ARSENIC_full report_APAD & DAYAT

EOH 4301INDUSTRIAL &

ENVIRONMENTAL TOXICOLOGY

Prepared By:Wan Noorhidayat bt Wan Jusoh

141931Nur Fadhilah binti Rosli

141466

Lecturer:Associate Prof. Dr. Mohd Yusoff Adon

Bachelor of Science Environmental & Occupational Health

1.0 Introduction

Arsenic is an element that is widely distributed in the earth’s crust. The elemental

arsenic is known ordinarily a steel grey metal which usually found in the environment

combined with other elements. The arsenic which combined with elements such as oxygen,

chlorine, and sulfur called inorganic arsenic while the other arsenic which combined with

carbon and hydrogen is referred to as organic arsenic.

Arsenic in the organic forms is usually less harmful than the inorganic forms. Most of

inorganic and organic arsenic compounds are white or colorless powders that do not

evaporate. They have no smell, and most have no special taste. Thus, it is usually

undetectable if present in food, water, or air. Arsine is a gas consisting of arsenic and

hydrogen. It is known that can extremely toxic to humans. Although EPA has not classify

arsine for carcinogenicity but the arsenic itself widely known as the carcinogenic agents.

Form Chemical Formula Name

Common valence states As0

As3+

As5+

As3-

metalloid arsenic

such as arsenites

such as arsenates

such as arsine gas

Examples of organic arsenicals

(CH3)2AsO(OH)

CH3AsO(ONa)2

C7H9AsN2O4

cacodylic acid (dimethylarsinic acid)

disodium methylarsenate (DSMA)

carbasone

Examples of inorganic arsenicals

H3AsO4

Na2HAsO4

NaAsO2

arsenic acid

disodium arsenate

sodium arsenite

Inorganic arsenic exists in four main chemical forms known as valency or oxidation

states. Valency is a measure of the ability of a compound to combine with other elements,

such as hydrogen. The dominant forms are arsenite, with a valency of 3, and arsenate, with a

valency of 5. The element arsenic itself is not soluble in water. Arsenic in combination with

other elements (as salts) has a wide range of solubilities depending on the surrounding acidity

and the presence of other chemicals.

Arsenic can be found naturally on earth in small concentrations. It occurs in soil and

minerals and it may enter air, water and land through wind-blown dust and water run-off.

Arsenic in the atmosphere comes from various sources: vulcanoes release about 3000 tonnes

per year and microorganisms release volatile methylarsines to the extent of 20.000 tonnes per

year, but human activity is responsible for much more: 80.000 tonnes of arsenic per year are

released by the burning of fossil fuels. Despite its notoriety as a deadly poison, arsenic is an

essential trace element for some animals, and maybe even for humans, although the necessary

intake may be as low as 0.01 mg/day.

Arsenic is a component that is extremely hard to convert to water-soluble or volatile

products. The fact that arsenic is naturally a fairly a mobile component, basically means that

large concentrations are not likely to appear on one specific site. This is a good thing, but the

negative site to it is that arsenic pollution becomes a wider issue because it easily spreads.

Arsenic cannot be mobilized easily when it is immobile. Due to human activities, mainly

through mining and smelting, naturally immobile arsenics have also mobilized and can now

be found on many more places than where they existed naturally. 

2.0 Physical and chemical properties

Arsenic is a chemical element that has the symbol As and atomic number 33. Its

Atomic Mass is 74.92. Arsenic appears in Group 15 (V) of the periodic table, below nitrogen

and phosphorus. Its Ionic Charge is (3-). Its position in the periodic table is shown at right.

Arsenic appears in three allotropic forms: yellow, black and grey; the stable form is a silver-

gray, brittle crystalline solid. Arsenic is classified chemically as a metalloid, having both

properties of a metal and a nonmetal; however, it is frequently referred to as a metal.

A rock containing an extremely high amount of arsenic.

The melting point for arsenic is 817 °C and the boiling point for arsenic is 614°C.

