Intended for healthcare professionals

Editorials

Fire retardants, biocides, plasticisers, and sudden infant deaths

BMJ 1994; 309 doi: https://doi.org/10.1136/bmj.309.6969.1594 (Published 17 December 1994) Cite this as: BMJ 1994;309:1594
  1. P J Fleming,
  2. M Cooke,
  3. S M Chantler,
  4. J Golding

    The message of the “back to sleep” campaign holds until the chemistry has been worked out

    Recent television programmes linking the sudden infant death syndrome to the antimony added to the plastic of cot mattresses has concerned the public and health care professionals alike. Unfortunately, the programmes and their fallout have been stronger on opinion and invective than on accurate information. There is a danger that the message of the government's “back to sleep” campaign, which has been followed by a dramatic fall in sudden infant deaths in Britain in the past three years,1 may be obscured by incomplete, inaccurate, and sensationalist reporting.

    Barry Richardson, a consulting scientist, proposed in 1989 that fire retardants in cot mattresses might contribute to the sudden infant death syndrome.2 The essential component of his hypothesis was that, under the right conditions of warmth and humidity and in the presence of traces of organic material (for example, from sweat or urine), certain fungi (such as Scopulariopsis brevicaulis) can metabolise constituents of infants' mattresses (phosphorus, arsenic, or antimony) and produce the highly toxic trihydrides—phosphine, arsine, and stibine. These trihydrides, by acting as anticholinesterases, might then kill infants by inducing cardiac or respiratory failure of rapid onset.

    S brevicaulis is common and can degrade nitrogen-containing compounds in organic material (for example, in meat, cheese, and leather), so that ammonia (nitrogen trihydride) is released. Phosphorus, arsenic, and antimony are—like nitrogen—in group V/Vb of the periodic table of the elements, and Richardson's hypothesis is that their trihydrides may be similarly produced. Such a degradation process was recognised in the 19th century as leading to deaths from arsine poisoning. (In damp conditions S brevicaulis degraded arsenic contained in wallpaper pigments and paste.3) Although cot mattresses do not usually contain arsenic, they commonly contain organophosphates and antimony trioxide, which are added during manufacture to the polyvinylchloride coverings (as plasticisers and fire retardants respectively). Although the foam and woven fabrics used in cot mattresses do not contain antimony, they often contain phosphates.34

    This hypothesis is compatible with many of the features of the sudden infant death syndrome in Western countries, particularly the association with the prone sleeping position and heavy wrapping, and with the pronounced falls in incidence when infants do not sleep prone.5 6 Stibine, being heavier than air, would be most likely to cause toxicity to infants sleeping face down under heavy wrapping. The association of the sudden infant death syndrome with social disadvantage and high maternal parity is explained by the suggestion that such families are more likely to use old mattresses (which are said to be more heavily colonised with S brevicaulis).

    But the characteristic age distribution of infants dying of the sudden infant death syndrome (peaking between 2 and 4 months), the seasonal incidence (with, until recently, a pronounced winter peak), and the strong association with parental cigarette smoking are not well explained by this hypothesis. Haemolysis, the most common finding in acute stibine toxicity in adults,4 is not seen in the sudden infant death syndrome. In Rihardson's laboratory, incubation of pieces of polyvinylchloride from mattresses with S brevicaulis on malt agar plates has been shown to produce colour changes in silver nitrate indicator papers, which he claims indicates the presence of stibine.

    The Turner committee, set up in in 1990 to investigate this hypothesis, commissioned studies in the laboratory of the government chemist; attempts to replicate these observations were unsuccessful.4 A controlled study commissioned by the Foundation for the Study of Infant Deaths (C F Simpson, personal communication), closely following Richardson's methods, failed to show evidence of production of stibine. While the studies in the laboratory of the government chemist have been criticised on methodological grounds, there has to date been no independent replication of Richardson's observations (B Richardson, personal communication).

    Antimony's role

    The most recent data produced in support of the hypothesis consists of the television description7 of concentrations of antimony in postmortem liver and serum from infants who were said to have died of the sudden infant death syndrome and from control infants who died of other causes, including trauma, infections, prematurity, and malformations (S Variend, personal communication). These data have not been published, but a summary of the results has been made available to us (A Taylor, personal communication) and shows detectable concentrations of antimony in the livers of 22 of the 41 children dying of the sudden infant death syndrome compared with only one of the 15 controls. Liver and blood concentrations correlated poorly; the infant with the highest liver concentration had no detectable antimony in the blood.

    No evidence exists that the concentrations that have been found are toxic, and the presence of antimony in liver suggests long term rather than short term exposure. Published results from women occupationally exposed to antimony have shown urine concentrations more than 1000 times higher than the serum concentrations observed in these infants.8 Several of the control infants died in hospital and may have received supported ventilation, which may have reduced environmental exposure. The presence of antimony in infants' hair9—if confirmed— represents evidence of environmental exposure but does not indicate toxicity. The concentrations quoted in the television programme are close to those previously reported for antimony in hair and much lower than those recorded after drugs containing antimony have been used to treat parasitic diseases.10

    The sudden infant death syndrome is not a “new” condition. Babies have died suddenly and unexpectedly in all societies since antiquity.11 Until this century such deaths most commonly occurred in bed with a parent and were attributed to overlying.12 In 1953 a committee was established by the Ministry of Health, which undertook studies on sudden death in infancy. The interim report published in 1957 estimated that 1400 such deaths occurred annually in England and Wales,13 a similar figure to that recorded in 1990, before the “back to sleep” campaign began.1 The dramatic fall in the incidence of the sudden infant death syndrome in many Western societies after “back to sleep” campaigns means that the incidence of the syndrome in these countries (in which mattresses covered with polyvinylchloride are widely used) is now similar to or lower1 6 than that reported from countries such as Japan and China where these mattresses are not commonly used.3 14 15 In Britain the incidence or the syndrome fell in the few years after many manufacturers increased the amount of antimony added to the polyvinylchloride coverings of mattresses (believing that this was necessary to meet the 1988 Furniture and Furnishings Fire Safety Regulations). Thus potential environmental exposure to antimony increased as rates of the syndrome fell.1 3 4 6

    The Richardson hypothesis has some biological plausibility and fits some, but not all of the known epidemiological features of the syndrome. Stibine, the trihydride of antimony, is highly toxic, and without compelling evidence of benefit from the addition to cot mattresses of (reportedly non-toxic) antimony trioxide we agree with the suggestion in the Turner report that its continued use should be seriously questioned.4 While Richardson's observations of release of stibine from polyvinylchloride have not been confirmed independently, the concentrations of antimony in infants suggest an environmental source. The dietary content of antimony is generally low,16 concentrations in tobacco are higher,17 and antimony is widely used as a fire retardant—in paper products as well as plastics16; information on its uptake and excretion in infants, however, is scarce.

    The two year case-control study on all sudden unexpected deaths in infancy in three health regions (with a population of about 17 million), funded by the Department of Health, is due to complete the collection of data early next year and will provide important information on any association between particular types or ages of mattress and the risk of the sudden infant death syndrome. Further studies are needed of the concentrations of antimony in infants and the relations to various environmental sources. Of particular urgency is the need for independent replication of Richardson's observations of the generation of stibine from polyvinylchloride.

    For the immediate future, it is important to stress that the advice contained in the “back to sleep” campaign of 1991 still holds and has been followed by a remarkable fall in the incidence of the sudden infant death syndrome in Britain and elsewhere.1 6

    References

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    View Abstract