Exposure to outdoor fine particulate matter (PM₂.₅)-bound polycyclic aromatic hydrocarbons (PAHs) is linked to reproductive dysfunction. However, it is unclear which component of PAHs is responsible for the adverse outcomes. In the Male Reproductive Health in Chongqing College Students (MARHCS) cohort study, we measured the exposure levels of 16 PAHs by collecting air PM₂.₅ particles and assessed eight PAHs metabolites from four parent PAHs, including naphthalene, fluorene, phenanthrene, and pyrene in urine samples. We investigated compositional profiles and variation characteristics for 16 PAHs in PM₂.₅, and then assessed the association between PAHs exposure and semen routine parameters, sperm chromatin structure, and serum hormone levels in 1452 samples. The results showed that naphthalene (95% CI: −17.989, −8.101), chrysene (95% CI: −64.894, −47.575), benzo[a]anthracene (95% CI: −63.227, −45.936) and all the high molecular weight (HMW) PAHs in PM₂.₅ were negatively associated with sperm normal morphology. Most of the low molecular weight (LMW) PAHs, such as acenaphthylene, fluorene, phenanthrene, fluoranthene, pyrene, chrysene, benzo[a]anthracene, ∑LMW PAHs and ∑16 PAHs, were correlated with increased sperm motility (all corrected P < 0.05). On the other hand, sperm normal morphology was all negatively associated with urinary metabolites of ∑OH-Nap (95% CI: −5.611, −0.536), ∑OH-Phe (95% CI: −5.741, −0.957), and ∑OH-PAHs (95% CI: −5.274, −0.361). Urinary concentrations of ∑OH-PAHs were found to be negatively associated with sperm high DNA stainability (HDS) (P = 0.023), while ∑OH-Phe were negatively associated with serum testosterone level and sperm HDS (P = 0.004). Spearman correlation analysis showed that except for the urinary OH-Nap metabolites, the rest of the urinary OH-PAHs metabolites were negatively correlated with their parent PAHs in air. The results of this study suggest that various PAHs’ components may affect reproductive parameters differently. Inhalation of PAHs in air, especially HMW PAHs, may be a potential risk factor for male reproductive health.

Seven perfluorinated and polyfluorinated substances (PFASs), namely perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluoroheptanoic acid (PFHpA), perfluorohexanoic acid (PFHxA), and perfluoro-1,10-decanedicarboxylic acid (PFDDA), were evaluated in urine and hair samples from children (age: 4–6 years, N = 53), airborne particles sampled at 17 kindergartens, and tap water and bottled water samples. All samples were collected in Hong Kong. The analytical results suggested widespread PFAS contamination. All target PFASs were detected in at least 32% of urine samples, with geometric mean (GM) concentrations ranging from 0.18 to 2.97 ng/L, and in 100% of drinking water samples at GM concentrations of 0.18–21.1 ng/L. Although PFOS and PFDDA were not detected in hair or air samples, the other target PFASs were detected in 48–70% of hair samples (GM concentrations: 2.40–233 pg/g) and 100% of air samples (GM concentrations: 14.8–536.7 pg/m³). In summary, the highest PFAS concentrations were detected in airborne particles measured in kindergartens. PFOA was the major PFAS detected in hair, urine, and drinking water samples, while PFOA, PFDA, and PFHpA were dominant in airborne particles. Although a significant difference in PFAS concentrations in hair samples was observed between boys and girls (p < .05), no significant sex-related difference in urinary PFAS or paired PFAS (hair/urine) concentrations was observed.