Elemental arsenic, which is also referred to as metallic arsenic, (As(0)) normally occurs as

the α-crystalline metallic form, which is a steel gray and brittle solid. The β-form is a dark

gray amorphous solid. Other allotropic forms of arsenic may also exist. In compounds,

arsenic typically exists in one of three oxidation states, -3, +3, and +5. Arsenic compounds

can be categorized as inorganic, compounds without an arsenic-carbon bond, and organic,

compounds with an arsenic-carbon bond. The metallic form is brittle, tarnishes and when

heated it rapidly oxidizes to arsenic trioxide, which has a garlic odor. The non metallic form

is less reactive but will dissolve when heated with strong oxidizing acids and alkalis. Arsenic

and its compounds are poisonous.

Arsenic and its compounds occur in crystalline, powder, amorphous or vitreous forms.

They usually occur in trace quantities in all rock, soil, water and air. However, concentrations

may be higher in certain areas as a result of weathering and anthropogenic activities including

metal mining and smelting, fossil fuel combustion and pesticide use. There are many arsenic

compounds of environmental importance. Inorganic compounds include the trivalent arsenic

trioxide, arsenic trichloride, arsenic trisulphide and sodium arsenite. Pentavalent ones include

arsenic pentoxide, arsenic acid and sodium arsenate. Representative organic compounds are

monomethyl-, dimethyl- and trimethylarsine, and arsenobetaine.

3.0 Occupational Industrial Usage

Occupational exposures to arsenic can be encountered in smelting and also in the

manufacture of various pesticides, glass, paints, pigments, and wood preservatives. A more

recently developed use of gallium arsenide occurs in various types of electronics

manufacturing, including use as a semiconductor and infrared detector.

Main occupational exposures as summarized are the following:

i. Workers (mainly roaster workers) engaged in the smelting industries: copper, gold,

lead, silver and zinc ores, where arsenic is present as a contaminant or by-product of

ores containing lead, gold, zinc, cobalt, and nickel.

ii. Workers engaged in the manufacturing of pesticides, herbicides and other agricultural

products using arsenic preparations and industrial or agricultural workers using them.

iii. Arsenic in wood processing plants.

iv. Arsenic as desiccant or defoliant for the preparation of cotton fields for harvesting.

v. Various metallurgical or industrial activities like the electrolysis of copper, or

cadmium, with arsenic as a contaminant.

vi. Arsine is used in the microelectronics industry and in semiconductor manufacture.

4.0 Classification

5.0 Occupational Exposure Limit (TLV/PEL)

The current Occupational Safety and Health Administration (OSHA) permissible

exposure limit (PEL) for inorganic arsenic (except arsine) is 0.01 miligrams of arsenic per

cubic meter of air (mg/m³) as a time-weighted average (TWA) over an 8-hour work shift. The

National Institute for Occupational Safety and Health (NIOSH) recommends that arsenic and

all its inorganic compounds be controlled and handled as potential human carcinogens in the

workplace and that exposure be minimized to the lowest feasible limit. The NIOSH

recommended exposure limit (REL) for arsenic and all its inorganic compounds is 0.002

mg/m³ as a ceiling concentration determined in any 15-minute sampling period. The

American Conference of Governmental Industrial Hygienist (ACGIH) threshold limit value

(TLV) for soluble arsenic compounds is 0.2 mg/m³ as a TWA for a normal 8-hour workday

and a 40-hour workweek.

6.0 Health Effects

The symptoms of the adverse health effects can be divided up into the acute health

effects and the chronic effects. Acute health effects are characterized by sudden and severe

exposure and rapid absorption of the substance. Normally, a single large exposure is

involved. Acute health effects are often reversible.

Chronic health effects are characterized by prolonged or repeated exposures over

many days, months or years. Symptoms may not be immediately apparent. Chronic health

effects are often irreversible.

