Reference values should not be confused with limit values, which generally are the legal limits or guidelines for occupational and environmental exposure Alessio et al. When it is necessary to compare the results of group analyses, the distribution of the values in the reference group and in the group under study must be known because only then can a statistical comparison be made.
In these cases, it is essential to attempt to match the general population reference group with the exposed group for similar characteristics such as, sex, age, lifestyle and eating habits. To obtain reliable reference values one must make sure that the subjects making up the reference group have never been exposed to the toxic substances, either occupationally or due to particular conditions of environmental pollution. In assessing exposure to toxic substances one must be careful not to include subjects who, although not directly exposed to the toxic substance in question, work in the same workplace, since if these subjects are, in fact, indirectly exposed, the exposure of the group may be in consequence underestimated.
Another practice to avoid, although it is still widespread, is the use for reference purposes of values reported in the literature that are derived from case lists from other countries and may often have been collected in regions where different environmental pollution situations exist. Periodic monitoring of individual workers is mandatory when the levels of the toxic substance in the atmosphere of the working environment approach the limit value. Where possible, it is advisable to simultaneously check an indicator of exposure and an indicator of effect. The data thus obtained should be compared with the reference values and the limit values suggested for the substance under study ACGIH Analysis of a group becomes mandatory when the results of the biological indicators used can be markedly influenced by factors independent of exposure diet, concentration or dilution of urine, etc.
In order to ensure that the group study will furnish useful results, the group must be sufficiently numerous and homogeneous as regards exposure, sex, and, in the case of some toxic agents, work seniority. The more the exposure levels are constant over time, the more reliable the data will be. An investigation carried out in a workplace where the workers frequently change department or job will have little value. For a correct assessment of a group study it is not sufficient to express the data only as mean values and range. The frequency distribution of the values of the biological indicator in question must also be taken into account.
Data obtained from biological monitoring of groups of workers can also be used in cross-sectional or prospective epidemiological studies. Cross-sectional studies can be used to compare the situations existing in different departments of the factory or in different industries in order to set up risk maps for manufacturing processes. A difficulty that may be encountered in this type of application depends on the fact that inter-laboratory quality controls are not yet sufficiently widespread; thus it cannot be guaranteed that different laboratories will produce comparable results.
Prospective studies serve to assess the behaviour over time of the exposure levels so as to check, for example, the efficacy of environmental improvements or to correlate the behaviour of biological indicators over the years with the health status of the subjects being monitored.
The results of such long-term studies are very useful in solving problems involving changes over time. A given level of exposure considered safe today may no longer be regarded as such at some point in the future. Some ethical considerations arise in connection with the use of biological monitoring as a tool to assess potential toxicity. One goal of such monitoring is to assemble enough information to decide what level of any given effect constitutes an undesirable effect; in the absence of sufficient data, any perturbation will be considered undesirable.
The regulatory and legal implications of this type of information need to be evaluated. Therefore, we should seek societal discussion and consensus as to the ways in which biological indicators should best be used. In other words, education is required of workers, employers, communities and regulatory authorities as to the meaning of the results obtained by biological monitoring so that no one is either unduly alarmed or complacent.
There must be appropriate communication with the individual upon whom the test has been performed concerning the results and their interpretation. Further, whether or not the use of some indicators is experimental should be clearly conveyed to all participants. See the chapter Ethical Issues for further discussion and the text of the Code. Biological monitoring can be carried out for only a limited number of environmental pollutants on account of the limited availability of appropriate reference data.
This imposes important limitations on the use of biological monitoring in evaluating exposure. The World Health Organization WHO , for example, has proposed health-based reference values for lead, mercury, and cadmium only. These values are defined as levels in blood and urine not linked to any detectable adverse effect.
This is especially so in the case of biological monitoring data and it is therefore the responsibility of any laboratory undertaking analytical work on biological specimens from working populations to ensure the reliability, accuracy and precision of its results. This responsibility extends from providing suitable methods and guidance for specimen collection to ensuring that the results are returned to the health professional responsible for the care of the individual worker in a suitable form. All these activities are covered by the expression quality assurance.
The central activity in a quality assurance programme is the control and maintenance of analytical accuracy and precision. Biological monitoring laboratories have often developed in a clinical environment and have taken quality assurance techniques and philosophies from the discipline of clinical chemistry. Indeed, measurements of toxic chemicals and biological effect indicators in blood and urine are essentially no different from those made in clinical chemistry and in clinical pharmacology service laboratories found in any major hospital. A quality assurance programme for an individual analyst starts with the selection and establishment of a suitable method.
