Concerns over implementation of the plan for the gas assault include considerations both as to the sheer quantity employed and as to the manner of injection.

A determination of the effects of the quantity employed is rendered difficult by inability to fix the amount with any certainty. The number of injections can be deduced from the FLIR tapes: how much was delivered by each injection is unknown. The Justice report states that a "Mark 5" injector was employed. This could describe either of two devices: one delivers slightly over an ounce of CS, the other delivers over fifty pounds. The calculations of Failure Analysis Associates indicate that even assuming the smaller device was used, the gas assault marked the most massive use of CS against civilians in the history of the nation.

CS is an extremely powerful lung and mucous membrane irritant. Biochemists believe that it acts by causing tissues to release bradykinens, substances which cause pain, tissue swelling (edema) and leakage of fluid from the capillaries. Cucinell, et al., Biochemical Interactions and Metabolic Fate of Riot Control Agents, 30 Feder. Proceedings 86, 89-90 (1971). The biochemical process is similar to that employed by "mustard gas" and the more deadly lewisite. Id. at 86-87. Symptoms of exposure, even at low levels, include sensations of chemical burning on the eyes (sometimes described as "it was as if my eyes were on fire"), burning in the nose and throat, constriction in the chest, and respiratory difficulty. CS's power is illustrated by its ability to cause severed animal muscle tissue to involuntarily contract. Id. at 90.

The agency witnesses described it as the safest riot control agent--but its safety is due largely to its capacity to cause pain at a lower threshold, leading to a greater gap between the effective (i.e., painful) dose and the lethal one. It is "less dangerous" only if those who use it in fact employ a lower dose in light of its potency. If it is simply poured on, regardless of concentration, its potency makes it more deadly rather than less.

The agency witnesses implied that CS is some manner of marvelous irritant which (1) becomes effective at a low dose and (2) does not inflict increasing damage at any higher dose. All studies of the gas conclude otherwise: while there is a sizeable gap between the effective and the lethal dose, there certainly is a lethal dose. If breathed in a confined space, where one must inhale CS into the lungs if one is to inhale air into the lungs, the edema and capillary leakage will cause pneumonia and death. The lack of human volunteers for such death precludes determining the human lethal dose by experimentation. Among test animals, it has been shown to vary widely. Guinea pigs die at half the dose necessary to kill rats or rabbits, for instance. Ballantyne & Callaway, Inhalation Toxiciology and Pathology of Animals Exposed to 0-Chlorobenzylidene Malononitrile (CS), 12 Med., Science & the Law 43, 45 (1972). Other studies indicate that guinea pigs die at one-fifth the dose required to kill mice, and rabbits at half the dose required to kill rats. Punte, et al. Toxicologic Studies on o-Chlorobenzylidene Malononitrile, 4 Toxicology and Applied Pharmacology 656, 660 (1962).

The lethal dose is not merely a question of how much gas, but also a question of how long the victim was exposed to it: tissue injury keeps accumulating as the substance is inhaled. A low dose for a longer period may be more lethal than a high dose for a short one. Thus:


Dose Time Exposed ......Deaths Effects

(per m3 air)

750 mg half hour ........ 0 of 240..............5 of 240 showed "minimal lung pathology"


480 mg one hour ........ 40 of 226 ............Dead had "extensive damage to lung and kidney"


Ballentyne & Callaway, supra  at 58. It was also obvious that there are individual variations. 150 mg/m3, a very mild dose by these standards, still killed a few especially susceptible specimens. Id. The primary killing mechanism was lung damage:

All rats and the majority of hamsters which died within 48 hours of exposure presented with moderately severe damage to the lungs and kidney. Damage to the lung generally took the form of moderately severe congestion, alveolar haemorrhage, and in some cases oedema.

Id. at 57. At the same time, a few animals died without evidence of much lung damage: "The few hamsters which died within 48 hours and had minimal or no lung damage, also had little kidney damage." Id. The occurence of deaths with no discernable cause may be an important consideration in potential effects upon children, which we will now explore.

That children are more sensitive than adults to respiratory conditions is no secret to any parent. Their smaller breathing passages are more easily obstructed, so that a pneumonia which leave an adult walking can kill a child. Further, children are prone to an ocular-cardiac reflex of unknown origin, by which severe eye pain can cause heart failure. It would stand to reason that exposure to CS poses special dangers to children, especially where the exposure is prolonged. As noted above, animals which can withstand a large dose of CS for a half hour may die when given a smaller dose for a full hour. The original attorney general's plan envisioned exposure of children for as much as 48 hours; as it turned out they were exposed for approximately six hours.

The agency experts stated that an infant, exposed to an unknown concentration of CS for two hours, had recovered with no lasting harm. We have located the article referring to this case and it appears grossly misconstrued. Park & Giammona, Toxic Effects of Tear Gas on an Infant, 123 Am. J. Diseases of the Child 245 (1972). The authors note that immediately after exposure the child was seen by an emergency room and "required suctioning to relieve upper airway obstruction." The following day the child had an episode of cyanosis (turning purple from lack of oxygen) which required further suctioning. Despite antibiotics, coughing and fever continued through the seventh day of hospitalization, and x-rays revealed lung infiltration (pneuomonia). The infant also developed first-degree chemical burns of the skin. He was discharged on the 12th day, but readmitted into the ER within 24 hours with worsening pneumonia. He had to be placed on a respirator (indicating he was in respiratory failure: the hope was that with lessened work for the lungs they might be able to repair the tissue damage) and finally released after four weeks of hospitalization.

