Environmental exposure

The health and unhealth of individuals reflects that daily interactions with the air, land, and sea.

There are diseases which have a large environmental component.

The lungs take in as much as 5000 gallons of air every 24 hours and with that air comes bacteria, viruses, mold, fungus and pollutants.

In a healthy young adult tidal volume is approximately 500 mL per inspiration, or  7 mL per kilogram, and at 12 to 14 breaths per minute they process 10,000 L of air each day, or nearly 4,000,000 L each year.

Throughout the respiratory pathway, pseudostratified epithelium cilia line trachea, bronchi and bronchioles.

The large in small airways remove tremendous amounts of inhaled toxicants by mucocilliary mechanisms and molecular detoxication processes carried out by the pulmonary epithelium and the immune system.

Depending upon the patient,, the toxicant and patients genetic architecture, their defense mechanisms of airway reactivity and parenchymal changes can cause fibrosis and result in maladaptive processes that lead to disease.

We are constantly exposed to environmental toxicants through inhalation, ingestion and transdermal absorption.y

Air quality impacts the rate of progression for inflammatory lung diseases.

Water quality is a strong determinant of kidney disease when combined with climate in certain geographic regions.

More than 80,000 chemicals currently utilized in the U.S.

Approximately 1500 pesticides and 5500 food additives are utilized.

Only about 600 chemicals used have been tested and 10% of these produce malignancy in rodents (Carpenter).

Social determinants of health or societal root derived and relate to conditions in which people are born, live, learn, work, play, worship, and age.

Economic stability, education quality, neighborhood resources social context and healthcare access in quality or determinants of health.

Black communities have higher rates of air pollution levels associated with increased incidence of associated diseases.

Exposures to particular matter  is associated with higher incidence of COPD, heart disease, asthma, stroke, preterm labor, and death along with lung, breast, and prostate cancer linked to nitrogen dioxide and now the measures of traffic exposure.

Most of the variance in COPD is attributed to the interaction of the  environment and specific gene alleles.

COPD has been associated with exposure to cigarette smoke, and nearly 25% of the mortality associated with COPD in low income countries has been attributed to smoke exposure from other sources such as coal, kerosene, and biomass fuels (wood, charcoal).

In higher income countries there is a measurable impact on COPD burden disease from industrial emissions, vehicle emissions and wildfires.

Smoke from any source contains components that can induce cough, alter mucus production, and activate bronchial reactivity: ozone, sulfur dioxide, nitrogen dioxide, volatile organic compounds, and particulate matter.

Particles less than 10µm in diameter such as dust, pollen, and mold, can get deep into the lungs and particles as small as 2. 5 µm including combustion products, organic matter, and heavy metals, can cross the pulmonary epithelium into the systemic circulation.

Kidney diseasecan be caused or accelerated by exposure to environmental toxicants.

Mechanisms for chronic kidney disease include pathophysiological manifestations to the glomeruli, the interstitium, and the tubules.

There are geographic differences in the distribution of kidney disease that cannot be explained by the usual  hemodynamic and metabolic risk factors:agricultural workers in some equatorial communities develop a rapid decline in GFR that is  independent of all risk factors,  and is expected environmental factors including agricultural chemicals, industrial waste products, and viruses play a role.

In patients  of African ancestry the presence of APOL1 gene has been shown to be consistently associated with a change in glomerular filtration rate, and these  variants may alter patient vulnerability to environmental nephrotoxins.

In patients with glomerular diseases characterized by a gradual loss of nephrons, such as with hypertension and diabetes, the remaining healthy nephrons typically undergo changes that compensate for such losses.

In the presence of  nephrotoxins, additional renal parenchymal changes of tubo interstitial fibrosis results in a failure of normal compensatory changes, shifting the slope in GFR downward overtime.

Nephrotoxins capable of causing tubular injury include numerous pollutants in the environment and patients in agricultural communities frequently exposed to fertilizers, herbicides, and pesticides, and heavy metals.

Soil conditions, climate, and runoff of these agricultural chemicals can appear in drinking water.

Water quality can also be altered in the presence of the petroleum industry, and the mining industry, as well.

The amount of metal cations like calcium, magnesium, and iron in drinking water impacts the severity of heavy metal induced nephrotoxicity.

More than half of domestic wells  have agricultural pesticides and solvents detected, albeit they rarely exceed human health benchmarks.








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