The next stage is the development of an internal quality control procedure to maintain precision; the laboratory needs then to satisfy itself of the accuracy of the analysis, and this may well involve external quality assessment see below. It is important to recognize however, that quality assurance includes more than these aspects of analytical quality control.
There are several texts presenting analytical methods in biological monitoring. Although these give useful guidance, much needs to be done by the individual analyst before data of a suitable quality can be produced. Central to any quality assurance programme is the production of a laboratory protocol that must specify in detail those parts of the method which have most bearing on its reliability, accuracy and precision.
Development of a suitable protocol is usually a time-consuming process.
If a laboratory wishes to establish a new method, it is often most cost-effective to obtain from an existing laboratory a protocol that has proved its performance, for example, through validation in an established international quality assurance programme. Should the new laboratory be committed to a specific analytical technique, for example gas chromatography rather than high-performance liquid chromatography, it is often possible to identify a laboratory that has a good performance record and that uses the same analytical approach. Laboratories can often be identified through journal articles or through organizers of various national quality assessment schemes.
The quality of analytical results depends on the precision of the method achieved in practice, and this in turn depends on close adherence to a defined protocol. For example, for control of blood lead analyses, quality control samples are introduced into the run after every six or eight actual worker samples.
More stable analytical methods can be monitored with fewer quality control samples per run. The quality control samples for blood lead analysis are prepared from ml of blood human or bovine to which inorganic lead is added; individual aliquots are stored at low temperature Bullock, Smith and Whitehead Before each new batch is put into use, 20 aliquots are analysed in separate runs on different occasions to establish the mean result for this batch of quality control samples, as well as its standard deviation Whitehead These two figures are used to set up a Shewhart control chart figure The results from the analysis of the quality control samples included in subsequent runs are plotted on the chart.
The analyst then uses rules for acceptance or rejection of an analytical run depending on whether the results of these samples fall within two or three standard deviations SD of the mean. A sequence of rules, validated by computer modelling, has been suggested by Westgard et al. This approach to quality control is described in textbooks of clinical chemistry and a simple approach to the introduction of quality assurance is set forth in Whitehead It must be emphasized that these techniques of quality control depend on the preparation and analysis of quality control samples separately from the calibration samples that are used on each analytical occasion.
This approach can be adapted to a range of biological monitoring or biological effect monitoring assays. Batches of blood or urine samples can be prepared by addition of either the toxic material or the metabolite that is to be measured. Similarly, blood, serum, plasma, or urine can be aliquotted and stored deep-frozen or freeze-dried for measurement of enzymes or proteins. However, care has to be taken to avoid infective risk to the analyst from samples based on human blood. Careful adherence to a well-defined protocol and to rules for acceptability is an essential first stage in a quality assurance programme.
Any laboratory must be prepared to discuss its quality control and quality assessment performance with the health professionals using it and to investigate surprising or unusual findings. This is a difficult exercise for a laboratory to do on its own but can be achieved by taking part in a regular external quality assessment scheme. These have been an essential part of clinical chemistry practice for some time but have not been widely available for biological monitoring. The exception is blood lead analysis, where schemes have been available since the s e.
Several national and international quality assessment schemes are available. Many of these schemes welcome new laboratories, as the validity of the mean of the results of an analyte from all the participating laboratories taken as a measure of the actual concentration increases with the number of participants. Schemes with many participants are also more able to analyse laboratory performance according to analytical method and thus advise on alternatives to methods with poor performance characteristics. In some countries, participation in such a scheme is an essential part of laboratory accreditation.
Guidelines for external quality assessment scheme design and operation have been published by the WHO In the absence of established external quality assessment schemes, accuracy may be checked using certified reference materials which are available on a commercial basis for a limited range of analytes. The advantages of samples circulated by external quality assessment schemes are that 1 the analyst does not have fore-knowledge of the result, 2 a range of concentrations is presented, and 3 as definitive analytical methods do not have to be employed, the materials involved are cheaper.
Effort spent in attaining good laboratory accuracy and precision is wasted if the samples presented to the laboratory have not been taken at the correct time, if they have suffered contamination, have deteriorated during transport, or have been inadequately or incorrectly labelled. It is also bad professional practice to submit individuals to invasive sampling without taking adequate care of the sampled materials. Although sampling is often not under the direct control of the laboratory analyst, a full quality programme of biological monitoring must take these factors into account and the laboratory should ensure that syringes and sample containers provided are free from contamination, with clear instructions about sampling technique and sample storage and transport.