Health Effect characteristics of Arsenic:

Toxic by ingestion, inhalation and skin absorption

Corrosive

Short-term inhalation may cause cough, sore throat, breathlessness and wheezing

Short-term ingestion causes sickness, diarrhea and abdominal pain

Inorganic arsenic is irritant to the eye and skin

Following long-term ingestion the lungs, nervous system, liver, kidneys or stomach

may be affected

Long-term inhalation may cause inflammation of the eyes and nose

Inorganic arsenic compounds have mutagenic potential and human carcinogen

6.1 Acute Health Effects

Symptoms of acute arsenic poisoning may develop minutes to hours after ingestion

and consists of nausea, vomiting, abdominal pain, and copious blood-tinged diarrhea. Cold,

clammy skin, muscle cramps, and facial edema may be present. Seizures, coma and

circulatory collapse precede death. A dose of 120 mg arsenic trioxide may be fatal. Liver

enlargement and oliguria also may occur.

Persons who recover may develop delayed peripheral neuropathy, presenting after

several weeks as symmetric distal sensory loss. The lower extremities usually are more

affected than the upper. Motor involvement extending to total paralysis also may occur.

Acute exposure to arsine results in intravascular hemolysis. Other complaints include

headache, nausea, and chest tightness. Exposure to 10 ppm rapidly causes delirium, coma,

and death. The triad of abdominal pain, jaundice, and oliguria should strongly suggest arsine

exposure. Physical examination may reveal bronzing of the skin and hepatosplenomegaly.

The acute health effects differ according to the target organs and routes of exposure of

the compound.

a) Ingestion

Ingestion of large doses of arsenic may lead to acute symptoms within 30-60 min;

effects may be delayed when the arsenic is taken with food. An acute gastrointestinal

syndrome is the most common presentation of acute arsenic poisoning characterised by a

metallic or garlic-like taste associated with dry mouth, burning lips and dysphagia. Violent

vomiting may ensue and may eventually lead to haematemesis. Central Nervous System

findings may include headaches, weakness and delirium. Gastrointestinal symptoms caused

by paralysis of the capillary control in the intestinal tract may include profuse watery diarrhea

and may lead to a decrease in blood volume, lowered blood pressure and electrolyte

imbalance. Thus, after the initial gastrointestinal problems, rhabdomyolysis and multi-organ

failure may occur, including renal failure, respiratory failure, failure of vital cardiovascular

and brain functions, and death.

b) Inhalation

In inhalation route (respiratory tract) Arsenic compounds are irritant to the upper

airways. Features include cough, sore throat, breathlessness, wheeze, pulmonary oedema and

respiratory failure. Features of systemic toxicity may also occur.

c) Dermal/Ocular Exposure

For dermal exposure, Arsenic compounds such as trivalent arsenic compounds are

well absorbed through the skin and may lead to features of systemic toxicity. Arsenic trioxide

is irritant to the skin and mucous membranes. In ocular exposure, pain, lacrimation,

blepharospasm, conjunctivitis and corneal damage may occur after exposure to dusts or

vapours containing inorganic arsenic.

6.2 Chronic Health Effects

Chronic arsenic (As) poisoning has become a worldwide public health issue. Most

human arsenic exposure occurs from consumption of drinking water containing high amounts

of inorganic Arsenic. Signs of chronic toxicity may be difficult to diagnose: a number of

body systems may be affected and to different extents.

Signs of chronic arsenicalism, including pigmentation and development of keratoses,

peripheral neuropathy, skin cancer, peripheral vascular disease, hypertensive heart disease,

cancers of internal organs (bladder, kidney, liver, and lung), and alterations in gastrointestinal

function (non-cirrhotic hypertension). Dermal lesions, such as hyperpigmentation

(Melanosis), warts, and hyperkeratosis (thickening of the skin) of the palms and soles, are the

most commonly observed symptoms.

System or Organ Effect

Respiratory Tract Inflammation and tracheobronchitis

Dermal Hyperkeratosis, hypigmentation (Melanosis), skin cancer

Vascular Peripheral vascular disease; ("Blackfoot disease"), myocardial injury

Haematological Bone marrow depression (resulting in leucopenia and anaemia)

Neurological Peripheral neuropathy, encephalopathy

Reproductive Spontaneous abortion, congenital malformation

Liver Hepatomegaly, cirrhosis, angiosarcoma, altered haem metabolism

Kidneys Proximal tubule degeneration, papillary and cortical necrosis

Gastrointestinal Diarrhoea, vomiting

Summary of Arsenic Chronic Effects

a) Gastrointestinal, Hepatic, and Renal Effects

Gastrointestinal effects are seen primarily after arsenic ingestion, and less often after

inhalation or dermal absorption.

