review of hydrogen sulfide and sour gas effects on the eye - a historical perspective

7/29/2019 Review of hydrogen sulfide and sour gas effects on the eye - a historical perspective

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Review

Hydrogen sulfide (H2S) and sour gas effects on the eye.

A historical perspective

Timothy William Lamberta,, Verona Marie Goodwin b,Dennis Stefani a, Lisa Stroshera

a Environmental Health, Calgary Health Region, 1509 Centre St SW, Calgary Alberta, T2G 2E6, Canadab VM Goodwin Research and Consulting Ltd., Canada

Received 18 May 2005; received in revised form 19 December 2005; accepted 16 January 2006Available online 2 May 2006

Abstract

The toxicology of hydrogen sulfide (H2S) and sour gas on the eye has a long history beginning at least with Ramazzini's

observations [Ramazzini B. Diseases of WorkersDe Morbis Artificum Diatriba1713. Wright WC (trans). New York, C. Hafner

Publishing Co Inc.; 1964.9899 pp.]. In contrast, a recent review by Alberta Health andWellness (AHW Report) concluded that there

is little evidence of eye irritation following short-term exposures to H2S at concentrations up to 100ppm and that the H2S literature on

the eye is a series of unsubstantiated claims reproduced in review articles dating back to the 1930s [Alberta Health and Wellness

(AHW report). Health effects associated with short-term exposure to lowlevels of hydrogensulfide: a technical review, Alberta Health

and Wellness, October 2002, 81pp.]. In this paper, we evaluated this claim through a historical review of the toxicology of the eye.Ramazzini noted the effects of sewer gas on the eye [Ramazzini B. Diseases of Workers De Morbis Artificum Diatriba1713.

Wright WC (trans). New York, C. Hafner Publishing Co Inc. 1964.9899 pp.]. Lehmann experimentally showed eye effects in men at

7090ppmH2S and also in animals [Lehmann K. Experimentalle Studien uber den Einfluss technisch und hygienisch wichtiger Gase

und Dampfe auf den Organismus. Arch Hyg 1892;14:135189]. In 1923, Sayers, Mitchell and Yant reported eye effects in animals

and men at 50ppm H2S. Barthelemy showed eye effects in animals and men at 20ppm H2S [Barthelemy HL. Ten years' experience

with industrial hygiene in connection with the manufacture of viscose rayon. J Ind Hyg Toxicol 1939;21:14151]. Masure

experimentally showed that H2S is the causative agent of eye impacts in animals and men [Masure R. La Keratoconjunctivite des

filatures de viscose; etude clinique and experiementale. Rev Belge Pathol 1950;20:297341]. Michal upon microscopic examination

of the rat's cornea, found nuclear pyknosis, edema andseparation of cells in the eye following exposures for 3h at 36ppm H2S [Michal

FV. Eye lesions caused by hydrogen sulfide. Cesk Ophthalmol 1950;6;58]. In 1975, in Alberta, irreversible eye damage and

photophobia were experimentally produced in calves exposed to 20ppm H2S for 1week [Nordstrom GA. A study of calf response of

ammonia and hydrogen sulfide gases. Thesis, University of Alberta, Department of Agricultural Engineering, Edmonton Alberta;

1975, 218 pp.]. Alberta Environmental Centre documented clinical irritation of the eye at 40ppm H 2S in 6 hours in rats [Alberta

Environmental Centre. Morphological observations in rats exposed for six hours to an atmosphere of 0, 56, or 420mg/m 3 hydrogen

sulfide. AECV86-A1. Alberta Environmental Centre, Vegreville, Alberta; 1986b. 28 pp.]. In two sour gas blow-outs in Alberta, in the

early 1980s, eye injury was documented in humans and animals at 0.5 ppm H2S. Community studies in the United States, Europe and

New Zealand suggest that acute exposure to 25ppb H2S is the lowest concentration to irritate the eyes; with chronic exposure, serious

eye effects are suggested. In contrast to the conclusion, all of the studies, except one, cited in the AHW Report indicate toxic effects on

the eye below 100ppm H2S [Alberta Health and Wellness (AHW report). Health effects associated with short-term exposure to low

Science of the Total Environment 367 (2006) 1 22

www.elsevier.com/locate/scitotenv

Corresponding author. Tel.: +1 403 943 8048; fax: +1 403 943 8056.

E-mail address: [email protected] (T.W. Lambert).

0048-9697/$ - see front matter 2006 Elsevier B.V. All rights reserved.doi:10.1016/j.scitotenv.2006.01.034


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levels of hydrogensulfide (H2S): a technical review, Alberta Health andWellness, October 2002, 81pp.]. In addition, theAHW Report

(2002) mis-presented two studies as clinical studies, claiming they reported no evidence of eye effects in humans from 2 and 30 ppm

H2S for 3040 minutes [Alberta Health and Wellness (AHW report). Health effects associated with short-term exposure to low levels

of hydrogen sulfide (H2S): a technical review, Alberta Health and Wellness, October 2002, 81pp.].

2006 Elsevier B.V. All rights reserved.

Keywords: Hydrogen sulfide; H2S; Sour gas; Eye; Conjunctivitis; Historical review; Mechanism

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

2. Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

3. An historical perspective of hydrogen sulfide and the eye . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

3.1. Lehmann (1892) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

3.2. U.S. Bureau of Mines: Sayers et al. (1923), Mitchell and Davenport (1924), Mitchell and Yant (1925),

Aves et al. (1929) and Yant (1930) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

3.3. Sjorgen (1939) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73.4. Viscose rayon spinning rooms: Kranenburg and Kessener (1925), Lewey (1938), McDonald (1938),

Barthelemy (1939), Rubin and Arieff (1945), Masure (1950), Nyman (1954), Nesswetha (1969) and Vanhoorne

et al. (1995) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

3.5. Occupational, experimental and community exposures: Michal (1950), Ahlborg (1950), Carson (1963),

Beasley (1963), US Department of Public Health Service, Terre Haute (1964), Luck and Baye (1989) and

Schiffman et al. (2005). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

3.6. Chronology of Alberta studies: Nordstrom (1975), Burnett et al. (1977), Lodgepole Blowout Report (1984),

Drummond Blow-Out (Alberta Environmental Centre, 1984), Arnold et al. (1985), Alberta Environmental

Centre (1986a,b) and Lefebvre et al. (1991) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

3.7. South Karelia air pollution studies: Haahtela et al. (1992) and Marttila et al. (1994, 1995) . . . . . . . . . . . 14

3.8. Community study in Rotorua: Bates et al. (1998, 2002). . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

4. Critique of Alberta Health and Wellness Report (2002) of H2S . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

4.1. Comparison of AHW Report (2002) review of H2S effects on the eye with other major reviews . . . . . . . . . . 15

4.2. Review of the scientific studies to support AHW Report (2002) conclusion that there is bvery little evidence

of eye irritation following short-term exposures to H2S at concentrations up to 100ppmQ. . . . . . . . . . . . 17

4.2.1. Non-clinical studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

4.2.2. Clinical studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

4.2.3. Case-control and observational studies from sour gas releases . . . . . . . . . . . . . . . . . . . . . 18

4.3. AHW Report (2002) critique of Alberta Health (1988) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

5. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

1. Introduction

Public and occupational exposure to hydrogen sulfide

(H2S) can result from many industries, including petroche-

mical, agricultural and wastewater treatment. Eye irritation

from hydrogen sulfide has been described as the first health

effect to manifest at low concentrations. Ramazzini (1713)

made an articulate observation of the effect of privy gas

on the eyes in his book the Diseases of Workers:

I pitied him at that filthy work and asked himwhy he was working so strenuously and why he

did not take it more quietly so as to avoid the fatigue

that follows overexertion. The poor wretch lifted his

eyes from the cavern and gazed at me, and said: No

one who has not tried it can imagine what it costs to

stay more than four hours in this place; it is the same

thing as being struck blind.

Later when he had come up from the cesspit, I

examined his eyes carefully and observed that they

were extremely bloodshot and dim. I asked whether

cleaners of privies regularly used any particularremedy for this trouble.

2 T.W. Lambert et al. / Science of the Total Environment 367 (2006) 122


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Only this he replied, they go back at once to their

homes as I shall do presently, shut themselves in a

dark room, stay there for a day and bathe their eyes

now and then with lukewarm water; by this means

they are able to relieve the pain somewhat.

Then I asked him: Had they a burning sensation in

the throat or any respiratory troubles or attacks of

headache? Did that stench hurt their nostrils or cause

nausea?

Nothing of that sort he replied, in this work our

eyes only are injured and no other part. If I

consented to go on with it any longer I should very

soon become blind as has happened to others.

Thereupon he wished me good-day and went home,keeping his hands over his eyes

I am inclined to think that some volatile acid is given

off by this camerine of filth when they disturb it, and

what makes this probable is the fact that copper and

silver coins carried by these scavengers in their

purses turn black. (Ramazzini, 1713, pp. 9899)

Ramazzini did not have knowledge of H2S. Howev-

er, Ramazzini presumed the release of a molecule from

the tarnishing of the silver coins; this observation

formed the basis of technical measurements of H2S wellinto this century. At the concentration of the gas

experienced, only the eyes were afflicted. Furthermore,

the observation detailed that, with increasing time, the

severity of the effect increased, such that a 4-h exposure

was the maximum someone could endure and that

continued exposure risked blindness. Ramazzini ob-

served the characteristic signs described today from H2S

exposure: conjunctivitis, photophobia and, in the

extreme, loss of vision.

