Is Acute High-Dose Secondhand Smoke Exposure Always Harmful to Microvascular Function in Healthy Adults?

Prev Cardiol.Long-term exposure to secondhand smoke (SHS) is associated with impaired vascular function. The authors investigated the vascular and blood pressure (BP) reactions to acute SHS exposure. Twenty-five healthy nonsmoking adults underwent a 1-hour exposure to SHS (mean fine particulate matter <2.5 μm level=315±116 μg/m 3 ). Microvascular endothelial-dependent vasodilatation (EDV) (EndoPAT, Itamar Medical, Caesarea, Israel) and aortic hemodynamics/compliance (SphygmoCor, AtCor Medical, West Ryde, Australia) were measured before and after the SHS exposure with BP measured every 15 minutes during and for a 24-hour period before and after the exposure. SHS exposure did not change EDV, aortic hemodynamics, arterial compliance, or 24-hour BP. However, diastolic BP significantly increased during the SHS exposure period by 3.4±5.6 mm Hg. Our brief SHS exposure did not impair microvascular endothelial function or arterial compliance in healthy nonsmoking adults, but brachial diastolic BP increased.Prev Cardiol. 2010;13:175–179. © 2010 Wiley Periodicals, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/79199/1/j.1751-7141.2010.00074.x.pd

PM2.5-induced cardiovascular dysregulation in rats is associated with elemental carbon and temperature-resolved carbon subfractions

Abstract Background We tested the hypothesis that cardiovascular responses to PM2.5 exposure will be enhanced in hypertensive rats and linked to specific carbonaceous pollutants in an urban industrial setting. Methods Spontaneously hypertensive rats were exposed by inhalation to concentrated PM2.5 in an industrial area of Dearborn, Michigan, for four consecutive summer days. Blood pressure (BP), heart rate (HR) and HR variability (HRV) metrics (SDNN, RMSSD) were assessed by radiotelemetry and compared to 1 h- and 8 h-averaged fluctuations in PM2.5 composition, with a focus on elemental and organic carbon (EC and OC, respectively), and temperature-resolved subfractions (EC1-EC5, PC (pyrolized carbon), and OC1-OC4), as well as other major and minor PM components. Results Mean HR and BP were increased, while HRV was decreased over 4 days of exposure. Using 1 h averages, EC (1 μg/m3 increase) was associated with increased HR of 11-32 bpm (4-11% increase), 1.2-1.5 ms (22-27%) decreases in SDNN, 3-14 mmHg (1.5-8%) increases in systolic BP, and 5-12 mmHg (4-9%) increases in diastolic BP. By comparison, associations with OC were negligible. Using 8 h averages, EC subfractions were linked with increased heart rate (EC1: 13 bpm; EC2, EC3, PC:  > EC2 > EC3, EC4, PC), but with decreased RMSSD (EC2, EC5 > EC3, EC4). Minimal effects were associated with OC and OC1. Associations between carbon subfractions and BP were negligible. Associations with non-carbonaceous components and trace elements were generally non-significant or of negligible effect size. Conclusions These findings are the first to describe associations between acute cardiovascular responses and thermally resolved carbon subfractions. We report that cardiovascular responses to PM2.5 carbonaceous materials appear to be driven by EC and its EC1 fraction.http://deepblue.lib.umich.edu/bitstream/2027.42/115867/1/12989_2014_Article_306.pd

An intensive multi-site pilot study investigating atmospheric mercury in Broward County, Florida

An intensive multi-site pilot study of atmospheric Hg was conducted in Broward County, Florida in August and September of 1993. Broward County, which contains the city of Fort Lauderdale, is located in southeastern Florida. The county borders the Florida Everglades on the west and the Atlantic Ocean on the east. A network of four sampling sites was set up for 20 days throughout Broward County to measure Hg in both the vapor phase and the particle phase as well as Hg in precipitation. The mean concentrations of total vapor phase Hg measured at two inland sites were found to be significantly higher (3.3 and 2.8 ng/m 3 ) than that measured at a site located on the Atlantic shore (1.8 ng/m 3 ). The mean concentrations of particle phase Hg collected at the two inland sites (51 and 49 pg/m 3 ) were found to be 50% greater than that measured at the coastal site (34 pg/m 3 ). In addition, event precipitation samples were collected at four sampling sites over the 20 day study period and were analyzed for both reactive and total Hg. The mean concentration of total Hg in the precipitation samples was found to be 44 ng/L, with a range of 14 to 130 ng/L. It was determined that further meteorological analysis and a more complete characterization of the aerosol and precipitation composition are needed to identify the probable source(s) contributing to the increased deposition of Hg.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/43910/1/11270_2005_Article_BF01189665.pd

