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PubMed2000

Maternal copper supplementation protects the neonatal rat lung against the adverse effects of maternal nicotine exposure.

Maternal nicotine exposure interferes with the extracellular formation of the connective tissue framework of the neonatal lung, a process that is dependent on copper-dependent lysyl oxidase. It has been shown that, during the phase of lung development associated with alveolarization, maternal nicotine exposure resulted in a reduction in the copper content and thus conceivably in the activity of lysyl oxidase of the neonatal lung. Therefore the aims of this study were (a) to determine the effects of maternal nicotine exposure during gestation and lactation on neonatal lung development, and (b) to establish whether maternal copper supplementation during gestation and lactation prevented the effect of maternal nicotine exposure on neonatal lung development. Pregnant rats were randomly divided into four groups: the control group received saline; the second group received 1 mg nicotine (kg bodyweight)(-1) day(-1) subcutaneously; the third group received 1 mg copper (kg bodyweight)(-1) day(-1); and the fourth group received both nicotine and copper in the same quantities as the previous two groups. Lung tissue of 14- and 42-day-old rat pups were processed for light microscopy. Maternal nicotine exposure during gestation and lactation resulted in (a) decreased alveolar number, (b) reduced internal surface area and (c) increased alveolar volume. Copper supplementation during gestation and lactation prevented the adverse effects of maternal nicotine exposure during gestation and lactation on the development of the alveolar region of the rat lung.

Animals↗

PubMed2002

Effects of maternal exposure to cadmium on pregnancy outcome and breast milk.

OBJECTIVE: The effects of cadmium (Cd) on birth weight have been discussed in the scientific literature. However, investigations on the effects of maternal body burden of Cd on the next generation during pregnancy and lactation have been limited. The relation between maternal exposure to Cd and pregnancy outcome or Cd in breast milk in Japanese mothers was investigated. METHODS: Cd concentrations in urine and colostrum milk samples of 57 mothers were measured by atomic absorption spectrophotometery. The relations between maternal urinary Cd and infant growth, gestational age at birth, and Cd in breast milk were investigated. RESULTS: The rate of perterm deliveries of mothers with higher urinary Cd (> or =2 nmol/mmol creatinine (Cr)) was higher than that of mothers with lower urinary Cd (<2 nmol/mmol Cr). The gestational age was significantly correlated with urinary Cd even after adjustment for maternal age. The height and weight of newborn infants of mothers with higher urinary Cd were significantly lower than those of the newborn infants of mothers with lower urinary Cd, but these decreases were ascribed to early delivery induced by Cd. The Cd in breast milk of mothers with higher urinary Cd was significantly higher than that of mothers with lower urinary Cd. A significant positive correlation was found between maternal urinary Cd and Cd in breast milk. CONCLUSION: Maternal exposure to Cd seems to increase early delivery, which leads to a lower birth weight. Also, the Cd is transferred in part to the next generation through breast milk after birth.

Adult↗

PubMed1997

Maternal exposure to delta 9-tetrahydrocannabinol (delta 9-THC) alters indolamine levels and turnover in adult male and female rat brain regions.

Perinatal exposure to delta 9-THC has been shown to produce effects on brain development. In this study we evaluated the changes induced by maternal exposure to delta 9-THC (5 mg/kg per day) from gestational day 5 to postnatal day 24 in eight discrete brain areas on the central serotoninergic system in both adult male and female rats. These result show that maternal exposure to delta 9-THC from gestational day 5 to postnatal day 24 affects development of the various central indoleaminergic system of the offsprings brain. Perinatal exposure to delta 9-THC decreased the levels of 5-HT in hypothalamus and rostral neostriatum in exposed males, and also decreased the levels of 5-HT in ventral hippocampus, septum, and midbrain raphe nuclei in both exposed males and females. Perinatal exposure to delta 9-THC increased the levels of 5-HIAA in dorsal hippocampus, hypothalamus, septum, midbrain raphe nuclei, and rostral neostriatum in exposed males and females. We have also found differences between nonexposed males and females in several brain regions. Our results confirm a regional and sexual specificity in endogenous levels of indoleamine after perinatal delta 9-THC treatment, being the midbrain raphe nuclei the most affected area.

Animals↗

PubMedDate not supplied

Maternal exposure to genistein during pregnancy increases carcinogen-induced mammary tumorigenesis in female rat offspring.