Ramazzini's account is consistent with that presented

by Grant (1974) in his book on the toxicology of the eye:

Effects of hydrogen sulfide on the eyes are notable

only at sublethal concentrations, most commonly at

concentrations so low that they have no discernable

systemic effect. At least 120 articles have been

published describing the highly characteristic super-

ficial injury of the cornea and conjunctiva occurring

in workmen exposed to low concentrations of

hydrogen sulfide in sewers, caissons, tunnels, sugar

beet refineries, rayon and artificial silk manufacture,

sulfur baths, refining of sulfur containing petroleum,tanneries and sulfur mining. (Grant, 1974, p. 561)

In contrast to the observations of Ramazzini (1713)

and Grant (1974), a recent Alberta Health and Wellness

Surveillance Branch (AHW Report) (2002) claimed

that:

There is very little evidence of eye irritationfollowing short-term exposures to H2S at concentra-

tions up to 100ppm. This is in sharp contrast to the

earlier report (Alberta Health, 1988), wherein it was

concluded that the eye is susceptible to the irritant

action of H2S and irreversible eye tissue damage can

occur at 20ppm H2S. This discrepancy may be

explained in part by reliance placed on review

articles in the earlier assessment. It would appear

that the earlier conclusions relied heavily on

statements made by Milby (1962) and Gosselin et

al. (1976) attesting to irreversible eye tissue damageat concentrations > 20ppm for several hours ex-

posure. Neither statement represents original re-

search. Instead the following statement by Milby

cites Yant (1930), exposure to concentrations above

50ppm for a period exceeding 1 hour may produce

irritation of the conjunctival and corneal tissues.

The statement does not suggest irreversible eye

damage, nor does it make reference to effects at

20ppm. Moreover the report by Yant also does not

represent original research. Alberta Health (1988)

also reported blurred vision at 0.08 ppm (Kleinfeld

et al., 1964); however, this exposure concentrationwas not stated in the cited document. Thus it appears

that unsubstantiated opinions have been propagated

through several review articles, dating as far back as

1930. (AHW Report, 2002, p. 58)

The first part of this paper presents a historical review

of the literature and the latter half a critique of the AHW

Report (2002) claims. This historical review addresses

the question of the likelihood that the eye will respond to

H2S at concentrations below 100ppm H2S. The review

develops the observations of Ramazzini, providingdetails of the signs of exposure, the different environ-

ments in which they have been experienced and the

specific levels of H2S.

2. Methods

Toxline and Pubmed databases were searched for all

papers relating to H2S. All papers cited in review articles

were obtained including English and other languages. The

review focuses primarily on English papers published in

the last 100 years and emphasizes the key findings on thetoxicological effects on the eye. Three key papers in non-

3T.W. Lambert et al. / Science of the Total Environment 367 (2006) 1 22


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English were translated into English: Lehmann (1892),

Masure (1950) and Michal (1950). There are a large

number of studies in non-English which were not

translated due to financial limitations. The specific details

of each paper are presented such that the reader can

understand the scientific quality of the particular study.We obtained and compared all of the literature cited

in the AHW Report (2002). We also compared the AHW

Report (2002) citations with NIOSH (1977), Alberta

Health (1988) and WHO (2003), to illustrate the

citations which the AHW Report (2002) is relying on

for its conclusions.

In contrast to the AHW Report (2002) method, our

approach to the historical perspective was not to simply

select the best scientific papers. We did not simply

collect the harmonious statements to suggest the defin-

itive perspective

on H2S effects on the eye. Our approachhas been to present the papers such that a reader can

appreciate the divergence, consistency and coherence of

the perspectives and observations of H2S eye toxicity.

3. An historical perspective of hydrogen sulfide and

the eye

Mitchell and Davenport (1924) reviewed much of the

early literature from 1773 to 1924. Most of the early

reports were conducted in France and they note the

following in their paper with respect to the eye. In 1785,

Halle identified two toxicological observations in sewerworkers: a condition called mitte, inflammation of the

eyes and mucous membranes, and plomb, a type of

asphyxia. In 1832, Christison observed that these two

types of toxicological effects were due to H2S and that

the eye effects were related to sub-acute exposures. In

1911, Oliver reported numerous cases of conjunctivitis

in the workmen in the sulfur mines of Sicily.

3.1. Lehmann (1892)

One of the earliest experimental studies is that ofLehmann (1892), who conducted a series of acute

chamber study exposures on men and animals. Lehmann

(1892) conducted experiments on six men at a range of

H2S concentrations; observations of eye effects that he

tabulated are presented in Table 1.

Lehmann described eye effects of one subject and

himself: Kwilecki's (subject) observation of mucous

membrane irritation symptoms both before and after the

onset of headache is notable. I also noted the onset of a

most pronounced and painful irritation of the nasal and

eye mucous membranes, even before any sign ofheadache. Lehmann noted thatno significant observa-

tions were noted for any of the animals that Kwilecki

regularly took into the test chamber with him.

Lehmann had difficulty with measurement of the H2S

concentrations and observed his method tended to over-

predict the concentrations. After adjusting his experi-

mental apparatus to improve H2S measurement, Leh-mann noted the following from exposure of two

additional subjects: The trial results indicated that a

H2S concentration of 0.020.04 per thousand [20

40ppm H2S] over a 1-h exposure period did not yet

induce any symptoms of irritation. A concentration of

0.070.09 parts per thousand [7090ppm H2S] induced

a mild biting sensation in the throat and eyes. Similarly,

0.140.15 per thousand [140150ppm H2S] and 0.12

0.13 parts per thousand [120130ppm H2S ] i n a

different trial also caused uncomfortable, pronounced

and immediate biting sensation in the eyes and throat

.One observation which Lehmann reported in many

trials was the sudden decrease in eye pain during the

exposure (Table 1); this suggests development of nerve

effects very similar to olfactory fatigue described from

H2S exposure. Even with only a few test subjects, Leh-

mann reported different sensitivity in the men to the

effects of H2S and varying health effects aside from the

eye. In summary, Lehmann noted that all test subjects

showed symptoms of intense irritation targeting the eyes,

nose, and tracheal mucous membranes. Lehmann ob-

served similar effects in animal experiments, and claims

his results were in agreement with Eulenberg (1865).

3.2. U.S. Bureau of Mines: Sayers et al. (1923),

Mitchell and Davenport (1924), Mitchell and Yant

(1925), Aves et al. (1929) and Yant (1930)

A series of papers were produced by the Bureau of

Mines in the United States on health effects from H2S in

the petroleum industry from 1923 to 1930. Two papers,

Sayers et al. (1923) and Mitchell and Yant (1925), might

be of the same experimental results. It is unclear if men

were exposed to 50ppm H2S by Sayers et al. (1925) andif additional experiments at 100ppm H2S were con-

ducted by Mitchell and Yant (1925). The experiments on

animals began at 3550ppm H2S (Table 1).

Sayers et al. (1923) stated:

a few experiments were carried out on men, using

low percentages of hydrogen sulfide (Sayers et al.,

1923, p. 2).

In a table of effects under sub-acute exposures,

they all begin at 0.005 per cent (50ppm H2S). In theconclusion, the paper says: the exact low limit of



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Table 1

Select experimental studies of hydrogen sulfide on the eye

Study Experiment design and H2S

concentration

Observations/comments

Lehmann, 1892 Men and animals were exposed None of the tabulated trials specifically mention the 2040ppm and

7090ppm exposures; the trials only document Mr. Kwilecki andMr. Greulich symptoms

Men were exposed to 2040ppm, 7090ppm and

100138ppm. Several other exposure regimes

and times were reported

Mr. Kwilecki test subjecteye observations

Test 1: 100150ppm: after 18min mucous membranes, nose,

throat and larynx irritated, followed by eye inflammation and

tearing. Symptoms were increased with time. Irritation continued

after the trial for some time

5 men in total were exposed in different trials,

for up to 4 h

Test III: 200ppm for 1h: after 5min irritation of mucous membranes,

eyes irritated

Method of H2S analysis was reaction with

potassium iodide; the H2S concentration in

the 29m3 room was mixed via a ceiling fan.

Lehmann notes the ceiling fan carried away the

iodine vapours, which resulted in

over-estimation of the H2S concentrations.A constant value of H2S could not be obtained

because of leakage in the room

Test IVa: 210ppm for 3h: irritation of mucous membranes led

to marked inflammation and swelling of conjunctiva

Thus, H2S concentrations were not accurate

and concentration varied within the test room.

Test VIII: 530ppm for 40min: after 11min biting pain in the eyes,

after 14min eye catarrh

Test IX: 575ppm 3h: after 14min biting pain in eyes, 35min

strong eye catarrh persisting for duration of trial; after test symptomsof eye catarrh increasing accompanied with lively pain.

Lehmann suggested Mr. Kwilecki was the least sensitive of all subjects.

