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BACKGROUND: Interest in the health effects of particulate matter (PM) has focused on identifying sources of PM, including biomass burning, power plants, and gasoline and diesel emissions that may be associated with adverse health risks. Few epidemiologic studies, however, have included source-apportionment estimates in their examinations of PM health effects. We analyzed a time-series of chemically speciated PM measurements in Atlanta, Georgia, and conducted an epidemiologic analysis using data from three distinct source-apportionment methods. OBJECTIVE: The key objective of this analysis was to compare epidemiologic findings generated using both factor analysis and mass balance source-apportionment methods. METHODS: We analyzed data collected between November 1998 and December 2002 using positive-matrix factorization (PMF), modified chemical mass balance (CMB-LGO), and a tracer approach. Emergency department (ED) visits for a combined cardiovascular (CVD) and respiratory disease (RD) group were assessed as end points. We estimated the risk ratio (RR) associated with same day PM concentrations using Poisson generalized linear models. RESULTS: There were significant, positive associations between same-day [PM.sub.2.5] (PM with aerodynamic diameter [less than or equal to] 2.5 [micro]m) concentrations attributed to mobile sources (RR range, 1.018-1.025) and biomass combustion, primarily prescribed forest burning and residential wood combustion, (RR range, 1.024-1.033) source categories and CVD-related ED visits. Associations between the source categories and RD visits were not significant for all models except sulfate-rich secondary [PM.sub.2.5] (RR range, 1.012-1.020). Generally, the epidemiologic results were robust to the selection of source-apportionment method, with strong agreement between the RR estimates from the PMF and CMB-LGO models, as well as with results from models using single-species tracers as surrogates of the source-apportioned [PM.sub.2.5] values. CONCLUSIONS: Despite differences among the source-apportionment methods, these findings suggest that modeled source-apportioned data can produce robust estimates of acute health risk. In Adanta, there were consistent associations across methods between [PM.sub.2.5] from mobile sources and biomass burning with both cardiovascular and respiratory ED visits, and between sulfate-rich secondary [PM.sub.2.5] with respiratory visits. KEY WORDS: acute, Atlanta, cardiovascular, chemical mass balance, emergency department visits, fine particulate matter, positive matrix factorization, respiratory, source apportionment, tracer. Environ Health Perspect 116:459-466 (2008). doi:10.1289/ehp.10873 available via http://dx.doi.org/ [Online 14 January 2008], Recent interest in the health effects of particulate matter (PM) has focused on identifying sources of PM that pose the greatest health risks. Because it is likely that not all [...]

Since the U.S. Environmental Protection Agency began widespread monitoring of [PM.sub.2.5] (particulate matter < 2.5 [micro] in diameter) concentration levels in the late 1990s, the epidemiological community has performed several observational studies directly relating [PM.sub.2.5] concentration to various health endpoints including mortality and morbidity. However, recent research suggests that human exposure to the constituents of [PM.sub.2.5] may differ significantly from ambient (or outdoor) [PM.sub.2.5] concentration measured by monitors because people spend a great deal of time in environments, such as various indoor environments, where they are partially shielded from ambient sources of PM and are exposed to nonambient sources of PM. Recent research has provided some ways to include exposure information, but little has been done to determine the impact of including such information in a statistical model. To address this concern, we develop a three-stage Bayesian hierarchical model based on the Poisson regression model that is traditionally used to characterize the relationship between [PM.sub.2.5] concentration and health endpoints. Our approach includes a spatial model relating monitor readings to average county [PM.sub.2.5] concentration and an exposure simulator that links average ambient [PM.sub.2.5] concentration to average personal exposure using activity pattern data. We apply our model to a study population in North Carolina and explore the impact of various exposure modeling assumptions on the conclusions that can be drawn about the link between [PM.sub.2.5] exposure and cardiovascular mortality. KEY WORDS: Bayesian hierarchical modeling; Markov chain Monte Carlo; [PM.sub.2.5]; Poisson regression; Spatial statistics.

