Environmental Articles Archive: Pollution/Toxic Waste
Web version prepared by BCAS
June, 2008

The pollution in our rivers
Immediate action is a must

Our rivers are in a bad state, have been for a long time. That is not surprising, seeing that we have been concerned about the situation for years. What now appears to give it a new twist is the result of a survey carried out on some of the rivers, 25 in total. Predictably, the quality of the water in the rivers has dwindled to a precarious state. Worse is the knowledge that some of these rivers may actually have reached a point where they are no longer capable of nurturing or supporting aquatic life forms in them. The pollution in the Buriganga, Turag and Norai -- and these flow by the nation's capital -- has grown to an extent where no life forms can survive in their waters. That is the stark finding by a group of researchers after a three-year survey of the 25 rivers in question. Obviously, the oxygen levels in the Buriganga and in parts of the Turag and Norai have declined to a dangerous level. Where 4 to 6 levels of oxygen are required for local fish species to survive, the oxygen level in these rivers has now declined precipitously to less than one per microgram.

The water resources department of the Bangladesh University of Engineering and Technology has surely done a commendable job of acquainting us with the issues involved. The 25 rivers surveyed all are at risk of losing their life forms. Of course, the Buriganga, Balu, Turag and Sitalakhya are the worst affected rivers, but the problems afflicting them could also, and soon, come to characterise other rivers. And that is where the question of dealing with the problem comes in. A major reason behind the pollution of the rivers has been the dumping of effluents and myriad industrial waste by factories situated on the banks or nearby. That has been a worry for years together, with periodic calls for action on the part of those responsible for such conditions going unheeded. Add to that the careless dumping of waste matter by the municipal authorities. These lead to faecal contamination and other difficulties for the rivers. A bleak picture is thus before us: if meaningful and firm action is not taken now to roll back the damage already done, it may be too late to save these rivers. Moreover, with large numbers of people still using the waters of these rivers for drinking and washing purposes, there is a clear and present danger to public health. 

An immediate and well thought-out action plan involving the government, industrial units and environment experts is today called for. Surveys and studies must now lead to concrete action. Rivers are a lifeline to a society. Inaction on our polluted rivers will thus be seen as a clear invitation to suicide. Briefly, creating awareness of the danger at the mass level must now be the priority. 

Source: The Daily Star, June 17, 2008

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Save life from plastic pollution 
Dr Hossain Shahriar

The history of plastics goes back more than 100 years - however, compared to other materials, plastics are relatively modern. Their usage over the past century has enabled society to make huge technological advances to take us towards the new Millennium.

Although we think of plastic as a modern invention, there have always been "natural polymers" such as amber, tortoiseshell and horn. These materials behaved very much like manufactured plastics and were often put to similar uses to today's materials - for example, horn, which becomes transparent and pale yellow when heated, was used to replace glass in the 18th century. The original breakthrough for the first semi-synthetic plastics material - cellulose nitrate - occurred in the late 1850s and involved the modification of cellulose fibers with nitric acid. Cellulose nitrate had many false starts and financial failures following its invention by a Briton, Alexander Parkes, who exhibited it as the world's first plastic in 1862. Firstly known as Parkesine, then Xylonite, it began to find success in the production of objects such as ornaments, knife handles, boxes and more flexible products such as cuffs and collars. The American Hyatt brothers were attempting to develop a substitute for the ivory billiard ball and in so doing came up with a process for manufacturers using a nitrate cellulose composition. Celluloid was thus born and was patented in 1870 - its early commercial success lay in dental plates for false teeth.

In 1912, German chemist Fritz Klatte at Greisheim Electron unknowingly made the first PVC in an attempt to create uses for large quantities of acetylene gas fuel lamps just before the new technology of electric lights made them obsolete. He had reacted acetylene with hydrochloric acid (HCl). Not knowing what to do with the new material, it was stored for some time, and polymerization took place. Their patent expired in 1925 without them ever knowing what to do with it. Independently, in 1926, chemist Waldo Semon at the American company B.F. Goodrich invented PVC. And again, it was patented.

