Document QNZEmexK5mrZ5oENmDogeV5k

*V CONFIDENTIAL 2.j/'4'/ 1o COT DEATHS Draft submission bo the Department of Health, 3rd May 1. First use of PVC mattress Covers y Due to breaks in record keeping therory G the evolution of companies the exact date for the introduction of PVC mattress covers is not known. They were certainly in use in the early 1950's. 2. Dates on the first use of foam fillings Information to be supplied by the British Rubber Manufacturers Association but their origins draw similar comments to the response In ,(1), . J J> ^ 3- The composition of materials used for covers. lUy, I 1 60 (PoLjUJl Over the years the composition of PVC materials used in the manufacture of cot mattress has evolved to reflect changing technologies, regulations and their attendant standards. Typical formulations at different stages would be as follows: 1960's PVC polymer Octyl phthalate Epoxy plasticizers Baruium/cadmium/zinc stabiliser Titanium Dioxide pigment 60* 30* 2* 1.25* 6-6.25% 1980's Pvc polymer DIDP Epoxy plasticiser Barium/zinc Stabiliser Titanium Dioxide Autimany Trloxide - < ^ 59* 33* 1.8* 1.25* 6* 1.2* 0 /a / JU fU c n-V, 1990 ,, f. The level of Autimany Tiroxide has been increased to enable materials to meet the'match test' requirement. 60 fIjk'fcO.s) 22480040 C (j.\- CP^l^l' Jk rn U JL cXrtv cP e.j . 6j y S V S' CuA w 0~ r /i i.~\C O. P 0 c ri>l(* r|j Q : vovJS rn i vAc ^. u c u/o -">0^ t.ltl.l u Phiu,4i~ & if p^uJc l ^. The compositon of materials used for fillings Information to be supplied by the British Rubber Manufacturers. 5. Changes in the compositon of there materials, particularly in the use of fire retardants which might have takensplace in 1986 and 1987 We are unaware of any chages in the composition of PVC mattress covers in this period^ C. /{*. ii.K. - j Cm*. ^ lit. *. bj Sales levels of PVC cot mattress in the UK together with any regional variations Our beat estimates of the total UK market sizes for the different types of PVC cot mattress are as follows: - Cot mattresses : 90,000 - 100,000 units Carry oot mattresses: 80,000 - 100,000 units Push chairs: 250,000 No statistics are available on the regional pattern of sales. From qualitative data we are unaware of any departure from what could be described as normal distribution. 22480041 H 'ji t U U J e*rry A ftichkrd** W con^iVe *< J* r^*> <* f' * Jscrfc^^sH +Si w +* #' Fhosphine, arsine ind stibine gas from plasticised polyvinyl chloride; a possible explanation for sudden infant death syndrome f E^a.rry A, Richardson Technical Director, Penarth Research International Limited PO G'cx 1-42i C'V Pc-tor P*=-r**i, Guernsey, CKai*ivicl izlsntJc Introduction Sudden infant death, commonly described as cot death, accounts for a significant " proportion of pcstneonatal mortalities, usually involving infants 4ih,ich are not observably ill prior to death. The causes remain unexplained despite extensive research, many recent studies concentrating on statistical interpretations of th circumstances of death as obvious explanations seem to have been elirn inated. It has been generally established that sudden infant death syndrome is the commonest cause of death between 1 and 12 months, and accounts for about 2 deaths per 1,000 live births in Vie United Kingdom, 2 to 4 per 1,000 generally in western countries, and about 6 per- 1,000 in New Zealand, but only about 0.3 per 1,000 in Hong Kong, and very lew incidence in Russia, China, Indie, and Africa, and amongst infants of African or Asian origin in England and We.lestl ,2,3,4,5,Cl. The very high death rate in New Zealand is due to exceptional rates ot scout i i ,o per I ,UiX' amongst riaon infants, the rate tor Caucasian infants at about 1.5 per 1,000 being lower than most western countries!??, Deaths occur unexpectedly during sleep, 80X of the deaths affecting infants between 1 and 5 months. There are proportionally more deaths in the winter and more at weekends, with