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

Professor 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:

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
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
Role
Principal Investigator
Start Date
End Date

Prospective Evaluation of Air Pollution, Cognition, and Autism from Birth Onward (PEACABO)

Administered By
Duke Global Health Institute
Awarded By
Johns Hopkins University
Role
Principal Investigator
Start Date
End Date

Publications:

Effects of personal air pollutant exposure on oxidative stress: Potential confounding by natural variation in melatonin levels.

Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA) are commonly used biomarkers of oxidative stress. However, their associations with air pollutant exposure have not been consistent across studies. We hypothesize that the inconsistency is partly due to confounding of circulating melatonin. We analyzed urinary 6-sulfatoxymelatonin (aMT6s), a surrogate of circulating melatonin, along with 8-OHdG and MDA, in 159 healthy adults who had not taken melatonin supplementation. Within the natural range of endogenously-generated aMT6s (0.3-93.5 ng/mg creatinine) measured in this study, increasing aMT6s levels were significantly associated with increasing concentrations of 8-OHdG and MDA. Measurements of PM2.5, ozone (O3), and nitrogen dioxide (NO2), coupled with time-activity data, were used to calculate time-averaged personal exposures 12 -hour (12h) and 24-hour (24h) prior to urine collection. Without controlling for aMT6s, the relationships between pollutant exposure and 8-OHdG or MDA were not clear. After controlling for aMT6s, an interquartile range (IQR) increase in 12h PM2.5 and 12h NO2 exposure was associated with 6.1% [95%CI: 1.6%-10.8%] and 8.6% [1.3%-16.5%] increase in MDA, respectively. An IQR increase in 12h O3 exposure was associated with a 5.7% [1.9%-9.7%] in 8-OHdG. The findings suggest the need for controlling for aMT6s as a confounder in using urinary 8-OHdG and MDA as biomarkers of oxidative stress related to short-term air pollution exposure.
Authors
He, L; Cui, X; Xia, Q; Li, F; Mo, J; Gong, J; Zhang, Y; Zhang, JJ
MLA Citation
He, Linchen, et al. “Effects of personal air pollutant exposure on oxidative stress: Potential confounding by natural variation in melatonin levels..” International Journal of Hygiene and Environmental Health, vol. 223, no. 1, Jan. 2020, pp. 116–23. Epmc, doi:10.1016/j.ijheh.2019.09.012.
URI
https://scholars.duke.edu/individual/pub1415098
PMID
31588015
Source
epmc
Published In
International Journal of Hygiene and Environmental Health
Volume
223
Published Date
Start Page
116
End Page
123
DOI
10.1016/j.ijheh.2019.09.012

Associations of county-level cumulative environmental quality with mortality of chronic obstructive pulmonary disease and mortality of tracheal, bronchus and lung cancers.

Chronic obstructive pulmonary disease (COPD) and tracheal, bronchus, and lung (TBL) cancers are among the leading causes of mortality worldwide. Many environmental factors have been linked to COPD and TBL cancers. This study examined the associations of cumulative environmental quality indices with COPD mortality and TBL cancers mortality, respectively. Environmental Quality Index (EQI) was constructed to represent cumulative environmental quality for the overall environment and 5 major environmental domains (e.g., air, water, built). Associations of each EQI indices with COPD mortality and TBL cancers mortality, across 3109 counties in the 48 contiguous states of the US, were examined using simultaneous autoregressive (SAR) models. Stratified analyses were conducted in females versus males and according to rural-urban continuum codes (RUCC) to assess the heterogeneity across the overall population. Overall poor environmental quality was associated with a percent difference (PD) of 0.75 [95% confidence intervals (95% CI), 0.46, 1.05] in COPD mortality and an PD of 1.22 (95% CI, 0.97, 1.46) in TBL cancers mortality. PDs were higher in females than in males for both COPD and TBL cancers. The built domain had the largest effect on COPD mortality (PD, 0.85; 95% CI, 0.58, 1.12) while the air domain had the largest effect on TBL cancers mortality (PD, 1.54; 95% CI, 1.31, 1.76). The EQI-mortality associations varied among different RUCCs, but no consistent trend was found. This result suggests that poor environmental quality, particularly poor air quality and built environment quality may increase the mortality risk for COPD and that for TBL cancers. Females appear to be more susceptible to the effect of cumulative environmental quality. Our findings highlight the importance of improving overall and domain-specific cumulative environmental quality in reducing COPD and TBL cancer mortalities in the United States.
Authors
Li, X; Xiao, J; Huang, M; Liu, T; Guo, L; Zeng, W; Chen, Q; Zhang, J; Ma, W
MLA Citation
Li, Xing, et al. “Associations of county-level cumulative environmental quality with mortality of chronic obstructive pulmonary disease and mortality of tracheal, bronchus and lung cancers..” The Science of the Total Environment, Nov. 2019. Epmc, doi:10.1016/j.scitotenv.2019.135523.
URI
https://scholars.duke.edu/individual/pub1422575
PMID
31767293
Source
epmc
Published In
The Science of the Total Environment
Published Date
Start Page
135523
DOI
10.1016/j.scitotenv.2019.135523

