Recent Posts

All solutions you need - A Blog for your needs

If you want answers/informatiom for on any subject, it may be related to computers or health care, common issues, you may come to our blog for all your solutions. If you are not able to find your solution; let us know. You may contact us by commenting or emailing to out more by exploring...

Following are the some of the Advantages of our blog :-

  • Easy to use.
  • never miss our posts by subscribeing.
  • You can join us by contacting

Sunday, 15 April 2018

// // Leave a Comment

Illustrated Toxicology 1st Edition With Study Questions- 2018

Illustrated Toxicology - 1st Edition - ISBN: 9780128132135, 9780128132142 Authors: PK Gupta
eBook ISBN: 9780128132142
Paperback ISBN: 9780128132135
Imprint: Academic Press
Published Date: 19th April 2018
Page Count: 640


Illustrated Toxicology: With Study Questions is an essential, practical resource for self-study and guidance catering to a broad spectrum of students. This book covers a range of core toxicological areas, including pesticides, radioactive materials and poisonous plants, also presenting a section on veterinary toxicology. Across 16 chapters, the book presents key concepts with the aid of over 250 detailed, full-color illustrations. Each section is supplemented with practical exercises to support active learning. This combination of clear illustrations and sample testing will help readers gain a deeper understanding of toxicology.
This book is useful for toxicology, pharmacy, medical and veterinary students, and also serves as a refresher for academics and professionals in the field, including clinical pharmacists, forensic toxicologists, environmentalists and veterinarians.

Key Features

  • Includes comprehensive coverage of key toxicological concepts for study and revision
  • Provides a visual learning aid with over 250 full-color illustrations
  • Enhances understanding and memory retention of core concepts with the use of practical exercises


Advanced undergraduates and graduates in toxicology; examiners. This will also be of interest to academics in the field of toxicology, clinical pharmacists, forensic toxicologists and veterinarians

Table of Contents

  1. 1. General Toxicology
    2. Disposition and Toxicokinetics of Toxicants
    3. Metals and Micronutrients
    4. Pesticides (Agrochemicals)
    5. Non-metallics and micronutrients
    6. Solvents, Vapors and Gases
    7. Poisonous Plants
    8. Poisons of Animal Origin
    9. Poisonous Foods and Food Poisoning
    10. Drugs of Use, Dependence and Abuse
    11. Environmental Toxicology
    12. Radioactive Materials
    13. Veterinary Toxicology
    14. Clinical Toxicology
    15. Organs and Mechanism of Toxicity
    16. Brain Storming Questions
  2. For more details, visit


No. of pages:
© Academic Press 2018
Academic Press
eBook ISBN:
Paperback ISBN:

Read More

Monday, 26 March 2018

// // Leave a Comment

Toxicity of Fungicides


Fungicides are agents that are used to prevent or eradicate fungal infections from plants or seeds. Numerous substances having widely varying chemical constituents are used as fungicides (Gupta, 1988; Gupta, 2016).Fungicides have been classified according to chemical structures or have been categorized agriculturally and horticulturally according to the mode of action (Ballantyne, 2004). According to the mode of application, fungicides are grouped as foliar, soil and dressing fungicides. Foliar fungicides are applied as liquids or powders to the aerial green parts of plants, producing a protective barrier on the cuticular surface and systemic toxicity in the developing fungus. Soil fungicides are applied as liquids, dry powders, or granules, acting either through the vapor phase or by systemic properties. Dressing fungicides are applied to the postharvest crop as liquids or dry powders to prevent fungal infestation of the crop, particularly if stored under less than optimum conditions of temperature and humidity. Thus, effective fungicides must be protective, curative, or eradicative and should possess the following properties: (1) low toxicity to the plant/animal but high toxicity to the particular fungus; (2) activity per se or the ability to convert themselves (by plant or fungal enzymes) into toxic intermediates; (3) the ability to penetrate fungal spores or the developing mycelium to reach the site of action; (4) low ecotoxicity; and (5) the ability to form a protective, tenacious deposit on the plant surface that will be resistant to weathering by sunlight, rain and wind (Phillips, 2001). With a few exceptions, most of the newly developed chemicals have a low order of toxicity to mammals. Public concern has focused on the positive mutagenicity tests obtained with many fungicides and the predictive possibility of both teratogenic and carcinogenic potential. The quantity of fungicides used on major crops is estimated to have increased 2.3-fold between 1964 and 1997. Use of inorganics (primarily copper compound) and dithiocarbamates has declined since the 1960s, but captan, chlorothalonils and other organic materials account for 90% of fungicide use. Newer groups, such as benzimidazoles, conazoles, dicarboximides and metal organic compounds, account for approximately 10% of fungicide use (Osteen and Padgitt, 2002). In this chapter, fungicides are discussed using a chemical classification system.


