The molecular mechanism of evaluating 17β-estradiol (E₂)-induced toxicity in female Daphnia magna has not been determined. In this study, the transcriptome of D. magna was analyzed after exposure to three different concentrations (0, 10, and 100 ng L⁻¹) of E₂ at 3, 6, and 12 h. The results showed 351–17,221 significantly up-regulated and 505–10,282 significantly down-regulated genes (P < 0.05). Overall, the selected largest 10,282 (10 ng L⁻¹vs control at 12 h) down-regulated and 17,221 (100 vs 10 ng L⁻¹) up-regulated genes were identified; following annotation, pathways in cancer and RNA transport were found to be enriched according to the interaction network. Among all completed comparisons, KEGG pathways related to the immune system, cancer, disease infection, and active compound metabolism were identified by short time series expression miner analysis. A different set of genes fluctuated in a “U”-shaped pattern over time and at different concentrations of E₂, whereas some genes associated with disintoxication showed a reverse “U”-shaped response as E₂ administration was increased. These results suggest that E₂ exposure caused transcriptional changes in the immune system, disintoxication, disease prevention, and the protein degradation pathway.

Limited research has examined the impacts of coal mine fire smoke on human health. The aim of this study was to assess the association between prolonged smoke PM₂.₅ exposure from a brown coal mine fire that burned over a seven week period in 2014 and medications dispensed across five localities in South-eastern Victoria, Australia. Spatially resolved PM₂.₅ concentrations were retrospectively estimated using a dispersion model coupled with a chemical transport model. Data on medications dispensed were collected from the national Pharmaceutical Benefits Schedule database for 2013–2016. Poisson distributed lag time series analysis was used to examine associations between daily mine fire-related PM₂.₅ concentrations and daily counts of medications dispensed for respiratory, cardiovascular or psychiatric conditions. Factors controlled for included: seasonality, long-term trend, day of the week, maximum ambient temperature and public holidays. Positive associations were found between mine fire-related PM₂.₅ and increased risks of medications dispensed for respiratory, cardiovascular and psychiatric conditions, over a lag range of 3–7 days. A 10 μg/m³ increase in coal mine fire-related PM₂.₅ was associated with a 25% (95%CI 19–32%) increase in respiratory medications, a 10% (95%CI 7–13%) increase in cardiovascular medications and a 12% (95%CI 8–16%) increase in psychiatric medications dispensed. These findings have the potential to better prepare for and develop more appropriate public health responses in the event of future coal mine fires.

The use of an integrative molecular approach can actively improve the evaluation of environmental health status and impact of chemicals, providing the knowledge to develop sentinel tools that can be integrated in risk assessment studies, since gene and protein expressions represent the first response barriers to anthropogenic stress.This work aimed to determine the mechanisms of toxic action of a widely applied fungicide formulation (chlorothalonil), following a time series approach and using a soil model arthropod, Folsomia candida. To link effects at different levels of biological organization, data were collected on reproduction, gene expression and protein levels, in a time series during exposure to a natural soil.Results showed a mechanistic mode of action for chlorothalonil, affecting pathways of detoxification and excretion, immune response, cellular respiration, protein metabolism and oxidative stress defense, causing irregular cell signaling (JNK and NOD ½ pathways), DNA damage and abnormal cell proliferation, leading to impairment in developmental features such as molting cycle and reproduction. The omics datasets presented highly significant positive correlations between the gene expression levels at a certain time-point and the corresponding protein products 2–3 days later. The integrated omics in this study has provided useful insights into pesticide mechanisms of toxicity, evidencing the relevance of such analyses in toxicological studies, and highlighting the importance of considering a time-series when integrating these datasets.

As the frequency, intensity, and duration of heatwaves increases, emergency health serviceutilization, including ambulance service, has correspondingly increased across the world. The negative effects of air pollution on health complicate these adverse health effects. This research work is the first known study to analyze the joint effects of heatwaves and air quality on the ambulance service in Western Australia (WA). The main objective is to investigate the potential joint effects of heatwaves and air quality on the ambulance service for vulnerable populations in the Perth metropolitan area. A time series design was used. Daily data on ambulance callouts, temperature and air pollutants (CO, SO₂, NO₂, O₃, PM₁₀ and PM₂.₅) were collected for the Perth metropolitan area, WA from 2006 to 2015. Poisson regression modeling was used to assess the association between heatwaves, air quality, and ambulance callouts. Risk assessments on age, gender, socio-economic status (SES), and joint effects between heatwaves and air quality on ambulance callouts were conducted. The ambulance callout rate was higher during heatwave days (14.20/100,000/day) compared to non-heatwave days (13.95/100,000/day) with a rate ratio of 1.017 (95% confidence interval 1.012, 1.023). The ambulance callout rate was higher in males, people over 60 years old, people with low SES, and those living in coastal areas during period of heatwaves. Exposure to CO, SO₂, O₃ and PM₂.₅ increased risk on ambulance callouts and exposure to NO₂ showed joint effect with heatwave and increased risk of ambulance callouts by 3% after adjustment of all other risk factors. Ambulance callouts are an important indicator for evaluating heatwave-related emergency morbidity in WA. As the median concentrations of air pollutants in WA were lower than the Australian National Standards, the interactive effects of heatwaves and air quality on ambulance service need to be further examined, especially when air pollutants exceed the standards.

