Malaysia: Pesticide Poisoning

ACCIDENTAL POISONING : SELECTED ASPECTS OF ITS EPIDEMIOLOGY AND PREVENTION
John T Arokiasamy, MPH, Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur

Pesticides, insecticides and rodenticides are major agents of unintentional poisoning too, both directly as well as indirectly. In recent years, pesticides have caused numerous cases of poisoning, many of whom are children. Worldwide, an estimated half a million poisonings per year are said to be caused by exposure to agricultural pesticides. This occurs when pesticides are left in open containers in homes or in areas where children play.

The use of pesticides on commercial vegetable crops is often extensive in order to obtain higher yields and better returns. Indiscriminate, excessive spraying of stronger dosages of these chemicals are often resorted to achieve this end. In 1993, there were about 400 deaths due to pesticide poisoning from over 1400 reported cases, of which 45% were non-suicidal in nature. Ministry of Health figures based on government hospitals data revealed that in 1992, 138 cases of pesticide poisoning were unintentional in nature, mostly at work, with two deaths.

Elsewhere, reports of organophosphorous toxicity due to absorption through the skin has been reported. Organophosphates, found in pesticides, were commonly implicated in cases seen in Jordan with an annual mortality rate of about 35.3%.

It was also reported that 74% of the cases were among children less than 10 years. Aplastic anemia, pure red cell aplasia, leukemia, lymphoma and other hematologic disorders following exposure to the pesticide pentachlorophenol (PCP) has been reported, suggesting that exposure to chemicals that linger long in the environment can lead to mutagenic, hemolytic and carcinogenic effects.

Arsenic commonly found in insecticides, herbicides and industrial materials are involved in heavy metal poisonings and most commonly in children. A herbicide of importance in unintentional poisoning, resulting from accidental ingestion, is paraquat. A 9-year-old is reported to have been poisoned after using an empty bottle of paraquat for drinking water from a water tank.

Rodenticides too are known to give rise to poisoning. A superwarfarin compound (brodifacoum) used as a rodenticide resulted in a child being poisoned.

Ke Arah Melaksanakan Pertanian Ekologi

Berita Harian, 12 Nov 2002
Oleh Junita Mat Rasid

SEKTOR pertanian hari ini menghadapi cabaran serius untuk meningkatkan hasil bagi memenuhi keperluan makanan selaras dengan populasi penduduk. Hasil pertanian perlu sentiasa ditingkatkan dan pada masa yang sama kita perlu memastikan sumber alam semula jadi tidak dieksploitasi secara keterlaluan yang boleh menyebabkan kerosakan.Bagaimana, proses meningkatkan pengeluaran pertanian yang diamalkan sentiasa terdedah kepada kerosakan habitat sehingga menyebabkan pelbagai spesies musnah.Di negara ini, dalam tempoh 1955 hingga 2000, pengeluaran makanan meningkat 2.6 peratus setahun, berbanding keperluan makanan meningkat antara 6 hingga 7 peratus setahun. Bagaimanapun peningkatan kegiatan pengeluaran pertanian seperti yang diamalkan di kebanyakan negara di dunia, menimbulkan ancaman kepada sebahagian besar sistem ekologi semula jadi.Pertanian tidak boleh dihentikan tetapi jika polisi pertanian yang diamalkan sekarang tidak diubah, tidak mustahil biodiversiti akan musnah dalam tempoh 50 tahun akan datang. Hari ini biodiversiti terancam dan mungkin pupus kerana kegiatan manusia sendiri. Walaupun Malaysia adalah antara negara di dunia yang kaya dengan biodiversiti, tanpa pengurusan sistematik dan kesedaran semua pihak, biodiversiti akan musnah begitu saja.Bidang ini perlu ada keseimbangan antara usaha untuk memulihara biodiversiti yang selalu dilaung-laungkan negara maju dengan hak negara membangun yang kaya dengan khazanah ini untuk menggunakan secara mapan.Biodiversiti merujuk kepada unsur semula jadi yang meliputi haiwan, tumbuhan dan mikro organisma yang membantu sistem ekologi. Ia membantu mengekalkan kepentingan keseimbangan atmosfera bumi, melindungi tadahan air, memperbaharui tanah dan mengitar semula nutrien.Kepentingan biodiversiti tidak dapat dinafikan, malah di sesetengah kawasan yang mempunyai jumlah biodiversiti yang sedikit seperti di gurun, kehadiran beberapa spesies di kawasan itu masing-masing mempunyai peranan penting kepada semua hidupan di kawasan itu.Penyelidik Pemodelan Ekologi Pusat Penyelidikan Strategik, Alam Sekitar dan Sumber Semula Jadi di Institut Penyelidikan dan Pembangunan Pertanian Malaysia (Mardi), Dr Mohd Norowi Hamid, berkata haiwan termasuk serangga sebenarnya membantu produktiviti tumbuhan, selain menyumbang kepada kesuburan tanah dan mengatur populasi serangga perosak. Katanya, tumbuhan serta rumput pula membantu memastikan sumber air bersih dan mengawal banjir, manakala mikro organisma memainkan peranan mengurai bahan organik termasuk membentuk tanah, membantu pergerakan udara dan air serta memusnahkan serangga perosak. Banyak kajian mendapati ada langkah yang boleh dijalankan untuk mengendalikan pewujudan bersama antara hidupan alam sekitar dan pertanian.Dr Mohd Norowi berkata, serangga turut menyumbang kepada ekologi, tanpanya fungsi ekosistem mungkin tidak seimbang.“Serangga adalah antara binatang yang mula memproses tumbuhan kepada protein dan menyediakan makanan dalam rantai makanan dan turut bertindak sebagai ejen kitar semula.“Malah serangga turut membantu meningkatkan tahap kesuburan tanah dan menjadi ejen pengawalan biologi serta ejen pendebungaan,” katanya.Katanya, tanpa pengurusan sempurna, pertanian akan menghapuskan habitat hidupan liar.Beliau berkata, kehilangan habitat yang disebabkan pembangunan pertanian dan perubahan tanah pertanian menjadi bandar dikenal pasti sebagai ancaman moden yang serius terhadap pengekalan biodiversiti.Katanya, separuh daripada hutan, kawasan tropika digunakan untuk pembangunan, manakala lebih satu pertiga padang rumput dan savana turut digunakan untuk kegiatan pertanian. Di Asia Tenggara, penggunaan tanah pertanian meningkat 11 juta hektar tanah dalam tempoh 1980-an hingga awal 1990-an dengan kebanyakannya adalah tanah hutan yang diterokai. Selain itu pertanian turut menyebabkan pencemaran bahan kimia yang akhirnya boleh mengurangkan biodiversiti.Setiap tahun, negara membelanjakan kira-kira RM300 juta untuk racun serangga dengan 75 hingga 85 peratus daripadanya adalah racun rumpai. Kebanyakan daripada racun serangga ini menyumbang kepada hasil tanaman.“Dianggarkan separuh daripada pengeluaran gandum akan musnah jika petani tidak menggunakan racun serangga.“Malangnya, kebanyakan racun serangga juga mempunyai kesan buruk terhadap biodiversiti, sama ada melalui racun kimia oleh haiwan atau melalui pencemaran air dan habitatnya,” katanya.Sisa racun serangga boleh mengganggu hidupan dalam air dan pesisiran pantai, termasuk batu karang, hutan paya bakau dan rumpai laut.Pertanian perlu diuruskan dengan baik bagi melindungi biodiversiti, nilai habitat dan pada masa sama menyediakan bekalan makanan serta pendapatan kepada penduduk.Pengurusan ekosistem yang dijalankan dengan gabungan strategi untuk menyediakan sumber makanan dan pada masa sama melindungi haiwan boleh menjadi langkah berkesan pengekalan biodiversiti.Pertanian berasaskan ekologi adalah sistem pertanian yang tidak bergantung sepenuhnya kepada bahan kimia, sebaliknya menggunakan tindak balas ekologi sedia ada untuk meningkatkan produktiviti dan perlindungan.Melalui pengurusan kegunaan biodiversiti ini, dunia tidak perlu lagi bergantung sepenuhnya kepada bahan kimia.Sebagai pusat mega biodiversiti, Malaysia mempunyai banyak pilihan ejen biologi yang lebih selamat digunakan termasuk bakteria, tumbuhan, haiwan dan bahan galian.Ejen biologi secara amnya mempunyai sasaran yang terhad dan mekanisme tindak balas yang khusus untuk menghapuskan perosak. Ada tiga jenis ejen biologi bagi mengawal makhluk perosak iaitu ejen tumbuhan, biokimia dan mikrob. Ejen tumbuhan dihasilkan daripada bahan biak baka yang dimasukkan dalam sesuatu pokok.Ejen biokimia pula adalah bahan asli yang mempunyai mekanisme tindak balas tidak bersifat toksik, manakala ejen mikrob terdiri daripada bakteria, kulat, virus dan protozoa sebagai bahan aktif.Pertanian organik adalah antara pertanian ekologi yang bergantung kepada sumber semula jadi untuk meningkatkan hasil pertanian dan pemprosesan makanan.Dr Norowi berkata, antara strategi mewujudkan dasar pertanian ekologi ialah dengan mengurangkan kemusnahan habitat melalui peningkatan produktiviti pertanian dan pengekalan tanah pertanian sedia ada.Katanya, jika produktiviti ditingkatkan, keperluan untuk membuka kawasan pertanian baru menurun dan secara tidak langsung mengelak daripada pemusnahan habitat biodiversiti.Selain itu, katanya, penyediaan sebahagian kecil kawasan pertanian bertujuan mengekalkan habitat tumbuhan dan haiwan sedia ada turut menyumbang kepada pertanian ekologi.Sebagai contoh, katanya, negara Eropah turut memberikan bayaran kepada petani yang mengekalkan habitat semula jadi di ladang mereka.Beliau berkata, kita juga perlu melindungi lebih banyak kawasan berhampiran tanah pertanian yang mengekalkan habitat asal kerana ia boleh bertindak meningkatkan produktiviti pertanian, selain menjadi kawasan tadahan hujan.Pelaksanaan kaedah pertanian yang mengurangkan pencemaran perlu diamalkan bagi mewujudkan pertanian ekologi.Sistem pertanian intensif melalui penggunaan racun serangga dan baja boleh meningkatkan hasil tetapi penggunaan yang berlebihan tanpa pengurusan cekap boleh menyebabkan pencemaran alam sekitar melalui sisa penggunaan racun dan baja.Contohnya di Wilayah Yunnan, selatan China, petani berjaya mengurangkan penggunaan racun serangga melalui penanaman pelbagai jenis padi dalam satu kawasan yang boleh mengawal masalah penyakit.Kajian menunjukkan melalui kaedah itu membantu mencegah penyakit dan secara tidak langsung meningkatkan hasil sehingga 89 peratus.Peningkatan kaedah pengurusan sumber semula jadi juga membantu banyak spesies liar yang berbeza hidup. Contohnya kaedah pembalakan yang baik akan mencegah kerosakan dan meningkatkan pokok yang ada terus hidup. Pertanian berasaskan ekologi menyediakan garis panduan untuk membangunkan kepelbagaian kaedah yang memberikan kelebihan kepada kesan gabungan tumbuhan dan haiwan biodiversiti.Pertanian ekologi berupaya meningkatkan ekonomi dan mengekalkan agrosistem melalui sistem pengurusan yang selaras dengan keadaan alam sekitar dan sosio ekonomi.Dalam strategi pertanian berasaskan ekologi ini, komponen pengurusan mementingkan pengekalan dan perkembangan sumber pertanian seperti tanah, fauna, tumbuhan dan biodiversiti dengan menitikberatkan kaedah pembangunan yang menggalakkan petani turut bekerjasama menjalankan kegiatan pertanian yang selaras dengan keperluan sosio ekonomi dan keadaan alam sekitar.Peningkatan kesedaran di kalangan orang ramai dan masyarakat mengenai isu biodiversiti penting dengan setiap orang mempunyai tanggungjawab untuk menghormati kewujudan makhluk di dunia, di samping mengurangkan tindakan yang boleh merosakkan alam sekitar kerana setiap organisme mempunyai fungsi tersendiri dan saling berkait rapat dalam memastikan dunia ini terus sejahtera. Tidak salah jika masyarakat turut menghormati alam sekitar yang menyumbang kepada kesempurnaan kehidupan.Biodiversiti berpotensi untuk dimajukan, misalnya, tumbuh-tumbuhan dan mikro organisme jadi produk berguna seperti ubat-ubatan dan produk industri.Biodiversiti berfungsi penting dalam memastikan alam sekitar di sesebuah negara atau tempat itu terus stabil dan tidak tercemar.Contohnya, dengan adanya hutan yang dijaga baik, kita juga dapat memperoleh sumber air bersih di samping memastikan udara bersih dan suhu panas tidak meningkat secara mendadak.Biodiversiti yang diurus secara baik juga boleh mendatangkan pendapatan tinggi kepada negara. Sebagai contoh, hasil balak yang diuruskan secara mapan, ikan di laut yang terus boleh ditangkap oleh nelayan serta tumbuh-tumbuhan, mikro organisme yang berpotensi dijadikan bahan industri atau ubat-ubatan.Langkah pemuliharaan alam sekitar harus dijalankan dengan rasional dan pragmatik iaitu mengambil kira kemampuan dan juga kepentingan sesebuah negara.Tidak dinafikan negara perlu meningkatkan pembangunan demi kepentingan ekonomi tetapi khazanah alam semula jadi perlu dipulihara demi kepentingan bersama dan warisan untuk generasi akan datang

