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Toxic Exposures (toxic + exposure)
Selected AbstractsToxic Exposures: contested illnesses and the environmental health movementAUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 2 2010Article first published online: 8 APR 2010 No abstract is available for this article. [source] Integrated condition indices as a measure of whole effluent toxicity in zebrafish (Danio rerio)ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 1 2002Roel Smolders Abstract Toxic exposure of organisms interferes with organismal integrity at the biochemical level and ultimately gives rise to effects at the individual level. These effects may result in reductions in ecologically relevant characteristics such as growth, reproduction, and survival. A chronic toxicity test with zebrafish (Danio rerio) was conducted where fish were exposed to 50, 75, and 100% effluent for 28 d under flow-through conditions. Effects of effluent exposure were determined using endpoints of physiological (respiration during swimming), growth (condition, length, and weight), and reproductive (spawning and hatching) processes within the same population. Results clearly indicate that the condition and growth of zebrafish is depressed by exposure to the effluent. Also, increased oxygen consumption was found after 14, 21, and 28 d of exposure. Reproduction proved to correlate well with the condition of the motherfish in the control, and spawning and hatching were significantly depressed by effluent exposure. These results indicate that the evaluation of endpoints describing different ecologically relevant processes provides a rational assessment of the cause,effect relationships of effluent toxicity. This approach can quantify effects on different biological processes and can determine the interactions that occur between these different processes. [source] Adverse health effects of children's exposure to pesticides: What do we really know and what can be done about itACTA PAEDIATRICA, Issue 2006JOANNA JUREWICZ Abstract Children may be exposed to pesticides in several ways, such as by transplacental transfer during foetal life, by intake of contaminated breast milk and other nutrients, or by contact with contaminated subjects and areas in the environment such as pets treated with insecticides, house dust, carpets and chemically treated lawns and gardens. Exposure early in life, and particularly during periods of rapid development, such as during foetal life and infancy, may have severe effects on child health and development by elevating the risk of congenital malformations, cancer, malabsorption, immunological dysfunction, endocrine disease, and neurobehavioural deficiencies. As pesticides can also interfere with parental reproductive health, exposure of parents may have consequences for the offspring leading to reduced chance of male birth and increased risk of childhood cancer. Conclusions: Current knowledge about tolerable levels and consequences of toxic exposure to pesticides during human development is rather scarce. Owing to the high risk of exposure to pesticides, particularly in less developed countries, further elucidation by well-controlled epidemiological studies in this field it is urgently needed. The Policy Interpretation Network on Children's Health and Environment (PINCHE), which is financed by the EU DG research has suggested actions against pesticide exposure. They have been presented and discussed in this paper. Several suggestions of PINCHE concerning action needed regarding pesticides were presented in the paper. [source] ESI+ MS/MS confirmation of canine ivermectin toxicity,JOURNAL OF MASS SPECTROMETRY (INCORP BIOLOGICAL MASS SPECTROMETRY), Issue 1 2009A. F. Lehner Abstract Ivermectin is a semisynthetic macrocyclic lactone anthelmintic of the avermectin family derived from Streptomyces fermentation products. Avermectins are used as antiparasitic agents in domestic animals; although considered relatively safe, one must consider animal species, breed, weight, and age in dosage determinations. In January 2006, two canines were presented to the UK Livestock Disease Diagnostic Center after dying from suspected ivermectin overdoses [30,50 mg/kg body weight]. To confirm this clinical diagnosis we developed a rapid, sensitive semiquantitative ElectroSpray Ionization,Mass Spectrometry (ESI/MS) method for ivermectin in canine tissue samples. Pharmaceutical ivermectin contains two ivermectins differing by a single methyl group, and each compound forms interpretation-confounding adducts with tissue Na+ and K+ ions. We now report that ivermectin administration was clearly confirmed by comparison with standard and dosage forms of ivermectin, and simple proportionalities based on mass spectral intensity of respective molecular ions allowed semiquantitative estimates of injection site tissue concentrations of 20 and 40 µg/g tissue (wet weight) in these animals, consistent with the history of ivermectin administration and the clinical signs observed. There