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EDITORIAL

Over the past five decades, a dominant role of tobacco smoke in lung cancer has been demonstrated. In fact, tobacco is one of the main contributors to total mortality, in many developed countries and has become a major contributor in developing countries as well. In India at present, lung cancer ranks among the top three killers in men in almost every metropolis. The situation is more alarming in other developing countries where the problem is further compounded by the lack of data on usage and dependence of economies of these countries on tobacco.

To formulate and carry out effective tobacco control activities, it is important to assess the relative incidence of tobacco-related cancers in different social strata and the prevalence of tobacco use across strata. Despite many years of data gathering, the information base is far from complete, especially in developing countries, where tobacco use is increasing rapidly and where aggressive marketing by the transcational tobacco industry is occurring. But as important as it is to continue to improve the information base on tobacco use and its health consequences, it is even more urgent to interpret and channel these findings into prevention strategies. Health advocates can learn to export successful smoking and cessation programmes too from the tobacco industries.


ODDS AND ENDS
Smoking Associated With Thyroid Disease

An association has been found between smoking and increased risk of developing clinically overt thyroid disease. Data from a study based on the Danish Twin Register suggest that the cumulative cigarettes consumption is also a risk factor. This effect is more pronounced in autoimmune thyroid diseases such as Graves' disease and autoimmune thyroiditis.

Danish researchers used a population-based national twin register to enroll 132 same-sex twin pairs. Established in 1991, the register includes 20,888 twin pairs born between 1953 and 1981. The 264 individuals enrolled in the thyroid study were discordant for overt thyroid disease. Questionnaires were used to gather information on thyroid disease in the pairs and on participants' smoking habits. Physicians verified the thyroid information.

Researchers report that they associated smoking with an increased risk of clinical overt thyroid disease irrespective of zygosity and phenotype. The association remained statistically significant whether the twins were monozygotic or dizygotic, although the effect of smoking was more pronounced in monozygotic pairs. Overall, cumulative smoking as measured in pack-years was significantly higher for twins with overt thyroid disease than for their healthy co-twins. When researchers restricted the sample to women twins, the results did not change.

When the twin pairs were subdivided into groups discordant for autoimmune (49 pairs) and non-autoimmune (83 pairs) thyroid disease, results were essentially similar. But when both twins smoked (51 pairs), the twins with clinically overt autoimmune thyroid disease were found to smoke significantly more than their healthy co-twins. Probands with non-autoimmune thyroid disease, on the other hand, did not.

(Archives of Internal Medicine, March 2000)

Killing cancer cells with tapioca

The cassava plant, which is the basis of the well known tapioca pudding, has now provided British and Spanish genetic scientists with a new method of killing cancer cells. The dual country team based at Newcastle University, North East England, believes the cassava plant may well hold the key to a powerful anticancer drug. Genes isolated from the plant have already been used to eradicate brain tumours in laboratory rats.

Taking the project a stage further, it is reported that tests on human tissues are also going well. Cassava is a staple crop for people in rural Africa, Asia and South America. However, the plant can be dangerous to eat as it exhibits cyanogenesis - the manufacture of cyanide to deter grazing animals from eating it. This means that if the cook is not careful, the meal could contain a dangerous dose of cyanide.

The plant achieves this deterrent effect by producing a chemical called linamarin that releases hydrogen cyanide when it is broken down by linamarase, an enzyme produced by the plant. It is the plant's roots that contain the poisonous cyanoglucoside. The latex contains the enzyme that breaks down the poison, but the enzyme and the poison do not come into contact within the living plant. This contact only happens when the plant is processed in some way, thus allowing the enzyme to reach the cyanoglucoside and convert it to poisonous hydrogen cyanide gas.
The gas escapes, leaving the root safe to eat. Professor Monica Hughes, a plant geneticist at New Castle University, has been studying the plant for many years. Her team has now cloned the genes for two enzymes which break down the poisons. 

Professor Hughes said that the team also hoped to develop genetically modified strains of cassava in which the cyanide production is switched off in some root tissues, to reduce ill health in the developing world. A longer term strategy is to alter genes in the cassave plant itself so that the roots produce more of the neutralising enzyme. (Chemical Weekly, January 11, 2000, p. 134).

Ginger may help fight cancer
Scientists have found that two kinds of ginger roots contain substances which can inhibit spontaneous mutations. Usually, such mutations lead to the development of cancer. However, the Japan International Research Centre for Agricultural Sciences has identified eight anticancer substances in the two ginger roots native to Thailand called galanga and kra-chai.

