Longitudinal associations of long-term exposure to ultrafine particles with blood pressure and systemic inflammation in Puerto Rican adults.

BACKGROUND: Few longitudinal studies have examined the association between ultrafine particulate matter (UFP, particles < 0.1 µm aerodynamic diameter) exposure and cardiovascular disease (CVD) risk factors. We used data from 791 adults participating in the longitudinal Boston Puerto Rican Health Study (Massachusetts, USA) between 2004 and 2015 to assess whether UFP exposure was associated with blood pressure and high sensitivity C-reactive protein (hsCRP, a biomarker of systemic inflammation). METHODS: Residential annual average UFP exposure (measured as particle number concentration, PNC) was assigned using a model accounting for spatial and temporal trends. We also adjusted PNC values for participants' inhalation rate to obtain the particle inhalation rate (PIR) as a secondary exposure measure. Multilevel linear models with a random intercept for each participant were used to examine the association of UFP with blood pressure and hsCRP. RESULTS: Overall, in adjusted models, an inter-quartile range increase in PNC was associated with increased hsCRP (ß = 6.8; 95% CI = - 0.3, 14.0%) but not with increased systolic blood pressure (ß = 0.96; 95% CI = - 0.33, 2.25 mmHg), pulse pressure (ß = 0.70; 95% CI = - 0.27, 1.67 mmHg), or diastolic blood pressure (ß = 0.55; 95% CI = - 0.20, 1.30 mmHg). There were generally stronger positive associations among women and never smokers. Among men, there were inverse associations of PNC with systolic blood pressure and pulse pressure. In contrast to the primary findings, an inter-quartile range increase in the PIR was positively associated with systolic blood pressure (ß = 1.03; 95% CI = 0.00, 2.06 mmHg) and diastolic blood pressure (ß = 1.01; 95% CI = 0.36, 1.66 mmHg), but not with pulse pressure or hsCRP. CONCLUSIONS: We observed that exposure to PNC was associated with increases in measures of CVD risk markers, especially among certain sub-populations. The exploratory PIR exposure metric should be further developed.

Combustion-Derived Nanoparticles in Key Brain Target Cells and Organelles in Young Urbanites: Culprit Hidden in Plain Sight in Alzheimer's Disease Development.

Millions of children and young adults are exposed to fine particulate matter (PM2.5) and ozone, associated with Alzheimer's disease (AD) risk. Mexico City (MC) children exhibit systemic and brain inflammation, low cerebrospinal fluid (CSF) Aß1-42, breakdown of nasal, olfactory, alveolar-capillary, duodenal, and blood-brain barriers, volumetric and metabolic brain changes, attention and short-term memory deficits, and hallmarks of AD and Parkinson's disease. Airborne iron-rich strongly magnetic combustion-derived nanoparticles (CDNPs) are present in young urbanites' brains. Using transmission electron microscopy, we documented CDNPs in neurons, glia, choroid plexus, and neurovascular units of young MC residents versus matched clean air controls. CDNPs are associated with pathology in mitochondria, endoplasmic reticulum (ER), mitochondria-ER contacts (MERCs), axons,and dendrites. There is a significant difference in size and numbers between spherical CDNPs (>85%) and the angular, euhedral endogenous NPs (<15%). Spherical CDNPs (dogs 21.2±7.1 nm in diameter versus humans 29.1±11.2 nm, p = 0.002) are present in neurons, glia, choroid plexus, endothelium, nasal and olfactory epithelium, and in CSF at significantly higher in numbers in MC residents (p < 0.0001). Degenerated MERCs, abnormal mitochondria, and dilated ER are widespread, and CDNPs in close contact with neurofilaments, glial fibers, and chromatin are a potential source for altered microtubule dynamics, mitochondrial dysfunction, accumulation and aggregation of unfolded proteins, abnormal endosomal systems, altered insulin signaling, calcium homeostasis, apoptotic signaling, autophagy, and epigenetic changes. Highly oxidative, ubiquitous CDNPs constitute a novel path into AD pathogenesis. Exposed children and young adults need early neuroprotection and multidisciplinary prevention efforts to modify the course of AD at early stages.