Components of surfactant act as opsonins and enhance phagocytosis of bacteria; whether this process occurs with atmospheric fine particles has not been shown. We have studied the interactions of fine particles (urban [PM.sub.2.5]) and surfactant removed from normal human lungs by lavage, using a surface analysis technique. The aim was to identify which of the chemical components of brochoalveolar lavage (BAL) deposit on the surfaces of urban [PM.sub.2.5]. Deposition of surfactant components on urban [PM.sub.2.5] surfaces was reported in previous studies, but molecular identification and relative quantification was not possible using simple data analysis. In this study, we were able to identify adsorbed components by applying an appropriate statistical technique, factor analysis. In this study, the most strongly associated mass fragment on [PM.sub.2.5] surfaces exposed to BAL (and undetected on both untreated samples and saline controls) was di-palmitoyl-phosphatidylcholine, a component of lung surfactant. Amino acids were also strongly associated with BAL-exposed [PM.sub.2.5] surfaces and not other sample types. Thirteen mass fragments were identified, diagnostic of the amino acids alanine, arginine, asparagine, aspartic acid, glutamic acid, glutamine, glycine, histidine, isoleucine, leucine, lysine, methionine, serine, and valine. This study provides evidence that lung surfactant and amino acids related to opsonin proteins adsorb to nonbiological particle surfaces exposed to human lung lining fluid. Disruption of normal surfactant function, both physical and immunological, is possible but unproven. Further work on this PM-opsonin interaction is recommended. bronchoalveolar lavage

BACKGROUND: Particulate matter, especially ultrafine particles (UFPs), may cause health effects through generation of oxidative stress, with resulting damage to DNA and other macromolecules. OBJECTIVE: We investigated oxidative damage to DNA and related repair capacity in peripheral blood mononuclear cells (PBMCs) during controlled exposure to urban air particles with assignment of number concentration (NC) to four size modes with average diameters of 12, 23, 57, and 212 nm. DESIGN. Twenty-nine healthy adults participated in a randomized, two-factor cross-over study with or without biking exercise for 180 min and with exposure to particles (NC 6169-15362/[cm.sup.3]) or filtered air (NC 91-542/[cm.sup.3]) for 24 hr. METHODS: The levels of DNA strand breaks [SB.sub.s), oxidized purines as formamidopyrimidine DNA glyco]lase (FPG) sites, and activity of 7,8-dihydro-8-oxoguanine-DNA glycosylase (OGG1) in PBMCs were measured by the Comet assay. mRNA levels of OGG1, nucleoside diphosphate linked moiety X-type motif 1 (NUDT1), and heme oxygenase-1 (HO1) were determined by real-time reverse transcriptase-polymerase chain reaction. RESULTS: Exposure to UFPs for 6 and 24 hr significantly increased the levels of SBs and FPG sites, with a further insignificant increase after physical exercise. The OGG1 activity and expression of OGG1, NUDT1, and HO1 were unaltered. There was a significant dose-response relationship between NC and DNA damage, with the 57-nm mode as the major contributor to effects. Concomitant exposure to ozone, nitrogen oxides, and carbon monoxide had no influence. CONCLUSION: Our results indicate that UFPs, especially the 57-nm soot fraction from vehicle emissions, causes systemic oxidative stress with damage to DNA and no apparent compensatory up-regulation of DNA repair within 24 hr. KEY WORDS: air pollution, biomarkers, Comet assay, DNA repair, oxidative DNA damage, ultrafine particles. Environ Health Perspect 115:1177-1182 (2007). doi:10.1289/ehp.9984 available via http://dx.doi.org/ [Online 27 April 2007], Particulate matter (PM) in ambient air is an important risk factor for acute and long-term adverse effects related to pulmonary and cardiovascular diseases, cancer, and mortality (Pope and Dockery 2006). [...]

BACKGROUND: Many studies have shown that airborne particles are associated with increased risk of death, but attention has more recently focused on the differential toxicity of particles from different sources. [...]

INTRODUCTION: We investigated whether markers of airway and systemic inflammation, as well as heart rate variability (HRV) in asthmatics, change in response to fluctuations in ambient particulate matter (PM) in [...]

