DDT May Have A Substantial Impact On Infant Mortality
From: Robina Suwol
Date: 14 Aug 2003
Time: 19:09:42
Remote Name: 66.141.118.149
Comments
Nonmalarial infant deaths and DDT use for malaria control
Chen, A and WJ Rogan. 2003. Nonmalarial infant deaths and DDT use for malaria
control. Emerging Infectious Diseases 9(8):960-964.
A growing body of scientific evidence indicates that DDT may have a
substantial impact on infant mortality, by increasing the risk of pre-term
birth and by decreasing the duration of breast-feeding after birth. In this
paper, Chen and Rogan conclude that DDT may cause a comparable increase in
infant mortality through these mechanisms as the decrease in infant mortality
it causes by killing mosquitoes and thus reducing malaria cases.
They conclude that debates over the value of using DDT for malaria control
should incorporate consideration of the unintended consequences of exposure.
The authors acknowledge uncertainty in their calculations because the
available research does not yet prove conclusively that DDT causes the effects
on pre-term birth and breast-feeding. They argue, nonetheless, that the
findings are sufficiently plausible that they must be factored into decisions
about whether or not to use DDT for malaria control.
Coincidentally, this article appeared just as an op-ed was published in the
New York Times recommending that DDT be used in the US to fight West Nile
Virus (WNV). While Chen and Rogan do not address WNV in their paper, the
analysis they advance is equally, if not even more relevant here. In this
case, the increases in infant mortality due to DDT use would dramatically
outweigh any possible benefits that might result from using DDT to fight West
Nile Virus, because the number of deaths due to WNV is so low.
What did they do? Chen and Rogan began with data from African studies of
DDT/DDE levels in people documenting the increase in DDT/DDE levels that are
caused by living in homes treated in malaria control programs. They then
calculated, based on the elevation in DDE levels produced by treatment, how
much infant mortality would be expected to increase because of maternal DDT
exposure based on the following findings from the scientific literature.
The risk of preterm birth increases with the level of DDE measured in the
mother's serum. This finding, reported by a team of scientists from the
National Institute of Environmental Health Sciences and they US Centers for
Disease Control, found over a 3-fold increase in preterm birth in the most
exposed group.
Preterm birth, in turn, has a strong link to infant mortality. Babies born
before term are significantly more likely to die.
[They also are at risk to a range of adverse health conditions through life (a
cost not included in Chen and Rogan's
calculation.]
The duration of lactation decreases as serum DDE levels increase. Two studies
(data combined in graph at right, from Chen and Rogan) both show that mothers
with higher serum DDE levels nurse their babies 40%-50% less than mothers with
little or no DDE.
As shown in the graph to the left (from Chen and Rogan; data from World Health
Organization) An infant that is not breast feeding at under two months of age
is 5.8 times more likely to die than an infant that is breast feeding. Several
factors contribute to this pattern. For example, children still breast feeding
are less likely to contract diarrheal diseases through exposure to polluted
water.
What did they find?
Chen and Rogan calculated that infant mortality would increase by 9% because
of preterm births, and by 20% because of shortened lactation.
Combining the effect of preterm birth and shortened lactation, Chen and Rogan
calculated an overall increase of 20.5 deaths per 1000 infants. By comparison,
data from Africa indicate that malaria itself causes 20% of infant deaths in
Africa (175 deaths per 1000 infants), with additional deaths caused by
maternal transmission of malaria (3-8%).
What does it mean? The increase in infant deaths estimated by Chen and Rogan
to result from maternal DDE exposure is smaller but comparable in magnitude to
the number of children that die from malaria. Therefore, according to Chen and
Rogers, "the side effects of DDT spraying might reduce or abolish its benefits
from the control of malaria in infants."
In evaluating this comparison, several factors must be considered. Chen and
Rogan used conservative assumptions in their calculations. Hence the side
effects of DDT spraying could be substantially more adverse, even through just
these two mechanims (shortened lactation, increased preterm birth).
Use of DDT does not eliminate all childhood malaria. Hence the comparison to
total infant deaths caused by malaria is somewhat misleading; the actual
number of malarial deaths prevented by DDT would be lower.
Other health effects of DDT/DDE (for example, the recent indication that DDT
exposure in the womb reduces fertility in women 30 years later) would decrease
DDT's net benefit further.
Just as they don't include adverse impacts of DDT use other than increased
infant mortality, they don't include beneficial impacts of DDT use that result
from decreased cases of childhood and adult malaria.
The studies on which Chen and Rogan base their research were carried out in
the US and Mexico. They may not provide an accurate basis for calculations
extrapolated to Africa. The extrapolation could be biased in either direction,
high or low. As noted above, Chen and Rogan used conservative procedures in
the calculations to avoid inflating the possible adverse effects of DDT.
These studies have not established a causal relationship between DDE serum
levels and either preterm birth or shortened lactation. The effects may be
causal, and Chen and Rogan's calculations make sense only if they are causal,
but the nature of the epidemiological methods used do not allow causal
conclusions. This is a common situation in epidemiology.
