Applying a Phase-Separation Parameterization in Modeling Secondary Organic Aerosol Formation from Acid-Driven Reactive Uptake of Isoprene Epoxydiols under Humid Conditions.

Secondary organic aerosol (SOA) from acid-driven reactive uptake of isoprene epoxydiols (IEPOX) contributes up to 40% of organic aerosol (OA) mass in fine particulate matter. Previous work showed that IEPOX substantially converts particulate inorganic sulfates to surface-active organosulfates (OSs). This decreases aerosol acidity and creates a viscous organic-rich shell that poses as a diffusion barrier, inhibiting additional reactive uptake of IEPOX. To account for this "self-limiting" effect, we developed a phase-separation box model to evaluate parameterizations of IEPOX reactive uptake against time-resolved chamber measurements of IEPOX-SOA tracers, including 2-methyltetrols (2-MT) and methyltetrol sulfates (MTS), at ~ 50% relative humidity. The phase-separation model was most sensitive to the mass accommodation coefficient, IEPOX diffusivity in the organic shell, and ratio of the third-order reaction rate constants forming 2-MT and MTS ( k M T / k M T S ). In particular, k M T / k M T S had to be lower than 0.1 to bring model predictions of 2-MT and MTS in closer agreement with chamber measurements; prior studies reported values larger than 0.71. The model-derived rate constants favor more particulate MTS formation due to 2-MT likely off-gassing at ambient-relevant OA loadings. Incorporating this parametrization into chemical transport models is expected to predict lower IEPOX-SOA mass and volatility due to the predominance of OSs.

Indoor monoterpene emission rates from commercial cannabis cultivation facilities in Colorado.

In 2019, an air emissions field sampling study was conducted by the Colorado Department of Public Health and Environment's Air Pollution Control Division (APCD) at four commercial cannabis cultivation facilities. Measurements of ambient biogenic volatile organic compounds (VOC) concentrations were collected from various growing stages of cannabis (vegetative and flowering) and during post-harvest activities (drying and trimming). These data were then used to determine room-specific biogenic VOC emission rates for three of the facilities from the vegetative stage of the life cycle through post-harvest activities. This study shows that the magnitude of biogenic VOC emissions within a cannabis cultivation facility varies widely with the highest emission rates of up to 7.18E-1 kg/hr found during mechanical trimming and up to 2.33E-1 kg/hr in the drying rooms. These were up to an order of magnitude higher than emission rates found in the cultivation rooms. For example, Facility A vegetative room had an emissions rate of 1.46E-2 kg/hr. Normalized by the amount of biomass present, the drying rooms had the highest VOC emissions rates, with a maximum rate of 1.6E-3 kg/hr/kg biomass. The flowering room rates were found to be up to 3.25E-4 kg/hr/kg biomass and drying rooms up to 1.16E-3 kg/hr/kg biomass. When normalized by plant count, emission rates in the flower rooms ranged from 8.11E-6 to 3.62E-4 kg/hr/plant. The dominant monoterpenes from sampling were ß-myrcene, terpinolene, and D-limonene. These data suggest that the variability in emission rates across cannabis production will create a challenge in establishing a generalized emission factor for all facilities. Across the industry, cannabis cultivation conditions and strategies can vary widely impacting the amount and type of VOC emissions. Minimizing uncertainties for VOC emission from cannabis facilities requires site-specific information on air exchange rates, plant counts, cannabis strains, biomass, and if hand or mechanical processing is used.Implications: This study found that the magnitude of biogenic VOC emissions within a cannabis cultivation varies widely throughout rooms found in the facility, with the highest emissions found during post-harvest activities (i.e. trimming) and the lowest rates in the vegetative room. These data suggest that the large emission sources of VOCs are found post-harvest and emission inventories based solely on cultivation emissions will underestimate total biogenic VOC emissions from indoor cannabis cultivation facilities. The dominant measured terpenes throughout all facilities from cultivation to post harvest were: ß-myrcene, terpinolene, and D-limonene.

"Skunky" Cannabis: Environmental Odor Troubleshooting and the "Need-for-Speed".

