Archive for the ‘science’ Category

Is Hair Cell Regeneration in Humans Possible?

September 5th, 2010 Comments off


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Hair cell damage in the inner ear is becoming increasingly more common. More children, and adults, are exposing themselves to loud noises via concerts or headphones, and there are other various environmental factors as well. There are medicines and ototoxins, diseases, and overstimulization issues that also contribute to hair cell damage. Since this is becoming a more common issue, researchers are developing ways to regenerate the hair cells within the inner ear. This is necessary because the loss of hair cells can lead to hearing loss. Additionally, it can lead to problems with balance and the overall quality of life. While hair cell regeneration in humans is a possibility of the future, it will not be successful without further research and development.


The loss of hair cells in the inner ear leads to a sensorineural hearing loss. This type of loss usually occurs in the cochlea, which is within the inner ear and it is vital to processing sound as it is the primary organ of hearing (Cotanche, 2008). This type of loss is very difficult to treat as hair cells do not reproduce on their own, so once they are lost, the loss is permanent. Sensorineural hearing loss occurs due to hair cell loss, damage, hair cell degeneration, and other various sources (Izumikawa, Minoda, Kawamoto, Abrashkin, Swiderski, Dolan, et al. 2005).

To explain the difficulty in regenerating hair cells, it is best to cover some of the anatomy of how the cochlea works in the hearing process. This will provide a better understanding of treatment. Once sound enters the ear, it changes from acoustic to mechanical energy in the middle ear. From the middle ear, it is sent to the inner ear where it changes from mechanical to hydraulic energy. When the wave of energy reaches the cochlea, it changes back to mechanical energy, and then chemical energy within the hair cells. The transduction process is vital for hearing, as the brain cannot process acoustic energy. If the chemical process is absent or minimal, the brain cannot process the sound, and thus hearing will be impaired. (Hume, Oesterlie, Raible, Rubel, & Stone, 2010).

In cell development, there are sensory and nonsensory supporting cells (Ozeki, Oshima, Senn, Kurihara, & Kaga, 2007).   They alternate in their development, with nonsensory supporting cells at the bottom holding the sensory hair cells into place.   According to the lateral inhibition theory of cell development, the supporting cells replace the hair cells when they are damaged, and then more supporting cells are recreated as needed.   The supporting cells divide without assistance to replace the missing cells.   This is the ideal cure to hair cell regeneration and knowledge of how this process works is vital to researchers.   With this information, it enables them to find a way to recreate this cell division process.   In the bird’s organ of hearing, they are capable of this self repair.   However, in humans it is still being assessed as merely a possibility.   The problem is that this type of cell division does not happen spontaneously in the human organ of hearing.   Researchers are still developing ways to make this event happen through the use of growth hormones, stem cells, genes, etc.   (Walshe, et al. 2003)

            As mentioned, human hair cells do not regenerate on their own, and this was because not all cells have the ability to divide (White, Doetzlhofer, Yun Shain, Groves, & Segil, 2006).   One of the biggest challenges for researchers was getting cells to divide that normally do not possess this ability.   Once the hair cells were damaged or lost, it resulted in hearing loss, or even the possibility of a cochlear implant to enable hearing.   Again, hearing loss may cause balance issues as there are hair cells in the vestibular system.   (Ozeki, et al. 2007)

            Why are birds able to regenerate cells and humans cannot?   Birds, however, had the ability to regenerate hair cells automatically, once they were lost or damaged.   Researchers are currently still studying these animals to find out why they possess this ability.   Thus far, they have discovered that birds were able to restore neural connections as a functional unit.   This means that instead of having different cells, performing various functions and regenerating separately, in birds they regenerated as a whole. (Walshe, et al. 2003).

            A more in-depth look at bird’s regenerative ability revealed that once a bird’s hair cell was lost or damaged, the auditory nerve retreated from the cell (Matsui & Ryals, 2005).   Once the innervation was removed, the process of replacing the cell could begin.   A signal came down from the Notch, notifying the bird’s organ of hearing to begin the replacement process (Stone & Rubel, 2000).   Bird’s have a different organ of hearing than humans.   The basilar papilla in a bird is similar to the cochlea in a human.   It controls the hearing process and in their case, hair cell regeneration.   (Hume, Oesterlie, Raible, Rubel, & Stone, 2010). Their hair cells then had the ability to proliferate, or to multiply excessively as needed to repair themselves.   After the cells multiply, they transdifferated or replaced the dead cells, and then they were re-innervated by the auditory nerve.   This is an amazing process that occurs automatically within birds. (Stone & Rubel, 2000)

            When looking at possibilities for hair cell regeneration within humans, proliferation and transdifferation are two proposed options for repair and both are dependent upon each other.   During the proliferation process, cells multipled rapidly in order to replace the damaged or dead cells.   However, in the transdiffereration process, the proliferated cells were stimulated in an attempt to repair the damaged cell.   Stimulation allowed the cell to divide, and while the new division replaced the supporting cell, the supporting cell took place of the damaged hair cell.   One of the main concerns with this process was the restructuring of the cells.   Would this change alter the organ of Corti in humans?   If it does, what is the affect this would have on hearing?   The only way this process will be effective is if the transdifferated cell replaces itself.   What could happen if the cell does not replace itself?   Would there be a bunching of supporting cells, or even possibly missing supporting cells?   If supporting cells are missing, will there be a space and nothing to hold on to the newly generated hair cell?   These are questions that researchers are still trying to answer before conducting experiments in humans, and most definitely before approving this type of resolution as valid for hair cell regeneration. (Mastui, et al. 2005).

                To recreate the proliferation process in humans, genes must be present or injected as this does not happen naturally (Matsui, et al. 2005).     Additionally, Kopke, Jackson, Geming, Rasmussen, Hoffer, & Frenz (2001) found that insulin can increase the cell response.   Thus, if the cell does not proliferate after being exposed to the gene, insulin can be added to increase the likelihood that it will divide.

            The primary gene involved in proliferation is Atoh1.   Once injected into the organ of Corti, it can function as a non-expressing supporting cell, an expressing hair cell, or it can even be expressed but not function as a sensory cell (Ozeki, et al. 2007).   Atoh1 regulates “common cellular precursor’s” in cell differentiation, which is why it is seen as the primary gene in hair cell regeneration.   (Izumikawa, et al. 2005).