Effects of ambient ozone concentrations with different averaging times on asthma exacerbations: A meta-analysis.

BACKGROUND:Mounting evidence suggests that short-term exposure to ozone increases the risk of asthma exacerbations. However, ozone exposures have been assessed using ambient ozone concentrations averaged over different time periods in different studies. OBJECTIVE:To evaluate the risks for asthma exacerbations related to ambient ozone measured as 1-hour or 8-hour daily maximum and 24-hour average concentrations. METHODS:Based on a literature search in PubMed, EMBASE and Web of Science, we identified all time-series studies as of December 4th, 2018 and included 47 eligible studies in our analyses. Asthma exacerbation is defined as the risk for emergency room visits or hospital admissions. Pooled relative risks (RRs) and 95% confidence intervals (95%CIs) for a 10 μg/m3 increase in daily ozone concentration were estimated using random effect models. Subgroup analyses and sensitivity analyses were also performed to examine the risks for different seasons, regions and age groups and for the robustness of our main findings. RESULTS:Significant and similar associations were found for O3-1 h max (RR,1.012; 95%CI, 1.005-1.019) and O3-8 h max (RR, 1.011; 95%CI, 1.007-1.014), while marginal effect was identified for O3-24 h average (RR, 1.005; 95%CI, 0.996-1.014). No significant publication bias but high heterogeneities were observed. During the warm season, ozone was significantly associated with asthma exacerbation. O3-1 h max had the highest RR of 1.014 (95%CI, 1.005-1.024), followed by O3-8 h max (RR, 1.012; 95%CI, 1.009-1.016), while marginal association was identified for O3-24 h avg (RR, 1.008; 95%CI, 0.998-1.017). During the cold season, null associations were identified for all the three averaging times. Variations were also observed in region and age. CONCLUSION:Ozone exposure measured as 1-hour or 8-hour daily max were more consistently associated with asthma exacerbations than 24-hour average exposure during the warm season.
Authors
Li, X; Chen, Q; Zheng, X; Li, Y; Han, M; Liu, T; Xiao, J; Guo, L; Zeng, W; Zhang, J; Ma, W
MLA Citation
Li, Xing, et al. “Effects of ambient ozone concentrations with different averaging times on asthma exacerbations: A meta-analysis..” The Science of the Total Environment, vol. 691, Nov. 2019, pp. 549–61. Epmc, doi:10.1016/j.scitotenv.2019.06.382.
URI
https://scholars.duke.edu/individual/pub1397879
PMID
31325855
Source
epmc
Published In
The Science of the Total Environment
Volume
691
Published Date
Start Page
549
End Page
561
DOI
10.1016/j.scitotenv.2019.06.382

Differential Health Effects of Constant versus Intermittent Exposure to Formaldehyde in Mice: Implications for Building Ventilation Strategies.