The earliest fungicides were inorganic materials such as sulfur, lime, copper and mercury compounds. The use of element sulfur as a fungicide was recommended as early as 1803. It has become an important component of integrated pest management systems because it can be used in “organic farming.” There are an increasing number of instances of dermatitis in human farmworkers and diseases in ruminants caused by exposure to high levels of sulfur (Gammon et al., 2010). The mercury-containing fungicides have been responsible for many deaths or permanent neurological disability. Some of the earlier inorganic metallic fungicides have been withdrawn in many countries because of their toxicity and adverse environmental effects (Ballantyne, 2004). Another compound, hexachlorobenzene (HCB), was extensively used from the 1940s through the 1950s as a fungicidal dressing applied to seed grains as a dry powder. Between 1955 and 1959, an epidemic of poisoning occurred in Turkey and resulted in a syndrome called black sore and caused more than 4000 deaths. Although this agent has largely fallen by the wayside, it is still being used in developing countries. It is a highly toxic compound and can lead to severe skin manifestations including hypersensitivity (Hayes, 1982; Gupta, 2010a). Since that time, many compounds have been developed and used to control fungal diseases in plants, seeds and produce. Carbamic acid derivatives, including ethylenebisdithiocarbamates (EBDCs), are a group of fungicides that have been used widely throughout the world since the 1940s. The important members of this class include mancozeb, maneb, metiram, zineb and nabam. All the members have an EBDC backbone, with different metals associated with the individual compounds. Captan, folpet and captafol have been in use for more than 55 years. These compounds belong to the chloroalkylthiodicarboximide class of fungicides due to the presence of chlorine, carbon and sulfur in the side chain. Related compounds associated with this fungicide class are dichlofluanid and tolylfluanid. These two compounds have a fluorine atom substituted for one of the terminal chlorine atoms. Another compound, chlorothalonil, which is a halogenated benzonitrile fungicide, was first registered for use as an agrochemical in the United States in 1966. Chlorothalonil also has wider biocidal applications, including use in paints and lubricant fluids. The benzimidazole fungicides, benomyl and carbendazim, have been in use for more than 40 years, whereas anilinopyrimidines, a new class of fungicides (cyprodinil, mepanipyrim and pyrimethanil), were introduced in 1993 (cyprodinil by Ciba in France) for application on cereal grains (Ollinger et al., 2010).


