Document 6RzBBg7oeQNB7GpM0waK6jOqo

*-v 2h-A~^ CONFIDENTIAL 'rkJ^-p W-^. ''to cLyvC^SS-^-^ * i*J^Ss -^jCVfc. V ***--iaJ5 c^yf^rS^. &-A f"Oiic COT DEATHS Draft submission to the Department of Health, 3rd May 1. First use of PVC mattreaa Covers Due to breaks in record keeping theory 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 19fc0' s. fo*s!4. V}5o'<. 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). 3. The composition of materials used for covers. 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 1980's 1990 PVC polymer Octyl phthalate Epoxy plasticizers Bar|lium/cadmium/zinc stabiliser Titanium Dioxide pigment 60* 301 2< 1.25* 6-6.25* (XmjVc3L Pvc polymer DIDP Epoxy plasticiser Barium/zinc Stabiliser Titanium Dioxide Antimeny Trioxide c*^Ta~~ io 59* 33* 1.8* 1.25* 6* 1.2* 4.5'i |o"i, pUS" UfZK M*o the'match test' requirement. ) o U7 CO The compositon of materials used for fillings Information to be supplied by the British Rubber Manufacturers. 5. Changes in the composlton of there materials, particularly in the use of fire retardants which might have taken, place in 1986 and 1987. n - l* We are unaware of any chages in the composition ofiPVC mattress covers in thi3 period. pb&A-iU* (V 6* Sales levels of PVC cot mattress in the UK together with any regional variations --- Our best estiraates-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 cot 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.- -------- / V Mr P.G Dibb l Department of Health Hannibal House Elephant and Castle London SE1 6TE The British Plastics Federation 5 Belgrave Square London SW1X 8PD 071-235 9483 Telex 8951528 Plafed G Fax 071-235 8045 2nd May 1990 STRICTLY CONFIDENTIAL Dear Mr Dibb I am responding to your request for information on several points relating to the usage of PVC cot mattresses and foam fillings. I understand that you will be passing these data to the Expert Working Group convened by the Chief Medical Officer to advise him on Mr Barry Richardson's hypothesis on the cause of Sudden Infant Death Syndrome (SIDS). A delegation from the British Plastics Federation will of course be meeting the Expert Working Group on the afternoon of May 3rd when we will be pleased to discuss this issue further and to add any necessary amplification. I I should add that owing to the structure of the industry and its trade bodies it is the British Rubber Manufacturers Association (BRMA) which is the focal point for matters relating to foam. We cannot therefore offer detailed comments here on foam but we expect that a representative of the BRMA will Join our delegation on May 3rd. To revert to your specific questions: 1. First U3e of PVC mattress covers Due to breaks in record keeping during the evolution of companies and changes which have affected the structure of the industry the exact date for the introduction of PVC mattress covers is not known. They were certainly in use in the early 1960's and their origins probably lie in the late 1950*3. 2. Dates on the first use of foam fillings This information will be supplied by the British Rubber Manufacturers Association but the origins of foam fillings draw similar comments to the response in (1). 3. The composition of materials used for PVC mattress covers 0 Over the years the composition'of PVC materials Used in the manufacture of cot mattresses has evolved to reflect changing technologies, regulations and their attendant standards. Typical formulations at different stages in the history of the product would be as follows: Director -DR Jones A company limited by guarantee Registered in England No. 282883 / I960'3 PVC Polymer Octyl Phthalate Plasticiser Epoxidised Soya Bean Oil as Plasticiser Barium/Cadmiura/Zinc stabiliser Titanium Dioxide pigment 60* 30* 2* 1.25* 6-6.25* 1980*3 - two formulations in common use: (A) PVC Polymer Di-isodecyl phthalate plasticicer Epoxy plasticiser -- Barium/Zinc Stabiliser ! Titanium Dioxide __ Antimony Trioxide 59* 33* 1.8* 1.25* 6* 1.2* (B) PVC Polymer Di-isodecyl phthalate plasticiser Phosphate Plasticiser - Epoxidised Soya Bean Ester as Plasticiser and Co-stabiliser Calcium/zinc stabiliser Phospite Stabiliser booster Titanium Dioxide _ z 58* 23.5* 8.5* 1.1* 1.1* 1.1* 6.8* 1990 -- The level of Antimony Tioxide in formulation (A) above has been increased to_a level of 4.5*_enable materials to meet the 'match test1 requirement. It is worth mentioning in this-context that PVC sheet is widely used in hospitals for mattress covers and pillow cases and that fire retardants have been used in these applications to meet DHSS requirements for many years. 4. The composition of materials used for fillings This information will be supplied by the British Rubber Manufacturers Association. 5. Changes in the compostlon of these materials< particularly in the use of fire retardants which might have taken place in 1986 and 1987 We are unaware of any changes either in the composition of PVC mattress covers or the fire retardant systems used in this period. 6. Sales levels of PVC cot mattresses in the UK together with any regional variations Our best estimates of the total UK market sizes for different types of PVdM cot mattress are as follows: ,2480061 Cot mattresses: 90,000 - 100,000 Units Carry cot mattresses: 80,000 - 100|000 units Push Chairs: 250,000 units (UK manufacturers have th6 major share of thd market) (There is a substantial leVel of imports of thd sheet Used itt this category particularly emanatihg dt thd moment from East Germany fthd Israel) (UK manufacturers havfi fchA major shara bf thft market) Ho 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> More broadly Mr Richardson's study haS bflSH Subjected td close Scrutihy by tfill industrial companies involved. They and otheh organisations have been Unabifi td reproduce his work. A full appraisal of hiS initial paper carried oUt by th8 British Plastics Federation is attached As Appendix A; A detailed report of experimental work carried out by the British PlasticS Federation is also attached as Appendix B. The British Plastics Federation is extremely inxioUS to co-operate fully With the Department of Health's Expert Working GroUp in its investigation to see Sri early vindication of our productsi We did irt fact at A much earlier poiht provide detailed information to the Laboratory of thd Government Chemist but unfortunately we have not yet had a fdrmdl indication of its reSUltsi We now look forward to some positive feedback from the Department and Should y8U require any further information pldase dc hot hdsitdtd td Contact mej With best wishes Yours sincerely Philip Law Head of Planning and Membership Activities 22480062 i The British Plastics Federation 5 Belgrave Square London SW1X 8PD 071-235 9483 Telex 8951528 Plated G Fax 071-235 8045 APPENDIX I BRITISH PLASTICS FEDERATION'S REVIEW OF MR B.A. RICHARDSON'S REPORT, 'COT MATTRESS BIODETERIORATION AND SUDDEN INFANT DEATH' (JUNE 1989) AUGUST 24TH 1989 9 0 0 8 V IZ V Director - D R Jones A company limited by guarantee Reaislered in Enaland No. 282883 If >* 24ihAnf<i^ i irmn COT MATTRESS BIODETERIORATION AND SUDDEN INFANT DEATH 1 . Introduction In early June 19^9 considerable media coverage focused oti the conclusions of a report entitled 'Cot Mattress Biodeterioration and Sudden Infant heath' published liy Mr II.A. Richardson oT Fenarth Research Intehnational Ltd, thid attempted to demonstrate a link between the Use oF PVC materials In cot mattress and the tragic phenomenon commonly known ad 'cot death't This report has been subjected to detailed investigation by the Laboratory oT the Government Chemist. This paper summarises the examination of the report separately carried out by the manufacturing companies concerned - the PVC resin manufacturers, additive suppliers and calendered FVC sheet manufacturers - and It approaches the subject from three principal .standpoints: - - analytical, chemistry - microbiology - medical The principal, plications which Mr Richardson's report raises are as follows: A) What are the constituents of PVC materials Used In FVC cot mattresses? H) Can emissions oT arsine, phosphine and stibine take place? C) Do these emissions actually take place? D) If so are the emissions injurious to health? G) is there any link between the emissions and cot death? ?.. What are the constituents of PVC materials Used In PVC cot mattresses? Mr Richardson1s report states that "all cot FVC contains antimohy trioJcide and phosphate plasticisers" (p.'l). It is certainly trUe that triaryl phosphate is used up to 12X weight/weight fihal compound and antimony tr.loxi.de incorporated up to about 1.3< weight/weight final compound. However, they are never used together in a formulation. Mr Richardson is wrong in his assertion that 'manufacturers are how Using a timony trioxlde as a filler pigment at concentrations vtell above those Used for fire re ta rdancy 1 ( p. 'I) . it is also untrue, as Mr Richardson implies (p.'l) that 10,10' oxybi sphenoxyarsinn (OFIPA) is used as a biocide (p.ll) in PVC cot mattress for mi 11 a t ions . Mr Richardson has not produced any evidence to indicate that he has analysed the PVC coverings to determine their hrtspMstHons. i i J t 9 0 0 d 'k t t Can emissions of arsine, phosphine and stibine bake place? Hr Richardson's conclusions rest on the role of a particular fungus, 'Scopulerop3is brevicaulis', in developing on PVC cot mattresses 'if adequate moisture and protein are present, perspiration providing these requirements' (p.M). It is this, he says, which liberates arsine, phosphine and stibine. The strong implication is that he had carried out laboratory investigations hims-e-lf (p.5). However, he gives no information about the time-scale of the experiments detect the presence of phosphine, arsine or stibine through the colour changes experienced by stiver nitrate and silver diethyldithiocarbamate, particular the length of time taken for colour to develop. to in The use of silver nitrate test paper itself provides only a qualitative means of detecting the hydrides of phosphorous, arsenic and antimony. Thi3 method is by no means _spe_sific for these hydrides. A positive test is only -indicative of a reducing agent being present. Hydrogen sulphide also-gives a__colouration with silver nitrate, test paper. If sulphate-reducing bacteria" are present, hydrogen sulphide could be-- generated. The absence of hydrogen sulphide would have to be proved - lead acetate test paper would probably suffice. Mr Richardson also claims ammonia can be evolved by a variety of bacteria. Again, the absence of ammonia would have to be proved - it could also discolour silver nitrate test papers. Richardson is adding protein (a source of nitrogen) to the culture dishes. If there i-s-any degradation of P. V. C. itself then there i3 a possibility of hydrogen chloride evolution - another potential interference to silver nitrate test papers. Nowhere in Mr Richardson's paper is there scientific evidence to show the absence-of these potential interfering substances. Mr Richardson's detection method is inadequate if phosphorus, antimony and arsenic are present together. More fundamentally there were no adequate controls in the investigations and the following issues need to be addressed: what happens with fungi growing on the medium with no added PVC ? what happens with the indicator strip incubated over uninoculated medium? what happens with the indicator strip incubated with infected and sterile Pvc alone in the absence of a growth medium and added fungus? These controls are particularly important since one of the references cited, 32, indicates that the organism can release arsine from laboratory media. His result therefore may just be an artefact of his methodology. 32480065 t There is no evidence of identification of the fungus from infected samples. Fie claims the fungus has been detected but gives no quantitative data such as number per square millimetre or amount of hypha per square millimetre. 4. Do these emissions actually take place? Mr Richardson's investigations were carried out in a laboratory where the fungus was developed under optimal conditions ,for its growth. They do not show that these gases could be produced 'in vivo'. The temperature under a baby in a cot would be at about body temperature of 37C, possibly higher in situations where bed clothes act as insulation. It is not established that the fungus will grow or remain metabolically active at that temperature as many fungi will not grow at 37*C. 5. Are the emissions injurious to health? The quanities of gases generated in cots under normal conditions are likely to be extremely small and uninjurious to health. This is further supported by the configuration of cots, most of which are open-sided with rails rather than panels. Additionally, mattresses currently manufactured have holes cut into the foam at the head end to facilitate a child's breathing. In these cirumstance3, if phosphine, arsine and stibine were generated in the way described by Mr Richardson they would be well diluted. This Is graphically illustrated by the following example. If we assume that the densest of the three gases, stibine was present at the extraordinarily high level of 1000 ppm even then the density of the air/stibine mixture would only be 1.003 compared to air = 1. This is a trivial difference and the stibine would rapidly disperse in normal air movements such as convection currents. Lethal concentrations cannot accumulate. 6. 13 there a link between the emissions and cot death? Mr nichardson's report only remains a hyphthesis. The statistical information he cites on the incidence of cot deaths (ppl-2) is not based on authoritative source material. Some fundamental weaknesses are illustrated by the following: his statement that most cot deaths occur at week-ends is not totally corroborated as several studies do no demonstrate a correlation. he does not mention that the incidence in the USA is equivalent to that of Australia and the UK. the lower incidence of cot deaths in Scandinavia is more probably due to their higher level of health education and social conditions. the rate for Hong Kong of 0.3 per 1000 is more likely to be due to the over-crowded conditions in which large families live, producing a greater awareness of subtle changes in a baby's condition. 99008k j / statistics on this subject are notoriously inadequate, this is due to the lack of a post-mortem and death certification, a post mortem being essential to produce a diagnosis of cot death. Statistics are probably at their weakest in Russia, China and India where Hr Richardson quotes a low incidence of cot death (pi). Authoritative organisations and close students of cot deaths such as the Foundation for the Study of Infact Death believe that there has been no increase in cot deaths and that cot deaths occured in antiquity. It is additionally, a well known fact that babies who die from 'cot death1 do not necessarily die in a cot and are known to die even when in the arms of their parents. Although there is probably no one single cause of cot death, perhaps one possible cause of cot death relates to the sleeping patterns of babies. Two-thirds of cot deaths take place during the first six months of life. baby has a deep sleep pattern in this phase, which then changes. A We have to conclude that there is no direct evidence of an association between gaseous intoxication and Sudden Infant Death. 9008kZ2 I f (~) The British Plastics Federation 5 Belgrave Square London SW1X 8PD 071-235 9483 Telex 8951528 Plafed G Fax 071-235 8045 X APPENDIX II t EXPERIMENTAL WORK CARRIED OUT BY THE BRITISH PLASTICS FEDERATION ON THE BIODETERIORATION OF PVC COT MATTRESS COVERS. JULY 12TH 1989 890081^3 V Director -DR Jones A company limited by guarantee Realstered in England No. 282883 J t BIODETERIORATION OF FVC COT MATTRESS COVERS INTRODUCTION A recent rejport by B.A. RichArdSon b feAharth -Research inter* national Ltd., Guernsey stated that jpboSphin6} Arsine And stilbene can be released from pldstici id PVC cot mattress covers by biodeterioration .caused by reaction of the fungus - Scopulariopsis Brevicaulls, _ A set of experiments were- performed to test this hypothesis,~ EXPERIMENTAL An authentic sample of the fungus SaopUl&riopSiS brevicauliS No. 049528 was obtained from C.A.S, international Mycological Institute, Ferry Lane, Kew, Surrey, TW9 3AF, Culture media utilised during, the investigation Were malt extract-agar (Oxoid, CM 59). With the Addition of 10 g pet litre soy peptone (Lab M, MC3) and malt extract-broth (oxoid CM 57) with an identical addition of Soy peptone, -The" media were prepared and StAtiiisAd According to the manufacturer's instructions. The agdt medium WaS dispensed in ~20-ml velumes-into 90-mm single vent pAtri dishesi The broth medium was stored in 50-ml volumes Itt 100 ml Dtlran ScrAW-feApped bottles. Silver nitrate and mercuric chloride test paperg Were prepared as in B.A. Richardson's report. Preparation of Starter CulturA A starter culture was prepared by inoculating Soy-enriched malt extract broth with scopulariopsis brAVicdUliS and ineubAtihg on a shaking water bath for 72 hours at 23*C, Subsequent Viable counting, after suitable serial dilUtibh, indicated -thAt the resulting suspension contained Approximately 61S X 103 colony* forming units per millilitre. Investigation in liquid medium In order to investigate whether Any phbsphorug ArSAnic or antimony hydrides were liberated ftom Appropriately doped broths by the action of SdopulAtiopSiS IvevicAuliS thA following experiment was performedJ Four bottles of broth were ASfepticAily ihoclllatAd With d;S fiii of a starter culture. One o these bottles WAS used AS A control, with no further Additions< (ThA other three WAtA supplemented by the addition of One bf the following 1 i 6900nvtz--- (a) Corvic S71/102 PVC powder ((3,5 g) (b) Antimony Oxide powder (0,5 g) (c) Triaryl Phosphate (2.0 till) Suspended from the top of each bottle WAte Strips (30 K 5 tom) of silver nitrate test paper Ahd mercuric chloride test pApeti The bottles were incubated for 144 hours At 23 #c, After Which A dense micelial growth Was observed ih Ach Simple, Investigation on solid medium In order to investigate whether the hydrides of phosphtotUA, arsenic ahd antimony were released from the materials under investigation by the action of the fungus When grown On & Solid medium, the following experiments Were Set Upi I Sixteen petri-dishes .containing Soy peptone-enriched mAlt extract agar were inoculated With 02 ml Of the ScopulatiopAiS brevicaulis starter culture. This ihoculum WAS then Spread uniformly over the surface of the agar. Two plates were used as controls. To the remainder, thfi following Additions Were made: (1) TRIARYL PHOSPHATE (0,5 tali WAS feprSAd OVAr thfe AgAt, (2) corvic S71/102 (0.5 g) was Sprinkled over the agar. (3) Antimony Oxide (0.5 g) WAS feprihkied over the agAr. (4-14) 25 x 50 mm samples of PVC sheet WAS plAeed on the agar, See Table 1 for the composition of thi PVC Formulations R6f 7631-7641. % *' * Widely separated strips of ftilVSt nitrate And metbUtio Chloride test paper (ioo x 5 mm) were now placed in the lid of the petti dish, the paper was stretched over the ihOCUlAted And impreg nated agar surface. All the piatCS weti ihcubatfed at 23 4C fot 144 hours, after which a dense lAWn of fungal mycelium Coveted most of the plate. EXAMINATION OF TEST STRIPS AFTER TESTS No stains were observed on the metcUric chloride test papfetS from both the liquid and Solid cultures, i,Ai ho positive t68t for arsenic. There was some yellowing of the test Strip from the cdhtrol but only on the edge of the strip overhanging the edges of the petri-dish. it was noticeable that the only Area of the piatis where dense fungal growth had not occurred Was that tone immediately below the mercuric chloride teat strip. This is presumably because of the potent fungicidal properties of mercury compounds. No stains were observed on the silver nitrate test papers 6h the area of strip across the diameter of the petri-diShAS, There was a general discoloration of All the Silver nitrite test strips which is probably the effect of daylight, l i3c Black stains were observed ort the Silver nitrate test papers ih the area which was bent over the 4dg#S of thd petri-difihes> These black stains were also observed in the controls. As there was no staining of the pipits ih the 4be48 Where fungal growth was taking plies> these Stains an the edges Of the test papers cannot be taken as a positive test of hydride generation especially aS the S4m phhom6non OeeurS in the controls. on the plates where triaryi phoSphite* antimony okidd Ahd PV6 powder had been placed in the agar Surface> the fuhgdl growth had completely invaded the impregnated areas* On the plates where plasticised PVC Strips had been placed bh the agar surface , the fungus did not appear to invade the fcVC strips. h i There was also no staining of the test strips ftbm the iiguid broth experiments. ' CONCLUSION This repeat of Richardson'S WOtk WaS Unable to give a positive identification of hydride generation ftort pVc cot mattress materials. The stains on the test pipet9 at the overhanging outside edges cannot be taken &S a positive test 4S this 4165 occurs in the controls. Even in the more^rigoroue conditions of fungal growth ih liguid cultures were we/^abie to detect phosphine> arsine bti stiibene using Richardson's detection methods* J !j .J, # T W 08VZZ I Fo" 00 cn\T? C\? t rJ ri ff.' if 1r ti l!. oHo 1 1 fS 1 i ii o vn i1 m 100 50 i rs i ii Oo o H 1 i ri m i I 1> i vo oN o H P I i I m i o m o o m <N o H I w I | i i I m o o a# H "T m O o H r (N o I in o o (N H ? o o o m <N HI o o m M rH o i i i nr* i vo fsj | I l o 10 I lo I I o I I I to II Q I mi I I i o Imi I I l i o r) o H *t o i I I I I I VO r* o V(-O* en r>1 vo r oo m vo r> r- vo t*' vo vmo r- mvmo p* pi vo r* m vmo p< IN vmo t" n vo ! I i / r~ 12.4.90 To: BPF MEMBERS INVOLVED IN COT DEATH ISSUE The British Plastics Federation 5 Belgrave Square London SW1X 0PD 071-235 9483 Telex 8951528 Plafed G Fax 071-235 8045 \ Gentlemen, As you know the Chief Medical Officer has asked a group of experts to advise him on Barry Richardson's hypothesis. The Federation has been invited to attend a meeting of this group on May 3rd (time and location to be advised to us) and has been specifically asked to present the following data in as much detail as possible in the form of a paper:- 1. Dates on the first use of PVC mattress covers. /';_ 2. Dates on the first use of foam fillings. 