Association Of Air Pollution Exposure Research Articles

Impact of Short-Term Air Pollution Exposure on Acute Coronary Syndrome in Two Cohorts of Industrial and Non-Industrial Areas: A Time Series Regression with 6,000,000 Person-Years of Follow-Up (ACS - Air Pollution Study)

Background: There is a lack of data on the effect of air pollution on acute coronary syndrome (ACS) in industrial and non-industrial areas. Objectives: A comparison of association of air pollution exposure with ACS in two cohorts of industrially different areas. Materials and Methods: The study covered 6,000,000 person-years of follow-up and five types of air pollution between 2008 and 2017. A time series regression analysis with 7-lag was used to assess the effects air pollution on ACS. Results: The daily concentrations of PM2.5, PM10, NO2, SO2, CO were higher in industrial than in non-industrial area(P<0.001). In non-industrial area, an increase of 10 µg/m3 of NO2 concentration (Relative Risk (RR)=1.126, 95%CI=1.009–1.257;P=0.034, lag-0) and an increase of 1 mg/m3 in CO concentration (RR=1.055, 95%CI=1.010–1.103;P=0.017, lag-0) were associated with an increase in the number of hospitalization due to Non-ST segment elevation myocardial infarction (NSTEMI) (for industrial area increase of 10 µg/m3 in NO2 (RR=1.062, 95%CI=1.020–1.094;P=0.005, lag-0), SO2 (RR=1.061, 95%CI=1.010–1.116;P=0.018, lag-4), PM10 (RR=1.010, 95%CI=1.001–1.030;P=0.047, lag-6). In ST-segment elevation myocardial infarction (STEMI) patients in industrial area, an increased hospitalization was found to be associated with an increase of 10 µg/m3 in SO2 (RR=1.094, 95%CI=1.030–1.162;P=0.002, lag-1), PM2.5 (RR=1.041, 95%CI=1.020–1.073;P<0.001, lag-1), PM10 (RR=1.030, 95%CI=1.010–1.051;P<0.001, lag-1). No effects of air pollution on the number of hospitalization due to STEMI were noted from non-industrial area. Conclusion: The effect of NO2 on the incidence of NSTEMI was observed in both areas. In industrial area, the effect of PMs and SO2 on NSTEMI and STEMI were also observed. A negative clinical effect was more delayed in patients with NSTEMI, especially after exposure to PM10 . Chronic exposure to air pollution causes destabilization of atheroscleroticplaque and may underlie the differences in the short-term effect between particulate air pollution impact on the incidence of STEMI. Trial Registration: This study was registered at ClinicalTrials.gov (NCT04539925). Funding Statement: No external funding. Declaration of Interests: Not declared. Ethics Approval Statement: The study was approved by the bioethics committee of the Medical University of Bialystok (Approval No.: R-1-002/18/2019).

Differential association of air pollution exposure with neonatal and postneonatal mortality in England and Wales: A cohort study.

BackgroundMany but not all studies suggest an association between air pollution exposure and infant mortality. We sought to investigate whether pollution exposure is differentially associated with all-cause neonatal or postneonatal mortality, or specific causes of infant mortality.Methods and findingsWe separately investigated the associations of exposure to particulate matter with aerodynamic diameter ≤ 10 μm (PM10), nitrogen dioxide (NO2), and sulphur dioxide (SO2) with all-cause infant, neonatal, and postneonatal mortality, and with specific causes of infant deaths in 7,984,366 live births between 2001 and 2012 in England and Wales. Overall, 51.3% of the live births were male, and there were 36,485 infant deaths (25,110 neonatal deaths and 11,375 postneonatal deaths). We adjusted for the following major confounders: deprivation, birthweight, maternal age, sex, and multiple birth. Adjusted odds ratios (95% CI; p-value) for infant deaths were significantly increased for NO2, PM10, and SO2 (1.066 [1.027, 1.107; p = 0.001], 1.044 [1.007, 1.082; p = 0.017], and 1.190 [1.146, 1.235; p < 0.001], respectively) when highest and lowest pollutant quintiles were compared; however, neonatal mortality was significantly associated with SO2 (1.207 [1.154, 1.262; p < 0.001]) but not significantly associated with NO2 and PM10 (1.044 [0.998, 1.092; p = 0.059] and 1.008 [0.966, 1.052; p = 0.702], respectively). Postneonatal mortality was significantly associated with all pollutants: NO2, 1.108 (1.038, 1.182; p < 0.001); PM10, 1.117 (1.050, 1.188; p < 0.001); and SO2, 1.147 (1.076, 1.224; p < 0.001). Whilst all were similarly associated with endocrine causes of infant deaths (NO2, 2.167 [1.539, 3.052; p < 0.001]; PM10, 1.433 [1.066, 1.926; p = 0.017]; and SO2, 1.558 [1.147, 2.116; p = 0.005]), they were differentially associated with other specific causes: NO2 and PM10 were associated with an increase in infant deaths from congenital malformations of the nervous (NO2, 1.525 [1.179, 1.974; p = 0.001]; PM10, 1.457 [1.150, 1.846; p = 0.002]) and gastrointestinal systems (NO2, 1.214 [1.006, 1.466; p = 0.043]; PM10, 1.312 [1.096, 1.571; p = 0.003]), and NO2 was also associated with deaths from malformations of the respiratory system (1.306 [1.019, 1.675; p = 0.035]). In contrast, SO2 was associated with an increase in infant deaths from perinatal causes (1.214 [1.156, 1.275; p < 0.001]) and from malformations of the circulatory system (1.172 [1.011, 1.358; p = 0.035]). A limitation of this study was that we were not able to study associations of air pollution exposure and infant mortality during the different trimesters of pregnancy. In addition, we were not able to control for all confounding factors such as maternal smoking.ConclusionsIn this study, we found that NO2, PM10, and SO2 were differentially associated with all-cause mortality and with specific causes of infant, neonatal, and postneonatal mortality.

