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PubMed2005

Mechanisms and consequences of paternally-transmitted chromosomal abnormalities.

Paternally-transmitted chromosomal damage has been associated with pregnancy loss, developmental and morphological defects, infant mortality, infertility, and genetic diseases in the offspring, including cancer. There is epidemiological evidence linking paternal exposure to occupational or environmental agents with an increased risk of abnormal reproductive outcomes. There is also a large body of literature on germ cell mutagenesis in rodents showing that treatment of male germ cells with mutagens has dramatic consequences on reproduction, producing effects such as those observed in human epidemiological studies. However, we know very little about the etiology, transmission, and early embryonic consequences of paternally-derived chromosomal abnormalities. The available evidence suggests that: 1) there are distinct patterns of germ cell-stage differences in the sensitivity of induction of transmissible genetic damage, with male postmeiotic cells being the most sensitive; 2) cytogenetic abnormalities at first metaphase after fertilization are critical intermediates between paternal exposure and abnormal reproductive outcomes; and 3) there are maternal susceptibility factors that may have profound effects on the amount of sperm DNA damage that is converted into chromosomal aberrations in the zygote and that directly affect the risk for abnormal reproductive outcomes.

Aneuploidy↗
PubMed1996

Paternally inherited chromosomal structural aberrations detected in mouse first-cleavage zygote metaphases by multicolour fluorescence in situ hybridization painting.

We describe a fluorescence in situ hybridization (FISH) procedure for assessing zygotic risk of paternal exposure to endogenous or exogenous agents. The procedure employs multicolour FISH with chromosome-specific DNA painting probes plus DAPI staining for detecting both balanced and unbalanced chromosomal aberrations in mouse first-cleavage (1-Cl) zygote metaphases. Four composite probes specific for chromosomes 1, 2, 3 or X, each labelled with biotin, plus a composite probe specific for chromosome Y labelled with digoxigenin, were used. We applied this method to evaluate the effects of paternal exposure to acrylamide, a model germ cell clastogen. First-cleavage zygote metaphases, collected from untreated females mated to males whose sperm or late spermatids were treated with acrylamide, were scored for the induction of structural aberrations using both chromosome painting (PAINT analysis) and DAPI analysis. Structural chromosomal aberrations were observed in the sperm-derived, but not in the egg-derived, pronuclei. While 59.4% of the zygotes had structural aberrations by DAPI analysis, 94.1% of the same zygotes had structural aberrations by PAINT analysis (P < 0.001), illustrating the increased sensitivity for detecting translocations and insertions obtained by adding chromosome painting. These findings show that FISH painting of mouse 1-Cl zygotes when used in conjunction with DAPI analysis is a powerful model for investigating the cytogenetic defects transmitted from father to offspring.

Animals↗
PubMed1989

Effects of paternal subacute exposure to Tordon 202c on fetal growth and development in CD-1 mice.

Male CD-1 mice were exposed to Tordon 202c (a picloram and 2,4-D combination herbicide) in the drinking water at concentrations of 0.21, 0.42, and 0.84% solutions for 60 days prior to mating with untreated females. Subsequently there was no exposure to Tordon 202c during gestation. Fetal weight and crown-rump length were reduced in the highest dosage group. The incidence of malformed fetuses (e.g., ablepharon, cleft palate, and unilateral agenesis of the testes) was increased in the middle dosage group while the incidence of fetuses with variants was increased in the lowest (e.g., an extra pair of ribs) and the highest dosage groups (e.g., incomplete ossification of the skeleton). The frequency of pregnancy failure was increased in the middle dosage group. Indices of paternal toxicity included increased lethality and decreased water consumption in the highest dosage group and increased relative spleen weights in the lowest and middle dosage groups. The results suggest paternally mediated reproductive toxicity.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2004

[A case-control study on risk factors of hypospadias].

