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

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:

Changes in children's lung function over two decades in relation to socioeconomic, parental and household factors in Wuhan, China.

<h4>Background</h4>It is important to identify risk and beneficial factors for children's lung function. This study aims to ascertain potential changes in children's lung function in relation to changes in socioeconomic, parental and household factors, based on a comparison between two periods spanning 25 years in Wuhan, the largest metropolis in central China.<h4>Methods</h4>In two cross-sectional studies, lung function measurements and questionnaire surveys were conducted on school-age children in 1993-1996 (Period I) and in 2018 (Period II). Children of 6-12 years old from elementary schools were selected by a multistage sampling method. Demographic information, socioeconomic status, feeding methods, parental illness and behavior patterns, as well as household characteristics, were collected through a questionnaire survey. Spirometric lung function was measured, including forced vital capacity (FVC), forced expiratory volume in the first second (FEV<sub>1</sub>), forced expiratory flow at 25% and 75% of the pulmonary volume (FEF25-75), and peak expiratory flow (PEF). Wilcoxon analysis of variances was used to assess the differences in lung function indexes between Period I and Period II. Multiple linear regression models were used to estimate the association of lung function with regard to socioeconomic, parental and household factors, respectively.<h4>Results</h4>Significant prevalence reductions were observed for household coal use, paternal smoking and maternal asthma, while the prevalence increased significantly for children sleeping in their own rooms or own beds and breastfeeding, ventilation use during cooking, and parental education level from Period I to Period II. When adjusted for age, height, weight, sex and other factors assessed in the study, children had significant lower values of FVC, FEV<sub>1</sub>, and PEF in Period II than in Period I. Enclosed kitchen was significantly associated with lower lung function in children in Period I. Urban living condition and higher maternal education level were each associated with a higher FVC, while father having no fixed income was associated with a lower FVC and a lower FEV<sub>1</sub>, respectively, in Period II. In comparison with Period I, the beneficial impact of urban living and that of breastfeeding were enhanced and the detrimental effect of poor household condition was weakened in Period II.<h4>Conclusions</h4>Lung function was lower in 2018 than in 1993-1996 in school-age children living in Wuhan. Although improvements in urban living and household environmental conditions as well as increased breastfeeding in Period II could have contributed to increased lung function, other unmeasured risk factors may have played a more dominant role in leading to a net decrease in lung function from Period I to Period II. Future studies are needed to identify these risk factors.
Authors
Cao, S; Wen, D; Li, S; Guo, Q; Duan, X; Gong, J; Xu, X; Meng, X; Qin, N; Wang, B; Zhang, JJ
MLA Citation
Cao, Suzhen, et al. “Changes in children's lung function over two decades in relation to socioeconomic, parental and household factors in Wuhan, China.Journal of Thoracic Disease, vol. 13, no. 7, July 2021, pp. 4601–13. Epmc, doi:10.21037/jtd-21-158.
URI
https://scholars.duke.edu/individual/pub1493475
PMID
34422385
Source
epmc
Published In
Journal of Thoracic Disease
Volume
13
Published Date
Start Page
4601
End Page
4613
DOI
10.21037/jtd-21-158

Population ageing and deaths attributable to ambient PM<sub>2·5</sub> pollution: a global analysis of economic cost.

