Gabriel D. Shapiro

Dr. Gabriel D. Shapiro


Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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31 October 2017 in Archives of Physical Medicine and Rehabilitation
Verified
Journal Article
Closed access
BGBrian Grieve
Brian Grieve
GSGabriel D. Shapiro
Gabriel D. Shapiro
LWLucy Wibbenmeyer
Lucy Wibbenmeyer
AAAmy Acton
Amy Acton
ALAustin Lee
Austin Lee
TTTaryn Travis
Taryn Travis

JAJillian Ashley-Martin
Jillian Ashley-Martin
LDLinda Dodds
Linda Dodds
TATye E. Arbuckle
Tye E. Arbuckle
AMAnne-Sophie Morisset
Anne-Sophie Morisset
MFMandy Fisher
Mandy Fisher
WFWilliam Donald Fraser
William Donald Fraser
Perfluoroalkyl substances (PFASs) are ubiquitous, persistent pollutants widely used in the production of common household and consumer goods. There is a limited body of literature suggesting that these chemicals may alter metabolic pathways and growth trajectories. The relationship between prenatal exposures to these chemicals and gestational weight gain (GWG) has received limited attention. One objective was to analyze the associations among maternal plasma levels of three common perfluoroalkyl substances (perfluorooctanoate (PFOA), perfluorooctanesulfonate (PFOS), perfluorohexanesulfanoate (PFHxS)) and GWG. Additionally, we explored whether GWG was associated with cord blood PFAS levels. This study utilized data collected in the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, a trans-Canada cohort study of 2001 pregnant women. Our analysis quantified associations between (1) maternal PFAS concentrations and GWG and (2) GWG and cord blood PFAS concentrations. Maternal PFOS concentrations were positively associated with GWG (β = 0.39 95% CI: 0.02, 0.75). Interquartile increases in GWG were significantly associated with elevated cord blood PFOA (OR = 1.33; 95% CI: 1.13 to 1.56) and PFOS (OR = 1.20; 95% CI: 1.03 to 1.40) concentrations. No statistically significant associations were observed between GWG and either measure of PFHxS. These findings warrant elucidation of the potential underlying mechanisms.

25 October 2016 in Paediatric and Perinatal Epidemiology
Verified
Journal Article
Open access
PDF file
WFWilliam Donald Fraser
William Donald Fraser
GSGabriel D. Shapiro
Gabriel D. Shapiro
FAFrançois Audibert
François Audibert
LDLise Dubois
Lise Dubois
JPJean‐Charles Pasquier
Jean‐Charles Pasquier
ZLZhong‐Cheng Luo
Zhong‐Cheng Luo
Background: The 3D Cohort Study (Design, Develop, Discover) was established to help bridge knowledge gaps about the links between various adverse exposures during pregnancy with birth outcomes and later health outcomes in children.Methods: Pregnant women and their partners were recruited during the first trimester from nine sites in Quebec and followed along with their children through to 2 years of age. Questionnaires were administered during pregnancy and post‐delivery to collect information on demographics, mental health and life style, medical history, psychosocial measures, diet, infant growth, and neurodevelopment. Information on the delivery and newborn outcomes were abstracted from medical charts. Biological specimens were collected from mothers during each trimester, fathers (once during the pregnancy), and infants (at delivery and 2 years of age) for storage in a biological specimen bank.Results: Of the 9864 women screened, 6348 met the eligibility criteria and 2366 women participated in the study (37% of eligible women). Among women in the 3D cohort, 1721 of their partners (1704 biological fathers) agreed to participate (73%). Two thousand two hundred and nineteen participants had a live singleton birth (94%). Prenatal blood and urine samples as well as vaginal secretions were collected for ≥98% of participants, cord blood for 81% of livebirths, and placental tissue for 89% of livebirths.Conclusions: The 3D Cohort Study combines a rich bank of multiple biological specimens with extensive clinical, life style, and psychosocial data. This data set is a valuable resource for studying the developmental etiology of birth and early childhood neurodevelopmental outcomes.