boys more at risk in countries wh^re high death rates occur, The risk is higher with premature births at low birth_ weights, twins, smoking mothers, unemployed fathers, single mothers and poor housing conditions, DeaVis some times follow observations of general malaise when infants have digestive disorders, refuse to feed or are difficult to wake, Page 1 b JUII 'tod 1 x : 1 to k K *J 11 LiH fci 1 J 1 I hK H PAGE.010 B*r^y O Riahrdion j j Plmi>tc id f'VC nc^ puddan infant ^k*U- * * ' ! J --. Recent hypotheses have concentrated on the upper respiratory tract. It has been . /' noted that there has been a threefold increase in sudden infant deaths In The ' ' 1 'Netherlands front 0,46 per 1,000 for 1563-71 to about 1,31 per 1,000 since C'1, '1970(6?, This increase has been attributed to the general adoption of a prone or face-down sleeping position following recommendations that it was preferable at a paediatric conference in 1371', It has been suggested that sleeping in the [ ' , prone position presents more risk, of obstruction of the upper respiratory I ' tract(9,10), Viral and bacterial infections have-also been reported, and may be !. associated with this prone sleeping position (11,12), In a recent review it was pointed out that sleeping in this supine position may avoid some problems but . . create others(13). It has also been suggested that the prone position might- result in hyperthermia as this face is the most important cooling surface and f h , .. temperature control element, particularly in Infants protected in /tf?e winter by extra coverings( 14,15), .j. 1 Another possibility with heavy bed coverings and cots with high impermeable ; 1 sides is that the infant is affected by an heavier-than-*ir gas accumulating at ' V the bottom of the cot, the prone position aggravating exposure and the most !*tv obvious gas being carbon dioxide generated by the Infant itself. High carbon >f. dioxide concentrations would normally stimulate hyperventilation, although infants at risk may suffer longer attacks of apnoea and may not be able to hyperventilate to a sufficient extent to clear, the accumulating carbon dioxide! 16,17). In such circumstances the carbon dioxide would be converted eventually to toxic carbon monoxide, such a conversion p-erhaps explaining why sudden infant deaths are particularly associated with week-ends when an infant may remain unchecked in the cot for a longer period<6). Carbon monoxide poisoning has not been reported but such an explanation would also be consistent with the slow release or formation of any ether- toxic heavier-than- air gas, This paper therefore considers tire risks associated with this possible generation of phosphine, arsine and stibine through biodeterioration of the plasticisers in polyvinyl chloride mattress covers, cot sides and nappy pants, I ! , \ j: :. ` ,' I ..E fcQ Q & M Z . Page 2 b I w 1 1 Hf` H G^rry pi(jhnrf^ PRGE.011 * ' rvc *>\r-Jd n irt f knt Phosphine,arsine and stibine Group lsn-?wn V/Vb S elements form L'Cr-l f_.l gaseous trlh.ydrides, N 1 trogen trihydride is best . ?.<!'. lrin.T>Tri'- *!*$, lervVj ""T f.O liT "Jjf uJSpf ill fT 1 arsine and stibine gases which are' 1,17, 2,68 and 4,29 times heavier than air respectively. The threshold limit, values for phosphine, arsine and stibine are usually quoted ac 0,2, 0,01? and 0,1 ppm rocpo^iively, about 300, 3000 arvd 10OO times more toxic than carbon monoxide which has a TLV of lOOppm, All three gases are colourless, Fhosphine bias & 'dead fish' or 'garlic' odour, arsine is more distinctly 'garlic', and stibine odour is usually described only S3 Very unpleasant'; with arsine the garlic odour is only detectable at air concentrations well in excess of the TLV, a Arsine The typical symptoms of acute arsine poisoning in adults, which usually develop between 2 and 24 hours after exposure, are headache and dizziness with general weakness and malaise, followed by