Particulate matter (PM) induces oxidative stress and cardiovascular adverse health effects, but the mechanistic link between the two is unclear. We hypothesized that PM enhanced oxidative stress in vascular endothelial cells and investigated the enzymatic sources of reactive oxygen species and their effects on mitogen-activated protein kinase (MAPK) activation and vasoconstriction. We measured the production of extracellular [H.sub.2][O.sub.2], activation of extracellular signal-regulated kinases1/2 (ERK1/2) and p38 MAPKs in human pulmonary artery endothelial cells (HPAEC) treated with urban particles (UP; SRM1648), and assessed the effects of [H.sub.2][O.sub.2] on vasoconstriction in pulmonary artery ring and isolated perfused lung. Within minutes after UP treatment, HPAEC increased [H.sub.2][O.sub.2] production that could be inhibited by diphenyleneiodonium (DPI), apocynin (APO), and sodium azide (Na[N.sub.3]). The water-soluble fraction of UP as well as its two transition metal components, Cu and V, also stimulated [H.sub.2][O.sub.2] production. Na[N.sub.3] inhibited [H.sub.2][O.sub.2] production stimulated by Cu and V, whereas DPI and APO inhibited only Cu-stimulated [H.sub.2][O.sub.2] production. Inhibitors of other [H.sub.2][O.sub.2]-producing enzymes, including [N.sup.[omega]]-methyl-L-argnine, indomethacin, allopurinol, cimetidine, rotenone, and antimycin, had no effects. DPI but not Na[N.sup.3] attenuated UP-induced pulmonary vasoconstriction and phosphorylation of ERK1/2 and p38 MAPKs. Knockdown of p47phox gene expression by small interfering RNA attenuated UP-induced [H.sub.2][O.sub.2] production and phosphorylation of ERK1/2 and p38 MAPKs. Intravascular administration of [H.sub.2][O.sub.2] generated by glucose oxidase increased pulmonary artery pressure. We conclude that UP induce oxidative stress in vascular endothelial cells by activating NAD(P)H oxidase and the mitochondria. The endothelial oxidative stress may be an important mechanism for PM-induced acute cardiovascular health effects. mitogen-activated protein kinase; extracellular signal-regulated kinase; p38; vasoconstriction doi:10.1152/ajpcell.00365.2005

Exposure to zinc-laden particulate matter in ambient and occupational settings has been associated with proinflammatory responses in the lung. IL-8 is an important proinflammatory cytokine in the human lung and is induced in human airway epithelial cells exposed to zinc. In this study, we examined the cellular mechanisms responsible for [Zn.sup.2+]-induced IL-8 expression. [Zn.sup.2+] stimulation resulted in pronounced increases in both IL-8 mRNA and protein expression in the human airway epithelial cell line (BEAS-2B). IL-8 promoter activity was significantly increased by [Zn.sup.2+] exposure in BEAS-2B cells, indicating that [Zn.sup.2+]-induced IL-8 expression is transcriptionally mediated. Mutation of the activating protein (AP)-1 response element in an IL-8 promoter-enhanced green fluorescent protein construct reduced [Zn.sup.2+]-induced IL-8 promoter activity. Moreover, [Zn.sup.2+] exposure of BEAS-2B cells induced the phosphorylation of the AP-1 proteins c-Fos and c-Jun. We observed that [Zn.sup.2+] exposure induced the phosphorylation of ERK, JNK, and p38 MAPKs, whereas inhibition of ERK or JNK activity blocked IL-8 mRNA and protein expression in BEAS-2B cells treated with [Zn.sup.2+]. In addition, we investigated the role of protein tyrosine phosphatases in the activation of signaling by [Zn.sup.2+] * [Zn.sup.2+] treatment inhibited ERK- and JNK-directed phosphatase activities in BEAS-2B cells. These results suggested that [Zn.sup.2+] -induced inhibition of phosphatase activity is an initiating event in MAPK and AP-1 activation that leads to enhanced IL-8 expression by human airway epithelial cells. interleukin-8; zinc; activating protein-1; c-Jun N[H.sub.2]-terminal kinase; extracellular signal-regulated kinase; mitogen-activated protein kinase phosphatase; metal; particulate matter

The hypothesis that subchronic exposure to environmentally relevant particulate matter, even at low concentrations, potentiates atherosclerosis and alters vasomotor tone is tested in a mouse model. The findings suggest that mice exposed to environmentally relevant concentrations of particulate matter had more atherosclerosis and vascular inflammation and a heightened vasococonstrictive response than mice exposed to filtered air.