The importance of the correct sampling time within the shift or working week and its dependence on the toxicokinetics of the sampled material are now recognized ACGIH ; HSE , and this information should be made available to the health professionals responsible for collecting the samples. High-quality analytical results may be of little use to the individual or health professional if they are not communicated to the professional in an interpretable form and at the right time.
Each biological monitoring laboratory should develop reporting procedures for alerting the health care professional submitting the samples to abnormal, unexpected, or puzzling results in time to allow appropriate action to be taken. Interpretation of laboratory results, especially changes in concentration between successive samples, often depends on knowledge of the precision of the assay.
Toxic metals and organometallic compounds such as aluminium, antimony, inorganic arsenic, beryllium, cadmium, chromium, cobalt, lead, alkyl lead, metallic mercury and its salts, organic mercury compounds, nickel, selenium and vanadium have all been recognized for some time as posing potential health risks to exposed persons. One problem in seeking precise and accurate measurements of metals in biological materials is that the metallic substances of interest are often present in the media at very low levels. Expression of the results per gram of creatinine is the method of standardization most frequently used.
Analyses performed on too dilute or too concentrated urine samples are not reliable and should be repeated. In industry, workers may be exposed to inorganic aluminium compounds by inhalation and possibly also by ingestion of dust containing aluminium. Aluminium is poorly absorbed by the oral route, but its absorption is increased by simultaneous intake of citrates.
The rate of absorption of aluminium deposited in the lung is unknown; the bioavailability is probably dependent on the physicochemical characteristics of the particle. Urine is the main route of excretion of the absorbed aluminium. The concentration of aluminium in serum and in urine is determined by both the intensity of a recent exposure and the aluminium body burden.
Data on welders suggest that the kinetics of aluminium excretion in urine involves a mechanism of two steps, the first one having a biological half-life of about eight hours. In workers who have been exposed for several years, some accumulation of the metal in the body effectively occurs and aluminium concentrations in serum and in urine are also influenced by the aluminium body burden. Aluminium is stored in several compartments of the body and excreted from these compartments at different rates over many years.
High accumulation of aluminium in the body bone, liver, brain has also been found in patients suffering from renal insufficiency. Inorganic antimony can enter the organism by ingestion or inhalation, but the rate of absorption is unknown. Absorbed pentavalent compounds are primarily excreted with urine and trivalent compounds via faeces.
Retention of some antimony compounds is possible after long-term exposure. A preliminary study on workers exposed to pentavalent antimony indicates that a time-weighted average exposure to 0. Inorganic arsenic can enter the organism via the gastrointestinal and respiratory tracts.
The absorbed arsenic is mainly eliminated through the kidney either unchanged or after methylation. Inorganic arsenic is also excreted in the bile as a glutathione complex. Following occupational exposure to inorganic arsenic, the proportion of the arsenical species in urine depends on the time of sampling. The organoarsenicals present in marine organisms are also easily absorbed by the gastrointestinal tract but are excreted for the most part unchanged. Long-term toxic effects of arsenic including the toxic effects on genes result mainly from exposure to inorganic arsenic.
Therefore, biological monitoring aims at assessing exposure to inorganic arsenic compounds. For this purpose, the specific determination of inorganic arsenic As i , monomethylarsonic acid MMA , and cacodylic acid DMA in urine is the method of choice. However, since seafood consumption might still influence the excretion rate of DMA, the workers being tested should refrain from eating seafood during the 48 hours prior to urine collection.
Higher values can be found in geographical areas where the drinking water contains significant amounts of arsenic. In the case of exposure to less soluble inorganic arsenic compounds e. Arsenic in hair is a good indicator of the amount of inorganic arsenic absorbed during the growth period of the hair. Organic arsenic of marine origin does not appear to be taken up in hair to the same degree as inorganic arsenic.
Determination of arsenic concentration along the length of the hair may provide valuable information concerning the time of exposure and the length of the exposure period. However, the determination of arsenic in hair is not recommended when the ambient air is contaminated by arsenic, as it will not be possible to distinguish between endogenous arsenic and arsenic externally deposited on the hair. Arsenic in nails has the same significance as arsenic in hair.
