Substances Included Synonyms

Therapeutic Toxic Class

A)

B)

C)

Specific Substances

1) Hydraulic cement
2) Concrete
3) Portland cement silicate
4) Clinker
5) CAS 65997-15-1
6) CONCRETE MIX
7) DI-CALCIUM SILICATE
8) PORTLAND CEMENT
9) SILICATE, PORTLAND CEMENT
10) TETRA-CALCIUM ALUMINOFERRITE
11) TRI-CALCIUM ALUMINATE
12) TRI-CALCIUM SILICATE

Available Forms Sources

A)

1) Cement is available in many products intended for commercial and home use. It may be purchased in "pure" form, in premixed sacks with sand (mortar), or with gravel (concrete). It may also be mixed with heavy metals to form colored mortars (iron).

B)

1) Cement is frequently stated to consist of 60% to 67% calcium oxide, 17% to 25% silicon dioxide, 3% to 5% aluminum oxide, with smaller amounts of iron oxide, chromium, potassium, sodium, sulfur, and magnesium oxide (Finkel, 1983; Sax & Lewis, 1989; Harbison, 1998).

a) Pike et al (1988) state that dry cement consists of a variety of complex silicates and that the stated calcium oxide content is an artifact of the convention of reporting elemental analysis in terms of oxides (Pike et al, 1988).
b) The complex silicates react with proper amounts of water to yield a watery residue that is essentially slaked lime saturated in water. The pH of this residue is reported to range from 10 to 12 (Pike et al, 1988).
c) The pH may continue to rise to 12 to 14 as hydration continues and as water penetrates the cement particles (Pike et al, 1988).
d) MORTAR: On hardening, residual calcium hydroxide react with atmospheric carbon dioxide to form non-caustic compounds.
e) HYDRAULIC CEMENT: On hardening, only small amounts, if any, of residual lime reacts with carbon dioxide (Pike et al, 1988).

2) Concrete is 15% cement diluted with sand and other coarse particles. In mixed concrete, the approximate calcium hydroxide content is 3.75% (Greening & Tonry, 1978).
3) SPECIAL-PURPOSE CEMENTS: May contain additives such as plastics, resins, and waterproofing agents.

C)

1) Portland cement is used as a binding agent in mortar and concrete (Sittig, 1985).

Overview

Life Support

A)

Clinical Effects

0.2.1)

A) TOPIC DESCRIPTION: Cement consists of 60% to 67% calcium oxide, 17% to 25% silicon dioxide, 3% to 5% aluminum oxide, with smaller amounts of iron oxide, chromium, potassium, sodium, sulfur, and magnesium oxide. The pH of cement is greater than or equal to 12 when it is in contact with water. Concrete is cement (approximately 15%) mixed with water, air, sand, and gravel or other coarse particles. The approximate calcium hydroxide content of concrete is 3.75%.
B) USES: Cement is available in many products intended for commercial and home use. It may be purchased in "pure" form, in premixed sacks with sand (mortar), or with gravel (concrete). It may also be mixed with heavy metals to form colored mortars (iron). Portland cement is used as a binding agent in mortar and concrete.
C) TOXICOLOGY: Cement's toxicity is primarily due to the formation of calcium hydroxide. This forms when calcium oxide in cement comes in contact with moisture or is mixed with water.
D) EPIDEMIOLOGY: Cement or concrete poisoning is rarely reported, with 920 exposures reported to US poison centers in 2013. Severe poisoning is uncommon, with 171 patients (approximately 18%) experiencing moderate clinical outcomes or major clinical outcomes, and there were no reported deaths.
E) WITH POISONING/EXPOSURE

1) INGESTION: Mucosal burns of the mouth, esophagus, and stomach may occur with ingestion. Bezoars can also form in the stomach and intestines.
2) DERMAL EXPOSURE: Dry skin, erythema, and contact dermatitis can occur with dermal exposure. Prolonged dermal contact with wet cement may cause severe second or third degree burns.
3) INHALATION EXPOSURE: Acute inhalation may cause irritation, wheezing, and coughing. Chronic inhalation has been associated with chest tightness, coughing, restrictive lung disease, and emphysema.
4) OCULAR EXPOSURE: Splash contact can result in conjunctivitis, burns, and corneal edema.

Laboratory Monitoring

A)

B)

Treatment Overview

0.4.2)

A) As there is little data on exposure to cement, the following treatment information is based on experience with other alkaline corrosive agents.
B) MANAGEMENT OF MILD TO MODERATE ORAL TOXICITY

1) Perform early (within 12 hours) endoscopy in patients with stridor, drooling, vomiting, significant oral burns, difficulty swallowing or abdominal pain, and in all patients with deliberate ingestion. If burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation.

C) MANAGEMENT OF SEVERE ORAL TOXICITY

1) Resuscitate with 0.9% saline; blood products may be necessary. Early airway management in patients with upper airway edema or respiratory distress. Early (within 12 hours) gastrointestinal endoscopy to evaluate for burns. Early bronchoscopy in patients with respiratory distress or upper airway edema. Early surgical consultation for patients with severe grade II or grade III burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation.

D) DECONTAMINATION

1) DILUTION: In patients without vomiting or respiratory distress who are able to swallow, dilute with 4 to 8 ounces of milk/water if possible shortly after ingestion; then NPO until after endoscopy. Neutralization, gastric lavage, and activated charcoal all contraindicated.

E) AIRWAY MANAGEMENT

1) Aggressive airway management in patients with deliberate ingestions or any indication of upper airway injury.

F) ANTIDOTE

1) None

G) ENDOSCOPY

1) Should be performed as soon as possible (preferably within 12 hours, not more than 24 hours) in any patient with deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after inadvertent ingestion. Endoscopy should also be considered in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion. Children and adults who are asymptomatic after inadvertent ingestion do not require endoscopy. The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns.

H) CORTICOSTEROIDS

1) The use of corticosteroids to prevent stricture formation is controversial. Corticosteroids should not be used in patients with grade I or grade III injury, as there is no evidence that they are effective. Evidence for grade II burns is conflicting, and the risk of perforation and infection is increased with steroid use, so routine use is not recommended.

I) STRICTURE

1) A barium swallow or repeat endoscopy should be performed several weeks after ingestion in any patient with grade II or III burns or with difficulty swallowing to evaluate for stricture formation. Recurrent dilation may be required. Some authors advocate early stent placement in these patients to prevent stricture formation.

J) SURGICAL MANAGEMENT

1) Immediate surgical consultation should be obtained on any patient with grade III or severe grade II burns on endoscopy, significant abdominal pain, metabolic acidosis, hypotension, coagulopathy, or a history of large ingestion. Early laparotomy can identify tissue necrosis and impending or unrecognized perforation, early resection and repair in these patients is associated with improved outcome.

