Assessment of internal exposure risk from metals pollution of occupational and non-occupational populations around a non-ferrous metal smelting plant.

Non-ferrous metal smelting poses significant risks to public health. Specifically, the copper smelting process releases arsenic, a semi-volatile metalloid, which poses an emerging exposure risk to both workers and nearby residents. To comprehensively understand the internal exposure risks of metal(loid)s from copper smelting, we explored eighteen metal(loid)s and arsenic metabolites in the urine of both occupational and non-occupational populations using inductively coupled plasma mass spectrometry with high-performance liquid chromatography and compared their health risks. Results showed that zinc and copper (485.38 and 14.00 µg/L), and arsenic, lead, cadmium, vanadium, tin and antimony (46.80, 6.82, 2.17, 0.40, 0.44 and 0.23 µg/L, respectively) in workers (n=179) were significantly higher compared to controls (n=168), while Zinc, tin and antimony (412.10, 0.51 and 0.15 µg/L, respectively) of residents were significantly higher than controls. Additionally, workers had a higher monomethyl arsenic percentage (MMA%), showing lower arsenic methylation capacity. Source appointment analysis identified arsenic, lead, cadmium, antimony, tin and thallium as co-exposure metal(loid)s from copper smelting, positively relating to the age of workers. The hazard index (HI) of workers exceeded 1.0, while residents and control were approximately at 1.0. Besides, all three populations had accumulated cancer risks exceeding 1.0 × 10-4, and arsenite (AsIII) was the main contributor to the variation of workers and residents. Furthermore, residents living closer to the smelting plant had higher health risks. This study reveals arsenic exposure metabolites and multiple metals as emerging contaminants for copper smelting exposure populations, providing valuable insights for pollution control in non-ferrous metal smelting.

Association between machine learning-assisted heavy metal exposures and diabetic kidney disease: a cross-sectional survey and Mendelian randomization analysis.

Background and objective: Heavy metals, ubiquitous in the environment, pose a global public health concern. The correlation between these and diabetic kidney disease (DKD) remains unclear. Our objective was to explore the correlation between heavy metal exposures and the incidence of DKD. Methods: We analyzed data from the NHANES (2005-2020), using machine learning, and cross-sectional survey. Our study also involved a bidirectional two-sample Mendelian randomization (MR) analysis. Results: Machine learning reveals correlation coefficients of -0.5059 and - 0.6510 for urinary Ba and urinary Tl with DKD, respectively. Multifactorial logistic regression implicates urinary Ba, urinary Pb, blood Cd, and blood Pb as potential associates of DKD. When adjusted for all covariates, the odds ratios and 95% confidence intervals are 0.87 (0.78, 0.98) (p = 0.023), 0.70 (0.53, 0.92) (p = 0.012), 0.53 (0.34, 0.82) (p = 0.005), and 0.76 (0.64, 0.90) (p = 0.002) in order. Furthermore, multiplicative interactions between urinary Ba and urinary Sb, urinary Cd and urinary Co, urinary Cd and urinary Pb, and blood Cd and blood Hg might be present. Among the diabetic population, the OR of urinary Tl with DKD is a mere 0.10, with a 95%CI of (0.01, 0.74), urinary Co 0.73 (0.54, 0.98) in Model 3, and urinary Pb 0.72 (0.55, 0.95) in Model 2. Restricted Cubic Splines (RCS) indicate a linear linkage between blood Cd in the general population and urinary Co, urinary Pb, and urinary Tl with DKD among diabetics. An observable trend effect is present between urinary Pb and urinary Tl with DKD. MR analysis reveals odds ratios and 95% confidence intervals of 1.16 (1.03, 1.32) (p = 0.018) and 1.17 (1.00, 1.36) (p = 0.044) for blood Cd and blood Mn, respectively. Conclusion: In the general population, urinary Ba demonstrates a nonlinear inverse association with DKD, whereas in the diabetic population, urinary Tl displays a linear inverse relationship with DKD.

Combined Exposures and Mixtures Research: An Enduring NIEHS Priority.

BACKGROUND: The National Institute of Environmental Health Sciences (NIEHS) continues to prioritize research to better understand the health effects resulting from exposure to mixtures of chemical and nonchemical stressors. Mixtures research activities over the last decade were informed by expert input during the development and deliberations of the 2011 NIEHS Workshop "Advancing Research on Mixtures: New Perspectives and Approaches for Predicting Adverse Human Health Effects." NIEHS mixtures research efforts since then have focused on key themes including a) prioritizing mixtures for study, b) translating mixtures data from in vitro and in vivo studies, c) developing cross-disciplinary collaborations, d) informing component-based and whole-mixture assessment approaches, e) developing sufficient similarity methods to compare across complex mixtures, f) using systems-based approaches to evaluate mixtures, and g) focusing on management and integration of mixtures-related data. OBJECTIVES: We aimed to describe NIEHS driven research on mixtures and combined exposures over the last decade and present areas for future attention. RESULTS: Intramural and extramural mixtures research projects have incorporated a diverse array of chemicals (e.g., polycyclic aromatic hydrocarbons, botanicals, personal care products, wildfire emissions) and nonchemical stressors (e.g., socioeconomic factors, social adversity) and have focused on many diseases (e.g., breast cancer, atherosclerosis, immune disruption). We have made significant progress in certain areas, such as developing statistical methods for evaluating multiple chemical associations in epidemiology and building translational mixtures projects that include both in vitro and in vivo models. DISCUSSION: Moving forward, additional work is needed to improve mixtures data integration, elucidate interactions between chemical and nonchemical stressors, and resolve the geospatial and temporal nature of mixture exposures. Continued mixtures research will be critical to informing cumulative impact assessments and addressing complex challenges, such as environmental justice and climate change. https://doi.org/10.1289/EHP14340.

