Associations of polycyclic aromatic hydrocarbons exposure with serum uric acid and hyperuricemia in US adults: The role of systemic inflammation.

The associations of polycyclic aromatic hydrocarbon (PAH) exposure with serum uric acid (SUA) or hyperuricemia have been rarely assessed. We aimed to investigate the relationships between urinary PAH metabolites and SUA or hyperuricemia among US adults and to explore the mediating role of systemic inflammation in the associations. A total of 10,307 US adults were conducted to assess the associations of seven urinary hydroxy­PAH with SUA and hyperuricemia and evaluate the role of C-reactive protein (CRP), a biomarker of systemic inflammation, in such associations. Results showed that each 1-unit increase in ln-transformed 2-hydroxynaphthalene (2-OHNa), 1-hydroxyphenanthrene (1-OHPh), 2&3-hydroxyphenanthrene (2&3-OHPh) and total hydroxyphenanthrene (ΣOHPh) was associated with a 1.68 (95% confidence interval (CI): 0.19 to 3.17), 2.46 (0.78 to 4.13), 3.34 (1.59 to 5.09), and 2.99 (1.23 to 4.75) µmol/L increase in SUA, and a 8% (odds ratio (OR): 1.08, 1.02 to 1.15), 9% (OR: 1.09, 1.02 to 1.18), 13% (OR: 1.13, 1.05 to 1.22), and 12% (OR: 1.12, 95% CI: 1.03, 1.21) increase in hyperuricemia, respectively. Co-exposure of seven PAHs was positively associated with SUA and hyperuricemia, with 2&3-OHPh showing the highest weight (components weights: 0.83 and 0.78, respectively). The CRP mediated 11.47% and 10.44% of the associations of ΣOHPh and 2&3-OHPh with SUA and mediated 8.60% and 8.62% in associations of ΣOHPh and 2&3-OHPh with hyperuricemia, respectively. In conclusion, internal levels of PAH metabolites were associated with elevated SUA levels and the increased risk of hyperuricemia among US adults, and CRP played a mediating role in the associations.

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.

Exposure of individuals aged 18-44 years to personal care products in Beijing, China: Exposure profiles, possible influencing factors, and risk assessment.

Personal care products (PCPs) are a class of emerging pollutants that have attracted public concern owing to their harmful effects on humans and the environment. Biomonitoring data is valuable for insight the levels of PCPs in the human body and can be crucial for identifying potential health hazards. To gain a better understanding of timely exposure profiles and health risk of reproductive-age population to PCPs, we determined six parabens, six benzophenone-type ultraviolet filters, and three disinfectants in 256 urine samples collected from young adults aged 18-44 years in Beijing, China. The urinary levels of benzophenone-3 (BP-3) and 4-hydroxybenzophenone (4-OHBP) were significantly higher in summer compared to winter, suggesting these compounds have different seasonal usage patterns. Moreover, the total concentration of 15 PCPs in female was 430 ng/mL, approximately two times higher than that in male. P­chloro-m-xylenol (PCMX), as a new type of antibacterial agent, has the greatest level among all target analytes, indicating the increasingly use of this antibacterial alternative recently. Five potential influencing factors that lead to the elevated exposure level of PCPs were identified. Over 19% of the target population had a high hazard index value (greater than 1) which was attributed to exposure to propyl paraben (PrP), benzophenone-1 (BP-1), BP-3 and PCMX, indicating that PCPs may pose a relatively high exposure risk at environmental levels that should be a cause for concern.

Machine learning approaches to identify the link between heavy metal exposure and ischemic stroke using the US NHANES data from 2003 to 2018.

Purpose: There is limited understanding of the link between exposure to heavy metals and ischemic stroke (IS). This research aimed to develop efficient and interpretable machine learning (ML) models to associate the relationship between exposure to heavy metals and IS. Methods: The data of this research were obtained from the National Health and Nutrition Examination Survey (US NHANES, 2003-2018) database. Seven ML models were used to identify IS caused by exposure to heavy metals. To assess the strength of the models, we employed 10-fold cross-validation, the area under the curve (AUC), F1 scores, Brier scores, Matthews correlation coefficient (MCC), precision-recall (PR) curves, and decision curve analysis (DCA) curves. Following these tests, the best-performing model was selected. Finally, the DALEX package was used for feature explanation and decision-making visualization. Results: A total of 15,575 participants were involved in this study. The best-performing ML models, which included logistic regression (LR) (AUC: 0.796) and XGBoost (AUC: 0.789), were selected. The DALEX package revealed that age, total mercury in blood, poverty-to-income ratio (PIR), and cadmium were the most significant contributors to IS in the logistic regression and XGBoost models. Conclusion: The logistic regression and XGBoost models showed high efficiency, accuracy, and robustness in identifying associations between heavy metal exposure and IS in NHANES 2003-2018 participants.

Air Pollution and Parkinson Disease in a Population-Based Study.

