Indicators of human health in ecosystems: what do we measure?

Increasingly, scientists are being called upon to assist in the development of indicators for monitoring ecosystem health. For human health indicators, they may draw on environmental exposure, human morbidity/mortality or well-being and sustainability approaches. To improve the rigour of indicators, we propose six scientific criteria for indicator selection: (1) data availability, suitability and representativeness (of populations), (2) indicator validity (face, construct, predictive and convergent) and reliability; (3) indicator responsiveness to change; (4) indicator desegregation capability (across personal and community characteristics); (5) indicator comparability (across populations and jurisdictions); and (6) indicator representativeness (across important dimensions of concern). We comment on our current capacity to adhere to such criteria with examples of measures of environmental exposure, human health and sustainability. We recognize the considerable work still required on documenting environment-human health relationships and on monitoring potential indicators in similar ways over time. Yet we argue that such work is essential in order for science to inform policy decisions which affect the health of ecosystems and human health.

Fish consumption by Vietnamese women immigrants: a comparison of methods.

In this study, the measurement properties of an interview-administered fish consumption frequency questionnaire, used with a pilot study of 20 Vietnamese immigrant women, were described. Reproducibility across two summer interviews and one winter interview for estimates of seasonal and yearly intake of Great Lakes fish was moderate (intraclass correlation coefficients: .51-.61). Detailed questioning, by species, resulted in higher estimates of mean overall consumption (44.6-57.8 meals/y) than did asking about any fresh-water fish consumed (33.5-46.1; differences 5.1-15.7). Estimates based on the fish consumption frequency questionnaire (i.e., 6.2+/-2.0 meals per winter season) were comparable with those based on extrapolation from a 1-mo calendar (5.8+/-5.6); however, both estimates of consumption were far less than a weighed record (29.1+/-22.2). The results of this study suggest that measurement variation in fish consumption estimates should be detailed in research reports and should be discussed with respect to risk assessments.

Purification of carboxypeptidase B by zinc chelate chromatography.

A method is described to purify pancreatic carboxypeptidases B (CPB), removing contaminating endoproteinases that interfere with use of CPB for carboxy-terminal analysis or modification of proteins. The separation uses zinc chelate chromatography and is based on the property that CPB has higher affinity for immobilized zinc ions than do serine proteinases such as trypsin and chymotrypsin, which are abundant endoproteolytic activities in pancreas. CPB preparations are loaded onto a column of iminodiacetic acid-Sepharose that has been saturated with ZnCl2. A step gradient with buffers of decreasing pH is used to elute bound proteins. CPB elutes at a lower pH than do the serine proteinases.

Alpha 2-antiplasmin's carboxy-terminal lysine residue is a major site of interaction with plasmin.

alpha 2-Antiplasmin (AP) inhibits plasmin in a two-step reaction in which AP reversibly binds to lysine-binding sites of plasmin and, then, more slowly complexes covalently with the enzyme's active site. Here, we show that the C-terminal lysine residue of AP has a key role in binding of the inhibitor to plasmin. A synthetic peptide corresponding to the C-terminal 26 amino acid residues of AP blocked association of AP with plasmin, but this activity of the peptide was lost when its C-terminal lysine residue was removed with carboxypeptidase B. The essential role of this lysine residue was shown more directly by treating AP with carboxypeptidase B and observing that AP lost its ability to inhibit plasmin rapidly.

Mg2+ reduces N-methyl-D-aspartate neurotoxicity in embryonic chick neural retina in vitro.

N-Methyl-D-aspartate (NMDA) is a potent neurotoxin that affects cells in the inner layers of the embryonic chick retina exposed in vitro. After exposure of the embryonic day 12 neural retina to 0.5-10.0 mM NMDA for 30 min, 50-80% of the cells in the inner region of the inner nuclear layer and 50-100% of the cells in the ganglion cell layer were hypochromatic. When retinas were incubated with Mg2+ (0.5-10.0 mM) for 15 min and then incubated with Mg2+ and NMDA (0.5 mM) for 30 min, the NMDA effect in the inner layers was dramatically reduced but not abolished. Removal of Mg2+ before NMDA exposure produced retinas as seriously affected as retinas not exposed to Mg2+. Studying the effects of NMDA inhibitors, such as Mg2+, may help elucidate the mechanism of the cytotoxic events that occur in the retina in response to certain excitatory acidic amino acids.