Formaldehyde, an air pollutant in the indoor environment, may have severe effects on human health. The aim of this study is to compare the health effects caused by intermittent exposure to formaldehyde (based on real monitoring) to those caused by exposures at constant concentration. Health effects explored in this study including the oxidative stress, histopathological changes, inflammatory responses, etc. Mice were divided into three groups and exposed to intermittent concentration formaldehyde (0.8 ppm for 12 h and 0 ppm for another 12 h), or constant concentration formaldehyde (0.4 ppm for 24 h) or zero concentration formaldehyde (reference) per day for 7, 14, and 28 days. Following these exposures, bronchoalveolar lavage fluid (BALF), lung tissue and lung tissue homogenate were prepared to measure biomarkers of oxidative stress (ROS, MDA, GSH), histopathological changes, inflammatory responses (EOS, NEU, LYM, IL-4, IL-5, IL-13, IL-6, IL-17A, NF-κB, IL-1β) and apoptosis (caspase-3). Compared to the constant exposure, intermittent exposure to fluctuating formaldehyde concentrations resulted in more profound increases in numbers of inflammatory cells in the BALF, greater biological alterations including apoptosis. The findings imply that with the same average indoor formaldehyde concentrations over the same time, a ventilation strategy to avoid higher peak concentrations would lead to lower health risks.
Authors
Zhang, X; Zhao, Y; Song, J; Yang, X; Zhang, J; Zhang, Y; Li, R
MLA Citation
Zhang, Xu, et al. “Differential Health Effects of Constant versus Intermittent Exposure to Formaldehyde in Mice: Implications for Building Ventilation Strategies..” Environmental Science & Technology, vol. 52, no. 3, Feb. 2018, pp. 1551–60. Epmc, doi:10.1021/acs.est.7b05015.
URI
https://scholars.duke.edu/individual/pub1300325
PMID
29293324
Source
epmc
Published In
Environmental Science & Technology
Volume
52
Published Date
Start Page
1551
End Page
1560
DOI
10.1021/acs.est.7b05015

Association of air pollution sources and aldehydes with biomarkers of blood coagulation, pulmonary inflammation, and systemic oxidative stress.

Using data collected before, during, and after the 2008 Summer Olympic Games in Beijing, this study examines associations between biomarkers of blood coagulation (vWF, sCD62P and sCD40L), pulmonary inflammation (EBC pH, EBC nitrite, and eNO), and systemic oxidative stress (urinary 8-OHdG) with sources of air pollution identified utilizing principal component analysis and with concentrations of three aldehydes of health concern. Associations between the biomarkers and the air pollution source types and aldehydes were examined using a linear mixed effects model, regressing through seven lag days and controlling for ambient temperature, relative humidity, gender, and day of week for the biomarker measurements. The biomarkers for pulmonary inflammation, particularly EBC pH and eNO, were most consistently associated with vehicle and industrial combustion, oil combustion, and vegetative burning. The biomarkers for blood coagulation, particularly vWF and sCD62p, were most consistently associated with oil combustion. Systemic oxidative stress biomarker (8-OHdG) was most consistently associated with vehicle and industrial combustion. The associations of the biomarkers were generally not significant or consistent with secondary formation of pollutants and with the aldehydes. The findings support policies to control anthropogenic pollution sources rather than natural soil or road dust from a cardio-respiratory health standpoint.
Authors
Altemose, B; Robson, MG; Kipen, HM; Ohman Strickland, P; Meng, Q; Gong, J; Huang, W; Wang, G; Rich, DQ; Zhu, T; Zhang, J
MLA Citation
Altemose, Brent, et al. “Association of air pollution sources and aldehydes with biomarkers of blood coagulation, pulmonary inflammation, and systemic oxidative stress..” Journal of Exposure Science & Environmental Epidemiology, vol. 27, no. 3, May 2017, pp. 244–50. Epmc, doi:10.1038/jes.2016.38.
URI
https://scholars.duke.edu/individual/pub1146955
PMID
27436693
Source
epmc
Published In
Journal of Exposure Science & Environmental Epidemiology
Volume
27
Published Date
Start Page
244
End Page
250
DOI
10.1038/jes.2016.38