Importance: The role of air pollution in risk and progression of Parkinson disease (PD) is unclear. Objective: To assess whether air pollution is associated with increased risk of PD and clinical characteristics of PD. Design, Setting, and Participants: This population-based case-control study included patients with PD and matched controls from the Rochester Epidemiology Project from 1998 to 2015. Data were analyzed from January to June 2024. Exposures: Mean annual exposure to particulate matter with a diameter of 2.5 µm or less (PM2.5) from 1998 to 2015 and mean annual exposure to nitrogen dioxide (NO2) from 2000 to 2014. Main Outcomes and Measures: Outcomes of interest were PD risk, all-cause mortality, presence of tremor-predominant vs akinetic rigid PD, and development of dyskinesia. Models were adjusted for age, sex, race and ethnicity, year of index, and urban vs rural residence. Results: A total of 346 patients with PD (median [IQR] age 72 [65-80] years; 216 [62.4%] male) were identified and matched on age and sex with 4813 controls (median [IQR] age, 72 [65-79] years, 2946 [61.2%] male). Greater PM2.5 exposure was associated with increased PD risk, and this risk was greatest after restricting to populations within metropolitan cores (odds ratio [OR], 1.23; 95% CI, 1.11-1.35) for the top quintile of PM2.5 exposure compared with the bottom quintile. Greater NO2 exposure was also associated with increased PD risk when comparing the top quintile with the bottom quintile (OR, 1.13; 95% CI, 1.07-1.19). Air pollution was associated with a 36% increased risk of akinetic rigid presentation (OR per each 1-µg/m3 increase in PM2.5, 1.36; 95% CI, 1.02-1.80). In analyses among patients with PD only, higher PM2.5 exposure was associated with greater risk for developing dyskinesia (HR per 1-µg/m3 increase in PM2.5, 1.42; 95% CI, 1.17-1.73), as was increased NO2 exposure (HR per 1 µg/m3 increase in NO2, 1.13; 95% CI, 1.06-1.19). There was no association between PM2.5 and all-cause mortality among patients with PD. Conclusions and Relevance: In this case-control study of air pollution and PD, higher levels of PM2.5 and NO2 exposure were associated with increased risk of PD; also, higher levels of PM2.5 exposure were associated with increased risk of developing akinetic rigid PD and dyskinesia compared with patients with PD exposed to lower levels. These findings suggest that reducing air pollution may reduce risk of PD, modify the PD phenotype, and reduce risk of dyskinesia.

PFAS Levels, Early Life Factors, and Mammographic Breast Density in Premenopausal Women.

BACKGROUND: Mammographic breast density (MBD) is a strong risk factor and an intermediate phenotype for breast cancer, yet there are limited studies on how environmental pollutants are associated with MBD. OBJECTIVE: We investigated associations of perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), and perfluorohexane sulfonate (PFHxS) levels with measures of MBD and evaluated if early life factors modified any associations. METHODS: Metabolon performed metabolomics analysis using ultrahigh-performance liquid chromatography/tandem accurate mass spectrometry in fasting blood from 705 premenopausal women completing their annual screening mammogram in St. Louis, Missouri. We calculated least square means (LSM) of mammographic volumetric percent density (VPD), dense volume (DV), and nondense volume (NDV) by quartiles (Q) of PFOS, PFOA, and PFHxS from multivariable linear regression modeling overall and stratified by recruitment period, race, age at menarche, and body shape at age 10. Models were adjusted for age, age at menarche, body fat percentage, race, family history of breast cancer, oral contraceptive use, alcohol consumption, parity/age at first birth, and body shape at age 10. RESULTS: PFOS, PFOA, and PFHxS were not significantly associated with VPD or NDV. PFHxS was significantly positively associated with DV (Q1=67.64 cm3, Q2=69.91 cm3, Q3=69.06 cm3, Q4=75.79 cm3; p-trend=0.03). PFOS was positively associated with DV (Q1=65.45 cm3, Q2=70.74 cm3, Q3=73.31 cm3, Q4=73.52 cm3; p-trend=0.06) with DV being 8.1%, 12%, and 12.3% higher in Q2, Q3, and Q4 compared to Q1. Among women who were underweight/normal weight at age 10, PFOS was positively associated with VPD (Q1=9.02%, Q2=9.11%, Q3=9.48%, Q4=9.92%; p-trend=0.04) while there was an inverse association among women who were overweight/obese at age 10 (Q1=7.46%, Q2=6.94%, Q3=6.78%, Q4=5.47%; p-trend=0.005) (p-interaction=0.04). DISCUSSION: We report novel associations of PFHxS and PFOS with DV in premenopausal women. PFOS, PFOA, and PFHxS were not associated with VPD and NDV. In addition, body shape at age 10 may modify the associations of PFOS with MBD. Further studies are needed to validate our findings and to evaluate the associations of other per- and polyfluoroalkyl substances (PFAS), as well as mixtures of PFAS, with MBD. https://doi.org/10.1289/EHP14065.

Widespread exposure to anticoagulant rodenticides among common urban mesopredators in Chicago.

