Science

Methyl Bromide Recapture/Scrubber Technologies

F.A.S.T. (FUMIGATION ABATEMENT AND DESTRUCTION) SYSTEM

P. SWORDS*, D. MUELLER AND A. VANRYCKEGHEM

Insects Limited, Inc. and Fumigation Service & Supply

16950 Westfield Park Road

Westfield, IN 46074 USA;  O: (317) 896-9300 | C: (317) 306-0160 | F: (317) 867–5757

*Corresponding author e-mail: p.swords@insectslimited.com

Abstract: The F.A.S.T. System scrubber accompanies a fumigation chamber/area by functioning to capture and destroy fumigant gases such as methyl bromide, sulfuryl fluoride, methyl iodide and any other alkyl halides.  The F.A.S.T. system contains a depository holding scrubbing material that causes a substantially complete chemical breakdown of the fumigant introduced.  The solution is non-carbon based and is mostly aqueous containing chemical degradation properties.  Any alkyl halide such as methyl bromide or sulfuryl fluoride agitated through the depository can be broken down through the scrubbing solution by a SN2 chemical reaction.  By-products of the reaction are retained in the scrubber depository leaving only ambient air to be released into the atmosphere.

INTRODUCTION

              Many native and non-native species of moths, beetles, borers, parasites, nematodes, other microorganisms, and rodents have the ability to damage a wide range of agricultural and non-agricultural commodities and stored products.  Such items can include grain, seed, flour, processed foods, cut wood, logs and a wide variety of other perishable and non-perishable goods and products.  Fumigation using specialized gases with lethal properties to a broad spectrum of pests, especially insects, rodents, and pest microorganisms, are a fast and effective eradication method to prevent damage to stored commodities (Mueller, 2010).  Fumigations can take place in any gas/air tight chamber, building or structure to eliminate infestations.  Sealed containers, trailers, boxcars, import and export shipments, grain bins, homes and other free standing structures, where fumigant gas can be introduced and held for a long enough periods of time to, make for desirable fumigation areas and permit eradication.  Other more unique situations where fumigations may take place include libraries, restaurants, ship holds, museums, and rare and/or high value artifacts.

For many years, methyl bromide (MeBr) has been widely used as a pesticide fumigant.  However, because bromine released from methyl bromide has been found to contribute to depletion of the ozone layer in the troposphere, its use is being eliminated under both U.S. laws and international treaties.  Nevertheless, until such time as those fully take effect, methyl bromide is still being used as a fumigant, particularly in the U.S. for quarantine and pre-shipment purposes (Mueller, 2010).  From an environmental standpoint, there is therefore a strong incentive to develop systems that will ensure that fumigations performed with methyl bromide will not result in its escape into ambient atmosphere.

Because of the ozone-depleting drawbacks associated with the use of methyl bromide as a fumigant, efforts have been made to find and/or develop non-ozone depleting substitute pesticide fumigants.  One such substitute is sulfuryl fluoride (SF).  Although not an ozone depletor, SF is a colorless and odorless gas which is toxic if inhaled (MeBr gas is also toxic if inhaled).  SF is therefore a hazardous gas, and it is necessary to take stringent safety precautions and perform fumigations using only properly trained personnel using proper safety techniques.

Most fumigant systems in present use offer little, if any, control of the spent fumigant gas, even those involving the use of toxic and/or ozone depleting substances like MeBr and SF.  Frequently, all that is done is to maintain a safety perimeter (about 15 m) around the location so that any persons in the area will be at a safe inhalation distance when the spent fumigant is simply exhausted to the atmosphere (Swords et al., 2011).  Other systems offer some recovery of the spent fumigant; however, these systems use carbon absorption techniques that require activated carbon based filters and/or beds to capture the fumigant.2  The activated carbon does not destroy the fumigant but instead only holds the fumigant for a short time, eventually allowing it to be let back into the atmosphere.  Moreover, carbon based systems are only able to be used with MeBr and are ineffective when the fumigant is SF.  Thus, there is a need for improvement in this field.

 

MATERIALS AND METHODS

 

The scrubber functions to capture and destroy any harmful fumigant gas by a nucleophilic-substitution reaction. The F.A.S.T. system removes fumigant from a variety of fumigation situations including agricultural and non-agricultural commodities and/or stored products, structures and articles of value.  The system includes a fumigation chamber enclosing in a substantially gastight manner an area containing an object to be fumigated therein.  A fumigant gas having environmentally hazardous and/or toxic-to-humans properties is provided for introduction into the chamber.  A fumigant gas scrubber containing fumigant destruction properties is also provided.  A delivery system is employed for delivering the fumigant gas into the fumigation chamber and for delivering spent fumigant gas under pressure to the fumigant gas scrubber after the object has been fumigated. The scrubber functions to capture and destroy any harmful fumigant gas, such as for example methyl bromide or sulfuryl fluoride, which might otherwise be released to the atmosphere after fumigations (Swords et al., 2011).  The system can be used with pallets, shipping containers, fumigation chambers, trailers and is able to fumigate small buildings and bins from a truck-based mobile system.  Methyl bromide (MeBr) or sulfuryl fluoride (SF) is drawn out of the area fumigated by a regenerative air blower that forces contact with the scrubbing liquid through a multi-prong filter head.  The spent fumigant gas is agitated through the solution causing a chemical breakdown of the fumigant gas into liquid and other non-hazardous by-products (Swords et al., 2011).

 

SN2 Substitution Reaction:

The destruction process proceeds by the SN2 substitution reaction.  This can be explained as a reaction of an electron pair donor, which would be a nucleophile (Nu), with an electron pair acceptor, which is the electrophile.  The key to this reaction is that the electrophile must have a leaving group in order for the reaction to take place.  In this case it is the halide (X) shown in Fig. 1. The halides in fumigants are bromide (Br) and fluoride (F) in methyl bromide and sulfuryl fluoride.  The nucleophile that causes the breakdown is within the scrubbing solution.

Fig. 1 – Reaction of an electron pair donor, a nucleophile (Nu), with an electron pair acceptor, which is the electrophile and a leaving group halide (X).

The electron pair from the nucleophilic scrubbing solution attacks the electrophile which can be methyl bromide, sulfuryl fluoride or any other alkyl halide.  This nucleophilic attack takes place at the carbon or sulfur molecule at the center forming a new bond, while the leaving group, Br or F, departs with an electron pair.

 

System Workings

Following fumigation, the system is switched on from a 110 or 220 volt power source providing the necessary energy to run the system. The system employs a regenerative air blower that operates to draw out fumigant through a network of 4 and 2 inch piping to be delivered under pressure scrubbing solution depository. Once the air blower is running, the spent fumigant gas is drawn into the scrubber system inlet and travels through flexible tubing.  At the other end of the flexible tubing, a reducer reduces the diameter of the inlet opening.  At this point, the fumigant gas flows through piping and into the blower inlet.  At the air blower inlet, the fumigant gas then moves through the regenerative air blower building pressure and then is forced through the blower outlet.