Air pollution and IgE sensitization in 4 European birth cohorts—the MeDALL project

Whether long-term exposure air to pollution has effects on allergic sensitization is controversial. Our aim was to investigate associations of air pollution exposure at birth and at the time of later biosampling with IgE sensitization against common food and inhalant allergens, or specific allergen molecules, in children aged up to 16 years. A total of 6163 children from 4 European birth cohorts participating in the Mechanisms of the Development of ALLergy [MeDALL] consortium were included in this meta-analysis of the following studies: Children, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) (Sweden), Influences of Lifestyle-Related Factors on the Human Immune System and Development of Allergies in Childhood (LISA)/German Infant Study on the Influence of Nutrition Intervention PLUS Environmental and Genetic Influences on Allergy Development (GINIplus) (Germany), and Prevention and Incidence of Asthma and Mite Allergy (PIAMA) (The Netherlands). The following indicators were modeled by land use regression: individual residential outdoor levels of particulate matter with aerodynamic diameters less than 2.5 μm, less than 10 μm, and between 2.5 and 10 μm; PM2.5 absorbance (a measurement of the blackness of PM2.5 filters); and nitrogen oxides levels. Blood samples drawn at ages 4 to 6 (n= 5989), 8 to 10 (n= 6603), and 15 to 16 (n= 5825) years were analyzed for IgE sensitization to allergen extracts by ImmunoCAP. Additionally, IgE against 132 allergen molecules was measured by using the MedALL microarray chip (n= 1021). Air pollution was not consistently associated with IgE sensitization to any common allergen extract up to age 16 years. However, allergen-specific analyses suggested increased risks of sensitization to birch (odds ratio [OR]= 1.12 [95% CI= 1.01-1.25] per 10-μg/m3 increase in NO2 exposure). In a subpopulation with microarray data, IgE to the major timothy grass allergen Phleum pratense 1 (Phl p 1) and the cat allergen Felis domesticus 1 (Fel d 1) greater than 3.5 Immuno Solid-phase Allergen Chip standardized units for detection of IgE antibodies were related to PM2.5 exposure at birth (OR= 3.33 [95% CI= 1.40-7.94] and OR= 4.98 [95% CI= 1.59-15.60], respectively, per 5-μg/m3 increase in exposure). Air pollution exposure does not seem to increase the overall risk of allergic sensitization; however, sensitization to birch as well as grass pollen Phl p 1 and cat Fel d 1 allergen molecules may be related to specific pollutants.

Association Between Cardiovascular Disease and Long-term Exposure to Air Pollution With the Risk of Dementia

