Background:Phthalates are ubiquitous environmental contaminants and established endocrine disruptors with disproportionate exposure among disadvantaged populations. Food insecurity, a marker of socioeconomic deprivation, may be a modifiable contributor to disparate phthalate exposure among adults. Still, associations between food insecurity and phthalate concentrations remain unclear. Methods:We analyzed cross-sectional data from 13,024 adults in eight cycles of the National Health and Nutrition Examination Survey (2003-2018). Using multivariable linear regression models, we assessed associations between food security status (four categories) and percent difference in urinary phthalate metabolite concentrations (spot sample), adjusting for sociodemographic factors, survey year, and urinary creatinine. We assessed effect modification by sex and race/ethnicity. Results:Compared with adults with high food security (70.5%), those experiencing very low food security (7.1%) had significantly higher urinary concentrations of monobenzyl phthalate (MBzP: 25.1%; 95% confidence interval [CI]: 13.2%, 38.2%), mono-n-butyl phthalate (MnBP: 9.6%; 95% CI: 1.1%, 18.8%), higher ∑di-2-ethylhexyl phthalate (12.1%; 95% CI: 2.4%, 22.7%), ∑Butyls (11.4%; 95% CI: 3.9%, 19.4%), and ∑Plastic-associated metabolites (16.0%; 95% CI: 6.4%, 26.4%). Sex and race/ethnicity, respectively, modified the food security-metabolite associations. Stronger associations were observed among females (MBzP, ∑di-2-ethylhexyl phthalate, ∑Butyls, and ∑Plastics), as well as non-Hispanic White, non-Hispanic Black, and other race individuals (MnBP and MBzP). Conclusion:Lower food security was associated with elevated concentrations of several phthalate biomarkers among US adults, with stronger associations seen in certain population subgroups. These findings highlight the need to further investigate food insecurity as a modifiable risk factor to decrease phthalate exposure disparities.
Background:In urban areas, transportation and industry-related combustion processes release large quantities of outdoor ultrafine particles (UFPs; <0.1 µm). Due to their small size, UFPs can cross biological barriers, including the placenta, and reach vital organs. Exposure during critical windows of development may increase the risk of adverse health outcomes in children, including cancer. Methods:We conducted a cohort study of over 965,000 children born in Canada between 1999 and 2020 whose birthing parent resided in Montreal or Toronto during pregnancy. Vital status and cancer incidence were obtained from the Canadian Vital Statistics Databases and the Canadian Cancer Registry. High-resolution estimates of outdoor UFP number concentrations and UFP size (i.e., mean particle diameter for a given UFP number concentration) were assigned to children's six-digit residential postal codes from annual tax records. We estimated hazard ratios (HRs) between outdoor UFP number concentrations and childhood cancer using Cox proportional hazards models, adjusting for UFP size, sociodemographic factors, and co-pollutants. Results:Children were followed from 0 to 14 years old for a mean of 9.1 years. In total, 1,625 children were diagnosed with cancer. For each 10,000 particles/cm3 increase in prenatal UFP exposure, we observed positive associations with acute lymphoblastic leukemia (ALL) (HR: 1.12; 95% confidence interval [CI]: 0.94, 1.34) and neuroblastoma (HR: 1.15; 95% CI: 0.85, 1.57), although estimates were imprecise and included the null. Consistent associations were also observed for these outcomes across different exposure windows and multiple sensitivity analyses. In contrast, null associations were observed for central nervous system tumors, and an inverse association was observed for lymphoma. Conclusion:Overall, our findings varied depending on the cancer diagnostic group evaluated. Positive associations observed between outdoor UFPs and ALL and neuroblastoma warrant further research.
