Dietary Habits Related to Food Packaging and Population Exposure to PFASs
2019; National Institute of Environmental Health Sciences; Volume: 127; Issue: 10 Linguagem: Inglês
10.1289/ehp4092
ISSN1552-9924
AutoresHerbert Susmann, Laurel A. Schaider, Kathryn M. Rodgers, Ruthann A. Rudel,
Tópico(s)Toxic Organic Pollutants Impact
ResumoVol. 127, No. 10 ResearchOpen AccessDietary Habits Related to Food Packaging and Population Exposure to PFASsis companion ofPFAS in Food Packaging: A Hot, Greasy Exposure Herbert P. Susmann, Laurel A. Schaider, Kathryn M. Rodgers, and Ruthann A. Rudel Herbert P. Susmann Silent Spring Institute, Newton, Massachusetts, USA Department of Biostatistics, University of Massachusetts Amherst, Amherst, Massachusetts, USA Search for more papers by this author , Laurel A. Schaider Address correspondence to Laurel Schaider, Silent Spring Institute, 320 Nevada St., Suite 302, Newton, MA 02460 USA. Telephone: (617) 332-4288. Email: E-mail Address: [email protected] Silent Spring Institute, Newton, Massachusetts, USA Search for more papers by this author , Kathryn M. Rodgers Silent Spring Institute, Newton, Massachusetts, USA Search for more papers by this author , and Ruthann A. Rudel Silent Spring Institute, Newton, Massachusetts, USA Search for more papers by this author Published:9 October 2019CID: 107003https://doi.org/10.1289/EHP4092Cited by:37AboutSectionsPDF Supplemental Materials ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InRedditEmail AbstractBackground:Per- and polyfluoroalkyl substances (PFASs) are common industrial and consumer product chemicals with widespread human exposures that have been linked to adverse health effects. PFASs are commonly detected in foods and food-contact materials (FCMs), including fast food packaging and microwave popcorn bags.Objectives:Our goal was to investigate associations between serum PFASs and consumption of restaurant food and popcorn in a representative sample of Americans.Methods:We analyzed 2003–2014 serum PFAS and dietary recall data from the National Health and Nutrition Examination Survey (NHANES). We used multivariable linear regressions to investigate relationships between consumption of fast food, restaurant food, food eaten at home, and microwave popcorn and serum levels of perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluorohexanesulfonic acid (PFHxS), and perfluorooctanesulfonic acid (PFOS).Results:Calories of food eaten at home in the past 24 h had significant inverse associations with serum levels of all five PFASs; these associations were stronger in women. Consumption of meals from fast food/pizza restaurants and other restaurants was generally associated with higher serum PFAS concentrations, based on 24-h and 7-d recall, with limited statistical significance. Consumption of popcorn was associated with significantly higher serum levels of PFOA, PFNA, PFDA, and PFOS, based on 24-h and 12-month recall, up to a 63% (95% CI: 34, 99) increase in PFDA among those who ate popcorn daily over the last 12 months.Conclusions:Associations between serum PFAS and popcorn consumption may be a consequence of PFAS migration from microwave popcorn bags. Inverse associations between serum PFAS and food eaten at home—primarily from grocery stores—is consistent with less contact between home-prepared food and FCMs, some of which contain PFASs. The potential for FCMs to contribute to PFAS exposure, coupled with concerns about toxicity and persistence, support the use of alternatives to PFASs in FCMs. https://doi.org/10.1289/EHP4092IntroductionPer- and polyfluoroalkyl substances (PFASs) are a diverse group of synthetic compounds with dual hydrophobic and hydrophilic properties and characteristic carbon–fluorine bonds that are extremely resistant to degradation even at high temperatures. They are widely used in nonstick, grease- and water-proof, and stain-resistant consumer products; firefighting foams; paints; and a range of industrial processes (U.S. EPA 2009). PFASs were first produced in the late 1940s (Lindstrom et al. 2011), and at least 4,700 PFASs are estimated to be on the global market (OECD 2018). Worldwide, PFASs have been detected in surface water, drinking water, and wildlife (Kelly et al. 2009; Weiss et al. 2015).Human exposure in the general population can