Moving from the blower outlet, the spent fumigant gas then travels through piping into the scrubber inlet in the depository and through an agitator having a filter head positioned inside and towards the bottom of the depository. The depository, containing the special scrubbing liquid, may be a wide variety of volumes (currently the largest is 950 L [250 gal]).  The filter head, which is multi-pronged, is designed so that on each prong contains small apertures that allow the spent fumigant to bubble through (Swords et al., 2011).  Size of apertures may vary to provide the optimum range of bubbling size and/or agitation action so that the fumigant gas can be broken down chemically much easier as it travels through the scrubbing solution from the multi-prong filter head.  Spent fumigant gas bubbles through the scrubbing solution creating agitation and complete chemical breakdown of the gas introduced.  Ambient air is allowed to travel up and through the exhaust and non-toxic and environmentally non hazardous or ozone depleting by products are contained within the depository (Swords et al., 2011). Gas concentrations can be monitored throughout the entire scrubbing process.  The monitoring equipment provides readings of how much fumigant is left in the fumigation chamber, when the reading from the equipment within the chamber reads 0-0.0353 g m-3 (0-1 g/ft3), the process has been completed and sealing may be removed.  Two other locations are monitored for fumigant concentration including the exhaust from the scrubbing system and another monitoring line measuring ambient air surrounding the chamber and system.  Overall, the system within 10-15 minutes can completely remove fumigant from 28.3 m3 (1000ft3) but is subject to change with up scaling and further testing.  Our most common 950 L (250 gal) system allows more than 4 air exchanges per hour on land/sea containers or trailers and runs at a minimum of 6 m3/min (215 ft3/min).

Fig. 2-  Recent F.A.S.T. System Scrubber installed at Chicago O’Hare International Airport.

 

RESULTS FROM SCRUBBING PROCESS

 

Example 1:  F.A.S.T. System removing MeBr from  90 m3 (3200 ft3) trailer.

Date:  6/14/2011              Start Time:  4:00pm

MeBr:  6.8 kg (15 lb)                    Trailer:   90 m3 (3200 ft3)

Note:  Concentration measured in units of g m3 (oz/1000 ft3)

Filter:  Multi-head Filter

 

Table 1- F.A.S.T. System removing MeBr from  90 m3 trailer.

 

Time (min) Conc. Trailer

(g   m-3)Conc. Exhaust

(g   m-3)Conc. Air

(g   m-3)Corrected Conc.

(g   m-3)

0

128

0

0

0

5

67

2

2

0

10

28

3

2

1

15

27

1

2

0

20

24

2

1

1

25

20

1

1

0

30

14

1

1

0

35

7

1

1

0

40

5

1

1

0

45

2

1

1

0

50

1

1

1

0

 

 

Example 2:  F.A.S.T. System removing MeBr from 28 m3 (1000 ft3)fumigation chamber.

Date:  8/17/2011              Start Time:  3:45pm

MeBr:  0.7 kg (1.5 lb)                   Chamber:  28 m3 (1000 ft3)

Note:  Concentration measured in units of g m-3 (oz/1000 ft3)

Filter:  Multi-head Filter

 

Table 2- F.A.S.T. System removing MeBr from  28 m3 fumigation chamber.

 

Time (min) Conc. Chamber

(g   m-3)Conc. Exhaust

(g   m-3)Conc. Air

(g   m-3)Corrected Conc.

(g   m-3)

0

111

0

0

0

5

30

0

0

0

10

7

0

0

0

15

0

0

0

0

 

 

Example 3:  F.A.S.T. System removing SF from a 90 m3 (3200 ft3)trailer.

Date:  6/14/2011              Start Time:  5:25pm

SF:  6.4 kg  (14 lb)           Trailer:  90 m3 (3200 ft3)

Note:  Concentration measured in units of g m-3 (oz/1000 ft3)

Filter:  Multi-head Filter

 

 

Table 3- F.A.S.T. System removing SF from  90 m3 fumigation trailer.

 

Time (min) Conc. Trailer

(g   m-3)Conc. Exhaust

(g   m-3)Conc. Air

(g   m-3)Corrected Conc.

(g   m-3)

0

30

0

0

0

5

18

1

2

0

10

12

2

1

1

15

11

2

1

1

20

9

1

0

1

25

8

1

1

0

30

7

0

0

0

35

3

2

1

1

40

3

1

0

1

45

1

1

1

0

 

 

Example 4:  F.A.S.T. System removing SF from 28 m3 (1000 ft3)trailer.

Date:  7/1/2011  Start Time:  2:00pm

SF:  0.7 kg (1.5 lb)           Chamber:  28 m3 (1000 ft3)

Note:  Concentration measured in units of g m-3 (oz/1000 ft3)

Filter:  Multi-head Filter

 

Table 4- F.A.S.T. System removing SF from  28 m3 fumigation trailer.

 

Time (min.) Conc. Chamber

(g   m-3)Conc. Exhaust

(g   m-3)Conc. Air

(g   m-3)Corrected Conc.

(g   m-3)

0

70

0

0

0

5

20

2

2

0

10

5

2

2

0

15

3

0

0

0

20

1

0

0

0

 

 

Example 5:  Gas chromatograph analysis of F.A.S.T. System exhaust (small scale).

Fig. 3 represents the concentration of methyl bromide from the exhaust as a function of time.  This study was done on small scale within the lab hood using gas chromatograph analysis to determine the concentration of methyl bromide by peak area after gas has been scrubbed and allowed to flow through the exhaust.

 

Fig. 3- Gas chromatograph analysis of F.A.S.T. system exhausts showing concentration of methyl bromide as a function of time.

 

As can be seen in the above graph 100% methyl bromide has a concentration / peak area of over 1,000,000 units.  After scrubbing, the gas/air flow from exhaust is analyzed showing miniscule amounts of methyl bromide present.

 

Example 6:  Gas chromatograph (GC) analysis of scrubber exhaust from 794 L system (210 gal).

              Fig. 4 shows the results of GC analysis for the scrubber exhaust of the large scale 794 L system (210 gal) F.A.S.T. system.  The grey trace represents concentrated methyl bromide with overlays of the scrubber exhaust (the dotted line) and ambient air surrounding the system (solid black line). The results show no indications of methyl bromide present from the F.A.S.T. System exhaust as well as the surrounding ambient air.

 

 

Fig. 4  Gas chromatograph analysis and comparison of scrubber exhaust, ambient air and concentrated methyl bromide. The darker grey trace represents the peaks created from concentrated methyl bromide with overlays of the scrubber exhaust ( solid black line) and ambient air surrounding the system ( solid light grey line).

