Department Of Bioinformatics And Biotechnology

Published Date: 02 Nov 2017

Environmental Toxins

Submitted To: Mr.Waseem Sarwar

Submitted By: Muhammad Bilal (1041)

BS BNB 3rd Afternoon 2011-2015

Govt. College University, Faisalabad

Department of Bioinformatics and Biotechnology,

Environmental Toxins

Definition:

(Environmental toxin) Pollution is the introduction of contaminants into a natural environment that causes instability, disorder, harm or discomfort to the ecosystem i.e. physical systems or living organisms.

Etiology:

Chemicals are ingested through food or water, inhaled or pass through the skin. Frequently toxicity is found in artists, researchers, or individuals who are exposed through their work in industry and agriculture. Exposure may be limited to small amounts over long periods or through massive amounts over a shorter time. Current research also implicates household products and

Cosmetics. Dental work can also be a source of toxicity.

Symptoms:

The most pronounced symptom is fatigue, frequently encountered even in young people. Joint pain and skin problems such as eczema and psoriasis are frequently found. Other serious heath conditions such as neoplastic processes and severe environmental sensitivity should be considered. We believe that further research will elucidate a more complete picture.

Common Environmental Toxins:

* Hydrocarbons

* Inhaled toxins

* Pesticides

* Heavy Metals

Hydrocarbons:

Introduction:

One of most frequently reported poisonings.

Presentation to ED classified into 4 types:

1.) Accidental ingestion,

- Most common.

- In children less 5 years.

2.) Intentional inhalation,

- Abuse of volatile hydrocarbons.

- Recreational.

3.) Accidental inhalation / exposure,

- Household or workplace.

4.) Massive oral ingestion,

- Suicide attempts.

Pharmacology:

Diverse group of organic compounds.

Contain hydrogen and carbon.

Most are petroleum distillates (e.g. gasoline)

- derived from crude oil and coal

- Turpentine derived from pine oil

Pathophysiology:

3 main target organs effected:

1) CNS

2) Lungs

3) Heart

Most acute damage in the lungs.

LUNG DISEASE:

Mechanisms:

Penetrates lower airways ~ produces bronchospasm + inflammation

Displaces alveolar O2 (volatile hydrocarbon)

Inhibits surfactant

Damaging alveoli and capillaries

These effects cause:

Alveolar disfx

Vent / Perfusion mismatch

Hypoxia

Resp. failure

CNS:

Narcotic – like effects:

~ Euphoria

~ Disinhibition

~ Confusion

Usually substance abusers - recreational use.

Single exposure with rapid onset of intoxication + recovery.

Chronic use causes:

~ Peripheral neuropathy

~ Cerebellar degeneration

~ Neuropsychiatric disorders

~ Dementia

~ Chronic encephalopathy

CARDIAC:

Sudden death.

Sudden physical activity during / after intentional inhalation.

Myocardial sensitization to endogenous + exogenous catecholamines.

Precipitates vent. dysrythmias + myocardial dysfx.

Clinical presentation:

4 typical presentations:

1.) Accidental ingestion:

Usually toddlers.

Reused beverage containers storing hydrocarbon.

Mild Sx include ~ tachypnoea.

~ Dyspnoea

~ Bronchospasm

~ fever within 6 hours

Severe poisonings ~ early resp. Sx

~ Cyanosis

~ grunting

~ coughing

~ Repeated vomiting

~ These findings suggests aspiration

Change in mental status ~ direct CNS effect OR

~ caused by hypoxia

2.) Intentional inhalation:

Substance abuse

Mechanisms include: - "bagging"- hydrocarbon poured into bag/container

+ deeply inhaled.

- "Huffing" - inhaling through a saturated cloth.

- "sniffing"

Mostly volatile hydrocarbons – petrol.

- Paint

- Glue

3.) Accidental dermal exposure or inhaled resp. exposure:

In workplace / home.

Not life threatening.

Asymptomatic or transient non-specific symptoms.

Sx resolve with fresh air / removal from offending environment.

4.) Intentional ingestion / intravenous injection:

Suicide attempts.

Used in combination with other substances.

Massive oral ingestion not associated with significant morbidity.

INHALED TOXINS:

* Smoke inhalation

* Cyanide

* Carbon monoxide

Smoke inhalation:

Inhalation injury common.

Fires in enclosed spaces like homes / factories.

Injury typically irritant in nature.

Heated particulate matter + absorbed toxins injure normal mucosa.

Carbon monoxide + Cyanide poisoning often associated with smoke inhalation.

- These are systemic (not resp.) toxins.

Clinical presentation:

Morbidity + mortality related to resp. tract damage

- Thermal / irritant in nature

Time between smoke exposure + onset of Sx – highly variable

May always be delayed

Depend on degree + nature of exposure

Cough + stridor

- Thermal + irritant induced laryngeal injury

Cough stridor + bronchospasm

- caused by soot + irritant toxins in the airways

Subsequently – a cascade of:

- Airway inflammation

- Acute lung injury with pulm. Edema

- Resp. failure

Burned nasal hair + soot in the sputum suggest substantial exposure

Always consider CO + cyanide inhalation

- in pt`s exposed to filtered / distant smoke (different room) OR

- Relatively smokeless combustion

Cyanide:

One of the most rapidly acting poisons.

