Fertility of Male Workers Exposed to Cadmium, Lead, or Manganese

Gennart, J P; Buchet, Jean‐Pierre; Roels, Harry; Ghyselen, Patrick; Ceulemans, E.; Lauwerys, Robert

doi:10.1093/oxfordjournals.aje.a116227

Cited by 156 publications

(68 citation statements)

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“…No difference was found in fertility between men occupationally exposed to Cd and an appropriately matched control group (n = 118) by assessing birth experiences of their wives (Gennart et al 1992). …”

Section: Reproductionmentioning

confidence: 95%

Cadmium exposure in the population: from health risks to strategies of prevention

et al. 2010

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We focus on the recent evidence that elucidates our understanding about the effects of cadmium (Cd) on human health and their prevention. Recently, there has been substantial progress in the exploration of the shape of the Cd concentrationresponse function on osteoporosis and mortality. Environmental exposure to Cd increases total mortality in a continuous fashion without evidence of a threshold, independently of kidney function and other classical factors associated with mortality including age, gender, smoking and social economic status. Pooled hazard rates of two recent environmental population based cohort studies revealed that for each doubling of urinary Cd concentration, the relative risk for mortality increases with 17% (95% CI 4.2-33.1%; P \ 0.0001). Tubular kidney damage starts at urinary Cd concentrations ranging between 0.5 and 2 lg urinary Cd/g creatinine, and recent studies focusing on bone effects show increased risk of osteoporosis even at urinary Cd below 1 lg Cd/g creatinine. The non-smoking adult population has urinary Cd concentrations close to or higher than 0.5 lg Cd/g creatinine. To diminish the transfer of Cd from soil to plants for human consumption, the bioavailability of soil Cd for the plants should be reduced (external bioavailability) by maintaining agricultural and garden soils pH close to neutral (pH-H 2 O of 7.5; pH-KCL of 6.5). Reducing the systemic bioavailability of intestinal Cd can be best achieved by preserving a balanced iron status. The latter might especially be relevant in groups with a lower intake of iron, such as vegetarians, and women in reproductive phase of life. In exposed populations, house dust loaded with Cd is an additional relevant exposure route. In view of the insidious etiology of health effects associated with low dose exposure to Cd and the current European Cd intake which is close to the tolerable weekly intake, one should not underestimate the importance of the recent epidemiological evidence on Cd toxicity as to its medical and public health implications.

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Section: Reproductionmentioning

confidence: 95%

Cadmium exposure in the population: from health risks to strategies of prevention

et al. 2010

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“…The experimental protocol followed the Guide for Care and Use of Laboratory Animals. The rats were divided into four groups (6 rats per group) as follows: [1] cadmium only, [2] cadmium and lithium, [3] lithium only and [4] control. Cadmium (5 mg) was administered intraperitoneally in a single dose while lithium was administered orally (0.1 mg/100 gm body weight was added to the drinking water daily) for 6 weeks.…”

Section: Animals and Experimental Designmentioning

confidence: 99%

“…It is released into water as a by-product of smelting, into air by combustion of coal and oil, and into soils as impurities [1]. Cadmium is absorbed via the lungs in significant quantities from cigarette smoke and it has toxic effects on the male reproductive system [2][3][4][5] which may account for the recent declining fertility in men in developed countries. The role of cadmium in the modulation of male reproductive health stems from the observations that high levels of cadmium in seminal fluid are associated with asthenozoospermia in infertile males [6].…”

Section: Introductionmentioning

confidence: 99%

Lithium protects against toxic effects of cadmium in the rat testes

Al-Azemi

Omu

Kehinde

et al. 2010

J Assist Reprod Genet

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Purpose To investigate the protective effect of Lithium against the toxic effect of Cadmium in the rat testes. Methods Twenty four adult male Sprague-Dawley rats were treated with four different regimens: Cadmium only, Cadmium and lithium, lithium only and controls. Rats were sacrificed after 6 weeks and testicular levels of proinflammatory cytokine (IL-4), anti-inflammatory cytokine (TNF-α), Pro-apoptotic protein (Bax) and anti-apoptotic protein (Bcl-2) were measured by ELISA while serum levels of FSH, LH, Prolactin and Testosterone were measured using the Vidas parametric system. Antioxidant status (MDA, SOD) was also assessed in serum. Histopathological changes of testes were examined using light and electron microscopy. Immunohistochemical staining for Bax, Bcl-2 and Caspase 3 were performed. Results Treatment with lithium was associated with significant reduction in the toxic effects of Cadmium as shown by reduced testicular levels of TNF-α, serum levels of Malondialdehyde and testicular level of Bax, and increased levels of IL-4, Zn-Cu SOD, Bcl-2 and Testosterone. Testicular histopathology showed that Cadmium produced an extensive germ cells apoptosis and the addition of lithium in Cadmium-treated rats significantly reduced cadmium-induced testicular damage. Conclusion(s) Lithium has a protective effect against cadmium-induced testicular apoptosis in the rat.

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“…The increased generation of ROS often observed in older men [37][38][39], may be due to several factors and include routine medical prescription and environmental pollutants [58]. The generation of ROS could be made worse by infection, prolonged stasis and abnormal spermatozoa, environmental and life style changes [44,45,[59][60][61] .…”

Section: Extrinsic Factorsmentioning

confidence: 99%