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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↗
PubMed2002

Paternal alcohol exposure affects sperm cytosine methyltransferase messenger RNA levels.

BACKGROUND: Although paternal alcohol exposure has been shown to affect the growth and behavior of offspring, the mechanisms underlying these effects still remain to be elucidated. This study examines one possible mechanism, namely, altered genomic imprinting as reflected by changes in sperm cytosine methyltransferase messenger RNA (mRNA) levels. METHODS: Male rats were treated with alcohol for 9 weeks before breeding. Resulting fetuses were counted and weighed, and paternal sperm was examined for changes in cytosine methyltransferase mRNA levels. RESULTS: Alcohol did not affect mating, fecundity, or litter size, but it did result in significantly decreased mean fetal weight, increased fetal runt incidence in offspring, and decreased cytosine methyltransferase mRNA levels in paternal sperm, compared with pair-fed and ad libitum controls. CONCLUSIONS: Alcohol-induced reductions in cytosine methyltransferase mRNA levels may reflect altered genomic imprinting caused by reduced DNA methylation, which, in turn, may lead to the expression of normally silent paternal alleles and may be a mechanism for paternal alcohol effects.

Alcohol Drinking↗
PubMed1998

Paternal alcohol exposure: developmental and behavioral effects on the offspring of rats.

The effect of paternal alcohol exposure on neurochemical and behavioral parameters was investigated using as a model system glial cells derived from newborn rat brain and cultured for 4 weeks. The total brain neurochemical parameters from rats born to mothers sired by an alcohol treated father were also investigated. Enzymatic markers of nerve cell development (enolase isoenzymes and glutamine synthetase) and the defense system (superoxide dismutase) against free radicals formed during alcohol degradation were measured in order to evaluate nerve cell damage. Behavioral locomotor tests (open-field, novelty-seeking, light/dark) were carried out to show long-lasting effects of paternal alcoholization on the offspring. Behavioral and developmental alterations were found until 1 year of age in the offspring and a significant growth retardation was observed in the males. Our results suggest that paternal alcohol exposure produces developmental and behavioral effects in the offspring. The consequence of either alcohol withdrawal during stage one spermatogenesis, or maternal diet supplementation with manganese during pregnancy were investigated. It was observed that some of the effects of paternal alcohol exposure on the offspring may be reversed by these treatments.

Animals↗
PubMed2001

Peripubertal paternal EtOH exposure.

Fetal alcohol syndrome usually implies effects on the offspring of maternal EtOH consumption during gestation, with fewer reports addressing the impact of paternal exposure on the progeny. One previous report has dealt with the impact of EtOH exposure on peripubertal male rats as a model of teenage drinking and the deleterious effects on the offspring. We report here findings examining the effect of 2 mo of EtOH feeding on male animals as they progressed through puberty on their ability to impregnate EtOH-naive female rats and characteristics of the subsequent litters. The EtOH-imbibing fathers weighed significantly less than pairfed controls and animals ingesting a non-EtOH liquid diet ad libitum. Nevertheless, they were able to mate successfully, although fecundity was significantly reduced. The number of successful pregnancies, defined as carried to term, was diminished from 92% in controls to 75% in EtOH-fed animals (p < 0.05). There was increased paternal testicular oxidative injury demonstrated by enhanced lipid peroxidation, protein oxidation, and decreased ratio of reduced to oxidized glutathione. The litter size of the EtOH-exposed males was reduced by 46%. The average litter size was 12.4+/-1.5 pups/litter in ad libitum animals, virtually identical to the 12.5+/-0.6 pups/litter in the pair fed controls. This is in sharp contrast to the 6.7+/-0.1 pups/litter from the paternal EtOH matings (p < 0.001). There was an increase in the average individual weight of pup offspring of paternally EtOH-exposed animals (p < 0.01 vs pair-fed controls and p < 0.05 vs ad libitum). Curiously, the male-to-female pup ratio was altered with a higher preponderance of male offspring from EtOH-fed fathers. There were no gross malformations noted among the pups. Insulin-like growth factor-1 levels in the pups at 10 d of age were unaltered between the groups. However, leptin was significantly elevated in the EtOH offspring. It appears that chronic EtOH exposure in the peripubertal fathers subsequently decreases fecundity and that this may be mediated by testicular oxidative injury, perhaps leading to accelerated germ cell apoptosis.