A high estrogenic environment in utero may increase subsequent breast cancer risk. It was therefore determined whether a maternal exposure during pregnancy to the phytoestrogen genistein or zearalenone, both of which exhibit estrogenic activities in vitro and in vivo, alters breast cancer risk among female offspring. Pregnant rat dams were treated daily with subcutaneous injections of 20, 100 or 300 microgram genistein, 20 microgram zearalenone, or vehicle between days 15 and 20 of gestation. The offspring were given 7, 12-dimethylbenz(a)anthracene (DMBA) at the age of 2 months to induce mammary tumors. The results indicate that in utero exposure to genistein, but not to zearalenone, dose-dependently increased the incidence of DMBA-induced mammary tumors, when compared with the controls. Tumor growth characteristics were not altered. Prior to the carcinogen administration, the number of estrogen receptor (ER) binding sites, determined using a ligand binding assay, were significantly elevated in the mammary glands of genistein offspring. In contrast, the mammary protein kinase C (PKC) activity was significantly reduced in the genistein offspring. Our results suggest that a maternal exposure to subcutaneous administration of genistein can increase mammary tumorigenesis in the offspring, mimicking the effects of in utero estrogenic exposures. Further, increased ER protein levels and reduced PKC activity in the mammary gland may be involved in increasing susceptibility to carcinogen-induced mammary tumorigenesis in rats exposed to genistein in utero.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1991

Effect of maternal exposure to nicotine in the rat on level and binding of somatostatin in brain of developing offspring.

The effect of maternal exposure to nicotine on the level of somatostatin and specific binding in frontoparietal cortex and hippocampus of developing offspring was investigated. Sprague-Dawley rats were injected subcutaneously, throughout the pregnancy and the nursing period, with either: 3 mg/kg nicotine base or saline vehicle. In the offspring of control rats, the level of somatostatin-like immunoreactivity peaked at day 10 in the frontoparietal cortex, whereas the level of immunoreactivity in the hippocampus was the highest on day 30. Maternal exposure to nicotine caused enhanced levels of immunoreactivity in the frontoparietal cortex, on the day of birth and in the hippocampus, up to day 10. The maximum specific binding of somatostatin to the receptors in membranes from the frontoparietal cortex, peaked at 10 days of age in the offspring of control rats. The number of somatostatin receptors in cortical (but not in hippocampal) membranes was significantly decreased in the 0- to 10-day-old offspring of the nicotine-treated rats. Despite transient alterations in the number of somatostatin receptors, the affinity of the sites for somatostatin was consistently unchanged. The levels of somatostatin-like immunoreactivity and the number of somatostatin receptors in the frontoparietal cortex and hippocampus was comparable in the 30-day-old offspring of the control and nicotine-treated rats.

Aging↗

PubMedDate not supplied

Achieving environmentally relevant organochlorine pesticide concentrations in eggs through maternal exposure in Alligator mississippiensis.

Alligator mississippiensis eggs from organochlorine pesticide (OCP) contaminated sites in Florida exhibit high rates of embryonic mortality compared to reference sites (P < 0.05). The objective of the present study was to use captive adult alligators to test the hypotheses that maternal exposure to OCPs results in increased OCP concentrations in eggs, and that increased exposure is associated with increased embryonic mortality. A total of 24 adult alligators (8 males and 16 females) were housed in eight pens. Eight females in four pens were dosed with a mixture of p,p'-DDE, toxaphene, dieldrin, and chlordane at a rate of 0.2+/-0.01 mg/kg/day for 274+/-8 days. Treated females produced eggs containing higher OCP concentrations (12,814+/-813 ng/g yolk) than controls (38+/-4 ng/g yolk). Eggs of treated females exhibited decreased viability (13+/-22%) as compared to controls (45+/-20%). Results indicated that 0.6% of administered OCPs were maternally transferred to the eggs of American alligators, and that maternal exposure is associated with decreased egg/embryo viability in this species.

Alligators and Crocodiles↗

PubMed2002

The influence of maternal exposure to volatile organic compounds on the cytokine secretion profile of neonatal T cells.