The gastrointestinal (GI) effects of arsenic generally result from exposure via

ingestion; however, GI effects may also occur after heavy exposure by other routes. The

fundamental GI lesion appears to be increased permeability of the small blood vessels,

leading to fluid loss and hypotension. Extensive inflammation and necrosis of the mucosa and

submucosa of the stomach and intestine may occur and progress to perforation of the gut

wall. A hemorrhagic gastroenteritis may develop, with bloody diarrhea as a presenting

symptom.

Chronic arsenic ingestion may lead to cirrhotic portal hypertension. Case reports have

also linked chronic high-level arsenic exposure with hepatic angiosarcoma, a rare form of

cancer.

Arsenic is capable of causing chronic renal insufficiency from cortical necrosis has

also been reported. The actual cause of injury may be hypotensive shock, hemoglobinuric or

myoglobinuric tubular injury, or direct effects of arsenic on tubule cells. Glomerular damage

can result in proteinuria. The kidney is not a major target organ for chronic toxicity.

b) Cardiovascular Effects

Long-term ingestion of arsenic in drinking water has resulted in pronounced

peripheral vascular changes. Epidemiological evidence indicates that chronic arsenic

exposure is associated with vasospasm and peripheral vascular insufficiency. Gangrene of the

extremities, known as Blackfoot disease, has been associated with drinking arsenic-

contaminated well water in Taiwan, where the prevalence of the disease increased with

increasing age and well-water arsenic concentration (10 to 1,820 ppb). Persons with

Blackfoot disease also had a higher incidence of arsenic-induced skin cancers. However,

investigators believe other vasoactive substances found in the water may have been

contributory.

Raynaud's phenomenon and acrocyanosis resulted from contamination of the city's

drinking water supply in Antofagasta, Chile, at arsenic concentrations ranging from 20 to 400

ppb. Autopsies of Antofagasta children who died of arsenic toxicity revealed fibrous

thickening of small and medium arteries and myocardial hypertrophy. Similar vascular

disorders, as well as abnormal electrocardiographs (ECGs), have been noted in vineyard

workers exposed to arsenical pesticides.

c) Neurologic Effects

Arsenic-exposed patients develop destruction of axonal cylinders, leading to

peripheral neuropathy. Peripheral neuropathy is a common complication of arsenic poisoning.

The classic finding is a peripheral neuropathy involving sensory and motor nerves in a

symmetrical, stocking-glove distribution. Sensory effects, particularly painful dysesthesia,

occur earlier and may predominate in moderate poisoning, whereas ascending weakness and

paralysis may predominate in more severe poisoning. Encephalopathy has been reported after

both acute and chronic exposures.

Onset may begin within 24 to 72 hours following acute poisoning, but it more often

develops slowly as a result of chronic exposure. The neuropathy is primarily due to

destruction of axonal cylinders (axonopathy). Nerve conduction and electromyography

studies can document severity and progression. Subclinical neuropathy, defined by the

presence of abnormal nerve conduction with no clinical complaints or symptoms, has been

described in chronically exposed individuals.

Recovery from neuropathy induced by chronic exposure to arsenic compounds is

generally slow, sometimes taking years, and complete recovery may not occur. Follow-up

studies of Japanese children who chronically consumed arsenic-contaminated milk revealed

an increased incidence of severe hearing loss, mental retardation, epilepsy, and other brain

damage. Hearing loss as a sequela of acute or chronic arsenic intoxication has not been

confirmed by other case reports or epidemiologic studies.

d) Dermal Effects

Pigment changes and palmoplantar hyperkeratosis are characteristic of chronic arsenic

exposure and benign arsenical keratoses may progress to malignancy. The types of skin

lesions occurring most frequently in arsenic-exposed humans are hyperpigmentation,

hyperkeratosis, and skin cancer. Patchy hyperpigmentation, a pathologic hallmark of chronic

exposure, may be found anywhere on the body, but occurs particularly on the eyelids,

temples, axillae, neck, nipples, and groin. The classic appearance of the dark brown patches

with scattered pale spots is sometimes described as "raindrops on a dusty road." In severe

cases, the pigmentation extends broadly over the chest, back, and abdomen. Pigment changes

have been observed in populations chronically consuming drinking water containing 400 ppb

or more arsenic.