Emerging yet contrasting evidence associates air pollution with incident dementia, and the potential role of cardiovascular disease (CVD) in this association is unclear. To investigate the association between long-term exposure to air pollution and dementia and to assess the role of CVD in that association. Data for this cohort study were extracted from the ongoing Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a longitudinal population-based study with baseline assessments from March 21, 2001, through August 30, 2004. Of the 5111 randomly selected residents in the Kungsholmen district of Stockholm 60 years or older and living at home or in institutions, 521 were not eligible (eg, due to death before the start of the study or no contact information). Among the remaining 4590 individuals, 3363 (73.3%) were assessed. For the current analysis, 2927 participants who did not have dementia at baseline were examined, with follow-up to 2013 (mean [SD] follow-up time, 6.01 [2.56] years). Follow-up was completed February 18, 2013, and data were analyzed from June 26, 2018, through June 20, 2019. Two major air pollutants (particulate matter ≤2.5 μm [PM2.5] and nitrogen oxide [NOx]) were assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. The hazard of dementia was estimated using Cox proportional hazards regression models. The potential of CVD (ie, atrial fibrillation, ischemic heart disease, heart failure, and stroke) to modify and mediate the association between long-term exposure to air pollution and dementia was tested using stratified analyses and generalized structural equation modeling. At baseline, the mean (SD) age of the 2927 participants was 74.1 (10.7) years, and 1845 (63.0%) were female. Three hundred sixty-four participants with incident dementia were identified. The hazard of dementia increased by as much as 50% per interquartile range difference in mean pollutant levels during the previous 5 years at the residential address (hazard ratio [HR] for difference of 0.88 μg/m3 PM2.5, 1.54 [95% CI, 1.33-1.78]; HR for difference of 8.35 μg/m3 NOx, 1.14 [95% CI, 1.01-1.29]). Heart failure (HR for PM2.5, 1.93 [95% CI, 1.54-2.43]; HR for NOx, 1.43 [95% CI, 1.17-1.75]) and ischemic heart disease (HR for PM2.5, 1.67 [95% CI, 1.32-2.12]; HR for NOx, 1.36 [95% CI, 1.07-1.71]) enhanced the dementia risk, whereas stroke appeared to be the most important intermediate condition, explaining 49.4% of air pollution-related dementia cases. This study found that long-term exposure to air pollution was associated with a higher risk of dementia. Heart failure and ischemic heart disease appeared to enhance the association between air pollution and dementia, whereas stroke seemed to be an important intermediate condition between the association of air pollution exposure with dementia.

Associations between long-term exposure to air pollution and blood pressure and effect modifications by behavioral factors

BackgroundStudies on the hypertensive effect of long-term air pollution exposure were inconclusive and showed scarce evidence from rural areas in developing countries. In this context, we examined the associations of air pollution exposure with hypertension and blood pressure, and their effect modifiers in rural Chinese adults. MethodsWe studied 39,259 participants from a cohort established in five rural regions of central China. Individual exposures to PM2.5 and PM10 (particulate matter with an aerodynamic diameter less than or equal to 2.5 μm and 10 μm) and nitrogen dioxide (NO2) was evaluated using satellite-based spatiotemporal models. Mixed-effect regression models were applied to examine the associations of long-term exposure to air pollution with hypertension and four blood pressure component measurements, including systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP). Several potential effect modifiers related to demographic and behavioral factors were also examined. ResultsThe results showed that for each 1 μg/m3 increase in PM2.5, PM10 and NO2, the adjusted odds ratio of hypertension was 1.029 (95%CI: 1.001,1.057), 1.015 (95%CI: 1.001, 1.029) and 1.069 (95%CI: 1.038, 1.100), respectively. These three air pollutants were also associated with increased SBP (except for PM10), DBP and MAP. The hypertensive effects of air pollution were more pronounced among males, smokers, drinkers, individuals with a high-fat diet, and those with high-level physical activity. ConclusionLong-term exposure to PM2.5, PM10 and NO2 was associated with increased blood pressure and hypertension in rural Chinese adults, and the associations were modified by several behavioral factors.

Air Pollution Exposure and Lung Function Until Age 16 Years: The PIAMA Birth Cohort Study

Evidence for the effects of air pollution exposure on lung function growth into adolescence is scarce. Therefore, the purpose of this study was to investigate the associations of air pollution exposure from birth with lung function growth from ages 8 to 16 and lung function at age 16. Potential confounders (sex and asthma diagnosis) were also explored.The study was performed within the Dutch population-based Prevention and Incidence of Asthma and Mite Allergy birth cohort. From the 3963 pregnant women initially enrolled, 915 children (mean age: 16.3 years) had sufficient longitudinal data for this study.Both longitudinal (n = 915) and cross-sectional (n = 721) analyses were conducted. Researchers estimated residential concentrations of nitrogen dioxide, “soot,” and particulate matter (PMx, where x is the 50% cutoff aerodynamic diameter in μm) with diameters of <2.5 μm (PM2.5), <10 μm (PM10), and 2.5 to 10 μm (PMcoarse) during the preschool, primary school, and secondary school time windows by land use regression models. Associations with (growth in) forced expiratory volume in 1 second (FEV1) and forced vital capacity were analyzed by linear (mixed effects) regression.Greater air pollution exposure was associated with reduced FEV1 growth (eg, adjusted difference: −0.26% [95% confidence interval: −0.49 to −0.03%] per interquartile range increase in secondary school PM2.5) and lower FEV1 (adjusted difference: −2.36% [95% confidence interval: −3.76 to −0.94%]) but was not adversely associated with forced vital capacity. Associations with FEV1 were stronger in boys than girls and were not modified by asthma status.Greater air pollution exposure may lead to increased airway obstruction but not reduced lung volume in adolescence.This study supports previous longitudinal studies that have reported an association between air pollution exposure and reduced lung function growth. The association between lower FEV1 and PM2.5 exposure during the secondary school time window suggests that exposure during this time frame is critical. This study was limited by a lack of racial diversity, which could create differing results because of epigenetic changes. Future longitudinal studies should address this issue.

