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PubMed1998

Time to pregnancy among the wives of men exposed to organic solvents.

OBJECTIVES: To assess whether paternal exposure to organic solvents is associated with decreased fertility. METHODS: A retrospective time to pregnancy study was conducted among men biologically monitored for organic solvents. The workers were classified into exposure categories on the basis of work description and the use of solvents as reported in the questionnaires, and on biological exposure measurements. The relative fecundability density ratios (FDR--an analogue of incidence density ratio of clinically recognised pregnancies) were calculated with discrete proportional hazards regression. RESULTS: After three mailings 316 (72.1%) wives of the monitored men participated. The final study population consisted of 282 couples who did not use contraception at the beginning of pregnancy. The FDRs, adjusted for potential confounders, were 0.80 (95% confidence interval (95% CI) 0.57 to 1.11) and 0.74 (95% CI 0.51 to 1.06) for high or frequent and low or intermediate exposure, respectively. High or frequent and low or intermediate exposure were related to decreased fecundability among primigravida (FDRs 0.36; 95% CI 0.19 to 0.66 and 0.53; 95% CI 0.27 to 1.04) but not among couples with at least one previous pregnancy (FDRs 0.96; 95% CI 0.62 to 1.49 and 0.77; 95% CI 0.47 to 1.24). CONCLUSIONS: The findings of the study provide limited support for the hypothesis that paternal exposure to organic solvents might be associated with decreased fertility. Further studies with careful design are warranted.

Adolescent↗
PubMed2002

[Study on risk factors of cryptorchidism].

OBJECTIVE: Cryptorchidism is the most common urogenital congenital malformations in males, which increases male infertility and testicular tumors. It is necessary to identify its risk factors. METHODS: A hospital-based case-control study was conducted. Cases were 99 boys with cryptorchidism with two matched controls per case were randomly selected. Both cases and controls were interviewed with a uniformed questionnaire by face to face. Conditional logistic regression model was used for univariable and multivariate analysis by SAS6.12 computer software was used to estimate odds ratios (OR) and their 95 per cent confidence internals (95% CI). RESULTS: Multiple conditional logistic regression analysis showed that cryptorchidism was positively associated with maternal common cold accompanied fever in the first trimester (OR = 9.37, 95% CI: 2.25 - 39.09), with threatened abortion in the first and/or second trimester (OR = 4.66, 95% CI: 2.02 - 10.74), maternal preeclampsia during pregnancy (OR = 16.33, 95% CI: 1.40 - 191.20), paternal exposure to pesticides occupationally (OR = 12.79, 95% CI: 2.90 - 56.43), neonatal low birth weight (OR = 5.77, 95% CI: 1.39 - 23.98), and maternal age under 24 years (OR = 2.89, 95% CI: 1.29 - 4.06). CONCLUSIONS: The risk factors of cryptorchidism were maternal common cold accompanied fever in the first trimester, threatened abortion in the first and/or second trimester, maternal preeclampsia during pregnancy, paternal exposure to pesticides occupationally, neonatal low birth weight, maternal age under 24 years.

Case-Control Studies↗
PubMed1990

Paternal occupational exposure to electromagnetic fields and neuroblastoma in offspring.

Investigators in Texas have reported an association between paternal employment in jobs linked with exposure to electromagnetic fields and risk of neuroblastoma in offspring. In an attempt to replicate this finding, the authors conducted a case-control study in Ohio. A total of 101 incident cases of neuroblastoma were identified through the Columbus (Ohio) Children's Hospital Tumor Registry. All cases were born sometime during the period 1942-1967. From a statewide roster of birth certificates, four controls were selected for each case, with individual matching on the case's year of birth, race, and sex, and the mother's county of residence at the time of the (index) child's birth. Multiple definitions were employed to infer the potential for paternal occupational exposure to electromagnetic fields from the industry/occupation statements on the birth certificates. Case-control comparisons revealed adjusted odds ratios ranging in magnitude from 0.5 to 1.9. For two of the exposure definitions employed--both of which are similar to one used by the Texas investigators--the corresponding odds ratios were modestly elevated (odds ratios = 1.6 and 1.9). Notably, the magnitude of these odds ratios is not inconsistent with the Texas findings, where the exposure definition referred to yielded an odds ratio of 2.1. Because the point estimates in this study are imprecise, and because the biologic plausibility of the association is uncertain, the results reported here must be interpreted cautiously. However, the apparent consistency between two independent studies suggests that future evaluation of the association is warranted.

