Citation:

Martin, B., L. Thompson, Y. Kim, W. Williams, S. Snow, M. Schladweiler, P. Phillips, C. King, J. Richards, N. Coates, M. Higuchi, Ian Gilmour, U. Kodavanti, M. Hazari, AND A. Farraj. Acute Peat Smoke Inhalation Sensitizes Rats to the Postprandial Cardiometabolic Effects of a High Fat Oral Load. SCIENCE OF THE TOTAL ENVIRONMENT. Elsevier BV, AMSTERDAM, Netherlands, 643:378-391, (2018). https://doi.org/10.1016/j.scitotenv.2018.06.089

Impact/Purpose:

Epidemiological studies of the health effects of ambient air pollution largely indicate that exposure causes few immediate measurable clinical effects, with undesirable cardiovascular outcomes instead arising hours or even days following exposure. This time-lag represents a significant challenge to controlled exposure studies that rely on measures of spontaneous alterations in cardiovascular function that may be missed due to monitoring constraints and other limitations. The findings from the study indicate that t that non-specific stressors of the cardiovascular system like high fat meal consumption may reveal effects of air pollution that would otherwise be imperceptible, particularly at low exposure levels, and when modeled experimentally, may limit the potential for mis-characterization and/or or underestimation of the impacts of exposure. This may in the long-term help reduce uncertainty in standard setting.

Description:

Wildland fire emissions cause adverse cardiopulmonary outcomes, yet controlled exposure studies to characterize health impacts of specific biomass sources have been complicated by the often latent effects of air pollution. The aim of this study was to determine if postprandial responses after a high fat challenge, long used clinically to predict cardiovascular risk, would unmask latent cardiometabolic responses in rats exposed to peat smoke, a key wildland fire air pollution source. Male Wistar Kyoto rats were exposed once (1 hr) to filtered air (FA), or low (0.36 mg/m3 particulate matter) or high concentrations (3.30 mg/m3) of peat smoke, generated by burning peat from an Irish bog. Rats were then fasted overnight, and then administered an oral gavage of a HF suspension (60 kcal% from fat), mimicking a HF meal, 24 hr post-exposure. In one cohort, cardiac and superior mesenteric artery function were assessed using high frequency ultrasound 2 hr post gavage. In a second cohort, circulating lipids and hormones, pulmonary and systemic inflammatory markers, and circulating monocyte phenotype using flow cytometry were assessed before or 2 or 6 hr after gavage. HF gavage alone elicited increases in circulating lipids characteristic of postprandial responses to a HF meal. Few effects were evident after peat exposure in un-gavaged rats. By contrast, exposure to low or high peat caused several changes relative to FA-exposed rats 2 and 6 hr post HF gavage including increased heart isovolumic relaxation time, decreased serum glucose and insulin, increased CD11 b/c-expressing blood monocytes, increased serum total cholesterol, alpha-1 acid glycoprotein, and alpha-2 macroglobulin (p = 0.063), decreased serum corticosterone, and increased lung gamma-glutamyl transferase. In summary, these findings demonstrate that HF challenge reveals effects of air pollution that may otherwise be imperceptible, particularly at low exposure levels, and suggest exposure may sensitize the body to mild inflammatory triggers.

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