Schizophrenia is a devastating neuropsychiatric disorder with increasing concern. Limited studies have been conducted to assess the relationship between short-term exposure to ambient air pollution and schizophrenia attacks. This study aimed to investigate the associations between short-term air pollution exposure and schizophrenia outpatient visits based on a time-series study performed in China. Daily data of schizophrenia outpatient admissions and air pollution from 1 October 2010 to 31 December 2013 were collected in Xi'an, a heavily-polluted city in China. We utilized a time-series Poisson regression model to examine the associations between short-term air pollution and schizophrenia outpatient visits with different lag days. A total of 34,865 outpatient-visits for schizophrenia were identified. A 10 μg/m³ increase of PM₁₀, SO₂, and NO₂ concentrations corresponded to 0.289% (95% Cl: 0.118%, 0.460%), 1.374% (95% Cl: 0.723%, 2.025%), and 1.881% (95% Cl: 0.957%, 2.805%) elevation in outpatient-visits for schizophrenia at lag 0, and the associations appeared to be stronger, although not statistically significantly, in females and in middle and older age adults (40 and over). The most significant associations were observed on the concurrent day in different lag models. In conclusion, short-term exposure to ambient air pollution (PM₁₀, SO₂, and NO₂) can be associated with increased risk of daily outpatient visits for schizophrenia, which may contribute to the further understanding of the potential adverse effects of air pollution in schizophrenia and other neuropsychiatric disorders.

The associations between bisphenol analogues (BPs) exposure and oxidative damage was explored in this 3-year longitudinal study of 275 school children in East China. Nine BPs in first morning urine samples were measured to assess BPs exposure, and 8-hydroxydeoxyguanosine (8-OHdG) and 8-oxo-7,8-dihydroguanosine (8-OHG) were measured as biomarkers of oxidative DNA and RNA damage. Linear mixed model (LMM) was used for repeated measures analysis. School children were mainly exposed to BPA, BPS, BPF, and BPAF (detection frequencies: 97.9%, 42.2%, 13.3%, and 12.8%) with median concentrations of 1.55, 0.355, 0.236 and 0.238 μg g⁻¹Cᵣₑ, respectively. An interquartile range (IQR) increase in urinary BPA was significantly associated with 12.9% (95% CI: 6.1%, 19.6%) increase in 8-OHdG and 19.4% (95% CI: 11.7%, 27.1%) increase in 8-OHG, and for total of BPs (the sum of BPA, BPS, BPF, and BPAF), they were 17.4% (95% CI: 8.9%, 26.0%) for 8-OHdG and 25.9% (95% CI: 16.1%, 35.7%) for 8-OHG, respectively. BPS was positively associated with 8-OHG, but not with 8-OHdG. The study found positive associations of urinary levels of BPA and total BPs with 8-OHdG and 8-OHG and indicated that BPs exposure might cause oxidative RNA damage.

Ambient fine particulate matter (PM2.5) pollution has been implicated in the development of hypertensive disorders of pregnancy. However, evidence on the effects of PM2.5-derived chemical constituents on gestational blood pressure (BP) is limited, and the potential mechanisms underlying the association remain unclear. In this study, we repeated three consecutive 72-h personal air sampling and BP measurements in 215 pregnant women for 590 visits during pregnancy. Individual PM2.5 exposure level was assessed by gravimetric method and 28 PM2.5 chemical constituents were analyzed by ED-XRF method. Plasma biomarkers of endothelial function and inflammation were measured using multiplexed immunoassays. Robust multiple linear regression models were used to estimate the associations among personal PM2.5 exposure and chemical constituents, BP changes (compared with pre-pregnancy BP) and plasma biomarkers. Mediation analyses were performed to evaluate underlying potential pathways. Result showed that exposure to PM2.5 was significantly associated with increases in systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) in the early second trimester. Meanwhile, elevated concentration of lead (Pb) constituent in PM2.5 was significant associated with increases in DBP and MAP after adjusting for PM2.5 total mass. PM2.5 and Pb constituent also presented positive associations with plasma biomarkers of endothelial function (ET-1, E-selectin, ICAM-1) and inflammation (IL-1β, IL-6, TNFα) significantly. After multiple adjustment, elevated ET-1 and IL-6 were significantly correlated with increased gestational BP, and respectively mediated 1.24%–25.06% and 7.01%–10.69% of the increased BP due to PM2.5 and Pb constituent exposure. In conclusion, our results suggested that personal exposure to PM2.5 and Pb constituent were significantly associated with increased BP during pregnancy, and the early second trimester might be the sensitive window of PM2.5 exposure. The endothelial dysfunction and elevated inflammation partially mediated the effect of PM2.5 and Pb constituent on BP during pregnancy.