Indoor VOC (volatile organic compound) exposure has been shown to be correlated with airway symptoms and allergic manifestations in children. An investigation was conducted within an ongoing birth cohort study (LISA: Lifestyle-Immune System-Allergy) of the association between maternal exposure to VOCs and immune status at birth, in particular the cytokine secretion profile of cord-blood T cells. In a randomly selected group of 85 neonates, cytokine-producing cord-blood T cells were analyzed using intracellular cytokine detection. VOC exposure was measured in children's dwellings by passive sampling, while parents were asked to complete questionnaires about possible sources of VOC exposure. Adjusted odds ratios (ORs) were calculated by logistic regression based on categorized quartiles. A positive association was found between elevated percentages of interleukin-4-producing (IL-4) type 2 T cells and exposure to naphthalene (OR = 2.9) and methylcyclopentane (OR = 3.3). Exposure to tetrachloroethylene was associated with reduced percentages of interferon-gamma-producing (IFN-gamma) type 1 T cells (OR = 2.9). In addition, smoking during pregnancy was correlated with a higher indoor air concentration of naphthalene (OR = 3.8), new carpets in infants' bedrooms with elevated methylcyclopentane concentrations (OR = 4.1), and home renovation with a higher trichloroethylene burden (OR = 4.9). Our data suggest that maternal exposure to VOC may have an influence on the immune status of the newborn child.

Adult↗

PubMed1989

Fetal lung growth: influence of maternal exposure to cold and exercise in rats.

The consequences of maternal exposure to low ambient temperature and exercise on maternal and fetal lung growth and in particular on the relationship between the three gas exchange organs (lungs and placenta) were studied in albino rats. Pregnant rats were subjected to 10 degrees C ambient temperature or to daily 10 min swimming exercise beginning at day 3 or day 11 of pregnancy till day 21 when they were sacrificed. Maternal lung growth was assessed by measuring the lung weight, lung air volume and lung DNA content, and the fetal lung growth by lung DNA content. Comparisons were made in rats with litter sizes of 9-14. The major findings were as follows. Cold increased: (1) the maternal lung, liver, kidney and heart size, and fetal body weight, in both groups, but to a greater degree in rats exposed to cold at day 3; and (2) fetal lung DNA content in rats subjected to cold at late gestation. It abolished the relationship between maternal and fetal lung DNA content which exists in large litter size pregnancies. Exercise did not enlarge the maternal lungs; it decreased the placental weight and fetal lung DNA content and abolished the relationship between maternal and fetal lung DNA content in rats subjected to exercise at early gestation. Neither cold nor exercise had an effect on fetal lung maturation. It is postulated that reduction in fetal lung DNA content with maternal exercise may result from the effects of hypoxemia which may be the consequence of reduced uterine blood flow; and that abolition of normally existing direct relationship between maternal and fetal lung DNA content may be the outcome of the effects of alterations in metabolic and endocrine functions, in both the mother and the fetus, in response to cold temperature and exercise, offsetting the influence the growing maternal lung may have on fetal lung growth.

Animals↗

PubMed1998

Maternal exposure to low doses of delta9-tetrahydrocannabinol facilitates morphine-induced place conditioning in adult male offspring.

The possible existence of an increased susceptibility to the reinforcing properties of morphine was analyzed in male and female rats born from mothers exposed to delta9-tetrahydrocannabinol (THC, 1, 5, or 20 mg/kg) during gestation and lactation. Maternal exposure to low doses of THC (1 and 5 mg/kg), relevant for human consumption, resulted in an increased response to the reinforcing effects of a moderate dose of morphine (350 microg/kg), as measured in the place-preference conditioning paradigm (CPP) in the adult male offspring. These animals also displayed an enhanced exploratory behavior in the defensive withdrawal test. However, only females born from mothers exposed to THC 1 mg/kg exhibited a small increment in the place conditioning induced by morphine. The possible implication of the hypothalamo-pituitary-adrenal axis (HPA) was analyzed by monitoring plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone in basal and moderate-stress conditions (after the end of the CPP test). Female offspring perinatally exposed to THC (1 or 5 mg/kg) displayed high basal levels of corticosterone and a blunted adrenal response to the HPA-activating effects of the CPP test. However, male offspring born from mothers exposed to THC (1 or 5 mg/kg) displayed the opposite pattern: normal to low basal levels of corticosterone, and a sharp adrenal response to the CPP challenge. The present study reveals that maternal exposure to low doses of THC results in an increased sensitivity to the reinforcing effects of morphine in the adult male offspring, and in sexually dimorphic behavioral and endocrine alterations in the adaptative responses to stressors such as novelty or place-preference testing. These results support the growing evidence of the importance of monitoring the long-term consequences of maternal consumption of cannabis derivatives.

