DDT and Breast Cancer in Young Women: Significance of Age at Exposure
DDT and Breast Cancer in Young Women: Significance of Age at Exposure
Background: Previous studies of DDT and breast cancer assessed exposure later in life when the breast may not have been vulnerable, after most DDT had been eliminated, and after DDT had been banned.
Objectives: We investigated whether DDT exposure in young women during the period of peak DDT use predicts breast cancer.
Methods: We conducted a prospective, nested casecontrol study with a median time to diagnosis of 17 years using blood samples obtained from young women during 19591967. Subjects were members of the Child Health and Development Studies, Oakland, California, who provided blood samples 13 days after giving birth (mean age, 26 years). Cases (n = 129) developed breast cancer before the age of 50 years. Controls (n = 129) were matched to cases on birth year. Serum was assayed for p,p´-DDT, the active ingredient of DDT ; o,p´-DDT, a low concentration contaminant ; and p,p´-DDE, the most abundant p,p´-DDT metabolite.
Results: High levels of serum p,p´-DDT predicted a statistically significant 5-fold increased risk of breast cancer among women who were born after 1931. These women were under 14 years of age in 1945, when DDT came into widespread use, and mostly under 20 years as DDT use peaked. Women who were not exposed to p,p´-DDT before 14 years of age showed no association between p,p´-DDT and breast cancer (p = 0.02 for difference by age).
Conclusions: Exposure to p,p´-DDT early in life may increase breast cancer risk. Many U.S. women heavily exposed to DDT in childhood have not yet reached 50 years of age. The public health significance of DDT exposure in early life may be large.
Most previous studies do not support the hypothesis that exposure to DDT is an important risk factor for breast cancer (Lopez-Cervantes et al. 2004). However, previous studies were limited by the inability to measure exposure in young women during periods of the heaviest DDT use. Consequently most of these studies observed very low levels of p,p´-DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] and o,p´-DDT [1,1,1-trichloro-2-(p-chlorophenyl)-2-(o-chloro-phenyl)ethane], the primary constituents of commercial DDT ( Table 1 ). The conclusions of these studies apply to the effects of p,p´-DDE [1,1´-dichloro-2,2´-bis(p-chlorophenyl)ethylene], the primary metabolite of p,p´-DDT (Lopez-Cervantes et al. 2004), which is more persistent in the environment and in biological systems and can therefore be measured years after DDT use had declined (Stehr-Green 1989).
In the present study we investigated whether serum p,p´-DDT and o,p´-DDT are associated with breast cancer, using blood samples obtained before DDT was banned and when use of this pesticide was very high (1960s). The median year of blood sampling in the present study was 1963, not long after the peak use of DDT in the United States in 1959 [U.S. Environmental Protection Agency (EPA) 1975] and near the peak dietary content of DDT estimated around 1965 (Wolff et al. 2005). Exposure declined considerably thereafter, even before the DDT ban in 1972 (Kutz et al. 1991).
This is the first study to measure blood levels in young adulthood (mean age of 26 years). In other studies, blood was collected when women were of middle age or older ( Table 1 ). The present study is also the first study specifically designed, a priori, to consider whether age at exposure may modify DDT effects on breast cancer. Because DDT was first widely introduced in the United States beginning in 1945 (U. S. EPA 1975), a woman's age in 1945 is a proxy for the youngest possible age at exposure to DDT and for her age when DDT use was peaking. A range of ages in 1945 is represented among women in the Child Health and Development Studies (CHDS). Moreover, these women could be observed prospectively. These data permit a unique design that tests the hypothesis that DDT associations with breast cancer are larger for birth cohorts in which women could have been most heavily exposed in early life.
Background: Previous studies of DDT and breast cancer assessed exposure later in life when the breast may not have been vulnerable, after most DDT had been eliminated, and after DDT had been banned.
Objectives: We investigated whether DDT exposure in young women during the period of peak DDT use predicts breast cancer.
Methods: We conducted a prospective, nested casecontrol study with a median time to diagnosis of 17 years using blood samples obtained from young women during 19591967. Subjects were members of the Child Health and Development Studies, Oakland, California, who provided blood samples 13 days after giving birth (mean age, 26 years). Cases (n = 129) developed breast cancer before the age of 50 years. Controls (n = 129) were matched to cases on birth year. Serum was assayed for p,p´-DDT, the active ingredient of DDT ; o,p´-DDT, a low concentration contaminant ; and p,p´-DDE, the most abundant p,p´-DDT metabolite.
Results: High levels of serum p,p´-DDT predicted a statistically significant 5-fold increased risk of breast cancer among women who were born after 1931. These women were under 14 years of age in 1945, when DDT came into widespread use, and mostly under 20 years as DDT use peaked. Women who were not exposed to p,p´-DDT before 14 years of age showed no association between p,p´-DDT and breast cancer (p = 0.02 for difference by age).
Conclusions: Exposure to p,p´-DDT early in life may increase breast cancer risk. Many U.S. women heavily exposed to DDT in childhood have not yet reached 50 years of age. The public health significance of DDT exposure in early life may be large.
Most previous studies do not support the hypothesis that exposure to DDT is an important risk factor for breast cancer (Lopez-Cervantes et al. 2004). However, previous studies were limited by the inability to measure exposure in young women during periods of the heaviest DDT use. Consequently most of these studies observed very low levels of p,p´-DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] and o,p´-DDT [1,1,1-trichloro-2-(p-chlorophenyl)-2-(o-chloro-phenyl)ethane], the primary constituents of commercial DDT ( Table 1 ). The conclusions of these studies apply to the effects of p,p´-DDE [1,1´-dichloro-2,2´-bis(p-chlorophenyl)ethylene], the primary metabolite of p,p´-DDT (Lopez-Cervantes et al. 2004), which is more persistent in the environment and in biological systems and can therefore be measured years after DDT use had declined (Stehr-Green 1989).
In the present study we investigated whether serum p,p´-DDT and o,p´-DDT are associated with breast cancer, using blood samples obtained before DDT was banned and when use of this pesticide was very high (1960s). The median year of blood sampling in the present study was 1963, not long after the peak use of DDT in the United States in 1959 [U.S. Environmental Protection Agency (EPA) 1975] and near the peak dietary content of DDT estimated around 1965 (Wolff et al. 2005). Exposure declined considerably thereafter, even before the DDT ban in 1972 (Kutz et al. 1991).
This is the first study to measure blood levels in young adulthood (mean age of 26 years). In other studies, blood was collected when women were of middle age or older ( Table 1 ). The present study is also the first study specifically designed, a priori, to consider whether age at exposure may modify DDT effects on breast cancer. Because DDT was first widely introduced in the United States beginning in 1945 (U. S. EPA 1975), a woman's age in 1945 is a proxy for the youngest possible age at exposure to DDT and for her age when DDT use was peaking. A range of ages in 1945 is represented among women in the Child Health and Development Studies (CHDS). Moreover, these women could be observed prospectively. These data permit a unique design that tests the hypothesis that DDT associations with breast cancer are larger for birth cohorts in which women could have been most heavily exposed in early life.