Anticoagulant rodenticides (ARs) are currently the most common method to control rats in cities, but these compounds also cause morbidity and mortality in non-target wildlife. Little attention has been focused on AR exposure among mesopredators despite their ecological role as scavengers and prey for larger carnivores, thus serving as an important bridge in the biomagnification of rodenticides in food webs. In this study, we sampled liver tissue from raccoons (Procyon lotor; n = 37), skunks (Mephitis mephitis; n = 15), and Virginia opossums (Didelphis virginiana; n = 45) euthanized by pest professionals and brown rats (Rattus norvegicus; n = 101) trapped in alleys in Chicago, USA to evaluate how often these species are exposed to ARs. We tested whether mesopredators had a higher prevalence of ARs and to more AR compounds compared to rats and calculated biomagnification factors (mean concentration in mesopredators/rats) as indicators of biomagnification. Of 93 sampled mesopredators, 100 % were exposed to at least one AR compound, mainly brodifacoum (≥80 %), and 79 % were exposed to multiple AR compounds. We also documented teal stomach contents consistent with the consumption of rat bait and altricial young tested positive to the same AR as their mother, suggesting mammary transfer. Of the 101 rats, 74 % tested positive to at least one AR compound and 32 % were exposed to multiple AR compounds. All mesopredator species had biomagnification factors exceeding 1.00 for brodifacoum (6.57-29.07) and bromadiolone (1.08-4.31). Our results suggest widespread exposure to ARs among urban mesopredators and biomagnification of ARs in mesopredators compared to rats. Policies that limit AR availability to non-target species, such as restricting the sale and use of ARs to licensed professionals in indoor settings, education on alternatives, and more emphasis on waste management may reduce health risks for urban wildlife and people in cities around the world.

Distribution, bioaccumulation and human exposure risk of bisphenol analogues, bisphenol A diglycidyl ether and its derivatives in the Dongjiang River basin, south China.

Bisphenols, bisphenol A diglycidyl ether (BADGE), and bisphenol F diglycidyl ether (BFDGE) are commonly used as raw materials or additives in the production of several industrial and consumer products. However, information regarding the occurrence and distribution of these industrial chemicals in freshwater ecosystem is limited. In this study, four bisphenols, six BADGEs, and three BFDGEs were determined in abiotic and biotic samples collected from the Dongjiang River basin in southern China. Among the four bisphenols, BPA was widely present in all samples analyzed including surface water (median: 1.81 ng/L), sediment (3.1 ng/g dw), aquatic plants (3.69 ng/g dw), algae (7.57 ng/g dw), zooplankton (6.17 ng/g dw), and fish muscle (5.28 ng/g dw). Among the nine BADGEs and BFDGEs analyzed, BADGE, BADGE•H2O, BADGE·HCl·H2O and BADGE•2H2O was found in all sample types. Although the median concentration of BADGE•2H2O in surface water was below LOQ, this compound was found at median concentrations of 2.61, 3.59, 1.03, 1.69, and 49.8 ng/g dw in sediment, plants, algae, zooplankton, and fish muscle, respectively. Significant positive linear correlations were found among logarithmic transformed concentrations of BPA, BADGE, BADGE•H2O, BADGE•HCl•H2O, and BADGE•2H2O in sediment. The bioconcentration factor (logBCF) values of BADGE, BADGE•H2O, BADGE•HCl, BADGE•HCl•H2O, BADGE•2H2O, and BADGE•2HCl in fish, plants, algae, and zooplankton were > 3.3 L/kg (wet weight), indicating that these chemicals possess moderate bioaccumulation potential. The estimated daily total intake of bisphenols and BADGEs through fish consumption was 75.1 ng/kg bw/day for urban adult residents. The study provides baseline information on the occurrence of bisphenols, BADGEs, and BFDGEs in a freshwater ecosystem.

Serum arsenic augments gallstone risk in Henan rural cohort with multiple metal exposure.

BACKGROUND: People are exposed to metals in various ways during their daily lives. However, the association between metal exposure and gallstones remains unclear. OBJECTIVES: To investigate the relationship between serum elemental concentrations and the risk of gallstones. METHODS: Participants (n = 4204) were drawn from the Henan Rural Cohort. Gallstone diagnosis was based on abdominal ultrasound reports during follow-up. Baseline serum elemental concentrations were measured using inductively coupled plasma mass spectrometry. The relationship between serum elemental levels and gallstones was evaluated using robust Poisson regression, restricted cubic spline (RCS), quantile g-computation (Qgcomp), grouped weighted quantile sum (GWQS) and Bayesian kernel machine regression (BKMR). RESULTS: 121 individuals were diagnosed with gallstone (incidence rate of 2.88 %). In robust Poisson regression, after adjusting for confounding factors, the highest quartile of arsenic concentration compared to the lowest quartile had a 1.90 times higher relative risk (RR) [95 % confidence interval (CI): 1.05, 3.44]. Conversely, the highest quartile of zinc concentration compared to the lowest quartile had a 0.50 times lower RR (95 % CI: 0.28, 0.89). RCS showed an approximately "S"-shaped nonlinear relationship between serum arsenic levels and gallstones, with increasing arsenic concentration leading to a higher risk of gallstones; however, the risk plateaued when arsenic concentration exceeded 0.62 µg/L. Both the Qgcomp and GWQS indicated that arsenic plays a significant role in increasing the risk of gallstones, whereas zinc plays a significant role in reducing the risk of gallstones. BKMR showed that raising arsenic exposure from the 25th to the 75th percentile increased the risk of gallstones, while raising serum zinc concentration reduced it. CONCLUSIONS: Higher serum arsenic concentration increases the risk of gallstones, whereas higher zinc concentration may reduce the risk. Effective prevention of gallstones may require further reduction of arsenic exposure and appropriate increases in zinc intake.