Environmental Toxicant Exposure and Depressive Symptoms.

Importance: Recognizing associations between exposure to common environmental toxicants and mental disorders such as depression is crucial for guiding targeted mechanism research and the initiation of disease prevention efforts. Objectives: To comprehensively screen and assess the associations between potential environmental toxicants and depressive symptoms and to assess whether systemic inflammation serves as a mediator. Design, Setting, and Participants: A total of 3427 participants from the 2013-2014 and 2015-2016 waves of the National Health and Nutrition Examination and Survey who had information on blood or urine concentrations of environmental toxicants and depression scores assessed by the 9-item Patient Health Questionnaire (PHQ-9) were included. Statistical analysis was performed from July 1, 2023, to January 31, 2024. Exposures: Sixty-two toxicants in 10 categories included acrylamide, arsenic, ethylene oxide, formaldehyde, iodine, metals, nicotine metabolites, polycyclic aromatic hydrocarbons, volatile organic compound (VOC) metabolites; and perchlorate, nitrate, and thiocyanate. Main Outcomes and Measures: An exposome-wide association study and the deletion-substitution-addition algorithm were used to assess associations with depression scores (PHQ-9 ≥5) adjusted for other important covariates. A mediation analysis framework was used to evaluate the mediating role of systemic inflammation assessed by the peripheral white blood cell count. Results: Among the 3427 adults included, 1735 (50.6%) were women, 2683 (78.3%) were younger than 65 years, and 744 (21.7%) were 65 years or older, with 839 (24.5%) having depressive symptoms. In terms of race and ethnicity, 570 participants (16.6%) were Mexican American, 679 (19.8%) were non-Hispanic Black, and 1314 (38.3%) were non-Hispanic White. We identified associations between 27 chemical compounds or metals in 6 of 10 categories of environmental toxicants and the prevalence of depressive symptoms, including the VOC metabolites N-acetyl-S-(2-hydroxy-3-butenyl)-l-cysteine (odds ratio [OR], 1.74 [95% CI, 1.38, 2.18]) and total nicotine equivalent-2 (OR, 1.42 [95% CI, 1.26-1.59]). Men and younger individuals appear more vulnerable to environmental toxicants than women and older individuals. Peripheral white blood cell count mediated 5% to 19% of the associations. Conclusions and Relevance: In this representative cross-sectional study of adults with environmental toxicant exposures, 6 categories of environmental toxicants were associated with depressive symptoms with mediation by systemic inflammation. This research provides insight into selecting environmental targets for mechanistic research into the causes of depression and facilitating efforts to reduce environmental exposures.

Using Parametric g-Computation for Time-to-Event Data and Distributed Lag Models to Identify Critical Exposure Windows for Preterm Birth: An Illustrative Example Using PM2.5 in a Retrospective Birth Cohort Based in Eastern Massachusetts (2011-2016).

BACKGROUND: Parametric g-computation is an attractive analytic framework to study the health effects of air pollution. Yet, the ability to explore biologically relevant exposure windows within this framework is underdeveloped. OBJECTIVES: We outline a novel framework for how to incorporate complex lag-responses using distributed lag models (DLMs) into parametric g-computation analyses for survival data. We call this approach "g-survival-DLM" and illustrate its use examining the association between PM2.5 during pregnancy and the risk of preterm birth (PTB). METHODS: We applied the g-survival-DLM approach to estimate the hypothetical static intervention of reducing average PM2.5 in each gestational week by 20% on the risk of PTB among 9,403 deliveries from Beth Israel Deaconess Medical Center, Boston, Massachusetts, 2011-2016. Daily PM2.5 was taken from a 1-km grid model and assigned to address at birth. Models were adjusted for sociodemographics, time trends, nitrogen dioxide, and temperature. To facilitate implementation, we provide a detailed description of the procedure and accompanying R syntax. RESULTS: There were 762 (8.1%) PTBs in this cohort. The gestational week-specific median PM2.5 concentration was relatively stable across pregnancy at ∼7µg/m3. We found that our hypothetical intervention strategy changed the cumulative risk of PTB at week 36 (i.e., the end of the preterm period) by -0.009 (95% confidence interval: -0.034, 0.007) in comparison with the scenario had we not intervened, which translates to about 86 fewer PTBs in this cohort. We also observed that the critical exposure window appeared to be weeks 5-20. DISCUSSION: We demonstrate that our g-survival-DLM approach produces easier-to-interpret, policy-relevant estimates (due to the g-computation); prevents immortal time bias (due to treating PTB as a time-to-event outcome); and allows for the exploration of critical exposure windows (due to the DLMs). In our illustrative example, we found that reducing fine particulate matter [particulate matter (PM) with aerodynamic diameter ≤2.5µm (PM2.5)] during gestational weeks 5-20 could potentially lower the risk of PTB. https://doi.org/10.1289/EHP13891.

