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Nonlinear low dose hematotoxicity of benzene; a pooled analyses of two studies among Chinese exposed workers

Vermeulen, Roel; Lan, Qing; Qu, Qingshan; Linet, Martha S; Zhang, Luoping; Li, Guilan; Portengen, Lutzen; Vlaanderen, Jelle; Sungkyoon, Kim; Hayes, Richard B; Yin, Songnian; Smith, Martyn T; Rappaport, Stephen M; Rothman, Nathaniel
BACKGROUND:Impairment of the hematopoietic system is one of the primary adverse health effects from exposure to benzene. We previously have shown that exposure to benzene at low levels (<1 ppm) affects the blood forming system and that these effects were proportionally stronger at lower versus higher levels of benzene exposure. This observation is potentially explained by saturation of enzymatic systems. METHODS:Here we extend these analyses by detailed modeling of the exposure response association of benzene and its major metabolites (i.e. catechol, muconic acid, phenol, and hydroquinone) on peripheral white blood cell (WBC) counts and its major cell-subtypes (i.e. granulocytes, lymphocytes, and monocytes) using two previously published cross-sectional studies among occupationally exposed Chinese workers. RESULTS:Supra-linear exposure response associations were observed between air benzene concentrations (range ∼ 0.1 - 100 ppm) and WBC counts and its cell-subtypes, with a larger than proportional decrease in cell counts at lower than at higher levels of benzene exposure. The hematotoxicity associations were largely similar in shape when the analyses were repeated with benzene urinary metabolites suggesting that enzymatic saturation is not a full explanation of the observed non-linearity with WBC endpoints. DISCUSSION:We hypothesize that the flattening of the exposure response curve especially at higher benzene exposure levels may reflect a response by the bone marrow to maintain hematopoietic homeostasis. Toxicity to the bone marrow and an induced hyper-proliferative response could both contribute to risk of subsequently developing a hematopoietic malignancy. Additional work is needed to explore this hypothesis.
PMID: 37290291
ISSN: 1873-6750
CID: 5533562

A prediction model of delayed graft function in deceased donor for renal transplant: a multi-center study from China

Xue, Wujun; Wang, Changxi; Chen, Jianghua; Sun, Xuyong; Wu, Xiaotong; Peng, Longkai; Chen, Zhishui; Qu, Qingshan; Zhang, Xiaodong; Fu, Yaowen; Dong, Zhen; Chen, Zheng; Feng, Guiwen; Lin, Tao; Men, Tongyi; Yu, Lixin; Sun, Qiquan; Zhao, Yongheng; Zhou, Jiangqiao; Zeng, Li; Zhao, Ming; Tan, Jianming; Ye, Qifa; Shi, Bingyi; Ming, Yingzi; Zhu, Tongyu; Sui, Weiguo; Huang, Chibing; Fu, Yingxin
BACKGROUND/UNASSIGNED:Kidneys obtained from deceased donors increase the incidence of delayed graft function (DGF) after renal transplantation. Here we investigated the influence of the risk factors of donors with DGF, and developed a donor risk scoring system for DGF prediction. METHODS/UNASSIGNED:transplants in 29 centers in China. We quantified DGF associations with donor clinical characteristics. A donor risk scoring system was developed and validated using an independent sample set. RESULTS/UNASSIGNED:The incidence of DGF from donors was 19.0%. Six of the donor characteristics analyzed, i.e., age, cause of death, history of hypertension, terminal serum creatinine, persistence of hypotension, and cardiopulmonary resuscitation (CPR) time were risk factors for DGF. A 49-point scoring system of donor risk was established for DGF prediction and exhibited a superior degree of discrimination. External validation of DGF prediction revealed area under the receiver-operating characteristic (AUC) curves of 0.7552. CONCLUSIONS/UNASSIGNED:Our study determined the deceased donor risk factors related to DGF after renal transplantation pertinent to the Chinese cohort. The scoring system developed here had superior diagnostic significance and consistency and can be used by clinicians to make evidence-based decisions on the quality of kidneys from deceased donors and guide renal transplantation therapy.
PMCID:7971200
PMID: 33719820
ISSN: 1525-6049
CID: 4850992

Association of cardiovascular responses in mice with source-apportioned pm2.5 air pollution in beijing

