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Sudden Infant Death syndrome discovery

The great 80% decline in British SIDS deaths began exactly when this discovery/hypothesis booklet (see below) was sent by mail to government and SIDS organisations in Britain and all the world in November 1988.

I also sent it to all SIDS Foundation addresses found in the 1986 published book Cot Deaths by Jacquelynn Luben (Thornsons).

I was able to prove for the first time that SIDS deaths shared the same mechanism as adult forms of Sudden deaths. My narcotic/stress related discovery revealed the actual cause of SIDS deaths because the same cause in adults was already well Known.

The decline in Britain was spectacular down around 40% the decline  began in January 1989 three years before the governments December 1991 "Back to sleep campaign"

There was another spectacular decline following the discovery published in August 1997

As submitted to Medical Hypotheses 1986  and accepted for publication in September 1987

It was evetually published as a discovery in Medical Hypotheses Vol. 49 August 1997. Pp 177-179. A R Parish.


A.R. Parish


Many incidences of sudden unexplained death that occur in adolescents and adults are preceded by exposure to certain central nervous system gases or drugs e.g., the most commonly abused drug used by glue sniffers is Trichloroethylene, a form of which, TRILENE, is still used as an analgesic gas in childbirth. The great majority of the drugs and gases which are known to cause toxic poisoning in workers exposed to them industrially and in victims of Sudden Sniffing Death Syndrome are also used or related to the drugs and gases used in perinatal medication. Sudden Infant Death Syndrome can, therefore, be logically regarded as the result of exposure to those same toxins. A mechanism for delayed death due to latent perinatal medication poisoning can be demonstrated.INTRODUCTION

The term "cot death" was first used in the 1950"s to cover the sudden unexpected death of an apparently healthy baby in its sleeping accommodation. Sudden Infant Death Syndrome (SIDS) was first defined in 1969 in the USA as the sudden death of any infant or young child which is unexpected by history and in which a thorough post mortem examination fails to demonstrate an adequate cause of death.

Over a two year period of studying the literature relating to TRICHLOROETHYLENE (TCE), I became quite familiar with the subject of sudden death from TCE poisoning. I examined many reports of the phenomenon of delayed death which occurred on rare occasions, usually a few hours or even the day following industrial exposure to TCE. I saw a logical possible connection with SIDS and the analgesic gas TCE used in childbirth. During subsequent investigations, I discovered a known delayed effect from other gases and insecticides that resembled the delayed effect I was searching [or. Could a similar mechanism he responsible for SIDS from exposure to analgesic gases in childbirth, affecting the infant but not the mother? Are longer and lesser amounts of TCE more harmful than larger acute doses, as is known to be the case with CO poisoning? Can the same mechanism that is responsible for a delayed effect from CO poisoning he applied to infant exposure to analgesic gas? (I) Is Sudden Infant Death Syndrome a delayed toxic effect? This hypothesis proposes that SIDS is caused primarily by exposure to analgesic gases used in long periods of labour, and that exposure is followed by a "symptom-free" interval; the latent poisoning "matures in the infant and begins to manifest three to four weeks after exposure, this delayed process can he reactivated by illness.


It is proposed that Sudden Infant Death Syndrome (S1DS) is caused by a delayed toxic effect from latent perinatal medication poisoning. The main culprits are the CNS gases used as analgesics; these gases are often inhaled over long periods during labour. On the following pages is a brief description of one anaesthetic/analgesic still in use in Great Britain for the relief of pain in childbirth: TRICHLOROETHYLENE. For simplicity, I have concentrated on this one anaesthetic gas. A similar description could he prepared for any volatile anaesthetic gas.


TCE is a Chlorinated Hydrocarbon.

Percentage Composition:


CARBON 18.28%


Thermal decomposition produces HCI and PHOSGENE

CHLORINE and PHOSGENE were the two most notorious chemicals used in the First World War.

TCE is an anaesthetic all anaesthetics can kill by paralysing the Central Nervous System. In anaesthesia, sub-lethal doses are administered to maintain unconsciousness,

TCE is an insecticide (6) and belongs to a group known as Organo-Chlorines. The organo-chiorine insecticides are derived from CHLORINATED HYDROCARBONS. (7) The most infamous of the organochlorine insecticides is DDT, now banned because the chemical was found to accumulate in the fatty tissues of animal and man. The banning of DDT was mainly brought about by the publication of the book SILENT SPRING. This book is recommended together with this document as evidence of the harmful effects of the Chlorinated Hydrocarbons.

