Displaying all 18 publications

  1. Norsa'adah B, Salinah O
    Malays J Med Sci, 2014 Mar;21(2):44-53.
    PMID: 24876807 MyJurnal
    There was strong evidence from studies conducted in developed countries that second-hand smoke (SHS) exposure is detrimental to the birth weight of newborn. This study was conducted to determine the effect of exposure to SHS smoke during pregnancy on the weight of newborns.
    Matched MeSH terms: Maternal Exposure
  2. Sreeramareddy CT, Shidhaye RR, Sathiakumar N
    BMC Public Health, 2011;11:403.
    PMID: 21619613 DOI: 10.1186/1471-2458-11-403
    BACKGROUND: Observational epidemiological studies and a systematic review have consistently shown an association between maternal exposure to biomass smoke and reduced birth weight. Our aim was to further test this hypothesis.
    METHODS: We analysed the data from 47,139 most recent singleton births during preceding five years of 2005-06 India Demographic Health Survey (DHS). Information about birth weight from child health card and/or mothers' recall) was analysed. Since birth weight was not recorded for nearly 60% of the reported births, maternal self-report of child's size at birth was used as a proxy. Fuel type was classified as high pollution fuels (wood, straw, animal dung, and crop residues kerosene, coal and charcoal), and low pollution fuels (electricity, liquid petroleum gas (LPG), natural gas and biogas). Univariate and multivariable logistic regression models were developed using SURVEYLOGISTIC procedure in SAS system. We used three logistic regression models in which child factors, maternal factors and demographic factors were added step-by-step to the main exposure variable. Adjusted Odds Ratios (AORs) and their 95% CI were calculated. A p-value less than 0.05 was considered as significant.
    RESULTS: Child's birth weight was available for only 19,270 (41%) births; 3113 from health card and 16,157 from mothers' recall. For available data, mean birth weight was 2846.5 grams (SD = 684.6). Children born in households using high pollution fuels were 73 grams lighter than those born in households using low pollution fuels (mean birth weight 2883.8 grams versus 2810.7 grams, p < 0.001). Use of biomass fuels was associated with size at birth. Unadjusted OR was 1.41 (95% CI, 1.27 1.55). Adjusted OR after controlling for child factors was 1.41 (95% CI 1.29, 1.57). AOR after controlling for both child and maternal factors was 1.21 (95% CI 1.06, 1.32). In final model AOR was 1.07 (95% 0.94, 1.22) after controlling for child, maternal and demographic factors. Gender, birth order, mother's BMI, haemoglobin level and education were significant in all three models.
    CONCLUSIONS: Use of biomass fuels is associated with child size at birth. Future studies should investigate this association using more direct methods for measurement of exposure to smoke emitted from biomass fuels and birth weight.
    Matched MeSH terms: Maternal Exposure/adverse effects*
  3. Hinwood AL, Stasinska A, Callan AC, Heyworth J, Ramalingam M, Boyce M, et al.
    Environ Pollut, 2015 Sep;204:256-63.
    PMID: 25984984 DOI: 10.1016/j.envpol.2015.04.024
    Most studies of metals exposure focus on the heavy metals. There are many other metals (the transition, alkali and alkaline earth metals in particular) in common use in electronics, defense industries, emitted via combustion and which are naturally present in the environment, that have received limited attention in terms of human exposure. We analysed samples of whole blood (172), urine (173) and drinking water (172) for antimony, beryllium, bismuth, cesium, gallium, rubidium, silver, strontium, thallium, thorium and vanadium using ICPMS. In general most metals concentrations were low and below the analytical limit of detection with some high concentrations observed. Few factors examined in regression models were shown to influence biological metals concentrations and explained little of the variation. Further study is required to establish the source of metals exposures at the high end of the ranges of concentrations measured and the potential for any adverse health impacts in children.