2nd series of tests with Mr. Greulich

Test 1: 230ppm: irritation of conjunctiva in 13min; 19min tearing;

27min pain in the eyes and lots of tearing; 33min increasing

pain and light sensitivity; 40 min eyes open only with difficulty;

46min pain and secretion in eyes almost completely disappears

Test 2 (2 weeks later): 490ppm for 30min and 400ppm for

60min: after 18min eye irritation. 45min no complaints, 1.5h eye

itching after trial: 3min significant eye soreness, strong tear

secretion, cramping closure of eyes, light sensitivity, swelling of

eyelids, redness of conjuctiva; several hourspain in eyes when

subject to light

Test 3: 300ppm for 2h: 38min eye irritation, 52min painful tear

secretion, light sensitivity; 1h. Immediately afterinfection of the

conjunctiva, 15min extreme pain in eyes for next 2h; at

nightinterruptions in sleep because pain in eyes; light sensitivity

Test 4: 532ppm for 30min: 10min irritation of conjunctiva; 20min

significant eye soreness, difficulty opening eyes, completely adverse

to light; 30min extreme pain in eyes. After test: 10min lesioning

eye soreness

Test 5: 100ppm for 2 and 3 h sessions in 1 day: 48min slight

irritation of eyes, light sensitivity; 1h 25min eye soreness and

sensitivity almost completely vanished; 2h light sensitivity

with continuous increasing frequency of stabbing sensation in

eyes; 2h 15min blurred vision

2nd exposure 4h later: 5min stabbing in eyes; 15min start lightsensitivity; 29min burning pain in eyes; 1h 45min significant eye

irritation. Left eye hurts; 2h no irritation in eyes

After: 1h blurred vision, light sensitivity, eye soreness; at night 5 h

latersudden awakening due to eye pain, continuous tears, can only

open eyes with force and extreme pain; following morning, eye clinic

examinationextreme conjunctivitis, continued development of

conjunctivitis, advise to keep eyes closed for hours; 4 pm first

lesioning of eye pain but remain closed; next morning conjunctiva

still red, minor stabbing sensation; 4th dayblurred vision continues,

squinting to improve vision causes tear secretion

(continued on next page)



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hydrogen-sulfide concentration at which it ceases to

act as a poison has not as yet been determined, but it

is evidently below 0.005 per cent. (Sayers et al.,

1923, p. 5). There is no experimental detail in thepaper.

Mitchell and Davenport (1924) stated in their

review:

In an experimental study on the effects of hydrogensulfide upon animals (canary birds, white rats,

Table 1 (continued)

Study Experiment design and H2S

concentration

Observations/comments

Mitchell and

Yant, 1925

Experiments conducted within a 1000ft3 chamber Rats:

H2S produced with a Kipp generator charged

with FeS and HCl

3565ppm: 48h irritation of eyes, 1848h pus in eyes

H2S mixed in chamber with a fan. H2S analyzed

periodically CaCl method

310350ppm: 230min eyes closed

Control experiments were conducted and all were

negative

Guinea pigs:

3565ppm: 1848h pus in eyes

Dogs:

100ppm: 48h lacrimation, 816h pus in eyes, death intense

350ppm: 230min lacrimation

Men: (Mitchell and Yant note: compiled from the Work of Lehmann (1892)

and the writers of this report)

100150ppm: 215min irritation to eyes, loss of smell; 1530min pain

in eyes; 14h sharp pain in eyes

150200ppm: 1530min eye irritation; 14h indistinct vision, light shy;

48h serious irritating effect

Masure, 1950 A. H2S, CS2 and H2SO4 alone and in combination A. Concentrated H2S alone resulted in keratitis after 2h.

With 36 to 71ppm H2S, no lesions were observed. When 40 to 70 mg/m3 CS2

was added, they observed lesions in 3 days. With 1429ppm H2S and

70mg/m3 CS2, no lesions were observed after 5 days.

Exposed rabbits and guinea pigs

No effect was observed with 70 mg/m3 CS2 and 300mg/m3 H2SO4 alone.

B. Exposed rabbits and guinea pigs to the rayon

spinning room at three different levels where

worker effects observed (50cm, 1.6m and 2.4m),

three animals per level B. First assay 10h/day for 6 days. Only rabbits at the high level had eye

effects observed with the slit lamp.Evaluated the mechanism of H2S eye toxicity.

Second assay was 5 days continuously. All animals had eye effects

but those at top levels had greater effect even though H2S concentration

C. Investigated local or general action; sutured

one eye closed with three rabbits and three

guinea pigs and exposed them for 5days in the

spinning room

was similar or slightly higher at lower levels. Suggested denser aerosols

at higher levels lower the threshold of H2S.

D. After acute and after 5-day exposure, treated

cells with fixing agent and colouring agent to

conduct cell histology.

C. Found that only the eye exposed to the gas was affected and not the

eye sutured closed. The action of H2S is therefore local impact on the

eye and not a general affect.

Treated eyes with ferricyanure ferrique which is

reduced by SH groups and forms Prussian blue.

D. With exposure in the spinning room, they observed reduction of the

epithelium to the basal layer and a flattening of the epithelium, mainly

in the central part of the cornea but on the periphery it was a normal

thickness. Observed an increase in mitosis at the basal layer suggesting

regeneration of the cells. They observed a decrease in attachment to

the Bowman's capsule.

Masure used a lead acetate colour technique to

analyze H2S

With pure H2S, observed desquamification process by formation of

slits between epithelial layers. Observed individual cylindrical cells

that remain individually attached to the Bowman's membrane.

Observed this after 2h of exposure to pure H2S which shows the

speed of action.

After 5-day exposure, observed the central part of the cornea a lossof colourability, translating as a decrease in SH groups. A transition

zone of colourability to the edge of unit where it was coloured normally.

With concentrated H2S, they did not observe the colour effect and

thus the mechanism for acute eye injury and total desquamification is

different. No colour change was noted with just CS2 or H2SO4.



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guinea pigs, dogs, and goats) and upon men by

Sayers, Mitchell and Yant, it was found that as low a

concentration as 0.005 per cent (50ppm H2S) would

cause toxic symptoms and on continued exposure

covering a number of days, with a concentration of

0.02 percent (200ppm H2S) death occurred.(Mitchell and Davenport, 1924, p. 9)

Sayers et al. (1925) stated in a review:

the toxic action of H2S has been studied on animals

and men. H2S has been found to be toxic in

concentrations as low as 0.005 percent (50ppm H2S)

and men exposed daily to such percentages would in

all probability suffer irritation of the eyes and

respiratory tract, or subacute poisoning. (Sayers et

al., 1925, p. 5)

Mitchell and Yant's (1925) experimental results on

men are difficult to understand as they report them

compiled' with Lehmann's (1892) experimental results

in a table (see Table 1). In the text Mitchell and Yant

(1925) stated:

some men were exposed for short periods to H2S

in low concentrations (p. 64), and the lowest

concentration of H2S to which men were subjected

was 0.01 percent, which was definitely irritating.

From the experience with canaries and animals,symptoms of irritation were observed in 0.005

percent, and in all probability further experiments

will demonstrate that exposures to even lower

concentrations over long periods will cause poison-

ings. (Mitchell and Yant, 1925, p. 73)

With respect to occupational exposure, Sayers et al.

(1923) presented a typical sub-acute case of H2S

poisoning:

A laborer worked all night in an atmospherecontaining a small amount of hydrogen sulfide. He

complained that it pained his eyes, and the following

day his cornea was lusterless and pained exceed-

ingly; he suffered marked lacrimation (tears in eyes)

and photophobia (pain on exposure to light) existed.

He was placed under the care of a specialist. The

exposed part of the cornea became cloudy, and later

peeled. For several days the patient was unable to

use his eyes, but at the end of a week the

conjunctivitis cleared up, and his eyes were not

permanently affected. He was able to return to workafter 10 days treatment. (Sayers et al., 1923, p. 2)

Mitchell and Yant (1925) have virtually the same

paragraph as above, but described this as a severe case

from a man working several hours in a tank steamed

and declared safe. There is no documentation on how it

was determined that the eye was not permanently

affected, i.e., no comment that the eye was examinedwith a microscope.

Sayers et al. (1923) provided a general description of

eye damage. The paper reported:

the cases of conjunctivitis range from mild to

severe. The eyes itch and smart, and the lids feel dry

and rough. The eyes become red and swollen due to

inflammation of the conjunctiva. The secretion is

increased and may become mucoid or muco-

purulent (pus). Photophobia (pain caused by light)

is usually marked. In the severe cases the cornea(transparent membrane over the coloured part of the

eye) may become cloudy, and the outer cell layer

may be destroyed with accompanying pain, photo-

phobia, lacrimation and blurring of vision (Sayers

et al., 1923, p. 4).

Mitchell and Yant (1925) concluded their paper with

a definition of conjunctivitis, which is virtually the same

as the above description by Sayers et al. (1923).

Mitchell and Yant (1925) stated with respect to

occupational exposures that:

conjunctivitas, pharyngitis, or bronchitis usually

occurred after exposure to low concentrations (0.005

to 0.02 percent) (50 to 200ppm H2S) of the gas for

several hours; occasionally however, they resulted

from an exposure of 510 minutes to a relatively

high concentration 0.05 to 0.06 percent of gas.

