Defining Cyber Security and Cyber Security Risk within a Multidisciplinary Context using Expert Elicitation.

It is important to have and use standardized terminology and develop a comprehensive common understanding of what is meant by cyber security and cyber security risk given the multidisciplinary nature of cyber security and the pervasiveness of cyber security concerns throughout society. Using expert elicitation methods, collaborating cyber researchers from multiple disciplines and two sectors (academia, government-military) were individually interviewed and asked to define cyber security and cyber security risk. Data-driven thematic analysis was used to identify the most salient themes within each definition, sector, and cyber expert group as a whole with results compared to current standards definitions. Network analysis was employed to visualize the interconnection of salient themes within and across sectors and disciplines. When examined as a whole group, "context-driven," "resilient system functionality," and "maintenance of CIA (confidentiality, integrity, availability)" were the most salient themes and influential network nodes for the definition of cyber security, while "impacts of CIA vulnerabilities," "probabilities of outcomes," and "context-driven" were the most salient themes for cyber security risk. We used this expert elicitation process to develop comprehensive definitions of cyber security (cybersecurity) and cyber security risk that encompass the contextual frameworks of all the disciplines represented in the collaboration and explicitly incorporates human factors as significant cyber security risk factors.

Parameterization Framework and Quantification Approach for Integrated Risk and Resilience Assessments.

A growing challenge for risk, vulnerability, and resilience assessment is the ability to understand, characterize, and model the complexities of our joint socioecological systems, often delineated with differing natural (e.g., watershed) and imposed (e.g., political) boundaries at the landscape scale. To effectively manage such systems in the increasingly dynamic, adaptive context of environmental change, we need to understand not just food web interactions of contaminants or the flooding impacts of sea level rise and storm surges, but rather the interplay between social and ecological components within the inherent and induced feedforward and feedback system mechanisms. Risk assessment, in its traditional implementation, is a simplification of a complex problem to understand the basic cause-and-effect relationships within a system. This approach allows risk assessors to distill a complex issue into a manageable model that quantifies, or semiquantifies, the effects of an adverse stressor. Alternatively, an integrated risk and resilience assessment moves toward a solution-based assessment with the incorporation of adaptive management practices as 1 of 4 parts of system resilience (i.e., prepare, absorb, recover, and adapt), and directly considers the complexities of the systems being modeled. We present the Multilevel Risk and Resilience Assessment Parameterization framework for the systematic parameterization and deconstruction of management objectives and goals into assessment metrics and quantifiable risk measurement metrics and complementary resilience measurement metrics. As a proof-of-concept, the presented framework is paired with the Bayesian Network-Relative Risk Model for a human-focused subset of a larger risk and resilience assessment of climate change impacts within the Charleston Harbor Watershed of South Carolina. This new parameterization framework goes beyond traditional simplification and embraces the complexity of the system as a whole, which is necessary for a more representative analysis of an open, dynamic complex system. Integr Environ Assess Manag 2021;17:131-146. © 2020 The Authors. Integrated Environmental Assessment and Management published by Wiley Periodicals LLC on behalf of Society of Environmental Toxicology & Chemistry (SETAC).

Characterizing and Measuring Maliciousness for Cybersecurity Risk Assessment.

