- Email: [email protected]
Meeting report—Dioxins revisited
Fd Chem. Toxic. Vol. 29, No. 12, pp. 863-864, 1991
Pergamon Press plc. Printed in Great Britain
Information Section MEETING REPORT--DIOXINS The Swedish have been at the forefront of research on dioxins in the environment, and their recent efforts have shown that the contribution of incinerators to dioxin formation is shrinking, while dioxin emissions from steel works and related metallurgical processes have either remained constant or increased to become the main source of environmental contamination compared with the 1970s. The pattern of PCDD and PCDF isomer formation (as shown by gas chromatograph-total ion chromatograms) from steel mills was typical of dioxins formed by combustion sources (including car emissions), and the origins of the chlorine ring substituents are thought to include PVC, cutting oil and inorganic chloride (CaC12). The anthropogenic source of dioxins is now accepted, but Professor Rappe and co-workers are investigating the recently reported in vitro enzymic formation of dioxins (L. G. ~)berg et al., "Biogenic Dioxin Formation", presented at the 9th International Conference on Dioxins and Related Compounds, Toronto, 1989). Chlorophenols in the presence of horseradish peroxidase and H202 at pH7 gave measurable amounts of PCDDs (103-104rig PCDD/g phenol) plus much lower amounts of PCDFs (typically the PCDD/PCDF ratio was 470: 1). The products depended, in part, on the pattern of chlorine substitution in the phenol, but rearrangement, dechlorination and chlorination reactions also contributed to the composition of the final products. There seems to be scope for exploring this enzyme reaction: does it occur in vitro with other sources of peroxidase? Could it account for the environmental formation of dioxins? Turning to another aspect of dioxin analysis, Professor Rappe reviewed the data on UK historical rural soil and herbage samples collected from 1846 to 1986. Dioxins were present in all samples; a base level was found for the 1870-1935 samples followed by a steady increase to 1986, with recent herbage samples containing approximately twice the PCDD/PCDF level of 19th century samples. Statistical analysis (including principal component analysis) revealed the pattern for 1846-1940 was consistent with incineration as the main source of PCDDs and PCDFs. From 1940 to 1970 increased amounts of hepta- and octaCDDs indicated the contribution of environmental pentachlorophenol to dioxin formation. The restriction on the use of pentachlorophenol, introduced in 1970, was discernible from the change in the PCDD/PCDF profile since then. Vegetation responded more quickly than soil to changes in dioxin emissions in the environment. Differences between actual and predicted environmental dioxin levels provided the topic for the fourth *TEQ = 2,3,7,8--TCDD toxic equivalent.
REVISITED
part of Professor Rappe's talk. Analysis of snow samples collected in Sweden showed discrepancies between actual levels of PCDDs and PCDFs and those expected from the deposition of combustion products. Representative snow samples contained 2-10 ng TEQ*/m 3, giving a net deposition of 2250 g TEQ per annum. This compared with an estimated emission from incineration and other sources of 100-200g TEQ per annum (Swedish EPA data). Similarly, calculations based on measured air concentrations of PCDDs and PCDFs (30 fg TEQ/m 3) were l0 times higher than dioxin levels produced by incineration. Professor Rappe suggested various reasons for these differences (overestimation of dioxins in snow samples, lack of reproducibility in collecting representative samples from emission sources, longrange transport of dioxins) but thought (perhaps wishfully?) that enzymic formation might be responsible in part. Diet is the main route for human exposure to dioxins (loc. cit.) and analysis of human milk had shown that exposure to PCDDs and PCDFs is a worldwide problem. Milk samples revealed not only differences in the disposition of dioxins in different countries, but, the isomer profile also gave clues about the origin of PCDDs and PCDFs in human tissue. The highest levels (30 pg TEQ/g milk fat) were found in Belgium, W. Germany (E. German data were not available), Holland and the UK, while the lowest levels (10pg TEQ/g milk fat) were seen in Hungary and Yugoslavia. Middle-range values occurred in the USA, Canada, New Zealand, Japan and Scandinavia. Professor Rappe described the correlation of blood levels of PCDDs and PCDFs with fish consumption in Swedish subjects (B.-G. Svensson et al., New England Journal of Medicine 1991, 324, 8). In particular there was a strong correlation between plasma levels of pentaCDFs and serum n-3 polyunsaturated fatty acid concentration (a marker of fish consumption). PentaCDFs, and especially 2,3,4,7,8pentaCDF, possibly arising from PCB manufacture, are the most prevalent dioxin congeners found in herring and salmon samples from the Baltic, where the high-intake group for this study obtained their fish. Fish was not, however, implicated in the relatively high amounts of octaCDD found in Japanese human milk. Fish is a staple part of the Japanese diet, but contains low levels of OCDD compared with other PCDDs and PCDFs, and dermal exposure has been suggested as an alternative route of exposure. PentaCDD, thought to be a marker of dioxins formed during incineration, occurred in the highest concentrations in human milk samples from
863
864
Information section--Fd Chem. Toxic. Vol. 29, No. 12
Germany, Sweden and Japan, while tetraCDDs were found in samples from Birmingham, UK and New Zealand. Professor Rappe postulated that the presence of these dioxins in New Zealand breast milk
