Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 39
Filter
Add more filters

Country/Region as subject
Affiliation country
Publication year range
1.
Hum Genet ; 134(3): 333-41, 2015 Mar.
Article in English | MEDLINE | ID: mdl-25566987

ABSTRACT

We previously carried out a multi-stage genome-wide association study (GWAS) on lung cancer among never smokers in the Female Lung Cancer Consortium in Asia (FLCCA) (6,609 cases, 7,457 controls) that identified novel susceptibility loci at 10q25.2, 6q22.2, and 6p21.32, and confirmed two previously identified loci at 5p15.33 and 3q28. Household air pollution (HAP) attributed to solid fuel burning for heating and cooking, is the leading cause of the overall disease burden in Southeast Asia, and is known to contain lung carcinogens. To evaluate the gene-HAP interactions associated with lung cancer in loci independent of smoking, we analyzed data from studies participating in FLCCA with fuel use information available (n = 3; 1,731 cases; 1,349 controls). Coal use was associated with a 30% increased risk of lung cancer (OR 1.3, 95% CI 1.0-1.6). Among the five a priori SNPs identified by our GWAS, two showed a significant interaction with coal use (HLA Class II rs2395185, p = 0.02; TP63 rs4488809 (rs4600802), p = 0.04). The risk of lung cancer associated with coal exposure varied with the respective alleles for these two SNPs. Our observations provide evidence that genetic variation in HLA Class II and TP63 may modify the association between HAP and lung cancer risk. The roles played in the cell cycle and inflammation pathways by the proteins encoded by these two genes provide biological plausibility for these interactions; however, additional replication studies are needed in other non-smoking populations.


Subject(s)
Adenocarcinoma/genetics , Air Pollutants/toxicity , Lung Neoplasms/genetics , Adenocarcinoma/chemically induced , Adult , Aged , Air Pollution, Indoor , Case-Control Studies , Female , Gene-Environment Interaction , Genetic Markers , Genetic Predisposition to Disease , Genome-Wide Association Study , Humans , Lung Neoplasms/chemically induced , Middle Aged , Polymorphism, Single Nucleotide , Risk
2.
Allergy Asthma Proc ; 36(4): 59-64, 2015.
Article in English | MEDLINE | ID: mdl-26108072

ABSTRACT

BACKGROUND: Many studies have shown the relationship between serum Club cell secretory protein-16 (CC16) and respiratory diseases. However, little research has been done to study urinary CC16 in relation to respiratory diseases. Our objective was to examine the association of urinary CC16 and physician-diagnosed asthma or lung function measurements in Chinese children. METHODS: A total of 147 physician-diagnosed children with asthma, ages 9-15 years, were recruited from our cross-sectional study population in northeast China. The 390 healthy children who were not asthmatic and not smokers were selected at random from the population according to 10% proportional sampling. Lung function values, including forced expiratory volume in 1 second and forced vital capacity were measured with two portable spirometers. Urine CC16 was determined by using an enzyme-link immunoassay kit. The relationships between urine CC16 levels and asthma, lung function were assessed by multiple regression models. RESULTS: The geometric mean (95% confidence interval [CI]) creatinine-adjusted urine CC16 level was, for creatinine, 9.77 ng/mg (95% CI, 8.12-12.02 ng/mg). After adjustments for sex, age, body mass index, parental education, and smoking status, lower urine CC16 levels were found to be associated with asthma (odds ratio 0.782 [95% CI, 0.617- 0.990]). A positive association was found between urine CC16 and forced vital capacity (beta 0.064 [95% CI, 0.008-0.119]). CONCLUSION: Our study demonstrated lower levels of urine CC16 and lung function in patients with asthma than in those patients without asthma. CC16 in urine may be a useful tool or biomarker for investigating lung epithelium integrity among children with asthma or lung injury.


Subject(s)
Asthma/physiopathology , Asthma/urine , Forced Expiratory Volume , Uteroglobin/urine , Adolescent , Asian People , Asthma/epidemiology , Biomarkers , Case-Control Studies , Child , China , Female , Humans , Male , Respiratory Function Tests , Risk Factors
3.
J Epidemiol ; 23(4): 280-7, 2013.
Article in English | MEDLINE | ID: mdl-23728483

ABSTRACT

BACKGROUND: Concentrations of ambient air pollution and pollutants in China have changed considerably during the last decade. However, few studies have evaluated the effects of current ambient air pollution on the health of kindergarten children. METHODS: We studied 6730 Chinese children (age, 3-7 years) from 50 kindergartens in 7 cities of Northeast China in 2009. Parents or guardians completed questionnaires that asked about the children's histories of respiratory symptoms and risk factors. Three-year concentrations of particles with an aerodynamic diameter ≤10 µm (PM10), sulfur dioxide (SO2), and nitrogen dioxides (NO2) were calculated at monitoring stations in 25 study districts. A 2-stage regression approach was used in data analyses. RESULTS: The prevalence of respiratory symptoms was higher among children living near a busy road, those living near chimneys or a factory, those having a coal-burning device, those living with smokers, and those living in a home that had been recently renovated. Among girls, PM10 was associated with persistent cough (odds ratio [OR]PM10 = 1.44; 95% CI, 1.18-1.77), persistent phlegm (ORPM10 = 1.36; 95% CI, 1.02-1.81), and wheezing (ORPM10 = 1.31; 95% CI, 1.04-1.65). NO2 concentration was associated with increased prevalence of allergic rhinitis (OR = 1.96; 95% CI, 1.27-3.02) among girls. In contrast, associations of respiratory symptoms with concentrations of PM10, SO2, and NO2 were not statistically significant among boys. CONCLUSIONS: Air pollution is particularly important in the development of respiratory morbidity among children. Girls may be more susceptible than boys to air pollution.