Using the Ames test, the researchers have been able to gauge the cancer fighting abilities of the ginger's substances. In the Ames test-generally used to determine the carcinogenicity of chemicals bacteria are exposed to a test sample to measure the extent to which mutations arise. (Australasian Biotechnology, January 2000, p. 18).

Smoking Induced Leukemia is Benzene to Blame?
Benzene, known to cause leukemia is present in cigarette smoke. However, although smokers are one and a half to two times more likely to develop leukemia than nonsmokers, the degree to which the risk of leukemia can be attributed to the low doses of benzene in cigarette smoke is uncertain. Also uncertain is the validity of linear models of dose response with respect to benzene and leukemia, particularly at doses lower than those encountered in the workplace (and studied) in the past.

The researchers determined the proportion of smoking induced leukemia deaths caused by benzene by following a five step process in which they calculated the lifetime leukemia risk from smoking, determined the potency of benzene in causing leukemia, estimated the benzene dose from smoking, characterized the low dose risk of leukemia from benzene, and compared the predicted lifetime risk of leukemia from benzene in cigarettes with the observed risk due to smoking. They applied their calculations to light (20 cigarettes daily) and heavy (40 or more cigarettes daily) smokers, with comparisons to those who never smoked.

When applying linear models to these steps, the researchers calculated that benzene is responsible for 8-58% of all smoking induced leukemia deaths and 12-58% of smoking induced AML deaths. These results the researchers say, are reasonable, compared to published data on the numbers of such deaths.

The study not only provides information on the quantitative contribution of benzene to cancer deaths from cigarette smoking, it also helps demonstrate the validity of linear models in extrapolating to low doses of benzene. Benzene is an important industrial chemical used in making nylon, film developer, and solvents. Industrial workers are exposed to benzene concentrations that are 10-100 times greater than those encountered by smokers.

The researchers caution, however, that benzene is not the only leukemia causing chemical in cigarette smoke. They note that 1,3-butadiene, styrene, N-nitrosodi-n-butylamine, urethane, and radioactive elements are also suspected of being leukemogenic. Benzene, however, appears to cause a substantial proportion of the leukemia deaths induced by smoking - (Environ. Hlth. Persp. April, 2000).

An Evaluation of the Roadside Plants as Bioindicators of Atmospheric Lead Pollution

Lead is heavy metal and highly toxic when present in excessive amounts in the environment. Several reports are available for effect of lead on human health and commercially important agriculture crops. The monitoring of atmospheric lead pollution is, therefore, very essential to protect human health hazards. Lead containing petrol is the major source of the environmental lead accumulation, roadside ecosystems are natural targets of such lead pollution. Assessment monitoring systems, therefore, would prove very useful to control the atmospheric lead contamination.

Plants are known to absorb lead and accumulation of metals has been reported in roots, stem, leaves, root nodules and seeds. Naik & Deshpande of SRTM University, Nanded have undertaken studies to assess the atmospheric lead pollution using plants as bioindicators. Various leaf samples were collected from plants near the densely populated, high density automobile traffic roads of Nanded city.

Of the various plants species screened leaves of Polyalthia longifolia (Ashoka), Steculia foetida (Badam), Zizypus rotundifolia (Ber), Mangifera indica (Mango) and eucaena latisiliqua (Subhabul), Polyalthia longifolia showed accumulation of lead. P. longifolia leaves showed maximum accumulation of atmospheric lead of the plants tested. P. longifolia is a sensitive plant and responds to atmospheric lead levels.

The potential hazardous effect of CS poses an alarming public health problem. The best way of prevention is to stop smoking. However, cigarette smoking is extremely addictive and approaches to cessation of smoking have had limited success. So it is highly desirable to find the means to prevent the deleterious effects of CS. The observations made by Panda et al of Dr. B.C. Guha, Centre for Genetic Engineering and Biotechnology and Chatterjee of Calcutta University using guinea pig as the experimental animal indicate that the major oxidative damage caused by CS, such as oxidative degradation of proteins and lipid peroxidation, is almost completely prevented by large doses of vitamin C (15 mg ascorbate/animal/day). The amount of vitamin C considered to be adequate to maintain good health of the guinea pigs (5 mg ascorbate/animal/day) under normal physiological condition is not sufficient to prevent the deleterious effects of CS. If the results obtained with guinea pigs are extrapolated to humans, it would appear that comparatively large doses of vitamin C may protect smokers from CS induced oxidative damage and the associated diseases (Ind. J. Environ. Hlth, April, 2000).