Although the "skunky" odor characteristic of cannabis has been widely referenced, its cause has been historically misassigned to unspecified "skunky terpenes". Recent reports from two independent research groups, the Koziel team (March and April 2021) and Oswald team (August and November 2021), have corrected this misassignment by linking the "skunky" character of industrial hemp and cannabis to 3-methyl-2-butene-1-thiol (321MBT). A recent USPTO patent application review clearly indicated that the Oswald team should take full credit for the discovery of this link with respect to cannabis. However, the August 19, 2021 publication of their patent application appears to be their formal public disclosure of 321MBT as the primary source odorant which is responsible for the targeted "skunky" odor. This date is well after the March and April 2021 public disclosures by the Koziel team for the 321MBT/"skunky" odor link relative to both cannabis and industrial hemp. This Viewpoint summarizes the investigative strategy leading to the public disclosure of this historically elusive link. It is presented from the perspective of the rapid multidimensional-gas chromatography-mass spectrometry-olfactometry (i.e., MDGC-MS-O) based odorant-prioritization "screening" approach, as applied by the Koziel team.

Meteorological based parameters and ozone exceedances in Houston and other cities in Texas.

In the Houston-Galveston-Beaumont (HGB) region considerable scientific effort has been directed at elucidating the relationships among atmospheric circulations and urban mixed-layer ozone concentrations. These studies of the HGB region have provided guidance on the conditions that are used herein to identify specific meteorological parameters that relate with observed exceedances of the National Ambient Air Quality Standard for ozone. These parameters were developed using 15 years of ozone concentrations and localized wind conditions enhanced by incorporating data from a private monitoring network. Using these data, several key parameters were found that described the most common meteorological conditions for an exceedance day in HGB. The most relevant parameters included: the wind direction at midnight, wind speeds from 0 to 6 LST, and the extent of wind direction rotation in a 24-hour period. These parameters, and the meteorological conditions they describe, were also found to occur in an analysis of observational data throughout the state of Texas suggesting large scale forces beyond the influence of a sea breeze. A mixed layer model was developed and shown to illustrate the large-scale synoptic forces found in the observational data. The meteorological parameters, and conditions they describe, could be part of a diagnostic model performance evaluation to assure that accurate predictions of ozone for Texas were not the result of compensating errors.Implications: This study identified meteorological-based parameters that coincided with observed exceedances of the National Ambient Air Quality Standard for ozone across the state of Texas. These parameters can be used in support of regulatory model performance evaluations to assure accuracy in predicting ozone conducive conditions. In Houston, the vast majority of meteorlogical ozone conducive days did not produce an exceedance, suggesting other as yet unidentified conditions that are necessary such as an intermittent emission of precursors.

B vitamin intakes modify the association between particulate air pollutants and incidence of all-cause dementia: Findings from the Women's Health Initiative Memory Study.

INTRODUCTION: Particulate air pollutants may induce neurotoxicity by increasing homocysteine levels, which can be lowered by high B vitamin intakes. Therefore, we examined whether intakes of three B vitamins (folate, B12 , and B6 ) modified the association between PM2.5 exposure and incidence of all-cause dementia. METHODS: This study included 7183 women aged 65 to 80 years at baseline. B vitamin intakes from diet and supplements were estimated by food frequency questionnaires at baseline. The 3-year average PM2.5 exposure was estimated using a spatiotemporal model. RESULTS: During a mean follow-up of 9 years, 342 participants developed all-cause dementia. We found that residing in locations with PM2.5 exposure above the regulatory standard (12 µg/m3 ) was associated with a higher risk of dementia only among participants with lower intakes of these B vitamins. DISCUSSION: This is the first study suggesting that the putative neurotoxicity of PM2.5 exposure may be attenuated by high B vitamin intakes.

Racial/Ethnic Disparities in Alzheimer's Disease Risk: Role of Exposure to Ambient Fine Particles.

