR, previous studies have not fully controlled for its effect in the association between AP and IR. We investigated the association between exposure to AP and IR in Korean adults in the general population and whether this association is maintained even after controlling for the effects of abdominal fat, particularly visceral fat. This was a cross-sectional study. Data were obtained for Korean adults who participated in screening health checkups at Seoul National University Health Examination Center from 2006 to 2014. A total of 4251 men and women aged 22–84 years were included. IR was represented by the homeostasis model assessment of insulin resistance (HOMA-IR). Adiposity traits such as visceral adipose tissue (VAT) and subcutaneous adipose tissue areas were measured by computed tomography. We assessed the annual mean concentrations of air pollutants, including particulate matter with an aerodynamic diameter of 10 µm or less (PM10), nitrogen dioxide, sulfur dioxide, and carbon monoxide. HOMA-IR was significantly associated with increased annual mean exposure to PM10 in both men (β = 0.15; 95% CI 0.09, 0.22) and women (β = 0.16; 95% CI 0.09, 0.23), and these associations were maintained even after controlling for VAT area (both p < 0.05). The adjusted mean HOMA-IR increased gradually with the level of long-term PM10 exposure (low, intermediate, and high exposure) (all p for trend < 0.001) in the subgroup analysis. After adjusting for possible confounding factors, including VAT area, the annual mean exposure to PM10 was significantly associated with the presence of IR in both men (OR 1.18; 95% CI 1.03, 1.35) and women (OR 1.44; 95% CI 1.18, 1.76). Other air pollutants, such as NO2, SO2 and CO, did not show any significant associations with HOMA-IR or the presence of IR. Persistent exposure to PM10 is the main independent risk factor for IR and exhibits a dose-dependent association regardless of visceral fatness in both men and women.

The use of snapshot personal exposure monitoring in estimating annual exposure to air pollutants for epidemiological studies

Background While advancements in sensor technology have broadened the use of personal monitors to estimate individual exposure to air pollution in recent years, significant challenges remain in extending their use for application in epidemiological studies. By collating measurements from several personal exposure (PE) campaigns in London, we aimed to develop a method for extending snapshot PE monitoring to estimates of annual mean exposure to pollution from outdoor sources at individual level. Methods Our conceptual model for annual extrapolation included three factors: a) variation in ambient concentrations, b) variation in infiltration efficiency of residence and other frequently inhabited buildings, and c) mobility behaviour. We utilised a dataset of 200+ million PE measurements from 427 participants of diverse demographics - school children, COPD patients, professional drivers and healthy adults - to characterise these three factors during snapshot monitoring (varying from four days to six months). Location-adjusted ambient concentrations, coupled with seasonal infiltration factors were used to extend results to annual mean personal exposure estimates for PM2.5, NO2, O3 and BC. Methods described elsewhere were used to censor exposure to indoor sources from the measurements. Results Residential infiltration factors did not show significant variation between seasons, suggesting that ventilation behaviour was not a major determinant. Each demographic exhibited distinct patterns in mobility behaviour, although impact was limited by relatively small proportion of time spent travelling. Behaviour modelling of participants with at least four months’ PE measurements showed that some participants had repeated routines, but others were unpredictable. Conclusions The extension of snapshot PE monitoring to annual mean exposure estimates requires assumptions relating to participant behaviour over time, notably mobility and residential ventilation. The impact of these assumptions will vary between individuals and demographics. Extrapolation of snapshot monitoring is more robust for those with predictable routines. Keywords Air pollution, personal exposure, sensors, measurement error

Lung cancer and annual mean exposure to outdoor air pollution in Crete, Greece. Reflections from a two decades big-database

Lung cancer and annual mean exposure to outdoor air pollution in Crete, Greece. Reflections from a two decades big-database

Long-term exposure to elemental components of fine particulate matter and natural and cause-specific mortality in a Danish nationwide administrative cohort

BACKGROUND AND AIM: Fine particulate matter (PM₂.₅) is an established risk factor for premature death, but it remains unclear which components and sources are most responsible. We investigated the associations between long-term exposure to PM₂.₅ components and mortality from all-natural causes, cardiovascular disease (CVD), respiratory diseases (RD), lung cancer, diabetes, chronic kidney disease (CKD), dementia, and psychiatric disorders in a Danish nationwide administrative cohort. METHODS: We followed all Danish residents aged &amp;#x2265;30 at January 1, 2000 (3,081,244) until December 31, 2017. Residential annual mean exposure PM₂.₅ components levels (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by Europe-wide land-use regression models at a 100×100m scale, developed within the &amp;#x22;Effects of Low-Level Air Pollution: A Study in Europe” project, with two modeling approaches: supervised linear regression (SLR) and random forest (RF). We used Cox proportional hazard models to evaluate the associations between each component and mortality, adjusting for demographic, socioeconomic factors, and PM₂.₅ mass. RESULTS: The cohort accumulated 46,992,890 person-years, and 803,373 died from natural causes. For natural mortality, we observed significant positive associations [hazard ratios (HRs); 95% confidence intervals per interquartile range increase] with SLR-silicon (1.04; 1.03-1.05) and SLR-potassium (1.03; 1.02-1.04) and with RF- iron (1.02; 1.01-1.02), RF-zinc (1.02; 1.01-1.03), RF-nickel (1.01; 1.00-1.02), RF-vanadium (1.02; 1.01-103), RF-silicon (1.01; 1.00-1.02), and RF-potassium (1.06; 1.05-1.07). Potassium and silicon were most strongly associated with all causes of death except CKD and diabetes, respectively, with the highest HRs observed for psychiatric disorders. Furthermore, iron was associated with RD, lung cancer, CKD, and psychiatric disorders, zinc with RD, CKD, and lung cancer, and nickel and vanadium with lung cancer. CONCLUSIONS: We present novel findings that different PM₂.₅ components were relevant to different causes of death. Potassium and silicon seemed most consistently associated with mortality in Denmark. KEYWORDS: Long-term exposure, PM₂.₅ components, mortality

Effect of simultaneous exposure to inhalational anesthetics and radiation on the adaptive response in operating room personnel.

Some operating room personnel, such as orthopedic surgeons, are exposed simultaneously to inhalational anesthetics (IAs) and radiation that both can cause DNA damage. Some studies have shown that low doses of radiation reduce DNA damage when the cells are followed by a higher dose of the same or related agent. This study, therefore, set out to compare DNA damage in the anesthesiologists, radiologists, orthopedic surgeons, and healthcare staff (non-exposed group). In this cross-sectional study, breathing zone concentrations of anesthetic gas nitrous oxide (N2O) were measured in the studied groups using standard method. Additionally, DNA damage was measured by micronucleus (MN) assay. The mean concentrations of N2O in the anesthesiologists and orthopedic surgeons were 450.27 ± 327.44ppm and 313.64 ± 216.14ppm, respectively. The mean annual exposure to X-rays radiation in radiologists and orthopedic surgeons was 15.65 ± 8.46 mSy/year and 3.56 ± 1.32 mSy/year, respectively. MN frequencies were significantly higher in anesthesiologists and radiologists exposed to IAs and X-rays radiation respectively than in the non-exposed healthcare staff. While, there were no statistically significant differences between MN frequencies of orthopedic surgeons exposed to both IAs and radiation and healthcare staff.These findings suggest that an earlier exposure of orthopedic surgeons to a small dose of ionizing radiation can increase their resistance to genotoxicity caused by high doses of N2O, a phenomenon that is called adaptive response.