is a distinct need for both rapid detection and confirmation of toxic exposures in veterinary diagnostics, whether for interpretation of clinical cases antemortem or for forensic reasons postmortem. It is vital that interpreters of analytical results have appropriate guidance in the scientific literature and elsewhere so as to enable clear-cut answers. The method presented here is suitable for routine diagnostic work in that it allows rapid extraction of ivermectin from tissue samples, avoids the need for high-performance liquid chromatography and allows ready interpretation of the multiple ivermectin species seen by ESI+ MS/MS in samples originating from veterinary dosage forms. Copyright © 2008 John Wiley & Sons, Ltd. [source] Policy on Acute Toxic Ingestion or Dermal or Inhalation ExposureJOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 7 2003ANP-C FAANP, Mary Jo Goolsby EdD ABSTRACT Many nurse practitioners (NPs) practice in emergency and urgent-care settings, and fir more practical remote settings. NPs in each of these settings should be familiar with the assessment, stabilization, and treatment of patients who seek treatment for suspected intentional or accidental poisoning. This month's Clinical practice guideline (CPG) column reviews the "Clinical Policy for the Initial Approach to Patients Presenting With Acute Toxic Ingestion or Dermal or Inhalation Exposure." SUMMARY The ACEP "Clinical Policy for the Initial Approach to Patients Presenting With Acute Toxic Ingestion or Dermal or Inhalation Exposure" includes several helpful resources. In addition to recommending specific clinical actions in response to patient variables, the document includes a table identifying the antidote for many of the most commonly ingested drugs. These include digoxin, iron, opioids, salicylates, acetaminophen, and tricyclic antidepressants. The table also includes both the adult and pediatric dose of each listed antidote. A quick reference is included. This form can be used to guide the history, physical examination, and subsequent actions for treating patients with acute toxic ingestion or dermal or inhalation exposure. Finally, there is a quality assurance form to guide chart reviews. Many of the attributes of a well-developed guideline are identified in the report. The authors clearly identify the situations for which the recommendations are intended as well as those in which they do not apply. For instance, the guidance is not intended for use when patients are unstable and stabilization is the primary focus. It is also not intended for cases of radiation, parenteral, or eye exposure or of food poisoning. The authors describe the process used to develop the recommendations and identify the strength of the evidence on which each recommendation is based. The role of provider judgment in application of the guidance is addressed. Prior to its dissemination, the CPG was subjected to external review by dinical experts. This ACEP policy has applicability for the growing number of NPs working in emergency and urgent cafe settings as well as for those who must provide front line emergency care in remote settings. It provides a framework for responding to acute toxic exposures and provides several useful resources to assist the clinician in responding to situations in which accidental or intentional poisoning is suspected. [source] One agent, many diseases: Exposure-response data and comparative risks of different outcomes following silica exposure,AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 1 2005Kyle Steenland Abstract Background Evidence in recent years indicates that silica causes lung cancer, and probably renal disease, in addition to its well-known relationship to silicosis. There is also suggestive evidence that silica can cause arthritis and other auto-immune diseases. Silica has, therefore, joined a handful of other toxic exposures such as tobacco smoke, dioxin, and asbestos which cause multiple serious diseases. Methods The available exposure-response data for silica and silicosis, lung cancer, and renal disease are reviewed. We compare the corresponding excess risks (or absolute risks in the case of silicosis) of death or disease incidence by age 75 for these three diseases, subsequent to a lifetime (45 years) of exposure to silica at current US standard (0.1 mg/m3 respirable crystalline silica). Results The absolute risk of silicosis, as defined by small opacities greater than or equal to ILO classification 1/1 on an X-ray, ranges from 47% to 77% in three cohort studies with adequate follow-up after employment. The absolute risk of death from silicosis is estimated at 1.9% (0.8%,2.9%), based on a pooled analysis of six cohort studies. The excess risk of lung cancer death, assuming US male background rates, is 1.7% (0.2%,3.6%), based on a pooled analysis of ten cohort studies. The excess risk of end-stage renal disease (assuming male background rates) is 5.1% (2.2%,7.3%), based on a single cohort. The excess risk of death from renal disease is estimated to be 