Lead exposure in Chinese children: Urbanization lowers children's blood lead levels (BLLs).

Lead is a toxic metal that can pose a huge threat to children's health. China has experienced rapid urbanization since the reform in 1978; however, there has been no examination of the potential influence of this urbanization on children's blood lead levels (BLLs). This study is the initial investigation to explore the correlation between urbanization and BLLs in Chinese children. Five windows of time are considered: pre-2000, 2001-2005, 2006-2010, 2011-2015 and 2016-2021. The results show that urbanization affected lead distribution in urban soil and agricultural soil during the above periods, especially in northern China. The higher non-carcinogenic risk of lead for children is consistent with the lead pollution in soil (3 < Igeo ≤ 4). Urban children's BLLs are slightly higher than those of rural children in 2001-2010, but rural children's BLLs in 2011-2021 are higher than those of urban children during China's urbanization. The areas of rural decline and the areas of urban growth increased across all the window periods. However, the BLLs decrease in all rural and urban areas during all window periods, especially in urban areas. Children's BLLs have a significantly negative correlation with urban areas (p < 0.01). Therefore, China's urbanization has a significant effect on the decrease in children's BLLs. The significance of this study is to provide a fresh perspective and innovative strategy for policymaking in order to reduce children's BLLs and prevent lead exposure. This can be achieved by transforming their external living environment from a rural lifestyle to an urban one, while also ensuring access to well education and maintaining a balanced nutrient intake.

Partitioning indoor-generated and outdoor-generated PM2.5 from real-time residential measurements in urban and peri-urban Beijing.

Limited number of projects have attempted to partition and quantify indoor- and outdoor-generated PM2.5 (PM2.5ig and PM2.5og) where strong indoor sources (e.g., solid fuel, tobacco smoke, or kerosene) exist. This study aimed to apply and refine a previous recursive model used to derive infiltration efficiency (Finf) to additionally partition pollution concentrations into indoor and outdoor origins within residences challenged by elevated ambient and indoor combustion-related sources. During the winter of 2016 and summer of 2017 we collected residential measurements in 72 homes in urban and peri-urban Beijing, 12 of which had additional paired residential outdoor measurements during the summer season. Local ambient measurements were collected throughout. We then compared the calculated PM2.5ig and using (i) outdoor and (ii) ambient measurements as model inputs. The results from outdoor and ambient measurements were not significantly different, which suggests that ambient measurements can be used as a model input for pollution origin partitioning when paired outdoor measurements are not available. From the results calculated using ambient measurements, the mean percentage contribution of indoor-generated PM2.5 was 19 % (σ = 22 %), and 7 % (11 %) of the total indoor PM2.5 for peri-urban and urban homes respectively during the winter; and 18 % (18 %) and 6 % (10 %) of the total indoor PM2.5 during the summer. Partitioning pollution into PM2.5ig and PM2.5og is important to allow investigation of distinct associations between health outcomes and particulate mixes, often with different physiochemical composition and toxicity. It will also inform targeted interventions that impact indoor and outdoor sources of pollution (e.g., domestic fuel switching vs. power generation), which are typically radically different in design and implementation.

Exposure to Elevated Nitrogen Dioxide Concentrations and Cardiac Remodeling in Patients With Dilated Cardiomyopathy.

BACKGROUND: Empirical evidence suggests a strong link between exposure to air pollution and heart failure incidence, hospitalizations, and mortality, but the biological basis of this remains unclear. We sought to determine the relationship between differential air pollution levels and changes in cardiac structure and function in patients with dilated cardiomyopathy. METHODS AND RESULTS: We undertook a prospective longitudinal observational cohort study of patients in England with dilated cardiomyopathy (enrollment 2009-2015, n = 716, 66% male, 85% Caucasian) and conducted cross sectional analysis at the time of study enrollment. Annual average air pollution exposure estimates for nitrogen dioxide (NO2) and particulate matter with diameter of 2.5 µm or less (PM2.5) at enrolment were assigned to each residential postcode (on average 12 households). The relationship between air pollution and cardiac morphology was assessed using linear regression modelling. Greater ambient exposure to NO2 was associated with higher indexed left ventricular (LV) mass (4.3 g/m2 increase per interquartile range increase in NO2, 95% confidence interval 1.9-7.0 g/m2) and lower LV ejection fraction (-1.5% decrease per interquartile range increase in NO2, 95% confidence interval -2.7% to -0.2%), independent of age, sex, socioeconomic status, and clinical covariates. The associations were robust to adjustment for smoking status and geographical clustering by postcode area. The effect of air pollution on LV mass was greatest in women. These effects were specific to NO2 exposure. CONCLUSIONS: Exposure to air pollution is associated with raised LV mass and lower LV ejection fraction, with the strongest effect in women. Although epidemiological associations between air pollution and heart failure have been established and supported by preclinical studies, our findings provide novel empirical evidence of cardiac remodeling and exposure to air pollution with important clinical and public health implications.