One of the first uses for PVC was insulation on electric cables in 1930. Mass production, facilitated by improved injection molding, and automation, greatly reduced its price. PVC has been commercially available since 1942. By 1950, there were five companies producing PVC. And by 1980, there were twenty. Today, vinyl is the second largest-selling plastic in the world, and the industry employs more than 100,000 people in just the US. PVC is the second largest volume thermoplastic only to polyethylene. Production capacity has almost doubled over the last 20 years, currently 27 million tons/year worldwide. Current worldwide uses of PVC by percent are as follows: Building 56%; Packaging 15%; Consumer goods 10%; Electronics industries 9%; Agriculture 5%; others 5%.

Health Hazard

Dioxin is created during all phases of PVC production, as well as in its disposal by incineration or accidental fire. There is no "threshold" dose, meaning that the lowest dose that has hormonal action has not been found yet. Researchers have been unable to find the threshold using the most up-to-date advanced systems.

PVC plastic is the largest single use of chlorine in the U.S., accounting for about 34 percent of all chlorine production. In 1996, the US and Canada alone produced 6.61 million tons of PVC and copolymers. A large body of evidence suggests that the greatest share of the nation's dioxin burden stems from the manufacture, use, recycling, and disposal of this enormous quantity of PVC plastic.

The US Environmental Protection Agency (EPA) has known since the 1980's, that dioxin is an unavoidable by product created during the production and heating or incineration of many materials containing chlorine such as PVC and paper. One can be fairly safe in assuming that the PVC industry's knowledge of dioxin being created by the manufacture of was prior to that of the EPA. Since they continued to manufacture PVC even after knowing this, it is therefore an intentional action placing profits above people. Industry also knows that PCBs are an unavoidable byproduct of PVC production.

Dioxin has been found in PVC process waste in concentrations as high as 200,750 parts per billion (ppb), which compares closely with that found in Agent Orange production wastes. Making the production of PVC free of dioxin is highly unlikely. One industry officially stated in 1994, "It is difficult to see how any of these conditions could be modified so as to prevent PCDD/PCDF formation without seriously impairing the reaction for which the process is designed." PVC is the largest single use of chlorine in the US, and is most likely the largest source of the dioxin in the US. It accounts for about 34 percent of all chlorine production.

According to the EPA, incineration of municipal and medical waste, which is heavily loaded with PVC, is the largest source. Dioxin has no commercial value and is extremely toxic, long-lived and ubiquitous in both the environment and our bodies. It is hormonally active in concentrations as low as 5 parts per trillion (ppt). The EPA has labeled dioxin a known carcinogen.

It is also unavoidable when PVC is incinerated or heated. PVC is the largest contributor of the world's dioxin burden and it is highly persistent in the environment, traveling up the food chain, and accumulating in body fat.

Much of the discarded PVC is burned knowingly in municipal incinerators or accidentally in building fires, sending minute but extremely potent quantities of dioxin into the air. How to prevent the creation of dioxin when certain organic materials are incinerated in the presence of a source of chlorine (PVC and other chlorinated materials) and oxygen is still unknown. When airborne this potent chemical travels a few feet or thousands of miles. After making its way to the upper atmosphere, it condenses in colder regions of the globe. According to a study by Barry Commoner at Queens College, CUNY, dioxin concentrations in Inuit mothers' milk are twice the levels observed in southern Quebec, even though no significant sources of dioxin are located nearby.

In 1994, the nonprofit organization Green peace sampled the sediment downstream the discharge of the Geon Corporation (formerly BF Goodrich) in La Porte, Texas. They found it to contain a dioxin concentration of greater 2,911 parts per trillion (ppt). This is about five times higher than what the EPA reported in their draft dioxin reassessment. From that reading, Green peace estimates that the quantity of dioxin discharged into U.S. waterways from EDC/VCM facilities may rival that discharged from all U.S. pulp and paper mills.