occur through diet, drinking water, air, dust, and direct contact with products (Trudel et al. 2008). Long-chain PFASs (carboxylates with ≥7 perfluorinated carbon atoms, sulfonates with ≥6 perfluorinated carbon atoms), particularly perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS), have been associated with cancer, immunotoxicity, weight gain, altered thyroid function, and reproductive and developmental toxicity (Wolf et al. 2007; Hines et al. 2009; Grandjean et al. 2012; Lopez-Espinosa et al. 2012; Barry et al. 2013). Concerns about persistence, bioaccumulation, and toxicity have led manufacturers to phase out production of long-chain PFASs and their precursors in North America and Europe, although production continues in other regions (Liu et al. 2017). As a way to prevent further exposures, the U.S. EPA issued Significant New Use Rules (SNURs) for a number of legacy PFASs, including PFOA and PFOS, requiring any new uses and imports of these chemicals to first be evaluated by the U.S. EPA (2019). Although alternative PFAS compounds, including short-chain PFASs, may be less bioaccumulative than long-chain compounds, they raise similar concerns in terms of persistence, mobility, and toxicity (Olsen et al. 2009; Butenhoff et al. 2012; Blaine et al. 2013; Rosenmai et al. 2016; Rushing et al. 2017).Long-chain PFASs can persist in the human body for years. The human half-lives for PFOA, PFOS, and perfluorohexanesulfonic acid (PFHxS) in blood are approximately 3.5, 4.8, and 7.3 y, respectively (Olsen et al. 2007). The U.S. National Health and Nutrition Examination Survey (NHANES) detected these three PFASs, as well as perfluorononanoic acid (PFNA), in the blood of >98% of Americans tested in 2003–2004 (Calafat et al. 2007), as well as in all children 3–11 y of age tested in 2013–2014 (Ye et al. 2018). Some short-chain replacement compounds, such as perfluorobutanesulfonic acid (PFBS) and perfluorohexanoic acid (PFHxA), have half-lives of about 1 month in blood (Olsen et al. 2009; Russell et al. 2013). Human half-lives for other short-chain compounds have not been evaluated, although they are also highly resistant to degradation (Danish Ministry of the Environment 2015).Diet is considered a major route of PFAS exposure (Tittlemier et al. 2007; Trudel et al. 2008; Vestergren and Cousins 2009). PFASs have been found in many foods; a market basket study in Canada found PFASs in fish, meat, pizza, and microwave popcorn (Tittlemier et al. 2007). In particular, consumption of fish and shellfish has been positively associated with serum PFAS concentrations in studies in the United States, Europe, and Asia (Rylander et al. 2010; Bjermo et al. 2013; Manzano-Salgado et al. 2016; Christensen et al. 2017). An analysis of 2007–2014 NHANES data found positive associations between fish and shellfish consumption and serum PFAS concentrations (Christensen et al. 2017).Migration of PFASs from food-contact materials (FCMs) into foods may also contribute to dietary exposure. PFASs have been used in FCMs for their grease- and water-resistant properties since the 1960s (Posner et al. 2013; Wang et al. 2017). PFASs that have been detected in fast food packaging, microwave popcorn bags, and other FCMs in North America, Europe, Asia, and Africa include PFOA and other perfluoroalkyl carboxylates (PFCAs), PFOS and other perfluoroalkyl sulfonates (PFSAs), fluorotelomer alcohols (FTOHs), and polyfluoroalkyl phosphate esters (PAPs) (Trier et al. 2011; Poothong et al. 2012; Gebbink et al. 2013; Shoeib et al. 2016; Yuan et al. 2016; Schaider et al. 2017). A 2017 survey of 400 FCMs collected from U.S. fast food restaurants (primarily large fast food chains with ≥100 U.S. stores) found fluorinated chemicals in 46% of food-contact papers and 20% of paperboard samples, and a compound-specific analysis of a subset of samples detected 27 PFASs, including PFOA, PFHxA, and PFBS (Schaider et al. 2017). Compared with other types of FCMs, microwave popcorn bags have among the highest concentrations of PFASs, including PFCAs, PFOS, PAPs, fluorotelomer saturated carboxylic acids (FTCAs), and fluorotelomer unsaturated carboxylic acids (FTUCAs) (Poothong et al. 2012; Moreta and Tena 2014; Zabaleta et al. 2016, 2017).PFASs in FCMs have been shown to migrate out of packaging and into food. PFAS