Chronic social stress and susceptibility to concentrated ambient fine particles in rats.
BACKGROUND
Epidemiologic evidence suggests that chronic stress may alter susceptibility to air pollution. However, persistent spatial confounding between these exposures may limit the utility of epidemiologic methods to disentangle these effects and cannot identify physiologic mechanisms for potential differential susceptibilities.


OBJECTIVE
Using a rat model of social stress, we compared respiratory responses to fine concentrated ambient particles (CAPs) and examined biological markers of inflammation.


METHODS
Twenty-four 12-week-old male Sprague-Dawley rats were randomly assigned to four groups [stress/CAPs, stress/filtered air (FA), nonstress/CAPs, nonstress/FA]. Stress-group animals were individually introduced into the home cage of a dominant male twice weekly. Blood drawn at sacrifice was analyzed for immune and inflammatory markers. CAPs were generated using the Harvard ambient particle concentrator, which draws real-time urban ambient fine particles, enriching concentrations approximately 30 times. CAPs/FA exposures were delivered in single-animal plethysmographs, 5 hr/day for 10 days, and respiratory function was continuously monitored using a Buxco system.


RESULTS
Stressed animals displayed higher average C-reactive protein, tumor necrosis factor-alpha, and white blood cell counts than did nonstressed animals. Only among stressed animals were CAPs exposures associated with increased respiratory frequency, lower flows, and lower volumes, suggesting a rapid, shallow breathing pattern. Conversely, in animals with elevated CAPs exposures alone, we observed increased inspiratory flows and greater minute volumes (volume of air inhaled or exhaled per minute).


CONCLUSIONS
CAPs effects on respiratory measures differed significantly, and substantively, by stress group. Higher CAPs exposures were associated with a rapid, shallow breathing pattern only under chronic stress. Blood measures provided evidence of inflammatory responses. Results support epidemiologic findings that chronic stress may alter respiratory response to air pollution and may help elucidate pathways for differential susceptibility.
Clougherty
Jane E
JE
Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02215, USA. jcloughe@hsph.harvard.edu
Rossi
Christina A
CA
Lawrence
Joy
J
Long
Mark S
MS
Diaz
Edgar A
EA
Lim
Robert H
RH
McEwen
Bruce
B
Koutrakis
Petros
P
Godleski
John J
JJ
D000818:Animals; D002097:C-Reactive Protein / Q000378:metabolism; D004198:Disease Susceptibility / Q000209:etiology*; D007958:Leukocyte Count; D008297:Male; D052638:Particulate Matter / Q000032:analysis / Q000633:toxicity*; D010991:Plethysmography; D051381:Rats; D017207:Rats, Sprague-Dawley; D012120:Respiration Disorders / Q000139:chemically induced* / Q000473:pathology; D056152:Respiratory Rate / Q000187:drug effects; D013315:Stress, Psychological / Q000150:complications*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D052638:Particulate Matter; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein