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Nicotine levels in non fruit/edible parts of plants (that are not tobacco)

Nicotine levels in non fruit/edible parts of plants (that are not tobacco)


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I am an ex smoker who now vapes (uses e-cigs). Various authorities are equating vaping with smoking by calling it a 'tobacco product' - which is in a sense true given that the majority of nicotine sold is extracted from the leaves of tobacco. I am interested in the practicality (or otherwise) of extracting nicotine from other botanical sources.

Of course, it is not just tobacco that contains nicotine, it is common in other plants of the nightshade family, as suggested by The Nicotine Content of Common Vegetables & Nicotine: Occurrence and biosynthesis. The second source notes:

Nicotine is a natural product of tobacco, occurring in the leaves in a range of 0.5 to 7.5% depending on variety.[84] Nicotine also naturally occurs in smaller amounts in plants from the family Solanaceae (such as potatoes, tomatoes, and eggplant).[85]

Reference 85 points back to the first link, which shows this table.

But looking at the numbers, it seems unlikely. At even .5%, the 'low nicotine' tobacco leaf comes in at 5 mg/g, which is 5,000,000 ng/g - around 50,000 times more concentrated than eggplant. In fact, here is a graph of the log10 value (2 is ten times larger than 1) of each.

On the other hand, the ability of a plant to produce nicotine is retained and handed down to ancestors because nicotine is a pesticide that… discourages insects from eating the plant, and larger herbivores will also get sick if they eat too much of it. Logically, levels of nicotine would be higher in the leaves and stems of a plant than in the fruits/food that we & animals are more interested in eating. That again makes sense, since most fruits are 'designed' to be put through the stomach of a larger animal as part of the process of regeneration.

That logic seems to be borne out by the levels of nicotine in tomatoes, that start around 40 ng/g in green tomatoes, but end up at just over 4 ng/g in ripe tomatoes (not sure what's going on with that 'pureed tomato' level of over 50 ng!). The drop suggests to me that's the plant's way of preventing consumption while the fruits are still developing, but making them safe(r) to eat once ripe.

But what about the nicotine content in the leaves of those plants? Logically they might have a higher nicotine content. Does anyone know of studies of the levels of nicotine in the other parts of plants of the nightshade family?


Tomato leaves have something like 184 ng/g of nicotine, in the same ballpark as tomatoes (the fruit) and not close to tobacco. I think this is not peer-reviewed, but it cites other papers that are: Nicotine Analysis in Several Non-Tobacco Plant Materials And this is a PDF of a slide deck providing a simple presentation of the results from the same article: Nicotine Analysis in Several Non-Tobacco Plant Materials - PDF


I take issue with the previous answerer's assertion that it is extremely unlikely that previous research on nicotine concentrations has ever been performed; in fact, it was very well established decades ago that alkaloids in Nicotiana (and other Solanaceaes) are predominantly synthesized in the roots and, in the case of grafting studies, translocated through the stalk into the scion, which findings rest on measurements of alkaloid levels throughout the plant. The research is very much out there.

Reference
G. R. Waller and E. K. Nowacki,“Alkaloid Biology and Metabolism in Plants,” Plenum Press, New York, NY, 1978. Pages 121-141 for the nicotiana grafting discussion. No doubt there is more recent work out there, though.


… I'm not aware of large nicotine levels in other parts of plants. I assume tobacco will still have the highest nicotine levels, because that's what people have been selecting for for centuries.… - user137

That logic seems compellingly sound.

Based on that, why would a researcher even bother to measure the nicotine content of the other parts of non-tobacco plants?

  1. They are not being eaten by consumers & thereby have little or no risk of poisoning them.
  2. The levels of nicotine would be expected to be so far lower than the 'commercially viable' tobacco leaves as to be of no interest (purely for their nicotine content).

So in answer to my own question.

Does anyone know of studies of the levels of nicotine in the other parts of plants of the nightshade family?

No, because it is unlikely any such research has been performed.


