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This chapter describes the application of specific principles to the practice of surveillance of noninfectious diseases and events, specifically chronic diseases, injuries, and birth defects. It outlines the importance and contribution of public health surveillance to the prevention and control of non-communicable health outcomes. It reviews the need for accurate and timely data in order to design and implement prevention programs, the need for baseline measures for risk factors and disease prevalence in order to monitor progress toward health goals and objectives, and the ultimate goal of better guiding planning, policy creation, and decision making. It describes specific surveillance programs in each area, outlining innovative methods and uses of data, special challenges, and opportunities for improvement.

This chapter discusses nutritional aspects of birth defects, including physical, biochemical, and other abnormalities; nutritional factors (specifically of neural tube defects); and nutritional management, such as use of folic acid, vitamin A, and vitamin A analogs.

Today, alcohol is recognized as one of the leading preventable causes of birth defects and developmental disorders. It is now established that there are a range of effects on the developing foetus and that the severity of these effects are the result of timing and amount of alcohol exposure, as well as genetic vulnerabilities, environmental factors such as nutrition, and epigenetic changes. This chapter discusses foetal alcohol spectrum disorders (FASD); alcohol-related birth defects and alcohol-related neurodevelopmental disorders; intervention strategies for FASD; incidence and prevalence of foetal alcohol syndrome and FASD; and maternal risk factors for FASD and the need for effective prevention strategies.

Binary data is often an important type of data. The description of twin pairs presents an extensive example. Also introduced are the statistical consequences of random pairs illustrated by the analysis of the occurrence of twins with birth defects.

This chapter describes reproductive disorders and developmental disorders, with a focus on their recognition and prevention. Certain hazardous exposures at sufficient doses during preconception among men and women have been shown to increase the risk for infertility, miscarriage (spontaneous abortion) and birth defects. Women’s exposures during pregnancy can cause fetal death, congenital anomalies, and neurodevelopmental disorders. Fathers’ occupational exposures can secondarily expose pregnant women through contamination of the home environment. Numerous chemical pollutants readily cross the placenta and are transmitted into breast milk. Prenatal and perinatal exposures have been linked to abnormal development of the immune system, childhood cancer, and learning disabilities. Specific examples, such as lead and dibromochloropropane, are provided in the chapter to illustrate general concepts. A final section addresses evaluation and control of risk.

In 1996, when I was working with Channi as a psychiatry trainee, we were both struck by how often we were seeing women with psychotic disorders in the outpatient clinic who were seeking advice on whether or not they should try to conceive and have a family. Although there was a small amount of literature on the parenting difficulties some of these women would experience, there was a very limited evidence base on their risk of adverse obstetric outcomes. We felt we needed to know more about the outcome of pregnancy for women with pre-existing psychotic disorders, and this led to my PhD, funded by a Wellcome Trust Clinical Training Fellowship, with Channi as my primary supervisor. Channi became too ill to continue working on this project, but our work together led to my perinatal mental health research programme, for which I will always be in his debt. This chapter describes this early PhD research, and the research it has led on to, over the subsequent years. We initially thought about collecting detailed clinical outcome data from the women we were seeing locally, who came from a large catchment area. However, to obtain a large enough sample size would take many years and it became clear we needed large epidemiological datasets in order to optimize statistical power and minimize bias. We therefore started to look for such data, with the first dataset available coming from colleagues at the Institute of Psychiatry—the PriSM psychosis study (Thornicroft et al. 1998). The PRiSM psychosis study research team conducted the complete ascertainment of all prevalent cases of psychosis in the two study catchment areas in the index year (1991–1992) providing us with a representative population of mothers with psychotic disorders. We found that 63% of women with psychotic disorders (n = 155) were mothers, and that these women were more likely to be older and live in unsupported accommodation than women who had not had children, although they had similar levels of disability and health and social care needs (Howard et al. 2001).

