Virginia Buchner

Neurotoxic Effects and Biomarkers of Lead Exposure: A Review

Lead, a systemic toxicant affecting virtually every organ system, primarily affects the central nervous system, particularly the developing brain. Consequently, children are at a greater risk than adults of suffering from the neurotoxic effects of lead. To date, no safe lead-exposure threshold has been identified. The ability of lead to pass through the blood-brain barrier is due in large part to its ability to substitute for calcium ions. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurologic disorders. At the molecular level, lead interferes with the regulatory action of calcium on cell functions and disrupts many intracellular biological activities. Experimental studies have also shown that lead exposure may have genotoxic effects, especially in the brain, bone marrow, liver, and lung cells. Knowledge of the neurotoxicology of lead has advanced in recent decades due to new information on its toxic mechanisms and cellular specificity. This paper presents an overview, updated to January 2009, of the neurotoxic effects of lead with regard to children, adults, and experimental animals at both cellular and molecular levels, and discusses the biomarkers of lead exposure that are useful for risk assessment in the field of environmental health.

Health effects of uranium: new research findings.

Abstract Recent plans for a nuclear renaissance in both established and emerging economies have prompted increased interest in uranium mining. With the potential for more uranium mining worldwide and a growth in the literature on the toxicology and epidemiology of uranium and uranium mining, we found it timely to review the current state of knowledge. Here, we present a review of the health effects of uranium mining, with an emphasis on newer findings (2005–2011). Uranium mining can contaminate air, water, and soil. The chemical toxicity of the metal constitutes the primary environmental health hazard, with the radioactivity of uranium a secondary concern. The update of the toxicologic evidence on uranium adds to the established findings regarding nephrotoxicity, genotoxicity, and developmental defects. Additional novel toxicologic findings, including some at the molecular level, are now emerging that raise the biological plausibility of adverse effects on the brain, on reproduction, including estrogenic effects, on gene expression, and on uranium metabolism. Historically, most epidemiology on uranium mining has focused on mine workers and radon exposure. Although that situation is still overwhelmingly true, a smaller emerging literature has begun to form around environmental exposure in residential areas near uranium mining and processing facilities. We present and critique such studies. Clearly, more epidemiologic research is needed to contribute to causal inference. As much damage is irreversible, and possibly cumulative, present efforts must be vigorous to limit environmental uranium contamination and exposure.

Exploring the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity: a literature review

Abstract Nickel, a naturally occurring element that exists in various mineral forms, is mainly found in soil and sediment, and its mobilization is influenced by the physicochemical properties of the soil. Industrial sources of nickel include metallurgical processes such as electroplating, alloy production, stainless steel, and nickel-cadmium batteries. Nickel industries, oil- and coal-burning power plants, and trash incinerators have been implicated in its release into the environment. In humans, nickel toxicity is influenced by the route of exposure, dose, and solubility of the nickel compound. Lung inhalation is the major route of exposure for nickel-induced toxicity. Nickel can also be ingested or absorbed through the skin. The primary target organs are the kidneys and lungs. Other organs such as the liver, spleen, heart, and testes can also be affected to a lesser extent. Although the most common health effect is an allergic reaction, research has also demonstrated that nickel is carcinogenic to humans. The focus of the present review is on recent research concerning the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity. We first present a background on the occurrence of nickel in the environment, human exposure, and human health effects.