3. The composition of materials used for covers. 4. The composition of materials used for fillings. 5. Any changes in the compositions of these materials, particularly in the use of fire retardants which might have taken place in 1986 and 1987. 6. Sales levels of PVC cot mattresses in the UK together with any regional variations. The Department Of Health have pledged their confidential treatment of this information. I have naturally accepted the invitation, and I am now taking 3teps to prepare this paper. Not all of this data will be available from Federation sources, for example The British Rubber Manufacturers Association will be the fount of knowledge on foam fillings. I will be contacting those companies I feel will be best placed to provide this information directly. I wish to invite you to a meeting of the interested manufacturers at the BPF at 11.00 a.m. Monday 23rd April to review the information which we can collate, determine the compostion of our delegation to the Department Of Health and our approach to the Meeting on May 3rd. Would you please send me a fax advising me of your attendance. 2Lm m zz Head Of Planning and Membership Activities V ___________________________ _____________________ Director -OR Jones A company limited by guarantee Registered in England No. 282883 ___________ J (St^ J&. '-. qjhO- o- S<P. 3jZ\ o^ ... - fL^i^U ^ JU'te^Jegh*-- ^ ^ oo (u6> Qm c$kd <3S - 2&ju> wo S^LO^QA, a} CjS^-wvA. t-SW^A. <x ^JLnAfM. ^) |M><S/^- C*Ab.QL^ VSrS^ v-s p|iS. o^fL^a. c.) M-jAvu*fl2_ uJ3iL^**3$ % JvA^> ^ -AJtft^ uio^ A-OvAi^?. A*Wt\< (<VJ ^fi> la!bC*M CSftwv-) i*-<Sl.. _______ Uc^g4 /HfU>3AsA :_________________ ____________ k-**.p jffir(4>) -<*- gRt^^ *_ *"$$ Wj 1 BPF _3^0-'<S<us^ (^VAA-Sl _\ ^JC.^ ob> ? ^- __ (^(Lv^fct.'i ^-Aj)_____ _+X^r l**^V V ~ t -V ^AS^S>j. cKyy/^T .- V*A^|^ USl*\V OfL^. -"T^U GsPF" C^L<yAA ECN/tA %tiS\ O^rCTvu!^ ^ 0*^e^3r" <BP^~~ ^oi^so^J^aJ^ i"i>S<*_ ^BF^-^ \4a5^J ^___ -re- ... g.. oo o ^4&> PF ^ A{J Zi*- f IViLp LoUjd* QSr -s^S. EfA- ^5 t*W iN*.' ? g)H tos^eA' VJe^V* ^ -5u- -- _-- ^wil^ clU*^ ^&a*eU^) 1^*-. ^W^4|oo\ -- ^J)csr. o*-^> Orui" K-^). UJ&mKU Mqo Wl)Sa. jbbt1 WP^~ Cm*>| (Vdrct. 'f*aA ^ox) | i^Sbi}*^.e*rK3^, cJ>Tl fW6WS. _._Z"'_ ^Vi^fe^VcLvw) $$}**riasL+.' ~~-- ^A.Jj>oX'Yt_ C^U^<>TOj^6-^-^ l*v*3S_/i 5C_^a.-"&c*5A_ OirjUj^iA WjcM. ^tWv Q3^ ____ ___ _ . Rt-t^ovA^r-i C^\*oJ^*A. ^ --- -- "K^C3-e ^osAJUjX fUro^ __ 'y-rCarX^ _ Q^aQsJ -^1 '*V\3'*. fo&rtfea sr} ^ k cj~vJ ~^ M.*1 ^u^53i ^x^\ttJ>lt^'5^v CXA-Jt T^Ji "^v ^tA* U^- ^'lt*'-____ _ UtfJlX Js^ fe_',**3-2.J$ Jl^. _________________ jMA V>\Qji **j*^*jft \A&T (Sfaji- ^o ^i^JUr" ._ - *^) t'-S" aS cya!| * <A*r>?T' eJB^InxC **| iJh+s. <5^~4-^^M3s3_v t-W*. ^Jo Co--sp-^C. 0S&. ?*^a^c>PS" '3=^^ ^ 3** (Aji^k^c^ VWa^Cjsz^ c^'^ojC'j-o ^ ^ l^roV. 7^ sv^iSLjxi^ Wc U^*A Ei^ ^ ^ ~~ 3^vSr^-^ > ~^c Ct~t%^ CoV" >J?rt- CO OT^-'5,I^oCX^ ( WV" 3Kco*i- -K>*P> JDD_ o o OC\ ^<oaV^~ U\ ^3>-V" Au^"-Qil\^c^ te^E_ ^i*SS ^A---^jro ^60 ______ ___________ ^jp S^l***r> fet ^ " *......................................................... ------ T?JlA.-. gcfe <1^A gft^CaH flJk*-c~tA.W .>4ri--ft /< ................................................................... The Foundation for the Study of Infant Deaths 35 Belgrave Square London SW1X 8QB Telephone: 071-235 1721 / 071-235 0965 / 071-823 2216 <An**i Fax: 071-823 1986 PMrotv.! M ttovnl 1 \w. Duclirs? of CWuic.cMcr 13th March 1990 STATEMENT TO ALL FSID STj^FF FOR INFORMATION "Sir Donald Acheson, the Chief Medical Officer, announced today (9th March 1990) that he has asked a group of independent experts to investigate the claim that the emission of toxic gases from fungal growth on some cot mattresses is a cause of sudden infant death. The group will be chaired by Professor Paul Turner who is Chairman of the Government's' independent expert advisory committee on toxicity and will include experts in toxicology, neonatal pathology, mycology, epidemiology and analytical chemistry. Announcing the review, Sir Donald said that the sudden infant death syndrome was almost certainly due to many causes and these are little understood. Any new hypothesis therefore warranted careful consideration. The hypothesis - put forward bv Mr B A Richardson, Director of Penarth Research International and Mr P R Mitchell, Director of Mitchell Marquees - is that due to the action of certain fungi, soiled cot mattresses may emit toxic gases. Sir Donald went on: 'The death of an infant is a shattering blow to parents. We have a duty to investigate possible causes. But this needs to be done in a way which, on the one hand avoids alarming parents unnecessarily before claims can be properly assessed and on the other, raising hopes that a 'preventable cause' of sudden infant death has been found". "Mr Richardson's and Mr Mitchell's work which has not been published in the scientific literature, and therefore has not been subject to the usual scrutiny and discussion, is al ready being assessed by the Laboratory ot the Government Chemist. The independent experts will be examining the laboratory findings as well as the work done by Mr Richard son and Mr Mitchell, f have asked the group to report as soon as possible and will make public their recommendations". In the meantime, Sir Donald has taken advice from a range of experts including neonatal pathologists and paediatricians. He has been advised that no case of cot death in this country due to the toxic gases arsine, stibine and phosphine has been reported. Nor is there any need for parents to take any special action in respect of cot mattresses. Never theless, as a matter of prudence he has invited an independent assessment of the evidence". The above extract is taken from a Department of Health press release, and follows articles in the Daily Express in February 1990. These articles stated that "startling evidence by government scientists has confirmed a possible new link between cot death syndrome ana fire resistant mattresses", that "Ministers begin a scries of crisis meetings in Whitehall", that "Health Secretary Kenneth Clarke (has) ordered an immediate enquiry into the possible link between cot deaths and fireproof mattresses" and that "Mr Clarke is prepared to order tens of thousands of baby mattresses to be withdrawn from sale if Government scientists confirm a possible link". 22480076 IWjKtorrd n* Olvtnby No. The articles correspond to a theory of a cause of sudden infant death syndrome (SIDS) that was widely reported on television, radio and in the press at the beginning of June 1989. Laboratory work by a chemical analyst, Mr Barry Richardson, suggested that toxic gases were being released when biocides (substances acting against infecting organisms) and fire retardants contained in cot mattress coverings of plasticised polyvinyl chloride (PVC) were acted on by a normal household fungus. He believed that the gases might be a significant cause of SIDS and informed both the Foundation for the Study of Infant Deaths and the Department of Health of his views. Mr Richardson told amneeting of the Scientific Advisory Committee of the Foundation for the Study of Infant Deaths about his work, and was questioned about it by members. After careful consideration, the Committee formed the view that this was an unproven hypothesis for which no direct evidence-existed and that this was unlikely to be a major cause of SIDS. The infant mortality rate (all first year deaths) has continued to fall since plasticised poly vinyl chloride (PVC) was introduced while the SIDS rate has stayed relatively constant. However, the toxic gas theory was widely publicised on radio and television and in the press before any scientific confirmation of the laboratory work had been undertaken. The Foundation was concerned that .any possible such link with SIDS should be quickly and appropriately investigated and forJhat reason is at present funding a project in London (10,000 over 6 months) to undertake^uitable tests. - -- Advice to parents: if'-' The Foundation for the Study of Infant Deaths advises parents that they need not feet that they should take any special action following these claims, and warns them NOT to endan ger their baby by wrapping polythene around the mattress as has been suggested by Mr Richardson. For further information please_contact: '-- Erica De'Ath (Chief Executive) or Tracy Lamb (Research and Information Officer) The Foundation for the Study of Infant Deaths 35 Belgrave Square London SW1X8QB Phone: 01-235 0965/1721. Fax: 01-823 1986 (ENDS) Z i/ jC K ) f r2* PENARTH RESEARCH INTERNATIONAL LIMITED Consulting and Research Scientists Castle Emplacement. P.O. Box 142 St. Peter Port. Guernsey. C.l. Tel: 0481-28559 Research Mote January 1990 Cot mattress biodeterioration and sudden infant death \ 1. Introduction 1.01 FRIL research in 1988 included an investigation into deterioration of reinforced polyvinyl chloride (PVC) fabric used as tentage. The fabric was found to be infected by various fungi which were utilising the plasticisers as nutrient, particularly Aspergillus niger which causes grey staining along the reinforcement fibres and St.reptonyces rubrlretlculi which causes patches of pink staining, despite the presence of the arsenical biocide 10,10'- oxybisphenoxyarsine (OBPA). The clients sponsoring the research were warned by the project, director B A Richardson that other fungi might develop such as Scopulariopsis brevicaulls which could convert the OBPA biocide into toxic arsine gas, and that accumulations of this gas might occur in folded tentage in winter.storage. One of the clients, P R Mitchell of Mitchell Marquees, enquired: whether similar infections might occur on PVG cot mattress coverings end whether generated arsine might be the cause of unexplained sudden infant death. 1.02 The fungus Sccpularicpsis brevicaulls is commonly found infecting protein substrates such os meat, milk and cheese, as well as damp wool, leather and silk 0,2' It has been known since about 1890 that this fungus is able to convert arsenic compounds into arsine (arsenic trihydride) and related alkyl compounds 0-17). Gosio and Sanger reported that some mystery illnesses and deaths were due to arsine generation through this fungus infecting wallpaper printed with the arsenical pigments Paris green and Scheele's green, although another source of arsine on papered walls was horse-hoof size which often contained white arsenic (arsenious oxide) as a rodent repellent. In the United Kingdom the last deaths from these causes were reported in 1932 02). 1.03 Investigations on PVC cot mattress coverings show that all used mattresses are naturally infected by the fungus . Scopulariopsis brevicaulls in the area affected by the warmth and perspiration of the sleeping infant. Arsine generation is not usually identified as OBPA biocide is not generally used in PVC cot mattress coverings. However, phosphine (phosphorus trihydride) and particularly stibine (antimony trihydride) and related alkyl compounds are frequently identified, originating from the phosphate plasticisers and antimony trioxide that are used to improve fire retardency. Exposed foam mattresses ore infected by a wide range of micro-organisms where they are affected by dribble and vomit, Including Sccpulariopsis brevicaulls which generates phosphine if phosphate fire retardents are present. .viOCl*^ g ldo svzz C'-> t. n.m t t.-*.' i fc< t ion >'* Inf.nt ^aCt <Vi <r*- 2. Research observations 201 All used cot mattress coverings are infected by a wide range of the micro organisms that--are commonly found in the domestic environment. 2.02 PVC cot mattress coverings are generally affected by surface soilage infections but Scopulariopsis brevlcaulls always develops on the area affected by the warmth and perspiration of the sleeping Infant^ This infection, which is apparently prompted by the nitrogen content in the perspiration, develops in the plasticiser within the PVC sheet and is invisible, the only evidence being progressive loss of plasticity and the development of brittleness and splits. Phosphine, arsine and stibine--or related alkyl gaseous compounds are usually detected when samples are incubated. Stibine, originating from the antimony trioxide fire retardent-component in the PVC, is most often detected. Phosphine from fire retardent phosphate plasticisers is also often detected. Arsine from the arsenical biocide OBPA~is rarely detected but traces of arsine are sometimes detected" which are attributable to arsenical impurities in antimony- trioxide. Fungal activity and gas generation vary with temperature, the rate of generation at 40C being about 100 times that at 20C. Phenolic compounds, released when aryl phosphate plasticisers are degraded by the infection, sometimes cause pink staining in the shape of the sleeping infant. iv r _2.03 Exposed foam mattresses, that is mattresses which comprise foam alone, or covered with net, or. partly covered with PVC, are usually infected by a wide range of infections, including many fungi which--produce spores or support mites which can prompt allergic respiratory reactions- such as asthma. Scopulariopsis brevicaulis_ infections on foams are usually associated with phosphate fire retardents and phosphine generation. tfe. food ? 1 2.04 Unexplained sudden infant deaths or cot deaths usually involve infants in the-prone~dr face down position with generous coverings. Death usually occurs after the infant has remained undisturbed for six hours or more. Death is usually attributed to sudden infant death syndrome or SIDS. The prone position and heavy coverings maximises exposure to any gas generation from the mattress, and hyperthermia in the infant caused by the heavy coverings also increases the rate of gas generation through both the higher temperature and the increased persp irat ion. 2.05 50 mattresses from 45 SID incidents have been examined, including 1 cotton covered, 26 PVC covered, 15 PVC covered with exposed foam at one or both ends, and 8 exposed foam; 2 mattresses were involved in 5 incidents. All the PVC and foam mattresses were infected by the fungus Scopulariopsis brevicaulis and, when samples were incubated, all generated phosphine, arsine or stibine gas. Mattresses had generally been used for a previous -infant, the mattresses varying from apparently excellent clean condition to grubby surfaces with brittle and split PVC coverings or heavily stained foam. Five mattresses were involved which had not been used for previous infants. Two of the mattresses involved PVC coverings which were brittle, pink stained and generating phosphine; purchase dates are also known for some of the used mattresses, those generating phosphine and therefore containing phosphate plasticisers apparently deteriorating more rapidly than those containing other plasticisers. Another *0 mattress was exposed foam, pink stained and generating phosphine from a JO phosphate fire retardent treatment. In all cases the infection and gas GO r.l . .:i . r. . < I. 1... i frm-J Page 2 O .p > 5-> i<>*> b I'.Klfl <r I'.'ii'ft *. tori ni.i'H^n Inf n't -3 ^ generation were restricted to the area affected by the warmth and perspiration of the sleeping infant. Bed coverings were also sometimes examined. Cotton sheets covering the mattresses were always found to be saturated with perspiration if examined shortly after death. 3. Notes 3.01 Incubation of naturally infected samples of PVC and foam at high humidity is sufficient to cause phosphine, arsine or stibine gas generation. However, incubation of small samples on nutrient plates is necessary for the infection to spread from the samples so that it can be identified. Samples are therefore examined routinely by plating on agar plates containing 57. malt and 57. soya flour, the protein in the soya flour encouraging Scopulariopsis brevicaulls ^ growth. Samples are incubated at 22 to 25'"-'C in order to restrict activity and < limit the rate of gas generation to avoid danger to staff; headaches are the first indication of excessive gas concentrations. CJ--^ 3.02 Silver nitrate and mercuric bromide cor chloride) papers are used for gas detection; gold compounds can also be used. With silver nitrate phosphine gives a yellow colour, whilst arsine gives a brown or mauve colour and stibine a pink or Frown colour; high concentrations eventually cause darkening to grey or black with all three gases. With mercuric bromide phosphine and stibine cause'-n<r colour change as white complexes are formed but arsine gives a yellow colour, darkening to orange and red, with high gas concentrations. These reactions are quantltative and sensitivity can be improved by the use of optimum loadings on the detection paper and by limiting the size of the paper strips; high humidity is also essential as the reactions do not occur if the papers are too dry. Routine studies involve placing small samples of PVC or foam on malt/soya agar plates in Petri dishes and incubating for several days at 22 to 25'=C until active Scopulariopsls brevicaulls growth develops, either as beige coloured hyphal growth or the buff coloured slime form which develops under stress. With PVC the fungus develops only on the nutrient medium and the edge of the PVC. Small strips of detection paper about 5mm wide and 25mm long are then slipped over the edge of the dishes and secured with the lid, the colour generated after 1 to 3 hours identifying any phosphine, arsine or stibine generation. Hydrogen sulphide interference, which is indicated by early darkening of the silver nitrate, does not normally occur. Alkyl compounds are also generated by Scopulariopsis brevicaulls and account for the characteristic garlic odour associated with phosphine, arsine and stibine, but the silver, mercury and gold complexing method of detection is more sensitive to the trihydrides. 3.03 The increase in the rate of gas generation at higher temperatures can be observed by placing well established open plates in a desiccator in a water bath, conditioning to the required temperature for an hour or more, flushing with air, and determining the rate of gas generation by introducing test paper and observing the rate of development of the detection colour. Silver nitrate and mercuric bromide papers can be used but greater detection sensitivity can be achieved using paper treated with mercuric chloride and a pH indicator, the trihydride gases complexing with mercury forming hydrochloric acid. 0 0 0 0 8 bZZ r-.>rw*-u. r;.r l_ Lim t Page 3 t to Ira'd** t' t ion nd nuddn in f n 3.04 The gases can also be detected using, for example, the termite Reficulitermes sarttcnsnsis. Termites placed on well developed plates with PVC samples generating easily detectable arsine and stibine are generally killed within two hours but phosphine is distinctly less toxic. 