Adolescent↗
PubMed2000

Birth defects and paternal occupational exposure. Hypotheses tested in a record linkage based dataset.

UNLABELLED: MAIN QUESTION: To test previously established hypotheses on associations of birth defects with paternal occupation on the basis of a Norwegian registry material. METHODS: The study comprised all births in Norway 1970 -1993 for which linkage with population censuses 1970, -80 and -90 on parents' job title could be obtained--about 1 million births (75% all births). The reference population was offspring of the group that did not belong to the actual occupation. RESULTS: Vehicle mechanics had an association with hypospadias--OR 5.19 (CI 1.31-14.24), painters had a non-significant association with spina bifida--OR 2.03 (CI 0.99-3.75) and printers with club foot--OR 1.61 (CI 0.89-2.90). Associations observed previously in off-spring of fathers in large occupational groups such as teachers, drivers, electricity related occupations, sales related occupations and agricultural workers were not confirmed in this dataset. CONCLUSIONS: The study gave further evidence of cause effect relationships in the confirmed positive associations, though without any clarification of possible mechanisms involved. Possible false negative findings might be caused by low statistical power due to small occupational groups or non-differential misclassification of exposure.

Adult↗
PubMedDate not supplied

Review of experimental male-mediated behavioral and neurochemical disorders.

Paternal exposures to exogenous agents have been reported to produce a variety of developmental defects in the offspring. In experimental animals, these effects include decreased litter size and weight, increased stillbirth and neonatal death, birth defects, tumors, and functional/behavioral abnormalities-some of these effects being transmitted to the second and third generations. This article reviews the exogenous agents that have reportedly caused behavioral or neurochemical alterations in offspring of experimental animals following paternal exposures, including advanced age, alcohols, cyclophosphamide, ethylene dibromide, lead, opiates, and a few miscellaneous chemicals. Based upon the consistency of effects in several of these agents in a variety of studies in experimental animals, the conclusion is that paternal exposures may contribute to the incidence of neurobehavioral disorders in humans.

Age Factors↗
PubMedDate not supplied

Paternal alcohol exposure and Turner syndrome.

AIMS: Turner syndrome (TS) is a sex chromosome aneuploidy that occurs as a result of a non-disjunctional error in meiosis I or anaphase lag; however, the aetiology of this disorder remains unknown. Anecdotal evidence suggests that paternal alcoholism may play an unidentified role in the aetiology of TS. Accordingly, the primary objective of this study was to determine the potential association between paternal alcohol exposure and TS. METHODS: The questionnaire was designed to solicit information about the parents' health and lifestyle habits occurring 1 year prior to and throughout the pregnancy of their daughter with TS. Alcohol dependence was assessed by the Brief Michigan Alcohol Screening Test (BMAST). The study population was solicited from the Turner's Syndrome Society of Canada and included any parent(s) having a child with TS who was of any age. Two hundred and twelve families completed and returned the survey. RESULTS: This provided a response rate of 86.5%. Six of the fathers (3.6%; n = 166) and six of the mothers (3.6%; n = 165) had scores of 5 or more on the BMAST (scores of 5+ are considered to be in the 'alcoholic range'). This is considerably lower than the population norm of 9.5%. CONCLUSIONS: Our study has suggested there is no association between paternal or maternal alcohol consumption and TS.

Adolescent↗
PubMed2002

Risk of birth defects by parental occupational exposure to 50 Hz electromagnetic fields: a population based study.