The increasing use of artificial light at night (ALAN) has led to exposure of freshwater ecosystems to light pollution worldwide. Simultaneously, the spectral composition of nocturnal illumination is changing, following the current shift in outdoor lighting technologies from traditional light sources to light emitting diodes (LED). LEDs emit broad-spectrum white light, with a significant amount of photosynthetically active radiation, and typically a high content of blue light that regulates circadian rhythms in many organisms. While effects of the shift to LED have been investigated in nocturnal animals, its impact on primary producers is unknown. We performed three field experiments in a lowland agricultural drainage ditch to assess the impacts of a transition from high-pressure sodium (HPS) to white LED illumination (color temperature 4000 K) on primary producers in periphyton. In all experiments, we compared biomass and pigment composition of periphyton grown under a natural light regime to that of periphyton exposed to nocturnal HPS or, consecutively, LED light of intensities commonly found in urban waters (approximately 20 lux). Periphyton was collected in time series (1–13 weeks). We found no effect of HPS light on periphyton biomass; however, following a shift to LED the biomass decreased up to 62%. Neither light source had a substantial effect on pigment composition. The contrasting effects of the two light sources on biomass may be explained by differences in their spectral composition, and in particular the blue content. Our results suggest that spectral composition of the light source plays a role in determining the impacts of ALAN on periphyton and that the ongoing transition to LED may increase the ecological impacts of artificial lighting on aquatic primary producers. Reduced biomass in the base of the food web can impact ecosystem functions such as productivity and food supply for higher trophic levels in nocturnally-lit ecosystems.

Propranolol (PRO), a human β-AR (β-adrenergic receptor) antagonist, is considered to result in specific effects in a non-target species, D. magna, based on our previous studies. The present study investigated the effects of β-AR agents, including an antagonist and agonist using pharmacologically relevant endpoints as well as a more holistic gene expression approach to reveal the impacts and potential mode of actions (MOAs) in the model non-target species. Results show that the responses in cardiac endpoints and gene expression in D. magna are partially similar but distinguishable from the observations in different organisms. No effect was observed on heart size growth in PRO and isoprenaline (ISO) exposure. The contraction capacity of the heart was decreased in ISO exposure, and the heart rate was decreased in PRO exposure. Time-series exposures showed different magnitudes of effect on heart rate and gene expression dependent on the type of chemical exposure. Significant enrichment of gene families involved in protein metabolism and biotransformation was observed within the differentially expressed genes, and we also observed differential expression in juvenile hormone-inducible proteins in ISO and PRO exposure, which is suspected of having endocrine disruption potential. Taken together, deviation between the effects of PRO and ISO in D. magna and other organisms suggests dissimilarity in MOAs or attributes of target bio-molecules between species. Additionally, PRO and ISO may act as endocrine disruptors based on the gene expression observation. Results in the present study confirm that it is challenging to predict ecological impact of active pharmaceutical ingredients (APIs) based on the available data acquired through human-focused studies. Furthermore, the present study provided unique data and a case study on the impact of APIs in a non-target organism.

Substantial evidence has linked short-term exposure to ambient fine particulate matter (PM2.5) with increased cardiovascular mortality, however, the specific chemical constituent and emission source responsible for this effect remained largely unclear. A time series Poisson model was employed to quantify the association of cardiovascular mortality with two sets of shipping pollution emission: nickel (Ni), vanadium (V) (the indices of shipping emission) and estimated shipping emission using a source apportionment approach in Guangzhou, China in 2014. We observed that Ni, V, and estimated shipping emission in PM2.5 were associated with increased cardiovascular mortality, an inter-quartile range (IQR) increase in lag2 Ni was associated with 4.60% (95% CI: 0.14%, 9.26%) increase in overall cardiovascular mortality, and 13.35% (95% CI: 5.54%, 21.75%) increase in cerebrovascular mortality; each IQR increase of lag1 V was correlated with 6.01% (95% CI: 1.83%, 10.37%) increase in overall cardiovascular mortality, and 11.02% (95% CI: 3.15%, 19.49%) increase in cerebrovascular mortality; and each IQR increase in lag1 shipping emission was associated with 5.55% (95% CI: 0.78%, 10.54%) increase in overall cardiovascular mortality, and 10.39% (95% CI: 1.43%, 20.14%) increase in cerebrovascular mortality. The results remained robust to adjustment for PM2.5 mass and gaseous air pollutants. This study suggests that shipping emission is an important detrimental factor of cardiovascular mortality, and should be emphasized in air pollution control and management in order to protect the public health in Guangzhou, China.