Traffic-Related Air Pollution Exposure and Altered Fatty Acid Oxidation among Adolescents and Young Adults – the Interplay with Obesity

S01: Mapping the Air Pollution Metabolome: Applications, Limitations, and the Path Forward, Room 217, Floor 2, August 26, 2019, 10:30 AM - 12:00 PM Background/Aim: Air pollution exposure has been shown to increase the risk of obesity and metabolic dysfunction in animal models and human studies. However, the metabolic pathways altered by air pollution exposure are unclear, especially in adolescents and young adults who are at a critical period for developing cardio-metabolic diseases. The aim of this study was to examine the associations of exposures to traffic-related and regional air pollutants with indices of fatty acid and amino acid metabolism. Methods: A total of 173 young adults (18-23 years) from eight Children’s Health Study (CHS) Southern California communities were examined from 2014-2018. Exposures to traffic-related [freeway and non-freeway nitrogen oxides (NOx)] and regional air pollutants (nitrogen dioxide, ozone and particulate matter) were estimated based on participants’ residential addresses. Serum concentrations of 64 targeted metabolites including amino acids, acylcarnitines, ketones and total non-esterified fatty acid (NEFA) were measured in fasting serum samples. Principal component analysis (PCA) of metabolites was performed to identify metabolite clusters that represent key metabolic pathways. Mixed effects models were used to analyze the associations of air pollution exposure with metabolomic principal component (PC) scores and individual metabolite concentrations adjusting for potential confounders. Results: Higher long-term (lagged one-year average) exposure to non-freeway NOx was associated with higher concentrations of NEFA oxidation byproducts and higher NEFA-related PC score (all p’s<0.01). The effect sizes were larger among obese and Non-Hispanic White individuals (interaction p’s≤0.002). Among females, higher exposure to freeway NOx was associated with a higher NEFA-related PC score (p=0.006). Additionally, among all participants, higher exposure to freeway NOx was associated with a lower PC score for lower concentrations of short- and median-chain acylcarnitines (p=0.042). Conclusions: Results of this study indicate that traffic-related air pollution exposure is associated with altered fatty acid metabolism, which contributes to the metabolic perturbation in obese youth.

Near-roadway air pollution exposure and altered fatty acid oxidation among adolescents and young adults – The interplay with obesity

BackgroundAir pollution exposure has been shown to increase the risk of obesity and metabolic dysfunction in animal models and human studies. However, the metabolic pathways altered by air pollution exposure are unclear, especially in adolescents and young adults who are at a critical period in the development of cardio-metabolic diseases. ObjectivesThe aim of this study was to examine the associations between air pollution exposure and indices of fatty acid and amino acid metabolism. MethodsA total of 173 young adults (18–23 years) from eight Children's Health Study (CHS) Southern California communities were examined from 2014 to 2018. Near-roadway air pollution (NRAP) exposure (freeway and non-freeway) and regional air pollution exposure (nitrogen dioxide, ozone and particulate matter) during one year before the study visit were estimated based on participants' residential addresses. Serum concentrations of 64 targeted metabolites including amino acids, acylcarnitines, non-esterified fatty acid (NEFA) and glycerol were measured in fasting serum samples. Principal component analysis of metabolites was performed to identify metabolite clusters that represent key metabolic pathways. Mixed effects models were used to analyze the associations of air pollution exposure with metabolomic principal component (PC) scores and individual metabolite concentrations adjusting for potential confounders. ResultsHigher lagged one-year averaged non-freeway NRAP exposure was associated with higher concentrations of NEFA oxidation byproducts and higher NEFA-related PC score (all p's ≤ 0.038). The effect sizes were larger among obese individuals (interaction p = 0.047). Among females, higher freeway NRAP exposure was also associated with a higher NEFA-related PC score (p = 0.042). Among all participants, higher freeway NRAP exposure was associated with a lower PC score for lower concentrations of short- and median-chain acylcarnitines (p = 0.044). ConclusionsResults of this study indicate that NRAP exposure is associated with altered fatty acid metabolism, which could contribute to the metabolic perturbation in obese youth.