 

Scrubbing Solution Quenching:

After repeated use the scrubbing solution depletes and needs to be replaced.  This is the saturation point of the solution which is directly dependent on the molar ratio of fumigant to scrubbing material.  Our 946 L system (250 gal)system will destroy approximately 363 – 454 kg (800 – 1000 lb ) of methyl bromide or sulfuryl fluoride; however this is subject to change depending on the size of the system which can be customized to be more or less.  Upon reaching the saturation point, an over the counter – food grade neutralizing product is used as an additive to quench the scrubbing solution before disposal.  This quenching process lowers the pH of the solution making the scrubbing solution neutral.  The spent solution then has a low neutral pH and has a flash point of greater than 82.2oC (180°F) making it extremely non-flammable and non hazardous. Saturated material can be disposed of at a local waste management facility for a low, economical cost of less than $40 per 208 L (55 gal ) drum.

 

REFERENCES

 

Mueller, D. K. (2010). Reducing Customer Complaints in Stored Products. Carmel, Indiana: UN Communications.

 

Swords, P., VanRyckeghem, A., Mueller, D. (2011)  Current Methyl Bromide Recapture Technologies     and Uses.  MBAO Conference. San Diego, California, October 2011.

 

Methyl Bromide Recapture Slideshow

 

 

 

UN Decision on Recapturing/Recycling and Destruction of Methyl Bromide

Decision XVII/11: Recapturing/recycling and destruction of methyl bromide from space fumigation


prev-arrow up-arrow http://ozone.unep.org/new_site/en/Treaties/treaties_decisions-hb.php?nav_id=1239

Brain damage caused by hydrogen sulfide – American Journal of Industrial Medicine

Brain Damage Caused by Hydrogen Sulfide: A Follow-Up Study of Six Patients
by Bjarrn Tvedt, MA, Knut Skyberg, MD, Olaf Aaserud, MD, Anund Hobbesland, MD, and Tove Mathiesen, MA

Published in the American Journal of Industrial Medicine

Abstract

Hydrogen sulfide (H2S) poisoning involves a risk of hypoxic brain damage. Six patients who lost consciousness due to H2S poisoning are described. The symptoms varied from anosmia in the patient with the shortest but highest exposure to delayed neurological deterioration in the patient with the longest exposure. The two patients with the most serious symptoms developed pulmonary edema, which may have prolonged the hypoxia. The patients were reexaminated 5 years or more after the poisoning. The five patients who had been unconscious in H2S atmosphere for from 5 to 15-20 min showed persisting impairment at neurological and neuropsychological re-examination. Memory and motor function were most affected. One patient was seriously demented. Recent reports of large groups of H2S-poisoned workers probably underestimate the risk of sequelae, due to the inclusion of cases with exposure of short duration and lack of follow-up.

…..
Above abstract available from the US National Library of Medicine, National Institute of Health:  http://www.ncbi.nlm.nih.gov/pubmed/1867221.

Full document available from the California State University website:  http://www.csun.edu/~dorsogna/byron/H2Snew.pdf.

 

 

Basics of Landfill Gas (discusses human olfactory sensitivity to hydrogen sulfide)

Published by the Massachusetts Department of Environmental Protection (http://www.mass.gov/dep/recycle)

…..

Hydrogen Sulfide and Sulfides:
Sulfides are naturally occurring gasses that often give a landfill gas mixture its rotten egg smell. Sulfides
can cause unpleasant odors even at very low concentrations. Hydrogen sulfide is a colorless, flammable
gas and is one of the most common sulfides responsible for landfill odors. Some people can smell
hydrogen sulfide (individual’s odor threshold) at concentrations as low as 0.5 parts per billion (ppb).
However, the odor threshold can vary significantly among individuals based on the olfactory sensitivity of
the person. For many compounds, including hydrogen sulfide, there is a wide variability in published odor
thresholds (refer to Table 1). Odors alone cannot be relied upon as providing an early warning for
elevated concentrations of hydrogen sulfide. “At concentrations around 100 ppm,” (parts per million)
“no odor is detected due to a loss of olfactory sensation, resulting in loss of warning properties at lethal
levels.” (Integrated Risk Information System (IRIS)). Hydrogen sulfide is more dense than air, and
therefore, more likely to pool at lower elevations under still conditions, depending upon topography.

……..

Above paragraph is an excerpt from  Appendix A – Basics of Landfill Gas (Methane, Carbon Dioxide, Hydrogen Sulfide and Sulfides):  http://www.mass.gov/dep/recycle/laws/lfgasapp.pdf 

The full document is Control of Odorous Gas at Massachusetts Landfills (http://www.mass.gov/dep/recycle/laws/lfgaspol.pdf) published on the website of the

COMMONWEALTH OF MASSACHUSETTS
EXECUTIVE OFFICE OF ENVIRONMENTAL AFFAIRS
DEPARTMENT OF ENVIRONMENTAL PROTECTION

Toxicological Profile for Hydrogen Sulfide – U.S. Department Of Health And Human Services

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service
Agency for Toxic Substances and Disease Registry

July 2006

(The document introduction “Public Health Statement” is shown below.   The Table of Contents and a link to the full 253-page document are listed further down.)

1. PUBLIC HEALTH STATEMENT

This public health statement tells you about hydrogen sulfide and the effects of exposure to it.

The Environmental Protection Agency (EPA) identifies the most serious hazardous waste sites in
the nation. These sites are then placed on the National Priorities List (NPL) and are targeted for
long-term federal clean-up activities. Hydrogen sulfide has been found in at least 35 of the
1,689 current or former NPL sites. Although the total number of NPL sites evaluated for this
substance is not known, the possibility exists that the number of sites at which hydrogen sulfide
is found may increase in the future as more sites are evaluated. This information is important
because these sites may be sources of exposure and exposure to this substance may harm you.

When a substance is released either from a large area, such as an industrial plant, or from a
container, such as a drum or bottle, it enters the environment. Such a release does not always
lead to exposure. You can be exposed to a substance only when you come in contact with it.
You may be exposed by breathing, eating, or drinking the substance, or by skin contact.

If you are exposed to hydrogen sulfide, many factors will determine whether you will be harmed.
These factors include the dose (how much), the duration (how long), and how you come in
contact with it. You must also consider any other chemicals you are exposed to and your age,
sex, diet, family traits, lifestyle, and state of health.

…..

