TABLE 2.

The principal causes and factors associated with FEV₁ decline, COPD and asthma, as established from observational studies

Cause	Effect on FEV1 decline and/or COPD
1. Smoking	The only environmental risk factor whose contribution to COPD is entirely undisputed [48–50]; up to half of all smokers eventually develop fixed airflow limitation [54]. Smoking during pregnancy increases risk of low birth weight and decreased lung function at birth, leading to lower maximum FEV1 and increased risk of impaired pulmonary function and developing COPD in later life [55–58]. Adolescents who smoke show reduced development of lung function [59].
2. Occupational exposure to dust and gases	Leads to accelerated decline in FEV1 and increased incidence of COPD [60–62]. Dose–effect relationship between the number of agents to which subjects were exposed and decline in FEV1 [63].
3. Burning of solid fuels/biomass	Linked to an increased risk of developing respiratory symptoms and airflow limitation [64, 65]; rate of FEV1 decline slower and more homogeneous versus smokers [66].
4. Socioeconomic status and poverty	Strong risk factor for obstructive lung disease [67–69]. Specific link not known, but likely to include multiple aspects throughout life, including environment, diet, housing conditions and other lifestyle and occupational factors [70].
5. Chronic bronchitis	Strong association between chronic bronchitis/chronic mucus hypersecretion and FEV1 decline, COPD-related morbidity and both overall and COPD-related mortality [71–73]. Most important in patients <50 years of age [74].
6. Airway hyper-responsiveness	Known independent risk factor for COPD [75, 76]. Occurrence during young adult life associated with an increased risk of COPD 20 years later [75].
7. Asthma	Uncontrolled asthma leads to airway remodelling and fixed airflow obstruction that may lead to an incorrect diagnosis of COPD [77] .
Cause	Effect on asthma
1. Exposure to microorganisms	Viral infection is one of the most common causes of asthma exacerbations [53]. Exposure in early life is associated with an increased risk of developing persistent asthma in later life [53]; however, reduced exposure during childhood may be contributing to the global increase in allergy and asthma [52].
2. Allergen exposure	Childhood asthma is typically attributed to an allergic sensitisation [52, 53]. The risk of allergic sensitisation may differ between allergens and may be related to the dose and duration of exposure [52, 53, 78].
3. Smoking (active and passive)	Passive smoking, both pre- and post-natal, is associated with an increased risk of asthma in children [79]. Passive smoking is also associated with a higher prevalence of asthma and bronchial responsiveness in adults [80]. An association between active smoking and onset of asthma may be stronger in younger than older adults [81].
4. Air pollution	Exposure to traffic-related air pollution during early childhood is associated with a higher risk of developing asthma in later life [53]. An association between outdoor nitrogen levels and the onset of asthma has been observed in adults [82].
5. Indoor environment	Dampness in residential buildings has been associated with the onset of asthma in both children [83] and adults [84]; this problem may well extend to the workplace [84].
6. Occupation	Occupational exposure is estimated to account for approximately 15% of new asthma diagnoses in adults [85]. Cleaners, welders and farm workers in particular are at increased risk [86–88].
7. Diet	Low intake of vitamin C and fruit has been associated with a higher risk of asthma [89]. A lower prevalence of wheeze and risk of asthma has been observed in children receiving a Mediterranean diet and fish in early childhood [89].
8. Obesity	Obesity is a risk factor for developing asthma in both children and adults [90, 91]. The mechanism is not completely understood, but obesity-induced systemic inflammation [90, 92] and decreased physical activity may both play a role [93].

COPD: chronic obstructive pulmonary disease; FEV₁: forced expiratory volume in 1 s.