BACKGROUND: Whether racial/ethnic disparities in Alzheimer's disease (AD) risk may be explained by ambient fine particles (PM2.5) has not been studied. METHOD: We conducted a prospective, population-based study on a cohort of Black (n = 481) and White (n = 6 004) older women (aged 65-79) without dementia at enrollment (1995-1998). Cox models accounting for competing risk were used to estimate the hazard ratio (HR) for racial/ethnic disparities in AD (1996-2010) defined by Diagnostic and Statistical Manual of Mental Disorders, 4th edition and the association with time-varying annual average PM2.5 (1999-2010) estimated by spatiotemporal model. RESULTS: Over an average follow-up of 8.3 (±3.5) years with 158 incident cases (21 in Black women), the racial disparities in AD risk (range of adjusted HRBlack women = 1.85-2.41) observed in various models could not be explained by geographic region, age, socioeconomic characteristics, lifestyle factors, cardiovascular risk factors, and hormone therapy assignment. Estimated PM2.5 exposure was higher in Black (14.38 ± 2.21 µg/m3) than in White (12.55 ± 2.76 µg/m3) women, and further adjustment for the association between PM2.5 and AD (adjusted HRPM2.5 = 1.18-1.28) slightly reduced the racial disparities by 2%-6% (HRBlack women = 1.81-2.26). The observed association between PM2.5 and AD risk was ~2 times greater in Black (HRPM2.5 = 2.10-2.60) than in White (HRPM2.5 = 1.07-1.15) women (range of interaction ps: <.01-.01). We found similar results after further adjusting for social engagement (social strain, social support, social activity, living alone), stressful life events, Women's Health Initiative's clinic sites, and neighborhood socioeconomic characteristics. CONCLUSIONS: PM2.5 may contribute to racial/ethnic disparities in AD risk and its associated increase in AD risk was stronger among Black women.

Adherence to a MIND-Like Dietary Pattern, Long-Term Exposure to Fine Particulate Matter Air Pollution, and MRI-Based Measures of Brain Volume: The Women's Health Initiative Memory Study-MRI.

BACKGROUND: Previous studies suggest that certain dietary patterns and constituents may be beneficial to brain health. Airborne exposures to fine particulate matter [particulate matter with aerodynamic diameter ≤2.5µm (PM2.5)] are neurotoxic, but the combined effects of dietary patterns and PM2.5 have not been investigated. OBJECTIVES: We examined whether previously reported association between PM2.5 exposure and lower white matter volume (WMV) differed between women whose usual diet during the last 3 months before baseline was more or less consistent with a Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND)-like diet, a dietary pattern that may slow neurodegenerative changes. METHODS: This study included 1,302 U.S. women who were 65-79 y old and free of dementia in the period 1996-1998 (baseline). In the period 2005-2006, structural brain magnetic resonance imaging (MRI) scans were performed to estimate normal-appearing brain volumes (excluding areas with evidence of small vessel ischemic disease). Baseline MIND diet scores were derived from a food frequency questionnaire. Three-year average PM2.5 exposure prior to MRI was estimated using geocoded participant addresses and a spatiotemporal model. RESULTS: Average total and temporal lobe WMVs were 0.74 cm3 [95% confidence interval (CI): 0.001, 1.48) and 0.19 cm3 (95% CI: 0.002, 0.37) higher, respectively, with each 0.5-point increase in the MIND score and were 4.16 cm3 (95% CI: -6.99, -1.33) and 1.46 cm3 (95% CI: -2.16, -0.76) lower, respectively, with each interquartile range (IQR) (IQR=3.22 µg/m3) increase in PM2.5. The inverse association between PM2.5 per IQR and WMV was stronger (p-interaction<0.001) among women with MIND scores below the median (for total WMV, -12.47 cm3; 95% CI: -17.17, -7.78), but absent in women with scores above the median (0.16 cm3; 95% CI: -3.41, 3.72), with similar patterns for WMV in the frontal, parietal, and temporal lobes. For total cerebral and hippocampus brain volumes or WMV in the corpus callosum, the associations with PM2.5 were not significantly different for women with high MIND scores and women with low MIND scores. DISCUSSION: In this cohort of U.S. women, PM2.5 exposure was associated with lower MRI-based WMV, an indication of brain aging, only among women whose usual diet was less consistent with the MIND-like dietary pattern at baseline. https://doi.org/10.1289/EHP8036.

PM2.5 associated with gray matter atrophy reflecting increased Alzheimers risk in older women.

