TL: GREENPEACE BRIEFING ON CHEMICAL WEAPONS (GP) SO: Greenpeace QMC DT: 18-JAN-91 Keywords: toxics chemical weapons greenpeace gp reports gulf wars middle east / INTRODUCTION Chemical weapons were first used in World War I. The fledgling chemical industry of the early 1900s quickly found ways to adapt known compounds such as pesticides for weapons use and to develop progressively more toxic war gases. Although in the Second World War, no official deployment of these weapons took place, there were accidents due to their transport, and at the end of the conflict, large stockpiles were disposed of, generally by sea dumping. Some of the captured stockpiles of chemical agents are thought to have been assimilated into the Allied stockpiles. Since then chemical weapons are known or thought to have been employed in South East Asia, by Libya against Chad and in Afghanistan. Most recently, chemical agents (mustard and nerve gases) were used in the Iran/Iraq conflict and in Iraq against the Kurdish ethnic minority. The spectre of chemical weapons use in the current conflict in the Gulf arises then, from the known possession of such agents by Iraq. Retaliatory action is possible through the large stockpiles held by the US. The US Senate did not ratify the terms of the 1925 Geneva Protocol, designed to outlaw these chemicals, until 1975. While highly effective, chemical weapons are relatively easy to make. Many facilities using glass lined production vessels can be rapidly (perhaps as little as 12 hours) configured and reconfigured to allow the manufacture of these materials. Production is relatively cheap. Add to this the overwhelming problems in policing and enforcing compliance of a global ban, and it becomes clear why chemical agents are favoured as a weapon by smaller countries with no nuclear capability. The toxicology of the major unitary agents is well known. That of the new generation of binary agents, where two relatively harmless chemicals are mixed together to produce a toxic agent, less so since this information is often subject to various provisions of secrecy. This extends to the manufacturing processes also. Iraq is thought to possess only unitary chemical agents and possibly some bacterial weapons. Members of the multinational force currently deployed in the Gulf arena have been issued with antidotes to nerve agents, inoculated against anthrax in some cases and issued with nuclear, biological and chemical protection suits. There are two scenarios whereby chemical weapons could be released to the environment. One is through attack on a chemical weapons manufacturing facility. Pinpoint bombing on identified targets has been carried out during the present conflict. If a facility was attacked in this way, then stored and stockpiled chemicals and the chemicals used in the manufacturing process could be released. Strategic release against advancing ground troops is another possibility. The following considers the types of chemical agent likely to be involved, and the effects of deployment or accidental release. TYPES OF CHEMICAL WARFARE AGENTS The chemical warfare agents possessed by Iraq are likely to include nerve agents, vesicants, the blood gases and asphyxiants. These will be held in a variety of weapons ranging from rockets and missiles to shells for conventional artillery pieces from the calibre of mortars upwards. Some may also be held in spray tanks. 1) Nerve Agents The nerve agents are all organophosphate compounds designed to enter the body through the skin or by inhalation. All these agents exhibit strong anticholinesterase activity. This means that they work by inhibiting the activity of the nervous system causing paralysis and eventual death by suppression of the respiratory system. In addition some effects are apparently unrelated to nerve transmission. The major agents are GA (Tabun), GB (Sarin), Soman and VX. All are liquid at normal temperatures and can be delivered as the warhead of a weapons system or sprayed from tanks. Variants of the basic formulae of the agents also exist. Weapon payload of examples from the US stockpile ranges from around 0.7 kilos in the M360 105mm projectile to 157 kilos in the MK-116 Weteye bomb to 615 kilos in the TMU-28/B spray tank. It can be assumed that the Iraqi forces have similarly configured chemical weapons. The nerve gases are extremely toxic. The human skin LD50 of VX agent is 0.04 mg/kg body weight. Effective inhalation doses range from 45 mg-min/cubic metre for VX to 100 mg- min/cubic metre for Sarin. In other words an ambient concentration in the air of 100 mg per cubic metre of Sarin, breathed for one minute can cause death. Similarly, 200 mg per cubic metre breathed for half a minute can cause death. Symptoms of exposure include, on an increasing scale: drooling, increased lung secretion, narrowing of the pupils, excessive sweating, vomiting, diarrhoea, involuntary urination, irregular heartbeat, convulsions and coma. Death results from respiratory failure. There is some evidence that apart from the acute toxic effects, delayed neuropathies (malfunction of the nervous system) may occur. Certainly, changes in brain current (EEG) patterns are known to result from exposure and anxiety, confusion and restlessness are recognised as symptoms. 