migration from food-contact paper increases with higher temperatures, longer contact time, and the presence of emulsifiers (Begley et al. 2008). The extent of migration is compound-specific, and short-chain PFASs have higher migration efficiencies than longer-chain analogs (Yuan et al. 2016). A PAP surfactant was found in popcorn after heating in a microwave popcorn bag (Begley et al. 2008); however, another study did not find migration of four PFCAs from microwave popcorn bags into the popcorn after cooking (Moreta and Tena 2014). PFASs, especially volatile PFCA precursors such as FTOHs, have been found in the vapors from cooked microwave popcorn bags, indicating the potential for inhalation exposure (Sinclair et al. 2007). These findings indicate that migration of PFASs used in FCM formulations, such as PAPs and FTOHs, may occur at a higher rate than PFCAs, which are present in the additives as impurities (D’eon and Mabury 2011). PAPs and FTOHs are PFCA precursors and can contribute indirectly to PFCA exposure via in vivo biotransformation (Fasano et al. 2006; D’eon and Mabury 2007).At a population level, the extent of PFAS exposure attributable to migration from FCMs is not well characterized. Several studies of the relationship between diet and PFAS blood concentrations have included popcorn and other foods likely to have been in contact with FCMs. Consumption of snacks (including popcorn) was positively associated with PFOS levels in the Danish National Birth Cohort (Halldorsson et al. 2008), and popcorn was among the foods associated with blood PFAS levels in four additional cohort studies (Halldorsson et al. 2008; Wu et al. 2015; Zong et al. 2018; Boronow et al. 2019). However, these studies did not more broadly investigate associations between the extent of food packaging, food sources (e.g., restaurants, grocery stores), and population PFAS exposures.In this paper, we report our investigation of whether consumption of microwave popcorn, fast food, and other food consumed outside and within the home is associated with population exposure to PFASs. We analyzed associations between serum PFAS concentrations and consumption of fast food, restaurant food, nonrestaurant food eaten at home, and microwave popcorn across multiple recall periods (24-h, 7- and 30-d, and 12-month) from six cycles of NHANES from 2003 to 2014. We included fish and shellfish consumption in our models because prior research found significant associations for these foods with serum PFASs (Christensen et al. 2017). Understanding sources of dietary exposures to PFASs can inform exposure assessment and identify intervention strategies to reduce exposure.MethodsSerum PFAS DataNHANES is an ongoing national survey that combines biomonitoring, physical examinations, and interviews to assess the health and nutrition of U.S. residents over time. The Centers for Disease Control and Prevention (CDC) has conducted the survey in biennial cycles beginning in 1999 and uses a complex survey design in which selected demographic subpopulations are oversampled and survey weights are used to construct a nationally representative sample. The study protocol was approved by the National Center for Health Statistics (NCHS) Research Ethics Review Board, and participants provided consent. For participants under 18, consent was provided by parents or guardians.The NHANES biomonitoring program has measured PFAS serum concentrations since 1999. We compiled NHANES PFAS data from six cycles covering 2003–2014, including a subsample of 639 children (3–11 y of age) in the 2013–2014 cycle. We did not include data from the 1999–2000 cycle because PFAS data for that cycle were only available from surplus serum samples, which were treated differently than serum in later years, nor from the 2001–2002 cycle because only pooled data were available. Ten PFASs were analyzed in blood in all six cycles: perfluoroheptanoic acid (PFHpA), PFOA, PFNA, perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnDA), perfluorododecanoic acid (PFDoDA), PFBS, PFHxS, PFOS, and 2-(N-methylperfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH). Serum concentrations were reported in nanograms per milliliter. Details of analytical methods are described in CDC (2014) and include solid-phase extraction coupled to