Subject(s)
Air Pollutants/adverse effects , Air Pollution, Indoor/adverse effects , Air Pollution/adverse effects , Environmental Exposure/adverse effects , Respiratory Tract Diseases/epidemiology , Air Pollutants/analysis , Child , Child, Preschool , China/epidemiology , Cross-Sectional Studies , Female , Humans , Male , Risk Factors , Sex Distribution , Surveys and Questionnaires
4.
Zhonghua Yu Fang Yi Xue Za Zhi ; 47(1): 49-54, 2013 Jan.
Article in Zh | MEDLINE | ID: mdl-23601523

ABSTRACT

OBJECTIVE: To study the effects of indoor air pollution and individual susceptible factors on prevalence of children's asthma and asthma-related symptoms in Shenyang city. METHODS: On April, 2007, 8733 Han children who were under age of 12 and lived for more than 2 years in Shenyang city, were selected from five administrative areas (one primary school and two kindergartens for each area) through cluster random sampling method. Information on children's general condition, asthma and related symptoms (including stridor, stridor symptoms, persistent cough, persistent phlegm), indoor air pollution, and susceptibility history were obtained by a standard questionnaire from the American Thoracic Society. The effects of indoor air pollution on asthma and asthma-related symptoms was analyzed through χ(2) test. Logistic regression was used to research the effects of risk factors on the prevalence of asthma and asthma-related symptoms of both susceptible and non-susceptible children. RESULTS: Among the 8733 subjects, 4420 (50.6%) were boy and 4313 (49.4%) were girl, with the age of (8.08 ± 2.88) years old. The prevalence of asthma, current asthma, cough, persistent phlegm, stridor and stridor symptom were 6.4% (559 cases), 2.5% (215 cases), 9.6% (836 cases), 4.4% (386 cases), 17.5% (1524 cases) and 2.6% (229 cases) respectively. The prevalence of asthma the boys and girls were among 7.1% (313 cases) and 5.7% (246 cases) (χ(2) = 6.916, P < 0.05); and stridor symptom for them were 19.2% (850 cases), 15.6% (674 cases) (χ(2) = 19.678, P < 0.05), respectively. Passive smoking before two years old, house decoration and pet were related to asthma of children, and there was significant difference between the two groups. The prevalence of asthma of exposed children were 7.7% (312 cases), 9.5% (159 cases), 8.0% (270 cases), 9.0% (114 cases), respectively. Compared with the non-exposed children who had asthma, the prevalence of asthma were 5.7% (400 cases), 5.4% (289 cases), 6.0% (445 cases), the value of χ(2) were 33.646, 23.944 and 16.527 respectively (all P values < 0.05). Children who had family history of asthma, family history of allergy and allergy history were also related with asthma, the prevalence of asthma were 17.3% (106 cases), 13.1% (85 cases), 22.0% (147 cases), compared with the non-exposed children who had asthma, the prevalence of asthma were 5.5% (453), 5.9% (474), 5.1% (412), and there was significant difference between the two groups, the value of χ(2) were 130.522, 59.929 and 293.997, respectively (all P values < 0.05). Logistic regression analysis showed that passive smoking (OR = 1.7, 95%CI: 1.2 - 2.4), house decoration (OR = 1.5, 95%CI: 1.1 - 1.9) and pet (OR = 1.6, 95%CI: 1.1 - 2.3) were statistically significant to asthma in non-susceptible children. While passive smoking (OR = 1.3, 95%CI: 1.0 - 1.7) and house decoration (OR = 1.4, 95%CI: 1.1 - 1.7) were increased the risk of asthma. CONCLUSION: Indoor air pollution is a risk factor of children' s asthma. Family history of asthma and physical susceptible children are high risk to asthma, and susceptible children are easily influenced by other risk factors.