                Matsui et al. (2005) used microarray to establish which gene was expressed and its location.   This assessment was great for inner ear analysis given the specificity and intricate structures.   Additionally, they were able to look at transcription factors to determine which genes played specific roles.   Their results found that there were six-hundred factors in both the vestibular and auditory system, and only forty in one organ.  

            Another theory involved in hair cell regeneration or cell development, is the use of growth factors.   They are associated with the differentiation and proliferation process, but suggest that instead of genes, these growth factors cause the regeneration (Kopke, et al. 2001). Matsui et al. (2001) suggests that macrophages, or white blood cells, are housed within tissue and they go to the dying cells.   Once in the vicinity, they either repair or remove the dying cell.   This process most frequently occurs after some type of trauma.   A flaw with this theory was that the researchers were unclear of the current function of the macrophages within the inner ear of humans.   Obviously, this process was not currently working spontaneously, as humans cannot regenerate cells without assistance.   However, researchers would like to better understand this process within the inner ear to determine if hair cell regeneration is possible by the production of growth factors in general. (Oregon Health & Sciences University, 2008).

                Other significant contributors to the process of proliferation are leukocytes-activators or “progenitor cell proliferation” (Stone & Rubel, 2000).   There were three subtypes of progenitors that may play a role in this process.   The first was the neuronal-colony-forming type which were the most similar to stem cells (Stone, Choi, Wooley, Yamashita, Rubel, 1999).   The second and third type were the progency and mash1 which had very little proliferate ability. These variances in progenitor cells may explain the differences in regeneration.   Furthermore, it may also explain why other animals can regenerate while humans cannot.   Additional research needs to be conducted to determine the exact role these ‘activators’ play in the proliferation process.   (Stone & Rubel, 2000).

            The transdifferation process, in comparison to proliferation, is about as complex.   In this process, the cells are transformed from supporting cells into hair cells (Ozeki, et al. 2007).   This process can be initiated by the use of the gene Atoh1 as well as Retinoic acid (Kopke, et al. 2001) and (White, et al. 2006).   One flaw in this process is that the hair cell may not always be functional after transformation (Kopke, et al. 2001).   This is because the cell needs a brain-derived neurotrophic factor which is provides a neurological connection and lack of it can prevent function of the generated hair cell.     Furthermore, it is important for vestibular ganglion neurons to survive, it protects neurons from ototoxins which may cause future damage to the cell, and when combined with insulin and retinoic it is known to cause vestibular function.   Ideally, this means once we get control of how this process works, we could possibly treat some balance disorders.   Given all of this information, it is important to note that neural elements are not needed for the regeneration process itself and it does not affect the production of hair cells; it is only necessary for function and innervations of the hair cell (Stone & Rubel, 2000).

            Now that there is a better understanding of the anatomical process involved in the inner ear, it is best to assess the proposed treatments for human hair cell regeneration.   The first treatment was the reconstruction of the organ of Corti.   Ideally, Ozeki et al. (2007) found that doctors should inject progenitor cells into the inner ear.   After the injections, the hope was that the cells would differentiate on their own into supporting or hair cells as necessary.   This meant that the supporting cells would differentiate into hair cells, and more supporting cells would be created.

The second proposed treatment was stem cell transplant. This became a possibility because stem cells had many properties that were beneficial to humans. Additionally, they had very similar properties to supporting cells, could generate in large numbers, and could take the form of different types of cells (Matsui, et al. 2005). One drawback of this treatment was the uncertainty if the new cell would be functional. An additional avenue of this type of treatment was to find out if progenitor cells could act like stem cells (Stone & Rubel, 2000).

As researchers progress in finding a successful treatment for regenerating hair cells within the inner ear, there are still many questions to be answered about the process. For one, why do only our vestibular cells show the possibility of regeneration (Matsui, et al. 2005)? This is interesting because Matsui et al. (2005) found that hair cells regenerate spontaneously in the vestibule but not in the cochlea. Is it possible that vestibular cells do not need a replacement cell? Why is it that the auditory system cells do not regenerate (Rubel, 2005)? Do supporting cells lack a replacement cell; are there unknown gene functions; are signals being blocked that regulate cell regeneration (White, et al. 2006)? Until these questions are answered, significant research still needs to be conducted in this area of treatment.

The possibility that hair cell regeneration will someday lead to the restoration of hearing still exists. Many avenues have been addressed by various researchers ranging in everything from genes, growth factors, and stem cell replacement. However, if research reaches the point where hair cell regeneration is successful, this does not resolve the issue of whether hair cell regeneration alone can restore hearing in a hearing impaired individual. There is still the idea that not all regenerated cells will be functional and innervated, and the regeneration process may not provide full regeneration. Thus, the result will still be a hearing impairment. Unless hair cell regeneration can overcome all of these obstacles, the need for a cochlear implant may still be necessary.


1. Cotanche, D. (2008). Genetic and pharmacological intervention for treatment/prevention of hearing loss. Journal of Communication Disorders, 41(5): 421-43.

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Is Hair Cell Regeneration in Humans Possible? (Part 2)

September 5th, 2010 Comments off


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2. Hume, Oesterlie, Raible, Rubel, & Stone. (2010). Inner ear hair cell regeneration. Virginia Merrill Bloedel Hearing Research Center. Retrieved March 20, 2010 from http:// depts. washington. edu/hearing/InnerEarHairCellRegeneration. php

3. Izumikawa, M. Minoda, R. Kawamoto, K. Abrashkin, K. Swiderski, D. Dolan, D. et al.

(2005). Auditory hair cell replacement and hearing improvement by Atoh1 gene therapy in deaf mammals. Nature Medicine, 11(3), 271-276.

4. Kopke, R. Jackson, R. Geming, L. Rasmussen, M. Hoffer, M. Frenz, D. et al. (2001). Growth factor treatment enhances vestibular hair cell renewal and results in improved vestibular. Proceedings of the National Academy of Sciences of the United States of America, 98(10), 5886.

5. Matsui, J. & Ryals, B. (2005). Hair cell regeneration: An exciting phenomenon … But will restoring hearing and balance be possible? Journal of Rehabilitation Research & Development, 42187-198. Doi:10. 1682/JRRD. 2005. 01. 0008.

6. Oregon Health & Sciences University. (2008). Treatment for hearing loss? Scientists grow hair cells involved in hearing. ScienceDaily. Retrieved March 20, 2010 from www. sciencedaily. com/releases/2008/08/080830005613. htm

7. Ozeki, H. Oshima, K. Senn, P. Kurihara, H. & Kaga, K. (2007). Development and regeneration of hair cells. Acta Oto-Laryngologica (Supplement), 12738-44. Doi: 10. 1080/03655230701597200

8. Rubel, E. (2005). Hair cell regeneration: look into the future. Journal of Acoustical Society of America, 117(4), 2377-2377.