Tobacco Induced Cancer: Challenges Ahead

Y. Shukla

Tobacco is smoked as cigarette, cigar, biri, hookah and chewed in beetel or lime flavored pan masala etc. Among addicted people, it has been implicated as the cause of cancer oral cavity and upper digestive tract. Smoking of manufactured cigarettes has been linked to respiratory tract cancer. Several epidemiological and experimental evidences indicate greater incidences of lung, larynx, mouth, esophagus and bladder cancers among tobacco users. The production distribution, marketing and use of tobacco continues to grow in every corner of world. About 3 million deaths (0.6 million in India) occur annually in world due to tobacco. Numerous prospective studies conducted over the past 40 years have documented multifarious disease risks associated with its smoking and oral consumption. Tobacco is a complex chemical mixture that contains diverse types of carcinogens, cocarcinogens accelerators and promotors. These include nicotine, polycyclic aromatic hydrocarbons, beta-naphthylamine, nitrosamines, catechols and trace metals like polonium, nickel arsenic etc. In addition to these tobaccos contains significant quantities of nicotine which are responsible for addition and nervous system abnormalities.

There is a clear relationship between lung cancer risk and daily cigarette consumption, people who smoke more than a pack of cigarettes a day have 20 times higher risk than of non smokers. The four major histolytic types of lung cancer squamous cell, adenocarcinoma, small cell and large cell are associated with smoking. Squamous cell cancer is most common form among men and in women adenocarcinoma pre dominates. From 1960s to 1990, death rates from lung cancer increased six fold among women and nearly double among males of smoke. By 1990, lung cancer had displaced coronary heart disease as the leading single most cause of excess of mortality in developed and developing nations. Worldwide 85% of 6,76,000 annually newly diagnosed cases of lung tumors are attributed to cigarette smoke. In India more than 20% of all cancer cases reported are of respiratory tract associated to smoking. The majority of deaths due to respiratory tract cancers occur in individuals between ages of 40 and 70;s. The case of Laryngeal cancers are also seen among tobacco addicts. In a population case control study smoking accounted for 95% of all laryngeal cancer. In South East Asia region, tobacco chewing in combination with reca nut and or lime, beetle, pan masala is a very prevalent. This has been shown to be strongly associated with cancers of mouth, esophagus and buccal cavity which is predominant type of cancer among males in India. In one study of Indian rural population 21.8% of 4,829 males tobacco habitue's and 12.3% of 3,151 female habitues had oral and pre cancerous lesions. Tobacco chewing causes tumors of lip, tongue, salivary gland mouth and pharynx accounting for 90% of tumours of oral caviery in men and 60% among women. Spitting tobacco is significant cause of leukoplakia, an abnormal thickening and keratinization of oral mucosa recognized as precursor of malignancy. The problem is aggravated in persons who smoke in addition to tobacco's oral consumption. Continued smoking after radiation therapy for cancer of larynx has been associated with significantly greater risk of recurrence.

Two thirds of the smoke from burning cigarette never reach the smokers lung but go directly in the air forming environmental tobacco smoke (ETS) which expose the non smokers as well. Involuntary or passive smokers due to ETS also suffer from adverse effects of tobacco smoke. The adverse effects of tobacco have been found to be enhanced among tobacco user/smokers and alcoholics. This synergistic and multiplicative effect may possibly be the result of alcohol acting as a solvent of carcinogens in tobacco or result of alteration of liver metabolism. Such individuals are at higher risk of head and neck cancers. Miners who smoke are more susceptible and hence at a greater risk indicating possibly potentiating interaction between ore dust, radiation and cigarette smoking.

Tobacco pandemic is extending throughout the world. There is a need of generating awareness and educating people towards serious hazardous health effects of tobacco. Number of international agencies like IARC, WHO, FDA and AMA are taking measures to curtail use and promotion of tobacco. A number of NGO's are also playing an important role in this direction.

