Title
Lead Poisoning and Reproduction: Effects on Pituitary and Serum Gonadotropins in Neonatal Rats
Author
Peter Petrusz, Catharina M. Weaver, Lester D. Grant, Paul Mushak, Martin R. Krigman
Publication
Environmental Research. Volume 19, Issue 2, August 1979, Pages 383–391
Link
http://www.sciencedirect.com/science/article/pii/001393517990063X
Abstract
In order to investigate the effects of neonatal lead poisoning on pituitary gonadotropic function, newborn rats were given daily doses of lead (25, 100, and 200 mg/kg) by gastric gavage. Control rats were given deionized water. Groups of animals were sacrificed at 10, 15, and 20 days of age and serum and pituitary levels of the gonadotropins follicle stimulating hormone (FSH) as well as pituitary contents of luteninizing hormone (LH) were determined by radioimmunoassay. Lead concentrations in blood, bone, brain, and pituitary tissues of similarly treated 15-day-old rats were determined by atomic absorption spectrometry. Lead content in bone (femur) and brain showed dose-dependent elevations throughout the dose range; in blood, it reached a plateau of about 1000 μg% already at the dose of 100 mg/kg/day. Lead remained at undetectable levels (<0.01 μg/g) in pituitary tissue regardless of the dose. There were no significant differences between lead-treated and control rats in body weights, pituitary weights, pituitary LH contents in either sex, and serum FSH levels in males. Lead exposure increased pituitary FSH content in male rats at all ages studied, and suppressed serum FSH levels in 15-day-old females. These results suggest that the effects of subclinical neonatal lead poisoning on gonadal development and subsequent function, especially in the female, may be mediated by central neuroendocrine mechanisms.
Title
Male reproductive toxicity of lead in animals and humans. ASCLEPIOS Study Group
Author
- Apostoli, P. Kiss, S. Porru, J. P. Bonde & M. Vanhoorne
Publication
Occupational & Environmental Medicine, 55(6): 364–374, Jun 1998
Link
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1757597/
Abstract
OBJECTIVE: To critically review the literature on male reproductive toxicity of lead in animals and humans. METHODS: A systematic literature search identified a total of 32 experimental studies in animals and 22 epidemiological studies, one case report on humans and five review articles or documents. The studies were evaluated by paying attention mainly to sample size, study design, exposure, and dose characterisation, analytical method standardisation, and quality assurance. RESULTS: Several studies on rats and other rodents indicated that blood lead concentrations > 30-40 micrograms/dl were associated with impairment of spermatogenesis and reduced concentrations of androgens. However, other animal studies, mainly about histopathological, spermatozoal, and hormonal end points, indicated that certain species and strains were quite resistant to the reproductive toxicity of lead and that different testicular lead concentrations could account for these differences. The human studies focused mainly on semen quality, endocrine function, and birth rates in occupationally exposed subjects, and showed that exposure to concentrations of inorganic lead > 40 micrograms/dl in blood impaired male reproductive function by reducing sperm count, volume, and density, or changing sperm motility and morphology. No relevant effects were detected on endocrine profile. CONCLUSION: Several factors make it difficult to extrapolate the animal data to the human situation. The difficulties are mainly due to differences between species in reproductive end points and to the level of exposure. Concentrations of blood lead > 40 micrograms/dl seemed to be associated with a decrease in sperm count, volume, motility, and morphological alterations and a possible modest effect on endocrine profile. Dose-response relation, in particular at a threshold level, is poorly understood, and site, mode, or mechanism of action are unknown. Also, the effects were not always the same or associated in the same on sperm count and concentration. Some methodological issues and indications for future studies are discussed.
Title
Adverse Reproductive Effects in Female Workers of Lead Battery Plants
Author
Ning Tang & Zi Zhu
Publication
International Journal of Occupational Medicine and Environmental Health, 16(4): 359-361, 2003
Link
http://www.imp.lodz.pl/upload/oficyna/artykuly/pdf/full/Tang9-04-03.pdf
Abstract
Fifty seven female workers at mean age 32 years (range, 23–45 years), employed in a storage battery plant and a capacitor factory were investigated. The lead exposure period was 7.4 years (range, 1–17 years). The retrospective method was used to analyse reproductive functions of women: menses, libido, abortion and delivery. The results were compared with the control group (62 female workers, mean age 32 years; range, 24–45 years). The incidence of polymenorrhea, prolonged and abnormal menstruations, hypermenorrhea was significantly higher in the lead exposed group than in controls. The incidence of spontaneous abortions was reported by 6 exposed female workers whereas it was not observed in the control group (p = 0.01). The authors conclude that occupational lead exposure of female workers could lead to the impairment of the functions of reproductive system, however poor working conditions and workload may prove to be additional factors responsible for functional disorders in the subjects under study.
Title
Lead, Endocrine Disruption and Reproductive Outcomes
Publication
BioPortfolio, December 20, 2014
Abstract
This prospective cohort study of 400 lead exposed and 400 non-lead exposed women and their husbands assesses endocrine dysfunction and adverse reproductive outcomes. Residing in two study areas in Shenyang, China, the women are married, 20 and 34 years of age, never smokers, have obtained permission to have a child, and have attempted to become pregnant over the course of the study. Lead exposure is defined by lead levels in blood samples collected at the baseline survey (both women and their husbands), first and second trimesters, and at delivery (both maternal and cord blood). Endocrine dysfunction is monitored by urinary hormone metabolites including follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrone conjugates (E1C), and pregnanediol-3-glucuronide (PdG). Reproductive endpoints include menstrual disturbance, time to conception, spontaneous abortion, preterm delivery, and low birth weight.