The lipophilic nature of dioxin allows it to be readily assimilated in the lipid (fat) stores of plants and animals. It rapidly enters the food of all creatures on earth. Bioaccumulation is the result of its presence and persistence at many locations on the web of life. It is not broken down in the systems of various organisms, and is accumulated in the organism that consumes it. The pace of accumulation increases with the level of the organism on the food chain.

The higher level, the more organisms of the lower levels it must consume to survive. Because humans are at the top of the web of life, we accumulate the most dioxin, PCBs, and other bioaccumulating contaminants. Children are at an even higher level than their parents.

Effects:

Sexual ambiguity of both internal and external genitalia, cryptorchidism (testicular maldescent), hypospadias, cleft phallus, suprainguinal (cryptorchid) ectopic testes, abnormal spermatogenesis, lowered sperm count and motility, genital abnormalities, deformed and reduced penis, abnormal concentrations of steroid and peptide hormones instrumental in reproduction, reduced levels of testosterone, elevated levels of estradiol-17ß, males born with neutral or female genitalia, 20-year-old women dying of breast cancer.

Mothers:

All mothers have had many years of exposures. Many of the chemicals accumulate faster than they are cleared and are attracted to the fatty cells of the body. When pregnant, these stored toxins can affect the embryo in a number of ways. It is now understood that the placenta does not protect the embryo from all harm. It acts as an efficient barrier to bacteria, but not to most synthetic chemicals. Some cross the placenta with ease, some are changed into even more toxic chemicals called metabolites, and others damage the functioning of the placenta.

Dioxin is just one of hundreds of contaminants stored in the mother's fat. It is consumed by nursing infants at a rate of 35-100 pg/kg (picograms per kilogram of body weight per day. A picogram is one-trillionth of a gram). The World Health Organization's acceptable daily intake of dioxin is 1-4 pg/kg. The EPA "Risk Specific Dose" is 0.01 pg/kg, which is 10,000 times lower than that the nursing child receives.

Fathers:

Dioxin is also stored in the father's fatty tissues. Dioxin is what made Agent Orange such a nightmare for Vietnam vets and their offspring. Its legacy continues today in US veterans, Vietnamese citizens, and their offspring, decades after its use.

It and many other contaminants can cause problems related to his sperm that are passed on to the child. Besides lowering the quantity and quality of sperm, the DNA carried by the sperm can be damaged, the sperm can be coated in toxins, and the semen entering the vagina can carry the toxicants that are flowing throughout the body of the father. His own sperm production could have been limited while he was an embryo. Decreasing sperm counts in many industrialized nations are about 1.5% annually.

Children:

Considering the facts above, it follows that our children that take the largest hit of dioxin, PCBs, and other toxic chemicals that are the result of the manufacture, use or disposal of PVC and other synthetic chemicals and products.

Dioxin is the most powerful endocrine disruptor (ED). An ED is generally a manmade synthetic chemical that has been proven to have many deleterious effects on the endocrine system of animals by mimicking, blocking, and/or disturbing in some other way, the messages of hormones that guide the complex processes of the endocrine system. There is no human hormone that dioxin does not disrupt.

Accidental building and forest fires release some unknown quantities of dioxin. In the case of the building fires, the creation of dioxin is from the abundant supply of PVC materials in and on the building. The windows, flooring, garden hoses, raincoats, umbrellas, toys, wall and floor coverings, furniture, and all the other PVC items in a building add up to a significant source of chlorine to be burned. In the case of forest fires, the dioxin originated with the advent of chlorinated chemicals and did not exist in the massive quantities recorded today. This fact is borne out because of the analysis of mummies showing little or no traces of dioxin. Therefore, it is not true when Industry states that forest fires are the cause of dioxin and that dioxin has always been on earth in great quantities.