Cyber attacks have been increasingly detrimental to networks, systems, and users, and are increasing in number and severity globally. To better predict system vulnerabilities, cybersecurity researchers are developing new and more holistic approaches to characterizing cybersecurity system risk. The process must include characterizing the human factors that contribute to cyber security vulnerabilities and risk. Rationality, expertise, and maliciousness are key human characteristics influencing cyber risk within this context, yet maliciousness is poorly characterized in the literature. There is a clear absence of literature pertaining to human factor maliciousness as it relates to cybersecurity and only limited literature relating to aspects of maliciousness in other disciplinary literatures, such as psychology, sociology, and law. In an attempt to characterize human factors as a contribution to cybersecurity risk, the Cybersecurity Collaborative Research Alliance (CSec-CRA) has developed a Human Factors risk framework. This framework identifies the characteristics of an attacker, user, or defender, all of whom may be adding to or mitigating against cyber risk. The maliciousness literature and the proposed maliciousness assessment metrics are discussed within the context of the Human Factors Framework and Ontology. Maliciousness is defined as the intent to harm. Most maliciousness cyber research to date has focused on detecting malicious software but fails to analyze an individual's intent to do harm to others by deploying malware or performing malicious attacks. Recent efforts to identify malicious human behavior as it relates to cybersecurity, include analyzing motives driving insider threats as well as user profiling analyses. However, cyber-related maliciousness is neither well-studied nor is it well understood because individuals are not forced to expose their true selves to others while performing malicious attacks. Given the difficulty of interviewing malicious-behaving individuals and the potential untrustworthy nature of their responses, we aim to explore the maliciousness as a human factor through the observable behaviors and attributes of an individual from their actions and interactions with society and networks, but to do so we will need to develop a set of analyzable metrics. The purpose of this paper is twofold: (1) to review human maliciousness-related literature in diverse disciplines (sociology, economics, law, psychology, philosophy, informatics, terrorism, and cybersecurity); and (2) to identify an initial set of proposed assessment metrics and instruments that might be culled from in a future effort to characterize human maliciousness within the cyber realm. The future goal is to integrate these assessment metrics into holistic cybersecurity risk analyses to determine the risk an individual poses to themselves as well as other networks, systems, and/or users.

Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation.

This review aims to cover experimental data on oxidative effects of low-intensity radiofrequency radiation (RFR) in living cells. Analysis of the currently available peer-reviewed scientific literature reveals molecular effects induced by low-intensity RFR in living cells; this includes significant activation of key pathways generating reactive oxygen species (ROS), activation of peroxidation, oxidative damage of DNA and changes in the activity of antioxidant enzymes. It indicates that among 100 currently available peer-reviewed studies dealing with oxidative effects of low-intensity RFR, in general, 93 confirmed that RFR induces oxidative effects in biological systems. A wide pathogenic potential of the induced ROS and their involvement in cell signaling pathways explains a range of biological/health effects of low-intensity RFR, which include both cancer and non-cancer pathologies. In conclusion, our analysis demonstrates that low-intensity RFR is an expressive oxidative agent for living cells with a high pathogenic potential and that the oxidative stress induced by RFR exposure should be recognized as one of the primary mechanisms of the biological activity of this kind of radiation.

GSM 900 MHz cellular phone radiation can either stimulate or depress early embryogenesis in Japanese quails depending on the duration of exposure.

PURPOSE: Our study was designed to assess the effects of low intensity radiation of a GSM (Global System for Mobile communication) 900 MHz cellular phone on early embryogenesis in dependence on the duration of exposure. MATERIALS AND METHODS: Embryos of Japanese Quails were exposed in ovo to GSM 900 MHz cellular phone radiation during initial 38 h of brooding or alternatively during 158 h (120 h before brooding plus initial 38 h of brooding) discontinuously with 48 sec ON (average power density 0.25 µW/cm(2), specific absorption rate 3 µW/kg) followed by 12 sec OFF intervals. A number of differentiated somites were assessed microscopically. Possible DNA damage evoked by irradiation was assessed by an alkaline comet assay. RESULTS: Exposure to radiation from a GSM 900 MHz cellular phone led to a significantly altered number of differentiated somites. In embryos irradiated during 38 h the number of differentiated somites increased (p < 0.001), while in embryos irradiated during 158 h this number decreased (p < 0.05). The lower duration of exposure led to a significant (p < 0.001) decrease in a level of DNA strand breaks in cells of 38-h embryos, while the higher duration of exposure resulted in a significant (p < 0.001) increase in DNA damage as compared to the control. CONCLUSION: Effects of GSM 900 MHz cellular phone radiation on early embryogenesis can be either stimulating or deleterious depending on the duration of exposure.

GSM 900 MHz microwave radiation affects embryo development of Japanese quails.