As with urine levels, blood arsenic levels may reflect the amount of arsenic recently absorbed, but the relation between the intensity of arsenic exposure and its concentration in blood has not yet been assessed. Inhalation is the primary route of beryllium uptake for occupationally exposed persons.
Long-term exposure can result in the storage of appreciable amounts of beryllium in lung tissues and in the skeleton, the ultimate site of storage. Elimination of absorbed beryllium occurs mainly via urine and only to a minor degree in the faeces. Beryllium levels can be determined in blood and urine, but at present these analyses can be used only as qualitative tests to confirm exposure to the metal, since it is not known to what extent the concentrations of beryllium in blood and urine may be influenced by recent exposure and by the amount already stored in the body.
Furthermore, it is difficult to interpret the limited published data on the excretion of beryllium in exposed workers, because usually the external exposure has not been adequately characterized and the analytical methods have different sensitivities and precision. However, the finding of a normal concentration of beryllium in urine is not sufficient evidence to exclude the possibility of past exposure to beryllium. Indeed, an increased urinary excretion of beryllium has not always been found in workers even though they have been exposed to beryllium in the past and have consequently developed pulmonary granulomatosis, a disease characterized by multiple granulomas, that is, nodules of inflammatory tissue, found in the lungs.
In the occupational setting, absorption of cadmium occurs chiefly through inhalation. However, gastrointestinal absorption may significantly contribute to the internal dose of cadmium. In tissues, cadmium is mainly bound to metallothionein. In blood, it is mainly bound to red blood cells. In view of the property of cadmium to accumulate, any biological monitoring programme of population groups chronically exposed to cadmium should attempt to evaluate both the current and the integrated exposure.
By means of neutron activation, it is currently possible to carry out in vivo measurements of the amounts of cadmium accumulated in the main sites of storage, the kidneys and the liver. However, these techniques are not used routinely. So far, in the health surveillance of workers in industry or in large-scale studies on the general population, exposure to cadmium has usually been evaluated indirectly by measuring the metal in urine and blood.
The detailed kinetics of the action of cadmium in humans is not yet fully elucidated, but for practical purposes the following conclusions can be formulated regarding the significance of cadmium in blood and urine. In newly exposed workers, the levels of cadmium in blood increase progressively and after four to six months reach a concentration corresponding to the intensity of exposure.
In persons with ongoing exposure to cadmium over a long period, the concentration of cadmium in the blood reflects mainly the average intake during recent months. The relative influence of the cadmium body burden on the cadmium level in the blood may be more important in persons who have accumulated a large amount of cadmium and have been removed from exposure.
After cessation of exposure, the cadmium level in blood decreases relatively fast, with an initial half-time of two to three months. Depending on the body burden, the level may, however, remain higher than in control subjects. Several studies in humans and animals have indicated that the level of cadmium in urine can be interpreted as follows: in the absence of acute overexposure to cadmium, and as long as the storage capability of the kidney cortex is not exceeded or cadmium-induced nephropathy has not yet occurred, the level of cadmium in urine increases progressively with the amount of cadmium stored in the kidneys.
Under such conditions, which prevail mainly in the general population and in workers moderately exposed to cadmium, there is a significant correlation between urinary cadmium and cadmium in the kidneys. If exposure to cadmium has been excessive, the cadmium-binding sites in the organism become progressively saturated and, despite continuous exposure, the cadmium concentration in the renal cortex levels off. From this stage on, the absorbed cadmium cannot be further retained in that organ and it is rapidly excreted in the urine.
Then at this stage, the concentration of urinary cadmium is influenced by both the body burden and the recent intake. If exposure is continued, some subjects may develop renal damage, which gives rise to a further increase of urinary cadmium as a result of the release of cadmium stored in the kidney and depressed reabsorption of circulating cadmium. However, after an episode of acute exposure, cadmium levels in urine may rapidly and briefly increase without reflecting an increase in the body burden. Recent studies indicate that metallothionein in urine has the same biological significance.
Good correlations have been observed between the urinary concentration of metallothionein and that of cadmium, independently of the intensity of exposure and the status of renal function. The normal levels of cadmium in blood and in urine are usually below 0.
They are higher in smokers than in nonsmokers. An accumulation of cadmium in the body which would lead to a urinary excretion exceeding this level should be prevented. For blood, a biological limit of 0. It is possible, however, that in the case of the general population exposed to cadmium via food or tobacco or in the elderly, who normally suffer a decline of renal function, the critical level in the renal cortex may be lower.
