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Published on: September 27, 2017
Prenatal exposure to perfluoroalkyl and polyfluoroalkyl substances and childhood atopic dermatitis: a prospective
Qian Chen1, Rong Huang1, Li Hua2
1Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, China.
Insights
Prenatal exposure to certain PFASs, like PFOA and PFNA, significantly increases the risk of atopic dermatitis (AD) in infant girls. These findings highlight potential environmental health risks for children exposed to these common chemicals.
Area of Science:
- Environmental Health
- Pediatric Allergy
- Toxicology
Background:
- Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are widespread environmental contaminants.
- Previous research on prenatal PFAS exposure and offspring allergic disorders yielded inconsistent results.
- Immune-suppressive effects of PFASs are documented, necessitating further investigation into their role in allergic diseases.
Purpose of the Study:
- To investigate the association between prenatal exposure to various PFASs and the development of childhood atopic dermatitis (AD).
- To assess this association in offspring up to 24 months of age.
- To determine if sex influences the relationship between prenatal PFAS exposure and AD.
Main Methods:
- A prospective birth cohort study included 1056 pregnant women in Shanghai (2012-2015).
- Prenatal PFAS levels were measured in umbilical cord blood plasma.
- Children were followed for AD diagnosis at 6, 12, and 24 months using standardized criteria and logistic regression analysis.
Main Results:
- AD was diagnosed in 25.2% of 687 children with complete follow-up and PFAS data.
- Prenatal exposure to perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA) significantly increased AD risk in female infants.
- Elevated risks were also observed for perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluorohexane sulfonic acid (PFHxS) in girls, with no significant associations found in boys.
Conclusions:
- Prenatal exposure to specific PFASs (PFOA, PFDA, PFDoA, PFHxS) is linked to a higher risk of childhood AD in female offspring.
- The association between prenatal PFNA exposure and AD risk approached statistical significance.
- These findings underscore the potential sex-specific impact of prenatal PFAS exposure on allergic disease development.
Background:
Perfluoroalkyl and polyfluoroalkyl substances (PFASs) have been reported to suppress immune function. However, previous studies on prenatal exposure to PFASs and allergic disorders in offspring provided inconsistent results. We aimed to examine the association between prenatal exposure to PFASs and childhood atopic dermatitis (AD) in offspring up to 24 months of age.
Methods:
A prospective birth cohort study involving 1056 pregnant women was conducted in two hospitals in Shanghai from 2012 to 2015. Prenatal information was collected by an interview with the women and from medical records. Fetal umbilical cord blood was collected at birth. Cord blood plasma PFASs were measured. Children were followed at 6, 12 and 24 months and information on the development of AD was recorded. AD was diagnosed by 2 dermatologists independently based on the questionnaires. Multiple logistic regression was used to compute odds ratio (OR) and corresponding 95% confidence interval (CI) for the association between AD and each PFASs, adjusting for potential confounders.
Results:
A total of 687 children completed a 2-year follow-up visit and had PFASs measurement. AD was diagnosed in 173 (25.2%) children during the first 24 months. In female children, a log-unit increase in perfluorooctanoic acid (PFOA) was associated with a 2.1-fold increase in AD risk (AOR 2.07, 95% CI 1.13-3.80) after adjusting for potential confounders. The corresponding risk was 2.22 (1.07-4.58) for perfluorononanoic acid (PFNA). The highest PFOA quartile was significantly associated with AD (2.52, 1.12-5.68) compared with the lowest quartile. The highest quartile of PFNA, perfluorodecanoic acid (PFDA) and perfluorohexane sulfonic acid (PFHxS) were associated with AD with AOR (95% CI) being 2.14 (0.97-4.74), 2.14 (1.00-4.57), and 2.30 (1.03-5.15), respectively. Additionally, the second quartile of perfluorododecanoic acid (PFDoA) was associated with a 3.2-fold increase in AD risk (3.24, 1.44-7.27). However, no significant associations were found in male children.
Conclusions:
Prenatal exposure to PFOA, PFDA, PFDoA and PFHxS significantly increased the risk of childhood AD in female children during the first 24 months of life. In addition, the associations between AD with prenatal exposure to PFNA were close to statistical significance.
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