Assessing personal PM2.5 exposure using a novel neck-mounted monitoring device in rural Rwanda.

There is growing global concern regarding the detrimental health impacts of PM2.5 emissions from traditional stoves that utilize polluting fuels. Conventional methods for estimating daily personal PM2.5 exposure involve personal air samplers and measuring devices placed in a waist pouch, but these instruments are cumbersome and inconvenient. To address this issue, we developed a novel neck-mounted PM2.5 monitoring device (Pocket PM2.5 Logger) that is compact, lightweight, and can operate continuously for 1 week without recharging. Twelve participants who utilized charcoal, firewood, or propane gas for cooking in rural regions of Rwanda wore the Pocket PM2.5 Logger continuously for 1 week, and time-series variations in personal PM2.5 exposure were recorded at 5-min intervals. Individual daily exposure concentrations during cooking differed significantly among users of the different fuel types, and PM2.5 exposure was at least 2.6 and 3.4 times higher for charcoal and firewood users, respectively, than for propane gas users. Therefore, switching from biomass fuels to propane gas would reduce daily individual exposure by at least one-third. An analysis of cooking times showed that the median cooking time per meal was 30 min; however, half the participants cooked for 1.5 h per meal, and one-third cooked for over 4.5 h per meal. Reducing these extremely long cooking times would reduce exposure with all fuel types. The Pocket PM2.5 Logger facilitates the comprehensive assessment of personal PM2.5 exposure dynamics and is beneficial for the development of intervention strategies targeting household air pollution.

Assessing Self-Rated Physical Health Scores Following Repeat Exposure to Anthropogenic and Natural Hazards in Houston, TX.

BACKGROUND: Research connects health outcomes to hazard exposures but often neglects the nature of the exposure or repeated events. METHODS: We undertook a cross-sectional study (N = 1,094) from a representative sample in the Houston Metropolitan Statistical Area (HMSA). Respondents were recruited using Qualtrics panels, targeting individuals reflecting the population of the HMSA. Physical composite scores (PCS) were calculated using the SF-12v2. RESULTS: Among the hazards (hurricanes, flooding, tornadoes, chemical spills, industrial fires), only chemical spills showed a dose-response: physical health scores declined significantly with repeated exposures. This decline persisted after multiple linear regression. Covariates including sex, race, age, education, and chemical exposure affected PCS, but chemical spill exposure remained the most significant, negatively affecting PCS even after adjusting for other factors (coef =-2.24, 95% CI, -3.33 to -1.15). CONCLUSION: Grasping the effects of hazards, especially repeated ones, can guide emergency management in mitigation, recovery, and preparedness efforts.

The Effect of Long-Term Particulate Matter Exposure on Respiratory Mortality: Cohort Study in China.

Background: Particulate matter (PM), which affects respiratory health, has been well documented; however, substantial evidence from large cohorts is still limited, particularly in highly polluted countries and for PM1. Objective: Our objective was to examine the potential causal links between long-term exposure to PMs (PM2.5, PM10, and more importantly, PM1) and respiratory mortality. Methods: A total of 580,757 participants from the Guangzhou area, China, were recruited from 2009 to 2015 and followed up through 2020. The annual average concentrations of PMs at a 1-km spatial resolution around the residential addresses were estimated using validated spatiotemporal models. The marginal structural Cox model was used to estimate the associations of PM exposure with respiratory mortality, accounting for time-varying PM exposure. Results were stratified by demographics and lifestyle behaviors factors. Results: Among the participants, the mean age was 48.33 (SD 17.55) years, and 275,676 (47.47%) of them were men. During the follow-up period, 7260 deaths occurred due to respiratory diseases. The annual average concentrations of PM1, PM2.5, and PM10 showed a declining trend during the follow-up period. After adjusting for confounders, a 6.6% (95% CI 5.6%-7.6%), 4.2% (95% CI 3.6%-4.7%), and 4.0% (95% CI 3.6%-4.5%) increase in the risk of respiratory mortality was observed following each 1-µg/m3 increase in concentrations of PM1, PM2.5, and PM10, respectively. In addition, older participants, nonsmokers, participants with higher exercise frequency, and those exposed to a lower normalized difference vegetation index tended to be more susceptible to the effects of PMs. Furthermore, participants in the low-exposure group tended to be at a 7.6% and 2.7% greater risk of respiratory mortality following PM1 and PM10 exposure, respectively, compared to the entire cohort. Conclusions: This cohort study provides causal clues of the respiratory impact of long-term ambient PM exposure, indicating that PM reduction efforts may continuously benefit the population's respiratory health.

Associations between co-exposure to per- and polyfluoroalkyl substances and metabolic diseases: The mediating roles of inflammation and oxidative stress.

