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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 ( PM 10 , PM 2.5 , and PM 2.5 absorbance), accumulation mode particle number ( PN AM ), and nitrogen dioxide ( NO 2 ) was estimated applying land-use regression and chemistry transport models. Noise exposures were assessed as weighted 24-h ( L den ) and nighttime ( L night ) 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 PM 2.5 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. https://doi.org/10.1289/EHP9737.

Background: Residential exposure to air pollution (AP) has been shown to activate the immune system (IS). Although innate immune responses to AP have been studied extensively, investigations on the adaptive IS are scarce., Objectives: The aim of this study was to investigate the association between short- to long-term AP exposure and polyclonal free light chains (FLC) produced by plasma cells., Methods: We used repeated data from three examinations ( t 0 : 2000-2003; t 1 : 2006-2008; and t 2 : 2011-2015) of the population-based German Heinz Nixdorf Recall cohort of initially 4,814 participants (45-75 y old). Residential exposure to total and source-specific particulate matter (PM) with an aerodynamic diameter of 10 or 2.5 μ m ( PM 10 and PM 2.5 respectively), nitrogen dioxide ( NO 2 ), and particle number concentrations (accumulation mode; PN AM ) was estimated using a chemistry transport model with different time windows (1- to 365-d mean ± standard deviation) before blood draw. We applied linear mixed models with a random participant intercept to estimate associations between total, traffic- and industry-related AP exposures and log-transformed FLC, controlling for examination time, sociodemographic and lifestyle variables, estimated glomerular filtration rate and season., Results: Analyzing 9,933 observations from 4,455 participants, we observed generally positive associations between AP exposures and FLC. We observed strongest associations with middle-term exposures, e.g., 3.0% increase in FLC (95% confidence interval: 1.8%, 4.3%) per interquartile range increase in 91-d mean of NO 2 ( 14.1 μ g / m ³ ). Across the different pollutants, NO 2 showed strongest associations with FLC, followed by PM 10 and PN AM . Effect estimates for traffic-related exposures were mostly higher compared with total exposures. Although NO 2 and PN AM estimates remained stable upon adjustment for PM, PM estimates decreased considerably upon adjustment for NO 2 and PN AM ., Discussion: Our results suggest that middle-term AP exposures in particular might be positively associated with activation of the adaptive IS. Traffic-related PM, PN AM , and NO 2 showed strongest associations. https://doi.org/10.1289/EHP7164.

Objectives: Due to inconsistent epidemiological evidence on health effects of air pollution on progression of atherosclerosis, we investigated several air pollutants and their effects on progression of atherosclerosis, using carotid intima media thickness (cIMT), coronary calcification (CAC), and thoracic aortic calcification (TAC)., Methods: We used baseline (2000-2003) and 5-y follow-up (2006-2008) data from the German Heinz Nixdorf Recall cohort study, including 4,814 middle-aged adults. Residence-based long-term air pollution exposure, including particulate matter (PM) with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ), ( PM 10 ), and nitrogen dioxide ( NO 2 ) was assessed using chemistry transport and land use regression (LUR) models. cIMT was quantified as side-specific median IMT assessed from standardized ultrasound images. CAC and TAC were quantified by computed tomography using the Agatston score. Development (yes/no) and progression of atherosclerosis (change in cIMT and annual growth rate for CAC/TAC) were analyzed with logistic and linear regression models, adjusting for age, sex, lifestyle variables, socioeconomic status, and traffic noise., Results: While no clear associations were observed in the full study sample (mean age 59.1 ( ± 7.6 ) y; 53% female), most air pollutants were marginally associated with progression of atherosclerosis in participants with no or low baseline atherosclerotic burden. Most consistently for CAC, e.g., a 1.5   μ g / m 3 higher exposure to PM 2.5 (LUR) yielded an estimated odds ratio of 1.19 [95% confidence interval (CI): 1.03, 1.39] for progression of CAC and an increased annual growth rate of 2% (95% CI: 1%, 4%)., Conclusion: Our study suggests that development and progression of subclinical atherosclerosis is associated with long-term air pollution in middle-aged participants with no or minor atherosclerotic burden at baseline, while overall no consistent associations are observed. https://doi.org/10.1289/EHP7077.

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 n = 615 participants from the population-based 1000BRAINS study, based on the German Heinz Nixdorf Recall study, we assessed residential exposures to particulate matter ( PM 10 , PM 2.5 , PM 2.5 abs ), accumulation mode particle number ( PN AM ), and nitrogen oxides ( NO x , NO 2 ), 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 ( n = 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 - μ g / m 3 PM 10 , 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. https://doi.org/10.1289/EHP5859.