Subject(s)
Air Pollution, Indoor/adverse effects , Asthma/etiology , Air Pollution, Indoor/analysis , Asthma/epidemiology , Child , China/epidemiology , Environment , Female , Humans , Male , Risk Factors
5.
Environ Toxicol ; 27(5): 285-96, 2012 May.
Article in English | MEDLINE | ID: mdl-20737580

ABSTRACT

Previous studies indicate that exposure to perfluorooctanesulfonate (PFOS), a ubiquitous and highly persistent environmental contaminant, induces immunotoxicity in mice. However, few studies have specifically assessed the effects of PFOS on inflammation. This study utilized a standard 60-day oral exposure period to assess the effects of PFOS on the response of inflammatory cytokines [tumor necrosis factor α (TNF-α), interleukin-1 ß (IL-1ß), and interleukin-6 (IL-6)]. Adult male C57BL/6 mice were dosed daily by oral gavage with PFOS at 0, 0.0083, 0.0167, 0.0833, 0.4167, 0.8333 or 2.0833 mg/kg/day to yield a targeted Total Administered Dose (TAD) over 60 days of 0, 0.5, 1, 5, 25, 50, or 125 mg PFOS/kg, respectively. The percentage of peritoneal macrophages (CD11b+ cells) was significantly increased at concentrations ≥ 1 mg PFOS/kg TAD in a dose-dependent manner. Ex vivo IL-1ß production by peritoneal macrophages was elevated substantially at concentrations of ≥ 5 mg PFOS/kg TAD. Moreover, PFOS exposure markedly enhanced the ex vivo production of TNF-α, IL-1ß and IL-6 by peritoneal and splenic macrophages when stimulated either in vitro or in vivo with lipopolysaccharide (LPS). The serum levels of these inflammatory cytokines observed in response to in vivo stimulation with LPS were elevated substantially by exposure to PFOS. PFOS exposure elevated the expression of pro-inflammatory cytokines TNF-α, IL-1ß, IL-6, and proto-oncogene, c-myc, in the spleen. These data suggest that exposure to PFOS modulates the inflammatory response, and further research is needed to determine the mechanism of action.


Subject(s)
Alkanesulfonic Acids/toxicity , Fluorocarbons/toxicity , Animals , Cytokines/blood , Cytokines/metabolism , Dose-Response Relationship, Drug , Inflammation/blood , Inflammation/chemically induced , Inflammation/metabolism , Interleukin-1beta/blood , Interleukin-1beta/metabolism , Interleukin-6/blood , Interleukin-6/metabolism , Macrophages, Peritoneal/drug effects , Male , Mice , Mice, Inbred C57BL , Spleen/drug effects , Spleen/metabolism , Tumor Necrosis Factor-alpha/blood , Tumor Necrosis Factor-alpha/metabolism
6.
Apoptosis ; 16(12): 1195-204, 2011 Dec.
Article in English | MEDLINE | ID: mdl-21910009

ABSTRACT

In vitro and in vivo studies have demonstrated that lung cell apoptosis is associated with lung fibrosis; however the relationship between apoptosis of alveolar macrophages (AMs) and human silicosis has not been addressed. In the present study, AM apoptosis was determined in whole-lung lavage fluid from 48 male silicosis patients, 13 male observers, and 13 male healthy volunteers. The relationships between apoptosis index (AI) and silica exposure history, soluble Fas (sFas)/membrane-bound Fas (mFas), and caspase-3/caspase-8 were analyzed. AI, mFas, and caspase-3 were significantly higher in lung lavage fluids from silicosis patients than those of observers or healthy volunteers, but the level of sFas demonstrated a decreasing trend. AI was related to silica exposure, upregulation of mFas, and activation of caspase-3 and -8, as well as influenced by smoking status after adjusting for confounding factors. These results indicate that AM apoptosis could be used as a potential biomarker for human silicosis, and the Fas/FasL pathway may regulate this process. The present data from human lung lavage samples may help to understand the mechanism of silicosis and in turn lead to strategies for preventing or treating this disease.


Subject(s)
Apoptosis , Fas Ligand Protein/metabolism , Macrophages, Alveolar/cytology , Signal Transduction , Silicosis/metabolism , fas Receptor/metabolism , Adult , Bronchoalveolar Lavage Fluid/chemistry , Case-Control Studies , Caspase 3/genetics , Caspase 3/metabolism , Caspase 8/genetics , Caspase 8/metabolism , Cells, Cultured , Fas Ligand Protein/genetics , Humans , Macrophages, Alveolar/metabolism , Male , Middle Aged , Occupational Exposure/adverse effects , Silicon Dioxide/toxicity , Silicosis/enzymology , Silicosis/genetics , Silicosis/physiopathology , fas Receptor/genetics
7.
Respiration ; 81(3): 179-85, 2011.
Article in English | MEDLINE | ID: mdl-21051869

ABSTRACT

BACKGROUND: Experimental data suggest that asthma exacerbation by allergens is enhanced by exposure to environmental tobacco smoke (ETS); however, there is little supporting epidemiologic evidence. To our knowledge, few studies have assessed respiratory symptoms and allergies in this context. OBJECTIVES: To evaluate whether the association of exposure to animals (indicators of allergen and endotoxin exposure) with asthma-related symptoms is modified by ETS exposure in Chinese children. METHODS: A cross-sectional study of 8,819 children in kindergarten was conducted in 25 districts in northern China. Information on respiratory health and exposure to indoor allergens was obtained using a standard questionnaire from the American Thoracic Society. RESULTS: Among the children with ETS exposure in utero, the effects of exposure to animals were significant with respect to persistent cough [adjusted odds ratio (OR) 1.83; 95% confidence interval (CI) 1.12-2.99] and persistent phlegm (adjusted OR 2.40; 95% CI 1.28-4.54). The combined effect of in utero ETS exposure and animal exposure on doctor-diagnosed asthma was approximately as expected on the basis of their independent effects on an additive scale. There was no interaction between animal exposure and ETS exposure in the first 2 years of life or current ETS exposure. CONCLUSIONS: This study provides evidence that animal and ETS exposure increases the risk of asthma-related symptoms in children in kindergarten. ETS exposure in utero did modify the effect of animal exposure on persistent phlegm and persistent cough but not on doctor-diagnosed asthma among children.