CONTENTS
DISCLAIMER ……………………………………………………………………………………………………………………………ii
UPDATE STATEMENT ……………………………………………………………………………………………………………..iii
FOREWORD …………………………………………………………………………………………………………………………….. v
QUICK REFERENCE FOR HEALTH CARE PROVIDERS…………………………………………………………..vii
CONTRIBUTORS……………………………………………………………………………………………………………………..ix
PEER REVIEW …………………………………………………………………………………………………………………………xi
CONTENTS…………………………………………………………………………………………………………………………….xiii
LIST OF FIGURES …………………………………………………………………………………………………………………xvii
LIST OF TABLES……………………………………………………………………………………………………………………xix
1. PUBLIC HEALTH STATEMENT……………………………………………………………………………………………. 1
1.1 WHAT IS HYDROGEN SULFIDE?……………………………………………………………………………… 1
1.2 WHAT HAPPENS TO HYDROGEN SULFIDE WHEN IT ENTERS THE
ENVIRONMENT? ………………………………………………………………………………………………………. 2
1.3 HOW MIGHT I BE EXPOSED TO HYDROGEN SULFIDE? …………………………………………. 2
1.4 HOW CAN HYDROGEN SULFIDE ENTER AND LEAVE MY BODY? ………………………… 3
1.5 HOW CAN HYDROGEN SULFIDE AFFECT MY HEALTH? ……………………………………….. 4
1.6 HOW CAN HYDROGEN SULFIDE AFFECT CHILDREN?…………………………………………… 5
1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO HYDROGEN
SULFIDE?…………………………………………………………………………………………………………………. 6
1.8 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN
EXPOSED TO HYDROGEN SULFIDE? ………………………………………………………………………. 6
1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO
PROTECT HUMAN HEALTH?……………………………………………………………………………………. 7
1.10 WHERE CAN I GET MORE INFORMATION? …………………………………………………………….. 8
2. RELEVANCE TO PUBLIC HEALTH ……………………………………………………………………………………… 9
2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO HYDROGEN
SULFIDE IN THE UNITED STATES …………………………………………………………………………… 9
2.2 SUMMARY OF HEALTH EFFECTS………………………………………………………………………….. 10
2.3 MINIMAL RISK LEVELS (MRLs) …………………………………………………………………………….. 14
3. HEALTH EFFECTS…………………………………………………………………………………………………………….. 21
3.1 INTRODUCTION…………………………………………………………………………………………………….. 21
3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE ……………………………. 21
3.2.1 Inhalation Exposure ……………………………………………………………………………………………….. 22
3.2.1.1 Death ……………………………………………………………………………………………………………. 22
3.2.1.2 Systemic Effects …………………………………………………………………………………………….. 26
3.2.1.3 Immunological and Lymphoreticular Effects……………………………………………………… 61
3.2.1.4 Neurological Effects……………………………………………………………………………………….. 62
3.2.1.5 Reproductive Effects ………………………………………………………………………………………. 68
3.2.1.6 Developmental Effects ……………………………………………………………………………………. 70
3.2.1.7 Cancer………………………………………………………………………………………………………….. 71
3.2.2 Oral Exposure……………………………………………………………………………………………………….. 72
3.2.2.1 Death ……………………………………………………………………………………………………………. 72
3.2.2.2 Systemic Effects …………………………………………………………………………………………….. 72
3.2.2.3 Immunological and Lymphoreticular Effects……………………………………………………… 73

3.2.2.4 Neurological Effects……………………………………………………………………………………….. 73
3.2.2.5 Reproductive Effects ………………………………………………………………………………………. 73
3.2.2.6 Developmental Effects ……………………………………………………………………………………. 73
3.2.2.7 Cancer………………………………………………………………………………………………………….. 73
3.2.3 Dermal Exposure……………………………………………………………………………………………………. 73
3.2.3.1 Death ……………………………………………………………………………………………………………. 73
3.2.3.2 Systemic Effects …………………………………………………………………………………………….. 74
3.2.3.3 Immunological and Lymphoreticular Effects……………………………………………………… 74
3.2.3.4 Neurological Effects……………………………………………………………………………………….. 74
3.2.3.5 Reproductive Effects ………………………………………………………………………………………. 75
3.2.3.6 Developmental Effects ……………………………………………………………………………………. 75
3.2.3.7 Cancer………………………………………………………………………………………………………….. 75
3.3 GENOTOXICITY ……………………………………………………………………………………………………… 75
3.4 TOXICOKINETICS………………………………………………………………………………………………….. 75
3.4.1 Absorption……………………………………………………………………………………………………………. 76
3.4.1.1 Inhalation Exposure………………………………………………………………………………………… 76
3.4.1.2 Oral Exposure………………………………………………………………………………………………… 76
3.4.1.3 Dermal Exposure ……………………………………………………………………………………………. 77
3.4.2 Distribution …………………………………………………………………………………………………………… 77
3.4.2.1 Inhalation Exposure………………………………………………………………………………………… 77
3.4.2.2 Oral Exposure………………………………………………………………………………………………… 79
3.4.2.3 Dermal Exposure ……………………………………………………………………………………………. 79
3.4.2.4 Other Routes of Exposure ……………………………………………………………………………….. 79
3.4.3 Metabolism…………………………………………………………………………………………………………… 79
3.4.4 Elimination and Excretion……………………………………………………………………………………….. 82
3.4.4.1 Inhalation Exposure………………………………………………………………………………………… 82
3.4.4.2 Oral Exposure………………………………………………………………………………………………… 82
3.4.4.3 Dermal Exposure ……………………………………………………………………………………………. 83
3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models …………. 83
3.5 MECHANISMS OF ACTION …………………………………………………………………………………….. 84
3.5.1 Pharmacokinetic Mechanisms………………………………………………………………………………….. 84
3.5.2 Mechanisms of Toxicity………………………………………………………………………………………….. 86
3.5.3 Animal-to-Human Extrapolations …………………………………………………………………………….. 88
3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS…………………….. 88
3.7 CHILDREN’S SUSCEPTIBILITY………………………………………………………………………………. 89
3.8 BIOMARKERS OF EXPOSURE AND EFFECT ………………………………………………………….. 91
3.8.1 Biomarkers Used to Identify or Quantify Exposure to Hydrogen Sulfide ………………………. 92
3.8.2 Biomarkers Used to Characterize Effects Caused by Hydrogen Sulfide ………………………… 93
3.9 INTERACTIONS WITH OTHER CHEMICALS ………………………………………………………….. 93
3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE……………………………………….. 95
3.11 METHODS FOR REDUCING TOXIC EFFECTS…………………………………………………………. 95
3.11.1 Reducing Peak Absorption Following Exposure …………………………………………………….. 96
3.11.2 Reducing Body Burden……………………………………………………………………………………….. 97
3.11.3 Interfering with the Mechanism of Action for Toxic Effects ……………………………………. 97
3.12 ADEQUACY OF THE DATABASE……………………………………………………………………………. 98
3.12.1 Existing Information on Health Effects of Hydrogen Sulfide …………………………………… 98
3.12.2 Identification of Data Needs ………………………………………………………………………………. 100
3.12.3 Ongoing Studies……………………………………………………………………………………………….. 107