Background:Non-Hispanic Black women have almost double the risk of preterm birth compared with non-Hispanic White women in the United States, and the disparity is not fully explained by sociodemographic factors, health behaviors, or medical factors. Thus, it is critical to look beyond these "traditional" risk factors and evaluate contributions from psychosocial stressors, chemical exposures, and features of residential environments where pregnant women live. Methods:This study was conducted among 1,847 Black and White women recruited at the time of delivery between 2021 and 2023 in greater Houston, Texas to examine the contribution of individual- and neighborhood-level factors to the Black/White disparity in preterm birth using two-fold Blinder-Oaxaca decomposition. We evaluated the contribution from variables within the following domains: sociodemographics; perinatal history; comorbidities and health behaviors; chemical exposures; social factors; and neighborhood characteristics. We present the results as percent contributions to the disparity for each covariate and by domain. Results:With a 6.6% higher prevalence of preterm birth among Black mothers compared with White mothers, variables included in our decomposition analysis explained 63.0% of the preterm birth disparity, with perinatal history explaining the highest proportion (36.3%), followed by neighborhood characteristics (32.8%). Individual variables with the highest contributions included residing in a more racially minoritized and economically disadvantaged neighborhood (19.2%) and having a previous pregnancy complication (18.5%), a hypertensive disorder in the index pregnancy (16.7%), or chronic hypertension before pregnancy (16.8%). Conclusion:Our study underscores the importance of perinatal history and neighborhood factors in explaining disparities in preterm birth, which should be further explored in other populations.
Background: In urban areas, transportation and industry-related combustion processes release large quantities of outdoor ultrafine particles (UFPs; <0.1 µm). Due to their small size, UFPs can cross biological barriers, including the placenta, and reach vital organs. Exposure during critical windows of development may increase the risk of adverse health outcomes in children, including cancer. Methods: We conducted a cohort study of over 965,000 children born in Canada between 1999 and 2020 whose birthing parent resided in Montreal or Toronto during pregnancy. Vital status and cancer incidence were obtained from the Canadian Vital Statistics Databases and the Canadian Cancer Registry. High-resolution estimates of outdoor UFP number concentrations and UFP size (i.e., mean particle diameter for a given UFP number concentration) were assigned to children’s six-digit residential postal codes from annual tax records. We estimated hazard ratios (HRs) between outdoor UFP number concentrations and childhood cancer using Cox proportional hazards models, adjusting for UFP size, sociodemographic factors, and co-pollutants. Results: Children were followed from 0 to 14 years old for a mean of 9.1 years. In total, 1,625 children were diagnosed with cancer. For each 10,000 particles/cm 3 increase in prenatal UFP exposure, we observed positive associations with acute lymphoblastic leukemia (ALL) (HR: 1.12; 95% confidence interval [CI]: 0.94, 1.34) and neuroblastoma (HR: 1.15; 95% CI: 0.85, 1.57), although estimates were imprecise and included the null. Consistent associations were also observed for these outcomes across different exposure windows and multiple sensitivity analyses. In contrast, null associations were observed for central nervous system tumors, and an inverse association was observed for lymphoma. Conclusion: Overall, our findings varied depending on the cancer diagnostic group evaluated. Positive associations observed between outdoor UFPs and ALL and neuroblastoma warrant further research.
Background: Phthalates are ubiquitous environmental contaminants and established endocrine disruptors with disproportionate exposure among disadvantaged populations. Food insecurity, a marker of socioeconomic deprivation, may be a modifiable contributor to disparate phthalate exposure among adults. Still, associations between food insecurity and phthalate concentrations remain unclear. Methods: We analyzed cross-sectional data from 13,024 adults in eight cycles of the National Health and Nutrition Examination Survey (2003–2018). Using multivariable linear regression models, we assessed associations between food security status (four categories) and percent difference in urinary phthalate metabolite concentrations (spot sample), adjusting for sociodemographic factors, survey year, and urinary creatinine. We assessed effect modification by sex and race/ethnicity. Results: Compared with adults with high food security (70.5%), those experiencing very low food security (7.1%) had significantly higher urinary concentrations of monobenzyl phthalate (MBzP: 25.1%; 95% confidence interval [CI]: 13.2%, 38.2%), mono-n-butyl phthalate (MnBP: 9.6%; 95% CI: 1.1%, 18.8%), higher ∑di-2-ethylhexyl phthalate (12.1%; 95% CI: 2.4%, 22.7%), ∑Butyls (11.4%; 95% CI: 3.9%, 19.4%), and ∑Plastic-associated metabolites (16.0%; 95% CI: 6.4%, 26.4%). Sex and race/ethnicity, respectively, modified the food security–metabolite associations. Stronger associations were observed among females (MBzP, ∑di-2-ethylhexyl phthalate, ∑Butyls, and ∑Plastics), as well as non-Hispanic White, non-Hispanic Black, and other race individuals (MnBP and MBzP). Conclusion: Lower food security was associated with elevated concentrations of several phthalate biomarkers among US adults, with stronger associations seen in certain population subgroups. These findings highlight the need to further investigate food insecurity as a modifiable risk factor to decrease phthalate exposure disparities.
