土壤微量元素测试及其应用

土壤微量元素测试在其发展历史过程中,不断改进技术,逐渐深入地揭示土壤供给微量元素的能力,对指导施肥和保护生态环境起着积极的作用。现代测试手段发展到广泛采用原子吸收光谱(AA)和电感耦合等离子体发射光谱(ICP),但比色法(光度法)和极谱法不仅设备比较简便,而且新的显色剂、催化系统等方面的研究进展,使其对某些元素的测定灵敏度和准确度超过AA和ICP,从而在微量元素测试技术中仍占据一定地位。土壤溶液抽取技术虽然有所改进,但有效态微量元素仍然主要是选用适当提取剂来提取测定。临界值和分级标准的确定是应用测定值的桥梁。作者曾采用全幅分级标准分级制图,确定缺素面积和需肥区域,再根据土壤含量水平和增产幅度之间的函数关系预测增产效果和投入的经济效益。     

Are the young more sensitive than adults to the effects of radiofrequency fields? An examination of relevant data from cellular and animal studies

It has sometimes been assumed that children are more sensitive than adults to the effects of radiofrequency (RF) fields associated with cellular wireless telephones. However, relatively few in vitro or animal models have examined this possibility.In vitro studies have used several cell types, from both humans and rodents, including primary cells, embryonic cell lines, undifferentiated cancer cell lines, and stem cells. Overall, the balance of evidence does not suggest that field-related effects occur in any cell type: gene and protein expression were not significantly changed by exposure in nine out of 15 studies; genotoxicity was evaluated in 13 papers and in most, of these studies, no damage to DNA was detected; eight studies failed to demonstrate induction of apoptosis; and three studies reported lack of oxidative stress induction by RF-exposures. Five of eight studies investigating the effects of combined exposures to RF fields and chemical or physical agents reported a lack of field-related effects.In addition, few papers have been published on the effects of low level exposure of immature animals. The available results are very limited, both in terms of signals used and biological endpoints investigated, but the evidence does not indicate that prenatal or early postnatal exposures are associated with acute adverse responses or the development of detrimental changes in the long-term. Overall, this suggests that young animals may not be significantly more sensitive than adults, but there is clearly a need for further studies to be carried out.     

Environmental epigenomics and disease susceptibility

Epidemiological evidence increasingly suggests that environmental exposures early in development have a role in susceptibility to disease in later life. In addition, some of these environmental effects seem to be passed on through subsequent generations. Epigenetic modifications provide a plausible link between the environment and alterations in gene expression that might lead to disease phenotypes. An increasing body of evidence from animal studies supports the role of environmental epigenetics in disease susceptibility. Furthermore, recent studies have demonstrated for the first time that heritable environmentally induced epigenetic modifications underlie reversible transgenerational alterations in phenotype. Methods are now becoming available to investigate the relevance of these phenomena to human disease.     

Neurobehavioral Dysfunction as a Possible Sentinel of Methylmercury Exposure

The main concern regarding methylmercury neurotoxicity relates to adverse effects on the brain during development. Many environmental chemicals may act as developmental neurotoxicants, but solid documentation from epidemiological studies exists only on methylmercury, lead, and polychlorinated biphenyls (PCBs). Neurobehavioral tests may reveal subtle dysfunctions, but the tests chosen must be valid and appropriate for the setting. In a prospective study in the Faroe Islands, the main neuropsychological functions affected by prenatal methylmercury exposure were attention, language and memory. Deficits in visuospatial function were mainly related to postnatal exposures. These associations were stable after adjustment for confounders and exclusion of the children with the highest exposures to methylmercury and PCBs. Tests with good psychometric properties were more likely to show an association with mercury exposure. Greater sensitivity was also seen with tests administered by specialized academic staff rather than a trained technician. Despite highly significant effects on nervous system function, the deficits were subtle, and mercury exposure explained only a small part of the variation. Available evidence suggests that neurotoxicity may have severe implications on public health, but current methods are not amenable to application as sentinels of adverse health effects in environmental health surveillance.     

Aspects of trace element interactions during development

The origins of nutritional trace element deficiencies are summarized. Inadequate intake results in primary deficiency, whereas secondary or conditioned deficiencies can arise in several ways including trace element interactions. Evidence is presented and discussed for interactions of essential trace elements during prenatal and early postnatal development. Diets of widely different zinc and copper concentrations and ratios were fed to pregnant rats. Analysis of fetal outcome and copper and zinc concentrations of maternal and fetal livers showed that although there is an interaction between these metals it occurs only at levels of dietary copper deficiency. Iron and manganese interact so that high levels of one depress absorption of the other. Mice fed iron-supplemented diets had liver manganese concentrations lower than those of unsupplemented mice. Iron supplements at high but not low levels also depressed absorption of zinc. Conversely, zinc deficiency in pregnant rats caused higher than normal concentrations of iron in maternal and fetal liver. Trace element analyses of proprietary infant formulas indicate that in some, concentrations and ratios of these trace elements may be incorrect. The effects of essential trace element interactions during development should be further investigated. Caution is urged in considering levels of trace element supplements during pregnancy, lactation, or early childhood.     