    Matched MeSH terms: Maternal Exposure*
  4. Mohamed NN, Loy SL, Lim PY, Al Mamun A, Jan Mohamed HJ
    Sci Total Environ, 2018 Jan 01;610-611:147-153.
    PMID: 28803192 DOI: 10.1016/j.scitotenv.2017.08.030
    Exposure to secondhand smoke (SHS) can affect fetal brain development as well as subsequent neurodevelopment. This study aimed to determine the association between prenatal and postnatal SHS exposure with children's neurodevelopment at 2years of age. Among 107 mother-child pairs from a Malaysia prospective cohort, prenatal and postnatal SHS exposure was determined based on maternal and child hair nicotine concentrations. Multiple linear regressions were used to determine the association between prenatal and postnatal levels of nicotine in maternal and children's' hair with children's neurodevelopment. After adjustment for confounders, prenatal nicotine concentration levels were negatively associated with communication (β=-2.059; p=0.015) and fine motor skills (β=-2.120; p=0.002) while postnatal nicotine concentration levels were inversely associated with fine motors (β=-0.124; p=0.004) and problem solving skills (β=-0.117; p=0.013). In conclusion, this study suggests that early life exposure to SHS may affect children's neurodevelopment.
    Matched MeSH terms: Maternal Exposure/adverse effects*
  5. Singh HJ, Keah LS, Kumar A, Sirajudeen KN
    Exp. Toxicol. Pathol., 2012 Nov;64(7-8):751-2.
    PMID: 21354772 DOI: 10.1016/j.etp.2011.01.011
    This report documents an incidental finding during a study investigating the effects of melatonin supplementation on the development of blood pressure in SHR. Administration of 10 mg/kg/day of melatonin in drinking water during pregnancy to Wistar-Kyoto (WKY) dams caused a loss of more than 50% of the pups by the age of three weeks and 95% by the age of 6 weeks. There was no maternal morbidity or mortality in the two strains or death of any of the SHR pups. No obvious physical defects were present but mean body weight was lower in the surviving WKY rats when compared to that of melatonin supplemented SHR or non-supplemented WKY pups. The reason for the high mortality in WKY pups is uncertain and appears to be strain if not batch specific. There is a need for caution in its use, particularly during pregnancy, and clearly necessitates more detailed studies.
    Matched MeSH terms: Maternal Exposure/adverse effects*
  6. Lim WL, Soga T, Parhar IS
    Dev Neurosci, 2014;36(2):95-107.
    PMID: 24713635 DOI: 10.1159/000360416
    Migration and final positioning of gonadotropin-releasing hormone (GnRH) neurons in the preoptic area (POA) is critical for reproduction. It is known that maternal dexamethasone (DEX) exposure impairs reproductive function and behaviour in the offspring. However, it is still not known whether maternal DEX exposure affects the postnatal GnRH neurons in the offspring. This study determined the neuronal movement of enhanced green fluorescent protein (EGFP)-tagged GnRH neurons in slice culture of postnatal day 0 (P0), P5 and P50-60 transgenic male rats. Effect of maternal DEX treatment on EGFP-GnRH neuronal movement and F-actin distribution on GnRH neurons at P0 stage were studied. Time-lapse analysis of P0 and P5 EGFP-GnRH neurons displayed active cellular movement within the POA compared to young adult P50-60 stages, suggesting possible fine-tuning movement for positioning of early postnatal GnRH neurons. The DEX-treated EGFP-GnRH neurons demonstrated decreased motility in the POA and reduced F-actin distribution in the GnRH neurons at 60 h culture compared to the vehicle-treated. These results suggest that the P0 GnRH neuronal movement in the POA is altered by maternal DEX exposure, which possibly disrupts the fine-tuning process for positioning and development of early postnatal GnRH neurons in the brain, potentially linked to reproductive dysfunction in adulthood.
