A potential association between environmental exposure and the incidence of a disease.

Briefly describe how the authors conducted their study and how they evaluated a potential association between environmental exposure and the incidence of a disease. What primary tool did they use? 

2) The authors refer to primary air pollutants and secondary air pollutants. What is the difference between a primary air pollutant and a secondary air pollutant? 

3) What are the three primary air pollutants? 

4) What are two secondary pollutants? 

5) What pollutant is referred to as a “silent killer” in the paper?

19616 Environ Sci Pollut Res (2021) 28:19615-19628 Environ Sci Pollut Res (2021) 28:19615-19628 19617 General air pollution Outdoor (ambient) air pollutants In China, a systematic review and meta-analysis by Sun as benzene, toluene, styrene, ethylbenzene, and xylene, as et al. identified a positive correlation between short-term am- well as aliphatic hydrocarbons (mostly n-alkanes), dichloro- Air pollutants are classified into two main categories: primary Sulfur dioxide bient exposure to NO2 and pulmonary diseases. A 10-ug/m’ methane, and disulfide carbon (Ciganek and Neca 2008). air pollutants (pollutants emitted directly into the atmosphere) increase in NO2 concentration was associated with an increase Oxidative stress and decreased lung function are related to and secondary air pollutants (pollutants that are formed within Sulfur dioxide (SO2) and PM come from the process of burn- of 1.4% in mortality due to respiratory disease and 1.0% in exposure to low levels of VOCs. Additionally, airway inflam- the atmosphere itself) (World Health Organization 2005) ing fossil fuels and represent the essential components of air hospital admission. Elderly individuals had an even higher mation could be related to exposure to increased levels of Mannucci et al. 2015). pollution. Sulfurous and sulfuric acids are formed as a result of susceptibility (Sun et al. 2017). VOCs in everyday life (Kwon et al. 2018). those released from a direct the oxidation process of SO2. Natural sources include volca- In a national cross-sectional representative survey that was source, such as exhaust pipes from a mobile vehicle, or noes, but significant concerns have been encountered in large Carbon monoxide conducted by the Indoor Air Quality Observatory, N- from a stationary source, such as factory chimneys. At metropolitan regions where coal is being used for domestic undecane and 1,2,4-trimethylbenzene were correlated with the same time, contaminated dust can also be distributed heating or for poorly controlled combustion for industrial in- The most important source of environmental CO is incom- asthma in 8.6% of cases, while trichloroethylene, ethylben- by the wind to uncontaminated areas. These pollutants can stallations (World Health Organization 2005). plete combustion of traffic-related fossil fuels, leading to zene, and m/p- and o-xylene were associated with rhinitis be calculated by measuring the amounts emitted by the Exacerbation of respiratory symptoms has been shown to 50% of emissions in urban areas, other sources (such as (Billionnet et al. 2011). source itself. Primary air pollutants are represented by ox- be related to exposure to SO2 emitted by coal-burning power manufacturing and natural processes, etc.) being less promi- In a French cross-sectional study on farmers, indoor mean ides of nitrogen, carbon monoxide (CO), sulfur dioxide plants, and lower concentrations were associated with respira- nent (World Health Organization 2005). VOC concentrations were smaller in workplaces than in (SO2), volatile organic compounds (VOCs), and carbona- tory deaths. The major anthropogenic sources of SO2 are Carbon monoxide is considered to be a "silent killer" due to dwellings. Working in a rural environment involves a degree ceous and non-carbonaceous primary particles. The found in developing countries and come from burning fossil its toxicity arising from its ability to bind hemoglobin more of exposure to various risk factors such as agricultural machin- International Agency for Research on Cancer (IARC) has fuels that contain sulfur. The reason for burning fossil fuels is strongly than oxygen, increasing the risk of asphyxia-related ery and fires, exposure to capricious weather, agricultural land classified emissions from burning coal in an indoor envi- due to heating homes, use in power plants, and powering deaths at high levels of exposure or hypoxic tissue damage at working, and exposure to various organic compounds. ronment as potentially carcinogenic to humans. These were vehicles (Kravchenko and Lyerly 2018). Sulfur dioxide con- low levels of exposure (World Health Organization 2005). Following this study, individuals mentioned that respiratory observed with sufficient evidence in both animals and centrations are lower since indoor concentrations are absorbed Asthma, bronchiectasis, and pneumonia have been associ- symptoms, such as dyspnea, cough, sneezing, and wheezing, humans (Barone-Adesi et al. 2012) by walls, furniture, and inhalation systems (World Health ated with ambient short-term exposure to CO (Zhao et al. were the most common. They were present in 44% of people There are many sources of primary air pollutants, but the Organization 2005). 