The associations of air pollution exposure during pregnancy with fetal growth and anthropometric measurements at birth: a systematic review and meta-analysis.

Fetal growth has been demonstrated to be an important predictor of perinatal and postnatal health. Although the effects of maternal exposure to air pollution during pregnancy on fetal growth have been investigated using ultrasound in many previous studies, the results were inconsistent and disputable. We aimed to qualitatively and quantitatively investigate the associations of air pollution exposure during different periods of pregnancy with fetal growth and anthropometric measurements at birth. We searched for all studies investigating the associations of air pollution exposure during pregnancy with fetal growth and birth anthropometric measurements in English and Chinese databases published before July 31, 2017. A random-effects model was employed in the meta-analysis to estimate the pooled effects of each 10μg/m3 increment in air pollutant exposure. The ACROBAT-NRSI tool was applied to assess the quality of each included study, and the GRADE tool was employed to assess the overall quality of the meta-analysis. Maternal PM2.5 exposure (10μg/m3) during the entire pregnancy was negatively associated with head circumference at birth (β = - 0.30cm, 95% CI - 0.49, - 0.10), and NO2 exposure during the entire pregnancy was significantly linked to shorter length at birth (β = - 0.03cm, 95% CI - 0.05, - 0.02). Maternal exposure to higher NO2 and PM2.5 during pregnancy may impair neonatal head circumference and length development, respectively. More studies are needed to confirm the effects of NO2 and PM2.5 and to identify the sources and major toxic components of PMs.

Association of Air Pollution Exposure With Psychotic Experiences During Adolescence

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. 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. 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. 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. At 18 years of age, participants were privately interviewed regarding adolescent psychotic experiences. Urbanicity was estimated using 2011 census data. 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. 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.

Air pollution exposure and lung function until age 16 years: the PIAMA birth cohort study.

Evidence for the effects of air pollution exposure on lung function growth into adolescence is scarce. We investigated associations of air pollution exposure with lung function and lung function growth until age 16.We conducted both longitudinal (n=915) and cross-sectional (n=721) analyses of associations of air pollution exposure with forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) growth from ages eight to 16 and FEV1 and FVC at age 16. We estimated residential concentrations of nitrogen dioxide (NO2), "soot" and particulate matter (PMx, where x is the 50% cut-off aerodynamic diameter in µm) with diameters of <2.5 µm (PM2.5), <10 µm (PM10) and 2.5-10 µm (PMcoarse) during the preschool, primary school and secondary school time windows by land use regression models. Associations with (growth in) FEV1 and FVC were analysed by linear (mixed effects) regression.Higher air pollution exposure was associated with reduced FEV1 growth (e.g. adjusted difference -0.26% (95% CI -0.49 to -0.03%) per interquartile range increase in secondary school PM2.5) and lower FEV1 (adjusted difference -2.36% (95% CI -3.76 to -0.94%)), but was not adversely associated with FVC. Associations with FEV1 were stronger in boys than girls and were not modified by asthma status.Higher air pollution exposure may lead to increased airway obstruction, but not reduced lung volume in adolescence.

Developmental exposures to ultrafine particle air pollution reduces early testosterone levels and adult male social novelty preference: Risk for children’s sex-biased neurobehavioral disorders

Epidemiological studies have reported associations of air pollution exposures with various neurodevelopmental disorders such as autism spectrum disorder (ASD), attention deficit and schizophrenia, all of which are male-biased in prevalence. Our studies of early postnatal exposure of mice to the ultrafine particle (UFP) component of air pollution, considered the most reactive component, provide support for these epidemiological associations, demonstrating male-specific or male-biased neuropathological changes and cognitive and impulsivity deficits consistent with these disorders. Since these neurodevelopmental disorders also include altered social behavior and communication, the current study examined the ability of developmental UFP exposure to reproduce these social behavior deficits and to determine whether any observed alterations reflected changes in steroid hormone concentrations. Elevated plus maze, social conditioned place preference, and social novelty preference were examined in adult mice that had been exposed to concentrated (10-20x) ambient UFPs averaging approximately 45 ug/m3 particle mass concentrations from postnatal day (PND) 4–7 and 10–13 for 4 h/day. Changes in serum testosterone (T) and corticosterone where measured at postnatal day (P)14 and approximately P120. UFP exposure decreased serum T concentrations on PND 14 and social nose-to-nose sniff rates with novel males in adulthood, suggesting social communication deficits in unfamiliar social contexts. Decreased sniff rates were not accounted for by alterations in fear-mediated behaviors and occurred without overt deficits in social preference, recognition or communication with a familiar animal or alterations in corticosterone. Adult T serum concentrations were positively correlated with nose to nose sniff rates. Collectively, these studies confirm another feature of male-biased neurodevelopmental disorders following developmental exposures to even very low levels of UFP air pollution that could be related to alterations in sex steroid programming of brain function.

