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BACKGROUND: Evidence suggests that prenatal air pollution exposure alters DNA methylation (DNAm), which could go on to affect long-term health. It remains unclear whether DNAm alterations present at birth persist through early life. Identifying persistent DNAm changes would provide greater insight into the molecular mechanisms contributing to the association of prenatal air pollution exposure with atopic diseases. OBJECTIVES: This study investigated DNAm differences associated with prenatal nitrogen dioxide (NO2) exposure (a surrogate measure of trafficrelated air pollution) at birth and 1 y of age and examined their role in atopic disease. We focused on regions showing persistent DNAm differences from birth to 1 y of age and regions uniquely associated with postnatal NO2 exposure. METHODS: Microarrays measured DNAm at birth and at 1 y of age for an atopy-enriched subset of Canadian Health Infant Longitudinal Development (CHILD) study participants. Individual and regional DNAm differences associated with prenatal NO2 (푛= 128) were identified, and their persistence at age 1 y were investigated using linear mixed effects models (푛= 124). Postnatal-specific DNAm differences (푛= 125) were isolated, and their association with NO2 in the first year of life was examined. Causal mediation investigated whether DNAm differences mediated associations between NO2 and age 1 y atopy or wheeze. Analyses were repeated using biological sex-stratified data. RESULTS: At birth (푛= 128), 18 regions of DNAm were associated with NO2, with several annotated to HOX genes. Some of these regions were specifically identified in males (푛= 73), but not females (푛= 55). The effect of prenatal NO2 across CpGs within altered regions persisted at 1 y of age. No significant mediation effects were identified. Sex-stratified analyses identified postnatal-specific DNAm alterations. DISCUSSION: Regional cord blood DNAm differences associated with prenatal NO2 persisted through at least the first year of life in CHILD participants. Some differences may represent sex-specific alterations, but replication in larger cohorts is needed. The early postnatal period remained a sensitive window to DNAm perturbations. [ABSTRACT FROM AUTHOR]

The article explores the direct health effects of gas stove emissions. Topics discussed include association of childhood asthma cases in the U.S. to gas stove use, association of natural gas connections in residential and commercial construction to carbon emissions and climate change, pollutants produced by gas burners such as volatile organic compounds and liquefied petroleum gas or propane, and concentration of nitrogen dioxide in kitchens with overhead range hood versus sealed off kitchens.

The article presents a study of households with electric induction and gas stoves which assessed nitrogen dioxide exposures when the same individual used each stove type. Topics include effect of stove randomization on exposure in panel fixed effects regressions via ordinary least squares (OLS), background pollution variations, and effect of cooking events on changes to natural log-transformed and nontransformed kitchen nitrogen dioxide concentrations and personal particulate matter exposure.

BACKGROUND: Air pollutants may contribute to the development of Parkinson's disease (PD), but empirical evidence is limited and inconsistent. OBJECTIVES: This study aimed to prospectively investigate the associations of PD with ambient exposures to fine particulate matter with aerodynamic diameter = 2.5μm (PM2.5) and nitrogen dioxide (NO2). METHODS: We analyzed data from 47,108 US women from the Sister Study, enrolled from 2003–2009 (35–80 years of age) and followed through 2018. Exposures of interest included address-level ambient PM2.5 and NO2 in 2009 and their cumulative averages from 2009 to PD diagnosis with varying lag-years. The primary outcome was PD diagnosis between 2009 and 2018 (푛 = 163). We used multivariable Cox proportional hazards and time-varying Cox models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: NO2 exposure in 2009 was associated with PD risk in a dose-response manner. The HR and 95% CI were 1.22 (95% CI: 1.03, 1.46) for one interquartile [4.8 parts per billion (ppb)] increment in NO2, adjusting for age, race and ethnicity, education, smoking status, alcohol drinking, caffeine intake, body mass index, physical activity, census region, residential area type, area deprivation index (ADI), and self-reported health status. The association was confirmed in secondary analyses with time-varying averaged cumulative exposures. For example, the multivariable adjusted HR for PD per 4.8 ppb increment in NO2 was 1.25 (95% CI: 1.05, 1.50) in the 2-year lag analysis using cumulative average exposure. Post hoc subgroup analyses overall confirmed the association. However, statistical interaction analyses found that the positive association of NO2 with PD risk was limited to women in urban, rural, and small town areas and women with = 50th percentile ADI but not among women from suburban areas or areas with < 50th percentile ADI. In contrast, PM2.5 exposure was not associated with PD risk with the possible exception for women from the Midwest region of the US (HRinterquartile-range = 2.49, 95% CI: 1.20, 5.14) but not in other census regions. DISCUSSION: In this nationwide cohort of US women, higher level exposure to ambient NO2 is associated with a greater risk of PD. This finding needs to be independently confirmed and the underlying mechanisms warrant further investigation. [ABSTRACT FROM AUTHOR]

BACKGROUND: Heart failure (HF) poses a significant global disease burden. The current evidence on the impact of air pollution on HF remains inconsistent. OBJECTIVES: We aimed to conduct a systematic review of the literature and meta-analysis to provide a more comprehensive and multiperspective assessment of the associations between short- and long-term air pollution exposure and HF from epidemiological evidences. METHODS: Three databases were searched up to 31 August 2022 for studies investigating the association between air pollutants (PM2.5, PM10, NO2, SO2, CO, O3) and HF hospitalization, incidence, or mortality. A random effects model was used to derive the risk estimations. Subgroup analysis was conducted by geographical location, age of participants, outcome, study design, covered area, the methods of exposure assessment, and the length of exposure window. Sensitivity analysis and adjustment for publication bias were performed to test the robustness of the results. RESULTS: Of 100 studies covering 20 countries worldwide, 81 were for short-term and 19 were for long-term exposure. Almost all air pollutants were adversely associated with the risk of HF in both short- and long-term exposure studies. For short-term exposures, we found the risk of HF increased by 1.8% [relative risk (RR)=1.018, 95% confidence interval (CI): 1.011, 1.025] and 1.6% (RR=1.016, 95% CI: 1.011, 1.020) per 10-μg/m³ increment of PM2.5 and PM10, respectively. HF was also significantly associated with NO2, SO2, and CO, but not O3. Positive associations were stronger when exposure was considered over the previous 2 d (lag 0–1) rather than on the day of exposure only (lag 0). For long-term exposures, there were significant associations between several air pollutants and HF with RR (95% CI) of 1.748 (1.112, 2.747) per 10-μg/m³ increment in PM2.5, 1.212 (1.010, 1.454) per 10-μg/m³ increment in PM10, and 1.204 (1.069, 1.356) per 10-ppb increment in NO2, respectively. The adverse associations of most pollutants with HF were greater in low- and middle-income countries than in high-income countries. Sensitivity analysis demonstrated the robustness of our results. DISCUSSION: Available evidence highlighted adverse associations between air pollution and HF regardless of short- and long-term exposure. Air pollution is still a prevalent public health issue globally and sustained policies and actions are called for to reduce the burden of HF. [ABSTRACT FROM AUTHOR]

BACKGROUND: Ambient air pollution exposure has been associated with childhood asthma, but previous studies have primarily focused on prevalence of asthma and asthma-related outcomes and urban traffic-related exposures. OBJECTIVE: We examined nationwide associations between pre- and postnatal exposure to ambient air pollution components and asthma incidence in children age 0–19 y. METHODS: Asthma incidence was identified from hospital admission, emergency room, and outpatient contacts among all live-born singletons born in Denmark between 1998 and 2016. We linked registry data with monthly mean concentrations of particulate matter (PM) with aerodynamic diameter ≤2.5 μm (PM2.5) and PM with aerodynamic diameter ≤10 μm (PM10), nitrogen dioxide (NO2), nitrogen oxides, elemental carbon, and organic carbon (OC), sulfur dioxide, ozone, sulfate, nitrate, ammonium, secondary organic aerosols, and sea salt. Associations were estimated with Cox proportional hazard models using fixed prenatal exposure means and time-varying postnatal exposures. RESULTS: Of the 1,060,154 children included, 6.1% had asthma during the mean follow-up period of 8.8 y. The risk of asthma increased with increasing prenatal exposure to all pollutants except for O3 and sea salt. We also observed increased risk after restriction to asthma after age 4 y, after additional adjustment for area-specific socioeconomic status, and for postnatal exposure to most pollutants. The hazard ratio (HR) associated with an interquartile range increase of 2.4 and 8.7 µg/m³ in prenatal exposure was 1.06 [95% confidence interval (CI): 1.04, 1.08] for PM2.5 and 1.04 (95% CI: 1.02, 1.05) for NO2, respectively. This association with PM2.5 was stable after adjustment for NO2, whereas it attenuated for NO2 to 1.01 (95% CI: 0.99, 1.03) after adjustment for PM2.5. For a 0.5-µg/m³ increase in prenatal OC exposure, for which biomass is an important source, the HR was 1.08 (95% CI: 1.06, 1.10), irrespective of adjustment for PM2.5. DISCUSSION: These findings suggest that early-life exposure to ambient air pollution from multiple sources contributes to asthma development. [ABSTRACT FROM AUTHOR]

The article discusses research which analyzed the association between long-term air pollution exposure and mitochondrial DNA copy number (mtDNA-CN) using data from UK Biobank. The study estimated and compared differences in mtDNA-CN by quintiles of air pollutant concentrations. It measured concentrations of particulate matter, black carbon and nitrogen dioxide and examined their association with the prevalence of hypertension, diabetes, hyperlipidemia, or cardiovascular disease.