Animals↗
PubMed1995

Effects of parental occupational exposure to lead and other metals on spontaneous abortion.

The aim of this article was to summarize the epidemiologic studies on the possible impact of parental occupational exposure to lead or other metals on spontaneous abortion. For paternal exposure, the total number of abortions in the studies with adequate exposure contrast were 340 for lead, 240 for mercury, and 90 for unspecified metals and, correspondingly, for maternal exposure, about 80 for lead, 80 for mercury, 70 for nickel, and 130 for exposure to unspecified metals. Epidemiologic studies indicate that paternal exposure to lead or mercury might be associated with the risk of spontaneous abortion. For maternal exposure, no clear conclusion could be reached. In particular, paternal occupational exposure levels to metals were substantial compared with population values. Even though there are shortcomings in the present knowledge, protective goals for paternal exposure to lead and mercury are warranted. More well-designed studies on metals are needed.

Abortion, Spontaneous↗
PubMed1998

Paternal dioxin, preterm birth, intrauterine growth retardation, and infant death.

We studied paternal exposure to Agent Orange and its dioxin contaminant (2,3,7,8-tetrachlorodibenzo-p-dioxin) and preterm birth, intrauterine growth retardation, or infant death in veterans of Operation Ranch Hand, the unit responsible for spraying herbicides during the Vietnam war. A Comparison group of Air Force veterans who served in Southeast Asia during the same time period and who were not occupationally exposed to herbicides was included. We studied children conceived during or after the father's service in Southeast Asia and based exposure on paternal dioxin measured in 1987 or 1992 extrapolated to the time of conception of the child. We assigned each child to one of four exposure categories: Comparison and three Ranch Hand categories (Background, Low, High). Children in the High (relative risk = 1.3) and Background (relative risk = 1.4) categories were at increased risk of preterm birth. The risk of intrauterine growth retardation was not increased in any exposure category. The risk of infant death was increased in all Ranch Hand children, with the greatest increases in the High (relative risk = 4.5) and Background (relative risk = 3.2) categories. These patterns indicate that the increases in the relative risk of preterm birth and infant death may not be related to paternal dioxin level.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1997

Paternal occupational exposure around conception and spina bifida in offspring.

A multi-center case-referent study was conducted on the relation between paternal occupational exposure and spina bifida in offspring. Cases were born between 1980 and 1992 in The Netherlands. Referents were recruited from hospitals and from the general population. Postal questionnaires were used to gather information on occupation and potential confounders. Through job-specific telephone interviews with 122 case fathers and 411 referent fathers, detailed exposure information was collected on specific tasks, the use of chemical or physical agents, frequency of exposure, and use of protective equipment. The study yielded statistically significant associations between spina bifida and low exposure to welding fumes (OR = 1.6, 95% CI: 1.0-2.6) and low exposure to UV radiation during welding (OR = 2.6, 95% CI: 1.2-5.6), and suggestive findings of an association between spina bifida and moderate or high exposure to cleaning agents, moderate or high pesticide exposure (OR = 1.7, 95% CI: 0.7-4.0), and stainless steel dust (OR = 2.0, 95% CI: 0.8-5.2). No associations were identified for other paternal occupational exposures, such as organic solvents.

Case-Control Studies↗
PubMed2006

Maternal and paternal occupational exposure to agricultural work and the risk of anencephaly.