OBJECTIVE: To examine whether late-life exposure to PM2.5 (particulate matter with aerodynamic diameters <2.5-µm) contributes to progressive brain atrophy predictive of Alzheimer's disease (AD) using a community-dwelling cohort of women (aged 70-89) with up to two brain MRI scans (MRI-1: 2005-6; MRI-2: 2010-11). METHODS: AD pattern similarity (AD-PS) scores, developed by supervised machine learning and validated with MRI data from the AD Neuroimaging Initiative, was used to capture high-dimensional gray matter atrophy in brain areas vulnerable to AD (e.g., amygdala, hippocampus, parahippocampal gyrus, thalamus, inferior temporal lobe areas and midbrain). Based on participants' addresses and air monitoring data, we implemented a spatiotemporal model to estimate 3-year average exposure to PM2.5 preceding MRI-1. General linear models were used to examine the association between PM2.5 and AD-PS scores (baseline and 5-year standardized change), accounting for potential confounders and white matter lesion volumes. RESULTS: For 1365 women aged 77.9±3.7 years in 2005-6, there was no association between PM2.5 and baseline AD-PS score in cross-sectional analyses (ß=-0.004; 95% CI: -0.019, 0.011). Longitudinally, each interquartile range increase of PM2.5 (2.82-µg/m3) was associated with increased AD-PS scores during the follow-up, equivalent to a 24% (hazard ratio=1.24; 95% CI: 1.14, 1.34) increase in AD risk over 5-years (n=712; aged 77.4±3.5 years). This association remained after adjustment for socio-demographics, intracranial volume, lifestyle, clinical characteristics, and white matter lesions, and was present with levels below US regulatory standards (<12-µg/m3). CONCLUSIONS: Late-life exposure to PM2.5 is associated with increased neuroanatomical risk of AD, which may not be explained by available indicators of cerebrovascular damage.

Identifying the Transcriptional Response of Cancer and Inflammation-Related Genes in Lung Cells in Relation to Ambient Air Chemical Mixtures in Houston, Texas.

Atmospheric pollution represents a complex mixture of air chemicals that continually interact and transform, making it difficult to accurately evaluate associated toxicity responses representative of real-world exposure. This study leveraged data from a previously published article and reevaluated lung cell transcriptional response induced by outdoor atmospheric pollution mixtures using field-based exposure conditions in the industrialized Houston Ship Channel. The tested hypothesis was that individual and co-occurring chemicals in the atmosphere relate to altered expression of critical genes involved in inflammation and cancer-related processes in lung cells. Human lung cells were exposed at an air-liquid interface to ambient air mixtures for 4 h, with experiments replicated across 5 days. Real-time monitoring of primary and secondary gas-phase pollutants, as well as other atmospheric conditions, was simultaneously conducted. Transcriptional analysis of exposed cells identified critical genes showing differential expression associated with both individual and chemical mixtures. The individual pollutant identified with the largest amount of associated transcriptional response was benzene. Tumor necrosis factor (TNF) and interferon regulatory factor 1 (IRFN1) were identified as key upstream transcription factor regulators of the cellular response to benzene. This study is among the first to measure lung cell transcriptional responses in relation to real-world, gas-phase air mixtures.

Predicting secondary organic aerosol phase state and viscosity and its effect on multiphase chemistry in a regional-scale air quality model.

Atmospheric aerosols are a significant public health hazard and have substantial impacts on the climate. Secondary organic aerosols (SOAs) have been shown to phase separate into a highly viscous organic outer layer surrounding an aqueous core. This phase separation can decrease the partitioning of semi-volatile and low-volatile species to the organic phase and alter the extent of acid-catalyzed reactions in the aqueous core. A new algorithm that can determine SOA phase separation based on their glass transition temperature (T g), oxygen to carbon (O : C) ratio and organic mass to sulfate ratio, and meteorological conditions was implemented into the Community Multiscale Air Quality Modeling (CMAQ) system version 5.2.1 and was used to simulate the conditions in the continental United States for the summer of 2013. SOA formed at the ground/surface level was predicted to be phase separated with core-shell morphology, i.e., aqueous inorganic core surrounded by organic coating 65.4 % of the time during the 2013 Southern Oxidant and Aerosol Study (SOAS) on average in the isoprene-rich southeastern United States. Our estimate is in proximity to the previously reported ~ 70 % in literature. The phase states of organic coatings switched between semi-solid and liquid states, depending on the environmental conditions. The semi-solid shell occurring with lower aerosol liquid water content (western United States and at higher altitudes) has a viscosity that was predicted to be 102-1012 Pa s, which resulted in organic mass being decreased due to diffusion limitation. Organic aerosol was primarily liquid where aerosol liquid water was dominant (eastern United States and at the surface), with a viscosity < 102 Pa s. Phase separation while in a liquid phase state, i.e., liquid-liquid phase separation (LLPS), also reduces reactive uptake rates relative to homogeneous internally mixed liquid morphology but was lower than aerosols with a thick viscous organic shell. The sensitivity cases performed with different phase-separation parameterization and dissolution rate of isoprene epoxydiol (IEPOX) into the particle phase in CMAQ can have varying impact on fine particulate matter (PM2.5) organic mass, in terms of bias and error compared to field data collected during the 2013 SOAS. This highlights the need to better constrain the parameters that govern phase state and morphology of SOA, as well as expand mechanistic representation of multiphase chemistry for non-IEPOX SOA formation in models aided by novel experimental insights.

