Environews
FOCUS | The Carbon Footprint of Biofuels: Can We Shrink It Down to Size in Time?
With excessive carbon emissions cited as a chief culprit in anthropogenic climate change, our dependence on fossil fuel energy is affecting more than our wallets. The urgent need to curb carbon emissions is driving the search for cleaner, more sustainable sources of energy. Biofuels are being held up as one such source. But how much more environmentally sound are these fuels, anyway? This article (p. A246) discusses the carbon impact of various biofuels, and examines agricultural trends and possible policies that could affect future development and use of these fuels.
SPHERES OF INFLUENCE | Food vs. Fuel: Diversion of Crops Could Cause More Hunger
Recent grain shortages around the globe are shining the spotlight on how we distribute the world's food supply to its population. As more grain crops are earmarked for biofuel production, some fear that access to food—especially for those in poorer developing countries—could become even more difficult than it already is. Others argue that diverting grains to biofuels provides needed relief from gasoline use and need not result in food scarcity. This article (p. A254) takes a look at both sides of the debate.
Review
AUTOIMMUNE DISEASE | Lupus: Environment and Mechanisms of Disease
In this review Cooper et al. (p. 695) summarize the research on mechanisms of environmental agents that may be involved in the pathogenesis of lupus, noting three exposures that have been the focus of research in this area. To further understand the environmental influences on lupus and other autoimmune diseases, the authors recommend the development and use of animal models with varying degrees of penetrance and manifestations of disease; identification of molecular or physiologic targets of specific exposures; development and use of improved exposure assessment methodologies; multisite collaborations designed to examine understudied environmental exposures in humans; and further study of gene–environment interactions in humans and animals.
Research
CARCINOGENESIS | Selenium Inhibition of Arsenic Cocarcinogenesis
Arsenite, which is carcinogenically inactive, enhances ultraviolet radiation (UVR) carcinogenesis in hairless mice. Dietary organoselenium blocked the enhancement of UVR carcinogenesis by arsenic but did not affect UVR cancer induction. Burns et al. (p. 703) examined whether coincident or divergent tissue distributions in mouse skin explain how selenium blocks As enhancement. Supplemental Se prevented even a trace of As in skin. Traces of the seleno-bis arsinium ion in the liver suggest that formation of this compound is more likely to be responsible for the As-blocking effect of Se than is a mechanism based on antioxidation.
CARDIOVASCULAR DISEASE | CAPs and Vascular Function
Exposure to fine particulate air pollution is associated with increased cardiovascular morbidity and mortality, and exposure to dilute diesel exhaust causes vascular dysfunction in humans. Mills et al. (p. 709) investigates whether exposure to concentrated ambient particles (CAPS) causes vascular dysfunction. Although there were marked increases in particulate matter, exposure to CAPs (low in combustion-derived particles) did not affect vasomotor or fibrinolytic function in either healthy volunteers or patients with coronary heart disease. These findings contrast with previous exposures to dilute diesel exhaust and highlight the importance of particle composition in determining the vascular effects of particulate matter in humans.
NEUROTOXICITY | Developmental Neurotoxicity of Perfluorinated Chemicals
The widespread detection of perfluoroalkyl acids and their derivatives in wildlife and humans—and their entry into the immature brain—raise increasing concern about whether these agents might be developmental neurotoxicants. In an investigation of the effects of perfluorooctane sulfonate, perfluorooctanoic acid, perfluorooctane sulfonamide, and perfluorobutane sulfonate in undifferentiated and differentiating PC12 cells, a neuronotypic line used to characterize neurotoxicity, Slotkin et al. (p. 716) found that all perfluorinated chemicals are not the same in their impact on neurodevelopment and that it is unlikely that there is one simple, shared mechanism by which they all produce their effects. In vitro models can aid in the rapid and cost-effective screening for developmental neurotoxicity.
Also see Science Selections, p. A258
CANCER | Asbestos and Survival in Mesothelioma
Malignant pleural mesothelioma (MPM) is a rapidly fatal asbestos-associated malignancy with a median survival time of < 1 year after diagnosis. Treatment strategy is determined in part using known prognostic factors. To advance the understanding of the contribution of asbestos exposure to MPM prognosis, Christensen et al. (p. 723) examined the relationship between asbestos exposure and survival outcome in MPM. They found independent, significant associations between male sex and reduced survival, and between nonepithelioid tumor histology and reduced survival. Data suggest that patient survival is associated with asbestos fiber burden in MPM and is perhaps modified by susceptibility.
