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Echo Rock Plaza 概要 解説 概要 日本語：エコーロックプラザ 業種：商業施設 所在地：バインウッド - アルタ - ハウィックアベニューとアルタストリートの交差点。 解説 施設一覧 24/7 エコーロックプラザ店 エコーロック バイト！ エコーロックプラザ店 Walk of Fame Talon Scout Nails Molar Flair Dentist
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https://w.atwiki.jp/pipopipo777/pages/29.html
TOXICOLOGICAL PROFILE FOR WHITE PHOSPHORUS -index 2 HEALTH EFFECTS 2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 2.2.2 Oral Exposure -3 2.2.2 Oral Exposure(2.2.2.0 preface) 2.2.2.1 Death 2.2.2 Oral Exposure -22.2.2.2 Systemic Effects 2.2.2 Oral Exposure -32.2.2.3 Immunological and Lymphoreticular Effects 2.2.2.4 Neurological Effects 2.2.2.5 Reproductive Effects 2.2.2.6 Developmental Effects 2.2.2.7 Genotoxic Effects 2.2.2.8 Cancer 2.2.2.3 Immunological and Lymphoreticular Effects There is limited information on the immunotoxicity of white phosphorus; however, there is some information that suggests that the immune system may be a target. Thymic hemorrhages were observed in two young children accidentally ingesting white phosphorus-containing fireworks (Dwyer and Helwig 1925; Humphreys and Halpert 1931). In one of these children, hyperplasia of lymphoid tissue in the intestinal wall and abdominal lymph nodes and hyperplastic lymphoid corpuscles in the spleen were observed (Humphreys and Halpert 193 1). Decreases in leukocyte levels were reported in a number of case reports involving acute ingestion of rat poison or fireworks containing white phosphorus (Diaz-Rivera et al. 1950; Ehrentheil 1957; Fletcher and Galambos 1963; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968). A decrease (Pietras et al. 1968) or an increase in the percentage of polymorphonuclear leukocytes (neutrophils) (McCarron et al. 1981) were also observed in individuals ingesting white phosphorus. Because the individuals vomited shortly after ingesting the white phosphorus and/or received gastric lavage, doses could not be estimated. In workers exposed to an unknown level of white phosphorus via inhalation, oral, and dermal routes, a decrease in leukocyte levels was observed (Ward 1928). No studies were located regarding immunological or lymphoreticular effects in animals after oral exposure to white phosphorus. 2.2.2.4 Neurological Effects A number of case reports of individuals accidentally or intentionally ingesting a single dose of white phosphorus have reported neurological effects. Nonspecific neurological effects including lethargy (Dathe and Nathan 1946; Fletcher and Galambos 1963; McCarron et al. 1981; Rao and Brown 1974; Rubitsky and Myerson 1949; Simon and Pickering 1976; Talley et al. 1972), sleepiness (Dwyer and Helwig 1925; Ehrentheil 1957; McCarron et al. 1981; McIntosh 1927), irritability (McCarron et al. 1981), restlessness (Diaz-Rivera et al. 1950; Ehrentheil 1957; Harm and Veale 1910), and hypoactivity (Humphreys and Halpert 1931) have been observed. Other symptoms of neurotoxicity that have been observed include coma or semi-coma (Caley and Kellock 1955; Ehrentheil 1957; Hann and Veale 1910; McCarron et al. 1981; McIntosh 1927; Wechsler and Wechsler 1951), toxic delirium and psychosis (Diaz-Rivera et al. 1950), hemiplegia (Humphreys and Halpert 1931; McCarron et al. 1981), abnormal reflexes (Wechsler and Wechsler 1951), hyperesthesia (Humphreys and Halpert 1931), coarse muscle fasciculations (Caley and Kellock 1955), unresponsiveness to painful stimuli (Simon and Pickering 1976), and marked asterixis (flapping tremor) (Greenberger et al. 1964). In addition to these overt signs of neurotoxicity, histological damage in the brain was observed in four individuals ingesting a single dose of white phosphorus. Based on this limited information, the types of cellular damage can be grouped into four categories (1) cellular changes resulting from ischemic damage found in the Purkinje cells and cerebral cortical cells of the second and third layer of the cortex (Wertham 1932); (2) direct white phosphorus-induced cellular damage to the dentate nucleus and inferior olives (Wertham 1932); (3) fatty infiltration in the ganglion cells of the cortex, neuroglial cells, Golgi cells of the cerebellum, and the cells in the pia-arachnoid space (Humphreys and Halpert 1931; Wertham 1932); and (4) cerebral edema (Rao and Brown 1974). It is not known if the cerebral edema observed in this one individual was secondary to the other types of damage. A child treated with 0.083 mg/kg/day white phosphorus for an intermediate duration became lethargic 3 months after beginning treatment and remained lethargic until treatment was discontinued .70 days later. Following cessation of treatment, the child recovered very rapidly (Sontag 1938). Overt signs of neurotoxicity were observed in a cat ingesting a single lethal dose (Fry and Cucuel 1969) and in pregnant rats exposed to a lethal dose (0.075 mg/kg/day) of white phosphorus for an intermediate duration (effects only observed during late gestation of parturition) (Bio/dynamics 1991). Tonoclonic convulsions, increased salivation and weakness were observed in the cat (Frye and Cucuel1969), and tremors were observed in pregnant rats (Bio/dynamics 1991). In another developmental toxicity study (IRDC 1985), no signs of neurotoxicity were observed in pregnant rats. All LOAEL values from each reliable study for neurological effects in each species and duration category are recorded in Table 2-2 and plotted in Figure 2-2. Because vomiting occurred or the individuals received gastric lavage shortly after ingestion, reliable dose estimations could only be made for one individual acutely exposed to 2 mg/kg/day white phosphorus (Hann and Veale 1910). 2.2.2.5 Reproductive Effects Extensive uterine hemorrhaging was observed in a 2-month pregnant woman following the intentional ingestion of 2 mg/kg white phosphorus in rat poison (Hann and Veale 1910). Autopsy results showed that the uterus was enlarged containing a hemorrhagic mole, which was consistent with a 2-month pregnancy. No effects on reproductive performance or histological alterations in the ovaries, uterus, testis, or epididymis were observed in rats administered 0.075 mg/kg/day or less in a one-generation reproduction study (Bio/dynamics 1991; IRDC 1985). The highest NOAEL value and all LOAEL values from each reliable study for effects in each species and duration category are recorded in Table 2-2 and plotted in Figure 2-2. 2.2.2.6 Developmental Effects A healthy infant was administered phosphorized cod liver oil (reported to contain 1.1 mg “pure” phosphorus per fluid ounce) from ages l-7 months (Sontag 1938). The phosphorized cod liver oil was apparently administered for the prevention of rickets. The time-weighted average dose for the 6-month exposure was 0.083 mg/kg/day. During the first 3 months of treatment, the child appeared clinically normal and grew at a normal rate. From the ages of .4 to 6 months, the child became clinically ill, gained essentially no weight, and the rate of growth in height decreased from .0.1 to 0.04 cm/day. Following replacement of the treatment with normal, nonphosphorized cod liver oil, the child appeared to recover quickly, and began to grow at a normal rate. Radiograms taken at 6 months of age showed bands of increased density at the end of all the long bones with increased thickness and density also observed in the zones of calcification. Radiograms taken between 9 months and 5 years of age showed bands of increased density in the diaphyses of the long bones, and in the pelvic, metacarpal, and metatarsal bones. This study describes formation of “phosphorus” bands of increased density in the ends of long bones and possible decreased growth in a child exposed to 0.083 mg/kg/day phosphorus for 6 months (Sontag 1938). It should be noted that radiologic densities are common at the growing points of long bones in children. However, lead poisoning, administration of nickel, certain chronic diseases like anemia, and hypervitaminosis D may also produce bands in the ends of bones, but these are much thicker and heavier (Sontag 1938). A child with Perthes’ disease was administered 0.056 mgkg/day of phosphorus for two periods of intermediate duration, separated by a period with no exposure (Phemister 1918). “Phosphorus” bands of increased density developed in the ends in the tibia, fibula, and femur during the two exposure periods, without any improvement in the child’s condition. A male child with dyschondroplasia was administered 0.026 and 0.046 mg/kg/day white phosphorus for 3 and 8 months, respectively. “Phosphorus” bands of increased density developed in the tibia, fibula, and femur. The density and thickness of the bands were greater at the high-dose level and longer-treatment period. A male child with osteogenesis imperfecta was administered 0.078, 0.063, and 0.059 mg/kg/day phosphorus for 26,3, and 18 months, respectively, separated by a period of time with no white phosphorus exposure. Treatment with white phosphorus produced marked changes, including bands of increased density at the ends of bones and increased transverse diameters of the shafts of bones in the legs and arms (Phemister 1918). Four children with moderate to severe cases of rickets were treated orally with 0.110-0.158 mg/kg/day white phosphorus for durations ranging from 64 to 