Coupling atmospheric mercury isotope ratios and meteorology to identify sources of mercury impacting a coastal urban‐industrial region near Pensacola, Florida, USA

Identifying the anthropogenic and natural sources of mercury (Hg) emissions contributing to atmospheric mercury on local, regional, and global scales continues to be a grand challenge. The relative importance of various direct anthropogenic emissions of mercury, in addition to natural geologic sources and reemission of previously released and deposited mercury, differs regionally and temporally. In this study, we used local‐scale, mesoscale, and synoptic‐scale meteorological analysis to couple the isotopic composition of ambient atmospheric mercury with potential sources of mercury contributing to a coastal urban‐industrial setting near a coal‐fired power plant in Pensacola, Florida, USA. We were able to broadly discern four influences on the isotopic composition of ambient atmospheric mercury impacting this coastal urban‐industrial region: (1) local to regional urban‐industrial anthropogenic emissions (mean δ202Hg = 0.44 ± 0.05‰, 1SD, n = 3), (2) marine‐influenced sources derived from the Gulf of Mexico (mean δ202Hg = 0.77 ± 0.15‰, 1SD, n = 4), (3) continental sources associated with north‐northwesterly flows from within the planetary boundary layer (mean δ202Hg = 0.65 ± 0.04‰, 1SD, n = 3), and (4) continental sources associated with north‐northeasterly flows at higher altitudes (i.e., 2000 m above ground level; mean δ202Hg = 1.10 ± 0.21‰, 1SD, n = 8). Overall, these data, in conjunction with previous studies, suggest that the background global atmospheric mercury pool is characterized by moderately positive δ202Hg values; that urban‐industrial emissions drive the isotopic composition of ambient atmospheric mercury toward lower δ202Hg values; and that air‐surface exchange dynamics across vegetation and soils of terrestrial ecosystems drive the isotopic composition of ambient atmospheric mercury toward higher positive δ202Hg values. The data further suggest that mass‐independent fractionation (MIF) of both even‐mass‐ and odd‐mass‐number isotopes, likely generated by photochemical reactions in the atmosphere or during reemission from terrestrial and aquatic ecosystems, can be obscured by mixing with anthropogenic emissions having different MIF signatures.Key PointsIsotopic composition of TGM differed among meteorologically identified sourcesBackground atmospheric TGM displayed moderately positive δ202Hg valuesAnthropogenic emissions drive TGM isotopic composition to lower δ202Hg valuesPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/136364/1/gbc20349-sup-0001-Supplementary.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/136364/2/gbc20349.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/136364/3/gbc20349_am.pd

Exposures to Airborne Particulate Matter and Adverse Perinatal Outcomes: A Biologically Plausible Mechanistic Framework for Exploring Potential Effect Modification by Nutrition

OBJECTIVES: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. METHODS: We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. CONCLUSIONS: Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts

Air Pollution–Associated Changes in Lung Function among Asthmatic Children in Detroit

In a longitudinal cohort study of primary-school–age children with asthma in Detroit, Michigan, we examined relationships between lung function and ambient levels of particulate matter ≤ 10 μm and ≤ 2.5 μm in diameter (PM(10) and PM(2.5)) and ozone at varying lag intervals using generalized estimating equations. Models considered effect modification by maintenance corticosteroid (CS) use and by the presence of an upper respiratory infection (URI) as recorded in a daily diary among 86 children who participated in six 2-week seasonal assessments from winter 2001 through spring 2002. Participants were predominantly African American from families with low income, and > 75% were categorized as having persistent asthma. In both single-pollutant and two-pollutant models, many regressions demonstrated associations between higher exposure to ambient pollutants and poorer lung function (increased diurnal variability and decreased lowest daily values for forced expiratory volume in 1 sec) among children using CSs but not among those not using CSs, and among children reporting URI symptoms but not among those who did not report URIs. Our findings suggest that levels of air pollutants in Detroit, which are above the current National Ambient Air Quality Standards, adversely affect lung function of susceptible asthmatic children

Social and Physical Environments and Disparities in Risk for Cardiovascular Disease: The Healthy Environments Partnership Conceptual Model