Silent Spring

Silent Spring is a book written by Rachel Carson and published by Houghton Mifflin in September 1962. The book is widely credited with launching the environmentalism movement in the West.When Silent Spring was published, Rachel Carson was already a well-known writer on natural history, but had not previously been a social critic. The book was widely read (especially after its selection by the Book-of-the-Month Club and an endorsement by Supreme Court Justice William O. Douglas), spending several weeks on the New York Times best-seller list, and inspired widespread public concerns with pesticides and pollution of the environment. Silent Spring facilitated the ban of the pesticide DDT in 1972 in the United States.The book claimed detrimental effects of pesticides on the environment, particularly on birds. Carson accused the chemical industry of spreading disinformation, and public officials of accepting industry claims uncritically. She proposed a biotic approach to pest control as an alternative to DDT, claiming that DDT had been found to cause thinner egg shells and result in reproductive problems and death.Silent Spring has made many lists of the best nonfiction books of the twentieth century. In the Modern Library List of Best 20th-Century Nonfiction it was at #5, and it was at #78 in the conservative National Review's. Most recently, Silent Spring was named one of the 25 Greatest Science Books of All-Time by the editors of Discover MagazineA follow-up book, Beyond Silent Spring, co-authored by H.F. van Emden and David Peakall, was published in 1986.

Even before Silent Spring was published by Houghton Mifflin in 1962, there was strong opposition to it. According to Time in 1999:Carson was violently assailed by threats of lawsuits and derision, including suggestions that this meticulous scientist was a "hysterical woman" unqualified to write such a book. A huge counterattack was organized and led by Monsanto, Velsicol, American Cyanamid—indeed, the whole chemical industry—duly supported by the Agriculture Department as well as the more cautious in the media.In the 1960s, biochemist and former chemical industry spokesman Robert White-Stevens stated, "If man were to follow the teachings of Miss Carson, we would return to the Dark Ages, and the insects and diseases and vermin would once again inherit the earth."Industry and agribusiness advocates continue to criticize Silent Spring. In a 2005 essay, "The Harm That Pressure Groups Can Do", British politician Dick Taverne was damning in his criticism of Carson:Carson didn't seem to take into account the vital role (DDT) played in controlling the transmission of malaria by killing the mosquitoes that carry the parasite (...) It is the single most effective agent ever developed for saving human life (...) Rachel Carson is a warning to us all of the dangers of neglecting the evidence-based approach and the need to weight potential risk against benefit: it can be argued that the anti-DDT campaign she inspired was responsible for almost as many deaths as some of the worst dictators of the last century. However, DDT has never been banned for anti-malaria use, and Carson argued in "Silent Spring" that:No responsible person contends that insect-borne disease should be ignored. The question that has now urgently presented itself is whether it is either wise or responsible to attack the problem by methods that are rapidly making it worse. The world has heard much of the triumphant war against disease through the control of insect vectors of infection, but it has heard little of the other side of the story—the defeats, the short-lived triumphs that now strongly support the alarming view that the insect enemy has been made actually stronger by our efforts. Even worse, we may have destroyed our very means of fighting. ... What is the measure of this setback? The list of resistant species now includes practically all of the insect groups of medical importance. ... Malaria programmes are threatened by resistance among mosquitoes. ... Practical advice should be 'Spray as little as you possibly can' rather than 'Spray to the limit of your capacity' ..., Pressure on the pest population should always be as slight as possible.In 2002, Reason Magazine (part of the Reason Foundation) published an essay by economist Ronald Bailey, a former fellow with the libertarian Competitive Enterprise Institute, marking the book's 40th anniversary. Both the Reason Foundation and the CEI have received substantial funding from corporations in regulated industries. Bailey argued that the book had a mixed legacy;The book did point to problems that had not been adequately addressed, such as the effects of DDT on some wildlife. And given the state of the science at the time she wrote, one might even make the case that Carson's concerns about the effects of synthetic chemicals on human health were not completely unwarranted. Along with other researchers, she was simply ignorant of the facts. But after four decades in which tens of billions of dollars have been wasted chasing imaginary risks without measurably improving American health, her intellectual descendants don't have the same excuse.

