Association of perfluoroalkyl substances exposure with impaired lung function in children
Introduction
Asthma is one of the most common chronic diseases throughout the world, especially among children (Lai et al., 2009). Although many asthma risk factors have been identified, reasons for its rising prevalence remain poorly understood (Beasley et al., 2015) and emerging environmental exposures may bear a portion of the attributable risk (Guarnieri and Balmes, 2014, Miller and Marty, 2010).
Perfluoroalkyl substances (PFASs) are a diverse class of chemicals with unique properties like extremely high thermal and chemical stability. They have long serum half-lives (in years) of 5.4 (perfluorooctane sulfonate, PFOS), 3.8 (perfluoronanoic acid, PFOA), and 8.3 (perfluorohexanesulfonate, PFHxS) years (Buck et al., 2011, Olsen et al., 2007). These properties are responsible for the accumulation of PFASs in the environment, wildlife, and humans (Fromme et al., 2007, Schecter et al., 2012, Zhou et al., 2014), but also make them ideal for applications such as firefighting foams, paints, semiconductors, photographic films, and pesticides, for which they have been widely used since the 1950s (Lindstrom et al., 2011). In addition, both human and animal studies have found that the lungs are likely a target organ of PFASs (Borg et al., 2010, Perez et al., 2013).
Animal evidence indicates that exposure to PFOA and PFOS cause a variety of asthma-related outcomes. Fairley et al. (2007) revealed that PFOA caused increased serum immunoglobulin E (IgE) and an exaggerated response to ovalbumin. The evidence suggests exposure to PFOA may intensify the IgE response to allergens in a murine model of asthma (Fairley et al., 2007). Furthermore, two animal studies show that prenatal PFOA and PFOS exposure may adversely affect lung development (Loewen et al., 2011, Ryu et al., 2014). One study noted that PFOS exposure lowered baseline airway resistance but significantly increased airway responsiveness in an allergic murine model of pups (Loewen et al., 2011). Another study did not identify maternal exposure to PFOA or PFOS as a risk factor for more severe asthma-like symptoms in pups, but found that PFOA induced airway inflammation and altered airway function (Ryu et al., 2014).
Epidemiologic evidence suggests that exposure to PFASs is positively associated with asthma, but results are inconsistent. Dong et al. (2013) reported a positive association between PFASs and asthma, asthma severity, and immune markers in Taiwanese children. Using 1999–2000 and 2003–2008 National Health and Nutrition Examination Survey (NHANES) data, Humblet et al. (2014) provided modest evidence for positive associations between exposure to PFASs and asthma-related outcomes among children. In the INUENDO birth cohort study from Greenland and Ukraine, however, Smit et al. (2015) did not find an association.
No study has examined whether PFAS exposure is associated with objective measures of lung function such as spirometry, which provides information on airway obstruction by measuring forced expiratory volume in one second (FEV1), forced vital capacity (FVC), peak expiratory flow rate (PEF), and forced expiratory flow at 25–75% of FVC (FEF25–75) (Pellegrino et al., 2005). These tools not only have utility for diagnosing and monitoring asthma (Gaffin et al., 2010, Pijnenburg et al., 2015), but also are the most commonly employed pulmonary function tests for assessing effects of environmental chemicals on lung function (Barraza-Villarreal et al., 2008, Miller and Marty, 2010). The objective of the present study was to test the association between PFAS exposure and lung function in a case-control study of asthmatic and non-asthmatic children, by using data from the Genetic and Biomarkers study for Childhood Asthma (GBCA).
Section snippets
Study participants
Study participants were from the Genetic and Biomarkers study for Childhood Asthma (GBCA) in Taiwan during 2009–2010. Study methods are available elsewhere (Dong et al., 2013). One hundred and thirty-two non-smoking children aged 10–15 with physician-diagnosed asthma were recruited from the cross-sectional component of GBCA from two hospitals in northern Taiwan. The 168 controls, without asthma and non-smokers, were randomly selected from seven public schools in northern Taiwan. The cases and
Results
Table 1 shows detailed information about the study sample. Participants ranged in age from 10.11 to 16.39 years (mean±SD, 12.78±1.58) for cases and 11.95–15.06 years (13.46±0.69) for controls. Children with asthma were shorter, younger and less likely to report environmental tobacco smoke (ETS) exposure, compared to controls. Asthmatic children had lower means of pulmonary function measurements FEV1 and FEF25–75, as well as higher median serum PFASs concentrations, except for PFBS, PFHxA and
Discussion
In this case-control study, multiple lung function index (FVC, FEV1, PEF and FEF25–75) was measured to assess the health impact of PFASs exposure. We found that serum PFASs concentrations were significantly associated with lung function reduction among asthmatics aged 10–15. To our knowledge, this is the first report of associations between PFASs exposure and lung function.
Contextualization of our results proves difficult due to a paucity of literature on the subject. In a systematic Medline
Conclusion
We found that serum PFAS concentrations were negatively associated with lung function in children with asthma, and that small airway obstruction is a possible mechanism of this effect. Moreover, the reduction in lung function projected across a population may have important implications in long term lung function and lung health.
Funding sources
This work was supported by the National Natural Science Foundation of China [81472936, 81172630], Major Program of National Natural Science Foundation of China (91543208), the National Science Council in Taiwan [98-2314-B-002-138-MY3, 101-2621-M-002-005], the Fundamental Research Funds for the Central Universities [16ykzd02], and the Guangdong Province Natural Science Foundation [2016A030313342, 2014A030313021].
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