2)1 cU> 3.05 Although the fungus Scopulariopsis brevicaulls can survive on simple carbohydrate media such as malt agar, a source of nitrogen will greatly enhance activity and enable the fungus to compete strongly with other organisms. This fungus is often therefore the dominant 'species on substrates containing protein such as meat, milk and cheese, but substrates containing nitrogen sources such as ammonium compounds and urea are equally suitable. Extracellular enzymes are produced by invading hyphae which convert the nitrogen sources to ammonia (nitrogen trihydride) gas which is then absorbed by the hyphae and utilised for protein formation. However, the extracellular enzymes do not act on nitrogen sources alone but also on other Group V/Vb compounds, generating phosphine, arsine and stibine which are apparently liberated into the atmosphere as they cannot be absorbed by the hyphae. The fungus has an affinity for Group V/Vb compounds; if they are sprinkled on plain agar plates to form a distinctive pattern the fungus will follow the pattern. If the fungus is under stress, usually due to inadequate nitrogen in the substrate, the beige hyphal growth degenerates to a buff coloured slime, reverting when plated onto a more suitable medium. The infection is invisible in PVC fabric because it is in this structureless slime form and causes only slight distortion of the PVC; the infection does not spread over the surface of the PVC. 3.06 Phosphine, arsine and stibine poisoning cannot be readily detected on post mortem investigation. Normal lethal doses will cause increases in phosphorus, arsenic and antimony levels in blood and tissue but these increases are smaller than normal ambient variations and therefore undetectable. 3.07 Standard toxicological references Indicate that chronic exposure to phosphine, arsine or stibine causes death by haemolytic anaemia in adults, although a headache is an early symptom of poisoning (32-36). It is suggested that these gases are accumulative but this is not strictly correct; chronic exposure simply causes the anaemia to become progressively more severe. However, SIDS is not normally associated with haemolytic anaemia, although colour changes in the lungs may result from local haemolysis in lung tissue. Infants are sometimes reported to be irritable in their cot several hours prior to death which may indicate headaches.Infants are sometimes provided with monitors which detect cessation of respiration but prompt attempts at resuscitation are apparently unsuccessful. These observations may indicate a poisoning action causing cessation of respiration, perhaps acting through the respiratory centre in the medulla, although the trihydrides are likely to degrade in the blood before reaching the brain, and respiration in young infants is controlled by the carotid sinus rather than the respiratory centre. Whilst the trihydrides may block the carotid sinus, the circumstances of sudden infant death are also consistent with damage to sensitive cells due to oxygen or blood sugar deprivation. The trihydrides are reducing agents and may obstruct oxygen transport by blocking the oxygen acceptor sites on erythrocyte haemoglobin. Alternatively phosphine, arsine and stibine m3y form phosphonium, arsonium and stibonium hydroxide which may condense onto blood sugar hydroxyl groups, preventing blood sugar utilisation by cells. Research by PRIL in 1969 showed that poisoning by organotin compounds, which caused numerous deaths and brain ix. 1 U tin 1 Page 4 T8009frZ t. I b> io-J' r- t-r>11' injuries in France in the Stallnon affair, involves similar condensation on blood sugar hydroxyl groups (40-42). 4. Further information 4.01 This Research Mote will be revised as this project progresses. Revised issues will be distributed only to bona fide research teams. Further information on this project is available from the director B A Richardson. 4.02 This project is not sponsored. PRIL has provided laboratory facilities for the microbiological and entomological work. The project consultants are B A Richardson, T R G Cox and J 0 Watt. The culture of Scopulariopsis brevicaulis involved in the initial work was provided by Dr D Allsopp of the International Mycological Institute at (few; subsequent research involved cultures front naturally infected samples. 5. References Smith 0. An introduction to Industrial Mycology. London, Edward Arnold, 6th edition, 1969. 2. Morton F J & Smith G. The genera Scopulariopsis Bainer, Microsacus Zukal, and Doratomyces Corda. Mycol Paper 86, 1963 3. Thom C & Raper K B. The arsenic fungi of Gosio. Science 1932, 76, 548-550. 4. Cosio B. Azione di alcune muffe sui composti fissi d'arsenico. Rlv d'lglene e San Publ 1892, 3, 201-230, 261-273. 5. Gosio B. Action de quelques moisissures sur les composes fixes d'arsenic.Arch Ital Biol 1893, 18, 253-265. 6. Gosio B. Zur Frage, wodurch die Giftigkeit arsenhaltiger Tapeten bedingt wird. Ber Deuts Ghent Ges 1897, 30, 1024-1026. 7. Schmidt H R. Uber verschimmelte Tapeten. Dlss Erlangen, 1899 8. Bub-Bodmar F & Tilger B. Die Konservierung des Holies in Theorle und Praxis, Berlin, 1922. 9. Richardson B A Wood Preservation London, Construction Press & Longmans, 1978. 10 Broese van Groenou H, Rischen H W L & van den Berge J. Wood Preservation during the last 50 years. Leiden, Sijthoffs, 1952. 1 1 Hamilton A. Indus trial Poisons in the United States Mew York, 1925 12. Anon. Gaseous arsenic from wall-plaster,The Analyst 1932, 57, 163-164. 13. Sanger C R. On formation of volatile compounds of arsenical wall papers.Free Am Acad Arts <5 Sci 1894, 21, 1 12-147. 14. Sanger C R. On chronic arsenical poisoning from wall papers and fabrics. Froc Am Acad Arts A Sci 1894, 21, 148-177. 15. Biginelli P. Composizione e costituzione chimica de gas arsenicale delle tappezerie. Atti R Accad Lincel Rendic Cl Sc Fis Math e Mat 1900, 9, 210- 214, 242-249. 16. Maasen A. Die biologische Methode Gosio's zum Nachueis des Arsens und die Bildung organischer Arsen-, Selen- und Tellurverbindungen durch Schimmelpilze und Bakterien. Arb a d kalserl Gesundh ambt 1902, 18, 475489. i ~ Huss H. Zur Kenutnis der biologischen Zersetzung von Arsenverbindungen.Z f Hyg u Infekt krankh, 1914, 75, 361-406. i l I. i>.. 1 bod Page 5 28009 kZ2 t C- ** lz> Ur.ci' t; i--*.-. 18. Lerrign A F. The biological method for the detection of arsenic. The Analyst 1932, 57, 155-158. 19. Challenger F, Higginbottom C & Ellis L J Chem Soc 1933, 95. 20. Challenger F Chem Rev 1945, 36, 315. 2-tr Braman R "S' & Foreback C C Science 1973, 102, 1247. 22. Cullen W R & Reimer K J. Arsenic speciation in the environment. Chen Rev~ 1989, 89, 713-764. 23. Cox 0 P & Alexander M Ball Environ Contam Toxicol 1973, 9, 84. 24. Mahlke F & Troschel E. Handbuch de^Holzkonservierung Berlin, 1928 25. Berge- J van den. Beoordeeling van de -waarde van fungicide stoffen voor houtconserveering.Piss Delft, 1934. (Testing the suitability of fungicides for wood preservation. Publ Int Adv Off Wood Pres, The Hague). 26. Klausmeier R E. Results of the second interlaboratory experiemnt in biodeterioration_of plastics.Int Biodet Bull 1972; 8<1): 3-7 27. Yeager C C. Pink staining in polyvinylchloride.Plastics World 1962; 20:14. 28. Yeager C C. Laboratory and service tests for PVC Proc 1st Int Biodet Symp 1968; 151-16TT ~ 29. Klausmeier R E & Jones W A. Microbial degradation of plasticizers.Pev Ind Microbiol 1961; 2:47-53. 30. Klausmeier R E. The effect of extraneous nutrients on the biodeterioration of plastics.Monograph 23, Soc Chem Ind 1966; 232-243. __31. Hollo J & Kollai--Volgyesi M. Resistance of plastics to microbiological corrosion.Sioch Exp Biol 1975; 11:163-173. . --32. Plunkett E R Handbook of Industrial Toxicology 3rd edition, Edward Arnold, London 1987. 33.~ Dreisbach R H Handbook of_Polsonlng 11-th-edition, Lange, Los Altos, 1983. 34.__ -Gooper P Poisoning by Drugs and Chemicals 3rd edition, Alchemist, London, ___ 1974t-- 35. _ Poison C J, Green M A & Lee M R Clinical Toxicology 3rd edition, Pitman, London, 1983. -- 36. Kleijifeld M J. Arsine poisoning J o M 1980; 22:820. 37. Wilson R, Lovejoy F H, Jaeger R J & Landrigan P L. Acute phosphine poisoning aboard a grain freighter. JAMA 1980, 244, 148-150. 38. Nelson E A S, Taylor B J & Weatherall I L. Sleeping position and infant death bedding may predispose to hyperthermia and the Sudden Infant Death Syndrome. Lancet 1989; i: 199-200. 39. Stanton A N, Scott P J J Downham MAPS. Is overheating a factor in some unexpected infant deaths? Lancet 1989;1:1054-7. 40. Richardson B A. Action mechanisms of some organometallic preservatives. Froc 1st Int Biodet Sym 1969,498-505. 41. Richardson B A. Tributyltin wood preservatives. Rec Ann Conv BWPA 1970. 42. Richardson B A. Organotin wood preservatives; activity and safety in relation to structure. Froc AWPA 1988. BAR/JR PI 9008 f 'j -> ..- I \ t . * tL l-,... ... L t_ !,, t Page 6 670 THE LA Cot mattress biodeterioration and SIDS Sir,--In 1988, various fungi were identified in industrial plasticised polyvinyl chloride (PVQ despite the presence of the preservative 10, lO'-oxybbphenoxyaisinc (OBPA). Warnings were given that the PVC might aiso become infected by arsenic-tolerant organisms which might convert OBPA to toxic arsine gas. Mr P. R. Mitchell, a client of our company, inquired whether arsine generation through biodeterioration ofsuch coverings might be a cause of sudden infant' death syndrome (SIDS). 50 mattresses used in fony-fivc SIDS incidents were examined, including t cotton covered, 26 PVC covered, 15 PVC covered with exposed foam at one or both ends, and 8 exposed foam; in five incidents 2 mattresses had been used. All mattresses contained Scopuiariopsii brtvieaulis, but only in the area beneath the infant affected by warmth and perspiration. Incubated samples of the infected materials all generated toxic trihydride gases. PVC coverings usually generate sdbine (SbHj) from a fire retardant additive, antimony trioxide, but also phosphine (PH,) from the phosphate plasticisers that are used when fire resistance is required. Although OBPA b not generally used in cot mattress PVC, tests indicated arsine (AsH,) generation when it was used; and small amounts of arsine were sometimes identified when it was not, presumably from arsenical impurities in antimony trioxide. Mixtures of gases were often detected. Phosphine generation from PVC was sometimes sssoented with the development of a pink stain, usually in the shape ofthe sleeping infant, apparently caused by liberation of phenol compounds from decomposition of phenyl phosphate plasticisers. Only phosphine was generated from infected cotton and foam samples, apparently through biodeterioration of phosphate fire-retardant treatments. Foam samples and the 1 cotton sample were also infected by various other fungi, especially in the area affected by dribble; many of these fungi produce asthmatic reactions. The generation of highly toxic trihydride gases from cot mattresses is a serious threat to health. The gases are heavier than air, and infants roost at risk are those who remain for long periods in their cota, sleep prone in carry-cots, or are heavily wrapped such that they are in long and dote bceathing contact with accumulations of gas. Heavy wrapping also induces hyperthermia, which prompts an increase in gas generation. Some infants probably survive because the first symptom ofpoisoning b headache, which results in irritability, dislodgment of bedding, and improved ventilation; infants of low weight cannot dislodge bedding. SIDS occurs mainly in infants up to age 5 months who sleep prone with heavy wrapping and have indications of hyperthermia. SIDS is only reported in western-style communities where foam and PVC covered cot mattresses arc used, and hasonly been recognised since about 1969, following introduction of these materials during the previous 10--15 years. fr8008& g H\-sS It has been reported that SIDS is less likdy to occur in first bom children, perhaps because mans esses are new and do not become infected while the infant is young and most at risk. 5 first children were involved in the 45 incidents investigated. 2 died on previously used mattresses; 1 of these 2 slept on a mattress immediately after use by an older child. I infant died on a new foam mattress that was generating phosphine and 2 died on new PVC mattresses which were affected by exceptionally active fungus and were generating phosphine; two other new mattresses were implicated, both of which were similarly affected. Infection by 5 brcvicauta is not readily visible in PVC Severe deterioration, usually associated with phosphate plasticisers, results in brittleness and splitting. In the home the fungus is usually found in protein-containing substances such as cheese and meat, and in damp wool and leather; however, its extracellular enzymes can convert a wide range of compounds containing the elements nitrogen, phosphorus, arsenic, and antimony into the trihydrides ammonia, phosphine, arsine, and sdbine. The preferential development ofthis fungus in cot mattresses should be attributed to the presence of nitrogen compounds in the perspiration. The generation of arsine in this way has been recognised for about 100 years since Go$k>* discovered that death in children and illnesses in adults were sometimes caused by arsine generated by the action of 5 brtvicaulu on arsenical wallpaper pigments, although it is now known that arsine could be similarly generated from the horse-hoof size that was commonly used at that time and which contained white arsenic to discourage rodent damage.2 Phosphine, arsine, and sdbine are exceedingly toxic with threshold limit values of 0-3, 0-5 and 01 ppm, respectively, compared with 100 ppm for carbon monoxide. Relatively high ambient levels prevent the detection of phosphorus, arsenic, and antimony residues at necropsy. However, some pathologists have commented that they usually associate SIDS wiih abnormal lung colour; this could be associated with local erythrocyte haemolysis due to exposure to these trihydride gases. hnnih Nmasrch toMMWttonal. PO Box 142 St P<Port GuontMT. Channot Wand* B. A. RlO IAKUSON I. (jono B. AxjnncdlaiciOTX tnuOt *uicnmfmuftui d'arscnH" Krr JIfimt t .Van IIW2; X 201-00,26I-7V 2-Thom C. Rxpcr KK. The amic fungi of G*a Samct W4-S0. */A Government inquiry, prompted by these findings, was announced on March 9. The inquiry will be chaired by Prof Paul Turner. THE LANCET MARCH 17, 1990 $8008 bZZ vO QD C & Recorder James Crcspi Q sentenced Neequaye, o f W,- worth, south-east London, to fo" years. The judge said he ter A STEPFATHER who kicked a girl of four about " I i foot- ball"r , dumpedi ,, her in i~.j baths,, , ,, ----- 1 i,,, r i h naked in a more than 10 milliSieverts in one year, and no more than J mSv in anv six-month period, the unions ;2o r.1 * H &1-! O "O2 `JS -. 5 'rt cVo) -wC js2 ' -O 3O r/t> S o 2?J i- ^ > C I U uOi SS^-g: . *>S.J 1 ics 'e5j- _y o fi/ji o* E >0>.0 GJgsS 2uC c--u "eO *: 2c *c "c(24 z<U* S?-~.'.b^e ww- 5- ? 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B 5,,E o 5 ^ Z% 2& U *3 . 2o.Ei 8 sbe i 'g'S* g| O^ 4^> V Sh T5 <D <D vH -4--1 r--( QQ So O co "cS ^ &r Cw co a Sh .2 cd ^ a> T3 ^3 S3 cd s? ^ Ofc - ^ 01 A REDl ION in radiation dose limits to one fifth of the cur........... i R L ^ in c rR m n m lrd hv 01 235 8045 . '90-02-2? 13:58 BRITISH PLASTICS FED 01-235-6045 r PKL/AC/26.02.90 COT DEATH Th British Plastics Federation 5 Belgrava Square London SW1X8PD 01-235 9463 Telex 8951528 Plated G Fax 01-235 8045 The British Plastics Federation is aware of the article, 'New Glue probed over cot deaths' which appeared in the 'Exclusive' column of the Daily Express on 26th February 1990. To test the accuracy of the statement made in the article we have been ihitouch with the Department of Trade and Industry and the Laboratory of the Government Chemist. From these enquiries it is apparent that a report has not been issued on the subject of.an asserted link between the phenomenon of,cot death syndroms ____ ______ 'and'>fire retari?an f^emftalg 'by e`nhef'1hS^fi^TO^t^^h8*l^boratotyf^^BS!^^** Crisis meetings, involving government ministers, ss reported in the Express article, have not taken place. The Laboratory of the Government ChemiBt is proceeding with its investigation in this field. We are ewalting a full report from the Laboratory but we do understand that the allegations made in the article, whatever their source, cannot be substantiated. For further information contact: Philip Law 01 235 9483 V Director - O R Jonea A oompany limited by guarantee PO CO o 00 -sj J code for parents. He urged: |? All new mattresses should be washed down once a week with disinfectant. All old and second-hand i.mattresses should be - securely wrapped in a dear t polythene sheet, obtainable (ram ironmongers. The polythene should wrapped tightly and prop erty secured with adhesive tape oo the bottom.'- i? "I: advise' people with earry-eot mattresses . to throw them away and use a doubled-up cotton sheet Instead,* be said. He tested 45 mattresses on which babies bad died. They-were made from foam, PVC and cotton. All had been fire-proofed. In tests all gave off t lethal doses of poison gases. Bottomtey: Probe But the Daily Express can reveal that results of at least two experiments confirm independent research to which the Government was first alerted 12 months ago. Ministers were also told yesterday that cot deaths rose 12 to 15 percent in 1986 By PETER HOOLEY Whitehall and have continued increased since. It was then that foam manufacturers, increasingly worried about toxic fumes given off in household fires, started treating their prod ucts with fire retardants. Mr Clarke is prepared to order tens of thousands of baby mattresses to be withdrawn from sale if Government scientists con firm a possible link. "He is determined to find out wbat la going on and will not hesitate to act.' an aide said last night Sir Donald Acheson was under pressure to issue urgent guidelines to parents who have already bought fireproof mattresses, which have to conform to new fire safety laws from September. The Government's failure to grasp the nettle over this is simply frightening,' said independent biochemist Barry Richardson. He has spent 50.000 of his own cash and thousands of hours since he discovered the cot death link by chance. "Wbat I dlacovtred la not remarkable. It is so blind ingly obvious that it is amaz ing it was not considered before," he said Danger "I now hope the Govern ment will take note and ensure all new mattresses do not contain the fire retar dants that give rise to danger." Mr Richardson's findings link cot deaths with a chemi cal reaction between a com mon invisible household fungus and phosphorus and antimony compounds used in fire-retardant mattresses. . ,, V'.-. ^ - - The reaction can also be triggered bv preservatives used in PVC mattresses, which some scientists now say may be responsible for the huge rise in British cot deaths since 1971. The Department of Trade and Industry was urged last night by baby product firms to make a statement. "We are in a cleft stick." said Nursery Shop boss Corrine Flounders, a quali fied health visitor. "Mtany of us are extremely worried about this. But if we do not comply with govern ment regulations we will be breaking the law." Now Bush guns for Castro New IRA warning From Page One lation were bom after he took over in 1959. almost 11 years in power. U.S. intelli gence reports indicated the result will .lave a pulverising effect in Havana, already quaking over the worldwide dis He has erected signs along country roads exhorting. "Long five rigidity!" and "'Socialism or Death". integration of Communism. His rhetoric was beginning to sound Cuba's state-run radio, TV and news' papers had predicted a near-certain win: for Ortega's Leftist Sandlnista move like a death-rattle, especially in Wash ington- where hlax every move- ia moni tored. _ " . t Austerityment. Castro. 