Haulbowline Opinion

Dust to dust… Part 1

2008-08-21T14:24:00.003+01:00

Toxic waste

By Marcus O’Garvey (Haulbowline) with thanks for the info to Metal Man (Sligo IT), Boffin Island (Haulbowline), Pat the Barker (Limerick), Tralee Rose and Others, 21 August 2008.

Note: This blog entry grew exponentially! Due to its large eventual size (it links out to a separate web page below) we have also made it available as a PDF file for download together with Part 2: Health risk.

DEPENDING on wind direction, humidity and rainfall (or lack of), the County Cork residents of Cobh, Ringaskiddy, Monkstown as well as Naval Service personnel, Irish Steel/Ispat and other civilian workers on Haulbowline Island itself have all suffered the horrors of airborne pollution from the Cork Harbour steelworks and all its associated industrial activities over the years.

To the great shame of this country and of its present Green-tinged government in particular, the air pollution from the site is an ongoing threat to human health. This despite the cessation of smelting by Irish Ispat in 2001 – which went into voluntary liquidation to deliberately avoid the costs of cleaning-up their act and paying damages, and got away with it by passing the buck to a government stupid enough to take it.

Haulbowline continues to tarnish the image of County Cork and the mighty Cork Harbour, scene of the illustrious Cork Week sailing races and port of call for luxury cruise liners. Forget the clean and green image; former Ispat is a toxic brownfield site resembling the worst industrial blackspots of Soviet era Eastern Europe. The legacy of importing by road and sea, from Ireland and across Europe, breaking-up and smelting scrap metal – meaning anything from ‘end of life vehicles’ to old factory fittings – is the dumping of great volumes of hazardous waste residue. This is a mixture of ferrous and non-ferrous metals, plastics, PVC, rubber, glass, asbestos, tyres, lead batteries, battery acid, engine oil, oil filters, hydraulic fluids, and electric arc furnace wastes (EAF dust, refractory linings, slag, cinders, soot, mill scale, and reject metal), plus other industrial rubbish such as oily sludge and acid waste from the metal curing and zinc galvanising baths.

The East Tip is composed of this dangerous muck cocktail. That is, the 9 hectares of the 35 hectare Haulbowline Island that ‘grew’ (by 2.5 hectares) during Ispat’s race to profit before EU legislation kicked-in in 2002 that required scrap metal, old vehicles and metal shredder residues to be classified as hazardous waste and to be recycled and disposed of in a manner that didn’t harm the environment and human health. That is, the tip levelled in part to make a football pitch for the Navy. That is, the tip which lies right next to naval vessels berthed at the Naval Basin, and to the nearby Naval Service Headquarters. That is, the tip, which on dry, windy days spreads its toxic dust like a shroud across the area’s inhabitants.

Is it any wonder that Naval Service personnel talk of cars parked on the Haulbowline Base covered in dust on dry days? Or of the taste and smell of metal when jogging in the ‘fresh’ Haulbowline air?

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Dust to dust… Part 2: Health risk follows

Dust to dust… Part 2

2008-08-21T14:20:00.005+01:00

Health risk

By Marcus O’Garvey (Haulbowline) with thanks for the info to Metal Man (Sligo IT), Boffin Island (Haulbowline), Pat the Barker (Limerick), Tralee Rose and Others, 21 August 2008.

This blog entry grew exponentially! Due to its large size we have made it available as a PDF file for download together with Part 1: Toxic waste.

Introduction

Haulbowline Island is a notorious toxic waste (“brownfield”) site smack-bang in the centre of Cork Harbour, on Ireland’s south coast. And it’s not just a dumping ground covered with heavy metal dust, aromatic hydrocarbons and PCBs. Part of the island itself, the East Tip, is actually made of the stuff. Nearly 9 hectares to be precise. That’s a hell of a lot of toxic waste. It also means (and sorry to ignore the poor old marine ecosystem for now) a hell of a lot of dust blowing around in the environment.

Part 1 of this diatribe showed that the dust, or “fugitive emissions” or “particulate matter” or “immissions” as it is otherwise called, did not just stop being produced and go away with the cessation of smelting in 2001 when Irish Ispat Ltd went into receivership. It continues to be liberated from the East Tip by the recent (and future) contaminated site remediation activities, with help from the wind on dry days. Whether you get a lungful/skinful or not depends on where you live and/or work (Cobh, Ringaskiddy or on Haulbowline itself) and which way the wind is blowing. Sort of Russian Roulette with nanogram (parts per billion) sized bullets of lead, zinc, chromium six, cadmium, arsenic, manganese, etc. etc.

What, then, does this heavy metal cocktail do to you? That is the question this Part 2 briefly addresses.

We are not even going to attempt to go near the cocktail mixers of dioxins, furans, polycyclic aromatic hydrocarbons, and polychlorinated biphenyls (PCBs). That is a job for our local (well paid) biomedical experts at Cork’s very own University Hospital and University College (not that they have had anything to say so on the subject far!!).

Part 2 variously borrows, copies and steals information from all over the Web and pastes it together to, well, scare the hell out of you! It is after all what the scientific experts and international health organisations have to say.

Bias? Yes, we have edited stuff to bring you the juicy “bad news”. But, we hope you may then be in a better position to both inform yourself and regurgitate biochemistry facts all over those nicey politicians who will want your vote next year during the local council elections. Give ‘em hell on the doorstep. They did, after all, give us Irish Ispat!

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No Minister! Some things you should know

2008-08-17T10:29:00.004+01:00

This entry was orginally posted on 28 July 2008 on the Irish Military Online (IMO) Discussion Board for the Navy & Naval Reserve in the Irish Steel Mill thread by "Boffin Island" Recruit.

As a civilian employee at the naval base: How dare he? The Minister’s strident assertion that “There is currently no indication that the situation at the former Ispat site represents any risk to the health of Naval Service personnel or civilian employees at the naval base” is untrue and unacceptable.

There is plenty that currently indicates high risk to health and Willie O’Dea does and should know it. If he lacks the relevant reports, he could ask his cabinet colleague John Gormley for copies! For example:

2002 Enviros Aspinwall report to DCMNR

According to the qualitative risk assessment contained in the October 2002 report (‘Phase One Investigation and Assessment at Haulbowline Island, Cork Harbour, Cork’) by Enviros Aspinwall to the then Department of Communications, Marine and Natural Resources:

The East Tip (i.e. the area covered by slag, mill scale, bag house dust and other waste that was subject to intensive dust-creating work between November 2007 and April 2008) posed “high risks to humans, groundwater, surface water, marine ecosystem from leached metals, hydrocarbons and PCBs” and “high risks to humans from windblown dust” (p3).

The Main Site (i.e. where the now demolished former Irish Steel/Ispat steelworks buildings stood, adjoining the Naval Base) posed “high risk to humans from PCBs spills; high risk to marine ecosystem from metals from dust; high/moderate risks to humans from windblown dust” among others (p4).

The report specifically identifies “People – Naval personnel and other site neighbours” as being at risk from “Direct contact/ingestion of wind blown dust” (p32).

Table 6.2 Risk Assessment matrix for Irish Ispat is detailed and includes: “Human residents (neighbours sited on Naval base and Cobh)” are at risk from “Windblown dust” with associated hazard of “Long term health risks [Severe]” with likelihood of occurrence described as “Likely. The tip is unvegetated, dusts present on the tip may be mobilised and blown by the wind” which may or may not blow towards human residents. The potential significance is rated as “High Risk” (p33).

Also, the marine ecosystem was at “High Risk” and any humans without personal protective equipment on the East Tip were at “High Risk” with “High Likelihood” of “Direct contact, ingestion of soil, inhalation of particulates” with associated “Health risk [Medium]” (p33).

* The term “high risk” is used to mean “Harm is likely to arise to a designated receptor [i.e. human] from an identified hazard at the site without appropriate remedial action” (p29).

The 2002 report for DCMNR clearly points to heavy metals in the bag house furnace dust “including zinc and lead” which was “deposited on the East Tip until 1980 as a dust” (p22).

“This material comprises a fine dust which will require some form of treatment to facilitate handling and disposal or recycling on or off site” (p69).

2003 Bord na Móna report to Naval Service

The November 2003 report (‘An ambient air quality survey for selected parameters at the Naval Service Base, Haulbowline Island on behalf of the Naval Service undertaken over a six month period’ from March 2003 to September 2003) by Bord na Móna Environmental Ltd Technical Services is considered a baseline survey as “All of the results were obtained during a period of inactivity at both the east tip and the steel works” (p41).

Nevertheless, sampling of airborne dust (particulate matter or PM10) carried out at the football pitch (location PM-01) exceeded the standard 50 μg/m³ limit value on seven occasions over a 10 day period in March 2003. The report states that “any breach of the 50 μg/m³ daily limit value may be considered significant” (p2).

“The most obvious source of PM10 particles is the material located to the east of the sampling location on the east tip… during an easterly wind there is a significant probability of increased particulate levels impacting on the basin area” (p37).

“The exceedences correspond to a high number of recorded easterly wind hours during that time and significant machinery activity on the east tip. After this period, activity on the east tip reduced” (p2).

The implications are, of course, that when there is significant machinery activity on East Tip –- such as when the site was being cleared recently by contractors, especially between November 2007 and April 2008 –- and the wind is from the East (and presumably it is dry weather), then dust levels over the Naval Base are likely to be significantly higher than the daily limit.

On page 3 the Bord na Móna report states: “The level of activity at the east tip and the steel works during the sampling period was generally low apart from a period of machinery movement and scrap steel recovery on the east tip during the early phase of the sampling period. The results obtained from the selected parameters reflect this low level of activity. Therefore, the levels recorded for each of the parameters would be considered baseline levels.”

It then concludes: “Based on these results and comparison to the appropriate standards, there is no significant impact on ambient air quality in the basin and headquarters area of the island arising from the steel works and the east tip.”

If this conclusion is quoted out of context by a politician, it would sound like everything is hunky-dory. But it also means that there is a significant impact on ambient air quality in the basin and headquarters area when there is a high level of activity of the East Tip. Which the 2002 report goes on to warn:

“However, should the level of activity in these areas change due to removal of material on the east tip or structural alteration/remediation of the steel works area, it is probable that ambient air quality in the area will suffer a significant impact, particularly with regard to PM10 levels. This would be based on the impact of machinery movement on the recorded PM10 levels during the early phase of the sampling period” (p3).

Oh, and it says this about why “PM10” is so important, regardless of any chemical heavy metal cocktail it may be made of:

“PM10 is defined as particulate matter with an aerodynamic diameter less than 10 μm. This description is restricted to this physical characteristic and no particular chemical composition is implied. The size is of importance because it is this that determines where in the human respiratory tract a particle deposits when inhaled. Most concern is given to particles small enough to penetrate into the lungs to reach the alveoli. When inhaled almost all particles larger than 7 μm are deposited in the nose and throat, and only 20-30% of particles between 1 and 7 μm are deposited in the alveoli. The measurement of PM10 relies on the use of a size-selective instrument, which collects small particles preferentially” (p6).

2008 AWN Consulting report to Cork County Council

If the Minister isn’t satisfied yet, he can look at the 30 May 2008 report (‘Dust deposition monitoring in the region of the former Irish ISPAT plant, Haulbowline, Co. Cork (01/04/08 – 01/05/08)’) by AWN Consulting Ltd for Cork County Council.

Since July 2005, continuous monitoring of dust deposition has taken place at four locations: on Haulbowline Island (A) Naval Base Dockyard and (B) Naval Base Church, and at (C) Ringaskiddy (until 5/6/07) and (D) Cobh Town Centre. The AWN report “details the results of monitoring over the period 01/04/08 – 01/05/08 (i.e. April 2008)”. The standard daily limit of dust deposited is 350 mg/m²/day.

During April 2008, the average monthly levels of deposited dust per day were:

(A) Dockyard ------ 114 mg/m²/day

(B) Church --------- 1267 mg/m²/day

(D) Cobh ----------- 47 mg/m²/day

“The dustfall levels at one of the three measured locations for the April 2008 period exceeded the TA Luft annual limit of 350 mg/m²/day, reaching 362% of the limit at the Naval Base Church on Haulbowline Island. The monthly deposition level at the Naval base dockyard and at Cobh reached 33% and 13% of the TA Luft limit vales respectively” (p2).

TA Luft is an international limit for air pollution. Clearly there was a huge amount of dust in the air over the Base in April when the contractors were removing heaps from the East Tip. From the 2005 White Young Green report (see below) released by the Dept. of Environment, we know that the ‘soil’ they were digging up and shaking to separate dust for shipping to Germany was a cocktail of heavy metals and other toxic substances. The other thing for sure is that if it was in the air, it was capable of being breathed in by anyone on the Base in April.

And it’s not just April 2008 that had high dust levels. At the Church on the Base (location B) the 350 mg/m²/day limit (monthly average) was exceeded in March 2007, February 2008 and March 2008 as well:

6/3/07 to 2/4/07 ----- 494 mg/m²/day

4/2/08 to 3/3/08 ----- 583 mg/m²/day

3/3/08 to 1/4/08 ----- 428 mg/m²/day

2005 White Young Green report to Cork County Council

Now that Minister O’Dea knows it was very dusty on the Naval Base, and that the Government was warned in 2002 of the “high risks to humans from windblown dust”, and that a study in 2003 found significant breaches of airborne dust (PM10) limits, what did he and his Cabinet colleagues know about the chemical substances in East Tip that was turned into dust by machinery and activities in clearing the site?

The September 2005 report (‘Factual Geo-Environmental Report: Contamination and Geotechnical Assessment, Former Irish Steel Site, Haulbowline Island’) by White Young Green Ireland Ltd for Cork County Council first of all refers to environmental investigations by KT Cullen & Co in 1995 and 1998 as well as O’Callaghan Moran & Associates (May 2002) and Enviros Aspinwall (October 2002):

“All of the reports highlighted the potential risks to humans and the environment from materials dumped and spilled on site. This included potential heavy metal contamination leached from waste slag and furnace dust, waste oils, organic solvents, PCBs, PAHs and radioactive material. Historical site activities may have disposed sludges containing high levels of metals and mill scale on-site” (p1).

“According to the KTC report 1995, the East Tip is predominantly comprised of slag (approximately 45 000 tonnes/year) with laboratory chemicals, hot flume dust, oil and grease and domestic waste. Prior to the 1980 s the fine filter dust was deposited with the slag without being processed, but was palletised and exported from the early 1980’s. In 1994 a part of the East Tip was reclaimed for the development of a Naval football pitch” (p6).

The 1995 KT Cullen & Co report concluded:

“The materials dumped on the East Tip are a significant potential source of heavy metal contamination of sediment and groundwater as demonstrated by the laboratory analyses” (WYG p7).

The 1998 KT Cullen & Co report concluded:

“…observations at the site suggest that the uncompacted waste near the ground surface has a high permeability. The permeability of the waste is expected to be highly variable due to the following factors: The nature of the deposited materials varied from fine dust or sludge to coarse metal fragments; The shallow waste was much less compacted than the deeper waste; and The waste below the water table was flushed by the tide which may have allowed some dissolving and washing of the finer particles” (WYG p8).

The 2002 O’Callaghan Moran & Associates report for KPMG Corporate Recovery (i.e. the receivers for Irish Ispat Ltd production facility on Haulbowline Island) identified:

“Hazardous waste was disposed of at three separate locations; the former dock and waterway, the South Tip and the East Tip. That there is documentary evidence to confirm or strongly suggest disposal of furnace dust, waste oils, organic solvents and PCBs at the South and East Tips. That there is a possibility that similar wastes were disposed at the dock and waterway.

Process wastewater treatment sludge containing high levels of metals may have been deposited on-site.

A coal gasification plant was demolished ca. 1960. Such plants are recognized as sources of PAHs and can be a significant contaminant. There is a strong possibility that the contaminated demolition debris from the gasification plant has been disposed of on the site.

The furnace dust assessment established that it readily leaches lead and zinc and in sufficient quantities is toxic to marine organisms.

The East Tip was used for disposal of production wastes. The primary contaminants identified were heavy metals, oils and PCBs. However the investigation by OCM did not assess all potential contaminants and there was no investigation on the South Tip.” (WYG p8-9).

The OCM survey of Contaminated Soil and Groundwater identified the following:

“Contaminated demolition debris from the former coal gasification plant and possibly the galvanizing plant may have been used as fill. No site investigation data for the main plant is available to confirm the nature of the fill material.

Furnace dust emissions with high levels of zinc and lead and lower levels of other metals would have been deposited in the vicinity of the main plant prior to installation of the furnace dust collector. Such dust, which is susceptible to leaching zinc and lead by rainwater, could result in elevated metals in exposed soils on the site. …” (WYG p9).

Appendix I of the 2005 WYG report (600k pdf) lists results of laboratory chemical testing on 'soil' sample from trial pits and bore holes on the Base. It looks like a nightmare to me!

Arsenic, Cadmium, Chromium (including the infamous Chromium 6 or Hexavalent Chromium), Copper, Lead, Nickel, Vanadium and Zinc all have very high levels in many of the trial (i.e. surface) pits. There is also lots of hydrocarbons –- if this was an offshore oil rig like the Brent Spar, the thing would have been shut down by the authorities and Greenpeace would be all over it by now! Then there are the PCBs –- any they are bad.