A wide range of non thermal biological effects of microwave radiation (MW) was revealed during the last decades. A number of reports showed evident hazardous effects of MW on embryo development in chicken. In this study, we aimed at elucidating the effects of MW emitted by a commercial model of GSM 900 MHz cell phone on embryo development in quails (Coturnix coturnix japonica) during both short and prolonged exposure. For that, fresh fertilized eggs were irradiated during the first 38 h or 14 days of incubation by a cell phone in "connecting" mode activated continuously through a computer system. Maximum intensity of incident radiation on the egg's surface was 0.2 µW/cm2.The irradiation led to a significant (p<0.001) increase in numbers of differentiated somites in 38-hour exposed embryos and to a significant (p<0.05) increase in total survival of embryos from exposed eggs after 14 days exposure. We hypothesized that observed facilitating effect was due to enhancement of metabolism in exposed embryos provoked via peroxidation mechanisms. Indeed, a level of thiobarbituric acid (TBA) reactive substances was significantly (p<0.05-0.001) higher in brains and livers of hatchlings from exposed embryos. Thus, observed effects of radiation from commercial GSM 900 MHz cell phone on developing quail embryos signify a possibility for non-thermal impact of MW on embryogenesis. We suggest that the facilitating effect of low doses of irradiation on embryo development can be explained by a hormesis effect induced by reactive oxygen species (ROS). Future studies need to be done to clarify this assumption.

Acceleration of the meckel syndrome by near-infrared light therapy.

BACKGROUND/AIMS: Phototherapy using a narrow-band, near-infrared (NIR) light (using a light-emitting diode, LED) is being used to treat certain medical conditions. This narrow-band red light has been shown to stimulate cytochrome c oxidase (CCO) in mitochondria that would stimulate ATP production and has the ability to stimulate wound healing. LED treatment also decreases chemical-induced oxidative stress in tested systems. As renal cystic diseases are known to have evidence of oxidative stress with reduced antioxidant protection, we hypothesized that NIR light therapy might ameliorate the renal pathology in renal cystic disease. METHODS: Wistar-Wpk/Wpk rats with Meckel syndrome (MKS) were treated with light therapy on days 10-18 at which time disease severity was evaluated. Wpk rats were either treated daily for 80 s with narrow-band red light (640-690 nm wavelength) or sham treated. At termination, renal and cerebral pathology was evaluated, and renal expression and activity of enzymes were assessed to evaluate oxidative stress. Blood was collected for blood urea nitrogen (BUN) determination, the left kidney frozen for biochemical evaluation, and the right kidney and head fixed for morphological evaluation. RESULTS: There were no significant effects of LED treatment on body weight (BW) or total kidney weight in non-cystic rats. Total kidney weight was increased and anephric BW was decreased in cystic versus non-cystic controls. LED reduced BW and total kidney weight in cystic rats compared to non-light-treated cystic (control) rats. BUN was already increased almost 6-fold in cystic rats compared to control rats. BUN was further increased almost 2-fold with NIR treatment in both non-cystic and cystic rats compared to cystic and control rats. The hydrocephalus associated with Wpk/Wpk (ventricular volume expressed as total volume and as percent of anephric BW) was also more severe in NIR-treated cystic rats compared to the normal control rats. Renal glutathione peroxidase and catalase (CAT) were reduced in the cystic kidney while superoxide dismutase and CCO were increased. NIR increased CAT and CCO, marginally decreased glutathione S-transferase and slightly decreased glutathione reductase in cystic rats compared to the normal control rats. The detrimental effects of NIR may be related to reduced renal blood flow associated with progression of cystic pathology. Compression by cysts may not allow sufficient oxygen or nutrient supply necessary to support the increased oxidative phosphorylation-associated cellular activity, and the increased demand induced by NIR-increased CCO may have created further oxidative stress. CONCLUSION: LED phototherapy initiated after the onset of symptoms was detrimental to MKS-induced pathology. NIR stimulates CCO thereby increasing the kidney's need for oxygen. We hypothesize that cystic compression of the vasculature impairs oxygen availability and the enhanced CCO activity produces more radicals, which are not sufficiently detoxified by the increased CAT activity.

Effects of low-level light therapy on streptozotocin-induced diabetic kidney.

