Environmental Health Sciences Faculty Publication Series

Permanent URI for this collection

Recent Submissions

Now showing 1 - 5 of 38
  • Publication
    Roadside Exposure and Inflammation Biomarkers among a Cohort of Traffic Police in Kathmandu, Nepal
    (2019-01-01) Shakya, Kabindra M.; Peltier, Richard E.; Zhang, Yimin; Pandey, Basu D.
    Air pollution is a major environmental problem in the Kathmandu Valley. Specifically, roadside and traffic-related air pollution exposure levels were found at very high levels exceeding Nepal air quality standards for daily PM2.5. In an exposure study involving traffic police officers, we collected 78 blood samples in a highly polluted spring season (16 February 2014–4 April 2014) and 63 blood samples in the less polluted summer season (20 July 2014–22 August 2014). Fourteen biomarkers, i.e., C-reactive protein (CRP), serum amyloid A (SAA), intracellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), interferon gamma (IFN-γ), interleukins (IL1-β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-13), and tumor necrosis factor (TNF-α) were analyzed in collected blood samples using proinflammatory panel 1 kits and vascular injury panel 2 kits. All the inflammatory biomarker levels were higher in the summer season than in the spring season, while particulate levels were higher in the spring season than in the summer season. We did not find significant association between 24-hour average PM2.5 or black carbon (BC) exposure levels with most of analyzed biomarkers for the traffic volunteers working and residing near busy roads in Kathmandu, Nepal, during 2014. Inflammation and vascular injury marker concentrations were generally higher in females, suggesting the important role of gender in inflammation biomarkers. Because of the small sample size of female subjects, further investigation with a larger sample size is required to confirm the role of gender in inflammation biomarkers.
  • Publication
    Ambient PM2.5 and risk of emergency room visits for myocardial infarction: impact of regional PM2.5 oxidative potential: a case-crossover study
    (2016-01-01) Weichenthal, Scott; Lavigne, Eric; Evans, Greg; Pollitt, Krystal; Burnett, Rick T.
    Background Regional differences in the oxidative potential of fine particulate air pollution (PM2.5) may modify its impact on the risk of myocardial infarction. Methods A case-crossover study was conducted in 16 cities in Ontario, Canada to evaluate the impact of regional PM2.5 oxidative potential on the relationship between PM2.5and emergency room visits for myocardial infarction. Daily air pollution and meteorological data were collected between 2004 and 2011 from provincial monitoring sites and regional estimates of glutathione (OPGSH) and ascorbate-related (OPAA) oxidative potential were determined using an acellular assay based on a synthetic respiratory tract lining fluid. Exposure variables for the combined oxidant capacity of NO2 and O3 were also examined using their sum (Ox) and a weighted average (Ox wt) based on their redox potentials. Results In total, 30,101 cases of myocardial infarction were included in the analysis. For regions above the 90th percentile of OPGSH each 5 μg/m3 increase in same-day PM2.5 was associated with a 7.9 % (95 % CI: 4.1, 12) increased risk of myocardial infarction whereas a 4.1 % (95 % CI: 0.26, 8.0) increase was observed in regions above the 75th percentile and no association was observed below the 50th percentile (p-interaction = 0.026). A significant 3-way interaction was detected with the strongest associations between PM2.5 and myocardial infarction occurring in areas with high regional OPGSH and high Ox wt (p-interaction < 0.001). Conclusions Regional PM2.5 oxidative potential may modify the impact of PM2.5 on the risk of myocardial infarction. The combined oxidant capacity of NO2 and O3 may magnify this effect.
  • Publication
    A glance into how the cold war and governmental loyalty investigations came to affect a leading U.S. radiation geneticist: Lewis J. Stadler’s nightmare
    (2017-01-01) Calabrese, Edward J.
    This paper describes an episode in the life of the prominent plant radiation geneticist, Lewis J. Stadler (1897–1954) during which he became a target of the Federal Bureau of Investigation (FBI) concerning loyalty to the United States due to possible associations with the communist party. The research is based on considerable private correspondence of Dr. Stadler, the FBI interrogatory questions and Dr. Stadler’s answers and letters of support for Dr. Stadler by leading scientists such as, Hermann J. Muller.
  • Publication
    A proposed framework for the systematic review and integrated assessment (SYRINA) of endocrine disrupting chemicals
    (2016-01-01) Vandenberg, Laura N.; Ågerstrand, Marlene; Beronius, Anna; Beausoleil, Claire; Bergman, Åke; Bero, Lisa A.; Bornehag, Carl-Gustaf; Boyer, C. Scott; Cooper, Glinda S.; Cotgreave, Ian; Gee, David; Grandjean, Philippe; Guyton, Kathryn Z.; Hass, Ulla; Heindel, Jerrold J.; Jobling, Susan; Kidd, Karen A.; Kortenkamp, Andreas; Macleod, Malcolm R.; Martin, Olwenn V.; Norinder, Ulf; Scheringer, Martin; Thayer, Kristina A.; Toppari, Jorma; Whaley, Paul; Woodruff, Tracey J.; Rudén, Christina