What does this cocktail do to you? If just one of these metals and chemicals cab be carcinogenic, what does breathing in all of them in one go do to you?

~~~

Maybe Minister O’Dea should come down to Haulbowline Naval Base and get himself a good long lungful of dust on a dry day with the wind blowing from the tip, whilst the contractors resume their digging and shaking (poor devils!)? Maybe he should come work here for several months, even years? In fact, why doesn’t he relocate his Department to Haulbowline Island? I’m sure the unions would have something to say about it then! He too can then take this toxic dust back home on his clothes to his wife and kids!

Now let's hear him dare to say: “There is currently no indication that the situation at the former Ispat site represents any risk to the health of Naval Service personnel or civilian employees at the naval base.” Wake up and smell the chromium Minister!

Me? I’m off on me hols to Chernobyl. I hear it’s a lot safer there!

Everyone duck! There's a pink elephant flying over Haulbowline Island!

2008-08-17T10:13:00.005+01:00

This entry was originally posted on 28 July 2008 on the Irish Military Online (IMO) Discussion Board for the Navy & Naval Reserve in the Irish Steel Mill thread by "Boffin Island" Recruit.

These extracts are from Irish Examiner 28 July 2008:

Moustache forever? O’Dea answers your questions
By Paul O’Brien, Political Correspondent

THE need to “tighten the belt” because of the economic squeeze should not mean cutting anybody’s wages — politicians included, Defence Minister Willie O’Dea has said.

In the first of a new series in which Irish Examiner readers get to quiz members of the Cabinet, Mr O’Dea answers questions on a wide range of issues today — from the Lisbon Treaty to The Simpsons television show. … Elsewhere, Mr O’Dea says there are no indications that the toxic waste at the former Irish Ispat/Steel plant in Haulbowline, Co Cork, poses a threat to those working on the naval base which is in close proximity.

When demolition of the steelworks at the plant commenced in 2005, dust-monitoring equipment was installed.

“The data collected to date does not suggest that activities on the steelworks site have had a significant impact on the environment or might pose a threat to the Naval Services at Haulbowline,” Mr O’Dea says.

As a precaution, the Department of Defence has hired consultants to carry out soil and air analysis across the naval base. …

Can you give assurances that the toxic waste buried on the old Irish Steel/Ispat site on Haulbowline poses no threat to the navy?
D McCARTHY, Bishopstown, Cork city

O'Dea answers: “The health and safety of all Defence Force personnel and employees is of primary concern to me. There is currently no indication that the situation at the former Ispat site represents any risk to the health of Naval Service personnel or civilian employees at the naval base.

When demolition of the steelworks at Haulbowline commenced in the summer of 2005, it was agreed by all interested parties that dust monitoring equipment be installed on the naval base. The monitoring equipment selected and installed in two locations on the base includes Bergerhoff dust deposition gauges, to record total dust fall-out on a monthly basis, and PM-10 monitors to record the respirable fraction of fine dust in real time. In layman’s terms, this means that dust-generating events on the steelworks site can be identified and controlled as they happen.

The data collected to date does not suggest that activities on the steelworks site have had a significant impact on the environment or might pose a threat to the Naval Services at Haulbowline.

Purely as a precautionary measure — following the excavations on the East Tip — we have engaged environmental consultants RPS Group plc. They will carry out sampling and conduct soil and air analysis across the naval base checking for heavy metals and other species. This investigation has already commenced. It is expected to be completed by the end of August.”

No place to be a dolphin

2008-08-12T23:09:00.002+01:00

By Karlos Marx

PCBs, Cadmium, Chromium 6, Copper, Lead, Nickel, poly-aromatic hydrocarbons… Is this anyway to treat our cetacean cousins?

The scandalous saga of former Irish Ispat and the toxic slag heap from hell (East Tip) on Haulbowline Island is not just a human health disaster. It is also a very real threat to the several species of protected marine mammals which frequent Cork Harbour.

The Irish Whale and Dolphin Group (IWDG) has recorded schools of bottlenose dolphins (Tursiops truncatus) on numerous occasions. Also harbour porpoises (Phocoena phocoena) and orca (Orcinus orca). Other species sighted within Cork Harbour include common dolphin (Delphinus delphis) and even the odd stray Risso’s dolphin (Grampus griseus) and pilot whale (Globicephala melas). Neither should we forget the seals: the harbour seal (Phoca vitulina) and grey seal (Halichoerus grypus).

Bottlenose dolphins were observed off Ringaskiddy in August 2003 when 20 or so animals including a calf remained in the vicinity for nearly a fortnight. According to the IWDG they were using an area between East Ferry, Spike Island, Haulbowline, Roche’s Pt. and outside the harbour from Myrtleville (IWDG). Similar bottlenose activity was reported in Cork Harbour in August 2002. In September 2005 a group of between 20-30 bottlenose dolphins were seen bow-riding a container ship in front of Cobh, and between Spike Island and Whitegate refinery (IWDG).

In May 2007 a school of bottlenose dolphins was seen bow-riding the naval vessel LE Aisling, east of Cobh Town, near the Cork Harbour pilots station (IWDG). They were also seen in the Passage West/Lough Mahon inner harbour area and feeding on grey mullet alongside the LE Ciara off Whitepoint. On previous days they were sighted between Passage West and Great Island, Cobh and between Whitepoint and Ringaskiddy, where they have been observed feeding in water as shallow as 2-3m depth (14/5/07).

Local IWDG members, Conor Ryan and Peter Wilson have been monitoring a school of six ‘resident’ bottlenose dolphins, which in favourable weather can be seen on a near daily basis from places like Roche’s Point, Camden and Carlisle Forts.

The IWDG states: ‘In common with all 24 Irish cetacean species, bottlenose dolphins are afforded full protection under the Irish Wildlife Act 1976. In addition, along with the much smaller harbour porpoise (Phocoena phocoena), they are also an Annex II species on the EU habitats directive, which means that both the animals and their habitats are afforded priority protection under EU law.’

All marine mammals are protected in Irish waters under the 1976 and 2000 Wildlife Acts. Under the 1992 EU Habitats Directive, all cetaceans are included in Annex IV of the Directive as species ‘in need of strict protection’. Bottlenose dolphins, harbour porpoises, grey and harbour seals are all additionally included in Annex II of the directive as species requiring the establishment of Special Areas of Conservation (marine SAC).

Clearly, this raises questions about the threat to the conservation status of these species posed by the former Ispat site and toxic East Tip that forms a significant intertidal part of Haulbowline Island. The Island is known to be surrounded by marine sediments contaminated with high levels of heavy metals, complex aromatic hydrocarbons, endocrine-system disrupting PCBs and other hazardous organic substances that were introduced into the Cork Harbour marine ecosystem and food web by the ongoing industrial (including brownfield remediation) activity on Haulbowline.

Is it time that higher authorities (the European Commission, OSPAR Commission, Convention on Migratory Species?) become involved and demand that the Irish Government stop their delaying tactics, corner-cutting, penny-pinching and procrastination and just get on with the job of securing and cleaning up this toxic threat to the marine ecosystem and its protected species?

Told you the shrimp was off!

2008-08-12T20:41:00.001+01:00

By Seriously Concerned (& Others) of Cobh/Haulbowline

Until recently, it was common to see the lads of various ages fishing with rod and tackle from the bridge between Ringaskiddy and Haulbowline Island. Also down on the shore at both Paddy’s Point and Rocky Island.

In the middle of July 2008, even after the Chromium 6 had hit the fan (front page Irish Examiner 26/6/08), at least two local potting boats were seen by Cobh residents fishing off the toxic East Tip. Apart from the obvious likelihood of heavy metal poisoning for anyone eating the shrimp, green crab or lobster catch, the pots probably disturb the sediments and help redistribute the heavy metals and other contaminants around Cork Harbour.

Why are there no “fishing prohibited” notices around Ringaskiddy, Cobh, Rocky Island and Haulbowline to warn anglers (including the large number of visitors to Cork Harbour from elsewhere in Ireland and from overseas who wouldn’t be aware of the local dangers of the Ispat legacy)?

Why are fishing boats still potting, especially off the East Tip? We thought there was supposed to be a ban on fishing these toxic grounds anyway?

What happened to the catch? Did the shrimps and/or other crustaceans get sold locally (to posh restaurants) or was it exported and is now poisoning some Spanish kid?

What does BIM and the Marine Institute have to say about this travesty?

According to Evin McGovern PhD (Senior Chemist, Marine Environment and Food Safety at the Marine Institute) there is an environmental monitoring station for wild mussels (Mytilis edulis)* at Ringaskiddy near the bridge to Haulbowline.

On 11 July 2008 she told Mark Masterson (Senior Scientist with White Young Green Environmental (Ireland) Ltd) who is currently investigating sediment contamination around Haulbowline Island as part of WYG consultancy report to the Department of the Environment, due in late August:

“You will note high lead (Pb) at the site near Ringaskiddy - shoreline on the channel opposite Spike Island”

That would be Paddy’s Point and the West Channel then.

The Marine Institute spreadsheet data highlighted in red clearly show that mussels at Ringaskiddy are contaminated with lead (Pb) and in the past (when Ispat was active) with Cadmium, Zinc and probably other metals as well. Note that not all the toxic metals known to be in East Tip (Appendix I of WYG 2005 report) are being monitored!

The limits (i.e. “strictest standard and guidance values applied by various OSPARCOM countries for contaminants in shellfish for the assessment of the possible hazards to human health”) that we added to the spreadsheet are taken from Department of the Marine July 1995 document.

* Mussels are sedentary filter-feeders which readily accumulate contaminants from the surrounding seawater and are recommended indicators of marine environmental quality.

Sediment contamination

It is, of course, unsurprising that the marine sediments both around Haulbowline and within the Naval Base Dockyard are contaminated with the full range of toxic waste and settled dust emissions from the former Irish Steel/Ispat site on the Island.

The ‘Report of Seabed Samples - Naval Base Haulbowline, June 2003’ by Hydrographic Surveys Ltd of Crosshaven for the Department of Defence at Haulbowline clearly shows high levels of sediment contamination at the Naval Basin (locations 1-5), near Spencer’s Jetty (locations 6-7) and in front of the recently burned out Glucksman Marine Building, which housed the UCC Coastal and Marine Resources Centre overlooking Rat Island (location 8).

The samples were collected on 23 June 2003 and analysed by Mercury Analytical Ltd, Limerick. Note: 1 ‘part per million’ (ppm) is the same as 1 ‘mg/kg’.

	OSPAR BC* mg/kg (or ppm)	Haulbowline mg/kg (or ppm)	Sample Location
Cadmium	0.20	0.08	5 Basin
Chromium	60.00	14.50	5 Basin
Copper	20.00	45.00	5 Basin
Lead	35.00	85.40	5 Basin
Mercury	0.05	0.49	5 Basin
Nickel	30.00	12.40	5 Basin
Zinc	90.00	679.00	5 Basin

* BC or “Background concentrations” are OSPAR assessment tools intended to represent the concentrations of certain hazardous substances that would be expected in the North-East Atlantic if certain industrial developments had not happened. They represent the concentrations of those substances at “remote” sites, or in “pristine” conditions based on contemporary or historical data respectively, in the absence of significant mineralisation and/or oceanographic influences. In this way they relate to the background values referred to in the OSPAR Hazardous Substances Strategy. BCs do not represent target values and should not be used as such. Source: Agreement on Background Concentrations for Contaminants in Seawater, Biota and Sediment (OSPAR Agreement 2005-6).

This is not new knowledge. A 1992 report ‘Analysis of sediments from Haulbowline’ by EOLAS for the Department of Defence at the Naval Base. In June 1997 the report ‘Haulbowline Naval Base - Analysis of Sediment Prior to Dredging and Disposal by Dumping at Sea’ commissioned by the Department of the Marine and carried out by UCC Aquatic Services Unit, gives the following (highest) levels of metals in sediments (mg/kg) in the Naval Basin:

	1992	1997
Arsenic	9.1	50
Cadmium	<0.9	<1
Chromium	45.1	147
Copper	46.2	114
Lead	53	68
Manganese	401.4	509
Mercury	<0.15	0.217
Nickel	26.1	57
Zinc	191.9	337

It is not just around Haulbowline Island that the sediments are contaminated. Analyses of sediment grab samples taken just off Cobh deepwater quay (west of the Heritage Centre and railway station) by Glover Site Investigations Ltd in June 2007 and September 2007 in connection with dredging on either side of the existing berthing basin for the giant cruise ships found similarly (highest) levels of metals (mg/kg):

	June 2007	Sept 2007
Arsenic	6.45	12.9
Cadmium	<0.1	0.045
Chromium	45.8	21.7
Copper	19.6	7.1
Lead	78.2	10.6
Mercury	<2.0	<0.05
Nickel	50.6	18.0
Zinc	125	47.9

So, anyone fancy fish for supper?

SCIENCE: Provisional Assessment of Recent Studies on Health Effects of Particulate Matter Exposure

2008-08-12T09:27:00.001+01:00

US EPA report (EPA/600/R-06/063) July 2006

Executive Summary

In the proposed rule on the National Ambient Air Quality Standards for particulate matter (PM), EPA committed to conduct a review and assessment of the numerous studies relevant to assessing the health effects of PM that were published too recently to be included in the 2004 PM Air Quality Criteria Document (AQCD). This report presents the findings of EPA’s survey and provisional assessment of such studies. EPA has screened and surveyed the recent literature and developed a provisional assessment that places those studies of potentially greatest relevance in the context of the findings of the 2004 PM AQCD. The focus is on: (a) epidemiologic studies that used PM2.5 or PM10-2.5 and were conducted in the U.S. or Canada, and (b) toxicology or epidemiologic studies that compared effects of PM from different sources, PM components, or size fractions. Given the limited time available, the provisional assessment presented here does not attempt to critically review individual studies or to provide the kind of full integration found in a typical AQCD.

This survey and assessment finds that that the new studies expand the scientific information and provide important insights on the relationships between PM exposure and health effects of PM. Taken in context, however, the new information and findings do not materially change any of the broad scientific conclusions regarding the health effects of PM exposure made in the 2004 PM AQCD. In brief, this report finds the following:

• Recent epidemiologic studies, most of which are follow-ups or extensions of earlier work, continue to find that long-term exposure to fine particles is associated with both mortality and morbidity, as was stated in the 2004 PM AQCD. Notably, a follow-up to the Six Cities study shows that an overall reduction in PM2.5 levels results in reduced long-term mortality risk. Both this study and the analysis of the ACS cohort data in Los Angeles suggest that previous studies may have underestimated the magnitude of mortality risks. Some studies provide more mixed results, including the suggestion that higher traffic density may be an important factor. In addition, the California Children’s Health Study reported that measures of PM2.5 exposure and PM components and gases were associated with reduction in lung function growth in children, increasing the evidence for increased susceptibility early in life, as was suggested in the 2004 PM AQCD. The results of recent epidemiologic and toxicology studies have also reported new evidence linking long-term exposure to fine particles with a measure of atherosclerosis development and, in a cohort of individuals with cystic fibrosis, respiratory exacerbations.

• Recent epidemiologic studies have also continued to report associations between acute exposure to fine particles and mortality and morbidity health endpoints. These include three multi-city analyses, the largest of which (in 204 counties) shows a significant association between acute fine PM exposures and hospitalization for cardiovascular and respiratory diseases, and suggestions of differential cardiovascular effects in eastern U.S. as opposed to western U.S. locations. The new studies support previous conclusions that short-term exposure to fine PM is associated with both mortality and morbidity, including a substantial number of studies reporting associations with cardiovascular and respiratory health outcomes such as changes in heart rhythm or increases in exhaled NO.

• New toxicology and epidemiologic studies have continued to link health outcomes with a range of fine particle sources and components. Several new epidemiologic analyses and toxicology studies have included source apportionment techniques, and the results indicated that fine PM from numerous sources, including traffic-related pollution, regional sulfate pollution, combustion sources, resuspended soil or road dust, are associated with various health outcomes. Toxicology studies continue to indicate that various components, including metals, sulfates, and elemental and organic carbon, are linked with health outcomes, albeit at generally high concentrations. Recent epidemiologic studies have also linked different fine PM components with a range of health outcomes; new studies indicate effects of the organic and elemental carbon fractions of fine PM that were generally not evaluated in earlier analyses.

• The recent epidemiologic studies greatly expand the more limited literature on health effects of acute exposure to thoracic coarse particles (PM10-2.5). The 2004 PM AQCD conclusion that PM10-2.5 exposure was associated with respiratory morbidity is substantially strengthened with these new studies; several epidemiologic studies, in fact, report stronger evidence of associations with PM10-2.5 than for PM2.5. In two new casecrossover studies, associations with thoracic coarse particles are robust to the inclusion of gaseous copollutants. For mortality, many studies do not report statistically significant associations, though one new analysis reports a significant association with cardiovascular mortality in Vancouver, Canada.

• Evidence of associations between long-term exposure to thoracic coarse particles and either mortality or morbidity remains limited.

• New toxicology studies have demonstrated that exposure to thoracic coarse particles, or PM sources generally representative of this size fraction (e.g., road dust), can result in inflammation and other health responses. Clinical exposure of healthy and asthmatic humans to concentrated ambient air particles comprised mostly of PM10-2.5 showed changes in heart rate and heart rate variability measures. The results are still too limited to draw conclusions about specific thoracic coarse particle components and health outcomes, but it appears that endotoxin and metals may play a role in the observed responses. Two studies comparing toxicity of dust from soils and road surfaces found variable toxic responses from both urban and rural locations.

• Significant associations between improvements in health and reductions in PM and other air pollutants have been reported in intervention studies or “found experiments.” One new study reported reduced mortality risk with reduced PM2.5 concentrations. In addition, several studies, largely outside the U.S., reported reduced respiratory morbidity with lowered air pollutant concentrations, providing further support for the epidemiological evidence that links PM exposure to adverse health effects.

SCIENCE: Vanadium pentoxide inhalation

2008-08-12T09:21:00.002+01:00

Review article in Indian Journal of Occupational and Environmental Medicine (2007) Vol 11, Issue 3, pages 97-103 by Ross G. Cooper at Division of Physiology, UCE Birmingham, UK.

Abstract

Context: This mini-review describes the toxic effects of vanadium pentoxide inhalation principally in the workplace and associated complications with breathing and respiration. Although there are some material safety data sheets available detailing the handling, hazards and toxicity of vanadium pentoxide, there are only two reviews listed in PubMed detailing its toxicity. Aim: To collate information on the consequences of occupational inhalation exposure of vanadium pentoxide on physiological function and wellbeing. Materials and Methods: The criteria used in the current mini-review for selecting articles were adopted from proposed criteria in The International Classification of Functioning, Disability and Health. Articles were classifi ed from an acute and chronic exposure and toxicity thrust. Results: The lungs are the principal route through which vanadium pentoxide enters the body. It can injure the lungs and bronchial airways possibly involving acute chemical pneumonotis, pulmonary edema and/or acute tracheobronchitis. It may adversely influence cardiac autonomic function. It stimulates the secretion of cytokines and chemokines by hepatocytes and disrupts mitochondria function. It disrupts the permeability of the epithelium and promotes access of inflammatory mediators to the underlying neuronal tissue causing injury and neuronal death. When renal brush border membrane vesicles are exposed to vanadium pentoxide, there is a time-dependent inhibition of citrate uptake and Na+K+ATPase in the membrane possibly contributing to nephrotoxicity. Exposure results in necrosis of spermatogonium, spermatocytes and Sertoli cells contributing to male infertility. Conclusion: Vanadium pentoxide certainly has adverse effects on the health and the well-being and measures need to be taken to prevent hazardous exposure of the like.

Extracts

This mini-review describes the toxic effects of vanadium pentoxide inhalation principally in the workplace and associated complications with breathing and respiration.[1] Vanadium is a by-product of oil-burning furnaces when vanadium pentoxide (MR 181.88) is deposited in the flues. It is an odorless gas.[2] Inhalation is the principal route of entry into the body and may result acutely in severe pneumonitis with associated mucus membrane irritation and gastrointestinal disturbances. Ambient vanadium pentoxide dust produces irritation of the eyes, nose and throat.[3] Over long periods, inhalation may potentiate chronic bronchitis, eczematous skin lesions, fine tremors of the extremities and greenish discoloration of the tongue.[1] As it has a rapid renal clearance, it may be monitored in urine specimens to determine exposure to vanadium pentoxide (American Conference of Governmental Industrial Hygienists, ACGIH and British Education Index, BEI) 50 ìg.g-1 creatinine for an end-ofshift, end-of-workweek sample.[1] Most absorbed vanadium is excreted in the urine within one day after a long-term moderate exposure to vanadium dust.[4] ... The workplace exposure limit for vanadium pentoxide is according to the Health and Safety Executive (HSE), 0.05 mg.m-3/8h.[1] MSDS[2] details airborne exposure limits of 0.5 mg.m-3 (ceiling) for vanadium respirable dust and 0.1 mg.m-3 (ceiling) for vanadium fumes. ...

Although there are some material safety data sheets available detailing the handling, hazards and toxicity of vanadium pentoxide,[2,24] there are only two reviews listed in PubMed detailing its toxicity.[25,26] The aim of this article therefore was to collate information on the consequences of occupational inhalation exposure of vanadium pentoxide on physiological function and wellbeing. An attempt to classify the like according to functionality of certain selected organ systems was decided. ...

Lungs: Vanadium pentoxide is regarded as a less soluble form of vanadium and is therefore eliminated from the lungs at a slow rate.[28] Inhalation of vanadium pentoxide can injure the lungs and bronchial airways,[2] possibly involving acute chemical pneumonotis, pulmonary edema and/or acute tracheobronchitis.[25] Symptoms include irritation and inflammation of the mucus membranes, nasal passages and pharynx.[2] Clinical complications include a persistent cough, shortness of breath, bronchiolar constriction, tightness of the chest and a pseudo-asthmatic inflammation.[2] In a study of 40 plant workers previously free of lung disease and exposed to vanadium pentoxide, 12 had bronchial hyper-reactivity and symptoms of asthma.[29] Vanadate acts directly on human bronchial smooth muscle promoting the release of Ca2+ from intracellular store via the production of inositol phosphate second messengers and inhibition of Ca2+-ATPase and causing spasms.[30] Occasionally pulmonary edema and/or pneumonia may result with fatal consequences.[2] First aid measures following inhalation include removing the patient into fresh air and applying artificial respiration if breathing has expired. Oxygen is needed if breathing is labored and it is essential to seek medical attention.[2] Vanadium pentoxide dust may be a potential mutagen via induced chromosomal aberrations in man[31] and hamsters.[32] ... There may be a pathological pattern within the lung which may be associated with the pattern and/or extent of vanadium deposition.[40] Its cumulative effect in lung tissue possibly contributes to the development lung cancer. ...

Circulatory system: Chronically, exposure to airborne metals including vanadium may result in alterations in cardiac autonomic function.[43] Vanadium induces thrombocytosis and may be associated with various thromboembolic diseases.[44] Acute studies of vanadium pentoxide inhalation on the heart in experimental animals revealed that there was myocardial vascular congestion was observed, with focal perivascular haemorrhages.[6] Studies in humans has revealed palpitation of the heart, high incidence of extrasystoles, changes in the blood picture (anemia, leukopenia, punctatebasophilia of the erythrocytes) and reduced levels of cholesterol in the blood.[45] Limited studies have suggested a positive correlation between vanadium inhalation in urban air and mortality from cardiac failure, despite an absence of lifestyle determination.[46]

Liver: Acutely, vanadium is a potent inhibitor of many enzymes, while it stimulates adenylate cyclase. It has been shown to inhibit cholesterol biosynthesis and lower plasma cholesterol levels. Vanadium can also directly influence glucose metabolism in vitro and may play a role in its regulation. Lipid peroxidation of rat liver microsomes and mitochondria was induced by sulphite and accelerated by the presence of vanadium compounds.[6] Severe acute exposure (tens of mg/m3) is responsible for systemic effects. Most frequent findings in animal experiments were in the liver, kidneys, gonads and the nervous, hematological and cardiovascular systems.[45] Chronically, histopathological changes observed in the liver following the higher level of inhalation exposure (27 ìg/m3 for 70 days) included central vein congestion with scattered small hemorrhages and granular degeneration of hepatocytes.[6] ...

CNS: Severe acute exposure to vanadium pentoxide has major patho-physioloogical manifestations on the nervous system.[6] Inhalation thereof produces a time-dependent loss of dendritic spines, necrotic-like cell death and considerable alterations of the hippocampus CA1 neurophile, all associated with spatial memory impairment.[51] Additionally, there is a decrease in the number of tyrosine hydroxylase immunreactive neurones in the substatia nigra pars compacta.[52] Within the ependymal epithelium, cilia loss, cell sloughing and cell layer detachment occur after vanadium pentoxide inhalation.[53] The damage results in disrupted permeability of the epithelium and promotes access of inflammatory mediators to the underlying neuronal tissue causing injury and neuronal death.[53] In humans, severe chronic exposure results in general symptomatology including nervous disturbances, neurasthenic or vegetative symptoms.[6]

Kidneys: Severe acute exposure (tens of mg/m3) is responsible for aberrations in renal function.[6] Vanadium concentrations of 25 μg/g dwt. in the kidneys are associated with mortality in ducks acutely exposed to sodium metavanadate.[47] Chronic exposure to increasing dietary concentrations of sodium metavanadate (38.5-2651 ppm) over 67 days resulted in vanadium accumulation in the kidneys of 13.6 μg/g dw.[47] It is unlikely though that such concentrations would have been achieved via inhalation. ...

Testicles: Chronic ingestion of vanadium may have significant consequences for infertility by damaging spermatogenesis. Studies in mice have demonstrated that inhalation of vanadium pentoxide results in necrosis of spermatogonium, spermatocytes and Sertoli cells.[58] Vanadium accumulates in the testes and attenuates the percentage of gammatubulin in all analysed testicular cells, suggesting changes in microtubules used in cell division.[59] Vanadium also induces DNA damage.[60] Leydig cells may not be affected by vanadium pentoxide as testosterone levels remain unchanged.[61]

Discussion

This mini-review has contributed to a brief synthesis of the literature which is currently rather scattered in nature into a compact format. Its main thrust was from both an acute and chronic exposure and toxicity angle. Vanadium pentoxide has adverse effects on health and well-being and measures need to be taken to prevent hazardous exposure of the like. Medical monitoring of workers exposed to the dust or fumes; workplace monitoring and measurement of ambient concentrations; dealing with contaminated attire and establishing personal hygienic procedures; dealing with emergency spills of dust; enforcing protocols for emergencies and hazardous waste management; and the use of inspected respiratory and personal protective equipment, are all essential in reducing toxic exposure.