Organic Pesticides

You may prefer to use a "natural" or "organic" pesticide when you need to control a pest. Organic pesticides are usually considered as those pesticides that come from natural sources. These natural sources are usually plants, as is the case with pyrethrum (pyrethins), rotenone or ryania (botanical insecticides), or minerals, such as boric acid, cryolite, or diatomaceous earth. Organic pesticides are largely insecticides.
Even if a product is considered to be organic, it is still a pesticide. It is important to be careful when using any pesticide, even organic or natural pesticides. Just because a product is thought to be organic, or natural, does not mean that it is not toxic. Some organic pesticides are as toxic, or even more toxic, than many synthetic chemical pesticides. Organic pesticides have specific modes of action, just as do synthetic pesticides.
To determine the relative toxicity of any pesticide to humans, check the signal word given on the pesticide label. Least toxic products carry the signal word CAUTION on their label. Products with the signal word WARNING on the label are more toxic. The most toxic pesticides have the signal word DANGER on their labels. Signal words are not an indication of the potential for environmental harm.
While some organic pesticides may be nontoxic or are only slightly toxic to people, they may be very toxic to other animals. For instance, the organic pesticide ryania is very toxic to fish. Also, some organic pesticides may be toxic to beneficial insects, such as honeybees, if they are combined with other materials, such as combining pyrethrins with rotenone.
All pesticides, according to law, can only be used EXACTLY according to label directions. Be sure to carefully read the label of ANY pesticide you use and follow the instructions exactly as they are written. Be sure you use all pesticide products only when and where the label says they can be used.

BIOPESTICIDES
Biopesticides are an important group of pesticides that can reduce pesticide risks. Biopesticides, in general:
Have a narrow target range and a very specific mode of action;
Are slow acting;
Have relatively critical application times;
Suppress, rather than eliminate, a pest population;
Have limited field persistence and a short shelf life;
Are safer to humans and the environment than conventional pesticides;
Present no residue problems.
The two types of biopesticides are biochemical and microbial. Biochemical pesticides may have a similar structure to, and function like, naturally occurring chemicals, and have nontoxic modes of action.
Insect pheromones, for example, are naturally-occurring chemicals that insects use to locate mates. Man-made pheromones are used to disrupt insect mating by creating confusion during the search for mates, or can be used to attract male insects to traps. Pheromones are often used to detect or monitor insect populations, or in some cases, to control them.
Microbial insecticides are another kind of biopesticide. They come from naturally-occurring or genetically altered bacteria, fungi, algae, viruses or protozoans. They suppress pests by:
Producing a toxin specific to the pest;
Causing a disease;
Preventing establishment of other microorganisms through competition; or
Other modes of action.
An example of a microbial pesticide is Bacillus thuringiensis, or "Bt." Bacillus thuringiensis is a naturally occurring soil bacteria that is toxic to the larvae of several species of insects but not toxic to nontarget organisms. Bacillus thuringiensis can be applied to plant foliage or incorporated into the genetic material of crops. Bacillus thuringiensis, as discovered, is toxic to the caterpillars (larvae) of moths and butterflies. Several strains of Bt have been developed and now strains are available that control fly larvae. These can be used in controlling mosquitoes and blackflies.

Malaysia issue- Time to weed out POPs from Malaysia

Time to weed out POPs from Malaysia
Beginning October 1, 1998, chlordane - a chemical used mainly by pest control companies for the treatment of termites will be banned according to the Malaysian Pesticide Board recently. This move is indeed very appropriate since the US Environmental Protection Agency has done so ten years ago in 1988. The substance has been known for it hazardous effects both short-term and long-term. The former included gastrointestinal and neurological problems like tremors and convulsions in humans.

The long-term effects also involved other organs: the heart, the lungs and even the blood. Chronic neurotoxic effects associated with low-level exposures to the chlordane were further substantiated in a study in 1995 on protracted neurotoxicity from chlordane sprayed to kill termites. The deficits identified included that of balance, reaction time, and verbal recall. Studies too have confirmed that in animals the chemicals can cause reduced fertility and caused neurological defects in their offsprings.

In Malaysia, the choice for using chlordane is said to be because of its relative cost as compared to other available alternatives. Also, it is perceived as effective since its residue can persist in the ground for up to 40 years once it is pumped in. On the contrary this is in fact one of the major setback of chlordane because of the risk that Malaysians could be exposed to due its persistent nature in the environment. It is therefore high time that such chemicals be removed from our market as soon as possible.

The ban on the manufacture and importation of chlordane however has also raised some larger questions. Foremost, chlordane belongs to a group of chemicals generally known as "persistent organic pollutants" or POPs for short. They include similar organochlorine compounds like DDT, PCBs, furans, heptachlor, aldrin, dieldrin and endrin. Some of these are still common found in Malaysia. Many of them are used in or arise from industry, agriculture and disease vector control. They may also be created unintentionally, as by-products. As such all of them can result in environmental health risks. Because of their persistent nature, over a period of time, their concentrations can increase to levels that eventually effect health.

Dangers of other POPs
The best known example is perhaps DDT, which has been widely used for many years for vector control around the world. It has a low acute toxicity in humans and for a while was regarded as 'safe'. However, it is now recognised that DDT has a number of long-term effects including acting as "endocrine disruptor" namely in mimicking steroid hormones in the human body. Moreover, the reports of high concentrations of DDT found in human breast milk especially in developing countries point to the possibility of environmental accumulation of DDT. One prospective study based on the New York University Women's Health Study in fact, showed a significant association between body stores of the DDT metabolite, DDE, and breast cancer.

On the other hand, eldrin, another POP, is even more hazardous. As a comparison, it is reported to be between two to four times more toxic than DDT (LD 50: 16-43 mg/kg in rats), despite endrin being more readily meta-bolised. Food contamination with endrin has caused several clusters of illness worldwide especially with regard to poisoning in children. But these are often overlooked because the symptoms resembles those of encephilitis, making the cause not immediately apparent.

Yet another group of great concern is the polychlorinated biphenyls (PCBs). They have been around since 1929 but was banned more that 20 years ago in the US. PCBs are made up of more than 200 related compounds which because of their many ideal characteristics are used in a number of industrial applications, especially as insulators. Their wide acceptance have "insulated" them from being made a focus of potential health and environmental problems.
The extent to which PCBs can affect us today cannot be overemphasied since at time of their discovery as environmental and health hazards, they had been produced and used extensively for more than 3 decades.

Like most POPs, PCBs too can accumulate in the fatty tissue, and over the years it becomes clear that PCBs have been detected in food samples from all over the world. They can enter the food chains and disrupted them. The higher the level of the food chain, the greater the concentration of PCBs. Some have been passed on to eggs (for birds and fishes) as well as milk (for mammals), and eventually humans. Indeed, PCBs can be traced to humans by consuming such contaminated food, and through breast milk in the case of infants. One report submitted to the UK Department of Health stated the "[b]reast fed infants are receiving up to 17 times the tolerable amounts of dioxins and polychlorinated biphenyls (PCBs)."

PCBs and IQ
One of the most alarming exposure effects of PCBs, however is the lowering of IQ, a subtle and devastating impact. It was recently confirmed that children exposed to the low levels of PCBs in the womb grow up with low IQs, poor reading comprehension, attention deficit as well as memory problems. Even at the age of 11, maternal exposures to PCBs were correlated with lower overall IQ and lower verbal IQ score. About 11 percent of the children whose mothers has highest exposures now have IQs 6.2 points lower than average. Other researchers suggested that the mechanism of harm of PCB involves with interference with the thyroid hormones, which are essential for development of the brain.

Children exposed to PCBs in the womb at levels regarded as "background levels" in the US have also been reported to experience loss of muscle tone, poor reflexes at birth, delays in psychomotor development at ages of 6 and 12 months, and diminished visual recognition memory at 7 months. Others have reported of findings like "balky, uncooperative behaviour" suspected to be linked to exposure of higher levels of PCBs. All these invariably are related to the presence of PCBs in the environment - be it in storage, landfills, in sediment of lakes, rivers, or even oceans - apart of the larger proportion that are in use, estimated at 70 percent of the total. Given all these findings, it is therefore not suprising that a ban was imposed on PCBs by the US Congress - outlawing the manufacture, sale and distribution - as early as 1976, except in "totally enclosed" systems. Even then, although their use in heat transfer and hydraulic systems can be regarded as "closed," there is always the risk of leakage and exposure.

The question of safety
Thus, while the banning of chlordane can be seen as a step in the right direction, it by not means the only substance of concern. Many more should follow suit in the immediate future. We must continue to weed out as many POPs as possible in the shortest time frame possible until they no longer pose potential risks to the population. In fact, in a recent WHO report (1997) as part of the review five years after the Earth Summit, considerable attention has recently been focused on POPs (see box). The report commented that the use of such substances cannot be considered sustainable. Increasing evidence of the long-range transport in the environment of these substances and the consequent threats they pose to the whole globe, has prompted the international community to call for urgent global action to reduce and eliminate releases and emissions of these chemicals.

Among the twelve POPs under initial consideration for international action, DDT is the only insecticide still in use for public health purposes, notably vector control. DDT has made major impact to the eradication, or virtual eradication of malaria from a number of countries, including Malaysia. Even then the use has declined following development of vector-resistance, reduction in its global production and adverse recent findings.
In other words, the POPs is fast losing its 'popularity' and Malaysians should be spared of any potential hazardous that could arise from being accessible to such hazardous substances. The only way that this can happen for certain is by eliminating all of them from our mwrektt as soon as possible.N

Agriculture Subsidies

It's raining agriculture subsidies in the USA and Europe, causing drought in Africa!
Nicholson Cartoons.