    Background The issue of endocrine disrupting chemicals (EDCs) is receiving wide attention from both the scientific and regulatory communities. Recent analyses of the EDC literature have been criticized for failing to use transparent and objective approaches to draw conclusions about the strength of evidence linking EDC exposures to adverse health or environmental outcomes. Systematic review methodologies are ideal for addressing this issue as they provide transparent and consistent approaches to study selection and evaluation. Objective methods are needed for integrating the multiple streams of evidence (epidemiology, wildlife, laboratory animal, in vitro, and in silico data) that are relevant in assessing EDCs. Methods We have developed a framework for the systematic review and integrated assessment (SYRINA) of EDC studies. The framework was designed for use with the International Program on Chemical Safety (IPCS) and World Health Organization (WHO) definition of an EDC, which requires appraisal of evidence regarding 1) association between exposure and an adverse effect, 2) association between exposure and endocrine disrupting activity, and 3) a plausible link between the adverse effect and the endocrine disrupting activity. Results Building from existing methodologies for evaluating and synthesizing evidence, the SYRINA framework includes seven steps: 1) Formulate the problem; 2) Develop the review protocol; 3) Identify relevant evidence; 4) Evaluate evidence from individual studies; 5) Summarize and evaluate each stream of evidence; 6) Integrate evidence across all streams; 7) Draw conclusions, make recommendations, and evaluate uncertainties. The proposed method is tailored to the IPCS/WHO definition of an EDC but offers flexibility for use in the context of other definitions of EDCs. Conclusions When using the SYRINA framework, the overall objective is to provide the evidence base needed to support decision making, including any action to avoid/minimise potential adverse effects of exposures. This framework allows for the evaluation and synthesis of evidence from multiple evidence streams. Finally, a decision regarding regulatory action is not only dependent on the strength of evidence, but also the consequences of action/inaction, e.g. limited or weak evidence may be sufficient to justify action if consequences are serious or irreversible.
  • Publication
    Developmental Exposure to 2,2′,4,4′-Tetrabromodiphenyl Ether Permanently Alters Blood-Liver Balance of Lipids in Male Mice
    (2018-01-01) Khalil, Ahmed; Cevik, Sebnem Eren; Hung, Stephanie; Kolla, Sridurgadevi; Roy, Monika; Suvorov, Alexander
    Polybrominated diphenyl ethers (PBDEs) were used as flame-retardant additives starting 1965 and were recently withdrawn from commerce in North America and Europe. Approximately 1/5 of the total U.S. population were born when environmental concentrations of PBDE plateaued at their maximum. Accumulating evidence suggests that developmental exposures to PBDE may result in long-lasting programming of liver metabolism. In this study, CD-1 mice were exposed prenatally or neonatally to 1 mg/kg body weight of 2,2′ ,4,4′ -tetrabromodiphenyl ether (BDE-47), and changes in liver histology, transcriptome, and liver-blood balance of triglycerides were analyzed in 10 months old male offspring. In both exposure groups, long-term reprogramming of lipid metabolism was observed, including increased liver triglycerides and decreased blood triglycerides, and altered expression of metabolic genes in the liver. Significant upregulation of lipid influx transporter Cd36 2.3- and 5.7-fold in pre- and neonatal exposure groups, respectively was identified as a potential mechanism of blood/liver imbalance of triglycerides. Analysis of our and previously published all-genome gene expression data identified changes in expression of ribosomal protein genes as a transcriptomic signature of PBDE exposure. Further comparison of our new data and published data demonstrate that low doses (0.2 mg/kg body weight) of PBDE induce long-lasting up-regulation of ribosomal genes, suppression of Cd36 in liver and increase circulating triglycerides in blood, while moderated doses (≥1 mg/kg body weight) produce opposite long-lasting effects. To conclude, this study shows that an environmentally relevant developmental exposures to BDE-47 permanently alter lipid uptake and accumulation in the liver, with low and moderate doses having opposite effect on liver transcriptomics and triglyceride balance. Similar effects of pre- and neonatal exposures point at hepatocyte maturation as a sensitive window of the liver metabolism programming. These results suggest that PBDE exposure may be an important factor increasing risks of cardio-vascular disease and non-alcoholic fatty liver disease via modulation of liver/blood balance of lipids. The translational relevance of these findings for human remain to be studied.