Microplastic occurrence in settled indoor dust in schools.

This study examines for the first time the characteristics and human exposure of microplastics (MPs) in settled indoor dust in schools. An average of 195 MPs·g-1 of dust were detected in settled indoor composite dust samples from 28 schools in Shiraz. White-transparent microfibres with lengths 500-1000 µm were the most abundant type of MP found among the samples examined. Polyethylene terephthalate and polypropylene MPs were dominant across all types of MP found including microfibres. MPs had generally smooth morphology with sharp or regular edges which could have been released to the environment as primary MPs. Among all sampling sites, higher concentrations of MPs were found in the south and centre of the city. These were areas affected by high population density, high traffic load and high presence of industrial units and workshops. Principal Component Analysis (PCA) showed a positive strong correlation between sampling sites and MP physical characteristics. The PCA plots revealed that MP sheets and fragments were prevalent in sites in the North of Shiraz, whereas microfibres were mainly associated with sites in the South. The levels of MPs in the South of Shiraz were greater than in the rest of the country and the wind direction and topography were found to be important factors affecting the MP distribution observed. Compared to other population groups, elementary school students had relatively high exposure risk to MPs. This study reveals that microfibres are widespread in Shiraz' schools and pose a high exposure risk to MPs for young students.

Source attribution and quantification of atmospheric nickel concentrations in an industrial area in the United Kingdom (UK).

Pontardawe in South Wales, United Kingdom (UK), consistently has the highest concentrations of nickel (Ni) in PM10 in the UK and repeatedly breaches the 20 ng m-3 annual mean EU target value. Several local industries use Ni in their processes. To assist policy makers and regulators in quantifying the relative Ni contributions of these industries and developing appropriate emission reduction approaches, the hourly concentrations of 23 elements were measured using X-ray fluorescence alongside meteorological variables and black carbon during a four-week campaign in November-December 2015. Concentrations of Ni ranged between 0 and 2480 ng m-3 as hourly means. Positive Matrix Factorization (PMF) was used to identify sources contributing to measured elements. Cluster analysis of bivariate polar plots of those factors containing Ni in their profile was further used to quantify the industrial processes contributing to ambient PM10 concentrations. Two sources were identified to contribute to Ni concentrations, stainless-steel (which contributed to 10% of the Ni burden) and the Ni refinery (contributing 90%). From the stainless-steel process, melting activities were responsible for 66% of the stainless-steel factor contribution.

Association of PM 2.5 Reduction with Improved Kidney Function: A Nationwide Quasiexperiment among Chinese Adults.

Background. Increasing evidence from human studies has revealed the adverse impact of ambient fine particles (PM 2.5) on health outcomes related to metabolic disorders and distant organs. Whether exposure to ambient PM 2.5 leads to kidney impairment remains unclear. The rapid air quality improvement driven by the clean air actions in China since 2013 provides an opportunity for a quasiexperiment to investigate the beneficial effect of PM 2.5 reduction on kidney function.Methods. Based on two repeated nationwide surveys of the same population of 5115 adults in 2011 and 2015, we conducted a difference-in-difference study. Variations in long-term exposure to ambient PM 2.5 were associated with changes in kidney function biomarkers, including estimated glomerular filtration rate by serum creatinine (GFR scr) or cystatin C (GFR cys), blood urea nitrogen (BUN), and uric acid (UA).Results. For a 10 µg/m 3 reduction in PM 2.5, a significant improvement was observed for multiple kidney functional biomarkers, including GFR scr, BUN and UA, with a change of 0.42 (95% confidence interval [CI]: 0.06, 0.78) mL/min/1.73m 2, -0.38 (-0.64, -0.12) mg/dL, and -0.06 (-0.12, -0.00) mg/dL, respectively. A lower socioeconomic status, indicated by rural residence or low educational level, enhanced the adverse effect of PM 2.5 on kidney function.Conclusions. These results support a significant nephrotoxicity of PM 2.5 based on multiple serum biomarkers and indicate a beneficial effect of improved air quality on kidney function.

