Particulate air pollution is a continuing challenge in China, and its adverse effects on chronic obstructive pulmonary disease (COPD) have been widely reported. However, epidemiological evidence on the associations between size-fractionated particle number concentrations (PNCs) and COPD mortality is limited. In this study, we utilized a time-series approach to investigate the associations between PNCs of particles at 0.25–10 μm in diameter and COPD mortality in Shanghai, China. Quasi-Poisson regression generalized additive models were applied to evaluate these associations, with adjustment of time trend, day of week, holidays, temperature and relative humidity. Stratification analyses were performed by season and gender. There were a total of 3238 deaths due to COPD during the study period. We found that daily COPD deaths were significantly associated with PNCs of particles <0.5 μm, and the magnitude of associations increased with decreasing particle size. An interquartile range (IQR) increase in PNC₀.₂₅—₀.₂₈, PNC₀.₂₈—₀.₃, PNC₀.₃—₀.₃₅, PNC₀.₃₅—₀.₄, PNC₀.₄—₀.₄₅ and PNC₀.₄₅—₋₀.₅ was associated with increments of 7.51% (95%CI: 2.45%, 12.81%), 7.22% (95%CI: 2.16%, 12.53%), 6.95% (95%CI: 1.81%, 12.35%), 6.26% (95%CI: 1.25%, 11.52%), 5.24% (95%CI: 0.56%, 10.13%) and 4.15% (95%CI: 0.14%, 8.32%), respectively. The associations remained robustness after controlling for the mass concentrations of gaseous air pollutants. In stratification analyses, significant associations between PNCs and COPD mortality were observed in the cold seasons, and in males. Our results suggested that particles <0.5 μm in diameter might be most responsible for the adverse effects of particulate air pollution on COPD mortality, and COPD patients are more susceptible to PM air pollution in the cold seasons, especially for males.

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.

In ecological risk assessment, acute to chronic ratio (ACR) uncertainty factors are routinely applied to acute mortality benchmarks to estimate chronic toxicity thresholds. To investigate variability of aquatic ACRs, we first compiled and compared 56 and 150 pairs of acute and subchronic/chronic growth/reproductive toxicity data for fishes (Pimephales promelas (53), Danio rerio (2), and Oryzias latipes (1)) and the crustacean Daphnia magna, respectively, for 172 chemicals with different modes of action (MOA). We found that there were only significant relationships between P. promelas acute median lethal concentrations and growth lowest-observed effect concentrations for class 1 (nonpolar narcosis) chemicals, though significant relationships were demonstrated for D. magna to all Verhaar et al. MOA classes (Class 1: nonpolar narcosis, Class 2: polar narcosis, Class 3: reactive chemicals, and Class 4: AChE inhibitors and estrogenics). Probabilistic ecological hazard assessment using chemical toxicity distributions was subsequently employed for each MOA class to estimate acute and chronic thresholds, respectively, to identify MOA and species specific ecological thresholds of toxicological concern. Finally, novel MOA and species specific ACRs using both chemical toxicity distribution comparison and individual ACR probability distribution approaches were identified using representative MOA and chemical categories. Our data-driven approaches and newly identified ACR values represent robust alternatives to application of default ACR values, and can also support future research and risk assessment and management activities for other chemical classes when toxicity information is limited for chemicals with specific MOAs within invertebrates and fish.

The active use of solid fossil fuels (coal) in the production of heat and electricity has led to significant pollution, climate change, environmental degradation, and an increase in morbidity and mortality. Many countries (in particular, European ones, China, Japan, the USA, Canada, etc.) have launched programs for using plant and agricultural raw materials to produce heat and electricity by burning them instead of or together with traditional fuels. It is a promising solution to produce slurry fuels, based on a mixture of coal processing, oil refining and agricultural waste. This paper presents the results of experimental research into the formation and assessment of the most hazardous emissions (sulfur and nitrogen oxides) from the combustion of promising coal slurry fuels with straw, sunflower and algae additives, i.e. the most common agricultural waste. A comparative analysis has been carried out to identify the differences in the concentrations of sulfur and nitrogen oxides from the combustion of typical coal, coal processing waste, as well as fuel slurries with and without plant additives. It has been shown that the concentration of sulfur and nitrogen oxides can be reduced by 62–87% and 12–57%, respectively, when using small masses of plant additives (no more than 10 wt%) and maintaining high combustion heat of the slurry fuel. However, the use of algae and straw in the slurry composition can increase the HCl emissions, which requires extra measures to fight corrosion. A generalizing criterion of slurry fuel vs. coal efficiency has been formulated to illustrate significant benefits of adding plant solid waste to coal-water slurries containing petrochemicals. Straw and sunflower waste (10 wt%) were found to be the best additives to reduce the air pollutant emissions.