4. CHEMICAL AND PHYSICAL INFORMATION…………………………………………………………………… 109
4.1 CHEMICAL IDENTITY…………………………………………………………………………………………… 109
4.2 PHYSICAL AND CHEMICAL PROPERTIES……………………………………………………………. 109
5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL…………………………………………………. 113
5.1 PRODUCTION ……………………………………………………………………………………………………….. 113
5.2 IMPORT/EXPORT ………………………………………………………………………………………………….. 113
5.3 USE……………………………………………………………………………………………………………………….. 114
5.4 DISPOSAL…………………………………………………………………………………………………………….. 114
6. POTENTIAL FOR HUMAN EXPOSURE …………………………………………………………………………….. 115
6.1 OVERVIEW…………………………………………………………………………………………………………… 115
6.2 RELEASES TO THE ENVIRONMENT…………………………………………………………………….. 118
6.2.1 Air …………………………………………………………………………………………………………………….. 118
6.2.2 Water…………………………………………………………………………………………………………………. 119
6.2.3 Soil ……………………………………………………………………………………………………………………. 120
6.3 ENVIRONMENTAL FATE………………………………………………………………………………………. 121
6.3.1 Transport and Partitioning……………………………………………………………………………………… 121
6.3.2 Transformation and Degradation ……………………………………………………………………………. 122
6.3.2.1 Air……………………………………………………………………………………………………………… 122
6.3.2.2 Water ………………………………………………………………………………………………………….. 122
6.3.2.3 Sediment and Soil…………………………………………………………………………………………. 123
6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT…………………………. 123
6.4.1 Air …………………………………………………………………………………………………………………….. 124
6.4.2 Water…………………………………………………………………………………………………………………. 127
6.4.3 Sediment and Soil ………………………………………………………………………………………………… 127
6.4.4 Other Environmental Media…………………………………………………………………………………… 128
6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE ………………………………. 129
6.6 EXPOSURES OF CHILDREN………………………………………………………………………………….. 131
6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ……………………………………. 132
6.8 ADEQUACY OF THE DATABASE………………………………………………………………………….. 132
6.8.1 Identification of Data Needs ………………………………………………………………………………….. 133
6.8.2 Ongoing Studies …………………………………………………………………………………………………… 135
7. ANALYTICAL METHODS ………………………………………………………………………………………………… 137
7.1 BIOLOGICAL MATERIALS……………………………………………………………………………………. 137
7.2 ENVIRONMENTAL SAMPLES……………………………………………………………………………….. 143
7.3 ADEQUACY OF THE DATABASE………………………………………………………………………….. 151
7.3.1 Identification of Data Needs ………………………………………………………………………………….. 151
7.3.2 Ongoing Studies …………………………………………………………………………………………………… 152
8. REGULATIONS AND ADVISORIES ………………………………………………………………………………….. 153
9. REFERENCES ………………………………………………………………………………………………………………….. 159
10. GLOSSARY ……………………………………………………………………………………………………………………. 201

……

Full document:  http://www.atsdr.cdc.gov/toxprofiles/tp114-p.pdf

Toxicological Review of Hydrogen Sulfide – U.S. Environmental Protection Agency

Link to Full Document:  http://www.epa.gov/IRIS/toxreviews/0061tr.pdf

…..

MAJOR CONCLUSIONS IN THE CHARACTERIZATION OF HAZARD AND DOSE RESPONSE

6.1. HAZARD IDENTIFICATION

Hydrogen sulfide is a colorless gas and has a strong odor of rotten eggs. Its primary uses include the production of elemental sulfur and sulfuric acid, the manufacture of heavy water and other chemicals, in metallurgy, and as an analytical reagent. Although quantitative data are lacking, toxicity studies suggest that H2S gas is absorbed rapidly through the lungs. Oral exposure is not likely to occur. In animals and humans, it distributes to the blood, brain, lung, heart, liver, spleen, and kidney. Oxidation is the primary metabolic pathway for H2S, with thiosulfate and sulfate as metabolites. Metabolism in laboratory animals and in humans appears to be similar. Hydrogen sulfide is excreted in the urine.

Human data pertaining to inhalation exposure (the expected route of ambient exposure) consist of a plethora of case reports and a variety of occupational epidemiological studies. Although these studies have limitations that preclude their use for quantitative risk assessment, they indicate that exposure to H2S (at high concentrations) has profound effects on the respiratory system leading to unconsciousness with attendant neurologic sequelae and, sometimes, death. An increase in cardiovascular-related deaths due, in part, to H2S exposure was reported in one occupational study.

Inhalation studies in adult rodents demonstrate sensitivity of nasal olfactory epithelium to low concentrations of H2S. The RfC is based on these lesions. Limited evidence suggests that exposure of humans to low concentrations may also cause neurologic symptoms although quantitative exposure-response data is lacking. Because of similar access of inhaled H2S to the olfactory tissues of humans, these lesions are likely of relevance to humans and a reasonable choice as a critical effect. Relevance to olfactory lesions seen in rodents to humans is also suggested by Hirsch and Zavala (1999) who reported decreased persistent olfactory function in workers exposed to hydrogen sulfide chronically. Whereas adverse nasal effects are of relevance and concern in adult human exposure scenarios, inhalation studies of perinatal or neonatal exposure in rats demonstrates abnormal cellular development in the brain as well as significant alterations in neurotransmitter levels; the toxicological significance of these findings is uncertain.

Relevant quantitative human oral toxicity data are not available and ingestion is not a likely route of exposure. An RfD based on GI disturbances in pigs consuming feed containing hydrogen sulfide was derived in the previous IRIS entry. A review of the RfD (see Section 4.2.1) indicates that the effects on which that value were based are not reproducible and probably not related to H2S. Therefore the previous RfD will be withdrawn and a new RfD will not be derived based on data base deficiencies.

The indicators of a possible effect noted in the developing brain cells of newborn rats indicate the possibility that the developing human fetus could also be at risk. The exposure levels producing these effects, however, are in the same range or somewhat higher than those producing the critical sentinel clearly adverse effect (nasal tract lesions) in adult animals, thereby ameliorating the concern that young animals (and possibly children) may be especially susceptible to the effects from relatively low-level chronic exposures to hydrogen sulfide. Other observations in the data base do indicate a possible concern regarding the susceptibility of children exposed to high levels of H2S, i.e., > 600 ppb. However, the relevance of this apparent susceptibility at environmental levels of H2S where toxicity is not likely to occur, such as the RfC value derived herein, is not at all clear.

There is no evidence indicating that H2S exposure is associated with carcinogenesis. Under the Draft Revised Guidelines for Carcinogen Risk Assessment (U.S. EPA, 1999), data are inadequate for an assessment of the carcinogenic potential of hydrogen sulfide.

…..

