The impact of reality shock on professional identity among junior nurses: a latent profile analysis.
Authors: Li X, Liu XY, Li YW, Zhou P, Jiang F
Journal: Frontiers in medicine
mental health
psychology
open access
Abstract
Organophosphate ester flame retardants
and plasticizers (OPEs)
are synthetic chemicals of emerging concern. Human exposure to OPEs
has increased rapidly since these compounds replaced polybrominated
diphenyl ether (PBDE) flame retardants, which were phased out in the
early 2000s due to health risks. Today,
the production and environmental concentrations of OPEs exceed those
of PBDEs at their peak use. Similar to
PBDEs, OPEs are not chemically bound to the many consumer products
and textiles to which they are added; therefore, they gradually volatilize
into indoor air and contaminate indoor dust. Human exposures mainly
occur through ingestion of indoor dust and consumption of contaminated
drinking water and food, although inhalation and dermal exposure are
also important. Most Americans, including pregnant
women, have detectable levels of OPEs in their bodies. OPEs are also present in placental tissues, suggesting that transfer
to the fetus is possible. Although the
biological half-life of OPEs (on the order of hours to days) is much
shorter than the half-life of the PBDEs (years) they replaced, they
appear to be similarly or even more toxic with continuous and ubiquitous
exposure. In vitro and animal
studies have demonstrated that exposure to
OPEs has developmental, reproductive, and neurological effects. A limited number of epidemiological studies
have found that early life OPE exposure is associated with adverse
child development, including shorter gestational duration, greater risk of childhood obesity, and adverse neurodevelopment. Specifically,
studies across the United States, Norway, and China have linked prenatal
exposure to OPEs such as diphenyl phosphate (DPHP) and bis(1,3-dichloro-2-propyl)
phosphate (BDCPP) to multiple adverse neurodevelopmental outcomes,
including decreases in cognitive and psychomotor functioning and greater
problems with executive function, attention-deficit/hyperactivity
disorder (ADHD)-related symptoms, and internalizing and externalizing
behaviors. Toxicological and some human studies indicate that OPEs can
alter
sex steroid physiology; neuroendocrine signaling; pathways of inflammation
and oxidative stress, including via induction of peroxisome proliferator-activated
receptors (PPARs); and thyroid function. Interference with these critical pathways of fetal development is
the same mechanism of action for other known developmental toxicants
such as PBDEs, phthalates, and per- and polyfluoroalkyl substances
(PFASs), suggesting that OPEs could similarly
exert neurotoxic effects on the fetus during pregnancy. Further, evidence
of sex-specific effects of OPEs, including potential antiandrogenic
activity, has been noted in several human and animal studies. Some have found poorer neuropsychological functioning with OPE exposure
in males relative to that in females. These potential sex differences warrant examination in larger samples.
and plasticizers (OPEs)
are synthetic chemicals of emerging concern. Human exposure to OPEs
has increased rapidly since these compounds replaced polybrominated
diphenyl ether (PBDE) flame retardants, which were phased out in the
early 2000s due to health risks. Today,
the production and environmental concentrations of OPEs exceed those
of PBDEs at their peak use. Similar to
PBDEs, OPEs are not chemically bound to the many consumer products
and textiles to which they are added; therefore, they gradually volatilize
into indoor air and contaminate indoor dust. Human exposures mainly
occur through ingestion of indoor dust and consumption of contaminated
drinking water and food, although inhalation and dermal exposure are
also important. Most Americans, including pregnant
women, have detectable levels of OPEs in their bodies. OPEs are also present in placental tissues, suggesting that transfer
to the fetus is possible. Although the
biological half-life of OPEs (on the order of hours to days) is much
shorter than the half-life of the PBDEs (years) they replaced, they
appear to be similarly or even more toxic with continuous and ubiquitous
exposure. In vitro and animal
studies have demonstrated that exposure to
OPEs has developmental, reproductive, and neurological effects. A limited number of epidemiological studies
have found that early life OPE exposure is associated with adverse
child development, including shorter gestational duration, greater risk of childhood obesity, and adverse neurodevelopment. Specifically,
studies across the United States, Norway, and China have linked prenatal
exposure to OPEs such as diphenyl phosphate (DPHP) and bis(1,3-dichloro-2-propyl)
phosphate (BDCPP) to multiple adverse neurodevelopmental outcomes,
including decreases in cognitive and psychomotor functioning and greater
problems with executive function, attention-deficit/hyperactivity
disorder (ADHD)-related symptoms, and internalizing and externalizing
behaviors. Toxicological and some human studies indicate that OPEs can
alter
sex steroid physiology; neuroendocrine signaling; pathways of inflammation
and oxidative stress, including via induction of peroxisome proliferator-activated
receptors (PPARs); and thyroid function. Interference with these critical pathways of fetal development is
the same mechanism of action for other known developmental toxicants
such as PBDEs, phthalates, and per- and polyfluoroalkyl substances
(PFASs), suggesting that OPEs could similarly
exert neurotoxic effects on the fetus during pregnancy. Further, evidence
of sex-specific effects of OPEs, including potential antiandrogenic
activity, has been noted in several human and animal studies. Some have found poorer neuropsychological functioning with OPE exposure
in males relative to that in females. These potential sex differences warrant examination in larger samples.