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

Airborne particulate matter exposure and urinary albumin excretion: The Multi-Ethnic Study of Atherosclerosis

Objectives: Understanding mechanistic pathways linking airborne particle exposure to cardiovascular health is important for causal inference and setting environmental standards. We evaluated whether urinary albumin excretion, a subclinical marker of microvascular function which predicts cardiovascular events, was associated with ambient particle exposure. Methods: Urinary albumin and creatinine were measured among members of the Multi-Ethnic Study of Atherosclerosis at three visits during 2000-2004. Exposure to PM2.5 and PM10 (g/m3) was estimated from ambient monitors for one month, two months and two decades before visit one. We regressed recent and chronic (20 year) PM exposure on urinary albumin/creatinine ratio (UACR) (mg/g) and microalbuminuria at first exam, controlling for age; race/ethnicity; sex; smoking; secondhand smoke exposure; body mass index; and dietary protein (n=3,901). We also evaluated UACR changes and development of microalbuminuria between the first, and second and third visits which took place at 1.5 to 2 year intervals in relation to chronic PM exposure prior to baseline using mixed models. Results: Chronic and recent particle exposures were not associated with current UACR nor microalbuminuria {per 10 g/m3 increment of chronic PM10 exposure, mean difference in log UACR = -0.02 (CI: -0.07, 0.03) and relative probability of having microalbuminuria = 0.92 (CI: 0.77, 1.08)} We found only weak evidence that albuminuria was accelerated among those chronically exposed to particles: each 10 g/m3 increment in chronic PM10 exposure was associated with a 1.14 relative probability of developing microalbuminuria over 3-4 years, though 95% confidence intervals (CI) included the null (0.96, 1.36). Conclusions: UACR is not a strong mechanistic marker for air pollution¡¦s possible influence on cardiovascular health in this sample.http://deepblue.lib.umich.edu/bitstream/2027.42/57886/1/Airborne particulate matter exposure and urinary albumin excretion THe Multi Ethnic Study if Atherosclerosis.pd

Recent exposure to particulate matter and C-reactive protein concentration in the Multiethnic Study of Atherosclerosis (MESA)

http://deepblue.lib.umich.edu/bitstream/2027.42/55422/1/Diez Roux et al Sep 2006 Recent exposure to particulate matter and C-reactive protein concentration in the multi-ethnic study of atherosclerosis.pd

Associations between recent exposure to ambient fine particulate matter and blood pressure in the Multi-Ethnic Study of Atherosclerosis

This EHP-in-Press article has been peer-reviewed, revised, and accepted for publication. The EHP-in-Press articles are completely citable using the assigned DOI code for the article. This document will be replaced with the copyedited and formatted version as soon as it is available. Through the DOI number used in the citation, you will be able to access this document at each stage of the publication process. Environ Health Perspect doi:10.1289/ehp.10899 available via http://dx.doi.org/ [Online 24 January 2008http://deepblue.lib.umich.edu/bitstream/2027.42/58000/1/Associations between recent exposure to ambient fine particulate matter and blood pressure in the Multi Ethnic Study of Atherosclerosis.pd

Exposure to road traffic and railway noise and associations with blood pressure and self-reported hypertension: a cohort study