<h4>Background</h4>The health impacts of ambient air pollution impose large costs on society. Although all people are exposed to air pollution, the older population (ie, those aged ≥60 years) tends to be disproportionally affected. As a result, there is growing concern about the health impacts of air pollution as many countries undergo rapid population ageing. We investigated the spatial and temporal variation in the economic cost of deaths attributable to ambient air pollution and its interaction with population ageing from 2000 to 2016 at global and regional levels.<h4>Methods</h4>In this global analysis, we developed an age-adjusted measure of the value of a statistical life-year (VSLY) to estimate the economic cost of deaths attributable to ambient PM<sub>2·5</sub> pollution using Global Burden of Diseases, Injuries, and Risk Factors Study 2017 data and country-level socioeconomic information. First, we estimated the global age-specific and cause-specific mortality and years of life lost (YLLs) attributable to PM<sub>2·5</sub> pollution using the global exposure mortality model and global estimates of exposure at 0·1° × 0·1° (about 11 km × 11 km at the equator) resolution. Second, for each year between 2000 and 2016, we translated the YLLs within each age group into a health-related cost using a country-specific, age-adjusted measure of VSLY. Third, we decomposed the major driving factors that contributed to the temporal change in health costs related to PM<sub>2·5</sub>. Finally, we did a sensitivity test to analyse the variability of the estimated health costs to four alternative valuation measures. We identified the uncertainty intervals (UIs) from 1000 draws of the parameters and concentration-response functions by age, cause, country, and year. All economic values are reported in 2011 purchasing power parity-adjusted US dollars. All simulations were done with R, version 3.6.0.<h4>Findings</h4>Globally, in 2016, PM<sub>2·5</sub> was estimated to have caused 8·42 million (95% UI 6·50-10·52) attributable deaths, which was associated with 163·68 million (116·03-219·44) YLLs. In 2016, the global economic cost of deaths attributable to ambient PM<sub>2·5</sub> pollution for the older population was US$2·40 trillion (1·89-2·93) accounting for 59% (59-60) of the cost for the total population ($4·09 trillion [3·19-5·05]). The economic cost per capita for the older population was $2739 (2160-3345) in 2016, which was 10 times that of the younger population (ie, those aged <60 years). By assessing the factors that contributed to economic costs, we found that increases in these factors changed the total economic cost by 77% for gross domestic product (GDP) per capita, 21% for population ageing, 16% for population growth, -41% for age-specific mortality, and -0·4% for PM<sub>2·5</sub> exposure.<h4>Interpretation</h4>The economic cost of ambient PM<sub>2·5</sub> borne by the older population almost doubled between 2000 and 2016, driven primarily by GDP growth, population ageing, and population growth. Compared with younger people, air pollution leads to disproportionately higher health costs among older people, even after accounting for their relatively shorter life expectancy and increased disability. As the world's population is ageing, the disproportionate health cost attributable to ambient PM<sub>2·5</sub> pollution potentially widens the health inequities for older people. Countries with severe air pollution and rapid ageing rates need to take immediate actions to improve air quality. In addition, strategies aimed at enhancing health-care services, especially targeting the older population, could be beneficial for reducing the health costs of ambient air pollution.<h4>Funding</h4>National Natural Science Foundation of China, China Postdoctoral Science Foundation, and Qiushi Foundation.
Authors
Yin, H; Brauer, M; Zhang, JJ; Cai, W; Navrud, S; Burnett, R; Howard, C; Deng, Z; Kammen, DM; Schellnhuber, HJ; Chen, K; Kan, H; Chen, Z-M; Chen, B; Zhang, N; Mi, Z; Coffman, D; Cohen, AJ; Guan, D; Zhang, Q; Gong, P; Liu, Z
MLA Citation
Yin, Hao, et al. “Population ageing and deaths attributable to ambient PM2·5 pollution: a global analysis of economic cost.The Lancet. Planetary Health, vol. 5, no. 6, June 2021, pp. e356–67. Epmc, doi:10.1016/s2542-5196(21)00131-5.
URI
https://scholars.duke.edu/individual/pub1485894
PMID
34119010
Source
epmc
Published In
The Lancet. Planetary Health
Volume
5
Published Date
Start Page
e356
End Page
e367
DOI
10.1016/s2542-5196(21)00131-5

Malondialdehyde in dried blood spots: a biomarker of systemic lipid peroxidation linked to cardiopulmonary symptoms and risk factors.

