Health Consequences of Environmental Exposures: Changing Global Patterns of Exposure and Disease.

Environmental pollution is a major cause of disease and death. Exposures in early life are especially dangerous. Patterns of exposure vary greatly across countries. In low-income and lower middle income countries (LMICs), infectious, maternal, neonatal, and nutritional diseases are still major contributors to disease burden. By contrast, in upper middle income and high-income countries noncommunicable diseases predominate. To examine patterns of environmental exposure and disease and to relate these patterns to levels of income and development, we obtained publically available data in 12 countries at different levels of development through a global network of World Health Organization Collaborating Centres in Children's Environmental Health. Pollution exposures in early life contribute to both patterns. Chemical and pesticide pollution are increasing, especially in LMICs. Hazardous wastes, including electronic waste, are accumulating. Pollution-related chronic diseases are becoming epidemic. Future Global Burden of Disease estimates must pay increased attention to the short- and long-term consequences of environmental pollution.

Children's Environmental Health Indicators in Australia.

BACKGROUND: Adverse environmental exposures in early life increase the risk of chronic disease but do not attract the attention nor receive the public health priority warranted. A safe and healthy environment is essential for children's health and development, yet absent in many countries. A framework that aids in understanding the link between environmental exposures and adverse health outcomes are environmental health indicators-numerical estimates of hazards and outcomes that can be applied at a population level. The World Health Organization (WHO) has developed a set of children's environmental health indicators (CEHI) for physical injuries, insect-borne disease, diarrheal diseases, perinatal diseases, and respiratory diseases; however, uptake of steps necessary to apply these indicators across the WHO regions has been incomplete. A first indication of such uptake is the management of data required to measure CEHI. OBJECTIVES: The present study was undertaken to determine whether Australia has accurate up-to-date, publicly available, and readily accessible data on each CEHI for indigenous and nonindigenous Australian children. FINDINGS: Data were not readily accessible for many of the exposure indicators, and much of the available data were not child specific or were only available for Australia's indigenous population. Readily accessible data were available for all but one of the outcome indicators and generally for both indigenous and nonindigenous children. Although Australia regularly collects data on key national indicators of child health, development, and well-being in several domains mostly thought to be of more relevance to Australians and Australian policy makers, these differ substantially from the WHO CEHI. CONCLUSIONS: The present study suggests that the majority of these WHO exposure and outcome indicators are relevant and important for monitoring Australian children's environmental health and establishing public health interventions at a local and national level and collection of appropriate data would inform public health policy in Australia.

Children's environmental health indicators in Australia: are we collecting the right information?

In order to assess progress in improving children's health objectively standardized measurements are required. The World Health Organization (WHO) undertook a pilot project to develop and implement a series of children's environmental health indicators (CEHI) to facilitate this process. No countries in Oceania were included in this pilot. This project was undertaken to determine whether data collected and publicly available in Australia were sufficient to address the CEHI. Government documents and websites were searched to obtain publicly available data. These data adequately reflected outcome indicators but data addressing many exposure indicators were either missing or not available in a child-specific format. Australia does collect data on child health and well-being but not in a form compatible with the WHO CEHI.

Special vulnerability of children to environmental exposures.

Fetal life and childhood are the periods most vulnerable to the harmful effects of exposure to environmental insults. This is because, during these periods, there is rapid cell division,organs are being formed, and growth is rapid. Thus, disruption of these processes may result in life-long abnormalities.Of particular concern are exposures that alter cognitive function and behavior, but exposures that alter growth, development,and reproductive and immune system function and that may increase risk of development of diseases like cancer later in life are also especially important. Exposure to environmental chemicals as well as infectious agents occurs via air, food,water, and absorption through the skin. Therefore, the environment in which fetal and childhood development occurs is very important. Unfortunately, poverty is a major risk factor for both exposures and childhood and later-life disease resulting from exposures to both environmental chemicals and infectious agents. It is very important to protect children because they are the future generation.

Syrian Hamster Embryo (SHE) cell transformation assay with and without X-ray irradiation of feeder cells using Di(2-ethylhexyl)phthalate (DEHP) and N-nitroso-N-methylnitroguanidine (MNNG).

