Luoping Zhang

Dr. Luoping Zhang

Division of Environmental Health Sciences, School of Public Health, University of California at Berkeley, Berkeley, CA 94720, USA
orcid

Research Focus & Metrics

Academic Career Length

22Years (2005-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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7 January 2019 in Environmental Health
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Journal Article
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CGChristina Gillezeau
Christina Gillezeau
Maaike van GerwenMaaike van Gerwen
Maaike van Gerwen
RSRachel M. Shaffer
Rachel M. Shaffer
IRIemaan Rana
Iemaan Rana
LZLuoping Zhang
Luoping Zhang
emanuela taioliemanuela taioli
emanuela taioli
Despite the growing and widespread use of glyphosate, a broad-spectrum herbicide and desiccant, very few studies have evaluated the extent and amount of human exposure. We review documented levels of human exposure among workers in occupational settings and the general population. We conducted a review of scientific publications on glyphosate levels in humans; 19 studies were identified, of which five investigated occupational exposure to glyphosate, 11 documented the exposure in general populations, and three reported on both. Eight studies reported urinary levels in 423 occupationally and para-occupationally exposed subjects; 14 studies reported glyphosate levels in various biofluids on 3298 subjects from the general population. Average urinary levels in occupationally exposed subjects varied from 0.26 to 73.5 μg/L; environmental exposure urinary levels ranged from 0.16 to 7.6 μg/L. Only two studies measured temporal trends in exposure, both of which show increasing proportions of individuals with detectable levels of glyphosate in their urine over time. The current review highlights the paucity of data on glyphosate levels among individuals exposed occupationally, para-occupationally, or environmentally to the herbicide. As such, it is challenging to fully understand the extent of exposure overall and in vulnerable populations such as children. We recommend further work to evaluate exposure across populations and geographic regions, apportion the exposure sources (e.g., occupational, household use, food residues), and understand temporal trends.

1 July 2019 in Mutation Research - Reviews in Mutation Research
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Journal Article
Closed access
LZLuoping Zhang
Luoping Zhang
IRIemaan Rana
Iemaan Rana
RSRachel M. Shaffer
Rachel M. Shaffer
ETEmanuela Taioli
Emanuela Taioli
LSLianne Sheppard
Lianne Sheppard

1 March 2009 in Mutation Research - Reviews in Mutation Research
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Journal Article
Closed access
LZLuoping Zhang
Luoping Zhang
CSCraig Steinmaus
Craig Steinmaus
DEDavid A. Eastmond
David A. Eastmond
XXXianjun K. Xin
Xianjun K. Xin
MSMartyn T. Smith
Martyn T. Smith

1 November 2011 in Mutation Research - Reviews in Mutation Research
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Journal Article
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ADAnh Duong
Anh Duong
CSCraig Steinmaus
Craig Steinmaus
CMCliona M. McHale
Cliona M. McHale
CVCharles P. Vaughan
Charles P. Vaughan
LZLuoping Zhang
Luoping Zhang

1 January 2010 in Cancer Epidemiology, Biomarkers & Prevention
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Journal Article
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LZLuoping Zhang
Luoping Zhang
XTXiaojiang Tang
Xiaojiang Tang
NRNathaniel Rothman
Nathaniel Rothman
RVRoel Vermeulen
Roel Vermeulen
ZJZhiying Ji
Zhiying Ji
QLQing Lan
Qing Lan
There are concerns about the health effects of formaldehyde exposure, including carcinogenicity, in light of elevated indoor air levels in new homes and occupational exposures experienced by workers in health care, embalming, manufacturing, and other industries. Epidemiologic studies suggest that formaldehyde exposure is associated with an increased risk of leukemia. However, the biological plausibility of these findings has been questioned because limited information is available on the ability of formaldehyde to disrupt hematopoietic function. Our objective was to determine if formaldehyde exposure disrupts hematopoietic function and produces leukemia-related chromosome changes in exposed humans. We examined the ability of formaldehyde to disrupt hematopoiesis in a study of 94 workers in China (43 exposed to formaldehyde and 51 frequency-matched controls) by measuring complete blood counts and peripheral stem/progenitor cell colony formation. Further, myeloid progenitor cells, the target for leukemogenesis, were cultured from the workers to quantify the level of leukemia-specific chromosome changes, including monosomy 7 and trisomy 8, in metaphase spreads of these cells. Among exposed workers, peripheral blood cell counts were significantly lowered in a manner consistent with toxic effects on the bone marrow and leukemia-specific chromosome changes were significantly elevated in myeloid blood progenitor cells. These findings suggest that formaldehyde exposure can have an adverse effect on the hematopoietic system and that leukemia induction by formaldehyde is biologically plausible, which heightens concerns about its leukemogenic potential from occupational and environmental exposures. Cancer Epidemiol Biomarkers Prev; 19(1); 80–8.

9 June 2015 in International Journal of Cancer
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Journal Article
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HBHelen Bailey
Helen Bailey
CIClaire Infante‐Rivard
Claire Infante‐Rivard
CMCatherine Metayer
Catherine Metayer
JCJacqueline Clavel
Jacqueline Clavel
TLTracy Lightfoot
Tracy Lightfoot
JSJoachim Schüz
Joachim Schüz
Some previous studies have suggested that home pesticide exposure before birth and during a child's early years may increase the risk of childhood leukemia. To further investigate this, we pooled individual level data from 12 case–control studies in the Childhood Leukemia International Consortium. Exposure data were harmonized into compatible formats. Pooled analyses were undertaken using multivariable unconditional logistic regression. The odds ratio (ORs) for acute lymphoblastic leukemia (ALL) associated with any pesticide exposure shortly before conception, during pregnancy and after birth were 1.39 (95% confidence interval [CI]: 1.25, 1.55) (using 2,785 cases and 3,635 controls), 1.43 (95% CI: 1.32, 1.54) (5,055 cases and 7,370 controls) and 1.36 (95% CI: 1.23, 1.51) (4,162 cases and 5,179 controls), respectively. Corresponding ORs for risk of acute myeloid leukemia (AML) were 1.49 (95% CI: 1.02, 2.16) (173 cases and 1,789 controls), 1.55 (95% CI: 1.21, 1.99) (344 cases and 4,666 controls) and 1.08 (95% CI: 0.76, 1.53) (198 cases and 2,655 controls), respectively. There was little difference by type of pesticide used. The relative similarity in ORs between leukemia types, time periods and pesticide types may be explained by similar exposure patterns and effects across the time periods in ALL and AML, participants' exposure to multiple pesticides, or recall bias. Although some recall bias is likely, until a better study design can be found to investigate the associations between home pesticide use and childhood leukemia in an equally large sample, it would appear prudent to limit the use of home pesticides before and during pregnancy, and during childhood.