pool and escrete it (Wynder & Reddy. Diy. Dis. 1974, 19, 937) and that changes limited to dietary cholcs- terol have a small effect on serum cholesterol (Key er trl. Mercrbolism 1965. 14, 759). They therefore suggest that the level of strum cholesterol may not be the most appropriate parameter ror future investigations or colon carcinogenesis; additional dietary studies ol cholesterol intake along with further analysis ol steroid mctabolitcs in the large bowel may be of more value.

Another look at the carcinogenicity of 2.4,5-T

Eriksson. M.. Hardell, L., Berg. N. 0.. MGller. T. & Axelson. 0. (19s I). Sort-tissue sarcomas and exposure to chemical substances: a case-rel’erent study. Br. J. id. 114 ed. 38, 17.

Phenosy acids are present in many of the hcrbi- tides used in agriculture. horticulture and l’orestry. A case-control study in northcrn Sweden suggested that exposure to phenoxy acids and chlorophcnols may be associated with a sis-cold increase in the risk of devel- oping sort-tissue sarcoma although the role played by impurities such as dioxin or dibcnzofuran could not be ascertained (Cirerl irr F.C.7: 19SO. 18. 541). The same group or workers has now conducted a rurther case-control study of sort-tissue sarcomas with the aim or confirming the earlier lindings and obtaining inrormation on the erects or din‘ercnt phenoxy acids. This study was carried out in southern Sweden where csposure to phenosy acid herbicides is likely to be through their agricultural use rather than through [orestry, as in the north.

Each of I IO cases (38 deceased) with sort-tissue sar- comas was compared with two carerully selected con- trols for exposure to phenosy acids other than 2.45trichlorophenosyacctic acid (2.4.5-T). to phe- nosy acids including 2.4.5-T and to chlorophenols. Esposure was assessed initially by a sell-completed questionnaire which was followed up by a telephone interview by a ‘blind‘ interviewer and contact with employers etc. if this was judged necessary. Individ- uals esposed to phenosy acids for a total of less than I day were considered to be unesposed. and separate analyses were perrormed [or individuals exposed to phenosy acids Tar more or less than 30 days. Risk

ratios rOr sort-tiss~~~ sarcomas calculated ror the various exposure groups were as rOli0~vs: phenosy acids or chlorophenols 4.7.; phenosy acids wept 1.4.5-T 4.2: phcnosy acids including 2.4,5-T 17.0 (> 30 days 8.5. <30 days 57); all esposures to phenosy acids 6,s; chlorophcnols 3.3. The authors conclude that their results indicate that esposure 10 phenosy acids and chlorophenols might constitute a risk ractor in the development or soft-tissue sarcomas and that this risk relates not only to 2.4,5-T which. like certain chlorophenols. may contain polychlorinatcd dibenzo- diosins and dibenzorurans but also to other phenosy acids such as 2,4-dichlorophenosyacetic acid. 4-chloro- 2-methvlohenoxvacetic acid and the analogous phe- noxypri&onic ;;cids which are less prone to contain such contaminants. They also conclude that individ- uals with IOW exposure to chlorophenols (defined as 21 masimum or one continuous week or rcpcated short-

term exposures amounting at the most to I month in all) are not subject to an increased risk of developing soft-tissue sarcomas. Smoking habits and exposure to organic solvents, asbestos, glass fibre, power saws and various pesticides did not appear to be associated with an increased risk of developing soft-tissue sar- comas.

[The results or this study are similar to those of the previous investigation (Cited irl F.C.7: 1980. 18, 541) which was criticized on a number of counts by the UK Advisory Committee on Pesticides (Furtlle, Reuieu, ofr/w Sufer.~~,/br Use irl rllr U.K. c~/‘ rhe Herbi- cidr Z,J,j-T; December 19SO; pp. 71). The methods used in the present study were very thorough in many respects and the authors have gone to considerable lengths to assess exposure to phcnosy acids and other compounds. They have also taken great care in select- ing the controls. However some ol” the Committee’s criticisms are probably also applicable to the present study. The accuracy with which workers (or their rela- tives or colleagues) can recall the type or duration or esposurc to chemicals is likely to be limited. and, OIICC again. the types or tumours observed covered a wide range.