The Healthy Environments Partnership (HEP) is a community-based participatory research effort investigating variations in cardiovascular disease risk, and the contributions of social and physical environments to those variations, among non-Hispanic black, non-Hispanic white, and Hispanic residents in three areas of Detroit, Michigan. Initiated in October 2000 as a part of the National Institute of Environmental Health Sciences’ Health Disparities Initiative, HEP is affiliated with the Detroit Community–Academic Urban Research Center. The study is guided by a conceptual model that considers race-based residential segregation and associated concentrations of poverty and wealth to be fundamental factors influencing multiple, more proximate predictors of cardiovascular risk. Within this model, physical and social environments are identified as intermediate factors that mediate relationships between fundamental factors and more proximate factors such as physical activity and dietary practices that ultimately influence anthropomorphic and physiologic indicators of cardiovascular risk. The study design and data collection methods were jointly developed and implemented by a research team based in community-based organizations, health service organizations, and academic institutions. These efforts include collecting and analyzing airborne particulate matter over a 3-year period; census and administrative data; neighborhood observation checklist data to assess aspects of the physical and social environment; household survey data including information on perceived stressors, access to social support, and health-related behaviors; and anthropometric, biomarker, and self-report data as indicators of cardiovascular health. Through these collaborative efforts, HEP seeks to contribute to an understanding of factors that contribute to racial and socioeconomic health inequities, and develop a foundation for efforts to eliminate these disparities in Detroit

Central IKKβ inhibition prevents air pollution mediated peripheral inflammation and exaggeration of type II diabetes

Abstract Background Prior experimental and epidemiologic data support a link between exposure to fine ambient particulate matter (<2.5 μm in aerodynamic diameter, PM2.5) and development of insulin resistance/Type II diabetes mellitus (Type II DM). We investigated the role of hypothalamic inflammation in PM2.5-mediated diabetes development. Methods KKay mice, a genetically susceptible model of Type II DM, were assigned to either concentrated PM2.5 or filtered air (FA) for 4–8 weeks via a versatile aerosol concentrator and exposure system, or administered intra-cerebroventricular with either IKKβ inhibitor (IMD-0354) or TNFα antibody (infliximab) for 4–5 weeks simultaneously with PM2.5 exposure. Glucose tolerance, insulin sensitivity, oxygen consumption and heat production were evaluated. At euthanasia, blood, spleen, visceral adipose tissue and hypothalamus were collected to measure inflammatory cells using flow cytometry. Standard immunohistochemical methods and quantitative PCR were used to assess targets of interest. Results PM2.5 exposure led to hyperglycemia and insulin resistance, which was accompanied by increased hypothalamic IL-6, TNFα, and IKKβ mRNA expression and microglial/astrocyte reactivity. Targeting the NFκB pathway with intra-cerebroventricular administration of an IKKβ inhibitor [IMD-0354, n = 8 for each group)], but not TNFα blockade with infliximab [(n = 6 for each group], improved glucose tolerance, insulin sensitivity, rectified energy homeostasis (O2 consumption, CO2 production, respiratory exchange ratio and heat generation) and reduced peripheral inflammation in response to PM2.5. Conclusions Central inhibition of IKKβ prevents PM2.5 mediated peripheral inflammation and exaggeration of type II diabetes. These results provide novel insights into how air pollution may mediate susceptibility to insulin resistance and Type II DM.http://deepblue.lib.umich.edu/bitstream/2027.42/109486/1/12989_2014_Article_53.pd

Prevalence and Determinants of Mucous Membrane Irritations in a Community Near a Cement Factory in Zambia: A Cross Sectional Study

Exposure to cement dust has been associated with deleterious health effects in humans. This study investigated whether residing near a cement factory increases the risk of irritations to the mucous membranes of the eyes and respiratory system. A cross sectional study was conducted in Freedom Compound, a community bordering a cement factory in Chilanga, Zambia and a control community, Bauleni, located 18 km from the cement plant. A modified American Thoracic Society questionnaire was administered to 225 and 198 respondents aged 15–59 years from Freedom and Bauleni, respectively, to capture symptoms of the irritations. Respondents from Freedom Compound, were more likely to experience the irritations; adjusted ORs 2.50 (95% CI: 1.65, 3.79), 4.36 (95% CI (2.96, 6.55)) and 1.94 (95% CI (1.19, 3.18)) for eye, nose and sinus membrane irritations respectively. Cohort panel studies to determine associations of cement emissions to mucous membrane irritations and respiratory symptoms, coupled with field characterization of the exposure are needed to assess whether the excess prevalence of symptoms of mucous membrane irritations observed in Freedom compound are due to emissions from the cement factory

Investigation of Local Mercury Deposition from a Coal-Fired Power Plant Using Mercury Isotopes

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/155708/1/Sherman_et_al_2012_Investigation_of_local.pd