Phthalate exposure and markers of biological aging: The mediating role of inflammation and moderating role of dietary nutrient intake.

Limited evidence has suggested a relationship between phthalate exposure and biological aging. This study investigated the association between phthalate exposure and biological aging, focusing on the mediating role of inflammation and the interaction with dietary nutrient intake. Data were analyzed from a nationwide cross-sectional survey comprising 12,994 participants aged 18 and above. Eight phthalate metabolites were detected in spot urine samples. Biological aging was assessed using the Klemera-Doubal method-biological age (KDM-BA) acceleration, phenotypic age (PA) acceleration, and homeostatic dysregulation (HD). The systemic immune-inflammation index (SII) evaluated systemic inflammation. The individual and combined associations between phthalate exposure and biological aging were assessed using linear regression, weighted quantile sum (WQS) regression, and quantile g-computation (qgcomp). The participants had a mean age of 47 years, with 50.7 % male and 44.8 % non-Hispanic white. Most phthalate metabolites were positively correlated with KDM-BA acceleration (ß = 0.306-0.584), PA acceleration (ß = 0.081-0.281), and HD (ß = 0.016-0.026). Subgroup analysis indicated that men, older individuals, and non-Hispanic whites are particularly sensitive populations. WQS regression and qgcomp analyses consistently indicated a positive association between mixed phthalate exposure and HD, highlighting MEHHP as the most significant contributing metabolite. Mediation analyses showed inflammation partially mediated the association between phthalate metabolites and biological aging. Significant interactions regarding biological aging were found between specific phthalate metabolites and dietary nutrients (carotenoids, vitamins A, B1, B2, B6, B12, niacin, and selenium) intake. These findings indicated that the association between phthalate exposure and biological aging was mediated by inflammation, with nutrient intake mitigating this effect.

Road traffic noise pollution and prevalence of ischemic heart disease: modelling potential association and abatement strategies in noise-exposed areas.

In many developing countries with surging vehicular traffic and inadequate traffic management, excessive road traffic noise exposure poses substantial health concerns, linked to increased stress, insomnia and other metabolic disorders. This study aims to assess the linkage between sociodemographic factors, traffic noise levels in residential areas and health effects using a cross-sectional study analyzing respondents' perceptions and reports. Noise levels were measured at 57 locations in Srinagar, India, using noise level meter. Sound PLAN software was employed to generate noise contour maps, enabling the visualization of noise monitoring locations and facilitating the assessment of noise levels along routes in proximity to residential areas. Correlation analysis showed a strong linear relationship between field-measured and modelled noise (r2 = 0.88). Further, a questionnaire-based survey was carried out near the sampling points to evaluate the association of ischemic heart disease with traffic noise. Residents exposed to noise levels (Lden > 60 dB(A)) were found to have a 2.24 times higher odds ratio. Compared to females, males reported a 16% higher prevalence of the disease. Multi-faceted policy strategies involving noise mapping initiatives, source noise standards, traffic flow urban mobility optimization, smart city initiatives and stringent litigatory measures could significantly reduce its detrimental impact on public health. Finally, this study envisions a region-specific strong regulatory framework for integrating noise pollution mitigation strategies into the public health action plans of developing nations.

Exposure to Air Pollution, Genetic Susceptibility, and Psoriasis Risk in the UK.

Importance: Psoriasis is a common autoinflammatory disease influenced by complex interactions between environmental and genetic factors. The influence of long-term air pollution exposure on psoriasis remains underexplored. Objective: To examine the association between long-term exposure to air pollution and psoriasis and the interaction between air pollution and genetic susceptibility for incident psoriasis. Design, Setting, and Participants: This prospective cohort study used data from the UK Biobank. The analysis sample included individuals who were psoriasis free at baseline and had available data on air pollution exposure. Genetic analyses were restricted to White participants. Data were analyzed between November 1 and December 10, 2023. Exposures: Exposure to nitrogen dioxide (NO2), nitrogen oxides (NOx), fine particulate matter with a diameter less than 2.5 µm (PM2.5), and particulate matter with a diameter less than 10 µm (PM10) and genetic susceptibility for psoriasis. Main Outcomes and Measures: To ascertain the association of long-term exposure to NO2, NOx, PM2.5, and PM10 with the risk of psoriasis, a Cox proportional hazards model with time-varying air pollution exposure was used. Cox models were also used to explore the potential interplay between air pollutant exposure and genetic susceptibility for the risk of psoriasis incidence. Results: A total of 474 055 individuals were included, with a mean (SD) age of 56.54 (8.09) years and 257 686 (54.36%) female participants. There were 9186 participants (1.94%) identified as Asian or Asian British, 7542 (1.59%) as Black or Black British, and 446 637 (94.22%) as White European. During a median (IQR) follow-up of 11.91 (11.21-12.59) years, 4031 incident psoriasis events were recorded. There was a positive association between the risk of psoriasis and air pollutant exposure. For every IQR increase in PM2.5, PM10, NO2, and NOx, the hazard ratios (HRs) were 1.41 (95% CI, 1.35-1.46), 1.47 (95% CI, 1.41-1.52), 1.28 (95% CI, 1.23-1.33), and 1.19 (95% CI, 1.14-1.24), respectively. When comparing individuals in the lowest exposure quartile (Q1) with those in the highest exposure quartile (Q4), the multivariate-adjusted HRs were 2.01 (95% CI, 1.83-2.20) for PM2.5, 2.21 (95% CI, 2.02-2.43) for PM10, 1.64 (95% CI, 1.49-1.80) for NO2, and 1.34 (95% CI, 1.22-1.47) for NOx. Moreover, significant interactions between air pollution and genetic predisposition for incident psoriasis were observed. In the subset of 446 637 White individuals, the findings indicated a substantial risk of psoriasis development in participants exposed to the highest quartile of air pollution levels concomitant with high genetic risk compared with those in the lowest quartile of air pollution levels with low genetic risk (PM2.5: HR, 4.11; 95% CI, 3.46-4.90; PM10: HR, 4.29; 95% CI, 3.61-5.08; NO2: HR, 2.95; 95% CI, 2.49-3.50; NOx: HR, 2.44; 95% CI, 2.08-2.87). Conclusions and Relevance: In this prospective cohort study of the association between air pollution and psoriasis, long-term exposure to air pollution was associated with increased psoriasis risk. There was an interaction between air pollution and genetic susceptibility on psoriasis risk.