K) PATIENT DISPOSITION

1) OBSERVATION CRITERIA: Patients with alkaline corrosive ingestion should be sent to a health care facility for evaluation. Patients who remain asymptomatic over 4 to 6 hours of observation, and those with endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged home.
2) ADMISSION CRITERIA: Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.

L) PITFALLS

1) The absence of oral burns does NOT reliably exclude the possibility of significant esophageal burns.
2) Patients may have severe tissue necrosis and impending perforation requiring early surgical intervention without having severe hypotension, rigid abdomen, or radiographic evidence of intraperitoneal air.
3) Patients with any evidence of upper airway involvement require early airway management before airway edema progresses.
4) The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn. All patients with corrosive eye injury should be evaluated by an ophthalmologist.

M) DIFFERENTIAL DIAGNOSIS

1) Acid ingestion, gastrointestinal hemorrhage, or perforated viscus.

0.4.3)

A) DECONTAMINATION

1) Administer oxygen as necessary. Monitor for respiratory distress.

B) AIRWAY MANAGEMENT

1) Manage airway aggressively in patients with significant respiratory distress, stridor or any evidence of upper airway edema. Monitor for hypoxia or respiratory distress.

C) BRONCHOSPASM

1) Treat with oxygen, inhaled beta agonists and consider systemic corticosteroids.

0.4.4)

A) DECONTAMINATION

1) Exposed eyes should be irrigated with copious amounts of 0.9% saline for at least 30 minutes, until pH is neutral and the cul de sacs are free of particulate material.
2) An eye examination should always be performed, including slit lamp examination. Ophthalmologic consultation should be obtained. Antibiotics and mydriatics may be indicated.

0.4.5)

A) OVERVIEW

1) DECONTAMINATION

a) Remove contaminated clothes. Irrigate exposed skin with copious amounts of water for at least 15 minutes or longer (until the slippery feeling is gone), depending on amount and duration of exposure to cement. A physician may need to examine the area if irritation or pain persist.
b) Irrigation usually prevents any burns from developing. Once the cement is hardened, debridement and even skin grafting has been necessary.

Range Of Toxicity

A)

Clinical Effects

Summary Of Exposure

A)

B)

C)

D)

E)

1) INGESTION: Mucosal burns of the mouth, esophagus, and stomach may occur with ingestion. Bezoars can also form in the stomach and intestines.
2) DERMAL EXPOSURE: Dry skin, erythema, and contact dermatitis can occur with dermal exposure. Prolonged dermal contact with wet cement may cause severe second or third degree burns.
3) INHALATION EXPOSURE: Acute inhalation may cause irritation, wheezing, and coughing. Chronic inhalation has been associated with chest tightness, coughing, restrictive lung disease, and emphysema.
4) OCULAR EXPOSURE: Splash contact can result in conjunctivitis, burns, and corneal edema.

Heent

3.4.3)

A) WITH POISONING/EXPOSURE

1) CONJUNCTIVITIS and keratitis may occur (ITI, 1988; Alakija, 1988).
2) BURNS: Splash contacts in the eyes from Portland cement may cause pain, burning, and corneal edema (Grant & Schumann, 1993).

a) VISUAL DISTURBANCE: Halos or colored rings may be visible about lights immediately after Portland cement exposure (Grant & Schumann, 1993).

3) MORTAR: "Lime burns" may occur from mortar. Mortar contains a greater amount of free calcium hydroxide and is more alkaline than Portland cement (Grant & Schumann, 1993).
4) FOREIGN BODY: In one study, cement-exposed workers were more likely to have a corneal foreign body than non-exposed workers (Alakija, 1988).
5) PTERYGIUM: In one study, cement-exposed workers were more likely to have a pterygium (a patch of hypertrophied bulbar subconjunctival tissue extending from the inner canthus to the cornea) than non-exposed workers (Alakija, 1988).

3.4.5)

A) WITH POISONING/EXPOSURE

1) SEPTAL PERFORATION: Perforation of the nasal septum may occur (ITI, 1988).

3.4.6)

A) WITH POISONING/EXPOSURE

1) BURNS: If ingested in either powder or liquid form, caustic burns may occur in the mouth.

a) CASE REPORT: A 46-year-old woman developed erythema and swelling of the lips and buccal mucosa after ingesting a few mouthfuls of cement powder (22% CaO, 7% silica, and 66% granite) (Shibata et al, 1995).

Respiratory

3.6.2)

A) EMPHYSEMA

1) WITH POISONING/EXPOSURE

a) The actual danger of inhaling cement dust (especially in cement manufacture) is somewhat controversial. Bronchitis and emphysema, after many years of exposure in cement manufacturing, were reported by Kalacic (1973a) (Kalacic, 1973a).

B) PNEUMOCONIOSIS

1) WITH POISONING/EXPOSURE

a) Pneumoconiosis was reported by Doig (1955)(Doig, 1955). This data seems to be contradicted by Davis & Nagelschmidt (1956) who found no pneumoconiosis (Davis & Nagelschmidt, 1956).
b) One study indicated that occupational exposure in cement plants may lead to predominantly obstructive ventilatory impairment (Kalacic, 1973b).
c) Some of the differences seen in these studies may have to do with the calcium oxide or silica content of raw cement.

C) PNEUMONITIS

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Pulmonary alveolar proteinosis occurred in a 29-year-old man within 2 years of working as a cement truck driver (McCunney & Godefroi, 1989). Lung biopsy indicated the presence of silica particles within the alveolar fluid and macrophages.

D) DISORDER OF RESPIRATORY SYSTEM

1) WITH POISONING/EXPOSURE

a) RADIOLOGICAL STUDIES: Radiological evidence of pneumoconiosis was low in Portland cement workers, but a dose-response relationship was present between the length of exposure and degree of radiographic abnormalities, specifically rounded and irregular opacities and pleural abnormalities (Abrons et al, 1988). History of smoking appeared to increase the risk of radiographic changes, but it did not completely explain the difference observed between smokers in the exposed group and those in the control group.

E) RESPIRATORY FINDING

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Subacute respiratory toxicity was reported in a woman following an unintentional spill of dry cement into a truck cab where she was sitting. Inhalation of a large amount of the dry powder occurred. The following day she developed cough, dyspnea, and sore throat, which progressed to respiratory insufficiency with wheezing (Turchen et al, 1993).