Nicotine uptake by peppermint plants as a possible source of nicotine in plant-derived products

Recently, nicotine has been detected in a large number of food crops and plant-derived products such as spices and herbal teas, but the origin of this nicotine is unknown. This study aimed to elucidate the putative sources of nicotine. We investigate the uptake of nicotine from nicotine-contaminated soils and tobacco smoke using peppermint plants, Mentha × piperita, as a model system in mulching and fumigation experiments. Results show that all the peppermint plants contain minor amounts of nicotine before treatment, but the experiments revealed that the plants also incorporate nicotine considerably from the soil as well as from tobacco smoke. These findings demonstrate for the first time that the reported occurrence of nicotine indeed may originate from tobacco. The incorporated nicotine was subsequently metabolised by the plants. Apart from the nutritional aspects, the results on nicotine uptake may also affect basic plant biology, because they demonstrate that alkaloids can be transferred from one plant, after its death, to another plant species.


Food from Tobacco A Well Kept Secret

It must come as no small surprise that tobacco, whose current worldwide use as a smoking material kills some three million people every year, "may in time become one of the world's principal sources of protein for human consumption and livestock feed." So stated no less an authority than the World Health Organization's Farm and Agriculture Organization in 1981. Nevertheless, tobacco as a protein source has received so little publicity over the years that most of us are still largely unaware of it's potential to feed a hungry world.

Protein From Tobacco

Among the protein extracts that were prepared from a variety of green plants and forage crops, those originating from the leaves of the tobacco plant, Nicotiana tabacum, according to Wildman, a leading protein chemist, had "properties which make them uniquely desirable as sources of edible leaf protein".

Tobacco was the only plant from which the Fraction-1-protein (F-1-p a single, large, homogenous protein that makes up half of the plant's soluble protein) could be obtained in pure, crystalline form. It has no taste or odor, is colorless and non-allergenic and exhibits an optimal amino acid composition which lowers cholesterol. Its functional characteristics (e.g. solubility, stability, foaming, gelling and emulsifying ability) are superior to those of egg white, casein and soy protein. In feeding experiments, tobacco F-1-p significantly exceeded casein, soy, corn and other cereal proteins in protein efficiency, i.e., the weight increment of growing rats per gram of protein ingested. All in all, tobacco F-1-p may be the best nutritional and functional food protein. It has also been recommended for a variety of medical uses (e.g., for kidney dialysis patients and as artificial milk for infants).

F-2-proteins (a mixture of low molecular weight soluble proteins) from tobacco also have favorable characteristics and could be added to soups and beverages to boost nutritional quality. The insoluble proteins, could be used to enrich solid foods for human consumption or used as feed for poultry and non-ruminants.

Can It be Done?

Leaf Protein International (LPI) was founded in 1979 as a joint venture between the North Carolina Farm Bureau Federation and General Foods (prior to its incorporation into Philip Morris Industries). In spite of severe budgetary limitations, LPI built and operated a pilot plant in North Carolina's tobacco region. During 1981 and 1982, LPI demonstrated that the extraction process for obtaining crystalline F-1-p and other raw materials from tobacco was commercially feasible. The yield of F-1-p was estimated at 530 lbs/acre (600 kg/hectare).

LPI's goal was to transform tobacco into a commodity used on a large scale for human food as well as for smoking. Cigarettes made from the fibrous residue remaining after protein extraction (more than 5 tons per acre) would produce much lower amounts of toxins and carcinogens during burning than conventional cigarettes. The residue could also serve as ruminant feed.

Grown for food, tobacco plants could be more densely spaced and generate about four times as much protein per acre as soybeans or corn and about five times as much smoking material as conventional tobacco crops. At the same time, labor input could be halved. The total yield value could exceed $6,000 per acre as compared to $2,500 per acre for conventional tobacco. In comparison, corn brings $100-150 per acre.