Vinyl chloride monomer

Vinyl chloride monomer (VC) is a gas that is currently produced in the United States by 10 companies at 12 facilities, which are as follows: Westlake Monomers Corporation in Calvert City, Kentucky; Borden Chemicals and Plastics in Geismar, Louisiana; Dow Chemical in Oyster Creek, Texas, and in Plaquemine, Louisiana; Georgia Gulf Corporation in Plaquemine, Louisiana; PPG Industries in Lake Charles, Louisiana; Vista Chemical Company in Lake Charles, Louisiana; The Geon Company in La Porte, Texas; Formosa Plastics Corporation in Baton Rouge, Louisiana, and in Point Comfort, Texas; Occidental Chemical Corporation in Deer Park, Texas; and Oxymar in Ingleside, Texas. VC was used as an aerosol propellant and as an ingredient of drug and cosmetic products such as hair sprays, until the EPA banned it in 1974.

Monomers are very reactive and biologically aggressive. The health effects of VC are many. It is toxic in the short- and long-term. It is an immunotoxicant, reproductive toxic VC is a known human carcinogen, and has been associated with tumors of the liver, brain, lung, and hematolymphopoietic system. There is a causal association to angiosarcoma of the liver. Exposure to VC also causes other forms of cancer, such as melanoma, hepatocellular carcinoma, brain tumors, lung tumors, and malignancies of the lymphatic and hematopoietic system. Exposure to PVC dust was associated with an increased incidence of lung tumors. There are slightly elevated risks for gastric and gastrointestinal cancer (other than liver cancer).

Recycling

Of the tens of millions of tons of PVC manufactured each year, practically none is recycled. According to the American Plastics Council, in 1995, less than less than 2 hundredths of a percent was recycled. Much of it makes its way to landfills of less fortunate countries such as India. Even the .02% that is recycled isn't done so in the true sense of the word. In this case, recycling means to use over a few times before being discarded in any number of ways including incineration or land filling.

Switch to PVC-free materials

Hoping to avoid litigation, many major corporations are now eliminating the use of PVC. Proctor and Gamble, Mattel, LEGOs, Little Tikes (Newell Rubbermaid),[55] Baxter[56] and several others have made this commitment.

More than 80% of the IV bags used in the U.S. are PVC plastic manufactured mainly by Baxter Healthcare Corp., Deerfield, IL, and Abbott Laboratories, North Chicago, IL. Harm to Workers Exposed To PVC

There is a six-fold increase in the risk for seminoma, one type of testicular cancer, among plastic workers exposed to polyvinyl chloride (PVC).

In September 1973, the US Department of Health Education and Welfare, National Institute for Occupational Safety and Health (NIOSH) determined that air contaminants generated by the thermal cutting of polyvinyl chloride (PVC) packaging films in conjunction with the wrapping of meat are potentially toxic to some meat wrapping employees PVC meat wrap. At that time this would have had an effect on 75,000 meat-wrapping employees in the United States, according to union and industry estimates. The testing by NIOSH found hydrogen chloride (HCl) as one of the air contaminants generated by the hot wire cutting of PVC film in the meat wrapping. Other contaminants included chlorinated hydrocarbons and breakdown products of film additives.

NIOSH's predecessor the Bureau of Occupational Safety and Health began getting complaints about PVC wrap from meat wrappers in the summer of 1969, and continued coming from several cities across the nation at least until the time of the NIOSH report cited.

"Sixteen of the eighteen meat wrappers interviewed in the preliminary survey were known to have suffered ill effects from air contaminants from PVC films. Only two workers were free of any clinical symptomatology. Eight had similar case histories and admitted experiencing varying degrees of sneezing, rhinorrhea, and eye irritation. Most individuals gave a like story that the ill effects came on from one to three hours after the commencement of meat' wrapping it the morning. The workers stated that as the workday progressed the prodromal manifestations increased. in intensity. The sneezing, rhinorrhea, rind threat and eye irritation would abate in the evening hours and would be non-existent during weekends and vacations."

In 1974, the FDA was considered revoking the "prior sanction" for use of polyvinyl chloride in food packaging and ban its use for packaging alcoholic beverages because of the migration of VC. "Trade secret" considerations prevented the investigations that were needed.

