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.

Public health is threatened by air pollution and high temperature, especially in urban areas and areas impacted by climate change. Well-designed urban forms have co-benefits on promoting human health and mediating atmospheric environment-related threats (e.g., high temperature and air pollution). Previous studies overlooked these mediating effects of urban form on suicide mortality. This study used partial least squares modeling and countywide data in Taiwan to identify the crucial influences and pathways of urban environment, socioeconomic status, and diseases on suicide mortality. The model considered the impact of the characteristics of urban form (i.e., urban development intensity, land mix, and urban sprawl), urban industrial status (i.e., industrial level), urban greening (i.e., green coverage), disease (i.e., important diseases morbidity of human immunodeficiency virus [HIV], cerebrovascular disease [CVD], chronic liver disease and cirrhosis [CLDC], nephritis, nephrotic syndrome and nephrosis [NNSN], malignant tumor [MT]), socioeconomic status (i.e., income level and aging population rate), and the atmospheric environment (i.e., air pollution and high temperature) on suicide mortality. Optimizing land mix and minimizing urban development intensity and urban sprawl have been found to reduce suicide mortality. The mediating effect of urban form on suicide mortality originated from air pollution and high temperature, and mediating air pollution was greater than high temperature. Furthermore, industrial level, important diseases (HIV, CVD, CLDC, NNSN, and MT) morbidity, an aging population rate, air pollution, and high temperature were associated with an increase in suicide mortality, whereas green coverage and income level were associated with a reduction in suicide rates. The findings demonstrate that appropriate urban policy and urban planning may lower suicide mortality, be useful strategies for suicide prevention, and be a foundation for building a healthy city. Moreover, this study provides clarity on the complex relationship of suicide and the urban environment while identifying crucial factors.

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.

Accelerating evidence of endocrine-related morbidity has raised alarm about the ubiquitous use of phthalates in the human environment, but studies have not directly evaluated mortality in relation to these exposures. To evaluate associations of phthalate exposure with mortality, and quantify attributable mortality and lost economic productivity in 2013–4 among 55–64 year olds. This nationally representative cohort study included 5303 adults aged 20 years or older who participated in the US National Health and Nutrition Examination Survey 2001–2010 and provided urine samples for phthalate metabolite measurements. Participants were linked to mortality data from survey date through December 31, 2015. Data analyses were conducted in July 2020. Mortality from all causes, cardiovascular disease, and cancer. Multivariable models identified increased mortality in relation to high-molecular weight (HMW) phthalate metabolites, especially those of di-2-ethylhexylphthalate (DEHP). Hazard ratios (HR) for continuous HMW and DEHP metabolites were 1.14 (95% CI 1.06–1.23) and 1.10 (95% CI 1.03–1.19), respectively, with consistently higher mortality in the third tertile (1.48, 95% CI 1.19–1.86; and 1.42, 95% CI 1.13–1.78). Cardiovascular mortality was significantly increased in relation to a prominent DEHP metabolite, mono-(2-ethyl-5-oxohexyl)phthalate. Extrapolating to the population of 55–64 year old Americans, we identified 90,761–107,283 attributable deaths and $39.9–47.1 billion in lost economic productivity. In a nationally representative sample, phthalate exposures were associated with all-cause and cardiovascular mortality, with societal costs approximating $39 billion/year or more. While further studies are needed to corroborate observations and identify mechanisms, regulatory action is urgently needed.

Sensing of pathogens by specialized receptors is the hallmark of the innate immunity. Innate immune response also mounts a defense response against various allergens and pollutants including particulate matter present in the atmosphere. Air pollution has been included as the top threat to global health declared by WHO which aims to cover more than three billion people against health emergencies from 2019 to 2023. Particulate matter (PM), one of the major components of air pollution, is a significant risk factor for many human diseases and its adverse effects include morbidity and premature deaths throughout the world. Several clinical and epidemiological studies have identified a key link between the PM existence and the prevalence of respiratory and inflammatory disorders. However, the underlying molecular mechanism is not well understood. Here, we investigated the influence of air pollutant, PM₁₀ (particles with aerodynamic diameter less than 10 μm) during RNA virus infections using Highly Pathogenic Avian Influenza (HPAI) – H5N1 virus. We thus characterized the transcriptomic profile of lung epithelial cell line, A549 treated with PM₁₀ prior to H5N1infection, which is known to cause severe lung damage and respiratory disease. We found that PM₁₀ enhances vulnerability (by cellular damage) and regulates virus infectivity to enhance overall pathogenic burden in the lung cells. Additionally, the transcriptomic profile highlights the connection of host factors related to various metabolic pathways and immune responses which were dysregulated during virus infection. Collectively, our findings suggest a strong link between the prevalence of respiratory illness and its association with the air quality.

