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Background: The growing consensus links exposure to fine particulate matter (PM2.5) with an increased risk of respiratory diseases. However, little is known about the additional effects of particulate matter on brainstem function in allergic rhinitis (AR). Furthermore, it is unknown to what extent the PM2.5-induced effects in the brainstem affect the inflammatory response in AR. This study aimed to determine the effects, mechanisms and consequences of brainstem neural activity altered by allergenic stimulation and PM2.5 exposure. Methods: Using an AR model of ovalbumin (OVA) elicitation and whole-body PM2.5 exposure, the metabolic profile of the brainstem post-allergen stimulation was characterized through in vivo proton magnetic resonance imaging (1H-MRS). Then, the transient receptor potential vanilloid-1 (TRPV1) neuronal expression and sensitivity in the trigeminal nerve in AR were investigated. The link between TRPV1 expression and brainstem differential metabolites was also determined. Finally, we evaluated the mediating effects of brainstem metabolites and the consequences in the brain-spleen axis in the inflammatory response of AR. Results: Exposure to allergens and PM2.5 led to changes in the metabolic profiles of the brainstem, particularly affecting levels of glutamine (Gln) and glutamate (Glu). This exposure also increased the expression and sensitivity of TRPV1+ neurons in the trigeminal nerve, with the levels of TRPV1 expression closely linked to the brainstem metabolism of Glu and Gln. Moreover, allergens increased the activity of p38, while PM2.5 led to the phosphorylation of p38 and ERK, resulting in the upregulation of TRPV1 expression. The brainstem metabolites Glu and Gln were found to partially mediate the impact of TRPV1 on AR inflammation, which was supported by the presence of pro-inflammatory changes in the brain-spleen axis. Conclusion: Brainstem metabolites are altered under allergen stimulation and additional PM2.5 exposure in AR via sensitization of the trigeminal nerve, which exacerbates the inflammatory response via the brain-splenic axis.

BackgroundCooking oil fumes are closely related to immune response, and adipose tissue also plays an important role in immune regulation. At present, the biological effect and mechanism of inflammation of adipose tissue induced by oil fume exposure are not clear yet.ObjectiveTo investigate the inflammatory effect of different exposure duration of cooking fumes on adipose tissue in mice and explore the role of Nod-like receptor pyrin domain 3 (NLRP3)/cysteinyl aspartate specific proteinase 1 (Caspase 1)/interleukin (IL)-1β signaling pathway.MethodsForty 8-week-old female C57BL/6J mice were randomly divided into 3-day control group (CON3 group), 7-day control group (CON7 group), 3-day oil fume exposure group (COF3 group), and 7-day oil fume exposure group (COF7 group), with 10 mice in each group. The mice were exposed to oil fumes in a cooking oil fume formation and exposure equipment (COFFEE) for 20 min, followed by a 10-min pause, 1 h a day for consecutive 3 d or 7 d. General condition of mice was observed and body weight was measured every day. After exposure, blood was sampled from the eyeball. Serum levels of IL-6, IL-27, and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA). The adipose tissue of mice was collected and observed after hematoxylin-eosin (HE) staining. The percentages of CD4+ and CD8+T cells in adipose tissue were detected by flow cytometry. Real-time quantitative PCR (RT-qPCR) was used to detect the expression levels of nuclear factor-κB (NF-κB), NLRP3, Caspase 1, and IL-1β in adipose tissue. Western blot was used to detect the expression levels of NLRP3, Caspase 1, and IL-1β in adipose.ResultsCompared with the corresponding control group, serum IL-6, IL-27, and IL-1β contents in the COF3 group and the COF7 group were significantly increased (P

