Download or read book NTP Technical Report on the Toxicity Studies of Trimethylsilyldiazomethane CASRN 18107 18 1 Administered by Nose only Inhalation to Sprague Dawley Hsd Sprague Dawley r SD r Rats and B6C3F1 N Mice written by and published by . This book was released on 2021 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Trimethylsilyldiazomethane (TMSD) is a methylating reagent widely used in organic chemistry. TMSD is structurally related to the compound diazomethane, which is a known lethal respiratory toxicant in humans and in animal models. TMSD is less reactive (with lower explosive potential) than diazomethane and is considered a safer, less toxic alternative. Few toxicity data are available to support this claim, however, and TMSD is readily available commercially from chemical suppliers. Concern over the inhalation toxicity of TMSD originates from reports of the death of two chemists resulting from lung injury and acute respiratory distress syndrome following exposure to TMSD in the workplace. Other concerns include the known inhalation toxicity of diazomethane and the absence of inhalation toxicity data for TMSD. The National Toxicology Program (NTP) conducted this study to evaluate the acute inhalation toxicity of TMSD in vivo. Groups of eight male Sprague Dawley (Hsd:Sprague Dawley(r) SD(r)) rats and eight male B6C3F1/N mice were exposed by nose-only inhalation to targeted vapor concentrations of 0 s(air), 0 s(hexanes), or 10 sppm TMSD (in hexanes) for 1 day (30 sminutes) with or without a 9-day recovery period following exposure (1-day exposure or 1-day exposure - recovery). Groups of eight male rats and eight male mice were also exposed to 0 s(air), 0 s(hexanes), 0.3, 1, 3, or 10 sppm TMSD (in hexanes) by nose-only inhalation for up to 5 sdays (30 sminutes/day) with or without a 5-day recovery period following exposure (5-day exposure or 5-day exposure - recovery). Animals were either euthanized the day after the single or last exposure or held for 9 sor 5 days postexposure, respectively, and euthanized to assess recovery and delayed effects in the absence of TMSD exposure. All TMSD-exposed rats survived until scheduled termination. In the 5-day exposure - recovery group exposed to 10 sppm, 4/8 (50%) of the rats exhibited labored breathing. Final mean body weights for the 1-day exposure and 1-day exposure - recovery group rats were similar to those of the air control group, but they were significantly decreased in the 5-day exposure (11.7% lower) and 5-day exposure - recovery rat groups (10.4% lower) at 10 sppm TMSD relative to the air control group. Final mean body weight gains in the 5-day exposure and 5-day exposure - recovery rat groups at 10 sppm TMSD were also significantly decreased relative to the air control groups. Absolute and relative lung weights were significantly decreased in the 1-day exposure rat group at 10 sppm TMSD. Absolute and relative lung weights of rats were significantly increased in the three other exposure groups at the same or lower exposure concentrations: 1-day exposure - recovery group at 10 sppm TMSD, 5-day exposure group at 3 sand 10 sppm TMSD, and 5-day exposure - recovery group at ≥0.3 sppm TMSD exposure concentrations. No exposure-related histopathological lesions were present in the 1-day exposure and 1-day exposure - recovery rat groups at 10 sppm TMSD. In the 5-day exposure and 5-day exposure - recovery groups, increased incidences of lung histopathological lesions included chronic-active inflammation (≥3 sppm), histiocyte (alveolar macrophage) infiltration (3 sppm), interstitial fibrosis (10 sppm), pulmonary edema (10 sppm), acute hemorrhage (10 sppm), and alveolar and bronchiolar epithelial hyperplasia (10 sppm). Alveolar and bronchiolar epithelial hyperplasia were also noted at 3 sppm TMSD in the 5-day exposure group. In addition, increased incidences of histiocyte infiltration in the mediastinal lymph nodes were observed in all rats exposed to 10 sppm TMSD in the 5-day exposure and 5-day exposure - recovery groups. Inhaled TMSD was more toxic in mice than in rats. Five mice in the 1-day exposure - recovery group and all mice in the 5-day exposure and 5-day exposure - recovery groups died or were euthanized prior to scheduled termination after only one to three exposures, and 19/24 (79%) of the 10 sppm-exposed mice exhibited labored breathing. In the 5-day exposure - recovery group exposed to 3 sppm, all mice (8/8) exhibited labored breathing. Final mean body weights for the 1-day exposure group were similar to the air control group. In the 1-day exposure - recovery group, final mean body weights of the three mice remaining at study day s9 were significantly decreased (26.8% less than the air control group); final mean body weight gain was also significantly decreased in this group. Final mean body weights were significantly decreased in the 5-day exposure group mice at 3 sppm (10.2% lower) and 10 sppm (16.5% lower) and also in the 5-day exposure - recovery group mice at 3 sppm (21.7% lower) and 10 sppm (18.4% lower). Final mean body weight gains were also significantly decreased in both the 5-day