BACKGROUND: Recent studies have reported the association between air pollution exposure and reduced kidney function. However, it is unclear whether air pollution is associated with an increased risk of acute kidney injury (AKI). OBJECTIVES: To address this gap in knowledge, we investigated the effect estimates of long-term exposures to fine particulate matter [PM ≤ 2.5 μm in aerodynamic diameter (PM2.5)], nitrogen dioxide (NO2), and ozone (O3) on the risk of first hospital admission for AKI using nationwide Medicare data. METHODS: This nationwide population-based longitudinal cohort study included 61,300,754 beneficiaries enrolled in Medicare Part A fee-for-service (FFS) who were ≥65 years of age and resided in the continental United States from the years 2000 through 2016. We applied Cox-equivalent Poisson models to estimate the association between air pollution and first hospital admission for AKI. RESULTS: Exposure to PM2.5, NO2, and O3 was associated with increased risk for first hospital admission for AKI, with hazard ratios (HRs) of 1.17 (95% CI: 1.16, 1.19) for a 5-μg/m³ increase in PM2.5, 1.12 (95% CI: 1.11, 1.13) for a 10-ppb increase in NO2, and 1.03 (95% CI: 1.02, 1.04) for a 10-ppb increase in summer-period O3 (June to September). The associations persisted at annual exposures lower than the current National Ambient Air Quality Standard. DISCUSSION: This study found an association between exposures to air pollution and the risk of the first hospital admission with AKI, and this association persisted even at low concentrations of air pollution. Our findings provide beneficial implications for public health policies and air pollution guidelines to alleviate health care expenditures and the disease burden attributable to AKI. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure to air pollution has been associated with a higher risk of type 2 diabetes (T2D), but studies investigating whether deprived groups are more susceptible to the harmful effects of air pollution are inconsistent. OBJECTIVES: We aimed to investigate whether the association between air pollution and T2D differed according to sociodemographic characteristics, comorbidity, and coexposures. METHODS: We estimated residential exposure to PM2.5, ultrafine particles (UFP), elemental carbon, and NO2 for all persons living in Denmark in the period 2005–2017. In total, 1.8 million persons 50–80 y of age were included for main analyses of whom 113,985 developed T2D during follow-up. We conducted additional analyses on 1.3 million persons age 35–50 y. Using Cox proportional hazards model (relative risk) and Aalens additive hazard model (absolute risk), we calculated associations between 5-y time-weighted running means of air pollution and T2D in strata of sociodemographic variables, comorbidity, population density, road traffic noise, and green space proximity. RESULTS: Air pollution was associated with T2D, especially among people age 50-80 y, with hazard ratios of 1.17 [95% confidence interval (CI): 1.13, 1.21] per 5 μg/m³ PM2.5 and 1.16 (95% CI: 1.13, 1.19) per 10,000 UFP/cm³. In the age 50-80 y population, we found higher associations between air pollution and T2D among men in comparison with women, people with lower education vs. individuals with high education, people with medium income vs. those with low or high income, people cohabiting vs. those living alone, and people with comorbidities vs. those without comorbidities. We observed no marked changes according to occupation, population density, road noise, or surrounding greenness. In the age 35-50 y population, similar tendencies were observed, except in relation to sex and occupation, where we observed associations with air pollution only among women and blue-collar workers. DISCUSSION: We found stronger associations between air pollution and T2D among people with existing comorbidities and weaker associations among people with high socioeconomic status in comparison with those with lower socioeconomic status. [ABSTRACT FROM AUTHOR]

BACKGROUND: Metabolic syndrome (MetS), a major contributor to cardiovascular and metabolic diseases, has been linked with exposure to air pollution. However, the relationship between air pollutants and the five components of MetS [abdominal obesity, elevated triglyceride, decreased high-density lipoprotein cholesterol (HDL-C), elevated blood pressure, and elevated fasting blood glucose levels], has not been clearly described. OBJECTIVE: We examined the association between long-term exposure to air pollutants and the occurrence of MetS and its components by using a longitudinal cohort in Taiwan. METHODS: The MJ Health Research Foundation is a medical institute that conducts regular physical examinations. The development of MetS, based on a health examination and the medical history of an MJ cohort of 93,771 participants who were enrolled between 2006 and 2016 and had two or more examinations, was compared with estimated exposure to air pollutants in the year prior to health examination. The exposure levels to fine particulate matter [PM with an aerodynamic diameter of ≤2.5 μm (PM2.5)] and nitrogen dioxide (NO2) in the participants' residential areas were estimated using a hybrid Kriging/land-use regression (LUR) model executed using the XGBoost algorithm and a hybrid Kriging/LUR model, respectively. Cox regression with time-dependent covariates was conducted to estimate the effects of annual air pollutant exposure on the risk of MetS and its components. RESULTS: During the average follow-up period of 3.4 y, the incidence of MetS was 38.1/1,000 person-years. After mutual adjustment and adjustments for potential covariates, the results indicated that every 10-μg/m³ increase in annual PM2.5 concentration was associated with an increased risk of abdominal obesity [adjusted hazard ratio (aHR)=1.07; 95% confidence interval (CI): 1.01, 1.14], hypertriglyceridemia (aHR=1.17; 95% CI: 1.11, 1.23), low HDL-C (aHR=1.09; 95% CI: 1.02, 1.17), hypertension (aHR=1.15; 95% CI: 1.09, 1.21), and elevated fasting blood glucose (aHR=1.15; 95% CI: 1.10, 1.20). Furthermore, PM2.5 and NO2 may increase the risk of developing MetS among people who already “have” some components of MetS. DISCUSSION: Our findings suggest that in apparently healthy adults undergoing physical examination, exposure to PM2.5 and NO2 might be associated with the occurrence of MetS and its components. [ABSTRACT FROM AUTHOR]

BACKGROUND: Older adults show a high variability in cognitive performance that cannot be explained by aging alone. Although research has linked air pollution and noise to cognitive impairment and structural brain alterations, the potential impact of air pollution and noise on functional brain organization is unknown. OBJECTIVE: This study examined the associations between long-term air pollution and traffic noise with measures of functional brain organization in older adults. We hypothesize that exposures to high air pollution and noise levels are associated with age-like changes in functional brain organization, shown by less segregated brain networks. METHODS: Data from 574 participants (44.1% female, 56–85 years of age) in the German 1000BRAINS study (2011–2015) were analyzed. Exposure to particulate matter (PM10, PM2.5, and PM2.5 absorbance), accumulation mode particle number (PNAM), and nitrogen dioxide (NO2) was estimated applying land-use regression and chemistry transport models. Noise exposures were assessed as weighted 24-h (Lden) and nighttime (Lnight) means. Functional brain organization of seven established brain networks (visual, sensorimotor, dorsal and ventral attention, limbic, frontoparietal and default network) was assessed using resting-state functional brain imaging data. To assess functional brain organization, we determined the degree of segregation between networks by comparing the strength of functional connections within and between networks. We estimated associations between air pollution and noise exposure with network segregation, applying multiple linear regression models adjusted for age, sex, socioeconomic status, and lifestyle variables. RESULTS: Overall, small associations of high exposures with lesser segregated networks were visible. For the sensorimotor networks, we observed small associations between high air pollution and noise and lower network segregation, which had a similar effect size as a 1-y increase in age [e.g., in sensorimotor network, -0.006 (95% CI: -0.021, 0.009) per 0.3 × 10-5/m increase in PM2.5 absorbance and -0.004 (95% CI: -0.006, -0.002) per 1-y age increase]. CONCLUSION: High exposure to air pollution and noise was associated with less segregated functional brain networks. [ABSTRACT FROM AUTHOR]

The article discusses a study that provides additional support for an association between exposure to the air pollutant nitrogen dioxide and risk of developing Parkinson's disease (PD). It describes the researchers' use of data from the Sister Study that investigated environmental and genetic risk factors for breast cancer and other chronic diseases. It examines the discovery of a positive dose-response association between nitrogen dioxide exposure and PD risk by the researchers.

The authors discuss an article by M. Johnson and colleagues, published in the issue which reported results from their study of respiratory distress in a sample of mother-child dyads across ten Canadian cities. Topics include common risk factors for severe respiratory distress, finding on particulate matter exposure, and role of air pollution in the burden of neonatal respiratory stress.

BACKGROUND: Air pollution disparities by socioeconomic status (SES) are well documented for the United States, with most literature indicating an inverse relationship (i.e., higher concentrations for lower-SES populations). Few studies exist for China, a country accounting for 26% of global premature deaths from ambient air pollution. OBJECTIVE: Our objective was to test the relationship between ambient air pollution exposures and SES in China. METHODS: We combined estimated year 2015 annual-average ambient levels of nitrogen dioxide (NO2) and fine particulate matter [PM =2.5 µm in aerodynamic diameter (PM2.5)] with national demographic information. Pollution estimates were derived from a national empirical model for China at 1-km spatial resolution; demographic estimates were derived from national gridded gross national product (GDP) per capita at 1-km resolution, and (separately) a national representative sample of 21,095 individuals from the China Health and Retirement Longitudinal Study (CHARLS) 2015 cohort. Our use of global data on population density and cohort data on where people live helped avoid the spatial imprecision found in publicly available census data for China. We quantified air pollution disparities among individual’s rural-to-urban migration status; SES factors (education, occupation, and income); and minority status. We compared results using three approaches to SES measurement: individual SES score, community-averaged SES score, and gridded GDP per capita. RESULTS: Ambient NO2 and PM2.5 levels were higher for higher-SES populations than for lower-SES population, higher for long-standing urban residents than for rural-to-urban migrant populations, and higher for the majority ethnic group (Han) than for the average across nine minority groups. For the three SES measurements (individual SES score, community-averaged SES score, gridded GDP per capita), a 1-interquartile range higher SES corresponded to higher concentrations of 6–9 µg/m³ NO2 and 3–6 µg/m³ PM2.5; average concentrations for the highest and lowest 20th percentile of SES differed by 41–89% for NO2 and 12–25% for PM2.5. This pattern held in rural and urban locations, across geographic regions, across a wide range of spatial resolution, and for modeled vs. measured pollution concentrations. CONCLUSIONS: Multiple analyses here reveal that in China, ambient NO2 and PM2.5 concentrations are higher for high-SES than for low-SES individuals; these results are robust to multiple sensitivity analyses. Our findings are consistent with the idea that in China’s current industrialization and urbanization stage, economic development is correlated with both SES and air pollution. To our knowledge, our study provides the most comprehensive picture to date of ambient air pollution disparities in China; the results differ dramatically from results and from theories to explain conditions in the United States. [ABSTRACT FROM AUTHOR]

BACKGROUND: Population studies support the adverse associations of air pollution exposures with child behavioral functioning and cognitive performance, but few studies have used spatiotemporally resolved pollutant assessments. OBJECTIVES: We investigated these associations using more refined exposure assessments in 1,967 mother–child dyads from three U.S. pregnancy cohorts in six cities in the ECHO-PATHWAYS Consortium. METHODS: Pre- and postnatal nitrogen dioxide (NO2) and particulate matter (PM) ≤2.5 µm in aerodynamic diameter (PM2.5) exposures were derived from an advanced spatiotemporal model. Child behavior was reported as Total Problems raw score using the Child Behavior Checklist at age 4–6 y. Child cognition was assessed using cohort-specific cognitive performance scales and quantified as the Full-Scale Intelligence Quotient (IQ). We fitted multivariate linear regression models that were adjusted for sociodemographic, behavioral, and psychological factors to estimate associations per 2- unit increase in pollutant in each exposure window and examined modification by child sex. Identified critical windows were further verified by distributed lag models (DLMs). RESULTS: Mean NO2 and PM2.5 ranged from 8.4 to 9.0 ppb and 8.4 to 9.1 µg/m³, respectively, across pre- and postnatal windows. Average child Total Problems score and IQ were 22.7 [standard deviation (SD): 18.5] and 102.6 (SD: 15.3), respectively. Children with higher prenatal NO2 exposures were likely to have more behavioral problems [b: 1.24; 95% confidence interval (CI): 0.39, 2.08; per 2 ppb NO2], particularly NO2 in the first and second trimester. Each 2-µg/m³ increase in PM2.5 at age 2–4 y was associated with a 3.59 unit (95% CI: 0.35, 6.84) higher Total Problems score and a 2.63 point (95% CI: -5.08, -0.17) lower IQ. The associations between PM2.5 and Total Problems score were generally stronger in girls. Most predefined windows identified were not confirmed by DLMs. DISCUSSION: Our study extends earlier findings that have raised concerns about impaired behavioral functioning and cognitive performance in children exposed to NO2 and PM2.5 in utero and in early life. [ABSTRACT FROM AUTHOR]

The article discusses a 2022 French study on whether outdoor air pollution exposure is linked to poor hand grip strength (HGP). Results showed significant interaction between pollutants and sex, with links to poorer HGP in men 65 years old and above, who had low education, and who are nonsmokers in comparison with other study participants. Also noted is the absence of significant interaction with age for women.