BackgroundIt is unclear if there is any combined effect of air pollutants and non-optimal temperature on metabolic syndrome, or any molecular mechanisms of related signaling pathways in the process, which requires urgent systematic research. ObjectiveTo observe the effects of combined exposure to PM2.5 and non-optimal temperature on metabolic damage at gene and protein levels in mice, and elucidate the role of related signaling pathway in crucial organs. MethodsA total of 60 six-week-old male C57BL/6J mice were randomly divided into six groups: a normal temperature-filter air group (TN-FA), a normal temperature-concentrated PM2.5 group (TN-PM), a heat-filter air group (TH-FA), a heat-concentrated PM2.5 group (TH-PM), a cold-filter air group (TC-FA), and a cold-concentrated PM2.5 group (TC-PM). The Shanghai Meteorological and Environmental Animal Exposure System (Shanghai-METAS) was used to provide combined exposure settings of air types [concentrated PM2.5 and filter air (FA)] and temperatures [normal (22°C), cold (4°C), and heat (30°C)] for 4 weeks. Skeletal muscle and white adipose tissue (WAT) of the mice were sampled at the end of exposure, and transcriptomics and Western blot (WB) assay were adopted to observe selected gene and protein expression levels in the samples respectively. ResultsThe transcriptomics results indicated that the PM2.5 exposure enhanced the number of differentially expressed genes. Specifically, 4820 genes were differentially expressed in the TN-PM mice compared to the TN-FA mice at normal temperature, and 1143 genes were differentially expressed in the Tc-PM mice compared to the Tc-FA mice in the cold environment. The phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway and the endoplasmic reticulum protein processing pathway were identified as the most significant pathways in metabolic injury resulting from combined exposure to PM2.5 and non-optimal temperature exposure. The WB results showed that exposure to PM2.5 in the normal temperature and the cold environments led to a significant increase in the expression of p-AKT in WAT (P

BackgroundAtmospheric fine particulate matter (PM2.5) can disrupt the metabolic homeostasis of the liver and accelerate the progression of liver diseases, but there are few studies on the effects of sub-chronic PM2.5 exposure on the liver metabolome. ObjectivesTo investigate the effects of sub-chronic exposure to concentrated PM2.5 on hepatic metabolomics in mice by liquid chromatography-mass spectrometry (LC-MS), and to identify potentially affected metabolites and metabolic pathways. MethodsTwelve male C57BL/6J (6 weeks old) mice were randomly divided into two groups: a concentrated PM2.5 exposure group and a clean air exposure group. The mice were exposed to concentrated PM2.5 using the "Shanghai Meteorological and Environmental Animal Exposure System" at Fudan University. The exposure duration was 8 h per day, 6 d per week, for a total of 8 weeks. The mice's liver tissues were collected 24 h after the completion of exposure. LC-MS was performed to assess changes in the hepatic metabolome. Orthogonal partial least squares discriminant analysis and t-test were employed to identify differentially regulated metabolites between the two groups under the conditions of variable important in projection (VIP)≥1.0 and P

Abstract While it is known that air borne ultrafine particulate matter (PM) may pass through the pulmonary circulation of blood at the alveolar level between lung and heart and cross the air-blood barrier, the mechanism and effects are not completely clear. In this study the imaging method fluorescence lifetime imaging microscopy is adopted for visualization with high spatial resolution and quantification of ultrafine PM particles in mouse lung and heart tissues. The results showed that the median numbers of particles in lung of mice exposed to ultrafine particulate matter of diameter less than 2.5 µm was about 2.0 times more than that in the filtered air (FA)-treated mice, and about 1.3 times more in heart of ultrafine PM-treated mice than in FA-treated mice. Interestingly, ultrafine PM particles were more abundant in heart than lung, likely due to how ultrafine PM particles are cleared by phagocytosis and transport via circulation from lungs. Moreover, heart tissues showed inflammation and amyloid deposition. The component analysis of concentrated airborne ultrafine PM particles suggested traffic exhausts and industrial emissions as predominant sources. Our results suggest association of ultrafine PM exposure to chronic lung and heart tissue injuries. The current study supports the contention that industrial air pollution is one of the causative factors for rising levels of chronic pulmonary and cardiac diseases.

The coexistence of temperature changes and air pollution poses a severe global environmental issue, exacerbating health burdens. The aim of this study was to clarify the combined effects of ambient PM2.5 and cold exposure on the development of metabolic disorders. Male C57BL/6 mice were randomly divided into four groups: TN-FA, TN-PM, TC-FA and TC-PM. The mice were then exposed to concentrated PM2.5 or filtered air (FA) under normal (22 °C) or cold (4 °C) environment conditions for 4 weeks. Metabolic-disorder-related indicators, blood pressure, serous lipids, fasting blood glucose and insulin, energy metabolism, mitochondria and protein expression in tissues were detected for comprehensively assessing metabolic disorder. The results showed that, compared to being exposed to PM2.5 only, when mice were exposed to both PM2.5 and the cold (non-optimal), they exhibited more significant metabolic disorders regarding glucose tolerance (p < 0.05), insulin resistance (p < 0.05), lipid metabolism, adipocytes (p < 0.01) and mitochondrial function. This study suggested that a cold environment might substantially exacerbate PM2.5-induced metabolic disorder. The interaction between temperature changes and air pollution implied that implementing the necessary environment-related policies is a critical and complex challenge.