In 1983, the U.S. Office on Technology Assessment convened a workshop on protein extraction. The general tenor regarding protein extraction from tobacco is reflected in the preface of the proceedings:
The risk involved in investment in this technology is perceived to be high, and a considerable concern exists that products would have limited marketability because of:

* the health concerns that some (italics added) attach to tobacco, and
* the changed character of cigarettes and chewing tobacco made from protein-extracted tobacco may not satisfy consumers.
In due course funding for the protein project dried up, the pilot plant ceased operating and LPI was disbanded.

Paradoxically, the project suffered defeat at the very juncture when one would have expected the green light for a large-scale trial. The negative arguments cited in the OTA Proceedings must have existed before the pilot study began. However, they were only brought to bear when the project was proving successful. The language used unmistakably betrays its provenance. Obviously, the powerful tobacco lobby is jealously guarding the status quo, for conventional cigarettes are still the most lucrative commodity sold on world markets.

Realistic constraints, however, do exist. The need for prompt processing of harvested leaves to forestall loss in F-1-p will require duplication of equipment which raises initial investment cost. Tobacco, unable to utilize atmospheric nitrogen, is hard on soils, demanding more fertilizer than legumes. However, since tobacco has recently become a favorite object of biogenetic manipulation, it is conceivable that a nitrogen-fixing variety can be created.

Consumers in developed nations may be surprised when offered protein supplements from tobacco, which most (not some) view as a killer weed. The protein extracts are, of course, freed of poisons. Nicotine is present in a concentration of 20 ppb, many times lower than that normally found in tomatoes, potatoes or green peppers. Nevertheless, a painstaking scrutiny of both food and pharmaceutical products from tobacco would precede the Food and Drug Administration's approval for marketing. (The prospect of FDA involvement with tobacco is anathema to an industry that has successfully kept it out of the agency's grip). While the market for protein supplements might be disappointing in affluent countries which thrive on meat, the benefit to the protein-starved third world may be considerable.

Tobacco for a Hungry World

For over 25 years tax-supported tobacco was dispatched to hungry nations under the auspices of America's Food for Peace program. When mounting criticism prompted the suspension of this practice in 1980, the ground was already prepared for the transnational tobacco corporations' onslaught of third world markets. Nicotine addiction spread, inflated profits lured farmers away from tending food crops, and ravaged forests provided new land for planting and fuel for curing tobacco. The maxim "Whenever tobacco is grown, food is not" has become the grim characterization of the third world's current predicament.

Today we know that there is another side to the coin. With projections based on North Carolina's pilot study, the third world's almost 4.5 million hectares under tobacco cultivation could deliver over 2.5 million tons of high quality F-1-p, about half as much F-2-p and 20 million tons of insoluble protein, leaving another 60 million tons of deproteinized residue for use in cigarettes and/or ruminant feed. Indeed, this may just be the beginning, because tobacco could later replace some food crops with lesser yields of high quality protein.

Tobacco is Not the Enemy

It may be unrealistic to expect tobacco's complete elimination, the avowed goal of a smoke-free society. However, the prospect of turning a deadly harvest into one which supports life would preserve, if not enrich, the livelihood of tobacco farmers and win them over as allies in the just cause of the pro-health forces.

It's ironic that the same plant which has killed millions of people should also possess the potential to feed a protein-starved world. Tobacco is not inherently evil, nor for that matter is anything else in our environment. In the final analysis, it depends on what we, individually and collectively, make of it.

K.H. Ginzel, M.D., is Professor Emeritus of Pharmacology and Toxicology at the University of Arkansas. Most of his work is in the area of nicotine and its effects. He wishes to acknowledge the invaluable input of Dr. Shuh J. Sheen, a leading authority in the field of protein extraction from tobacco.

Protein from Plants

Plants are the primary and most prolific manufacturers of proteins on earth. But, in order for us to enjoy animal food, plant proteins must first be converted into animal proteins at a substantial loss in food efficiency (20 pounds of grain produce one pound of beef). Most of the less developed countries cannot afford this luxury. They must depend solely on plant proteins which their dietary staples often fail to provide in adequate amount, composition or quality. Hence, protein deficiencies abound in the third world.