exposure group (3 sppm) and the 5-day exposure - recovery group (1 and 3 sppm). Absolute and relative lung weights were significantly increased in the 1-day exposure and 1-day exposure - recovery mouse groups at 10 sppm TMSD, in the 5-day exposure group mice at ≥0.3 sppm, and in the 5-day exposure - recovery group mice at ≥1 sppm. Increased incidences of lung histopathological lesions in mice were similar to those observed in rats, but also included necrosis and acute inflammation and were observed at greater incidences in the 1 and 3 sppm groups. In addition, lesions occurred in the larynx of mice exposed to 3 and 10 sppm TMSD, which included squamous epithelial hyperplasia and ulceration and acute inflammation. Lung and laryngeal lesions in the 1-day exposure - recovery mouse group at 10 sppm TMSD were similar to those in the 5-day exposure - recovery mouse group but occurred at lower incidences. This in vivo study showed that inhaled TMSD at low vapor concentrations (≤10 sppm) caused acute and progressive lung injury, as reported in human case studies (in particular, pulmonary edema), and that these effects can occur after a single 30-minute exposure to the chemical. These data provide useful information for mitigating exposure risks in the workplace and alerting chemical suppliers to the dangers of TMSD.SYNONYMS: (trimethylsilyl) diazomethane; diazo((trimethylsilyl))methane; diazomethyl(trimethyl)silane; (diazomethyl)trimethylsilane; diazomethyltrimethyl silane; silane, (diazomethyl)trimethyl-; TMS-diazomethane; TMSCHN2.

Download or read book NTP Technical Report on the Toxicity Studies of Trimethylsilyldiazomethane CASRN 18107 18 1 Administered by Nose only Inhalation to Sprague Dawley Hsd Sprague Dawley SD Rats and B6C3F1 N Mice written by and published by . This book was released on 2021 with total page 89 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book NTP Technical Report on the Toxicity Studies of O Phthalaldehyde CASRN 643 79 8 Administered by Inhalation to Sprague Dawley Hsd Sprague Dawley SD Rats and B6C3F1 N Mice Toxicity Report 84 written by and published by . This book was released on 2018 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book NTP Technical Report on the Toxicity Studies of 1020 Long Multiwalled Carbon Nanotubes Administered by Inhalation to Sprague Dawley Hsd Sprague Dawley SD Rats and B6C3F1 N Mice Toxicity Report 94 written by and published by . This book was released on 2019 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book NTP Technical Report on the Toxicology and Carcinogenesis Studies of Di n butyl Phthalate CASRN 84 74 2 Administered in Feed to Sprague Dawley Hsd Sprague Dawley r SD r Rats and B6C3F1 N Mice written by National Toxicology Program and published by . This book was released on 2021 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book NTP Technical Report on the Toxicity Studies of 1020 Long Multiwalled Carbon Nanotubes Administered by Inhalation to Sprague Dawley Hsd sprague Dawley SD Rats and B6C3F1 N Mice written by and published by . This book was released on 2019 with total page 120 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book NTP Technical Report on the Toxicity Studies of Triethylamine CASRN 121 44 8 Administered by Inhalation to F344 N Rats and B6C3F1 N Mice written by and published by . This book was released on 2018 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Triethylamine is used primarily as a catalyst to cure the resin systems incorporated into sand cores for foundry molds. It is also used as a curing catalyst in phenol-formaldehyde particle board adhesives, for the precipitation and purification of penicillin and cephalosporin antibiotics, and in the interfacial polymerization process for the production of polycarbonate resins. Triethylamine was nominated by the United Auto Workers Union for long-term toxicity and carcinogenicity studies based on its high production volume, the large number of occupationally exposed workers, and the lack of carcinogenicity data. Male and female F344/N rats and B6C3F1/N mice were exposed to triethylamine (greater than 99% pure) by whole body inhalation for 2 weeks or 3 months. Genetic toxicology studies were conducted in Salmonella typhimurium and mouse peripheral blood erythrocytes. In the 2-week toxicity studies, groups of five male and five female F344/N rats and B6C3F1/N mice were exposed to triethylamine at concentrations of 0, 100, 200, 400, 800, or 1,000 ppm, 6 hours plus T90 (12 minutes) per day, 5 days per week for 16 (rats) or 17 (mice) days. All rats exposed to 800 or 1,000 ppm died after exposure on day 1; all mice exposed to 800 or 1,000 ppm died between day 1 (postexposure) and day 11. The final mean body weights of all surviving groups of exposed male rats and 200 and 400 ppm female rats were significantly less than those of the chamber controls. In mice, the final mean body weights of 400 ppm males and females were significantly less than those of the chamber controls. Possible chemical-related clinical findings in 400 ppm rats and mice included lethargy, abnormal breathing, ataxia, tremor, nasal discharge (rats), and thinness (mice). Kidney weights of 100 ppm female rats were significantly greater than those of the chamber controls. In the nose of male rats, there were significantly increased incidences of respiratory epithelium hyperplasia in all surviving exposed groups; significantly increased incidences of suppurative inflammation in the 200 and 400 ppm groups; significantly increased incidences of turbinate necrosis, squamous metaplasia of the respiratory epithelium, and respiratory epithelium ulcer in the 400 ppm group; and a significantly increased incidence of olfactory epithelium atrophy in the 200 ppm group. In the nose of female rats, there were significantly increased incidences of suppurative inflammation, squamous metaplasia of the respiratory epithelium, and respiratory epithelium ulcer in the 400 ppm group; significantly increased incidences of respiratory epithelium hyperplasia in the 100 and 200 ppm groups; and a significantly increased incidence of olfactory epithelium atrophy in the 200 ppm group. All rats that died early had necrosis of the respiratory epithelium of the nose and necrosis of the bronchus. In the lung of surviving groups of male and female rats, there were significantly increased incidences of bronchus degeneration in the 200 and 400 ppm groups and significantly increased incidences of suppurative inflammation and regeneration of the bronchus in the 400 ppm groups. Rats dying early often showed corneal degeneration or necrosis, and a few rats in the 100 and 200 ppm groups exhibited subepithelial vesicles of the cornea. Turbinate necrosis occurred in the nose of all exposed mice except the 100 ppm groups. There were significantly increased incidences of olfactory epithelium atrophy in the nose of all surviving groups of exposed mice, and significantly increased incidences of acute inflammation and squamous metaplasia of the respiratory epithelium in 200 and 400 ppm mice. Lung lesions observed only in the groups with early mortality included necrosis of the bronchus in male and female mice and cytoplasmic vacuolization of the bronchus in females. In 400 ppm mice, incidences of chronic active inflammation of the bronchus were increased. Groups of mice with early mortality also had corneal necrosis and cataracts. In the 3-month toxicity studies, groups of 10 male and 10 female F344/N rats and B6C3F1/N mice were exposed to triethylamine at concentrations of 0, 12.5, 25, 50, 100, or 200 ppm, 6 hours plus T90 (12 minutes) per day, 5 days per week for 14 weeks. All exposed rats and mice survived to the end of the studies. Body weights of 200 ppm rats and mice were significantly less than those of the chamber controls. In male rats, differences in reproductive parameters included decreased spermatozoa motility at 50 ppm or greater and increased spermatid heads per mg testis in the 100 and 200 ppm groups. In the olfactory epithelium of the nose of rats, there were significantly increased incidences of atrophy in males exposed to 50 ppm or greater and in females exposed to 25 ppm or greater. In the respiratory epithelium of the nose of rats, there were significantly increased incidences of hyperplasia in males and females exposed to 25 ppm or greater. In the lung of female rats, there were significantly increased incidences of histiocyte cellular infiltration of the alveolus in the 100 and 200 ppm groups. Corneal lesions of the eye were noted in four males and six females exposed to 200 ppm. In the olfactory epithelium of the nose of mice, there were significantly increased incidences of atrophy in males and females exposed to 50 ppm or greater and significantly increased incidences of cytoplasmic vacuolization in 50 ppm males and females. In the respiratory epithelium of the nose of mice, there were significantly increased incidences of squamous metaplasia in 200 ppm males and females. There were significantly increased incidences of turbinate hyperostosis in all exposed groups of male and female mice and significantly increased incidences of turbinate necrosis in 200 ppm males and females. Triethylamine was not mutagenic in any of four strains of S. typhimurium, with or without exogenous metabolic activation. An equivocal increase, based on a trend test analysis, in the frequency of micronucleated erythrocytes was observed in peripheral blood of male mice sampled at the end of the 3-month study; no increase in micronucleated erythrocytes was seen in female mice. Under the conditions of the 3-month inhalation studies, there were treatment-related lesions in male and female rats and mice. The major targets of triethylamine exposure in rats and mice included the nose and eyes. In rats, the most sensitive measure of triethylamine exposure was respiratory epithelium hyperplasia of the nasal cavity with a lowest-observed-effect level (LOEL) of 12.5 ppm in males and females. In mice, the most sensitive measure of triethylamine exposure was turbinate hyperostosis of the nasal cavity with a LOEL of 12.5 ppm in males and females. Synonyms: (Diethylamino) ethane; ethanamine, N,N-diethyl- (9CI); N,N-diethylethanamine; triethyl-(diethylamino) ethaneamine.

