Nitric acid. General information

Nitric acid General information Key Points Fire Non-flammable under normal conditions, but may ignite other flammable materials Highly reactive Releases toxic and irritating fumes when heated In the event of fire involving nitric acid, use fine water spray and liquid-tight chemical protective suit with breathing apparatus Gas-tight protective suits with breathing apparatus are required for fuming nitric acid Health Exposure can occur through ingestion, inhalation, or absorption through the skin or eyes Highly corrosive Short-term inhalation may result in a dry throat and nasal passages, cough, chest pain, shortness of breath, headache and difficulty breathing Long-term inhalation may lead to the development of lung diseases such as bronchitis and can cause tooth erosion Short-term ingestion can cause burns to the lips, tongue, mouth, throat and stomach. Swelling of the airways can cause difficulty breathing and swallowing. Skin exposure can result in severe burns, blisters and permanent scarring Exposure of the eyes can result in severe injury leading to permanent blindness Nitric acid or nitric acid solutions are not considered to cause cancer Nitric acid is not thought to cause damage to the unborn child Environment Avoid release into the environment Inform Environment Agency of substantial release incidents Prepared by J C Wakefield CHAPD HQ, HPA 2007 Version 1

NITRIC ACID GENERAL INFORMATION Nitric acid is a highly corrosive liquid which is colourless to yellow, with an acrid, choking odour. Nitric acid can be produced by mixing nitrogen dioxide with water in the presence of oxygen. However, commercial production of nitric acid, known as the Ostwald process, commonly involves the oxidation of ammonia. Nitric acid has widespread uses in industry, with over one million tons per year being produced in the UK alone. It is an important component for the manufacture of fertilisers, dyes and some pharmaceuticals. Nitric acid is also used for the production of semiconductors, in electroplating, etching and for the cleaning of many metals. Nitric acid can react violently when mixed with other organic compounds, and for this reason is a major component in some rocket fuels. It is also used in the manufacture of some explosives, such as nitroglycerin and trinitrotoluene (TNT). Background pollutant, in the atmosphere, and is one of the constituents of acid-rain. Nitric acid is highly corrosive. Drinking a solution of nitric acid will result in burns to the mouth, throat and stomach and can, in some cases, cause death. Inhalation of air containing high levels of nitric acid can cause dryness of the throat and nasal passages, cough, shortness of breath, difficulty breathing and chest pain. In some cases the inhalation of high concentrations of nitric acid can cause death. Repeated inhalation of air containing nitric acid over a long time can damage the lungs and erode the outer coating (enamel) from teeth. People with breathing problems such as asthma may be more sensitive to the damage caused by breathing air containing nitric acid. Nitric acid is also capable of causing burns, blisters, ulcers and permanent scarring following skin contact. The depth of the burn depends upon the strength of the acid and the duration of contact. If nitric acid comes into contact with the eyes, the resulting burns can lead to permanent injury and blindness, depending on the length of exposure. Nitric acid is not commonly present in household products, therefore exposure of the general public is not common. However, the widespread industrial use of nitric acid, means that exposure may potentially occur in a variety of occupational settings. Nitric acid does not accumulate in the environment and is rapidly neutralised in soil. However, nitric acid may be formed readily from nitrogen dioxide, which is a common air Children exposed to nitric acid will display similar effects to exposed adults. However, the effects seen in children may possibly be more severe. Exposure of a pregnant mother to nitric acid is not likely to cause damage to the unborn child, as the acid is toxic only at the point of contact and is also rapidly broken down. Solutions of nitric acid are not considered to be carcinogenic. General information: Page 2 of 5

NITRIC ACID GENERAL INFORMATION Production and Uses Key Points Nitric acid is an important industrial chemical, with over 1 million tons being produced annually in the UK The main commercial use of nitric acid is in the production of nitrate-containing fertilisers Nitric acid is also used in the manufacture of dyes, fungicides, explosives and some pharmaceuticals In the UK, over 1 million tons of nitric acid are produced annually. The Ostwald process is the main method used for the commercial production of nitric acid. In this process, ammonia is converted into nitric acid. This involves heating ammonia with oxygen to first form nitrogen dioxide. The nitrogen dioxide is then readily absorbed by water to produce dilute nitric acid. The acid can then be concentrated to the required strength by distillation. The principle commercial use for nitric acid is in the production of nitrate-containing fertilisers. Nitric acid is also a common component used in the manufacture of dyes, pharmaceuticals, explosives and fungicides and is also used for water treatment, the manufacture of fibres and polymers, such as nylon and can be used for the reprocessing of spent nuclear fuels. As nitric acid reacts and corrodes most metals it is widely used for cleaning and plating metal surfaces. General information: Page 3 of 5