More than 40 years ago, Pirie first pioneered protein extraction. He insisted that the technique could offer a more efficient way than does the ruminant to convert leaf protein into food suitable for human consumption with equivalent nutritional value to meat. During the following decades great progress was achieved by different research teams toward extracting, purifying and characterizing leaf proteins as well as developing technologies which promised practical commercial utility.


Pharmacology

Nicotine in its base form is an odour and colourless liquid. It is metabolized hepatically with a half-life of app 2 hours and the protein binding is <5%. Bioavailability is route dependent with the highest app 90% when inhaled (e.g. cigarettes) and approximately 60% when used orally (e.g. smokeless tobacco) (Jacob, Benowitz & Shulgin, Reference Jacob, Benowitz and Shulgin 1988 Lunell & Lunell, Reference Lunell and Lunell 2005).

The fundamental pharmacological effect of nicotine is its action on the nicotinic acetylcholinergic receptors (nAChRs). Although nicotine directly activates only the nicotinic and not the muscarinic receptors, the end result is often a complex pattern of indirect effects on other transmitter systems such as the dopamine glutamate and adrenergic systems. Activation of central nAChRs may result in beneficial effects of nicotine such as cognitive enhancement and increased control over arousal and negative emotions (Sherwood, Reference Sherwood 1993). An exception to the primary role of brain nAChR beneficial effects may be the metabolic and lipolytic processes involved in weight control, which seem to be more peripherally mediated (Perkins, Reference Perkins 1993). Like acetylcholine, nicotine stimulates the nAChRs, but when the nicotine molecule is bound to the receptor, it seems to keep the receptors depolarized for longer than what happens with acetylcholine. Nicotine therefore has a dual effect: stimulation of the receptor – agonist function, followed by a receptor blockade – antagonist function. These effects interfere with normal functioning in nicotine intolerant individuals, therefore the CNS needs to adapt to the disrupting effects of nicotine. Blocking appears to be a more significant effect than stimulation since the brain adjusts and overcomes blocking, rather than stimulation, by upregulating the number of nicotine receptors (Benwell Balfour & Birrell, Reference Benwell, Balfour and Birrell 1995). Neuroadaptation can be seen as the organism's mean of defence against the toxic effects of nicotine.

The upregulation is dependent on the mode of administration. Chronic infusion of nicotine has been associated with greater upregulation than injections (Ulrich, Hargreaves, & Flores, Reference Ulrich, Hargreaves and Flores 1997), and it is thought that those who smoke more often and with shorter intervals are administering nicotine in a way that is more conducive to receptor upregulation, compared with those smoking just a few cigarettes per day with long intervals between. If nicotine administration is finally stopped, the system has too many nAChRs to function properly, which often results in withdrawal symptoms. The objective for the cholinergic nervous system when nicotine administration stops is to readapt to the nicotine-free state. This readaptation differ for individuals but some data for the important nAChR subtype beta 2 subunit suggest that it normalizes to nonsmoker levels by 6–12 weeks of abstinence from tobacco smoking (Cosgrove et al., Reference Cosgrove, Batis, Bois, Maciejewski, Esterlis and Kloczynski 2009).


Nicotine levels in non fruit/edible parts of plants (that are not tobacco) - Biology


1 Tar in cigarette smoke contains carcinogens and is mostly deposited in the bronchi.


What is the effect of these carcinogens?

2 Which component of tobacco smoke binds with haemoglobin to form carboxyhaemoglobin?

A carbon monoxide
B carcinogens
C nicotine
D tar


3 What is not a symptom of emphysema?

A alveoli burst
B alveoli lose elastic fibres
C bronchi are blocked by tumours
D the total surface area of the alveoli is reduced

4 Two lifelong cigarette smokers, X and Y, both have persistent coughs. X also has difficulty breathing out and Y is getting much thinner. From these symptoms it is possible that:

A X has bronchitis and Y has emphysema.
B X has emphysema and Y has chronic obstructive pulmonary disease.
C X has chronic obstructive pulmonary disease and Y has lung cancer.
D X has lung cancer and Y has bronchitis.