Hyperglycemia causes oxidative damage in tissues prone to complications in diabetes. Low-level light therapy (LLLT) in the red to near infrared range (630-1000nm) has been shown to accelerate diabetic wound healing. To test the hypothesis that LLLT would attenuate oxidative renal damage in Type I diabetic rats, male Wistar rats were made diabetic with streptozotocin (50mg/kg, ip), and then exposed to 670nm light at a dose of 9J/cm(2) once per day for 14weeks. The activity and expression of catalase and the activity of Na K-ATPase increased in kidneys of light-treated diabetic rats, whereas the activity and expression of glutathione peroxidase and the expression of Na K-ATPase were unchanged. LLLT lowered the values of serum BUN, serum creatinine, and BUN/creatinine ratio. In addition, LLLT augmented the activity and expression of cytochrome c oxidase, a primary photoacceptor molecule in the mitochondrial respiratory chain, and reduced the formation of the DNA adduct 8-hydroxy-2'-deoxyguanosine in kidney. LLLT improved renal function and antioxidant defense capabilities in the kidney of Type I diabetic rats. Thus, 670nm LLLT may be broadly applicable to the amelioration of renal complications induced by diabetes that disrupt antioxidant defense mechanisms.

The Pine River statement: human health consequences of DDT use.

OBJECTIVES: Dichlorodiphenyltrichloroethane (DDT) was used worldwide until the 1970s, when concerns about its toxic effects, its environmental persistence, and its concentration in the food supply led to use restrictions and prohibitions. In 2001, more than 100 countries signed the Stockholm Convention on Persistent Organic Pollutants (POPs), committing to eliminate the use of 12 POPs of greatest concern. However, DDT use was allowed for disease vector control. In 2006, the World Health Organization and the U.S. Agency for International Development endorsed indoor DDT spraying to control malaria. To better inform current policy, we reviewed epidemiologic studies published from 2003 to 2008 that investigated the human health consequences of DDT and/or DDE (dichlorodiphenyldichloroethylene) exposure. DATA SOURCES AND EXTRACTION: We conducted a PubMed search in October 2008 and retrieved 494 studies. DATA SYNTHESIS: Use restrictions have been successful in lowering human exposure to DDT, but blood concentrations of DDT and DDE are high in countries where DDT is currently being used or was more recently restricted. The recent literature shows a growing body of evidence that exposure to DDT and its breakdown product DDE may be associated with adverse health outcomes such as breast cancer, diabetes, decreased semen quality, spontaneous abortion, and impaired neurodevelopment in children. CONCLUSIONS: Although we provide evidence to suggest that DDT and DDE may pose a risk to human health, we also highlight the lack of knowledge about human exposure and health effects in communities where DDT is currently being sprayed for malaria control. We recommend research to address this gap and to develop safe and effective alternatives to DDT.

Effects of low-level light therapy on hepatic antioxidant defense in acute and chronic diabetic rats.

Diabetes causes oxidative stress in the liver and other tissues prone to complications. Photobiomodulation by near infrared light (670 nm) has been shown to accelerate diabetic wound healing, improve recovery from oxidative injury in the kidney, and attenuate degeneration in retina and optic nerve. The present study tested the hypothesis that 670 nm photobiomodulation, a low-level light therapy, would attenuate oxidative stress and enhance the antioxidant protection system in the liver of a model of type I diabetes. Male Wistar rats were made diabetic with streptozotocin (50 mg/kg, ip) then exposed to 670 nm light (9 J/cm(2)) once per day for 18 days (acute) or 14 weeks (chronic). Livers were harvested, flash frozen, and then assayed for markers of oxidative stress. Light treatment was ineffective as an antioxidant therapy in chronic diabetes, but light treatment for 18 days in acutely diabetic rats resulted in the normalization of hepatic glutathione reductase and superoxide dismutase activities and a significant increase in glutathione peroxidase and glutathione-S transferase activities. The results of this study suggest that 670 nm photobiomodulation may reduce, at least in part, acute hepatic oxidative stress by enhancing the antioxidant defense system in the diabetic rat model.

