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Tobacco Smoking and Psychotic-Like Experiences in a General Population Sample

J Clin Psychiatry 2018;79(6):17m11994
10.4088/JCP.17m11994

Objective: Recent findings suggest an association between tobacco and psychosis, but whether this association is mediated by confounding factors is unknown. Psychosis-like experiences (PLEs) are a subclinical expression of psychosis. To disentangle the association of tobacco with PLEs, we examined data from a large US population–based, nationally representative sample.

Methods: Analysis was conducted on Wave 2 of the National Epidemiologic Survey of Alcohol and Related Conditions (N = 34,653 adults, conducted from 2004 to 2005). Participants were assessed with the Alcohol Use Disorder and Associated Disabilities Interview Schedule-IV. Twenty-two PLEs previously described as observed indicators of psychosis were used. Participants were stratified according to their smoking status (never/former/current) for 5 different types of tobacco.

Results: There was a significant association (ie, with 95% CIs for which the lower value was ≥ 1) between smoking status and 14 of the 22 assessed PLEs. These associations remained significant after adjustment for sociodemographic variables (including urbanicity or ethnicity), lifetime drug use disorder, and past-year cannabis use. While 26.33% of nonsmokers reported at least 1 PLE, this prevalence was slightly higher in former smokers (27.48%) and rose as high as 39.09% in current smokers (for current smokers vs lifetime abstainers, adjusted OR = 1.33; 95% CI, 1.23–1.45). All 22 PLEs had higher prevalence in smokers than in former smokers or lifetime abstainers. A total of 8.56% of smokers reported at least 5 PLEs, compared to 3.42% in lifetime abstainers (aOR = 1.56; 95% CI, 1.32–1.84).

Conclusions: In a large population-based, nationally representative sample, smoking status was associated with various PLEs. This association was not explained only by other known risk factors of PLEs or schizophrenia. There is a need to identify the potential neurobiological mechanisms by which smoking and PLEs are associated, for patients and from a public health perspective.