Environmental and Workplace Lung Disease

major atmospheric pollutants

carbon monoxide, nitrogen oxides, sulphur oxides, heavy metals, hydrocarbons, photochemical oxidants, particulate matter

carbon monoxide pollutant

largest pollutant by weight; produced by incomplete combustion of carbon in fuels, mainly cars

binds to hemoglobin, with 200x greater affinity than O2

commuter using a busy urban road may have 5-10% of their Hb bound to CO

evidence that it impairs mental skills, reduced by catalytic converters

nitrogen oxides

produced when fossil fuels burned at high temps in power stations and cars

cause inflammation of eyes and upper respiratory tract during smoggy conditions

high concentration can cause acute tracheitis, acute bronchitis, and pulmonary edema

sulphur oxide pollutant

corrosive, poisonous gases produced when sulphur containing fuels are burned, mainly by power stations

cause inflammation of mucous membranes, eyes, upper respiratory tract, and bronchial mucosa

short term exposure to high concs can cause edema

hydrocarbon pollutant

product of unburned fuel waste

not usually toxic at concentrations found in atmosphere, but can sunlight triggers conversion into photochemical oxidants

photochemical oxidants pollutant

ozone, peroxyacyl nitrates, aldehydes, and acrolein

produced by actions of sunlight on hydrocarbons and nitrogen oxides

cause inflammation of eyes and respiratory tract

high concentration ozone causes pulmonary edema

particulate matter pollutant

particles with range of sizes, up to visible smoke and soot

sources are power stations, industrial plants

although air pollution can occur due to natural causes such as volcanoes,

increased combustion of fossil fuels is the largest culprit for the deterioration of our planet’s air

effects of climate change

increased temp, increased cardio-respiratory attacks, changes in frequency of respiratory disease, altered distribution of allergens and infectious disease vectors, increased wildfires, increased drought conditions

effects of climate change- increased temperature

increased number of deaths and acute morbidity, especially among respiratory patients, due to heat waves

for every 1 degree C rise, the risk of premature death among respiratory patients is up to 6 times higher than in the rest of the population

effects of climate change- increased cardio-respiratory attacks

due to higher concentrations of ground-level ozone

effects of climate change- changes in frequency of respiratory disease

due to transboundary long-range air pollution

effects of climate change- altered distribution of allergens/infectious disease vectors

e.g. more pollen due to rapid growth of plants, longer pollen seasons, and high allergen content during thunderstorms

effects of climate change- increased wildfires

this activity is increasing with climate change

decreased air quality, smoke can travel great distances

at risk population include adults 65+, children, pregnant woman and developing fetuses, pre-existing lung disease (asthma, COPD)

one recent worldwide estimate is that 339,000 deaths annually may be attributed to landscape fire smoke

effects of climate change- increased drought conditions

multiple health challenges: in dry conditions, more pollen, dust, particulates (and wildfire smoke) which can irritate respiratory epithelium, exacerbate chronic respiratory illnesses, and asthma, and increase risks for acute respiratory infection

components of fire smoke that cause issues

vary depending on fuel tupe, landscape, meteorological conditions, etc

include asphyxiants, respiratory irritants, systemic toxins

wildfire components- asphyxiants

produce hypoxia by displacing oxygen, e.g. CO2, CO, and methane

wildfire components- respiratory irritants

produce hypoxia by causing tracheobronchitis, upper airway obstruction, pneumonia

e.g. ammonia, acrolein/aldehyde, sulphur dioxide

wildfire components- systemic toxins

cause inhalation injury

e.g. particulate matter- depends on particle size, concentration, respiratory rate, pre-existing conditions, time exposure

of all the things the components of wildfires can cause, what does this ultimately result in?

decreased lung function, exacerbation of asthma and COPD, increased respiratory infections which means increased ER units and hospitalizations

effects of air pollutants on upper airway disease

epidemiological studies have shown that these aggravate airway diseases including asthma, COPD, bronchitis, as well as these type of diseases such as allergic and non-allergic rhinitis, sinusitis, and otitis media

diesel exhaust particles, nitrogen dioxide and cigarette smoke, photochemical pollutants/ozone are worst offenders

young children and obese most vulnerable

more studies needed on long term effects of lower dose exposures

many pollutants trigger the generation of

ROS, which induce apoptosis and increase inflammation and mucin production

ozone effects

exposure impairs lung function, even in healthy individuals, where it causes reductions in vital capacity, FEV1, and resistance

effects of exposure increase with physical exercise

patients with respiratory diseases are more susceptible to its effects, e.g. it can cause difficulty of breathing (e.g. shortness of breath and pain when taking a deep breath)

long term exposure implicated in asthma development and under conditions of oxidizing air pollution (such as summer), exposure may lead to asthma exacerbations

exposure likely to cause premature deaths

children seem at increased risk from exposure, as they have a relatively higher dose per body mass and their lungs are still developing

high levels of ozone are due to

photochemical reactions involving volatile organic compounds (VOCs) and oxides of nitrogen (NOx)

anthropogenic emissions

fossil fuel combustion

responsible for NOx and mainly responsible for VOCs and CO

air pollution has been proposed to contribute to the development and exacerbation specifically of

asthma

main mechanisms of air pollution worsening asthma

1. oxidative stress and damage

2. airway remodelling

3. inflammatory pathways and immunological response

4. enhancement of respiratory sensitization to aeroallergens

variation in the genes that regulate mechanisms between air pollution and asthma

could confer increased susceptibility to development of new-onset asthma or exacerbations of existing disease with exposure to air pollution

cigarette smoke

important pollutant because it is inhaled, therefore concentrations are very much higher than atmospheric pollutants

approx 4% CO, which is enough to raise carboxyHb level in a person who does this’s blood to 10%

sufficient to impair exercise and mental performance

contains nicotine, which stimulates the ANS producing tachycardia, hypertension, and sweating

