EOH 4301

INDUSTRIAL &
ENVIRONMENTAL TOXICOLOGY

Prepared By:
Wan Noorhidayat bt Wan Jusoh
141931
Nur 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 metalloid arsenic
As3+ such as arsenites
As5+ such as arsenates
As3- such as arsine gas
Examples of organic (CH3)2AsO(OH) cacodylic acid (dimethylarsinic acid)
arsenicals CH3AsO(ONa)2 disodium methylarsenate (DSMA)
C7H9AsN2O4 carbasone
Examples of inorganic H3AsO4 arsenic acid
arsenicals Na2HAsO4 disodium arsenate
NaAsO2 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.

A rock containing an
extremely high amount of

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.

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.

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
The Risk Assessment Information System: Toxicity Summary for Arsenic
http://rais.ornl.gov/tox/profiles/arsenic.shtml
ii) Case Studies in Environmental Medicine (CSEM): Arsenic Toxicity Physiologic
Effects http://www.atsdr.cdc.gov/csem/arsenic/physiologic_effects.html
 iii) Chronic Toxicity Summary: Arsenic And Arsenic Compounds
http://www.oehha.ca.gov/air/chronic_rels/pdf/arsenics.pdf
iv) Arsenic Toxicity http://www.manbir-online.com/diseases/arsenic.htm
v) Arsenic toxicity http://pages.swcp.com/~tanman/ho/ArsenicToxicity.txt
vi) Toxicity arsenic http://emedicine.medscape.com/article/812953-overview
vii) Evidence On Developmental And Reproductive Toxicity Of Inorganic Arsenic
http://www.oehha.ca.gov/Prop65/pdf/AS-HID.pdf
viii) Case Studies in Environmental Medicine (CSEM): Arsenic Toxicity Clinical
Evaluation: History and Physical Evaluation
http://www.atsdr.cdc.gov/csem/arsenic/clinical_evaluation.html
ix) Safety and Health Topics: Arsenic
http://www.osha.gov/SLTC/arsenic/index.html
x) Arsenic toxicity http://www.knowledgebank.irri.org/wheat/factsheets/arsenic
%20toxicity.pdf