Thallium, a highly toxic heavy metal and priority pollutant, has been widely reported to cause neurodevelopmental toxicity in animals. However, accessible epidemiological studies concerning the neurodevelopmental toxicity of early-life thallium exposure in humans are limited. In a prospective birth cohort including 2164 mother-child pairs, we explored the effect of prenatal serum thallium exposure on cognitive development among preschool-aged children born in Ma'anshan, Anhui, China. Serum thallium concentrations were measured in the first trimester, second trimester, third trimester, and cord blood by inductively coupled plasma mass spectrometry (ICP-MS). Child cognitive development was appraised by the Chinese version of the Wechsler Preschool and Primary Scale of Intelligence-Fourth Edition (WPPSI-IV) at 4.5 years old. Multiple informants generalized estimating equations (GEEs) were fit to jointly estimate the association between the four repeated measurements of thallium concentrations and the preschool-aged children's cognitive test scores. After adjusting for potential confounders, the visual spatial index (VSI) was 1.45 points lower in the highest tertile of serum thallium during the first trimester than in the lowest tertile (p for trend = 0.04). Moreover, children in the highest tertile of serum thallium during the third trimester had a significantly lower full-scale intelligence quotient (FSIQ) (β = −1.51, 95% CI: −2.68, −0.35), VSI (β = −1.79, 95% CI: −3.16, −0.42), fluid reasoning index (FRI) (β = −1.41, 95% CI: −2.73, −0.10), and processing speed index (PSI) (β = −1.47, 95% CI: −2.71, −0.24) scores than the children in the lowest tertile. When performing stratified analysis by child sex, the associations of first- and third-trimester thallium concentrations with cognitive test scores were more prominent in boys than in girls. Our findings revealed that maternal serum thallium exposure during the first and third trimesters, but not other periods, had detrimental effects on preschoolers' cognitive development, and these effects showed sex differences.

As the underlying mechanisms of the adverse effects of cold spells on cardiac events are not well understood, we explored the effects of cold spells on plasma viscosity, a blood parameter linked to cardiovascular disease. This cross-sectional study involved 3622 participants from the KORA S1 Study (1984–1985), performed in Augsburg, Germany. Exposure data was obtained from the Bavarian State Office for the Environment. Cold spells were defined as two or more consecutive days with daily mean temperatures below the 3ʳᵈ, 5ᵗʰ, or 10ᵗʰ percentile of the distribution. The effects of cold spells on plasma viscosity were explored by generalized additive models with distributed lag nonlinear models (DLNM). We estimated cumulative effects at lags 0–1, 0–6, 0–13, 0–20, and 0–27 days separately. Cold spells (mean temperature <3ʳᵈ, <5ᵗʰ or <10ᵗʰ percentile) were significantly associated with an increase in plasma viscosity with a lag of 0–1 days [%change of geometric mean (95% confidence interval): 1.35 (0.06–2.68), 1.35 (0.06–2.68), and 2.49 (0.34–4.69), respectively], and a lag of 0–27 days [18.81 (8.97–29.54), 17.85 (8.29–28.25), and 7.41 (3.35–11.0), respectively]. For the analysis with mean temperature <3ʳᵈ or 10ᵗʰ percentile, we also observed significant associations at lag 0–20 days [8.34 (0.43–16.88), and 4.96 (1.68, 8.35), respectively]. We found that cold spells had significant immediate and longer lagged effects on plasma viscosity. This finding supports the complex interplay of multiple mechanisms of cold on adverse cardiac events and enriches the knowledge about how cold exposure acts on the human body.

Previous studies have indicated that maternal exposure to particles with aerodynamic diameter <2.5 μm (PM₂.₅) is associated with adverse birth outcomes. However, the critical exposure windows remain inconsistent. A retrospective cohort study was conducted in Huai River Basin, Henan, China during 2013–2018. Daily PM₂.₅ concentration was collected using Chinese Air Quality Reanalysis datasets. We calculated exposures for each participant based on the residential address during pregnancy. Binary logistic regression was used to examine the trimester-specific association of PM₂.₅ exposure with preterm birth (PTB), low birth weight (LBW) and term LBW (tLBW), and we further estimated monthly and weekly association using distributed lag models. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated for each 10 μg/m³ increase in PM₂.₅ exposure. Stratified analyses were performed by maternal age, infant gender, parity, and socioeconomic status (SES). In total, 196,780 eligible births were identified, including 4257 (2.2%) PTBs, 3483 (1.8%) LBWs and 1770 (0.9%) tLBWs. Maternal PM₂.₅ exposure during the second trimester were associated with the risk of PTB and LBW. At the monthly level, the PTB and LBW risks were associated with PM₂.₅ exposure mainly in the 4th -6th month. By estimating the weekly-specific association, we observed that critical exposure windows of PM₂.₅ exposure and PTB were in the 18th- 27th gestational weeks. Stronger associations were found in younger, multiparous mothers and those with a female baby and in low SES. In conclusion, the results indicate that maternal PM₂.₅ exposure during the second trimester was associated with PTB and LBW. Younger, multiparous mothers and those with female babies and in low SES were susceptible.