A 1997 study found that while the food and water intake of VCM cannot accumulate in hazardous quantities, inhalation in workplace (heat cutting and sealing of PVC wrap) settings can accumulate VCM in the blood to form carcinogenic and mutagenic metabolites.

Ethylene dichloride

The largest single use of EDC, also known as 1,2-dichloroethane, 1,2-DCE, C2H2Cl2, is the production of VC used to produce PVC. EDC can also be used in the manufacture paint removers, pharmaceuticals, electronics, metal degreasers, aerosols, and urethane foam. In test animals, EDC decreased litter size, decreased fertility, disrupted estrous cycle, increased incidence of congenital cardiac lesions, increased incidence of testicular lesions, and increased embryo mortality significantly decreased antibody-forming cells of the spleen. Acute (short-term) inhalation exposure of humans to EDC can induce neurotoxic, nephrotoxic, and hepatotoxic effects, as well as respiratory distress, cardiac arrhythmia, nausea, and vomiting. No information is available on the reproductive or developmental effects of EDC in humans. EDC is metabolized into epoxides by enzymes, which can yield dichloroacetaldehyde (DCAld), dichloroethanol, and dichloroacetic acid. It is categorized by the EPA as a Group B2 probable human carcinogen, and by IARC as a Group 2B (possibly carcinogenic to humans). All forms of EDC usage in agriculture, including pesticides and fumigants, are banned in 5 countries (Austria, Belize, Canada, Slovenia and the United Kingdom) and in the European Union.

Other Toxicants with Similar Actions

EDC Metabolites

One of the metabolites of EDC, dichloroacetic acid, is also one of the metabolites of trichloroethylene (TCE). Because of the pervasiveness of TCE in the environment, most people are likely to have some exposure via one or more of the following pathways: ingestion of drinking water, inhalation of ambient air, or ingestion of food. The National Institute for Occupational Safety and Health (NIOSH) conducted a survey of various industries from 1981 to 1983 and estimated that approximately 401,000 U.S. employees in 23,225 plants are potentially exposed to TCE. Relatively little information is available in regard to environmental levels and exposure. Background exposure to related compounds may influence the effect of small incremental exposures of TCE. Releases of TCE into the environment occur during its manufacture, use, and disposal.

The major use of TCE is as a degreaser for metal cleaning operations. It is also used in paint stripper, adhesive solvent, ingredient in paints and varnishes, in the manufacture of organic chemicals, silk screening, taxidermy, electronic cleaning, wood stains, varnishes, finishes, lubricants, adhesives, typewriter correction fluids, paint removers, and cleaners. More data are needed on the levels of TCE in private wells, indoor air, soil, food, blood across all ages, and mother's milk.

Vinyldene chloride (VDC)

VDC is used to make Saran-type (Johnson Wax, Racine, Wisconsin) plastics and as a degreasing agent. It has contaminated groundwater in many areas, and is ranked 11th among the hazardous chlorinated organic compounds found in US drinking water. 50% of the US population obtains their drinking water from a groundwater source. The major method of drinking water disinfection in the United States is by chlorination. Monochloroacetic acid (MCA) is formed as a result of chlorination of drinking water for disinfection and can be present at concentrations of approximately 1 µg/l. Coexposure of humans to these chemicals is possible. VDC and MCA are both hepatotoxic and interact with each other. VDC causes centrilobular necrosis of the liver and the elevation of serum enzymes, indicating hepatocellular damage. In animal studies of VDC that included MCA, there was a significant increase in VDC hepatotoxicity. Fasting and other conditions can enhance the injury caused by VDC, putting the poor at greater risk. — NewsNetwork

(The writer is journalist and ecologist) 

Source: The Financial Express, June 21, 2008

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Tropospheric ozone and air pollution

Ozone is one of the highly reactive gases, which is photo chemically active. It is composed of three atoms of oxygen (O3) and its role depends on its location in the atmosphere. This gas plays a different role in the lowest two layers of the atmosphere, known as the stratosphere and troposphere. In the stratosphere, above the tropopause about 90 percent of the ozone protects life on earth from the sun's dangerous ultraviolet radiation. In contrast, the layer surrounding the earth's surface is the troposphere where the presence of ozone is harmful for the environment as well as for human health. 