    Matched MeSH terms: Maternal Exposure/adverse effects*
  7. Imam MU, Ismail M, Ooi DJ, Sarega N, Ishaka A
    Mol Nutr Food Res, 2015 Jan;59(1):180-4.
    PMID: 25329877 DOI: 10.1002/mnfr.201400396
    White rice (WR) is a major staple food for people in developing countries and it may be responsible for the growing incidence of type 2 diabetes. Nonpregnant Female Sprague Dawley rats fed with WR or brown rice (BR) for 8 weeks were mated with age-matched male rats maintained on normal pellet over the same period. Offsprings were fed normal pellet after weaning until 8 weeks postdelivery. Rats fed with WR and their offsprings showed worsened oral glucose tolerance test, lower serum adiponectin levels, and higher weights, homeostatic model assessment of insulin resistance, serum retinol binding protein-4 levels, and leptin levels, compared with the normal and BR groups, suggesting an increased risk of insulin resistance. Furthermore, transcriptional levels of genes involved in insulin signaling showed different expression patterns in the liver, muscle, and adipose tissues of mothers and offsprings in both WR and BR groups. The results propose that the cycle of WR-induced insulin resistance in offsprings due to prenatal exposure, followed by their consumption of WR later in life may contribute to diabetes incidents. These findings are worth studying further.
    Matched MeSH terms: Maternal Exposure*
  8. Sudaryanto A, Kunisue T, Tanabe S, Niida M, Hashim H
    Arch Environ Contam Toxicol, 2005 Oct;49(3):429-37.
    PMID: 16132420
    This study determined the concentrations of polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs), polychlorinated biphenyls (PCBs), organochlorine (OC) pesticides, and tris(4-chlorophenyl) methane (TCPMe) in human breast milk samples collected in 2003 from primipara mothers living in Penang, Malaysia. OCs were detected in all the samples analyzed with DDTs, hexachlorocyclohexane isomers (HCHs), and PCBs as the major contaminants followed by chlordane compounds (CHLs), hexachlorobenzene (HCB), and TCPMe. The residue levels of DDTs, HCHs, and CHLs were comparable to or higher than those in general populations of other countries, whereas PCBs and HCB were relatively low. In addition, dioxins and related compounds were also detected with a range of dioxin equivalent concentrations from 3.4 to 24 pg-TEQs/g lipid wt. Levels of toxic equivalents (TEQs) were slightly higher than those in other developing countries but still much lower than those of industrialized nations. One donor mother contained a high TEQs level, equal to the mean value in human breast milk from Japan, implying that some of the residents in Malaysia may be exposed to specific pollution sources of dioxins and related compounds. No association was observed between OCs concentrations and maternal characteristics, which might be related to a limited number of samples, narrow range of age of the donor mothers, and/or other external factors. The recently identified endocrine disrupter, TCPMe, was also detected in all human breast milk samples of this study. A significant positive correlation was observed between TCPMe and DDTs, suggesting that technical DDT might be a source of TCPMe in Malaysia. The present study provides a useful baseline for future studies on the accumulations of OCs in the general population of Malaysia.
    Matched MeSH terms: Maternal Exposure*
  9. Daud ANA, Bergman JEH, Kerstjens-Frederikse WS, van der Vlies P, Hak E, Berger RMF, et al.
    Pharmacogenomics, 2017 Jul;18(10):987-1001.
    PMID: 28639488 DOI: 10.2217/pgs-2017-0036
    AIM: To explore the role of pharmacogenetics in determining the risk of congenital heart anomalies (CHA) with prenatal use of serotonin reuptake inhibitors.

