The environment affects children differently than adults. Because their bodies are still growing, children are at greater risk if they are exposed to environmental contaminants. A toddler playing in dirt contaminated with high levels of lead can become sick from lead poisoning. A child with asthma playing outside when the air quality is bad may have an asthma attack. Environmental hazards are not just outside, but can also be found inside a child’s home or school. Children living in older homes with lead-based paint can get sick from breathing lead dust or swallowing chipping paint. Drinking water from a private well and even a community water system is also a concern if it’s contaminated. Bacteria and other harmful chemicals can be a threat to anyone’s health, but especially to young children. Because they are small and still developing, they are more easily exposed to environmental contaminants and here’s why: Children breathe more air, drink more water, and eat more food per pound of body weight than adults. Children are more likely to put their hands in their mouth. A child’s body may not be able to break down and get rid of harmful contaminants that enter their body. Health problems from an environmental exposure can take years to develop. Because they are young, children have more time to develop health conditions and diseases than adults who are exposed later in their life. Prenatal and postnatal passive smoking have a wide range of effects on mortality and morbidity in children. Prenatal passive smoking has lifetime consequences since it influences placental and fetal development, reduces birth weight, and affects lung and brain development. A low birth weight is associated with an increase in the incidence of coronary heart disease, stroke, hypertension, type 2 diabetes mellitus, insulin resistance, serum lipids, and premature pubarche. Lung function tests in infants and older children born to smoking mothers show reduced airway patency, probably reflecting underdevelopment of lungs and airways. The reduced lung growth and the increased risk for respiratory infections due to passive smoking are possible explanations for the increased risk for SIDS. Furthermore, prenatal passive smoking is thought to be a risk factor for a variety of neurodevelopmental and behavioural problems, such as reduced general intellectual ability and attention deficit and hyperactivity disorder. Epidemiological studies show that maternal smoking during pregnancy and postnatal ETS exposure could cause subtle changes in children’s neurodevelopment and behaviour, such as reduced general intellectual ability and attention deficit and hyperactivity disorder (ADHD). However, studies to date are difficult to interpret because of the unknown influence of uncontrolled confounding factors. The precise impact of prenatal or postnatal exposure is not clear, however, there is consistent support for an aetiological role of prenatal smoking in the onset of antisocial behaviour. Moreover, there is a dose-response relation between maternal prenatal smoking and both criminal arrest and psychiatric hospitalisations for substance abuse in male and female offspring. Animal studies showed that the relation between nicotine and adverse developmental outcome is causal, and that prenatal nicotine exposure elicits abnormalities of cell proliferation and differentiation leading to shortfalls in the number of cells and altered synaptic activity. Possibly, these functional and structural adverse developments of the brain also occur in humans.