12 research outputs found

    Modifying effect of a common polymorphism in the interleukin-6 promoter on the relationship between long-term exposure to traffic-related particulate matter and heart rate variability

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    Exposure to particulate matter (PM) has been associated with an increase in many inflammatory markers, including interleukin 6 (IL6). Air pollution exposure has also been suggested to induce an imbalance in the autonomic nervous system (ANS), such as a decrease in heart rate variability (HRV). In this study we aimed to investigate the modifying effect of polymorphisms in a major proinflammatory marker gene, interleukin 6 (IL6), on the relationship between long-term exposure to traffic-related PM10 (TPM10) and HRV.; For this cross-sectional study we analysed 1552 participants of the SAPALDIA cohort aged 50 years and older. Included were persons with valid genotype data, who underwent ambulatory 24-hr electrocardiogram monitoring, and reported on medical history and lifestyle. Main effects of annual average TPM10 and IL6 gene variants (rs1800795; rs2069827; rs2069840; rs10242595) on HRV indices and their interaction with average annual exposure to TPM10 were tested, applying a multivariable mixed linear model.; No overall association of TPM10 on HRV was found. Carriers of two proinflammatory G-alleles of the functional IL6 -174 G/C (rs1800795) polymorphism exhibited lower HRV. An inverse association between a 1 µg/m3 increment in yearly averaged TPM10 and HRV was restricted to GG genotypes at this locus with a standard deviation of normal-to-normal intervals (SDNN) (GG-carriers: -1.8%; 95% confidence interval -3.5 to 0.01; pinteraction(additive) = 0.028); and low frequency power (LF) (GG-carriers: -5.7%; 95%CI: -10.4 to -0.8; pinteraction(dominant) = 0.049).; Our results are consistent with the hypothesis that traffic-related air pollution decreases heart rate variability through inflammatory mechanisms

    Adjusted<sup>a</sup> estimates of the mean percent difference of HRV associated with a 1 µg/m<sup>3</sup> increase in average exposure to traffic-related PM10<sup>b</sup> by <i>IL6</i>-174 G/C genotypes (N = 1549).

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    <p>HRV indicates heart rate variability: SDNN indicates standard deviation of all NN intervals (units ms); TP, total power (ms<sup>2</sup>); HF, high frequency power (ms<sup>2</sup>); LF, low frequency power (ms<sup>2</sup>).</p>a<p>adjusted for gender, age, age squared, BMI, BMI squared, smoking status, environmental tobacco smoke exposure, alcohol consumption, physical activity, high-sensitivity C-reactive protein, uric acid levels, hypertension, heart disease, diabetes, street and railway noise, seasonal effects and area.</p>b<p>Annual average over 10 years previous to the study.</p>c<p>p-values for the genotype- specific TPM<sub>10</sub> effect estimate.</p>d<p>p-values of interaction effects of the <i>IL6</i>-174 G/C polymorphism with TPM<sub>10</sub> on HRV were tested for additive, dominant and recessive genetic models; p-values of the most significant mode of inheritance are presented (additive<sup>1</sup> or dominant<sup>2</sup>).</p

    Characteristics of the study population (N = 1552).

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    <p>ETS indicates environmental tobacco smoke exposure; SBP, systolic blood pressure; DBP, diastolic blood pressure; BMI, body mass index;</p>a<p>Annual average over 10 years previous to the study.</p>b<p>average over 3 days previous to the HRV measurement.</p

    Unadjusted and adjusted<sup>a</sup> geometric means of the HRV indices and percent differences in HRV indices by traffic-related PM<sub>10</sub> (TPM<sub>10</sub>) and by <i>IL6</i>-174G/C genotypes (N = 1549).

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    <p>HRV indicates heart rate variability: SDNN indicates standard deviation of all NN intervals (units ms); TP, total power (ms<sup>2</sup>); HF, high frequency power (ms<sup>2</sup>); LF, low frequency power (ms<sup>2</sup>).</p>a<p>adjusted for gender, age, age squared, BMI, BMI squared, smoking status, environmental tobacco smoke exposure, alcohol consumption, physical activity, high-sensitivity C-reactive protein, uric acid levels, hypertension, heart disease, diabetes, street and railway noise, seasonal effects and area.</p>b<p>p-values of genotype-specific main effects of the <i>IL6</i>-174G/C polymorphism and TPM<sub>10</sub> on HRV (codominant genetic model).</p>c<p>p-values of main effects of the <i>IL6</i> -174G/C polymorphism on HRV indices were tested for additive, dominant and recessive genetic models; p-values of the most significant mode of inheritance are presented (<sup>1</sup>additive or <sup>2</sup>dominant).</p>d<p>per 1 µg/m<sup>3</sup> TPM<sub>10</sub> increase.</p>e<p>compared to reference genotype G/G.</p