149 days (Compere 1930a). “Phosphorus” bands of increased thickness and density were observed in the long bones of 1 of 2 of the children examined. An arachitic child was treated with 0.119 mg/kg/day white phosphorus for 82 days (Compere 1930b). Following treatment, the child had a “heavy phosphorus line” and increased density of cortices. Treatment with white phosphorus did not generally improve the condition of the bones in children with rickets. Because these children were sickly, the relevance of the observed effects to potential effects of white phosphorus in normal, healthy children could not be ascertained. Young, growing rabbits exposed to 0.3 mg/kg/day white phosphorus given as a pill for an acute duration had transverse bands of increased density in metaphyseal regions of the tibia and fibula, compared to a control group (Adams 1938a). However, the percentage of calcium and phosphorus, and the calcium/phosphorus ratio in the metaphyseal and cortical regions of the right tibia was similar between treated and control animals. Young, growing rabbits exposed to 0.3 mg/kg/day white phosphorus given as a pill for an intermediate duration had average growth of the tibia of 0.27 mm/day, compared to 0.36 mm/day in the control group; however, no statistical analysis of the results was reported (Adams and Samat 1940). One rabbit had histological abnormalities in the tibia including decreased size of epiphyseal cartilage plate, as well as increased density in the metaphyseal zone with trabeculae that were greater in number and extended further into the diaphysis to a greater extent, compared to a control rabbit. The trabeculae were associated with a greater amount of calcified cartilage matrix. These effects probably resulted from a decrease in the normal rate of bone resorption during bone growth, resulting in decreased rate of growth of the tibia. Weanling rats exposed to 1.25 mg/kg/day white phosphorus in the feed for an intermediate duration had widening of the metaphyseal trabeculae, broadened metaphysis, and a slightly convex lateral contour of the proximal tibia, compared to a control group (Whalen et al. 1973). Osteocytes were small and elongated compared to those in the control group, and osteocytic osteolysis and chondrolysis were decreased or missing. In the treated rats, metaphyseal trabeculae extended deeper into the diaphysis than in the controls. These effects probably resulted from decreased bone resorption during bone growth, resulting in widening trabeculae and a denser metaphysis. Very similar results were observed in studies on growing rats (Adams and Sarnat 1940) and rabbits, but not in an adult rabbit (Adams 1938b). In rats, the doses varied from 0.002% to 0.05% yellow phosphorus (Adams and Sarnat 1940) and in rabbits, from 0.6 to 6 mg (Adams 1938b; Adams and Samat 1940). A decrease in the number of viable pups and an increase in the number of stillborn pups was observed in the F1a and F1b offspring of rats exposed to 0.075 mg/kg/day; however, the incidence was not significantly (p 0.05) different from controls (IRDC 1985). These effects were not seen in a similarly designed reproduction study in which rats were administered 0.075 mg/kg/day (Bio/dynamics 1991). Neither of these studies found any significant differences in the occurrence of malformations or anomalies. These NOAEL and LOAEL values from each reliable study for developmental effects in rats are recorded in Table 2-2 and plotted in Figure 2-2. 2.2.2.7 Genotoxic Effects No studies were located regarding genotoxic effects in humans or animals after oral exposure to white phosphorus. Genotoxicity studies are discussed in Section 2.5. 2.2.2.8 Cancer No studies were located regarding cancer in humans or after oral exposure to white phosphorus. In the only chronic duration oral study in animals, no treatment-related histopathological lesions were observed in the lungs or other organs (not otherwise specified) in rats given .1.6 mg/kg/day white phosphorus in the diet for up to 479 days (Fleming et al. 1942). Only six rats per dose group were used. 2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE
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TOXICOLOGICAL PROFILE FOR WHITE PHOSPHORUS -index ▼2 HEALTH EFFECTS ▼▼2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 2.2.2 Oral Exposure 2.2.2 Oral Exposure(2.2.2.0 preface) 2.2.2.1 Death 2.2.2 Oral Exposure -22.2.2.2 Systemic Effects 2.2.2 Oral Exposure -32.2.2.3 Immunological and Lymphoreticular Effects 2.2.2.4 Neurological Effects 2.2.2.5 Reproductive Effects 2.2.2.6 Developmental Effects 2.2.2.7 Genotoxic Effects 2.2.2.8 Cancer (2.2.2.0 preface) Studies reporting acute oral exposure of humans to white phosphorus were limited to case reports of intentional or accidental ingestion of match heads, rat poison, cockroach poison, firecrackers, or from military operations. Manufacturers of white phosphorus-containing rat poison have claimed that the only active ingredient in the rat poison was white phosphorus (Peacock 1993). It is likely that white phosphorus was the agent producing toxicity following ingestion of cockroach poison, match heads, and fireworks, although the presence of other toxic compounds cannot be ruled out. Many of the case reports involving acute oral exposure of humans to white phosphorus did not report intake levels. High doses of white phosphorus nearly always induced vomiting, expelling much of the ingested white phosphorus from the body. In addition, gastric lavage to remove white phosphorus from the stomach was performed on many poisoned patients. Thus, doses could not be estimated for end points other than vomiting for all but one of the case reports for humans receiving acute oral exposure to white phosphorus. Several studies reporting intermediate oral exposure of children to white phosphorus were located. In most cases the white phosphorus was administered as a treatment for rickets, but in some cases white phosphorus was administered to healthy children to prevent the development of rickets. In studies reporting the effects of white phosphorus on bones in children, the doses of white phosphorus.. administered (0.026-0.158 mg/kg/day) were several orders of magnitude lower than those reported following intentional or accidental white phosphorus poisoning. Humans exposed to white phosphorus in the workplace probably ingested some airborne white phosphorus. One retrospective study indicated that oral exposure to white phosphorus passed from hand to mouth was likely, because the workers constantly handled a paste containing 4-6% white phosphorus, and washroom facilities at the plants were inadequate. No studies were located regarding health effects in human or animals after oral exposure to white phosphorus smoke. 2.2.2.1 Death Numerous case reports of death following acute oral exposure of humans to white phosphorus were located (Diaz-Rivera et al. 1950,196l; Dwyer and Helwig 1925; Hann and Veale 1910; Humphreys and Halpert 1931; McCarron et al. 1981; Rao and Brown 1974; Rubitsky and Myerson 1949; Simmon and Pickering 1976; Talley et al. 1972; Torrielli et al. 1974; Wechsler and Wechsler 1951; Wertham 1932; Winek et al. 1973). In one case report, circumstances following ingestion of white phosphorus allowed for estimation of dose (Hann and Veale 1910). A woman consumed .3.9 g of rat poison containing 4% white phosphorus, but did not vomit until the second day after the poisoning, and the vomitus at that time was clear. Thus, little or none of the white phosphorus ingested was lost due to vomiting. The estimated single dose was 2 mg/kg/day. Four days after ingesting the rat poison, the woman died. The cause of death was not reported, but autopsy revealed fatty degeneration and cell transformation in the liver (Hann and Veale 1910). In case reports of 56 individuals intentionally ingesting large quantities of white phosphorus (0.19-6.3 g) in rat poison, 48.2% of the individuals died, with a 90% death rate in patients ingesting .1.57 g of phosphorus (Diaz-Rivera et al. 1950). Because white phosphorus at these oral exposure levels induced rapid vomiting, the doses for these case reports could not be estimated. In patients that died, symptom prior to death included irreversible vascular collapse; cyanosis, ashen skin color, and deep pallor (probably secondary to vascular collapse); coma; abnormal electrocardiogram readings; evidence of extreme liver and kidney damage, and hypoglycemia (possible secondary to liver damage); and delirium, psychosis, and hallucinations (possibly secondary to brain damage). The cause of death was not reported for each patient, but appeared in most cases to be related to irreversible failure of the liver, kidney, brain, and/or cardiovascular system (Diaz-Rivera et al. 1950). In other case reports, autopsy of patients dying from white phosphorus poisoning nearly always revealed severe damage to one or more of those four systems (Diaz-Rivera et al. 1961; Dwyer and Helwig 1925; Hann and Veale 1910; Humphreys and Halpert 1931; McCarron et al. 1981; Rao and Brown 1974; Wechsler and Wechsler 1951; Wertham 1932). In some cases, pulmonary edema and/or congestion were observed at autopsy (Rao and Brown 1974; Wechsler and Wechsler 1951). In studies reporting the specific cause of death, death was attributed