Vanadium pentoxide exposure (acutely and chronically) in both experimental animal and human studies indicates a systemic patho-physiological and pathological influence on cell metabolism and tissue function. Therefore procedures need to be implemented in environments which potentially expose workers to vanadium pentoxide including influences on respiratory function and appropriate quality guidelines enforced. The lungs are likely to accumulate more vanadium particles than elsewhere particularly from polluted air. The lowest observed-adverse-effect level for acute exposure can be considered to be 60 μg vanadium per m3. Indeed, chronic exposure emanates as slight changes in the upper respiratory tract, with irritation, coughing and injection of pharynx, to more serious effects such as chronic bronchitis and pneumonitis. Persons suffering from lung problems including asthma and cystic fibrosis would need to ensure that they take adequate measures to prevent vanadium irritation of the mucosae. Obviously, however, a systemic assessment via renal and liver function tests needs to be completed in order to make an accurate clinical assessment of the influence of vanadium on body function and ultimately the efficient maintenance of homeostasis. More research is required to establish and add to the limited existing knowledge on the toxicokinetic and toxicological database on vanadium pentoxide. Indeed, there is limited understanding of the potential for dermal absorption and the potential long term effects as a result of sequestration in body tissues such as bone.

SCIENCE: Assessing Cumulative Health Risks from Exposure to Environmental Mixtures—Three Fundamental Questions

2008-08-12T09:20:00.001+01:00

Article in Environmental Health Perspectives (2007) Vol 115 No. 5, Pages 825-832 by Ken Sexton of University of Texas School of Public Health, Brownsville, Texas, USA and Dale Hattis of The George Perkins Marsh Institute, Clark University, Worcester, Massachusetts, USA.

Abstract

Differential exposure to mixtures of environmental agents, including biological, chemical, physical, and psychosocial stressors, can contribute to increased vulnerability of human populations and ecologic systems. Cumulative risk assessment is a tool for organizing and analyzing information to evaluate the probability and seriousness of harmful effects caused by either simultaneous and/or sequential exposure to multiple environmental stressors. In this article we focus on elucidating key challenges that must be addressed to determine whether and to what degree differential exposure to environmental mixtures contributes to increased vulnerability of exposed populations. In particular, the emphasis is on examining three fundamental and interrelated questions that must be addressed as part of the process to assess cumulative risk: a) Which mixtures are most important from a public health perspective? and b) What is the nature (i.e., duration, frequency, timing) and magnitude (i.e., exposure concentration and dose) of relevant cumulative exposures for the population of interest? c) What is the mechanism (e.g., toxicokinetic or toxicodynamic) and consequence (e.g., additive, less than additive, more than additive) of the mixture’s interactive effects on exposed populations? The focus is primarily on human health effects from chemical mixtures, and the goal is to reinforce the need for improved assessment of cumulative exposure and better understanding of the biological mechanisms that determine toxicologic interactions among mixture constituents.

Extracts

It is well established that people are exposed to a diverse and dynamic mixture of environmental stressors as a routine part of their existence, and there is clear evidence that toxicity can be modified by simultaneous or sequential exposure to multiple environmental agents (Carpenter et al. 2002; Hertzberg and Teuschler 2002). We know, for example, that exposure to tobacco smoke and asbestos (Erren et al. 1999) or radon (Morrison et al. 1998) multiplicatively increases the risk of lung cancer over what would be expected from simple addition of the effects from the agents acting separately. Similarly, exposure to aflatoxin-contaminated food and hepatitis B infection greatly increases the risk of hepato-cellular carcinoma (Kuper et al. 2001), exposure to noise and toluene results in higher risk of hearing loss than from either stressor alone (Franks and Thais 1996), exposure to poly-cyclic aromatic hydrocarbons and ultraviolet radiation increases toxicity to aquatic organisms (Oris and Geisy 1985), and adults with increased perceived stress (Cohen et al. 1999) and children of parents experiencing stress (Boyce et al. 1995) are more susceptible to viral respiratory infections.

Risk assessments have, nevertheless, focused mainly on the narrow question of harm from exposure to individual chemicals in a specific environmental medium via a single route or pathway [U.S. Environmental Protection Agency (EPA) 2003]. Although there is an expanding body of work on cumulative exposures and combined effects on people (Agency for Toxic Substances and Disease Registry 2002; Carpenter et al. 2002; Monosson 2005; U.S. EPA 2000; Yang 1994) and on ecosystems (Bryce et al. 1999; Dale et al. 1998; U.S. EPA 1998), adequate and appropriate data are rarely available to conduct a rigorous assessment of cumulatve risk. In this article, we briefly review three fundamental and interrelated questions that must be addressed as part of the cumulative risk assessment process. Which environmental mixtures are most important from a public health perspective? What is the nature and magnitude of cumulative exposures for populations of interest? What is the mechanism and consequence of combined effects on exposed populations? ...

Conclusions

Cumulative risk assessment is currently hampered by three interrelated problems: a) Relatively little is known about the magnitude, duration, frequency, and timing of cumulative exposure to important environmental mixtures. b) Scant evidence is available on whether mixture-related effects are antagonistic, synergistic, or additive at exposure levels typically encountered by people. c) There is inadequate knowledge and insufficient understanding about interactive mechanisms of toxicity that occur among mixture constituents. In the near-term, quantitative assessment of cumulative risks depends not only on targeted research but also on development of science-based methods and procedures for using existing exposure and effects data to characterize mixture-related health risks with an acceptable degree of precision. This will unavoidably involve science policy decisions about how best to bridge the gap between the scarcity of hard scientific evidence and the need to estimate cumulative risks as an integral part of risk management decisions.

Cumulative risk assessment will be most useful to decision makers when it can help answer a fundamental question: “Do the uncertainty/safety factors built into the conventional risk assessment process adequately protect public health and ecologic resources from cumulative effects with a sufficient margin of safety?” To be relevant, therefore, cumulative risk assessment must provide guidance about which, if any, of the innumerable environmental mixtures that are part of our day-to-day lives represent important health risks, where “important” means there is a reasonable likelihood that combined effects of mixture constituents at realistic exposure levels constitute a serious health risk that is not adequately accounted for by traditional risk assessment methods.

SCIENCE: Vascular Effects of Ambient Pollutant Particles and Metals

2008-08-12T09:17:00.001+01:00

Article in Current Vascular Pharmacology, (2006) 4, 199-203 by Yuh-Chin T. Huang and Andrew J. Ghio of National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, USA and Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA.

Abstract

Exposure to ambient pollutant particle (APP) is associated with increased cardiovascular morbidity and mortality. Recent evidence indicates that APP-induced vasoconstriction may be an important mechanism. APP constricts systemic arteries and increases blood pressure in human. APP decreases the diameter of pulmonary arterioles in animals. Intratracheal instillation of APP increases pulmonary artery resistance in isolated buffer-perfused lungs, and APP constricts isolated arterial rings. APP-induced vasoconstriction may be secondary to the release of inflammatory mediators from lung cells, which then activate vascular endothelial and smooth muscle cells. The vasoconstriction may also be caused by alterations in autonomic nervous system balance. Some soluble metals (e.g., vanadium) can produce acute vasoconstriction in in vitro and in vivo systems, and contribute to the systemic health effects of APP since they can more easily permeate the alveolar-capillary membrane than the whole particle. Both APP and its associated metals have been shown to enhance the release of endothelin 1 and reactive oxygen species, activate epithelial growth factor receptor and mitogenactivated protein kinases, and inhibit nitric oxide vasodilator activity. The vasoactive properties of APP and metals raised the possibility that patients with vascular diseases may be more susceptible to APP-induced adverse health effects, and that people who are regularly exposed to high amount of metals, e.g., vanadium contained in certain dietary and musclebuilding regimens or in the air of boiler making plants, may have increased risk for vascular diseases. Understanding how metals induce vasoconstriction may lead to the development of novel vasodilator therapies for vascular diseases.

Extracts

... The present review will focus on how ambient pollutant particle (APP) and its metal constituents affect vascular function. ...

APP AND ADVERSE CARDIOVASCULAR HEALTH EFFECTS

APP is a complex mixture of solid and liquid particles suspended in air. APP varies in size and chemical composition depending on the source and age as well as the surrounding gases. APP can come from anthropogenic (e.g., combustion of fossil fuels), or natural (e.g., soil resuspension) sources with secondary modification by physicochemical reactions between gas and particles in the atmosphere [3]. Consequently APP contains multiple chemical constituents, including metals in the forms of oxides and salts, soluble salts (e.g., ammonium nitrate and sulfates), and organic materials (e.g., elemental carbon and hydrocarbon compounds) [4]. The specific composition and relative abundance of these constituents in APP depend on the sources and thus can vary from place to place. For example, APP from fossil fuel combustion emissions (e.g., oil fly ash) contains large amount of soluble transition metal in additional to a relatively inert carbonaceous matrix. This is in contrast to APP derived from soil (e.g., Mount St. Helen dust) which has almost no transition metals [5].

Over the last decade, a growing body of epidemiological and clinical evidence has raised the possibility of the potentially deleterious effects of ambient pollutant particles on cardiovascular health. Exposure to APP has consistently been associated with increased hospitalization and mortality due to cardiovascular diseases [2,6,7]. It is estimated that the daily cardiopulmonary mortality in the short term increased by 0.3% for each 10-µm/m3 increase in PM10 (particulate matter [PM] <>.

The causes for the short term cardiovascular morbidity and mortality have been investigated. In Sweden, workers with exposure to products from non-vehicular combustion processes had increased risk of myocardial infarction [11]. In Helsinki, Finland, APP was associated with increased risk for hospital admission for transient myocardial ischemic attacks [12]. Elevated concentrations of PM2.5 were associated with a transient risk of developing acute myocardial infarction within hours after exposure [13]. Exposure to PM has also been associated with the development of cerebrovascular disorders [14]. The pathophysiological mechanisms for the increased cardiovascular morbidity and mortality have been proposed, including increases in heart rate and blood pressure [15], fibrinogen [16,17] and blood coagulation factors; decreased heart rate variability [18]; release of inflammatory mediators [19,20]; and endothelial injury/dysfunction and arterial vasoconstriction [21,22]. …

CONCLUSIONS

Studies on the cardiovascular adverse effects of APP have had tremendous public health impact. The effects of APP-associated metals on vascular reactivity provide a biologically plausible mechanism for the adverse cardiovascular effects associated with APP. These effects are likely more detrimental in patients with compromised cardiovascular conditions, including congestive heart failure, coronary artery disease and vascular disease (e.g., in diabetes). In addition, the vascular effects of exogenous metals also raise the concerns that people who regularly consume certain weight-reduction and muscle building supplements that contain high amount of vanadyl sulfate (e.g., Satieté®) may be at risk for developing cardiovascular diseases. Future research will be needed to determine the metabolic fate of these environmental metals in the cell and how cellular defense mechanisms are activated to combat the toxicity induced by these metals. Understanding how metals induce vascular changes may lead to development of novel therapy for vascular diseases.

SCIENCE: Metal ions and carcinogenesis

2008-08-12T09:11:00.001+01:00

Chapter in book ‘Cancer: Cell Structures, Carcinogens and Genomic Instability’ (edited by Leon P. Bignold (2006) Birkhäuser Verlag/Switzerland, pages 97-130) by Troy R. Durham and Elizabeth T. Snow of the Centre for Cellular and Molecular Biology, School of Biological and Chemical Sciences, Deakin University, Victoria, Australia.

Abstract

Metals are essential for the normal functioning of living organisms. Their uses in biological systems are varied, but are frequently associated with sites of critical protein function, such as zinc finger motifs and electron or oxygen carriers. These functions only require essential metals in minute amounts, hence they are termed trace metals. Other metals are, however, less beneficial, owing to their ability to promote a wide variety of deleterious health effects, including cancer. Metals such as arsenic, for example, can produce a variety of diseases ranging from keratosis of the palms and feet to cancers in multiple target organs. The nature and type of metal-induced pathologies appear to be dependent on the concentration, speciation, and length of exposure. Unfortunately, human contact with metals is an inescapable consequence of human life, with exposures occurring from both occupational and environmental sources. A uniform mechanism of action for all harmful metals is unlikely, if not implausible, given the diverse chemical properties of each metal. In this chapter we will review the mechanisms of carcinogenesis of arsenic, cadmium, chromium, and nickel, the four known carcinogenic metals that are best understood. The key areas of speciation, bioavailability, and mechanisms of action are discussed with particular reference to the role of metals in alteration of gene expression and maintenance of genomic integrity.

Extracts

Introduction

The association of metal exposure with cancer is a well-documented phenomenon. Metals such as arsenic (As), cadmium (Cd), chromium (Cr), and nickel (Ni) are part of an ever growing list of environmental agents that have been formally classified by the International Agency for Cancer Research (IARC) as being known carcinogens [1–4]. For other metals such as iron, copper, beryllium, lead, and mercury there exists an ever increasing body of evidence to support their inclusion in the IARC listings [5–8]. Iron [8] and copper [7], in particular, are carcinogenic in excess, but are highly regulated and generally only produce cancer in animal models or in people with genetic diseases that prevent appropriate metabolic regulation. There is even less information on beryllium carcinogenesis, and no definitive studies that indicate the species, conditions or length of exposure by which lead and mercury metals cause cancer in humans. For these reasons, this review will focus on the known carcinogenic metals: As, Cd, Cr and Ni.

Despite increasing numbers of researchers in the field and the expanding role of metals in environmental health issues, the nature of cancer induction by metals remains a complex and poorly understood process. However, what is known is that metals can promote change in normal cellular functions, leading to aberrant cell growth and development [6]. All metals are now thought to promote cancer by a number of common mechanisms. These include the formation of free radicals, either actively as key players in redox reactions, or through less direct means such as biomethylation [5, 6, 9, 10]. Similarly, many metals can also influence cell control by altering gene regulation [7, 11–14]. In terms of direct damage to DNA, most metals are only weakly mutagenic; however, many are strong co-carcinogens, promoting a synergistic effect in the presence of other cancer-causing agents [5, 6, 15]. Hence, the ability of metals to promote cellular alterations may be far more dynamic than has been classically assumed. Thus, it is the purpose of this review to evaluate mechanisms that are central to the role of metals as carcinogenic agents. This review outlines current evidence related to the mechanisms of genotoxicity and gene expression, as well as other mechanisms unique to specific metals. The principle focus is on those metals for which the IARC has deemed there to be sufficient evidence to classify as carcinogens, and that there is the most information regarding genotoxic mechanisms. Because of the great amount of data now available on this topic, this chapter does not claim to be exhaustive, but will hopefully provide a useful survey of the field, with selected references focusing heavily on recent reviews. ...

Speciation, uptake and health effects of specific metals

Arsenic

... Occupational exposure to arsenic is greatest in mining and metal smelting industries; ...

Arsenic in the environment can take a range of forms, both organic and inorganic. Inorganic arsenic has two possible valencies, arsenite, or As(III) and arsenate, As(V). Arsenite is the more toxic of the two species with cell viability assays indicating that concentrations anywhere from 1 to 10 µM and upwards are able to promote toxicity [5]. Arsenate is approximately three to fivefold less toxic than arsenite, presumably because As(V) requires reduction to As(III) to exert its toxicity. Organoarsenic species can also be formed by biometabolism. Many organoarsenic species are significantly less toxic than inorganic As(III). However, methyl As(III) species can be significantly more toxic than inorganic As(III) [40] and may contribute to arsenic carcinogenesis. The relative toxicity of the different forms of arsenic is predominantly the result of their different chemical properties, but may also relate to the relative efficiency of their uptake [41, 42], the duration of the exposure, and the time when the toxicity assay is performed [42, 43]. Arsenic excretion rates vary, but it is generally accepted that arsenic, unlike other carcinogenic metals, is rapidly excreted by the body, to the extent that more than 50% is removed within 2 days in acute poisoning cases [33]. ...

Arsenic pathology is complex. ... At very low doses, arsenic appears to have minimal short-term effect however, over longer periods a range of pathologies are seen [2]. Chronic low-dose exposure initially produces blotching of the skin, followed by hyperkeratosis of the palms and soles of the feet. If exposure continues, alterations to peripheral vasculature are seen along with the formation of skin lesions, which left untreated, can become cancerous [47, 48]. Arsenic is also associated with an increased risk for cancer of the lungs, liver and bladder [47].

Induction of cancer by arsenic is not thought to originate from a single exposure, but rather is the result of gradual changes to a variety of processes within the cell. Different arsenic species enter cells by different mechanisms. Arsenate is able to mimic phosphate, and hence is able to enter cells using phosphate transport proteins. Arsenite, however, is thought to enter through aquaglyceroporins [49]. Once in the blood stream, arsenic is taken to the liver where biometabolism occurs. This process involves the progressive methylation of arsenic, with As(III) converted to the less toxic methyl As(V) species. The ingested arsenic is excreted predominantly in the urine as inorganic As(III) and As(V), methyl As(V), and dimethyl As(V), with the proportions of these being variable and related to arsenic dose [50–52]. Some intermediate trivalent arsenic metabolites are also produced, and can be found in the urine [53]. Despite their greater toxicity, relative to either inorganic As or organic As(V) species, it is yet to be determined whether these methyl As(III) and dimethyl As(III) species play a significant role in carcinogenesis.

Cadmium

Unlike many other metals, cadmium is found in only one valence state, that of Cd(II). Exposure to cadmium has also been far less common than other carcinogenic metals. Of greatest note was the historical use of cadmium as a paint additive giving rise to the bright yellows seen in many paintings, such as those of Claude Monet [54]. Industrial use of cadmium is only a recent phenomenon, beginning in the 1940s. Cadmium is now most commonly encountered in cadmium- nickel battery production [10], although it continues to be used in paints, as well as in plastic production where it is an effective stabilizing agent. Like arsenic, occupational exposure to cadmium can occur through metal refining processes, where cadmium is often associated with copper and can be released into the atmosphere during heating [55]. The greatest exposure to cadmium, however, comes from cigarette smoke [10]. Particulate cadmium in cigarette smoke collects in the lungs where it can be transported into the bloodstream across the alveoli. Unlike arsenic, cadmium has a long biological half life, considered to be somewhere between 15 and 25 years [4, 56]. This means cadmium can accumulate to levels many times greater than an individual would be subjected to in a single exposure. Cadmium is only a weak mutagen, but is a strong co-mutagen [4, 57, 58]. This is of particular concern for cigarette smokers who simultaneously inhale cadmium and benzo[a]pyrene, as well as a range of other chemicals, including arsenic and other metals.

Health effects of cadmium are quite dissimilar to other metals. Non-toxic doses of cadmium produce a wide variety of effects, many of which are related to bone development and maintenance. Individuals exposed to cadmium can develop osteoporosis, anemia, eosinophilia, emphysema, and renal tubular damage [59]. Long-term cadmium toxicity can produce Itai-Itai disease, in which individuals suffer from bone fractures, severe pain, proteinuria and severe osteomalacia [59]. Acute high-level exposure to cadmium is also able to produce severe lung damage. However, like other metals, prolonged repeated exposures are required to induce carcinogenesis. Target organs for cadmium are varied however, lung cancers predominate [4]. Other tissues subject to malignant transformation by cadmium include the prostate, pancreas and kidney. The testes are also thought to be a site of cadmium carcinogenesis; however, this has only been shown in animal models. Like arsenic, cadmium is only a weak mutagen. This suggests that tumors result from either epigenetic or co-carcinogenic effects, particularly in cases of smoking-induced lung cancer [10].

Chromium

Chromium is widely available, complex in action, and used industrially in a myriad of applications including, pigment production, chrome plating, welding, production of ferrochrome metals, leather tanning and as a dietary supplement [3, 60]. Dietary supplementation is of particular interest because of the critical nature of Cr(III) for optimum insulin binding [61]. Occupational exposure to Cr(VI) is a well-established source of human carcinogenesis; however, occupational health initiatives have had a considerable impact in reducing incidence levels. Non-occupational sources of exposure are thought to originate from engine emissions, atmospheric particles released from smelting and refining industries, as well as through cigarette smoke [13]. Chromium speciation is complex, and chromium is often found in compounds with other metals. Environmental chromium is generally found in two principle valency states, the more toxic and carcinogenic Cr(VI) [60] and the essential Cr(III). Cr(VI) species are readily taken up into cells by phosphate/sulfate anion channels [62–64]. Cr(III), however, cannot move into cells by the same mechanism, and is required at considerably higher concentrations to produce toxicity in cells. It must be noted, however, that not all Cr(VI) species are of equal carcinogenic risk. Animal models have shown that the largely insoluble chromium compounds are far more carcinogenic than their soluble counterparts [3, 65]. It appears that particulate matter containing insoluble chromium is deposited on the epithelial surface of the lung where it accumulates to levels high enough to produce cancer [66]. ...

Unlike arsenic and cadmium, chromium is an essential trace element in its trivalent form. That said, Cr(VI) species can be highly toxic to humans [13]. Inhalation of particulate Cr(VI) can cause irritation to the nasal tissue, leading to nose bleeds, ulceration and formation of lesions in the nasal passage [60]. Damage to lung tissue is also not uncommon [70, 71]. Ingestion of Cr(VI) can cause nausea, vomiting, ulceration of the stomach, damage to the liver and kidney, and finally death [60]. Both species of chromium can cause contact hypersensitivity, leading to rashes, swelling and ulcerations. Cr(VI) is the most carcinogenic form of chromium, with insoluble particulate chromium compounds being the most persistent [66] and the most hazardous [72].

Nickel

Nickel has many common industrial uses, thanks largely to its unique chemical properties. Industrially, it is used in electroplating, electroforming, in circuitry, and in nickel-cadmium batteries. Nickel alloys, including stainless steel, are used in a wide variety of objects, from kitchen knives to building tools [73]. Nickel is also used in jewelry and medical implements. Metallic nickel is non-carcinogenic to humans; however, all other nickel compounds, such as nickel sulfides, oxides, and silicates, and other soluble salts, are known carcinogens [12]. Carcinogenic nickel exposure is greatest through the inhalation of nickel-containing particulates. The burning of fossil fuels, as well as the refining of metals such as copper, introduces considerable amounts of nickel into the atmosphere [12]. Like arsenic, nickel can also be leached from soils and rock, thereby contaminating water supplies. In lower organisms such as bacteria, nickel is an essential trace element found in up to seven different enzymes [74]. Higher organisms, however, have failed to show any definitive role for nickel in normal cellular function. That said, studies in the 1970s and 80s showed that the removal of nickel from the diet of rats had significant effects both physically and mentally, which, with continued exclusion of nickel from the diet, were more profound in the subsequent generations [75]. It may be that nickel is not required for normal cellular function in humans, but rather is essential for our intestinal microflora. Like both arsenic and chromium, nickel occurs in different oxidation states, ranging from I to IV, with Ni(II) being most common in biological systems.

As with chromium, particulate nickel is most harmful to humans, especially in the lung where crystalline nickel becomes lodged in the mucous prior to being phagocytized by both epithelial cells and macrophages [76]. Once inside the cells, the nickel compounds are gradually broken down releasing reactive nickel ions. The phagocytic nature of nickel uptake means considerable amounts of nickel are able to accumulate over time, damaging lung tissue and frequently causing latent effects in individuals who may have been exposed to nickel many years earlier [76].

Nickel is not overly toxic to individuals at low doses; however, nickel-containing jewelry can produce contact hypersensitivity in many people [73]. This normally results in rashes and inflammation of the region of contact. However, 104 T.R. Durham and E.T. Snow in more extreme reactions, individuals can suffer from asthma attacks. Individuals who inhale nickel fumes for prolonged periods of time frequently develop bronchitis and chronic lung infections. While ingestion of large quantities of nickel is not normally fatal, it can produce stomach aches, kidney pain and blood in the urine [73]. Nickel carcinogenesis is generally limited to the lung, because phagocytosis is necessary to bring the nickel ions to the DNA in the target tissue [12, 77].

Metals and oxidative stress

Most, if not all, of the carcinogenic metals, have the capacity to produce a variety of radical species that can damage cells. Arsenic, chromium, copper, iron, nickel and, to a lesser extent, cadmium, have all been shown to be able to participate in reactions resulting in the formation of reactive oxygen, sulfur or nitrogen species (for reviews see [6, 7, 11, 14, 27, 76–79]). In most cases these metals produce either radicals based on oxygen species or those based on nitrogen species; however, the formation of oxygen species appears to predominate. The formation of radical species can originate from a variety of sources, from redox cycling, through Fenton/Haber-Weiss chemistry, as products of biometabolism, as messengers in signal cascades, and as normal products of cellular metabolism [6, 80, 81]. Essential transition metals, such as iron and copper, are most likely to participate in redox cycling and Fenton/Haber- Weiss chemistry; however, these metals are highly regulated and are of less concern with regard to carcinogenesis. Nevertheless, other carcinogenic metals may also react in similar fashion and thereby produce reactive species that can cause DNA damage and mutations. Some of the key reactions responsible for the metal-related formation of reactive oxygen species (ROS) are described briefly below. ...

Mechanisms of metal induced alterations in DNA repair

DNA is a dynamic molecule, constantly under assault from both endogenous and exogenous agents, which can often facilitate mutational changes to its sequence. DNA replication also causes changes in genetic material through the infidelity of replication enzymes, most notably during bypass of DNA lesions. The error rate of replication and repair of endogenous base damage has been shown to lead to the formation of lesions with a frequency of one in every 104–109 bases per cell per day [147]. To combat this, cells have developed a variety of DNA repair mechanisms. In mammalian cells these repair processes fall within several distinct pathways: mismatch repair (MMR), homologous and non-homologous rejoining, nucleotide excision repair, base excision repair, and direct reversion of damage. Alterations in the regulation and activity of repair processes have been shown to occur through interactions of cells with a variety of agents, including many metals. Interference by metal ions with DNA repair has the capacity to increase the potential for mutations, which then persist in the genome. A major consequence of this is the initiation of carcinogenesis. The following paragraphs outline the repair processes that have been shown to be affected by As, Cr, Cd, and Ni. ...

DNA and protein interactions

