01 August 2008

SCIENCE: Human health effects of air pollution

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)."

2 comments:

Jeremy dePots said...

Examination of Emission Testing Data for Dioxins
from A Steel Works at Haulbowline , County Cork

R.P. Finegan 1 June 1998

Examination of Emission Testing Data for Dioxins
from A Steel Works at Haulbowline , County Cork

R.P. Finegan 1 June 1998

A brief report prepared on behalf of Cork Environmental Alliance
Emission tests carried out by ENTEC on the furnace exhaust of Irish Ispat (formerly Irish Steel) steel works at Haulbowline , County Cork , showed that the presence of polychlorinated dibenzodioxins ( PCDD ) and polychlorinated dibenzofurans ( PCDF ) at levels which showed a substantial increase from 1992 to 1997 . The available data is shown in table 1 below :

Table 1. Particulate Matter , PCDD Levels and PCDF Levels
in Furnace Exhaust Emissions

Parameter Year Levels

Particulates mg/Nm3 Run 1 Run 2 Run 3
Particulate Gaseous Total
PCDD ng/Nm3 1992 0.06 0.01 0.07
1997 0.3639 0.3333 0.6972
PCDF ng/Nm3 1992 0.51 0.1 0.61
1997 0.9433 1.5813 2.5246
PCDD + PCDF ng/Nm3 1992 0.57 0.11 0.68
1997 1.3072 1.9146 3.2218
Lacking from the available data are figures for the volume of emissions , so that the actual amounts of polychlorinated dibenzodioxins and furans emitted from the furans emitted from the furnace cannot be calculated . Also lacking is information concerning the composition of the PCDD and PCDF fractions , important in estimating the toxic qualities of the emissions . Thus it is desirable to know the concentrations of 2, 3, 7, 8-tetrachlorinated dibenzodioxin ( 2378-TCDD ) , the most toxic of these compounds , and to translate the emissions into TCDD equivalents . Nevertheless , inferences can be drawn from the measurements , the most important of which is that these important environmental contaminants are present in significant amounts in the emissions , seemingly at levels which have increased since 1992 . This is illustrated by the ratios derived from the data , shown in Table 2.

Table 2. Ratios Derived from Furnace Emission Data
Ratio Type Parameter Year
1992 1997 1992:1997
PCDF:PCDD particulate 8.50:1 2.59:1 3.28:1
gas 10.0:1 4.74:1 2.11:1
total 8.71:1 3.62:1 2.41:1
Inference : The proportion of PCDF has decreased since 1992 and
the proportion of PCDD has increased .

Part. : Gas PCDD 6.00:1 1.11:1 5.41:1
PCDF 5.10:1 0.60:1 8.50:1
total 5.18:1 0.68:1 7.51:1
Inference : The proportion of dioxins to furans in particulates has
decreased since 1992 , and the proportion in gas has
correspondingly increased .

It can be seen from these tables that there has been a large increase in measured concentrations of PCDD and PCDF between 1992 and 1997 . The percentage increase in total PCDD concentrations is 996% , and the percentage increase in total PCDF concentrations is 414% . An explanation may be sought for this in the possibility that more sensitive analytical techniques were employed in 1997 than in 1992 . That is something that can be determined by further enquiry . However , that would not explain the shift to the relatively higher concentrations in the gaseous phase , or the increased amounts of PCDD relative to PCDF . In general PCDDs are more toxic than PCDFs so that the change is in an unfavourable direction . Moreover , the shift to higher concentrations in the gaseous phase has serious implications for cleanup procedures . The ENTEC view was expressed in these terms :
‘The results for the Dioxins and Furans show that a high proportion of emissions are in the particulate phase . Sampling was carried out upstream of the bag filtration system . The bag filter will abate most of the dioxins in the particulate phase thereby reducing the emissions .’

For 1997 the figures show that the combined dioxin an furan concentration in the particulate phase was 1.3072 ng/Nm3 compared with 1.9146 ng/Nm3 in the gaseous phase , or 40.6% . If all of this was removed by bag filters the conclusion is that the remaining 59.4% in the gaseous phase escaped to the atmosphere .