NITRIC ACID GENERAL INFORMATION Frequently Asked Questions What is nitric acid? Nitric acid is a clear liquid, which appears colourless to yellow. It has a choking odour and is highly corrosive. Nitric acid is used in many industries. For example, it is commonly used for the production of fertilisers, dyes, some pharmaceuticals, explosives and fungicides. It is also used to clean or etch metal. How does nitric acid get into the environment? Nitric acid may be present in the environment as a break-down product of nitrogen dioxide, which is a common pollutant released into the environment from commercial and industrial processes. Nitrogen dioxide in the environment, in the presence of water, can readily form nitric acid. It is also one of the components present in acid-rain, which can cause environmental damage. How could I be exposed to nitric acid? Nitric acid is not commonly present in household products, so the most likely place people might be exposed is in the workplace. Small amounts of nitric acid may also be breathed in from polluted air. If there is nitric acid in the environment will I have any adverse health effects? The presence of nitric acid in the environment does not always lead to exposure. Clearly, in order for it to cause any adverse health effects you must come into contact with it. You may be exposed by breathing, eating, or drinking the substance or by skin contact. Following exposure to any chemical, the adverse health effects you may encounter depend on several factors, including the amount to which you are exposed (dose), the way you are exposed, the duration of exposure, the form of the chemical and if you were exposed to any other chemicals. Strong solutions of nitric acid are highly corrosive and can cause burns to any part of the body it comes into contact with. More dilute solutions of nitric acid may cause irritation to the skin, eyes and throat. Can nitric acid cause cancer? Nitric acid and its solutions are not considered to be cancer causing substances. Does nitric acid affect children or damage the unborn child? Children will be affected by nitric acid in the same way as adults. Nitric acid is not likely to cause damage to the unborn child if the mother is exposed, as nitric acid only causes toxicity at the point of contact and breaks down rapidly on contact with skin and other tissues. General information: Page 4 of 5

NITRIC ACID GENERAL INFORMATION What should I do if I am exposed to nitric acid? It is very unlikely that the general population will be exposed to a level of nitric acid high enough to cause adverse health effects. This document from the HPA Centre for Radiation, Chemical and Environmental Hazards reflects understanding and evaluation of the current scientific evidence as presented and referenced in this document. General information: Page 5 of 5

Nitric acid Incident management Key Points Fire Non-flammable, but may ignite other flammable materials Oxidising Highly reactive with organic, combustible and reducible materials, reacts violently with bases Emits toxic fumes of nitrogen oxide fumes when heated to decomposition In the event of a fire involving nitric acid, use fine water spray and liquid and gas tight chemical protective clothing with breathing apparatus Health Toxic by all routes Ingestion may result in ulceration of the upper GI tract, haemorrhage, metabolic acidosis, cardiovascular collapse, acute renal failure and coagulation disorders Inhalation may cause irritation of eyes and nose with sore throat, cough, chest tightness, headache, ataxia and confusion. Pulmonary oedema with increasing breathlessness, wheeze, hypoxia and cyanosis may take up to 36h to develop Dermal exposure causes coagulation burns Ocular exposure can result in corneal burns, pain, blepharospasm, lacrimation, conjunctivitis, palpebral oedema and photophobia Environment Avoid release into the environment Inform Environment Agency of substantial incidents CRCE HQ, HPA 03/2012 Version 2

Hazard Identification Standard (UK) Dangerous Goods Emergency Action Codes (a) UN 1826 EAC 2X Nitrating acid mixture, spent, with not more than 50 % nitric acid, packaging group II Use fine water spray. Wear liquid-tight chemical protective clothing in combination with breathing apparatus*. Spillages and decontamination run-off should be prevented from entering drains and watercourses. APP - Hazards Class 8 Corrosive substance Sub risks - HIN 80 Corrosive or slightly corrosive substance UN 1826 EAC 2W Nitrating acid mixture spent, with more than 50 % nitric acid, packaging group I Use fine water spray. Wear liquid-tight chemical protective clothing in combination with breathing apparatus*. Danger that the substance can be violently or explosively reactive. Spillages and decontamination run-off should be prevented from entering drains and watercourses. APP B Gas-tight chemical protective suit with breathing apparatus**. Class 8 Corrosive substance Hazards Sub risks 5.1 Oxidising substance HIN 885 Highly corrosive substance, oxidising (fire-intensifying) a Dangerous Goods Emergency Action Code List 2011. National Chemical Emergency Centre (NCEC). The Stationary Office, London. Incident management: Page 2 of 16