high-performance liquid chromatography–turbo ion spray ionization–tandem mass spectrometry. With the exception of PFBS and PFHpA, these compounds are all considered long-chain PFASs according to Buck et al. (2011). Table S1 provides additional information about each analyte.Diet Recall DataWe compiled dietary information covering four timescales: 24-h diet recall, 7-d and 30-d meal recall, and 12-month food frequency questionnaires (FFQs). Table S2 shows available PFAS and dietary data for each NHANES cycle. Starting in 1999, 24-h dietary recall data were collected through an in-person interview at a Mobile Examination Center that was open to all ages (CDC 2009). Participants were asked to list every food or beverage item consumed, including portion size, in the previous day (midnight to midnight). Each item was later annotated by U.S. Department of Agriculture (USDA) analysts with nutritional information including caloric content, USDA food type code, and food source from 30 possible categories (including “Don’t Know”). For 24-h diet recall data, we assigned each meal to one of four categories: “Fast food and pizza restaurants,” “Other restaurants,” “Other sources—eaten at home,” and “Other sources—eaten outside the home.” For “fast food and pizza restaurants,” we used the NHANES definition of fast food as food from the “Restaurant fast food/pizza place” category. Lack of waiter/waitress service distinguishes fast food and pizza restaurants from other restaurants. Fast food does not include food from other similar categories such as “Vending machine,” “Bar/tavern/lounge,” and “Street vendor, vending truck.” This definition was used by Zota et al. (2016) in a previous study of chemical exposures and fast food consumption. “Other restaurants” included food from non-fast food restaurants, which we defined as any food items in the categories “Restaurant with waiter/waitress” and “Restaurant, no additional information.” “Other sources” included all other NHANES food source categories (including “Store grocery/supermarket,” “Cafeteria in a K-12 school,” and “Store—convenience type”). We further categorized meals from “Other sources” into those eaten at home and those eaten outside the home based on the field named “Did you eat this meal at home?” Any items without a food source specified were excluded.We compiled information separately about several specific types of food that we hypothesized might contribute substantially to PFAS exposure. We classified microwave popcorn as any food item that had a USDA food code associated with microwave popcorn (see Table S3 for specific food codes). This excluded other types of popcorn, such as air popped popcorn. In addition, because a previous study using NHANES data found associations with serum PFAS and consumption of fish and shellfish, we also compiled data on consumption of fish and shellfish food items using USDA food codes for each food group (see Table S4).Data from the 24-h diet recall were used to calculate caloric intake associated with certain food types and food sources. We calculated the total caloric intake over 24 h from microwave popcorn and from fish/shellfish for each participant by summing the total kilocalories (kcal) from each microwave popcorn or fish/shellfish food item in the recall data. Total caloric intake from fast food, restaurants, and other sources was calculated similarly, with each source category excluding any kilocalories from microwave popcorn or fish/shellfish.From 2007 to 2014, NHANES included a consumer behavior module in the household interview that included questions on food consumption patterns over 7- and 30-d recall periods. Specifically, it asked the number of meals consumed in the last 7 d that were prepared outside the home (not including school breakfast or lunch, or from community programs) and how many of these meals were from fast food or pizza restaurants. The number of meals from other sources consumed in the past week was not gathered in the survey. These data were included in a separate analysis because they may be more representative of long-term fast food consumption than data from the 24-h diet recall (Willett 1998). The 30-d recall asked participants how many servings of various species of fish and shellfish they consumed over the past 30 d; we summed these