Discussion

The emission figures for PCDDs and PCDFs raise a number of questions concerning the cause of the increase between 1992 and 1997 , and the corresponding effects on the surrounding area , and the welfare of its animal and human inhabitants . Those questions include :
* Has there been a change in the volume of emissions as well as an increase in the
concentrations of dioxins and furans ?
* Has there been a change in the furnace design or functioning ?

* Has there been an increase in the input , or change in the nature of raw or recycled materials , and the corresponding output of steel ?

* Has there been a change in the type or quality of steel produced ?

* Has there been a change in measuring technology or analytical procedures ?

* Has there been a change in fuels used in stoking the furnace ?

* Has there been a change in the filtering or scrubbing systems ?

* Has there been any change in worker health ?

Answers to questions such as these need to be determined with some urgency , on account of the potential danger to human health and the contamination of food resources.

An important factor relating to the increased emissions is the effect of bioaccumulation in concentrating PCDDs and PCDFs in the living components of the ecosystem (4,p.B11), including human tissues ( 11 ) . The eventual fallout of atmospheric emissions onto land or water , and the subsequent attachment of contained PCDDs and PCDFs to soils or sediments in the terrestrial and aquatic environments provides a toxic reservoir from which the contaminants pose a continuing threat to the well being of human society in the vicinity . The danger of these particular types of contaminant is well indicated by the disastrous consequences which have resulted from their escape to the environment even in relatively tiny amounts . That includes not only damage to human health , of which there are abundant examples ( 6,9,11 ) , but also economic consequences affecting the industrial sources . Thus in 1963 an explosion at the Philips Duphar 245-T herbicide factory in the Netherlands resulted in the release of an estimated 30 to 200 grams ( 1 to 7 ounces ) of TCDD . The factory was sealed off for 10 years then dismantled , embedded in concrete , and dumped into a deep part of the Atlantic ocean ( 6.p.54 ) . This is testimony to the precautions that are needed to mitigate the extreme toxic hazard represented by 2378-TCDD and related compounds . That being the case it is only sensible to view a 996% increase in PCDD emissions from the steel works alarm , inasmuch as it may represent an unacceptable health risk to the inhabitants of the surrounding area . To bring this into focus it must be remembered that dioxins and furans are persistent in the environment ( 3 ) , so that each year’s increment is added to an only slightly diminished burdan in soils and sediments derived from previous fallout . It was claimed by Professor Rappe that the levels previously measured in soils in the Cork area had arrived by long range transport from emissions elsewhere ( 1 ) . That is a matter beyond the power of local authorities to remedy , but the present findings in the ENTEC report dispel any idea that there is not also a local problem , made worse by the fact that the local emissions will be additive from fallout elsewhere .

It may be maintained that the actual amounts emitted are still very small , that the concentrations achieved in foodstuffs or in ambient air fall within guidelines established by the World Health Organisation , or countries with a tolerant attitude to environmental contamination . Some other jurisdictions , such as the United States Environmental Protection Agency which sets the acceptable dioxin intake at 0.006 pg/Kg/day , are less tolerant , and set higher standards (9,p.26 ) . Knowing the concentrations in emissions is important in the sense that it gives a measure of toxic potential , but if the emissions are small and the dilution after emission is great then the actual hazard may be negligible . In the case of a steel works it is unlikely that the amount of emission is small , but that essential piece of data is lacking in the document that has been examined . To gain some idea of the dimension of contamination a calculation can be made based on the modest assumption that the daily volume of emission is 2,000,000 Nm3 , applied to the known mean values for PCDD concentrations .
At 0.3333 ng/Nm3 for the gaseous phase the output would be 0.6666 mg/d or 0.243 grams per year ; and at 0.3639 for the particulate phase the output would be 0.7278 mg/d or 0.265 grams per year . This is , the combined output of PCDDs would be approximately half a gram per year , or a gram in 2 years . If it is borne in mind that an estimated amount of between 30 and 200 grams of dioxins accidentally released in the case of Philips Duphar factory was sufficient for the plant to be sealed off , dismantled , embedded in concrete , and dumped in the ocean , this is a very significant amount .

