Description
Introduction: Major Depressive Disorder (MDD) is one of the most prevalent medical conditions worldwide, accounting for relevant disability and high economic social costs. Different factors were found to play a role in the aetiology of this condition, including genetic predisposition, alterations in biological systems and social/natural environmental factors (including air pollution).
Objective: Purpose of the present research was to study the interplay between air pollution, biological markers, and severity of MDD.
Methodology: The study population includes 416 adult subjects affected by MDD. Patients with severe medical comorbidities associated with prominent inflammation or behavioural disturbances, subjects with current substance use disorders or pregnant women were excluded. The included subjects were assessed by a socio-demographic questionnaire and by rating scales to measure MDD severity and related disability: Montgomery-Asberg Depression Rating Scale (MADRS); Hamilton Depression Rating Scale (HAM-D); Clinical Global Impression-severity of illness (CGI); Sheehan Disability Scale (SDS); Global assessment of functioning (GAF). The mean exposure to particulate matter (PM10 and PM2.5) and nitrogen dioxide (NO2) in the two weeks preceding recruitment was studied. The methylation of the following clock or clock-related genes was assessed by pyrosequencing: CLOCK, BMLA1, PER1, PER2, OX1R, CRY1, CRY2, OXTR, FOXp3, HERV-W. The associations between air pollution and MDD severity, and between MDD severity and DNA methylation were assessed by multivariate regression models. Hypersusceptibility was defined as the presence of medical comorbidities characterized by low-grade inflammation (e.g., diabetes) or active smoking.
Results: An increase in NO2 exposure was associated with more severe depressive symptoms as shown by increments in HAM-D scores (β=2.09, p=0.005) as well as with a loss of social functioning as shown by a decrease in GAF scores (β=-1.96, p=0.019). On the contrary, an increase in PM exposure caused a worsening of depressive symptoms as measured by MADRS but only in hypersusceptible subjects (interaction p-value=0.019 for PM10 and 0.011 for PM2.5). Hypermethylation of CLOCK was associated with lower HAM-D scores (β=-3.40, p=0.040), thus allowing us to interpret a hypomethylation of this gene as associated with an increased MDD severity. Hypermethylation of oxytocin receptor gene (OXTR) was associated with more severe depressive symptoms in subjects with melancholic and psychotic depressive subtype (MADRS: β=0.16, p=0.031; HAM-D: β=0.17, p=0.030).
Discussion: This study shows that air pollution has a negative impact on mental health with potential direct or indirect (i.e., mediated by alterations on biological systems such as over-inflammation) toxic effects on the Central Nervous System. On the other hand, the findings of this study support the evidence of a relationship between MDD severity and biological systems such as those regulating circadian rhythms or neuropeptides (oxytocin).
Conclusions: Our study confirms the detrimental effects of air pollution on mental health; as such, actions to ameliorate quality of air (e.g., limitation of pollution sources such as road traffic or implementation of green areas in the urban environment) are warranted.
Acknowledgments: this research was funded by Cariplo Foundation and dissemination was supported by 4EU+ Alliance that includes University of Milan.
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