There are over 100,000 similar synthesised compounds, all with molecular differences; but in reality many are almost identical - one is often substituted for the other. For example, note the following extract from E. M. Waters" et al TRICHLOROETHYLENE: AN IMPACT OVERVIEW: Apparently, lessons taught us by asbestos, vinyl chloride and chloredecone are neither easily learned nor remembered. No sooner is one chemical spotlighted and removed from use than another of equally unknown hazard often becomes a less-than-completely-tested surrogate. The substitution of methylene chloride and perchloroethylene for TCE arc cases in fact." (8)

TCE as an analgesic/anaesthetic is no longer is use in the USA its use was abandoned in l985.

By studying one anaesthetic with abundance of evidence regarding human exposure one can begin to understand all anaesthetics.
The sudden deaths described here are not confined to Trichloroethylene.

The delayed toxic effect from perinatal medication is really a latent poisoning that can he reactivated in the same way that aspirin effects REYES Syndrome or alcohol affects Trichloroethylene (TCE) poisoned subjects, (9) If the toxic burden is great enough, death may occur around the time of exposure, infection or vaccination, but more frequently it happens at an unsuspecting time long after the toxic insult. The gases, combined with other forms of medication given at birth, have a profound effect on the central nervous system. The delayed effect, or latent poisoning, may contribute to all post-natal deaths, especially deaths attributed to respiratory deaths (Graph) as these deaths often present the physician with a dilemma in diagnosis. Sometimes the term "viral pneumonia" is mentioned on the death certificate even though it may not, in the pathologist's view, wholly explain the cause of death.

With growth and development the threat of death diminishes but, paradoxically, during the first months of life the toxic burden increases. Dr. Tesh of Life Science Research believes that a child"s central nervous system continues to develop after birth for perhaps two years. (10) The newborn infant is clearly not a miniature adult. The delayed effect is very subtle. Adults exposed to anaesthetics can easily survive exposure without sequelae: the only indication of a delayed effect is post-natal or post-operative depression. In the infant this subtle effect is magnified and is responsible for the hulk of deaths that occur in the second and third months of life.

Compare Graph A with Graph B. In animal experiments with inhalation gases designed to determine lethal doses, the results often reveal that a percentage die on exposure and a percentage of the remainder die over the following few weeks. If the dose was lowered, instant death would disappear, leaving only delayed deaths, Reduce the exposure yet further and the delayed death ratio that is found in SIDS is reached, without any deaths occurring at the time of exposure. Note the similarity of initial delay after exposure. Observe that lesser amounts of poison increase the exposure - death interval. Examination of deaths described here reveals that they are not dying from anaesthetic death or asphyxiating death but that another mechanism is in action: that mechanism is identical to the mechanism found in SIDS.

The following graphs and quotations have been extracted from:
- Bitron MD: Aharonson EF
- Israel Institute for Biological Research, Ness-Ziona, Israel.
- Delayed mortality of mice following inhalation of acute doses of CH203, SO2Cl2 and Br.

- American Industrial Hygiene Association Journal. VOL. 39, 1SS 2, 1978. P 129-38.


Mortality of mice, exposed to either 290 or 170-ppm chlorine for various durations, as a function of time elapsed after exposure. For each group of combined experiments, the range of exposure durations and number of animals are specific in the figure.



Mortality of mice, exposed to either 750 or 240 ppm bromine for various durations, as a function of lime elapsed after exposure. For each group of combined experiments, the range of exposure durations and number of animals are specified in the figure.


"Values of acute toxicities often are derived from experiments, in which inhalation of the investigated materials was continued until death occurred to all the exposed animals - a procedure that fails to account for delayed mortality following inspiration of substantially smaller doses, which is more meaningful in many cases of hazard analysis".

Age in weeks

The fact that subsequent births are more at risk than first births supports my hypothesis that there is an accumulative poisoning effect; the higher risk associated with smoking also supports the hypothesis of chemical poisoning since Nicotine was one of the first generation of insecticides. Similarly, the expanding use of certain drugs appears to he related to the expanding recognition of SIDS: Benzodiazepines, for example in the same year that Valium became the number one prescription drug in America, SIDS was clinically defined as a disease entity. All the chemicals referred to in this paper are related to sudden/delayed death; all the chemicals referred to are, or are related to, perinatal medication, Therefore, if all the chemicals and all the sudden/delayed deaths arc related, then Sudden lnfant Death is caused by perinatal medication.