These symptoms of poisoning may not appear for

some hours after exposure. (Mitchell and Yant,

1925, p. 60)

Aves et al. (1929) described cases of eye damage inthe Mexican sour gas industry. Similar to Mitchell and

Yant (1925), they distinguished between eye damage

from exposure to low concentrations over time and acute

reactions from high concentrations during blow-outs.

Yant (1930) published a review of the Bureau of

Mines experimental work citing verbatim wording of

the earlier papers.

3.3. Sjorgen (1939)

Sjorgen (1939) presented case reports of workersexposed to sulfurated hydrogen in a paper mill and a brief



8/22

review of the literature on eye damage from H2S. There

is no indication that Sjorgen had knowledge of the work

by Ramazzini (1713), Lehmann (1892), Sayers et al.

(1923) or Mitchell and Yant (1925). In this respect, the

paper provided a relatively independent account of eye

damage from H2S from the previous papers reviewed.The source of the H2S exposure was process water

that was being used. There were no recordings of the

H2S concentration in the air but the room had a

pronounced smell. When the plant ceased using the

water with H2S, all the health symptoms on the eyes

ceased suggesting that the causative agent was H2S.

Sjorgen stated the onset of symptoms in the one case

were:

diffuse annoyance, burning and friction. At an early

stage he had symptoms of dimness and saw rainbowhaloes around flames of light. By and by the

symptoms became enhanced, with abundant lachry-

mation, dread of light, and redness of the eyes.

Finally the burning and friction got so bad he had to

leave his work. These symptoms attain their

maximum either after one day or after several days .

(Sjorgen, 1939, p. 166)

Sjorgen stated:

it is emphasized by all that keratitis cannot be

observed with the naked eye but only with a pocket-lens or microscope. The picture one then discovers is

marked by a grayish muddy or a fine tiny pin point

stippling of the outermost corneal layers within the

rima area. According to Strebel it is due to a

cystiform swelling of the epithelian cells which are

filled with an opalescent exudiation. Later on there

are blister formations which burst and leave behind

epithelian defects colourable with fluorescein, some-

time forming large continuous erosions. (Sjorgen,

1939, p. 169)

This is the first record that we found of using

fluorescein as a stain to observe the keratitis (although

perhaps it is mentioned in the early German papers

which we have not translated). The emphasis on the

need of using a microscope to see the eye damage was

not mentioned by Lehmann (1892), Sayers et al. (1923)

or Mitchell and Yant (1925).

Sjorgen (1939) stated that people do not become

accustomed to the effect of H2S and there has often

been observed after the lapse of time increased

sensitivity in persons who work in air polluted withH2S (Sjorgen, 1939, p. 170). Lehmann (1892) also

commented that they did not observe any development

of habituation and that older workers show heightened

sensitivity to the effects of H2S.

3.4. Viscose rayon spinning rooms: Kranenburg and

Kessener (1925), Lewey (1938), McDonald (1938),Barthelemy (1939), Rubin and Arieff (1945), Masure

(1950), Nyman (1954), Nesswetha (1969) and Van-

hoorne et al. (1995)

There are several papers that presented eye problems

in the spinning industry where exposure to H2S occurs

with other compounds present, most notably carbon

disulfide (CS2) and sulfuric acid (H2SO4).

Kranenburg and Kessener (1925) reported eye pain,

photophobia and inability to open eyes as a result of H2S

exposure. Based on differential air monitoring data, aconcentration of 1625ppm H2S was associated with

conjunctivitis and at 1115ppm H2S was not associated

with symptoms.

A report by Lewey (1938) reviewed the literature on

eye effects from H2S and suggested that the workplace

limit of H2S exposure should be 10ppm H2S to protect the

eyes. McDonald (1938) discussed eye damage from H2S

noting the variability of eye effects: The workers first

notice a slight blurring of vision; they see haloes about

lights, and have pain in their eyeballs. Their eyes soon

begin to tear, and because of the pain and tearing are

obliged to stop work. Many of the workers are apparentlyimmune and we frequently heard the story that they were

free from sore eyes but that the man next to them would

be hardly able to work because pain and tearing

(McDonald, 1938, p. 39). McDonald also notes the

development of sensitivity that was suggested by

Lehmann (1892). McDonald says: once they [the

symptoms] have appeared, they are likely to occur

repeatedly and some claimed that they [the workmen] had

been moved to other parts of the plant because they were

susceptible to sore eyes (McDonald, 1938, p. 39).

McDonald noted that the blisters in the epithelium healrapidly as a rule without leaving any scar or impairment

of vision and the workers are able to return to work.

Barthelemy (1939) presented concentrations of H2S

and CS2 that were found to cause keratoconjunctivitis

and reported on an experiment with rabbits which

reproduced the eye injury observed in workers.

Barthelemy recounted a specific incident in the

spinning room, when the ventilation system was not

adequate to handle the vapours and resulted in many

cases of conjunctiva at once. The eye specialist said:

none of the patients presented symptoms of CS2poisoning, but each case has the following symptoms,



9/22

varying in degree: intense photophobia, spasm of the

lids, excessive tearing, intense congestion, pain, blurred

vision, the pupils were contracted and reacted sluggish-

ly, the cornea was hazy and sometimes numerous

blisters could be seen. The acute symptoms subsided

rapidly and the corneal epithelium regenerated withoutscarring (Barthelemy, 1939, pp. 148149).

Barthelemy discounted CS2 as the causative agent:

We were indeed very much puzzled because we

knew that in many instances operators had been

accidentally exposed for a few hours in another

department of the plant to a concentration as high as

0.40mg CS2 per litre [400mg/m3] without apparent

detrimental effect (Barthelemy, 1939, p. 149).

H2S is produced in the spinning room only while CS2is found in the churn and spinning rooms.

Barthelemy presented measurements of air concen-

tration with eye cases (Table 2). The reduction of eye

cases from December 1933 to December 1934 was the

result of installing a ventilation system. The increases in

cases in December 1936 were a result of an increase in

H2S and CS2 concentrations. From this data, Barthel-

emy concluded a threshold for eye injury: it was found

that if CS2 was kept below 0.1mg/L [or less than

30ppm] and H2S below 0.03 [or less than 20ppm], no

trouble whatever was experienced (Barthelemy, 1939,

p. 151). Barthelemy stated: we are now inclined tobelieve that the simultaneous presence of CS2 and

atomized particles of spinning bath promote a hyper-

sensitiveness of the conjunctiva and cornea to H2S

which gas was recognized long ago as capable of

causing severe eye cases (Barthelemy, 1939, p. 150).

To confirm their observations on workers, Barthel-

emy reported an experiment conducted with white

rabbits in an environment that reproduced as closely as

possible the spinning room conditions. Barthelemy

stated that: Dr. Smith found a marked reaction in the

conjunctiva and cornea of both eyes of each rabbit

treated, with considerable cornea deposit (Barthelemy,

1939, p. 149), and one of the rabbits was given a very

severe exposure and developed a very cloudy cornea

with a slight loss of corneal epithelium, probably the

beginning of ulcerative process. However, after 8 days,

the rabbit had recovered completely (Barthelemy,1939, p. 150). There is no discussion of the number of

rabbits used, nor the eye examination to determine that

the rabbit recovered completely.

Rubin and Arieff (1945) described a clinical study,

although it is perhaps a symptom survey, of 100 workers

exposed to low concentrations of CS2 (517ppm) and

H2S (23ppm). Of the entire group, 1% reported

inflamed lids, 1% burning sensation in the eyes, and

1% pain in eyes and circles before eyes, 2%

occasional blurring of vision and 1% cloudiness of

vision. They found that the day shift reported moreburning of eyes (4.5% or 1 of 22 persons) than the shift

operators (1.3% or 1 person of 78). However, the other

eye symptoms were found only with the shift operators.

Rubin and Arieff (1945) noted that 16% of the group

had diminished or absent corneal reflexes compared

with 12% in the control group. Potential exposures of

the control group were not described.

Masure (1950) conducted a detailed investigation into

eye injury in the viscose rayon industry in Belgium,

including animal experiments to identify the causative

agents, and the mechanism of H2S eye toxicity (Table 1).

Masure described similar symptoms: perception oflooking through fog or veil, coloured rings around

lamps, lively pains in the eyes, feeling of grains of sand

in the eyes, tugging on the eyeball, tearing and

photophobia. With a microscope, Masure (1950) de-

scribed fine superficial lesions of the anterior epithelium

of the eye, developed at the level of the centre of the

pupil. The lesions were present as fine punctuation,

tinged light whitish by fluorescein, corresponding to a

desquamation of the epithelium. In most cases, the

symptoms were bilateral although 17% of cases were

unilateral. Masure (1950) noted human variability.

Table 2

Data reproduced from Barthelemy (1939) of cases of conjunctivitis in the spinning room, December 19321937, and gas concentrations

Year Cases reported including

recurrent ones

Average air analysis (mg/L) [ppm] Remarks

H2SO4 CS2 H2S

December 1932 None 0.031 0.066 [21] 0.012 [9]

December 1933 332 0.055 0.162 [51] 0.041 [30] Increased production

December 1934 85 0.043 0.122 [38] 0.032 [23]

December 1935 None 0.032 0.063 [20] 0.019 [14]

December 1936 71 Not made 0.120 [38] 0.032 [23] Increased production

December 1937 None Not made 0.103 [32] 0.025 [18]



10/22

At the concentrations in the spinning room, it was

suggested that two to four successive workdays were

required for symptoms to manifest. Masure (1950)

noted the frequency of eye cases varied with the

concentration of H2S and not CS2 (Table 3). The

concentration of CS2 remained relatively constant inall five factories. At 0.005mg/L [5mg/m3 or

3.6ppm] H2S, there were no cases of eye injury

despite the same concentration of CS2 as in factory

A where the greatest number of cases of eye injury

were observed.

