TY - JOUR
T1 - The cross-sectional and longitudinal association between air pollution and salivary cortisol
T2 - Evidence from the Multi-Ethnic Study of Atherosclerosis
AU - Hajat, A.
AU - Hazlehurst, Marnie F.
AU - Golden, Sherita Hill
AU - Merkin, Sharon Stein
AU - Seeman, Teresa
AU - Szpiro, Adam A.
AU - Kaufman, Joel D.
AU - Roux, Ana Diez
N1 - Funding Information:
Not Applicable. AH was supported by R00ES023498 and AS was supported in part by R21ES024894 from the National Institute of Environmental Health Sciences, USE. MESA Stress Study was supported by R01HL076831 and R01HL101161 (PI: ADR) from the National Heart, Lung and Blood Instiute and partially supported by funding from the UCLA Older Americans Independence Center supported by the National Institute on Aging (P30-AG028748). This publication was developed under two STAR research assistance agreements, No. RD831697 (MESA Air) and No. RD83830001 (MESA Air Next Stage), awarded by the U.S Environmental Protection Agency. The EPA does not endorse any products or commercial services mentioned in this publication. This research was supported by contracts HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168 and N01-HC-95169 from the National Heart, Lung, and Blood Institute, and by grants UL1-TR-000040, UL1-TR-001079, and UL1-TR-001420 from National Center for Advancing Translational Sciences. This study has not been formally reviewed by the funding agencies and the views expressed in this document are solely those of the authors.
Funding Information:
AH was supported by R00ES023498 and AS was supported in part by R21ES024894 from the National Institute of Environmental Health Sciences, USE. MESA Stress Study was supported by R01HL076831 and R01HL101161 (PI: ADR) from the National Heart, Lung and Blood Instiute and partially supported by funding from the UCLA Older Americans Independence Center supported by the National Institute on Aging (P30-AG028748). This publication was developed under two STAR research assistance agreements, No. RD831697 (MESA Air) and No. RD83830001 (MESA Air Next Stage), awarded by the U.S Environmental Protection Agency. The EPA does not endorse any products or commercial services mentioned in this publication. This research was supported by contracts HHSN268201500003I , N01-HC-95159 , N01-HC-95160 , N01-HC-95161 , N01-HC-95162 , N01-HC-95163 , N01-HC-95164 , N01-HC-95165 , N01-HC-95166 , N01-HC-95167 , N01-HC-95168 and N01-HC-95169 from the National Heart, Lung, and Blood Institute , and by grants UL1-TR-000040 , UL1-TR-001079 , and UL1-TR-001420 from National Center for Advancing Translational Sciences . This study has not been formally reviewed by the funding agencies and the views expressed in this document are solely those of the authors.
Publisher Copyright:
© 2019 The Authors
PY - 2019/10
Y1 - 2019/10
N2 - Background: Cortisol, a stress hormone released by the activation of the hypothalamic-pituitary-adrenal (HPA) axis, is critical to the body's adaptive response to physiological and psychological stress. Cortisol has also been implicated in the health effects of air pollution through the activation of the sympathetic nervous system. This study evaluates the cross-sectional and longitudinal association between several air pollutants and salivary cortisol. Methods: We used data from the Multi-Ethnic Study of Atherosclerosis (MESA), a cohort of 45–85 years old participants from six US cities. Salivary cortisol was evaluated at two time points between 2004 and 2006 and then again from 2010 to 2012. Cortisol samples were taken several times per day on two or three consecutive days. Particulate matter <2.5 μm in diameter (PM2.5), nitrogen dioxide (NO2) and nitrogen oxides (NOx) in the year prior to cortisol sampling were examined. We used piecewise linear mixed models that were adjusted for demographics, socioeconomic status and cardiovascular risk factors to examine both cross-sectional and longitudinal associations. Longitudinal models evaluated change in cortisol over time. Results: The pooled cross-sectional results revealed largely null results with the exception of a 9.7% higher wake-up cortisol associated with a 10 ppb higher NO2 (95% CI, −0.2%, 20.5%). Among all participants, the features of the cortisol curve became flatter over 5 years. The wake-to-bed slope showed a more pronounced flattening over time (0.014, 95% CI, 0.0, 0.03) with a 10 ppb higher NO2 level. Other air pollutants were not associated with change in cortisol over time. Conclusions: Our results suggest only a moderate association between traffic related air pollution and cortisol. Very few epidemiologic studies have examined the long-term impact of air pollution on the stress response systems, thus warranting further exploration of these findings.
AB - Background: Cortisol, a stress hormone released by the activation of the hypothalamic-pituitary-adrenal (HPA) axis, is critical to the body's adaptive response to physiological and psychological stress. Cortisol has also been implicated in the health effects of air pollution through the activation of the sympathetic nervous system. This study evaluates the cross-sectional and longitudinal association between several air pollutants and salivary cortisol. Methods: We used data from the Multi-Ethnic Study of Atherosclerosis (MESA), a cohort of 45–85 years old participants from six US cities. Salivary cortisol was evaluated at two time points between 2004 and 2006 and then again from 2010 to 2012. Cortisol samples were taken several times per day on two or three consecutive days. Particulate matter <2.5 μm in diameter (PM2.5), nitrogen dioxide (NO2) and nitrogen oxides (NOx) in the year prior to cortisol sampling were examined. We used piecewise linear mixed models that were adjusted for demographics, socioeconomic status and cardiovascular risk factors to examine both cross-sectional and longitudinal associations. Longitudinal models evaluated change in cortisol over time. Results: The pooled cross-sectional results revealed largely null results with the exception of a 9.7% higher wake-up cortisol associated with a 10 ppb higher NO2 (95% CI, −0.2%, 20.5%). Among all participants, the features of the cortisol curve became flatter over 5 years. The wake-to-bed slope showed a more pronounced flattening over time (0.014, 95% CI, 0.0, 0.03) with a 10 ppb higher NO2 level. Other air pollutants were not associated with change in cortisol over time. Conclusions: Our results suggest only a moderate association between traffic related air pollution and cortisol. Very few epidemiologic studies have examined the long-term impact of air pollution on the stress response systems, thus warranting further exploration of these findings.
KW - Cortisol
KW - Hypothalamic-pituitary-adrenal axis
KW - NO
KW - PM
KW - Sympathetic nervous system
KW - Traffic related air pollution
UR - http://www.scopus.com/inward/record.url?scp=85070544472&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85070544472&partnerID=8YFLogxK
U2 - 10.1016/j.envint.2019.105062
DO - 10.1016/j.envint.2019.105062
M3 - Article
C2 - 31491811
AN - SCOPUS:85070544472
SN - 0160-4120
VL - 131
JO - Environment international
JF - Environment international
M1 - 105062
ER -