Chen and Rogan's calculations challenge a prevailing assumption in
considerations about using DDT to control malaria, that the adverse effects of
DDT use are small compared to the benefits in avoided deaths. Instead, Chen
and Rogan show that the adverse effects are plausibly the same order of
magnitude as the benefits. Their work, while far from definitive, raises a
series of new questions about the wisdom of building malaria control programs
on DDT use, when not only are there likely to be substantial adverse effects,
but there are also affordable alternatives.
Chen and Rogan's work is also of immediate relevance to a proposal that DDT be
used to fight West Nile Virus in the United States. In this case, the possible
benefits of DDT use are numerically tiny compared to the likely adverse
effects, even if the only adverse effect of DDT is increased infant mortality.
By one calculation, from the lead scientist at the National Institute of
Health who carried out the study linking DDE to increased preterm birth, up to
15% of infant mortality in the US during the 1950's and 1960's, may have been
caused by DDT. If that estimate is correct, elimination of DDT use in the US
is today avoiding approximately 66,000 infant deaths each year. Even if that
estimate is high by a factor of 10, that would be 6,600 deaths, and this
calculation does not include any contribution of decreased lactation period.
By comparison, West Nile Virus last year caused approximately 300 deaths in
the US.
Gladen, BC and WJ Rogan. 1995. DDE and shortened duration of lactation in a
northern Mexican town. American Journal of Public Health 85:504-508.
Rogan, WJ, BC Gladen, JD McKinney, N Carreras, P Hardy, and J Thullen, J
Tingelstad and M Tully. 1987. Polychlorinated biphenyls (PCBs) and
dichlorodiphenyl dichloroethene (DDE) in human milk: effects on growth,
morbidity, and duration of lactation. American Journal of Public Health
77:1294-1297.
Schecter, A, M Pavuk, O P??pke, JJ Ryan, L Birnbaum and R Rosen 2003.
Polybrominated diphenyl ethers (PBDEs) in U.S. mothers' milk.
Environmental Health Perspectives doi:10.1289/ehp.6466 (available at
Background on PBDEs
Schecter et al. report they find comparatively high levels of PBDEs in breast
milk from mothers in Texas. The levels measured are comparable to those found
by other recent US studies in breast fat and maternal and cord serum. They are
up to 100 times higher than recent measurements of PBDEs in European breast
milk.
While a definitive answer for the high levels in the US compared to Europe
awaits further systematic study, it most likely relates to differences in the
use of brominated flame retardants in various consumer products, combined with
recent European moves to decrease exposures.
Policy makers have recently begun to consider reductions in PBDE exposures in
the US. As of August 2003, only the State of California has taken concrete
steps.
What did they do? Schecter et al. obtained breast milk from volunteers at two
health centers in Texas (Austin and Dallas). Samples were then shipped to two
World Health Organization-certified laboratories in Canada and Germany for
analysis of PBDE levels. In all, measurements of 13 different PBDE congeners
were obtained from 47 individuals, few if any of whom were
exposed occupationally.
What did they find? This first-ever study of PBDE levels in American's breast
milk finds extremely elevated levels of PBDEs compared to European levels.
As seen in the graph to the right, the 10 women (21% of those sampled) had
PBDE concentrations above 100 ppb, with the highest milk level at 419 ppb.
Fifteen women (32% of sample) had levels over 50 ppb.
The scientists found no relationship between PBDE levels and the age of the
woman measured, nor did they observe any racial differences in PBDE
concentrations.
As shown in the graph to the left, the Texas measurements made by Schecter et
al. were dramatically higher than those reported
in recent studies from Europe, and somewhat higher than recent data from
Canada. Levels in Canada appear to have risen over the past decade.
Graphs adapted from Schecter, et al.
What does it mean? This study of 47 Texas women adds to the growing body of
scientific evidence demonstrating high levels of PBDEs in Americans at levels
10 to 100 times that seen in Europe. It is the first study undertaken of PBDEs
in breast milk in the US.
The sources of exposure responsible for these high PBDE body burdens are
uncertain. PBDEs are widely used in a variety of consumer products and can be
found in food, household dust and sewage sludge, among many places. Swedish
levels appear to be declining following implentation of a ban. Coincidentally,
the week that Schecter et al.'s study appeared online (8 August 2003),
California's Governor signed a law banning some PBDEs in California.
The main concern about PBDEs is their ability to disrupt thryoid function, and
thus interfere with proper brain development, at least as indicated by
experiments with laboratory animals and cells in culture. No published
epidemiological studies have examined the impact of PBDEs on people. Yet over
the same time period that PBDE body burdens have been increasing dramatically
Americans, we have also witnessed apparent increases in the frequency of a
number of neurobehavioral abnormalities in people, including autism and
attention deficit hyperactivity disorder. Surely this coincidence warrants
investigation.
Last changed: March 14, 2006