thirst, nausea, vomiting, diarrhoea and abdominal pain, often with, a burning sensation of the face and chest discomfort accompanying dyspnea and pulmonary oedema1IS>. Red urine may develop 4 to 6 hours after exposure, followed by oliguria, anuria' and anaemia, Hepatomegaly and jaundice follow after 24 to 49 hours. Polyneuropathy and encephalopathy hav& also been reported. Chronic exposure is usually reported to have a cumulative effect, This is not slilcLly cun ec l as arsine is .l im ! ia IfJ by cui ivyrs lvi i arid excretion in the urine, but anaemia caused by chronic exposure obviously becomes progressively mure severe-; at very low sir concentrations poisoning is Characterised -at i :n:r^hC32 rrcbvi cvna -gcntrca wcutu..,i>s .<-. i-v*' vmi Vhi3'*anaC(i ie\, 1 Y(*C by of poisoning includes ervthrocyte haemolysis through glutathione reduction which continues after exposure ceases, followed by haemorrhagic hepatitis and nephritis with tubule,!- necrosis, Arsine is a depressant of the central nervous system, and severe exposure may affect this bone marrow, Exposure to 1Oppm for Page 3 H-009LZ2 r n ui t r~> n t n . or j. r n am AT II Ui 4U. nrrr r o B*rry A ftlchrd*on 1c Immd Fva iuddn infni 1, Vl 1 .i :i ,1 toinuts or 3ppm for 30 minutes is sufficient to cause fatal or severe toxic ::Vi| reactions, and 1 ppm for long periods can bo exceedingly dangerous, I 1 *tl. * ' >,: ./f . Arsine poisoning is CJstJally diagnosd ' through acute haemolitic anaemia with ghost erythrocytes and increased plasma haemoglobin, Arsinic in the urine usually exceeds 0.05ma/l in acute poisoning, although in chronic poisoning continuous elimination usually means that the arsenic concentration does not exceed normal ambient levels, It has long been advised that cases of 'toxic jaundice1 and 'haemolytic anaemia' should be investigated for possible arsine . poisoning Cl 9), Mild chronic arsine poisoning may be easily missed and ' attributed to food poisoning(20), Phosphine and stibine ii Phosphorus trihydride or phosphine and antimony trihydride or stibine are nul--=rs------ well known as arsine, but 'they are exceedingly poisonous hea.vier-th&n-air gases!V ;\;j with the same mode of action and symptoms as arsine, The main differences are y\. aEsoconly v 1 to. differences in density and toxicity, ` i 1 i t Phosphine, arsine and stibine from plasticised polyvinyl chloride Phosphine, arsine and stibine can be generated by biodeterioration of organic . and inorganic phosphorus, arsenic and antimony compounds; alkyl compounds may . also be produced whic.h are also exceedingly toxic gases, Scopulariopsis and Paecilomyces fungi are usually involved but some bacteria can also act in this way. These organisms can only convert phosphorus, arsenic and antimony compounds to hydrides if sufficient energy is available, Scopi/laj'i'Opsis breyicaulis, also known as F&nicillium brevicauie, is the fungus species which . is most frequently reported as acting in this way in domestic situations, It is usually described as protein tolerant but it is actually n protein dependent, and was more readily recognised in the past as causing biodeterioration of silk, a protein fibre, Several classical cases of arsine ' poisoning have been attributed to this fungus causing biodeterioration of old'. Page 4 shooed b J UH ' ay Ic'.dl FkUll UH - B 1 3 1 1 HFH PAGE.013. :l t: Pi.r rv A p-VC nd uddn i r f n -t ^th f wallpaper printed -with Scheele's green or Paris green arsenical pigments; a ' u* mystery illness c-c* f ^ c red b*;` UO ArftbtiSSCidv- e Oi> -to J t^).y WCX3 tttt -1t t'J ,; chronic arsine poisoning caused in this way. . Aithuuyh Uis--fungus is ysuaH>T~-- ; associated with biod^terioration of silk, it probably occurs in domestic situations on other protein sources, such as wool in carpets on damp floors or " clothing stored in damp wardrobes. Scopuiariopsis hreviesulis can develop on polyvinyl chloride in an infant cot if the