The gaseous phase escapes filtration and exits to the environment , while the particulate phase may be captured 85% to 99% by the bag-house filtration system so that only 1% to 15% ( 2.65 - 39.75 mg/y ) would be directly emitted to the environment , still significant in view of the extreme toxicity of PCDDs . The question then remaining is the fate of the PCDDs retained by the filters , and that is a subject not dealt with in the ENTEC data that was examined .

The conclusion reached is that the large increase in PCDD and PCDF content of emissions in the steel works furnace exhaust requires explanation ; and because of the toxicity of these products and the implications for public health , that consideration should be given to the setting up of a task force to deal with the matter of PCDD and PCDF contamination of the environment in the area of Cork Harbour .

A short bibliography is included to provide additional information concerning environmental and health effects of dioxins and furans .










Bibliography
1. A Pollution Overview of the Chemical /Pharmaceutical Industry in Cork : Cork Environmental Alliance , April 1994 . 195 pp . Section 9. Dioxin investigation in Ringaskiddy .
p.137-139. Professor Rappe’s Report . Data from two sources of dioxins in the area , Irish Steel and Penn Chemicals , were sent by Cork County Council to Professor Rappe in Sweden .
p.138. Soil samples , from a Sandoz study , contained elevated levels of International Toxic Equivalents ( TEQ ) of dioxin : (a) North of Sandoz 23.7 (b) Ringaskiddy 21.6 (c) East of Shanbally 10.0 . Four other sites had levels from 0.2 to 0.7.
p.144-145. Memo dated 13 May 1992 to Cork County Manager from the Chief Environmental Officer . ‘Analysis of dioxin emissions were carried out on the two local point sources - Penn Chemicals and Irish Steel ‘. The figures cited above are contained in this memo .

2. Dioxins in the Environment : Report of an Interdepartmental Working Group on polychlorinated dibenzo-para-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) : Department of the Environment , Central Directorate of Environmental Protection : Pollution Paper No. 27 . HMSO , London . 1989 .
p.5. Table 2 provides International Toxic Equivalent factors , I-TEF, in which the most toxic , 2378-TCDD equals 1, as shown below :

2378-TCDD 1 2378-TCDF 0.1
12378-PeDD 0.5 23478-PeCDF 0.05
123478-HxCDD 123478-HxCDF
123678-HxCDD 0.1 123789-HxCDF 0.1
123789-HxCDD 123678-HxCDF
234678-HxCDF
1234678-HpCDD 0.01 1234678-HpCDF 0.01
1234789-HpCDF
OCDD 0.001 OCDF 0.001
p.10-11. Metallurgical processes : ‘Work in Sweden has shown that PCDDs and PCDFs are formed at steel mills recycling and smelting scrap iron . In studies of processes recovering metals coated with PVC or other chlorinated plastics , measurable quantities of PCDDs and PCDFs were found on dust released into the workplace and in the flue gas.’ ( C. Rappe is a co-author of a paper ( 1of 3) cited )
p.14. Emissions from a chemical waste incinerator in South Wales ranged from 0.005 to 1.78 ng/m3 , with a mean of 0.69 ng/m3 for total PCDD/PCDF . The mean value for TCDD was 0.06 ng/m3 .
p.77. ‘ In laboratory animals 2378-TCDD affects the immune system and the reproductive system and is a carcinogen .’ See pages 85-102 for Survey of the Immunotoxicity of Polychlorinated Dibenzo-p-Dioxins .

3. David A. Barna and Gary A. Amendola : Michigan Dioxin Studies : Screening Survey of Surface Water Supplies , Potable Ground Water and Dow Chemical Brine Operations : US EPA , Westlake , Ohio.1985 .
p.4. ‘Likely sources ( in brine pond sediments ) of the PCDDs and PCDFs are fallout from atmospheric emissions....’
p.31. Background levels of TCDD occur in blank samples of nearly every laboratory method . The half-life in soils is given as 12 years .

4. The National Dioxin Study : Tiers 3,5,6 and 7 . US EPA : Office of Water Regulations and Standards , Monitoring and Data Support Division . Washington , DC.1987.
p.B-11. Bioaccumulation in animals . Bioconcentration factors in fish are given as 2000 (catfish ) , 6600 (rainbow trout ) , 24,000 ( mosquito Fish ) . Milk samples from dairy farms near the ICMESA plant at Seveso harvested near the contaminated zone . ( The Seveso factory was involved in an accident which released dioxins in 1976 )
Appendix A provides health assessments for TCDD .