In the new millenium preventive and curative strategies should be applied over the continuum of general population. The anti tobacco campaign is one of the most practical and rational measures for cancer prevention. A holistic approach is essential with improvement in life style and avoidance of cigarette smoking and other sources of carcinogens as integral elements. Prevention is always better than cure. Hence, all efforts be made to educate people about the adverse effects of tobacco in any form. Free sale "guthka" pan masala should not be allowed as children have free access. Regulatory measures be taken so that children do not have free access to tobacco and tobacco containing material. A comprehensive programme should be launched aimed at reducing tobacco use among young people. In this context, public awareness campaigns, social service, advertising and public icons warning against effects of tobacco become more imperative. One option would be to negate cigarette advertising with counter propaganda, pointing out the adverse effects of smoking on health.
Deaddiction and rehabilitation centres be set up. One should demythologize certain beliefs that smoking relieves stress and creates pleasure.

CURRENT CONCERNS

On 2 October 1999, the Bangladesh government announced it is implementing a three step plan to stop widespread arsenic poisoning in its nation, where groundwater contaminated by naturally occurring arsenic is found in over 90% of the districts and 20 million people are at risk for poisoning.

The government's plan, already launched in six districts, calls for nationwide testing of tubewells for contamination, identifying arsenicosis suffers and referring them to health centers, and educating the community through television and radio commercials, manuals, brochures, posters and music and dance performance in villages.

Over 34 support agencies, including the World Bank and UNICEF, have joined the government on this project. Field schools have been set up to train agency workers, and a database has been developed to supply information about arsenic screening results.
(EHP, Vol. 108# 2, Feb 2000)


REGULATORY TRENDS

India seeks review of Basel ban on export of wastes
After years of campaigning for a ban on the movement of hazardous waste, India is pushing for a review of the United Nations Environment Programme's (UNEP) Basel Convention rules on exports of wastes.

Metals recyclers said the Indian Government's change of position was a major development and could signal developing nations taking a greater role in the framing of new Basel rules. The economic impact of the ban had made India alter its position.

Many scrap materials are classed as hazardous waste under Basel rules and lead and zinc smelters in India have been crippled by the inability to import scrap as a secondary raw material. India recently lifted a block on zinc ash scrap and is now giving active consideration to allowing lead scrap imports.
(Chemical Industry Digest, March 2000)


IN A LIGHTER VEIN

Okhit Chandra Sen, wrote a letter to the Divisional Traffic Superintendent, Sahabgunj Divisional Office in 1909, complaining about how he missed the train when he got down to attend the call of nature. The Times of India reproduced the unedited letter:

Beloved Sir,
I am arrive by passenger train at ahmedpore station and my belly is too much swelling with jackfruit. I am therefore sent to privy. Just as I am doing the nuisance that guard making whistle blow for train to go off and I am running with lota in one hand and dhoti in the next when I fall over and expose all my shockings to many female women on the platform. I got leaved on Ahmedpore station.
This is too much bad in passengers to make dung that dam guard not wait train five minutes for him. I am therefore pray otherwise I am making big report to papers . Pray Your honour to make big fine on that dam guard for public sake otherwise I am making big report to papers.

Yours faithfully

(Sd/- Okhit Chandra Sen

MINIPROFILE OF ANILINE

Aniline is the simplest and the most important primary aromatic amine. It was obtained from the destruct, distillation of Indigo in 1826. It is generally manufactured by the catalytic hydrogenation of nitrobenzene. The demand of aniline is growing worldwide at 4-5% per year.

Synonyms: Amino benzene, phenylamine, blue oil, aniline oil, benzenamine, aminophen.

NIOSH# : BW 6650000

Uses:
Strong oxidizer. Manufacture of dyes polymers rubber accelerators, drugs, photographic chemicals, herbicides, fungicides, isocyanates, explosives, paints, pharmaceuticals, plastics, varnishes, pigment.

Properties;
Oily, clear, colourless brown liquid with a weak amine odour. Turns brown on exposure to air, b.p. 184 °C; m.p. -6 °C; f.p. 70 °C; a.p. 530 °C; r.d. (water=1) 1.02; r.v.d (air=1) 3.2; v.p. in mbar at 20 °C : 0.4; soluble in water, g/100 ml at 20 °C; e.l.vol. % in air: 1.3-20.

Violet reaction with acids. Decomposes on heating forming highly toxic flammable fumes of Nox. Reacts vigorously with oxidants; corrosive to Al, Zn. Moderate to violent reactions with acetic anhydride, ozone, oleum, perchromate, F2, trichloronitro methane

Hazards:
Fire: MOD, when exposed to heat or flame.
Explosion: above 70 °C
Hazard rating: Moderately dangerous

Occupational Risk:
Epidemiological data: Acute toxicity, cyanosis and death by asphyxiation in acetanilide production workers (1).

