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: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.