Causes:

1.) Smoke inhalation:

- Most common

- Compounds containing carbon + nitrogen produce hydrogen CN

Gas when burned

- Natural compounds (silk + wood) produces HCN as combustion

product

- burning of household furniture + plastics also causes HCN gas

2.) Intentional poisoning:

- Uncommon.

- Cyanide salts in hospitals + labs.

3.) Industrial exposure:

- Occupations with easy access to cyanide

* Chemists

* Jewelers

* Pest control

* Mineral refining

* Photography

* electroplating

* Dying + printing

Pathophysiology:

Cyanide inhibits mitochondrial cytochrome oxidase + blocks electron transport (binding with ferric iron Fe3+)

Aerobic metabolism + O2 utilization decreases

Lactic acidosis occurs as a consequence of anaerobic metabolism

O2 metabolism @ cellular level is grossly hampered

Cyanide rapidly absorbed from:

- Stomach

- Lungs

- Mucosal surfaces

- Skin

Clinical presentation:

Sx appear seconds to minutes after exposure

HCN gas can lead to cardioresp. arrest + death within minutes

Onset of effects after ingestion / skin contamination:

- Much slower (several hours)

- Early signs:

i) Dizziness

ii) Bronchospasm

iii) Dyspnoea

iv) Confusion

v) Paresis

- Later:

i) Cardiovasc. Collapse

ii) Seizers

iii) Coma

Pathophysiology:

Intense tissue hypoxia + cell injury caused by

2 mechanisms:

1.) Interrupts electron transport in the mitochondria (like cyanide),

Leading to anaerobic metabolism

2.) Reduces O2 delivery by:

- competing with O2 for binding to Hb (CO has much higher affinity for

Hb, than O2!)

- Shifting the HbO2 dissociation curve to the left

Clinical presentation:

Hypoxia without cyanosis.

Myocardium + Brain mostly affected (high O2 consumption).

Sx include:

- Dizziness - convulsions

- Headaches - coma

- Confusion - cardio/resp. dysfx + death

- Chest pain

- Dyspnoea

- Palpitations

- Syncope

Pesticides:

1.) Organophosphates + Carbamates

2.) Paraquat + Diquat Poisoning

Organophosphates + Carbamates:

Introduction:

Potent cholinesterase inhibitors.

Accumulation of acetylcholine (Ach).

Indirect stimulation of nicotinic + muscarinic receptors

Absorbed through: - skin

- Inhalation

- Ingestion

Carbamate + OP poisoning clinically indistinguishable

Differences: - OP forms irreversible complex with cholinesterase

- Carbamate complex reversible, with shorter duration of

action (less than 24 h)

- Carbamates penetrates blood-brain barrier poorly,

therefore less CNS effects

Clinical presentation:

Minutes to 12 hours after exposure

1.) Muscarinic effects: (post ganglionic)

- Hyper secretion (sweating, salivation + bronchial secretions)

- constricted pupils

- Bradycardia + hypotension

- vomiting + diarrhoea

- Urinary incontinence

- Bronchoconstriction

- Also commonly referred to SLUDGE syndrome:

2.) Nicotinic effects: (preganglionic)

- Muscle weakness

- Fasciculations

- Resp. muscle weakness

Paraquat + Diquat:

Most toxic herbicide known (weed-killers)

Multiorgan toxicity

Death due to delayed pulm. fibrosis + resp. failure.

Pathophysiology:

- Cytotoxic O2 radicals generated

- Selectively accumulates in the lungs

- Lungs major target organs (except diquat)

- Also liver, kidneys, heart + CNS

- Absorption: * skin

* GIT

* Resp. tract

Clinical presentation:

1.) Chemical burns of oropharynx

2.) Esophageal perforation + mediastinitis (extreme cases)

3.) N + V

4.) Skin irritation

5.) Resp. injury:

- High doses cause dyspnoea, ARDS + rapid multiorgan failure

- Progressive pulm. Injury over 1 – 3 weeks with irreversible

pulm. fibrosis

Heavy Metal Toxicity:

Uncommon dx

Exceptions: 1.) acute iron toxicity (intentional / unintentional)

2.) Lead exposure

Unrecognized / inappropriately Rx result in significant morbidity + mortality

Other examples: arsenic, mercury, cadmium.

Toxicity depends on:

1.) Metal

2.) Total dose absorbed

3.) Acute/Chronic exposure

4.) Age – children more susceptible to toxic effects + prone to

accidental exposures

5.) Route of exposure - e.g. Elemental mercury, not dangerous

if ingested / absorbed through skin

Sources:

Exposure through:

* Diet supplements

* Medications (herbal remedies)

* Environment

* Occupational / Industrial

(Most acute presentation)

* Ingestion of non food items e.g. Toys, paint chips, ballistic

devices, fishing sinkers, curtain, weights

* Retained bullets (rarely causes lead toxicity)

Pathophysiology:

Remains relatively constant for all heavy metal toxidromes

Binds to O2, Nitrogen + sulphydryl groups in proteins

Result in: ALTERATIONS OF ENZYMATIC ACTIVITY

Nearly all organ systems involved:

* CNS

* PNS

* Haemapoietic

* GIT

* Cardiovasc.

* Renal