In a polluted urban atmosphere ozone acts as a more powerful photochemical oxidant than other oxidants such as Nitrogen dioxide (NO2), Hydrogen peroxide (H2O2), and Peroxy Nitrogen (PAN). Moreover, ozone in the troposphere is designated as a greenhouse gas due to its absorption in the infrared, visible, and ultraviolet spectral region. Enhancement of ozone in the middle and upper troposphere could have significant climatic consequences. In addition, enhanced ozone levels in the boundary layer of polluted regions have adverse effects on human health and crop yields. The phototoxic nature of tropospheric ozone in relation to photochemical air pollution is discussed in this write-up. Photo chemically produced ozone may affect crop yield, plant growth, and the respiratory system and lung function of humans. Furthermore, it may also damage the building materials. 

Formation of tropospheric ozone

Tropospheric ozone is not directly emitted into the troposphere; rather its presence depends on stratospheric intrusion and complex photochemical reactions. It is considered as a secondary or transformation pollutant rather than a primary pollutant. Primary pollutants that are involved in the formation of secondary pollutants are often referred to as precursors. The formation of tropospheric ozone depends on some precursors such as oxides of nitrogen (NOx), Volatile Organic Compounds (VOCs), and carbon monoxide (CO). Aromatic and olefin hydrocarbons contribute significantly to ozone formation. These precursors act in the presence of sunlight to produce ozone. Since, these reactions are stimulated by sunlight and temperature, the peak ozone levels typically occur in the warmer times of the year during daytime. 

Due to the increase of anthropogenic emissions in the atmosphere, the growth of carbon and nitrogen compounds are rising dramatically. As a result, the enhanced level of tropospheric ozone has become an issue of concern in terms of photochemical air pollution. Tropospheric ozone was first measured over 100 years ago. Reports mentioned that the average daily maximum of tropospheric ozone in North America was approximately 0.019 ppm, and in Europe 0.017-0.23 ppm. But now this amount exceeds 0.2-0.3 ppm in some cities the world in peak pollution periods. 

Impacts

Impacts of ozone on humans and the environment vary with the emission patterns, meteorological transport and chemical and physical processes. The effects associated with levels of ozone have been monitored in many areas of the world. 

Effects on human health

It is hardly surprising that oxidant like ozone can be damaging to health. Ozone exposure experiments on human health began in the mid 1960s. That exposure data provide a foundation for the interpretation of epidemiological studies and indicate what concentrations are likely to impact on the normal population. It is the potentially serious effects on human health that have caused many countries to adopt air quality standards.

Numerous studies indicate that there is an adverse effect on health associated with short-term, prolonged or sub chronic, and chronic exposure to ozone. There has also been growing concern about long-term exposure to elevated ozone levels -- may be cause of irreversible chronic lung injury. 

Photochemical oxidant can damage respiratory tissues through inhalation. Ozone has been linked to tissue decay, promotion of scar tissue formation, and cell damage by oxidation. Ozone can impair an athlete's performance, create attack that is more frequent for individuals with asthma, cause eye irritation, chest pain, coughing, nausea, headache and chest congestion and discomfort. It can worsen heart disease, bronchitis, and emphysema. 

On Vegetation

Research and analysis indicate that the impacts of ozone on vegetation have also been observed in several regions in the world. Ozone may damage forests and crops. This slows down photosynthesis and plant growth. Ozone can lead to plant tissue injury and reduction in growth and productivity because of its phytotoxic nature. If a sufficient amount reaches sensitive cellular sites within the leaf, ozone exerts a phytotoxic effects.

However, ozone injury will not occur if the rate of ozone uptake is slow enough, to allow plants to respond to ozone by defensive reactions, such as avoidance by stomatal closure, detoxification of ozone by chemical reaction, adjustment by alteration of metabolic pathways, and repair of injured tissue. However, these factors depend on the intensity of ozone exposure. 

