Pesticides exposure a serum organochlorine residuals among testicular cancer patients and heathy controls

Department of Public Health and Infectious Diseases, University of Rome Sapienza, Rome, Italy.
Journal of Environmental Science and Health Part B Pesticides Food Contaminants and Agricultural Wastes (Impact Factor: 1.2). 11/2011; 46(8):780-7. DOI: 10.1080/03601234.2012.597704
Source: PubMed


The incidence of testicular cancer (TC) has been increasing worldwide during the last decades. The reasons of the increase remains unknown, but recent findings suggest that organochlorine pesticides (OPs) could influence the development of TC. A hospital-based case-control study of 50 cases and 48 controls was conducted to determine whether environmental exposure to OPs is associated with the risk of TC, and by measuring serum concentrations of OPs, including p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) isomer and hexachlorobenzene (HCB) in participants. A significant association was observed between TC and household insecticide use (odds ratio [OR] = 3.01, 95 % CI: 1.11-8.14; OR(adjusted) = 3.23, 95 % CI: 1.15-9.11). Crude and adjusted ORs for TC were also significantly associated with higher serum concentrations of total OPs (OR = 3.15, 95 % CI: 1.00-9.91; OR(adjusted) = 3.34, 95 % CI: 1.09-10.17) in cases compared with controls. These findings give additional support to the results of previous research that suggest that some environmental exposures to OPs may be implicated in the pathogenesis of TC.

Download full-text


Available from: Roberta Turci, Aug 03, 2015
  • Source
    • "Eight studies investigated environmental exposure to organochlorines using blood samples [19,27–29,42,44,78,79] or questionnaires [42,44]. The study by McGlynn et al. suggested that p,p’-DDE, oxychlordane, cis-nonachlor, trans-nonachlor and total chlordane serum levels are associated with TGCT risk, especially with seminomas [28]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Testicular germ cell tumours (TGCT) are the most common cancers in men aged between 15 and 44 years and the incidence has increased steeply over the past 30 years. The rapid increase in the incidence, the spatial variation and the evolution of incidence in migrants suggest that environmental risk factors play a role in TGCT aetiology. The purpose of our review is to summarise the current state of knowledge on occupational and environmental factors thought to be associated with TGCT. A systematic literature search of PubMed. All selected articles were quality appraised by two independent researchers using the 'Newcastle-Ottawa Quality Assessment Scale'. After exclusion of duplicate reports, 72 relevant articles were selected; 65 assessed exposure in adulthood, 7 assessed parental exposures and 2 assessed both. Associations with occupation was reported for agricultural workers, construction workers, firemen, policemen, military personnel, as well as workers in paper, plastic or metal industries. Electromagnetic fields, PCBs and pesticides were also suggested. However, results were inconsistent and studies showing positive associations tended to had lower quality ranking using the assessment scale (p=0.02). Current evidence does not allow concluding on existence of any clear association between TGCT and adulthood occupational or environmental exposure. The limitations of the studies may partly explain the inconsistencies observed. The lack of association with adulthood exposure is in line with current hypotheses supporting the prenatal origin of TGCT. Future research should focus on prenatal or early life exposure, as well as combined effect of prenatal and later life exposure. National and international collaborative studies should allow for more adequately powered epidemiological studies. More sophisticated methods for assessing exposure as well as evaluating gene-environment interactions will be necessary to establish clear conclusion.
    PLoS ONE 10/2013; 8(10):e77130. DOI:10.1371/journal.pone.0077130 · 3.23 Impact Factor
  • Source
    • "Moreover, evidences suggest that exposures to pesticides could be risk factor of TC development. Indeed, a recent study reported a significant association between TC development and use of insecticides such as organochlorine pesticides, namely dichlorodiphenyldichloroethylene (p,p′-DDE) isomer and hexachlorobenzene (Giannandrea et al., 2011). "
    [Show abstract] [Hide abstract]
    ABSTRACT: In the last decades, studies in rodents have highlighted links between in utero and/or neonatal exposures to molecules that alter endocrine functions and the development of genital tract abnormalities, such as cryptorchidism, hypospadias, and impaired spermatogenesis. Most of these molecules, called endocrine disrupters exert estrogenic and/or antiandrogenic activities. These data led to the hypothesis of the testicular dysgenesis syndrome which postulates that these disorders are one clinical entity and are linked by epidemiological and pathophysiological relations. Furthermore, infertility has been stated as a risk factor for testicular cancer (TC). The incidence of TC has been increasing over the past decade. Most of testicular germ cell cancers develop through a pre-invasive carcinoma in situ from fetal germ cells (primordial germ cell or gonocyte). During their development, fetal germ cells undergo epigenetic modifications. Interestingly, several lines of evidence have shown that gene regulation through epigenetic mechanisms (DNA and histone modifications) plays an important role in normal development as well as in various diseases, including TC. Here we will review chromatin modifications which can affect testicular physiology leading to the development of TC; and highlight potential molecular pathways involved in these alterations in the context of environmental exposures.
    Frontiers in Endocrinology 11/2012; 3:150. DOI:10.3389/fendo.2012.00150
  • Source
    • "Evidence of incidence peak of TC among young adults suggests that causal factors operate very early in life (Bray et al., 2006). One theory attributes it to the increase in endogenous estrogen levels during prenatal life and/or later exposures to various occupational and environmental estrogenic chemicals, termed endocrine-disrupting chemicals (EDCs) (Toppari et al., 1996; Sharpe, 2003; Cook et al., 2011; Giannandrea et al., 2011). "
    [Show abstract] [Hide abstract]
    ABSTRACT: The etiology of testicular germ cell tumors (TGCTs) is poorly understood. Recent epidemiological findings suggest that, TGCT risk is determined very early in life, although the available data are still conflicting. The rapid growth of the testes during puberty may be another period of vulnerability. Body size has received increasing attention as possible risk factor for TC. To clarify the relation of body size and its anthropometric variables to TGCT risk, the authors analyzed data from 272 cases and 382 controls with regard to height (cm), weight (Kg), and body mass index (BMI; kg/m(2)). Overall, participants in the highest quartile of height were more likely to be diagnosed with TGCTs than participants in the lowest quartile of height, OR 2.22 (95% confidence intervals (CI): 1.25-3.93; adjusted; p(trend) = 0.033). Moreover, histological seminoma subgroup was significantly associated with tallness, very tall men (>182 cm) having a seminoma TGCT risk of OR = 2.44 (95% confidence intervals (CI): 1.19-4.97; adjusted; p(trend) = 0.011). There was also a significant inverse association of TGCT with increasing BMI (p(trend) = 0.001; age-adjusted analysis) and this association was equally present in both histological subgroups. These preliminary results indicate that testicular cancer (TC) is inversely associated with BMI and positively associated with height, in particular with seminoma subtype. Several studies have reported similar findings on body size. As adult height is largely determined by high-calorie intake in childhood and influenced by hormonal factors at puberty, increased attention to postnatal exposures in this interval may help elucidate the etiology of TGCTs.
    Frontiers in Endocrinology 11/2012; 3:144. DOI:10.3389/fendo.2012.00144
Show more