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    <title>Pierik, F.H.</title>
    <link>http://repub.eur.nl/res/aut/892/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Air pollution, blood pressure, and the risk of hypertensive complications during pregnancy: The generation r study (Article)</title>
      <link>http://repub.eur.nl/res/pub/33709/</link>
      <pubDate>2011-03-01T00:00:00Z</pubDate>
      <description>Exposure to air pollution is associated with elevated blood pressure and cardiovascular disease. We assessed the associations of exposure to particulate matter (PM10) and nitrogen dioxide (NO2) levels with blood pressure measured in each trimester of pregnancy and the risks of pregnancy-induced hypertension and preeclampsia in 7006 women participating in a prospective cohort study in the Netherlands. Information on gestational hypertensive disorders was obtained from medical records. PM10 exposure was not associated with first trimester systolic and diastolic blood pressure, but a 10-μg/m increase in PM10 levels was associated with a 1.11-mm Hg (95% confidence interval [CI] 0.43 to 1.79) and 2.11-mm Hg (95% CI 1.34 to 2.89) increase in systolic blood pressure in the second and third trimester, respectively. Longitudinal analyses showed that elevated PM10 exposure levels were associated with a steeper increase in systolic blood pressure throughout pregnancy (P&lt;0.01), but not with diastolic blood pressure patterns. Elevated NO2exposure was associated with higher systolic blood pressure levels in the first, second, and third trimester (P&lt;0.05), and with a more gradual increase when analyzed longitudinally (P&lt;0.01). PM10 exposure, but not NO2exposure, was associated with an increased risk of pregnancy-induced hypertension (odds ratio 1.72 [95% CI 1.12 to 2.63] per 10-μg/m increase). In conclusion, our results suggest that air pollution may affect maternal cardiovascular health during pregnancy. The effects might be small but relevant on a population level. </description>
    </item> <item>
      <title>Residential traffic exposure and pregnancy-related outcomes: A prospective birth cohort study (Article)</title>
      <link>http://repub.eur.nl/res/pub/25340/</link>
      <pubDate>2009-12-01T00:00:00Z</pubDate>
      <description>Background. The effects of ambient air pollution on pregnancy outcomes are under debate. Previous studies have used different air pollution exposure assessment methods. The considerable traffic-related intra-urban spatial variation needs to be considered in exposure assessment. Residential proximity to traffic is a proxy for traffic-related exposures that takes into account within-city contrasts. Methods. We investigated the association between residential proximity to traffic and various birth and pregnancy outcomes in 7,339 pregnant women and their children participating in a population-based cohort study. Residential proximity to traffic was defined as 1) distance-weighted traffic density in a 150 meter radius, and 2) proximity to a major road. We estimated associations of these exposures with birth weight, and with the risks of preterm birth and small size for gestational age at birth. Additionally, we examined associations with pregnancy-induced hypertension, (pre)eclampsia, and gestational diabetes. Results. There was considerable variation in distance-weighted traffic density. Almost fifteen percent of the participants lived within 50 m of a major road. Residential proximity to traffic was not associated with birth and pregnancy outcomes in the main analysis and in various sensitivity analyses. Conclusions. Mothers exposed to residential traffic had no higher risk of adverse birth outcomes or pregnancy complications in this study. Future studies may be refined by taking both temporal and spatial variation in air pollution exposure into account. </description>
    </item> <item>
      <title>Levels of metabolites of organophosphate pesticides, phthalates, and bisphenol A in pooled urine specimens from pregnant women participating in the Norwegian Mother and Child Cohort Study (MoBa) (Article)</title>
      <link>http://repub.eur.nl/res/pub/16059/</link>
      <pubDate>2009-09-01T00:00:00Z</pubDate>
      <description>Concerns about reproductive and developmental health risks of exposure to organophosphate (OP) pesticides, phthalates, and bisphenol A (BPA) among the general population are increasing. Six dialkyl phosphate (DAP) metabolites, 3,5,6-trichloro-2-pyridinol (TCPy), BPA, and fourteen phthalate metabolites were measured in 10 pooled urine samples representing 110 pregnant women who participated in the Norwegian Mother and Child Birth Cohort (MoBa) study in 2004. Daily intakes were estimated from urinary data and compared with reference doses (RfDs) and daily tolerable intakes (TDIs). The MoBa women had a higher mean BPA concentration (4.50 μg/L) than the pregnant women in the Generation R Study (Generation R) in the Netherlands and the National Health and Nutrition Examination Survey (NHANES) in the United States. The mean