F) CHRONIC OBSTRUCTIVE LUNG DISEASE

1) WITH POISONING/EXPOSURE

a) An increased incidence of restrictive lung disease was found in some cement-exposed workers (Pimentel & Menezes, 1978; Oleru, 1984). Exposed workers were also more likely to complain of chest tightness, cough, and phlegm. Highly exposed workers had decreased FEV1 and FVC compared with controls, and revealed a moderate degree of restrictive ventilatory defect.
b) CASE SERIES: In a cross-sectional survey of 348 Portland cement workers, approximately 42% of the workers complained of chronic symptoms, which most often included respiratory tract irritation such as cough, dyspnea, and asthma (18.7%, 17.5%, and 15.8%, respectively) (AbuDhaise et al, 1997). Despite an increased risk of lung irritation in cement workers, pulmonary function indices were normal. In addition, cement workers who smoked were found to have more frequent symptoms than non-smokers.

G) PNEUMONIA

1) WITH POISONING/EXPOSURE

a) CASE SERIES: In a series of 6 patients evaluated after swallowing cement, 1 adult developed bronchopneumonia and a child developed aspiration pneumonitis (Visvanathan, 1986).

H) LACK OF EFFECT

1) VENTILATORY FUNCTION: No significant difference in symptoms or ventilatory function were found in a controlled epidemiological study of respiratory effects of Portland cement plant dust (Abrons et al, 1988). Personal dust samples contained a geometric mean concentration of respirable dust and total dust of 0.57 mg/m(3) and 2.9 mg/m(3), respectively.

Gastrointestinal

3.8.2)

A) CHEMICAL BURN

1) WITH POISONING/EXPOSURE

a) Ingestion of either the powder or liquid forms may cause burns of the esophagus and/or stomach.
b) CASE REPORT: A 46-year-old woman developed erythema and swelling of the lips and buccal mucosa after ingesting a few mouthfuls of cement powder (22% CaO, 7% silica, and 66% granite) (Shibata et al, 1995). Endoscopy revealed mild esophageal erythema.
c) CASE SERIES: In a series of 6 patients evaluated after swallowing cement, 2 had oropharyngeal burns or inflammation (Visvanathan, 1986).

B) BEZOAR

1) WITH POISONING/EXPOSURE

a) Cement ingestion may cause bezoar formation (Visvanathan, 1986). Smaller bezoars may pass spontaneously, but larger ones may cause obstruction and require surgical removal.

Dermatologic

3.14.2)

A) CHEMICAL BURN

1) WITH POISONING/EXPOSURE

a) SEVERITY: First, second and third degree burns may occur after exposure to wet cement (Fisher, 1979; Flowers, 1978).
b) LOCATION: The most common areas where burns are seen are the hands, feet, knees, legs, and ankles (McGeown, 1984; Peters, 1984; Feldberg et al, 1992; Fisher, 1998).
c) ONSET: The damage is usually delayed in onset and if washed off soon after exposure, burns do not usually occur (Skiendzielewski, 1980). Serious symptoms usually result from exposures of 1 to 6 hours. Soon after exposure there is erythema, which may proceed to ulcers and third degree burns in 12 to 48 hours (Hannuksela et al, 1976; Flowers, 1978).

1) Burns may arise without obvious pain at the time of exposure, and it is often 12 to 48 hours before the initial mild erythema proceeds to burns (Flowers, 1978; Feldberg et al, 1992). Patients may delay seeking treatment for up to 10 days (Feldberg et al, 1992).

d) MECHANISM: Wet cement (including ready-mixed cement used by nonprofessionals) causes alkaline burns; mechanical abrasion may add to the injury (Feldberg et al, 1992; Xiao & Cai, 1995; Lofgren et al, 1996). Factors affecting burn production include alkalinity, duration of contact, and the abrasive nature of the cement particles (e.g., calcium oxide, silica and other metal and alkali oxides) (Winder & Carmody, 2002).

1) Wet cement has a pH of approximately 12.5, due mainly to the hydration of calcium oxide (also known as quicklime) causing an exothermic reaction which may seem negligible initially. Persistent exposure to wet cement decreases the amount of surface lipids on the skin, which can promote drying and cracking of the skin. Abrasions allow the alkali to enter and persist within the skin causing progressive and slow burns to the skin (Boyce & Dickson, 1993). Skin exposure to this compound can produce not only chemical burns with potential sloughing of the skin, but also dermatitis, ulcers, vesicular rash, and urticaria (Winder & Carmody, 2002).
2) Cement powder may cause thermal burns during manufacturing as it is "cooled" only to 1000 C before leaving the kiln (Xiao & Cai, 1995; Onuba & Essiet, 1986). Cement in the dry form will not cause an alkaline burn (Saydjari et al, 1986).
3) Prolonged contact with the water used to wash cement off shoes has caused significant burns (Koo et al, 1992).

e) COMPLICATIONS: Cellulitis may be a complication. Healing may be prolonged.
f) SEQUELAE: Permanent scarring and pain may develop after severe cement burns (Lane & Hogan, 1985; Kelsey & Alvey, 1995).
g) CASE REPORT: A 28-year-old man developed second and third degree burns on the anterior aspects of both shins. He had kneeled on premixed Portland cement, wearing only cotton trousers, for approximately 30 minutes (Tosti et al, 1989).

1) He initially experienced burning and pain over his knees and shins and noticed redness of the skin. By the following day, the affected area had become blistered with some areas of necrosis.

h) CASE REPORT: A 47-year-old man developed partial and full thickness burns with bilateral lower leg pain, erythema and edema after standing in a wet cement mixture intermittently while working for approximately 4 hours. Although he washed off the cement with water during his work, this may have exacerbated his condition by increasing the production of calcium hydroxide. Following debridement and skin grafting, he recovered and was discharged after 10 days of hospitalization (Sherman & Larkin, 2005).
i) CASE REPORT: A 53-year-old woman developed severe full-thickness burns of both ankles after standing in wet cement with bare feet for approximately 4 hours. Initially, the patient presented with pain and erythema, with complete development of the burns over a period of 8 to 10 hours post-exposure. The patient recovered following excision of the necrotic areas and application of skin grafts (Seyhan et al, 2012).
j) OTHER: Although not commonly reported in the United States, explosions have developed during the manufacture of cement which have resulted in serious injury (Morley et al, 1996).

B) DERMATITIS

1) WITH POISONING/EXPOSURE

a) Dermatologic reactions may be due to heavy metals in the mixture, the most important being chromium, but cobalt and nickel may also contribute to this reaction (Perone et al, 1974; Pirila, 1954; Garcia & Armisen, 1985; El Sayed & Bazex, 1994).
b) The main types of skin reactions seen are dermatitis of the hands, forearms, and feet, with erythema and vesicles, seborrheic eczema, irritant dermatitis, allergic contact dermatitis, stasis dermatitis, hyperkeratosis, and occasionally, exfoliative dermatitis (Calnan, 1960; Avnstorp, 1991; Goh et al, 1986a) Goh et al, 1986b; (Kiec-Swierczynska, 1990).
c) Allergic contact dermatitis appears to carry a worse prognosis than irritant dermatitis. Patients with allergic contact dermatitis from cement exposure have more frequent episodes, longer duration of disease and are more likely to require steroid therapy (Avnstorp, 1991). Once sensitized, patients with allergic contact dermatitis often do not improve despite a change in job or retirement (Avnstorp, 1991a; Halbert et al, 1992; Winder & Carmody, 2002).