9. Stone, J. Choi, Y. Wooley, S. Yamashita, H. Rubel, E. (1999). Progenitor cell cycling during hair cell regeneration in the vestibular and auditory epithelia of the chick. Journal of Neurocytology, 28, 863-876.

10. Stone, J. & Rubel, E. (2000). Cellular studies of auditory hair cell regeneration in birds. Proceedings of the National Academy of Sciences of the United States of America, 97(22), 11714.

References Continued

11. Walshe, P. Walsh, M. & McConn Walsh, R. (2003). Hair cell regeneration in the inner ear: a review. Clinical Otolaryngology & Allied Sciences, 28(1), 5-13. Doi:10. 1046/j. 1365-2273. 2003. 00658. x.

12. White, P. Doetzlhofer, A. Yun Shain, L. Groves, A. & Segil, N. (2006). Mammalian cochlear supporting cells can divide and trans-differentiate into hair cells. Nature, 441(7096), 984-987. Doi: 10. 1038/nature04849.

13. Viastarakos, P. Nikolopoulos, T. Tavoulari, E. Papacharalambous, G. (2008). Sensory cell regeneration and stem cells: what we have already achieved in the management of deafness. Otology & Neurotology, 29(6): 758-68.

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Early Detection of Autism in Infants and Toddlers

June 15th, 2010 Comments off


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At this very moment, thousands of infants and toddlers throughout the United States exhibit worrisome behavior. They are being managed by perplexed parents and remain unclassified by family practioners, but the developmental outcome of these very young children may brighten as the early diagnosis and consequential expedience of intervention becomes a reality. Anecdotal reports imply that children diagnosed with autism display characteristics of abnormal behavior at an early age, possibly from birth, and in fact, this early onset of such behaviors (prior to thirty-six months) is a diagnostic criterion (Young, Brewer, & Pattison, 2003). According to Trevarthen & Aitken, (2001) fifty percent of parents of children with suspected autism report a strong suspicion of abnormal development prior to the age of one. However, as Kalb asserts, most children will not even be seen by specializing clinicians until they have reached their second birthday with many of these waiting on the appropriate diagnosis until at least the age of three (2005). Further research suggests that anywhere between thirty-one and fifty-five percent of children with autistic disorder show at least some defining behavioral characteristics in the first year of life, and seventy-five to eighty-eight percent have some of these abnormal responses by the first two years of life (Young et al. 2003). For example, in this same data analysis conducted, it was determined that despite these qualitative and quantitative differences in development, the average age of diagnosis for children living in the United Kingdom in 1994 was not until forty-four months even when parents became first concerned about their child’s development at an average age of seventeen months (Young et al. 2003). Additional research has demonstrated a lag between twenty-four and thirty months from the first expression of apprehension by parents about their child’s development to the actual obtainment of a diagnosis.

Over the past decade, researchers have been working toward increasing the accuracy and sensitivity for the interpretation of minute behavioral characteristics in distinguishing autism from the typically developing population. As part of a ten year plan, the National Institute of Mental Health has set the goal of actually “reducing the frequency of autism in school-aged children through early diagnosis and intervention,” (Volkmar, Chawarska, & Klin, 2005). To do this, diagnostic criteria must be tweaked to accommodate the earliest observable behaviors of this disorder. The current definition outlined by the DSM-IV-TR was not researched for children under the age of three, and therefore, is clearly not applicable to toddlers and infants, particularly involving criteria for peer relationships and conversational skills (Klin, Charwarska, Paul, Rubin, Morgan, Wiesner, & Volkmar, 2004). As stated by Young et al. “Many of the behaviors included in [this] classification system relate to secondary behaviors often developed to compensate for underlying neurological deficits,” (2003). For example, stereotyped behaviors such as adherence to routines and rituals are much more common in older children and are rarely noted in children under two years of age. In this paper I will review the observed signs and symptomology reported by parents, observed during clinical diagnostics, and investigated within in the research setting of very young children with suspected autism spectrum disorders.

Parental Observations of Early Symptomology

Parents are often the first to become aware of behavioral deviations their children display from the expected norm, and as a result, these observations become critically vital for the development of early diagnostic tools in clinical evaluation. In a study conducted by Young et al. in 2003, the researcher found the mean age in which parents first notice abnormal developmental signs to be approximately 15. 1 months with a standard deviation of 11. 2 months. Ninety-five percent of these same parents noted anomalies in social development by the age of two. By their first birthdays, children have been noted by their parents to show patterns of extreme reactivity, either getting upset when a new toy or activity is presented or barely noticing this novelty at all. In case reports of classic autism, parents often report their babies have failed to coo or babble by their first birthday or words that they have developed inexplicably disappear (Kalb, 2005). A substantial proportion of others also exhibit repetitive behaviors characteristic of autism such as rocking back and forth or becoming fixated on an object, as well as unusual preoccupations and stereotypy emerging around twenty to thirty months (Kalb, 2005). Parents predominantly report that speech delays or worries about hearing are common concerns, and also may worry that their child is too well behaved or is highly irritable (Volkmar et al. 2005). Additionally, infants with autism may display limited eye contact, diminished social responsiveness, and show little facial expression. Children may be less likely to engage in motor or vocal imitation and are more likely to exhibit difficulties in regulating arousal levels and organizing sensory responses.

By thirty months, Volkmar et al. determined that differences from typical peers in areas of “both person-to-person behaviors (anticipatory postures, turn taking, intensity of eye contact)” and “behaviors in which an object is the focus of joint interest (joint attentional skills such as pointing to materials, following a point of another person, or giving objects),” (2005) have become readily apparent to many adults the children interact with, particularly parents. A minority of children with autism, however, (approximately one in five) show a normal course of development during infancy but begin to lose or regress in social and communication skills and instead manifest autistic symptoms of attention and preservative behavior between the ages of eighteen and thirty-six months (Osterling, Dawson, & Munson, 2002). This and other variations in the acquisition of symptomology of infants and toddlers with autism present significant difficulties in relying solely on parental observation, and thus require further evaluation and scientific study by trained clinicians.

