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.

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.

Exposure to polycyclic aromatic hydrocarbons (PAHs) has been linked to the development of certain diseases. However, the relationship between PAH exposure and thyroid disorders remains unknown. We measured 10 of the most common hydroxylated PAHs (OH-PAHs) in the urine of thyroid nodular goiter (NG) patients, papillary thyroid carcinoma (PTC) patients, and healthy controls by gas chromatography-triple-quadrupole mass spectrometry (GC-MS/MS). We found that the concentrations of 2-hydroxyfluorene (2-OH-FLU), 2-hydroxydibenzofuran (2-OH-DBF), and 1-hydroxyphenanthrene (1-OH-PHE) in the NG group, and of 2-hydroxynaphthalene (2-OH-NAP), 2-OH-DBF, and 1-OH-PHE in the PTC group were significantly higher than those in controls. In addition, participants in the high tertiles of 2-OH-FLU and 1-OH-PHE had higher risk of NG. Besides these two OH-PAHs, elevated risk of NG was observed in women in the high tertiles of 1-hydroxynaphthalene (1-OH-NAP), 2-OH-NAP, 2-OH-DBF, and 3-hydroxyfluorene (3-OH-FLU). Furthermore, participants in the high tertiles of seven OH-PAHs, namely, 1-OH-NAP, 2-OH-NAP, 2-OH-DBF, 2-OH-FLU, 3-OH-FLU, 3/9-hydroxyphenanthrene (3/9-OH-PHE), and 1-OH-PHE, had elevated risk of PTC, and females in these high tertiles had an even higher risk of PTC. Our findings suggest that PAH exposure may increase the risk of NG/PTC, and there may be a gender-specific effect of PAH exposure on the development of NG/PTC.

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.

Lipophilic marine algal toxins (LMATs) pose a potential threat to the health of marine shellfish consumers and marine breeding industries. In this study, LMATs in dissolved phases (DP) and particulate phases (PP) in the seawater of Jiaozhou Bay were accurately determined over four seasons to understand their composition, level, phase partitioning, spatiotemporal variation, and potential sources in aquatic environments of a typical semi-closed mariculture bay. Various LMATs, such as okadaic acid (OA), dinophysistoxin-1 (DTX1), dinophysistoxin-2 (DTX2), gymnodimine (GYM), 13-desmethyl spirolide C (SPX1), pectenotoxin-2 (PTX2), pectenotoxin-2 seco acid (PTX2 SA), and pectenotoxin-11 (PTX11), were detected in DP and PP; of these, OA and PTX2 were the dominant LMATs in DP and PP, respectively. The average proportion of ΣLMATs in DP (97.5%) was significantly higher than that in PP (2.5%), which indicates that LMATs are predominantly partitioned into DP. The total concentrations of LMATs in DP ranged from 4.16 ng/L to 23.19 ng/L (mean, 13.35 ng/L) over four seasons. The highest levels of LMATs in DP and PP were found in summer (mean, 16.71 ng/L) and spring, respectively, while the maximum variety of LMATs was found in autumn. This result suggests that seasonal changes could influence the composition, concentration, and phase partitioning of LMATs in aquatic environments of a coastal semi-closed mariculture bay. ΣLMAT concentrations were higher in the western region than in the eastern region of the bay, where shellfish may have a greater risk of exposure. Dinophysis acuminata, Dinophysis fortii, and Prorocentrum minimum were the potential sources of LMATs in the aquaculture seawater. Overall, various LMATs occurred in the semi-closed mariculture bay, and the persistence and bioavailability of these toxins in aquaculture seawater should be determined in future research.

Numerous epidemiological studies have indicated the adverse cardiovascular effects of air pollution on heart failure (HF) risk. However, little data are available directly evaluating the association of ambient volatile organic compounds (VOCs) with HF risk. We aimed to estimate the short-term effects of ambient VOCs on HF emergency hospitalizations in Hong Kong and to evaluate whether the associations were modified by sex and age.We collected the daily VOCs concentrations from the Hong Kong Environmental Protection Department between April 2011 to December 2014. HF emergency hospital admission data were obtained from the Hospital Authority of Hong Kong. Generalized additive model (GAM) integrated with the distributed lag model (DLM) was used to estimate the excess risks of HF emergency hospitalizations with ambient concentrations of each VOCs groups – alkane, alkene, alkyne, benzene and substituted benzene.We observed short-term effects of alkyne and benzene on an increased risk of HF emergency hospitalizations. The cumulative effect over 0–6 lag days (dlm₀₋₆) for an IQR increment of alkyne (1.17 ppb) was associated with 4.2% (95% CI: 1.18%–7.26%) increases of HF emergency hospitalizations, while the corresponding effect estimate over dlm₀₋₂ for benzene per IQR (0.43 ppb) was 2.7% (95% CI: 0.39%–5.04%). Each VOCs groups was significantly associated with HF emergency hospitalizations in men.Ambient volatile organic compounds, particularly alkyne and benzene, were associated with increased risks of heart failure in the Hong Kong population.