Exposure to air pollutants has been associated with respiratory and cardiovascular mortality, but the underlying molecular mechanisms remain inadequately understood. We aimed to examine molecular-level inflammatory and oxidative stress responses to personal air pollutant exposure. Fifty-three healthy adults aged 22–52 were measured three times for their blood inflammatory cytokines and urinary malondialdehyde (MDA, an oxidative stress biomarker) within 2 consecutive months. Pollutant concentrations monitored indoors and outdoors were combined with the time-activity data to calculate personal O₃, PM₂.₅, NO₂, and SO₂ exposures averaged over 12 h, 24 h, 1 week, and 2 weeks, respectively, prior to biospecimen collection. Inflammatory cytokines and MDA were associated with pollutant exposures using linear mixed-effects models controlling for various covariates. After adjusting for a co-pollutant, we found that concentrations of proinflammatory cytokines were significantly and negatively associated with 12-h O₃ exposures and significantly but positively associated with 2-week O₃ exposures. We also found significant and positive associations of proinflammatory cytokines with 12-h and 24-h NO₂ exposures, respectively. However, we did not find clear associations of PM₂.₅ and SO₂ exposure with proinflammatory cytokines and with MDA. The removal of an O₃-generating electrostatic precipitator in the mechanical ventilation systems of the offices and residences of the subjects was associated with significant decreases in IL-1β, IL-2, IL-6, IL-8, IL-17A, and TNF-α. These findings suggest that exposure to O₃ for different time durations may affect systemic inflammatory responses in different ways.

Evidence is available about the associations of phthalates or their metabolites with blood lipids, however, the mixture effects of multiple phthalate metabolites on blood lipid traits remain largely unknown. In this pilot study, 106 individuals at three age groups of <18, 18- and ≥60 years were recruited from the residents (n = 1240) who were randomly selected from two communities in Wuhan city, China. The participants completed the questionnaire survey and physical examination as well as provided urine samples in the winter of 2014 and the summer of 2015. We measured urinary levels of nine phthalate metabolites using a high-performance liquid chromatography-tandem mass spectrometry. We estimated the associations of individual phthalate metabolite with blood lipid traits by linear mixed effect (LME) models, and assessed the overall association of the mixture of nine phthalate metabolites with blood lipid traits using Bayesian kernel machine regression (BKMR) models. LME models revealed the negative association of urinary mono-2-ethylhexyl phthalate (MEHP) with total cholesterol (TC) as well as of urinary mono-benzyl phthalate or urinary MEHP with low density lipoprotein cholesterol (LDL-C). BKMR models revealed the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C, and DEHP metabolites (especially MEHP) had a greater contribution to TC or LDL-C levels than non-DEHP metabolites. The findings indicated the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C. Among nine phthalate metabolites, MEHP was the most important component for the changes of TC or LDL-C levels, implying that phthalates exposure may disrupt lipid metabolism in the body.

Urban environments are characterized by multiple exposures that may influence body mass index (BMI) growth in early life. Previous studies are few, with inconsistent results and no evaluation of simultaneous exposures. Thus, this study aimed to assess the associations between exposure to air pollution, green spaces and built environment characteristics, and BMI growth trajectories from 0 to 5 years. This longitudinal study used data from an electronic primary care health record database in Catalonia (Spain), including 79,992 children born between January 01, 2011 and December 31, 2012 in urban areas and followed until 5 years of age. Height and weight were measured frequently during childhood and BMI (kg/m²) was calculated. Urban exposures were estimated at census tract level and included: air pollution (nitrogen dioxide (NO₂), particulate matter <10 μm (PM₁₀) and <2.5 μm (PM₂.₅₎), green spaces (Normalized Difference Vegetation Index (NDVI) and % green space) and built environment (population density, street connectivity, land use mix, walkability index). Individual BMI trajectories were estimated using linear spline multilevel models with several knot points. In single exposure models, NO₂, PM₁₀, PM₂.₅, and population density were associated with small increases in BMI growth (e.g. β per IQR PM₁₀ increase = 0.023 kg/m², 95%CI: 0.013, 0.033), and NDVI, % of green spaces and land use mix with small reductions in BMI growth (e.g. β per IQR % green spaces increase = −0.015 kg/m², 95%CI: −0.026, −0.005). These associations were strongest during the first two months of life. In multiple exposure models, most associations were attenuated, with only those for PM₁₀ and land use mix remaining statistically significant. This large longitudinal study suggests that early life exposure to air pollution, green space and built environment characteristics may be associated with small changes in BMI growth trajectories during the first years of life, and that it is important to account for multiple exposures in urban settings.