63, was devastated as the first returns came in. His gloom deepened when Ortega conceded defeat Cuba's Radio Rebelde described his surrender of power as "one of the bravest political "People who lived through the revolu tion had a sense of what they were fight ing against." said a State Department analyst. "The kids who have grown up since style, is only 90 miles away in Florida. Yesterday's pounding of the Commu nists in Nicaragua was beamed to them from U.S. radio and TV stations inMiami where 700,000 Cuban exiles are growing increasingly optimistic about Castro's downfall. -The-US. Congress, gave, motber-offoar.Mrr Chamorro morethan 1 mlF oon for ber low-key campaign end ahe is believed to have received five times that amount through the backdoor. Almost everyone in Nicaragua is on the poverty line. It has been tom by war for most or the past decade with the U.S. ploughing in millions of pounds in aid to THE GANG responsible for two town centre blasts in a week may go for civilian targets next, security chiefs warned last night. The alert followed the expfosfcMM-at a. Arair icciiUtlag-centrrhi Hali fax. West Yorkshire, late on Sunday night. Nobody was hurt. Ponce are Unk ing it with the IRA bomb ing of an Army van in Leicester last week. inrl.fawn.l.t .klxfe EXCLUSIVE New clue probed over cot deaths By PETER HOOLEY Whitehall Correspondent STARTLING evidence by government scientists has confirmed a possible new link between cot-death syndrome and (ire-reststent mattresses. It could lead to emer gency guidelines to par ents "-- or the recall of tens of thousands of recently-sold fire-retar dant baby mattresses. Ministers begin a series of crisis meetings in Whitehall today after it was found that chemicals used in fire-proofing to comply with new fire laws, designed to make cots safer, could actually cause the deaths of babies. Scientists have found the fire retardants can form part of a chemical reaction which emits minute quantities of some of the most deadly gases known to man and create an invisible cloud of death around a sleeping intent Many thousands of such Page 2 Column 1 [Target 36^ Sftflrt; 38.:. 44& 2 DAILY EXPRESS Monday F PR Eric Forth: Talks Cot death: New clue From Page One mattresses have already By OA . and R< PR r readiness for new fire safety laws on babies' furniture which come into force from Septem ber 1 this year. The findings could force Consumer Minister Eric Forth to change bis mind nd give a Mat-minute emergency exemption from the new match-test rules for all nursery furniture. And Health Ministet Virginia Bottomley will be pressed to issue urgent new guidelines The cot-death syn drome. which results in the death of 2.000 of the 80.000 babies bom in Bri tain every year, has never been fully explained. Reaction Scientists have noted an increase in victim num bers since the fire retar dant chemicals became widely used. Whitehall sources said yesterday research by Laboratory of the Gov ernment Chemist is believed to have con firmed the possible link. A chemical reaction occurs between an invisi ble and common house hold fungus, usually pres ent on mattresses, and the chemicals used in the fire retardant, phospho rous and antimony com pounds. Fungal activity was made worse by the nitro gen content in perspira tion and babies' urine. A young mother's tragic mistake with an electric blanket led to the deaths of her four-weekold twin boys. Kurt and Damon Hardman died from heat exhaustion after Mrs Karen Hard man, of Klrkham. Lanca shire forgot to switch off the blanket. unity. Follow call from America i total wit from Ge West mi events. He pubI West Gern after spen him at Cat MrKoh. on the toe tiers until But Bus warn of instability. `It is foi tgreed set tiere was s Ganges th last year? `What v meriting cl Vestern E "Eastern hrowing o [he policy io6ody ca rill come a oeourgoc rith Nato He said rould no urope. The Pre Bat From F promised: going to gr He went o we are goin period ol unpopular^ are pursui against infli it meant mortgage r 5 GO C Daily Express 12____Hampshire Chronicle. Friday, February 9.1990 Speed up cot death research, Prime Minister urged - "WINCHESTER M.P., Mr. John Browne has asked the Prime Minister to speed up the Government chem"ist's inquiry into the cause of cot deaths. In the meantime, he has show that stronger babies were ; called for a Government warn- able to throw open some of i-ing to be issued to parents as their bedding and escape the '...a matter of urgency. effect of the toxic fumes. -- Mrs. Margaret Thatcher, the Mr. Browne said: "I realise "'Prime Minister, replied this that the Government is looking il'week: "I share the great con- into the matter, but there is ; cent of parents and Health need for more urgency. I -Service staff about the incidence myself have friends who have '.' of unexplained cot deaths, the suffered the trauma of a cot -/suddenness of which is especial death and I know the anguish ly tragic for the families. that this causes, especially for ' "The Department of Health the mother. " has promptly commissioned the " In the meantime 1 think the ..laboratory of the Government Government should issue a '."chemist to undertake a sden- warning to parents advising .. tiAc assessment, which is under them to be careful of second wav." hand or previously used cot ___Continued Mrs. Thatcher: "1 mattresses, that may have been understand that, ao far, those soiled and may contain the tests have not reproduced the deadly fungus." result obtained by the indepen dent researcher who proposed a link with Are resistant chemic als." She added that the Govern ment weald consider whether if would be right to issue warnings in the light of the scientific assessments now going on. Afterwards, Mr. Browne said one of his constituents, Mr. Peter Mitchell had raised the nucslion with him al a meeting and had referred to the research of another constituent, Mr Barry Richardson. Mr. Browne said: "Mr. Richardson's researches show that when a baby's bodv- liquids come into contact with fire resistant additives <e.g. antimony trioxide) and pre servative additives (e-g. OBPA) the resulting reaction can, over a period of time, cause the growth of a fungus. If this fungus is then heated by the body.' temperature of a subse quent baby, highly toxic gases can be given off such as Stibine, Phosphine and Arsine." Mr. Browne added: "It appears, and I stress the word appears from samples provided by Mr. Mitchell and studied by Mr. Richardson, that these gases were the likely cause of the majority of cot deaths, current- Iv about 2000 each year in the United Kingdom. " Obviously, a used mattress was much more dangerous because the fungus had time to grow before being heated bv .subsequent babies. It was interesting to note that the inci dence^ of cot deaths increased -in-.-winter when babies arc heavily wrapped and central . heating switdird on. The im. JCF/AC 24 August 1989 The British Plastics Federation 5 Belgrave Square London SW1X 8PD 01-235 9483 Telex 8951528 Plafed G Fax 01-235 8045 Status and publication details of the Laboratory of the Government Chemist research into the allegations made by Mr Richardson __ The 8PF has been advised to liaise directly, with Dr Raymond Cooke of the LGC every 2 months (links-have aXready been established) and it is anticipated that the LGC work will take approximately 4 months to complete. -- It is likely that the research will be described in an article in Chase Bulletin however, no conclusions will be drawn. Conclusions will only be made available . to_the DTI'3 CSU directly and will not be made public. The CSU may well retain a statement in its files which could, for instance, be used to respond to Parliamentary questions. Details "of the research may also appear in the-house journal of the LGC, ` published_quarterly. This information is then passed on to the DTI, the Government Research Establishment and other academic/research bodies. " If an industry has been closely involved in a particular-issue being researched by the LGC then it is usual for them to be consulted before details of the report-are finalised. "It is therefore probable that the BPF will have sight of the LGC's draft report. _ It is the current view of the CSU and Department of-Health that Mr Richards reports is very much a 'dead-letter' with little, if any, foundation on fact. Jacky Freer Group Executive V Director - D R'Jones A company limited by guarantee n A DtvMonot The Society of The Plastics Industry, Inc. TELECOPY TRANSMITTAL FORM TO: Harold Clayton 9 Hydro Polymers FROM: Roy T. Gottccman j,DATE: April 1 1990 I/PAGES J SUBJECT: British Report on "Cot Deaths" / One Plus cover COMMENTS: Harold: i have lust learned that there was a radio report on NBC by a Roger Field dealing with the Lancet report on "cot deaths" and the interpretation that stlbene, arsine, etc, liberated by fungi acting on the fire retardants in PVC cot mattresses are suspects in causing these deaths. Today# Pat Toner, V.P. Technical of SPI, talked with Mr. Field who la now working on a story on this for -the New York Times. In response ho Mr. Field's inquiries, Pat Toner eidvised Fields that all wo have seen is a "letter Lo the Editor11 In Lancet which is lacking in technical details and that until our technical experts have an opportunity to review the technical work on which this report is based, we'd have no comment._______________________ o rnirstcnoiiu. Continued ................. Wayne Interchange Plaza II 155 Route 40 West Wayne, NJ 07470 * (201) 800-9298 Fax # (201) 890-7020 tB O dS H Z RPR-17-'90 10:38 ID:THE UINYL INSTITUTE TEL NG:201 890-7029 8782 P02 Mr. Harold Clayton @ Hydro Polymers April 17, 1990 Page 2 Would you please gather together copies of all information you have on this subject and bring them with you to the Brighton Conference? I'd greatly appreciate that as it will provide Pat and me a total_ package of information for our review. Also I would look-forward to the opportunity of discussing this with you at Brighton. ~~ Thanks in advance for your assistance in this and I look forward to seeing-you next week. Kindest personal regards. cc: H. Patrick Toner, SPI -Washington g6U 08fr2! V )c)cp PVC Stuurgroep PVC & Milieu PJC. Ou-Jl EivW'^cn i PRESS RELEASE Cot Deaths As a result of reports concerning a possible connection between cot mattresses having a lining of PVC and cot deaths we make the following statement: The first publications concerning the possible connection between flame retardants made of PVC and cot deaths came out early In 1989 in England, when a scientific investigator at Penearth Research International Indicated a possible connection between cot death and flame retarding additives to the PVC lining on cot mattresses. A publication of the results of research work was rejected by the British Medical Journal due to Insufficient scientific foundation. Consequently, the British Ministry of Health, Safety and Environment dismissed the line of reasoning put forward by the researcher. The British Government likewise saw no reason to take any action regarding flame retardants used in the Industry. In June 1989 It was however decided that the laboratory of the British Government should carry out an Investigation since It has been considered that every possible indication, no matter how small, should be Investigated If It may help to solve the as yet unexplained problem of cot deaths. Up to the present time no Indications have been found concerning a possible connection. In view of the Information now known the Stuurgroep PVC it Milieu looks forward with confidence to the outcome of the British investigation. Should however the results not Indicate anything positive or be available within the envisaged 6 weeks the Stuurgroep and the Dutch government will together decide to carry out their own investigation. It need hardly be said that the Stuurgroep PVC & Milieu takes very seriously reports concerning a possible connecting existing between PVC and cot deaths. It is of the utmost importance that all possible efforts be made to solve this mysteryl All the same It Is also very important that In a matter which Involves, understandably, a great deal of emotion the facts must be relegated*f1rst consideration. Note for the editor: You may obtain more Information from H.J. Moonen, .chairman of Stuurgroep PVC en Milieu on tel.no. 020-934844. t 0 0 8 bZ Stuurgroep PVC & Milieu PERSBERICHT Wiegedood Near aanleiding van berichten over een mogelijk verband cusaen kindermatrasjes met een PVC bekleding en wiegedood hec volgende: De eerste publieatiea over het mogelijk verband cussen in PVC toegepaste brandvertragers en wiegedood verscbenen begin. 1989 in Engeland, waar een onderzoeker van Penearth Research International een mogelijk verband aangaf tuscen wiegedood en brandvertragende toevoegingen aan de PVC omhulling van kindermatrasjes. Een publicatie van de nderzoekeresultaten weed door de British Medical Journal geveigerd op grond van Ce magere vetenschappelijke onderbouving. Het Engelse Ministerie voor gezondheid en veiligheid en milieu(HSE) verwierp vervolgens de door de onderzoeker naac voren gebrachte argumentatie. De gepresenteerde onderzoeksreeultaten waren dan ook voor de Britse overheid geen reden om eniga maatregel te nemen tegen de door de industrie gebruikte brandvertragers. In juni 1989 werd echter alsnog beeloten tot onderzoek door hec laboracorlun van de Engelse overheid, daar men terechc van mening vas dat elke mogelijk* eanwijzing, hoe gering ook, die tot de oplossing van een cot nu toe onverklaarbaar probleem kon leiden in ieder geval onderzocht diende ta vorden. Tot op heden heefc men geen aanwijzingen kunnen vinden voor een mogelijk verband. Gezien de nu bekende gegevens ziet de Stuurgroep PVC (x Milieu de uitkomsten van het in Engeland uitgevoerde onderzoek met vertrouven tegemoet. Indien echter de resultaten niet tot een duidelijke conclusle leiden, of na de nu voorziene ca. 6 weken niet bekend zijn, zal de Stuurgroep, eventueel saroen met de NederlAndsc overhoid, tot een eigen onderzoek besluiten. Het spreekt vanzelf dat de Stuurgroep FVC & Milieu berichten over een mogelijk verband cusaen PVC on wiegedood zeer serieue neemt. Het is buitengewoon belangrijk dat alle mogelijke inspanningen vorden verrichc om het mysterie tot een oplossing ta brengen. Het is echter van groot belang dat Juisc in een zaak waar, begrijpeiijkervijs, emoties een groce rol spelen de feiten een hoofdrol blijven vervullen. Noot voor de redactie: voor near informatie kune U zich wonden tot H.J. Moonon, voorzitter van de Stuurgroep PVC on Milieu, Tel. 020- 934844 p.. NFK Potoerbian IS 3440 AH Woerden 22480095 JF/AC 24 August 1989 The British Plastics Federation 5 Belgrave Square London SW1X 8PD 01-235 9483 Telex 8951528 Plafed G Fax 01-235 8045 STRICTLY CONFIDENTIAL 1 To: Participants in BPF Forum on Cot Mattress Biodetioration You will recall that at our meeting on 12th June a Task Force was established to produce a critique of Mr Barry Richardson's study. Initial work has now been completed and the second draft is attached for your information. Would you please study the report and, if you feel that there are any questions still to be addressed or areas which require clarification or revision, please contact me immediately. Obviously, as this is such a sensitive issue the report is strictly confidential to member companies involved. Please do not discuss it outside your company. Also attached are brief notes to a conversation with a representative of the DTI's Consumer Safety Unit which outline the status and intended publication details of the Laboratory of the Government Chemist's research. A meeting of interested parties will be called in approximately 4 weeks to take stock of the situation. I will be contacting you shortly to establish a convienent date. Jacky Freer Group Executive l i 94()U9>ZZ l Director - D R Jones A company limited by guarantee Registered in England No. 282883 COT MATTRESS BIODETERIORATION AND SUDDEN INFANT DEATH - 2ND DRAFT 1. Introduction In early June 1989 considerable media coverage focused on the conclusions of a report entitled 'Cot Mattress Biodeterioration and Sudden Infant Death' published by Mr B.A. Richardson of Penarth Research International Ltd. This attempted to demonstrate a link between the use of pPVC materials in cot mattress and the tragic phenomenon commonly known as 'cot death'. His report is the subject of detailed investigation by the Laboratory of the Government Cheimist. This paper summarises the examination of the report separately carried out by the manufacturing companies concerned - the PVC resin manufacturers, additive suppliers and calendered PVC sheet manufacturers - and it approaches the subject from three principal standpoints: - analytical chemistry - microbiology - medicine Five principal questions are raised by Mr Richardson's report: i) What are the constituents of PVC materials used in pPVC cot mattresses? ii) Can emissions of arsine, phosphine and stibine take place? iii) Do these emissions actually take place in situ? iv) If so, are the emissions injurious to health? v) Is there any link between the emissions and cot death? 2. What are the constituents of PVC materials used in PVC cot mattre33es? Mr Richardson has not produced any evidence to indicate that he has analysed the pPVC cot mattress coverings to determine their composition - he has assumed their composition only from the results of his experiments. The report states that "all cot PVC contains antimony trioxide and phosphate plasticisers" (p.4). Whilst it is certainly true that triaryl phosphate is used up to 12% weight/weight final compound and antimony trioxide incorporated up to about 1.3% weight/weight final compound they are never used together in a formulation. Mr Richardson is wrong in his assertion that 'manufacturers are now using antimony trioxide as a filler pigment at concentrations well above those used for fire retardancy' (p.U). It is also untrue, as Mr Richardson implies (p.4) that 10,10' oxybisphenoxyarsine (OBPA) is used as a biocide (p.4) in PVC cot mattress formulations. tSOOSfrzz 3. Can emissions of arsine, phosphine and stibine bake place? Mr Richardson's conclusions rest on the role of a particular fungus, 'Scopulariopsis brevicaulis1, which he says develops on pPVC cot mattressds 'if adequate moisture and protein are present, perspiration providing these requirements'. It is this, he says, which liberates arsine, phosphine and stibine and the strong implication is that he has carried out laboratory investigations (however vague) (p.5) to verify this (p.1)). However, he presents no evidence of identification of the fungus from samples of infected mattresses. He claims the fungus has been detected but gives no -- quantitative data about its presence, such as numbers per square millimetre or amount of hypha per square millimetre. All experiments to which Mr Richardson refers and from whose results he bases his conclusions are dated, crude and not specific to the detection of the gases in question. He gives no information about the time-scale of the experiments or the particular- length of time taken for colour to develop. His use of silver nitrate test paper to indicate the presence of the hydrides of phosphine, "arsine and stibine is very crude. Silver nitrate only provides a qualitative means of detecting the presence of hydrides. Hydrogen sulphate, ammonia-or hydrogen chloride -(whose absence would have be positively ascertained) can also discolour silver nitrate and, in addition, this paper naturally turns black in the atmosphere over time anyway. to ~"Mr Richardson does" not scientifically prove the absence of potential interfering substances (for which credible sources in his experiments exist) and in addition has no adequate controls in his experiment which could address the following important points: _____ - what happens with fungi growing on the medium with no added PVC? ~~ - "what happens with the indicator -strip incubated over uninoculated medium? what happens with the indicator strip incubated with infected and sterile PVC alone in the absence of a growth medium and added fungus? These controls are particularly important since one of the references cited, 32, indicates that the organism can release arsine from laboratory media. His results therefore may just be artefacts of his methodology. 