Toxicokinetic studies provide important data on the amount of toxicant delivered to a target as well as species-specific metabolism. Animals are exposed to fungicides through ingestion or they are absorbed through the skin or the respiratory system. Different factors regulate their absorption, distribution, metabolism and excretion. In general, the liver is the primary site for biotransformation and may include detoxification as well as activation reactions (Gupta, 1986). Some fungicides do not undergo any metabolism and bind with other active binding sites. The aryl organomercurials methyl- and ethylmercury chloride are poorly excreted and tend to accumulate in muscle, brain and other tissues, whereas the aryl organomercurial phenylmercury is more readily excreted via the kidney and less likely to accumulate in brain and muscles. Similarly, HCB possesses all the properties of chemical stability, slow degradation and biotransformation, environmental persistence and bioaccumulation in adipose tissue and organs containing a high content of lipid membranes (Costa, 2008). The newly introduced class of fungicides are rapidly absorbed, metabolized and excreted and do not accumulate in tissues, but some of them are partially absorbed from the gastrointestinal (GI) tract. For example, absorption of chlorothalonil from the GI tract is on the order of 30–32% of the administered dose. At least 80% of the administered dose is excreted in feces within 96 h. The highest concentrations are observed in the kidneys – approximately 0.1% of the dose. In this case, gut microflora plays a role in the disposition and metabolism in rats. Glutathione conjugation plays a central role in the metabolism and subsequent complex metabolic processing of these conjugates, resulting in selective renal uptake and urinary excretion of thiol-derived metabolites. Hepatic glutathione levels are decreased, and renal glutathione levels are elevated. The depletion of hepatic glutathione is considered a direct consequence of glutathione conjugation within the liver utilizing tissue resources. The increase in renal glutathione content is more difficult to explain, but it may be a consequence of urinary excretion of glutathione conjugates (Parsons, 2010).
The captan is rapidly degraded to 1,2,3,6-tetrahydrophthalimide (THPI) and thiophosgene (via thiocarbonyl chloride) in the stomach before reaching the duodenum. THPI has a half-life of 1–4 s, and thiophosgene is detoxified by reaction with cysteine or glutathione and is rapidly excreted. No captan is detected in blood or urine. It is therefore unlikely that these compounds or even thiophosgene would survive long enough to reach systemic targets such as the liver, uterus, or testes. Due to rapid elimination, meat, milk, or eggs from livestock/poultry would be devoid of the parent materials. Humans appear to metabolize captan in a similar manner to other mammals (Krieger and Thongsinthusak, 1993; JMPR, 2004; Gordon, 2010).
Cyprodinil, an anilinopyrimidine class fungicide, is rapidly absorbed from the GI tract into systemic circulation in rats. Approximately 48–68% of the administered dose is excreted in the urine, whereas 29–47% is found in the feces. Total excretions reach 92–97% of the administered dose within 48 h. Cyprodinil is almost completely metabolized. No unchanged parent molecule is found in urine, whereas minor amounts of unchanged cyprodinil are found in feces. Most of the administered cyprodinil is metabolized by sequential oxidation of the phenyl and pyrimidine ring (Figure 48.1). In urine and feces, there is no difference in the metabolite patterns of the phenyl or pyrimidyl labeled cyprodinil. Seven urinary, two biliary and two fecal metabolites have been identified, which in total account for 65–80% of the administered dose. Cyprodinil is absorbed in goats to a lesser extent and more slowly than in rats. The major route of excretion is in urine and feces, whereas excretion via milk is minimal. In laying hens, cyprodinil is rapidly and completely eliminated. Residues in eggs and edible tissues are very low. The metabolic pathways of cyprodinil in lactating goats and laying hens are similar to those observed in rats (Waechter et al., 2010).
Carbamic acid derivative fungicides, such as EBDCs, are only partially absorbed, and then they are rapidly metabolized and excreted with no evidence of long-term bioaccumulation. Absorption of oral doses is rapid, and doses are excreted within 24 h with approximately half eliminated in the urine and half in the feces. Their common metabolite is ethylenethiourea (ETU). Only low-level residues are found in tissues, particularly the thyroid. Another compound in this class, propamocarb, is rapidly and nearly completely absorbed and distributed with a concentration reaching peak levels within 1 h. Elimination from tissues is rapid; with a half-life ranging from 11 to 26 h, urine is the main route of excretion (~75–91% within 24 h). Up to 6% of the administered dose is excreted in feces. Propamocarb is extensively metabolized, and only small quantities are unchanged in urine. Metabolism involves aliphatic oxidation of the propyl chain (to form hydroxyl propamocarb) and N-oxidation and N-demethylation of the tertiary amine resulting in propamocarb N-oxide and mono demethyl propamocarb, respectively. Both benomyl and carbendazim are well absorbed after oral exposure (80–85%) but poorly absorbed after dermal exposure (1 or 2%) in rats, mice, dogs and hamsters. The major pathway of clearance is urinary elimination in rats and mice, but in dogs the majority of the dose (83.4%) is eliminated via feces, with only 16.2% of the dose eliminated in the urine after 72h of dosing. In animals, benomyl is converted into carbendazim through the loss of the n-butylcarbamyl side chain prior to further metabolism. In dogs and rats, carbendazim undergoes aryl hydroxylation–oxidation at the 5 and 6 positions of the benzimidazole ring, followed by sulfate or glucuronide conjugation before elimination. The urinary excretion half-life of carbendazim in both male and female rats is approximately 12 h. Benomyl or carbendazim or their metabolites are cleared rapidly from blood and exhibit minimal potential for bioaccumulation in rats exposed orally or intravenously (Gardiner et al., 1974; JMPR, 2005).
Similarly, amide fungicides are rapidly absorbed and eliminated. Metalaxyl-M and metalaxyl can lead to stimulation of hepatic and renal cytochrome P450 and some other drug metabolizing enzymes. Tolylfluanid is rapidly and extensively absorbed, followed by rapid metabolism and almost complete excretion, mainly in the urine and to a lesser extent in the bile, within 48 h. High tissue concentration has been seen soon after dosing in the kidney and liver, with lower concentrations in the perirenal fat, brain, gonads and thyroid. In most species, the concentration of fluoride in the bone and teeth increases in a dose-related manner (JMPR, 2002, 2005).
After oral dose, conazole fungicides such as triadimenol and triadimefon are rapidly absorbed and widely distributed in liver and kidney. Excretion and metabolism is rapid and extensive, predominantly through oxidation of the t-butyl methyl group. Propiconazole indicates rapid and extensive absorption (80% of the administered dose) and is widely distributed, having the highest concentration in liver and kidney. Excretion is more than 95% in the urine and feces within 48 h. There is extensive enterohepatic recirculation. The compound is extensively metabolized with oxidation of propyl side chain, hydroxylation of phenyl and triazole rings, and conjugation. The cleavage of dioxolane is significantly different according to species and sex (JMPR, 2004). The other compound, fludioxonil, is rapidly and extensively (80%) absorbed, widely distributed, extensively metabolized and rapidly excreted, primarily in feces (80%), with a small amount being excreted in the urine (20%). The maximum blood concentration is reached within 1 h after administration. Elimination is biphasic, with half-lives of between 2 and 5 h for the first phase and between 30 and 60 h for the second phase. The compound is extensively metabolized, involving primarily oxidation of the pyrrole ring (57% of the administered dose) and a minor oxo-pyrrole metabolite (4% of the administered dose), followed by glucuronyl and sulfate conjugation. There is no potential of accumulation in the tissues. Trifloxystrobin is rapidly absorbed (66%) in 48 h and is widely distributed, with highest concentrations in blood, liver and kidney. Within 72 h, 72–96% of the administered dose is eliminated in the urine and feces. Metabolism is extensive, and the compound undergoes hydroxylation, O-demethylation, oxidation, conjugation, chain shortening and cleavage between glyoxylphenyl and trifluoromethyl moieties (JMPR, 2004).