On crop yield

Ozone may reduce the intended use or value of the plant species, plant communities, or ecosystem. The impact of ozone on crop yield was identified through foliar injury symptoms in the 1960s. Injury symptoms and crop yield are usually not directly proportional because of the importance of variation in allocation processes and metabolic factors in determining plant yield. For instance, much more loss of yield can occur with little foliar injury; on the other hand, foliar injury can be much greater than yield loss. This means the injury -- yield loss relationship may depend on the ozone exposure. 

As an example, for corn, foliar injury occurred at lower ozone concentration than yield reduction; but as the ozone concentration increased, yield is reduced to a greater extent than the increasing foliar injury. Numerous studies indicate that ambient oxidants reduced the yield and quality of citrus, grape, tobacco, cotton, and potato. The impacts of ambient ozone of oxidants are comparatively much higher than other oxidants. However, studies confirmed that ambient ozone levels are sufficient to reduce crop yields. Higher losses depend on several factors such as ozone concentrations, environmental conditions, and crops that are more susceptible to ozone. Table shows typical ozone injury symptoms of some crops. 

In fact, ozone can change the integrity of the cells through entering inside a leaf. If the cells collapse and die, then symptoms occur on the leaf surface. 

Conclusion

Intrusion from stratospheric ozone and photochemical production are the two main sources of ozone in the troposphere. The photochemical formation of ozone depends on some precursors as discussed earlier -- VOCs, NOx, and CO. Due to world expansion in agriculture, transportation, and industry, huge amounts of these precursors are emitted into the troposphere. The concentrations of ozone have risen from pre-industrial times to the present because of increased emissions from anthropogenic sources. Ozone, like other pollutants, does not stay in the source region, rather it can transport throughout the global atmosphere. As the fossil fuel emissions are mainly responsible for the photochemical production of ozone, it is therefore important to control the emissions from anthropogenic sources because the global atmosphere is common to all countries and all lives. 

Khorsheda Yasmeen is UNO, Dhamrai. 

Source: The Daily Star, June 21, 2008

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Can Indian Jamuna be brought back to life?

Money and expensive technology are not the solutions. We have already spent close to Rs 1,500 crore on cleaning the Yamuna -- and the river has become dirtier. New Delhi, April 18, 2007: Delhi has spent a whopping Rs 1,188-1,491 crore on cleaning the Yamuna till 2006. Or, Rs 71-85 crore per km in the 22-km stretch of the river as it passes through the city. But in spite of this massive investment, the river Yamuna runs dirtier. 

"There is obviously something fundamentally wrong in the way we are managing our river cleaning programmes. Our planners believe in spending money without understanding the connection between sewage and its disposal and river pollution," said Sunita Narain, director, Centre for Science and Environment (CSE) here today. She was speaking at the release function of CSE's latest publication, Sewage Canal: How to Clean the Yamuna. The book was released by the Union minister for water resources, Saifuddin Soz and the chief minister of Delhi, Sheila Dikshit. 

CSE also premiered a 32-minute video on the subject, Faecal Attraction: Political Economy of Defecation, which explodes various myths about river cleaning. "The film is our way of connecting the river to our water and sewage," says its director, Pradip Saha. Becoming dirtier all along "The Yamuna has become dirtier, and so have the towns along its stretch. And Delhi is its biggest polluter, followed by Agra, Ghaziabad and Faridabad. The Yamuna's 22-km stretch in Delhi is barely 2 per cent of the length of the river, but contributes over 70 per cent of the pollution load," said S V Suresh Babu, deputy coordinator, river pollution campaign, CSE. 

Delhi, with only 5 per cent of the nation's urban population, has 40 per cent of India's sewage treatment capacity. Despite this huge investment, the Yamuna remains as dirty as ever. The river, in fact, is relatively clean till it enters Delhi at Wazirabad. It leaves the city transformed into a murky sewer. In Delhi, the river has virtually no freshwater for nine months. Delhi impounds all its water at Wazirabad, where the dammed up river practically ceases to exist; what flows subsequently is only sewage and waste from Delhi's 22 drains. There is just no water available to dilute this waste. 

