Harmful algal blooms (HABs) are recurrent in the NW Patagonia fjords system and their frequency has increased over the last few decades. Outbreaks of HAB species such as Alexandrium catenella, a causal agent of paralytic shellfish poisoning, and Protoceratium reticulatum, a yessotoxins producer, have raised considerable concern due to their adverse socioeconomic consequences. Monitoring programs have mainly focused on their planktonic stages, but since these species produce benthic resting cysts, the factors influencing cyst distributions are increasingly gaining recognition as potentially important to HAB recurrence in some regions. Still, a holistic understanding of the physico-chemical conditions influencing cyst distribution in this region is lacking, especially as it relates to seasonal changes in drivers of cyst distributions, as the characteristics that favor cyst preservation in the sediment may change through the seasons. In this study, we analyzed the physico–chemical properties of the sediment (temperature, pH, redox potential) and measured the bottom dissolved oxygen levels in a “hotspot” area of southern Chile, sampling during the spring and summer as well as the fall and winter, to determine the role these factors may play as modulators of dinoflagellate cyst distribution, and specifically for the cysts of A. catenella and P. reticulatum. A permutational analysis of variance (PERMANOVA) showed the significant effect of sediment redox conditions in explaining the differences in the cyst assemblages between spring-summer and fall-winter periods (seasonality). In a generalized linear model (GLM), sediment redox potential and pH were associated with the highest abundances of A. catenella resting cysts in the spring-summer, however it was sediment temperature that most explained the distribution of A. catenella in the fall-winter. For P. reticulatum, only spring-summer sediment redox potential and temperature explained the variation in cyst abundances. The implications of environmental (physico-chemical) seasonality for the resting cysts dynamics of both species are discussed.

The link between zinc exposure and glucose metabolism or the development of type 2 diabetes (T2D) is controversial, and underlying mechanisms are unclear. This study aimed to explore the associations of zinc exposure with glucose-insulin homeostasis traits and the long-term effects of zinc on the development of T2D, and further to estimate the potential roles of inflammation and oxidative damage in such relationships. We investigated 3890 urban adults from the Wuhan-Zhuhai cohort, and followed up every three years. Mixed linear model was applied to estimate dose-response associations between urinary zinc and glycemia traits [fasting plasma insulin (FPI), fasting plasma glucose (FPG), insulin resistance (homeostasis model assessment of insulin resistance, HOMA-IR), and β-cell dysfunction (homeostasis model assessment of β-cell function, HOMA-B)], as well as zinc and biomarkers for systemic inflammation (C-reactive protein) and oxidative damage (8-isoprostane and 8-hydroxy-2′-deoxyguanosine). Logistic regression model and Cox regression model were conducted to evaluate the relationships between urinary zinc and prevalence and incidence of T2D, respectively. We further performed mediation analysis to assess the roles of inflammation and oxidative damage biomarkers in above associations. At baseline, we observed significant dose-response relationships of elevated urinary zinc with increased FPI, FPG, HOMA-IR, and T2D prevalence and decreased HOMA-B, and such associations could be strengthened by increased C-reactive protein, 8-isoprostane, and 8-hydroxy-2′-deoxyguanosine. Elevated C-reactive protein significantly mediated 9.09% and 17.67% of the zinc-related FPG and HOMA-IR increments, respectively. In longitudinal analysis, a significantly positive association between urinary zinc and T2D incidence was observed among subjects with persistent high urinary zinc levels when compared with those with persistent low zinc levels. Our results suggested that high levels of zinc exposure adversely affected on glucose-insulin homeostasis and further contributed to increased risk of T2D cross-sectionally and longitudinally. Moreover, inflammatory response might play an important role in zinc-related glucose metabolic disorder.

Air pollution has been an important risk factor for female reproductive health. However, epidemiological evidence of ambient air pollution on the predictor for ovarian reserve (antral follicle count, AFC) is deficient. We aim to comprehensively evaluate the association of long-term exposure to ambient air pollution with AFC among women of reproductive age in Shanxi of north China. 600 women with spontaneous menstrual cycle, not using controlled ovarian stimulation, were enrolled in the retrospective study. Two distinct periods of antral follicle development were designed as exposure windows. Generalized linear model was employed to estimate the change of AFC associated with exposure of atmospheric pollutants (SO₂, NO₂, PM₁₀, PM₂.₅, CO and O₃). Stratification analysis based on age (<30, ≥30 years), university degree (yes, no), years of exposure (2013–2016, 2017–2019) and duration of infertility (<2, 2–5, >5 years) along with two pollutants model were employed to further illustrate the association. We found every 10 μg/m³ increase in SO₂ concentration level during the entire development stage of antral follicle was associated with a −0.01 change in AFC (95% confidence interval: −0.016, −0.002) adjusting for the confounders including age, BMI, parity and infertility diagnosis factors. The significant association of increased SO₂ level with decreased AFC was particularly observed during the early transition from primary follicle to preantral follicle stage by 10 μg/m³ increase in SO₂ exposure level with a −0.01 change (95% CI: -0.015, −0.002) in AFC. The negative association was pronounced among women aged ≥30 years old, and also significant in two pollutants model after adjusting the confounders. No significant associations between other air pollutants and AFC were observed. Our finding suggests that long-term exposure to air pollutant SO₂ is associated with lower AFC, raising our concern that atmospheric SO₂ exposure may have potential adverse impact on women ovarian reserve.

