AMMONIA TESTING METHODS

The Hydrion Ammonia Test Paper is designed and calibrated to measure the amount of ammonia in the air. These strips can be used to detect trace amounts of ammonia in poultry houses or animal rooms, where levels as low as 25 ppm can be detrimental. Also helps to identify contamination from processing equipment.
Features:

Sharp color changes at each whole value Each kit contains one roll of paper in a protective plastic dispenser with a matching color chart To use simply tear off a strip of paper, moisten and expose to air - wait 15 seconds and then compare to the calibrated color chart

Specifications:

Range: 0 - 100 ppm Scale: 0, 5, 10, 20, 50, 100 Roll Length: 15 ft. Each roll is sufficient for 75 - 100 tests

The ToxiRAE II ammonia monitor is perfect for spot checks in poultry operations and much more. It continuously displays measurements and costs just a little more than disposable meters, although it is loaded with features. This unit couldnt be simpler to use, as it just has one button, so all you have to do is turn it on.

Features: Field-replaceable filter and battery Large, easy-to-read display shows continuous readings Displays STEL, TWA, peak values, and alarms

User-adjustable alarms Varying audio alarm signals for different conditions Bright red flashing alarm and 90 dB buzzer Durable, impact-resistant, carbon-loaded ABS housing 2-year warranty for instrument and 1-year for sensors Supplied with operation and maintenance manual, stainless-steel alligator clip (installed), stainlesssteel belt clip, wrist strap, calibration gas test adapter, high-capacity Lithium battery (installed)

Specifications: Range (NH3): 0 to 50 ppm Resolution: 1 ppm IP Rating: IP-65, protected against dust and low-pressure water Power: User-replaceable 2/3 AA high-capacity Lithium battery (use only RAE batteries) Dimensions: 3.6" x 1.9" x 0.9" Weight: 3.6 oz (102 g)

LETS UNDERSTAND AMMONIA

At room temperature, ammonia (NH3) is a highly water-soluble, colorless, irritant gas with a unique pungent odor. Ammonia has a boiling point of -33C and an ignition temperature of 650C. Anhydrous ammonia is one of the most widely produced chemicals in the United States, one third of which is used by the farming industry as a component of fertilizer and animal feed. Before the 1970s, liquid ammonia stored under high pressure was widely used for refrigeration. Although Freon largely has replaced ammonia as a refrigerant, ammonia refrigeration is still used and numerous case reports exist of severe toxicity following unintentional exposure. Ammonia also is used in the production of explosives, pharmaceuticals, pesticides, textiles, leather, flame-retardants, plastics, pulp and paper, rubber, petroleum products, and cyanide. Furthermore, ammonia is a major component of many common household cleaning and bleaching products (eg, glass cleaners, toilet bowel cleaners, metal polishes, floor strippers, wax removers, smelling salts). Permissible levels of exposure to toxic gases are defined by time-weighted average (TWA), short-term exposure limit (STEL), and concentration at which toxic gasses are immediately dangerous to life or health (IDLH). The TWA is defined as the concentration for an 8-hour workday of a 40-hour workweek that nearly all workers can be exposed to without adverse effects. Similarly, the STEL is the concentration to which an exposure of longer than 15 minutes is potentially dangerous and may produce immediate or chronic compromise to health. Anhydrous ammonia has a TWA of 25 ppm, an STEL of 35 ppm, and an IDLH of 500 ppm. Although injury from ammonia most commonly is caused by inhalation, it also may follow ingestion or direct contact with eyes or skin. The clinical presentations of these injuries and their investigation and treatment are discussed in this article; chloramine gas inhalation injury also is discussed.