Urban street dust in the Middle East oldest oil refinery zone: Oxidative potential, source apportionment، and health risk assessment of potentially toxic elements.

The current study is the intented to investigate the intensity of pollution, source characterization, oxidative potential, and human health risks of fourteen potentially toxic elements in the street dust of the Middle East oldest oil refinery zone. Thirty five street dust samples were collected from various regions in Abadan and Khorramshahr cities. The mean concentration of As, Mo, Cu, Pb, Hg, Zn, Cd, and Sb in Abadan street dust were 5.55, 3.39, 83.68, 49.82, 4493.54, 281.24, 1.15,and 1.17, while in Khorramshahr As, Mo, Cu, Pb, Hg, Zn, Cd, and Sb were.14, 2.58, 74.35, 56.50, 0.74, 214.26, 0.62, and 1.18, respectively. The concentration of these elements in both cities is higher than the local background values. Potential ecological risk index and pollution load index at all stations of both cities are greater than 1, indicating a high pollution load in the study area. Calculated enrichment factor showed high enrichment of Hg, Sb, Cd, Mo, Cu, Pb, and Zn in both areas. Of particular concern is the enrichment factor for mercury which proved to be 3370.54 ppb in the vicinity of the petrochemical unit in Abadan city (EF > 40). The results of positive matrix factorization receptor model together with geochemical maps and multivariate statistics indicated that industrial activities (especially petrochemical industries) are responsible for Hg, Cu, and Zn pollution, while exhaust emissions are responsible for Mo, Pb, Cd, and Sb, and natural sources for Al, Cr, Mn, Fe, Co, and Ni. The percentage of OPAA in the region ranged from 15.1 to 26.4 and OPGSH ranged from 9.5 to 24.4. The percentage of OPTOTAL/µg (OPAA/µg + OPGSH/µg) values varied between 0.6 and 1. The health risk evaluation models indicated that specific attention should be paid to Hg, Cd, Pb, and Zn and that the higher oxidative potential of street dust recovered from polluted locations is also a matter of concern in Abadan and Khorramshahr Cities.

Difference in ambient-personal exposure to PM2.5 and its inflammatory effect in local residents in urban and peri-urban Beijing, China: results of the AIRLESS project.

Measurement of ambient fine particulate matter (PM2.5) is often used as a proxy of personal exposure in epidemiological studies. However, the difference between personal and ambient exposure, and whether it biases the estimates of health effects remain unknown. Based on an epidemiological study (AIRLESS) and simultaneously launched intensive monitoring campaigns (APHH), we quantified and compared the personal and ambient exposure to PM2.5 and the related health impact among residents in Beijing, China. In total, 123 urban and 128 peri-urban non-smoking participants were recruited from two well-established cohorts in Beijing. During winter 2016 and summer 2017, each participant was instructed to carry a validated personal air monitor (PAM) to measure PM2.5 concentration at high spatiotemporal resolution for seven consecutive days in each season. Multiple inflammatory biomarkers were measured, including exhaled NO, blood monocytes counts and C-reactive protein. Linear mixed-effect models were used for the associations between exposure and health outcomes with adjustment for confounders. The average level of daily personal exposure to PM2.5 was consistently lower than using corresponding ambient concentration, and the difference is greater during the winter. The personal to ambient (P/A) ratio of exposure to PM2.5 exhibited an exponentially declining trend, and showed larger variations when ambient PM2.5 levels < 25 µg m-3. Personal exposure to PM2.5 was significantly associated with the increase in respiratory and systemic inflammatory biomarkers; however, the associations were weaker or became insignificant when ambient concentrations were used. Exposure to ambient PM2.5 might not be a good proxy to estimate the health effect of exposure to personal PM2.5.