Kitchen emissions are mixed indoor air pollutants with adverse health effects, but the large-scale assessment is limited by costly equipment and survey methods. This study aimed to discuss the application of backpropagation (BP) neural network models in the assessment of kitchen emissions based on the exposure marker. A total of 3686 participants were recruited for the kitchen survey, and their sleep quality was measured by the Pittsburgh sleep quality index (PSQI). After excluding the confounders, 365 participants were selected to assess their urinary hydroxy polycyclic aromatic hydrocarbons (OH-PAHs) concentrations by ultra-high-performance liquid chromatography/tandem mass spectrometry. Two BP neural network models were then set up using the survey and detection data from the 365 participants and used to predict the total urinary OH-PAHs concentrations of all participants. The total urinary OH-PAHs and 1-hydroxy-naphthalene (1-OHNap) concentrations were significantly higher among the 365 participants with poor sleep quality (global PSQI score > 5; P < 0.05). Results from internal and external validation showed that our model has high credibility (model 2). Further, the participants with higher predicted total urinary OH-PAHs concentrations were associated with the global PSQI score of >5 (odds ratio (OR) = 1.284, 95% confidence interval (CI) = 1.082–1.525 for participants with predicted total urinary OH-PAHs concentrations of over 1.897 μg/mmol creatinine in model 1, and OR = 1.467, 95% CI = 1.240–1.735 for participants with predicted total urinary OH-PAHs concentrations of over 2.253 μg/mmol creatinine in model 2) after adjusting for the confounders. Findings suggest that the BP neural network model is suitable for assessing kitchen emissions, and the urinary OH-PAHs concentrations can be taken as the model outlay.

Pesticides used in agriculture are some of the most common pollutants in the world. This study aimed to investigate the effects of Organophosphorus Pesticides (OPPs) and Organochlorine Pesticides (OCPs) on the families of farmworkers in the southeast of Iran.In the present case-control study, 141 family members of farmworkers (as the case group) and 59 family members of non-farmworkers (as the controls) were recruited. Serum levels of OCPs such as α-HCH, β-HCH, γ-HCH, 2,4-DDE, 4,4-DDE, 2,4-DDT, and 4,4-DDT were determined. In addition, erythrocyte acetylcholinesterase (AChE) activity, malondialdehyde (MDA), total antioxidant capacity (TAC), protein carbonyl (PC), nitric oxide (NO) serum levels, arylesterase activity of paraoxonase 1 (PON-1), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity were determined in all participants. Furthermore, distance to farmlands, education, crops, type, and the number of consumed fruits were evaluated for each individual separately.The erythrocyte AChE activity and serum activities of GPx, SOD, and PON-1 and TAC levels were significantly decreased, whereas the concentration of MDA, PC, NO, and seven OCPs were significantly increased in the farmworkers’ families as compared to the controls. Spearman correlation and linear regression suggest that OCPs increase the oxidative stress in farmworkers’ family members. Moreover, distance, education, farming precedence, products, and ventilation had significant effects on the OCP levels and increased the odds ratio of OCP levels in farmworkers’ families.With regards to the data obtained in this study, it was revealed that OCPs as illegal pesticides and OPPs were higher than expected in the farmworkers’ family members. Furthermore, exposure to OCPs and OPPs, apart from the other effects on the body, leads to oxidative stress (OS) that may cause serious diseases in the exposed populations.