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Early Detection of Autism in Infants and Toddlers (Part 2)

June 15th, 2010 Comments off


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Problems Associated with the Reliability of Parental Report of Early Symptoms

Due to the fact that parents spend the most time with their young children, both mother and father are considered to be in the best position logically to provide historical background information pertaining to developmental delays, skill regression, patterns of behavior, and behavioral difficulties shown by their children with suspected autism. Despite this remark, Goin & Myers determined that parent and family caregivers, as the most intimate observers of their own children, can deviate from objectivity in their recall of behaviors (2004). Moreover, due to the fact that twenty to forty percent of parents report a normal developmental course for their child up until an observed regression point, the examination of extremely early symptoms of infants later diagnosed with autism becomes limited to a smaller percent who have experienced consistently slow developmental milestones (Volkmar et al. 2005). Less frequently, evidence of autistic symptoms may be apparent in children under the age of three, and thus, compiled in data to determine the earliest diagnostic criteria, but these behaviors may become less obvious as the child matures. Finally, due to the fact that seventy-five percent of children with autism are mentally retarded, it is possible that the symptoms parents report in infants with autism are more so related to mental retardation and not at all autism specifically (Osterling et al. 2002). These weaknesses in terms of the reliability of parental report necessitate further investigation before an exact definition of autism can be developed in very early infants.

Overview of Early Symptomology as Assessed by Experienced Clinicians

Parents are often asked to participate in the systematic study of their children’s autistic behaviors by experienced researchers, even when direct observational reports are not requested in the form of parental interview as were described previously. With the technological revolution in the past decades in the United States, video cameras have become increasing accessible to families across the nation, and therefore, many parents inadvertently provide detailed documentation of their child’s development which can be utilized in research. According to Baranek in 1999, “retrospective video analysis has shown success as an ecologically valid methodological tool for earlier identification of children with various psychopathologies,” (220), and consequently can provide significant reliability and validity to parental report of behaviors.

Such is the case in an experiment conducted by Volkmar et al. (2005) where age-matched infants with autism were compared to typically developing infants, and differences in visual attention to social stimuli, smile frequency, vocalization, and object exploration engagement were examined. At twenty months of age, behaviors in facial expression, use of conventional gesture, and pointing to indicate interest were distinguishing criteria. In a follow-up retrospective video analysis between twelve and fifteen months later, groups were identified by social activities such as seeking shared enjoyment, social reciprocity, use of another person as a tool, interest in other children, and in communicative tasks, (e. g. attending to voice, pointing, using and understanding gesture). A similar study determined that by the age of three, finger mannerisms, attention to voice, pointing, and the use of other person’s body were able to correctly classify all subjects recruited in the experiment as either autistic or typically developing by examining videotaped interactions of young infants (Cox, Charman, Baron-Cohen, Drew, Klein, Baird, Swettenham, & Wheelwright, 1999). When first birthday party video tapes were viewed by Osterling & Dawson, a significant main effect of the diagnostic group was found for the category of social behavior, including looking at the face of another, seeking contact, imitating, and for the category of joint attention behaviors, pointing vague pointing, showing, as well, but not for the category of communicative behaviors of following directions and babbling (1994). In these videos, it was determined that the autistic subjects showed significantly more abnormal systems such as ear covering and self-stimulation, and as a result, ninety-one percent of all cases were correctly identified, providing solid evidence that professionals should thoroughly evaluate infantile use of eye contact, joint attention behaviors, and orientating to speech when determining appropriate diagnostic measures. Baranek found similar results when comparing infants with mentally retarded participants, in that those with autism exhibited poor visual attention, required more prompts to respond to their name, excessively mouthed objects, and more frequently showed aversion to social touch (1999). Furthermore, in a study aimed to characterize infants with autism spectrum disorders under the age of one, five behavior abnormalities were documented through retrospective video analysis which included poor social attention, lack of social smiling and appropriate facial expressions, hypotonia, and unstable attention (Werner, Dawson, Osterling, & Dinno, (2000).

Neurological Abnormalities as Diagnostic Criteria

To evaluate the significance of the previously reported behavioral characteristics found in various research studies, one must examine the neurological abnormalities occurring in the brains of those with autism. In determining the rationale for each observed behavior, it is important to establish that many core deficit behaviors can be linked to underlying neurological problems, whereas “secondary manifestations may be a product of an individual’s approach to coping with the disorder or other disorders that may coexist,” (Young et al. 2003), such as an intellectual disability. The cerebellum, medial temporal structures, and prefrontal cortex have been recognized as possible core regions of abnormality in autism spectrum disorders (Dawson, Meltzoff, Osterling, & Rinaldi, 1998), and perhaps the imaging process of an fMRI, MRI, or CT scan of the brain during infancy could diagnose children very early before symptoms appear, as brain differences would most likely precede observed behaviors. Further evidence supporting the notion that the medial temporal lobe of an individual’s brain is a primary player in the manifestation of autistic symptoms is found when lesions are made in the hippocampus and amygdala early in the development of monkeys.

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Early Detection of Autism in Infants and Toddlers (Part 3)

June 15th, 2010 Comments off


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These animal subjects subsequently displayed the persistent and severe cognitive and social impairments as well as stereotyped and self-stimulatory behaviors that are defining features of autism (Dawson et al. 1998). However, this discovery does contrast a recent case study evaluation of a young autistic girl by Dawson, Osterling, Meltzoff, and Kuhl which determined that in this specific child at one year of age, impairments did not exist in the domains of immediate memory of actions, working memory, and response inhibition linked to frontal lobe functioning as core features of autism (2000).