2019). The study of Zhao et al. conducted over 4 and 1/2 when manipulating plants that had been harvested. Asthma most significant are road traffic and power plants. years, with a daily mean ambient CO of 0.88 mg/m’, varying and early airway obstruction were linked with exposure to Additionally, industrial and residential heating based on Nitrogen dioxide from 0.40 to 3.13 mg/m’, reported an increased risk for daily VOCs and PM and in farmers (Maesano et al. 2019). wood, coal. or oil contributes to increasing the degree of air outpatient visits for respiratory disease, with a higher effect on pollution (World Health Organization 2005) (Guarnieri and There are many species of nitrogen oxides, but the one with women and elderly patients (Zhao et al. 2019). Ozone Balmes 2014) (Kravchenko and Lyerly 2018) (Minichilli the most important effect on human health is NO2. NO2 is a In different studies, a positive association between daily et al. 2019). gas with a brown color, having a distinctive powerful scent. exposure to PM2.5, SO2, and CO and an increased risk of Ozone (03) is a chemical compound that is not directly emit- Secondary air pollutants are formed through chemical re- Nitric oxide spontaneously produces dioxide when it is ex- mortality from respiratory diseases and lung cancer was re- ted into the air but is formed through a series of complex actions in the atmosphere, with natural components such as posed to air. It is a powerful oxidant that produces nitric acid ported. For a 1-mg/m’ increase in CO and a 10-ug/m’ increase reactions. Atomic oxygen and nitric oxide are formed after water and oxygen. Secondary air pollutants include ozone and nitric oxide by reacting with water, and it is an important in PM10, there has been a 1.9% and 4.8% increase in total NO2 splits. Atomic oxygen later combines with oxygen- (03), oxides of nitrogen, and particulate matter (PM) (World trace gas affecting human health. It absorbs solar radiation, deaths, respectively (Xue et al. 2018) (Table 1). forming ozone. Ozone is disintegrated by reacting with nitric Health Organization 2005) (Guarnieri and Balmes 2014) contributing to low visibility in the atmosphere and plays a oxide, resulting in NO2 and oxygen. Ambient concentrations (Mannucci et al. 2015) direct role in global climate change. Volatile organic compounds depend on several factors: the concentration of NO2 and The chemical composition of air pollutants is diverse and NO2 undergoes further transformations, and after the pho- VOCs, sunshine intensity, atmospheric convection, and the depends on the source. Additionally, a seasonal pattern is tochemical reaction sequence is initiated by its solar radiation- Volatile organic compounds (VOCs) are compounds with a proportion of VOCs to nitrogen oxides (World Health observed, with higher average daily concentration levels of induced activation, newly generated pollutants are created, high vapor pressure of one or more carbon atoms, which will Organization 2005) (Guarnieri and Balmes 2014). nitrogen dioxide (NO2), CO, PM10, and fine particulate mat- containing organic, nitrate, and sulfate particles, all measured lead to their release in the atmosphere (Ciganek and Neca Daily concentrations of air pollutants are higher in the cool ter (PM2.5) during the cold season, while O3 concentration at PM2.5 and PM10. Among natural sources, the represented 2008). Compounds from the atmosphere, in a state of a vapor seasons than in the warm seasons, except for O3, which is levels tended to be higher during the warm season (Bernardini sources include lightning, inclusion of stratospheric nitrogen phase, such as oxygenates, hydrocarbons, halogenates, and higher during warm seasons (Wang et al. 2019d). Ground- et al. 2019) oxides, and bacterial and volcanic actions. The major anthro- other carbon compounds, are the main components of VOC’s level ozone (03) is considered one of the most dangerous air Air pollutants released by coal-fired power plants have pogenic sources are mobile sources (combustion engines) and World Health Organization 2005). pollutants in the USA and the European Union, being a strong raised concerns about their impact on public health. PM2.5 stationary combustion sources (power generation sources) There are different sources of VOCs. They can arise from oxidizing compound. In recent years, O3 levels have remained can have both short-term and long-term consequences on hu- (World Health Organization 2005) (Kravchenko and Lyerly natural causes, such as forest fires, vegetation, and animals, high without showing any decline and will remain a constant man health. In a study conducted by Cheng-Kuan Lin et al., a 2018) but also from artificial causes, such as vehicles. Natural public health problem, especially with the progression of strong association was observed between the increase in coal Patients with asthma and chronic obstructive pulmonary sources of VOCs represent a higher percentage, but anthropo- global warming (Guarnieri and Balmes 2014) (Wang et al. capacity per person and an increase in the relative risk for lung disease (COPD) have been associated with an increased risk genic sources contribute significantly to reducing air quality. 2019c ) . cancer, both in men and women. These were observed by a of respiratory hospitalization after exposure to NO2 The most important sources of VOCs are released by in Concentrations of O3 can increase during late spring and factor of 85% among women and 59% among men. Based on (Kravchenko and Lyerly 2018). In addition, exposure to air dustrial and agricultural sources. At the same time, handling summer months due to photochemical reactions, along with these data, it is predicted that in 2025, a total of 1.37 million pollution due to traffic vehicles increases the risk of develop solvents or solvent-based products contributes significantly to its precursors, such as VOCs. High concentrations of O, can cases of lung cancer will be correlated with coal-fired power ing bronchiolitis obliterans post-lung transplant syndrome VOC concentrations. Samples that were collected from road be associated with various local and long-range transports plants (Lin et al. 2019). (Johannson et al. 2015). dust or soil were based on volatile organic compounds, such of anthropogenic emissions. In winter, lower Springer 2 Springer