5 Both carbon monoxide and nicotine are absorbed into the blood from tobacco smoke.

What describes their effects on the body?


6 What is the sequence of events leading to atherosclerosis?

1 blood clot forms at site of plaque
2 phagocytes attracted to site of damage
3 low density lipoproteins transport cholesterol to artery
4 damage to the lining of an artery
5 atheroma builds up and breaks through the endothelium

7 Which of the following explains the increased risk of stroke, caused by smoking tobacco?

A CO increases the blood pressure and increases the chance of a blood vessel in the brain bursting.
B Carcinogens increase the blood pressure and increase the chance of a blood vessel in the brain bursting.
C Nicotine increases the chance of a blood clot blocking a blood vessel in the brain.
D Tars increase the chance of a blood clot blocking a blood vessel in the brain.

8 Which observation is experimental evidence that smoking tobacco causes lung cancer?

A Most people who develop cancer are smokers.
B Death rates from lung cancer are highest in people who smoke more than 25 cigarettes per day.
C Lung cancer was a rare disease until smoking became common in the 20th century.
D When substances extracted from tar in cigarette smoke were painted onto the skin of mice, the mice developed tumours.

9 Which dietary factors increase the risk of coronary heart disease?

A high intake of fruit and vegetables
B high intake of saturated fat and cholesterol
C low intake of sodium chloride and alcohol
D moderate intake of unsaturated fat

10 What would not form part of an effective screening programme for CHD?

A screening for high blood pressure
B screening for high cholesterol
C monitoring heart rhythms
D screening blood samples for bacterial infection a


Answers to Multiple choice test

2. End-of-chapter questions

1 C
2 A
3 B
4 D

5 a tar stimulates, goblet cells/mucous glands, to secrete more mucus
paralyses/destroys, cilia
mucus not moved up the, bronchioles/bronchi, trachea/airways
mucus accumulates in the airways
bacteria multiply within the airways
(leads to) chronic bronchitis
tar contains, carcinogens/named carcinogen e.g. benzpyrene
(tar) settles on bronchial, epithelial cells/epithelium
mutation(s)/change to DNA
growth of tumour
bronchial carcinoma/lung cancer

b nicotine: increases heart rate
increases blood pressure
increases chance of blood clotting/promotes thrombosis
decreases fl ow of blood to, extremities/fi ngers/ toes
carbon monoxide: combines (irreversibly) with haemoglobin
forms carboxyhaemoglobin
reduces oxygen-carrying capacity of, haemoglobin/ blood
damages lining of arteries
promotes atherosclerosis

6 a fewer alveoli
larger air spaces
fewer capillaries
scar tissue in bronchioles/bronchi
few/no cilia
few/no goblet cells
enlarged mucous glands
enlarged smooth muscle
may be pre-cancerous/cancerous cells
tumour/bronchial carcinoma [max. 4]

b i difficulty breathing/breathlessness
wheezing
tiredness
not able to do (much) exercise [max. 4]

ii small(er) surface area for gas exchange
less oxygen absorbed
poor oxygenation of the blood
bronchi/bronchioles/airways blocked by mucus
increased resistance to fl ow of air [max. 3]
[Total: 11]

7 a (tar) settles on bronchial epithelial cells/epithelium
carcinogens/named carcinogen (in tar) e.g. benzpyrene
causes mutation(s)/change to DNA (in epithelial cells)
in (proto onco)genes that control cell division/ mitosis
cancer cells do not respond to signals/growth factors/other cells
cancer cells divide uncontrollably
no programmed cell death/apoptosis
cells do not diff erentiate/become specialised
cells form tumour/bronchial carcinoma
tumour supplied with blood vessels/lymph vessels [max. 6]

b i data are standardised
populations diff er from year to year
allows valid comparisons [max. 2]