BACKGROUND: Per- and polyfluoroalkyl substances (PFAS) pose potential risks to human health. In real-world settings, humans are exposed to various PFAS through numerous pathways. OBJECTIVES: This study evaluated the associations between co-exposure to PFAS and obesity and its comorbidities, along with the mediating roles of inflammation and oxidative stress. METHODS: We analyzed 11,090 participants from National Health and Nutrition Examination Survey (NHANES), 2003-2018. Linear regression, logistic regression, and generalized additive models were used to assess the individual effects of PFAS exposure on obesity and its comorbidities. The environmental risk score (ERS) was calculated using the adaptive elastic-net model to assess the co-exposure effects. Linear and logistic regression models explored the associations between ERS and obesity and its comorbidities. Mediation analyses explored the roles of inflammatory (neutrophils, lymphocytes, and alkaline phosphatase) and oxidative stress (gamma-glutamyl transferase, total bilirubin, and uric acid) markers in the associations between ERS and obesity and its comorbidities. RESULTS: For each unit increase in ERS, the odds of obesity and type 2 diabetes mellitus (T2DM) increased 3.60-fold (95 % CI: 2.03, 6.38) and 1.91-fold (95 % CI: 1.28, 2.86), respectively. For each unit increase in ERS, BMI increased by 2.36 (95 % CI: 1.24, 3.48) kg/m2, waist circumference increased by 6.47 (95 % CI: 3.56, 9.37) cm, and waist-to-height ratio increased by 0.04 (95 % CI: 0.02, 0.06). Lymphocytes, alkaline phosphatase, and total bilirubin were significantly associated with both ERS and obesity, with mediation proportions of 4.17 %, 3.62 %, and 7.37 %, respectively. Lymphocytes, alkaline phosphatase, total bilirubin, and uric acid were significantly associated with both ERS and T2DM, with the mediation proportions of 8.90 %, 8.74 %, 29.73 %, and 38.19 %, respectively. CONCLUSIONS: Co-exposure to PFAS was associated with obesity and T2DM, and these associations may be mediated by inflammation and oxidative stress. Further mechanistic and prospective studies are required to verify these associations.

Association between PFAS exposure and thyroid health: A systematic review and meta-analysis for adolescents, pregnant women, adults and toxicological evidence.

A burgeoning body of epidemiological and toxicological evidence suggests that thyroid health may be significantly impacted by exposure to both long- and short-chain perfluoroalkyl substances (PFAS) compounds. We conducted a meta-analysis to examine the association between 16 PFAS compounds and five thyroid hormones (TSH, TT3, TT4, FT3, and FT4) in the serum of a pregnant women, adolescents, and adults. The dose-response relationship between some PFAS and thyroid hormones in different population subpopulation was found and the model was fitted. We also amalgamated data from 18 animal experiments with previously published in vitro studies to elucidate the toxicological mechanisms underlying the impact of PFAS on the thyroid gland. The results of the study showed that (a) both conventional and emerging PFAS compounds were identified in human samples and exhibited associations with thyroid health outcomes; (b) in animal studies, PFAS have been found to impact thyroid gland health through two primary mechanisms: by influencing the hypothalamic-pituitary-thyroid axis and by binding to thyroid receptors. This study provides a systematic description of the health effects and risk assessment associated with PFAS exposure on the thyroid gland. Furthermore, dose-response relationships were established through the Hill model in python.

Neonicotinoid residues in fruits and vegetables in Shenzhen: Assessing human exposure and health risks.

The extensive use of neonicotinoids (NEOs) in agricultural production has led to their pervasive presence in various environmental matrices, including human samples. Given the central role of fruits and vegetables in daily human diets, it is crucial to evaluate the levels of NEOs residues and their potential health risks. In this study, 3104 vegetable samples and 1567 fruit samples from the Shenzhen city were analyzed. Using the relative potency factor (RPF) method, the residue levels of six representative neonicotinoids, including imidacloprid (IMI), acetamiprid (ACE), thiamethoxam (THM), dinotefuran (DIN), clothianidin (CLO), thiacloprid (THI), were systematically evaluated. The estimated daily intake (EDI), hazard quotient (HQ), and hazard index (HI) for both children and adults were calculated to gauge the prevalence and potential health risks of NEOs in fruits and vegetables. Acetamiprid (ACE) was the most frequently detected NEO in vegetables (69.4%) and fruits (73.9%), making it the predominant contributor to total residues. Further analyses indicated notably higher levels of imidacloprid-equivalent total neonicotinoids (IMIRPF) in root and tuber vegetables (3025 µg/kg) and other fruits (243 µg/kg). A significant strong positive correlation (r = 0.748, P < 0.05) was observed between thiamethoxam (THM) and clothianidin (CLO), possibly due to their shared metabolic pathways. Although the mean HI values for adults and children from daily fruit (adults: 0.02, children: 0.01) and vegetable (adults: 0.02, children: 0.03) intake were generally below safety thresholds, some maximum HI values exceeded these limits, indicating that the potential health risks associated with NEOs exposure should not be overlooked.

NMR-based metabolomics analysis reveals the effect of environmental contamination exposure on fishermen living around the Mundaú Lagoon in Maceió (Alagoas, Brazil).