Subject(s)
Allergens/adverse effects , Asthma/etiology , Tobacco Smoke Pollution/adverse effects , Animals , Asthma/epidemiology , Child , Child, Preschool , China/epidemiology , Cough/epidemiology , Cough/etiology , Cross-Sectional Studies , Female , Humans , Male , Pets/immunology , Pregnancy , Respiratory Sounds/etiology , Rhinitis, Allergic, Seasonal/epidemiology , Rhinitis, Allergic, Seasonal/etiology
8.
Int J Environ Health Res ; 21(3): 173-88, 2011 Jun.
Article in English | MEDLINE | ID: mdl-21547813

ABSTRACT

To assess the interaction of environmental tobacco smoke (ETS) exposure and allergic predisposition regarding respiratory health among Chinese children, a sample of 23,474 children (6-13 years old) was studied from 25 districts in Liaoning province, China. The results showed that children without allergic predisposition were more susceptible to ETS than children with allergic predisposition. Among children without allergic predisposition, ETS exposure was associated with more respiratory symptoms and diseases in boys than in girls; In utero ETS exposure was associated with history of asthma (OR, 1.86; 95% CI, 1.44-2.40) and current asthma (OR, 2.25; 95% CI, 1.48-3.44) only among boys without allergic predisposition. Among children with allergic predisposition, more associations between ETS exposure and respiratory symptoms and diseases were detected in girls. In conclusion, ETS exposure was more evident in boys without family atopy history and more associations were detected in girls with family atopy history.


Subject(s)
Disease Susceptibility/ethnology , Environmental Exposure/analysis , Hypersensitivity/etiology , Respiratory Tract Infections/etiology , Sex Characteristics , Tobacco Smoke Pollution/analysis , Adolescent , Asthma/epidemiology , Asthma/etiology , Child , China/epidemiology , Cities/epidemiology , Disease Susceptibility/classification , Disease Susceptibility/epidemiology , Female , Health Surveys , Humans , Hypersensitivity/epidemiology , Male , Respiratory Tract Infections/epidemiology
9.
Chin J Cancer Res ; 23(1): 21-4, 2011 Mar.
Article in English | MEDLINE | ID: mdl-23467677

ABSTRACT

OBJECTIVE: To assess economic cost-effects for the screening programs of gastric cancer in a high risk population in northeastern China. METHODS: The data were collected from November 2001 to December 2003. The multi-stage sampling to define the screening group and the control group was applied in this study. Two stage screening programs were used in the study. An epidemiological survey and serum PG test were carried out in the first stage. The endoscopy and pathological examination were performed in the second stage screening. Effectiveness was assessed by the increased quality adjusted life-year (QALY) because of reduced gastric cancer deaths in screening. RESULTS: A total of 27,970 participants (n=7,128 screening group, n=20,842 control group) were enrolled in the survey. Twenty nine gastric cancer cases were detected in the screening group with 20 cases in the early stage and 9 cases in the advanced stage, respectively. Eighty six gastric cancer cases were detected in the control group, all of whom were in the advanced stage and had died before the study finished. The screening and treatment of 29 cases cost $152,227 and $5,249 per each case, respectively. The costs were $459 to gain per QALY. CONCLUSION: The screening program of gastric cancer used in our study is an economic and society-beneficial measure to detect gastric cancer in high risk area. The methods fit China's present economic development level.

10.
Environ Int ; 147: 105975, 2021 02.
Article in English | MEDLINE | ID: mdl-33385923

ABSTRACT

We previously identified 10 lung adenocarcinoma susceptibility loci in a genome-wide association study (GWAS) conducted in the Female Lung Cancer Consortium in Asia (FLCCA), the largest genomic study of lung cancer among never-smoking women to date. Furthermore, household coal use for cooking and heating has been linked to lung cancer in Asia, especially in Xuanwei, China. We investigated the potential interaction between genetic susceptibility and coal use in FLCCA. We analyzed GWAS-data from Taiwan, Shanghai, and Shenyang (1472 cases; 1497 controls), as well as a separate study conducted in Xuanwei (152 cases; 522 controls) for additional analyses. We summarized genetic susceptibility using a polygenic risk score (PRS), which was the weighted sum of the risk-alleles from the 10 previously identified loci. We estimated associations between a PRS, coal use (ever/never), and lung adenocarcinoma with multivariable logistic regression models, and evaluated potential gene-environment interactions using likelihood ratio tests. There was a strong association between continuous PRS and lung adenocarcinoma among never coal users (Odds Ratio (OR) = 1.69 (95% Confidence Interval (CI) = 1.53, 1.87), p=1 × 10-26). This effect was attenuated among ever coal users (OR = 1.24 (95% CI: 1.03, 1.50), p = 0.02, p-interaction = 6 × 10-3). We observed similar attenuation among coal users from Xuanwei. Our study provides evidence that genetic susceptibility to lung adenocarcinoma among never-smoking Asian women is weaker among coal users. These results suggest that lung cancer pathogenesis may differ, at least partially, depending on exposure to coal combustion products. Notably, these novel findings are among the few instances of sub-multiplicative gene-environment interactions in the cancer literature.