5. US EPA / Paper Industry Cooperative Dioxin Screening : NCASI Technical Bulletin No. 545. New York. 1988 .
p.52. Validation experiment results . Concentrations of 0.015 ppt (ng/Kg) were measured. A level of 0.0034 ppt was classified as not detected .

6. Chlorinated Dibenzodioxins : IARC Monographs of the Carcinogenic Risk of Chemicals to Man , Volume 15. IARC, WHO, Lyon . August 1977.
in inducing AHH ( aryl hydrocarbon Hydroxylase ) activity in rat liver .
p.54. In 1963 an explosion at the Philips Duphar 245-T factory in the Netherlands released an estimated 30 to 200 grams of TCDD . The factory was sealed off for 10 years, then dismantled , embedded in concrete , and dumped into a deep part of the Atlantic ocean .
p.76. TCDD increases renal and hepatic glutathione -S transferase .
p.77. TCDD is 30,000 times as potent as 3- methyl cholanthrene in inducing AHH ( aryl hydrocarbon hydroxylase ) activity in rat liver .
p.84 Waste oil as a source of dioxins : In 1971 TCDD was identified in waste oil used for dust control , poisoning animals and humans .
Note that if such oil was used as a fuel it would contribute dioxins to atmospheric emissions .

7. Soil Screening Survey at Four Midwestern Sites : EPA-905 / 4-85-005:
US EPA Region 5 , Chicago , Illinois . 1985.
Attachment 2. Chlorinated Dioxins Workgroup Position Document , March 16 1985 . Risk Assessment for Mixtures of Chlorinated Dioxins and - dibenzofurans (CDDs and CDFs ) ;Draft .
This document explains methods for generating TCDD equivalents . Table 1 on page 20 of the attachment shows the potencies of dioxins relative to 2378-TCDD . Table II on page 21 shows CDD/CDF isomers of most toxic concern , using TEF = toxic equivalency factor . The figures provided differ to some extent from the I - TEF figures shown above .

8. Gary A. Amendola and David A. Barna : Dow Chemical Wastewater Characterization Study : Tittabawassee River Sediments and Native Fish : United States Environmental Protection Agency . 1986. The annual release of approximately 1/80 oz =0.36 grams of 2378-TCDD contaminated sediment in the Tittabawassee River (Michigan) for a distance of 19,5 miles =32.5 km below the point of discharge , and contaminated fish to the extent that a single meal of 9oz =255 grams constituted a significant cancer risk .

9. Lois Mary Gibbs , CCHW et al .: Dying From Dioxin : Southend Press , Boston , MA. 1995.
p.26. Table 1.1 provides the following ‘acceptable’ dioxin intakes in pg/kg/day : USEPA 0.006 ; California 0.007 ; Centers for Disease Control 0.03 ; US Food and Drug Administration 0.06; National Research Council of Canada 0.07 ; Germany 1-10 ; Netherlands 4; Canada and Ontario 10 ; World Health Organisation 10 ; Washington State 20-80 .
p.30-31 . ‘ Much of the research that came out of the e1991 Symposium on Dioxin supported the findings of the EPA’s original 1985 health assessment and provided the basis for the current reassessment report :
1. Dioxin -related health problems other than cancer -causing effects of dioxin .
2. The EPA’s conclusion that dioxin causes cancer in people was reaffirmed and strengthened by the data . The EPA estimated that at current exposure levels , the dioxin related cancer risk is between 1 in 1,000 and 1 in 10,000 . This risk is 100 to 1000 times higher than the generally ‘acceptable ‘ risk level of one in a million . This risk estimate makes dioxin the most important cancer causing chemical for the general population .
3. Dioxin accumulates in biological tissues , and the average level of dioxin in our bodies is at or just below levels that cause some adverse health effects .
4. The major route of human exposure is through the ingestion of a wide variety of common foods containing small amounts of dioxin . Dioxin has been found in very high levels in human breast milk , the top of the food chain .
5. Some health effects of dioxin ( suppression of the immune system ; reduced testosterone levels , which affects fertility ; and reduced glucose tolerance , which increases the risk of diabetes ) were found to occur ‘at or near levels to which people in the general population are exposed .’
6. The principle sources of dioxin in the environment are combustion and incineration , chemical manufacturing , pulp and paper mills , metal refining and smelting , and ‘reservoir’ sources .(dioxin - contaminated soils and sediments ) (USEPA, 1994) .