Maciejczyk, P; Jin, L; Hwang, J-S; Guo, X; Zhong, M; Thurston, G; Qu, Q; Zhang, J; Sun, Q; Chen, L-C
In this study, factor analysis and mass regression were used to identify four fine particulate matter sources and estimate their contributions to the ambient air pollution in Beijing. The identified sources were traffic re-suspended soil, mixed industrial sources, oil combustion, and secondary sulfate. The estimated source contributions were then introduced into two models as exposure variables to explore the relationships between cardiovascular responses in mice and PM exposures. We observed that PM2.5 has a small negative acute effect on heart rate, but the individual source factors showed much more significant effects. Traffic re-suspended soil had the most significant effect on heart rate, with a positive contribution on the day of exposure and a negative one on day lag 1. Acute heart rate variability outcomes were better explained by the total PM2.5 than by the source components. Chronic effects were observed as a decreased heart rate but an increased number of heart rate variability outcomes
SCOPUS:85055034730
ISSN: 1680-8584
CID: 3409402

Improving Knowledge about Children's Environmental Health in Northwest China

Niu, Jingping; Qu, Qingshan; Li, Juansheng; Liu, Xingrong; Zhang, Benzhong; Li, Zhilan; Ding, Guowu; Sun, Yingbiao; Shi, Yanrong; Wan, Yaxiong; Hu, Xiaobin; Chen, Lung-Chi; Mendelsohn, Alan; Chen, Yu; Trasande, Leonardo
The main purpose of this study was to identify policy maker opinions and attitudes towards children's environmental health (CEH), potential barriers to child-specific protective legislation and implementation in northwest China, and evaluate knowledge and attitudes about CEH before and after an educational conference. We conducted seventy-two interviews with regional officials, researchers and non-governmental organization representatives from five provinces, and surveyed participants (forty-seven) before and after an educational conference in northwest China about CEH. Interviews identified general consensus among participants of the adverse effects of air pollution on children, yet few participants knew of policies to protect them. Barriers identified included limited funding and enforcement, weak regional governments and absence of child-specific policy-making. After the conference, substantially greater self-efficacy was identified for lead, mercury, air pollution and polychlorinated biphenyls (+0.57-0.72 on a 1-5 Likert scale, p = 0.002-0.013), and the scientific knowledge for the role of environment in children's health (+0.58, p = 0.015), and health care provider control (+0.52, p = 0.025) were rated more strongly. We conclude that policy makers in Northwest China appreciate that children are uniquely vulnerable, though additional regulations are needed to account for that vulnerability. Further research should examine effectiveness of the intervention on a larger scale and scope, and evaluate the usefulness of such interventions in translating research into improved care/reduced exposure to environmental hazards.
PMCID:4730471
PMID: 26712775
ISSN: 1660-4601
CID: 1894472

Metal rich particulate matter impairs acetylcholine-mediated vasorelaxation of microvessels in mice

Cuevas, Azita K; Niu, Jingping; Zhong, Mianhua; Liberda, Eric N; Ghio, Andrew; Qu, Qingshan; Chen, Lung Chi
BACKGROUND: Exposure to PM2.5 (particulate matter <2.5 mum) has been associated with changes in endothelial function. PM2.5 was collected from two Chinese cities, Jinchang (JC) and Zhangye (ZH), both with similar PM2.5 concentrations. However, JC had levels of nickel (Ni), selenium (Se), copper (Cu), and arsenic (As) that were 76, 25, 17, and 7 fold higher than that measured in ZH, respectively. We used this unique PM sample to delineate the chemical components that drive pulmonary and systemic effects and explore the mechanism(s) by which vascular dysfunction is caused. METHODS: Male FVB/N mice received oropharyngeal aspiration of water or PM2.5 from JC, ZH or ZH spiked with one of the following elements at the same concentrations found in the JC PM (Ni = 4.76; As = 2.36; Se = 0.24; Cu = 2.43 mug/mg) followed by evaluation of markers of pulmonary and systemic inflammation. Mesenteric arteries were isolated for gene expression or functional response to various agonists (Phenylephrine, Acetylcholine, and Sodium Nitroprusside) and inhibitors (L-NAME, Apocynin, and VAS2870) ex vivo. RESULTS: Protein and total cell counts from lung lavage revealed significant pulmonary inflammation from ZH (p < 0.01) and JC and ZH + NiSO4 (p < 0.001) as compared to control and a significant decrease in mesenteric artery relaxation (p < 0.001) and this decrease is blunted in the presence of NADPH oxidase inhibitors. Significant increases in gene expression (TNF-alpha, IL-6, Nos3; p < 0.01; NOX4; p < 0.05) were observed in JC and ZH + NiSO4, as well as significantly higher concentrations of VEGF and IL-10 (p < 0.01, p < 0.001; respectively). CONCLUSIONS: Our results indicate that the specific toxicity observed in PM from JC is likely due to the nickel component in the PM. Further, since VAS2870 was the most successful inhibitor to return vessels to baseline relaxation values, NADPH Oxidase is implicated as the primary source of PM-induced O2 (*-).
PMCID:4456050
PMID: 26041432
ISSN: 1743-8977
CID: 1616592