Background:Extreme temperatures affect health, but nationwide evidence on injury-related hospitalization and economic burden in East Asia is scarce. We aimed to quantify the nonlinear and lagged associations between ambient temperature and injury-related hospitalization and the attributable economic burden. Methods:This nationwide time-stratified case-crossover study used the National Health Insurance Service-National Sample Cohort (2010-2019) of adults (≥20 years). The exposure was the district-specific percentile of daily mean temperature, and the outcome was inpatient hospital admission for injury. Conditional logistic regression with distributed lag nonlinear models (7-day lag, 3 degrees of freedom) was used to estimate relative risks (RRs) and 95% confidence intervals (CIs) at the 1st and 99th percentiles, each relative to the minimum injury temperature, adjusting for holidays, particulate matter concentrations (lag 0-1), and humidity. Analyses were stratified by age, sex, economic activity, residential area, and injury type. Societal economic burden was estimated using a human capital-based cost-of-illness approach. Results:On analyzing 198,937 hospitalizations, a distinct U-shaped relationship emerged. At the 1st percentile (cold), the RR was 1.151 (95% CI = 1.091, 1.214) with delayed effects (lags 1-6) primarily affecting limb injuries. Conversely, at the 99th percentile (heat), the RR was 1.157 (95% CI = 1.081, 1.239) with acute risks (lags 0-3) associated with severe injuries, such as multiple trauma (RR = 2.434, 95% CI = 0.886, 6.687) and burns (RR = 1.995, 95% CI = 1.272, 3.129). The total heat-related economic burden (24,649 million South Korean Won) exceeded that of cold (7,853 million South Korean Won). Individuals with low income, economically active groups, and provincial residents exhibited increased vulnerability to extreme heat, whereas females and the economically inactive population exhibited susceptibility to extreme cold. Conclusions:Nonoptimal temperatures increase injury risk and economic burdens while exacerbating inequalities. Integrating economic evaluations and targeted interventions into climate adaptation strategies is thus essential.
Background:Lung function, expressed as forced expiratory volume in 1 second (FEV1), reaches its maximum at 20-30 years of age. A lower maximal lung function has been associated with a higher risk of chronic obstructive pulmonary disease in later adulthood, but the impact of smoking and indoor environmental exposures on this maximum remains unclear. Methods:Using data from 858 participants of the Dutch PIAMA birth cohort (mean age: 25.7 years), we investigated associations between smoking, second-hand smoke (SHS), dampness or mold, furry pets, and gas cooking exposure with maximal lung function. Exposure data were collected via questionnaires from pregnancy through early adulthood, and life-course exposure trajectories were derived using latent class growth modeling. We assessed associations with FEV1 and forced vital capacity (FVC) using linear regression, adjusting for potential confounders. Results:Pre- and post-bronchodilator spirometry was available for 846 and 806 participants, respectively. We found no associations between exposure to dampness or mold, furry pets, or gas cooking and lung function. Current and life-course active smoking was associated with higher post-bronchodilator FEV1, and pre- and post-bronchodilator FVC [regression coefficient β for pre-bronchodilator FVC (ml) (95% confidence interval): current (yes vs. no) 175 (68, 281), life-course (regular vs. occasional or none) 168 (55, 281)]. Current SHS was positively associated with post-bronchodilator FVC. Conclusion:No associations were found between indoor environmental exposures and maximal lung function in early adulthood. The observed positive associations with active smoking likely reflect bias arising from a selective uptake of smoking by individuals with higher pre-existing lung function, rather than a true physiological effect.
