Patton Khuu Nguyen

All Publications

• Mapping the key characteristics of carcinogens for glyphosate and its formulations: A systematic review. Chemosphere Rana, I., Nguyen, P. K., Rigutto, G., Louie, A., Lee, J., Smith, M. T., Zhang, L. 2023; 339: 139572

  Abstract

  Glyphosate was classified as a probable human carcinogen (Group 2A) by the International Agency for Research on Cancer (IARC) partially due to strong mechanistic evidence in 2015. Since then, numerous studies of glyphosate and its formulations (GBF) have emerged. These studies can be evaluated for cancer hazard identification with the newly described ten key characteristics (KC) of carcinogens approach. Our objective was to assess all in vivo, ex vivo, and in vitro mechanistic studies of human and experimental animals (mammals) that compared exposure to glyphosate/GBF with low/no exposure counterparts for evidence of the ten KCs. A protocol with our methods adhering to PRISMA guidelines was registered a priori (INPLASY202180045). Two blinded reviewers screened all in vivo, ex vivo, and in vitro studies of glyphosate/GBF exposure in humans/mammals reporting any KC-related outcome available in PubMed before August 2021. Studies that met inclusion criteria underwent data extraction conducted in duplicate for each KC outcome reported along with key aspects of internal/external validity, results, and reference information. These data were used to construct a matrix that was subsequently analyzed in the program R to conduct strength of evidence and quality assessments. Of the 2537 articles screened, 175 articles met inclusion criteria, from which we extracted >50,000 data points related to KC outcomes. Data analysis revealed strong evidence for KC2, KC4, KC5, KC6, KC8, limited evidence for KC1 and KC3, and inadequate evidence for KC7, KC9, and KC10. Notably, our in-depth quality analyses of genotoxicity (KC2) and endocrine disruption (KC8) revealed strong and consistent positive findings. For KC2, we found: 1) studies conducted in humans and human cells provided stronger positive evidence than counterpart animal models; 2) GBF elicited a stronger effect in both human and animal systems when compared to glyphosate alone; and 3) the highest quality studies in humans and human cells consistently revealed strong evidence of genotoxicity. Our analysis of KC8 indicated that glyphosate's ability to modulate hormone levels and estrogen receptor activity is sensitive to both exposure concentration and formulation. The modulations observed provide clear evidence that glyphosate interacts with receptors, alters receptor activation, and modulates the levels and effects of endogenous ligands (including hormones). Our findings strengthen the mechanistic evidence that glyphosate is a probable human carcinogen and provide biological plausibility for previously reported cancer associations in humans, such as non-Hodgkin lymphoma. We identified potential molecular interactions and subsequent key events that were used to generate a probable pathway to lymphomagenesis.

  View details for DOI 10.1016/j.chemosphere.2023.139572

  View details for PubMedID 37474029

• Elevator Ventilation and SARS-CoV-2-Relevant Particulate Matter Removal in Three Older California Elevators INDOOR AIR Kado, M. J., Perttula, K., Noth, E. M., Moore, D., Nguyen, P., Perrino, C., Nicas, M., Hammond, S. 2023; 2023

  View details for DOI 10.1155/2023/7664472

  View details for Web of Science ID 001076700400001

• Fine Particulate Matter Exposure From Secondhand Cannabis Bong Smoking. JAMA network open Nguyen, P. K., Hammond, S. K. 2022; 5 (3): e224744

  Abstract

  This cohort study quantifies the levels of secondhand cannabis smoke from social bong smoking in a home environment.

  View details for DOI 10.1001/jamanetworkopen.2022.4744

  View details for PubMedID 35353170

  View details for PubMedCentralID PMC8968464

• A pilot study comparing T-regulatory cell function among healthy children in different areas of Gansu, China. Environmental science and pollution research international Gou, P., Chang, X., Ye, Z., Yao, Y., Nguyen, P. K., Hammond, S. K., Wang, J., Liu, S. 2017; 24 (28): 22579-22586

  Abstract

  Immune system is critical to protecting human health from toxic substances. Our previously published research had found an important link between polycyclic aromatic hydrocarbons (PAHs) in ambient air and changes at the DNA level in immune cells that led to impaired function of regulatory T (Treg) cells in children living in California, USA. But molecular and cellular pathways of these changes remain unclear. The present study aims to explore whether exposure to PAHs leads to changes in Treg cells functions of children living in Gansu, China, where ambient air pollution levels are much higher than those in California, and to explore potential mechanisms of PAH-induced immunological dysfunctions. Air pollutions in Lanzhou and Lintao, Gansu Province, were measured from December 2015 to June 2016. Healthy children were recruited from both cities and enrolled in this pilot study. Demographic information was collected by questionnaires. Blood samples were collected. Peripheral blood Treg cells were analyzed for Treg cells percentage by flow cytometry. Gene expression of forkhead box transcription factor 3 (Foxp3), transforming growth factor-β (TGF-β), and interleukin 35 (IL35) were examined by reverse transcription-polymerase chain reaction (RT-PCR). The results indicated PAH concentration (as sum of 16 PAHs) in Lintao was over two times higher than that was in Lanzhou (707 vs. 326 ng/m3), whereas PM2.5 concentration was comparable in two cities (55.3 in Lintao vs. 65.7 μg/m3 in Lanzhou). Notably, we observed lower gene expressions for Foxp3 (P < 0.05), IL35 (P < 0.05), and TGF-β, in children living in Lintao, suggesting an impairment of Treg cells function potentially associated with higher PAH exposure in Lintao. However, no significant difference was observed in Treg cells % among CD4+ T cells between Lanzhou and Lintao groups.

  View details for DOI 10.1007/s11356-017-9907-3

  View details for PubMedID 28808862