Reproductive paternal effects

Because both males and females are treated in this type of study design, it is not possible to distinguish between maternal and paternal effects in the reproductive performance. To permit this separation, it is necessary to dose additional animals to the stage of mating and then breed them to untreated members of the opposite sex. Similarly, if effects are seen postnatally, it may not be possible to distinguish between effects mediated in utero or mediated by lactation. This distinction can be made by cross-fostering the offspring of treated females to untreated females, and vice versa. 

The February 1987 update of the October 1985 RTECS list of chemicals which cause reproductive hazards, had 6,917 entries. We selected the following T codes T01-T09 (paternal effects), T25 (postimplantation mortality), T31-T59 (effects on embryo or fetus, and specific developmental abnormalities), and T65 (transplacental tumorigenesis). All but the first ones (T01-T09) would fit into a classical definition of teratogens. The paternal effects were included in line with the recommendation by Schardein (vide supra), and also to incorporate the newest data on this long neglected subject. 

It exhibited reproductive toxicity in animals, indicating paternal effects and specific developmental abnormalities in the central nervous system, eyes, and ears. Ethylenimine is a mutagen, testing positive in the histidine reversion-Ames test as well as in the... 

The acute oral toxicity of this compound is low. It is, however, more toxic, than the phthalic acid diaUcyl esters discussed in the preceding sections. The toxic symptoms include nausea, dizziness, somnolence, and hallucination. The oral LD50 value in mice is within the range of 4200 mg/kg. Oral administration produced reproductive toxicity in male mice (paternal effects). At a dose of 2% in diet, it caused maternal and developmental toxicity and an increased incidence... 

Methyl chloride caused adverse reproductive effects in test animals. These include embryo toxicity, fetal death, developmental abnormalities, and paternal effects in rats and mice. It tested positive to the histidine reversion-Ames test for mutagenicity. The carcinogenic properties of this compound have not been established. The evidence in animals and humans is inadequate. 

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. 

A complete and up-to-date reproductive history should be obtained and available for all naval personnel (men and women active duty and reservists). Such a history should be updated annually or after a reproductive outcome. This would provide important baseline information and permit study of maternally and paternally mediated effects. The reproductive history should address sexual activity and inactivity, sexual libido, sexual dysfunction, semen analysis, menstruation history, pregnancy intentions, time-to-pregnancy (conception delays, fecundability, infertility), and pregnancy outcomes (e.g., ectopic pregnancy, spontaneous loss, fetal demise, birth size, secondary sex ratios, birth defects, mental retardation, developmental disabilities). Recording this information is in keeping with the definition for reproductive health and the need to address all health aspects of individuals. 

In further analysis of the Buck et al. (1999) study summarized above and the Buck et al. (1997) study summarized in Section 3.2.5.2.1 (Female Reproductive Effects), Buck et al. (2000) combined maternal and paternal fish consumption into one model looking at fecundability ratios as the outcome, rather than TTP (continuous variable used in 1997 paper) or conception delay (>12 months unprotected intercomse used in 1999 paper). The sample included 606 women with known and unknown TTP who discontinued... 

Parental Hazards (Effects). For assessment of reproductive and developmental risk, parental hazards, both paternal and maternal, must be identified and evaluated. Parental hazards can be expressed as altered nutritional state, functional impairment, and systemic toxicity. Because of possible indirect affects, knowledge and evaluation of non-reproductive/non-developmental toxicity studies are useful. This information is available by examination of subchronic and chronic toxicity studies. 

There is considerable uncertainly about the number of workers actually exposed to harmful levels of workplace reproductive hazards and the number of resulting adverse health effects. However, a substantial number of scientific studies have found these effects in specific groups of workers following both maternal and paternal exposure. 

Experimental evaluations of acrylonitrile have not produced any clear evidence of adverse effects on reproductive fimction or development of offspring at doses below those producing paternal toxicity. The results of genotoxicity evaluations of acrylonitrile have been mixed. Positive findings in vitro have occurred mainly at exposures associated with cellular toxicity, and the most reliable in vitro tests have been negative. 

Overall, Pb exposure appears to have some effect on reproductive histories for families with paternal Pb contact histories. Lin et al. (1996) reported... 

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