Global professional football (soccer in the United States) is increasingly integrated with fossil fuel-derived capital through club ownership, expansive sponsorship deals, and tournament hosting. While often discussed in ethical or political terms, these developments have received limited attention from an environmental health perspective. This commentary examines the growing alignment between fossil fuel-derived wealth and global football, focusing primarily on club ownership, while situating it within a broader ecosystem of commercial and geopolitical influence. We argue that these relationships function as a commercial determinant of health by shaping social norms, legitimizing carbon-intensive industries, and delaying policy action on climate change. Drawing parallels to the historical regulation of tobacco sponsorship, we highlight how such dynamics contribute to the persistence of exposures that drive climate-related health risks. Climate change is the great public health challenge of the 21st century, just as tobacco was in the 20th century. Greater scrutiny, transparency, and leadership from the public health community with regard to fossil fuel-derived funding of sport are warranted. It is no longer acceptable for major sporting bodies and events to accept tobacco industry funding. It should also be unacceptable for them to accept fossil fuel-derived funding.
Background:Air quality in New York City has improved substantially in the past 2 decades due to reductions in both transported aerosols and local emissions. We estimated the short-term risk changes for three criteria air pollutants and corresponding attributable burdens. Methods:Trends in percent excess risk (PER) per same pollution increment and attributable counts and fractions for fine particles (PM2.5), nitrogen dioxide (NO2), and ozone (warm season only) were examined for Emergency Department (ED) visits (2005-2019) and hospitalizations (2000-2019) for youth asthma (ages 5-17), adult cardiovascular disease (CVD) (ages 40+), and older adult respiratory causes (ages 65+). Time-series models considered up to 3-day lag, adjusted for seasonal trends, day of week, holidays, and concurrent and delayed temperature. Results:Most pollutant-outcome pairs did not exhibit trends in PERs over time. NO2-attributable burden was higher than PM2.5 burden for asthma and CVD outcomes. We estimated about 4500 (17%) youth asthma ED visits and 1000 (2%) CVD hospitalizations on average annually (2005-2019) attributable to NO2 compared with 1900 (7%) youth asthma ED visits and 450 (1%) CVD hospitalizations attributable to PM2.5. NO2- and PM2.5-attributable health impacts declined about 50%-70%, driven by decreasing pollution levels and total morbidity burden depending on outcome, pollutant, and season. Ozone-attributable burden was mostly unchanged over time. Conclusion:With less decline and greater attributable impact than PM2.5, NO2 is increasingly important for measuring morbidity impacts from local sources (i.e., traffic and buildings) in New York City. Ozone impacts from regional source emissions persist.
Background:Dengue incidence has increased significantly in recent decades, especially in areas undergoing rapid urbanization and frequent flooding. Floods can promote dengue transmission by creating favorable mosquito breeding sites, yet the timing and strength of this association remain unclear, particularly in Vietnam, where flood-prone areas overlap with a high dengue burden. Methods:This study assessed the relationship between flood exposure and dengue incidence across Vietnam and in Ho Chi Minh City (HCMC), a densely populated, flood-prone urban center. Time-series analyses were conducted using monthly data from 63 provinces (2011-2019) and weekly data from 24 districts in HCMC. Generalized additive mixed models with a negative binomial distribution were used, incorporating distributed lag linear functions to estimate cumulative and delayed effects. Analyses were stratified by season (rainy vs. dry). Results:At the national level, flooding was associated with a 17% higher dengue incidence (relative risk [RR] = 1.17; 95% confidence interval [CI] = 0.94, 1.47), with the strongest effect observed 2 months after flooding (RR = 1.11; 95% CI = 1.03, 1.20). Associations were more pronounced during the rainy season (RR = 1.65; 95% CI = 1.17, 2.32). In HCMC, floods were linked to a 10.4% increase in dengue cases (RR = 1.10; 95% CI = 1.03, 1.18), with effects peaking at week 9 (RR = 1.03; 95% CI = 1.02, 1.04). Seasonal analysis revealed short-term declines in risk during the rainy season and delayed increases during the dry season, peaking at week 9 (RR = 1.03; 95% CI = 1.01, 1.04). Conclusions:These findings highlight the delayed and seasonal nature of flood-related dengue risk and support the integration of flood metrics into early warning systems and climate-informed vector control strategies.