to derive the total number of fish servings and total number of shellfish servings consumed.A 12-month FFQ was included in the 2003–2004 and 2005–2006 NHANES cycles. Participants were mailed a questionnaire that asked how often they ate a number of different food types. The categorical responses were converted by NHANES, using the Diet*Calc software, to a continuous daily frequency measure that ranges from 0 (never) to 2 (two or more times per day). The factors for these conversions are listed in Table S5. We selected popcorn food frequency results (microwave popcorn was not differentiated in the questionnaire), and summed all seafood-related categories to form a combined “seafood” frequency measure. The data did not include frequency of fast food consumption over the last 12 months. We included these data as an indicator of long-term consumption habits to supplement the shorter-term recall data.In addition, we compiled data for potential confounders that were previously included in related studies (Zota et al. 2016; Christensen et al. 2017), including age, gender, race/ethnicity, poverty–income ratio (PIR; ratio of family income to the U.S. Department of Health and Human Services poverty guideline; CDC 2015), and body mass index (BMI). Race/ethnicity was categorized as Hispanic (including both Mexican American and other Hispanic), non-Hispanic white, and non-Hispanic black. Age, PIR, and BMI were included as continuous variables.Data AnalysisWe combined data from six NHANES survey cycles covering 2003–2014, excluding the 2013–2014 child subsample, which was analyzed separately. The raw data set contained survey and laboratory results from 13,933 participants. We identified 10,578 qualifying participants by removing anyone who was missing PFAS serum concentration data (n=1,317), missing race/ethnicity or reported as mixed race/other (n=1,030), or missing household PIR data (n=870) or BMI data (n=138). The 2013–2014 subsample of children 3–11 y of age was analyzed separately due to its use of special subsample survey weights that could not be combined with data from other subsamples. We identified 517 qualifying participants in the child subsample using the same criteria as the adolescent and adult data set.We estimated associations between serum PFAS and dietary exposures that were derived using data from the four recall instruments (see Table S6). For participants ≥12y of age, we estimated exposures based on: 24-h dietary recall from 10,106 NHANES participants during 2003–2014 who also had serum PFAS data; 7-d and 30-d meal recall data from NHANES consumer behavior modules for 5,261 participants during 2007–2014 (after excluding 1,407 participants missing data for weekly fast food consumption and fish/shellfish consumption); and 12-month FFQ data for 2,788 participants during 2003–2006 (after excluding 1,028 participants missing these data). We used separate models to estimate associations between serum PFAS and dietary exposures in children (3–11 y of age) based on 24-h recall data (n=437 from the 2013–2014 NHANES cycle) and on 7- and 30-d recall data (n=365 from the 2013–2014 NHANES cycle).All analyses incorporated NHANES’ complex survey design and sample weights. We computed new sample weights according to NCHS guidelines for combining data from multiple cycles (Johnson et al. 2013). Concentrations below the lower limit of detection (LLOD) were substituted with a value of LLOD divided by the square root of 2. Analyses were only conducted on analytes with a high detection frequency (>70%) in order to avoid bias from substituted values.We used a series of multivariable linear regression models to investigate the association between log-transformed PFAS serum concentrations and metrics of restaurant food and popcorn consumption in three data sets. All regressions included age, gender, race/ethnicity, cycle year, BMI, and PIR as covariates. Percent increase in the response variable was calculated from the regression coefficient β and standard error (SE) by the formula (exp (β)−1)×100%, with a 95% confidence interval (CI) given by (exp (β±critical value×SE)−1)×100%. A significance level of α=0.05 was set prior to analysis. Because gender was frequently a significant predictor and because of the potential for gender-specific differences in diet