Postnatal penile growth concurrent with mini-puberty predicts later sex-typed play behavior: Evidence for neurobehavioral effects of the postnatal androgen surge in typically developing boys

The masculinizing effects of prenatal androgens on human neurobehavioral development are well established. Also, the early postnatal surge of androgens in male infants, or mini-puberty, has been well documented and is known to influence physiological development, including penile growth. However, neurobehavioral effects of androgen exposure during mini-puberty are largely unknown. The main aim of the current study was to evaluate possible neurobehavioral consequences of mini-puberty by relating penile growth in the early postnatal period to subsequent behavior. Using multiple linear regression, we demonstrated that penile growth between birth and three months postnatal, concurrent with mini-puberty, significantly predicted increased masculine/decreased feminine behavior assessed using the Pre-school Activities Inventory (PSAI) in 81 healthy boys at 3 to 4 years of age. When we controlled for other potential influences on masculine/feminine behavior and/or penile growth, including variance in androgen exposure prenatally and body growth postnally, the predictive value of penile growth in the early postnatal period persisted. More specifically, prenatal androgen exposure, reflected in the measurement of anogenital distance (AGD), and early postnatal androgen exposure, reflected in penile growth from birth to 3 months, were significant predictors of increased masculine/decreased feminine behavior, with each accounting for unique variance. Our findings suggest that independent associations of PSAI with AGD at birth and with penile growth during mini-puberty reflect prenatal and early postnatal androgen exposures respectively. Thus, we provide a novel and readily available approach for assessing effects of early androgen exposures, as well as novel evidence that early postnatal aes human neurobehavioral development.     

Trends in trace element determinations in blood,serum, and urine of the dutch population,and the role of neutron activation analysis

A critical review on the quality of literature data on trace elements in human blood, serum, and urine of inhabitants in the Netherlands has shown that many of the currently available data have been established 15–20 years ago. Only in a few publications are quality indicators mentioned, which should be considered typical—and minimal —for studies resulting at reference values. The use of neutron activation analysis for determination of trace elements in human body fluids was restricted to a few studies in the 1970s. However, although it is frequently assumed that the sensitivity of NAA might be insufficient, it is demonstrated that modern, large, well-type Ge detectors may serve well for the determination of trace elements in human body fluids via radiochemical NAA, for example.     

Role of endocannabinoids in brain development.

In addition to those functions that have been extensively addressed in this special issue, such as nociception, motor activity, neuroendocrine regulation, immune function and others, the endogenous cannabinoid system seems to play also a role in neural development. This view is based on a three-fold evidence. A first evidence emerges from neurotoxicological studies that showed that synthetic and plant-derived cannabinoids, when administered to pregnant rats, produced a variety of changes in the maturation of several neurotransmitters and their associated-behaviors in their pups, changes that were evident at different stages of brain development. A second evidence comes from studies that demonstrated the early appearance of elements of the endogenous cannabinoid system (receptors and ligands) during the brain development. The atypical location of these elements during fetal and early postnatal periods favours the notion that this system may play a role in specific molecular events related to neural development. Finally, a third evidence derives from studies using cultures of fetal glial or neuronal cells. Cannabinoid receptors are present in some of these cultured cells and their activation produced a set of cellular effects consistent with a role of this system in the process of neural development. All this likely supports that endocannabinoids, early synthesized in nervous cells, play a role in events related to development, by acting through the activation of second messenger-coupled cannabinoid receptors.     

In vitro and in vivo genotoxicity of radiofrequency fields

There has been growing concern about the possibility of adverse health effects resulting from exposure to radiofrequency radiations (RFR), such as those emitted by wireless communication devices. Since the introduction of mobile phones many studies have been conducted regarding alleged health effects but there is still some uncertainty and no definitive conclusions have been reached so far. Although thermal effects are well understood they are not of great concern as they are unlikely to result from the typical low-level RFR exposures. Concern rests essentially with the possibility that RFR-exposure may induce non-thermal and/or long-term health effects such as an increased cancer risk. Consequently, possible genetic effects have often been studied but with mixed results. In this paper we review the data on alleged RFR-induced genetic effects from in vitro and in vivo investigations as well as from human cytogenetic biomonitoring surveys. Attention is also paid to combined exposures of RFR with chemical or physical agents. Again, however, no entirely consistent picture emerges. Many of the positive studies may well be due to thermal exposures, but a few studies suggest that biological effects can be seen at low levels of exposure. Overall, however, the evidence for low-level genotoxic effects is very weak.     