Arsenical hyperkeratosis occurs most frequently on the palms and soles. Keratoses

usually appear as small corn-like elevations, 0.4 to 1 cm in diameter. In most cases, arsenical

keratoses show little cellular atypia and may remain morphologically benign for decades. In

other cases, cells develop marked atypia (precancerous) and appear indistinguishable from

Bowen disease, which is an in situ squamous cell carcinoma discussed in Carcinogenic

Effects.

e) Respiratory Effects

Inhalation of high concentrations of arsenic compounds produces irritation of the

respiratory mucosa. Smelter workers experiencing prolonged exposures to high

concentrations of airborne arsenic at levels rarely found today had inflammatory and erosive

lesions of the respiratory mucosa, including nasal septum perforation. Lung cancer has been

associated with chronic arsenic exposure in smelter workers and pesticide workers.

f) Hematopoietic Effects

Bone marrow depression may result from acute or chronic arsenic intoxication.

Anemia and leukopenia are common in chronic arsenic toxicity, and are often accompanied

by thrombocytopenia and mild eosinophilia. The anemia may be normocytic or macrocytic,

and basophilic stippling may be noted on peripheral blood smears.

g) Reproductive Effects

Increased frequency of spontaneous abortions and congenital malformations has been

linked to arsenic exposure. Arsenic is a reproductive toxicant and a teratogen. It is readily

transferred across the placenta, and concentrations in human cord blood are similar to those

in maternal blood. A study of women working at or living near a copper smelter where

ambient arsenic levels were elevated reported increased frequencies of spontaneous abortions

and congenital malformations. The frequency of all malformations was twice the expected

rate and the frequency of multiple malformations was increased fivefold. However, a number

of other chemicals, including lead, cadmium, and sulfur dioxide were also present, and thus it

is difficult to assess the role of arsenic in the etiology of these effects.

h) Carcinogenic Effects

IARC have classified inorganic arsenic as a known human carcinogen. Chronic

inhalation of inorganic arsenic can cause cancer in humans. A number of studies have shown

good correlations between occupational exposure to arsenic and cancer in workers in such

environments as copper smelting plants. In one study, an almost ten-fold increase in the

incidence of lung cancer was found in workers most heavily exposed to arsenic. Smelter

workers are however, exposed to other factors in the working environment, some of which

may be carcinogenic. An attempt was made to control for exposure to sulphur dioxide,

copper, lead, nickel, selenium, antimony and bismuth in one case-control study, and the

excess lung cancer remained. Smoking habits have also been considered in two studies and

could not account for the excess of lung cancer noted. With regard to histological type of

lung cancer, a significant, relative excess of adenocarcinomas and a slight excess of oat-cell

cancers were seen among smelter workers.

Long-term ingestion of drinking water contaminated with inorganic arsenic has been causally

linked to an increased risk of a number of other cancers [1]. However, in the most recent

IARC review in 2004 there was considered to be sufficient evidence in humans that arsenic in

drinking-water causes cancers of the urinary bladder, lung and skin only.

i) Skin Cancer

Latency for skin cancer associated with ingestion of arsenic may be 3 to 4 decades,

whereas the noncarcinogenic skin effects typically develop several years after exposure. An

increased risk of skin cancer in humans is associated with chronic exposure to inorganic

arsenic in medication, contaminated water, and the workplace. Arsenic-induced skin cancer is

frequently characterized by lesions over the entire body, mostly in unexposed areas such as

the trunk, palms, and soles. More than one type of skin cancer may occur in a patient. Most of

the Taiwanese who developed skin cancer in association with ingestion of arsenic-

contaminated drinking water had multiple cancer types. The most commonly reported types,

in order of decreasing frequency, were intraepidermal carcinomas (Bowen disease),

squamous cell carcinomas, basal cell carcinomas, and "combined forms." Seventy-two

percent of the Taiwanese with skin cancer also had hyperkeratosis, and 90% had

hyperpigmentation.