We evaluated the short-term effect of mixtures of ambient air pollutants on respiratory and circulatory morbidity in four Colombian cities.Daily Emergency Department (ED) visit records for respiratory and circulatory selected diagnosis and daily concentrations for six criteria air pollutant were obtained in four of the five major cities in Colombia: Bucaramanga, Bogota, Cali, and Medellin during 2011–2014. Using conditional Poisson time series analysis with fixed effects, we assessed the effect of air pollutants on health outcomes using single-pollutant, two-pollutant and specific mixtures-of-pollutant models controlling for meteorology and time trends. The percentages of change in the rate of ED visits and their 95% confidence interval were estimated for the joint effect of pollutants.In single-pollutant models increases in gases concentrations were associated with increases in ED visits for respiratory and circulatory diseases. The two-pollutant models for respiratory diseases showed that the effect of NO₂ alone (% change 2.86 95% CI 1.87–3.85) is higher than the joint effect of any of its combinations except for its combination with SO₂ (% change 3.05 95%CI 1.04–5.05). The two-pollutant models for circulatory diseases showed synergistic effects between NO₂ and PM₂.₅ (% change 2.13 95%CI 0.001–4.26). Specific mixtures models showed that the mixture of “traffic-related pollutants” has the higher joint effect on circulatory morbidity and respiratory morbidity.The results show the dominant effect of NO₂ in air pollution mixtures on respiratory and circulatory morbidity, and the synergistic effect of NO₂ and SO₂ in air pollution mixtures on respiratory morbidity.

Concerning PM2.5 concentrations, rapid industrialization, along with increase in cardiovascular disease (CVD) were recorded in Pakistan, especially in urban areas. The degree to which air pollution contributes to the increase in the burden of CVD in Pakistan has not been assessed due to lack of data. This study aims to describe the characteristics of PM2.5 constituents and investigate the impact of individual PM2.5 constituent on cardiovascular morbidity in Karachi, a mega city in Pakistan. Daily levels of twenty-one constituents of PM2.5 were analyzed using samples collected at two sites from fall 2008 to summer 2009 in Karachi. Hospital admission and emergency room visits due to CVD were collected from two large hospitals. Negative Binominal Regression was used to estimate associations between pollutants and the risk of CVD. All PM2.5 constituents were assessed in single-pollutant models and selected constituents were assessed in multi-pollutant models adjusting for PM2.5 mass and gaseous pollutants. The most common CVD subtypes among our participants were ischemic heart disease, hypertension, heart failure, and cardiomyopathy. Extremely high levels of PM2.5 constituents from fossil-fuels combustion and industrial emissions were observed, with notable peaks in winter. The most consistent associations were found between exposure to nickel (5–14% increase per interquartile range) and cardiovascular hospital admissions. Suggestive evidence was also observed for associations between cardiovascular hospital admissions and Al, Fe, Ti, and nitrate. Our findings suggested that PM2.5 generated from fossil-fuels combustion and road dust resuspension were associated with the increased risk of CVD in Pakistan.

There have been few large multicity studies to evaluate the acute health effects of ambient air pollution on morbidity risk in developing counties. In this study, we examined the short-term associations of air pollution with daily hospital admissions in China. We conducted a nationwide time-series study in 218 Chinese cities between 2014 and 2016. Data on daily hospital admissions counts were obtained from the National Health Insurance Database for Urban Employees covering 0.28 billion enrollees. We used generalized additive model with Poisson regression to estimate the associations in each city, and we performed random-effects meta-analysis to pool the city-specific estimates. More than 60 million hospital admissions were analyzed in this study. At the national-average level, each 10 μg/m³ increase in PM₁₀, SO₂, and NO₂, and 1 mg/m³ increase in CO at lag 0 day was associated with a 0.29% (95% CI, 0.23%–0.36%), 1.16% (95% CI, 0.92%–1.40%), 1.68% (95% CI, 1.40%–1.95%), and 2.59% (95% CI, 1.69%–3.50%) higher daily hospital admissions, respectively. The associations of air pollution with hospital admissions remained statistically significant at levels below the current Chinese Ambient Air Quality Standards. The effect estimates were larger in cities with lower air pollutants levels or higher air temperatures and relative humidity, as well as in the elderly. In conclusion, our findings provide robust evidence of increased hospital admissions in association with short-term exposure to ambient air pollution in China.

Previous studies have suggested that ambient temperature is associated with the mortality and morbidity of myocardial infarction (MI) although consistency among these investigations is lacking. We performed a meta-analysis to investigate the relationship between ambient temperature and MI. The PubMed, Web of Science, and China National Knowledge Infrastructure databases were searched back to August 31, 2017. The pooled estimates for different temperature exposures were calculated using a random-effects model. The Cochran's Q test and coefficient of inconsistency (I2) were used to evaluate heterogeneity, and the Egger's test was used to assess publication bias. The exposure-response relationship of temperature-MI mortality or hospitalization was modeled using random-effects meta-regression. A total of 30 papers were included in the review, and 23 studies were included in the meta-analysis. The pooled estimates for the relationship between temperature and the relative risk of MI hospitalization was 1.016 (95% confidence interval [CI]: 1.004–1.028) for a 1 °C increase and 1.014 (95% CI: 1.004–1.024) for a 1 °C decrease. The pooled estimate of MI mortality was 1.639 (95% CI: 1.087–2.470) for a heat wave. The heterogeneity was significant for heat exposure, cold exposure, and heat wave exposure. The Egger's test revealed potential publication bias for cold exposure and heat exposure, whereas there was no publication bias for heat wave exposure. An increase in latitude was associated with a decreased risk of MI hospitalization due to cold exposure. The association of heat exposure and heat wave were immediate, and the association of cold exposure were delayed. Consequently, cold exposure, heat exposure, and exposure to heat waves were associated with an increased risk of MI. Further research studies are required to understand the relationship between temperature and MI in different climate areas and extreme weather conditions.

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.