Association of Air Pollution Exposure and Interleukin-13 Haplotype with the Risk of Aggregate Bronchitic Symptoms in Children

Interleukin-13(IL-13) might play an important role in driving aggregate bronchitic symptoms pathogenesis. However, none of the studies assessed the interaction between air pollutants exposure and IL-13 gene on the risk of aggregate bronchitic symptoms in non-asthma children. To assess the independent and joint effects of the exposure to air pollution and IL-13 haplotypes on the risk of aggregate bronchitic symptoms, we conducted a cross-sectional study and focused on non-asthma children. The study population consisted of 2944 children. The effect of each air pollutant on the risk of aggregate bronchitic symptoms was estimated as odds ratios per interquartile range (IQR) change. In the multiple logistic regressions, adjusted for confounding factors, the risk of chronic phlegm was associated with PM2.5 exposure (aOR, 1.59; 95% CI, 1.07–2.37 per 12.51μg/m3 change), O3 exposure (aOR, 1.54 95% CI, 1.05–2.27 per 8.28ppb change) and SO2 exposure (aOR, 1.19; 95% CI, 1.02–1.39 per 0.98ppb change). Our study further provides the evidence that gene-environment interactions between IL-13 haplotype and O3 exposure on chronic phlegm (95% CI for interaction, 1.01–1.38). Identifying children who are more sensitive to air pollution helps us to provide them an efficient prevention to avoid aggregate bronchitic symptoms.

Is physical activity a modifier of the association between air pollution and arterial stiffness in older adults: The SAPALDIA cohort study.

Air pollution and insufficient physical activity have been associated with inflammation and oxidative stress, molecular mechanisms linked to arterial stiffness and cardiovascular disease. There are no studies on how physical activity modifies the association between air pollution and arterial stiffness. We examined whether the adverse cardiovascular effects of air pollution were modified by individual physical activity levels in 2823 adults aged 50-81 years from the well-characterized Swiss Cohort Study on Air Pollution and Lung and Heart Diseases (SAPALDIA). We assessed arterial stiffness as the brachial-ankle pulse wave velocity (baPWV [m/s]) with an oscillometric device. We administered a self-reported physical activity questionnaire to classify each subject's physical activity level. Air pollution exposure was estimated by the annual average individual home outdoor PM10 and PM2.5 (particulate matter <10μm and <2.5μm in diameter, respectively) and NO2 (nitrogen dioxide) exposure estimated for the year preceding the survey. Exposure estimates for ultrafine particles calculated as particle number concentration (PNC) and lung deposited surface area (LDSA) were available for a subsample (N=1353). We used mixed effects logistic regression models to regress increased arterial stiffness (baPWV≥14.4m/s) on air pollution exposure and physical activity while adjusting for relevant confounders. We found evidence that the association of air pollution exposure with baPWV was different between inactive and active participants. The probability of having increased baPWV was significantly higher with higher PM10, PM2.5, NO2, PNC and LDSA exposure in inactive, but not in physically active participants. We found some evidence of an interaction between physical activity and ambient air pollution exposure for PM10, PM2.5 and NO2 (pinteraction=0.06, 0.09, and 0.04, respectively), but not PNC and LDSA (pinteraction=0.32 and 0.35). Our study provides some indication that physical activity may protect against the adverse vascular effects of air pollution in low pollution settings. Additional research in large prospective cohorts is needed to assess whether the observed effect modification translates to high pollution settings in mega-cities of middle and low-income countries.

Gene expression network analyses in response to air pollution exposures in the trucking industry.

