The human health impacts caused due to exposure to criteria outdoor air pollutants PM2.5, PM10 and NO2 were assessed in present study. The human health effects associated with exposure to atmospheric air pollution in NCT Delhi were estimated utilizing the AirQ+ v1.3 software tool integrated with Ri-MAP during the study period 2013-2018 considering 80% of the whole population subjected to air pollution exposure. Taking into account the World Health Organization (WHO) (2016) guidelines, the inter-annual average concentrations of PM2.5, PM10, and NO2, concentration response relationships and population attributable fraction (AF) or impact fraction (IF) concepts were adopted. The excess number of cases (ENCs) of Mortality (all) natural cases 30+ years, acute lower respiratory infection (ALRI), lung cancer (LC), ischaemic heart disease (IHD), stroke, incidence of chronic bronchitis in children, postneonatal infant mortality, chronic obstructive pulmonary disease (COPD), prevalence of bronchitis in children, incidence of asthma symptoms in asthmatic children in the year 2013 were 48332, 2729, 5645, 26853, 22737, 120754, 34510, 5125, 9813, 3054, 17203 and 682, respectively. Within half of a decade i.e. in year 2018, the ENCs of Mortality (all) natural cases 30+ years, ALRI, COPD, LC, IHD, stroke, incidence of chronic bronchitis in children, postneonatal infant mortality, prevalence of bronchitis in children, incidence of asthma symptoms in asthmatic children increased significantly and were 72254, 3471, 6547, 7568, 32358, 28233, 150110, 50810, 9019, 862, 29570 and 1189, respectively.

The UN Sustainable Development Goal, SDG 7.3, is to double the global rate of improvement in energy efficiency by 2030. To meet this and other energy targets, countries encourage the development and adoption of energy-efficient products. An extensively researched phenomenon in this context is the energy rebound effect, especially in transportation. However, the direct relationship between the energy rebound effect and car emission levels has barely been investigated. Understanding this relationship is important, because energy-related emissions are closely linked to mortality, morbidity, and climate change. We assess the emission consequences in the private car market in Israel of a rebound effect associated with a policy promoting energy-efficient cars. We find that the baseline rebound before introduction of the policy was 40%. In the following three periods marked by policy changes, it grew to 54%, 69%, and 88%. Using household data with specific car characteristics and usage, we calculate the added greenhouse gas (GHG) emission consequences of this rebound by the end of the studied period to be about 5% of the country's per-capita target. Notably, estimates for the emission consequences using “average car” values were almost twice as high. The reason for this gap derives from the co-dependance between car usage and car efficiency. We discuss the implications of this gap in meeting emission goals.

Household air pollution (HAP) arising from combustion of biomass fuel (BMF) is a leading cause of morbidity and mortality in low-income countries. Air pollution may stimulate pro-inflammatory responses by activating diverse immune cells and cyto/chemokine expression, thereby contributing to diseases. We aimed to study cellular immune responses among women chronically exposed to HAP through use of BMF for domestic cooking. Among 200 healthy, non-smoking women in rural Bangladesh, we assessed exposure to HAP by measuring particulate matter 2.5 (PM₂.₅), black carbon (BC) and carbon monoxide (CO), through use of personal monitors RTI MicroPEM™ and Lascar CO logger respectively, for 48 h. Blood samples were collected following HAP exposure assessment and were analyzed for immunoprofiling by flow cytometry, plasma IgE by immunoassay analyzer and cyto/chemokine response from monocyte-derived-macrophages (MDM) and -dendritic cells (MDDC) by multiplex immunoassay. In multivariate linear regression model, a doubling of PM₂.₅ was associated with small increments in immature/early B cells (CD19⁺CD38⁺) and plasmablasts (CD19⁺CD38⁺CD27⁺). In contrast, a doubling of CO was associated with 1.20% reduction in CD19⁺ B lymphocytes (95% confidence interval (CI) = -2.36, −0.01). A doubling of PM₂.₅ and BC each was associated with 3.12% (95%CI = −5.85, −0.38) and 4.07% (95%CI = −7.96, −0.17) decrements in memory B cells (CD19⁺CD27⁺), respectively. Exposure to CO was associated with increased plasma IgE levels (beta(β) = 240.4, 95%CI = 3.06, 477.8). PM₂.₅ and CO exposure was associated with increased MDM production of CXCL10 (β = 12287, 95%CI = 1038, 23536) and CCL5 (β = 835.7, 95%CI = 95.5, 1576), respectively. Conversely, BC exposure was associated with reduction in MDDC-produced CCL5 (β = −3583, 95%CI = −6358, −807.8) and TNF-α (β = −15521, 95%CI = −28968, −2074). Our findings suggest that chronic HAP exposure through BMF use adversely affects proportions of B lymphocytes, particularly memory B cells, plasma IgE levels and functions of antigen presenting cells in rural women.