BACKGROUND: School classrooms, where students spend the majority of their time during the day, are the second most important indoor microenvironment for children. OBJECTIVE: We investigated factors influencing classroom exposures to fine particulate matter (PM2.5.), black carbon (BC), and nitrogen dioxide (NO2) in urban schools in the northeast United States. METHODS: Over the period of 10 y (2008–2013; 2015–2019) measurements were conducted in 309 classrooms of 74 inner-city schools during fall, winter, and spring of the academic period. The data were analyzed using adaptive mixed-effects least absolute shrinkage and selection operator (LASSO) regression models. The LASSO variables included meteorological-, school-, and classroom-based covariates. RESULTS: LASSO identified 10, 10, and 11 significant factors (푝<0.05) that were associated with indoor PM2.5, BC, and NO2 exposures, respectively. The overall variability explained by these models was R² =0.679, 0.687, and 0.621 for PM2.5, BC, and NO2, respectively. Of the model’s explained variability, outdoor air pollution was the most important predictor, accounting for 53.9%, 63.4%, and 34.1% of the indoor PM2.5, BC, and NO2 concentrations. School-based predictors included furnace servicing, presence of a basement, annual income, building type, building year of construction, number of classrooms, number of students, and type of ventilation that, in combination, explained 18.6%, 26.1%, and 34.2% of PM2.5, BC, and NO2 levels, whereas classroom-based predictors included classroom floor level, classroom proximity to cafeteria, number of windows, frequency of cleaning, and windows facing the bus area and jointly explained 24.0%, 4.2%, and 29.3% of PM2.5, BC, and NO2 concentrations, respectively. DISCUSSION: The adaptive LASSO technique identified significant regional-, school-, and classroom-based factors influencing classroom air pollutant levels and provided robust estimates that could potentially inform targeted interventions aiming at improving children’s health and well-being during their early years of development. [ABSTRACT FROM AUTHOR]

BACKGROUND: Although short-term ozone (O3) exposure has been associated with a series of adverse health outcomes, research on the health effects of chronic O3 exposure is still limited, especially in developing countries because of the lack of long-term exposure estimates. OBJECTIVES: The present study aimed to estimate the spatiotemporal distribution of monthly mean daily maximum 8-h average O3 concentrations in China from 2005 to 2019 at a 0.05° spatial resolution. METHODS: We developed a machine learning model with a satellite-derived boundary-layer O3 column, O3 precursors, meteorological conditions, land-use information, and proxies of anthropogenic emissions as predictors. RESULTS: The random, spatial, and temporal cross-validation 푅² of our model were 0.87, 0.86, and 0.76, respectively. Model-predicted spatial distribution of ground-level O3 concentrations showed significant differences across seasons. The highest summer peak of O3 occurred in the North China Plain, whereas southern regions were the most polluted in winter. Most large urban centers showed elevated O3 levels, but their surrounding suburban areas may have even higher O3 concentrations owing to nitrogen oxides titration. The annual trend of O3 concentrations fluctuated over 2005-2013, but a significant nationwide increase was observed afterward. DISCUSSION: The present model had enhanced performance in predicting ground-level O3 concentrations in China. This national data set of O3 concentrations would facilitate epidemiological studies to investigate the long-term health effect of O3 in China. Our results also highlight the importance of controlling O3 in China’s next round of the Air Pollution Prevention and Control Action Plan. [ABSTRACT FROM AUTHOR]

BACKGROUND: Olfactory impairment is increasingly common with older age, which may be in part explained by cumulative effects of exposure to inhaled toxins. However, population-based studies investigating the relationship between air pollution and olfactory ability are scarce. OBJECTIVES: We aimed to investigate associations between exposure to common air pollutants and longitudinal change in odor identification. METHODS: Our study of 2,468 participants (mean age = 72.3 y; 61.1% female), of which 1,774 participants (mean age = 70.5 y; 61.9% female) had at least two olfactory assessments over 12 y of follow-up from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), Stockholm, Sweden. Participants were free from cognitive impairment and neurodegenerative disease at baseline. Odor identification ability was assessed with Sniffin’ Sticks. Change in olfactory performance was estimated with linear mixed models. Exposure to two major airborne pollutants [particulate matter with aerodynamic diameter =2.5 μm (PM2.5) and nitrogen oxides (NOx)] for the 5 y preceding baseline was assessed using spatiotemporal dispersion models for outdoor levels at residential addresses. RESULTS: Participants showed significant decline in odor identification ability for each year in the study {β= -0.20 [95% confidence interval (CI): -0.22, 0.18; 푝< 0.001]}. After adjustment for all covariates, residents of third [β= -0.09 (95% CI: -0.14, -0.04; 푝< 0.001)] and fourth [β= -0.07 (95% CI: -0.12, -0.02; 푝= 0.005)] exposure quartiles of PM2.5 had faster rates of olfactory decline than residents from the first quartile. Similar results were observed for the third [β= -0.05 (95% CI: -0.10, -0.01; 푝= 0.029)] and fourth [β= -0.07 (95% CI: -0.11, -0.02; 푝= 0.006) quartiles of NOx]. DISCUSSION: Our results suggest an association between air pollution exposure and subsequent olfactory decline. We speculate that cumulative effects of airborne pollutants on the olfactory system may be one underlying cause of olfactory impairment in aging. [ABSTRACT FROM AUTHOR]

BACKGROUND: Mounting evidence has shown that long-term exposure to fine particulate matter [PM ≤ 2.5 μm in aerodynamic diameter (PM2.5)] and ozone (O3) can increase mortality. However, the health effects associated with long-term exposure to nitrogen dioxide (NO2) are less clear, in particular the evidence is scarce for NO2 at low levels that are below the current international guidelines. METHODS: We constructed a population-based full cohort comprising all Medicare beneficiaries (aged ≥65, 푁 =13,590,387) in the southeastern United States from 2000 to 2016, and we then further defined the below-guideline cohort that included only those who were always exposed to low-level NO2, that is, with annual means below the current World Health Organization guidelines (i.e., ≤21 ppb). We applied previously estimated spatially and temporally resolved NO2 concentrations and assigned annual means to study participants based on their ZIP code of residence. Cox proportional hazards models were used to examine the association between long-term exposure to low-level NO2 and all-cause mortality, adjusting for potential confounders. RESULTS: About 71.1% of the Medicare beneficiaries in the southeastern United States were always exposed to low-level NO2 over the study period. We observed an association between long-term exposure to low-level NO2 and all-cause mortality, with a hazard ratio (HR)= 1.042 (95% CI: 1.040, 1.045) in single-pollutant models and a HR= 1.047 (95% CI: 1.045, 1.049) in multipollutant models (adjusting for PM2.5 and O3), per 10-ppb increase in annual NO2 concentrations. The penalized spline indicates a linear exposure–response relationship across the entire NO2 exposure range. Medicare enrollees who were White, female, and residing in urban areas were more vulnerable to long-term NO2 exposure. CONCLUSION: Using a large and representative cohort, we provide epidemiological evidence that long-term exposure to NO2, even below the national and global ambient air quality guidelines, was approximately linearly associated with a higher risk of mortality among older adults, independent of PM2.5 and O3 exposure. Improving air quality by reducing NO2 emissions, therefore, may yield significant health benefits. [ABSTRACT FROM AUTHOR]

BACKGROUND: Few studies have investigated air pollution exposure disparities by race/ethnicity and income across criteria air pollutants, locations, or time. OBJECTIVE: The objective of this study was to quantify exposure disparities by race/ethnicity and income throughout the contiguous United States for six criteria air pollutants, during the period 1990 to 2010. METHODS: We quantified exposure disparities among racial/ethnic groups (non-Hispanic White, non-Hispanic Black, Hispanic (any race), non-Hispanic Asian) and by income for multiple spatial units (contiguous United States, states, urban vs. rural areas) and years (1990, 2000, 2010) for carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), particulate matter with aerodynamic diameter =2.5 µm (PM2.5; excluding year-1990), particulate matter with aerodynamic diameter =10 µm (PM10), and sulfur dioxide (SO2). We used census data for demographic information and a national empirical model for ambient air pollution levels. RESULTS: For all years and pollutants, the racial/ethnic group with the highest national average exposure was a racial/ethnic minority group. In 2010, the disparity between the racial/ethnic group with the highest vs. lowest national-average exposure was largest for NO2 [54% (4.6 ppb)], smallest for O3 [3.6% (1.6 ppb)], and intermediate for the remaining pollutants (13%–19%). The disparities varied by U.S. state; for example, for PM2.5 in 2010, exposures were at least 5% higher than average in 63% of states for non-Hispanic Black populations; in 33% and 26% of states for Hispanic and for non-Hispanic Asian populations, respectively; and in no states for non-Hispanic White populations. Absolute exposure disparities were larger among racial/ethnic groups than among income categories (range among pollutants: between 1.1 and 21 times larger). Over the period studied, national absolute racial/ethnic exposure disparities declined by between 35% (0.66 µg/m³; PM2.5) and 88% (0.35 ppm; CO); relative disparities declined to between 0.99 × (PM2.5; i.e., nearly zero change) and 0.71 × (CO; i.e., a ~29% reduction). DISCUSSION: As air pollution concentrations declined during the period 1990 to 2010, absolute (and to a lesser extent, relative) racial/ethnic exposure disparities also declined. However, in 2010, racial/ethnic exposure disparities remained across income levels, in urban and rural areas, and in all states, for multiple pollutants. [ABSTRACT FROM AUTHOR]

The article discusses the results of a study on the link of nitrogen oxides and fine particulates with the risk of patients with inflammatory bowel disease (IBD) for gastrointestinal surgeries and gastrointestinal cancer. Topics mentioned include the assessment of patients' long-term exposure to nitrogen dioxide and fine particulates, the analysis of a patient's diet, and the benefit of environmental health to long-term prognosis of patients with IBD.