1.8% (0.8%,9.7%), based on a pooled analysis of three cohorts. Conclusions Keeping in mind that the usual OSHA acceptable excess risk of serious disease or death for workers is 0.1%, it is clear that the current standard is far from sufficiently protective of workers' health. Perhaps surprisingly, kidney disease emerges as perhaps a higher risk than either mortality from silicosis or lung cancer, although the data are based on fewer studies. Am. J. Ind. Med. 48:16,23, 2005. © 2005 Wiley-Liss, Inc. [source] Mortality among unionized construction plasterers and cement masons,AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 4 2001Frank Stern Abstract Background Plasterers perform a variety of duties including interior and exterior plastering of drywall, cement, stucco, and stone imitation; the preparation, installation, and repair of all interior and exterior insulation systems; and the fireproofing of steel beams and columns. Some of the current potential toxic exposures among plasterers include plaster of Paris, silica, fiberglass, talc, and 1,1,1-trichloroethylene; asbestos had been used by the plasterers in the past. Cement masons, on the other hand, are involved in concrete construction of buildings, bridges, curbs and gutters, sidewalks, highways, streets and roads, floors and pavements and the finishing of same, when necessary, by sandblasting or any other method. Exposures include cement dust, silica, asphalt, and various solvents. Methods Proportionate mortality ratios (PMRs) and proportionate cancer mortality ratios (PCMRs) were calculated for 99 causes of death among 12,873 members of the Operative Plasterers' and Cement Masons' International Association who died between 1972 and 1996 using United States age-, race-, and calender-specific death rates. Statistical significance (P value) of results was based upon the Poisson distribution. Results Among plasterers, statistically significant elevated mortality was observed for asbestosis, where the PMR reached 1,657 (P,<,0.01) with eleven observed deaths and less than one death expected, for lung cancer (PCMR,=,124, P,<,0.01), and for benign neoplasms (PMR,=,210, P,<,0.05). Among cement masons, statistically significant elevated mortality was observed for cancer of the stomach (PCMR,=,133, P,<,0.01), benign neoplasms (PMR,=,132, P,<,0.01), and poisonings (PMR,=,159, P,<,0.05). Except for poisonings, which were not thought to be occupationally related, all of the statistically significant results occurred among those members who entered the union prior to 1950. However, the risk for lung cancer among plasterers was still elevated among those entering the union after 1970 as was the risk for stomach cancer among cement masons who entered the union after 1950. Conclusions The present study suggests that plasterers and cement masons still have elevated risks for certain diseases, especially lung and stomach cancer. Therefore, union members currently living should be screened for asbestos-related diseases and educated about the future risks for these diseases. Am. J. Ind. Med. 39:373,388, 2001. Published 2001 Wiley-Liss, Inc. [source] Hypothesis: Could Epstein-Barr virus play a role in the development of gastroschisis?BIRTH DEFECTS RESEARCH, Issue 2 2010Martha M. Werler BACKGROUND: The strong inverse association between maternal age and risk of gastroschisis in offspring has spurred many investigators to hypothesize that behaviors among younger females are the cause. Examples include cigarette smoking, illicit drugs, genitourinary infections, and sexually transmitted diseases, each of which has been reported to be associated with gastroschisis. Although these exposures are more common in young women, recent studies have shown that cigarette smoking, genitourinary infections, and sexually transmitted diseases are most strongly associated with gastroschisis in older women. There is both anecdotal and published evidence showing that gastroschisis sometimes (but not always) occurs in clusters, raising the possibility that an infectious agent might be involved in its pathogenesis. RESULTS: One such agent whose epidemiologic characteristics parallel those of gastroschisis is Epstein-Barr virus (EBV). Primary EBV infection in early childhood has been decreasing over time, leaving a greater proportion of adolescents at risk, as reflected by increased rates of infectious mononucleosis over time. During the childbearing years, risk of primary EBV infection decreases dramatically, as does risk of gastroschisis. The stronger risks of gastroschisis associated with cigarette smoking, genitourinary infections, and sexually transmitted diseases in older women might be explained by EBV reactivation resulting from multiple challenges to immune response such as pregnancy, age, toxic exposures, and genitourinary and sexually transmitted infections. CONCLUSION: EBV and other herpes viruses should be added to the research agenda for gastroschisis. Birth Defects Research (Part A) 2010. © 2009 Wiley-Liss, Inc. [source] | |||||||||||||