The formation of metal complexes with amino acids, proteins and DNA is common in cells. Interactions of this nature have been speculated to have a wide range of consequences, including initiation of signal cascades, constitutive activation or inactivation of enzymes, as well as inhibition of both DNA repair and replication. Arsenic, chromium and nickel all exhibit the capacity to create or become part of a variety of complexes in cells. Cadmium and other metals may also form protein complexes, although the role of these complexes in carcinogenesis is less well understood. ...

Effects on gene regulation: direct and epigenetic changes

Metals have been shown to alter the expression of a great number of genes, too many to cover in detail here. These changes in gene expression are generally 114 T.R. Durham and E.T. Snow transient, and can be produced or caused by a multitude of different factors. Accordingly, this section looks at a limited number of genes that best illustrate the effects of carcinogenic metals on gene expression. For more detailed information on gene expression, the following recent reviews cover each metal in detail [10, 12–14]. Changes in gene expression are often thought to be the indirect result of signal cascades, DNA methylation changes and ROS; however, metals may also be directly responsible for changes in transcription factor activity. Epigenetic mechanisms are heritable changes that can impart effects on the regulation of genes without altering the genomic sequence itself. Hypermethylation generally causes genes to be downregulated or effectively switched off, while hypomethylation often results in increased levels of gene expression. A number of agents that induce carcinogenesis, such as X-rays, have been shown to affect cells in this manner [224]. Similarly, nickel, arsenic, and, to a lesser extent, cadmium and chromium, are able to produce extensive alterations in genomic methylation [10, 23, 25, 97, 225–228]. ...

Summary

Agents responsible for human carcinogenesis are grossly varied in their properties, and metals are no exception. However, it seems likely that metals share several common means by which to induce cancer. Critically, the most important of these appears to be the generation of oxidative stress and deregulation of key maintenance genes within cells. That said, the nature of the dose of each of these metals, as well as confounding variables required to produce a carcinogenesis, remain at best an unresolved issue. However, with time, and as research progresses, it is likely that a more complete picture will emerge on metal-induced carcinogenesis.

Source

SCIENCE: Atmospheric levels and cytotoxicity of PAHs and heavy metals in TSP and PM2.5 at an electronic waste recycling site in southeast China

2008-08-12T09:09:00.001+01:00

Article in Atmospheric Environment 40 (2006) 6945–6955 by W.J. Deng, P.K.K. Louie, W.K. Liu, X.H. Bi, J.M. Fu, M.H. Wong (Croucher Institute for Environmental Sciences and Department of Biology, Hong Kong Baptist University, Kowloon, Hong Kong, China & other institutes).

Abstract

Twenty-nine air samples of total suspended particles (TSP, particles less than 30–60 μm) and thirty samples of particles with aerodynamic diameter smaller than 2.5 μm (PM2.5) were collected at Guiyu, an electronic waste (e-waste) recycling site in southeast China from 16 August 2004 to 17 September 2004. The results showed that mass concentrations contained in TSP and PM2.5 were 124±44.1 and 62.12±20.5 μgm-3, respectively. The total sum of 16 USEPA priority polycyclic aromatic hydrocarbons (PAHs) associated with TSP and PM2.5 ranged from 40.0 to 347 and 22.7 to 263 ngm-3, respectively. Five-ring and six-ring PAHs accounted for 73% of total PAHs. The average concentration of benzo(a) pyrene was 2–6 times higher than in other Asian cities. Concentrations of Cr, Cu and Zn in PM2.5 of Guiyu were 4–33 times higher than in other Asian countries. In general, there were significant correlations between concentrations of individual contaminants in TSP with PM2.5 (i.e. PAHs, Cd, Cr, Cu, Pb, Zn, Mn except Ni and As). The high concentrations of both PAHs and heavy metals in air of Guiyu may impose a serious environmental and health concern. Cytotoxicity of the extract of TSP and PM2.5 of ten 24 h samples collected against human promonocytic leukemia cell line U937 (ATCC 1593.2) was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cytotoxicity assay. The results showed that under the same concentrations of extract, PM2.5 cytotoxicity was 2–4 times higher than TSP.

Extracts

... The uncontrolled combustion of electronic scraps has the potential to produce highly toxic heavy metals and metalloids, such as lead (Pb), cadmium (Cd), chromium (Cr), arsenic (As), as well as polyhalogenated pollutants, including Polycyclic aromatic hydrocarbons (PAHs) (Qiu et al., 2004). Our previous studies have shown the contamination of the terrestrial environment of Guiyu by persistent organic pollutants and heavy metals (Leung et al., 2006; Wang et al., 2005). PAHs are known to be persistent, bio-accumulative, carcinogenic and mutagenic. High levels of PAHs and heavy metals in air will impose serious environmental and biological problems (Park et al., 2002). Increased risks of mortality and morbidity have been associated with elevated levels of total suspended particles (TSP) in ambient air, especially for fine particles with aerodynamic diameter less than 2.5 mm (PM2.5) (Schwartz et al., 1996). ...

... The World Health Organization (WHO World Health Organization, 2000) regards BaP [Benzo(a)pyrene] as an indicator of carcinogenic risk. ...

... Size distribution of PAHs determines the degree of human respiratory system penetration. Small sizes (<>. ...

SCIENCE: Evaluation of toxic metals in biological samples (scalp hair, blood and urine) of steel mill workers by electrothermal atomic absorption ...

2008-08-12T09:06:00.001+01:00

SCIENCE: Evaluation of toxic metals in biological samples (scalp hair, blood and urine) of steel mill workers by electrothermal atomic absorption spectrometry

Article in Toxicology and Industrial Health (2006), 22: 381-393 by Hassan I Afridi, Tasneem G Kazi, Mohammad K Jamali, Gul H Kazi, Mohammad B Arain, Nusrat Jalbani, Ghulam Q Shar and Raja A Sarfaraz of Center of Excellence in Analytical Chemistry, University of Sindh, Jamshoro , Pakistan.

Abstract

The determination of toxic metals in the biological samples of human beings is an important clinical screening procedure. This study aimed to assess the possible influence of environmental exposure on production workers (PW) and quality control workers (QCW) of a steel mill, all male subjects aged 25-55 years. In this investigation, the concentrations of Pb, Cd, Ni and Cr were determined in biological samples (blood, urine and scalp hair samples) from these steel mill workers in relation to controlled unexposed healthy subjects of the same age group. After pre-treatment with nitric acid-hydrogen peroxide, the samples were digested via a microwave oven, and for comparison purposes, the same samples were digested by the conventional wet acid digestion method. The samples digested were subjected to graphite furnace atomic absorption spectrometry (GFAAS). To assess the reliability of these methods, critical factors, such as detection limit(s), calibration range(s), accuracy and precision, were studied. Quality control for these procedures was established with certified sample of human hair, urine and whole blood. The results indicate that the level of lead, cadmium and nickel in scalp hair, blood and urine samples were significantly higher in both groups of exposed workers (QW and PW) than those of the controls. The possible connection of these elements with the etiology of disease is discussed. The results also show the need for immediate improvements in workplace ventilation and industrial hygiene practices.

Extracts

Introduction

Human biomonitoring for toxic metals continues to receive considerable attention as the effort to reduce the uncertainty in health risk assessment increases. The primary goal of biomonitoring studies is to evaluate human exposure by comparing the measured concentrations of toxic elements with those of control groups or with literature-based ‘background’ values. Thus, in the assessment of health risk, the knowledge of reference values (RVs) in human tissues and fluids provides a meaningful insight into the extent of the exposure, and is of fundamental importance in environmental pollution control. A number of heavy metals as well as dust fumes and gases are found in these working environments. The exposure may have both acute and long term effects.

Cadmium, lead and nickel are toxic metals with a long history of detrimental effects. Exposure to these toxic metals is common in industry, where the metals are used in a wide range of manufacturing processes. The presence of heavy metals, such as Pb and Cd, replaces Ca and Zn, respectively, by competition with binding sites in biological systems. It is also known that these toxic metals and their compounds can be toxic if their concentrations exceed certain limits (Smith-Sivertsen et al., 1997). ...

Cadmium exposure has been associated with many physiological disorders, such as hypertension, and many studies show that hair levels of Cd in hypertensive patients are higher than controls (Engvall et al., 1985). The Cd concentration in urine (U-Cd) is mainly influenced by the body burden, being proportional to the kidney concentration. The urine level of cadmium is also a good measure of body stores (Lauwerys et al., 1994). Cigarette smokers and people living in contaminated areas have higher level of Cd in blood and urine, but smokers have more than twice as high concentration as non-smokers. Blood-Cd generally reflects current exposure, but partly also lifetime body burden (Waalkes et al., 1992; Jarup et al., 1998).

Although the role of Cr and Ni as essential trace elements in humans is no longer debated, the interest in these metals is mainly dictated by their noxious potential as industrial and environmental pollutants. Individual Ni exposure, in turn, seems also to be associated with the level of urbanisation. This may be traced back to Ni content in automobile exhausts and bitumen, the main component of asphalt. Nickel occurs also in road dust; Ni containing particles may thus easily make their way into the respiratory tract. Nickel accumulates with age and smoking, perhaps explaining why tissue levels are highest in patients who died of cardiovascular disease. Nickel’s ability to cause contact dermatitis, and its observed perturbation of immunoglobulin levels was investigated that elevated levels of nickel in hair may serve as an indicator of possible immune dysfunction, as well as a potentially useful marker of cardiovascular problems (Vienna et al., 1995).

Occupational exposure to chromium occurs from chromate and stainless-steel production, chromeplating, and working in tanning industries; occupational exposure can be two orders of magnitude higher than exposure to the general population (Agency for Toxic Substances and Disease Registry, 1998). The trivalent Cr is the more common form. However, the hexavalent form, such as chromate compound, is of great industrial importance. The major source of Cr is from chromites ore. Metallurgical grade chromite is usually converted into one of several types of ferrochromium or other Cr alloy containing Co or Ni. Ferrochrome is used in the production of stainless steel. Over review of Cr exposures and health effect have been reviewed (WHO, 1998).

Scalp hair and urine samples are easily sampled and provide a useful indicator of exposure to toxic and heavy metals for several diseases. Blood analysis is also important to monitor the immediate effects of environmental exposure.

Hair has the potential of being an excellent biomonitor due to its historical representation of intake over prior weeks to years, depending on its unique features, hair can also be utilised for investigating the exposure of individuals or populations to toxins and pollutants, such as heavy metals (Bencko, 1995; Martin et al., 2005). Its popularity lies in the fact that it can be collected easily and non-traumatically and can be stored easily. Most trace elements have higher concentration in hair than other body compartment, which helps in the analytic process (IAEA Review, 1994). Profiling for toxic metals has been used to identify the origins of exposure to mercury (Toribara, 2001) or monitoring medical treatments (Nicolis et al., 2000). Many studies have shown a correlation between heavy metals concentration in hair and blood (Chlopicka, 1998). Significant elevations of toxic element levels are also observed in human hair, particularly cadmium, lead, and nickel (Chattopadhyay et al., 1990; Wolfsperger et al., 1994).

The standard clinical procedure for the measurement of toxic elements in biological samples is very simple and is based on the use of highly sensitive GFAAS instrumentation. Several analytical techniques have been commonly used for heavy metals in blood measurement. The recommended method is graphite furnace atomic absorption spectrometry (GFAAS) (Parsons et al., 1993; Mido et al., 1995; Zhang et al., 1997).

The biological monitoring of toxic metals in biological samples has become a matter of wide interest owing to the toxicity of these metals and their influence in controlling the course of biological processes. Karachi is the most important metropolitan city of Pakistan, having many big industrial areas, and it is also the most affected by air pollution and industrial wastes (most of the pollutants being heavy metals), which are detrimental to human health. The aim of this study was to investigate the concentration of cadmium, chromium, lead and nickel in the biological samples (scalp hair, blood and urine) of long-term exposed steel production (PW) and quality control (QCW) workers to evaluate the degree of their exposure in these working environments. The obtained results have been compared with those of same age groups, healthy persons not exposed to industrial environmental pollution. The tissue concentrations related to a number of other variables, eg, age, employment time, health and habits (smoking or chewing tobacco) have been studied. These data can provide guiding references to occupational diseases and pollution control. ...

Results and discussion

Heavy metals of considerable toxicological importance pose a challenge for authorities in the public health and industrial hygiene sectors. A number of heavy metals, as well as dust, fumes and gases, are found in these working environments. The exposure may have both acute and long term health effects (Mikac-Devic et al., 1977).

Heavy metal toxicity generally results in gastrointestinal irritation, renal toxicity and multi-organ toxicity. Gastrointestinal irritation is the most common complaint, and may manifest as nausea, vomiting, diarrhea and abdominal pain. Renal toxicity is the second most common adverse event, and may be caused by acute and subacute exposure to heavy metals. On the other hand, interstitial nephritis is more likely cause by chronic exposure to heavy metals. Multi-organ toxicity may affect the skin and central nervous system as well (Adeloju et al., 1985). ...

Conclusions

We have established the analytical procedure to determine lead, chromium, cadmium, and nickel in biological samples (blood, urine and scalp hair) by a technique that is not only easier to follow and less expensive to run, but also more rapid and accurate than other techniques, thus providing a useful tool to screen large number of individuals that are at a risk of exposure to these and perhaps other metals.

The results show that in steel production, the workers assigned to the production and QC areas are indeed exposed to these metals, presenting significantly elevated levels in all three biological samples when compared to normal controls. The significantly high level of all these metals under consideration was observed with respect to duration of exposure. This suggests the need for immediate improvement of workplace ventilation and industrial hygiene practices.

SCIENCE: Concentrations of Ni and V, other heavy metals, arsenic, elemental and organic carbon in atmospheric fine particles (PM2.5) from Puerto Rico

2008-08-12T09:02:00.000+01:00

Article in Toxicology and Industrial Health (2006); 22: 87-99 by David Acevedo Figueroa, Carlos J Rodriguez-Sierra and Braulio D Jimenez-Velez of Center for Environmental and Toxicological Research, Department of Biochemistry, University of Puerto Rico, Medical Sciences Campus, San Juan, Puerto Rico & Department of Environmental Health, Medical Sciences Campus, University of Puerto Rico, San Juan, Puerto Rico.

Abstract

Fine atmospheric particulate PM2.5 (particles with diameters of <2.5>

Extracts

Particulate air pollutants have been associated with increased respiratory, cardiovascular and cancer mortality and morbidity, and with other health problems (Dockery et al., 1993; Reichhardt, 1995). The fine fraction of the atmospheric particulate matter is of great concern because it is predominantly deposited in the alveolar region of the lung where absorption efficiency is higher and the overall removal of particles is relatively inefficient (Hlavay et al., 1992; Lippmann et al., 1980). Only about 20% of particles deposited in the alveolar region are cleared in the first day, and the remaining portion is cleared very slowly (Rozman and Klassen, 1996). The fine fraction includes particles with aerodynamic diameters of <2.5>. In addition, several studies suggest an association between motorized traffic-related air pollution and diminished pulmonary function and/or increased respiratory symptoms in children (Kim et al., 2004; Weiland et al., 1994).

PM2.5 is mainly produced by particles emitted directly into the atmosphere and particles formed in the air from the chemical transformation of gaseous pollutants (secondary particles) (Kim et al., 2005). The principal types of directly emitted particles are soil related, elemental/organic carbon (EC/OC) and other particles from the combustion of fossil fuels and biomass materials. However, PM2.5 has a low level of soil particle components, and the main anthropogenic source is a product of the combustion of fossil fuels (Ohlstro¨m et al., 2000). Principal sources of PM2.5 include combustion of coal, oil, gasoline, diesel or wood, atmospheric transformation products of NOx, SO2and organic compounds, natural and anthropogenic (WHO, 2000).

It is well known that fine particles have high concentrations of many potentially toxic trace metals, such as cadmium (Cd), chromium (Cr), copper (Cu), iron (Fe), manganese (Mn), nickel (Ni), lead (Pb), vanadium (V) and zinc (Zn), that can be incorporated into the body through inhalation (Singh et al., 2002). The metal content on fine particles has been suggested as causative agents associated with adverse respiratory health effects (Dreher et al., 1997; Ghio et al., 1996). Most of the toxic metals in the air are in the form of fine particles, with a size distribution equivalent to that of aerosols (1.0 mm or less in diameter). It is suggested that these metals can produce lung tissue damage by catalyzing oxidant formation (Fang et al., 1999) and promoting the release of inflammatory mediators and cytotoxicity (Frampton et al., 1999). Recent epidemiological studies have linked low DNA repair activity with lung cancer (Paz-Elizur et al., 2003), showing that there is a component of the population with a higher cancer risk. The studies showed that this population may have a genetic predisposition to lung damage and is more susceptible to metal exposure from airborne particulates. ...

Toxicological effects of metals

Although there is no consistent evidence for the carcinogenicity of arsenic compounds in animals (WHO, 2000), there is sufficient evidence to indicate that inorganic arsenic compounds are skin and lung carcinogens in humans (WHO, 2000). Inorganic arsenic seems to affect DNA repair mechanisms (Rossman, 1981). Teratogenic effects in the hamster, rat and mouse were detected at high exposure levels (WHO, 2000). Chronic exposure to arsenic causes neurotoxic effects in human (Lagerkvist and Zetterlund, 1994). Increased mortality from cardiovascular diseases has been observed in epidemiological studies of smelter workers exposed to high levels of airborne arsenic (WHO, 2000). In addition, spontaneous abortions and lower mean birth weights have been registered in smelter workers and among subjects living in the vicinity of the smelter (WHO, 2000). …

Nickel compounds induce respiratory tract irritation, chemical pneumonia, emphysema, varying degrees of hyperplasia in pulmonary cells, and fibrosis (pneumoconiosis) in animals by inhalation (WHO, 2000). Ottolenghi et al. (1974) described a significant increase in the number of lung tumors in rats following inhalation exposure to nickel subsulfide for about two years. Nickel carbonyl inhalation in rats has produced lung tumors in one of three reported experiments compared to none in corresponding control groups (WHO, 2000). Acute inhalation exposure to nickel carbonyl has also caused lung damage, mucosal irritation, and asthma in workers exposed to inorganic nickel compounds (WHO, 2000). There is no epidemiological information on nickel uptake from the environment or relations with cancer incidence in the general population. However, nickel refinery workers exposed through inhalation to various nickel compounds have a higher risk of lung cancer and nasal cavity cancers than the non-occupationally exposed population (ICNCM, 1990; WHO, 2000). Some studies show a correlation between nickel workers and incidence of laryngeal, kidney, prostate or bone cancer (ICNCM, 1990). There is no need to emphasize the significance and need to learn more about the relevant environmental exposure concentrations of nickel, which would exert a health effect on the exposed community. …

Vanadium compounds present different toxicities which are related to the balance of the vanadium compound. The toxicity of vanadium is intermediate in the case of respiratory exposure (Vouk, 1979). Acute exposure to vanadium (tens of mg/m3) is responsible for systemic effects in animals. Damage to the liver, kidneys, gonads, haematological, cardiovascular and nervous systems have been reported (Vouk, 1979). In addition, systemic effects at very low levels of exposure have also been reported (WHO, 2000). Carter et al. (1997) showed that metals in airborne particles can induce the secretion of inflammatory cytokines in respiratory airway cells. These findings demonstrate that exposure to this metal may be associated with respiratory illness problems. Positive correlations were obtained between V concentrations in urban air and mortality from bronchitis, pneumonia, cancer and heart disease (Stocks, 1960). …

The intake for As, Ni and V were within the range of that reported by WHO (2000) - As 20- 200 ng/day, Ni 100-800 ng/day and V 1.5 µg/day. Although the levels of Ni and V were found to be relatively high in Guaynabo, they are comparable to the WHO (2000) report. However, one should consider the fact that the combined toxicity of metals is many times greater than the single metal (Shubert et al., 1978). Consequently, the need to analyze these individual constituents in ambient air is evident in order to incorporate such interactions in future epidemiological studies. ...

SCIENCE: Airborne Particulate Matter and Human Health: A Review

2008-08-12T09:00:00.001+01:00

Article in Aerosol Science and Technology (2005), 39:8, 737-749 by Cliff I. Davidson,1 Robert F. Phalen,2 and Paul A. Solomon,3 (1 Department of Civil & Environmental Engineering and Public Policy, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA & 2 Department of Community and Environmental Medicine, University of California, Irvine, California & 3 United States Environmental Protection Agency, Las Vegas, Nevada, USA.)

Abstract

Results of recent research show that particulate matter (PM) composition and size vary widely with both space and time. Despite the variability in PM characteristics, which are believed to influence human health risks, the observed relative health risk estimates per unit PM mass falls within a narrow range of values. Furthermore, no single chemical species appears to dominate health effects; rather the effects appear to be due to a combination of species. Non-PM factors such as socioeconomic status and lifestyle are also believed to affect the health risk, although accounting for these confounding factors is challenging. Airborne PM is also responsible for a number of effects aside from human health, such as alterations in visibility and climate. Because the PM problem is associated with a range of societal issues such as energy production and economic development, making progress on reducing the effects of PM will require integrated strategies that bring together scientists and decision makers fromdifferent disciplines to consider tradeoffs holistically.

Extracts

Particulate matter refers to small particles consisting of solid or liquid droplets suspended in air. EPA currently regulates particles in two size ranges to help protect public health. These include PM10 and PM2.5. PM10 refers to particles less than 10µm in aerodynamic diameter (about 1/10th the diameter of a human hair), while PM2.5 (fine particles) refers to particles less than 2.5 µm in aerodynamic diameter. Because PM10 includes PM2.5, EPA is in the process of promulgating new standards for coarse particles (PMc). This refers to particles with aerodynamic diameters between 2.5 µm and 10 µm. ...

CONCLUSIONS

Reducing the health (and welfare) effects associated with ambient PM is not a simple undertaking. It involves understanding not only the effects of PM, but also the linkages between PM (or precursors) emitted from sources and how that PM makes its way through the air and into the human body. Each step along the way between source and health effect is complicated and makes it difficult to link the observed effect back to the specific source or even source type. For example, roughly half the total global emissions of PM2.5 and precursor species (~500 Tg/year) are emitted from anthropogenic sources with the other half from natural sources. The distribution of those emissions in air and resulting PM varies greatly in size and composition, and thus, PM2.5 concentrations vary widely over space and time.

The health effects of PM are thought to be strongly associated with particle size, composition, and concentration, even though relative risk estimates indicate that the risk per unit PM mass falls within a limited range of values for these parameters. As well, a combination of species and daily variations in PM mass and composition are believed to contribute to the toxicity of the particulate matter air pollution. Furthermore, measuring the relevant parameters and quantifying the health effects are extremely challenging, as numerous external factors, including meteorology and socioeconomic aspects of the human lifestyle, strongly affect human morbidity and mortality. Identifying and correcting for the effects of confounding factors remain a difficult task.

People are exposed to PM2.5 from many sources as they go about their daily activities, spending time in their homes, at work, in recreation, and in traveling. This is further complicated by the knowledge that some individuals or segments of the population are more susceptible to PM exposures, due to factors such as respiratory habits (e.g., mouth breathing versus nose breathing), pre-existing diseases, or genetics. Given all these complications, it is interesting to note that fixed monitoring stations at a central urban site seem to provide reasonable estimates of total exposure of an individual to PM2.5 mass and some secondary species like SO2. 4 . However, determining concentrations of other species such as metals and organic compounds may require measurements in each microenvironment. …

SCIENCE: Cr(VI) containing electric furnace dusts and filter cake from a stainless steel waste treatment plant: Part 2 – Formation mechanisms and ...

2008-08-06T22:35:00.001+01:00

SCIENCE: Cr(VI) containing electric furnace dusts and filter cake from a stainless steel waste treatment plant: Part 2 – Formation mechanisms and leachability

Article in Ironmaking and Steelmaking (2006) Vol 33 No 3 by G. Ma(1) and A. M. Garbers-Craig(2) at (1)Department of Metallurgical Engineering, Wuhan University of Science and Technology, China and (2)Department of Materials Science and Metallurgical Engineering, University of Pretoria, South Africa.

The present study describes the formation mechanisms and leachability of Cr(VI) from electric furnace dust and filter cake from the ferrochromium and stainless steel industries. The results show that stainless steel dust is formed by the entrainment of charge materials, volatilisation of elements and ejection of slag and metal by spitting or bursting of gas bubbles. Ferrochrome dust is formed by the ejection of slag and metal from the electrode holes, the entrainment of charge fines, vaporisation as well as the precipitation of reaction products in the off gas duct. Toxicity characteristics leaching procedure (TCLP) and American Society for Testing and Materials (ASTM) D3987–85 tests show that these wastes are all hazardous materials according to South African legislation, owing to the high degree of Cr (VI) leachability. Cr(VI) in the wastes is easily leached by distilled water, and cannot be stockpiled without prior treatment.

Introduction

Emissions from ferrochromium and stainless steel plants, which consists of NOx, COx , SOx , organic compounds, particulate dusts and filter cake, pose a potential threat to human health and the environment. The US EPA has classified the dusts as hazardous materials (K061), as it exceeds the Toxicity Characteristics Leaching Procedure (TCLP) test limits for Pb, Cd and Cr,1 which imply that these elements can leach into the groundwater. Filter cake, which is the precipitate after the treatment of waste pickling acid (classified as K062) in stainless steel plants also contains significant levels of Cr(VI) species and inorganic salts.2 These particulate materials therefore need to be treated before it can be stockpiled or land filled.

Between 18 and 25 kg of dust or slurry per ton of ferrochrome produced is collected by the abatement systems in ferrochromium plants, and about 18–33 kg bag house filter dust are generated per ton of stainless steel produced.3–7 The South African ferrochromium industry produces ,100 000 t bag house filter dust and slurry, while the stainless steel industry produces 24 000 t dust annually.4,8,9 According to Cox et al.,10 ,20% of the total chromium in the ferrochrome dust is present as Cr(VI), which is leachable. Table 1 illustrates the maximum acceptable concentrations of Cr species, Zn and Pb in the leachate from these wastes, as specified by different countries.11–16 It shows that the limits and test methods vary from country to country. However, the Cr(VI) species has the lowest limits (0.02– 1.5 mg L21) and is considered to be the most harmful species in the dusts owing to its high solubility in water and carcinogenic properties.

In order to minimise the generation of the wastes and develop the appropriate method to treat them, the formation mechanisms and the leachability of the wastes need to be known and understood. The present paper subsequently describes the formation mechanisms and the leachability of the dust and filter cake. ...

Conclusions