Polycyclic aromatic hydrocarbons (PAHs) are compounds with two or more benzene rings whose hydroxylated metabolites (OH-PAHs) are excreted in urine. Human PAH exposure is therefore commonly estimated based on urinary OH-PAH concentrations. However, no study has compared PAH exposure estimates based on urinary OH-PAHs to measurements of PAH levels in blood samples. Estimates of PAH exposure based solely on urinary OH-PAHs may thus be subject to substantial error. To test this hypothesis, paired measurements of parent PAHs in serum and OH-PAHs in urine samples from 480 participants in Guangzhou, a typical developed city in southern China, were used to investigate differences in the estimates of human PAH exposure obtained by sampling different biological matrices. The median PAH concentration in serum was 4.05 ng mL⁻¹, which was lower than that of OH-PAHs in urine (8.33 ng mL⁻¹). However, serum pyrene levels were significantly higher than urinary levels of its metabolite 1-hydroxypyrene. Concentrations of parent PAHs in serum were not significantly correlated with those of their metabolites in urine with the exception of phenanthrene, which exhibited a significant negative correlation. Over 28% of the participants had carcinogenic risk values above the acceptable cancer risk level of 10⁻⁶. Overall, estimated human exposure and health risks based on urinary 1-hydroxypyrene levels were only 13.6% of those based on serum pyrene measurements, indicating that estimates based solely on urine sampling may substantially understate health risks due to PAH exposure.

Coke oven emissions (COEs), usually composed of polycyclic aromatic hydrocarbons (PAHs) and so on, may alter the relative telomere length of exposed workers and have been linked with adverse health events. However, the relevant biological exposure limits of COEs exposure has not been evaluated from telomere damage. The purpose of this study is to estimate benchmark dose (BMD) of urinary PAHs metabolites from COEs exposure based on telomere damage with RTL as a biomarker. A total of 544 exposed workers and 238 controls were recruited for participation. High-performance liquid chromatography and qPCR were used to detect concentrations of urinary mono-hydroxylated PAHs and relative telomere length in peripheral blood leukocytes for all subjects. The benchmark dose approach was used to estimate benchmark dose (BMD) and its lower 95% confidence limit (BMDL) of urinary OH-PAHs of COEs exposure based on telomere damage. Our results showed that telomere length in the exposure group (0.75 (0.51, 1.08)) was shorter than that in the control group (1.05 (0.76,1.44))(P < 0.05), and a dose-response relationship was shown between telomere damage and both 1-hydroxypyrene and 3-hydroxyphenanthrene in urine. The BMDL of urinary 1-hydroxypyrene from the optimal model for telomere damage was 1.96, 0.40, and 1.01 (μmol/mol creatinine) for the total, males, and females group, respectively. For 3-hydroxyphenanthrene, the BMDL was 0.94, 0.33, and 0.49 (μmol/mol creatinine) for the total, males, and females. These results contribute to our understanding of telomere damage induced by COEs exposure and provide a reference for setting potential biological exposure limits.

Bisphenol A and its alternatives are frequently detected in environmental and human samples, but studies associated with the pattern of combined health hazards from the exposure to the bisphenol mixtures are lacking, particularly for pregnant women. Here, we recruited 941 pregnant women with a full set of urine samples in the three trimesters collected under a cohort study project in Wuhan, China, between 2014 and 2015. We measured the concentrations of 8 bisphenols in 2823 urine samples, and calculated the average concentrations of bisphenols, which were detected in over 50% of samples, once during each trimester of pregnancy. We calculated the maximum cumulative ratio (MCR) on basis of estimated daily intake (EDI), hazard quotient (HQ), hazard index (HI) of three major bisphenols, including bisphenol A (BPA), bisphenol F (BPF), and bisphenol S (BPS), to find which one or mixtures drive risks. Participants were categorized into four groups according to their maximum HQ, HI and MCR values. We found negative relationships between log(MCR-1) and log(HI) with the slope (−0.6431). Percentage of HQ of BPA in HI ranged from 37.1% (<25th percentiles of HI) to 75.5% (>95th percentiles of HI) indicating the upward trend of dominance by BPA at increasing HI ranges. The cumulative health risks of bisphenol exposures largely originated from the health hazards of BPA and BPS, particularly BPA. The intervention for regulation on the production and application of BPA and its alternatives are urgent, and China should consider national regulation on these chemicals based on its risk to human health.