Derepression of glomerular filtration, renal blood flow and antioxidant defence in patients with type 2 diabetes at high-risk of cardiorenal disease.

BACKGROUND: The role of antioxidant status on microvascular blood flow and glomerular filtration (eGFR) in patients with type 2 diabetes and hypertension whose risk of progressive renal disease varies by ethnicity is unknown. METHODS: Adult, non-Caucasian (n = 101) and Caucasian (n = 69) patients with type 2 diabetes, hypertension and/or microalbuminuria and an eGFR > 45 mL/min/1.73 m2 were randomised to receive 400 IU vitamin E and/or 20 µg selenium daily or matching placebo. eGFR (CKD-EPI) was measured at baseline, 3,6 and 12 months and renal blood flow by contrast-enhanced ultrasonography in a sub-group (n = 9) at baseline and 3 months by assessing the area under the time intensity curve (TIC). Circulating glutathione peroxidase 3 (GPx-3) activity was measured as a biomarker of oxidative defence status. RESULTS: The time to change in eGFR was shortest with combined vitamin E and selenium than usual care (5.6 [4.0-7.0] vs 8.9 [6.8-10.9 months]; p = 0.006). Area under the TIC was reduced compared to baseline (38.52 [22.41-90.49] vs 123 [86.98-367.03]dB.s; P ≤ 0.05 and 347 [175.88-654.92] vs 928.03 [448.45-1683]dB.s; P ≤ 0.05, respectively] at 3 months suggesting an increase in rate of perfusion. The proportional change in eGFR at 12 months was greater in the group whose GPx-3 activity was above, compared with those below the cohort median (360 U/L) in the non-Caucasian and the Caucasian groups (19.1(12.5-25.7] % vs 6.5[-3.5 to 16.5] % and 12.8 [0.7 to 24] % vs 0.2 [-6.1 to 6.5] %). CONCLUSION: In these patients with type 2 diabetes and early CKD, antioxidant treatment derepresses renal blood flow and a rise in eGFR correlated directly with GPx-3 activity. SIGNIFICANCE: Diabetes mellitus is the world's leading cause of end-stage renal disease which has a predilection for black and minor ethnic groups compared with Caucasians. The differences in risk despite the benefits of conventional care may be related to oxidative stress. We found that glomerular filtration and renal blood flow is suppressed when renal function is preserved in high-risk patients with type 2 diabetes. Conventional care supplemented with selenium - the co-factor for glutathione peroxidase-3 (GPx-3) - improves renal perfusion and increase glomerular filtration according to host antioxidant defence determined by GPx-3 activity. Circulating GPx-3 activity warrants further investigation as a novel biomarker of reversible haemodynamic changes in early diabetic kidney disease to better enable targeting of renoprotective strategies.

Association of Air Pollution Exposure With Psychotic Experiences During Adolescence.

Importance: Urbanicity is a well-established risk factor for clinical (eg, schizophrenia) and subclinical (eg, hearing voices and paranoia) expressions of psychosis. To our knowledge, no studies have examined the association of air pollution with adolescent psychotic experiences, despite air pollution being a major environmental problem in cities. Objectives: To examine the association between exposure to air pollution and adolescent psychotic experiences and test whether exposure mediates the association between urban residency and adolescent psychotic experiences. Design, Setting, and Participants: The Environmental-Risk Longitudinal Twin Study is a population-based cohort study of 2232 children born during the period from January 1, 1994, through December 4, 1995, in England and Wales and followed up from birth through 18 years of age. The cohort represents the geographic and socioeconomic composition of UK households. Of the original cohort, 2066 (92.6%) participated in assessments at 18 years of age, of whom 2063 (99.9%) provided data on psychotic experiences. Generation of the pollution data was completed on October 4, 2017, and data were analyzed from May 4 to November 21, 2018. Exposures: High-resolution annualized estimates of exposure to 4 air pollutants-nitrogen dioxide (NO2), nitrogen oxides (NOx), and particulate matter with aerodynamic diameters of less than 2.5 (PM2.5) and less than 10 µm (PM10)-were modeled for 2012 and linked to the home addresses of the sample plus 2 commonly visited locations when the participants were 18 years old. Main Outcomes and Measures: At 18 years of age, participants were privately interviewed regarding adolescent psychotic experiences. Urbanicity was estimated using 2011 census data. Results: Among the 2063 participants who provided data on psychotic experiences, sex was evenly distributed (52.5% female). Six hundred twenty-three participants (30.2%) had at least 1 psychotic experience from 12 to 18 years of age. Psychotic experiences were significantly more common among adolescents with the highest (top quartile) level of annual exposure to NO2 (odds ratio [OR], 1.71; 95% CI, 1.28-2.28), NOx (OR, 1.72; 95% CI, 1.30-2.29), and PM2.5 (OR, 1.45; 95% CI, 1.11-1.90). Together NO2 and NOx statistically explained 60% of the association between urbanicity and adolescent psychotic experiences. No evidence of confounding by family socioeconomic status, family psychiatric history, maternal psychosis, childhood psychotic symptoms, adolescent smoking and substance dependence, or neighborhood socioeconomic status, crime, and social conditions occurred. Conclusions and Relevance: In this study, air pollution exposure-particularly NO2 and NOx-was associated with increased odds of adolescent psychotic experiences, which partly explained the association between urban residency and adolescent psychotic experiences. Biological (eg, neuroinflammation) and psychosocial (eg, stress) mechanisms are plausible.