Link to Full Document:  http://www.epa.gov/IRIS/toxreviews/0061tr.pdf

Hydrogen sulfide needs Hazardous Air Pollutant listing under CAA Title III – Sierra Club letter to EPA administrator Lisa Jackson

Nonprofit sign-on letter to EPA administrator Lisa Jackson
Published: March 30, 2009

Intro/Letter excerpt:  (from http://www.earthworksaction.org/library/detail/hydrogen_sulfide_needs_hazardous_air_pollutant_listing_under_caa_title_iii)

The community, environmental, and public health organizations named below request that you formally list Hydrogen Sulfide (H2S) as a hazardous air pollutant (HAP), as defined in Title III, section 112(b) of the 1990 Clean Air Act Amendments (CAA). We assert that EPA must act to address adverse H2S impacts based on evidence of harmful exposures in numerous communities and its toxicological effects at low concentrations such as non-cancer effects and emerging evidence that H2S is a genotoxic agent, meaning it damages DNA. EPA has assessed the need to list H2S as a HAP, but no formal listing action has been taken. H2S is clearly an unlisted hazardous air pollutant.

……
(Full letter can be viewed at: http://www.earthworksaction.org/files/publications/H2SLetterToEPA.pdf)
……

Conclusion  

Public health scientists have recognized for over a decade that hydrogen sulfide is a potent neurotoxin, and chronic
exposure to low ambient levels causes irreversible damage to the brain and central nervous system. Ultra-low levels
of H2S down to 25 ppb have been associated with acute exposure causing eye irritation in community settings in the
United States, Europe and New Zealand. Now emerging scientific evidence supports H2S causes neuron death,
confirming findings by Kilburn of irreversible brain damage. The latest scientific findings suggest H2S causes DNA
damage as a genotoxic agent, which EPA can no longer ignore. The potential carcinogenic implications of H2S
demand that EPA act to protect public health.

Children are among the most susceptible to this poison gas, and EPA needs to do a more effective job of protecting
schoolchildren from H2S impacts. Today, it is unacceptable for communities to have to continue suffering the ill
effects of H2S when the technology to monitor and control H2S emissions exists. As EPA has learned in the last four
decades, environmental injustice is a significant fact of life for thousands of communities in this nation and these
residents all have a right to clean, safe air.

It’s time for the EPA to take action to formally acknowledge hydrogen sulfide’s clear toxicity at low concentrations.
As Administrator, you have CAA authority under section 112(b)(2) to act based on a pollutant that poses or may
pose “…a threat of adverse human health effects…” Health studies confirm the need for EPA to list H2S under
section 112(b) of the CAA and Title III, since routine daily exposure effects are not addressed under the accidental
release provisions in section 112(r) of the CAA, where H2S is currently regulated. However, section 112(r) is not
designed or intended to address daily exposures at sublethal concentrations, but section 112(b) can bridge this gap.

EPA, in addition, needs to require annual reporting of H2S as a toxic substance under the Toxic Release Inventory
(TRI) reporting program, since H2S is not reported due to an administrative stay issued August 22, 1994 evidently
under a legal threat by the American Petroleum Institute. It’s extraordinary that industry has delayed reporting of
H2S for twenty years. EPA needs a TRI reporting threshold of 1.0 pound for H2S and not 10,000 pounds as was
originally the requirement. We request that EPA immediately lift the administrative stay on H2S and require TRI
reporting in the next TRI submission cycle. The TRI data would also help EPA compile more accurate H2S data.

Please respond to this request for EPA to take action to list H2S under section 112(b) of the CAA. Address the
EPA’s response to Neil Carman at the contact information listed below.

Respectfully yours,

Neil J. Carman, Ph.D.
Sierra Club’s Clean Air Team and the
Lone Start Chapter of the Sierra Club
1202 San Antonio St, Austin, TX 78701
Tel 512-472-1767; Fax 512-477-8526

(This letter was also sent/signed by the following organizations:   National Environmental Justice and Community Partnerships Director; Citizens for Environmental Justice; Community In-Powerment and Development Association; Earthjustice Legal Defense Fund; Environmental Integrity Project; Galveston Houston Association for Smog Prevention & Mothers for Clean Air; Global Community Monitor, National Refinery Reform Campaign & National Bucket Brigade Coalition; Downwinders At Risk; Groups Allied to Stop Pollution; The People’s Advocate; Lower Mississippi Riverkeeper; Louisiana Environmental Action Network; EARTHWORKS’, and Oil & Gas Accountability Project; San Juan Citizens Alliance; Sustainable Energy & Economic Development Coalition; Citizens Against Environmental Destruction; Northeast Ohio Gas Accountability Project; Huron Environmental Activist League; Don’t Waste Arizona; Cook Inletkeeper; Protect All Children’s Environment.)

Long-term effects on the olfactory system of exposure to hydrogen sulphide

Published in the journal of “Occupational & Environmental Medicine” (http://oem.bmj.com)

Abstract (with author affiliations & other articles citing this article):  http://oem.bmj.com/content/56/4/284.abstract)
Full document:  http://oem.bmj.com/content/56/4/284.full.pdf+html

By Alan R Hirsch, Gilberto Zavala

Abstract 

Objective—To study chronic effects of hydrogen sulphide (H2S) on cranial nerve I (nervi olfactorii), which have been only minimally described.

Methods—Chemosensations (smell and taste) were evaluated in eight men who complained of continuing dysfunction 2–3 years after the start of occupational exposure to H2S. Various bilateral (both nostrils) and unilateral (one nostril at a time) odour threshold tests with standard odorants as well as the Chicago smell test, a three odour detection and identification test and the University of Pennsylvania smell identification test, a series of 40 scratch and sniff odour identification tests were administered.

Results—Six of the eight patients showed deficits of various degrees. Two had normal scores on objective tests, but thought that they continued to have problems. H2S apparently can cause continuing, sometimes unrecognised olfactory deficits.

Conclusion—Further exploration into the extent of such problems among workers exposed to H2S is warranted.

(Occup Environ Med 1999;56:284–287)

 

Occupational and Environmental Medicine (OEM) is an international peer reviewed journal covering current developments in occupational and environmental health worldwide. Original contributions include: epidemiological studies of health concerns related to exposures in the workplace and the environment; human studies employing biological and genomic techniques to investigate the effects of such exposures; exposure assessment studies; evidence based research on the practice of occupational medicine, and new research methods.

Hydrogen Sulfide, Oil and Gas, and People’s Health

Document obtained from the “Energy and Resources Group” (http://erg.berkeley.edu) of The University of California, Berkeley

By Lana Skrtic

Submitted in partial satisfaction of the requirements for the degree of
Master’s of Science
May 2006
Energy and Resources Group
University of California, Berkeley

Full Document:  PDF File

 

8. Concluding Remarks

The literature on human health and hydrogen sulfide reveals serious and lasting physiological and neurological effects associated  with acute exposure.  The health effects of chronic exposure to lower levels of H2S, as documented in several studies, also include persistent physiological and neurological disturbances.   Oil and gas facilities can be expected to accidentally and routinely emit hydrogen sulfide in concentrations that span a wide range and are associated with a variety of health effects.  Academic studies, my conversations with health department staff, and available data from monitoring projects help establish that hydrogen sulfide is indeed present near oil and gas facilities.

