Authors
Chen, A. and Rogan, W.J.

Title
Nonmalarial infant deaths and DDT use for malaria control.

Journal
Emerging Infectious Diseases. 9(8):960-964. 2003.

Summary
DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane) has been classified as a Persistent Organic Pollutant (POPs) of "historical concern" by the United Nations Environment Programme (UNEP). The production and use of DDT has been banned in most countries around the world due to the potential damage it exerts on wildlife and human health. However, due to the malaria endemic in some parts of the world, the use of DDT as an insecticide is still permitted for "disease vector control" with the permission of the United Nations. The campaign against DDT and other synthetic chemicals is the result of laboratory and epidemiological experiments reporting associations between DDT exposure and human toxicity. Some evidence suggests that DDT may increase the rate of infant mortality by increasing the risk of preterm birth and by decreasing the duration of lactation after birth. The study by Chen and Rogan sought to determine whether the increase in infant deaths caused by DDT exposure is comparable to the decrease in infant deaths resulting from reduced malaria cases following prophylactic DDT spraying.

The investigators combined published data from North American studies on preterm delivery or duration of lactation and DDE exposure with African data on DDT spraying and the effect of preterm birth or lactation duration on infant deaths to estimate infant mortality rates (IMR). Specifically, Chen and Rogan wanted to compare malaria-specific IMR with DDT-induced IMR. The increase in infant mortality due to maternal DDT exposure was calculated based on the following findings from the scientific literature: (I) The National Institute of Environmental Health Sciences and the US Centers for Disease Control reported an increase in the rate of preterm birth with increasing levels of DDE in maternal serum; (ii) Two birth cohort studies reported a negative relationship between lactation duration and DDE levels. Specifically, mothers with higher concentrations of serum DDE breastfed their infants 40%-50% less than those mothers with low or undetectable levels of DDE. African data was then used to correlate the IMR with preterm birth (RR=2.0; preterm births accounted for 17% infant deaths in sub-Saharan Africa) and WHO-Africa data was used to correlate the IMR with shortened lactation duration (Senegal, estimated that DDT-induced shorted lactation from 19 months to 11 months would result in RR=2.0). The North American data was used to further estimate the proportion of preterm births due to DDT exposure. Using the assumption that DDT spraying increased the preterm delivery rate from approximately 15% in Africa before DDT spraying to 25% after spraying (RR=1.7 for preterm birth, RR=2.0 preterm birth leading to infant death), DDT-induced preterm births increase the IMR by 9%.

Using these estimates and reported IMRs for sub-Saharan African countries, Chen and Rogan then compared malaria-induced IMR with DDT-induced IMR. DDT was estimated to increased IMR because of preterm births (9%) and due to increased infectious diseases acquired because of shortened lactation (20%) with approximately 20.5/1000 infant deaths. Maternal malaria causes 3-8% infant deaths and 20% deaths in children less than 5 years of age (175/1000), with malaria-specific deaths representing 30% of infant deaths (52.5/1000). Thus, infant mortality rates due to DDT-related complications (preterm births, and shortened lactation) are comparable to IMRs due to malaria.

These findings lead to some very important questions regarding the use of prophylactic DDT use to control malaria in Africa, given that DDT exposure itself is a risk for infant death. Several factors must be considered in evaluating these findings. First, Chen and Rogan employed conservative assumptions by only using data pertaining to preterm births and duration of lactation. Thus, the adverse side effects of DDT spraying could be even more substantial. Second, the data used to show that DDE exposure shortened lactation duration were not obtained from Africa, nor have studies from Africa demonstrated such a link. Rather, North American and Mexican studies were used to correlate the risk of DDE exposure with lactation duration. DDE exposure reducing lactation duration is biologically plausible as DDE, a weak estrogen, may inhibit the stimulatory effect of prolactin on milk synthesis. Similarly, no studies from Africa show relationships between DDE exposure and preterm births. Finally, the impact of HIV transmission through breast-feeding as opposed to bottle feeding has not been fully accounted for in this analysis.

Chen and Rogan conclude that the increase in infant mortality due to DDT exposure is less than, but comparable to, the magnitude of infant deaths caused by malaria. In particular, they state that "the side effects of DDT spraying might reduce or abolish its benefits from the control of malaria in infants". Their analysis raises concerns about the use of DDT for controlling malaria for infants. It is important to note, however, that the benefits of DDT use to reduce malaria-induced mortality rates in children and adults should be taken into consideration. Mortality rates in children and adults were not taken into account in this study. Similarly, additional adverse effects due to DDT exposure in infants, children or adults may also become apparent in future studies with broader scopes of investigation. Therefore, the development and employment of affordable alternative methods for malaria prevention may become necessary as we learn more about the health risks due to DDT exposure.