to cardiopulmonary arrest (Diaz-Rivera et al. 1950; Rao and Brown 1974; Simon and Pickering 1976; Winek et al. 1973), peripheral vascular collapse (Diaz-Rivera et al. 1950,1961), liver failure (Diaz-Rivera et al. 1961; McCarron et al. 1981), hypoglycemia (Diaz-Rivera et al. 1961), and gastrointestinal hemorrhage and hemorrhagic bronchopneumonia (Winek et al. 1973). No deaths were reported in children treated with 0.0264.158 mg/kg/day white phosphorus for as much as 26 months (Compere 1930a; Phemister 1918). An infant became seriously ill during treatment with 0.083 mg/kg/day white phosphorus (timed-weighted average dose for 6 months), but recovered entirely following discontinuation of the dose (Sontag 1938). Humans occupationally exposed to phosphorus probably ingested some airborne white phosphorus. In a study of 71 humans occupationally exposed to fumes/vapors and paste containing white phosphorus, oral exposure to phosphorus passed from hand to mouth was likely, because the workers constantly handled a paste containing 4-6% white phosphorus, and washroom facilities at the plants were inadequate (Ward 1928). White phosphorus-related deaths occurred in 0 of 44 and 2 of 27 of the workers exposed for intermediate and chronic durations, respectively. In the two cases of death, the workers died from complications related to phossy jaw, a degenerative condition affecting the soft tissue, bones, and teeth of the oral cavity. In this condition, the toxic effects of white phosphorus probably result from the local irritant action of white phosphorus on tissues in the mouth. Thus, white phosphorus paste passed from hand to mouth and the local action of airborne white phosphorus on the oral cavity may have contributed to the development of phossy jaw, and subsequent death, of these two workers. It is not known whether white phosphorus ingested and absorbed into the systemic circulation contributed to the development of phossy jaw in the two workers that died (Ward 1928). Details of this study are provided in Section 2.2.2.2. A mortality rate of 30% was observed in Wistar rats treated by gavage with 6 mg/kg white phosphorus (Torrielli et al. 1974). The oral LD50 value for Charles-River rats was 3.03 mg/kg for females and 3.76 mg/kg for males (Lee et al. 1975). A mortality rate of 20-35% was observed in mice treated by gavage with 5-6 mg/kg (Hurwitz 1972). LD50 values of 4.82 mg/kg and 4.85 mg/kg were reported for female and male mice, respectively (Lee et al. 1975). In two separate one-generation reproduction studies in rats (IRDC 1985; Bio/dynamics 1991), 30-47% and 53%, respectively, of pregnant females treated by gavage with 0.075 mg/kg/day for 145-204 days (intermediate duration) died (or were killed due to morbidity) in late gestation or during parturition; dams exposed to 0.015 mg/kg/day for similar durations did not have an increased mortality rate (IRDC 1985). Compound-related deaths were not observed in male rats exposed to 0.075 mg/kg/day for similar durations (Bio/dynamics 1991; IRDC 1985). Mortality was observed in 9 of 21 dogs treated once by gavage with an unknown quantity of white phosphorus from firecrackers (Dwyer and Helwig 1925). A cat died 2 hours after ingesting an unknown amount of white phosphorus (Frye and Cucuel 1969). The LD50 values and doses associated with death in each species and duration category are recorded in Table 2-2 and plotted in Figure 2-2. 2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE
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STEALTH Yo Yo Yo I wanna destroy I m a saint slave in a maze Joy and pain My heart easy to break Got a dark face Art for art s sake Live STEALTH My dayz without a trace I destroy but I was born to create Ball and chain My soul s lost its place Got a dark face Art for art s sake I never can explain my fuckin wayz Somethin changes I think it again but down down and down but back on my feet again Funny tragic comic callin my name again Callin ones They really mean it I got thing Fixed dynamics Wishful panic I mean I meant this ain t a game in strength Sunny black in sonic Callin my name again Chosen ones really need it I got thing I GOT THING I GOT THING WHEN I HAVE NEVER SEEN IT I GOT THING Yeah I GOT THING WHEN I HAVE NEVER SEEN IT Givin back tha same amount given Interaction through bipolar livin Livin in purple Inner circle Why you attracted to lost chaos? Livin I never do this just to please ya Tha world causes me a seizure just for your leisure Preacher That s tha sort of symbolic disappearer Catch a cold blooded fever This trigger-happy scene Nothin in-between I thought you saw a star blink Sympathizers believin in If I could give you anythin I would give you fixed statics is difficult to understand Given strings to pull and play withstand Full of monotonous choices a colorful blend Cut off all distorted sounds Live STEALTH Just once and never again Yea Ye-yea I GOT THING I GOT THING WHEN I HAVE NEVER SEEN IT Yea I GOT THING I GOT THING WHEN I HAVE NEVER SEEN IT I GOT THING I GOT THING WHEN I HAVE NEVER SEEN IT I GOT THING Yea I GOT THING WHEN I HAVE NEVER SEEN IT I GOT THING Yea Yo Somethin changes I think it again but down down and down but back on my feet again Funny tragic comic callin my name again Callin ones They really mean it I got thing Fixed dynamics Wishful panic I mean I meant this ain t a game in strength Sunny black in sonic Callin my name again Chosen ones really need it I got thing Everyone changes I think it again Tha values I would kill for in this modest scene Beautiful sick laughter out on tha beat again Fallin ones They really mean it I got thing Everythin changes I think it again and again Tha values I would live for in this freak scene Similar here after doubtin foe and friend Rollin ones really need it I got thing I GOT THING Yea I GOT THING WHEN I HAVE NEVER SEEN IT Yea I GOT THING I GOT THING WHEN I HAVE NEVER SEEN IT I GOT THING I GOT THING WHEN I HAVE NEVER SEEN IT Yea I GOT THING I GOT THING WHEN I HAVE NEVER SEEN IT I GOT THING I GOT THING WHEN I HAVE NEVER SEEN IT I GOT THING Yea I GOT THING WHEN I HAVE NEVER SEEN IT I GOT THING Yea I GOT THING WHEN I HAVE NEVER SEEN IT I GOT THING ア アラララァ ア アァ Live STEALTH
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Scott's Health Record Google Health Out of pocket healthcare spending Tinnitus Music theropy Acyclovir 1998 - Lasik 1997 - gum graft 2003 - bike accident Past Doctors Cook Dailey Kessler Magee John Greenwood 23450 College Blvd Phone 913-764-7788 Audiologist- Larry Ruder 498-2827 Optometrist- Dr. Matt Lowenstein 397-9111 (119th I-35) Last visit 12/29/09 Greenwood 11750 W 135th 913-851-1280 Resources Kansas City Enhance Magazine "We spend the first half of our lives wasting our health to gain wealth, and the second half of our lives spending our wealth to regain our health" Signs of Dementia (Sep/Oct2010) Memory Lose disrupts daily life Challenges plan or problem solving. Difficulty completing familiar tasks Confusion with time or place Trouble with visual images and spatial relationships New problems with words in speaking or writing Misplace things and lose the ability to retrace Decreased or poor judgment Withdrawl from work or social activities Changes in mood and personality Aging Telomeres (like the end of a shoelace) Cell TurnoverSkin Cells once a month Liver Cells once every 6 weeks. Stomach lining every 5 days. Healthful Diet Sugar, white flour, and saturated fatts cause blood sugar to spike, which triggers oxidative stress, then inflamation, and finally telomere burn rate speeds up. Keys vit D which reduces inflamation exercise stress can cause inflamation omega-3 foods salmon,kale,blueberries,qunioa, black beans, walnuts. 10 tips for mental health Join a club Do the Sunday crossword, read, etc. Find your spiritual side Spend time with friends Exercise Laugh, every day. Take care of yourself first focus on your sexual needs. get a phyisical get a mental checkup