Download or read book National Toxicology Program Annual Report for Fiscal Year written by National Toxicology Program (U.S.) and published by . This book was released on 1994 with total page 320 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book NTP Technical Report on the Toxicology and Carcinogenesis Studies of Di n butyl Phthalate CASRN 84 74 2 Administered in Feed to Sprague Dawley Hsd Sprague Dawley r SD r Rats and B6C3F1 N Mice written by and published by . This book was released on 2021 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Di-n-butyl phthalate (DBP) is a phthalate used in the manufacture of consumer products such as plastics and personal care products. Widespread exposure in the population occurs throughout life, including during pregnancy and lactation. Because limited data are available in both animals and humans to evaluate DBP as a human carcinogen, the National Toxicology Program conducted 2-year studies of DBP in rats and mice. Time-mated female Sprague Dawley (Hsd:Sprague Dawley(r) SD(r)) rats were exposed to 0, 300, 1,000, 3,000, or 10,000\sppm DBP in feed during gestation and lactation. Postweaning, F1\soffspring consumed diets with the same exposure concentrations as the dam for 2\syears (n\s=\s50/sex/exposure group). Male and female adult B6C3F1/N mice were exposed to 0, 1,000, 3,000, or 10,000\sppm DBP in feed for 2\syears (n\s=\s50/sex/exposure group). Estimated average chronic chemical consumption was 16-17, 54-57, 152-169, and 510-600\smg DBP/kg body weight/day (mg/kg/day) in rats in the 300, 1,000, 3,000, and 10,000\sppm groups, respectively, and 105-112, 329-347, and 1,306-1,393\smg/kg/day in mice in the 1,000, 3,000, and 10,000\sppm groups, respectively.TWO-YEAR STUDIES: In rats, no exposure-related effect in mortality between exposed and control groups was observed. DBP did not affect rat reproductive or littering parameters. Marginal F0\sweight effects (≤6% difference from the control group) were observed during gestation and by the end of lactation; F1\smale and female pup weights in the 10,000\sppm group were significantly decreased by 12% and 13%, respectively, compared to the control groups upon weaning. Throughout the postweaning period, F1\sbody weights were approximately within 20% of the control animals. At 2\syears, the incidence of pancreatic acinus adenomas was slightly higher in the 10,000\sppm group compared to the control group in male rats only. Because pancreatic acinus adenomas and carcinomas are associated with peroxisome proliferator-activated receptor alpha activation--and have been observed with exposure to other phthalates--the marginal increase observed could have been related to chemical exposure. The male reproductive tract was a primary target system of DBP in rats. A high incidence of small or absent organs of the male reproductive tract and undescended testes occurred only in the 10,000\sppm group. Some gross lesions correlated with microscopic lesions in the testes (germinal epithelium atrophy), epididymis (hypospermia), and prostate and seminal vesicles (decreased secretory fluid) in the 10,000\sppm groups. Additional microscopic lesions in the reproductive tract in rats included seminiferous tubule dysgenesis, testicular interstitial cell hyperplasia, testicular edema, and fibrosis and granuloma of the rete testis. In mice, there were no exposure-related effects on survival, and mean body weights were lower only in the 10,000\sppm groups compared to the control groups. There was no exposure-related increase in neoplasms. No gross lesions were observed in the male reproductive tract, but significantly increased incidences of germinal epithelium degeneration in the testes and exfoliated germ cells in the epididymal duct were observed microscopically. The lesions generally occurred only in the 10,000\sppm group and were fewer and less severe in the mouse study, which did not include perinatal exposure, compared to the rat study. Other nonneoplastic lesions observed were generally limited to the 10,000\sppm group. These lesions were found in the liver (hepatocyte cytoplasmic alteration in male and female rats and mice and multinucleated hepatocytes in male mice), in the pituitary gland (pars distalis hypertrophy in male rats), and in the kidney (renal tubule hyperplasia in female mice). CONCLUSIONS: Under the conditions of these 2-year feed studies, there was equivocal evidence of carcinogenic