Are noise and air pollution related to the incidence of dementia? A cohort study in London, England.

OBJECTIVE: To investigate whether the incidence of dementia is related to residential levels of air and noise pollution in London. DESIGN: Retrospective cohort study using primary care data. SETTING: 75 Greater London practices. PARTICIPANTS: 130 978 adults aged 50-79 years registered with their general practices on 1 January 2005, with no recorded history of dementia or care home residence. PRIMARY AND SECONDARY OUTCOME MEASURES: A first recorded diagnosis of dementia and, where specified, subgroups of Alzheimer's disease and vascular dementia during 2005-2013. The average annual concentrations during 2004 of nitrogen dioxide (NO2), particulate matter with a median aerodynamic diameter ≤2.5 µm (PM2.5) and ozone (O3) were estimated at 20×20 m resolution from dispersion models. Traffic intensity, distance from major road and night-time noise levels (Lnight) were estimated at the postcode level. All exposure measures were linked anonymously to clinical data via residential postcode. HRs from Cox models were adjusted for age, sex, ethnicity, smoking and body mass index, with further adjustments explored for area deprivation and comorbidity. RESULTS: 2181 subjects (1.7%) received an incident diagnosis of dementia (39% mentioning Alzheimer's disease, 29% vascular dementia). There was a positive exposure response relationship between dementia and all measures of air pollution except O3, which was not readily explained by further adjustment. Adults living in areas with the highest fifth of NO2 concentration (>41.5 µg/m3) versus the lowest fifth (<31.9 µg/m3) were at a higher risk of dementia (HR=1.40, 95% CI 1.12 to 1.74). Increases in dementia risk were also observed with PM2.5, PM2.5 specifically from primary traffic sources only and Lnight, but only NO2 and PM2.5 remained statistically significant in multipollutant models. Associations were more consistent for Alzheimer's disease than vascular dementia. CONCLUSIONS: We have found evidence of a positive association between residential levels of air pollution across London and being diagnosed with dementia, which is unexplained by known confounding factors.

Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter.

BACKGROUND: Particulate matter (PM) pollutant exposure, which induces oxidative stress and inflammation, and vitamin D insufficiency, which compromises immune regulation, are detrimental in asthma. OBJECTIVES: Mechanistic cell culture experiments were undertaken to ascertain whether vitamin D abrogates PM-induced inflammatory responses of human bronchial epithelial cells (HBECs) through enhancement of antioxidant pathways. METHODS: Transcriptome analysis, PCR and ELISA were undertaken to delineate markers of inflammation and oxidative stress; with comparison of expression in primary HBECs from healthy and asthmatic donors cultured with reference urban PM in the presence/absence of vitamin D. RESULTS: Transcriptome analysis identified over 500 genes significantly perturbed by PM-stimulation, including multiple pro-inflammatory cytokines. Vitamin D altered expression of a subset of these PM-induced genes, including suppressing IL6. Addition of vitamin D suppressed PM-stimulated IL-6 production, although to significantly greater extent in healthy versus asthmatic donor cultures. Vitamin D also differentially affected PM-stimulated GM-CSF, with suppression in healthy HBECs and enhancement in asthmatic cultures. Vitamin D increased HBEC expression of the antioxidant pathway gene G6PD, increased the ratio of reduced to oxidised glutathione, and in PM-stimulated cultures decreased the formation of 8-isoprostane. Pre-treatment with vitamin D decreased CXCL8 and further decreased IL-6 production in PM-stimulated cultures, an effect abrogated by inhibition of G6PD with DHEA, supporting a role for this pathway in the anti-inflammatory actions of vitamin D. CONCLUSIONS: In a study using HBECs from 18 donors, vitamin D enhanced HBEC antioxidant responses and modulated the immune response to PM, suggesting that vitamin D may protect the airways from pathological pollution-induced inflammation.