Mechanism of action

There are a series of biochemical changes or free radical-mediated processes; some may also be produced by other mechanisms that have been used to assess tissue injury. This is exemplified by the phenomenon of lipid peroxidation, which has been invoked as a toxic mechanism in many situations and also occurs subsequent to cell death and membrane lysis. However, in most situations, it is difficult to identify the exact mechanism of action. For example, in fungicides containing mercury, the mercury ions inhibit the sulfhydryl group of enzymes involved in the transfer of amino acids across the blood–brain barrier and then interfere with protein synthesis. Organomercurials can also release some mercury ions in the body, but their toxicity is not believed to be a primary action of mercury ions (Sandhu and Brar, 2009). There are several theories regarding the mechanism by which sulfur produces its toxic action. The oxidized sulfur theory attributes toxicity to its oxidation products, such as sulfur dioxide, sulfur trioxide, thiosulfuric acid, or pentathionic acid. The reduced sulfur theory ascribes toxicity to hydrogen sulfide. Direct action theory suggests toxicity due to crosslinking of proteins, formation of other cellular components by free radicals of sulfur or polysulfides, or extensive oxidation of thiol groups leading to loss of function or structural integrity of proteins. Pentachlorophenol (PCP), a halogenated substituted monocyclic aromatic, acts cellularly to uncouple oxidative phosphorylation, with the target enzyme being Na+/K+-ATPase. Oxygen consumption is increased, whereas adenosine triphosphate (ATP) formation is decreased. The energy is lost as heat instead of being stored as high-energy phosphate bonds. The electron transport chain responds by using increasingly more available oxygen (increased oxygen demand) in an effort to produce ATP, but much of the free energy is lost as body heat. This leads to depletion of energy reserves (Eaton and Gallagher, 1997). Similarly, organotin compounds, particularly triethyltin, uncouple oxidative phosphorylation, whereas other agents (e.g., sulfur) in the presence of sulfiting agents such as sulfur dioxide uncouple oxidative phosphorylation. Thiamine is cleaved into its constituent pyrimidine and thiazole moieties, rendering it inactive.
Although the biochemical and molecular mechanism(s) by which captan and its analogs exert their cellular toxicity has not been fully established, captan is known to react with cellular thiols to produce thiophosgene, a potent and unstable chemical capable of reacting with sulfhydryl-, amino-, or hydroxyl-containing enzymes (Cremlyn, 1978). Thiols reduce the potency of captan. A volatile product of captan is responsible for mutagenic activity, the intermediate being short-lived and formed more quickly at higher levels at an alkaline pH. There are several other mechanisms by which these chemicals can induce cellular toxicity. For example, mouse tumors develop with oral administration above a threshold if maintained for at least 6 months. As shown in Figure 48.1, epithelial cells that comprise the villi are damaged by exposure to captan and sloughed off into the intestinal lumen at an increased rate. Second, the basal cells in the crypt compartment that normally divide at a rate commensurate with the normal loss of villi cells from the tips of the villi increase, resulting in high cell proliferation, which is not carcinogenic per se but does play a role in tumor development. However, there appears to be no treatment-related duodenal tumor incidence of captan in rats or dogs. Some of the data have been compiled in reviews, and a task force and framework have been evolving for evaluation of the mode of toxicity and tumorogenicity findings in mice bioassay and human relevance for risk assessment purposes (Arce et al., 2010; Cohen et al., 2010; Gordon, 2010).