plasticiser in the PVC is a. p-rote-in, such as epoxidised soya bean oil, or through soilage by food, vomit or faeces which has been inadequately cleaned . from a. textured FVC- surface. Other fungi and bacteria can deteriorate PVC plasticisers, particularly Qspgrgilltjs nicer which causes grey discolouration and Si-"`apivmy:ss rubrire ticauii which- causes bright pink staining; these organisms have no toxic effect but their presence indicates that conditions are suitable for the development of S. bre^icaulis and other organisms that can generate :`i;. phosphine, arsine and stlbine. : .. The arsenic source in plasticised PVf: is usually 1 Q..1 iV--r*>i/h-l=phen=-fs</=.rc ins(OBPfil, a biocide that is incorporated to prevent biodeterioration of the plasticiser in tentage and similar PVC fabric exposed to the weather, although it is also sometimes used in PVC furniture coverings for hospitals as a .sanitizina agent ClfiPA will I'linf.rnl mnst organisms at nra-msl biocidal uco> concentrations but it is slightly volatile and it is also degraded by ultra violet light, concentrations progressively decreasing until colonisation by arsenic-resistant organisms such as ?. hreviczulis becomes possible. The- antimony source is usually antimony trioxide, a. white pigment which is added to PVC to improve fire retardency as it acts with the chlorine in the PVQ as a flame suppressant, but it appears that many manufacturers are now using antimony trioxide as a filler pigment at concentrations well above those, . ' required for fire retardency. Antimony trioxide is not particularly biocidal and . stlbine can be generated If conditions are otherwise suitable for microbial. development, The phosphorous source Is usually & phosphate plasticiser, used in preference to phthsilate and similar compounds when fire retardency is required. Regulations Introduced in the United Kingdom in March )9B3 require PVC for : Page 5 ;> 9frOG9tZZ 6 JUM '89 12:21 FROM DH - B1311 AFH 01 407 4384 PAGE.014 I I -l B^rry A RlehrJ>vn ^ id rvc >n<d tnTnt i .nursery purposes to be fire retardent and this will mean that all cot PVC will contain antimony trioxide and/or phosphate plast.lri=*r3 in tl,* fwKir, v^ Sufficient moisture is essential for microbial activity, but breathing will be an adequate source in a ; cot, and in 'winter conditions in houses without central heating there will be s tendency for moisture to. condense on the inner surface of PVC cot sides. A nutrient is also necessary which is usually the plasticiser in the PVC formulation, although surface soiling may be essential to initiate fungal or bacterial infection capable'of phosphine, arsine or stibine generation. i Investigations l1 Phosphine, arsine and stibine generation by Scopu1sricps-is brevicaulis can be demonstrated in the laboratory. This fungus is protein dependent and will not develop strongly in the absence of a protein nutrient source, ft convenient culture medium can be prepared by stirring 5% soya flour into E7. malt agar, If a phosphorus, arsenic or antimony source"is added in the medium or as a patch of material such as impregnated filter paper or fabric, generation of phosphine, arsine or stibine will occur. These gases are reducing agents and can be detected by their reactions with silver nitrate (black) or mercuric chloride or bromide (yellow to red, depending On concentration), Mercuric chloride or bromide oaoer. preoared hv semiring (111*1' f'Jfer in =. 4'/ ;<leol>il con be used .