    METHODS: We included 33 case-mother dyads and 2 mother-only (child deceased) cases of CHA in a case-only study. Ten genes important in determining fetal exposure to serotonin reuptake inhibitors were examined: CYP1A2, CYP2C9, CYP2C19, CYP2D6, ABCB1, SLC6A4, HTR1A, HTR1B, HTR2A and HTR3B.

    RESULTS: Among the exposed cases, polymorphisms that tended to be associated with an increased risk of CHA were SLC6A4 5-HTTLPR and 5-HTTVNTR, HTR1A rs1364043, HTR1B rs6296 and rs6298 and HTR3B rs1176744, but none reached statistical significance due to our limited sample sizes.

    CONCLUSION: We identified several polymorphisms that might potentially affect the risk of CHA among exposed fetuses, which warrants further investigation.

    Matched MeSH terms: Maternal Exposure/adverse effects*
  10. Sakai N, Alsaad Z, Thuong NT, Shiota K, Yoneda M, Ali Mohd M
    Chemosphere, 2017 Oct;184:857-865.
    PMID: 28646768 DOI: 10.1016/j.chemosphere.2017.06.070
    Arsenic and 5 heavy metals (nickel, copper, zinc, cadmium and lead) were quantitated in surface water (n = 18) and soil/ore samples (n = 45) collected from 5 land uses (oil palm converted from forest, oil palm in peat swamp, bare land, quarry and forest) in the Selangor River basin by inductively coupled plasma mass spectrometry (ICP-MS). Geographic information system (GIS) was used as a spatial analytical tool to classify 4 land uses (forest, agriculture/peat, urban and bare land) from a satellite image taken by Landsat 8. Source profiling of the 6 elements was conducted to identify their occurrence, their distribution and the pollution source associated with the land use. The concentrations of arsenic, cadmium and lead were also analyzed in maternal blood (n = 99) and cord blood (n = 87) specimens from 136 pregnant women collected at the University of Malaya Medical Center for elucidating maternal exposure as well as maternal-to-fetal transfer. The source profiling identified that nickel and zinc were discharged from sewage and/or industrial effluents, and that lead was discharged from mining sites. Arsenic showed a site-specific pollution in tin-tungsten deposit areas, and the pollution source could be associated with arsenopyrite. The maternal blood levels of arsenic (0.82 ± 0.61 μg/dL), cadmium (0.15 ± 0.2 μg/dL) and lead (2.6 ± 2.1 μg/dL) were not significantly high compared to their acute toxicity levels, but could have attributable risks of chronic toxicity. Those in cord blood were significantly decreased in cadmium (0.06 ± 0.07 μg/dL) and lead (0.99 ± 1.2 μg/dL) but were equivalent in arsenic (0.82 ± 1.1 μg/dL) because of the different kinetics of maternal-to-fetal transfer.
    Matched MeSH terms: Maternal Exposure/statistics & numerical data
  11. Mahzabin T, Pillow JJ, Pinniger GJ, Bakker AJ, Noble PB, White RB, et al.
    Pediatr Res, 2017 Sep;82(3):509-517.
    PMID: 28388600 DOI: 10.1038/pr.2017.99
    BackgroundPregnant women at a high risk of preterm delivery receive glucocorticoids to accelerate fetal lung maturation and surfactant synthesis. However, the effect of antenatal steroids on the developing diaphragm remains unclear. We hypothesized that maternal betamethasone impairs the fetal diaphragm, and the magnitude of the detrimental effect increases with longer duration of exposure. We aimed to determine how different durations of fetal exposure to maternal betamethasone treatment influence the fetal diaphragm at the functional and molecular levels.MethodsDate-mated merino ewes received intramuscular injections of saline (control) or two doses of betamethasone (5.7 mg) at an interval of 24 h commencing either 2 or 14 days before delivery. Preterm lambs were killed after cesarean delivery at 121-day gestational age. In vitro contractile measurements were performed on the right hemidiaphragm, whereas molecular/cellular analyses used the left costal diaphragm.ResultsDifferent durations of fetal exposure to maternal betamethasone had no consistent effect on the protein metabolic pathway, expression of glucocorticoid receptor and its target genes, cellular oxidative status, or contractile properties of the fetal lamb diaphragm.ConclusionThese data suggest that the potential benefits of betamethasone exposure on preterm respiratory function are not compromised by impaired diaphragm function after low-dose maternal intramuscular glucocorticoid exposure.
