Junfeng Zhang

Overview:

Dr. Zhang joined the Duke Faculty in fall 2013 from the University of Southern California where he had been a professor of environmental and global health and the director of Environmental and Biomarkers Analysis Laboratory since 2010. His prior positions include professor, department chair, and associate dean at the Rutgers School of Public Health. Dr. Zhang has more than 140 peer-reviewed publications. His work has been featured in major international media such as the Time, the New York Times, BBC, ABC, CBS, Yahoo News, etc. His early work on characterizing sources of non-methane greenhouse gases made him one of the officially recognized contributor to the 2007 Nobel Peace Prize awarded to IPCC. He is the 2012 recipient of the Jeremy Wesolowski Award, the highest award of the International Society of Exposure Science. He also received a Distinguished Alumni Award from the Rutgers Graduate School.

Dr. Zhang’s research interests include developing novel biomarkers of human exposure and health effects, assessing health and climate co-benefits of air pollution interventions, and examining biological mechanisms by which environmental exposures exert adverse health effects. Dr. Zhang has led a number of international collaborations to study air pollution health effects and underlying pathophysiologic mechanisms. He is currently leading two multidisciplinary, multi-institutional centers studying the health impact of engineered nanomaterials.

Positions:

Professor of Global and Environmental Health

Environmental Sciences and Policy
Nicholas School of the Environment

Research Professor of Global Health

Duke Global Health Institute
Institutes and Provost's Academic Units

Professor of Global and Environmental Health at Duke Kunshan University

DKU Faculty
Duke Kunshan University

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

Ph.D. 1994

Rutgers University

Grants:

Cooperative Program in Nanomaterials Hazard and Exposure Assessment Traineeships (NanoHEAT)

Administered By
Pratt School of Engineering
Awarded By
Environmental Protection Agency
Role
Mentor
Start Date
End Date

Duke University Program in Environmental Health

Administered By
Environmental Sciences and Policy
Awarded By
National Institute of Environmental Health Sciences
Role
Mentor
Start Date
End Date

Effects of perfluorobutane sulfonate (PFBS) exposure on adverse pregnancy outcomes and fetal development

Administered By
Obstetrics and Gynecology, Reproductive Sciences
Awarded By
National Institutes of Health
Role
Mentor
Start Date
End Date

The effect of household air pollution on the health outcomes of infants in Botswana

Administered By
Medicine, Pulmonary, Allergy, and Critical Care Medicine
Awarded By
Thrasher Research Fund
Role
Co-Mentor
Start Date
End Date

Measurement of urinary 8-isoprostane and 11-dehydrothromboxane

Administered By
Duke Global Health Institute
Awarded By
University of California - San Francisco
Role
Principal Investigator
Start Date
End Date

Publications:

Inhibition of TRPA1 reduces airway inflammation and hyperresponsiveness in mice with allergic rhinitis.

This study was conducted to investigate whether a transient receptor potential ankyrin 1 (TRPA1) antagonist (HC-030031) can reduce airway inflammation and hyperresponsiveness in a murine allergic rhinitis (AR) model. BALB/c mice were sensitized and challenged by ovalbumin (OVA) to induce AR. HC-030031 or vehicle was administrated to mice via intraperitoneal injection prior to OVA challenges. Nose-scratching events, histopathologic alterations of the airways, and bronchial hyperresponsiveness (BHR) were assessed. Differential cells and proinflammatory cytokines in the nasal lavage (NAL) and bronchoalveolar lavage (BAL) fluid were measured. Expressions of TRPA1 in nasal mucosa were examined by immunohistochemistry. TRPA1-expressing vagal neurons were labeled by immunofluorescent staining. HC-030031-treated AR mice had markedly reduced type-2 inflammation in nasal mucosa and ameliorated-nose-scratching events than AR mice received vehicle. HC-030031 treatment also dramatically reduced leucocyte numbers and IL-8 level in the BAL fluid, inhibited lower airway remodeling and fibrosis, and nearly abolished BHR. HC-0300031 treatment significantly inhibited the upregulated number of TRPA1 expressing nasal epithelial cells and TRPA1 expressing sensory neurons, leading to downregulation of SP in both upper and lower airways. Targeting TRPA1 may represent a promising strategy for treating AR and AR-related asthma.
Authors
Fang, Z; Yi, F; Peng, Y; Zhang, JJ; Zhang, L; Deng, Z; Chen, F; Li, C; He, Y; Huang, C; Zhang, Q; Lai, K; Xie, J
MLA Citation
Fang, Zhangfu, et al. “Inhibition of TRPA1 reduces airway inflammation and hyperresponsiveness in mice with allergic rhinitis.Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, vol. 35, no. 5, May 2021, p. e21428. Epmc, doi:10.1096/fj.201902627r.
URI
https://scholars.duke.edu/individual/pub1477414
PMID
33774861
Source
epmc
Published In
Faseb Journal
Volume
35
Published Date
Start Page
e21428
DOI
10.1096/fj.201902627r

Metabolomic Changes after Subacute Exposure to Polycyclic Aromatic Hydrocarbons: A Natural Experiment among Healthy Travelers from Los Angeles to Beijing.

