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At least 19 recordsLinked to original sources
PubMed1988

Human mutagens: evidence from paternal exposure?

The importance of inherited mutations as a cause of human disease has been established clearly through examples of well-defined genetic anomalies, such as Down syndrome and retinoblastoma. Furthermore, it is suspected that environmental contaminants induce mutations resulting in increased risk for such defects in subsequent generations of persons exposed. The present lack of direct evidence for induced inherited genetic disorders in human beings hampers the development of risk estimation techniques for extrapolation from animal models. The most extensive prospective epidemiologic studies of inherited genetic effects have involved survivors of atomic bomb detonations and patients treated with cancer chemotherapy. In neither case has a significant elevation in inherited genetic effects or cancer been detected in the offspring of exposed individuals. Epidemiologic studies of subjects receiving chronic exposure may be confounded by the effect of maternal exposure during pregnancy. Consideration of only paternal exposure can minimize the confounding influence of teratogenicity, enhancing the resolving power of studies for inherited effects. Using this approach, retrospective (case-control) studies of childhood cancer patients have provided limited but suggestive evidence for inheritance of induced effects. Endpoints, such as congenital malformations and spontaneous abortion following paternal exposure, can also be considered as indicators of heritable mutagenic effects. For example, there is limited evidence suggesting that paternal exposure to anaesthetic gases may cause miscarriage and congenital abnormalities as a result of induced male germ cell mutations. By comparing male-exposure endpoints for which there are human data, as described above, with parallel or similar animal endpoints, such as dominant lethal, inherited cancer and "male teratogenic" effects, it is possible that suitable models for extrapolating to human risk can be developed. In order to establish a clearer relationship between induced mutation and genetic disease, the current surveillance systems should be expanded to include endpoints relevant to genetic study. The relaxation of regulations regarding access to census data could improve the chances of documenting such an association.

Abortion, Spontaneous↗
PubMedDate not supplied

Effects of limited paternal exposure to xenobiotic agents on the development of progeny.

This report represents a series of investigations of the postnatal functional sequelae of paternal exposure to opioids and other xenobiotic agents. In separate studies, young adult male mice were exposed to (1) morphine; (2) levorphanol or its nonanalgesic isomer dextrorphan; or (3) 80% nitrous oxide/20% oxygen. Males (5-8/group) were injected twice daily for 5 1/2 or 8 1/2 days with opioids or saline, or received a single 4 hour inhalation exposure to nitrous oxide/oxygen or compressed air. At 6-8 1/2 days post-treatment, each male was housed with 3 drug-naive nulliparous females. With the exception of birth weights of litters, no alterations in reproductive indices were observed. Changes in reproductive endocrine parameters included marked attenuation of serum luteinizing hormone response to castration in both young adult (8 week) and older (18 week) F1 morphine offspring, when compared with saline-derived groups. The morphine progeny showed decrements in body weight and delayed onset of maturational indices through four generations of selective inbreeding. Similar developmental delays occurred in F1 offspring originating from paternal levorphanol, dextrorphan and nitrous oxide groups, when compared with their respective controls. Behavioral study of F1 offspring revealed alterations in: water maze performance and learning, if preceded by unavoidable footshock, in morphine offspring at 8 and 18 weeks; aberrant swim patterns in both levorphanol and dextrorphan progeny at 6 1/2 and 8 1/2 weeks. Nitrous oxide progeny showed a blunting of hypothermic response to pharmacologic challenge at 16 weeks, in comparison to compressed air controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Lack of birth defects among offspring conceived during or after paternal exposure to dibromochloropropane (DBCP).

The present study describes birth defects and health status of offspring of men with dibromochloropropane (DBCP) induced testicular dysfunction. One case with a major anomaly (urinary bladder extrophy and epispadias) and 2 cases of minor birth defects were observed among the 34 children evaluated. This rate was similar and not significantly different (p = 0.80) from that observed in a control group of 51 children conceived during pre-exposure in the same families. The health status of all the children was unremarkable. It is concluded that paternal exposure to DBCP, severe enough to cause azoospermia or oligozoospermia, did not increase the rate of congenital malformations or of impaired health status of offspring conceived during or after exposure.