The human circulating miRNome reflects multiple organ disease risks in association with short-term exposure to traffic-related air pollution.

Traffic-related air pollution is a complex mixture of particulate matter (PM) and gaseous pollutants, such as nitrogen dioxide (NO2). PM exposure contributes to the pathogenesis of many diseases including several types of cancer, as well as pulmonary, cardiovascular and neurodegenerative diseases. Also exposure to NO2 has been related to increased cardiovascular mortality. In search of an early diagnostic biomarker for improved air pollution-associated health risk assessment, recent human studies have shown that certain circulating miRNAs are altered upon exposure to traffic-related air pollutants. Here, we present for the first time a global analysis of the circulating miRNA genome in an experimental cross-over study of a human population exposed to traffic-related air pollution. By utilizing next-generation sequencing technology and detailed real-time exposure measurements we identified 54 circulating miRNAs to be dose- and pollutant species-dependently associated with PM10, PM2.5, black carbon, ultrafine particles and NO2 already after 2 h of exposure. Bioinformatics analysis suggests that these circulating miRNAs actually reflect the adverse consequences of traffic pollution-induced toxicity in target tissues including the lung, heart, kidney and brain. This study shows the strong potential of circulating miRNAs as novel biomarkers for environmental health risk assessment.

Cys34 Adductomes Differ between Patients with Chronic Lung or Heart Disease and Healthy Controls in Central London.

Oxidative stress generates reactive species that modify proteins, deplete antioxidant defenses, and contribute to chronic obstructive pulmonary disease (COPD) and ischemic heart disease (IHD). To determine whether protein modifications differ between COPD or IHD patients and healthy subjects, we performed untargeted analysis of adducts at the Cys34 locus of human serum albumin (HSA). Biospecimens were obtained from nonsmoking participants from London, U.K., including healthy subjects (n = 20) and patients with COPD (n = 20) or IHD (n = 10). Serum samples were digested with trypsin and analyzed by liquid chromatography-high resolution mass spectrometry. Effects of air pollution on adduct levels were also investigated based on estimated residential exposures to PM2.5, O3 and NO2. For the 39 adducts with sufficient data, levels were essentially identical in blood samples collected from the same subjects on two consecutive days, consistent with the 28 day residence time of HSA. Multivariate linear regression revealed 21 significant associations, mainly with the underlying diseases but also with air-pollution exposures (p-value < 0.05). Interestingly, most of the associations indicated that adduct levels decreased with the presence of disease or increased pollutant concentrations. Negative associations of COPD and IHD with the Cys34 disulfide of glutathione and two Cys34 sulfoxidations, were consistent with previous results from smoking and nonsmoking volunteers and nonsmoking women exposed to indoor combustion of coal and wood.

Oxidative potential (OP) and mineralogy of iron ore particulate matter at the Gol-E-Gohar Mining and Industrial Facility (Iran).

