The authors reply:
Acquavella and Burns raise two issues regarding exposure assessment in studies of residential proximity to agricultural pesticide applications and birth outcomes: the magnitude of drift from pesticide applications to residential areas, and whether a biologically-active dose level would harm vegetation and insect populations. Several studies have shown that, when compared to the general population, individuals living near agricultural crops have an increased exposure to agricultural pesticides due to drift at the time of application. 1–3 These studies have measured detectable levels of pesticides in house dust from homes located within mile of agricultural crops. However, detection decreased as the distance between the homes and crops increased.
In our study, we assigned proximity to exposure by using the “TRS” (township, range, and section) from the USGS (US Geological Survey) to define a fixed unit of one square mile. 4 If a woman’s residence was near the edge of the TRS in which she lived, and an application occurred near her home but in the adjacent TRS, then our narrow definition of exposure would classify her as “unexposed.” Therefore, we used the broad definition, which included her TRS of residence and the eight surrounding TRSs, in order to increase the sensitivity of the exposure categorization. By using this definition, we could have misclassified some individuals outside the range of drift as exposed. However, given that nondifferential exposure misclassification tends to bias estimates toward the null, it is unlikely that the observed increase in risk was due to exposure misclassification. At the time of our study, we were limited to a resolution of 1 square mile. Recently, geographic-based exposure metrics have been developed that can be linked to the California pesticide use database in order to more precisely estimate the proximity of agricultural pesticide applications to residences. 5 These new methods could serve as valuable exposure assessment tools in future studies.
The authors also suggest that the validity of our exposure model is dependent upon having an environmentally relevant dose (ie, the insect population and vegetation between the application and residence would be noticeably damaged). Given that the agricultural pesticides are applied to crops in order to control for insects or weeds, we can assume that this criterion would be met for mothers living in very close proximity to agricultural crops. However, this criterion assumes that the biologically and environmentally relevant doses are equal. Several studies have shown that the risk of adverse birth outcomes (birth defects in particular) is a factor of both dose and fetal age at the time of exposure. 6–8 Thus, we cannot rule out the possibility that the environmentally safe dose is greater than the biologically relevant dose for a fetus, particularly when the exposure occurs during a vulnerable period of fetal development.
We agree with Acquavella and Burns that studies of residential proximity to agricultural pesticide applications would benefit from an improved measure of exposure. Nevertheless, our study represented a significant improvement in the exposure assessment over the majority of studies evaluating reproductive health effects of pesticides. Geographic proximity was not subject to recall bias, and gestational age at the time of exposure was known. As discussed above, methods that incorporate geographic mapping techniques in conjunction with pesticide application data have been developed that could improve the specificity of exposure classification. Finally, biomonitoring studies that characterize pesticide exposure due to drift, controlling for variability in wind and weather conditions, would lead to better understanding of environmental exposure to agricultural pesticides.
Erin M. Bell
James J. Beaumont
1. Fenske RA, Lu C, Simcox NJ, et al. Strategies for assessing children’s organophosphorus pesticide exposures in agricultural communities. J Exposure Anal Environ Epidemiol 2000; 10: 662–671.
2. Loewenhertz C, Fenske RA, Simcox NJ, Bellamy G, Kalman D. Biological monitoring of organophosphorous pesticide exposure among children of agricultural workers in central Washington State. Environ Health Perspect 1997; 105 (12): 1344–1353.
3. Simcox NJ, Fenske RA, Wolz S, Lee I, Kalman DA. Pesticides in household dust and soil: exposure pathways for children of agricultural families. Environ Health Perspect 1995; 03: 126–1134.
4. Bell EM, Hertz-Picciotto I, Beaumont JJ. A case-control study of pesticides and fetal death due to congenital anomalies. Epidemiology 2001; 12: 148–156.
5. Nuckols JR, Miller R, Weigel S, Gunier R, Hearst A, Reynolds P. Agricultural chemical exposures and childhood cancers. Progress Report. NCI-RO3 CA83071. National Cancer Institute, July 2000.
6. Klassen C. Cassarett and Doull’s Toxicology: The Basic Science of Poisons. New York: McGraw-Hill, Inc, 1996.
7. Kurzel RB, Cetrulo CL. Chemical teratogenesis and reproductive failure. Obstet Gynecol Surv 1985; 40: 397–424.
8. Sadler TW. Langman’s Medical Embryology. Baltimore: Williams & Wilkins, 1995.