OBJECTIVE: Hypospadias is one of the most commonly seen urogenital congenital malformations in males and to identify its etiological factors. METHODS: A hospital-based case-control study was conducted, with 107 hypospadias cases. Two matched controls per case were randomly selected. Both cases and controls were face to face interviewed with a uniformed questionnaire. Conditional logistic regression model was used for univariable and multivariate analysis on SAS 6.12 to estimate odds ratios (OR) and 95 per cent confidence internals (95% CI). RESULTS: Data from multiple conditional logistic regression analysis showed that hypospadias was positively associated with maternal history of spontaneous abortion (OR = 3.87, 95% CI: 1.60 - 9.39), with threatened abortion in the first or second trimester (OR = 3.57, 95% CI: 1.31 - 9.64), with common cold accompanied fever in the first trimester (OR = 7.63, 95% CI: 2.50 - 23.24), with maternal drug (antibiotic, analgesiscs) exposure during the second trimester (OR = 16.46, 95% CI: 3.46 - 78.21), with paternal exposure to pesticides occupationally (OR = 3.70,95% CI: 1.49 - 9.16), with neonatal low birth weight (OR = 12.62, 95% CI: 2.97 - 53.67), but was negatively associated with maternal diet supplemented with protein in the first trimester (OR = 0.33, 95% CI: 0.15 - 0.74). CONCLUSIONS: The risk factors of hypospadias seemed to include maternal history of spontaneous abortion, threatened abortion in the first or second trimester, maternal common cold accompanied fever in the first trimester, maternal drug exposure during the second trimester, paternal occupational exposure to pesticides, neonatal low birth weight. However, maternal diet supplemented with protein probably acted as the protective factor for neonatal hypospadias in the first trimester.

Adolescent↗
PubMed1981

Maternal and paternal chronic exposure to enflurane and halothane: fetal and histological changes in the rat.

Adult male and female rats were exposed chronically to halothane 10 p.p.m., enflurane 20 p.p.m. or air for up to 64 days before mating and subsequently throughout the pregnancy of the females. The parents, progeny and, in a few cases, the subsequent generation, were studied. No abortifacient effect was seen with either agent. The groups exposed to anaesthetic had larger litters with lighter fetuses compared with their control groups. Skeletal examination did not reveal any major teratological effects for either agent. No consistent organ injury could be associated with chronic exposure to the agents under the conditions of this study.

Abnormalities, Drug-Induced↗
PubMed1992

Ewing's bone sarcoma, paternal occupational exposure, and other factors.

To determine risk factors for Ewing's bone sarcoma, the authors interviewed mothers of 43 patients diagnosed between January 1978 and August 1986 and 193 controls in the San Francisco Bay Area, California, regarding medical and occupational history of parents and other factors related to the subjects and their immediate families. Controls were selected by using random digit dial telephone methods. Adjusted relative risk estimates suggest that risks were elevated for children whose fathers were engaged in agricultural occupations during the period from 6 months prior to conception of the subject up to the time of diagnosis for the patients or interview for the controls (relative risk (RR) = 8.8, 95% confidence interval (CI) 1.8-42.7) and for children whose fathers had occupational exposure to herbicides, pesticides, or fertilizers (RR = 6.1, 95% CI 1.7-21.9, p = 0.002). Prior ingestion of poison or an overdose of medication was more common in patients than in controls (RR = 4.4, 95% CI 1.4-13.5). These and other findings should be investigated in larger population-based studies to determine specific factors that may account for the associations.

Adolescent↗
PubMed1991

Leukaemia and paternal radiation exposure.

OBJECTIVE: Recently, Gardner and colleagues inferred, from a case-control study of leukaemia incidence in young people near the Sellafield nuclear facility in West Cumbria, that an increase near Sellafield was real, and was probably caused by occupational exposure of the father to ionising radiation at the Sellafield plant. The intent of this paper is to dispute that attribution, and to suggest that confirmation of such an alarming and prejudicial conclusion should precede its dissemination. MATERIAL CONSIDERED: Critical comment is limited to the paper by the Gardner group presenting their results, the accompanying paper outlining their methods, a review from Mathews that provides some support for the Gardner proposal by suggesting a pathogenetic mechanism, and some observations on inherited tumours by Nomura that are quoted by Gardner et al. and Mathews in support of their beliefs. Other material quoted is from the general medical literature of the past 20 years relating to radiation biology, mutagenesis and carcinogenesis with some relevance to the Gardner contention; it is not exhaustive. MAIN RESULTS: Statistical arguments suggest that it is almost impossible to be sure that a specific leukaemia "cluster", such as that near Sellafield, is not a chance finding. The study by Gardner et al. provides only weak statistical evidence for an association between leukaemia in children and parental occupational radiation exposure at Sellafield. The postulate of a causal relation between parental exposure at Sellafield and leukaemia in progeny is incompatible with what is known of the role of genetic mechanisms in leukaemia, with current views on the quantitative relation between radiation dose and mutagenetic effect, and with observations on the children of people exposed to radiation by the nuclear bombs used in Japan in 1945. CONCLUSIONS: The suggestion that occupational exposure to ionising radiation of a father may be responsible for an increased risk of leukaemia in his children cannot be substantiated. It would be proper to seek confirmation from other groups of occupationally exposed persons before undertaking precipitous, and inevitably disturbing, action to remedy the supposed problem.