Masure (1950) presented a number of animal

experiments conducted on rabbits and guinea pigs

both in the spinning room and laboratory (Table 1).

Using a slit lamp, fine and central punctuations that

quickly became marked ulcers, and that infiltrated the

stroma of the cornea, were observed with fluorescein.Masure sutured an eye closed and demonstrated the eye

injury was a result of topical rather than inhaled H2S;

this also demonstrated that closing the eye provides

protection from exposure.

In the spinning room experiment, animals were

placed at three heights, as the concentrations changed

with height. In the first experiment, the concentration

was 38mg/m3 (27ppm) H2S at the top and 49mg/m3

(35ppm) H2S at the bottom level. There was only eye

damage observed at the top level. In the second

experiment, the concentration was 22 and 28 mg/m3

(15.720ppm) H2S at the top and bottom; eye damagewas observed at all three levels; however, eye damage

was more intense at the top levels.

Masure (1950) tested each gas individually (Table 1).

After 5 consecutive days of exposure to 70mg/m3 or

150mg/m3 CS2 alone (no H2S), no lesions were

observed using a slit lamp. At 300mg/m3 H2SO4 (10

times higher than in the spinning room) after 5

consecutive days, lesions were not observed with the

slit lamp. These findings suggest that CS2 and H2SO4were not the causal factors in eye lesion formation.

With pure H2S, Masure (1950) observed lesions in

the animal eyes after 2h. With 50 to 100mg/m3 [36 to

71ppm] H2S after 5 full days, lesions were not observed

in the animals with the slit lamp. With the addition of 40

to 70mg/m3 CS2 and the same concentration of H2S,

lesions were observed after 3 days. When the concen-tration of H2S was reduced to 20 to 40mg/m

3 [14 to

29ppm] H2S with 70mg/m3 CS2, lesions were not

observed after 5 days. They increased the concentration

of H2S on day 5 to 75 to 100mg/m3 [54 ppm and

71ppm] H2S and observed lesions on the next day.

Masure (1950) conducted histological experiments

to gain some insight into the mechanism of the H2S

induced eye damage. Masure (1950) used ferricya-

nide stain to evaluate effects on the formaldehyde

fixed eye tissue. Ferricyanide salts are mild oxidants

that react with reducing substances including sulfhy-dryl groups forming a blue colour known as Prussian

blue. Animal eyes exposed to CS2 and H2SO4 did

not show any decrease in staining. Animal eyes that

were exposed to low levels of H2S alone for several

days showed markedly decreased staining for sulf-

hydryl groups in the central portion of the exposed

eye, and a transition zone to colour formation at the

periphery. In contrast, eyes exposed acutely to high

concentrations of H2S did not result in significant

formation of Prussian blue. Masure (1950) concluded

that the decrease in free sulfhydryl groups was

related to low H2S exposure after several days andthat other mechanisms were responsible for the acute

high dose effects.

Nyman (1954) emphasized the clinical picture of eye

effects caused by H2S and treatment of 237 patents with

cortisone. From a historical perspective, a key point is

the distinction Nyman made between conjunctivitis and

keratitis:

Both acute and chronic hydrogen sulfide and

carbon disulfide poisoning occurs in such plants,

acute conjunctivitis induced by hydrogen sulfidebeing the most frequent. Some patients, in addition

develop keratitis. Sometimes this occurs only after

the conjunctivitis has persisted for a few days, but

occasionally its onset is simultaneous with the

conjunctivitis. This type of keratitis has been studied

by an ophthalmologist who diagnosed it as keratitis

punctata superficilialis. According to the literature a

characteristic of this keratitis is that the corneal

epithelium remains intact.

I have followed such cases of keratitis for sevenyears, both early and late stages, and found that the

Table 3

Data reproduced from Masure (1950) of cases of conjunctivitis in the

spinning room, in different Belgium factories in 1948, and gas

concentrations

Machine CS2(mg/L)

H2S

(mg/L)

H2SO4(mg/L)

SO2(mg/L)

Number of

case per

month

% attained

spinners

A 0.063 0.03 0.023 54 41

B 0.044 0.03 13 6

C 0.09 0.017 6 4

D 0.06 0.008 2 1

E 0.066 0.005 0.19 0 0



11/22

epithelium of the cornea is often readily broken and

the surface of the cornea hence rough. It is as if a

small or large epithelial vesicle had developed on the

cornea and then ruptured. The edge of such a

ruptured vesicle is readily discernable, and it is not

unusual for the broken surface to cover practicallythe whole cornea.

At this stage the patient has such severe pain in his

eyes that he can neither sit nor lie but walks to and

fro with his head bent, covers his eyes with his

hands, and complains all the time. He is practically

completely blind. He is unable to open his eyes and

cannot move outside his room without help. He is

afraid of having lost his sight. The disease picture is

highly dramatic. (Nyman, 1954, p. 161)

Nyman (1954) did not present any concentrations of

H2S, which resulted in the above clinical picture. Nyman

(1954) suggested three types of eye disease: (1) a pure

conjunctivitis, (2) conjunctivitis developing into keratitis

in a few days and (3) an immediate keratitis.

After Nymans (1954) terminology, the potential for

irreversible eye effect can be appreciated as keratitis

where healing is accompanied with scar formation. In

the case of cornea, a scar or tissue may form during the

healing process and can result in partial loss of vision or

destroy eye function completely, in particular, when

compounded by secondary infection (Gosselin et al.,1976; Potts, 1986).

Nesswetha (1969) studied etiologic factors in 6500

cases of keratitis superficialis punctata (spinner's eye),

attributed to occupational exposure to H2S. At 15mg/m3

(10 ppm) H2S, eye irritation occurred after 67 h o f

exposure. At 20mg/m3 (14ppm) H2S, symptoms

developed after 45h. Note, this summary is based on

NIOSH (1977) and Alberta Health (1988) as we have

not translated the paper.

Vanhoorne et al. (1995) conducted a cross-sectional

study on eye injury in viscose rayon industry. A keydistinguishing feature from the cases described by

Barthelemy (1939) and Masure (1950) is that H2SO4was not detected in the work place. The highest H2S was

8.9mg/m3 [6.4ppm H2S] and occurred only in the

spinning room, and it always occurred simultaneously

with CS2. However, there was no discussion of

conjunctivitis and no eye examination of impacted

workers.

Some workers only had CS2 exposure and the highest

concentration exceeded 90mg/m3 [64ppm]. Consider-

ing the group exposed to CS2 without H2S, versuscontrols, statistically significant differences were ob-

served only for exposure to 3190mg/m3 CS2 for eye

tension (P5 mg/m3

[3.6 ppm] H2S.

In addition, to assess possible bias, a mail out survey

to former workers found that 25% spontaneously

responded leaving the workplace because of eyecomplaints, which suggests the data underestimated

the health problems. Vanhoorne et al. (1995) suggested

that their study could not distinguish the primary

causative agent for the injury.

3.5. Occupational, experimental and community ex-

posures: Michal (1950), Ahlborg (1950), Carson

(1963), Beasley (1963), US Department of Public

Health Service, Terre Haute (1964), Luck and Baye

(1989) and Schiffman et al. (2005)

Michal (1950) reported the sudden emergence of 27people with eye disease after washing beets using

wastewater: blepharospasm, dacryorrhea, photody-

shoria and oedema of corneal epithelium. The people

reported seeing coloured rings around lights, sharp

stabbing pain in the eyes, delacrimation, eyelid spasms

and obvious redness. Most people affected returned to

work after 5 days. The odour of H2S was present in the

room and was the suspected cause of the eye disease.

The problem went away when they switched to artesian

well water.

To investigate the cause, Michal (1950) experimen-tally evaluated acute and chronic eye exposure effects

from H2S. At 860ppm H2S, they observed rubbing of

eyes and the rat died in 10 min. Microscopic

examination showed pycnosis of the epithelium cell

nucleus, occasional cell spacing, and oedema reaching

all the way to the surface layers of the corneal stroma.

Michal reported the same effects as in the acute toxicity

experiment with a rat exposed for 3h at 36ppm H2S.

Our calculation suggests that testing was done by

exposing a rat to 50 vol.% (50g/m3) (36ppm) for 3h,

which is similar to the concentration calculated byNIOSH (1977). Beauchamp et al. (1983) and Alberta



12/22

Environmental Centre (1986b) suggested that the

experiment was conducted with 54ppm H2S.

Ahlborg (1950) described occupational cases of

keratoconjunctivitis from brief exposure and the typical

scenario as follows:

a thin jet of gas has suddenly shot out against the

face of the man working with pipes or pumps.

Automatically he had held his breath and gone to get

his gas mask. The exposure, therefore, has been

extremely intense but brief. Within 12 to 24 hours

keratoconjunctivitis has developed, with pain, itch-

ing, photophobia and other eye disturbances.

