Bisphenol A is extensively used in the manufacturing of epoxy resins and polycarbonate plastics, whereas several brominated and chlorinated analogues are used as flame retardants and intermediates in the plastic industry. Due to the structural relationship between these chemicals and the high production volumes, we wanted to characterize and compare their potential oestrogen-like potency using several end-points in MCF-7 cells: induction of pS2 protein and progesterone receptor, reduction of oestrogen receptor level, and stimulation of cell growth. Bisphenol A, tetrachloro-and tetrabromobisphenol A, 4-hydroxybiphenyl and 4,4ø-dihydroxybiphenyl all showed oestrogen-like properties in MCF-7 cells. The chemicals tested had affinity to the oestrogen receptor isolated from MCF-7 cells, although their EC 50 s were 1,000 to 80,000 times higher than the EC 50 of 17b-oestradiol. Bisphenol A and 4-hydroxybiphenyl induced cell growth in MCF-7 cells, and the highest test concentrations induced responses, apparently exceeding the cell growth induced by 17b-oestradiol. The other chemicals tested induced less than 50% of the maximum 17b-oestradiol-stimulated cell growth. Bisphenol A, 4-hydroxybiphenyl, tetrabromobisphenol A and tetrachlorobisphenol A all increased the level of the oestrogen-regulated proteins, progesterone receptor and pS2, whereas 4,4ø-dihydroxybiphenyl showed no such effect. Bisphenol A was the only chemical tested that clearly mimicked 17b-oestradiol in its ability to reduce the level of cytosolic oestrogen receptors in MCF-7 cells. By measuring several oestrogen-dependent endpoints it seems that some xeno-oestrogens cause an imbalanced oestrogen-response. Their ability and potency in mimicking 17b-oestrogen in one parameter is not necessarily accompanied by a similar effect in another oestrogen-linked parameter.

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The presence of Volatile Organic Compounds (VOC) in indoor air has in past decades often been associated with adverse health effects such as sensory irritation, odour and the more complex set of symptoms called the Sick Building Syndrome (SBS). More recently, a possible link between the increase in the prevalence of allergies throughout the industrialized areas of the world and exposure to elevated concentrations of VOCs has been suggested. In many cases, the total VOC (TVOC) is used as a measure of the concentration of air pollution and, by extension, as a measure of the health risk in non‐industrial buildings. However, the TVOC concept has been questioned for a number of reasons, including the facts that it is an ambiguous concept, that individual VOCs making up the whole can be expected to give rise to different effects in people and that researchers have been using different definitions and interpretations of TVOC. This means that simple addition of the quantities of individual VOCs may not be relevant from a health point of view. Twelve researchers from the Nordic countries have reviewed the literature on VOC/TVOC and health. A search of the literature resulted in the identification of about 1100 articles, of which 120 were selected for further examination. A final review of the articles reduced their number to 67 that contained data on both exposure and health effects. The group concluded that indoor air pollution including VOC is most likely a cause of health effects and comfort problems in indoor environments in non‐industrial buildings. However, the scientific literature is inconclusive with respect to TVOC as a risk index for health and comfort effects in buildings. Consequently, there is at present an inadequate scientific basis on which to establish limit values/guidelines for TVOC, both for air concentrations, and for emissions from building materials. The group concluded that continued research is required to establish a risk index for health and comfort effects for VOC in non‐industrial buildings.

Phthalates are found in numerous consumer products, including interior materials like polyvinyl chloride (PVC). Several studies have identified phthalates in indoor air. A recent case-control study demonstrated associations between allergic symptoms in children and the concentration of phthalates in dust collected from their homes. Here we have analyzed the content of selected phthalates in particulate matter (PM): PM(10) and PM(2.5) filter samples collected in 14 different indoor environments. The results showed the presence of the phthalates di-n-butyl phthalate (DBP), butyl benzyl phthalate (BBP), dicyclohexyl phthalate (DCHP) and diethyl hexyl phthalate (DEHP) in the samples. The dominating phthalate in both PM(10) and PM(2.5) samples from all locations was DBP. More than a 10-fold variation in the mean concentration of total phthalates between sampling sites was observed. The highest levels of total phthalates were detected in one children's room, one kindergarten, in two primary schools, and in a computer room. The relative contribution of total phthalates in PM(10) and PM(2.5) was 1.1 +/- 0.3% for both size fractions. The contribution of total phthalates in PM(2.5) to total phthalates in PM(10) ranged from 23-81%, suggesting different sources. Of the phthalates that were analyzed in the PM material, DBP was found to be the major phthalate in rubber from car tyres. However, our analyses indicate that tyre wear was of minor importance for indoor levels of both DBP as well as total phthalates. Overall, these results support the notion that inhalation of indoor PM contributes to the total phthalate exposure.

Hepatocytes isolated from Aroclor 1254 (PCB) pretreated rats metabolized 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) to a reactive metabolite that induced DNA damage measured by alkaline elution or as increased unscheduled DNA synthesis. PhIP induced mutations in Salmonella typhimurium TA98 and DNA strand breaks and sister chromatid exchange(s) in Chinese hamster V79 cells co-incubated with PCB-hepatocytes. No, or only minor genotoxic, effects were observed when hepatocytes from non-induced rats were used. The bacterial mutagenicity could be inhibited by alpha-naphthoflavone, indicating a role of P-450 in the activation of PhIP. At least eight different metabolites could be separated on HPLC after PhIP had been incubated with PCB-hepatocytes. All of the directly acting mutagenicity towards S.typhimurium TA98 co-eluted with one of the metabolites. The identity of this metabolite was concluded to be 2-hydroxamino-PhIP based on the following evidence: (i) it reduced ferric ion to ferrous ion as hydroxylamines do, (ii) it had an identical UV spectrum and chromatographic properties as a species formed upon reduction of 2-nitro-PhIP by NADPH P-450 reductase. This product displayed a major peak at m/z 241 during thermospray mass spectrometry in the positive-ion mode as would be expected from 2-hydroxamino-PhIP. 2-Hydroxamino-PhIP was directly genotoxic both to TA98 and V79 cells. The genotoxic activity of the medium after removing the hepatocytes remained stable for several hours. Compared to 2-amino-3,4-dimethylimidazo[4,5-f]quinolone (MeIQ), PhIP caused a much larger increase in DNA damage in V79 cells (with hepatocyte activation), whereas MeIQ was more potent with respect to DNA damage induced in hepatocytes and bacteria.