Health effects of natural dust

This article reviews the health effects of trace elements carried in natural dusts of geologic or geochemical origin. The sources of these dusts are diverse, including volcanoes, dust storms, long-range transport of desert dust, and displacement through natural processes such as landslides and earthquakes. The primary focus is dust exposures affecting communities rather than occupational groups (which have been comprehensively explored in other publications). The principal elements and compounds reviewed are trace metals (including As, Hg, Cd, and Fe), radioactive elements, fluoride, silicates, natural asbestiform compounds, and alkali salts. The pathways by which such agents affect human populations are explored, including carriage through water, air, soil, and the food chain. The mechanisms of biotoxicity and the acute and chronic consequences on health associated with these elements are described. The discussion explores problems inferring risk and disease causation from natural dust exposures using standard epidemiological indicators, particularly for chronic outcomes, and will argue for the importance of the ecological perspective in assessing pathogenesis. The authors stress the global scale of the problem, which remains underevaluated and underreported in terms of health implications.     

Developmental programming of reproduction and fertility: what is the evidence?

The concept of the foetal/developmental origins of adult disease has been around for ~20 years and from the original epidemiological studies in human populations much more evidence has accumulated from the many studies in animal models. The majority of these have focused upon the role of early dietary intake before conception, through gestation and/or lactation and subsequent interactions with the postnatal environment, e.g. dietary and physical activity exposures. Whilst a number of theoretical models have been proposed to place the experimental data into a biological context, the underlying phenomena remain the same; developmental deficits (of single (micro) nutrients) during critical or sensitive periods of tissue growth alter the developmental pathway to ultimately constrain later functional capacity when the individual is adult. Ageing, without exception, exacerbates any programmed sequelae. Thus, adult phenotypes that have been relatively easy to characterise (e.g. blood pressure, insulin sensitivity, body fat mass) have received most attention in the literature. To date, relatively few studies have considered the effect of differential early environmental exposures on reproductive function and fecundity in predominantly mono-ovular species such as the sheep, cow and human. The available evidence suggests that prenatal insults, undernutrition for example, have little effect on lifetime reproductive capacity despite subtle effects on the hypothalamic-pituitary-gonadal axis and gonadal progenitor cell complement. The postnatal environment is clearly important, however, since neonatal/adolescent growth acceleration (itself not independent from prenatal experience) has been shown to significantly influence fecundity in farm animals. The present paper will expand these interesting areas of investigation and review the available evidence regarding developmental programming of reproduction and fertility. However, it appears there is little strong evidence to indicate that offspring fertility and reproductive senescence in the human and in farm animal species are overtly affected by prenatal nutrient exposure. Nevertheless, it is clear that the developing gonad is sensitive to its immediate environment but more detailed investigation is required to specifically test the long-term consequences of nutritional perturbations during pregnancy on adult reproductive well-being.     

Potential risk of asthma associated with in utero exposure to xenobiotics

The incidence of asthma, a complex disease and significant public health problem, has been increasing over the last 30 years for unknown reasons. Changes in environmental exposures or lifestyle may be involved. In some cases asthma may originate in utero or in early life. Associations have been found between in utero exposures to several xenobiotics and increased risk of asthma. There is convincing evidence that maternal smoking and/or in utero and perinatal exposure to environmental tobacco smoke are associated with increased risk of asthma. Similar effects have been demonstrated in animal models of allergic asthma. Evidence also suggests that in utero and/or early‐life exposures to various ambient air pollutants may increase the risk of asthma although supporting animal data are very limited. A few studies have suggested that in utero exposure to acetaminophen is associated with increased risk of asthma; however, animal data are lacking. Various vitamin deficiencies and supplements during pregnancy have been studied. In general, it appears that vitamins A, C, and E have protective effects and vitamins D and B may, in some instances, increase the risk, but the data are not conclusive. Some studies related to in utero exposures to polychlorinated biphenyls and bisphenol A and asthma risk are also reported. The underlying mechanisms for an association between xenobiotic exposures and asthma remain a matter of speculation. Genetic predisposition and epigenetic changes have been explored. The developing immune, respiratory, and nervous systems are potential targets. Oxidative stress and modulation of inflammation are thought to be involved. Birth Defects Research (Part C) 99:1–13, 2013. © 2013 Wiley Periodicals, Inc.     

Trace elements in animals.

