C. de Jager

II. The effect of p‐nonylphenol on the fertility potential of male rats after gestational, lactational and direct exposure

Summary. There is growing concern that abnormalities in male reproductive health are becoming more frequent. The most fundamental change has been the striking decline in sperm counts and semen quality. The effect of maternal exposure of rats to the oestrogenic environmental substance p‐nonylphenol (p‐NP) was determined in this study. Exposure to p‐NP for the experimental period impaired general growth. The lower testicular mass indicated a direct toxic effect on the testis in animals exposed to p‐NP during foetal life, the postnatal period and after weaning until termination at 10 weeks of age. The epididymal mass was also negatively affected by p‐NP; this was supported by the decrease in the epididymal ratio. The total cauda epididymal sperm count was significantly lower in the 250 mg kg−1 p‐NP dosage group compared to the control and 100 mg kg−1 p‐NP groups. The overall lower sperm count with increased p‐NP concentrations corresponded with the decreased testicular and epididymal masses. This emphasized the toxicity of p‐NP on both testis and epididymis. Seminiferous tubule diameter, lumen diameter and seminiferous epithelium thickness were smaller in the exposed groups, even at the low dose level. These histological measurements further supported the finding of a low testicular mass. In spite of the measurements being smaller, p‐NP had no effect on the stages of spermatogenesis except for one animal with disrupted spermatogenesis in some tubules, while others were normal.

I. The effect of p-nonylphenol, an environmental toxicant with oestrogenic properties, on fertility potential in adult male rats

Summary. Infertility is a sad reality and it is now evident that several aspects of male reproductive health have changed for the worse over the past 30–50 years. para‐nonylphenol (p‐NP), an environmental toxicant with oestrogenic properties, was tested for its effect on male fertility potential. When adult male rats were exposed to 100 mg kg−1 p‐NP the histological parameters of the seminiferous tubules were adversely affected. Although spermatogenesis was already established in these males at the time exposure commenced, p‐NP still had an effect on the histology of the seminiferous tubules. Increasing the level to 250 mg kg−1 additionally resulted in a smaller weight gain and signs of epididymal toxicity, while 400 mg kg−1 also impaired testicular mass and sperm count. In the last two groups spermatogenesis was also affected in some animals. Because p‐NP had an effect on established spermatogenesis in the rat, one could speculate that the same effects might also occur in humans. It would appear that p‐NP had toxic effects on both the testis and epididymis and both structures might be important in impairing male fertility. Bio‐accumulation may enhance the negative effects at even lower p‐NP concentrations over longer exposure periods than reported here.

Simultaneous exposure to low concentrations of dichlorodiphenyltrichloroethane, deltamethrin, nonylphenol and phytoestrogens has negative effects on the reproductive parameters in male Spraque-Dawley rats

Many reports suggest that male reproductive health has deteriorated over the last decades, possibly due to environmental contaminants that act as endocrine disruptors. This hypothesis was tested in Sprague‐Dawley rats using a modified Organization for Economic Cooperation and Development 415 one‐generation test. Group A received cottonseed oil as control, and Groups B, C and D received deltamethrin (DM); DM and dichlorodiphenyltrichloroethane (DDT); and DM, DDT, phytoestrogens and p‐nonylphenol, respectively. Rats were exposed in utero and then received the substances for 10 weeks. The seminal vesicle mass (Group B; P = 0.046) and sperm count [Groups C (P = 0.013) and D (P = 0.003)] were lower and the anogenital distance [Group B (P = 0.047) C (P = 0.045) and D (P = 0.002)] shorter compared with the control group. The seminiferous tubule diameter [Groups B (P = <0.001), C (P = <0.001) and D (P = <0.001)] and epithelium thickness [Groups B (P = 0.030), C (P = <0.001) and D (P = <0.001)] were smaller compared with the control. The histology of the testes showed signs of apical sloughing and vacuolisation. Liver weights [Groups C (P = 0.013) and D (P = 0.005)] and liver enzymes [Group D (P = 0.013)] were also affected. These findings may indicate that simultaneous exposure to endocrine disrupting compounds contributes to the deterioration observed in male reproductive health.

LETHAL DOSE AND REPRODUCTIVE PARAMETERS OF p-NONYLPHENOL IN RATS

Male reproductive abnormalities may be due to an increased level of maternal estrogens affecting the developing fetus. Man is exposed to environmental estrogens in multiple ways: diet, drinking water, air, and skin. para-Nonylphenol (p-NP), an alkylphenol, has estrogenic properties. This study was performed to evaluate the potency and workable concentrations before reproductive tests could be performed. The oral LD50 (median lethal dose) value for rats was 1475 mg/kg. For both males in the reproductive test the litter size after long-term treatment at 50 mg/kg p-NP was smaller than that in the breeding records. Five females did not conceive at all.Male reproductive abnormalities may be due to an increased level of maternal estrogens affecting the developing fetus. Man is exposed to environmental estrogens in multiple ways: diet, drinking water, air, and skin, para-Nonylphenol (p-NP), an alkylphenol, has estrogenic properties. This study was performed to evaluate the potency and workable concentrations before reproductive tests could be performed. The oral LD50 (median lethal dose) value for rats was 1475 mg/kg. For both males in the reproductive test the litter size after long-term treatment at 50 mg/kg p-NP was smaller than that in the breeding records. Five females did not conceive at all.

Preliminary assessment of oestrogenic activity in water sources in Rietvlei Nature Reserve, Gauteng, South Africa

A preliminary assessment was made of oestrogenic activity in water sources in the Rietvlei Nature Reserve, from which water is supplied to the metropolitan area of Pretoria. Single samples were extracted from seven sites using a solid phase C18 cartridge and the extracts assessed for oestrogenic activity using the Recombinant Yeast Screen bio-assay. Estradiol equivalents ranged from 0.31–2.1 ng l−1, which are comparable to those reported for rivers near Paris (1.0–32 ng l−1) and for environmental water in Korea (0.5 pg l−1 and 7.4 ng l−1). The oestrogenic activity found in Rietvlei water samples is supported by a report of intersex in catfish, Clarias gariepinus, in the reserve. Further studies are required to determine whether this phenomenon is consistent, to determine the chemical(s) responsible for this activity and to characterise the potential effects on human, aquatic, and wildlife health in the area.

Endocrine Disruptors and Health Effects in Africa: A Call for Action

Background: Africa faces a number of unique environmental challenges. Unfortunately, it lacks the infrastructure needed to support the comprehensive environmental studies that could provide the scientific basis to inform environmental policies. There are a number of known sources of endocrine-disrupting chemicals (EDCs) and other hazardous chemicals in Africa. However, a coordinated approach to identify and monitor these contaminants and to develop strategies for public health interventions has not yet been made. Objectives: This commentary summarizes the scientific evidence presented by experts at the First African Endocrine Disruptors meeting. We describe a “call to action” to utilize the available scientific knowledge to address the impact of EDCs on human and wildlife health in Africa. Discussion: We identify existing knowledge gaps about exposures to EDCs in Africa and describe how well-designed research strategies are needed to address these gaps. A lack of resources for research and a lag in policy implementation slows down intervention strategies and poses a challenge to advancing future health in Africa. Conclusion: To address the many challenges posed by EDCs, we argue that Africans should take the lead in prioritization and evaluation of environmental hazards, including EDCs. We recommend the institution of education and training programs for chemical users, adoption of the precautionary principle, establishment of biomonitoring programs, and funding of community-based epidemiology and wildlife research programs led and funded by African institutes and private companies. https://doi.org/10.1289/EHP1774