Abnormalities, Drug-Induced↗
PubMed2026

Paternal exposure to polystyrene nanoplastics induces inter- and transgenerational bronchopulmonary dysplasia-like damage in male offspring by FtMt hypermethylation-mediated ferroptosis.

Bronchopulmonary dysplasia (BPD) is a major cause of chronic lung disease in both preterm infants and adults, but its etiology remains incompletely understood. In this study, F0 generation mice were exposed to polystyrene nanoplastics (PS-NPs), and F1 to F3 generations were obtained by breeding. Multi-omics sequencing including whole genome methylation sequencing, single cell transcriptome sequencing and transcriptome sequencing was performed on the lungs of offspring. The levels of Fe2+, lipid peroxidation products and key gene expression were determined. Male mice exposed to PS-NPs at environmentally relevant doses produced offspring (F1 and F2) that exhibited a typical BPD-like phenotype. Meanwhile, the F0 males showed diminished sperm motility, demonstrating that paternal PS-NPs exposure constituted an etiological factor for BPD in descendants. Mechanistic studies showed that PS-NPs exposure upregulated the expression of DNA methyltransferase Dnmt3a, leading to global hypermethylation of the sperm genome. Importantly, the hypermethylated promoter signature of the mitochondrial ferritin (FtMt) gene partially resisted epigenetic reprogramming and was transmitted to the lungs of offspring, resulting in persistently low FtMt expression in F1 and F2 lungs. This led to increased intracellular Fe2+ levels, subsequently triggered ferroptosis in alveolar epithelial cells, and ultimately impaired alveolarization. Knockdown of FtMt confirmed that FtMt deficiency was sufficient to induce ferroptosis and BPD-like lung injury both in vitro and in vivo. Furthermore, using in vitro fertilization of F0 sperm combined with Dnmt3a siRNA microinjection, we directly demonstrated that Dnmt3a is a key driver for FtMt to escape reprogramming and maintain its hypermethylation. In summary, this study reveals for the first time that paternal PS-NPs exposure causes BPD through a Dnmt3a-FtMt hypermethylation intergenerational and transgenerational axis, providing an epigenetic basis for understanding paternal derived chronic lung disease and potential targets for early intervention.

Animals↗
PubMed1991

Paternal exposure to mercury and spontaneous abortions.

The potential reproductive toxicity of mercury vapour was investigated by comparing the rate of spontaneous abortions among the wives of 152 workers occupationally exposed to mercury vapour with the rate among the wives of 374 controls in the same plant. The results indicate an increase in the rate of spontaneous abortions with an increasing concentration of mercury in the fathers' urine before pregnancy. At concentrations above 50 micrograms/l the risk of spontaneous abortion doubles (odds ratio (OR) = 2.26; 95% confidence interval (95% CI) = 0.99-5.23). Special care was taken to avoid bias in reporting abortions and known risk factors of spontaneous abortions do not seem to explain the results. Several biological mechanisms might account for them including, in particular, direct action of mercury on the paternal reproductive system and indirect toxicity to the mother or embryo through transport of mercury from the father. These indications could be of practical importance and should therefore be further documented.

Abortion, Spontaneous↗
PubMed1990

Reversibility of the effects of chronic paternal exposure to cyclophosphamide on pregnancy outcome in rats.

Low-dose chronic treatment of the male rat with the antitumor drug cyclophosphamide causes a time- and dose-dependent increase in pre- and post-implantation loss in the untreated females to which he is mated. The objective of the present study was to determine whether such effects are reversed, and if so at what time after cessation of drug treatment. Adult male Sprague-Dawley rats were gavage fed daily, 6 times per week for 9 weeks, with saline (control) or with 1 of 3 doses of cyclophosphamide, 1.4, 3.4 or 5.1 mg/kg/day. After the 9 weeks of treatment and at 2-week intervals thereafter, each male was mated with 2 females in proestrus. The females were caesarian sectioned 20 days later and pregnancy outcome assessed. After 9 weeks of drug treatment, pre-implantation loss increased more than 3-fold from 6% in the control group to 21% in the 5.1 mg/kg/day cyclophosphamide treatment group. Post-implantation loss increased in a dose dependent fashion from 5% in the control group to 74% in the 5.1 mg/kg/day cyclosphosphamide treatment group. Pre-implantation loss rapidly decreased upon cessation of treatment with cyclophosphamide: within 2 weeks it had returned to within the control range. Within just 2 weeks after termination of drug treatment in the 5.1 mg/kg/day cyclophosphamide treatment group, post-implantation loss decreased by half to 44%; it had decreased to 11% by 4 weeks and then was maintained at 4-6% thereafter. In the 3.4 mg/kg/day cyclophosphamide treatment group, post-implantation loss returned to the control range by 4 weeks. Thus, the effects of paternally administered cyclophosphamide on progeny outcome are reversible. The timing of reversal suggests that the effects on pre-implantation loss are due to a drug effect on spermatozoa either in the epididymis or near the time of spermiation while those on post-implantation loss are due to an additional effect on spermatids in the seminiferous tubules.

