Air pollution poses a present and growing danger to physical and mental health. A new review paper published in the Journal of Clinical Medicine shows strong associations between air pollution and poor perinatal health, especially postpartum depression and stress.
Study: Air Pollution and Perinatal Mental Health: A Comprehensive Overview. Image Credit: NadyGinzburg/Shutterstock.com
The perinatal period influences the mother's health and the bond developed between the mother and her infant postnatally. It is also, unfortunately, a key vulnerability point for the mother, often marking the onset of various maternal mental illnesses.
About 12 in every hundred women become depressed in the perinatal period, while about one in three (30%) have clinical anxiety symptoms. Meanwhile, an initial episode of postpartum psychosis occurred in 25 to 60 cases per 100,000 births.
Biological, psychological, social, and environmental factors have all been thought to play a role in the genesis of postpartum psychosis.
Air pollution is among the top five risk factors for deaths that can be directly traced to exposure and would not have happened without such exposure. Air pollutants are associated with multiple morbidities, including respiratory, cardiovascular, and metabolic diseases.
Recent research indicates that depression risk could be higher in populations exposed to air pollution, especially particulate matter of diameter 2.5 microns (PM2/5).
The mechanisms of mental illness following exposure to air pollution could involve inflammatory responses via microglia or epigenetic modifications involving the circadian genes that regulate basic physiological processes such as appetite and sleep.
Such genes include CLOCK-BMAL, CRY1, and CRY2. A delay in circadian rhythms could affect the success of breastfeeding. Again, air pollution could modulate oxytocin release, which is critical in maternal-infant bonding and breastfeeding. Its anti-inflammatory effects are just as valuable, inhibiting depression-induced inhibition of biological functions.
Stress can disrupt the hypothalamo-pituitary-adrenal (HPA) axis by increasing cortisol levels, which may cause dysregulation of the mother's immune system.
With increased levels of corticotropic releasing factor (CRF) from the hypothalamus, higher levels of glucocorticoids flood the brain, causing responsive changes in the microglia and neurons. Oxytocin is key to inhibiting such disruptive effects by its paracrine actions.
Air pollution could thus cause increased levels of systemic inflammation via various pathways. Chronic inflammation may cause tryptophan levels to drop in the brain, leading to reduced production of serotonin, a molecule key to positive mood.
PM2.5 is also known to be directly neurotoxic. Such effects could also be caused secondary to chronic injury to the peripheral parts of the body, reflecting as skull marrow changes that produce sustained brain inflammation. Immune dysregulation is another outcome of hyper-inflammation in women with perinatal PPD.
Pregnant women have higher ventilation rates due to their increased need for oxygen, the relative drop in oxygen-binding capacity, and heavy metabolic demands in the brain. This makes them sitting targets for air pollution and the resulting effects on the central nervous system and the whole body system.
The current study aimed to collate and summarize available evidence for the harmful effect of air pollution on women's mental health in the perinatal period.
The various pollutants of interest included PM10 (particulate matter of 10 microns diameter), carbon monoxide (CO), nitrogen dioxide (NO2), polybrominated diphenyl ethers (PBDEs), per- and polyfluoroalkyl substances (PFAS) and sulfur dioxide (SO2).
What did the study show?
The researchers included nine studies in their review. Most of them focused on tracing a link between air pollution exposure and postpartum depression (PPD) risk.
Short-term risk of PPD at six weeks postpartum was found to be associated with exposure to PM10, CO, and NO2, either in combination or singly, varying between studies. The exposure period was over the first, second, third, or all trimesters.
Second-trimester exposure to NO2/PM2.5, or NO2 over the whole pregnancy, was related to PPD within a year of childbirth. The level of PM2.5 in mid-pregnancy was associated with PPD of increased severity, especially in Black women.
Such associations were reported in two studies, the first with PM2.5 and the second with both PM2.5 and NO2 exposure. A third study found a positive link between PPD risk six months after childbirth and NO2 exposure.
PBDE levels were related in a dose-responsive way to the severity of depression. These substances are ubiquitous, emitted from car interiors, firefighting foams, and textiles. The molecules of interest included BDE-4 and perfluorooctanoate (PFOA), and perfluorooctane sulfonate (PFOS).
The former was linked to increased severity of symptoms at four weeks after delivery, but the latter showed both acute and chronic effects.
Finally, the investigators showed that stress symptoms are associated with specific exposure to PM2.5, and PM10, during pregnancy. Women exposed to stress were less likely to tolerate it well in late pregnancy when subjected to higher levels of PM2.5 and PM10 over the whole pregnancy and ozone in late pregnancy. This effect was more severe in women with less educated.
Also, spring exposures to PM10 were more strongly linked with increased susceptibility to stress, but no link was found with NO2. Perinatal psychotic disorders, including anxiety or bipolar disorder, were not associated with air pollution exposure.
PM10 and sulfur dioxide (SO2) may also be linked to PPD, pending further validation. Contradictory findings were reported regarding ozone, probably because this chemical's concentration and toxic effects vary with the temperature and climatic factors.
What are the implications?
The review included papers with widely varying parameters and different designs. Even so, the analysis showed a small to medium effect regarding increased PPD risk when the woman was exposed to PM2.5 during pregnancy.
Interestingly, PM2.5 exposure also might make women less able to tolerate stress with resilience in late pregnancy.
Both NO2 and PM2.5 exposure is linked to a higher risk of PPD, with the duration of exposure being associated with greater symptom severity, suggesting a dose-dependent association. The effects of other molecules, such as SO2, ozone, PDBEs, and PFAs, require further studies.
Some promising data support the impact of air pollution on mental health of women during the perinatal period."
The long period of follow-up involved in screening for delayed-onset PPD may cause confusion between causal and coincident associations by facilitating the activity of multiple confounding factors in the intervening months before the outcome was assessed.
These could include lactation-associated hormonal fluctuations, maternal stress due to neurodevelopmental anomalies in the offspring linked to air pollution, seasonal factors, geographic variations, and poverty.
Future studies with a rigorous methodology are needed to confirm the preliminary positive associations between air pollution and poor perinatal mental health."
The immune dysregulation observed because of inflammation in women with perinatal PPD and the adverse outcomes associated with mood disorders in pregnancy emphasizes the need for such research to help identify and mitigate or prevent such risk factors.