4. Do these emissions actually take place? Mr Richardson's investigations were carried out in a laboratory where the fungus was developed under optimal conditions for its growth. They do not show that these gases could be produced 'in vivo'. The temperature under a baby in a cot would be at about 37*C, possibly higher in situations where bed clothes act as insulation. It is not established that the fungus will grow or remain metabolically active at such a temperature as many fungi will not grow at 37'C. sG oos^e: 5. Are the emissions injurious to health? n The quantities of gases generated in cots under normal conditions are likely to be extremely small and uninjurious to health (Mr. Richardson did not measure these). Mattresses currently manufactured have holes cut into the foam at the head end to facilitate a child's breathing and in these cirumstances, if phosphine, arsine and stibine were generated in the way described by Mr Richardson, they would be well diluted in air. This is graphically illustrated by the following example: If we assume that the densest of the three gases, stibine, was present at the extraordinarily high level of 1000 ppm even then the density of the air/stibine mixture would only be 1.003 compared to air's density of 1. Such a difference is trivial and the stibine would rapidly disperse in normal air movements such as convection currents. Lethal concentrations cannot accumulate. Is there a link between the emissions and cot death? Mr Richardson's report only remains a hypothesis. The statistical information he cites on the incidence of cot deaths (ppl-2) is not based on authoritative source material. Some fundamental weaknesses are illustrated by the following: his statement that most cot deaths occur at week-ends is not totally corroborated as several studies do not demonstrate a correlation. he does not mention that the incidence in the USA is equivalent to that of Australia and the UK. the lower incidence of cot deaths in Scandinavia is probably due to their higher level of health education and social conditions. the rate for Hong Kong of 0.3 per 1000 is likely to be due to the over-crowded conditions in which large families live, producing a greater awareness of subtle changes in a baby's condition. statistics on this subject are notoriously inadequate. This is due to the lack of a post-mortem and death certification, a post mortem being essential to produce a diagnosis of cot death. Statistics are probably at their weakest in Russia, China and India where Mr Richardson quotes a low incidence of cot death (pi). One would expect a post-mortem to indicate the presence of toxins in a Childs body and Mr Richardson's argument around this is spurions. Authoritative organisations and close students of cot deaths, such as the Foundation for the Study of Infant Death, believe that there has been no increase in cot deaths and that cot deaths occured in antiquity. It is additionally, a well known fact that babies who die from 'cot death' do not necessarily die in a cot and are known to die even when in the arms of their parents. Although there is probably no one single cause of cot death, perhaps one possible contributory factor in its cause relates to the sleeping patterns of babies. Two-thirds of cot deaths take place during the first six months of life. A baby has a deep sleep pattern in this phase, which then changes. We conclude that there is no direct evidence of an association between gaseous intoxication and sudden infant death. r JCF/AC 24 August 1989 The British Plastics Federation 5 Belgrave Square London SW1X8PD 01-235 9483 Telex 8951528 Plated G Fax 01-235 8045 \ Status and publication details of the Laboratory of the Government Chemist research Into the allegations made by Mr Richardson The BPF has been advised to liaise directly with Dr Raymond Cooke of the LGC every 2 months (links have already been established) and it is anticipated that the LGC work will take approximately 4 months to complete. It is likely that the research will be described in an article in Chase Bulletin however, no conclusions will be drawn. Conclusions will only be made available to the DTI's CSU directly and will not be made public. The CSU may well retain a statement in its files which could, for instance, be used to respond to Parliamentary questions. Details of the research may also appear in the house journal of the LGC, published quarterly. This information is then passed on to the DTI, the Government Research Establishment and other acaderaic/research bodies. If an industry has been closely involved in a particular issue being researched by the LGC then it is usual for them to be consulted before details of the report are finalised. It is therefore probable that the BPF will have sight of the LGC's draft report. It is the current view of the CSU and Department of Health that Mr Richards reports is very much a 'dead-letter' with little, if any, foundation on fact. Jacky Freer Group Executive eorosfec l Director - D R'Jones A company limited by guarantee Registered in England No. 282883 6 J O 79 --T9 5? 3 O liffOC e w = " N|L'&t ||I|I I&e:; s?si! tra'8?*. a2. 3 = t?2 "g " -csa 3 g - s3n >-rs*as So o8 _"g- fcoi? ?=3*<^ c* < ^ jr cr o srg. 3 cr 0 r5CsrO< OO22b iis-.aS SrSiT*?* 5< p ic first to pro ach for w ith s o f al- Ucpcn- 2,0 o oo-<-- no nft --o |B*oT n E2 1 S3& _5!<fat--O'' n--sr 2n 001" V0H 2," ,P 2 "M 5 3 ft's 5 " 3 " 3 ft = 1 < w 5fl 3J" 2 C --4" 75 XsOVc 3 =* 33 C/ln" ?- *" ~ 2.? S Sfl,,** --la2, ?i^a Ejs s*' E SE o 3 fcuO'C *^ = i 3 o s E s = E&3 w s" 3 ^ CT 5* V 79 O < CD 5="0C*0 3 3u " .3 = &J5 rs '*c ne S<j 3nIS3 3 gg?^ J7 s*ei e--sto --n n o 5III? to CO l g.5 i*3 Ea I O 95 o CD --J *T3 "a sf- * s- V- 3 O gf & 3 fr 3- Hj 0 ocrq i <Sj w|?<* m to 2 -- ?r Oo10 2 gSLo*'goo cK8P-jrtjrsar3^'l^<*oU5j:Hj 0iS 3xS2B =3=a y> ^ 0, OC. c5O3Tt 3X" CPaD rM3 = nf Eb. 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' 39 *v 02 HO. 0328628 Thi Britlih Pintle* Fidtratlon 5 Belgrave Square Lonoon SW1X8PQ 01-235 8463 Telex 8951528 Plafed G Fax 01-235 6045 Thi Britlih Plastics Ftdaratlon 1 awari of tht risiarch report thtt h bain produced which 11nk$ the Incldenca of Suddtn Infnt Oaath Syndrom* ("cot daithj") with certain addltlves'appllad to PVC used In ] tha manuractura of children* bedding, M < \ j i Tha 6PF It obviously concerned md has requested in 1 Independent assessment of thi report's findings is will i / 40 obtaining Ito own experts' opinion, Aftir initial reading, the rport ippotri not to Involve PYC directly with thee* tregedlee. An ImmedUte apprilail of the materiel* uiod la being cirrlid out with the manufteturers. In the meantime concirnod perants should follow tha quit! normal hygiene procedures whtn dialing with Infants and if in any doubt ink medical advlci. ------------------------------- ---------------For mori Inforwtioni Philip Law British Plastics Fidiritlon 5 Bflgriva Squire London SW1X 9PH England Til! (01) 235 9483 Dir.Clor - 0 R Jon* M eoto8&z '?0M *3S*-36f35v 42*^9 BRITISH PLASTICS FED 0l-235-(3j^| -------------------- j.------------------------------------------------ Tha British Plastic# Fadaratlon 5Be!grav Square London SW 1X0PH 01-235 9483 Telex 8951528 Plated G \ TC: NO. OF PAGES (INCLUDING FRONT): IF ANY DIFFICULTIES ARE ENCOUNTERED DURING TRANSMISSION. OUR FAX NUNBEE IS; 01-235 8045 t>i*ciof - a iwi oae A COmpiny Mld by guin! bQToSPzS "OH Hv8Sff0pH05Ni^49 BRITISH PIPSTJCS fZD 0r-7?ffi&-------------------- -------------- r.C'j CnOH) s. S.39 13:04 N 0 . 2 0 8 2 8 6 2 8 1 2 PQGE 2 "-cw*. ^XPv. ILf 4* ,3T. i Xilu^ vm oVv. GLV-* ^Wv L L^(*kAJUs (L u< (v^-v>4. C-IJL-*. /^Ay^k v. y, (^^\J>^rXjk sfr. fit* /2rt Qr> tv^u. t(jx3*A/> 'XL^A' $ C <^ Ofi" J'UojbL^f /W*e fl ^7T ^ ^ oiT i^La'cX , (LjUsjJuf'l^ C*-V I o UI ~\/ -90 tI H / ae _ ft--}%!* oV*uVv ----v " ClY fTt^ 5 ~ BRITISH FLfiSTICS Ftu Ul-^i5-ey<35 < no N ) 5. S.'S? 13:05 / r-.o^o NO.2082862312 PAGE ftTM M*- { iAKQ_ hjijL***--- C*--* /^o( ^ Ow Mb -T\ 0*j**jh-t\ f' ^u( /vC OaxsI i ('ipj^SIiArl t clutedLt e*_ f* bx^x. 0<--w. OiAQj '^ftr t^<sU'^kJ[ 1$jjJ[- \sla_ Ljuu< fVJ&v-vrVvvr-j^-Jl iy b"tj/ (\Jair ' I\j^'i^vi/- y&-v 9 o T o S >2:K t volume linkto'ii cot deaths dismissed By Pearce Wright Science Editor A theory that cot deaths arc linked to poisonous fumes released from PVC plastic cot mattresses has been widely dismissed by experts. The Department of Health says there is "no adequate validation" for the idea, which has caused alarm among many parents. The scientific advisory co mmittee to the Foundation for the Study of Infant Deaths, which has spent 4 million in the past 17 years on research, says the hypothesis contra dicts the findings of painstak ing investigations into factors 'that may trigger the deaths. jThe British Medical Journal 'also rejected the theory. : Dr John Grange, consultant jbacteriologisi at the Brampton ' Hospital, west London, said in a devastating assessment of | the report for The Times, 'which was circulated this `week, that more detailed stud ies were needed to provide a 'more definitive answer. The controversy centres on the details of a report by Mr Barry Richardson, director of a scientific consultancy ser vice, which describes the lab oratory experiments on which the suggestions about cot deaths are based. Dr Grange described the ex perimental methods as "using crude equipment, lacking an obvious control experiment that would reveal flaws and irrelevant as a representation of a cot mattress". Mr Richardson maintains that a particular type ofmicro organism common in homes can react with traces ofchemi cals used in the manufacture of PVC to generate poisonous fumes. A key to the process is mattresses must also have a protein content on which the micro-organisms thrive. The laboratory experiments involved placing strips ofPVC and organisms on a rich j nutrient mixture of soya flour ' and malt Dr Grange said that ! that bore no relation to mat tress conditions and traces of protein it might contain. Moreover, advanced in struments would be needed to identify the type and amount of gases generated. The report 1 contains no figures of the quantity of gases which came from heating those cultures. Dr Grange said they could have been generated from the nutrient mixture rather than the PVC. He suggested that Mr Richardson had con ducted for the best of motives I a completely irrelevant -ot--n> G A <D 6 i-y Bo o JG CT> 00 CD *0 ^ 04 OJ P? > I s.tS cu <D --' ON tm x cn .a c-pq oa G O Co CuO (2 So o 'u O CC//33 < C/3 ior<nu2>3tT <U *_* C/3 me 3 T3 c OONN <3 S 15 O aG OJ X3 u 'to go ooi .2o 0.. 00' "3 c mx & -cr JOui -,tM<Su >. KcO- +co<-D> cS Tf roH *sH ss EC Q s, o +J T03) H u : Mr Mr a 3 l3<o of s 3 2 H 5 ^DP7J"bm Lr,oO- *ouao^a, a :h TELLEX THE BROADCAST REPORTING SERVICE , REPORT PVC - LINKS WITH COT DEATHS For : Prog : Date : BRITISH PLASTICS FEDERATION KEITH HANMAN -- S Qp harald fuchs 8.6.8 9 Time: 1200 Service : Duration: BBC SHROPSHIRE Serial : 066232/JD o "03" 3 minutes 10 seconds H TELLEX 36 Paradise Street; Birmingham B1 2AJ Telephone: 021*643 4177 `1 1 >\ r t HARALD FUCHS: PVC mattresses could be the cause of cot deaths, according to a British research company. Penarth Research Laboratory tested twenty one mattresses, including some from Shropshire, on whichccot deaths occurred. Jonathan Beale asked the Tech nical Director of the company, Barry Richardson, what his N investigations had revealed. BARRY RICHARDSON: Our research was part of a programme of investigating i deterioration of PVC fabric and we became aware that a particular fungus might infect fabric and might attack some of the additives that are commonly put into the fabric ;as preservatives and fire retardents (sic). And this fungus would then cause toxic gases to be produced from the fabric. JONATHAN BEALE: So what would actually happen to the baby then'lying on the bed? B.R; Well in the case of the cot mattresses investigations that we did we found that the infection is always naturally present underneath the baby. It develops after a few months. The... depending upon how long a baby is left on the mattresses actually, and it only develops just beneath the baby where the mattress is warm and moist from perspiration. The gas, we find, is always produced from the in...from infected mattresses. Every one that we have examined is producing this gas when we incubate it. That means we put it in conditions that are 1 similar to cot conditions. The gas is produced, the main one is called dibean* and it's exceedingly toxic., A thousand times more toxic than carbon monoxide. So I'm afraid I'm not talking about anything that is mildly toxic or anything like that. We're talking about one of the most toxic gases we know. What we actually have is the babies who are dying are generally sleeping apparently in the face down position,' and they're generally quite heavily wrapped during cool weather. J.B: (Phrase inaudible)...to the incidence of cot death, particularly in relation to Shropshire? eotostz: *Phonetic spelling . u . i imli.\1 [ i -vT'j-Tr TT. When deaths have occurred some of the coroners offices who have heard of our work have asked the parents whether they could provide us with the mattresses on which the infants were lying. We've received mattresses, including mattresses from Shropshire. -- J.B: What's your reaction to people who've actually disclaimed this theory? For example, the Foundation for the Study of Infant Deaths.says that your work is'unproven. , What's your reaction to that? __ B.R: _ __ The work that I have done on the generation of the gas from plastic is quite fixmly proven. What is unproven is_the significance that this work may have, or this poisoning may have in relation to actual dot deaths. That's not my job. I'm i afraid the medical people must take my work into account and " see whether it does relate to the cot deaths that they're _investigating. J.B: - _ ----------- - What precautions can' parents take? B.R: Well 1 think in the long term, of course, parents will have to replace mattresses with safe mattresses. There's no objection; to PVC, I'must emphasise that. The problem lies with the additives that are used in current PVC. So obviously the mattress manufacturers will producing safe mattresses I imagine quite shortly. H.F: Barry Richardson of Penarth Research Laboratory talking about his investigations into cot deaths. '89-06-09 10:23 BRITISH PLASTICS FED 01-235-8045 P. 1'14 The British Plastics Federation 5 Belgrave Square London SW1X 8PO 01-235 9483 Telex 8951528 Plafed G Fax 01-235 8045 'l 7G : 'ROM : DATE: *V - NO, OF PAGES (INCLUDING FRONT): . . IF ANY DIFFICULTIES ARE ENCOUNTERED DURING TRANSMISSION CUR FAX NUMBER IS: 014-235 80^5 MESSAGE: . .(S^ . .......... >fe. .v'Tyc*--* r>9i''rr^sph. tV' ____ Vnt rtV-v , . j/W*. .. 'N .r. .-^rhfr. .\.................... I V Director - D R Jones A company ^mitea by guarantee --'stared in England No. 282983 5 turn#. ' 89-08- ?= 10:24 BRITISH PLASTICS FED 01-235-8045 P.2/14' P.R.I. L. TCCKNiCAL MKVJCKt PENARTH RESEARCH INTERNATIONAL ConU Itf.nq And R*Mirh P.0. Box ME, St. Peter Port Guernsey, Channel Islands LIMITED REPORT COT MATTRESS BIODETERIORATION AND ' SUDDEN INFANT-DEATH Barry A Richardson P1 June 1989 ZTTG&trZZ 89-06-09 10=24 BRITISH PLASTICS FED 01-235-8045 P.3/14 Cot wi tti tirast cr> lioidwtiaM-* n<t uwid4n os#%%n COT MATTRESS BIODETERIORATION AND SUDDEN INFANT DEATH Barry A. Richardson Introduction Sudden Infant deethr commonly described as cot death, accounts for a significant proportion of postneonetal- mortalities, usually involving infants which ere not observably ill priocJto death*. The causes remain unexplained despite extensive research,-- many recent studies- concentrating on statistical interpretation* of the circumstances of death as obvious explanations seem to have been eliminated. 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 the United Kingdom, 2 to 4 per 1,000 generally irr western countries, and about 6 per 1,000 in New Zeeland, but only about 0.3 per 1,000 In Hong Kong, and very' low incidence in Russia, China, India and Africa, and amongst infants of African--or "Hsian origin in England end Wales <172,3,4,3,5). The very- high death rate in New Zealand is due to exceptionalTrates of about 11.5 per 1,000 amongst Maori infants, the rate for _ -Caucasian infants at - about 1.6 per 1,000 being lower then most western countries<7). Deaths occur unexpectedly during sleep,-80% 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 where high death rates occur. The riek-is higher with premature births at low birth weights, twins, smoking mothers, unemployed fathers, single mothers and poor housing conditions, perhaps because all these factors tend to result in infants with lower weights than normal for their age. Deaths sometimes follow observations of general malaise when infants have digestive disorders, refuse to feed or are difficult to woke. Recent hypotheses have concentrated on the upper respiratory tract. It has been noted that there hee been a threefold increeee in sudden infant deaths in The Netherlands from 0.46 per 1,000 for 1969-71 to about 1.31 per 1,000 sines 1978(8), The obvious explanation for this increase is that sudden infant death syndrome is now recognised statistically, but this increase has been attributed instead to the general adoption of a prone or face-down sleeping position following recommendations that it was preferable at a paediatric conference in 1971. It has been suggested that sleeping in the prone position presents mors risk of obstruction of the upper respiratory tract<9,10), Viral end bacterial infections have also been reported, and may be associated with the prone sleeping position (11,12). In a recent review it was pointed out that sleeping in the supine position may avoid these problems but crests others(13). It has also been suggested that the prone position might result in hyperthermia as ths face is ths most important cooling surface and temperature control element, particularly in infants protected in the winter by extra coverings(14,15). .P. F?. JC.L.. Tehnil l.r.U.. Page 1 trro sn z '89-05-09 10:25 BRITISH PL-STICS FED 01-235-8045 P.4/14 Cet, * ttrwiifi l? liAdntnr !or *tton art-cl uddtn in f *n * ***1H"i Another possibility with heavy bed coverings end cots with high impermeable sides is that the infant is affected by accumulations of an heevier-than-air gas, the prone position aggravating exposure. The mo6t obvious gas is carbon dioxide generated by the infant itself. High carbon 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 gas from a cot and bedclothes reservoir<16,175. In such circumstances the carbon dioxide would be converted eventually to toxic carbon monoxide, euch a conversion parheps explaining why sudden infant deaths ere particularly associated with week-ends when en infant mey remain unchecked in the cot for a longer period <6>. ` Carbon monoxide poisoning has not been reported and is unlikely as this gas is lighter than air end likely to disperse, but such an explanation would be consistent with the slow release or formation of a toxic heavier-thsn-air gas. Recent investigations by Penarth Research International Limited into biodeterioration of the plasticisers in polyvinyl chloride indicated that three extremely toxic heevier-than-air gases phosphine, arsine and atibine might be generated, and this report therefore considers the possibility that these toxic gases from mattress covers, cot aides snd nappy pants might be a cause of sudden infant death. Phosphine, arsine and atibine Group V/Vb elements form gaseous trihydrides. Nitrogen trihydride is beet known as ammonia, but phosphorus, arsenic and antimony similarly form phosphine, arsine end etlbine gases which are 1.17, 2.66 and 4.29 times heavier than air respectively. The threshold limit values for phosphine, arsine and etlbine are usually quoted as 0.3, 0.05 and O.lppm respectively, about 300, 2000 and 1000 times more toxic than carbon monoxide which has a TLV of lOOppm. All three gases are colourless. Phosphine has a 'dead fish1 or `garlic1 odour, arsine is more distinctly 'garlic', end stibine odour is usually described only as 'very unpleasant') with arsine the garlic odour, which may be associated with the formation of alkyl compounds, is only detectable at concentrations well in excess of the TLV, Arsine The typical symptoms of scute 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 oedema(16). Red urine may develop 4 to 6 hours after exposure, followed by oliguria, anuria and anaemia. Hepatomegaly and jaundice follow after 24 to 48 hours. Polyneuropathy and encephalopathy have also been reported. Chronic exposure is usually reported to have a cumulative effect. This is not strictly correct as arsine is eliminated by conversion and excretion in the urine, but anaemia caused by chronic exposure obviously becomes progressively more severe; at very low air concentrations poisoning is characterised by shortness of brsath and general weakness reeulting from this anaemia. The mode of poisoning includes erythrocyte haemolysis through glutathione reduction which continues after exposure ceases, followed by haemorrhagic hepatitis and F>. FI . X. I-- . B.rvl... Page 2 F T T ()8 h Z 2 '88-05-09 10=25 epitish plastics fed 01-235-8045 P.5/14/''' C4 % hm tti*aia U>' i)i' tion uaain nephritis with tubular necrosis. Arsine ia a depressant of the central nervous ayGtem, and prolonged exposure may affect the bone marrow. Exposure to lOppm for 1 minute or 3ppm for 30 minutes is sufficient to cause fatal or severe toxic reactions, and ippm for long periods can be exceedingly dangerous. Arsine poisoning is usually diagnosed through acute haemolitic anaemia with ghoet erythrocytes and increased plasma haemoglobin. Arsenic in the urine usually exceeds 0.05mg/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 jaundice' and 'haemolytic anaemia* should be investigated for possible arsine poisoning<19). Mild chronic arsine poisoning may be easily missed end attributed to food poisoning<20). This description of arsine poisoning is based on observations in adults. Young Infants can be expected to be more susceptible because of their low body weight but there may be other physiological factors which may further increase susceptibly such as sluggish respiration and blood circulation in deeply sleeping infante, end which may cause local rather than general anaemia in cases of acute poisoning. Phosphine and etibine Phosphorus trihydride or phosphine end antimony trihydride or stibine are not as well known ae arsine, but they are exceedingly poisonous heavier-then-eir gases with the aame mode of action and symptoms as arsine. The mein differences are associated only with differences in density and toxicity, Phosphine, eraine and stibine from plasticised polyvinyl chloride Phosphine, arsina end stibine can be generated by biodeterioration of organic and inorganic phosphorus, arsenic and antimony compounds*, alkyl compounds may also be produced which are also exceedingly toxic gases. Scopulariopais fungi are usually involved but Poecilomycea species and some wood destroying fungi such as Lent in us squemoaua and some bacteria can also act in this way (32-52). Published reports refer only to ereine generation but phosphine and stibine can be similarly formed. Micro-organisms can only convert phosphorus, arsenic and antimony compounds to hydrides if an adequate nutrient source is also available which will provide the necessary energy. Scopulariopals brevlcaulls, also known as Penlcllllum brevicaule, is the fungus species which is most frequently reported as generating arsine in this way in domestic situations. It is usually described as protein tolerant but it is actually protein dependent, end we6 usually identified in the past on eilk, a protein fibre. Several classical case6 of arsine poisoning have been attributed to thie fungus causing biodeterioration of old wallpaper printed with Scheele'a green or Paria green arsenical pigments. Napoleon's death and a mystery illness suffered a few years ago by the US Ambassadress to Italy have both been attributed to chronic arsine poisoning caused in this way, and this could be en explanation for some of the unexplained sudden infant deaths reported in the 19th century. Although this fungue is usually associated in reference books with biodaterioration of silk, it actually occurs in normal domestic air and will Page 3 C TTnakw '89-06-09 10:27 BRITISH PLfiSTICS FED 01-235-0045 P.S/14-^ C*-t t laa (t tw r l>:> r 11 a n a**!