    Matched MeSH terms: Maternal Exposure*
  12. Lim WL, Idris MM, Kevin FS, Soga T, Parhar IS
    PMID: 27630615 DOI: 10.3389/fendo.2016.00117
    Maternal dexamethasone [(DEX); a glucocorticoid receptor agonist] exposure delays pubertal onset and alters reproductive behavior in the adult offspring. However, little is known whether maternal DEX exposure affects the offspring's reproductive function by disrupting the gonadotropin-releasing hormone (GnRH) neuronal function in the brain. Therefore, this study determined the exposure of maternal DEX on the GnRH neuronal spine development and synaptic cluster inputs to GnRH neurons using transgenic rats expressing enhanced green fluorescent protein (EGFP) under the control of GnRH promoter. Pregnant females were administered with DEX (0.1 mg/kg) or vehicle (VEH, water) daily during gestation day 13-20. Confocal imaging was used to examine the spine density of EGFP-GnRH neurons by three-dimensional rendering and synaptic cluster inputs to EGFP-GnRH neurons by synapsin I immunohistochemistry on postnatal day 0 (P0) males. The spine morphology and number on GnRH neurons did not change between the P0 males following maternal DEX and VEH treatment. The number of synaptic clusters within the organum vasculosum of the lamina terminalis (OVLT) was decreased by maternal DEX exposure in P0 males. Furthermore, the number and levels of synaptic cluster inputs in close apposition with GnRH neurons was decreased following maternal DEX exposure in the OVLT region of P0 males. In addition, the postsynaptic marker molecule, postsynaptic density 95, was observed in GnRH neurons following both DEX and VEH treatment. These results suggest that maternal DEX exposure alters neural afferent inputs to GnRH neurons during early postnatal stage, which could lead to reproductive dysfunction during adulthood.
    Matched MeSH terms: Maternal Exposure
  13. Ayu, A., Samsudin, A.R., Ismail, N.M., Isa, M.N.
    The prevalence of cleft lip and palate in human is 1 in 500 live births worldwide. Non·syndromic clefts are a complex trait with both genetic and environmental etiology. The aim ofthe study was to assess the association between maternal exposure to second-hand smoke during pregnancy and ruk of having cleft child. Unmatched case-control study was carried out among Malays in Kelantan.
    1 Case and control subjects were denned as mothers of cleft children and mothers of normal children respectively. The cleft children were recruited from the Combined Cleft Clinic at Kota Bharu Dental Clinic. Normal chiMren were selected at Orthodontic Clinic, Kota Bharu. A total of 184 cases and controb with age range from 17 to 50 years were interviewed using the standard craniofacial
    registration form. Multiple Logistic Regression modeling was used to estimate adjusted odds ratio of factors associated with non-syndromic oral cleft. Signijicant factors include history of miscarriage (OR: 3.40; 95% C1:1.05, 11 .08) p=0.042; duration of exposure to second-hand smoke for 15-30 minutes (OR: 2.41; 95% C1:1.42, 4.09) p 30 minutes (OR: 5.16; 95% C1:Z.87, 9.28) p
    Matched MeSH terms: Maternal Exposure
  14. Kishi R, Zhang JJ, Ha EH, Chen PC, Tian Y, Xia Y, et al.
    Epidemiology, 2017 10;28 Suppl 1:S19-S34.
    PMID: 29028672 DOI: 10.1097/EDE.0000000000000698
    BACKGROUND: The environmental health of children is one of the great global health concerns. Exposures in utero and throughout development can have major consequences on later health. However, environmental risks or disease burdens vary from region to region. Birth cohort studies are ideal for investigating different environmental risks.

