168 research outputs found
The Role of Health Inequality in Achieving Universal Primary Education: A Cross-National Panel Analysis
Throughout the latter half of the 20th century, cross-national primary education has improved substantially, even when considering remaining inequalities between nations. In order to further tease apart the complex mechanisms that have facilitated this growth, the present study posits that global reductions in health inequality (defined as a country’s distribution of age at death) has played a key role in increasing primary school enrollment. Health inequality is theorized to negatively affect primary school enrollment by acting as a collective proxy of distinct phenomena within a population, such as prevalence of mortality, prevalence of poor childhood health, and prevalence of parental health shocks. To test the relationship between health inequality and primary school enrollment, this study employed a cross-national unbalanced panel dataset of 806 observations across 142 nations from 1970 to 2015. Across random and fixed effects models as well as sensitivity analyses, higher levels of health inequality were significantly associated with lower primary school enrollment. Therefore, evidence suggests that improvements in cross-national health equality contributed in part to the substantial increase in global access to primary education
Use of kinetic and mechanistic data in species extrapolation of bioactivation: Cytochrome P-450 dependent trichloroethylene metabolism at occupationally relevant concentrations
Abstract: Use of Kinetic and Mechanistic Data in S p e c i e s E x t r a p o l a t i o n o f B i o a c t i v a t i o n : Cytochrome P-450 Dependent Trichloroethylene M e t a b o l i s m a t O c c u p a t i o n a l l y R e l e v a n t Concentrations: John C. LIPSCOMB, et al. United States Air Force, Armstrong Laboratory, Toxicology Division-Trichloroethylene (TRI) is an industrial solvent and environmental contaminant; therefore exposure to TRI occurs in diverse human populations. TRI causes hepatocellular carcinoma in B6C3F1 mice, but not rats; this suggests that TRI may be metabolized differently in the two species. We investigated the metabolism of TRI and the effect of TRI on enzymatic activities indicative of specific cytochrome P450 (CYP) forms in hepatic microsomes from mice, rats and humans. Studies in microsomes estimated MichaelisMenten kinetic parameters by saturation analysis. K m values were 35.4, 55.5 and 24.6 µM and V max values were 5,425, 4,826 and 1,440 pmol/min/mg in pooled mouse, rat and human microsomes, respectively. TRI (1,000 ppm) inhibited CYP2E1 dependent activity in all three species and BROD activity in mice and rats; TRI (1,000 ppm) increased CYP1A1/1A2 activity, and had no effect on CYP2A activity. Inhibition studies with mouse hepatic microsomes demonstrated that TRI was a competitive inhibitor of CYP2E1, with K i of 50 ppm. TRI noncompetitively inhibited CYP2B-dependent activities in the rat and mouse. Preincubation of microsomes with TRI and NADPH decreased the absorbence of CO-bound CYP in all three species, but the dose-dependence was most evident in mouse hepatic microsomes. These results have quantified the interspecies difference in CYP-dependent TRI bioactivation and indicate that under both equivalent and occupationally relevant (hepatic) exposure conditions the human is at less risk of forming toxic Trichloroethylene (TRI) is an unsaturated, chlorinated hydrocarbon widely used as an industrial solvent and is now a relatively common ground water pollutant 1) . TRI produces liver and lung toxicity in mice TRI concentrations as low as 10 µM, in vitro, inhibit gap junction mediated intercellular communication in mouse but not rat hepatocytes, and effect which is blocked by CYP inhibitio
Systemic Exposure to PAHs and Benzene in Firefighters Suppressing Controlled Structure Fires
Turnout gear provides protection against dermal exposure to contaminants during firefighting; however, the level of protection is unknown. We explored the dermal contribution to the systemic dose
of polycyclic aromatic hydrocarbons (PAHs) and other aromatic hydrocarbons in firefighters during suppression and overhaul of controlled structure burns. The study was organized into two rounds, three controlled burns per round, and five firefighters per burn. The firefighters wore new or laundered turnout gear tested before each burn to ensure lack of PAH contamination. To ensure that any increase in
systemic PAH levels after the burn was the result of dermal rather than inhalation exposure, the firefighters did not remove their self-contained breathing apparatus until overhaul was completed and they
were >30 m upwind from the burn structure. Specimens were collected before and at intervals after the burn for biomarker analysis. Urine was analyzed for phenanthrene equivalents using enzyme-linked
