Maternal Exposure to Drinking-water Chlorination By-products and Small-for-gestational-age Neonates

Levallois, Patrick; Gingras, Suzanne; Marcoux, Sylvie; Legay, Christelle; Catto, Cyril; Rodriguez, Manuel J.; Tardif, Robert

doi:10.1097/ede.0b013e3182468569

Cited by 67 publications

(48 citation statements)

References 30 publications

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“…2,3,6,[8][9][10][11] Exposure to trihalomethanes and other volatile disinfection by-products occurs predominantly through inhalation and absorption, during activities such as showering, bathing, and swimming. 12,13 For non-volatile disinfection by-products, such as haloacetic acids, ingestion is the main route of exposure.…”

Section: Introductionmentioning

confidence: 99%

Drinking Water Disinfection By-products, Genetic Polymorphisms, and Birth Outcomes in a European Mother–Child Cohort Study

et al. 2016

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Section: Introductionmentioning

confidence: 99%

Drinking Water Disinfection By-products, Genetic Polymorphisms, and Birth Outcomes in a European Mother–Child Cohort Study

et al. 2016

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“…Participants were from a previous study on the association between exposure to THMs and HAAs during pregnancy and the occurrence of SGA (Levallois et al 2012). Among the 2647 women (and their child) participating to the original study, 2517 (95%) accepted to be contacted for a follow-up study.…”

Section: Study Design and Populationmentioning

confidence: 99%

“…Also, because our focus was the effect of the DBPs exposure in the third trimester and in accordance to our previous study (Levallois et al 2012), only term babies were considered for this study (see Figure 1).…”

Section: Study Design and Populationmentioning

confidence: 99%

“…Details are given in the original study (Levallois et al 2012). In brief, THM and HAA were monitored monthly during the study at 53 sites within the 16 water distribution systems serving the residence of participants.…”

Section: Dbps Exposure Assessmentmentioning

confidence: 99%

“…Our exposure assessment was optimized with monthly sampling of DBPs in the drinking water systems serving the residences of participants, high quality DBPs laboratory analysis and detailed description of water consumption as well as correction for the effectiveness of home treatment devices and other handling for DBP removal. All routes of exposure were also considered for THMs which are volatiles and lipophilic and internal dose was estimated using a PBPK model taking into consideration personal anthropometric characteristics of each participant (Levallois et al 2012). Also, it is important to consider that our higher exposure levels to THMs (nearly the double than the levels evaluated in previous studies) are normally more favourable to detect an association.…”

Section: Strengths and Limitations Of The Studymentioning

confidence: 99%

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Disinfection by-products exposure and intra-uterine growth restriction: Do genetic polymorphisms of CYP2E1or deletion of GSTM1 or GSTT1 modify the association?

Levallois

Giguère

Nguilé-Makao

et al. 2016

Environment International

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Background-Exposure to disinfection by-products (DBPs) during pregnancy was associated with reduced fetal growth. Genetic susceptibility might play a role, especially for genes encoding for the Cytochrome P450 (CYP2E1) and Glutathione S-Transferase (GST) enzymes, involved in metabolism and activation of DBPs. Few epidemiological studies evaluated these geneenvironment interactions and their results were never replicated.Objective-This study aims to examine interactions between trihalomethanes (THM) or haloacetic acids (HAA) exposure and genetic polymorphisms on small for gestational age (SGA) neonates by investigating single nucleotide polymorphisms (SNPs) in CYP2E1 gene and GSTM1 and GSTT1 deletions in mothers-children pairs.Methods-A population-based case-control study of 1549 mothers and 1455 children was conducted on SGA and THM/HAA exposure. DNA was extracted from blood or saliva cells. Targeted SNPs and deletions were genotyped. Statistical interaction between SNPs/deletions and THMs or HAAs in utero exposure with regard to SGA occurrence was evaluated by unconditional logistic regression with control of potential confounders.Results-Previously reported positive modification of the effect of THM uterine exposure by mothers or newborns CYP2E1 rs3813867 C allele or GSTM1 deletion was not replicated. However interactions with CYP2E1 rs117618383 and rs2515641 were observed but were not statistically significant after correction for multiple testing. Conclusions-Previous positive interactions betweenTHMs exposure and CYP2E1 and GSTM1 were not replicated but interactions with other CYP2E1 polymorphisms are reported.

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Impact of chloroform exposures on reproductive and developmental outcomes: A systematic review of the scientific literature

Williams

Bates

Pace

et al. 2018

Birth Defects Research

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Aims:We assessed the animal and epidemiological data to determine if chloroform exposure causes developmental and/or reproductive toxicity. Results and Discussion: Initial scoping identified developmental toxicity as the primary area of concern. At levels producing maternal toxicity in rats and mice, chloroform caused decrements in fetal weights and associated delays in ossification. In a single mouse inhalation study, exposure to a high concentration of chloroform was associated with small fetuses and increased cleft palate. However, oral exposure of mice to chloroform at a dose 4 times higher was negative for cleft palate; multiple inhalation studies in rats were also negative. Epidemiologic data on low birth weight and small for gestational age were generally equivocal, preventing conclusions from being drawn for humans. The animal data also show evidence of very early (peri-implantation) total litter losses at very high exposure levels. This effect is likely maternally mediated rather than a direct effect on the offspring. Finally, the epidemiologic data indicate a possible association of higher chloroform exposure with lower risk of preterm birth (<37 weeks gestation). Conclusions: The available animal data suggest that exposures lower than those causing maternal toxicity should be without developmental effects in the offspring. Also, most studies in humans rely on group-level geographic exposure data, providing only weak epidemiologic evidence for an association with development outcomes and fail to establish a causal role for chloroform in the induction of adverse developmental outcomes at environmentally relevant concentrations. K E Y W O R D Sbirth defects, chloroform, developmental toxicity, epidemiology, teratogenicity

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Maternal Exposure to Drinking-water Chlorination By-products and Small-for-gestational-age Neonates

Abstract: Oral exposure to high levels of chlorination by-products in drinking water could be a risk factor for term SGA.

Cited by 67 publications

References 30 publications

Drinking Water Disinfection By-products, Genetic Polymorphisms, and Birth Outcomes in a European Mother–Child Cohort Study

Drinking Water Disinfection By-products, Genetic Polymorphisms, and Birth Outcomes in a European Mother–Child Cohort Study

Disinfection by-products exposure and intra-uterine growth restriction: Do genetic polymorphisms of CYP2E1or deletion of GSTM1 or GSTT1 modify the association?

Impact of chloroform exposures on reproductive and developmental outcomes: A systematic review of the scientific literature

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