10. Fact Sheet on the State of the Marine Environment of the St. Lawrence : Contamination of Baie des Anglais : Fisheries & Oceans Canada , Ottawa . April 1997 .
p.4 Table 1. This table shows mean levels of dioxins and furans in surface sediments at Baie des Anglais in the Lower St. Lawrence Estuary and in the Gulf of St. Lawrence , measured in 1995. Figures are also provided for Baie des Anglais whelks . The units are in 2378-TCDD toxic equivalents (TEQ) expressed as ng/g (ppt) . The estuarine location can be compared with Haulbowline in the Lee Estuary .
Dioxins ng/g Furans ng/g
Gulf of St. Lawrence Sediments 209 87 (dry wt.)
Baie des Anglais Sediments 92 338 (dry wt.)
Whelks 1.8 (wet wt.)
p.6 Research has detected anomalies in the reproductive and immune systems of American plaice Hippoglossoides platessoides exposed to contaminated sediments from this location . High levels of PCB and PAH were also present in Baie des Anglais sediments .

11. Kay Teshcke , Shona J. Kelly , Michelle Wiens , Clyde Hertzman , Helen D. Ward , John E.H.Ward & Jay C.Van Oostam : Chlorinated Dibenzo-p-dioxins and Dibenzofurans in the Adipose Tissue of British Columbia Residents : Ministry of Environment , Lands & Parks ; Industrial Waste & Hazardous Contaminants Branch , Victoria , B.C..March 1992.
p.16. Table 9. Summary of statistics for dioxin and furan concentrations ( pg/g in lipid ) in B.C. residents :
Min. Max Mean Median
2378-TCDD 1.8 9.2 4.2 3.8
Int. TEQ 8.4 56.4 29.1 28.1
p.26. ‘In conclusion , dioxin and furan levels in this sample of the British Columbia populations not known to have been exposed , with a similar congener profile . Populations from agricultural economies such as Vietnam tend to have lower levels . Populations with known exposures appear to have higher adipose concentrations , especially of 2378-T4CDD. Of the population characteristics measured in the B.C. study group , age showed the most consistent effect . PCDD/PCDF concentrations increased with increasing age .....
Note : Tables 10 and 11 compared B.C. residents with other Canadian residents , American veterans not exposed to herbicides , North Vietnamese not exposed to herbicides , German workers exposed to a trichlorophenol plant release in 1953, and American and south Vietnamese and lower than for other groups . The position of Cork residents in relation to these groups would be of interest .

















Mr Liam Cashman
European Commission
Directorate General for Environment, Nuclear Safety and Civil Protection
Rue de la Loi 200
B-1049 Brussels
Belgium

30th November, 1998


Complaint re failure of the Irish State, its Central and Local Government Agencies to enforce EU Air Emission Standards for dioxins as specified in Council Directive 94/67/EC (Article 7.2) and lead emissions as specified in Council Directive 82/884/EEC.


Dear Sir,

Cork Environmental Alliance Ltd wish to bring to your attention the failure of the Irish State and its Competent Authorities to regulate emissions from the Irish Ispat steel smelting/sintering facility at Haulbowline Island, Cork Harbour, Co Cork in accordance with the EU Directives outlined above.

We would respectfully request the Commission to initiate an investigation into the current situation regarding the unregulated emissions, and the associated contamination of air, soil and surface waters, from Irish Ispat and direct the Irish State to comply with the requirements of the relevant Commission Directives.

For purposes of clarity this complaint comprises of two parts. The first, dealing with breaches of EU Standards for emissions of dioxins to the atmosphere. The second outlines breaches of EU Standards for emissions of lead to the atmosphere.