19618 Environ Sci Pollut Res (2021) 28:19615-19628 Environ Sci Pollut Res (2021) 28:19615-19628 19619 Table 1 Associations between air pollutants and respiratory diseases respiratory airways, primarily in the small airways and alveoli, An investigation of the origin of wintertime high PM2.5 Authors Disease Air pollutant association Ethnicity/nationality while ultrafine PM (<0.1 um) is stored in the alveoli (World pollution days revealed that in addition to traffic emissions, Health Organization 2005) (Guarnieri and Balmes 2014) another significant source that helped increase PM2.5 in win- Liang et al. (2019) COPD PM2.5 China Liang et al. 2019). ter was a mixed factor represented by local industry and agri- Huang et al. (2019) COPD PM2.5 Taiwan PM2.5 are primarily formed from gases. These particles culture (deduced as gas emission sources and upstream oil) Havet et al. (2019) Asthma PM10, O3 France usually emerge as ultrafine particles created by the formation (Bari and Kindzierski 2017) Cadelis et al. (2014 ) Asthma PM10, PM2.5-10 Caribbean of very small particles (nuclei) by condensation-nucleation of Akpinar-Elci et al. (2015) Asthma PM10, PM2.5-10 Caribbean ow vapor pressure substances generated by chemical reaction Guarnieri and Balmes (2014) Asthma PM2.5, PM 10 Meta-analyses into the atmosphere or by high-temperature vaporization Indoor air pollutants Xing et al. (2019 Lung cancer PM2.5, PM10, O3 China World Health Organization 2005) (Mannucci et al. 2015) Hamra et al. (2014) Lung cancer PM2.5 Meta-analyses (Kravchenko and Lyerly 2018). The principal precursor gases Biomass smoke Gharibvand et al. (2017) Lung cance PM2.5 USA, Canada are represented by nitrogen oxides, ammonia, SO2, and Wang et al. (2019a) Lung cancer PM2.5 Chin VOCs. At the same time, fluctuations in the concentrations Biomass smoke is a major public health problem (Balcan et al. Winterbottom et al. (2018) IPF PM10 USA of these compounds may alter ambient PM concentrations. 2016). Coal and biomass fuels are used by almost 3 billion Johannson et al. (2018) IPF NO2, PM2.5, PM10 USA On the days when PM10 concentration exceeds 50 ug/m’ people worldwide. A large part of the world’s population still Johannson et al. (2014) IPF 03, NO2 South Korea PM, nitrate becomes the main compound of PM10 and depends on solid fuel for cooking, firewood, and charcoal Nsoh et al. (2019) Respiratory infections PM2.5 Cameroon PM2.5 (World Health Organization 2005)(Kravchenko and (Nsoh et al. 2019). Individuals generally use different types Z. Zhang et al. (2019) Respiratory infections PM2.5, PM2.5-PM10 China Lyerly 2018). of fuels for heating and cooking, such as "smoky coal" (bitu- Zheng et al. (2017) Respiratory infections PM10, NO2, SO2 China There are numerous sources of both human activity and minous), "smokeless coal" (anthracite), and wood (Barone- Goeminne et al. (2018) Bronchiectasis PM10, NO2 UK natural source-related particles. Specific sources impact dif- Adesi et al. 2012). Garcia-Olive et al. (2018) Bronchiectasis SO2 Spain ferent regions of the world, but more than two-thirds of PM Compounds emitted from smoky coal combustion are pres- Popovic et al. (2019) Tuberculosis PM2. Asia, Europe, North America 2.5 is due to industrialization in developed areas. ent in abundance, such as polycyclic aromatic hydrocarbons Zhu et al. (2018) Tuberculosis PM10, NO2, SO2 China The origin of PM2.5 is variable. It can come from several (PAHs), methylated PAHs, and heterocyclic aromatic com- Lai et al. (2016) Tuberculosis PM2. Taiwan sources, such as vehicle traffic, followed by dust generation, pounds containing nitrogen. Following an incomplete com- Jassal et al. (2012) Tuberculosis PM2.5 USA aerosols from regional transport, agricultural activities, and bustion process, solid fuel releases a significant amount of Li et al. (2019) Tuberculosis PM2.5 China the burning of biomass for cooking or heating. It is difficult toxic particles. These will then be inhaled and cause multiple Yao et al. (2019) Tuberculosis PM2.5, PM10, 03, CO China to appreciate the contribution of each source and to further respiratory symptoms. Symptoms may include upper respira- recognize the PM formation mechanism (Zhang and Cao tory tract conditions, such as cough, nasal obstruction, vocal 2015). dysfunction, rhinorrhea, laryngeal spasm, and lower respira- Photochemical conversion of secondary pollutants (SO4-, tory tract symptoms, such as dyspnea, wheezing, and cough photochemical processes result in a