= small strips over Petri dish cultures and is this most convenient technique, but if greater sensitivity is required air can be passed through silver diethyldlthiecarbamate reagent (21 ). PVC is often naturally infected and deteriorated by organisms, particularly Asp&rgilius nicer and Streptomyces rubrireticuli, a.nd laboratory experiments have demonstrated that these infections can 'develop if the arsenical biocide 0E3PA is present at an inadequate concentration and even if antimony trioxide is present at high concentrations, provided that a suitable nutrient source is available externally or within the PVC as plasticiser, It has also--been demonstrated in laboratory experiments that the fungus Sccpulariopsis brevicaulis can develop on the same PVC- samples in similar conditions, a high Page 6 \ * ' I ; i I i V : : JO A'tOO9P0 6 JUN '83 12:22 ! FROM DH - B1311 AFH PAGE.015 A l^ichMrdn D1ilcl*d FVC mrtd *xuWW*r> tnfnt . protein nutrient source being necessary such as an epoxldised soya bean oil i - ' plasticiser or external soiling, a high protein soya/malt agar medium being the i i Meet dopt/onic-n-fe wo-;- iritr-;*du.- -ni trxtwciiai protein source in routine 1 ~ '` X\ I laboratory experiments . I Exposing small discs of FVC fabric to 5. brevicauiis Petri dish cultures c>n soya/malt agar with mercuric chloride paper detection is a simple means for checking whether samples contain arsenic, antimony or phosphorus sources which .might cmot u-'.-.ic yas generation urlder appropriate blodetericration conditions, Checking FVC involved in sudden infant death to confirm whether toxic gas generation was probable can involve a similar technique, but using small discs of the fabric to inoculate soya/agar plates with mercuric chloride paper to detect any generated arsine, stibi.ne or phosphine gas, This meihcyd; may not be sufficiently sensitive but with cultures in jars air can be circulated through silver diethyldithioca.rbamate reagent. Suspect fabric can also be checked for natural contamination end gas generation by placing samples in large jars with closed sir circulation passing through this reagent and returning to the culture jar through a water wash bottle to maintain humidity, Discussion Phosphine, arsine or stibine gas generation through biodeterioration of plastiser in polyvinyl chloride fabric is a possible explanation for sudden infant death, particularly if death occurs in closed cots which can form a reservoir for a toxic heavier-than-air gas, Toxic poisoning in this way is consistent with the reported circumstances of cot death syndrome, A prone sleeping position, heavy coverings in the winter, and longer sleeping times at week-ends all increase the risk of poisoning from a heavis>r-'then-lr gas, The increasing incidence over " the last 20 to 30 years would be consistent with the increasing use of plasticised FVC In nursery products, and significantly lower incidence in some countries may.be associated with failure to use FVC products in this way, The frequently reported malaise, digestive disorders and anorexia prior to death would be consistent with such poisoning, although it might be expected that some darkening of the urine would also be reported,' Page. 7 22480043 JUW '83 .12:23 FROM DH - B1311 AFH 81 48 F 4384 PAGE. 0 IS i ii DAfry A R Ict-iAfdAon FM tic ld PV C hd tuddAA Inf n \ Ua* fc Vn The symptom3 of phosphine, arsine and stibine poisoning have been generally ` reported for adults w ith the cautions that poisoning is not easily suspected or diagnosed*! 19), Children would be affected by lower concentrations because of their lower body weight; in an accident on the rherntopylia, a ship carrying grain fumigated with phosphine, 29 crew and 2 children were affected and one of the children died <22), Infants with low birth weights might be expected to be more susceptible, whatever the cause of low birth weight, The high incidence at less than 12 months is probably associeted with low body weight coupled with minimal ventilation due to body disturbance during sleep, but the peak incidence bf.t.w&e.n i and 5 months might he sssnrlateii__ with, physiological tea.toues t-.CS-t.A ic.'tiid poisoning. widh h-l^c-d. or rotpiraiion which n.igh-t infrcMC s>c-n 11 tv i -fcy 4o / Hydride formation by micro-organisms is well known, Sulphate reducing bacteria such as fossulfovibrie. Species can convert sulphates to sulphur