(Ahlborg, 1950, p. 260)

Carson (1963) and Beasley (1963) described the

exposure of five men to H2S and ammonia (NH3), in awell ventilated room. Beasley (1963) specifically

distinguished the H2S and NH3 eye effects, to suggest

that three of five men developed symptoms associated

with H2S. Carson (1963) described many of the

symptoms of H2S exposure. Carson noted that none of

the three men complained of their symptoms or the

atmosphere in the plants, and, unfortunately, therefore,

the measurement of H2S was not made. Carson suggested

that the incident provides further support that ocular

affects are the earliest symptom of H2S exposure.

In Terre Haute, Indiana (USDH, 1964), June

1964, a release from a chemical lagoon resulted incommunity levels of H2S recorded as 0.022

0.125ppm for 7h. Citizens complained about burning

eyes. It is stated in the NIOSH report: this study

did suggest that hydrogen sulfide can irritate the eyes

and respiratory system at concentrations below

1ppm (NIOSH, 1977, p. 44).

Luck and Baye (1989) presented case reports of

several people acutely exposed to H2S while making

sausages: bilateral blepharospasm, photophobia and

lacrimation, intense conjunctival infection, and superfi-

cial punctate corneal erosions (Luck and Baye, 1989, p.748). Slit lamp biomicroscopy showed resolution of the

superficial punctate corneal erosions. There were no

other health conditions reported from the exposure.

Schiffman et al. (2005) exposed 48 healthy partici-

pants to a complex mixture containing 24 ppb H2S,

817ppb NH3, 0.024mg/m3 total suspended particulates

and 7.4EU/m3 endotoxin for 1 h. Eleven participants

reported eye irritation after the exposure and seven

participants 2 h later. Two reported eye irritation prior to

exposure. A control group was exposed to filtered air;

two reported eye irritation. NH3 is not reported to causeeye irritation until concentrations reach 50ppm.

Particulate matter is generally not thought to be an eye

irritant unless in concentrations exceeding 5 mg/m3.

Endotoxin is also not known to be an eye irritant. 24ppb

H2S appears to be the responsible agent.

3.6. Chronology of Alberta studies: Nordstrom (1975),Burnett et al. (1977), Lodgepole Blowout Report

(1984), Drummond Blow-Out (Alberta Environmental

Centre, 1984), Arnold et al. (1985), Alberta Environ-

mental Centre (1986a,b) and Lefebvre et al. (1991)

Nordstrom (1975) designed a study of calves which

specifically evaluated the effects of H2S on the eye,

among other end-points. Alberta Health (1988) cited the

study as Nordstrom and McQuitty (1975). A specific

chamber was built for exposure, to allow for constant

and monitored concentration of H2S. A total of 8 calveswere continuously exposed to 20ppm H2S or 150ppm

H2S for 7 days. Other calves were exposed to NH3 and a

combination of the gases. Background concentrations of

13ppm NH3 were noted in all trials. A 7-day control

group was also included.

Nordstrom concluded:

exposure to 20ppm H2S for one week apparently

caused permanent tissue damage to the cornea. At

150ppm H2S induced severe corneal opacity and

rupture of the eye appeared possible toward the end of

the gas-exposure period (Nordstrom, 1975, p. iv).

Calves' eyes were clinically examined by Dr. Beck, a

veterinarian with Alberta Agriculture, who concluded

the damage at 20ppm H2S was irreversible.

Nordstrom stated:

bH2S appeared to have a direct degenerating effect

through cytotoxic mechanisms on the viability of the

exposed membranes of the eye the conjunctiva

and cornea, and of the nasal mucous membranes. At

both levels of H2S, definite detrimental effects wereapparent. At times the calves appeared lethargic and

stood with heads lowered, eyes closed and at

both levels of H2S, signs of photophobia were

evidenced by strabismus and refusal to open the

eyesQ (Nordstrom, 1975, p. 112).

On day 2 of the 20ppm H2S exposure, one calf

demonstrated definite cloudiness of the cornea and

anotherslight dullness of the eyes. At the higher levels

of H2S corneal opacity was severe. Nordstrom com-

mented that in two calves, it appeared they had becomeblind.



13/22

Burnett et al. (1977) presented cases of H2S

poisoning, typically acute exposure, in Alberta from

1969 to 1973. 92% of the cases occurred in the oil, gas,

and petrochemical industries. Of 221 cases, conjuncti-

vitis was observed in 5% of cases at the accident site,

9% at physician's office and 11% at the emergencyroom. Two case reports were presented. One case at the

accident site had tearing of the eyes and photophobia

and, at the hospital, he had severe photophobia, with

blepharospasm but no obvious conjunctivitis. A second

worker, who eventually died 34 days after vital system

support, was described at the hospital as having florid

conjunctivitis.

In Alberta, Canada, the 1982 Lodgepole sour gas well

blowout resulted in wide-spread exposure to H2S. The

time of exposure is difficult to determine but occurred on

and off for 28 days. The maximum concentrations of H2Sin the area were 3.5ppm in Drayton Valley, 14.5ppm in

Lodgepole, 14ppm in Cynthia and 6 ppm in Violet Grove

(Alberta Environment, 1982).

Alberta Health reported complaints of eye and lung

irritation in Cynthia after a maximum potential exposure

of 14ppm H2S for 2h (Alberta Health, 1988). In the

Lodgepole area, 43% of 189 people involved in a health

survey reported eye problems and 33% of the total

population (Win Consulting, 1983, p. 319). Residents

described their eyes as feeling sandy orburning and

several people reported having blurred vision. It was

reported that: mucopurulent exudate, which is reportedto accompany inflamed conjunctiva, occurred in several

children of Pembina area members. These young

children had to have the exudate wiped from their

eyelids before they could open their eyes in the

morning (Win Consulting, 1983, p. 55).

Further away, in the Edmonton area, 25% of

respondents reported eye irritation where the concen-

trations were 0.5ppm H2S and, in Drayton Valley,

37% reported eye irritation where the concentrations

were up to 2.6ppm H2S (Edmonton Board of Health,

1983).The Alberta Government Lodgepole public hearing

report noted that animals in the vicinity were affected in

a similar manner as humans, i.e., runny eyes and noses

and that the younger animals were affected more than

the older ones (Lodgepole Blowout Report, 1984,

p. 72). The report stated: the panel accepts that the

high rate of ocular and respiratory symptoms reflecting

mucous membrane irritation in different species of

animals simultaneously and the disappearance of birds

and small animals was unique and cannot be explained

on the basis of natural causes

(Lodgepole BlowoutReport, 1984, p. 72).

In the 1984 Drummond 6-30 sour gas well blow-out,

many animals were exposed to sour gas (Alberta

Environmental Centre, 1986a). The sour gas was

released from September 2428, 1984. On one farm

located 2 km from the wellhead the maximum H2S

concentration measured was 0.60.7 ppm (1 houraverage), with most levels


14/22

(400ppm) for 4h and 2100mg/m3 (1500ppm) H2S for

4min. The % of exfoliated cells was compared with

controls. Corneal epithelial cells represented the major-

ity of exfoliated cells followed by conjunctival epithelial

cells. There were few exfoliated polymorphonuclear

leukocytes. Masure (1950) also suggested that there wasno infiltration to the leukocytes.

Guidotti (1994) discussed the possibility of a linear

doseresponse curve for eye injury. From Lefebvre et al.

(1991), an approximation of the toxic load equation for

eye toxicity can be inferred. If we assume linearity and

that the two treatments had equivalent toxic load and

effect, where toxic load = (concentration)n time, then

the exponent on concentration would be n =3.1. This is

in the range ofn values for H2S lethality, where a value

of n =2.5 has been used and justified based on animal

and human data (ERCB, 1990), and an n =4.4 calculatedfrom rat lethality (EPA, 2002). However, Lefebvre et al.

(1991) observed that 560mg/m3 for 240min resulted in

more exfoliated cells than 2100mg/m3 at 4min, i.e., the

toxic load at 560mg/m3 for 4h was greater than

2100mg/m3 at 4min. This suggests that the n value

should be smaller than n =3.1. Relative to this point,

concentration becomes less important and time of

exposure more significant in the H2S toxic load on the

eye. However, Masure (1950) inferred different toxico-

logical mechanisms may be involved for acute and

chronic toxicity. This limits the extrapolation of this

toxic load equation to low concentrations for longperiods of time.

In two studies on adult Sprague-Dawley rats, there

were no observations of conjuctivitis from exposure to

100 ppm H2S for 3 hours (Skranjy et al., 1996) and 125

ppm H2S for 4 hours, 5 days week (Partlo et al., 2001).

Since the studies were designed to evaluate the effect of

H2S on the hippocamal EEG activity and memory in

rats, and not designed to study the effects on the eye, the

observations on the eye should be considered secondary

and not a critical portion of the studies (Roth SH, 2006,

personal communication).

3.7. South Karelia air pollution studies: Haahtela et al.

(1992) and Marttila et al. (1994, 1995)

The South Karelia air pollution studies documented

public exposures to low levels of H2S and other reduced

sulfides (methyl mercaptan, dimethyl sulfide and

dimethyl disulfide) from pulp mills in Finland.

