Diesel And Fracking: Pollutants' Link To Pulmonary Embolism

Diesel engines and fracking are major sources of air pollution. Air pollution has been linked to a wide range of health issues, including respiratory and cardiovascular illnesses, and even premature death.

Diesel engines, for instance, emit fine particulate matter and nitrogen oxides, which are harmful to human health even at low concentrations and through short-term exposure. Fracking, on the other hand, involves injecting sand, water, and chemicals into underground rock formations to release natural gas and oil. This process can worsen air and water quality, leading to potential health risks for nearby communities.

While the specific link between pollutants from diesel engines and fracking and pulmonary embolism requires further investigation, the available evidence suggests that air pollution can indeed increase the risk of pulmonary embolism. Therefore, it is reasonable to assume that pollutants from diesel engines and fracking may contribute to this health condition.

Diesel exhaust particles can cause acute effects like nose and eye irritation, lung function changes, respiratory changes, headache, fatigue and nausea

Diesel Exhaust Particles and Their Acute Effects

Diesel exhaust particles are among the most prevalent anthropogenic pollutants worldwide, and their adverse health effects are well-documented. Here is a detailed overview of the acute effects of diesel exhaust particles, including nose and eye irritation, lung function changes, respiratory changes, headache, fatigue, and nausea:

Nose and Eye Irritation:

Diesel exhaust particles can cause irritation and discomfort in the nose and eyes. The complex mixture of solid, liquid, and gaseous fractions in diesel exhaust can lead to nasal congestion, watery eyes, and other symptoms associated with irritation of the mucous membranes.

Lung Function and Respiratory Changes:

Diesel exhaust particles can have immediate effects on lung function and respiratory patterns. Inhalation of these particles can lead to coughing, shortness of breath, and changes in breathing patterns, such as rapid breathing or tachypnea. The particles can also cause lung inflammation and affect gas exchange in the alveoli, the tiny air sacs in the lungs where oxygen and carbon dioxide are exchanged.

Headache, Fatigue, and Nausea:

Exposure to diesel exhaust particles can result in non-specific symptoms such as headache, fatigue, and nausea. These symptoms may be due to the body's response to the irritant effects of the particles or the overall impact on the respiratory and cardiovascular systems.

Other Acute Effects:

In addition to the above-mentioned acute effects, diesel exhaust particles can also cause changes in heart rate, chest pain, and coughing up blood. The particles can trigger inflammatory responses and affect the cardiovascular system, leading to an increased risk of cardiovascular diseases and thrombosis.

It is important to note that the effects of diesel exhaust particles can vary depending on individual factors, duration of exposure, and the concentration of particles inhaled. While some people may experience more severe acute effects, others may have milder or no noticeable symptoms at all.

Furthermore, it is worth mentioning that diesel exhaust particles are not the only contributors to air pollution. Other sources, such as gasoline engines, industrial emissions, and natural sources, also play a role in air pollution and can have similar acute effects.

Diesel exhaust particles can cause chronic effects like cough, sputum production and lung function decrements

Diesel exhaust particles are a major component of fine particulate matter in the atmosphere of urban areas. Exposure to diesel exhaust particles has been associated with acute short-term symptoms, such as headache, dizziness, coughing, difficult or laboured breathing, and irritation of the eyes, nose, and throat.

Chronic exposure to diesel exhaust particles can lead to the development of cough and sputum. In addition, chronic bronchitis may be partially responsible for some of the exacerbations of asthma. The biological response to inhaled particles is aggravated during chronic exposure to diesel exhaust particles in a dose-dependent manner.

Chronic exposure to diesel exhaust particles can also lead to increased airway responsiveness and inflammatory cell infiltration, cytokine changes, collagen deposition, and goblet cell hyperplasia, indicating that long-term exposure to diesel exhaust particles may be associated with airway hyperresponsiveness, inflammation, and lung fibrosis.

Diesel exhaust particles can cause inflammation in the airways

Diesel exhaust particles (DEPs) are a major component of fine particulate matter in the atmosphere of urban areas. DEPs can induce and trigger airway hyperresponsiveness and inflammation. DEPs are related to allergic diseases, including asthma and allergic rhinitis, and act as an adjuvant during allergen exposure and effect acute asthma exacerbations, bronchitis, or chronic obstructive pulmonary disease.

The gaseous exhaust fraction of DEPs consists of more than 99% by volume of non-toxic inorganic gases such as nitrogen, water and oxygen. Toxic inorganic gases such as carbon dioxide (CO2), carbon monoxide (CO), nitric oxide (NO) and nitrogen dioxide (NO2), and a complex mixture of organic compounds account for the rest. The organic fraction consists of small molecules such as methanol, ethylene or formaldehyde but mainly of larger aliphatic compounds and more complex molecules such as benzene, naphthalene, pyrene, anthracene and their various functionalized derivatives, collectively referred to as polycyclic aromatic hydrocarbons (PAHs), nitrated polyaromatic hydrocarbons (NPAHs) and heterocyclic aromatic compounds (HACs).

The inflammatory effects of DEPs seem to be attributable to the soluble organic fraction, but questions still remain with respect to what fraction and components that are most important for the inflammatory responses. The mechanisms are still unclear, but receptors in the plasma membrane, including the PAR-2 receptor, vanilloid-1 receptor, RAGE-receptor, and the EGF-receptor, seem to be involved. DEPs are known to induce acellular as well as cell-mediated ROS-formation, oxidative stress and deplete the levels of antioxidants, which seem to be involved in the inflammatory effects of DEPs.