UN United Nations number; EAC Emergency Action Code; APP Additional Personal Protection; HIN - Hazard Identification Number UN 1796 EAC 2P Nitrating acid, mixture, with more than 50 % nitric acid, packaging I Use fine water spray. Wear liquid-tight chemical protective clothing in combination with breathing apparatus*. Danger that the substance can be violently or explosively reactive. Spillages and decontamination run-off may be washed to drains with large quantities of water. Due care must however still be exercised to avoid unnecessary pollution to watercourses. APP B Gas-tight chemical protective suit with breathing apparatus**. Class 8 Corrosive substance Hazards Sub risks 5.1 Oxidising substance HIN 885 Highly corrosive substance, oxidising (fire-intensifying) UN 1796 Nitrating acid, mixture, with not more than 50 % nitric acid, EAC 2R APP - Use fine water spray. Wear liquid-tight chemical protective clothing in combination with breathing apparatus*. Spillages and decontamination run-off may be washed to drains with large quantities of water. Due care must however still be exercised to avoid unnecessary pollution to watercourses. Hazards Class 8 Corrosive substance Sub risks - HIN 80 Corrosive or slightly corrosive substance Incident management: Page 3 of 16

UN 2031 EAC 2P Nitric acid, other than red fuming, with more than 70 % nitric acid Use fine water spray. Wear liquid-tight chemical protective clothing in combination with breathing apparatus *. Danger that the substance can be violently or explosively reactive. Spillages and decontamination run-off may be washed to drains with large quantities of water. Due care must however still be exercised to avoid unnecessary pollution to watercourses. APP B Gas-tight chemical protective suit with breathing apparatus**. Class 8 Corrosive substance Hazards Sub risks 5.1 Oxidising substance HIN 885 Highly corrosive substance, oxidising (fire-intensifying) UN 2031 EAC 2R APP - Nitric acid, other than red fuming, with at least 65% but not more than 70% nitric acid Use fine water spray. Wear liquid-tight chemical protective clothing in combination with breathing apparatus*. Spillages and decontamination run-off may be washed to drains with large quantities of water. Due care must however still be exercised to avoid unnecessary pollution to watercourses. Class 8 Corrosive substance Hazards Sub risks 5.1 Oxidising substance HIN 85 Corrosive or slightly corrosive substance, oxidising (fireintensifying) Incident management: Page 4 of 16

UN 2031 EAC 2R APP - Nitric acid, other than red fuming, with less than 65% nitric acid Use fine water spray. Wear liquid-tight chemical protective clothing in combination with breathing apparatus*. Spillages and decontamination run-off may be washed to drains with large quantities of water. Due care must however still be exercised to avoid unnecessary pollution to watercourses. Hazards Class 8 Corrosive substance Sub risks - HIN 80 Corrosive or slightly corrosive substance UN 2032 Nitric acid, red fuming EAC 2PE Use fine water spray. Wear liquid-tight chemical protective clothing in combination with breathing apparatus *. Danger that the substance can be violently or explosively reactive. Spillages and decontamination run-off may be washed to drains with large quantities of water. Due care must however still be exercised to avoid unnecessary pollution to watercourses. There may be a public safety hazard outside the immediate area of the incident***. APP B Gas-tight chemical protective suit with breathing apparatus **. Class 8 Corrosive substance Hazards 5.1 Oxidising substance Sub risks 6.1 Toxic substance Corrosive or slightly corrosive substance, oxidising (fireintensifying) and toxic HIN 856 UN United Nations number; EAC Emergency Action Code; APP Additional Personal Protection; HIN - Hazard Identification Number Incident management: Page 5 of 16

*Liquid-tight chemical protective clothing (BS 8428) in combination with self-contained open circuit positive pressure compressed air breathing apparatus (BS EN 137). **Gas-tight chemical protective clothing (BS EN 943) in combination with self-contained open circuit positive pressure compressed air breathing apparatus (BS EN 137) *** People should stay indoors with windows and doors closed, ignition sources should be eliminated and ventilation stopped. Non-essential personnel should move at least 250 m away from the incident. Incident management: Page 6 of 16