The toxicity of chromium is attributable chiefly to its hexavalent compounds. The absorption of hexavalent compounds is relatively higher than the absorption of trivalent compounds. Elimination occurs mainly via urine. In persons non-occupationally exposed to chromium, the concentration of chromium in serum and in urine usually does not exceed 0.
Recent exposure to soluble hexavalent chromium salts e. Studies carried out by several authors suggest the following relation: a TWA exposure of 0. This relation is valid only on a group basis. Following exposure to 0. Hexavalent chromium readily crosses cell membranes, but once inside the cell, it is reduced to trivalent chromium.
The concentration of chromium in erythrocytes might be an indicator of the exposure intensity to hexavalent chromium during the lifetime of the red blood cells, but this does not apply to trivalent chromium. To what extent monitoring chromium in urine is useful for health risk estimation remains to be assessed.
Once absorbed, by inhalation and to some extent via the oral route, cobalt with a biological half-life of a few days is eliminated mainly with urine. Exposure to soluble cobalt compounds leads to an increase of cobalt concentration in blood and urine. The concentrations of cobalt in blood and in urine are influenced chiefly by recent exposure. For TWA exposures of 0. Sampling time is important as there is a progressive increase in the urinary levels of cobalt during the workweek.
In workers exposed to cobalt oxides, cobalt salts, or cobalt metal powder in a refinery, a TWA of 0. Inorganic lead, a cumulative toxin absorbed by the lungs and the gastrointestinal tract, is clearly the metal that has been most extensively studied; thus, of all the metal contaminants, the reliability of methods for assessing recent exposure or body burden by biological methods is greatest for lead.
In a steady-state exposure situation, lead in whole blood is considered to be the best indicator of the concentration of lead in soft tissues and hence of recent exposure. However, the increase of blood lead levels Pb-B becomes progressively smaller with increasing levels of lead exposure. When occupational exposure has been prolonged, cessation of exposure is not necessarily associated with a return of Pb-B to a pre-exposure background value because of the continuous release of lead from tissue depots.
These levels may be influenced by the dietary habits and the place of residence of the subjects. In children, lower blood lead concentrations have been associated with adverse effects on the central nervous system. Lead level in urine increases exponentially with increasing Pb-B and under a steady-state situation is mainly a reflection of recent exposure.
The amount of lead excreted in urine after administration of a chelating agent e. It seems that under constant exposure, chelatable lead values reflect mainly blood and soft tissues lead pool, with only a small fraction derived from bones. An x-ray fluorescence technique has been developed for measuring lead concentration in bones phalanges, tibia, calcaneus, vertebrae , but presently the limit of detection of the technique restricts its use to occupationally exposed persons.
Determination of lead in hair has been proposed as a method of evaluating the mobilizable pool of lead. However, in occupational settings, it is difficult to distinguish between lead incorporated endogenously into hair and that simply adsorbed on its surface. The determination of lead concentration in the circumpulpal dentine of deciduous teeth baby teeth has been used to estimate exposure to lead during early childhood.
Parameters reflecting the interference of lead with biological processes can also be used for assessing the intensity of exposure to lead. After the termination of occupational exposure to lead, the erythrocyte protoporphyrin remains elevated out of proportion to current levels of lead in blood.
In this case, the EP level is better correlated with the amount of chelatable lead excreted in urine than with lead in blood. Slight iron deficiency will also cause an elevated protoporphyrin concentration in red blood cells. In some countries, tetraethyllead and tetramethyllead are used as antiknock agents in automobile fuels. Lead in blood is not a good indicator of exposure to tetraalkyllead, whereas lead in urine seems to be useful for evaluating the risk of overexposure.
In the occupational setting, manganese enters the body mainly through the lungs; absorption via the gastrointestinal tract is low and probably depends on a homeostatic mechanism. Manganese elimination occurs through the bile, with only small amounts excreted with urine. It seems that, on an individual basis, neither manganese in blood nor manganese in urine are correlated to external exposure parameters.
There is apparently no direct relation between manganese concentration in biological material and the severity of chronic manganese poisoning. It is possible that, following occupational exposure to manganese, early adverse central nervous system effects might already be detected at biological levels close to normal values. Inhalation represents the main route of uptake of metallic mercury.