Chlorothalonil fungicide is a reactive molecule toward thio (–SH) groups. It is a soft electrophile with a preference for sulfur nucleophiles rather than nitrogen/oxygen nucleophiles. Such chemicals tend to show reactivity toward protein containing critical S electrophiles rather than toward DNA (containing critical O and N nucleophiles). A mechanistic interpretation for the carcinogenicity of chlorothalonil has been published by Wilkinson and Killeen (1996). Repeated administration of chlorothalonil causes hyperplasia in the forestomach of rats and mice. The data are consistent with a temporal sequence of events starting with increased cell proliferation, multifocal ulceration and erosion of the forestomach mucosa, regenerative hyperplasia and hyperkeratosis, and ultimately progressing to the formation of gastric tumors within the forestomach. In dogs, there is no evidence of either neoplastic development or the occurrence of pre-neoplastic lesions in the kidney or stomach. The absence of stomach lesions in dogs is attributable to the anatomical differences between rodents and dogs – dogs do not possess a forestomach. Continued administration of chlorothalonil leads to the development of a regenerative hyperplasia within the renal proximal tubular epithelium. Continued regenerative hyperplasia ultimately results in progression of the kidney lesion to tubular adenoma and carcinoma. Initial cytotoxicity and regenerative hyperplasia within the proximal tubular epithelium are essential prerequisites for subsequent tumor development. The proposed mode of action for the induction of renal toxicity in rodents is outlined in Figure 48.2.
Fig 48.2 here (plz insert fig 55.3 from 2nd edition of Vety Toxicology)

The toxicology database supporting mechanism of action of carbamic acid derivatives such as EBDCs and their common metabolite ETU has been explained using modern studies with mancozeb, maneb and metiram because the principal target organ is the thyroid. These compounds inhibit the synthesis of thyroid hormone, thyroxine (T4), and triiodothyronine (T3), leading to elevated levels of thyroid-stimulating hormone (TSH) via feedback stimulation of the hypothalamus and pituitary (Atterwill and Aylard, 1995). Prolonged and continuous elevation of TSH levels results in hypertrophy and hyperplasia of the thyroid follicular cells in rats, mice, hamsters, monkeys and dogs, leading to development of follicular nodular hyperplasia, adenoma and/or carcinoma in rats and mice (Ollinger et al., 2010). Conazoles such as propiconazole have phenobarbital-type mode of action, leading to cell proliferation, increased liver weight and microsomal enzyme induction (JMPR, 2004).

For details read full article

Gupta PK, (2018) Toxicity of fungicides. In Veterinary Toxicology- Basic and Clinical Principals, Gupta RC (ed.) 3nd ed. Elsevier, USA pp 569-582.
Read More

Sunday, 25 March 2018

// // Leave a Comment

Health for all: Overview of Herbicide Poisoning

Health for all: Overview of Herbicide Poisoning: prevention is better than cure
Herbicides are used routinely to control noxious plants. Most of these chemicals, particularly the more recently developed synthetic organic herbicides, are quite selective for specific plants and have low toxicity for mammals; other less selective compounds (eg, sodium arsenite, arsenic trioxide, sodium chlorate, ammonium sulfamate, borax, and many others) were formerly used on a large scale and are more toxic to animals.
Vegetation treated with herbicides at proper rates normally will not be hazardous to animals, including humans. Particularly after the herbicides have dried on the vegetation, only small amounts can be dislodged. When herbicide applications have been excessive, damage to lawns, crops, or other foliage is often evident.
The residue potential for most of these agents is low. However, runoff from agricultural applications and entrance into drinking water cannot be ruled out. The possibility of residues should be explored if significant exposure of food-producing animals occurs. The time recommended before treated vegetation is grazed or used as animal feed is available for a number of products.
Most health problems in animals result from exposure to excessive quantities of herbicides because of improper or careless use or disposal of containers. When used properly, problems of herbicide poisoning in veterinary practice are rare. With few exceptions, it is only when animals gain direct access to the product that acute poisoning occurs. Acute signs usually will not lead to a diagnosis, although acute GI signs are frequent. All common differential diagnoses should be excluded in animals showing signs of a sudden onset of disease or sudden death. The case history is critical. Sickness following feeding, spraying of pastures or crops adjacent to pastures, a change in housing, or direct exposure may lead to a tentative diagnosis of herbicide poisoning. Generally, the nature of exposure is hard to identify because of storage of herbicides in mis- or unlabeled containers. Unidentified spillage of liquid from containers or powder from torn or damaged bags near a feed source, or visual confusion with a dietary ingredient or supplement, may cause the exposure. Once a putative chemical source has been identified, an animal poison control center should be contacted for information on treatments, laboratory tests, and likely outcome.
Chronic disease caused by herbicides is even more difficult to diagnose. It may include a history of herbicide use in proximity to the animals or animal feed or water source, or a gradual change in the animals’ performance or behavior over a period of weeks, months, or even years. Occasionally, it involves manufacture or storage of herbicides nearby. Samples of possible sources (ie, contaminated feed and water) for residue analysis, as well as tissues from exposed animals taken at necropsy, are essential. Months or even years may be required to successfully identify a problem of chronic exposure.
In order to recognize whether a subject is exposed to herbicides, or even accidental poisoning, now standardized analytical procedure for diagnostic investigation of biological materials have become established and these are subsumed under the term“biomonitoring”. Accurately biomonitoring is an important tool that can be used to evaluate human or animal exposure to such herbicides by measuring the levels of these chemicals, their metabolites or altered biological structures or functions in biological media such as urine, blood or blood components, exhaled air, hair or nails, and tissues  The use of urine has advantage because of ease of availability.  As such urine has been used for biomonitoring of several herbicides such as 2,4-D, 2,4,5-T, MCPA (2-methyl-4-chlorophenoxyacetic acid), atrazine, diuron, alachlor, metolachlor, paraquat, diquat, imazapyr, imazapic,  imazethapyr, imazamox,  imazaquin and  imazamethabenz-methyl with the objective to assess exposure and health risk to exposed subjects.