Environmental Toxicology and Health Effects Associated with Hexachlorobenzene Exposure

The synthetic industrial chemical hexachlorobenzene (HCB) is a white crystalline solid compound. The substance is a bioaccumulative, persistent, and toxic pollutant. Historically HCB was commonly used as a pesticide and fungicide. Although HCB production and use has ceased in many countries, the compound is still generated inadvertently, as a byproduct and/or impurity in the manufacture of various chlorinated compounds, and released into the environment. Hexachlorobenzene is ubiquitous in air, water, soil, and biological matrices, as well as in major environmental compartments. Exposure to this substance is a public health concern because of its association with a wide range of adverse health effects. The International Agency for Research on Cancer and the United States Environmental Protection Agency classify HCB as a probable human carcinogen. Although globally the consumption of HCB-contaminated food is the principal source of environmental exposure, exposure can also occur through the inhalation of HCB-contaminated air, by dermal contact, or through in utero exposure and breast milk. In addition to cancer, the human health effects associated with HCB exposure involve systemic impairment (thyroid, liver, bone, skin), as well as damage to the kidneys and blood cells and the immune, endocrine, developmental, and nervous systems. In this review, we discuss the sources of HCB and the potential for human exposure, as well as systemic, carcinogenic, and teratogenic health effects.

Radium in the environment: exposure pathways and health effects.

Abstract Radium is a naturally occurring radioactive element in the environment that can exist as several isotopes. Little information is available on the acute (short-term) non-cancer effects in humans. Radium exposure has resulted in acute leukopenia, anemia, necrosis of the jaw, and other effects. Cancer is the major effect of concern. Radium, via oral exposure, is known to cause bone, head, and nasal passage tumors in humans. The US Environmental Protection Agency has not classified radium for carcinogenicity.

Climbing a Ladder: A Step-by-Step Approach to Understanding the Concept of Agroecosystem Health

Population and individual health is linked to agroecosystem health. To comprehend the concept of agroecosystem health, one should climb a ladder consisting of several successive steps, each rung presenting a certain degree of instability (conceptual difficulty and uncertainty) in an advisable but not inevitable order. Here we suggest a ladder consisting of the following concepts: ecosystem, agroecosystem, biodiversity, sustainability, ecosystem health, and agroecosystem health. Although these concepts are to a certain extent well understood and grasped by scientists, politicians, natural resource managers, and environmentalists, some steps are still highly debatable, unclear, and present a considerable degree of reluctance to be defined and understood. Consequently, much empirical and theoretical effort must be made to construct solid conceptual ladders made up of such steps. In this enterprise, a traditional reductionistic approach confining interpretations to narrow scientific disciplines is unadvisable. Holistic, transdisciplinary approaches are required to reach the desired goal.

Letter from the Editor: Introducing our new publisher

No abstract available

Methodological lessons and pilot data on the effect of proximity of homes and schools to highways on pediatric asthma and lung function

Abstract Purpose: Numerous studies have found that either living or attending school near highways or exposure to pollutants associated with heavy motor vehicle traffic are associated with a high prevalence of asthma and reduced lung function. Yet, few investigations have assessed school and home exposure in the same study. Methods: We recruited children aged 5–19 years from a pediatric clinic in an urban center (Boston Chinatown) for many of whom housing and school were located immediately adjacent to two major highways. A questionnaire was used to assess self-report of diagnosis of asthma and the proximity of schools and homes to highways, as well as basic demographic information. Spirometric lung function data were obtained and reviewed by a pediatric pulmonologist blinded to survey responses. During this review, we excluded lung function tests of low quality. Results: The analyses did not demonstrate any associations or mean differences between near-highway exposure at school, at home, or both with diagnosed asthma (p>0.10, n=124). For the lung function data (n=87), neither direct measures (FEV1, FVC, and FEF25–75) nor ratio measures (FEV1/FVC and FEF25–75/FVC) had a significant association with near-highway exposure (p>0.10). Certain predisposing factors, such as diagnosed allergies and family history of asthma, were strongly associated with diagnosed asthma (p<0.05 and p=0.001, respectively), findings we have seen consistently in other work with children recruited from the same clinic. We also found that exposure to pests was significantly correlated with a smaller FEF25–75/FVC ratio (p=0.02). Conclusions: Our findings suggest that either limitations in our study design restricted our ability to see the associations reported by others or that such associations do not exist in this population. One possibility is that in this community, with heavy street traffic and many street canyons, the gradient of exposure next to the highway is not very well delineated by simple proximity.