Used infant mattresses and sudden infant death syndrome in Scotland: case-control studyBMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7371.1007 (Published 02 November 2002) Cite this as: BMJ 2002;325:1007
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Cause and Prevention of Cot Death (SIDS)
Cause. Ubiquitous, ordinarily harmless household fungi and certain
microorganisms cohabit in bed with baby. Consuming legally required fire
retardant and other chemicals in mattress and bedding and whipped into
greater activity by remnants of detergents and similar chemicals, these
organisms generate neurotoxic gases about 1,000 times more poisonous than
T. James Sprott, OBE MSc PhD, proposed a toxic gas explanation for SIDS in
1986. (SUNDAY STAR-TIMES, 1986: April 6). In 1988/89 Barry A. Richardson
BSc FIWSc ACIArb of Great Britain, a physiologist and biochemist
specializing in action mechanisms, independently reached and refined the
same conclusion. (Richardson BA. Cot mattress biodeterioration and SIDS.
Lancet 1990; 335: 670). (Richardson BA. Sudden infant death syndrome: A
possible primary cause. Jour Forensic Sci Soc 1994; 34:199-204). (Sprott,
T. James, OBE, PhD. The Cot Death Cover-up? Auckland, NZ: Penguin
Environmental, 1996.). (Smith, Lendon H, MD, with Hattersley, Joseph. The
Infant Survival Guide: Protecting Your Baby from the Dangers of Crib
Death, Vaccines, and Other Environmental Hazards. Petaluma, CA: Smart
Publications, 2000.). (Smith LH with Hattersley JG. Victory over crib
death. Townsend Ltr Doc/Patients 2000; Aug/Sept 50-54, 126-131). Sprott
and Richardson were originally looking at different toxic gases, although
now they both are concerned with the gases that Richardson identified in
They are heavier than air, and so a baby sleeping face-up is less likely
to inhale a lethal dose. This explains why the worldwide campaign for “on
back” sleeping lowered the SIDS rate in Western countries by one-third or
more. (Gibson AAM. Current epidemiology of SIDS. Jour Clinical Pathology
1992; 45 (suppl): 7-10).
These heavier than air gases, typically phosphines, arsines, (Cullen WR,
Reimer KJ. Arsenic speciation in the environment. Chem Rev 1989: 713-764),
and stibines are nearly odorless. They quickly dissipate unnoticed by
parent or caregiver. A child older than about one year or an adult so
exposed would react to the severe headache the gases cause.(Sprott TJ. The
Cot Death Cover-up? Op cit.).
The chemicals which are formed and the toxic gases are also present in
sheepskins and other "natural" bedding such as tea-tree bark fibers,
widely used in Australia and New Zealand. Depending on the soils on which
the sheep graze, their skins can contain phosphorus, arsenic and/or
antimony, often in sufficient concentration. Tea-tree bark normally
contains phosphorus, since the trees excrete toxins into their bark.
(Sprott TJ. Personal communication, 1999).
Fungal spores remain after a baby has slept in a crib, and so on arrival
of a second baby gas production starts sooner and in greater volume.
Consequently, a mother’s second baby has double, and the third (still
using the same mattress) has quadruple the sudden infant death syndrome
risk of her firstborn. For later infants and for those of low-income
single mothers the risk is higher still. (Tappin D, Brooke H, Ecob R,
Gibson A, Used infant mattresses and infant death syndrome in Scotland:
case-control study. BMJ 2002; 325: 1007. ) (Sprott TJ, The Cot Death Cover
-up? Op. cit.)
The risk of re-use of mattresses is graphically shown by the statistic
that when there has been a cot death in a family the risk of a second cot
death is 1 in 65, that is 50 to 100 times the risk of the first cot death.