Head Circumference Growth as a Predictor of Autism

A recent discovery in human physiology and brain development research has led to the involvement of the Baby Sibs consortium in an effort to determine the earliest physical markers of autism, particularly abnormal head circumference growth (Kalb, 2005). It is presumed that if a significant increase in head growth during infancy is a risk factor for autism, the mechanism that triggers this onset of growth would actually precede any manifestation of the disorder. Post-mortem brain studies described by Lainhart suggest that brain abnormalities begin before birth in at least a percentage of cases of autism, and therefore, provide further evidence to this claim (2003). According to this same author, between birth and six to fourteen months of age, head circumference has been shown to increase at a significantly greater rate in children with autism than in an control or reference sample (Lainhart, 2003); fifty-nine percent of children with autism and only six percent of typically developing children show an increase of two or more standard deviations in head circumference during this developmental time. In another study of this same type with consistently similar results, it was determined that approximately ninety percent of two and three year old children had brain volumes larger than the healthy average in addition to abnormally large head circumferences (Courchesne, Carper, & Akshoomoff, 2003). In comparison to growth charts produced by the Center for Disease Control, average head size in recruited participants increased from the twenty-fifth percentile at birth to the eighty-four percentile in six to fourteen month old babies with autism spectrum disorders (Courchesne, et al. 2003), well before the typical onset of clinically significant behavioral symptoms. By late childhood, however, a follow-up study of participants between the ages of eight and forty-six yielded MRI results demonstrating that this extreme brain overgrowth is time limited and that eventually brain size between control and autistic individuals becomes approximately equal (Courchesne, et al. 2003). An additional study by Torrey, Dhavale, Lawlor, and Yolken discovered a pattern of significantly larger body weight and length in four month old infants later diagnosed with autism in comparison to control subjects, inferring that an abnormality in metabolism, growth factors, and hormone levels may indeed be the culprit (2004). Accelerated rate in head circumference growth is associated during infancy with overall increased brain volume and gray matter, as well as increased cerebral gray matter. Scientists have not come to a conclusive decision as to what exactly accounts for this increase, but theory suggests that the sudden growth could result from an over abundance of neuronal connections, which pruning fails to eliminate (Kalb, 2005).

The discovery that an overgrowth of head circumference occurs frequently during the early months of life for those later diagnosed with autism holds a very promising clinical role in the detection of this disorder. An inexpensive and noninvasive assessment technique, the tracking of brain size development may be a key to early diagnosis and consequently, even earlier intervention practices. If these results are further confirmed by subsequent studies, physicians and psychologists in the future may be able to quickly assess the risk for developing autism based on physical examination alone.

Communication Abnormalities: Nonverbal Gestures and Speech

Parents frequently express initial concern over their child’s speech and communication development, and thus this often becomes the first complaint of autism-related behavior that sends parents to seek out an evaluation. Although typically developing newborn infants possess immature brains, limited cognition, and weak bodies, it has been established that most are very motivated beyond an instinctual drive to attract parental care for immediate biological needs, and thus “to communicate intricately with the expressive forms and rhythms of interest and feeling displayed by other humans,” (Trevarthen & Aitken, 2001). This drive does not seem to be as strong in young children with autism as in most instances they communicate less frequently than matched developmentally delayed children. These children are also less likely to use contact and conventional gestures in requesting an object, but are, in fact, more likely to use unconventional gestures to make up for this deficit in such ways as manipulating the hand of the individual with whom they are interacting to the desired object (Volkmar et al. 2005). In an article by Werner et al. it was demonstrated that at two months of age, infants start to implement their vocalizations in a semi-social manner, and this distinction further aids in subsequent speech and language development (2000). From these results, one can determine that perhaps differences in these areas of vocalization between typically developing and impaired infants become evident by the age of twelve months. Also between the ages of six months to one year, meaningful differences become more pronounced in the communicative criteria, especially noted when these children develop a general lack of orientation toward verbalization and their own names. These differences, however, are often not utilized in evaluation of development and assessment for autism in individual children because most parents fail to recognize these communication difficulties until spoken language is more apparently delayed.

Within this same realm of communicative impairment, very young children with autism have also be distinguished in various studies from typically developing controls on the basis of response to name calling.

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Early Detection of Autism in Infants and Toddlers (Part 4)

June 15th, 2010 Comments off


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The process of learning to orient to one’s own name involves aspects of both social and communication domains as well as attention (Werner et al. 2000), and therefore, difficulties in responding to this specific vocalization indicates a broad range of dysfunction. Potentially a powerful estimate of impairment on the autism disorder spectrum, typically developing infants orient to their name being called approximately seventy-five percent of the time, whereas only thirty-seven percent of autistic infants oriented to their names between the ages of eight and ten months using retrospective home video footage in a study by Werner et al. (2000). Fewer differences were noted in terms of social response to name calling than in the Osterling and Dawson study (1994) of infants at one year of age, perhaps due to the fact that between nine and twelve months of age, many new behaviors are just beginning to develop. Although many complex social, emotional, and communicative behaviors emerge during the eight to nine months of life, skills within these categories do not begin to solidify until after the age of one.

Joint Attention as a Predictor for Social Impairment

The previous example of response to name calling in very young children also draws upon the difficulties that most autistic infants experience in their development of joint attention skills. During the first year of life, children with autism spectrum disorders may fail to follow a point and in many instances, will not gaze switch between interesting objects and an adult’s face or coordinate responses to emotional displays by an adult (Charman, Baron-Cohen, Swettenham, Cox, Baird, & Drew, 1997). Moreover, gaze monitoring in joint attention, which provides relevant information concerning interests and dangers in the environment, is essential for the active participation of social learning opportunities for all infants (Charwarska, Klin, & Volkmar, 2003). As such, deficits in spontaneous gaze monitoring are widely recognized at this point in current research as early signs of autism, although we are unaware of the neurological mechanisms to produce these problems. Kalb has determined through eye-tracking technology that when affected toddlers view the videos of their caregivers or other babies within the same nursery of which they are familiar, they tend to focus more on the individual’s mouth or an object located directly behind the individual than his or her eyes (2005). This finding was confirmed when Charwarska et al. demonstrated in 2003 that although face recognition improves with age in those with autism, older individuals employ feature-based rather than holistic strategies in face processing, and therefore, “recruit different neural substrates in face processing than their typical controls,” (1985).

In terms of pointing behavior, typically developing children will follow a pointed index finger when they have achieved a developmental level of twelve months old, but children with autism from the time they are born are significantly less likely, according to Young et al. to switch their gaze as a means of following a point by another individual (2003). Despite these findings, many infants with autism at two years of age show intact performance relative to typically developing controls in the area of nonsocial use of gaze to obtain information about objects and the environment surrounding them. Charman et al. suggest that these abilities remain intact in those with autism although social gaze is not initiated because they are not a feature of the central social communicative deficit in autism (1997). This discovery asserts that there may indeed be a key difference between the growth of social and nonsocial use of gaze in broad development of all infants.