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Market Scenario The global Smart Contracts For Healthcare Market is likely to grow at a healthy 48.2% CAGR in the forecast period 2020- 2027, according to the latest Market Research Future (MRFR) analysis. Though smart contracts possess the potential of benefitting any sector, it is extremely helpful in the healthcare industry. Managing patients’ data, records, and health information has become a huge task for most practitioners. Besides, there has been an increase in fraud cases owing to the vulnerability of the outdated systems that are currently in use. These issues cannot be solved alone by practitioners. It is here where smart contracts acts as a savior. The three ways in which smart contracts are used in the healthcare industry include health insurance, health records, and telemedicine. Various factors are fuelling the global smart contracts in healthcare market share. As per the recent MRFR market estimates, such factors include the increase in data breaching cases in the healthcare industry, improved visibility offered by distributed ledger technology, increase in threat of forged medicines in the pharmaceutical industry, increasing popularity of Blockchain technology, growing awareness of its different benefits such as transparency and accuracy, secure, time-saving, and cost-effective, supportive government initiatives, and increasing use for scalable and secure COVID-19 diagnostics and data management. On the contrary, lack of systems integration capabilities and lack of technical expertise associated with smart contracts in healthcare may limit the global smart contracts in healthcare market growth in the forecast period. COVID-19 Analysis The COVID-19 pandemic has proven to be a valid testing ground for all digital technologies as blockchain aims to provide an additional moat of security to healthcare organizations. Smart contracts can be used in providing solutions for COVID-19 testing and data management. The ability to attain the right data from state agencies, insurance companies, and health clinics to get insurance and provide the right equipment to patients in time constraints can be achieved rapidly. Request a Free Sample @ https //www.marketresearchfuture.com/sample_request/8074 Competitive Outlook The notable players profiled in the global smart contracts in healthcare market report include Medicalchain (UK), Guardtime (Netherlands), Microsoft Corporation (US), Blockpharma (France), FarmaTrust (UK), iSolve (US), smartData Enterprises (India), Chronicled (US), Hashed Health (US), PokitDok, Inc (US), Gem (US), SimplyVital Health (US), Proof.Work (UK), Factom (US), Patientory (US), and IBM Corporation (US), among others. Segmentation The MRFR report throws light on an inclusive segmental analysis of the global smart contracts in healthcare market based on end user, blockchain platform, and application. By blockchain platform, the global smart contracts in healthcare market is segmented into ethereum, NXT, sidechains, and bitcoin. Of these, the ethereum segment will lead the market over the forecast period. By application, the global smart contracts in healthcare market is segmented into claims adjudication billing management, supply chain management, clinical data exchange interoperability, electronic health records, patient data management, and others. Of these, the supply chain management segment will dominate the market over the forecast period for the rise in cases of forged medicines. By end user, the global smart contracts in healthcare market is segmented into healthcare payers, healthcare providers, pharmaceutical companies, and others. Of these, the pharmaceutical companies will spearhead the market over the forecast period. Regional Analysis By region, the global smart contracts in healthcare market covers the recent trends and growth opportunity across Europe, the Asia Pacific (APAC), South America, North America, and the Middle East and Africa (MEA). Of these, North America will sway the market over the forecast period. Increased investment by tier 1 companies, research and academic institutions contributing significantly to develop smart contract solutions, increased backing by the trade bodies and government, the robust marketing activities by contenders, the presence of leading players that are investing capital and fortifying their assets along with their competencies, and increase in focus in R D activities are adding to the global smart contracts in healthcare market growth in the region. In Europe, the global smart contracts in healthcare market is predicted to hold the second-largest share over the forecast period for the increase in healthcare expenditure in Western Europe’s developed economies. In the APAC region, the global smart contracts in healthcare market is predicted to have promising growth in the forecast period for the rising government initiatives to promote the perks of smart contracts in the healthcare market. In Rest of the World, the global smart contracts in healthcare market is predicted to have steady growth over the forecast period. Access Report Details @ https //www.marketresearchfuture.com/reports/smart-contracts-healthcare-market-8074 Table of Contents 1Executive Summary 2Scope of the Report 2.1Market Definition 2.2Scope of the Study 2.2.1Research objectives 2.2.2Assumptions Limitations 2.3Markets Structure Continued…. Similar Report Application Management Services Market By Service-Type (System Integration, Consulting Services, Modernization Services, And Others), By Organization Size, By Deployment, And By End-Users Open Source Intelligence (OSINT) Market By Security Type (Human Intelligence, Content Intelligence, Dark Web Analysis, Link/Network Analysis, Data Analytics, Text Analytics, Artificial Intelligence, Big Data, Others), Technology (Bid Data Software, Video Analytics, Text Analytics, Visualization Tool, Cyber Security, Web Analysis, Social Media Analysis, Others), Application (Military Defense, Homeland Security, Private Sector, Public Sector, National Security, Others) About Market Research Future Market Research Future (MRFR) has created a niche in the world of market research. It is counted among the top market research companies that offer well-researched and updated market research reports and insights to businesses of all sizes. What sets us apart is our super-responsive team that offers quality work keeping clients abridged of the prospective challenges and opportunities in various markets. Our team is adept in their space as well as patiently listens to every client. The best part is they know their work inside out and possess the expertise to guide the client in the right direction and achieve results on a tight deadline. We are a one-stop solution for all your data research needs. Our team does not believe in the “one size fits all” approach to creating a report that is detailed and concise. We handle 13 industry verticals including Healthcare, Chemicals and Materials, Information and Communications Technology, Semiconductor and Electronics, Energy and Power, Food, Beverages Nutrition, Automobile, Consumer and Retail, Aerospace and Defense, Industrial Automation and Equipment, Packaging Transport, Construction, and Agriculture. With our unique approach for every market report, we aim to reach the zenith in qualitative business intelligence and syndicated market research. Contact Market Research Future (Part of Wantstats Research and Media Private Limited) 99 Hudson Street, 5Th Floor New York, NY 10013 United States of America 1 628 258 0071 (US) 44 2035 002 764 (UK) Email sales@marketresearchfuture.com Website https //www.marketresearchfuture.com #market #research #industry #data #growth #trend #report #analyis #share #marketing #forecast #digital #geographic #demographic #gnews Plugin Error キーワードを入力してください。 #tech #researchreport #marketreport #futrue
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Clinical Tests Total Cholesterol 200 mg/dl HDL 60 mg/dl LDL 130mg/dl Triglycerides 150 mg/dl Glossary leptin (the hormone that tells us we re full) ghrelin (the hormone that tells us we re hungry) alkaline promoting -Fruits, vegetables, tofu, beans and some nuts and seeds are alkaline-promoting foods. acid promoting - Dairy, eggs, meat, most grains, processed foods, and many convenience, packaged foods tend to be more acidic Ginger, an alkaline spice, is also an anti-inflammatory. Multiple studies using ginger have shown it to be effective in reducing muscle pain and soreness after workouts. Capsicum, the spice found in chilies and hot peppers, also has anti-inflammatory properties, and is alkaline in nature. Training Plans Trifuel Magazines, etc. LifeTime Fitness US Masters Exercise Barefoot running Think like a pro Train thru the pain USA Triathlon Create a training plan 4 ways to avoid a bonk 6 tips for running in the heat 3 drills for open swim Strength Training for running Role of HR training 3 bike workouts 5 Laws of weight training Active.com main triathlon page 3 Things I liked from yoga class Rowing (can do anywhere and great for abs) Side Squart (good groin stretch and strengthener) Hip Stretch (great for outer hip. Start from push up) 48 hours prerace Swim Strength Training Fun treadmill workouts Improve your run all day long Push past those last few miles 5k - 8 points Build your running endurance Improve your stride 6 Solutions to midrun issues Perfect Pacing Survive the open water swim Race Recap Running Form Slay the fatigue monster Cycle Training secrets 20 cycling questions Health SuperShakes Pre-/Post-Meals in 15 minutes Exercise helps avoid aging Eat every 3 hours 5-6p of fish oil-How will you die? Chocolate Good Milk good for recovery Eggs good Hydration articles Smoothie and other stuff Telomerase extend your life? Spirulina 4 snack recipes 7 drinks to improve your performance Power of antioxidants Boost immune system Structure Your Workouts The same basics apply here as in any workout. Start with a warm-up of 10-12 minutes. Put in some technical focus for three to five minutes. Perform the main body of your workout, and then follow with seven to 10 minutes of cool-down. Three rides a week in the winter will keep you in shape and improve your bike ability. Drill ride. The main body consists of four sets of 30-second one-footers, with two minutes of recovery. To perform a one-footer, remove one cleat from the pedal and rest that foot safely on the frame of the trainer. Concentrate on 30 seconds of smooth, fluid circles using just one foot. Switch feet and take two minutes of easy spin with both feet as recovery. The next drill is four 30-second spin-ups with two