RISK ASSESSMENT | Microbial Risk Assessment
Although the U.S. Environmental Protection Agency has a long history of using risk-based approaches for regulatory purposes, pollutant limits for pathogens in biosolids are not currently based on quantitative risk assessments. Eisenberg et al. (p. 727) developed a risk-based methodology for assessing the risk to human health from exposure to pathogens via biosolids. Their risk-based approach provides a tool to a) help biosolids producers interpret the results of biosolids monitoring data in terms of its health implications; b) help treatment plant engineers evaluate the risk-based benefits of operational changes to existing or projected treatment processes; and c) help environmental managers evaluate potential capital improvements and/or land application site placement issues.
Also see Science Selections, p. A258
GENE POLYMORPHISM | Genetic Variation in Glutathione-Related Genes and MeHg Body Burden
Exposure to toxic methylmercury (MeHg) through fish consumption is a large problem worldwide, and it has led to governmental recommendations of reduced fish consumption and blacklisting of mercury-contaminated fish. Hereditary differences in MeHg metabolism may explain some of the variation in elimination kinetics of MeHg among individuals. Because MeHg is eliminated from the body as a glutathione (GSH) conjugate, Schläwicke Engström et al. (p. 734) investigated the influence of polymorphisms in GSH-synthesizing or GSH-conjugating genes on MeHg retention. Their results suggest a role of GSH-related polymorphisms in MeHg metabolism.
ENDOCRINE SYSTEM | Styrene Trimer May Affect Thyroid Hormone via AhR
Styrene trimers (STs) are polystyrene-container–eluted materials that are sometimes detected in packaged foods. Possible endocrine-disrupting effects of STs, such as estrogenic activity, have been reported, but their potential thyroid toxicity, such as that caused by the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has not been studied in detail. Using wild-type and aryl hydrocarbon receptor (Ahr)–null mice, Yanagiba et al. (p. 740) found that although 2,4,6-triphenyl-1-hexene (ST-1) treatment might cause an increase in AhR levels in the nucleus by inhibiting AhR export, it down-regulated AhR mRNA, thus leading to down-regulation of AhR target genes and an increase in plasma thyroxin levels.
NEUROTOXICITY | Delayed Toxicity of Perinatal Methylmercury in Mice
A long latency period of toxicity after methylmercury (MeHg) exposure exists in humans, but few animal studies have addressed this issue. A delay in MeHg toxicity in animals would affect the risk evaluation of MeHg. To demonstrate the existence of a latency period in a rodent model in which the toxicity of perinatal MeHg exposure becomes apparent only later in life, Yoshida et al. (p. 746) exposed pregnant metallothionein (MT)-null and wild-type C57Bl/6J mice to MeHg through the diet during gestation and early lactation and examined behavioral functions of the offspring. Few effects were seen at 12 weeks of age, but at 52 weeks of age, the MeHg-exposed groups showed poorer performance. The results suggest the existence of a long latency period after perinatal exposure to low-level MeHg, in which the behavioral effects emerged long after the leveling-off of brain Hg levels, which occurred by 13 weeks of age.
Also see Science Selections, p. A259
NEURODEVELOPMENT | Developmental Perchlorate Exposure and Hippocampal Function
Perchlorate, an environmental contaminant, blocks iodine uptake into the thyroid gland and reduces thyroid hormones. Because thyroid hormones play crucial roles in the development and maturation of the central system, this action of perchlorate raises significant concern over its effects on brain development. To evaluate neurologic function in rats after developmental exposure to perchlorate, Gilbert and Sui (p. 752) exposed pregnant rats to various concentrations of perchlorate in the drinking water, and assessed adult male offspring in a series of behavioral tasks and neurophysiologic measures of synaptic function in the hippocampus. Dose-dependent deficits in hippocampal synaptic function were detectable with relatively minor perturbations of the thyroid axis, indicative of an irreversible impairment in synaptic transmission in response to developmental perchlorate exposure.