2) Vesicant or Blister Agents. These agents are cellular poisons that destroy individual cells in target tissues. They fall into two major categories: the mustard gases and lewisite. i) Mustard gases Mustard gases such as HD and HT are liquid until temperatures reach 1-14 o C depending upon formulation. US munition specifications indicate that they are designed to be delivered by a variety of artillery projectiles and mortar shells. Substantial stocks are also held in one ton containers. Cells exposed to mustard gases are destroyed by the reaction of the chemical with cellular proteins, enzymes and nucleic acids. These are somewhat less toxic than the nerve agents with skin LD50 of around 100 mg/kg. The incapacitating dose is considered to be between 12-70 mg-min/cubic metre for H/HD. This translates to around 32 mg/man and 4 mg/man for H/HD an HT respectively. Exposure to 140 mg/cubic metre H/HD agent for ten minutes is fatal while 64 mg/kg body weight applied to the skin also causes death. Upon exposure to mustard gases, humans usually undergo a latency period of some hours before the onset of toxic symptoms. The symptoms include (at the lowest effective doses) eye inflammation, skin irritation, rash or blisters, and irritation of the respiratory tract. Recovery from these short term disabling symptoms may take days to weeks and special case management is required to prevent subsequent infection of the irritated tissue setting in. The mustard agents can also cause problems years after exposure. Permanent vision impairment may occur as may chronic bronchitis following severe doses. Epidemiological evidence indicates that cancers of the respiratory tract and the skin are one result of exposure. There is evidence of mutagenic activity. Skin lesions caused by exposure to the mustards can show permanent changes in pigmentation and remain hypersensitive to mechanical injury. ii) Lewisite Lewisite is another vesicant, but exerts its effect by fatally altering critical cellular enzyme systems. There is no latency period with lewisite, which causes immediate excruciating pain on contact with the skin and the eyes. It is also a systemic poison (liver and kidneys being the target organ) and can cause a slowly growing non-fatal form of skin cancer. The effective dose is estimated at 95 microgrammes per man. Severe systemic effects are estimated to be caused by 13 mg/kg body weight. Death can result from the inhalation of a concentration of 48 mg/cubic metre of air for just 30 minutes. ii) Blood Gases and asphyxiants. The blood gases include hydrogen cyanide. This compound exerts its action by interrupting the cellular respiratory chain. The oral LD50 is 3.7 mg/kg body weight, while the inhalation LC50 is 120 ppm in air breathed for 60 minutes. It is relatively non-persistent. The best known asphyxiants are chlorine gas and phosgene. Chlorine gas was the first chemical weapon to be used in WWI. It is an intensely irritating greenish yellow gas which attacks the lungs leading to copious secretion of fluid and thickening of the blood. In the attack of 22nd April 1915 some 168 tonnes of chlorine were released in a light, steady wind along 7km of front. 20% of the 27,000 troops affected died. Phosgene was also extensively used in WWI. It is more toxic than chlorine and exerts its effects in a similar way except that there is frequently a latent period between exposure and onset of toxic symptoms. Death, as with chlorine, is caused by drowning in the fluid secreted by the blood into the lung. PROTECTION AND DECONTAMINATION Protection from chemical weapons is usually by preventing skin absorption and inhalation. The NBC suits supplied to ground forces are supplemented with a variety of decontamination and sealed treatment facilities. The most likely decontaminant solutions are supertropical bleach (STB) and decontaminating solution no.2 (DS-2 containing diethylene triamine). The by- production during use of chloroform and the highly toxic cyanogen chloride would be of most concern. Routine precautions in use would during decontamination would, however, provide adequate protection from these and the irritant acetic and butanoic acids also produced. Some of the natural breakdown products of agents are highly toxic in their own right. Antidotes to nerve gases are of questionable value, the most common being atropine and pralidoxime with some other oximes in use in countries other than the US. Both can have fatal side effects and even their use is unlikely to protect against high exposure. Artificial respiration and anticonvulsant treatments are probably indicated. In the case of the mustard gases no specific antidotes have been developed. Once the chemical/biological interaction commences the process is irreversible. Minimisation of effects can be achieved by thorough washing with detergent and/or hypochlorite bleach. A synthetic dithiol known as British AntiLewisite injected intravenously up to an hour after exposure can significantly reduce skin blistering by this compound. The administration must be closely monitored, however, because