smaller contribution of Particulate matter (PM) is represented by a complex NO3 , and NH4+) represents 3.7% of PM2.5 and 2.4% of (Nsoh et al. 2019). this factor to PM2.5 mass (18%) (Bari and Kindzierski mixture containing components with diverse physical and PM10 (Lee et al. 2018). Concentrations of NH4 , NO3 , and Approximately half of the world’s population cooks and 2017). Human exposure to ozone is correlated with a high chemical characteristics. The potential for these particles to SO43-on days with higher pollution can be two to four times heats using unprocessed biomass fuels and coal. Several dis- risk of respiratory disorders, such as asthma exacerbation cause injury varies due to their chemical composition and higher than on unpolluted days (p < 0.01), according to the eases are associated with exposure to solid fuel smoke, include and lung inflammation, loss of lung function, and cystic source. Additionally, their size and physical characteristics study of Pan et al, where PM2.5 samples were gathered from ing lung cancer, chronic obstructive pulmonary disease, and fibrosis (Johannson et al. 2014). Additionally, it has been represent major concerns for public health (World Health two metropolitan areas (Beijing and Shanghai) on polluted respiratory infections (Barone-Adesi et al. 2012). In the study shown to interact with cerebral blood vessels by modulating Organization 2005). and unpolluted days in the fall of 2017 (Pan et al. 2019). by Barone-Ades et al., it was observed that mortality due to the expression of genes involved in brain vasoreactivity, Particles are classified in general by their aerodynamic di- Additionally, seasonal variations in PM2.5 have been de- lung cancer was higher in people who used smoked charcoal irritating mucous membranes, altering the levels of seroto- ameter. PM can generally be classified into three major frac- scribed in different regions of the world. than in those who used no-smoke charcoal throughout their nin, and affecting the immune system (Bernardini et al. tions: coarse particles, exceeding 2.5 um in aerodynamic di- In a Canadian study conducted by Md. Aynul Bari from lives. In the study, 9962 people used smokeless coal, and 2019). ameter; fine particles, which are smaller than 2.5 um; and May 2009 to December 2015, the overall mean and median 27,310 used smoked coal. The absolute risk of death from ultrafine particles, which are smaller than 0.1 um (100 nm) concentrations of PM2.5 were comparatively higher in winter lung cancer in individuals who used smoked charcoal was Particulate matter PM10 contains PM2.5 and thoracic coarse mass (the distinct than in summer (Bari and Kindzierski 2017). The same obser higher for women (20%) than men (18%). As a comparison, tion between PM10 and PM2.5 is generally presented as vation was reported in the Chinese study of Yan-Lin Zhang the percentage of people who used smokeless charcoal and According to the World Health Organization (WHO), the coarse mass). In general, PM10 mass contains 40-90% of et al., with remarkable seasonal variability in PM2.5, which developed lung cancer was only 0.5%. These values are sim- standard for daily PM2.5 concentration is 25 ug/m , while the PM2.5, the rest being considered coarse PM (World was highest during winter and lowest during summer. On the ilar to those observed in heavy smokers in Western countries, the annual average is 10 ug/m’. Approximately 92% of the Health Organization 2005) (Guarnieri and Balmes 2014) other hand, increased levels of PM2.5 are also found in the with a value between 20 and 26% (Barone-Adesi et al. 2012). world’s population lives in locations where the mean PM2.5 (Mannucci et al. 2015). spring and autumn due to the contribution of dust particles and Lung function begins to deteriorate after exposure to smoke mass concentration surpasses this amount. Approximately 3 PM with a 2.5-10-um aerodynamic diameter, also known the start of burning biomass. In addition, the lowest and for more than 15 years. The chance of having modified pulmo- million persons die from outdoor air pollution each year as coarse PM, is stored particularly in the head and in the highest PM2.5 concentrations frequently occur in the after- nary function increases as the duration of exposure increases. In (Wang et al. 2019b). upper respiratory tract. PM2.5 is usually stored in the deep noon and evening hours (Johannson et al. 2014). rural areas, women are generally more exposed due to their Springer 2 Springer