OBESITY | PCB-77 Promotes Obesity-Associated Atherosclerosis
Obesity, an inflammatory condition linked to cardiovascular disease, is associated with expansion of adipose tissue. Highly prevalent coplanar polychlorinated biphenyls (PCBs), such as 3,3´,4,4´-tetrachlorobiphenyl (PCB-77), accumulate in adipose tissue because of their lipophilicity and increase with obesity. However, the effects of PCBs on adipocytes, obesity, and obesity-associated cardiovascular disease are unknown. Arsenescu et al. (p. 761) examined in vitro and in vivo effects of PCB-77 on adipocyte differentiation, proinflammatory adipokines, adipocyte morphology, body weight, serum lipids, and atherosclerosis. Results suggest that PCB-77 may contribute to the development of obesity and obesity-associated atherosclerosis.
PROSTATE CANCER | Transcriptome Analysis in Cd-Treated Prostatic Epithelial Cells
Although cadmium s implicated in prostate carcinogenesis, its oncogenic action remains unclear. Bakshi et al. (p. 769) examined changes in cell growth and the transcriptome in an immortalized human normal prostate epithelial cell line (NPrEC) after exposure to low-dose Cd. Synchronized NPrEC cells were exposed to different doses of Cd and then assayed for cell viability and cell-cycle progression. Changes in transcriptome were investigated by global profiling. The authors found that noncytotoxic, low-dose Cd has growth-promoting effects on NPrEC cells and induces transient overexpression of tumor necrosis factor, leading to up-regulation of genes with oncogenic and immunomodulation functions.
BONE AND CARTILAGE | Bone Resorption and Cadmium
Environmental exposure to cadmium decreases bone density indirectly through hypercalciuria resulting from renal tubular dysfunction. To find evidence for a direct osteotoxic effect of cadmium in women, Schutte et al. (p. 777) measured 24-hr urinary cadmium and blood cadmium as indexes of lifetime and recent exposure, respectively, in women who were randomly recruited from a Flemish population with environmental cadmium exposure. In the absence of renal tubular dysfunction, environmental exposure to cadmium increased bone resorption in women, suggesting a direct osteotoxic effect with increased calciuria and reactive changes in calciotropic hormones.
BONE AND CARTILAGE | Relations of Bone Mineral Density with Lead Biomarkers
Theppeang et al. (p. 784) used cross-sectional analysis to evaluate the relationship between bone mineral density (BMD) and lead in blood, tibia, and patella and to investigate how BMD modifies these lead biomarkers in older women. BMD represents the capacity of bone to store lead by substituting for calcium; therefore, the findings may have relevance for effect-size estimates in individuals with higher BMD. The results suggest that aging affects lead kinetics and thus the related risk of health effects associated with substantial early- and midlife lead exposure in older persons.
REPRODUCTIVE HEALTH | Atmospheric Pollution and Human Reproduction
Associations between atmospheric pollutants and reproductive outcomes, in particular birth weight and gestational duration, are increasingly being reported in the epidemiologic literature. Slama et al. (p. 791) report on an international workshop convened to discuss the current evidence, to identify the strengths and weaknesses of published epidemiologic studies, and to suggest future directions for research. The authors suggest that input from toxicology, exposure assessment, and clinical research will aid in identifying and assessing exposure of fetotoxic agents in ambient air, in the developing of early markers of adverse reproductive outcomes, and in identifying relevant biological pathways.
Environmental Medicine
RESPIRATORY DISEASE | Fluticasone Propionate Protects against Airway Inflammation
Ozone exposure induces airway neutrophilia and modifies innate immune monocytic cell-surface phenotypes in healthy individuals. High-dose inhaled corticosteroids can reduce O3-induced airway inflammation, but their effect on innate immune activation is unknown. Alexis et al. (p. 799) used a human O3 inhalation challenge model to examine the effectiveness of clinically relevant doses of inhaled corticosteroids on airway inflammation and markers of innate immune activation in healthy volunteers. The study confirmed and extended data demonstrating the protective effect of FP against O3-induced airway inflammation and immune cell activation.
