[Risk of stillbirths and paternal occupational exposure to ionizing radiation].
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Animals↗
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Results for “Paternal Exposure”
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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↗
The stress response in gametes and embryos after paternal chemical exposures.
There is increasing concern that paternal exposure to toxic chemicals impacts negatively on progeny outcome. Exposure of male rats to a model male-mediated developmental toxicant and anticancer alkylating agent, cyclophosphamide, resulted in increased pre- and post-implantation loss, as well as in malformations. We hypothesize that the stage specificity of the effects of paternal cyclophosphamide exposure on progeny depends on the ability of germ cells to respond to stress, repair DNA or undergo apoptosis. Acute high dose exposure of male rats to cyclophosphamide increased the expression of heat shock proteins and DNA repair genes, predominantly in round spermatids. In contrast, chronic low dose treatment dramatically decreased the expression of stress response genes in pachytene spermatocytes and round spermatids, but not in elongated spermatids; this reduced ability to respond to stress may allow damage to accumulate, resulting in altered sperm function. Increased DNA damage was maximal 3 weeks after drug exposure, during spermiogenesis, a key point in sperm chromatin remodelling. Drug exposure for 9 weeks increased the frequency of spermatozoa with chromosome 4 disomy and nullisomy. DNA damage found in cyclophosphamide-exposed spermatozoa was imparted to the newly fertilized zygote. Drug-exposed spermatozoa decondensed more rapidly than control spermatozoa and male pronuclear formation was earlier. RNA synthesis was higher in 1-cell embryos sired by drug-treated fathers than in controls. Significantly, the profile of gene expression was altered in embryos sired by drug-treated males as early as the 1-cell stage. Thus, exposure of male rats to cyclophosphamide altered male germ cell quality with a consequent temporal and spatial disruption of the zygotic genome activation.
Animals↗
Paternal occupational exposures and embryo implantation rates after IVF.
OBJECTIVE: To investigate any influence of paternal occupational exposures on implantation rates after IVF. DESIGN: Cohort study of couples who sought IVF treatment. SETTING: University Hospital Utrecht, The Netherlands. PATIENT(S): The study population was composed of 726 couples pursuing IVF treatment. INTERVENTION(S): Only the earliest IVF treatment cycle with ET was selected for the analysis. All couples filled in a generic questionnaire on lifestyle factors and details about their occupation. In addition, more detailed exposure information was obtained for pesticides with use of job-specific questionnaires and a subsequent telephone interview. MAIN OUTCOME MEASURE(S): The implantation rate was defined as the number of gestational sacs seen with ultrasound at 6-7 weeks of pregnancy, divided by the number of embryos replaced. RESULT(S): A significantly reduced implantation rate was seen among couples with male partners working in occupations with presumably high levels of organic solvent exposure. Conversely, paternal pesticide exposure was significantly associated with an increased implantation rate. Paternal exposures to metal dust or fumes and welding fumes were not related to the probability of implantation. CONCLUSION(S): The findings suggested that paternal organic solvent exposure decreased the implantation rate among couples undergoing IVF-ET treatment.
Adult↗
Behavioral and neurochemical alterations in the offspring of rats after maternal or paternal inhalation exposure to the industrial solvent 2-methoxyethanol.
The industrial solvent 2-methoxyethanol (2ME) has antifertility effects in male rats at 300 ppm and is teratogenic in rats and rabbits at 50 ppm. The present research investigated if exposure of paternal or maternal animals to 25 ppm 2ME, the current U.S. permissible occupational exposure limit, would produce detectable effects in the offspring. Eighteen male young-adult Sprague-Dawley rats were exposed to 25 ppm 2ME 7 hr/day, 7 days/week for 6 weeks; they were then mated with untreated females which were allowed to deliver and rear their young. In addition, groups of 15 pregnant rats were exposed 7 hr/day on gestation days 7-13 or 14-20 and allowed to deliver and rear their young. At birth, litters were culled to 4 females and 4 males for behavioral testing of neuromotor function, activity, and simple learning ability on days 10 through 90. In addition, brains from newborn and 21-day-old offspring were analyzed for neurochemical deviations from controls. No effects on paternal or maternal animals, nor on the number or weight of live offspring, were noted. Behavioral testing revealed significant differences from controls only in avoidance conditioning of offspring of mothers exposed on days 7-13. In contrast, neurochemical deviations were observed in brains from 21-day-old offspring from the paternally exposed group as well as from both maternally exposed groups; changes were numerous in the brainstem and cerebrum but were fewer in the cerebellum and midbrain. Thus it appears that both paternal and maternal inhalation of 25 ppm 2ME produces some effect which is reflected in neurochemical deviations in the offspring.