Some hyperkeratinized lesions can develop into intraepidermal carcinoma, which may

ultimately become invasive. The lesions are sharply demarcated round or irregular plaques

that tend to enlarge; they may vary in size from 1 millimeter to >10 centimeters. Arsenical

basal cell carcinomas most often arise from normal tissue, are almost always multiple, and

frequently occur on the trunk. The superficial spreading lesions are red, scaly, atrophic, and

are often indistinguishable from Bowen disease by clinical examination. Arsenic-associated

squamous cell carcinomas are distinguished from UV-induced squamous cell carcinomas by

their tendency to occur on the extremities (especially palms and soles) and trunk rather than

on sun-exposed areas such as the head and neck. However, it may be difficult to distinguish

other arsenic-induced skin lesions from those induced by other causes.

j) Lung Cancer

In arsenic-exposed workers, there is a systematic gradient in lung cancer mortality

rates, depending on duration and intensity of exposure. An association between lung cancer

and occupational exposure to inorganic arsenic has been confirmed in several epidemiologic

studies. A higher risk of lung cancer was found among workers exposed predominantly to

arsenic trioxide in smelters and to pentavalent arsenical pesticides in other settings. Neither

concomitant exposure to sulfur dioxide nor cigarette smokes was determined to be essential

co-factors in these studies.

6.3 Summary of Health Effects

Single doses of inorganic arsenic may be highly toxic by ingestion and inhalation (70-

180 mg orally has been fatal). Trivalent arsenic is, in general, more toxic than pentavalent

arsenic.

Inorganic arsenic is a known human carcinogen which acts via a genotoxic

mechanism. It is assumed, therefore, that there is no threshold for such effects and that risk

management measures should ensure that exposures are as low as reasonably practical. There

is sufficient evidence that chronic exposure to inorganic arsenic in drinking water causes non-

melanoma skin cancers and an increased risk of bladder and lung cancers in humans.

The effects of inorganic arsenic on the vascular periphery are well documented. Long-

term ingestion of contaminated drinking water may lead to, Raynaud's phenomenon and

acrocyanosis and progression to endarteritis obliterans and gangrene of the lower extremities

("Black foot disease"). An increased incidence of cardiovascular disease has also been noted.

Haematologically, anaemia and leucopenia may occur together with disturbances in haem

synthesis.

Chronic exposure to inorganic arsenic compounds may lead to peripheral and central

neurotoxicity. Early events may include paresthesiae followed by muscle weakness. In the

periphery, both motor and sensory neurones are affected.

Characteristic dermal lesions after chronic oral or inhalation exposure may include

hyper pigmentation and hyperkeratosis.

Other toxic effects associated with chronic exposure to inorganic arsenic include liver

injury, cardiovascular disease and diabetes mellitus.

There is limited data from epidemiology to suggest that inorganic arsenic may be a

human developmental toxicant, but it is not possible to draw any definitive conclusions.

Administration of high doses of inorganic arsenic by oral, intraperitoneal or intravenous

routes may cause embryolethality or foetal malformations in laboratory animals.

Inorganic arsenic may cause irritation of the mucous membranes leading to

conjunctivitis and pharyngitis and rhinitis after inhalation. Skin irritation and allergic contact

dermatitis may occur after exposure to inorganic arsenic compounds.

7.0 Health Surveillance

Health surveillance can be divided into biological monitoring and medical

surveillance. Health surveillance means any examination and investigations which may be

necessary to detect exposure levels and early biological effects and responses, and includes

biological monitoring, biological effect monitoring, medical surveillance, enquires about

symptoms of occupational poisoning or occupational disease and review of records and

occupational history. Biological monitoring is a measurement and assessment of agents or

their metabolites either in tissues, secreta, excreta, expired air or any combination of these to

evaluate exposure and health risk compared to an appropriate reference. While medical

surveillance means the monitoring of a person for the purpose of identifying changes in

health status due to occupational exposure to chemicals hazardous to health.