BACKGROUND: Studies of the effects of prenatal environmental exposures on postnatal outcomes are particularly vulnerable to live birth bias; i.e., the bias that arises from the necessary restriction of the analysis to live births when that is influenced by both the exposure under study A and unmeasured factors U that also affect the outcome. OBJECTIVES: In the context of a recent publication of nitrogen dioxide (NO2) and autism spectrum disorder (ASD) that found an odds ratio (OR) of 0.77 per 5:85 ppb NO2 during pregnancy, we aimed to examine what parameters would be needed to account for this protective association through live birth bias. METHODS: We simulated the magnitude of bias under two selection mechanisms and when both mechanisms co-occur, assuming a true null effect. Simulation input parameters were based on characteristics of the original study and a range of plausible values for the prevalence of unmeasured factor U and the ORs for the selection effects (i.e., the effects of NO2 and U on loss and of U on ASD). Each scenario was simulated 1,000 times. RESULTS: We found that the magnitude of bias was small when NO2 and 푈 independently influenced pregnancy loss (collider-stratification without interaction), was stronger when NO2-induced loss preferentially occurred in 푈 = 1 (depletion of susceptibles), and was strongest when both mechanisms worked together. For example, ORs of 3.0 for NO2-loss, U-loss, U-ASD, and 푈 prevalence = 0.75 yielded NO2-ASD ORs per 5.85 ppb NO2 of 0.95, 0.89, and 0.75 for the three scenarios, respectively. The bias is amplified with multiple Us, yielding ORs as low as 0.51. DISCUSSION: Our simulations illustrate that live birth bias may lead to exposure–outcome associations that are biased downward, where the extent of the bias depends on the fetal selection mechanism, the strength of that selection, and the prevalence of U. [ABSTRACT FROM AUTHOR]

BACKGROUND: Limited data suggest air pollution exposures may contribute to pediatric high blood pressure (HBP), a known predictor of adult cardiovascular diseases. METHODS: We investigated this association in the Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) study, a sociodemographically diverse pregnancy cohort in the southern United States with participants enrolled from 2006 to 2011. We included 822 mother–child dyads with available address histories and a valid child blood pressure measurement at 4–6 y. Systolic (SBP) and diastolic blood pressures (DBP) were converted to age-, sex-, and height-specific percentiles for normal-weight U.S. children. HBP was classified based on SBP or DBP =90th percentile. Nitrogen dioxide (NO2) and particulate matter =2.5 μm in aerodynamic diameter (PM2.5) estimates in both pre- and postnatal windows were obtained from annual national models and spatiotemporal models, respectively. We fit multivariate Linear and Poisson regressions and explored multiplicative joint effects with maternal nutrition, child sex, and maternal race using interaction terms. RESULTS: Mean PM2.5 and NO2 in the prenatal period were 10.8 [standard deviation (SD): 0.9] μm/m³ and 10.0 (SD: 2.4) ppb, respectively, and 9.9 (SD: 0.6) μmg/m³ and 8.8 (SD: 1.9) ppb from birth to the 4-y-old birthday. On average, SBP percentile increased by 14.6 (95% CI: 4.6, 24.6), and DBP percentile increased by 8.7 (95% CI: 1.4, 15.9) with each 2-μmg/m³ increase in second-trimester PM2.5. PM2.5 averaged over the prenatal period was only significantly associated with higher DBP percentiles [Β= 11.6 (95% CI: 2.9, 20.2)]. Positive associations of second-trimester PM2.5 with SBP and DBP percentiles were stronger in children with maternal folate concentrations in the lowest quartile (푝interaction = 0.05 and 0.07, respectively) and associations with DBP percentiles were stronger in female children (푝interaction = 0.05). We did not detect significant association of NO2, road proximity, and postnatal PM2.5 with any outcomes. CONCLUSIONS: The findings suggest that higher prenatal PM2.5 exposure, particularly in the second trimester, is associated with elevated early childhood blood pressure. This adverse association could be modified by pregnancy folate concentrations. [ABSTRACT FROM AUTHOR]

BACKGROUND: Air pollution-attributable disease burdens reported at global, country, state, or county levels mask potential smaller-scale geographic heterogeneity driven by variation in pollution levels and disease rates. Capturing within-city variation in air pollution health impacts is now possible with high-resolution pollutant concentrations. OBJECTIVES: We quantified neighborhood-level variation in air pollution health risks, comparing results from highly spatially resolved pollutant and disease rate data sets available for the Bay Area, California. METHODS: We estimated mortality and morbidity attributable to nitrogen dioxide (NO2), black carbon (BC), and fine particulate matter [PM =2.5 µm in aerodynamic diameter (PM2.5)] using epidemiologically derived health impact functions. We compared geographic distributions of pollution-attributable risk estimates using concentrations from a) mobile monitoring of NO2 and BC; and b) models predicting annual NO2, BC and PM2.5 concentrations from land-use variables and satellite observations. We also compared results using county vs. census block group (CBG) disease rates. RESULTS: Estimated pollution-attributable deaths per 100,000 people at the 100-m grid-cell level ranged across the Bay Area by a factor of 38, 4, and 5 for NO2 [mean = 30 (95% CI: 9, 50)], BC [mean = 2 (95% CI: 1, 2)], and PM2.5, [mean = 49 (95% CI: 33, 64)]. Applying concentrations from mobile monitoring and land-use regression (LUR) models in Oakland neighborhoods yielded similar spatial patterns of estimated grid-cell–level NO2-attributable mortality rates. Mobile monitoring concentrations captured more heterogeneity [mobile monitoring mean = 64 (95% CI: 19, 107) deaths per 100,000 people; LUR mean = 101 (95% CI: 30, 167)]. Using CBG-level disease rates instead of county-level disease rates resulted in 15% larger attributable mortality rates for both NO2 and PM2.5, with more spatial heterogeneity at the grid-cell–level [NO2 CBG mean = 41 deaths per 100,000 people (95% CI: 12, 68); NO2 county mean = 38 (95% CI: 11, 64); PM2.5 CBG mean = 59 (95% CI: 40, 77); and PM2.5 county mean = 55 (95% CI: 37, 71)]. DISCUSSION: Air pollutant-attributable health burdens varied substantially between neighborhoods, driven by spatial variation in pollutant concentrations and disease rates. [ABSTRACT FROM AUTHOR]

BACKGROUND: The impact of nitrogen dioxide (NO2) and particulate matter with an aerodynamic diameter of less than or equal to 2.5. microns (PM2.5) exposures on lung function has been investigated mainly in children and less in adults. Furthermore, it is unclear whether short-term deviations of air pollutant concentration need to be considered in long-term exposure models. OBJECTIVES: The aims of this study were to investigate the association between short-term air pollution exposure and lung function and to assess whether short-term deviations of air pollutant concentration should be integrated into long-term exposure models. METHODS: Short-term (daily averages 0–7 d prior) and long-term (1- and 4-y means) NO2 and PM2.5 concentrations were modeled using satellite, land use, and meteorological data calibrated on ground measurements. Forced expiratory volume within the first second (FEV1) of forced exhalation and forced vital capacity (FVC) were measured during a LuftiBus assessment (2003–2012) and linked to exposure information from the Swiss National Cohort for 36,085 adults (ages 18–95 y). We used multiple linear regression to estimate adjusted associations, and additionally adjusted models of long-term exposures for short-term deviations in air pollutant concentrations. RESULTS: A 10 µg/m³ increase in NO2 and PM2.5 on the day of the pulmonary function test was associated with lower FEV1 and FVC (NO2: FEV1 -8.0 ml [95% confidence interval: -13.4, -2.7], FVC -16.7 ml [-23.4, -10.0]; PM2.5: FEV1 -15.3 ml [-21.9, -8.7], FVC -18.5 ml [-26.5, -10.5]). A 10 µg/m³ increase in 1-y mean NO2 was also associated with lower FEV1 (-7:7 ml; -15.9, 0.5) and FVC (-21.6 ml; -31.9, -11.4), as was a 10 µg/m³ increase in 1-y mean PM2.5 (FEV1: -42.2 ml; -56.9, -27.5; FVC: -82.0 ml; -100.1, -63.9). These associations were robust to adjustment for short-term deviations in the concentration of each air pollutant. CONCLUSIONS: Short- and long-term air pollution exposures were negatively associated with lung function, in particular long-term PM2.5 exposure with FVC. Our findings contribute substantially to the evidence of adverse associations between air pollution and lung function in adults. [ABSTRACT FROM AUTHOR]

BACKGROUND: Despite the importance of understanding associations of air pollution and noise exposure with loss of neurocognitive performance, studies investigating these exposures and local brain structure are limited. OBJECTIVE: We estimated associations of residential air pollution and noise exposures with neurocognitive test performance and the local gyrification index (lGI), a marker for local brain atrophy, among older adults. METHODS: For 푛= 615 participants from the population-based 1000BRAINS study, based on the German Heinz Nixdorf Recall study, we assessed residential exposures to particulate matter (PM10, PM2.5, PM2.5abs), accumulation mode particle number (PNAM), and nitrogen oxides (NOx, NO2), using land-use regression and chemistry transport models. Weighted 24-h and nighttime noise were modeled according to the European noise directive. We evaluated associations of air pollution and noise exposure at the participants' 2006-2008 residential addresses with neurocognitive test performance and region-specific lGI values (푛= 590) from magnetic resonance imaging, both assessed in 2011-2015, using linear regression and adjusting for demographic and personal characteristics. RESULTS: Air pollution and noise were associated with language and short-term/working memory and with local atrophy of the fronto-parietal network (FPN), a functional resting-state network associated with these cognitive processes. For example, per 2-ϕg/m³ PM10, local brain atrophy was more pronounced in the posterior brain regions of the FPN, with a -0.02 [95% confidence interval (CI): -0.04, 0.00] lower lGI. In contrast, in the anterior regions of the FPN, weighted 24-h and nighttime noise were associated with less local brain atrophy [e.g., 0.02 (95% CI: 0.00, 0.04) for 10 dB(A) 24-h noise]. CONCLUSIONS: Air pollution and noise exposures were associated in opposite directions with markers of local atrophy of the FPN in the right brain hemisphere in older adults, suggesting that both chronic air pollution and noise exposure may influence the physiological aging process of the brain. [ABSTRACT FROM AUTHOR]

