Developmental toxicity in white leghorn chickens following in ovo exposure to perfluorooctane sulfonate (PFOS)

Peden‐Adams, Margie M.; Stuckey, Joyce E.; Gaworecki, Kristen M.; Berger-Ritchie, Jennifer; Bryant, K.; Jodice, Patrick G. R.; Scott, Thomas R.; Ferrario, Joseph; Guan, Bing Cai; Vigo, Craig; Boone, J. Scott; McGuinn, W. David; DeWitt, Jamie C.; Keil, Deborah E.

doi:10.1016/j.reprotox.2008.10.009

Cited by 75 publications

(49 citation statements)

References 96 publications

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“…The role of PPARa in the avian hepatocyte response to PFOS exposure is addressed further below under Interaction networks and potential regulatory molecules. The large number of dysregulated genes involved in cellular growth and proliferation, hepatic system disease, and DNA replication, as well as an enrichment of cancer-related genes in the L40 and T10 groups, is consistent with the hepatomegaly, hepatocellular adenoma, and hyperplasia that have been observed in mammals [10,40,47] and birds [12][13][14]16] exposed to PFOS. Several genes in the hepatic system and disease category were also associated with intrahepatic cholestasis (Supplemental Data, Table S4A-C), which, as previously discussed, may be a result of Myh6 overexpression.…”

Section: Functional Analysissupporting

confidence: 77%

“…Effects from such studies include interference with lipid and carbohydrate metabolism, increased liver weight, hepatomegaly, disruption of the neuroendocrine system, and decreased reproductive success [8][9][10][11]. For birds, exposure to T-PFOS can cause hepatic lesions, reduced hatching success, and reduced survivability of hatchlings [12][13][14][15][16]. These experiments, however, might not accurately reflect natural exposure conditions experienced by wildlife because they do not consider PFOS isomer kinetics and therefore may lead to poor estimations of exposure effects.…”

Section: Introductionmentioning

confidence: 99%

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Technical‐grade perfluorooctane sulfonate alters the expression of more transcripts in cultured chicken embryonic hepatocytes than linear perfluorooctane sulfonate

O’Brien

Austin

Williams

et al. 2011

Enviro Toxic and Chemistry

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Recently it was discovered that the perfluorooctane sulfonate (PFOS) detected in wildlife, such as fish-eating birds, had a greater proportion of linear PFOS (L-PFOS) than the manufactured technical product (T-PFOS), which contains linear and branched isomers. This suggests toxicological studies based on T-PFOS data may inaccurately assess exposure risk to wildlife. To determine whether PFOS effects were influenced by isomer content, we compared the transcriptional profiles of cultured chicken embryonic hepatocytes (CEH) exposed to either L-PFOS or T-PFOS using Agilent microarrays. At equal concentrations (10 µM), T-PFOS altered the expression of more transcripts (340, >1.5-fold change, p < 0.05) compared with L-PFOS (130 transcripts). Higher concentrations of L-PFOS (40 µM) were also less transcriptionally disruptive (217 transcripts) than T-PFOS at 10 µM. Functional analysis showed that L-PFOS and T-PFOS affected genes involved in lipid metabolism, hepatic system development, and cellular growth and proliferation. Pathway and interactome analysis suggested that genes may be affected through the RXR receptor, oxidative stress response, TP53 signaling, MYC signaling, Wnt/β-catenin signaling, and PPARγ and SREBP receptors. In all functional categories and pathways examined, the response elicited by T-PFOS was greater than that of L-PFOS. These data show that T-PFOS elicits a greater transcriptional response in CEH than L-PFOS alone and demonstrates the importance of considering the isomer-specific toxicological properties of PFOS when assessing exposure risk.

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Section: Functional Analysissupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Technical‐grade perfluorooctane sulfonate alters the expression of more transcripts in cultured chicken embryonic hepatocytes than linear perfluorooctane sulfonate

O’Brien

Austin

Williams

et al. 2011

Enviro Toxic and Chemistry

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“…Both PBDEs and PFCs exhibit persistent and bioaccumulative properties similar to legacy POPs, and they are now recognized as globally pervasive contaminants Hites, 2004). Laboratory studies that indicate exposure to these compounds can induce deleterious effects on avian immune function (Fernie et al, 2005), development (Peden-Adams et al, 2009), courtship behaviors (Fernie et al, 2008), and reproductive success (Fernie et al, 2009); yet, despite the potential risks to birds of prey, few exposure data exist for wild populations, particularly those utilizing terrestrial food webs (Chen and Hale, 2010). To address the need for baseline exposure data and assess relationships with foraging ecology in wild birds of prey, we measured levels of PCBs, PBDEs, PFCs, and 14 legacy pesticides in bird-of-prey species spanning multiple trophic levels as determined by stable isotope analysis.…”

