The health impacts of air pollution manifest through both immediate acute effects and gradual chronic damage
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Peer-reviewed literature and scientific evidence establish that exposure to air pollution results in both immediate acute health effects, such as acute respiratory morbidity and short-term symptom exacerbations, and gradual chronic damage, including long-term cardiovascular and pulmonary diseases.
<h4>Background</h4>It is well known that air pollution causes respiratory morbidity and mortality by inducing airway inflammation. However, whether long-term exposure to air pollution is associated with increased incidence of chronic obstructive pulmonary disease (COPD) is controversial.<h4>Methods</h4>We conducted a systematic review and meta-analysis with a random-effects model to calculate the pooled risk estimates of COPD development per 10 μg/m<sup>3</sup> increase in individual air pollutants. PubMed, Embase, and Cochrane Library were searched from the date of their inception to August 2019 to identify long-term (at least three years of observation) prospective longitudinal studies that reported the risk of COPD development due to exposure to air pollutants. The air pollutants studied included particulate matter (PM<sub>2.5</sub> and PM<sub>10</sub>) and nitrogen dioxide (NO<sub>2</sub>).<h4>Results</h4>Of the 436 studies identified, seven met our eligibility criteria. Among the seven studies, six, three, and five had data on PM<sub>2.5</sub>, PM<sub>10</sub>, and NO<sub>2</sub>, respectively. The meta-analysis results showed that a 10 μg/m<sup>3</sup> increase in PM<sub>2.5</sub> is associated with increased incidence of COPD (pooled HR 1.18, 95% CI 1.13-1.23). We also noted that a 10 μg/m<sup>3</sup> increase in NO<sub>2</sub> is marginally associated with increased incidence of COPD (pooled HR 1.07, 95% CI 1.00-1.16). PM<sub>10</sub> seems to have no significant impact on the incidence of COPD (pooled HR 0.95, 95% CI 0.83-1.08), although the number of studies was too small. Meta-regression analysis found no significant effect modifiers.<h4>Conclusions</h4>Long-term exposure to PM<sub>2.5</sub> and NO<sub>2</sub> can be associated with increased incidence of COPD.
Abstract Existing evidence suggests that ambient air pollution has serious adverse effects on respiratory diseases, yet there is little direct evidence from China regarding corresponding economic losses. Here we quantified air pollution–related acute health effects and related economic losses of the most common two respiratory diseases in southwestern China, acute bronchitis and chronic obstructive pulmonary disease (COPD). We applied a distributed lag non-linear model to analyse the relationship between ambient air pollutants and hospital admissions of acute bronchitis and COPD, then applied the cost of illness method to explore the attributing economic burden. During the study period, 528 334 and 99 419 hospital admissions of acute bronchitis and COPD, respectively, were recorded. As a result, during the study period the total hospitalization economic losses attributable to air pollution were 486.40 and 254.74 million yuan for acute bronchitis and COPD, respectively, accounting for 0.015% of local gross domestic product. Our research provides intuitive evidence on the health and economic impacts of short-term exposure to air pollution, which is a key basis for the formulation of environmental policies.
India's rapid urbanization, population growth, and reliance on climate-sensitive sectors make it highly vulnerable to the mental health impacts of climate change. Extreme weather events and environmental degradation disproportionately affect vulnerable populations, yet mental health consequences remain under-addressed in policies and interventions. This narrative review examines the effects of climate change on mental health in India, highlighting risks for vulnerable groups and underscoring the need for climate-sensitive mental health policies and interventions. A comprehensive literature search was conducted using PubMed, Scopus, Google Scholar, and Web of Science. Searches covered the period 2000-2024, and included articles reported in English; we included empirical studies, reviews, case reports and government documents focused on Indian populations and excluded non-India studies and papers without mental-health outcomes. Study quality was appraised using standard checklists, and data were synthesized thematically to identify population-specific vulnerabilities and psychosocial outcomes. Climate change exacerbates anxiety, depression, PTSD, and stress among children, women, the older adults, and rural and urban communities. Mental health must be integrated into India's climate adaptation and disaster management strategies. Strengthening community-based interventions, awareness programs, and mental health infrastructure will enhance resilience against climate-induced psychological distress. The review applies an eco-social framework to conceptualize pathways linking climate stressors, displacement, and socio-economic disruption to mental health outcomes and identifies the need for longitudinal, culturally validated, and implementation-oriented research.