Diseases: papillomatous growths of the bladder, liver cirrohosis, anoxemia.

Accidents: A psychotic adult ingested 80 ml of reagent grade aniline; the victim was found in coma and shock. The skin, mucous membranes and retinal blood vessels were a deep state blue (2).

Occupational Safety Parameters:
Personal Protective Equipments: Reasonably proper clothing, safety goggles, butyl rubber or PVA gloves, face shield and breathing apparatus.

TLV: 2 ppm; STEL: 5 ppm.

Toxicity Data:
Unk-hmn LDLo: 357 mg/kg
Unk-hmn LDLo: 150 mg/kg

Treatment: 
Periodical medical examination according to degree of exposure. In case of methemoglobinemia specific first aid treatment essential. Methylene blue and Vit. C iv. 

Special high risk groups:
Anemic persons, pregnant women. Persons with cardiovascular or pulmonary diseases.

Prevention:
No open flames, no sparks no smoking, closed system, ventillation explosion protected electrical equipment. Do not eat, drink or smoke during work, Strict Hygiene. Routine checking of lips, and nail beds of exposed personnel for signs or cyanosis.
Disaster Management:
Collect leaking liquid in sealable containers. Absorb spilled liquid in sand or inert absorbants, remove to safe place. Extinguish fire with alcohol foam, CO2, powder chemicals, water spray.

Packaging & Labelling:
Unbreakable packaging
UN: 1547
Label: Poison
Storage: Fire proof separated from oxidants and strong acids.

DO YOU KNOW?

India has 80 thermal power plants. A 2000 megawatt thermal power plant with an annual consumption of 8 million tonnes of coal which produces 1600 tonnes of Pb, 800 tonnes of Zn, 80 tonnes of Cd and 40 tonnes of U.

ON THE WEB

http://www.wef.org/   

The Water Environment Federation (WEF) helps professionals at wastewater treatment plants in this country and abroad exchange information and keep abreast of new technologies and regulations. In addition, the organization works to raise public awareness of water pollution and ways to fight it. 

http://www.orf-facts.org/ 

This is the homepage for the authors of the book "Our Stolen Future", published in 1996 that explores endocrine disruption. The site contains many links to existing and new research in this field.
www.igidr.ac.in            

To meet the challenges of this century in India, the UNDP initiated the capacity 21 Project in 1995. Its goal is to build understanding and capacity for environmental economics in research institutions, government agencies, NGOs and the private sector, and to promote concern for sustainability among decision and policy makers in government and industry. The project focuses on the four main areas of air quality, water quality, land resources and biodiversity. As part of the project, the Indira Gandhi Institute of Development Research (IGIDR) has prepared strategy briefs for these four areas.

www.epa.gov/tri 

As part of the Toxic Release Inventory (TRI) programme of EPA, it publishes industry-specific and chemical-specific guidance documents and conducts an ongoing dialogue among stakeholders. Extensive information concerning the programme is available on the TRI web site.

This is a multiauthor review of carbon monoxide covering 23 topics of varied nature-physical, physiological, mechanistic, clinical, therapeutic, regulatory and relating to quality of life. Each chapter is a focussed mini review and provide a thorough careful review for those toxicologists specializing in pulmonary or combustion toxicology.

Brush with Death: A Social History of Lead Poisoning

An excellent knowledge source for anyone interested in lead poisoning, it is also an informative historical account of an industry gone bad. Presented in a novel/documentary format, the author unwinds a story beginning 5000 years ago when ancient metallurgists first separated lead from silver. Each chapter begins with brief statements from individuals in varying occupations documenting the progressive awareness of leads lethality.

This book has multiple sections which include models of toxicology, assessment of cell toxicity, biotransformation, toxicokinetics, glutathione, heme synthesis and breakdown, nitric oxide, neurotoxicology and molecular neurotoxicology. It provides numerous laboratory procedures and references. Each protocol is given in the standard operating procedure format that is very useful to laboratory workers. Alternate protocols are also provided. Approximate equipment and reagent are also included.

Neurotoxicology In vitro

Extensive reviews are presented of the potential use of fundamental and advanced methods for neurotoxicological in vitro --in vivo extrapolation, risk assessment and mechanistic studies. The book has 11 chapters written by some of the most distinguished experts in the field. A book on neurotoxicology in vitro which stands out as the obvious reference for investigators planning neurotoxicity studies.

CONFERENCE DIARY