7.1 Biological Monitoring

Arsenic levels in blood, urine, hair, and nails have all been investigated and used as

biological indicators of exposure to arsenic.

Most arsenic that is absorbed from the lungs or the gastrointestinal tract is excreted in

the urine, mainly within 1–2 days. For this reason, measurement of urinary arsenic levels is

generally accepted as the most reliable indicator of recent arsenic exposure, and this approach

has proved useful in identifying above-average exposures in populations living near industrial

point sources of arsenic (e.g., Milham and Strong 1974; Polissar et al. 1990). The best

specimen is a 24 hour urine collection. Normal total urinary arsenic values are <50 µg arsenic

per liter (As/L) in the absence of consumption of seafood in the past 48 hours; values in

excess of 200 µg As/L are considered abnormal (ATSDR 2000a). Person must not consume

any seafood for 1 or 2 days before sampling, this due to that the sea food have high

concentration of organoarsenicals, where if that person does so consume may affect the result

of the test.

Since arsenic is cleared from blood within a few hours (Tam et al. 1979b; Vahter

1983), measurements of blood arsenic reflect exposures only within the very recent past.

Blood test for arsenic level are less efficient compare to urine test, because arsenic in blood

more rapidly undergone the absorption process. Other than that, the test are measure the

arsenic level in whole blood volume where actual test must measure the arsenic level in red

blood cell only. Typical values in nonexposed individuals are <1 µg /L (Heydorn 1970;

Hindmarsh and McCurdy 1986; Valentine et al. 1979). Consumption of medicines containing

arsenic is associated with blood values of 100–250 µg /L, while blood levels in acutely toxic

and fatal cases may be 1,000 µg /L or higher (Driesback 1980).

Long after urine levels have returned to baseline, the arsenic content of hair and nails

may be the only clue of arsenic exposure. Arsenic tends to accumulate in hair and nails, and

measurement of arsenic levels in these tissues may be a useful indicator of past exposures.

Normal levels in hair and nails are 1 ppm or less (Choucair and Ajax 1988; Franzblau and

Lilis 1989). These values may increase from several-fold to over 100-fold following arsenic

exposure (Agahian et al. 1990; Bencko 2005; Bencko et al. 1986; de Peyster and Silvers

1995; EPA 1977a, 1981b; Karagas et al. 1996; Milham and Strong 1974; Valentine et al.

1979; Yamauchi et al. 1989) and remain elevated for 6–12 months (Choucair and Ajax 1988).

Minimum exposure levels that produce measurable increases in arsenic levels in hair and

nails have not been precisely defined. However, because the arsenic content of hair and nails

may be increased by external contamination, caution must be exercised in using the arsenic

content of these specimens to diagnose arsenic intoxication.

7.2 Medical Surveillance

Any occupational exposure to arsenic and its compounds > 50% PEL or possibility of

excessive absorption.

a) Pre-Placement Medical Examinations for Inorganic Arsenic:

Clinical examination & baseline data with particular emphasis on the:

Nervous system

Liver, liver function tests (Serum bilirubin, alkaline phosphatase, alanine and

aspartate transaminases and gamma-glutamyl transpeptidase)

Skin

Nasal septum, lungs and lymph nodes.

History of smoking, medicines taken, alcohol consumption, previous job.

Estimation of urinary arsenic content in an early morning urine specimen (with

creatinine correction). Ensure that worker avoids seafood for three days prior to urine

collection.

Fish and shellfish contain very large amounts of organically bound arsenic and these

are readily absorbed from the GIT and quickly excreted in the urine.

Full-sized chest x-ray examination (at pre-employment examination only).

b) Periodic Medical Examination for Inorganic Arsenic:

Done annually. Detect early skin changes, (hyperpigmentation and thickening).