Adult↗
PubMed1992

Leukemia in children and paternal radiation exposure at the Sellafield nuclear site.

Childhood cancer around nuclear installations has been studied in recent years, particularly in the United Kingdom but also in other countries. The early studies were prompted by the suggestion of a 10-fold raised level of childhood leukemia around the Sellafield nuclear site in England, which was confirmed and followed by the identification of generally smaller excesses around some (but not all) other nuclear sites in the United Kingdom. Marked excesses have not been reported in other countries. The increased leukemia rate around Sellafield has been further investigated by examining individual cases in detail in epidemiological cohort and case-control studies. The raised incidence seems to have been concentrated in children born in the local area but not among children who moved in after birth and was particularly associated with fathers who had experienced higher levels of occupational external ionizing radiation exposure at Sellafield before their children's conception. The underlying cause of this statistical association is not yet clear, but the findings have important potential implications for radiobiology and for protection of radiation workers and their children.

Adult↗
PubMed1992

Parental occupation and childhood astrocytoma: results of a case-control study.

Parental occupations were investigated as possible risk factors for astrocytoma, the most frequently occurring brain tumor in children. A case-control study of 163 pairs was performed. Cases under 15 years of age at diagnosis in 1980-1986 were identified through the tumor registries of eight hospitals in Pennsylvania, New Jersey, and Delaware. Controls were selected by random-digit dialing and were matched to cases on age, race, and telephone area code. Occupations before the child's conception, during the pregnancy, and after the child's birth were studied separately. We did not observe any strong associations. Significantly more fathers of cases were electrical or electronic repairmen, a subgroup of an occupational category previously associated with increased risk. An excess of case mothers employed as nurses was observed, which was significant for mothers of children diagnosed before 5 years of age. Elevated although not significant odds ratios were observed for some white collar and professional occupations in case parents; for paternal exposure to paint and paternal occupation in the paper and pulp mill industry, both in the period after the child's birth; and for maternal occupation as a hairdresser. The lack of strong associations may have resulted from low statistical power for some job groupings. Our study, unlike previous studies, focused on a single type of brain tumor: childhood astrocytoma. Thus our results suggest that some parental occupations associated with childhood brain tumors in previous studies may not be risk factors for childhood astrocytoma.

Adolescent↗
PubMed1999

Preconception urethane or chromium(III) treatment of male mice: multiple neoplastic and non-neoplastic changes in offspring.

Increase in neoplasia in offspring after preconception exposure of parents presents puzzling features such as high frequency of effects and lack of Mendelian inheritance. The present study examined the hypothesis that preconception carcinogenesis involves an increase in the rate of occurrence of neoplasms with a spontaneous incidence. Male NIH Swiss mice (12 per group) were exposed 2 weeks before mating (once, ip) to urethane (1.5 g/kg) or chromium(III) chloride (1 mmol/kg). Offspring (48-78/sex/group) were examined for all grossly apparent changes when moribund or at natural death, followed by histopathological diagnosis and statistical analysis. Significant exposure-related changes occurred in multiple organs. Ten to 20 percent of offspring showed changes related to paternal exposure, including at least one sired by most treated males. Pheochromocytomas occurred in both male and female offspring after both treatments, with none in controls. These neoplasms are rare in mice and suggest endocrine dysfunction as a component of preconception carcinogenesis. This was supported by increases in thyroid follicular cell and Harderian gland tumors, ovarian cysts, and uterine abnormalities. Lung tumors were increased in female offspring only. Effects seen in offspring only after paternal urethane exposure were an increase in preneoplasia/neoplasia in the glandular stomach (males) and in females, increased lymphoma but decreased incidence of histiocytic sarcoma. Increases in incidence of male reproductive gland tumors and of renal non-neoplastic lesions occurred only after chromium exposure. Thus, preconception exposure of fathers to toxicants had a significant impact on both neoplastic and non-neoplastic changes in almost all tissues in which these lesions often occur naturally during the aging process.

Adenoma↗
PubMed2004

Reproductive effects of occupational DDT exposure among male malaria control workers.

