Allows clinician to look at specific aspects of children's environmental health longitudinally throughot childhood. Children may serve as environmental health sentinels for our society, as they are becoming the first to manifest adverse response to environmental exposures.

ETS and other environmental exposures are used as examples of how a child's susceptibility to a toxicant varies at each developmental stage. Nicotines metabolite cotinine with a half life of days in serum has become the biological marker of choice of measuring ETS exposure.

Childrens and adults living in the same environment maty experience very different environment within that space. E.g. proximity to the floor and floor level,thus increasing chances of exposure.

Compared to adults children in postnatal development stages have higher consumption of air,water and food per kilogram body weight Hence have a higher rate of exposure at each stage of development-newborn,infancy,childhood and adolescence.

Foetal harm can result from prior parental exposure to toxicants either directly affecting the maternal or paternal reproductive organs or getting stored in the body and later mobuilised during pregnancy.

Congenital lead poisoning has been diagnosed in infants born to women who were themselves lead-poisoned as children Poly chlorinated biphenyls(PCB) have a long half life, stored in fat,consequently accumulate in the food chain-proved animal foetal toxicity

Placenta does not block some compounds from reaching the foetus for e.g.carbon monoxide,ethanol,lead etc. Eg.Association between maternal use of DI-ETHYL STILBESTROL(DES) and eventual development of vaginal adeno carcinoma in offspring exposed in utero

In japan,maternal exposure to Mercury through eating fish contaminated with mercury lead to large number of children with cerebral palsy, mental retardation, diffused brain atrophy and visual defects

Epidimiological studies of pregnancies complicated by both active & passive maternal smoking have shown increased rate of spontaneous abortion,intrauterine growth retardation, cleft lip & palate, and poor cognitive &beh. Development.

The neonatal stage is characterised by highly permeable gastrointestinal tract and skin and hence higher chances of exposure to toxins. dermal exposure-recent example of percutaneous poisoning is that of hexachlorophene induced neurotoxicity in babies.

Toxic substancestransported to the home environment on clothes can affect newborn e.g. documented case report of lead poisoning Environmental Tobacco Smoke-babies exposed to ETS have been shown to have smaller lung volumes,general developmental delay and reduction in somatic growth.

Oral exposure: biting toys leading to lead poisoning. acceptable levels of food additives for adults may be grossly in error for an infant Less variety in food increase chance of consuming one particular possibly contaminated food item e.g.milk.

There is chance of exposure to pesticides through commonly used fruits and vegetables inhaled exposures: infants and toddlers inhale more air per kilogram than adults resulting in higher exposure rates.

Crawling or walking on floor increases risk of exposure e.g. formaldehyde from new synthetic carpeting. contaminants that tend to be found in higher concentration near the floor include mercury vapour from old formulations of latex paints & radon, found in highest concentrations in the lowest elevations of the house.

Radon is a natural by product of uranium decay, by itself is harmless but its progeny attach to particulates in the air and are taken into the lung,exposing the bronchial stem cells to radiation, with an increased risk of lung cancer after a latency period of many years.

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