1 July 2018 in International Journal of Hygiene and Environmental Health
Verified
Journal Article
Open access
JAJillian Ashley-Martin
Jillian Ashley-Martin
LDLinda Dodds
Linda Dodds
TATye E. Arbuckle
Tye E. Arbuckle
AEAdrienne S. Ettinger
Adrienne S. Ettinger
GSGabriel D. Shapiro
Gabriel D. Shapiro
MBMaryse Bouchard
Maryse Bouchard
Epidemiological studies have hypothesized that both insufficient and excess blood manganese (Mn) levels during pregnancy are associated with reduced fetal growth. This literature is characterized by inconsistent results and a limited focus on women with exposures representative of the general North American population. We examined the relationship between maternal and cord blood Mn levels and fetal growth among women enrolled in the Maternal-Infant Research on Environmental Chemicals Study (MIREC). Mothers with singleton, term infants and complete maternal first and third trimester blood Mn data were eligible for inclusion in the present study (n = 1519). Mean birth weight and odds ratios of small for gestational age (SGA) births according to maternal and cord blood Mn levels (low (<10), referent (10-<90), high (≥90) percentiles) were estimated. We also evaluated the association between the ratio of cord and maternal blood Mn and birth weight. Women with low (<0.82 μg/dL) maternal blood third trimester Mn levels had infants that weighed an average of 64.7 g (95% CI: -142.3,12.8) less than infants born to women in the referent exposure group. This association was strengthened and became statistically significant when adjusted for toxic metals (lead, mercury, arsenic, and cadmium) [-83.3 g (95% CI: -162.4, -4.1)]. No statistically significant associations were observed in models of maternal first trimester or cord blood Mn. A one unit increase in the cord/maternal blood Mn ratio was associated with a 29.4 g (95% CI: -50.2, -8.7), when adjusted for maternal and neonatal characteristics. Our findings motivate additional research regarding the relation between Mn exposure and fetal growth. Further inquiry is necessary to determine whether an exposure threshold exists, how growth related effects of maternal and fetal Mn may differ, and how concurrent exposure to other toxic metals may impact the association between Mn and growth.

24 June 2016 in Journal of Epidemiology and Community Health
Verified
Journal Article
Closed access
PDF file
GSGabriel D. Shapiro
Gabriel D. Shapiro
TBTracey Bushnik
Tracey Bushnik
ASAmanda J Sheppard
Amanda J Sheppard
MKMichael S Kramer
Michael S Kramer
JKJay S Kaufman
Jay S Kaufman
SYSeungmi Yang
Seungmi Yang
Background Research on predictors of adverse birth outcomes has focused on maternal characteristics. Much less is known about the role of paternal factors. Paternal education is an important socioeconomic marker that may predict birth outcomes over and above maternal socioeconomic indicators. Methods Using data from the 2006 Canadian Birth-Census Cohort, we estimated the associations between paternal education and preterm birth, small-for-gestational-age (SGA) birth, stillbirth and infant mortality in Canada, controlling for maternal characteristics. Binomial regression was used to estimate risk ratios and risk differences for adverse birth outcomes associated with paternal education, after controlling for maternal education, age, marital status, parity, ethnicity and nativity. Results A total of 131 285 singleton births were included in the present study. Comparing the lowest to the highest paternal education category, adjusted risk ratios (95% CIs) were 1.22 (1.10 to 1.35) for preterm birth, 1.13 (1.03 to 1.23) for SGA birth, 1.92 (1.28 to 2.86) for stillbirth and 1.67 (1.01 to 2.75) for infant mortality. Consistent patterns of associations were observed for absolute risk differences. Conclusions Our study suggests that low paternal education increases the risk of adverse birth outcomes, and especially of fetal and infant mortality, independently from maternal characteristics.

1 August 2018 in Annals of Epidemiology
Verified
Journal Article
Closed access
GSGabriel D. Shapiro
Gabriel D. Shapiro
TBTracey Bushnik
Tracey Bushnik
RWRussell Wilkins
Russell Wilkins
MKMichael S. Kramer
Michael S. Kramer
JKJay S. Kaufman
Jay S. Kaufman
SYSeungmi Yang
Seungmi Yang