minutes’ recovery. To perform a spin-up, start at 90 rpm in a moderate gear. Gradually increase your cadence to 95, 100, 105 rpm and so on while still in that same gear. After 15 seconds of increasing cadence, get to your fastest spin which is still very smooth (no hopping around in the saddle) and hold that for 15 seconds. Take a full two minutes of easy circles between each for recovery. Interval ride. After a solid warm-up, shift into a higher gear and commit to going very strong for two minutes. You can determine how intense that effort should be with a heart rate monitor, by rate of perceived effort or by breath rate. Then, spin easy for three minutes. Start with three rounds, and as fitness develops, go to four or five rounds. After that, increase the duration of the effort. Eventually, reduce the recovery time. Steady state. After a solid warm-up, settle into a pace that will last 15-30 minutes. Make this a challenge, but not nearly as intense as the effort in the interval ride. Again, use either heart rate, perceived effort or breath rate to decide on the intensity. Hold this effort steady and strong for the full duration, and concentrate on good pedaling mechanics. Be sure to leave plenty of time for a quality cool-down. Vitamins Name Amt %DV True Need A 3500 UI 70% C 90mg 150% D 400 IU 100% E 30 IU 100% K 25cg 31% B1 1.5mg 100% B2 1.7mg 100% Niacin 20mg 100% B6 2mg 100% Folic Acid 500 mcg 125% B12 6mcg 100% Biotin 30mcg 10% Pantothenic Acide 10mg 100% Calcium 200mg 20% Iron 18mg 100% Phosphorus 109 mg 11% Iodine 150mcg 100% Magnesium 100g 25% Zinc 11mg 73% Selenium 55mcg 79% Copper .9mg 45% Manganese 2.3mg 115% Chromium 35mc 29% Molybdenum 45 mcg 60% Chloride 72mg 2% Potassium 80mg 2% Lutein 250mcg Lycopene 300mcg Diagnostic/Lab Tests Heart Test Range Notes Total Cholesterol 200 HDL+LDL+(Trig/5) HDL 59 LDL 100 Triglycerides 150 CHOL/HDLC 3.5 Total/HDL-Important Cardio CRP 1-3 Important Thyroid TSH/T3 .4-.4.5 Kidney Creatinine .5-1.3 EGFR 60 Bone Calcium 8.6-10.2 Pancreas Glucose 65-99 Hemoglobin A1C 6% EAG Liver Alkaline phosphatase 40-115 Bilirubin, Direct .2 Bilirubin, Total .2-1.2 GGT 3-70 AST 10-35 ALT 9-60 Protein, total 6.2-8.3 Guided Imagery Guided Imagery works best when you can close your eyes and listen to another voice. The following script was adapted from a stress-buster exercise available at www.thehealingmind.org. a site that offers many similar resoureces. Begin by getting comfortable where you are...take a couple of slow, deep breaths...when you breathe in, notice that you re bringing in fresh air, oxygen and energy, which can help you fuel and recharge your body...and when you breathe out, let go of any unnecessary tension, discomfort or worry...give yourself permission to relax...as you relax, let your eyes close and begin to focus inside. Imagine yourself in a place you love...somewhere beautiful, peaceful, comfortable and safe...somewhere you know or somewhere that feels good for you to be in...imagine it is yours... Intice the colors and sounds there...notice the air, the fragrances...notice the time of year or time of day...nitce the temperature and how you ve dressed...this is a place where your body can relax and revitalize...take the time to enojoy it...if your mind wanders for time to time, focus on your breatha dn bring yourself back to your beautiful place...remember you can come back here whenever you like. When you re ready to return to the outer worlkd, slowly let the images fade and go back inside...bring the feelings of safety, relaxation and revitalization with you...let yourself return energized and refreshed, ready to make the best of the day ahead. See also http //www.healthjourneys.com http //www.simplyaudiobooks.com http //www.learnoutloud.com
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TOXICOLOGICAL PROFILE FOR WHITE PHOSPHORUS -index ▼2 HEALTH EFFECTS ▼▼2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 2.2.2 Oral Exposure -2 2.2.2 Oral Exposure(2.2.2.0 preface) 2.2.2.1 Death 2.2.2 Oral Exposure -22.2.2.2 Systemic Effects(preface) Respiratory Effects. Cardiovascular Effects. Gastrointestinal Effects. Hematological Effects. Musculoskeletal Effects. Hepatic Effects. Renal Effects. Dermal Effects. Other Systemic Effects. 2.2.2 Oral Exposure -32.2.2.3 Immunological and Lymphoreticular Effects 2.2.2.4 Neurological Effects 2.2.2.5 Reproductive Effects 2.2.2.6 Developmental Effects 2.2.2.7 Genotoxic Effects 2.2.2.8 Cancer 2.2.2.2 Systemic Effects (preface) Systemic effects of white phosphorus in humans and animals after oral exposure are discussed below. The highest NOAEL value and all reliable LOAEL values from each reliable study for systemic effects in each species and duration category are recorded in Table 2-2 and plotted in Figure 2-2. No studies were located regarding ocular effects in humans or animals after oral exposure to white phosphorus. Respiratory Effects. Studies on respiratory effects following acute oral exposure of humans to white phosphorus were limited to case reports of intentional or accidental consumption of materials containing white phosphorus. Although intake of phosphorus was often reported, dose could be estimated for only one study (Hann and Veale 1910), because vomiting and/or gastric lavage nearly always occurred soon after poisoning, expelling much of the ingested phosphorus from the body. Tachypnea (increased respiratory rate; 48 breaths/minute) was observed in a woman consuming rat poison containing 4% white phosphorus (Hann and Veale 1910); the woman apparently did not vomit until the second day, and the vomitus was clear. The estimated dose was 2 mg/kg. Four days after ingesting the rat poison, the woman died, apparently from liver failure. Autopsy showed that the pleural cavity was filled with a dark fluid, but no histological abnormalities were observed in the lungs (Hann and Veale 1910). In the following studies, no doses could be estimated for respiratory effects because of vomiting and/or gastric lavage. In a case report involving ingestion of rat poison containing white phosphorus, the patient arrived at a hospital in a coma and displayed Cheyne-Stokes respirations and rales (Wechsler and Wechsler 1951). The Cheyne-Stokes respirations increased to an extreme degree, and the patient died. Autopsy revealed pulmonary congestion and edema throughout the stroma. Increased respiratory rate (56 breaths/minute) and rales also were observed in an infant ingesting rat poison containing white phosphorus (Rao and Brown 1974). The child died, and autopsy revealed evidence of pulmonary edema. Rales were observed in a child ingesting a fatal dose of white phosphorus in fireworks; autopsy indicated that the lungs were normal except for some fibrous adhesions (Dwyer and Helwig 1925). Hemorrhagic bronchopneumonia was observed following autopsy of a man ingesting a fatal dose of rat poison containing white phosphorus (Winek et al. 1973). Autopsy of a child who died following ingestion of a firecracker revealed fatty deposition in parenchyma, bronchial epithelium, and tracheal epithelium and cartilage (Humphreys and Halpert 1931). Death from cardiopulmonary failure was reported for a 63-year-old woman (Winek et al. 1973), a 2-year-old boy (Simon and Pickering 1976), and a 3-year-old girl (Simon and Pickering 1976) following ingestion of white phosphorus in rat poison; a respiratory rate of 44 breaths/minute was initially observed in the girl (Simon and Pickering 1976). Increased respiratory rate was observed prior to death in two case reports involving ingestion of rat poison (Talley et al. 1972; Winek et al. 1973). Shallow respirations and cyanosis were observed prior to death in an adult female following ingestion of rat/roach poison containing white phosphorus (Rubitsky and Myerson 1949). Rales were observed 1 day after intentional ingestion of rat poison by a 30-year-old man; 2 days later the patient went into shock but survived the poisoning and eventually recovered (Pietras et al. 1968). No treatment-related respiratory effects were reported in children treated with white phosphorus for intermediate durations. No treatment-related microscopic changes were observed in the lungs of rats exposed to 0.2 mg/kg/day white phosphorus in the diet for a chronic duration (Fleming et al. 1942) or 0.075 mg/kg/day phosphorus by gavage for an intermediate duration (LRDC 1985). Heavy breathing and apnea were reported following ingestion of a fatal quantity of white phosphorus by a cat (Frye and Cucuell969). Necropsy revealed hyperemia, hemorrhage and edema in the lungs. Cardiovascular Effects. Alterations in electrocardiograms, such as altered or inverted T waves and changes in the QRS complex, and other cardiac changes, such as tachycardia, arrhythmias, atrial fibrillation, and decreased ventricular contractility, have been observed in individuals accidentally or intentionally ingesting a single dose of white phosphorus (Dathe and Nathan 1946; Diaz-Rivera et al. 1950, 1961; Dwyer and Helwig 1925; Ehrentheil 1957; Matsumoto et al. 1972; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968; Rao and Brown 1974; Simon and Pickering 1976; Talley et al. 1972). Damage to the myocardium was verified by a number of cases in which histological examination of the heart was performed. Prominent cross striations in the