<p>Abstract</p> <p>Background</p> <p>Epidemiological studies suggest that long-term exposure to transport noise increases the risk for cardiovascular disorders. The effect of transport noise on blood pressure and hypertension is uncertain.</p> <p>Methods</p> <p>In 1993-1997, 57,053 participants aged 50-64 year were enrolled in a population-based cohort study. At enrolment, systolic and diastolic blood pressure was measured. Incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. Residential long-term road traffic noise (L_den) was estimated for 1- and 5-year periods preceding enrolment and preceding diagnosis of hypertension. Residential exposure to railway noise was estimated at enrolment. We conducted a cross-sectional analysis of associations between road traffic and railway noise and blood pressure at enrolment with linear regression, adjusting for long-term air pollution, meteorology and potential lifestyle confounders (N = 44,083). Incident self-reported hypertension was analyzed with Cox regression, adjusting for long-term air pollution and potential lifestyle confounders.</p> <p>Results</p> <p>We found a 0.26 mm Hg higher systolic blood pressure (95% confidence intervals (CI): -0.11; 0.63) per 10 dB(A) increase in 1-year mean road traffic noise levels, with stronger associations in men (0.59 mm Hg (CI: 0.13; 1.05) per 10 dB(A)) and older participants (0.65 mm Hg (0.08; 1.22) per 10 dB(A)). Road traffic noise was not associated with diastolic blood pressure or hypertension. Exposure to railway noise above 60 dB was associated with 8% higher risk for hypertension (95% CI: -2%; 19%, P = 0.11).</p> <p>Conclusions</p> <p>While exposure to road traffic noise was associated with systolic blood pressure in subgroups, we were not able to identify associations with hypertension.</p

Particulate air pollution, systemic oxidative stress, inflammation, and atherosclerosis

Air pollution has been associated with significant adverse health effects leading to increased overall morbidity and mortality of worldwide significance. Epidemiological studies have shown that the largest portion of air pollution-related mortality is due to cardiovascular diseases, predominantly those of ischemic nature. Human studies suggest an association with atherosclerosis and increasing experimental animal data support that this association is likely to be causal. While both gasses and particles have been linked to detrimental health effects, more evidence implicates the particulate matter (PM) components as major responsible for a large portion of the proatherogenic effects. Multiple experimental approaches have revealed the ability of PM components to trigger and/or enhance free radical reactions in cells and tissues, both ex vivo as well as in vivo. It appears that exposure to PM leads to the development of systemic prooxidant and proinflammatory effects that may be of great importance in the development of atherosclerotic lesions. This article reviews the epidemiological studies, experimental animal, and cellular data that support the association of air pollutants, especially the particulate components, with systemic oxidative stress, inflammation, and atherosclerosis. It also reviews the use of transcriptomic studies to elucidate molecular pathways of importance in those systemic effects

Long-term Atmospheric Mercury Wet Deposition at Underhill, Vermont

Section 112(m) of the 1990 Clean Air Act Amendments, referred to as the Great Waters Program, mandated an assessment of atmospheric deposition of hazardous air pollutants (HAPs) to Lake Champlain. Mercury (Hg) was listed as a priority HAP and has continued to be a high priority for a number of national and international programs. An assessment of the magnitude and seasonal variation of atmospheric Hg levels and deposition in the Lake Champlain basin was initiated in December 1992 which included event precipitation collection, as well as collection of vapor and particle phase Hg in ambient air. Sampling was performed at the Proctor Maple Research Center in Underhill Center, VT. The range in the annual volume-weighted mean concentration for Hg in precipitation was 7.8–10.5 ng/l for the 11-year sampling period and the average amount of Hg deposited with each precipitation event was 0.10 μg/m 2 . The average amount of Hg deposited through precipitation each year from 1993 to 2003 was 9.7 μg/m 2 /yr. A seasonal pattern for Hg in precipitation is clearly evident, with increased Hg concentrations and deposition observed during spring and summer months. While a clear trend in the 11-year event deposition record at Underhill was not observed, a significant decrease in the event max-to-monthly ratio was observed suggesting that a major source influence was controlled over time. Discrete precipitation events were responsible for significant fractions of the monthly and annual loading of Hg to the forested ecosystem in Vermont. Monthly-averaged temperatures were found to be moderately correlated with monthly volume-weighted mean Hg concentrations ( r 2 =0.61) and Hg deposition ( r 2 =0.67) recorded at the Vermont site. Meteorological analysis indicated the highest levels of Hg in precipitation were associated with regional transport from the west, southwest, and south during the warmer months.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44444/1/10646_2004_Article_6260.pd