of the considerable contra-indications to the use of this drug. ENVIRONMENTAL RISK Considerable evaluation of risk to the wider environment of accidental release of chemical agents has been carried out as a consequence of the US Army disposal programme. This information can be used to estimate effects upon exposed human populations and the wider effects of liberation of chemical agent to terrestrial and aquatic ecosystems. These models are complex and largely untested. They incorporate such factors as meteorological conditions, population density and a variety of release scenarios with appropriate scaling factors for uncertainties. The effect exerted will depend upon the properties of the agent and the medium into which it is released. All the agents considered can undergo a variety of hydrolysis and oxidation reactions which will eventually cause them to be rendered harmless albeit in some cases extremely slowly. i) Atmospheric release. Most air dispersion models in use have a number of shortcomings. These include not accounting for topography, changes in wind direction and other spatial changes in atmospheric conditions. This is generally considered to result in conservative estimates. The table below gives 50%, 1% and 0% fatality rates at given distances downwind of GB and VX agent released instantaneously, semicontinuously, and from spill evaporation. The figures are kg of agent that would cause the specified mortality at the specified distance Downwind Release distance (km) (kg) 50% 1% 0% FATALITIES GB Instant release worst case 0.5 18 3 2 2.0 320 45 27 10.0 9,000 1,600 900 GB Semicontinuous 0.5 90 14 7 release over 60 min 2.0 1,100 180 90 10.0 36,400 7,000 3,000 GB spill evaporation 0.5 45 4 2.7 over 60 min, worst 2.0 650 70 36.0 case 10.0 2,300 400 230.0 VX agent, semi- 0.5 4 0.7 0.4 continous release, 2.0 39 7.0 3.6 worst case 10.0 700 90.0 70.0 HD Evaporation from 0.5 13,600 1,400 900.0 over 60 min. 2.0 180,000 18,000 13,600 10.0 - - 270,000 It should be noted that the model used incorporated certain correction factors for metabolic effects. The agent will be dispersed into an elliptical plume. Worst case conditions result in narrow ellipses. Under these conditions the plume ellipse could measure 15x5 km with the 50 % ellipse being some 5km long. If a weapons manufacturing plant were destroyed without fire taking hold, then the effect upon the surrounding population will depend upon its density, the amount of agent released and whether release is instantaneous or evaporative. What is clear is that relatively small amounts of chemical have the capacity to cause death on a widespread scale in an unprotected population. It should be noted too, that these are fatalities and not a representation of any sub-acute effects. At the 50% fatality level it is probable that 100% of the population exposed to the chemical would be affected in some sub- acute way. No effect distances are some seven times greater than the no death distances, assuming that the no effect concentration for both VX and GB is 0.000003 mg/cubic metre of agent. Since the mustards are carcinogenic and have no threshold, no effect levels cannot be estimated. With most of the agents, young children and infants are considered to be most at risk. If fire took hold of an attacked facility, several toxic gases could be generated. These include hydrogen cyanide from GA, hydrogen fluoride from GB, nitrogen dioxide from GA, sulphur dioxide from VX, hydrogen chloride from HD and chlorine from Lewisite. These gases would be of immediate local concern while others such as the PAHs and PCDDs/PCDFs would be of concern in the longer term. If used offensively, the weapons would probably be deployed in order to result in a toxic level over a wide front. In this case effects would depend very much on the methods used to deliver the toxins. Toxic effects would be very much mitigated due to the protective clothing of combatants involved. Non- combatants would still be highly vulnerable. The major factors governing diminution of toxicity in air are simple dilution and deposition in droplet form. Chemical reactions with other air pollutants may play a role. For the most part detailed knowledge of such chemical reactions involving CW agents is extremely limited. ii) Aquatic Systems The behaviour of chemical weapons in aquatic systems may well result in them being carried well outside an impact area defined by simple aerial modelling. Contamination of drinking water may occur which will require supplies to be treated. There are two major routes through which contamination can occur. Firstly, deposition of agent from atmospheric aerosol and secondly, a direct spill into a watercourse. Aquatic insects are likely to be more sensitive than fish to the effects of the nerve agents based on the known impacts of OP pesticides in aquatic systems. There could thus be long term effects on the base of the food web supporting fish in an impacted stream. There are a number of variables which are agent dependent. GB is similar in density to water and is miscible with it, but evaporates more rapidly than either VX or mustard. Mustard hydrolyses rapidly in water if it is