1) DISEASE PROGRESSION

a) Workplace allergic contact dermatitis occurs in a stepwise progression.

1) INDUCTION: a period of initial contact where the worker is continually exposed to the allergen. No symptoms develop, but complete allergic sensitization occurs.
2) SECOND PHASE: skin is fully sensitized, and further contact can result in rapid and severe dermal symptoms. Although the levels of sensitivity can decrease over time, sensitization is usually life long.
3) ACUTE VS CHRONIC: Skin lesions may appear as acute (e.g., erythematous, vesicular, bulbous, edema or swelling usually lasting several days to weeks) or chronic (e.g., may have some of the same features as acute, along with thickened, scaly, and fissured skin).

2) Allergic contact dermatitis to chromate may also be more likely to require absence from work (Goh, 1986). The chromate found in cement is in the form of chromium (VI) or hexavalent chromium, which can be found in the material used to manufacture the cement or from the kiln used during processing of bricks (Winder & Carmody, 2002).

d) The addition of ferrous sulfate to cement reduces the chromate content (via precipitation) of cement to not more than 2 ppm of water-soluble chromate (Avnstorp, 1989; Winder & Carmody, 2002).

1) The use of cement with ferrous sulfate was associated with reduction in allergic contact dermatitis, but not irritant dermatitis, in workers engaged in the manufacture of pre-fabricated concrete building components (Avnstorp, 1989).
2) The degree of exposure to wet cement appears to have an effect on the risk of developing irritant cement eczema. The use of gloves and creams does not seem to reduce the development of irritant cement eczema (Avnstorp, 1991).

e) CASE REPORT: Three workers developed allergic contact dermatitis from chromate associated with exposure to cement containing iron sulfate. High concentrations of chromate were found in many samples of cement manufactured with iron sulfate (Bruze et al, 1990).
f) RISK FACTORS: Based on a review of the literature, it appears that cement dermatitis evolves over many years. Some factors which may influence the overall poor prognosis with this condition is that workers tend to be unskilled and have less opportunity to work in other fields, provide temporary labor, are older, and seek medical care less often (Winder & Carmody, 2002).

C) DRY SKIN

1) WITH POISONING/EXPOSURE

a) Cement workers may develop xerosis with erythema and scaling of the skin due to the dehydrating nature of the cement (Perone et al, 1974).

D) BULLOUS ERUPTION

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 71-year-old man with longstanding contact dermatitis from cement developed pemphigoid (Miyachi et al, 1985).

Carcinogenicity

3.21.1)

A) IARC Carcinogenicity Ratings for CAS65997-15-1 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):

1) Not Listed

3.21.3)

A) CARCINOMA

1) There have been several epidemiological studies suggesting an association between chronic exposure to Portland cement and cancers.

a) Two studies have found a possible association with lung cancer (Farebrother et al, no date; (Rafnsson & Johannesdottir, 1986), and one with stomach cancer (McDowall, 1984).
b) A survey of workers at 23 cement plants in the US found no increased mortality from stomach cancer, based on standard mortality ratios (Amandus, 1986; Amandus, 1986a), but this may be a relatively insensitive epidemiological method and did not take into account possible regional differences in mortality (McDowall, 1986).
c) A survey of 546 Portland cement workers found no increased risk of overall cancer or lung cancer when compared with white collar workers from the local reference population, using a Cox regression model controlling for age and smoking habits (Vestbo et al, 1991).
d) In a case control study, cancer of the supraglottis was associated with occupational exposure to cement (odds ratio 4.2) ( Cauvin et al, 1990).
e) A retrospective cohort study found an increased risk of colorectal cancer in workers exposed to cement dust (Jakobsson et al, 1993). The increase was primarily in tumors of the right side of the colon.
f) A study of 2498 Portland cement workers reported an increased incidence of lung and bladder cancer. Among males, there were indications of an increased risk of lung and stomach cancer with increasing cumulated exposure to cement dust (Smailyte et al, 2004).

Laboratory Monitoring

Monitoring Parameters Levels

4.1.1)

A) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise indicated.
B) If respiratory tract irritation is present, monitor pulse oximetry, pulmonary function tests, and chest x-ray.

Radiographic Studies

A)

1) Obtain an abdominal x-ray of patients suspected of ingesting cement. Radiopaque bezoars may be visible in the stomach or intestines (Visvanathan, 1986).

Methods

A)

1) Laboratory measures are unlikely to be useful.
2) Luck & Jentsch (1988) described an in vitro test method for detecting the presence of chromate, with a detection limit between 0.5 and 1 ppm for fresh concrete (Luck & Jentsch, 1988).

a) A solution is prepared consisting of 970 mL ethanol (96%) and 30 mL 8 normal hydrochloric acid saturated with diphenylcarbazide.
b) A strip of filter paper (0.5 x 5 cm) is used to pick up 1 cm of liquid.
c) The reactant (concrete) is applied to the liquid-soaked filter paper.
d) If chromate is present, a red-violet color change will be noted.

Treatment

Life Support

A)

Patient Disposition

6.3.1)

6.3.1.1) ADMISSION CRITERIA/ORAL

A) Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.

6.3.1.5) OBSERVATION CRITERIA/ORAL

A) Patients with alkaline corrosive ingestion should be sent to a health care facility for evaluation. Patients who remain asymptomatic over 4 to 6 hours of observation, and those with endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged home.

Monitoring

A)

B)

Oral Exposure

6.5.1)

A) GENERAL

1) As there is little data on exposure to cement, the following treatment information is based on experience with other alkaline corrosive agents.

B) DILUTION

1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994a; Homan et al, 1995), this has not been adequately studied in humans.
3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994a; Homan et al, 1993).
4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).

C) ACTIVATED CHARCOAL/NOT RECOMMENDED

1) Since the hazard of alkaline corrosive ingestion stems from local tissue injury and not from systemic absorption of toxicant, activated charcoal is of no benefit. Charcoal administration may worsen injury by causing vomiting and may interfere with the ability to visualize burns at endoscopy.

6.5.2)

A) DILUTION

1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994a; Homan et al, 1995), this has not been adequately studied in humans.
3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994a; Homan et al, 1993).
4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).