Air pollution causes a great disease burden worldwide. Recent evidences suggested that PM2.5 contributes to intestinal disease. The objective of present study was to investigate the influence of ambient PM2.5 on intestinal tissue and microbiome via whole-body inhalation exposure. The results showed that high levels and prolonged periods exposure to concentrated ambient PM2.5 (CAPM) could destroy the mucous layer of the colon, and significantly alter the mRNA expression of tight junction (Occludin and ZO-1) and inflammation-related (IL-6, IL-10 and IL-1β) genes in the colon, comparing with exposure to the filtered air (FA). The composition of intestinal microbiome at the phylum and genus levels also varied along with the exposure time and PM2.5 levels. At the phylum level, Bacteroidetes was greatly decreased, while Proteobacteria was increased after exposure to CAPM, comparing with exposure to FA. At the genus level, Clostridium XlVa, Akkermansia and Acetatifactor, were significantly elevated exposure to CAPM, comparing with exposure to FA. Our results also indicated that high levels and prolonged periods exposure to CAPM altered metabolic functional pathways. The correlation analysis showed that the intestinal inflammation was related to the alteration of gut microbiome induced by CAPM exposure, which may be a potential mechanism that elucidates PM2.5-induced intestinal diseases. These results extend our knowledge on the toxicology and health effects of ambient PM2.5.

Mice were exposed to ambient PM particles 8 h per day, 6 days per week, for twenty-four weeks in enrichment chambers, with real-time mass concentration of PM2.5 around 70 µg/m3, and the number of PM0.1 about 10,000-20,000/m3. The component analysis of PM particles by inductive coupled plasma emission spectrometer detected low concentrations of species associated with crustal materials, metalloid, transition metals, and heavy metals originating from industrial emission. High-performance liquid chromatography (HPLC) detected 22 polycyclic aromatic hydrocarbons originating from traffic exhausts. We found that PM particles from dirty air entered mouse brain which were visualized by field emission scanning electron microscopy (FE-SEM) and were counted by femtosecond pulsed laser illumination microscopy. FE-SEM of brain tissues from dirty air (n=8), and filtered air (control) (n=8) revealed ultrastructural hallmarks of neuroinflammation, enlarged perivascular space, and the attachment of inflammatory cells to the endothelium of blood vessels in brain. Exposure to dirty air containing ambient PM particles resulted in amyloid deposits and formation of neurofibrillary tangles and plaques. Desorption electrospray ionization mass spectrometry imaging enabled label-free elucidation of the spatial distribution of metabolites and lipids in brain tissue samples without any pretreatment. Ceramide Cer(t18:0/34:0(34OH)), m/z 822.54, and sulfatides, ST18:0, m/z 806.54; ST(d18:1/h22:0), m/z 878.60; ST(24:1), m/z 888.62, and ST(d18:1/h24:0), m/z 906.62 showed upregulation with significant differences in brain tissue from mice exposed to dirty air as compared to filtered air (control). The upregulation of ceramide resulted in formation of neurofibrillary tangles and plaques. Moreover, upregulation of sulfatides might enhance the leakiness of the blood brain barrier by weakening myelin sheaths. Although limited by sample number, our results strongly suggest that prolonged exposure to dirty air contributes to the observed increase in the incidence of cognitive decline and dementia, such as Alzheimer's disease.

