Reproductive Effects of Occupational DDT Exposure Among Male
To assess potential effects of human DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] exposure, we evaluated the reproductive history of 2,033 workers in the antimalaria campaign of Mexico. Data on occupational exposure to DDT and reproductive outcomes were gathered through a questionnaire, and workers provided information about 9,187 pregnancies. We estimated paternal exposure to DDT before each pregnancy using three approaches: a) a dichotomous indicator for pregnancies before and after exposure began, b) a qualitative index of four exposure categories, and c) an estimation of the DDT metabolite DDE [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene] accumulated in fat. To assess associations, we used logistic regression models that accounted for correlated observations and adjusted for parents' age at each child's birth, exposure to other pesticides, exposure to chemical substances in other employment, smoking, and alcohol consumption. The odds ratio for birth defects comparing pregnancies after and before the first exposure was 3.77 [95% confidence interval (95% CI), 1.19-9.52]. Compared with the lowest quartile of estimated DDE in fat, the ORs were 2.48 (95% CI, 0.75-8.11), 4.15 (95% CI, 1.38-12.46), and 3.76 (95% CI, 1.23-11.44) for quartiles 2, 3, and 4, equivalent to p,p´-DDE in fat of 50, 82, and 298 µg/g fat, respectively. No significant association was found for spontaneous abortion or sex ratio. We found an increased risk of birth defects associated with high occupational exposure to DDT in this group of workers. The significance of this association at lower exposure levels found in the general population remains uncertain.
DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane or dichlorodiphenyltrichloroethane was widely used to control malaria during the last half of the 20th century in many countries in the world. Most developed countries banned its use in the 1970s and 1980s because of its long persistence in the environment, unusual bioaccumulation, effects on wildlife, and the possibility of long-term adverse effects on human health [Turusov et al. 2002; U.S. Environmental Protection Agency (EPA) 1997; van Wendel de Joode et al. 2001]. In other countries, where malaria is a long-standing public health problem, however, DDT is still the main pesticide used for mosquito control. Mexico used DDT in malaria campaigns until 1999, not only because of its effectiveness but also because of its low cost and lack of acute toxicity to sprayers and exposed populations compared with alternative chemical pesticides.
Although the ban on DDT use provoked a serious debate (Schofield 2001; Walker 2000), the Mexican program has recently shown that malaria can be effectively controlled without the use of DDT. The operation of a comprehensive malaria control program has reduced the incidence of this disease substantially while gradually decreasing the reliance on DDT (Chanon et al. 2003). Although epidemiologic studies have yet to determine conclusively that DDT contributes to human disease, recent evidence emphasizes the need for further research aimed at assessing the risks of reproductive health impairment and cancer development related to DDT exposure (Cocco et al. 1997; Longnecker et al. 2001).
Mexican vector control workers were subjected to high levels of DDT exposure as detected in adipose tissue over the extended time period when they worked applying the pesticide during the antimalaria campaign (Rivero-Rodriguez et al. 1997). However, the overall impact on the health of exposed workers has not been quantified. This report is part of an extensive evaluation that Mexico is performing in support of the merits of banning DDT use.
Previous studies of potential reproductive effects of DDT in human populations have focused on maternal exposure (Cohn et al. 2003; Korrick et al. 2001; Longnecker et al. 2002), based on the antiandrogenic and estrogenic properties of the DDT metabolite p,p´-DDE (1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene) (Kelce et al. 1995). Studies of men have measured hormones and semen parameters (Hauser et al. 2003; Martin et al. 2002), but there are no reports on paternal exposure to DDT and reproductive outcomes such as congenital malformations, spontaneous abortion, and alteration of the sex ratio, which are indicators of teratogenicity, embryotoxicity, and endocrine disruption, respectively.
To assess potential effects of human DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] exposure, we evaluated the reproductive history of 2,033 workers in the antimalaria campaign of Mexico. Data on occupational exposure to DDT and reproductive outcomes were gathered through a questionnaire, and workers provided information about 9,187 pregnancies. We estimated paternal exposure to DDT before each pregnancy using three approaches: a) a dichotomous indicator for pregnancies before and after exposure began, b) a qualitative index of four exposure categories, and c) an estimation of the DDT metabolite DDE [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene] accumulated in fat. To assess associations, we used logistic regression models that accounted for correlated observations and adjusted for parents' age at each child's birth, exposure to other pesticides, exposure to chemical substances in other employment, smoking, and alcohol consumption. The odds ratio for birth defects comparing pregnancies after and before the first exposure was 3.77 [95% confidence interval (95% CI), 1.19-9.52]. Compared with the lowest quartile of estimated DDE in fat, the ORs were 2.48 (95% CI, 0.75-8.11), 4.15 (95% CI, 1.38-12.46), and 3.76 (95% CI, 1.23-11.44) for quartiles 2, 3, and 4, equivalent to p,p´-DDE in fat of 50, 82, and 298 µg/g fat, respectively. No significant association was found for spontaneous abortion or sex ratio. We found an increased risk of birth defects associated with high occupational exposure to DDT in this group of workers. The significance of this association at lower exposure levels found in the general population remains uncertain.
DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane or dichlorodiphenyltrichloroethane was widely used to control malaria during the last half of the 20th century in many countries in the world. Most developed countries banned its use in the 1970s and 1980s because of its long persistence in the environment, unusual bioaccumulation, effects on wildlife, and the possibility of long-term adverse effects on human health [Turusov et al. 2002; U.S. Environmental Protection Agency (EPA) 1997; van Wendel de Joode et al. 2001]. In other countries, where malaria is a long-standing public health problem, however, DDT is still the main pesticide used for mosquito control. Mexico used DDT in malaria campaigns until 1999, not only because of its effectiveness but also because of its low cost and lack of acute toxicity to sprayers and exposed populations compared with alternative chemical pesticides.
Although the ban on DDT use provoked a serious debate (Schofield 2001; Walker 2000), the Mexican program has recently shown that malaria can be effectively controlled without the use of DDT. The operation of a comprehensive malaria control program has reduced the incidence of this disease substantially while gradually decreasing the reliance on DDT (Chanon et al. 2003). Although epidemiologic studies have yet to determine conclusively that DDT contributes to human disease, recent evidence emphasizes the need for further research aimed at assessing the risks of reproductive health impairment and cancer development related to DDT exposure (Cocco et al. 1997; Longnecker et al. 2001).
Mexican vector control workers were subjected to high levels of DDT exposure as detected in adipose tissue over the extended time period when they worked applying the pesticide during the antimalaria campaign (Rivero-Rodriguez et al. 1997). However, the overall impact on the health of exposed workers has not been quantified. This report is part of an extensive evaluation that Mexico is performing in support of the merits of banning DDT use.
Previous studies of potential reproductive effects of DDT in human populations have focused on maternal exposure (Cohn et al. 2003; Korrick et al. 2001; Longnecker et al. 2002), based on the antiandrogenic and estrogenic properties of the DDT metabolite p,p´-DDE (1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene) (Kelce et al. 1995). Studies of men have measured hormones and semen parameters (Hauser et al. 2003; Martin et al. 2002), but there are no reports on paternal exposure to DDT and reproductive outcomes such as congenital malformations, spontaneous abortion, and alteration of the sex ratio, which are indicators of teratogenicity, embryotoxicity, and endocrine disruption, respectively.
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