indicated the relatively late (1988) legislative control on the use of the herbicide 2,4,5-T in that country. [Rupert Purchase--BIBRA]
INDOOR AIR POLLUTION The House of Commons Environment Committee has concluded that firm facts on indoor air quality are elusive, and responsibility for its control is fragmented among a large number of Government departments. Yet people spend on average 90% of their time indoors, and exposure to pollutants within buildings may therefore have a greater impact on health than exposure from any other source. -To improve the situation the Committee makes some 29 recommendations, both general and targeted on specific problems such as sick building syndrome, environmental tobacco smoke and radon. The Government should clarify and simplify existing responsibilities for indoor air quality, and should commission a review of present policies on matters such as building design and construction, maintenance, leakage and ventilation rates. Guidelines and codes of practice should be developed that set exposure limits for pollutants based on possible total exposure (ambient, home and workplace). Statistics on indoor air quality should be collectedand published, to provide a sound basis for future policy development. The costs of environmentally-triggered asthma and other allergies, and the numbers of people who might be affected by these disorders, should be assessed. Emission characteristics and indoor pollution should be included, where relevant, among the criteria whereby
applications for award of an eco-label are to be judged. Research on sick building syndrome should be given increased priority, and a best practice guide on the operation of buildings should be produced. A self-financing inspection system, initially for commercial buildings, should be established. The building regulations should be amended to ensure that designers pay greater attention to indoor air quality, and to require the use of building materials and surface finishes with the lowest pollutant emission properties. The Government should accelerate the promised guidance on segregation of smokers and non-smokers and the right to smoke-free air, and this should be integrated with other guidance given under health and safety at work and building regulations. The rate of progress in identifying homes affected by radon should be greatly accelerated, as should the production of advice on radon-proofing. Those who are exposed to high radon levels at work should be advised to have surveys at home. [Indoor Pollution. Volume I. Report, together with the Proceedings of the Committee relating to the Report. House of Commons Session 1990-91. Environment Committee Sixth Report. 61-I. HMSO, London 1991, pp. xliv. £9.80.] The minutes of evidence and appendices are published separately as Volume II (61-II, pp. viii + 430. £35.00).
Pergamon Press plc. Printed in Great Britain
Information Section MEETING REPORT--DIOXINS The Swedish have been at the forefront of research on dioxins in the environment, and their recent efforts have shown that the contribution of incinerators to dioxin formation is shrinking, while dioxin emissions from steel works and related metallurgical processes have either remained constant or increased to become the main source of environmental contamination compared with the 1970s. The pattern of PCDD and PCDF isomer formation (as shown by gas chromatograph-total ion chromatograms) from steel mills was typical of dioxins formed by combustion sources (including car emissions), and the origins of the chlorine ring substituents are thought to include PVC, cutting oil and inorganic chloride (CaC12). The anthropogenic source of dioxins is now accepted, but Professor Rappe and co-workers are investigating the recently reported in vitro enzymic formation of dioxins (L. G. ~)berg et al., "Biogenic Dioxin Formation", presented at the 9th International Conference on Dioxins and Related Compounds, Toronto, 1989). Chlorophenols in the presence of horseradish peroxidase and H202 at pH7 gave measurable amounts of PCDDs (103-104rig PCDD/g phenol) plus much lower amounts of PCDFs (typically the PCDD/PCDF ratio was 470: 1). The products depended, in part, on the pattern of chlorine substitution in the phenol, but rearrangement, dechlorination and chlorination reactions also contributed to the composition of the final products. There seems to be scope for exploring this enzyme reaction: does it occur in vitro with other sources of peroxidase? Could it account for the environmental formation of dioxins? Turning to another aspect of dioxin analysis, Professor Rappe reviewed the data on UK historical rural soil and herbage samples collected from 1846 to 1986. Dioxins were present in all samples; a base level was found for the 1870-1935 samples followed by a steady increase to 1986, with recent herbage samples containing approximately twice the PCDD/PCDF level of 19th century samples. Statistical analysis (including principal component analysis) revealed the pattern for 1846-1940 was consistent with incineration as the main source of PCDDs and PCDFs. From 1940 to 1970 increased amounts of hepta- and octaCDDs indicated the contribution of environmental pentachlorophenol to dioxin formation. The restriction on the use of pentachlorophenol, introduced in 1970, was discernible from the change in the PCDD/PCDF profile since then. Vegetation responded more quickly than soil to changes in dioxin emissions in the environment. Differences between actual and predicted environmental dioxin levels provided the topic for the fourth *TEQ = 2,3,7,8--TCDD toxic equivalent.