OBJECTIVES: To study the risk of birth defects by parental occupational exposure to 50 Hz electromagnetic fields. METHODS: The Medical Birth Registry of Norway was linked with census data on parental occupation. An expert panel constructed a job exposure matrix of parental occupational exposure to 50 Hz magnetic fields. Exposure to magnetic fields was estimated by combining branch and occupation into one of three exposure levels: <4 hours, 4-24 hours, and >24 hours/week above approximately 0.1 mu T. Risks of 24 categories of birth defects were compared across exposure levels. Out of all 1.6 million births in Norway in the period 1967-95, 836,475 and 1,290,298 births had information on maternal and paternal exposure, respectively. Analyses were based on tests for trend and were adjusted for parents' educational level, place of birth, maternal age, and year of birth. RESULTS: The total risk of birth defects was not associated with parental exposure. Maternal exposure was associated with increased risks of spina bifida (p=0.04) and clubfoot (p=0.04). A negative association was found for isolated cleft palate (p=0.01). Paternal exposure was associated with increased risks of anencephaly (p=0.01) and a category of "other defects" (p=0.02). CONCLUSION: The present study gives an indication of an association between selected disorders of the central nervous system and parental exposure to 50 Hz magnetic fields. Given the crude exposure assessment, lack of comparable studies, and the high number of outcomes considered, the results should be interpreted with caution.

Adult↗
PubMed1998

Parental occupational exposures and risk of childhood cancer.

Occupational exposures of parents might be related to cancer in their offspring. Forty-eight published studies on this topic have reported relative risks for over 1000 specific occupation/cancer combinations. Virtually all of the studies employed the case-control design. Occupations and exposures of fathers were investigated much more frequently than those of the mother. Information about parental occupations was derived through interviews or from birth certificates and other administrative records. Specific exposures were typically estimated by industrial hygienists or were self-reported. The studies have several limitations related to the quality of the exposure assessment, small numbers of exposed cases, multiple comparisons, and possible bias toward the reporting of positive results. Despite these limitations, they provide evidence that certain parental exposures may be harmful to children and deserve further study. The strongest evidence is for childhood leukemia and paternal exposure to solvents, paints, and employment in motor vehicle-related occupations; and childhood nervous system cancers and paternal exposure to paints. To more clearly evaluate the importance of these and other exposures in future investigations, we need improvements in four areas: a) more careful attention must be paid to maternal exposures; b) studies should employ more sophisticated exposure assessment techniques; c) careful attention must be paid to the postulated mechanism, timing, and route of exposure; and d) if postnatal exposures are evaluated, studies should provide evidence that the exposure is actually transferred from the workplace to the child's environment.

Brain Neoplasms↗
PubMed1995

Effects of parental exposure to solvents on pregnancy outcome.

The findings and methodological issues of epidemiologic studies on adverse developmental effects of parental occupational exposure to organic solvents are reviewed. The studies on maternal effects suggest that high exposure to solvents may increase the risk of spontaneous abortion, but the findings on congenital malformations are inconsistent. Suggestive associations of spontaneous abortions have also been observed with some particular solvents. The evidence appears to be most adequate for toluene. Evidence on the effects of paternal exposure to solvents on pregnancy outcome is limited and inconsistent. Suggestive results link paternal exposure to spontaneous abortion, congenital malformation, and low birth weight or preterm birth. A common methodological weakness in these studies is the inaccurate data on exposure. Positive findings encourage further studies with an improved study design and methods, particularly with improved assessment of exposure.

Abortion, Spontaneous↗
PubMed1990

Paternal alcohol exposure: paradoxical effect in mice and rats.

Male mice consumed liquid alcohol diets containing 25%, 10% or 0% ethanol-derived calories (EDC). Animals receiving the 10 and 0% EDC diets were pair fed to those consuming the 25% EDC diet. After 7 or 14 weeks of consumption, males were bred to non-treated females. Offspring were tested for swimming behavior at 75 days of age. Offspring sired by alcohol-consuming males were more immobile regardless of duration of paternal alcohol consumption or housing conditions (group or isolated). Imipramine (5, 15 mg/kg) reversed this effect such that after drug treatment, alcohol-sired offspring were less immobile than controls. Propranolol (1, 3 mg/kg) eliminated the group differences. Yohimbine (1, 10 mg/kg) significantly increased immobility in all groups but did not reverse the effects of paternal alcohol consumption. Metergoline (1 mg/kg) increased immobility in all groups but did not reverse the effects of paternal alcohol exposure. When rat offspring of alcohol-consuming fathers were tested, their swimming behavior was opposite to that of mice (i.e., rats were less immobile). However, as observed in mice, the effect was reversed by imipramine. These results extend the evidence for paternally mediated behavioral mutagenesis. They also indicate that the direction of induced changes are species dependent and that some of these effects, regardless of direction of change, are mediated by neurochemical changes sensitive to imipramine.

