A growing body of evidence has investigated the association between maternal exposure to PM2.5 (particulate matter with aerodynamic diameter 2.5 μm) during pregnancy and adverse pregnancy outcomes. However, the results of those studies are not consistent. To synthetically quantify the relationship between maternal exposure to PM2.5 during pregnancy and pregnancy outcomes (the change in birth weight, low birth weight (LBW), preterm birth (PTB), small for gestational age (SGA), and stillbirth), a meta-analysis of 25 published observational epidemiological studies that met our selection criteria was conducted. Results suggested a 10 μg/m(3) increase in PM2.5 was positively associated with LBW (odds ratio (OR) = 1.05; 95 % confidence interval (CI), 1.02-1.07), PTB (OR = 1.10; 95 % CI, 1.03-1.18), and SGA (OR = 1.15; 95 % CI, 1.10-1.20) based on entire pregnancy exposure, and pooled estimate of decrease in birth weight was 14.58 g (95 % CI, 9.86-19.31); however, there was no evidence of a statistically significant effect of per 10 μg/m(3) increase in PM2.5 exposure on the risk of stillbirth (OR = 1.18; 95 % CI, 0.69-2.04). With respect to three different gestation periods, no significant risks were found in PTB, stillbirth, and the first trimester on the change of birth weight with a 10 μg/m(3) increase in PM2.5. In this study, a comprehensive quantitative analysis of the results show that PM2.5 can increase the risk of LBW, PTB, and SGA; pregnant women need to take effective measures to reduce PM2.5 exposure.

The objective of this study was to investigate the role of intracellular calcium overload in the in vitro apoptosis of C6 glioma cells mediated by low level ultrasound and hematoporphyrin monomethyl ether (HMME) therapy. The frequency of ultrasound was optimized by the cell viability assay using 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). The apoptotic rate, reactive oxygen species (ROS) and decreased mitochondrial membrane potential (MMP) were determined by flow cytometry. Morphological changes were observed by the transmission electron microscope. Concentrations of intracellular Ca2+, [Ca2+]i were detected by a confocal microscopic laser scanning, and the release of cytochrome-c (cyt-c) was measured by western blotting. Results: The SDT-mediated apoptotic effect involved an overload of [Ca2+]i derived from the intra- and extracellular sources during the early progression of apoptotosis. The process was associated with an increased ROS production, a decreased MMP, and a release of cyt-c. In conclusion,the combined use of low level ultrasound and HMME improved the apoptotic rate of C6 glioma cells mediated by ultrasound alone. The [Ca2+]i overload involving activation of mitochondrial signaling played a pivotal role in the SDT-induced apoptosis.

Epidemiological studies demonstrate a linkage between morbidity and mortality and particulate matter (PM), particularly fine particulate matter (PM2.5) that can readily penetrate into the lungs and are therefore more likely to increase the incidence of respiratory and cardiovascular diseases. The present study investigated the compositions of cooking oil fume (COF)-derived PM2.5, which is the major source of indoor pollution in China. Furthermore, oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest induced by COF-derived PM2.5 in primary fetal alveolar type II epithelial cells (AEC II cells) were also detected. N-acetyl-L-cysteine (NAC), a radical scavenger, was used to identify the role of oxidative stress in the abovementioned processes. Our results suggested that compositions of COF-derived PM2.5 are obviously different to PM2.5 derived from other sources, and COF-derived PM2.5 led to cell death, oxidative stress, apoptosis, and G0/G1 cell arrest in primary fetal AEC II cells. Furthermore, the results also showed that COF-derived PM2.5 induced apoptosis through the endoplasmic reticulum (ER) stress pathway, which is indicated by the increased expression of ER stress-related apoptotic markers, namely GRP78 and caspase-12. Besides, the induction of oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest was reversed by pretreatment with NAC. These findings strongly suggested that COF-derived PM2.5-induced toxicity in primary fetal AEC II cells is mediated by increased oxidative stress, accompanied by ER stress which results in apoptosis.

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