In a recent review Coggon s( Acheson l?om the MRC Environmental Epidemiology Unit (Ltrrmt 1982. I, 1057) also point out the possibility or bias

resulting rrom ditl’erences in the recall of distant events. particularly between patients and healthy con- trols. They report. howcvcr, that one of the Swedish authors (Hardell. Sctr~ltl. J. H/d LWP~V. 1-1111~ I9S I 1 7, I 19) has compared the cases with soft-tissue sarcomas

with tl cwtrol group 0r patients with colonic cancer ancl obtained a similar (five-fold) increased risk ol soft-tissue sarcoma after exposure to phenosy acids and chlorophcnols. Coggon Sr Achcson (lot. cir.) con- clude that “there is suggcstivc evidence of a biological association bet\veen phenosy herbicides (or their con- taminants) and sort-tissw sarcomas”.]

Aluminium and impaired breeding in wild birds

Nyholm. N. E. I. (I9SO). Evidence or involvement or aluminium in causation or dcfcctive rormation of egg-

shells and of impaired breeding in wild passerine birds. Euuir. RPS. 26, 363.

Severe eggshell defects and reduced clutch sizes indicated a breeding impairment among birds nesting along the shores of two lakes in Swedish Lapland. Such impairment was not noticed in birds breeding further rrom the shores of these lakes nor in birds breeding along the shore of a lake in a similar en- vironment rurther north. Extensive analysis of various tissues indicated that neither biocides such as DDT nr -. polychlorinated biphenyls nor heavy metals such as cadmium. chromium, copper. lcad or mercury were likely to be causal rxtors.

The medullary tissue or humeri from nineteen remale pied Ilycatchcrs (Ficedulrr /~~~/w/euctr Pallas) were subjected to multi-element analysis. Spccimcns were obtained during the laying phase (when the birds were about to lay their second egg) or during the incubation period. Thirteen of the birds laid at least one egg with a derective shell and were classified as

974 Abstracts and comments-Fd C/~ern. Tosic. Vol. 10. no. 6

‘affected’. Four birds nesting far from any lake and two birds nesting along the shore of the northern lake showed no signs of impaired breeding and were classi- fied as ‘normal’. The affected birds suffered from incomplete filling of the bone marrow cavity during the laying phase and laid increasingly defective eggs. Small clutch sizes and a decreased number of devel- oping egg follicles demonstrated the lower laying ca- pacity of the affected birds. Two of the affected birds laid only one egg each, had no developing egg follicles and were found dead in their nests. The defective egg- shells were more porous and were made or coarser crystals than were the normal eggshells and they had incorporated blood cells which indicated that intra- uterine bleeding had occurred during eggshell forma- tion.

Under normal circumstances, calcium and phos- phorus (probably in the form of apatite) are the prin- cipal elements present in medullary tissue and these become depleted during the incubation period. In the affected birds. the levels of calcium and phosphorus were relatively low and varied widely throughout the tissue, suggesting abnormal deposition and/or mobil- ization of apatite. Aluminium was present in the med- ullary tissue of the humeri ol’ the affected birds but none was found in ‘normal’ birds. The aluminium levels were similar during the laying phase and incu- bation. suggesting that the aluminium was not subject to the calcium mobilization mechanism which oper- ates during the laying phase. It is possible that aluminium exerts a toxic effect by interfering with normal phosphate metabolism. perhaps as a result of interactions between aluminium and enzyme systems that require other metals. Such disruption of phos- phate metabolism could result in low bone-marrow levels of apatite. and thus decreased levels of calcium available for eggshell production. Low calcium avail- ability may also inhibit the development of ovarian follicles. Phosphate depletion could also occur by binding of orally ingested aluminium with dietary phosphate resulting in the excretion of unabsorbed aluminium phosphate.