and physiological uptake of PFAS, we also conducted an additional set of analyses to investigate effects by gender (referred to below as gender effect modification models) in which we added interaction terms between gender and all other variables (including confounders), according to the augmented product term method described by Buckley et al. (2017). All analyses were conducted in R (version 3.4.0; R Development Core Team). Complex survey analyses were conducted using the survey R package (Lumley 2004). The R scripts used to conduct these analyses are provided in the R source zip file “FinalPaperCode” in the Supplemental Material.ResultsPFOA, PFNA, PFDA, PFHxS, and PFOS were detected in more than 70% of samples collected in 2003–2014 (see Table S7). All subsequent analyses are restricted to these five analytes. Median serum PFOS and PFOA concentrations decreased by a factor of 4 and 2, respectively, over the study period, whereas concentrations of PFNA, PFDA, and PFHxS were fairly constant or showed slight decreases.As shown in Table 1, fast food consumption was common from 2003 to 2014, especially among adolescents: 35% of adults and 41% of adolescents (12–17 y of age) reported eating fast food in the last 24 h, and 70% of adults and 84% of adolescents ate at least one fast food meal in the past 7 d (2007–2014 data). Among participants who ate fast food in the last 24 h, median caloric intake from fast food was 745 kcal for adults and 791 kcal for adolescents (see Table S8). Microwave popcorn consumption was less common than fast food consumption in the 24-h recall; 5% of adults and 7% of adolescents reporting consuming microwave popcorn in the past 24 h, although 86% of participants reported eating popcorn of any kind in the past 12 months (2003–2006 data). Frequencies of microwave popcorn consumption in the 24-h recall were similar across demographic subgroups, ranging from 4% to 8%. Fish and shellfish consumption were common: 10% and 5% of participants reported fish and shellfish consumption, respectively, in the past 24 h (2003–2014), and 68% and 55% reported fish and shellfish consumption in the last month (2007–2014). The 12-month FFQ did not distinguish between fish and shellfish, but 89% of participants reported general seafood consumption in the past 12 months (2003–2006).Table 1 Consumption of fast food and pizza restaurant food and popcorn by demographic group in NHANES 2003–2014.Table 1 lists demographic group and n values in the first and second columns, respectively. The adjacent columns list percentage of consumers for fast food and pizza restaurant food; food from other restaurant; other food outlet, eaten at home; other food outlet, not eaten at home; and microwave popcorn within a 24-hour period (2003–2014). These columns are followed by n values and percentage consumers of meals from fast food or pizza restaurant within a 7-day period (2007–2014) and n values and percentage consumers of popcorn (any kind) within a 12-month period (2003–2006).Demographic group24-h (2003–2014)7-d (2007–2014)12-month (2003–2006)nFast food and pizza restaurant foodFood from other restaurantOther food outlet, eaten at homeOther food outlet, not eaten at homeMicrowave popcornnMeals from fast food/pizza restaurantnPopcorn (any kind)Consumers (%)Consumers (%)Consumers (%)Consumers (%)Consumers (%)Consumers (%)Consumers (%)All10,1063623955655,261712,78886Female5,1153422955352,630701,45986Male4,9913824955952,631721,32986Adults (≥18 y of age)8,4193524955554,551702,18386Non-Hispanic white adults4,3093425955552,385681,23387Non-Hispanic black adults1,8844315925359988046081Hispanic adults2,2263722945841,1687249078Adolescents (12–17 y of age)1,6874117936377108460588Non-Hispanic white adolescents5074020936482348418089Non-Hispanic black adolescents538427946161928822082Hispanic adolescents6424114955952848220587Note: NHANES, National Health and Nutrition Examination Survey.Children (3–11 y of age) in 2013–2014 ate fast food at a similar frequency as adults and adolescents, with 39% reporting eating fast food in the last 24 h, and a median caloric intake from fast food of 543 kcal (see Table S9). A slightly higher proportion of children (11%) in 2013–2014 reported consuming microwave popcorn in the past 24 h, and a slightly lower proportion reported consuming