Section: Introductionmentioning

confidence: 99%

Levels of Chlorinated, Brominated, and Perfluorinated Contaminants in Birds of Prey Spanning Multiple Trophic Levels

Yordy

Rossman

Ostrom

et al. 2013

Journal of Wildlife Diseases

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ABSTRACT:Birds of prey occupy high trophic levels and can consequently bioaccumulate high levels of environmental contaminants. To evaluate exposure to past-and current-use pollutants, we measured legacy contaminants (i.e., polychlorinated biphenyls [PCBs]; organochlorine pesticides, e.g., DDT), contaminants of emerging concern (polybrominated diphenyl ethers N) ranged from 5.2% to 13.7%, indicating the birds of prey spanned two to three trophic levels. Legacy contaminant levels were highly variable but generally comparable to levels reported previously for birds of prey in the southeast US, suggesting exposure has not declined substantially over the past 40 yr. Despite their status as newly emerging environmental contaminants, PFC levels were within the same order of magnitude as legacy contaminants. Although PBDEs were less prevalent, levels were among the greatest observed in wildlife to date (SPBDEs max. 200 mg/g lipid). Relative contaminant profiles also varied between birds of prey utilizing low and high trophic levels; specifically PFCs contributed to a larger proportion of the contaminant burden in birds utilizing high trophic levels, whereas the legacy pesticide mirex was a larger contributor in low-trophic-level birds, indicating that relative exposure is in part dependent on foraging ecology. This study demonstrates that birds of prey continue to face exposure to legacy contaminants as well as newly emerging contaminants at levels of concern.

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“…But when environmentally-induced immune insult occurs developmentally, it has the potential to result in a dysfunctional immune response pattern that may persist across a lifetime. Concern for the ramifications of developmental immunotoxicity (DIT) extends beyond humans (Dietert 2009) to include both agricultural (Bunn, Marsh, and Dietert 2000; Lavoie and Grasman 2007; Peden-Adams et al 2009) and wildlife species (Grasman and Fox 2001). In a prior review, the ramifications of developmental immunotoxicity (DIT) on the risk of pediatric asthma and allergy were discussed (Dietert and Zelikoff 2008).…”

Section: Introductionmentioning

confidence: 99%

Early life environment and developmental immunotoxicity in inflammatory dysfunction and disease

Leifer

Dietert

2011

Toxicological & Environmental Chemistry

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Components of the innate immune system such as macrophages and dendritic cells are instrumental in determining the fate of immune responses and are, also, among the most sensitive targets of early life environmental alterations including developmental immunotoxicity (DIT). DIT can impede innate immune cell maturation, disrupt tissue microenvironment, alter immune responses to infectious challenges, and disrupt regulatory responses. Dysregulation of inflammation, such as that observed with DIT, has been linked with an increased risk of chronic inflammatory diseases in both children and adults. In this review, we discuss the relationship between early-life risk factors for innate immune modulation and promotion of dysregulated inflammation associated with chronic inflammatory disease. The health risks from DIT-associated inflammation may extend beyond primary immune dysfunction to include an elevated risk of several later-life, inflammatory-mediated diseases that target a wide range of physiological systems and organs. For this reason, determination of innate immune status should be an integral part of drug and chemical safety evaluation.

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Developmental toxicity in white leghorn chickens following in ovo exposure to perfluorooctane sulfonate (PFOS)

Cited by 75 publications

References 96 publications

Technical‐grade perfluorooctane sulfonate alters the expression of more transcripts in cultured chicken embryonic hepatocytes than linear perfluorooctane sulfonate

Technical‐grade perfluorooctane sulfonate alters the expression of more transcripts in cultured chicken embryonic hepatocytes than linear perfluorooctane sulfonate

Levels of Chlorinated, Brominated, and Perfluorinated Contaminants in Birds of Prey Spanning Multiple Trophic Levels

Early life environment and developmental immunotoxicity in inflammatory dysfunction and disease

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