In the present study, the formation mechanisms and leachability of Cr(VI) containing EF dust and filter cake were studied. The following conclusions can be drawn.

1. Stainless steel dust is formed by the entrainment of charge materials, evaporation or volatilisation of elements and ejection of slag and metal by spitting or the bursting of gas bubbles.

2. Ferrochrome dusts are formed by the ejection of slag and metal droplets from the electrode hole, the entrainment of charge materials, vaporisation as well as the formation and precipitation of compounds from vaporised species in the off gas duct.

3. TCLP and ASTM D3987–85 tests show that all the wastes are hazardous materials according to South African legislation. They therefore pose a threat to the environment.

4. Leaching experiments on the stainless steel dust show that ~65% of the Cr(VI) leaches out within 5 min under the current experiment conditions, but that the Cr(VI) leaches out more easily in acidic and basic solutions than in DW.

5. Approximately 72 and 62% of Cr(VI), present respectively in ferrochrome fine dust samples FCD1 and FCD2, leach out by DW in 1 min, while ~57% of the Cr(VI) in the filter cake leaches out under the current experimental conditions in 1 min.

6. Owing to the fact that high concentrations of Cr(VI) are easily leached in short periods of time from the ferrochrome fine dust, these dusts can be put through a washing stage whereby the immediate impact on the environment can be reduced. However, this treatment is only a temporary solution, as Cr(VI) continues to leach (but to a lesser extent), and gradual oxidation of Cr(III) to Cr(VI) occurs under ambient conditions in the presence of Ca containing phases (such as CaO, Ca(OH)2, CaCO3 and CaF2) and alkali oxides.38–40

SCIENCE: Cr(VI) containing electric furnace dusts and filter cake from a stainless steel waste treatment plant: Part 1 - Characteristics and microstru

2008-08-06T22:29:00.001+01:00

Article in Ironmaking and Steelmaking (2006) Vol 33 No 3 by G. Ma(1) and A. M. Garbers-Craig(2) at (1)Department of Metallurgical Engineering, Wuhan University of Science and Technology, China and (2)Department of Materials Science and Metallurgical Engineering, University of Pretoria, South Africa.

Electric furnace dust and filter cake collected from a stainless steel plant as well as EF dust collected from a ferrochrome plant were characterised. Electric furnace dusts consist of very fine particles, from which Cr(VI) can be leached by shallow groundwater. When heated in air H2O, CO2, SO2, SO3, fluorine, calcium and silicon are expelled from these materials, while metallic particles oxidise. The main phases present in the stainless steel plant dust are the (Mg,Fe,Mn,Cr)3O4 spinel phase, quartz, Ca(OH)2 and nickel. The coarse fraction of ferrochrome dust mainly contains chromite and partly altered chromite, quartz and carbon, while the main components of the fine fractions of ferrochrome dust are chromite, SiO2, ZnO, NaCl and Mg2SiO4. CaF2 is the major phase in the filter cake. Cr(VI) containing phases are possibly generated at the top of the submerged arc furnace or in the off gas duct, as Cr(VI) is found on the surface of the dust.

Extracts

Introduction
Stainless steel is typically smelted in an electric arc furnace (EAF) from scrap, molten or lump ferrochrome and slag formers (lime, fluorspar and dolomite), after which it is refined in an argon oxygen decarburisation (AOD) vessel or Creusot–Loire Uddeholm (CLU) converter. Ferrochrome on the other hand, is produced by the carbothermic reduction of chromite ore in a submerged arc furnace (SAF) or direct current (DC) furnace. Emissions from these processes are cooled and the particulate matter collected by dust treatment systems. Figure 1 schematically shows the dust treatment systems of the ferrochromium and stainless steel plants. In the ferrochromium plant (Fig. 1a), the coarse dust is collected by a cyclone separator, while the bag house filters gather the fine dusts. The particulate matter from the EAF and refining converter are also collected by the bag house filter in the stainless steel plant (Fig. 1b). These electric furnace (EF) dusts contain valuable components (e.g. chromium, zinc and iron) as well as toxic substances (e.g. chromium (VI) and lead), which can leach into the groundwater when stockpiled or land filled. Of these toxic substances, chromium(VI) is also carcinogenic, and is present in the dusts at levels which exceed the regulation thresholds for the disposal of hazardous waste in many countries.1 The EF dust is therefore considered to be a hazardous material and it needs to be treated before being stockpiled or land filled.

Stainless steel plants also produce filter cake that contains significant levels of Cr(VI) and fluoride, which is also potentially harmful to human health and the environment. This filter cake is produced in the waste pickling acid treatment plant from a neutral solution of sodium sulphate as well as a mixture of nitric acid and hydrofluoric acid, which are used to dissolve the oxide scale on the surface of the stainless steel by electrochemical and chemical ways in order to improve the surface quality of the stainless steel (Fig. 2). The waste pickling acid is highly acidic (typically at pH of y1) and contains high concentrations of fluorine, iron, nickel, Cr(III) and Cr(VI). These waste acids are treated through neutralisation with lime, followed by iron sulphate addition to reduce Cr(VI) species to Cr(III), and then the precipitation of metals by lime (typically at pH of y9.5). Finally, the precipitate is pressed into a filter cake.2

The existence and treatment of wastes from stainless steel and ferrochrome production remain a challenge and an issue of concern. The increase of environmental legislation globally and the trend towards sustainable development are drives for alternatives to landfill.

In the past decades, a number of alternative technologies have been developed to handle EF dusts and other metallurgical wastes. These technologies can be divided into three categories, i.e. direct recycling processes,3,4 recovery processes5–10 and solidification/stabilisation processes.11–14 Direct recycling of dust back to the EF or blast furnace is the easiest way to treat the EF dusts. However, the alkaline metals and zinc in the dust could increase the energy consumption in the EF.5 The recovery processes include pyrometallurgical methods,7–9 which mostly recover Cr, Ni, Fe, Zn, Pb and Cd, and hydrometallurgical methods that focus on the recovery of zinc.10 The pyrometallurgical recovery processes require high investment costs, while in the hydrometallurgical recovery processes it is often difficult to both economically recover the valuable elements and let the treated residue meet the toxicity limits.10 Solidification/ stabilisation processes are therefore widely considered to be an effective method that can encapsulate, glassify or combine the toxic elements, and simultaneously add value to the wastes.

In order to develop a technique whereby the Cr(VI) containing EF dust and filter cake can successfully be stabilised, it is important to first comprehensively characterise these waste materials. The present paper subsequently describes the characteristics and microstructures of Cr(VI) containing EF dust and filter cake from a stainless steel and ferrochromium plant.

The mechanisms of formation of the dusts and a more detailed study of their leaching behaviour are presented in a later paper. ...

Results

Particle size distribution, bulk density, moisture content and Ph

The EF dusts are very fine particles, with d50 values of 3.2, 2.9, 5.5 and 79.8 µm for samples SPD, FCD1, FCD2 and FCD3 respectively. The bulk density, moisture content and pH of these wastes are presented in Table 1. It can be seen from Table 1 that sample FCD3 has the highest density (2.42 g cm23) while sample FCD1 (0.49 g cm23) has the lowest density of the examined waste materials. The moisture contents of the dusts range between 0.4 and 1.06%. The leaching behaviour of Cr species by ground water is related to the pH of the environment and the redox potential (EMF) of the aqueous solution.18 In natural groundwater chromium has two stable oxidation states, i.e. Cr (III) and Cr(VI). Cr(VI) is the stable species under oxidising conditions that are found in shallow ground waters, whereas Cr(III) is thermodynamically stable under reducing conditions in deeper ground waters.18 The dominant species of Cr(VI) are highly soluble HCrO4 2 and CrO4 22. Under oxidising conditions, in natural groundwater with a pH value between 6 and 8, the predominant species is CrO4 22.18 CrO4 22 prevails at higher pH.18 It was found that the EF dusts and filter cake all generate basic solutions (pH.8) when leached in water. The CrO4 22 species can therefore potentially be leached from these materials in shallow groundwater. A more detailed study on the leachability of Cr(VI) from the electric furnace dusts and filter cake is presented in a later paper.

Chemical composition and phase composition of EF dusts and filter cake

The chemical compositions of the EF dusts and filter cake are given in Table 2. The SPD is iron oxide, chromium oxide and CaO rich, but also contains some MgO, MnO, SiO2, ZnO and nickel. The fine fractions of the ferrochrome plant dust (FCD1 and FCD2) contain high concentrations of SiO2, ZnO, MgO and alkali metal oxides, but also some sulphur and chlorine, while the coarse fraction (FCD3) is SiO22Cr oxide–iron oxide2Al2O32MgO2C based. The concentrations of calcium, fluorine, iron and sulphur are high in the filter cake.

X-ray diffraction (Fig. 3) and EDS analyses indicated that the SPD mainly contains a (Mg,Fe,Mn,Cr)3O4 spinel phase, quartz, CaF2, pure Ni particles, stainless steel particles, Ca(OH)2 and a glassy slag phase. The major phases that are present in dust samples FCD1 and FCD2 include NaCl, ZnO, MgO, Mg2SiO4, chromite particles, cristobalite, ferrochrome particles and a glassy slag phase. Small amounts of zinc hydroxychlorosulphate hydrate [NaZn4(SO4)Cl(OH)6.6H2O] and zinc sulphate hydroxide hydrate [Zn4SO4(OH)6.5H2O] could also be detected by XRD. The coarse ferrochrome dust sample (FCD3) contains chromite and partially altered chromite (PAC) particles, carbon, quartz, (Ca,Mg)(CO3)2 and a glassy slag phase from which anorthite ((Ca,Na)(Si,Al)4O8) precipitated. Fluorite (CaF2) is the major phase in the filter cake, while CaSO4, an amorphous metal oxide rich phase, a few lime particles and stainless steel scale are also present. ...

Microstructure of EF dusts and filter cake

Steel plant dust

More than 85% of the SPD particles are smaller than 40 mm in diameter. These dust particles are of varying microstructure, and can be divided into three categories:

(i) particles that are irregular in shape
(ii) spherical or near spherical particles
(iii) particles coated with slag or oxides.

The particles that are spherical or near spherical, as well as the spherical particles that are coated with slag or oxides, are the most abundant in the SPD sample.

The particles that are irregular in shape include pure nickel (Fig. 5), quartz, lime, fluorspar and ferrochrome particles. It is clear that these particles were captured by the off gas during charging.

The spherical or near spherical particles include metal particles (Fig. 6) and slag particles. These particles range from submicron to ≥ 200 μm in diameter. The slag particles are either hollow (Fig. 7) or consist of a glassy silicate based matrix that contain oxide crystals (Figs. 8– 10) and metal droplets (Fig. 11). The oxide crystals are either cubic (Fig. 8), dendritic (Fig. 9) or needle like (Fig. 10). EDS analysis indicated that the cubic and dendritic crystals are (Mg,Fe,Mn)(Cr,Al)2O4 spinel crystals, while the needles are CaCr2O4. Spherical stainless steel particles (Fe–3.0Cr–7.2Ni–3.9Mo) that are coated with slag were also found (Fig. 11).

Slag particles that are covered with an oxide layer, which is of different chemical composition to the centre of the particle, could also be distinguished. Such slag particles are shown in Figs. 12 and 13. X-ray mapping of one of these particles (Fig. 13) indicated that the centre of the particle is enriched in Cr, Ca and Al, while the rim is rich in Zn and Fe.

Ferrochrome plant dust

The fine fractions of ferrochrome dust (FCD1 and FCD2) mostly consist of agglomerated particles that formed clusters (Fig. 14). Approximately 90, 75 and 20% of the particles are ( 40 μm diameter in samples FCD1, FCD2 and FCD3, respectively. Such clusters typically contain chromite and partly altered chromite (PAC) particles, reductant (C based particles), hollow metallic ferrochrome droplets, flux (quartz) and SiO2 based slag droplets that are embedded in a matrix of very fine particles. This matrix is mainly SiO2–MgO– ZnO–(Na, K)2O based.

The coarse fraction (FCD3) mostly contains particles that are irregular in shape, but also spherical or near spherical particles and particles coated with a slag layer (Fig. 15). The particles that are irregular in shape include chromite ore particles, quartz particles and carbon based particles. The spherical particles include metal particles, Si–Ca–Mg–Fe based slag particles, particles that contain spinel crystals and ferrochrome droplets that are embedded in a porous sodium rich silicate slag layer (Fig. 16), as well as chromite particles that are surrounded with a porous layer that contains some very small Cr–Fe based metal droplets, followed by a more solid layer of Mg2SiO4 (Fig. 17).

Filter cake

The filter cake consists of very finely intergrown areas that are Ca–F–S–O based, and areas that contain high concentrations of metal oxides of iron, chromium and nickel (Fig. 18). XRD analysis indicated that the Ca–F– S–O based areas consist of a mixture of CaF2 and CaSO4 while the metal rich oxide phase is amorphous. The Ca–F–S–O based precipitate presumably formed owing to supersaturation of the waste acid with respect to CaF2 and CaSO4 (solubility limits of 0.016 and 2.09 g L21 respectively24) in the neutralisation and reduction steps. It is assumed that the metal oxide rich precipitate is the reaction product between the metal ions and the lime particles during the final precipitation step. Free lime particles could also be distinguished in the filter cake (Fig. 19). ...

Conclusions

The size distribution, bulk density, moisture content, pH, thermal properties, chemical composition, phase composition and microstructure of chromium containing EF dusts and filter cake were characterised. The following conclusions can be drawn.

1. The EF dusts are very fine particles, have bulk densities that vary between 0.49 and 2.42 g cm23, and have low moisture contents.

2. On leaching in water the examined EF dusts and filter cake produce alkaline solutions (pH.8). Since water soluble Cr(VI) species are associated with shallow ground water where conditions are oxidising and alkaline (pH.6), it can be expected that Cr(VI) species will leach from these materials.

3. The main phases that are present in the SPD are the (Mg,Fe,Mn,Cr)3O4 spinel phase, quartz, Ca(OH)2 and nickel. The dominant phases of the coarse fraction of ferrochrome plant dust are chromite, partly altered chromite, quartz and carbon, while the main components of the fine fractions include chromite, SiO2, ZnO, NaCl and Mg2SiO4. The major phase present in the filter cake is CaF2.

4. TG/DTA analysis in air indicated that mass losses and gains occur during heating of these waste materials owing to reactions in which H2O, CO2, SO2, SO3, fluorine, calcium and silicon are driven off, and metallic particles oxidise.

5. It is assumed that Cr(VI) containing species in ferrochrome dust are generated at the top of the SAF or in the off gas duct, as Cr(VI) is found on the surface of the dust.

SCIENCE: Characterization and leachability of electric arc furnace dust made from remelting of stainless steel

2008-08-06T22:24:00.002+01:00

Article in Journal of Hazardous Materials B135 (2006) 156–164 by Guylaine Laforest, Josée Duchesne at Centre de Recherche sur les Infrastructure en Béton (CRIB), Département de géologie et de génie géologique, Université Laval, Québec, Canada.

Abstract

Electric arc furnace dust (EAFD) is a toxic waste product made in the remelting of scrap steel. The results of a Toxicity Characteristic Leaching Procedure (TCLP) conducted on a sample of EAFD originating from the remelting of stainless steel scrap showed that the total Cr and Cr (VI) liquor concentrations (9.7 and 6.1 mg/L, respectively) exceeded the Toxicity Characteristic Regulatory Level (TCRL). The EAFD showed a complex heterogeneous mineralogy with spinel minerals group predominance. A sequential extractions method has permitted the determination of the amount of available metals (potentially mobile component) from the EAFD as follows: Cr (3%), Ni (6%), Pb (49%) and Zn (40%). Solubility controls on Cr, Pb, Zn and Ni were identified in the EAFD. This means that the Cr, Pb, Zn and Ni concentrations in solution were controlled by the solubility of some phases from EAFD. The concentrations of Ni and Zn, which are metals not regulated by TCRL were below 0.41 and 1.3 mg/L, respectively. The solubility control on Pb was sufficient to decrease its concentration (<0.24>

Extracts

One of the most important problems in the secondary steel mill industry throughout the world is the disposition of dusts produced from electric arc furnaces [1]. A large quantity (10-20 kg) of electric arc furnace dust (EAFD) is generated per tonne of steel produced and around 700,000 and 50,000 tonnes of EAFD are generated each year in the United States and Canada, respectively [2,3]. The cost of EAFD disposal is not negligible. For example, 200 million dollars per year are necessary to dispose EAFD in the United States [4]. Moreover, the EADF is listed hazardous waste under Resource Conservation and Recovery ACT (RCRA) in United States and under the Transportation of dangerous Goods Regulations (TDGR) in Canada. Also, high levels of several contaminants cause it to fail the Ontario Regulation 347 leachate extraction procedure [5]. Thus, the disposal of these industrial solid toxic wastes can cause environmental risk due to the mobility of toxic elements. Some heavy metals of EAFD like chromium are toxic and have high solubility. Chromium (VI) is particularly problematic because it must initially be reduced before being fixed in an insoluble phase. A solubility control by a material implies that the concentration of some constituent elements in solution will be controlled by the solubility of the secondary precipitates. Reardon et al. [6] recommended conducting leaching tests on a particular waste material at least at two different water/solid ratios. They point out that if an element's concentration does not double when the water/solid ratio is halved, there must be a solid phase control on its concentration in solution.

... The chemical composition of dusts varies according to the type of steel produced and the variation’s range of compositions is considerable. For example, the Fe, which is the major element, can vary from 15 to 62% and represents around 43% in the EAFD from the stainless steel industry [3]. ... The concentrations of heavy metals are given in Table 2 along with some comparisons with data from the literature. The particle size distribution of the EAFD established by a Sedigraph particle size analyser (SediGraph 5000ET by Micromeritics) at 36 °C in an adequate liquid (density: 0.829 g/cc, viscosity: 9.14 cp) is presented in Table 3. The EAFD contains two major size fractions: a very fine-grained portion and a coarser part. Particle sizes range from less than 2.8 µm to more than 176 µm. The majority (94%) of the particles are smaller than 5.5 µm in diameter. ...

5.3. Leaching test results

5.3.1. TCLP results

The TCLP results presented in Table 6 show that the EAFD is a toxic waste. The total Cr (9.7 mg/L) and the Cr (VI) (6.1 mg/L) liquor concentrations after leaching are over the value of Toxicity Characteristic Regulatory Level (Table 7). The Pb concentration is under the regulatory level. The Ni and Zn concentrations are not regulated by the TCLP but it is important to note the high Zn concentration reached (93.9 mg/L). The EAFD is a toxic waste according to its high Cr concentration and must be treated. Stabilization/solidification (S/S) processes could be used to treat EAFD. This will be the subject of further research. The following section tries to evaluate the long-term leaching behaviour of EAFD in a neutral initial environment. ...

Conclusions

The EAFD particles appear as elongated grains, spherical, fine-grained and irregular particles. The predominance of spinel group minerals was determined. Magnetite is the main phase present in the EAFD together with chromite. Most grains are franklinite–magnetite–jacobsite solid solutions. No phase containing Zn or Pb was observed, but the hydroxides, carbonates and iron release Pb and Zn according to the sequential extraction results. These results revealed evidence of Zn in iron oxides. The Ni was found in Fe–Ni oxides (magnetite). The chromium appears both in chromium carbonate and chromite (spinel mineral). Many EAFD particles present different textures (zonation, exsolution and degassing phenomena). The EAFD is a toxic waste. The total Cr and Cr (VI) concentrations (9.7 and 6.1 mg/L, respectively) exceeded the Toxicity Characteristic Regulatory Level. A solubility control on Cr, Pb, Zn and Ni was identified in the EAFD. However, this control was not sufficient to decrease the Cr concentration to below the regulatory level. Future works may include analysis of leachates from the different granular sizes-fraction of EAFD.

SCIENCE: Properties of steel foundry electric arc furnace dust solidified/stabilized with Portland cement

2008-08-06T22:21:00.001+01:00

Article in Journal of Environmental Management 85 (2007) 190–197 by Guray Salihoglu, Vedat Pinarli, Nezih Kamil Salihoglu, Gizem Karaca atDepartment of Environmental Engineering, Faculty of Engineering-Architecture, Uludag University, Bursa, Turkey.

Abstract

Electric arc furnace dust from steel production is generated in considerable amounts worldwide and needs to be treated as hazardous waste. The aim of this study was to investigate the properties of electric arc furnace dust solidified/stabilized by using Portland cement. Mortar and paste samples were prepared with varying waste-to-binder ratios between 0% and 90%. A comprehensive experimental program was designed including XRF characterization, setting time, unconfined compressive strength, and toxicity characteristics leaching procedure (TCLP), synthetic precipitation leaching procedure (SPLP), and acid neutralization capacity (ANC) tests. The results were evaluated in order to determine if the solidified /stabilized product can be disposed of at a landfill site with domestic waste or at a segregated landfill. The effect of using sand on S/S performance was also investigated. The results indicated that the solidification /stabilization process using PC helps the heavy metals to be bound in the cement matrix, but the TCLP leaching results exceeded the EPA landfilling limits. The SPLP leaching results conformed to the limits implying that the waste or S/S products can be disposed of at a segregated landfill; however the low ANC of the S/S products reveals that there may be leaching in the long-term. The sand used in the mortar samples adversely affected the S/S performance, causing higher heavy metal leaching levels, and lower pH levels in the leachate after the TCLP extraction than those measured in the leachate of the paste samples.

Extracts

Electric arc furnace dust (EAFD) is generated in considerable amounts by the electric arc steelmaking process. During melting in an electric arc furnace, certain elements volatilize, and after cooling, these elements form a fine dust. This dust, called EAFD, is collected in a baghouse and amounts to approximately 2% of the steel produced (AISI, 2001). In Turkey 20.961 million tons of steel was produced in 2005 (IISI, 2006) with 64% of plants equipped with electric arc furnaces (Orhan, 2005), generating 268,300 tons of electric arc furnace dust in Turkey in 1 year.

The chemical composition of EAFD was investigated by several researchers, and the most abundant heavy metals in EAFD were found to be Zn, Pb, Cr, and Cd (Pereira et al., 2001; Pelino et al., 2002; Sofilic et al., 2004; Orhan, 2005). Because of the leaching potential of the heavy metals it contains, EAFD has been designated by Turkey, the European Union (EU), and the EPA (United States Environmental Protection Agency) as a hazardous waste, which means that it cannot be disposed of at landfills without treatment.

... EAFD can vary greatly in composition depending on the composition of the scrap charge, the furnace additives used, and the type of steel being manufactured. For example, use of galvanized steel scrap would increase the zinc content in the EAFD. Zinc content in EAFD may vary between 7% and 40%, and lead content between 4–9% (Orhan, 2005). ...

SCIENCE: Characterization of steel mill electric-arc furnace dust

2008-08-06T22:11:00.004+01:00

Article in Journal of Hazardous Materials B109 (2004) 59–70 by Tahir Sofilic, Alenka Rastovcan-Mioc, Stefica Cerjan-Stefanovic, Vjera Novosel-Radovic , Monika Jenko of Željezara Sisak Ltd., Sisak, Croatia & Faculty of Metallurgy, University of Zagreb, Croatia & Faculty of Chemical Engineering and Technology, University of Zagreb, Zagreb, Croatia & Institute of Metals and Technology, Ljubljana, Slovenia.

Abstract

In order to make a complete characterization of electric-arc furnace (EAF) dust, as hazardous industrial waste, and to solve its permanent disposal and/or recovery, bearing in mind both the volumes formed in the Croatian steel industry and experiences of developed industrial countries, a study of its properties was undertaken. For this purpose, samples of EAF dust, taken from the regular production process in the Željezara Sisak Steel Mill between December 2000 and December 2001, were subjected to a series of tests. The chemical composition of EAF dust samples was investigated by means of a several different analytical methods. The results from the chemical analysis show that the approximate order of abundance of major elements in EAF dusts is as follows: Fe, Zn, Mn, Ca, Mg, Si, Pb, S, Cr, Cu, Al, C, Ni, Cd, As and Hg. Granular-metric composition of single samples was determined by applying sieve separation. Scanning electron micro-structural examination of EAF dust microstructure was performed and results indicated that all twelve EAF dusts were composed of solid spherical agglomerates with Fe, Zn, Pb, O, Si and Ca as the principal element. The investigation of grain morphology and the mineralogical composition of EAF dust were taken by combination of high resolution Auger electron spectroscopy (HR AES), X-ray photoelectron spectroscopy (XPS) and X-ray powder diffraction analysis. The analysis of XPS-spectra determined the presence of zinc in the form of ZnO phase and the presence of lead in the form of PbO phase, i.e. PbSO3/PbSO4 forms. The results of the X-ray diffraction phase analysis show that the basis of the examined EAF dust samples is made of a mixture of metal oxides, silicates and sulphates. The metal concentration, anions, pH value and conductivity in water eluates was determined in order to define the influence of EAF dust on the environment.

Extracts

Major pollution that is released into the atmosphere during the steel making process includes solid particles (dust), carbon (II) oxide, nitrogen oxides, and volatile organic compounds. …

Due to its chemical and physical properties, the electric-arc furnace dust was categorized as hazardous waste according to the US EPA classification of 1980 [2]. Being treated as hazardous waste, it is partly disposed of permanently at appropriate, regulation-prescribed waste dumps, or it can be used as secondary raw material in the production of zinc, iron, lead, etc. ...

3. Results and discussion
3.1. Characterization of samples
3.1.1. Chemical analysis

The chemical composition of electric-arc furnace dust depends on the quality of steel scrap processed, the type of steel being produced, technological and operating conditions and the degree of return of the dust into the process. Reference data [11–24] imply that the prevailing elements in EAF dust vary in concentration: Fe 10–45%, Zn 2–46%, Pb 0.40–15.14%, Cr 0.2–11%, Cd 0.01–0.30%, Mn 1–5%, Cu <>

The results of the chemical analysis of the EAF dust samples are shown in Table 1. ...

The results of granular-metric analysis have shown that a sample of electric furnace dust basically consists of 100–125µm particles, while 90–100 µm particles are least represented. Although the results of granular-metric analysis show that the smallest measured fraction has the grain size <50µm,>particles with grain diameter = 1µm which mostly form agglomerates, the size of which can exceed 200 µm, Fig. 3. ...

Conclusion

The obtained research results show that the volume of EAF dust formed per tonne of crude steel in Croatia does not differ from the volumes of EAF dust formed in other steel mills in the world using the electric-arc furnace procedure.

The chemical composition of the domestic EAF dust is mostly identical to the chemical composition of EAF dust of other steel producers. Major differences refer to the zinc content, which has a mass share not greater than 10% in EAF dust samples from domestic steel mills. This is a direct consequence of applying high-quality steel scrap (containing very little galvanized steel). …

SCIENCE: Chemical, physical, structural and morphological characterization of the electric arc furnace dust

2008-08-06T00:12:00.004+01:00

Article in Journal of Hazardous Materials B136 (2006) 953–960 by Janaina G.M.S. Machado, Feliciane Andrade Brehm, Carlos Alberto Mendes Moraes, Carlos Alberto dos Santos, Antonio Cezar Faria Vilela , Joao Batista Marimon da Cunha, Laboratorio de Siderurgia/LASID, Universidade Federal do Rio Grande do Sul, UFRGS/PPGEM Centro de Tecnologia, Porto Alegre, RS, Brazil ans other Institutes.

Abstract

Electric arc furnace dust (EAFD) is a hazardous industrial waste generated in the collection of particulate material during steelmaking process via electric arc furnace. Important elements to the industry such as, Fe and Zn are the main ones in EAFD. Due to their presence, it becomes very important to know how these elements are combined before studying new technologies for its processing. The aim of this work was to carry out a chemical, physical, structural and morphological characterization of the EAFD. The investigation was carried out by using granulometry analysis, chemical analysis, scanning electron microscopy (SEM), energy dispersive spectroscopy via SEM (EDS), X-ray mapping analysis via SEM, X-ray diffraction (XRD) and M¨ossbauer spectroscopy. By XRD the following phases were detected: ZnFe2O4, Fe3O4, MgFe2O4, FeCr2O 4, Ca0.15Fe2.85O4, MgO, Mn3O4, SiO2 and ZnO. On the other hand, the phases detected by M¨ossbauer spectroscopy were: ZnFe2O4, Fe3O4, Ca0.15Fe2.85O4 and FeCr2O4. Magnesium ferrite (MgFe2O4), observed in the XRD pattern as overlapped peaks, was not identified in theM¨ossbauer spectroscopy analysis.

Extracts