Because people live near oil and gas sites, emissions of H2S may be routinely compromising human health.  The interviews I conducted with people who live close to oil and gas facilities, as well as some research reported in the Literature  Review section, provide evidence of health impacts from exposure to H2S emitted by oil and gas development.  Although the anecdotal  evidence from my interviews is vulnerable to criticism that other pollutants or individual health factors may be responsible for the symptoms, the reported health effects are consistent with hydrogen sulfide exposure.  The fact that concentrations of H2S to which people are exposed are often not known does not imply that hydrogen sulfide is  not the cause of the observed health effects.  The lack of precise exposure data is,  however, one area that future research should address.

……..

As I show in the Regulations and Recommendations section, at the federal level, the oil and gas industry and the paper and pulp industry have exerted their influence to prevent H2S from being included on the Clean Air Act’s Hazardous Air Pollutants (HAPs) list, and to exempt it from reporting under the EPA’s Toxic Release Inventory (TRI).  At the time of writing, the EPA is reviewing both decisions, which at the very least indicates that some concern exists over the lack of stricter regulation of hydrogen sulfide at the federal level.  The level of regulation of hydrogen sulfide varies widely across the states that have established an ambient standard in the absence of a federal one, but again, the very  existence of ambient standards suggests that hydrogen sulfide is a concern.

Monitoring of ambient H2S is necessary to determine exactly how much is being emitted and to clarify the link between exposure and health effects.  Enough evidence of routine H2S emissions at oil and gas facilities emerges from my conversations with health department personnel, interviews with people living near oil and gas sites, several studies summarized in the Literature Review section, and state monitoring projects to merit more comprehensive monitoring.  The lack of federal standards for ambient H2S levels or for emissions of H2S is one reason for sparse monitoring even at state level, since state health / environmental departments largely depend on federal funding for their projects.  More routine and special project monitoring would facilitate conducting community health studies, by providing accurate exposure data that could be matched with observed health effects.

In light of the information presented here on the health effects associated with exposure to hydrogen sulfide, even though rigorous data on the dose-response relationship is lacking, it is irresponsible and callous to delay making some public policy decisions that would help protect human health.

Human Impairment From Living Near Confined Animal (Hog) Feeding Operations (CAFO’S)

Research Article published in the Journal of Environmental and Public Health (http://www.hindawi.com/journals/jeph/aip/565690/)

Full PDF file

HUMAN IMPAIRMENT FROM LIVING NEAR CONFINED ANIMAL (HOG) FEEDING OPERATIONS (CAFO’S)

Kaye H. Kilburn, M.D.

Ralph Edgington Professor of Internal Medicine
University of Southern California
Keck School of Medicine (ret.)
President- Neuro-test Inc.

ABSTRACT

Problem  To determine whether neighbors around manure lagoons and massive hog confinement buildings who complained of offensive odors and symptoms had impaired brain and lung function.

Method  We compared near hog manure neighbors of lagoons to people living beyond 3 kilometers in Ohio and to unexposed people controls in a nearby state for neurophysiological, cognitive, recall and memory functions, and pulmonary performance.

Results  The 25 exposed subjects averaged 4.3 neurobehavioral abnormalities, significantly different from 2.5 for local controls and 2.3 for Tennessee controls. Exposed subjects mean forced vital capacity and expiratory volume in 1 sec. were reduced significantly compared to local and regional controls.

Conclusions  Near neighbors of hog enclosures and manure lagoon gases had impaired neurobehavioral functions and pulmonary functions and these effects extended to nearby people thought to be controls. Hydrogen sulfide must be abated because people living near lagoons can not avoid rotten egg gas.

Hydrogen Sulfide: Health Effects (from “Agency for Toxic Substance & Disease Registry” – CDC)

This 88-page document is “Chapter 3″ pulled from the “Agency for Toxic Substance & Disease Registry” (http://www.atsdr.cdc.gov/toxprofiles/index.asp) provided by the government’s “Centers for Disease Control and Prevention” (http://www.cdc.gov).

3. HEALTH EFFECTS

3.1 INTRODUCTION

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and
other interested individuals and groups with an overall perspective on the toxicology of hydrogen sulfide.
It contains descriptions and evaluations of toxicological studies and epidemiological investigations and
provides conclusions, where possible, on the relevance of toxicity and toxicokinetic data to public health.

3.2 Discussion of health effects by route of exposure
3.3 Genotoxicity
3.4 Health effects in wildlife potentially relevant to human health
3.5 Toxicokinetics
3.5 Mechanisms of action
3.6 Toxicities mediated through the neuroendocrine axis
3.7 Children’s susceptibility
3.8 Biomarkers of exposure and effect
3.9 Interactions with other chemicals
3.10 Populations that are unusually susceptible
3.11 Methods for reducing toxic effects
3.12 Adequacy of the database

…..

The full chapter on Health Effects can be read online:  http://www.atsdr.cdc.gov/toxprofiles/tp114-c3.pdf.

The full Toxicological Profile for Hydrogen Sulfide (all chapters) can be referenced at:  http://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=389&tid=67 

Health Effects and Evaluation of Human Health Risks – Air Quality Guidelines (Ch 6: Hydrogen Sulfide)

Below is an excerpt of the chapter on Hydrogen Sulfide from “Air Quality Guidelines for Europe, Second Edition” published by the World Health Organization, Regional Office for Europe, Copenhagen.

6.6 Hydrogen sulfide

Exposure evaluation
Typical symptoms and signs of hydrogen sulfide intoxication are most
often caused by relatively high concentrations in occupational exposures.
There are many occupations where there is a potential risk of hydrogen
sulfide intoxication and, according to the US National Institute for Occupational
Safety and Health (1), in the United States alone approximately
125 000 employees are potentially exposed to hydrogen sulfide. Low-level
concentrations can occur more or less continuously in certain industries,
such as in viscose rayon and pulp production, at oil refineries and in geothermal
energy installations.

In geothermal areas there is a risk of exposure to hydrogen sulfide for the
general population (2). The biodegradation of industrial wastes has been
reported to cause ill effects in the general population (2). An accidental
release of hydrogen sulfide into the air surrounding industrial facilities can
cause very severe effects, as at Poza Rica, Mexico, where 320 people were
hospitalized and 22 died (2). The occurrence of low-level concentrations of
hydrogen sulfide around certain industrial installations is a well known fact.

