Garcia AM, Benavides FG, Fletcher T, Orts E. Paternal exposure to pesticides and congenital malformations Scand J Work Environ Health 1998;24(6):473-480.Objectives A case-referent study with 261 matched pairs was carried out in 8 hospitals of Comunidad Valenciana, Spain, to assess the relation between occupatioilal cxposure to pesticides and selccted congenital malfor~nations. In this paper, the rcsults concerning patcnlal exposure are presented.
MethodsThe parents of the case patients and the referents were interviewed to collect inforination about exposure to pesticides and potential confounding variables. Detailed information on direct involve~nent in the handling of pesticides was collected for the interviewees involved in agricultural activities during a previously defined period in relation to conception and pregnancy. Exposure data were reviewed by 2 experts who assigned ordinal scores for the probability and intensity of exposure to pesticide classes and active ingredients.
ResultsThe dichotoinous analysis of exposure (absent, present) yiclded some increased risks, although not statistically significant, for aliphatic hydrocarbons [adjusted odds ratio (adjusted OR) 2.05, 95% confidence interval (95% CI) 0.62-6.801, inorganic compounds (adjusted OR 2.02, 95% CI 0.53-7.72), and glufosinate (adjusted OR 2.45, 95% CI 0.78-7.70), and a significant association for pyridil derivatives (adjusted OR 2.77, 95% CI 1.19-6.44). The analysis bascd on the experts' scores (2 levels of exposure) showed some consistent associations for these compounds.C O~~~U S~O~S This research indicates a possible risk of congenital malformations for paternal exposure to some pesticides, notably, pyridils, aliphatic hydrocarbons, inorganic compounds, and glufosinate. It did not find an increased risk for paternal exposure to pesticides in the classes of organophosphates, carbamates, organochlorines, chloroalkylthio fungicides and organosulfurs. These findings warrant further investigation.
Background:Colorectal cancer (CRC) is the second cause of cancer-related death in the Western world. Much of the CRC genetic risk remains unidentified and may be attributable to a large number of common, low-penetrance genetic variants. Genetic linkage studies in CRC families have reported additional association with regions 9q22–31, 3q21–24, 7q31, 11q, 14q and 22q. There are several plausible candidate genes for CRC susceptibility within the aforementioned linkage regions including PTCH1, XPA and TGFBR1 in 9q22–31, and EPHB1 and MRAS in 3q21–q24.Methods:CRC cases and matched controls were from EPICOLON, a prospective, multicentre, nationwide Spanish initiative, composed of two independent phases. Phase 1 corresponded to 515 CRC cases and 515 controls, whereas phase 2 consisted of 901 CRC cases and 909 controls. Genotyping was performed for 172 single-nucleotide polymorphisms (SNPs) in 84 genes located within regions 9q22–31 and 3q21–q24.Results:None of the 172 SNPs analysed in our study could be formally associated with CRC risk. However, rs1444601 (TOPBP1) and rs13088006 (CDV3) in region 3q22 showed interesting results and may have an effect on CRC risk.Conclusions:TOPBP1 and CDV3 genetic variants on region 3q22 may modulate CRC risk. Further validation and meta-analysis should be undertaken in larger CRC cohorts.
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