AIMS: To evaluate the association between parental occupational exposure to agricultural work and the risk of anencephaly in three Mexican states. METHODS: A paired case control study (1:1) was done based on records of the Epidemiological Surveillance System of Neural Tube Defects in Mexico; 151 cases of anencephaly of more than 20 weeks' gestation were selected between March 2000 and February 2001. Controls were selected from the same maternity services as those of the cases and were born alive without congenital malformations. Information was obtained from both parents by means of a general questionnaire, a food frequency questionnaire, and a specific questionnaire on occupational exposure to pesticides. Exposures were analysed with emphasis on the three months before and one month after the last menstruation periods (acute risk period (ARP)), as well as exposure prior to the above mentioned period (non-acute risk period (NARP)). RESULTS: The children of mothers who worked in agriculture in the ARP had a greater risk of anencephaly (OR = 4.57, 95% CI 1.05 to 19.96). The risk of fathers having a child with anencephaly was greater in those who applied pesticides irrespective of whether it was done in the ARP or the NARP (OR = 2.50, 95% CI 0.73 to 8.64; and OR = 2.03, 95% CI 0.58 to 7.08, respectively). CONCLUSIONS: These results support the hypothesis of the effect of maternal exposure to agricultural work on anencephaly and suggest that exposure of the father to pesticides in the periconceptional period or prior to this can also increase the risk of having an anencephalic child.

Adolescent↗
PubMed2006

Paternal occupational exposure to radiofrequency electromagnetic fields and risk of adverse pregnancy outcome.

BACKGROUND: During the last decades, public concern that radiofrequency radiation (RFR) may be related to adverse reproductive outcomes has been emerging. Our objective was to assess associations between paternal occupational exposure to RFR and adverse pregnancy outcomes including birth defects using population-based data from Norway. METHODS: Data on reproductive outcomes derived from the Medical Birth Registry of Norway were linked with data on paternal occupation derived from the general population censuses. An expert panel categorized occupations according to exposure. Using logistic regression, we analyzed 24 categories of birth defects as well as other adverse outcomes. RESULTS: In the offspring of fathers most likely to have been exposed, increased risk was observed for preterm birth (odds ratio (OR): 1.08, 95% confidence interval (CI): 1.03, 1.15). In this group we also observed a decreased risk of cleft lip (OR: 0.63, 95% CI: 0.41, 0.97). In the medium exposed group, we observed increased risk for a category of "other defects" (OR: 2.40, 95% CI: 1.22, 4.70), and a decreased risk for a category of "other syndromes" (OR: 0.75, 95% CI: 0.56, 0.99) and upper gastrointestinal defects (OR: 0.61, 95% CI: 0.40, 0.93). CONCLUSION: The study is partly reassuring for occupationally exposed fathers.

Abnormalities, Radiation-Induced↗
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↗
PubMed2007

Paternal occupational exposure to electro-magnetic fields as a risk factor for cancer in children and young adults: a case-control study from the North of England.

BACKGROUND: Numerous studies have implied that paternal occupational exposures, in particular electromagnetic fields (EMF) and ionizing radiation, may be involved in the etiology of childhood cancers. We investigated whether an association exists between paternal occupations at birth involving such exposures and cancer risk in offspring, using data from the Northern Region Young Persons' Malignant Disease Registry (NRYPMDR). PROCEDURE: Cases (n=4,723) were matched, on sex and year of birth, to controls from two independent sources: (i) all other patients from the NRYPMDR with a different cancer, (ii) 100 cancer-free individuals per case from the Cumbrian Births Database. An occupational exposure matrix was used to assign individuals to exposure groups. RESULTS: There was an increased risk of leukemia among the offspring of men employed in occupations likely to be associated with EMF or radiation exposures (OR 1.31, 95% CI 1.02-1.69), particularly in males aged less than 6 years (OR 1.81, 95% 1.19-2.75). No significant association was seen in females. Increased risks were also seen for chondrosarcoma (OR 8.7, 95% CI 1.55-49.4) and renal carcinoma (OR 6.75, 95% CI 1.73-26.0). These associations were consistent between control groups and remained after adjustment for socio-economic status. CONCLUSIONS: This large case-control study identified a significantly increased risk of leukemia among the offspring of men likely to have been occupationally exposed to EMF, with differing associations between males and females. Increased risks of chondrosarcoma and renal carcinoma were also seen, although based on smaller numbers. Further detailed investigations in this area are required to understand this association.

Adolescent↗
PubMed2006

Consequences of paternal cocaine exposure in mice.