The microscopic dust that comes off tyres contains unique combinations of known carcinogens, neurotoxins, heavy metals and other poisons that are linked to serious diseases such as heart failure. Humans are not the only ones to be affected since animals are also prone to the particulate, inhalation of which can damage both the hearts and the lungs of living beings.

Increases in the levels of environmental particulate matter with a diameter of interleukin-8; histone acetylation; particulate matter with diameter of

Background: It is unknown if ambient fine particulate matter ([PM.sub.2.5]) is associated with lower renal function, a cardiovascular risk factor. OBJECTIVE: We investigated whether long-term [PM.sub.2.5] exposure was associated with estimated glomerular filtration rate (eGFR) in a cohort of older men living in the Boston Metropolitan area. METHODS: This longitudinal analysis included 669 participants from the Veterans Administration Normative Aging Study with up to four visits between 2000 and 2011 (n = 1,715 visits). Serum creatinine was measured at each visit, and eGFR was calculated according to the Chronic Kidney Disease Epidemiology Collaboration equation. One-year exposure to [PM.sub.2.5] prior to each visit was assessed using a validated spatiotemporal model that utilized satellite remote-sensing aerosol optical depth data. eGFR was modeled in a time-varying linear mixed-effects regression model as a continuous function of 1-year [PM.sub.2.5], adjusting for important covariates. RESULTS: One-year [PM.sub.2.5] exposure was associated with lower eGFRs; a 2.1-µg/[m.sup.3] interquartile range higher 1-year [PM.sub.2.5] was associated with a 1.87 mL/min/1.73 [m.sup.2] lower eGFR [95% confidence interval (CI): -2.99, -0.76]. A 2.1 µg/[m.sup.3]-higher 1-year [PM.sub.2.5] was also associated with an additional annual decrease in eGFR of 0.60 mL/min/1.73 [m.sup.2] per year (95% CI: -0.79, -0.40). CONCLUSIONS: In this longitudinal sample of older men, the findings supported the hypothesis that long-term [PM.sub.2.5] exposure negatively affects renal function and increases renal function decline. http://dx.doi.org/10.1289/ehp.1510269, Introduction Chronic exposure to ambient fine particulate matter ([PM.sub.2.5]) is a well-known risk factor for cardiovascular-related morbidity and mortality (Brook et al. 2010). Although the underlying mechanisms have not been [...]

Exposure to fine particulate matter ([PM.sub.2.5]) is associated with cardiovascular health impacts including increased risk of irregular heartbeat and pulmonary embolism (arterial blockage). (1) However, the relationship between [PM.sub.2.5] and [...]