Chemical Hazard Information and Packaging for Supply Classification (a) O Oxidising Classification C Corrosive Risk phrases Safety phrases R8 R35 Contact with combustible material may cause fire Causes severe burns S1/2 Keep locked up and out of the reach of children S23 S26 S36 S45 Do not breathe gas/fumes/vapour/spray (appropriate wording to be specified by the manufacturer) In case of contact with eyes, rinse immediately with plenty of water and seek medical advice Wear suitable protective clothing In case of accident or if you feel unwell seek medical advice immediately (show the label where possible) Specific concentration limits Concentration Classification C 20 % C; R35 5 % C 20 % C; R34 C 70 % O:R8 a Annex VI to Regulation (EC) No 1272/2008 on Classification, Labelling and Packaging of Substances and Mixtures- Table 3.2. http://esis.jrc.ec.europa.eu/index.php?pgm=cla (accessed 03/2012) Incident management: Page 7 of 16

Globally Harmonised System of Classification and Labelling of Chemicals (GHS) (a) Ox. Liq. 3 Oxidizing liquid, category 3 Hazard Class and Category Skin Corr. 1A Skin corrosion, category 1A Hazard Statement H272 H314 May intensify fire; oxidiser Causes severe skin burns and eye damage Signal Words DANGER Implemented in the EU on 20 January 2009. Specific concentration limits Concentration Hazard Class and Category Hazard Statement C 20 % Skin Corr. 1A H314 Causes severe skin burns and eye damage 5 % C < 20 % Skin Corr. 1B H314 Causes severe skin burns and eye damage C 65 % Ox. Liq. 3 H272 May intensify fire; oxidiser a Annex VI to Regulation (EC) No 1272/2008 on Classification, Labelling and Packaging of Substances and Mixtures- Table 3.1. http://esis.jrc.ec.europa.eu/index.php?pgm=cla (accessed 03/2012) Incident management: Page 8 of 16

Physicochemical Properties CAS number 7697-37-2 Molecular weight 63 Empirical formula HNO 3 Common synonyms State at room temperature Hydrogen nitrate Liquid Volatility Vapour pressure: 4.1 mm Hg at 25 C Specific gravity 1.6 at 25 C (water = 1) Flammability Lower explosive limit Upper explosive limit Non-flammable, but may ignite other flammable materials Not applicable Not applicable Water solubility Soluble in water at 25 C Reactivity Reaction or degradation products Odour Highly reactive. Nitric acid reacts violently with organic, combustible and reducible materials, reacts violently with bases and is corrosive to metals Emits toxic fumes of nitrogen oxides when heated to decomposition Characteristic choking odour Structure References (a,b,c) a Nitric acid (HAZARDTEXT Hazard Management). In: Klasco RK (Ed): TOMES System, Thomson Micromedex, Greenwood Village, Colorado, USA. (electronic version). RightAnswer.com, Inc., Midland, MI, USA, Available at: http://www.rightanswerknowledge.com/data/dt/dt721.htm (accessed 01/2012) b The Merck Index (14 th Edition). Entry 6577: Nitric acid, 2006. c The Dictionary of Substances and their Effects. Ed. S Gangolli. Second Edition, Volume 5, 1999. Incident management: Page 9 of 16

Threshold Toxicity Values EXPOSURE VIA INHALATION ppm mg m -3 SIGNS AND SYMPTOMS - - Data not available Incident management: Page 10 of 16

Published Emergency Response Guidelines Emergency Response Planning Guideline (ERPG) Values (a) Listed value (ppm) Calculated value (mg m -3 ) ERPG-1* 1 3 ERPG-2** 6 16 ERPG-3*** 78 201 * Maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hr without experiencing other than mild transient adverse health effects or perceiving a clearly defined, objectionable odour. ** Maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hr without experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual's ability to take protective action. *** Maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hr without experiencing or developing life-threatening health effects. Interim Acute Exposure Guideline Levels (AEGLs) (b) ppm 10 min 30 min 60 min 4 hr 8 hr AEGL-1 0.53 0.53 0.53 0.53 0.53 AEGL-2 43 30 24 6.0 3.0 AEGL-3 170 120 92 23 11 The level of the chemical in air at or above which the general population could experience notable discomfort. The level of the chemical in air at or above which there may be irreversible or other serious longlasting effects or impaired ability to escape. The level of the chemical in air at or above which the general population could experience lifethreatening health effects or death. a American Industrial Hygiene Association (AIHA). 2011 Emergency Response Planning Guideline Values. http://www.aiha.org/insideaiha/guidelinedevelopment/erpg/documents/2011erpgweelhandbook_tabl e-only.pdf (accessed 03/2011). b U.S. Environmental Protection Agency. Acute Exposure Guideline Levels, http://www.epa.gov/oppt/aegl/pubs/chemlist.htm (accessed 03/2011). Incident management: Page 11 of 16