Subject(s)
Adenocarcinoma of Lung , Air Pollution, Indoor , Lung Neoplasms , Adenocarcinoma of Lung/epidemiology , Adenocarcinoma of Lung/genetics , Asia , Case-Control Studies , China/epidemiology , Coal , Female , Genome-Wide Association Study , Humans , Lung Neoplasms/epidemiology , Lung Neoplasms/genetics , Risk Factors , Smoking , Taiwan
11.
Int J Cancer ; 125(12): 2936-44, 2009 Dec 15.
Article in English | MEDLINE | ID: mdl-19521963

ABSTRACT

There has been conflicting evidence concerning the possible association between tuberculosis (TB) and subsequent risk of lung cancer. To investigate whether currently published epidemiological studies can clarify this association, we performed a systematic review of 37 case-control and 4 cohort studies (published between January 1966 and January 2009) and a meta-analysis of risk estimates, with particular attention to the role of smoking, passive smoking and the timing of diagnosis of TB on this relationship. Data for the review show a significantly increased lung cancer risk associated with preexisting TB. Importantly, the association was not due to confounding by the effects of tobacco use (RR=1.8, 95% confidence interval (CI)=1.4-2.2, among never smoking individuals), lifetime environmental tobacco smoke exposure (RR=2.9, 95%CI=1.6-5.3, after controlling) or the timing of diagnosis of TB (the increased lung cancer risk remained 2-fold elevated for more than 20 years after TB diagnosis). Interestingly, the association was significant with adenocarcinoma (RR=1.6, 95%CI=1.2-2.1), but no significant associations with squamous and small cell type of lung cancer were observed. Although no causal mechanism has been demonstrated for such an association, present study supports a direct relation between TB and lung cancer, especially adenocarcinomas.


Subject(s)
Adenocarcinoma/epidemiology , Lung Neoplasms/epidemiology , Tuberculosis, Pulmonary/complications , Humans , Risk Factors
12.
BMC Cancer ; 9: 439, 2009 Dec 15.
Article in English | MEDLINE | ID: mdl-20003463

ABSTRACT

BACKGROUND: Excision repair cross-complementing group 1 (ERCC1) and group 2 (ERCC2), and X-ray repair cross-complementing group 1 (XRCC1) proteins play important roles in the repair of DNA damage and adducts. Single nucleotide polymorphisms (SNPs) of DNA repair genes are suspected to influence treatment effect and survival of cancer patients. This study aimed to investigate the relationship between polymorphisms in ERCC2, ERCC1 and XRCC1 genes and survival of non-smoking female patients with lung adenocarcinoma. METHODS: We used polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method to evaluate SNPs in ERCC2, ERCC1 and XRCC1 genes among 257 patients. RESULTS: The overall median survival time (MST) was 13.07 months. Increasing numbers of either ERCC1 118 or XRCC1 399 variant alleles were associated with shorter survival of non-smoking female lung adenocarcinoma patients (Log-rank P < 0.001). The adjusted hazard ratios (HRs) for individuals with CT or TT genotype at ERCC1 Asn118Asn were 1.48 and 2.67 compared with those with CC genotype. For polymorphism of XRCC1 399, the HRs were 1.28 and 2.68 for GA and AA genotype. When variant alleles across both polymorphisms were combined to analysis, the increasing number of variant alleles was associated with decreasing overall survival. Using the stepwise Cox regression analysis, we found that the polymorphisms in ERCC1 and XRCC1, tumor stage and chemotherapy or radiotherapy status independently predicted overall survival of non-smoking female patients with lung adenocarcinoma. CONCLUSIONS: Genetic polymorphisms in ERCC1 and XRCC1 genes might be prognostic factors in non-smoking female patients with lung adenocarcinoma.