Part 1 - Dioxin Emissions to Atmosphere


Background


1

Breaches of Pollution Control Regulations Governing Atmospheric Emissions
of dioxins from the Irish Ispat facility and related issues.


1.1 Atmospheric emissions from the Irish Ispat facility are controlled under planning
condition (1907/77), issued by Cork County Council, the Competent Authority
under present Irish legislation. No emission monitoring has been conducted by the
Competent Authority to date....

“....as there are no licensed vents/emission points”.

(Appendix A, letter from Cork County Council, 13th May, `98)

1.2 Recent independent monitoring for dioxin emissions, commissioned by Irish Ispat,
indicate that dioxin emissions from the facility are considerably in excess of the
0.1ng/M3 specified at Article 7.2 of Council Directive 94/67/EC. (see Appendix B,
Entec Report No D/98009)

1.3 Cork Environmental Alliance Ltd commissioned the Conservation Advisory Service
of Vancouver, British Colombia, Canada to prepare a brief overview of the Entec
(consultants to Irish Ispat) Report in May, 1998. This Review is attached for your
information as Appendix C.

1.4 While Council Directive 94/67/EC is primarily intended to limit emissions from
hazardous waste incineration plants it is the opinion of Cork Environmental
Alliance Ltd that the Irish Ispat facility falls within the provisions of Article 3.3 of
the Directive for the following reasons.




i ) The raw materials utilised by Irish Ispat consist entirely of `scrap metal`. This is
smelted using an electric arc furnace. Consequently it is not possible that the
smelter fuel (i.e. the electricity supplied by the Irish Electricity Supply Board )
would give rise to dioxins in stack emissions at the Haulbowline site. It therefore
follows that hazardous dioxin precursors, as listed in Annex 1 &11 of EU Directive
91/689/EEC, are present in the raw materials processed at the Irish Ispat site.

ii) Much of the scrap raw materials utilised by Irish Ispat is supplied by a local scrap
metal supplier, Hammond Lane Ltd. The ferrous and non-ferrous waste material is
separated by a magnetic separation process at the Hammond Lane plant at
Ringaskiddy, Cork Harbour. Further supplies of scrap raw material is sourced both
within and outside the Irish State. It has not been possible for Cork Environmental
Alliance Ltd to establish with any degree of accuracy the quantity of the non
-ferrous and potentially hazardous nature of the raw material fed to the arc furnace.

iii) Because of the dearth of information regarding emissions, raw material composition
etc. at the Irish Ispat facility it has proved impossible to establish whether the
resulting heat release is higher than the 40% inclusive of the total heat released in
the plant in accordance with Article 3.3 of 94/67/EC. We would ask the
Commission to direct the Irish Authorities to establish the actual position.

1.5 Efforts by Cork Environmental Alliance Ltd to obtain a rational explanation as to
why Irish Ispat is not required to apply for an Integrated Pollution Control licence
under the EPA Act 1992 have had limited success. In June 1996 the Environmental
Protection Agency stated that.........

“The activities of Irish Steel (former name of Irish Ispat) are listed in the first
schedule of the EPA Act under Class 3. Under the terms of an order issued by
the Minister, new activities after April 3rd, 1995 in their class require an IPC
licence before commencing production. Irish Steel as an existing activity will
be licensed under the terms of a new order yet to be issued. The prescribed date
for existing activities in their class is set at the discretion of the Minister.”

(Correspondence, Appendix D)

Furthermore, the Environmental Protection Agency have intimated in their letter
of the 24th April, `98 (Appendix D) that they were not aware of the high levels of
dioxin in emissions from the Irish Ispat facility and consequently did not
recommend that the Minister issue an order under the EPA Act with a view to
including Irish Ispat, as an existing activity, under the IPC licensing system.




Had the EPA advised the Minister and had the Minister signed the commencement
order requiring Irish Ispat, as an existing activity under the first schedule, Class 3,
the emissions from Irish Ispat would then have been subject to the terms of the
Integrated Pollution Control licensing system under the terms of the EPA Act.

The standard emission limit value adopted by the EPA in all IPC licenses issued to
date by the Agency has been 0.1nG/M3, i.e. the standard stipulated in EU
Directive 94/67/EC.