Trace element deficiency and toxicity in animals induces a wide variety of clinical effects although few are sufficiently specific to permit diagnosis without supporting investigation of changes in tissue trace element content or of the activity of metabolic processes influenced by trace element supply. Study of such trace element dependent processes has shown that extensive changes often arise before overt signs of disease appear. Some of these subclinical effects have pathological consequences and thus cannot be ignored when seeking correlations between geochemical anomalies and disease incidence. Many past estimates of the quantitative requirements of animals for the essential trace elements are imprecise. Although recent work is providing clearer definition of requirements, many common dietary components have a marked influence upon the efficiency with which such elements can be utilized from the diet. Recent evidence indicates that such antagonists influence both the absorption and the subsequent fate of essential and toxic elements in body tissues and these processes have to be taken into account when investigating the aetiology of disorders believed to be attributable to anomalies in trace element supply. Their existence is not always detectable if attention is confined to the trace element analysis of body tissues or to the nature of clinical lesions. Provided the complexity of soil-plant-animal relations with respect to trace element supply is fully recognized in the interpretation of data, the geochemical approach to the initial recognition of areas associated with a high risk of anomalies in trace element supply to animals and man has considerable potential value. This is already apparent from investigations upon the incidence of trace element problems in animals. As yet, its validity for similar purposes in man is less fully established.     

Trace elements in coal

Trace elements can have profound adverse effects on the health of people burning coal in homes or living near coal deposits, coal mines, and coal-burning power plants. Trace elements such as arsenic emitted from coal-burning power plants in Europe and Asia have been shown to cause severe health problems. Perhaps the most widespread health problems are caused by domestic coal combustion in developing countries where millions of people suffer from fluorosis and thousands from arsenism. Better knowledge of coal quality characteristics may help to reduce some of these health problems. For example, information on concentrations and distributions of potentially toxic elements in coal may help delineate areas of a coal deposit to be avoided. Information on the modes of occurrence of these elements and the textural relations of the minerals in coal may help to predict the behavior of the potentially toxic trace metals during coal cleaning, combustion, weathering, and leaching.     

A generalized physiologically-based toxicokinetic modeling system for chemical mixtures containing metals

Background  

Humans are routinely and concurrently exposed to multiple toxic chemicals, including various metals and organics, often at levels that can cause adverse and potentially synergistic effects. However, toxicokinetic modeling studies of exposures to these chemicals are typically performed on a single chemical basis. Furthermore, the attributes of available models for individual chemicals are commonly estimated specifically for the compound studied. As a result, the available models usually have parameters and even structures that are not consistent or compatible across the range of chemicals of concern. This fact precludes the systematic consideration of synergistic effects, and may also lead to inconsistencies in calculations of co-occurring exposures and corresponding risks. There is a need, therefore, for a consistent modeling framework that would allow the systematic study of cumulative risks from complex mixtures of contaminants.     

Update on new developments in the study of human teratogens

BACKGROUND AND METHODS: The purpose of this annual article is to highlight and briefly review new and significant information on agents that may be teratogenic in pregnant women. Various sources of on-line and printed information are given. RESULTS: The following topics have been discussed: 1) lithium medication: decreased estimate of risk; 2) cigarette smoking and genotype as contributors to oral-facial clefts and clubfoot; 3) trimethoprim; 4) methimazole syndrome?; 5) glucocorticoids and oral-facial clefts; 6) binge drinking; 7) fetal valproate syndrome; and 8) carbamazepine. CONCLUSIONS: We have highlighted several maternal exposures during pregnancy that are associated with small but increased rates of birth defects, generally only a few cases per 1,000 infants. These exposures include cigarette smoking, and treatment with lithium, trimethoprim, methimazole, or corticosteroids. This weak teratogenic effect was usually identified by the linkage of an uncommon treatment with an unusual birth defect outcome. The use of modern epidemiologic techniques, especially prospective multicenter studies that provide increased numbers, has helped to strengthen the evidence for these associations. We discuss how teratogenic risks that are small in comparison to the background risk can be presented to at-risk women and their doctors. We have briefly listed some elements that might be used in prioritizing further studies of suspected teratogenic exposures. Various existing methods for expressing the strength of evidence for human teratogenicity are also given.     

Evaluation of time-to-pregnancy as a measure in environmental epidemiology

Since the late 80's, time to pregnancy has been used in environmental epidemiology to explore adverse effects of different exposures. The advantages of this measure and additional elements to be considered in the performance of this type of studies are reviewed. Study design includes the following steps: population selection, sample size, outcome measurement, statistical analyses and sources of bias. Guidelines were suggested for the properly development of this type of study.     

Trace Elements in Human Nutrition

A number of trace elements are required by man, but clear-cut evidence of deficiency has been observed for only iodine and iron. Despite the fact no evidence exists that human diets may be deficient in trace minerals other than iron and iodine, there is an increasing tendency to add more and more minerals to vitamin-mineral preparations. Since potassium iodide is a mandatory constituent of table salt in Canada, iron is apparently the only trace element which may not be consumed in adequate amounts under Canadian conditions, and whose addition to dietary supplements for sale to the general public can be justified. It is suggested that trace elements other than iron should not be advertised to the general public, but should be administered only on the advice of a physician, who is in a position to judge the merit of available products in each specific situation.