Acetylcholine↗
Paternal occupational exposure and spontaneous abortions: a closer look at paternal recall and vinyl chloride.
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Abortion, Spontaneous↗
Male-mediated spontaneous abortion among spouses of stainless steel welders.
OBJECTIVES: Male-mediated spontaneous abortion has never been documented for humans. The welding of stainless steel is associated with the pulmonary absorption of hexavalent chromium, which has genotoxic effects on germ cells in rodents. Clinical and early subclinical spontaneous abortions were examined among spouses of stainless-steel welders. METHODS: A cohort of first-pregnancy planners was recruited from members of the union of metal workers and 3 other trade unions. The cohort was followed for 6 menstrual cycles from the cessation of contraceptive use. Altogether, 280 pregnancies were conceived, of which 35 were detected by human chorionic gonadotrophic hormone analysis and did not survive to a clinically recognized pregnancy. Information on exposure was collected prospectively in relation to the outcome and was available for all cycles resulting in a pregnancy. Information on pregnancy outcome was collected for all 245 clinically recognized pregnancies. RESULTS: Increased risk of spontaneous abortion was found for pregnancies with exposure to paternal stainless-steel welding (adjusted relative risk 3.5, 95% confidence interval 1.3-9.1). The results were consistent in analyses of both biochemically and clinically recognized abortions. There was no increased risk for spontaneous abortion in pregnancies with paternal exposure to the welding of metals other than stainless steel. CONCLUSIONS: Male welding of stainless steel was associated with an increased risk of spontaneous abortion in spouses. A mutagenic effect of hexavalent chromium has been found previously in both somatic and germ cells, and the findings could be due to mutations in the male genome.
Abortion, Spontaneous↗
Review of epidemiologic studies of paternal occupational exposure and spontaneous abortion.
The question of whether paternal exposures influence risk of spontaneous abortion is of great public interest, with the possibility supported by laboratory investigations. Thirty-nine studies of male occupational exposure and risk of spontaneous abortion were examined, with the methods and results tabulated. Many of those reports were limited by exposure data based on maternal report of the father's job title or by potentially inaccurate paternal reports of spontaneous abortion, though the quality of more recent studies is markedly enhanced. Mercury has been implicated most strongly based on recent studies that included quantitative exposure estimates; a number of studies showing associations for exposure to anesthetic gases. Suggestive associations have also been found inconsistently for exposure to lead, rubber manufacturing, selected solvents, and some pesticides. Further study is encouraged, but with more intensive effort to measure accurately both spontaneous abortion and occupational exposures.
Abortion, Spontaneous↗
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↗
Maternal pesticide exposure from multiple sources and selected congenital anomalies.
We explored the relation between various potential sources of maternal periconceptional pregnancy exposures to pesticides and congenital anomalies in offspring. Data were derived from a case-control study of fetuses and liveborn infants with orofacial clefts, neural tube defects, conotruncal defects, or limb anomalies, among 1987-1989 California births and fetal deaths. We conducted telephone interviews with mothers of 662 (85% of eligible) orofacial cleft cases, 265 (84%) neural tube defect cases, 207 (87%) conotruncal defect cases, 165 (84%) limb cases, and 734 (78%) nonmalformed controls. The odds ratio (OR) estimates did not indicate increased risk for any of the studied anomaly groups among women whose self-reported occupational tasks were considered by an industrial hygienist likely to involve pesticide exposures. Paternal occupational exposure to pesticides, as reported by the mother, revealed elevated ORs for only two of the cleft phenotypes [OR = 1.7 [95% confidence interval (CI) = 0.9-3.4] for multiple cleft lip with/without cleft palate and OR = 1.6 [95% CI = 0.7-3.4] for multiple cleft palate]. Use of pesticide products for household gardening, by mothers or by professional applicators, was associated with ORs > or =1.5 for most of the studied anomalies. Use of pesticide products for the control of pests in or around homes was not associated with elevated risks for most of the studied anomalies, although women who reported that a professional applied pesticides to their homes had increased risks for neural tube defect-affected pregnancies [OR = 1.6 (95% CI = 1.1-2.5)] and limb anomalies [OR = 1.6 (95% CI = 1.0-2.7)]. Having a pet cat or dog and treating its fleas was not associated with increased anomaly risk. Women who reported living within 0.25 miles of an agricultural crop revealed increased risks for offspring with neural tube defects [OR = 1.5 (95%CI = 1.1-2.1)]. For many of the comparisons, data were sparse, resulting in imprecise effect estimation. Despite our investigating multiple sources of potential pesticide exposures, without more specific information on chemical and level of exposure, we could not adequately discriminate whether the observed effects are valid, whether biased exposure reporting contributed to the observed elevated risks, or whether nonspecific measurement of exposure was responsible for many of the observed estimated risks not being elevated.
