Maternal Pregnancy Levels of
            <i>trans</i>
            -Nonachlor and Oxychlordane and Prevalence of Cryptorchidism and Hypospadias in Boys

Trabert, Britton; Longnecker, Matthew P.; Brock, John W.; Klebanoff, Mark A.; McGlynn, Katherine A.

doi:10.1289/ehp.1103936

Cited by 36 publications

(19 citation statements)

References 24 publications

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“…The general lack of association agrees with recent studies indicating that hypospadias is not associated with maternal occupations that involve pesticide exposure [13][14][15] or serum levels of the persistent pesticides chlordane 21 and DDE. [16][17][18][19][20] We are aware of 1 other study that examined residential proximity to agriculture-related pesticide applications.…”

Section: Discussionsupporting

confidence: 89%

“…12 Three subsequent large maternal occupation-based studies have not suggested elevated risk. [13][14][15] Studies examining maternal serum levels of persistent pesticides DDE [16][17][18][19][20] and chlordane 21 and 1 study that estimated exposure based on residential proximity to certain crops 22 also do not provide evidence for association. These studies are limited by relatively crude measures of exposure, small sample sizes, or investigation of a limited set of specific compounds.…”

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confidence: 99%

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Hypospadias and Residential Proximity to Pesticide Applications

2013

PEDIATRICS

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WHAT'S KNOWN ON THIS SUBJECT: Some studies suggest a contribution of environmental exposures such as pesticides to risk of hypospadias, whereas others do not. One of the challenges that has limited current knowledge is the lack of detailed exposure data. WHAT THIS STUDY ADDS:This study examined a more detailed assessment of exposure to pesticides than previous studies. Exposure assignments, whether to groups of chemicals, specific chemicals, or a composite involving a number of chemicals, showed a general lack of association with hypospadias. abstract BACKGROUND: Experimental evidence suggests pesticides may be associated with hypospadias.OBJECTIVE: Examine the association of hypospadias with residential proximity to commercial agricultural pesticide applications. METHODS:The study population included male infants born from 1991 to 2004 to mothers residing in 8 California counties. Cases (n = 690) were ascertained by the California Birth Defects Monitoring Program; controls were selected randomly from the birth population (n = 2195). We determined early pregnancy exposure to pesticide applications within a 500-m radius of mother' s residential address, using detailed data on applications and land use. Associations with exposures to physicochemical groups of pesticides and specific chemicals were assessed using logistic regression adjusted for maternal race or ethnicity and age and infant birth year.RESULTS: Forty-one percent of cases and controls were classified as exposed to 57 chemical groups and 292 chemicals. Despite .500 statistical comparisons, there were few elevated odds ratios with confidence intervals that excluded 1 for chemical groups or specific chemicals. Those that did were for monochlorophenoxy acid or ester herbicides; the insecticides aldicarb, dimethoate, phorate, and petroleum oils; and adjuvant polyoxyethylene sorbitol among all cases; 2,6-dinitroaniline herbicides, the herbicide oxyfluorfen, and the fungicide copper sulfate among mild cases; and chloroacetanilide herbicides, polyalkyloxy compounds used as adjuvants, the insecticides aldicarb and acephate, and the adjuvant nonyl-phenoxy-poly(ethylene oxy)ethanol among moderate and severe cases. Odds ratios ranged from 1.9 to 2.9.CONCLUSIONS: Most pesticides were not associated with elevated hypospadias risk. For the few that were associated, results should be interpreted with caution until replicated in other study populations.

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Section: Discussionsupporting

confidence: 89%

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confidence: 99%

Hypospadias and Residential Proximity to Pesticide Applications

2013

PEDIATRICS

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“…(2007)USA (12 centers)Collaborative Perinatal Project219/564Third trimester serum75–90 percentile versus 0–10 percentileb-HCCH2.081.08–4.0190HCE0.820.41–1.65HCB0.850.52–1.40McGlynn et al . (2009a)USA (12 centers)Collaborative Perinatal Project230/593Third trimester serumHighest quartile versus lowestPCB (sum of 11 congeners)1.410.90–2.2080Trabert et al . (2012)USA (12 centers)Collaborative Perinatal Project217/557Third trimester serumHighest quartile versus lowest trans -nonachlor1.220.70–2.1290Oxychlordane0.950.55–1.64Bhatia et al .…”

Section: Methodsmentioning

confidence: 99%

The epidemiologic evidence linking prenatal and postnatal exposure to endocrine disrupting chemicals with male reproductive disorders: a systematic review and meta-analysis