dissolved but does not in fact dissolve readily and will tend to form a surface slick. The persistence of this will then depend upon wind and wave action. VX agent and some mustards are more dense than water and could form globules which sink to the bottom or are transported downstream. If the mustard was spilled into cold water, it would solidify and sink to the bottom. These globules have the potential to persist for between several months and several years and there is little information on toxic action involving contact with slicks or globules. The conclusion is that aquatic resources in streams up to a medium size could be severely affected by spills of around 5kg of agent for most of their length. This again raises the problem of drinking water abstracted from these. This would need to be subjected to treatment before drinking. iii) Terrestrial systems. Most of the impact models constructed to predict the effects of releases are based upon human toxicology. Accordingly, the downwind no effect distance is the distance beyond which there are no overt effects on humans. There may, however be effects on ecological resources. Both direct and indirect effects could be expected. Death of animals might result from inhalation of agent or grooming activities, absorption through the skin nose or eyes, and ingestion of contaminated vegetation. Indirect effects include the closure and restriction of areas. Crops and arable areas would be unusable for a year or more depending upon the agent involved. GB is volatile and disperses relatively readily while VX is less volatile and much more persistent. The mustards can remain active in the environment for years and can adsorb onto soils and vegetation. This is why they are recommended by military strategists as "terrain denial" material. On the basis of ingestion toxicity, steer and sheep are most sensitive to VX, rats and rabbits the least sensitive. There is evidence that chemical agents and their breakdown products are accumulated by plants and deaths in grazing animals could occur for a considerable time after the event. Although it is considered that the consumption of meat and dairy produce from animals exposed but not killed by the nerve agents should be safe, this is not certain. Animals killed by nerve agents would be unfit for consumption, those acutely affected would have to be destroyed. Precautions to prevent residual contamination problems would need to be carried out for all animals slaughtered for consumption from an area affected by a release. It would be necessary to quarantine all forage and grains until proved safe by testing. Birds and insects may be particularly sensitive to the effects of chemical weapons. In practice, in a combat zone, it may be extremely difficult to arrange for these tests to be carried out due to lack of an infrastructure. Substantial mortality could be expected, therefore, due to the consumption of contaminated food in the aftermath of a chemical attack. Another factor is the decontamination of buildings and personal effects. Depending on the extent of the attack and the agent used, the inability to prevent public access to contaminated areas will result in civilian populations being inadequately protected. Many of the decontamination methods may prove destructive to many common building materials since they involve heating to temperatures of 1000 o C. Hence buildings contaminated with the persistent mustards or VX agent may have to be subject to indefinite access restrictions. In practice these effects are likely to be exacerbated by the unavailability of decontaminating agents to the civilian population. The input of resources would need to be considerable to even begin to partially address the problem. CONCLUSION Chemical warfare agents are highly potent toxins designed to kill and incapacitate. In some cases they perform a "terrain denial" role for some time after release due to their persistence in soils and water. The major groupings likely to be used are the unitary nerve gases and vesicants although phosgene and chlorine could be used. Release of agents could result from attack on a manufacturing facility or from strategically motivated release. The use of chemical warfare agents in addition to causing immediate casualties, both military and civilian, would result in a number of wider environmental effects. These would include the contamination of water supplies and arable lands resulting in most foods from the affected areas being unfit for human consumption. Persistent chemical agents could result in areas being restricted for some years after release. Both soils and water can be affected in this way. Buildings contaminated by chemical agents would be extremely difficult to decontaminate and it is likely that large numbers of the population would be made homeless. Agricultural animals would also be killed by the agents, while the natural flora and fauna would also be severely affected. Deposition of agent on vegetation could cause poisoning in animals consuming it. Precise effects of a chemical weapon attack will depend on the chemical used, the quantities released, weather conditions and pouplation density. =ENDS=