ArticleEnvironmental health perspectives2008
Effects of maternal exposure to di-(2-ethylhexyl) phthalate during fetal and/or neonatal periods on atopic dermatitis in male offspring.
Article in Environmental health perspectives, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- A systematic review on the adverse health effects of di-2-ethylhexyl phthalate.Environmental science and pollution research international · 2016Pooled it
- Atopic Dermatitis and Autism Spectrum Disorders: Common Role of Environmental and Clinical Co-Factors in the Onset and Severity of Their Clinical Course.International journal of molecular sciences · 2024Review
- Maternal Exposure to Polychlorinated Biphenyls and Asthma, Allergic Rhinitis and Atopic Dermatitis in the Offspring: The Environmental Health Fund Birth Cohort.Frontiers in pharmacology · 2022Article
- Associations of prenatal environmental phenol and phthalate biomarkers with respiratory and allergic diseases among children aged 6 and 7 years.Environment international · 2018Article
- Prenatal Exposure to Phthalates and the Development of Eczema Phenotypes in Male Children: Results from the EDEN Mother-Child Cohort Study.Environmental health perspectives · 2018Article
- Screening forFrontiers in microbiology · 2018Article
- Environmental pollution and allergies.Journal of toxicologic pathology · 2017Review
- Pregnant women's navigation of information on everyday household chemicals: phthalates as a case study.BMC pregnancy and childbirth · 2015Article
- Prenatal exposure to butylbenzyl phthalate and early eczema in an urban cohort.Environmental health perspectives · 2012Article
- ICAM-1 and IL-8 are expressed by DEHP and suppressed by curcumin through ERK and p38 MAPK in human umbilical vein endothelial cells.Inflammation · 2012Article
- Effects of diisononyl phthalate on atopic dermatitis in vivo and immunologic responses in vitro.Environmental health perspectives · 2010Article
- Phthalates, Pesticides, and Bisphenol-A Exposure and the Development of Nonoccupational Asthma and Allergies: How Valid Are the Links?The open allergy journal · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDi-(2-ethylhexyl) phthalate (DEHP) has been widely used in polyvinyl chloride products and is ubiquitous in developed countries. Although maternal exposure to DEHP during fetal and/or neonatal periods reportedly affects reproductive and developmental systems, its effects on allergic diseases in offspring remain to be determined.
objectivesIn the present study, we examined whether maternal exposure to DEHP during fetal and/or neonatal periods in NC/Nga mice affects atopic dermatitis-like skin lesions related to mite allergen in offspring.
methodsWe administered DEHP at a dose of 0, 0.8, 4, 20, or 100 microg/animal/week by intraperitoneal injection into dams during pregnancy (gestation days 0, 7, and 14) and/or lactation (postnatal days 1, 8, and 15). Eight-week-old male offspring of these treated females were injected intradermally with mite allergen into their right ears. We then evaluated clinical scores, ear thickening, histologic findings, and protein expression of eotaxin in the ear.
resultsMaternal exposure to a 100-microg dose of DEHP during neonatal periods, but not during fetal periods, enhanced atopic dermatitis-like skin lesions related to mite allergen in males. The results were concomitant with the enhancement of eosinophilic inflammation, mast cell degranulation, and protein expression of eotaxin in overall trend.
conclusionMaternal exposure to DEHP during neonatal periods can accelerate atopic dermatitis-like skin lesions related to mite allergen in male offspring, possibly via T helper 2 (T(H)2)-dominant responses, which can be responsible, at least in part, for the recent increase in atopic dermatitis.
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