B) NEUTRALIZATION

1) The use of neutralizing agents after caustic ingestion is NOT recommended. Neutralization has the potential to generate gas and cause exothermic reactions which might worsen injury.
2) Experimental studies suggest that neutralization generates heat, does not limit injury unless performed immediately and that very large volumes of fluid are required to reach neutral pH (Homan et al, 1995a) Maull et al, 1985; (Rumack & Burrington, 1977a).

C) ACTIVATED CHARCOAL

1) Since the hazard of alkaline corrosive ingestion stems from local tissue injury and not from systemic absorption of toxicant, activated charcoal is not of benefit. Charcoal administration may worsen injury by causing vomiting and may interfere with the ability to visualize burns at endoscopy.

6.5.3)

A) SUPPORT

1) As there is little data on exposure to cement, the following treatment information is based on experience with other alkaline corrosive agents.
2) MANAGEMENT OF MILD TO MODERATE ORAL TOXICITY

a) Perform early (within 12 hours) endoscopy in patients with stridor, drooling, vomiting, significant oral burns, difficulty swallowing or abdominal pain, and in all patients with deliberate ingestion. If burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation.

3) MANAGEMENT OF SEVERE ORAL TOXICITY

a) Resuscitate with 0.9% saline; blood products may be necessary. Early airway management in patients with upper airway edema or respiratory distress. Early (within 12 hours) gastrointestinal endoscopy to evaluate for burns. Early bronchoscopy in patients with respiratory distress or upper airway edema. Early surgical consultation for patients with severe grade II or grade III burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation.

B) MONITORING OF PATIENT

1) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise indicated.
2) If respiratory tract irritation is present, monitor pulse oximetry, pulmonary function tests, and chest x-ray.

C) DILUTION

1) Do not exceed 8 ounces in adults and 4 ounces in children (Consensus, 1988), as vomiting may occur with excessive fluid. Contraindications include perforations and patients at risk of vomiting. Keep patient NPO following initial dilution until after medical/surgical evaluation.

a) Immediate dilution with milk or water decreased the extent of tissue injury induced by 50% sodium hydroxide in isolated rat esophagi (Homan et al, 1994).

D) ENDOSCOPIC PROCEDURE

1) Because of the high pH (12) and calcium hydroxide concentration in cement, caustic injury to the gastrointestinal tract is possible. Endoscopy should be reserved for patients with large deliberate ingestions or signs and symptoms such as drooling, stridor, pain, or vomiting. Concrete ingestion poses less of a risk for severe gastrointestinal burns due to the decreased cement concentration (approximately 15%) with approximately 3.75% calcium hydroxide content. .
2) SUMMARY: Obtain consultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.
3) INDICATIONS: Endoscopy should be performed in adults with a history of deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after unintentional ingestion (Crain et al, 1984). Endoscopy should also be performed in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion (Gaudreault et al, 1983; Nuutinen et al, 1994). Children and adults who are asymptomatic after accidental ingestion do not require endoscopy (Gupta et al, 2001; Lamireau et al, 2001; Gorman et al, 1992).
4) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.

a) REFERENCES: (Dogan et al, 2006; Symbas et al, 1983; Crain et al, 1984a; Gaudreault et al, 1983a; Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992)

5) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):

a) Advancing across the cricopharynx under direct vision
b) Gently advancing with minimal air insufflation
c) Never retroverting or retroflexing the endoscope
d) Using a pediatric flexible endoscope
e) Using extreme caution in advancing beyond burn lesion areas
f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).

6) GRADING

a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding, and perforation is related to the severity of the initial burn (Zargar et al, 1991):
b) Grade 0 - Normal examination
c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation or gastrointestinal bleeding may occur.
g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.

7) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
8) SCINTIGRAPHY - Scans utilizing radioisotope labelled sucralfate (technetium 99m) were performed in 22 patients with caustic ingestion and compared with endoscopy for the detection of esophageal burns. Two patients had minimal residual isotope activity on scanning but normal endoscopy and two patients had normal activity on scan but very mild erythema on endoscopy. Overall the radiolabeled sucralfate scan had a sensitivity of 100%, specificity of 81%, positive predictive value of 84% and negative predictive value of 100% for detecting clinically significant burns in this population (Millar et al, 2001). This may represent an alternative to endoscopy, particularly in young children, as no sedation is required for this procedure. Further study is required.
9) MINIPROBE ULTRASONOGRAPHY - was performed in 11 patients with corrosive ingestion . Findings were categorized as grade 0 (distinct muscular layers without thickening, grade I (distinct muscular layers with thickening), grade II (obscured muscular layers with indistinct margins) and grade III (muscular layers that could not be differentiated). Findings were further categorized as to whether the worst appearing image involved part of the circumference (type a) or the whole circumference (type b). Strictures did not develop in patients with grade 0 (5 patients) or grade I (4 patients) lesions. Transient stricture formation developed in the only patient with grade IIa lesions, and stricture requiring repeated dilatation developed in the only patient with grade IIIb lesions (Kamijo et al, 2004).

E) CORTICOSTEROID

1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
8) STUDIES

a) ANIMAL

1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).

b) HUMAN

1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
2) META ANALYSIS

a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).

3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).

a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).

6) ADVERSE EFFECTS

a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).

F) SURGICAL PROCEDURE

1) SUMMARY: Initially if severe esophageal burns are found a string may be placed in the stomach to facilitate later dilation. Insertion of a specialized nasogastric tube after confirmation of a circumferential burn may prevent strictures. Dilation is indicated after 2 to 4 weeks if strictures are confirmed. If dilation is unsuccessful colonic intraposition or gastric tube placement may be needed. Early laparotomy should be considered in patients with evidence of severe esophageal or gastric burns on endoscopy.
2) STRING - If a second degree or circumferential burn of the esophagus is found a string may be placed in the stomach to avoid false channel and to provide a guide for later dilation procedures (Gandhi et al, 1989).
3) STENT - The insertion of a specialized nasogastric tube or stent immediately after endoscopically proven deep circumferential burns is preferred by some surgeons to prevent stricture formation (Mills et al, 1978; (Wijburg et al, 1985; Coln & Chang, 1986).

a) STUDY - In a study of 11 children with deep circumferential esophageal burns after caustic ingestion, insertion of a silicone rubber nasogastric tube for 5 to 6 weeks without steroids or antibiotics was associated with stricture formation in only one case (Wijburg et al, 1989).

4) DILATION - Dilation should be performed at 1 to 4 week intervals when stricture is present(Gundogdu et al, 1992). Repeated dilation may be required over many months to years in some patients. Successful dilation of gastric antral strictures has also been reported (Hogan & Polter, 1986; Treem et al, 1987).
5) COLONIC REPLACEMENT - Intraposition of colon may be necessary if dilation fails to provide an adequate sized esophagus (Chiene et al, 1974; Little et al, 1988; Huy & Celerier, 1988).
6) LAPAROTOMY/LAPAROSCOPY - Several authors advocate laparotomy or laparoscopy in patients with endoscopic evidence of severe esophageal or gastric burns to evaluate for the presence of transmural gastric or esophageal necrosis (Cattan et al, 2000; Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993).

a) STUDY - In a retrospective study of patients with extensive transmural esophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (esophagoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).