The most common mechanism by which ammonia gas causes damage occurs when anhydrous ammonia (liquid or gas) reacts with tissue water to form the strongly alkaline solution, ammonium hydroxide. NH3 + H2 O NH4 OH This reaction is exothermic and capable of causing significant thermal injury. Ammonium hydroxide can cause severe alkaline chemical burns to skin, eyes, and especially the respiratory system. Mild exposures primarily affect the upper respiratory tract, while more severe exposures tend to affect the entire respiratory system (see Clinical). The gastrointestinal tract also may be affected if ammonia is ingested. Tissue damage from alkali is caused by liquefaction necrosis and theoretically can penetrate deeper than that caused by an equipotent acid. In the case of ammonium hydroxide, the tissue breakdown liberates water, thus perpetuating the conversion of ammonia to ammonium

hydroxide. In the respiratory tract, this results in the destruction of cilia and the mucosal barrier to infection. Furthermore, secretions, sloughed epithelium, cellular debris, edema, and reactive smooth muscle contraction cause significant airway obstruction. Airway epithelium can regain barrier integrity within 6 hours following exposure if the basal cell layer remains intact. However, damaged epithelium often is replaced by granular tissue, which may be one of the etiologies leading to chronic lung disease following ammonia inhalation injury. Liquid anhydrous ammonia (-33C) freezes tissue on contact. To put this in perspective, critical skin damage begins at -4C and becomes irreversible at -20C. The degree of tissue injury, however, is proportional to the duration and concentration of exposure. Similarly, damage to the respiratory system is proportional to depth of inhalation, duration of exposure, concentration, and pH of the gas or liquid. Ammonia is a product of protein catabolism and is metabolized by the liver. Normal blood ammonia levels range from 10-40 mol/L. This increases 10% with exposure to 25 ppm but is not considered harmful. Theoretically, patients with liver dysfunction are at increased risk for ammonia toxicity; however, currently no sufficient clinical evidence can confirm this.

The literature on ammonia toxicity in humans largely consists of case reports. In a 1996 literature review, de la Hoz et al found only 94 previously reported cases; of these cases, 20 resulted in fatality and only 35 had clinical follow-up of one year or more.[3] Despite lack of data, most literature is consistent regarding clinical presentation and treatment of ammonia toxicity. Gaseous ammonia effects at various concentrations are as follows:

25 ppm or less - TWA 25-50 ppm - Detectable odor; unlikely to experience adverse effects 50-100 ppm - Mild eye, nose, and throat irritation; may develop tolerance in 1-2 weeks with no adverse effects thereafter 140 ppm - Moderate eye irritation; no long-term sequelae in exposures of less than 2 hours 400 ppm - Moderate throat irritation 500 ppm - IDLH 700 ppm - Immediate eye injury 1000 ppm - Directly caustic to airway 1700 ppm - Laryngospasm 2500 ppm - Fatality (after half-hour exposure) 2500-6500 ppm - Sloughing and necrosis of airway mucosa, chest pain, acute lung injury (ALI), and bronchospasm 5000 ppm - Rapidly fatal exposure

Inhalation injury
Because of its high water solubility, ammonia has a tendency to be absorbed by the water-rich mucosa of the upper respiratory tract. However, unlike most highly water-soluble irritant gases that tend to affect exclusively the upper respiratory tract, ammonia can damage proximally and distally. In 1941, Caplin was the first to classify victims of unintentional ammonia exposure; he described them as mild, moderate, and severe. Patients in the mild group presented with conjunctival and upper respiratory inflammation and pain but showed no signs of respiratory distress.[4] The moderate group presented similarly but with more exaggerated symptoms. The severe group presented in frank respiratory distress with productive cough, acute lung injury (ALI), and dysphagia. Following a brief ammonia exposure, damage generally is limited to the upper airway mucosa. Brief exposures at very high concentrations, however, can be overwhelming and affect the entire respiratory system. People who are capable of escaping their environment usually are not subject to severe exposures, because they can flee upon detection of ammonia's pungent odor; furthermore, absence of symptoms following inhalational exposure to ammonia essentially rules out significant injury.