Subject(s)
Adenocarcinoma/genetics , Adenocarcinoma/mortality , DNA Repair/genetics , Lung Neoplasms/genetics , Lung Neoplasms/mortality , Polymorphism, Single Nucleotide , Adenocarcinoma/diagnosis , Adolescent , Adult , Aged , DNA-Binding Proteins/genetics , Endonucleases/genetics , Female , Follow-Up Studies , Genetic Linkage , Genotype , Humans , Lung Neoplasms/diagnosis , Middle Aged , Prognosis , Smoking , Survival Analysis , X-ray Repair Cross Complementing Protein 1 , Young Adult
13.
Arch Toxicol ; 83(7): 679-89, 2009 Jul.
Article in English | MEDLINE | ID: mdl-19015834

ABSTRACT

Perfluorooctanesulfonate (PFOS) is a widespread contaminant in the environment, as well as in wildlife and in humans. Toxicity tests in rodents have raised concerns about potential developmental, reproductive, and systemic effects of PFOS. However, there is little information about the effect of PFOS on immune system. In this study, adult male C57BL/6 mice were given by gavage 0, 5, 20 or 40 mg PFOS/kg day(-1) for 7 days. The results showed that PFOS exposure decreased food intake and body weight and increased liver mass and serum corticosterone levels in a dose-dependent manner. Flow cytometry analysis showed that the number of lymphocytic subpopulation cells decreased significantly in 20 or 40 mg PFOS/kg day(-1) group in comparison with normal C57BL/6 mice. Treatment with PFOS also markedly depressed the natural killer (NK) cell activity, lymphocyte proliferation and the plaque-forming cell (PFC) response. These results indicate that PFOS exposure can affect the immunity function in mice.


Subject(s)
Alkanesulfonic Acids/toxicity , Cell Proliferation/drug effects , Fluorocarbons/toxicity , Immune System/drug effects , Killer Cells, Natural/drug effects , Lymphocytes/drug effects , Administration, Oral , Alkanesulfonic Acids/blood , Animals , Body Weight/drug effects , Corticosterone/blood , Dose-Response Relationship, Drug , Drug Administration Schedule , Eating/drug effects , Fluorocarbons/blood , Liver/drug effects , Male , Mice , Mice, Inbred C57BL , Organ Size/drug effects , Spleen/cytology , Spleen/drug effects , Thymus Gland/cytology , Thymus Gland/drug effects , Viral Plaque Assay/methods
14.
Arch Toxicol ; 83(9): 805-15, 2009 Sep.
Article in English | MEDLINE | ID: mdl-19343326

ABSTRACT

A paucity of data exists to corroborate the few studies that report immune suppression after exposure to perfluorooctanesulfonate (PFOS). In this study, adult male C57BL/6 mice were exposed to PFOS daily via gavage for 60 days [0, 0.5, 5, 25, 50, or 125 mg/kg total administered dose (TAD)]. The results showed that liver mass was significantly increased at > or =5 mg PFOS/kg TAD and in a dose-dependent manner. Lymphocyte proliferation and natural killer cell activity were altered in male mice. Plaque forming cell (PFC) response was suppressed beginning at 5 mg/kg TAD. Based on the liver mass and PFC response, the no observed adverse effect level and lowest observed adverse effect level for male mice exposed PFOS for 60 days was 0.5 and 5 mg/kg TAD, respectively. Measured PFOS serum concentrations at these dose levels were 0.674 +/- 0.166 and 7.132 +/- 1.039 mg/l, respectively. These results indicate that PFOS exposure can affect the immunity function in mice at levels approximately 50-fold for highly exposed human populations.


Subject(s)
Alkanesulfonic Acids/toxicity , Fluorocarbons/toxicity , Immune System/drug effects , Administration, Oral , Alkanesulfonic Acids/blood , Animals , Body Weight/drug effects , Cell Proliferation/drug effects , Cells, Cultured , Dose-Response Relationship, Drug , Drug Administration Schedule , Fluorocarbons/blood , Formazans/metabolism , Hemolytic Plaque Technique , Kidney/drug effects , Killer Cells, Natural/drug effects , Killer Cells, Natural/immunology , Liver/drug effects , Liver/immunology , Lymphocyte Subsets/drug effects , Lymphocytes/drug effects , Lymphocytes/immunology , Male , Mice , Mice, Inbred C57BL , No-Observed-Adverse-Effect Level , Organ Size/drug effects , Organ Size/immunology , Random Allocation , Spleen/cytology , Spleen/drug effects , Spleen/growth & development , Spleen/immunology , Tetrazolium Salts/metabolism , Thymus Gland/cytology , Thymus Gland/drug effects , Time Factors
15.
Lung Cancer ; 62(2): 145-51, 2008 Nov.
Article in English | MEDLINE | ID: mdl-18407370