Imitation and Pretend Play

Significant delays in the production of imitation in very young infants as well as pretend play schemes in their slightly older counterparts are important warning signs to monitor in developing criterion for early assessment strategies. Imitation by typically developing and developmentally delayed infants is not merely a superficial repetition of movements made by another person but is instead a complex tool for developing interpersonal relationships with parents (Trevarthen & Aitken, 2001). Trevarthen and Aitken continue in this explanation in stating, “[imitation] is, even for newborns, an emotionally charged mutual influence of motive states in which certain salient expressive actions of the other are identified and repeated to further an ongoing communication,” (2001). A study by Charman et al. produced confirming results in suggesting that although basic level of imitation is apparent in school-age children with autism, those under the age of twenty months show considerable difficulty and unresponsiveness in this area (1997). After the mastery of a significant degree of gross and fine motor skills has been obtain through imitation, most children will begin to establish play activities progressing from simple object exploration to functional object use and finally pretend play. Between the ages of nine and twelve months, however, distinguishable abnormalities become evident and progressively more deviant in those with autism spectrum disorder in comparison to typically developing peers (Volkmar et al. 2005). In this same study, it was determined that by the second birthday of many children with autism, differences in functional play abilities and routines are striking, particularly in terms of purposefulness, symbolism, and complexity (Volkmar et al. 2005). As functional play ability continues to be impeded throughout the early years of life, pretend play is further hindered, and thus, many children with autism do not begin to develop a concept of such imaginative behavior until they have been taught specific strategies and skills within an early intervention setting (Charman, Swettenham, Baron-Cohen, Cox, Baird, & Drew, 1998).

Implications of Early Diagnosis

Early detection and diagnosis of autism in young infants may be crucial to the future outcome of these individuals because early behavioral intervention has been shown to provide a substantial impact on the long-term prognosis (Osterling et al.

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Early Detection of Autism in Infants and Toddlers (Part 5)

June 15th, 2010 Comments off


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2002). According to Moore and Goodson, as a result of eligibility for participation in early intervention programs being limited to those with a formal documented diagnosis, early identification and accurate assessment have become increasing important (2003). Research suggests that intervention provided before the age of three and a half has a greater impact than does after the age of five. Therefore, if we could screen all children at birth for autism, clinicians and educational specialists could perhaps retrain the brain and consequentially avoid the development of afore mentioned social impairments that develop in subsequent months (Wetherby, Woods, Allen, Cleary, Dickinson, & Lord, 2004). In the past two months, the Center for Disease Control and Prevention has launched a $2. 5 million autism-awareness campaign known as “Learn the Signs. Act Early”, with an ambitious goal to educate all health-care providers and parents about the warning signs in this disorder so that early intervention can be implemented as soon as possible “to give kids with autism a shot at productive, satisfying, and emotionally connected lives,” (Kalb, 2005). With the identification of discrete and precise symptoms in very young infants within the scope of neurological abnormalities, atypical head growth fluctuations, communication delays, joint attention difficulties, and inabilities to attend to imitation and engage in pretend play, I believe that early intervention would become a possibility and thus make a significant impact for all children diagnosed with autism spectrum disorders.


Baird, G. Charman, T. Baron-Cohen, S. Cox, A. Swettenham, J. Wheelwright, S. ,

Drew, A. (2000). A screening instrument for autism at 18 months of age: A 6-year

follow-up study. Journal of American Academy of Child Adolescent Psychiatry,

39, 694-702.

Baranek, G. (1999). Autism during infancy: A retrospective video analysis of sensory-

motor and social behaviors at 9-12 months of age. Journal of Autism and

Developmental Disorders, 29, 213-224.

Charman, T. Baron-Cohen, S. Swettenham, J. Cox, A. Baird, G. Drew, A. (1997).

Infants with autism: An investigation of empathy, pretend play, joint attention,

and imitation. Developmental Psychology, 33, 781-789.

Charman, T. Swettenham, J. Baron-Cohen, S. Cox, A. Baird, G. Drew, A. (1998). An

experimental investigation of social-cognitive abilities in infants with autism:

Clinical implications. Infant Mental Health Journal, 19, 260-275.

Charwarska, K. Klin, A. Volkmar, F. (2003). Automatic attention cueing through eye

movement in 2-year-old children with autism. Child Development, 74, 1108-112.

Courchesne, E. Carper, R. & Akshoomoff, N. (2003). Evidence of brain overgrowth in

the first year of life in autism. Journal of American Medical Association, 290,


Cox, A. Charman, T. Baron-Cohen, S. Drew, A. Klein, K. Baird, G. Swettenham, J. ,

Wheelwright, S. (1999). Autism spectrum disorders at 20 and 42 months of age:

Stability of clinical and ADI-R diagnosis. Journal of Child Psychology and

Psychiatry, 40, 719-732.

Dawson, G. Meltzoff, A. Osterling, J. Rinaldi, J. (1998). Neuropsychological correlates

of early symptoms of autism. Child Development, 69, 1276-1285.

Dawson, G. Osterling, J. Meltzoff, A. Kuhl, P. (2000). Case study of the development

of an infant with autism from birth to two years of age. Journal of Applied

Developmental Psychology, 21, 299-313.

Dawson, G. Webb, S. Carver, L. Panagitotides, H. McPartland, J. (2004). Young

children with autism show atypical brain responses to fearful versus neutral facial

expressions of emotion. Developmental Science, 7, 340-359.

Eaves, L. Ho, H. (2004). The very early identification of autism: outcome to age 4 ½-5.

Journal of Autism and Developmental Disorders, 34, 367-378.

Goin, R. Myers, B. (2004). Characteristics of infantile autism: Moving towards earlier

detection. Focus on Autism and Other Developmental Disabilities, 19, 5-12.

Kalb, C. (2005). Where does autism start? Newsweek, 28 Feb, 45-55.

Moore, V. Goodson, S. (2003). How well early diagnosis of autism stand the test of

time? Follow-up study of children assessed for autism at age 2 and development

of an early diagnostic service. Autism, 7, 47-63.

Klin, A. Charwarska, K. Paul, R. Rubin, E. Morgan, T. Wiesner, L. Volkmar, F.

(2004). Autism in a 15-month-old child. American Journal of Psychiatry, 161, 1981-1988.

Lainhart, J. (2003). Increased rate of head growth during infancy in autism. Journal of

the American Medical Association, 290, 393-394.

Osterling, J. Dawson, G. (1994). Early recognition of children with autism: A study of

first birthday home videotapes. Journal of Autism and Developmental Disorders, 24, 247-257.

Osterling, J. Dawson, G. Munson, J. (2002). Early recognition of 1-year-old infants with

autism spectrum disorder versus mental retardation. Development and

Psychopathology, 14, 239-251.

Sheinkopf, S. Mundy, P. Oller, D. & Steffens, M. (2000). Vocal atypicalities of

preverbal autistic children. Journal of Autism and Developmental Disorders, 30, 345-353.