Microplastics (MPs) as carriers of various contaminants have attracted more attentions in water environments. However, the interactions between typical MPs and norfloxacin (NOR) in natural water environments were still not systematically studied. In this study, the adsorption of NOR onto four typical types of MPs (polyethylene (PE), polypropylene (PP), polystyrene (PS), and polyvinyl chloride (PVC)) was investigated in simulated natural water and real surface water, and the adsorption mechanisms were deeply explored to provide fundamental understandings of the MPs-NOR complicated pollution. The results showed that the kinetics of NOR onto all MPs obeyed pseudo-second-order model, and was greatly slowed down at lower temperature or higher salinity. The intrinsic structure and surface area of MPs played important roles in the adsorption behaviors of NOR on these four types of MPs. The adsorption isotherm of NOR onto all MPs could be well described by linear model, with the Kd values following the order of PVC > PS > PE > PP (i.e. 6.229–11.901 L/μg) in simulated natural water. However, in surface water the adsorption isotherms of NOR on all MPs could be well fitted by Freundlich model. For all MPs, the adsorption of NOR was quite pH-dependent due to the electrostatic interactions. Furthermore, the salinity and the presence of dissolved organic matter (DOM) had significantly hindered the NOR adsorption. More importantly, compared with adsorption behaviors in simulated natural water, the competition of coexisting substances such as cations and NOM for adsorption sites and higher water pH dramatically reduced the adsorption of NOR onto all types of MPs in Jiang'an River, with the reduction rate of 19.7–41.2%. Finally, the mechanism studies indicated that the electrostatic attractions played a key role in the adsorption of NOR onto MPs, and π-π, H-bonding, polar-polar, and Van Der Waals interactions were also involved in adsorption processes.

Previous studies assessing excessive proliferation of phytoplankton (EPP) in lakes are generally based on single investigation and focused on limited environmental factors; meanwhile, less attention has been paid to lakes susceptibility to EPP. Here, we identify the priority of lakes for EPP control in a basin by assessing EPP in multiple lakes and identify the key factors related to lakes’ vulnerability to EPP. Field measurements, as well as multi-source survey data acquisition were conducted for 63 shallow lakes in the middle-lower Yangtze River basin. Resource-use efficiency by phytoplankton (RUE) was then used to represent lake susceptibility to EPP. Generalized linear models were used to assess the relative importance of environmental factors for RUE. We found that most lakes (76.19 %) were not suitable for recreation, due to health concern attributed to irritative or allergenic risk caused by EPP. Phosphorus was the primary limiting nutrient for EPP (74.60 % of lakes) which should be limited to < 0.09 mg/L. The linear model that included latitude, particulate matter 10, and precipitation explained 27.60 % of the variation of RUETP among lakes. In contrast, the linear model that included ozone, Secchi depth, and wind speed explained 19.41 % of the variation of RUETN among lakes. The key factor related to RUETP and RUETN was particulate matter 10 and ozone, respectively, both of which potentially increase RUE or reflect it. Our results suggest that integrating multiple survey datasets is critical for lakes EPP assessment in a basin, while lakes impacted by air pollution are a high priority for EPP control.

The knowledge about the effects of environmental temperature on human epigenome is a potential key to understand the health impacts of temperature and to guide acclimation under climate change. We performed a systematic review on the epidemiological studies that have evaluated the association between environmental temperature and human epigenetic modifications. We identified seven original articles on this topic published between 2009 and 2019, including six cohort studies and one cross-sectional study. They focused on DNA methylation in elderly people (blood sample) or infants (placenta sample), with sample size ranging from 306 to 1798. These studies were conducted in relatively low temperature setting (median/mean temperature: 0.8–13 °C), and linear models were used to evaluate temperature-DNA methylation association over short period (≤28 days). It has been reported that short-term ambient temperature could affect global human DNA methylation. A total of 15 candidate genes (ICAM-1, CRAT, F3, TLR-2, iNOS, ZKSCAN4, ZNF227, ZNF595, ZNF597, ZNF668, CACNA1H, AIRE, MYEOV2, NKX1-2 and CCDC15) with methylation status associated with ambient temperature have been identified. DNA methylation on ZKSCAN4, ICAM-1 partly mediated the effect of short-term cold temperature on high blood pressure and ICAM-1 protein (related to cardiovascular events), respectively. In summary, epidemiological evidence about the impacts of environment temperature on human epigenetics remains scarce and limited to short-term linear effect of cold temperature on DNA methylation in elderly people and infants. More studies are needed to broaden our understanding of temperature related epigenetic changes, especially under a changing climate.

