Endocrine disrupting chemicals are believed to play a role in the development of the testicular dysgenesis syndrome. Many pesticides are known to have endocrine disrupting abilities. In a previous study, sons of women who were occupationally exposed to non-persistent pesticides in early pregnancy showed signs of impaired reproductive function (reduced genital size and altered serum hormone concentrations) at three months of age. To assess the possible long-term effects of prenatal pesticide exposure, the boys were re-examined at 6–11 years. The 94 boys (59 exposed, 35 unexposed) underwent genital examinations including ultrasound of testicular volumes, puberty staging (Tanner), anthropometry, and blood sampling. Only a few of the boys had reached puberty (n = 3). Among prepubescent boys, testicular volume and penile length (age- and weight-adjusted) were reduced if mothers were exposed to pesticides. The effects were associated with the maternal exposure levels, so that high-exposed boys had smaller genitals than medium-exposed boys, who had smaller genitals than those who were unexposed. Boys of mothers in the high exposure group (n = 23) had 24.7% smaller testes (95% CI: −62.2; −10.1) and 9.4% shorter penile length (95% CI: −16.8; −1.1) compared with the unexposed. The testicular volume and penile length at school age could be tracked to measures from the same boys made at 3 months, e.g. those that had small testes at school age also had small testes at 3 months. Pituitary and testicular hormone serum concentrations did not differ between exposed and unexposed boys. Eight prenatally exposed boys had genital malformations (no unexposed). These boys had smaller testis, shorter penile length and lower inhibin B concentrations than prepubertal boys without genital malformations. The findings support the results obtained at three months of age and indicate that prenatal pesticide exposure has long-term effects on reproductive function in boys.