Organophosphate_Types of Pesticides

One of the products of the reaction of Fc2P2S4 with dimethyl cyanamide

An organophosphate (sometimes abbreviated OP) is the general name for esters of phosphoric acid and is one of the organophosphorus compounds. They can be found as part of insecticides, herbicides, and nerve gases, amongst others. Some less-toxic organophosphates can be used as solvents, plasticizers, and EP additives.
Early pioneers in the field include Jean Louis Lassaigne (early 1800s) and Philip de Clermount (1854). In 1932, German chemist Willy Lange and his graduate student, Gerde von Krueger, first described the cholinergic nervous system effects of organophosphates, noting a choking sensation and a dimming of vision after exposure. This discovery later inspired German chemist Gerhard Schrader at company I.G. Farben in the 1930s to experiment with these compounds as insecticides. Their potential use as chemical warfare agents soon became apparent, and the Nazi government put Schrader in charge of developing organophosphate (in the broader sense of the word) nerve gases. Schrader's laboratory discovered the G series of weapons, which included Sarin, Tabun, and Soman. The Nazis produced large quantities of these compounds, though did not use them during World War II (likely because they feared the Allies possessed similar weapons). British scientists experimented with an anticholinergic organophosphate of their own, called diisopropylfluorophosphate (DFP), during the war. The British later produced VX nerve gas, which was many times more potent than the G series, in the early 1950s.
After World War II, American companies gained access to some information from Schrader's laboratory, and began synthesizing organophosphate pesticides in large quantities. Parathion was among the first marketed, followed later by malathion and azinphosmethyl. The popularity of these insecticides increased after many of the organochlorine insecticides like DDT, dieldrin, and heptachlor were banned in the 1970s.

Organophosphate pesticides
In health, agriculture, and government, the word "organophosphates" refers to a group of insecticides or nerve agents acting on the enzyme acetylcholinesterase (the pesticide group Carbamates also act on this enzyme, but through a different mechanism). Organophosphate pesticides (as well as Sarin and VX nerve gas) irreversibly inactivate acetylcholinesterase, which is essential to nerve function in insects, humans, and many other animals. Organophosphate pesticides have tremendous variation in their ability to affect this enzyme, and thus in their potential for poisoning. For instance, parathion, one of the first OPs discovered, is many times more potent than malathion, an insecticide used in combatting the Mediterranean fruit fly (Med-fly) and West Nile Virus-transmitting mosquitoes.
Organophosphate pesticides tend to degrade rapidly on exposure to sunlight, air, and soil, though small amounts can persist and end up in food and drinking water. Their ability to degrade made them an attractive alternative to the persistent organochlorine pesticides, such as DDT, aldrin, and dieldrin, which were widely publicized in Rachel Carson's Silent Spring. While organophosphates degrade faster than the organochlorines, they have much greater acute toxicity, posing risks to farmworkers, pesticide applicators, and anyone else who may be exposed to large amounts. OP poisoning can be very serious and even cause death. See the Toxicity section below for the effects. Their toxicity is not limited to the acute phase, however, and chronic effects have long been noted. Neurotransmitters such as acetylcholine (which is affected by organophosphate pesticides) are profoundly important in the brain's development, and many OPs have neurotoxic effects on developing organisms even from low levels of exposure.
Commonly used organophosphates have included Parathion, Malathion, Methyl parathion, Chlorpyrifos, Diazinon, Dichlorvos, Phosmet, Azinphos methyl.

Example
A good example of this chemistry are the P-thiocyanate compounds which use an aryl (or alkyl) group and an alkylamino group as the lipophilic groups. The thiocyanate is the leaving group.

It was claimed in a German patent that the reaction of 1,3,2,4-dithiadiphosphetane 2,4-disulfides with dialkyl cyanamides formed plant protection agents which contained six membered (P-N=C-N=C-S-) rings. It has been proven in recent times by the reaction of diferrocenyl 1,3,2,4-dithiadiphosphetane 2,4-disulfide (and Lawesson's reagent) with dimethyl cyanamide that in fact a mixture of several different phosphorus-containing compounds is formed. Depending on the concentration of the dimethyl cyanamide in the reaction mixture either a different six membered ring compound (P-N=C-S-C=N-) or a nonheterocylic compound (FcP(S)(NR2)(NCS)) is formed as the major product, the other compound is formed as a minor product.
In addition small traces of other compounds are also formed in the reaction. It is unlikely that the ring compound (P-N=C-S-C=N-) {or its isomer} would act as a plant protection agent, but (FcP(S)(NR2)(NCS)) compounds can act as nerve poisons in insects.

Agent Orange

Vietnam. Defoliation Mission. A UH-1D helicopter from the 336th Aviation Company sprays a defoliation agent on a dense jungle area in the Mekong delta., July 26, 1969

Agent Orange and "Super Orange" were the nicknames given to a herbicide and defoliant used by the U.S. military in its Herbicidal Warfare program during the Vietnam War.
Agent Orange was used from 1961 to 1971, and was by far the most used of the so-called "rainbow herbicides" utilized during the program. Degradation of Agent Orange (as well as Agents Purple, Pink, and Green) released dioxins, which have caused harm to the health of those exposed during the Vietnam War. Agents Blue and White were part of the same program but did not contain dioxins.
Studies of populations highly exposed to dioxin, though not necessarily Agent Orange, indicate increased risk of various types of cancer and genetic defects; the effect of long-term low-level exposure has not been established.
Since the 1980s, several lawsuits have been filed against the companies who produced Agent Orange, among them being Dow Chemical, Monsanto and Diamond Shamrock (produced only 5% ). U.S. veterans obtained a $180 million settlement in 1984, most affected veterans receiving a one-time lump sum payment of $1,200. American veterans of the war on Vietnam were seeking recognition of Agent Orange, compensation and treatment for maladies that they and their children suffered from; many Vietnam veterans exposed to Agent Orange have not been able to receive promised medical care through the VA medical system and only with rare exception have their affected children received healthcare assistance from the government. Vietnam veterans and their families who brought the original Agent Orange lawsuit stated 25 years ago that the government "is just waiting for us all to die". They alleged that most of those still alive will succumb to the effects of toxic exposure over the next several years, before age 65. Elsewhere, Australian, Canadian and New Zealand veterans obtained compensation in an out-of-court settlement that same year. In 1999, South Korean veterans filed a lawsuit in Korea; in January 2006, the Korean Appeal Court ordered Monsanto and Dow to pay $62 million in compensation. However, no Vietnamese have obtained compensation, and on March 10, 2005 Judge Jack Weinstein of Brooklyn Federal Court dismissed the lawsuit filed by the Vietnamese victims of Agent Orange against the chemical companies that produced the defoliants/herbicides.

Description
Agent Orange, given its name from the 55 US gallon orange-striped barrels it was shipped in, is a roughly 1:1 mixture of two phenoxy herbicides in ester form, 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T). These herbicides were developed during the 1940s by independent teams in England and the United States for use in controlling broad-leaf plants. Phenoxy agents work by mimicking a plant growth hormone, indoleacetic acid (IAA). When sprayed on broad-leaf plants they induce rapid, uncontrolled growth, eventually defoliating them. When sprayed on crops such as wheat or corn, it selectively kills just the broad-leaf plants in the field - the weeds - leaving the crop relatively unaffected. First introduced in 1946, these herbicides were in widespread use in agriculture by the middle of the 1950s and was first introduced in the agricultural farms of Aguadilla, Puerto Rico.
At the time Agent Orange was sold to the U.S. government for use in Vietnam, internal memos of its manufacturers reveal it was known that a dioxin, 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD), is produced as a byproduct of the manufacture of 2,4,5-T, and was thus present in any of the herbicides that used it. The National Toxicology Program has classified TCDD to be a human carcinogen, frequently associated with soft-tissue sarcoma, Non-Hodgkin's lymphoma, Hodgkin's disease and chronic lymphocytic leukemia (CLL). 2,4,5-T has since been banned for use in the US and many other countries.
Although the herbicide 2,4-D does not contain dioxin, its impact on health and environment has not been thoroughly studied, and it remains one of the most-used herbicides in the world today.
Diseases associated with dioxin, again not necessarily Agent Orange, exposure are chloracne, soft tissue sarcomas, Hodgkin's lymphoma, and non-Hodgkin's lymphoma. A link has also been found to diabetes, in a study by the Institute of Medicine. Diseases with limited evidence of an association with Agent Orange are respiratory cancers, prostate cancer, multiple myeloma, Porphyria cutanea tarda (a type of skin disease), acute and subacute transient peripheral neuropathy, spina bifida, Type 2 diabetes, and acute myelogenous leukemia found only in the second or third generation. Diseases with inadequate or insufficient evidence of an association are hepatobiliary cancers, nasal or nasopharyngeal cancers, bone cancer, female reproductive cancers, renal cancer, testicular cancer, leukemia, spontaneous abortion, birth defects, neonatal or infant death and stillbirths, low birth weight, childhood cancers, abnormal sperm parameters, cognitive neuropsychiatric disorders, ataxia, peripheral nervous system disorders, circulatory disorders, respiratory disorders, skin cancers, urinary and bladder cancer. Diseases with limited or suggestive evidence of no association are gastrointestinal tumors such as stomach cancer, pancreatic cancer, colon cancer, and rectal cancer, and brain tumors.
Agent orange is currently used in the United States as a defoliant for cotton before it is harvested. Therefore it is found in small amounts in cottonseed oil, which is not regulated by the United States Food and Drug Administration (FDA). Cottonseed oil is a cheap oil that is commonly used by snack chip manufacturers.