ii death rate for men always higher than for women
use of the data to make a comparison between death rates for men and women
death rate for men rises to a maximum in 1966 and then decreases
death rate for women increases later than for men
death rate for women increases to a maximum in late 1980s/1990 and then decreases
decrease in death rate for women not as steep as for men
use of the data to show increase or decrease in death rate for men or women [max. 4]

iii men started smoking earlier than women
more men smoked than women
smoking became less popular among men from 1950s/1960s onwards
increase in number of women who smoked from the same time
link made between smoking and cancer
anti-smoking campaigns
lung cancer takes a long time to develop/be diagnosed
decrease in death rate did not happen until many years after decrease in popularity of smoking [max. 4]

8 a CHD: narrowing of coronary arteries that supply oxygenated blood to heart muscle
stroke: interruption of blood supply to part of the brain as a result of blockage or bursting of an artery (or arteries), leading to death of brain cells [2]

b vein taken from the chest, arm or leg
attached to coronary artery either side of blockage
may be one or more by-passes if there are several blockages in the coronary arteries [max. 2]

c health promotion campaigns/publicity/leafl ets/ advertising
provide information about maintaining fitness/ healthy eating/stopping smoking/reducing alcohol intake
increase tax on tobacco/alcohol to reduce consumption
provide health warnings on foods that are high in saturated fat
print health warnings on tobacco products
ban smoking in public places
provide drugs for, hypertension/high blood cholesterol
provide screening for, risk factors/high blood pressure/high blood cholesterol
in people at greatest risk
provide, leisure facilities/fi tness centres [max. 6]


Nicotine levels in non fruit/edible parts of plants (that are not tobacco) - Biology

livecontent

I want to ask a serious question of people who have been around tobacco farms and culture. Has anyone eaten green tabacco leaves? Can one eat the green leaves or the flowers? Are there types of tobacco plants that are more suited for eating than smoking.

My question is not to mean eating tobacco for the nicotine but eating tobacco as a salad green or a cooked green. I am not talking about cured tobacco products or eating any sort of cured dried tobacco.

I have only seen a green tobacco leave a few times. I am from New York and have not spend much time in the south and I would assume some people would have eaten green tobacco.

If you gather tobacco to eat, does it make sense to pick the new leaves which may be tender. Do you gather green leaves at certain times of the year.

What are the preparations for green tobacco. I have a feeling in talking about southern cuisine, they must deep fried or slathered with pork fat or bacon, as other greens are eaten.

If Tobacco leaves are not eaten, why? Are they not nutritious. I would have to believe people tried to eat it. Certainly if it could feed the slaves, it would have been tried.

I can see another source for the crop and another market for tobacco companies.

Can you make tea out of the green leaves and/or flowers--I assume they have flowers.

I can imagine different recipes of stuffed tobacco, tobacco pesto, tobacco with corned beef, tobacco with grits, tobacco salad waldorf, mixed tobacco salad greens, tobacco wrapped baked catfish etc.

We could market organic, free ranged, pesticide fee tobacco, non gmo-- gathered by young virgins as a overpriced product to the yuppies and the gourmands.

Can you flavor wine or beer with tobacco. Can it be certified and grown in a delimited area for the discriminating consumer as a QBA or VDQS, or first growth, second growth, with selected vintage years? That is another point: why is not tobacco moved out of a commodity product and be distinguished as value added as grown in a specific area when it is included in a product.


Alkaloid Content in Different Nicotiana Species

The alkaloid composition within Nicotiana is species specific and extremely variable (62, 78). The major alkaloids in Nicotiana are nicotine, nornicotine, anatabine, and anabasine, but a single alkaloid usually predominates in each species (62, 80). Nicotiana tabacum typically produces nicotine as the most abundant alkaloid (87).