G) FLUID/ELECTROLYTE BALANCE REGULATION

1) Fluid and electrolyte replacement may be necessary in cases of hypovolemia or lactic acidosis due to severe tissue burns and shock.

H) ANTIBIOTIC

1) Antibiotics may be indicated for specific infections.

Inhalation Exposure

6.7.1)

A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

6.7.2)

A) GENERAL TREATMENT

1) Manage airway aggressively. Intubate any patient with significant stridor, respiratory distress or upper airway edema. Be prepared to perform cricothyroidotomy as intubation may be difficult secondary to edema.
2) CAUSTIC INHALATION: Administer humidified oxygen, and remove from exposure. Monitor patient for respiratory distress; if a cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, and pneumonitis.
3) Patients with upper airway burns may develop significant edema abruptly; early intubation is advised.
4) Determine pulse oximetry and/or blood gases, obtain chest x-ray, perform endotracheal intubation and provide mechanical ventilation as clinically indicated.
5) Administer inhaled beta2-adrenergic agonists in patients with bronchospasm (National Heart,Lung,and Blood Institute, 2007). If acute lung injury develops, consider PEEP (Haas, 2011; Leaver & Evans, 2007; Stolbach & Hoffman, 2011).
6) Evaluate for esophageal, dermal and eye burns as indicated.

B) ACUTE LUNG INJURY

1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

C) BRONCHOSPASM

1) BRONCHOSPASM SUMMARY

a) Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.

2) ALBUTEROL/ADULT DOSE

a) 2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).

3) ALBUTEROL/PEDIATRIC DOSE

a) 0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).

4) ALBUTEROL/CAUTIONS

a) The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.

5) CORTICOSTEROIDS

a) Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).

D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

6.8.1)

A) Begin irrigation immediately with copious amounts of water or sterile 0.9% saline, which ever is more rapidly available. Lactated Ringer's solution may also be effective. Once irrigation has begun, instill a drop of local anesthetic (eg, 0.5% proparacaine) for comfort; switching from water to slightly warmed sterile saline may also improve patient comfort (Singh et al, 2013; Spector & Fernandez, 2008; Ernst et al, 1998; Grant & Schuman, 1993a). In one study, isotonic saline, lactated Ringer's solution, normal saline with bicarbonate, and balanced saline plus (BSS Plus) were compared and no difference in normalization of pH were found; however, BSS Plus was better tolerated and more comfortable (Fish & Davidson, 2010).

1) Continue irrigation for at least an hour or until the superior and inferior cul-de-sacs have returned to neutrality (check pH every 30 minutes), pH of 7.0 to 8.0, and remain so for 30 minutes after irrigation is discontinued (Spector & Fernandez, 2008; Brodovsky et al, 2000). After severe alkaline burns, the pH of the conjunctival sac may only return to a pH of 8 or 8.5 even after extensive irrigation (Grant & Schuman, 1993a). Irrigating volumes up to 20 L or more have been used to neutralize the pH (Singh et al, 2013; Fish & Davidson, 2010). Immediate and prolonged irrigation is associated with improved visual acuity, shorter hospital stay and fewer surgical interventions (Kuckelkorn et al, 1995; Saari et al, 1984).
2) Search the conjunctival sac for solid particles and remove them while continuing irrigation (Grant & Schuman, 1993a).
3) For significant alkaline or concentrated acid burns with evidence of eye injury irrigation should be continued for at least 2 to 3 hours, potentially as long as 24 to 48 hours if pH not normalized, in an attempt to normalize the pH of the anterior chamber (Smilkstein & Fraunfelder, 2002). Emergent ophthalmologic consultation is needed in these cases (Spector & Fernandez, 2008).

B) Sticky lime (calcium hydroxide) paste may be removed from the conjunctiva or cul-de-sac by using a cotton tipped applicator soaked in 0.01 M sodium EDTA (Pfister & Koski, 1982) Burns & Peterson, 1989).
C) DEPOSITS

1) Remove deposits immediately via vigorous irrigation with water or saline to dislodge particles mechanically. A pulsatile jet stream irrigation (Grant, 1986) or other devices which provide continuous irrigation (Burns et al, 1989) may be useful.
2) Swab or brush material from the fornices after double everting the lids. This procedure may be facilitated by application of a local anesthetic and use of a 0.01 to 0.05 M disodium edetate (EDTA) at pH 4.6 to 7 (Grant & Schuman, 1993) Burns et al, 1989).

6.8.2)

A) SUPPORT

1) There is little information specifically about the treatment of ophthalmic exposure to cement. The following recommendations are based on information about ocular exposure to other alkaline corrosives.

B) EDETATE CALCIUM DISODIUM

1) Sticky lime (calcium hydroxide) paste may be removed from the conjunctiva or cul-de-sac by using a cotton tipped applicator soaked in 0.01 M sodium EDTA (Pfister & Koski, 1982).

C) BURN

1) EYE ASSESSMENT: The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn.

D) INJURY OF GLOBE OF EYE

1) EVALUATION

a) ASSESSMENT CAUSTIC EYE BURNS: It may take 48 to 72 hours after the burn to assess correctly the degree of ocular damage (Brodovsky et al, 2000a).
b) The 1965 Roper-Hall classification uses the size of the corneal epithelial defect, the degree of corneal opacification and extent of limbal ischemia to evaluate the extent of the chemical ocular injury (Brodovsky et al, 2000a; Singh et al, 2013):

1) GRADE 1 (prognosis good): Corneal epithelial damage; no limbal ischemia.
2) GRADE 2 (prognosis good): Cornea hazy; iris details visible, ischemia less than one-third of limbus.
3) GRADE 3 (prognosis guarded): Total loss of corneal epithelium; stromal haze obscures iris details; ischemia of one-third to one-half of limbus.
4) GRADE 4 (prognosis poor): Cornea opaque; iris and pupil obscured, ischemia affects more than one-half of limbus.

c) A newer classification (Dua) is based on clock hour limbal involvement as well as a percentage of bulbar conjunctival involvement (Singh et al, 2013):

1) GRADE 1 (prognosis very good): 0 clock hour of limbal involvement and 0% conjunctival involvement.
2) GRADE 2 (prognosis good): Less than 3 clock hour of limbal involvement and less than 30% conjunctival involvement.
3) GRADE 3 (prognosis good): Greater than 3 and up to 6 clock hour of limbal involvement and greater than 30% to 50% conjunctival involvement.
4) GRADE 4 (prognosis good to guarded): Greater than 6 and up to 9 clock hour of limbal involvement and greater than 50% to 75% conjunctival involvement.
5) GRADE 5 (prognosis guarded to poor): Greater than 9 and less than 12 clock hour of limbal involvement and greater than 75% and less than 100% conjunctival involvement.
6) GRADE 6 (very poor): Total limbus (12 clock hour) involved and 100% conjunctival involvement.