fish and shellfish (5% and 2%, respectively, in the past 24 h).The models included demographic and temporal variables as predictors to control for differences in exposure among subpopulations and over time. In the 24-h recall model, PFOS was lower in every cycle relative to the first cycle (2003–2004), and all five PFASs were lower in the last cycle (2013–2014) relative to the first cycle (see Table S10), reflecting the U.S. population’s generally declining exposures to long-chain PFASs. We found some evidence of different exposures among demographic subgroups. Both income and age were positively associated with all five PFASs and with their total concentration (ΣPFAS). Females had lower levels of all five PFASs and ΣPFAS compared with males. Compared with Non-Hispanic whites, Hispanics had lower levels of PFOA, PFHxS, and PFOS, whereas Non-Hispanic blacks were lower in PFOA and PFHxS and higher in the other three PFASs. Four of the five PFASs had statistically significant inverse relationships with BMI, with the exception of PFNA. Similar associations have been reported in prior analyses of NHANES data (Calafat et al. 2007; Christensen et al. 2017).Consumption of microwave popcorn had significant positive associations with serum concentrations of PFOA, PFNA, and PFOS, as well as ΣPFAS, in the 24-h recall model, and significant associations were also observed for consumption of popcorn (any type) with these PFASs, in addition to PFDA, in the 12-month recall model (Table 2 and Figure 1). Based on 24-h recall data, serum concentrations for these PFASs changed 3.0% (95% CI: 0.53, 5.5) for PFNA to 5.0% (95% CI: 1.5, 8.6) for PFOS per 100 kcal of microwave popcorn consumed daily, and the largest increases were observed for PFOS and PFOA (Table 2). For context, the median caloric intake from microwave popcorn among microwave popcorn consumers in the 24-h diet recall was 165 kcal (see Table S8). In the 12-month recall model, eating popcorn once a day was associated with 39% higher levels for PFNA (95% CI: 13, 73) up to 63% higher levels for PFDA (95% CI: 34, 99). Although we could not distinguish between microwave popcorn and other types of popcorn in the 12-month data, analysis of the 24-h recall data shows that microwave popcorn on average accounted for 85% (95% CI: 81, 89%) of overall popcorn consumption in the NHANES population. In our gender effect modification model, we did not find significant gender-specific differences in associations between popcorn consumption and serum PFAS levels (see Table S11 and Figure S1).Table 2 Percentage difference in serum PFASs (95% CI) in association with self-reported consumption of food from fast food or pizza restaurants, other restaurants, or other food outlets, and of microwave popcorn, fish, and shellfish among NHANES participants ≥12y of age.Table 2 lists recall period and types of food consumed for the 24-hour recall, a 7-day and 30-day recall, and a 12-month food frequency questionnaire in the first column. The adjacent columns list percentage difference in serum PFASs in association with self-reported consumption of food for PFOA; PFNA; PFDA; PFHxS; PFOS; and sigma PFAS.Recall period/food consumedPFOAPFNAPFDAPFHxSPFOSΣPFAS24-h recalla Fast food or pizza restaurant0.35 (0.087, 0.62)p=0.0180.25 (−0.014, 0.52)p=0.0990.087 (−0.21, 0.38)p=0.65−0.12 (−0.52, 0.28)p=0.650.078 (−0.20, 0.35)p=0.650.066 (−0.17, 0.30)p=0.65 Other restaurant0.29 (−0.081, 0.65)p=0.170.25 (−0.16, 0.66)p=0.30.19 (−0.24, 0.61)p=0.480.17 (−0.33, 0.66)p=0.60.15 (−0.23, 0.53)p=0.520.11 (−0.25, 0.47)p=0.64 Other food outlet, eaten at home−0.33 (−0.52, −0.14)p=0.002−0.32 (−0.53, −0.11)p=0.0062−0.36 (−0.57, −0.14)p=0.0043−0.50 (−0.81, −0.18)p=0.0053−0.46 (−0.67, −0.26)p=6.7×10–5−0.48 (−0.67, −0.28)p=2×10–5 Other food outlet, not eaten at home−0.025 (−0.30, 0.25)p=0.88−0.033 (−0.30, 0.23)p=0.84−0.0011 (−0.31, 0.31)p=0.99−0.29 (−0.63, 0.040)p=0.13−0.27 (−0.59, 0.051)p=0.15−0.26 (-0.54, 0.012)p=0.096 Microwave popcorn4.7 (2.2, 7.2)p=0.000793.0 (0.53, 5.5)p=0.0313.4 (0.25, 6.6)p=0.0582.2 (−1.3, 5.6)p=0.295.0 (1.5, 8.6)p=0.0114.8 (1.8, 7.9)p=0.005 Fish−0.066 (−1.4, 1.3)p=0.941.3 (−0.28, 2.8)p=0.162.2 (0.65, 3.7)p=0.011−0.062 (−2.3, 2.2)p=0.970.44 (−1.0, 1.9)p=0.650.31 (−1.1, 1.7)p=0.72 Shellfis
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