Fluoride mediated disruption of sex steroid hormones has been demonstrated in animals. However, evidence from humans was limited and contradictory, especially for children and adolescents. Based on data of the National Health and Nutrition Survey (NHANES) 2013–2016, a total of 3392 subjects aged 6–19 years were analyzed in this cross-sectional study. Both plasma and water fluoride levels were quantified electrometrically using the ion-specific electrode. Sex steroid hormones of total testosterone, estradiol and sex hormone-binding globulin (SHBG) were tested in serum. Percent changes and 95% confidence intervals (CIs) in sex steroid hormones associated with tertiles of fluoride levels (setting the first as reference) were estimated using adjusted linear regression models by stratification of gender and age. Compared with subjects at the first tertile of plasma fluoride, percent changes (95% CIs) in testosterone were −8.08% (−17.36%, 2.25%) and −21.65% (−30.44%, −11.75%) for the second and third tertiles, respectively (P ₜᵣₑₙd <0.001). Male adolescents at the third tertile of plasma fluoride had decreased levels of testosterone (percent change = −21.09%, 95% CIs = −36.61% to −1.77%). Similar inverse associations were also found when investigating the relationships between plasma fluoride and estradiol. Besides, the data indicated decreased levels of SHBG associated with water and plasma fluoride among the male adolescents (percent change of the third tertile = −9.39%, 95% CIs = −17.25% to −0.78%) and female children (percent change of the second tertile = −10.78%, 95% CIs = −17.55% to −3.45%), respectively. The data indicated gender- and age-specific inverse associations of fluoride in plasma and water with sex steroid hormones of total testosterone, estradiol and SHBG in U.S. children and adolescents. Prospective cohort studies are warranted to confirm the causality.

Evidence suggests that residential greenness may be protective of high blood pressure, but there is scarcity of evidence on the associations between greenness around schools and blood pressure among children. We aimed to investigate this association in China. Our study included 9354 children from 62 schools in the Seven Northeastern Cities Study. Greenness around each child’s school was measured by NDVI (Normalized Difference Vegetation Index) and SAVI (Soil-Adjusted Vegetation Index). Particulate matter ≤ 1 μm (PM1) concentrations were estimated by spatiotemporal models and nitrogen dioxide (NO2) concentrations were collected from air monitoring stations. Associations between greenness and blood pressure were determined by generalized linear and logistic mixed-effect models. Mediation by air pollution was assessed using mediation analysis. Higher greenness was consistently associated with lower blood pressure. An increase of 0.1 in NDVI corresponded to a reduction in SBP of 1.39 mmHg (95% CI: 1.86, −0.93) and lower odds of hypertension (OR = 0.76, 95% CI: 0.69, 0.82). Stronger associations were observed in children with higher BMI. Ambient PM1 and NO2 mediated 33.0% and 10.9% of the association between greenness and SBP, respectively. In summary, greater greenness near schools had a beneficial effect on blood pressure, particularly in overweight or obese children in China. The associations might be partially mediated by air pollution. These results might have implications for policy makers to incorporate more green space for both aesthetic and health benefits.

Mosaic loss of chromosome Y (mLOY) is the most common structure somatic event that related to increased risks of various diseases and mortality. Environmental pollution and genetic susceptibility were important contributors to mLOY. We aimed to explore the associations of polycyclic aromatic hydrocarbons (PAHs) exposure, as well as their joint effects with age, smoking, and genetic variants on peripheral blood mLOY. A total of 1005 male coke-oven workers were included in this study and their internal PAHs exposure levels of 10 urinary PAH metabolites and plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts were measured. mLOY was defined by the median log R ratio(mLRR) of 1480 probes in male-specific region of chromosome-Y from genotyping array. We found that the PAHs exposure levels were linearly associated with mLOY. A 10-fold increase in urinary 1-hydroxynaphthalene (1-OHNa), 1-hydroxyphenanthrene (1-OHPh), 2-OHPh, 1-hydroxypyrene (1-OHP), ΣOH-PAHs, and plasma BPDE-Alb adducts could generate 0.0111, 0.0085, 0.0069, 0.0103, 0.0134, and 0.0152 decrease in mLRR-Y, respectively. Additionally, mLOY accelerated with age, smoking pack-years, and TCL1A rs1122138-C allele, and we observed the most severe mLOY among subjects carrying more than 3 of the above risk factors. Our results revealed the linear dose-effect associations between PAHs exposure and mLOY. Elder male smokers carrying rs1122138CC genotype were the most susceptible subpopulations to mLOY, who should be given protections for PAHs exposure induced chromosome-Y aberration.