Children's Health
ENDOCRINE SYSTEM | PCBs and Thyroid Hormone Levels in Youth
Acute exposure to high levels of persistent organic pollutants, such as polychlorinated biphenyls (PCBs), p,p´-dichlorophenyldichloroethylene (p,p´-DDE), and hexachlorobenzene (HCB), can affect human health including thyroid function. Chronic exposure to multiple toxicants is common but difficult to analyze, and most prior studies have focused on adults or newborns, creating a gap in our understanding of multitoxicant effects among adolescents. Schell et al. (p. 806) investigated whether levels of PCBs, p,p´-DDE, HCB, mirex, lead, and mercury that reflect past chronic exposure are associated with alterations in levels of thyroid-stimulating hormone, triiodothyronine, total thyroxine, and free thyroxine among older children and adolescents from the Akwesasne Mohawk Nation who lived near several contaminated sites.
Also see Science Selections, p. A259
FETAL DEVELOPMENT | PCE-Contaminated Water and Adverse Birth Outcomes
Prior studies of prenatal exposure to tetrachloroethylene (PCE) have shown mixed results regarding its effect on birth weight and gestational age. Aschengrau et al. (p. 814) examined whether PCE contamination of public drinking water supplies in Massachusetts influenced the birth weight and gestational duration of children whose mothers were exposed before the child's delivery. The study included 1,353 children whose mothers were exposed to PCE-contaminated drinking water and a comparison group of 772 children of unexposed mothers. The researchers found no meaningful associations between PCE exposure and birth weight or gestational duration.
DENTAL HEALTH | Cadmium and Pediatric Dental Caries
Animal experiments have shown that cadmium exposure results in severe dental caries, but limited epidemiologic data are available on this issue. Arora et al. (p. 821) examined the relationship between environmental cadmium exposure and dental caries in children 6–12 years of age using cross-sectional data, including urine cadmium concentrations and counts of decayed or filled tooth surfaces, from the third National Health and Nutrition Examination Survey (NHANES III). Approximately 56% of children experienced caries in their deciduous teeth and almost 30% were affected by caries in their permanent teeth. The authors observed a positive, but statistically nonsignificant, association between environmental cadmium exposure and dental caries in deciduous teeth.
ASTHMA | Ambient Zinc Increases Pediatric Asthma Morbidity
Recent studies indicate that the composition of fine particulate matter [≤ 2.5 µm in aerodynamic diameter (PM2.5)] is associated with increased hospitalizations for cardiovascular and respiratory diseases. The metal composition of PM2.5 influences allergic and/or inflammatory reactions, and ambient zinc contributes to worsening pulmonary function in susceptible adults. However, information is limited concerning associations between ambient air zinc levels and health care utilization for asthma, especially among children. Hirshon et al. (p. 826) investigated the relationship between outdoor ambient PM2.5 zinc levels and emergency department (ED) visits for children living in the Greater Baltimore, Maryland, area. Results suggest that high zinc levels in ambient PM2.5 are associated with an increase in ED visits/hospital admissions for asthma on the following day among children living in an urban area.
RESPIRATORY DISEASE | Airway Inflammation, Lung Function and Air Pollutants
The biological mechanisms involved in inflammatory response to air pollution are not clearly understood. Barraza-Villarreal et al. (p. 832) examined the association of short-term air pollutant exposure with inflammatory markers and lung function in a cohort of 158 asthmatic and 50 nonasthmatic school-age children, followed an average of 22 weeks. They conducted spirometric tests, measurements of fractional exhaled nitric oxide, interleukin-8 in nasal lavage, and pH of exhaled breath condensate every 15 days during follow-up and analyzed data using linear mixed-effects models. Exposure to particulate matter < 2.5 µm in aerodynamic diameter resulted in acute airway inflammation and decreased lung function in both asthmatic and nonasthmatic children.
CARDIOVASCULAR DISEASE | Heritability and Household Estimates in Children with Stroke
Nowak-Göttl et al. (p. 839) used blood samples from 1,002 individuals with 282 stroke pedigrees to estimate the phenotypic variation within lipid concentrations and coagulation factor levels, as well as the proportions attributable to heritability (h2r) and shared environmental effects (c2), in pediatric stroke families. Using h2r and c2 in one model adjusted for age, blood group, sex, smoking, and hormonal contraceptives, they found significant h2r estimates for lipoprotein (a), low-density lipoprotein, fibrinogen, protein C, and protein Z. This research stresses the importance of research on the genetic variability and lifestyle modifications of risk factors associated with pediatric stroke.