Perfluoroalkyl substances in umbilical cord serum and gestational and postnatal growth in a Chinese birth cohort

Cao, Wencheng; Liu, Xiao; Liu, Xiaofang; Zhou, Yan; Zhang, Xiaotian; Tian, He; Wang, Jin; Shi, Feng; Wu, Yongning; Bhatti, Parveen; Wen, Shi Wu; Sun, Xin

doi:10.1016/j.envint.2018.04.015

Cited by 50 publications

(42 citation statements)

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“…PFAS are hard to be degraded under natural environmental conditions and can also be detected in the environment, plants, and wildlife 2 , 3 . Human populations are exposed to PFAS via ingestion of drinking water and food, inhalation of air and dust, and contact with contaminated media 2 , 4 . Emerging evidence has suggested an accumulation of PFAS in the human body is associated with adverse health effects, including immune-related health conditions (like allergic diseases, infection, and vaccine response), metabolic dysregulation (like nonalcoholic fatty liver disease, chronic kidney diseases), and neurodevelopmental delays 5 – 9 .…”

Section: Introductionmentioning

confidence: 99%

Perfluoroalkyl substance pollutants activate the innate immune system through the AIM2 inflammasome

et al. 2021

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Perfluoroalkyl substances (PFAS) are widely used in various manufacturing processes. Accumulation of these chemicals has adverse effects on human health, including inflammation in multiple organs, yet how PFAS are sensed by host cells, and how tissue inflammation eventually incurs, is still unclear. Here, we show that the double-stranded DNA receptor AIM2 is able to recognize perfluorooctane sulfonate (PFOS), a common form of PFAS, to trigger IL-1β secretion and pyroptosis. Mechanistically, PFOS activates the AIM2 inflammasome in a process involving mitochondrial DNA release through the Ca2+-PKC-NF-κB/JNK-BAX/BAK axis. Accordingly, Aim2−/− mice have reduced PFOS-induced inflammation, as well as tissue damage in the lungs, livers, and kidneys in both their basic condition and in an asthmatic exacerbation model. Our results thus suggest a function of AIM2 in PFOS-mediated tissue inflammation, and identify AIM2 as a major pattern recognition receptor in response to the environmental organic pollutants.

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Section: Introductionmentioning

confidence: 99%

Perfluoroalkyl substance pollutants activate the innate immune system through the AIM2 inflammasome

et al. 2021

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“…The only study that reported any significant associations between prenatal exposure and postnatal length was by Cao et al, in which length at 19 months of age was positively associated with the highest tertiles of cord blood PFDoDA (in boys) and PFUnDA (in girls). However, the results were not consistent, as the same study also noted an inverse association between higher exposure to PFDS and postnatal length (77). Only one cross-sectional study, in which growth parameters was analyzed according to the children's PFAS concentrations, showed consistent doseresponse inverse associations of PFOA, PFNA, PFDA, PFOS, and PFHxS with height at 2 years of age (71).…”

Section: Postnatal Length/heightmentioning

confidence: 91%

“…In a study of 334 infants with repeated anthropometric measurements from 4 weeks to 2 years of age, prenatal PFOA exposure was inversely associated with weight-for-age or weight-for-height (74). PFOA was also inversely associated with postnatal weight in boys at 19.7 ± 3.2 months of age, however the association was significant only between the second and first tertiles of PFOA (77). For PFOS, there were more studies that suggested associations with weight in the first 2 years (32,48,(73)(74)(75) as opposed to null associations (76)(77)(78).…”

Section: Postnatal Weightmentioning

confidence: 98%

“…Six studies assessed for associations between prenatal PFAS exposures and length/height within the first 2 years of life. All of the studies that assessed for gestational PFOA and PFOS exposures by sampling maternal blood or cord blood showed null associations with measures of the child's length after birth to 2 years (48,73,74,(76)(77)(78).…”

Section: Postnatal Length/heightmentioning

confidence: 99%

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Early-Life Exposure to Per- and Poly-Fluorinated Alkyl Substances and Growth, Adiposity, and Puberty in Children: A Systematic Review