Animals↗
PubMed2005

Paternal organic solvent exposure and adverse pregnancy outcomes: a meta-analysis.

BACKGROUND: Organic solvents are widely used, but conflicting reports exist concerning paternal exposure and adverse pregnancy outcomes. We conducted a meta-analysis to assess the risks of spontaneous abortions (SAs) and major malformations (MMs) after paternal exposure to organic solvents. METHODS: Medline, Toxline, Reprotox, and Embase from 1966 to 2003 were searched. Two independent reviewers searched for cohort and case-control studies in any language on adult human males exposed chronically to any organic solvent. Two non-blinded independent extractors used a standardized form for data extraction; disagreements were resolved through consensus discussion. RESULTS: Forty-seven studies were identified; 32 exclusions left 14 useable studies. Overall random effects odds ratios and 95% confidence intervals (CI95%) were 1.30 (CI95%: 0.81-2.11, N=1,248) for SA, 1.47 (CI95%: 1.18-1.83, N=384,762) for MMs, 1.86 (CI95%: 1.40-2.46, N=180,242) for any neural tube defect, 2.18 (CI95%: 1.52-3.11, N=107,761) for anencephaly, and 1.59 (CI95%: 0.99-2.56, N=96,517; power=56.3%) for spina bifida. CONCLUSIONS: Paternal exposure to organic solvents is associated with an increased risk for neural tube defects but not SAs.

Abnormalities, Drug-Induced↗
PubMed2002

Sex ratios of children of Russian pesticide producers exposed to dioxin.

We investigated the sex ratio of children of pesticide workers who produced the biocide trichlorophenol and the herbicide 2,4,5-trichlorophenoxy acetic acid from 1961 to 1988 in the city of Ufa, Bashkortostan, Russia. We measured exposure of the two related cohorts to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dioxins by analyzing 84 blood samples, which produced median TCDD toxic equivalents blood lipid values of 240 ng/kg, which are more than 30 times higher than background or normal exposure from the region. The sex ratio (fraction male) of the combined cohort of 227 children from 150 male and 48 female workers was 0.40, significantly lower (z-test for proportions = 3.21; p < 0.001) than those for the city of Ufa (0.512) and elsewhere worldwide. When we analyzed the sex ratio of the children according to maternal or paternal exposure, we observed a decrease in the number of boys (ratio 0.38) for fathers and a normal number (ratio 0.51) for the mothers. Human exposure of these pesticide producers to high levels of dioxins is associated with the birth of more girls, but only for paternal exposures.

Adult↗
PubMed1994

Paternal cyclophosphamide exposure causes decreased cell proliferation in cleavage-stage embryos.

Exposure of the male germ cell to cyclophosphamide during spermatogenesis and sperm maturation can interfere with development of the embryo. When male rats were treated with a chronic low dose of cyclophosphamide for 4 wk there was a dramatic increase in early postimplantation loss in their progeny, characterized by implantation sites selectively lacking in embryonic tissues. The present study was designed to determine the earliest appearance of a paternal effect of cyclophosphamide treatment and to examine whether the embryonic lineage was selectively affected. Male Sprague-Dawley rats were orally dosed for 4-5 wk with saline or 6 mg/kg per day of cyclophosphamide; their progeny were obtained on Days 2, 2.5, 3, 4, and 4.5 of gestation. Paternal cyclophosphamide treatment had no effect on the mean number of embryos per pregnant female. However, as early as Day 3 of gestation, there was a significant decrease in cell number among the embryos sired by cyclophosphamide-treated males, increasing to a greater than 50% decrease in cell number by Day 4. The cell doubling time in embryos sired by treated males (16 h) was longer than that of controls (12 h). This decreased proliferation rate was confirmed by a dramatic decrease in the capacity of both Day 3 and Day 4 embryos sired by cyclophosphamide-treated males to incorporate [3H]thymidine over a 26-h culture period. Cytogenetic analysis in a limited number of blastomeres entering metaphase revealed no evidence of chromosomal abnormalities. Both the trophectoderm and the inner cell mass cells were proportionally decreased in Day 4.5 embryos sired by cyclophosphamide-treated males. Thus, paternal cyclophosphamide exposure affected both cell lineages in the conceptus as early as Day 3 of gestation.