When gas and air was first introduced in childbirth, it was observed that newborn babies were often born in a sleepy state. This is now so common that it is accepted as normal. Toxicology is a comparatively new science: recommended ambient levels of exposure in industry are continuously being reduced. All the delayed deaths display the same mode of action - ventricular fibrillation - without evidence of cause of death. The general belief that the effects of anaesthetics are reversible is only partly true. (11) These chemicals do not possess any magical powers: anaesthesia and analgesia are merely states of chemical poisoning - for example, narcosis, convulsions, post-operative vomiting, toxic comas etc.

Schwartz describes a possible pathogenic link with cardiac sympathetic enervation and SIDS. (12) Ludomirsky, Klein et al refer to ventricular arrhythmia's associated with organophosphorus insecticide poisoning and describe an insidious complication of Delayed Sudden Death which can occur 3-15 days after exposure. (13) Bass, in his article on Sudden Sniffing Death, states that 'The general impression has been that Sniffers die as a result of plastic bag suffocation. It is now clear that a rapidly rising number are dying suddenly and unexpectedly without suffocation." (14) Other reports confirm this strange mode of death. (15) King, Smialek and Troutman report on four deaths, three of which were delayed. (16)

Stolman, referring to the interaction of drugs and chemicals, slates that "interest in the combined effects of drugs in the toxicological field was originally aroused by the observations of the suddenness of death in some known instances or where the available evidence suggested that death may have supervened after several drugs in small quantities were ingested. Workers have observed that in persons, who had taken both alcohol, and barbiturates, death was more rapid and the clinical picture different from that produced by either one acting alone. They were impressed with the relative suddenness at which the onset of death occurred. (17)

Some anaesthetics are used in the manufacture of chemical warfare agents (18) - for example, TCE is used to make phosgene. Phosgene can also produce delayed death. (19) Merewether reports on peculiar cases of sudden deaths from neurotropic poisons in dry-cleaning establishments and describes the development of a psycho-organic syndrome in the same workers exposed toTCE. (20) Finkle and McCloskey describe sudden death from cocaine users (local anaesthetic); they state that "sudden unexplained deaths are the subject of extensive medical and circumstantial investigation to determine manner and cause of death. (21) McConnell reports that examination of autopsy tissue from persons with no known exposure to TCE confirmed TCE present in most organs (22) (TCE is not a naturally occurring substance. (23))

Rementaria and Bhatt state an apparent increase in the incidence of SIDS among infants of narcotic-addicted women and describe the sudden death of an infant born to a mother taking diazepam. (24) Diazepam levels in newborn infants have been reported to be double that of their mothers. (25)

Protestos, Carpenter et al, in their paper on the obstetric and perinatal histories of children who died unexpectedly (cot deaths) found a highly significant difference in the length of second stage labour, (26) the very time when gas and air is most used. This difference adds strong support to this hypothesis.


The toxicology of a human adult is a giant step away from the toxicology of a newborn infant; likewise, anaesthetics are a giant step away from nerve gases. However, a clear connection exists. Nag, Siungh and Senon describe an epilepsy epidemic from organochlorine insecticides and write "the Germans first introduced nerve gases and related compounds, now used in pesticides, in World War II." (27) Aleksandrowicz describes a chronic brain syndrome developing from an acute exposure to oraganochlorine insecticides and refers to a "residual phase" two years later. (28) TCE is an effective organochlorine insecticide and fumigant.

(29) Hundreds of references with positive TCE poisoning finding can be found on the British library"s medical computer. Waters et al (30) also cite over 50 summaries of positive findings: one random example is Shertoli, involving 67 cases. (31) Carbon disulphide is another industrial solvent with high anaesthetic properties. Like TCE, its dangers were only recognised after many years of industrial use. Hanninen demonstrates that the psychological syndrome of carbon disulphide exposure is not limited to subjective experiences alone and that "latent poisoning" exists among healthy exposed workers or those suspected of having the disease without clinical manifestation of the disease. (32) The entire area of the interaction of various chemicals, their additive, synergistic and inhibiting effects on the biological system are virtually unexplored. The probability of aggravation of effects, of the biological interaction from prior, current and subsequent exposures to the same and other toxins and stresses, emphasises the importance of such combined accumulative exposures. S. Castellino warns of possible active lesions resulting from exposure to TCE in workers that are employed in the chemical warfare industry. (33)

Both Carson and Lahani and Souheil confirm that TCE freely crosses the placenta. (34) Waters et al confirms that it freely crosses the blood-brain barrier. (35) Elkington, in THE POISONED WOMB, reports embryo-toxic or teterogenic effects from TCE exposure in mice and in humans: female anaesthetists and pharmaceutical and chemical workers are found to have an increased risk of spontaneous abortions (36); a leak into the water supply from TCE storage tanks caused an increase in spontaneous abortion, amongst a group of residents in Silicone Valley California. (37)

Stewart describes a well known phenomenon call "Degreaser"s Flush" - a rather spectacular flushing of the skin that appears after ingestion of alcohol, found in workers exposed to TCE. The mechanism responsible for this is unknown, but it clearly demonstrates how one chemical can reactivate another in an unsuspecting way. (38) Lohs describes latent poisoning this way in the SIPRI Monograph on the delayed Toxic effects of chemical warfare agents.

