INHALED
POISONS
the LUNGS
             large surface area and
              good blood supply
             excellent route for
              absorption and
              distribution of toxic gases
             Absorption occurs via the
              capillary-alveolar
              membrane in the lungs
                     INHALED GASES
            CLASES                                  EXAMPLES
                         Ammonia, chlorine, suphur dioxide, ozone, phosgene,
Irritants
                         halogens, acrolein
                         Nitrogen, hydrogen, methane, liquid petroleum gas,
Simple Asphyxiants
                         propane, carbon dioxide, dichlorotetraflouroethane
                         Carbon monoxide, hydrogen, cyanide, nitriles, hydrogen
Chemical Asphyxiants
                         sulphides
Central nervous system   Aliphatic hydrocarbons, chlorinated hydrocarbons,
depressants              acetone, ethyl ether, benzene
                         Carbon disulphide, mercury, acrylamide, n-hexane, methyl
Neurotoxic agents
                         n-butyl ketone
                         Carbon tetrachloride, chloroform, allyl alcohol,
Hepatotoxic agents
                         bromobenzene
Nephrotoxic agents       Carbon tetrachloride, chloroform, trichloroethylene
Agents damaging blood    Nitrobenzene, arsine, naphthalene
Agents damaging bone
                         Benzene, trinitrotoluene
marrow
Carcinogens              Vinyl chloride, 2-naphthylamine, bis(chloromethyl)ether
 Besides causing irritation and injury to the lungs,
  inhalation of gases in some, may even lead to
  significant systemic poisoning involving vital organs
  such as the brain, kidney and liver.
 Exposure to these substances however may produce
  varied effects.
 The nature, extent and severity of the effects to be
  observed may depend on:
      the types of gas involved
      its solubility
      concentration
      extent and duration of exposure
 Poorly ventilated exposure site will very likely cause
  more significant effects especially in individuals
  who have preexisting lung diseases.
ASPHYXIANTS
Simple & Chemical asphyxiants
Simple asphyxiants
 nonirritating, chemically inert gases
 naturally occurring atmospheric components
 When present in high concentration, they displace
  oxygen in inspired air with the gas, causing a
  decrease in oxygen concentration available for gas
  exchange
 Examples: carbon dioxide and methane
Carbon dioxide (CO2)
 Colorless, odorless gas
 used in the food industry in the carbonation of
  beverages, in fire extinguishers as an 'inerting'
  agent and in the chemical industry
Signs and symptoms of toxicity
 increased respiratory rate, tachycardia, cardiac
  arrhythmias and impaired consciousness (higher
  concentrations)
 Concentrations >10% may cause convulsions, coma
  and death.
Clinical management
 removal of the casualty from the toxic environment
 administration of oxygen
 In severe cases, assisted ventilation may be
  required.
 Dry ice burns are treated similarly to other
  cryogenic burns, requiring thawing of the tissue
  and suitable analgesia.
Methane
 colorless, odorless and flammable gas
 utilized as fuel and in chemical reactions to produce
  commercially used chemicals such as carbon
  tetrachloride, carbon black and as a source of
  hydrogen
 reacts at high temperatures with steam to yield the
  hydrogen used in the manufacturing of explosives
  and ammonia-based fertilizers
Signs and symptoms of toxicity
 headaches
 heart palpitations
 cognitive impairment (poor judgement, memory
  loss)
 dizziness
 loss of motor coordination
 flu-like symptoms (mental uneasiness, lethargy,
  discomfort)
Clinical management
 removal of the casualty from the toxic environment
 administration of oxygen
Chemical asphyxiants
 interfere with the body's ability to utilise oxygen
 They either prevent oxygen delivery or inhibit the
  utilization of oxygen by the cells
Carbon monoxide (CO)
 highly toxic, colourless, odourless, flammable gas
 produced industrially for use in the manufacture of
  numerous organic and inorganic chemical products
 present in the exhaust gases of internal-
  combustion engines and furnaces as a result of
  incomplete conversion of carbon or carbon-
  containing fuels to carbon dioxide
Mechanism of toxicity
 Following inhalation,       Bound carbon          Prevention of unloading
  carbon monoxide         monoxide increases           of oxygen at the
   rapidly binds to      hemoglobin affinity for       tissues, further
hemoglobin to produce     oxygen at the other         reducing oxygen
 carboxyhemoglobin        oxygen-binding sites             delivery
Signs and symptoms of toxicity
 headache, dyspnea, lethargy, confusion, and
  drowsiness
 seizures, coma, and death (higher exposure levels)
Clinical management
 prompt removal from the source of carbon
  monoxide
 institution of 100% oxygen by nonrebreathing face
  mask or endotracheal tube
 In patients with severe intoxication, oxygenation in
  a hyperbaric chamber is recommended.