Association of heavy metals exposure with lower blood pressure in the population aged 8-17 years: a cross-sectional study based on NHANES.

Background: The existing evidence regarding the joint effect of heavy metals on blood pressure (BP) in children and adolescents is insufficient. Furthermore, the impact of factors such as body weight, fish consumption, and age on their association remains unclear. Methods: The study utilized original data from the National Health and Nutrition Examination Survey, encompassing 2,224 children and adolescents with complete information on 12 urinary metals (barium, cadmium, cobalt, cesium, molybdenum, lead, antimony, thallium, tungsten, uranium, mercury and arsenic), BP, and core covariates. Various statistical methods, including weighted multiple logistic regression, linear regression, and Weighted Quantile Sum regression (WQS), were employed to evaluate the impact of mixed metal exposure on BP. Sensitivity analysis was conducted to confirm the primary analytical findings. Results: The findings revealed that children and adolescents with low-level exposure to lead (0.40 µg/L, 95%CI: 0.37, 0.42), mercury (0.38 µg/L, 95%CI: 0.35, 0.42) and molybdenum (73.66 µg/L, 95%CI: 70.65, 76.66) exhibited reduced systolic blood pressure (SBP) and diastolic blood pressure (DBP). Conversely, barium (2.39 µg/L, 95%CI: 2.25, 2.54) showed a positive association with increased SBP. A 25th percentile increase in the WQS index is significantly associated with a decrease in SBP of 0.67 mmHg (95%CI, -1.24, -0.10) and a decrease in DBP of 0.59 mmHg (95% CI, -1.06, -0.12), which remains statistically significant even after adjusting for weight. Furthermore, among individuals who consume fish, heavy metals have a more significant influence on SBP. A 25 percentile increase in the WQS index is significantly associated with a decrease of 3.30 mmHg (95% CI, -4.73, -1.87) in SBP, primarily attributed to mercury (27.61%), cadmium (27.49%), cesium (17.98%), thallium (8.49%). The study also identified a declining trend in SBP among children aged 10-17, whereas children aged 11-18 exhibited lower levels of systolic and diastolic blood pressure, along with a reduced risk of hypertension. Conclusion: Some heavy metals demonstrate an inverse association with the BP of children and adolescents, particularly notable in groups with fish consumption and older children and adolescents. Future studies are warranted to validate these findings and delve deeper into the interplay of heavy metals.

An analysis of exogenous harmful substance exposure as risk factors for COPD and hypertension co-morbidity using PSM.

Background: Some occupational and environmental exposures could increase the risk of chronic obstructive pulmonary disease (COPD) and hypertension in various work and living environments. However, the effect of exposure to multiple exogenous harmful substances on COPD and hypertension co-morbidities remains unclear. Methods: Participants were selected from eight hospitals in five provinces in China using a multistage cluster sampling procedure. Participants' demographic, exposure, and disease information were collected through questionnaires, spirometry, and blood pressure examinations. Demographic data were used as matching factors, and 1:1 matching between the exposed and non-exposed groups was performed by employing propensity score matching (PSM) to minimize the influence on the results. A one-way chi-squared analysis and multifactorial logistic regression were used to analyze the association between the exposure to exogenous harmful substances (metals and their compound dust, inorganic mineral dust, organic chemicals, and livestock by-products) and the co-morbidity of COPD and hypertension. Results: There were 6,610 eligible participants in the final analysis, of whom 2,045 (30.9%) were exposed to exogenous harmful substances. The prevalence of co-morbidities of COPD and hypertension (6.0%) in the exposure group was higher than their prevalence in the total population (4.6%). After PSM, exogenous harmful substance exposure was found to be a risk factor for the co-morbidity of COPD and hypertension [odds ratio (OR) = 1.347, 95% confidence interval (CI): 1.011-1.794], which was not statistically significant before PSM (OR = 1.094, 95% CI: 0.852-1.405). Meanwhile, the results of different outcomes showed that the association between hypertension and exogenous harmful substance exposure was not statistically significant (OR = 0.965, 95% CI: 0.846-1.101). Smoking (OR = 4.702, 95% CI: 3.321-6.656), history of a respiratory disease during childhood (OR = 2.830, 95% CI: 1.600-5.006), and history of respiratory symptoms (OR = 1.897, 95% CI: 1.331-2.704) were also identified as risk factors for the co-morbidity of COPD and hypertension. Conclusion: The distribution of exogenous harmful substance exposure varies in the population, and the prevalence of co-morbidities is generally higher in susceptible populations. Exposure to exogenous harmful substances was found to be a key risk factor after adjusting for demographic confounders.