Living in walkable neighborhoods has been reported to be associated with a lower risk of cardiovascular disease. Features of walkable neighborhoods, however, may be related to particulate matter with an aerodynamic diameter ≤2.5 μm (PM₂.₅), which could increase risk of cardiovascular disease. The interaction effect between walkability and PM₂.₅ on risk of ischemic stroke remains to be elucidated. In this study, we recruited a total of 27,375 participants aged ≥40 years from Yinzhou District, Ningbo, Zhejiang Province, China to investigate the associations of walkability and PM₂.₅ with risk of ischemic stroke. We used amenity categories and decay functions to evaluate walkability and high-spatiotemporal-resolution land-use regression models to assess PM₂.₅ concentrations. We used Cox proportional hazards regression models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). During a median follow-up of 4.08 years, we identified a total of 637 incident cases of ischemic stroke in the entire cohort. Higher walkability was associated with a lower risk of ischemic stroke (quartile, Q4 vs. Q1 walkability: HR = 0.59, 95% CI: 0.47–0.75), whereas PM₂.₅ was positively associated with risk of ischemic stroke (Q4 vs. Q1 PM₂.₅: HR = 1.70, 95% CI: 1.29–2.25). Furthermore, we observed a significant interaction between walkability and PM₂.₅ on risk of ischemic stroke. Walkability was inversely associated with risk of ischemic stroke at lower PM₂.₅ concentrations, but this association was attenuated with increasing PM₂.₅ concentrations. Although walkable neighborhoods appear to decrease the risk of ischemic stroke, benefits may be offset by adverse effects of PM₂.₅ exposure in the most polluted areas. These findings are meaningful for future neighborhood design, air pollution control, and stroke prevention.

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.

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.

Allergic diseases have been one of the leading causes of chronic disorders in the United States. Animal studies have suggested that exposures to perchlorate, nitrate, and thiocyanate could induce allergic inflammation. However, the associations have not been examined among general populations. Here, we investigated data of 7030 participants aged ≥6 years from the National Health and Nutritional Examination Survey (NHANES) 2005–2006. Urinary levels of perchlorate, nitrate, and thiocyanate were measured by ion chromatography combined with electrospray tandem mass spectrometry. Information on allergic symptoms (hay fever, allergy, rash, sneeze, wheeze, eczema, and current asthma) was collected by questionnaire. Allergic sensitization was defined by a concentration ≥150 kU/L for total immunoglobulin E (IgE) levels. The associations were estimated using multivariate-adjusted logistic regression models. A positive association was observed for urinary nitrate and eczema (p < 0.001 for the trend). Compared with quartile 1 (lowest quartile), the odds ratios of eczema with 95% confidence intervals [ORs (95% CIs)] from quartiles 2 to 4 were 1.72 (95% CI, 1.41, 2.09), 1.94 (1.53, 2.47) and 2.10 (1.49, 2.97) for urinary nitrate. In addition, urinary thiocyanate was positively related to sneeze (ORQ₄ ᵥₛ. Q₁: 1.25, 95% CI: 1.01, 1.55; p = 0.015 for the trend). However, urinary perchlorate was not correlated with any allergic-related outcome. Additionally, the associations were different among subgroups in a four-level polytomous model. Thus, our results suggested that exposures to nitrate and thiocyanate may be associated with allergic symptoms. Further investigations are warranted to concentrate on the practical strategies to monitor exposure levels and the latent mechanisms of the relationship between exposure and allergy.