Studies have documented that exposure to organochlorine pesticides (OCPs) is linked with breast cancer, but the underlying biological mechanisms are still unknown. This study included 313 women diagnosed with breast cancer and 313 controls in Wuhan, China, and measured 18 OCPs in serum and 3 oxidative stress biomarkers in urine. Multivariable adjusted regression models were used to evaluate the associations among OCPs, oxidative stress biomarkers, and breast cancer. The mediating effect of oxidative stress was assessed by mediation analysis. We observed that most OCPs were positively associated with risk of breast cancer (all FDR-P values < 0.05 or 0.10). Moreover, we found that p,p'-DDT, p,p'-DDD, dieldrin, heptachlor, and heptachlor epoxide were positively associated with 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA) and 8-iso-prostaglandin F₂α (8-isoPGF₂α), which in turn were positively associated with risk of breast cancer. Mediation analysis indicated that HNE-MA and 8-isoPGF₂ɑ mediated the positive associations between these OCPs and risk of breast cancer, with mediating proportion ranging from 6.23% to 19.9%. Our results suggest that lipid peroxidation may mediate the positive associations between OCP exposures and risk of breast cancer.

Due to worldwide regulations on the application of the high production volume industrial chemical bisphenol A (BPA) in various consumer products, alternative bisphenols such as bisphenol F (BPF) and bisphenol S (BPS) are increasingly used. To assess human exposure to these chemicals, biomonitoring of urinary concentrations is frequently used. However, the short-term variability of alternative bisphenols has not been evaluated thoroughly yet, which is essential to achieve a correct estimation of exposure. In this study, we collected all spot urine samples from ten healthy adults for five consecutive days, and an additional 24 h pooled sample. We measured the concentrations of seven bisphenols (BPAF, BPF, BPA, BPB, BPZ, BPS and BPAP) in these samples using gas chromatography coupled to tandem mass spectrometry. BPA, BPF and BPS were frequently found in spot samples (>80%), while bisphenol AP (BPAP) was detected in 43% of spot samples. Calculations of intra-class correlation coefficients (ICCs) showed that reproducibility of these four bisphenols was relatively poor (<0.01–0.200) but improved when concentrations were corrected for urine dilution using creatinine levels (0.128–0.401). Of these four bisphenols, BPF showed the best reproducibility (ICC 0.200–0.439) and BPS the most variability (ICC <0.01–0.128). In general, the within-participant variability of bisphenol levels was the largest contributor to the total variance (47–100%). We compared repeated first morning voids to 24 h pooled urine and found no significantly different concentrations for BPA, BPF, BPS, or BPAP. Levels of BPA and BPF differed significantly depending on the sampling time throughout the day. The findings in this study suggest that collecting multiple samples per participant over a few days, in predefined time windows throughout the day, could result in a more reliable estimation of internal exposure to bisphenols.

Agricultural plastic greenhouse (PG) production can extend the growing season of crops to satisfy domestic consumption in countries such as China. Workers in PGs have potential higher phthalate exposure risks than the general population as phthalate accumulation has been observed in greenhouse soil, air, and crops. To date, biomonitoring tests of phthalates for the working population have not been carried out. To address this shortage, we conducted a pilot study in Shaanxi Province, China, among 35 healthy PG workers by follow-up recording their seasonal dietary habits and work activities and urine sample collection and measurement between 2018 and 2019. The objectives were to uncover the association between phthalate metabolites and the population characteristics, seasonal and diurnal variations and causes, and to estimate exposure risks and contributions of exposure pathways from PG production systems. A total of 13 phthalate metabolite concentrations (Σ₁₃ phthalate metabolites) ranged from 102 to 781 (5th-95th) ng/mL (median: 300 ng/mL). Mono-n-butyl phthalate (MNBP) made up 51.3% of Σ₁₃ phthalate metabolites, followed by the sum of four di-2-ethylhexyl phthalate (DEHP) metabolites (24.2%), mono-2-isobutyl phthalate (MIBP) (13.4%), and mono-ethyl phthalate (MEP) (9.8%). The concentrations of MNBP and MIBP in summer were significantly higher than the levels in winter (p < 0.0001). A total of 62.3% of the PG worker population was shown to have exposure risks, and the proportion was as high as 79.4% in summer. Phthalate exposure of the workers from PG production systems constituted over 20% of the total creatinine-based daily intake, and consuming vegetables and fruit planted in PGs and inhalation in PGs were the two largest exposure pathways. Our findings demonstrate that it is important to protect workers in PGs from phthalate exposure risks, and phasing out the use of plastic materials containing phthalates in PGs is imperative, to guarantee food safety in PGs.