Although neither the origin nor transport route of the aluminium found in the tissues of afected birds has been confirmed. the author suggests that acidic precipitation may leach out relatively high levels of aluminium from the gneiss. which is the prevalent bedrock in the area in which the affected birds were found. The area around the northern lake where im- paired breeding was not noted consists largely of cal- careous deposits which have a high buffering capacity and therefore a low risk ol aluminium leaching. The postulated route ol transfer of aluminium to the birds is by the consumption of the insects that swarm along the lake shores. However, although it was confirmed that such insects make up a significant proportion ol’ the birds’ diet, no attempt was made to assess the aluminium content of these insects.

Flare-op dermatitic reactions induced by ingested nickel

Christensen, 0. B., Lindstriim, C., LGfberg, H. & MGller, H. (1981). Micromorphology and specificity of

orally induced flare-up reactions in nickel-sensitive patients. Am derrn.-ww.. Srockh. 61, 505.

Nickel is said to be responsible for more instances or allergic dermatitis than all the other metals com- bined (Fischer. Corlrrrcl Derrn~~iris. 2nd Ed., p. 96. Lea & Febiger. Philadelphia. PA, 1973) and is one of the most common causes of contact dermatitis (Citc’rl in F.C.7: 1976. 14, 217). Activation of hand dermatitis in nickel-sensitive patients and flare-up reactions at earlier patch-test or contact-dermatitis sites following ingestion of nickel have been reported (Christensen & MGller. Corrt~tcr Dermritis 1975. 1. 136; Cronin et rrl. in Nick4 To.sico/o!/~. p. 149. Edited by S. S. Brown and F. W. Sunderman, Jr. Academic Press. London. 1974). The micromorphology and specificity of flare- up reactions induced by oral ingestion of nickel some 4-7 wk after patch testing have now been investi- gated.

Patch testing with nickel sulphate (Y,, in petrola- turn) was carried out on five adult women. all of whom had been hypersensitive to nickel l-or several years and were periodically affected by hand eczema. Patch testing with benzalkonium chloride (I”,, in water) and an intradermal test with tuberculin 2TU served as controls. These controls provided examples of substances known to induce toxic dermatitis and a delayed hypersensitivity reaction. respectively. The tests were read at 72 hr after application and the mar- gins of the inflammatory reactions carefully marked. When the reactions had virtually disappeared 4-7 wk later punch biopsies were removed from the benz- alkonium chloride and nickel test sites and from the palms of the hands and examined by light microscopy and direct immunofluorescence. The patients were examined closely for 24 hr following oral ingestion of 5.6 mg nickel (as nickel sulphate) and punch biopsies were then taken rrom the test sites and palms. Ecze- matous reactions at the nickel test sites with eryth- ema, infiltration. papules and/or vesicles were ob- served in all five patients IO-24 hr after oral provoca- tion. The areas of the reaction sites were 2-3 times greater than the original patch-test reactions. Flare- ups of hand eczema were evident in four patients and the fifth reported itching of the palms. Flare-ups also occurred at sites of earlier contact dermatitis. Three of the patients were certain that they had had no derma- titis in these areas for the previous 24 yr. No clinical or histopathological changes were elicited at the benz- alkonium chloride or tuberculin test sites following oral ingestion of nickel, indicating that the oral anti- gen had no effect on the inflammatory process per SC nor on any type IV reaction other than nickel allergy. The authors suspect that degrdnulation of the mast cells plays some part in the flare-up reactions but doubt that humoral antibodies play a pathogenic role since neither immunoglobulins of the IgG, IgA and IgM class, nor complement 3 nor fibrinogen could be detected at the test sites using the direct immuno- fluorescence technique.

[This paper highlights the ract that contact sensi- tizers are capable of eliciting reactions even when ad- ministered by routes other than dermal. It seems that tests in guinea-pigs do not reflect the situation in man. The authors of the present study cite a test (Pollk & Turk, Ch. esp. Imrmr~. 1968, 3, 253) in