The Mundaú lagoon in Maceió (Alagoas, Brazil) is a crucial resource for the local population, particularly fishing communities. Recent studies have revealed potential toxic metal contamination in the lagoon, particularly with mercury (Hg) levels exceeding the maximum regulated values. This inorganic contaminant may be impacting the health of fishermen and the local population. In this context, metabolomics, a study of small-molecule metabolites, can offer insights into the physiological impact of environmental contamination on humans. Thus, volunteers from the control and exposed groups were selected, considering the main exposure criteria primarily defined by their proximity and interaction with the lagoon. Blood and urine samples were collected from the volunteers and subjected to analysis using NMR spectroscopy. The data underwent Principal Component Analysis (PCA) and Orthogonal Partial Least-Squares Discriminant Analysis (OPLS-DA) based on metabolic patterns to establish group discrimination or identification. Metabolic pathways were assessed through enrichment analysis. The study revealed several metabolic disturbances in the exposed group's urine and plasma samples compared to control group. Noteworthy findings included arginine and proline metabolism disruptions, indicative of ammonia recycling and urea cycle impairment. These changes suggest compromised ammonia detoxification in the exposed group. Disturbances in the tricarboxylic acid (TCA) cycle and the transfer of acetyl groups into mitochondria suggested systemic metabolic stress in energy metabolism. Furthermore, elevated carnitine and ketone levels may indicate compensatory responses to low TCA cycle activity. Alterations in glutamate and glutathione metabolism and imbalances in glutathione levels indicate oxidative stress and impaired detoxification. This study highlights significant metabolic changes in fishermen exposed to contaminated environments, which can affect various metabolic pathways, including energy metabolism and antioxidant processes, potentially making individuals more vulnerable to the adverse effects of environmental contaminants. Finally, this work highlights insights into the relationship between environmental contamination and metabolic pathways, particularly in regions with limited studies.

Early-life ozone exposure and childhood otitis media: Unveiling critical windows of risk.

BACKGROUND: Despite increasing evidence of a strong correlation between air pollution and otitis media (OM), the impact of early-life ozone (O3) exposure on the development of OM in children remains uncertain. OBJECTIVES: To explore the connection between early-life O3 exposure and OM, and to identify the critical time period(s) during which O3 exposure significantly influences the development of OM in children. METHODS: We conducted a study involving 8689 children living in Changsha, China. Information regarding personal factors, health conditions, and the indoor environment was gathered using questionnaires. Personal exposure to outdoor O3 and other major pollutants at the place of residence during the periods before conception, prenatal periods, and after birth was calculated by applying the inverse distance weighted (IDW) method with data gathered from ten air quality monitoring stations. Multiple logistic regression analyses were employed to investigate the associations between O3 exposure and children's OM. RESULTS: After controlling for covariates and ambient temperature, exposure to O3 during the year preceding pregnancy was correlated with childhood lifetime OM, showing ORs (95 % CI) of 1.28 (1.01-1.64). O3 exposures in the 10th-12th, 7th-9th, and 4th-6th months before pregnancy were all linked to children's lifetime OM. Within the multi-window model, we detected that O3 exposure in the 10th to 12th month prior to pregnancy was significantly related to lifetime OM, showing ORs (95 % CI) of 1.28 (1.05-1.55). A significant link was discovered between childhood OM and O3 exposure after controlling for six other pollutants (SO2, PM2.5, NO2, PM2.5-10, CO, and PM10) during the 10th to 12th month prior to conception. Exposure to O3 during the 36th gestational week significantly raised the likelihood of childhood lifetime OM. There is a significant interaction between O3 and temperature exposure during the first trimester of pregnancy and one year before pregnancy on childhood lifetime OM. CONCLUSIONS: Preconceptional O3 exposure and its interaction with low temperature played critical roles in children's OM development, backing the hypothesis of "(pre) fetal origins of childhood OM".

The effect of exposure to radiofrequency fields on cancer risk in the general and working population: A systematic review of human observational studies - Part I: Most researched outcomes.