BACKGROUND: Air pollution has been related to brain structural alterations, but a relationship with white matter microstructure is unclear. OBJECTIVES: We assessed whether pregnancy and childhood exposures to air pollution are related to white matter microstructure in preadolescents. METHODS: We used data of 2,954 children from the Generation R Study, a population-based birth cohort from Rotterdam, Netherlands (2002–2006). Concentrations of 17 air pollutants including nitrogen oxides (NOX), particulate matter (PM), and components of PM were estimated at participants’ homes during pregnancy and childhood using land-use regression models. Diffusion tensor images were obtained at child’s 9–12 years of age, and fractional anisotropy (FA) and mean diffusivity (MD) were computed. We performed linear regressions adjusting for socioeconomic and lifestyle characteristics. Single-pollutant analyses were followed by multipollutant analyses using the Deletion/Substitution/Addition (DSA) algorithm. RESULTS: In the single-pollutant analyses, higher concentrations of several air pollutants during pregnancy or childhood were associated with significantly lower FA or higher MD (p<0.05). In multipollutant models of pregnancy exposures selected by DSA, higher concentration of fine particles was associated with significantly lower FA [-0.71 (95% CI: -1.26, -0.16) per 5 µg/m³ fine particles] and higher concentration of elemental silicon with significantly higher MD [0.06 (95% CI: 0.01, 0.11) per 100 ng/m³ silicon]. Multipollutant models of childhood exposures selected by DSA indicated significant associations of NOX with FA [-0.14 (95% CI: -0.23, -0:04) per 20-µg/m³ NOX increase], and of elemental zinc and the oxidative potential of PM with MD [0.03 (95% CI: 0.01, 0.04) per 10-ng=m3 zinc increase and 0.07 (95% CI: 0.00, 0.44) per 1-nmol DTT/min/m³ oxidative potential increase]. Mutually adjusted models of significant exposures during pregnancy and childhood indicated significant associations of silicon during pregnancy, and zinc during childhood, with MD. DISCUSSION: Exposure in pregnancy and childhood to air pollutants from tailpipe and non-tailpipe emissions were associated with lower FA and higher MD in white matter of preadolescents. [ABSTRACT FROM AUTHOR]

Background: Particulate matter (PM) is a comp lex mixture. Geograp hic variations in PM may exp lain the lack of consistent associations with breast " color:blue;" >cancer. Objective: We aimed to evaluate the relationship between air p ollution, PM comp onents, and breast cancer risk in a United States-wide p rosp ective " color:blue;" >cohort. Methods: We estimated annual average ambient residential levels of p articulate matter <2.5 p m and <10 p m in aerodynamic diameter (PM2.5 and PM10, resp ectively) and nitrogen dioxide (NO2) using land-use regression for 47,433 Sister Study p articip ants (breast " color:blue;" >cancer-free women with a sister with breast cancer) living in the contiguous United States. Cox p rop ortional hazards regression was used to estimate hazard ratios (HRs) and 95% " color:blue;" >con- fidence intervals (Cis) for risk associated with an interquartile " color:blue;" >range (IQR) increase in p ollutants. Predictive £-means were used to assign p articip ants to clusters derived from " color:blue;" >PM2.5 comp onent p rofiles to evaluate the imp act of heterogeneity in the " color:blue;" >PM2.5 mixture. For " color:blue;" >PM2.5, we investigated effect measure modification by comp onent cluster membership and by geograp hic region without regard to air p ollution mixture. Results: During follow-up (mean = 8.4y), 2,225 invasive and 623 ductal carcinoma in situ (DCIS) cases were identified. PM2.5 and NO2 were associated with breast cancer " color:blue;" >over all " color:blue;" >[HR= " color:blue;" >1.05 (95% CI:0.99, 1.11) and 1.06 (95% " color:blue;" >CI: " color:blue;" >1.02, " color:blue;" >1.11), " color:blue;" >resp ectively] " color:blue;" >and with " color:blue;" >DCIS " color:blue;" >but " color:blue;" >not " color:blue;" >with " color:blue;" >invasive cancer. Invasive breast cancer was associated with " color:blue;" >PM2.5 only in the Western United States " color:blue;" >[HR " color:blue;" >=1.14 (95% " color:blue;" >CI: " color:blue;" >1.02,1.27)] and NO2 only in the Southern United States " color:blue;" >[HR " color:blue;" >=1.16 (95% " color:blue;" >CI: " color:blue;" >1.01, " color:blue;" >1.33)]. " color:blue;" >PM2.5 " color:blue;" >was " color:blue;" >associated " color:blue;" >with " color:blue;" >a " color:blue;" >higher " color:blue;" >risk " color:blue;" >of " color:blue;" >invasive " color:blue;" >breast " color:blue;" >cancer " color:blue;" >among " color:blue;" >two " color:blue;" >of " color:blue;" >seven " color:blue;" >identified comp osition- " color:blue;" >based clusters. A higher risk was observed " color:blue;" >[HR " color:blue;" >= " color:blue;" >1.25 " color:blue;" >(95% " color:blue;" >CI: " color:blue;" >0.97, " color:blue;" >1.60)] " color:blue;" >in " color:blue;" >a " color:blue;" >Ca lifornia-based " color:blue;" >cluster " color:blue;" >characterized " color:blue;" >by " color:blue;" >low " color:blue;" >S and " color:blue;" >high " color:blue;" >Na and nitrate " color:blue;" >(NO3" ) fractions and for another Western United States cluster " color:blue;" >[HR " color:blue;" >= " color:blue;" >1.60 (95% CI: " color:blue;" >0.90, 2.85)], characterized by high fractions of Si, Ca, K, and Al. Conclusion: Air p ollution measures were related to both invasive breast cancer and DCIS within certain geograp hic regions and PM comp onent " color:blue;" >clusters, http s://doi.org/10.1289/EHP5131 [ABSTRACT FROM AUTHOR]

BACKGROUND: Lung cancer rates among never-smoking women in Xuanwei and Fuyuan in China are among the highest in the world and have been attributed to the domestic use of smoky (bituminous) coal for heating and cooking. However, the key components of coal that drive lung cancer risk have not been identified. OBJECTIVES: We aimed to investigate the relationship between lifelong exposure to the constituents of smoky coal (and other fuel types) and lung cancer. METHODS: Using a population-based case-control study of lung cancer among 1,015 never-smoking female cases and 485 controls, we examined the association between exposure to 43 household air pollutants and lung cancer. Pollutant predictions were derived from a comprehensive exposure assessment study, which included methylated polycyclic aromatic hydrocarbons (PAHs), which have never been directly evaluated in an epidemiological study of any cancer. Hierarchical clustering and penalized regression were applied in order to address high colinearity in exposure variables. RESULTS: The strongest association with lung cancer was for a cluster of 25 PAHs [odds ratio (OR): 2.21; 95% confidence interval (CI): 1.67, 2.87 per 1 standard deviation (SD) change], within which 5-methylchrysene (5-MC), a mutagenic and carcinogenic PAH, had the highest individual observed OR (5.42; 95% CI: 0.94, 27.5). A positive association with nitrogen dioxide (NO2) was also observed (OR: 2.06; 95% CI: 1.19, 3.49). By contrast, neither benzo(a)pyrene (BaP) nor fine particulate matter with aerodynamic diameter =2:5 lm (PM2:5) were associated with lung cancer in the multipollutant models. CONCLUSIONS: To our knowledge, this is the first study to comprehensively evaluate the association between lung cancer and household air pollution (HAP) constituents estimated over the entire life course. Given the global ubiquity of coal use domestically for indoor cooking and heating and commercially for electric power generation, our study suggests that more extensive monitoring of coal combustion products, including methylated PAHs, may be warranted to more accurately assess health risks and develop prevention strategies from this exposure. [ABSTRACT FROM AUTHOR]

BACKGROUND: Telomere length is a molecular marker of biological aging. OBJECTIVE: Here we investigated whether early-life exposure to residential air pollution was associated with leukocyte telomere length (LTL) at 8 y of age. METHODS: In a multicenter European birth cohort study, HELIX (Human Early Life Exposome) (n=1,396), we estimated prenatal and 1-y childhood exposure to nitrogen dioxide (NO2), particulate matter with aerodynamic diameter ≤2:5 lm (PM2:5), and proximity to major roads. Average relative LTL was measured using quantitative real-time polymerase chain reaction (qPCR). Effect estimates of the association between LTL and prenatal, 1-y childhood air pollution, and proximity to major roads were calculated using multiple linear mixed models with a random cohort effect and adjusted for relevant covariates. RESULTS: LTL was inversely associated with prenatal and 1-y childhood NO2 and PM2:5 exposures levels. Each standard deviation (SD) increase in prenatal NO2 was associated with a −1:5% (95% CI: −2:8, −0:2) change in LTL. Prenatal PM2:5 was nonsignificantly associated with LTL (−0:7% per SD increase; 95% CI: −2:0, 0.6). For each SD increment in 1-y childhood NO2 and PM2:5 exposure, LTL shortened by −1:6% (95% CI: −2:9, −0:4) and −1:4% (95% CI: −2:9, 0.1), respectively. Each doubling in residential distance to nearest major road during childhood was associated with a 1.6% (95% CI: 0.02, 3.1) lengthening in LTL. CONCLUSION: Lower exposures to air pollution during pregnancy and childhood were associated with longer telomeres in European children at 8 y of age. These results suggest that reductions in traffic-related air pollution may promote molecular longevity, as exemplified by telomere length, from early life onward. [ABSTRACT FROM AUTHOR]