The acute exposure effects of inhaled nickel nanoparticles on murine endothelial progenitor cells

Liberda, Eric N; Cuevas, Azita K; Qu, Qingshan; Chen, Lung Chi
Abstract Introduction: The discovery of endothelial progenitor cells (EPCs) may help to explain observed cardiovascular effects associated with inhaled nickel nanoparticle exposures, such as increases in vascular inflammation, generation of reactive oxygen species, altered vasomotor tone and potentiated atherosclerosis in murine species. METHODS: Following an acute whole body inhalation exposure to 500 microg/m(3) of nickel nanoparticles for 5 h, bone marrow EPCs from C57BL/6 mice were isolated. EPCs were harvested for their RNA or used in a variety of assays including chemotaxis, tube formation and proliferation. Gene expression was assessed for important receptors involved in EPC mobilization and homing using RT-PCR methods. EPCs, circulating endothelial progenitor cells (CEPCs), circulating endothelial cells (CECs) and endothelial microparticles (EMPs) were quantified on a BD FACSCalibur to examine endothelial damage and repair associated with the exposure. RESULTS AND CONCLUSIONS: Acute exposure to inhaled nickel nanoparticles significantly increased both bone marrow EPCs as well as their levels in circulation (CEPCs). CECs were significantly elevated indicating that endothelial damage occurred due to the exposure. There was no significant difference in EMPs between the two groups. Tube formation and chemotaxis, but not proliferation, of bone marrow EPCs was impaired in the nickel nanoparticle exposed group. These results coincided with a decrease in the mRNA of receptors involved in EPC mobilization and homing. These data provide new insight into how an acute nickel nanoparticle exposure to half of the current Occupational Safety & Health Administration (OSHA) permissible exposure limit may adversely affect EPCs and exacerbate cardiovascular disease states.
PMCID:4212263
PMID: 25144474
ISSN: 0895-8378
CID: 1161512

Regulation of microRNA expression in the lungs by exposure to air pollution & antigen [Meeting Abstract]

Lucas, B; Chen, W -C; Bleck, B; Reibman, J; Rom, W; Narayanan, N; Qu, Q; Park, S -H; Grunig, G
Pulmonary Hypertension is characterized by pulmonary arterial remodeling and increased pressure in the pulmonary circulation. It is often associated with inflammation in the lungs and can lead to right heart failure. Our work shows that urban ambient pollution exacerbates the experimental pulmonary hypertension phenotype just like other types of inflammatory lung conditions. We aimed to identify microRNAs (miRNAs) that are differentially expressed in our mouse model. In addition, we examined plasma samples from individuals occupationally exposed to high levels of air pollution or cigarette smoke, and from controls. Our study is the first to show significantly de-regulated expression of three microRNA species (miR-135a, miR-21, miR-204) in the lungs of mice that were exposed to antigen and particulate matter and developed pulmonary hypertension. De-regulated levels of miR-21 and miR-204 have been reported in human pulmonary hypertension and in experimental pulmonary hypertension. MiR-135a is targeting STAT6 and upregulated expression has been reported in experimental asthma. Using human samples, our study showed that plasma levels of miR-21 and miR-135a, but not levels of miR-204, clustered individuals with high dose exposures and individuals with low dose environmental exposures. Current studies are aimed at identifying the cytokines that control these miRNAs' expression. The long range goal is to identify miRNAs that indicate an at-risk state of the pulmonary vasculature
EMBASE:71472718
ISSN: 0022-1767
CID: 1058342