Use Outside of Vietnam
In September 2000, the United States Veteran's Association (VA) recognized that Agent Orange was used in Korea in the late 1960s. Republic of Korea troops are reported to have done the spraying, which occurred along the DMZ with North Korea. The VA has also acknowledged that Agent Orange was used domestically by U.S. forces, as well as in Canada during the same time period

Effects of the program
The New Jersey Agent Orange Commission
In 1980, New Jersey created the New Jersey Agent Orange Commission, the first state commission created to study its effects. The Commission's research project in association with Rutgers University was called "The Pointman Project". It was disbanded by governor Christine Todd Whitman in 1996. New York Times, 3 July 1996.
During Pointman I, Commission researchers devised ways to determine small dioxin levels in blood. Prior to this, such levels could only be found in the adipose (fat) tissue. The project compared dioxin levels in a small group of Vietnam veterans who had been exposed to Agent Orange with a group of matched veterans who had not served in Vietnam. The results of this project were published in the Journal of the American Medical Association (JAMA) in 1988. (Vol. 259 No. 11, 18 March 1988).
The second phase of the project continued to examine and compare dioxin levels in various groups of Vietnam veterans including Army, Marines and brown water riverboat Navy personnel. In addition, the Commission was the only agency to examine such levels in women who served in Vietnam.

Lawsuits
In 1984, Agent Orange manufacturers paid Australian, Canadian and New Zealand veterans in an out-of-court settlement.

U.S. Vietnamese victims class action lawsuit
On January 31, 2004, a victim's rights group, the Vietnam Association for Victims of Agent Orange/Dioxin (VAVA), filed a lawsuit in a US Federal District Court in Brooklyn, New York, against several US companies, for liability in causing personal injury, by developing and producing the chemical. Dow Chemical and Monsanto were the two largest producers of Agent Orange for the US military, and were named in the suit along with the dozens of other companies (Diamond Shamrock, Uniroyal, Thompson Chemicals, Hercules, etc.). A number of lawsuits by American GIs were settled out of court - without admission of liability by the chemical companies - in the years since the Vietnam War. In 1984, some chemical companies that manufactured Agent Orange paid $180 million into a fund for United States veterans following a lawsuit.
On March 10, 2005, the District Court judge Jack Weinstein - who had defended the US veterans victims of Agent Orange - dismissed the suit, ruling that there was no legal basis for the plaintiffs' claims. The judge concluded that Agent Orange was not considered a poison under international law at the time of its use by the US; that the US was not prohibited from using it as an herbicide; and that the companies which produced the substance were not liable for the method of its use by the government. The US government is not a party in the lawsuit, claiming sovereign immunity.

On September 30, 2005, the Vietnamese victims lodged an appeal in the Second Circuit Court of Appeals; it is expected that the Court of Appeals will hold an oral argument sometime in Fall 2006. At this point the appeal is focused on whether or not the case will be reinstated and go to trial.

In order to assist those who have been impacted by Agent Orange/Dioxin, the Vietnamese have established "Peace villages", which each host between 50 to 100 victims, giving them medical and psychological help. As of 2006, there were 11 such Peace villages, thus granting some social protection to fewer than a thousand victims. US veterans of the war in Vietnam, NGOs and individuals who are aware and sympathetic to the impacts of Agent Orange have also supported these programs in Vietnam. An international group of Veterans from the US and its allies during the Vietnam war working together with their former enemy - veterans from the Vietnam Veterans Association - established the Vietnam Friendship Village located outside of Hanoi. The center provides medical care, rehabilitation and vocational training for children and veterans from Vietnam who have been impacted by Agent Orange.
The US Department of Veterans Affairs has listed prostate cancer, respiratory cancers, multiple myeloma, type II diabetes, Hodgkin’s disease, non-Hodgkin’s lymphoma, soft tissue sarcoma, chloracne, porphyria cutanea tarda, peripheral neuropathy, and spina bifida in children of veterans exposed to Agent Orange as side effects of the herbicide.

South Korean lawsuit
In 1999, about 20,000 South Koreans filed two separated lawsuits against US companies, seeking more than $5 billion in damages. After losing a decision in 2002, they filed an appeal. In January 2006, the South Korean Appeals Court ordered Dow Chemical and Monsanto to pay $62 million in compensation to about 6,800 people. The ruling acknowledged that "the defendants failed to ensure safety as the defoliants manufactured by the defendants had higher levels of dioxins than standard", and, quoting the U. S. National Academy of Science report, declared that there was a "causal relationship" between Agent Orange and 11 diseases, including cancers of the lung, larynx and prostate. However, the judges failed to acknowledge "the relationship between the chemical and peripheral neuropathy, the disease most widespread among Agent Orange victims" according to the Mercury News.

Minamata disease

Minamata disease (水俣病, Minamata-byō?), sometimes referred to as Chisso-Minamata disease (窒素水俣病, Chisso-Minamata-byō?), is a neurological syndrome caused by severe mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, general muscle weakness, narrowing of the field of vision and damage to hearing and speech. In extreme cases, insanity, paralysis, coma and death follow within weeks of the onset of symptoms. A congenital form of the disease can also affect fetuses in the womb.
Minamata disease was first discovered in Minamata city in Kumamoto prefecture, Japan in 1956. It was caused by the release of methyl mercury in the industrial wastewater from the Chisso Corporation's chemical factory, which continued from 1932 to 1968. This highly toxic chemical bioaccumulated in shellfish and fish in Minamata Bay and the Shiranui Sea, which when eaten by the local populace resulted in mercury poisoning. While cat, dog, pig and human deaths continued over more than 30 years, the government and company did little to prevent the pollution.
As of March 2001, 2,265 victims had been officially recognised (1,784 of whom had died) and over 10,000 had received financial compensation from Chisso.Lawsuits and claims for compensation continue to this day.
A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965. Both the original Minamata disease and Niigata Minamata disease are considered two of the Four Big Pollution Diseases of Japan.

Background, 1908-1955


Wastewater discharge from the Chisso factory in Minamata
The Chisso Corporation first opened a chemical factory in Minamata in 1908. Initially producing fertilisers, the factory followed the nationwide expansion of Japan's chemical industry, branching out into production of acetylene, acetaldehyde, acetic acid, vinyl chloride and octanol, among others. The Minamata factory became the most advanced in all Japan, both before and after World War II. The waste products resulting from the manufacture of these chemicals were released into Minamata Bay in the factory wastewater. Inevitably these pollutants had an environmental impact. Fisheries were damaged in terms of reduced catches and in response Chisso reached two separate compensation agreements with the fishery cooperative in 1926 and 1943.
The rapid expansion of the Minamata factory spurred on the local economy and as Chisso prospered, so did Minamata. This fact, combined with the lack of other industry, meant that Chisso had great influence in Minamata. At one stage over half of the tax revenue of Minamata City authority came from Chisso and its employees and the company and its subsidiaries were responsible for creating a quarter of all jobs in Minamata.Minamata was even dubbed Chisso's "castle town", in reference to the capital cities of feudal lords who ruled Japan during the Edo period.
The Chisso Minamata factory first started acetaldehyde production in 1932, producing 210 tons that year. By 1951 production had jumped to 6,000 tons per year: over 50% of Japan's total output. The chemical reaction used to produce the acetaldehyde used mercury sulfate as a catalyst. A side reaction of the catalytic cycle led to the production of a small amount of an organic mercury compound, namely methyl mercury.This highly toxic compound was released into Minamata Bay from the start of production in 1932 until 1968 when this production method was discontinued.

