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

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

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

Air Pollution Particle Effects on Human Lung Antimycobacterial Immunity

Administered By
Duke Global Health Institute
Awarded By
Rutgers, The State University of New Jersey
Role
Principal Investigator
Start Date
End Date

Publications:

Boiler Briquette Coal versus Raw Coal: Part II-Energy, Greenhouse Gas, and Air Quality Implications.

The objective of this paper is to conduct an integrated analysis of the energy, greenhouse gas, and air quality impacts of a new type of boiler briquette coal (BB-coal) in contrast to those of the raw coal from which the BB-coal was formulated (R-coal). The analysis is based on the source emissions data and other relevant data collected in the present study and employs approaches including the construction of carbon, energy, and sulfur balances. The results show that replacing R-coal with BB-coal as the fuel for boilers such as the one tested would have multiple benefits, including a 37% increase in boiler thermal efficiency, a 25% reduction in fuel demand, a 26% reduction in CO2 emission, a 17% reduction in CO emission, a 63% reduction in SO2 emission, a 97% reduction in fly ash and fly ash carbon emission, a 22% reduction in PM2.5 mass emission, and a 30% reduction in total emission of five toxic hazardous air pollutant (HAP) metals contained in PM10. These benefits can be achieved with no changes in boiler hardware and with a relatively small amount of tradeoffs: a 30% increase in PM10 mass emission and a 9-16% increase in fuel cost.
Authors
Zhang, J; Ge, S; Bai, Z
MLA Citation
Zhang, Junfeng, et al. “Boiler Briquette Coal versus Raw Coal: Part II-Energy, Greenhouse Gas, and Air Quality Implications.Journal of the Air & Waste Management Association (1995), vol. 51, no. 4, Apr. 2001, pp. 534–41. Epmc, doi:10.1080/10473289.2001.10464294.
URI
https://scholars.duke.edu/individual/pub1446681
PMID
28072240
Source
epmc
Published In
Journal of the Air & Waste Management Association (1995)
Volume
51
Published Date
Start Page
534
End Page
541
DOI
10.1080/10473289.2001.10464294

Endogenous melatonin mediation of systemic inflammatory responses to ozone exposure in healthy adults.

BACKGROUND/AIM: Melatonin is a free radical scavenger and an anti-inflammatory biomolecule. Air pollution exposure has been associated with increased inflammatory responses. We hypothesize that endogenous melatonin plays a role in inflammatory responses to air pollution exposure. METHODS: We tested this hypothesis in a cohort of 53 healthy adults (22-52 years old, 16 women), none of whom were on melatonin supplementation. Early morning urine and fasting blood were collected from each participant longitudinally up to three times. We analyzed urinary 6-sulfatoxymelatonin (aMT6s), as a surrogate of circulating melatonin, and pro- and anti-inflammatory cytokines in the plasma samples. Indoor and outdoor air pollutants were measured and combined with participants' time-activity patterns to calculate personal exposure to O3, PM2.5, NO2, and SO2 averaged over 12-hour, 24-hour, 1-week, and 2-week periods prior to biospecimen collection, respectively. Linear mixed-effects models were used to examine the relationships among urinary aMT6s, personal pollutant exposure, and plasma cytokines. A mediation analysis was conducted to examine the role of aMT6s in the relationships between pollutant exposures and inflammatory cytokines. RESULTS: One interquartile range (4.2 ppb) increase in 2-week O3 exposure was associated with a -26.2% (95% CI: -43.9% to -2.8%) decrease in aMT6s. Within the range of endogenous aMT6s concentrations (0.5-53.0 ng/ng creatinine) across the participants, increased aMT6s was associated with decreased pro-inflammatory cytokines including IL-1β, IL-8, IL-17A, IFN-γ, and TNF-α. These cytokines were significantly and positively associated with 2-week average O3 exposure. Furthermore, 7.4% to 17.4% of the O3-cytokine associations were mediated by aMT6s. We did not find similar effects for the other pollutants. CONCLUSIONS: Pro-inflammatory responses to O3 exposure in the preceding 2 weeks partly resulted from the depletion of endogenous melatonin by O3.
Authors
He, L; Hu, X; Gong, J; Day, D; Xiang, J; Mo, J; Zhang, Y; Zhang, J
MLA Citation
He, Linchen, et al. “Endogenous melatonin mediation of systemic inflammatory responses to ozone exposure in healthy adults.Sci Total Environ, vol. 749, Aug. 2020, p. 141301. Pubmed, doi:10.1016/j.scitotenv.2020.141301.
URI
https://scholars.duke.edu/individual/pub1456257
PMID
32829269
Source
pubmed
Published In
The Science of the Total Environment
Volume
749
Published Date
Start Page
141301
DOI
10.1016/j.scitotenv.2020.141301

Health effects of air pollution: what we need to know and to do in the next decade.