The present study examined the potential neuroteratological effects of paternal cocaine (COC) exposure using the novel mouse model of inhalational drug administration. In this model, mice were trained to self-administer COC in multi-hour daily inhalation sessions reminiscent of crack binges. The controls included males pair-fed with COC-inhaling animals as well as ad-lib-fed males. All males were bred with drug-naive females. The newborn pups sired by COC-inhaling males had a reduced biparietal head diameter, suggesting a decreased cerebral volume. When the pups reached adulthood, their sustained visuo-spatial attention and spatial working memory were tested using a 5-arm maze paradigm. During the attention tests, the percentage of correct trials at the shortest stimulus duration employed in the study (0.5 s) was significantly lower for the male offspring of COC-inhaling fathers as compared to the offspring of both pair-fed and ad-lib-fed controls. For the females sired by COC-inhaling fathers, the deficit was observed at light stimulus durations of 0.5 and 0.75 s. Also, during the working memory tests, the male offspring of COC-inhaling fathers required more sessions than the offspring of either pair-fed or ad-lib-fed fathers to reach the selected criterion at retention intervals of 16 min and longer. The impairment of working memory in female offspring of COC-inhaling fathers was even stronger, as the offspring needed more sessions to reach the criterion as compared to their control counterparts, even at retention intervals as short as 4 min. These findings suggest that paternal COC abuse prior to coitus may impact the development of the offspring, particularly if they are females. We further showed that chronic COC exposure in male mice does not result in substantial breakage of spermatozoal DNA, but significantly alters expression of DNA methyltransferases 1 and 3a in the germ cell-rich seminiferous tubules of the testis. Since these enzymes are essential for generating and maintaining parental gene imprinting in germ cells, our observations point to an intriguing possibility that COC may cause paternally induced neuroteratological effects by interfering with gene-imprinting patterns in male gametes.

Administration, Inhalation↗
PubMed1995

Adverse effects of paternal opiate exposure on offspring development and sensitivity to morphine-induced analgesia.

We have shown previously that chronic morphine administration to adolescent male rats produced a number of gender specific deficits in their offspring. The purpose of the present studies was to extend our earlier observations by examining the acute, direct effects of morphine exposure to male rats on their fertility and the development of viable offspring. Sexually mature male rats were injected with a single dose of morphine (25 mg/kg) and 24 hr later were bred with drug-naive females. Fertility rates (vaginal plugs and pregnancies) were monitored throughout the breeding period as was the development of the offspring. Our results showed that a large, acute dose of morphine given to drug-naive male rats 24 hr before the initiation of breeding had no effect on fertility rates, but produced several adverse effects on fetal outcome. Litter sizes in morphine-derived offspring were considerably smaller than in controls and mortality rates were more than 6 times higher. Moreover, morphine-derived male, but not female, offspring had a significantly enhanced sensitivity to the antinociceptive effects of morphine. Collectively, these data suggest that acute paternal morphine exposure just before breeding with drug-naive females had no effect on fertility, but exerted negative effects on the viability and development of their offspring. These results represent the most compelling evidence to date that paternal opiate exposure can adversely affect fetal outcome and are particularly striking in that they were produced by a single injection of morphine. We are aware of no animal studies, clinical cases or anecdotal reports in humans in which such a phenomenon has been described.

Analgesia↗
PubMed1995

Parental exposures to pesticides and risk of Wilms' tumor in Brazil.