Effects of socioeconomic status and regional inequality on the association between PM2.5 and its components and cardiometabolic multimorbidity: A multicenter population-based survey in eastern China.

BACKGROUND: Despite evidence linking fine particulate matter (PM2.5) to cardiometabolic multimorbidity (CMM), the impact of its components remains unclear. Socioeconomic status (SES) and regional disparities may confound their association. We aim to evaluate the associations between PM2.5 components and CMM and explore how socioeconomic status and regional disparities affect these relationships. METHODS: We recruited 108,941 participants aged 35-76 years from ten cities in eastern China. Individual exposure was assessed using Tracking Air Pollution in China (TAP) data, including PM2.5 and five components: ammonium (NH4+), black carbon (BC), nitrates (NO3-), organic matter (OM), and sulfates (SO42-). Generalized linear models and quantile g-computation models were employed to quantify the effects of PM2.5 components on CMM and to identify key components. Stratified analyses were performed to investigate the modifying effect of SES and regional disparities. RESULTS: For each increase in interquartile range (IQR), BC (odds ratio [OR] 1.37, 95 % CI 1.29-1.47), OM (1.38, 1.29-1.48), NH4+ (1.31, 1.21-1.40), NO3- (1.34, 1.25-1.44), and SO42- (1.28, 1.20-1.38) were positively associated with CMM. Joint exposure to five components was significantly positively associated with CMM (OR: 1.27, 95 % CI: 1.21-1.33), with SO42- having the highest estimated weight, followed by NO3- and BC. These associations were stronger for participants from low socio-economic status and poor regions. CONCLUSION: In summary, we found a stronger hazard effect of PM2.5 and its components on CMM, compared to those suffering from CMDs, particularly among participants with low socioeconomic status and in poor regions. SO42- may be a primary contributor to the association between PM2.5 components and CMM. These findings underscore the importance of prioritizing CMM and targeting SO42-related pollution sources in health policies, particularly amid China's aging population, reducing environmental health inequalities is critical.

Midlife Residential Greenness and Late-Life Cognitive Decline among Nurses' Health Study Participants.

BACKGROUND: Midlife residential exposure to greenspace may slow cognitive decline by increasing opportunities for physical activity and social connection, restoring attention, or reducing stress or adverse environmental exposures. However, prospective studies on the association between greenness and cognitive decline are sparse. OBJECTIVE: We investigated the prospective association between greenness at midlife and cognitive decline later in life. We explored effect measure modification by apolipoprotein E (APOE)-ɛ4 carrier status, neighborhood socioeconomic status (NSES), and rural/urban regions. METHODS: The Nurses' Health Study (N=121,700) started in 1976 with married female nurses, 30-55 years of age, located across 11 US states. We examined 16,962 nurses who were enrolled in a substudy starting in 1995-2001 (mean age=74y) through 2008. We assessed average summer residential greenness in a 270-m buffer using Landsat Normalized Difference Vegetation Index data from 1986-1994. Starting in 1995-2001, participants underwent up to four repeated measures of five cognitive tests. A global composite score was calculated as the average of all z-scores for each task to evaluate overall cognition. We used linear mixed models to evaluate the association of average greenness exposure at midlife with cognitive decline in later life, adjusted for age, education, NSES, and depression. RESULTS: In adjusted models, higher midlife greenness exposure [per interquartile range (IQR): 0.18] was associated with a 0.004-unit (95% CI: 0.001, 0.006) slower annual rate of cognitive decline. For comparison, we found that 1 year of age is related to a -0.006 mean annual difference for global cognition in the full sample; thus, higher midlife greenness appeared equivalent to slowing cognitive decline by ∼8 months. In analysis exploring gene-environment interactions, we found that among APOE-ɛ4 carriers, an IQR increase in greenness was associated with a rate of decline that was slower by 0.01 units of global composite score (95% CI: 0.0004, 0.02). This association was attenuated among APOE-ɛ4 noncarriers. We did not observe associations between greenness and baseline or annual rate of cognitive decline of verbal memory. DISCUSSION: Higher midlife greenness exposure is associated with slower cognitive decline later in life. Future research is necessary to confirm these findings. https://doi.org/10.1289/EHP13588.

Beyond lung cancer: air pollution and bladder, breast and prostate cancer incidence.