Adrenocorticotropic Hormone↗

PubMed1997

Effects of maternal exposure to 3,3',4,4'-tetrachlorobiphenyl or propylthiouracil in rats trained to discriminate apomorphine from saline.

In the present experiment drug discrimination was examined in rats after maternal exposure to 3,3',4,4'-tetrachlorobiphenyl (PCB 77) using apomorphine (APO) as the training drug at a dose reported to act on dopamine D2 receptors. A group with maternal exposure to 6n-propyl-2-thiouracil (PTU) was included as a positive control for effects induced by PCB 77 on thyroid hormones. On gestational day (GD) 19 reduced levels of free and total thyroxine (FT4, TT4) and free triiodothyronine (FT3) were detected in dams exposed to PCB 77 or PTU. In the offspring decreases in levels of FT4 and TT4 were found in both treated groups on postnatal day (PND) 21, while reductions of FT3 were observed only in the PTU group. PTU-treated rats needed more daily sessions for successful discrimination between apomorphine and saline. There were no differences between groups in generalization tests and sessions with the D2/D3 agonist quinpirole, the D2 antagonist haloperidol plus APO, or with the GABAergic drug pentobarbital and only minor differences in sessions with the D1 agonist SKF-38393. Differences between controls and groups exposed to PCB 77 or PTU were detected in a blocking test using the mixed serotonin 5-HT1A agonist and partial D2 antagonist buspirone. This outcome suggests long-lasting effects by developmental exposure to PCB 77 on the interaction between dopaminergic and serotonergic processes which may be mediated by effects on thyroid hormone levels.

Animals↗

PubMed2000

Role of maternal exposures and newborn genotypes on newborn chromosome aberration frequencies.

Maternal exposures may induce chromosome damage and birth defects in the fetus. Polymorphic variation in genes coding for enzymes involved in metabolic activation and detoxification of environmental procarcinogens may account for some of the differences in chromosome aberration frequencies in newborns. In this study, 40 mothers completed questionnaires regarding exposures they received during their pregnancy. Umbilical cord blood samples were analyzed for chromosome aberrations. An average of 1020 metaphase cell equivalents (equal to 1020 G-banded cells) were examined from each newborn. In 26 of the newborns, genotyping analysis was performed for genes functioning in metabolic activation and detoxification (cytochrome P450 genes: CYP2D6 and CYP1A1, and phase II genes: NAT1, NAT2, GSTT1, GSTM1, GSTP1, and epoxide hydrolase). A significant association between the CYP1A1 MspI polymorphism and chromosome aberration frequencies was observed in the newborns (p=0.02), with heterozygotes showing higher aberration frequencies than the wild type homozygotes. Some large differences in chromosome aberration frequencies for other genotypes were also noted, but these were not statistically significant. Exposure to tobacco smoke in utero also appeared to increase translocation frequencies. The mean frequency of translocations per 100 cell equivalents from newborns of mothers who smoked during pregnancy was significantly higher than that of newborns whose mothers did not smoke (0.21 vs. 0.11, respectively, p=0.045).

Acetyltransferases↗

PubMed1996

Maternal exposure to potential inhibitors of DNA topoisomerase II and infant leukemia (United States): a report from the Children's Cancer Group.

Nearly 80 percent of infant leukemias present with an abnormality involving the MLL gene at 11q23. Moreover, secondary acute myeloid leukemias (AML) that occur as the result of chemotherapy agents, which are known to inhibit DNA topoisomerase II, often manifest the same MLL abnormalities. It has been hypothesized that de novo infant leukemias may occur as a result of maternal exposure to agents in diet and medications that inhibit DNA topoisomerase II. Three epidemiologic studies of childhood leukemia with similar methodologies were conducted in the United States and Canada over the past 10 years by the Children's Cancer Group (CCG). Of the total 771 mothers of infants diagnosed at one year of age or less (< 12.5 months) who originally were interviewed (303 infant cases and 468 matched controls) across the three studies, follow-up questionnaire data on maternal exposure to potential DNA topoisomerase II inhibitors during pregnancy were available on 84 cases and 97 matched controls in the US. For maternal diet, a composite variable was created that consisted of 10 foods identified alpha priori as containing DNA topoisomerase II inhibitors. There were no significant trends with increasing maternal consumption for either the overall group, or the acute lymphoblastic leukemia (ALL) stratum. However, within the AML stratum, there was a statistically significant positive association (P trend = 0.04) with increasing consumption of DNA topoisomerase II-inhibitor containing foods (odds ratio [OR] = 9.8, 95 percent confidence interval [CI] = 1.1-84.8; OR = 10.2, CI = 1.1-96.4; for medium and high consumption, respectively). Other potential topoisomerase II inhibitors were explored; no significant findings were found. Results of this preliminary study, in combination with molecular data, should be used in future investigations of childhood leukemia (particularly, infant) to justify the incorporation of a detailed dietary history.