dihydride, mors commonly known as hydrogen sulphide, but only usually in anaerobic conditions in. * which the bacteria utilises sulphate in this way as a source of oxygen. Nitrogen tr (hydride or ammonia can be generated from nitrogen sources such as. nitrates and urea by a. variety of bacteria, some acting In aerobic situations end some also capable of converting suitable phosphorus, arsenic and antimony sources into the trihyd'Md-iS phosphine, arsine and stibine, In all cases these bacteria also require a suitable nutrient carbon source. Fungi can also generate phosphine, arsine and stibine, Faecilomyces and particularly Scopulariopsis species being the most likely cause in domestic nursey situations in which the protein-dependent Scopulariopsis breyicsulis is likely to be present as an infection of damp wool carpeting or clothing, The spread of this infection to FVC and its phosphorus, arsenic and antimony sources is most likely to be through food, vomit or faeces contamination which is very difficult to completely remove from a deeply textured FVC- surface, although some PVC formulations contain epoxidised soya bean oil plasticiser which will provide this fungus with a convenient protein source and encourage particularly rapid deterioration of the plasticiser coupled with toxic gas generation from env phosphorus, arsenic and antimony compounds that may be present. 22480049 Page ? 6 JUN '89 12:23 . .J FROM DH B1311 RFH kJl 4U, 4yb4 PfiGE.017 6arry A Richrdon PVC`j fcrvcl udd*m inf'ni ' j; : Conclusions iv . i. >' .. s Fhosphine, arsine find stibine gas generation through biodet-erioration of plasticised PVC is a possible cense of sudden infant death. Infants are particularly at risk because of their low body weight which makes it easier to ;r. ; " accumulate a lethal dope. Poisoning is difficult to detect as ary throcyte haemolysis, the most important diagnostic feature, is also a normal postmortem' . feature, and the phosphorus, arsenic or antimony introduced into an infant body through phosphine, arsine or stibine poisoning would not increase levels beyond- : normal ranges. It is recommended that infant death investigators should npte- whether the deaths occur in enclosed cots which might act as reservoirs for toxic heavier1 "> than-air gases, and any PVC cot sides, mattress coverings and nappy pants should , </' be examined microbiologically. Small discs of fabric should be incubated on.' high protein agar plates, such as normal malt agar witti the addition of soya flour, to check for the presence of infections. Positive identification of:organisms is not essential, but it is necessary to confirm whether an infection' is present which may cause phosphine, arsine . or stibine generation by inoculating isolates onto high protein plates with 3 suitable PVC source of ' phosphorus, arsenic and antimony, and detecting phosphine, arsine or stibine generation using 3 chemical method, such as the formation of a yellow or orange colour on mercuric chloride- or bromide test paper, or a red colour in silver diethyIdithlocerbatne te reagontiJl ?. Acknowledgements These investigations ar~ an extension of a seris of projects on biodeterioration;; of plasticised FVC. I am particularly grateful to Hr P R Mitchell of Mitchell'' Marquees who, when warned that arsine generation might occur in stored tentage/ containing OEPA, prompted these investigations by enquiring whether sudden': infant death might be caused in this way. My assistant Mrs 9 A R Kelly was'; responsible for the myoo logical work, and Mr T R G Cox advised on chemical'- Page 9 : Q&008FZ b JUN ' b'd ii:a4 mull L>H - B131I HP H PAGE.018 V f: : A **** l*d PVC *pj tuddn in f m.r*> \ P matters, Dr 0 Allsopp o f 'the Commonwealth Myco log ice 1 Institute at Kew supplied the original sample of Scopulariopsis 6>-?vicaulis which enabled us to establish that phosphine, arsine and stibin* could be generated through biodeteriotaion