BACKGROUND: The carcinogenicity of air pollution and its impact on the risk of lung cancer is well known; however, there are still knowledge gaps and mixed results for other sites of cancer. METHODS: The current study aimed to evaluate the associations between ambient air pollution [fine particulate matter (PM2.5) and nitrogen oxides (NOx)] and cancer incidence. Exposure assessment was based on historical addresses of >900 000 participants. Cancer incidence included primary cancer cases diagnosed from 2007 to 2015 (n = 30 979). Cox regression was used to evaluate the associations between ambient air pollution and cancer incidence [hazard ratio (HR), 95% CI]. RESULTS: In the single-pollutant models, an increase of one interquartile range (IQR) (2.11 µg/m3) of PM2.5 was associated with an increased risk of all cancer sites (HR = 1.51, 95% CI: 1.47-1.54), lung cancer (HR = 1.73, 95% CI: 1.60-1.87), bladder cancer (HR = 1.50, 95% CI: 1.37-1.65), breast cancer (HR = 1.50, 95% CI: 1.42-1.58) and prostate cancer (HR = 1.41, 95% CI: 1.31-1.52). In the single-pollutant and the co-pollutant models, the estimates for PM2.5 were stronger compared with NOx for all the investigated cancer sites. CONCLUSIONS: Our findings confirm the carcinogenicity of ambient air pollution on lung cancer and provide additional evidence for bladder, breast and prostate cancers. Further studies are needed to confirm our observation regarding prostate cancer. However, the need for more research should not be a barrier to implementing policies to limit the population's exposure to air pollution.

[Occurrence and Risk Assessment of N-nitrosamines and Their Precursors in Qingjiang River Basin].

N-nitrosamines are a type of nitrogen-containing organic pollutant with high carcinogenicity and mutagenicity. In the main drinking water sources of small and medium-sized towns in China, the contamination levels of N-nitrosamines remain unclear. In addition, there is still lack of research on the concentration of N-nitrosamines and their precursors in tributary rivers. In this study, eight N-nitrosamines and their formation potentials （FPs） were investigated in the Qingjiang River, which is a primary tributary of the Yangtze River. The sewage discharge sites were also monitored, and the environmental influencing factors, carcinogenic and ecological risks caused by N-nitrosamines, and their precursors were evaluated. The results showed that six N-nitrosamines were detected in water samples of the Qingjiang River, among which NDMA [（10 ±15） ng·L-1], NDEA [（9.3 ±9.3） ng·L-1], and NDBA [（14 ±7.8） ng·L-1] were the dominant N-nitrosamines, whereas seven N-nitrosamines were detected in chloraminated water samples, among which NDMA-FP [（46 ±21） ng·L-1], NDEA-FP [（26 ±8.3） ng·L-1], and NDBA-FP [（22 ±13） ng·L-1] were the dominant N-nitrosamine FPs. The concentrations of N-nitrosamines in the middle reaches of the Qingjiang River were higher than those in the upper and lower reaches. Furthermore, the concentrations of N-nitrosamines in the sample sites of sewage discharge and tributaries were significantly higher than those in other sampling sites. The monitoring results at the direct sewage discharge points indicated that the main source of N-nitrosamines in river water was the sewage carrying N-nitrosamines and their precursors. In addition, the concentrations of the three dominant N-nitrosamines including NDMA, NDBA, and NDEA were positively correlated with each other, mainly because of their similar sewage sources. The average carcinogenic risk to residents due to N-nitrosamine in drinking water sources was 2.4×10-5, indicating a potential carcinogenic risk. Moreover, due to the high concentrations of N-nitrosamine formation potentials in the Qingjiang River, the carcinogenic risk of drinking water may be even higher. The ecological risk assessment showed that the ecological risk quotient values of N-nitrosamines in the Qingjiang River watershed were lower than 0.002, which was negligible.

Assessing the spatiotemporal evolution and socioeconomic determinants of PM2.5-related premature deaths in China from 2000 to 2021.

China's swift socioeconomic development has led to extremely severe ambient PM2.5 levels, the associated negative health outcomes of which include premature death. However, a comprehensive explanation of the socioeconomic mechanism contributing to PM2.5-related premature deaths has not yet to be fully elucidated through long-term spatial panel data. Here, we employed a global exposure mortality model (GEMM) and the system generalized method of moments (Sys-GMM) to examine the primary determinants contributing to premature deaths in Chinese provinces from 2000 to 2021. We found that in the research period, premature deaths in China increased by 46 %, reaching 1.87 million, a figure that decreased somewhat after the COVID-19 outbreak. 62 thousand premature deaths were avoided in 2020 and 2021 compared to 2019, primarily due to the decline in PM2.5 concentrations. Premature deaths have increased across all provinces, particularly in North China, and a discernible spatial agglomeration effect was observed, highlighting effects on nearby provinces. The findings also underscored the significance of determinants such as urbanization, import and export trade, and energy consumption in exacerbating premature deaths, while energy intensity exerted a mitigating influence. Importantly, a U-shaped relationship between premature deaths and economic development was unveiled for the first time, implying the need for vigilance regarding potential health impact deterioration and the implementation of countermeasures as the per capita GDP increases in China. Our findings deserve attention from policymakers as they shed fresh insights into atmospheric control and Health China action.

Residential air pollution, greenspace, and adverse mental health outcomes in the U.S. Gulf Long-term Follow-up Study.

