Human health risks due to airborne polychlorinated biphenyls are highest in New Bedford Harbor communities living closest to the harbor

Heiger-Bernays, Wendy; Tomsho, Kathryn S.; Basra, Komal; Petropoulos, Zoe E.; Crawford, Kathryn A.; Martínez, Andrés; Hornbuckle, Keri C.

doi:10.1016/j.scitotenv.2019.135576

Cited by 19 publications

(11 citation statements)

References 49 publications

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“…44 PCB exposures led to hypothyroidism and thyroid hormone (total T4 and T3) inhibition. 45,46 However, in our study, no significant changes in total T4 or T3 were observed in PCB-treated rats suggesting that thyroid hormone disruption may not be the most sensitive toxicity endpoint for PCBs. Our previously conducted study showed a significant reduction of total T4 using a mixture of Aroclor 1242 and Aroclor 1254 supplemented with PCB 11.…”

Section: ■ Materials and Methodscontrasting

confidence: 74%

Comprehensive Subchronic Inhalation Toxicity Assessment of an Indoor School Air Mixture of PCBs

Wang

Adamcakova‐Dodd

Flor

et al. 2020

Environ. Sci. Technol.

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Few in vivo inhalation studies have explored the toxicity of environmentally relevant mixtures of polychlorinated biphenyls (PCBs). The manufacture of industrial PCBs was banned in 1978, but PCBs continue to be formed in industrial and consumer products. Schools represent a significant source of airborne exposures to legacy and nonlegacy PCBs, placing children at risk. To evaluate the impact of these exposures, we generated an airborne mixture of PCBs, called the School Air Mixture (SAM), to match the profile of an older school from our adolescent cohort study. Female Sprague− Dawley rats were exposed either to SAM or filtered air in nose-only exposure systems, 4 h/day for 4 weeks. Congener-specific air and tissue PCB profiles were assessed using gas chromatography with tandem mass spectrometry (GC−MS/MS). PCB exposures recapitulated the target school air profile with a similarity coefficient, cos θ of 0.83. PCB inhalation yielded μg/g ∑ 209 PCB levels in tissues. Neurobehavioral testing demonstrated a modest effect on spatial learning and memory in SAM-exposed rats. PCB exposure induced oxidative stress in the liver and lungs, affected the maturational stages of hematopoietic stem cells, reduced telomerase activity in bone marrow cells, and altered the gut microbiota. This is the first study to emulate PCB exposures in a school and comprehensively evaluate toxicity.

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Section: ■ Materials and Methodscontrasting

confidence: 74%

Comprehensive Subchronic Inhalation Toxicity Assessment of an Indoor School Air Mixture of PCBs

Wang

Adamcakova‐Dodd

Flor

et al. 2020

Environ. Sci. Technol.

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“…It needs to be determined whether these in vitro effects of PCB 11 are predictive of in vivo effects, and whether they extend to other LC-PCBs. This point is underscored by a recent risk assessment that detected several airborne LC-PCBs for which there are limited to no toxicological data [290].…”

Section: Conclusion Data Gaps and Directions For Future Studymentioning

confidence: 99%

Evidence Implicating Non-Dioxin-Like Congeners as the Key Mediators of Polychlorinated Biphenyl (PCB) Developmental Neurotoxicity

Klocke

Lein

2020

IJMS

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Despite being banned from production for decades, polychlorinated biphenyls (PCBs) continue to pose a significant risk to human health. This is due to not only the continued release of legacy PCBs from PCB-containing equipment and materials manufactured prior to the ban on PCB production, but also the inadvertent production of PCBs as byproducts of contemporary pigment and dye production. Evidence from human and animal studies clearly identifies developmental neurotoxicity as a primary endpoint of concern associated with PCB exposures. However, the relative role(s) of specific PCB congeners in mediating the adverse effects of PCBs on the developing nervous system, and the mechanism(s) by which PCBs disrupt typical neurodevelopment remain outstanding questions. New questions are also emerging regarding the potential developmental neurotoxicity of lower chlorinated PCBs that were not present in the legacy commercial PCB mixtures, but constitute a significant proportion of contemporary human PCB exposures. Here, we review behavioral and mechanistic data obtained from experimental models as well as recent epidemiological studies that suggest the non-dioxin-like (NDL) PCBs are primarily responsible for the developmental neurotoxicity associated with PCBs. We also discuss emerging data demonstrating the potential for non-legacy, lower chlorinated PCBs to cause adverse neurodevelopmental outcomes. Molecular targets, the relevance of PCB interactions with these targets to neurodevelopmental disorders, and critical data gaps are addressed as well.

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“…PCBs have also been linked to deleterious changes in other health outcomes such as reproductive and immune function [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 ]. Detectable levels of PCBs are present in serum and tissue samples from humans [ 9 , 19 ] and livestock [ 20 ], as well as commercial milk [ 20 , 21 ], air [ 22 , 23 ] and water [ 24 ]. While the manufacture of PCBs is banned, exposure continues due to persistence of PCBs in the environment (legacy sources), as well as release of contemporary PCBs as unintentional byproducts during manufacturing processes such as paint pigment production [ 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

The Bladder Is a Novel Target of Developmental Polychlorinated Biphenyl Exposure Linked to Increased Inflammatory Cells in the Bladder of Young Mice

Kennedy

Spiegelhoff

Wang

et al. 2021

Toxics

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Bladder inflammation is associated with several lower urinary tract symptoms that greatly reduce quality of life, yet contributing factors are not completely understood. Environmental chemicals are plausible mediators of inflammatory reactions within the bladder. Here, we examine whether developmental exposure to polychlorinated biphenyls (PCBs) leads to changes in immune cells within the bladder of young mice. Female mice were exposed to an environmentally relevant mixture of PCBs through gestation and lactation, and bladders were collected from offspring at postnatal day (P) 28–31. We identify several dose- and sex-dependent PCB effects in the bladder. The lowest concentration of PCB (0.1 mg/kg/d) increased CD45+ hematolymphoid immune cells in both sexes. While PCBs had no effect on CD79b+ B cells or CD3+ T cells, PCBs (0.1 mg/kg/d) did increase F4/80+ macrophages particularly in female bladder. Collagen density was also examined to determine whether inflammatory events coincide with changes in the stromal extracellular matrix. PCBs (0.1 mg/kg/d) decreased collagen density in female bladder compared to control. PCBs also increased the number of cells undergoing cell division predominantly in male bladder. These results implicate perturbations to the immune system in relation to PCB effects on the bladder. Future study to define the underlying mechanisms could help understand how environmental factors can be risk factors for lower urinary tract symptoms.

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Human health risks due to airborne polychlorinated biphenyls are highest in New Bedford Harbor communities living closest to the harbor

Cited by 19 publications

References 49 publications

Comprehensive Subchronic Inhalation Toxicity Assessment of an Indoor School Air Mixture of PCBs

Comprehensive Subchronic Inhalation Toxicity Assessment of an Indoor School Air Mixture of PCBs

Evidence Implicating Non-Dioxin-Like Congeners as the Key Mediators of Polychlorinated Biphenyl (PCB) Developmental Neurotoxicity

The Bladder Is a Novel Target of Developmental Polychlorinated Biphenyl Exposure Linked to Increased Inflammatory Cells in the Bladder of Young Mice

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