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Background Common cold is a frequent upper respiratory tract infection, but the role of ambient temperature in the infection is unclear. Objective We investigated the role of prenatal exposure to diurnal temperature variation (DTV), the difference between the daily maximal and minimal temperatures, in the risk of common cold in children. Methods We conducted a cohort study of 2598 preschool children in Changsha, China. Occurrence of common cold during the past year was surveyed using questionnaire. We then estimated each child's prenatal exposure to DTV during pregnancy. Multivariate logistic regression model was used to examine the association between occurrence of common cold and prenatal exposure to DTV in terms of odds ratios (OR) and 95% confidence interval (CI). Results About 45% children have common cold (≥3 times) during the past year. We found that common cold in children was associated with maternal DTV exposure during pregnancy, particularly during the first trimester with adjusted OR (95% CI) = 1.27 (1.10–1.46). Male and atopic children were more susceptible to the effect of DTV during pregnancy. The risk of common cold due to DTV is higher in children living in the suburban areas and the bigger houses and in those exposed to environmental tobacco smoke, mold/dampness, new furniture and redecoration. We observed that the risk of common cold in children has been increased in recent years due to increasing DTV. Conclusions Common cold in children was associated with maternal exposure to temperature variation during pregnancy, suggesting that the risk of common cold may originate in pregnancy. [ABSTRACT FROM AUTHOR]

Numerous epidemiological studies have recently observed that exposure to traffic-related air pollution (TRAP) is associated with increased risk of various respiratory diseases. Major gaps in knowledge remain regarding the toxicological effects. We examined the toxicological effects of the gasoline exhaust particles (GEP), a paradigm of TRAP, in rats, with an objective to provide the evidence, obtain the biomarkers, and suggest effective intervention measure. We measured the airway hyperresponsiveness (AHR), inflammatory cells in the bronchoalveolar lavage (BAL) fluid, histological changes in the lung tissues, and the biomarkers so as to systematically examine the toxicological effects of GEPs at different dose levels (0.5, 2.5, 5 mg/kg BW). The intervention of vitamin E (VE), a natural antioxidant, on the toxicological effects was investigated. The lung injury caused by GEP exposure was first indicated by the airway hyperresponsiveness (AHR). Compared with the control group, GEP exposure significantly increased the airway resistances and decreased the lung compliance; the higher the dose of GEP, the more serious the lung injury. Lung injury was also revealed by the increase of inflammatory cells, including the lymphocytes and neutrophils, in the BAL fluid. With the increase of GEP dose, histological changes in the lung tissues were further observed: inflammatory cell infiltration increased and alveolar wall thickened. The toxicology of GEP was demonstrated by the increase of the biomarkers of the oxidative stress, the pro-inflammatory cytokines and the apoptosis cytokine. However, administration of VE was found to be effective in restoring airway injury. The toxicological effects of traffic-related air pollution (TRAP) on rat lungs are supported by evidence and biomarkers, and vitamin E intervention is feasible. [Display omitted] • Epidemiological studies observed that traffic-related air pollution increases the risk of respiratory diseases. • We examined the toxicological effects of the gasoline exhaust particles (GEP) on rat lungs. • We found the evidence in the airway hyperresponsiveness, the inflammatory cells in the bronchoalveolar lavage fluid, and histological changes in the lung tissues. • We found the biomarkers of the oxidative stress, the pro-inflammatory cytokines and the apoptosis cytokine. • Vitamin E was found to be effective in reducing the toxicological effects. [ABSTRACT FROM AUTHOR]

Abstract Although ambient particulate matter or particles have been found to be associated with morbidity and mortality all over the world, specific health effects of particles from different sources need further elucidation. The objective of this work is to predict the deposition of particles from different sources in the human lung. The whole lung, consisting of 24 generations of branches from trachea to alveoli, was approximated using a one-dimensional lumped "trumpet" model with a variable cross-sectional area. The aerosol dynamics equation was numerically solved using a finite difference method to investigate the transport and deposition of particles in the lung model. Particles from various sources were assumed to be different in both size and density. We found that in general, coarse particles (> 2.5 µm) were mainly deposited in the tracheobronchial (TB) region by impaction, and fine particles (< 2.5 µm) were mainly deposited in the pulmonary (P) region by sedimentation and diffusion. However, the coarse particles with low density can be deposited in P region by sedimentation. As a comparison, our results found that soil particles, which are coarse with low density, were deposited in the deep lung more than traffic particles, which are fine with high density. Modeling of particle deposition in the human lung indicated that coarse particles generated by crustal sources may have adverse health effects as strong as those resulting from fine particles generated from combustion sources. Graphical abstract fx1 Highlights • We examined particle deposition in the human lung using a one-dimensional "trumpet" model. • Particles from various sources differ in both size and density. • Coarse particles with low density can be deposited deep in the lungs as fine particles with high density. • The health effects of soil dust may be strong as those caused by traffic particles. • Health effects of coarse particles cannot be ignored. [ABSTRACT FROM AUTHOR]

The physiologically based pharmacokinetic (PBPK) model is a useful tool to predict the pharmacokinetics of various types of nanoparticles (NPs). The endocytosis mechanism plays a key role in pharmacokinetics of NPs. However, the effect of endocytosis mechanism both in the blood and tissue are seldom considered in PBPK model. To investigate the biodistribution of intravenously injected pegylated AuNPs in mice and human using PBPK model considering the endocytosis mechanism both in the blood and tissue. Taking polyethylene glycol-coated gold nanoparticles (AuNPs) as an example, we developed a PBPK model to explore biodistribution of different size AuNPs. In the model, we considered the role of endocytosis mechanism both in the blood and tissue. In addition, the size-dependent permeability coefficient, excretion rate constant, phagocytic capacity, uptake rate, and release rate were derived from literatures. The mice PBPK model was extrapolated to the human by changing physiology parameters and the number of phagocytic cell (PCs). AuNPs were primarily distributed in the blood, liver, and spleen regardless of particle size, and almost all captured by the PCs in the liver and spleen, while few was captured in the blood. There are more organ distribution and longer circulation for smaller NPs. The 24-h accumulation of AuNPs decreased with increasing size in the most organ, while the accumulation of AuNPs showed an inverted U-shaped curve in the liver and slight U-shaped curve in the blood. The human results of model-predicted displayed a similar tendency with those in mice. Size, partition coefficients, and body weight were the key factors influencing the organ distribution of AuNPs. The size played an important role on the distribution and accumulation of AuNPs in various tissues. Our PBPK model was well predicted the NPs distribution in mice and human. A better understanding of these mechanisms could provide effective guides for nanomedine delivery. • Endocytosis was considered both in the blood and tissue. • The size-dependent phagocytic capacity, uptake rate, and release rate were derived. • The number concentration of AuNPs was adopted in the model. • Accumulation of AuNPs decreased with increasing size in the most organ. [ABSTRACT FROM AUTHOR]