Bonde

Flachs

Rimborg

et al. 2016

Hum. Reprod. Update

253

128

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BACKGROUNDMore than 20 years ago, it was hypothesized that exposure to prenatal and early postnatal environmental xenobiotics with the potential to disrupt endogenous hormone signaling might be on the causal path to cryptorchidism, hypospadias, low sperm count and testicular cancer. Several consensus statements and narrative reviews in recent years have divided the scientific community and have elicited a call for systematic transparent reviews. We aimed to fill this gap in knowledge in the field of male reproductive disorders.OBJECTIVE AND RATIONALEThe aim of this study was to systematically synthesize published data on the risk of cryptorchidism, hypospadias, low sperm counts and testicular cancer following in utero or infant exposure to chemicals that have been included on the European Commission's list of Category 1 endocrine disrupting chemicals defined as having documented adverse effects due to endocrine disruption in at least one intact organism.SEARCH METHODSA systematic literature search for original peer reviewed papers was performed in the databases PubMed and Embase to identify epidemiological studies reporting associations between the outcomes of interest and exposures documented by biochemical analyses of biospecimens including maternal blood or urine, placenta or fat tissue as well as amnion fluid, cord blood or breast milk; this was followed by meta-analysis of quantitative data.OUTCOMESThe literature search resulted in 1314 references among which we identified 33 papers(28 study populations) fulfilling the eligibility criteria. These provided 85 risk estimates of links between persistent organic pollutants and rapidly metabolized compounds (phthalates and Bisphenol A) and male reproductive disorders. The overall odds ratio (OR) across all exposures and outcomes was 1.11 (95% CI 0.91–1.35). When assessing four specific chemical subgroups with sufficient data for meta-analysis for all outcomes, we found that exposure to one of the four compounds, p,p′-DDE, was related to an elevated risk: OR 1.35 (95% CI 1.04–1.74). The data did not indicate that this increased risk was driven by any specific disorder.WIDER IMPLICATIONSThe current epidemiological evidence is compatible with a small increased risk of male reproductive disorders following prenatal and postnatal exposure to some persistent environmental chemicals classified as endocrine disruptors but the evidence is limited. Future epidemiological studies may change the weight of the evidence in either direction. No evidence of distortion due to publication bias was found, but exposure–response relationships are not evident. There are insufficient data on rapidly metabolized endocrine disruptors and on specific exposure–outcome relations. A particular data gap is evident with respect to delayed effects on semen quality and testicular cancer. Although high quality epidemiological studies are still sparse, future systematic and transparent reviews may provide pieces of evidence contributing to the narrative and weight of the evidence assessments in th...

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“…Studies assessing individual-level exposure using pesticide bio-markers (Bhatia et al, 2005; Brucker-Davis et al, 2008; Carmichael et al, 2010; Chevrier et al, 2011; Damgaard et al, 2006; Fernandez et al, 2007; Giordano et al, 2010; Longnecker et al, 2002; Michalakis et al, 2014; Pierik et al, 2007; Trabert et al, 2012) yielded conflicting results (Table 6). Most of them failed to detect an association (Bhatia et al., 2005; Brucker-Davis et al, 2008; Carmichael et al, 2010; Chevrier et al, 2011; Longnecker et al, 2002; Pierik et al, 2007; Toft et al, 2016; Trabert et al, 2012) while some of them directly linked UGAs risk with DDE and/or DDT (Bhatia et al, 2005; Brucker-Davis et al, 2008; Longnecker et al, 2002).…”

Section: Urogenital Abnormalitiesmentioning

confidence: 99%

“…Most of them failed to detect an association (Bhatia et al., 2005; Brucker-Davis et al, 2008; Carmichael et al, 2010; Chevrier et al, 2011; Longnecker et al, 2002; Pierik et al, 2007; Toft et al, 2016; Trabert et al, 2012) while some of them directly linked UGAs risk with DDE and/or DDT (Bhatia et al, 2005; Brucker-Davis et al, 2008; Longnecker et al, 2002). Some others detected just a positive association (Damgaard et al, 2006; Fernandez et al, 2007; Giordano et al, 2010; Michalakis et al., 2014).…”

Section: Urogenital Abnormalitiesmentioning

confidence: 99%

Association of pesticide exposure with human congenital abnormalities

Kalliora

Mamoulakis

Vasilopoulos

et al. 2018

Toxicology and Applied Pharmacology

109

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Human pesticide exposure can occur both occupationally and environmentally during manufacture and after the application of indoor and outdoor pesticides, as well as through consumption via residues in food and water. There is evidence from experimental studies that numerous pesticides, either in isolation or in combination, act as endocrine disruptors, neurodevelopmental toxicants, immunotoxicants, and carcinogens. We reviewed the international literature on this subject for the years between 1990 and 2017. The studies were considered in this review through MEDLINE and WHO resources. Out of the n = 1817 studies identified, n = 94 were reviewed because they fulfilled criteria of validity and addressed associations of interest. Epidemiological studies have provided limited evidence linking pre- and post-natal exposure to pesticides with cancers in childhood, neurological deficits, fetal death, intrauterine growth restriction, preterm birth, and congenital abnormalities (CAs). In this review, the potential association between pesticide exposure and the appearance of some human CAs (including among others musculoskeletal abnormalities; neural tube defects; urogenital and cardiovascular abnormalities) was investigated. A trend towards a positive association between environmental or occupational exposure to some pesticides and some CAs was detected, but this association remains to be substantiated. Main limitations of the review include inadequate exposure assessment and limited sample size. Adequately powered studies with precise exposure assessments such as biomonitoring, are warranted to clarify with certainty the potential association between pesticide exposure and human CAs.

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Maternal Pregnancy Levels of trans -Nonachlor and Oxychlordane and Prevalence of Cryptorchidism and Hypospadias in Boys

Cited by 36 publications

References 24 publications

Hypospadias and Residential Proximity to Pesticide Applications

Hypospadias and Residential Proximity to Pesticide Applications

The epidemiologic evidence linking prenatal and postnatal exposure to endocrine disrupting chemicals with male reproductive disorders: a systematic review and meta-analysis

Association of pesticide exposure with human congenital abnormalities

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