Air pollution and greenness are environmental determinants of mental health, though existing evidence typically considers each exposure in isolation. We evaluated relationships between co-occurring air pollution and greenspace levels and depression and anxiety. We estimated cross-sectional associations among 9015 Gulf Long-term Follow-up Study participants living in the southeastern U.S. who completed the Patient Health Questionnaire-9 (depression: score ≥ 10) and Generalized Anxiety Disorder Questionnaire-7 (anxiety: score ≥ 10). Participant residential addresses were linked to annual average concentrations of particulate matter (1 km PM2.5) and nitrogen dioxide (1 km NO2), as well as satellite-based greenness (2 km Enhanced Vegetation Index (EVI)). We used adjusted log-binomial regression to estimate prevalence ratios (PR) and 95 % confidence intervals (CI) for associations between exposures (quartiles) and depression and anxiety. In mutually adjusted models (simultaneously modeling PM2.5, NO2, and EVI), the highest quartile of PM2.5 was associated with increased prevalence of depression (PR = 1.17, 95 % CI: 1.06-1.29), whereas the highest quartile of greenness was inversely associated with depression (PR = 0.89, 95 % CI: 0.80-0.99). Joint exposure to greenness mitigated the impact of PM2.5 on depression (PRPM only = 1.20, 95 % CI: 1.06-1.36; PRPM+green = 0.98, 95 % CI: 0.83-1.16) and anxiety (PRPM only = 1.10, 95 % CI: 1.00-1.22; PRPM+green = 0.95, 95 % CI: 0.83-1.09) overall and in subgroup analyses. Observed associations were stronger in urbanized areas and among nonwhite participants, and varied by neighborhood deprivation. NO2 exposure was not independently associated with depression or anxiety in this population. Relationships between PM2.5, greenness, and depression were strongest in the presence of characteristics that are highly correlated with lower socioeconomic status, underscoring the need to consider mental health as an environmental justice issue.

Childhood and adolescent residential and farm pesticide exposures and inflammatory bowel disease incidence in a U.S. cohort of women.

BACKGROUND AND AIMS: There are few known risk factors for inflammatory bowel disease (IBD), an autoimmune disease characterized by chronic intestinal inflammation. Use of specific pesticides has been associated with higher incidence of IBD among pesticide applicators and their spouses, but no study has examined pesticide exposure in early life, a period where the human immune system undergoes rapid changes. We evaluated pesticide use during childhood and adolescence and incidence of IBD among US women enrolled in the Sister Study. METHODS: Incident IBD diagnoses between enrollment (2003-2009) and 2021 were identified and validated with medication use and colectomy/colostomy surgery. We estimated hazard ratios (HR) and 95 % confidence intervals (CI) for the relationship of childhood/adolescent residential and farm pesticide exposures with IBD incidence using Cox models, accounting for age, race and ethnicity, education, smoking, and birth year. RESULTS: We identified 277 incident IBD cases among 48,382 eligible participants. IBD hazard was elevated among those whose childhood residence was regularly treated with pesticides, especially among those who ever personally applied pesticides (HR = 1.39, 95%CI: 0.65, 2.99). We observed a positive association between IBD and exposure to broadcast pesticide sprays before DDT was banned (>6 times vs. never HR = 1.56, 95%CI: 1.06, 2.31). Among participants who lived on a farm during childhood/adolescence for ≥1 year (N = 9162), IBD hazards were higher among those who were in crop fields during pesticide application (HR = 2.06, 95%CI: 0.94, 4.51) and who ever personally applied pesticides on crops (HR = 1.85, 95%CI: 0.81, 4.18) or livestock (HR = 2.58, 95%CI: 1.14, 5.83). CONCLUSION: Early-life pesticide exposure may be a novel risk factor for IBD. Practices that reduce pesticide exposure during early life may help reduce the burden of this disease.

The Association between Exposure to Fine Particulate Matter and MRI-Assessed Locus Coeruleus Integrity in the Vietnam Era Twin Study of Aging (VETSA).

BACKGROUND: Increased exposure to ambient air pollution, especially fine particulate matter ≤2.5µm (PM2.5) is associated with poorer brain health and increased risk for Alzheimer's disease (AD) and related dementias. The locus coeruleus (LC), located in the brainstem, is one of the earliest regions affected by tau pathology seen in AD. Its diffuse projections throughout the brain include afferents to olfactory areas that are hypothesized conduits of cerebral particle deposition. Additionally, extensive contact of the LC with the cerebrovascular system may present an additional route of exposure to environmental toxicants. OBJECTIVE: Our aim was to investigate if exposure to PM2.5 was associated with LC integrity in a nationwide sample of men in early old age, potentially representing one pathway through which air pollution can contribute to increased risk for AD dementia. METHODS: We examined the relationship between PM2.5 and in vivo magnetic resonance imaging (MRI) estimates of LC structural integrity indexed by contrast to noise ratio (LCCNR) in 381 men [mean age=67.3; standard deviation (SD)=2.6] from the Vietnam Era Twin Study of Aging (VETSA). Exposure to PM2.5 was taken as a 3-year average over the most recent period for which data were available (average of 5.6 years prior to the MRI scan). We focused on LCCNR in the rostral-middle portion of LC due to its stronger associations with aging and AD than the caudal LC. Associations between PM2.5 exposures and LC integrity were tested using linear mixed effects models adjusted for age, scanner, education, household income, and interval between exposure and MRI. A co-twin control analysis was also performed to investigate whether associations remained after controlling for genetic confounding and rearing environment. RESULTS: Multiple linear regressions revealed a significant association between PM2.5 and rostral-middle LCCNR (ß=-0.16; p=0.02), whereby higher exposure to PM2.5 was associated with lower LCCNR. A co-twin control analysis found that, within monozygotic pairs, individuals with higher PM2.5 exposure showed lower LCCNR (ß=-0.11; p=0.02), indicating associations were not driven by genetic or shared environmental confounds. There were no associations between PM2.5 and caudal LCCNR or hippocampal volume, suggesting a degree of specificity to the rostral-middle portion of the LC. DISCUSSION: Given previous findings that loss of LC integrity is associated with increased accumulation of AD-related amyloid and tau pathology, impacts on LC integrity may represent a potential pathway through which exposure to air pollution increases AD risk. https://doi.org/10.1289/EHP14344.