Haahtela et al. (1992) presented survey results from

a community that experienced low level acute H2S

exposure: the maximum 4-h concentration 135g/m

3

(96ppb) H2S and the 24-h average of 35 and 43g/m3

(25 and 31ppb H2S). During the peak emissions, the

SO2 mean 1-h average was only 3g/m3 and therefore

not a significant confounder. The authors concluded

that the observed symptoms correspond to the

physiological effects of acute exposure of H2S,

suggesting direct irritative effect on mucous mem-branes and eye conjunctivitis but at lower concentra-

tions than described previously (Haahtela et al., 1992,

p. 605).

The major confounding exposure was the release of

mesityl oxide and there were no concentrations

presented (Haahtela et al., 1992). Mesityl oxide is a

liquid at 25C with a low vapor pressure (8.7mm Hg at

25C). Its vapor is reported to have a distinct pep-

permint odor and induce sensation of irritation, which is

detectableat 25ppm in air (Hazardous Substances

Database, 2005). These properties suggest that theeffects observed were more likely due to H2S.

Marttila et al. (1994) reported in the most polluted

Karelia area that the annual mean H2S concentration

was calculated as 8g/m3 (5.7ppb) H2S, the highest

24-h concentration was calculated as 100g/m3

(71.4 ppb) H2S and the maximum 4-h average was

measured as 56g/m3 (40ppb) H2S. The other major

compound was methylmercaptan (CH3SH), with an

annual mean of 25g/m3 and a maximum 24-

h concentration of 150g/m3. CH3SH is considered

mildly irritating at concentrations two orders of

magnitude higher, 10mg/m3 (NIOSH, 1989). Sulfurdioxide annual mean levels were low (2g/m3)

because the plants use natural gas for energy (Haahtela

Haahtela et al., 1992). In the moderately polluted area,

the levels were much less for H2S and CH3SH. Of

note, there was no CS2 present which was the main

confounder in understanding the effect of H2S in the

viscose rayon industry.

Marttila et al. (1995) conducted surveys of the

community in a reference (non-polluted) area, medium

polluted and high polluted areas evaluating daily

symptom intensity in relation to exposure levels. Withrespect to eye symptoms, they found significant

differences between the medium and reference commu-

nities (OR 3.17, 1.217.47) and high vs. reference (OR

5.0, 1.6612.65). They observed a similar increase in

reporting of intensity of nasal and pharyngeal symptoms.

The intensity of eye symptoms was significantly higher

during days of TRS > 10 g/m3.

The parents reported their children's eye symptoms

over the past 12 months (OR 1.15, 95% CI 0.43-3.05) in

the three communities (reference n=7/30, medium n=20/

62, and high n=5/42) (Marttila et al., 1994). Onlyparents in the medium (n=2) and high (n=4) pollution



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areas reported children's eye symptoms over the

previous 4 weeks, so the risk could not be calculated.

Marttila et al. (1994) commented parents have problems

evaluating eye symptoms for their children compared

with more noticeable symptoms like wheezing. They

concluded the eye symptoms were consistent with thepresence of H2S.

3.8. Community study in Rotorua: Bates et al. (1998,

2002)

In Rotorua, New Zealand, seeps from a natural

geotherm result in ambient levels of H2S. The median

concentration was reported as 20g/m3 (14ppb) with

35% of the measurements >70g/m3 (50ppb) and 10%

>400g/m3 (286ppb) H2S. It was suggested that the

highest exposure group in the 2002 study was exposedregularly to at least 143ppb H2S, with highest

concentrations at 1ppm H2S for 30-min average (Fisher,

Fisher, 1999).

An early study in Rotorua reported several cases of

conjunctivitis and one case of blindness lasting three

days from H2S exposure (McDougal and Garland,

1945). Bates et al. (1998) conducted an ecological

study of health effects from hospital discharge data

from 1981 to 1990. They observed a statistically

significant increase in disease of the eye and adnexa

(SIR 1.12, 1.051.19), cataracts (SIR 1.26, 1.141.38),

disorders of the conjunctiva (SIR 2.09, 1.662.59) anddisorder of the orbit (SIR 1.69, 1.122.44). The

limitation of the study was that all people were treated

equally exposed.

Bates et al. (2002) conducted an ecological study of

health effects from 1993 to 1996 morbidity data

comparing the community by H2S exposure: high,

medium and low. They observed statistically significant

disorders of the eye and adnexa comparing the

communities: high (SIR 2.27, 1.972.61), medium

(SIR 1.57, 1.301.89) and low (SIR 1.47, 1.331.63).

They also observed statistical significance for a trendfrom high to low; P for trend


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Table 5

Comparison of studies cited for effects of hydrogen sulfide on the eye

Reports by date [H2S], time, eye effect:a

yes or no

Cited in review

Alberta Health

and Wellness,

2002

Alberta

Health,

1988

National Institute of

Occupational Health

(NIOSH), 1977

World Health

Organization

(WHO), 2003Ramazzini, 1713 no data, 4h, yes No No Yes No

Mitchell and Davenport,

1924

Review No No Yes No

Sayers et al., 1923 50ppm, hours, yes No Yes No No

Mitchell and Yant, 1925 Dogs 3550ppm,

13h, yes

Yes Yes No No

Men> 50ppm, hours, yes

Kranenburg and

Kessener, 1925

1626 ppm, hours, yes No Yes No

1015ppm, hours, no

Yant, 1930 Review Yes Yes No No

Legge, 1934 1424 ppm, hours, yes No No Yes No

Lewey, 1938,

McDonald, 1938

No data, yes No Yes No No

Barthelemy, 1939 > 20ppm, hours, yes No Yes Yes No

Elkins, 1939 > 20ppm, hours, yes

(no actual data provided)

No Yes Yes No

Sjorgen, 1939 No data, yes No No No No

Larsen, 1944 29132ppm, 30min

to hours, yes

No Yes No

Howes, 1943 No data, yes No No Yes No

Rubin and Arieff, 1945 15 ppm, hours, yes No Yes No No

Ahlborg, 1950 20ppm, hours, yes No Yes Yes

Masure, 1950 14ppm, hours, yes No Yes Yes No

Michal, 1950 36ppm, 3 h, yes No No Yes No

Zander, 1950 No data, yes No No Yes No

McCabe and Clayton,

1952

Up to >1000ppm,

minutes, yes

No No Yes No

Deveze, 1956 100 ppm, hours, yes No Yes No

Loginova, 1957 0.0040.021ppm, chronic, yes No Yes No No

Duan, 1959 0.0070.009ppm,

5min, yes

No Yes No No

Carson, 1963, Beasley,

1963

No data, yes No Yes Yes No

Grant, 1974 Review No No Yes No

Milby, 1962 Review No

Baikov, 1963 0.0080.009ppm,

40min, yes

No Yes No No

United States

Health Department,

Terre Haute, 1964

0.0220.125ppm,

7h, yes

No Yes Yes No

Kleinfeld et al., 1964 No comment in

paper of effect on the

eye

No Yes No No

Poda, 1966 < 10ppm, hours, yes No No Yes No

Benini and Colamussi,

1969

510 ppm, years, yes No Yes No

Brown, 1969 100 ppm, hours, yes No No Yes No

Nesswetha, 1969 1121ppm, 67 h, yes No Yes Yes No

Hays, 1972 20ppm, 24h, yes No Yes Nob No

Kosmider et al., 1971 71ppm, 1 h, yes Yes No Nob No

Nordstrom, 1975;

Nordstrom and

McQuitty, 1975

20ppm, 7 days, yes No Yes No No

Gosselin et al., 1976 Review Yes Yes No No



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4.2. Review of the scientific studies to support AHW

Report (2002) conclusion that there is very little

evidence of eye irritation following short-term expo-

sures to H2S at concentrations up to 100ppm

AHW Report (2002) concluded there was little

information available suggesting eye involvement

following short-term exposure up to 100ppm H2S.The

findings on the eye were discussed in three sections:

non-clinical, clinical and case-control studies (AHWReport 2002, pp. 2829).

4.2.1. Non-clinical studies

AHW report (2002) stated that most of the non-

clinical study effects were typically non-descript, and

less than 10% of studies reported eye irritation at less

than 100ppm H2S.

Only one study cited in the AHW Report (2002),

Skranjy et al. (1996), reported no effect of H2S on

the SpragueDawley rat eye at an exposure concen-

tration of 100 ppm H2S for 3h. The full context of

their comment is:

exposure to 50ppm causes severeeye irritation or gas eye in humans. However, eye

Table 5 (continued)

Reports by date [H2S], time, eye effect:a

yes or no

Cited in review

Alberta Health

and Wellness,

2002

Alberta

Health,

1988

National Institute of

Occupational Health

(NIOSH), 1977

World Health

Organization

(WHO), 2003

NIOSH, 1977 Review No Yes YesHaider et al., 1980 20 ppm, 1h, yes Yes No NAc Yes

IPCS, 1981 Review No No NA Yes

CIIT, 1983 10:20:80ppm, 6 h/day,

5days/week for 90 days,

yes

No Yes NA No

Alberta Lodgepole

Blowout, 1984


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irritation was never observed in the rats in the present

experiments which suggests that the rat may be more

resistant to the effects of H2S (Skranjy et al., 1996,

p. 52).

