Calamba, Micah Lou C. MD2 MAY 12,2022 PHARMA- Toxicology Dr.

Salvador
CHEMICAL DESCRIPTION MECHANISM OF ACTION
a colorless, tasteless, CO combines tightly but reversibly
odorless, and with the oxygen-binding sites of
nonirritating gas, a hemoglobin and has an affinity for
byproduct of incomplete hemoglobin that is about 220 times
combustion. that of oxygen. Forming
Carbon Carboxyhemoglobin which is unable
to transport oxygen and interferes
Monoxide with the dissociation of oxygen
from the remaining oxyhemoglobin
because of Bohr effect.
Thus, reducing the transfer and
supply of oxygen to the tissues.
CLINICAL EFFECTS TREATMENT
Intoxication & Hypoxia 1. The patient must be removed
progress in the following sequence: from the exposure source
1) psychomotor impairment immediately
2) headache and tightness in 2. Respiration must be
the temporal area maintained, and high flow and
3) confusion and loss of visual
acuity
concentration of oxygen should
be administered promptly
4) tachycardia, tachypnea,
syncope, and coma;
5) deep coma, convulsions, shock,
and respiratory failure

a colorless irritant gas At room temperature, the solubility This acid has severe irritant Treatment is not specific for SO2
generated primarily of SO2 is approximately 200 g SO2/L effects on the eyes, mucous but depends on therapeutic
Sulfur by the combustion of
sulfur-containing fossil
of water. Because of its high
solubility, when SO2 contacts moist
membranes, skin and throat, reflex
bronchoconstriction and increased
maneuvers used to treat
irritation of the respiratory tract
Dioxide fuels. membranes, it transiently forms bronchial secretions and asthma.
sulfurous acid.

a brownish irritant gas capable of producing pulmonary Acute exposure to NO2 include: There is no specific treatment for
sometimes associated edema and acute adult respiratory → irritation of the eyes and nose acute intoxication by NO2;.
with fires. It is formed distress syndrome (ARDS). → cough Measures Include
also from fresh silage; Inhalation damage the lung → mucoid o frothy sputum → maintenance of gas exchange
exposure of farmers to infrastructure that produces the production with adequate oxygenation and
NO2 in the confines of a surfactant necessary to → dyspnea alveolar ventilation.
silo can lead to silo- allow smooth and low-effort lung → chest pain → Drug therapy may include
filler’s disease, a severe alveolar expansion. Pulmonary edema may appear bronchodilators, sedatives, and
Nitrogen and potentially lethal within 1–2 hours. antibiotics.
form of acute respiratory
Oxide distress syndrome.
→ New approaches to the
management of NO2-induced
Chronic exposure of laboratory ARDS have been developed and
animals to 10–25 ppm NO2 has considerable controversy now
resulted in emphysematous exists about the precise
changes: thus, chronic effects in respiratory protocol to use in
humans are of concern. any given patient.
 bluish irritant gas found Ozone is an irritant of mucous Airway hyperresponsiveness and There is no specific treatment for
in the earth’s membranes. Mild exposure produces airway inflammation have acute O3 intoxication.
atmosphere, where it is upper respiratory tract irritation. been observed in humans. Management depends on
an important absorbent Severe exposure can cause deep lung therapeutic measures used for
of ultraviolet light at irritation, with pulmonary edema Chronic bronchitis, bronchiolitis, deep lung irritation and
Ozone high altitude. when inhaled at sufficient fibrosis, and emphysematous noncardiogenic pulmonary edema
concentrations. changes have been reported in that have resulted in ARDS.
a variety of species, including
humans, exposed to
concentrations above 1 ppm.

These “halohydrocarbon” cause central nervous system (CNS) • can cause cardiac arrhythmias in There is no specific treatment for
agents once found wide depression, liver injury, kidney injury, humans, particularly in situations acute intoxication resulting from
use as industrial and some degree of cardiotoxicity. involving sympathetic excitation exposure to halogenated
solvents, degreasing and norepinephrine release. hydrocarbons. Management
Halogena- agents, and cleaning Several are also carcinogenic in • Hepatotoxicity depends on the organ system
ted agents. animals and are considered probable • Nephrotoxicity involved.
Includes: human carcinogens. • Carcinogenicity
Aliphatic → carbon tetrachloride • Non-Hodgkin’s lymphoma
Hydro- → chloroform
→ trichloroethylene
carbons → tetrachloroethylene
(perchloroethylene)
1,1,1-trichloroethane
(methyl chloroform)