Emerging epidemiological evidence has associated exposure to polycyclic aromatic hydrocarbons (PAHs) with chronic diseases including cardiometabolic diseases and neurodegeneration. However, little information is available about their subacute effects, which may accumulate over years and contribute to chronic disease development. To fill this knowledge gap, we designed a natural experiment among 26 healthy young adults who were exposed to elevated PAHs for 10 weeks after traveling from Los Angeles to Beijing in 2014 and 2015. Serum was collected before, during, and after the trip for metabolomics analysis. We identified 50 metabolites that significantly changed 6-8 weeks after the travel to Beijing (FDR < 5%). The network analysis revealed two main independent modules. Module 1 was allocated to oxidative homeostasis-related response and module 2 to delayed enzymatic deinduction response. Remarkably, the module 1 metabolites were recovered 4-7 weeks after participants' return, while the module 2 metabolites were not. Urinary hydroxylated PAHs were significantly associated with metabolites from both modules, while PAH carboxylic acids, likely metabolites of alkylated PAHs, were only associated with antioxidation-related metabolites. These results suggested differential subacute effects of unsubstituted and alkylated PAHs. Further studies are warranted to elucidate the role of the reversibility of metabolite changes in adverse health effects of PAHs.
Authors
Lu, X; Lin, Y; Qiu, X; Liu, J; Zhu, T; Araujo, JA; Zhang, J; Zhu, Y
MLA Citation
Lu, Xinchen, et al. “Metabolomic Changes after Subacute Exposure to Polycyclic Aromatic Hydrocarbons: A Natural Experiment among Healthy Travelers from Los Angeles to Beijing.Environmental Science & Technology, vol. 55, no. 8, Apr. 2021, pp. 5097–105. Epmc, doi:10.1021/acs.est.0c07627.
URI
https://scholars.duke.edu/individual/pub1475831
PMID
33683876
Source
epmc
Published In
Environmental Science & Technology
Volume
55
Published Date
Start Page
5097
End Page
5105
DOI
10.1021/acs.est.0c07627

Prevalence of respiratory diseases in relation to smoking rate in adults living in four Chinese cities: a comparison between 2017-2018 and 1993-1996.

<h4>Background</h4>The sustained high prevalence of smoking in China has contributed substantially to the burden of chronic diseases, including respiratory diseases. This study compared the prevalence of smoking and respiratory diseases in Chinese adults between two time periods spanning over 25 years.<h4>Methods</h4>Cross-sectional surveys were performed in four Chinese cities of Chongqing, Lanzhou, Wuhan, and Guangzhou in 1993-1996 (Period 1) and in 2017-2018 (Period 2). Participants completed questionnaires asking smoking status, the presence of asthma and chronic bronchitis, education attainment and household characteristics. Logistic regression models were used to estimate the odds ratios of disease prevalence with regard to active smoking status for men and passive smoking status for women.<h4>Results</h4>Prevalence of asthma, prevalence of chronic bronchitis, and smoking rate, all decreased from Period 1 to Period 2. We observed strong evidence that active smoking increased prevalence for both asthma and chronic bronchitis in men during Period 1, with spatial heterogeneity and modifying effect by college-level education. Home exposure to passive smoking was associated with increased odds of having chronic bronchitis among female participants in Chongqing during Period 2, although the association was not statistically significant.<h4>Conclusions</h4>The prevalence for asthma and chronic bronchitis were lower in 2017-2018 compared to 25 years ago in the same four Chinese cities. Decreased smoking rate may have contribution to the improvement of these respiratory diseases. Male smokers, especially those without college-level education, showed higher prevalence of chronic bronchitis compared to nonsmokers during Period 1.
Authors
Yan, M; Gong, J; Liu, Q; Li, W; Duan, X; Cao, S; Li, S; He, L; Yin, Z; Lin, W; Zhang, JJ
MLA Citation
Yan, Meilin, et al. “Prevalence of respiratory diseases in relation to smoking rate in adults living in four Chinese cities: a comparison between 2017-2018 and 1993-1996.Journal of Thoracic Disease, vol. 12, no. 10, Oct. 2020, pp. 6315–26. Epmc, doi:10.21037/jtd-19-crh-aq-002.
URI
https://scholars.duke.edu/individual/pub1465310
PMID
33209471
Source
epmc
Published In
Journal of Thoracic Disease
Volume
12
Published Date
Start Page
6315
End Page
6326
DOI
10.21037/jtd-19-crh-aq-002

Respiratory health effects of residential individual and cumulative risk factors in children living in two cities of the Pearl River Delta Region, China.