The AHW Report (2002) cited Lopez et al.

(1986), which is the Alberta Environmental Centre(1986b) study (see Section 3.6). The AHW Report

(2002) stated that researchers observed lacrimation

at 40ppm H2S.

AHW Report (2002) stated that Mitchell and Yant

(1925) (see Section 3.2, Table 1) reported irritation of

the eyes progressing to pus in the eyes among rats,

guinea pigs and dogs following continuous exposure to

35 to 100ppm H2S for 8 to 48 hours, and that

lacrimation was also noted among dogs.

Haider et al. (1980) evaluated the effect of H2S on the

levels of total lipids in the brain of guinea pigs. Guineapigs were exposed to 20ppm H2S for 1h/day for 11days.

The publication has one sentence that includes the eye:

following exposure of guinea pigs to H2S such signs as

fatigue, somnolence, dizziness, itching and eye irritation

were observed (Haider et al., 1980, p. 419). WHO (2003)

cited this study as providing information of the lowest

concentration showing effects from short-term exposure.

Kosmider et al. (1971) evaluated the effect of vitarel,

a vitamin and mineral supplement, on mineral and

enzyme disturbances as a result of H2S. Kosmider et al.

(1971) exposed rabbits to 71 ppm for 1 h/day for 14days.

There is one statement in the paper that references theeye: quicker breathing and pulse-rate as well as conges-

tion of the conjunctivas could be observed (Kosmider et

al., 1971, p. 67). Thus, the effect on the eye was a result of

a brief exposure to H2S. WHO (2003) cited this paper but

did not mention the eye effect in its review.

The AHW Report (2002) stated that none of the other

non-clinical studies showed eye effects; there is no

indication of which studies these are.

In contrast to the AHW Report (2002) conclusion,

four of five non-clinical studies cited in the report

provided evidence of eye irritation from short-termexposure below 100ppm H2S. The lowest concentration

and time indicating eye irritation was 20ppm H2S after

1h (Haider et al., 1980).

4.2.2. Clinical studies

The AHW Report (2002) stated: Jappinen et al.

(1990) found no evidence of eye irritation following

controlled whole body exposure of asthmatics at 2ppm

H2S for 30 minutes, nor did Kangas and Savolainen

(1987) report eye irritation among subjects exposed to

H2S at con centrations up t o 3 0 ppm for 30 to40minutes (AHW Report, 2002, p. 28).

In Jappinen et al. (1990), the eye is mentioned in one

sentence in the discussion: malodorous sulfur com-

pounds existing in the ambient air have been shown to

cause mucosal and conjunctival irritation even at low

concentrations (Jappinen et al., 1990, p. 827).

Kangas and Savolainen (1987) evaluated the use ofthiosulfate as a urinary biomarker of H2S exposure.

There is no mention of the eye in the paper.

AHW Report (2002) presented the results of

Mitchell and Yant (1925) (see Section 3.2). The

report stated subjects reported eye irritation in as

little as 2 to 15min after exposure to 100 to 150ppm

H2S and that sharp pain in the eyes was reported

after 1 to 4h.

Only one of the three studies cited was a clinical

study evaluating effects on the eye and it provided

evidence of eye irritation from short-term exposure at100ppm H2S.

4.2.3. Case-control and observational studies from sour

gas releases

AHW Report (2002) reviewed two studies by

Kilburn (1997, 1999) from accidental releases of sour

gas. The AHW Report (2002) commented that: Kilburn

(1997) found that eye effects were not reported by

subjects exposed to 1 to 50ppm H2S for up to 24 hours

at the time of exposure; however, upon evaluation 2 to 6

years later, eye involvement was evidenced by abnormal

colour vision, and reduced fields as well as complaintsof eye irritation.

In Kilburn (1997), the only possible inference of eye

irritation or conjuctivitis at the time of exposure is the

category of mucous irritation in the symptom survey,

which was reported as significantly elevated over

controls.

The AHW Report (2002) stated: Kilburn reported

eye effects among individuals allegedly exposed to

H2S at concentrations ranging from 1 to 40ppm for

up to one week as a result of emissions from refinery

explosion and fire. The effects presented as abnormalcolour vision and impaired visual fields based on

testing performed three years after the event.

Kilburn (1999) presented findings from a neurobe-

havioural battery and the comments of impaired visual

field are in relation to neurological effects. We could

not find any statements in the paper with respect to eye

irritation or conjuctivitis.

AHW Report (2002) cited the Lodgepole Blowout

Report (1984) (see Section 3.6) and stated that:

witnesses testified experiencing eye irritation at the

time of the incident

. The Alberta Social Service Report(1983) report was cited, indicating a: relatively high



19/22

incidence of eye effects, including burning eyes and

double vision.

Of the case-control studies cited by Alberta Health

(2002), only the Alberta Lodgepole blowout report

supports eye effects at concentrations significantly

less than 100ppm H2S (see Section 3.6) and it isunclear if Kilburn (1997) results indicate eye

irritation.

4.3. AHW Report (2002) critique of Alberta Health

(1988)

The AHW Report (2002, p. 55) stated its con-

clusions are in sharp contrast to the earlier 1988

report. The AHW Report (2002) claimed that Alberta

Health (1988) relied heavily on the review by Milby

(1962), and Gosselin et al. (1976), which relied uponthe review by Yant (1930), none of which can be

substantiated by original research and none of it

suggesting that H2S at 20ppm H2S causes irreversible

eye damage (see Section 1 for the full quotation).

Table 5 indicates that Alberta Health (1988) did not

rely heavily on Milby (1962) and Gosselin et al. (1976).

Alberta Health (1988) cited Nordstrom and

McQuitty (1975) for irreversible eye effects at 20ppm

H2S (see Section 3.6). Of particular importance is that

the AHW Report (2002) did not reference this study

(Table 5), yet they referenced other Alberta gray

literature.In the Alberta Health (1988) report, Milby (1962)

was not cited in the description of the irreversible

damage to the eye from 20ppm H2S:

As acute conjunctivitis develops, characteristic

signs and symptoms include pain, mucopurulent

exudation, lacrimation, hyperemia, retroorbital ach-

ing, blepharospasm, blurred vision, photophobia,

and the illusion of rainbow-like colors around the

incandescent lights (Beasley, 1963). As this condi-

tion progresses vesiculation and ulceration of thecorneal epithelium may result in scar formation and

permanent impairment of vision (Mitchell and Yant,

1925; Yant, 1930; Gosselin et al., 1976). At H2S

concentrations below 50ppm increased exposure

duration is required to elicit these effects. For

example, Nordstrom and McQuitty (1975) con-

cluded that permanent corneal tissue damage could

be elicited in calves exposed to 20 ppm for 7 days.

Others have reported inflammation of eye tissues

(spinner's eye) after 67 hours of exposure to 11

21ppm H2S (Elkins, 1939; Nesswetha, 1969)

.(Alberta Health, 1988, pp. 1314)

In conclusion, the Alberta Health (1988) report

stated: to conclude, irreversible eye tissue damage can

occur at 20ppm H2S, but on the basis of animal data

(Alberta Health, 1988, p. 14).

Milby (1962) is only cited once in the 1988 report:

The current Alberta OEL for H2S is 10ppm.

Like ACGIH, the basis for this OEL is primarily

the greater incidence in irreversible eye tissue

damage at concentrations >20 ppm for several

hours exposure. For example, at concentrations

greater than 50ppm for 1 hour, irritation and

inflammation of the conjunctival and corneal

tissues may occur, a condition called gas eye.

(Milby, 1962; Gosselin et al., 1976; Alberta

Health, 1988, pp. 26)

The Alberta Health (1988) report did not reference

the 20ppm H2S effect to Milby (1962). In fact, the

Alberta Health (1988) citation is similar to the excerpt

from the AHW Report (2002, p. 55): exposure to

concentrations above 50ppm for a period exceeding 1

h may produce irritation of the conjunctival and corneal

tissues.

Contrary to AHW Report (2002) statement that there

is no original research to support the Yant (1930) review,

the original research paper, Mitchell and Yant (1925),

was actually cited in the AHW Report (2002). Yant

(1930) provided a review and rewording of thestatements from Sayers et al. (1923) and Mitchell and

Yant (1925) (Section 3.2). Milby (1962) referenced the

Yant (1930) paper. Therefore, the original research for

citing 50ppm H2S resulting in eye effects is Sayers et al.

(1923) or Mitchell and Yant (1925).

Therefore, quite clearly the AHW Report (2002)

claims that in sharp contrast to the earlier report

(Alberta Health, 1988) which relied heavily on

statements made by Milby (1962) cannot be

substantiated.

5. Conclusion

The AHW Report (2002) conclusion that there is

little evidence of eye irritation up to concentrations of

100ppm H2S is not supported by the non-clinical,

clinical and case-control studies that were cited in

their report. Almost all the scientific studies we found

that discussed the eye, reported eye effects below

100ppm H2S in a variety of environmental contexts

(Table 5). Ramazzini's observations in 1700 appear to

be an accurate description of the health effects ofH2S on the eye and consistent with scientific studies


7/29/2019 Review of hydrogen sulfide and sour gas effects on the eye - a historical pers

review of hydrogen sulfide and sour gas effects on the eye - a historical perspective

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