Perfluorooctanoate: Placental and lactational transport pharmacokinetics in rats

Hinderliter, Paul M.; Mylchreest, Eve; Gannon, Shawn A.; Butenhoff, John L.; Kennedy, Gerald L.

doi:10.1016/j.tox.2005.03.010

Cited by 78 publications

(52 citation statements)

References 21 publications

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“…Infants and young children may have proportionately greater exposure to water-borne pollutants since they drink more water per kg of body weight than do adults (28). The levels in the very young may also represent additional exposures as PFOA has been shown to cross the placenta and to be present in breast milk (at approximately 1/10 of the serum concentration) in Sprague Dawley rats (29), although comparable studies in humans are lacking. We are performing further studies to elucidate PFOA exposures in maternal milk and infant formula.…”

Section: Discussionmentioning

confidence: 99%

Community Exposure to Perfluorooctanoate: Relationships Between Serum Concentrations and Exposure Sources

Emmett

Shofer

Zhang

et al. 2006

Journal of Occupational and Environmental Medicine

320

300

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Objective-To determine serum [PFOA] in residents near a fluoropolymer production facility: the contributions from air, water and occupational exposures, personal and dietary habits, and relationships to age and gender.Methods-Questionnaire and serum PFOA measurements in a stratified random sample and volunteers residing in locations with the same residential water supply but with higher and lower potential air PFOA exposure. [PFOA] greatly exceeded general population medians. Occupational exposure from production processes using PFOA and residential water had additive effects, no other occupations contributed. Serum [PFOA] depended on the source of residential drinking water, and not potential air exposure. For public water users the best-fit model included age, tap water drinks per day, servings of home-grown fruit and vegetables, and carbon filter use. Results-SerumConclusions-Residential water source was the primary determinant of serum [PFOA].

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Section: Discussionmentioning

confidence: 99%

Community Exposure to Perfluorooctanoate: Relationships Between Serum Concentrations and Exposure Sources

Emmett

Shofer

Zhang

et al. 2006

Journal of Occupational and Environmental Medicine

320

300

View full text Add to dashboard Cite

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“…Animal studies as well as human studies have demonstrated that PFCs can cross the placental barrier and thereby expose the foetus (Apelberg et al 2007;Hinderliter et al 2005;Inoue et al 2004a;Monroy et al 2008). PFCs have also been detected in breast milk, and in a limited study on 12 primiparous Swedish mothers, PFOS concentrations in breast milk of around 1% of those in serum were found (Kärrman et al 2007).…”

Section: Human Biomonitoring (Internal Dose)mentioning

confidence: 99%

Characterisation of human exposure pathways to perfluorinated compounds — Comparing exposure estimates with biomarkers of exposure

Haug

Huber

Becher

et al. 2011

Environment International

339

215

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“…Both chemicals have been detected in blood samples collected from the general public, with human half-lives for PFOS and PFOA of 3.8 and 5.4 yr, respectively (28). They are readily absorbed, are not metabolized in humans, and cross the placental barrier to accumulate in the developing fetus (2,17,20). Newborns are exposed to PFCs through breastfeeding (21).…”

mentioning

confidence: 99%

Chronic exposure to perfluorinated compounds: Impact on airway hyperresponsiveness and inflammation

Ryu

Jha

Ojo

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

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Emerging epidemiological evidence reveals a link between lung disease and exposure to indoor pollutants such as perfluorinated compounds (PFCs). PFC exposure during critical developmental stages may increase asthma susceptibility. Thus, in a murine model, we tested the hypothesis that early life and continued exposure to two ubiquitous household PFCs, perfluorooctanoic acid (PFOA) and perflurooctanesulfonic acid (PFOS), can induce lung dysfunction that exacerbates allergen-induced airway hyperresponsiveness (AHR) and inflammation. Balb/c mice were exposed to PFOA or PFOS (4 mg/kg chow) from gestation day 2 to 12 wk of age by feeding pregnant and nursing dams, and weaned pups. Some pups were also sensitized and challenged with ovalbumin (OVA). We assessed lung function and inflammatory cell and cytokine expression in the lung and examined bronchial goblet cell number. PFOA, but not PFOS, without the OVA sensitization/challenge induced AHR concomitant with a 25-fold increase of lung macrophages. PFOA exposure did not affect OVA-induced lung inflammatory cell number. In contrast, PFOS exposure inhibited OVA-induced lung inflammation, decreasing total cell number in lung lavage by 68.7%. Interferon-γ mRNA in the lung was elevated in all PFC-exposed groups. Despite these effects, neither PFOA nor PFOS affected OVA-induced AHR. Our data do not reveal PFOA or PFOS exposure as a risk factor for more severe allergic asthma-like symptoms, but PFOA alone can induce airway inflammation and alter airway function.

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Perfluorooctanoate: Placental and lactational transport pharmacokinetics in rats

Cited by 78 publications

References 21 publications

Community Exposure to Perfluorooctanoate: Relationships Between Serum Concentrations and Exposure Sources

Community Exposure to Perfluorooctanoate: Relationships Between Serum Concentrations and Exposure Sources

Characterisation of human exposure pathways to perfluorinated compounds — Comparing exposure estimates with biomarkers of exposure

Chronic exposure to perfluorinated compounds: Impact on airway hyperresponsiveness and inflammation

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