Pollution levels in the Yamuna have risen. BOD load has increased 2.5 times between 1980 and 2005 -- from 117 tonne per day (tpd) in 1980 to 276 tpd in 2005. Dissolved oxygen (DO) - to check if the river is alive -- in the upper segments, considered pristine, is dipping, indicating an increase in organic pollution. By the time the river is midway through Delhi, the total coliform count is so high that it is difficult to count the zeroes. Pesticides and heavy metals are also present in the river. 

In fact, the river does not meet minimum standards for bathing even after treatment. There has been no change in pollution levels in Delhi from 1996. On April 10, 2001, the Supreme Court had directed that DO levels were to be maintained at a minimum concentration of 4 mg/l -- but five years after, the river is still dead.

It is clear that all the money spent to clean the Yamuna has literally flown down the drain, say the writers of Sewage Canal. In spite of that, in 2006, the Delhi government submitted another grand Rs 4,000 crore proposal under the Jawaharlal Nehru National Urban Renewal Mission. If approved, investment per km under this programme would be Rs 235-250 crore. 

Investment not enough Pollution of the river is directly linked to the inefficient water planning and management in Delhi. Our planners have no clue about how much water the city uses, and neither do they know how much waste the city generates. It is not surprising, therefore, that the growth in sewage treatment capacity has not kept pace with the increase in population and waste. Treatment capacity has increased almost eight-fold in the last 40 years, but wastewater generation has grown 12-fold in the same period. 

"We also suffer from under-utilisation. Delhi has a sewage treatment capacity of 2,330 mld -- 17 STPs -- of its own. But only 68 per cent of this capacity is utilised," says Suresh. The reasons are many: sewage has to be transported over long distances for treatment, through largely defunct conveyance systems. In 2001, only 15 per cent of Delhi's sewerage system was functional. On top of this, almost 45 per cent of Delhi lives in unauthorised colonies, generating 'illegal' sewage, which is unaccounted for. 

The sheer mindlessness of Delhi's pollution control efforts is evident from one example: a major portion of whatever Delhi manages to treat is released back into the city's drains. This treated effluent mixes with untreated and 'illegal' waste flowing in from large parts of the city, thereby nullifying all efforts to clean it. Also, efforts at reuse have been completely insufficient, to say the least. According to the DJB, about 535 mld is supplied for reuse. 

Needed: a Revival Action Plan "What we need is to maximise utilisation of the existing treatment facilities and ensure reuse of treated effluents," says Narain. All waste -- legal and illegal, sewered and unsewered -- must be trapped and treated and not mixed with untreated sewage. Centralised STPs cannot be the only option --- the cost of transporting waste to the treatment facility and transporting treated effluent back to the point of reuse makes them too expensive to run. Therefore, treatment facilities need to be constructed close to the source of sewage generation. Based on these principles, a detailed plan for the top six drains of the city, which contribute 90 per cent of the pollution in the river, should be made and implemented.

Simultaneously, steps should also be taken to achieve dilution in the river -- mainly by reducing the city's demand for freshwater. The river needs water for a minimum flow to keep it alive. Fiscal instruments - like taxing water-guzzling flush toilets -- can work. Simultaneously an attempt needs to be made to revive the waterbodies and their catchment areas to store maximum run-off, which could then be used for local water needs or could be released into the river for dilution. Says Narain, "We must remember that whatever amount of waste we manage to treat will be inadequate, and the technology to treat the waste is hugely expensive. It will be a battle which we will never win if we continue fighting it the way that we have been doing all this while. The only way out is to rethink our approach." The book and the film expose the political economy of defecation, where the rich are subsidised to defecate in convenience and the poor pay for pollution with their ill health because of dirty water. This is not acceptable, says CSE.

Source: The New Nation, June 23, 2008

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