of \N plasticised polyvinyl chloride fabric. References 1, Golding J, Limerick S 1 MacFarlane A, Sudden infant death; patterns, puzzles . and proble.as.Shepton Mallet: Open Book Publishing, 1935, 2, Eecroft 0 M 0 ti Mitchell E A, Trends in unexpected infant deaths, Lancet 1339;SE-39:673. , ^ 3, Lee N N Y, Chan Y F, Davies D P, L&n E Si Yip D C P, Sudden infant death syndrome in Hong Kong; confirmation of low incidence E'r Med rf 1939;293:721, 4, Gordon R R,Trends in unexpected deaths in Sheffield Lancet 1939:3629:106 5, Balarajan R, Son! Rsleigh V & Sotting B, Sudden infant death syndrome and i postneonate.l mortality in immigrants in England and Dales, Pr Med J 1989:238:7 I 3-720. 6, Morris J A, Increased risk of sudden infant death syndrome in older infants at weekends. Pr Med J 1386;233;5S8, 7, Mitchell E A, Hassall t B i Peeredt D M 0, Postneonatal mortality review in Auckland; two years Srxperience. NS Med J 19871100:239-272 3, de Jonge G A, Engelberts A 0, Koornen-Liefting A J M fi Kostense P J. Cot dea th and prone sleeping position in The Nether lands,Pr Med J 1989:233:722. 9, Beal S, Prone or supine for pre-term babies7 Lancet 1938;ii;5!2. 10, Southall D P, Croft C, Stebbins V, et al. Detection of sleep associated dysfunctional pharyngeal obstruction in infants, Fur J Pediatr 1969:148:353-9. 1 1 , Morris J A, Haran 0 Ii Smith A. Hypothesis! Common bacterial toxins are. a possible cause of the sudden infant death syndrome, Med Hypotheses 1937;22:211-222. 12. Morris J A. Sudden infant death syndrome, Pr Med J 1939! 298:353, 13. Milner A 0 Si Rnggins N, Sudden infant death syndrome. Br Me'd J 1989; 299:593-690. ! Page 10 TS008PZ 6 JUN '89 12:25 FROM DH - B1311 flFH Ul <4Ur 4d'd4 PAGE.019 B*i* r-v A Rich#r*don PVC ^ricJ JeJ* i.t-> r .rvt d** Vi 11, Nelson E P ? Te.y.1or B -T i; Waatherall I L, Sleeping position and infant death bedding in ay predispose to hyperthermia and the Sudden Infant Death 1 Syndrom* Lancet 199?', 1:19?-200. 15. Stanton A N, Scott D J S Downham MAP S, Is overheating, a factor in some unexpected infant deaths? Lancet 13'3?;i:l 054-7, 16. Kelly D H, Golub H, Car lev. D k Shannon D, FYieuwograifis in infants who subsequently died of Sudden Infant Death Syndrome. J Fedistr 1386:103:249- 254. ,. 17. Kahn A, Blum 0, Rebuffat. et si, Folysoinhographic studies of Infants who subsequently died of Sudden .Infant DeathSyndrome, Pediatrics 19SS;S2:721727. 13, tile inf eld M J, Arsine poisoning J o M 1 9s30:22;320, '3, Dolg A T. Lsncot 1354:ii;S3~32, 20. Hunter D. Fhsrm J 1936;! 37:61 4-1 5, // 21, Anon, Arsine Nc,r/-,vO'" f.-,r jj-,s detection of toxic Substances in sir,' BookJet No ?, Ministry of Labour, H M Factory Inspectorate; London, HMS0. 1355, 22, Wilson R, lovs-.ioy F H, Jaeger R J & Landrlgan P L, Acute phosphine poisoning abroad a grain freighter. SANA 2d4; 143-1 SO, 248005 : I Mr* in--,.. .... Page 11 JO K CC( HYDRO IfiBfit POLYMERS Vinyls Division Dr R K Hinderer B F Goodrich Co 3925 Embassy Parkway AKRON OHIO 4413-1799 USA Your ref. Our ref. HMC/PAM Your letter of Date 30 May 1990 Dear Bob, PVC AND COT DEATHS In reply to your fax of 29 May, a copy of the principal file items going back to early 1989 is enclosed. Most of the items were given to Roy Gottesman during the course of his visit to Brighton at the end of April. The relatively low order of priority that the Laboratory of the Government Chemist originally gave to the investigation of these claims has not been helpful. Please let me know if you have any queries on the file documents. We will keep you informed of public statements. Yours sincerely, ii n vi ajr iuii Senior Environmental Advisor zsm Btzz. Hydro Polymers Ltd. Newton Aycliffe, Co. Durham. DL5 6EA, England. Registered Telephone: Telex. 58322. in England National: (0325) 300555 FFaaxx:: No. 1631120 Internat: (44 325) 300555 (0325)300215 Registered Office: School Aycliffe Lane. Newton Aycliffe. Co. Durham. DL5 6EA, England