activity of di-n-butyl phthalate (DBP) in male Hsd:Sprague Dawley(r) SD(r) rats based on marginal increases in the incidence of pancreatic acinus adenomas. There was no evidence of carcinogenic activity of DBP in female Hsd:Sprague Dawley(r) SD(r) rats at exposure concentrations of 300, 1,000, 3,000, or 10,000\sppm. There was no evidence of carcinogenic activity of DBP in male or female B6C3F1/N mice at exposure concentrations of 1,000, 3,000, or 10,000\sppm. Exposure to DBP increased incidences of gross lesions in the male reproductive system in rats and of nonneoplastic microscopic lesions in the male reproductive system (rats and mice), liver (male and female rats and mice), pituitary gland pars distalis (male rats), and kidney (female mice).SYNONYMS: dibutyl benzene-1,2-dicarboxylate; 1,2-benzenedicarboxylic acid, dibutyl ester; di-n-butylorthophthalate.

Download or read book Alternative Toxicological Methods written by Harry Salem and published by CRC Press. This book was released on 2003-03-26 with total page 616 pages. Available in PDF, EPUB and Kindle. Book excerpt: Bringing together the recent and relevant contributions of over 125 scientists from industry, government, and academia in North America and Western Europe, Alternative Toxicological Methods explores the development and validation of replacement, reduction, and refinement alternatives (the 3Rs) to animal testing. Internationally recognized scientist

Download or read book Validation of Alternative Methods for Toxicity Testing written by Chantra Eskes and published by Springer. This book was released on 2016-09-26 with total page 418 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book provides information on best practices and new thinking regarding the validation of alternative methods for toxicity testing. It covers the validation of experimental and computational methods and integrated approaches to testing and assessment. Validation strategies are discussed for methods employing the latest technologies such as tissue-on-a-chip systems, stem cells and transcriptomics, and for methods derived from pathway-based concepts in toxicology. Validation of Alternative Methods for Toxicity Testing is divided into two sections, in the first, practical insights are given on the state-of-the-art and on approaches that have resulted in successfully validated and accepted alternative methods. The second section focuses on the evolution of validation principles and practice that are necessary to ensure fit-for-purpose validation that has the greatest impact on international regulatory acceptance of alternative methods. In this context validation needs to keep pace with the considerable scientific advancements being made in toxicology, the availability of sophisticated tools and techniques that can be applied in a variety of ways, and the increasing societal and regulatory demands for better safety assessment. This book will be a useful resource for scientists in the field of toxicology, both from industry and academia, developing new test methods, strategies or techniques, as well as Governmental and regulatory authorities interested in understanding the principles and practicalities of validation of alternative methods for toxicity testing.

Download or read book Translational Toxicology written by Claude L. Hughes and published by Humana Press. This book was released on 2016-03-23 with total page 384 pages. Available in PDF, EPUB and Kindle. Book excerpt: Bringing together a distinguished interdisciplinary team of contributors, this volume provides a comprehensive exploration of translational toxicology—a systematic approach to developing therapeutic interventions that can protect against, mitigate, or reverse the effects of exposures. In particular, the book addresses modes of action and biomarkers, developmental risks of exposures, and potential translational toxicology therapeutics. The result is a compelling application of developmental toxicology in a new therapeutic discipline that is destined to become part of standard medical practice. Translational Toxicology: Defining a New Therapeutic Discipline is an essential text for regulatory authorities, scientists, and physicians who are concerned with environmental exposures, public health, nutrition, and pharmaceutical research and development. Basic science, epidemiological, and clinical investigators will also find this book a significant resource.