Objectives: Traffic-related particulate matter (PM) is one of the major sources of air pollution in metropolitan areas. This study is to observe the interactive effects of gene and fine particles (particles smaller than 2.5 μm – PM2.5) on the respiratory system and explore the mechanisms linking PM2.5 and pulmonary injury. Material and Methods: The participants include 110 traffic policemen and 101 common populations in Shanghai, China. Continuous 24 h individual-level PM2.5 is detected and the pulmonary function, high-sensitivity C-reactive protein (hs-CRP), Clara cell protein 16 (CC16) and the polymorphism in CXCL3, NME7 and C5 genes are determined. The multiple linear regression method is used to analyze the association between PM2.5 and health effects. Meanwhile, the interactive effects of gene and PM2.5 on lung function are analyzed. Results: The individual PM2.5 exposure for traffic policemen was higher than that in the common population whereas the forced expiratory volume in 1 s (FEV1), the ratio of FEV1 to forced vital capacity (FEV1/FVC) and lymphocytes are lower. In contrast, the hs-CRP level is higher. In the adjusted analysis, PM2.5 exposure was associated with the decrease in lymphocytes and the increase in hs-CRP. The allele frequencies for NME7 and C5 have significant differences between FEV1/FVC ≤ 70% and FEV1/FVC > 70% participants. The results didn’t find the interaction effects of gene and PM2.5 on FEV1/FVC in all the 3 genes. Conclusions: The results indicated that traffic exposure to high levels of PM2.5 was associated with systemic inflammatory response and respiratory injury. Traffic policemen represent a high risk group suffering from the respiratory injury.

Although the mechanisms linking cardiopulmonary diseases to ambient fine particles (PM2.5) are still unclear, inflammation and oxidative stress play important roles in PM2.5-induced injury. It is well known that inflammation and oxidative stress could be restricted by vitamin E (Ve) or omega-3 fatty acids (Ω-3 FA) consumption. This study investigated the effects of Ve and Ω-3 FA on PM2.5-induced inflammation and oxidative stress in vascular endothelial cells. The underlying mechanisms linking PM2.5 to vascular endothelial injury were also explored. Human umbilical vein endothelial cells (HUVECs) were treated with 50 μg/mL PM2.5 in the presence or absence of different concentrations of Ve and Ω-3 FA. The inflammatory cytokines and oxidative stress markers were determined. The results showed that Ve induced a significant decrease in PM2.5-induced inflammation and oxidative stress. Malondialdehyde (MDA) in supernatant and reactive oxygen species (ROS) in cytoplasm decreased by Ve, while the superoxide dismutase (SOD) activity elevated. The inflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) also reduced by Ve. Moreover, Ω-3 FA played the same role on decreasing the inflammation and oxidative stress. IL-6 and TNF-α expressions were significantly lower in combined Ve with Ω-3 FA than treatment with Ve or Ω-3 FA alone. The Ve and Ω-3 FA intervention might abolish the PM2.5-induced oxidative stress and inflammation in vascular endothelial cells. There might be an additive effect of these two nutrients in mediating the PM2.5-induced injury in vascular endothelial cells. The results suggested that inflammation and oxidative stress might be parts of the mechanisms linking PM2.5 to vascular endothelial injury.

Objectives: Traffic-related particulate matter (PM) is one of the major sources of air pollution in metropolitan areas. This study is to observe the interactive effects of gene and fine particles (particles smaller than 2.5 μm - PM2.5) on the respiratory system and explore the mechanisms linking PM2.5 and pulmonary injury. Material and Methods: The participants include 110 traffic policemen and 101 common populations in Shanghai, China. Continuous 24 h individual-level PM2.5 is detected and the pulmonary function, high-sensitivity C-reactive protein (hs-CRP), Clara cell protein 16 (CC16) and the polymorphism in CXCL3, NME7 and C5 genes are determined. The multiple linear regression method is used to analyze the association between PM2.5 and health effects. Meanwhile, the interactive effects of gene and PM2.5 on lung function are analyzed. Results: The individual PM2.5 exposure for traffic policemen was higher than that in the common population whereas the forced expiratory volume in 1 s (FEV1), the ratio of FEV1 to forced vital capacity (FEV1/FVC) and lymphocytes are lower. In contrast, the hs-CRP level is higher. In the adjusted analysis, PM2.5 exposure was associated with the decrease in lymphocytes and the increase in hs-CRP. The allele frequencies for NME7 and C5 have significant differences between FEV1/FVC ≤ 70% and FEV1/FVC > 70% participants. The results didn't find the interaction effects of gene and PM2.5 on FEV1/FVC in all the 3 genes. Conclusions: The results indicated that traffic exposure to high levels of PM2.5 was associated with systemic inflammatory response and respiratory injury. Traffic policemen represent a high risk group suffering from the respiratory injury. [ABSTRACT FROM AUTHOR]

