Paternal exposure

Adams PM, Legator MS, Fanini D. 1983. The effect of paternal exposure to ethylene dibromide on the behavior of the FI progeny [Abstract]. Teratology 27 27A. 

Hsu LL, Adams PM, Fanini D, et al. 1985. Ethylene dibromide Effects of paternal exposure on the neurotransmitter enzymes in the developing brain of FI progeny. Mutat Res 147 197-203. 

There is a practical point to be considered here, since there are safety regulations which prevent women of childbearing age from exposure to suspected chemicals, and these regulations seem to be based on the premise that paternal exposure would not be expressed for some reason. This irrational regulatory status may be based on the belief that, since human sperm develop to maturity in about two weeks, exposed sperm will somehow disappear or possibly be killed. However, this approach ignores the fact that the basal germ cell stays there, and remembers all of its unrepaired, non-lethal chemical insults. 

There are no specific reports on turpentine carcinogenicity or mutagenicity. However, in one case control study, paternal exposure to turpentine was one of several substances associated with an increased risk of neuroblastoma in offspring. ... 

Anderson D (2000) Does paternal exposure result in congenital abnormalities in offspring and a predisposition to cancer In Anderson D, Karakaya AE, Sram RJ ed. Human monitoring after environmental and occupational exposure to chemical and physical agents. Amsterdam, IOS Press, pp 151-160 (NATO Science Series). 

Garcia AM, Benavides FG, Fletcher T, Orts E (1998) Paternal exposure to pesticides and congenital malformations. Scand J Work Environ Health, 24 473-480. 

Savitz DA (1994) Paternal exposures and pregnancy outcome miscarriage, stillbirth, low birth weight, preterm delivery. In Olshan AF Mattison DR ed. Male-mediated developmental toxicity. New York, Plenum Press, pp 177-198. 

Seveso births. There was none, indicating that there is no connection between maternal or paternal exposures to dioxin and spina bifida. 

Although this has been shown to occur in experimental animals after exposure of males to foreign compounds such as cyclophosphamide, there is only inconclusive evidence that this occurs in humans. Thus, studies of exposure of human males to vinyl chloride, dibromo-chloropropane, and anesthetic gases, for example, have revealed only equivocal evidence of developmental toxicity in the offspring. There now seems to be some evidence that the leukemia occurring in children, which appears to be clustered around nuclear fuel-reprocessing plants such as Sellafield in the United Kingdom, may be due to paternal exposure to radiation. 

A number of studies have examined pregnancy outcomes following paternal exposure or paternal and maternal exposure to 2,3,7,8-TCDD. No significant alterations in the incidence of spontaneous abortions were found in several studies of Vietnam veterans. In a case-control study conducted by Aschengrau and Monson (1989), no association was observed between paternal military service in Vietnam and the risk of spontaneous abortion (odds ratio [OR] of 0.88, 95% confidence interval [Cl] of 0.42-1.86). A limitation of this study is that service in Vietnam is not an adequate exposure surrogate for 2,3,7,8-TCDD exposure ... 

In an earlier study by Wolfe et al. (1985) of Air Force personnel involved in Operation Ranch Hand, a significant increase in the number of reported neonatal deaths (no additional details provided), as compared to a comparison group of Air Force military employees not stationed in Vietnam, was observed. The incidence of major defects, prematurity, learning disabilities, or infant deaths was not increased in the Ranch Hand personnel. A significant increase in the incidence of minor health effects such as birth marks, rashes, and neonatal jaundice was reported by the Ranch Hand veterans. It should be noted that the pregnancy outcomes were self-reported, and this finding was not corroborated by the follow-up study (Wolfe et al. 1995) which used birth certificates, medical records, and death certificates to assess possible relationships between paternal exposure to 2,3,7,8-TCDD and developmental effects in offspring. 

Dimich-Ward H, Hertzman C, Teschke K, et al. 1996. Reproductive effects of paternal exposure to chlorophenate wood preservatives in the sawmill industry. Scand J Work Environ Health 22 267-273. 

Stacker I, Mandereau L, Aubert-Berleur MP, et al. 1994. Occupational paternal exposure to benzene and risk of spontaneous abortion. Occupational Environ Med 51 475-478. 

Ishihara, K., Warita, K., Tanida, T., Suga Wara, T., Kitagawa, H., Hoshi, N. (2007). Does paternal exposure to 2,3,7,8-tetra-chlorodibenzo-p-dioxin (TCDD) affect the sex ratio of offspring J. Vet Med. Set 69(4) 347-52. 

Potashnik G and Phillip M (1988) Lack of birth defects among offspring conceived during or after paternal exposure to dibromochloropropane (DBCP). Andrologia 20(1) 90-94. 

Several studies have linked paternal exposure to organic solvents with infertility. I67 711 Two of these studies related increased infertility with exposures to mixtures of aromatic solvents (benzene, toluene, ethyl benzene, and toluene) J72-73 One study reported significantly decreased implantation rates after in vitro fertilization following paternal exposure to unspecified organic solvents. I74l... 

All these occupations have exposures to chemical mixtures associated with them. For most, the specific causative agents are unknown. Examples of paternal exposures leading to teratogenic effects are given in Section 24.5. 

It has been recently established that paternal exposures to teratogenic effects can be transgenerationally transmitted. The following example illustrates this effect. 

In one case study, it was shown that paternal exposure to pyridil herbicides (paraquat and diquat) was associated with congenital malformations... 

In occupational exposure studies, paternal exposure to metallic Hg does not appear to cause infertility or malformations (Alcser et al. 1989 Lauwerys et al. 1985). However, a study of pregnancy outcomes among the wives of 152 Hg-exposed men revealed an increased incidence of spontaneous abortions (Cordier et al. 1991). Preconception paternal urinary Hg concentrations above 50 pg/L were associated with a doubling of the spontaneous abortion risk. 

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