BACKGROUND: Surrounding green, air pollution, and noise have been associated with cardiometabolic diseases, but most studies have assessed only one of these correlated exposures. OBJECTIVES: We aimed to evaluate associations of combined exposures to green, air pollution, and road traffic noise with cardiometabolic diseases. METHODS: In this cross-sectional study, we studied associations between self-reported physician-diagnosed diabetes, hypertension, heart attack, and stroke from a Dutch national health survey of 387,195 adults and residential surrounding green, annual average air pollutant concentrations [including particulate matter with aerodynamic diameter ≤10 lm (PM10), PM with aerodynamic diameter ≤2:5 lm (PM2:5), nitrogen dioxide (NO2), and oxidative potential (OP) with the dithiothreitol (DTT) assay (OPDTT)] and road traffic noise. Logistic regression models were used to analyze confounding and interaction of surrounding green, air pollution, and noise exposure. RESULTS: In single-exposure models, surrounding green was inversely associated with diabetes, while air pollutants (NO2, OPDTT) and road traffic noise were positively associated with diabetes. In two-exposure analyses, associations with green and air pollution were attenuated but remained. The association between road traffic noise and diabetes was reduced to unity when adjusted for surrounding green or air pollution. Air pollution and surrounding green, but not road traffic noise, were associated with hypertension in single-exposure models. The weak inverse association of surrounding green with hypertension attenuated and lost significance when adjusted for air pollution. Only PM2:5 was associated with stroke and heart attack. CONCLUSIONS: Studies including only one of the correlated exposures surrounding green, air pollution, and road traffic noise may overestimate the association of diabetes and hypertension attributed to the studied exposure. [ABSTRACT FROM AUTHOR]

BACKGROUND: A few studies suggest that air pollution may decrease fertility, but prospective studies and examinations of windows of susceptibility remain unclear. OBJECTIVE: We aimed to examine the association between time-varying exposure to nitrogen dioxide (NO2), ozone (O3), fine particulate matter <2:5 lm (PM2:5), and black carbon (BC) on in vitro fertilization (IVF) outcomes. METHODS: We included 345 women (522 IVF cycles) for the NO2, O3, and PM2:5 analyses and 339 women (512 IVF cycles) for the BC analysis enrolled in a prospective cohort at a Boston fertility center (2004-2015). We used validated spatiotemporal models to estimate daily residential exposure to NO2, O3, PM2:5, and BC. Multivariable discrete time Cox proportional hazards models with four periods [ovarian stimulation (OS), oocyte retrieval to embryo transfer (ET), ET to implantation, implantation to live birth] estimated odds ratios (OR) and 95% confidence intervals (CI) of failing at IVF. Time-dependent interactions were used to identify vulnerable periods. RESULTS: An interquartile range (IQR) increase in NO2, PM2:5, and BC throughout the IVF cycle was associated with an elevated odds of failing at IVF prior to live birth (OR=1:08, 95% CI: 0.95, 1.23 for NO2; OR=1:06, 95% CI: 0.88, 1.28 for PM2:5; and OR=1:16, 95% CI: 0.96, 1.41 for BC). This relationship significantly varied across the IVF cycle such that the association with higher exposure to air pollution during OS was strongest for early IVF failures. An IQR increase in NO2, PM2:5, and BC exposure during OS was associated with 1.42 (95% CI: 1.20, 1.69), 1.26 (95% CI: 0.96, 1.67), and 1.23 (95% CI: 0.96, 1.59) times the odds of failing prior to oocyte retrieval, and 1.32 (95% CI: 1.13, 1.54), 1.27 (95% CI: 0.98, 1.65), and 1.32 (95% CI: 1.10, 1.59) times the odds of failing prior to ET. CONCLUSION: Increased exposure to traffic-related pollutants was associated with higher odds of early IVF failure. [ABSTRACT FROM AUTHOR]

BACKGROUND: Evidence on the association between road traffic noise and diabetes risk is sparse and inconsistent with respect to how confounding by air pollution was treated. OBJECTIVES: In this study, we aimed to examine whether long-term exposure to road traffic noise over 25 years is associated with incidence of diabetes, independent of air pollution. METHODS: A total of 28,731 female nurses from the Danish Nurse cohort (>44 years old at recruitment in 1993 or 1999) were linked to the Danish National Diabetes Register with information on incidence of diabetes from 1995 until 2013. The annual mean weighted levels of 24-h average road traffic noise (Lden) at nurses' residences from 1970 until 2013 were estimated with the Nord2000 method and annual mean levels of particulate matter (PM) with diameter <2.5 and 10 nm (PM2.5 and PM10), nitrogen dioxide (NO2), and nitrogen oxide (NOx) with the Danish AirGIS modeling system. Cox proportional hazards regression models were used to examine the association between residential Lden in four different exposure windows (1-, 5-, 10-, and 25-years) and the incidence of diabetes, adjusted for lifestyle factors and air pollutants. RESULTS: Of 23,762 nurses free of diabetes at the cohort baseline, 1,158 developed diabetes during a mean follow-up of 15.2 years. We found weak positive associations between 5-y mean exposure to Lden (per 10 dB increase) and diabetes incidence in a crude model [hazard ratio (HR): 1.07; 95% confidence interval (CI): 0.99, 1.12], which attenuated in a model adjusted for lifestyle factors (HR:1.04; 95% CI: 0.97, 1.12), and reached unity after additional adjustment for PM2.5 (HR: 0.99; 0.91, 1.08). In analyses by level of urbanization, we found a positive association between noise and diabetes in urban areas (HR:1.27; 95% CI: 0.98, 1.63) that was unchanged after adjusting for PM2.5 (HR: 1.25; 95% CI: 0.97, 1.62), but we found no apparent association in provincial (HR: 1.02; 95% CI: 0.88, 1.18) or rural areas (HR: 0.97; 95% CI: 0.87, 1.08). CONCLUSION: In the nationwide cohort of Danish nurses 44 years of age and older, we found no association between long-term exposure to road traffic noise and diabetes incidence after adjustment for PM2.5 but found suggestive evidence of an association limited to urban areas. [ABSTRACT FROM AUTHOR]

BACKGROUND: There is growing evidence that exposure to ultrafine particles (UFP; particles smaller than 100 nm) may play an underexplored role in the etiology of several illnesses, including cardiovascular disease (CVD). OBJECTIVES: We aimed o investigate the relationship between long-term exposure to ambient UFP and incident cardiovascular and cerebrovascular disease (CVA). As a secondary objective, we sought to compare effect estimates for UFP with those derived for other air pollutants, including estimates from two-pollutant models. METHODS: Using a prospective cohort of 33,831 Dutch residents, we studied the association between long-term exposure to UFP (predicted via land use regression) and incident disease using Cox proportional hazard models. Hazard ratios (HR) for UFP were compared to HRs for more routinely monitored air pollutants, including particulate matter with aerodynamic diameter =10 lm (PM10), PM with aerodynamic diameter =2:5 (PM2:5), and NO2. RESULTS: Long-term UFP exposure was associated with an increased risk for all incident CVD [HR=1:18 per 10,000 particles=cm3; 95% confidence interval (CI): 1.03, 1.34], myocardial infarction (MI) (HR=1:34; 95% CI: 1.00, 1.79), and heart failure (HR=1:76; 95% CI: 1.17, 2.66). Positive associations were also estimated for NO2 (HR for heart failure=1:22; 95% CI: 1.01, 1.48 per 20 lg=m3) and coarse PM (PMcoarse; HR for all CVD=1:21; 95% CI: 1.01, 1.45 per 10 lg=m3). CVD was not positively associated with PM2:5 (HR for all CVD=0:95; 95% CI: 0.75, 1.28 per 5 lg=m3). HRs for UFP and CVAs were positive, but not significant. In two-pollutant models (UFP+NO2 and UFP+PMcoarse), positive associations tended to remain for UFP, while HRs for PMcoarse and NO2 generally attenuated towards the null. CONCLUSIONS: These findings strengthen the evidence that UFP exposure plays an important role in cardiovascular health and that risks of ambient air pollution may have been underestimated based on conventional air pollution metrics. [ABSTRACT FROM AUTHOR]

BACKGROUND: Asthma is the most prevalent chronic respiratory disease worldwide, affecting 358 million people in 2015. Ambient air pollution exacerbates asthma among populations around the world and may also contribute to new-onset asthma. OBJECTIVES: We aimed to estimate the number of asthma emergency room visits and new onset asthma cases globally attributable to fine particulate matter (PM2.5), ozone, and nitrogen dioxide (NO2) concentrations. METHODS: We used epidemiological health impact functions combined with data describing population, baseline asthma incidence and prevalence, and pollutant concentrations. We constructed a new dataset of national and regional emergency room visit rates among people with asthma using published survey data. RESULTS: We estimated that 9-23 million and 5-10 million annual asthma emergency room visits globally in 2015 could be attributable to ozone and PM2.5, respectively, representing 8-20% and 4-9% of the annual number of global visits, respectively. The range reflects the application of central risk estimates from different epidemiological meta-analyses. Anthropogenic emissions were responsible for ~37% and 73% of ozone and PM2.5 impacts, respectively. Remaining impacts were attributable to naturally occurring ozone precursor emissions (e.g., from vegetation, lightning) and PM2.5 (e.g., dust, sea salt), though several of these sources are also influenced by humans. The largest impacts were estimated in China and India. CONCLUSIONS: These findings estimate the magnitude of the global asthma burden that could be avoided by reducing ambient air pollution. We also identified key uncertainties and data limitations to be addressed to enable refined estimation. [ABSTRACT FROM AUTHOR]

Background: Epidemiological evidence on the health effects of ultrafine particles (UFP) remains insufficient to infer a causal relationship that is largely due to different size ranges and exposure metrics examined across studies. Moreover, evidence regarding the association between UFP and cardiovascular disease at a sub-daily timescale is lacking. Objective: We investigated the relationship between different particle metrics, including particle number (PNC), length (PLC), and surface area (PSC) concentrations, and myocardial infarction (MI) at an hourly timescale. METHODS: We collected hourly air pollution and meteorological data from fixed urban background monitoring sites and hourly nonfatal MI cases from a MI registry in Augsburg, Germany, during 2005-2015. We conducted a time-stratified case-crossover analysis with conditional logistic regression to estimate the association between hourly particle metrics and MI cases, adjusted for air temperature and relative humidity. We also examined the independent effects of a certain particle metric in two-pollutant models by adjusting for copollutants, including particulate matter (PM) with an aerodynamic diameter of [less than or equal to] 10 [micro]m or 2.5 [micro]m ([PM.sub.10] and [PM.sub.2.5], respectively), nitrogen dioxide, ozone, and black carbon. RESULTS: Overall, a total of 5,898 cases of nonfatal MI cases were recorded. Exploratory analyses showed similar associations across particle metrics in the first 6-12 h. For example, interquartile range increases in PNC within the size range of 10-100 nm, PLC, and PSC were associated with an increase of MI 6 h later by 3.27% [95% confidence interval (CI): 0.27, 6.37], 5.71% (95% CI: 1.79, 9.77), and 5.84% (95% CI: 1.04, 10.87), respectively. Positive, albeit imprecise, associations were observed for PNC within the size range of 10-30 nm and 100-500 nm. Effect estimates for PLC and PSC remained similar after adjustment for PM and gaseous pollutants. Conclusions: Transient exposure to particle number, length, and surface area concentrations or other potentially related exposures may trigger the onset of nonfatal myocardial infraction. https://doi.org/10.1289/EHP5478, Introduction Ultrafine particles (UFP) are hypothesized to have adverse health effects due to their small size, their large active surface areas, and their ability to penetrate into the alveoli and [...]