*! uddi*ii I.nfan1 CS Wt develop on any suitable protein source, such as wool In carpets on damp floors or clothing stored In damp wardrobes, as well as on leather (53-58). Scopulariopsis brevicaulie can develop on polyvinyl chloride cot mattress -- coverings if adequate moisture and protein are present, perspiration usually providing these requirements. Other fungi and bacteria can deteriorate PVC plasticisers, particularly Aspergillus rtlger which causes grey discolouration and Streptomyces rubrireticuli which causes bright pink staining; these organisms have no toxic affect but their presence indicates that conditions are suitable for the development of 5. brevicaulis and other organisms that can generate phosphine, arsine end stibine(23*24,25,26,27,31). The arsenic source In--plasticised PVC is usually i0,10'-oxybisphanoxyarsine (OBPA), a biocide that -is incorporated to prevent biodsterioration_ of the plasticiser in tentage and--similar PVC fabric exposed to the weather, although it is trlso sometimes used--in PVC furniture coverings for hospitals as a sanitizing agent. OBPA will control most organisms at normal biocidal use concentrations but it is slightly volatile and it is also degraded by ultra violet light, concentrations typically decreasing progressively until colonisation by arsenic-resistant organisms such as S. brevicaulis becomes possible, The antimony source ia usually antimony trioxide, a white pigment which is added to PVC to improve fire retardency as it ects with the chlorine in the PVC 86 a flame suppressant by formation of antimony chlorides, but it appears that some manufacturers are now using antimsny tr-ioxide as a filler pigment at concentrations well above those required for fire retardency. Antimony trioxide is~not significantly biocidal and stibine can be generated if conditions are otherwise suitable for microbial development. The phoaphm-us source is usually a phosphate plasticiser, used in preference to phthalste and similar compounds when fire -retardency-is required. Regulations introduced in the United Kingdom in March 1989 require PVC for nursery purposes to be fire retardent end this means that all cot PVC contains-antimony trioxide end phosphate plasticisers; this is an unfortunats response to firs risk as fire rarely initiates in PVC items, and fire retardent PVC heated by-fire from another source will generate much more toxic smoke then ordinary PVC. Investigations Phosphine, areine and stibine generation by Scopulariopsis brevicaulis can be demonstrated in the laboratory. This fungus is protein dependent and will not develop etrongly in the absence of a protein nutrient source. A convenient culture medium can be prepared by stirring 5% soya flour into 6% malt agar, although the 6oyo flour can be replaced by other nitrogen sources such as ammonium citrate. Incubation should be at about 23C. If a phosphorus, arsenic or antimony source Is added to 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 derkening of silver nitrate; phosphine initially forms a lemon yellow complex, and arsine and stibine form brown complexes before black silver deposits are formed at higher concentrations. If greater sensitivity is required the culture air can be circulated through silver diethyldithiocarbamate reagent, producing a brown or orange colour for phosphine and red colours for arsine and stibine (21). F'.fJ.X.JL. ttfvt... Page 4 9TT08'le2 '89-06-09 10:23 EPITISH PLASTICS FED 01-235-8045 P.7/14 CO % m /> V t' e? m lorttOn u`td Mercuric chloride or bromide will react with arsine to produce yellow to red complexes, depending on concentration, but phosphine and stlbine do not produce coloured products- with these reagents. The most convenient method of detection of those gases from Petri dieh cultures is to use two small strips of detection -- paper tucked over the edge of each dish after the growth has become strongly established, a silver nitrate paper which will turn initially yellow with phosphine and brown-with arsine or stlbine and eventually black with all three gaaes, and a- mercuric chloride or bromide paper- which will turn yellow or red if arsine is present. Silver nitrate paper is prepared by soaking filter paper in a 5% aqueous eolution and mercuric chloride or' bromide paper is prepared by soaking filter paper in a 5% alcohol solution. PVC is often naturally- infected and deteriorated by organisms, particularly Aspergillus niger and SVreptoayces rubriretlculi, and laboratory experiments have demonstrated "that these infections can develop if the arsenical biocide OBPA 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 hae also been demonstrated in laboratory experiments that the fungus Scopulariopmls _J>revicaulis can develop on the same PVC samples in similar conditions, a high protein nutrient source being necessary, a soye/melt agar medium being the most convenient way to introduce an external protein source in routine laboratory experiments. Exposing email discs of PVC fabric to ST"brevicoulis Petri dish cultures on soya/malt .agar with silver nitrate and mercuric chloride' paper detection is a eimple means for checking whether samples contain phosphorus, arsenic or antimony sources which might cause- toxic hydride -gas generation under appropriate biodeterioration conditions. Checking PVC involved in eudden infant death to "confirm whether toxic gas generation was probable can involve a similar technique but without inoculation, relying upon the natural infection on the fabric. ~ Initial cot inveetigatlona were on PVC fabric from a new mattress which did not contain any biocide, according to the manufacturer. Samples were inoculated with . brevicoulis end generated gas gave a brown colour with silver nitrate and a faint yellow colour with mercuric chloride, indicating a reducing gas, probably stlbine from antimony trioxide, with some arsine, probably from the arsenic contamination that is usually present in antimony trioxide. A doctor who had lost an Infant then provided the mattress on which it had died. The mattress was a Viaivent carry cot type mattress comprising foam with the lower two-thirda covered with PVC end the upper third covered only with a net. The mattress had been used for a previous infant but was in excellent clean condition, The PVC fabric was eemplad and placed on soya/malt plates, producing the normal Penicillium, Aspergillus end other fungal cultures that are normal from domestic articles, but heavy growth of Scopulsriopsis brevicaulis also developed, generating gas causing brown or black colouration with silver nitrate but no detectable colouration with mercuric chloride, probably etibine from antimony trioxide. Foam wee sampled under the net, that is under the head of the infant, giving heavy S. brevicaulis infection but no colour change with silver nitrate; several other micro-organisms were alao found on the foam, including Streptomycee rubrireticuli which 1q a pink staining organism which is often associated with deterioration of plasticised PVC. F*. JR. I.L.. Tnnu*i Page 5 nxi& T rzz 89-0t-O9 10:29 BRITISH PLASTICS RED 01-235-9045 P.8/14 C.ca-t mkt'trttii* b iflffction wfldn tnf*nt The Initiel investigations included 21 mattresses from audden infent death incidents, including one cotton covered mattress but all others Involving PVC and some with exposed foam areas covered only by net. All PVC covers were infected with 5. brevicaulia which was particularly heavy at stitching, although also always present in the PVC covering immediately beneath the Infant', all samples infected with S. brevicavUs also generated gas which caused brown or black colouration with silvsr nitrate, probably etibine from antimony trioxlde, Home samples were also infected by S. rubrlreticull, although the characteristic pink stain was not always visibles in one case on a mattress only 2 years old the pink stain had clearly formed under the infant and followed the body shape, Foam samples from areas covered only by net were heavily infected with a number of fungi, including S, bravicaulia although gas generation was not detected) the foam does not contain suitable sources of phosphorus, arsenic or antimony, It was observed that some of the fungi on the foam produce spores which are well known as causes of allergic reactions and which might cause fatal asthmatic attacks in sensitized infants<53,57,59-64). Phosphine, arsine or stibine gas generation through biodeterioration of plastlser in polyvinyl chloride fabric is a possible explanation for sudden infant death, particularly if infants are in closed cots or heavily wrapped, Toxic poisoning in this way is consistsnt with the reported circumstances of sudden infant death syndrome. A prone sleeping position, heavy coverings in cool weather, and longer undisturbed periods in the cot at week-ends all increase the risk of chronic poisoning from a heavier-than-air gae, The increasing incidence over the last 20 to 30 years is consistent with the increasing use of plasticised PVC in nursery products, end significantly lower incidence in some countries such as Russia may be aasociatsd with lack of uss of PVC products in this way. The frequently reported malaise, digestive disorders end anorexia prior to death are consistent with chronic poisoning; it might be expected that some darkening of the urine would be reported in euch circumstances but It is possible that death occurs before It develops, The riek is least with new cots and mattresses as they are less likely to be supporting infection, The symptoms of phosphine, arsine and stibine poisoning have been generally reported for adults with the cautions that poisoning is not easily suspected or diagnosed(18,19). Infants are more susceptible because of their lower body weight) in an accident on the Thermopylia, a ship carrying grain fumigated with phosphine, 29 crew and 2 children were affected but it was a child that died (22). Infants with low birth weight6 might be expected to be particularly susceptible, whatever the cause of their low birth weight, because of their lower weight in relation to age during subeequent development. The high incidence at less than 12 months is probably associated with low body weight coupled with minimal ventilation due to lack of body disturbance during sleep, but the peak incidence between 1 and 5 months might be associated with physiological blood or respiration features associated with that age group. Hydride formation by micro-organisms is well known. Sulphate reducing bacteria such as Dasulfovibrle species can convert sulphates to aulphur dihydride, more commonly known as hydrogen sulphide, but only usually in anaerobic conditions in which the bacteria utilises sulphate as a source of oxygen; hydrogen sulphide is P.R. J.L. Thnlc*l Page 6 6 T T 0 apzz '39-06-03 10:29 BRITISH PLfiSTICS FED 01-235-8045 P.9/14 Ci: x mr\es nudeian meant cau**kiw-> generated In faeces in this way. Nitrogen trihydride or ammonia can be generated from nitrogen sources such as nitrates and urea by a variety of bacteria such as Thiobaclllus denltrlflcans, some acting in aerobic situations; ammonia Is generated in this way from urine soilage of nappies and clothing. Some bacteria are capable of converting suitable arsenic sources into the trihydrida arsine <28,29,30>. In all cases these bacteria also require a suitable nutrient carbon source. Fungi can also generate phosphine, arsine and stibine, Paacilomyces and particularly Scopulariopsis species being the most likely cause in domestic nursery situations in which the protein-dependant S. brevicaulis is likely to be present as an infection of damp wool carpeting or clothing. Infection of plaaticised PVC is opparently dspsndent on perspiration end .. develops mainly on the ares immediately beneath the infant, infection being followed by toxic gas generation if suitable sources of phosphorus, arssnic or antimony ars present; 6tibine formed from antimony trioxids seems to be the most commonly generated gas. The risk of infection on PVC in this way is higher on older materials which ara more likely to bs affected by established infections, although an infection will only generate significant amounts of gas when it la particularly active, perhaps not until several weeks after the mattress is first used. , i | j j ; ; Vented mattresses in which the foam at the heed end is covered only with a net support massive mixed fungal infections which produce spores which can cause allergic reactions, including severe asthmatic attacks in sensitized infants. Conclusions Phosphine, arsins and stibine gas generation through biodeterioration of plasticised PVC is a possible cause of sudden infant death. Infants are more susceptible than adults because of their low body weight which makes it easier to accumulate a lethal dose end particularly if sleeping in the prone position with the face close to the gas accumulating on the mattress. Poisoning is difficult to detect, as the phosphorus, arsenic or antimony introduced into the body through phosphine, arsine or stibine poisoning would not, increase levels beyond normal ranges. Investigations should involve incubation of samples of PVC mattress coverings at about 23C on high protein agar plates, such as 5% malt agar with the addition of 5% soya flour. Positive identification of organisms is not essential, but it is necessary to confirm whether an infection is present which may be generating phosphine, arsine or stibine, most conveniently by incubating the samples on Petri dish plates with silver nitrate end mercuric chloride or bromide test paper strips tucked over the edge of each dish when sn active infection has developedssilver nitrate paper changes initially to yellow with phosphine and brown for arsine and stibine, and subsequently to black with all three gases, arsine alBo causing yellow or red colouration of mercuric chloride or bromide paper. It should be appreciated that heavy fungal infections on exposed foam in vented mattreaeee may produce eporee that can cause allergic reactions, including severe asthmatic attacks in sensitized infants. P. R.I.L. Ttehfittu H'.Ull Page 7 e rv o s ^ rs '89-08-05 10:30 BPITISH PLPSTICS FED 01-235-8045 P.10/14 /: C&% f* lodaXvt\- 1 ctwcUi-\ intuit *ri Recommendations Sudden infant death investigators should recognise phosphine, ar6ine and stibine_ poisoning from PVC biodeterioration, and asthmatic reactions to fungal spores, as possible causes of death. PVC mattress coverings should be checked for fungal infections "and. gas generation, and exposed foam and porous mattress fabrics .should be checked for fungal infections. PVC used in mattress coverings, cot sides and nappy covers should be resistant to fungal and bacterial infections. Resistance can be achieved most reliably and permanently by using resistant plasticisers, rather than by adding biocides. Components containing--phosphorus, arsenic and antimony must not be used} the present limits for arsenic end antimony in British Standard BS 1877:Pari 10:1362 Domestic betidlngt--Pert 6,- Specification for mattresses for children's cote, perambulators and similar .domestic articles are too high and there are no limits for phosphorus. Exposed foam mattresses should not be used. ~Temporary protection against gas and spore generation can be achieved by wrapping mattresses in clear polythene sheet, secured on the underside ueing adhesive tape. Carry cot mattresses can be replaced with a folded large sheet. Acknowledgements These investigations are an extension of a series of projects on biodeterioration of plasticised PVC. I am particularly grateful to Mr P R Mitchell Mitchell Marquees who, when warned that arsine generation might occur in stored tentage containing OBPA, prompted these investigations by enquiring whether sudden infant death might be caused in this way. My assistant Mrs S A R Kelly was responsible for the mycological work, and Mr T R G Cox advised on chemical matters. Dr D Allsopp of the CAB International Mycology Institute at Kew supplied theoriginal sample of Scopulariopele breviceulls which enabled us to establish that phosphine, arsine end stibine could be generated through biodateriotaion of plasticised polyvinyl chloride fabric. References 1. Golding J, Limerick S & MacFarlane A. Sudden infant death; patterns, puzzles and probleras.Shepton Mallet: Open Book Publishing, 1985. 2. Secroft D M 0 & Mitchell E A. Trends in unexpected infant deaths, Lancet 1989;8S39;673. . 3. Lee N N Y, Chan Y F, Davies D P, Len E & Yip D C P. Sudden infant death syndrome in Hong Kong; confirmation of low incidence Br Med J 1989,298:721. 4. Gordon R R. Trends in unexpected deaths in Sheffield Lancet 1989:8629:106 Page 8 22460120 '89-06-Q9 10:31 BRITISH PLASTICS FED 01-235-6045' P.11/14 l C'3 < and auddon < nf curt 5. Balarajan R, Soni Raleigh V 4 Botting 8, Sudden infant death syndrome and po8tneonatal mortality in immigrants in England and Wales. Br Med 7 1989;298:74-6- 720, 6. Morris J A. Increased risk of 6udden infant death syndrome in older infants at weekends. Br Med 7 1986;293:566. 7. Mitchell E A, HbsssII I B 4 Becroft D M Or Postnaonatal mortality review in Auckland; two years experience. NZ Med 7 1987|100i269-272 8. de Jongs 0 A, Engelberts--A C, Koomen-Liefting A J M 4 Kostense P J. Cot death and ^rone sleeping position in The Netherlands.Br Med 7 1989;298:722. -- 9. Beal S. Prone-or supine~for pre-term babies? Lancet 1983:11:512. 10, Southall D P, Croft C, Stsbbins V, et al, Detection of sleep associated dysfunctional pharyngeal obstruction in Infants. ur J Pediatr 19891148:353-9. 11. Morris J A, Haran D 4 Smith A. Hypothesis! Common bacterial toxins are a poesible cause of the sudden Infant death eyndrome. Med Hypotheses 1987)22:21 1-222. . 12. Morris J A. Sudden infant death syndrome. Br Med 7 1969|29Q:958. 131~Milner A D- 4 Ruggine N, Sudden infant death syndrome. Br Med J 1989; "298:689-690. .- 14.-- Nelsorr-E A S, -Taylor B J 4 Weatherall I L. Sleeping position and infant death bedding may predispose to hyperthermia and the Sudden Infant Death Syndrome Lancet 19Q9ii: 199-2TCJO. 15. Stanton A N, Scott D J 4 Downhem M A P S. Is overheating a factor in some unexpected infant deaths? Lancet 1989;1:1054--7. 16, Kelly D H, Golub H, Carley D 4 Shannon D. Pneumograms in infants who subsequently died of Sudden Infant Death Syndrome. 