Studies of pollution from incinerators and power stations have generally focused on acid gases, particulates and dioxins. Polyaromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) have generally been ignored, even though PCBs may be formed in combustion processes by the same mechanisms that produce dioxins.
The study, conducted by specialist consultants and Agency staff, set out to shed light on whether emissions may be significant. A literature survey showed that municipal incinerators had been found to produce between 0.01 and 5ng/m3 of PCBs, measured as a toxic equivalent (TEQ) of the most potent dioxin, 2,3,7,8-TCDD. This compares with an EU standard of 0.1ng TEQ/m3 for dioxin emissions.
Results are difficult to compare and interpret because of international variations in both measurement protocols and incineration technologies. However, the authors note that where dioxin emissions were also measured, PCB levels were generally only 5-10% of these, even in modern plant capable of meeting the new EU dioxin limits.
The researchers went on to make PCB measurements at two municipal incinerators, a medical waste incinerator, a sewage sludge incinerator and a power station. In half of the tests, PCBs were below the detection limits of around 0.012-0.018ng TEQ/m3.
Where PCBs were detected, levels were a little higher, up to 0.022ng TEQ/m3, but always well below dioxin levels where these were measured.
The study recommends further studies to characterise PCB emissions from incineration processes - noting evidence that PCB levels in foods like meat, oils and dairy products actually increased between 1992 and 1997. UK diet studies show that PCB exposure did not decline over this period, despite a fall in fat consumption (ENDS Report 308, pp 13-14 ).
Measurements of PAHs were also made in the stack gases of the sewage sludge and clinical waste incinerators. Surprisingly, this appears to have been rarely attempted and there are no verified methods. The results showed that naphthalene dominated emissions in both cases, and there were traces of many other PAHs.
The Government's Advisory Committee on the Carcinogenicity of Chemicals ranks PAHs according to the level of concern over carcinogenicity. Group A includes likely genotoxic carcinogens such as benzo(a)pyrene (BaP), benz(a)anthracene (BaA) and dibenz(ah)anthracene (DbahA). Group B compounds are also suspected carcinogens but the evidence is incomplete and the toxic mechanisms unclear.
All group A and B PAHs emitted by the sludge incinerator were below the limits of detection, but group B compounds were present in emissions from the clinical waste incinerator. In particular, the study found that four rarely measured group B PAHs contributed the majority of the substances of concern.
One of the authors, Colin Foan of the Environment Agency, explained: "This work starts to raise the question of which PAHs are important. BaP is often measured because it is associated with transport, but the chemistry of combustion processes is very different."
PAHs are a much more diverse group of compounds than PCBs or dioxins. Mr Foan commented that the widespread practice of measuring BaP as a surrogate for all PAHs might be flawed, and many more measurements were needed before PAH profiles of various sources could be established. He also believes that much more attention needs to be given to identifying the PAHs most harmful to health.
Most exposure to PAHs in the diet comes from vegetable oils, fish and cereals. Analysis of pooled food samples collected in 2000 shows that the average adult received a dose of 69ng per kilogram of bodyweight per day.
These results can be compared with a less comprehensive study in 1979. Although this did not produce a value for total PAH exposure, it did measure three of the most dangerous PAHs classified as genotoxic carcinogens: BaP, BaA and DBahA.
Dietary levels of BaP and BaA fell by 33% and 69%, respectively, between 1979 and 2000. Levels of DBahA increased by 67%, albeit from a low baseline.
Levels of these PAHs in milk, dairy produce and beverages appear to have increased - for some compounds by up to five times. However, the FSA points out that the 1979 data are "lower bound" estimates where results at the limit of detection were counted as zero. Totals from analyses across many food groups are therefore likely to be significantly lower than the 2000 data. In the latter, case the totals are "upper bound" estimates, where results at the detection limit are counted as being equal to the detection limit.