This study assessed the human health risk of exposure to legacy PAHs in the Nwaenebo River sediments that received effluents for over two decades from the Nigeria National Petroleum Corporation (NNPC) petroleum product Depot in Emene, Enugu, Nigeria. The study went further to estimate economic costs of the sediment PAHs pollution based on the human health risk of exposure. The human health risks were determined by estimating carcinogenic and mutagenic risks via Benzo[a]pyrene total potential equivalent (BaP TPE) and mutagenic equivalent quotient (MEQ). The economic costs of the sediment pollution comprised costs due to mortality and those due to morbidity and were estimated using the value of statistical lives (VSLs) and cost of illness (CoI), respectively. The study, with an appropriate selection of sampling points established that the NNPC petroleum Depot was responsible for the Nwaenebo River sediment PAHs pollution with ƩPAHs concentration 14.3–163 mg/kg. The carcinogenic and mutagenic risks varied from 1.3*10^-5 to 4.7*10^-5 and 1.4*10^-5 to 6.0*10^-5 respectively. Based on risk threshold of 10^-6, these risks were high. The long term economic costs of pollution of the sediments by the PAHs were estimated at 60.5 million USD and 0.46 million USD for mortality and morbidity costs, respectively.

Exposure to particulate air pollution has been associated with a variety of respiratory, cardiovascular and neurological problems, resulting in increased morbidity and mortality worldwide. Brake-wear emissions are one of the major sources of metal-rich airborne particulate pollution in roadside environments. Of potentially bioreactive metals, Fe (especially in its ferrous form, Fe²⁺) might play a specific role in both neurological and cardiovascular impairments. Here, we collected brake-wear particulate emissions using a full-scale brake dynamometer, and used a combination of magnetic measurements and electron microscopy to make quantitative evaluation of the magnetic composition and particle size of airborne emissions originating from passenger car brake systems. Our results show that the concentrations of Fe-rich magnetic grains in airborne brake-wear emissions are very high (i.e., ~100–10,000 × higher), compared to other types of particulate pollutants produced in most urban environments. From magnetic component analysis, the average magnetite mass concentration in total PM₁₀ of brake emissions is ~20.2 wt% and metallic Fe ~1.6 wt%. Most brake-wear airborne particles (>99 % of particle number concentration) are smaller than 200 nm. Using low-temperature magnetic measurements, we observed a strong superparamagnetic signal (indicative of ultrafine magnetic particles, < ~30 nm) for all of the analysed size fractions of airborne brake-wear particles. Transmission electron microscopy independently shows that even the larger size fractions of airborne brake-wear emissions dominantly comprise agglomerates of ultrafine (<100 nm) particles (UFPs). Such UFPs likely pose a threat to neuronal and cardiovascular health after inhalation and/or ingestion. The observed abundance of ultrafine magnetite particles (estimated to constitute ~7.6 wt% of PM₀.₂) might be especially hazardous to the brain, contributing both to microglial inflammatory action and excess generation of reactive oxygen species.

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.

Aspergillus fumigatus is the primary agent of invasive aspergillosis (IA) causing high morbidity and mortality in immunocompromised patients. Triazole resistance in A. fumigatus and its sources have gained wide attention. For several years, environmental fungicides use has been proposed as the major cause for triazole resistance in A. fumigatus. However, there are few studies on azole-resistant A. fumigatus (ARAF) selected by triazole fungicides in agricultural systems. We studied the possible emergence of ARAF in the field after exposure to triazole fungicide tebuconazole. Our results showed that exposure to tebuconazole in soil selects for resistance to triazoles in A. fumigatus. The probability of ARAF developing in soils depends upon the concentrations of tebuconazole after application. We suggest that tebuconazole applications should be minimized to reduce selective pressure for the generation of ARAFs.

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.

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.

While numerous studies worldwide have evaluated the short-term associations of fine and coarse particulate matter (PM) air pollution with mortality and morbidity, these studies may be susceptible to short-term harvesting effect. We aimed to investigate the short-term association between mortality and PM with aerodynamic diameter less than 2.5 μm (PM2.5) and those between 2.5 and 10 μm (PMc) within a month prior to death, and assess the mortality displacement by PM2.5 and PMc among elderly population in Hong Kong.We obtained air pollution data from January 2011 to December 2015 from Environmental Protection Department, and daily cause-specific mortality data from Census and Statistical Department of Hong Kong. We performed generalized additive distributed lag model to examine the acute, delayed and long-lasting effects of PM2.5 and PMc within one month on mortality.We observed a statistically significant association of PM2.5 and PMc exposure over lags 0–6 days with all natural mortality and cardio-respiratory mortality. The overall cumulative effect of PM2.5 over 0–30 lag days was 3.44% (95% CI: 0.30–6.67%) increase in all natural mortality and 6.90% (95% CI: 0.58–13.61%) increase of circulatory mortality, which suggested the absence of mortality displacement by PM2.5. On the other hand, no significant cumulative association with mortality was found for PMc over 0–30 lag exposure window, and thus mortality displacement by PMc cannot be ruled out. Findings remained robust in various sensitivity analyses.We found adverse effect of both PM2.5 and PMc exposure within one week prior to death. While there was no evidence of mortality displacement in the association of PM2.5 exposure over one month prior with all natural and circulatory mortality, mortality displacement by PMc cannot be ruled out. PM2.5 may contribute more to the longer term effect of particulate matter than PMc.