Exposure Standards, Guidelines or Regulations Occupational standards WEL (a) http://www.hse.gov.uk/ LTEL (8 hour reference period): No guideline value specified STEL (15 min reference period): 1ppm (2.6 mg m -3 ) Public health guidelines DRINKING WATER QUALITY GUIDELINE Data not available AIR QUALITY GUIDELINE Data not available SOIL GUIDELINE VALUE AND HEALTH CRITERIA VALUES Data not available WEL Workplace exposure limit; LTEL - Long-term exposure limit; STEL Short-term exposure limit a EH40/2005 Workplace Exposure Limits (second edition, published 2011). http://www.hse.gov.uk/pubns/priced/eh40.pdf (accessed 01/2012) Incident management: Page 12 of 16

Major route of exposure (a) Health Effects Toxic by ingestion, inhalation, dermal and ocular absorption. (b-e) b,c,d,e) Immediate signs or symptoms of acute exposure Ingestion may can cause immediate pain with burning in the mouth, throat and stomach. This may be followed by abdominal pain, vomiting, haematemesis and dyspnoea. Pain and oedema may make swallowing difficult, causing drooling. Haemorrhagic or hypovolaemic shock and airway obstruction from laryngeal and/or epiglottic oedema are features of severe cases. Stridor and respiratory complications (including pneumonitis, pulmonary oedema, ARDS and pulmonary necrosis) can develop following aspiration of corrosive materials. Systemic effects following ingestion include circulatory collapse, metabolic acidosis, hypoxia, respiratory failure, acute renal failure, haemolysis and disseminated intravascular coagulation (DIC). Inhalation can cause irritation of eyes and nose with sore throat, cough, chest tightness, headache, fever, wheeze, tachycardia and confusion. Chemical pneumonitis, tachypnoea, dyspnoea and stridor due to laryngeal oedema may follow. Pulmonary oedema with increasing breathlessness, wheeze, hypoxia and cyanosis may take up to 36h to develop. Optic neuropathy has been reported following acute inhalation. Dermal contact may cause pain, blistering, ulceration and penetrating necrosis. Coagulation burns may develop, which can be self-limiting and superficial with the destruction of the surface epithelium and sub mucosa forming a leathery crust which limits the spread of the product. Ocular exposure may cause pain, blepharospasm, lacrimation, conjunctivitis, palpebral oedema and photophobia. Acidic solutions may cause corneal burns. TOXBASE - http://www.toxbase.org (accessed 01/2012) a TOXBASE: Nitric acid, 2004 b TOXBASE: Corrosives - ingestion, 2010. c TOXBASE: Corrosives - inhalation, 2010. d TOXBASE: Skin decontamination corrosives, 2010. e TOXBASE: Chemicals splashed or sprayed into the eyes, 2007. Incident management: Page 13 of 16