19620 Environ Sci Pollut Res (2021) 28:19615-19628 Environ Sci Pollut Res (2021) 28:19615-19628 19621 conventional lifestyle. In a case-control study, from a total of inflammation can be induced by specific pollutants (03, NO2, factor incriminated in developing lung cancer is active lung cancer in correlation to PM2.5 exposure (Wang et al. 115 women exposed to biomass smoke, 23.8% had small air- PM2.5), while airway hyperresponsiveness can be induced by smoking, but exposure to environmental occupational carcin- 2019a). way disease, 19.1% had obstruction, and 17.3% had a restrict 03 and NO2 (Johannson et al. 2014) (Kravchenko and Lyerly ogens, residential radon, and passive smoke is also recognized tion pattern on pulmonary function tests (Balcan et al. 2016). 2018). as risk factors (Raaschou-Nielsen et al. 2013). Idiopathic pulmonary fibrosis The EGEA study conducted on 204 adult asthmatic pa- Although the association between lung cancer and long- tients revealed important data about the role of oxidative stress term exposure to air pollution has been clarified, the link be- Idiopathic pulmonary fibrosis (IPF) is defined as a specific Public health focus on respiratory disease in the association between air pollution and asthma. The levels tween lung cancer mortality and short-term exposure to air form of chronic, progressive fibrosing interstitial pneumonia of fluorescent oxidation products (FIOPs), an oxidative stress- pollution remains unknown. The number of lung cancer cases of unknown cause, occurring primarily in older adults, and Chronic obstructive pulmonary disease related biomarker, increased with PM10 and O3, and the risk is expected to increase due to continuous exposure to air pol- limited to the lungs. It is a progressive lung disease with a of persistent asthma increased with plasma FIOP levels (Havet lution in regard to massive industrialization, an aging popula- complex etiology (Johannson et al. 2018) characterized by COPD is a multifactorial condition characterized by chronic et al. 2019) tion and constant high smoking prevalence (Wang et al. progressive worsening of dyspnea and lung function and is airway obstruction that is incompletely reversible, progres- Air pollution represents one of the most important factors 2019d). PM2.5, PM10, and O3 contribute to oxidative stress associated with poor prognosis (Raghu et al. 2011). sive, and associated with an abnormal inflammatory response aggravating asthma in children, with higher incidences in within the respiratory system and therefore potentially facili- There are not enough studies to certify the effects of air of the lung to harmful particles or gases (Singh et al. 2019). European and Caribbean regions (Cadelis et al. tate pulmonary inflammation and could initiate or promote the pollution on interstitial lung disease. However, in a study con- Ambient air pollution is associated with COPD morbidity 2014)(Akpinar-Elci et al. 2015). One of the contributing fac- mechanisms of carcinogenesis (Xing et al. 2019). PM2.5 is ducted by Johansson, it was shown that acute exacerbations of and mortality. From systemic analyses, it was observed that tors is Saharan dust (Gyan et al. 2005). Saharan particles are considered the most relevant pollutant (Hamra et al. 2014). IPF were associated with an increase in the mean level, the morbidity from COPD is correlated with a short-term increase composed of mineral origins. They are composed of a multi- In 2010, cancers of the trachea, bronchial tree, or lungs maximum level, and the number of exceedances above ac- in air pollution (Adar et al. 2014)(Zhang et al. 2016) (Tian tude of particles, such as clay, quartz, silicon oxide, and car- attributable to exposure to PM2.5 accounted for approximate- cepted standards of O, and NO2 (Johannson et al. 2014). Of et al. 2018). bonates. They are lined with organic matter represented by y 7% of total mortality. The mechanisms that have been in- the six criteria regulated by the US Environmental Protection The body’s response may differ from person to person. The bacteria and spores or pollen grains. Saharan dust contains criminated in the association between PM2.5 and lung cancer Agency, particulate matter (PM), ground level (03), and NO2 ability of each person to react to air pollution may differ in the PM10 and PM2.5-10, which can further predispose to an include DNA deterioration and cell cycle changes (Longhin were strongly related to adverse respiratory effects (Johannson Chinese population compared with the North American or increase in visits to the emergency service for patients aged et al. 2013). PM2.5 was also related to increased production of et al. 2015). European population due to differences in air pollution con- 5-15 years (Cadelis et al. 2014). reactive oxidative species. One potential mechanism by which ambient air pollution centration and the composition of the polluted air. At the same In a retrospective study of 5 years conducted by Muge A correlation was observed between the aerodynamic di- may cause interstitial lung disease is oxidative stress through time, the pre-existing pathology of one population may be Akpinar-Elci, the relationship between Saharan dust and ex- ameter of the fine particles in the medium – 2.5 (PM2.5) and the generation of excess reactive oxygen species (ROS), such different from another. In a study conducted in Beijing, posure, climatic variables, and asthma was analyzed. There the incidence and mortality from lung cancer. Based on a as radical hydroxide and superoxide anion. IPF patients ex- China, a reduction in the average concentration of PM2.5 up were 441 1 recorded asthma-related emergency visits, and var- meta-analysis of 18 studies, the