concentration of total DAP metabolites (24.20 μg/L) in MoBa women was higher than that in NHANES women but lower than that in Generation R women. The diethyl phthalate metabolite mono-ethyl phthalate (MEP) was the dominant phthalate metabolite in all three studies, with the mean concentrations of greater than 300 μg/L. The MoBa and Generation R women had higher mean concentrations of mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) than the NHANES women. The estimated average daily intakes of BPA, chlorpyrifos/chlorpyrifos-methyl and phthalates in MoBa (and the other two studies) were below the RfDs and TDIs. The higher levels of metabolites in the MoBa participants may have been from intake via pesticide residues in food (organophosphates), consumption of canned food, especially fish/seafood (BPA), and use of personal care products (selected phthalates).</description>
    </item> <item>
      <title>Response: the hypothalamus–pituitary–testis axis in cryptorchid boys (Letter To Editor)</title>
      <link>http://repub.eur.nl/res/pub/16543/</link>
      <pubDate>2009-08-20T00:00:00Z</pubDate>
      <description></description>
    </item> <item>
      <title>Urinary metabolite concentrations of organophosphorous pesticides, bisphenol A, and phthalates among pregnant women in Rotterdam, the Netherlands: The Generation R study (Article)</title>
      <link>http://repub.eur.nl/res/pub/18121/</link>
      <pubDate>2008-09-05T00:00:00Z</pubDate>
      <description>Concern about potential health impacts of low-level exposures to organophosphorus (OP) pesticides, bisphenol A (BPA), and phthalates among the general population is increasing. We measured levels of six dialkyl phosphate (DAP) metabolites of OP pesticides, a chlorpyrifos-specific metabolite (3,5,6-trichloro-2-pyridinol, TCPy), BPA, and 14 phthalate metabolites in urine samples of 100 pregnant women from the Generation R study, the Netherlands. The unadjusted and creatinine-adjusted concentrations were reported, and compared to National Health and Nutrition Examination Survey and other studies. In general, these metabolites were detectable in the urine of the women from the Generation R study and compared with other groups, they had relatively high-level exposures to OP pesticides and several phthalates but similar exposure to BPA. The median concentrations of total dimethyl (DM) metabolites was 264.0 nmol/g creatinine (Cr) and of total DAP was 316.0 nmol/g Cr. The median concentration of mono-ethyl phthalate (MEP) was 222.0 μg/g Cr; the median concentrations of mono-isobutyl phthalate (MiBP) and mono-n-butyl phthalate (MnBP) were above 50 μg/g Cr. The median concentrations of the three secondary metabolites of di-2-ethylhexyl phthalate (DEHP) were greater than 20 μg/g Cr. The data indicate that the Generation R study population provides a wide distribution of selected environmental exposures. Reasons for the relatively high levels and possible health effects need investigation.</description>
    </item> <item>
      <title>Maternal pregnancy serum level of heptachlor epoxide, hexachlorobenzene, and β-hexachlorocyclohexane and risk of cryptorchidism in offspring (Article)</title>
      <link>http://repub.eur.nl/res/pub/35124/</link>
      <pubDate>2007-11-01T00:00:00Z</pubDate>
      <description>Prenatal exposure to environmental endocrine disrupters has been postulated to cause adverse effects on male reproductive health. Exposure to organochlorine pesticides with anti-androgenic and estrogenic potency has been shown to interfere with the sex-hormone-dependent process of testicular descent in animal models. We examined the relation between serum levels of the pesticides heptachlor epoxide (HCE), hexachlorobenzene (HCB), and β-hexachlorocyclohexane (β-HCCH) in pregnant women, and the occurrence of cryptorchidism in their sons. These three pesticides were previously suggested as risk factors for cryptorchidism. In a nested case-control design, we compared serum levels between mothers of cases (n=219) and controls (n=564), selected from the Collaborative Perinatal Project, a US birth cohort study of pregnancies in 1959-1966. The offspring of mothers with HCE levels above the 90th percentile compared to those below the 10th percentile had an adjusted odds ratio of cryptorchidism of 1.2 (95% confidence interval 0.6-2.6); for β-HCCH the odds ratio was 1.6 (0.7-3.6). For HCB the adjusted odds ratio was near one. These results provide little support for an association of cryptorchidism with exposure to low levels of HCE or HCB. For β-HCCH the findings were somewhat suggestive of an association but were inconclusive.</description>
    </item> <item>
      <title>Maternal and paternal risk factors for cryptorchidism and hypospadias: a case-control study in newborn boys (Article)</title>
      <link>http://repub.eur.nl/res/pub/10368/</link>
      <pubDate>2004-01-01T00:00:00Z</pubDate>
      <description>Little is known on environmental risk factors for cryptorchidism and
      hypospadias, which are among the most frequent congenital abnormalities.