Abnormalities, Drug-Induced↗
PubMed1985

Ethylene dibromide: effects of paternal exposure on the neurotransmitter enzymes in the developing brain of F1 progeny.

The effects of ethylene dibromide (EDB) exposure to male rats on several neurotransmitter enzymes have been examined in various brain regions of the F1 progeny, from 7 to 90 days of age. The choline acetyltransferase activity was significantly increased at 21 days old, in most brain regions studied in the F1 progeny of the EDB-treated males, but not at 7, 14 or 90 days old. The acetylcholinesterase activity was altered in different brain regions of the F1 progeny of the EDB-exposed males at both 14 and 21 days old but not at 7 or 90 days old. Glutamic acid decarboxylase activity was increased in corpus striatum but decreased in frontal cortex only at 21 days of age. These neurochemical changes in the developing brain of F1 progeny of EDB-treated males at low doses may be associated with behavioral abnormalities observed early in their development.

Acetylcholinesterase↗
PubMed1987

Cyclophosphamide: effects of paternal exposure on the brain chemistry of the F1 progeny.

The effects of acute and chronic cyclophosphamide (CP) exposure to male rats on several neurotransmitter enzymes have been examined in various brain regions of the F1 progeny at 90 d old. The acute postmeiotic CP exposure to male rats induced significant biphasic changes in the choline acetyltransferase (ChAT) activity in various brain regions of F1 progeny; significant decreases in the cerebellar acetylcholinesterase (AChE) activity of the male (47%) and the female (14%) F1 progeny, and moderate decrease (26%) in the hippocampal AChE activity in the female F1 progeny; and a moderate increase (29%) in the temporo-cortical glutamic acid decarboxylase (GAD) activity of the female F1 rats. The chronic CP-exposed male rats resulted in a slight but significant decrease (16%) in the temporo-cortical ChAT activity in the female F1 progeny; a marked increase (51%) in the hypothalamic AChE activity in the male F1 progeny; and a marked decrease (32%) in cerebellar GAD activity and a slight increase (13%) in the striatal GAD activity in the female F1 progeny. These enzymatic changes in the adult brain of F1 progeny of CP-treated males may be associated with the behavioral abnormalities observed previously. Results suggest that these neurochemical parameters may be useful markers for analysis of the potential neurotoxicity of CP.

Acetylcholinesterase↗
PubMed1991

Paternal exposure to radiation and offspring cancer in mice: reanalysis and new evidence.

Parental exposure to radiation could induce various kinds of tumors in the next generation. In ICR mice, a large and significant increase of adult types tumor was observed in the F1 offspring after X-ray exposure at spermatozoa and spermatid stages, and less clear increase was observed after spermatogonial exposure. Mature oocytes were resistant upto 1 Gy, but very sensitive to tumor induction at higher doses. While there was no difference in the tumor incidence between acute and fractionated (0.36 Gy at 2 hr intervals) irradiation at post-gonial stages, a large reduction of tumor incidence was observed after spermatogonial and mature oocyte exposure, suggesting some repairs of X-ray damages in these germ cells. Acute lymphocytic leukemia was not induced in ICR and LT mice after spermatogonial exposure, while a large increase of adult type cancers was observed in F1 offspring. However, 1.9-3.2 fold and 4.5-7.4 fold increases of leukemia incidence were observed in ICR and LT mice, when spermatozoa stage was treated with the X-ray doses of 0.36-5.04 Gy and 3.6-5.04 Gy, respectively, indicating the large difference in the sensitivity of developing germ cells to leukemia induction by radiation in the F1 offspring. In contrast to ICR and LT mice, N5 strain developed about 10 or 18 times higher incidence of leukemia in the offspring after spermatogonial or spermatozoa exposure to 5.04 Gy of X-rays, respectively, showing a marked difference in the sensitivity to the leukemia induction by radiation between mouse strains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of paternal occupational exposure on spontaneous abortions.