correlation between PM2.5 hibit evidence of reduced antioxidant capacity, suggesting that to 58 ug/m’ was observed in 2017 compared with 2013 when iation in asthma was correlated with dust concentration and PM10 and the incidence and mortality of lung cancer were they may have an increased vulnerability to excess ROS the average concentration was 87 ug/m . Although a signifi- (Akpinar-Elci et al. 2015). Additionally, in a study conducted studied. Following the analysis, it was observed that the meta- (Johannson et al. 2015). Another explanation for the progres- cant reduction was observed, the value was still high, given by Cadelis et al., there were 836 visits for asthma, with 514 relative risk was 1.09 for lung cancer related to PM2.5 and sive evolution of the disease was highlighted by the study of that the reference value was 10 ug/m’ according to the WHO. boys and 322 girls (Cadelis et al. 2014). 1.09 for PM10. Additionally, the risk of adenocarcinoma as- Winterbottom et al. on 135 subjects evaluated between 2007 However, it was observed that there were 161,613 hospitali- In a study that took place in 10 European cities, the inci- sociated with PM 10 was 1.29, while for PM2.5, it was 1.4. and 2013. The results showed a strong association between zations for exacerbations of COPD (most patients were men dence of asthma among children was 14%, and after exposure These results can help us better analyze the pathology of PM10 levels and a decrease in forced vital capacity (FVC). over 65 years of age). Short-term exposure to air pollutants to air with polluting compounds from road traffic, children bronchopulmonary cancer in connection with air pollution With each ug/m increase in PM10, there was an additional 46 was correlated with hospital visits in the COPD emergency with exacerbated asthma constituted 15% of the cohort. (Hamra et al. 2014). cc/year decline in FVC. The significant relationship observed sections, resulting in subsequent hospitalizations and mortal- Asthma symptoms have been correlated with short-term ex- In the Ahsmong-2 study, it was shown that for each 10 ug/ between the exposure to coarse (PM10) and the decline rate of ty (Liang et al. 2019). posure to ambient PM2.5 and PM10 in prospective cohorts, m’ increase in ambient PM2.5, the incidence of lung cancer FVC was not reported for PM2.5, showing an inverse rela- In a population-based study involving 3941 nonsmoking particularly in children with allergic sensitivity (Guarnieri and increased, although the individuals from the study were ex- tionship between the diameter size of the particle and penetra- Taiwanese adults, 791 had COPD. Exposure to PM2.5 at con- Balmes 2014). In a cohort study conducted by Bowatte et al., posed to low levels of ambient PM2.5 and had never smoked. tion into the airways. Each 5 ug/m’ increase in ambient centrations higher than 38.98 ug/m’ was associated with in- exposure to traffic-related air pollution (TRAP) was associat- The percentage was higher for individuals who had a longer PM2.5 concentration at residences corresponded with an ad- creased predisposition to COPD among nonsmokers in ed with both persistent and new-onset asthma in adults. Living period of residence and who had spent more than 1 h/day ditional 1.15 L/year increase in oxygen use on the 6-min walk Taiwan. However, exposures to concentrations of 32.07- <200 m from a major road was correlated with greater odds of outside. The predominant type of cancer was adenocarci ing test (6MWT) (Winterbottom et al. 2018). The results are 38.98 ug/m’ and 29.38-32.07 ug/m’ were not significant new asthma for middle-aged persons who never had asthma nomas, with a percentage of 66.4% (Gharibvand et al. 2017). equivocal, because the study conducted by Kerri A (Huang et al. 2019). by 45 years. Asthmatic participants at 45 years had an in- Wang et al. suggested that the carcinogenic effects of Johannson et al. showed that PM10, PM2.5, and NO2 were From the multitude of studies that have shown a link be- creased risk of persistent asthma up to 53 years if they were PM2.5 vary by gender as well as by the environment in which associated with reduced lung function, but the changes were tween COPD and air pollution, we selected this study living < 200 m from a major road compared with asthmatic individuals live, i.e., rural or urban. It has also been observed independent of air pollution exposure (Johannson et al. 2018). participants living > 200 m from a major road (Bowatte et al. that younger people have a lower sensitivity than elderly peo- There were no significant relationships between mean Asthma 2018) ple. For individuals in rural areas, it was observed that with a weekly change in air pollutant levels and concurrent weekly growth level of the average concentration of PM2.5 by 10 ug/ changes in forced vital capacity (FVC), forced expiratory vol- At high concentrations, air pollutants have a direct inflamma Lung cancer m’, the incidence and mortality from lung cancer were 15% ume during the first second (FEV1), University of California tory effect on airway neuroreceptors and the epithelium. In and 23% among men, compared with 22% and 24% among San Diego Shortness of Breath Questionnaire (UCSD- addition, oxidative stress has been associated with pollutant Lung cancer represents one of the most common types of women, respectively. Thus, following this study, the results SOBQ), or visual analog scale (VAS) scores. Nevertheless. exposure (03, NO2, PM2.5) (Johannson et al. 2014). Airway cancer and has a poor prognosis. The most important risk showed that women have a meaningful risk of developing regarding the duration or interval of assessment periods, there Springer 2 Springer