The SHE cell transformation assay has traditionally been conducted with a feeder layer of X-ray irradiated cells to provide growth support to the target cells seeded in low numbers. The need for an X-ray irradiated feeder cell layer necessitates the maintenance of an X-ray machine and the additional step to seed feeder cells prior to plating target cells. This laboratory has previously reported a method allowing target cells to be seeded in conditioned media prepared from the stock culture flasks in lieu of plating them on a feeder layer (Pant et al. [1,2,4]). In order to expand the data base for chemicals tested using this method, we describe in this paper the results obtained testing Di(2-ethylhexyl)phthalate (DEHP) and N-nitroso-N-methylnitroguanidine (MNNG) which are known to give positive responses in the standard SHE cell transformation assay. With freshly prepared conditioned medium (used within 2 weeks of preparation), there was essentially no difference in the number of target cell colonies in the conditioned medium and in the plates with the X-ray irradiated feeder cell layer. The plating efficiencies of the vehicle controls were within the historical range for the standard SHE cell transformation assay. In more than ten experiments the positive control benzo(a)pyrene [B(a)P] elicited a significant increase in morphological transformation frequency (MTF), with or without X-ray irradiated feeder cells. Compounds, DEHP and MNNG, were tested in the SHE cell transformation assay with and without an X-ray irradiated feeder layer and using a 7-day exposure regimen. The results were comparable between experiments performed using either method. These results demonstrate the feasibility of conducting the SHE cell transformation assay without the use of an X-ray irradiated feeder layer, thereby simplifying the test procedure and assisting the scoring of morphologically transformed colonies.

Piloting a web-based continuing professional development program for asthma education.

PURPOSE: Continuing professional development is an integral component of modern medical practice, yet traditional educational methods are impractical for many Primary Care Physicians. Web-based programs may fulfill the requirements of busy practitioners who have difficulty attending formal education sessions. METHODS: We piloted the use of a learning management system to deliver asthma education materials to Primary Care Physicians in both Australia and Italy in their native languages. Each group of Physicians accessed an education module which contained content pages, self-tests, a quiz and a survey. Details of how the Physicians used the system, their preferences and performance on the assessment were monitored. RESULTS: The learning management system was well received by both Italian and Australian Physicians. Thirty-eight (18 Australian, 20 Italian) Physicians used the system. Participants visited an average of 8.8 pages, with a mean time per hit of 2.9 min. Formative assessment was undertaken by 63.2% and summative assessment by 68.4% of participants. There were no substantial differences in performance between Physicians from both countries. Italian physicians tended to use the system after hours whereas Australian Physicians appear to do so between patient visits. CONCLUSIONS: Simple web-based systems are suitable for delivering educational materials to Primary Care Physicians in a manner likely to be used.

The olfactory detection of sodium and lithium salts by sodium deficient cattle.

With development of Na+ depletion in cattle enhancement in the specific ability to smell very low concentrations of salt occurs. At the same time a behaviour pattern develops, in which increased locomotory activity is seen, directed towards searching for sodium salts. Following the initial successful location of a sodium source the pattern once learned, is consolidated by repetition and by consummation of the salt reward. Our data shows that olfactory and gustatory receptors are able to detect minute amounts of sodium salts as biochemical disruption develops with Na+ depletion but the central input from smell and taste receptors remain distinct. Salt appetite does not appear to be pleasurable (hedonic) in cattle, for salt appetite which is a feature of Na+ depletion does not persist when the ionic deficit is restored. The innate behaviour which develops with increased salt appetite in cattle may account for the evolutionary success and worldwide distribution of ruminants.

The effect on salt appetite and the renin-aldosterone system on replacing the depleted ions to sodium-deficient cattle.