Background:Pattern recognition in high-dimensional mixture data is of increasing interest in environmental health (EH), as researchers often aim to identify sources or behaviors leading to potentially harmful exposures. Principal component pursuit (PCP)-a robust dimensionality reduction technique-has been successfully utilized for pattern recognition in a number of EH studies. PCP decomposes an exposure matrix into a low-rank matrix encoding consistent exposure patterns and a sparse matrix isolating outlying exposure events. However, PCP's application has been hindered by a lack of available software tailored specifically to EH research. Methods:We introduce an open-source R package, pcpr, enabling easy PCP deployment in EH research. The package provides functions to fit and fine-tune PCP models with three EH-specific extensions: (1) a non-negativity constraint on the low-rank matrix, enhancing interpretability; (2) procedures to accommodate missingness; and (3) a specialized penalty for observations below the analytic limit of detection. We illustrate core functionality by conducting a fully reproducible source-apportionment analysis of an air pollution mixture of 26 PM2.5 constituents measured every few days in Queens, New York City (2015-2021). Results:The functions in pcpr autonomously extracted four consistent exposure patterns (secondary signal and tailpipe emissions, traffic, crustal dust, and salt) and 211 outlying exposure events (including July Fourth firework-related spikes) from the Queens PM2.5 mixture. If found to be associated with adverse health outcomes in downstream health models, these exposure patterns and extreme events can support targeted regulatory action. Conclusion:The pcpr package facilitates robust, reproducible, and accessible exposure pattern recognition tailored to environmental epidemiology.
Background:There is limited evidence of the associations between transportation noise and dementia risk. We examined associations of road and aircraft noise with cognitive function, cognitive decline, and Alzheimer's dementia (AD) in a cohort of older adults. Methods:We set our study in the Chicago Health and Aging Project, a longitudinal cohort of community-dwelling older adults from four Chicago, Illinois, neighborhoods, followed from 1993 to 2012. Every 3 years, participants underwent in-home cognitive assessments (episodic memory, perceptual speed, global cognition). A stratified random sample underwent clinical evaluation for AD diagnosis. We estimated 5-year time-weighted day-night average sound levels before baseline for road and, in analyses, we considered exploratory because of a limited exposure range, aircraft noise. We fit covariate-adjusted linear mixed models to estimate associations with cognitive performance and decline, and a multiple logistic regression model weighted by the sampling design to estimate incident AD odds ratios. Results:Of the 10,681 participants, an interquartile range increment in road noise (8.5 dBA) corresponded to a 0.06-SD unit lower baseline global cognitive score (95% confidence interval: -0.08, -0.03); there were no differences in cognitive decline. In exploratory analyses limited by power, higher aircraft noise was associated with a higher baseline score yet a faster rate of cognitive decline. Among 2147 participants evaluated for dementia (460 cases), road noise was not noticeably associated with greater AD risk, as there was substantial uncertainty (odds ratio per interquartile range = 1.17 [95% confidence interval: 0.86, 1.59]). Conclusion:We observed mixed associations of transportation noise with cognitive functioning and dementia across noise sources. These findings underscore the need to better characterize noise sources relevant to the cognitive health of older adults.
Background:Older adults, children, and low-income populations are recognized as vulnerable to climate-related health risks. However, evidence on morbidity risks by functional status remains limited. This study investigated the association between ambient temperature and all-cause hospitalization by functional dependency in Japan. Methods:We obtained daily hospitalization data from the Diagnosis Procedure Combination database and meteorological data for nine Japanese prefectures between 2012 and 2019, comprising over 10 million admissions. Functional status at admission was assessed using the Barthel Index (0-100), with scores >60 classified as functionally independent and ≤60 as functionally dependent. A time-stratified case-crossover design with conditional quasi-Poisson regression was applied to estimate temperature-hospitalization associations. Results:Among functionally independent individuals, relative risks (RRs) were 0.93 (95% confidence interval [CI]: 0.90, 0.96) at extreme cold (5th percentile) and 1.02 (95% CI: 1.01, 1.04) at extreme heat (95th percentile), with the temperature of peak risk (cold) (TPR [cold]) at the 35th percentile (TPR [cold] RR: 1.08 [1.05, 1.10]). Functionally dependent people showed higher risks at extreme cold (RR: 1.11; 95% CI: 1.07, 1.15), comparable risks at TPR (cold) (23rd percentile), and extreme heat (RR: 1.03; 95% CI: 1.02, 1.04). Compared with independent individuals, functionally dependent individuals had higher cold risks, with ratios of RR of 1.20 (95% CI: 1.14, 1.26) at extreme cold and 1.05 (95% CI: 1.01, 1.09) at TPR (cold). These disparities persisted across age and sex subgroups. Conclusions:Temperature-related hospitalization risks vary by functional status. Functionally dependent individuals are particularly vulnerable to cold exposure, highlighting the importance of targeted cold-weather preparedness strategies.