Wilms' tumor is one of the most common abdominal childhood malignancies. Wilms' tumor rates in Brazil are among the highest in the world. This prompted the Brazilian Wilms' Tumor Study Group to conduct a hospital-based, multicenter, case-control investigation of environmental risk factors for the disease. Between April 1987 and January 1989, the authors collected information on relevant occupational exposures by interviewing the parents of 109 Wilms' tumor cases admitted to hospitals in Sao Paulo, Salvador, Belo Horizonte, and Jau. Also interviewed were the parents of 218 age- and sex-matched control children who had been admitted for treatment of nonneoplastic diseases to the same or nearby hospitals. Odds ratios (ORs) adjusted for income and education were calculated by conditional logistic regression. Consistently elevated risks were seen for farm work involving frequent use of pesticides by both the father (OR = 3.24, 95% confidence interval (CI) 1.2-9.0) and the mother (OR = 128.6, 95% CI 6.4-2,569). These risk elevations were restricted to cases diagnosed after 2 years of age (ORs > 4), for paternal exposure, and after 4 years of age (OR = 14.8, 95% CI 2.2-98.8), for maternal exposure. Risk elevations were also more pronounced among boys (paternal exposure OR = 8.56, 95% CI 2.1-35.1; maternal exposure OR = 4.60, 95% CI 0.8-26.4) than among girls (paternal exposure OR = 1.31, 95% CI 0.4-4.1; maternal exposure OR = 2.03, 95% CI 0.5-8.9).

Age Factors↗
PubMed1982

Survey of reproductive events of wives of employees exposed to chlorinated dioxins.

To determine whether paternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or other polychlorinated dioxins might be associated with adverse pregnancy outcomes, an interviewer-administered questionnaire survey was conducted among wives of Dow Michigan Division employees in the Midland, Michigan, area who had been potentially exposed to dioxins. A control group consisted of wives of employees who had no dioxins exposure and whose hire dates were comparable to those of the men in the exposed group. A total of 737 conceptions, which resulted in 637 live births and 10 stillbirths and spontaneous abortions, were identified as having paternal exposure; 2031 conceptions, resulting in 1785 live births and 246 stillbirths and spontaneous abortions, were identified as having no paternal exposure to any isomer of dioxin. Odds ratios were calculated for dependent variables consisting of spontaneous abortions, stillbirths, infant deaths and several categories of congenital malformations. Trend analysis was performed for duration-of-paternal-exposure of 12 months or less, or more than 12 months. Overall, no statistically significant associations were found between any exposure and pregnancy outcome, either before or after stratification by pertinent sets of up to nine covariables.

Abnormalities, Drug-Induced↗
PubMed2006

Exposure to paternal alcoholism does not predict development of alcohol-use disorders in offspring: evidence from an offspring-of-twins study.

OBJECTIVE: Using an offspring-of-twins design, we tested the hypothesis that exposure to paternal alcoholism during the child's first 12 years will increase offspring risk for subsequent alcohol-use disorders (AUD). METHOD: Structured psychiatric interviews assessed history of psychiatric and substance-use disorders in Vietnam Era Twin Registry fathers (n = 512), their offspring (n = 877), and mothers of the offspring (n = 507). Exposure was defined as the fathers' endorsement of any Diagnostic and Statistical Manual of Mental Disorders (DSM), Fourth Edition, AUD symptom, according to the Lifetime Drinking History assessment (administered in 1999), at any time between off- spring ages 0-12 years; all fathers had satisfied DSM, Third Edition, Revised (DSM-III-R), criteria for alcohol dependence in a 1992 diagnostic interview. Cox proportional hazards models were fit to predict time to first symptom of abuse/dependence in offspring. RESULTS: Off- spring exposed to paternal alcoholism were significantly more likely to develop an AUD when compared with offspring of nonalcoholic fathers (hazard ratio [HR] = 1.51; 95% confidence interval [CI]: 1.10-2.07). Although offspring unexposed to paternal alcoholism did not significantly differ from control offspring (HR = 1.50, 95% CI: 0.93-2.41), the magnitude of association was similar to that in the exposed offspring. There were no significant differences in AUD between offspring of alcoholics who were exposed and those who were not exposed to paternal alcoholism, as long as fathers had satisfied DSM-III-R criteria for alcohol dependence at some point in their lives. CONCLUSIONS: There does not appear to be a relationship between exposure to paternal alcoholism during childhood and development of an AUD in offspring. Genetic and high-risk environmental factors that are correlated with lifetime paternal alcoholism may be stronger predictors of offspring AUD than fathers' problem drinking. Future research should be encouraged, using more comprehensive analyses, to examine the role of family genetic influences and other family environmental influences on offspring alcohol outcomes.

Adult↗