This chapter describes the methodological issues involved in outbreak detection and gives examples from a range of statistical techniques. It focuses on infectious disease detection because most outbreak detection systems have been applied to infectious disease. However, the methods described apply more generally, and examples are drawn from related areas, such as monitoring birth defects.

This chapter begins with a clinical description of “spina bifida.” Literally, spina bifida means a split or divided spine. It is a birth defect that occurs within the first month of pregnancy, when the embryo is about the length of a grain of rice. The cause of spina bifida is not known with certainty, but it is likely that folic acid deficiency during the crucial early weeks of pregnancy sometimes contributes to the problem. The defect in the spine may occur anywhere along the spinal column but is usually found in the midback (thoracic), in the lower back (lumbar), or at the base of the spine (sacral). Spina bifida may be open or closed. Closed spina bifida, or “spina bifida occulta,” is a fairly common condition, in which the bones of the spine may be incomplete but the defect is covered by skin and the spinal cord is usually normal.

Children are exquisitely vulnerable to health threats in the environment. The World Health Organization estimates that 36% of all deaths in children worldwide are caused by harmful environmental exposures. Environmental exposures are major causes of non-communicable diseases in children—asthma, birth defects, preterm birth, neurodevlopemental disorders, cancer, obesity, and diabetes. This chapter reviews the historical origins of children’s environmental health, which is the branch of pediatric medicine and public health that studies the influence of the environment on children’s health, development, and risk of disease. It describes the evolution of research in this growing field. It describes the global spread of environmental hazards, especially toxic chemicals and pesticides to rapidly industrializing low- and middle-income countries where these materials have resulted in major episodes of disease and death in children. The chapter concludes with a discussion of strategies for prevention of environmental disease in children.

Developmental toxicity studies investigate birth defects caused by toxic chemicals. This chapter develops a Bayesian nonparametric modelling approach for risk assessment in developmental toxicity studies. The model is built from a mixture with a product Binomial kernel, to capture the nested structure of the responses, and a dependent Dirichlet process (DDP) prior for the dose-dependent mixing distributions. The resulting nonparametric DDP mixture model provides rich inference for the response distributions as well as for the dose-response curves. Data from a toxicity experiment involving a plasticizing agent were used to illustrate the scientifically relevant features of the DDP mixture model with regard to estimation of different dose-response relationships for different endpoints, including non-monotonic dose-response curves.

As the seasons turned and a new year passed, Love Canal remained a whirlwind of remediation activity. “A plan is being set in motion now to implement technical procedures designed to meet the seemingly impossible job of detoxifying the Canal area,” EPA administrator Eckardt C. Beck declared in January 1979. Though a cold Western New York winter had set in, Beck explained that everything remained on track. “The plan calls for a trench system to drain chemicals from the Canal. It is a difficult procedure, and we are keeping our fingers crossed that it will yield some degree of success.” Beck reiterated that securing Love Canal’s poisons, rather than evacuating all area residents, remained the key to the neighborhood’s future. While conceding that no “one has paid more dearly already than the residents,” Beck commented that the Love Canal “tragedy” was well on its way to a successful resolution. Beck was wrong. In February, New York declared homes beyond the inner ring potential health hazards to pregnant women and children under age 2. Health officials recommended temporary evacuation but no more home buyouts. While roughly two dozen families exited, remaining residents exploded. If the broader neighborhood was deemed unsafe, they clamored, then everyone should be evacuated. The LCHA, several of whose members had been arrested in December for blocking remediation vehicles, intensified its protests but to no avail. Most Love Canal residents remained in a toxic environment. As one person put it dimly, the neighborhood itself had become a chemical “prison.” A local punk band called the Vores captured the area’s dark mood. “Contaminated. We’re all contaminated. Don’t get near us, or you’ll turn blue,” the band growled in a tune entitled simply “The Love Canal.” “Contaminated. We’re all contaminated. Don’t let us move in or you’ll get it too.” The troubling tenor of the times notwithstanding, Love Canal residents refused to give up.