However, despite being a natural allotetraploid derived from interspecific hybridization between ancestral N. sylvestris and N. tomentosiformis, N. tabacum remarkably presents an alkaloid profile different from both of its progenitor species (19). Dewey and Xie (14) proposed a model of molecular evolution of N. tabacum alkaloid content to try to explain these differences. Nicotiana tomentosiformis primarily accumulates nornicotine, whereas nicotine and nornicotine are the predominant alkaloids in N. sylvestris green and senescing leaves, respectively (78).

Nicotine and nornicotine are the major alkaloids in Nicotiana spp., and the insecticidal activity of these alkaloids varies widely depending on the insect species (17). Additionally, in some Nicotiana wild species, nornicotine has an important role as a precursor of N-acyl-nornicotine (NacNN), an alkaloid that exhibits 1,000-fold higher activity against nicotine-resistant Manduca sexta (tobacco hornworm) than nicotine (29, 40).

NacNN was found in the trichome exudate produced at the epidermis of Nicotiana repanda, Nicotiana stocktonii, and Nicotiana nesophila aerial parts (29, 40, 97). It was suggested as a route by which nicotine is N-demethylated to nornicotine in leaves, followed by its mobilization to the trichomes upon herbivory in these species (97 Figure 2). Then, nornicotine is acylated with straight-chain fatty acids, forming hydrophobic NacNN, which is secreted from the gland to the coat of leaf surface (63, 97 Figure 2).


Akhtar, M.: 1993, ‘Utilization of plant origin (tobacco) waste material for the control of plant-parasitic nematods’, Bioresource Technology 46(3), 255–257.

APHA-AWWA-WPCF: 1992, Standard Methods for the Examination of Water and Wastewater, 18th ed., Washington D.C., U.S.A.

Bick, I. R. C.: 1985, Alkoloids, in the Chemistry of Natural Products, R.H. Thomson (ed.), New York, U.S.A., pp. 298–386.

Borgerding, M. F. and Leyden, C.: 1999, Determination of Nicotine in Tobacco, Tobacco Processing Environments and Tobacco Products, Nicotine and related compounds.

Chiu-Yang Chen and Jun-Nen Chen: 1999, ‘Toxicity assessment of industrial wastewater by microbial testing method’, Wat. Sci. Tech. 39, 10–11, 139–143.

Civilini, M., Domenis, C., Sebastianutto, N. and Bertoldi, M.: 1997, ‘Nicotine Decontamination of Tobacco Agro-Industrial Waste and its Degradation by Microorganisms’, Waste Management and Research 15, 349–358.

Clarke, A. B. and Stanley, J.: 1964, ‘Process for Selective Extraction of Alkoloid’, United States Patent, No. 3.319.435.

De Lucas, A., Canizares, P., Garcia, M. A., Gomez, J. and Rodrigez, J. F.: 1998, ‘Recovery of nicotine from aqueous extracts of tobacco wastes’, Industrial and Engineering Chemistry Research 37(12), 4783–4791.

DFG, Deutsche Forschungsgemeinschaft, VCH, Verlagsgessellschaft mbH, D-6940 Weinheim: 1992, Manual of Pesticide Residue Analysis, Vols. 1 and 2, Method S-19, Hans-Peter Thier and Hans Zeumer (eds), Working Group Analysis, ISBN 3-527-27010-8, Federal Republic of Germany, pp. 317–322.

Dokuz Eylül University Report: 1994, ‘Increase the Treatment Efficiency in a Tobacco Industry Wastewater Treatment Plant in İzmir’, Turkey’.

Dugan, P. R. and Lundgren, D. C.: 1968, ‘Isolation of activated sludge microorganisms’, Appl. Microbiol. 8, 357–361.

Gorrod, J. W. and Jacob, P.: 1999, ‘Analytical Determination of Nicotine and Related Compounds and their Metabolites’, Part: Environments and Tobacco Products, ISBN: 0-444-50095-2, Elsevier, 732 p.

Gravely, L. E., Geiss, V. L. and Newton, R. P.: 1977, ‘Process for Maximizing the Growth and Nicotine Degrading Activity of Microorganisms’, United States Patent No. 4.011.141.