Regular self-inspection of skin by workers is appropriate.

c) Pre-Placement Medical Examinations for Arsine:

Clinical examination & baseline data with particular emphasis on the:

Liver, liver function tests (Serum bilirubin, alkaline phosphatase, serum transaminases

e.g. SGOT, SGPT, gamma-glutamyl transpeptidase)

Renal -Urine dipstick examination for protein and blood.

Hematological systems - Hemoglobin estimation and peripheral blood film

examination to look for basophilic stippling.

To exclude workers with cardiac or renal disease and those with hypersensitivity to hemolytic

agents.

Estimation of urinary arsenic content in an early morning urine specimen (with

creatinine correction). Ensure that the worker avoids seafood for 3 days prior to urine

collection as it may contain arsenic.

d) Periodic Medical Examination for Arsine

Annually as for pre-employment.

Renal function tests.

8.0 Prevention And Control

In order to prevent and control the hazard from the arsenic, we can use hierarchy of control.

8.1 Hierarchy of Control

Firstly is the elimination step, which getting rid of any hazardous job, tool, process,

machine, or substance is perhaps the best way of protecting workers. For example, try to

eliminate anything that in the workplace that use arsenic so that the workers are not expose to

the arsenic.

Secondly, we also can use substitution which means replace hazardous chemical with

something less dangerous. For example, try to substitute the arsenic usage in the company

with other chemical that less hazardous or not hazardous at all, if possible.

Thirdly, we can use the engineering control. Engineering control means structural

changes to the environment or process to interrupt the path between the person and the

hazard. For example, modified or create work environment that decrease the level or risk to

get the arsenic hazardous effect. The other example such as the enclosure of work operations

and local exhaust so that the arsenic concentration in the workplace air is under level of

which may produce effect; 0.01 mg/m³ of air as a time-weighted average (TWA) over an 8-

hour work shift.

Fourthly is administrative control which includes changes in work procedures with

the goal of reducing the duration, frequency and severity of exposure to hazardous chemical.

For example, reductions in time spent in arsenic-exposed work areas and alternate work will

reduce the exposure to hazard.

The last step in hierarchy of control is by using personal protective equipment (PPE).

The employer must provide the PPE to their workers. Other than that, Employers are required

to train each employee who must use PPE. Employees must be trained to know when PPE is

necessary, what PPE is necessary, how to properly put on, take off, adjust and wear the PPE,

the limitations of the PPE, and know the proper care, maintenance, useful life and disposal of

PPE. The examples of PPE such as protective clothing, gloves, goggles, safety hoods to

protect the head and neck, shoe covers, as well as respirators.

9.0 References

[online: 04 April 2009]

i) Toxicological Profile for Arsenic: August 2007.

http://www.atsdr.cdc.gov/toxprofiles/tp2.pdf

ii) The Risk Assessment Information System: Toxicity Summary for Arsenic

http://rais.ornl.gov/tox/profiles/arsenic.shtml

iii) Case Studies in Environmental Medicine (CSEM): Arsenic Toxicity Physiologic

Effects http://www.atsdr.cdc.gov/csem/arsenic/physiologic_effects.html

iv) Chronic Toxicity Summary: Arsenic And Arsenic Compounds

http://www.oehha.ca.gov/air/chronic_rels/pdf/arsenics.pdf

v) Arsenic Toxicity http://www.manbir-online.com/diseases/arsenic.htm

vi) Arsenic toxicity http://pages.swcp.com/~tanman/ho/ArsenicToxicity.txt

vii) Toxicity arsenic http://emedicine.medscape.com/article/812953-overview

viii) Evidence On Developmental And Reproductive Toxicity Of Inorganic Arsenic

http://www.oehha.ca.gov/Prop65/pdf/AS-HID.pdf

ix) Case Studies in Environmental Medicine (CSEM): Arsenic Toxicity Clinical

Evaluation: History and Physical Evaluation

http://www.atsdr.cdc.gov/csem/arsenic/clinical_evaluation.html

x) Safety and Health Topics: Arsenic http://www.osha.gov/SLTC/arsenic/index.html

xi) Arsenic toxicity http://www.knowledgebank.irri.org/wheat/factsheets/arsenic

%20toxicity.pdf