Authors
Zhang, JJ; Adcock, IM; Bai, Z; Chung, KF; Duan, X; Fang, Z; Gong, J; Li, F; Miller, RK; Qiu, X; Rich, DQ; Wang, B; Wei, Y; Xu, D; Xue, T; Zhang, Y; Zheng, M; Zhu, T
MLA Citation
Zhang, Junfeng Jim, et al. “Health effects of air pollution: what we need to know and to do in the next decade.Journal of Thoracic Disease, vol. 11, no. 4, Apr. 2019, pp. 1727–30. Epmc, doi:10.21037/jtd.2019.03.65.
URI
https://scholars.duke.edu/individual/pub1385741
PMID
31179119
Source
epmc
Published In
Journal of Thoracic Disease
Volume
11
Published Date
Start Page
1727
End Page
1730
DOI
10.21037/jtd.2019.03.65

Exposure to Silver Nanospheres Leads to Altered Respiratory Mechanics and Delayed Immune Response in an in Vivo Murine Model.

Here we examine the organ level toxicology of both carbon black (CB) and silver nanoparticles (AgNP). We aim to determine metal-specific effects to respiratory function, inflammation and potential interactions with lung lining fluid (LLF). C57Bl6/J male mice were intratracheally instilled with saline (control), low (0.05 μg/g) or high (0.5 μg/g) doses of either AgNP or CB 15 nm nanospheres. Lung histology, cytology, surfactant composition and function, inflammatory gene expression, and pulmonary function were measured at 1, 3, and 7 days post-exposure. Acutely, high dose CB resulted in an inflammatory response, increased neutrophilia and cytokine production, without alteration in surfactant composition or respiratory mechanics. Low dose CB had no effect. Neither low nor high dose AgNPs resulted in an acute inflammatory response, but there was an increase in work of breathing. Three days post-exposure with CB, a persistent neutrophilia was noted. High dose AgNP resulted in an elevated number of macrophages and invasion of lymphocytes. Additionally, AgNP treated mice displayed increased expression of IL1B, IL6, CCL2, and IL10. However, there were no significant changes in respiratory mechanics. At day 7, inflammation had resolved in AgNP-treated mice, but tissue stiffness and resistance were significantly decreased, which was accompanied by an increase in surfactant protein D (SP-D) content. These data demonstrate that the presence of metal alters the response of the lung to nanoparticle exposure. AgNP-surfactant interactions may alter respiratory function and result in a delayed immune response, potentially due to modified airway epithelial cell function.
Authors
Botelho, D; Leo, BF; Massa, C; Sarkar, S; Tetley, T; Chung, KF; Chen, S; Ryan, MP; Porter, A; Atochina-Vasserman, EN; Zhang, J; Schwander, S; Gow, AJ
MLA Citation
Botelho, Danielle, et al. “Exposure to Silver Nanospheres Leads to Altered Respiratory Mechanics and Delayed Immune Response in an in Vivo Murine Model.Frontiers in Pharmacology, vol. 9, Jan. 2018, p. 213. Epmc, doi:10.3389/fphar.2018.00213.
URI
https://scholars.duke.edu/individual/pub1311168
PMID
29632485
Source
epmc
Published In
Frontiers in Pharmacology
Volume
9
Published Date
Start Page
213
DOI
10.3389/fphar.2018.00213

Triggering of Myocardial Infarction by Ambient Fine Particle Concentration, Differences in Response by MI Type and Presence of Chronic Obstructive Pulmonary Disease

Authors
Rich, DQ; Kipen, HM; Zhang, J; Kamat, L; Wilson, A; Kostis, J
MLA Citation
Rich, David Q., et al. “Triggering of Myocardial Infarction by Ambient Fine Particle Concentration, Differences in Response by MI Type and Presence of Chronic Obstructive Pulmonary Disease.” Circulation, vol. 119, no. 10, LIPPINCOTT WILLIAMS & WILKINS, 2009, pp. E365–66.
URI
https://scholars.duke.edu/individual/pub1440476
Source
wos
Published In
Circulation
Volume
119
Published Date
Start Page
E365
End Page
E366