19622 Environ Sci Pollut Res (2021) 28:19615-19628 Environ Sci Pollut Res (2021) 28:19615-19628 19623 was no significant association between the mean level of air exhibited lower values in the warmer period. Young children the incidence of tuberculosis by spreading pathogens (Zhang risk for ambient PM2.5, PM10, O3, and CO exposure. The pollutants and subsequent changes in lung function. have a higher degree of susceptibility than older individuals and Zhang 2019). Fine particulate matter and traffic-related air most significant association for PM2.5 was noticed at 540 Additionally, neither higher cumulative mean exposures nor due to their less developed immune system, tighter airways, pollution might be associated with an increased risk of devel- days of exposure, for O3 was noticed at 180 days of exposure, maximal exposures to air pollution were associated with a higher frequency of respiration, and higher long-term expo- oping tuberculosis. This association is not due to direct expo- and for PM10 and CO, it was noted from 90 to 540 days of more rapid decline in FVC or FEV1 over the study period. sure to air pollutants of the lower respiratory tract. Due to the sure but rather to the impairment of the individual’s immunity exposure. Of the 752 cases, 18.8% were first-line drug-resis- However, in patients with IPF, average exposures to NO2, excessive use of coal for heating during the colder season, Lai et al. 2016). Popovic et al. showed in a systematic review tant cases with streptomycin having the highest rate of resis- PM2.5, and PM10 were associated with lower FVC, indicat- winds also contribute to increased concentrations of air pol- that the pollutant most frequently associated with tuberculosis tance (15.3%), 13% were second-line resistant, ing that air pollution may influence the severity of disease in lutants (P. Zheng et al. 2017). s PM2.5 (Popovic et al. 2019). fluoroquinolones having the highest rate of resistance some individuals (Johannson et al. 2018). The Chengdu study also documented that exposure to am- (11.3%), 12.3% were resistant to more than 1 drug but not In a study with 436 patients performed by Johannson et al., Bronchiectasis bient PM10, NO2, and SO2 was linked to increased tubercu MDR, and 3.3% were MDR-TB (Yao et al. 2019). 75 of them had at least one acute exacerbation, and a subgroup losis morbidity in China, but the lag time was 28 days for NO2 nitrogen dioxide, SO2 sulfur dioxide, PM2.5 particu- of 13 patients had more than one exacerbation. During the Bronchiectasis is defined as inappropriate and permanent di- PM10 and 5 days for SO2 and NO2, which can only be attrib- late matter with diameter < 2.5um in diameter, PM10 partic- exposure period, acute exacerbation of IPF was correlated latation of the bronchi. It is a chronic respiratory disease, with uted to short-term effects (Zhu et al. 2018). Another study ulate matter with diameter < 10um in diameter, O; ozone, CO significantly with increased mean rates, maximum levels, many patients having frequent exacerbations. Due to their conducted by Lai et al. highlighted that an increased risk of carbon monoxide, COPD chronic obstructive pulmonary dis- and amounts of O3 and NO2 exceedances. Increased exposure exacerbations, lung function will subsequently decrease, fur- active tuberculosis is related to exposure to fine particulate ease, IPF idiopathic pulmonary fibrosis to O3 and NO2 over the preceding 6 weeks was associated thermore, increasing mortality (Garcia-Olive et al. 2018). matter PM2.5. Furthermore, traffic-related air pollution, in with a high risk of acute exacerbation of IPF. This suggests Infectious pathogens are often incriminated in the majority cluding nitrogen dioxide, nitrogen, and carbon monoxide, Animal experiments that air pollution could be correlated with the development of of bronchiectasis exacerbations, but frequently, no pathogen was associated with tuberculosis risk. On the other hand, this clinically significant event. At the same time, there were can be identified. In a study conducted by C. Pieter Goeminne PM10 was not linked with active tuberculosis, and Os was Animal experiments have opened up new perspectives on air no consistent relationships between PM10, SO2, or CO and et al. on 432 patients diagnosed through high-resolution com- inversely associated with the risk of TB (Lai et al. 2016). pollution (Edwards et al. 2020). Air pollution contributes to acute exacerbation of IPF compared with NO2, O3, and PM2.5 puted tomography (HRCT) and clinically confirmed bronchi- Similar to the last results, O3 levels could not be signifi- increased inflammation. When polluted air is inhaled, its first (Johannson et al. 2014). ectasis, for a 10 ug/m’ increase in PM10 and NO2, the chance cantly correlated with acid fast bacilli (AFB)-positive smears stop is the lungs. This is where oxidation-reduction first oc- of developing an exacerbation in that same day increased by in the retrospective study of Jamal et al. Medical records of curs (Gangwar et al. 2020). Oxidative stress arises from alter- Respiratory infections 4.5% and 3.2%. In total, 11.2% for PM10 and 4.7% for NO2 196 individuals diagnosed with TB positivity at Los Angeles ing the balance between oxidants and antioxidants. Altering were the risk of having an exacerbation for a 10-ug/m’ in- County and University of Southern California Medical Center this balance will increase oxidative stress and cause the in- In the cross-sectional study of Nsoh et al., 1849 patients diag- crease in the concentration of air pollutants. Subanalysis Hospital were analyzed. A total of 11 1 had smear positivity, crease of lung pathologies through promoting inflammation nosed from January 2013 to April 2016 with acute respiratory showed considerably higher relative risks through spring and while 85 had smear negativity. There was a significant corre- of the airways. PM consists of a number of components capa- infections (ARIs) were registered. Of the selected patients, summer due to increased expected outdoor air pollution expo- lation in single pollutant models analyzing PM2.5 levels and ble of generating ROS, which subsequently increase inflam- more than 70% used