Erythrocyte omega-3 index, ambient fine particle exposure, and brain aging.

OBJECTIVE: To examine whether long-chain omega-3 polyunsaturated fatty acid (LCn3PUFA) levels modify the potential neurotoxic effects of particle matter with diameters <2.5 µm (PM2.5) exposure on normal-appearing brain volumes among dementia-free elderly women. METHODS: A total of 1,315 women (age 65-80 years) free of dementia were enrolled in an observational study between 1996 and 1999 and underwent structural brain MRI in 2005 to 2006. According to prospectively collected and geocoded participant addresses, we used a spatiotemporal model to estimate the 3-year average PM2.5 exposure before the MRI. We examined the joint associations of baseline LCn3PUFAs in red blood cells (RBCs) and PM2.5 exposure with brain volumes in generalized linear models. RESULTS: After adjustment for potential confounders, participants with higher levels of RBC LCn3PUFA had significantly greater volumes of white matter and hippocampus. For each interquartile increment (2.02%) in omega-3 index, the average volume was 5.03 cm3 (p < 0.01) greater in the white matter and 0.08 cm3 (p = 0.03) greater in the hippocampus. The associations with RBC docosahexaenoic acid and eicosapentaenoic acid levels were similar. Higher LCn3PUFA attenuated the inverse associations between PM2.5 exposure and white matter volumes in the total brain and multimodal association areas (frontal, parietal, and temporal; all p for interaction <0.05), while the associations with other brain regions were not modified. Consistent results were found for dietary intakes of LCn3PUFAs and nonfried fish. CONCLUSIONS: Findings from this prospective cohort study among elderly women suggest that the benefits of LCn3PUFAs on brain aging may include the protection against potential adverse effects of air pollution on white matter volumes.

Particulate matter and episodic memory decline mediated by early neuroanatomic biomarkers of Alzheimer's disease.

Evidence suggests exposure to particulate matter with aerodynamic diameter <2.5 µm (PM2.5) may increase the risk for Alzheimer's disease and related dementias. Whether PM2.5 alters brain structure and accelerates the preclinical neuropsychological processes remains unknown. Early decline of episodic memory is detectable in preclinical Alzheimer's disease. Therefore, we conducted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also explored the potential mediating role of increased neuroanatomic risk of Alzheimer's disease associated with exposure. Participants included older females (n = 998; aged 73-87) enrolled in both the Women's Health Initiative Study of Cognitive Aging and the Women's Health Initiative Memory Study of Magnetic Resonance Imaging, with annual (1999-2010) episodic memory assessment by the California Verbal Learning Test, including measures of immediate free recall/new learning (List A Trials 1-3; List B) and delayed free recall (short- and long-delay), and up to two brain scans (MRI-1: 2005-06; MRI-2: 2009-10). Subjects were assigned Alzheimer's disease pattern similarity scores (a brain-MRI measured neuroanatomical risk for Alzheimer's disease), developed by supervised machine learning and validated with data from the Alzheimer's Disease Neuroimaging Initiative. Based on residential histories and environmental data on air monitoring and simulated atmospheric chemistry, we used a spatiotemporal model to estimate 3-year average PM2.5 exposure preceding MRI-1. In multilevel structural equation models, PM2.5 was associated with greater declines in immediate recall and new learning, but no association was found with decline in delayed-recall or composite scores. For each interquartile increment (2.81 µg/m3) of PM2.5, the annual decline rate was significantly accelerated by 19.3% [95% confidence interval (CI) = 1.9% to 36.2%] for Trials 1-3 and 14.8% (4.4% to 24.9%) for List B performance, adjusting for multiple potential confounders. Long-term PM2.5 exposure was associated with increased Alzheimer's disease pattern similarity scores, which accounted for 22.6% (95% CI: 1% to 68.9%) and 10.7% (95% CI: 1.0% to 30.3%) of the total adverse PM2.5 effects on Trials 1-3 and List B, respectively. The observed associations remained after excluding incident cases of dementia and stroke during the follow-up, or further adjusting for small-vessel ischaemic disease volumes. Our findings illustrate the continuum of PM2.5 neurotoxicity that contributes to early decline of immediate free recall/new learning at the preclinical stage, which is mediated by progressive atrophy of grey matter indicative of increased Alzheimer's disease risk, independent of cerebrovascular damage.