Pain (oropharyngeal, retrosternal) Dyspnea, hemoptysis - As expected, individuals with reactive airway disease, such as asthmatics, are particularly sensitive to ammonia inhalation. Hoarseness Dysphagia Loss of consciousness

Farming industry
Industrial injury most often results from either ammonia leaks in fertilizer tanks and hoses or toxic ammonia levels in animal confinement buildings, where ammonia is adsorbed by dust particles that transport it more directly to small airways. Because of this synergistic effect, symptoms have reportedly developed within minutes of entering animal confinement buildings. Symptoms include rhinorrhea, scratchy throat, chest tightness, cough, dyspnea, and eye irritation and usually subside within 24-48 hours. Farmers exposed to high levels of ammonia may also have a higher likelihood of developing chronic bronchitis and COPD, particularly those with underlying atopy.[5]

Firefighters
Firefighters are at risk for exposure to this irritant gas, as ammonia is liberated during combustion of nylon, silk, wood, and melamine.

Contact - Burns and cold injury

Gaseous ammonia combines with water of the skin, eyes, and airways to form ammonium hydroxide. This exothermic reaction results in both heat and chemical burns. Liquid ammonia freezes tissue on contact and may cause full-thickness tissue damage that penetrates deeper than the more conspicuous superficial chemical burns. Concentrations greater than 10,000 ppm are required to cause skin damage. The eyes begin to feel irritated at concentrations of 50-100 ppm; at 700 ppm, immediate eye damage occurs.

Ingestion
Typical household ammonia products (3-10% ammonium hydroxide) have a pH less than 12.5, although the pH of industrial solutions (up to 30% ammonium hydroxide) is often greater than 13. Because caustic alkali burns generally are thought to occur when pH is greater than 12.5, ammonia ingestions in the home usually do not lead to significant damage. However, Klein et al reported 3 cases of oropharyngeal and esophageal injury following intentional ingestion of household solutions with a pH less than 12.[6] Patients present with oropharyngeal, epigastric, and retrosternal pain. Abdominal pain and other gastroenterologic symptoms may occur if ingestion causes viscus perforation (perforation may occur up to 24-72 hours postingestion). Respiratory symptoms may be present if aspiration pneumonia or pneumonitis complicates ingestion. Smelling salts are a less common source of household ammonia ingestion. Often in capsule form, smelling salts, which contain approximately 20% ammonia, release a pungent odor when broken. Smelling salts are found in many first-aid kits as a treatment for syncope; unfortunately, children sometimes bite into them, resulting in minor esophageal burns and mild respiratory symptoms.

Inhalation injury

Head, ears, eyes, nose, throat (HEENT) - Facial and oral burns and ulcerations Respiration - Tachypnea, oxygen desaturation, stridor, drooling, cough, wheezing, rhonchi, and decreased air entry Central nervous system (CNS) - Loss of consciousness (if exposure is massive)

Contact - Burns and cold injury

Skin - Alkali burns to the skin are yellow, soapy, and soft in texture. When burns are severe, skin turns black and leathery. HEENT - Burns to the eye penetrate particularly deeply and rapidly, leading to destruction of the inner structures within 2-3 minutes; this may progress to globe perforation. Ammonia typically causes more corneal epithelium and lens damage than other alkalis. Intraocular pressure and pH

of the anterior chamber rise, resulting in a syndrome similar to acute narrow-angle glaucoma. Other symptoms include iritis, corneal edema, semi-dilated fixed pupil, and eventual cataract formation.

Ingestion

Cardiovascular - With intentional ingestion, hypovolemic shock may occur because of vomiting and third-spacing of intravascular fluid. HEENT - Symptoms include edema of the lips, oropharynx, and upper airway. GI - Patient may experience epigastric tenderness; mediastinitis and peritoneal signs may be present with viscus perforation, which can occur as late as 24-72 hours postingestion. Respiratory -Aspiration pneumonia and pulmonary edema may occur.

HARMFUL HEALTH EFFECTS OF AMMONIA