Health and Cellular Impacts of Air Pollutants: From Cytoprotection to Cytotoxicity
Air pollution as one of the ravages of our modern societies is primarily linked to urban centers, industrial activities, or road traffic. These atmospheric pollutants have been incriminated in deleterious health effects by numerous epidemiological and in vitro studies. Environmental air pollutants are a heterogeneous mixture of particles suspended into a liquid and gaseous phase which trigger the disruption of redox homeostasis—known under the term of cellular oxidative stress—in relation with the establishment of inflammation and cell death via necrosis, apoptosis, or autophagy. Activation or repression of the apoptotic process as an adaptative response to xenobiotics might lead to either acute or chronic toxicity. The purpose of this paper is to highlight the central role of oxidative stress induced by air pollutants and to focus on the subsequent cellular impacts ranging from cytoprotection to cytotoxicity by decreasing or stimulating apoptosis, respectively.
Published in Biochemistry Research International
Sympathetic Nerve Activation Evoked by Diesel Exhaust Exposure
The adverse effects of air pollution on cardiovascular and respiratory health have been demonstrated in an extensive series of epidemiological, observational and experimental studies. In the current project the investigators aim to determine whether an acute exposure to diesel exhaust causes impacts on sympathetic nervous system activation in healthy volunteers. Brief as well as chronic exposures to air pollution have been linked with increases in cardiovascular morbidity and mortality. Evidence suggests that the strongest associations between air pollution exposure and adverse cardiovascular effects are found for combustion-derived particulate matter, especially in the fine and ultrafine ranges such as is found in diesel engine emissions. Despite a greater understanding of the cardiovascular effects of air pollution, the underlying mechanism through which exposure to fine particulate air pollution alters vascular function has yet to be determined. Microneurography is a method that records nerve impulse traffic in human peripheral nerves, allowing for the assessment of sympathetic nervous activity.
Pollution remains a major global public health concern increasingly associated with cancer incidence. This systematic review and meta-analyses examined the association between cancer risk and pollution across air, water, and land following the PRISMA guidelines. From 26,367 records initially identified in PubMed, Web of Science, and Scopus (January 2014-June 2025), 168 studies met the eligibility criteria. Meta-analyses conducted on 11 groups of studies revealed significant associations of lung cancer with fine particulate matter (HR<sub>pooled</sub> = 1.347; 95% CI: 1.158-1.536), black carbon (HR<sub>pooled</sub> = 1.096; 95% CI: 1.014-1.179) and ozone (HR<sub>pooled</sub> = 0.941; 95% CI: 0.908-0.975), and breast cancer with nitrogen dioxide (HR<sub>pooled</sub> = 1.064; 95% CI: 1.011-1.117). The association of ozone with cancer risks was inconsistent. While 155 studies reported on cancer risks from air pollution, only 10 studies focused on water pollutants and two on land pollutants, primarily heavy metals. Also, 79% of reviewed studies originated from only six high-income countries. The findings suggest that while particulate matter is a consistent risk factor, the global evidence base remains imbalanced based on pollution type and economic status of countries. Addressing these data gaps through targeted research in underrepresented regions and prioritizing the reduction of exposure to identified carcinogenic pollutants could reduce the global cancer burden.
Although the international community collectively seeks to reduce global temperature rise to less than 1.5°C before 2100, irreversible environmental changes have already occurred, and as the planet warms, these changes will continue to occur. As we witness the effects of a warming planet on human health, it is imperative that neurologists anticipate how the epidemiology and incidence of neurologic disease may change. In this review, we organized our analysis around 3 key themes related to climate change and neurologic health: extreme weather events and temperature fluctuations, emerging neuroinfectious diseases, and pollutant impacts. Across each of these themes, we appraised and reviewed recent literature relevant to neurologic disease and practice. Studies were identified using search terms relating to climate change, pollutants, and neurologic disease in PubMed, OVID MEDLINE, EMBASE, PsycInfo, and gray literature. Studies published between 1990 and 2022 were included if they pertained to human incidence or prevalence of disease, were in English, and were relevant to neurologic disease. We identified a total of 364 articles, grouped into the 3 key themes of our study: extreme weather events and temperature fluctuations (38 studies), emerging neuroinfectious diseases (37 studies), and pollutant impacts (289 studies). The included studies highlighted the relationships between neurologic symptom exacerbation and temperature variability, tick-borne infections and warming climates, and airborne pollutants and cerebrovascular disease incidence and severity. Temperature extremes and variability both associated with stroke incidence and severity, migraine headaches, hospitalization in patients with dementia, and multiple sclerosis exacerbations. Exposure to airborne pollutants, especially PM2.5 and nitrates, associated with stroke incidence and severity, headaches, dementia risk, Parkinson disease, and MS exacerbation. Climate change has demonstrably expanded favorable conditions for zoonotic diseases beyond traditional borders and poses the risk of disease in new, susceptible populations. Articles were biased toward resource-rich regions, suggesting a discordance between where research occurs and where changes are most acute. As such, 3 key priorities emerged for further study: neuroinfectious disease risk mitigation, understanding the pathophysiology of airborne pollutants on the nervous system, and methods to improve delivery of neurologic care in the face of climate-related disruptions.