BackgroundExposure to air pollution, including traffic-related pollutants, has been associated with a variety of adverse health outcomes, including increased cardiopulmonary morbidity and mortality, and increased lung cancer risk.MethodsTo better understand the cellular responses induced by air pollution exposures, we performed genome-wide gene expression microarray analysis using whole blood RNA sampled at three time-points across the work weeks of 63 non-smoking employees at 10 trucking terminals in the northeastern US. We defined genes and gene networks that were differentially activated in response to PM2.5 (particulate matter ≤ 2.5 microns in diameter) and elemental carbon (EC) and organic carbon (OC).ResultsMultiple transcripts were strongly associated (padj < 0.001) with pollutant levels (48, 260, and 49 transcripts for EC, OC, and PM2.5, respectively), including 63 that were statistically significantly correlated with at least two out of the three exposures. These genes included many that have been implicated in ischemic heart disease, chronic obstructive pulmonary disease (COPD), lung cancer, and other pollution-related illnesses. Through the combination of Gene Set Enrichment Analysis and network analysis (using GeneMANIA), we identified a core set of 25 interrelated genes that were common to all three exposure measures and were differentially expressed in two previous studies assessing gene expression attributable to air pollution. Many of these are members of fundamental cancer-related pathways, including those related to DNA and metal binding, and regulation of apoptosis and also but include genes implicated in chronic heart and lung diseases.ConclusionsThese data provide a molecular link between the associations of air pollution exposures with health effects.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-016-0187-z) contains supplementary material, which is available to authorized users.

Association between air pollution and emergency room admissions for atrial fibrillation

INTRODUCTION: Recent studies have pointed out also the possible association of air pollution exposure with atrial fibrillation (AF), the most frequent cardiac arrhythmia diagnosed in clinical practice. We investigated the association between air pollution levels and emergency room visits for AF. METHODS: We conducted a 14 years time-series study to evaluate the association between daily levels of air pollution (particulate matter, PM10 and PM2.5 and nitrogen dioxide, NO2) and daily count of emergency access for AF (ICD-9 code: 427.31) for the city of Rome (Italy). We applied over-dispersed conditional Poisson model to analyze the associations at different lags after controlling for seasonality, day of the week, influenza epidemics, holiday periods, temperature and relative humidity. Additionally, we evaluated bi-pollutant models by including the other pollutant in turn and the influence of several effect modifiers such as personal characteristics and pre-existing medical conditions on a subset of data. RESULTS: In total 79,892 admissions were recorded in emergency room departments of Rome hospitals in the study period. At lag of 0-1 days, the increased risk of admission for 10 ug/m3 increase in PM10 was 1.45% (0.65, 2.26), 3.00% (1.35-4.67) for PM25 and 1.19% (0.27, 2.13) for NO2.The NO2 effect is consistent when also PM10 concentration is high, showing an increase in AF emergency admissions between 0.6% and 1.8%, depending on the lag. Presence of previous cardiovascular conditions, but not other effect modifiers, increase pollution effects by 5-8% depending on the lag. CONCLUSION: We found that high concentrations of air pollution may trigger AF emergency room visits in the short term

Association between pregnancy exposure to air pollution and birth weight in selected areas of Norway.

BackgroundExposure to air pollution has adverse effects on cardiopulmonary health of adults. Exposure to air pollution in pregnancy may affect foetal development. However, the evidence of such effect remains inconsistent. We investigated the effects of exposure to air pollution during pregnancy on birth outcomes.MethodsThis study, based within the Norwegian Mother and Child Cohort Study (MoBa), includes 17,533 participants living in the two largest cities in Norway: Oslo and Bergen, and their two surrounding counties: Akershus and Hordaland. Air pollution levels at residential addresses were estimated using land use regression models and back-extrapolated to the period of each pregnancy using continuous monitoring station data. Birth outcomes were birth weight, low birth weight, gestational age, and preterm delivery obtained from the Medical Birth Registry of Norway. Information on lifestyle factors was collected from MoBa questionnaires completed by mothers during pregnancy. Linear and logistic regression models were used to analyse the associations between pregnancy NO2 exposure and birth outcomes.ResultsWe found a statistically significant negative association between pregnancy exposure to NO2 and birth weight −43.6 (95%CI −55.8 to −31.5) g per 10 μg/m3 NO2. However, after adjusting for either area or the combination of parity and maternal weight, no substantive effects of air pollution exposure were evident.ConclusionsExposure to air pollution during pregnancy was associated with decrease in birth weight, but area-related and lifestyle factors attenuated this association. We found no statistically significant associations of air pollution exposure with gestational age, low birth weight or preterm delivery.Electronic supplementary materialThe online version of this article (doi:10.1186/s13690-016-0138-8) contains supplementary material, which is available to authorized users.

Associations of air pollution exposure with blood pressure and heart rate variability are modified by oxidative stress genes: A repeated-measures panel among elderly urban residents.

