Interactive Effects of TCDD andp,p′-DDE on Male Reproductive Tract Development inin Uteroand Lactationally Exposed Rats

Prostate cancer in US Air Force veterans of the Vietnam war

“…Our findings clearly highlight the need for a more comprehensive exposure assessment of this cohort, especially due to the availability of frozen specimens for most of these veterans. These could be used for the chemical analysis of an expanded battery of organochlorine compounds including those suspected to be associated with prostate cancer development in animal studies (Faqi et al, 1998;Loeffler and Peterson, 1999;Tessier and Matsumura, 2001). …”

“…Prenatal or postnatal exposures may cause reductions in the weight of the ventral, dorsolateral, and anterior prostate lobes, plasma testosterone concentrations, decreases in epididymal sperm reserves (Roman et al, 1995;Abbott et al, 2003;Simanainen et al, 2004), and inhibit prostatic epithelial bud formation (Abbott et al, 2003;Ko et al, 2004;Lin et al, 2004). Interactive effects of TCDD and DDE on male reproductive tract development were also observed in rats suggesting that exposure to both these chemicals may potentiate their individual actions although by different mechanism since DDE is not an Ah-receptor agonist (Loeffler and Peterson, 1999). Other studies suggest that TCDD exposure impairs prostate growth and androgen responsiveness by inhibiting prostatic epithelial cell differentiation and morphogenesis (Theobald et al, 2000;Ko et al, 2002;Timms et al, 2002).…”

Developmental variations in environmental influences including endocrine disruptors on pubertal timing and neuroendocrine control: Revision of human observations and mechanistic insight from rodents

“…Although both fetal and early postnatal periods of exposure fall into the so-called "programming window", there may be differences in sensitivity to endocrine disruption even within this particular period. The dose of EDC plays a critical role since, when investigated at a given period of life, higher doses appear to be more effective such as shown after prenatal exposure for DDE (Loeffler and Peterson, 1999) and phthalates (Saillenfait et al, 2008;Salazar et al, 2004), or after lactational exposure for DDE, vinclozolin or DES (Yoshimura et al, 2005) or following exposure after weaning for DDE (Ashby and Lefevre, 2000;Yoshimura et al, 2005), vinclozolin (Yoshimura et al, 2005;Monosson et al, 1999), DES (Yoshimura et al, 2005;Shin et al, 2009), phthalates (Ge et al, 2007;Noriega et al, 2009) and PBDE (Stoker et al, 2004). It is noteworthy that in two studies using phthalates, opposing effects are observed since lower doses are associated with early puberty and higher doses with delayed puberty (Ge et al, 2007;Saillenfait et al, 2008).…”

Prenatal DDT Exposure in Relation to Anthropometric and Pubertal Measures in Adolescent Males

“…There are reports of neurotoxic and immunotoxic effects in young children (Dewailly et al 2000; Ribas-Fitó et al 2003), although not all studies show such effects (Gladen et al 1988; Rogan et al 1987). At even later ages, prenatal and lactational exposure to p,p ′-DDE in animals has been associated with delayed male puberty in some but not all studies (Loeffler and Peterson 1999; You et al 1998). …”