Of the threats to public health linked to climate change, exposures to heightened air pollution and elevated temperatures rank high in national and international assessments. Climatic effects on air quality are well documented, especially for ozone, a secondary pollutant that increases in concentration with warmer temperatures. There is less certainty regarding the effects of climate change on fine particulate matter, air pollutant most hazardous to human health, and how a changing climate will affect the public health burden of air pollution overall. This research augments health impact studi
Immune responses to pollutant mixtures from indoor sources. Indoor air pollution occurs as an undesirable consequence of urbanization, energy conservation, indoor bioaerosol contamination, and use of synthetic materials and new technologies, and has become a worldwide concern. It is important to comprehend not only the diversity of pollutant hazards but also to develop novel methods and approaches that establish dose-response relationships, cause-and-effect relationships, and clinical relevance. Coincident with heightened public concern over indoor air pollution and its health consequences, a revolution in immunology has occurred. The immune system is recognized as an essential defensive and homeostatic mechanism. Unfortunately, the immune apparatus is exquisitely sensitive to toxic damage. Equally important, among the disciplines available to assess the health impact of indoor air pollutants, immunology has the capability to provide sensitive and specific tools that may accurately measure relevant clinical effects at tissue, cellular, and molecular levels.
System interactions of air pollutants.
The impact of system interactions and simultaneous or sequential exposure to various air pollutants, both man-made and natural ones, requires greater concern in the interpretation of the total adverse impact of various air pollutants. It is clear that there are highly significant system interactions with exposure to various air pollutants, and these must be considered very carefully in the evaluation of their adverse health effects.
Published in Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery (1992)
of its toxicity. Benzene is a volatile organic compound. Benzene is classified as a carcinogen. Its particular effects on human health, such as the long-term
Benzene is an organic chemical compound with the molecular formula C6H6. The benzene molecule is composed of six carbon atoms joined in a planar hexagonal ring with one hydrogen atom attached to each. As it contains only carbon and hydrogen atoms, benzene is a hydrocarbon.
Benzene is a natural constituent of petroleum and is one of the elementary petrochemicals. Because of the cyclic continuous pi
Benzene is classified as a carcinogen, which increases the risk of cancer and other illnesses, and is also a notorious cause of bone marrow failure. Substantial quantities of epidemiologic, clinical, and laboratory data link benzene to aplastic anemia, acute leukemia, bone marrow abnormalities and cardiovascular disease. The specific hematologic malignancies that benzene is associated with include: acute myeloid leukemia (AML), aplastic anemia, myelodysplastic syndrome (MDS), acute lymphoblastic leukemia (ALL), and chronic myeloid leukemia (CML).
Carcinogenic activity of benzene was discovered by Swedish pharmacologist C. G. Santesson in 1897 on female workers of a tire-making factory. The American Petroleum Institute (API) stated in 1948 that "it is generally considered that the only absolutely safe concentration for benzene is zero". There is no safe exposure level; even tiny amounts can cause harm. The US Department of Health and Human Services (DHHS) classifies benzene as a human carcinogen. Long-term exposure to excessive levels of benzene in the air causes leukemia, a potentially fatal cancer of the blood-forming organs. In particular, acute myeloid leukemia or acute nonlymphocytic leukemia (AML & ANLL) is caused by benzene. IARC rated benzene as "known to be carcinogenic to humans" (Group 1).
As benzene is ubiquitous in gasoline and hydrocarbon fuels that are in use everywhere, human exposure to benzene is a global health problem. Benzene targets the liver, kidney, lung, heart and brain and can cause DNA strand breaks and chromosomal damage, therefore it is mutagenic. Benzene causes cancer in animals including humans. Benzene has been shown to cause cancer in both sexes of multiple species of laboratory animals exposed via various routes.
Introduction. Man is the only being that has created an artificial environment, or civilization. The development of civilization entails changes in the environment. The rapid growth of the impact of human economic activity has led to such changes that are able to threaten not only other living creatures but also themselves. Increasing environmental pollution are well-known factors negative influencing on human environment. Is now a global problem. Anthropogenic pollution contribute to the unfavorable demographic changes and grooving number of health problems of the population. Unfavourable demographic changes manifest themselves as not only increment in the number of deaths and malformations (defects in the reproductive organs), but also as decrement in the fertility rates being the consequence of increasing the growing problem of couples infertility. There is observed the increasing role of male factor in the couple infertility problem. In some developed countries its participation rate reaches 50%. Objective. The aim of the study is to assess the impact of environmental pollution on human development and reproductive function of male gonads. Material and methods. The study was carried out using the method of data analysis published in the works and scientific reports. Current state of knowledge. The paper presents information on identified environmental pollution with proven adverse effects on the development of the gonads and the their reproductive function. There are also
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