This study was conducted to explore the effect of fine particulate matter on Th17 related lung and systematic inflammation in atherosclerotic-susceptible ApoE-/- mice. Eight-weeks old ApoE-/- mice were fed with high-fat diet for 8 weeks to induce the atherosclerosis model. Then the ApoE-/- mice and their littermates C57BL/6 mice were exposed by intratracheal instillation to fine particulate matters with the dose of 0.0 (control), 3.0, 10.0, 30.0 mg/kg b.w. respectively. The exposure was conducted once a day, every other day, for three days. Twenty-four hours after thelast exposure, the mice were sacrificed. Lung lavage was collected to conduct cell differentiate counts. Inflammatory cytokines (IL-6, IL-17, TNF-α) in Bronchoalveolar lavage fluid (BALF) were assessed by Elisa kits. Systematic inflammation characterized by C-reactive protein (CRP) and Th-17 related cytokines IL-6, IL-17A, IL-21 and transforming growth factor-β (TGF-β) were assessed by ELISA kits in the serum of mice. The IL-6, IL-17A, IL-21 and TGF-β mRNA expression and Th17-related transcription factors retinoic acid-related orphan receptor-γt (RORγt) was assessed in thoracic aorta of mice using realtime PCR. The proportion of Th17 and Th1 cells in the spleen of mice was assessed by flow cytometry. The results demonstrated a dose-dependent increase of key inflammatory markers (IL-6, IL-17, TNF-α) in the BALF of ApoE-/- mice. ApoE-/- mice with atherosclerosis received significantly increased secretion of CRP and Th17 related cytokines IL-6, IL-17A and IL-21 and TGF-β levels as compared with age-matched C57BL/6 mice. Meanwhile, the gene expression of Th17 related IL-6, IL-17A and IL-21 and TGF-β and transcription factor RORγt was substantially higher in the arterial wall of ApoE-/- mice than in the arterial wall of their littermates. Importantly, the gene expression of Th17 related cytokines and transcription factor RORγt were up-regulated in the thoracic wall of ApoE-/- mice with a dose-dependent manner. However, the proportion of Th17 cells in the spleen of mice has no significantdifference. These data indicated that acute exposure of fine particulate matter could induce more serious Th17 related lung and systematic inflammation in ApoE-/- mice than in C57BL/6 mice. [ABSTRACT FROM AUTHOR]

Epidemiological studies have found that individuals with diabetes mellitus (DM) display an increased susceptibility for adverse cardiovascular outcomes when exposed to air pollution. This study was conducted to explore the potential mechanism linking ambient fine particles (PM2.5) and heart injury in a Type 2 DM (T2DM) animal model. The KKay mouse, an animal model of T2DM, was exposed to concentrated ambient PM2.5 or filtered air for 8 weeks via a versatile aerosol exposure and concentrator system. Simultaneously, an inhibitor of IκB kinase-2 (IKK-â) (IMD-0354), which is a blocker of nuclear factor κB (NF-κB) nuclear translocation, was administrated by intracerebroventricular injection (ICV) to regulate the NF-êB pathway. The results showed that ambient PM2.5 induced the increase of, NF-êB, cyclooxygenase-2 (COX-2) and mitogen activated protein kinase (MAPK) expression in cardiac tissue, and that IMD-0354 could alleviate the inflammatory injury. The results suggested that the NF-êB pathway plays an important role in mediating the PM2.5-induced cardiovascular injury in the T2DM model. Inhibiting NFκB may be a therapeutic option in air-pollution-exacerbated cardiovascular injury in diabetes mellitus. [ABSTRACT FROM AUTHOR]