BACKGROUND: Survivors of acute myocardial infarction (AMI) are at increased risk of dying within several hours to days following exposure to elevated levels of ambient air pollution. Little is known, however, about the influence of long-term (months to years) air pollution exposure on survival after AMI. OBJECTIVE: We conducted a population-based cohort study to determine the impact of long-term exposure to fine particulate matter [less than or equal to] 2.5 µm in diameter ([PM.sub.2.5]) on post-AMI survival. METHODS: We assembled a cohort of 8,873 AMI patients who were admitted to 1 of 86 hospital corporations across Ontario, Canada in 1999-2001. Mortality follow-up for this cohort extended through 2011. Cumulative time-weighted exposures to [PM.sub.2.5] were derived from satellite observations based on participants' annual residences during follow-up. We used standard and multilevel spatial random-effects Cox proportional hazards models and adjusted for potential confounders. RESULTS: Between 1999 and 2011, we identified 4,016 nonaccidental deaths, of which 2,147 were from any cardiovascular disease, 1,650 from ischemic heart disease, and 675 from AMI. For each 10-µg/[m.sup.3] increase in [PM.sub.2.5], the adjusted hazard ratio ([HR.sub.10]) of nonaccidental mortality was 1.22 [95% confidence interval (CI): 1.03, 1.45]. The association with [PM.sub.2.5] was robust to sensitivity analyses and appeared stronger for cardiovascular-related mortality: ischemic heart ([HR.sub.10] = 1.43; 95% CI: 1.12, 1.83) and AMI ([HR.sub.10] = 1.64; 95% CI: 1.13, 2.40). We estimated that 12.4% of nonaccidental deaths (or 497 deaths) could have been averted if the lowest measured concentration in an urban area (4 µg/[m.sup.3]) had been achieved at all locations over the course of the study. CONCLUSIONS: Long-term air pollution exposure adversely affects the survival of AMI patients. http://dx.doi.org/10.1289/EHP185, Introduction Acute myocardial infarction (AMI) is one of the most common cardiovascular events, affecting ~7.9 million adults in the United States (Roger et al. 2011) and 540,000 in Canada (Chow [...]

BACKGROUND: Telomere length and mitochondrial DNA (mtDNA) content are markers of aging and aging-related diseases. There is inconclusive evidence concerning the mechanistic effects of airborne particulate matter (PM) exposure on biomolecular markers of aging. OBJECTIVE: The present study examines the association between short- and long-term PM exposure with telomere length and mtDNA content in the elderly and investigates to what extent this association is mediated by expression of genes playing a role in the telomere-mitochondrial axis of aging. METHODS: Among 166 nonsmoking elderly participants, we used qPCR to measure telomere length and mtDNA content in leukocytes and RNA from whole blood to measure expression of SIRT1, TP53, PPARGC1A, PPARGC1B, NRF1, and NFE2L2. Associations between PM exposure and markers of aging were estimated using multivariable linear regression models adjusted for sex, age, BMI, socioeconomic status, statin use, past smoking status, white blood cell count, and percentage of neutrophils. Mediation analysis was performed to explore the role of age-related markers between the association of PM exposure and outcome. Annual [PM.sub2.5] exposure was calculated for each participant's home address using a high-resolution spatialtemporal interpolation model. RESULTS: Annual [PM.sub2.5] concentrations ranged from 15 to 23 µg/[m.sup.3]. A 5-µg/[m.sup.3] increment in annual [PM.sub2.5] concentration was associated with a relative decrease of 16.8% (95% CI: -26.0%, -7.4%, p = 0.0005) in telomere length and a relative decrease of 25.7% (95% CI: -35.2%, -16.2%, p < 0.0001) in mtDNA content. Assuming causality, results of the mediation analysis indicated that SIRT1 mediated 19.5% and 22.5% of the estimated effect of [PM.sub2.5] exposure on telomere length and mtDNA content, respectively. CONCLUSIONS: Our findings suggest that the estimated effects of [PM.sub2.5] exposure on the telomere-mitochondrial axis of aging may play an important role in chronic health effects of [PM.sub2.5]. http://dx.doi.org/10.1289/ehp.1509728, Introduction Telomeres are complexes of hexameric repeats at the distal end of chromosomes where they provide stability and protection to the coding DNA. Telomere length declines with each cell division [...]

