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.

The potential leakage from marine CO2 storage sites is of increasing concern, but few studies have evaluated the probable adverse effects on marine organisms. Fish, one of the top predators in marine environments, should be an essential representative species used for water column toxicity testing in response to waterborne CO2 exposure. In the present study, we conducted fish life cycle toxicity tests to fully elucidate CO2 toxicity mechanism effects. We tested sub-lethal and lethal toxicities of elevated CO2 concentrations on marine medaka (Oryzias melastigma) at different developmental stages. At each developmental stage, the test species was exposed to varying concentrations of gaseous CO2 (control air, 5%, 10%, 20%, and 30%), with 96 h of exposure at 0–4 d (early stage), 4–8 d (middle stage), and 8–12 d (late stage). Sub-lethal and lethal effects, including early developmental delays, cardiac edema, tail abnormalities, abnormal pigmentation, and mortality were monitored daily during the 14 d exposure period. At the embryonic stage, significant sub-lethal and lethal effects were observed at pH < 6.30. Hypercapnia can cause long-term and/or delayed developmental embryonic problems, even after transfer back to clean seawater. At fish juvenile and adult stages, significant mortality was observed at pH < 5.70, indicating elevated CO2 exposure might cause various adverse effects, even during short-term exposure periods. It should be noted the early embryonic stage was found more sensitive to CO2 exposure than other developmental stages of the fish life cycle. Overall, the present study provided baseline information for potential adverse effects of high CO2 concentration exposure on fish developmental processes at different life cycle stages in marine ecosystems.

There is increasing concern that standard laboratory toxicity tests may be misleading when assessing the impact of toxicants, because they lack ecological realism. Both warming and biotic interactions have been identified to magnify the effects of toxicants. Moreover, while biotic interactions may change the impact of toxicants, toxicants may also change the impact of biotic interactions. However, studies looking at the impact of biotic interactions on the toxicity of pesticides and vice versa under warming are very scarce. Therefore, we tested how warming (+4 °C), intraspecific competition (density treatment) and exposure to the pesticide chlorpyrifos, both in isolation and in combination, affected mortality, cannibalism, growth and heat tolerance of low- and high-latitude populations of the damselfly Ischnura elegans. Moreover, we addressed whether toxicant exposure, potentially in interaction with competition and warming, increased the frequency of autotomy, a widespread antipredator mechanism. Competition increased the toxicity of chlorpyrifos and made it become lethal. Cannibalism was not affected by chlorpyrifos but increased at high density and under warming. Chlorpyrifos reduced heat tolerance but only when competition was high. This is the first demonstration that a biotic interaction can be a major determinant of ‘toxicant-induced climate change sensitivity’. Competition enhanced the impact of chlorpyrifos under warming for high-latitude larvae, leading to an increase in autotomy which reduces fitness in the long term. This points to a novel pathway how transient pesticide pulses may cause delayed effects on populations in a warming world. Our results highlight that the interplay between biotic interactions and toxicants have a strong relevance for ecological risk assessment in a warming polluted world.

Adult coho salmon (Oncorhynchus kisutch) prematurely die when they return from the ocean to spawn in urban watersheds throughout northwestern North America. The available evidence suggests the annual mortality events are caused by toxic stormwater runoff. The underlying pathophysiology of the urban spawner mortality syndrome is not known, and it is unclear whether closely related species of Pacific salmon are similarly at risk. The present study co-exposed adult coho and chum (O. keta) salmon to runoff from a high traffic volume urban arterial roadway. The spawners were monitored for the familiar symptoms of the mortality syndrome, including surface swimming, loss of orientation, and loss of equilibrium. Moreover, the hematology of both species was profiled by measuring arterial pH, blood gases, lactate, plasma electrolytes, hematocrit, and glucose. Adult coho developed behavioral symptoms within a few hours of exposure to stormwater. Various measured hematological parameters were significantly altered compared to coho controls, indicating a blood acidosis and ionoregulatory disturbance. By contrast, runoff-exposed chum spawners showed essentially no indications of the mortality syndrome, and measured blood hematological parameters were similar to unexposed chum controls. We conclude that contaminant(s) in urban runoff are the likely cause of the disruption of ion balance and pH in coho but not chum salmon. Among the thousands of chemicals in stormwater, future forensic analyses should focus on the gill or cardiovascular system of coho salmon. Because of their distinctive sensitivity to urban runoff, adult coho remain an important vertebrate indicator species for degraded water quality in freshwater habitats under pressure from human population growth and urbanization.