1.6 The failure of the EPA to inform the Minister, based on their contention that they
were unaware of the situation vis a vis dioxin emissions from Irish Ispat, is
untenable in light of the facts.

1.7 Prior to the establishment of the Environmental Protection Agency in 1993, Mr.
Iain McLean, now a Director with the Agency, was employed as its Chief
Environmental Officer with Cork County Council. Mr. Kieran O`Brien, now
Regional Inspector with the EPA, was employed by Cork County Council as
Assistant Environmental Officer.

1.8 In 1991 Mr. McClean, assisted by Mr. O`Brien, coordinated an investigation into
the discovery of relatively high levels of contamination of soil with dioxins in
close proximity to the Irish Ispat site at Ringaskiddy in Cork Harbour.

(Appendix E, Dioxin Survey, 1991)

1.9 Mr. McLean was instrumental in commissioning Professor Christopher Rappe of
Umea University, Sweden, (an acknowledged expert in the study of dioxins) to
examine possible dioxin sources in the Cork Harbour area.

1.10 Prof Rappe, in a letter dated December 12th 1991, (Appendix F) to Mr. McLean,
stated that..........

“In my opinion the most important potential source (of dioxins) in this region
might be the steel mill at Cobh (Irish Ispat)............”

Further comments of Professor Rappe are included as Appendix G.







1.11 In a letter dated 13th April, 1992 to the Carrigaloe Environmental Group, a
constituent member of the Cork Environmental Alliance, Mr. McLean suggested
that ..........

“All the indications are that these dioxins have arisen as a result of long range
transportant and deposition. There are absolutely no indications of any
localised point sources.”

On February 27th, 1992, Mr. McLean wrote to Friends of Cork Harbour,
Another constituent group of Cork Environmental Alliance, the contents of
which are quoted in full below.......

“The Council do not believe that there is a problem with dioxins in Cork
Harbour (Appendix H)

During this period public access to relevant Cork County Council documents
was at the sole discretion of the County Council. Efforts to secure copies of the
dioxin survey results and Prof Rappe`s investigation were denied by Council
officials. Therefore Mr. McLean`s version of Prof Rappe`s assessment was the
only information available to members of the public.

1.12 However, following the implementation of Directive 90/313 EC - Freedom of
Access to Information on the Environment, in May 1993, Cork Environmental
Alliance Ltd succeeded in securing discovery of documents relating to the Dioxin
studies in Cork Harbour during 1991/`92.

One such document, an internal memorandum dated 13th, May 1992, between
Mr.Kieran O`Brien and the Acting County Manager, makes it quite clear that the
situation regarding dioxin sources in Cork Harbour, as outlined in Mr. McLean`s
letter quoted above was a deliberate attempt to mislead the public. This
memorandum refers specifically to Mr. McLean`s letter of the 13th April, 1992
to the Carrigaloe Environmental Group and concludes by stating that..........

“This (Mr. McLean`s letter) in no way addressed the high levels at locations
5, 6 and 7 ..........I feel that until these chromatograms are evaluated, any
statement on dioxins in the harbour area would be unwise.”

(Appendix I)




Conclusion.

1.13 It is clear that significant levels of dioxins are being emitted from the Irish Ispat
facility at Haulbowline Island, Cork Harbour.

1.14 Significant and unexplained dioxin contamination of soil has occurred in the
vicinity of Irish Ispat in Cork Harbour.

1.15 Such dioxin emissions are considerably in excess of the limits laid down in
Directive 94/67/EC.

1.16 The competent Authority/ies, Cork County Council and/or the Environmental
Protection Agency have failed to take action to enforce the EU atmospheric
emission standard of 0.1nG/M3 for dioxins - see Appendix A, letter from Cork
County Council to Cork Environmental Alliance Ltd, 13th May,1998, last
paragraph......

“To the best of our knowledge a Notice under Section 26 of the Air Pollution
Act, 1987 was not served by Cork County Council on Irish Steel/Ispat in the
last 10 years.”

1.17 The Environmental Protection Agency was derelict in its duty to inform the
Minister that such breaches of EU Standards were/are occurring.

