COPD causes breathing problems that worsen over time. People with COPD have episodes called exacerbations where breathing gets much worse than usual, and they may need to be admitted to the hospital.
Routine screening with specialists familiar with Agent Orange complications is recommended. Patients who report exposure should undergo a head-to-toe examination with special consideration of potential dioxin-related problems.
Smoking
Inhaling tobacco smoke (from cigarettes, cigars, or pipes) is the primary risk factor for COPD. This toxin-laden smoke destroys the walls of many of the air sacs in the lungs, causes them to make more mucus, and limits airflow. It also leads to the development of chronic bronchitis and emphysema. Long-term exposure to other lung irritants may also lead to the development of COPD. This can include chemical fumes and dust from the workplace, cooking with gas or using fuel in the home without ventilation, and secondhand smoke from other people smoking.
Other significant factors causing COPD include genetics, older age, and respiratory infections such as pneumonia. Symptoms of COPD include coughing, wheezing, and shortness of breath. You may receive a COPD diagnosis after a doctor evaluates your symptoms and medical history, performs a physical exam, and conducts breathing tests, such as spirometry. COPD sufferers often experience exacerbations when their symptoms worsen significantly for several days.
Genetics
COPD from Agent Orange exposure is a condition that affects the lungs and airways. Exposure to chemicals in the workplace or to pollution in the environment can cause it, but some people are also genetically predisposed.
The underlying cause of COPD is chronic lung inflammation. Researchers evaluate genetic markers that measure this inflammation and have promising predictive value.
In up to 5 percent of people with COPD, the disease is hereditary and caused by a defective gene coding for alpha-1-antitrypsin (AAT). AAT deficiency cannot be prevented but can be managed with medications to prevent exacerbations.
Several genome-wide association studies have identified variants associated with COPD phenotypes. These include variations in the FEV1/FVC gene (CHRNA3/5 and IREB2) and variations on chromosomes 12 and 17. These variants impact COPD risk independently of smoking behavior. Researchers are pooling resources to perform collaborative genetic studies of multiple cohorts with genotype and phenotype data. These extensive collaborative genetic studies are expected to provide greater power than a single case-control study and may identify additional genetic variants.
Occupational Exposure
While smoking is the most recognized risk factor for COPD, several other environmental and occupational factors contribute to this disease. These include exposure to biological dusts, gas fumes, and pesticides. In cross-sectional studies, occupational exposure has been associated with COPD, which yields an additive effect when combined with smoking.
However, these studies are prone to recall bias.
Environmental Exposure
Air pollution, especially long-term exposure to dust and chemical vapors, can damage the lungs. This also increases your chances of developing COPD. People working in specific industries relying on chemical-based products, such as metal molders or coal miners, are more likely to develop lung problems because of their exposure to these fumes. In some cases, even those who have never smoked or had prolonged exposure to particulate matter can develop COPD due to genetic conditions like a lack of the protein alpha 1 (a1)-antitrypsin, which affects how the lungs take in oxygen.
One of the chemicals used in the Vietnam War was Agent Orange. This toxic herbicide contained dioxins, particularly 2,3,7,8-TCDD, which take a while to break down and accumulate in fatty tissues in animals and humans, entering the food chain. COPD from Agent Orange exposure causes various health issues, including cancer, immune system disturbances, and endocrine problems. Over a prolonged period of exposure to dioxins can increase the risk of cardiovascular and vascular diseases.
