Alteration of pregnancy related hormones and fetal survival in F-344 rats exposed by inhalation to benzo(a)pyrene

Archibong, Anthony E.; Inyang, Frank; Ramesh, Aramandla; Greenwood, Michael; Nayyar, Tultul; Kopsombut, Prapaporn; Hood, Darryl B.; Nyanda, Alfred M.

doi:10.1016/s0890-6238(02)00058-8

Cited by 137 publications

(83 citation statements)

References 52 publications

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“…It was recently shown, in rats, that mid-gestation inhalation of aerosolized BaP resulted in decreased fetal survival in a dose-dependent manner [Archibong et al 2002]; similar results have also been reported in pregnant rats [Bui et al 1986] and mice [Mackenzie and Angevine 1981] exposed to BaP. Resorption of the entire litter was observed in pregnant mice orally exposed to carbon black oil, which is a petroleum refinery by-product, containing several classes of hydrocarbons, including PAHs [Hansen et al 2000].…”

Section: Polycyclic Aromatic Hydrocarbonssupporting

confidence: 52%

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

Detmar

Jurisicova

2010

Systems Biology in Reproductive Medicine

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Polycyclic aromatic hydrocarbons (PAHs) are released into the environment as a result of incomplete fossil fuel combustion from industrial furnaces, woodburning stoves, and automobile exhaust fumes; however, the primary source of human exposure to these compounds is cigarette smoke. Embryonic and fetal loss after treatment with high doses of PAHs have been well documented in animal studies; however, few studies have addressed the reproductive consequences of long-term, low-level exposure to these chemicals. We previously reported that low doses of PAHs administered to ICR mice over a period of 9 weeks prior to conception resulted in early embryonic resorptions, whereby treated dams lost approximately 50% of their litter. During the course of these studies, we observed greater numbers of infiltrating uterine natural killer (uNK) cells into the placenta of PAH-exposed conceptuses. While exposure to high levels of PAHs has been shown to be immunosuppressive, increasing evidence suggests that chronic, low-dose exposure to PAHs may stimulate immune cells. Thus, we hypothesized that low-dose, chronic PAH exposure in our mouse model is mediating embryonic resorption by hyperstimulating maternal immune cells. In this review of the literature, we outline the rationale of our argument and present preliminary data, focussing upon PAH-mediated alterations in uNK cell dynamics and how these changes may be linked to early embryonic resorptions.

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Section: Polycyclic Aromatic Hydrocarbonssupporting

confidence: 52%

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

Detmar

Jurisicova

2010

Systems Biology in Reproductive Medicine

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“…Teratogenicity has not been reported based on gross examination, and none of the studies conducted detailed skeletal or visceral examinations of pups. Inhalation studies with benzo [a]pyrene in pregnant rats have demonstrated decreased fetal survival, which resulted from a reduction of luteotropic hormone synthesis and release (Archibong et al, 2002). Similar studies in male rats showed reduced reproductive capacity due to changes in sperm parameters, impaired epididymal function and disturbed hormonal regulation in the testes (Inyang et al, 2003).…”