Discovery and Investigation, 1956-1959
On April 21, 1956, a five-year-old girl was examined at the Chisso Corporation's factory hospital in Minamata, Japan, a town on the west coast of the southern island of Kyūshū. The physicians were puzzled by her symptoms: difficulty walking, difficulty speaking and convulsions. Two days later her younger sister also began to exhibit the same symptoms and she too was hospitalised. The girls' mother informed doctors that her neighbour's daughter was also experiencing similar problems. After a house-to-house investigation eight further patients were discovered and hospitalised. On May 1, the hospital director reported to the local public health office the discovery of an "epidemic of an unknown disease of the central nervous system", marking the official discovery of Minamata disease.
To investigate the epidemic, the city government and various medical practitioners formed the Strange Disease Countermeasures Committee (奇病対策委員会, Kibyō Taisaku Iinkai?) at the end of May, 1956. Owing to the localised nature of the disease, it was suspected to be contagious and as a precaution patients were isolated and their homes disinfected. Unfortunately, this contributed to the stigmatisation and discrimination experienced by Minamata victims from the local community. During their investigations the committee uncovered surprising anecdotal evidence of the strange behaviour of cats and other wildlife in the areas surrounding patient's homes. From around 1950 onwards cats had been seen to have convulsions, go mad and die. Locals called it the "cat dancing disease", owing to their erratic movement. Crows had fallen from the sky, seaweed no longer grew on the sea bed and fish floated dead on the surface of the sea. As the extent of the outbreak was understood, the committee invited researchers from Kumamoto University to help in the research effort.
The Kumamoto University Research Group was formed on August 24, 1956. Researchers from the School of Medicine began visiting Minamata regularly and admitted patients to the university hospital for detailed examinations. Gradually a more complete picture of the symptoms exhibited by patients was uncovered. The disease developed without any prior warning, with patients complaining of a loss of sensation and numbness in their hands and feet. They became unable to grasp small objects or fasten buttons. They could not run or walk without stumbling, their voices changed in pitch and many patients complained of difficulties seeing, hearing and swallowing. In general these symptoms deteriorated and were followed by severe convulsions, coma and eventually death. By October 1956, 40 patients had been discovered, 14 of whom had died: an alarming mortality rate of 36.7%.

Finding the cause
Researchers from Kumamoto University also began to focus on the cause of the strange disease. They found that the victims, often members of the same family, were clustered in fishing hamlets along the shore of Minamata Bay. The staple food of victims was invariably fish and shellfish from Minamata Bay. The cats in the local area, who tended to eat scraps from the family table, had died with symptoms similar to those now discovered in humans. This led the researchers to believe that the outbreak was caused by some kind of food poisoning, with contaminated fish and shellfish the prime suspects.
On November 4 the research group announced their initial findings: "Minamata disease is rather considered to be poisoning by a heavy metal... presumably it enters the human body mainly through fish and shellfish."

Identification of mercury

Methylmercury, an organic mercury compound released in factory wastewater and the cause of Minamata disease
As soon as the investigation identified a heavy metal as the causal substance, the wastewater from the Chisso plant was immediately suspected as the origin. The company's own tests revealed that its wastewater contained many heavy metals in concentrations sufficiently high to bring about serious environmental degradation including lead, mercury, manganese, arsenic, selenium, thallium and copper. Identifying which particular poison was responsible for the disease proved to be extremely difficult and time consuming. During the years 1957 and 1958 many different theories were proposed by different researchers. Initially manganese was thought to be the causal substance due to the high concentrations found in fish and the organs of the deceased. Thallium, selenium and a multiple contaminant theory were also proposed but it was not until March 1958, when visiting British neurologist Douglas McAlpine suggested that Minamata symptoms resembled those of organic mercury poisoning, that the focus of the investigation centred on mercury.
In February 1959 the mercury distribution in Minamata Bay was investigated. The results shocked the researchers involved. Large quantities of mercury were detected in fish, shellfish and sludge from the bay. The highest concentrations were centred around the Chisso factory wastewater canal in Hyakken Harbour and decreased going out to sea, clearly identifying the plant as the source of contamination. At the mouth of the wastewater canal a figure of 2 kg of mercury per ton of sediment was measured: a level which would be economically viable to mine, (indeed, Chisso did later set up a subsidiary to reclaim and sell the mercury recovered from the sludge).
Hair samples were taken from the victims of the disease and also from the Minamata population in general. In patients the maximum mercury level recorded was 705 ppm (parts per million), indicating very heavy exposure and in non-symptomatic Minamata residents the level was 191 ppm. This compared to an average level of 4 ppm for people living outside the Minamata area.
On November 12, 1959 the Ministry of Health and Welfare's Minamata Food Poisoning Subcommittee published its results:
"Minamata disease is a poisoning disease that affects mainly the central nervous system and is caused by the consumption of large quantities of fish and shellfish living in Minamata Bay and its surroundings, the major causative agent being some sort of organic mercury compound."

Chisso's responses, 1959


The Chisso factory and its wastewater routes
During the investigation by researchers at Kumamoto University, the causal substance had been identified as a heavy metal and it was widely presumed that the Chisso plant was the source of the contamination. Chisso was coming under closer scrutiny and in order to deflect criticism the wastewater output route was changed. Chisso knew the environmental damage caused by its wastewater and was well aware that it was the prime suspect in the Minamata disease investigation. Despite this, from September 1958, instead of discharging its waste into Hyakken Harbour (the focus of investigation and source of original contamination), it discharged wastewater directly into Minamata River. The immediate effect was the death of fish at the mouth of the river, and from that point on new Minamata disease victims began to appear in other fishing villages up and down the coast of the Shiranui Sea, as the pollution spread over an even greater area.
Chisso failed to co-operate with the investigation team from Kumamoto University. It withheld information on its industrial processes, leaving researchers to speculate what products the factory was producing and by what methods. The Chisso factory's hospital director, Hajime Hosokawa, established a laboratory in the research division of the plant to carry out his own experiments into Minamata disease in July 1959. Food to which factory wastewater had been added was fed to healthy cats. 78 days into the experiment cat 400 exhibited symptoms of Minamata disease and pathological examinations confirmed a diagnosis of organic mercury poisoning. The company did not reveal these significant results to the investigators and ordered Hosokawa to stop his research.
In an attempt to undermine Kumamoto University researcher's organic mercury theory, Chisso and other parties with a vested interest that the factory remain open (including the Ministry of International Trade and Industry and the Japan Chemical Industry Association) funded research into alternative causes of the disease, other than its own waste.

Compensation of fishermen and patients, 1959
Polluting wastewater had damaged the fisheries around Minamata ever since the opening of the Chisso factory in 1908. The Minamata Fishing Cooperative had managed to win small payments of "sympathy money" (見舞い金, mimaikin?) from the company in 1926 and again in 1943, but after the outbreak of Minamata disease the fishing situation was becoming critical. Fishing catches had declined by 91% between the years 1953 and 1957. The Kumamoto prefectural government issued a partial ban on the sale of fish caught in the heavily polluted Minamata Bay, but not an all-out ban, which would have legally obliged it to compensate the fishermen. The fishing cooperative protested against Chisso and angrily forced their way into the factory on 6 August and 12 August, demanding compensation. A committee was set up by Minamata Mayor Todomu Nakamura to mediate between the two sides but this committee was stacked heavily in the company's favour. On 29 August the fishing cooperative agreed to the mediation committee's proposal, stating: "In order to end the anxiety of the citizens, we swallow our tears and accept". The company paid the cooperative JPY20 million (USD55,600) and set up a JPY15 million (USD41,700) fund to promote the recovery of fishing.


Protestors at the gates of the Chisso factory (W. E. Smith)
Since the change of route of wastewater output in 1958, pollution had spread up and down the Shiranui Sea, damaging fisheries there too. Emboldened by the success of the small Minamata cooperative, the Kumamoto Prefectural Alliance of Fishing Cooperatives also decided to seek compensation from Chisso. On 17 October, 1,500 fishermen from the alliance descended on the factory to demand negotiations. When this produced no results the alliance members took their campaign to Tokyo, securing an official visit to Minamata by members of the Japanese Diet. During the visit on 2 November alliance members forced their way into the factory and rioted, causing many injuries and JPY10 million (USD27,800) worth of damage. The violence was covered widely in the media, bringing the nation's attention to the Minamata issue for the first time since the outbreak began. Another mediation committee was set up, an agreement hammered out and signed on 17 December. JPY25 million "sympathy money" was paid to the alliance and a JPY65 million fishing recovery fund established.
In 1959, the victims of Minamata disease were in a much weaker position than the fishermen. The recently-formed Minamata Disease Patients Families Mutual Aid Society was much more divided than the fishing cooperatives. Patients' families were the victim of discrimination and ostracism from the local community. Local people felt that the company (and their city that depended upon it) was facing economic ruin. To some patients this ostracism by the community represented a greater fear than the disease itself. After beginning a sit-in at the factory gates in November 1959 the patients asked Kumamoto Prefecture Governor Hirosaku Teramoto to include the patients' request for compensation with the mediation that was ongoing with the prefectural fishing alliance. Chisso agreed and after a few weeks' further negotiation, another "sympathy money" agreement was signed. Patients who were certified by a Ministry of Health and Welfare committee would be compensated: adult patients received JPY100,000 (USD278) per year; children JPY30,000 (USD83) per year and families of dead patients would receive a one-off JPY320,000 (USD889) payment.