2) MINOR INJURY

a) SUMMARY

1) If ocular damage is minor, artificial tears/lubricants, topical cycloplegics, and antibiotics may be all that are needed.

b) ARTIFICIAL TEARS

1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).

c) TOPICAL CYCLOPLEGIC

1) Use to guard against development of posterior synechiae and ciliary spasm (Brodovsky et al, 2000b; Grant & Schuman, 1993a). Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).

d) TOPICAL ANTIBIOTICS

1) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000b; Grant & Schuman, 1993a). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008).

e) PAIN CONTROL

1) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993a). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).

3) SEVERE INJURY

a) SUMMARY

1) If the damage is minor, the above may be all that is needed. For grade 3 or 4 injuries, one or more of the following may be used, only with ophthalmologic consultation: acetazolamide, topical timolol, topical steroids, citrate, ascorbate, EDTA, cysteine, NAC, penicillamine, tetracycline, or soft contact lenses.

b) ARTIFICIAL TEARS

1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).

c) PAIN CONTROL

1) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993a). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).

d) CARBONIC ANHYDRASE INHIBITOR

1) Acetazolamide (250 mg orally 4 times daily) may be given to control increased intraocular pressure (Singh et al, 2013; Tuft & Shortt, 2009; Spector & Fernandez, 2008).

e) TOPICAL STEROIDS

1) DOSE: Dexamethasone 0.1% ointment 4 times daily to reduce inflammation. If persistent epithelial defect is present, discontinue dexamethasone by day 14 to reduce the risk of stromal melt (Tuft & Shortt, 2009). Other sources suggest that corticosteroids should be stopped if the epithelium has not covered surface defects by 5 to 7 days (Grant & Schuman, 1993b).
2) Topical prednisolone 0.5% has also been used. A further increase in corneoscleral melt may occur if topical steroids are used alone. In one study, topical prednisolone 0.5% was used in combination with topical ascorbate 10%; no increase in corneoscleral melt was observed when topical steroids were used until re-epithelization (Singh et al, 2013; Fish & Davidson, 2010).
3) In one retrospective study, fluorometholone 1% drops were administered every 2 hours initially, then decreased to four times daily when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete (Brodovsky et al, 2000).

a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000).

f) ASCORBATE

1) Oral or topical ascorbate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
2) DOSE: Ascorbate 10% 4 times daily topically or 1 g orally (2 g/day) (Singh et al, 2013; Tuft & Shortt, 2009).
3) Ascorbate is needed for the formation of collagen and the concentration of ascorbate in the anterior chamber is decreased when the ciliary body is damaged by alkali burns (Tuft & Shortt, 2009; Grant & Schuman, 1993b). In one retrospective study, ascorbate drops (10%) were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received 500 mg of oral ascorbate 4 times daily, until discharge from the hospital (Brodovsky et al, 2000).

a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000).

g) CITRATE

1) Topical citrate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
2) DOSE: Potassium citrate 10% 4 times daily topically (Tuft & Shortt, 2009).
3) Citrate chelates calcium, and thereby interferes with the harmful effects of neutrophil accumulation, such as release of proteolytic enzymes and superoxide free radicals, phagocytosis and ulceration (Grant & Schuman, 1993b). In one retrospective study, 10% citrate drops were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received a urinary alkalinizer containing 720 mg of citric acid anhydrous and 630 mg of sodium citrate anhydrous 3 times daily, until discharge from the hospital (Brodovsky et al, 2000).

a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000).

h) COLLAGENASE INHIBITORS

1) Inhibitors of collagenase can inhibit collagenolytic activity, prevent stromal ulceration, and promote wound healing. Several effective agents, such as cysteine, n-acetylcysteine, sodium ethylenediamine tetra acetic acid (EDTA), calcium EDTA, penicillamine, and citrate, have been recommended (Singh et al, 2013; Tuft & Shortt, 2009; Perry et al, 1993; Seedor et al, 1987).
2) TETRACYCLINE: Has been found to have an anticollagenolytic effect. Systemic tetracycline 50 mg/kg/day reduced the incidence of alkali-induced corneal ulcerations in rabbits (Seedor et al, 1987).
3) DOXYCYCLINE: Decreased epithelial defects and collagenase activity in a rabbit model of alkali burns to the eye (Perry et al, 1993). DOSE: 100 mg twice daily (Tuft & Shortt, 2009).

i) ANTIBIOTICS

1) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000b; Grant & Schuman, 1993a). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008). In patients with severe burns, a topical fluoroquinolone antibiotic drop 4 times daily may also be used (Tuft & Shortt, 2009). A topical fourth generation fluoroquinolone has been recommended as an antimicrobial prophylaxis in patients with large epithelial defect (Fish & Davidson, 2010).

j) TOPICAL CYCLOPLEGIC

1) Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).

k) SOFT CONTACT LENSES

1) A bandage contact lens (eg, silicone hydrogel) may make the patient more comfortable and protect the surface (Fish & Davidson, 2010; Tuft & Shortt, 2009). Hydrophilic high oxygen permeability lenses are preferred (Singh et al, 2013). Soft lenses with intermediate water content and inherent rigidity may facilitate reepithelialization. The use of 0.5 normal sodium chloride drops hourly and artificial tears or lubricant eyedrops instilled 4 times a day may help maintain adequate hydration and lens mobility.

4) SURGICAL THERAPY

a) SURGICAL THERAPY CAUSTIC EYE INJURY

1) Early insertion of methylmethacrylate ring or suturing saran wrap over palpebral and cul-de-sac conjunctiva may prevent fibrinosis adhesions and reduce fibrotic contracture of conjunctiva, but the advantage of such treatments is not clear.
2) Limbal stem cell transplantation has been used successfully in both the acute stage of injury and the chronically scarred healing phase in patients with persistent epithelial defects after chemical burns (Azuara-Blanco et al, 1999; Morgan & Murray, 1996; Ronk et al, 1994).
3) In some patients, amniotic membrane transplantation (AMT) has been successful in improving corneal healing and visual acuity in patients with persistent epithelial defects after chemical burns. It can restore the conjunctival surface and decrease limbal stromal inflammation (Fish & Davidson, 2010; Sridhar et al, 2000; Su & Lin, 2000; Meller et al, 2000; Azuara-Blanco et al, 1999).
4) Control glaucoma. Remove any cataracts formed (Fish & Davidson, 2010; Tuft & Shortt, 2009).
5) In patients with severe injury, tenonplasty can be performed to promote epithelialization and prevent melting (Tuft & Shortt, 2009).
6) A keratoprosthesis placement has also been indicated in severe cases (Fish & Davidson, 2010). Penetrating keratoplasty is usually delayed as long as possible as results appear to be better with a greater lag time between injury and keratoplasty (Grant & Schuman, 1993a).

E) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

6.9.1)

A) DERMAL DECONTAMINATION

1) Remove contaminated clothing. Irrigate exposed skin with copious amounts of water for at least 15 minutes or longer, depending on the concentration, amount and duration of exposure to the chemical. A physician may need to examine the area if irritation or pain persists after washing.
2) Patients exposed dermally should immediately rinse the area with water until the slippery feeling is gone (Saydjari et al, 1986).
3) Rinsing the exposed area with 50% dextrose water may slow down the hardening process, allowing more of the cement to be washed off (Cuomo & Sobel, 1989). If 50% dextrose water is not readily available, normal saline may be used to rinse the exposed area.
4) pH testing the skin 15 minutes after the end of irrigation allows alkali time to diffuse to the skin surface and helps guide the need for further irrigation (Moran et al, 1987). Continue irrigation until skin pH is neutral.
5) Irrigation will usually, but not always (Whiting, 1977), prevent any burns from developing.
6) Irrigation with buffered phosphate solution is recommended by some authors (Feldberg et al, 1992). If buffered phosphate solution is not available, normal saline may be used for irrigation.
7) Remove any solid particles form the skin with forceps (Herbert & Lawrence, 1989).

6.9.2)

A) WOUND CARE

1) Once the cement has hardened, debridement and even skin grafting has been necessary (Fisher, 1979). Dried on cement is extremely difficult to remove. Water-mineral oil soaks may aid in removing material from the skin. In many cases, a surgical debridement has been necessary.

B) ACUTE ALLERGIC REACTION

1) Those patients sensitive to hexachromium salts should avoid cements, or use one of the low chromium salt cements made available by adding iron which chelates the chromium (Fregert et al, 1979).
2) Treatment with topical corticosteroids is recommended in allergic contact dermatitis to cement (Avenstorp, 1992).

C) BURN

1) Several authors recommend early excision and grafting of full thickness cement burns (Feldberg et al, 1992; Cooke, 1984).
2) One study found that early excision of full thickness caustic burns reduced the time necessary for eschar separation and allowed immediate skin grafting and diminished length of hospitalization (Early & Simpson, 1985).
3) Institute intravenous fluid resuscitation as with any burn (Saydjari et al, 1986).
4) Patients with second or third degree burns involving significant body surface area, hands, feet, face, or genitalia should be referred to a burn center.

D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Case Reports

A)

1) Dextrose water, 50%, has been reported (Cuomo & Sobel, 1989) to be useful in disimpacting concrete from the external auditory canal. After unsuccessful normal saline irrigations, D50W was used in a construction worker who had told medical personnel that sugar was frequently added to ready-made cement to prolong its setting time. Dextrose irrigation was successful and the patient no longer complained of otalgia or decreased auditory activity.

Range Of Toxicity

Summary

A)

Maximum Tolerated Exposure

A)

1) The primary danger with cement is its alkalinity. The pH of cement is greater than or equal to 12 when it is in contact with moisture (eg, on skin or mucous membranes) or when mixed with water. The alkalinity is produced by calcium hydroxide, and trace amounts of sodium and potassium hydroxide. Cement (or concrete) is usually only an alkaline hazard in its plastic state.
2) These compounds, in decreasing order of alkalinity, are cement, concrete, dried cement or concrete.
3) Although exposure limits for cement have not been established, the accepted TLV-TWA is 5 mg/m(3) for calcium hydroxide (ACGIH, 2000).

Workplace Standards

A)

1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

a) Adopted Value

1) Portland cement

a) TLV:

1) TLV-TWA: 1 mg/m(3)
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: A4
2) Codes: E, R
3) Definitions:

a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
b) E: The value is for particulate matter containing no asbestos and less than 1% crystalline silica.
c) R: Respirable fraction; see Appendix C, paragraph C (of TLV booklet).

c) TLV Basis - Critical Effect(s): Pulm func; resp symptoms; asthma
d) Molecular Weight:

1) For gases and vapors, to convert the TLV from ppm to mg/m(3):

a) [(TLV in ppm)(gram molecular weight of substance)]/24.45

2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:

a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

e) Additional information:

B) NIOSH REL and IDLH Values for CAS65997-15-1 (National Institute for Occupational Safety and Health, 2007):

1) Listed as: Portland cement
2) REL:

a) TWA: 10 mg/m(3) (total) 5 mg/m(3) (resp)
b) STEL:
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

3) IDLH:

a) IDLH: 5000 mg/m3
b) Note(s): Not Listed

C) Carcinogenicity Ratings for CAS65997-15-1 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Portland cement

a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Portland cement
5) MAK (DFG, 2002): Not Listed
6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

D) OSHA PEL Values for CAS65997-15-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Listed as: Portland cement (Total dust)
2) Table Z-1 for Portland cement (Total dust):

a) 8-hour TWA:

1) ppm:

a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

2) mg/m3: 15

a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

3) Ceiling Value:
4) Skin Designation: No
5) Notation(s): Not Listed

3) Listed as: Portland cement (Respirable fraction)
4) Table Z-1 for Portland cement (Respirable fraction):

a) 8-hour TWA:

1) ppm:

a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

2) mg/m3: 5

a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

3) Ceiling Value:
4) Skin Designation: No
5) Notation(s): Not Listed

Pharmacology Toxicology

Toxicologic Mechanism

A)

1) the gritty nature of the product
2) allergic dermatitis to chromate contaminants
3) alkaline burns (Skiendzielewski, 1980)

B)

C)

Physicochemical

Physical Characteristics

A)

Ph

A)

Molecular Weight

A)

Animal Toxicology

References

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CEMENT

Classification | Detailed evidence-based information

Therapeutic Toxic Class

Specific Substances

Available Forms Sources

Life Support

Clinical Effects

Laboratory Monitoring

Treatment Overview

Range Of Toxicity

Summary Of Exposure

Heent

Respiratory

Gastrointestinal

Dermatologic

Carcinogenicity

Monitoring Parameters Levels

Radiographic Studies

Methods

Life Support

Patient Disposition

Monitoring

Oral Exposure

Inhalation Exposure

Eye Exposure

Dermal Exposure

Case Reports

Summary

Maximum Tolerated Exposure

Workplace Standards

Toxicologic Mechanism

Physical Characteristics

Ph

Molecular Weight

General Bibliography