BACKGROUND: Numerous studies have examined associations between air pollution and pregnancy outcomes, but most have been restricted to urban populations living near monitors. OBJECTIVES: We examined the association between pregnancy outcomes and fine particulate matter in a large national study including urban and rural areas. METHODS: Analyses were based on approximately 3 million singleton live births in Canada between 1999 and 2008. Exposures to [PM.sub.2.5] (particles of median aerodynamic diameter ≤ 2.5 µm) were assigned by mapping the mother's postal code to a monthly surface based on a national land use regression model that incorporated observations from fixed-site monitoring stations and satellite-derived estimates of [PM.sub.2.5]. Generalized estimating equations were used to examine the association between [PM.sub.2.5] and preterm birth (gestational age < 37 weeks), term low birth weight (< 2,500 g), small for gestational age (SGA; < 10th percentile of birth weight for gestational age), and term birth weight, adjusting for individual covariates and neighborhood socioeconomic status (SES). RESULTS: In fully adjusted models, a 10-µg/[m.sup.3] increase in [PM.sub.2.5] over the entire pregnancy was associated with SGA (odds ratio = 1.04; 95% CI 1.01, 1.07) and reduced term birth weight (-20.5 g; 95% CI -24.7, -16.4). Associations varied across subgroups based on maternal place of birth and period (1999-2003 vs. 2004-2008). CONCLUSIONS: This study, based on approximately 3 million births across Canada and employing [PM.sub.2.5] estimates from a national spatiotemporal model, provides further evidence linking [PM.sub.2.5] and pregnancy outcomes. http://dx.doi.org/10.1289/ehp.1408995, Introduction Numerous studies have examined the association between air pollution and pregnancy outcomes. Meta-analyses and pooled multicenter analyses suggest that particulate matter is associated with low birth weight and preterm [...]

BACKGROUND: Both short- and long-term exposures to fine particulate matter (< 2.5 pm; [PM.sub.2.5]) are associated with mortality. However, whether the associations exist at levels below the new U.S. Environmental Protection Agency (EPA) standards (12 µg/[m.sup.3] of annual average [PM.sub.2.5], 35 µg/[m.sup.3] daily) is unclear. In addition, it is not clear whether results from previous time series studies (fit in larger cities) and cohort studies (fit in convenience samples) are generalizable. OBJECTIVES: We estimated the effects of low-concentration [PM.sub.2.5] on mortality. METHODS: High resolution (1 km x 1 km) daily [PM.sub.2.5] predictions, derived from satellite aerosol optical depth retrievals, were used. Poisson regressions were applied to a Medicare population ([greater than or equal to] 65 years of age) in New England to simultaneously estimate the acute and chronic effects of exposure to [PM.sub.2.5], with mutual adjustment for short- and long-term exposure, as well as for area-based confounders. Models were also restricted to annual concentrations < 10 µg/[m.sup.3] or daily concentrations < 30 µg/[m.sup.3]. RESULTS: [PM.sub.2.5] was associated with increased mortality. In the study cohort, 2.14% (95% CI: 1.38, 2.89%) and 7.52% (95% CI: 1.95, 13.40%) increases were estimated for each 10-[miro]g/[m.sup.3] increase in short- (2 day) and long-term (1 year) exposure, respectively. The associations held for analyses restricted to low-concentration [PM.sub.2.5] exposure, and the corresponding estimates were 2.14% (95% CI: 1.34, 2.95%) and 9.28% (95% CI: 0.76, 18.52%). Penalized spline models of long-term exposure indicated a larger effect for mortality in association with exposures ≥ 6 µg/[m.sup.3] versus those < 6 µg/[m.sup.3]. In contrast, the association between short-term exposure and mortality appeared to be linear across the entire exposure distribution. CONCLUSIONS: Using a mutually adjusted model, we estimated significant acute and chronic effects of [PM.sub.2.5] exposure below the current U.S. EPA standards. These findings suggest that improving air quality with even lower [PM.sub.2.5] than currently allowed by U.S. EPA standards may benefit public health. http://dx.doi.org/10.1289/ehp.1409111, Introduction Many studies have found associations between fine particulate matter [PM with aerodynamic diameter < 2.5 pm ([PM.sub.2.5])] and increased mortality (Dockery et al. 1993; Franklin et al. 2007; Pope [...]

