Abstract
BackgroundHypothalamic-pituitary-adrenal (HPA)-axis dysfunction has been associated with a variety of mental health and cardio-metabolic disorders. While causal models of HPA-axis dysregulation have been largely focused on either pre-existing health conditions or psychosocial stress factors, recent evidence suggests a possible role for central nervous system activation via air pollutants, such as nitrogen dioxide (NO2), ozone (O3) and particulate matter (PM). Therefore, in an observational study of Latino youth, we investigated if monthly ambient NO2, O3, and PM with aerodynamic diameter ≤ 2.5 (PM2.5) exposure were associated with morning serum cortisol levels.MethodsIn this cross-sectional study, morning serum cortisol level was assessed after a supervised overnight fast in 203 overweight and obese Latino children and adolescents (female/male: 88/115; mean age: 11.1 ± 1.7 years; pre-pubertal/pubertal/post-pubertal: 85/101/17; BMI z-score: 2.1 ± 0.4). Cumulative concentrations of NO2, O3 and PM2.5 were spatially interpolated at the residential addresses based on measurements from community monitors up to 12 months prior to testing. Single and multi-pollutant linear effects models were used to test the cumulative monthly lag effects of NO2, O3, and PM2.5 on morning serum cortisol levels after adjusting for age, sex, seasonality, social position, pubertal status, and body fat percent by DEXA.ResultsSingle and multi-pollutant models showed that higher O3 exposure (derived from maximum 8-h exposure windows) in the prior 1–7 months was associated with higher serum morning cortisol (p < 0.05) and longer term PM2.5 exposure (4–10 months) was associated with lower serum morning cortisol levels (p < 0.05). Stratification by pubertal status showed associations in pre-pubertal children compared to pubertal and post-pubertal children. Single, but not multi-pollutant, models showed that higher NO2 over the 4–10 month exposure period associated with lower morning serum cortisol (p < 0.05).ConclusionsChronic ambient NO2, O3 and PM2.5 differentially associate with HPA-axis dysfunction, a mechanism that may serve as an explanatory pathway in the relationship between ambient air pollution and metabolic health of youth living in polluted urban environments. Further research that uncovers how ambient air pollutants may differentially contribute to HPA-axis dysfunction are warranted.
Highlights
Elevated levels of circulating cortisol resulting from hypothalamic-pituitary-adrenal (HPA)-axis dysfunction have been associated with a variety of mental health [1,2,3,4], cardiovascular [5], and metabolic disorders, such as type 2 diabetes [6]
While causal models of HPA-axis dysregulation have been largely focused on either chronic psychosocial stressors [7,8,9], pre-existing clinical conditions (i.e., Cushing syndrome) [10], or fetal programming [11], recent experimental evidence suggests that exposure to air pollutants may play a role in central nervous system activation and may have downstream effects on HPA-axis activity, assessed via cortisol concentrations or diurnal patterning [12]
Among all Latino children, cumulative 1 to 7-month O3 8-h exposures were associated with higher morning serum cortisol levels before and after adjusting for potentially important confounders
Summary
Elevated levels of circulating cortisol resulting from hypothalamic-pituitary-adrenal (HPA)-axis dysfunction have been associated with a variety of mental health [1,2,3,4], cardiovascular [5], and metabolic disorders, such as type 2 diabetes [6]. While causal models of HPA-axis dysregulation have been largely focused on either chronic psychosocial stressors [7,8,9], pre-existing clinical conditions (i.e., Cushing syndrome) [10], or fetal programming [11], recent experimental evidence suggests that exposure to air pollutants may play a role in central nervous system activation and may have downstream effects on HPA-axis activity, assessed via cortisol concentrations or diurnal patterning [12]. In an observational study of Latino youth, we investigated if monthly ambient NO2, O3, and PM with aerodynamic diameter ≤ 2.5 (PM2.5) exposure were associated with morning serum cortisol levels
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