Download or read book Adverse Effects of Engineered Nanomaterials written by Bengt Fadeel and published by Academic Press. This book was released on 2012-01-27 with total page 367 pages. Available in PDF, EPUB and Kindle. Book excerpt: An essential reference that discusses occupational exposure and the adverse health effects of engineered nanomaterials and highlights current and future biomedical applications of these nanomaterials in relation to nanosafety.

Download or read book Significant New Use Rules on Certain Chemical Substances Us Environmental Protection Agency Regulation Epa 2018 Edition written by Law Library and published by Createspace Independent Publishing Platform. This book was released on 2018-09 with total page 68 pages. Available in PDF, EPUB and Kindle. Book excerpt: Significant New Use - Rules on Certain Chemical Substances (US Environmental Protection Agency Regulation) (EPA) (2018 Edition) The Law Library presents the complete text of the Significant New Use - Rules on Certain Chemical Substances (US Environmental Protection Agency Regulation) (EPA) (2018 Edition). Updated as of May 29, 2018 EPA is promulgating significant new use rules (SNURs) under the Toxic Substances Control Act (TSCA) for 57 chemical substances which were the subject of premanufacture notices (PMNs). The applicable review periods for the PMNs submitted for these 57 chemical substances all ended prior to June 22, 2016 (i.e., the date on which President Obama signed into law the Frank R. Lautenberg Chemical Safety for the 21st Century Act which amends TSCA). Thirty-four of these chemical substances are subject to TSCA section 5(e) consent orders issued by EPA. This action requires persons who intend to manufacture (defined by statute to include import) or process any of these 57 chemical substances for an activity that is designated as a significant new use by this rule to notify EPA at least 90 days before commencing that activity. The required notification initiates EPA's evaluation of the intended use within the applicable review period. Manufacture and processing for the significant new use is unable to commence until EPA has conducted a review of the notice, made an appropriate determination on the notice, and take such actions as are required with that determination. This book contains: - The complete text of the Significant New Use - Rules on Certain Chemical Substances (US Environmental Protection Agency Regulation) (EPA) (2018 Edition) - A table of contents with the page number of each section

Download or read book Chemical Status Report written by and published by . This book was released on 1992 with total page 40 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Atlas of Histology of the Juvenile Rat written by George A Parker and published by Academic Press. This book was released on 2016-05-04 with total page 464 pages. Available in PDF, EPUB and Kindle. Book excerpt: Atlas of Histology of the Juvenile Rat should be of interest to toxicologic pathologists, toxicologists, and other biological scientists who are interested in the histomorphology of juvenile rats. For several decades the laboratory rat has been used extensively in nonclinical toxicology studies designed to detect potential human toxicity of drugs, agrochemicals, industrial chemicals, and environmental hazards. These studies traditionally have involved young adult rats that are 8-10 weeks of age as studies are started. It is becoming increasingly apparent that children and young animals may have different responses to drug/chemical exposures, therefore, regulatory agencies are emphasizing toxicology studies in juvenile animals. While the histologic features of organs from young adult and aged laboratory rats are well known, less is known about the histologic features of organs from juvenile rats. Final histologic maturity of many organs is achieved postnatally, thus immature histologic features must be distinguished from chemical- or drug-related effects. While this postnatal organ development is known to exist as a general concept, detailed information regarding postnatal histologic development is not readily available. The Atlas includes organs that are typically sampled in nonclinical toxicology studies and presents the histologic features at weekly intervals, starting at birth and extending through postnatal day 42. Written and edited by highly experienced, board-certified toxicologic pathologists Includes more than 700 high-resolution microscopic images from organs that are typically examined in safety assessment toxicology studies Detailed figure legends and chapter narratives present the salient features of each organ at each time interval Figures are available for further study via Elsevier’s Virtual Microscope, which allows viewing of microscopic images at higher magnification Valuable resource for toxicologic pathologists who are confronted with interpretation of lesions in juvenile rats in situations where age-matched concurrent controls are not available for comparison, e.g., with unscheduled decedents Figures are available for further study on ScienceDirect with Virtual Microscope, which allows viewing of microscopic images at higher magnification