Adult↗
An application of hierarchical regression in the investigation of multiple paternal occupational exposures and neuroblastoma in offspring.
BACKGROUND: We used hierarchical regression to study the effects of 46 paternal occupational exposures on the incidence of neuroblastoma in offspring. METHODS: The study population included 405 cases and 302 controls. The effect of each exposure was estimated using both conventional maximum likelihood and hierarchical regression. RESULTS: Using hierarchical regression, overall precision was greatly enhanced compared to the conventional analysis. In addition, adjustment of effect estimates based on prespecified prior distributions of the true effect parameters allowed a more consistent interpretation across the entire panel of exposures. Estimates for several metals and solvents were shrunk close to the null value, whereas estimates for several thinner solvents, diesel fuel, solders, wood dust, and grain dust remained moderately elevated. CONCLUSIONS: Hierarchical regression may mitigate some of the problems of the conventional approach by controlling for correlated exposures, enhancing the precision of estimates, and providing some adjustment of estimates based on prior knowledge.
Adult↗
Paternal occupational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and birth outcomes of offspring: birth weight, preterm delivery, and birth defects.
Agent Orange is a phenoxy herbicide that was contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). We studied pregnancy outcomes among wives of male chemical workers who were highly exposed to chemicals contaminated with TCDD and among wives of nonexposed neighborhood referents. For exposed pregnancies, we estimated serum TCDD concentration at the time of conception using a pharmacokinetic model. The mean TCDD concentration for workers' births was 254 pg/g lipid (range, 3-16,340 pg/g). The mean referent concentration of 6 pg/g was assigned to pregnancies fathered by workers before exposure. A total of 1,117 live singleton births of 217 referent wives and 176 worker wives were included. Only full-term births were included in the birth weight analysis (greater than or equal to 37 weeks of gestation). Mean birth weight among full-term babies was similar among referents' babies (n = 604), preexposure workers' babies (n = 221), and exposed workers' babies (n = 292) (3,420, 3,347, and 3,442 g, respectively). Neither continuous nor categorical TCDD concentration had an effect on birth weight for term infants after adjustment for infant sex, mother's education, parity, prenatal cigarette smoking, and gestation length. An analysis to estimate potential direct exposure of the wives during periods of workers' exposure yielded a nonstatistically significant increase in infant birth weight of 130 g in the highest exposure group (TCDD concentration > 254 pg/g) compared with referents (p = 0.09). Mothers' reports of preterm delivery showed a somewhat protective association with paternal TCDD (log) concentration (odds ratio = 0.8; 95% confidence interval, 0.6-1.1). We also include descriptive information on reported birth defects. Because the estimated TCDD concentrations in this population were much higher than in other studies, the results indicate that TCDD is unlikely to increase the risk of low birth weight or preterm delivery through a paternal mechanism. Key words: birth defects, birth weight, congenital anomalies, dioxin, occupation, paternal exposure, preterm birth, TCDD.
Adult↗
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↗
Paternal occupational exposures and childhood cancer.
The objective of the study described here was to test the hypothesis that paternal occupational exposure near conception increases the risk of cancer in the offspring. We conducted a cohort study based on a population of 235,635 children born shortly after two different censuses in Sweden. The children were followed from birth to 14 years, and cases of cancer were identified in the Swedish Cancer Registry. Occupational hygienists assessed the probability of exposure to different agents in each combination of the father's industry and occupation as reported in the censuses. We also analyzed individual job titles. We compared the cancer incidence among children of exposed fathers to that among children of unexposed fathers using Cox proportional hazards modeling. The main findings were an increased risk of nervous system tumors related to paternal occupational exposure to pesticides [relative risk (RR) = 2.36; 95% confidence interval (CI), 1.27-4.39] and work as a painter (RR = 3.65; 95% CI, 1.71-7.80), and an increased risk of leukemia related to wood work by fathers (RR = 2.18; 95% CI, 1.26-3.78). We found no associations between childhood leukemia and paternal exposure to pesticides or paint. Our results support previous findings of an increased risk of childhood brain tumors and leukemia associated with certain paternal occupational exposures. Some findings in previous studies were not confirmed in this study.