Acute Disease↗

PubMedDate not supplied

Maternal exposure to trichloroethylene in drinking water and birth-weight outcomes.

An ecological epidemiological study was conducted with data obtained from an environmental dose-reconstruction study and the Arizona Birth Information Tapes. Before 1981, a portion of the city of Tucson water-distribution system was contaminated with trichloroethylene (i.e., < 5 micrograms per liter of water to 107 micrograms per liter of water). Target and comparison populations were selected with a Geographic Information System. Logistical-regression analysis revealed an association between maternal exposure to trichloroethylene via drinking water and very-low-birth-weight babies (i.e., < 1,501 grams) (odds ratio = 3.3; 95% confidence interval = 0.5, 20.6; and Wald chi-square p value = 0.2). No association was found between maternal exposure to trichloroethylene via drinking water and low birth weight or full-term low-birth-weight infants (gestational period > 35 wk and < 46 wk).

Arizona↗

PubMed2000

Maternal exposure to the synthetic cannabinoid HU-210: effects on the endocrine and immune systems of the adult male offspring.

Natural and synthetic cannabinoid receptor agonists have been described to exert profound effects on both the neuroendocrine integration and the functional responses of the immune system. In the present study, Wistar rats were exposed to the highly potent cannabinoid agonist HU-210 (1, 5 and 25 microg/kg) during gestation and lactation and the ensuing effects on several endocrine and immune parameters of the adult male offspring were analyzed. Perinatal exposure to HU-210 partially affected the distribution of lymphocyte subpopulations in the spleen and peripheral blood. The major changes observed occur after maternal exposure to the 25 microg/kg dose of HU-210. There was a reduction in the T-helper subpopulation in the spleen and a dose-related decrease in the rate of T(helper)/T(cytotoxic) in peripheral blood lymphocytes. Concanavalin-A and lipopolysaccharide-induced proliferation were normal in all the groups tested. In the same animals, perinatal exposure to HU-210 did not affect basal levels of growth hormone, IGF-1, prolactin, or follicle-stimulating hormone. Basal values of luteinizing hormone were elevated in animals given the 1 microg/kg dose of HU-210. Corticosterone levels were reduced in the animals exposed to the higher dose of HU-210 during gestation and lactation. These animals exhibited a decreased responsiveness of the hypothalamo-pituitary-adrenal (HPA) axis to the stimulation with a single injection of HU-210 (20 microg/kg, i.v.) at adult ages, which may reflect the onset of long-lasting tolerance to the HPA-activating properties of cannabinoids. The opposite pattern of response was found in the animals given the 1 microg/kg dose, in which a sensitization of the corticosterone response to acute HU-210 was observed. The present work reveals that maternal exposure to cannabinoids results in minor changes in the development of the immune system, but may induce long-lasting alterations in the functional status of the HPA axis.

Administration, Oral↗

PubMedDate not supplied

Ethological methods to study the effects of maternal exposure to estrogenic endocrine disrupters: a study with methoxychlor.

There has been increasing interest, both at the scientific and regulatory level, in the use of ethological methods for evaluating neural effects of endocrine disrupters. We present a series of ethological studies on the effects of maternal exposure to low, environmentally relevant doses (0.02, 0.2, and 2 microg/g mother bw/day) of the estrogenic pesticide methoxychlor (MXC) on behavior. From gestation day 11 to 17, female mice spontaneously drank oil with or without MXC; their maternal behavior was examined from postpartum days 2 to 15. MXC treatment during pregnancy produced slight changes in the expression of maternal behavior: females fed the lower MXC dose spent less time nursing the pups as compared to control dams. Their maternally exposed offspring were subjected to a series of behavioral tests at different ages. Maternal exposure to MXC affected behavioral responses to novelty in both sexes at periadolescence. The onset of male intrasex aggression was delayed in males prenatally exposed to low doses of MXC, since exposed males showed low levels of aggressive interactions during early adolescence but not after they reached adulthood. When adults, MXC-exposed females, but not males showed increased exploration in an unfamiliar open-field. While a sex difference was observed in the control group, with males being significantly more active in the open field than females, prenatal treatment with some MXC doses tended to decrease the sexual dimorphism in activity levels in the novel environment. Ethology, as the evolutionary study of behavior, may provide a framework for integrating a functional perspective (i.e., evolutionary significance) to studies on proximate mechanisms that can account for behavioral alterations induced by developmental exposure to endocrine disrupters.