Electric arc furnace dust (EAFD) is a solid waste generated during the steelmaking process. It is classified according to NBR 10005 [1] as dangerous solid waste-class I, because the elements Pb & Cd leach in water exceeding the maximum limits permitted by the NBR 10004 [2,3]. The State Foundation for Environmental Protection of Rio Grande do Sul – FEPAM – requires that this waste must be stored in an appropriate place protected from rain. Due to the great amount generated, 12–14 kg of dust per ton of steel, an evaluation of the steel recycling alternatives is necessary.

When galvanized scrap is used in the EAF, most of the zinc from the steel scrap ends up in the dust and fume due to its very low solubility in molten steel and slag, and, especially, because zinc vapor pressure is higher than iron vapor pressure at steelmaking temperature. Vapor zinc is carried out the furnace with other gaseous or particulate compounds generated during steelmaking reactions, generating compounds like ZnO and ZnFe2O4. According to Leclerc [5], when some zinc particles are in contact with iron particles at high temperatures in an oxidizing atmosphere, zinc ferrite formation will occur in the furnace and in the evacuation system. The problem is that zinc does not comes out alone, other elements evaporate and are collected in the dedusting system originating the EAFD. ...

3. Results and discussion
3.1. Granulometric analysis

The granulometric distribution analysis of the EAFD is shown in Fig. 2. The mean particle diameter of EAFD determined by laser granulometer was 1.88µm. It can be seen from Fig. 2 that the EAFD has a heterogeneous distribution of particle size, where 60% have size between 0.90 and 4.30µm. Such an irregular granulometric distribution is in agreement with that published by Mantovani et al. [9]. Probably, this is due to the agglomerated state of the particles because this material is well known to have fine granulometry.

Xia and Pickles [10] also pointed out that the particles in EAFD tend to exist as aggregates consisting of very fine individual particles. Most of the individual particles were lower than 1µm. Takano et al. [6] determined in two different types of EAFD that almost 90% of the particles are lower than 10 µm.

Menad et al. [11] analyzed the particle size distribution of EAFD with two screen sizes (i.e., 500 and 15µm). They observed that the dust is very fine; more than 70% of particles are lower than 15 µm. They also observed that the metals are more concentrated in the fine fraction of the waste. 3.2. Chemical characterization The result of the chemical analysis of EAFD is presented in Table 1. ...

4. Conclusions

• The mean particle diameter of EAFD was 1.88 µm. The EAFD has a heterogeneous distribution of particles, where 60% have size between 0.90 and 4.30 µm;

• Fe and Zn are present in the EAFD with 49.96 and 9.24%, respectively;

• XRD technique detected in the EAFD the following phases: ZnFe2O4, Fe3O4, MgFe2O4, FeCr2O4, Mn3O4, MgO, SiO2, Ca0.15Fe2.85O4 and ZnO. However, except for SiO2 and ZnO, the signals from all the phases exhibit overlapping. Because of such overlapping the presence of these phases cannot be unequivocally assured;

• The ferrous oxide phases detected by M¨ossbauer spectroscopy were: ZnFe2O4, Fe3 O4, Ca0.15Fe2.85O4 and FeCr2O4; ...

In conclusion, the characterization of a solid waste using many techniques increase the reliability in the results and also give more conditions to decide about the best feasible recycling method.

SCIENCE: Mineral phases of weathered and recent electric arc furnace dust

2008-08-06T00:05:00.004+01:00

Article in Journal of Hazardous Materials 154 (2008) 417–425 by Fernanda Machado Martins, José Manoel dos Reis Neto, Carlos Jorge da Cunha, Laboratorio de Quimica Mineral Aplicada, Departamento de Quimica, Universidade Federal do Parana (UFPR), Curitiba-PR, Brazil.

Abstract

A weathered and a recent sample of electric arc furnace dust (EAFD), generated in a southern Brazilian steel industry, were characterized by X-ray fluorescence spectroscopy (XFA), powder X-ray diffraction (XRD), thermogravimetric analysis (TG), scanning electron microscopy (SEM) with energy dispersive spectroscopy (EDS) probe and Fourier transform infrared spectroscopy (FTIR). A quantitative phase composition model, that accounts for the observed data and for the physico-chemical conditions of formation, was postulated for each material. One sample, in the form of a wet paste, was collected from the lowest part of a landfill and corresponds to a weathered material whereas the other sample was collected from the top portion of the landfill and corresponds to a recently produced material. The dominant cations present in both samples are iron, zinc and lead with minor amounts of manganese, calcium and silicon. The dominant mineralogical phases identified in both materials are Magnetite, Franklinite and Zincite. The recent sample has Laurionite whereas the weathered sample has Hydrocerussite and Hydrozincite.

Extracts

The steel plant under study is located in Paraná State and uses EAF process in which iron scrap is the main source of iron and pig iron is a secondary source. Oxygen is injected during the melting process and act on decarburization and on the burning of natural gas and coal. Dolomitic or calcitic lime is added to make slag. An extra energy input is obtained from the combustion of natural gas and pulverized coal. The electrodes are made of carbon and are slowly consumed in the process. The fused material in the EAF reaches temperatures of 1600 °C, the molten steel is then poured in a ladle furnace for refining. Lime, to make slag, and alloying elements are added in this stage. The molten refined steel is directed to a continuous molding system where the ingots are water cooled and cut. The EAF processing generates gases, volatile organic compounds, slag and particulates known as EAF dust or simply EAFD. The EAFD is directed to a bag filter system that is periodically washed with water generating a sludge. In past plant operations this wet sludge was placed in a hazardous waste landfill. Nowadays this sludge is directed to a pelletizer that considerably reduces the humidity and material volume. No chemicals are added to make the EAFD pellets that are being landfilled on top of the sludge. The estimated generation of EAFD in this plant is 9.6 thousand tonnes/ year.

According to Brazilian standards [3], the EAFD is classified as a dangerous residue due to the potential leaching of toxic metal ions. Its disposal in controlled landfills is the main form of final destination in Brazil.

Recent work has been dedicated to the characterization of EAFD from different steel plants with focus on the solid EAFD [4,5] or on its leaching products [6,7]. Various applications for the EAFD are been suggested such as the study of its vitrification product [8], the recovery of zinc and iron [9–16], soil fertilization [17], recycling to the EAF [18–21], incorporation in cement [22,23] and incorporation in glass [24].

According to a recent study [25] the EAFD formation takes place in two steps: first, the emission of dust “precursors” (vapors, metal droplets, and solid particles) inside the furnace; second, the conversion of those precursors into dust by agglomeration and physico-chemical transformations. Out of the five possible emission mechanisms evaluated the two most important were found to be the projection of fine metal droplets by bursting of CO bubbles (coming from the decarburization of the steel bath) and volatilization at the hot spots in the arc zone, in the oxygen jet zone and in the CO bubbles. The direct fly-off of solid particles from the EAF feed, such as coal powder and lime powder depend on operational conditions and may even be absent in optimized furnaces. The projection of metal droplets at the impact points of the arc and at the impact points of the oxygen jet were found to be an unlikely mechanism because the large particles projected return to the molten bath. The so generated air-borne precursors can undergo physical transformations in their way out of the EAF and into the filtration system such as condensation of the vapors, rapid solidification of the fine metal droplets, in-flight agglomeration and coalescence of dust particles [25].

In the present work a recent and a weathered EAFD sample were collected, from a landfill of a southern Brazilian steel plant, and were characterized by means of an integrated approach, developed by our research team, that takes into account diffractometry, electron microscopy, spectroscopy, thermal analysis and the physico-chemical conditions of residue formation. This integrated approach has recently been applied to various types of industrial residues [26] including four residues of a pulp and paper plant [27]. The authors hope that this methodology can be useful to help finding industrial uses for this material and to improve EAF process control. This is the first work, to the authors’ knowledge, to characterize a recent and a weathered EAFD sample generated in the same steel mill. ...

2.1. Sampling

Sampling of the two residues was performed according to a Brazilian standard [28]. The weathered material, representative of past operations of the industry, was collected from the lowest part of a landfill, whereas the recently generated material was collected from the topmost part of the landfill.

3. Results and discussion
3.1. EAFD characterization
3.1.1. Elemental analysis

The elemental chemical composition of the weathered and recent EAFD samples can be seen in Table 1. The weathered sample and the recent sample have Fe, Zn and Pb as the major electropositive elements, intermediate amounts of Mn, Ca and Si and trace amounts of other elements. A comparison between EAFD from different origins reveals a significant variation in the elemental composition. The EAFD samples studied here have Fe, Zn, Pb, Mn, Ca, Cr and Ni percentages close to those related by Leclerc et al. [14], whereas the Fe percentage in the weathered sample is close to that reported by Sofilic et al. [4], the percentages of Zn in both samples are close to that reported by Yamada and Hara [10]. The percentage of Pb in both samples agrees with that reported by Sekula et al. [11]. These variations in compositions are mainly due to the different types of iron and steel scrap consumed in the EAF, to the type of steel being produced and to particular operations performed during the steel production. The EAFD zinc originates form the galvanized iron scrap, lead comes from the paint present in the scrap pieces, manganese, chromium, silicon, nickel, phosphorus and titanium are present in steel alloys, chromium may also come from metalized steel pieces, calcium, magnesium, barium, potassium and strontium originate from the calcitic and dolomitic lime used in the EAF, copper comes from wiring mixed with the scrap and tin comes from solder. Al is commonly present in the zinc layer of galvanized iron and steel. In the weathered EAFD Al may also come from environmental clay contamination. ...

Conclusions

A recent and a weathered sample of EAFD, generated in the same steel mill, were characterized by means of an integrated approach and a mineral phase composition model was estimated for each sample. The major chemical composition of the weathered and recent EAFD samples are similar being Fe, Zn and Pb the most dominant electropositive elements.The major phases present in both samples are also similar being spinels (Franklinite and Magnetite) and Zincite the most dominant ones. The recent sample has Laurionite as the main lead bearing phase. The weathered material has two hydroxicarbonates, Hydrozincite and Hydrocerussite, typical weathering products of zinc and lead. The pH of the samples is compatible with the presence of the assigned phases. Clay and some type of ester (or polyester) are also part of the weathered sample. Calcination of the samples, at 1000 .C for 3 h, promotes the decomposition of the hydroxicarbonates into oxides, the sublimation of lead oxide, the oxidation of iron(II) and the reaction between zincite and iron oxides to form Franklinite. The recent sample displays agglomerates of spherulitic granules being the submicrometric ones composed of Franklinite and the micrometric ones composed of Magnetite. The observed lead bearing phase in the electron micrographies of recent sample is consistent with the proposed precipitation of Laurionite. In the weathered sample the granules are completely loose and well mixed as told from the electron micrographies. During the course of the present work it was realized that the thermal treatment of EAFD may be a useful source of synthetic Franklinite, a rare mineral, whose applications in materials science are appealing. The prospect use of this EAFD as a source of synthetic Franklinite is currently being evaluated. ...

SCIENCE: Study of occupational health impact of atmospheric pollution on exposed workers at an iron and steel complex ...

2008-08-05T23:54:00.004+01:00

SCIENCE: Study of occupational health impact of atmospheric pollution on exposed workers at an iron and steel complex by using neutron activation analysis of scalp hair

Article in Journal of Radioanalytical and Nuclear Chemistry, Vol. 259, No. 1 (2004) 153.156 by Z. F. Chai, Q. F. Qian, X. Q. Feng, P. Q. Zhang, N. Q. Liu, W. Y. Feng, M. X. Kuang, H. Y. Wang, Y. Z. Zhang of Laboratory of Nuclear Analytical Techniques, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, P.R. China & General Hospital of Capital Steel and Iron Company, Beijing, P.R. China.

Abstract

The occupational health impact of atmospheric pollution on exposed workers at one iron and steel complex was studied by instrumental neutron activation analysis of workers’ hair samples and medical examination. The experimental results indicate that there is a positive correlation between the high inhalation amounts of iron and other trace elements by the exposed workers and the symptom of their high blood pressure and hypoglycemia, which implies that the atmospheric environment polluted by iron and steel industry has an adverse health impact on the exposed workers. The measures to relieve and abate the occupational diseases caused by air-borne particulate matter should be taken.

Extracts

More and more attention has been paid to occupational health impact at workplace,1 especially in mining, metal refining and metal working industries.2 Excessive exposure to trace metals released by iron and steel industry has become one of the major environmental pollution problems, especially in developing and economically-emerging countries. However, the related report on the correlation between the chronic or acute exposure of chemical elements and workers’ health effect is scarce. For better understanding the health impact of this industrious activity, a representative iron and steel company in Beijing, China, i.e., Capital Iron and Steel Company (CISC) was selected as a target working area, which was one of the biggest industrious enterprises in China. Its annual steel output is up to 10 million tons. The atmospheric particle matter (APM) released by this company in the eighties constituted about 55% of the total APM in the metropolitan city.3,4 The local government and people are more and more concerned about the atmospheric pollution, especially herein heavy metals and toxic elements, caused by CISC and the health impact on occupational workers at workplace and on population living in its surrounding regions. As a part of the municipal environmental monitoring and health survey and the coordinated research project on ‘Assessment of Levels and Health Effects of Airborne Particulate Matter in Mining, Metal Refining and Metal Working Industries Using Nuclear and Related Analytical Techniques’ organized by the International Atomic Energy Agency, we systematically studied the status of environmental pollution and health impact on furnace workers at workplace caused by CISC. In order to monitor the status of environmental pollution, various biological indicators or biomarkers have been developed.5 In this paper, the human hair was utilized as biomonitoring specimen and analyzed by instrumental neutron activation analysis, by which the evaluation of health impact of environmental pollution caused by iron and steel complex on exposed workers was made.

Results and discussion

Content of trace elements in the hair samples of the exposed workers, staff members and control group

... From the average contents of trace elements in the hair samples of the 3 different groups, it can be seen that the contents of some pollution elements (e.g., Fe, Cr, Co and Mn, etc.) in the hair samples of the exposed workers and staff members at the workplace of CISC are very high compared with those of the control group. The most serious pollution element at CISC is iron. The hair of the exposed workers contains 10 times higher Fe concentrations than of the controls.

... As a basic principle of the biological effects of trace elements, any element is harmful to human health, if its amount of intake is overor ill-dose (e.g., Reference 11). The excessive intake of iron by the workers may play an adverse role of their health.

Health impact of the atmospheric pollution on the exposed workers
To assess the health impact of atmospheric pollution caused by iron and steel smelters at CISC on humans, a medical survey for the young workers and staff members (50 each, 20.35 years old) working there was carried out, along with 35 individuals at the same age range living at a relatively clean area as controls. The statistical treatment indicates that more workers and staff members suffer the symptoms of high blood pressure, hypoglycemia and other chronic diseases than the controls. The percentages of the high blood pressure and hypoglycemia for the workers, staff members and controls are 46, 24 and 11% of total specimen numbers, respectively, which implies that the inhalation of excess Fe and other metallic elements may cause adverse health impact.

Until now, the report on the health impact of atmospheric pollution at workplace is available, but the quantitative evaluation of this effect is very difficult. Based on our results of atmospheric monitoring at CISC, the inhalation amounts of trace elements in 0.4 and 8 µm air particles by the exposed workers can be estimated and listed in Table 4, together with the total amount of the air-borne particles with the size over 0.4 µm. It is evident from Table 4 that the inhaled amount of Fe is very high, up to 144 (0.4 µm), 398 (8 µm) and total 542 µg per day. The same is also for other trace elements, such as As, Pb, Rb, Sb, Se and Zn. As medical observation described, the inhalation of excessive ferrous oxide will cause poisonous reactions of respiratory tract,12 including nasal itching, aqueous nasal discharge, abnormal mucous, pharynx itching and irritation, cough, sputum, dyspnoea, chest tightness and pain, etc. Further, the long-term inhalation of ironbearing air particles results in the chronic diseases, even lung cancer.12 As to the relationship between the high iron uptake and cardiovascular diseases, until now no direct evidence is available. This work provides an experimental observation to show the adverse health impact of the atmospheric environment polluted by iron and steel industry on the exposed workers. Nevertheless, more study on the mechanism of its biological effect, especially at the molecular level, is highly needed.

SCIENCE: Surface Enrichment of Trace Elements in Electric Steel Furnace Dust

2008-08-05T23:51:00.001+01:00

Article in Environmental Science & Technology (1983) 17, 435-439 by Marc J. Van Craen, Erlc A. Denoyer, David F. S. Natusch, and F. Adams (Department of Chemistry, University of Antwerp, Belgium).

Secondary ion mass spectrometry (SIMS) and laser microprobe mass analysis (LAMMA) have been used to study the surface enrichment of trace elements in dusts emitted from an electric steel making furnace. It is demonstrated that the elements Na, P, S, C1, K, Cr, Mn, Co, Cu, Zn, and Pb are preferentially enriched on the particle surfaces and that several of these elements are appreciably leachable by water. In several cases the chemical forms of the elements are indicated.

Introduction
A number of workers have reported the observation that certain trace elements increase in specific concentration (micrograms per gram) with decreasing particle size in particles emitted to the atmosphere from high-temperature combustion or conversion processes (1-5). The mechanism that gives rise to this phenomenon has not been fully established; however it has been suggested (1,6) that certain trace elements, or their compounds, are volatilized at the elevated temperatures encountered during particle formation and then condense onto the surfaces of coentrained particles during emission. Such a mechanism would give rise to surface enrichment of the volatilized elements, and this has been observed for coal fly ash and for automobile exhaust particles (7, 8).

The environmental significance of surface enrichment of potentially toxic species is several fold. First, if it occurs as a result of the proposed volatilization-condensation mechanism, small particles will contain higher concentrations of trace elements than large particles, and this will promote emission to the atmosphere, atmospheric enrichment, and pulmonary deposition following inhalation (1, 9). Second, surface enrichment results in enhanced concentrations of potentially toxic species being in immediate contact with the external environment (e.g., body fluids). Finally, if the surface-enriched species are soluble, as is the case for coal fly ash and automobile exhaust particles, then they can be readily mobilized to produce possibly adverse environmental or toxicological effects.

In order to explore further the universality of the surface- enrichment phenomenon, we have chosen to study dust derived from an electric steel making furnace. The trace elements present are derived from the original ore used, and the high temperatures (1500 “C) involved in the furnace operation are sufficient to volatilize several of the elements known to be present. The techniques employed include secondary ion mass spectrometric (SIMS) determination of elemental depth profiles in particle conglomerates, laser microprobe mass analysis (LAMMA) of individual particles, and X-ray fluorescence spectrometry (XRF) of the bulk particulate sample. In all cases analyses are performed before and after the particles have been leached with water to determine the extent of solubility of surface-enriched species. …

[The rest of article was unavailable: IF ANYONE HAS A COPY, CAN YOU PLEASE EMAIL to ChromiumHarbour@gmail.com]

SCIENCE: Utilization of Electric Arc Furnace Dust as Raw Material for the Production

2008-08-05T23:42:00.002+01:00

Article in Journal of Environmental Science and Health, Part A, (2006) 41:9, 1943-1954 by Constantine Sikalidis and Manassis Mitrakas, Department of Chemical Engineering, Aristotle University of Thessaloniki, Thessaloniki, Greece.

... Following the EAF process, dust is generating and is usually collected by evacuation into a baghouse. In accordance with the increase of steel production by EAF process, the Electric Arc Furnace Dust (EAFD) production is also constantly increasing. The specific dust portion per ton of crude steel in the electric steel process is about 10 to 15 kilos,[2] or approximately 1.5% of the scrap steel charged to the EAF. This dust contains most of the zinc, lead, cadmium and halides contained in the charge.[3–5] Table 1 shows the worldwide occurrence of EAFD and moreover the output forecast for the year 2007.[2] Consequently, the administration of millions of tons of dust becomes increasingly difficult the greater their bulk. ...

EAFD is classified as an environmentally hazardous waste in most regions of the world, mainly because of its relatively high levels of Pb, Cd and Cr and in general because of its chemical and physical properties.[2,4] Most of the currently developed and commercialised processes are predominantly applied to the recycling of EAFD and to a lesser extent, to its inactivation prior to permanent disposal in landfills.[2,3] Currently, about 55% of EAFD is processed by high temperature metal recovery processes, mainly for Zn and Pb recovery. ...

RESULTS AND DISCUSSION

The chemical analyses of clayey material and EAFD samples are given in Tables 2 and 3, respectively. Clayey material is typical for such applications. Main elements in EAFD were found to be Fe and Zn, which is common in EAFD.[8] The sum of their oxides almost exceeds the 50 wt% of the dust. The toxic metal which presented the highest concentration, ranging between 64 mg kg‾1 and 104 x 10³ mg kg‾1 (Table 3), was Pb.

Among the other toxic metals, Cu and Cr showed one order of magnitude lower concentration than Pb (27-32 x 10² mg kg‾1 and 14-37 x 10³ mg kg‾1, respectively). Furthermore, Cd and Ba presented two orders of magnitude lower concentration than Pb (43-60 x 10 mg kg‾1 and 25-61 x 10 mg kg‾1, respectively). The extremely low concentration of Hg does not create considerable environmental problems. Main phases identified within EAFD (Fig. 1) were, Fe3O4, ZnO, Mn3O4 and PbO.[9] This suggests that EAFD could be used as raw material for the production of ceramics. The particles’ size of EAFD (>125 μm 0.4%; <125>100 μm 0.7%; <100>63 μm 9% <63>50 μm 28.4%; <50>) is similar to the one (100% <>

... The disposal to the environment of EAFD presents serious problems due to the extremely high leachability mainly because of Pb and secondly of Se and Sb presence. In addition, due to high concentrations of Cl- and SO4 2-, environmental restrictions arise (compare column 3 and 4 of Table 5). The results of leaching experiments (Table 5) indicate that hazardous elements in EAFD can be stabilized completely within a sintered ceramic body being strong enough to be used in bricks production. The concentrations of heavy metals and soluble salts in the leachates of ceramic specimens, were found to be extremely low (compare columns 3 and 6 of Table 5), fulfilling even the EU standards for potable water. ...

CONCLUSIONS

EAFD studied presents certain but not big differences from other EAFD formed in other similar steel plants. Main problem for the environmental disposal of this dust is the high leachability mainly of Pb but also of Se and Sb. By mixing of EAFD and clayey material and following the conventional forming process of ceramic plastic mass extrusion, followed by drying and firing, the heavy metals of the dust can be stabilized in the glassy phase resulting to a sintered ceramic body, having enough strength to be used as brick or other similar ceramic products. Leaching experiments support the utilization of EAFD as raw material in the production of ceramic bricks. The product obtained was found to be environmentally accepted resulting also in profitable economics. On the contrary, the addition of EAFD in dolomite-concrete products might result to not environmentally accepted products due to Pb leachability. Further research is needed concerning the presuppositions under which the leachability, especially of Pb introduced by EAFD addition in dolomite-concrete products can be reduced.

SCIENCE: Leaching properties of electric arc furnace dust prior/following alkaline extraction

2008-08-05T23:38:00.001+01:00

Article in Journal of Environmental Science and Health Part A (2007) 42, 323-329 by Visnja Orescanin, Ruder Boskovic and others, Institute, Laboratory for Radioecology, Bijenicka cesta, Zagreb, Croatia.

Extracts

This study was carried out to determine the appropriate treatment of electric arc furnace (EAF) dust prior to permanent disposal. The total heavy metal content as well as heavy metal leaching from EAF dust was investigated in five composite samples obtained from three Croatian and Slovenian steelworks. ... The results of the study indicate that permanent disposal of EAF dust require the following procedure: alkaline digestion (followed by leachate purification and alkaline zinc electrolyses), chromate reduction (if necessary), solidification of leaching residue and its testing using the leaching analyses. ...

Electric arc furnace (EAF) dust is a major by-product hazardous waste generated by the secondary steelmaking industry. It is a complex, fine-grained, high-density material. The composition of EAF dust is directly associated with the chemistry of the metallic charges used in process. Phase analysis showed that EAF dust was composed mostly of metal oxides, silicates and sulfates.[1,2] According to its chemical composition and leaching properties, the material was classified as hazardous waste which requires special treatment prior to permanent disposal. Generally, there are two main ways of the handling of this sort of waste material. The first is oriented on the conversion of EAF dust into a non-hazardous waste by the solidification/stabilization procedure, which results in reduced heavy metal leaching. For that purpose, zeolitised ashes as well as the original coal fly ash were used.[3,4] Additionally, leachability/toxicity of EAF dust was also decreased by embedding it into the mixture for the production of concrete[5] and Portland cement.[6] The secondway of the handling of EAF dust is oriented toward the recycling of its valuable constituents like zinc and lead. For that purpose, various technologies were developed. They include magnetic and mechanical separation of EAF dust particles,[7] alkaline leaching withNaOH[8,9] and alkaline leaching with NaOH followed by fusion leaching residues with caustic soda,[10,11] microwave assisted caustic leaching[12] and high temperature metal recovery.[13] Acid leaching method gave also promising results.[14] ...

Results and discussion

Major components of electric arc furnace (EAF) dust (Table 1) were iron (ranging from 210.1 to 397.5 g/kg), zinc (ranging from 57.7 to 218.0 g/kg), manganese (ranging from 25.3 to 63.9 g/kg), calcium (ranging from 27.00 to 33.00 mg/kg) and lead (ranging from 5.4 to 16.4 g/kg). From an inspection of these values it is evident that all EAF dust samples highly differ among each other in elemental concentrations as well as in pH values. Generally, samples from Slovenian steelworks (SL-1 and SL-2) had almost two times lower iron concentrations, significantly higher pH values and higher content of zinc, lead, nickel, total chromium and chromium (VI) compared to Croatian steelworks (SK- 1, SK-2 and ST). Concentrations of Ni and Cr (VI) were negligible in the samples SK-1, SK-2 and ST. Significant differences in the composition of all five EAF dust samples are connected with the composition of steel scrap material used in steel production, the type and proportion of nonmetal additive, the type and proportion of ferroalloys and technological parameters as well as techniques and dynamic of slag separation. ...

Conclusion

Electric arc furnace (EAF) dust in its original form presents in the same time a hazardous waste material as well as a valuable secondary raw material for the production of zinc. Due to its origin (a by-product of steel production from the steel scrap) this material significantly varied in its composition.

High concentrations of zinc and lead were determined in the TCLP extracts of initial EAF dust samples, having maximum values 204 mg/L and 42.2 mg/L respectively. Zn values were more than 15-fold lower and Pb values more than 200-fold lower following alkaline digestion of EAF dust in comparison with the TCLP extracts of initial EAF dust. As regards the DIN 38414-S4 extracts of either initial or alkaline digested dust, only Cr( VI) exceeded permissible level, and its reduction to Cr(III) using FeSO4·7H2O is required prior to permanent disposal.NaOH-extractable zinc ranged from 50.3% to 73.2%. Removal efficiency largely depended on the zincite/franklinite ratio.