Ambient ozone is one of the most important air pollutants with respect to its impacts on human health and its increasing concentrations globally. However, studies which explored the burden of ozone pollution on chronic obstructive pulmonary disease (COPD) and estimated the relevant economic loss were rare.We explored the relationships between ambient ozone exposure and years of life lost (YLL) from COPD mortality and estimated the relevant economic loss in Ningbo, in the Yangtze River Delta of China, 2011–2015.A time-series study was conducted to explore the effects of ozone on YLL from COPD. Seasonal stratified analyses were performed, and the effect modification of demographic factors was estimated. In addition, the related economic loss was calculated using the method of the value per statistical life year (VSLY).Averaged daily mean maximum 8-h average ozone concentration was 40.90 ppb in Ningbo, China, 2011–2015. The effect of short term ambient ozone exposure on COPD YLL was more pronounced in the cool season than in the warm season, with 10 ppb increment of ozone corresponding to 7.09(95%CI: 3.41, 10.78) years increase in the cool season and 0.31 (95%CI: −2.15, 2.77) years change in the warm season. The effect was higher in the elderly than the young. Economic loss due to excess COPD YLL related to ozone exposure accounted for 7.30% of the total economic loss due to COPD YLL in Ningbo during the study period.Our findings highlight that ozone exposure was related to tremendous disease burden of COPD in Ningbo, China. The effects were more pronounced in the cool season, and the elderly were more susceptible populations.

Osteoporosis or enhanced bone loss is one of the most commonly occurring bone conditions in the world, responsible for higher incidence of fractures leading to increased morbidity and mortality in adults. Bone loss is affected by various environmental factors including diet, age, drugs, toxins etc. Microcystins are toxins produced by cyanobacteria with microcystin-LR being the most abundantly found around the world effecting both human and animal health. The present study demonstrates that MC-LR treatment induces bone loss and impairs both trabecular and cortical bone microarchitecture along with decreasing the mineral density and heterogeneity of bones in mice. This effect of MC-LR was found due to its immunomodulatory effects on the host immune system, wherein MC-LR skews both T cell (CD4+ and CD8+ T cells) and B cell populations in various lymphoid tissues. MC-LR further was found to significantly enhance the levels of osteoclastogenic cytokines (IL-6, IL-17 and TNF-α) along with simultaneously decreasing the levels of anti-osteoclastogenic cytokines (IL-10 and IFN-γ). Taken together, our study for the first time establishes a direct link between MC-LR intake and enhanced bone loss thereby giving a strong impetus to the naïve field of “osteo-toxicology”, to delineate the effects of various toxins (including cyanotoxins) on bone health.

How to evaluate the ecological risk of transgenic technology is a focus of scientists because of the safety concerns raised by genetically modified (GM) organisms. Nevertheless, most studies are based on individual chemicals and always analyze the GM organism as a type of toxicant. In this study, we changed the approach and used GM organisms as the test objects with normal chemical exposure. Three types of chemicals (two substituted phenols, 4-chlorophenol and 4-nitrophenol; two ionic liquids, 1-butylpyridinium chloride and 1-butylpyridinium bromide; two pesticides, dichlorvos and glyphosate) were used to construct a six-component mixture system. The lethality to wild-type (N2) and sod-3::GFP (SOD-3) Caenorhabditis elegans was determined when they were exposed to the same mixture system after 12 and 24 h. The results showed that the pEC50 values of all of the single chemicals on SOD-3 were greater than those on N2 at 24 h. The toxicities of the single chemicals and nine mixture rays on the two strains increased with time. Notably, we discovered a significant difference between the two strains; time-dependent synergism occurred in mixtures on N2, but time-dependent antagonism occurred in mixtures on SOD-3. Finally, the strength of the synergism or antagonism turned to additive action on the two strains as the exposure time increased. These findings illustrated that the GM factor of the nematode influenced the mixture toxicological interaction at some exposure times. Compared with N2, SOD-3 were more sensitive to stress or toxic reactions. Therefore, the influence of the GM factor on mixture toxicological interactions in environmental risk assessment must be considered.