1. Sodium depletion which occurred in cattle following exteriorization of a parotid duct produced depression of both plasma and salivary sodium, acidosis, elevated plasma aldosterone and renin activity. Increased sodium appetite, characteristic of sodium depletion, was assessed by operant behaviour where scoring of panel pressing for NaHCO(3) rewards showed change in sodium appetite.2. Sodium-depleted calves readily drank the calculated ionic deficit as a hypertonic solution (4 l.) in a few minutes, or as an isotonic solution (16 l.) usually within 30 min.3. When the ionic deficit was restored by either i.v. infusion or drinking, sodium appetite was reduced significantly. The suppression of sodium appetite was more rapid when the depleted ions were replaced by drinking (30 min) than by i.v. infusion (2 hr) but in both circumstances the effect was short lived since sodium appetite redeveloped within 3 hr.4. The rapid return of sodium appetite following restoration of the ionic deficit occurred even when the plasma sodium level was normal. Other biochemical changes resulting from sodium depletion, such as acidosis and reduced salivary sodium, could not be correlated with variation in sodium appetite.5. Rapid infusion of Ringer saline (4 l.) did not inhibit the sodium appetite, which suggests that neither vascular volume changes per se nor vascular baroreceptors control sodium appetite in sodium-deficient calves.Plasma aldosterone fell rapidly following infusion of the hypertonic solution but only slightly with the isotonic infusion. The change in plasma hormone level was not related to changes in sodium appetite.6. Drinking the hypertonic solution produced a marked reduction in panel pressing for NaHCO(3) with a rapid rise in plasma sodium. Consumption of the larger volume of isotonic solution also inhibited sodium intake but plasma sodium remained low. A secondary increase in plasma renin activity (p.r.a.) occurred following ingestion of the hypertonic solution, but both p.r.a. and aldosterone fell to normal levels over the next 6 hr when the cattle again showed marked sodium appetite. It is possible that these effects may be due to ion and fluid movement between gut and extracellular fluid and reflect osmolality changes or tissue dehydration.7. It is concluded that the sodium appetite of sodium deficient cattle is only temporarily alleviated by restoration of the depleted ionic loss, and that the behavioural response to seek sodium rewards is independent of plasma sodium, p.r.a., aldosterone and volume changes in the gut and vascular system.8. Recent reports suggest that sodium appetite may be controlled by receptors in the hypothalamus or by angiotensin II in the brain. In cattle the capacious gut may also be involved, since sodium appetite is inhibited more rapidly when the depleted ions are taken orally than by i.v. infusion.

A study of olfaction and gustatory senses in sheep after olfactory bulbectomy.

The importance of taste and smell in discrimination of sodium salts was examined in normal and anosmic sheep. To test for anosmia, faeces of pig, calf and sheep were used as noxious odours. Intact sheep, and sheep with one olfactory bulb removed avoided the aversive stimulus whereas following total bulbectomy, the faecal odour was no longer a deterrent. Olfactory bulbectomy did not affect food intake but changes in fluid intake, urinary loss and electrolyte excretion were apparent. In two-choice preference tests, normal sheep showed a marked aversion for 0.48 M NaHCO3 and 0.51 M NaCl when compared to water. Following either unilateral or bilateral olfactory bulbectomy the aversion for sodium salts persisted but was less extreme. This suggests that in the final discrimination of sodium salts the sense of taste is dominant but olfaction or the olfactory bulb may have a minor role.

The metabolic effects of sodium depletion in calves on salt appetite assessed by operant methods.

1. Sodium deficiency was induced in calves by unilateral exteriorization of the parotid duct, the continual loss of alkaline saliva from the body to the environment causing negative sodium balance. 2. The metabolic effect of negative sodium balance was seen in statistically significant reduction in plasma sodium and blood bicarbonate, together with marked acidosis and reduced plasma osmolality. 3. The homoeostatic response to sodium depletion was associated with a reversal of sodium/potassium ratio in parotid saliva and a reduction of the rate of secretion. Appetite diminished. The extracellular fluid was halved as marked diuresis developed with considerable weight loss. Urinary and faecal sodium was reduced to zero. 4. On restoration of sodium balance by allowing the calves to drink sodium bicarbonate solutions the metabolic deviations were eliminated. 5. During sodium depletion the parotid gland was able to respond to transient reflex stimulation by increasing flow rate and the sodium concentration of the saliva. 6. When sodium depleted, the calves became restless and agitated and would run from the home pen to the operant procedure stand. The sodium depleted animals readily pressed a panel for sodium bicarbonate rewards in direct proportion to the degree of sodium imbalance. When the balance was restored the motivation to work for sodium bicarbonate disappeared. 7. The motivation which developed during sodium depletion was directed specifically towards the sodium ion. Lithium was an exception to this rule and sodium carbonate was aversive. 8. It is possible that in sodium depletion the glottal sodium taste receptors develop an enhanced threshold for sodium ions because of the reduced sodium content of the saliva. This effect would be abolished when the content of sodium was restored in saliva. 9. The correlation of operant reactions and sodium depletion suggests that the consequential metabolic effects activate changes in the central nervous system. 10. The metabolic changes which develop in parallel with the severity of the sodium deficit appear to be able to evoke behavioural changes with increase in salt appetite directed towards restoration of sodium balance.