<h4>Background</h4>There are few oxidative biomarkers that can be used in resource-limited settings (e.g., rural Africa) where blood collection facilities are lacking. This study aims to evaluate the potential of malondialdehyde (MDA) in dried blood spots (DBS) as a useful biomarker to monitor cardiopulmonary health.<h4>Methods</h4>We first conducted a cross-validation comparison of matched capillary DBS, plasma, and whole venous blood collected from nine healthy volunteers for the measurement of total MDA (free + conjugated) and C-reactive protein (CRP), a well-established biomarker of systemic inflammation. Then a field study was conducted in a rural Senegal with a population of 441 women routinely exposed to severe household air pollution, examining associations of MDA and CRP levels in 882 DBS with self-reported cardiopulmonary symptoms.<h4>Results</h4>In the cross-validation study, CRP levels were strongly correlated across DBS, plasma, and whole blood. MDA levels were correlated between DBS and whole blood and were 1-2 orders of magnitude lower in plasma, suggesting that DBS MDA may reflect total oxidation levels in intracellular and extracellular compartments. In the field study, we observed significantly higher MDA levels in women with secondhand smoke exposure. An interquartile range increase in MDA concentration was associated with 27.0% (95% CI: 3.1-56.5%) and 21.1% (95% CI: -3.5% to 52.0%) increases in the incidence of chest tightness and breath difficulty, respectively. In contrast, CRP levels were not associated with worse outcomes or risk factors.<h4>Conclusions</h4>These results support the use of DBS as a convenient alternative to venous blood when MDA is measured as a biomarker for cardiopulmonary health risk.
Authors
Lin, Y; Wang, X; Lenz, L; Ndiaye, O; Qin, J; Wang, X; Huang, H; Jeuland, MA; Zhang, JJ
MLA Citation
Lin, Yan, et al. “Malondialdehyde in dried blood spots: a biomarker of systemic lipid peroxidation linked to cardiopulmonary symptoms and risk factors.Journal of Thoracic Disease, vol. 13, no. 6, June 2021, pp. 3731–40. Epmc, doi:10.21037/jtd-21-604.
URI
https://scholars.duke.edu/individual/pub1487637
PMID
34277064
Source
epmc
Published In
Journal of Thoracic Disease
Volume
13
Published Date
Start Page
3731
End Page
3740
DOI
10.21037/jtd-21-604

DNA Methylation in Babies Born to Nonsmoking Mothers Exposed to Secondhand Smoke during Pregnancy: An Epigenome-Wide Association Study.

BACKGROUND: Maternal smoking during pregnancy is related to altered DNA methylation in infant umbilical cord blood. The extent to which low levels of smoke exposure among nonsmoking pregnant women relates to offspring DNA methylation is unknown. OBJECTIVE: This study sought to evaluate relationships between maternal prenatal plasma cotinine levels and DNA methylation in umbilical cord blood in newborns using the Infinium HumanMethylation 450K BeadChip. METHODS: Participants from the Newborn Epigenetics Study cohort who reported not smoking during pregnancy had verified low levels of cotinine from maternal prenatal plasma (0 ng/mL to <4 ng/mL), and offspring epigenetic data from umbilical cord blood were included in this study (n=79). Multivariable linear regression models were fit to the data, controlling for cell proportions, age, race, education, and parity. Estimates represent changes in response to any 1-ng/mL unit increase in exposure. RESULTS: Multivariable linear regression models yielded 29,049 CpGs that were differentially methylated in relation to increases in cotinine at a 5% false discovery rate. Top CpGs were within or near genes involved in neuronal functioning (PRKG1, DLGAP2, BSG), carcinogenesis (FHIT, HSPC157) and inflammation (AGER). Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses suggest cotinine was related to methylation of gene pathways controlling neuronal signaling, metabolic regulation, cell signaling and regulation, and cancer. Further, enhancers associated with transcription start sites were enriched in altered CpGs. Using an independent sample from the same study population (n=115), bisulfite pyrosequencing was performed with infant cord blood DNA for two genes within our top 20 hits (AGER and PRKG1). Results from pyrosequencing replicated epigenome results for PRKG1 (cg17079497, estimate=-1.09, standard error (SE)=0.45, p=0.018) but not for AGER (cg09199225; estimate=-0.16, SE=0.21, p=0.44). DISCUSSION: Secondhand smoke exposure among nonsmoking women may alter DNA methylation in regions involved in development, carcinogenesis, and neuronal functioning. These novel findings suggest that even low levels of smoke exposure during pregnancy may be sufficient to alter DNA methylation in distinct sites of mixed umbilical cord blood leukocytes in pathways that are known to be altered in cord blood from pregnant active smokers. https://doi.org/10.1289/EHP8099.
Authors
Fuemmeler, BF; Dozmorov, MG; Do, EK; Zhang, JJ; Grenier, C; Huang, Z; Maguire, RL; Kollins, SH; Hoyo, C; Murphy, SK
MLA Citation
Fuemmeler, Bernard F., et al. “DNA Methylation in Babies Born to Nonsmoking Mothers Exposed to Secondhand Smoke during Pregnancy: An Epigenome-Wide Association Study.Environ Health Perspect, vol. 129, no. 5, May 2021, p. 57010. Pubmed, doi:10.1289/EHP8099.
URI
https://scholars.duke.edu/individual/pub1483191
PMID
34009014
Source
pubmed
Published In
Environ Health Perspect
Volume
129
Published Date
Start Page
57010
DOI
10.1289/EHP8099