To assess potential effects of human DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] exposure, we evaluated the reproductive history of 2,033 workers in the antimalaria campaign of Mexico. Data on occupational exposure to DDT and reproductive outcomes were gathered through a questionnaire, and workers provided information about 9,187 pregnancies. We estimated paternal exposure to DDT before each pregnancy using three approaches: a) a dichotomous indicator for pregnancies before and after exposure began, b) a qualitative index of four exposure categories, and c) an estimation of the DDT metabolite DDE [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene] accumulated in fat. To assess associations, we used logistic regression models that accounted for correlated observations and adjusted for parents' age at each child's birth, exposure to other pesticides, exposure to chemical substances in other employment, smoking, and alcohol consumption. The odds ratio for birth defects comparing pregnancies after and before the first exposure was 3.77 [95% confidence interval (95% CI), 1.19-9.52]. Compared with the lowest quartile of estimated DDE in fat, the ORs were 2.48 (95% CI, 0.75-8.11), 4.15 (95% CI, 1.38-12.46), and 3.76 (95% CI, 1.23-11.44) for quartiles 2, 3, and 4, equivalent to p,p -DDE in fat of 50, 82, and 298 microg/g fat, respectively. No significant association was found for spontaneous abortion or sex ratio. We found an increased risk of birth defects associated with high occupational exposure to DDT in this group of workers. The significance of this association at lower exposure levels found in the general population remains uncertain.

Abortion, Spontaneous↗
PubMed1992

Male-mediated teratogenesis and other reproductive effects: biologic and epidemiologic findings and a plea for clinical research.

This paper reviews biologic and epidemiologic evidence that prefertilization and perifertilization exposures to fathers influence a variety of reproductive outcomes, including fertilization, miscarriage, low birth weight, congenital anomalies, cancer, and neurodevelopmental and other childhood health problems. Males and females bring an equal number of chromosomes to their progeny, but their genomes may affect different aspects of reproduction. While the key male role principally ends at fertilization, there is growing experimental and human evidence that factors relating both to prefertilization and perifertilization exposure also play a role post fertilization. Some negative human epidemiologic findings reflect the fact that routinely gathered information usually generates detailed descriptions of maternal exposures and does not collect records regarding prefertilization paternal exposures. The absence of extensive human evidence should be interpreted as a deficiency in research rather than an absence of male-mediated adverse reproductive outcomes. More than 60 different compounds or industrial processes have been identified as increasing defects in human sperm and possibly increasing the risk to offspring from male-mediated exposures. Further research needs to include better characterizations of both maternal and paternal prefertilization and perifertilization exposures, in order to assess more accurately their relative effects. Pediatricians confronted with adverse pregnancy and antenatal health outcomes should obtain detailed information on relevant prefertilization exposures of both parents.

Abnormalities, Drug-Induced↗
PubMed1997

Parental occupation, occupational exposure to solvents and polycyclic aromatic hydrocarbons and risk of childhood brain tumors (Italy, France, Spain)

The role of parental occupational exposure in childhood brain tumors was investigated in a population-based case-control study grouping 251 cases and 601 controls from three European centers: Milan (Italy), Paris (France), and Valencia (Spain). Parental occupational exposure to solvents and polycyclic aromatic hydrocarbons (PAH) during the five-year period before birth was estimated using a job-exposure matrix developed earlier in the same countries. Odds ratios (OR) of brain tumors for each occupation and occupational exposure were estimated by logistic regression, adjusting for child's age, gender, exposure to tobacco smoke and ionizing radiation, mother's age and years of schooling, and center. The risk of childhood brain tumors rose when fathers worked in agriculture (OR = 2.2, 95 percent confidence interval [CI] = 1.0-4.7) and motor-vehicle-related occupations. In the latter group, the risk increased for primitive neuroectodermal tumors in particular (OR = 2.7, CI = 1.1-6.6). Astroglial tumors were more frequent among children of mothers in health services (OR = 2.2, CI = 1.0-4.9). Paternal exposure to PAHs was associated with an increased, but not dose-related, risk of primitive neuroectodermal tumors (OR = 2.0, CI = 1.0-4.0), and maternal exposure to solvents at a high level was associated with an increased risk of both astroglial (OR = 2.3, CI = 0.9-5.8) and primitive neuroectodermal tumors (OR = 3.2, CI = 1.0-10.3).

Adolescent↗