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Air pollution ups psychosis risk in teens

Tristan Manalac
12 Jun 2019
In the first 10 days of May 2017 alone, air pollution reached ‘very high’ and ‘serious’ levels in six out of Hong Kong’s 13 monitoring stations.

Exposure to air pollution appears to raise the odds of experiencing psychosis episodes during adolescence, according to a recent study.

“Associations were not explained by a range of potential individual-, family- and neighbourhood-level confounders. Levels of nitrogen dioxide (NO2) and nitrogen oxides (NOx) statistically explained 60 percent of the association between urban residency and adolescent psychotic experiences,” said researchers.

Linking a population-based cohort of 2,232 children (52.5 percent female) with high-resolution annualized pollution data, researchers assessed exposure to four pollutants: NO2, NOx, and particulate matter with aerodynamic diameters <2.5 µm (PM2.5) and <10 µm (PM10). Urban environments were found to have significantly higher levels of all pollutants, according to unstandardized linear regression analysis. [JAMA Psychiatry 2019;doi:10.1001/jamapsychiatry.2019.0056]

Ordinal logistic regression modelling further revealed a link between pollution exposure and adolescent psychosis. For instance, those in the topmost quartile of NO2 exposure were significantly more likely to develop psychosis than their counterparts in lower quartiles (odds ratio [OR], 1.83, 95 percent CI, 1.42–2.36; p<0.001).

The same was true for exposures to NOx (OR, 1.84, 1.42–2.36; p<0.001), PM2.5 (OR, 1.58, 1.23–2.03; p<0.001) and PM10 (OR, 1.39; 1.08–1.79; p<0.05).

After adjusting simultaneously for all covariates, such as family factors, childhood psychotic symptoms, substance use during adolescence and neighbourhood characteristics, the effects of NO2 (OR, 1.71, 1.28–2.28; p<0.001), NOx (OR, 1.72, 1.30–2.29; p<0.001) and PM2.5 (OR, 1.45, 1.11–1.90; p<0.01) remained significant, but not of PM10 (OR, 1.27, 0.98–1.65).

In sensitivity analysis, while the magnitude and direction of the associations remained, statistical significance was not achieved when clinically verified adolescent psychosis was set as the outcome.

In subsequent mediation modelling, researchers found that both NO2 (OR, 1.25, 1.07–1.45) and NOx (OR, 1.26, 1.08–1.47) each significantly mediated the link between living in an urban setting and adolescent psychotic experiences, explaining 55 percent and 58 percent of the correlation, respectively.

PM2.5, in comparison, explained a smaller proportion of the association between urbanicity and adolescent psychotic symptoms (25 percent; OR, 1.11, 0.99–1.23), as did PM10 (5 percent; OR, 1.02, 0.99–1.06).

Different biological mechanisms may account for the relationship between air pollution exposure and adolescent psychosis, said researchers, noting that “[a]ir pollutants have potent oxidative effects on lipids and proteins.”

Previous studies have found small changes in the brain structure of patients with psychosis, they continued. “Thus, air pollution could increase the risk for psychotic experiences by directly influencing the brain. Such influences are likely to be cumulative.”

“This study demonstrates the feasibility and value of linking high-resolution data on air pollution with rich phenotypic data,” researchers added. “Our findings require replication. Further research is needed in this and other cohorts to explore the association of early-life exposure to air pollution with psychotic symptoms, psychotic disorders, and other psychiatric problems such as depression and anxiety to examine specificity.”

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