The gastrointestinal absorption of metallic mercury is negligible. Inorganic mercury salts can be absorbed through the lungs inhalation of inorganic mercury aerosol as well as the gastrointestinal tract. The cutaneous absorption of metallic mercury and its inorganic salts is possible. The biological half-life of mercury is of the order of two months in the kidney but is much longer in the central nervous system. Inorganic mercury is excreted mainly with the faeces and urine. Small quantities are excreted through salivary, lacrimal and sweat glands.
Mercury can also be detected in expired air during the few hours following exposure to mercury vapour. Under chronic exposure conditions there is, at least on a group basis, a relationship between the intensity of recent exposure to mercury vapour and the concentration of mercury in blood or urine.
These values can be influenced by fish consumption and the number of mercury amalgam fillings in the teeth. The organic mercury compounds are easily absorbed by all the routes. A distinction must be made, however, between the short chain alkyl compounds mainly methylmercury , which are very stable and are resistant to biotransformation, and the aryl or alkoxyalkyl derivatives, which liberate inorganic mercury in vivo.
For the latter compounds, the concentration of mercury in blood, as well as in urine, is probably indicative of the exposure intensity. Under steady-state conditions, mercury in whole blood and in hair correlates with methylmercury body burden and with the risk of signs of methylmercury poisoning. Nickel is not a cumulative toxin and almost all the amount absorbed is excreted mainly via the urine, with a biological half-life of 17 to 39 hours. The concentrations of nickel in plasma and in urine are good indicators of recent exposure to metallic nickel and its soluble compounds e. Values within normal ranges usually indicate nonsignificant exposure and increased values are indicative of overexposure.
In workers exposed to slightly soluble or insoluble nickel compounds, increased levels in body fluids generally indicate significant absorption or progressive release from the amount stored in the lungs; however, significant amounts of nickel may be deposited in the respiratory tract nasal cavities, lungs without any significant elevation of its plasma or urine concentration. Selenium is an essential trace element. Soluble selenium compounds seem to be easily absorbed through the lungs and the gastrointestinal tract. Selenium is mainly excreted in urine, but when exposure is very high it can also be excreted in exhaled air as dimethylselenide vapour.
The concentration of selenium in urine is mainly a reflection of recent exposure. The relationship between the intensity of exposure and selenium concentration in urine has not yet been established. It seems that the concentration in plasma or serum and urine mainly reflects short-term exposure, whereas the selenium content of erythrocytes reflects more long-term exposure.
Measuring selenium in blood or urine gives some information on selenium status. Currently it is more often used to detect a deficiency rather than an overexposure. Since the available data concerning the health risk of long-term exposure to selenium and the relationship between potential health risk and levels in biological media are too limited, no biological threshold value can be proposed. In industry, vanadium is absorbed mainly via the pulmonary route. Vanadium is excreted in urine with a biological half-life of about 20 to 40 hours, and to a minor degree in faeces.
Urinary vanadium seems to be a good indicator of recent exposure, but the relationship between uptake and vanadium levels in urine has not yet been sufficiently established. It has been suggested that the difference between post-shift and pre-shift urinary concentrations of vanadium permits the assessment of exposure during the workday, whereas urinary vanadium two days after cessation of exposure Monday morning would reflect accumulation of the metal in the body.
Organic solvents are volatile and generally soluble in body fat lipophilic , although some of them, e. They have been extensively employed not only in industry but in consumer products, such as paints, inks, thinners, degreasers, dry-cleaning agents, spot removers, repellents, and so on. If the address matches an existing account you will receive an email with instructions to retrieve your username. Skip to Main Content. Rosen MD,. First published: 19 July About this book Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 8th Edition is the comprehensive revision of the field-leading reference on bone and mineral health.
The eighth edition has been fully revised by the leading researchers and clinicians in the field to provide concise coverage of the widest possible spectrum of metabolic bone diseases and disorders of mineral metabolism. Chapters look to explain basic biological factors of healthy development and disease states and make it easily translatable to clinical interventions. Moe received his medical degree from the University of Toronto where he also did his internal medicine residency and clinical nephrology fellowship.
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Orson Moe conducts both basic science and patient-oriented research on renal physiology and metabolism, and epithelial biology. I would definitely recommend this book to anyone in the nephrology community, whether clinical or research oriented. Praise for the Previous Edition: "This is an excellent in-depth compilation of all aspects of renal physiology in health and disease, presented in well-balanced in chapters with high-quality figures and ample references…This book clearly represents an excellent, useful, usable, and in view of recent rapid scientific progress needed update of the previous edition and will have a prominent place on my bookshelf as well as those of many others in the field.
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