et al. 2021

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Per- or polyfluoroalkyl substances (PFAS), a family of synthetic polyfluorinated compounds, are widely used in consumer products. Ubiquitous exposures to PFAS, in consideration of their persistence, bioaccumulation potential, and toxicities have led to concerns regarding possible harmful effects during critical periods of development in early-life and long-term consequences on health. The potential effects of PFAS depend on various factors including the type of PFAS and the timing and level of exposure. We performed a systematic review of the epidemiologic literature to assess the effects of early-life PFAS exposure on prenatal and postnatal growth, adiposity, and puberty in children and adolescents. For birth size, most studies indicated that prenatal PFAS exposure, in particular long-chain PFAS, may impair fetal growth, albeit some reports of null associations with maternal PFAS. For growth within 2 years of age, prenatal PFAS exposure showed no associations with height and either null or negative associations with weight. However, postnatal PFAS exposures were inversely related to height and weight at 2 years in a cross-sectional study. For postnatal adiposity, prenatal PFAS may mostly have negative associations with body mass index in the first 2 years of life, but positive relationships with adiposity in childhood and adolescence, although some studies showed null associations. For puberty, the evidence for associations between early-life PFAS exposure and pubertal development or sex hormone levels were limited and inconclusive. From experimental studies, plausible mechanisms through which PFAS may affect early-life growth and puberty include PFAS-induced activation of peroxisome proliferator-activated receptor, alterations of thyroid or steroid hormone synthesis and metabolism, and their weak estrogenic or anti-androgenic properties. Although the published literature suggests possible effects of PFAS exposures on early-life growth, adiposity, and puberty, current human evidence is limited in establishing PFAS-induced effects on early-life physical development. Further investigation is warranted to clarify PFAS-induced effects on growth and physical development in consideration of the critical time-window of exposure, concomitant exposure to chemical mixtures including various PFAS types, and possible non-monotonic dose-response relationship for growth and adiposity trajectories.

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“…Exposure to environmental endocrine disruptors during fetal life is a well‐known cause of reproductive abnormalities in males (Rouiller‐Fabre et al, ). PFAAs are measured in the umbilical cord blood sample in several studies; e.g., in the Chinese population the median concentration of perfluorooctanoic acid, perfluorooctane sulfonate and perfluorononanoic acid (PFNA) was 1.59, 1.43 and 0.11 ng/mL respectively (Cao et al, ), while in Taiwanese participants the concentration of these three PFAAs was 1.86, 5.67 and 3.00 ng/mL, respectively (Lien et al, ). Studies in laboratory animals have shown that PFAAs can cross the placental barrier and be transferred from mother to fetus (Das et al, ; Lai et al, ); therefore, the gestational exposure to these compounds can influence the developing fetus and produce diseases in later life.…”

Section: Introductionmentioning

confidence: 99%

Effect of gestational exposure to perfluorononanoic acid on neonatal mice testes

Singh

2019

J of Applied Toxicology

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Perfluoroalkyl acids (PFAAs) are widely used in commercial products and are found in many goods of daily use. Perfluorononanoic acid (PFNA) is one of the PFAAs that possesses endocrine disrupting properties and we have recently shown that PFNA affects testicular functions in Parkes mice. Exposure to environmental endocrine disruptors during fetal life is believed to affect gonadal development and they might produce reproductive abnormalities in males. Therefore, the present study examined the effect of gestational exposure to PFNA on the testes of neonatal mice offspring. Pregnant Parkes mice were orally administered PFNA (2 and 5 mg/kg body weight) or distilled water from gestational day 12 until parturition. Male pups were killed on postnatal day 3. PFNA treatment decreased testosterone biosynthesis by inhibiting expression of steroidogenic acute regulatory protein, cytochrome P450scc, and 3β‐ and 17β‐hydroxysteroid dehydrogenase; proliferation of testicular cells was also affected in treated mice. Furthermore, a marked decrease in expression of Wilms tumor 1, steroidogenic factor 1 and insulin‐like factor 3 was noted in neonatal mice testes, indicating that the PFNA treatment may affect the development of the testis. Moreover, observation of the dose‐related expression of anti‐müllerian hormone and c‐Kit in neonatal mice testes is also suggestive of an interference with gonadal development by PFNA exposure. In conclusion, the results suggest that the gestational exposure to PFNA decreased testosterone biosynthesis and altered the expression of critical factors involved in the development of the testis, thereby advocating a potential risk of PFNA to male reproductive health.

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Perfluoroalkyl substances in umbilical cord serum and gestational and postnatal growth in a Chinese birth cohort

Cited by 50 publications

References 50 publications

Perfluoroalkyl substance pollutants activate the innate immune system through the AIM2 inflammasome

Perfluoroalkyl substance pollutants activate the innate immune system through the AIM2 inflammasome

Early-Life Exposure to Per- and Poly-Fluorinated Alkyl Substances and Growth, Adiposity, and Puberty in Children: A Systematic Review

Effect of gestational exposure to perfluorononanoic acid on neonatal mice testes

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