Torrey, E. Dhavale, D. Lawlor, J. & Yolken, R. (2004). Autism and head circumference

in the first year of life. Journal of Biopsychiatry, 56, 892-894.

Trevarthen, C. Aitken, K. (2001). Infant intersubjectivity: Research, theory, and clinical

applications. Journal of Child Psychology and Psychiatry, 42, 3-48.

Volkmar, F. Chawarska, K. Klin, A. (2005). Autism in infancy and early childhood.

Annual Review of Psychology, 56, 315-36.

Werner, E. Dawson, G. Osterling, J. Dinno, N. (2000). Brief report: Recognition of

autism spectrum disorder before one year of age: A retrospective study based on

home videotapes. Journal of Autism and Developmental Disorders, 30, 157-162.

Wetherby, A. Woods, J. Allen, L. Cleary, J. Dickinson, H. Lord, C. (2004). Early

indicators of autism spectrum disorders in the second year of life. Journal of Autism and Developmental Disorders, 34, 473-493.

Wimpory, D. Hobson, P. Williams, M. Nash, S. (2000). Are infants with autism

socially engaged? A study of recent retrospective parental reports. Journal of Autism and Developmental Disorders, 30, 525-536.

Young, R. Brewer, N. Pattison, C. (2003). Parental identification of early behavioral

abnormalities in children with autistic disorder. Autism, 7, 125-143.

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Human Exposure and Risk Assessment for Naturally Occurring Asbestos

May 21st, 2010 Comments off


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Asbestos is a general name given to a group of naturally occurring silicate minerals with a tendency to separate into fibers or fiber bundles. The fibers have high tensile strength, low heat transfer, chemical resistance, and heat resistance. These properties make asbestos useful for a number of industrial applications, including thermal insulations and fireproofing, friction materials such as automotive brake pads, and fiber reinforcement in cementitious materials…


Although asbestos is a versatile material with many commercial applications, it also a known human carcinogen. Epidemiological data consistently indicate an increased incidence of cancer in occupationally exposed individuals. Asbestos exposure occurs primarily through inhalation of fibers in asbestos dust. Animal inhalation studies show consistently similar findings for lung cancer and mesothelioma. Animal and epidemiological ingestion study data are insufficient to judge carcinogenicity due to ingestion. Asbestos regulation has been based on a linear dose-response relationship between exposure and adverse health effects (risk increases as total dose increases) and on the lack of a known exposure threshold below which no asbestos-related health effects have been observed. Much of the available epidemiological data cover occupational exposures, which are frequently higher than environmental exposures.

Since asbestos is a naturally-occurring mineral, however, there are areas of the United States in which geological deposits of asbestos minerals pose a potential environmental exposure risk. Asbestos also occurs as a contaminant in some commercially mined minerals, such as vermiculite. The most well-known case of exposure to naturally-occurring asbestos may be the case of Libby, Montana. Asbestos-contaminated vermiculite was mined in Libby from 1919 until the mine was closed in 1990. In response to local concerns and media coverage of the local population’s exposure to the asbestos-contaminated vermiculite, EPA sent an emergency response team to Libby in 1999 to collect air, soil, dust, and insulation samples from businesses and homes. Libby was added to EPA’s Superfund National Priorities List in 2002. Asbestos-related lung diseases have been observed in the Libby population. Exposure scenarios in this case include occupational exposures in the mining process, exposure of family members through “take-home” dust, environmental exposures due to ambient airborne asbestos concentrations, and exposure of residents due to vermiculite-containing insulations and soil conditioners used in and around their homes.

Although the Libby, Montana, situation may be the best known case of exposure to naturally occurring asbestos in the United States, there are other areas of the country in which asbestos deposits result in potential exposure. The presence of naturally occurring asbestos in exposed soils in El Dorado Hills, California, has been well documented by State and Federal agencies. In response to a citizen’s petition to evaluate asbestos-related health risks in the community, EPA contracted to conduct a multimedia assessment of the area in 2003 to evaluate the potential for inhalation exposure to naturally occurring asbestos in disturbed soils. That assessment concluded through activity-based sampling that airborne asbestos concentrations were elevated in the breathing zone for both children and adults when soils were disturbed (Ladd, 2005).

Unlike occupational asbestos exposures, which may be controlled with personal protective equipment and specialized work practices, exposure to naturally occurring asbestos in native soils is not easily controlled. Exposed individuals may not even realize they have been exposed during outdoor activities. While occupational exposures generally affect adults of working age, exposure to naturally occurring asbestos minerals may also affect children and the elderly. Adverse health effects resulting from exposure to asbestos have been anecdotally documented as far back as ancient Rome, where slaves weaving asbestos fibers into textile products became weakened due to breathing problems and suffered premature death. More recent awareness of escalating asbestos-related respiratory disorders in the 1960s and early 1970s led EPA to add asbestos in 1971 to the list of materials regulated by the National Emissions Standard for Hazardous Air Pollutants (NESHAP), and to promulgate regulation under the Asbestos Hazard Emergency Response Act (AHERA) in 1986 to address asbestos in schools. AHERA covers asbestos-containing materials inside school buildings and, therefore, works to protect a susceptible subpopulation (children).

While there is strong evidence of a causal link between inhalation of asbestos particles and the development of debilitating respiratory disease and cancers, the specific mechanisms by which asbestos minerals cause disease are still not fully understood. The roles that morphology, fiber length, chemistry, and solubility in biological fluids (biopersistence) play in asbestos toxicity are still an area of vigorous debate. As noted by Fubini and Fenoglio (2007), particle toxicology is a distinct study area. Particle toxicants, in which surface chemistry and surface topography play a significant role in interaction with living tissues, behave differently than molecular toxicants. A particle’s surface structure and surface chemistry are affected by factors such as the mechanical processes that generate the particle, weathering processes, and adsorption of chemical contaminants onto the particle surface. For this reason, two particles with the same general chemical composition may have different surface chemistry.

In the case of mineral particles, properties relevant to toxicity include fibrous morphology, surface features such as sharp edges or fracture faces, surface reactivity related to covalent and ionic bonds, the presence of surface contaminants, and biopersistence. Asbestos particles have some toxicity characteristics that are different from other mineral dusts. Although fibrous morphology plays a part in toxicity, not all mineral fibers are equally toxic. There is some evidence that carcinogenic potency varies with asbestos mineral type and the geographic area from which the asbestos originates (EPA IRIS). It is generally agreed that chrysotile asbestos is less toxic than the other regulated asbestos minerals in relationship to mesothelioma, a cancer of the lining of the lungs and abdominal cavity.