ABSTRACT

X-ray repair cross-complementing group 1 (XRCC1) is one of the major DNA repair proteins involved in the base excision repair (BER) and single-strand break repair (SSBR) pathway. Single nucleotide polymorphisms (SNPs) in XRCC1 may alter protein function and repair capacity, thus lead to genetic instability and carcinogenesis. To establish our understanding of possible relationships between XRCC1 polymorphisms (5'UTR -77T>C, Arg194Trp, Arg280His and Arg399Gln) and the susceptibility to lung cancer among women nonsmokers, we performed a hospital-based case-control study of 350 patients with newly diagnosed lung cancer and 350 cancer-free controls, frequency matched by age. Our results showed that exposure to cooking oil fume was associated with increased risk of lung cancer in Chinese women nonsmokers [odds ratio (OR)=2.51, 95% confidence interval (CI) [1.80-3.51], P<0.001]. Individuals with homozygous XRCC1 399Gln/Gln genotype (OR=1.75, 95% CI [1.02-3.01]) and XRCC1 -77 combined TC and CC genotype (OR=1.66, 95% CI [1.13-2.42]) showed a slightly higher risk for lung cancer overall. In the subgroup of adenocarcinoma cases, adjusted ORs were increased for individuals with homozygous XRCC1 399Gln/Gln genotype (OR=2.62, 95% CI [1.44-4.79]) and XRCC1 -77 combined TC and CC genotype (OR=1.85, 95% CI [1.19-2.86]). Haplotype analysis showed that T-Trp-Arg-Gln haplotypes were associated with an increased risk of lung cancer among women nonsmokers (OR=2.26, 95% CI [1.38-3.68]), however, we did not observe a statistically significant joint effect of cooking oil fume and 399Gln or -77C variant allele on lung cancer among women nonsmokers. In conclusion, XRCC1 Arg399Gln and T-77C polymorphisms may alter the risk of lung cancer in women nonsmokers in China.


Subject(s)
DNA-Binding Proteins/genetics , Environmental Exposure/adverse effects , Genetic Predisposition to Disease , Lung Neoplasms/genetics , Oils/adverse effects , Asian People/genetics , Case-Control Studies , Cooking/methods , DNA Repair/genetics , Female , Humans , Middle Aged , Polymorphism, Single Nucleotide , Smoking , X-ray Repair Cross Complementing Protein 1
16.
Respiration ; 76(1): 82-91, 2008.
Article in English | MEDLINE | ID: mdl-18337632

ABSTRACT

BACKGROUND: Only few studies have assessed the relative impact of housing characteristics and home environmental factors on asthma and asthma-related symptoms in Chinese children, and to our knowledge, few studies have elaborated respiratory symptoms and allergies in this context. OBJECTIVE: It was the aim of this study to assess the effects of housing characteristics, pet keeping, home decorations and other indoor environmental factors on respiratory health of Chinese children. METHODS: We studied 10,784 children (6-13 years old) from 12 districts in Liaoning province, Northeast China. Information on respiratory health, housing characteristics and environmental pollution was obtained by a standard questionnaire from the American Thoracic Society. RESULTS: Prevalence of asthma-related symptoms was higher for those living along the main stem of traffic, and for those with a house nearby a pollution source. Lower prevalence rates of respiratory morbidity were associated with households with a bigger area of residence and more rooms. Pet keeping was associated with doctor-diagnosed asthma (OR = 1.52; 95% CI 1.25-1.84). Home decorations also increased the risk of doctor-diagnosed asthma (OR = 1.72; 95% CI 1.45-2.04) and current asthma (OR = 1.43; 95% CI 1.06-1.93). Environmental tobacco smoke, pests and visible mold on walls were associated with the occurrence of asthma symptoms. CONCLUSION: Home environmental factors are particularly important for the development of respiratory morbidity among children.


Subject(s)
Residence Characteristics , Respiratory Tract Diseases/epidemiology , Adolescent , Air Pollution, Indoor , Animals , Animals, Domestic , Asthma/epidemiology , Asthma/etiology , Child , China , Environmental Pollution/adverse effects , Female , Housing , Humans , Male , Respiratory Tract Diseases/etiology , Surveys and Questionnaires
17.
J Investig Allergol Clin Immunol ; 18(3): 207-13, 2008.
Article in English | MEDLINE | ID: mdl-18564633

ABSTRACT

BACKGROUND: The relationship between exposure to animals and allergic respiratory diseases in childhood is controversial, and there is little information about how exposure to pets affects the respiratory health of Chinese children, who have lower rates of asthma. OBJECTIVE: To study the association between exposure to pets and doctor-diagnosed asthma and asthma-related symptoms in Chinese children. We also investigated whether genetic propensity as a result of parental atopy modifies these relations. METHODS: A cross-sectional study of 16 789 children was conducted at 24 randomly selected kindergartens and 12 elementary schools in Liaoning province, China. Information on respiratory health and exposure to indoor allergens was obtained by a standard questionnaire from the American Thoracic Society. RESULTS: In children, exposure to animals was associated with a diagnosis of asthma (adjusted odds ratio [OR], 1.49; 95% confidence interval [CI], 1.30-1.70), wheezing (adjusted OR, 1.37; 95% CI, 1.18-1.60), persistent cough (adjusted OR, 1.71; 95% CI, 1.52-1.91), and persistent phlegm (adjusted OR, 2.26; 95% CI, 1.94-2.64). Parental atopy increased the risk of a diagnosis of asthma (adjusted OR, 3.12; 95% CI, 2.61-3.73) and asthma-related symptoms. There was an interaction between parental atopy and pet exposure in persistent cough and persistent phlegm, but not in doctor-diagnosed asthma. CONCLUSIONS: Pet keeping and parental atopy increased the risk of asthma and allergic respiratory diseases in children. Parental atopy modified the effect of pet exposure in persistent cough and persistent phlegm but not in doctor-diagnosed asthma.