7 Pedletr 1986;109:24-9-- 254. 17. Kahn A, Blum D, Rebuffat, et el. Polyaomnographic studies of infants who subsequently died of Sudden Infant Death Syndrome. Pediatrics 19B8|82:721727. 18. Kleinfeld M J. Arsine poisoning 7 o M 1980;22:820. 19. Doig A T. Lancet 1954111:88-92. 20. Hunter D, Pharm 7 1936j 137:514-15. 21. Anon. Arsine Methods for the detection of toxic substances in air; Booklet No 9, Ministry of Labour, H M Factory Inspectorate! London, HMSO, 1966. .P-7?. X. Z-. *pvic.. Page 9 22460JM 89-06-09 10:31 BRITISH PLASTICS FED 01-235-8045 P. 12/14-, I-? Col 19 lor*uclc<n Infunt 22. Wilson R, LoveJoy F H, Jaeger R J & Landrigan P L. Acute phosphine poisoning abroad a grain freighter. JAMA 244:148-150. 23. Klauameiar R E, Results of the second interlaboratory experiment in biodeterioration of plastics. Int Bioctet Bull 1972;8 (1 >:3-7, 24. Yeager C C, Pink staining in polyvinylchloride. Plastics World 1962;20:14, 25. Yeager C C. Laboratory and service tests for PVC. Proc 1st Int Blodet Symp 19S8;151-161. 26. Kleusmeier R E & Jones W A. Microbial degradation of plasticizers. Dev Ind Microbiol 1961;2:47-53. 27. Klauameier R E. The effect of extraneous nutrients on the biodeterioration of plastics. Monograph 23, Soc Cham Indl966;232-243. 28. Stainer R Y, Doudoroff M 4 Adelber E A. General Microbiology, London,Macmillan, 2nd edition, 1971. 29. Bergey, Manual of Determinative Bacteriology, 8th edition, 1975. 30. Engvall A-0. Ammonium release at the sediment-water interface; in situ studies of a Baltic sediment during negative redox turnover. Microbial Geochem 1978;2:1-39. 31. Hollo J 4 Kollar-Volgyesi M. Resistance of plastics to microbiological corrosion. Bioch Exp Biol 1975;11:163-173. 32. Smith G. An introduction to Industrial Mycology. London,Edward Arnold, 6th edition, 1969. 33. Morton F J 4 Smith G. The genera Scopulariopsla Beinsr, Microsacus Zukal, and Doratomyces Corda. Mycol Paper 86, 1963. 34. Richardson B A. Wood Preservation. London, Construction Frees 4 Longmans, 1978. 35. Broese van Groenou H, Rischen H W L & van den Borge J. Wood Preservation during the lost 50 years. Leiden, Sijthoffs, 1952. 36. Hamilton A. Industrial Poisons in the United States. New York, 1925. 37. Bub-Bodmer F 4 Tilger B. Die Konservlerung des Maizes in Theoria und Praxis. Berlin, 1922. 38. Gosio B. Azione di alcune muffs eui composti fisei d'arsanico. Rlv d'lglene e San Publ 3,201-230, 261-273, 1892. 39. Goaio B. Action de quelques moisissurea sur las composes fixes d'arsenic. Arch Ital Biol 18.253-265,1893. <* Page 10 Z Z T W lrZ Z '89-06-09 10:32 5RITISH PLASTICS FED 01-235-8045 P.13/14 7? Cot rnro totdv*w*r n* ncicici'ftn da<*k*t" *0. Goalo B. Zur Frage, wodurch die Giftigkeit arsenhaltiger Tape^en bedingt wird, Ber Deuts Chem Ges 30, 1024-1026,1897, 41. Schmidt H R. Uber verschimmelte Tapeten. Dies Erlangen, 1899. 42. Thom C & Paper K B. The arsenic fungi of Gosio, Science 76, 548-550,1932. 43. Mahlka F & Troschel E, Handbuch der Molzkonservierung. Berlin, 192S 44. Barge J van den. Baoordeeling van de waarde van fungicide atoffen voor houteonserveering. Dies Delft, 1934. (Testing the suitability of fungicides for wood preservation. Publ Int Adv Off Wood Pres, The Hogue). 45. Anon, Gaseous arsenic from wall-plaster. The Analyst 57,163-164,1932, 46. Larrigo A F,The biological method for the detection of Analyst 57,155-158,1932. arsenic. The 47. Sanger C R, On the formation of volatile compounds of arsenical well papers. Proc Am Acad Arts A Scl, 21,112-147,1894. 48. Sanger C R, On chronic areenicel poisoning from well papers and fabrics. Proc Am Acad Arts A Sci, 21,148-177,1894, 49. Biginelll P. Composizione a costituziona chimlca del gas arsenlcale dalle tappezerie. Atti R Accad Lincei Rendic Cl Sc Fis Math e Mat, 9,210-214,242249,1900. 50. Maasen A. Die biologische Methode Gosio'e zum Nechweis des Arsens und die Sildung organiseher Arsen-, Selen- and Tellurverbindungen durch Schimmelpilze und Bakterien. Arb a d kaiserl Gesundh ambt, 18,475-489,1902. 51. Hu66 H. Zur Kenutnis der. biologischen Zersetzung von Arsenverbindungen. Z f Myg u Infekt krenkh, 76,361-406,1914. 52. Legge T M. Arsenic poisoning. Ann Rep Chief Tnsp Fact Worksh Gr Brit, 6768,1918. 53. Milberg P. Mikroorganismer i byggnader, en litterarurstudie over arter, forekomst och miljokrav. Sv Lantbruksunlv, Inst f vlrkeslara, Uppseta 164, 1987. 54. Davies RR. Viable moulds in house dust. Trans Brit Myc Soc, 43,617630,1960. 55. Gravesan S, Identification end quantification of indoor airborne micro fungi during 12 months from 44 Danish homes. Acta allergologies, 27, 337354,1972. 58. Gravesen S. Identification and prevalence of culturabla mesophilic microfungi in house dust from 100 Danish homes. Allergy, 33,266-272,1978. ft?* J2T--L T**hni#l Page 11 Z T 0 8 frZ Z '89-36-39 10:33 BRITISH PLASTICS FED 31-235-6045 P.14/14. I CC * Loctiv-tor r>d ituddon infant <a* th 57. Kolmberg K. Halsoeffekter av mogelkontaminering i sveneka Byggforskni.ngsroctet rapport R36,99s.l985. bostader. 5&j_ Morton L-H 0 & Eggins HOW. The effect of moisture content in wood on the surface growth and penetration of fungi. Mot u Org, 11,279-294,1576. -- 59. Anon. Mogel i byggnader; en kunskapsoversikt. Soclslstyrelsen redovisar, 11,378,1984. ---- 60. Oravesen S. Fungi as a cause of allergic disease. Allergy, 34,135-154,1979. 61. Holmberg K 4 Kallings--L-0, Allergisk alveolit oraekad av mogel och termofila ektinomyceter, Lokortidningen, 77,39-44, 1980, 62. Sundin B. Fukt och mogel i byggnader. Medicinska effekteri - VVS och energi, 12.45-+S, 1983 ~- 63. Barr ARM, Hutchens M E & David J, Mycotoxinsi 8 potential hazard to health indomestic dwellings, J Inst Wood Sci, 10,120-121,1985. 64. Croft W A, Jarvis BBS Yatawara C S. Airborne outbreak of Trichothecene toxicosis. Atmos Env, 20,549-552,1986. t'Z tc e W Z ^* Ft . JT. JL* * rvli Page 12 fbHMJMij Sfa*dajj ' gas" THE mystery cot~death syndrome may be caused by Alan Massam-** ..- by babies breathing toxic gases generated Irom PVC mattress coverings, scientists now believe. ing by gas heavier than air accumulating in bedding. Infants usually died face A team of researcher*-- down when they were have come up with the ex heavily wrapped against the planation lor sudden infant cold. death syndrome, which kills 2000 babies each year in Bri tain. Deaths often occurred on mattresses which were not new and in which fungi or The discovery was an ganisms could have become nounced today by Guernsey- established. based Penarth Research In ternational. But Britain's leading research body into the problem. The Founder lion lor the Study of Infant ' Deaths, condemned It be Mattresses supplied by parents who had recently lost babies were contami nated with Ibe fungus scopulXTTbpsls brevlcmuUs, par ticularism stitching. cause it was 'only an un- proven hypothesis". The researchers also con "We have been inundated-- with calls from worried par- sidered that, loam coverings of the top half of mattresses supported fungal infections ents.Tspokeswoman said. which could provoke aller Penarth claim that mat gic reactions. tresses tested included The Foundation for the those only half covered with Study of Infant Deaths* PVC. It was found that they*- - stressed that epidemiologi-. were likely to harbour fungi cal evidence did not support 4: which were capable of giv the Penarth claims because- ing off gases like arsenic cot deaths occurred long be-.. trichloride when they re fore PVC was used on mat-- acted with the plastlcisers- tresses. --------- - _V used to make PVC Oeadblle. The Penarth research Is * The company .believed supported by Dr Peter Flero- - that the usual clrcum-..:. ing of Bristol. Maternity stances of sudden cot deaths Hospital's Department of ;vrere consistent with poison- Child Health.. .. k_ ______ C?iTSfh,Sy will be examined By Our Health Services StafT Health officials are "taking seri ously" a theory that some cot deaths may be caused by PVC in mattresses emitting heavierthan-airnoxious gases.' The Department of Health said yesterday that the claim, by a Guernsey research company, would be evaluated scieniifically, but a spokesman added'. "Currerit thinking is that cot deaths are due to more than one cause and the possible explans. tion that has been put forward is just another possibility." Hope.for;par'e.nts:::i OT deaths -bring ' tragedy to _ thousands .of .parents every year. They are ail the more dis-v1-' dressing for being shrouded in such;`,; Tmystery. * . .- "Researchers are not sure whether 7 * they stem from one cause or many.' .All of which does nothing to reassure- * millions of anxious mothers. Moreover the mystery helps create . suspicion , in the.minds;.-of outsid ers-- thus increasing .the'agonyrof -' the grieving parents. ..^rrV. ../:> JT*: - For these-reasons'the prospect of major breakthrough Into the cause of ' cot death is a matter for rejoicing. If -' the research!:.team on- the.'Channel . ' Islands really, has come up with the ., answer; they 7 will - deserve all our *7 thanks.. .... .?. ,v.. .-..*- ZT>"43mYW Fragus" poison r . .TifrisfUf gaslink deaths*1. By MARK VOULE : BRITISH - scientists claimed yesterday to - '.'.Risk..- hnvc trucked down a lie advised parents' (q/ major cruise - of .cot throw away all fVC coy*;, denth) which kills more ered mattresses andf'- than 1,000 babies a year. rcplace them:? with Jn.v' Rcscnfchers .the folded cotton sliccl." -n.'.r* ; sard:-7~^.yeryChannel Islands hKre dlj- . ; M.r, ' Richard' ofj.- covered a fungus' which attacks PVC .mattress covers, giving off a cock tail o( deadly gases. -arwenhleycao(tsu'Jendti,'tj;-b:gmqefty!\v< >:p#;|fi' Af .The scientists said the . wr^W.l>.||i*ferfvtn* amount of poisonous gas i ecoudsult** - to \to if has increased because of ' I d.OrtrUiif* Aiwtfffca?. chemicals added to PVC : M'the.pdlnJs.li t. to comply with recent bhuW* always sceln toilie * lire lvs.. 'In (dee down positions - Laboratory tests on 21 . where thqy `are closn to -mattresses on which the liberated gas." babies died were carried, The news caused pjtnle '. out by Penarth Research hmont parents after Mr. ey. International In' Gt'crn-. Richardson was Iqlcr-viewed on Radio Four's . t Twenty had pVC cover Today programme:- . ings and each of these Hundreds Jammed had ` lungnV -Infections ' phone line* to the Foun* which .were generating datlon for the Study of ' the lethal gases arsine Infant Deaths pleading nd sllblne. ' I. The . scientfsts said more Investigation: was needed, but researchcompany director Barry . Richardson! was ."bso- lor.help on how iti pro-, tecl their babies. Many' callers were In tear*. The Department of Health promised an Investigation -- and hilely convinced" he has . advised parents not to . discovered ono o( the start ripping oil rvc causes of .col dertlh. mattress covers. * I> ; X:& A". ,, COT DEATH. Is one of-the*moat > > ' traumatic ` tragedies that', a young-'- I. 7 1 .family can suffer. The distress and -. f i shock can be so devastating .that..-. ` 'JLT'jL.some parents have been driven, to.' * commit suicide as a result.- > - the news that Scientists have coma-up'.-1 with a hew and plausible reason (or Sudden: ` intent Death Syndrome tSIDS) Is very wel-. v; . come.-The findings show that the PVC-cov- /ered-mattress on the-cot itself could be /responsible.-'"-- Research by Barry Richardson;-of. Penarth Research - International in Guernsey. .; .rdvealed yesterday, suggests cot death vic tims may'be being literally gassed by their `own cots as fungi, growing on-PVC-clad mat tresses, give off toxic fumes. The fungi can- not be killed by ordinary disinfectant and are paturally present in the home, especially in wools. It is a terrible irony that many parents 1 bare switched to PVC-covered mattresses to beat other-possible causes of eot death.' -. Cot death still remalns an enigma. Dr Eli- ' tabeth Taylor, senior lecturer in.. - . community paediatrics at Shef-- ~'V Held University,'is one of the foremost researchers In theheld. She says: "Cot death Is. flVircPNaBMH probably due to a lot of factors which come together and then hit a baby who is already vulner able. We've got to look at every thing.". ..L LITTLE David '.Fellowe* .used 4e. although there wa i a alight inlcc- : wake so regularly In Ihe morning .- tion of the lung. - ' "that he was like an alarm clock for._; "One ef the worst things afler- * hts parents Sue and Graham.*...' ' wards Is the guilt you led." Sue .-' Cot death wms only officially classed as a cause of death in . . 1971. Before then, the syndrome . -was not commonly recognised. .. ./: Vulnerability . it is now thought that about * . one In $00 babies die from col . O-W.. I. r~r i*TM-^ 2u*K ..pL Theft !4.been'.no Urm. Octobtr.thrill.d but w.r- ^k. Sue *tnl Inlb u,e nunerr. ; rie<l 'h,ve , ,h, Graham was horrified (e hear her scream. "I couldn't see David at first, he was under the covers." Sue sbbaeeyiinsn.g;uu"Hnnded<ee-rrwhbali<ss qqsuutUiillLLl IIwtmraieremdn gpfiyrvo,innmgC' cot wwhhii^chh sounds iIrf itkhe* kbakbvv'-s ' T.-.wbriellaathlsinogshleeInpteInrruthpeteirdr.-oTohme. baby I: -rj conML 'death..Two thirds of tlhcse . deaths occur In babies of four to *1$ weeks old. and tUghty more boys are victims than girls. Research has shown that 6 per . cent of ell eot deaths happen , Sue Feflowes .. ; gulh r..-him muuth U, m.u.h re^C-/l-n -. and massaging - his heart," Graham. But David was dead. Mart, tel d-dj3J3J or`09J/-"j 1IJ111 or on their. 24 hour hetplme ; The post mortem said that there * OlJW/Wlfl. was nothing wrong with David ROSEMARY CARPENTER J -between October and March.. ' The high winter rates have led - problem associated with the (Bloomsbury. 9.99), writer - researchers to believe that over-, heating may be a cause, or even By JANET MENZ1ES after-effects of a minor respira tory tract Infection.' Deborah Jackson-says that In the first year, of life, a baby's `auflocatlon because of overwrapped babies. Children under . three months old have dllllculty in regulating their temperature- '.control mechanism. But the 1 researcher* came to a halt when.. . looking at Older victims. . S'-'' " The oew. research links the Incidence of.chlldren lying fsc.^ downwards * and - swaddled- In.'* Dr Taylor confirms:' "Breath breathing slows from 17 to PVC * and eventually give off toric gas can also be found In woot -. -.; ing Is very -important. The mechanism which controls.the/ baby's breathing can be Inter, A common theory Is that the . rupted. Sof baby's oxygen auppfy U In some ..- utests this U because of respl- around 17 breaths per minute. "And between' two and lour months; the Ume when a baby Is changing breathing patterns, he is most susceptible to SIDS." ; way - Inhibited, either from'out- *-' ratory infection. Allergy has . taping_ r l to an adult c aide, by gasses perhaps or from '.-`-Mao been put forward as a poaal- .- -cumulate regular breathing In a internal problems^ " ;ble reason." . * *. .n , ba^y and gas exchange may also covers with their Increased vul~- Dr Kevin Forsyth.of Lhe lnsU- - ' Cu'ecpnttble-k' nerablUty to' fumes eccumulal---. lute of Child Health ln-London. ^ .-oUSCeptlDie, Ing In the PVC bedding. * * Further support for the the ory appears to come -from New Zealand, which has one of the has conducted a survey.which he believes shows -respiratory Infection, as .a. factor. .HU research revealed that many cot A new book published tomor*' nU br*y In can rqw suggests that parents anx-- Jxm <?***?' a chemical atimu- lous about COt death could take .: 10 !*** next breath., . t--he b--a---bjy --to -s--l-e--ep --lo -t-h---e--t--r----w---n-- * -_-S- fud-J-a-* ^-guot.ed In Three In 4 ' highest cot dedlh rates In .the death vicUma bad had minor . bed wilhAhem. This, an age-old .. Bed show that babies sleepin* wrkfVhT custom 'thTre"u"lo respiratory infections..-.- . . . practice in Africa.- India .and-.;. with their mothers display dll, pIL^U* baby face down on a - Six babies died wlthlng .30 -- J*P*n, U linked io tha balpr fol-. (cent breathing paoerru Iroq fhJSpsWn nig covered with hours In the Home Counties In . lowing the proximity, ol"the;/.. ^Wldreo blankets -- and the mlcro-organlsms which can contaminate January IhU year. Researchers, mother s breathing patterns. fell that Jt was caused by a lung . -x;In her book Three In-A-Bedi- a waotuhldlngapfpoellaorwtshatht ethme oethhUedr'sf 22480125 Mothercare rap boffin -- Ey SUM REPORTER ! P scientist landed In a row last night w.. .. he claimed to have discovered one of the main causes of cot deaths. Dr Barry Richardson said mattresses covered by PVC were to blame for many of the.cot tragedies which have baffled research* ers for years. But bosses of the giant which stockj rang* of . Pt/C*covcr<l foam - mat* j tresses, w*r fitrioui. I A spokesman said: "We don't want parnts to worry about something that is not proven." j Mothercan store chain, Makers Dr Richardson, Si, head of a research firm In Guernsey, **d he found that 20 mattress covers on whleh babies had died were affected by a fungus : living off toxic gases. Mothereare WILL dls* cuss his findings with ' mattress makers. The Little Ones cot death charity said: "Wt remain sceptical:" |xh6i3HSH6?!B _ HOUSAHDS of ancjcious m---------yesterday laced the dilemma of rthrowing away tbtlr babies' J*vc. mattreasea, which. bav .bean nkad*wlth coi deaths. 7he oowUuassy has brvusbt mUUcttog- >**. CflbdHia tMCbilM Vt. IKpT tt -tUst Parry waeaaro-r 4or "folee pub ;* . wUl> *bOCk cswtta attar *U, oeUu-oi matftb n --** rvc was. imm stadacMs i Bvy6MUALER-K_- *. rim SCIENTISTS faced' an .'angry---, backiash-^yesterdajr^after claiming, to have discovered-a- r* major cause^tjf the?mysterious - cot`death- syndrome. ; The Mothercare chain eras besieged by calls from parents anxious:about the report that PVC-covered mattresses might be to blame, r Doctors were furious tiut the researchers bad Jumped the run.and revealed their,findings In. advance of more atnngeot tests. , .. . ,. . . But 'last night the director* of Penarth Research international Bj UN JENKINS was ataoding by > faU . claim of a - possible Oreaktbough In tbe hmfninf syadrwme which kills one ' heavier than air. could accumulate baby In every 500. / in bedding and wws more common Mr Barry Richardson explained f; In older mattresses.,- ; ` bow, dunsc * research into fabrics % `tbe ptnarth report * has been ''Vice-chairman Lady Limerick- -. aalcL Ideas like this which are - unsubstantiated should not be thrown at the public. It Is very irresponsible and will cause eoor- motu. distress. Got death has been with us a lot longer than PVC mittWEIEE ' for 'marquees and tests, his <*aua * -. submitted to'the British Medic*/ Medical experts are sceptical accidentally stumbled across a .. Journal where tt Is being examined about the theory because It would fungus in PVC-oovered mattreasea ..by'a referee * to * decide U H .1* ..not account for the fact that more which gives olf highly toxic aUblne. suitable lor publication. . boys than girls die In oot deaths, gas when tn contact with elements But the Foundation for the Study of tbe PVC.. The mettresses of.-cot'death victims were then studied and it was found that the fu. which Is ... of. Infant Death. wboae - experts bare studied the findings, dismissed ^be *UQpn7vea hypdthesis'. that second-born children are more ' susceptible and that the risk is greatest between the ages of two and four months. Mothercare sells three types mattress ineluding one covered w PVC which bas been oo sale sii the . *We hare had lots of calls fn worried parents,-but we arc tetil them there Is no rUX.' a spokesm said. *Our PVC is supplied by a leadl European nursery specialist a our mattresses meet striogr requirements relating to tomtity. Mr Richardson said:. T faced real dilemma in whether to t people. As a adentist 1 would vt to prove it Outright, and 1 Ooi want to be accused of scau mongenng. But we ha Theories add to grief, say: mothers-j;found something that nee f Investigation. *PVC came in - betwe. 1M0 and 1910. and It w A MOTHER who lost her "flelds -to'tb* baby Weeping covering. But gho said: 'My.'.lag'so many different news flve-mooth-old daughter'- thc^wroog .way. vpand - two.other children flept on As to why their child died.'* : iJcnDon- aflaic*t-i-cncogott t`hddeeeoraaietthhs a-- s.drdaaelidddT-*."-"*d*.r,w'Aus1lleK.tsVht.hVee>a.s'e...,..vd**if''feyrent--vv>it>eeww**t ,i-ic-*am*e%mno hm*aofat*o>Uo.*r*h-e.atsrtsa.--'n- d : ;; O-OwBw*tauU*ttmp..ooaoAourrl,.wlBBunee.-rr-kk- sKheireeg:awwnbb..oaoeef tn v,.r ............................. - arej-very. worrying- fo> -CJ lf***--** |M*--vghf(fy, o.f f seixix--iDmOoOnth-oolldd ssoonn BBeenn ddieiedd " .F, `/parents. I believe tot deaths Belfast, who lost bet baby . in -January, welooortd the Only around 1970 that une plained .Infant.. dean reached such- a*level th the- syndrome was reco niaed. Tor the past 30 yea the figures have remain* one In ttXL . ^rions' Katiler/ 'irom ' are caused by a ootdbins- :.