Background:Gestational exposure to phthalates is higher among non-Hispanic black (NHB) women than non-Hispanic white (NHW) women and may contribute to racial/ethnic differences in birthweight z-scores. Objective:We aimed to investigate whether gestational phthalate and replacement biomarkers mediate the association between race/ethnicity and birthweight z-scores. Methods:We analyzed data from 271 pregnancies in the Human Placenta and Phthalates study, a prospective cohort recruited from 2017 to 2020. Urinary phthalate metabolite concentrations were measured at up to eight time points during pregnancy and averaged to represent gestational exposure. Metabolites were grouped by parent compound. Linear regression models estimated associations in phthalate biomarkers by race and ethnicity, between race and ethnicity and birthweight z-scores, and between phthalate biomarkers and birthweight z-scores. Mediation analyses assessed whether phthalate biomarkers mediate the association between race/ethnicity and birthweight z-scores. Results:NHB participants exhibited higher concentrations of most phthalate biomarkers than NHW participants. For example, monoethyl phthalate concentrations were 250% higher (95% confidence interval [CI] = 173, 349). NHB participants had 0.43 lower birthweight z-scores (95% CI = -0.67, -0.19) than NHW participants. Monoethyl phthalate and summed metabolites of di-iso-butyl phthalate (ΣDiBP) and di-n-butyl phthalate were inversely associated with birthweight z-scores. ΣDiBP was associated with 0.16 (95% CI = -0.32, -0.002) lower birthweight z-scores. Mediation by phthalate biomarkers was modest and not statistically significant, with a ≤5% mediated effect. Conclusions:Racial/ethnic differences in phthalate exposure and birthweight z-scores were evident, and some phthalate biomarkers were associated with lower birthweight z-scores. However, phthalate exposures explained only a small, nonsignificant portion of the association between race and ethnicity and birthweight z-scores, underscoring the need to investigate additional contributors.
Background:Whether residential greenness affects cancer outcomes across the cancer continuum and whether comorbid coronary heart disease (CHD) confers differential vulnerability remains an open question. We evaluated greenness-cancer associations and CHD effect modification in a pooled multicohort study. Methods:Four cohorts were pooled: two CHD patient registries and two Israeli National Health and Nutrition Surveys. Cancer and mortality data were obtained from national registries. Greenness was estimated using the Normalized Difference Vegetation Index (NDVI) within a 300 m buffer. Incident cancer cases were 1:1 matched to cancer-free controls by age, sex, cohort, and enrollment year and followed for second primary cancer incidence and mortality. Conditional logistic and Cox regression models estimated hazard ratios (HRs) per 1- standard deviation NDVI increase; CHD effect modification was tested. Results:Overall, 17,047 individuals were pooled, including 1,661 prevalent cancer cases. Over a median of 13.6 years, 2,481 incident cancer cases [age 74 (11.3) years, 27% females] were identified; 1,387 died. Prevalent cases [age 75 (10.9) years, 33% females] had 1,125 deaths over a median of 15.0 years. Greenness associations were specific to postcancer survival: NDVI-300 was not associated with first or second primary cancer incidence [HRs (95% confidence intervals) = 0.96 (0.90, 1.02) and 1.04 (0.93, 1.16), respectively]. NDVI-300 was inversely associated with postcancer mortality [HRs (95% confidence intervals) = 0.93 (0.88, 0.99) and 0.92 (0.86, 0.98) in incident and prevalent groups]. The association was consistent regardless of CHD status (all P-for-effect-modification > 0.05). Conclusions:While no association was observed for cancer incidence, residential greenness was consistently associated with lower postcancer mortality, regardless of CHD status.