Ireland, M. S., Larson, T. M. and Moring, T. M.: 1980, ‘Nicotine Transfer Process’, United States Patent No. 4.215.706.

Kaesler, R. L., Herricks, E. E. and Crossman, J. S.: 1978, Use of Indices of Diversity and Hierarchical Diversity in Stream Surveys, Biological Data in Water Pollution Assessment, Quantitative and Statistical Analysis, ASTM STP 652, K. L. Dickson, Jhon Cairns and J. Livingston (eds), American Society for Testing and Materials, pp. 92–112.

Lenkey, A. A.: 1989, ‘Nicotine Removal Process and Product Thereby Mixing with Alkaline Agent in Aerobic Environment’, United States Patent No. 4.848.373.

Meher, K. K., Panchwagh, A. M., Rangrass, S. and Gollakota, K. G.: 1995, ‘Biomethanation of Tobacco Waste’, Environmental Pollution 90(2), 199–202.

Metcalf and Eddy: 1991, Wastewater Engineering, Treatment, Disposal and Reuse,3rd ed., McGraw-Hill International Editions.

Moghissi, A. A.: 1994, ‘Tobacco Industry’, Editorial, Environment International, V.20, No. 4., pp. 427–428.

Munari, M.: 1986, ‘Quantitative Determination of Nicotine Content in Protein Extracted from Tobacco’, Tobacco Journal International 2, 128–132.

Palmer, W. E. and Browley, P. T.: 1992, Pesticides-Tobacco-Toxicity, Department of Biology and Entomology, NCSU, Web 3–95.

Pelezar, M. T. and Chan, E. C. S.: 1972, Laboratory Experiences in Microbiology, 3rd ed., McGraw-Hill Book Company.

Pielou, E. C.: 1975, Ecological Diversity, Wiley-Interscience, New York, pp. 1–165.

Radhakrishna, P.: 1986, ‘Studies on the Production of Biogas from Non-edible Oil Cakes’, Ph.D. Thesis, Dept. Biochemistry, Osmania University, Hyderabad, India.

Rincan, J., De Lucas, A., Garcia, M. A., Garcia, A., Alvarez, A. and Carnicer, A.: 1998, ‘Preliminary study on the supercritical carbon dioxide extraction of nicotine from tobacco wastes’, Separation Sciences and Technology 33(3), 411–123.

Ryan, T. A., Joiner, B. L. and Ryan, B. F.: 1982, Minitab Manual, The Pennsylvania State University, U.S.A.

Saunders, J. A. and Blume, D. E.: 1981, ‘Quantitation of Major Tobacco Alkaloids by High Performance Liquid Chromatography’, Journal of Chromatography 205, 147–154.

Sax, N. I. and Lewis, R. J.: 1989, Dangerous Properties of Industrial Materials, New York U.S.A., pp. 2486–2487.

Simpkin, T. J.: 1988, ‘The diversity of activated sludge microbial communities as described by the fundamental niche concept’, Wat. Sci. Tech. 20, 39–44.

Shannon, C. E. and Weaver W.: 1949, The Mathematical Theory of Communication, University of Illinois Press, Urbana, pp. 1–25.

Slabbert, J. L. and Venter, E. A.: 1999, ‘Biological assay for aquatic toxicity testing’, Wat. Sci. Tech. 39(10–11), 367–373.

Tchobanoglous, G. and Eliassen, R.: 1969, ‘The Indirect Cycle of Water Reuse’, Water Wastes Eng. 6(2).

Tchobanoglous, G. and Schroeder, E. D.: 1985, Water Quality: Characteristics, Modeling, Modification, Addison-Wesley, Reading, MA.


Biology - Endocrine System

The endocrine system is study of the glands of an organism that secrete hormones directly into the circulatory system.

The organs through which the life running hormones are secreted are known as endocrine glands or simply ductless glands.

The hormone secreting glands are located in different parts of a human body (see the image given below).

The scientific study of the endocrine system and its disorders is known as endocrinology.


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