Per-and polyfluoroalkyl substances (PFASs) are highly persistent in the environment and may cause depressed immune function. Previous studies have linked PFAS exposure to lower vaccine responses in children, but research in adults is limited. Therefore, the present study evaluated the associations between exposure to PFASs and serum antibody concentrations in adults vaccinated at age 28 years in the Faroe Islands. PFAS concentrations were determined from cord-blood collected at birth and serum samples collected at ages 7, 14, 22, and 28 years. Serum antibody concentrations against hepatitis type A and B, diphtheria, and tetanus were analyzed from blood samples collected about 6 mo after the first vaccine inoculation at age 28 years. Linear regression models were used to estimate changes in antibody concentration for each doubling of PFAS concentration. Potential effect modification by sex was assessed by including an interaction term between PFAS and sex. Although the 95% confidence intervals contain the null value, inverse trends were observed between serum perfluorooctanoate (PFOA) at ages 14 and 28 years and hepatitis type A antibody (anti-HAV) concentrations, as revealed by an estimated decrease of 0.71 (95% CI: À1.52, 0.09) and 0.24 (95% CI: À0.59, 0.10) signal-to-cutoff ratio for each doubling of exposure, respectively. Inverse trends were also observed between serum PFOA at ages 22 and 28 years and hepatitis type B antibody (anti-HBs) concentration, with an estimated decrease of 21% (95% CI: À42.20%, 7.34%) and of 17% (95% CI: À35.47%, 7.35%) in anti-HBs for each doubling of exposure, respectively. Sexspecific associations with anti-HAV were observed for cord-blood PFASs and serum PFAS concentrations at ages 7 and 14 years. No inverse associations of PFAS exposure were found with diphtheria and tetanus antibody concentrations. Future studies are needed to confirm these findings and further investigate the effects of PFASs on adult immune function.

Inhaling radon and its progeny is associated with adverse health outcomes. However, previous studies of the health effects of residential exposure to radon in the United States were commonly based on a county-level temporally invariant radon model that was developed using measurements collected in the mid- to late 1980s. We developed a machine learning model to predict monthly radon concentrations for each ZIP Code Tabulation Area (ZCTA) in the Greater Boston area based on 363,783 short-term measurements by Spruce Environmental Technologies, Inc., during the period 2005–2018. A two-stage ensemble-based model was developed to predict radon concentrations for all ZCTAs and months. Stage one included 12 base statistical models that independently predicted ZCTA-level radon concentrations based on geological, architectural, socioeconomic, and meteorological factors for each ZCTA. Stage two aggregated the predictions of these 12 base models using an ensemble learning method. The results of a 10-fold cross-validation showed that the stage-two model has a good prediction accuracy with a weighted R 2 of 0.63 and root mean square error of 22.6 Bq/m3. The community-level time-varying predictions from our model have good predictive precision and accuracy and can be used in future prospective epidemiological studies in the Greater Boston area.

BackgroundThe cardiovascular effects of low‐level environmental radiation exposures are poorly understood. Although particulate matter (PM) has been linked to cardiovascular morbidity and mortality, and elevated blood pressure (BP), the properties promoting its toxicity remain uncertain. Addressing a knowledge gap, we evaluated whether BP increased with higher exposures to radioactive components of ambient PM, herein referred to as particle radioactivity (PR).Methods and ResultsWe performed a repeated‐measures analysis of 852 men to examine associations between PR exposure and BP using mixed‐effects regression models. As a surrogate for PR, we used gross β activity, measured by the US Environmental Protection Agency's radiation monitoring network. Higher PR exposure was associated with increases in both diastolic BP and systolic BP, for exposures from 1 to 28 days. An interquartile range increase in 28‐day PR exposure was associated with a 2.95–mm Hg increase in diastolic BP (95% confidence interval, 2.25–3.66; P<0.001) and a 3.94–mm Hg increase in systolic BP (95% confidence interval, 2.62–5.27; P<0.001). For models including both PR and PM ≤2.5 µm, the PR‐BP associations remained stable and significant. For models including PR and black carbon or PR and particle number, the PR‐BP associations were attenuated; however, they remained significant for many exposure durations.ConclusionsThis is the first study to demonstrate the potential adverse effects of PR on both systolic and diastolic BPs. These were independent and similar in magnitude to those of PM ≤2.5 µm, black carbon, and particle number. Understanding the effects of particle‐bound radionuclide exposures on BP may have important implications for environmental and public health policy.

Numerous studies have reported a positive association between ambient fine particles and daily mortality, but little is known about the particle properties or environmental factors that may contribute to these effects. This study assessed potential modification of radon on PM 2.5 (particulate matter with an aerodynamic diameter <2.5 μm)-associated daily mortality in 108 U.S. cities using a two-stage statistical approach. First, city-and season-specific PM 2.5 mortality risks were estimated using over-dispersed Poisson regression models. These PM 2.5 effect estimates were then regressed against mean city-level residential radon concentrations to estimate overall PM 2.5 effects and potential modification by radon. Radon exposure estimates based on measured short-term basement concentrations and modeled long-term living-area concentrations were both assessed. Exposure to PM 2.5 was associated with total, cardiovascular, and respiratory mortality in both the spring and the fall. In addition, higher mean city-level radon concentrations increased PM 2.5-associated mortality in the spring and fall. For example, a 10 µg/m 3 increase in PM 2.5 in the spring at the 10th percentile of cityaveraged short-term radon concentrations (21.1 Bq/m 3) was associated with a 1.92% increase in total mortality (95% CI: 1.29, 2.55), whereas the same PM 2.5 exposure at the 90th radon percentile (234.2 Bq/ m 3) was associated with a 3.73% increase in total mortality (95% CI: 2.87, 4.59). Results were robust to adjustment for spatial confounders, including average planetary boundary height, population age, percent poverty and tobacco use. While additional research is necessary, this study suggests that radon enhances PM 2.5 mortality. This is of significant regulatory importance, as effective regulation should consider the increased risk for particle mortality in cities with higher radon levels. Implications: In this large national study, city-averaged indoor radon concentration was a significant effect modifier of PM 2.5-associated total, cardiovascular, and respiratory mortality risk in the spring and fall. These results suggest that radon may enhance PM 2.5-associated mortality. In addition, local radon concentrations partially explain the significant variability in PM 2.5 effect estimates across U.S. cities, noted in this and previous studies. Although the concept of PM as a vector for radon progeny is feasible, additional research is needed on the noncancer health effects of radon and its potential interaction with PM. Future air quality regulations may need to consider the increased risk for particle mortality in cities with higher radon levels.

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