The Environment and Children's Health Care in Northwest China

Trasande, Leonardo; Niu, Jingping; Li, Juansheng; Liu, Xingrong; Zhang, Benzhong; Li, Zhilan; Ding, Guowu; Sun, Yingbiao; Chen, Meichi; Hu, Xiaobin; Chen, Lung-Chi; Mendelsohn, Alan; Chen, Yu; Qu, Qingshan
BACKGROUND: Industrialization in the northwest provinces of the People's Republic of China is accelerating rapid increases in early life environmental exposures, yet no publications have assessed health care provider capacity to manage common hazards. METHODS: To assess provider attitudes and beliefs regarding the environment in children's health, determine self-efficacy in managing concerns, and identify common approaches to managing patients with significant exposures or environmentally-mediated conditions, a two-page survey was administered to pediatricians, child care specialists, and nurses in five provinces (Gansu, Shaanxi, Xinjiang, Qinghai, and Ningxia). Descriptive and multivariable analyses assessed predictors of strong self-efficacy, beliefs or attitudes. RESULTS: 960 surveys were completed with <5% refusal; 695 (72.3%) were valid for statistical analyses. The role of environment in health was rated highly (mean 4.35 on a 1-5 scale). Self-efficacy reported with managing lead, pesticide, air pollution, mercury, mold and polychlorinated biphenyl exposures were generally modest (2.22-2.52 mean). 95.4% reported patients affected with 11.9% reporting seeing >20 affected patients. Only 12.0% reported specific training in environmental history taking, and 12.0% reported owning a text on children's environmental health. Geographic disparities were most prominent in multivariable analyses, with stronger beliefs in environmental causation yet lower self-efficacy in managing exposures in the northwestern-most province. CONCLUSIONS: Health care providers in Northwest China have strong beliefs regarding the role of environment in children's health, and frequently identify affected children. Few are trained in environmental history taking or rate self-efficacy highly in managing common hazards. Enhancing provider capacity has promise for improving children's health in the region.
PMCID:3986873
PMID: 24670157
ISSN: 1471-2431
CID: 867162

Micro-Rna Regulation By Exposure To Air Pollution And Antigen [Meeting Abstract]

Grunig, G.; Lucas, B.; Kazeros, A.; Reibman, J.; Rom, W. N.; Qu, Q.; Park, S. -H.; Park, S. -H.
ISI:000209838202550
ISSN: 1073-449x
CID: 2960072

Plasma Anti-Glycan Antibody Profiles Associated with Nickel level in Urine

Vuskovic, Marko; Barbuti, Anna-Maria; Goldsmith-Rooney, Emma; Glassman, Laura; Bovin, Nicolai; Pass, Harvey; Tchou-Wong, Kam-Meng; Chen, Meichi; Yan, Bing; Niu, Jingping; Qu, Qingshan; Costa, Max; Huflejt, Margaret
Nickel (Ni) compounds are widely used in industrial and commercial products including household and cooking utensils, jewelry, dental appliances and implants. Occupational exposure to nickel is associated with an increased risk for lung and nasal cancers, is the most common cause of contact dermatitis and has an extensive effect on the immune system. The purpose of this study was two-fold: (i) to evaluate immune response to the occupational exposure to nickel measured by the presence of anti-glycan antibodies (AGA) using a new biomarker-discovery platform based on printed glycan arrays (PGA), and (ii) to evaluate and compile a sequence of bioinformatics and statistical methods which are specifically relevant to PGA-derived information and to identification of putative "Ni toxicity signature". The PGAs are similar to DNA microarrays, but contain deposits of various carbohydrates (glycans) instead of spotted DNAs. The study uses data derived from a set of 89 plasma specimens and their corresponding demographic information. The study population includes three subgroups: subjects directly exposed to Nickel that work in a refinery, subjects environmentally exposed to Nickel that live in a city where the refinery is located and subjects that live in a remote location. The paper describes the following sequence of nine data processing and analysis steps: (1) Analysis of inter-array reproducibility based on benchmark sera; (2) Analysis of intra-array reproducibility; (3) Screening of data - rejecting glycans which result in low intra-class correlation coefficient (ICC), high coefficient of variation and low fluorescent intensity; (4) Analysis of inter-slide bias and choice of data normalization technique; (5) Determination of discriminatory subsamples based on multiple bootstrap tests; (6) Determination of the optimal signature size (cardinality of selected feature set) based on multiple cross-validation tests; (7) Identification of the top discriminatory glycans and their individual performance based on nonparametric univariate feature selection; (8) Determination of multivariate performance of combined glycans; (9) Establishing the statistical significance of multivariate performance of combined glycan signature. The above analysis steps have delivered the following results: inter-array reproducibility rho=0.920 +/- 0.030; intra-array reproducibility rho=0.929 +/- 0.025; 249 out of 380 glycans passed the screening at ICC>80%, glycans in selected signature have ICC >/= 88.7%; optimal signature size (after quantile normalization)=3; individual significance for the signature glycans p=0.00015 to 0.00164, individual AUC values 0.870 to 0.815; observed combined performance for three glycans AUC=0.966, p=0.005, CI=[0.757, 0947]; specifity=94.4%, sensitivity=88.9%; predictive (cross-validated) AUC value 0.836.
PMCID:3984841
PMID: 24737927
ISSN: 0974-276x
CID: 899372