Cyanide
 one of the toxic products of combustion produced
  during house fires
 used in electroplating
 hydrogen cyanide may be produced during
  photographic developing and petroleum refining
Mechanism of toxicity
                                      Respiratory arrest
inactivation of the
                                         of oxidative
     enzyme           inhibition of
                                       phosphorylation
   cytochrome            cellular                          Death
                                      and production of
      oxidase          respiration
                                         adenosine
 (cytochrome a3)
                                        triphosphate
Clinical management
 Hydroxocobalamin (vitamin B12a) is administered
  intravenously to bind the cyanide and produce
  cyanocobalamin (vitamin B12)
 cyanide antidote kit
    sodium nitrite to form cyanomethemoglobin
    sodium thiosulfate to accelerate the production of
     thiocyanate, which is much less toxic than cyanide and is
     also quickly excreted in urine.
IRRITANTS
Irritants
 Primary irritants - produce little systemic effects
 Secondary irritants - produce both respiratory and
  systemic toxicity
    include hydrogen sulphide, ozone, acetylene,
     methylated halogens and metal fumes
Irritants
 have the ability to cause injury and induce
  inflammation of the mucous membranes upon
  contact
 Individuals exposed to these gases may develop
  signs and symptoms that are either predominantly
  associated with upper or lower respiratory tract.
 These depend on the solubility of the gas.
Irritants
 Highly water soluble gases like ammonia affect
  mainly the upper respiratory tract
 Low water soluble gases like phosgene affects the
  lower respiratory tract
Signs and symptoms of irritation
          URT                 LRT
 rhinitis           pneumonitis
 pharyngitis        pulmonary edema
 cough              hypovolemic shock
 laryngeal edema
 Signs of lower respiratory tract involvement may
  not necessarily be preceded by signs of upper
  respiratory tract involvement.
 However, injury to the upper respiratory tract may
  be extended to involve the lower respiratory tract if
  the exposure is prolonged.
    e.g. Sulphur dioxide
Ammonia
 found in refrigerators, fertilisers, household
  cleaning and bleaching agents, and liniments
 available as industrial ammonia solution (28%
  solution) and household ammonia (5-10% solution)
 has a strong penetrating odour and this can be
  detected at 5 ppm
 The threshold limit value (TLV), which is the
  maximum tolerable concentration at an average of
  8 hours workday without giving symptoms, is about
  50 ppm.
 effects are mostly local, causing mild irritation to
  severe corrosion of the mucous membranes
 400-700 ppm - skin, eyes, nose, throat and lungs
  may become irritated immediately
 >1000 ppm - violent coughing, sore throat,
  lacrimation, dyspnea, restlessness, blurred vision,
  pulmonary edema
 5,000-10,000 ppm - lose consciousness, develop
  severe epiglottis, larynx and trachea, caustic burns
  of edema the skin/eyes, blindness and purulent
  bronchitis/pneumonia
Chlorine
 yellowish-green gas with an irritating odour
 used in the manufacture of plastics, as bleaching
  agents and for purifying water.
 Exposure to the gas usually follows a leak from a
  storage tank or at home as a result of accidentally
  mixing sodium hypochlorite (Clorox) with industrial
  acid cleaners, such as sodium acid sulphate.
 TLV = 1 ppm
 3-6 ppm - irritation of the skin, eyes, nose, throat and
  lungs
    nausea, vomiting, diaphoresis, headache, coughing, tightness
     of chest, redness/watery eyes, blurred vision, agitation,
     excitement, increase heart rate and blood pressure can also
     develop
 >50 ppm - pulmonary edema/pneumonitis, purulent
  bronchitis/ pneumonia, ulcerations and necrosis of skin
  and eyes
 Both severe mucosal irritation and pulmonary
  parenchymal damage can occur within 10 minutes of
  exposure
 1000 ppm - respiratory failure, coma, shock and death
Sulphur dioxide
 by-product of gasoline combustion, oil refining and
  paper production
 a colourless gas
 upon contact with water at the mucosal
  membranes of the eyes and upper respiratory tract
  will form sulphuric acid that produces a severe
  irritation
 10 to 15 ppm (for 5 to 15 minutes) - irritation of the
  eyes, nose, throat; rhinorrhea, choking, cough
 high concentration  death
 Prolonged exposure - irreversible bronchiolar
  obstruction or restrictive lung disease
Hydrogen sulphide
 by-product of many industrial processes and decay
  of organic matter
 may be found in areas around petroleum refineries,
  tunnels and mines
 has a "rotten eggs" odour that is easily detected at
  concentration of 1 ppm.
 TLV = 10 ppm
 50 ppm - irritation of the eyes and respiratory tract
 1000 ppm - respiratory paralysis and death