The agency witnesses--and apparently those advising the Attorney General--construed the case to mean "the child survived with no permanent effects." A fairer reading would be "despite immediate treatment and full life support, the child came very close to dying." If the child had been inside the compound--with no medical equipment available to suction its mouth and throat open--it probably would not have survived the first onslaught of effects. The degree of exposure is hard to assess, but the concentration cannot have been high: it apparently took two hours to force an adult, without gas mask, out of the building. Extrapolation of the documented effects to a dose sufficient to drive out protected adults, and to exposure to 6-48 hours of that dose, would suggest, not that infant deaths were unlikely, but rather that they were inevitable.

In brief, the published literature, apparently consulted by the testifying experts, would have supported the following advice to the Attorney General and to the subcommittees:

CS can kill: the only question is the exposure and the individual. We have little idea of the lethal dose for adult humans, and none of the lethal dose for infants. Length of exposure is more important than concentration: and here we are discussing hours or days rather than minutes. Moreover, there may be a mechanism of death quite independent of lung damage, of particular relevance to children, and upon which we have no usable data at all. It does appear that a dose insufficient to stop an unprotected adult nearly killed one child despite immediate life support. That was 2 hours' exposure, and here we are discussing 6-48 hours.

We can now proceed to the secondary question: did the CS actually kill children? At the hearings, Rep. Schumer and others argued that it did not, since the autopsies did not mention it. The argument is, to say the least, disingenuous: as the Justice report correctly notes, any CS particles present would have broken down long before the bodies were examined. We must accordingly determine what symptoms we would expect to find on autopsy which would (1) be consistent with death from CS and (2) inconsistent with death from other causes such as smoke inhalation.

Animal studies indicate that certain lung damage is indicative of CS-caused death. Prominent among these are (1) congestion and edema--fluid in the lungs: (2) occasional hemorrhage and bleeding into the lung and throat. "Damage to the lung generally took the form of moderately severe congestion, alveolar haemorrhage, and in some cases oedema." Ballantyne & Callender at 57. "The congestion and stasis of blood in the lungs, together with the presence of exudates, suggests that the main cause of death in these animals was pulmonary damage." Id. at 49. Similar results were found upon autopsy of an adult apparently killed by a combination of CS and CN. Chapman & White, Death Resulting from Lacrimatory Agents, 23 Journal of Forensic Sciences 527 (1978).

Death from smoke inhalation, on the other hand, would be characterized by extensive deposits of soot in the bronchi and high carbon monoxide levels in the blood. These signs are quite striking, and were noticed by the coroners. The autopsy of David Koresh, for instance, reports "a dense black soot deposition over the mucosa of the tracheobronchial tree extending to the smaller airways," and 24% carbon monoxide saturation. Jane Doe 65, who died in the bunker, is assigned asphyxia due to smoke inhalation based on carbon monoxide saturation of 73%.

With these standards in mind, we can look at the autopsies of the children dying in the bunker.

The body of Jane Doe 57 was among the best preserved. Cause of death is assigned to asphyxia, with no mention of smoke. The respiratory system is thus described:

The larynx and hyloid are intact. The trachea and major bronchi contain blood debris admixed with variable (generally small amounts) soot deposits. The lungs are congested and autolyzed [decomposing] (no weight available).

Jane Doe 55 is listed as dead due to suffocation. Decomposition prevents analysis of the lungs, but the blood was able to be recovered and is negative for carbon monoxide. This would suggest death before any smoke reached her.

Other deceased are likewise listed as dying of suffocation or asphyxia rather than burns and smoke inhalation. Decomposition prevented any detailed examination of the bodies. The total roster of dead due to non-smoke suffocation include:

Doe No. Name (if known) Age

55 Audrey Martinez 13

57 Star Howell 4-6

62 ? 1

67-2 C. Howell 8

67-6 R. Silvia 13

70 Mayanna Schneider 1

51B J. Schneider 41

67-3 R. Howell 24

75 Ruth Morrison 29

For lack of any other explanation of suffocation deaths occuring without characteristic soot deposits, the coroners assigned "burial in structural collapse" as the reason. Yet this can easily be discounted. All these dead were found inside the concrete "bunker." That the bunker did not collapse is proven: photographs of the roof show it secure, with the exception of one hole about two feet in diameter. Photographs inside the bunker show only a small amount of concrete debris, and that mostly as dust or pebbles along one wall. Since even this debris is found atop the piles of exploded ammunition, it would have fallen late in the fire, long after all inside the bunker were dead of other causes. The fact remains that (1) many individuals are dead of simple suffocation or asphyxia; (2) evidenced by congested lungs; (3) without soot deposits indicative of smoke-caused death and (4) composed largely of children. While we will never be able to state positively that these were killed by CS effects on their lungs, the evidence is consistent with this explanation and with no other.

In sum, it is clear that CS can cause death by lung damage and asphyxia, and that it poses special dangers for children and in confined areas. The danger rapidly escalates as the exposure continues, and here the exposure was approximately six hours. The deaths of several children in the bunker area are explicable as reaction to CS overdose and inexplicable by another other known cause.