Exposure to fine particulate matter and temporal dynamics of episodic memory and depressive symptoms in older women.

BACKGROUND: Emerging data suggests PM2.5 (particulate matter with aerodynamic diameter <2.5 µm) may be associated with both earlier declines in episodic memory (EM) and increased depressive symptoms in older adults. Although late-life depressive symptoms are associated with EM, no longitudinal studies have examined the inter-relationship among PM2.5, depressive symptoms and EM. METHODS: Older women (n = 2,202; aged 67-83 in 1999) enrolled in the Women's Health Initiative Study of Cognitive Aging completed up to eight annual assessments of depressive symptoms (15-item Geriatric Depression Scale) and EM (California Verbal Learning Test). A nationwide spatiotemporal model (1999-2010) was used to estimate ambient PM2.5 exposure at residential locations. Univariate and bivariate structural equation models (SEMs) for latent-change scores were used to examine how 3-year average PM2.5 preceding each assessment affects the temporal dynamics and bidirectional relations of annual changes in depressive symptoms and EM. RESULTS: In univariate SEMs, one inter-quartile (4.04 µg/m3) increment of 3-year PM2.5 was significantly (p < 0.05) associated with accelerated declines in verbal learning (List A trials 1-3: ß = -1.48) and free-recall memory (short-delay: ß = -1.43; long-delay: ß = -1.11), but not with change in depressive symptoms (ß = 0.12; p = 0.71). In bivariate SEMs, significant associations were observed between PM2.5 and accelerated declines in EM measures (ß = -1.44 to -0.99; p < 0.05) and between EM performance and changes in depressive symptoms (ß = -0.08 to -0.05; p < 0.05), with significant indirect PM2.5 effects on changes in depressive symptoms (ß = 0.08-0.10; p < 0.05). These findings were robust with adjustment for multiple demographic, lifestyle, and clinical factors, and remained after excluding subjects with dementia or mild cognitive impairment. No associations were found between PM2.5 and change in depressive symptoms or depressive symptoms and subsequent EM decline. CONCLUSIONS: Findings suggest that PM2.5 neurotoxicity may damage brain areas implicated in EM, followed by manifestation of depressive symptoms. Our data did not support depressive symptoms as the neuropsychological mediator of accelerated brain aging associated with PM2.5 exposure.

Particulate Air Pollutants and Trajectories of Depressive Symptoms in Older Women.

OBJECTIVES: Although several environmental factors contribute to the etiology of late-life depressive symptoms, the role of ambient air pollution has been understudied. Experimental data support the neurotoxicity of airborne particulate matter with aerodynamic diameter of ≤2.5 µm (PM2.5), but it remains unclear whether long-term exposure is associated with late-life depressive symptoms. Our secondary aim was to explore whether the observed associations between exposure and depressive symptoms are explained by dementia risk. DESIGN, SETTING, AND PARTICIPANTS: Prospective community-dwelling cohort study from the Women's Health Initiative Study of Cognitive Aging (1999-2010). Our analyses included 1,989 older women (baseline age 73.3 ± 3.75) with no prior depression or cognitive impairment. MEASUREMENTS: Participants completed annual assessments of depressive symptoms (15-item Geriatric Depression Scale). Average ambient PM2.5 exposure at the residential location was estimated by spatiotemporal modeling for the 3-years preceding each neuropsychological assessment. Participants underwent separate annual examinations for incident dementia defined by DSM-IV. Latent-class mixture models examined the association between PM2.5 and identified trajectories of symptoms. RESULTS: Six trajectories of depressive symptoms were identified. Across all women, PM2.5 exposure was positively associated with depressive symptoms. The effect was especially strong in two clusters with sustained depressive symptoms (n = 625 sustained-mild [31%]; n = 125 sustained-moderate; [6%]). Among those with sustained-moderate symptoms, the estimated adverse effect of PM2.5 exposure was greater than that of hypertension. Among women without dementia, associations were modestly attenuated. CONCLUSION: Long-term exposure to ambient fine particles was associated with increased depressive symptoms among older women without prior depression or cognitive impairment.