    Reconciliation of energy use disparities in brick production in India

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    Abstract Energy conservation in brick production is crucial to achieving net-zero carbon emissions from the building sector, especially in countries with major expansions in the built environment. However, widely disparate energy consumption estimates impede benchmarking its importance relative to the steel and cement industries. Here we modelled Indian brick production and its regional energy consumption by combining a nationwide questionnaire survey on feedstock, process variables and practices with remote sensing data on kiln enumeration. We found a large underreporting in current official estimates of energy consumption, with actual energy consumption comparable to that in the steel and cement industries in the country. With a total estimated production of 233 ± 15 billion bricks per year, the brick industry consumes 990 ± 125 PJ yr −1 of energy, 35 ± 6 Mt yr −1 coal and 25 ± 6 Mt yr −1 biomass. The main drivers of energy consumption for brick production are the kiln technology, the production capacity and the fuel mix used. The results suggest that improving operating practices would be a first step in making brick production more energy efficient

    Heating and lighting: understanding overlooked energy-consumption activities in the Indian residential sector

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    Understanding the climate impact of residential emissions starts with determining the fuel consumption of various household activities. While cooking emissions have been widely studied, non-cooking energy-consumption activities in the residential sector such as heating and lighting, have been overlooked owing to the unavailability of data at national levels. The present study uses data from the Carbonaceous Aerosol Emissions, Source Apportionment and Climate Impacts (COALESCE) project, which consists of residential surveys over 6000 households across 49 districts of India, to understand the energy consumed by non-cooking residential activities. Regression models are developed to estimate information in non-surveyed districts using demographic, housing, and meteorological data as predictors. Energy demand is further quantified and distributed nationally at a 4 × 4 km resolution. Results show that the annual energy consumption from non-cooking activities is 1106 [201] PJ, which is equal to one-fourth of the cooking energy demand. Freely available biomass is widely used to heat water on traditional stoves, even in the warmer regions of western and southern India across all seasons. Space heating (51%) and water heating (42%) dominate non-cooking energy consumption. In comparison, nighttime heating for security personnel (5%), partly-residential personal heating by guards, dominant in urban centers and kerosene lighting (2%) utilize minimal energy. Biomass fuels account for over 90% of the non-cooking consumption, while charcoal and kerosene make up the rest. Half of the energy consumption occurs during winter months (DJF), while 10% of the consumption occurs during monsoon, when kerosene lighting is the highest. Firewood is the most heavily used fuel source in western India, charcoal in the northern hilly regions, agricultural residues and dung cake in the Indo-Gangetic plains, and kerosene in eastern India. The study shows that ∼20% of residential energy consumption is on account of biomass-based heating and kerosene lighting activities

    Adult lung function and long-term air pollution exposure. ESCAPE : a multicentre cohort study and meta-analysis

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    The chronic impact of ambient air pollutants on lung function in adults is not fully understood. The objective of this study was to investigate the association of long-term exposure to ambient air pollution with lung function in adult participants from five cohorts in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Residential exposure to nitrogen oxides (NO2, NOx) and particulate matter (PM) was modelled and traffic indicators were assessed in a standardised manner. The spirometric parameters forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) from 7613 subjects were considered as outcomes. Cohort-specific results were combined using meta-analysis. We did not observe an association of air pollution with longitudinal change in lung function, but we observed that a 10 μg·m(-3) increase in NO2 exposure was associated with lower levels of FEV1 (-14.0 mL, 95%CI -25.8- -2.1) and FVC (-14.9 mL, 95% CI -28.7- -1.1). An increase of 10 μg·m(-3) in PM10, but not other PM metrics (PM2.5, coarse fraction of PM, PM absorbance), was associated with a lower level of FEV1 (-44.6 mL, 95% CI -85.4- -3.8) and FVC (-59.0 mL, 95% CI -112.3- -5.6). The associations were particularly strong in obese persons. This study adds to the evidence for an adverse association of ambient air pollution with lung function in adults at very low levels in Europe

    Adult lung function and long-term air pollution exposure. ESCAPE : a multicentre cohort study and meta-analysis

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    The chronic impact of ambient air pollutants on lung function in adults is not fully understood. The objective of this study was to investigate the association of long-term exposure to ambient air pollution with lung function in adult participants from five cohorts in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Residential exposure to nitrogen oxides (NO2, NOx) and particulate matter (PM) was modelled and traffic indicators were assessed in a standardised manner. The spirometric parameters forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) from 7613 subjects were considered as outcomes. Cohort-specific results were combined using meta-analysis. We did not observe an association of air pollution with longitudinal change in lung function, but we observed that a 10 μg·m(-3) increase in NO2 exposure was associated with lower levels of FEV1 (-14.0 mL, 95%CI -25.8- -2.1) and FVC (-14.9 mL, 95% CI -28.7- -1.1). An increase of 10 μg·m(-3) in PM10, but not other PM metrics (PM2.5, coarse fraction of PM, PM absorbance), was associated with a lower level of FEV1 (-44.6 mL, 95% CI -85.4- -3.8) and FVC (-59.0 mL, 95% CI -112.3- -5.6). The associations were particularly strong in obese persons. This study adds to the evidence for an adverse association of ambient air pollution with lung function in adults at very low levels in Europe
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