(Fleming et al. Sudden death in infancy: the CESDI SUDI Studies, Table
3.15 on page 30. 1993-1996, 2000: p. 43.) Judges hearing “Shaken baby
syndrome” cases should take note. (See Al-Bayati Mohammed A., PhD DABT
DABVT. Analysis of causes that led to Baby Alan Ream Yurko’s Cardiac
Arrest and Death in November of 1997. http://www.redflagsweekly.com Dec.
Any increase in temperature of baby, mattress and bedding makes the fungi
more active; they then generate gases faster. Warming mattress and
bedding, in contact with the baby, from 98.6oF to 104oF can increase toxic
gas generation tenfold or more. And some vaccines create recurring fevers
(Landrigan PJ, Witte JJ. Neurological disorders following live measles-
virus vaccination. Jour Amer Med Assoc. 1973; 223; 13: 1459-1462.),
possibly explaining bunching of SIDS deaths at predictable intervals
Prevention. In 1996 Dr. Jim Sprott perfected a gas-impermeable membrane
called BabeSafe® to separate the gases from the baby. Through December
1999, the New Zealand Ministry of Health had no record of any cot death in
a baby sleeping on a BabeSafe cover. (New Zealand Ministry of Health,
statement, 1999; Dec.). Dr. Sprott estimates the number of babies who have
been so protected, in New Zealand and elsewhere, now totals at least
120,000. There has still been no report of a cot death in a baby who was
By contrast, during the six years in which BabeSafe covers have been in
use, about 520 New Zealand babies not sleeping on such covers have died of
cot death. The BabeSafe intervention has been 100% successful in
preventing cot death.
Joseph G. Hattersley, MA.
7031 Glen Terra Court SE, Olympia, WA 98503.
T. James Sprott, OBE, PhD.
10 Combes Rd., Remuera, Auckland 5, New
Competing interests: No competing interests
The study by Tappin et al. (2 Nov 2002) found an increased risk
of SIDS for infants who
slept on used mattresses and this was further increased if the used
mattress on which the infant
slept was from another home. In relation to cause and effect, the
authors suggest that the increased
risk might be associated with the presence of toxigenic species of
bacteria such as Staphylococcus
aureus that have been demonstrated to grow well in body fluids that
contaminate the mattresses.
We have identified pyrogenic toxins of S. aureus in over half of
tissue samples from SIDS infants
sent for examination from five different countries [1,2]. The
increased risk for SIDS associated
with used mattresses might be due in part to colonisation of infants
by toxigenic strains against
which they have no passive immunity from the mother or active
immunity acquired by natural
exposure while protected by maternal antibodies.
The higher risk associated with mattresses obtained from other homes
might be related to
introduction of strains producing toxins different from those
colonising the members of the infant’s
immediate family. Young infants obtain their normal flora mainly from
their mothers from whom
they also obtain passive antibody protection against these
microorganisms and their toxins. We
examined 116 pairs of S. aureus isolates from healthy infants and
their mothers. Among these pairs
of isolates, 59 (51%) isolates from mother and baby had the same
pattern of toxin production,
e.g., no detectable toxin or the same toxin. When toxin production of
strains isolated from SIDS
infants and healthy infants was compared, the proportions of strains
producing the different toxins
examined varied significantly between the two groups (X2 = 16.2, df =
4, p = 0.00003) (Table)
The increased risk associated with used cot mattresses might be due
in part to increased exposure
to toxigenic strains against which the infant lacks antibody;
however, these observations must be
assessed in relation to other major risk factors such as the prone
sleeping position. The
staphylococcal toxins cannot be dismissed as postmortem contamination
as the toxins are
produced only between 37-40°C which is above the normal
nasopharyngeal temperature of
children. Overheating or minor respiratory infection might increase
the nasopharyngeal temperature
to the range in which toxins are produced. Previous studies found
that children in the prone
position have significant increases in nasal temperatures, and in a
proportion of those tested,
temperatures of 37°C or higher were recorded after 30 min in the
prone position .