1.18 Ireland, through the present Minister for the Environment Mr. Noel Dempsey,
TD and his predecessors continues to be in breach of EU Directive 94/67/EC in
permitting such exceedances of the 0.1nG/M3 standard outlined in the above
quoted EU Directive continue.

1.19 There has been a deliberate policy of obfuscation carried out by the Competent
Authorities and their officers which has resulted in confusion surrounding the
true dioxin situation pertaining in Cork Harbour since the discovery of significant
dioxin contamination of agricultural land in1991.












Part 2 - Lead Emissions to Atmosphere

Background

2. Breaches of Pollution Control Standards Governing Atmospheric Emissions
of Lead from the Irish Ispat Facility at Cork Harbour.

2.1 The Competent Authority are those as defined within the Statutory Instrument
and EU Directive 82/884/EEC. ie, Cork County Council and/or the
Environmental Protection Agency.

2.2 The air quality standard for lead is that specified in EU Directive 82/884/EEC,
i.e., 2u G/M3 (Mean of daily values measured during a period beginning on
January 1st to the following December 31st, as outlined in the Air Pollution Act
1987 - Air Quality Standards - Regulations, 1987)

(Appendix J)


2.3 Forbairt, the Irish State`s scientific advisory agency, was requested to carry out
an atmospheric monitoring programme between 28/12/`95 and 26/12/`97 in order
to establish ground level concentrations of lead in ambient air at the Irish Ispat
site. Weekly average lead concentrations for the period 28/12/`95 - 2/1/`07
show an annual mean reading of 3.6u G/M3. However this annual mean result
does not take cognizance of the requirement for daily monitoring nor the 9
weeks for which no monitored results were declared. This report is included with
other related reports as Appendix K.


Conclusion


2.4 The limited data collated by the Competent Authority would suggest that
emissions of lead in excess of the standards laid down in EU Directive
82/884/EEC are occurring regularly at the Irish Ispat site.




2.5 Efforts to date by the Competent Authority to correct this situation have been
ineffective.

2.6 The competent Authority/ies, Cork County Council and/or the Environmental
Protection Agency have failed to take action to enforce the EU atmospheric
emission standard of 2uG/M3 for lead - see Appendix A, letter from Cork
County Council to Cork Environmental Alliance Ltd, 13th May,1998, last
paragraph......

“To the best of our knowledge a Notice under Section 26 of the Air Pollution
Act, 1987 was not served by Cork County Council on Irish Steel/Ispat in the
last 10 years.”

2.7 The Environmental Protection Agency was derelict in its duty to inform the
Minister that such breaches of EU Standards were/are occurring.

2.8 Ireland, through the present Minister for the Environment Mr. Noel Dempsey, TD
and his predecessors continues to be in breach of EU Directive 94/67/EC in
permitting such exceedances of the 2uG/M3 standard outlined in the above
quoted EU Directive continue.


Should you require further information or clarification on any of the issues raised in this complaint please do not hesitate to contact me.


Yours sincerely,






____________________
Derry Chambers
(on behalf of CEA Ltd)

Jeremy dePots said...

Hello,

Came across your site by accident and was pleasantly surprised to see that someone is concerned (rather than the normal posturing) about the goings at at the former steel plant. You may be aware that several hundred tonnes of radioactive waste (ceasium 137) was stored on Rocky Island under license from the Radiological Protection Institute of Ireland from 1990 onwards. In June '95 this waste was found spilled alongside the public roadway at the entrance to what is now the crematorium. Though this was in blatant breach of the licence conditions, as usual, no one was prosecuted. I have had no success in tracking down the final resting place of this material. The Examiner covered the issue extensively in the summer of '95 but their online archives don't stretch that far back.

There was also significant dioxin emissions from the site (and one could assume that the waste at the slag heap is contaminated with same) throughout the 1990s at least. The authorities refused to take any action to curtail these emissions. Dioxin has been described as the most toxic substance known and has a half life of between 7 and 20 years. Once metabolised by living tissue it remains for life. Human beings have simply no way of ridding themselves of it once they are contaminated unless they get pregnant, then it's removed via the newborn infant.

The attached may be of interest. The site is excellent,

Keep up the good work,