immunosorbent assay and a benzene metabolite (s-phenylmercapturic acid) using liquid chromatography/tandem mass spectrometry; both were adjusted by creatinine. Exhaled breath collected on thermal
desorption tubes was analyzed for PAHs and other aromatic hydrocarbons using gas chromatography/mass spectrometry. We collected personal air samples during the burn and skin wipe samples (corn oil medium) on several body sites before and after the burn. The air and wipe samples were analyzed for PAHs using a liquid chromatography with photodiode array detection. We explored possible changes in external exposures or biomarkers over time and the relationships between these variables using non-parametric sign tests and Spearman tests, respectively. We found significantly elevated (P < 0.05) post-exposure breath concentrations of benzene compared with pre-exposure concentrations for both rounds. We also found significantly elevated post-exposure levels of PAHs on the neck compared with pre-exposure levels for round 1. We found statistically significant positive correlations between external exposures (i.e. personal air concentrations of PAHs) and biomarkers (i.e. change in urinary PAH metabolite levels in round 1 and change in breath concentrations of benzene in round 2). The results
suggest that firefighters wearing full protective ensembles absorbed combustion products into their bodies. The PAHs most likely entered firefighters’ bodies through their skin, with the neck being the
primary site of exposure and absorption due to the lower level of dermal protection afforded by hoods. Aromatic hydrocarbons could have been absorbed dermally during firefighting or inhaled during the
doffing of gear that was off-gassing contaminants.National Institute for Occupational Safety and Health (NIOSH) by intramural award under the National Occupational Research AgendaOpe
Muscular contractions in the zebrafish embryo are necessary to reveal thiuram-induced notochord distortions
Author Posting. © The Authors, 2006. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Toxicology and Applied Pharmacology 212 (2006): 24-34, doi:10.1016/j.taap.2005.06.016.Dithiocarbamates form a large group of chemicals that have numerous uses in agriculture and medicine. It has been reported that dithiocarbamates, including thiuram (tetramethylthiuram disulfide), cause wavy distortions of the notochord in zebrafish and other fish embryos. In the present study, we investigated the mechanism underlying the toxicity of thiuram in zebrafish embryos. When embryos were exposed to thiuram (2-1,000 nM: 0.48-240 µg/L) from 3 hours post fertilization (hpf) (30% epiboly) until 24 hpf (Prim-5), all embryos develop wavy notochords, disorganized somites, and have shortened yolk sac extensions. The thiuram response was specific and did not cause growth retardation or mortality at 24 hpf. The thiuram-dependent responses showed the same concentration dependence with a waterborne EC50 values of approximately 7 nM. Morphometric measurements revealed that thiuram does not affect the rate of notochord lengthening. However, the rate of overall body lengthening was significantly reduced in thiuram exposed animals. Other dithiocarbamates, such as ziram, caused similar malformations to thiuram. While expression of genes involved in somitogenesis was not affected, the levels of notochord specific transcripts were altered before and after the onset of malformations. Distortion of the notochord started precisely at 18 hpf, which is concomitant with onset of spontaneous rhythmic trunk contractions. Abolishment of spontaneous contractions using tricaine, α-bungarotoxin, and a paralytic mutant sofa potato, resulted in normal notochord morphology in the presence of thiuram. These results indicate that muscle activity is necessary to reveal the underlying functional deficit and suggest that the developmental target of dithiocarbamates impairs trunk plasticity through an unknown mechanism.This work was supported by grants-in-aid for scientific research from the Japanese Ministry of Education, Culture, Sports, Science and Technology (T.H. and H.T.), and grant-in-aid for JSPS fellows from the Japanese Ministry of Education, Culture, Sports, Science and Technology (W. D.), a grant-in-aid for High Technological Research Center (Rakuno Gakuen University) from the Ministry of Education, Science, Sports and Culture of Japan (H.T.), Technology, cooperative research from active research in Rakuno Gakuen University 2004-7 (H.T.), and NIH/NIEHS grants ES00210 and ES03850 (RT)
The evaluation of a system of reporting school progress as used in the junior high section of St. Benedict's School, Evansville, Indiana
There is no abstract available for this research paper.Thesis (M.A.E.
A Cross-National Analysis of Lifespan Inequality, 1950–2015: Examining the Distribution of Mortality Within Countries
- …
