Our Stolen Futurea book by Theo Colborn, Dianne Dumanoski, and John Peterson Myers
 
 

 

  Bell, EM, I Hertz-Picciotto and JJ Beaumont. 2001. A case-control study of pesticides and fetal death due to congenital anomalies. Epidemiology 12:148-156.
 
 

This study reports a strong association between exposure to commercially applied agricultural pesticides during a crucial period in fetal development and the likelihood of fetal death due to congenital defects. Associations were found for mothers living within a 9-square mile area around the home. That is, fetal death is more likely among mothers who are living within a 9-square mile area in which commercial pesticide spraying takes place during pregnancy.

What did they do? Bell et al.carried out a case-control study of the risk of fetal death in relation to pesticide exposure. Their work built upon two independent data sets:

  • birth/fetal death/death certificates obtained from the California State Vital Statistics Registry, including mother's address, cause of death, data on the pregnancy and the parents, etc.; and
  • the California State Pesticide Use Report (183-1984), which includes information on the application of all restricted-use agricultural pesticides, including specific chemicals used, amount applied, date and location for each application. Bell et al. broke the pesticides examined in their study into five categories: phosphates, carbamates, pyrethroids, halogenated hydrocarbons, and endocrine disruptors. Increases in risk were observed for all 5 categories.

Because both data sets included information on place and time, Bell et al. break new ground in their work in several important ways.

  • First, their measurement of exposure, while imperfect (see below), does not depend upon memories of the mothers and comes from a source independent of the assessment of the birth outcome, a governmental database of pesticide applications. Most epidemiological studies depend upon recall. This makes them vulnerable to vagaries of memory and it also means the asessment of exposure and outcome are not truly independent. Bell et al. have avoided this problem.
  • Second, they use a more refined approach to the timing of exposure and vulnerability, focusing their attention on the period of fetal development during which many of the most basic aspects of fetal differention are taking place, weeks 3-8 (the period of "organogenisis"). Toxicological studies have clearly established that the timing of exposure during fetal development is crucial to determining the outcome. But the data are usually not available in sufficient detail to allow the most vulnerable period in human development, weeks 3-8, to be examined separately. Studies are at best usually able to study the effects of during different trimesters, and often cannot consider timing at all, other than simply that exposure took place sometime during pregnancy. This refinement by Bell et al. is very important because it decreases the chance that irrelevant or less relevant exposures (outside the period of maximum vulnerability) will dilute their ability to detect real effects. They demonstrate the value of this approach by showing that the calculated risk increases as they focus their analysis: risk of fetal death is greater for exposures in week 3-8 compared to week 1-20.

To calculate the effect of exposure on risk, Bell et al. compared the cases of fetal and neonatal deaths due to congenital defects that they found in the health records with controls selected randomly from normal live births in the same California counties in which the deaths occurred. The bottom line of their analysis is that if pesticide exposure has no impact on risk, then the mothers whose pregnancies resulted in fetal death should not be any more likely to have been exposed to pesticides during pregnancy than mothers whose babies were born normally. As noted above, for each of the categories of pesticide studied, they found that exposure increased the risk of fetal death.

The use of the California state Pesticide Use Report in this study is an important breakthrough, but it has significant limitations. It is good because, as noted above, it provides an assessment of the likelihood of exposure that is independent of the mother's recall and is specific to a time and place. The weakness is that it is only a surrogate index of exposure. Clearly, if no pesticide use took place within the mother's geographic area, then no exposure to these agricultural chemicals should have been possible. But the fact that pesticides were applied does not mean that exposure to that mother actually took place. This limitation is likely to have weakened Bell et al.'s ability to detect real effects.

 

 

 

 

 

 

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