Altered Heart Rate Variability in Spontaneously Hypertensive Rats Is Associated with Specific Particulate Matter Components in Detroit, Michigan

Rohr, Annette; Kamal, Ali; Morishita, Masako; Mukherjee, Bhramar; Keeler, Gerald J.; Harkema, Jack R.; Wagner, James G.

doi:10.1289/ehp.1002831

Cited by 31 publications

(22 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In similar PM 2.5 field exposures in urban areas we have previously identified associations of health effects with a number of trace elements that are linked to industrial activities in the Midwest [21,40]. In the current analyses, several elements had statistically significant associations with HR, HRV and BP, but we interpret the effect sizes as having questionable biological relevance (e.g., < 0.1 bpm HR).…”

Section: Discussioncontrasting

confidence: 48%

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

et al. 2014

Self Cite

View full text Add to dashboard Cite

BackgroundWe 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.MethodsSpontaneously 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.ResultsMean 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: <5 bpm) and SDNN (EC1> > 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.ConclusionsThese 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.

show abstract

Section: Discussioncontrasting

confidence: 48%

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

et al. 2014

Self Cite

View full text Add to dashboard Cite

show abstract

“…These data will be used in future analyses to investigate the role of PM composition and interactions with other co-pollutant on outcomes. Interestingly, several recent studies have reported on this issue; for example, a recent animal inhalation study in a nearby exposure site location in Detroit indicated that modulation of cardiac function was most strongly linked to local industrial sources including iron/steel manufacturing (Rohr, et al 2011). Similarly, determining if there are factors altering subjects’ susceptibilities (e.g.…”

Section: Discussionmentioning

confidence: 99%

Reduced metabolic insulin sensitivity following sub-acute exposures to low levels of ambient fine particulate matter air pollution

Brook

Bard

et al. 2013

Science of The Total Environment

Self Cite

161

124

View full text Add to dashboard Cite

Epidemiological studies suggest that fine particulate matter (PM2.5) may increase the risk for developing diabetes mellitus (DM). To evaluate possible mechanisms explaining these associations, we investigated if sub-acute ambient-level exposures can impair insulin sensitivity. Twenty-five healthy adults living in rural Michigan were transported to an urban location for 5 consecutive days (exposure-block) of daily 4- to 5-hour-long ambient air pollution exposures. Health outcomes, including the homeostasis model assessment of insulin resistance (HOMA-IR) the primary outcome of insulin sensitivity, were measured at 3 time points in relation to exposure-blocks: 7 days prior to start; on the last exposure-day; and 7 days after completion. PM2.5 was monitored at the urban exposure site and at community monitors near subjects’ residences. We calculated 3 “sub-acute” exposure periods (approximately 5-days-long) starting retrospective from the time of health outcome measurements (PM2.5 ranges: 9.7±3.9 to 11.2±3.9 µg•m−3). A 10 µg•m−3 increase in sub-acute PM2.5 exposures was associated with increased HOMA-IR (+0.7, 95% confidence interval (CI) 0.1 to 1.3; p=0.023) and reduced heart rate variability (standard deviation of normal-to-normal intervals [−13.1 msec, 95%CI −25.3 to −0.9; p=0.035]). No alterations in other outcomes (inflammatory markers, vascular function) occurred in relation to PM2.5 exposures. Our findings suggest that ambient PM2.5, even at low levels, may reduce metabolic insulin sensitivity supporting the plausibility that air pollution could potentiate the development of DM.

show abstract

“…Sample extracts were then analyzed for a suite of trace elements using inductively coupled plasma-mass spectrometry (ICP-MS) (ELEMENT2, Thermo Finnigan, San Jose, CA) as detailed previously [38]. To estimate the contribution of urban dust in southwest Michigan, we used the equation 1.89*Al + 1.4*Ca + 1.43*Fe + 2.14*Si, where Si is estimated by K/0.15 [42]. …”

Section: Methodsmentioning

confidence: 99%

Ambient fine particulate matter and ozone exposures induce inflammation in epicardial and perirenal adipose tissues in rats fed a high fructose diet

Sun

Liu

et al. 2013

Part Fibre Toxicol

Self Cite

View full text Add to dashboard Cite

BackgroundInflammation and oxidative stress play critical roles in the pathogenesis of inhaled air pollutant-mediated metabolic disease. Inflammation in the adipose tissues niches are widely believed to exert important effects on organ dysfunction. Recent data from both human and animal models suggest a role for inflammation and oxidative stress in epicardial adipose tissue (EAT) as a risk factor for the development of cardiovascular disease. We hypothesized that inhalational exposure to concentrated ambient fine particulates (CAPs) and ozone (O3) exaggerates inflammation and oxidative stress in EAT and perirenal adipose tissue (PAT).MethodsEight- week-old Male Sprague–Dawley rats were fed a normal diet (ND) or high fructose diet (HFr) for 8 weeks, and then exposed to ambient AIR, CAPs at a mean of 356 μg/m3, O3 at 0.485 ppm, or CAPs (441 μg/m3) + O3 (0.497 ppm) in Dearborn, MI, 8 hours/day, 5 days/week, for 9 days over 2 weeks.ResultsEAT and PAT showed whitish color in gross, and less mitochondria, higher mRNA expression of white adipose specific and lower brown adipose specific genes than in brown adipose tissues. Exposure to CAPs and O3 resulted in the increase of macrophage infiltration in both EAT and PAT of HFr groups. Proinflammatory genes of Tnf-α, Mcp-1 and leptin were significantly upregulated while IL-10 and adiponectin, known as antiinflammatory genes, were reduced after the exposures. CAPs and O3 exposures also induced an increase in inducible nitric oxide synthase (iNOS) protein expression, and decrease in mitochondrial area in EAT and PAT. We also found significant increases in macrophages of HFr-O3 rats. The synergetic interaction of HFr and dirty air exposure on the inflammation was found in most of the experiments. Surprisingly, exposure to CAPs or O3 induced more significant inflammation and oxidative stress than co-exposure of CAPs and O3 in EAT and PAT.ConclusionEAT and PAT are both white adipose tissues. Short-term exposure to CAPs and O3, especially with high fructose diet, induced inflammation and oxidative stress in EAT and PAT in rats. These findings may provide a link between air-pollution exposure and accelerated susceptibility to cardiovascular disease and metabolic complications.

show abstract

Altered Heart Rate Variability in Spontaneously Hypertensive Rats Is Associated with Specific Particulate Matter Components in Detroit, Michigan

Cited by 31 publications

References 24 publications

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

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

Reduced metabolic insulin sensitivity following sub-acute exposures to low levels of ambient fine particulate matter air pollution

Ambient fine particulate matter and ozone exposures induce inflammation in epicardial and perirenal adipose tissues in rats fed a high fructose diet

Contact Info

Product

Resources

About