Previous studies have suggested that short-term exposure to ambient air pollution was associated with pediatric hospital admissions and emergency room visits for certain respiratory diseases; however, there is limited evidence on the association between short-term air pollution exposure and pediatric outpatient visits. Our aim was to quantitatively assess the short-term effects of ambient air pollution on pediatric outpatient visits for respiratory diseases. We conducted a time-series study in Yichang city, China between Jan 1, 2014 and Dec 31, 2015. Daily counts of pediatric respiratory outpatient visits were collected from 3 large hospitals, and then linked with air pollution data from 5 air quality monitoring stations by date. We used generalized additive Poisson models to conduct linear and nonlinear exposure-response analyses between air pollutant exposures and pediatric respiratory outpatient visits, adjusting for seasonality, day of week, public holidays, temperature, and relative humidity. Each interquartile range (IQR) increase in PM2.5 (lag 0), PM10 (lag 0), NO2 (lag 0), CO (lag 0), and O3 (lag 4) concentrations was significantly associated with a 1.91% (95% CI: 0.60%, 3.23%), 2.46% (1.09%, 3.85%), 1.88% (0.49%, 3.29%), 2.00% (0.43%, 3.59%), and 1.91% (0.45%, 3.39%) increase of pediatric respiratory outpatient visits, respectively. Similarly, the nonlinear exposure-response analyses showed monotonic increases of pediatric respiratory outpatient visits by increasing air pollutant exposures, though the associations for NO2 and CO attenuated at higher concentrations. These associations were unlikely modified by season. We did not observe significant association for SO2 exposure. Our results suggest that short-term exposures to PM2.5, PM10, NO2, CO, and O3 may account for increased risk of pediatric outpatient visits for respiratory diseases, and emphasize the needs for reduction of air pollutant exposures for children.

Ambient air pollution ranks high among the risk factors that increase the global burden of disease. Previous studies focused on assessing mortality risk and were sparsely performed in populous developing countries with deteriorating environments. We conducted a time-series study to evaluate the air pollution-associated years of life lost (YLL) and mortality risk and to identify potential modifiers relating to the season and demographic characteristics. Using linear (for YLL) and Poisson (for mortality) regression models and controlling for time-varying factors, we found that an interquartile range (IQR) increase in a three-day average cumulative (lag 0–2 day) concentrations of PM2.5, PM10, NO2 and SO2 corresponded to increases in YLL of 12.09 (95% confidence interval [CI]: 2.98–21.20), 13.69 (95% CI: 3.32–24.07), 26.95 (95% CI: 13.99–39.91) and 24.39 (95% CI: 8.62–40.15) years, respectively, and to percent increases in mortality of 1.34% (95% CI: 0.67–2.01%), 1.56% (95% CI: 0.80–2.33%), 3.36% (95% CI: 2.39–4.33%) and 2.39% (95% CI: 1.24–3.55%), respectively. Among the specific causes of death, cardiovascular and respiratory diseases were positively associated with gaseous pollutants (NO2 and SO2), and diabetes was positively correlated with NO2 (in terms of the mortality risk). The effects of air pollutants were more pronounced in the cool season than in the warm season. The elderly (>65 years) and females were more vulnerable to air pollution. Studying effect estimates and their modifications by using YLL to detect premature death should support implementing health risk assessments, identifying susceptible groups and guiding policy-making and resource allocation according to specific local conditions.

In April of 2010, the Macondo well blowout in the northern Gulf of Mexico resulted in an unprecedented release of oil into the water column at a depth of approximately 1500 m. A time series of surface and subsurface sediment samples were collected to the northwest of the well from 2010 to 2013 for molecular biomarker and bulk carbon isotopic analyses. While no clear trend was observed in subsurface sediments, surface sediments (0–3 cm) showed a clear pattern with total concentrations of n-alkanes, unresolved complex mixture (UCM), and petroleum biomarkers (terpanes, hopanes, steranes) increasing from May to September 2010, peaking in late November 2010, and strongly decreasing in the subsequent years. The peak in hydrocarbon concentrations were corroborated by higher organic carbon contents, more depleted Δ14C values and biomarker ratios similar to those of the initial MC252 crude oil reported in the literature. These results indicate that at least part of oil discharged from the accident sedimented to the seafloor in subsequent months, resulting in an apparent accumulation of hydrocarbons on the seabed by the end of 2010. Sediment resuspension and transport or biodegradation may account for the decrease in sedimented oil quantities in the years following the Macondo well spill.