BACKGROUND: The objective of this review was to assess the quality and strength of the evidence provided by human observational studies for a causal association between exposure to radiofrequency electromagnetic fields (RF-EMF) and risk of the most investigated neoplastic diseases. METHODS: Eligibility criteria: We included cohort and case-control studies of neoplasia risks in relation to three types of exposure to RF-EMF: near-field, head-localized, exposure from wireless phone use (SR-A); far-field, whole body, environmental exposure from fixed-site transmitters (SR-B); near/far-field occupational exposures from use of hand-held transceivers or RF-emitting equipment in the workplace (SR-C). While no restrictions on tumour type were applied, in the current paper we focus on incidence-based studies of selected "critical" neoplasms of the central nervous system (brain, meninges, pituitary gland, acoustic nerve) and salivary gland tumours (SR-A); brain tumours and leukaemias (SR-B, SR-C). We focussed on investigations of specific neoplasms in relation to specific exposure sources (i.e. E-O pairs), noting that a single article may address multiple E-O pairs. INFORMATION SOURCES: Eligible studies were identified by literature searches through Medline, Embase, and EMF-Portal. Risk-of-bias (RoB) assessment: We used a tailored version of the Office of Health Assessment and Translation (OHAT) RoB tool to evaluate each study's internal validity. At the summary RoB step, studies were classified into three tiers according to their overall potential for bias (low, moderate and high). DATA SYNTHESIS: We synthesized the study results using random effects restricted maximum likelihood (REML) models (overall and subgroup meta-analyses of dichotomous and categorical exposure variables), and weighted mixed effects models (dose-response meta-analyses of lifetime exposure intensity). Evidence assessment: Confidence in evidence was assessed using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach. RESULTS: We included 63 aetiological articles, published between 1994 and 2022, with participants from 22 countries, reporting on 119 different E-O pairs. RF-EMF exposure from mobile phones (ever or regular use vs no or non-regular use) was not associated with an increased risk of glioma [meta-estimate of the relative risk (mRR) = 1.01, 95 % CI = 0.89-1.13), meningioma (mRR = 0.92, 95 % CI = 0.82-1.02), acoustic neuroma (mRR = 1.03, 95 % CI = 0.85-1.24), pituitary tumours (mRR = 0.81, 95 % CI = 0.61-1.06), salivary gland tumours (mRR = 0.91, 95 % CI = 0.78-1.06), or paediatric (children, adolescents and young adults) brain tumours (mRR = 1.06, 95 % CI = 0.74-1.51), with variable degree of across-study heterogeneity (I2 = 0 %-62 %). There was no observable increase in mRRs for the most investigated neoplasms (glioma, meningioma, and acoustic neuroma) with increasing time since start (TSS) use of mobile phones, cumulative call time (CCT), or cumulative number of calls (CNC). Cordless phone use was not significantly associated with risks of glioma [mRR = 1.04, 95 % CI = 0.74-1.46; I2 = 74 %) meningioma, (mRR = 0.91, 95 % CI = 0.70-1.18; I2 = 59 %), or acoustic neuroma (mRR = 1.16; 95 % CI = 0.83-1.61; I2 = 63 %). Exposure from fixed-site transmitters (broadcasting antennas or base stations) was not associated with childhood leukaemia or paediatric brain tumour risks, independently of the level of the modelled RF exposure. Glioma risk was not significantly increased following occupational RF exposure (ever vs never), and no differences were detected between increasing categories of modelled cumulative exposure levels. DISCUSSION: In the sensitivity analyses of glioma, meningioma, and acoustic neuroma risks in relation to mobile phone use (ever use, TSS, CCT, and CNC) the presented results were robust and not affected by changes in study aggregation. In a leave-one-out meta-analyses of glioma risk in relation to mobile phone use we identified one influential study. In subsequent meta-analyses performed after excluding this study, we observed a substantial reduction in the mRR and the heterogeneity between studies, for both the contrast Ever vs Never (regular) use (mRR = 0.96, 95 % CI = 0.87-1.07, I2 = 47 %), and in the analysis by increasing categories of TSS ("<5 years": mRR = 0.97, 95 % CI = 0.83-1.14, I2 = 41 %; "5-9 years ": mRR = 0.96, 95 % CI = 0.83-1.11, I2 = 34 %; "10+ years": mRR = 0.97, 95 % CI = 0.87-1.08, I2 = 10 %). There was limited variation across studies in RoB for the priority domains (selection/attrition, exposure and outcome information), with the number of studies evenly classified as at low and moderate risk of bias (49 % tier-1 and 51 % tier-2), and no studies classified as at high risk of bias (tier-3). The impact of the biases on the study results (amount and direction) proved difficult to predict, and the RoB tool was inherently unable to account for the effect of competing biases. However, the sensitivity meta-analyses stratified on bias-tier, showed that the heterogeneity observed in our main meta-analyses across studies of glioma and acoustic neuroma in the upper TSS stratum (I2 = 77 % and 76 %), was explained by the summary RoB-tier. In the tier-1 study subgroup, the mRRs (95 % CI; I2) in long-term (10+ years) users were 0.95 (0.85-1.05; 5.5 %) for glioma, and 1.00 (0.78-1.29; 35 %) for acoustic neuroma. The time-trend simulation studies, evaluated as complementary evidence in line with a triangulation approach for external validity, were consistent in showing that the increased risks observed in some case-control studies were incompatible with the actual incidence rates of glioma/brain cancer observed in several countries and over long periods. Three of these simulation studies consistently reported that RR estimates > 1.5 with a 10+ years induction period were definitely implausible, and could be used to set a "credibility benchmark". In the sensitivity meta-analyses of glioma risk in the upper category of TSS excluding five studies reporting implausible effect sizes, we observed strong reductions in both the mRR [mRR of 0.95 (95 % CI = 0.86-1.05)], and the degree of heterogeneity across studies (I2 = 3.6 %). CONCLUSIONS: Consistently with the published protocol, our final conclusions were formulated separately for each exposure-outcome combination, and primarily based on the line of evidence with the highest confidence, taking into account the ranking of RF sources by exposure level as inferred from dosimetric studies, and the external coherence with findings from time-trend simulation studies (limited to glioma in relation to mobile phone use). For near field RF-EMF exposure to the head from mobile phone use, there was moderate certainty evidence that it likely does not increase the risk of glioma, meningioma, acoustic neuroma, pituitary tumours, and salivary gland tumours in adults, or of paediatric brain tumours. For near field RF-EMF exposure to the head from cordless phone use, there was low certainty evidence that it may not increase the risk of glioma, meningioma or acoustic neuroma. For whole-body far-field RF-EMF exposure from fixed-site transmitters (broadcasting antennas or base stations), there was moderate certainty evidence that it likely does not increase childhood leukaemia risk and low certainty evidence that it may not increase the risk of paediatric brain tumours. There were no studies eligible for inclusion investigating RF-EMF exposure from fixed-site transmitters and critical tumours in adults. For occupational RF-EMF exposure, there was low certainty evidence that it may not increase the risk of brain cancer/glioma, but there were no included studies of leukemias (the second critical outcome in SR-C). The evidence rating regarding paediatric brain tumours in relation to environmental RF exposure from fixed-site transmitters should be interpreted with caution, due to the small number of studies. Similar interpretative cautions apply to the evidence rating of the relation between glioma/brain cancer and occupational RF exposure, due to differences in exposure sources and metrics across the few included studies. OTHER: This project was commissioned and partially funded by the World Health Organization (WHO). Co-financing was provided by the New Zealand Ministry of Health; the Istituto Superiore di Sanità in its capacity as a WHO Collaborating Centre for Radiation and Health; and ARPANSA as a WHO Collaborating Centre for Radiation Protection. REGISTRATION: PROSPERO CRD42021236798. Published protocol: [(Lagorio et al., 2021) DOI https://doi.org/10.1016/j.envint.2021.106828].