Background:This pilot study aimed to examine associations between recent occupational exposure to per- and polyfluoroalkyl substances (PFAS) and domain-specific cognitive performance and explore whether cumulative perfluorooctane sulfonic acid (PFOS) modified these associations. Methods:Sixty-five actively serving firefighters in Central Texas (June 2023-March 2025) participated. Recent exposure was assessed using total concentrations (pg/µl) of perfluorobutanoic acid, perfluorobutane sulfonic acid, and PFOS measured in single post-incident wash-water samples from three sites (June-August 2024), with site-specific results extrapolated to all firefighters at each site. Cumulative exposure was measured using PFOS concentrations (pg/µl) in whole blood collected from February to March 2025. Cognitive outcomes included standardized z-scores for processing speed and global cognition derived from the NIH Toolbox Cognition Battery. Linear regression models evaluated PFAS-cognition associations, adjusting for covariates and testing interaction effects. Results:After adjustment, each doubling of cumulative PFOS corresponded to an estimated 11.1-point decline in processing speed (β = -1.07, 95% confidence interval = -1.59, -0.55, P < 0.001). Among firefighters with lower cumulative PFOS, higher recent PFAS exposure was associated with a 7.5-point reduction in processing speed. This effect was amplified with increasing cumulative PFOS (interaction β = 0.74, P = 0.01). No significant associations were observed for global cognition. Conclusion:PFAS exposure may differentially relate to cognitive domains in firefighters. Cumulative PFOS was associated with reduced processing speed and modified the impact of recent exposure. These preliminary findings warrant confirmation in larger studies and highlight the need to evaluate exposure mitigation strategies, including decontamination practices.
Background: Prolonged exposure to both occupational and recreational noise can lead to noise-induced hearing loss. This study aimed to determine annual noise exposure (ANE) levels among Malaysian young adults using the Noise Exposure Questionnaire and to examine differences in ANE by gender, race, and medical background. Methods: A culturally modified Noise Exposure Questionnaire was validated and distributed to 205 healthy young adults (mean age = 22.9, SD = 3.0). ANE values were computed based on participants’ reported frequency and duration of exposure, combined with predetermined mid-intensity levels for each activity. Test-retest reliability was assessed in 20 randomly selected participants after a 3-month interval. Results: The median ANE was 71.4 dBA (95% confidence interval [CI] = 70.5, 72.1). A total of 16.5% (n = 34) of participants exceeded the National Institute for Occupational Safety and Health-recommended limit of 79.0 dBA. Subgroup analyses using bootstrap CIs suggested a possible difference in ANE between males (73.8 dBA, 95% CI = 71.7, 76.1) and females (70.5 dBA, 95% CI = 69.2, 71.3), with the wider interval in males reflecting the smaller male sample (n = 49). ANE estimates were comparable between racial groups (Chinese: 70.8 dBA, 95% CI = 69.7, 71.7; Malay: 71.9 dBA, 95% CI = 66.9, 77.5), though the considerably wider CI in the Malay subgroup (n = 25) limits the interpretability of this comparison. ANE was similarly comparable between participants with (70.9 dBA, 95% CI = 69.7, 71.9) and without (71.5 dBA, 95% CI = 69.0, 73.3) a medical background. Approximately 85% of participants reported never using hearing protection during motorized vehicle use, amplified events, and musical instrument playing. Test-retest reliability showed a moderate intraclass correlation coefficient (ICC3 = 0.60, 95% CI = 0.22, 0.82), though the wide CI warrants cautious interpretation. Conclusion: Recreational and daily lifestyle habits among young adults may contribute to elevated noise exposure, increasing the risk of noise-induced hearing loss. These findings underscore the importance of promoting hearing health awareness and safe listening practices among youth to mitigate preventable hearing loss.