BACKGROUND: [PM.sub.2.5] (particulate matter [less than or equal to] 2.5 µm) has been associated with adverse cardiovascular outcomes, but it is unclear whether specific [PM.sub.2.5] components, particularly metals, may be responsible for cardiovascular effects. OBJECTIVES: We aimed to determine which [PM.sub.2.5] components are associated with blood pressure in a longitudinal cohort. METHODS: We fit linear mixed-effects models with the adaptive LASSO penalty to longitudinal data from 718 elderly men in the Veterans Affairs Normative Aging Study, 1999-2010. We controlled for [PM.sub.2.5] mass, age, body mass index, use of antihypertensive medication (ACE inhibitors, non-ophthalmic beta blockers, calcium channel blockers, diuretics, and angiotensin receptor antagonists), smoking status, alcohol intake, years of education, temperature, and season as fixed effects in the models, and additionally applied the adaptive LASSO method to select [PM.sub.2.5] components associated with blood pressure. Final models were identified by the Bayesian Information Criterion (BIC). RESULTS: For systolic blood pressure (SBP), nickel (Ni) and sodium (Na) were selected by the adaptive LASSO, whereas only Ni was selected for diastolic blood pressure (DBP). An interquartile range increase (2.5 ng/[m.sup.3]) in 7-day moving-average Ni was associated with 2.48-mmHg (95% CI: 1.45, 3.50 mmHg) increase in SBP and 2.22-mmHg (95% CI: 1.69, 2.75 mmHg) increase in DBP, respectively. Associations were comparable when the analysis was restricted to study visits with [PM.sub.2.5] below the 75th percentile of the distribution (12 µg/[m.sup.3]). CONCLUSIONS: Our study suggested that exposure to ambient Ni was associated with increased blood pressure independent of [PM.sub.2.5] mass in our study population of elderly men. Further research is needed to confirm our findings, assess generalizability to other populations, and identify potential mechanisms for Ni effects. http://dx.doi.org/10.1289/ehp.1409021, Introduction Studies have shown that exposure to fine particulate matter ([PM.sub.2.5]; particles ≤ 2.5 µm in aerodynamic diameter) is associated with cardiovascular morbidity and mortality (Franklin et al. 2008; Laden [...]

BACKGROUND: Long-term exposure to fine particles (particulate matter ≤ 2.5 µm; [PM.sub.2.5]) has been consistently linked to heart and lung disease. Recently, there has been increased interest in examining the effects of air pollution on the nervous system, with evidence showing potentially harmful effects on neurodegeneration. OBJECTIVE: Our objective was to assess the potential impact of long-term [PM.sub.2.5] exposure on event time, defined as time to first admission for dementia, Alzheimer's (AD), or Parkinson's (PD) diseases in an elderly population across the northeastern United States. METHODS: We estimated the effects of [PM.sub.2.5] on first hospital admission for dementia, AD, and PD among all Medicare enrollees ≥ 65 years in 50 northeastern U.S. cities (1999-2010). For each outcome, we first ran a Cox proportional hazards model for each city, adjusting for prior cardiopulmonary-related hospitalizations and year, and stratified by follow-up time, age, sex, and race. We then pooled the city-specific estimates by employing a random effects meta-regression. RESULTS: We followed approximately 9.8 million subjects and observed significant associations of long-term [PM.sub.2.5] city-wide exposure with all three outcomes. Specifically, we estimated a hazard ratio (HR) of 1.08 (95% CI: 1.05, 1.11) for dementia, an HR of 1.15 (95% CI: 1.11, 1.19) for AD, and an HR of 1.08 (95% CI: 1.04, 1.12) for PD admissions per 1-µg/[m.sup.3] increase in annual [PM.sub.2.5] concentrations. CONCLUSIONS: To our knowledge, this is the first study to examine the relationship between longterm exposure to [PM.sub.2.5] and time to first hospitalization for common neurodegenerative diseases. We found strong evidence of association for all three outcomes. Our findings provide the basis for further studies, as the implications of such exposures could be crucial to public health. http://dx.doi.org/10.1289/ehp.1408973, Introduction Long-term exposure to [PM.sub.2.5], particles with aerodynamic diameter ≤ 2.5 µm, has been consistently associated with a series of outcomes including but not limited to mortality (Krewski et al. [...]