BACKGROUND: Paternal exposure to mutagenic agents has been suggested to affect pregnancy outcome adversely. METHODS: A nationwide data base of medically diagnosed spontaneous abortions and other pregnancies and national census data was used to evaluate the effects of men's occupational exposures on risk of spontaneous abortion in 99,186 pregnancies in Finland. Census data from the years 1975 and 1980 provided information about the occupation, industry, and socioeconomic status. A job-exposure classification was developed to classify women and their husbands according to possible occupational exposures on the basis of their occupational title and industry. RESULTS: In 10% of the pregnancies, the husband was exposed to one or more of the mutagens, and the rate of spontaneous abortion was unaffected (OR = 1.0). Of the 25 specific mutagenic exposures evaluated, paternal exposure to four (ethylene oxide, rubber chemicals, solvents used in refineries, and solvents used in the manufacturing of rubber products) was associated with an increased relative risk of spontaneous abortion. In addition, the risk of spontaneous abortion was higher among wives of rubber products workers than among unexposed men. CONCLUSIONS: Although there is some biological rationale for the findings of this study, these findings need to be confirmed by studies in which individual exposures can be measured directly.

Abortion, Spontaneous↗
PubMed1987

Childhood nervous system tumors--an evaluation of the association with paternal occupational exposure to hydrocarbons.

Paternal occupational exposures to hydrocarbons have been associated with childhood nervous system cancer, but study results have not been consistent. This population-based case-control study was designed to examine this association using a large sample size to increase the precision of risk estimates. The birth certificates of 499 children who died in Texas from intracranial and spinal cord tumors were compared with 998 control certificates randomly selected from all Texas live births. Information on parental job title and industry at the time of birth was obtained from the birth certificates. No significant associations were identified for the dichotomized variable of all hydrocarbon-related occupations combined, as variously defined in previous studies, or for most of the specific jobs affiliated with exposures to hydrocarbons. Significant, relatively stable odds ratios (OR) were found for printers and graphics arts workers (OR = 4.5; 95% confidence interval (CI) = 1.4-14.7) and chemical and petroleum workers with high exposure levels (OR = 3.0; CI = 1.1-8.5). A discussion of the biases involved in this type of study design is presented.

Adolescent↗
PubMedDate not supplied

Neurochemical, but not behavioral, deviations in the offspring of rats following prenatal or paternal inhalation exposure to ethanol.

In addition to its widespread social use, ethanol is used extensively as an industrial solvent. Inhalation exposures to ethanol which produce narcosis in maternal rats are not teratogenic. The present study sought to extend the previous research by including offspring from paternal exposures, and testing for behavioral disorders in the offspring following maternal or paternal exposures. Groups of 18 male (approximately 450 g) and 15 female (200-300 g) Sprague-Dawley rats were exposed 7 hours/day for six weeks or throughout gestation to 16000, 10000, or 0 ppm ethanol by inhalation and then mated with untreated rats. Litters were culled to 4 males and 4 females, and were fostered within 16 hours after birth to untreated dams which had delivered their litters within 48 hours previously. Offspring from paternally or maternally exposed animals performed as well as controls on days 10-90 in tests of neuromotor coordination (ascent on a wire mesh screen, rotorod), activity levels (open field, modified-automated open field, and running wheel), and learning ability (avoidance conditioning and operant conditioning). In addition, brains of 10 21-day-old pups were analyzed for neurochemical differences from controls in concentrations of protein and the neurotransmitters acetylcholine, dopamine, norepinephrine, 5-hydroxytryptamine, substance P, Met-enkephalin, and beta-endorphin. Levels of acetylcholine, dopamine, substance P, and beta-endorphin were essentially unchanged in the offspring of rats exposed to ethanol. Complex, but significant changes in levels of norepinephrine occurred only in paternally exposed offspring. 5-Hydroxytryptamine levels were reduced in the cerebrum, and Met-enkephalin levels were increased in all brain regions of offspring from both maternally and paternally exposed rats.