Diesel exhaust particles can cause cardiovascular issues like increased blood coagulability, blood clotting and ischaemic heart disease

Diesel exhaust particles are a substantial cause of the negative health effects traced to air pollution, especially in traffic environments. The solid fraction of diesel exhaust contains metal and metal-oxides originating from lubrication and fuel additives and from engine wear. The gaseous exhaust fraction consists of toxic inorganic gases such as carbon dioxide (CO2), carbon monoxide (CO), nitric oxide (NO) and nitrogen dioxide (NO2), and a complex mixture of organic compounds. The organic fraction consists of small molecules such as methanol, ethylene or formaldehyde, but mainly of larger aliphatic compounds and more complex molecules such as benzene, naphthalene, pyrene, anthracene and their various functionalized derivatives, collectively referred to as polycyclic aromatic hydrocarbons (PAHs), nitrated polyaromatic hydrocarbons (NPAHs) and heterocyclic aromatic compounds (HACs).

The inhalation of diesel exhaust particles can induce pulmonary oxidative stress, (pro-)inflammation and genotoxicity, which ultimately may result in respiratory diseases such as chronic obstructive pulmonary disease (COPD), asthma and lung cancer. The exposure to diesel exhaust can also affect the vascular function in a group of healthy individuals and cause a decrease in two important and complementary blood-vessel functions: the regulation of the width of the blood vessels and the body’s ability to dissolve blood clots (fibrinolysis).

The exposure to diesel exhaust can also lead to a lowered capacity to dissolve blood clots, together with an impaired ability of blood vessels to expand. These effects can be observed in individuals with clinically stable coronary artery disease, and they are consistent with a shortage of oxygen in the heart muscle.

The exact causal connection between air pollution and adverse health effects is still not fully understood, but certain molecular and cellular mechanisms are generally assumed to play a key role. The most well-described cellular responses upon interaction with diesel exhaust are the induction of pulmonary oxidative stress and (pro-)inflammation, both of which are known to be involved in the onset or exacerbation of respiratory diseases such as COPD, but also in the (air pollution-related) development of systemic effects such as cardiovascular diseases or thrombosis. A further relevant reaction is the induction of genotoxicity, which is partly also linked to oxidative stress and (pro-)inflammation and may ultimately result in the onset of lung cancer.

Diesel exhaust particles can cause allergies and asthma

Diesel exhaust particles (DEPs) are a complex mixture of solid, condensed, and gaseous fractions. They are released by diesel-fuelled compression-ignition engines and are among the most prevalent anthropogenic pollutants worldwide. DEPs can act as nonspecific airway irritants at relatively high levels. However, at lower levels, they can promote the release of specific cytokines, chemokines, immunoglobulins, and oxidants in the upper and lower airway. This initiates a cascade that can culminate in airway inflammation, mucus secretion, serum leakage into the airways, and bronchial smooth muscle contraction.

DEPs have been linked to the onset and exacerbation of respiratory and allergic diseases, including asthma. Exposure to diesel exhaust particles can induce allergic inflammation and allergic immune responses, with most of these immune responses mediated by the carbon core of DEPs. Polyaromatic hydrocarbons (e.g., anthracene, fluoranthene, pyrene, phenanthrene) are major chemical components of DEPs and have been shown to enhance the production of immunoglobulin E.

Several epidemiological studies have demonstrated a strong association between exposure to motor vehicle traffic emissions and allergic symptoms and reduced lung function. However, the evidence for the development of allergic sensitization from DEPs is less abundant. Recent comparisons of the prevalence of hay fever and positive skin-prick tests between citizens of former West and East Germany and between Hong Kong and China civilians have demonstrated marked differences, which may be attributed to crucial variations in the level of particulate air pollution from motor vehicles in these countries.

DEPs appear to have greater immunologic effects in the presence of environmental allergens than they do alone. This immunologic evidence may help explain the epidemiologic studies indicating that children living along major trucking thoroughfares are at increased risk for asthmatic and allergic symptoms and are more likely to have objective evidence of respiratory dysfunction.

The health effects of exposure to DEPs are not trivial. Within the respiratory tract, they can exacerbate pre-existing, predominantly house dust mite-driven asthma, COPD, or rhinitis. The inhalation of diesel engine fumes is also implicated in myocardial ischaemia, thrombotic sequelae, the development of childhood asthma, and lung cancer.

Case Study: Diesel Engine Exhaust Emissions Exposure (DEEE) Mimicking Allergic Asthma and Rhinitis

A 36-year-old female bank employee presented with symptoms suggestive of asthma and rhinitis, for which she had previously required Accident and Emergency (A&E) treatment. The symptoms only occurred at work or after work and had coincided with changing offices to one located proximal to a diesel-powered electricity generator. A diagnosis of asthma was made, and the patient was prescribed inhaled fluticasone and salbutamol, which provided limited relief. Skin prick testing was weakly positive for seasonal pollen and house dust mite allergens, while tests for 16 regionally relevant aeroallergens were negative.

Upon further investigation, it was determined that the symptoms were triggered by DEEE exposure. Following a 10-day discontinuation of work exposure, the symptoms abated, and lung function improved. The recent onset of asthma in a non-atopic adult, with workday-related symptoms and improvement upon discontinuation of exposure, was attributed to passive occupational exposure to DEEE. The diesel generator was relocated, and the patient was prescribed a short course of inhaled fluticasone and oral prednisolone, leading to symptom resolution.

This case highlights the importance of considering occupational exposure in the evaluation of patients with asthma-like symptoms, even in office workers who do not meet the standard occupational risk profile. Serial monitoring of lung function values is recommended for diagnostic and monitoring purposes. Additionally, the increasing use of diesel generators in households and offices should prompt healthcare providers to include exposure to diesel fumes in the differential diagnoses of unexplained respiratory symptom exacerbations.

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