myocardium (Dwyer and Helwig 1925), fatty infiltration of muscle (Diaz-Rivera et al. 1961; Humphreys and Halpert 1931; Wertham 1932), necrosis of myocardium (Wechsler and Wechsler 1951), markedly dilated cardiac chamber (Rao and Brown 1974), and interstitial edema of the myocardium and vacuolation of cells (Talley et al. 1972) have been observed. Because of vomiting and gastric lavage, doses cannot be calculated from the human studies. No cardiac effects were reported in longer term human studies. In addition to the effects on the heart, a number of vascular effects have been observed in humans acutely exposed to white phosphorus. A markedly decreased or undetectable blood pressure (Caley and Kellock 1955; Dathe and Nathan 1946; McCarron et al. 1981; Rubitsky and Myerson 1949; Simon and Pickering 1976; Wechsler and Wechsler 1951), vascular collapse (Diaz-Rivera et al. 1950, 1961), undetectable or decreased pulse (Dwyer and Helwig 1925; Rubitsky and Myerson 1949), and increased pulse (Dathe and Nathan 1946; Hann and Veale 1910; McCarron et al. 1981; Wechsler and Wechsler 1951) have been observed. In addition, individuals have died following cardiopulmonary arrest (Simon and Pickering 1976; Winek et al. 1973), which may be due to effects on the heart or vascular system. A dose of 2 mg/kg/day for vascular effects was identified from the Hann and Veale (1910) report of a woman ingesting a single dose of white phosphorus. Dose levels cannot be estimated for the other case reports. Hemorrhaging in internal organs, as well as the appearance of petechial hemorrhages on the skin, have been reported in a number of acute human exposure cases (Hann and Veale 1910; Humphreys and Halpert 1931; Winek et al. 1973). It is not known whether these effects are due to impairment of the integrity of the blood vessels or due to damage of the affected organ (e.g., liver, stomach) itself. In rats administered 0.075 mg/kg/day white phosphorus for an intermediate duration, no histological alterations were observed in the heart (Bio/dynamics 1991; IRDC 1985). In rats exposed for an intermediate duration to an unknown concentration of airborne white phosphorus from the furnace room of a phosphorus factory, an increase in permeability of capillary walls, lesions in the walls of blood vessels and evidence of impaired microcirculation were observed in the mouth (Ruzuddinov and Rys-Uly 1986). These effects probably resulted from the local action of white phosphorus on the oral cavity. Gastrointestinal Effects. Most of the human case reports listed vomiting as an early effect following ingestion of a single high dose of white phosphorus (Caley and Kellock 1955; Dathe and Nathan 1946; Diaz-Rivera et al. 1950; Dwyer and Helwig 1925; Ehrentheil 1957; Fletcher and Galambos 1963; Greenberger et al. 1964; Hann and Veale 1910; Humphreys and Halpert 193 1; Matsumoto et al. 1972; McCarron et al. 1981; McIntosh 1927; Newburger et al. 1948; Pietras et al. 1968; Rubitsky and Myerson 1949; Simon and Pickering 1976; Wechsler and Wechsler 1951; Winek et al. 1973). The doses that induced vomiting ranged from 2 to 23 mg/kg (Caley and Kellock 1955; Ehrentheil 1957; Fletcher and Galambos 1963; Harm and Veale 1910; Matsumoto et al. 1972; McCarron et al. 1981; Newburger et al. 1948; Rubitsky and Myerson 1949). Vomiting generally started within hours after ingesting the white phosphorus, and sometimes continued for many days. Other gastrointestinal effects included abdominal cramps or pain (often severe) (Dwyer and Helwig 1925; Ehrentheil1957; Fletcher and Galambos 1963; Greenberger et al. 1964; Humphreys and Halpert 1931; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968), vomiting blood and/or pieces of the gastric mucosa (Dathe and Nathan 1946; Diaz-Rivera et al. 1950; Rubitsky and Myerson 1949), necrosis and erosion of mucosa in the esophagus, stomach, duodenum, and jejunum (Wechsler and Wechsler 1951), and gastrointestinal hemorrhage (Dwyer and Helwig 1925; Hann and Veale 1910; Humphreys and Halpert 1931; Wertham 1932, Winek et al. 1973). These effects, with the exception of necrosis, were probably due to the irritating effects of white phosphorus on the mucosa of the gastrointestinal tract. Vomitus often contained white phosphorus, indicating that vomiting generally occurred before all white phosphorus and/or its oxidation products had been absorbed. No gastrointestinal effects were reported in children receiving treatment with 0.026-0.158 mg/kg/day white phosphorus for as much as 26 months (Phemister 1918; Compere 1930a). An infant became seriously ill during treatment with 0.083 mg/kg/day white phosphorus (6-month time-weighted average dose), but recovered entirely following discontinuation of the treatment (Sontag 1938). No vomiting or diarrhea was observed during the treatment period. Gastrointestinal effects were not reported in studies examining longer term occupational exposure to white phosphorus (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Ward 1928). Erosion and hemorrhages in tissue in the esophagus and stomach were observed following ingestion of a fatal unknown quantity of white phosphorus by a cat (Frye and Cucuel 1969). Vomiting was observed in 6 of 21 dogs treated by gavage with an unknown quantity of white phosphorus from firecrackers (Dwyer and Helwig 1925). No gross or microscopic alterations were observed in the gastrointestinal tract of rats treated by gavage with 0.075 mg/kg/day for 204 days (IRDC 1985). Hematological Effects. Hematological effects have been reported in a number of case histories of individuals accidentally or intentionally ingesting a single dose of white phosphorus contained in rat (and cockroach) poisons or fireworks. Because most of the individuals vomited or received gastric lavage shortly after ingestion, the amount of white phosphorus available for absorption is not known. Increases in erythrocyte levels (Diaz-Rivera et al. 1950) and hemoglobin levels (Diaz-Rivera et al. 1950; McIntosh 1927); decreases in erythrocyte levels (Dwyer and Helwig 1925) and hemoglobin and/or hematocrit levels (Simon and Pickering 1973); and anemia (Caley and Kellock 1955) have been observed in some of these individuals. A number of individuals had no change in erythrocyte parameters (Ehrentheil 1957; Fletcher and Galambos 1963; Newburger et al. 1948; Simon and Pickering 1976). The decreases in erythrocyte parameters may be a reflection of the hemorrhages observed in specific tissues (e.g., gastrointestinal tract, liver, skin) (Dathe and Nathan 1946; Hann and Veale 1910; Humphreys and Halpert 1931; Wechsler and Wechsler 1951; Winek et al. 1973). In addition to these changes in erythrocyte parameters, changes in total or differential leukocyte levels were reported in a number of individuals acutely exposed to white phosphorus. Decreases in total leukocyte levels (Diaz-Rivera et al. 1950; Ehrentbeil 1957; Fletcher and Galambos 1963; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968) and decreases or increases in the percentage of polymorphonuclear leukocytes (neutrophils) have been reported (Ehrentheil 1957; McCarron et al. 1981; Pietras et al. 1968). No changes in leukocyte parameters were observed in a number of individuals (Fletcher and Galambos 1963; Newburger et al. 1948; Simon and Pickering 1976). Abnormally low protbrombin times or levels (hypo-prothrombinemia) and a moderate decrease in platelets were observed in a number of individuals ingesting single doses of white phosphorus (Caley and Kellock 1955; Dathe and Nathan 1946; Ehrentheil 1957; Fletcher and Galambos 1963; McCarron et al 1981). Most of the patients developed hypoprothrombinemia within 4-8 days (McCarron et al. 1981). This is probably secondary to the liver damage rather than a direct effect on platelets. No changes in hematological parameters were observed in a child ingesting phosphorized cod liver oil (0.083 mg/kg/day phosphorus) for 184 days (Sontag 1938). Anemia and leukopenia were observed in individuals occupationally exposed to white phosphorus chronically (Ward 1928). It is likely that workers were exposed by the inhalation, oral, and dermal routes. Because there is very little consistency regarding the length of time that elapsed between ingestion and measurement of hematological parameters and the doses cannot be calculated, it is difficult to compare the results of different studies. There is insufficient information to determine whether white phosphorus has a direct effect on erythrocytes and/or leukocytes. The effects observed may be secondary effects. The decrease in erythrocyte, hemoglobin, hematocrit and leukocyte levels may be secondary to hemorrhaging or hematoemesis (Diaz-Rivera et al. 1950; Rubitsky and Myerson 1949) and the increase in erythrocytes and hemoglobin may be a compensatory mechanism due to tissue anoxia. However, since red blood cell synthesis takes 3-5 days, the observed effects may be direct if they are occurring within l-2 days. A slight decrease in hemoglobin levels and increase in eosinophil levels were observed in a 30-year-old man who performed magic shows that involved placing white phosphorus pellets in the mucobuccal folds of his mouth for 15 years. He had no other personal habits that might adversely affect his health except for occasional bidi smoking for about 8 years (Jakhi et al. 1983). Information on hematological effects in animals is limited to one study in which a marked increase in total leukocyte levels and the percentage of monocytes were observed in a guinea pig acutely exposed to 0.9-2.4 mg/kg/day of white phosphorus in a complex dosing regimen (Lawrence and Huffman 1929). The study authors did not specify at which doses the effects occurred. Musculoskeletal Effects. Following ingestion of a fatal dose of rat poison containing white phosphorus by a woman, autopsy revealed fatty infiltration of essentially all tissues, including the musculature (Wertham 1932). Similar effects were reported following the death of a male child who accidentally ingested a firecracker containing white phosphorus; autopsy revealed fatty deposition in many tissues, included the diaphragmic muscle (Humphreys and Halpert 1931). Humans occupationally exposed to white phosphorus probably ingested some airborne white phosphorus. In a study of 71 humans occupationally exposed to white phosphorus, oral exposure to white phosphorus via hand-to-mouth activity was likely because the workers constantly handled a paste containing 4-6% white phosphorus and washroom facilities were inadequate (Ward 1928). In workers exposed to white phosphorus for intermediate durations, 2 of 44 developed phossy jaw, described as slight necrosis in the lower jaw. In workers exposed to white phosphorus for chronic durations, 12 of 27 developed phossy jaw, with necrosis ranging from slight to severe; 2 of the 12 workers developing phossy jaw died from complications related to the necrosis. The progression of the disease was similar in the cases described, usually beginning with the extraction of one or more teeth, poor healing of the socket, followed by necrosis of tissue in the jaw with severe pain and infection. Treatment consisted of repeated removal of destroyed bone tissue and teeth, draining of abscesses, and reconstructive surgery. In severe cases, extensive removal of necrotic bone tissue led to permanent disfigurement. However, exposure levels of white phosphorus were not reported (Ward 1928). Case reports of development of phossy jaw following intermediate or chronic occupational exposure to unreported levels of white phosphorus and phosphorus compounds describe a similar progression of symptoms, with similar results; even in cases of early diagnosis and prompt, intensive treatment of phossy jaw, recovery often took several years (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944). It is likely that the effect of white phosphorus in the oral cavity is local, resulting from contact of “inhaled”white phosphorus particles with tissue in the mouth. White phosphorus may affect the oral mucosa. Dull, red spots in the oral mucosa, an early sign of phossy jaw, have been reported to precede its development in occupationally exposed workers (Kennon and Hallam 1944). The oral mucosa of workers exposed to white phosphorus has been described as having a dull, red, unhealthy appearance (Hughes et al. 1962). Exposed bones may be especially susceptible to the irritating affects of white phosphorus. It is not known whether white phosphorus ingested and absorbed into the systemic circulation contributed to the development of phossy jaw. Not all workers exposed to white phosphorus for longer-term durations developed phossy jaw. In a study of 71 workers exposed to airborne white phosphorus for intermediate or chronic durations, 4.5% and 44%, respectively, developed phossy jaw (Ward 1928). Forty-eight male workers with exposure to white phosphorus ranging from 1 to 17 years were found to be normal and healthy with regards to many parameters, including serum levels of calcium and phosphorus, and bone density; none of the men developed phossy jaw (Hughes et al. 1962). Tooth loss often precedes and accompanies the progression of development of phossy jaw (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Ward 1928). Tooth loss during the later stages of phossy jaw clearly results from destruction of the-bone structure supporting the teeth (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Legge 1920; Ward 1928). It is not known if tooth loss prior to diagnosis of phossy jaw or early in the development of the condition is related to the white phosphorus exposure. Poor dental hygiene alone can result in tooth loss, and in several case reports some of the workers were described as having poor dental hygiene (Kennon and Hallam 1944). Tooth loss followed by poor healing of the socket often precedes development of the necrosis (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Ward 1928), suggesting that poor dental hygiene and exposure to white phosphorus may both be contributing factors to the development of phossy jaw. In a case report, five men developed “precursor signs” (delayed healing of extracted tooth sites and residual sepsis) of phossy jaw developed following tooth extraction and occupational exposure to white phosphorus (Hughes et al. 1962). However, the condition did not develop into “classical” phossy jaw. A man was repeatedly exposed to white phosphorus pellets, placed in the right mucobuccal cavity for magic shows, for . 15 years (Jakhi et al. 1983). After . 14.5 years of this type of exposure to white phosphorus, right maxillary molars became loose, and were subsequently lost. This was followed by a lack of healing and development of fistulae in the sockets of the right maxillary molars. White phosphorus necrosis of the jaw developed, with massive necrosis of the maxilla and floor of the antrum on the right side of the mouth; perforations were present through which the maxillary sinus and nasal cavity were visible. No effects were observed on the left side of the maxilla or on the mandible. Radiographs revealed no evidence of pathology in the chest and long bones. The damage to the jaw was probably caused by direct local contact of phosphorus with the soft tissue and bone in the oral cavity. No microscopic or histological abnormalities were observed in the bone of rats treated by gavage with 0.075 mg/kg/day for 204 days (IRDC 1985). Rats exposed for a chronic duration to 0.2 mg/kg/day white phosphorus in the diet had epiphyseal line thickening and greater extension of trabeculae into the diaphysis of unspecified bones, compared to a control group (Fleming et al. 1942). This study is limited by the failure to specify incidences of effects at interval during dosing and by the failure to state the dosing duration explicitly. Bone effects were observed in children (Compere 1930a; Phemister 1918; Sontag 1938) and young animals (Adams 1938a, 1938b; Adams and Sarnat 1940; Whalen et al. 1973) following acute and intermediate oral exposure to white phosphorus. Because white phosphorus-related effects were observed in growing bones, these effects were considered developmental effects, and are discussed in. Section 2.2.2.6. Hepatic Effects. Hepatic effects have been observed in most individuals accidentally or intentionally ingesting a single dose of white phosphorus. These effects include jaundice (Caley and Kellock 1955; Diaz-Rivera et al. 1950, 1961; Ehrentheil 1957; Greenberger et al. 1964; Humphreys and Halpert 1931; McCarron et al. 1981), hepatomegaly (Diaz-Rivera et al. 1950; Fletcher and Galambos 1963; Humphreys and Halpert 1931; Rao and Brown 1974; Simon and Pickering 1976; Wechsler and Wechsler 1951), increased levels of serum bilirubin (Caley and Kellock 1955; Fletcher and Galambos 1963; McCarron et al. 1981; Pietras et al. 1968), impaired liver function test results (Fletcher and Galambos 1963; Newburger et al. 1948; Pietras et al. 1968; Rubitsky and Myerson 1949), and increases in AST, ALT, and/or lactate dehydrogenase (Ehrentheil 1957; Matsumoto et al. 1972; McCarron et al. 1981; Pietras et al. 1968). In addition to these effects, autopsies or liver biopsies have revealed a number of histological alterations in these individuals. Necrosis (Fletcher and Galambos 1963; Rao and Brown 1974; Wechsler and Wechsler 1951), degeneration (Dwyer and Helwig 1925; Greenberger et al. 1964; Wechsler and Wechsler 1951), fibrosis (Greenberger et al. 1964), hemorrhages (Wechsler and Wechsler 1951), and fatty infiltration (Dwyer and Helwig 1925; Hann and Veale 1910; Humphreys and Halpert 1931; Wertham 1932) have been observed in the liver. In addition to these effects, altered prothrombin time or level has been observed in a number of individuals ingesting a single dose of white phosphorus (Caley and Kellock 1955; Dathe and Nathan 1946; Ehrentheill957; Fletcher and Galambos 1963; McCarron et al. 1981). Prothrombin and other plasma proteins that are required for the efficient progression and regulation of blood coagulation are primarily synthesized in the liver. A deficiency of these proteins is often observed in individuals with severe liver disease. A prolongation of prothrombin time is in part due to this impaired synthesis. Liver function tests were normal in workers chronically exposed to unreported levels of airborne phosphorus (Hughes et al. 1962). Similar hepatic alterations have been observed in animals acutely exposed to white phosphorus. Increases in AST and ALT levels (Paradisi et al. 1984), impaired liver function tests (Ghoshal et al. 1969; Hurwitz 1972; Sigal et al. 