Administration, Inhalation↗
PubMed1989

Parental occupational lead exposure and lead concentration of newborn cord blood.

The purpose of this study was to determine the influence of parental occupational lead exposure on the lead levels of newborn cord blood in the Taipei area. From September 1984 to June 1985, 5,000 pregnant women voluntarily participated in the study at the Taipei Municipal Maternal and Child Hospital. Each woman was interviewed regarding her and her husband's occupational exposures; 2,948 successfully delivered healthy newborns, and cord blood samples were obtained using Terumo Venoject, and 242 samples were analyzed by graphite furnace atomic absorption spectrometry using an Instrumentation Laboratory 251 instrument. Nine cord blood samples were from newborns with both parents exposed, 26 samples had maternal exposure only, 105 samples had paternal exposure only, and 102 were nonexposed. The results showed that the average lead level of cord blood with both parents exposed was 8.9 +/- 2.9 micrograms%, maternal exposure 9.0 +/- 3.8 micrograms%, paternal exposure 8.3 +/- 3.4 micrograms%, and 6.9 +/- 3.2 micrograms% in the nonexposed group. There were significant differences between the nonexposed and the maternal exposure groups, and also between the nonexposed and paternal exposure groups. All 26 maternal exposures were from lead soldering operations. Multivariate analysis revealed that, after control of father's exposure status, newborn cord blood lead level increased 0.27 micrograms% for each hour the mother spent on lead soldering during a normal working day, thus suggesting that soldering during pregnancy may be hazardous to newborns. Paternal contribution to the cord blood lead levels seemed to be through either working at home with the pregnant mother also at home or bringing work clothes home for laundering.

Adolescent↗
PubMed1989

Paternal occupational exposures and the risk of Down syndrome.

An exploratory case-control study of paternal occupation as a risk factor for Down syndrome was conducted. With the use of the British Columbia Health Surveillance Registry, 1,008 cases of live-born Down syndrome were identified for the period 1952-73. Two controls were matched to each case by using the birth files of British Columbia. Paternal occupation was obtained from the birth notice. Elevated maternal age-adjusted relative risks of Down syndrome were found for fathers employed as janitors (odds ratio [OR] = 3.26; 95% confidence interval [C.I.] = 1.02-10.44); mechanics (OR = 3.27; C.I. = 1.57-6.80); farm managers/workers (OR = 2.03; C.I. = 1.25-3.03); material-moving equipment operators (OR = 1.88; C.I. = 0.93-3.82); food processors (OR = 1.79; C.I. = 0.96-3.31); sheet-metal workers, iron workers, and other metalworkers (OR = 1.57; C.I. = 0.92-2.69); and sawmill workers (OR = 1.43; C.I. = 0.90-2.66). This large study provides new leads for further evaluation of the role of paternal exposures in the etiology of Down syndrome.

British Columbia↗
PubMed1992

Adverse pregnancy outcome and childhood malignancy with reference to paternal welding exposure.

Welding may deteriorate spermatogenesis and increase reproductive failures. This study examines reproductive end points in a Danish cohort of 10,059 metalworkers who fathered 3,569 children in 1973 through 1986. Occupational histories were gathered by postal questionnaires. Information on pregnancy outcomes and offspring was obtained by record linkage to medical registers. The occurrence of reduced birthweight, preterm delivery, infant mortality, and congenital malformation was not increased among children at risk from paternal welding exposure in comparison with children not at risk. The overall incidence of childhood malignancies among 23,264 children born in 1968 through 1986 with a total of 259,113 person-years of follow-up was equal to national rates (relative risk 0.97, 95% confidence interval 0.63-1.42). However, pregnancies preceding a birth at risk from paternal exposure to stainless steel welding were more often terminated by spontaneous abortion (odds ratio 1.9, 95% confidence interval 1.1-3.2). This finding needs cautious interpretation and should be further investigated in future studies.

Child↗