While extreme high temperatures are an important aspect of global warming, their effects on organisms are relatively understudied, especially in ecotoxicology. Sequential exposure to heat spikes and pesticides is a realistic scenario as both are typically transient stressors and are expected to further increase in frequency under global warming. We tested the effects of exposure to a lethal heat spike and subsequently to an ecologically relevant lethal pulse exposure of the pesticide chlorpyrifos in the larvae of mosquito Culex pipiens. The heat spike caused direct and delayed mortality, and resulted in a higher heat tolerance and activity of acetylcholinesterase, and a lower fat content in the survivors. The chlorpyrifos exposure caused mortality, accelerated growth rate, and decreased the heat tolerance and the activity of acetylcholinesterase. The preceding heat spike did not change how chlorpyrifos reduced the heat tolerance. Notably, the preceding heat spike did lower the lethal effect of the pesticide, which makes an important novel finding at the interface of ecotoxicology and global change biology, and adds a new dimension to the “climate-induced toxicant sensitivity” (CITS) concept. This may be due to both survival selection and cross-tolerance, and therefore likely a widespread phenomenon. Our results emphasize the importance of including extreme high temperatures as an important transient global change stressor in ecotoxicology.

Per- and polyfluoroalkyl substances (PFASs) have been used for decades within industrial processes and consumer products, resulting in frequent detection within the environment. Using zebrafish embryos, we screened 38 PFASs for developmental toxicity and revealed that perfluorooctanesulfonamide (PFOSA) was the most potent developmental toxicant, resulting in elevated mortality and developmental abnormalities following exposure from 6 to 24 h post fertilization (hpf) and 6 to 72 hpf. PFOSA resulted in a concentration-dependent increase in mortality and abnormalities, with surviving embryos exhibiting a >12-h delay in development at 24 hpf. Exposures initiated at 0.75 hpf also resulted in a concentration-dependent delay in epiboly, although these effects were not driven by a specific sensitive window of development. We relied on mRNA-sequencing to identify the potential association of PFOSA-induced developmental delays with impacts on the embryonic transcriptome. Relative to stage-matched vehicle controls, these data revealed that pathways related to hepatotoxicity and lipid transport were disrupted in embryos exposed to PFOSA from 0.75 to 14 hpf and 0.75 to 24 hpf. Therefore, we measured liver area as well as neutral lipids in 128-hpf embryos exposed to vehicle (0.1% DMSO) or PFOSA from 0.75 to 24 hpf and clean water from 24 to 128 hpf, and showed that PFOSA exposure from 0.75 to 24 hpf resulted in a decrease in liver area and increase in yolk sac neutral lipids at 128 hpf. Overall, our findings show that early exposure to PFOSA adversely impacts embryogenesis, an effect that may lead to altered lipid transport and liver development.

In the previous publication “Can atmospheric pollution be considered a co-factor in extremely high level of SARS-CoV-2 lethality in Northern Italy?” Conticini et al. hypothesized that the surplus of lethality of the novel SARS-CoV-2 in Northern Italy may be at least in part explained by the evidence of highest pollution reported in this area, as both severe COVID-19 and smog exposure are correlated to an innate immune system hyper-activation with subsequent lung inflammation and injury. Since this hypothesis alone does not fully explain why specific subgroups of patients are at major risk, we hypothesized that obesity may be one of the links between COVID-19 severity and high level of air pollution. First, obesity is a predisposing factor for SARS-Cov-2 infection and worse COVID-19 outcomes, and unequivocal evidence demonstrated that fat mass excess is independently associated with several pulmonary diseases and lung inflammation. Moreover, it has been shown that obesity may intensify the detrimental effects of air pollution on the lungs, and this is not surprising if we consider that these conditions share an excessive activation of the immune system and a lung inflammatory infiltrate. Finally, fat mass excess has also been speculated to be itself a consequence of air pollutants exposure, which has been proved to induce metabolic disruption and weight gain in murine models. In conclusion, although many variables must be taken into account in the analysis of the pandemic, our observations suggest that obesity may act as effect modifier of smog-induced lung-injury, and the concomitant presence of these two factors could better explain the higher virulence, faster spread and greater mortality of SARS-CoV-2 in Northern Italy compared to the rest of the country.