Associations between time-weighted personal air pollution exposure and amino acid metabolism in healthy adults.

The molecular mechanisms underlying the associations between air pollution exposure and adverse cardiopulmonary effects remain to be better understood. Altered amino acid metabolism may plays an important role in the development of cardiopulmonary diseases and may be perturbed by air pollution exposure. To test this hypothesized molecular mechanism, we conducted an association analysis from an existing intervention study to examine the relations of air pollution exposures with amino acids in 43 Chinese healthy adults. Plasma levels of amino acids were measured using a UPLC-QqQ-MS system. Time-weighted personal exposure to O<sub>3</sub>, PM<sub>2.5</sub>, NO<sub>2</sub>, and SO<sub>2</sub> over four time windows, i.e., 12 h, 24 h, 1 week, and 2 weeks, were calculated using the measured indoor and outdoor concentrations coupled with the time-activity data for each participant. Linear mixed-effects models were used to estimate the associations between air pollutants at each exposure window and amino acids by controlling for potential confounders. We observed significant associations between exposures and plasma concentrations of amino acids, with the direction of associations varying by amino acid and air pollutant. While there is little evidence of associations for NO<sub>2</sub> and SO<sub>2</sub>, the associations with amino acids were fairly pronounced for exposure to PM<sub>2.5</sub> and O<sub>3</sub>. In particular, independent O<sub>3</sub> (12- and 24-hour) associations were observed with changes in the amino acids that were related to the urea cycle, including aspartate, asparagine, glutamate, arginine, citrulline, and ornithine. Our findings indicated that air pollution may cause acute perturbation of amino acid metabolism, and that O<sub>3</sub> and PM<sub>2.5</sub> may affect the metabolism of amino acids in different pathways. Main finding: Acute air pollution exposure might affect the perturbation of amino acid metabolism, and in particular, was associated with amino acids in relation to the urea cycle.
Authors
Hu, X; Yan, M; He, L; Qiu, X; Zhang, J; Zhang, Y; Mo, J; Day, DB; Xiang, J; Gong, J
MLA Citation
Hu, Xinyan, et al. “Associations between time-weighted personal air pollution exposure and amino acid metabolism in healthy adults.Environment International, vol. 156, Nov. 2021, p. 106623. Epmc, doi:10.1016/j.envint.2021.106623.
URI
https://scholars.duke.edu/individual/pub1482998
PMID
33993003
Source
epmc
Published In
Environment International
Volume
156
Published Date
Start Page
106623
DOI
10.1016/j.envint.2021.106623