    METHODS: The principal investigators of three birth cohorts in Asia including the Taiwan Birth Panel Study (TBPS), the Mothers and Children's Environmental Health Study (MOCEH), and the Hokkaido Study on Environment and Children' Health (Hokkaido Study) coestablished the Birth Cohort Consortium of Asia (BiCCA) in 2011. Through a series of five PI meetings, the enrolment criteria, aim of the consortium, and a first-phase inventory were confirmed.

    RESULTS: To date, 23 birth cohorts have been established in 10 Asian countries, consisting of approximately 70,000 study subjects in the BiCCA. This article provides the study framework, environmental exposure and health outcome assessments, as well as maternal and infant characteristics of the participating cohorts.

    CONCLUSIONS: The BiCCA provides a unique and reliable source of birth cohort information in Asian countries. Further scientific cooperation is ongoing to identify specific regional environmental threats and improve the health of children in Asia.

    Matched MeSH terms: Maternal Exposure
  15. Cheang HK, Wong HT, Ho SC, Chew KS, Lee WS
    Singapore Med J, 2013 Apr;54(4):224-6.
    PMID: 23624451
    INTRODUCTION: This study aimed to assess the immune response in infants who received the three-shot hepatitis B vaccine in Malaysia.

    METHODS: Consecutive infants born between March 2002 and April 2010 who received three doses of hepatitis B vaccine at a community clinic in Malaysia were enrolled in the study. Screening for hepatitis B surface antigen (HBsAg) and antibody against HBsAg (anti-HBs) was performed after the completion of primary immunisation, at approximately one year of age.

    RESULTS: A total of 572 infants (median age 9.3 ± 2.7 months; range 6.3-48 months) were screened for immune response to hepatitis B vaccination - 553 (96.7%) infants had adequate levels of anti-HBs (≥ 10 IU/L). Of the 440 mothers whose HBsAg status was known, 14 (3.2%) were positive for HBsAg. None of the 14 infants who were born to HBsAg-positive mothers were positive for HBsAg, and all but one infant had anti-HBs level ≥ 10 IU/L. Gender, gestational age and maternal HBsAg status were not found to significantly affect the subsequent immune response in infants following vaccination.

    CONCLUSION: The proportion of Malaysian mothers who are positive for HBsAg remains high. The three-shot hepatitis B vaccine, given as part of universal vaccination against hepatitis B, provides adequate anti-HBs in the vast majority of infants in a community setting in Malaysia.
    Matched MeSH terms: Maternal Exposure
  16. Shamsuddin K, Marmuji LZ
    Singapore Med J, 2010 Oct;51(10):800-5.
    PMID: 21103816
    Several strategies have been developed to reduce hepatitis B infections. These include antenatal screening, universal immunisation of newborns and immunoglobulin therapy for babies who are at risk. Antenatal screening for hepatitis B is not routinely performed, but all newborns in Malaysia are immunised against hepatitis B. We assessed the prevalence of hepatitis B and the factors associated with it among antenatal mothers in Ipoh. This information is useful in decision-making for future hepatitis B screening programmes for antenatal mothers, allowing for immunoglobulin therapies for newborns if their mother's hepatitis B virus (HBV) status is known.
    Matched MeSH terms: Maternal Exposure
  17. Leong YH, Azmi NI, Majid MIA, Wen S
    PMID: 34014804 DOI: 10.1080/19440049.2021.1922758
    An average 50 ml breast milk samples were collected from 21 lactating primiparous mothers (range 25 to 45 years, mean 33 years), 4-8 weeks after delivery in Penang Island, Malaysia. The geometric mean concentration of the most toxic congeners, 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) was 0.14 pg WHO2005-TEQ g-1 zlipid. The most abundant congeners of PCDD/Fs were octachlorodibenzo-p-dioxin (OCDD) (5.9-75.4%), followed by 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (1,2,3,4,6,7,8-HpCDD) (1.1-30.7%). The geometric mean level of total dioxins and dl-PCBs was 2.2 pg WHO2005-TEQ g-1 lipid, significantly lower than those in developed countries or highly contaminated areas. The total dioxins and dl-PCBs in pg WHO2005-TEQ levels in breast milk were significantly correlated with years of residence at potential contaminated site. The average daily intake of 11.8 pg WHO2005-TEQ kg-1 body weight was estimated for a breastfed infant at 6 months of age. This demonstrates the exposure risk to infants, especially from Penang region, to these pollutants from human milk intake are potentially high during the lactation period.
    Matched MeSH terms: Maternal Exposure
  18. David P, Subramaniam K
    PMID: 19452514 DOI: 10.1002/bdra.20593
    Clinical studies and research in animals have established that alcohol consumption during pregnancy produces irreversible developmental anomalies. Deficits in fine motor performance are often noted in infants diagnosed with fetal alcohol syndrome. However, the effects of alcohol on the spinal motoneurons have not been examined. In this study, the morphometric alterations in spinal motoneurons were assessed as a result of prenatal alcohol exposure.
    Matched MeSH terms: Maternal Exposure
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