"It must he emphasised that a lesion (of this kind) is not the same as one caused by chronic poisoning. By chronic is meant protracted, continuous or intermittent exposure to a small quantity of a poisonous substance. A delayed lesion results, however, from a single dose or a brief exposure, the onset of symptoms months or years later requiring no further intake of the substance in the meantime." (39)

SIDS occurs more in winter than in summer (40): seasonal distribution can he explained by the similar seasonal distribution of all infectious diseases and all infant mortalities as they are all synergistically connected to SIDS. Only CNS chemicals possess the innate power to cause sudden death. The interaction of chemicals with physical illness can be clearly demonstrated.


In SIDS the action is more subtle and reversed it is also delayed:



Death can he delayed or reactivated from any point in the chain reaction, but death is caused by the original poisoning because vaccines and illness do not possess the innate power to cause sudden death; they only have the power to synergistically reactivate or cause a physical illness with natural death. CNS drugs, on the other hand, do not only possess the innate power to cause unnatural sudden death but also possess the innate power to delay it.

An important observation to support this hypothesis was reported by S. Tonkin. She reports that there maybe two types of unexpected or "cot deaths", the one occurring between four and sixteen weeks of age and the other occurring after sixteen weeks of age. (41) Convincing graphical charts supports this. Similar graphic information can be found in the Netherlands report by Baak and Huber. (42) Although two types of deaths were not observed, the statistics speak for themselves. It is interesting to note that both of these reports are less distorted by high seasonal distribution of mortalities.


This hypothesis demonstrates the possibility that SIDS is the product of subtle latent CNS poisoning following exposure to medication at birth. The poisoning is followed by a "symptom-free" interval that occurs after delays, which are proportional to the duration and the density of the insult. If the infant survives the initial delayed effect the poison remains latent but can be reactivated by illness or vaccination etc. Once reactivated, if death is not the immediate outcome, the insult takes on the same course of delayed action as the original poisoning. Death can occur even when the infant is well on the way to recovery from what appeared to he an uneventful normal illness.

"All action is followed by reaction." It is thus proposed that sudden infant death is caused by a reaction to perinatal medication.


1     Two cases of acute carbon monoxide poisoning with delayed neurological sequelae after a "free" interval. Werner et al. Clinical Toxicology. Vol. 23 (4-6) 1985, pp. 249-265

2     Waters EM. Black SA. (Eds.) An Abstracted Literature Collection. 1907-1976. p. 8

3     ibid. p. 4

4     ibid. pp. 10-12

Holniherg B. Biological Aspects of Chemical and Biological Weapons in AMBIO; 4 (5-6), 1975 (Recd 1976) pp. 211-215

5     Seagrave S. Yellow Rain: Chemical Warfare—The Deadliest Arms Race 1981. pp. 36-81

6     Waters EM; Black SA. (Eds.) Op Cit. pp. 239/249

7     Carson R. Silent Spring. Pelican 1982. PP" 33-41

8     Waters EM; Gerstner HB; Luff JE. "I"richloroethylene: An Impact Overview. 1976. p. 68

9     Stewart RD; Hake CL; Peterson JR.. "Degreasers" Flush: Dermal Response to Triehloroethylene arid Ethanol" in Archives of Environ,nental Health. Vol. 29. July 1974.

10   Elkington J. The Poisoned Womb. Penguin; 1985. p. 116

II     Lehmann KB; Flury F. Toxicology and Hygiene of Industrial Solvents. 1943. pp. 51-85

12   Schwartz. P. Cardiac Sympathetic Enervation and the Sudden Infant Death Syndrome in The American Journal of Medicine. Vol. 60. February 1976. p. 176.

13   Ludomirsky A; Klein HO; Sarelli P; Becker B; Hoffmann S; Taitelman U; Barzilai J; Lang R; David D; Disegni E and Kaplinsky E. Q-T Prolongation and Polymorphous ("Torsade de Pointes") Ventricular Arrythmias Associated with Organophosphorus Insecticide Poisoning in The American Journal of Cardiology. Vol. 49. May 1982. pp. 1654-1657.