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Human Exposure and Risk Assessment for Naturally Occurring Asbestos (Part 2)

May 21st, 2010 Comments off


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There is not clear evidence of lower chrysotile toxicity in relationship to lung cancer and asbestosis, a debilitating scarring of the lung tissues. Evidence, such as that reviewed by Hardy in 1995, suggests that iron also plays a part in asbestos toxicity. Iron is present in all asbestos minerals. Iron ions on the surface of asbestos fibers may be catalytic sites for free radical and reactive oxygen species (ROS) generation, resulting in the initiation or promotion of cancer.

EPA’s carcinogenicity assessment dates back to 1986. The lung cancer model in that assessment (Nicholson, 1986) assumes a linear function of cumulative asbestos exposure in units of fibers-years/ml as measured with phase contrast microscopy, and can be expressed as follows: IL IE(1+KL*f*d), where: IL lung cancer incidence observed or projected in an exposed population IE lung cancer expected in the absence of exposure KL= proportionality constant measure of the carcinogenic potency of exposure f intensity of exposure (fibers/ml) d duration of exposure (years) The model assumes equal potency for all six regulated asbestos types and all asbestos fibers greater than 5 μm in length. The 1986 assessment document does point out that fiber size distribution varies with asbestos type and mineral processing, and accepts that length and width are important variables in fiber carcinogenicity in animal studies. Stanton et al (1981) developed the “Stanton Hypothesis,” which suggested that long thin fibers were the most toxic. Later studies, such as those reviewed by Dodson et al, suggested that all fiber sizes may contribute, to some extent, to asbestos toxicity. One source of uncertainty in asbestos exposure estimates is the uncertainty of conversions between analytical measurements performed with PCM and measurements performed with transmission electron microscopy (TEM).

Asbestos unit risk is based on fiber counts made with PCM because PCM is typically the method used for measurements in the occupational environment. Unfortunately, PCM is not fiber specific. All fibers are counted, regardless of identity. PCM also does not have the resolution necessary to image smaller fibers, generally resolving fibers longer than 5 μm and greater than 0. 4 μm in diameter. Transmission electron microscopy (TEM) resolves much shorter and thinner fibers and allows for identification of fibers based on chemical composition and selected area electron diffraction (SAED) of the mineral’s crystal structure. The correlation between PCM and TEM is highly uncertain. Asbestos measurement techniques and the level of understanding of asbestos toxicity have improved substantially since EPA’s 1986 assessment document.

A proposed updated methodology for conducting asbestos risk assessments (Berman and Krump, 2003) is under review at this time. The proposed methodology, which distinguishes between asbestos types and fiber sizes in assessing risk, is a topic of debate. The report on EPA’s peer consultation workshop to discuss the proposed methodology (Eastern Research Group, 2003) documents several discussion topics. Issues under discussion include fiber diameter and length (what size cut-off points to use in considering fibers), the use of different carcinogenic potency factors for different asbestos fiber types for lung cancer versus mesothelioma, how to address mineral cleavage fragments of equal dimension and biopersistence as fibers, the potency of unregulated asbestos minerals, statistical analysis methods, consideration of the synergistic impact of cigarette smoking, and localized exposures to naturally occurring asbestos such as that in California. The potential for health risks associated with exposure to asbestos minerals continues to be a public concern. Much of the epidemiological asbestos data studied over the past several decades has focused on occupational exposure. Since asbestos is a generic term used to identify a group of naturally-occurring minerals, however, there are areas of the United States in which geological deposits of asbestos minerals pose a potential environmental exposure risk. Unlike occupational asbestos exposures, which can be controlled with personal protective equipment and specialized work practices, exposure to naturally occurring asbestos may not be easily controlled and may impact susceptible subpopulations. Given the asbestos toxicity questions that remain and the vigorous research debate, it is obvious that asbestos is still a relevant exposure and risk assessment topic.


Berman, D. W. and Krump, K. (2003). “Technical Support Document for a Protocol to Assess Asbestos-Related Risk – Final Draft. ” Report No. EPA 935. 4-06600/8-84/003F, Prepared for U. S. EPA Office of Solid Waste and Emergency Response, Washington, DC.

Bernarde, M. (1990). Asbestos The Hazardous Fiber. CRC Press: Florida.

Dodson, R. Atkinson, M. and Levinson, J. (2003). “Asbestos Fiber Length as Related to Potential Pathogenicity: A Critical Review,” American Journal of Industrial Medicine, 44: 291-297.

Eastern Research Group, Inc. (2003). “Report on the Peer Consultation Workshop to Discuss a Proposed Protocol to Assess Asbestos-Related Risk. ” Contract No. 68-C-98-148, Prepared by Eastern Research Group, Inc. for U. S. EPA Office of Solid Waste and Emergency Response, Washington, DC.

Fubini, B. and Fenoglio, I. (2007). “Toxic Potential of Mineral Dusts,” Elements, 3: 407-414. Hardy, J. and

Aust, A. (1995). “Iron in Asbestos Chemistry and Carcinogenicity,” Chemical Reviews, 95(1): 97-118.

Ladd, K. (2005). “El Dorado Hills Naturally Occurring Asbestos Multimedia Exposure Assessment, Preliminary Assessment and Site Inspection Report Interim Final. ” Contract No. 68-W-01-012, Prepared by Ecology and Environment, Inc. Superfund Technical Assessment and Response Team (START) for U. S. EPA Region IX. Nicholson, W. J. (1986). “Airborne Asbestos Health Assessment Update. ” Report No. EPA/600/8-84/003F, Prepared for U. S. EPA Environmental Criteria and Assessment Office, Research Triangle Park, NC.

Stanton M. F. Layard M. Tegeris E. Miller E. May M. Morgan E. and Smith A. (1981). “Relation of Particle Dimension to Carcinogenicity in Amphibole Asbestoses and Other Fibrous Minerals. ” Journal of the National Cancer Institute, 67: 965-975.

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Human Exposure and Risk Assessment for Naturally Occurring Asbestos (Part 3)

May 21st, 2010 Comments off


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Summary/Toxicological Review for Asbestos (CASRN 1332-21-4) viewed at Integrated Risk Information System (IRIS) website, USEPA, http://www. epa. gov/ncea/iris/subst/0371. htm, viewed February 1, 2008.

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