Background: Ambient fine particulate air pollution with aerodynamic diameter [less than or equal to] 2.5 [micro]m ([PM.sub.2.5]) is an important contributor to the global burden of disease. Information on the shape of the concentration-response relationship at low concentrations is critical for estimating this burden, setting air quality standards, and in benefits assessments. Objectives: We examined the concentration-response relationship between [PM.sub.2.5] and nonaccidental mortality in three Canadian Census Health and Environment Cohorts (CanCHECs) based on the 1991, 1996, and 2001 census cycles linked to mobility and mortality data. Methods: Census respondents were linked with death records through 2016, resulting in 8.5 million adults, 150 million years of follow-up, and 1.5 million deaths. Using annual mailing address, we assigned time-varying contextual variables and 3-y moving-average ambient [PM.sub.2.5] at a 1x1 km spatial resolution from 1988 to 2015. We ran Cox proportional hazards models for [PM.sub.2.5] adjusted for eight subject-level indicators of socioeconomic status, seven contextual covariates, ozone, nitrogen dioxide, and combined oxidative potential. We used three statistical methods to examine the shape of the concentration-response relationship between [PM.sub.2.5] and nonaccidental mortality. Results: The mean 3-y annual average estimate of [PM.sub.2.5] exposure ranged from 6.7 to 8.0 [micro]g/[m.sup.3] over the three cohorts. We estimated a hazard ratio (HR) of 1.053 [95% confidence interval (CI): 1.041, 1.065] per 10-[micro]g/[m.sup.3] change in [PM.sub.2.5] after pooling the three cohort-specific hazard ratios, with some variation between cohorts (1.041 for the 1991 and 1996 cohorts and 1.084 for the 2001 cohort). We observed a supralinear association in all three cohorts. The lower bound of the 95% CIs exceeded unity for all concentrations in the 1991 cohort, for concentrations above 2 [micro]g/[m.sup.3] in the 1996 cohort, and above 5 [micro]g/[m.sup.3] in the 2001 cohort. Discussion: In a very large population-based cohort with up to 25 y of follow-up, [PM.sub.2.5] was associated with nonaccidental mortality at concentrations as low as 5 [micro]g/[m.sup.3]. https://doi.org/10.1289/EHP5204, Introduction Exposure to ambient fine particulate air pollution with aerodynamic diameter [less than or equal to] 2.5 [micro]m ([PM.sub.2.5]) consistently ranks among the leading risk factors for premature death and [...]

BACKGROUND: Despite the importance of understanding the connection between air pollution exposure and diabetes, studies investigating links between air pollution and glucose metabolism in nondiabetic adults are limited. OBJECTIVE: We aimed to estimate the association of medium-term air pollution exposures with blood glucose and glycated hemoglobin A1c (HbA1c) among nondiabetics. METHODS: This study included observations from nondiabetic participants (nobs =7,108) of the population-based Heinz Nixdorf Recall study at baseline (2000-2003) and follow-up examination (2006-2008). Daily fine particulate matter (aerodynamic diameter≤2.5 lm,PM2.5; aerodynamic diameter ≤10 μm,PM10), accumulation mode particle number (PNAM), and nitrogen dioxide (NO2) exposures were estimated at participants' residences using the spatiotemporal European Air Pollution Dispersion (EURAD) chemistry transport model. We evaluated the associations between medium-term air pollution exposures (28- and 91-d means) and glucose metabolism measures using mixed linear regression and adjusting for season, meteorology, and personal characteristics. Arange of other exposure windows (1-, 2-, 3-, 7-, 14-, 45-, 60-, 75-, 105-, 120-, and 182-d means) were also evaluated to identify potentially relevant biological windows. RESULTS: We observed positive associations between PM2.5 and PNAM exposures and blood glucose levels [e.g., 28-d PM2.5: 0.91 mg/dL (95% CI: 0.38, 1.44) per 5.7 μg/m3]. PM2.5, PM10, and PNAM exposures were positively associated with HbA1c [e.g., 91-d PM2.5: 0.07 p.p: (95% CI: 0.04, 0.10) per 4.0 μg/m3]. Mean exposures during longer exposure windows (75- to 105-d) were most strongly associated with HbA1c, whereas 7- to 45-d exposures were most strongly associated with blood glucose. NO2 exposure was not associated with blood glucose or with HbA1c. CONCLUSIONS: Medium-term PM and PNAM exposures were positively associated with glucose measures in nondiabetic adults. These findings indicate that reducing ambient air pollution levels may decrease the risk of diabetes. [ABSTRACT FROM AUTHOR]

BACKGROUND: There is growing evidence suggesting an association between air pollution and suicide. However, previous findings varied depending on the type of air pollutant and study location. OBJECTIVES: We examined the association between air pollutants and suicide in 10 large cities in South Korea, Japan, and Taiwan. METHODS: We used a two-stage meta-analysis. First, we conducted a time-stratified case-crossover analysis to estimate the short-term association between nitrogen dioxide (NO2), sulfur dioxide (SO2), and particulate matter [aerodynamic diameter =10 lm (PM10), aerodynamic diameter =2:5 lm (PM2:5), and PM10-2:5] and suicide, adjusted for weather factors, day-of-week, long-term time trends, and season. Then, we conducted a meta-analysis to combine the city-specific effect estimates for NO2, SO2, and PM10 across 10 cities and for PM2:5 and PM10-2:5 across 3 cities. We first fitted single-pollutant models, followed by two-pollutant models to examine the robustness of the associations. RESULTS: Higher risk of suicide was associated with higher levels of NO2, SO2, PM10, and PM10-2:5 over multiple days. The combined relative risks (RRs) were 1.019 for NO2 (95% confidence interval [CI]: 0.999, 1.039), 1.020 for SO2 (95% CI: 1.005, 1.036), 1.016 for PM10 (95% CI: 1.004, 1.029), and 1.019 for PM10-2:5 (95% CI: 1.005, 1.033) per interquartile range (IQR) increase in the 0-1 d average level of each pollutant. We found no evidence of an association for PM2:5. Some of the associations, particularly for SO2 and NO2, were attenuated after adjusting for a second pollutant. CONCLUSIONS: Our findings suggest that higher levels of air pollution may be associated with suicide, and further research is merited to understand the underlying mechanisms. [ABSTRACT FROM AUTHOR]

BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women. METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts - Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2:5 μm, ≤10 μm, and 2:5-10 μm in diameter (PM2.5, PM10, and PMcoarse, respectively); PM2.5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. RESULTS: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM2.5 {hazard ratio (HR)=1:08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg = m3}, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg = m3], PMcoarse [1.20 (95% CI: 0.96, 1.49 per 5 μg = m3], and NO2 [1.02 (95% CI: 0.98, 1.07 per 10 μg = m3], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg = m3, p = 0:04]. CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. [ABSTRACT FROM AUTHOR]

BACKGROUND: Recently, there has been increasing evidence that exposure to air pollution is linked to neurodegenerative diseases, but little is known about the association with amyotrophic lateral sclerosis (ALS). OBJECTIVES: We investigated the association between long-term exposure to air pollution and risk of developing ALS. METHODS: A population-based case-control study was conducted in Netherlands from 1 January 2006 to 1 January 2013. Data from 917 ALS patients and 2,662 controls were analyzed. Annual mean air pollution concentrations were assessed by land use regression (LUR) models developed as part of the European Study of Cohorts for Air Pollution Effects (ESCAPE). Exposure estimates included nitrogen oxides (NO2, NOx), particulate matter (PM) with diameters of <2.5 μm (PM2.5), <10 μm (PM10), between 10 μm and 2.5 μm (PMcoarse), and PM2.5 absorbance. We performed conditional logistic regression analysis using two different multivariate models (model 1 adjusted for age, gender, education, smoking status, alcohol use, body mass index, and socioeconomic status; model 2 additionally adjusted for urbanization degree). RESULTS: Risk of ALS was significantly increased for individuals in the upper exposure quartile of PM2.5 absorbance [OR = 1:67; 95% confidence interval (CI): 1.27, 2.18], NO2 (OR = 1:74; 95% CI: 1.32, 2.30), and NOx concentrations (OR = 1:38; 95% CI: 1.07, 1.77). These results, except for NOx, remained significant after adjusting additionally for urbanization degree. CONCLUSIONS: Based on a large population-based case-control study, we report evidence for the association between long-term exposure to trafficrelated air pollution and increased susceptibility to ALS. Our findings further support the necessity for regulatory public health interventions to combat air pollution levels and provide additional insight into the potential pathophysiology of ALS. [ABSTRACT FROM AUTHOR]

BACKGROUND: Although air pollution and road traffic noise have been associated with higher risk of cardiovascular diseases, associations with heart failure have received only little attention. OBJECTIVES: We aimed to investigate whether long-term exposure to road traffic noise and nitrogen dioxide (NO2) were associated with incident heart failure. METHODS: In a cohort of 57,053 people 50-64 y of age at enrollment in the period 1993-1997, we identified 2,550 cases of first-ever hospital admission for heart failure during a mean follow-up time of 13.4 y. Present and historical residential addresses from 1987 to 2011 were found in national registers, and road traffic noise (Lden) and NO2 were modeled for all addresses. Analyses were done using Cox proportional hazard model. RESULTS: An interquartile range higher 10-y time-weighted mean exposure for Lden and NO2 was associated with incidence rate ratios (IRR) for heart failure of 1.14 (1.08-1.21) and 1.11 (1.07-1.16), respectively, in models adjusted for gender, lifestyle, and socioeconomic status. In models with mutual exposure adjustment, IRRs were 1.08 (1.00-1.16) for Lden and 1.07 (1.01-1.14) for NO2. We found statistically significant modification of the NO2-heart failure association by gender (strongest association among men), baseline hypertension (strongest association among hypertensive), and diabetes (strongest association among diabetics). The same tendencies were seen for noise, but interactions were not statistically significant. CONCLUSIONS: Long-term exposure to NO2 and road traffic noise was associated with higher risk of heart failure, mainly among men, in both singleand two-pollutant models. High exposure to both pollutants was associated with highest risk. [ABSTRACT FROM AUTHOR]