BackgroundOxidative stress has been suggested as a major cause of elevated blood pressure (BP) and reduced heart rate variability (HRV) due to air pollution. We hypothesized that the associations of air pollution exposure with BP and HRV are modified by oxidative stress gene polymorphisms.MethodsBetween 2008 and 2010, we conducted up to 5 surveys of 547 elderly participants, measured their BP and HRV, and genotyped 47 single nucleotide polymorphisms (SNPs) in 18 oxidative stress genes. Linear mixed models were constructed to evaluate the associations of particulate matter ≤10 μm, nitrogen dioxide, and sulfur dioxide with BP and HRV, as well as the modifications of these associations by the genotyped SNPs.ResultsSingle-SNP analyses revealed interactions between air pollution and 15 SNPs (for BP) and 33 SNPs (for HRV) (all, P for interaction < 0.05). When we generated genetic risk scores for BP and HRV, using the SNPs with interactions in the single-SNP models, we found that associations of air pollution exposure with BP and HRV were modified by the genetic risk scores (P for interaction < 0.05).ConclusionsThese results strongly suggest that the associations of air pollution with BP and HRV are mediated by oxidative stress pathways.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-016-0130-3) contains supplementary material, which is available to authorized users.

Exposure to air pollution and development of asthma and rhinoconjunctivitis throughout childhood and adolescence: a population-based birth cohort study

Previous published analyses have focused on the effect of air pollution on asthma and rhinoconjunctivitis throughout early and middle childhood. However, the role of exposure to air pollution in the development of childhood and adolescent asthma and rhinoconjunctivitis remains unclear. We aimed to assess the longitudinal associations between exposure to air pollution and development of asthma and rhinoconjunctivitis throughout childhood and adolescence. We did a population-based birth cohort study of 14 126 participants from four prospective birth cohort studies from Germany, Sweden, and the Netherlands with 14–16 years of follow-up. We linked repeated questionnaire reports of asthma and rhinoconjunctivitis with annual average air pollution concentrations (nitrogen dioxide [NO2], particulate matter [PM] with a diameter of less than 2·5 μm [PM2·5], less than 10 μm [PM10], and between 2·5 μm and 10 μm [PMcoarse], and PM2·5 absorbance [indicator of soot]) at the participants' home addresses. We analysed longitudinal associations of air pollution exposure at participants' birth addresses and addresses at the time of follow-up with asthma and rhinoconjunctivitis incidence and prevalence in cohort-specific analyses, with subsequent meta-analysis and pooled analyses. Overall, the risk of incident asthma up to age 14–16 years increased with increasing exposure to NO2 (adjusted meta-analysis odds ratio [OR] 1·13 per 10 μg/m3 [95% CI 1·02–1·25]) and PM2·5 absorbance (1·29 per 1 unit [1·00–1·66]) at the birth address. A similar, albeit non-significant, trend was shown for PM2·5 and incident asthma (meta-analysis OR 1·25 per 5 μg/m3 [95% CI 0·94–1·66]). These associations with asthma were more consistent after age 4 years than before that age. There was no indication of an adverse effect of air pollution on rhinoconjunctivitis. Exposure to air pollution early in life might contribute to the development of asthma throughout childhood and adolescence, particularly after age 4 years, when asthma can be more reliably diagnosed. Reductions in levels of air pollution could help to prevent the development of asthma in children. The European Union.

Association of air pollution with cognitive functions and its modification by APOE gene variants in elderly women

BackgroundEpidemiological studies have shown effects of long-term exposure to air pollution on cardiovascular and respiratory health. However, studies investigating the effects of air pollution on cognition and brain function are limited.We investigated if neurocognitive functions are associated with air pollution exposure and whether apolipoprotein E (ApoE) alleles modify the association of air pollution exposure with cognition. MethodsWe investigated 789 women from the SALIA cohort during the 22-year follow-up examination (2008–2009). Exposure to particulate matter (PM) size fractions and nitrogen oxides (NOx) were assigned to home addresses. Traffic indicators were used to assess residential proximity to high traffic load. Level of cognitive performance was assessed using the CERAD-Plus test. Air pollution effects on cognitive functioning were estimated cross-sectionally using adjusted linear regression models. ResultsAir pollution was negatively associated with cognitive function and cognitive performance in the subtests for semantic memory and visuo-construction. Significant associations could be observed for figure copying with an interquartile range increase of NO2 (β=–0.28 (95%CI:–0.44;–0.12)), NOx (β=–0.25 (95%CI:–0.40;–0.09)), PM10 (β=–0.14 (95%CI:–0.26;–0.02)) and PM2.5 (β=–0.19 (95%CI:–0.36;–0.02)). The association with traffic load was significant in carriers of one or two ApoE ɛ4 risk alleles. ConclusionIn this study of elderly women, markers of air pollution were associated with cognitive impairment in the visuospatial domain. The association of traffic exposure is significant in participants carrying the ApoE ε4 risk allele.