Animals↗

PubMed1990

Cardiovascular malformations and maternal exposure to video display terminals during pregnancy.

The possible effects of working with video display terminals (VDTs) during pregnancy on the occurrence of cardiovascular malformations in the offspring was studied in 500 cases and 1055 controls. The cases represented all registered cardiovascular malformations reported in Finland during 1982-84, excluding those with chromosomal anomaly or known genetic syndrome. The controls were randomly selected from all babies born during the same period. Both the case and control mothers were interviewed by midwives using a structured questionnaire approximately three months after delivery. In this interview the mother's occupation, job description and employer during the first trimester were noted, as were large number of other exposures to chemical and physical factors. An industrial hygienist examined all these records for information indicating exposure to VDTs, unaware of case/control status. Work with VDTs during the first trimester of pregnancy was ascertained for 30 case mothers (6.0%, 30/500) and 53 control mothers (5.0%, 53/1055). In logistic regression analysis maternal exposure to VDTs for at least 20h a week during the first trimester of pregnancy showed a point estimate of odds ratio of 1.4 with 95% confidence limits of 0.5 and 3.8, when adjusted for age and alcohol use. Maternal exposure to VDTs was not associated with indicators of fetal growth such as birthweight, placental weight or length of gestation.

Computer Systems↗

PubMed1996

Maternal exposure to paternal HLA does not explain the postpartum increase in rheumatoid arthritis.

The postpartum period, particularly after the first pregnancy, represents a time of increased risk for the development of rheumatoid arthritis (RA). The present study was undertaken to investigate whether this increase in risk may be due to maternal exposure to fetally inherited paternal HLA-DR antigens that were either 1) similar to their own or 2) had an increased likelihood of being one of the two specific types, HLA-DR1 and DR4, implicated in the etiology of RA. We recruited 94 families where the mother had developed RA within 12 months of a pregnancy, and HLA typed the mother, father, and relevant child of each family. Mothers were not more likely to share HLA-DR genes with their partners than would be expected, and children whose parents shared one HLA-DR gene were not more likely to inherit the shared gene from their father as opposed to the non-shared gene. Further, those children whose fathers were heterozygous for HLA-DR1 or DR4 were not more likely to inherit these genes as opposed to the non-DR1/DR4 gene. In conclusion, maternal exposure during pregnancy to either fetally inherited paternal HLA-DR1 and DR4 genes or to paternal DR genes similar to their own does not appear to contribute to postpartum maternal susceptibility of RA.

Arthritis, Rheumatoid↗

PubMed1995

Maternal exposure to N-nitrosatable drugs as a risk factor for childhood brain tumours.

BACKGROUND: Animal models suggest that compounds containing a nitrosyl group (N-nitroso compounds (NNO)) can act as potent transplacental carcinogens. Many common drug formulations have the potential to undergo nitrosation in vivo. The association between maternal use of nitrosatable drugs during pregnancy and development of brain tumours in the offspring was examined in a SEER-based case-control study. METHODS: Maternal exposure to nitrosatable drugs during pregnancy was compared among 361 childhood brain tumour cases and 1083 matched controls recruited through random-digit dialing. RESULTS: There was no increase in risk observed for childhood brain tumours overall (OR = 1.15; 95% CI: 0.69-1.94) or for astrocytomas individually (OR = 1.16; 95% CI: 0.50-2.69). A slight elevation in risk was noted for medulloblastomas (OR = 1.47; 95% CI: 0.28-7.62) and 'other' tumours (OR = 1.27; 95% CI: 0.56-2.86), however, both estimates were based on small numbers. CONCLUSIONS: Our findings suggest that no increased risk of childhood brain tumours was associated with maternal exposure to nitrosatable drugs. The study results should be viewed with caution given the imprecision of the point estimates as well as the lack of data on specific timing and dosage of exposure and degree of nitrosatability of drugs taken.

Astrocytoma↗