<h4>Background</h4>Indoor environment is complex, with many factors potentially interacting with each other to affect health. However, previous studies have usually focused on effect of a single factor. Assessment of the combined effects of multiple factors can help with understanding the overall health risk.<h4>Methods</h4>A cross-sectional study was conducted among 2,306 school children in Guangzhou and Shenzhen. Questionnaire data on respiratory symptoms and diseases were collected along with sociodemographic and residential environmental information. A subset of children (N=987) were measured for their lung function. A random forest algorithm was applied to screen the top-ranked indoor environmental exposure variables and to form a composite index for cumulative risk of indoor pollution (CRIP). Logistic regressions were conducted to analyze the independent effect of single indoor environmental risk factors and the combined effect of CRIP on children's respiratory health. Multiple linear regressions were used to examine the independent and combined effects of indoor environmental exposure on lung function.<h4>Results</h4>We found that home dampness and molds as well as environmental tobacco smoke (ETS) were significantly and independently associated with increased prevalence of children's respiratory symptoms and diseases and with reduced lung function. A higher CRIP level was significantly associated with increased risk of cough with cold (OR =1.37, 95% CI: 1.05-1.79) and wheeze (OR =2.71, 95% CI: 1.16-6.34). A higher CRIP level was also associated with reduced lung function measured as FVC, FEV<sub>1</sub>, PEF, FEF<sub>25%</sub>, FEF<sub>25-75%</sub> and VC.<h4>Conclusions</h4>In children living in the subtropical region of the Pearl River Delta, home dampness and the presence of mold as well as ETS were individual risk factors for children's respiratory health. The composite CRIP index was associated with respiratory symptoms and lung function, suggesting the utility of this index for predicting the combined effects of multiple risk factors.
Authors
Lin, J; Lin, W; Yin, Z; Fu, X; Mai, D; Fu, S; Zhang, JJ; Gong, J; Feng, N; He, L
MLA Citation
Lin, Jianqing, et al. “Respiratory health effects of residential individual and cumulative risk factors in children living in two cities of the Pearl River Delta Region, China.Journal of Thoracic Disease, vol. 12, no. 10, Oct. 2020, pp. 6342–55. Epmc, doi:10.21037/jtd.2020.03.92.
URI
https://scholars.duke.edu/individual/pub1465311
PMID
33209473
Source
epmc
Published In
Journal of Thoracic Disease
Volume
12
Published Date
Start Page
6342
End Page
6355
DOI
10.21037/jtd.2020.03.92

Nitrated Polycyclic Aromatic Hydrocarbons and Arachidonic Acid Metabolisms Relevant to Cardiovascular Pathophysiology: Findings from a Panel Study in Healthy Adults.

Concerns on nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) in the environment have mainly arisen from their mutagenic and carcinogenic effects. The objective of this study is to investigate whether nitro-PAH exposures are associated with biomarkers of cardiovascular pathophysiology. In a panel study design, urines and blood samples were collected up to four times with a 2-week interval from 89 healthy adults. We measured 1-naphthylamine, 2-naphthylamine, 9-aminophenanthrene, 2-aminofluorene, and 1-aminopyrene as biomarkers of nitro-PAH exposures. We measured three urinary metabolites of arachidonic acid (AA) including 20-hydroxyeicosatetraenoic acid (20-HETE) from the cytochrome P450 (CYP) pathway, 8-isoprostane from the nonenzymatic pathway, and 11-dehydro-thromboxane B2 (11-dhTXB<sub>2</sub>) from the cyclooxygenase (COX) pathway. Urinary malondialdehyde, 8-hydroxy-2'-deoxyguanosine (8-OHdG), and 6-sulfatoxymelatonin (aMT6s) were measured to reflect systemic oxidative stress. Plasma concentrations of the soluble P-selectin and von Willebrand factor (vWF) were measured as biomarkers of platelet activation and endothelial dysfunction. We found that increased urinary concentrations of amino-PAHs were significantly associated with increased 20-HETE, 11-dhTXB<sub>2</sub>, and 8-OHdG and with decreased 8-isoprostane and aMT6s. Increased amino-PAHs were positively associated with P-selectin and vWF, respectively. These results suggest that exposure to nitro-PAHs increases systemic oxidative stress and alters AA metabolism toward CYP and COX pathways, leading to an increased cardiovascular disease risk.
Authors
He, L; Lin, Y; Day, D; Teng, Y; Wang, X; Liu, XL; Yan, E; Gong, J; Qin, J; Wang, X; Xiang, J; Mo, J; Zhang, Y; Zhang, JJ
MLA Citation
He, Linchen, et al. “Nitrated Polycyclic Aromatic Hydrocarbons and Arachidonic Acid Metabolisms Relevant to Cardiovascular Pathophysiology: Findings from a Panel Study in Healthy Adults.Environmental Science & Technology, vol. 55, no. 6, Mar. 2021, pp. 3867–75. Epmc, doi:10.1021/acs.est.0c08150.
URI
https://scholars.duke.edu/individual/pub1474673
PMID
33621071
Source
epmc
Published In
Environmental Science & Technology
Volume
55
Published Date
Start Page
3867
End Page
3875
DOI
10.1021/acs.est.0c08150