The cause of the development of<unk>  is the exposure to harmful particles or gases that irritate the lung causing inflammation that interacts with a number of host factors. Such exposure needs to be significant or long-term. The greatest risk factor for the development of<unk>  is tobacco smoke. However, less than 50 percent of heavy smokers develop<unk> , so other factors including exposure to indoor and outdoor pollutants, allergens, occupational exposure, and host factors need to be considered. Host factors include a genetic susceptibility, factors associated with poverty, aging and physical inactivity. Asthma and tuberculosis are also recognized as risk factors, as the cormorbidity of<unk>  is reported to be 12 times higher in patients with asthma after adjusting for smoking history. In Europe airway hyperresponsiveness is rated as the second most important risk factor after smoking. A host factor of an airway branching variation arising during development has been described. The respiratory tree is a filter for harmful substances and any variant has the potential to disrupt this. A variation has been found to be associated with the development of<unk>  bronchitis, and another with the development of emphysema. A branch variant in the central airway is specifically associated with an increased susceptibility for the later development of<unk> . A genetic association for the variants has been sometimes found with FGF10. Alcohol abuse can lead to alcoholic lung<unk>  and is seen to be an independent risk factor for<unk> . Mucociliary clearance is disrupted by<unk>  exposure to alcohol; macrophage activity is diminished and an inflammatory response promoted. The damage leads to a susceptibility for infection, including COVID-19, more so when combined with smoking; smoking induces the upregulation of the expression of ACE2 a recognized factor in the development of COVID-19. Smoking The primary risk factor for<unk>  globally is tobacco smoking with an increased rate of developing<unk>  shown in smokers and ex-smokers. Of those who smoke, about 20% will get<unk> , increasing to less than 50% in heavy smokers. In the United States and United Kingdom, of those with<unk> , 80–95% are either current or previous smokers. Several studies indicate that women are more susceptible than men to the harmful effects of tobacco smoke. For the same amount of cigarette smoking, women have a higher risk of<unk>  than men. In non-smokers, exposure to passive smoking (second-hand smoke) is the cause of 1.2 million deaths from the more than 8 million deaths worldwide due to tobacco smoke. Women who smoke during pregnancy and in early life of the child is a risk factor for the later development of<unk>  in their child. Inhaled smoke triggers the release of excessive proteases in lungs, which then degrades elastin, the major component of aveoli (which allows rapid gas exchange in the lungs). Smoke also impairs the action of cilia, inhibiting the cilia from clearing the bronchi of mucus, cellular debris, and unwanted fluid. Other types of tobacco smoke, such as from cigar, pipe, water-pipe and hookah use, also confer a risk. Water-pipe or hookah smoke appears to be as harmful or even more harmful as smoking cigarettes. Marijuana is the second most commonly smoked substance, but evidence linking its use to<unk>  is very limited. Limited evidence shows that marijuana does not accelerate lung function decline. A low use of marijuana gives a bronchodilatory effect rather than the bronchoconstrictive effect from tobacco use, but it is often smoked in combination with tobacco or on its own by tobacco smokers. Higher use however has shown a decline in the FEV1. There is evidence of it causing some respiratory problems, and its use in combination may have a cumulative toxic effect suggesting it as a risk factor for spontaneous pneumothorax, bullous emphysema,<unk> , and lung cancer. A noted difference between marijuana use and tobacco was that respiratory problems were resolved with stopping usage unlike the continued decline with stopping tobacco smoking. Respiratory symptoms reported with marijuana use included<unk>  cough, increased sputum production, and wheezing but not shortness of breath. Also these symptoms were typically reported ten years ahead of their affecting tobacco smokers. Another study found that<unk>  marijuana smokers even with the additional use of tobacco developed similar respiratory problems, but did not seem to develop airflow limitation and<unk> . Pollution Access to clean fuel and clean cooking facilities as of 2016. Poorly ventilated fires used for cooking and heating, are often fueled by coal or biomass such as wood and dry dung, leading to indoor air pollution and are one of the most common causes of<unk>  in developing countries. Women are affected more as they have a greater exposure. These fuels are used as the main source of energy in 80% of homes in India, China and sub-Saharan Africa. People who live in large cities have a higher rate of<unk>  compared to people who live in rural areas. While urban air pollution is a contributing factor in exacerbations, its overall role as a cause of<unk>  is unclear. However, urban air significantly effects the developing lung and its maturation, and contributes a potential risk factor for the development of<unk> . Areas with poor outdoor air quality, including that from exhaust gas, generally have higher rates of<unk> . The overall effect in relation to smoking, is believed to be small. Occupational exposure Intense and prolonged exposure to workplace dusts, chemicals, and fumes increases the risk of<unk>  in smokers, nonsmokers, and never-smokers. Substances implicated in occupational exposure and listed in the UK, include organic and inorganic dusts such as cadmium, silica, dust from grains and flour, and fumes from cadmium and welding that promote respiratory symptoms. Workplace exposure is believed to be the cause in 10–20% of cases, and in the United States, it is believed to be related to around 30% of cases among never smokers, and probably represents a greater risk in countries without sufficient regulations. The negative effects of dust exposure and cigarette smoke exposure appear to be cumulative. Genetics Genetics play a role in the development of<unk> . It is more common among relatives of those with<unk>  who smoke than unrelated smokers. The most well known genetic risk factor is alpha-1 antitrypsin deficiency (AATD), and this is the only genotype (genetic subtype) with a specific treatment. This risk is particularly high if someone deficient in alpha-1 antitrypsin (AAT) also smokes. It is responsible for about 1–5% of cases and the condition is present in about three to four in 10,000 people. The<unk> Gene study is an ongoing longitudinal study into the epidemiology of<unk> , identifying phenotypes and looking for their likely association with susceptible genes. Genome wide analyses in concert with the International<unk>  Genetics Consortium has identified more than 80 genome regions associated with<unk> , and further studies in these regions has been called for. Whole genome sequencing is an ongoing collaboration (2019) with the National Heart, Lung, and Blood Institute (NHLBI) to identify rare genetic determinants.
Chronic obstructive pulmonary disease
Tracheobronchomalacia
Asthma
Bronchiectasis
Reactive airway disease
Pneumonia
End stage pulmonary disease
Acute bronchitis