BACKGROUND: Disparities in exposure to air pollution by race-ethnicity and by socioeconomic status have been documented in the United States, but the impacts of declining transportation-related air pollutant emissions on disparities in exposure have not been studied in detail. OBJECTIVE: This study was designed to estimate changes over time (2000 to 2010) in disparities in exposure to outdoor concentrations of a transportation-related air pollutant, nitrogen dioxide (NO2), in the United States. METHODS: We combined annual average NO2 concentration estimates from a temporal land use regression model with Census demographic data to estimate outdoor exposures by race-ethnicity, socioeconomic characteristics (income, age, education), and by location (region, state, county, urban area) for the contiguous United States in 2000 and 2010. RESULTS: Estimated annual average NO2 concentrations decreased from 2000 to 2010 for all of the race-ethnicity and socioeconomic status groups, including a decrease from 17.6ppb to 10.7ppb (-6.9ppb) in nonwhite [non-(white alone, non-Hispanic)] populations, and 12.6ppb to 7.8ppb (-4.7 ppb) in white (white alone, non-Hispanic) populations. In 2000 and 2010, disparities in NO2 concentrations were larger by race-ethnicity than by income. Although the national nonwhite-white mean NO2 concentration disparity decreased from a difference of 5.0ppb in 2000 to 2.9 ppb in 2010, estimated mean NO2 concentrations remained 37% higher for nonwhites than whites in 2010 (40% higher in 2000), and nonwhites were 2.5 times more likely than whites to live in a block group with an average NO2 concentration above the WHO annual guideline in 2010 (3.0 times more likely in 2000). CONCLUSIONS: Findings suggest that absolute NO2 exposure disparities by race-ethnicity decreased from 2000 to 2010, but relative NO2 exposure disparities persisted, with higher NO2 concentrations for nonwhites than whites in 2010. [ABSTRACT FROM AUTHOR]

BACKGROUND: Fetal stress has been proposed to be associated with diseases in both children and adults. Epidemiological studies suggest that maternal exposure to nitrogen dioxide (NO2) contributes to increased morbidity and mortality of offspring with allergic asthma later in life. OBJECTIVES: We aimed to test whether maternal NO2 exposure causes allergic asthma-related consequences in offspring absent any subsequent lung provocation and whether this exposure enhances the likelihood of developing allergic asthma or the intensity of developed allergic airway disease following postnatal allergic sensitization and challenge. In addition, if such consequences and enhancements occurred, we sought to determine the mechanism( s) of these responses. METHODS: Pregnant BALB/c mice were exposed to either NO2 (2:5 ppm, 5 h/day) or air daily throughout the gestation period. Offspring were sacrificed on postnatal days (PNDs) 1, 7, 14, 21, and 42, and remaining offspring were sensitized by ovalbumin (OVA) injection followed by OVA aerosol challenge during postnatal wk 7-9. We analyzed the lung histopathology, inflammatory cell infiltration, airway hyper-responsiveness (AHR), immune responses, and gene methylation under different treatment conditions. RESULTS: Maternal exposure to NO2 caused a striking increase in inflammatory cell infiltration and the release of type 2 cytokines in the lungs of offspring at PNDs 1 and 7; however, these alterations were reversed during postnatal development. Following OVA sensitization and challenge, the exposure enhanced the levels of allergic asthma-characterized OVA-immunoglobulin (Ig) E, AHR, and airway inflammation in adult offspring. Importantly, differentiation of T-helper (Th) 2 cells and demethylation of the interleukin-4 (IL4) gene occurred during the process. CONCLUSIONS: Maternal exposure to indoor environmental NO2 causes allergic asthma-related consequences in offspring absent any subsequent lung provocation and potentiates the symptoms of allergic asthma in adult offspring following postnatal allergic sensitization and challenge; this response is associated with the Th2-based immune response and DNA methylation of the IL4 gene. [ABSTRACT FROM AUTHOR]

BACKGROUND: Evidence for an association between transportation noise and cardiovascular disease has increased; however, few studies have examined metabolic outcomes such as diabetes or accounted for environmental coexposures such as air pollution, greenness, or walkability. OBJECTIVES: Because diabetes prevalence is increasing and may be on the causal pathway between noise and cardiovascular disease, we examined the influence of long-term residential transportation noise exposure and traffic-related air pollution on the incidence of diabetes using a populationbased cohort in British Columbia, Canada. METHODS: We examined the influence of transportation noise exposure over a 5-y period (1994-1998) on incident diabetes cases in a populationbased prospective cohort study (n=380,738) of metropolitan Vancouver (BC) residents who were 45-85 y old, with 4-y of follow-up (1999-2002). Annual average transportation noise (Lden), air pollution [black carbon, particulate matter with aerodynamic diameter <2:5 lm (PM2.5), nitrogen oxides], greenness [Normalized Difference Vegetation Index (NDVI)], and neighborhood walkability at each participant's residence were modeled. Incident diabetes cases were identified using administrative health records. RESULTS: Transportation noise was associated with the incidence of diabetes [interquartile range (IQR) increase, 6.8 A-weighted decibels (dBA); OR=1:08 (95% CI: 1.05, 1.10)]. This association remained after adjustment for environmental coexposures including traffic-related air pollutants, greenness, and neighborhood walkability. After adjustment for coexposure to noise, traffic-related air pollutants were not associated with the incidence of diabetes, whereas greenness was protective. CONCLUSION: We found a positive association between residential transportation noise and diabetes, adding to the growing body of evidence that noise pollution exposure may be independently linked to metabolic health and should be considered when developing public health interventions. [ABSTRACT FROM AUTHOR]

Background: It has been widely demonstrated that air pollution can affect human health and that certain pollutant gases lead to adverse obstetric outcomes, such as preeclampsia and fetal growth restriction. OBJECTIVES: We evaluated the influence of individual maternal exposure to air pollution on placental volume and vascularization evaluated in the first trimester of pregnancy. METHODS: This was a cross-sectional study on low-risk pregnant women living in São Paulo, Brazil. The women carried passive personal NO[sub 2] and O[sub 3] monitors in the week preceding evaluation. We employed the virtual organ computer-aided analysis (VOCAL) technique using three-dimensional power Doppler ultrasound to evaluate placental volume and placental vascular indexes [vascularization index (VI), flow index (FI), and vascularization flow index (VFI)]. We analyzed the influence of pollutant levels on log-transformed placental vascularization and volume using multiple regression models. RESULTS: We evaluated 229 patients. Increased NO[sub 2] levels had a significant negative association with log of VI (p = 0.020 and beta = -0.153) and VFI (p = 0.024 and beta = -0.151). NO[sub 2] and O[sub 3] had no influence on the log of placental volume or FI. CONCLUSIONS: NO[sub 2], an estimator of primary air pollutants, was significantly associated with diminished VI and VFI in the first trimester of pregnancy. CITATION: Hettfleisch K, Bernardes LS, Carvalho MA, Pastro LD, Vieira SE, Saldiva SR, Saldiva P, Francisco RP. 2017. Short-term exposure to urban air pollution and influences on placental vascularization indexes. Environ Health Perspect 125:753-759; http://dx.doi.org/10.1289/EHP300 [ABSTRACT FROM AUTHOR]

BACKGROUND: Prenatal exposure to air pollution is considered to be associated with adverse effects on child health. This may partly be mediated by mechanisms related to DNA methylation. OBJECTIVES: We investigated associations between exposure to air pollution, using nitrogen dioxide (NO2) as marker, and epigenome-wide cord blood DNA methylation. METHODS: We meta-analyzed the associations between NO2 exposure at residential addresses during pregnancy and cord blood DNA methylation (Illumina 450K) in four European and North American studies (n = 1,508) with subsequent look-up analyses in children ages 4 (n = 733) and 8 (n = 786) years. Additionally, we applied a literature-based candidate approach for antioxidant and anti-inflammatory genes. To assess influence of exposure at the transcriptornics level, we related mRNA expression in blood cells to NO2 exposure in 4- (n = 111) and 16-year-olds (n = 239). RESULTS: We found epigenome-wide significant associations [false discovery rate (FDR) p < 0.05] between maternal NO2 exposure during pregnancy and DNA methylation in newborns for 3 CpG sites in mitochondria-related genes: cgl2283362 (LONP1), cg24l72570 (3.8 kbp upstream of HIBADH), and cg08973675 (SLC25A28). The associations with cg08973675 methylation were also significant in the older children. Further analysis of antioxidant and anti-inflammatory genes revealed differentially methylated CpGs in CAT and TPO in newborns (FDR p < 0.05). NO2 exposure at the time of biosampling in childhood had a significant impact on CAT and TPO expression. CONCLUSIONS: NO2 exposure during pregnancy was associated with differential offspring DNA methylation in mitochondria-related genes. Exposure to NO2 was also linked to differential methylation as well as expression of genes involved in antioxidant defense pathways. CITATION: Gruzieva O, Xu CJ, Breton CV, Annesi-Maesano I, Antó JM, Auffray C, Ballereau S, Bellander T, Bousquet J, Bustamante M, Charles MA, de Kluizenaar Y, den Dekker HT, Duijts L, Felix JF, Gehring U, Guxens M, Jaddoe VV, Jankipersadsing SA, Merid SK, Kere J, Kumar A, Lemonnier N, Lepeule J, Nystad W, Page CM, Panasevich S, Postma D, Slama R, Sunyer J, Söderhäll C, Yao J, London SJ, Pershagen G, Koppelman GH, Melen E. 2017. Epigenome-wide meta-analysis of methylation in children related to prenatal NO2 air pollution exposure. Environ Health Perspect 125:104-110; http://dx.doi.org/10.1289/EHP36 [ABSTRACT FROM AUTHOR]

BACKGROUND: Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (OBJECTIVE: We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 μm in diameter (PM10) and < 2.5 μm in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk. METHODS: Our nested case--control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders. RESULTS: We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORq5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations. CONCLUSIONS: Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. CITATION: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765; http://dx.doi.org/10.1289/EHP135 [ABSTRACT FROM AUTHOR]