REVISITED
part of Professor Rappe's talk. Analysis of snow samples collected in Sweden showed discrepancies between actual levels of PCDDs and PCDFs and those expected from the deposition of combustion products. Representative snow samples contained 2-10 ng TEQ*/m 3, giving a net deposition of 2250 g TEQ per annum. This compared with an estimated emission from incineration and other sources of 100-200g TEQ per annum (Swedish EPA data). Similarly, calculations based on measured air concentrations of PCDDs and PCDFs (30 fg TEQ/m 3) were l0 times higher than dioxin levels produced by incineration. Professor Rappe suggested various reasons for these differences (overestimation of dioxins in snow samples, lack of reproducibility in collecting representative samples from emission sources, longrange transport of dioxins) but thought (perhaps wishfully?) that enzymic formation might be responsible in part. Diet is the main route for human exposure to dioxins (loc. cit.) and analysis of human milk had shown that exposure to PCDDs and PCDFs is a worldwide problem. Milk samples revealed not only differences in the disposition of dioxins in different countries, but, the isomer profile also gave clues about the origin of PCDDs and PCDFs in human tissue. The highest levels (30 pg TEQ/g milk fat) were found in Belgium, W. Germany (E. German data were not available), Holland and the UK, while the lowest levels (10pg TEQ/g milk fat) were seen in Hungary and Yugoslavia. Middle-range values occurred in the USA, Canada, New Zealand, Japan and Scandinavia. Professor Rappe described the correlation of blood levels of PCDDs and PCDFs with fish consumption in Swedish subjects (B.-G. Svensson et al., New England Journal of Medicine 1991, 324, 8). In particular there was a strong correlation between plasma levels of pentaCDFs and serum n-3 polyunsaturated fatty acid concentration (a marker of fish consumption). PentaCDFs, and especially 2,3,4,7,8pentaCDF, possibly arising from PCB manufacture, are the most prevalent dioxin congeners found in herring and salmon samples from the Baltic, where the high-intake group for this study obtained their fish. Fish was not, however, implicated in the relatively high amounts of octaCDD found in Japanese human milk. Fish is a staple part of the Japanese diet, but contains low levels of OCDD compared with other PCDDs and PCDFs, and dermal exposure has been suggested as an alternative route of exposure. PentaCDD, thought to be a marker of dioxins formed during incineration, occurred in the highest concentrations in human milk samples from
863
864
Information section--Fd Chem. Toxic. Vol. 29, No. 12
Germany, Sweden and Japan, while tetraCDDs were found in samples from Birmingham, UK and New Zealand. Professor Rappe postulated that the presence of these dioxins in New Zealand breast milk
indicated the relatively late (1988) legislative control on the use of the herbicide 2,4,5-T in that country. [Rupert Purchase--BIBRA]
INDOOR AIR POLLUTION The House of Commons Environment Committee has concluded that firm facts on indoor air quality are elusive, and responsibility for its control is fragmented among a large number of Government departments. Yet people spend on average 90% of their time indoors, and exposure to pollutants within buildings may therefore have a greater impact on health than exposure from any other source. -To improve the situation the Committee makes some 29 recommendations, both general and targeted on specific problems such as sick building syndrome, environmental tobacco smoke and radon. The Government should clarify and simplify existing responsibilities for indoor air quality, and should commission a review of present policies on matters such as building design and construction, maintenance, leakage and ventilation rates. Guidelines and codes of practice should be developed that set exposure limits for pollutants based on possible total exposure (ambient, home and workplace). Statistics on indoor air quality should be collectedand published, to provide a sound basis for future policy development. The costs of environmentally-triggered asthma and other allergies, and the numbers of people who might be affected by these disorders, should be assessed. Emission characteristics and indoor pollution should be included, where relevant, among the criteria whereby
applications for award of an eco-label are to be judged. Research on sick building syndrome should be given increased priority, and a best practice guide on the operation of buildings should be produced. A self-financing inspection system, initially for commercial buildings, should be established. The building regulations should be amended to ensure that designers pay greater attention to indoor air quality, and to require the use of building materials and surface finishes with the lowest pollutant emission properties. The Government should accelerate the promised guidance on segregation of smokers and non-smokers and the right to smoke-free air, and this should be integrated with other guidance given under health and safety at work and building regulations. The rate of progress in identifying homes affected by radon should be greatly accelerated, as should the production of advice on radon-proofing. Those who are exposed to high radon levels at work should be advised to have surveys at home. [Indoor Pollution. Volume I. Report, together with the Proceedings of the Committee relating to the Report. House of Commons Session 1990-91. Environment Committee Sixth Report. 61-I. HMSO, London 1991, pp. xliv. £9.80.] The minutes of evidence and appendices are published separately as Volume II (61-II, pp. viii + 430. £35.00).