Air Pollution Linked to Psychosis in Urban-Dwelling Teens

Batya Swift Yasgur, MA, LSW

March 29, 2019

Air pollution exposure is associated with a significantly increased risk of adolescent psychosis, new research shows.

Investigators followed over 2000 youngsters from birth through age 18, assessing their exposure to four common air pollutants and interviewing them regarding possible psychotic episodes during adolescence.

Investigators found psychotic experiences were significantly more common among adolescents with the highest exposure to nitrogen dioxide (NO2), nitrogen oxides (NOx), and very small particulate matter (PM2.5), even after adjusting for known risk factors for psychosis.

In particular, NO2 and NOx together accounted for 60% of the association between living in an urban setting and experiencing psychosis during adolescence.

"We found that psychotic experiences were significantly more common among adolescents living in areas with the highest — top quartile — annual exposure to NO2, NOx, and particulate matter with a very small aerodynamic diameter, than those living in areas with lower levels of these pollutants," senior author Helen Fisher, PhD, reader in developmental psychopathology, Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology, and Neuroscience, King's College, London, UK, told Medscape Medical News.

"There are not any conclusive messages for clinicians or larger societal systems at this stage, [since] this is the first study to explore a potential association between air pollution and psychotic experiences, and therefore we need to investigate if these findings are replicated in a large number of other studies before we could draw any firm conclusions about this," she said.

The study was published online March 27 in JAMA Psychiatry.

Seeking Clues

Previous research has suggested that an urban upbringing is associated with a twofold higher risk for psychosis in adulthood, but has mostly examined adverse social features in the urban environment, the authors write.

Air pollution, which is a "key feature of the urban environment" and a "major worldwide health problem, particularly in cities," remains "under-researched."

A "handful of studies" investigating the association between air pollution and adult psychotic disorders have yielded "inconsistent" findings.

Additionally, few studies have used high-resolution measures of air pollution to examine associations with psychosis, and none have focused specifically on adolescent psychotic experiences.

"Adolescents who have psychotic experiences are at higher risk of going on to develop a psychotic disorder in adulthood," Fisher observed.

"Therefore, by improving our understanding of what leads to these lower-level psychotic phenomena occurring in adolescence, we can develop interventions to prevent and treat them early to reduce the incidence of psychotic disorders in adulthood," she said.

She noted that it is a "well-replicated finding that growing up in a city is associated with increased likelihood of developing psychosis — both milder psychotic experiences and clinical-level psychotic disorders."

Her group previously explored whether a variety of social factors could explain this link but found that only around half of the association between urbanicity and adolescent psychotic experiences could be explained by these factors.

They therefore "turned to other aspects of the urban environment for clues as to why psychotic experiences may occur more frequently in these settings" and decided to investigate the potential role of air pollution, which has previously been shown to cause major physical health problems.

Representative Sample

To investigate the question, the researchers used data from the Environmental Risk (E-Risk) Longitudinal Twin study, which tracked the development of a nationally representative cohort of 2232 children born from January 1, 1994 to December 4, 1995 across England and Wales.

Participants were initially interviewed at age 5 years and then followed at ages 7, 10, 12, and 18 years, using a battery of phenotypic and family- and neighborhood-level measures.

Participants were considered to be "representative of UK households across the spectrum of neighborhood socioeconomic conditions."

The study focused on 2063 participants (47.5% male), of whom 71.4% had lived at the same address from age 12 to 18 years.

Symptoms of psychosis were measured using a prodromal psychosis instrument (Prevention Through Risk Identification, Management, Education [PRIME]).

The researchers estimated high-resolution levels of NO2, NOx, and particulate matter with aerodynamic diameters of < 2.5 μm (PM2.5) and < 10 μm (PM10) that were linked to the adolescents' addresses in 2012.

Pollution data for two additional addresses where the adolescents spent their time were also included.

The most common locations were home, school, work, and shops.

Pollution exposure estimates were modeled through the local-scale Community Multiscale Air Quality (CMAQ-urban) modeling system.

The analyses controlled for a wide range of potential confounding covariates, including family socioeconomic status, family psychiatric history, maternal psychosis, childhood psychotic symptoms, adolescent smoking, cannabis and/or alcohol dependence, neighborhood socioeconomic status, neighborhood crime, and neighborhood social conditions.

Neuroinflammation, Noise Levels

Higher mean levels of all four pollutants were estimated in urban versus rural neighborhoods, with mean levels of NOx (40.6 μm) and PM2.5 (12.9 μm) in urban settings that exceeded WHO guidelines (40 μm and 10 μm, respectively).