Concentrations of total suspended particulate matter, particulate matter with aerodynamic diameter <2.5 µm (PM2.5), particulate matter <10 µm (PM10), and fallout dust were measured at the Iranian Gol-E-Gohar Mining and Industrial Facility. Samples were characterized in terms of mineralogy, morphology, and oxidative potential. Results show that indoor samples exceeded the 24-h PM2.5 and PM10 mass concentration limits (35 and 150 µg m-3, respectively) set by the US National Ambient Air Quality Standards. Calcite, magnetite, tremolite, pyrite, talc, and clay minerals such as kaolinite, vermiculite, and illite are the major phases of the iron ore PM. Accessory minerals are quartz, dolomite, hematite, actinolite, biotite, albite, nimite, laumontite, diopside, and muscovite. The scanning electron microscope structure of fibrous-elongated minerals revealed individual fibers in the range of 1.5 nm to 71.65 µm in length and 0.2 nm to 3.7 µm in diameter. The presence of minerals related to respiratory diseases, such as talc, crystalline silica, and needle-shaped minerals like amphibole asbestos (tremolite and actinolite), strongly suggests the need for detailed health-based studies in the region. The particulate samples show low to medium oxidative potential per unit of mass, in relation to an urban road side control, being more reactive with ascorbate than with glutathione or urate. However, the PM oxidative potential per volume of air is exceptionally high, confirming that the workers are exposed to a considerable oxidative environment. PM released by iron ore mining and processing activities should be considered a potential health risk to the mine workers and nearby employees, and strategies to combat the issue are suggested.

Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study.

BACKGROUND: Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. METHODS: In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. FINDINGS: Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited. Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park. Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park. In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk. By contrast, these beneficial responses were attenuated after walking on Oxford Street. In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5-20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles. In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles. INTERPRETATION: Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases. Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease. Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects. FUNDING: British Heart Foundation.

Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes.

Epidemiological studies have consistently shown associations between elevated concentrations of urban particulate matter (UPM) air pollution and exacerbations of asthma and chronic obstructive pulmonary disease, which are both associated with viral respiratory infections. The effects of UPM on dendritic cell (DC) -stimulated CD4 T lymphocytes have been investigated previously, but little work has focused on CD8 T-lymphocyte responses despite their importance in anti-viral immunity. To address this, we examined the effects of UPM on DC-stimulated naive CD8 T-cell responses. Expression of the maturation/activation markers CD83, CCR7, CD40 and MHC class I on human myeloid DCs (mDCs) was characterized by flow cytometry after stimulation with UPMin vitro in the presence/absence of granulocyte-macrophage colony-stimulating factor (GM-CSF). The capacity of these mDCs to stimulate naive CD8 T-lymphocyte responses in allogeneic co-culture was then assessed by measuring T-cell cytokine secretion using cytometric bead array, and proliferation and frequency of interferon-γ (IFN-γ)-producing T lymphocytes by flow cytometry. Treatment of mDCs with UPM increased expression of CD83 and CCR7, but not MHC class I. In allogeneic co-cultures, UPM treatment of mDCs enhanced CD8 T-cell proliferation and the frequency of IFN-γ+ cells. The secretion of tumour necrosis factor-α, interleukin-13, Granzyme A and Granzyme B were also increased. GM-CSF alone, and in concert with UPM, enhanced many of these T-cell functions. The PM-induced increase in Granzyme A was confirmed in a human experimental diesel exposure study. These data demonstrate that UPM treatment of mDCs enhances priming of naive CD8 T lymphocytes and increases production of pro-inflammatory cytokines. Such UPM-induced stimulation of CD8 cells may potentiate T-lymphocyte cytotoxic responses upon concurrent airway infection, increasing bystander damage to the airways.

Associations of night-time road traffic noise with carotid intima-media thickness and blood pressure: The Whitehall II and SABRE study cohorts.

BACKGROUND: Road traffic noise has been linked to increased risk of stroke, for which hypertension and carotid intima-media thickness (cIMT) are risk factors. A link between traffic noise and hypertension has been established, but there are few studies on blood pressure and no studies on cIMT. OBJECTIVES: To examine cross-sectional associations for long-term exposure to night-time noise with cIMT, systolic blood pressure (SBP), diastolic blood pressure (DBP) and hypertension. METHODS: The study population consisted of 2592 adults from the Whitehall II and SABRE cohort studies living within Greater London who had cIMT, SBP and DBP measured. Exposure to night-time road traffic noise (A-weighted dB, referred to as dBA) was estimated at each participant's residential postcode centroid. RESULTS: Mean night-time road noise levels were 52dBA (SD=4). In the pooled analysis adjusted for cohort, sex, age, ethnicity, marital status, smoking, area-level deprivation and NOx there was a 9.1µm (95% CI: -7.1, 25.2) increase in cIMT in association with 10dBA increase in night-time noise. Analyses by noise categories of 55-60dBA (16.2µm, 95% CI: -8.7, 41.2), and >60dBA (21.2µm, 95% CI: -2.5, 44.9) vs. <55dBA were also positive but non-significant, expect among those not using antihypertensive medication and exposed to >60dBA vs. <55dBA (32.6µm, 95% CI: 6.2, 59.0). Associations for SBP, DPB and hypertension were close to null. CONCLUSIONS: After adjustments, including for air pollution, the association between night-time road traffic noise and cIMT was only observed among non-medication users but associations with blood pressure and hypertension were largely null.