Exposome-Wide Ranking to Uncover Environmental Chemicals Associated with Dyslipidemia: A Panel Study in Healthy Older Chinese Adults from the BAPE Study.

BACKGROUND: Environmental contaminants (ECs) are increasingly recognized as crucial drivers of dyslipidemia and cardiovascular disease (CVD), but the comprehensive impact spectrum and interlinking mechanisms remain uncertain. OBJECTIVES: We aimed to systematically evaluate the association between exposure to 80 ECs across seven divergent categories and markers of dyslipidemia and investigate their underpinning biomolecular mechanisms via an unbiased integrative approach of internal chemical exposome and multi-omics. METHODS: A longitudinal study involving 76 healthy older adults was conducted in Jinan, China, and participants were followed five times from 10 September 2018 to 19 January 2019 in 1-month intervals. A broad spectrum of seven chemical categories covering the prototypes and metabolites of 102 ECs in serum or urine as well as six serum dyslipidemia markers [total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, apolipoprotein (Apo)A1, ApoB, and ApoE4] were measured. Multi-omics, including the blood transcriptome, serum/urine metabolome, and serum lipidome, were profiled concurrently. Exposome-wide association study and the deletion/substitution/addition algorithms were applied to explore the associations between 80 EC exposures detection frequency >50% and dyslipidemia markers. Weighted quantile sum regression was used to assess the mixture effects and relative contributions. Multi-omics profiling, causal inference model, and pathway analysis were conducted to interpret the mediating biomolecules and underlying mechanisms. Examination of cytokines and electrocardiograms was further conducted to validate the observed associations and biomolecular pathways. RESULTS: Eight main ECs [1-naphthalene, 1-pyrene, 2-fluorene, dibutyl phosphate, tri-phenyl phosphate, mono-(2-ethyl-5-hydroxyhexyl) phthalate, chromium, and vanadium] were significantly associated with most dyslipidemia markers. Multi-omics indicated that the associations were mediated by endogenous biomolecules and pathways, primarily pertinent to CVD, inflammation, and metabolism. Clinical measures of cytokines and electrocardiograms further cross-validated the association of these exogenous ECs with systemic inflammation and cardiac function, demonstrating their potential mechanisms in driving dyslipidemia pathogenesis. DISCUSSION: It is imperative to prioritize mitigating exposure to these ECs in the primary prevention and control of the dyslipidemia epidemic. https://doi.org/10.1289/EHP13864.

A randomized controlled trial of a housing intervention to reduce endocrine disrupting chemical exposures in children.

Few studies have considered household interventions for reducing endocrine disrupting chemical (EDC) exposures. We conducted a secondary analysis of a randomized controlled trial, originally designed to reduce lead exposure, to evaluate if the intervention lowered EDC exposures in young children. Study participants were children from the Cincinnati, Ohio area (n = 250, HOME Study). Prenatally, families received a housing intervention that included paint stabilization and dust mitigation, or as a control, injury prevention measures. At 24-months, we measured organophosphate esters (OPEs) and phthalates or their metabolites in dust and urine. We measured perfluoroalkyl substances (PFAS) in dust and serum at 24- and 36-months, respectively. We assessed associations between dust and biomarker EDCs using Spearman correlations, characterized EDC mixtures via principal components analysis, and investigated treatment effects using linear regression. To mitigate selection bias, we fit statistical models using inverse probability of retention weights. Correlations between dust EDCs and analogous biomarkers were weak-to-moderate (ρ's ≤ 0.3). The intervention was associated with 23 % (95 % CI: -38, -3) lower urinary DEHP metabolites and, in a per-protocol analysis, 34 % lower (95 % CI: -55, -2) urinary MBZP. Additionally, among Black or African American children, the intervention was associated with lower serum concentrations of several PFAS (e.g., -42 %; 95 % CI: -63, -8 for PFNA). Household interventions that include paint stabilization and dust mitigation may reduce childhood exposures to some phthalates and PFAS in Blacks/African Americans. These findings highlight the need for larger studies with tailored and sustained housing interventions.