      The aim of our study was to identify risk factors for cryptorchidism and
      hypospadias, with a focus on potential endocrine disruptors in parental
      diet and occupation. In a case-control study nested within a cohort of
      8,698 male births, we compared 78 cryptorchidism cases and 56 hypospadias
      cases with 313 controls. The participation rate was 85% for cases and 68%
      for controls. Through interviews, information was collected on pregnancy
      aspects and personal characteristics, lifestyle, occupation, and dietary
      phytoestrogen intake of both parents. Occupational exposure to potential
      endocrine disruptors was classified based on self-reported exposure and
      ratings of occupational hygienists based on job descriptions. Our findings
      indicate that paternal pesticide exposure was associated with
      cryptorchidism [odds ratio (OR) = 3.8; 95% confidence interval (95% CI),
      1.1-13.4]. Smoking of the father was associated with hypospadias (OR =
      3.8; 95% CI, 1.8-8.2). Maternal occupational, dietary, and lifestyle
      exposures were not associated with either abnormality. Both abnormalities
      were associated with suboptimal maternal health, a lower maternal
      education, and a Turkish origin of the parents. Being small for
      gestational age was a risk factor for hypospadias, and preterm birth was a
      risk factor for cryptorchidism. Because paternal pesticide exposure was
      significantly associated with cryptorchidism and paternal smoking was
      associated with hypospadias in male offspring, paternal exposure should be
      included in further studies on cryptorchidism and hypospadias risk
      factors.</description>
    </item> <item>
      <title>A high hypospadias rate in The Netherlands (Article)</title>
      <link>http://repub.eur.nl/res/pub/9880/</link>
      <pubDate>2002-01-01T00:00:00Z</pubDate>
      <description>BACKGROUND: Reports on increasing hypospadias trends are based on birth
      defect registries, which are prone to inaccuracy. We assessed the
      prevalence of hypospadias precisely, by prospective examination of all
      newborns in Rotterdam over a 2-year period. METHODS: A total of 7292
      consecutive male births were examined for the presence of hypospadias,
      classified by severity. RESULTS: The frequency of hypospadias in newborn
      boys was 0.73% (53/7292). The rate among live births was 38 per 10 000,
      which is 6 times the previously reported rate for the Southwestern
      Netherlands (6.2) (P &lt; 0.0001). This registry excludes glandular
      hypospadias. Without glandular cases, our rate is 26 per 10 000, which is
      still 4-fold higher (P &lt; 0.0001). The ratio of minor to major hypospadias
      was 0.3. In 79% of cases, surgery was indicated. CONCLUSIONS: We found a
      4-fold higher than expected hypospadias rate, which may be explained by
      case ascertainment differences. The proportion of major cases was higher
      than generally assumed. This study provides evidence for substantial
      geographical differences. Explanations for temporal and geographical
      differences need to be explored. To monitor hypospadias rates and trends
      accurately, complete case ascertainment, including standardized
      classification of severity, is warranted.</description>
    </item> <item>
      <title>Structured data collection in clinical andrology (Doctoral Thesis)</title>
      <link>http://repub.eur.nl/res/pub/20035/</link>
      <pubDate>1999-10-06T00:00:00Z</pubDate>
      <description></description>
    </item> <item>
      <title>Serum inhibin B as a marker of spermatogenesis (Article)</title>
      <link>http://repub.eur.nl/res/pub/8902/</link>
      <pubDate>1998-01-01T00:00:00Z</pubDate>
      <description>Inhibin B is produced by Sertoli cells, provides negative feedback on FSH
          secretion, and may prove to be an important marker for the functioning of
          seminiferous tubules. The purpose of the present study was to examine the
          relationship between the spermatogenic function of the testis of
          subfertile men and the plasma concentrations of inhibin B and FSH. These
          parameters were estimated in a group of 218 subfertile men. Serum inhibin
          B levels were closely correlated with the serum FSH levels (r = -0.78, P &lt;
          0.001), confirming the role of inhibin B as feedback signal for FSH
          production. The spermatogenic function of the testis was evaluated by
          determining testicular volume and total sperm count. Inhibin B levels were
          significantly correlated with the total sperm count and testicular volume
          (r = 0.54 and r = 0.63, respectively; P &lt; 0.001). Testicular biopsies were
          obtained in 22 of these men. Inhibin B was significantly correlated with
          the biopsy score (r = 0.76, P &lt; 0.001). Receiver operating characteristic
          analysis revealed a diagnostic accuracy of 95% for differentiating
          competent from impaired spermatogenesis for inhibin B, whereas for FSH, a
          value of 80% was found. We conclude that inhibin B is the best available
          endocrine marker of spermatogenesis in subfertile men.</description>
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