The environmental contaminant, especially pesticides, threatened the amphibian population. In this assay, the enantioselective behavior of cyproconazole on Rana nigromaculata was studied. We found LC50 (lethal concentration causing 50% mortality) of 4-enantiomers was nearly twice as 3-enantiomers in 96 h acute toxicity test. Besides, the significant considerable variation of oxidative stress and LDH (lactic dehydrogenase) induced by the four enantiomers indicated that cyproconazole could enantioselectively affect enzymes in tadpoles. Bioaccumulation experiments showed the order of cyproconazole in the tadpoles was 4-enantiomers>3- enantiomers>2- enantiomers>1- enantiomers during the exposure for 28d. In tissue distribution test, cyproconazole was formed and accumulated in order of 4-enantiomers>2-enantiomers>3- enantiomers>1- enantiomers, except that in the gut. During the elimination experiment, cyproconazole was rapidly eliminated by 95% within the only 24 h. These results suggested that the influence of enantioselective behavior should consider when assessing ecological risk of chiral pesticides to amphibians.

Global burden of disease estimates reveal that people in Nigeria are living shorter lifespan than the regional or global average life expectancy. Ambient air pollution is a top risk factor responsible for the reduced longevity. But, the magnitude of the loss or the gains in longevity accruing from the pollution reductions, which are capable of driving mitigation interventions in Nigeria, remain unknown. Thus, we estimate the loss, and the gains in longevity resulting from ambient PM2.5 pollution reductions at the local sub-national level using life table approach. Surface average PM2.5 concentration datasets covering Nigeria with spatial resolution of ∼1 km were obtained from the global gridded concentration fields, and combined with ∼1 km gridded population of the world (GPWv4), and global administrative unit layers (GAUL) for territorial boundaries classification. We estimate the loss or gains in longevity using population-weighted average pollution level and baseline mortality data for cardiopulmonary disease and lung cancer in adults ≥25 years and for respiratory infection in children under 5. As at 2015, there are six “highly polluted”, thirty “polluted” and one “moderately polluted” States in Nigeria. People residing in these States lose ∼3.8–4.0, 3.0–3.6 and 2.7 years of life expectancy, respectively, due to the pollution exposure. But, assuming interventions achieve global air quality guideline of 10 μg/m3, longevity would increase by 2.6–2.9, 1.9–2.5 and 1.6 years for people in the State-categories, respectively. The longevity gains are indeed high, but to achieve them, mitigation interventions should target emission sources having the highest population exposures.

Air pollution is an important public health concern especially for children who are particularly susceptible. Latin America has a large children population, is highly urbanized and levels of pollution are substantially high, making the potential health impact of air pollution quite large. We evaluated the effect of air pollution on children respiratory mortality in four large urban centers: Mexico City, Santiago, Chile, and Sao Paulo and Rio de Janeiro in Brazil.Generalized Additive Models in Poisson regression was used to fit daily time-series of mortality due to respiratory diseases in infants and children, and levels of PM10 and O3. Single lag and constrained polynomial distributed lag models were explored. Analyses were carried out per cause for each age group and each city. Fixed- and random-effects meta-analysis was conducted in order to combine the city-specific results in a single summary estimate.These cities host nearly 43 million people and pollution levels were above the WHO guidelines. For PM10 the percentage increase in risk of death due to respiratory diseases in infants in a fixed effect model was 0.47% (0.09–0.85). For respiratory deaths in children 1–5 years old, the increase in risk was 0.58% (0.08–1.08) while a higher effect was observed for lower respiratory infections (LRI) in children 1–14 years old [1.38% (0.91–1.85)]. For O3, the only summarized estimate statistically significant was for LRI in infants. Analysis by season showed effects of O3 in the warm season for respiratory diseases in infants, while negative effects were observed for respiratory and LRI deaths in children.We provided comparable mortality impact estimates of air pollutants across these cities and age groups. This information is important because many public policies aimed at preventing the adverse effects of pollution on health consider children as the population group that deserves the highest protection.