In the context of global climate change, far less is known about the impact of long-term temperature variability (TV), especially in developing countries. The current study aimed to estimate the effect of long-term TV on the incidence of cardiovascular disease (CVD) in China. A total of 23,721 individuals with a mean age of 56.15 years were enrolled at baseline from 2012 to 2016 and followed up during 2017–2019. TV was defined as the standard deviation of daily temperatures during survey years and was categorized into tertiles (lowest≤ 8.78 °C, middle = 8.78–10.07 °C, highest ≥ 10.07 °C). The Cox proportional hazards regression was used to estimate the multivariable-adjusted hazard ratio (HR) between TV and CVD. During the median follow-up of 4.65 years, we ascertained 836 cases of incident CVD. For per 1 °C increase in TV, there was a 6% increase of CVD (HR = 1.06 [95% confidence interval (CI): 1.01–1.11]). A significant positive trend was observed between CVD risk and increasing levels of TV compared to the lowest tertile [HR = 1.34 (95% CI: 1.13–1.59) for the medium tertile, HR = 1.72 (95% CI: 1.35–2.19) for the highest tertile, Pₜᵣₑₙd < 0.001]. Exposure to high TV would lose 2.11 disease-free years for the population aged 35–65 years and 66 CVD cases (or 7.95% cases) could been attributable to TV higher than 8.11 °C in the current study. The current findings suggested that long-term TV was associated with a higher risk of CVD incidence, it is needed to reduce the TV-related adverse health effect.

Both air pollution and dyslipidemias contributed to large number of deaths and disability-adjusted life lost years. Long-term air pollution exposure was related to changed blood lipids and risk of dyslipidemias. This study was designed to evaluate relationships between air pollutants, blood lipids and prevalence of dyslipidemias in a Chinese rural population exposed to high-level air pollution based on baseline data of The Henan Rural Cohort study. An amount of 39,057 participants from rural areas in China were included. The 3-year average exposure of air pollutants (PM2.5, PM10, NO2) was estimated by a spatiotemporal model. Logistic and linear regression models were employed to explore relationships between air pollutants, blood lipids (TC, TG, HDL-C and LDL-C) and prevalence of dyslipidemias. The three-year concentration of PM2.5, PM10 and NO2 was 72.8 ± 2.3 μg/m3, 131.5 ± 5.7 μg/m3and 39.1 ± 3.1 μg/m3, respectively. Overall, increased air pollution exposure was related to increased TC and LDL-C, while decreased TG and HDL-C. Each 1-μg/m3 increment of PM2.5 was related to 0.10% (0.07%–0.19%) increase in TC, 0.63% (0.50%–0.77%) increase in LDL-C, 2.93% (2.70%–3.16%) decrease in TG, 0.49% (0.38%–0.60%) decrease in HDL-C; and 5.7% (95%CI: 3.7%–7.6%), 4.0% (95%CI: 2.1%–6.0%) and 3.8% (95%CI: 2.5%–5.1%) increase in odds for hypercholesterolemia, hyperbetalipoproteinemia and hypoalphalipoproteinemia, respectively. Stronger associations were found in male and older participants. Findings suggest that air pollutants were associated with changed blood lipid levels and higher risk of dyslipidemias among rural population. Male and elder people should pay more attention to personal safety protection.

Telomere length (TL) is an index of cellular aging and can predict the incidences of many age-related diseases. Change of TL might be affected by environmental pollution and individual's genetic background. In this cohort study, we aimed to evaluate the associations between polycyclic aromatic hydrocarbons (PAHs) exposure and longitudinal TL shortening, and investigate whether genetic variations in TERT-CLPTM1L can modify these associations. We measured the baseline concentrations of twelve urinary PAH metabolites and genotyped six variants at TERT-CLPTM1L among 1243 coke-oven workers. The relative leukocyte TL was detected in both baseline and follow-up (4 years later) visits. The TL shortening were estimated by TL decline and TL ratio. We found that the urinary level of 1-hydroxypyrene (1-OHP) had significant dose-response relationships with increased TL decline [β(95%CI) = 0.078(0.023, 0.133), P = 0.005] and TL ratio [β(95%CI) = 0.096(0.037, 0.155), P = 0.002]. Besides, urinary 1-hydroxynaphthalene (1-OHNa) was marginally dose-related with elevated TL decline [β(95%CI) = 0.053(-0.001, 0.107), P = 0.055] and TL ratio [β(95%CI) = 0.057(-0.002, 0.116), P = 0.058]. Analyses of TERT-CLPTM1L variants showed that the rs401681 and rs465498 could modify the effect of 1-OHP on increasing TL decline (Pᵢₙₜₑᵣₐcₜᵢₒₙ = 0.012 and 0.035, respectively) and TL ratio (Pᵢₙₜₑᵣₐcₜᵢₒₙ = 0.014 and 0.067, respectively), which were pronounced among rs401681TT and rs465498CC carriers, but not seen among rs401681TC + CC and rs465498CT + TT carriers. In conclusion, elevated exposure to PAHs can accelerate the TL shortening and this effect can be modified by TERT-CLPTM1L variants. These results may add potential evidence for gene-environment interactions on dynamic changes of telomere length. Further studies are warranted to validate these findings and uncover the underlying mechanisms.