Increasing Isoprene Epoxydiol-to-Inorganic Sulfate Aerosol Ratio Results in Extensive Conversion of Inorganic Sulfate to Organosulfur Forms: Implications for Aerosol Physicochemical Properties.

Acid-driven multiphase chemistry of isoprene epoxydiols (IEPOX), key isoprene oxidation products, with inorganic sulfate aerosol yields substantial amounts of secondary organic aerosol (SOA) through the formation of organosulfur compounds. The extent and implications of inorganic-to-organic sulfate conversion, however, are unknown. In this article, we demonstrate that extensive consumption of inorganic sulfate occurs, which increases with the IEPOX-to-inorganic sulfate concentration ratio (IEPOX/Sulfinorg), as determined by laboratory measurements. Characterization of the total sulfur aerosol observed at Look Rock, Tennessee, from 2007 to 2016 shows that organosulfur mass fractions will likely continue to increase with ongoing declines in anthropogenic Sulfinorg, consistent with our laboratory findings. We further demonstrate that organosulfur compounds greatly modify critical aerosol properties, such as acidity, morphology, viscosity, and phase state. These new mechanistic insights demonstrate that changes in SO2 emissions, especially in isoprene-dominated environments, will significantly alter biogenic SOA physicochemical properties. Consequently, IEPOX/Sulfinorg will play an important role in understanding the historical climate and determining future impacts of biogenic SOA on the global climate and air quality.

α-Pinene-Derived Organic Coatings on Acidic Sulfate Aerosol Impacts Secondary Organic Aerosol Formation from Isoprene in a Box Model.

Fine particulate matter (PM2.5) is known to have an adverse impact on public health and is an important climate forcer. Secondary organic aerosol (SOA) contributes up to 80% of PM2.5 worldwide and multiphase reactions are an important pathway to form SOA. Aerosol-phase state is thought to influence the reactive uptake of gas-phase precursors to aerosol particles by altering diffusion rates within particles. Current air quality models do not include the impact of diffusion-limiting organic coatings on SOA formation. This work examines how α-pinene-derived organic coatings change the predicted formation of SOA from the acid-catalyzed multiphase reactions of isoprene epoxydiols (IEPOX). A box model, with inputs provided from field measurements taken at the Look Rock (LRK) site in Great Smokey Mountains National Park during the 2013 Southern Oxidant and Aerosol Study (SOAS), was modified to incorporate the latest laboratory-based kinetic data accounting for organic coating influences. Including an organic coating influence reduced the modeled reactive uptake when relative humidity was in the 55-80% range, with predicted IEPOX-derived SOA being reduced by up to 33%. Only sensitivity cases with a large increase in Henry's Law values of an order of magnitude or more or in particle reaction rates resulted in the large statistically significant differences form base model performance. These results suggest an organic coating layer could have an impact on IEPOX-derived SOA formation and warrant consideration in regional and global scale models.

Regionalized PM2.5 Community Multiscale Air Quality model performance evaluation across a continuous spatiotemporal domain.

The regulatory Community Multiscale Air Quality (CMAQ) model is a means to understanding the sources, concentrations and regulatory attainment of air pollutants within a model's domain. Substantial resources are allocated to the evaluation of model performance. The Regionalized Air quality Model Performance (RAMP) method introduced here explores novel ways of visualizing and evaluating CMAQ model performance and errors for daily Particulate Matter ≤ 2.5 micrometers (PM2.5) concentrations across the continental United States. The RAMP method performs a non-homogenous, non-linear, non-homoscedastic model performance evaluation at each CMAQ grid. This work demonstrates that CMAQ model performance, for a well-documented 2001 regulatory episode, is non-homogeneous across space/time. The RAMP correction of systematic errors outperforms other model evaluation methods as demonstrated by a 22.1% reduction in Mean Square Error compared to a constant domain wide correction. The RAMP method is able to accurately reproduce simulated performance with a correlation of r = 76.1%. Most of the error coming from CMAQ is random error with only a minority of error being systematic. Areas of high systematic error are collocated with areas of high random error, implying both error types originate from similar sources. Therefore, addressing underlying causes of systematic error will have the added benefit of also addressing underlying causes of random error.

Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol.

Secondary organic aerosol (SOA) derived from the photochemical oxidation of isoprene contributes a substantial mass fraction to atmospheric fine particulate matter (PM2.5). The formation of isoprene SOA is influenced largely by anthropogenic emissions through multiphase chemistry of its multigenerational oxidation products. Considering the abundance of isoprene SOA in the troposphere, understanding mechanisms of adverse health effects through inhalation exposure is critical to mitigating its potential impact on public health. In this study, we assessed the effects of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B) through an air-liquid interface exposure. Gene expression profiling of 84 oxidative stress and 249 inflammation-associated human genes was performed. Our results show that the expression levels of 29 genes were significantly altered upon isoprene SOA exposure under noncytotoxic conditions (p < 0.05), with the majority (22/29) of genes passing a false discovery rate threshold of 0.3. The most significantly affected genes belong to the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor network. The Nrf2 function is confirmed through a reporter cell line. Together with detailed characterization of SOA constituents, this study reveals the impact of isoprene SOA exposure on lung responses and highlights the importance of further understanding its potential health outcomes.

Finely Resolved On-Road PM2.5 and Estimated Premature Mortality in Central North Carolina.

To quantify the on-road PM2.5 -related premature mortality at a national scale, previous approaches to estimate concentrations at a 12-km × 12-km or larger grid cell resolution may not fully characterize concentration hotspots that occur near roadways and thus the areas of highest risk. Spatially resolved concentration estimates from on-road emissions to capture these hotspots may improve characterization of the associated risk, but are rarely used for estimating premature mortality. In this study, we compared the on-road PM2.5 -related premature mortality in central North Carolina with two different concentration estimation approaches-(i) using the Community Multiscale Air Quality (CMAQ) model to model concentration at a coarser resolution of a 36-km × 36-km grid resolution, and (ii) using a hybrid of a Gaussian dispersion model, CMAQ, and a space-time interpolation technique to provide annual average PM2.5 concentrations at a Census-block level (∼105,000 Census blocks). The hybrid modeling approach estimated 24% more on-road PM2.5 -related premature mortality than CMAQ. The major difference is from the primary on-road PM2.5 where the hybrid approach estimated 2.5 times more primary on-road PM2.5 -related premature mortality than CMAQ due to predicted exposure hotspots near roadways that coincide with high population areas. The results show that 72% of primary on-road PM2.5 premature mortality occurs within 1,000 m from roadways where 50% of the total population resides, highlighting the importance to characterize near-road primary PM2.5 and suggesting that previous studies may have underestimated premature mortality due to PM2.5 from traffic-related emissions.

A Voxel-Based Morphometry Study Reveals Local Brain Structural Alterations Associated with Ambient Fine Particles in Older Women.

Objective: Exposure to ambient fine particulate matter (PM2.5: PM with aerodynamic diameters < 2.5 µm) has been linked with cognitive deficits in older adults. Using fine-grained voxel-wise analyses, we examined whether PM2.5 exposure also affects brain structure. Methods: Brain MRI data were obtained from 1365 women (aged 71-89) in the Women's Health Initiative Memory Study and local brain volumes were estimated using RAVENS (regional analysis of volumes in normalized space). Based on geocoded residential locations and air monitoring data from the U.S. Environmental Protection Agency, we employed a spatiotemporal model to estimate long-term (3-year average) exposure to ambient PM2.5 preceding MRI scans. Voxel-wise linear regression models were fit separately to gray matter (GM) and white matter (WM) maps to analyze associations between brain structure and PM2.5 exposure, with adjustment for potential confounders. Results: Increased PM2.5 exposure was associated with smaller volumes in both cortical GM and subcortical WM areas. For GM, associations were clustered in the bilateral superior, middle, and medial frontal gyri. For WM, the largest clusters were in the frontal lobe, with smaller clusters in the temporal, parietal, and occipital lobes. No statistically significant associations were observed between PM2.5 exposure and hippocampal volumes. Conclusions: Long-term PM2.5 exposures may accelerate loss of both GM and WM in older women. While our previous work linked smaller WM volumes to PM2.5, this is the first neuroimaging study reporting associations between air pollution exposure and smaller volumes of cortical GM. Our data support the hypothesized synaptic neurotoxicity of airborne particles.