Association between Personal Abiotic Airborne Exposures and Body Composition Changes among Healthy Adults (60-69 Years Old): A Combined Exposome-Wide and Lipidome Mediation Approach from the China BAPE Study.

BACKGROUND: Evidence suggested that abiotic airborne exposures may be associated with changes in body composition. However, more evidence is needed to identify key pollutants linked to adverse health effects and their underlying biomolecular mechanisms, particularly in sensitive older adults. OBJECTIVES: Our research aimed to systematically assess the relationship between abiotic airborne exposures and changes in body composition among healthy older adults, as well as the potential mediating mechanisms through the serum lipidome. METHODS: From September 2018 to January 2019, we conducted a monthly survey among 76 healthy adults (60-69 years old) in the China Biomarkers of Air Pollutant Exposure (BAPE) study, measuring their personal exposures to 632 abiotic airborne pollutions using MicroPEM and the Fresh Air wristband, 18 body composition indicators from the InBody 770 device, and lipidomics from venous blood samples. We used an exposome-wide association study (ExWAS) and deletion/substitution/addition (DSA) model to unravel complex associations between exposure to contaminant mixtures and body composition, a Bayesian kernel machine regression (BKMR) model to assess the overall effect of key exposures on body composition, and mediation analysis to identify lipid intermediators. RESULTS: The ExWAS and DSA model identified that 2,4,5-T methyl ester (2,4,5-TME), 9,10-Anthracenedione (ATQ), 4b,8-dimethyl-2-isopropylphenanthrene, and 4b,5,6,7,8,8a,9,10-octahydro-(DMIP) were associated with increased body fat mass (BFM), fat mass indicators (FMI), percent body fat (PBF), and visceral fat area (VFA) in healthy older adults [Bonferroni-Hochberg false discovery rate (FDRBH)<0.05]. The BKMR model demonstrated a positive correlation between contaminants (anthracene, ATQ, copaene, di-epi-α-cedrene, and DMIP) with VFA. Mediation analysis revealed that phosphatidylcholine [PC, PC(16:1e/18:1), PC(16:2e/18:0)] and sphingolipid [SM, SM(d18:2/24:1)] mediated a significant portion, ranging from 12.27% to 26.03% (p-value <0.05), of the observed increase in VFA. DISCUSSION: Based on the evidence from multiple model results, ATQ and DMIP were statistically significantly associated with the increased VFA levels of healthy older adults, potentially regulated through lipid intermediators. These findings may have important implications for identifying potentially harmful environmental chemicals and developing targeted strategies for the control and prevention of chronic diseases in the future, particularly as the global population is rapidly aging. https://doi.org/10.1289/EHP13865.

A Snapshot of Lead in Consumer Products Across Four US Jurisdictions.

BACKGROUND: Following the removal of lead from gasoline, paint and pipes were thought to be the main sources of lead exposure in the United States. However, consumer products, such as certain spices, ceramic and metal cookware, traditional health remedies, and cultural powders, are increasingly recognized as important sources of lead exposure across the United States. OBJECTIVE: This paper reviews data from four US jurisdictions that conduct in-home investigations for children with elevated blood lead levels (BLLs) to examine the prevalence of lead exposures associated with consumer products, in comparison with housing-related sources. METHODS: Authors reviewed investigation data (2010-2021) provided by California, Oregon, New York City, and King County, Washington, and compared the extent of lead exposures associated with housing-related vs. consumer products-related sources. DISCUSSION: The proportion of investigations identifying consumer products-related sources of lead exposure varied by jurisdiction (range: 15%-38%). A review of US CDC and US FDA alerts and New York City data indicates that these types of lead-containing products are often sourced internationally, with many hand carried into the United States during travel. Based on surveillance data, we believe that US immigrant and refugee communities are at an increased risk for lead exposures associated with these products. To engage health authorities, there is a need for evidentiary data. We recommend implementing a national product surveillance database systematically tracking data on consumer products tested by childhood lead poisoning prevention programs. The data repository should be centralized and accessible to all global stakeholders, including researchers and governmental and nongovernmental agencies, who can use these data to inform investigations. Effectively identifying and addressing the availability of lead-containing consumer products at their source can focus resources on primary prevention, reducing lead exposures for users abroad and in the United States. https://doi.org/10.1289/EHP14336.