The conclusion of a large study of SIDS in Scandinavia was that the
risk factors for SIDS increase
the “dangerousness of infection in infancy” . The findings by
Tappin et al. are another piece of
evidence to support this hypothesis.
C. Caroline Blackwell
Immunology and Microbiology, University of
Newcastle, NSW, Australia
Donald M. Weir
Medical Microbiology, University of Edinburgh,
Forensic Medicine Unit, University of Edinburgh,
1. Blackwell CC, Gordon AE, James VS et al. The role of bacterial
toxins in Sudden Infant Death
Syndrome (SIDS). Int J Med Microbiol 2002; 291: 561-570.
2. Zorgani AA, Essery SD, Al Madani O et al. Detection of pyrogenic
toxins of Staphylococcus
aureus in cases of sudden infant death syndrome. FEMS Immunol Med
Microbiol 1999; 25:
3. Molony N, Blackwell CC, Busuttil A. The effect of prone posture on
nasal temperature in
children in relation to induction of staphylococcal toxins implicated
in Sudden Infant Death
Syndrome. FEMS Immunol Med Microbiol 1999; 25: 109-113.
4. Helweg-Larsen K, Lundemose, JB, Oyen, N et al. Interaction of
infectious symptoms and
modifiable risk factors in sudden infant death syndrome. The Nordic
Epidemiological SIDS Study.
Acta Paediatr 1999; 88: 521-527.
Table 1. Detection of staphylococcal toxins SEA, SEB, SEC1 and TSST-1 produced by isolates from SIDS and control infants n (%) n (%) SEA 13 (12.3) 41 (27.3) SEB 34 (32.1) 48 (32.0) SEC1 35 (33.0) 34 (22.7) TSST-1 5 (4.7) 37 (24.7) Non-toxigenic 51 (48.1) 54 (36.0)
Competing interests: None declared
Competing interests: Table 1. Detection of staphylococcal toxins SEA, SEB, SEC1 and TSST-1produced by isolates from SIDS and control infants n (%) n (%)SEA 13 (12.3) 41 (27.3)SEB 34 (32.1) 48 (32.0)SEC1 35 (33.0) 34 (22.7)TSST-1 5 (4.7) 37 (24.7)Non-toxigenic 51 (48.1) 54 (36.0)
If a used infant mattress is associated with an increased risk of
sudden infant death syndrome then I suggest that this indicates a toxic
cause of death.
If the routine use of an infant mattress previously used by another child
was significantly associated with an increased risk of sudden infant death
syndrome then this also indicates a toxic cause of death.
In my view this is unlikely to be the result of bacterial toxins but is
more likely to be the result of the use of materials no longer in use and
this would also explain why covering the mattresses and keeping the
infants' airways clear of those mattresses considerably reduces Cot
However that would not reduce the exposures to toxins in the air or in the
food, water and milk and these also add to the toxic load, as do vaccines.
My health was destroyed directly by organophosphorus (OP) chemicals.
Friends, and many other people I know, have been similary harmed and many
have died either as the direct result of the poisoning, or from the
induced illnesses, and many have taken their own lives due to the adverse
effects which have devastated their lives.
Although few in the medical profession are brave enough to accept that
exposure to nerve-toxic chemicals caused our nervous disorders and deaths
it is perfectly clear that these effects have been known and recognised in
law, in this country, for most of the last century.
Our occupational exposures to OP pesticides and animal health products
will naturally be much higher than for an infant.
It is recognised, I understand, that for infants the harm caused by even
minute amounts of such a toxic nerve toxic chemical would be fatal if the
exposure was too much or for too long. Lesser exposures are likely to
adversely affect both the blood and the immune system in attempts to
counter the effects of the poison.
Some believe that OP action is predominantly more harmful to males
than females but ultimately all are susceptible and, as recent reports
demonstrate, some are genetically more susceptible than others as a result
of inherited enzyme deficiency. Infants are particularly vulnerable to
any given dose due to their relative mass and under-developed immune
systems, at least until about 6 months of age, when essential levels in
the blood are, I understand, then similar to those of adults.