Wastewater treatment
On 21 October Chisso was ordered by the Ministry of International Trade and Industry to switch back its wastewater drainage from the Minamata River to Hyakken Harbour and to speed up the installation of wastewater treatment systems at the factory. Chisso duly installed a Cyclator purification system on 19 December 1959, and opened it with a special ceremony. Chisso's president Kiichi Yoshioka dared to drink a glass of water supposedly treated through the Cyclator to demonstrate that it was safe. In fact, the wastewater from the acetaldehyde plant, which the company knew still contained mercury and led to Minamata disease when fed to cats, was not treated through the Cyclator at the time. The stunt was an outright deception. Testimony at a later Niigata Minamata disease trial proved that Chisso knew the Cyclator to be completely ineffective: "...the purification tank was installed as a social solution and did nothing to remove organic mercury."
The deception was wholly successful and almost all parties involved in Minamata disease were duped into believing that the factory's wastewater had been made safe from December 1959 on. This widespread assumption meant that doctors were not expecting new patients to appear, resulting in numerous problems in the years to follow, as the pollution continued. In most people's minds the issue of Minamata disease had been resolved.

Years of "silence" and change, 1959-69
The years between the first set of "sympathy money" agreements in 1959 and the start of the first legal action to be taken against Chisso in 1969 are often called the "ten years of silence". In fact, much activity on the part of the patients and fishermen took place during this period but nothing had a significant impact on the actions of the company or the coverage of Minamata in the national media.

Continued pollution
Despite the almost universal assumption to the contrary, the wastewater treatment facilities installed in December 1959 had no effect on the level of organic mercury being released into the Shiranui Sea. The pollution and the disease it caused continued to spread. The Kumamoto and Kagoshima prefectural governments conducted a joint survey in late 1960 and early 1961 into the level of mercury in the hair of people living around the Shiranui Sea. The results confirmed that organic mercury had spread all around the inland sea and that people were still being poisoned by contaminated fish. Hundreds of people were discovered to have levels greater than 50 ppm of mercury in their hair: the level at which people are likely to experience nerve damage. The highest result recorded was that of a lady from Goshonoura island who had 920ppm in her sample.
The prefectural governments did not publish the results and did nothing in response to these surveys. The participants who had donated hair samples were not informed of their result, even when they requested it. A follow-up study ten years later discovered that many had died from "unknown causes".

Congenital Minamata disease
Local doctors and medical officials had noticed for a long time an abnormally high frequency of cerebal palsy and other infantile disorders in the Minamata area. In 1961 a number of medical professionals including Masazumi Harada (later to receive an honour from the United Nations for his body of work on Minamata disease) set about re-examining children diagnosed with cerebral palsy. The symptoms of the children closely mirrored those of adult Minamata disease patients but many of their mothers did not exhibit symptoms. The fact that these children had been born after the initial outbreak and had never been fed contaminated fish also led their mothers to believe they were not victims. At the time the medical establishment believed the placenta to protect the foetus from toxins in the bloodstream, which is indeed the case with most chemicals. What was not known at the time was that exactly the opposite is the case with methylmercury: the placenta removes it from the mother's bloodstream and concentrates the chemical in the foetus.
After several years of study and the autopsies of two children, the doctors announced that these children were suffering from an as yet unrecognised congenital form of Minamata disease. The certification committee convened on 29 November 1962 and agreed that the two dead children and the 16 children still alive should be certified as patients, and therefore liable for "sympathy" payments from Chisso, in line with the 1959 agreement.

Outbreak of Niigata Minamata disease
Unfortunately, Minamata disease broke out again in 1965, this time along the banks of the Agano River in Niigata Prefecture. The polluting factory (owned by Showa Denko) employed a chemical process using a mercury catalyst very similar to that used by Chisso in Minamata. As in Minamata, from the autumn of 1964 to the spring of 1965, cats living along the banks of the Agano River had been seen to go mad and die. Before long patients appeared with identical symptoms to patients living on the Shiranui Sea, and the outbreak was made public on 12 June 1965. Researchers from the Kumamoto University Research Group and Hajime Hosokawa (who had retired from Chisso in 1962) used their experience from Minamata and applied it to the Niigata outbreak. In September 1966 a report was issued proving Showa Denko's pollution to be the cause of this second Minamata disease.
Unlike the patients in Minamata, the victims of Showa Denko's pollution lived a considerable distance from the factory and had no particular link to the company. As a result the local community was much more supportive of patients' groups and a lawsuit was filed against the company in March 1968, only three years after discovery.
The events in Niigata catalysed a change in response to the original Minamata incident. The scientific research carried out in Niigata forced a re-examination of that done in Minamata and the decision of Niigata patients to sue the polluting company allowed the same response to be considered in Minamata. Masazumi Harada has said that, "It may sound strange, but if this second Minamata disease had not broken out, the medical and social progress achieved by now in Kumamoto... would have been impossible."
Around this time two other pollution-related diseases were also grabbing headlines in Japan. Victims of Yokkaichi asthma and Itai-itai disease were forming citizen's groups and filed lawsuits against the polluting companies in September 1967 and March 1968 respectively. Collectively these diseases came to be known as the Four Big Pollution Diseases of Japan.
Slowly but surely the mood in Minamata and Japan as a whole was shifting. Minamata patients found the public gradually becoming more receptive and sympathetic as the decade wore on. This culminated in 1968 with the establishment in Minamata of the Citizens' Council for Minamata Disease Countermeasures which was to become the chief citizens' support group to the Minamata patients. A founding member of the citizens' council was Michiko Ishimure, a local housewife and poet who later that year published Pure Land, Poisoned Sea: Our Minamata disease (苦海浄土―わが水俣病, Kugai Jōdo: Waga Minamatabyō?) a book of poetic essays that received national acclaim.

The second solution, 1969-1973
Official government recognition
Finally on 26 September 1968 — twelve years after the discovery of the disease (and four months after Chisso had stopped production of acetaldehyde using its mercury catalyst) — the government issued an official conclusion as to the cause of Minamata disease:
"Minamata disease is a disease of the central nervous system, a poisoning caused by long-term consumption, in large amounts, of fish and shellfish from Minamata Bay. The causative agent is methyl mercury. Methyl mercury produced in the acetaldehyde acetic acid facility of Shin Nihon Chisso's Minamata factory was discharged in factory wastewater... Minamata disease patients last appeared in 1960, and the outbreak has ended. This is presumed to be due to the fact that consumption of fish and shellfish from Minamata Bay was banned in the fall of 1957, and the fact that the factory had waste-treatment facilities in place from January 1960."
The conclusion contained many factual errors: eating fish and shellfish from other areas of the Shiranui Sea, not just Minamata Bay, could cause the disease; eating small amounts, as well as large amounts of contaminated fish over a long time also produced symptoms; the outbreak had not in fact "ended" in 1960 nor had mercury-removing wastewater facilities been installed in January 1960. Nevertheless, the government announcement brought a feeling of relief to a great many victims and their families. Many felt vindicated in their long struggle to force Chisso to accept responsibility for causing the disease and expressed thanks that their plight had been recognised by their social superiors. The struggle now focused on to what extent the victims should be compensated.

Struggle for a new agreement
In light of the government announcement, the patients of the Mutual Aid Society decided to ask for a new compensation agreement with Chisso and submitted the demand on 6 October. The company replied that it was unable to judge what would be fair compensation and asked the national government to set up a binding arbitration committee to decide. This proposal split the members of the patients' society, many of whom were extremely wary of entrusting their fate to a third party, as they had done in 1959 with unfortunate results. At a meeting on 5 April 1969 the opposing views within the society could not be reconciled and the organisation split into the Arbitration Group (who were willing to accept binding arbitration) and the Litigation Group (who decided to sue the company). That summer Chisso sent gifts to the families who opted for arbitration rather than litigation.