Decontamination and First Aid Important Notes Ambulance staff, paramedics and emergency department staff treating chemicallycontaminated casualties should be equipped with Department of Health approved, gas-tight (Respirex) decontamination suits based on EN466:1995, EN12941:1998 and pren943-1:2001, where appropriate. Decontamination should be performed using local protocols in designated areas such as a decontamination cubicle with adequate ventilation. Dermal exposure (a,b) Remove patient from exposure. Do NOT apply neutralising chemicals as heat produced during neutralization reactions may cause thermal burns and increase injury. Contaminated clothing and any particulate matter adherent to skin should be removed and the patient washed with copious amounts of water under low pressure for at least 10-15 minutes, or until ph of skin is normal (ph of the skin is 4.5 6 although it may be closer to 7 in children, or after irrigation). The earlier irrigation begins, the greater the benefit. Pay special attention to skin folds, fingernails and ears. Recheck ph of affected areas after a period of 15-20 minutes and repeat irrigation if abnormal. Burns with strong solutions may require irrigation for several hours or more. Once the ph is normal and stabilised, treat as per a thermal injury. Burns totalling more than 15% of body surface area in adults (>10% in children) will require standard fluid resuscitation as for thermal burns. Moderate/severe chemical burns should be reviewed by a burns specialist. Excision or skin grafting may be required. Other measures as indicated by the patient's clinical condition Ocular exposure (c) Remove patient from exposure. Remove contact lenses if present and immediately irrigate the affected eye thoroughly with water or 0.9% saline for at least 10-15 minutes. Continue until the conjunctival sac ph is normal (7.5-8.0), retest after 20 minutes and use further irrigation if necessary.. Any particles lodged in the conjunctival recesses should be removed. Patients with corneal damage or those whose symptoms do not resolve rapidly should be referred for urgent ophthalmological assessment. Inhalation (d) Remove patient from exposure and give oxygen. Remove contaminated clothing to prevent further exposure Ensure a clear airway and adequate ventilation. TOXBASE - http://www.toxbase.org (accessed 01/2012) a TOXBASE: Nitric acid, 2004 b TOXBASE: Skin decontamination - corrosives, 2010. c TOXBASE: Chemicals splashed or sprayed into the eyes, 2007. d TOXBASE: Corrosives inhalation, 2010.. Incident management: Page 14 of 16

Apply other supportive measures as indicated by the patient's clinical condition. Ingestion (a) In severely affected patients rapid intervention is essential. Urgent assessment of the airway is required. A supraglottic-epiglottic burn with erythema and oedema is usually a sign that further oedema will occur which will lead to airway obstruction and is an indication for consideration of early intubation or tracheotomy. Do NOT attempt gastric lavage. Do NOT give neutralising chemicals as heat produced during neutralisation reactions may increase injury. The use of water or milk (maximum initial volume = 100-200 ml in an adult; 2 ml/kg in a child) as diluents in the management of corrosive ingestion may be of some symptomatic benefit (but caution is necessary following large ingestions where mucosal damage / perforation may have already developed). Monitor BP, pulse and oxygen saturation. Treat shock by replacing lost fluids intravenously. Apply other supportive measures as indicated by the patient's clinical condition. This document from the HPA Centre for Radiation, Chemical and Environmental Hazards reflects understanding and evaluation of the current scientific evidence as presented and referenced in this document. TOXBASE - http://www.toxbase.org (accessed 01/2012) a TOXBASE: Corrosives ingestion, 2010 Incident management: Page 15 of 16

Incident management: Page 16 of 16

Nitric acid Toxicological overview Kinetics and metabolism Key Points Nitric acid is corrosive at the site of contact and does not elicit systemic toxicity On contact with body tissues, nitric acid is rapidly broken down into its constituent ions and excreted in the urine Health effects of acute exposure Exposure to nitric acid can occur through all routes Nitric acid is irritating and corrosive to all tissues with which it comes into contact. The severity of effects is dependent upon concentration and duration of exposure Acute inhalation of nitric acid vapour can lead to symptoms such as ocular and nasal irritation, sore throat, cough, chest tightness, headache, ataxia and confusion In severe cases, pulmonary oedema may develop hours or days following exposure Acute ingestion may cause burns to the oesophagus and stomach which can include ulceration, haemorrhage and perforation. Abdominal pain, difficulty swallowing, nausea, salivation, vomiting, diarrhoea and haematemesis may also occur, and in some cases may be fatal Dermal exposure may result in deep burns, blisters and permanent scarring Ocular exposure may cause corneal burns, lacrimation, conjunctivitis, photophobia and, in severe cases, could lead to permanent blindness Health effects of chronic exposure Chronic inhalation exposure to nitric acid can cause respiratory irritation, leading to bronchitis and airways hyperreactivity and erosion of dental enamel Chronic ingestion is unlikely due to the adverse effect of acute ingestion Dermal exposure to low concentrations of nitric acid can result in dermatitis Nitric acid is not considered to be carcinogenic or mutagenic Prepared by J C Wakefield CHAPD HQ, HPA 2007 Version 1