Section: Reproductive and Developmental Toxicitymentioning

confidence: 94%

Integrating Field Analyses with Laboratory Exposures to Assess Ecosystems Health

Hellou¹,

Beach²,

Leonard³

et al. 2012

Polycyclic Aromatic Compounds

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initiated a programme on the evaluation of the carcinogenic risk of chemicals to humans involving the production of critically evaluated monographs on individual chemicals. The programme was subsequently expanded to include evaluations of carcinogenic risks associated with exposures to complex mixtures, life-style factors and biological and physical agents, as well as those in specific occupations. The objective of the programme is to elaborate and publish in the form of monographs critical reviews of data on carcinogenicity for agents to which humans are known to be exposed and on specific exposure situations; to evaluate these data in terms of human risk with the help of international working groups of experts in chemical carcinogenesis Publications of the World Health Organization enjoy copyright protection in accordance with the provisions of Protocol 2 of the Universal Copyright Convention. All rights reserved.The International Agency for Research on Cancer welcomes requests for permission to reproduce or translate its publications, in part or in full. Requests for permission to reproduce or translate IARC publications -whether for sale or for noncommercial distribution -should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; email: permissions@who.int).The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the World Health Organization concerning the legal status of any country, territory, city, or area or of its authorities, or concerning the delimitation of its frontiers or boundaries.The mention of specific companies or of certain manufacturers' products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.The IARC Monographs Working Group alone is responsible for the views expressed in this publication. IARC Library Cataloguing in Publication Data NOTE TO THE READERThe term 'carcinogenic risk' in the IARC Monographs series is taken to mean that an agent is capable of causing cancer under some circumstances. The Monographs evaluate cancer hazards, despite the historical presence of the word 'risks' in the title.Inclusion of an agent in the Monographs does not imply that it is a carcinogen, only that the published data have been examined. Equally, the fact that an agent has not yet been evaluated in a Monograph does not mean that it is not carcinogenic.The evaluations of carcinogenic risk are made by international working groups of independent scientists and are qualitative in nature. No recommendation is given for regulation or legislation.Anyone who is aware of published data that may alter the evaluation of the carcinogenic risk of an agent to humans is encouraged to make this information available to the Section of IARC Monographs, International Agency for...

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“…PAHs have been shown to be neurodevelopmental toxicants in experimental studies [19][20][21]. Suggested mechanisms include endocrine disruption [41][42][43], binding to receptors for placental growth factors resulting in decreased exchange of oxygen and nutrients [44], binding to the human Ah receptor to induce P450 enzymes, DNA damage resulting in activation of apoptotic pathways [45][46][47], epigenetic effects [48], or oxidative stress due to inhibition of the brain antioxidant scavenging system [49].…”

Section: Exposure To Gas Cooking and Children's Neurodevelopmentmentioning

confidence: 99%

Exposure to widespread environmental toxicants and children’s cognitive development and behavioral problems

Jurewicz¹,

Polańska²,

Hanke³

2013

International Journal of Occupational Medicine and Environmental Health

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Nowadays a special attention is focused on prenatal and childhood exposures to a variety of contaminants in the environment, especially toxicants widely present in the environment and their impact on children's health and neurodevelopment. This article aims at evaluating the impact of exposure to several widespread toxicants including: polycyclic aromatic hydrocarbons (PAHs), phthalates, bisphenol A, brominated flame retardants and gas cooking on children's cognitive development and behavioral problems by reviewing most recent published literature. Epidemiological studies focusing on exposure to widespread toxicants and children's development for the last eleven years were identified by a search of the PubMed, Medline, Ebsco and Toxnet literature bases. The combination of following key words was used: 1) referring to the exposure: pregnancy, prenatal exposure, postnatal exposure, gas cooking, exposure to phthalates, bisphenol A, brominated flame retardants, PAHs and 2) referring to outcome: neurodevelopment, neurobehavior, psychomotor development, behavioral problems, cognitive development, mental health, school achievements, learning abilities. The results from the presented studies suggest that there are strong and rather consistent indications that the developing nervous system is particularly vulnerable to insult from low levels of exposure to widespread environmental contaminants such as: phthalates, bisphenol A, brominated flame retardants, polycyclic aromatic hydrocarbons, gas cooking. Considering the suggested health effects, more epidemiologic data is urgently needed and, in the meantime, precautionary policies must be implemented.

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Alteration of pregnancy related hormones and fetal survival in F-344 rats exposed by inhalation to benzo(a)pyrene

Cited by 137 publications

References 52 publications

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

Integrating Field Analyses with Laboratory Exposures to Assess Ecosystems Health

Exposure to widespread environmental toxicants and children’s cognitive development and behavioral problems

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