described with a difficulty noted of determining the best treatment. the only genotype is the alpha-1 antitrypsin deficiency (aatd) genetic subtype and this has a specific treatment. cause the cause of the development of copd is the exposure to harmful particles or gases, including tobacco smoke, 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 copd is tobacco smoke. however, less than 50 percent of heavy smokers develop copd, so other factors need to be considered, including exposure to indoor and outdoor pollutants, allergens, occupational exposure, and host factors. one of the known causes of copd is the exposure to construction dust. the three main types of construction dust includes silica dust, non-silica dust (e.g, dust from gypsum, cement, limestone, marble and dolomite) and wood dust. 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 comorbidity of copd 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 chronic 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 copd. a genetic association for the variants has been sometimes found with fgf10. alcohol abuse can lead to alcoholic lung disease and is seen to be an independent risk factor for copd. mucociliary clearance is disrupted by chronic 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 receptor for the sars-cov-2 virus. smoking the primary risk factor for copd globally is tobacco smoking with an increased rate of developing copd shown in smokers and ex-smokers. of those who smoke, about 20% will get copd, increasing to less than 50% in heavy smokers. in the united states and united kingdom, of those with copd, 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 copd than men. in non-smokers, exposure to second-hand smoke (passive smoking) is the cause of 1.2 million deaths from the more than 8 million deaths worldwide each year due to tobacco smoke. women who smoke during pregnancy, and during the early life of the child is a risk factor for the later development of copd in their child. inhaled smoke triggers the release of excessive proteases in lungs, which then degrades elastin, the major component of alveoli (which allows rapid gas exchange in the lungs). smoke also impairs the action of cilia, inhibiting mucociliary clearance that clears 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 than smoking cigarettes. marijuana is the second most commonly smoked substance, but evidence linking its use to copd 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, copd 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 chronic 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 chronic marijuana smokers even with the additional use of tobacco developed similar respiratory problems, but did not seem to develop airflow limitation and copd. pollution