Quinolinate. A selective neurotoxin in embryonic and posthatching chicken retinas.

Quinolinate (QUIN), an endogenous dicarboxylic amino acid, structurally related to the putative retinal neurotransmitter aspartate, acts as a specific neurotoxin in the chick neural retina. Qualitative analysis of QUIN's neurotoxic effects reveals that sensitivity to the amino acid is first detected in the 9-day-old embryonic chick retina. Nuclei and cytoplasm of some cells in the inner region of the inner nuclear layer and in the ganglion cell layer appear hypochromatic or electron lucent when examined by light or electron microscopy, respectively. Between day 10 and 12, the sensitivity of the embryonic retina to QUIN increases and remains around the day 12 level throughout the remaining embryonic and initial posthatching period. Cells in the inner half of the inner nuclear layer continue to be the most severely affected throughout retinal development, ganglion cells less so. Photoreceptor and most cells in the outer region of the inner nuclear layer remain undamaged. QUIN effects are partially reversible: retinas exposed to QUIN briefly in vitro and then transferred to fresh QUIN-free medium are not as severely affected as those allowed no recovery time. In day 1 posthatching chick retinas, similar patterns of QUIN-toxicity were observed in vitro (0.5-5 mM QUIN; 5-30 min) and in vivo (200-600 micrograms QUIN/eye; 0.5-24 hr following intravitreal injection).

Airborne contact urticaria due to sodium benzoate in a pharmaceutical manufacturing plant.

Three workers exposed to airborne contact with sodium benzoate (SB) in a pharmaceutical plant developed transient urticaria related to skin contamination with SB. Patch test responses to SB and benzoic acid (BA), without occlusion, were similar to those of three previously unexposed controls in keeping with the nonimmunologic nature of the reaction. Sweating, which lowers skin pH and increases topical BA concentration, appeared to increase the susceptibility to urticaria in two of the three workers. Ventilation and hygiene control methods designed to reduce SB skin contamination eliminated the problem in the workplace.

In vitro effects of kainate on embryonic and posthatching chick retina.

The onset and developmental pattern of kainate effects were determined in isolated embryonic and posthatching chick neural retinas exposed to KA (0.01-0.24 mM; 1-30 min) in vitro. Damage was first apparent in day 8 embryonic retinas; cells in the inner region of the inner nuclear layer and neuronal processes in the inner plexiform layer were affected. In older embryonic retinas, cells in the inner region of the inner nuclear layer continued to be the most damaged although cells in the ganglion cell layer and the outer region of the inner nuclear layer, and neurites in the outer plexiform layer were also affected. Cells in the outer nuclear layer stained normally in both embryonic and posthatching retinas. Partial reversibility of kainate effects was observed in retinas which had been exposed briefly to kainate and then allowed to recover in kainate-free medium. The results of our in vitro experiments are consistent with those reported for a variety of neonatal and adult retinas treated with kainate in vivo.

Precocious retinal adhesion in the embryonic chick.

In the normal chick embryo the neural retina adheres firmly and irreversibly to the underlying retinal pigment epithelium (RPE) starting on day 17--18 of development, coincident with maturation of photoreceptor outer segments. Retinas from earlier embryos (days 13--16) became prematurely attached to the RPE within 30 minutes after death, if held at 37 degrees C, even though developed outer segments were not yet present. Lower temperatures, or failure to enucleate the eye, retarded but did not prevent this postmortem, precocious adhesion. The biochemical factors involved in this process were explored by altering the incubation medium; the factors appear different from those that help maintain retinal adhesion in the adult mammalian eye.