NITRIC ACID TOXICOLOGICAL OVERVIEW Toxicological Overview Summary of Health Effects Concentrated nitric acid is highly corrosive to all tissues with which it may come into contact and exposure can occur via all routes (ingestion, inhalation, dermal and ocular absorption). The toxicity of nitric acid is due to its effects at the point of contact, it readily dissociates into simple ions and systemic effects are unlikely. Inhalation exposure to nitric acid is a common occupational hazard as it readily forms a vapour at room temperature. Symptoms of an acute inhalation exposure to nitric acid include dry nose and throat, cough, chest pain, shortness of breath, headache and difficulty breathing. An acute exposure to a high dose of concentrated nitric acid can cause pulmonary oedema, which may take up to 48 hours to develop and can potentially be fatal [1, 2]. Ingestion of nitric acid can cause burns to the lips, tongue, mouth, throat and stomach. Other symptoms can include abdominal pain, nausea, vomiting and diarrhoea. In severe cases, the ingestion of a high dose of nitric acid may be fatal [1, 2]. Dermal exposure to nitric acid can result in severe burns, blisters and permanent scarring depending upon the concentration of the acid and the duration of exposure. Ocular exposure can cause severe eye burns which may lead to permanent injury and possibly blindness [1]. A long term inhalation exposure to nitric acid can lead to chronic respiratory irritation such as bronchitis and may also lead to dental erosion as the nitric acid deposits on the teeth and erodes the outer coating of enamel [1]. Repeated exposure of the skin to low concentrations of nitric acid may cause dermatitis. Nitric acid and its solutions are not considered to be carcinogenic or mutagenic in humans or experimental animals. Toxicological overview: Page 2 of 7

NITRIC ACID TOXICOLOGICAL OVERVIEW Kinetics and metabolism Nitric acid is a contact irritant that causes adverse effects at the site of exposure. The corrosive effects of nitric acid are due to the low ph. Aqueous solutions and vapours of nitric acid readily dissociate into hydrogen and nitrate ions. Nitric acid does not accumulate in the body as it is rapidly broken down into its constituent ions which are excreted in the urine. Exposure to nitric acid does not give rise to systemic toxicity as it is broken down at the point of contact and therefore causes adverse effects only at the site of exposure [1]. Sources and route of exposure Nitric acid exposure can occur through all routes [1, 3]. Nitric acid has a range of widespread uses in industry, but is not commonly found in household products. Exposure to nitric acid is therefore most likely to occur in an occupational setting. The most likely routes of occupational exposure are inhalation of nitric acid vapours and skin or eye contact of nitric acid solutions. In such occupations where nitric acid is used, personal protective equipment is recommended to reduce potential exposures [4]. Nitric acid is not expected to accumulate in the environment [1]. Low concentrations of nitric acid may be present in the atmosphere as it may be formed by the conversion of nitrogen dioxide, which is a common air pollutant released into the environment from many commercial and industrial processes [5]. Toxicological overview: Page 3 of 7

NITRIC ACID TOXICOLOGICAL OVERVIEW Health Effects of Acute / Single Exposure Human Data General toxicity Nitric acid is irritating and corrosive to any tissue with which it may come into contact. The severity of its effects are dependent upon the concentration of nitric acid and the duration of exposure [1]. The UK workplace exposure limit to nitric acid is 4 ppm (10.3 mg m -3 ) [6]. Inhalation Nitric acid readily forms a vapour at room temperature and so poses a potential inhalation hazard [1, 3]. Symptoms of inhalation exposure to nitric acid vapours include irritation of the nose, with sore throat, cough, chest tightness, headache, ataxia and confusion. Following these symptoms, dyspnoea and stridor can occur due to laryngeal oedema. After a severe inhalation exposure to nitric acid, pulmonary oedema may develop hours or even days after exposure, which may possibly be fatal, with increasing shortness of breath, wheeze, chest pain and cough [1-3]. Ingestion Ingestion of nitric acid can cause immediate burns to the lips, mouth and throat. Due to the immediate pain, strong nitric acid is not often swallowed. However, if nitric acid is swallowed, it can cause burns to the oesophagus and stomach which can include antral ulceration, haemorrhage and perforation. Extensive areas of the gastrointestinal tract may also be involved [2]. Nitric acid ingestion can also cause retrosternal and abdominal pain, dysphagia, nausea, hypersalivation, vomiting, diarrhoea and haematemesis [1, 2]. Additionally, ingestion of nitric acid may result in metabolic acidosis, shock, collapse, hypotension, acute renal failure and disseminated intravascular coagulation (DIC). Following ingestion of nitric acid, the larynx may also be burned causing oedema, airway obstruction and difficulty clearing bronchial secretions [2]. In some cases, ingestion of a strong solution of nitric acid can prove to be fatal [1]. Dermal / ocular exposure Nitric acid causes superficial coagulation burns (which may be self limiting) and destruction of the surface epithelium [2]. Other effects of dermal exposure to nitric acid may be blisters, ulcers and permanent scarring, dependent upon the concentration of the acid and the duration of exposure. Concentrated solutions of nitric acid cause burns to the skin, whereas dilute solutions can cause discolouration, mild irritation and hyperkeratosis [1, 7]. Eye contact with solutions of nitric acid may cause corneal burns. Symptoms of ocular exposure to nitric acid can also include pain, blepharospasm, lacrimation, conjunctivitis, Toxicological overview: Page 4 of 7