Background: Exposure to particulate matter ≤ 2.5 μm in diameter (PM2.5) increases blood pressure (BP) in humans and animal models. Abnormal activation of the sympathetic nervous system may have a role in the acute BP response to PM2.5exposure. The mechanisms responsible for sympathetic nervous system activation and its role in chronic sustenance of hypertension in response to PM2.5 exposure are currently unknown. Objectives: We investigated whether central nervous system inflammation may be implicated in chronic PM2.5 exposure-induced increases in BP and sympathetic nervous system activation. Methods: C57BL/6J mice were exposed to concentrated ambient PM2.5 (CAPs) for 6 months, and we analyzed BP using radioactive telemetric transmitters. We assessed sympathetic tone by measuring low-frequency BP variability (LF-BPV) and urinary norepinephrine excretion. We also tested the effects of acute pharmacologic inhibitors of the sympathetic nervous system and parasympathetic nervous system. Results: Long-term CAPs exposure significantly increased basal BP, paralleled by increases in LF-BPV and urinary norepinephrine excretion. The increased basal BP was attenuated by the centrally acting α2a agonist guanfacine, suggesting a role of increased sympathetic tone in CAPs exposure-induced hypertension. The increase in sympathetic tone was accompanied by an inflammatory response in the arcuate nucleus of the hypothalamus, evidenced by increased expression of pro-inflammatory genes and inhibitor kappaB kinase (IKK)/nuclear factor-kappaB (NF-κB) pathway activation. Conclusion: Long-term CAPs exposure increases BP through sympathetic nervous system activation, which may involve hypothalamic inflammation. [ABSTRACT FROM AUTHOR]

Background Ambient fine-particle particulate matter (PM2.5) exposure is associated with the decline in pulmonary function, prevalence of coronary heart disease and incidence of myocardial infarction. The study is to observe the effects of ambient PM2.5 on the cardiovascular system and to explore the potential inflammatory and immune mechanisms. Methods The subjects included 110 traffic policemen in Shanghai, China, who were aged 25-55 years. Two-times continuous 24 h individual-level PM2.5 measurements were performed in winter and summer, respectively. The inflammatory marker (high-sensitivity C-reactive protein, hs-CRP), immune parameters (IgA, IgG, IgM and IgE) and lymphocyte profiles (CD4 T cells, CD8 T cells, CD4/CD8 T cells) were measured in blood. The associations between individual-level PM2.5 and inflammatory marker and immune parameters were analysed by multiple linear regression. Results The average concentration of 24 h personal PM2.5 for participants was 116.98 μg/m³ and 86.48 μg/m³ in winter and summer, respectively. In the main analysis, PM2.5 exposure is associated with the increases in hs-CRP of 1.1%, IgG of 6.7%, IgM of 11.2% and IgE of 3.3% in participants, and decreases in IgA of 4.7% and CD8 of 0.7%, whereas we found no statistical association in CD4 T cells and CD4/CD8 T cells. In the adjusted model, the results showed that the increase of PM2.5 was associated with the changes of inflammatory markers and immune markers both in winter and summer. Conclusions Traffic policeman have been a high-risk group suffering inflammatory response or immune injury because of the high exposure to PM2.5. These findings provided new insight into the mechanisms linking ambient PM2.5 and inflammatory and immune response. [ABSTRACT FROM AUTHOR]

Background: The prevalence of allergic sensitization has increased all over the world during last years and allergic sensitization may be related to genetic or environmental factors or to both. The objective of this study was to estimate the prevalence rates of allergic sensitization and assess the familial aggregation of allergic sensitization to aeroallergens in asthma index families. Methods: The skin prick test (SPT) reactivity to 8 aeroallergens and the SPT reactivity-related risk factors were evaluated. The allergic sensitization was based on SPT. Univariate and multivariate logistic regressive models were used to estimate the effect size (odds ratio, OR) of correlation within families with positive SPT. Results: Of 4,213 analyzed subjects in 1,006 asthma index families, 40.9% had at least one positive SPT, 42.3% in parents (father: 43.3%; mother: 42.3%), 43.9% in first offspring, and 36.0% in subsequent offspring. The most common allergens were Dermatophagoides pteronyssinus (DP), cockroach and Dermatophagoides farinae (DF). Allergic sensitization status of both parents and first offspring was related to the risk of allergic sensitization for subsequent offspring. The OR for the positive (father)-positive (first offspring) group was 1.92 (p < 0.01), 3.26 (p < 0.01) for the positive (mother)-positive (first offspring) group, and 2.12 (p < 0.01) for the positive (father)-positive (mother) group, which were adjusted for age, sex, body mass index, history of asthma and smoking status. Conclusions: Our findings supported a significant familial aggregation of allergic sensitization in this Chinese population and highlighted the role of genetic factors in allergic sensitization. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]