It could be concluded that EAF dust should be treated prior to permanent disposal according to the following procedure: alkaline digestion (followed by leachate purification and alkaline zinc electrolyses), chromate reduction (if necessary), solidification of leaching residue and its testing using appropriate leaching procedures (TCLP, SPLP, DIN 38414-S4).

Gerdau AmeriSteel Steel Mill Electric Arc Furnace Dust (Baghouse Dust, KO61) Material Safety Data Sheet

2008-08-05T23:31:00.003+01:00

Gerdau AmeriSteel, Tampa, Florida, USA. 'Steel Mill Electric Arc Furnace Dust' (Baghouse Dust, KO61) Material Safety Data Sheet, 16 February 1993 (Reviewed 5/06)

Extracts

Section II - hazardous constituents

SECTION VI - HEALTH HAZARD DATA Routes of Entry

Inhalation: Yes
Skin: No
Ingestion: Yes

Health Hazards:
Acute - Inhalation of fumes may result metal fume fever, irritation to eyes, mucous membranes and respiratory system, pneumonia, bronchitis, sinusitis, laryngitis, chest pain, conjunctivitis, gingivitis, cardiopulmonary arrest. Skin exposure may result in dermatitis and skin lesions.
Chronic - Chronic bronchitis, chronic atrophic nasopharyngitis, pulmonary fibrosis, silicosis, insomnia, irritability, speech disorders, muscle incoordination, mucosal ulcerations, anemia, metallic taste, nausea, vomiting, weakness, headache, pallor, lead line on gums, chromitosis, anorexia, duodenal ulcer, colitis.
Carcinogenic -
NTP: Arsenic, nickel, chromium, cadmium, crystalline silica
IARC: Arsenic, nickel, chromium, lead, cadmium, crystalline silica
OSHA: Arsenic
Signs and Symptoms of Exposure - Nausea, tightness of chest, fever, cough, irritation of eyes, nose, and throat, metallic taste, photophobia, elevated blood lead level.
Medical Conditions Generally Aggravated by Exposure - Respiratory diseases, allergic conditions. ...

SECTION VII - PRECAUTIONS FOR SAFE HANDLING AND USE

Steps To Be Taken In Case of Release or Spill - Dust should be swept up and placed in suitable container. Prevent release to air, sinks, drains, sewers, or water runoff.
Waste Disposal Method - Material is a RCRA hazardous waste. Must be manifested and containerized for shipment to waste treatment or disposal facility.
Precautions to be Taken in Handling and Storing - Wear appropriate personal protective equipment. Use good housekeeping to prevent accumulation.

Electric Arc Furnace Dust (KO61) Material Safety Data Sheet

2008-08-05T23:27:00.002+01:00

Cascade Steel Rolling Mills, Inc., Oregon, USA. Electric Arc Furnace Dust (KO61) Material Safety Data Sheet, January 2001 (Revised: 4/03, 9/05)

Extracts

Chemical Name & Synonyms: Electric Arc Furnace Dust (KO61), Baghouse Dust
Chemical Family: Metal
Formula: Mixture

Section 3 Toxicology and Health Information

Effects of Overexposure: Electric Arc Furnace Dust under normal conditions does not present an inhalation, ingestion or contact health hazard. However, operations such as blowing, sweeping, or moving the dust may result in the following effects if exposure exceeds the exposure limits. Exposures to high concentrations of metallic dusts may result in irritation of the respiratory tract and/or sensitization of the lungs and other mucous membranes. Signs and symptoms of overexposure include redness, swelling, itching, and/or irritation of skin and eyes, respiratory difficulties such as coughing, wheezing, shortness of breath, central nervous system effects, flu-like symptoms, anorexia and/or weight loss.

Acute: Exposure to metal particulates can cause eye, skin, and respiratory tract irritation and/or sensitization. Ingestion of dust may result in increased levels of lead in the body, resulting in lead poisoning. Skin contact with dust may cause irritation or sensitization, possibly leading to dermatitis.

Chronic: Excessive and repeated exposures to dust may cause:

Allergic sensitization - dermatitis and asthma
Lung inflammation and damage - pneumonitis, pneumonia, bronchitis, siderosis, diffuse pulmonary firbrosis
Nasal perforation and nasal cavity damage
Eye inflammation
Central nervous system damage, possibly permanent
Kidney damage
Liver damage
Gout - inflammation of the joints
Lead poisoning
Target Organs: Respiratory tract
Route of Entry: Inhalation, ingestion

Carcinogenicity: The carcinogenicity of this product as a whole has not been tested. Individual components and some compounds of these elemental metals may have been associated with carcinogenicity by NTP and IARC. Iron - IARC Cancer Review Group 3. OSHA/ACGIH Not classifiable as a human carcinogen. Nickel - Confirmed carcinogen. ...

Section 6 Accidental Release Measures

Steps to be Taken in Case Material is Released or Spilled: Shut off ignition sources. Do not touch or walk through spilled material. Compressed air should not be used to clean up spills. During cleanup, skin and eye contact and inhalation of dust should be avoided as much as possible. Provide local exhaust or dilution ventilation as required. Appropriate PPE should be worn if exposure limits are exceeded. Collect material in compatible and appropriately labeled containers. For small dry spills, place material into clean dry container with a clean shovel, and cover loosely. ...

Section 7 Storage and Handling

... Handling Precautions: Avoid breathing of and contact with dusts. ...

Section 11 Toxicological Information

Data not available for the mixture.

Iron: Excessive exposure of eyes to airborne iron dust can cause conjunctivitis, choroiditis, and retinitis. Chronic inhalation of excessive concentrations of iron oxide fumes or dusts may result in development of a benign pneumoconiosis, called siderosis, which is observable via x-ray. Inhalation of excessive concentrations of iron oxide may enhance the risk of lung cancer development in workers exposed to pulmonary carcinogens. LD50 (oral, rat) - 30 gm/kg.

Zinc: High airborne concentrations of dust may cause temporary irritation of the nose and throat. Metal fume fever can be caused by inhalation of zinc oxide fume formed in air from welding or heating zinc metal. Zinc compounds have relatively low toxicity by ingestion.

Chromium: The health hazards associated with exposure to chromium are dependent upon its oxidation state. The metal form (chromium as it exists in this product) is of low toxicity.

Nickel: Nickel fumes are respiratory irritants and may cause pneumonitis. Exposure to nickel and its compounds may result in the development of a dermatitis known as "nickel itch" in sensitized individuals. The first symptom is usually itching, which occurs up to 7 days before skin eruption occurs. Nickel sensitivity, once acquired, appears to persist indefinitely. Nickel and certain nickel compounds have been listed by NTP as being reasonably anticipated to be carcinogens. IARC has listed nickel compounds within group 1 and nickel within group 2B. Nickel is not regulated as a carcinogen by OSHA.

Aluminum: Inhalation of finely divided aluminum and aluminum oxide powder has been reported as a cause of pulmonary fibrosis and lung damage.

Silicon: Elemental silicon is an inert material which appears to lack the property of causing fibrosis in lung tissue. Silicon dust has little adverse affect on lungs and does not appear to produce significant organic disease or toxic effects when exposures are below the permissible exposure limit. Silicon may cause chronic respiratory effects.

Manganese: Chronic manganese poisoning may result from prolonged inhalation of manganese dust and fumes. The central nervous system is the chief site of dmage from the disease, which may result permanent disability. Symptoms include languor, sleepiness, weakness, emotional disturbances, spastic gait, recurring leg cramps, and paralysis. LD50 (oral, rat) - 30 mg/mkg.

Copper: Industrial exposure to copper fumes, dusts, or mists may result in metal fume fever with atrophic changes in nasal mucous membranes. Chronic copper poisoning results in Wilson's Disease, characterized by a hepatic cirrhosis, brain damage, demyelination, renal disease, and copper deposition in the cornea. Copper fume (respirable) has appeared on the ACGIH Notice of Intended Changes (1996 & 1997). The intended ACGIH TLV for respirable copper fume is 0.05 mg/m3.

Section 12 Ecological Information

It is believed that this product, based on its components, will be hazardous to fish, animals, plants and the environment if released, the degree of which would depend on the particle size and quantity released. This material may persist in the environment for long periods, based upon its corrosion resistant, insoluble, and non-biodegradable properties. As with all foreign substances do not allow to enter the storm drainage systems.

Note regarding Electric Arc Furnace Dust (EAFD) and galvanising (zinc)

2008-08-05T23:16:00.002+01:00

The former Irish Steel/Ispat steelworks on Haulbowline Island underwent modernisation in 1972 when a 35 tonne Electric Arc Furnace (EAF) replaced the oil fired open hearth furnace. This required a large electrical current to power the furnace and an electrical substation and transformers with over 400 PCB filled capacitors were installed. In 1981 a 90 tonne EAF was installed and the plant reconfigured to combine fast melting in the EAF with continuous casting and rolling. A ladle furnace (used to keep molten metal from the EAF hot before it was cast) was installed in 1992.

Years	Approx. annual steel production
1972-1980	140,000 p.a.
1981-1992	300,000 p.a.
1992-2001	380,000 p.a.

The acid pickling and galvanising plant (used to coat metals with zinc), which opened in 1954, ceased operations in 1981.

From 1981 the steelworks produced steel sections from scrap steel sourced from Ireland and Europe until June 2001 when Irish Ispat Ltd production ceased.

Source: Enviros Aspinwall report to DCMNR, October 2002 (27MB)

See Wikipedia for further details on EAFs.

SCIENCE: Hazards of heavy metal contamination

2008-08-05T23:07:00.003+01:00

Contributed by Pat The Barker (Limerick)

Article in British Medical Bulletin 68:167-182 (2003) by Lars Järup, Department of Epidemiology and Public Health, Imperial College, London, UK.

Abstract

The main threats to human health from heavy metals are associated with exposure to lead, cadmium, mercury and arsenic. These metals have been extensively studied and their effects on human health regularly reviewed by international bodies such as the WHO. Heavy metals have been used by humans for thousands of years. Although several adverse health effects of heavy metals have been known for a long time, exposure to heavy metals continues, and is even increasing in some parts of the world, in particular in less developed countries, though emissions have declined in most developed countries over the last 100 years. Cadmium compounds are currently mainly used in re-chargeable nickel-cadmium batteries. Cadmium emissions have increased dramatically during the 20th century, one reason being that cadmium-containing products are rarely re-cycled, but often dumped together with household waste. Cigarette smoking is a major source of cadmium exposure. In non-smokers, food is the most important source of cadmium exposure. Recent data indicate that adverse health effects of cadmium exposure may occur at lower exposure levels than previously anticipated, primarily in the form of kidney damage but possibly also bone effects and fractures. Many individuals in Europe already exceed these exposure levels and the margin is very narrow for large groups. Therefore, measures should be taken to reduce cadmium exposure in the general population in order to minimize the risk of adverse health effects. … The general population is exposed to lead from air and food in roughly equal proportions. During the last century, lead emissions to ambient air have caused considerable pollution, mainly due to lead emissions from petrol. Children are particularly susceptible to lead exposure due to high gastrointestinal uptake and the permeable blood-brain barrier. Blood levels in children should be reduced below the levels so far considered acceptable, recent data indicating that there may be neurotoxic effects of lead at lower levels of exposure than previously anticipated. Although lead in petrol has dramatically decreased over the last decades, thereby reducing environmental exposure, phasing out any remaining uses of lead additives in motor fuels should be encouraged. The use of lead-based paints should be abandoned, and lead should not be used in food containers. In particular, the public should be aware of glazed food containers, which may leach lead into food. Exposure to arsenic is mainly via intake of food and drinking water, food being the most important source in most populations. Long-term exposure to arsenic in drinking-water is mainly related to increased risks of skin cancer, but also some other cancers, as well as other skin lesions such as hyperkeratosis and pigmentation changes. Occupational exposure to arsenic, primarily by inhalation, is causally associated with lung cancer. Clear exposure-response relationships and high risks have been observed.

Extracts

Although there is no clear definition of what a heavy metal is, density is in most cases taken to be the defining factor. Heavy metals are thus commonly defined as those having a specific density of more than 5 g/cm3. The main threats to human health from heavy metals are associated with exposure to lead, cadmium, mercury and arsenic (arsenic is a metalloid, but is usually classified as a heavy metal). ...

Emissions of heavy metals to the environment occur via a wide range of processes and pathways, including to the air (e.g. during combustion, extraction and processing), to surface waters (via runoff and releases from storage and transport) and to the soil (and hence into groundwaters and crops) (see Chapter 1). Atmospheric emissions tend to be of greatest concern in terms of human health, both because of the quantities involved and the widespread dispersion and potential for exposure that often ensues. The spatial distributions of cadmium, lead and mercury emissions to the atmosphere in Europe can be found in the Meteorological Synthesizing Centre-East (MSC-E) website (http://www.msceast.org/hms/emission.html#Spatial). Lead emissions are mainly related to road transport and thus most uniformly distributed over space. Cadmium emissions are primarily associated with non-ferrous metallurgy and fuel combustion, whereas the spatial distribution of anthropogenic mercury emissions reflects mainly the level of coal consumption in different regions.

People may be exposed to potentially harmful chemical, physical and biological agents in air, food, water or soil. However, exposure does not result only from the presence of a harmful agent in the environment. The key word in the definition of exposure is contact2. There must be contact between the agent and the outer boundary of the human body, such as the airways, the skin or the mouth. Exposure is often defined as a function of concentration and time: "an event that occurs when there is contact at a boundary between a human and the environment with a contaminant of a specific concentration for an interval of time"3. For exposure to happen, therefore, co-existence of heavy metals and people has to occur (see Chapter 1).

Cadmium
... Health effects

Inhalation of cadmium fumes or particles can be life threatening, and although acute pulmonary effects and deaths are uncommon, sporadic cases still occur9,10. Cadmium exposure may cause kidney damage. The first sign of the renal lesion is usually a tubular dysfunction, evidenced by an increased excretion of low molecular weight proteins [such as ß2-microglobulin and {alpha}1-microglobulin (protein HC)] or enzymes [such as N-Acetyl-ß-D-glucosaminidase (NAG)]4,6. It has been suggested that the tubular damage is reversible11, but there is overwhelming evidence that the cadmium induced tubular damage is indeed irreversible4.

WHO6 estimated that a urinary excretion of 10 nmol/mmol creatinine (corresponding to circa 200 mg Cd/kg kidney cortex) would constitute a 'critical limit' below which kidney damage would not occur. However, WHO calculated that circa 10% of individuals with this kidney concentration would be affected by tubular damage. Several reports have since shown that kidney damage and/or bone effects are likely to occur at lower kidney cadmium levels. European studies have shown signs of cadmium induced kidney damage in the general population at urinary cadmium levels around 2-3 µg Cd/g creatinine12,13.

The initial tubular damage may progress to more severe kidney damage, and already in 1950 it was reported that some cadmium exposed workers had developed decreased glomerular filtration rate (GFR)14. This has been confirmed in later studies of occupationally exposed workers15,16. An excess risk of kidney stones, possibly related to an increased excretion of calcium in urine following the tubular damage, has been shown in several studies4.

Recently, an association between cadmium exposure and chronic renal failure [end stage renal disease (ESRD)] was shown17. Using a registry of patients, who had been treated for uraemia, the investigators found a double risk of ESRD in persons living close to (<2>Cancer
The IARC has classified cadmium as a human carcinogen (group I) on the basis of sufficient evidence in both humans and experimental animals22. IARC, however, noted that the assessment was based on few studies of lung cancer in occupationally exposed populations, often with imperfect exposure data, and without the capability to consider possible confounding by smoking and other associated exposures (such as nickel and arsenic). Cadmium has been associated with prostate cancer, but both positive and negative studies have been published. Early data indicated an association between cadmium exposure and kidney cancer23. Later studies have not been able clearly to confirm this, but a large multi-centre study showed a (borderline) significant over-all excess risk of renal-cell cancer, although a negative dose-response relationship did not support a causal relation24. Furthermore, a population-based multicentre-study of renal cell carcinoma found an excess risk in occupationally exposed persons25. In summary, the evidence for cadmium as a human carcinogen is rather weak, in particular after oral exposure. Therefore, a classification of cadmium as 'probably carcinogenic to humans' (IARC group 2A) would be more appropriate. This conclusion also complies with the EC classification of some cadmium compounds (Carcinogen Category 2; Annex 1 to the directive 67/548/EEC).

Lead

... Occupational exposure to inorganic lead occurs in mines and smelters as well as welding of lead painted metal, and in battery plants. Low or moderate exposure may take place in the glass industry. High levels of air emissions may pollute areas near lead mines and smelters. Airborne lead can be deposited on soil and water, thus reaching humans via the food chain.

Up to 50% of inhaled inorganic lead may be absorbed in the lungs. Adults take up 10-15% of lead in food, whereas children may absorb up to 50% via the gastrointestinal tract. Lead in blood is bound to erythrocytes, and elimination is slow and principally via urine. Lead is accumulated in the skeleton, and is only slowly released from this body compartment. Half-life of lead in blood is about 1 month and in the skeleton 20-30 years35.

In adults, inorganic lead does not penetrate the blood-brain barrier, whereas this barrier is less developed in children. The high gastrointestinal uptake and the permeable blood-brain barrier make children especially susceptible to lead exposure and subsequent brain damage. Organic lead compounds penetrate body and cell membranes. Tetramethyl lead and tetraethyl lead penetrate the skin easily. These compounds may also cross the blood-brain barrier in adults, and thus adults may suffer from lead encephalopathy related to acute poisoning by organic lead compounds.

... Health effects

The symptoms of acute lead poisoning are headache, irritability, abdominal pain and various symptoms related to the nervous system. Lead encephalopathy is characterized by sleeplessness and restlessness. Children may be affected by behavioural disturbances, learning and concentration difficulties. In severe cases of lead encephalopathy, the affected person may suffer from acute psychosis, confusion and reduced consciousness. People who have been exposed to lead for a long time may suffer from memory deterioration, prolonged reaction time and reduced ability to understand. Individuals with average blood lead levels under 3 µmol/l may show signs of peripheral nerve symptoms with reduced nerve conduction velocity and reduced dermal sensibility. If the neuropathy is severe the lesion may be permanent. The classical picture includes a dark blue lead sulphide line at the gingival margin. In less serious cases, the most obvious sign of lead poisoning is disturbance of haemoglobin synthesis, and long-term lead exposure may lead to anaemia.

Recent research has shown that long-term low-level lead exposure in children may also lead to diminished intellectual capacity. Figure 3 shows a meta-analysis of four prospective studies using mean blood lead level over a number of years. The combined evidence suggests a weighted mean decrease in IQ of 2 points for a 0.48 µmol/l (10 µg/dl) increase in blood lead level (95% confidence interval from -0.3 points to -3.6 points)35.

Acute exposure to lead is known to cause proximal renal tubular damage35. Long-term lead exposure may also give rise to kidney damage and, in a recent study of Egyptian policemen, urinary excretion of NAG was positively correlated with duration of exposure to lead from automobile exhaust, blood lead and nail lead36. Despite intensive efforts to define the relationship between body burden of lead and blood pressure or other effects on the cardiovascular system, no causal relationship has been demonstrated in humans35. …

Blood lead levels in children below 10 µmg/dl have so far been considered acceptable, but recent data indicate that there may be toxicological effects of lead at lower levels of exposure than previously anticipated. There is also evidence that certain genetic and environmental factors can increase the detrimental effects of lead on neural development, thereby rendering certain children more vulnerable to lead neurotoxicity38.

IARC classified lead as a 'possible human carcinogen' based on sufficient animal data and insufficient human data in 1987. Since then a few studies have been published, the overall evidence for lead as a carcinogen being only weak, the most likely candidates are lung cancer, stomach cancer and gliomas39.

Arsenic

... Smelting of non-ferrous metals and the production of energy from fossil fuel are the two major industrial processes that lead to arsenic contamination of air, water and soil, smelting activities being the largest single anthropogenic source of atmospheric pollution41.

... Contaminated soils such as mine-tailings are also a potential source of arsenic exposure40.

... Absorption of arsenic in inhaled airborne particles is highly dependent on the solubility and the size of particles. Soluble arsenic compounds are easily absorbed from the gastrointestinal tract. However, inorganic arsenic is extensively methylated in humans and the metabolites are excreted in the urine40.

Arsenic (or metabolites) concentrations in blood, hair, nails and urine have been used as biomarkers of exposure. Arsenic in hair and nails can be useful indicators of past arsenic exposure, if care is taken to avoid external arsenic contamination of the samples. Speciated metabolites in urine expressed as either inorganic arsenic or the sum of metabolites (inorganic arsenic + MMA + DMA) is generally the best estimate of recent arsenic dose. However, consumption of certain seafood may confound estimation of inorganic arsenic exposure, and should thus be avoided before urine sampling40.

Health effects

Inorganic arsenic is acutely toxic and intake of large quantities leads to gastrointestinal symptoms, severe disturbances of the cardiovascular and central nervous systems, and eventually death. In survivors, bone marrow depression, haemolysis, hepatomegaly, melanosis, polyneuropathy and encephalopathy may be observed. Ingestion of inorganic arsenic may induce peripheral vascular disease, which in its extreme form leads to gangrenous changes (black foot disease, only reported in Taiwan).

Populations exposed to arsenic via drinking water show excess risk of mortality from lung, bladder and kidney cancer, the risk increasing with increasing exposure. There is also an increased risk of skin cancer and other skin lesions, such as hyperkeratosis and pigmentation changes.

Studies on various populations exposed to arsenic by inhalation, such as smelter workers, pesticide manufacturers and miners in many different countries consistently demonstrate an excess lung cancer. Although all these groups are exposed to other chemicals in addition to arsenic, there is no other common factor that could explain the findings. The lung cancer risk increases with increasing arsenic exposure in all relevant studies, and confounding by smoking does not explain the findings.

The latest WHO evaluation40 concludes that arsenic exposure via drinking water is causally related to cancer in the lungs, kidney, bladder and skin, the last of which is preceded by directly observable precancerous lesions. Uncertainties in the estimation of past exposures are important when assessing the exposure-response relationships, but it would seem that drinking water arsenic concentrations of approximately 100 µg/l have led to cancer at these sites, and that precursors of skin cancer have been associated with levels of 50-100 µg/l.

The relationships between arsenic exposure and other health effects are less clear. There is relatively strong evidence for hypertension and cardiovascular disease, but the evidence is only suggestive for diabetes and reproductive effects and weak for cerebrovascular disease, long-term neurological effects, and cancer at sites other than lung, bladder, kidney and skin40.

Conclusions

Recent data indicate that adverse health effects of cadmium exposure, primarily in the form of renal tubular damage but possibly also effects on bone and fractures, may occur at lower exposure levels than previously anticipated. Many individuals in Europe already exceed these exposure levels and the margin is very narrow for large groups. Therefore, measures should be taken to reduce cadmium exposure in the general population in order to minimize the risk of adverse health effects.

The general population does not face a significant health risk from methylmercury, although certain groups with high fish consumption may attain blood levels associated with a low risk of neurological damage to adults. Since there is a risk to the fetus in particular, pregnant women should avoid a high intake of certain fish, such as shark, swordfish and tuna. Fish, such as pike, walleye and bass, taken from polluted fresh waters should especially be avoided.

There has been a debate on the safety of dental amalgams and claims have been made that mercury from amalgam may cause a variety of diseases, but to date no studies have been able to show any associations between amalgam fillings and ill health.

Children are particularly vulnerable to lead exposure. Blood levels in children should be reduced below the levels so far considered acceptable, recent data indicating that there may be neurotoxic effects of lead at lower levels of exposure than previously anticipated. Although lead in petrol has dramatically declined over the last decades, thereby reducing environmental exposure, there is a need to phase out any remaining uses of lead additives in motor fuels. The use of lead-based paints should also be abandoned, and lead should not be used in food containers. In particular, the public should be aware of glazed food containers, which may leach lead into food.

Long-term exposure to arsenic in drinking water is mainly related to increased risks of skin cancer, but also some other cancers, and other skin lesions such as hyperkeratosis and pigmentation changes. Occupational exposure to arsenic, primarily by inhalation, is causally associated with lung cancer. Clear exposure-response relationships and high risks have been observed.

UCC researchers pointed to Ispat problems in 2001

2008-08-04T17:31:00.001+01:00

Contributed by Cobh resident (name withheld)

LOSPAN Phase 2 Report, January 2001 "Developing Monitoring Protocols for Spatial Policy Indicators" available from UCC Coastal and Marine Resources Centre (CMRC), Haulbowline Island, Cobh, Co. Cork

Cork Harbour: Eight principle issues of interest in the environs of Cork Harbour were identified as part of Phase 1. These include: agriculture; employment; water quality; tourism and recreational use; land use and development; fishing; atmospheric emissions and conservation. ...

Irish Ispat Ltd., situated on Haulbowline Island in the lower harbour, remains the only steelmaking and rolling plant in Ireland. In recent years it has been developed into one of Europe's most modern steel industries. Significant movement of seaborne traffic occurs at regular intervals at the Haulbowline plant, as 90% of its rolled steel output is exported. ...

Air Quality
Air quality monitoring in Ireland remains focused on the measurement of sulphur dioxide and particulates (smoke) with simultaneous measurements of daily values of the two pollutants at almost 60 monitoring sites throughout the country, mainly in urban areas. The standards currently in force in Ireland follow from EC Directive 80/779/EEC (CEC, 1980) on air quality limit values for SO2 and suspended particulates which specifies limit values for annual, winter and daily reference periods. The levels of both smoke and SO2 in 1998/1999 were very low and fully compliant with the Irish air quality standards (Air Quality Monitoring annual report 1998, EPA). The Air Quality Framework Directive 1996 (96/62/EC) provides a framework under which the European Commission is bringing into force a range of daughter directives to tackle a wide range of priority air pollutants throughout Member States.

Emissions from point sources typically arise in the context of industrial processes; ambient air quality monitoring is just one way of monitoring/assessing the impacts. Complementary stack emission monitoring is commonly carried out to ensure compliance with licensing requirements. Dispersion modelling allows the likely impacts of these emissions to be determined numerically, facilitating comparisons with limit and guideline values for ambient concentrations. As the accuracy of such predictions is uncertain, emissions monitoring and dispersion modelling cannot always provide reliable estimates of pollution effects. The measurement of atmospheric pollution concentrated at dispersion points in the vicinity of a point source remains the most reliable method of determining air quality. A complete assessment of air quality through monitoring alone requires a well distributed and maintained network of monitoring stations, employing reliable and accurate measurement equipment. However these are expensive and it is important that monitoring campaigns are carefully planned to ensure that as much useful information as possible is gathered with the available resources.