14 Bass M. Sudden Sniffing Death in The Journal of the American Medical Association. Vol. 212. June1970. pp. 2075-2079.

15   Derrick El-I and Johnson DW. Three Cases of Poisoning by Irrespirable Gases in The Medical Journal of Australia. 1943. p. 356.
Guberan E; Fryo 0; Robert M. Sudden Death from Ventricular Fibrillation After Voluntary Inhalation of Chlorothene in a Mechanics Apprentice in Schweitz Med Wochenschr  1976. Jan 24; 106 (4,):pp. 119-121.
Garriott J; Petty CS. Death From inhalant Abuse: Toxicological and Pathological Evaluation of 34 Cases in Clinical Toxicology. Vol. 16. 1980. pp. 305-315.

16   King GS; Smialek JE; Troutman WO. Sudden Deaths in Adolescents resulting From the Inhalation of Typewriter Correction Fluid in JAMA. 1985. Mar 15. 253 (Il):pp. 1604-1606.

17   Stolman A. Modifications in Toxicity from the Interactions of Drugs and Chemicals in Sundernian F U"

(Ed) Laboratory Diagnosis of Diseases Caused by Toxic Agents. 1970 pp. 71-73.

18   Reichert D; Ewald D; Henschler D. Generation and Inhalation of Dichloroacetylene in Food Cosmet Toxicol.   13 (5); 1975. pp. 511-515.
Seagrave S. Op. Cit. p. 51
" Castellino N. New Original Research Work on the Pathology of Certain Operations in the Chemical Warfare Industry in Folio Medca No. 6. March 1943. pp. 209-221

19   Seagrave S. Op. Cit. p. 51

20   Merewether ERA (ed). Industrial Medicine and Hygiene. Vol. 3. 1956. p. 530

21   Finkle BS, McCloskey KL, The Forensic Toxicology of Cocaine (1971-1976) in Journal of Forensic Science. Vol. 23. 1977. p. 173.

22   in Waters EM; Black SA (Eds). Op. Cit., pp. 28-3 1

23   Carson R. Op. Cit. pp. 31-49

24   Rementaria JL; Bhatt K. Paediatric Pharmacology and Therapeutics in The Journal of Paediatrics. Vol 90. No. 1 pp. 123-126.

25 ibid.

26   Protestos CD; Carpenter RG; McWeeny PM Emery JL. Obstetric and Perinatal Histories of Children Who Died Unexpectedly (Cot Death) in Archives of Disease in Childhood. 1973. VoL 48. p. 835.

27   Nag D; Singh GC; Senon S. Epilepsy Epidemic Due to Benzahexachlorine in Tropical and Geographical Medicine. 1976. pp. 22 9-232

28    Aleksandrowicz DR. Endosulfan. Poisoning and Chronic Brain Syndrome in Archives of Toxicology  vol. 43. 1979. pp. 65-68.

29   Waters EM: Black SA (Eds.) Op. Cit. pp. 249-253

30   ibid. pp. 215-233

31   Sbertoli C. Occupational trrichloroethylene Intoxication. 1964. (University Milan) Meo Lavoro, 55(12) 787-810 1964 (Italian)

32  Hanninen 11. Psychological picture of manifest and Latent Carbon Disulphide Poisoning in British Journal of Industrial Medicine. Vol 28. 1971. pp. 374-381.

33   Op. Cit. pp. 209-221

34   Carson It Op. Cit. pp. 31-49 - Laham; Southeil. Studies on Placental Transfer: Trichloroethylene in Ind. Med. Surg. 1970. Vol. 39. PP. 46-4 9.

35   Waters et al. Op. Cit. pp. 27-37

36   Elkington J. Op. Cit. pp. 65-68/211-212

37   ibid. pp. 211-212

38   Stewart RD et al. Op. Cit.

39   Lohs. The Delayed Toxic Effect of Chemical Warfare Agents. The Stockholm Peace Research institute. 1975. p. 1

40 Limerick S. in 'Cot Death Research and Support'. The SIDS Foundation. Newsletter . 28 August 1985. p. 2.

41   Tonkin S. Epidemiology of SIDS in Auckland, New Zealand in "SIDS 74" The Canadian Foundation for the Study of Infant Deaths. 1974. p. 169.

42   Biaak; Hubers in SIDS 1974" The Candian Foundadation for the studies of Infant Deaths. pp. 157-167. 1974.

Copyright 1986 Anthony R Parish Ph.D.

Contact Details

Anthony Parish PhD.
41/c Britannia House
Golding Place
Norfolk NR2 4BD

Tel: England (+44) (0) 1603 461316

Last updated 12/06/2000