at least one form of solid fuel for sure (Goeminne et al. 2018). smear-positive TB (Jassal et al. 2012). matory mediators in the lungs (Valavanidis et al. 2013). cooking. In poorly ventilated homes, the impact of this expo- Additionally, in a retrospective observational study con- The link between PM2.5 concentration, notably a 10 ug/m’ In a study conducted by Edward et al., it was observed that sure was irritation of the respiratory tract and eyes and an ducted in Badalona, SO2 was considerably related to an in- increase in PM2.5 levels, and active TB was also noted in a rats exposed to TRAP, compared with those not exposed, increased risk of cancers related to long-term inhalation of this crease in the hospitalization number (Garcia-Olive et al study conducted from 2014 to 2017 in Lianyungang. For the exhibited increased gene expression changes related to oxida- poor-quality air. The probability of developing ARI was 3.62 2018). Through our search of the literature, we noticed that single-pollutant model, the association between a 10-ug/m’ tive stress, inflammation, aging, and fibrosis in the heart times higher for people who were exposed to cooking indoors there are few studies on the connection between air pollution increase in PM10 concentration and SO2 concentration and (Edwards et al. 2020). While Zheng et al. showed that follow- than for those who were not exposed. Additionally, the and bronchiectasis. active TB was significant. Additionally, a potential correlation ing exposure to tracheal diesel particles, mice presented an chances of developing ARI were 1.91 times higher for those between relatively long-term outdoor exposure to PM2.5, increase in transient oxidative stress in the lungs, Sun et al. exposed to open fire than for those who were not exposed. Tuberculosis PM10, SO2, and NO2 and active TB was observed in the showed that PM2.5 accentuates the degree of atherosclerosis, Thus, PM2.5 values were 13.2 times higher than what the time-series study conducted in the northeastern region of degrades vasomotor tone, and determines vascular inflamma WHO recommends. Dry weather and dust also increase the According to the WHO, in the 2019 Global Tuberculosis Jiangsu Province, China. In the multipollutant models, ambi- tion in mice that have been chronically exposed to low con- risk of developing ARI (Nsoh et al. 2019). Report, approximately 10 million people worldwide fell ill ent PM10 and NO2 remained significant, and the association centrations of PM2.5 (Q. Sun et al. 2015) (X. Zheng et al. A study conducted in China found that with increasing with tuberculosis in 2018, and it is the leading cause of a was not altered in subgroups of different genders or ages (Li 2019) (Gangwar et al. 2020). Rats that were exposed to ozone concentrations of PM2.5 and PM2.5-10 compounds, the single infectious agent. Worldwide, tuberculosis is considered et al. 2019) showed 8-hydroxy-2′-deoxyguanosine (8-OHdG) and heme number of hospital visits for upper airway infections and to be the 10th leading cause of death (WHO-Global In addition, exposure to pollution over different periods of oxygenase-1 (HO-1) in macrophages, developing rigid lungs pneumonia meaningfully increased. The increase in the aver- Tuberculosis Report 2019 n.d.) Tuberculosis (TB) is a disease time may be associated with drug resistance. Exposure to with reduced function (Sunil et al. 2013) (Valavanidis et al. age concentration, which accumulated over 6 days, was 10 whose prevalence has been associated with socioeconomic PM2.5, PM10, O3, and CO has been associated with drug- 2013). ug/m’ (Z. Zhang et al. 2019). risk factors that has a stronger association with urban settings, resistant TB, including first-line monodrug resistance, Fibrosis and reversible cardiac dysfunction were observed Zheng P et al. constructed a seasonal model of cases of where there is greater exposure to air pollution (Jassal et al. polydrug resistance, and multidrug resistance (MDR), in both in mice after intratracheal exposure to PM2.5 (Gangwar et al. respiratory infections, revealing a higher preponderante in 2012). single- and multiregression models. In the retrospective study 2020). Oxidative stress in the myocardium is increased in the period with lower temperatures. While children aged 5- There is a direct correlation between air quality and tuber- of Yao et al., conducted in Jinan city, China, from January 1, those exposed to ultrafine particles (Cozzi et al. 2021). Qin 14 years had a higher chance of developing acute respiratory culosis incidence. Precipitation, atmospheric pressure, and rel- 2014 to December 31, 2015, 752 new culture-confirmed TB and all demonstrated that after intratracheal exposure to infections (55.1%), those under 5 years had a higher chance ative humidity affect the incidence of tuberculosis by indirect- cases reported in TB prevention and control institutions of PM2.5, the most sensitive were the extremes of age compared (60.5%) of developing lower acute respiratory infections. The ly reducing the quantity of inhalable PM and SO2 concentra- inan were included. The results showed significant with adult animals, developing heart dysfunction and revers- concentrations of air pollutants PM10, NO2, and SO2 tions. On the other hand, wind plays a major role by increasing monodrug resistance, and polydrug resistance increased the ible fibrosis (Qin et al. 2018) (Gangwar et al. 2020). Cozzi Springer 2 Springer

Collepals.com Plagiarism Free Papers

Are you looking for custom essay writing service or even dissertation writing services? Just request for our write my paper service, and we'll match you with the best essay writer in your subject! With an exceptional team of professional academic experts in a wide range of subjects, we can guarantee you an unrivaled quality of custom-written papers.

Get ZERO PLAGIARISM, HUMAN WRITTEN ESSAYS

Why Hire Collepals.com writers to do your paper?

Quality- We are experienced and have access to ample research materials.

We write plagiarism Free Content

Confidential- We never share or sell your personal information to third parties.

Support-Chat with us today! We are always waiting to answer all your questions.