Health risk evaluation
The first noticeable effect of hydrogen sulfide at low concentrations is its
unpleasant odour. Conjunctival irritation is the next subjective symptom
and can cause so-called “gas eye” at hydrogen sulfide concentrations of 70–
140 mg/m3. Table 16 shows the established dose–effect relationships for
hydrogen sulfide.

The hazards caused by high concentrations of hydrogen sulfide are relatively
well known, but information on human exposure to very low concentrations
is scanty. Workers exposed to hydrogen sulfide concentrations
of less than 30 mg/m3 are reported to have rather diffuse neurological and
mental symptoms (4) and to show no statistically significant differences
when compared with a control group. On the other hand, changes in haem
synthesis have been reported at hydrogen sulfide concentrations of less than
7.8 mg/m3 (1.5–3 mg/m3 average) (5). It is not known whether the inhibition
is caused by the low concentrations or by the cumulative effects of
occasional peak concentrations. Most probably, at concentrations below
1.5 mg/m3 (1 ppm), even with exposure for longer periods, there are very
few detectable health hazards in the toxicological sense. The malodorous

property of hydrogen sulfide is a source of annoyance for a large proportion
of the general population at concentrations below 1.5 mg/m3, but from the
existing data it cannot be concluded whether any health effects result. The
need for epidemiological studies on possible effects of long-term, low-level
hydrogen sulfide exposure is obvious. A satisfactory biological exposure
indicator is also needed.

The full text excerpt of the chapter on Hydrogen Sulfide can be read here:  AQG2ndEd_6_6Hydrogensulfide.
The full document can be read online:  http://www.euro.who.int/__data/assets/pdf_file/0005/74732/E71922.pdf.

 


U.S. Geological Survey: Materials Flow of Sulfur

By Joyce A. Ober

(from page 48)
…..

Losses during handling and shipping solid bulk sulfur have been significant in the past, although difficult to quantify. When sulfur was poured to block in the early days of the industry, the solid material was broken up and moved with bulldozers, creating a tremendous problem with fine sulfur dust. The fine particles were difficult to contain and could be blown great distances on the wind.  In addition to contaminating the area adjacent to the production locations, contamination was a problem along rail lines and at port facilities. Of even more concern than the dust contamination was the hazardous nature of the sulfur dust. Finely divided sulfur presents explosive and fire hazards, and the SO2 generated by such a fire is toxic (West, 1966).48

Because of these issues, regulations were established to limit shipments of crushed and broken sulfur. Several processes have been developed to minimize the loss and lessen the hazards in handling solid sulfur. Domestically, nearly all sulfur is shipped molten, avoiding any of the dusting problems associated with bulk sulfur. If sulfur is poured to block in the U.S. Gulf Coast area, then it is mechanically broken and passed through a melter before it is shipped from the storage site in molten form. During this processing, dust is kept to a minimum by containing dust inside the outer walls of the sulfur block. Most sulfur produced in California and Washington is shipped overseas. To make this material acceptable for bulk transport, the molten sulfur is processed in forming apparatus that solidifies the sulfur into distinct particles, such as granules, pastilles, prills, and slates, that resist breakage, significantly reducing the fines problems during handling. Additional dust suppression techniques include covered conveyors systems, dust collectors, and enclosed railcar unloading facilities with water sprays. These innovations have reduced losses during handling to a minimum.
…..

Open-File Report 02-298 [4.3-MB PDF file]
Full text version [178 KB]

Contact Information
For questions about the scientific content of this report, contact Joyce Ober.

U.S. Department of the Interior, U.S. Geological Survey
URL: http://pubs.usgs.gov/of/2002/of02-298/index.html
Maintained by Publishing Services
Last modified: 15:40:44 Thu 13 Feb 2003
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Wind Rose

Smith Field/Beaufort Windrose Plot

Wind rose

Fairy Tales and Facts and Omissions – Elisabeth Gray, Chemist

Elisabeth Gray (Chemist from Vanderbilt University) responds with factual rebuttals to erroneous (“fictional”) statements being circulated:

1. Fiction: For years, PCS Phosphate has been conducting the same operations at RadioIsland as they now propose to accomplish at the MHC state port facility.

2. Fiction: The annual emissions into the air will not be changed by the additional processesof moving and melting bulk formed solid sulfur.

3. Fiction: We already have phosphate dust. Sulfur dust is no different or worse than phosphate dust.

Omissions. The documents submitted by PCS to Air Quality seem to furnish contradictoryinformation about the operations that might be the most critical to our environment, theunloading of solid sulfur, the moving of solid sulfur from place to place and transferring solidsulfur to the melting pots.

Her detailed responses are found in the attached document:  PCS July 21-Elisabeth.

Elisabeth also poses some additional questions about issues that need to be specifically addressed by PCS Phosphates:

1. Why are the oxides of nitrogen not modeled? The primary EPA standard for nitrogen dioxide established in April 2010 is 100 ppb.  According to the PCS data in their environmental statement, over 121 times as many molecules of the oxides of nitrogen will be produced as molecules of sulfur dioxide.

2. How is the solid sulfur to be handled? In a closed or an open system?

3. If the system is closed, how much water/day will be used to achieve a 3% by mass of water to bulk sulfur?

4. How will this water be handled after it is sprayed on the sulfur?

5. If the system is an open one, how will the sulfur dust produced be prevented from entering the surrounding waters?

6. How will PCS dispose of this sulfur dust?

7. Will PCS fund a manned, fire station with well trained personnel in the event that a catastrophe occurs? Local capability does not exist.

8. Can we get an Environmental Impact Statement? How? Why not?

9. Is there a Hurricane Preparedness plan?

Sulfur Dioxide (general info) – Wisconsin Department of Health Services

Highlights…

“Sulfur dioxide dissolves easily in water to form sulfuric acid. Sulfuric acid is a major component of acid rain. Acid rain can damage forests and crops, change the acidity of soils, and make lakes and streams acidic and unsuitable for fish. Sulfur dioxide also contributes to the decay of building materials and paints, including monuments and statues.”

“People who live near industrial sources of sulfur dioxide may be exposed to it in the air.”

“Short term exposure to high enough levels of SO2 can be life threatening. Generally, exposures to SO2 cause a burning sensation in the nose and throat. Also, SO2 exposure can cause difficulty breathing, including changes in the body’s ability to take a breath or breathe deeply, or take in as much air per breath. Long term exposure to sulfur dioxide can cause changes in lung function and aggravate existing heart disease. Asthmatics may be sensitive to changes in respiratory effects due to SO2 exposure at even low concentrations.”

Full document…

Air pollutants from the planned sulfur melting project

Abbreviated synopsis of the human toxic potential of the most likely air pollutants as described in the environmental assessment from the planned sulfur melting project in Morehead City, NC – James E. Gibson, Ph.D., Fats Professor of Pharmacology and Toxicology the Brody School of Medicine at ECU

Scanned document