NITRIC ACID TOXICOLOGICAL OVERVIEW palpebral oedema, photophobia and in severe cases could lead to permanent blindness [1, 2]. Delayed effects following an acute exposure Pulmonary oedema may develop 24 to 48 hours after an inhalation exposure to nitric acid, which can potentially be life threatening, with increasing breathlessness, wheeze, chest pain, cough, hypoxia and cyanosis [1, 2]. Toxicological overview: Page 5 of 7

NITRIC ACID TOXICOLOGICAL OVERVIEW Health Effects of Chronic / Repeated Exposure Human Data General toxicity Long term exposure to nitric acid can cause skin and respiratory irritation which may develop into chronic bronchitis. Repeated exposure to vapours, mists or aerosols of nitric acid has been shown to cause dental erosion [1, 7]. Inhalation Long term inhalation exposures to nitric acid can cause chronic respiratory irritation, which may result in chronic bronchitis and airways hyperreactivity [1]. Repeated exposure to nitric acid vapours, mists or aerosols may cause dental erosion. As nitric acid is inhaled, it may be deposited on teeth and cause decalcification resulting in erosion of tooth enamel [1, 2]. Dermal exposure Repeated dermal exposures to low concentrations of nitric acid in solution, vapour or mist can result in dermatitis, characterised by erythema, itching and a dry scaly appearance [1]. Ingestion There is little human data on the effects of chronic or repeated ingestion of nitric acid, as chronic exposure by ingestion is unlikely due to the adverse acute effects. Genotoxicity There is no relevant human or animal information available regarding the genotoxicity of nitric acid. However, nitric acid dissociates into hydrogen and nitrate ions which can be predicted to be without mutagenic potential. It can therefore be assumed that nitric acid does not have any significant mutagenic potential. Carcinogenicity There are no relevant human or animal studies to assess the carcinogenicity of nitric acid. However, the toxicity of nitric acid is limited to its irritant and corrosive effects at the point of contact and it does not cause systemic toxicity. Provided that chronic irritant effects are avoided, it would not be expected to have any carcinogenic potential. The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of nitric acid [1]. Reproductive and developmental toxicity There is no human or animal data available on the reproductive and developmental toxicity of nitric acid. However, nitric acid is not expected to cause reproductive or developmental toxicity, as it is a contact irritant and exposure results in adverse effects only at the point of contact and not systemically [1]. Toxicological overview: Page 6 of 7

NITRIC ACID TOXICOLOGICAL OVERVIEW References [1] Canadian Centre for Occupational Health and Safety (CCOHS) (2004). Nitric acid, Cheminfo. [2] National Poisons Information Service (NPIS) (2004). Nitric acid. TOXBASE. [3] International Programme on Chemical Safety (IPCS) (1994). Nitric acid. International Chemical Safety Card: 0183. WHO. Geneva. [4] National Institute for Occupational Safety and Health (NIOSH) (2005). NIOSH Pocket Guide to Chemical Hazards. Nitric Acid. [5] Australian Government. Department of the Environment and Heritage (1999). National Pollutant Inventory Substance Profile. Nitric Acid. [6] Health and Safety Executive (HSE) (2005). EH40/2005 Workplace Exposure Limits. [7] National Institute for Occupational Safety and Health (NIOSH) (1976). Criteria for a recommended standard: occupational exposure to nitric acid. US Department of Health Education and Welfare. This document from the HPA Centre for Radiation, Chemical and Environmental Hazards reflects understanding and evaluation of the current scientific evidence as presented and referenced in this document. Toxicological overview: Page 7 of 7