Moreover, urbanicity was significantly associated with high levels of NO2 (unstandardized β, 8.68; 95% CI, 8.02 - 9.35), NOx (unstandardized β, 13.22; 95% CI, 12.03 - 14.42), PM2.5 (unstandardized β, 1.46; 95% CI, 1.30 - 1.63), and PM10 (unstandardized β, 0.98; 95% CI, 0.78 - 1.18).

Standardized βs (which may be interpreted as correlations and therefore compared across pollutants, the authors note) were 0.64, 0.58, 0.49, and 0.26 for NO2, NOx, PM2.5, and PM10, respectively.

Of the adolescents, 30% experienced psychosis between the ages of 12 and 18 years.

Psychotic experiences were significantly more common among adolescents residing in the most urban versus rural neighborhoods at age 18 years (OR, 1.93; 95% CI, 1.35 - 2.75).

Adolescents exposed to the highest quartile of annual air pollution levels reported higher rates of psychotic experiences compared with those exposed to lower levels of pollution.

In the unadjusted model, the odds ratio (95% CI) of the association between the top quartile of annualized mean levels of air pollutants and adolescent psychotic experiences for NO2, NOx, PM2.5, and PM10 were 1.83 (1.42 - 2.36), 1.84 (1.43 - 2.36), 1.58 (1.23 - 2.03), and 1.39 (1.08 - 1.79), respectively.

Although the associations were "slightly attenuated," they remained significant after adjusting for individual factors as well as all potential confounders simultaneously, although PM10 was no longer significant after these adjustments.

The associations were also not changed when the researchers adjusted for urbanicity or confined their analysis to adolescents who remained at the same address between ages 12-18 years.

Additional sensitivity analyses using different thresholds for pollution variables yielded similar findings.

Potential Mechanisms

NO2 and NOx significantly mediated the association between urbanicity and adolescent psychotic experiences, which remained significant even after considering potential confounders, with each accounting for 55% and 58% of the association, respectively.

When entered together, they statistically explained 60% of the adjusted association between most urban residency and adolescent psychotic experiences.

"This is the first study to link high-resolution estimates of air pollution to a general population sample of adolescents in the UK. These findings could not be explained by other common risk factors," Fisher said.

She speculated on two potential mechanisms for the association between pollution and psychosis.

"Air pollution has been suggested to lead to inflammation in the brain and stunted development that could then result in the emergence of psychotic experiences," she said.

Moreover, since "air pollution is largely due to heavy traffic in urban areas, it is actually the correlated level of noise pollution that may be driving the association because it disrupts sleep and is stressful, and these factors have also been linked to the onset of psychotic experiences," she added.

Fisher also noted that the team was unable to "rule out noise as a major confounder in this study and, as yet, there are no studies that have directly linked air pollution-related neuroinflammation or stunted brain development to psychotic phenomena in the same individuals."

For this reason, "although both mechanisms are plausible, they are just theories at present," she added.

Clean Up Our Cities

Commenting on the study for Medscape Medical News, Brendan Kelly, MD, PhD, professor of psychiatry, Trinity College Dublin, Trinity Centre for Health Sciences, Tallaght University Hospital, Ireland, who was not involved with the study, said the findings "support the idea of a causal link between the two [air pollution and psychotic illness and symptoms] — that pollution may cause, trigger, or worsen psychosis," he said.

He suggested that the authors "are wise to articulate possible biological links, such as neuroinflammation, and possible psychosocial links, such as stress, as responsible for the apparent link between pollution and psychosis," noting that these are not mutually exclusive.

"We know that pollution adversely affects our bodily health, and this paper provides evidence that it can affect mental health also," he noted.

"This makes perfect sense when you think about it, but the authors of this paper have demonstrated this point both powerfully and elegantly, and provide yet another argument for us to clean up our urban environments," he added.

Fisher noted that once there is "a weight of evidence about this correlation, then we would need to explore the mechanisms underlying this association and we could then hopefully utilize this information to develop preventive interventions and target them effectively at the most vulnerable youth."

However, "we're still quite a long way from that at present," she added.

The E-Risk Longitudinal Twin Study is funded by the UK Medical Research Council. The current study was additionally supported the National Institute of Child Health and Human Development; British Academy; Jacobs Foundation; Natural Environment Research Council, UK Medical Research Council, and Chief Scientist Office (pollution data). Additional funding for individual researchers is listed in the original article. Fisher, Kelly, and the authors have disclosed no relevant financial relationships.

JAMA Psychiatry. Published online March 27, 2019. Full text

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