Attenuation of TCDD-induced oxidative stress by 670 nm photobiomodulation in developmental chicken kidney.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a potent developmental teratogen inducing oxidative stress and sublethal changes in multiple organs, provokes developmental renal injuries. In this study, we investigated TCDD-induced biochemical changes and the therapeutic efficacy of photobiomodulation (670 nm; 4 J/cm(2)) on oxidative stress in chicken kidneys during development. Eggs were injected once prior to incubation with TCDD (2 pg/g or 200 pg/g) or sunflower oil vehicle control. Half of the eggs in each dose group were then treated with red light once per day through embryonic day 20 (E20). Upon hatching at E21, the kidneys were collected and assayed for glutathione peroxidase, glutathione reductase, catalase, superoxide dimutase, and glutathione-S-transferase activities, as well as reduced glutathione and ATP levels, and lipid peroxidation. TCDD exposure alone suppressed the activity of the antioxidant enzymes, increased lipid peroxidation, and depleted available ATP. The biochemical indicators of oxidative and energy stress in the kidney were reversed by daily phototherapy, restoring ATP and glutathione contents and increasing antioxidant enzyme activities to control levels. Photobiomodulation also normalized the level of lipid peroxidation increased by TCDD exposure. The results of this study suggest that 670 nm photobiomodulation may be useful as a noninvasive treatment for renal injury resulting from chemically induced cellular oxidative and energy stress.

Melatonin as a principal component of red light therapy.

Melatonin is well recognized for its role as a potent antioxidant and is directly implicated in the free radical theory of aging [1] [Reiter RJ, Pablos MI, Agapito TT, Guerrero JM. Melatonin in the context of the free radical theory of aging. Ann N Y Acad Sci 1996;786:362-78]. Moreover, melatonin has been shown to retard age-related increases in lipid peroxidation and oxidative damage [2] [Okatani Y, Wakatsuki A, Reiter RJ. Melatonin protects hepatic mitochondrial respiratory chain activity in senescence-accelerated mice. J Pineal Res 2002;32:143-8] and to act directly upon the immune system [3] [Poon AM, Liu ZM, Pang CS, Brown GM, Pang SF. Evidence for a direct action of melatonin on the immune system. Biol Signals 1994;3:107-17]. This report focuses on characterizing documented functions of melatonin in the context of red light therapy and proposes that melatonin is a potential mediator of red light's therapeutic effects, a hypothesis that is as yet untested. Red light therapy (670 nm, 4J/cm(2)) has been shown to restore glutathione redox balance upon toxicological insult and enhance both cytochrome c oxidase and energy production, all of which may be affected by melatonin. The red light treatment has also been successfully implemented in the clinical setting for its effectiveness in reducing both the number of incidences and severity of oral mucositis resulting in part from the chemotherapy and/or radiation administered prior to bone marrow transplants. Moreover, red light therapy improves wound healing and is being further tested for its ability to ameliorate toxicant-induced retinal and visual cortical neuron damage. Researchers in the growing field of light therapy may be in a position to draw from and collaborate with melatonin researchers to better characterize this alternative treatment.

670 nanometer light treatment attenuates dioxin toxicity in the developing chick embryo.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an acutely toxic anthropogenic chemical. Treatment with a red to near-infrared (630-1000 nm) light-emitting diode (LED) attenuates the toxicant-induced oxidative stress and energy deficit in neuronal cell culture. For this study, fertile chicken (Gallus gallus) eggs were injected once at the start of incubation with sunflower oil vehicle or 200 pg TCDD/g egg (200 parts per trillion), an environmentally relevant dose. Daily LED treatment after TCDD exposure reduced embryonic mortality by 47%. LED treatment of TCDD-exposed eggs also decreased the hepatic oxidized-to-reduced glutathione ratio by 88%. Activities of other hepatic indicators of oxidative stress, such as glutathione reductase and catalase, were increased after LED treatment of TCDD-exposed eggs. Our study demonstrates that 670 nm phototherapy can mitigate the oxidative stress and energy deficit resulting from developmental exposure to TCDD while reducing TCDD-induced embryo mortality. Moreover, LED treatment restores hepatic enzyme activities to control levels in TCDD-exposed embryos. The effective attenuation of TCDD-induced embryo toxicity by LED treatment could extend to mitigating the effects of other teratogens that induce oxidative and energy stress.

Brief report: embryonic growth and hatching implications of developmental 670-nm phototherapy and dioxin co-exposure.