Exposure to environmental metals has been reported to be associated with airway inflammation. Fractional exhaled nitric oxide (FeNO) is an important inflammatory biomarker of the airway. However, the associations between metal exposures and FeNO change and the underlying mechanisms remain unclear. To investigate the associations between urinary metals and FeNO, and the potential role of Club cell secretory protein (CC16), a lung epithelial biomarker, in these associations. We conducted a cross-sectional study from the Wuhan-Zhuhai cohort and measured eight urinary metals, plasma CC16 and FeNO among 3067 subjects by using inductively coupled plasma-mass spectrometry, enzyme-linked immunosorbent assay kit and Nano Coulomb Nitric Oxide Analyzer, respectively. Mixed linear models were used to quantify dose-relationships between urinary metals and FeNO, as well as urinary metals and plasma CC16. The potential role of plasma CC16 in the associations between urinary metals and FeNO was estimated using mediationanalyses. After adjusting for covariates, one percent increase in urinary vanadium, nickel or antimony was associated with a respective 6.60% (95% CI: 3.52%, 9.68%), 2.18% (0.45%, 3.91%), 4.87% (1.47%, 8.27%) increase in FeNO level. The adverse associations were much stronger among participants with low concentration of plasma CC16 than those with high CC16 level. Moreover, plasma CC16 decreased monotonically with increasing quartiles of urinary vanadium, nickel or antimony. Mediation analyses found that CC16 mediated the associations between urinary metals and FeNO by 5.64%, 39.06% and 25.18% for vanadium, nickel and antimony respectively. CC16 plays an important role in airway inflammation. General population with lower plasma CC16 concentration is more likely to suffer from airway inflammation when exposed to high levels of vanadium, nickel or antimony.

This study assessed the impact on air quality and health risk by long-range transported (LRT) PM2.5-10- and PM2.5-bound metals and PAHs in Taipei City, Taiwan. Several methods with receptor aerosol measurements were used to quantify the effect of LRT. The hybrid single particle lagrangian integrated trajectory model (HYSPLIT) was used in conjunction with the potential source contribution function (PSCF) to distinguish the LRT aerosols. By using a general linear model (GLM) with a marginal mean and positive matrix fraction (PMF), this study also evaluated the annual increased level of LRT (AIRLRT) for each source contribution to the concentration and the resultant health risk of particle-bound metals and polycyclic aromatic hydrocarbons (PAHs). The LRT influenced fine-sized metals and PAHs rather than coarse-sized ones. We found that the level of PM2.5-bound toxic metals (Pb, Cd, and As) and PAHs (Benzo[a]pyrene and dibenzo[a,e]pyrene) could increase by 90% under the influence of LRT in 2014, while an AIRLRT value of 25% for the PM2.5 mass concentration was observed. Overall, the excess cancer risk (ECR) resulting from PM2.5-bound metal and PAH exposures was 6.40 × 10−5 in relation to coal combustions (20.7%), traffic-related emissions (59.7%) and re-suspended aerosols (19.6%). Among these contributors, LRT-related metals and PAHs in PM2.5 accounted for 51% of the total ECR.

A mass balance approach to quantify methane (CH4) emission of four co-located landfills by means of airborne measurements and dispersion modelling was proposed and assessed. By flying grids at different heights above the landfills, atmospheric CH4 densities and wind components were measured along the edges and inside the study atmospheric volume, in order to calculate mass flows in the along- and across-wind directions. A steady-state Gaussian dispersion model was applied to build the concentration fields associated to unit emission from each landfill, while the contribution of each one to the total emission was assessed using a General Linear Model approach, minimizing the difference between measured and modeled mass flows. Results showed that wind spatial and temporal variability is the main factor controlling the accuracy of the method, as a good agreement between measured and modeled mass flows was mainly found for flights made in steady wind conditions. CH4 emissions of the entire area ranged from 213.5 ± 33.5 to 317.9 ± 90.4 g s−1 with a mean value of 252.5 ± 54.2 g s−1. Contributions from individual sources varied from 17.5 to 40.1 g m−2 day−1 indicating a substantial heterogeneity of the different landfills, which differed in age and waste composition. The proposed method was validated against tower eddy covariance flux measurements made at one of the landfills, revealing an overall agreement within 20%.

Temperature has been associated with population health, but few studies have projected the future temperature-related years of life lost attributable to climate change. To project future temperature-related disease burden in Tianjin, we selected years of life lost (YLL) as the dependent variable to explore YLL attributable to climate change. A generalized linear model (GLM) and distributed lag non-linear model were combined to assess the non-linear and delayed effects of temperature on the YLL of non-accidental mortality. Then, we calculated the YLL changes attributable to future climate scenarios in 2055 and 2090. The relationships of daily mean temperature with the YLL of non-accident mortality were basically U-shaped. Both the daily mean temperature increase on high-temperature days and its drop on low-temperature days caused an increase of YLL and non-accidental deaths. The temperature-related YLL will worsen if future climate change exceeds 2 °C. In addition, the adverse effects of extreme temperature on YLL occurred more quickly than that of the overall temperature. The impact of low temperature was greater than that of high temperature. Men were vulnerable to high temperature compared with women. This analysis highlights that the government should formulate environmental policies to reach the Paris Agreement goal.