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Toxics, Volume 1, Issue 1 (December 2013), Pages 1-76

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Editorial

Jump to: Research, Review

Open AccessEditorial Introducing Toxics
Toxics 2013, 1(1), 1; doi:10.3390/toxics1010001
Received: 21 March 2013 / Revised: 3 April 2013 / Accepted: 3 April 2013 / Published: 11 April 2013
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Abstract
With this inaugural issue, Toxics begins its life as a peer-reviewed, open access journal focusing on all aspects of toxic chemicals. We are interested in publishing papers that present a wide range of perspectives on toxicants and naturally occurring toxins, including exposure, [...] Read more.
With this inaugural issue, Toxics begins its life as a peer-reviewed, open access journal focusing on all aspects of toxic chemicals. We are interested in publishing papers that present a wide range of perspectives on toxicants and naturally occurring toxins, including exposure, biomarkers, kinetics, biological effects, fate and transport, treatment, and remediation. Toxics differs from many other journals in the absence of a page or word limit on contributions, permitting authors to present their work in as much detail as they wish. Toxics will publish original research papers, conventional reviews, meta-analyses, short communications, theoretical papers, case reports, commentaries and policy perspectives, and book reviews (Book reviews will be solicited and should not be submitted without invitation). Toxins and toxicants concern individuals from a wide range of disciplines, and Toxics is interested in receiving papers that represent the full range of approaches applied to their study, including in vitro studies, studies that use experimental animal or non-animal models, studies of humans or other biological populations, and mathematical modeling. We are excited to get underway and look forward to working with authors in the scientific and medical communities and providing them with a novel venue for sharing their work. [...] Full article

Research

Jump to: Editorial, Review

Open AccessArticle Genotoxicity of Silver Nanoparticles in Lung Cells of Sprague Dawley Rats after 12 Weeks of Inhalation Exposure
Toxics 2013, 1(1), 36-45; doi:10.3390/toxics1010036
Received: 3 October 2013 / Revised: 6 November 2013 / Accepted: 7 November 2013 / Published: 19 November 2013
Cited by 3 | PDF Full-text (498 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Due to the widespread use of silver nanoparticles in consumer products, the toxicity of silver nanoparticles has also been studied in relation to their application. However, most genotoxicity studies of silver nanoparticles have been performed in vitro. Therefore, this study evaluated [...] Read more.
Due to the widespread use of silver nanoparticles in consumer products, the toxicity of silver nanoparticles has also been studied in relation to their application. However, most genotoxicity studies of silver nanoparticles have been performed in vitro. Therefore, this study evaluated the DNA damage to lung cells caused by repeated inhalation of silver nanoparticles. Male Sprague Dawley rats were exposed to silver nanoparticles for 12 weeks in a whole-body inhalation chamber. The animals were divided into one control group and three dose groups that were exposed to silver nanoparticles (14–15 nm diameter) at concentrations of 0.66 × 106 particles/cm3 (49 μg/m3, low dose), 1.41 × 106 particles/cm3 (117 μg/m3, middle dose), and 3.24 × 106 particles /cm3 (381 μg/m3, high dose), respectively, for six hours/day over 12 weeks. The rats were sacrificed after the 12-week exposure period and the DNA damage assessed using a Comet assay of cells obtained from the right lungs. The olive tail moment values were 2.93 ± 0.19, 3.81 ± 0.23, 3.40 ± 0.22, and 5.16 ± 0.32 for the control, low-, middle-, and high-dose groups, respectively. Although no dose-dependent results were observed, a significant increase in the level of DNA damage was noted for the high-dose group. Full article
(This article belongs to the Special Issue Feature Papers)
Open AccessArticle Chronic Exposure to Particulate Nickel Induces Neoplastic Transformation in Human Lung Epithelial Cells
Toxics 2013, 1(1), 46-59; doi:10.3390/toxics1010046
Received: 16 October 2013 / Revised: 6 November 2013 / Accepted: 14 November 2013 / Published: 25 November 2013
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Abstract
Nickel is a well-known human lung carcinogen with the particulate form being the most potent; however, the carcinogenic mechanism remains largely unknown. Few studies have investigated the genotoxicity and carcinogenicity of nickel in its target cell, human bronchial epithelial cells. Thus, the [...] Read more.
Nickel is a well-known human lung carcinogen with the particulate form being the most potent; however, the carcinogenic mechanism remains largely unknown. Few studies have investigated the genotoxicity and carcinogenicity of nickel in its target cell, human bronchial epithelial cells. Thus, the goal of this study was to investigate the effects of particulate nickel in human lung epithelial cells. We found that nickel subsulfide induced concentration- and time-dependent increases in both cytotoxicity and genotoxicity in human lung epithelial cells (BEP2D). Chronic exposure to nickel subsulfide readily induced cellular transformation, inducing 2.55, 2.9 and 2.35 foci per dish after exposure to 1, 2.5 and 5 μg/cm2 nickel subsulfide, respectively. Sixty-one, 100 and 70 percent of the foci isolated from 1, 2.5, and 5 μg/cm2 nickel subsulfide treatments formed colonies in soft agar and the degree of soft agar colony growth increased in a concentration-dependent manner. Thus, chronic exposure to particulate nickel induces genotoxicity and cellular transformation in human lung epithelial cells. Full article
(This article belongs to the Special Issue Feature Papers)
Open AccessArticle Personal Exposure to Air Pollution in Office Workers in Ireland: Measurement, Analysis and Implications
Toxics 2013, 1(1), 60-76; doi:10.3390/toxics1010060
Received: 8 October 2013 / Revised: 13 November 2013 / Accepted: 14 November 2013 / Published: 2 December 2013
Cited by 7 | PDF Full-text (990 KB) | HTML Full-text | XML Full-text
Abstract
An experimental assessment of personal exposure to PM10 in 59 office workers was carried out in Dublin; Ireland. Two hundred and fifty five samples of 24 hour personal exposure were collected in real time over a 28 month period. The investigation [...] Read more.
An experimental assessment of personal exposure to PM10 in 59 office workers was carried out in Dublin; Ireland. Two hundred and fifty five samples of 24 hour personal exposure were collected in real time over a 28 month period. The investigation included an assessment of the uptake of pollutants in the lungs during various daily activities using a Human Respiratory Tract Model. The results of the investigation showed that indoor air quality was the overriding determinant of average daily personal exposure as participants in the study spent over 92% of their time indoors. Exposure in the workplace and exposure at home were the most important microenvironments in total uptake of particulate matter. Exposure while commuting or shopping were found to play a minor role in comparison. The investigation highlighted the importance of considering pollutant uptake as well as personal exposure among receptors where variations in levels of physical activity and duration of exposure are present. Full article
(This article belongs to the Special Issue Risk Assessment of Environmental Contaminants)