The European Air Quality Framework Directive requires that areas around significant point sources be defined as air quality zones and that the air quality is assessed at least every five years. This requires the completion of short monitoring campaigns in the vicinity of the point source (Optimal Monitoring of Air Quality in the Vicinity of Point Sources - report for EPA, Feb., 2000).

Air quality data are obtained largely from Local Authority monitoring programmes and also from the Environmental Protection Agencies monitoring activities. In order to comply with Integrated Pollution Control (IPC) license requirements, industrial companies must carry out their own emissions monitoring and incorporate the data in their license application. Data from the many industries in Cork harbour is held at the EPA regional office in Inniscarra, Co. Cork. It is evident that the majority of the industries situated in the harbour comply with the IPC license requirements. The EPA contacted the pharmaceutical company Warner Lambert, which is situated in Ringaskiddy in Cork harbour, in January 2001, commending them on having a compliant audit and noted the efforts made to comply with the requirements of the IPC license. This is not always the case however and much controversy surrounding air pollution from Irish Ispat (steel industry) in Cork Harbour has occurred over the past number of years. Numerous records exist of complaints from the naval base at Haulbowline and from local people in the area surrounding Ispat. These complaints refer to emissions causing significant environmental pollution. A letter sent to Ispat in January 2001 from the EPA required Ispat to cease all activities giving rise to these emissions and if this did not occur then the agency will apply to the High Court for injuncture relief against the facility. Irish Ispat responded to the EPA's 'Air monitoring report' of Jan. 23, 2001 and acknowledged that guideline limit values were exceeded on a number of occasions and that the probable cause of this was due to the castor fans. Irish Ispat proceeded to point out that an abatement system has been decided upon and instalment planned for April 2001 and that ambient levels of various pollutants will be reduced significantly.

In an EPA report on Ambient Air Monitoring at Haulbowline Naval Base June-August 2000, a mobile laboratory was used. Levels of lead, benzene, SO2, oxides of nitrogen and carbon monoxide were measured and none of these exceeded directive limits during the monitoring period. However concentrations of PM10 particles exceeded the annual limit value for the protection of human health. On three episodes where very high levels of PM10 particles were recorded, it was noted that easterly winds were blowing from the Irish Ispat steel plant to the Naval Base (information provided by the EPA, Cork). ...

Chromium 6: A Killer Compound With An Improbable Trigger

2008-08-04T17:27:00.002+01:00

Link

Chromium 6, the cancer-causing compound that sparked the legal crusade by Erin Brockovich, can be toxic in tiny doses. Brown University scientists have uncovered the unlikely culprit: vitamin C. In new research, the Brown team shows that when vitamin C reacts with even low doses of chromium 6 inside human cells, it creates high levels of cancer-causing DNA damage and mutations.

PROVIDENCE, R.I. [Brown University] - Even miniscule amounts of chromium 6 can cause cancer. Blame that do-gooder nutrient, vitamin C.

Brown University researchers have discovered that naturally occurring vitamin C reacts inside human lung cells with chromium 6, or hexavalent chromium, and causes massive DNA damage. Low doses of chromium 6, combined with vitamin C, produce up to 15 times as many chromosomal breaks and up to 10 times more mutations - forms of genetic damage that lead to cancer - compared with cells that lacked vitamin C altogether.

This finding is startling, said Anatoly Zhitkovich, an associate professor of medical science at Brown who oversaw the experiments. Outside cells, Zhitkovich said, vitamin C actually protects against the cellular damage caused by hexavalent chromium, the toxic chemical that starred as the villain in the true-to-life Hollywood drama, Erin Brockovich. In fact, vitamin C has been used as an antidote in industrial accidents and other instances when large amounts of chromium are ingested.

Vitamin C works protective wonders because it is a powerful antioxidant, blocking cellular damage from free radicals. Specifically, the vitamin rapidly "reduces," or adds electrons, to free radicals, converting them into harmless molecules. This electron transfer from vitamin C to chromium 6 produces chromium 3, a form of the compound that is unable to enter cells.

But what happens when chromium and vitamin C come together inside cells? Because vitamin C isn't found in cells grown in a lab, Zhitkovich and his team conducted experiments using human lung cells supplemented with vitamin C. They learned that when vitamin C is present, chromium reduction has a very different effect. Cellular vitamin C acted as a potent toxic amplifier, sparking significantly more chromosomal breaks and cellular mutations.

"When we increased the concentration of vitamin C inside cells, we saw progressively more mutations and DNA breaks, showing how seemingly innocuous amounts of chromium can become toxic," Zhitkovich said. "For years, scientists have wondered why exposure to small amounts of hexavalent chromium can cause such high rates of cancer. Now we know. It's vitamin C."

Hexavalent chromium is used to plate metals and to make paints, dyes, plastics and inks. As an anticorrosive agent, it is also added to stainless steel, which releases hexavalent chromium during welding. Hexavalent chromium causes lung cancer and is found in 40 percent of Superfund sites nationwide. This is the toxic metal, found in drinking water in a small California town, that Erin Brockovich campaigned against, successfully winning residents a record settlement of $333 million in 1996.

Zhitkovich said his team's research, published in Nucleic Acids Research, might have policy implications. When combined with vitamin C, chromium 6 caused genetic damage in cells in doses four times lower than current federal standards, Zhitkovich said. If additional research backs these findings, he said federal regulators might want to lower exposure standards.

Zhitkovich is part of a major Brown research initiative, the Superfund Basic Research Program, which addresses the health and environmental concerns created by hazardous waste contamination. As part of this program, funded by the National Institute of Environmental Health Sciences, Zhitkovich is conducting basic research that may result in a medical test that assesses DNA damage from hexavalent chromium. Former Brown graduate student Mindy Reynolds was lead author of the journal article. Brown research assistant Lauren Stoddard and postdoctoral research associate Ivan Bespalov also took part in the research. The National Institutes of Health funded the work.

Editors: Brown University has a fiber link television studio available for domestic and international live and taped interviews and maintains an ISDN line for radio interviews. For more information, call the Office of Media Relations at (401) 863-2476.

SCIENCE: Heavy metal pollution and human biotoxic effects

2008-08-02T12:50:00.005+01:00

Contributed by Marcus O'Garvey

Article in scientific journal by Duruibe, J.O., Ogwuegbu, M.O. and Egwurugwu, J.N. (2007) International Journal of Physical Sciences, Vol 2(5), pp 112-118.

Abstract
Some heavy metals have bio-importance as trace elements but, the biotoxic effects of many of them in human biochemistry are of great concern. Hence, there is the need for proper understanding of the conditions, such as the concentrations and oxidation states, which make them harmful, and how biotoxicity occurs. It is also important to know their sources, leaching processes, chemical conversions and their modes of deposition to pollute the environment, which essentially supports lives. Literature sources point to the fact that these metals are released into the environment by both natural and anthropogenic sources, especially mining and industrial activities, and automobile exhausts (for lead). They leach into underground waters, moving along water pathways and eventually depositing in the aquifer, or are washed away by run-off into surface waters thereby resulting in water and subsequently soil pollution. Poisoning and toxicity in animals occur frequently through exchange and co-ordination mechanisms. When ingested, they combine with the body's biomolecules, like proteins and enzymes to form stable biotoxic compounds, thereby mutilating their structures and hindering them from the bioreactions of their functions. This paper reviews certain heavy metals and their biotoxic effects on man and the mechanisms of their biochemical activities.

Extracts
The term "heavy metals" refers to any metallic element that has a relatively high density and is toxic or poisonous even at low concentration (Lenntech, 2004). "Heavy metals" is a general collective term, which applies to the group of metals and metalloids with atomic density greater than 4 g/cm3, or 5 times or more, greater than water (Huton and Symon, 1986; Battarbee et al., 1988; Nriagu and Pacyna 1988; Nriagu, 1989; Garbarino et al., 1995, Hawkes, 1997). However, being a heavy metal has little to do with density but concerns chemical properties. Heavy metals include lead (Pb), cadmium (Cd), zinc (Zn), mercury (Hg), arsenic (As), silver (Ag) chromium (Cr), copper (Cu) iron (Fe), and the platinum group elements. Environment is defined as the totality of circumstances surrounding an organism or group of organisms especially, the combination of external physical conditions that affect and influence the growth, development and survival of organisms (Farlex, 2005). It consists of the flora, fauna and the abiotic, and includes the aquatic, terrestrial and atmospheric habitats. The environment is considered in terms of the most tangible aspects like air, water and food, and the less tangible, though no less important, the communities we live in (Gore, 1997). A pollutant is any substance in the environment, which causes objectionable effects, impairing the welfare of the environment, reducing the quality of life and may eventually cause death. Such a substance has to be present in the environment beyond a set or tolerance limit, which could be either a desirable or acceptable limit. Hence, environmental pollution is the presence of a pollutant in the environment; air, water and soil, which may be poisonous or toxic and will cause harm to living things in the polluted environment.

Heavy metals occur as natural constituents of the earth crust, and are persistent environmental contaminants since they cannot be degraded or destroyed. To a small extent, they enter the body system through food, air, and water and bio-accumulate over a period of time (Lenntech, 2004; UNEP/GPA, 2004). ...

OCCUPATIONAL EXPOSURE

Heavy metal exposure occurs significantly by occupational exposure. Workers of the mining and production of cadmium, chromium, lead, mercury, gold and silver have been reported to be thus exposed; also inhabitants around industrial sites of heavy metal mining and processing, are exposed through air by suspended particulate matters (SPM) (Heyer, 1985; USDOL, 2004; Ogwuegbu and Muhanga, 2005). ...

HEAVY METAL POISONING AND BIOTOXICITY

The biotoxic effects of heavy metals refer to the harmful effects of heavy metals to the body when consumed above the bio-recommended limits. Although individual metals exhibit specific signs of their toxicity, the following have been reported as general signs associated with cadmium, lead, arsenic, mercury, zinc, copper and aluminium poisoning: gastrointestinal (GI) disorders, diarrhoea, stomatitis, tremor, hemoglobinuria causing a rust-red colour to stool, ataxia, paralysis, vomiting and convulsion, depression, and pneumonia when volatile vapours and fumes are inhaled (McCluggage, 1991). The nature of effects could be toxic (acute, chronic or sub-chronic), neurotoxic, carcinogenic, mutagenic or teratogenic.

Cadmium is toxic at extremely low levels. In humans, long term exposure results in renal dysfunction, characterized by tubular proteinuria. High exposure can lead to obstructive lung disease, cadmium pneumonitis, resulting from inhaled dusts and fumes. It is characterized by chest pain, cough with foamy and bloody sputum, and death of the lining of the lung tissues because of excessive accumulation of watery fluids. Cadmium is also associated with bone defects, viz; osteomalacia, osteoporosis and spontaneous fractures, increased blood pressure and myocardic dysfunctions. Depending on the severity of exposure, the symptoms of effects include nausea, vomiting, abdominal cramps, dyspnea and muscular weakness. Severe exposure may result in pulmonary odema and death. Pulmonary effects (emphysema, bronchiolitis and alveolitis) and renal effects may occur following subchronic inhalation exposure to cadmium and its compounds (McCluggage, 1991; INECAR, 2000; European Union, 2002; Young, 2005).

Lead is the most significant toxin of the heavy metals, and the inorganic forms are absorbed through ingestion by food and water, and inhalation (Ferner, 2001). A notably serious effect of lead toxicity is its teratogenic effect. Lead poisoning also causes inhibition of the synthesis of haemoglobin; dysfunctions in the kidneys, joints and reproductive systems, cardiovascular system and acute and chronic damage to the central nervous system (CNS) and peripheral nervous system (PNS) (Ogwuebgu and Muhanga, 2005). Other effects include damage to the gastrointestinal tract (GIT) and urinary tract resulting in bloody urine, neurological disorder and can cause severe and permanent brain damage. While inorganic forms of lead, typically affect the CNS, PNS, GIT and other biosystems, organic forms predominantly affect the CNS (McCluggage, 1991; INECAR, 2000; Ferner, 2001; Lenntech, 2004). Lead affects children by leading to the poor development of the grey matter of the brain, thereby resulting in poor intelligence quotient (IQ) (Udedi, 2003). Its absorption in the body is enhanced by Ca and Zn deficiencies. Acute and chronic effects of lead result in psychosis.

Zinc has been reported to cause the same signs of illness as does lead, and can easily be mistakenly diagnosed as lead poisoning (McCluggage, 1991). Zinc is considered to be relatively non-toxic, especially if taken orally. However, excess amount can cause system dysfunctions that result in impairment of growth and reproduction (INECAR, 2000; Nolan, 2003). The clinical signs of zinc toxicosis have been reported as vomiting, diarrhea, bloody urine, icterus (yellow mucus membrane), liver failure, kidney failure and anemia (Fosmire, 1990). ...

SCIENCE: Human health effects of air pollution

2008-08-01T09:58:00.004+01:00

Contributed by Boffin Island

Article on the effect of air pollutants on human health and underlying mechanisms of cellular action in scientific journal: Environmental Pollution 151 (2008) 362-367. By Marilena Kampa & Elias Castanas, Laboratory of Experimental Endocrinology, University of Crete, School of Medicine, Heraklion, Greece. Download (180k)

Abstract

Hazardous chemicals escape to the environment by a number of natural and/or anthropogenic activities and may cause adverse effects on human health and the environment. Increased combustion of fossil fuels in the last century is responsible for the progressive change in the atmospheric composition. Air pollutants, such as carbon monoxide (CO), sulfur dioxide (SO2), nitrogen oxides (NOx), volatile organic compounds (VOCs), ozone (O3), heavy metals, and respirable particulate matter (PM2.5 and PM10), differ in their chemical composition, reaction properties, emission, time of disintegration and ability to diffuse in long or short distances. Air pollution has both acute and chronic effects on human health, affecting a number of different systems and organs. It ranges from minor upper respiratory irritation to chronic respiratory and heart disease, lung cancer, acute respiratory infections in children and chronic bronchitis in adults, aggravating pre-existing heart and lung disease, or asthmatic attacks. In addition, short- and long-term exposures have also been linked with premature mortality and reduced life expectancy. These effects of air pollutants on human health and their mechanism of action are briefly discussed.

Extracts

1. Introduction

Although a number of physical activities (volcanoes, fire, etc.) may release different pollutants in the environment, anthropogenic activities are the major cause of environmental air pollution. Hazardous chemicals can escape to the environment by accident, but a number of air pollutants are released from industrial facilities and other activities and may cause adverse effects on human health and the environment. By definition, an air pollutant is any substance which may harm humans, animals, vegetation or material. As far as humans are concerned an air pollutant may cause or contribute to an increase in mortality or serious illness or may pose a present or potential hazard to human health. The determination of whether or not a substance poses a health risk to humans is based on clinical, epidemiological, and/or animal studies which demonstrate that exposure to a substance is associated with health effects. In the context of human health, ''risk'' is the probability that a noxious health effects may occur.

2. Pollutant categories

Persistent organic pollutants form a toxic group of chemicals. They persist in the environment for long periods of time, and their effects are magnified as they move up through the food chain (bio-magnification). They include pesticides, as well as dioxins, furans and PCBs. Generally, the generic term ''dioxins'' is used to cover polychlorinated dibenzo-dioxins (PCDDs) and polychlorinated dibenzo-furans (PCDFs) while polychlorinated biphenyls (PCB) are called ''dioxin like compounds'' and can act similarly in terms of dioxin-type toxicity (Schecter et al., 2006). Dioxins are formed during incomplete combustion and whenever materials containing chlorine (e.g. plastics) are burned. Emitted in the atmosphere, dioxins tend to deposit on soil and water but, being water-insoluble, they do not contaminate ground water sources. Most dioxins in plants come from air and dust or pesticides and enter the food chain where they bio-accumulate due to their ability to be stably bound to lipids.

Heavy metals include basic metal elements such as lead, mercury, cadmium silver nickel, vanadium, chromium and manganese. They are natural components of the earth's crust; they cannot be degraded or destroyed, and can be transported by air, and enter water and human food supply. In addition, they enter the environment through a wide variety of sources, including combustion, waste water discharges and manufacturing facilities. To a small extent they enter human bodies where, as trace elements, they are essential to maintain the normal metabolic reactions. However, at higher (although relatively low) concentrations they can become toxic (Jarup, 2003). Most heavy metals are dangerous because they tend to bio-accumulate in the human body. Bioaccumulation means an increase in the concentration of a chemical in a biological organism over time, compared to the chemical's concentration in the environment. Compounds accumulate in organisms any time they are taken in and stored faster than they are broken down (metabolized) or excreted.

Particulate matter (PM) is the generic term used for a type of air pollutants, consisting of complex and varying mixtures of particles suspended in the breathing air, which vary in size and composition, and are produced by a wide variety of natural and anthropogenic activities (Poschl, 2005). Major sources of particulate pollution are factories, power plants, refuse incinerators, motor vehicles, construction activity, fires, and natural windblown dust. The size of the particles varies (PM2.5 and PM10 for aerodynamic diameter smaller than 2.5 µm and 10 µm respectively) and different categories have been defined: Ultrafine particles, smaller than 0.1 µm in aerodynamic diameter, Fine particles, smaller than 1 µm, and Coarse particles, larger than 1 µm. The size of the particles determines the site in the respiratory tract that they will deposit: PM10 particles deposit mainly in the upper respiratory tract while fine and ultra fine particles are able to reach lung alveoli. So far, no single component has been identified that could explain most of the PM effects. Among the parameters that play an important role for eliciting health effects are the size and surface of particles, their number and their composition. The composition of PM varies, as they can absorb and transfer a multitude of pollutants. However, their major components are metals, organic compounds, material of biologic origin, ions, reactive gases, and the particle carbon core. There is strong evidence to support that ultra fine and fine particles are more hazardous than larger ones (coarse particles), in terms of mortality and cardiovascular and respiratory effects. In addition, the metal content, the presence of PAHs and other organic components such as endotoxins, mainly contribute to PM toxicity.

3. Routes of exposure

Humans enter in contact with different air pollutants primarily via inhalation and ingestion, while dermal contact represents a minor route of exposure. Air pollution contributes, to a great extent, to the contamination of food and water, which makes ingestion in several cases the major route of pollutant intake (Thron, 1996). Via the gastrointestinal and respiratory tract, absorption of pollutants may occur, while a number of toxic substances can be found in the general circulation and deposit to different tissues. Elimination occurs to a certain degree by excretion (Madden and Fowler, 2000).

4. Health effects

Sporadic air pollution events, like the historic London fog in 1952 and a number of short and long term epidemiological studies investigated the effects of air quality changes on human health. A constant finding is that air pollutants contribute to increased mortality and hospital admissions (Brunekreef and Holgate, 2002). The different composition of air pollutants, the dose and time of exposure and the fact that humans are usually exposed to pollutant mixtures than to single substances, can lead to diverse impacts on human health. Human health effects can range from nausea and difficulty in breathing or skin irritation, to cancer. They also include birth defects, serious developmental delays in children, and reduced activity of the immune system, leading to a number of diseases. Moreover, there exist several susceptibility factors such as age, nutritional status and predisposing conditions. Health effects can be distinguished to acute, chronic not including cancer and cancerous. Epidemiological and animal model data indicate that primarily affected systems are the cardiovascular and the respiratory system. However, the function of several other organs can be also influenced (Cohen et al., 2005; Huang and Ghio, 2006; Kunzli and Tager, 2005; Sharma and Agrawal, 2005).

4.1. Effects of air pollutants on different organs and systems

4.1.1. Respiratory system

Numerous studies describe that all types of air pollution, at high concentration, can affect the airways. Nevertheless, similar effects are also observed with long-term exposure to lower pollutant concentrations. Symptoms such as nose and throat irritation, followed by bronchoconstriction and dyspnoea, especially in asthmatic individuals, are usually experienced after exposure to increased levels of sulphur dioxide (Balmes et al., 1987), nitrogen oxides (Kagawa, 1985), and certain heavy metals such as arsenic, nickel or vanadium. In addition particulate matter that penetrates the alveolar epithelium (Ghio and Huang, 2004) and ozone initiate lung inflammation (Uysal and Schapira, 2003). In patients with lung lesions or lung diseases, pollutant-initiated inflammation will worsen their condition. Moreover air pollutants such as nitrogen oxides increase the susceptibility to respiratory infections (Chauhan et al., 1998). Finally chronic exposure to ozone and certain heavy metals reduces lung function (Rastogi et al., 1991; Tager et al., 2005), while the later are also responsible for asthma, emphysema, and even lung cancer (Kuo et al., 2006; Nawrot et al., 2006). Emphysema-like lesions have also been observed in mice exposed to nitrogen dioxide (Wegmann et al., 2005).

4.1.2. Cardiovascular system

Carbon monoxide binds to haemoglobin modifying its conformation and reduces its capacity to transfer oxygen (Badman and Jaffe, 1996). This reduced oxygen availability can affect the function of different organs (and especially high oxygenconsuming organs such as the brain and the heart), resulting in impaired concentration, slow reflexes, and confusion. Apart from lung inflammation, systemic inflammatory changes are induced by particulate matter, affecting equally blood coagulation (Riediker et al., 2004). Air pollution that induces lung irritation and changes in blood clotting can obstruct (cardiac) blood vessels, leading to angina or even to myocardial infraction (Vermylen et al., 2005). Symptoms such as tachycardia, increased blood pressure and anaemia due to an inhibitory effect on haematopoiesis have been observed as a consequence of heavy metal pollution (specifically mercury, nickel and arsenic) (Huang and Ghio, 2006). Finally, epidemiologic studies have linked dioxin exposure to increased mortality caused by ischemic heart disease, while in mice, it was shown that heavy metals can also increase triglyceride levels (Dalton et al., 2001).

4.1.3. Nervous system

The nervous system is mainly affected by heavy metals (lead, mercury and arsenic) and dioxins. Neurotoxicity leading to neuropathies, with symptoms such as memory disturbances, sleep disorders, anger, fatigue, hand tremors, blurred vision, and slurred speech, have been observed after arsenic, lead and mercury exposure (Ewan and Pamphlett, 1996; Ratnaike, 2003). Especially, lead exposure causes injury to the dopamine system, glutamate system, and N-methyl-D-Aspartate (NMDA) receptor complex, which play an important role in memory functions (Lasley and Gilbert, 2000; Lasley et al., 2001). Mercury is also responsible for certain cases of neurological cancer. Dioxins decrease nerve conduction velocity and impaired mental development of children (Thomke et al., 1999; Walkowiak et al., 2001).

4.1.4. Urinary system

Heavy metals can induce kidney damage such as an initial tubular dysfunction evidenced by an increased excretion of low molecular weight proteins, which progresses to decreased glomerular filtration rate (GFR). In addition they increase the risk of stone formation or nephrocalcinosis (Damek-Poprawa and Sawicka-Kapusta, 2003; Jarup, 2003; Loghman-Adham, 1997) and renal cancer (Boffetta et al., 1993; Vamvakas et al., 1993).

4.1.5. Digestive system

Dioxins induce liver cell damage (Kimbrough et al., 1977), as indicated by an increase in levels of certain enzymes in the blood (see following discussion on the underlying cellular mechanisms of action), as well as gastrointestinal and liver cancer (Mandal, 2005).

4.2. Exposure during pregnancy

It is rather important to mention that air pollutants can also affect the developing foetus (Schell et al., 2006). Maternal exposure to heavy metals and especially to lead, increases the risks of spontaneous abortion and reduced fetal growth (preterm delivery, low birth weight). There are also evidences suggesting that parental lead exposure is also responsible for congenital malformations (Bellinger, 2005), and lesions of the developing nervous system, causing important impairment in newborn's motor and cognitive abilities (Garza et al., 2006). Similarly, dioxins were found to be transferred from the mother to the fetus via the placenta. They act as endocrine disruptors and affect growth and development of the central nervous system of the foetus (Wang et al., 2004). In this respect, TCDD is considered as a developmental toxin in all species examined.

...The article then goes on to discuss cellular mechanisms involved in air pollutants and their adverse effects.

Heavy metals induce oxidative stress and inflammatory responses; their toxic effects are to do with their ability to subsititute other metals (such as calcium and magnesium) in the body tissues that are important catalysts and structural elements in the maintenance of proteins. Heavy metals accumulate in sub-cellular organelles (e.g. mitichondria) and interfere with their function. Moreover, metals bind to proteins (Goering, 1993) and inhibit a large number of enzymes, including the mitochondrial ones (Rossi et al., 1993). This also involves the cell nucleus and nucleic acid binding proteins. It has been shown that metals can also bind to DNA, affecting the expression of genes (i.e. mutagenic ~ genetic damage). For example nickel enters the nucleus, interacts with chromatin and silences the expression of genes such as tumor suppressor genes, inducing carcinogenesis (Costa et al., 2003). Finally, some heavy metals exert neurotoxic effects. As far as cancer is concerned, it becomes clear that most pollutants play an important role in the initiation, promotion and progression of cancer cells.

6. Natural protection

In our day-to-day life we are exposed in different kinds of pollutants. Health impacts, as already described above, depend on the pollutant type, its concentration, length of exposure, other coexisting pollutants and individual susceptibility. People living in cities are exposed to a greater extent, as a consequence of increased industrialization and demands for energy and motor vehicles. Occupational exposure is also an important factor that should be taken into consideration. During the last decade, health effects of air pollution are studied more in developed countries, while more and better environmental monitoring data are required in order to setup threshold levels. In addition efforts should be intensified by taking the appropriate measures, in order to reduce the possibility of human pollutant exposure. ...

7. Conclusion

This brief review presents the adverse effects of a number of (air) pollutants in human health. As shown, major impairments of different organs can be observed. The main conclusion drawn is that, in view of increased exposure of humans in a diversity of pollutants, dietary interventions, rich in plant-derived foods, may protect or decrease their effects on different organs. This conclusion is supported by a number of epidemiological studies on the beneficial effect of a Mediterranean- type diet on human health.

Boffin Island comments: "There you go folks, either move to the Med or change your diet to one rich in vegetables, fruits and olive oil - But before you whack down the Vit C, check out Chromium 6: A Killer Compound With An Improbable Trigger (Brown University, Providence RI, USA)."