A peer-reviewed open access journal published by the National Institute of Environmental Health Sciences

More 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. The 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. A 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. The 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. The 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 the field.

Background: Numerous studies describe the occurrence of post-traumatic stress disorder following disasters, but less is known about the risk of major depression.Aims: To review the risk of depressive disorder in people surviving disasters and in soldiers returning from military deployment.Method: A systematic literature search combined with reference screening identified 23 controlled epidemiological studies. We used random effects models to compute pooled odds ratios (ORs).Results: The average OR was significantly elevated following all types of exposures: natural disaster OR = 2.28 (95% CI 1.30–3.98), technological disaster OR = 1.44 (95% CI 1.21–1.70), terrorist acts OR = 1.80 (95% CI 1.38–2.34) and military combat OR = 1.60 (95% CI 1.09–2.35). In a subset of ten high-quality studies OR was 1.41 (95% CI 1.06–1.87).Conclusions: Disasters and combat experience substantially increase the risk of depression. Whether psychological trauma per se or bereavement is on the causal path is unresolved.

Objective Previous studies have indicated that shift work, long working hours, and prevalent workplace exposures such as lifting, standing, and physical workload increase the risk of miscarriage, but the evidence is conflicting. We conducted a systematic review of original research reports. Methods A search in Medline and EMBASE 1966–2012 identified 30 primary papers reporting the relative risk (RR) of miscarriage according to ≥1 of 5 occupational activities of interest. Following an assessment of completeness of reporting, confounding, and bias, each risk estimate was characterized as more or less likely to be biased. Studies with equivalent measures of exposure were pooled to obtain a weighted common risk estimate. Sensitivity analyses excluded studies most likely to be biased. Results Working fixed nights was associated with a moderately increased risk of miscarriage (pooled RR 1.51 [95% confidence interval (95% CI) 1.27–1.78, N=5), while working in 3-shift schedules, working for 40–52 hours weekly, lifting >100 kg/day, standing >6–8 hours/day and physical workload were associated with small risk increments, with the pooled RR ranging from 1.12 (3-shift schedule, N=7) to 1.36 (working hours, N=10). RR for working hours and standing became smaller when analyses were restricted to higher quality studies. Conclusions These largely reassuring findings do not provide a strong case for mandatory restrictions in relation to shift work, long working hours, occupational lifting, standing, and physical workload. Considering the limited evidence base, however, it may be prudent to advise women against work entailing high levels of these exposures and women with at-risk pregnancies should receive tailored individual counseling.

AJA publishes new findings in basic and clinical (including modern, traditional and epidemiological) research on Andrology.