Background: Parkinson’s Disease (PD) prevention and treatment are complicated because biological processes underlying PD may begin several years before diagnosis. Previous studies suggest that increased exposure to fine particulate matter (PM 2.5 ) and nitrogen dioxide (NO 2 ) air pollution increases PD morbidity. Methods: We analyzed data from 10,366,083 Medicare fee-for-service beneficiaries (age 65+) in the contiguous United States from 2000 to 2016. We defined “hospitalization with PD” as a beneficiary’s first hospitalization claim with diagnosis codes indicating PD. We linked 10-year exposure histories for PM 2.5 , NO 2 , and summer ozone (O 3 ). In a discrete-time survival analysis, we fitted distributed lag models and estimated the lagged associations between air pollution and the odds of first hospitalization with PD. Results: Increased PM 2.5 and NO 2 exposure at least 4 years before hospitalization was associated with increased odds of hospitalization with PD. Accounting for nonlinearities in exposure-response and 10 years of continuous exposure to PM 2.5 at the 90th versus the 0.5th percentile (i.e., 11.8 μg/m 3 vs. 3.0 μg/m 3 ), the odds ratio for hospitalization with PD was 1.634 (95% CI: 1.489, 1.792). Similarly, for 10 years of continuous exposure to NO 2 at the 90th versus the 0.5th percentile (i.e., 31.7 ppb vs. 3.7 ppb), the odds ratio for hospitalization with PD was 1.474 (95% CI: 1.379, 1.575). Evidence of a relationship between O 3 exposure and odds for hospitalization with PD was more limited. Conclusions: Air pollution at least 4 years before hospitalization may increase the odds of hospitalization with PD. Reducing air pollution exposure may have long-term effects on PD prevention.
Background: Preeclampsia (PE), characterized by hypertension and organ dysfunction during pregnancy, is a leading cause of maternal and fetal mortality. Residential greenness has been reported to be inversely associated with a broad range of health outcomes. However, evidence on the association between residential greenness and PE remains limited, particularly among East Asian populations. Methods: This study included 20,140 pregnancies among Japanese women from the Tohoku Medical Megabank Project Birth and Three-Generation Cohort Study. Residential greenness was assessed using the normalized difference vegetation index (NDVI) values calculated around the population-weighted centroid of each participant’s postal code area. PE was identified using a rule-based phenotyping algorithm applied to medical records. Poisson regression with robust variance was used to estimate risk ratios (RRs) and confidence intervals, adjusting for maternal age, educational attainment, household income, urbanization status, and areal deprivation index. Results: Moderate NDVI levels were associated with a lower risk of PE than low NDVI levels (RR = 0.81 [95% confidence interval = 0.66, 1.00]). For high NDVI levels, the point estimate was below 1.00, but the association was not statistically significant (RR = 0.88 [0.69, 1.11]). No clear dose-response pattern emerged across tertiles ( P for trend = 0.228). This inverse association was primarily observed in more-deprived areas. In subtype analysis, the associations were more evident in gestational hypertension and late-onset PE. Conclusion: Moderate residential greenness was associated with a lower risk of PE compared with low residential greenness.
Background: Metal exposures adversely impact prenatal neurodevelopment; however, their associations with child autism spectrum disorder (ASD) remain unclear. Methods: In the Environmental Influences on Child Health Outcomes Cohort, we analyzed prenatal blood (N = 479) and urinary (N = 482) metal concentrations in relation to Social Responsiveness Scale—Second Edition (SRS-2) total T-scores, SRS-2 subscale T-scores, and ASD diagnosis. Associations were examined using linear and logistic regression for individual metals and Bayesian Kernel Machine Regression for mixtures, adjusting for covariates. Results: Interquartile range increases in maternal blood lead and mercury were associated with higher SRS-2 total T-scores (lead: β = 0.11, 95% confidence interval [CI] = 0.03, 0.18; mercury: β = 0.19, 95% CI = 0.01, 0.37), and maternal blood cadmium was associated with higher odds of ASD diagnosis (OR = 2.42, 95% CI = 1.16, 5.03). Bayesian Kernel Machine Regression revealed joint effects of blood metal mixtures (arsenic, cadmium, mercury, and lead) on social awareness and cognition. Blood cadmium correlated with social awareness in females (raw score: β = 0.85, 95% CI = 0.09, 1.61) versus males ( p -interaction = 0.02). Urinary barium correlated with social motivation in females (raw score: β = 0.273, 95% CI = 0.067, 0.478) versus males ( p -interaction = 0.05). Conclusions: Future research should prioritize metal speciation, larger samples, and mechanistic studies to clarify sex-specific pathways.