Ecological risk assessment associated with seawater intrusions has been supported on the determination of lethal/sublethal effects following standard protocols that force exposure neglecting the ability of mobile organisms to spatially avoid salinized environments. Thus, this work aimed at assessing active emigration from climate change-caused seawater intrusion into freshwater habitats. To specific objectives were delineated: first, to compute median 12-h avoidance conductivities (AC₅₀,₁₂ₕ) for freshwater species, and second, to compare it with literature data (LC₅₀,₄₈ ₒᵣ ₉₆ₕ, EC₅₀,₆ ₒᵣ ₂₁d) to assess the relevance of the inclusion of stressor-driven emigration into risk assessment frameworks. Four standard test species, representing a broad range of ecological niches – Daphnia magna, Heterocypris incongruens, Danio rerio and Xenopus laevis – were selected. The salt NaCl was used as a surrogate of natural seawater to create the saline gradient, which was established in a 7-compartment system.At each specific LC₅₀, ₄₈ ₒᵣ ₉₆ₕ, the proportion of avoiders were well above 50%, ranging from 71 to 94%. At each LC₅₀, considering also avoiders, populations would decline by 85–97%. Furthermore, for D. magna and X. laevis it was noticed that at the lowest conductivities eliciting mortality, the avoidance already exceeded 50%.The results showed that the emigration from salinity-disturbed habitats exists and that can even be more sensitive than standard endpoints. Looking solely to standard endpoints involving forced exposure may greatly underestimate the risk of local population extinction, because habitat function can be severely disrupted, with subsequent stressor-driven emigration, before any adverse physiological effects at the organism level. Thus, the present study highlights the need to include non-forced exposure testing into ecological risk assessment, namely of salinity-menaced costal freshwaters.

The association between temperature and mortality has been widely reported. However, it remains largely unclear whether inflammation-related diseases, caused by excessive or inappropriate inflammatory reaction, may be affected by ambient temperature, particularly in low-income areas.To explore the association between ambient temperature and clinical visits for inflammation-related diseases in rural villages in the Ningxia Hui Autonomous Region, China, during 2012─2015.Daily data on inflammation-related diseases and weather conditions were collected from 258 villages in Haiyuan (161 villages) and Yanchi (97 villages) counties during 2012─2015. A Quasi-Poisson regression with distributed lag non-linear model was used to examine the association between temperature and clinical visits for inflammation-related diseases. Stratified analyses were performed by types of diseases including arthritis, gastroenteritis, and gynecological inflammations.During the study period, there were 724,788 and 288,965 clinical visits for inflammation-related diseases in Haiyuan and Yanchi, respectively. Both exposure to low (RR: 2.045, 95% CI: 1.690, 2.474) and high temperatures (RR: 1.244, 95% CI: 1.107, 1.399) were associated with increased risk of total inflammation-related visits in Haiyuan county. Low temperatures were associated with increased risks of all types of inflammation-related diseases in Yanchi county (RR: 4.344, 95% CI: 2.887, 6.535), while high temperatures only affected gastroenteritis (RR: 1.274, 95% CI: 1.040, 1.561). Moderate temperatures explained approximately 26% and 33% of clinical visits due to inflammation-related diseases in Haiyuan and Yanchi, respectively, with the burden attributable to cold exposure higher than hot exposure. The reference temperature values ranged from 17 to 19 in Haiyuan, and 12 to 14 in Yanchi for all types of clinical visits.Our findings add additional evidence for the adverse effect of suboptimal ambient temperature and provide useful information for public health programs targeting people living in rural villages.

The Deepwater Horizon (DWH) oil spill caused an estimated 100,000 bird mortalities. However, mortality estimates are often based on the number of visibly oiled birds and likely underestimate the true damage to avian populations as they do not include toxic effects from crude oil ingestion. Elevated susceptibility to disease has been postulated to be a significant barrier to recovery for birds that have ingested crude oil. Effective defense against pathogens involves integration of physiological and behavioral traits, which are regulated in-part by cytokine signaling pathways. In this study, we tested whether crude oil ingestion altered behavioral and physiological aspects of disease defense in birds. To do so, we used artificially weathered Mississippi Canyon 242 crude oil to orally dose zebra finches (Taeniopygia guttata) with 3.3 mL/kg or 10 mL/kg of crude oil or a control (peanut oil) for 14 days. We measured expression of cytokines (interleukin [IL]-1β, IL-6, IL-10) and proinflammatory pathways (NF-κB, COX-2) in the intestine, liver, and spleen (tissues that exhibit pathology in oil-exposed birds). We also measured heterophil:lymphocyte (H:L) ratio and complement system activity, and video-recorded birds to analyze sickness behavior. Finches that ingested crude oil exhibited tissue-specific changes in cytokine mRNA expression. Proinflammatory cytokine expression decreased in the intestine but increased in the liver and spleen. Birds exposed to crude oil had lower H:L ratios compared to the control on day 14, but there were no differences in complement activity among treatments. Additionally, birds exposed to 10 mL/kg crude oil had reduced activity, indicative of sickness behavior. Our results suggest cytokines play a role in mediating physiological and behavioral responses to crude oil ingestion. Although most avian population damage assessments focus on mortality caused by external oiling, crude oil ingestion may also indirectly affect survival by altering physiological and behavioral traits important for disease defense.