If poisoning is suspected, the first step in management is to halt further exposure. Animals should be separated from any possible source before attempting to stabilize and support them. If there are life-threatening signs, efforts to stabilize animals by general mitigation methods should be started. Specific antidotal treatments, when available, may help to confirm the diagnosis. As time permits, a more detailed history and investigation should be completed. The owner should be made aware of the need for full disclosure of facts in order to successfully determine the source of poisoning, eg, unapproved use or failure to properly store a chemical.
Toxicity and Management of Poisoning
There are >200 active ingredients used as herbicides; however, some of them are believed to be obsolete or no longer in use. Of these, several have been evaluated for their toxic potential and are discussed below. More specific information is available on the label and from the manufacturer, cooperative extension service, or poison control center. Selected information on herbicides, such as the acute oral toxic dose (LD50) in rat, the amount an animal can be exposed to without being affected (no adverse effect level), the likelihood of problems caused by dermal contact in rabbit (dermal LD50, eye and skin irritation), deleterious effects on avian species and toxicity to fish in water is included for some commonly used herbicides (TABLE 1). Comparative toxic doses (TD) and lethal doses (LD), of selected herbicides in domesticated species such as monkeys, cattle, sheep, pigs, cats, dogs, chickens is also summarized (TABLE 2). The information is only a guideline because the toxicity of herbicides may be altered by the presence of other ingredients (eg, impurities, surfactants, stabilizers, emulsifiers) present in the compound. With a few exceptions, most of the newly developed chemicals have a low order of toxicity to mammals. However, some herbicides such as atrazine, buturon, butiphos, chloridazon, chlorpropham, cynazine, 2,4-D and 2,4,5-T alone or in combination, dichlorprop dinoseb, dinoterb, linuron, mecoprop, monolinuron, MCPA (2-methyl-4-chlorophenoxyacetic acid), prometryn, propachlor, nitrofen, silvex, TCDD (a common contaminant during manufacturing process of some herbicides such as 2,4- D and 2,4,5-T), tridiphane and tridiphane are known to have adverse effects on development of

Overview of Herbicide Poisoning

By P. K. Gupta, PhD, Post Doc (USA), Hon DSc PGDCA, MSc VM & AH BVSc, FNA VSc, FASc, AW, FST, FAEB, FACVT (USA), Gold Medalist, Editor-in-Chief, Toxicology International
The Merck Veterinary Manual (2016). Chapter “Herbicide Poisoning” by PK GUPTA 11th edition, Merck & Co. Inc Whitehouse Station, NJ, USA  pp 2969-99
Read More