Air pollution, ethnicity and telomere length in east London schoolchildren: An observational study.

BACKGROUND: Short telomeres are associated with chronic disease and early mortality. Recent studies in adults suggest an association between telomere length and exposure to particulate matter, and that ethnicity may modify the relationship. However associations in children are unknown. OBJECTIVES: We examined associations between air pollution and telomere length in an ethnically diverse group of children exposed to high levels of traffic derived pollutants, particularly diesel exhaust, and to environmental tobacco smoke. METHODS: Oral DNA from 333 children (8-9years) participating in a study on air quality and respiratory health in 23 inner city London schools was analysed for relative telomere length using monochrome multiplex qPCR. Annual, weekly and daily exposures to nitrogen oxides and particulate matter were obtained from urban dispersion models (2008-10) and tobacco smoke by urinary cotinine. Ethnicity was assessed by self-report and continental ancestry by analysis of 28 random genomic markers. We used linear mixed effects models to examine associations with telomere length. RESULTS: Telomere length increased with increasing annual exposure to NOx (model coefficient 0.003, [0.001, 0.005], p<0.001), NO2 (0.009 [0.004, 0.015], p<0.001), PM2.5 (0.041, [0.020, 0.063], p<0.001) and PM10 (0.096, [0.044, 0.149], p<0.001). There was no association with environmental tobacco smoke. Telomere length was increased in children reporting black ethnicity (22% [95% CI 10%, 36%], p<0.001) CONCLUSIONS: Pollution exposure is associated with longer telomeres in children and genetic ancestry is an important determinant of telomere length. Further studies should investigate both short and long-term associations between pollutant exposure and telomeres in childhood and assess underlying mechanisms.

Short-term associations between particle oxidative potential and daily mortality and hospital admissions in London.

BACKGROUND: Particulate matter (PM) from traffic and other sources has been associated with adverse health effects. One unifying theory is that PM, whatever its source, acts on the human body via its capacity to cause damaging oxidation reactions related to its content of pro-oxidants components. Few epidemiological studies have investigated particle oxidative potential (OP) and health. We conducted a time series analysis to assess associations between daily particle OP measures and numbers of deaths and hospital admissions for cardiovascular and respiratory diseases. METHODS: During 2011 and 2012 particles with an aerodynamic diameter less than 2.5 and 10µm (PM2.5 and PM10 respectively) were collected daily on Partisol filters located at an urban background monitoring station in Central London. Particulate OP was assessed based on the capacity of the particles to oxidize ascorbate (OP(AA)) and glutathione (OP(GSH)) from a simple chemical model reflecting the antioxidant composition of human respiratory tract lining fluid. Particulate OP, expressed as % loss of antioxidant per µg of PM, was then multiplied by the daily concentrations of PM to derive the daily OP of PM mass concentrations (% loss per m(3)). Daily numbers of deaths and age- and cause-specific hospital admissions in London were obtained from national registries. Poisson regression accounting for seasonality and meteorology was used to estimate the percentage change in risk of death or admission associated with an interquartile increment in particle OP. RESULTS: We found little evidence for adverse associations between OP(AA) and OP(GSH) and mortality. Associations with cardiovascular admissions were generally positive in younger adults and negative in older adults with confidence intervals including 0%. For respiratory admissions there was a trend, from positive to negative associations, with increasing age although confidence intervals generally included 0%. CONCLUSIONS: Our study, the first to analyse daily particle OP measures and mortality and admissions in a large population over two years, found little evidence to support the hypothesis that short-term exposure to particle OP is associated with adverse health effects. Further studies with improved exposure assessment and longer time series are required to confirm or reject the role of particle OP in triggering exacerbations of disease.