OBJECTIVE: We assessed the effect of 670-nm light therapy on growth and hatching kinetics in chickens (Gallus gallus) exposed to dioxin. BACKGROUND DATA: Photobiomodulation has been shown to stimulate signaling pathways resulting in improved energy metabolism, antioxidant production, and cell survival. In ovo treatment with 670-nm light-emitting diode (LED) arrays improves hatching success and increases hatchling size in control chickens. Under conditions where developmental dioxin exposure is above the lethality threshold (100 ppt), phototherapy attenuates dioxin-induced early embryonic death. We hypothesized that 670-nm LED therapy would attenuate dioxin-induced developmental anomalies and increase hatching success. METHODS: Fertile chicken eggs were injected with control oil, 2, 20, or 200 ppt dioxin, or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prior to the start of incubation. Half of the eggs in each dose group were treated once per day from embryonic days 0-20 with 670-nm LED light at a fluence of 4 J/cm2. Hatchling size, organ weights, and energy parameters were compared between dose groups and LED treatment. RESULTS: LED therapy resulted in earlier pip times (small hole created 12-24 h prior to hatch), and increased hatchling size and weight in the 200 ppt dose groups. However, there appears to be an LED-oil interaction within the oil-treated controls that results in longer hatch times and decreased liver weight within the LED control dose groups in comparison to the non-LED control dose groups. CONCLUSION: Size and hatching times suggest that the hatching success and preparedness of chicks developmentally exposed to dioxin concentrations above the lethality threshold is improved by 670-nm LED treatment administered throughout the gestation period, but the relationship may be complicated by an LED-oil interaction.

Clinical and experimental applications of NIR-LED photobiomodulation.

This review presents current research on the use of far-red to near-infrared (NIR) light treatment in various in vitro and in vivo models. Low-intensity light therapy, commonly referred to as "photobiomodulation," uses light in the far-red to near-infrared region of the spectrum (630-1000 nm) and modulates numerous cellular functions. Positive effects of NIR-light-emitting diode (LED) light treatment include acceleration of wound healing, improved recovery from ischemic injury of the heart, and attenuated degeneration of injured optic nerves by improving mitochondrial energy metabolism and production. Various in vitro and in vivo models of mitochondrial dysfunction were treated with a variety of wavelengths of NIR-LED light. These studies were performed to determine the effect of NIR-LED light treatment on physiologic and pathologic processes. NIRLED light treatment stimulates the photoacceptor cytochrome c oxidase, resulting in increased energy metabolism and production. NIR-LED light treatment accelerates wound healing in ischemic rat and murine diabetic wound healing models, attenuates the retinotoxic effects of methanol-derived formic acid in rat models, and attenuates the developmental toxicity of dioxin in chicken embryos. Furthermore, NIR-LED light treatment prevents the development of oral mucositis in pediatric bone marrow transplant patients. The experimental results demonstrate that NIR-LED light treatment stimulates mitochondrial oxidative metabolism in vitro, and accelerates cell and tissue repair in vivo. NIR-LED light represents a novel, noninvasive, therapeutic intervention for the treatment of numerous diseases linked to mitochondrial dysfunction.

External heart deformities in passerine birds exposed to environmental mixtures of polychlorinated biphenyls during development.

Necropsy-observable cardiac deformities were evaluated from 283 nestling passerines collected from one reference site and five polychlorinated biphenyl (PCB)-contaminated sites around Bloomington and Bedford, Indiana, USA. Hearts were weighed and assessed on relative scales in three dimensions (height, length, and width) and for externally visible deformities. Heart weights normalized to body weight (heart somatic index) were decreased significantly at the more contaminated sites in both house wren (Troglodytes aedon) and tree swallow (Tachycineta bicolor). Heart somatic indices significantly correlated with log PCB concentrations in Carolina chickadee (Parus carolinesis) and tree swallow and with log 2,3,7,8-tetrachlorodibenzo-p-dioxin toxic equivalent values in tree swallow alone. Ventricular length was increased significantly in eastern bluebirds (Sialia sialis) and decreased significantly in Carolina chickadee and tree swallow from contaminated sites versus the reference site. Heart length regressed significantly against the log PCB concentrations (Carolina chickadee and tree swallow) or the square of the PCB concentrations (red-winged blackbird [Agelaius phoeniceus]) in a sibling bird. The deformities that were observed most at the contaminated sites included abnormal tips (pointed, rounded, or flattened), center rolls, macro- and microsurface roughness, ventricular indentations on the ventral or dorsal surface, lateral ventricular notches, visibly thin ventricular walls, and changes in overall heart shape. A pooled heart deformity index regressed significantly against the logged contaminant concentrations for all species except red-winged blackbird. These results indicate that developmental changes in heart morphometrics and shape abnormalities are quantifiable and may be sensitive and useful indicators of PCB-related developmental impacts across many avian species.