Saturday, 24 March 2018

// // Leave a Comment

Gupta’s Series 10: TOXICOLOGY Question and Answer bank

TOXICOLOGY Question and Answer bank is aimed to make the study of toxicology simple and understandable ----------------
Exercise 1
1.        Which one of the following statements regarding toxicology is true?
a. Modern toxic ology is concerned with the study of the adverse effects of chemicals on ancient forms of life.
b. Modern toxicology studies embrace principles from such disciplines as biochemistry, botany, chemistry, physiology, and physics.
c. Modern toxicology has its roots in the knowledge of plant and animal poisons, which predates recorded history and has been used to promote peace.
d. Modern toxicology studies the mechanisms by which inorganic chemicals produce advantageous as well as deleterious effects.
e. Modern toxicology is concerned with the study of chemicals in mammalian species.
2. Knowledge of the toxicology of poisonous agents was published earliest in the:
a. Ebers papyrus.
b. De Historia Plantarum.
c. De Materia Medica.
d. Lex Cornelia.
e. Treatise on Poisons and Their Antidotes.
3. Paracelsus, physician- alchemist, formulated many revolutionary reviews that remain integral to the structure of toxicology, pharmacology, and therapeutics today. He focused on the primary toxic agent as chemical entity and articulated the dose–response relation. Which one of the following statements is not attributable to Paracelsus?
a. Natural poisons are quick in their onset of actions.
b. Experimentation is essential in the examination of
responses to chemicals.
c. One should make distinction between the therapeutic and toxic properties of chemicals.
d. These properties are sometimes but not always indistinguishable except by dose.
e. One can ascertain a degree of specificity of chemicals and their therapeutic or toxic effects.
4. The art of toxicology requires years of experience to acquire, even though the knowledge base facts may be learned more quickly. Which modern toxicologist is credited with saying that “you can be toxicologist in two easy lesions, each of 10 years?”
a. Claude Bernard.
b. Rachel Carson.
c. Upton Sinclair.
d. Arnold Lehman.
e. Oswald Schmiedeberg.
5. Which of the following statements is correct?
a. Claude Bernard was a prolific scientist who trained over 120 students and published numerous contributions to the scientific literature.
b. Louis Lewin trained under Oswald Schmiedeberg
and published much of the early work on the toxicity
of narcotics, methanol, and chloroform.
c. An Introduction to the Study of Experimental Medicine was written by the Spanish physician Orfila.
d. Magendie used autopsy material and chemical analysis systematically as legal proof of poisoning.
e. Percival Potts was instrumental in demonstrating the chemical complexity of snake venoms.
1. b.
2. a.
3. a.
4. d.
5. b.
Exercise 2
1. Five identical experimental animals are treated with 1 mg of one of the following toxins. The animal treated with which toxin is most likely to die?
a. ethyl alcohol (LD50 = 10,000 mg/kg).
b. botulinum toxin (LD50 = 0.00001 mg/kg).
c. nicotine (LD50 = 1 mg/kg).
d. ferrous sulfate (LD50 = 1500 mg/kg).
e. picrotoxin (LD50 = 5 mg/kg).
2. Place the following mechanisms of toxin delivery in order from most effective to least effective—1: intravenous; 2: subcutaneous; 3: oral; 4: inhalation; 5: dermal.
a. 1, 5, 2, 4, 3.
b. 4, 1, 2, 3, 5.
c. 1, 4, 2, 3, 5.
d. 4, 2, 1, 5, 3.
e. 1, 4, 3, 2, 5.
3.A toxin with a half -life of 12 h is administered every 12 h. Which of the following is true?
a. The chemical is eliminated from the body before the next dose is administered.
b. The concentration of the chemical in the body will
slowly increase until the toxic concentration is attained.
c. A toxic level will not be reached, regardless of how many doses are administered.
d. Acute exposure to the chemical will produce immediate toxic effects.
e. The elimination rate of the toxin is much shorter than the dosing interval.
4. Urushiol is the toxin found in poison ivy. It must first react and combine with proteins in the skin in order for the immune system to recognize and mount a response against it. Urushiol is an example of which of the following?
a. antigen.
b. auto-antibody.
c. superantigen.
d. hapten.
e. cytokine.
5. Toxic chemicals are most likely to be biotransformed in which of the following organs?
a. central nervous system.
b. heart.
c. lung.
d. pancreas.
e. liver.
6. When chemicals A and B are administered simultaneously, their combined effects are far greater than the sum of their effects when given alone. The chemical interaction between chemicals A and B can be described as which of the following?
a. potentiative.
b. additive.
c. antagonistic.
d. unctionally antagonistic.
e. synergistic.
7. With respect to dose–response relationships, which of the following is true?
a. Graded dose–response relationships are often
referred to as “all or nothing” responses.
b. Quantal dose–response relationships allow for the
analysis of a population’s response to varying dosage.
c. Quantal relationships characterize the response of an individual to varying dosages.
d. A quantal dose–response describes the response of an individual organism to varying doses of a chemical.
e. The dose–response always increases as the dosage is increased.
8. When considering the dose–response relationship or an essential substance:
a. there are rarely negative effects of ingesting too much.
b. the curve is the same or all people.
c. adverse responses increase in severity with increasing or decreasing dosages outside of the homeostatic range.
d. the relationship is linear.
e. deficiency will never cause more harm than over- ingestion.
9. The therapeutic index of a drug:
a. is the amount of a drug needed to cure an illness.
b. is lower in drugs that are relatively safer.
c. describes the potency of a chemical in eliciting a
desired response.
d. describes the ratio of the toxic dose to the therapeutic dose of a drug.
e. explains the change in response to a drug as the dose is increased.
10. Penicillin interferes with the formation of peptidoglycan cross-links in bacterial cell walls, thus weakening the cell wall and eventually causing osmotic death of the bacterium. Which of the following is true?
a. Treatment with penicillin is a good example of selective toxicity.
b. Penicillin interferes with human plasma membrane structure.
c. Penicillin is a good example of a drug with a low
therapeutic index.
d. Penicillin is also effective in treating viral infections.
e. Penicillin is completely harmless to humans
1. b.
2. c.
3. b.
4. d.
5. e.
6. e.
7. b.
8. c.
9. d.
10. a.                                                                         