Subject(s)
Animals, Domestic , Asthma/epidemiology , Hypersensitivity, Immediate/epidemiology , Parents , Adolescent , Allergens/immunology , Animals , Animals, Domestic/immunology , Asthma/etiology , Child , Child, Preschool , China/epidemiology , Cross-Sectional Studies , Female , Humans , Male , Risk Factors , Surveys and Questionnaires
18.
Rev Epidemiol Sante Publique ; 56(2): 97-107, 2008 Apr.
Article in English | MEDLINE | ID: mdl-18486382

ABSTRACT

BACKGROUND: Very few studies have assessed the relative impact of housing characteristics and home environmental factors on asthma and asthma-related symptoms in Chinese children who have lower rates of asthma. To our knowledge few studies have assessed respiratory symptoms and allergies in this context. METHODS: To assess the effects of housing characteristics, pet keeping, home decorations and other indoor environmental factors on respiratory health of Chinese children. We studied a population of 14,729 children (1-13 years old) from 12 districts in Liaoning province, Northeast China. Information on respiratory health, housing characteristics, and environmental pollutions were obtained by a standard questionnaire from the American Thoracic Society. RESULTS: Housing conditions, house adjacent to traffic or not, house with or without pollution source nearby, pet keeping, presence of pests and mold/water damage in the home, home decorations and exposure to environmental tobacco smoke (ETS) were associated with doctor-diagnosed asthma and asthma-related symptoms both in boys and girls. The vulnerability towards exposure to housing conditions and environmental factors differed between males and females. Among boys, the risk of respiratory morbidity appeared to be reduced in households with larger surface areas and more rooms; use of a ventilation device was strongly protective against persistent phlegm (OR=0.68; 95%CI: 0.48, 0.96). Asthma-related symptoms were more associated with different pets among girls than among boys. The presence of a cat in the household was associated with doctor-diagnosed asthma (OR=1.89; 95% CI, 1.11-3.20), current wheeze (OR=2.64; 95% CI, 1.52-4.59), persistent cough (OR=1.84; 95% CI, 1.18-2.87) and persistent phlegm (OR=2.17; 95% CI, 1.21-3.87) only among girls. CONCLUSION: Living within the vicinity of a source of pollution, traffic, pet keeping, home decorations, pests, mold and ETS are important determinants of children's respiratory health in China.


Subject(s)
Asthma/epidemiology , Environment , Housing , Adolescent , Animals , Animals, Domestic , Child , Child, Preschool , China/epidemiology , Female , Health Surveys , Humans , Infant , Male
19.
Int J Environ Health Res ; 18(4): 267-82, 2008 Aug.
Article in English | MEDLINE | ID: mdl-18668415

ABSTRACT

The objective of the study was to assess the effects of housing characteristics and home environmental factors on respiratory symptoms of Chinese children. A cross-sectional study of 3945 children aged 1-6-years-old was conducted at 24 randomly selected kindergartens in Liaoning province, northeast China during April 2007. Information on respiratory symptoms (persistent cough, persistent phlegm, doctor-diagnosed asthma, current asthma, current wheeze and allergic rhinitis) and exposures to home environmental factors was obtained by a standard questionnaire from the American Thoracic Society. We used Chi-square tests, multivariate logistic regression models and adjusted odds ratios (ORs) with 95% confidence intervals (95% CI) for estimates of the risk of respiratory symptoms. Results suggested that the prevalence of asthma-related symptoms was higher for those who lived along the main stem of traffic, and houses near a pollution source. Lower prevalence rates of respiratory morbidity were associated with households with a larger area of residence and more rooms. Pet keeping was associated with doctor-diagnosed asthma (OR = 1.45; 95% CI, 1.03-2.06). Among boys, home decorations significantly increased the risk of doctor-diagnosed asthma (OR = 1.71; 95% CI, 1.21-2.41), current asthma (OR = 1.80; 95% CI, 1.10-2.94) and current wheeze (OR = 1.81; 95% CI, 1.31-2.50). Environmental tobacco smoke, pests and visible mold on walls were associated with the occurrence of asthma symptoms, especially in boys. Based upon the findings of this study, it is concluded that home environmental factors are particularly important for the development of respiratory morbidity among children. Boys may be more susceptible to home environmental factors than girls.


Subject(s)
Environment , Housing , Respiratory Tract Diseases/epidemiology , Air Pollution, Indoor , Child , Child, Preschool , China/epidemiology , Cross-Sectional Studies , Data Collection , Female , Humans , Infant , Male , Odds Ratio , Risk Factors , Surveys and Questionnaires
20.
Respiration ; 2007 May 02.
Article in English | MEDLINE | ID: mdl-17476094

ABSTRACT

RETRACTION: The paper entitled "Effects of Outdoor and Indoor Air Pollution on Respiratory Health of Children from Kindergarten in Northern China" by Guang-hui Dong et al, which was published online on 02 May 2007, has been withdrawn at the authors' request.

SELECTION OF CITATIONS
SEARCH DETAIL