Review

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Open AccessReview Inorganic Arsenic Exposure and Children’s Neurodevelopment: A Review of the Evidence
Toxics 2013, 1(1), 2-17; doi:10.3390/toxics1010002
Received: 19 August 2013 / Revised: 9 September 2013 / Accepted: 24 September 2013 / Published: 15 October 2013
Cited by 4 | PDF Full-text (429 KB) | HTML Full-text | XML Full-text
Abstract
Experimental studies suggest a myriad of mechanisms by which inorganic arsenic can interfere with central nervous system development, and, indeed, epidemiological studies published in the last dozen years suggest that exposure to arsenic impairs children’s cognitive development. Most of the studies have [...] Read more.
Experimental studies suggest a myriad of mechanisms by which inorganic arsenic can interfere with central nervous system development, and, indeed, epidemiological studies published in the last dozen years suggest that exposure to arsenic impairs children’s cognitive development. Most of the studies have been conducted in developing countries (e.g., Bangladesh, India, Mexico), where exposure to arsenic is thought to be considerably higher than it is in developed countries. This review summarizes the results of these studies, focusing in particular on issues pertinent to risk assessment, including the existence of critical windows of vulnerability, characteristics of the dose-effect relationships (e.g., the lowest adverse effect level, the functional form), the most sensitive neurodevelopmental endpoints, and potential effect modifiers such as host characteristics (e.g., methylation efficiency, sex) and co-exposures to other neurotoxicants (e.g., lead, manganese). At present, the epidemiological data do not permit firm conclusions to be drawn regarding these issues. Several factors that complicate an effort to compare the results of studies are identified, including use of a variety of indices of external and internal exposure, and inconsistency in the measurement of important potential confounders for neurodevelopmental outcomes. Full article
(This article belongs to the Special Issue Feature Papers)
Open AccessReview Ecotoxicology: The Challenges for the 21st Century
Toxics 2013, 1(1), 18-35; doi:10.3390/toxics1010018
Received: 27 September 2013 / Revised: 6 November 2013 / Accepted: 7 November 2013 / Published: 18 November 2013
Cited by 3 | PDF Full-text (584 KB) | HTML Full-text | XML Full-text
Abstract
The usual procedures for ecological risk assessment (ERA) have been based for decades on simplified approaches in order to provide basic information on the huge amount of chemicals introduced into the environment. These approaches allowed the development of international regulatory tools capable [...] Read more.
The usual procedures for ecological risk assessment (ERA) have been based for decades on simplified approaches in order to provide basic information on the huge amount of chemicals introduced into the environment. These approaches allowed the development of international regulatory tools capable of substantially reducing the adverse effects on ecosystems in developed countries. Nevertheless, these approaches suffer from a lack of ecological realism and are poorly suitable for understanding the actual consequences for ecosystem health. The need for more ecologically-based approaches is now recognized by the scientific community and has been highlighted by a recent document of the European Commission. In this paper, a synthesis is presented of the most important issues and the need for research to improve the ecological realism of exposure and effect assessment and the tools that should be developed to reach this objective. In particular, the major challenges are the following: the effects of variable exposure patterns; the vulnerability of ecosystems; the indirect ecological effects; the responses to multiple stress factors; the improvement of ecological modeling. The possibilities for using new scientific achievements in regulatory ERA are also discussed. Full article
(This article belongs to the Special Issue Feature Papers)

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