Lower Sperm Counts Following Prenatal Tobacco Exposure

Jensen, M.S.; Mabeck, L.M.; Toft, Gunnar; Thulstrup, A. M.; Bonde, Jens Peter

doi:10.1016/s0022-5347(05)00573-2

Cited by 17 publications

(36 citation statements)

References 1 publication

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“…Testicular biopsies from boys exposed in utero/neonatal to tobacco smoke demonstrated a decreased number of spermatogonia and gonocytes per tubule cross section (Thorup et al, 2006). Similarly, a large cross-sectional European study of 889 Danish men, 221 men from Norway, 313 Lithuanian men, and 190 men from Estonia reported reductions of sperm concentrations by 20% in sons exposed to prenatal tobacco smoke (Jensen et al, 2004), while a separate study described an inverse dose-dependent association between sperm concentration and prenatal tobacco exposure, measured in adult sons of 522 Danish women (Jensen et al, 2005). The association between impaired semen quality and smoking is fairly well established (Vine, 1996).…”

Section: Tobacco Smokementioning

confidence: 96%

Environmental Toxicants Induced Male Reproductive Disorders: Identification and Mechanism of Action

Jana¹,

Sen²

2012

Toxicity and Drug Testing

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Section: Tobacco Smokementioning

confidence: 96%

Environmental Toxicants Induced Male Reproductive Disorders: Identification and Mechanism of Action

Jana¹,

Sen²

2012

Toxicity and Drug Testing

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“…Contrary to expectations, males with birth weights within the normal range had a tendency to abnormal spermatogenesis in this study. Maternal smoking, which clearly can reduce birth weight, has a significant impact in reducing sperm counts subsequently in male offspring, an effect that is dose dependent (285,286).…”

Section: B Reproductive Functionmentioning

confidence: 99%

Small for Gestational Age: Short Stature and Beyond

et al. 2007

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Depending on the definitions used, up to 10% of all live-born neonates are small for gestational age (SGA). Although the vast majority of these children show catch-up growth by 2 yr of age, one in 10 does not. It is increasingly recognized that those who are born SGA are at risk of developing metabolic disease later in life. Reduced fetal growth has been shown to be associated with an increased risk of insulin resistance, obesity, cardiovascular disease, and type 2 diabetes mellitus. The majority of pathology is seen in adults who show spontaneous catch-up growth as children. There is evidence to suggest that some of the metabolic consequences of intrauterine growth retardation in children born SGA can be mitigated by ensuring early appropriate catch-up growth, while avoiding excessive weight gain. Implicitly, this argument questions current infant formula feeding practices. The risk is less clear for individuals who do not show catch-up growth and who are treated with GH for short stature. Recent data, however, suggest that long-term treatment with GH does not increase the risk of type 2 diabetes mellitus and the metabolic syndrome in young adults born SGA. (Endocrine Reviews 28: 219 -251, 2007)

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“…The fact that fetal exposure may indeed be important is demonstrated by several Danish studies that now consistently indicate that mothers' tobacco smoking during pregnancy is related to rather strong reduction in sperm counts in male offspring. It also seems that fetal exposure to tobacco smoking has stronger impact on semen quality than smoking during adult age [49][50][51][52][53]. Studies of twins, half and full siblings also indicate that early exposures taking place in-utero are important in causing cryptorchidism [54].…”

Section: Fetal Exposurementioning

confidence: 99%

Male reproductive organs are at risk from environmental hazards

Bonde¹

2009

Asian J Androl

106

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Male reproductive disorders that are of interest from an environmental point of view include sexual dysfunction, infertility, cryptorchidism, hypospadias and testicular cancer. Several reports suggest declining sperm counts and increase of these reproductive disorders in some areas during some time periods past 50 years. Except for testicular cancer this evidence is circumstantial and needs cautious interpretation. However, the male germ line is one of the most sensitive tissues to the damaging effects of ionizing radiation, radiant heat and a number of known toxicants. So far occupational hazards are the best documented risk factors for impaired male reproductive function and include physical exposures (radiant heat, ionizing radiation, high frequency electromagnetic radiation), chemical exposures (some solvents as carbon disulfide and ethylene glycol ethers, some pesticides as dibromochloropropane, ethylendibromide and DDT/DDE, some heavy metals as inorganic lead and mercury) and work processes such as metal welding. Improved working conditions in affluent countries have dramatically decreased known hazardous workplace exposures, but millions of workers in less affluent countries are at risk from reproductive toxicants. New data show that environmental low-level exposure to biopersistent pollutants in the diet may pose a risk to people in all parts of the world. For other toxicants the evidence is only suggestive and further evaluation is needed before conclusions can be drawn. Whether compounds as phthalates, bisphenol A and boron that are present in a large number of industrial and consumer products entails a risk remains to be established. The same applies to psychosocial stressors and use of mobile phones. Finally, there are data indicating a particular vulnerability of the fetal testis to toxicants-for instance maternal tobacco smoking. Time has come where male reproductive toxicity should be addressed form entirely new angles including exposures very early in life.

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Lower Sperm Counts Following Prenatal Tobacco Exposure

Cited by 17 publications

References 1 publication

Environmental Toxicants Induced Male Reproductive Disorders: Identification and Mechanism of Action

Environmental Toxicants Induced Male Reproductive Disorders: Identification and Mechanism of Action

Small for Gestational Age: Short Stature and Beyond

Male reproductive organs are at risk from environmental hazards

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