Adult↗
Association of paternal diagnostic X-ray exposure with risk of infant leukemia. Investigators of the Childrens Cancer Group.
Whether low level radiation exposure before conception increases the risk of leukemia in offspring has been much debated. No study has specifically evaluated the effect of parental preconception diagnostic X-ray exposure in the development of leukemia among infants. Mothers of 302 infant leukemia cases (diagnosed at < or = 18 months of age) and 558 individually matched regional controls, and fathers of 250 cases and 361 controls, were independently interviewed to obtain information on X-ray exposures. Paternal preconception X-ray exposure was associated with an increased risk of infant leukemia, higher risks being linked to exposures closer to conception. X-ray related leukemia risk varied with exposure site and histopathological type, the highest risk being for acute lymphocytic leukemia related to two or more X-rays of the lower gastrointestinal (GI) tract and lower abdomen (odds ratio, 3.78; 95% confidence interval, 1.49-9.64). A positive association was observed between acute lymphocytic leukemia and number of paternal X-rays of the lower GI and lower abdomen (trend test, P < 0.01), upper GI (P = 0.04), and chest (P = 0.08). Exposures of head and neck and limbs were unrelated to risk. The risk of acute myelogenous leukemia was unrelated to paternal X-ray exposure, except for a marginally significant association (trend test, P = 0.07) for upper GI X-rays. No consistent association between maternal X-ray exposure and infant leukemia was observed. The results of this study suggest that paternal low level radiation exposure before conception is associated with an increased risk of infant leukemia, although the nature of this association needs to be further evaluated.
Adult↗
Spontaneous abortion, sex ratio, and paternal occupational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.
There is conflicting research regarding an association between fetal death and paternal exposure to Agent Orange, a phenoxy herbicide widely used in Vietnam that was contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Men who worked in the U.S. factories that produced Agent Orange were exposed to TCDD at levels hundreds of times higher than TCDD levels in the general population. Wives of TCDD-exposed chemical workers and wives of nonexposed neighborhood referents were interviewed to determine reproductive history. Paternal serum TCDD level at time of conception was estimated for each pregnancy using serum samples taken in 1987. Estimated TCDD levels of workers during or after exposure were high (median, 254 ppt; range, 3-16,340 ppt) compared to referent levels (median, 6 ppt; range, 2-19 ppt). No association between paternal TCDD level at the time of conception and spontaneous abortion was observed among pregnancies fathered by workers with TCDD levels of < 20 ppt [odds ratio (OR) = 0.77; 95% confidence interval (CI), 0.48-1.22], 20 to < 255 ppt (OR = 0.81; 95% CI, 0.40-1.63), 255 to < 1,120, (OR = 0.69; 95% CI, 0.30-1.58), and >or= 1,120 ppt (OR = 0.95; 95% CI, 0.42-2.17) compared to pregnancies fathered by referents. The sex ratio [males/(males + females)] of offspring also did not differ by TCDD exposure (0.53 and 0.54 among workers and referents, respectively). We did not find an association between paternal serum TCDD level and spontaneous abortion or sex ratio of offspring in this population. The estimated TCDD levels in this exposed worker population were much higher than in other studies, providing additional evidence that paternal TCDD exposure does not increase the risk of spontaneous abortion at levels above those observed in the general population. The study could not evaluate the effect of father's childhood or prenatal TCDD exposure on subsequent sex ratio.
Abortion, Spontaneous↗
Reproductive male-mediated risk: spontaneous abortion among wives of pesticide applicators.
This study was conducted among 32 pesticide applicators occupationally exposed to pesticides to determine whether paternal exposure is associated with an increased risk of spontaneous abortion. The ratio of abortion was compared between applicators and a group of 51 food retailers (control population). The ratio of abortions/pregnancies for applicators was 0.27 and for retailers 0.07. OR for spontaneous abortion adjusted for age of wife and smoking of parents is 3.8 times greater than for the control population in the multiple logistic regression model and 7.6 times with interaction effects model.
Abortion, Spontaneous↗
Congenital malformations related to occupational reproductive hazards.
Occupational and environmental agents are the suspected cause of at least some of the approximately 60% of birth defects whose etiology is unknown. The author discusses studies of birth defects published since 1988. Studies that examine associations between congenital malformations and both maternal and paternal exposures are included.
Abnormalities, Drug-Induced↗