Background Few studies have explored the modifications by family stress and male gender in the relationship between early exposure to traffic-related air pollution (TRAP) and allergic rhinitis (AR) risk in preschool children. Methods We conducted a case-control study of 388 children aged 2–4 years in Shenyang, China. These children AR were diagnosed by clinicians. By using measured concentrations from monitoring stations, we estimated the exposures of particulate matter less than 10 μm in diameter (PM10), nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and sulfur dioxide (SO2) in preschool children aged 2–4 years. After adjusted potential confounding factors, we used logistic regression model to evaluate the odds ratio (OR) and 95% confidence interval (CI) for childhood AR with exposure to different air pollutants according to the increasing of the interquartile range (IQR) in the exposure level. Results The prevalence of AR in children aged 2–4 years (6.4%) was related to early TRAP exposure. With an IQR (20 μg/m3) increase in PM10 levels, an adjusted OR was significantly elevated by 1.70 (95% CI, 1.19 to 2.66). Also, with an IQR (18 μg/m3) increase in NO2, an elevated adjusted OR was 1.85 (95% CI, 1.52 to 3.18). Among children with family stress and boys, PM10 and NO2 were positively related to AR symptoms. No significant association was found among children without family stress and girls. Conclusions Family stress and male gender may increase the risk of AR in preschool children with early exposure to PM10 and NO2.

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The objective of this study was to evaluate the role of apoptosis in the development of the newborn cochlear structures and hearing loss caused by prenatal cis-diaminedichloroplatinum (cisplatin) exposure. Pregnant albino guinea pigs were intraperitoneally injected with 1.5 mg/kg body weight cisplatin once a day for seven consecutive days at gestational day (GD) 51 to GD 57. At postnatal day (PND) 14, pups were examined in the distortion product otoacoustic emission (DPOAE) task. The temporal bones were then removed and immunohistochemically stained for caspase 3, using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method. Cisplatin used during pregnancy could induce hearing loss in newborn and cochlear hair cell apoptosis. In conclusion, apoptosis may play an important role in the development of hearing impairment, caused by perinatal cisplatin exposure.

Maximal number of pre-synaptic ribbons is formed in the cochlear region of middle frequency in mice, coupling with the lowest ABR threshold and highest CAP amplitudes. Our study shows that the middle frequency (8-16 kHz) could be the most sensitive region to sound stimuli in mice.

We evaluated the role of βIII-tubulin in the morphology of olfactory receptor neuron (ORN) and olfactory dysfunction in offspring caused by prenatal and postnatal lanthanum exposure. Pregnant rats were exposed to 0.25% lanthanum chloride in drinking water from gestational day (GD) 7 until postnatal day 21. From postnatal day 23 until postnatal day 28, pups were examined with buried food pellet and olfactory maze test. The ultrastructural features of ORNs in the olfactory epithelium (OE) were observed by transmission electron microscope. The expression of βIII-tubulin and olfactory marker protein (OMP) in the tissue sections and homogenates of OE were, respectively, measured by immunodetection and western blot. Behavioral analysis of olfaction showed that lanthanum chloride exposure induced olfactory dysfunction. Offsprings exposed to lanthanum chloride showed enlarged ORN knobs and a decreased number of cilia. In addition, the levels of OMP and βIII-tubulin expression in lanthanum chloride exposure offsprings significantly decreased. Developmental lanthanum exposure could impair olfaction, and this deficit may be attributed to the downregulation of βIII-tubulin and OMP in the OE.