>#eU wight years ago, Affjwrfd investigation!.......... The fact that old -.ZlateacS. Surrey,.-who** . ttoo of factors add* If there - There hr* far too many of -Bed sleot on a - ft^m daughter Satie died in Jaxv-** was-* one' easy solUUOft. It these reports. I don't think mattress with PVC ebvertn* uumaaarrnyy.y. swaeJuxfp.cla7nahtaiovnes,heiatrd)u*a%o <- awgooui-.l'd-ha*ve been, >.fou.n.d?..lo..n.g. *..iuitmnhdtuiyl wihsheoyu-mAldJk btoe trptlutubllivctis. e-d aXLt atdhinegslowgaevre eljvnfdc.s *tlhf etnheiste -- ------ Her daughter AbrpV | ^eraAVed ^Artn(s ^ has to be good nws lor all PnU.- arli mattresses are more suscep tbla points to the higher rt among second-born nhildre Svttv with Qrst-born vlctin We found Ibe mattrMs Wert penrl on from faml thing from electro-magnetic r mattiws* with a partial f vc,. f /. or friends.'. ... 71a ~TiM6 *7-6? pS^C fume link to cot deaths dismissed Dr Grange described the ex By Pearce Weight Science EdUor- A theory that col deaths arc perimental methods as "using crude equipment, lacking an obvious., control experiment that would reveal Haws and linked to poisonous fume* released from PVC plastic col mattresses' has been widely irrelevant as a .representation of a eol mattress", - Mr Richardson maintains dismissed by experts. that a particular type of micro The Department-of Health say's there is' "no aricouaic organism.common in homes can react with tracts of chemi validation" for the idea, which cals used in the manufaetwre has caused alarm among of PVC to generate poisonous many parents. . fumes. < , .. The scientific advisory co mmittee (o the Foundation for A key to the proceis. is mattresses must alio have, a the Study of Infmti Deaths, which has spent 4 million in protein content on which the micro-organisms thrive. .7* ' the past 17 year* on research, .says the -hypothesis contraidicts the findings of painstak ing investigations into factors '.that may trigger the deaths. (The British Medico! Journal jalso rejected the theory. * Dr'John Grange, consultant Jbac/eooJogij! al the Drompton . The laboratory experiments involved placing strip* of TVCand . organisms on I a. rich nutrient mixture of soya flour and mall Dr Gra. je said that that bore no relation to mat-' Iress conditions and traces of protein it might contain. Moreover, advanced In Hospital; west London, said in struments would be needed to |a devastating assessment of identify the type and amotinl. jthc report for The Timet, of gases generated. The report; which* was circulated this contains rio figures of the* (week, that more detailed stud-- quantity of gases which came, lies were needed to provide a from heating those cultures. 1 -more definitive answer. , 1 Dr Grange *aid they could The controversy centres on have been generated from the the'details of * report by Mr nutricnl mixture rather lhan: Barry Richardson, director of the PVC He suggested that' a scientific consultancy ser- Mr Richardson had con-' v/ce. which describes the lab ducted for the best of motives oratory experiments on which a completely, irrelevant the suggestions about cot experiment. datitiiretaus: 22480126 s <c Q O h* n cot link.. as a father I had to warn >Ns*Uv\^V\>X\X'' CS : TTHHEE scientist at the centre of the cot death panic is a factually precise, mild- marmeredman, not given to dramatic or emotional statements. But when Barry Richardson, discovered that fungus growing on PVC: mattresses caused cot deaths, his Instincts as a parent took over.- -.' "You can Imagine the situation 1 was in," he says. "1 had a terrible dilemma. Should { g6 on as a scientist and completely prove a link 1 was ctthlne was generated when exposed to fungus. 'Medical research shows cot death risk is highest for babies lying face down during the winter months or cool summer days,- "This means these ba bies are well wrapped tip. The (bogus grows in certain existed or should ! warn people? I still the warmth and perspi didn't have proof, but as a father and potential ration. the well-wrapped grandfather I realised 1 had to let people know. Hundreds of panic- baby breathes in the gas and there is nowhere sttrrickken m---o*thers jammed a help hotline after Mr Richardson is sued his warning. "1 knew there might be a panic but 1 couldn't have lived with my con science If 1 had done nothing. 1 just hope It saves lives." A consultant and dir by PENNY WARK monoxide. "Out of an PVC cot death mat tresses we examined from Moses baskets, prims, cots, carry cots and of different types of PVC, every one was in YeeUMay** TODAY They were just two of (he 2.000 British babies who die.suddenly and mysteriously In their cots each year, victims of S7DS. sudden Infant death syndrome. Lethal for it to escape to." says Mr Richardson. And he maintains his theory Is backed up by statistics. "Cot deaths became more noticeable in 1970. They had in creased very rapidly during (he previous ten years, when t'VC began to be used as a mattress covering." ector of a scientific re fected with the fungus search company, Mr . In the surface beneath Richardson first discov the baby/ he says. ered in January that a common household fun gus reacted with chemi cals In PVC mattresses As he speaks ot his home in Winchester. Mr Richardson cradles two to produce the gas sti- small mattresses. Each bine, 1,090 times more was donated by the par Mr Richardson, 51, has spent 15.000 re searching his theory since the presence of arsenic preservative <n plastics first caught his attention last year. Testa proved the same He also points nut that SIDS, which affects between two and four babies per thousand, is a purely Western phe nomenon. In Russia and China, where cotton mattresses poisonous than carbon ents of children who died. chemical was not used in oot fabric, but closer are used, the syndrome is not recognised. examinations revealed Although (he Founda itniofanntfoDr etahtehs Shtausdy nootf accepted Mr Richard- fton'a findings, he insists Ihe results speak for 5,*km or Pvc dented k!r,PTOiucrf b*>y Hetyon, who ,uppi, "'k' ""d ,, cum unnecessary panic. " vl!ie*laa bl*`cd ad- vtce to ua folded up said a spokesman. "PVC does not cause cot death. themselves. "f hope PVC mattress manufacturers will change. the additives they use. It's as simple b.Db; food' elwln Mother- 5!*!" l'TPonibie caremongering". ?r,,i']\COn,r01 n,"n'd -M ? ,rd M** "* a * very dan gerous statement to ife?d .?rp0,^hene ln luSr *r' `o"r Relyon's Pvc . "We meet standards and do not feel re sponsible for making . an unsafe product, be cause we don't." as that," he says. "While we are still conducting tests to prove the link with ba bies' deaths, we have Hdl' ,W*ra`o Stored The Foundation for established ihat lethal rtdkuted the finding. " * Pret>otrou, teleracnt and will act everyone in a . Study into Infant Heaths said the report gas is generated by cot mattresses. was "unproven, pre* mature and lacked de- >\.exc"eWptiohnavyeent.'t found tailed research". f8ie |P C J .HM 2-s*-ga-sssa \ g?isc,, rt-rt--' o o - w-o J'fT&S c 9 ItUi* llasifil i3f"Vitalii I||1 S3 2" 48 2l>2a* zph- ? BSaS?. 'Mf-sgs'"ss U lfll 3|3f! s1lso gl-lqjaso C 4, > <U ..CO oQ) -2H C 3V 5"s.Se so^alg 2-S M -3 5asglis|:Vl52%MV 5sf30ot.E"0C9i 5thFa*1S3So-5 ijidSf.8 9 dSfia a"* et Ox: 2 ** -j <j o 8 O 153- is a . 3n aS)i C- . 4) 4> a s u> -Se-5 " 2 fta Sfl=| 3.= . i; a ac -- d. Sr2fil S ? 41 c6 Is 313 * l8? Jc S5 SfsiiS5fgtlSUi,2 --`wO'OQ.-C 5 4,>, o ioi"2"0n *;Scsiioo 22 fessiSe .> 8 | JZ i2i si C* 3ZXo (p"o -Sna --faSl,yuISu-Rce E E'oSf ''IS"*" Ioa COf >oV 2JZ v CO 0 CLJ= ^C"d5 ? o x ' ^2,3 oi 3O, t(oC 5 c CIWdO'S JZ,,oj 4a1a>)j,3rIi *0 CD * h-t >0 NEWSCUP/APCUT TODAY Daily *078 y 9m Vi <.vy\Vr. by ANDREW YOUNG HUNDREDS of panicstricken m o t h p_r s jammed a hotline yest erday after babies' mattresses were blamed for cot deaths. They pleaded lor advice alter scientists claimed the bedding's PVC covering could give ofT a gas 1.000 times ns lethal as carbon monoxide. The danger has soared since new (Ire-retardant linings were ^ introduced in March, research- . ers said. Flooded Horror spread as radio butledits announced the latrst the ory to explain why `1.000 babies every year die In their sleep. The leading cot death charity, the Foundation for the Study of Infant Deaths, was flooded with calls. A counsellor said: "Mums were extremely upset to hear the results of the study. Some were so distressed liiey were crying on the phone." All Infant mattresses are at least partly covered by PVC. Mr Dairy Iticlurdson. who led the research In Guernsey, urged parents to thrown away tiny ones used in carry cuts. "These should be replaced Turn to Page 2 Mothers panic over mattress link to cot deaths From Page 1 with a folded sheet," he said, "tn the case of a larger dropsided cot, the mattress should be covered in a jmlyIhene sheet and securely taped." Parents must also ensure that babies* rooms arc welt ventilated. But caution was urged by Peter Fleming of Bristol Maternity Hospital, con sidered one of the country's leading paediatricians. He said: "The mere possi bility that this has occurred, when all the products have been tested for safety, dearly gives us cause for concent. "The tests were carried out under controlled luLwrulory conditions and there is no hard evidence that this oc curs in the cot. "We must Ik cautious. It would be foolish for mothers to throw away PVC mat* nvsses or change the way they attend to their chil dren." Oik* of the biggest retail ers. Muthcrcarc, announced an immediate investigation. S|>okeswouian Jane Bookhain said: "The foam mat tress has lieen In our range since the 1960s and we have no record of any cot death attributed to the use of PVC. "We will investigate the report's conclusions with our manufacturers." The Foundation for (he Study of Infant Deaths ad mitted it had known abuul the research fora mouth. A spokeswoman said: "The hypothesis But cot deaths might be caused by the re lease of poisonous gages from PVC cot mattresses has been carefully considered by our Scientific Advisory* Com mittee. "It must remain as yet a completely unptvveo hy|oih esis which due* not III with what is known of sudden infant death syndrentc." There have been many the ories to explain cot death since it was first identified more than .10 years ago. Most of the young victims are uitdcr eight months old. with more tays dying than girls. The mortality rate soars during the winter months. Most previous explana tions Tor cite mystery centred on the tables themselves, with such causes as a miss ing enzyme, a lung malfunc tion. a deficiency of sleep hormone or abnormal red blood cells. Babies breathe in killer gas A SI.KKIMNG b.ilts could Ik* gassed lo death In a cunimon household tungus residing nidi the 1*VC on cot bedding. Scientists at I'cu^Tb Ueseurch liilcrtiaiioiuil on Guernsey stumbled on the breukthrough accid entally. . During tests on the de terioration of PVC fabrics they found that a micro organism scvpularlopts hreiaiulu reacted with chemicals used In produc tion methods. The bug cun give olT three lethal gases, all tif -which are heavier than air. Youngsters King Ian* down at- -i.uv.-tl of o\v gen as thev sleep, the srienlists suggest. Manul.irtuicis use an agent to kill oil tin- fun gus , during pi odtirtioii. Itul this drift unities vs til* age. The {Mttvntial danger has grown since .Maul* when a firc-relurdant chemical, untimom trioxIde. was iutiuducvd intu PVC ptaiduciion. The fungus leads with Oie chemical to pr<ducv fnlo the highly toxic gas slihim*. Itcsearci* base dtieclor Hurry Richardson said: \\ I..OM.I all OtallM sses lirn .<! old li.il Im.mi <-i| the limgus. "Slilooe Is l.'HMI HO.es more deadly than c.iiImoi luouuvtde atol attacks the n-d blood cells reudetiug them unable to ahsotl* o\ygen. "The e\at 1 cans** ul death would t*e auaemia. "The nk to infants is very high. It is onlv a hypothesis, J>ut ui- he- lievu it lu Ik* ki'rcui step forward in need of greater research." Mat tresses with foam pillow licadpircrs could also cause aslhiiiMs attacks, say duetors. 2 2 4 SQJ2 Q 05/17/90 MARKETING THE LANCET 001 MARCH 17, 1990 Cot mattress blodulerioration and SIDS Sir,--In 1988, various Amgj were idenuiied in industrial plasticised polyvinyl chloride (PVQ despite the presence of the preservative 10, lO'roxybijphCtidxyirsine (OBl'A). Warnings were given that the FVC mighl also become infected by at senic-tderant organisms which might convert ObPA to toxic arsine gas. Mr P. R. Mitchell, a client ofour company, inquired whether arsine generation through biodeterioradort ofsuch coverings might be l cause ofsudden infant death syndrome (SIDS). 50 uuumsa used in forty-live SIDS inddattx were examined, including 1 cotton covered, 26 PVC covered, 15 PVC covered with exposed foam at one or both ends, and fi exposed foam; in five incidents 2 mattresses had been used. All martretses contained Scopulampsii fatvicaullt, but only in the tree beneath the infant affected by warmth and perspiration. Incubated samples of the Wetted materials til generated toxic trihydride gases. PVC coverings usually generate stibinc (SbHj) from a fire retardant additive, antimony trioxide, but also phosphine (PH,) from the phosphate plasticisers that arc used when fire resistance it required. Although OBPA is not generally used in cot nusures* PVC, tests indicated arsine (AsH,) generation when it w* used; and small amounts of arsine were sometime* identified when it was not, presumably from arsenical impurities in antimony uioxidc. Mixtures of gases were often detcewd. Phosphine generation from PVC was sometimes associated with the development of a pink stain, usually in the shape of the sleeping infant, apparently caused by liberation of phenol compounds from decomposition of phenyl phosphate plasticscrs, Only phosphine was generated from infected Colton and foam samples, apparently through biodeterioration of phosphate fire-rctardaru treatments, Foam samples and the 1 ennon sample wereaho infected by various other fungi, especially in the area affected by dribble; many of these fungi produce asthmatic reactions. The generation of highly toxic trihydride gases from cot maUresses is i serious threat to health. The gases arc heavier than air, and infants most at risk art those who remain for long periods in 'their cots, sleep prone in carry-cots, or arc heavily wrapped such that they arc in long and close breathing contact with Huatmulations of gas. Heavy Wrapping also induces hyperthermia, which prompts an Increase in gas generation. Some infanta probably survive because the first symptom of poisoning is headache,which results in irritability, dislodgmcnt of bedding, and improved ventilation; infants oflow weight cannot dislodge bedding. SIDS occurs mainly in infanta up to age 5 months who sleep prune with heavy wrapping and have indications of hyperthermia. SIDS is only reported in western-style communities where foam and PVC covered cot mattresses arc used, and has only been recognised since about 1969, following introduction ofthese materials during the previous 10-15 years. It has been reported that SIDS it lets likely to wait in tint bom children, perhaps because mattresses are new and do not become infected while the infant is young and most at risk. 5 first children were involved in the 45 incidents investigated. 2 died on previously used mattresses; 1 of these 2 slept on a mattress immediately after use by an older child. 1 infant died on a new foam mattress that was generating phosphine and 2 died on new PVC mattresses which were affected by exceptionally active fungus and were generating phosphine; two other new mattresses were implicated, both of which were similarly affected. Infection by 5 brevicaulis is not readily visible in PVC Severe deteriorerion, usually associated with phosphate plasticisers, results in brittleness and spirting. In the home (he fungus is usually found in protein-containing substances such as cheese and meat, and in damp wool and leather; however, its extracellular enzymes can convert a wide range of compounds containing the elements nitrogen, phosphorus, arsenic, and antimony into the trihydrides ammonia, phosphine, arsine, and stibinc. The preferential development ofthii Bangui in cot mattresses should be attributed to the presence of nitrogen compounds in the perspiration. The generation of mine in this way has been recognised for about 106 years since Cotio' discovered that death in children and illnews in adults were sometimre caused by arsine generated by the action of S krtlnctlidis on arsenical wallpaper pigments, although it ij now known (hat arsine could be similarly generated from she horre-hoof tun that was commonly used at that time snd which contained white arsenic to discountjc rodent damage.' Phosphine, ursine, and stibinc ire exceedingly toxic with threshold limit values of 0-5, 0 5 and 0-1 ppm, respectively, compared with 100 ppm for carbon monoxide. Relatively high ambient levels prevent the detection of phosphorus, arsenic, and antimony residues at necropsy. However, some pathologists have commented that they usually associate SIDS with abnormal lung eokjur; this could be associated wuh local erythrocyte haemolysis due tu exposure to these triliydride gases. rsAarirt Bewateh !nt,nations!, R0BeU2 Straw ron. Gusmssr. Channel Isliftdr B, A. FjUt/dtDSON 1. t'Uuki H. U' t-v-a;nivfTTSMi WKXTOati ftfai (Tusavca. ftn> ttf .V*, 1*72; h SSl-30. Ml -73. 2. Thun C, Raptr KB. The irynv fungi o( Gouo. StMmu 1VU. 10; S4M-SQ. VA Covcnviwni inquiry, prompted by these findings, was announced on March 9. The inquiry will be chaired by Prof Paul Turner. Acute renal failure after colloidal bismuth subcitrate overdose Sir,--Nephropathy due to acute and chronic use of bismuth salts i$ well recognised,' but urai ingestion ofcolloidal hismuih is said to be wife sinus it is less readily absorbed than other salts.' Vi'c report a case of acute renal failure associated with an overdose of colloidal bismuth subdtrste. A 76-ycar-old man who had been taking tripotassium dicftrambisrowhaie CDa-Nol1) for four weeks for haemorrhagic gastritis and duodenitis was admitted having taken an overdote of 6 'Detroit/ (tetracycline hydrochloride 115-4 mg, chlortetraeyeline hydrochloride 115-4 mg, and demeelocyelinc hydrochloride 69 2 mg per tablet) and SO de-ool tablets 4 h earlier. The only other prescribed drug ingested in the month before admission was fluoxetine. His pulse pte was 84 per min and blood pressure was 170/90 mm Hr. He had mild epigastric tenderness and was Slightly coiffured. Fiascia creatinine was 145 pmol/l, serum sodium 137 liurvul/1, serum potassium 5-4 mmol/1 (hsemoivsed sample), haemoglobin 13 9 g/di, white cell count 22-8 x I0";l, and platelet count 212 x JO'/I. Bismuth was detectable in the blood (1600 jtg/1). An abdominal X-ray film showed opacification of the Colon by Ingested bismuth Acyi a chest X-ray film showed no evidence offree gas under the diapltnigm. Since the patient had vomited profusely at home ttnd in the accident and emergency department, gastric lavage was not done. After admission oo the ward he was noted to be oliguric and four hours later began passing bloody stools, but no source was seen at sigmgidoseopy. He was turned on ranitidine and regular antacid, and magnesium tulpiute enemas were prescribed to purge his colon ofbinnuih. He had a briefepisode of hypotension (80/35 man Hg lasting about 5 min) 12 h after admission, but mean blood pressure was-149/80 ram 1 Ig with a venous central presure of 1 10 on water. I ic was transfused with two unis of blood though hit haemoglobin never dropped below 11-3 g/dj. After 48 h of oliguria plasma creatinine was 516 pmol/J and serum poussiwn was 8-1 mmol/1 and h was dialysed for 3 days, during which time he continued to pass bloody stools and needed further transfusion. Acute abdominal pain then developed with absent bowel sounds but he wvu judged unfit for surgery and died 4 days later. Necropsy revealed perforated duodenal ulcer and "pale kidneys'1 which^-J proved to contain bismuth (11 mg/gond l$mg/g). tjsj) This patient had toxic scrum bismuth concentrations 4 h *Actkv_ ingestion of 60 de-nol tablets and bismuth proved to have accumulated in his renal tissue. Bismuth nephropathy probably contributed to weute ratal failure, although there was the additional'^ insult of gastrointestinal bleeding. We are aware of only one previously recorded case ofacute renal failure secondary to colloidal. q bismuth subdtrste ingestion,3 in which a 27-ycar-old man recovered following colonic purging and haemodialysis. Quunic