Summary points suggested to be of interest:
1 If there is a toxic action – then simple enzyme tests or that of a
simple blood count should indicate the infant's attempts to replace
inhibited blood and enzymes over a period of time. Were the enzyme levels
and WBC’s reported?
2 If there is a toxic action, figures are likely to show deaths at a
peak at birth, falling to low levels at 6 months, but there could also
possibly be peaks when infants are subjected to any further toxic action
If all deaths, and not just sudden death, are included then what are the
total number of deaths in infants for each of the first 6 months?
3 It must be as difficult to detect that the deaths are of toxic
cause as it has proven to be in adults regularly exposed to these
It appears that deaths from toxins were known in the 1970’s resulting from
the use of an antibiotic, which apparently killed hundreds of infants, but
only between 2% and 10% showed the clear signs of a toxic death. I am
informed that up to 98% were killed by the poison although the only
“proof” was found in the nurses' records of the exposure and subsequent
death from an “unascertained” cause.
Absence of evidence of a toxic death does not mean it was not a toxic
This may cast doubt over the quoted figures.
4 The more than 100 deaths apparently from the use of an anaesthetic
in a Moscow Theatre, possibly fentamyl, indicates another possibility.
The same or similar anaesthetic is used in some births and therefore other
toxic causes of death should be explored, including those to which the
infant is exposed before birth. Has any study been performed on the
exposures to life threatening chemicals before birth and possible links to
later Cot Death?
What are the numbers of epidurals using fentamyl?
What happened to these mothers and infants compared to those who didn’t
have the epidural or were given a different anaesthetic?
The work of the Scottish Group clearly demonstrates that toxins in a
mattress do kill so should we therefore be commissioning more work to look
into toxic actions and how to recognise them?
When will we begin to understand and recognise toxic causes for what they
are and stop pretending that we don't know and that we need more research
in order to re-discover "lost", or perhaps "overlooked", knowledge?
The evidence is clearly there for all to see and the lives of both the
infants and their distressed families could be saved.
Richard Bruce. 10/11/2002
Competing interests: No competing interests
A four-and-a-half year study by the Scottish Cot Death Trust(1) has
shown that the re-use of infant mattresses triples the risk of cot death.
This research finding cannot be ignored. It is crucial to cot death
From late 1994 I have publicised mattress-wrapping for cot death
prevention nationwide in New Zealand, and since that time a very large
number of babies have slept on wrapped mattresses. There has been no
reported cot death among those babies; the New Zealand cot death rate has
fallen by 48%(2), and the European/Pakeha ethnic rate has fallen by about
Wrapping mattresses in an chemically inert gas-impermeable diaphragm
prevents exposure of the baby to toxic gases which can be generated in
Earlier this year a German doctor published the results of the New
Zealand mattress-wrapping campaign in a journal of environmental
medicine(4), including statistical analysis carried out in conjunction
with the University of Munich. The statistics showed that the proof of
the validity of mattress-wrapping for cot death prevention was one billion
billion times(5) the level of proof which is generally accepted by the
medical community as proving a scientific proposition.
The 100% success of mattress-wrapping has been proved in New Zealand
over a period of nearly eight years. Now Scottish researchers have
confirmed that mattresses cause cot death, and a German doctor has
demonstrated that the proof of mattress-wrapping is vastly greater than
accepted medical standard of proof.
The New Zealand Ministry of Health, the New Zealand Cot Death
Association and the Royal New Zealand Plunket Society have been dithering
around over mattress-wrapping for nearly eight years. During that time
around 550 New Zealand babies have died needlessly of cot death. The
Ministry, Cot Death Association and Plunket have been informed time and
again about the efficacy of mattress-wrapping in preventing cot death -
yet they have failed to act on this life-saving information. I hold them
responsible for those 550 deaths.