Survivorship and mortality implications of developmental 670-nm phototherapy: dioxin co-exposure.

OBJECTIVE: We assessed the effect of 670-nm light therapy on dioxin-induced embryonic mortality in chickens (Gallus gallus). BACKGROUND DATA: Developmental photobiomodulation using 670-nm light-emitting diode (LED) arrays improves hatching success and increases body size in hatchling chickens. Photobiomodulation also stimulates signaling pathways resulting in improved energy metabolism, antioxidant production and cell survival. Dioxin causes embryonic mortality, including increases in the frequency of chicken embryos that pip but can't go to hatch. We hypothesized that 670-nm LED therapy would attenuate dioxin-induced embryo mortality. METHODS: Fertile chicken eggs were injected with control or 2, 20, or 200 ppt 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) prior to the start of incubation. Half of the eggs in each dose group were treated once per day from embryonic days 0-20 with 670-nm LED light at a fluence of 4 J/cm(2). In ovo survival and hatching success were compared between dose groups and LED treatment. RESULTS: LED therapy decreased the embryonic mortality rate by 41%, resulting in increased embryonic survival and improved hatching success in eggs exposed to 200 ppt dioxin. However, at sub-lethal dioxin concentrations and in oil-treated controls, LED therapy slightly increased mortality. CONCLUSION: Overall survivorship and hatching success of chicks developmentally exposed to dioxin concentrations above the lethality threshold (>100 ppt TCDD) is improved by 670-nm LED treatment administered throughout the gestation period, but the relationship may be complicated by an LED-oil interaction.

An investigation of the relationship between air emissions of volatile organic compounds and the incidence of cancer in Indiana counties.

Cancer is a health endpoint influenced by a multitude of factors, including genetic history, individual behavior, and environmental insults. The ubiquity of toxicants in the environment has raised questions about the extent of their role in causing cancer in humans. More specifically, it is desirable to understand the cancer incidence due to airborne toxicants in anthropogenic pollution. One particular class of such pollutants is volatile organic compounds (VOCs). This paper reports an epidemiological investigation of the incidence of cancer in the 92 counties of Indiana. We evaluated the relationship between the amount of VOCs released in each county, as reported by the Toxic Release Inventory, and the county-by-county incidence of various types of cancer, especially those of less common organ systems not directly associated with the absorption or distribution of toxicants. Our evaluation considered chlorinated versus nonchlorinated emissions as well as stack versus fugitive emissions. We evaluated three models: linear, quadratic, and polynomial. Of these, the quadratic model appeared to be the best predictor (highest r2) for most endpoints for which there was a positive correlation. However, the linear model was the most sensitive (lowest P-value) for skin, melanoma, and endocrine-related cancers, including female genital system cancers. Our results indicate a relationship between emissions of VOCs and the incidence of some types of cancers. Most notable were strong correlations between VOC emissions and cancers of the brain, nervous system, endocrine system, and skin.

Site specific PCB-correlated interspecies differences in organ somatic indices.

We correlated site specific differences in the organ somatic indices of nestlings of five passerine species (tree swallow, red-winged blackbird, house wren, Carolina chickadee, and eastern bluebird) with the degree of polychlorinated biphenyls (PCB) exposure in ovo and post-hatching. The birds were exposed to PCBs at or downstream of four PCB-contaminated sites. Of the organs evaluated for this paper, brain, bursa, heart, kidneys, lungs, pancreas, spleen, stomach, and thyroid varied significantly (p<0.05) or marginally significantly (0.05