Animals↗
PubMed1993

Paternal radiation exposure and leukaemia in offspring: the Ontario case-control study.

OBJECTIVES: To test the hypothesis that there is an association between childhood leukaemia and the occupational exposure of fathers to ionising radiation before a child's conception. DESIGN: Case-control study with eight matched controls per case. SETTING: Regions of Ontario, Canada, with an operating nuclear facility. SUBJECTS: Cases were children (age 0-14) who died from or were diagnosed as having leukaemia from 1950 to 1988 and were born to mothers living in the vicinity of an operating nuclear facility. Controls were identified from birth certificates, matched by date of birth and residence at birth. There were 112 cases and 890 controls. MAIN OUTCOME MEASURES: Paternal radiation exposure was determined by a record linkage to the Canadian National Dose Registry. RESULTS: Six fathers of cases and 53 fathers of controls had had a total whole body dose > 0.0 mSv before the child's conception, resulting in an odds ratio of 0.87 (95% confidence interval 0.32 to 2.34). There was no evidence of an increased leukaemia risk in relation to any exposure period (lifetime or six months or three months before conception) or exposure type (total whole body dose, external whole body dose, or tritium dose), except for radon exposure to uranium miners, which had a large odds ratio that was not significantly different from the null value. CONCLUSIONS: The findings of this study in Ontario did not support the hypothesis that childhood leukaemia is associated with the occupational exposure of fathers to ionising radiation before the child's conception.

Adolescent↗
PubMedDate not supplied

Acute treatment of paternal alcohol exposure produces malformations in offspring.

Male rats were intubated only once with either 6, 4, 2, or 0 g/kg alcohol. Food was removed from all animals for several hours after intubation. Males were bred with a single female until sperm was observed in the vaginal smear, for up to a maximum of 7 days after treatment. Females were sacrificed on gestation day 20. There were no significant effects on mating, fecundity, or litter size, but there were significant dose-response increases in "runts" and significant linear associations in the number of malformations in alcohol-sired offspring. A second study using the same methodology found similar results. The results indicate that a single acute treatment with alcohol just prior to breeding may have a significant effect on offspring.

Abnormalities, Drug-Induced↗
PubMed2001

K-ras mutations in mouse lung tumors of extreme age: independent of paternal preconceptional exposure to chromium(III) but significantly more frequent in carcinomas than adenomas.

Preconceptional exposure of male NIH Swiss mice to chromium(III) chloride resulted in increased incidence of neoplastic and non-neoplastic changes in their progeny, including lung tumors in females [Toxicol. Appl. Pharmacol. 158 (1999) 161-176]. Since mutations in the K-ras protooncogene are frequent, early changes in mouse lung tumors, we investigated possible mutational activation of this gene as a mechanism for preconceptional carcinogenesis by chromium(III). These offspring had lived until natural death at advanced ages (average 816+/-175 days for controls, 904+/-164 for progeny of chromium-treated fathers). Mutations of K-ras, analyzed by single-strand conformation polymorphism and sequencing, were, in codon 12, wild type GGT (glycine), to GAT (aspartic acid); to GTT (valine); and to CGT (arginine); and in codon 61, wild-type CAA (glutamine), to CGA (arginine). K-ras mutation frequencies in lung tumors were very similar in control progeny (4/14) and in progeny of chromium-treated fathers (5/15). Thus, germline mutation or tendency to spontaneous mutation in K-ras does not seem to be part of the mechanism of preconceptional carcinogenesis here. However, an additional interesting observation was that K-ras mutations were much more frequent in lung carcinomas (8/16) than in adenomas (1/13) (P=0.02), for all progeny combined. This was not related to age of the tumor-bearing mice or the size of the tumors. K-ras mutations may contribute to malignant tumor progression during aging, of possible relevance to the putative association of such mutations with poor prognosis of human lung adenocarcinomas.

Adenoma↗