Who is vulnerable to copd

Increased mortality in COPD among construction workers exposed to inorganic dust. Decline in FEV1 and airflow limitation related to occupational exposures in men of an urban community. Salvi S. Tobacco smoking and environmental risk factors for chronic obstructive pulmonary disease.

Clin Chest Med. Genetic influences on chronic obstructive pulmonary disease - a twin study. Respir Med. Alpha1-antitrypsin deficiency. DeMeo D, Silverman E. Stockley RA. Alpha-1antitrypsin review. Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Siblings of patients with severe chronic obstructive pulmonary disease have a significant risk of airflow obstruction.

Hum Mol Genet. Genetic susceptibility. Early-onset chronic obstructive pulmonary disease is associated with female sex, maternal factors, and African American race in the COPDGene study.

New Mexican hispanic smokers have lower odds of chronic obstructive pulmonary disease and less decline in lung function than non-Hispanic whites. Lancet Respir Med. A genome-wide association study of emphysema and airway quantitative imaging phenotypes. Genome-wide association analysis of blood biomarkers in chronic obstructive pulmonary disease. Repression of CC16 by cigarette smoke CS exposure. PLoS One. Gender and chronic obstructive pulmonary disease: why it matters. Female smokers beyond the perimenopausal period are at increased risk of chronic obstructive pulmonary disease: a systematic review and meta-analysis.

Sex differences in airway remodeling in a mouse model of chronic obstructive pulmonary disease. Sex differences in chronic obstructive pulmonary disease mechanisms. Am J Respir Crit Care. Assad NA, Sood A. Leptin, adiponectin and pulmonary diseases. Gender differences in the adipose secretome system in chronic obstructive pulmonary disease COPD : a pivotal role of leptin.

Massaro D, Massaro GD. Proc Am Thorac Soc. Prescott E, Vestbo J. Socioeconomic status and chronic obstructive pulmonary disease. Stebbings J. Chronic respiratory disease among nonsmokers in Hagerstown, Maryland.

Social class and chronic respiratory disease. Environ Res. Long-term care use and socio-economic status in Belgium: a survival analysis using health care insurance data. Arch Public Health. Socioeconomic status, race and COPD health outcomes. J Epidemiol Community Health. Martinez FD. The origins of asthma and chronic obstructive pulmonary disease in early life. Risk factors and early origins of chronic obstructive pulmonary disease.

Lancet ; : Bolton CE. COPD as a consequence of premature birth? Controversies in COPD. ERS Monogr. Relation of birth weight and childhood respiratory infection to adult lung function and death from chronic obstructive airways disease. Lower respiratory tract infection in the first year of life is associated with worse lung function in adult life: prospective results from the Barry Caerphilly Growth study.

Ann Epidemiol. Early life origins of chronic obstructive pulmonary disease. Airway hyperresponsiveness to histamine associated with accelerated decline in FEV1. Methacholine reactivity predicts changes in lung function over time in smokers with early chronic obstructive pulmonary disease. Reversible and irreversible airflow obstruction as predictor of overall mortality in asthma and chronic obstructive pulmonary disease.

Rate of decline of lung function in subjects with asthma. Postma DS, Timens W. Remodeling in asthma and chronic obstructive pulmonary disease. Jeffery PK. Remodeling and inflammation of bronchi in asthma and chronic obstructive pulmonary disease. Guerra S. There are studies analysing the impact of tobacco on people with COVID infection, and it has been observed that active smokers present a greater risk of serious complications compared to ex-smokers and people who have never smoked.

For all these reasons, it is very important for patients with chronic lung disease such as COPD to adopt more restrictive measures to avoid contact with suspected or confirmed cases, and to thus minimise any potential exposure to SARS-CoV Therefore, you are advised to maintain as much social distance as possible, wash your hands frequently for at least 30 seconds, use a face mask, and follow all other measures established by the health authorities.

Furthermore, you should continue regular treatment, including in case of contagion, unless a healthcare professional indicates otherwise. Author: Nuria Seijas, nurse and care coordinator for Home Hospitalisation. We have received your information. Check your inbox, in a few moments you will receive a confirmation email. Accept cookies. This link opens in a new tab. Picture: Francisco Avia. Smoking is the main cause of COPD and is thought to be responsible for around 9 in every 10 cases.

The harmful chemicals in smoke can damage the lining of the lungs and airways. Stopping smoking can help prevent COPD from getting worse. Some research also suggests that being exposed to other people's cigarette smoke passive smoking may increase your risk of COPD. Exposure to certain types of dust and chemicals at work may damage the lungs and increase your risk of COPD. Treatment of COPD requires a careful and thorough evaluation by a physician.

Treatment options that your physician may consider include:. Skip directly to site content Skip directly to page options Skip directly to A-Z link. Section Navigation. Facebook Twitter LinkedIn Syndicate. Minus Related Pages.

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