General population are concurrently and extensively exposed to many volatile organic compounds (VOCs), including some Group 1 human carcinogens, such as 1,3-butadiene. However, only a few studies assessed internal exposure levels of VOCs; particularly, very limited studies have examined associations between the urinary concentrations of multiple VOC metabolites (mVOCs) and oxidative stress biomarkers (OSBs) among the general population. In this study, 21 mVOCs and three OSBs including 8-hydroxy-2′-deoxyguanosine (8-OHdG; for DNA), 8-hydroxyguanosine (8-OHG; for RNA), and 4-hydroxy nonenal mercapturic acid (HNEMA; for lipid) were measured in 406 urine samples collected from 128 healthy adults during autumn and winter of 2018 in Wuhan, central China, including repeated samples taken in 3 d from 75 volunteers. Inter-day reproducibility for most mVOCs was good to excellent; urinary concentrations of mVOCs in winter were generally higher than those in autumn. Risk assessment was conducted by calculating hazard quotients for the parent compounds, and the results suggested that acrolein, 1,3-butadiene, and cyanide should be considered as high-priority hazardous ones for management. After false-discovery adjustment, 16 of the studied mVOCs were positively associated with 8-OHdG and 8-OHG (β values ranged from 0.04 to 0.48), and four mVOCs were positively associated with HNEMA (β values ranged from 0.21 to 0.78). Weighted quantile sum regression analyses were used to assess associations of mVOC mixture and OSBs, and we found significantly positive associations between the mixture index and OSBs, among which the strongest mVOC contributors for the associations were 2-methylhippuric acid for both DNA (20%) and RNA (17%) oxidative damage, and trans,trans-muconic acid (50%) for lipid peroxidation. This study firstly reported good to excellent short-term reproducibility, seasonal difference in autumn and winter, and possible health risk in urinary concentrations of multiple mVOCs among the general population.

Four most concerned heavy metal pollutants, arsenic, cadmium, lead, and mercury may share common mechanisms to induce metabolic syndrome (MetS). However, recent studies exploring the relationships between MetS and metal exposure presented inconsistent findings. We aimed to clarify the relationship between heavy metal exposure biomarkers and MetS using a meta-analysis and systematic review approach. Literature search was conducted in international and the Chinese national databases up to June 2020. Of selected studies, we extracted the relevant data and evaluated the quality of each study’s methodology. We then calculated the pooled effect sizes (ESs), standardized mean differences (SMDs), and their 95% confidence intervals (CIs) using a random-effect meta-analysis approach followed by stratification analyses for control of potential confounders. Involving 55,536 participants, the included 22 articles covered 52 observational studies reporting ESs and/or metal concentrations on specific metal and gender. Our results show that participants with MetS had significantly higher levels of heavy metal exposure [pooled ES = 1.16, 95% CI: 1.09, 1.23; n = 42, heterogeneity I² = 75.6%; and SMD = 0.22, 95% CI: 0.15, 0.29; n = 32, I² = 94.2%] than those without MetS. Pooled ESs in the subgroups stratified by arsenic, cadmium, lead, and mercury were 1.04 (95% CI: 0.97, 1.10; n = 8, I² = 61.0%), 1.10 (0.95, 1.27; 11, 45.0%), 1.21 (1.00, 1.48; 12, 82.9%), and 1.26 (1.06, 1.48; 11, 67.7%), respectively. Pooled ESs in the subgroups stratified by blood, urine, and the other specimen were 1.22 (95% CI: 1.08, 1.38; n = 26, I² = 75.8%), 1.06 (1.00, 1.13; 14, 58.1%), and 2.41 (1.30, 4.43; 2, 0.0%), respectively. In conclusion, heavy metal exposure was positively associated with MetS. Further studies are warranted to examine the effects of individual metals and their interaction on the relationship between MetS and heavy metals.