Tar

a largely aromatic hydrocarbon which is responsible for the high risk of bronchial carcinomas, found in cigarette smoke

cigarette smoking and risk factors

35 cigs/day →40 times risk of carcinoma

associated with increased risk for chronic bronchitis, emphysema, heart disease

one single cig increased airway resistance

why are occupational lung diseases likely underestimated?

lack of screening

physician’s inability to recognize these conditions

long latency time

major classifications of occupational lung diseases

hypersensitivity pneumonitis (HP) and pneumoconiosis

hypersensitivity penumonitis

extrinsic allergic alveolitis, an inflammatory disease of the lung parenchyma caused by inhalation of organic dusts

characterized by diffuse inflammation of the lung parenchyma in previously sensitized patients

organic dust sources

dairy and grain products, animal dander and protein, bark, water reservoir vaporizers

most common antigens in hypersensitivity pneumonitis

actinomycetes species (gram positive bacteria) and avian proteins

most common hypersensitivity pneumonitis diseases

farmer’s lung and bird fancier’s lung

farmer’s lung source of exposure

moldy hay

bird fancier’s lung source of exposure

pigeons, parakeets, fowl, rodents (avian or animal proteins)

pneumoconiosis

collection of interstitial lung diseases caused by breathing in certain kinds of inorganic material particles, such as mineral dust

usually takes years to develop

lungs fail to clear these particles, resulting in inflammation and eventually development of lead to scar tissue

coal worker’s lung

type of pneumoconiosis

fibrotic condition, coal dust enters alveoli and is ingested by macrophages which expel particles through mucus or via the lymphatic system

when system overwhelmed, accumulation of macrophages triggers an immune response leading to inflammation and fibrosis

result is lesions called coal dust macules, which can be seen as black area and are composed of coal-dust laden macrophages within the walls of the respiratory bronchioles and adjacent alveoli

often emphysemous tissue also apparent surrounding macule

in advanced disease, condensed masses of black fibrous tissue seen called nodules

silicosis

environmental pneumoconiosis

caused by inhalation of crystalline silica dust (SiO2) found in quartz and sand

acute →infiltration of the alveolar walls with plasma cells, lymphocytes, and fibroblasts, with some collagen deposition. alveoli fill with eosinophils, inflammation and scarring often more common in upper lobes of the lungs

widening of alveolar walls with collagen and clusters of type II cells

long latency period

patients particularly susceptible to TB infection possibly due to silica damaging alveolar macrophages, reducing ability to kill myobacteria

asbestos

family of naturally occurring hydrous silicates found in soil

fibers are either long and curly (serpentine) or straight and rodlike (amphibole)

serpentine fiber, chrysolite, most commonly used (95%)

due to heat resistance properties, it is used for heat insulation, pipe lagging, roofing material

asbestosis

type of pneumoconiosis

asbestos fibers deposit at branch points in the distal airways and alveolar ducts, resulting in inflammatory cascade of cellular activation, recruitment, and injury

damage to airway epithelial cells

early stage characterized by discrete foci of fibrosis within the respiratory bronchiole walls and alveolar duct bifurcations associated with the accumulation of asbestos bodies (AB)

asbestos bodies

fibrous structures with asbestos in its corse encased by mucopolysaccharides and iron-rich proteins (e.g. ferritin and hemosiderin)

proposed mechanism of asbestosis

asbestos elicits a macrophage response to phagocytize and clear the fibers, but fibers too large

asbestos triggers accumulation of AMs and other inflammatory cells resulting in inflammatory reaction, followed by more diffuse pulmonary involvement characterized by (a) loss of type I and II alveolar cells, (b) fibroblast proliferation, and (c) collagen deposition

pulmonary fibrosis of the disease associated with fibrosis of the walls of the respiratory bronchioles and alveolar ducts

bronchial carcinoma

asbestos related disease, often aggravated by cigarette smoke

pleural disease

asbestos related disease

may occur after trivial exposure

most common are pleural plaques (with or without calcification) and pleural thickening—benign

changes in pleura result in restrictive type in disease, with reduced VC, and reduced compliance

malignant mesothelioma may develop from cells lining pleura (mesothelium)

can develop up to 40 years after exposure

progressive restriction of lung movement, severe chest pain, low survival rate

occupational asthma

variable airflow obstruction or bronchial hyper-responsiveness resulting from conditions attributable to a particular working environment and not to stimuli encountered outside the workplace

5-15% adult-onset asthma patients report that their workplace makes symptoms worse

can be either immunologically or non-immunologically mediated

immunologically mediated occupational asthma

characterized by a latency period necessary for acquiring sensitization

caused by broad-spectrum of protein derived and natural and synthetic chemicals in workplace

e.g. animal derived allergens (handlers, pharmaceutical workers), cereals (bakers), wood ducts (carpenters), formaldehyde (hospital staff)

non-immunologically mediated occupational asthma

characterized by the lack of a latency period

underlying mechanism unclear, but maybe extensive denudation of epithelium results in airway inflammation and hyper-responsiveness due to loss of epithelium-derived relaxing factors, exposure of nerve endings to neurogenic inflammation and non-specific activation of mast cells, with release of mediators and cytokines