Further Reading

Andrew Patkinson and Brian W. Ogilvie (2013) Biotransformation of Xenobiotics. In: Klaassen, C. D (Ed.) Casarett and Doull’s Toxicology: The Basic Science of Poisons, 8th ed (pp 185-366), McGraw-Hill New York 
Danny, D, Shen (2013) Toxicokinetics. In: Klaassen, C. D (Ed) Casarett and Doull’s Toxicology: The Basic Science of Poisons, 8th ed (pp 367-390) McGraw-Hill New York.
Deon van der Merwe, Ronette Gehring and Jennifer L. Buur (2017) Toxicokinetics In. Gupta R.C (Ed.) Veterinary Toxicology: Basic and Clinical Principles.3rd ed. Academic Press/Elsevier: Amsterdam (in press)
Gupta P.K (2010): Absorption, Distribution, & Excretion of Xenobiotics. In: Gupta, PK (Ed.) Modern Toxicology: Basis of Organ and Reproduction Toxicity, Vol. 1, 2nd reprint (pp 71-92) PharmaMed Press, Hyderabad, India.. 
Gupta P.K. (2014) Essential concept in toxicology. BSP India (chapter 7)
Gupta P.K. (2016) Fundamental of Toxicology: Essential concept and applications. Elsevier/BSP USA (Chapter 8)
Gupta P.K. (2016) Fundamental of Toxicology: Essential concept and applications. Elsevier/BSP USA (Chapter 9)
Curtis D. Klaassen, CD; Watkins III, JB (2015) Casarett & Doull’s Essentials of Toxicology. 3rd ed McGraw-Hill, USA pp 1-524.
Krishnamurti, C. R (2010): Biotransformation of Xenobiotics. In: Gupta, PK (Ed.) Modern Toxicology: Basis of Organ and Reproduction Toxicity, Vol. 1, 2nd reprint (pp 95-129). PharmaMed Press, Hyderabad, India.
Lois D Lehman-McKeeman (2013) Absorption distribution and excretion of toxicants. In: Klaassen CD (Ed) Casarett and Doull’s toxicology: The basic science of poisons, 8th ed (pp 153-184) (New York), McGraw-Hill,
Mats Ehrnebo (2010) Kinetic Analysis of . In: Gupta, PK (Ed.) Modern Toxicology: Basis of Organ and Reproduction Toxicity, Vol. 1, 2nd reprint (pp 130-151). PharmaMed Press, Hyderabad, India
Randy L. Rose, Hodgson E (2010) Chemical and Physiological Influences on Xenobiotic Metabolism. In: Hodgson, E.A (Ed) A Textbook of Modern Toxicology 4th edition (pp 163-201), John Wiley, New Jersey.
Randy L. Rose and Ernest Hodgson (2010) Metabolism of Toxicants. In: Hodgson, E.A (Ed) A Textbook of Modern Toxicology 4th ed (pp 111- 148), John Wiley, New Jersey.
Randy L. Rose and Patricia E. Levi (2010) Reactive Metabolites. In: Hodgson, E.A (Ed) A Textbook of Modern Toxicology 4th ed (pp 149-161), John Wiley, New Jersey.
Renwick AG (2008) Toxicokinetic. In: Hays AW (Ed) Principles and methods of toxicology. 5th ed (179-230). Boca Tato Taylor and Francis.
Timbrell JA (2009) Factors affecting toxic responses: disposition. In: Timbrell JA (Ed) Principles of biochemical toxicology. 4th ed. (35-74), Informa, New York:
 Gupta PK (2018) SERIES 3: TOXICOLOGY Question and Answer bank | Dr Pawan ... 26, 2018 - 
Gupta PK (2018) Series 4: TOXICOLOGY Question and Answer bank | Dr Pawan Kumar ... 4, 2018 - Feb 4, 2018 Cont'd from series 3.
Gupta PK (2018) Series 5: Risk Assessment-TOXICOLOGY Question and Answer bank ... 5: Risk Assessment. Cont'd from series 4.
Gupta PK (2018) Series 6: (Multiple choice questions) TOXICOLOGY Question and Answer bank toxicology-question-gupta/
Gupta PK (2018) Dr Pawan K (PK) Gupta Series7: Multiple Choice Questions and fill in blanks TOXICOLOGY Question and Answer bank
Gupta PK (2018) Series 8: True and False, and Match the statements- TOXICOLOGY Questions by Dr Pawan K (PK) Gupta
To be Cont’d series 11
Read More


Enter your email address:

Delivered by FeedBurner