(1) Tappin et al, Used infant mattresses and sudden infant death
syndrome in Scotland: case-control study, British Medical Journal
(2) From 2.1 deaths per 1000 live births in 1994 to 1.1/1000 in
(3) Sprott, T J, "The Cot Death Cover-up?" (Penguin Books, 1996)
(4) Kapuste, H, Giftige Gase im Kinderbett (“Toxic Gases in Infants’
Beds”), Zeitschrift fuer Umweltmedizin No. 44; January-April 2002:18-20
(5) p < 1.9 x 10(exp minus 22). The generally accepted figure
for medical proof is p < 1.0 x 10(exp minus 3).
Competing interests: No competing interests
The Scottish research on the effect of a mattress on cot death, first
done in 1997 and now repeated in a more robust manner for publication in
2002, shows clearly a way of saving the lives of two thirds of those that
die. Your “toxic” mattress may kill your infant, comes through clearly.
Any practical way of reducing cot death is surely a cause for
celebration? No, according to the editorials of the BMJ and Peter Fleming
et al. Why?
A “toxic” mattress will by definition be more likely to kill than a
“non-toxic” mattress. The question which now needs addressing is what is
the “toxin” in the mattress?
As a chemist it is quite simple to find answers. Organophosphorus
(OP) nerve agents have been used since the 1930’s in home materials and
furnishings for flame retardants. Today, the position on the use of such
chemicals is not clear, without further chemical investigation and
But Peter Fleming himself denies that any testing of a mattress for
“toxins” should be done. The question must be asked of him and his team –
Are they sufficiently “unbiased” to admit what to them cannot be true,
even if research were to suggest it was true? They have been denying a
toxic mattress cause of cot death for a very long time. They also seem to
be “unclear” whether it is the more “toxic” PVC or a safe “non-toxic”
plastic such as polythene, that is used to cover mattresses to halt the
effect of any “toxic” material in the mattress proper..
Is it fair to condemn the work of David Tappin and others of 1997 and
again repeated, if the criticism is by doctors who refuse to allow even
the testing of mattresses to be commissioned after a cot death?
SIDS a suggested approach for police and coroner’s officers
· The hypothesis that the cot mattress may give off toxic gases has never
been substantiated and is not a reason to remove the mattress.
CESDI SUDI Studies, Sudden unexpected deaths in infancy. Editors, Peter
Fleming, Pete Blair, Chris Bacon and Jem Berry. The Stationery Office,
2000. ISBN 0-11-322299-8
Does this mean, that another baby is to use the mattress that may
have already taken a life?
Whenever toxins are measured for in cot deaths they are always found.
Whenever toxins are covered up the cot deaths fail to happen.
To deny a truth without proper scientific investigation is not
“sloppy” science it is “non”-science.
And sloppy science may well be superior that of doing no science.
But the answer to the cot death conundrum is to decide that from
today it is time to do some “proper” science.
John Fryer Chemist
Competing interests: No competing interests
Determining the cause(s) of SIDS
All deaths occur from an impairment of mitochondrial oxidative
phosphorylation. There are many exogenous agents that might have
impaired oxidative phosphorylation in babies with SIDS. These include
bacterial toxins, chemicals that might have contaminated their
mattresses, clothing, food or water and poisonous gases that might have
contaminated their living spaces. The effects of these agents are likely
to be additive for there are so many different ways in which oxidative
phosphorylation can be impaired. Some babies might in addition have
inherited or acquired mutant mitochondrial DNA.
Surely no conclusion can be drawn until all the possible agents that
might impair ox phos in babies have been identified, their relative
potencies established in animal studies using tissue pH as an end-point,
and their presence and outcome examined prospectively in a cohort of
babies, their mothers and their homes.
1. The real danger is in the mixing? Richard G Fiddian-Green
bmj.com/cgi/eletters/325/7367/736/c#26113, 7 Oct 2002
Competing interests: No competing interests