Minamata patients and family members hold photographs of their dead during a demonstration (W. E. Smith)
An arbitration committee was duly set up by the Ministry of Health and Welfare on 25 April, but it took almost a year to draw up a draft compensation plan. A newspaper leak in March 1970 revealed that the committee would ask Chisso to pay only JPY2 million (USD5,600) for dead patients and JPY140,000 to JPY200,000 (USD390 to USD560) per year to surviving patients. The Arbitration Group were dismayed by the sums on offer. They petitioned the committee, together with patients and supporters of the Litigation Group, for a fairer deal. The arbitration committee announced their compensation plan on 25 May in a disorderly session at the Ministry of Health and Welfare in Tokyo. Thirteen protesters were arrested. Instead of accepting the agreement as they had promised, the Arbitration Group asked for increases. The committee was forced to revise its plan and the patients waited inside the Ministry building for two days while they did so. The final agreement was signed on 27 May. Payments for deaths ranged from JPY1.7 million to JPY4 million (USD4,700 to USD11,100), one-time payments from JPY1 million to JPY4.2 million (USD2,760 to USD11,660) and annual payments of between JPY170,000 and JPY380,000 (USD470 to USD1,100) for surviving patients. On the day of the signing, the Minamata Citizens' Council held a protest outside the Minamata factory gates. One of the Chisso trade unions held an eight-hour strike in protest at the poor treatment of the Arbitration Group by their own company.
The Litigation Group, representing 41 certified patients (17 already deceased) in 28 families, submitted their suit against Chisso in the Kumamoto District Court on 14 June 1969. The leader of the group, Eizō Watanabe (a former leader of the Mutual Aid Society), declared that, "Today, and from this day forth, we are fighting against the power of the state". Those who decided to sue the company came under fierce pressure to drop their lawsuits against the company. One woman was visited personally by a Chisso executive and harassed by her neighbours. She was ignored, her family's fishing boat used without permission, their fishing nets cut and human faeces thrown at her in the street.
The Litigation Group and their lawyers were helped substantially by an informal national network of citizens' groups that sprung up around the country in 1969. The Associations to Indict [Those Responsible for] Minamata Disease (水俣病を告発する会, Minamata-byō o Kokuhatsu Suru Kai?) were instrumental in raising awareness and funds for the lawsuit. The Kumamoto branch in particular was especially helpful to the case. In September 1969 they set up a Trial Research Group which included law professors, medical researchers (including Masazumi Harada), sociologists and even the housewife and poet Michiko Ishimure to provide useful material to the lawyers to improve their legal arguments. In fact their report: Corporate Responsibility for Minamata Disease: Chisso's Illegal Acts, published in August 1970, formed the basis of the ultimately successful lawsuit.
The trial lasted almost four years. The Litigation Group lawyers sought to prove Chisso's corporate negligence. Three main legal points had to be overcome to win the case. First the lawyers had to show that methylmercury caused Minamata disease and that the company's factory was the source of pollution. The extensive research by Kumamoto University and the government conclusion meant that this point was proved quite easily. Secondly, could and should the company have anticipated the effect of its wastewater and should it have taken steps to prevent the tragedy (ie. was the company negligent in its duty of care)? Thirdly, was the "sympathy money" agreement of 1959, which forbade the patients from claiming any further compensation, a legally binding contract?
The trial heard from patients and their families but the most important testimony came from Chisso executives and employees. The most dramatic testimony came from Hajime Hosokawa who spoke on 4 July 1970 from his hospital bed where he was dying of cancer. He explained his experiments with cats, including the infamous cat 400 which developed Minamata disease after being fed factory wastewater. He also spoke of his opposition to the 1958 change in wastewater output route from Hyakken Harbour to Minamata River. His testimony was backed up by a colleague who also told how company officials had ordered them to halt their cat experiments in the autumn of 1959. Hajime Hosokawa died three months after giving his testimony. Former factory manager Eiichi Nishida admitted that the company put profits ahead of safety, resulting in dangerous working conditions and a lack of care with mercury. Former Chisso President Kiichi Yoshioka admitted that the company promoted a theory of dumped WWII explosives even though it knew it to be unfounded.
The verdict handed down on 20 March 1973 represented a complete victory for the patients of the Litigation Group:
"The defendant's factory was a leading chemical plant with the most advanced technology and... should have assured the safety of its wastewater. The defendant could have prevented the occurrence of Minamata disease or at least have kept it at a minimum. We cannot find that the defendant took any of the precautionary measures called for in this situation whatsoever. The presumption that the defendant had been negligent from beginning to end in discharging wastewater from its acetaldehyde plant is amply supported. The defendant cannot escape liability for negligence."
The "sympathy money" agreement was found to be invalid and Chisso was ordered to make one-time payments of JPY18 million (USD66,000) for each deceased patient and from JPY16 million to JPY 18 million (USD59,000 to USD66,000) for each surviving patient. The total compensation of JPY937 million (USD3.4 million) was the largest sum ever awarded by a Japanese court.

Uncertified patients fight to be recognised
While the struggles of the arbitration and litigation groups against Chisso were continuing, a new groups of Minamata disease sufferers emerged. In order to qualify for compensation under the 1959 agreement, patients had to be officially recognised by various ad hoc certification committees according to their symptoms. Unfortunately, in an effort to limit the liability and financial burden on the company, these committees were sticking to a rigid interpretation of Minamata disease. They required that patients must exhibit all symptoms of Hunter-Russell Syndrome - the standard diagnosis of organic mercury poisoning at the time, which originated from an industrial accident in the United Kingdom in 1940. The committee only certified patients exhibiting explicit symptoms of the British syndrome, rather than basing their diagnosis on the disease in Japan. This resulted in many applicants being rejected by the committee, leaving them understandably confused and frustrated.
A key figure in the fight for the uncertified patients was Teruo Kawamoto. Born in 1931, he was the seventh son of a Chisso worker and local fisherman. From 1959 onwards, Teruo's father began to exhibit the typical symptoms of Minamata disease: numbness in his hands and feet, slurred speech, impaired walking and restricted vision. His condition slowly deteriorated until he was admitted to the mental hospital at which Teruo himself had found a job. Hallucinating and suicidal, his father eventually became unable to recognise anyone around him and died with his son at his bedside in April 1965.

Victims
As of March 2001, 2,265 victims have been officially certified (1,784 of whom have died)[1] and over 10,000 people have received financial compensation from Chisso, although they are not recognised as official victims. The issue of quantifying the impact of Minamata disease is complicated as a full epidemiological study has never been conducted and patients were only ever recognised if they voluntarily applied to a Certification Council in order to seek financial compensation. Many victims of Minamata disease faced discrimination and ostracism from the local community if they came out into the open about their symptoms. Some people feared the disease to be contagious and many local people were fiercely loyal to Chisso, depending on the company for their livelihoods. In this atmosphere sufferers were understandably reluctant to come forward and seek certification. Despite these factors, over 17,000 people have applied to the Council for certification. Also, in recognising an applicant as a Minamata disease sufferer, the Certification Council qualified that patient to receive financial compensation from Chisso. As such, the Council has always been under immense pressure to reject claimants and minimise the financial burden placed on Chisso. Rather than being a Council of medical recognition, the decisions of the Council were always affected by the economic and political factors surrounding Minamata and the Chisso corporation. Furthermore, compensation of the victims led to continued strife in the community, including unfounded accusations that some of the people who sought compensation did not actually suffer from the disease.

Democratizing effects
According to Timothy S. George, the environmental protests that surrounded the disease appeared to aid in the democratization of Japan.[citation needed] When the first cases were reported and subsequently suppressed, the rights of the victims were not recognized, and they were given no compensation. Instead, the afflicted were ostracised from their community due to ignorance about the disease, as people were afraid that it was contagious.
The people directly impacted by the pollution of Minamata Bay were not originally allowed to participate in actions that would affect their future. Disease victims, fishing families, and company employees were excluded from the debate. Progress occurred when Minamata victims were finally allowed to come to a meeting to discuss the issue. As a result, postwar Japan took a small step towards democracy.
Through the evolution of public sentiments, the victims and environmental protesters were able to acquire standing and proceed more effectively in their cause. The involvement of the press also aided the process of democratization because it caused more people to become aware of the facts of Minamata disease and the pollution that caused it.
Although the environmental protests did result in Japan being more democratized, it did not completely rid Japan of the system that first suppressed the fishermen and victims of Minamata disease.

Media
Photographic documentation of Minamata started in the early 1960s. One photographer who arrived in 1960 was Shisei Kuwabara, straight from university and photo school. The first exhibition of his work in Minamata was held in the Fuji Photo Salon in Tokyo in 1962, and the first of his book-length anthologies Minamata was published in Japan in 1965. He has returned to Minamata many times since.
However, it was a dramatic photographic essay by W. Eugene Smith that brought world attention to Minamata disease. He and his Japanese wife lived in Minamata from 1971 to 1973. The most famous and striking photo of the essay, Tomoko Uemura in Her Bath, (1972) shows Ryoko Uemura, holding her severely deformed daughter, Tomoko, in a Japanese bath chamber. Tomoko was poisoned by methyl mercury while still in the womb. The photo was very widely published. It was posed by Smith with the cooperation of Ryoko and Tomoko in order to dramatically illustrate the consequences of the disease. It has subsequently been withdrawn from circulation at the request of Tomoko's family, and therefore does not appear in recent anthologies of Smith's works. Smith and his wife were extremely dedicated to the cause of the victims of Minamata disease, closely documenting their struggle for recognition and right to compensation. Smith was himself attacked and seriously injured by Chisso employees in an incident in Goi, Ichihara city, near Tokyo on January 7, 1972, in an attempt to stop the photographer from further revealing the issue to the world. The 54 year-old Smith survived the attack, but his sight in one eye deteriorated and his health never fully recovered before his death in 1978.



Minamata disease today
Minamata disease remains an important issue in contemporary Japanese society. Lawsuits against Chisso and the prefectural and national governments are still continuing and many regard the government responses to date as inadequate.
A memorial service was held at the Minamata Disease Municipal Museum on 1 May 2006 to mark 50 years since the official discovery of the disease. Despite bad weather the service was attended by over 600 people, including Chisso chairman Shunkichi Goto and Environment Minister Yuriko Koike.
Most congenital patients are now in their forties and fifties and their health is deteriorating. Their parents, who are often their only source of care, are into their seventies or eighties or already deceased. Often these patients find themselves tied to their own homes and the care of their family, in effective isolation from the local community. Some welfare facilities for patients do exist. One notable example is Hot House (ほっとはうす, Hotto Hausu?), a vocational training centre for congenital patients as well as other disabled people in the Minamata area. Hot House members are also involved in raising awareness of Minamata disease, often attending conferences and seminars as well as making regular visits to elementary schools throughout Kumamoto Prefecture.