1954) increased liver weight (Ghoshal et al. 1969; Seakins and Robinson 1964), increased hepatic triglyceride levels (Ghoshal et al. 1969; Pani et al. 1972; Paradisi et al. 1984; Seakins and Robinson 1964), decreased protein synthesis (Barker et al. 1963; Seakins and Robinson 1964), disaggregation of polyribosomes (Pani et al. 1972), fatty degeneration (Ghoshal et al. 1969) and necrosis (Ghoshal et al. 1969) have been observed. No NOAEL values for hepatic effects following acute animal exposure were identified. In rats, the LOAEL value for liver effects was 6 mg/kg (Barker et al. 1963); in mice it was 5 mgkglday (Hurwitz 1972); and in dogs it was 0.2 mg/kg/day (Sigal et al. 1954). The liver effects occurred shortly after dosing; 3 hours after dosing, a significant decrease in protein synthesis was observed in the liver (Barker et al. 1963), minimal hepatocytic fatty changes were observed after 4 hours (Ghoshal et al. 1969), and severe hepatocytic fatty changes were observed after 12 hours (Ghoshal et al. 1969). The following hepatic effects have been observed in animals orally exposed for an intermediate duration fatty infiltration in guinea pigs exposed to 0.75 mg/kg/day (Ashbum et al. 1948), presence of eosinophilic granules at 0.25 mg/kg/day and cirrhosis at 0.66 mg/kg/day in rabbits and guinea pigs (Mallory 1933), and fibrosis and cirrhosis in pigs exposed to 0.6 mg/kg for 5 days/week (Peterson et al. 1991). In the Peterson et al. (1991) study, no liver effects were observed after 4 weeks of exposure; after 8 weeks, there were early signs of fibrosis, and after 12 weeks, extensive fibrosis was observed. Exposure to 0.075 mg/kg/day for an intermediate duration resulted in slight-to-moderate liver necrosis in dying pregnant rats (Bio/dynamics 1991), but no hepatic effects in the surviving pregnant rats or in male rats (Bio/dynamics 1991). In another reproduction study, liver effects were not observed in dying pregnant rats exposed to 0.075 mg/kg/day (IRDC 1985). Both studies used similar exposure protocols and similar vehicles; the difference in the occurrence of liver damage between the studies cannot be explained. Renal Effects. Evidence of severe renal effects have been observed in a number of individuals intentionally or accidentally ingesting a single dose of white phosphorus contained in rat (or roach) poison or fireworks. Proteinuria (Matsumoto et al. 1972; Pietras et al. 1968; Rao and Brown 1974), albuminuria (Dathe and Nathan 1946; Diaz-Rivera et al. 1950; Dwyer and Helwig 1925; Fletcher and Galambos 1963; McCarron et al. 1981; Rubitsky and Myerson 1949), acetonuria (Pietras et al. 1968), increased urobilinogen (Matsumoto et al. 1972), oliguria (Dathe and Nathan 1946; McCarron et al. 1981; Rao and Brown 1974), increased blood levels of urea and/or nitrogen (Diaz-Rivera et al. 1950, 1961; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968; Rao and Brown 1974; Rubitsky and Myerson 1949), and increased blood creatinine levels (Dathe and Nathan 1946; McCarron et al. 1981) have been observed in these individuals. Renal insufficiency may be due to a direct toxic effect of phosphorus on the kidneys or to acute renal tubular necrosis from fluid loss and shock. Patients in shock may have a peculiar pallor and cyanosis. These probably reflect extensive cellular damage with poor perfusion of the capillary beds, and are a prognostic sign of serious health effects (Melamon et al. 1981). Several case reports have reported no alterations in kidney function (Ehrentheil 1957; Fletcher and Galambos 1963; Greenberger et al. 1964; Simon and Pickering 1976). Histological alterations have also been observed in a number of humans ingesting a single dose of white phosphorus. Fatty changes in the tubules and loop of Henle (Dwyer and Helwig 1925; Humphreys and Halpert 1931; Wertham 1932) and engorged glomeruli and intratubular capillaries (Wechsler and Wechsler 1951) have been observed. Because most individuals vomited shortly after ingesting the white phosphorus or were lavaged, accurate doses cannot be calculated except for one study (Harm and Veale 1910). Histological alterations in the kidney were observed in an individual ingesting 2 mg/kg/day, but the lesion was not described. Creatinine levels were similar among unexposed workers and workers exposed to white phosphorus for chronic durations (Hughes et al. 1962). In animals, fatty infiltration in the nephron and subcapsular hemorrhages were observed in dogs acutely exposed to an unspecified amount of white phosphorus (Dwyer and Helwig 1925). No renal effects were observed in rats exposed to 0.075 mg/kg/day for an intermediate duration (Bio/dynamics 1991; IRDC 1985). No chronic exposure animal studies examining renal effects were located. Dermal Effects. Transient toxic dermatitis (described as a scalartiniform rash) developed 9 days after a man ingested a near-fatal dose of rat poison (Dathe and Nathan 1946). Edema of eyelids was reported in a 13-month-old child after ingestion of a fatal dose of white phosphorus (Rao and Brown 1974). Subcutaneous hemorrhages were visible in the left foot in a woman after consumption of 3.9 g of rat poison containing 4% phosphorus (Hann and Veale 1910). The woman died 4 days after the initial poisoning. At this time, an enormous subcutaneous hemorrhage was visible below the waist line. In this case report, the woman apparently did not expel (via vomiting) any of the ingested dose. Thus, it is likely that the ingested dose (2 mg/kg) was representative of the effective dose. Scattered blue-green petechiae were observed on the abdomen of a male child following accidental ingestion of a fatal dose of white phosphorus mixed with other ingredients from a firecracker (Humphreys and Halpert 1931). The dose level in this study could not be determined; the firecracker was a red composition of phosphorus mixed with other ingredients and was thought to contain about 10% phosphorus (Humphreys and Halpert 1931). No studies were located regarding dermal effects in animals after oral exposure to white phosphorus. Other Systemic Effects. A number of other systemic effects have been observed in humans ingesting a single dose of white phosphorus. The effects that are observed most consistently are hypoglycemia (Diaz-Rivera et al. 1950; McCarron et al. 1981; McIntosh 1927; Wechsler and Wechsler 1951), an increase in body temperature (mild pyrexia or fever) (Dathe and Nathan 1946; McIntosh 1927), and a decrease in plasma calcium, potassium, and/or sodium levels (Caley and Kellock 1955; McCarron et al. 1981; Rao and Brown 1974). It is unclear whether the fever seen is a symptom of phosphorus poisoning or a result of the treatment involved. In addition to these effects, metabolic acidosis (Rao and Brown 1974), hypothermia (Simon and Pickering 1976), damage to the spleen (Greenberger et al. 1964), ascites (Fletcher and Galambos 1963), fatty infiltration of the pancreas (Humphreys and Halpert 193 l), and necrosis of the adrenal medulla and cortex (Wechsler and Wechsler 1951) have been observed. In a child ingesting 0.083 mg/kg/day white phosphorus for an intermediate duration, decreased appetite, impaired body weight gain, and poor turgor (fullness or tension produced by the fluid content of blood vessels, capillaries, and cells) were observed (Sontag 1938). Serum glucose levels were decreased in workers occupationally exposed to white phosphorus for a chronic duration. It is likely that the workers were exposed by the inhalation, oral, and dermal routes (Ward 1928). In dogs acutely exposed to an unspecified amount of white phosphorus, hypoglycemia was observed (Williamson and Mann 1923). Rats received intermittent exposure to the atmosphere in the furnace room of a phosphorus factory for 14 months (Ruzuddinov and Rys-Uly 1986). Histology of rats killed monthly revealed progressive morphological degeneration of the tongue and oral mucosa of the cheek, gum, and hard palate. Epithelium and connective tissue from different parts of the oral cavity responded similarly to the treatment. Changes in the epithelial layer, observed after only 1 month of exposure, included increases in keratinization and numbers of cell layers, resulting in thickening and hyperkeratosis in the epithelium of the mucosa. Over time, the thickening and hyperkeratosis in the epithelium increased and histological changes were observed in the subepithelial connective tissue base. Eventually, the oral cavity contained areas of thickening of the mucosa from hyperkeratosis and increased epithelial cell layers interspersed with areas of decreased thickness of the epithelial layer due to atrophy, dystrophy, and cellular necrosis. At this time, adverse changes in the subepithelial connective tissue were considered pronounced. These effects occurred in most of the animals exposed to the atmosphere. It is likely that the observed effects of phosphorus on the oral cavity were local rather than systemic, resulting from direct contact of white phosphorus with tissues in the mouth. The study presented essentially no quantitative data, and the types and exposure levels of chemicals in the atmosphere (thought to contain elementary phosphorus and its inorganic compounds) were not reported (Ruzuddinov and Rys-Uly 1986). 2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE